drug_id,text,molecular_weight,tpsa,clogp,group,state,has_text
14012,"Copper is a transition metal and a trace element in the body. It is important to the function of many enzymes including cytochrome c oxidase, monoamine oxidase and superoxide dismutase. Copper is commonly used in contraceptive intrauterine devices (IUD). For use in the supplementation of total parenteral nutrition and in contraception with intrauterine devices. Copper is incorporated into many enzymes throughout the body as an essential part of their function. Copper ions are known to reduce fertility when released from copper-containing IUDs. Copper is absorbed from the gut via high affinity copper uptake protein and likely through low affinity copper uptake protein and natural resistance-associated macrophage protein-2. It is believed that copper is reduced to the Cu1+ form prior to transport. Once inside the enterocyte, it is bound to copper transport protein ATOX1 which shuttles the ion to copper transporting ATPase-1 on the golgi membrane which take up copper into the golgi apparatus. Once copper has been secreted by enterocytes into the systemic circulation it remain largely bound by ceruloplasmin (65-90%), albumin (18%), and alpha 2-macroglobulin (12%). ",,,,Copper is approved and investigational.,Copper is a solid.,True
14013,"Oxygen is an element displayed by the symbol O, and atomic number 8. It is an essential element for human survival. Decreased oxygen levels may be treated with medical oxygen therapy. Treatment with oxygen serves to increase blood oxygen levels and also exerts a secondary effect of decreasing blood flow resistance in the diseased lung, leading to decreased cardiovascular workload in an attempt to oxygenate the lungs. Oxygen therapy is used to treat emphysema, pneumonia, some heart disorders (congestive heart failure), some disorders that cause increased pulmonary artery pressure, and any disease that impairs the body's ability to take up and use gaseous oxygen. Higher level of oxygen than ambient air (hyperoxia) can be introduced under normobaric or hyperbaric conditions. Oxygen therapy in clinical settings is used across diverse specialties, including various types of anoxia, hypoxia or dyspnea and any other disease states and conditions that reduce the efficiency of gas exchange and oxygen consumption such as respiratory illnesses, trauma, poisonings and drug overdoses. Oxygen therapy tries to achieve hyperoxia to reduce the extent of hypoxia-induced tissue damage and malfunction.  Oxygen therapy improves effective cellular oxygenation, even at a low rate of tissue perfusion. Oxygen molecules adjust hypoxic ventilatory drive by acting on chemoreceptors on carotid bodies that sequentially relay sensory information to the higher processing centers in brainstem. It also attenuates hypoxia-induced mitochondrial depolarization that generates reactive oxygen species and/or apoptosis. Oxygen therapy increases the arterial pressure of oxygen and is effective in improving gas exchange and oxygen delivery to tissues, provided that there are functional alveolar units. Oxygen plays a critical role as an electron acceptor during oxidative phosphorylation in the electron transport chain through activation of cytochrome c oxidase (terminal enzyme of the electron transport chain). This process achieves successful aerobic respiration in organisms to generate ATP molecules as an energy source in many tissues. Oxygen supplementation acts to restore normal cellular activity at the mitochondrial level and reduce metabolic acidosis. There is also evidence that oxygen may interact with O2-sensitive voltage-gated potassium channels in glomus cells and cause hyperpolarization of mitochondrial membrane. ",The molecular weight is 32.0.,Oxygen has a topological polar surface area of 34.14.,,Oxygen is approved and vet_approved.,Oxygen is a gas.,True
14014,"Flunisolide (marketed as AeroBid, Nasalide, Nasarel) is a corticosteroid with anti-inflammatory actions. It is often prescribed as treatment for allergic rhinitis and its principle mechanism of action involves activation of glucocorticoid receptors. For the maintenance treatment of asthma as a prophylactic therapy. Flunisolide is a synthetic corticosteroid. It is administered either as an oral metered-dose inhaler for the treatment of asthma or as a nasal spray for treating allergic rhinitis. Corticosteroids are naturally occurring hormones that prevent or suppress inflammation and immune responses. When given as an intranasal spray, flunisolide reduces watery nasal discharge (rhinorrhea), nasal congestion, postnasal drip, sneezing, and itching oat the back of the throat that are common allergic symptoms. Flunisolide is a glucocorticoid receptor agonist. The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. The immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. Flunisolide binds to plasma transcortin, and it becomes active when it is not bound to transcortin.",The molecular weight is 434.5.,Flunisolide has a topological polar surface area of 93.06.,The log p value of  is 2.41.,Flunisolide is approved and investigational.,Flunisolide is a solid.,True
14015,"Alclometasone is synthetic glucocorticoid steroid for topical use in dermatology as anti-inflammatory, antipruritic, antiallergic, antiproliferative and vasoconstrictive agent. For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Alclometasone is a synthetic corticosteroid for topical dermatologic use. The corticosteroids constitute a class of primarily synthetic steroids used topically as anti-inflammatory and antipruritic agents. Alclometasone is a selective glucocorticoid receptor agonist. The mechanism of the anti-inflammatory activity of the topical steroids, in general, is unclear. However, corticosteroids are thought to act by the induction of phospholipase A<sub>2</sub> inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor, arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A<sub>2</sub>. Alclometasone initially binds the corticosteroid receptor. This complex migrates to the nucleus where it binds to different glucocorticoid response elements on the DNA. This in turn enhances and represses various genes, especially those involved in inflammatory pathways.",,,,Alclometasone is approved.,Alclometasone is a solid.,True
14016,"Medrysone is a corticosteroid used in ophthalmology. For the treatment of allergic conjunctivitis, vernal conjunctivitis, episcleritis, and epinephrine sensitivity. Medrysone is a topical anti-inflammatory corticoidsteroids for ophthalmic use. In patients with increased intraocular pressure and in those susceptible to a rise in intraocular pressure, there is less effect on pressure with medrysone than with dexamethasone or betamethasone. Corticoidsteroids inhibit the edema, fibrin deposition, capillary dilation, and phagocytic migration of the acute inflammatory response, as well as capillary proliferation, deposition of collagen, and scar formation. There is no generally accepted explanation for the mechanism of action of ocular corticosteroids. However, corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor, arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2. Initially, the drug binds to the glucocorticoid receptor in the cytosol. This migrates to the nucleus and binds to genetic elements which cause activation and repression of the involved genes in the inflammatory pathway.",The molecular weight is 344.5.,Medrysone has a topological polar surface area of 54.37.,The log p value of  is 3.36.,Medrysone is approved.,Medrysone is a solid.,True
14017,"A glucocorticoid employed, usually as eye drops, in the treatment of allergic and inflammatory conditions of the eye. It has also been used topically in the treatment of various skin disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p732) For the ophthalmic treatment of corticosteroid-responsive inflammation of the palpebral and bulbar conjunctiva, cornea and anterior segment of the globe. Corticosteroids such as fluorometholone inhibit the inflammatory response to a variety of inciting agents and probably delay or slow healing. They inhibit the edema, fibrin deposition, capillary dilation, leukocyte migration, capillary proliferation, fibroblast proliferation, deposition of collagen, and scar formation associated with inflammation. There is no generally accepted explanation for the mechanism of action of ocular corticosteroids. However, corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor, arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2. Their primary target is the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes.",The molecular weight is 376.47.,Fluorometholone has a topological polar surface area of 74.6.,The log p value of  is 2.11.,Fluorometholone is approved and investigational.,Fluorometholone is a solid.,True
14018,"Beclomethasone dipropionate is a second-generation synthetic corticosteroid agent and a diester of beclomethasone, which is structurally similar to. It is a prodrug of an active metabolite beclomethasone 17-monopropionate (17-BMP) which acts on the glucocorticoid receptor to mediates its therapeutic action. Beclomethasone dipropionate itself posesses weak glucocorticoid receptor binding affinity and is rapidly converted into 17-BMP upon administration. Formulations for oral inhalation, intranasal, and topical use are available for beclomethasone dipropionate. Beclomethasone dipropionate became first available in a pressurized metered-dose inhaler in 1972 and later in a dry powder inhaler and an aqueous nasal spray. Due to its anti-inflammatory, antipruritic, and anti-allergy properties, beclomethasone dipropionate is used in various inflammatory conditions, such as asthma, allergic rhinitis, and dermatoses to reduce symptoms. When inhaled, it is proposed that beclomethasone dipropionate remains active locally in the lung without causing significant side effects associated with systemic corticosteroids. Compared to earlier corticosteroids such as and , beclomethasone dipropionate is reported to be less irritating to the nasal mucosa with a longer duration of action when administered intranasally. Indicated for oral inhalation use in the maintenance treatment of asthma as prophylactic therapy in patients 5 years of age and older. The aerosol form of beclomethasone diproprionate is not indicated for the relief of acute bronchospasm. Inflammatory conditions, including asthma, dermatoses, and allergic rhinitis, involve the activation of cascades by inflammatory mediators. Inflammation is a primary defense mechanism and the homeostatic response of the immune system; however, a prolonged inflammatory response in certain disorders may lead to tissue damage, pain, and swelling. Beclomethasone dipropionate works by attenuating the inflammatory responses associated with asthma, allergic rhinitis, nasal polyps, and corticosteroid-responsive dermatoses. It suppresses the actions of inflammatory cells, such as mast cells, eosinophils, basophils, lymphocytes, macrophages, and neutrophils. It also inhibits the release of inflammatory mediators, such as histamine, eicosanoids, leukotrienes, and cytokines. Beclomethasone dipropionate is reported to exhibit potent topical activity while possessing low systemic effects.  Beclomethasone dipropionate is a corticosteroid and prodrug that is rapidly activated by hydrolysis to the active monoester, 17 monopropionate (17-BMP), which mediates anti-inflammatory actions. 17-BMP has been shown _in vitro_ to exhibit a binding affinity for the human glucocorticoid receptor which is approximately 13 times that of dexamethasone and 25 times that of beclomethasone dipropionate. Upon binding of the ligand, the glucocorticoid receptors dimerize and translocate into the nucleus, where they subsequently bind to glucocorticoid response elements (GRE) on glucocorticoid-responsive genes, leading to changes in transcription. There are several proposed mechanisms for the anti-inflammatory action of corticosteroids. Corticosteroids may work by increasing the transcription of genes coding for anti-inflammatory proteins, including lipocortin-1 and interleukin-10. Corticosteroids were also shown to inhibit the expression of multiple genes that encode pro-inflammatory factors, such as cytokines, chemokines, and adhesion molecules, that are activated during the chronic inflammatory process. This is thought to be due to the direct inhibitory interaction between activated glucocorticoid receptors and activated pro-inflammatory transcription factors, such as nuclear factor-kappa B and activator protein-1. Chronic inflammation is often characterized by enhanced expression of these transcription factors that bind to and activate coactivator molecules, which then acetylate core histones to switch on gene transcription to further amplify the inflammatory process. Corticosteroids suppress the multiple inflammatory gene expression by promoting histone deacetylation, resulting in tighter coiling of DNA and reduced access of transcription factors to their binding sites. ",The molecular weight is 521.05.,Beclomethasone dipropionate has a topological polar surface area of 106.97.,The log p value of  is 4.26.,Beclomethasone dipropionate is approved and investigational.,Beclomethasone dipropionate is a solid.,True
14019,"Betamethasone is a long-acting corticosteroid with immunosuppressive and antiinflammatory properties. It can be used topically to manage inflammatory skin conditions such as eczema, and parenterally to manage several disease states including autoimmune disorders. Betamethasone has potent glucocorticoid activity and negligible mineralocorticoid activity. As a member of the corticosteroid family, betamethasone is indicated for the treatment of several inflammatory conditions. As topical monotherapy, betamethasone is indicated to relieve pruritic and inflammatory symptoms of corticosteroid-responsive-dermatoses. Betamethasone can be used topically in combination with a vitamin D analog such as calcipotriene to treat plaque psoriasis. The corticosteroid is also available as an injectable suspension and can be used to manage a range of inflammatory conditions including endocrine disorders, gastrointestinal disorders, and rheumatic disorders among other conditions. Corticosteroids bind to the glucocorticoid receptor inhibiting pro-inflammatory signals, while promoting anti-inflammatory signals. Corticosteroids have a wide therapeutic window as patients may require doses that are multiples of what the body naturally produces. Patients who require long-term treatment with a corticosteroid should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections. Glucocorticoids inhibit neutrophil apoptosis and demargination, and inhibit NF-Kappa B and other inflammatory transcription factors. They also inhibit phospholipase A2, leading to decreased formation of arachidonic acid derivatives. In addition, glucocorticoids promote anti-inflammatory genes like interleukin-10.",The molecular weight is 392.47.,Betamethasone has a topological polar surface area of 94.83.,The log p value of  is 1.79.,Betamethasone is approved and vet_approved.,Betamethasone is a solid.,True
14020,"Fluticasone propionate is a synthetic glucocorticoid. These drugs are available as inhalers, nasal, sprays, and topical treatments for various inflammatory indications. Fluticasone propionate was first approved in 1990. Fluticasone propionate is indicated as an inhaler for the treatment and management of asthma by prophylaxisas well as inflammatory and pruritic dermatoses. Fluticasone propionate nasal spray is indicated for managing allergic and nonallergic rhinitis. Systemically, fluticasone propionate activates glucocorticoid receptors, and inhibits lung eosinophilia in rats. Fluticasone propionate as a topical formulation is also associated with vasoconstriction in the skin. Fluticasone propionate works through an unknown mechanism to affect the action of various cell types and mediators of inflammation. Fluticasone propionate activates glucocorticoid receptors and inhibits lung eosinophilia in rats.",The molecular weight is 500.57.,Fluticasone propionate has a topological polar surface area of 80.67.,The log p value of  is 3.8.,Fluticasone propionate is approved.,Fluticasone propionate is a solid.,True
14021,"Fluocinolone acetonide, with the formula 6-alpha, 9-alpha-difluoro-16-alpha, 17 alpha-acetonide, is a corticosteroid that presents a high lipophilicity. It has been used extensively in dermatological preparations and it has also been investigated thoroughly for its use in implantable corticosteroid devices. This type of device containing fluocinolone acetonide was developed by Taro Pharmaceuticals and approved by FDA in May 2016. Fluocinolone acetonide has been used extensively in different medical areas. Fluocinolone acetonide is a synthetic anti-inflammatory corticosteroid and thus, the effect of its interaction with the body produces vasoconstriction and suppression of membrane permeability, mitotic activity, immune response and release of inflammatory mediators. Fluocinolone acetonide is a corticosteroid and thus, it can be inferred that it acts by inhibiting the edema, fibrin deposition, capillary dilation, leukocyte migration, capillary proliferation, fibroblast proliferation, collagen deposition, and scar formation. ",The molecular weight is 452.5.,Fluocinolone acetonide has a topological polar surface area of 93.06.,The log p value of  is 2.25.,Fluocinolone acetonide is approved and investigational and vet_approved.,Fluocinolone acetonide is a solid.,True
14022,"Ulobetasol is a highly potent corticosteroid. It is structurally related to. Due to its high potency, it is mainly prescribed in the treatment of severe plaque psoriasis and corticosteroid responsive dermatoses. Ulobetasol cream and ointment are indicated in the treatment of inflammatory and pruritic corticosteroid responsive dermatoses. Ulobetasol lotion is indicated in the treatment of plaque psoriasis. Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Ulobetasol has a moderate duration of action as it is applied once or twice daily. Corticosteroids have a wide therapeutic window as patients may require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections. The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.",,,,Ulobetasol is approved.,Ulobetasol is a solid.,True
14023,"Triamcinolone is a corticosteroid used to treat various inflammatory conditions in the body from allergic rhinitis to acute exacerbations of multiple sclerosis. Triamcinolone can be used as a one time adjunct treatment of osteoarthritic knee pain, or first line as a topical treatment of corticosteroid responsive dermatoses. Triamcinolone is more commonly seen in the forms triamcinolone hexacetonide, triamcinolone acetonide, and triamcinolone diacetate. Triamcinolone hexacetonide injections are indicated for intralesional administration in alopecia areata, discoid lupus erythematosus, keloids, and necrobiosis lipoidica diabeticorum. This formulation can also be used for localized hypertrophic infiltrated inflammatory lesions of granuloma annulare, lichen planus, lichen simplex chronicus, and psoriatic plaques. Triamcinolone is a corticosteroid with anti-inflammatory properties. These properties are used to treat inflammation in conditions that affect various organs and tissues. Triamcinolone should not be administered as an epidural injection. Corticosteroids like triamcinolone inhibit phospholipase A2 on cell membranes, preventing the breakdown of lysosomal membranes of leukocytes, which in turn prevent the formation of arachidonic acid, which decrease expression of cyclooxygenase and lipoxygenase, inhibiting synthesis of prostaglandins and leukotrienes. Anti-inflammatory activity occurs via reversal of vascular dilation and reducing permeability, which prevents macrophage and leukocyte migration. Triamcinolone also inhibits nuclear factor kappa-B, which decreases the production of pro-inflammatory signals such as interleukin-6, interleukin-8, and monocyte chemoattractant protein-1.",The molecular weight is 394.44.,Triamcinolone has a topological polar surface area of 115.06.,The log p value of  is 0.71.,Triamcinolone is approved and vet_approved.,Triamcinolone is a solid.,True
14024,"A synthetic anti-inflammatory glucocorticoid derived from. It is biologically inert and converted to in the liver. Prednisone is indicated as an anti-inflammatory or immunosuppressive drug for allergic, dermatologic, gastrointestinal, hematologic, ophthalmologic, nervous system, renal, respiratory, rheumatologic, infectious, endocrine, or neoplastic conditions as well as in organ transplant. Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Prednisone has a short duration of action as the half life is 2-3 hours. Corticosteroids have a wide therapeutic window as patients make require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections. Prednisone is first metabolized in the liver to its active form, prednisolone, a glucocorticoid agonist corticosteroid.",The molecular weight is 358.43.,Prednisone has a topological polar surface area of 91.67.,The log p value of  is 1.66.,Prednisone is approved and vet_approved.,Prednisone is a solid.,True
14025,"A derivative of the insecticide dichlorodiphenyldichloroethane that specifically inhibits cells of the adrenal cortex and their production of hormones. It is used to treat adrenocortical tumors and causes CNS damage, but no bone marrow depression. For treatment of inoperable adrenocortical tumours; Cushing's syndrome Mitotane is an oral chemotherapeutic agent indicated in the treatment of inoperable adrenal cortical carcinoma of both functional and nonfunctional types. Mitotane can best be described as an adrenal cytotoxic agent, although it can cause adrenal inhibition, apparently without cellular destruction. The administration of Mitotane alters the extra-adrenal metabolism of cortisol in man; leading to a reduction in measurable 17-hydroxy corticosteroids, even though plasma levels of corticosteroids do not fall. The drug apparently causes increased formation of 6-B-hydroxyl cortisol. Its biochemical mechanism of action is unknown, although data are available to suggest that the drug modifies the peripheral metabolism of steroids as well as directly suppressing the adrenal cortex.",The molecular weight is 320.03.,,The log p value of  is 6.06.,Mitotane is approved.,Mitotane is a solid.,True
14026,"Flumethasone is a moderately potent difluorinated corticosteroid ester with anti-inflammatory, antipruritic and vasoconstrictive properties. As it is a privalate salt, its anti-inflammatory action is concentrated at the site of application. This local effect on diseased areas results in a prompt decrease in inflammation, exudation and itching. For the treatment of contact dermatitis, atopic dermatitis, exczema, psoriasis, diaper rash and other skin conditions Flumethasone pivalate is a moderately potent difluorinated corticosteroid ester with anti-inflammatory, antipruritic and vasoconstrictive properties. As it is a privalate salt, its anti-inflammatory action is concentrated at the site of application. This local effect on diseased areas results in a prompt decrease in inflammation, exudation and itching. Flumethasone is a glucocorticoid receptor agonist. This complex binds to the nucleus causing a variety of genetic activation and repressions. The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. The immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. Flumethasone binds to plasma transcortin, and it becomes active when it is not bound to transcortin.",The molecular weight is 410.46.,Flumethasone has a topological polar surface area of 94.83.,The log p value of  is 1.83.,Flumethasone is approved and vet_approved.,Flumethasone is a solid.,True
14027,"Fludrocortisone is a synthetic mineralocorticoid used in conjunction with to replace missing endogenous corticosteroids in patients with adrenal insufficiency. It is functionally similar to , the body's primary endogenous mineralocorticoid, and is structurally analogous to , differing only by a fluorine atom at the 9-position of the steroid structure - this fluorination is thought to be crucial to fludrocortisone's significant mineralocorticoid potency. Fludrocortisone is indicated as partial replacement therapy for primary or secondary adrenocortical insufficiency in Addison's disease. It is also indicated for the treatment of salt-losing androgenital syndrome. Fludrocortisone is a synthetic mineralocorticoid used to replace endogenous in conditions resulting in missing or inadequate endogenous synthesis. It acts on the kidneys to increase both sodium reabsorption and potassium excretion. As its effects are exerted at the transcriptional level, a single dose of fludrocortisone may work over the course of 1-2 days despite a relatively short plasma half-life. Like other systemic corticosteroids, fludrocortisone may mask signs of infection by depressing the normal immune response - infections occurring during fludrocortisone therapy should be promptly treated with appropriate antimicrobial therapy. The main endogenous mineralocorticoid, aldosterone, is produced in the zona glomerulosa of the adrenal cortex - it acts on mineralocorticoid receptors in the kidneys to increase sodium reabsorption and potassium excretion, which in turn helps to regulate plasma electrolyte composition and blood pressure. In conditions of adrenal insufficiency, such as Addison’s disease, aldosterone is not produced (or is produced in insufficient quantities) and must be replaced by exogenous mineralocorticoids such as fludrocortisone.",,,,Fludrocortisone is approved and investigational.,Fludrocortisone is a solid.,True
14028,"Hydrocortisone, or cortisol, is a glucocorticoid secreted by the adrenal cortex. Hydrocortisone is used to treat immune, inflammatory, and neoplastic conditions. It was discovered in the 1930s by Edward Kendall and named Compound F, or 17-hydroxycorticosterone. Otic solutions are indicated for infections of the external auditory canal caused by susceptible organisms and with inflammation. Hydrocortisone tablets are indicated for certain endocrine, rheumatic, collagen, allergic, ophthalmic, respiratory, hematologic, neoplastic, edematous, gastrointestinal, and other conditions. A hydrocortisone enema is indicated for ulcerative colitis, a topical ointment with antibiotics is indicated for corticosteroid responsive dermatoses with infections, and a topical cream with is indicated to treat cold sores. Oral granules of hydrocortisone are used as a replacement therapy for Adrenocortical Insufficiency (AI) in children under 17 years of age. Hydrocortisone binds to the glucocorticoid receptor leading to downstream effects such as inhibition of phospholipase A2, NF-kappa B, other inflammatory transcription factors, and the promotion of anti-inflammatory genes. Hydrocortisone has a wide therapeutic index and a moderate duration of action. Patients should stop taking the medication if irritation or sensitization occurs. The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.",The molecular weight is 362.47.,Hydrocortisone has a topological polar surface area of 94.83.,The log p value of  is 1.89.,Hydrocortisone is approved and vet_approved.,Hydrocortisone is a solid.,True
14029,"A corticosteroid used topically in the treatment of various skin disorders. It is usually employed as a cream or an ointment, and is also used as a polyethylene tape with an adhesive. (From Martindale, The Extra Pharmacopoeia, 30th ed, p733) For relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses, particularly dry, scaling localized lesions Flurandrenolide is primarily effective because of its anti-inflammatory, antipruritic, and vasoconstrictive actions. Flurandrenolide is a topical corticosteroid. It is normally applied to a plastic tape called Cordran. Cordran is primarily effective because of its anti-inflammatory, antipruritic, and vasoconstrictive actions. Flurandrenolide, which is slowly released from the Cordran tape, binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. Cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In another words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. Like other glucocorticoid agents Fluocinolone acetonide acts as a physiological antagonist to insulin by decreasing glycogenesis (formation of glycogen). It also promotes the breakdown of lipids (lipolysis), and proteins, leading to the mobilization of extrahepatic amino acids and ketone bodies. This leads to increased circulating glucose concentrations (in the blood). There is also decreased glycogen formation in the liver.",The molecular weight is 436.52.,Flurandrenolide has a topological polar surface area of 93.06.,The log p value of  is 2.87.,Flurandrenolide is approved.,Flurandrenolide is a solid.,True
14030,"Prednisolone is a glucocorticoid similar to used for its anti-inflammatory, immunosuppressive, anti-neoplastic, and vasoconstrictive effects. Prednisolone is indicated to treat endocrine, rheumatic, and hematologic disorders; collagen, dermatologic, ophthalmic, respiratory, and gastrointestinal diseases; allergic and edematous states; and other conditions like tuberculous meningitis. Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Prednisolone has a short duration of action as the half life is 2.1-3.5 hours. Corticosteroids have a wide therapeutic window as patients make require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections. The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.",The molecular weight is 360.45.,Prednisolone has a topological polar surface area of 94.83.,The log p value of  is 1.42.,Prednisolone is approved and vet_approved.,Prednisolone is a solid.,True
14031,"Rimexolone is a 1% eye drop solution is a glucocorticoid steroid. It is used to treat inflammation in the eye. It is marketed as Vexol. For the treatment of postoperative inflammation following ocular surgery and in the treatment of anterior uveitis. Rimexolone is a glucocorticoid corticosteroid for systemic use. Corticosteroids suppress the inflammatory response to a variety of inciting agents of a mechanical, chemical, or immunological nature. They inhibit edema, cellular infiltration, capillary dilatation, fibroblastic proliferation, deposition of collagen and scar formation associated with inflammation. Rimexolone is a glucocorticoid receptor agonist. The antiinflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition of arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. By binding to the glucocorticoid receptor, this drug ultimately leads to changes in genetic transcription involving the lipocortins and prostaglandins.",The molecular weight is 370.53.,Rimexolone has a topological polar surface area of 54.37.,The log p value of  is 4.14.,Rimexolone is approved.,Rimexolone is a solid.,True
14032,"Clobetasol propionate is a prednisolone derivative with higher specificity for glucocorticoid receptors than mineralocorticoid receptors. It has demonstrated superior activity compared to and was first described in the literature in 1974. Clobetasol propionate is indicated to treat moderate to severe plaque psoriasis as well as inflammatory and pruritic manifestations of corticosteroid responsive dermatoses. Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Clobetasol propionate is generally applied twice daily so the duration of action is long. Corticosteroids have a wide therapeutic window as patients may require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections. The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.",The molecular weight is 466.97.,Clobetasol propionate has a topological polar surface area of 80.67.,The log p value of  is 3.49.,Clobetasol propionate is approved.,Clobetasol propionate is a solid.,True
14033,"A topical glucocorticoid used in the treatment of eczema. A topical anti-inflammatory product for the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Fluocinonide is a potent glucocorticoid steroid used topically as anti-inflammatory agent for the treatment of skin disorders such as eczema. It mediates its effects to relieve itching, redness, dryness, crusting, scaling, inflammation, and discomfort associated with inflammatory skin conditions.  Fluocinonide is a potent glucocorticoid steroid used topically as anti-inflammatory agent for the treatment of skin disorders such as eczema. Fluocinonide binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. Cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In another words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding. Like other glucocorticoid agents Fluocinolone acetonide acts as a physiological antagonist to insulin by decreasing glycogenesis (formation of glycogen). It also promotes the breakdown of lipids (lipolysis), and proteins, leading to the mobilization of extrahepatic amino acids and ketone bodies. This leads to increased circulating glucose concentrations (in the blood). There is also decreased glycogen formation in the liver.",The molecular weight is 494.53.,Fluocinonide has a topological polar surface area of 99.13.,The log p value of  is 2.79.,Fluocinonide is approved and investigational.,Fluocinonide is a solid.,True
14034,"Budesonide is a glucocorticoid that is a mix of the 22R and 22S epimer used to treat inflammatory conditions of the lungs and intestines such as asthma, COPD, Crohn's disease, and ulcerative colitis. Budesonide extended release capsules are indicated for the treatment and maintenance of mild to moderate Crohn’s disease. Various inhaled budesonide products are indicated for prophylactic therapy in asthma and reducing exacerbations of COPD. A budesonide nasal spray is available over the counter for symptoms of hay fever and upper respiratory allergies. Extended release capsules are indicated to induce remission of mild to moderate ulcerative colitis and a rectal foam is used for mild to moderate distal ulcerative colitis. Budesonide is a glucocorticoid used to treat respiratory and digestive conditions by reducing inflammation. It has a wide therapeutic index, as dosing varies highly from patient to patient. Patients should be counselled regarding the risk of hypercorticism and adrenal axis suppression. The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.",The molecular weight is 430.54.,Budesonide has a topological polar surface area of 93.06.,The log p value of  is 2.9.,Budesonide is approved.,Budesonide is a solid.,True
14035,"A glucocorticoid with the general properties of corticosteroids. It has been used by mouth in the treatment of all conditions in which corticosteroid therapy is indicated except adrenal-deficiency states for which its lack of sodium-retaining properties makes it less suitable than hydrocortisone with supplementary fludrocortisone. (From Martindale, The Extra Pharmacopoeia, 30th ed, p737) For the treatment of all conditions in which corticosteroid therapy is indicated except adrenal-deficiency states for which its lack of sodium-retaining properties makes it less suitable than hydrocortisone with supplementary fludrocortisone. Paramethasone is a glucocorticoid with the general properties of corticosteroids. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by having different receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. Glucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated. Glucocorticoids such as paramethasone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Paramethasone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",,,,Paramethasone is experimental.,Paramethasone is a solid.,True
14036,"Ciclesonide is a glucocorticoid used to treat obstructive airway diseases. It is marketed under the brand name Alvesco. For the treatment of nasal symptoms associated with seasonal and perennial allergic rhinitis in adults and adolescents 12 years of age and older. Ciclesonide is a pro-drug that is enzymatically hydrolyzed to a pharmacologically active metabolite, C21-desisobutyryl-ciclesonide (des-ciclesonide or RM1) following intranasal application. Des-ciclesonide has anti-inflammatory activity with affinity for the glucocorticoid receptor that is 120 times higher than the parent compound. The precise mechanism through which ciclesonide affects allergic rhinitis symptoms is not known. Corticosteroids have been shown to have a wide range of effects on multiple cell types (e.g., mast cells, eosinophils, neutrophils, macrophages, and lymphocytes) and mediators (e.g., histamine, eicosanoids, leukotrienes, and cytokines) involved in allergic inflammation. Glucocorticoids such as ciclesonide can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Ciclesonide reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Ciclesonide is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",The molecular weight is 540.7.,Ciclesonide has a topological polar surface area of 99.13.,The log p value of  is 5.25.,Ciclesonide is approved and investigational.,Ciclesonide is a solid.,True
14037,"CRx-119 is a novel synergistic combination drug candidate discovered using the CombinatoRx combination High Throughput Screening (cHTS(TM)) technology with potential therapeutic use in a broad range of immuno-inflammatory conditions. CRx-119 is a combination of a low dose of the steroid prednisolone, 3mg, and amoxapine. Investigated for use/treatment in periodontal disease and rheumatoid arthritis. CRx-119 is a novel orally available syncretic drug candidate in clinical development for immunoinflammatory diseases. A syncretic drug comprises two compounds that are designed to act together synergistically through multiple pathways to provide a novel therapeutic effect which neither component alone can achieve. CRx-119 contains a low dose of the steroid prednisolone and amoxapine. The target product profile for CRx-119 is to selectively amplify certain elements of prednisolone's anti-inflammatory and immunomodulatory effects, without replicating steroid toxicity. Amoxapine acts by decreasing the reuptake of norepinephrine and serotonin (5-HT). Glucocorticoids such as prednisolone can inhibit leukocyte infiltration at the site of inflammation, interfere with mediators of inflammatory response, and suppress humoral immune responses. The antiinflammatory actions of glucocorticoids are thought to involve phospholipase A2 inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Prednisolone reduces inflammatory reaction by limiting the capillary dilatation and permeability of the vascular structures. These compounds restrict the accumulation of polymorphonuclear leukocytes and macrophages and reduce the release of vasoactive kinins. Recent research suggests that corticosteroids may inhibit the release of arachidonic acid from phospholipids, thereby reducing the formation of prostaglandins. Prednisolone is a glucocorticoid receptor agonist. On binding, the corticoreceptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing an increase or decrease in expression of specific target genes, including suppression of IL2 (interleukin 2) expression.",,,,CRx-119 is investigational.,CRx-119 is a solid.,True
14038,"Fluticasone furoate is a synthetic glucocorticoid available as an inhaler and nasal spray for various inflammatory indications. Fluticasone furoate was first approved in 2007. Fluticasone furoate is indicated as an inhaler for the treatment and management of asthma by prophylaxis. The fluticasone furoate nasal spray is indicated for treating season and perennial allergic rhinitis. Systemically, in vitro experiments show fluticasone furoate activates glucocorticoid receptors, inhibits nuclear factor kappa b, and inhibits lung eosinophilia in rats. Fluticasone furoate works through an unknown mechanism to affect the action of various cell types and mediators of inflammation. In vitro experiments show fluticasone furoate activating glucocorticoid receptors, inhibiting nuclear factor kappa b, and inhibiting lung eosinophilia in rats.",The molecular weight is 538.58.,Fluticasone furoate has a topological polar surface area of 93.81.,The log p value of  is 4.26.,Fluticasone furoate is approved.,Fluticasone furoate is a solid.,True
14039,"Medrogestone (INN), also known as 6,17α-dimethyl-6-dehydroprogesterone, is a progestational agent derived from 17-methylprogesterone. It was conceived as an alternative for an orally effective contraceptive option. It was developed by Ayerst, approved in Canada in 1969 and its current status is cancelled post-marketing. It was never approved by the FDA. Medrogestone is indicated as adjunct to treat endometial shedding in menopausal women, to treat secondary amenorrhea, to induce menses and to treat dysfunctional uterine bleeding in adult and adolescent women. Medrogestone was created as a more potent and orally active option of progesterone. In pre-clinical trials, medrogestone was proven to have four times more progestational activity than progesterone with a similar duration effect than the one found for 17-hydroxyprogesterone. Medrogestone was also able to maintain pregnancy and prevented ovulation in ovariectomized rats. Administration of medrogestone, alone or with premarin, prevented pregnancy, as well as it suppressed ovarian weight increase by nearly 100% of the tested individuals. Medrogestone does not produce any androgenic effect but it presented a marked anti-androgenic effect. It did not present an oestrogenic effect, nor changes in organ weight or histological appearance in adrenal glands or thymus and it does not present any anti-inflammatory effects.  Medrogestone is a progestogen, thus its action is done under the same profile. These type of molecules are steroid hormones that bind and activate the progesterone receptor. Its action may involve the suppression of gonadotropic hormones from the anterior portion of the pituitary gland and secondary suppression of testosterone. Medrogestone presents structural similarities to testosterone which allows it to compete for the androgen-receptor-protein receptor sites in prostatic cells. Administration of medrogestone diminishes the response to endogenous hormones in tumor cells due to a reduction in hormone steroid receptors; this effect will translate into cytotoxic or antiproliferative effects.",The molecular weight is 340.51.,Medrogestone has a topological polar surface area of 34.14.,The log p value of  is 4.38.,Medrogestone is approved and withdrawn.,Medrogestone is a solid.,True
14040,"Fluticasone is a synthetic glucocorticoid available as 2 esters, and. These drugs are available as inhalers, nasal, sprays, and topical treatments for various inflammatory indications. was first approved in 1990 and was approved in 2007. Fluticasone's 2 esters are indicated as inhalers for the treatment and management of asthma by prophylaxisas well as inflammatory and pruritic dermatoses. A nasal spray is indicated for managing nonallergic rhinitis while the nasal spray is indicated for treating season and perennial allergic rhinitis. Systemically, in vitro experiments show activates glucocorticoid receptors, inhibits nuclear factor kappa b, and inhibits lung eosinophilia in rats. performs similar activity but is not stated to affect nuclear factor kappa b. as a topical formulation is also associated with vasoconstriction in the skin.  and work through an unknown mechanism to affect the action of various cell types and mediators of inflammation. In vitro experiments show activating glucocorticoid receptors, inhibiting nuclear factor kappa b, and inhibiting lung eosinophilia in rats. performs similar activity but is not stated to affect nuclear factor kappa b.",,,,Fluticasone is approved and experimental.,Fluticasone is a solid.,True
14041,"For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease. Hydrocortisone is the most important human glucocorticoid. It is essential for life and regulates or supports a variety of important cardiovascular, metabolic, immunologic and homeostatic functions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by having different receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. Glucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated. Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",The molecular weight is 460.57.,Hydrocortisone aceponate has a topological polar surface area of 106.97.,The log p value of  is 3.49.,Hydrocortisone aceponate is experimental and vet_approved.,,True
14042,"For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease. Hydrocortisone is the most important human glucocorticoid. It is essential for life and regulates or supports a variety of important cardiovascular, metabolic, immunologic and homeostatic functions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by having different receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. Glucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated. Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",The molecular weight is 404.5.,Hydrocortisone acetate has a topological polar surface area of 100.9.,The log p value of  is 2.42.,Hydrocortisone acetate is approved and vet_approved.,,True
14043,"For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease. Hydrocortisone is the most important human glucocorticoid. It is essential for life and regulates or supports a variety of important cardiovascular, metabolic, immunologic and homeostatic functions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by having different receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. Glucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated. Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",The molecular weight is 432.56.,Hydrocortisone butyrate has a topological polar surface area of 100.9.,The log p value of  is 3.48.,Hydrocortisone butyrate is approved and vet_approved.,,True
14044,"For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease. Hydrocortisone is the most important human glucocorticoid. It is essential for life and regulates or supports a variety of important cardiovascular, metabolic, immunologic and homeostatic functions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by having different receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. Glucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated. Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",The molecular weight is 486.65.,Hydrocortisone cypionate has a topological polar surface area of 100.9.,The log p value of  is 5.04.,Hydrocortisone cypionate is approved and investigational and vet_approved.,,True
14045,"For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease. Hydrocortisone is the most important human glucocorticoid. It is essential for life and regulates or supports a variety of important cardiovascular, metabolic, immunologic and homeostatic functions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by having different receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. Glucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated. Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",The molecular weight is 442.44.,Hydrocortisone phosphate has a topological polar surface area of 141.36.,The log p value of  is 0.42.,Hydrocortisone phosphate is approved and vet_approved.,,True
14046,"For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease. Hydrocortisone is the most important human glucocorticoid. It is essential for life and regulates or supports a variety of important cardiovascular, metabolic, immunologic and homeostatic functions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by having different receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. Glucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated. Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",The molecular weight is 488.62.,Hydrocortisone probutate has a topological polar surface area of 106.97.,The log p value of  is 4.55.,Hydrocortisone probutate is approved and vet_approved.,,True
14047,"For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders, such as arthritis, lupus, severe psoriasis, severe asthma, ulcerative colitis, and Crohn's disease. Hydrocortisone is the most important human glucocorticoid. It is essential for life and regulates or supports a variety of important cardiovascular, metabolic, immunologic and homeostatic functions. Topical hydrocortisone is used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by having different receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. Glucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated. Hydrocortisone binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",The molecular weight is 446.58.,Hydrocortisone valerate has a topological polar surface area of 100.9.,The log p value of  is 4.01.,Hydrocortisone valerate is approved and vet_approved.,,True
14048,"Prednisolone phosphate is a glucocorticoid similar to used for its anti-inflammatory, immunosuppressive, anti-neoplastic, and vasoconstrictive effects. Prednisolone phosphate is indication to a number of conditions including treat allergic states, dermatologic diseases, edematous states, endocrine disorders, gastrointestinal diseases, hematologic disorders, neoplastic diseases, nervous system, ophthalmic diseases, respiratory diseases, rheumatic disorders. Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Prednisolone has a short duration of action as the half life is 2-4 hours. Corticosteroids have a wide therapeutic window as patients make require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections. The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.",,,,Prednisolone phosphate is approved and vet_approved.,Prednisolone phosphate is a solid.,True
14049,"Betamethasone phosphate is a prodrug that is rapidly hydrolyzed, providing rapidly accessible to agonize glucocorticoid receptors. Betamethasone provides greater anti-inflammatory activity than with less sodium and water retention. Betamethasone phosphate is indicated intramuscularly to treat allergic states, dermatologic diseases, endocrine disorders, gastrointestinal diseases, hematologic disorders, neoplastic diseases, nervous system conditions, ophthalmic diseases, renal diseases, respiratory diseases, rheumatic disorders, trichinosis with neurologic or myocardial involvement, and tuberculous meningitis with subarachnoid block or impending block. It is also used intra-articularly in the treatment of acute gouty arthritis, acute and subacute bursitis, acute nonspecific tenosynovitis, epicondylitis, rheumatoid arthritis, and synovitis of osteoarthritis. Intralesional betamethasone phospahte is indicated in the treatment of alopecia areata, discoid lupus erythematosus, keloids, lichen planus, lichen simplex chronicus, psoriatic plaques, necrobiosis lipoidica diabeticorum, and localized hypertrophic, infiltrated, inflammatory lesions of granuloma annulare. Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Betamethasone phosphate has a short duration of action as it is rapidly hydrolyzed to betamethasone. Corticosteroids have a wide therapeutic window as patients may require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections. Betamethasone phosphate is a soluble ester prodrug of betamethasone. Betamethasone is rapidly de-esterified, allowing betamethasone to act as an agonist of the glucocorticoid receptor. The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.",,,,Betamethasone phosphate is approved and vet_approved.,Betamethasone phosphate is a solid.,True
14050,"Prednisolone acetate is a molecule bound to an acetate functional group by an ester bond. Prednisolone acetate is indicated as an anti-inflammatory or immunosuppressive agent for allergic, dermatologic, gastrointestinal, hematologic, ophthalmologic, nervous system, renal, respiratory, rheumatologic, or infectious conditions. Prednisolone acetate is also indicated in organ transplant patients, as well as endocrine or neoplastic conditions. Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Prednisolone acetate has a short duration of action as the half life is 2-3 hours. Corticosteroids have a wide therapeutic window as patients make require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections. The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.",The molecular weight is 402.49.,Prednisolone acetate has a topological polar surface area of 100.9.,The log p value of  is 1.96.,Prednisolone acetate is approved and vet_approved.,Prednisolone acetate is a solid.,True
14051,"Rubidium chloride Rb-82 injection is a sterile nonpyrogenic solutions of rubidium Rb 82 chloride. It is indicated for Positron Emission Tomography (PET) imaging of the myocardium under rest or pharmacologic stress conditions to evaluate regional myocardial perfusion in adult patients with suspected or existing coronary artery disease. Rubidium Rb 82 chloride injection is indicated for Positron Emission Tomography (PET) imaging of the myocardium under rest or pharmacologic stress conditions to evaluate regional myocardial perfusion in adult patients with suspected or existing coronary artery disease. In human studies, myocardial activity was noted within the first minute after peripheral intravenous injection of Rb-82. When areas of infarction or ischemia are present in the myocardium, they are visualized within 2-7 minutes after injection as photon-deficient, or “cold”, areas on the myocardial scan. Rb-82 is analogous to potassium ion (K+) in its biochemical behavior and is rapidly extracted by the myocardium proportional to the blood flow. Rb+ participates in the sodium-potassium (Na+/K+) ion exchange pumps that are present in cell membranes. The intracellular uptake of Rb-82 requires maintenance of ionic gradient across cell membranes. Rb-82 radioactivity is increased in viable myocardium reflecting intracellular retention, while the tracer is cleared rapidly from necrotic or infarcted tissue.",,,,Rubidium Rb-82 is approved and investigational.,,True
14052,"Retinol and derivatives of retinol that play an essential role in metabolic functioning of the retina, the growth of and differentiation of epithelial tissue, the growth of bone, reproduction, and the immune response. Dietary vitamin A is derived from a variety of carotenoids found in plants. It is enriched in the liver, egg yolks, and the fat component of dairy products. For the treatment of vitamin A deficiency. Vitamin A is effective for the treatment of Vitamin A deficiency. Vitamin A refers to a group of fat-soluble substances that are structurally related to and possess the biological activity of the parent substance of the group called all-<i>trans</i> retinol or retinol. Vitamin A plays vital roles in vision, epithelial differentiation, growth, reproduction, pattern formation during embryogenesis, bone development, hematopoiesis and brain development. It is also important for the maintenance of the proper functioning of the immune system. Vision:Vitamin A (all-<i>trans</i> retinol) is converted in the retina to the 11-<i>cis</i>-isomer of retinaldehyde or 11-<i>cis</i>-retinal. 11-<i>cis</i>-retinal functions in the retina in the transduction of light into the neural signals necessary for vision. 11-<i>cis</i>-retinal, while attached to opsin in rhodopsin is isomerized to all-<i>trans</i>-retinal by light. This is the event that triggers the nerve impulse to the brain which allows for the perception of light. All-<i>trans</i>-retinal is then released from opsin and reduced to all-<i>trans</i>-retinol. All-<i>trans</i>-retinol is isomerized to 11-<i>cis</i>-retinol in the dark, and then oxidized to 11-<i>cis</i>-retinal. 11-<i>cis</i>-retinal recombines with opsin to re-form rhodopsin. Night blindness or defective vision at low illumination results from a failure to re-synthesize 11-<i>cis</i> retinal rapidly. <br/>Epithelial differentiation: The role of Vitamin A in epithelial differentiation, as well as in other physiological processes, involves the binding of Vitamin A to two families of nuclear retinoid receptors (retinoic acid receptors, RARs; and retinoid-X receptors, RXRs). These receptors function as ligand-activated transcription factors that modulate gene transcription. When there is not enough Vitamin A to bind these receptors, natural cell differentiation and growth are interrupted.",The molecular weight is 286.46.,Vitamin A has a topological polar surface area of 20.23.,The log p value of  is 6.4.,Vitamin A is approved and nutraceutical and vet_approved.,Vitamin A is a solid.,True
14053,"Beta-carotene, with the molecular formula C40H56, belongs to the group of carotenoids consisting of isoprene units. The presence of long chains of conjugated double bonds donates beta-carotene with specific colors. It is the most abundant form of carotenoid and it is a precursor of the vitamin A. Beta-carotene is composed of two retinyl groups. It is an antioxidant that can be found in yellow, orange and green leafy vegetables and fruits. Under the FDA, beta-carotene is considered as a generally recognized as safe substance (GRAS). Beta-carotene is FDA approved to be used as a nutrient supplement and to be even added in infant formula as a source of vitamin A. It is also approved to be used as a color additive for food products, drugs (with the label of \only as a color additive\"") and cosmetics."" Oral administration of beta-carotene increases the serum concentration of beta-carotene by 60% but it does not change the concentration found in the heart, liver or kidneys. In vitro studies in hepatocytes have shown that beta-carotene ameliorates oxidative stress, enhances antioxidant activity and decreases apoptosis. Beta-carotene is an antioxidant that presents significant efficacy against the reactive oxygen species singlet oxygen. Beta-carotene acts as a scavenger of lipophilic radicals within the membranes of every cell compartments. It also presents an oxidative modification of LDL. The presence of long chains of conjugated double bonds is responsible for its antioxidative properties by allowing beta-carotene to chelate oxygen-free radicals and dissipate their energy. The chelation of free radicals inhibits the peroxidation of lipids.",The molecular weight is 536.89.,,The log p value of  is 15.23.,Beta carotene is approved and nutraceutical.,Beta carotene is a solid.,True
14054,"In 1922, vitamin E was demonstrated to be an essential nutrient. Vitamin E is a term used to describe 8 different fat soluble tocopherols and tocotrienols, alpha-tocopherol being the most biologically active. Vitamin E acts as an antioxidant, protecting cell membranes from oxidative damage. The antioxidant effects are currently being researched for use in the treatment of diseases causing bone loss, cardiovascular diseases, diabetes mellitus and associated comorbidities, eye diseases, inflammatory diseases (including skin conditions), lipid disorders, neurological diseases, and radiation damage. Though this research is so far inconclusive, vitamin E remains a popular supplement and is generally considered safe by the FDA. Vitamin E supplementation is indicated for treatment of vitamin E deficiency which can occur in cystic fibrosis, cholestasis and severe liver disease, abetalipoproteinemia or simply poor diet. Vitamin E is a collective term used to describe 8 separate fat soluble antioxidants, most commonly alpha-tocopherol. Vitamin E acts to protect cells against the effects of free radicals, which are potentially damaging by-products of the body's metabolism. Vitamin E deficiency is seen in persons with abetalipoproteinemia, premature, very low birth weight infants (birth weights less than 1500 grams, or 3&frac12; pounds), cystic fibrosis, and cholestasis and severe liver disease. Preliminary research suggests vitamin E may help prevent or delay coronary heart disease and protect against the damaging effects of free radicals, which may contribute to the development of chronic diseases such as cancer. It also protects other fat-soluble vitamins (A and B group vitamins) from destruction by oxygen. Low levels of vitamin E have been linked to increased incidence of breast and colon cancer. The mechanism of action for most of vitamin E's effects are still unknown. Vitamin E is an antioxidant, preventing free radical reactions with cell membranes. Though in some cases vitamin E has been shown to have pro-oxidant activity.",The molecular weight is 430.72.,Vitamin E has a topological polar surface area of 29.46.,The log p value of  is 12.05.,Vitamin E is approved and nutraceutical and vet_approved.,Vitamin E is a solid.,True
14055,N-Ethylretinamide is the ethylamide of all-trans B-retinoic acid.,,,,N-Ethylretinamide is experimental.,N-Ethylretinamide is a solid.,True
14056,"A synthetic retinoid that is used orally as a chemopreventive against prostate cancer and in women at risk of developing contralateral breast cancer. It is also effective as an antineoplastic agent. Investigated for use/treatment in macular degeneration. Fenretinide inhibits the growth of several human cancer cell lines, acting through both retinoid-receptor-dependent and retinoid-receptor-independent mechanisms.1In vivo, fenretinide selectively accumulates in breast tissue and is particularly active in inhibiting rat mammary carcinogenesis.1 An important feature of fenretinide is its ability to inhibit cell growth through the induction of apoptosis rather than through differentiation, an effect that is strikingly different from that of vitamin A.1 In contrast to tamoxifen, which inhibits only estrogen receptor (ER)-positive tumors, fenretinide induces apoptosis in both ER-positive and ER-negative breast cancer cell lines.2 All of these properties render fenretinide an attractive candidate for breast cancer chemoprevention.",,,,Fenretinide is investigational.,Fenretinide is a solid.,True
14057,,,,,2-piperidin-1-yl}carbonyl)amino]benzoic acid is experimental.,2-piperidin-1-yl}carbonyl)amino]benzoic acid is a solid.,False
14058,"A synthetic nonsteroidal estrogen used in the treatment of menopausal and postmenopausal disorders. It was also used formerly as a growth promoter in animals. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), diethylstilbestrol has been listed as a known carcinogen. (Merck, 11th ed) Used in the treatment of prostate cancer. Previously used in the prevention of miscarriage or premature delivery in pregnant women prone to miscarriage or premature delivery. Diethylstilbestrol is a synthetic estrogen that was developed to supplement a woman's natural estrogen production. In 1971, the Food and Drug Administration (FDA) issued a Drug Bulletin advising physicians to stop prescribing DES to pregnant women because it was linked to a rare vaginal cancer in female offspring. Estrogens diffuse into their target cells and interact with a protein receptor, the estrogen receptor. Target cells include the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. The effect of Estrogen binding their receptors causes downstream increases the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary. The combination of an estrogen with a progestin suppresses the hypothalamic-pituitary system, decreasing the secretion of gonadotropin-releasing hormone (GnRH).",The molecular weight is 268.36.,Diethylstilbestrol has a topological polar surface area of 40.46.,The log p value of  is 4.96.,Diethylstilbestrol is approved and investigational.,Diethylstilbestrol is a solid.,True
14059,"Liothyronine is a thyroidal hormone T3 which is normally produced by the thyroid gland in a ratio 4:1 when compared with T4: T3. Liothyronine is the active form of thyroxine which is composed in a basic chemical structure by a tyrosine with bound iodine. The exogenous liothyronine product was developed by King Pharmaceuticals and FDA approved in 1956. Liothyronine is officially approved for the following indications: In hormonal replacement, liothyronine is more potent and present a faster action when compared to levothyroxine but the time of action is significantly shorter. The type of treatment needs to be well evaluated as the fast correction of thyroid hormones in certain diseases presents additional risks such as heart failure. The onset of activity is observed a few hours after administration and the maximum effect is observed after 2-3 days. Liothyronine replaces endogenous thyroid hormone and then exerts its physiologic effects by controlling DNA transcription and protein synthesis. This effect on DNA is obtained by the binding of liothyronine to the thyroid receptors attached to DNA. Exogenous liothyronine exerts all the normal effects of the endogenous thyroid T3 hormone. Hence, it increases energy expenditure, accelerates the rate of cellular oxidation stimulating growth, maturation, and metabolism of the body tissues, aids in myelination of nerves and development of synaptic processes in the nervous system and enhances carbohydrate and protein metabolism.",The molecular weight is 650.98.,Liothyronine has a topological polar surface area of 92.78.,The log p value of  is 2.63.,Liothyronine is approved and vet_approved.,Liothyronine is a solid.,True
14060,"Levothyroxine is a synthetically produced form of thyroxine, a major endogenous hormone secreted by the thyroid gland. Also known as L-thyroxine or the brand name product Synthroid, levothyroxine is used primarily to treat hypothyroidism, a condition where the thyroid gland is no longer able to produce sufficient quantities of the thyroid hormones T<sub>4</sub> (tetraiodothyronine or thyroxine) and T<sub>3</sub> (triiodothyronine or ), resulting in diminished down-stream effects of these hormones. Without sufficient quantities of circulating thyroid hormones, symptoms of hypothyroidism begin to develop such as fatigue, increased heart rate, depression, dry skin and hair, muscle cramps, constipation, weight gain, memory impairment, and poor tolerance to cold temperatures. Levothyroxine is indicated as replacement therapy in primary (thyroidal), secondary (pituitary) and tertiary (hypothalamic) congenital or acquired hypothyroidism. It is also indicated as an adjunct to surgery and radioiodine therapy in the management of thyrotropin-dependent well-differentiated thyroid cancer. Oral levothyroxine is a synthetic hormone that exerts the same physiologic effect as endogenous T<sub>4</sub>, thereby maintaining normal T<sub>4</sub> levels when a deficiency is present.  Levothyroxine is a synthetically prepared levo-isomer of the thyroid hormone thyroxine (T<sub>4</sub>, a tetra-iodinated tyrosine derivative) that acts as a replacement in deficiency syndromes such as hypothyroidism. T<sub>4</sub> is the major hormone secreted from the thyroid gland and is chemically identical to the naturally secreted T<sub>4</sub>: it increases metabolic rate, decreases thyroid-stimulating hormone (TSH) production from the anterior lobe of the pituitary gland, and, in peripheral tissues, is converted to T<sub>3</sub>. Thyroxine is released from its precursor protein thyroglobulin through proteolysis and secreted into the blood where is it then peripherally deiodinated to form triiodothyronine (T<sub>3</sub>) which exerts a broad spectrum of stimulatory effects on cell metabolism. T<sub>4</sub> and T<sub>3</sub> have a relative potency of ~1:4. ",The molecular weight is 776.87.,Levothyroxine has a topological polar surface area of 92.78.,The log p value of  is 3.51.,Levothyroxine is approved.,Levothyroxine is a solid.,True
14061,"Diclofenac is a phenylacetic acid derivative and non-steroidal anti-inflammatory drug (NSAID). NSAIDs inhibit cyclooxygenase (COX)-1 and-2 which are the enzyme responsible for producing prostaglandins (PGs). PGs contribute to inflammation and pain signalling. Diclofenac, like other NSAIDs, is often used as first line therapy for acute and chronic pain and inflammation from a variety of causes. Diclofenac was the product of rational drug design based on the structures of , , and. The addition of two chlorine groups in the ortho position of the phenyl ring locks the ring in maximal torsion which appears to be related to increased potency. It is often used in combination with to prevent NSAID-induced gastric ulcers. Diclofenac was first approved by the FDA in July 1988 under the trade name Voltaren, marketed by Novartis (previously Ciba-Geigy). Diclofenac is indicated for use in the treatment of pain and inflammation from varying sources including inflammatory conditions such as osteoarthritis, rheumatoid arthritis, and akylosing spondylitis, as well as injury-related inflammation due to surgery and physical trauma. It is often used in combination with as a gastro-protective agent in patients with high risk of developing NSAID-induced ulcers. Diclofenac reduces inflammation and by extension reduces nociceptive pain and combats fever. It also increases the risk of developing a gastrointestinal ulcer by inhibiting the production of protective mucus in the stomach. Diclofenac inhibits cyclooxygenase-1 and -2, the enzymes responsible for production of prostaglandin (PG) G<sub>2</sub> which is the precursor to other PGs. These molecules have broad activity in pain and inflammation and the inhibition of their production is the common mechanism linking each effect of diclofenac.",The molecular weight is 296.15.,Diclofenac has a topological polar surface area of 49.33.,The log p value of  is 4.58.,Diclofenac is approved and vet_approved.,Diclofenac is a solid.,True
14062,"Diflunisal, a salicylate derivative, is a nonsteroidal anti-inflammatory agent (NSAIA) with pharmacologic actions similar to other prototypical NSAIAs. Diflunisal possesses anti-inflammatory, analgesic and antipyretic activity. Though its mechanism of action has not been clearly established, most of its actions appear to be associated with inhibition of prostaglandin synthesis via the arachidonic acid pathway. Diflunisal is used to relieve pain accompanied with inflammation and in the symptomatic treatment of rheumatoid arthritis and osteoarthritis. For symptomatic treatment of mild to moderate pain accompanied by inflammation (e.g. musculoskeletal trauma, post-dental extraction, post-episiotomy), osteoarthritis, and rheumatoid arthritis. Diflunisal is a nonsteroidal drug with analgesic, anti-inflammatory and antipyretic properties. It is a peripherally-acting non-narcotic analgesic drug. Habituation, tolerance and addiction have not been reported. Diflunisal is a difluorophenyl derivative of salicylic acid. Chemically, diflunisal differs from aspirin (acetylsalicylic acid) in two respects. The first of these two is the presence of a difluorophenyl substituent at carbon 1. The second difference is the removal of the 0-acetyl group from the carbon 4 position. Diflunisal is not metabolized to salicylic acid, and the fluorine atoms are not displaced from the difluorophenyl ring structure. The precise mechanism of the analgesic and anti-inflammatory actions of diflunisal is not known. Diflunisal is a prostaglandin synthetase inhibitor. In animals, prostaglandins sensitize afferent nerves and potentiate the action of bradykinin in inducing pain. Since prostaglandins are known to be among the mediators of pain and inflammation, the mode of action of diflunisal may be due to a decrease of prostaglandins in peripheral tissues.",The molecular weight is 250.2.,Diflunisal has a topological polar surface area of 57.53.,The log p value of  is 4.4.,Diflunisal is approved and investigational.,Diflunisal is a solid.,True
14063,"A highly polar organic liquid, that is used widely as a chemical solvent. Because of its ability to penetrate biological membranes, it is used as a vehicle for topical application of pharmaceuticals. It is also used to protect tissue during cryopreservation. Dimethyl sulfoxide shows a range of pharmacological activity including analgesia and anti-inflammation. For the symptomatic relief of patients with interstitial cystitis. Dimethyl Sulfoxide may have anti-inflammatory, antioxidant and analgesic activities. Dimethyl Sulfoxide also readily penetrates cellular membranes. The membrane-penetrating ability of dimethyl sulfoxide may enhance diffusion of other substances through the skin. For this reason, mixtures of idoxuridine and dimethyl sulfoxide have been used for topical treatment of herpes zoster in the United Kingdom. The mechanism of dimethyl sulfoxide's actions is not well understood. Dimethyl sulfoxide has demonstrated antioxidant activity in certain biological settings. For example, the cardiovascular protective effect of dimethyl sulfoxide in copper-deficient rats is thought to occur by an antioxidant mechanism. It is also thought that dimethyl sulfoxide's possible anti-inflammatory activity is due to antioxidant action.",The molecular weight is 78.13.,Dimethyl sulfoxide has a topological polar surface area of 17.07.,The log p value of  is -1.38.,Dimethyl sulfoxide is approved and vet_approved.,Dimethyl sulfoxide is a liquid.,True
14064,"Liotrix is a synthetically derived thyroid hormone replacement preparation. It consists of levothyroxine sodium (thyroxine, T4) and liothyronine sodium (triiodothyronine, T3) in a 4 to 1 ratio by weight. Liotrix was developed when it was believed that serum levels of both T4 and T3 were maintained by direct thyroidal secretion. It is now known that the thyroid gland secretes approximately ten times more T4 than T3 and that 80% of serum T3 is derived from deiodination of T4 in peripheral tissues. Administration of levothyroxine alone is sufficient for maintaining serum T4 and T3 levels in most patients and combination hormone replacement therapy generally offers no therapeutic advantage. In fact, administration of T3 may result in supratherapeutic levels of T3. May be used to treat primary, secondary or tertiary hypothyroidism. May also be used to suppress thyroid stimulating hormone (TSH) secretion in patients with simple (nontoxic) goiter, subacute or chronic lymphocytic thyroiditis multinodular goiter, and in the management of thyroid cancer. May be used in conjunction with other antithyroid agents to treat thyrotoxicosis to prevent goitrogenesis and hypothyroidism. May also be used for differential diagnosis of suspected mild hyperthyroidism or thyroid gland autonomy. Thyroid hormone drugs are natural or synthetic preparations containing T<sub>4</sub> or T<sub>3</sub> or both. T<sub>4</sub> and T<sub>3</sub> are produced in the human thyroid gland by the iodination and coupling of the amino acid tyrosine. Liotrix is a synthetic preparation of T4 and T3 in a 4:1 weight-based ratio. These hormones enhance oxygen consumption by most tissues of the body and increase the basal metabolic rate and the metabolism of carbohydrates, lipids and proteins. Thus, they exert a profound influence on every organ system in the body and are of particular importance in the development of the central nervous system. The hormones, T<sub>4</sub> and T<sub>3</sub>, are tyrosine-based hormones produced by the thyroid gland. Iodine is an important component in their synthesis. The major secreted form of thyroid hormone is T4. T4 is converted T3, the more active thyroid hormone, by deiodinases in peripheral tissues. T3 acts in the body to increase basal metabolic rate, alter protein synthesis and increase the body's sensitivity to catecholamines (such as adrenaline). Thyroid hormones are essential for proper development and differentiation of all cells of the human body. T<sub>4</sub> and T<sub>3</sub> regulate protein, fat and carbohydrate metabolism to varying extents. The most pronounced effect of the hormones is in altering how human cells use energetic compounds. The thyroid hormone derivatives bind to the thyroid hormone receptors initially to initiate their downstream effects.",,,,Liotrix is approved.,Liotrix is a solid.,True
14065,"An isoflavonoid derived from soy products. It inhibits protein-tyrosine kinase and topoisomerase-II (DNA topoisomerases, type II) activity and is used as an antineoplastic and antitumor agent. Experimentally, it has been shown to induce G2 phase arrest in human and murine cell lines. Currently Genistein is being studied in clinical trials as a treatment for prostate cancer.  Genistein may inhibit cancer cell growth by blocking enzymes required for cell growth. ",,,,Genistein is investigational.,Genistein is a solid.,True
14066,,,,,Tetraiodothyroacetic acid is experimental.,Tetraiodothyroacetic acid is a solid.,False
14067,,,,,"6,4'-Dihydroxy-3-Methyl-3',5'-Dibromoflavone is experimental.","6,4'-Dihydroxy-3-Methyl-3',5'-Dibromoflavone is a solid.",False
14068,,,,,O-Trifluoromethylphenyl Anthranilic Acid is experimental.,O-Trifluoromethylphenyl Anthranilic Acid is a solid.,False
14069,"An anthranilic acid derivative with analgesic, anti-inflammatory, and antipyretic properties. It is used in musculoskeletal and joint disorders and administered by mouth and topically. (From Martindale, The Extra Pharmacopoeia, 30th ed, p16)",The molecular weight is 281.23.,Flufenamic acid has a topological polar surface area of 49.33.,The log p value of  is 5.38.,Flufenamic acid is approved.,Flufenamic acid is a solid.,True
14070,,,,,"2,4,6-Tribromophenol is experimental.","2,4,6-Tribromophenol is a solid.",False
14071,,,,,"N-(M-Trifluoromethylphenyl) Phenoxazine-4,6-Dicarboxylic Acid is experimental.","N-(M-Trifluoromethylphenyl) Phenoxazine-4,6-Dicarboxylic Acid is a solid.",False
14072,"Resveratrol (3,5,4'-trihydroxystilbene) is a polyphenolic phytoalexin. It is a stilbenoid, a derivate of stilbene, and is produced in plants with the help of the enzyme stilbene synthase. It exists as cis-(Z) and trans-(E) isomers. The trans- form can undergo isomerisation to the cis- form when heated or exposed to ultraviolet irradiation. In a 2004 issue of Science, Dr. Sinclair of Harvard University said resveratrol is not an easy molecule to protect from oxidation. It has been claimed that it is readily degraded by exposure to light, heat, and oxygen. However, studies find that Trans-resveratrol undergoes negligible oxidation in normal atmosphere at room temperature. Being investigated for the treatment of Herpes labialis infections (cold sores). Resveratrol, a phytoalexin, has been found to inhibit herpes simplex virus types 1 and 2 (HSV-1 and HSV-2) replication in a dose-dependent, reversible manner, although this is only one of its many pharmaceutical properties. In some countries where there is higher consumption of red wine, there appears to be a lower incidence of heart disease. Other benefits of resveratrol include its anti-inflammatory and antioxidant effects. In preclinical studies, Resveratrol has been found to have potential anticancer properties. Resveratrol suppresses NF-kappaB (NF-kappaB) activation in HSV infected cells. Reports have indicated that HSV activates NF-kappaB during productive infection and this may be an essential aspect of its replication scheme. ",,,,Resveratrol is investigational.,Resveratrol is a solid.,True
14073,,,,,Pentabromophenol is experimental.,Pentabromophenol is a solid.,False
14074,,,,,"3',5'-Dinitro-N-Acetyl-L-Thyronine is experimental.","3',5'-Dinitro-N-Acetyl-L-Thyronine is a solid.",False
14075,,,,,"3,3',5,5'-tetrachlorobiphenyl-4,4'-diol is experimental.","3,3',5,5'-tetrachlorobiphenyl-4,4'-diol is a solid.",False
14076,,,,,"Dibenzofuran-4,6-Dicarboxylic Acid is experimental.","Dibenzofuran-4,6-Dicarboxylic Acid is a solid.",False
14077,,,,,8-anilinonaphthalene-1-sulfonic acid is experimental.,8-anilinonaphthalene-1-sulfonic acid is a solid.,False
14078,,,,,"2-HYDROXY-3,5-DIIODOBENZOIC ACID is experimental.","2-HYDROXY-3,5-DIIODOBENZOIC ACID is a solid.",False
14079,,,,,2-benzoic acid is experimental.,2-benzoic acid is a solid.,False
14080,"NRP409 is a triiodothyronine (T3) hormone, being investigated by New River Pharmaceuticals as a treatment for patients with primary hypothyroidism. For use in treatment of hypothyroidism. The company is hoping that NRP409 will mark a significant improvement in thyroid HRT by reducing the variability of the more active hormone's availability, while reducing the safety risk associated with other T3 based therapies. NRP409 is presumed to work like the endogenous thyroid hormone thyroxine (T<sub>4</sub>, a tetra-iodinated tyrosine derivative). In the liver and kidney, T<sub>4</sub> is converted to T<sub>3</sub>, the active metabolite. In order to increase solubility, the thyroid hormones attach to thyroid hormone binding proteins, thyroxin-binding globulin, and thyroxin-binding prealbumin (transthyretin). Transport and binding to thyroid hormone receptors in the cytoplasm and nucleus then takes place. Thus by acting as a replacement for natural thyroxine, symptoms of thyroxine deficiency are relieved.",,,,NRP409 is investigational.,NRP409 is a solid.,True
14081,"Fx-1006A is a small molecule compound with the potential to treat genetic disorders, such as familial amyloid cardiomyopathy (FAC) and familial amyloid polyneuropathy (FAP). Investigated for use/treatment in amyloidosis. Fx-1006A is a first-in-class, disease-modifying compound that is designed to inhibit the formation of amyloid deposits by preventing the misfolding and deposition of the transthyretin protein (TTR), which is associated with amyloidosis.",,,,Fx-1006A is investigational.,Fx-1006A is a solid.,True
14082,,,,,3-methylidene}amino)oxy]propanoic acid is experimental.,3-methylidene}amino)oxy]propanoic acid is a solid.,False
14083,,,,,"2-(2,6-DICHLOROPHENYL)-1,3-BENZOXAZOLE-6-CARBOXYLIC ACID is experimental.","2-(2,6-DICHLOROPHENYL)-1,3-BENZOXAZOLE-6-CARBOXYLIC ACID is a solid.",False
14084,,,,,"2',6'-DIFLUOROBIPHENYL-4-CARBOXYLIC ACID is experimental.","2',6'-DIFLUOROBIPHENYL-4-CARBOXYLIC ACID is a solid.",False
14085,,,,,"2',4'-DICHLORO-4-HYDROXY-1,1'-BIPHENYL-3-CARBOXYLIC ACID is experimental.","2',4'-DICHLORO-4-HYDROXY-1,1'-BIPHENYL-3-CARBOXYLIC ACID is a solid.",False
14086,,,,,1-Naphthylamine-5-sulfonic acid is experimental.,1-Naphthylamine-5-sulfonic acid is a solid.,False
14087,,,,,(2S)-3--2-methylpropanoic acid is experimental.,(2S)-3--2-methylpropanoic acid is a solid.,False
14088,,,,,3-propanoic acid is experimental.,3-propanoic acid is a solid.,False
14089,,,,,3-({amino}oxy)propanoic acid is experimental.,3-({amino}oxy)propanoic acid is a solid.,False
14090,,,,,"N-(3,5-dibromo-4-hydroxyphenyl)-2,6-dimethylbenzamide is experimental.","N-(3,5-dibromo-4-hydroxyphenyl)-2,6-dimethylbenzamide is a solid.",False
14091,,,,,"2,5-dichloro-N-(3,5-dibromo-4-hydroxyphenyl)benzamide is experimental.","2,5-dichloro-N-(3,5-dibromo-4-hydroxyphenyl)benzamide is a solid.",False
14092,,,,,"N-(3,5-dibromo-4-hydroxyphenyl)-4-hydroxy-3,5-dimethylbenzamide is experimental.","N-(3,5-dibromo-4-hydroxyphenyl)-4-hydroxy-3,5-dimethylbenzamide is a solid.",False
14093,,,,,"3',5'-DIFLUOROBIPHENYL-4-CARBOXYLIC ACID is experimental.","3',5'-DIFLUOROBIPHENYL-4-CARBOXYLIC ACID is a solid.",False
14094,,,,,"3',5'-DIBROMO-2',4,4',6'-TETRAHYDROXY AURONE is experimental.","3',5'-DIBROMO-2',4,4',6'-TETRAHYDROXY AURONE is a solid.",False
14095,,,,,METHYL N--BETA-ALANINATE is experimental.,METHYL N--BETA-ALANINATE is a solid.,False
14096,,,,,N--BETA-ALANINE is experimental.,N--BETA-ALANINE is a solid.,False
14097,,,,,"2,6-dimethyl-4-phenol is experimental.","2,6-dimethyl-4-phenol is a solid.",False
14098,,,,,"2,6-dibromo-4-phenol is experimental.","2,6-dibromo-4-phenol is a solid.",False
14099,,,,,"3,5-dibromobiphenyl-4-ol is experimental.","3,5-dibromobiphenyl-4-ol is a solid.",False
14100,,,,,"2,6-dibromo-4-phenoxyphenol is experimental.","2,6-dibromo-4-phenoxyphenol is a solid.",False
14101,,,,,"N-(3,5-dibromo-4-hydroxyphenyl)benzamide is experimental.","N-(3,5-dibromo-4-hydroxyphenyl)benzamide is a solid.",False
14102,,,,,"4-(1,3-BENZOXAZOL-2-YL)-2,6-DIMETHYLPHENOL is experimental.","4-(1,3-BENZOXAZOL-2-YL)-2,6-DIMETHYLPHENOL is a solid.",False
14103,,,,,"4-(1,3-BENZOXAZOL-2-YL)-2,6-DIBROMOPHENOL is experimental.","4-(1,3-BENZOXAZOL-2-YL)-2,6-DIBROMOPHENOL is a solid.",False
14104,,,,,"2-(3,5-DIMETHYLPHENYL)-1,3-BENZOXAZOLE is experimental.","2-(3,5-DIMETHYLPHENYL)-1,3-BENZOXAZOLE is a solid.",False
14105,"Thyroid extract is dried and powdered thyroid glands from pigs containing tiiodothyronine (T3) and thyroxine (T4) used to supplement low or absent thyroid activity. Thyroid extract has been described in literature to treat hypothyroidism since 1891 but its use dates back as far as the 6th century. Thyroid extract is no longer considered a first line therapy as it delivers a dose that is inconsistent with the stated strength of the tablet. Currently, patients are more likely to be treated with. Thyroid extract is indicated for replacement therapy in decreased or absent thyroid function. Thyroid extract increases the metabolic rate of patients with hypothyroidism. The therapeutic index of thyroid extract is wide, as patients can be given varying doses. The duration of action is long as thyroid extract is generally given once daily. Patients should not use thyroid extract for weight loss. T3 binding to the thyroid hormone receptor (TR), changes the conformation of the TR, allowing it to bind to the retinoid X receptor (RXR) and form a coactivator complex. The coactivator complex has histone acetyltransferase activity, which activates genes. In the absence of T3, TR and RXR form a corepressor complex with histone deacetylase activity, which represses genes. The macroscopic effects of thyroid hormones is an increase in the metabolic rate. T4 has similar but weaker activity to T3.",,,,"Thyroid, porcine is approved.","Thyroid, porcine is a solid.",True
14106,"Hydroxocobalamin, also known as vitamin B12a and hydroxycobalamin, is an injectable form of vitamin B 12 that has been used therapeutically to treat vitamin B 12 deficiency. It is also used in cyanide poisoning, Leber's optic atrophy, and toxic amblyopia. For treatment of pernicious anemia and the prevention and treatment of vitamin B12 deficiency arising from alcoholism, malabsorption, tapeworm infestation, celiac, hyperthyroidism, hepatic-biliary tract disease, persistent diarrhea, ileal resection, pancreatic cancer, renal disease, prolonged stress, vegan diets, macrobiotic diets or other restrictive diets. Also for the treatment of known or suspected cyanide poisoning. Hydroxocobalamin is a synthetic, injectable form of Vitamin B12. Hydroxocobalamin is actually a precursor of two cofactors or vitamins (Vitamin B12 and Methylcobalamin) which are involved in various biological systems in man. Vitamin B12 is required for the conversion of methylmalonate to succinate. Deficiency of this enzyme could therefore interfere with the production of lipoprotein in myelin sheath tissue and so give rise to neurological lesions. The second cofactor, Methylcobalamin, is necessary for the conversion of homocysteine to methionine which is essential for the metabolism of folic acid. Deficiency of tetrahydrafolate leads to reduced synthesis of thymidylate resulting in reduced synthesis of DNA which is essential for cell maturation. Vitamin B12 is also concerned in the maintenance of sulphydryl groups in reduced form, deficiency leading to decreased amounts of reduced SH content of erythrocytes and liver cells. Overall, vitamin B12 acts as a coenzyme for various metabolic functions, including fat and carbohydrate metabolism and protein synthesis. It is necessary for growth, cell replication, hematopoiesis, and nucleoprotein as well as myelin synthesis. This is largely due to its effects on metabolism of methionine folic acid, and malonic acid. Vitamin B12 exists in four major forms referred to collectively as cobalamins; deoxyadenosylcobalamin, methylcobalamin, hydroxocobalamin, and cyanocobalamin. Two of these, methylcobalamin and 5-deoxyadenosyl cobalamin, are primarily used by the body. Methionine synthase needs methylcobalamin as a cofactor. This enzyme is involved in the conversion of the amino acid homocysteine into methionine. Methionine in turn is required for DNA methylation. 5-Deoxyadenosyl cobalamin is a cofactor needed by the enzyme that converts L-methylmalonyl-CoA to succinyl-CoA. This conversion is an important step in the extraction of energy from proteins and fats. Furthermore, succinyl CoA is necessary for the production of hemoglobin, the substances that carries oxygen in red blood cells.",The molecular weight is 1346.38.,Hydroxocobalamin has a topological polar surface area of 508.94.,,Hydroxocobalamin is approved.,Hydroxocobalamin is a solid.,True
14107,"Glycyrrhizic acid is extracted from the root of the licorice plant; _Glycyrrhiza glabra_. It is a triterpene glycoside with glycyrrhetinic acid that possesses a wide range of pharmacological and biological activities. When extracted from the plant, it can be obtained in the form of ammonium glycyrrhizin and mono-ammonium glycyrrhizin. Glycyrrhizic acid has been developed in Japan and China as a hepatoprotective drug in cases of chronic hepatitis. From January 2014, glycyrrhizic acid as part of the licorice extract was approved by the FDA as an existing food sweetener. It was approved by Health Canada to be used in over-the-counter products but all the products are currently on the status canceled post marketed. Glycyrrhizic acid is widely applied in foods as a natural sweetener. As a therapeutic agent, is has been used in a vast variety of formulations as it is reported to be anti-inflammatory, anti-ulcer, anti-allergic, antioxidant, anti-tumor, anti-diabetic and hepatoprotective. Due to this properties, its indications have been: treatment of premenstrual syndrome, treatment of viral infections, anti-lipidemic and antihyperglycemic. It is also known to be used as a remedy for peptic ulcer and other stomach diseases. Glycyrrhizic acid was reported to present antiallergic, antiviral and anti-inflammatory activities as well as improvements in glucose tolerance.  Glycyrrhizic acid can be found in the alpha and beta forms. The alpha form is predominant in the liver and duodenum and thus, it is thought that the anti-inflammatory liver effect of this drug are mainly due to the action of this isomer. Glycyrrhizic acid anti-inflammatory effect is generated via suppression of TNF alpha and caspase 3. It also inhibits the translocation of NFkB into the nuclei and conjugates free radicals. Some studies have shown a glycyrrhizic-driven inhibition of CD4+ T cell proliferation via JNK, ERK and PI3K/AKT.",The molecular weight is 822.94.,Glycyrrhizic acid has a topological polar surface area of 267.04.,The log p value of  is 3.03.,Glycyrrhizic acid is approved and experimental.,Glycyrrhizic acid is a solid.,True
14108,"Ubidecarenone, also called coenzyme Q10, is a 1,4-benzoquinone. From his name (Q10), the Q refers to the constitutive quinone group, and 10 is related to the number of isoprenyl subunits in its tail. It is a powerful antioxidant, a lipid-soluble and essential cofactor in mitochondrial oxidative phosphorylation. The ubidecarenone is the coenzyme destined for mitochondrial enzyme complexes involved in oxidative phosphorylation in the production of ATP. It is fundamental for cells that have a high metabolic demand. Ubidecarenone is sold as a dietary supplement and is not FDA approved as a drug thus, it is not meant to treat, cure or prevent any disease. FDA does not approve this dietary supplements before sold nor regulate the manufacturing process. The diet supplements containing ubidecarenone are indicated, as stated in the product label, to assist individuals with cardiovascular complaints including congestive heart failure and systolic hypertension. In the product, ubidecarenone is used to increase the cardiac input as well as for the prevention of several other diseases like Parkinson, fibromyalgia, migraine, periodontal disease and diabetes, based on preclinical studies. It is important to highlight that these products are not FDA approved and it is recommended to use under discretion. Ubidecarenon has roles in many prysiological process including sulfide oxidation, regulation of mitochondrial permeability transition pore and translocation of protons and calcium ions accross biological membranes. Studies have shown its benefitial effect in treating cancer, statin myopathy, congestive heart failure and hypertension.  Ubidecarenone is an essential cofactor in the mitochondrial electron transport chain. Its functions are the acceptance of electrons from the complex I and II and this activity is vital for the production of ATP. It acts as a mobile redox agent shuttling electrons and protons in the electron transport chain. Ubidecarenone also presents antioxidant activity in mitochondria and cellular membranes, protecting against peroxidation of lipid membranes as well as inhibiting oxidation of LDL-cholesterol.",The molecular weight is 863.36.,Ubidecarenone has a topological polar surface area of 52.6.,The log p value of  is 20.43.,Ubidecarenone is approved and investigational and nutraceutical.,Ubidecarenone is a solid.,True
14109,"Tocopherol exists in four different forms designated as α, β, δ, and γ. They present strong antioxidant activities, and it is determined as the major form of vitamin E. Tocopherol, as a group, is composed of soluble phenolic compounds that consist of a chromanol ring and a 16-carbon phytyl chain. The classification of the tocopherol molecules is designated depending on the number and position of the methyl substituent in the chromanol ring. The different types of tocopherol can be presented trimethylated, dimethylated or methylated in the positions 5-, 7- and 8-. When the carbons at position 5- and 7- are not methylated, they can function as electrophilic centers that can trap reactive oxygen and nitrogen species. Tocopherols can be found in the diet as part of vegetable oil such as corn, soybean, sesame, and cottonseed. It is currently under the list of substances generally recognized as safe (GRAS) in the FDA for the use of human consumption. Tocopherol can be used as a dietary supplement for patients with a deficit of vitamin E; this is mainly prescribed in the alpha form. Vitamin E deficiency is rare, and it is primarily found in premature babies of very low birth weight, patients with fat malabsorption or patients with abetalipoproteinemia. The antioxidant effects of tocopherol can be translated into different changes at the pharmacodynamic level. In vitro studies have shown that this antioxidant activity can produce modification in protein kinase C (PKC) which will later be translated into an inhibition of cell death. Some other derivate effects are the anti-inflammatory properties of tocopherol which can be related to the modulation of cytokines or prostaglandins, prostanoids and thromboxanes. Tocopherol acts as a radical scavenger. It mainly acts as an antioxidant for lipid bilayers. Tocopherol's functions depend on the H-atom donating ability, location, and movement within the membrane, as well as the efficiency in the radical recycling by some cytosolic reductants such as ascorbate. Tocopherol actions are related to the trap of radicals, and it has been shown that even in the absence of substituents in the ortho-positions, tocopherol can trap more than two radicals. The type of radicals available for tocopherol are alkyl and peroxy. ",,,,Tocopherol is approved and investigational.,Tocopherol is a liquid.,True
14110,"Alpha-tocopherol is the primary form of vitamin E that is preferentially used by the human body to meet appropriate dietary requirements. In particular, the RRR-alpha-tocopherol (or sometimes called the d-alpha-tocopherol stereoisomer) stereoisomer is considered the natural formation of alpha-tocopherol and generally exhibits the greatest bioavailability out of all of the alpha-tocopherol stereoisomers. Moreover, RRR-alpha-tocopherol acetate is a relatively stabilized form of vitamin E that is most commonly used as a food additive when needed. The primary health-related use for which alpha-tocopherol acetate is formally indicated is as a dietary supplement for patients who demonstrate a genuine vitamin E deficiency. At the same time, vitamin E deficiency is generally quite rare but may occur in premature babies of very low birth weight (< 1500 grams), individuals with fat-malabsorption disorders (as fat is required for the digestive tract to absorb vitamin E), or individuals with abetalipoproteinemia - a rare, inherited disorder that causes poor absorption of dietary fat - who require extremely large doses of supplemental vitamin E daily (around 100 mg/kg or 5-10 g/day). In all such cases, alpha-tocopherol is largely the preferred form of vitamin E to be administered. Of the eight separate variants of vitamin E, alpha-tocopherol is the predominant form of vitamin E in human and animal tissues, and it has the highest bioavailability. This is because the liver preferentially resecretes only alpha-tocopherol by way of the hepatic alpha-tocopherol transfer protein (alpha-TTP); the liver metabolizes and excretes all the other vitamin E variants, which is why blood and cellular concentrations of other forms of vitamin E other than alpha-tocopherol are ultimately lower. Vitamin E's antioxidant capabilities are perhaps the primary biological action associated with alpha-tocopherol. In general, antioxidants protect cells from the damaging effects of free radicals, which are molecules that consist of an unshared electron. These unshared electrons are highly energetic and react rapidly with oxygen to form reactive oxygen species (ROS). In doing so, free radicals are capable of damaging cells, which may facilitate their contribution to the development of various diseases. Moreover, the human body naturally forms ROS when it converts food into energy and is also exposed to environmental free radicals contained in cigarette smoke, air pollution, or ultraviolet radiation from the sun. It is believed that perhaps vitamin E antioxidants might be able to protect body cells from the damaging effects of such frequent free radical and ROS exposure.",,,,alpha-Tocopherol acetate is approved.,alpha-Tocopherol acetate is a liquid.,True
14111,"An important regulator of gene expression during growth and development, and in neoplasms. Tretinoin, also known as retinoic acid and derived from maternal vitamin A, is essential for normal growth; and embryonic development. An excess of tretinoin can be teratogenic. It is used in the treatment of psoriasis; acne vulgaris; and several other skin diseases. It has also been approved for use in promyelocytic leukemia (leukemia, promyelocytic, acute). For topical treatment of cutaneous lesions in patients with AIDS-related Kaposi's sarcoma. Alitretinoin (9-<i>cis</i>-retinoic acid) is a naturally-occurring endogenous retinoid indicated for topical treatment of cutaneous lesions in patients with AIDS-related Kaposi's sarcoma. Alitretinoin inhibits the growth of Kaposi's sarcoma (KS) cells <i>in vitro</i>. Alitretinoin binds to and activates all known intracellular retinoid receptor subtypes (RARa, RARb, RARg, RXRa, RXRb and RXRg). Once activated these receptors function as transcription factors that regulate the expression of genes that control the process of cellular differentiation and proliferation in both normal and neoplastic cells.",The molecular weight is 300.44.,Alitretinoin has a topological polar surface area of 37.3.,The log p value of  is 6.74.,Alitretinoin is approved and investigational.,Alitretinoin is a solid.,True
14112,"Etretinate is a medication used to treat severe psoriasis. It is a synthetic aromatic retinoid. The mechanism of action of etretinate is still incompletely understood although, like retinoic acid, it is thought to interfere with the terminal differentiation of keratinocytes. It is thought to bind to the retinoic acid receptors. Etretinate is also believed to enhance the binding of cAMP to the regulatory RI subunit of cAMP dependent protein kinases. Etretinate was taken off the market in Canada in 1996 and America in 1998 due to the risk of birth defects. Etretinate is now used to treat T-cell lymphomas. It also appears to inhibit NADH oxidase activity. For the treatment of severe psoriasis in adults. The active metabolite responsible for etretinate's effects, acitretin, is a retinoid. Retinoids have a structure similar to vitamin A and are involved in the normal growth of skin cells. Acitretin works by inhibiting the excessive cell growth and keratinisation (process by which skin cells become thickened due to the deposition of a protein within them) seen in psoriasis. It therefore reduces the thickening of the skin, plaque formation and scaling. The mechanism of action of the active metabolite, acitretin, is unknown, however it is believed to work by targeting specific receptors (retinoid receptors) in the skin which help normalize the growth cycle of skin cells.",The molecular weight is 354.49.,Etretinate has a topological polar surface area of 35.53.,The log p value of  is 6.82.,Etretinate is withdrawn.,Etretinate is a solid.,True
14113,"Tamibarotene is a novel synthetic retinoid for acute promyelocytic leukaemia (APL). Tamibarotene is currently approved in Japan for treatment of recurrent APL, and is undergoing clinical trials in the United States. Investigated for use/treatment in leukemia (unspecified). Tamibarotene is a new synthetic retinoid drug recently approved for relapsed or refractory acute promyelocytic leukemia (APL) in Japan. It is a specific agonist for retinoic acid receptor alpha/beta. Compared to all-trans retinoic acid (ATRA), a natural retinoid indicated for a first-line treatment of APL, tamibarotene is chemically more stable and several times more potent as an inducer of differentiation in promyelocytic leukemia cells. In contrast to ATRA, whose plasma concentration declines considerably during daily administration, tamibarotene sustains plasma level probably due to a lower affinity for cellular retinoic acid binding protein. Furthermore, adverse side effects were milder than those of ATRA in clinical trials. Tamibarotene is a specific agonist for retinoic acid receptor alpha/beta with possible binding to retinoid X receptors (RXR).",The molecular weight is 351.45.,Tamibarotene has a topological polar surface area of 66.4.,The log p value of  is 6.38.,Tamibarotene is investigational.,Tamibarotene is a solid.,True
14114,"Iron dextran is a dark brown, slightly viscous liquid complex of ferric hydroxide and dextran for intravenous or intramuscular use. Iron Dextran is used for the treatment of patients with documented iron deficiency in which oral administration is unsatisfactory or impossible. For treatment of patients with documented iron deficiency in whom oral administration is unsatisfactory or impossible. Also used to replenish body iron stores in Non-Dialysis Dependent-Chronic Kidney Disease (NDD-CKD) patients receiving or not receiving erythropoietin and in Hemodialysis Dependent (HDD-CKD) and Peritoneal Dialysis Dependent (PDD-CKD) - Chronic Kidney Disease patients receiving an erythropoietin. Iron dextran is a dark brown, slightly viscous sterile liquid complex of ferric hydroxide and dextran for intravenous or intramuscular use. It is for treatment of patients with documented iron deficiency in whom oral administration is unsatisfactory or impossible. Iron is essential to the formation of hemoglobin and to the function and formation of other heme and nonheme compounds. Untreated depletion of iron stores leads to iron-deficient erythropoiesis and, in turn, to iron deficiency anemia. After iron dextran is injected, the circulating iron dextran is removed from the plasma by cells of the reticuloendothelial system, which split the complex into its components of iron and dextran. The iron is immediately bound to the available protein moieties to form hemosiderin or ferritin, the physiological forms of iron, or to a lesser extent to transferrin. This iron which is subject to physiological control replenishes hemoglobin and depleted iron stores.",,,,Iron Dextran is approved and vet_approved.,Iron Dextran is a solid.,True
14115,"Bismuth subsalicylate is the active ingredient in the popular medication Pepto-Bismol that is used to treat nausea, heartburn, indigestion, upset stomach, diarrhea, and other temporary discomforts of the stomach and gastrointestinal tract. It is also the main ingredient of Kaopectate. It displays anti-inflammatory action (due to salicylic acid) and also acts as an antacid and mild antibiotic. Used to treat nausea, heartburn, indigestion, upset stomach, diarrhea, and other temporary discomforts of the stomach and gastrointestinal tract. Bismuth subsalicylate displays anti-inflammatory action (due to salicylic acid) and also acts as an antacid and mild antibiotic. It can also cause a black tongue and black stools in some users of the drug, when it combines with trace amounts of sulfur in their saliva and gastrointestinal tract. This discoloration is temporary and harmless. As an antidiarrheal, the exact mechanism has not been determined. Bismuth subsalicylate may exert its antidiarrheal action not only by stimulating absorption of fluid and electrolytes across the intestinal wall (antisecretory action) but also, when hydrolyzed to salicylic acid, by inhibiting synthesis of a prostaglandin responsible for intestinal inflammation and hypermotility. In addition, bismuth subsalicylate binds toxins produced by Escherichia coli. Both bismuth subsalicylate and the intestinal reaction products, bismuth oxychloride and bismuth hydroxide, are believed to have bactericidal action. As an antacid, bismuth has weak antacid properties.",The molecular weight is 362.09.,Bismuth subsalicylate has a topological polar surface area of 55.76.,The log p value of  is 0.34.,Bismuth subsalicylate is approved and vet_approved.,Bismuth subsalicylate is a solid.,True
14116,"Gallium nitrate is a drug that is used to treat hyper-calcemia, or too much calcium in the blood. This condition may occur when individuals develop various types of cancer. Gallium nitrate is also known by the common brand name Ganite. For the treatment of hypercalcemia. Also intended for the treatment of non-hodgkin's lymphoma. Gallium nitrate exerts hypocalcemic effect by inhibiting calcium resorption from bone, possibly by stabilizing bone matrix, thereby reducing increased bone turnover. Gallium nitrate inhibits the growth of various lymphoma cell lines in vitro and exhibits antitumor activity in patients with lymphoma. The mechanism(s) of cytotoxicity is (are) only partly understood but appears to involve a two-step process: (1) targeting of gallium to cells, and (2) acting on multiple, specific intracellular processes. Gallium shares certain chemical properties with iron; therefore, it binds avidly to the iron transport protein transferrin. Transferrin-gallium complexes preferentially target cells that express transferrin receptors on their surface. Expression of transferrin receptors is particularly high on lymphoma cells. Cellular uptake of the gallium-transferrin complex leads to inhibition of cellular proliferation primarily via disruption of iron transport and homeostasis and blockade of ribonucleotide reductase. Recent studies have shown that cellular uptake of gallium leads to activation of caspases and induction of apoptosis. In phase II trials in patients with relapsed or refractory lymphoma, the antitumor activity of gallium nitrate is similar to, or better than, that of other commonly used chemotherapeutic agents.  Gallium nitrate is believed to exert a hypocalcemic effect by inhibiting calcium resorption from bone. Gallium nitrate localizes preferentially where bone resorption and remodeling is occurring, and inhibits osteoclast activity. Inhibition of resorption may occur via a reduction in increased bone turnover. It seems to enhance hydroxyapatite function, inhibit osteocalcin, and inhibit the vacuolar ATPase on the osteoclast ruffled membrane. All these aid in the reduction of bone resorption.",The molecular weight is 255.74.,Gallium nitrate has a topological polar surface area of 68.88.,,Gallium nitrate is approved and investigational.,Gallium nitrate is a solid.,True
14117,"Chromium is a transition element with the chemical symbol Cr and atomic number 24 that belongs to Group 6 of the periodic table. It is used in various chemical, industrial and manufacturing applications such as wood preservation and metallurgy. The uses of chromium compounds depend on the valency of chromium, where trivalent Cr (III) compounds are used for dietary Cr supplementation and hexavalent Cr (VI) compounds are used as corrosion inhibitors in commercial settings and are known to be human carcinogens. Humans can be exposed to chromium via ingestion, inhalation, and dermal or ocular exposure. Trivalent chromium (Cr(III)) ion is considered to be an essential dietary trace element as it is involved in metabolism of blood glucose, regulation of insulin resistance and metabolism of lipids. Clinical trials and other studies suggest the evidence of chromium intake improving glucose tolerance in patients with Type I and II diabetes, however its clinical application in the standard management of type II diabetes mellitus is not established. Chromium deficiency has been associated with a diabetic-like state, impaired growth, decreased fertility and increased risk of cardiovascular diseases. Indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN), to maintain chromium serum levels and to prevent depletion of endogenous stores and subsequent deficiency symptoms. Trivalent chromium is part of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Chromium increases insulin binding to cells, increases insulin receptor density and activates insulin receptor kinase leading to enhanced insulin sensitivity. In chromium deficiency, intravenous administration of chromium resulted in normalization of the glucose tolerance curve from the diabetic-like curve typical of chromium deficiency.  Chromium is an essential nutrient involved in the metabolism of glucose, insulin and blood lipids. Its role in potentiating insulin signalling cascades has been implicated in several studies. Chromium upregulates insulin-stimulated insulin signal transduction via affecting effector molecules downstream of the insulin receptor (IR). IR-mediated signalling pathway involves phoshorylation of multiple intracellular domains and protein kinases, and downstream effector molecules. Upon activation by ligands, intracellular β-subunit of IR autophosphorylates and activates tyrosine kinase domain of the IR, followed by activation and phosphorylation of regulatory proteins and downstream signalling effectors including phosphatidylinositol 2-kinase (PI3K). PI3K activates further downstream reaction cascades to activate protein kinase B (Akt) to ultimately promote translocation of glucose transporter-4 (Glut4)-vesicles from the cytoplasm to the cell surface and regulate glucose uptake. Chromium enhances the kinase activity of insulin receptor β and increases the activity of downstream effectors, pI3-kinase and Akt. ",,,,Chromium is approved.,Chromium is a solid.,True
14118,"Rose bengal is a pink stain derived as an analogue of fluorescein. Its disodium salt in ophthalmic solutions has been used as a diagnostic agent in suspected damage to conjunctival and corneal cells. It is also used in laboratory settings, including the preparation of Foraminifera for microscopic analysis and suppression of bacterial growth in several microbiological media. A direct cytotoxic effect of Rose bengal on microorganisms and cancer cells has been observed, questioning its potential antitumor actions via intralesional injections. The clinical applications of rose bengal as injectable formulation under the name PV-10 in melanoma, breast cancer and skin conditions such as eczema and psoriasis are being investigated in clinical trials. Indicated as a diagnostic agent in routine ocular examinations or when superficial conjunctiva or corneal tissue change is suspected, and as an aid in the diagnosis of keratoconjunctivitis sicca, keratitis, abrasions or corrosions as well as the detection of foreign bodies. Rose bengal is a staining agent that visualized ocular surfaces of both diseased and dead cells _in vivo_. It has also shown to stain healthy cultured cells, including rabbit corneal epithelial cells, in a rapid, dose-dependent manner. Various studies demonstrate the cytotoxic effects of rose bengal in different cell cultures, including smooth-muscle cells from human intestine, endothelial cells from bovinepulmonary artery, rabbit Tenon fibro-blasts, and rabbit and human corneal epithelial cells. Cellular morphological changes such as detachment, separation, loss of motility and disruption, in addition to swelling, intracytoplasmic vacuole formation and lysis have been manifested with the treatment of rose bengal , indicating that rose Bengal is not a vital dye.  Rose Bengal stains both the nuclei and cell walls of dead or degenerated epithelial cells of the cornea and conjunctiva, and stain the mucus of the precorneal tear film. It is proposed that the staining ability of rose bengal is dependent on the status of tear film protection rather than cell viability, as tear components such as albumin and mucin can block the rose bengal uptake. It induces intrinsic cytotoxic effects by causing cellular morphologic changes, subsequent loss of cellular motility, cell detachment, and cell death. It mediates inhibitory actions on bovine corneal endothelial cells and attenuates cell proliferation. ",,,,Rose bengal is approved and investigational.,Rose bengal is a solid.,True
14119,"Iron is a transition metal with a symbol Fe and atomic number 26. By mass, it is the most common element on Earth. Iron is an essential element involved in various metabolic processes, including oxygen transport, deoxyribonucleic acid (DNA) synthesis, and energy production in electron transport. Resulting from inadequate supply of iron to cells due to depletion of stores, iron deficiency is the most common nutritional deficiency worldwide, particularly affecting children, women of childbearing age, and pregnant women. Iron deficiency may be characterized without the development of anemia, and may result in functional impairments affecting cognitive development and immunity mechanisms, as well as infant or maternal mortality if it occurs during pregnancy. The main therapeutic preparation of iron is , and iron-sucrose may also be given intravenously. For the control of serum phosphorus levels in patients with chronic kidney disease on dialysis, as ferric citrate. When Fe3+ is converted to soluble Fe2+, it primarily exists in the circulation in the complex forms bound to protein (hemoprotein) as heme compounds (hemoglobin or myoglobin), heme enzymes, or nonheme compounds (flavin-iron enzymes, transferring, and ferritin). Once converted, Fe2+ serves to support various biological functions. Iron promotes the synthesis of oxygen transport proteins such as myoglobin and hemoglobin, and the formation of heme enzymes and other iron-containing enzymes involved in electron transfer and redox reactions. It also acts as a cofactor in many non-heme enzymes including hydroxylases and ribonucleotide reductase. Iron-containing proteins are responsible in mediating antioxidant actions, energy metabolism, oxygen sensing actions, and DNA replication and repair. Saturation of transferrin from high concentrations of unstable iron preparations may elevate the levels of weakly transferrin-bound Fe3+, which may induce oxidative stress by catalyzing lipid peroxidation and reactive oxygen species formation.  Iron is incorporated into various proteins to serve biological functions as a structural component or cofactor. Once ferric or ferrous cation from intestinal enterocytes or reticuloendothelial macrophages is bound to circulating transferrin, iron-transferrin complex binds to the cell-surface transferrin receptor (TfR) 1, resulting in endocytosis and uptake of the metal cargo. Internalized iron is transported to mitochondria for the synthesis of heme or iron-sulfur clusters, which are integral parts of several metalloproteins. Excess iron is stored and detoxified in cytosolic ferritin. Internalized Fe2+ exported across the basolateral membrane into the bloodstream via Fe+2 transporter ferroportin, which is coupled by reoxidation to Fe3+ via membrane-bound ferroxidase hephaestin or ceruloplasmin activity. Fe+3 is again scavenged by transferrin which maintains the ferric iron in a redox-inert state and delivers it into tissues.",,,,Ferric cation is approved.,Ferric cation is a solid.,True
14120,"Tetraferric tricitrate decahydrate is an iron containing phosphate binder used to treat hyperphosphatemia and iron deficiency anemia in adults with chronic kidney disease. Tetraferric tricitrate decahydrate is indicated to control serum phosphorous in adults with chronic kidney disease who require dialysis. Tetraferric tricitrate decahydrate is also indicated to treat iron deficiency anemia in adults with chronic kidney disease who are not on dialysis. Tetraferric tricitrate decahydrate is an iron containing product indicated to treat iron deficiency anemia and hyperphosphatemia. It has a wide therapeutic index, as doses can be varied significantly between patients. Tetraferric tricitrate decahydrate has a long duration of action in the treatment of iron deficiency anemia, due to the slow loss of iron from the body, and a moderate duration of action in the treatment of hyperphosphatemia, due to its action being dependant on residence time in the gastrointestinal tract. Patients should be counselled regarding the risk of iron overload. Ferric (Fe<sup>3+</sup>) iron is absorbed from the gastrointestinal tract by divalent metal transporter-1, and reduced to ferrous (Fe<sup>2+</sup>) iron by ferrireductase and cytochrome b reductase 1. Ferrous iron is stored intracellularly in ferritin and transported into the blood by ferroportin 1. Transport by ferroportin 1 is coupled with oxidation to ferric iron by hephaestin or ceruloplasmin. Ferric iron in plasma is bound to transferrin, which carries iron to other cells. Iron is transported to mitochondria for the synthesis of heme or iron-sulfur clusters, which are integral parts of several metalloproteins like hemoglobin.",,,,Tetraferric tricitrate decahydrate is approved.,Tetraferric tricitrate decahydrate is a solid.,True
14121,"Indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN), to maintain chromium serum levels and to prevent depletion of endogenous stores and subsequent deficiency symptoms. Trivalent chromium is part of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Chromium increases insulin binding to cells, increases insulin receptor density and activates insulin receptor kinase leading to enhanced insulin sensitivity. In chromium deficiency, intravenous administration of chromium resulted in normalization of the glucose tolerance curve from the diabetic-like curve typical of chromium deficiency.  Chromium is an essential nutrient involved in the metabolism of glucose, insulin and blood lipids. Its role in potentiating insulin signalling cascades has been implicated in several studies. Chromium upregulates insulin-stimulated insulin signal transduction via affecting effector molecules downstream of the insulin receptor (IR). IR-mediated signalling pathway involves phoshorylation of multiple intracellular domains and protein kinases, and downstream effector molecules. Upon activation by ligands, intracellular β-subunit of IR autophosphorylates and activates tyrosine kinase domain of the IR, followed by activation and phosphorylation of regulatory proteins and downstream signalling effectors including phosphatidylinositol 2-kinase (PI3K). PI3K activates further downstream reaction cascades to activate protein kinase B (Akt) to ultimately promote translocation of glucose transporter-4 (Glut4)-vesicles from the cytoplasm to the cell surface and regulate glucose uptake. Chromium enhances the kinase activity of insulin receptor β and increases the activity of downstream effectors, pI3-kinase and Akt. ",,,,Chromic citrate is experimental.,,True
14122,"Indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN), to maintain chromium serum levels and to prevent depletion of endogenous stores and subsequent deficiency symptoms. Trivalent chromium is part of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Chromium increases insulin binding to cells, increases insulin receptor density and activates insulin receptor kinase leading to enhanced insulin sensitivity. In chromium deficiency, intravenous administration of chromium resulted in normalization of the glucose tolerance curve from the diabetic-like curve typical of chromium deficiency.  Chromium is an essential nutrient involved in the metabolism of glucose, insulin and blood lipids. Its role in potentiating insulin signalling cascades has been implicated in several studies. Chromium upregulates insulin-stimulated insulin signal transduction via affecting effector molecules downstream of the insulin receptor (IR). IR-mediated signalling pathway involves phoshorylation of multiple intracellular domains and protein kinases, and downstream effector molecules. Upon activation by ligands, intracellular β-subunit of IR autophosphorylates and activates tyrosine kinase domain of the IR, followed by activation and phosphorylation of regulatory proteins and downstream signalling effectors including phosphatidylinositol 2-kinase (PI3K). PI3K activates further downstream reaction cascades to activate protein kinase B (Akt) to ultimately promote translocation of glucose transporter-4 (Glut4)-vesicles from the cytoplasm to the cell surface and regulate glucose uptake. Chromium enhances the kinase activity of insulin receptor β and increases the activity of downstream effectors, pI3-kinase and Akt. ",,,,Chromic nitrate is approved.,,True
14123,"Indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN), to maintain chromium serum levels and to prevent depletion of endogenous stores and subsequent deficiency symptoms. Trivalent chromium is part of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Chromium increases insulin binding to cells, increases insulin receptor density and activates insulin receptor kinase leading to enhanced insulin sensitivity. In chromium deficiency, intravenous administration of chromium resulted in normalization of the glucose tolerance curve from the diabetic-like curve typical of chromium deficiency.  Chromium is an essential nutrient involved in the metabolism of glucose, insulin and blood lipids. Its role in potentiating insulin signalling cascades has been implicated in several studies. Chromium upregulates insulin-stimulated insulin signal transduction via affecting effector molecules downstream of the insulin receptor (IR). IR-mediated signalling pathway involves phoshorylation of multiple intracellular domains and protein kinases, and downstream effector molecules. Upon activation by ligands, intracellular β-subunit of IR autophosphorylates and activates tyrosine kinase domain of the IR, followed by activation and phosphorylation of regulatory proteins and downstream signalling effectors including phosphatidylinositol 2-kinase (PI3K). PI3K activates further downstream reaction cascades to activate protein kinase B (Akt) to ultimately promote translocation of glucose transporter-4 (Glut4)-vesicles from the cytoplasm to the cell surface and regulate glucose uptake. Chromium enhances the kinase activity of insulin receptor β and increases the activity of downstream effectors, pI3-kinase and Akt. ",,,,Chromium gluconate is approved.,,True
14124,"Indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN), to maintain chromium serum levels and to prevent depletion of endogenous stores and subsequent deficiency symptoms. Trivalent chromium is part of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Chromium increases insulin binding to cells, increases insulin receptor density and activates insulin receptor kinase leading to enhanced insulin sensitivity. In chromium deficiency, intravenous administration of chromium resulted in normalization of the glucose tolerance curve from the diabetic-like curve typical of chromium deficiency.  Chromium is an essential nutrient involved in the metabolism of glucose, insulin and blood lipids. Its role in potentiating insulin signalling cascades has been implicated in several studies. Chromium upregulates insulin-stimulated insulin signal transduction via affecting effector molecules downstream of the insulin receptor (IR). IR-mediated signalling pathway involves phoshorylation of multiple intracellular domains and protein kinases, and downstream effector molecules. Upon activation by ligands, intracellular β-subunit of IR autophosphorylates and activates tyrosine kinase domain of the IR, followed by activation and phosphorylation of regulatory proteins and downstream signalling effectors including phosphatidylinositol 2-kinase (PI3K). PI3K activates further downstream reaction cascades to activate protein kinase B (Akt) to ultimately promote translocation of glucose transporter-4 (Glut4)-vesicles from the cytoplasm to the cell surface and regulate glucose uptake. Chromium enhances the kinase activity of insulin receptor β and increases the activity of downstream effectors, pI3-kinase and Akt. ",,,,Chromium nicotinate is approved and experimental.,,True
14125,"Indicated for use as a supplement to intravenous solutions given for total parenteral nutrition (TPN), to maintain chromium serum levels and to prevent depletion of endogenous stores and subsequent deficiency symptoms. Trivalent chromium is part of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Chromium increases insulin binding to cells, increases insulin receptor density and activates insulin receptor kinase leading to enhanced insulin sensitivity. In chromium deficiency, intravenous administration of chromium resulted in normalization of the glucose tolerance curve from the diabetic-like curve typical of chromium deficiency.  Chromium is an essential nutrient involved in the metabolism of glucose, insulin and blood lipids. Its role in potentiating insulin signalling cascades has been implicated in several studies. Chromium upregulates insulin-stimulated insulin signal transduction via affecting effector molecules downstream of the insulin receptor (IR). IR-mediated signalling pathway involves phoshorylation of multiple intracellular domains and protein kinases, and downstream effector molecules. Upon activation by ligands, intracellular β-subunit of IR autophosphorylates and activates tyrosine kinase domain of the IR, followed by activation and phosphorylation of regulatory proteins and downstream signalling effectors including phosphatidylinositol 2-kinase (PI3K). PI3K activates further downstream reaction cascades to activate protein kinase B (Akt) to ultimately promote translocation of glucose transporter-4 (Glut4)-vesicles from the cytoplasm to the cell surface and regulate glucose uptake. Chromium enhances the kinase activity of insulin receptor β and increases the activity of downstream effectors, pI3-kinase and Akt. ",,,,Chromous sulfate is approved.,,True
14126,"Highly purified sheep hyaluronidase for administration by injection into the vitreous of the eye. For increase of absorption and distribution of other injected drugs and for rehydration. Hyaluronidase hydrolyzes hyaluronic acid and increase diffusion of injected drugs, thus facilitating their absorption. Hyaluronidase is used for enhancing absorption and distribution of other injected drugs. Hyaluronidase is a spreading or diffusing substance. It increase the permeability of connective tissue through the hydrolysis of hyaluronic acid. Hyaluronidase hydrolyzes hyaluronic acid by splitting the glucosaminidic bond between C1 of the glucosamine moiety and C4 of glucuronic acid. This temporarily decreases the viscosity of the cellular cement and increases diffusion of injected fluids or of localized transudates or exudates, thus facilitating their absorption.",,,,Hyaluronidase (ovine) is approved and investigational.,Hyaluronidase (ovine) is a liquid.,True
14127,"Acromegaly is a disorder caused by excess growth hormone (GH), increasing the growth of body tissues and causing metabolic dysfunction. In most cases, it results from an anterior pituitary growth hormone-releasing tumor. Typically, the feet, hands, and face grow abnormally large; organomegaly and insulin resistance may also occur. Acromegaly is a life-threatening disease requiring life-long management. Octreotide by injection is used for the treatment of acromegaly and the reduction of flushing and diarrhea symptoms related to carcinoid tumors and/or vasoactive intestinal peptide (VIPoma) tumors. The delayed-release oral formulation is used for the long-term treatment of acromegaly in patients who tolerate and respond adequately to injectable octreotide and. Octreotide mimics the naturally occurring hormone known as somatostatin. Like somatostatin, it demonstrates activity against growth hormone and glucagon, treating the disordered tissue growth and insulin regulation in patients with acromegaly. In addition, octreotide relieves the flushing and diarrhea associated with gastrointestinal tumors by reducing splanchnic blood flow and various gastrointestinal hormones associated with diarrhea. Octreotide binds to somatostatin receptors coupled to phospholipase C through G proteins and leads to smooth muscle contraction in the blood vessels. Downstream effects that stimulate phospholipase C, the production of 1, 4,5-inositol triphosphate, and action on the L-type calcium channels lead to the inhibition of growth hormone, treating the various growth-hormone and metabolic effects of acromegaly.",The molecular weight is 1019.25.,Octreotide has a topological polar surface area of 332.22.,The log p value of  is 2.51.,Octreotide is approved and investigational.,Octreotide is a solid.,True
14128,"A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant. Used to treat vitamin C deficiency, scurvy, delayed wound and bone healing, urine acidification, and in general as an antioxidant. It has also been suggested to be an effective antiviral agent. Ascorbic Acid (vitamin C) is a water-soluble vitamin indicated for the prevention and treatment of scurvy, as ascorbic acid deficiency results in scurvy. Collagenous structures are primarily affected, and lesions develop in bones and blood vessels. Administration of ascorbic acid completely reverses the symptoms of ascorbic acid deficiency. In humans, an exogenous source of ascorbic acid is required for collagen formation and tissue repair by acting as a cofactor in the posttranslational formation of 4-hydroxyproline in -Xaa-Pro-Gly- sequences in collagens and other proteins. Ascorbic acid is reversibly oxidized to dehydroascorbic acid in the body. These two forms of the vitamin are believed to be important in oxidation-reduction reactions. The vitamin is involved in tyrosine metabolism, conversion of folic acid to folinic acid, carbohydrate metabolism, synthesis of lipids and proteins, iron metabolism, resistance to infections, and cellular respiration.",The molecular weight is 176.12.,Ascorbic acid has a topological polar surface area of 107.22.,The log p value of  is -1.76.,Ascorbic acid is approved and nutraceutical.,Ascorbic acid is a solid.,True
14129,"Lutein is an xanthophyll and one of 600 known naturally occurring carotenoids. Lutein is synthesized only by plants and like other xanthophylls is found in high quantities in green leafy vegetables such as spinach, kale and yellow carrots. In green plants, xanthophylls act to modulate light energy and serve as non-photochemical quenching agents to deal with triplet chlorophyll (an excited form of chlorophyll), which is overproduced at very high light levels, during photosynthesis. Xanthophylls are taken for nutritional supplementation, and also for treating dietary shortage or imbalance. Lutein was found to be present in a concentrated area of the macula, a small area of the retina responsible for central vision. The hypothesis for the natural concentration is that lutein helps protect from oxidative stress and high-energy light. Several studies show that an increase in macula pigmentation decreases the risk for eye diseases such as Age-related Macular Degeneration (AMD). Xanthophylls have antioxidant activity and react with active oxygen species, producing biologically active degradation products. They also can inhibit peroxidation of membrane phospholipids and reduce lipofuscin formation, both of which contribute to their antioxidant properties. Lutein is naturally present in the macula of the human retina. It filters out potentially phototoxic blue light and near-ultraviolet radiation from the macula. The protective effect is due in part, to the reactive oxygen species quenching ability of these carotenoids. Lutein is more stable to decomposition by pro-oxidants than are other carotenoids such as beta-carotene and lycopene. Lutein is abundant in the region surrounding the fovea, and lutein is the predominant pigment at the outermost periphery of the macula. Zeaxanthin, which is fully conjugated (lutein is not), may offer somewhat better protection than lutein against phototoxic damage caused by blue and near-ultraviolet light radiation. Lutein is one of only two carotenoids that have been identified in the human lens, may be protective against age-related increases in lens density and cataract formation. Again, the possible protection afforded by lutein may be accounted for, in part, by its reactive oxygen species scavenging abilities. Carotenoids also provide protection from cancer. One of the mechanisms of this is by increasing the expression of the protein connexin-43, thereby stimulating gap junctional communication and preventing unrestrained cell proliferation.",The molecular weight is 568.89.,Lutein has a topological polar surface area of 40.46.,The log p value of  is 11.23.,Lutein is approved and investigational and nutraceutical.,Lutein is a liquid.,True
14130,"Thiamine or thiamin, also known as vitamin B1, is a colorless compound with the chemical formula C12H17N4OS. It is soluble in water and insoluble in alcohol. Thiamine decomposes if heated. Thiamine was first discovered by Umetaro Suzuki in Japan when researching how rice bran cured patients of Beriberi. Thiamine plays a key role in intracellular glucose metabolism and it is thought that thiamine inhibits the effect of glucose and insulin on arterial smooth muscle cell proliferation. Thiamine plays an important role in helping the body convert carbohydrates and fat into energy. It is essential for normal growth and development and helps to maintain proper functioning of the heart and the nervous and digestive systems. Thiamine cannot be stored in the body; however, once absorbed, the vitamin is concentrated in muscle tissue. For the treatment of thiamine and niacin deficiency states, Korsakov's alcoholic psychosis, Wernicke-Korsakov syndrome, delirium, and peripheral neuritis. Thiamine is a vitamin with antioxidant, erythropoietic, cognition-and mood-modulatory, antiatherosclerotic, putative ergogenic, and detoxification activities. Thiamine has been found to protect against lead-induced lipid peroxidation in rat liver and kidney. Thiamine deficiency results in selective neuronal death in animal models. The neuronal death is associated with increased free radical production, suggesting that oxidative stress may play an important early role in brain damage associated with thiamine deficiency. Thiamine plays a key role in intracellular glucose metabolism and it is thought that thiamine inhibits the effect of glucose and insulin on arterial smooth muscle cell proliferation. Inhibition of endothelial cell proliferation may also promote atherosclerosis. Endothelial cells in culture have been found to have a decreased proliferative rate and delayed migration in response to hyperglycemic conditions. Thiamine has been shown to inhibit this effect of glucose on endothelial cells. It is thought that the mechanism of action of thiamine on endothelial cells is related to a reduction in intracellular protein glycation by redirecting the glycolytic flux. Thiamine is mainly the transport form of the vitamin, while the active forms are phosphorylated thiamine derivatives. Natural derivatives of thiamine phosphate, such as thiamine monophosphate (ThMP), thiamine diphosphate (ThDP), also sometimes called thiamine pyrophosphate (TPP), thiamine triphosphate (ThTP), and thiamine triphosphate (AThTP), that act as coenzymes in addition to their each unique biological functions. ",,,,Thiamine is approved and investigational and nutraceutical and vet_approved.,Thiamine is a solid.,True
14131,"Important polyunsaturated fatty acid found in fish oils. It serves as the precursor for the prostaglandin-3 and thromboxane-3 families. A diet rich in eicosapentaenoic acid lowers serum lipid concentration, reduces incidence of cardiovascular disorders, prevents platelet aggregation, and inhibits arachidonic acid conversion into the thromboxane-2 and prostaglandin-2 families. EPA can be used for lowering elevated triglycerides in those who are hyperglyceridemic. In addition, EPA may play a therapeutic role in patients with cystic fibrosis by reducing disease severity and may play a similar role in type 2 diabetics in slowing the progression of diabetic nephropathy. Eicosanoids are chemical messengers derived from 20-carbon polyunsaturated fatty acids that play critical roles in immune and inflammatory responses. Both 20-carbon omega-6 fatty acids (arachidonic acid) and 20-carbon omega-3 fatty acids (EPA) can be found in cell membranes. During an inflammatory response, arachidonic acid and EPA are metabolized by enzymes known as cyclooxygenases and lipoxygenases to form eicosanoids. Increasing omega-3 fatty acid intake increases the EPA content of cell membranes and decreases the arachidonic acid content, resulting in higher proportions of eicosanoids derived from EPA. Physiologic responses to arachidonic acid-derived eicosanoids differ from responses to EPA-derived eicosanoids. In general, eicosanoids derived from EPA are less potent inducers of inflammation, blood vessel constriction, and clotting than eicosanoids derived from arachidonic acid. The anti-inflammatory, antithrombotic and immunomodulatory actions of EPA is probably due to its role in eicosanoid physiology and biochemistry. Most eicosanoids are produced by the metabolism of omega-3 fatty acids, specifically, arachidonic acid. These eicosanoids, leukotriene B4 (LTB4) and thromboxane A2 (TXA2) stimulate leukocyte chemotaxis, platelet aggregation and vasoconstriction. They are thrombogenic and artherogenic. On the other hand, EPA is metabolized to leukotriene B5 (LTB5) and thromboxane A3 (TXA3), which are eicosanoids that promote vasodilation, inhibit platelet aggregation and leukocyte chemotaxis and are anti-artherogenic and anti-thrombotic. The triglyceride-lowering effect of EPA results from inhibition of lipogenesis and stimulation of fatty acid oxidation. Fatty acid oxidation of EPA occurs mainly in the mitochondria. EPA is a substrate for Prostaglandin-endoperoxide synthase 1 and 2. It also appears to affect the function and bind to the Carbohydrate responsive element binding protein (ChREBP) and to a fatty acid receptor (G-coupled receptor) known as GP40.",The molecular weight is 302.46.,Icosapent has a topological polar surface area of 37.3.,The log p value of  is 6.91.,Icosapent is approved and nutraceutical.,Icosapent is a liquid.,True
14132,"Pyridoxine is the 4-methanol form of vitamin B6, an important water-soluble vitamin that is naturally present in many foods. As its classification as a vitamin implies, Vitamin B6 (and pyridoxine) are essential nutrients required for normal functioning of many biological systems within the body. While many plants and microorganisms are able to synthesize pyridoxine through endogenous biological processes, animals must obtain it through their diet.  Pyridoxine is indicated for the treatment of vitamin B6 deficiency and for the prophylaxis of -induced peripheral neuropathy. It is also approved by Health Canada for the treatment of nausea and vomiting in pregnancy in a combination product with (as the commercially available product Diclectin). Vitamin B6 (pyridoxine) is a water-soluble vitamin used in the prophylaxis and treatment of vitamin B6 deficiency and peripheral neuropathy in those receiving isoniazid (isonicotinic acid hydrazide, INH). Vitamin B6 has been found to lower systolic and diastolic blood pressure in a small group of subjects with essential hypertension. Hypertension is another risk factor for atherosclerosis and coronary heart disease. Another study showed pyridoxine hydrochloride to inhibit ADP- or epinephrine-induced platelet aggregation and to lower total cholesterol levels and increase HDL-cholesterol levels, again in a small group of subjects. Vitamin B6, in the form of pyridoxal 5'-phosphate, was found to protect vascular endothelial cells in culture from injury by activated platelets. Endothelial injury and dysfunction are critical initiating events in the pathogenesis of atherosclerosis. Human studies have demonstrated that vitamin B6 deficiency affects cellular and humoral responses of the immune system. Vitamin B6 deficiency results in altered lymphocyte differentiation and maturation, reduced delayed-type hypersensitivity (DTH) responses, impaired antibody production, decreased lymphocyte proliferation and decreased interleukin (IL)-2 production, among other immunologic activities. Vitamin B6 is the collective term for a group of three related compounds, pyridoxine (PN), pyridoxal (PL) and pyridoxamine (PM), and their phosphorylated derivatives, pyridoxine 5'-phosphate (PNP), pyridoxal 5'-phosphate (PLP) and pyridoxamine 5'-phosphate (PMP). Although all six of these compounds should technically be referred to as vitamin B6, the term vitamin B6 is commonly used interchangeably with just one of them, pyridoxine. Vitamin B6, principally in its biologically active coenzyme form pyridoxal 5'-phosphate, is involved in a wide range of biochemical reactions, including the metabolism of amino acids and glycogen, the synthesis of nucleic acids, hemogloblin, sphingomyelin and other sphingolipids, and the synthesis of the neurotransmitters serotonin, dopamine, norepinephrine and gamma-aminobutyric acid (GABA).",The molecular weight is 169.18.,Pyridoxine has a topological polar surface area of 73.58.,The log p value of  is -0.35.,Pyridoxine is approved and investigational and nutraceutical and vet_approved.,Pyridoxine is a solid.,True
14133,"Torasemide is a high-ceiling loop diuretic. Structurally, it is a pyridine-sulfnyl urea used as an antihypertensive agent. On the FDA records, torasemide was developed and first introduced by the company Teva Pharmaceuticals and FDA approved in 2002. However, torasemide was first approved for clinical use by the FDA on 1993. Torasemide is indicated for the treatment of edema associated with congestive heart failure, renal or hepatic diseases. From this condition, it has been observed that torasemide is very effective in cases of kidney failure. It is widely known that administration of torasemide can attenuate renal injury and reduce the severity of acute renal failure. This effect is obtained by increasing urine output and hence, facilitating fluid, acid-base and potassium control. This effect is obtained by the increase in the excretion of urinary sodium and chloride. As mentioned above, torasemide is part of the loop diuretics and thus, it acts by reducing the oxygen demand in the medullary thick ascending loop of Henle by inhibiting the Na+/K+/Cl- pump on the luminal cell membrane surface. This action is obtained by the binding of torasemide to a chloride ion-binding site of the transport molecule.",The molecular weight is 348.42.,Torasemide has a topological polar surface area of 100.19.,The log p value of  is 3.21.,Torasemide is approved.,Torasemide is a solid.,True
14134,"Nelfinavir is a potent HIV-1 protease inhibitor. It is used in combination with other antiviral drugs in the treatment of HIV in both adults and children. Nelfinavir inhibits the HIV viral proteinase enzyme which prevents cleavage of the gag-pol polyprotein, resulting in noninfectious, immature viral particles. Used in combination with other antiviral drugs in the treatment of HIV in both adults and children. Nelfinavir is a protease inhibitor with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Protease inhibitors block the part of HIV called protease. HIV-1 protease is an enzyme required for the proteolytic cleavage of the viral polyprotein precursors into the individual functional proteins found in infectious HIV-1. Nelfinavir binds to the protease active site and inhibits the activity of the enzyme. This inhibition prevents cleavage of the viral polyproteins resulting in the formation of immature non-infectious viral particles. Protease inhibitors are almost always used in combination with at least two other anti-HIV drugs. Nelfinavir inhibits the HIV viral proteinase enzyme which prevents cleavage of the gag-pol polyprotein, resulting in noninfectious, immature viral particles.",The molecular weight is 567.79.,Nelfinavir has a topological polar surface area of 101.9.,The log p value of  is 5.84.,Nelfinavir is approved.,Nelfinavir is a solid.,True
14135,"Lovastatin, also known as the brand name product Mevacor, is a lipid-lowering drug and fungal metabolite derived synthetically from a fermentation product of _Aspergillus terreus_. Originally named Mevinolin, lovastatin belongs to the statin class of medications, which are used to lower the risk of cardiovascular disease and manage abnormal lipid levels by inhibiting the endogenous production of cholesterol in the liver. More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) Reductase, which catalyzes the conversion of HMG-CoA to mevalonic acid and is the third step in a sequence of metabolic reactions involved in the production of several compounds involved in lipid metabolism and transport including cholesterol, low-density lipoprotein (LDL) (sometimes referred to as \bad cholesterol\""), and very low-density lipoprotein (VLDL). Prescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD, such as those with Type 2 Diabetes. The clear evidence of the benefit of statin use coupled with very minimal side effects or long term effects has resulted in this class becoming one of the most widely prescribed medications in North America."" Lovastatin is indicated to reduce the risk of myocardial infarction, unstable angina, and the need for coronary revascularization procedures in individuals without symptomatic cardiovascular disease, average to moderately elevated total-C and LDL-C, and below average HDL-C. It is indicated as an intervention alternative in individuals presenting dyslipidemia at risk of developing atherosclerotic vascular disease. The administration of this agent should be accompanied by the implementation of a fat and cholesterol-restricted diet. Lovastatin is an oral antilipemic agent which reversibly inhibits HMG-CoA reductase. It is used to lower total cholesterol, low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apoB), non-high density lipoprotein-cholesterol (non-HDL-C), and trigleride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease and high ratios are associated with higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, lovastatin reduces the risk of cardiovascular morbidity and mortality. Lovastatin is a lactone which is readily hydrolyzed _in vivo_ to the corresponding β-hydroxyacid and strong inhibitor of HMG-CoA reductase, a hepatic microsomal enzyme which catalyzes the conversion of HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A ) to mevalonate, an early rate-limiting step in cholesterol biosynthesis. At therapeutic lovastatin doses, HMG-CoA reductase is not completely blocked, thereby allowing biologically necessary amounts of mevalonate to be available. Because the conversion of HMG-CoA to mevalonate is an early step in the biosynthetic pathway for cholesterol, therapy with lovastatin would not be expected to cause an accumulation of potentially toxic sterols.",The molecular weight is 404.55.,Lovastatin has a topological polar surface area of 72.83.,The log p value of  is 4.08.,Lovastatin is approved and investigational.,Lovastatin is a solid.,True
14136,"Enflurane is a halogenated inhalational anesthetic initially approved by the FDA in 1972. Since this date, it has been withdrawn from the US market. Unlike its other inhalational anesthetic counterparts including and , enflurane is known to induce seizure activity. In addition, it is known to cause increased cardio depressant effects when compared to other inhaled anesthetics. Enflurane may be used for both the induction and maintenance of general anesthesia. It can also be used to induce analgesia for vaginal delivery. Low concentrations of enflurane can also be used as an adjunct to general anesthetic drugs during delivery by Cesarean section. Enflurane rapidly induces anesthesia via the stimulation of inhibitory neural channels and the inhibition of excitatory neural channels. Muscle relaxation, obtundation of pharyngeal and laryngeal reflexes, and lowering of blood pressure are some of the main pharmacodynamic effects of this drug. Enflurane also decreases cardiac muscle contractility.  The mechanism of action of enflurane is not completely established. Studies on rats indicate that enflurane binds to GABAA and glycine receptors, causing depressant effects at the ventral neural horn. It has been reported that 30% of the central nervous system depressant effects on the spinal cord after enflurane is administered are caused by the (GABA-A) receptor while binding to glycine receptors is responsible for about 20 % of the depressant effects. The relevance of these findings to humans is unknown. Other studies have found that enflurane binds to the calcium channels in the cardiac sarcoplasmic reticulum causing cardio depressant effects. Other studies support that this drug potentiates glycine receptors, which results in central nervous system depressant effects. ",The molecular weight is 184.49.,Enflurane has a topological polar surface area of 9.23.,The log p value of  is 2.46.,Enflurane is approved and investigational and vet_approved.,Enflurane is a liquid.,True
14137,"Butabarbital, or Butisol, is a fast onset barbiturate with short duration of action compared to other barbiturates. This makes butabarbital a useful drug for treating severe insomnia and pre-operative anxiety. Butabarbital is less commonly used in recent years, as more patients are typically prescribed benzodiazepines. Its short duration of action gives butabarbital a high abuse potential, comparable to. Butabarbital is indicated for use as a sedative or hypnotic. Butabarbital should not be used to treat insomnia for longer than 2 weeks. Butabarbital potentiates GABAergic neurons while inhibiting neuronal acetylcholine and glutamate receptors to produce sedation. Butabarbital is an intermediate acting barbiturate with a duration of action of approximately 6-8 hours. The therapeutic index is quite wide as doses vary considerably from patient to patient. Patients should be counselled regarding the risk of worsening insomnia, drowsiness, falls, and complex behaviour while not fully awake. Barbiturates like butabarbital potentiate GABA-A receptors and inhibit receptors for neuronal acetylcholine, and kainate. GABA-A receptors are predominantly on the post-synaptic membrane, and upon activation, open chloride channels to hyperpolarize the neuron and decreased firing rate. Potentiation of GABAergic neurons produces sedation. Inhibition of neuronal acetylcholine receptors and glutamate receptors of the kainate subtype desensitize their respective neurons, producing sedation.",The molecular weight is 212.25.,Butabarbital has a topological polar surface area of 75.27.,The log p value of  is 1.58.,Butabarbital is approved and illicit.,Butabarbital is a solid.,True
14138,"A potent, non-nucleoside reverse transcriptase inhibitor (NNRTI) used in combination with nucleoside analogues for treatment of Human Immunodeficiency Virus Type 1 (HIV-1) infection and AIDS. Structurally, nevirapine belongs to the dipyridodiazepinone chemical class. For use in combination with other antiretroviral drugs in the ongoing treatment of HIV-1 infection. Nevirapine is a non-nucleoside reverse transcriptase inhibitor (nNRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). HIV-2 RT and eukaryotic DNA polymerases (such as human DNA polymerases alpha, beta, or sigma) are not inhibited by nevirapine. Nevirapine is, in general, only prescribed after the immune system has declined and infections have become evident. It is always taken with at least one other HIV medication such as Retrovir or Videx. The virus can develop resistance to nevirapine if the drug is taken alone, although even if used properly, nevirapine is effective for only a limited time. Nevirapine binds directly to reverse transcriptase (RT) and blocks the RNA-dependent and DNA-dependent DNA polymerase activities by causing a disruption of the enzyme's catalytic site. The activity of nevirapine does not compete with template or nucleoside triphosphates.",The molecular weight is 266.3.,Nevirapine has a topological polar surface area of 58.12.,The log p value of  is 2.65.,Nevirapine is approved.,Nevirapine is a solid.,True
14139,"Benztropine, with the chemical formula 3alpha-diphenylmethoxytropane, is a tropane-based dopamine inhibitor used for the symptomatic treatment of Parkinson's disease. It is a combination molecule between a tropane ring, similar to cocaine, and a diphenyl ether from the dialkylpiperazines determined to be a dopamine uptake inhibitor since 1970. The generation of structure-activity relationships proved that benztropine derivatives with the presence of a chlorine substituent in the para position in one of the phenyl rings produces an increased potency for dopamine uptake inhibition as well as a decreased inhibition of serotonin and norepinephrine. Benztropine was developed by USL Pharma and officially approved by the FDA on 1996. Benztropine is indicated to be used as an adjunct in the therapy of all forms of parkinsonism. It can also be used for the control of extrapyramidal disorders due to neuroleptic drugs. The inhibition of dopamine reuptake by benztropine produces a dose-dependent increase of dopamine in the nerve terminal of the dopaminergic system.  Benztropine is an agent with anti-muscarinic and antihistaminic effects. Its main mechanism of action is presented by the selective inhibition of dopamine transporters but it also presents affinity for histamine and muscarine receptors.",The molecular weight is 307.44.,Benzatropine has a topological polar surface area of 12.47.,The log p value of  is 3.52.,Benzatropine is approved.,Benzatropine is a solid.,True
14140,"Disorders such as schizophrenia and bipolar disorder can significantly impair mood, cognition, and behavior. These mental illnesses can often be accompanied by comorbidities such as depression and substance abuse, and can significantly impact the quality of life of patients and caregivers. Luckily, several treatment options for psychotic disorders have been introduced to market since the realization of chlorpromazine's antipsychotic properties in 1952.  In its oral form, ziprasidone is approved for the treatment of schizophrenia, as monotherapy for acute treatment of manic or mixed episodes related to bipolar I disorder, and as adjunctive therapy to lithium or valproate for maintenance treatment of bipolar I disorder. The injectable formulation is approved only for treatment of acute agitation in schizophrenia. Ziprasidone is classified as a \second generation\"" or \""atypical\"" antipsychotic and is a dopamine and 5HT2A receptor antagonist with a unique receptor binding profile. As previously mentioned, ziprasidone has a very high 5-HT2A/D2 affinity ratio, binds to multiple serotonin receptors in addition to 5-HT2A, and blocks monoamine transporters which prevents 5HT and NE reuptake. On the other hand, ziprasidone has a low affinity for muscarinic cholinergic M1, histamine H1, and alpha1-adrenergic receptors."" The effects of ziprasidone are differentiated from other antispychotics based on its preference and affinity for certain receptors. Ziprasidone binds to serotonin-2A (5-HT2A) and dopamine D2 receptors in a similar fashion to other atypical antipsychotics; however, one key difference is that ziprasidone has a higher 5-HT2A/D2 receptor affinity ratio when compared to other antipsychotics such as olanzapine, quetiapine, risperidone, and aripiprazole. Ziprasidone offers enhanced modulation of mood, notable negative symptom relief, overall cognitive improvement and reduced motor dysfunction which is linked to it's potent interaction with 5-HT2C, 5-HT1D, and 5-HT1A receptors in brain tissue. Ziprasidone can bind moderately to norepinephrine and serotonin reuptake sites which may contribute to its antidepressant and anxiolytic activity. Patient's taking ziprasidone will likely experience a lower incidence of orthostatic hypotension, cognitive disturbance, sedation, weight gain, and disruption in prolactin levels since ziprasidone has a lower affinity for histamine H1, muscarinic M1, and alpha1-adrenoceptors. ",The molecular weight is 412.94.,Ziprasidone has a topological polar surface area of 48.47.,The log p value of  is 4.21.,Ziprasidone is approved.,Ziprasidone is a solid.,True
14141,"Phenytoin is classified as a hydantoin derivative and despite its narrow therapeutic index, it is one of the most commonly used anticonvulsants. Since it's introduction about 80 years ago, phenytoin has not only been established as an effective anti-epileptic, but has also been investigated for several other indications such as bipolar disorder, retina protection, and wound healing. Phenytoin is indicated to treat grand mal seizures, complex partial seizures, and to prevent and treat seizures during or following neurosurgery. Injectable phenytoin and , which is the phosphate ester prodrug formulation of phenytoin, are indicated to treat tonic-clonic status epilepticus, and for the prevention and treatment of seizures occurring during neurosurgery. Phenytoin is an anticonvulsant with a narrow therapeutic index. Although the recommended therapeutic range is cited to be between 10-20 mg/L, differences in albumin levels, genetics, comorbidities, and body composition can make achieving an ideal phenytoin dose challenging. For example, studies have confirmed that phenytoin metabolism is impacted by CYP2C9 genotype polymorphisms and possibly by CYP2C19 genotype polymorphisms (the latter has not been as extensively studied). Although phenytoin first appeared in the literature in 1946, it has taken decades for the mechanism of action to be more specifically elucidated. Although several scientists were convinced that phenytoin altered sodium permeability, it wasn’t until the 1980’s that this phenomenon was linked to voltage-gated sodium channels. ",The molecular weight is 252.27.,Phenytoin has a topological polar surface area of 58.2.,The log p value of  is 2.08.,Phenytoin is approved and vet_approved.,Phenytoin is a solid.,True
14142,"Metoprolol is a selective beta-1 blocker commonly employed as the succinate and tartrate derivatives depending if the formulation is designed to be of immediate release or extended release. The possibility of the generation of these formulations comes from the lower systemic bioavailability of the succinate derivative. To this date, it is one of the preferred beta-blockers in general clinical guidelines and it is widely prescribed in the Netherlands, New Zealand, and the US. Metoprolol was developed since 1969 by US Pharmaceutical Holdings I and FDA approved in 1978. Metoprolol is indicated for the treatment of angina, heart failure, myocardial infarction, atrial fibrillation, atrial flutter and hypertension. Administration of metoprolol in normal subjects is widely reported to produce a dose-dependent reduction on heart rate and cardiac output. This effect is generated due to a decreased cardiac excitability, cardiac output, and myocardial oxygen demand. In the case of arrhythmias, metoprolol produces its effect by reducing the slope of the pacemaker potential as well as suppressing the rate of atrioventricular conduction. Metoprolol is a beta-1-adrenergic receptor inhibitor specific to cardiac cells with negligible effect on beta-2 receptors. This inhibition decreases cardiac output by producing negative chronotropic and inotropic effects without presenting activity towards membrane stabilization nor intrinsic sympathomimetics.",The molecular weight is 267.37.,Metoprolol has a topological polar surface area of 50.72.,The log p value of  is 1.49.,Metoprolol is approved and investigational.,Metoprolol is a solid.,True
14143,"Dicoumarol is an oral anticoagulant agent that works by interfering with the metabolism of vitamin K. In addition to its clinical use, it is also used in biochemical experiments as an inhibitor of reductases. For decreasing blood clotting. Often used along with heparin for treatment of deep vein thrombosis. Dicumarol is an coumarin-like compound found in sweet clover. It is used as an oral anticoagulant and acts by inhibiting the hepatic synthesis of vitamin K-dependent coagulation factors (prothrombin and factors VII, IX, and X).  Dicumarol inhibits vitamin K reductase, resulting in depletion of the reduced form of vitamin K (vitamin KH2). As vitamin K is a cofactor for the carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent proteins, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited. Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decresed prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots.",The molecular weight is 336.3.,Dicoumarol has a topological polar surface area of 93.06.,The log p value of  is 3.66.,Dicoumarol is approved.,Dicoumarol is a solid.,True
14144,"Topiramate is a anti-epileptic drug used to manage seizures and prevent migraines. It was initially approved by the FDA in 1996. In 2004, topiramate was approved for the prevention of migraine in adults. Since 2012, the extended-release formulation has been approved in combination with for chronic weight management therapy in adults.  Topiramate is indicated for the following conditions: 1)Monotherapy for partial onset or primary generalized tonic-clonic seizures for patients 2 years of age and above 2)Adjunctive therapy for partial onset seizures or primary generalized tonic-clonic seizures for both adult and pediatric patients above 2 years old 3)Adjunctive therapy for seizures associated with Lennox-Gastaut syndrome in patients above 2 years of age 4)Prophylaxis of migraine in children 12 years of age and older and adults. Topiramate prevents the occurrence of seizures and prevents migraine symptoms by reducing neural pathway excitability. It is important to note that this drug may cause metabolic acidosis, mood changes, suicidal thoughts and attempts, as well as kidney stones. When topiramate is combined with , it is known to cause hypothermia. A seizure is an abnormal and unregulated electrical discharge occurring in the brain. This leads to transient interruption in brain function, manifested by reduced alertness, abnormal sensations, and focal involuntary movements or convulsions. Several types of seizures exist, with common types including tonic-clonic seizures and partial onset seizures.",The molecular weight is 339.36.,Topiramate has a topological polar surface area of 115.54.,The log p value of  is 0.04.,Topiramate is approved.,Topiramate is a solid.,True
14145,"A semisynthetic cephamycin antibiotic with a broad spectrum of activity against both gram-positive and gram-negative microorganisms. It has a high rate of efficacy in many types of infection and to date no severe side effects have been noted. For the treatment of infections caused by susceptible organisms. Cefmetazole is a second-generation cephalosporin. The cephalosporins are bactericidal drugs with both gram-positive and gram-negative activity. They inhibit bacterial cell wall synthesis in a way similar to the penicillins. Cefmetazole is more active than 1st-generation cephalosporins against indole-positive <i>Proteus</i>, <i>Serratia</i>, anaerobic gram-negative bacilli (including <i>B. fragilis</i>), and some <i>E. coli</i>, <i>Klebsiella</i>, and <i>P. mirabilis</i>, but is less active than cefoxitin or cefotetan against most gram-negative bacilli. The bactericidal activity of cefmetazole results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs).",The molecular weight is 471.53.,Cefmetazole has a topological polar surface area of 163.33.,The log p value of  is -1.31.,Cefmetazole is approved and investigational.,Cefmetazole is a solid.,True
14146,"Argatroban is a direct, selective thrombin inhibitor. The American College of Cardiologists (ACC) recommend using bivalirudin or argatroban in patients who have had, or at risk for, heparin induced thrombocytopenia (HIT) and are undergoing percutaneous coronary intervention. Argatroban is a non-heparin anticoagulant shown to both normalize platelet count in patients with HIT and prevent the formation of thrombi. Parental anticoagulants must be stopped and a baseline activated partial thromboplastin time must be obtained prior to administering argatroban. Argatroban is indicated for prevention and treatment of thrombosis caused by heparin-induced thrombocytopenia (HIT). It is also indicated for use in patients with, or at risk for, HIT who are undergoing percutaneous coronary intervention. Argatroban is a synthetic direct thrombin inhibitor derived from L-arginine indicated as an anticoagulant for prophylaxis or treatment of thrombosis in patients with heparin-induced thrombocytopenia. Argatroban is a direct thrombin inhibitor that reversibly binds to the thrombin active site. Argatroban does not require the co-factor antithrombin III for antithrombotic activity. Argatroban exerts its anticoagulant effects by inhibiting thrombin-catalyzed or -induced reactions, including fibrin formation; activation of coagulation factors V, VIII, and XIII; protein C; and platelet aggregation. Argatroban is highly selective for thrombin with an inhibitory constant (K<sub>i</sub>) of 0.04 &micro;M. At therapeutic concentrations, Argatroban has little or no effect on related serine proteases (trypsin, factor Xa, plasmin, and kallikrein). Argatroban exerts its anticoagulant effects by inhibiting thrombin-catalyzed or -induced reactions, including fibrin formation; activation of coagulation factors V, VIII, and XIII; protein C; and platelet aggregation.",The molecular weight is 508.64.,Argatroban has a topological polar surface area of 177.71.,The log p value of  is -0.57.,Argatroban is approved and investigational.,Argatroban is a solid.,True
14147,"The conjugated estrogens are noncrystalline mixtures of purified female sex hormones obtained either by its isolation from the urine of pregnant mares or by synthetic generation from vegetal material. Both of these products are later conjugated to natrium sulfate by ester bonds in order to make them more water soluble.  The conjugated estrogens are indicated for several different conditions including: The binding of estrogens to the estrogen receptor produces the activation of nuclear receptors in order to bind to estrogen response elements in certain target genes. This mechanistic cascade results in histone acetylation, alteration of chromatin conformation and the initiation of transcription of certain specific drugs. The conjugated estrogens, equally to the normal physiological estrogen, work by agonistically binding to the estrogen receptors alpha and beta. The estrogen receptors vary in quantity and proportion according to the tissues and hence, the activity of this conjugated estrogens is very variable.",The molecular weight is 3556.05.,Conjugated estrogens has a topological polar surface area of 74.27.,,Conjugated estrogens is approved.,Conjugated estrogens is a solid.,True
14148,"Atomoxetine is a selective norepinephrine (NE) reuptake inhibitor used for the treatment of attention deficit hyperactivity disorder (ADHD). Also known as the marketed product Strattera, atomoxetine is used with other treatment modalities (psychological, educational, cognitive behaviour therapy, etc) to improve developmentally inappropriate symptoms associated with ADHD including distractibility, short attention span, hyperactivity, emotional lability, and impulsivity. Although the underlying pathophysiology that causes ADHD remains unclear, evidence suggests that dysregulation in noradrenergic and dopaminergic pathways plays a critical role in suboptimal executive functioning within prefrontal regions of the brain, which are involved in attention and memory. Atomoxetine has been shown to specifically increase NA and DA within the prefrontal cortex, but not in the nucleus accumbens (NA) or striatum. This is beneficial in the treatment of ADHD as DA activation in the subcortical NA and striatum is associated with many stimulant-associated side effects and an increase in abuse potential, which is a limiting factor associated with the use of stimulant medications such as , , and. Use of non-stimulant medications such as atomoxetine is therefore thought to offer a clinical advantage over the use of traditional medications for the management of ADHD. More recently, positron emission tomography (PET) imaging studies in rhesus monkeys have shown that atomoxetine also binds to the serotonin transporter (SERT), and blocks the N-methyl-d-aspartate (NMDA) receptor, indicating a role for the glutamatergic system in the pathophysiology of ADHD.  Atomoxetine is indicated for the treatment of attention deficit hyperactivity disorder (ADHD) in children and adults. Atomoxetine is a selective norepinephrine (NE) reuptake inhibitor used for the treatment of attention deficit hyperactivity disorder (ADHD). Atomoxetine has been shown to specifically increase norepinephrine and dopamine within the prefrontal cortex, which results in improved ADHD symptoms. Atomoxetine is known to be a potent and selective inhibitor of the norepinephrine transporter (NET), which prevents cellular reuptake of norepinephrine throughout the brain, which is thought to improve the symptoms of ADHD. More recently, positron emission tomography (PET) imaging studies in rhesus monkeys have shown that atomoxetine also binds to the serotonin transporter (SERT), and blocks the N-methyl-d-aspartate (NMDA) receptor, indicating a role for the glutamatergic system in the pathophysiology of ADHD. ",The molecular weight is 255.36.,Atomoxetine has a topological polar surface area of 21.26.,The log p value of  is 3.94.,Atomoxetine is approved.,Atomoxetine is a solid.,True
14149,"Etonogestrel molecule is a 3-ketodesogestrel or 19-nortestosterone which is a synthetic biologically active metabolite of progestin desogestrel. The first product including etonogestrel was developed by the Merck subsidiary Organon and FDA approved in 2001. Etonogestrel is administered in subdermal implants as long-acting reversible contraception. It is known to be effective in postpartum insertion including breastfeeding women. Etonogestrel attains its therapeutic effect inhibiting fertility by impairing the release of the luteinizing hormone which is one of the most important reproductive hormones for ovulation. As well, etonogestrel is known to increase the viscosity of the cervical mucus hindering the passage of the spermatozoa and altering the lining in the uterus to prevent the implantation of the fertilized eggs in the endometrium. Etonogestrel binds with high affinity to the progesterone and estrogen receptors in the target organs. From the target organs, they include the female reproductive tract, mammary gland, hypothalamus, and pituitary. Once bound, this drug changes the synthesis of different proteins which in order decreases the level of gonadotropin-releasing hormone and the luteinizing hormone.",The molecular weight is 324.46.,Etonogestrel has a topological polar surface area of 37.3.,The log p value of  is 3.35.,Etonogestrel is approved and investigational.,Etonogestrel is a solid.,True
14150,"Morphine, the main alkaloid of opium, was first obtained from poppy seeds in 1805. It is a potent analgesic, though its use is limited due to tolerance, withdrawal, and the risk of abuse. Morphine is still routinely used today, though there are a number of semi-synthetic opioids of varying strength such as , , , , , , and. Morphine is used for the management of chronic, moderate to severe pain. Morphine binding to opioid receptors blocks transmission of nociceptive signals, signals pain-modulating neurons in the spinal cord, and inhibits primary afferent nociceptors to the dorsal horn sensory projection cells. Morphine-6-glucuronide is responsible for approximately 85% of the response observed by morphine administration. Morphine and its metabolites act as agonists of the mu and kappa opioid receptors. The mu-opioid receptor is integral to morphine's effects on the ventral tegmental area of the brain. Morphine's activation of the reward pathway is mediated by agonism of the delta-opioid receptor in the nucleus accumbens, while modification of the respiratory system and addiction disorder are mediated by agonism of the mu-opioid receptor.",The molecular weight is 285.34.,Morphine has a topological polar surface area of 52.93.,The log p value of  is 0.57.,Morphine is approved and investigational.,Morphine is a solid.,True
14151,"Desogestrel, a prodrug, is a third generation progestogen and hence, a member of the gonane family which was largely used in Europe before being approved in the US and Canada. It was firstly generated from a study that showed that 11-beta and 11-alkylidene substituent in nortestosterone can enhance the biological activity. Desogestrel is now produced semi-synthetically from naturally occurred plant steroids. In the US, desogestrel is found only in combination with. The first approved drug containing desogestrel was developed by Organon USA Inc in 1972 and FDA approved in 1992. Oral desogestrel is used in combination with as a contraceptive agent for the prevention of pregnancy. The effects of desogestrel are divided on reproductive including modification of luteinizing hormone and follicle stimulating hormone, declines on the onset of menstruation, and increases the viscosity of the vaginal fluid; and on metabolic that includes increase insulin secretion and resistance, increased lipase activity, and increased fat deposition. The effect of desogestrel on the lipids has been studied extensively and the results are contradictory. Desogestrel enters the cell passively and acts by binding selectively to the progesterone receptor and generating low androgenic activity. Its binding produces an effect like a transcription factor and thus, it produces modifications in the mRNA synthesis.",The molecular weight is 310.48.,Desogestrel has a topological polar surface area of 20.23.,The log p value of  is 5.5.,Desogestrel is approved.,Desogestrel is a solid.,True
14152,"Chlorthalidone is a thiazide-like diuretic used for the treatment of hypertension and for management of edema caused by conditions such as heart failure or renal impairment. Chlorthalidone improves blood pressure and swelling by preventing water absorption from the kidneys through inhibition of the Na+/Cl− symporter in the distal convoluted tubule cells in the kidney. The exact mechanism of chlorthalidone's anti-hypertensive effect is under debate, however, it is thought that increased diuresis results in decreased plasma and extracellular fluid volume, decreased cardiac output and therefore overall reduction in blood pressure. Chlorthalidone is indicated in the management of hypertension either as the sole therapeutic agent or to enhance the effect of other antihypertensive drugs in the more severe forms of hypertension. Chlorthalidone prevents reabsorption of sodium and chloride through inhibition of the Na+/Cl- symporter in the cortical diluting segment of the ascending limb of the loop of Henle. Reduction of sodium reabsorption subsequently reduces extracellular fluid and plasma volume via an osmotic, sodium-driven diuresis. By increasing the delivery of sodium to the distal renal tubule, Chlorthalidone indirectly increases potassium excretion via the sodium-potassium exchange mechanism. The exact mechanism of chlorthalidone's anti-hypertensive effect is under debate, however, it is thought that increased diuresis results in decreased plasma and extracellular fluid volume which therefore requires decreased cardiac output and overall lowers blood pressure. Chlorthalidone has also been shown to decrease platelet aggregation and vascular permeability, as well as promote angiogenesis in vitro, which is thought to be partly the result of reductions in carbonic anhydrase–dependent pathways. These pathways may play a role in chlorthalidone's cardiovascular risk reduction effects.",The molecular weight is 338.76.,Chlorthalidone has a topological polar surface area of 109.49.,The log p value of  is 0.45.,Chlorthalidone is approved.,Chlorthalidone is a solid.,True
14153,"Valproic acid, or valproate, is an fatty acid derivative and anticonvulsant originally synthesized in 1881 by Beverly S. Burton. It enjoyed use as a popular organic solvent in industry and pharmaceutical manufacturing for nearly a century. In 1963, a serendipitous discovery was made by George Carraz during his investigations into the anticonvulsant effects of khelline when he found that all of his samples, dissolved in valproic acid, exerted a similar degree of anticonvulsive activity. It first received approval on February 28, 1978 from the FDA under the trade name Depakene. **Indicated** for:  Valproate has been shown to reduce the incidence of complex partial seizures and migraine headaches. It also improves symptom control in bipolar mania. Although the exact mechanisms responsible are unknown, it is thought that valproate produces increased cortical inhibition to contribute to control of neural synchrony. It is also thought that valproate exerts a neuroprotective effect preventing damage and neural degeneration in epilepsy, migraines, and bipolar disorder. The exact mechanisms by which valproate exerts it's effects on epilepsy, migraine headaches, and bipolar disorder are unknown however several pathways exist which may contribute to the drug's action.",The molecular weight is 144.21.,Valproic acid has a topological polar surface area of 37.3.,The log p value of  is 2.76.,Valproic acid is approved and investigational.,Valproic acid is a solid.,True
14154,"Acetaminophen (paracetamol), also commonly known as _Tylenol_, is the most commonly taken analgesic worldwide and is recommended as first-line therapy in pain conditions by the World Health Organization (WHO). It is also used for its antipyretic effects, helping to reduce fever. This drug was initially approved by the U.S. FDA in 1951 and is available in a variety of forms including syrup form, regular tablets, effervescent tablets, injection, suppository, and other forms. In general, acetaminophen is used for the treatment of mild to moderate pain and reduction of fever. It is available over the counter in various forms, the most common being oral forms. Animal and clinical studies have determined that acetaminophen has both antipyretic and analgesic effects. This drug has been shown to lack anti-inflammatory effects. As opposed to the _salicylate_ drug class, acetaminophen does not disrupt tubular secretion of uric acid and does not affect acid-base balance if taken at the recommended doses. Acetaminophen does not disrupt hemostasis and does not have inhibitory activities against platelet aggregation. Allergic reactions are rare occurrences following acetaminophen use.  According to its FDA labeling, acetaminophen's exact mechanism of action has not been fully established - despite this, it is often categorized alongside NSAIDs (nonsteroidal anti-inflammatory drugs) due to its ability to inhibit the cyclooxygenase (COX) pathways. It is thought to exert central actions which ultimately lead to the alleviation of pain symptoms.",The molecular weight is 151.16.,Acetaminophen has a topological polar surface area of 49.33.,The log p value of  is 0.49.,Acetaminophen is approved.,Acetaminophen is a solid.,True
14155,"Gefitinib (originally coded ZD1839) is a drug used in the treatment of certain types of cancer. Acting in a similar manner to erlotinib (marketed as Tarceva), gefitinib selectively targets the mutant proteins in malignant cells. It is marketed by AstraZeneca under the trade name Iressa. For the continued treatment of patients with locally advanced or metastatic non-small cell lung cancer after failure of either platinum-based or docetaxel chemotherapies. Gefitinib inhibits the intracellular phosphorylation of numerous tyrosine kinases associated with transmembrane cell surface receptors, including the tyrosine kinases associated with the epidermal growth factor receptor (EGFR-TK). EGFR is expressed on the cell surface of many normal cells and cancer cells. Gefitinib is an inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase that binds to the adenosine triphosphate (ATP)-binding site of the enzyme. EGFR is often shown to be overexpressed in certain human carcinoma cells, such as lung and breast cancer cells. Overexpression leads to enhanced activation of the anti-apoptotic Ras signal transduction cascades, subsequently resulting in increased survival of cancer cells and uncontrolled cell proliferation. Gefitinib is the first selective inhibitor of the EGFR tyrosine kinase which is also referred to as Her1 or ErbB-1. By inhibiting EGFR tyrosine kinase, the downstream signaling cascades are also inhibited, resulting in inhibited malignant cell proliferation. ",The molecular weight is 446.91.,Gefitinib has a topological polar surface area of 68.74.,The log p value of  is 5.45.,Gefitinib is approved and investigational.,Gefitinib is a solid.,True
14156,"Amitriptyline hydrochloride, also known as _Elavil_, is a tricyclic antidepressant (TCA) with analgesic properties, widely used to treat depression and neuropathic pain. It was originally approved by the FDA in 1977 and manufactured by Sandoz. This drug in indicated for the following conditions : **Effects in pain and depression** The mechanism of action of this drug is not fully elucidated. It is suggested that amitriptyline inhibits the membrane pump mechanism responsible for the re-uptake of transmitter amines, such as norepinephrine and serotonin, thereby increasing their concentration at the synaptic clefts of the brain ,.  These amines are important in regulating mood. The monoamine hypothesis in depression, one of the oldest hypotheses, postulates that deficiencies of serotonin (5-HT) and/or norepinephrine (NE) neurotransmission in the brain lead to depressive effects.  This drug counteracts these mechanisms, and this may be the mechanism of amitriptyline in improving depressive symptoms.",The molecular weight is 277.41.,Amitriptyline has a topological polar surface area of 3.24.,The log p value of  is 4.85.,Amitriptyline is approved.,Amitriptyline is a solid.,True
14157,"Hydromorphone is a pure opioid, a semi-synthetic hydrogenated ketone derivative of that has been available clinically since 1920. Structurally, hydromorphone derived from in the modification of the hydroxyl group in the carbon 6 to a carbonyl and the absence of a double bond between the carbon 7 and 8. Due to these modifications, it presents a very high potency and comparable side effect profile to the parent compound. Even though hydromorphone does not present a 6-hydroxyl group, it is categorized under the family of phenanthrenes and it is considered a chemical under the schedule II (medical purposes with high addiction potential). Hydromorphone is indicated for the management of moderate to severe acute pain and severe chronic pain. Due to its addictive potential and overdose risk, hydromorphone is only prescribed when other first-line treatments have failed. In clinical trials, hydromorphone has been shown to be suitable for pain relief in patients that do not tolerate the side effects of or that suffer from renal failure or asthma. It has been shown to be 5-7 times more potent than morphine with a shorter duration of analgesia. Hydromorphone is an opioid agonist that can bind to different types of opioid receptors. Its analgesic effect is suggested to be related to the effect on the mu-opioid receptors. It has been reported to also have a minor affinity for the delta and kappa receptor. On the other hand, it is known to act at the level of the medulla which allows it to depress the respiratory drive and suppress cough.",The molecular weight is 285.34.,Hydromorphone has a topological polar surface area of 49.77.,The log p value of  is 0.72.,Hydromorphone is approved and illicit.,Hydromorphone is a solid.,True
14158,"Indometacin, or indomethacin, is a non-steroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic, and antipyretic properties. NSAIDs consist of agents that are structurally unrelated; the NSAID chemical classification of indometacin is an indole-acetic acid derivative with the chemical name 1- (p-chlorobenzoyl)25-methoxy-2-methylindole-3-acetic acid. The pharmacological effect of indometacin is not fully understood, however, it is thought to be mediated through potent and nonselective inhibition of the enzyme cyclooxygenase (COX), which is the main enzyme responsible for catalyzes the rate-limiting step in prostaglandin and thromboxane biosynthesis via the arachidonic acid (AA) pathway. Indometacin was first discovered in 1963 and it was first approved for use in the U.S. by the Food and Drug Administration in 1965, along with other acetic acid derivatives such as and that were also developed during the 1960s. Since then, indometacin has been extensively studied in clinical trials as one of the most potent NSAIDs in blocking prostaglandin synthesis and was among the first NSAIDs to be used in the symptomatic treatment of migraine and for headaches that eventually became known as “indomethacin-responsive” headache disorders.  Oral indometacin is indicated for symptomatic management of moderate to severe rheumatoid arthritis including acute flares of chronic disease, moderate to severe ankylosing spondylitis, moderate to severe osteoarthritis, acute painful shoulder (bursitis and/or tendinitis) and acute gouty arthritis. Indometacin is an NSAID with analgesic and antipyretic properties that exerts its pharmacological effects by inhibiting the synthesis of factors involved in pain, fever, and inflammation. Its therapeutic action does not involve pituitary-adrenal stimulation. Indometacin primarily works by suppressing inflammation in rheumatoid arthritis by providing relief of pain as well as reducing fever, swelling, and tenderness. This effectiveness has been demonstrated by a reduction in the extent of joint swelling, the average number of joints displaying symptoms of inflammation, and the severity of morning stiffness. Increased mobility was demonstrated by a decrease in total walking time and by improved functional capability seen as an increase in grip strength. In clinical trials, indometacin was shown to be effective in relieving the pain, reducing the fever, swelling, redness, and tenderness of acute gouty arthritis. Due to its pharmacological actions, the use of indometacin is associated with the risk of serious cardiovascular thrombotic events, including myocardial infarction and stroke, as well as gastrointestinal effects such as bleeding, ulceration, and perforation of the stomach or intestines. Indometacin is a nonspecific and reversible inhibitor of the cyclo-oxygenase (COX) enzyme, or prostaglandin G/H synthase. There are two identified isoforms of COX: COX-1 is universally present in most body tissues and is involved in the synthesis of the prostaglandins and thromboxane A2, while COX-2 is expressed in response to injury or inflammation. Constitutively expressed, the COX-1 enzyme is involved in gastric mucosal protection, platelet, and kidney function by catalyzing the conversion of arachidonic acid to prostaglandin (PG) G2 and PGG2 to PGH2. COX-2 is constitutively expressed and highly inducible by inflammatory stimuli. It is found in the central nervous system, kidneys, uterus, and other organs. COX-2 also catalyzes the conversion of arachidonic acid to PGG2 and PGG2 to PGH2. In the COX-2-mediated pathway, PGH2 is further converted to PGE2 and PGI2 (also known as prostacyclin). PGE2 is involved in mediating inflammation, pain, and fever. Decreasing levels of PGE2 leads to reduced inflammatory reactions. Indometacin is known to inhibit both isoforms of COX, however, with greater selectivity for COX-1, which accounts for its increased adverse gastric effects relative to other NSAIDs. It binds to the active site of the enzyme and prevents the interaction between the enzyme and its substrate, arachidonic acid. Indometacin, unlike other NSAIDs, also inhibits phospholipase A2, the enzyme responsible for releasing arachidonic acid from phospholipids. The analgesic, antipyretic and anti-inflammatory effects of indomethacin as well as adverse reactions associated with the drug occur as a result of decreased prostaglandin synthesis. Its antipyretic effects may be due to action on the hypothalamus, resulting in increased peripheral blood flow, vasodilation, and subsequent heat dissipation.",The molecular weight is 357.79.,Indomethacin has a topological polar surface area of 68.53.,The log p value of  is 4.18.,Indomethacin is approved and investigational.,Indomethacin is a solid.,True
14159,"Ipratropium is a quaternary ammonium derivative of that acts as an anticholinergic agent. It is commonly administered through inhalation which allows producing a local effect without presenting a significant systemic absorption. Inhaled ipratropium is indicated in combination with inhaled beta-agonist systemic corticosteroids for the management of severe exacerbations of asthma flares requiring treatment. Ipratropium is a short-acting agent that inhibits the parasympathetic nervous system at the level of the airway which then produces bronchodilatation. The effect of this agent starts after 1-2 hours and it is known to last only from 4 to 6 hours. As part of the effect, ipratropium relaxes the bronchial airways which reverse the narrowing that accounts for wheezy breathing, chest tightness, cough and abnormal gas exchange. Ipratropium acts as an antagonist of the muscarinic acetylcholine receptor. This effect produces the inhibition of the parasympathetic nervous system in the airways and hence, inhibit their function. The function of the parasympathetic system in the airway is to generate bronchial secretions and constriction and hence, the inhibition of this action can lead to bronchodilation and fewer secretions.",The molecular weight is 332.46.,Ipratropium has a topological polar surface area of 46.53.,The log p value of  is -2.19.,Ipratropium is approved and experimental.,Ipratropium is a solid.,True
14160,"Methadone is a potent synthetic analgesic that works as a full µ-opioid receptor (MOR) agonist and N-methyl-d-aspartate (NMDA) receptor antagonist. As a full MOR agonist, methadone mimics the natural effects of the body's opioids, endorphins, and enkephalins through the release of neurotransmitters involved in pain transmission. It also has a number of unique characteristics that have led to its increased use in the last two decades; in particular, methadone has a lower risk of neuropsychiatric toxicity compared to other opioids (due to a lack of active metabolites), minimal accumulation in renal failure, good bioavailability, low cost, and a long duration of action.  Methadone is indicated for the management of pain severe enough to require an opioid analgesic and for which alternative treatment options are inadequate. It's recommended that use is reserved for use in patients for whom alternative treatment options (eg, nonopioid analgesics, opioid combination products) are ineffective, not tolerated, or would be otherwise inadequate to provide sufficient management of pain. Overall, methadone's pharmacological actions result in analgesia, suppression of opioid withdrawal symptoms, sedation, miosis (through binding to receptors in the pupillary muscles), sweating, hypotension, bradycardia, nausea and vomiting (via binding within the chemoreceptor trigger zone), and constipation. Like many basic drugs, methadone also enters mast cells and releases histamine by a non-immunological mechanism leading to flushing, pruritus, and urticaria, which can commonly be misattributed to an allergic reaction.  Methadone is a synthetic opioid analgesic with full agonist activity at the µ-opioid receptor. While agonism of the µ-opioid receptor is the primary mechanism of action for the treatment of pain, methadone also acts as an agonist of κ- and σ-opioid receptors within the central and peripheral nervous systems. Interestingly, methadone differs from (which is considered the gold standard reference opioid) in its antagonism of the N-methyl-D-aspartate (NMDA) receptor and its strong inhibition of serotonin and norepinephrine uptake, which likely also contributes to its antinociceptive activity. ",The molecular weight is 309.45.,Methadone has a topological polar surface area of 20.31.,The log p value of  is 4.17.,Methadone is approved.,Methadone is a solid.,True
14161,"Olanzapine is a thienobenzodiazepine classified as an atypical or second-generation antipsychotic agent. The second-generation antipsychotics were introduced in the 90s and quickly gained traction due to their impressive efficacy, reduced risk for extrapyramidal side effects and reduced susceptibility to drug-drug interactions. Olanzapine very closely resembles and only differs by two additional methyl groups and the absence of a chloride moiety. It was discovered by scientists at Eli Lilly and approved to be marketed in the US in 1996. Olanzapine was initially used orally and intramuscularly for the chronic treatment of schizophrenia in patients over 13 years old and other psychiatric disorders such as bipolar I disorder including mixed or manic episodes.  The effect of olanzapine in the D2 receptor is reported to produce the positive effects of this drug such as a decrease in hallucinations, delusions, disorganized speech, disorganized thought, and disorganized behavior. On the other hand, its effect on the serotonin 5HT2A receptor prevents the onset of anhedonia, flat affect, alogia, avolition and poor attention. Based on the specific mechanism of action, olanzapine presents a higher affinity for the dopamine D2 receptor when compared to the rest of the dopamine receptor isotypes. This characteristic significantly reduces the presence of side effects. The activity of olanzapine is achieved by the antagonism of multiple neuronal receptors including the dopamine receptor D1, D2, D3 and D4 in the brain, the serotonin receptors 5HT2A, 5HT2C, 5HT3 and 5HT6, the alpha-1 adrenergic receptor, the histamine receptor H1 and multiple muscarinic receptors.",The molecular weight is 312.44.,Olanzapine has a topological polar surface area of 30.87.,The log p value of  is 2.86.,Olanzapine is approved and investigational.,Olanzapine is a solid.,True
14162,"Atenolol is a cardioselective beta-blocker used in a variety of cardiovascular conditions.  **Indicated** for: Atenolol is a cardio-selective beta-blocker and as such exerts most of its effects on the heart. It acts as an antagonist to sympathetic innervation and prevents increases in heart rate, electrical conductivity, and contractility in the heart due to increased release of norepinephrine from the peripheral nervous system. Together the decreases in contractility and rate produce a reduction in cardiac output resulting in a compensatory increase in peripheral vascular resistance in the short-term. This response later declines to baseline with long-term use of atenolol. More importantly, this reduction in the work demanded of the myocardium also reduces oxygen demand which provides therapeutic benefit by reducing the mismatch of oxygen supply and demand in settings where coronary blood flow is limited, such as in coronary atherosclerosis. Reducing oxygen demand, particularly due to exercise, can reduce the frequency of angina pectoris symptoms and potentially improve survival of the remaining myocardium after myocardial infarction. The decrease in rate of sinoatrial node potentials, electrical conduction, slowing of potentials traveling through the atrioventricular node, and reduced frequency of ectopic potentials due to blockade of adrenergic beta receptors has led to benefit in arrhythmic conditions such as atrial fibrillation by controlling the rate of action potential generation and allowing for more effective coordinated contractions. Since a degree of sympathetic activity is necessary to maintain cardiac function, the reduced contractility induced by atenolol may precipitate or worsen heart failure, especially during volume overload. Atenolol is a cardioselective beta-blocker, called such because it selectively binds to the β1-adrenergic receptor as an antagonist up to a reported 26 fold more than β2 receptors. Selective activity at the β1 receptor produces cardioselectivity due to the higher population of this receptor in cardiac tissue. Some binding to β2 and possibly β3 receptors can still occur at therapeutic dosages but the effects mediated by antagonizing these are significantly reduced from those of non-selective agents. β1 and β2 receptors are G<sub>s</sub> coupled therefore antagonism of their activation reduces activity of adenylyl cyclase and its downstream signalling via cyclic adenosime monophosphate and protein kinase A (PKA). ",The molecular weight is 266.34.,Atenolol has a topological polar surface area of 84.58.,The log p value of  is -0.11.,Atenolol is approved.,Atenolol is a solid.,True
14163,"Diltiazem is a benzothiazepine derivative with antihypertensive and vasodilating properties. Approved in 1982 by the FDA, it is a member of the non-dihydropyridine calcium channel blockers drug class. It works through various mechanisms of action, but it primarily works by inhibiting the calcium influx into cardiac and vascular smooth muscle during depolarization. Compared to dihydropyridine drugs, such as , that preferentially act on vascular smooth muscle and that directly acts on the heart muscle, diltiazem displays an intermediate specificity to target both the cardiac and vascular smooth muscle. Being a potent vasodilator, diltiazem is used clinically as an antihypertensive, anti-arrhythmic, and as an anti-anginal agent for the management of cardiovascular conditions such as hypertension, chronic stable angina, atrial fibrillation, atrial flutter. Apart from its main FDA-approved indications, diltiazem has also been used for numerous off-label indications, such as anal fissures (in topical formulations), migraine prophylaxis, pulmonary hypertension, and rest-related cramps in the lower extremities. Typically available in extended-release oral and intravenous formulations, diltiazem is marketed under various brand names with Cardizem and Tiazac being the most common ones. **Oral** Diltiazem is an antihypertensive and vasodilating agent that works by relaxing the vascular muscle and reducing blood pressure. This is related to the long-term therapeutic effects, as lowering the blood pressure reduces the risk of fatal and non-fatal cardiovascular events, primarily strokes and myocardial infarctions. Diltiazem inhibits the influx of extracellular calcium ions across the myocardial and vascular smooth muscle cell membranes during depolarization. Diltiazem is classified as a negative inotrope (decreased force) and negative chronotrope (decreased rate). It is also considered a rate-control drug as it reduces heart rate. Diltiazem is exerts hemodynamic actions by reducing blood pressure, systemic vascular resistance, the rate-pressure product, and coronary vascular resistance while increasing coronary blood flow. Diltiazem decreases sinoatrial and atrioventricular conduction in isolated tissues and has a negative inotropic effect in isolated preparations. In supraventricular tachycardia, diltiazem prolongs AV nodal refractories. Excitation of cardiac muscle involves the activation of a slow calcium inward current that is induced by L-type slow calcium channels, which are voltage-sensitive, ion-selective channels associated with a high activation threshold and slow inactivation profile. L-type calcium channels are the main current responsible for the late phase of the pacemaker potential. Acting as the main Ca2+ source for contraction in smooth and cardiac muscle, activation of L-type calcium channels allows the influx of calcium ions into the muscles upon depolarization and excitation of the channel. It is proposed that this cation influx may also trigger the release of additional calcium ions from intracellular storage sites. Diltiazem is a slow calcium channel blocker that binds to the extracellular site of the alpha-1C subunit of the channel, which is thought to be the S5-6 linker region of the transmembrane domain IV and/or S6 segment of domain III. Diltiazem can get access to this binding site from either the intracellular or extracellular side, but it requires a voltage-induced conformational changes in the membrane. Diltiazem inhibits the influx of extracellular calcium across the myocardial and vascular smooth muscle cell membranes. In isolated human atrial and ventricular myocardium, diltiazem suppressed tension over the range of membrane potentials associated with calcium channel activity but had little effect on the tension-voltage relations at more positive potentials. This effect is thought to be mediated by the voltage-dependent block of the L-type calcium channels and inhibition of calcium ion release from the ER stores, without altering the sodium-calcium coupled transport or calcium sensitivity of myofilaments. Through inhibition of inward calcium current, diltiazem exerts a direct ionotropic and energy sparing effect on the myocardium. Diltiazem fslows atrioventricular nodal conduction, which is due to its ability to impede slow channel function.",The molecular weight is 414.52.,Diltiazem has a topological polar surface area of 59.08.,The log p value of  is 3.65.,Diltiazem is approved and investigational.,Diltiazem is a solid.,True
14164,"Alprazolam is a triazolobenzodiazepine indicated for the treatment of anxiety and panic disorders. It is mainly metabolized by CYP3As and so is contraindicated with CYP3A inhibitors like ketoconazole and itraconazole. Benzodiazepine treatment should be stopped gradually by tapering down a patient's dose to avoid withdrawal symptoms. Alprazolam's adverse effects are generally related to the sedation it can cause. Alprazolam has been mixed with alcohol as a drug of abuse to potentiate the sedative effects of the drug which may lead to coma and death. Alprazolam was given FDA approval on October 16, 1981. Alprazolam is indicated for the management of anxiety disorder, anxiety associated with depression, panic disorder, and panic disorder with agoraphobia. Alprazolam may also be prescribed off label for insomnia, premenstrual syndrome, and depression. Alprazolam is indicated to treat anxiety and panic disorders. The mechanism by which its cell receptor interactions translate to a clinical effect is not known. Alprazolam is a triazolobenzodiazepine used to treat certain anxiety and panic disorders. Alprazolam acts on benzodiazepine receptors BNZ-1 and BNZ-2. The active metabolites 4-hydroxyalprazolam acts on these receptors with 0.20 times the potency of alprazolam and alpha-hydroxyalprazolam acts on these receptors with 0.66 times the potency.",The molecular weight is 308.77.,Alprazolam has a topological polar surface area of 43.07.,The log p value of  is 2.55.,Alprazolam is approved and illicit and investigational.,Alprazolam is a solid.,True
14165,"Rosiglitazone is an anti-diabetic drug in the thiazolidinedione class of drugs. It is marketed by the pharmaceutical company GlaxoSmithKline as a stand-alone drug (Avandia) and in combination with metformin (Avandamet) or with glimepiride (Avandaryl). Like other thiazolidinediones, the mechanism of action of rosiglitazone is by activation of the intracellular receptor class of the peroxisome proliferator-activated receptors (PPARs), specifically PPARγ. Rosiglitazone is a selective ligand of PPARγ, and has no PPARα-binding action. Apart from its effect on insulin resistance, it appears to have an anti-inflammatory effect: nuclear factor kappa-B (NFκB) levels fall and inhibitor (IκB) levels increase in patients on rosiglitazone. Recent research has suggested that rosiglitazone may also be of benefit to a subset of patients with Alzheimer's disease not expressing the ApoE4 allele. This is the subject of a clinical trial currently underway. Rosiglitazone is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.  When rosiglitazone is used as monotherapy, it is associated with increases in total cholesterol, LDL, and HDL. It is also associated with decreases in free fatty acids. Increases in LDL occurred primarily during the first 1 to 2 months of therapy with AVANDIA and LDL levels remained elevated above baseline throughout the trials. In contrast, HDL continued to rise over time. As a result, the LDL/HDL ratio peaked after 2 months of therapy and then appeared to decrease over time.  Rosiglitazone acts as a highly selective and potent agonist at peroxisome proliferator activated receptors (PPAR) in target tissues for insulin action such as adipose tissue, skeletal muscle, and liver. Activation of PPAR-gamma receptors regulates the transcription of insulin-responsive genes involved in the control of glucose production, transport, and utilization. In this way, rosiglitazone enhances tissue sensitivity to insulin.",The molecular weight is 357.43.,Rosiglitazone has a topological polar surface area of 71.53.,The log p value of  is 3.02.,Rosiglitazone is approved and investigational.,Rosiglitazone is a solid.,True
14166,"A sulfonylurea hypoglycemic agent that is metabolized in the liver to 1-hydrohexamide. Acetohexamide has been discontinued in the US market. Used in the management of diabetes mellitus type 2 (adult-onset). Acetohexamide is an intermediate-acting, first-generation oral sulfonylurea. It lowers blood sugar by stimulating the pancreatic beta cells to secrete insulin and by helping the body use insulin efficiently. Due to its primary action on the pancreatic beta cells, the drug is only effective when there are functional pancreatic beta cells that can produce insulin granules. Acetohexamide has one-third the potency of chlorpropamide, and twice the potency of tolbutamide; however, similar hypoglycemic efficacy occurs with equipotent dosage of sulfonylureas. Sulfonylureas such as acetohexamide bind to an ATP-dependent K<sup>+</sup> channel on the cell membrane of pancreatic beta cells. This inhibits a tonic, hyperpolarizing outflux of potassium, which causes the electric potential over the membrane to become more positive. This depolarization opens voltage-gated Ca<sup>2+</sup> channels. The rise in intracellular calcium leads to increased fusion of insulin granulae with the cell membrane, and therefore increased secretion of (pro)insulin.",The molecular weight is 324.4.,Acetohexamide has a topological polar surface area of 92.34.,The log p value of  is 2.25.,Acetohexamide is approved and investigational and withdrawn.,Acetohexamide is a solid.,True
14167,"Ampicillin is a semi-synthetic derivative of penicillin that functions as an orally active broad-spectrum antibiotic. For treatment of infection (Respiratory, GI, UTI and meningitis) due to E. coli, P. mirabilis, enterococci, Shigella, S. typhosa and other Salmonella, nonpenicillinase-producing N. gononhoeae, H. influenzae, staphylococci, streptococci including streptoc Ampicillin is a penicillin beta-lactam antibiotic used in the treatment of bacterial infections caused by susceptible, usually gram-positive, organisms. The name \penicillin\"" can either refer to several variants of penicillin available, or to the group of antibiotics derived from the penicillins. Ampicillin has <i>in vitro</i> activity against gram-positive and gram-negative aerobic and anaerobic bacteria. The bactericidal activity of Ampicillin results from the inhibition of cell wall synthesis and is mediated through Ampicillin binding to penicillin binding proteins (PBPs). Ampicillin is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, and cephalosporinases and extended spectrum beta-lactamases."" By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, Ampicillin inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that Ampicillin interferes with an autolysin inhibitor.",The molecular weight is 349.41.,Ampicillin has a topological polar surface area of 112.73.,The log p value of  is -1.2.,Ampicillin is approved and vet_approved.,Ampicillin is a solid.,True
14168,"Spironolactone is a potassium sparing diuretic like that competitively inhibits mineralocorticoid receptors in the distal convoluted tubule to promote sodium and water excretion and potassium retention.. Spironolactone was originally developed purely for this ability before other pharmacodynamic properties of the drug were discovered. It is indicated to treat a number of conditions including heart failure, deem, hyperaldosteronism, adrenal hyperplasia, hypertension, and nephrotic syndrome. Off label uses of spironolactone involving its antiandrogenic activity include hirsutism, female pattern hair loss, and adult acne vulgaris. Spironolactone is also frequently used in medical gender transition. Spironolactone is indicated for the treatment of New York Heart Association Class III-IV heart failure, management of edema in cirrhotic adults not responsive to fluid and sodium restrictions, primary hyperaldosteronism short-term preoperatively, primary hyperaldosteronism long-term in patients with aldosterone producing adrenal adenomas that are not candidates for surgery or patients with bilarteral micro/macronodular adrenal hyperplasia, as an add-on therapy in hypertension, and in nephrotic syndrome when treatment of the disease as well as fluid and sodium restriction with other diuretics is inadequate. Originally spironolactone was only studied for its potassium sparing diuretic effect. Spironolactone competitively inhibits mineralocorticoid receptors in the distal convoluted tubule to promote sodium and water excretion and potassium retention.. Inhibition of this receptor leads to increased renin and aldosterone levels. Spironolactone competitively inhibits aldosterone dependant sodium potassium exchange channels in the distal convoluted tubule. This action leads to increased sodium and water excretion, but more potassium retention. The increased excretion of water leads to diuretic and also antihypertensive effects.",The molecular weight is 416.58.,Spironolactone has a topological polar surface area of 60.44.,The log p value of  is 2.84.,Spironolactone is approved.,Spironolactone is a solid.,True
14169,"Cefpiramide is a third-generation cephalosporin antibiotic. For treatment of severe infections caused by susceptible bacteria such as P. aeruginosa. Cefpiramide is a cephalosporin active against <i>Pseudomonas aeruginosa</i>. It has a broad spectrum of antibacterial activity. Cefpiramide works by inhibiting bacterial cell wall biosynthesis. The plasma half-lives of cefpiramide in rabbits, dogs, and rhesus monkeys were much longer than those of cefoperazone and cefazolin. The bactericidal activity of cefpiramide results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs).",The molecular weight is 612.64.,Cefpiramide has a topological polar surface area of 212.76.,The log p value of  is 1.94.,Cefpiramide is approved.,Cefpiramide is a solid.,True
14170,"Trifluridine is a fluorinated pyrimidine nucleoside that is structurally related to. It is an active antiviral agent in ophthalmic solutions used mainly in the treatment of primary keratoconjunctivitis and recurrent epithelial keratitis due to herpes simplex virus. It displays effective antiviral activity against Herpes simplex virus type 1 and 2.  Trifluridine is used for the treatment of primay keratoconjunctivitis and recurrent epithelial keratitis due to herpes simplex virus, types 1 and 2 in ophthalmic solutions. Trifluridine exhibits an antiviral effect against herpes simplex virus, types 1 and 2 and vacciniavirus both in vitro and in vivo. Some strains of adenovirus that contribute to the pathology of keratoconjunctivitis were shown to be susceptible to trifluridine _in vitro_. While there is evidence from a study that cross-resistance may develop between trifluridine and or , trifluridine was shown to effective in treating dendritic ulcers in patients with herpetic keratitis who are unresponsive to or based on the results from masked comparative trials. In nonclinical studies, trifluridine/tipiracil hydrochloride demonstrated antitumour activity against both 5-fluorouracil (5-FU) sensitive and resistant colorectal cancer cell lines. The cytotoxic activity of trifluridine and tipiracil against several human tumour xenografts show high correlation with the amount of trifluridine incorporated into DNA, indicating that the primary mechanism of action of trifluridine involves the direct incorporation into the cancer cell DNA. Trifluridine and tipiracil demonstrated anti-tumor activity against KRAS wild-type and mutant human colorectal cancer xenografts in mice.  The mechanism of action of trifluridine as an antiviral agent has not been fully elucidated, but appears to involve the inhibition of viral replication. Trifluridine gets incorporated into viral DNA during replication, which leads to the formation of defective proteins and an increased mutation rate. Trifluridine also mediates antineoplastic activities via this mechanism; following uptake into cancer cells, trifluridine is rapidly phosphorylated by thymidine kinase to its active monophosphate form. Subsequent phosphorylation produces trifluridine triphosphate , which is readily incorporated into the DNA of tumour cells in place of thymidine bases to perturb DNA function, DNA synthesis, and tumour cell proliferation. As trifluridine is subject to rapid degradation by TPase and readily metabolised by a first-pass effect following oral administration, tipiracil is added in the antineoplastic combination product as an inhibitor of TPase to increase the bioavailability of trifluridine. Trifluridine monophosphate also reversibly inhibits thymidylate synthetase (TS), an enzyme that is necessary for DNA synthesis and which levels are shown to be elevated different cancer cell lines. Up-regulation of the expression of the TS enzyme may also lead to the resistance to antineoplastic therapies, such as 5-fluorouracil (5-FU). However, this inhibitory effect is not considered to be sufficient enough to fully contribute to the cytotoxicity in cancer cells.",The molecular weight is 296.2.,Trifluridine has a topological polar surface area of 99.1.,The log p value of  is -0.41.,Trifluridine is approved and investigational.,Trifluridine is a solid.,True
14171,"A narcotic analgesic that can be used for the relief of most types of moderate to severe pain, including postoperative pain and the pain of labor. Prolonged use may lead to dependence of the morphine type; withdrawal symptoms appear more rapidly than with morphine and are of shorter duration. Used to control moderate to severe pain. Meperidine is a synthetic opiate agonist belonging to the phenylpiperidine class. Meperidine may produce less smooth muscle spasm, constipation, and depression of the cough reflex than equivalent doses of morphine. The onset of action is lightly more rapid than with morphine, and the duration of action is slightly shorter. The chemical structure of meperidine is similar to local anesthetics. Meperidine is recommended for relief of moderate to severe acute pain and has the unique ability to interrupt postoperative shivering and shaking chills induced by amphotericin B. Meperidine has also been used for intravenous regional anesthesia, peripheral nerve blocks and intraarticular, epidural and spinal analgesia. Meperidine is considered a second-line agent for the treatment of acute pain. Meperidine is primarily a kappa-opiate receptor agonist and also has local anesthetic effects. Meperidine has more affinity for the kappa-receptor than morphine. Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability.",The molecular weight is 247.34.,Meperidine has a topological polar surface area of 29.54.,The log p value of  is 2.23.,Meperidine is approved.,Meperidine is a solid.,True
14172,"Cefalotin is a cephalosporin antibiotic. Used to prevent infection during surgery and to treat many kinds of infections of the blood, bone or joints, respiratory tract, skin, and urinary tract. Cefalotin (INN) or cephalothin (USAN) is a semisynthetic first generation cephalosporin having a broad spectrum of antibiotic activity that is administered parenterally. The bactericidal activity of cefalotin results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs). The PBPs are transpeptidases which are vital in peptidoglycan biosynthesis. Therefore, their inhibition prevents this vital cell wall compenent from being properly synthesized.",The molecular weight is 396.43.,Cefalotin has a topological polar surface area of 113.01.,The log p value of  is 0.04.,Cefalotin is approved and investigational and vet_approved.,Cefalotin is a solid.,True
14173,"Imipramine, the prototypical tricyclic antidepressant (TCA), is a dibenzazepine-derivative TCA. TCAs are structurally similar to phenothiazines. They contain a tricyclic ring system with an alkyl amine substituent on the central ring. In non-depressed individuals, imipramine does not affect mood or arousal, but may cause sedation. In depressed individuals, imipramine exerts a positive effect on mood. TCAs are potent inhibitors of serotonin and norepinephrine reuptake. Tertiary amine TCAs, such as imipramine and amitriptyline, are more potent inhibitors of serotonin reuptake than secondary amine TCAs, such as nortriptyline and desipramine. TCAs also block histamine H<sub>1</sub> receptors, &alpha;<sub>1</sub>-adrenergic receptors and muscarinic receptors, which accounts for their sedative, hypotensive and anticholinergic effects (e.g. blurred vision, dry mouth, constipation, urinary retention), respectively. Imipramine has less sedative and anticholinergic effects than the tertiary amine TCAs, amitriptyline and clomipramine. Imipramine may be used to treat depression and nocturnal enuresis in children. Unlabeled indications include chronic and neuropathic pain (including diabetic neuropathy), panic disorder, attention-deficit/hyperactivity disorder (ADHD), and post-traumatic stress disorder (PTSD). For the relief of symptoms of depression and as temporary adjunctive therapy in reducing enuresis in children aged 6 years and older.  Imipramine is a tricyclic antidepressant with general pharmacological properties similar to those of structurally related tricyclic antidepressant drugs such as amitriptyline and doxepin. While it acts to block both, imipramine displays a much higher affinity for the serotonin reuptake transporter than for the norepinephrine reuptake transporter. Imipramine produces effects similar to other monoamine targeting antidepressants, increasing serotonin- and norepinephrine-based neurotransmission. Imipramine works by inhibiting the neuronal reuptake of the neurotransmitters norepinephrine and serotonin. It binds the sodium-dependent serotonin transporter and sodium-dependent norepinephrine transporter reducing the reuptake of norepinephrine and serotonin by neurons. Depression has been linked to a lack of stimulation of the post-synaptic neuron by norepinephrine and serotonin. Slowing the reuptake of these neurotransmitters increases their concentration in the synaptic cleft, producing knock-on effects in protein kinase signalling which is thought to contribute to changes in neurotransmission and brain physiology which relieves symptoms of depression. ",The molecular weight is 280.42.,Imipramine has a topological polar surface area of 6.48.,The log p value of  is 5.04.,Imipramine is approved.,Imipramine is a solid.,True
14174,"An oral retinoid effective in the treatment of psoriasis. It is the major metabolite of etretinate with the advantage of a much shorter half-life when compared with etretinate. For the treatment of severe psoriasis in adults. Acitretin is a retinoid. Retinoids have a structure similar to vitamin A and are involved in the normal growth of skin cells. Acitretin works by inhibiting the excessive cell growth and keratinisation (process by which skin cells become thickened due to the deposition of a protein within them) seen in psoriasis. It therefore reduces the thickening of the skin, plaque formation and scaling. The mechanism of action of acitretin is unknown, however it is believed to work by targeting specific receptors (retinoid receptors such as RXR and RAR) in the skin which help normalize the growth cycle of skin cells.",The molecular weight is 326.44.,Acitretin has a topological polar surface area of 46.53.,The log p value of  is 6.07.,Acitretin is approved.,Acitretin is a solid.,True
14175,"Nabumetone was originally developed as a non-acidic non-steroidal anti-inflammatory drug (NSAID). It was thought to avoid trapping of the drug in the stomach by making it unable to dissociate into ions which was believed to reduce GI toxicity by limiting local action. While slightly reduced, possibly due to a degree of cyclooxygenase-2 selectivity (COX-2), nabumetone still produces significant adverse effects in the GI tract. The molecule itself is a pro-drug with its 6-methoxy-2-naphthylacetic acid (6-MNA) metabolite acting as a potent COX inhibitor similar in structure to. Nabumetone was developed by Smithkline Beecham under the trade name Relafen and first received FDA approval in December, 1991. **Indicated** for: NSAIDs, like nabumetone, are well established as analgesics. NSAIDs reduce both peripheral and central sensitization of nociceptive neurons due to inflammation which contribute to hyperalgesia and allodynia. This sensitization occurs through reducing the action potential threshold in peripheral neurons, reducing the intensity of painful stimuli needed to produce a painful sensation. Centrally, activation of dorsal horn neurons occurs along with increased release of glutamate, calcitonin gene-related peptide (CGRP), and substance P which increase the transmission of painful stimuli. Coupled with this is an inhibition glycinergic neurons which normally inhibit pain transmission, a phenomenon known as disinhibition. Increased activity ofn-methyl d-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors leads to the establishment of central sensitization, allowing both mild painful and innocuous stimuli to produce action potentials in nociceptive projection neurons. NSAIDs are effective in reducing mild-moderate acute and chronic nociceptive pain, however, the usefulness of NSAIDs in neuropathic pain is limited. Nabumetone's active metabolite, 6-MNA, is an inhibitor of both COX-1 and COX-2 although it exhibits some COX-2 selectivity. Inhibition of COX-1 and COX-2 reduces conversion of arachidonic acid to PGs and thromboxane (TXA<sub>2</sub>). This reduction in prostanoid production is the common mechanism that mediates the effects of nambutone.",The molecular weight is 228.29.,Nabumetone has a topological polar surface area of 26.3.,The log p value of  is 2.98.,Nabumetone is approved.,Nabumetone is a solid.,True
14176,"Fluoxetine is a 2nd generation antidepressant categorized as a selective serotonin reuptake inhibitor (SSRI). It gained FDA approval in 1987 and although it was initially intended for the treatment of depression, today it is commonly prescribed to manage depression in addition to various other pathologies. Fluoxetine is indicated for both acute and maintenance treatment of major depressive disorder, obsessive compulsive disorder, and bulimia nervosa; however, it is only indicated for acute treatment of panic disorder independent of whether agoraphobia is present. Fluoxetine may also be used in combination with olanzapine to treat depression related to Bipolar I Disorder, and treatment resistant depression. Fluoxetine blocks the serotonin reuptake transporter in the presynaptic terminal, which ultimately results in sustained levels of 5-hydroxytryptamine (5-HT) in certain brain areas. However, fluoxetine binds with relatively poor affinity to 5-HT, dopaminergic, adrenergic, cholinergic, muscarinic, and histamine receptors which explains why it has a far more desirable adverse effect profile compared to earlier developed classes of antidepressants such as tricyclic antidepressants.  The monoaminergic hypothesis of depression emerged in 1965 and linked depression with dysfunction of neurotransmitters such as noradrenaline and serotonin. Indeed, low levels of serotonin have been observed in the cerebrospinal fluid of patients diagnosed with depression. As a result of this hypothesis, drugs that modulate levels of serotonin such as fluoxetine were developed.",The molecular weight is 309.33.,Fluoxetine has a topological polar surface area of 21.26.,The log p value of  is 4.57.,Fluoxetine is approved and vet_approved.,Fluoxetine is a solid.,True
14177,"Duloxetine is a dual serotonin and norepinephrine reuptake inhibitor. It was originally discovered in 1993 and developed by Eli Lilly and Company as LY248686. Duloxetine first received approval from the FDA in August, 2004 as Cymbalta for the treatment of Major Depressive Disorder. It has since received approval for a variety of indications including the treatment of neuropathic pain, Generalized Anxiety disorder, osteoarthritis, and stress incontinence. Duloxetine continues to be investigated for the treatment of pain in cancer, surgery, and more. **Indicated** for: Duloxetine, through increasing serotonin and norepinephrine concentrations in Onuf's nucleus, enhances glutamatergic activation of the pudendal motor nerve which innervates the external urethral sphinter. This enhanced signaling allows for stronger contraction. Increased contraction of this sphincter increases the pressure needed to produce an incontinence episode in stress urinary incontinence. Duloxetine has been shown to improve Patient Global Impression of Improvement and Incontinence Quality of Life scores. It has also been shown to reduce the median incontinence episode frequency at doses of 40 and 80 mg. Duloxetine is a potent inhibitor of neuronal serotonin and norepinephrine reuptake and a less potent inhibitor of dopamine reuptake. Duloxetine has no significant affinity for dopaminergic, adrenergic, cholinergic, histaminergic, opioid, glutamate, and GABA receptors.",The molecular weight is 297.42.,Duloxetine has a topological polar surface area of 21.26.,The log p value of  is 4.26.,Duloxetine is approved.,Duloxetine is a solid.,True
14178,"The prototypical phenothiazine antipsychotic drug. Like the other drugs in this class, chlorpromazine's antipsychotic actions are thought to be due to long-term adaptation by the brain to blocking dopamine receptors. Chlorpromazine has several other actions and therapeutic uses, including as an antiemetic and in the treatment of intractable hiccup. For the treatment of schizophrenia; to control nausea and vomiting; for relief of restlessness and apprehension before surgery; for acute intermittent porphyria; as an adjunct in the treatment of tetanus; to control the manifestations of the manic type of manic-depressive illness; for relief of intractable hiccups; for the treatment of severe behavioral problems in children (1 to 12 years of age) marked by combativeness and/or explosive hyperexcitable behavior (out of proportion to immediate provocations), and in the short-term treatment of hyperactive children who show excessive motor activity with accompanying conduct disorders consisting of some or all of the following symptoms: impulsivity, difficulty sustaining attention, aggressivity, mood lability, and poor frustration tolerance. Chlorpromazine is a psychotropic agent indicated for the treatment of schizophrenia. It also exerts sedative and antiemetic activity. Chlorpromazine has actions at all levels of the central nervous system-primarily at subcortical levels-as well as on multiple organ systems. Chlorpromazine has strong antiadrenergic and weaker peripheral anticholinergic activity; ganglionic blocking action is relatively slight. It also possesses slight antihistaminic and antiserotonin activity. Chlorpromazine acts as an antagonist (blocking agent) on different postsysnaptic receptors -on dopaminergic-receptors (subtypes D1, D2, D3 and D4 - different antipsychotic properties on productive and unproductive symptoms), on serotonergic-receptors (5-HT1 and 5-HT2, with anxiolytic, antidepressive and antiaggressive properties as well as an attenuation of extrapypramidal side-effects, but also leading to weight gain, fall in blood pressure, sedation and ejaculation difficulties), on histaminergic-receptors (H1-receptors, sedation, antiemesis, vertigo, fall in blood pressure and weight gain), alpha1/alpha2-receptors (antisympathomimetic properties, lowering of blood pressure, reflex tachycardia, vertigo, sedation, hypersalivation and incontinence as well as sexual dysfunction, but may also attenuate pseudoparkinsonism - controversial) and finally on muscarinic (cholinergic) M1/M2-receptors (causing anticholinergic symptoms like dry mouth, blurred vision, obstipation, difficulty/inability to urinate, sinus tachycardia, ECG-changes and loss of memory, but the anticholinergic action may attenuate extrapyramidal side-effects).",The molecular weight is 318.86.,Chlorpromazine has a topological polar surface area of 6.48.,The log p value of  is 5.5.,Chlorpromazine is approved and investigational and vet_approved.,Chlorpromazine is a liquid.,True
14179,"Raloxifene is a second generation selective estrogen receptor modulator (SERM) that mediates anti-estrogenic effects on breast and uterine tissues, and estrogenic effects on bone, lipid metabolism, and blood coagulation. Exhibiting tissue-specific effects distinct from , raloxifene is the first of the benzothiophene group of antiestrogens to be labelled a SERM. Available in many countries worldwide, raloxifene was initially approved by the FDA in December, 1997 under the market name Evista® for the management and prevention of osteoporosis in postmenopausal women and reduction in risk for invasive breast cancer in postmenopausal women with osteoporosis or those who are at high risk for invasive breast cancer. However, it has a negligible effect on altering the development and progression of breast cancer itself. The most common causes of osteoporosis include postmenopausal deficiency of estrogen and age-related deterioration in bone homeostasis. Due to the risk of bone fractures that may lead to morbidities and reduced quality of life, the management of osteoporosis in postmenopausal women with the use of therapeutic agents in addition to concurrent therapies is critical. Due to the decline in estrogen levels in postmenopausal osteoporosis, hormone replacement therapy (HRT), such as estradiol, has been used to ameliorate the condition. However, due to the off-target actions by HRT, newer non-hormonal agents such as raloxifene and have been developed to reduce adverse events through selective pharmacological actions on tissue-specific therapeutic targets. Indicated for the prevention and treatment of osteoporosis in postmenopausal women, as well as prevention and treatment of corticosteroid-induced bone loss. Raloxifene belongs to the selective estrogen receptor modulator (SERM) drug class that exhibits estrogenic effects on bone and lipid metabolism while mediating anti-estrogenic effects on uterine endometrium and breast tissues. On skeletal tissues, raloxifene stimulates bone-depositing osteoblasts and inhibits bone-resorbing osteoclasts to augument bone mineral density. Raloxifene produces estrogen-like effects on bone, reducing the resorption of bone and increasing bone mineral density in postmenopausal women, thus slowing the rate of bone loss. In three randomized, placebo-controlled trials in Europe, postmenopausal women receiving raloxifene at variable doses of 30 to 150 mg daily demonstrated significant increases in bone mineral density in the lumbar spine, total hip, femoral neck and total body compared to placebo. In the MORE and RUTH trials, there were fewer incidences of vertebral fractures in postmeopausal women receiving raloxifene compared to placebo. In a eight-week study evaluating short-term effects of raloxifene in healthy postmenopausal women, there was a decrease in the bone turnover markers, such as serum alkaline phosphatase level, serum osteocalcin level and urinary calcium excretion.  Raloxifene is a selective estrogen receptor modulator that acts as both an estrogen agonist and antagonist via differential effects on the tissue-specific estrogen receptors. Based on the findings of competitive binding assays, raloxifene displays binding affinity that is similar to that of , the predominant circulating estrogen. Estrogens play variable roles at different tissues in females, including the bone, breasts, uterus and liver, by binding to the steroid nuclear hormone receptors, Estrogen Receptor alpha (ERα) or Estrogen Receptor beta (ERβ). These receptors are normally bound to the Heat Shock Protein 90 (Hsp90) when unbound to the ligand. Ligand binding induces a conformational change in the receptor that promotes dissociation of the receptor from Hsp90, dimerization and translocation into the nucleus. This movement into the nucleus allows the receptor to bind to genomic locations based on sequence recognition of the DNA binding domain, also known as the Estrogen Response Elements (EREs). ",The molecular weight is 473.59.,Raloxifene has a topological polar surface area of 70.0.,The log p value of  is 6.86.,Raloxifene is approved and investigational.,Raloxifene is a solid.,True
14180,"Buspirone is a novel anxiolytic agent with a unique structure and a pharmacological profile. Belonging to the azaspirodecanedione drug class, buspirone is a serotonin 5-HT<sub>1A</sub> receptor agonist that is not chemically or pharmacologically related to benzodiazepines, barbiturates, and other sedative/anxiolytic drugs. Unlike many drugs used to treat anxiety, buspirone does not exhibit anticonvulsant, sedative, hypnotic, and muscle-relaxant properties. Due to these characteristics, buspirone been termed 'anxioselective'. First synthesized in 1968 then patented in 1975, it is commonly marketed under the brand name Buspar®. Buspirone was first approved in 1986 by the FDA and has been used to treat anxiety disorders, such as generalized anxiety disorder (GAD), and relieve symptoms of anxiety. It has also been used as a second-line therapy for unipolar depression when the use of selective serotonin reuptake inhibitors (SSRIs) is deemed clinically inadequate or inappropriate. The potential use of buspirone in combination with in depression and cognitive impairment via promoting neurogenesis has also been investigated. Indicated for the management of anxiety disorders or the short-term relief of the symptoms of anxiety. The clinical effect of buspirone in alleviating the symptoms of generalized anxiety disorders typically takes 2 to 4 weeks to achieve. The delayed onset of action of buspirone suggests that the therapeutic effectiveness in generalized anxiety may involved more than its molecular mechanism of action at the 5-HT<sub>1A</sub> receptors, or buspirone may induce adaptations of 5-HT<sub>1A</sub> receptors. Buspirone was not shown to alter the psychomotor or cognitive function in healthy volunteers, and the risk of developing sedation is relatively low compared to other anxiolytics, such as benzodiazepines. Unlike benzodiazepines and barbiturates used in anxiety disorders, buspirone is not associated with a risk for developing physical dependence or withdrawal, or any significant interaction with central nervous system depressants such as ethanol. This is due to the lack of effects on GABA receptors. Buspirone also does not exhibit any anticonvulsant or muscle-relaxing properties, but may interfere with arousal reactions due to its inhibitory action on the aactivity of noradrenergic locus coerulus neurons. The therapeutic action of buspirone in generalized anxiety disorders is thought to be mainly derived from its interaction with two major 5-HT<sub>1A</sub> receptor subtypes that are involved in the brain's anxiety and fear circuitry to enhance the serotonergic activity in these brain areas. Buspirone acts as a full agonist at presynaptic 5-HT<sub>1A</sub> receptors, or 5-HT<sub>1A</sub> autoreceptors, expressed at dorsal raphe while acting as a partial agonist at the postsynaptic 5-HT<sub>1A</sub> receptors expressed on hippocampus and cortex. 5-HT<sub>1A</sub> receptors function as inhibitory autoreceptors by being expressed on the soma or dendrites of serotonergic neurons or mediate postsynaptic actions of 5-HT by being highly expressed on the corticolimbic circuits. They are inhibitory G-protein coupled receptors that couple to Gi/Go proteins. When activated, presynaptic 5-HT<sub>1A</sub> autoreceptors causes neuron hyperpolarization and reduces the firing rate of the serotonergic neuron, thereby decreasing extracellular 5-HT levels in the neuron's projection areas. Activated postsynaptic 5-HT<sub>1A</sub> receptors promote hyperpolarization to released 5-HT on pyramidal neurons. ",The molecular weight is 385.51.,Buspirone has a topological polar surface area of 69.64.,The log p value of  is 2.19.,Buspirone is approved and investigational.,Buspirone is a solid.,True
14181,"A dideoxynucleoside compound in which the 3&#39;-hydroxy group on the sugar moiety has been replaced by an azido group. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA during reverse transcription. It improves immunologic function, partially reverses the HIV-induced neurological dysfunction, and improves certain other clinical abnormalities associated with AIDS. Its principal toxic effect is dose-dependent suppression of bone marrow, resulting in anemia and leukopenia.  Used in combination with other antiretroviral agents for the treatment of human immunovirus (HIV) infections. Zidovudine is a nucleoside reverse transcriptase inhibitor (NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Zidovudine is phosphorylated to active metabolites that compete for incorporation into viral DNA. They inhibit the HIV reverse transcriptase enzyme competitively and act as a chain terminator of DNA synthesis. The lack of a 3'-OH group in the incorporated nucleoside analogue prevents the formation of the 5' to 3' phosphodiester linkage essential for DNA chain elongation, and therefore, the viral DNA growth is terminated. Zidovudine, a structural analog of thymidine, is a prodrug that must be phosphorylated to its active 5′-triphosphate metabolite, zidovudine triphosphate (ZDV-TP). It inhibits the activity of HIV-1 reverse transcriptase (RT) via DNA chain termination after incorporation of the nucleotide analogue. It competes with the natural substrate dGTP and incorporates itself into viral DNA. It is also a weak inhibitor of cellular DNA polymerase α and γ. ",The molecular weight is 267.24.,Zidovudine has a topological polar surface area of 108.3.,The log p value of  is 0.04.,Zidovudine is approved.,Zidovudine is a solid.,True
14182,"Oxycodone is a semisynthetic opioid analgesic derived from thebaine in Germany in 1917. It is currently indicated as an immediate release product for moderate to severe pain and as an extended release product for chronic moderate to severe pain requiring continuous opioid analgesics for an extended period. The first oxycodone containing product, Percodan, was approved by the FDA on April 12, 1950. Oxycodone is indicated for the treatment of moderate to severe pain. There is also an extended release formulation indicated for chronic moderate to severe pain requiring continuous opioid analgesics for an extended period. Oxycodone acts directly on a number of tissues not related to its analgesic effect. These tissues include the respiratory centre in the brain stem, the cough centre in the medulla, muscles of the pupils, gastrointestinal tract, cardiovascular system, endocrine system, and immune system. Oxycodone's effect on the respiratory centre is dose dependant respiratory depression. The action on the cough centre is suppression of the cough reflex. Pupils become miopic or decrease in size, peristalsis of the gastrointestinal tract slows, and muscle tone in the colon may increase causing constipation. In the cardiovascular system histamine may be released leading to pruritis, red eyes, flushing, sweating, and decreased blood pressure. Endocrine effects may include increased prolactin, decreased cortisol, and decreased testosterone. It is not yet known if the effects of opioids on the immune system are clinically significant. The full mechanism of oxycodone is not known. Under conditions of inflammation or hyperalgesia, opioid receptors in the heart, lungs, liver, gastrointestinal tract, and reproductive system are upregulated and transported to nerve terminals. Oxycodone and its active metabolites, noroxycodone, oxymorphone, and noroxymorphone are opioid agonists. These compounds passively diffuse across the blood brain barrier or may be actively transported across by an unknown mechanism. Oxycodone and its active metabolites can selectively bind to the mu opioid receptor, but also the kappa and delta opioid receptors in the central nervous system and periphery, and induce a G protein coupled receptor signalling pathway. Activation of mu opioid receptors inhibits N-type voltage operated calcium channels, inhibiting responses to pain.",The molecular weight is 315.37.,Oxycodone has a topological polar surface area of 59.0.,The log p value of  is -0.04.,Oxycodone is approved and illicit and investigational.,Oxycodone is a solid.,True
14183,"A non-steroidal anti-inflammatory agent (anti-inflammatory agents, NON-steroidal) similar in mode of action to indomethacin. For the relief of signs and symptoms of rheumatoid arthritis and osteoarthritis, including the treatment of acute flares long-term management. Also for treatment of juvenile rheumatoid arthritis. Tolmetin is a nonsteroidal anti-inflammatory agent. Studies in animals have shown tolmetin to possess anti-inflammatory, analgesic and antipyretic activity. In the rat, tolmetin prevents the development of experimentally induced polyarthritis and also decreases established inflammation. In patients with either rheumatoid arthritis or osteaoarthritis, tolmetin is as effective as aspirin and indomethacin in controlling disease activity, but the frequency of the milder gastrointestinal adverse effects and tinnitus was less than in aspirin-treated patients, and the incidence of central nervous system adverse effects was less than in indomethacin-treated patients. In patients with juvenile rheumatoid arthritis, tolmetin is as effective as aspirin in controlling disease activity, with a similar incidence of adverse reactions. tolmetin has produced additional therapeutic benefit when added to a regimen of gold salts and, to a lesser extent, with corticosteroids. Tolmetin should not be used in conjunction with salicylates since greater benefit from the combination is not likely, but the potential for adverse reactions is increased. The mode of action of tolmetin is not known. However, studies in laboratory animals and man have demonstrated that the anti-inflammatory action of tolmetin is not due to pituitary-adrenal stimulation. Tolmetin inhibits prostaglandin synthetase in vitro and lowers the plasma level of prostaglandin E in man. This reduction in prostaglandin synthesis may be responsible for the anti-inflammatory action. Tolmetin does not appear to alter the course of the underlying disease in man.",The molecular weight is 257.29.,Tolmetin has a topological polar surface area of 59.3.,The log p value of  is 2.21.,Tolmetin is approved.,Tolmetin is a solid.,True
14184,"Ritonavir is an HIV protease inhibitor that interferes with the reproductive cycle of HIV. Although it was initially developed as an independent antiviral agent, it has been shown to possess advantageous properties in combination regimens with low-dose ritonavir and other protease inhibitors. It is now more commonly used as a booster of other protease inhibitors and is available in both liquid formulation and as capsules.  Indicated in combination with other antiretroviral agents for the treatment of HIV-1 infection. Ritonavir is a protease inhibitor with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Protease inhibitors block the part of HIV called protease. HIV-1 protease is an enzyme required for the proteolytic cleavage of the viral polyprotein precursors into the individual functional proteins found in infectious HIV-1. Ritonavir binds to the protease active site and inhibits the activity of the enzyme. This inhibition prevents cleavage of the viral polyproteins resulting in the formation of immature non-infectious viral particles. Protease inhibitors are almost always used in combination with at least two other anti-HIV drugs. Modern protease inhibitors require the use of low-dose ritonavir to boost pharmacokinetic exposure through inhibition of metabolism via the cytochrome P450 3A4 enzyme pathway.  Ritonavic inhibits the HIV viral proteinase enzyme that normally cleaves the structural and replicative proteins that arise from major HIV genes, such as *gag* and *pol*. *Gag* encodes proteins involved in the core and the nucleocapsid, while *pol* encodes the the HIV reverse transcriptase, ribonuclease H, integrase, and protease. The *pol*-encoded proteins are initially translated in the form of a larger precursoe polypeptide, *gag-pol*, and needs to be cleaved by HIV protease to form other complement proteins. Ritonavir prevents the cleavage of the *gag-pol* polyprotein, which results in noninfectious, immature viral particles. Ritonavir is a potent inhibitor of cytochrome P450 CYP3A4 isoenzyme present both in the intestinal tract and liver. It is a type II ligand that perfectly fits into the CYP3A4 active site cavity and irreversibly binds to the heme iron via the thiazole nitrogen, which decreases the redox potential of the protein and precludes its reduction with the redox partner, cytochrome P450 reductase. Ritonavir may also play a role in limiting cellular transport and efflux of other protease inhibitors via the P-glycoprotein and MRP efflux channels.",The molecular weight is 720.95.,Ritonavir has a topological polar surface area of 145.78.,The log p value of  is 4.94.,Ritonavir is approved and investigational.,Ritonavir is a solid.,True
14185,"Antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to ristocetin that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear. A variety of dosage forms (for example, oral, injections, etc.) exist for the treatment of serious or severe infections caused by susceptible strains of methicillin-resistant (beta-lactam-resistant) staphylococci. Vancomycin is a branched tricyclic glycosylated nonribosomal peptide often reserved as the \drug of last resort\"", used only after treatment with other antibiotics has failed. Vancomycin has been shown to be active against most strains of the following microorganisms, both in vitro and in clinical infections: <i>Listeria monocytogenes</i>, <i>Streptococcus pyogenes</i>, <i>Streptococcus pneumoniae</i> (including penicillin-resistant strains), <i>Streptococcus agalactiae</i>, <i>Actinomyces</i> species, and <i>Lactobacillus</i> species. The combination of vancomycin and an aminoglycoside acts synergistically in vitro against many strains of Staphylococcus aureus, Streptococcus bovis, enterococci, and the viridans group streptococci."" The bactericidal action of vancomycin results primarily from inhibition of cell-wall biosynthesis. Specifically, vancomycin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix, which forms the major structural component of Gram-positive cell walls. Vancomycin forms hydrogen bonds with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides, preventing the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, vancomycin alters bacterial-cell-membrane permeability and RNA synthesis. There is no cross-resistance between vancomycin and other antibiotics. Vancomycin is not active in vitro against gram-negative bacilli, mycobacteria, or fungi.                                                            ",The molecular weight is 1449.27.,Vancomycin has a topological polar surface area of 530.49.,The log p value of  is -1.14.,Vancomycin is approved.,Vancomycin is a solid.,True
14186,"Cisplatin, cisplatinum or cis-diamminedichloroplatinum(II) (CDDP) is a platinum-based chemotherapy drug used to treat various types of cancers, including sarcomas, some carcinomas (e.g. small cell lung cancer, and ovarian cancer), lymphomas and germ cell tumors. It was the first member of its class, which now also includes carboplatin and oxaliplatin. For the treatment of metastatic testicular tumors, metastatic ovarian tumors and advanced bladder cancer. Cisplatin is an antineoplastic in the class of alkylating agents and is used to treat various forms of cancer. Alkylating agents are so named because of their ability to add alkyl groups to many electronegative groups under conditions present in cells. They stop tumor growth by cross-linking guanine bases in DNA double-helix strands - directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. In addition, these drugs add methyl or other alkyl groups onto molecules where they do not belong which in turn inhibits their correct utilization by base pairing and causes a miscoding of DNA. Alkylating agents are cell cycle-nonspecific. Alkylating agents work by three different mechanisms all of which achieve the same end result - disruption of DNA function and cell death. Alkylating agents work by three different mechanisms: 1) attachment of alkyl groups to DNA bases, resulting in the DNA being fragmented by repair enzymes in their attempts to replace the alkylated bases, preventing DNA synthesis and RNA transcription from the affected DNA, 2) DNA damage via the formation of cross-links (bonds between atoms in the DNA) which prevents DNA from being separated for synthesis or transcription, and 3) the induction of mispairing of the nucleotides leading to mutations.",The molecular weight is 300.05.,,,Cisplatin is approved.,Cisplatin is a solid.,True
14187,"Erlotinib is an inhibitor of the epidermal growth factor receptor (EGFR) tyrosine kinase that is used in the treatment of non-small cell lung cancer, pancreatic cancer and several other types of cancer. It is typically marketed under the trade name Tarceva. Erlotinib binds to the epidermal growth factor receptor (EGFR) tyrosine kinase in a reversible fashion at the adenosine triphosphate (ATP) binding site of the receptor. Recent studies demonstrate that erlotinib is also a potent inhibitor of JAK2V617F, which is a mutant form of tyrosine kinase JAK2 found in most patients with polycythemia vera (PV) and a substantial proportion of patients with idiopathic myelofibrosis or essential thrombocythemia. This finding introduces the potential use of erlotinib in the treatment of JAK2V617F-positive PV and other myeloproliferative disorders. Erlotinib is indicated for: The mechanism of clinical antitumor action of erlotinib is not fully characterized. Erlotinib inhibits the intracellular phosphorylation of tyrosine kinase associated with the epidermal growth factor receptor (EGFR). Specificity of inhibition with regard to other tyrosine kinase receptors has not been fully characterized. EGFR is expressed on the cell surface of normal cells and cancer cells.",The molecular weight is 393.44.,Erlotinib has a topological polar surface area of 74.73.,The log p value of  is 4.19.,Erlotinib is approved and investigational.,Erlotinib is a solid.,True
14188,"Ciprofloxacin is a second generation fluoroquinolone that has spawned many derivative antibiotics. It is formulated for oral, intravenous, intratympanic, ophthalmic, and otic administration for a number of bacterial infections. Ciprofloxacin is only indicated in infections caused by susceptible bacteria. Ciprofloxacin is a second generation fluoroquinolone that is active against many Gram negative and Gram positive bacteria. It produces its action through inhibition of bacterial DNA gyrase and topoisomerase IV. Ciprofloxacin binds to bacterial DNA gyrase with 100 times the affinity of mammalian DNA gyrase. There is no cross resistance between fluoroquinolones and other classes of antibiotics, so it may be of clinical value when other antibiotics are no longer effective. Ciprofloxain and its derivatives are also being investigated for its action against malaria, cancers, and AIDS. Ciprofloxacin acts on bacterial topoisomerase II (DNA gyrase) and topoisomerase IV. Ciprofloxacin's targeting of the alpha subunits of DNA gyrase prevents it from supercoiling the bacterial DNA which prevents DNA replication.",The molecular weight is 331.35.,Ciprofloxacin has a topological polar surface area of 72.88.,The log p value of  is -0.73.,Ciprofloxacin is approved and investigational.,Ciprofloxacin is a solid.,True
14189,"Nortriptyline hydrochloride, the active metabolite of , is a tricyclic antidepressant (TCA). It is used in the treatment of major depression and is also used off-label for chronic pain and other conditions. Nortriptyline is indicated for the relief of the symptoms of major depressive disorder (MDD). Some off-label uses for this drug include treatment of chronic pain, myofascial pain, neuralgia, and irritable bowel syndrome. Nortriptyline exerts antidepressant effects likely by inhibiting the reuptake of serotonin and norepinephrine at neuronal cell membranes. It also exerts antimuscarinic effects through its actions on the acetylcholine receptor. Though prescribing information does not identify a specific mechanism of action for nortriptyline, is believed that nortriptyline either inhibits the reuptake of the neurotransmitter serotonin at the neuronal membrane or acts at the level of the beta-adrenergic receptors. It displays a more selective reuptake inhibition for noradrenaline, which may explain increased symptom improvement after nortriptyline therapy. Tricyclic antidepressants do not inhibit monoamine oxidase nor do they affect dopamine reuptake. As with other tricyclics, nortriptyline displays affinity for other receptors including mACh receptors, histamine receptors, 5-HT receptors, in addition to other receptors. ",The molecular weight is 263.38.,Nortriptyline has a topological polar surface area of 12.03.,The log p value of  is 4.31.,Nortriptyline is approved.,Nortriptyline is a solid.,True
14190,"A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the thymidylate synthetase conversion of deoxyuridylic acid to thymidylic acid. For the topical treatment of multiple actinic or solar keratoses. In the 5% strength it is also useful in the treatment of superficial basal cell carcinomas when conventional methods are impractical, such as with multiple lesions or difficult treatment sites. Fluorouracil injection is indicated in the palliative management of some types of cancer, including colon, esophageal, gastric, rectum, breast, biliary tract, stomach, head and neck, cervical, pancreas, renal cell, and carcinoid. Fluorouracil is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA. They prevent these substances from becoming incorporated into DNA during the \S\"" phase (of the cell cycle), stopping normal development and division. Fluorouracil blocks an enzyme which converts the cytosine nucleotide into the deoxy derivative. In addition, DNA synthesis is further inhibited because Fluorouracil blocks the incorporation of the thymidine nucleotide into the DNA strand."" The precise mechanism of action has not been fully determined, but the main mechanism of fluorouracil is thought to be the binding of the deoxyribonucleotide of the drug (FdUMP) and the folate cofactor, N5–10-methylenetetrahydrofolate, to thymidylate synthase (TS) to form a covalently bound ternary complex. This results in the inhibition of the formation of thymidylate from uracil, which leads to the inhibition of DNA and RNA synthesis and cell death. Fluorouracil can also be incorporated into RNA in place of uridine triphosphate (UTP), producing a fraudulent RNA and interfering with RNA processing and protein synthesis.",The molecular weight is 130.08.,Fluorouracil has a topological polar surface area of 58.2.,The log p value of  is -0.58.,Fluorouracil is approved.,Fluorouracil is a solid.,True
14191,"A cyclooxygenase inhibiting, non-steroidal anti-inflammatory agent (NSAID) that is well established in treating rheumatoid arthritis and osteoarthritis and used for musculoskeletal disorders, dysmenorrhea, and postoperative pain. Its long half-life enables it to be administered once daily. For treatment of osteoarthritis and rheumatoid arthritis. Piroxicam is in a class of drugs called nonsteroidal anti-inflammatory drugs (NSAIDs). Piroxicam works by reducing hormones that cause inflammation and pain in the body. Piroxicam is used to reduce the pain, inflammation, and stiffness caused by rheumatoid arthritis and osteoarthritis. The antiinflammatory effect of Piroxicam may result from the reversible inhibition of cyclooxygenase, causing the peripheral inhibition of prostaglandin synthesis. The prostaglandins are produced by an enzyme called Cox-1. Piroxicam blocks the Cox-1 enzyme, resulting into the disruption of production of prostaglandins. Piroxicam also inhibits the migration of leukocytes into sites of inflammation and prevents the formation of thromboxane A2, an aggregating agent, by the platelets.",The molecular weight is 331.35.,Piroxicam has a topological polar surface area of 99.6.,The log p value of  is 1.89.,Piroxicam is approved and investigational.,Piroxicam is a solid.,True
14192,"Lamotrigine is an antiepileptic drug belonging in the phenyltriazine class. It is used in the treatment of both epilepsy and as a mood stabilizer in bipolar disorder. Lamotrigine is the first medication since lithium granted Food and Drug Administration (FDA) approval for the maintenance treatment of bipolar type I.  It is approved for use in more than 30 countries. Lamotrigine is indicated as adjunctive therapy for the following seizure types in patients ≥2 years of age: partial seizures, primary generalized tonic-clonic seizures, and generalized seizures due to Lennox-Gastaut syndrome. Lamotrigine likely prevents seizures and prevents mood symptoms via stabilizing presynaptic neuronal membranes and preventing the release of excitatory neurotransmitters such as glutamate, which contribute to seizure activity.  The exact mechanism of action of lamotrigine is not fully elucidated, as it may exert cellular activities that contribute to its efficacy in a range of conditions. Although chemically unrelated, lamotrigine actions resemble those of phenytoin and carbamazepine, inhibiting voltage-sensitive sodium channels, stabilizing neuronal membranes, thereby modulating the release of presynaptic excitatory neurotransmitters. ",The molecular weight is 256.09.,Lamotrigine has a topological polar surface area of 90.71.,The log p value of  is 2.53.,Lamotrigine is approved and investigational.,Lamotrigine is a solid.,True
14193,"Hydroxyzine is a first-generation histamine H<sub>1</sub>-receptor antagonist of the dephenylmethane and piperazine classes that exhibits sedative, anxiolytic, and antiemetic properties. It was first developed in 1955, and has since remained a relatively common treatment for allergic conditions such as pruritus, urticaria, dermatoses, and histamine-mediated pruritus. The active metabolite of hydroxyzine, , is also available as an active ingredient in allergic medications, and is responsible for much of its hydroxyzine's antihistaminic effect. Hydroxyzine is also used for generalized anxiety disorder, tension caused by psychoneurosis, and other conditions with manifestations of anxiety. Hydroxyzine is indicated for the symptomatic relief of anxiety and tension associated with psychoneuroses, and as an adjunct in organic disease states in which anxiety is manifested. It is also indicated in the treatment of histamine-mediated pruritus and pruritus due to allergic conditions such as chronic urticaria. Hydroxyzine blocks the activity of histamine to relieve allergic symptoms such as pruritus. Activity at off-targets also allows for its use as a sedative anxiolytic and an antiemetic in certain disease states. The H<sub>1</sub> histamine receptor is responsible for mediating hypersensitivity and allergic reactions. Exposure to an allergen results in degranulation of mast cells and basophils, which then release histamine and other inflammatory mediators. Histamine binds to, and activates, H<sub>1</sub> receptors, which results in the further release of pro-inflammatory cytokines, such as interleukins, from basophils and mast cells. These downstream effects of histamine binding are responsible for a wide variety of allergic symptoms, such as pruritus, rhinorrhea, and watery eyes.",The molecular weight is 374.91.,Hydroxyzine has a topological polar surface area of 35.94.,The log p value of  is 4.0.,Hydroxyzine is approved.,Hydroxyzine is a solid.,True
14194,"Methotrexate is a folate derivative that inhibits several enzymes responsible for nucleotide synthesis. This inhibition leads to suppression of inflammation as well as prevention of cell division. Because of these effects, methotrexate is often used to treat inflammation caused by arthritis or to control cell division in neoplastic diseases such as breast cancer and non-Hodgkin's lymphoma. Methotrexate oral solution is indicated for pediatric acute lymphoblastic leukemia and pediatric polyarticular juvenile idiopathic arthritis. Methotrexate injections for subcutaneous use are indicated for severe active rheumatoid arthritis, polyarticular juvenile idiopathic arthritis and severe, recalcitrant, disabling psoriasis. Methotrexate inhibits enzymes responsible for nucleotide synthesis which prevents cell division and leads to anti-inflammatory actions. It has a long duration of action and is generally given to patients once weekly. Methotrexate has a narrow therapeutic index. Methotrexate enters tissues and is converted to a methotrexate polyglutamate by folylpolyglutamate.",The molecular weight is 454.45.,Methotrexate has a topological polar surface area of 210.54.,The log p value of  is -0.53.,Methotrexate is approved.,Methotrexate is a solid.,True
14195,"Cephalexin is the first of the first generation cephalosporins. This antibiotic contains a beta lactam and a dihydrothiazide. Cephalexin is used to treat a number of susceptible bacterial infections through inhibition of cell wall synthesis. Cephalexin was approved by the FDA on 4 January 1971. Cephalexin is indicated for the treatment of certain infections caused by susceptible bacteria. These infections include respiratory tract infections, otitis media, skin and skin structure infections, bone infections, and genitourinary tract infections. Cephalexin (also called Cefalexin) is a first generation cephalosporin antibiotic. It is one of the most widely prescribed antibiotics, often used for the treatment of superficial infections that result as complications of minor wounds or lacerations. It is effective against most gram-positive bacteria through its inihibition of the cross linking reaction between N-acetyl muramicacid and N-acetylglucosamine in the cell wall, leading to cell lysis. Cephalexin is a first generation cephalosporin antibiotic. Cephalosporins contain a beta lactam and dihydrothiazide. Unlike penicillins, cephalosprins are more resistant to the action of beta lactamase. Cephalexin inhibits bacterial cell wall synthesis, leading breakdown and eventualy cell death.",The molecular weight is 347.39.,Cephalexin has a topological polar surface area of 112.73.,The log p value of  is -1.84.,Cephalexin is approved and investigational and vet_approved.,Cephalexin is a solid.,True
14196,"Propranolol is a racemic mixture of 2 enantiomers where the S(-)-enantiomer has approximately 100 times the binding affinity for beta adrenergic receptors. Propranolol is used to treat a number of conditions but most commonly is used for hypertension.  Propranolol is indicated to treat hypertension. Propranolol is also indicated to treat angina pectoris due to coronary atherosclerosis, atrial fibrillation, myocardial infarction, migraine, essential tremor, hypertrophic subaortic stenosis, pheochromocytoma, and proliferating infantile hemangioma. Propranolol is a beta-adrenergic receptor antagonist used to treat hypertension. Propranolol has a long duration of action as it is given once or twice daily depending on the indication. When patients abruptly stop taking propranolol, they may experience exacerbations of angina and myocardial infarctions. Propranolol is a nonselective β-adrenergic receptor antagonist. Blocking of these receptors leads to vasoconstriction, inhibition of angiogenic factors like vascular endothelial growth factor (VEGF) and basic growth factor of fibroblasts (bFGF), induction of apoptosis of endothelial cells, as well as down regulation of the renin-angiotensin-aldosterone system.",The molecular weight is 259.35.,Propranolol has a topological polar surface area of 41.49.,The log p value of  is 2.75.,Propranolol is approved and investigational.,Propranolol is a solid.,True
14197,"An anti-inflammatory analgesic and antipyretic highly bound to plasma proteins. It is pharmacologically similar to aspirin, but causes less gastrointestinal bleeding. For relief of the signs and symptoms of rheumatoid arthritis and osteoarthritis. Also for the relief of mild to moderate pain. Fenoprofen is a propionic acid derivative with analgesic, antiinflammatory and antipyretic properties. Fenoprofen inhibits prostaglandin synthesis by decreasing the enzyme needed for biosynthesis. In patients with rheumatoid arthritis, the anti-inflammatory action of fenoprofen has been evidenced by relief of pain, increase in grip strength, and reductions in joint swelling, duration of morning stiffness, and disease activity (as assessed by both the investigator and the patient). In patients with osteoarthritis, the anti-inflammatory and analgesic effects of fenoprofen have been demonstrated by reduction in tenderness as a response to pressure and reductions in night pain, stiffness, swelling, and overall disease activity (as assessed by both the patient and the investigator). These effects have also been demonstrated by relief of pain with motion and at rest and increased range of motion in involved joints. In patients with rheumatoid arthritis and osteoarthritis, clinical studies have shown fenoprofen to be comparable to aspirin in controlling the aforementioned measures of disease activity, but mild gastrointestinal reactions (nausea, dyspepsia) and tinnitus occurred less frequently in patients treated with fenoprofen than in aspirin-treated patients. It is not known whether fenoprofen causes less peptic ulceration than does aspirin. In patients with pain, the analgesic action of fenoprofen has produced a reduction in pain intensity, an increase in pain relief, improvement in total analgesia scores, and a sustained analgesic effect. Fenoprofen's exact mode of action is unknown, but it is thought that prostaglandin synthetase inhibition is involved. Fenoprofen has been shown to inhibit prostaglandin synthetase isolated from bovine seminal vesicles.",The molecular weight is 242.27.,Fenoprofen has a topological polar surface area of 46.53.,The log p value of  is 3.82.,Fenoprofen is approved.,Fenoprofen is a solid.,True
14198,"Clonidine is an imidazole derivate that acts as an agonist of alpha-2 adrenoceptors. This activity is useful for the treatment of hypertension, severe pain, and ADHD. Clonidine tablets and transdermal systems are indicated for the treatment of hypertension alone or in combination with other medications. A clonidine injection is indicated for use with opiates in the treatment of severe cancer pain where opiates alone are insufficient. An extended release tablet of clonidine is indicated for the treatment of ADHD either alone or in combination with other medications. Clonidine functions through agonism of alpha-2 adrenoceptors which have effects such as lowering blood pressure, sedation, and hyperpolarization of nerves. It has a long duration of action as it is given twice daily and the therapeutic window is between 0.1mg and 2.4mg daily. Clonidine is primarily an alpha-2 adrenoceptor agonist which causes central hypotensive and anti-arrhythmogenic effects. The alpha-2 adrenoceptor is coupled to the G-proteins G<sub>o</sub> and G<sub>i</sub>. G<sub>i</sub> inhibits adenylyl cyclase and activates opening of a potassium channel that causes hyperpolarization. Clonidine binding to the alpha-2 adrenoceptor causes structural changes in the alpha subunit of the G-protein, reducing its affinity for GDP. Magnesium catalyzes the replacement of GDP with GTP. The alpha subunit dissociates from the other subunits and associates with an effector.",The molecular weight is 230.09.,Clonidine has a topological polar surface area of 36.42.,The log p value of  is 1.73.,Clonidine is approved.,Clonidine is a solid.,True
14199,"A sulfathiazole antibacterial agent. For the treatment of urinary tract infection Sulfamethizole is a sulfonamide antibiotic. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of <i>p</i>-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus. Sulfamethizole is a competitive inhibitor of bacterial enzyme dihydropteroate synthetase. The normal para-aminobenzoic acid (PABA) substrate is prevented from binding. The inhibited reaction is necessary in these organisms for the synthesis of folic acid.",The molecular weight is 270.33.,Sulfamethizole has a topological polar surface area of 97.97.,The log p value of  is 0.42.,Sulfamethizole is approved and investigational and vet_approved.,Sulfamethizole is a solid.,True
14200,"Enalapril is a prodrug belonging to the angiotensin-converting enzyme (ACE) inhibitor drug class that works on the renin-angiotensin-aldosterone system, which is responsible for the regulation of blood pressure and fluid and electrolyte homeostasis. Enalapril is an orally-active and long-acting nonsulphydryl antihypertensive agent that suppresses the renin-angiotensin-aldosterone system to lower blood pressure. It was developed from a targeted research programmed using molecular modelling. Being a prodrug, enalapril is rapidly biotransformed into its active metabolite, , which is responsible for the pharmacological actions of enalapril. The active metabolite of enalapril competitively inhibits the ACE to hinder the production of angiotensin II, a key component of the renin-angiotensin-aldosterone system that promotes vasoconstriction and renal reabsorption of sodium ions in the kidneys. Ultimately, enalaprilat works to reduce blood pressure and blood fluid volume. Indicated for the management of essential or renovascular hypertension as monotherapy or in combination with other antihypertensive agents, such as thiazide diuretics, for an additive effect. Enalapril is an antihypertensive agent that exhibits natriuretic and uricosuric properties. Enalapril lowers blood pressure in all grades of essential and renovascular hypertension, and peripheral vascular resistance without causing an increase in heart rate. Individuals with low-renin hypertensive population were still responsive to enalapril. The duration of hypertensive effect in the systolic and diastolic blood pressure persists for at least 24 hours following initial administration of a single oral dose, and repeated daily administration of enalapril confers an additional reduction in blood pressure and a steady-state antihypertensive response may take several weeks. In patients with severe congestive heart failure and inadequate clinical response to conventional antihypertensive therapies, treatment with enalapril resulted in improvements in cardiac performance as observed by a reduction in both preload and afterload, and improved clinical status long-term. Furthermore, enalapril was shown to increase cardiac output and stroke volume while decreasing pulmonary capillary wedge pressure in patients with congestive heart failure refractory to conventional treatment with digitalis and diuretics. In clinical studies, enalapril reduced left ventricular mass, and did not affect cardiac function or myocardial perfusion during exercise. Enalapril is not highly associated with the risk of bradycardia unlike most diuretics and beta-blockers and it does not produce rebound hypertension upon discontinuation of therapy.  The renin-angiotensin-aldosterone system (RAAS) is a signaling pathway that works in synergism with the sympathetic system to regulate blood pressure and fluid and electrolyte homeostasis. Activation of this system upon stimulation by different factors, such as low blood pressure and nerve impulses, leads to increased release of norepinephrine (NE) from sympathetic nerve terminals and effects on the vascular growth, vasoconstriction, and salt retention in the kidneys. Renin is released from ",The molecular weight is 376.45.,Enalapril has a topological polar surface area of 95.94.,The log p value of  is 0.67.,Enalapril is approved and vet_approved.,Enalapril is a solid.,True
14201,"A tetracycline analog isolated from the actinomycete streptomyces rimosus and used in a wide variety of clinical conditions. Oxytetracycline is indicated for treatment of infections caused by a variety of Gram positive and Gram negative microorganisms including <i>Mycoplasma pneumoniae, Pasteurella pestis, Escherichia coli, Haemophilus influenzae</i> (respiratory infections), and <i>Diplococcus pneumoniae</i>. Oxytetracycline is known as a broad-spectrum antibiotic due to its activity against such a wide range of infections. It was the second of the tetracyclines to be discovered. Oxytetracycline, like other tetracyclines, is used to treat many infections common and rare. Its better absorption profile makes it preferable to tetracycline for moderately severe acne, but alternatives sould be sought if no improvement occurs by 3 months. Oxytetracycline inhibits cell growth by inhibiting translation. It binds to the 30S ribosomal subunit and prevents the amino-acyl tRNA from binding to the A site of the ribosome. The binding is reversible in nature. Oxytetracycline is lipophilic and can easily pass through the cell membrane or passively diffuses through porin channels in the bacterial membrane.",The molecular weight is 460.44.,Oxytetracycline has a topological polar surface area of 201.85.,The log p value of  is -1.27.,Oxytetracycline is approved and investigational and vet_approved.,Oxytetracycline is a solid.,True
14202,"Labetalol is a racemic mixture of 2 diastereoisomers where dilevalol, the R,R' stereoisomer, makes up 25% of the mixture. Labetalol is formulated as an injection or tablets to treat hypertension. Labetalol injections are indicated to control blood pressure in severe hypertension. Labetalol tablets are indicated alone or in combination with antihypertensives like thiazides and loop diuretics to manage hypertension. Labetalol antagonizes various adrenergic receptors to decrease blood pressure. The duration of action is long as it is generally given twice daily, and the therapeutic window is wide as patients usually take 200-400mg twice daily. Patients susceptible to bronchospasms should not use labetalol unless they are unresponsive to or intolerant of other antihypertensives. Labetalol non-selectively antagonizes beta-adrenergic receptors, and selectively antagonizes alpha-1-adrenergic receptors. Following oral administration, labetalol has 3 times the beta-blocking ability than alpha-blocking ability. This increases to 6.9 times following intravenous administration. Antagonism of alpha-1-adrenergic receptors leads to vasodilation and decreased vascular resistance. This leads to a decrease in blood pressure that is most pronounced while standing. Antagonism of beta-1-adrenergic receptors leads to a slight decrease in heart rate. Antagonism of beta-2-adrenergic receptors leads to some of the side effects of labetalol such as bronchospasms, however this may be slightly attenuated by alpha-1-adrenergic antagonism. Labetalol leads to sustained vasodilation over the long term without a significant decrease in cardiac output or stroke volume, and a minimal decrease in heart rate.",The molecular weight is 328.41.,Labetalol has a topological polar surface area of 95.58.,The log p value of  is 2.5.,Labetalol is approved.,Labetalol is a solid.,True
14203,"Medroxyprogesterone acetate (MPA) is a derivative that is more resistant to metabolism for improved pharmacokinetic properties. MPA can be use to treat secondary amenorrhea, endometrial hyperplasia, abnormal uterine bleeding, osteoporosis, vasomotor symptoms in menopause, vulvar and vaginal atrophy, prevent pregnancy, manage pain in endometriosis, prevent pregnancy, and is also used in palliative care for endometrial and renal carcinoma. Medroxyprogesterone acetate (MPA) oral tablets are indicated to treat secondary amenorrhea, reduce the incidence of endometrial hyperplasia in postmenopausal women, and to treat abnormal uterine bleeding due to hormonal imbalance, not organic pathology. Oral tablets containing MPA and conjugated estrogens are indicated to prevent postmenopausal osteoporosis and to treat moderate to severe menopausal symptoms such as vasomotor symptoms, vulvar atrophy, and vaginal atrophy. Subcutaneous MPA is indicated to prevent pregnancy and manage pain associated with endometriosis. Intramuscular MPA is indicated to prevent pregnancy, and at higher concentrations for palliative treatment of endometrial or renal carcinoma. Medroxyprogesterone acetate (MPA) inhibits gonadotropin production, reduces nuclear estrogen receptors and DNA synthesis in epithelial cells of the endometrium, and induces p53 dependant apoptosis in cancer cell lines. MPA oral tablets have a half life of 40-60 hours and other formulations can have half lives that are considerably longer, so the duration of action is long. The therapeutic window is wide as patients may take doses ranging from 5mg orally daily to 1000mg as a depo injection weekly. Long term use of MPA is associated with a reduction in bone density and patients who taking MPA during adolescence may have lower peak bone mass than untreated patients, which can also increase the risk of osteoporosis and fractures in the future. Medroxyprogesterone acetate (MPA) inhibits the production of gonadotropin, preventing follicular maturation and ovulation, which is responsible for it’s ability to prevent pregnancy. This action also thins the endometrium. MPA reduces nuclear estrogen receptors and DNA synthesis in epithelial cells of the endometrium. MPA can also induce p53 dependant apoptosis in certain cancer cell lines, and inhibit GABA-A receptors.",The molecular weight is 386.53.,Medroxyprogesterone acetate has a topological polar surface area of 60.44.,The log p value of  is 4.2.,Medroxyprogesterone acetate is approved and investigational.,Medroxyprogesterone acetate is a solid.,True
14204,"Sulindac is a nonsteroidal anti-inflammatory drug (NSAID) of the arylalkanoic acid class that is marketed by Merck under the brand name Clinoril. Like other NSAIDs, it may be used in the treatment of acute or chronic inflammatory conditions. Sulindac is a prodrug, derived from sulfinylindene, that is converted _in vivo_ to an active sulfide compound by liver enzymes. There is evidence from some studies that sulindac may be associated with fewer gastrointestinal side effects than other NSAIDs, except for the cyclooxygenase-2 (COX-2) inhibitor drug class. This may be due to the sulfide metabolite undergoing enterohepatic circulation thus maintaining constant blood levels of the compound without inducing gastrointestinal effects, where the drug is excreted in the bile and then reabsorbed from the intestines. While its full mechanism of action is not fully understood, sulindac is thought to primarily mediate its action by inhibiting prostaglandin synthesis by inhibiting COX-1 and COX-2. For acute or long-term use in the relief of signs and symptoms of osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, acute painful shoulder (acute subacromial bursitis/supraspinatus tendinitis), and acute gouty arthritis. Sulindac is a non-steroidal anti-inflammatory indene derivative, also possessing analgesic and antipyretic activities. Sulindac's exact mechanism of action is unknown. Its antiinflammatory effects are believed to be due to inhibition of both COX-1 and COX-2 which leads to the inhibition of prostaglandin synthesis. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation.",The molecular weight is 356.41.,Sulindac has a topological polar surface area of 54.37.,The log p value of  is 3.16.,Sulindac is approved and investigational.,Sulindac is a solid.,True
14205,"A semi-synthetic antibiotic related to penicillin, Naficillin is a narrow-spectrum beta-lactam antibiotic drug. It is a beta-lactamase-resistant penicillin that is indicated for the treatment of Staphylococcal infections caused by strains that are resistant to other penicillins, except those caused by MRSA. It may be used as a first-line therapy in Methicillin-Sensitive *Staphylococcus aureus* infections. Indicated in the treatment of infections caused by penicillinase-producing staphylococci which have demonstrated susceptibility to the drug.  Nafcillin is a semisynthetic antibiotic substance derived from 6-amino-penicillanic acid. The drugs in this class are highly resistant to inactivation by staphylococcal penicillinase and are active against penicillinase-producing and non penicillinase-producing strains of Staphylococcus species.  Like other penicillins, nafcillin exerts a bactericidal action against penicillin-susceptible microorganisms during the state of active multiplication in the bacterial cell wall synthesis. It inhibits the biosynthesis of the bacterial cell wall by forming covalent bonds with penicillin-binding proteins that play a critical role in the final transpeptidation process. Binding to penicillin-binding proteins inhibits the transpeptidase and carboxypeptidase activities conferred by these proteins and prevents the formation of the crosslinks. ",The molecular weight is 414.48.,Nafcillin has a topological polar surface area of 95.94.,The log p value of  is 3.53.,Nafcillin is approved and investigational.,Nafcillin is a solid.,True
14206,"Chloroquine is an aminoquinolone derivative first developed in the 1940s for the treatment of malaria. It was the drug of choice to treat malaria until the development of newer antimalarials such as , , and. Chloroquine and its derivative have since been repurposed for the treatment of a number of other conditions including HIV, systemic lupus erythematosus, and rheumatoid arthritis. Chloroquine is indicated to treat infections of _P. vivax_, _P. malariae_, _P. ovale_, and susceptible strains of _P. falciparum_. It is also used to treat extraintestinal amebiasis. Chloroquine inhibits the action of heme polymerase, which causes the buildup of toxic heme in _Plasmodium_ species. It has a long duration of action as the half life is 20-60 days. Patients should be counselled regarding the risk of retinopathy with long term usage or high dosage, muscle weakness, and toxicity in children. Chloroquine inhibits the action of heme polymerase in malarial trophozoites, preventing the conversion of heme to hemazoin. _Plasmodium_ species continue to accumulate toxic heme, killing the parasite.",The molecular weight is 319.88.,Chloroquine has a topological polar surface area of 28.16.,The log p value of  is 5.06.,Chloroquine is approved and investigational and vet_approved.,Chloroquine is a solid.,True
14207,"Imatinib is a small molecule kinase inhibitor used to treat certain types of cancer. It is currently marketed by Novartis as Gleevec (USA) or Glivec (Europe/Australia) as its mesylate salt, imatinib mesilate (INN). It is occasionally referred to as CGP57148B or STI571 (especially in older publications). It is used in treating chronic myelogenous leukemia (CML), gastrointestinal stromal tumors (GISTs) and a number of other malignancies. For the treatment of Philadelphia chromosome positive chronic myeloid leukemia (Ph+ CML), Ph+ acute lymphoblastic leukaemia, myelodysplastic/myeloproliferative diseases, aggressive systemic mastocytosis, hypereosinophilic syndrome and/or chronic eosinophilic leukemia (CEL), dermatofibrosarcoma protuberans, and malignant gastrointestinal stromal tumors (GIST). Imatinib is an antineoplastic agent and a 2-phenylaminopyrimidine derivative that is used to treat chronic myelogenous leukemia. It works as a specific inhibitor of a number of tyrosine kinase enzymes. Chronic myelogenous leukemia is associated with the Philadelphia chromosome promoting the generation of BCR-ABL mutation, which results from the combination of two genes, known as BCR and ABL. BCR-ABL generates a fusion protein that acts as a constitutively active tyrosine kinase and imatinib works to inhibit this constitutive enzymatic activity.  Imatinib mesylate is a protein-tyrosine kinase inhibitor that inhibits the Bcr-Abl tyrosine kinase, the constitutive abnormal tyrosine kinase created by the Philadelphia chromosome abnormality in chronic myeloid leukemia (CML). It inhibits proliferation and induces apoptosis in Bcr-Abl positive cell lines as well as fresh leukemic cells from Philadelphia chromosome positive chronic myeloid leukemia. Imatinib also inhibits the receptor tyrosine kinases for platelet derived growth factor (PDGF) and stem cell factor (SCF) - called c-kit. Imatinib was identified in the late 1990s by Dr Brian J. Druker. Its development is an excellent example of rational drug design. Soon after identification of the bcr-abl target, the search for an inhibitor began. Chemists used a high-throughput screen of chemical libraries to identify the molecule 2-phenylaminopyrimidine. This lead compound was then tested and modified by the introduction of methyl and benzamide groups to give it enhanced binding properties, resulting in imatinib.",The molecular weight is 493.62.,Imatinib has a topological polar surface area of 86.28.,The log p value of  is 4.38.,Imatinib is approved.,Imatinib is a solid.,True
14208,"Testosterone is a steroid sex hormone indicated to treat primary hypogonadism and hypogonadotropic hypogonadism. Testosterone antagonizes the androgen receptor to induce gene expression that causes the growth and development of masculine sex organs and secondary sexual characteristics. Testosterone is indicated to treat primary hypogonadism and hypogonadotropic hypogonadism. Testosterone antagonizes the androgen receptor to induce gene expression that causes the growth and development of masculine sex organs and secondary sexual characteristics. The duration of action of testosterone is variable from patient to patient with a half life of 10-100 minutes. The therapeutic index is wide considering the normal testosterone levels in an adult man range from 300-1000ng/dL. Counsel patients regarding the risk of secondary exposure of testosterone topical products to children. The androgen receptor exists in the cytoplasm bound to the heat shock proteins HSP90, HSP70, and other chaperones. After binding to an androgen, the androgen receptor dissociates from HSP90 and undergoes a conformational change to slow the rate of dissociation from the androgen receptor. The androgen-receptor complex is transported into the nucleus where it binds to DNA and recruits other transcriptional regulators to form a pre-initiation complex and eventually induce expression of specific genes.",The molecular weight is 288.43.,Testosterone has a topological polar surface area of 37.3.,The log p value of  is 3.41.,Testosterone is approved and investigational.,Testosterone is a solid.,True
14209,"Efavirenz (brand names Sustiva® and Stocrin®) is a non-nucleoside reverse transcriptase inhibitor (NNRTI) and is used as part of highly active antiretroviral therapy (HAART) for the treatment of a human immunodeficiency virus (HIV) type 1. For use in combination treatment of HIV infection (AIDS) Efavirenz (dideoxyinosine, ddI) is an oral non-nucleoside reverse transcriptase inhibitor (NNRTI). It is a synthetic purine derivative and, similar to zidovudine, zalcitabine, and stavudine. Efavirenz was originally approved specifically for the treatment of HIV infections in patients who failed therapy with zidovudine. Currently, the CDC recommends that Efavirenz be given as part of a three-drug regimen that includes another nucleoside reverse transcriptase inhibitor (e.g., lamivudine, stavudine, zidovudine) and a protease inhibitor or efavirenz when treating HIV infection. Similar to zidovudine, efavirenz inhibits the activity of viral RNA-directed DNA polymerase (i.e., reverse transcriptase). Antiviral activity of efavirenz is dependent on intracellular conversion to the active triphosphorylated form. The rate of efavirenz phosphorylation varies, depending on cell type. It is believed that inhibition of reverse transcriptase interferes with the generation of DNA copies of viral RNA, which, in turn, are necessary for synthesis of new virions. Intracellular enzymes subsequently eliminate the HIV particle that previously had been uncoated, and left unprotected, during entry into the host cell. Thus, reverse transcriptase inhibitors are virustatic and do not eliminate HIV from the body. Even though human DNA polymerase is less susceptible to the pharmacologic effects of triphosphorylated efavirenz, this action may nevertheless account for some of the drug's toxicity.",The molecular weight is 315.68.,Efavirenz has a topological polar surface area of 38.33.,The log p value of  is 3.73.,Efavirenz is approved and investigational.,Efavirenz is a solid.,True
14210,"A dideoxynucleoside analog that inhibits reverse transcriptase and has in vitro activity against HIV. For the treatment of human immunovirus (HIV) infections. Stavudine is a nucleoside reverse transcriptase inhibitor (NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Stavudine is phosphorylated to active metabolites that compete for incorporation into viral DNA. They inhibit the HIV reverse transcriptase enzyme competitively and act as a chain terminator of DNA synthesis. The lack of a 3'-OH group in the incorporated nucleoside analogue prevents the formation of the 5' to 3' phosphodiester linkage essential for DNA chain elongation, and therefore, the viral DNA growth is terminated. Stavudine inhibits the activity of HIV-1 reverse transcriptase (RT) both by competing with the natural substrate dGTP and by its incorporation into viral DNA.",The molecular weight is 224.22.,Stavudine has a topological polar surface area of 78.87.,The log p value of  is -0.49.,Stavudine is approved and investigational.,Stavudine is a solid.,True
14211,"Estrone, one of the major mammalian estrogens, is an aromatized C18 steroid with a 3-hydroxyl group and a 17-ketone. It is produced in vivo from androstenedione or from testosterone via estradiol. It is produced primarily in the ovaries, placenta, and in peripheral tissues (especially adipose tissue) through conversion of adrostenedione. Estrone may be further metabolized to 16-alpha-hydroxyestrone, which may be reduced to estriol by estradiol dehydrogenase. For management of perimenopausal and postmenopausal symptoms. Estrone, a synthetically prepared or naturally occurring steroidal estrogen obtained from pregnant equine urine, is the primary circulating estrogen after menopause. Estrone is naturally derived from the peripheral conversion of androstenedione by an aromatase enzyme found in adipose tissues and is converted to estradiol in peripheral tissues. The estrogenic potency of estrone is one third that of estradiol. Estropipate is piperazine-stabilized estrone sulfate. Estrone, and estropipate are used to treat abnormalities related to gonadotropin hormone dysfunction, vasomotor symptoms, atrophic vaginitis, and vulvar atrophy associated with menopause, and for the prevention of osteoporosis due to estrogen deficiency. Estrogens enter the cells of responsive tissues (e.g. female organs, breasts, hypothalamus, pituitary) where they interact with estrogen receptors. Hormone-bound estrogen receptors dimerize, translocate to the nucleus of cells and bind to estrogen response elements (ERE) of genes. Binding to ERE alters the transcription rate of affected genes. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) release from the anterior pituitary.",The molecular weight is 270.37.,Estrone has a topological polar surface area of 37.3.,The log p value of  is 3.38.,Estrone is approved.,Estrone is a solid.,True
14212,"Verapamil is a phenylalkylamine calcium channel blocker used in the treatment of high blood pressure, heart arrhythmias, and angina, and was the first calcium channel antagonist to be introduced into therapy in the early 1960s. It is a member of the non-dihydropyridine class of calcium channel blockers, which includes drugs like and , but is chemically unrelated to other cardioactive medications. Verapamil is administered as a racemic mixture containing equal amounts of the S- and R-enantiomer, each of which is pharmacologically distinct - the S-enantiomer carries approximately 20-fold greater potency than the R-enantiomer, but is metabolized at a higher rate. Verapamil is indicated in the treatment of vasopastic (i.e. Prinzmetal's) angina, unstable angina, and chronic stable angina. It is also indicated to treat hypertension, for the prophylaxis of repetitive paroxysmal supraventricular tachycardia, and in combination with digoxin to control ventricular rate in patients with atrial fibrillation or atrial flutter. Given intravenously, it is indicated for the treatment of various supraventricular tachyarrhythmias, including rapid conversion to sinus rhythm in patients with supraventricular tachycardia and for temporary control of ventricular rate in patients with atrial fibrillation or atrial flutter. Verapamil is an L-type calcium channel blocker with antiarrhythmic, antianginal, and antihypertensive activity. Immediate-release verapamil has a relatively short duration of action, requiring dosing 3 to 4 times daily, but extended-release formulations are available that allow for once-daily dosing. As verapamil is a negative inotropic medication (i.e. it decreases the strength of myocardial contraction), it should not be used in patients with severe left ventricular dysfunction or hypertrophic cardiomyopathy as the decrease in contractility caused by verapamil may increase the risk of exacerbating these pre-existing conditions. Verapamil inhibits L-type calcium channels by binding to a specific area of their alpha-1 subunit,Cav1.2, which is highly expressed on L-type calcium channels in vascular smooth muscle and myocardial tissue where these channels are responsible for the control of peripheral vascular resistance and heart contractility. Calcium influx through these channels allows for the propagation of action potentials necessary for the contraction of muscle tissue and the heart's electrical pacemaker activity. Verapamil binds to these channels in a voltage- and frequency-dependent manner, meaning affinity is increased 1) as vascular smooth muscle membrane potential is reduced, and 2) with excessive depolarizing stimulus. ",The molecular weight is 454.61.,Verapamil has a topological polar surface area of 63.95.,The log p value of  is 4.47.,Verapamil is approved.,Verapamil is a solid.,True
14213,"Tamoxifen is a non-steroidal antiestrogen used to treat estrogen receptor positive breast cancers as well as prevent the incidence of breast cancer in high risk populations. Tamoxifen is used alone or as an adjuvant in these treatments. Tamoxifen may no longer be the preferred treatment for these types of cancers as patients generally have better survival, side effect profiles, and compliance with. Tamoxifen is indicated to treat estrogen receptor positive metastatic breast cancer in adults, as an adjuvant in the treatment of early stage estrogen receptor positive breast cancer in adults, to reduce the risk of invasive breast cancer after surgery and radiation in adult women with ductal carcinoma in situ. Tamoxifen is a selective estrogen receptor modulator that inhibits growth and promotes apoptosis in estrogen receptor positive tumors. It has a long duration of action as the active metabolite N-desmethyltamoxifen has a half life of approximately 2 weeks. It has a narrow therapeutic index as higher doses can lead to breathing difficulty or convulsions. Tamoxifen administration is also associated with an increased incidence of uterine malignancies. Tamoxifen competitively inhibits estrogen binding to its receptor, which is critical for it's activity in breast cancer cells. Tamoxifen leads to a decrease in tumor growth factor α and insulin-like growth factor 1, and an increase in sex hormone binding globulin. The increase in sex hormon binding globulin limits the amount of freely available estradiol. These changes reduce levels of factors that stimulate tumor growth.",The molecular weight is 371.52.,Tamoxifen has a topological polar surface area of 12.47.,The log p value of  is 6.82.,Tamoxifen is approved.,Tamoxifen is a solid.,True
14214,"An irreversible cholinesterase inhibitor with actions similar to those of echothiophate. It is a powerful miotic used mainly in the treatment of glaucoma. Its vapor is highly toxic and it is recommended that only solutions in arachis oil be used therapeutically. (From Martindale, The Extra Pharmacopoeia, 29th ed, p1330) For use in the eye to treat certain types of glaucoma and other eye conditions, such as accommodative esotropia. Isoflurophate is used as ocular drops in the treatment of chronic glaucoma. Isoflurophate is an organophosphorus compound that acts as an irreversible cholinesterase inhibitor. As such, it displays parasympathomimetic effects. Isoflurophate is used in the eye to treat certain types of glaucoma and other eye conditions, such as accommodative esotropia. They may also be used in the diagnosis of certain eye conditions, such as accommodative esotropia. Isoflurophate damages the acetylcholinesterase enzyme and is therefore irreversible, however, pralidoxime can displace organophosphates such as isoflurophate from acetylcholinesterase, but only if administered before isoflurophate damages (alkylates) the enzyme. The mechanism of isoflurophate's action involves the irreversible inhibition of cholinesterase.",The molecular weight is 184.15.,Isoflurophate has a topological polar surface area of 35.53.,The log p value of  is 1.01.,Isoflurophate is approved and investigational and withdrawn.,Isoflurophate is a liquid.,True
14215,"Losartan is an angiotensin II receptor blocker (ARB) used to treat hypertension. Angiotensin-converting enzyme (ACE) inhibitors are used for a similar indication but are associated with a cough. When patients with ACE inhibitor associated coughs are switched to ARBs like losartan, they have an incidence of cough similar to placebo or. Losartan is available as losartan potassium oral tablets as well as a combination tablet of losartan potassium and hydrochlorothiazide. Patients taking losartan should have their renal function and potassium levels monitored. Losartan was granted FDA approval on 14 April 1995. Losartan is indicated to treat hypertension in patients older than 6 years, reduce the risk of stroke in patients with hypertension and left ventricular hypertrophy (though this benefit may not extend to patients with African heritage), and to treat diabetic nephropathy with elevated serum creatinine and proteinuria in patients with type 2 diabetes and hypertension. Losartan with hydrochlorothiazide is indicated to treat hypertension and to reduce the risk of stroke in patients with hypertension and left ventricular hypertrophy (though this benefit may not extend to patients with African heritage). Losartan is an angiotensin II receptor blocker used to treat hypertension, diabetic nephropathy, and to reduce the risk of stroke. Losartan has a long duration of action as it is given once daily. Patients taking losartan should be regularly monitored for hypotension, renal function, and potassium levels. Losartan reversibly and competitively prevents angiotensin II binding to the AT<sub>1</sub> receptor in tissues like vascular smooth muscle and the adrenal gland. Losartan and its active metabolite bind the AT<sub>1</sub> receptor with 1000 times more affinity than they bind to the AT<sub>2</sub> receptor. The active metabolite of losartan is 10-40 times more potent by weight than unmetabolized losartan as an inhibitor of AT<sub>1</sub> and is a non-competitive inhibitor. Losartan's prevention of angiotensin II binding causes vascular smooth muscle relaxation, lowering blood pressure.",The molecular weight is 422.92.,Losartan has a topological polar surface area of 92.51.,The log p value of  is 3.85.,Losartan is approved.,Losartan is a solid.,True
14216,"Warfarin is an anticoagulant drug normally used to prevent blood clot formation as well as migration. Although originally marketed as a pesticide (d-Con, Rodex, among others), Warfarin has since become the most frequently prescribed oral anticoagulant in North America. Warfarin has several properties that should be noted when used medicinally, including its ability to cross the placental barrier during pregnancy which can result in fetal bleeding, spontaneous abortion, preterm birth, stillbirth, and neonatal death. Additional adverse effects such as necrosis, purple toe syndrome, osteoporosis, valve and artery calcification, and drug interactions have also been documented with warfarin use. Warfarin does not actually affect blood viscosity, rather, it inhibits vitamin-k dependent synthesis of biologically active forms of various clotting factors in addition to several regulatory factors. **Indicated** for: Warfarin is an anticoagulant, as such it disrupts the coagulation cascade to reduce frequency and extent of thrombus formation. In patients with deep vein thrombosis or atrial fibrillation there is an increased risk of thrombus formation due to the reduced movement of blood. For patients with cardiac valve disease or valve replacements this increased coagulability is due to tissue damage. Thrombi due to venous thrombosis can travel to the lungs and become pulmonary emboli, blocking circulation to a portion of lung tissue. Thrombi which form in the heart can travel to the brain and cause ischemic strokes. Prevention of these events is the primary goal of warfarin therapy. Warfarin is a antagonist which acts to inhibit the production of vitamin K by vitamin K epoxide reductase. The reduced form of vitamin K, vitamin KH<sub>2</sub> is a cofactor used in the γ-carboxylation of coagulation factors VII, IX, X, and thrombin. Carboxylation induces a conformational change allowing the factors to bind Ca<sup>2+</sup> and to phospholipid surfaces. Uncarboxylated factors VII, IX, X, and thrombin are biologically inactive and therefore serve to interrupt the coagulation cascade. The endogenous anticoagulation proteins C and S also require γ-carboxylation to function. This is particularly true in the case of thrombin which must be activated in order to form a thrombus. vitamin KH<sub>2</sub> is converted to vitamin K epoxide as part of the γ-carboxylation reaction catalyzed by γ-glutamyl carboxylase. Vitamin K epoxide is then converted to vitamin K<sub>1</sub> by vitamin K epoxide reductase then back to vitamin KH<sub>2</sub> by vitamin K reductase. Warfarin binds to vitamin K epoxide reductase complex subunit 1 and irreversibly inhibits the enzyme thereby stopping the recycling of vitamin K by preventing the conversion of vitamin K epoxide to vitamin K<sub>1</sub>. This process creates a hypercoagulable state for a short time as proteins C and S degrade first with half lives of 8 and 24 hours, with the exception of factor VII which has a half life of 6 hours. Factors IX, X, and finally thrombin degrade later with half lives of 24, 36, and 50 hours resulting in a dominant anticoagulation effect. In order to reverse this anticoagulation vitamin K must be supplied, either exogenously or by removal of the vitamin K epoxide reductase inhibition, and time allowed for new coagulation factors to be synthesized. It takes approximately 2 days for new coagulation factors to be synthesized in the liver. Vitamin K<sub>2</sub>, functionally identical to vitamin K<sub>1</sub>, is synthesized by gut bacteria leading to interactions with antibiotics as elimination of these bacteria can reduce vitamin K<sub>2</sub supply and result in a greater anticoagulation effect.",The molecular weight is 308.33.,Warfarin has a topological polar surface area of 63.6.,The log p value of  is 2.9.,Warfarin is approved.,Warfarin is a solid.,True
14217,"Furosemide is a potent loop diuretic that acts on the kidneys to ultimately increase water loss from the body. It is an anthranilic acid derivative. Furosemide is used for edema secondary to various clinical conditions, such as congestive heart failure exacerbation, liver failure, renal failure, and high blood pressure. It mainly works by inhibiting electrolyte reabsorption from the kidneys and enhancing the excretion of water from the body. Furosemide has a fast onset and short duration of action and has been used safely and effectively in both pediatric and adult patients. The use of furosemide is particularly beneficial in clinical settings that require a drug with a higher diuretic potential. In addition to oral formulations, the solution for intravenous and intramuscular administration is also available, which is typically limited to patients who are unable to take oral medication or for patients in emergency clinical situations. Furosemide is indicated for the treatment of edema associated with congestive heart failure, cirrhosis of the liver, and renal disease, including the nephrotic syndrome, in adults and pediatric patients.  Furosemide manages hypertension and edema associated with congestive heart failure, cirrhosis, and renal disease, including the nephrotic syndrome. Furosemide is a potent loop diuretic that works to increase the excretion of Na+ and water by the kidneys by inhibiting their reabsorption from the proximal and distal tubules, as well as the loop of Henle. It works directly acts on the cells of the nephron and indirectly modifies the content of the renal filtrate. Ultimately, furosemide increases the urine output by the kidney. Protein-bound furosemide is delivered to its site of action in the kidneys and secreted via active secretion by nonspecific organic transporters expressed at the luminal site of action.  Furosemide promotes diuresis by blocking tubular reabsorption of sodium and chloride in the proximal and distal tubules, as well as in the thick ascending loop of Henle. This diuretic effect is achieved through the competitive inhibition of sodium-potassium-chloride cotransporters (NKCC2) expressed along these tubules in the nephron, preventing the transport of sodium ions from the lumenal side into the basolateral side for reabsorption. This inhibition results in increased excretion of water along with sodium, chloride, magnesium, calcium, hydrogen, and potassium ions. As with other loop diuretics, furosemide decreases the excretion of uric acid. ",The molecular weight is 330.74.,Furosemide has a topological polar surface area of 122.63.,The log p value of  is 1.9.,Furosemide is approved and vet_approved.,Furosemide is a solid.,True
14218,"A reverse transcriptase inhibitor and zalcitabine analog in which a sulfur atom replaces the 3&#39; carbon of the pentose ring. It is used to treat Human Immunodeficiency Virus Type 1 (HIV-1) and hepatitis B (HBV). For the treatment of HIV infection and chronic hepatitis B (HBV). Lamivudine is a nucleoside reverse transcriptase inhibitor (NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1) and hepatitis B (HBV) to disrupt viral DNA synthesis. When phosphorylated, lamivudine can form active metabolites that compete for incorporation into viral DNA. Via DNA incorporation, lamivudine metabolites competitively inhibit the activity of the HIV reverse transcriptase enzyme and act as a chain terminator of DNA synthesis. Due to the lack of a 3'-OH group, incorporated nucleoside analogues prevent the formation of a 5' to 3' phosphodiester linkage that is essential for DNA chain elongation.  Lamivudine is a synthetic nucleoside analogue and is phosphorylated intracellularly to its active 5'-triphosphate metabolite, lamivudine triphosphate (L-TP). This nucleoside analogue is incorporated into viral DNA by HIV reverse transcriptase and HBV polymerase, resulting in DNA chain termination.",The molecular weight is 229.25.,Lamivudine has a topological polar surface area of 88.15.,The log p value of  is -1.46.,Lamivudine is approved and investigational.,Lamivudine is a solid.,True
14219,"Flurbiprofen, a propionic acid derivative, is a nonsteroidal anti-inflammatory agent (NSAIA) with antipyretic and analgesic activity. Oral formulations of flurbiprofen may be used for the symptomatic treatment of rheumatoid arthritis, osteoarthritis and anklylosing spondylitis. Flurbiprofen may also be used topically prior to ocular surgery to prevent or reduce intraoperative miosis. Flurbiprofen is structurally and pharmacologically related to fenoprofen, ibuprofen, and ketoprofen. Flurbiprofen tablets are indicated for the acute or long-term symptomatic treatment of rheumatoid arthritis, osteorarthritis and anklosing spondylitis. It may also be used to treat pain associated with dysmenorrhea and mild to moderate pain accompanied by inflammation (e.g. bursitis, tendonitis, soft tissue trauma). Topical ophthalmic formulations may be used pre-operatively to prevent intraoperative miosis.  Flurbiprofen, a nonsteroidal anti-inflammatory agent (NSAIA) of the propionic acid class, is structually and pharmacologically related to fenoprofen, ibuprofen, and ketoprofen, and has similar pharmacological actions to other prototypica NSAIAs. Flurbiprofen exhibits antiinflammatory, analgesic, and antipyretic activities. The commercially available flurbiprofen is a racemic mixture of (+)S- and (-) R-enantiomers. The S-enantiomer appears to possess most of the anti-inflammatory, while both enantiomers may possess analgesic activity. Similar to other NSAIAs, the anti-inflammatory effect of flurbiprofen occurs via reversible inhibition of cyclooxygenase (COX), the enzyme responsible for the conversion of arachidonic acid to prostaglandin G2 (PGG2) and PGG2 to prostaglandin H2 (PGH2) in the prostaglandin synthesis pathway. This effectively decreases the concentration of prostaglandins involved in inflammation, pain, swelling and fever. Flurbiprofen is a non-selective COX inhibitor and inhibits the activity of both COX-1 and -2. It is also one of the most potent NSAIAs in terms of prostaglandin inhibitory activity.",The molecular weight is 244.26.,Flurbiprofen has a topological polar surface area of 37.3.,The log p value of  is 3.75.,Flurbiprofen is approved and investigational.,Flurbiprofen is a solid.,True
14220,"Apomorphine is a non-ergoline dopamine D2 agonist indicated to treat hypomobility associated with Parkinson's. It was first synthesized in 1845 and first used in Parkinson's disease in 1884. Apomorphine has also been investigated as an emetic, a sedative, a treatment for alcoholism, and a treatment of other movement disorders. Apomorphine is indicated to treat acute, intermittent treatment of hypomobility, off episodes associated with advanced Parkinson's disease. Apomorphine is a dopaminergic agonist that may stimulate regions of the brain involved in motor control. It has a short duration of action and a wide therapeutic index as large overdoses are necessary for significant toxicity. Patients should be counselled regarding the risk of nausea, vomiting, daytime somnolence, hypotension, oral mucosal irritation, falls, hallucinations, psychotic-like behaviour, impulsive behaviour, withdrawal hyperpyrexia, and prolongation of the QT interval.p Apomorphine is a non-ergoline dopamine agonist with high binding affinity to dopamine D2, D3, and D5 receptors. Stimulation of D2 receptors in the caudate-putamen, a region of the brain responsible for locomotor control, may be responsible for apomorphine's action. However, the means by which the cellular effects of apomorphine treat hypomobility of Parkinson's remain unknown.",The molecular weight is 267.33.,Apomorphine has a topological polar surface area of 43.7.,The log p value of  is 2.49.,Apomorphine is approved and investigational.,Apomorphine is a solid.,True
14221,"Norethisterone, also known as norethindrone, is a synthetic progestational hormone belonging to the 19-nortestosterone-derived class of progestins. It is further classified as a second-generation progestin, along with and its derivatives, and is the active form of several other progestins including and. Norethisterone mimics the actions of endogenous , albeit with a greater potency, and is used on its own or in combination with estrogen derivatives in a variety of applications including contraception and hormone replacement therapy. First derived in 1951 in Mexico City, norethisterone was originally intended for use as a remedy for irregular menstruation and endometriosis, and was not marketed for use as an oral contraceptive until 1962. Norethisterone is indicated as an oral contraceptive when given as monotherapy or in combination with an estrogen component, such as or. In combination with an estrogen component, oral norethisterone is also indicated as a hormone replacement therapy in the treatment of postmenopausal osteoporosis and moderate-to-severe vasomotor symptoms arising from menopause. When applied via transdermal patch, the combination of norethisterone and estradiol is indicated for the treatment of hypoestrogenism, vulvovaginal atrophy, and moderate-severe vasomotor symptoms. Norethisterone is a synthetic oral progestin used for contraception or to treat other hormone-related conditions such as menopausal symptoms and endometriosis. As a synthetic progestin, norethisterone acts similarly to endogenous progesterone but with a much higher potency - it acts at the pelvic level to alter cervical and endometrial function, as well as via the inhibition of pituitary hormones that play a role in follicular maturation and ovulation. A small increase in the risk of developing breast cancer has been observed in patients using combined oral contraceptives, with some evidence also implicating progestin-only pills - patients starting hormonal contraception should be advised of this risk and should employ routine breast self-examinations to check for evidence of any developing masses. On a molecular level, progestins like norethisterone exert their effects on target cells via binding to progesterone receptors that result in downstream changes to target genes. Target cells are found in the reproductive tract, breast, pituitary, hypothalamus, skeletal tissue, and central nervous system. Contraceptive efficacy is derived mainly from changes to the cervical mucus, wherein norethisterone increases the cell content and viscosity of the mucous to impede sperm transport and migration. Norethisterone also induces a variety of changes to the endometrium - including atrophy, irregular secretion, and suppressed proliferation - that make it inhospitable for implantation. Working via a negative feedback loop, norethisterone also acts on both the hypothalamus and anterior pituitary to suppress the release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the anterior pituitary. Suppression of these hormones prevents follicular development, ovulation, and corpus luteum development. ",The molecular weight is 298.43.,Norethisterone has a topological polar surface area of 37.3.,The log p value of  is 2.79.,Norethisterone is approved.,Norethisterone is a solid.,True
14222,"Nateglinide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It belongs to the meglitinide class of short-acting insulin secretagogues, which act by binding to β cells of the pancreas to stimulate insulin release. Nateglinide is an amino acid derivative that induces an early insulin response to meals decreasing postprandial blood glucose levels. It should only be taken with meals and meal-time doses should be skipped with any skipped meal. Approximately one month of therapy is required before a decrease in fasting blood glucose is seen. Meglitnides may have a neutral effect on weight or cause a slight increase in weight. The average weight gain caused by meglitinides appears to be lower than that caused by sulfonylureas and insulin and appears to occur only in those naïve to oral antidiabetic agents. Due to their mechanism of action, meglitinides may cause hypoglycemia although the risk is thought to be lower than that of sulfonylureas since their action is dependent on the presence of glucose. In addition to reducing postprandial and fasting blood glucose, meglitnides have been shown to decrease glycosylated hemoglobin (HbA1c) levels, which are reflective of the last 8-10 weeks of glucose control. Meglitinides appear to be more effective at lowering postprandial blood glucose than metformin, sulfonylureas and thiazolidinediones. Nateglinide is extensively metabolized in the liver and excreted in urine (83%) and feces (10%). The major metabolites possess less activity than the parent compound. One minor metabolite, the isoprene, has the same potency as its parent compound. For the treatment of non-insulin dependent-diabetes mellitus in conjunction with diet and exercise. Insulin secretion by pancreatic β cells is partly controlled by cellular membrane potential. Membrane potential is regulated through an inverse relationship between the activity of cell membrane ATP-sensitive potassium channels (ABCC8) and extracellular glucose concentrations. Extracellular glucose enters the cell via GLUT2 (SLC2A2) transporters. Once inside the cell, glucose is metabolized to produce ATP. High concentrations of ATP inhibit ATP-sensitive potassium channels causing membrane depolarization. When extracellular glucose concentrations are low, ATP-sensitive potassium channels open causing membrane repolarization. High glucose concentrations cause ATP-sensitive potassium channels to close resulting in membrane depolarization and opening of L-type calcium channels. The influx of calcium ions stimulates calcium-dependent exocytosis of insulin granules. Nateglinide increases insulin release by inhibiting ATP-sensitive potassium channels in a glucose-dependent manner.  Nateglinide activity is dependent on the presence functioning β cells and glucose. In contrast to sulfonylurea insulin secretatogogues, nateglinide has no effect on insulin release in the absence of glucose. Rather, it potentiates the effect of extracellular glucose on ATP-sensitive potassium channel and has little effect on insulin levels between meals and overnight. As such, nateglinide is more effective at reducing postprandial blood glucose levels than fasting blood glucose levels and requires a longer duration of therapy (approximately one month) before decreases in fasting blood glucose are observed. The insulinotropic effects of nateglinide are highest at intermediate glucose levels (3 to 10 mmol/L) and it does not increase insulin release already stimulated by high glucose concentrations (greater than 15 mmol/L). Nateglinide appears to be selective for pancreatic β cells and does not appear to affect skeletal or cardiac muscle or thyroid tissue.",The molecular weight is 317.43.,Nateglinide has a topological polar surface area of 66.4.,The log p value of  is 4.3.,Nateglinide is approved and investigational.,Nateglinide is a solid.,True
14223,"Risperidone is a second-generation antipsychotic (SGA) medication used in the treatment of a number of mood and mental health conditions including schizophrenia and bipolar disorder. It is one of the most widely used SGAs. , another commonly used SGA, is the primary active metabolite of risperidone (i.e. 9-hydroxyrisperidone). Risperidone is indicated for the treatment of schizophrenia and irritability associated with autistic disorder. It is also indicated as monotherapy, or adjunctly with lithium or valproic acid, for the treatment of acute mania or mixed episodes associated with bipolar I disorder. The primary action of risperidone is to decrease dopaminergic and serotonergic pathway activity in the brain, therefore decreasing symptoms of schizophrenia and mood disorders. Though its precise mechanism of action is not fully understood, current focus is on the ability of risperidone to inhibit the D2 dopaminergic receptors and 5-HT2A serotonergic receptors in the brain. Schizophrenia is thought to result from an excess of dopaminergic D2 and serotonergic 5-HT2A activity, resulting in overactivity of central mesolimbic pathways and mesocortical pathways, respectively.",The molecular weight is 410.49.,Risperidone has a topological polar surface area of 61.94.,The log p value of  is 2.71.,Risperidone is approved and investigational.,Risperidone is a solid.,True
14224,"Meclizine is a histamine H1 antagonist with antiemetic and antivertigo properties. It is used in the symptomatic treatment of motion sickness and control of vertigo associated with vestibular system diseases. It also exhibits anticholinergic, central nervous system depressant, and local anesthetic effects. Commonly marketed under the brand name Antivert in the U.S., meclizine is available as oral tablets. Indicated for the symptomatic treatment of nausea, vomiting, and dizziness associated with motion sickness, and management of vertigo due to various causes, including radiation sickness, Meniere’s syndrome, labyrinthitis and other vestibular disturbances. Meclizine works on the higher centres of the brain to reduce nausea, vomiting, or vertigo. It is effective against nausea and vomiting arising from many causes, including motion sickness and disorders affecting the vestibular system. The onset of action of meclizine is about 1 hour, with effects lasting between 8 to 24 hours. Meclizine is reported to cause drowsiness due to its anticholinergic actions.  Vomiting is a centrally regulated reflex mechanism that initiates from the vomiting center and the chemoreceptor trigger zone (CTZ) located in the medulla. Motion sickness is also regulated by CTZ. The blood-brain barrier near the CTZ is relatively permeable to circulating mediators and CTZ can transmit impulses to vomiting center located in the brainstem. Different receptors responding to different factors, including histamine, 5-HT, enkephalins, substance P, and dopamine, are expressed along the brainstem to activate respective pathways and contribute to the control of vomiting. Histamine H1 receptors are expressed on the vestibular nuclei and nucleus of the solitary tract (NTS) that are activated by motion sickness and stimuli from the pharynx and stomach. When activated, H1 receptor signaling from these nuclei is transmitted to the CTZ and vomiting centre. ",The molecular weight is 390.96.,Meclizine has a topological polar surface area of 6.48.,The log p value of  is 6.73.,Meclizine is approved.,Meclizine is a solid.,True
14225,"Gadobenic acid (in the form of gadobenate dimeglumine) is an MRI contrast agent used primarily for MR imaging of the liver. It can also be used for visualizing the CNS and heart. In contrast to conventional extracellular fluid contrast agents, gadobenate dimeglumine is characterized by a weak and transient binding capacity to serum proteins. This binding leads to an increased relaxivity of gadobenate dimeglumine and, consequently, to a considerably increased signal intensity over that of other agents. Gadobenate Dimeglumine is an MRI contrast agent used primarily for MR imaging of the liver. It can also be used for MRI of the heart, as well as and central nervous system in adults to visualize lesions with abnormal brain vascularity or abnormalities in the blood brain barrier, the brain, spine, or other associated tissues. Gadobenate dimeglumine shares the pharmacokinetic properties of the ECF contrast agent gadopentetate dimeglumine; however, gadobenate differs in that is also selectively taken-up by hepatocytes and excreted via the bile (up to 5% of dose). The elimination half-life of gadobenate dimeglumine is approximately 1 hour. It is not metabolized. Based on the behavior of protons when placed in a strong magnetic field, which is interpreted and transformed into images by magnetic resonance (MR) instruments. Paramagnetic agents have unpaired electrons that generate a magnetic field about 700 times larger than the proton's field, thus disturbing the proton's local magnetic field. When the local magnetic field around a proton is disturbed, its relaxation process is altered. MR images are based on proton density and proton relaxation dynamics. MR instruments can record 2 different relaxation processes, the T1 (spin-lattice or longitudinal relaxation time) and the T2 (spin-spin or transverse relaxation time). In magnetic resonance imaging (MRI), visualization of normal and pathological brain tissue depends in part on variations in the radiofrequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in the T2. When placed in a magnetic field, Gadobenate Dimeglumine shortens both the T1 and the T2 relaxation times in tissues where it accumulates. At clinical doses, Gadobenate Dimeglumine primarily affects the T1 relaxation time, thus producing an increase in signal intensity. Gadobenate Dimeglumine does not cross the intact blood-brain barrier; therefore, it does not accumulate in normal brain tissue or in central nervous system (CNS) lesions that have not caused an abnormal blood-brain barrier (e.g., cysts, mature post-operative scars).",The molecular weight is 665.71.,,,Gadobenic acid is approved and investigational.,Gadobenic acid is a solid.,True
14226,"Leukotrienes are substances that induce numerous biological effects including augmentation of neutrophil and eosinophil migration, neutrophil and monocyte aggregation, leukocyte adhesion, increased capillary permeability, and smooth muscle contraction. These effects contribute to inflammation, edema, mucus secretion, and bronchoconstriction in the airways of asthmatic patients. Zileuton relieves such symptoms through its selective inhibition of 5-lipoxygenase, the enzyme that catalyzes the formation of leukotrienes from arachidonic acid. Specifically, it inhibits leukotriene LTB4, LTC4, LTD4, and LTE4 formation. Both the R(+) and S(-) enantiomers are pharmacologically active as 5-lipoxygenase inhibitors in in vitro systems. The immediate release tablet of Zileuton has been withdrawn from the US market. For the prophylaxis and chronic treatment of asthma in adults and children 12 years of age and older. Zileuton is an asthma drug that differs chemically and pharmacologically from other antiasthmatic agents. It blocks leukotriene synthesis by inhibiting 5-lipoxygenase, an enzyme of the eicosanoid synthesis pathway. Current data indicates that asthma is a chronic inflammatory disorder of the airways involving the production and activity of several endogenous inflammatory mediators, including leukotrienes. Sulfido-peptide leukotrienes (LTC4, LTD4, LTE4, also known as the slow-releasing substances of anaphylaxis) and LTB4, a chemoattractant for neutrophils and eosinophils, are derived from the initial unstable product of arachidonic acid metabolism, leukotriene A4 (LTA4), and can be measured in a number of biological fluids including bronchoalveolar lavage fluid (BALF) from asthmatic patients. In humans, pretreatment with zileuton attenuated bronchoconstriction caused by cold air challenge in patients with asthma. Leukotrienes are substances that induce numerous biological effects including augmentation of neutrophil and eosinophil migration, neutrophil and monocyte aggregation, leukocyte adhesion, increased capillary permeability, and smooth muscle contraction. These effects contribute to inflammation, edema, mucus secretion, and bronchoconstriction in the airways of asthmatic patients. Zileuton relieves such symptoms through its selective inhibition of 5-lipoxygenase, the enzyme that catalyzes the formation of leukotrienes from arachidonic acid. Specifically, it inhibits leukotriene LTB4, LTC4, LTD4, and LTE4 formation. Both the R(+) and S(-) enantiomers are pharmacologically active as 5-lipoxygenase inhibitors in <i>in vitro</i> systems. Due to the role of leukotrienes in the pathogenesis of asthma, modulation of leukotriene formation by interruption of 5-lipoxygenase activity may reduce airway symptoms, decrease bronchial smooth muscle tone, and improve asthma control.",The molecular weight is 236.29.,Zileuton has a topological polar surface area of 66.56.,The log p value of  is 2.48.,Zileuton is approved and investigational and withdrawn.,Zileuton is a solid.,True
14227,"Etodolac is a non-steroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic and antipyretic properties. Its therapeutic effects are due to its ability to inhibit prostaglandin synthesis. It is indicated for relief of signs and symptoms of rheumatoid arthritis and osteoarthritis. For acute and long-term management of signs and symptoms of osteoarthritis and rheumatoid arthritis, as well as for the management of pain. Etodolac is an anti-inflammatory agent with analgesic and antipyretic properties. It is used to treat osteoarthritis, rheumatoid arthritis and control acute pain. The therapeutic effects of etodolac are achieved via inhibition of the synthesis of prostaglandins involved in fever, pain, swelling and inflammation. Etodolac is administered as a racemate. As with other NSAIDs, the S-form has been shown to be active while the R-form is inactive. Both enantiomers are stable and there is no evidence of R- to S- conversion _in vivo_. Similar to other NSAIDs, the anti-inflammatory effects of etodolac result from inhibition of the enzyme cycooxygenase (COX). This decreases the synthesis of peripheral prostaglandins involved in mediating inflammation. Etodolac binds to the upper portion of the COX enzyme active site and prevents its substrate, arachidonic acid, from entering the active site. Etodolac was previously thought to be a non-selective COX inhibitor, but it is now known to be 5 – 50 times more selective for COX-2 than COX-1. Antipyresis may occur by central action on the hypothalamus, resulting in peripheral dilation, increased cutaneous blood flow, and subsequent heat loss.",The molecular weight is 287.36.,Etodolac has a topological polar surface area of 62.32.,The log p value of  is 3.43.,Etodolac is approved and investigational and vet_approved.,Etodolac is a solid.,True
14228,"A stable, non-explosive inhalation anesthetic, relatively free from significant side effects. For induction and maintenance of general anesthesia. Isoflurane is a general inhalation anesthetic used for induction and maintenance of general anesthesia. It induces muscle relaxation and reduces pains sensitivity by altering tissue excitability. It does so by decreasing the extent of gap junction mediated cell-cell coupling and altering the activity of the channels that underlie the action potential. Isoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Isoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. Also appears to bind the D subunit of ATP synthase and NADH dehydogenase. Isoflurane also binds to the GABA receptor, the large conductance Ca<sup>2+</sup> activated potassium channel, the glutamate receptor and the glycine receptor.",The molecular weight is 184.49.,Isoflurane has a topological polar surface area of 9.23.,The log p value of  is 1.76.,Isoflurane is approved and vet_approved.,Isoflurane is a liquid.,True
14229,"Tretinoin, also known as all-trans-retinoic acid (ATRA), is a naturally occurring derivative of vitamin A (retinol). Retinoids such as tretinoin are important regulators of cell reproduction, proliferation, and differentiation and are used to treat acne and photodamaged skin and to manage keratinization disorders such as ichthyosis and keratosis follicularis. Tretinoin also represents the class of anticancer drugs called differentiating agents and is used in the treatment of acute promyelocytic leukemia (APL). For the the induction of remission in patients with acute promyelocytic leukemia (APL), French-American-British (FAB) classification M3 (including the M3 variant); For the topical treatment of acne vulgaris, flat warts and other skin conditions (psoriasis, ichthyosis congenita, icthyosis vulgaris, lamellar icthyosis, keratosis palmaris et plantaris, epidermolytic hyperkeratosis, senile comedones, senile keratosis, keratosis follicularis (Darier's disease), and basal cell carcinomas.); For palliative therapy to improve fine wrinkling, mottled hyperpigmentation, roughness associated with photodamage. Tretinoin, also known as all-<i>trans</i>-retinoic acid (ATRA), is a naturally occurring derivative of vitamin A (retinol). Retinoids such as tretinoin are important regulators of cell reproduction, proliferation, and differentiation and are used to treat acne and photodamaged skin and to manage keratinization disorders such as ichthyosis and keratosis follicularis. Tretinoin also represents the class of anticancer drugs called differentiating agents and is used in the treatment of acute promyelocytic leukemia (APL). Tretinoin binds to alpha, beta, and gamma retinoic acid receptors (RARs). RAR-alpha and RAR-beta have been associated with the development of acute promyelocytic leukemia and squamous cell cancers, respectively. RAR-gamma is associated with retinoid effects on mucocutaneous tissues and bone. Although the exact mechanism of action of tretinoin is unknown, current evidence suggests that the effectiveness of tretinoin in acne is due primarily to its ability to modify abnormal follicular keratinization. Comedones form in follicles with an excess of keratinized epithelial cells. Tretinoin promotes detachment of cornified cells and the enhanced shedding of corneocytes from the follicle. By increasing the mitotic activity of follicular epithelia, tretinoin also increases the turnover rate of thin, loosely-adherent corneocytes. Through these actions, the comedo contents are extruded and the formation of the microcomedo, the precursor lesion of acne vulgaris, is reduced. Tretinoin is not a cytolytic agent but instead induces cytodifferentiation and decreased proliferation of APL cells in culture and in vivo. When Tretinoin is given systemically to APL patients, tretinoin treatment produces an initial maturation of the primitive promyelocytes derived from the leukemic clone, followed by a repopulation of the bone marrow and peripheral blood by normal, polyclonal hematopoietic cells in patients achieving complete remission (CR). The exact mechanism of action of tretinoin in APL is unknown.",The molecular weight is 300.44.,Tretinoin has a topological polar surface area of 37.3.,The log p value of  is 6.74.,Tretinoin is approved and investigational and nutraceutical.,Tretinoin is a solid.,True
14230,"Tetracycline is a broad spectrum polyketide antibiotic produced by the Streptomyces genus of Actinobacteria. It exerts a bacteriostatic effect on bacteria by binding reversible to the bacterial 30S ribosomal subunit and blocking incoming aminoacyl tRNA from binding to the ribosome acceptor site. It also binds to some extent to the bacterial 50S ribosomal subunit and may alter the cytoplasmic membrane causing intracellular components to leak from bacterial cells. Used to treat bacterial infections such as Rocky Mountain spotted fever, typhus fever, tick fevers, Q fever, rickettsialpox and Brill-Zinsser disease. May be used to treat infections caused by Chlamydiae spp., B. burgdorferi (Lyme disease), and upper respiratory infections caused by typical (S. pneumoniae, H. influenzae, and M. catarrhalis) and atypical organisms (C. pneumoniae, M. pneumoniae, L. pneumophila). May also be used to treat acne. Tetracycline may be an alternative drug for people who are allergic to penicillin. Tetracycline is a short-acting antibiotic that inhibits bacterial growth by inhibiting translation. It binds to the 30S ribosomal subunit and prevents the amino-acyl tRNA from binding to the A site of the ribosome. It also binds to some extent to the 50S ribosomal subunit. This binding is reversible in nature. Additionally tetracycline may alter the cytoplasmic membrane of bacteria causing leakage of intracellular contents, such as nucleotides, from the cell.  Tetracycline passively diffuses through porin channels in the bacterial membrane and reversibly binds to the 30S ribosomal subunit, preventing binding of tRNA to the mRNA-ribosome complex, and thus interfering with protein synthesis.",The molecular weight is 444.44.,Tetracycline has a topological polar surface area of 181.62.,The log p value of  is -0.9.,Tetracycline is approved and vet_approved.,Tetracycline is a solid.,True
14231,"Irinotecan is an antineoplastic enzyme inhibitor primarily used in the treatment of colorectal cancer. It is a derivative of camptothecin that inhibits the action of topoisomerase I. Irinotecan prevents religation of the DNA strand by binding to topoisomerase I-DNA complex, and causes double-strand DNA breakage and cell death. It is a derivative of camptothecin. Irinotecan was approved for the treatment of advanced pancreatic cancer in October, 2015 (irinotecan liposome injection, trade name Onivyde). For the treatment of metastatic colorectal cancer (first-line therapy when administered with 5-fluorouracil and leucovorin). Also used in combination with cisplatin for the treatment of extensive small cell lung cancer. Irinotecan is currently under investigation for the treatment of metastatic or recurrent cervical cancer. Also used in combination with fluorouracil and leucovorin for the treatment of patients with metastatic adenocarcinoma of the pancreas after disease progression following gemcitabine-based therapy.  Irinotecan is an antineoplastic enzyme inhibitor primarily used in the treatment of colorectal cancer. Irinotecan is a semisynthetic derivative of camptothecin. Camptothecins interact specifically with topoisomerase I, an enzyme in the cell nucleus that regulates DNA topology and facilitates nuclear processes such as DNA replication, recombination, and repair. During these processes, topoisomerase I relieves torsional strain in DNA by inducing reversible single-strand breaks, allowing single DNA strands to pass through the break. The 3'-DNA terminus of the broken DNA strands bind covalently with the topoisomerase enzyme to form a catalytic intermediate called a cleavable complex. After the DNA is sufficiently relaxed and the strand passage reaction is complete, DNA topoisomerase reattaches the broken DNA strands to form the chemically unaltered topoisomers that allow transcription to proceed. Irinotecan and its active metabolite SN-38 bind to the topoisomerase I-DNA complex and prevent religation of these single-strand breaks. Current research suggests that the cytotoxicity of irinotecan is due to double-strand DNA damage produced during DNA synthesis when replication enzymes interact with the ternary complex formed by topoisomerase I, DNA, and either Irinotecan or SN-38. Mammalian cells cannot efficiently repair these double-strand breaks. The precise contribution of SN-38 to the activity of irinotecan in humans is not known. Irinotecan is cell cycle phase-specific (S-phase). Irinotecan inhibits the action of topoisomerase I. Irinotecan prevents religation of the DNA strand by binding to topoisomerase I-DNA complex. The formation of this ternary complex interferes with the moving replication fork, which induces replication arrest and lethal double-stranded breaks in DNA. As a result, DNA damage is not efficiently repaired and apoptosis (programmed cell death) occurs.",The molecular weight is 586.69.,Irinotecan has a topological polar surface area of 112.51.,The log p value of  is 2.43.,Irinotecan is approved and investigational.,Irinotecan is a solid.,True
14232,"Olopatadine is a selective histamine H1 antagonist and mast cell stabilizer that works by attenuating inflammatory and allergic reactions. It is a structural analog of , which has a minimal anti-allergic activity. Olopatadine works by blocking the effects of histamine, which is a primary inflammatory mediator that causes inflammatory and allergic reactions. An ophthalmic solution of olopatadine was approved by the FDA and European Union for the treatment of seasonal and perennial allergic conjunctivitis in 1996 and 2002, respectively. In comparison to other anti-allergenic ophthalmic medications, olopatadine displays a good comfort and tolerability profile since it does not cause perturbation of cell membranes. Olopatadine is used for the symptomatic treatment of ocular itching associated with allergic conjunctivitis in ophthalmic formulations and seasonal allergic rhinitis in intranasal formulations. It is currently marketed under several brand names, including Pazeo, Patanase, and Opatanol. Olopatadine is indicated for the symptomatic treatment of ocular itching associated with allergic conjunctivitis as ophthalmic solution. Inflammatory reactions in response to various stimuli are mediated by endogenous mediators and other pro-inflammatory factors. Histamine receptor activation and mast cell degranulation are primary mechanisms that cause inflammatory reactions such as ocular itching, hyperemia, chemosis, eyelid swelling, and tearing of seasonal allergic conjunctivitis. Olopatadine is an anti-allergenic molecule and mast cell stabilizer that inhibits the _in vivo_ type 1 immediate hypersensitivity reaction. By blocking the effects of histamine, olopatadine works to reduce the symptoms of allergies and inflammation at various sites of administration, including the eyes and nose. It has shown to exert antihistaminic effects in isolated tissues, animal models, and humans. Olopatadine also demonstrated dose-dependent inhibition of immunologically-stimulated release of histamine from rat basophilic leukemia cells and human conjunctival mast cells _in vitro_. Olopatadine has a relatively rapid onset of action and prolonged duration, where it was shown to mediate anti-histaminic effects at 5 minutes to 24 hours post-administration. Histamine is a biogenic vasoactive amine that binds to its receptors, which are G-protein coupled receptors. Signaling through the histamine H1 receptor is thought to primarily promote the activation of inflammatory reactions, such as allergy, asthma, and autoimmune diseases. H1 receptor signaling activates the intracellular transcription factors, such as IP3, PLC, PKC, DAG, and intracellular calcium ions, which all work to activate further downstream cascades. Activated downstream cascades lead to the production of cytokines, the release of mast cell inflammatory mediators, synthesis of prostacyclins, activation of platelet factor, as well as the synthesis of nitric oxide, arachidonic acid, and thromboxane, which all contribute to inflammatory reactions. ",The molecular weight is 337.42.,Olopatadine has a topological polar surface area of 49.77.,The log p value of  is 1.09.,Olopatadine is approved.,Olopatadine is a solid.,True
14233,"A thiazide diuretic with actions and uses similar to those of hydrochlorothiazide. (From Martindale, The Extra Pharmacopoeia, 30th ed, p822) Used as adjunctive therapy in edema associated with congestive heart failure, hepatic cirrhosis, and corticosteroid and estrogen therapy. Also used in the management of hypertension either as the sole therapeutic agent or to enhance the effect of other antihypertensive drugs in the more severe forms of hypertension. Hydroflumethiazide is an oral thiazide used to treat hypertension and edema. High blood pressure adds to the workload of the heart and arteries. If it continues for a long time, the heart and arteries may not function properly. This can damage the blood vessels of the brain, heart, and kidneys, resulting in a stroke, heart failure, or kidney failure. High blood pressure may also increase the risk of heart attacks. Like other thiazides, Hydroflumethiazide promotes water loss from the body (diuretics). Thiazides inhibit Na+/Cl- reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue. Hydroflumethiazide is a thiazide diuretic that inhibits water reabsorption in the nephron by inhibiting the sodium-chloride symporter (SLC12A3) in the distal convoluted tubule, which is responsible for 5% of total sodium reabsorption. Normally, the sodium-chloride symporter transports sodium and chloride from the lumen into the epithelial cell lining the distal convoluted tubule. The energy for this is provided by a sodium gradient established by sodium-potassium ATPases on the basolateral membrane. Once sodium has entered the cell, it is transported out into the basolateral interstitium via the sodium-potassium ATPase, causing an increase in the osmolarity of the interstitium, thereby establishing an osmotic gradient for water reabsorption. By blocking the sodium-chloride symporter, Hydroflumethiazide effectively reduces the osmotic gradient and water reabsorption throughout the nephron.",The molecular weight is 331.28.,Hydroflumethiazide has a topological polar surface area of 118.36.,The log p value of  is -0.21.,Hydroflumethiazide is approved and investigational and withdrawn.,Hydroflumethiazide is a solid.,True
14234,"Oxcarbazepine is an anti-epileptic medication used in the treatment of partial onset seizures that was first approved for use in the United States in 2000. It is a structural derivative of and exerts a majority of its activity via a pharmacologically active metabolite, MHD, which exists as a racemate in the blood - a pro-drug of the more active (S)-enantiomer is also marketed as a separate anti-epileptic under the name. Compared to other anti-epileptic drugs, which are generally metabolized via the cytochrome P450 system, oxcarbazepine has a reduced propensity for involvement in drug-drug interactions owing to its primarily reductive metabolism. In the United States, oxcarbazepine is indicated as monotherapy in the treatment of partial-onset seizures in patients 4 years of age and older, and as adjunctive therapy in the treatment of partial-onset seizures in patients 2 years of age and older. In Canada, oxcarbazepine is indicated for use as monotherapy or adjunctive therapy in the treatment of partial-onset seizures in patients 6 years of age and older. Oxcarbazepine is an anticonvulsant drug that reduces the incidence of seizures in epilepsy by inhibiting abnormal electrical activity in the brain. The exact mechanism through which oxcarbazepine and its active metaoblite, MHD, exert their anti-epileptic effects is unclear, but is thought to primarily involve the blockade of voltage-gated sodium channels. The opening and closing of sodium channels allows for the propagation of action potentials along neurons - in epilepsy, these action potentials can occur in excess of that required for normal function, and the repetitive and pathological firing of these action potentials leads to seizure activity. Both oxcarbazepine and MHD are thought to inhibit seizure activity by binding to the inactive state of voltage-gated sodium channels, thus prolonging the period in which the receptor is unavailable for action potential propagation. This helps to stabilize hyperexcited neuronal membranes, inhibit repetitive neuron firing, and prevent the spread of seizure activity within the CNS without affecting normal neuronal transmission.",The molecular weight is 252.27.,Oxcarbazepine has a topological polar surface area of 63.4.,The log p value of  is 1.21.,Oxcarbazepine is approved.,Oxcarbazepine is a solid.,True
14235,"Estradiol is a naturally occurring hormone circulating endogenously in females. It is commercially available in several hormone therapy products for managing conditions associated with reduced estrogen, such as vulvovaginal atrophy and hot flashes. Some available forms of estradiol include oral tablets, injections, vaginal rings, transdermal patches, sprays, gels, and creams.  Estradiol is indicated in various preparations for the treatment of moderate to severe vasomotor symptoms and vulvar and vaginal atrophy due to menopause, for the treatment of hypoestrogenism due to hypogonadism, castration, or primary ovarian failure, and for the prevention of postmenopausal osteoporosis. It is also used for the treatment of breast cancer (only for palliation therapy) in certain men or women with metastatic disease, and for the treatment of androgen-dependent prostate cancer (only for palliation therapy). It is also used in combination with other hormones as a component of oral contraceptive pills for preventing pregnancy (most commonly as , a synthetic form of estradiol). Estradiol acts on the on the estrogen receptors to relieve vasomotor systems (such as hot flashes) and urogenital symptoms (such as vaginal dryness and dyspareunia). Estrogen is found in the the breast, uterine, ovarian, skin, prostate, bone, fat, and brain tissues. The main source of estrogen in adult women during the reproductive period of life is the ovarian follicle, which secretes 70 to 500 mcg of estradiol each day. After menopause, however, the majority of endogenous estrogen is produced by transformation of androstenedione (which is secreted by the adrenal cortex) to estrone in the peripheral tissues. Both estrone and its sulphate conjugated form, estrone sulphate, represent the most abundant estrogens found in postmenopausal women. ",The molecular weight is 272.39.,Estradiol has a topological polar surface area of 40.46.,The log p value of  is 3.78.,Estradiol is approved and investigational and vet_approved.,Estradiol is a solid.,True
14236,"A non-steroidal anti-inflammatory agent with analgesic, anti-inflammatory, and antipyretic properties. It is an inhibitor of cyclooxygenase. For the treatment of rheumatoid arthritis, osteoarthritis, dysmenorrhea, and mild to moderate pain, inflammation, and fever. Mefenamic acid, an anthranilic acid derivative, is a member of the fenamate group of nonsteroidal anti-inflammatory drugs (NSAIDs). It exhibits anti-inflammatory, analgesic, and antipyretic activities. Similar to other NSAIDs, mefenamic acid inhibits prostaglandin synthetase. Mefenamic acid binds the prostaglandin synthetase receptors COX-1 and COX-2, inhibiting the action of prostaglandin synthetase. As these receptors have a role as a major mediator of inflammation and/or a role for prostanoid signaling in activity-dependent plasticity, the symptoms of pain are temporarily reduced.",The molecular weight is 241.29.,Mefenamic acid has a topological polar surface area of 49.33.,The log p value of  is 5.14.,Mefenamic acid is approved.,Mefenamic acid is a solid.,True
14237,"Acyclovir is a nucleotide analog antiviral used to treat herpes simplex, _Varicella zoster_, herpes zoster, herpes labialis, and acute herpetic keratitis. Acyclovir is generally used first line in the treatment of these viruses and some products are indicated for patients as young as 6 years old. An acyclovir topical cream is indicated to treat recurrent herpes labialis in immunocompetent patients 12 years and older. Acyclovir oral tablets, capsules, and suspensions are indicated to treat herpes zoster, genital herpes, and chickenpox. An acyclovir topical ointment is indicated to treat initial genital herpes and limited non-life-threatening mucocutaneous herpes simplex in immunocompromised patients. An acyclovir cream with hydrocortisone is indicated to treat recurrent herpes labialis, and shortening lesion healing time in patients 6 years and older. An acyclovir buccal tablet is indicated for the treatment of recurrent herpes labialis. An acyclovir ophthalmic ointment is indicated to treat acute herpetic keratitis. Acyclovir is a nucleoside analog that inhibits the action of viral DNA polymerase and DNA replication of different herpesvirus. Acyclovir has a wide therapeutic window as overdose is rare in otherwise healthy patients. Acyclovir is becomes acyclovir monophosphate due to the action of viral thymidine kinase. Acyclovir monophosphate is converted to the diphosphate form by guanylate kinase. Acyclovir diphosphate is converted to acyclovir triphosphate by nucleoside diphosphate kinase, pyruvate kinase, creatine kinase, phosphoglycerate kinase, succinyl-CoA synthetase, phosphoenolpyruvate carboxykinase and adenylosuccinate synthetase. Acyclovir triphosphate has higher affinity for viral DNA polymerase than cellular DNA polymerase and incorporates into the DNA where the missing 2' and 3' carbons causes DNA chain termination. In other cases acyclovir triphosphate competes so strongly for viral DNA polymerase that other bases cannot associate with the enzyme, inactivating it.",The molecular weight is 225.21.,Acyclovir has a topological polar surface area of 114.76.,The log p value of  is -2.42.,Acyclovir is approved.,Acyclovir is a solid.,True
14238,"Naproxen is classified as a nonsteroidal anti-inflammatory dug (NSAID) and was initially approved for prescription use in 1976 and then for over-the-counter (OTC) use in 1994. It can effectively manage acute pain as well as pain related to rheumatic diseases, and has a well studied adverse effect profile. Given its overall tolerability and effectiveness, naproxen can be considered a first line treatment for a variety of clinical situations requiring analgesia. Naproxen is available in both immediate and delayed release formulations, in combination with sumatriptan to treat migraines, and in combination with esomeprazole to lower the risk of developing gastric ulcers. Naproxen is indicated for the management of rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, polyarticular juvenile idiopathic arthritis, tendinitis, bursitis, acute gout, primary dysmenorrhea, and for the relief of mild to moderate pain. Further, it is first-line therapy for osteoarthritis, acute gouty arthritis, dysmenorrhea, and musculoskeletal inflammation and pain. Naproxen is an established non-selective NSAID and is useful as an analgesic, anti-inflammatory and antipyretic. Similar to other NSAIDs, the pharmacological activity of naproxen can be attributed to the inhibition of cyclo-oxygenase, which in turn reduces prostaglandin synthesis in various tissues and fluids including the synovial fluid, gastric mucosa, and the blood.  As with other non-selective NSAIDs, naproxen exerts it's clinical effects by blocking COX-1 and COX-2 enzymes leading to decreased prostaglandin synthesis. Although both enzymes contribute to prostaglandin production, they have unique functional differences. The COX-1 enzymes is constitutively active and can be found in normal tissues such as the stomach lining, while the COX-2 enzyme is inducible and produces prostaglandins that mediate pain, fever and inflammation. The COX-2 enzyme mediates the desired antipyretic, analgesic and anti-inflammatory properties offered by Naproxen, while undesired adverse effects such as gastrointestinal upset and renal toxicities are linked to the COX-1 enzyme.",The molecular weight is 230.26.,Naproxen has a topological polar surface area of 46.53.,The log p value of  is 2.82.,Naproxen is approved and vet_approved.,Naproxen is a solid.,True
14239,"A short-acting opioid anesthetic and analgesic derivative of fentanyl. It produces an early peak analgesic effect and fast recovery of consciousness. Alfentanil is effective as an anesthetic during surgery, for supplementation of analgesia during surgical procedures, and as an analgesic for critically ill patients. For the management of postoperative pain and the maintenance of general anesthesia. Alfentanil is a synthetic opioid analgesic. Alfentanil interacts predominately with the opioid mu-receptor. These mu-binding sites are discretely distributed in the human brain, spinal cord, and other tissues. In clinical settings, alfentanil exerts its principal pharmacologic effects on the central nervous system. Its primary actions of therapeutic value are analgesia and sedation. Alfentanil may increase the patient's tolerance for pain and decrease the perception of suffering, although the presence of the pain itself may still be recognized. In addition to analgesia, alterations in mood, euphoria and dysphoria, and drowsiness commonly occur. Alfentanil depresses the respiratory centers, depresses the cough reflex, and constricts the pupils. Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Alfentanil's analgesic activity is, most likely, due to its conversion to morphine. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability.",The molecular weight is 416.53.,Alfentanil has a topological polar surface area of 81.05.,The log p value of  is 2.13.,Alfentanil is approved and illicit.,Alfentanil is a solid.,True
14240,"The most significant modifiable risk factor for cardiovascular disease and the most prominent contributor to all-cause mortality is hypertension. Characterized by an office blood pressure of ≥140/90, hypertension is pervasive and impacts an estimated 25% of adults globally. Treatment for hypertension should include a number of lifestyle changes (ie. reduced sodium intake) along with pharmacotherapy - it should be noted that treatment with several antihypertensive agents may be required in order to achieve blood pressure targets. Indapamide is a diuretic indicated for use as monotherapy or in combination with other blood pressure-lowering agents to treat hypertension. It may also be used to treat fluid and salt retention associated with congestive heart failure. Classified as a sulfonamide diuretic, indapamide is an effective antihypertensive agent and by extension, has shown efficacy in the prevention of target organ damage. Indapamide acts on the nephron, specifically at the proximal segment of the distal convoluted tubule where it inhibits the Na+/Cl- cotransporter, leading to reduced sodium reabsorption. As a result, sodium and water are retained in the lumen of the nephron for urinary excretion. The effects that follow include reduced plasma volume, reduced venous return, lower cardiac output, and ultimately decreased blood pressure.",The molecular weight is 365.83.,Indapamide has a topological polar surface area of 92.5.,The log p value of  is 2.96.,Indapamide is approved.,Indapamide is a solid.,True
14241,"Fentanyl, a potent opioid agonist, was developed in the 1950s to fill a need for strong and rapid analgesia. Because of these characteristics, fentanyl is commonly used to treat chronic cancer pain or in anesthesia. Fentanyl is related to other opioids like and. Fentanyl intravenous or intramuscular injections are indicated for short term analgesia during induction, maintenance, and recovery from general or regional anesthesia. These injections are also used with a neuroleptic for premedication, induction, and as an adjunct to maintenance of anesthesia. Finally, fentanyl intravenous or intramuscular injections are used with oxygen for anesthesia in high risk patients. Fentanyl produces strong analgesia through its activation of opioid receptors. It has a duration of action of several hours and a wider therapeutic index as patients develop tolerance to opioids. Fentanyl is associated with a risk of addiction and abuse and should not be mixed with alcohol or benzodiazepines. Fentanyl binds to opioid receptors, especially the mu opioid receptor, which are coupled to G-proteins. Activation of opioid receptors causes GTP to be exchanged for GDP on the G-proteins which in turn down regulates adenylate cyclase, reducing concentrations of cAMP. Reduced cAMP decreases cAMP dependant influx of calcium ions into the cell. The exchange of GTP for GDP results in hyperpolarization of the cell and inhibition of nerve activity.",The molecular weight is 336.48.,Fentanyl has a topological polar surface area of 23.55.,The log p value of  is 3.62.,Fentanyl is approved and illicit and investigational and vet_approved.,Fentanyl is a solid.,True
14242,"Meloxicam is a nonsteroidal anti-inflammatory drug (NSAID) used to relieve various types of pain, including pain caused by musculoskeletal conditions, osteoarthritis, and rheumatoid arthritis. With a longer half-life than most other NSAIDS, it is a favorable option for those who require once-daily dosing. Meloxicam is available in oral, transdermal, and intravenous formulations. It is a preferential COX-2 inhibitor, purportedly reducing the risk of adverse gastrointestinal tract effects, however, this is a topic of controversy. Meloxicam is indicated for the symptomatic treatment of arthritis and osteoarthritis. In addition, it is indicated for the pauciarticular and polyarticular course of Juvenile Rheumatoid Arthritis (JRA) in patients aged 2 years old or above. Off-label uses include the treatment of dental or post-surgical pain. In addition to the above, meloxicam has also been studied in the treatment of neuropathic pain.  Meloxicam is an anti-inflammatory, analgesic analgesic with antipyretic effects in fever. Prostaglandins are substances that contribute to inflammation. This drug also exerts preferential actions against COX-2, which may reduce the possible gastrointestinal effects of this drug.  Meloxicam inhibits prostaglandin synthetase (cylooxygenase 1 and 2) enzymes leading to a decreased synthesis of prostaglandins, which normally mediate painful inflammatory symptoms. As prostaglandins sensitize neuronal pain receptors, inhibition of their synthesis leads to analgesic and inflammatory effects. Meloxicam preferentially inhibits COX-2, but also exerts some activity against COX-1, causing gastrointestinal irritation.",The molecular weight is 351.4.,Meloxicam has a topological polar surface area of 99.6.,The log p value of  is 2.29.,Meloxicam is approved and vet_approved.,Meloxicam is a solid.,True
14243,"Sodium Lauryl Sulfate (SLS) is an anionic surfactant naturally derived from coconut and/or palm kernel oil. It usually consists of a mixture of sodium alkyl sulfates, mainly the lauryl. SLS lowers surface tension of aqueous solutions and is used as fat emulsifier, wetting agent, and detergent in cosmetics, pharmaceuticals and toothpastes. It is also used in creams and pastes to properly disperse the ingredients and as research tool in protein biochemistry. SLS also has some microbicidal activity. SLS is used as a surfactant in shampoos and toothpastes. SLS also has microbicidal activities against both enveloped (Herpes simplex viruses, HIV-1, Semliki Forest virus) and nonenveloped (papillomaviruses, reovirus, rotavirus and poliovirus) viruses, although it has not been approved for this use. SLS is an anionic surfactant. Its amphiphilic properties make it an ideal detergent.  Like other surfactants, SLS is amphiphilic. It thus migrates to the surface of liquids, where its alignment and aggregation with other SLS molecules lowers the surface tension. This allows for easier spreading and mixing of the liquid. SLS has potent protein denaturing activity and inhibits the infectivity of viruses by by solubilizing the viral envelope and/or by denaturing envelope and/or capsid proteins.",The molecular weight is 288.38.,Sodium lauryl sulfate has a topological polar surface area of 66.43.,,Sodium lauryl sulfate is experimental.,Sodium lauryl sulfate is a solid.,True
14244,"Propofol is an intravenous anaesthetic agent used for induction and maintenance of general anaesthesia. IV administration of propfol is used to induce unconsciousness after which anaesthesia may be maintained using a combination of medications. Recovery from propofol-induced anaesthesia is generally rapid and associated with less frequent side effects (e.g. drowsiness, nausea, vomiting) than with thiopental, methohexital, and etomidate. Propofol may be used prior to diagnostic procedures requiring anaesthesia, in the management of refractory status epilepticus, and for induction and/or maintenance of anaesthesia prior to and during surgeries. Used for induction and/or maintenance of anaesthesia and for management of refractory status epilepticus.  Propofol is a sedative-hypnotic agent for use in the induction and maintenance of anesthesia or sedation. Intravenous injection of a therapeutic dose of propofol produces hypnosis rapidly with minimal excitation, usually within 40 seconds from the start of an injection (the time for one arm-brain circulation). The action of propofol involves a positive modulation of the inhibitory function of the neurotransmitter gama-aminobutyric acid (GABA) through GABA-A receptors.",The molecular weight is 178.28.,Propofol has a topological polar surface area of 20.23.,The log p value of  is 3.93.,Propofol is approved and investigational and vet_approved.,Propofol is a liquid.,True
14245,"A benzodiazepine with anticonvulsant, anxiolytic, sedative, muscle relaxant, and amnesic properties and a long duration of action. Its actions are mediated by enhancement of gamma-aminobutyric acid activity. It is used in the treatment of severe anxiety disorders, as a hypnotic in the short-term management of insomnia, as a sedative and premedicant, as an anticonvulsant, and in the management of alcohol withdrawal syndrome. (From Martindale, The Extra Pharmacopoeia, 30th ed, p589) In general, diazepam is useful in the symptomatic management of mild to moderate degrees of anxiety in conditions dominated by tension, excitation, agitation, fear, or aggressiveness such as may occur in psychoneurosis, anxiety reactions due to stress conditions, and anxiety states with somatic expression. Diazepam is a benzodiazepine that exerts anxiolytic, sedative, muscle- relaxant, anticonvulsant and amnestic effects. Most of these effects are thought to result from facilitation of the action of gamma aminobutyric acid (GABA), an inhibitory neurotransmitter in the central nervous system. Diazepam is a benzodiazepine tranquilliser with anticonvulsant, sedative, muscle relaxant and amnesic properties.",The molecular weight is 284.74.,Diazepam has a topological polar surface area of 32.67.,The log p value of  is 2.96.,Diazepam is approved and illicit and investigational and vet_approved.,Diazepam is a solid.,True
14246,"Oxazepam is an intermediate-acting, 3-hydroxybenzodiazepine used in the treatment of alcohol withdrawal and anxiety disorders. Oxazepam, like related 3-hydroxybenzodiazepine , is considered less susceptible to pharmacokinetic variability based on patient-specific factors (e.g. age, liver disease) - this feature is advantageous as compared to other benzodiazepines, and is likely owing in part to oxazepam's relatively simple metabolism. It is an active metabolite of both and and undergoes very little biotransformation following absorption, making it unlikely to participate in pharmacokinetic interactions. Oxazepam is indicated for the management of anxiety disorders and for the short-term relief of symptoms of anxiety. It may also be used in the management of alcohol withdrawal symptoms. Benzodiazepines, including oxazepam, exert their sedative and anxiolytic effects by potentiating the effects of endogenous GABA, the primary inhibitory neurotransmitter in the CNS. Compared to other benzodiazepines, it has relatively low potency and a moderate duration of action. Oxazepam should be administered with caution to patients for whom a drop in blood pressure may lead to cardiac complications as, in rare cases, it may cause hypotension. Like other benzodiazepines, oxazepam exerts its anxiolytic effects by potentiating the effect of gamma-aminobutyric acid (GABA) on GABA(A) receptors, the main inhibitory neurotransmitter receptors in the mammalian brain. GABA(A) receptors are a component of GABA-gated ionotropic chloride channels that produce inhibitory postsynaptic potentials - following activation by GABA, the channel undergoes a conformational change that allows the passage of chloride ions through the channel. The inhibitory potentials produced by GABA neurotransmission play an integral role in the suppression and control of epileptiform nerve firing such as that seen in epilepsy, which makes the GABA system a desirable target in the treatment of epilepsy.",The molecular weight is 286.72.,Oxazepam has a topological polar surface area of 61.69.,The log p value of  is 2.31.,Oxazepam is approved.,Oxazepam is a solid.,True
14247,"Clofazimine is a highly lipophilic antimicrobial riminophenazine dye used in combination with other agents, such as , for the treatment of leprosy. It was originally described in 1957 and was the prototypical riminophenazine dye - a bright-red dye that, in its clinical use, results in long-lasting discoloration of the skin and bodily fluids. Although it carries _in vitro_ activity against other mycobacterium, such as _Mycobacterium tuberculosis_, it is generally considered an ineffective treatment in comparison to classic tuberculosis treatments such as and. Clofazimine is indicated for the treatment of lepromatous leprosy, including dapsone-resistant lepromatous leprosy and lepromatous leprosy complicated by erythema nodosum leprosum. To prevent the development of drug resistance, it should be used only in combination with other antimycobacterial leprosy treatments. Clofazimine exerts a slow bactericidal effect on <i>Mycobacterium leprae</i> (Hansen's bacillus) due primarily to its action on the bacterial outer membrane, though there is some evidence that activity on the bacterial respiratory chain and ion transporters may play a role. It also exerts anti-inflammatory properties due to the suppression of T-lymphocyte activity. Clofazimine has a relatively long duration of action owing to its long residence time in the body, but is still administered daily. Although the precise mechanism(s) of action of clofazimine have not been elucidated, its antimicrobial activity appears to be membrane-directed. It was previously thought that, due to its lipophilicity, clofazimine participated in the generation of intracellular reactive oxygen species (ROS) via redox cycling, specifically H<sub>2</sub>O<sub>2</sub> and superoxide, which then exerted an antimicrobial effect. A more recent and compelling theory involves clofazimine interacting with bacterial membrane phospholipids to generate antimicrobial lysophospholipids - bactericidal efficacy may, then, arise from the combined membrane-destabilizing effects of both clofazimine and lysophospholipids, which interfere with K+ uptake and, ultimately, ATP production.",The molecular weight is 473.4.,Clofazimine has a topological polar surface area of 39.99.,The log p value of  is 7.55.,Clofazimine is approved and investigational.,Clofazimine is a solid.,True
14248,"Cystinosis is a rare disease caused by mutations in the CTNS gene that encodes for cystinosin, a protein responsible for transporting cystine out of the cell lysosome. A defect in cystinosin function is followed by cystine accumulation throughout the body, especially the eyes and kidneys. The bitartrate salt of cysteamine is used for the oral treatment of nephropathic cystinosis and cystinuria in children 6 years old and above, and adults. The hydrochloride salt, used in eye drop preparations, is indicated for the treatment of corneal cystine crystal accumulation in patients with cystinosis. Cystine accumulation is the cause of organ damage in cystinosis. Cysteamine prevents the accumulation of cystine crystals in the body and is specifically prescribed to prevent kidney and eye damage. Cysteamine converts cystine into a form that may easily exit cells, preventing harmful accumulation. Individuals born without the ability to metabolize cystine suffer from cystinosis, a rare genetic disorder characterized by the widespread accumulation of cystine crystals throughout the body and eye tissues. The cystine crystals may cause considerable damage, particularly in the renal tissues and corneal tissues. In some cases, renal failure can occur during childhood if the condition is left untreated. Other organs that may be affected by cystinosis include the CNS, thyroid, pancreas, muscle tissues, and gonads. ",The molecular weight is 77.15.,Cysteamine has a topological polar surface area of 26.02.,The log p value of  is -0.25.,Cysteamine is approved and investigational.,Cysteamine is a solid.,True
14249,"Pseudoephedrine is structurally related to but exerts a weaker effect on the sympathetic nervous system. Both drugs naturally occur in in ephedra plant which have a history of use in traditional Eastern medicine and were first researched in the west in 1889. The decongestant effect of pseudoephedrine was described in dogs in 1927. Pseudoephedrine is a sympathomimetic amine used for its decongestant activity. Pseudoephedrine causes vasoconstriction which leads to a decongestant effect. It has a short duration of action unless formulated as an extended release product. Patients should be counselled regarding the risk of central nervous system stimulation. Pseudoephedrine acts mainly as an agonist of alpha adrenergic receptors and less strongly as an agonist of beta adrenergic receptors. This agonism of adrenergic receptors produces vasoconstriction which is used as a decongestant and as a treatment of priapism. Pseudoephedrine is also an inhibitor of norepinephrine, dopamine, and serotonin transporters.",The molecular weight is 165.24.,Pseudoephedrine has a topological polar surface area of 32.26.,The log p value of  is 0.89.,Pseudoephedrine is approved.,Pseudoephedrine is a solid.,True
14250,"Terbinafine hydrochloride (Lamisil) is a synthetic allylamine antifungal. It is highly lipophilic in nature and tends to accumulate in skin, nails, and fatty tissues. Like other allylamines, terbinafine inhibits ergosterol synthesis by inhibiting the fungal squalene monooxygenase (also called squalene epoxidase), an enzyme that is part of the fungal cell wall synthesis pathway. Terbinafine hydrochloride is indicated to treat fungal skin and nail infections caused by _Trichophyton_ species, _Microsporum canis_, _Epidermophyton floccosum_, and _Tinea_ species. Terbinafine hydrochloride also treats yeast infections of the skin caused by _Candida_ species and _Malassezia furfur_. Terbinafine is an allylamine antifungal that inhibits squalene epoxidase (also known as squalene monooxygenase) to prevent the formation of ergosterol and cause an accumulation of squalene, weakening the cell wall of fungal cells. Terbinafine distributes into tissues and has a long terminal elimination half life, so the duration of action is long. Overdose with terbinafine is rare, even above the therapeutic dose, so the therapeutic index is wide. Patients taking oral terbinafine should have liver function tests performed prior to treatment to reduce the risk of liver injury. Terbinafine inhibits the enzyme squalene monooxygenase (also called squalene epoxidase), preventing the conversion of squalene to 2,3-oxydosqualene, a step in the synthesis of ergosterol. This inhibition leads to decreased ergosterol, which would normally be incorporated into the cell wall, and accumulation of squalene.",The molecular weight is 291.44.,Terbinafine has a topological polar surface area of 3.24.,The log p value of  is 5.96.,Terbinafine is approved and investigational and vet_approved.,Terbinafine is a solid.,True
14251,"Tacrolimus (also FK-506 or Fujimycin) is an immunosuppressive drug whose main use is after organ transplant to reduce the activity of the patient's immune system and so the risk of organ rejection. It is also used in a topical preparation in the treatment of severe atopic dermatitis, severe refractory uveitis after bone marrow transplants, and the skin condition vitiligo. It was discovered in 1984 from the fermentation broth of a Japanese soil sample that contained the bacteria Streptomyces tsukubaensis. Tacrolimus is chemically known as a macrolide. It reduces peptidyl-prolyl isomerase activity by binding to the immunophilin FKBP-12 (FK506 binding protein) creating a new complex. This FKBP12-FK506 complex inhibits calcineurin which inhibits T-lymphocyte signal transduction and IL-2 transcription. For use after allogenic organ transplant to reduce the activity of the patient's immune system and so the risk of organ rejection. It was given FDA approval in 1994 for use in liver transplantation. Since then, this indication has expanded to kidney, heart, small bowel, pancreas, lung, trachea, skin, cornea, and limb transplants. It has also been used in a topical preparation in the treatment of severe atopic dermatitis. Tacrolimus acts by reducing peptidyl-prolyl isomerase activity by binding to the immunophilin FKBP-12 (FK506 binding protein) creating a new complex. This inhibits both T-lymphocyte signal transduction and IL-2 transcription. Tacrolimus has similar activity to cyclosporine but rates of rejection are lower with tacrolimus. Tacrolimus has also been shown to be effective in the topical treatment of eczema, particularly atopic eczema. It suppresses inflammation in a similar way to steroids, but is not as powerful. An important dermatological advantage of tacrolimus is that it can be used directly on the face; topical steroids cannot be used on the face, as they thin the skin dramatically there. On other parts of the body, topical steroid are generally a better treatment. The mechanism of action of tacrolimus in atopic dermatitis is not known. While the following have been observed, the clinical significance of these observations in atopic dermatitis is not known. It has been demonstrated that tacrolimus inhibits T-lymphocyte activation by first binding to an intracellular protein, FKBP-12. A complex of tacrolimus-FKBP-12, calcium, calmodulin, and calcineurin is then formed and the phosphatase activity of calcineurin is inhibited. This prevents the dephosphorylation and translocation of nuclear factor of activated T-cells (NF-AT), a nuclear component thought to initiate gene transcription for the formation of lymphokines. Tacrolimus also inhibits the transcription for genes which encode IL-3, IL-4, IL-5, GM-CSF, and TNF-, all of which are involved in the early stages of T-cell activation. Additionally, tacrolimus has been shown to inhibit the release of pre-formed mediators from skin mast cells and basophils, and to downregulate the expression of FceRI on Langerhans cells.",The molecular weight is 804.03.,Tacrolimus has a topological polar surface area of 178.36.,The log p value of  is 5.78.,Tacrolimus is approved and investigational.,Tacrolimus is a solid.,True
14252,"An ibuprofen-type anti-inflammatory analgesic and antipyretic. It inhibits prostaglandin synthesis and has been proposed as an anti-arthritic. It is no longer approved for use in the United States. Used as eye drops to inhibit the miosis (pupil constriction) that may occur during ocular surgery. Suprofen is a non-steroidal anti-inflammatory analgesic and antipyretic. Ophthalmic anti-inflammatory medicines are used in the eye to lessen problems that can occur during or after some kinds of eye surgery. Sometimes, the pupil of the eye gets smaller during an operation (pupil constriction), making it more difficult for the surgeon to reach some areas of the eye. Suprofen is used to help prevent this. Suprofen binds to the cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) isoenzymes, preventing the synthesis of prostaglandins and reducing the inflammatory response. Cyclooxygenase catalyses the formation of prostaglandins and thromboxane from arachidonic acid (itself derived from the cellular phospholipid bilayer by phospholipase A<sub>2</sub>). Prostaglandins act (among other things) as messenger molecules in the process of inflammation. The overall result is a reduction in pain and inflammation in the eyes and the prevention of pupil constriction during surgery. Normally trauma to the anterior segment of the eye (especially the iris) increases endogenous prostaglandin synthesis which leads to constriction of the iris sphincter.",The molecular weight is 260.31.,Suprofen has a topological polar surface area of 54.37.,The log p value of  is 2.54.,Suprofen is approved and withdrawn.,Suprofen is a solid.,True
14253,"Chlorhexidine is a broad-spectrum antimicrobial biguanide used as a topical antiseptic and in dental practice for the treatment of inflammatory dental conditions caused by microorganisms. It is one of the most common skin and mucous membrane antiseptic agents in use today. The molecule itself is a cationic bis-guanide consisting of two 4-chlorophenyl rings and two biguanide groups joined by a central hexamethylene chain. Topical chlorhexidine for disinfection, as well as oral rinses for dental use, carries activity against a broad range of pathogens including bacteria, yeasts, and viruses. Chlorhexidine is available over-the-counter in various formulations (e.g. solution, sponge, cloth, swab) as a topical antiseptic to sanitize prior to surgeries and/or medical procedures. Dental formulations, available by prescription only, include an oral rinse indicated for the treatment of gingivitis and a slow-release \chip\"" which is inserted into periodontal pockets and is indicated for the reduction of pocket depth in adult patients with periodontitis as an adjunct therapy to dental scaling and root planing procedures."" Chlorhexidine is a broad-spectrum antimicrobial with demonstrated activity against both gram-positive and gram-negative bacteria, yeasts, and viruses. Antimicrobial activity is dose-dependent - chlorhexidine is bacteriostatic at lower concentrations (0.02%-0.06%) and bactericidal at higher concentrations (>0.12%). Pharmacokinetic studies of oral chlorhexidine rinses indicate that approximately 30% of the active ingredient is retained in the mouth following rinsing, which is subsequently slowly released into oral fluids. This ability to adsorb to dentine, shared with tetracycline antibiotics such as , is known as \substantivity\"" and is the result of chlorhexidine's positive charge - it is likely that this substantivity plays at least some role in chlorhexidine's antimicrobial activity, as its persistence on surfaces such as dentine prevent microbial colonization."" Chlorhexidine’s broad-spectrum antimicrobial effects are due to its ability to disrupt microbial cell membranes. The positively charged chlorhexidine molecule reacts with negatively charged phosphate groups on microbial cell surfaces - this reaction both destroys the integrity of the cell, allowing leakage of intracellular material, and allows chlorhexidine to enter the cell, causing precipitation of cytoplasmic components and ultimately cell death. The specific means of cell death is dependent on the concentration of chlorhexidine - lower concentrations are bacteriostatic and result in leakage of intracellular substances such as potassium and phosphorous, whereas higher concentrations are bactericidal and cause cytoplasmic precipitation.",The molecular weight is 505.45.,Chlorhexidine has a topological polar surface area of 167.58.,The log p value of  is 4.81.,Chlorhexidine is approved and vet_approved.,Chlorhexidine is a solid.,True
14254,"Emtricitabine is a nucleoside reverse transcriptase inhibitor (NRTI) indicated for the treatment of HIV infection in adults or combined with for the prevention of HIV-1 infection in high risk adolescents and adults. Emtricitabine is a cytidine analogue. The drug works by inhibiting HIV reverse transcriptase, preventing transcription of HIV RNA to DNA. Emtricitabine is indicated in combination with other medications for the treatment of HIV-1 infections; treatment of HIV-1 infections in pediatric patients 25-35kg, treatment of HIV-1 infections in adult patients ≥35kg, for pre exposure prophylaxis of HIV-1 in adolescent and adult patients excluding those who have receptive vaginal sex; treatment of HIV-1 infections in pediatric and adult patients ≥17kg, pre exposure prophylaxis in adolescents and adults ≥35kg; treatment of HIV-1 in patients ≥12 years and ≥35kg; treatment of HIV-1 in patients weighing ≥35kg; treatment of HIV-1 in patients weighing ≥25kg; and treatment of HIV-1 in patients weighing ≥40kg. Emtricitabine is a cytidine analog that competes with the natural substrate of HIV-1 reverse transcriptase to be incorporated into newly formed DNA, terminating its transcription. It is administered once daily so it has a long duration of action. Patients should be counselled regarding the risk of lactic acidosis and hepatomegaly with steatosis. Emtricitabine is a cytidine analog which, when phosphorylated to emtricitabine 5'-triphosphate, competes with deoxycytidine 5'-triphosphate for HIV-1 reverse transcriptase. As HIV-1 reverse transcriptase incorporates emtricitabine into forming DNA strands, new nucleotides are unable to be incorporated, leading to viral DNA chain termination. Inhibition of reverse transcriptase prevents transcription of viral RNA into DNA, therefore the virus is unable to incorporate its DNA into host DNA and replicate using host cell machinery. This reduces viral load.",The molecular weight is 247.24.,Emtricitabine has a topological polar surface area of 88.15.,The log p value of  is -1.29.,Emtricitabine is approved and investigational.,Emtricitabine is a solid.,True
14255,"Quinapril is the ethyl ester prodrug of the non-sulfhydryl angiotensin converting enzyme inhibitor quinaprilat. It is used to treat hypertension and heart failure. ACE inhibitors are commonly used as a first line therapy in the treatment of hypertension, along with thiazide diuretics or beta blockers. Quinapril is indicated for the treatment of hypertension and as an adjunct therapy in the treatment of heart failure. Quinapril in combination with hydrochlorothiazide is indicated for the treatment of hypertension. Quinapril is a prodrug of an angiotensin converting enzyme (ACE) inhibitor used in the treatment of hypertension or adjunct in the treatment of heart failure. Quinapril has a wide therapeutic window and a long duration of action as it is given in doses of 10-80mg once daily. Angiotensin II constricts coronary blood vessels and is positively inotropic, which under normal circumstances, would increase vascular resistance and oxygen consumption. This action can eventually lead to myocyte hypertrophy and vascular smooth muscle cell proliferation. Angiotensin II also stimulates production of plasminogen activator inhibitor-1 (PAI-1), increasing the risk of thrombosis.",The molecular weight is 438.52.,Quinapril has a topological polar surface area of 95.94.,The log p value of  is 1.74.,Quinapril is approved and investigational.,Quinapril is a solid.,True
14256,"A dideoxynucleoside compound in which the 3&#39;-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. Didanosine is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase; ddI is then metabolized to dideoxyadenosine triphosphate, its putative active metabolite. For use, in combination with other antiretroviral agents, in the treatment of HIV-1 infection in adults. Didanosine is a nucleoside reverse transcriptase inhibitor (NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Didanosine is a hypoxanthine attached to the sugar ring, unlike other nucleoside analogues. Didanosine is phosphorylated to active metabolites that compete for incorporation into viral DNA. They inhibit the HIV reverse transcriptase enzyme competitively and act as a chain terminator of DNA synthesis. Didanosine is effective against HIV, and usually used in combination with other antiviral therapy. Switching from long term AZT treatment to didanosine has been shown to be beneficial. Didanosine has weak acid stability and therefore, it is often combined with an antacid. Didanosine (ddI) is metabolized intracellularly by a series of cellular enzymes to its active moiety, dideoxyadenosine triphosphate (ddATP), which inhibits the HIV reverse transcriptase enzyme competitively by competing with natural dATP. It also acts as a chain terminator by its incorporation into viral DNA as the lack of a 3'-OH group in the incorporated nucleoside analogue prevents the formation of the 5' to 3' phosphodiester linkage essential for DNA chain elongation, and therefore, the viral DNA growth is terminated.",The molecular weight is 236.23.,Didanosine has a topological polar surface area of 88.74.,The log p value of  is -1.92.,Didanosine is approved.,Didanosine is a solid.,True
14257,"A compound that inhibits symport of sodium, potassium, and chloride primarily in the ascending limb of Henle, but also in the proximal and distal tubules. This pharmacological action results in excretion of these ions, increased urinary output, and reduction in extracellular fluid. This compound has been classified as a loop or high ceiling diuretic. For the treatment of high blood pressure and edema caused by diseases like congestive heart failure, liver failure, and kidney failure. Ethacrynic acid is a monosulfonamyl loop or high ceiling diuretic. Ethacrynic acid acts on the ascending limb of the loop of Henle and on the proximal and distal tubules. Urinary output is usually dose dependent and related to the magnitude of fluid accumulation. Water and electrolyte excretion may be increased several times over that observed with thiazide diuretics, since ethacrynic acid inhibits reabsorption of a much greater proportion of filtered sodium than most other diuretic agents. Therefore, ethacrynic acid is effective in many patients who have significant degrees of renal insufficiency. Ethacrynic acid has little or no effect on glomerular filtration or on renal blood flow, except following pronounced reductions in plasma volume when associated with rapid diuresis. Ethacrynic acid inhibits symport of sodium, potassium, and chloride primarily in the ascending limb of Henle, but also in the proximal and distal tubules. This pharmacological action results in excretion of these ions, increased urinary output, and reduction in extracellular fluid. Diuretics also lower blood pressure initially by reducing plasma and extracellular fluid volume; cardiac output also decreases, explaining its antihypertensive action. Eventually, cardiac output returns to normal with an accompanying decrease in peripheral resistance. Its mode of action does not involve carbonic anhydrase inhibition.",The molecular weight is 303.14.,Etacrynic acid has a topological polar surface area of 63.6.,The log p value of  is 3.44.,Etacrynic acid is approved and investigational.,Etacrynic acid is a solid.,True
14258,"An optical isomer of , extracted from the bark of the Cinchona tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular action potential, and decreases automaticity. Quinidine also blocks muscarinic and alpha-adrenergic neurotransmission. For the treatment of ventricular pre-excitation and cardiac dysrhythmias Quinidine, a hydantoin anticonvulsant, is used alone or with phenobarbital or other anticonvulsants to manage tonic-clonic seizures, psychomotor seizures, neuropathic pain syndromes including diabetic neuropathy, digitalis-induced cardiac arrhythmias, and cardiac arrhythmias associated with QT-interval prolongation. Quinidine acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. The antiarrhythmic actions are mediated through effects on sodium channels in Purkinje fibers. Quinidine may also act on the slow inward calcium current (ICa), the rapid (IKr) and slow (IKs) components of the delayed potassium rectifier current, the inward potassium rectifier current (IKI), the ATP-sensitive potassium channel (IKATP) and Ito.",The molecular weight is 324.42.,Quinidine has a topological polar surface area of 45.59.,The log p value of  is 2.79.,Quinidine is approved and investigational.,Quinidine is a solid.,True
14259,"Repaglinide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It belongs to the meglitinide class of short-acting insulin secretagogues, which act by binding to β cells of the pancreas to stimulate insulin release. Repaglinide induces an early insulin response to meals decreasing postprandial blood glucose levels. It should only be taken with meals and meal-time doses should be skipped with any skipped meal. Approximately one month of therapy is required before a decrease in fasting blood glucose is seen. Meglitnides may have a neutral effect on weight or cause a slight increase in weight. The average weight gain caused by meglitinides appears to be lower than that caused by sulfonylureas and insulin and appears to occur only in those naïve to oral antidiabetic agents. Due to their mechanism of action, meglitinides may cause hypoglycemia although the risk is thought to be lower than that of sulfonylureas since their action is dependent on the presence of glucose. In addition to reducing postprandial and fasting blood glucose, meglitnides have been shown to decrease glycosylated hemoglobin (HbA1c) levels, which are reflective of the last 8-10 weeks of glucose control. Meglitinides appear to be more effective at lowering postprandial blood glucose than metformin, sulfonylureas and thiazolidinediones. Repaglinide is extensively metabolized in the liver and excreted in bile. Repaglinide metabolites do not possess appreciable hypoglycemic activity. Approximately 90% of a single orally administered dose is eliminated in feces and 8% in urine. As an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.  Insulin secretion by pancreatic &beta; cells is partly controlled by cellular membrane potential. Membrane potential is regulated through an inverse relationship between the activity of cell membrane ATP-sensitive potassium channels (ABCC8) and extracellular glucose concentrations. Extracellular glucose enters the cell via GLUT2 (SLC2A2) transporters. Once inside the cell, glucose is metabolized to produce ATP. High concentrations of ATP inhibit ATP-sensitive potassium channels causing membrane depolarization. When extracellular glucose concentrations are low, ATP-sensitive potassium channels open causing membrane repolarization. High glucose concentrations cause ATP-sensitive potassium channels to close resulting in membrane depolarization and opening of L-type calcium channels. The influx of calcium ions stimulates calcium-dependent exocytosis of insulin granules. Repaglinide increases insulin release by inhibiting ATP-sensitive potassium channels in a glucose-dependent manner.  Repaglinide activity is dependent on the presence functioning &beta; cells and glucose. In contrast to sulfonylurea insulin secretatogogues, repaglinide has no effect on insulin release in the absence of glucose. Rather, it potentiates the effect of extracellular glucose on ATP-sensitive potassium channel and has little effect on insulin levels between meals and overnight. As such, repaglinide is more effective at reducing postprandial blood glucose levels than fasting blood glucose levels and requires a longer duration of therapy (approximately one month) before decreases in fasting blood glucose are observed. The insulinotropic effects of repaglinide are highest at intermediate glucose levels (3 to 10 mmol/L) and it does not increase insulin release already stimulated by high glucose concentrations (greater than 15 mmol/L). Repaglinide appears to be selective for pancreatic &beta; cells and does not appear to affect skeletal or cardiac muscle or thyroid tissue. ",The molecular weight is 452.6.,Repaglinide has a topological polar surface area of 78.87.,The log p value of  is 5.3.,Repaglinide is approved and investigational.,Repaglinide is a solid.,True
14260,"Cyclobenzaprine, a centrally-acting muscle relaxant, was first synthesized in 1961 and has been available for human use since 1977. It was initially studied for use as antidepressant given its structural similarity to tricyclic antidepressants - it differs from by only a single double bond. Since its approval, it has remained relatively popular as an adjunctive, short-term treatment for acute skeletal muscle spasms secondary to musculoskeletal injury. Cyclobenzaprine is indicated as a short-term (2-3 weeks) adjunct therapy, along with rest and physical therapy, for relief of muscle spasm associated with acute, painful musculoskeletal conditions. It has not been found effective in the treatment of spasticity originating from cerebral or spinal cord disease, or spasticity in children with cerebral palsy. Cyclobenzaprine is also occasionally used off-label for reducing pain and sleep disturbances in patients with fibromyalgia. Cyclobenzaprine is a skeletal muscle relaxant that works on areas of the brainstem to reduce skeletal muscle spasm, though its exact pharmacodynamic behaviour is currently unclear. Despite its long half-life, it is relatively short-acting with a typical duration of action of 4-6 hours. Cyclobenzaprine has been reported to contribute to the development of serotonin syndrome when used in combination with other serotonergic medications. Symptoms of serotonin syndrome may include autonomic instability, changes to mental status, neuromuscular abnormalities, or gastrointestinal symptoms - treatment with cyclobenzaprine should be discontinued immediately if any of these reactions occur during therapy. The exact mechanism of action of cyclobenzaprine has not been fully elucidated in humans, and much of the information available regarding its mechanism has been ascertained from early animal studies. There is some evidence that cyclobenzaprine exerts its effects at the supraspinal level, specifically within the locus coeruleus of the brainstem, with little-to-no action at neuromuscular junctions or directly on skeletal musculature. Action on the brainstem is thought to result in diminished activity of efferent alpha and gamma motor neurons, likely mediated by inhibition of coeruleus-spinal or reticulospinal pathways, and ultimately depressed spinal cord interneuron activity.",The molecular weight is 275.4.,Cyclobenzaprine has a topological polar surface area of 3.24.,The log p value of  is 5.1.,Cyclobenzaprine is approved.,Cyclobenzaprine is a solid.,True
14261,"A broad-spectrum semisynthetic antibiotic related to tetracycline but excreted more slowly and maintaining effective blood levels for a more extended period. For the treatment of acute bacterial exacerbations of chronic bronchitis Methacycline is a tetracycline antibiotic. Similar to other tetracyclines, it has a wide spectrum of antimicrobial action. It is active against most Gram-positive bacteria (pneumococci, streptococci, staphylococci) and Gram-negative bacteria (E. coli, salmonella, shigella, etc.), and towards agents causing onithosis, psittacosis, trachoma, and some Protozoa. Like other tetracyclines, the general usefulness of methacycline has been reduced with the onset of bacterial resistance. Methacycline, a tetracycline antibiotic, is a protein synthesis inhibitors, inhibiting the binding of aminoacyl-tRNA to the mRNA-ribosome complex. Methacycline inhibits cell growth by inhibiting translation. It binds to the 16S part of the 30S ribosomal subunit and prevents the amino-acyl tRNA from binding to the A site of the ribosome. The binding is reversible in nature. Tetracyclines also have been found to inhibit matrix metalloproteinases. This mechanism does not add to their antibiotic effects, but has led to extensive research on chemically modified tetracyclines or CMTs (like incyclinide) for the treatmet of rosacea, acne, and various types of neoplasms.",The molecular weight is 442.42.,Metacycline has a topological polar surface area of 181.62.,The log p value of  is -0.8.,Metacycline is approved and investigational.,Metacycline is a solid.,True
14262,"A compound obtained from the bark of the white willow and wintergreen leaves, and also prepared synthetically. It has bacteriostatic, fungicidal, and keratolytic actions. Its salts, the salicylates, are used as analgesics. Key additive in many skin-care products for the treatment of acne, psoriasis, callouses, corns, keratosis pilaris and warts. Salicylic acid treats acne by causing skin cells to slough off more readily, preventing pores from clogging up. This effect on skin cells also makes salicylic acid an active ingredient in several shampoos meant to treat dandruff. Use of straight salicylic solution may cause hyperpigmentation on unpretreated skin for those with darker skin types (Fitzpatrick phototypes IV, V, VI), as well as with the lack of use of a broad spectrum sunblock. Subsalicylate in combination with bismuth form the popular stomach relief aid known commonly as Pepto-Bismol. When combined the two key ingredients help control diarrhea, nausea, heartburn, and even gas. It is also very mildly anti-biotic. Salicylic acid directly irreversibly inhibits COX-1 and COX-2 to decrease conversion of arachidonic acid to precursors of prostaglandins and thromboxanes. Salicylate's use in rheumatic diseases is due to it's analgesic and anti-inflammatory activity. Salicylic acid is a key ingredient in many skin-care products for the treatment of acne, psoriasis, calluses, corns, keratosis pilaris, and warts. Salicylic acid allows cells of the epidermis to more readily slough off. Because of its effect on skin cells, salicylic acid is used in several shampoos used to treat dandruff. Salicylic acid is also used as an active ingredient in gels which remove verrucas (plantar warts). Salicylic acid competitively inhibits oxidation of uridine-5-diphosphoglucose (UDPG) with nicotinamide adenosine dinucleotide (NAD) and noncompetitively with UDPG. It also competitively inhibits the transferring of the glucuronyl group of uridine-5-phosphoglucuronic acid (UDPGA) to a phenolic acceptor. Inhibition of mucopoly saccharide synthesis is likely responsible for the slowing of wound healing with salicylates.",The molecular weight is 138.12.,Salicylic acid has a topological polar surface area of 57.53.,The log p value of  is 2.19.,Salicylic acid is approved and investigational and vet_approved.,Salicylic acid is a solid.,True
14263,"Salmeterol is a long-acting beta-2 adrenergic receptor agonist drug that is currently prescribed for the treatment of asthma and chronic obstructive pulmonary disease COPD. It has a longer duration of action than the short-acting beta-2 adrenergic receptor agonist,. Salmeterol was first described in the literature in 1988. Salmeterol's structure is similar to salbutamol's with an aralkyloxy-alkyl substitution on the amine. Salmeterol is indicated in the treatment of asthma with an inhaled corticosteroid, prevention of exercise induced bronchospasm, and the maintenance of airflow obstruction and prevention of exacerbations of chronic obstructive pulmonary disease. Salmeterol is a long acting beta-2 adrenergic receptor agonist that binds to both the active and exo sites of the beta-2 adrenergic receptor. Salmeterol has a longer duration of action than other beta-2 agonists like. Patients should be counselled regarding the risks of long acting beta agonist (LABA) monotherapy, hypokalemia, hypoglycemia, and not to take this drug with another LABA. Beta-2 adrenoceptor stimulation causes relaxation of bronchial smooth muscle, bronchodilation, and increased airflow.",The molecular weight is 415.57.,Salmeterol has a topological polar surface area of 81.95.,The log p value of  is 3.06.,Salmeterol is approved.,Salmeterol is a solid.,True
14264,"A dideoxynucleoside compound in which the 3'-hydroxyl group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of 5' to 3' phosphodiester linkages, which are needed for the elongation of DNA chains, thus resulting in the termination of viral DNA growth. The compound is a potent inhibitor of HIV replication at low concentrations, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal toxic side effect is axonal degeneration resulting in peripheral neuropathy. For the treatment of Human immunovirus (HIV) infections in conjunction with other antivirals. Zalcitabine is an analog of 2'-deoxycytidine that is pharmacologically related to but structurally different from other nucleotide reverse transcriptase inhibitors (NRTIs). Zalcitabine inhibits the activity of HIV-1 reverse transcriptase (RT) both by competing with the natural substrate dGTP and by its incorporation into viral DNA. Zalcitabine is a nucleoside reverse transcriptase inhibitor (NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Within cells, zalcitabine is converted to its active metabolite, dideoxycytidine 5'-triphosphate (ddCTP), by the sequential action of cellular enzymes. ddCTP interferes with viral RNA-directed DNA polymerase (reverse transcriptase) by competing for utilization of the natural substrate deoxycytidine 5'-triphosphate (dCTP), as well as incorpating into viral DNA. Due to it's lack of a 3'-OH group, the formation of a 5' to 3' phosphodiester linkage that is necessary for DNA chain elongation is inhibited, thus leading to the termination of viral DNA growth.",The molecular weight is 211.22.,Zalcitabine has a topological polar surface area of 88.15.,The log p value of  is -1.25.,Zalcitabine is approved and investigational.,Zalcitabine is a solid.,True
14265,"Coumarin derivative that acts as a long-acting oral anticoagulant. Used for the prevention and treatment of thromboembolic disease including venous thrombosis, thromboembolism, and pulmonary embolism as well as for the prevention of ischemic stroke in patients with atrial fibrillation (AF). Phenprocoumon, a coumarin anticoagulant, thins the blood by antagonizing vitamin K which is required for the production of clotting factors in the liver. Anticoagulants such as phenprocoumon have no direct effect on an established thrombus, nor do they reverse ischemic tissue damage (damage caused by an inadequate blood supply to an organ or part of the body). However, once a thrombus has occurred, the goal of anticoagulant treatment is to prevent further extension of the formed clot and prevent secondary thromboembolic complications which may result in serious and possibly fatal sequelae. Phenprocoumon inhibits vitamin K reductase, resulting in depletion of the reduced form of vitamin K (vitamin KH2). As vitamin K is a cofactor for the carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent proteins, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited. Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decreased prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots.",The molecular weight is 280.32.,Phenprocoumon has a topological polar surface area of 46.53.,The log p value of  is 4.71.,Phenprocoumon is approved and investigational.,Phenprocoumon is a solid.,True
14266,"Fexofenadine is an over-the-counter second-generation antihistamine used in the treatment of various allergic symptoms. It is selective for the H<sub>1</sub> receptor, carries little-to-no activity at off-targets, and does not cross the blood-brain barrier - this is in contrast to previous first-generation antihistamines, such as , which readily bind to off-targets that contribute to side effects such as sedation. Fexofenadine is the major active metabolite of and is administered as a racemic mixture in which both enantiomers display approximately equivalent antihistamine activity. In the United States, fexofenadine is indicated for the symptomatic treatment of allergic rhinitis in patients ≥2 years old and chronic idiopathic urticaria in patients ≥6 months old. In Canada, fexofenadine carries the same indications but is approved only for patients ≥12 years old. Fexofenadine is also available in combination with for the symptomatic treatment of season allergic rhinitis in patients ≥12 years old. Fexofenadine relieves allergy symptoms by antagonizing the actions of histamine, an endogenous compound predominantly responsible for allergic symptomatology. The relatively long duration of action of fexofenadine (approximately 24 hours) allows for once or twice daily dosing, and its rapid absorption allows for an onset of action within 1-3 hours. Fexofenadine should not be taken with fruit juice, as this may impair its absorption. The H<sub>1</sub> histamine receptor is responsible for mediating hypersensitivity and allergic reactions. Exposure to an allergen results in degranulation of mast cells and basophils, which then release histamine and other inflammatory mediators. Histamine binds to, and activates, H<sub>1</sub> receptors, which results in the further release of pro-inflammatory cytokines, such as interleukins, from basophils and mast cells. These downstream effects of histamine binding are responsible for a wide variety of allergic symptoms, such as pruritus, rhinorrhea, and watery eyes.",The molecular weight is 501.67.,Fexofenadine has a topological polar surface area of 81.0.,The log p value of  is 1.96.,Fexofenadine is approved and investigational.,Fexofenadine is a solid.,True
14267,"Antibacterial agent used primarily as a tuberculostatic. It remains the treatment of choice for tuberculosis. For the treatment of all forms of tuberculosis in which organisms are susceptible. Isoniazid is a bactericidal agent active against organisms of the genus Mycobacterium, specifically <i>M. tuberculosis</i>, <i>M. bovis</i> and <i>M. kansasii</i>. It is a highly specific agent, ineffective against other microorganisms. Isoniazid is bactericidal when mycobacteria grow rapidly and bacteriostatic when they grow slowly. Isoniazid is a prodrug and must be activated by bacterial catalase. Specficially, activation is associated with reduction of the mycobacterial ferric KatG catalase-peroxidase by hydrazine and reaction with oxygen to form an oxyferrous enzyme complex. Once activated, isoniazid inhibits the synthesis of mycoloic acids, an essential component of the bacterial cell wall. At therapeutic levels isoniazid is bacteriocidal against actively growing intracellular and extracellular <i>Mycobacterium tuberculosis</i> organisms. Specifically isoniazid inhibits InhA, the enoyl reductase from <i>Mycobacterium tuberculosis</i>, by forming a covalent adduct with the NAD cofactor. It is the INH-NAD adduct that acts as a slow, tight-binding competitive inhibitor of InhA.",The molecular weight is 137.14.,Isoniazid has a topological polar surface area of 68.01.,The log p value of  is -0.67.,Isoniazid is approved and investigational.,Isoniazid is a solid.,True
14268,"Norgestimate was first described in the literature in 1977. It was developed by Ortho Pharmaceutical Corporation as part of an effort to develop new hormonal contraceptives with reduced adverse effects. It is commonly formulated with as a combined oral contraceptive that can also be used to treat moderate acne vulgaris. Norgestimate is formulated with as a combined oral contraceptive. It can also be given with low dose ethinylestradiol for contraception as well as the treatment of moderate acne vulgaris in women ≥15 years old. Norgestimate is a progestin that suppresses ovulation for contraception and reduces free testosterone to treat moderate acne vulgaris. The therapeutic index is wide as overdoses are rare. Patients should be counselled regarding the risk of vascular problems, liver disease, hypertension, metabolic effects, headaches, and bleeding irregularities. Progesterone analogs like norgestimate decrease the frequency of gonadotropin releasing hormone pulses from the hypothalamus, decreasing follicle stimulating hormone and luteinizing hormone. These actions prevent ovulation.",The molecular weight is 369.5.,Norgestimate has a topological polar surface area of 58.89.,The log p value of  is 5.06.,Norgestimate is approved and investigational.,Norgestimate is a solid.,True
14269,"Methylprednisolone is a derivative glucocorticoid with higher potency than. It was first described in the literature in the late 1950s. Oral and intramuscular methylprednisolone are indicated for a number of endocrine, rheumatic, collagen, dermatologic, allergic, ophthalmic, respiratory, hematologic, neoplastic, edematous, gastrointestinal, nervous system, and other disorders. Intra-articular and soft tissue injections are indicated for short term treatment of acute gouty arthritis, acute and subactute bursitis, acute nonspecific tenosynovitis, epicondylitis, rheumatoid arthritis, and synovitis of osteoarthritis. Intralesional injections are indicated for alopecia areata, discoid lupus erythematosus, keloids, lichen planus, lichen simplex chronicus and psoriatic plaques, necrobiosis lipoidica diabeticorum, and localized hypertrophic infiltrated inflammatory lesions of granuloma annulare. Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Corticosteroids have a wide therapeutic window as patients may require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections. The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.",The molecular weight is 374.48.,Methylprednisolone has a topological polar surface area of 94.83.,The log p value of  is 1.74.,Methylprednisolone is approved and vet_approved.,Methylprednisolone is a solid.,True
14270,"Ethinylestradiol was first synthesized in 1938 by Hans Herloff Inhoffen and Walter Hohlweg at Schering. It was developed in an effort to create an estrogen with greater oral bioavailability. These properties were achieved by the substitution of an ethinyl group at carbon 17 of. Ethinylestradiol soon replaced in contraceptive pills. Ethinylestradiol is combined with other drugs for use as a contraceptive, premenstrual dysphoric disorder, moderate acne, moderate to severe vasomotor symptoms of menopause, prevention of postmenopausal osteoporosis. Ethinylestradiol is a synthetic estrogen that decreases luteinizing hormone to decrease endometrial vascularization, and decreases gonadotrophic hormone to prevent ovulation. It has a long duration of action as it is taken once daily, and a wide therapeutic index as overdoses are generally not associated with serious adverse effects. Patients should be counselled regarding the risks of thrombotic events. Ethinylestradiol is a synthetic estrogenic compound. Use of estrogens have a number of effects on the body including reduced bone density. Combined oral contraceptives suppress ovulation by suppressing gonadotrophic hormone, thickening cervical mucus to prevent the travel of sperm, and preventing changes in the endometrium required for implantation of a fertilized egg. Ethinylestradiol decreases luteinizing hormone, decreasing vascularity in the endometrium. It also increases sex hormone binding globulin.",The molecular weight is 296.41.,Ethinylestradiol has a topological polar surface area of 40.46.,The log p value of  is 3.68.,Ethinylestradiol is approved.,Ethinylestradiol is a solid.,True
14271,"Isotretinoin is a retinoid derivative of vitamin A used in the treatment of severe recalcitrant acne. It was most widely marketed under the brand name Accutane, which has since been discontinued. Isotretinoin is associated with major risks in pregnancy and so it is only available under the iPLEDGE program in the United States. The first isotretinoin containing product was FDA approved on 7 May 1982. Isotretinoin is indicated to treat severe recalcitrant nodular acne and patients ≥12 years enrolled in the iPLEDGE program. The pharmacodynamics of isotretinoin are poorly understood. Isotretinoin produces its effects through altering progress through the cell cycle, cell differentiation, survival, and apoptosis. These actions reduce sebum production, preventing the blockage of pores, and growth of acne causing bacteria. Isotretinoin and 4-oxo-isotretinoin both significantly reduce the production of sebum. Isotretinoin has little to no affinity for retinol binding proteins (RBPs) and retinoic acid nuclear receptors (RARs). Tretinoin and 4-oxo-tretinion bind to the RAR-γ receptor, which is suspected to be part of the action of acne treatment by isotretinoin. Isotretinoin induces apoptosis in sebocytes, leading to a decrease in sebum production. Isotretinoin also reduces the formation of comedones by reducing hyperkeratinization through an unknown mechanism. Isotretinoin does not directly kill bacteria but it does reduce the size of sebum ducts and makes the microenvironment less hospitable to acne causing bacteria. It may also increase immune mechanisms and alter chemotaxis of monocytes to reduce inflammation.",The molecular weight is 300.44.,Isotretinoin has a topological polar surface area of 37.3.,The log p value of  is 6.74.,Isotretinoin is approved.,Isotretinoin is a solid.,True
14272,"Formoterol is an inhaled beta<sub>2</sub>-agonist used in the management of COPD and asthma that was first approved for use in the United States in 2001. It acts on bronchial smooth muscle to dilate and relax airways, and is administered as a racemic mixture of its active (R;R)- and inactive (S;S)-enantiomers. A major clinical advantage of formoterol over other inhaled beta-agonists is its rapid onset of action (2-3 minutes), which is at least as fast as , combined with a long duration of action (12 hours) - for this reason, treatment guidelines for asthma recommend its use as both a reliever and maintenance medication. It is available as a single-entity product and in several formulations in combination with both inhaled corticosteroids and long-acting muscarinic antagonists. Formoterol is indicated in various formulations for the treatment of asthma and COPD. For the treatment of COPD, formoterol is available as a single-entity inhalation solution, in combination with the long-acting muscarinic antagonists (LAMAs) and , and in combination with the corticosteroid. For the treatment of asthma, formoterol is available in combination with for patients 5 years and older and with budesonide for patients 6 years and older. Formoterol may also be used on an as-needed basis for prophylaxis against exercise-induced bronchospasm. Formoterol works locally in the lungs as a bronchodilator, relaxing smooth muscle and opening up the airways. It possesses both a rapid onset of action (approximately 2-3 minutes) and a long duration of action (up to 12 hours). The use of long-acting beta-agonists (LABAs), such as formoterol, without concomitant inhaled corticosteroids in asthmatic patients should be avoided, as LABA monotherapy has been associated with an increased risk of asthma-related death. Formoterol is a relatively selective long-acting agonist of beta<sub>2</sub>-adrenergic receptors, although it does carry some degree of activity at beta<sub>1</sub> and beta<sub>3</sub> receptors. Beta<sub>2</sub> receptors are found predominantly in bronchial smooth muscle (with a relatively minor amount found in cardiac tissue) whereas beta<sub>1</sub> receptors are the predominant adrenergic receptors found in the heart - for this reason, selectivity for beta<sub>2</sub> receptors is desirable in the treatment of pulmonary diseases such as COPD and asthma. Formoterol has demonstrated an approximately 200-fold greater activity at beta<sub>2</sub> receptors over beta<sub>1</sub> receptors.",The molecular weight is 344.41.,Formoterol has a topological polar surface area of 90.82.,The log p value of  is 1.26.,Formoterol is approved and investigational.,Formoterol is a solid.,True
14273,"Azathioprine is a prodrug of 6-mercaptopurine, first synthesized in 1956 by Gertrude Elion, William Lange, and George Hitchings in an attempt to produce a derivative of 6-mercaptopurine with a better therapeutic index. Azathioprine is used to treat inflammatory conditions like rheumatoid arthritis and as an immunosuppressant in the prevention of renal transplant rejection. Azathioprine is indicated to treat rheumatoid arthritis and prevent renal transplant rejection. Azathioprine is an immunosuppressive agent which functions through modulation of rac1 to induce T cell apoptosis, as well as other unknown immunosuppressive functions. It has a long duration of action as it is given daily, and has a narrow therapeutic index. Patients should be counselled regarding the risk of malignancies of the skin and lymphomas. Azathioprine's mechanism of action is not entirely understood but it may be related to inhibition of purine synthesis, along with inhibition of B and T cells.",The molecular weight is 277.26.,Azathioprine has a topological polar surface area of 115.42.,The log p value of  is 0.51.,Azathioprine is approved.,Azathioprine is a solid.,True
14274,"Auranofin is a gold salt that is capable of eliciting pharmacologic actions that suppress inflammation and stimulate cell-mediated immunity. It has subsequently been listed by the World Health Organization as a member of the antirheumatic agent category. Auranofin appears to induce heme oxygenase 1 (HO-1) mRNA. Heme oxygenase 1 is an inducible heme-degrading enzyme with anti-inflammatory properties. Used in the treatment of active, progressive or destructive forms of inflammatory arthritis, such as adult rheumatoid arthritis. Auranofin is a gold salt used in treating inflammatory arthritis. Gold salts are called second-line drugs because they are often considered when the arthritis progresses in spite of antiinflammatory drugs (NSAIDs and corticosteroids). Exactly how auranofin works is not well understood. It may act as an inhibitor of kappab kinase and thioredoxin reductase which would lead to a decreased immune response and decreased free radical production, respectively. In patients with inflammatory arthritis, such as adult and juvenile rheumatoid arthritis, gold salts can decrease the inflammation of the joint lining. This effect can prevent destruction of bone and cartilage.",The molecular weight is 678.48.,,,Auranofin is approved and investigational.,Auranofin is a solid.,True
14275,"Doxorubicin is a cytotoxic anthracycline antibiotic isolated from cultures of Streptomyces peucetius var. caesius. Doxorubicin binds to nucleic acids, presumably by specific intercalation of the planar anthracycline nucleus with the DNA double helix. Doxorubicin is used to produce regression in disseminated neoplastic conditions like acute lymphoblastic leukemia, acute myeloblastic leukemia, Wilms’ tumor, neuroblastoma, soft tissue and bone sarcomas, breast carcinoma, ovarian carcinoma, transitional cell bladder carcinoma, thyroid carcinoma, gastric carcinoma, Hodgkin’s disease, malignant lymphoma and bronchogenic carcinoma in which the small cell histologic type is the most responsive compared to other cell types. Doxorubicin is also indicated for use as a component of adjuvant therapy in women with evidence of axillary lymph node involvement following resection of primary breast cancer. Doxorubicin is an antineoplastic in the anthracycline class. General properties of drugs in this class include: interaction with DNA in a variety of different ways including intercalation (squeezing between the base pairs), DNA strand breakage and inhibition with the enzyme topoisomerase II. Most of these compounds have been isolated from natural sources and antibiotics. However, they lack the specificity of the antimicrobial antibiotics and thus produce significant toxicity. The anthracyclines are among the most important antitumor drugs available. Doxorubicin is widely used for the treatment of several solid tumors while daunorubicin and idarubicin are used exclusively for the treatment of leukemia. Doxorubicin may also inhibit polymerase activity, affect regulation of gene expression, and produce free radical damage to DNA. Doxorubicin possesses an antitumor effect against a wide spectrum of tumors, either grafted or spontaneous. The anthracyclines are cell cycle-nonspecific. Doxorubicin has antimitotic and cytotoxic activity through a number of proposed mechanisms of action: Doxorubicin forms complexes with DNA by intercalation between base pairs, and it inhibits topoisomerase II activity by stabilizing the DNA-topoisomerase II complex, preventing the religation portion of the ligation-religation reaction that topoisomerase II catalyzes.",The molecular weight is 543.52.,Doxorubicin has a topological polar surface area of 206.07.,The log p value of  is 0.32.,Doxorubicin is approved and investigational.,Doxorubicin is a solid.,True
14276,"Hydrochlorothiazide is the most commonly prescribed thiazide diuretic. It is indicated to treat edema and hypertension. Hydrochlorothiazide use is common but declining in favour of angiotensin converting enzyme inhibitors. Many combination products are available containing hydrochlorothiazide and angiotensin converting enzyme inhibitors or angiotensin II receptor blockers. Hydrochlorothiazide is indicated alone or in combination for the management of edema associated with congestive heart failure, hepatic cirrhosis, nephrotic syndrome, acute glomerulonephritis, chronic renal failure, and corticosteroid and estrogen therapy. Hydrochlorothiazide is also indicated alone or in combination for the management of hypertension. Hydrochlorothiazide prevents the reabsorption of sodium and water from the distal convoluted tubule, allowing for the increased elimination of water in the urine. Hydrochlorothiazide has a wide therapeutic window as dosing is individualized and can range from 25-100mg. Hydrochlorothiazide should be used with caution in patients with reduced kidney or liver function. Hydrochlorothiazide is transported from the circulation into epithelial cells of the distal convoluted tubule by the organic anion transporters OAT1, OAT3, and OAT4. From these cells, hydrochlorothiazide is transported to the lumen of the tubule by multidrug resistance associated protein 4 (MRP4).",The molecular weight is 297.73.,Hydrochlorothiazide has a topological polar surface area of 118.36.,The log p value of  is -0.36.,Hydrochlorothiazide is approved and vet_approved.,Hydrochlorothiazide is a solid.,True
14277,"Letrozole, or CGS 20267, is an oral non-steroidal type II aromatase inhibitor first described in the literature in 1990. It is a third generation aromatase inhibitor like and , meaning it does not significantly affect cortisol, aldosterone, and thyroxine. Letrozole is indicated to treat postmenopausal women with hormone receptor (HR) positive early breast cancer, postmenopausal women with early breast cancer who have periviously been treated with tamoxifen, and postmenopausal women with HR+ or unknown advanced breast cancer. Letrozole, given with ribociclib, is indicated to treat pre, peri, and postmenopausal women with HR+ and human epidermal growth factor 2 (HER2) negative advanced or metastatic breast cancer. Letrozole is an aromatase inhibitor used in the treatment of breast cancer. Aromatase inhibitors work by inhibiting the action of the enzyme aromatase, which converts androgens into estrogens by a process called aromatization. As breast tissue is stimulated by estrogens, decreasing their production is a way of suppressing recurrence of the breast tumor tissue. Letrozole is a non-steroidal type II aromatase inhibitor. It blocks the active site, and therefore the electron transfer chain of CYP19A1. This competitive inhibition prevents the conversion of androgens to estrogen. This action leads to a reduction in uterine weight and elevated leuteinizing hormone. In postmenopausal women, the action of aromatase is responsible for the majority of estrogen production. With reduced availability of estrogen, estrogen-dependant tumors regress. Third generation aromatase inhibitors do not significantly affect cortisol, aldosterone, and thyroxine levels.",The molecular weight is 285.31.,Letrozole has a topological polar surface area of 78.29.,The log p value of  is 1.43.,Letrozole is approved and investigational.,Letrozole is a solid.,True
14278,"Ketoprofen, a propionic acid derivative, is a nonsteroidal anti-inflammatory agent (NSAIA) with analgesic and antipyretic properties. For symptomatic treatment of acute and chronic rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, primary dysmenorrhea and mild to moderate pain associated with musculotendinous trauma (sprains and strains), postoperative (including dental surgery) or postpartum pain. Ketoprofen is a nonsteroidal anti-inflammatory agent (NSAIA) with analgesic and antipyretic properties. Ketoprofen has pharmacologic actions similar to those of other prototypical NSAIDs, which inhibit prostaglandin synthesis. Ketoprofen is used to treat rheumatoid arthritis, osteoarthritis, dysmenorrhea, and alleviate moderate pain. The anti-inflammatory effects of ketoprofen are believed to be due to inhibition cylooxygenase-2 (COX-2), an enzyme involved in prostaglandin synthesis via the arachidonic acid pathway. This results in decreased levels of prostaglandins that mediate pain, fever and inflammation. Ketoprofen is a non-specific cyclooxygenase inhibitor and inhibition of COX-1 is thought to confer some of its side effects, such as GI upset and ulceration. Ketoprofen is thought to have anti-bradykinin activity, as well as lysosomal membrane-stabilizing action. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation. ",The molecular weight is 254.28.,Ketoprofen has a topological polar surface area of 54.37.,The log p value of  is 2.76.,Ketoprofen is approved and vet_approved.,Ketoprofen is a solid.,True
14279,"Sulfamethoxazole is a bacteriostatic sulfonamide antibiotic that interferes with folic acid synthesis in susceptible bacteria. It is generally given in combination with , which inhibits a sequential step in bacterial folic acid synthesis - these agents work synergistically to block two consecutive steps in the biosynthesis of nucleic acids and proteins which are necessary for bacterial growth and division, and using them in conjunction helps to slow the development of bacterial resistance. In this combination, sulfamethoxazole is useful for the treatment of a variety of bacterial infections, including those of the urinary, respiratory, and gastrointestinal tracts. Sulfamethoxazole is indicated in combination with trimethoprim, in various formulations, for the following infections caused by bacteria with documented susceptibility: urinary tract infections, acute otitis media in pediatric patients (when clinically indicated), acute exacerbations of chronic bronchitis in adults, enteritis caused by susceptible _Shigella_, prophylaxis and treatment of _Pneumocystis jiroveci_ pneumonia, and travelers' diarrhea caused by enterotoxigenic _E. coli_. Sulfamethoxazole is a bacteriostatic sulfonamide antibiotic that inhibits a critical step in bacterial folate synthesis. It is generally given in combination with , a dihydrofolate reductase inhibitor, which inhibits the reduction of dihydrofolic acid to tetrahydrofolic acid. Studies have shown that bacterial resistance develops more slowly with the combination of the two drugs than with either trimethoprim or sulfamethoxazole alone, as together they inhibit sequential steps in the bacterial folate synthesis pathway. Sulfamethoxazole is a sulfonamide that inhibits bacterial dihydrofolic acid synthesis due to its structural similarity to an endogenous substrate, para-aminobenzoic acid (PABA). Most bacteria meet their need for folic acid by synthesizing it from PABA, as opposed to Animalia that require exogenous folic acid sources. Sulfamethoxazole competitively inhibits dihydropteroate synthase, the enzyme responsible for bacterial conversion of PABA to dihydrofolic acid. Inhibition of this pathway prevents the synthesis of tetrahydrofolate and, ultimately, the synthesis of bacterial purines and DNA, resulting in a bacteriostatic effect.",The molecular weight is 253.28.,Sulfamethoxazole has a topological polar surface area of 98.22.,The log p value of  is 0.56.,Sulfamethoxazole is approved.,Sulfamethoxazole is a solid.,True
14280,"Glyburide is a second generation sulfonylurea used to treat patients with diabetes mellitus type II. It is typically given to patients who cannot be managed with the standard first line therapy,. Glyburide stimulates insulin secretion through the closure of ATP-sensitive potassium channels on beta cells, raising intracellular potassium and calcium ion concentrations. Glyburide is indicated alone or as part of combination product with metformin, as an adjunct to diet and exercise, to improve glycemic control in adults with type 2 diabetes mellitus. Glyburide is a second generation sulfonylurea that stimulates insulin secretion through the closure of ATP-sensitive potassium channels on beta cells, raising intracellular potassium and calcium ion concentrations. Glibenclamide has a long duration of action as it is given once daily, and a wide therapeutic index as patients are started at doses as low as 0.75mg but that can increase as high as 10mg or more. Patients taking glyburide should be cautioned regarding an increased risk of cardiovascular mortality as seen with tolbutamide, another sulfonylurea. Glyburide belongs to a class of drugs known as sulfonylureas. These drugs act by closing ATP-sensitive potassium channels on pancreatic beta cells. The ATP-sensitive potassium channels on beta cells are known as sulfonylurea receptor 1 (SUR1).",The molecular weight is 494.0.,Glyburide has a topological polar surface area of 113.6.,The log p value of  is 4.24.,Glyburide is approved.,Glyburide is a solid.,True
14281,"Ketoconazole is an imidazole antifungal agent used in the prevention and treatment of a variety of fungal infections. It functions by preventing the synthesis of ergosterol, the fungal equivalent of cholesterol, thereby increasing membrane fluidity and preventing growth of the fungus. Ketoconazole was first approved in an oral formulation for systemic use by the FDA in 1981. At this time it was considered a significant improvement over previous antifungals, and , due to its broad spectrum and good absorption. However, it was discovered that ketoconazole produces frequent gastrointestinal side effects and dose-related hepatitis. These effects combined with waning efficacy led to its eventual replacement by triazole agents, , , , and. Ketoconazole and its predecessor continue to be used in topical formulations. Ketoconazole is used in the treatment or prevention of fungal infections including blastomycosis, candidiasis, coccidioidomycosis, histoplasmosis, chromomycosis, and paracoccidioidomycosis. In Europe, it is also used in the treatment of endogenous Cushing's syndrome. Ketoconazole, similarly to other azole antifungals, is a fungistatic agent which causes growth arrest in fungal cells thereby preventing growth and spread of the fungus throughout the body. Ketoconazole interacts with 14-&alpha;-sterol demethylase, a cytochrome P-450 enzyme necessary for the conversion of lanosterol to ergosterol. This results in inhibition of ergosterol synthesis and increased fungal cellular permeability due to reduced amounts of ergosterol present in the fungal cell membrane. This metabolic inhibition also results in accumulation of 14α-methyl-3,6-diol, a toxic metabolite. The increase in membrane fluidity is also thought to produce impairment of membrane-bound enzyme systems as components become less closely packed.",The molecular weight is 531.43.,Ketoconazole has a topological polar surface area of 69.06.,The log p value of  is 3.64.,Ketoconazole is approved and investigational.,Ketoconazole is a solid.,True
14282,"Irbesartan is an angiotensin receptor blocker (ARB) indicated to treat hypertension or diabetic nephropathy. It can also be used as part of a combination product with for patients not well controlled or not expected to be well controlled on monotherapy. Unlike angiotensin converting enzyme inhibitors, ARBs are not associated with a dry cough. Irbesartan is indicated to treat hypertension and diabetic nephropathy in hypertensive patients with type 2 diabetes, elevated serum creatinine, and proteinuria. A combination product with hydrochlorothiazide is indicated for hypertension in patients with uncontrolled hypertension with monotherapy or first line in patients not expected to be well controlled with monotherapy. Irbesartan is an angiotensin receptor blocker used to treat hypertension and diabetic nephropathy. It has a long duration of action as it is usually taken once daily and a wide therapeutic index as doses may be as low as 150mg daily but doses of 900mg/day were well tolerated in healthy human subjects. Irbesartan prevents angiotensin II binding to the AT<sub>1</sub> receptor in tissues like vascular smooth muscle and the adrenal gland. Irbesartan and its active metabolite bind the AT<sub>1</sub> receptor with 8500 times more affinity than they bind to the AT<sub>2</sub> receptor. Irbesartan's prevention of angiotensin II binding causes vascular smooth muscle relaxation and prevents the secretion of aldosterone, lowering blood pressure.",The molecular weight is 428.54.,Irbesartan has a topological polar surface area of 87.13.,The log p value of  is 6.04.,Irbesartan is approved and investigational.,Irbesartan is a solid.,True
14283,"The prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy. For the reduction of serum uric acid concentrations in chronic gouty arthritis and tophaceous gout in patients with frequent disabling gout attacks. Has also been effectively used to promote uric acid excretion in hyperuricemia secondary to the administration of thiazide and related diuretics.  Probenecid is a uricosuric and renal tubular blocking agent and is used in combination with colchicine to treat chronic gouty arthritis when complicated by frequent, recurrent acute attacks of gout. It inhibits the reabsorption of urate at the proximal convoluted tubule, thus increasing the urinary excretion of uric acid and decreasing serum urate levels. Effective uricosuria reduces the miscible urate pool, retards urate deposition, and promotes resorption of urate deposits. At the proximal and distal tubles, probenecid competitively inhibits the secretion of many weak organic acids including penicillins, most cephalosporins, and some other β-lactam antibiotics. This results in an increase in the plasma concentrations of acidic drugs eliminated principally by renal secretion, but only a slight increase if the drug is eliminated mainly by filtration. Thus, the drug can be used for therapeutic advantages to increase concentrations of certain β-lactam antibiotics in the treatment of gonorrhea, neurosyphilis, or pelvic inflammatory disease (PID). Probenecid inhibits the tubular reabsorption of urate, thus increasing the urinary excretion of uric acid and decreasing serum urate levels. Probenecid may also reduce plasma binding of urate and inhibit renal secretion of uric acid at subtherapeutic concentrations. The mechanism by which probenecid inhibits renal tubular transport is not known, but the drug may inhibit transport enzymes that require a source of high energy phosphate bonds and/or nonspecifically interfere with substrate access to protein receptor sites on the kidney tubules.",The molecular weight is 285.36.,Probenecid has a topological polar surface area of 74.68.,The log p value of  is 3.37.,Probenecid is approved and investigational.,Probenecid is a solid.,True
14284,"Fenofibrate is a fibric acid derivative like and. Fenofibrate is used to treat primary hypercholesterolemia, mixed dyslipidemia, severe hypertriglyceridemia. Fenofibrate is indicated as adjunctive therapy to diet to reduce elevated LDL-C, Total-C, Triglycerides, and Apo B, and to increase HDL-C adults with primary hypercholesterolemia or mixed dyslipidemia. Fenofibrate is also indicated to treat adults with severe hypertriglyceridemia. Fenofibrate is a fibrate that activates peroxisome proliferator activated receptor alpha (PPARα) to alter lipid metabolism and treat primary hypercholesterolemia, mixed dyslipidemia, and severe hypertriglyceridemia. Fenofibrate requires once daily dosing and has a half life of 19-27 hours so its duration of action is long. Fenofibrate capsules are given at a dose of 50-150mg daily so the therapeutic index is wide. Patients should be counselled about the risk of rhabdomyolysis, myopathy, and cholelithiasis when taking fibrates. Fenofibrate activates peroxisome proliferator activated receptor alpha (PPARα), increasing lipolysis, activating lipoprotein lipase, and reducing apoprotein C-III. PPARα is a nuclear receptor and its activation alters lipid, glucose, and amino acid homeostasis. Activation of PPARα activates transcription of gene transcription and translation that generates peroxisomes filled with hydrogen peroxide, reactive oxygen species, and hydroxyl radicals that also participate in lipolysis. This mechanism of increased lipid metabolism is also associated with increased oxidative stress on the liver. In rare cases this stress can lead to cirrhosis and chronic active hepatitis.",The molecular weight is 360.83.,Fenofibrate has a topological polar surface area of 52.6.,The log p value of  is 5.23.,Fenofibrate is approved.,Fenofibrate is a solid.,True
14285,"Gatifloxacin is an antibiotic agent and a member of the fourth-generation fluoroquinolone family. It works by inhibiting the bacterial enzymes DNA gyrase and topoisomerase IV. It was first introduced by Bristol-Myers Squibb in 1999 under the brand name Tequin® for the treatment of respiratory tract infections. Gatifloxacin is available as tablets and in various aqueous solutions for intravenous therapy. It is also available as eye drops under the brand name Zymar® marketed by Allergan. For the treatment of bronchitis, sinusitis, community-acquired pneumonia, and skin infections (abscesses, wounds) caused by S. pneumoniae, H. influenzae, S. aureus, M. pneumoniae, C. pneumoniae, L. pneumophila, S. pyogenes Gatifloxacin is a synthetic broad-spectrum 8-methoxyfluoroquinolone antibacterial agent for oral or intravenous administration. is bactericidal and its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Notably the drug has 100 times higher affinity for bacterial DNA gyrase than for mammalian. Gatifloxacin is a broad-spectrum antibiotic that is active against both Gram-positive and Gram-negative bacteria. It should be used only to treat or prevent infections that are proven or strongly suspected to be caused by bacteria. The bactericidal action of Gatifloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV, which are required for bacterial DNA replication, transcription, repair, and recombination.",The molecular weight is 375.4.,Gatifloxacin has a topological polar surface area of 82.11.,The log p value of  is -0.27.,Gatifloxacin is approved and investigational.,Gatifloxacin is a solid.,True
14286,"A semisynthetic antibiotic produced from Streptomyces mediterranei. It has a broad antibacterial spectrum, including activity against several forms of Mycobacterium. In susceptible organisms it inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme. It thus suppresses the initiation of RNA synthesis. Rifampin is bactericidal, and acts on both intracellular and extracellular organisms. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1160) For the treatment of Tuberculosis and Tuberculosis-related mycobacterial infections. Rifampin is an antibiotic that inhibits DNA-dependent RNA polymerase activity in susceptible cells. Specifically, it interacts with bacterial RNA polymerase but does not inhibit the mammalian enzyme. It is bactericidal and has a very broad spectrum of activity against most gram-positive and gram-negative organisms (including <i>Pseudomonas aeruginosa</i>) and specifically <i>Mycobacterium tuberculosis</i>. Because of rapid emergence of resistant bacteria, use is restricted to treatment of mycobacterial infections and a few other indications. Rifampin is well absorbed when taken orally and is distributed widely in body tissues and fluids, including the CSF. It is metabolized in the liver and eliminated in bile and, to a much lesser extent, in urine, but dose adjustments are unnecessary with renal insufficiency. Rifampin acts via the inhibition of DNA-dependent RNA polymerase, leading to a suppression of RNA synthesis and cell death.",The molecular weight is 822.95.,Rifampicin has a topological polar surface area of 220.15.,The log p value of  is 3.71.,Rifampicin is approved.,Rifampicin is a solid.,True
14287,"Ibuprofen is a non-steroidal anti-inflammatory drug (NSAID) derived from propionic acid and it is considered the first of the propionics. The formula of ibuprofen is 2-(4-isobutylphenyl) propionic acid and its initial development was in 1960 while researching for a safer alternative for aspirin. Ibuprofen was finally patented in 1961 and this drug was first launched against rheumatoid arthritis in the UK in 1969 and USA in 1974. It was the first available over-the-counter NSAID. Ibuprofen is the most commonly used and prescribed NSAID. It is very common over the counter medication widely used as an analgesic, anti-inflammatory and antipyretic. Ibuprofen has multiple actions in different inflammatory pathways involved in acute and chronic inflammation. The main effects reported in ibuprofen are related to the control of pain, fever and acute inflammation by the inhibition of the synthesis of prostanoids by COX-1 and COX-2. Pain relief is attributed to peripheral affected regions and central nervous system effects in the pain transmission mediated by the dorsal horn and higher spinothalamic tract. Some reports have tried to link the pain regulation with a possible enhancement on the synthesis of endogenous cannabinoids and action on the NMDA receptors. The effect on pain has been shown to be related to the cortically evoked potentials. The exact mechanism of action of ibuprofen is unknown. However, ibuprofen is considered an NSAID and thus it is a non-selective inhibitor of cyclooxygenase, which is an enzyme involved in prostaglandin (mediators of pain and fever) and thromboxane (stimulators of blood clotting) synthesis via the arachidonic acid pathway.",The molecular weight is 206.28.,Ibuprofen has a topological polar surface area of 37.3.,The log p value of  is 3.68.,Ibuprofen is approved.,Ibuprofen is a solid.,True
14288,"Benzylpenicillin (Penicillin G) is narrow spectrum antibiotic used to treat infections caused by susceptible bacteria. It is a natural penicillin antibiotic that is administered intravenously or intramuscularly due to poor oral absorption. Penicillin G may also be used in some cases as prophylaxis against susceptible organisms. For use in the treatment of severe infections caused by penicillin G-susceptible microorganisms when rapid and high penicillin levels are required such as in the treatment of septicemia, meningitis, pericarditis, endocarditis and severe pneumonia. Penicillin G is a penicillin beta-lactam antibiotic used in the treatment of bacterial infections caused by susceptible, usually gram-positive, organisms. The name \penicillin\"" can either refer to several variants of penicillin available, or to the group of antibiotics derived from the penicillins. Penicillin G has <i>in vitro</i> activity against gram-positive and gram-negative aerobic and anaerobic bacteria. The bactericidal activity of penicillin G results from the inhibition of cell wall synthesis and is mediated through penicillin G binding to penicillin binding proteins (PBPs). Penicillin G is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, and cephalosporinases and extended spectrum beta-lactamases."" By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, penicillin G inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that penicillin G interferes with an autolysin inhibitor.",The molecular weight is 334.39.,Benzylpenicillin has a topological polar surface area of 86.71.,The log p value of  is 1.75.,Benzylpenicillin is approved and vet_approved.,Benzylpenicillin is a solid.,True
14289,"An antiarrhythmic agent which exerts a potential- and frequency-dependent block of sodium channels. For the treatment of documented ventricular arrhythmias, such as sustained ventricular tachycardia, that, in the judgment of the physician, are life-threatening. Tocainide is a primary amine analog of lidocaine with antiarrhythmic properties useful in the treatment of ventricular arrhythmias. Tocainide, like lidocaine, produces dose dependent decreases in sodium and potassium conductance, thereby decreasing the excitability of myocardial cells. In experimental animal models, the dose-related depression of sodium current is more pronounced in ischemic tissue than in normal tissue. Tocainide is a Class I antiarrhythmic compound with electrophysiologic properties in man similar to those of lidocaine, but dissimilar from quinidine, procainamide, and disopyramide. Tocainide acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. Tocainide binds preferentially to the inactive state of the sodium channels.The antiarrhythmic actions are mediated through effects on sodium channels in Purkinje fibers.",The molecular weight is 192.26.,Tocainide has a topological polar surface area of 55.12.,The log p value of  is 0.26.,Tocainide is approved.,Tocainide is a solid.,True
14290,"A potent, long-acting irreversible cholinesterase inhibitor used as an ocular hypertensive in the treatment of glaucoma. Occasionally used for accomodative esotropia. For use in the treatment of subacute or chronic angle-closure glaucoma after iridectomy or where surgery is refused or contraindicated. Echothiophate Iodide is a potent, long-acting cholinesterase inhibitor used as a miotic in the treatment of glaucoma. Echothiophate iodide will depress both plasma and erythrocyte cholinesterase levels in most patients after a few weeks of eyedrop therapy. Echothiophate Iodide is a long-acting cholinesterase inhibitor for topical use which enhances the effect of endogenously liberated acetylcholine in iris, ciliary muscle, and other parasympathetically innervated structures of the eye. Echothiophate iodide binds irreversibly to cholinesterase, and is long acting due to the slow rate of hydrolysis by cholinesterase. It causes miosis, increase in facility of outflow of aqueous humor, fall in intraocular pressure, and potentiation of accommodation. ",The molecular weight is 256.32.,Echothiophate has a topological polar surface area of 35.53.,The log p value of  is -2.82.,Echothiophate is approved.,Echothiophate is a solid.,True
14291,"Amoxicillin, or BRL-2333, is a penicillin G derivative first described in the literature in 1972. Amoxicillin has similar activity to and , but leads to higher serum concentrations than ampicillin. Amoxicillin alone is indicated to treat susceptible bacterial infections of the ear, nose, throat, genitourinary tract, skin, skin structure, and lower respiratory tract. Amoxicillin is given with calvulanic acid to treat acute bacterial sinusitis, community acquired pneumonia, lower respiratory tract infections, acute bacterial otitis media, skin and skin structure infections, and urinary tract infections. Amoxicillin is given with omeprazole in the treatment of _H. pylori_. Amoxicillin competitively inhibit penicillin binding proteins, leading to upregulation of autolytic enzymes and inhibition of cell wall synthesis. Amoxicillin has a long duration of action as it is usually given twice daily. Amoxicillin has a wide therapeutic range as mild overdoses are not associated with significant toxicity. Patients should be counselled regarding the risk of anaphylaxis, _Clostridium difficile_ infections, and bacterial resistance. Amoxicillin competitively inhibits penicillin-binding protein 1 and other high molecular weight penicillin binding proteins. Penicillin bind proteins are responsible for glycosyltransferase and transpeptidase reactions that lead to cross-linking of D-alanine and D-aspartic acid in bacterial cell walls. Without the action of penicillin binding proteins, bacteria upregulate autolytic enzymes and are unable to build and repair the cell wall, leading to bacteriocidal action.",The molecular weight is 365.4.,Amoxicillin has a topological polar surface area of 132.96.,The log p value of  is -1.87.,Amoxicillin is approved and vet_approved.,Amoxicillin is a solid.,True
14292,"Overactive bladder (OAB) is a common condition negatively impacting the lives of millions of patients worldwide. Due to its urinary symptoms that include nocturia, urgency, and frequency, this condition causes social embarrassment and a poor quality of life.  Oxybutynin is indicated for the symptomatic treatment of overactive bladder, which causes urge urinary incontinence and frequency, and urgency. Oxybutynin may also be used for children aged 6 and above for the symptomatic management of detrusor muscle overactivity which has been found to be related to a neurological condition. Spina bifida is an example of a neurological condition in which oxybutynin may be used to control urinary symptoms. On occasion, oxybutynin may be used off-label to relieve bladder spasms associated with ureteral stents or urinary catheters. Oxybutynin exerts antispasmodic actions on the bladder, relieving the uncomfortable symptoms of overactive bladder, including urinary urgency and frequency. These actions occur through the inhibition of muscarinic receptors. Oxybutynin acts to relax the bladder by inhibiting the muscarinic action of acetylcholine on smooth muscle, and not skeletal muscle.",The molecular weight is 357.49.,Oxybutynin has a topological polar surface area of 49.77.,The log p value of  is 4.69.,Oxybutynin is approved and investigational.,Oxybutynin is a solid.,True
14293,"Glipizide is an oral hypoglycemic agent in the second-generation sulfonylurea drug class that is used to control blood sugar levels in patients with type 2 diabetes mellitus. It was first introduced in 1984 and is available in various countries including Canada and the U.S. According to the 2018 Clinical Practice Guidelines by Diabetes Canada, sulfonylurea drugs are considered a second-line glucose-lowering therapy following metformin. Because sulfonylureas require functional pancreatic beta cells for their therapeutic effectiveness, sulfonylureas are more commonly used for early-stage type 2 diabetes when there is no progressed pancreatic failure. Compared to the first-generation sulfonylureas, such as and , second-generation sulfonylureas contain a more non-polar side chain in their chemical structure, which enhances their hypoglycemic potency. Compared to other members of the sulfonylurea drug group, glipizide displays rapid absorption and onset of action with the shortest half-life and duration of action, reducing the risk for long-lasting hypoglycemia that is often observed with blood glucose-lowering agents. Glipizide was first approved by the FDA in 1994 and is available in extended-release tablets under the brand name Glucotrol®, as well as in combination with metformin under the brand name Metaglip®. Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.  Glipizide is a blood glucose-lowering agent. The initial onset of blood glucose-lowering effect occurs around 30 minutes post-administration with the duration of action lasting for about 12 to 24 hours. While the chronic use of glipizide does not result in elevations in the fasting insulin levels over time, the postprandial insulin response, or insulin response to a meal, is observed to be enhanced, even after 6 months of treatment. The main therapeutic actions of glipizide primarily occur at the pancreas where the insulin release is stimulated, but glipizide also mediates some extrapancreatic effects, such as the promotion of insulin signaling effects on the muscles, fat, or liver cells. Due to its action on the endogenous cells, sulfonylureas including glipizide is associated with a risk for developing hypoglycemia and weight gain in patients receiving the drug. Chronic administration of glipizide may result in down-regulation of the sulfonylurea receptors on pancreatic beta cells, which are molecular targets of the drug, leading to a reduced effect on insulin secretion.  Type 2 diabetes mellitus (T2DM) is a chronic metabolic disorder with increasing prevalence worldwide. Characterized by higher-than-normal levels of blood glucose, T2DM is a complex disorder that arises from the interaction between genetic, environmental and behavioral risk factors. Insulin is a peptide hormone that plays a critical role in regulating blood glucose levels. In response to high blood glucose levels, insulin promotes the uptake of glucose into the liver, muscle cells, and fat cells for storage. Although there are multiple events occurring that lead to the pathophysiology of T2DM, the disorder mainly involves insulin insensitivity as a result of insulin resistance, declining insulin production, and eventual failure of beta cells of pancreatic islets that normally produce insulin. Early management with lifestyle intervention, such as controlled diet and exercise, is critical in reducing the risk of long-term secondary complications, such as cardiovascular mortality.",The molecular weight is 445.54.,Glipizide has a topological polar surface area of 130.15.,The log p value of  is 2.57.,Glipizide is approved and investigational.,Glipizide is a solid.,True
14294,"A benzodiazepine used to treat various seizures, including myotonic or atonic seizures, photosensitive epilepsy, and absence seizures, although tolerance may develop. The agent has also been indicated for treating panic disorder. The mechanism of action appears to involve the enhancement of gamma-aminobutyric acid receptor responses. Clonazepam is indicated as monotherapy or as an adjunct in the treatment of Lennox-Gastaut syndrome (petit mal variant), akinetic, and myoclonic seizures. Furthermore, clonazepam may also be of some value in patients with absence spells (petit mal) who have failed to respond to succinimides. Additionally, clonazepam is also indicated for the treatment of panic disorder, with or without agoraphobia, as defined in the DSM-V. The pharmacodynamic properties of clonazepam are common among benzodiazepines and include anticonvulsive, sedative, muscle relaxing and anxiolytic effects. Animal data and electroencephalographic investigations in man have shown that clonazepam rapidly suppresses many types of paroxysmal activity including the spike and wave discharge in absence seizures (petit mal), slow spike wave, generalized spike wave, spikes with temporal or other locations, as well as irregular spikes and waves. Moreover, the agent can also decrease the frequency, amplitude, duration, and spread of discharge in minor motor seizures. Gamma-Aminobutyric acid (GABA) is considered the principal inhibitory neurotransmitter in the human body. When GABA binds to GABA(a) receptors found in neuron synapses, chloride ions are conducted across neuron cell membranes via an ion channel in the receptors. With enough chloride ions conducted, the local, associated neuron membrane potentials are hyperpolarized - making it more difficult or less likely for action potentials to fire, ultimately resulting in less excitation of the neurons. ",The molecular weight is 315.71.,Clonazepam has a topological polar surface area of 87.28.,The log p value of  is 2.38.,Clonazepam is approved and illicit.,Clonazepam is a solid.,True
14295,"Promethazine, originally known as 3,277 R.P., is an N-dimethylaminopropyl derivative of that was developed in France in 1946. Promethazine antagonizes a variety of receptors, allowing it to be used for a number of indications including allergic reactions, pain, sedation, nausea, and vomiting. Promethazine tablets and suppositories are indicated to treat rhinitis, allergic conjunctivitis, allergic reactions to blood or plasma, dermographism, anaphylactic reactions, sedation, nausea, vomiting, pain, motion sickness, and allergic skin reactions. Promethazine cough syrup with phenylephrine and codeine is indicated to relieve cough and upper respiratory symptoms, and nasal congestion associated with allergy or the common cold. Promethazine is is a histamine H1 antagonist that can be used for it's ability to induce sedation, reduce pain, and treat allergic reactions. Promethazine's effects generally last 4-6h but can last up to 12h. Patients should be counselled regarding CNS and respiratory depression, reduce seizure threshold, and bone marrow depression. Promethazine is a an antagonist of histamine H1, post-synaptic mesolimbic dopamine, alpha adrenergic, muscarinic, and NMDA receptors. The antihistamine action is used to treat allergic reactions. Antagonism of muscarinic and NMDA receptors contribute to its use as a sleep aid, as well as for anxiety and tension. Antagonism of histamine H1, muscarinic, and dopamine receptors in the medullary vomiting center make promethazine useful in the treatment of nausea and vomiting.",The molecular weight is 284.42.,Promethazine has a topological polar surface area of 6.48.,The log p value of  is 4.6.,Promethazine is approved and investigational.,Promethazine is a solid.,True
14296,"Atazanavir (formerly known as BMS-232632) is an antiretroviral drug of the protease inhibitor (PI) class. Like other antiretrovirals, it is used to treat infection of human immunodeficiency virus (HIV). Atazanavir is distinguished from other PIs in that it can be given once-daily (rather than requiring multiple doses per day) and has lesser effects on the patient's lipid profile (the amounts of cholesterol and other fatty substances in the blood). Like other protease inhibitors, it is used only in combination with other HIV medications. The U.S. Food and Drug Administration (FDA) approved atazanavir on June 20, 2003. Used in combination with other antiretroviral agents for the treatment of HIV-1 infection, as well as postexposure prophylaxis of HIV infection in individuals who have had occupational or nonoccupational exposure to potentially infectious body fluids of a person known to be infected with HIV when that exposure represents a substantial risk for HIV transmission. Atazanavir (ATV) is an azapeptide HIV-1 protease inhibitor (PI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). HIV-1 protease is an enzyme required for the proteolytic cleavage of the viral polyprotein precursors into the individual functional proteins found in infectious HIV-1. Atazanavir binds to the protease active site and inhibits the activity of the enzyme. This inhibition prevents cleavage of the viral polyproteins resulting in the formation of immature non-infectious viral particles. Protease inhibitors are almost always used in combination with at least two other anti-HIV drugs. Atazanivir is pharmacologically related but structurally different from other protease inhibitors and other currently available antiretrovirals. Atazanavir selectively inhibits the virus-specific processing of viral Gag and Gag-Pol polyproteins in HIV-1 infected cells by binding to the active site of HIV-1 protease, thus preventing the formation of mature virions. Atazanavir is not active against HIV-2.",The molecular weight is 704.87.,Atazanavir has a topological polar surface area of 171.22.,The log p value of  is 5.92.,Atazanavir is approved and investigational.,Atazanavir is a solid.,True
14297,"Atorvastatin (Lipitor®), is a lipid-lowering drug included in the statin class of medications. By inhibiting the endogenous production of cholesterol in the liver, statins lower abnormal cholesterol and lipid levels, and ultimately reduce the risk of cardiovascular disease. More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) Reductase, which catalyzes the conversion of HMG-CoA to mevalonic acid. This conversion is a critical metabolic reaction involved in the production of several compounds involved in lipid metabolism and transport, including cholesterol, low-density lipoprotein (LDL) (sometimes referred to as \bad cholesterol\""), and very-low-density lipoprotein (VLDL). Prescribing statins is considered standard practice for patients following any cardiovascular event, and for people who are at moderate to high risk of developing cardiovascular disease. The evidence supporting statin use, coupled with minimal side effects and long term benefits, has resulted in wide use of this medication in North America."" Atorvastatin is indicated for the treatment of several types of dyslipidemias, including primary hyperlipidemia and mixed dyslipidemia in adults, hypertriglyceridemia, primary dysbetalipoproteinemia, homozygous familial hypercholesterolemia, and heterozygous familial hypercholesterolemia in adolescent patients with failed dietary modifications. Atorvastatin is an oral antilipemic agent that reversibly inhibits HMG-CoA reductase. It lowers total cholesterol, low-density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apo B), non-high density lipoprotein-cholesterol (non-HDL-C), and triglyceride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease, and high ratios are associated with a higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, atorvastatin reduces the risk of cardiovascular morbidity and mortality.  Atorvastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis. Atorvastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low-density lipoprotein (LDL) receptors, which increases hepatic uptake of LDL. Atorvastatin also reduces Very-Low-Density Lipoprotein-Cholesterol (VLDL-C), serum triglycerides (TG) and Intermediate Density Lipoproteins (IDL), as well as the number of apolipoprotein B (apo B) containing particles, but increases High-Density Lipoprotein Cholesterol (HDL-C). ",The molecular weight is 558.65.,Atorvastatin has a topological polar surface area of 111.79.,The log p value of  is 4.46.,Atorvastatin is approved.,Atorvastatin is a solid.,True
14298,"Rosuvastatin, also known as the brand name product Crestor, is a lipid-lowering drug that belongs to the statin class of medications, which are used to lower the risk of cardiovascular disease and manage elevated lipid levels by inhibiting the endogenous production of cholesterol in the liver. More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) Reductase, which catalyzes the conversion of HMG-CoA to mevalonic acid and is the third step in a sequence of metabolic reactions involved in the production of several compounds involved in lipid metabolism and transport including cholesterol, low-density lipoprotein (LDL) (sometimes referred to as \bad cholesterol\""), and very low-density lipoprotein (VLDL). Prescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD, such as those with Type 2 Diabetes. The clear evidence of the benefit of statin use coupled with very minimal side effects or long term effects has resulted in this class becoming one of the most widely prescribed medications in North America."" The FDA monograph states that rosuvastatin is indicated as an adjunct to diet in the treatment of triglyceridemia, Primary Dysbetalipoproteinemia (Type III Hyperlipoproteinemia), and Homozygous Familial Hypercholesterolemia. Rosuvastatin is a synthetic, enantiomerically pure antilipemic agent. It is used to lower total cholesterol, low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apoB), non-high density lipoprotein-cholesterol (non-HDL-C), and trigleride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease and high ratios are associated with higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, rosuvastatin reduces the risk of cardiovascular morbidity and mortality. Rosuvastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis. Rosuvastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low density lipoprotein (LDL) receptors which increases hepatic uptake of LDL. Rosuvastatin also inhibits hepatic synthesis of very low density lipoprotein (VLDL). The overall effect is a decrease in plasma LDL and VLDL. ",The molecular weight is 481.54.,Rosuvastatin has a topological polar surface area of 140.92.,The log p value of  is 1.9.,Rosuvastatin is approved.,Rosuvastatin is a solid.,True
14299,"Sertraline is a popular antidepressant medication commonly known as a selective serotonin reuptake inhibitor (SSRI), and is similar to drugs such as and. Despite marked structural differences between compounds in this drug class, SSRIs exert similar pharmacological effects. Sertraline is indicated for the management of major depressive disorder (MDD), post-traumatic stress disorder (PTSD), obsessive-compulsive disorder (OCD), panic disorder (PD), premenstrual dysphoric disorder (PMDD), and social anxiety disorder (SAD). Common off-label uses for sertraline include the prevention of post stroke depression, generalized anxiety disorder (GAD), fibromyalgia, premature ejaculation, migraine prophylaxis, diabetic neuropathy, and neurocardiogenic syncope. Sertraline improves or relieves the symptoms of depression, OCD, post-traumatic stress disorder, obsessive-compulsive disorder, panic disorder, and premenstrual dysphoric disorder via the inhibition of serotonin reuptake. Clinical studies have shown that it improves cognition in depressed patients. It has less sedative, anticholinergic, and cardiovascular effects than the tricyclic antidepressant drugs because it does not exert significant anticholinergic, antihistamine, or adrenergic (alpha1, alpha2, beta) blocking activity. The onset of action and beneficial effects are usually noticed after 4-6 weeks, for reasons that are not fully understood and currently under investigation. Sertraline selectively inhibits the reuptake of serotonin (5-HT) at the presynaptic neuronal membrane, thereby increasing serotonergic activity. This results in an increased synaptic concentration of serotonin in the CNS, which leads to numerous functional changes associated with enhanced serotonergic neurotransmission. These changes are believed to be responsible for the antidepressant action and beneficial effects in obsessive-compulsive (and other anxiety related disorders). It has been hypothesized that obsessive-compulsive disorder, like depression, is also caused by the disregulation of serotonin.",The molecular weight is 306.23.,Sertraline has a topological polar surface area of 12.03.,The log p value of  is 5.35.,Sertraline is approved.,Sertraline is a solid.,True
14300,"Miconazole is a broad-spectrum azole antifungal with some activity against Gram-positive bacteria as well. It is widely used to treat mucosal yeast infections, including both oral and vaginal infections; although intravenous miconazole is no longer available, a wide variety of suppositories, creams, gels, and tablet-based products are available. Miconazole is thought to act primarily through the inhibition of fungal CYP450 14α-lanosterol demethylase activity. Miconazole is indicated for the local treatment of oropharyngeal candidiasis in adult patients and for the adjunctive treatment of diaper dermatitis complicated by candidiasis in immunocompetent patients aged four weeks and older. Miconazole is available as both a suppository and cream for the treatment of vaginal yeast infections and the relief of associated vulvar itching and irritation. Lastly, miconazole cream is effective in treating athlete's foot (tinea pedis), jock itch (tinea cruris), ringworm infections (tinea corporis), pityriasis (formerly tinea) versicolor, and cutaneous candidiasis. Miconazole is an azole antifungal that functions primarily through inhibition of a specific demethylase within the CYP450 complex. As miconazole is typically applied topically and is minimally absorbed into the systemic circulation following application, the majority of patient reactions are limited to hypersensitivity and cases of anaphylaxis. Patients using intravaginal miconazole products are advised not to rely on contraceptives to prevent pregnancy and sexually transmitted infections, as well as not to use tampons concurrently. Miconazole is an azole antifungal used to treat a variety of conditions, including those caused by _Candida_ overgrowth. Unique among the azoles, miconazole is thought to act through three main mechanisms. The primary mechanism of action is through inhibition of the CYP450 14α-lanosterol demethylase enzyme, which results in altered ergosterol production and impaired cell membrane composition and permeability, which in turn leads to cation, phosphate, and low molecular weight protein leakage.",The molecular weight is 416.12.,Miconazole has a topological polar surface area of 27.05.,The log p value of  is 5.81.,Miconazole is approved and investigational and vet_approved.,Miconazole is a solid.,True
14301,"Nifedipine, or BAY a 1040, is a first generation dihydropyridine L-type calcium channel blocker, similar to. Nifedipine was developed by Bayer and first described in the literature, along with other dihydropyridines, in 1972. Since nifedipine's development, second and third generation dihydropyridines have been developed with slower onsets and longer durations of action. The most popular of the third generation dihydropyridines is. Nifedipine capsules are indicated to treat vasospastic angina and chronic stable angina. Extended release tablets are indicated to treat vasospastic angina, chronic stable angina, and hypertension. Nifedipine is an inhibitor of L-type voltage gated calcium channels that reduces blood pressure and increases oxygen supply to the heart. Immediate release nifedipine's duration of action requires dosing 3 times daily. Nifedipine dosing is generally 10-120mg daily. Patients should be counselled regarding the risk of excessive hypotension, angina, and myocardial infarction. Nifedipine blocks voltage gated L-type calcium channels in vascular smooth muscle and myocardial cells. This blockage prevents the entry of calcium ions into cells during depolarization, reducing peripheral arterial vascular resistance and dilating coronary arteries. These actions reduce blood pressure and increase the supply of oxygen to the heart, alleviating angina.",The molecular weight is 346.34.,Nifedipine has a topological polar surface area of 110.45.,The log p value of  is 3.12.,Nifedipine is approved.,Nifedipine is a solid.,True
14302,"Amiodarone is a benzofuran derivative, anti-arrhythmic drug used commonly in a variety of settings. Most known for its approved indication in life-threatening ventricular arrhythmias, it is also used off-label in the outpatient and inpatient setting for atrial fibrillation. Because of its ability to cause serious toxicity and possibly death, amiodarone use should be reserved for its approved indications, according to prescribing information. The FDA approved indications for amiodarone are recurrent ventricular fibrillation (VF) After intravenous administration, amiodarone acts to relax smooth muscles that line vascular walls, decreases peripheral vascular resistance (afterload), and increases the cardiac index by a small amount. Administration by this route also decreases cardiac conduction, preventing and treating arrhythmias. When it is given orally, however, amiodarone does not lead to significant changes in the left ventricular ejection fraction. Similar to other anti-arrhythmic agents, controlled clinical trials do not confirm that oral amiodarone increases survival.  Amiodarone is considered a class III anti-arrhythmic drug. It blocks potassium currents that cause repolarization of the heart muscle during the third phase of the cardiac action potential. As a result amiodarone increases the duration of the action potential as well as the effective refractory period for cardiac cells (myocytes). Therefore, cardiac muscle cell excitability is reduced, preventing and treating abnormal heart rhythms.",The molecular weight is 645.32.,Amiodarone has a topological polar surface area of 42.68.,The log p value of  is 8.95.,Amiodarone is approved and investigational.,Amiodarone is a solid.,True
14303,"Gliclazide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It has been classified differently according to its drug properties in which based on its chemical structure, gliclazide is considered a first-generation sulfonylurea due to the structural presence of a sulfonamide group able to release a proton and the presence of one aromatic group. On the other hand, based on the pharmacological efficacy, gliclazide is considered a second-generation sulfonylurea which presents a higher potency and a shorter half-life. Gliclazide belongs to the sulfonylurea class of insulin secretagogues, which act by stimulating &beta; cells of the pancreas to release insulin. Sulfonylureas increase both basal insulin secretion and meal-stimulated insulin release. Medications in this class differ in their dose, rate of absorption, duration of action, route of elimination and binding site on their target pancreatic &beta; cell receptor. Sulfonylureas also increase peripheral glucose utilization, decrease hepatic gluconeogenesis and may increase the number and sensitivity of insulin receptors. Sulfonylureas are associated with weight gain, though less so than insulin. Due to their mechanism of action, sulfonylureas may cause hypoglycemia and require consistent food intake to decrease this risk. The risk of hypoglycemia is increased in elderly, debilitated and malnourished individuals. Gliclazide has been shown to decrease fasting plasma glucose, postprandial blood glucose and glycosolated hemoglobin (HbA1c) levels (reflective of the last 8-10 weeks of glucose control). Gliclazide is extensively metabolized by the liver; its metabolites are excreted in both urine (60-70%) and feces (10-20%). For the treatment of NIDDM in conjunction with diet and exercise.  Based on the pharmacological properties, gliclazide is a second generation sulphonylurea which acts as a hypoglycemic agent. It stimulates &beta; cells of the islet of Langerhans in the pancreas to release insulin. It also enhances peripheral insulin sensitivity. Overall, it potentiates insulin release and improves insulin dynamics. Gliclazide binds to the &beta; cell sulfonyl urea receptor (SUR1). This binding subsequently blocks the ATP sensitive potassium channels. The binding results in closure of the channels and leads to a resulting decrease in potassium efflux leads to depolarization of the &beta; cells. This opens voltage-dependent calcium channels in the &beta; cell resulting in calmodulin activation, which in turn leads to exocytosis of insulin containing secretorty granules.",The molecular weight is 323.41.,Gliclazide has a topological polar surface area of 78.51.,The log p value of  is 1.09.,Gliclazide is approved.,Gliclazide is a solid.,True
14304,"Tolbutamide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It is structurally similar to acetohexamide, chlorpropamide and tolazamide and belongs to the sulfonylurea class of insulin secretagogues, which act by stimulating β cells of the pancreas to release insulin. Sulfonylureas increase both basal insulin secretion and meal-stimulated insulin release. Medications in this class differ in their dose, rate of absorption, duration of action, route of elimination and binding site on their target pancreatic β cell receptor. Sulfonylureas also increase peripheral glucose utilization, decrease hepatic gluconeogenesis and may increase the number and sensitivity of insulin receptors. Sulfonylureas are associated with weight gain, though less so than insulin. Due to their mechanism of action, sulfonylureas may cause hypoglycemia and require consistent food intake to decrease this risk. The risk of hypoglycemia is increased in elderly, debilitated and malnourished individuals. Tolbutamide appears to be metabolized in the liver. Tolbutamide and its metabolites are excreted in urine (75-85%) and feces. For treatment of NIDDM (non-insulin-dependent diabetes mellitus) in conjunction with diet and exercise. Tolbutamide, a first-generation sulfonylurea antidiabetic agent, is used with diet to lower blood glucose levels in patients with diabetes mellitus type II. Tolbutamide is twice as potent as the related second-generation agent glipizide. Tolbutamide lowers blood sugar by stimulating the pancreas to secrete insulin and helping the body use insulin efficiently. The pancreas must be able to produce insulin for this drug to work. Sulfonylureas lower blood glucose in patients with NIDDM by directly stimulating the acute release of insulin from functioning beta cells of pancreatic islet tissue by an unknown process that involves a sulfonylurea receptor (receptor 1) on the beta cell. Sulfonylureas inhibit the ATP-potassium channels on the beta cell membrane and potassium efflux, which results in depolarization and calcium influx, calcium-calmodulin binding, kinase activation, and release of insulin-containing granules by exocytosis, an effect similar to that of glucose.",The molecular weight is 270.35.,Tolbutamide has a topological polar surface area of 75.27.,The log p value of  is 2.5.,Tolbutamide is approved and investigational.,Tolbutamide is a solid.,True
14305,"Dutasteride is an oral synthetic 4-azasteroid commonly marketed under the trade name Avodart. It is a novel dual 5α-reductase inhibitor that works by blocking both isoforms of 5α-reductase enzymes in a potent, selective, and irreversible manner. Type I and II 5α-reductase enzymes convert testosterone into dihydrotestosterone (DHT), a primary hormonal mediator that plays a role in the development and enlargement of the prostate gland. Dutasteride was approved by the FDA in 2001 for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men as monotherapy or in combination with the α-adrenergic antagonist to enhance the therapeutic response. Its clinical efficacy against benign prostate hyperplasia in male patients is comparable to that of , a specific type II 5α-reductase inhibitor. However, unlike finasteride, dutasteride is not yet indicated for the treatment of androgenic alopecia although it was demonstrated to be effective in several randomized, double-blind, placebo-controlled trials in androgenetic alopecia. Indicated for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate gland to improve symptoms, and reduce the risk of acute urinary retention and the need for BPH-related surgery alone or in combination with. Dutasteride is a synthetic 4-azasteroid compound that selectively inhibits both the type I and type II isoforms of steroid 5α-reductase, an intracellular enzyme that converts testosterone to 5α-dihydrotestosterone (DHT). Dutasteride works by reducing the levels of circulating DHT. It was also shown to reduce the size of the prostate gland, improve urinary flow, and symptoms of benign prostatic hyperplasia alone or in combination with tamsulosin. The effect of the reduction of DHT by dutasteride is dose-dependent, with the maximum effect observed within 1-2 weeks following initial administration.  The 5α-reductase is a nuclear-bound steroid intracellular enzyme primarily located in the prostatic stromal cell that converts the androgen testosterone into the more active metabolite, 5α-dihydrotestosterone (DHT). DHT is considered to be the primary androgen playing a role in the initial development and subsequent enlargement of the prostate gland. It serves as the hormonal mediator for the hyperplasia upon accumulation within the prostate gland. DHT displays a higher affinity towards androgen receptors in the prostate gland compared to testosterone and by acting on the androgen receptors, DHT modulates genes that are responsible for cell proliferation. Responsible for the synthesis of approximately one-third of circulating DHT, type I 5α-reductase is predominant in the sebaceous glands of most regions of skin, including the scalp, and liver. The type II 5a-reductase isozyme is primarily found in the prostate, seminal vesicles, epididymides, and hair follicles as well as liver, and is responsible for two-thirds of circulating DHT. Due to its dual inhibition of both isoenzymes of 5α-reductase, dutasteride causes a near-complete suppression of DHT. Compared to a 70% reduction of serum DHT levels caused by , a near-complete suppression of serum DHT-more than 90% is seen with dutasteride.",The molecular weight is 528.54.,Dutasteride has a topological polar surface area of 58.2.,The log p value of  is 4.94.,Dutasteride is approved and investigational.,Dutasteride is a solid.,True
14306,"Pioglitazone is an antihyperglycemic used as an adjunct to diet, exercise, and other antidiabetic medications to manage type 2 diabetes mellitus. It is administered as a racemic mixture, though there is no pharmacologic difference between the enantiomers and they appear to interconvert _in vivo_ with little consequence. The thiazolidinedione class of medications, which also includes and , exerts its pharmacological effect primarily by promoting insulin sensitivity and the improved uptake of blood glucose via agonism at the peroxisome proliferator-activated receptor-gamma (PPARγ). PPARs are ligand-activated transcription factors that are involved in the expression of more than 100 genes and affect numerous metabolic processes, most notably lipid and glucose homeostasis. Pioglitazone is indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. It is also available in combination with , , or for the same indication. Pioglitazone enhances cellular responsiveness to insulin, increases insulin-dependent glucose disposal, and improves impaired glucose homeostasis. In patients with type 2 diabetes mellitus, these effects result in lower plasma glucose concentrations, lower plasma insulin concentrations, and lower HbA1c values. Pioglitazone is a selective agonist at peroxisome proliferator-activated receptor-gamma (PPARγ) in target tissues for insulin action such as adipose tissue, skeletal muscle, and liver. Activation of PPARγ increases the transcription of insulin-responsive genes involved in the control of glucose and lipid production, transport, and utilization. Through this mechanism, pioglitazone both enhances tissue sensitivity to insulin and reduces the hepatic production of glucose (i.e. gluconeogenesis) - insulin resistance associated with type 2 diabetes mellitus is therefore improved without an increase in insulin secretion by pancreatic beta cells.",The molecular weight is 356.44.,Pioglitazone has a topological polar surface area of 68.29.,The log p value of  is 3.53.,Pioglitazone is approved and investigational.,Pioglitazone is a solid.,True
14307,"Tiludronate, or (4-chlorophenyl)thio-methylene-1,1-bisphosphonate, is a first generation bisphosphonate similar to and. These drugs were developed to mimic the action of pyrophosphate, a regulator of calcification and decalcification. Tiludronic acid was first described in the literature in 1988 as a potential treatment for Paget's disease of bone. Tiludronic acid is indicated to treat Paget's disease of bone in patients with serum alkaline phosphatase levels ≥2 times the upper limit of normal, with symptoms, or with risk of future complications. Tiludronic acid is a bisphosphonate that prevents osteoclasts from resorbing bone. The duration of action is quite long due to the slow clearance from the bone, and the therapeutic window is wide. Patients should be counselled regarding the risk of upper GI mucosal irritation as well as gastric and duodenal ulcers. Bisphosphonates are taken into the bone where they bind to hydroxyapatite. Bone resorption by osteoclasts causes local acidification, releasing the bisphosphonate, which is taken into the osteoclast by fluid-phase endocytosis. Endocytic vesicles become acidified, releasing bisphosphonates into the cytosol of osteoclasts where they act.",The molecular weight is 318.6.,Tiludronic acid has a topological polar surface area of 115.06.,The log p value of  is 0.26.,Tiludronic acid is approved and investigational and vet_approved.,Tiludronic acid is a solid.,True
14308,"Carvedilol is a racemic mixture where the S(-) enantiomer is a beta adrenoceptor blocker and the R(+) enantiomer is both a beta and alpha-1 adrenoceptor blocker. It is currently used to treat heart failure, left ventricular dysfunction, and hypertension. The dual action of carvedilol is advantageous in combination therapies as moderate doses of 2 drugs have a decreased incidence of adverse effects compared to high dose monotherapy in the treatment of moderate hypertension. Carvedilol is indicated to treat mild to severe heart failure, left ventricular dysfunction after myocardial infarction with ventricular ejection fraction ≤40%, or hypertension. Carvedilol reduces tachycardia through beta adrenergic antagonism and lowers blood pressure through alpha-1 adrenergic antagonism. It has a long duration of action as it is generally taken once daily and has a broad therapeutic index as patients generally take 10-80mg daily. Patients taking carvedilol should not abruptly stop taking this medication as this may exacerbate coronary artery disease. Carvedilol inhibits exercise induce tachycardia through its inhibition of beta adrenoceptors. Carvedilol's action on alpha-1 adrenergic receptors relaxes smooth muscle in vasculature, leading to reduced peripheral vascular resistance and an overall reduction in blood pressure. At higher doses, calcium channel blocking and antioxidant activity can also be seen. The antioxidant activity of carvedilol prevents oxidation of low density lipoprotein and its uptake into coronary circulation.",The molecular weight is 406.48.,Carvedilol has a topological polar surface area of 75.74.,The log p value of  is 4.04.,Carvedilol is approved and investigational.,Carvedilol is a solid.,True
14309,"Levofloxacin is a fluoroquinolone antibiotic and the optical S-(-) isomer of racemic. It reportedly carries 8 to 128-fold more activity against both gram-negative and gram-positive bacteria compared to R-(+)-ofloxacin and remains stereochemically stable following administration (i.e. it does not invert to the inactive isomer). Levofloxacin, along with other quinolones such as and , is a member of the third generation of fluoroquinolones, colloquially referred to as the \respiratory quinolones\"" due to improved activity against gram-positive bacteria commonly implicated in respiratory infections."" In oral and intravenous formulations, levofloxacin is indicated in adults for the treatment of various infections caused by susceptible bacteria, including infections of the upper respiratory tract, lower respiratory tract, skin, skin structures, urinary tract, and prostate. The oral formulation is also indicated in both adults and children 6 months of age and older for the post-exposure management of inhalational anthrax caused by _Bacillus anthracis_ and for the treatment and/or prophylaxis of plague caused by _Yersinia pestis_. Levofloxacin is bactericidal and exerts its antimicrobial effects via inhibition of bacterial DNA replication. It has a relatively long duration of action in comparison with other antibiotics that allows for once or twice daily dosing. Levofloxacin is associated with QTc-interval prolongation and should be used with caution in patients with other risk factors for prolongation (e.g. hypokalemia, concomitant medications). Levofloxacin, like other fluoroquinolone antibiotics, exerts its antimicrobial activity via the inhibition of two key bacterial enzymes: DNA gyrase and topoisomerase IV. Both targets are type II topoisomerases, but have unique functions within the bacterial cell. DNA gyrase is an enzyme found only in bacteria that introduces negative supercoils into DNA during replication - this helps to relieve torsional strain caused by the introduction of positive supercoils during replication, and these negative supercoils are essential for chromosome condensation and the promotion of transcription initiation. It is comprised of four subunits (two A subunits and two B subunits) of which the A subunits appear to be the target of fluoroquinolone antibiotics. Bacterial topoisomerase IV, in addition to contributing to the relaxation of positive supercoils, is essential at the terminal stages of DNA replication and functions to “unlink” newly replicated chromosomes to allow for the completion of cell division.",The molecular weight is 361.37.,Levofloxacin has a topological polar surface area of 73.32.,The log p value of  is -0.51.,Levofloxacin is approved and investigational.,Levofloxacin is a solid.,True
14310,"Doxepin is a psychotropic agent with antidepressant and anxiolytic properties. It is a tertiary amine that can be presented as (E) and (Z) stereoisomers with the (Z) stereoisomer corresponding to. Doxepin commonly produces a 5:1 (E):(Z) racemic mixture.  Oral doxepin is approved for the following indications: Similar to other tricyclic antidepressants, doxepin was shown, in preclinical trials, to decrease the electrical activity of the brain, prolong the hexobarbital-induced sleep and block avoidance behavior without affecting the conditioned emotional response. At high doses, it also produces symptoms of central nervous system depression. Doxepin exact mechanism of action is not very clear. However, doxepin is known to be a selective histamine H1 receptor blocker. This effect on histamine receptors indicates effectiveness in skin conditions.",The molecular weight is 279.38.,Doxepin has a topological polar surface area of 12.47.,The log p value of  is 4.09.,Doxepin is approved and investigational.,Doxepin is a solid.,True
14311,"A semi-synthetic antibiotic that is a chlorinated derivative of oxacillin. Used to treat infections caused by penicillinase-producing staphylococci, including pneumococci, group A beta-hemolytic streptococci, and penicillin G-sensitive and penicillin G-resistant staphylococci. Cloxacillin is a semisynthetic antibiotic in the same class as penicillin. Cloxacillin is for use against staphylococci that produce beta-lactamase. By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, cloxacillin inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that cloxacillin interferes with an autolysin inhibitor.",The molecular weight is 435.88.,Cloxacillin has a topological polar surface area of 112.74.,The log p value of  is 2.52.,Cloxacillin is approved and investigational and vet_approved.,Cloxacillin is a solid.,True
14312,"A nonflammable, halogenated, hydrocarbon anesthetic that provides relatively rapid induction with little or no excitement. Analgesia may not be adequate. nitrous oxide is often given concomitantly. Because halothane may not produce sufficient muscle relaxation, supplemental neuromuscular blocking agents may be required. (From AMA Drug Evaluations Annual, 1994, p178) For the induction and maintenance of general anesthesia Halothane is a general inhalation anesthetic used for induction and maintenance of general anesthesia. It reduces the blood pressure and frequently decreases the pulse rate and depresses respiration. It induces muscle relaxation and reduces pains sensitivity by altering tissue excitability. It does so by decreasing the extent of gap junction mediated cell-cell coupling and altering the activity of the channels that underlie the action potential. Halothane causes general anaethesia due to its actions on multiple ion channels, which ultimately depresses nerve conduction, breathing, cardiac contractility. Its immobilizing effects have been attributed to its binding to potassium channels in cholinergic neurons. Halothane's effect are also likely due to binding to NMDA and calcium channels, causing hyperpolarization.",The molecular weight is 197.38.,,The log p value of  is 2.27.,Halothane is approved and vet_approved.,Halothane is a liquid.,True
14313,"Arsenic trioxide is a chemotherapeutic agent of idiopathic function used to treat leukemia that is unresponsive to first line agents. It is suspected that arsenic trisulfide induces cancer cells to undergo apoptosis. In general, arsenic is known to be a naturally toxic substance capable of eliciting a variety of dangerous adverse effects. The enzyme thioredoxin reductase has recently been identified as a target for arsenic trioxide. For induction of remission and consolidation in patients with acute promyelocytic leukemia (APL), and whose APL is characterized by the presence of the t(15;17) translocation or PML/RAR-alpha gene expression Arsenic Trioxide is indicated for induction of remission and consolidation in patients with acute promyelocytic leukemia (APL) who are refractory to, or have relapsed from, retinoid and anthracycline chemotherapy. The mechanism of action of Arsenic Trioxide is not completely understood. Arsenic trioxide causes morphological changes and DNA fragmentation characteristic of apoptosis in NB4 human promyelocytic leukemia cells <i>in vitro</i>. Arsenic trioxide also causes damage or degradation of the fusion protein PML/RAR-alpha. It is suspected that arsenic trioxide induces cancer cells to undergo apoptosis.",The molecular weight is 197.84.,Arsenic trioxide has a topological polar surface area of 43.37.,,Arsenic trioxide is approved and investigational.,Arsenic trioxide is a solid.,True
14314,"Naloxone is an opioid antagonist medication used to block or reverse the effects of opioid drugs, particularly within the setting of drug overdoses which are rapidly becoming a leading cause of death worldwide. More specifically, naloxone has a high affinity for μ-opioid receptors, where it acts as an inverse agonist, causing the rapid removal of any other drugs bound to these receptors. When taken in large quantities, opioid medications such as , , , , or are capable of causing life-threatening symptoms such as respiratory depression, reduced heart rate, slurred speech, drowsiness, and constricted pupils. If untreated, this can progress to vomiting, absent pulse and breathing, loss of consciousness, and even death. Naloxone is indicated for the rapid reversal of these symptoms of central nervous system depression in opioid overdose. It's important to note that naloxone only works on opioid receptors within the body, and is therefore not capable of reversing the effects of non-opioid medications such as stimulants like or , or benzodiazepines like or.  For the complete or partial reversal of narcotic depression, including respiratory depression, induced by opioids including natural and synthetic narcotics, propoxyphene, methadone and the narcotic-antagonist analgesics: nalbuphine, pentazocine and butorphanol. It is also indicated for the diagnosis of suspected acute opioid overdose. It may also be used as an adjunctive agent to increase blood pressure in the management of septic shock. Naloxone is an opiate antagonist and prevents or reverses the effects of opioids including respiratory depression, sedation and hypotension. In the absence of narcotics or agonistic effects of other narcotic antagonists, it exhibits essentially no pharmacologic activity.  While the mechanism of action of naloxone is not fully understood, the preponderance of evidence suggests that naloxone antagonizes the opioid effects by competing for the same receptor sites, especially the mu-opioid receptor. Recently, naloxone has been shown to bind all three opioid receptors (mu, kappa and gamma) but the strongest binding is to the mu receptor.",The molecular weight is 327.38.,Naloxone has a topological polar surface area of 70.0.,The log p value of  is 0.16.,Naloxone is approved and vet_approved.,Naloxone is a solid.,True
14315,"Desflurane is a highly fluorinated methyl ethyl ether used for maintenance of general anaesthesia. Volatile agents such as desflurane may activate GABA channels and hyperpolarize cell membranes. In addition, they may inhibit certain calcium channels and therefore prevent release of neurotransmitters and inhibit glutamate channels. Volatile anesthetics easily partition into cellular membranes and could expand the volume of the cell membrane and subsequently distort channels necessary for sodium ion flux and the development of action potentials necessary for synaptic transmission. Desflurane preconditions human myocardium against ischemia through activation of mitochondrial K(ATP) channels, adenosine A1 receptor, and alpha and beta adrenoceptors. For use as an inhalation agent for induction and/or maintenance of anesthesia for inpatient and outpatient surgery in adults. Desflurane is a general inhalation anesthetic. It induces muscle relaxation and reduces pains sensitivity by altering tissue excitability. It does so by decreasing the extent of gap junction mediated cell-cell coupling and altering the activity of the channels that underlie the action potential. Desflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Desflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase. Desflurane also binds to and agonizes the GABA receptor, the large conductance Ca<sup>2+</sup> activated potassium channel, the glycine receptors, and antagonizes the glutamate receptors. ",The molecular weight is 168.04.,Desflurane has a topological polar surface area of 9.23.,The log p value of  is 1.32.,Desflurane is approved.,Desflurane is a liquid.,True
14316,"Flecainide is a Class I anti-arrhythmic agent like and. Flecainide’s development began in 1966 and was first synthesized in 1972 as an attempt to generate new anesthetics. It is used to prevent supraventricular and ventricular arrhythmias, as well as paroxysmal atrial fibrillation and flutter. In New Zealand and America, flecainide is indicated to prevent supraventricular arrhythmias and ventricular arrhythmias. In the United States, it is also indicated to prevent paroxysmal atrial fibrillation and flutter. Flecainide inhibits the action of sodium and potassium ion channels in the heart, raising the threshold for depolarization and correcting arrhythmias. Flecainide has a long duration of action, allowing for once daily dosing. The therapeutic index is narrow. Patients should not take this medication if there is already structural heart disease or left ventricular systolic dysfunction. Flecainide blocks fast inward sodium channels and slowly unbinds during diastole, prolonging the refractory period of the heart. This blockade also shortens the duration of action potentials through the Purkinjie fibers. Flecainide also prevents delayed rectifier potassium channels from opening, lengthening the action potential through ventricular and atrial muscle fibers. Finally, flecainide also blocks ryanodine receptor opening, reducing calcium release from sarcoplasmic reticulum, which reduces depolarization of cells.",The molecular weight is 414.35.,Flecainide has a topological polar surface area of 59.59.,The log p value of  is 3.66.,Flecainide is approved and withdrawn.,Flecainide is a solid.,True
14317,"Captopril is a potent, competitive inhibitor of angiotensin-converting enzyme (ACE), the enzyme responsible for the conversion of angiotensin I (ATI) to angiotensin II (ATII). ATII regulates blood pressure and is a key component of the renin-angiotensin-aldosterone system (RAAS). Captopril may be used in the treatment of hypertension. For the treatment of essential or renovascular hypertension (usually administered with other drugs, particularly thiazide diuretics). May be used to treat congestive heart failure in combination with other drugs (e.g. cardiac glycosides, diuretics, &beta;-adrenergic blockers). May improve survival in patients with left ventricular dysfunction following myocardial infarction. May be used to treat nephropathy, including diabetic nephropathy.  Captopril, an ACE inhibitor, antagonizes the effect of the RAAS. The RAAS is a homeostatic mechanism for regulating hemodynamics, water and electrolyte balance. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from the granular cells of the juxtaglomerular apparatus in the kidneys. In the blood stream, renin cleaves circulating angiotensinogen to ATI, which is subsequently cleaved to ATII by ACE. ATII increases blood pressure using a number of mechanisms. First, it stimulates the secretion of aldosterone from the adrenal cortex. Aldosterone travels to the distal convoluted tubule (DCT) and collecting tubule of nephrons where it increases sodium and water reabsorption by increasing the number of sodium channels and sodium-potassium ATPases on cell membranes. Second, ATII stimulates the secretion of vasopressin (also known as antidiuretic hormone or ADH) from the posterior pituitary gland. ADH stimulates further water reabsorption from the kidneys via insertion of aquaporin-2 channels on the apical surface of cells of the DCT and collecting tubules. Third, ATII increases blood pressure through direct arterial vasoconstriction. Stimulation of the Type 1 ATII receptor on vascular smooth muscle cells leads to a cascade of events resulting in myocyte contraction and vasoconstriction. In addition to these major effects, ATII induces the thirst response via stimulation of hypothalamic neurons. ACE inhibitors inhibit the rapid conversion of ATI to ATII and antagonize RAAS-induced increases in blood pressure. ACE (also known as kininase II) is also involved in the enzymatic deactivation of bradykinin, a vasodilator. Inhibiting the deactivation of bradykinin increases bradykinin levels and may sustain its effects by causing increased vasodilation and decreased blood pressure. There are two isoforms of ACE: the somatic isoform, which exists as a glycoprotein comprised of a single polypeptide chain of 1277; and the testicular isoform, which has a lower molecular mass and is thought to play a role in sperm maturation and binding of sperm to the oviduct epithelium. Somatic ACE has two functionally active domains, N and C, which arise from tandem gene duplication. Although the two domains have high sequence similarity, they play distinct physiological roles. The C-domain is predominantly involved in blood pressure regulation while the N-domain plays a role in hematopoietic stem cell differentiation and proliferation. ACE inhibitors bind to and inhibit the activity of both domains, but have much greater affinity for and inhibitory activity against the C-domain. Captopril, one of the few ACE inhibitors that is not a prodrug, competes with ATI for binding to ACE and inhibits and enzymatic proteolysis of ATI to ATII. Decreasing ATII levels in the body decreases blood pressure by inhibiting the pressor effects of ATII as described in the Pharmacology section above. Captopril also causes an increase in plasma renin activity likely due to a loss of feedback inhibition mediated by ATII on the release of renin and/or stimulation of reflex mechanisms via baroreceptors. Captopril’s affinity for ACE is approximately 30,000 times greater than that of ATI.",The molecular weight is 217.28.,Captopril has a topological polar surface area of 57.61.,The log p value of  is 0.89.,Captopril is approved.,Captopril is a solid.,True
14318,"Ceftriaxone is a broad-spectrum third-generation cephalosporin antibiotic. It has a very long half-life compared to other cephalosporins and is high penetrable into the meninges, eyes, and inner ear. Ceftriaxone has broader and stronger gram-negative coverage then first or second-generation cephalosporins, but worse activity against methicillin-susceptible S.aureus. Ceftriaxone is a commonly used antimicrobial due to its good activity against multi-drug resistant Enterobacteriaceae, its relatively safe adverse effect profile, and its long half-life which allows for the convenience of daily or twice-daily dosing. Ceftriaxone is used for the treatment of the infections (respiratory, skin, soft tissue, UTI, ENT) caused by susceptible organisms. Organisms that are generally susceptible to ceftriaxone include S. pneumoniae, S. pyogenes (group A beta-hemolytic streptococci), coagulase-negative staphylococci, Some Enterobacter spp, H. influenzae, N. gonorrhoeae, P. mirabilis, E. coli, Klebsiella spp, M. catarrhalis, B. burgdorferi, and some oral anaerobes.  Ceftriaxone is a cephalosporin/cephamycin beta-lactam antibiotic used in the treatment of bacterial infections caused by susceptible, usually gram-positive, organisms. Ceftriaxone has <i>in vitro</i> activity against gram-positive aerobic, gram-negative aerobic, and anaerobic bacteria. The bactericidal activity of ceftriaxone results from the inhibition of cell wall synthesis and is mediated through ceftriaxone binding to penicillin-binding proteins (PBPs). Ceftriaxone is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, and cephalosporinases and extended-spectrum beta-lactamases. However, resistance to ceftriaxone usually occurs through beta-lactamase hydrolysis, altered PBPs, or reduced bacterial cell permeability. Ceftriaxone should not be mixed with or giving in the same IV line as diluents/products containing calcium as they may cause ceftriaxone to precipitate. Ceftriaxone use may also cause biliary sludge or gallbladder pseudolithiasis.  Ceftriaxone works by inhibiting the mucopeptide synthesis in the bacterial cell wall. The beta-lactam moiety of ceftriaxone binds to carboxypeptidases, endopeptidases, and transpeptidases in the bacterial cytoplasmic membrane. These enzymes are involved in cell-wall synthesis and cell division. Binding of ceftriaxone to these enzymes causes the enzyme to lose activity; therefore, the bacteria produce defective cell walls, causing cell death.",The molecular weight is 554.57.,Ceftriaxone has a topological polar surface area of 208.98.,The log p value of  is 0.02.,Ceftriaxone is approved.,Ceftriaxone is a solid.,True
14319,"Saquinavir is an HIV-1 protease inhibitor used in combination with and other antiretrovirals for the treatment of human immunodeficiency virus-1 (HIV-1) infection. In 1995 it became the first protease inhibitor approved by the FDA, followed shortly by ritonavir in 1996, and remains in clinical use today due to a relatively benign adverse effect profile as compared to other antiretroviral therapies. While its efficacy was initially limited by exceptionally poor oral bioavailability (approximately 4%), its current indications require the co-administration of ritonavir - a potent enzyme inhibitor - that increases the bioavailability and subsequent serum concentrations of saquinavir, thus dramatically improving antiviral activity. Saquinavir is indicated, in combination with ritonavir and other antiretroviral agents, for the treatment of HIV-1 infection in patients 16 years of age and older. Saquinavir exerts its antiviral activity by inhibiting an enzyme critical for the HIV-1 viral lifecycle. Like other protease inhibitors, saquinavir has a propensity for participating in drug interactions - use caution when administering saquinavir to patients maintained on other pharmaceutical agents as pharmacodynamic and pharmacokinetic interactions are common. Saquinavir is known to increase the QTc-interval in otherwise healthy individuals, and should therefore be used with caution in patients maintained on other QTc-prolonging medications or for whom prolongation of the QTc-interval may be of particular consequence (e.g. patients with pre-existing heart disease). Careful and regular monitoring of patient bloodwork is recommended, as saquinavir has been associated with the development of metabolic complications (e.g. diabetes mellitus, hyperlipidemia) and worsening of pre-existing liver disease. The HIV lifecycle is comprised of 3 distinct stages: assembly, involving creation and packaging of essential viral components; budding, wherein the viral particle crosses the host cell plasma membrane and forms a lipid envelope; and maturation, wherein the viral particle alters its structure and becomes infectious. At the center of this lifecycle is the Gag polyprotein which, along with the products of its proteolysis, coordinate these stages and function as the major structural proteins of the virus. The HIV-1 protease enzyme, a dimeric aspartic protease, is the enzyme responsible for cleaving the Gag polyprotein and thus plays a critical role in many aspects of the HIV viral lifecycle.",The molecular weight is 670.86.,Saquinavir has a topological polar surface area of 166.75.,The log p value of  is 4.73.,Saquinavir is approved and investigational.,Saquinavir is a solid.,True
14320,"Dexamethasone, or MK-125, is a corticosteroid fluorinated at position 9 used to treat endocrine, rheumatic, collagen, dermatologic, allergic, ophthalmic, gastrointestinal, respiratory, hematologic, neoplastic, edematous, and other conditions. Developed in 1957, it is structurally similar to other corticosteroids like and. Dexamethasone and otic suspension is indicated for bacterial infections with inflammation in acute otitis media and acute otitis externa. Intramuscular and intravenous injections are indicated for a number of endocrine, rheumatic, collagen, dermatologic, allergic, ophthalmic, gastrointestinal, respiratory, hematologic, neoplastic, edematous, and other conditions. Oral tablets are indicated for the treatment of multiple myeloma. An intravitreal implant is indicated for some forms of macular edema and non-infectious posterior uveitis affecting the posterior of the eye. Various ophthalmic formulations are indicated for inflammatory conditions of the eye. Corticosteroids bind to the glucocorticoid receptor, inhibiting pro-inflammatory signals, and promoting anti-inflammatory signals. Dexamethasone's duration of action varies depending on the route. Corticosteroids have a wide therapeutic window as patients may require doses that are multiples of what the body naturally produces. Patients taking corticosteroids should be counselled regarding the risk of hypothalamic-pituitary-adrenal axis suppression and increased susceptibility to infections. The short term effects of corticosteroids are decreased vasodilation and permeability of capillaries, as well as decreased leukocyte migration to sites of inflammation. Corticosteroids binding to the glucocorticoid receptor mediates changes in gene expression that lead to multiple downstream effects over hours to days.",The molecular weight is 392.47.,Dexamethasone has a topological polar surface area of 94.83.,The log p value of  is 1.79.,Dexamethasone is approved and investigational and vet_approved.,Dexamethasone is a solid.,True
14321,"Levodopa is a prodrug of dopamine that is administered to patients with Parkinson's due to its ability to cross the blood-brain barrier. Levodopa can be metabolised to dopamine on either side of the blood-brain barrier and so it is generally administered with a dopa decarboxylase inhibitor like carbidopa to prevent metabolism until after it has crossed the blood-brain barrier. Once past the blood-brain barrier, levodopa is metabolized to dopamine and supplements the low endogenous levels of dopamine to treat symptoms of Parkinson's. The first developed drug product that was approved by the FDA was a levodopa and carbidopa combined product called Sinemet that was approved on May 2, 1975. Levodopa on its own is formulated as an oral inhalation powder indicated for intermittent treatment of off episodes in Parkinson's patients who are already being treated with carbidopa and levodopa. Levodopa is most commonly formulated as an oral tablet with a peripheral dopa decarboxylase inhibitor indicated for treatment of Parkinson's disease, post-encephalitic parkinsonism, and symptomatic parkinsonism following carbon monoxide intoxication or manganese intoxication. Levodopa is able to cross the blood-brain barrier while dopamine is not. The addition of a peripheral dopa decarboxylase inhibitor prevents the conversion of levodopa to dopamine in the periphery so that more levodopa can reach the blood-brain barrier. Once past the blood-brain barrier, levodopa is converted to dopamine by aromatic-L-amino-acid decarboxylase. Levodopa by various routes crosses the blood brain barrier, is decarboxylated to form dopamine. This supplemental dopamine performs the role that endogenous dopamine cannot due to a decrease of natural concentrations and stimulates dopaminergic receptors.",The molecular weight is 197.19.,Levodopa has a topological polar surface area of 103.78.,The log p value of  is -2.82.,Levodopa is approved.,Levodopa is a solid.,True
14322,"Sevoflurane, also called fluoromethyl, is an ether inhalation anaesthetic agent used for the induction and maintenance of general anesthesia. It is a volatile, non-flammable, non-irritant, and easy-to-administer compound with a low solubility profile and blood-to-gas partition coefficient. Used for induction and maintenance of general anesthesia in adult and pediatric patients for inpatient and outpatient surgery. Sevoflurane induces muscle relaxation and reduces pains sensitivity by altering tissue excitability with a fast onset of action. It does so by decreasing the extent of gap junction mediated cell-cell coupling and altering the activity of the channels that underlie the action potential. Sevoflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Sevoflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase and also binds to the GABA receptor, the large conductance Ca<sup>2+</sup> activated potassium channel, the glutamate receptor, and the glycine receptor.",The molecular weight is 200.06.,Sevoflurane has a topological polar surface area of 9.23.,The log p value of  is 1.45.,Sevoflurane is approved and vet_approved.,Sevoflurane is a liquid.,True
14323,"Aripiprazole is an atypical antipsychotic orally indicated for treatment of schizophrenia, bipolar I, major depressive disorder, irritability associated with autism, and Tourette's. It is also indicated as an injection for agitation associated with schizophrenia or bipolar mania. Aripiprazole exerts its effects through agonism of dopaminic and 5-HT1A receptors and antagonism of alpha adrenergic and 5-HT2A receptors. Aripiprazole was given FDA approval on November 15, 2002. Aripiprazole is indicated for manic and mixed episodes associated with bipolar I disorder, irritability associated with autism spectrum disorder, treatment of schizophrenia, treatment of Tourette's disorder, and as an adjunctive treatment of major depressive disorder. An injectable formulation of aripiprazole is indicated for agitation associated with schizophrenia or bipolar mania. Aripiprazole has high affinity for serotonin type 2 (5HT2), dopamine type 2 (D2), alpha1 and 2 adrenergic, and H1 histaminergic receptors. It also acts on a number of other receptors with lower affinity. The exact method by which aripiprazole's action on these receptors translates to a clinically relevant effect is not yet known. The antipsychotic action of aripiprazole is likely due to the agonism of D2 and 5-HT1A receptors though the exact mechanism has not been defined. Some adverse effects may be due to action on other receptors. For example, orthostatic hypotension may be explained by antagonism of the adrenergic alpha1 receptors.",The molecular weight is 448.39.,Aripiprazole has a topological polar surface area of 44.81.,The log p value of  is 5.31.,Aripiprazole is approved and investigational.,Aripiprazole is a solid.,True
14324,"Gemfibrozil is a fibric acid agent, similar to , used to treat Type IIb, IV, and V hyperlipidemias. Gemfibrozil is not a first line treatment and is prescribed to patients who have not responded adequately to weight loss, diet, exercise, and other medications. Gemfibrozil is indicated to treat patients with Types IV and V hyperlipidemia who have elevated serum triglycerides (usually above 2000mg/dL), elevated VLDL cholesterol, fasting chylomicrons, are at risk of developing pancreatitis, and do not adequately respond to dietary restrictions. Gemfibrozil is also indicated to reduce the risk of developing coronary heart disease in patients with Type IIb hyperlipidemia without history or symptoms of coronary heart disease; who do not adequately respond to weight loss, diet, exercise, and other medications; and have low HDL, raised LDL, and raised triglycerides. Gemfibrozil alters lipid metabolism to treat patients with hyperlipidemia. The duration of action requires twice daily dosing as the mean residence time of gemfibrozil is up to 9.6h in patients with chronic renal failure. Gemfibrozil has a wide therapeutic index as trials with twice the standard dose were not associated with severe side effects. Patients taking gemfibrozil may be at an increased risk of developing cholelithiasis and cholecystitis, as seen in patients taking. Gemfibrozil activates peroxisome proliferator-activated receptor-α (PPARα), which alters lipid metabolism. This activation leads to increased HDL, apo AI, apo AII, lipoprotein lipase (LPL), inhibition of apo B synthesis, peripheral lipolysis, decreased removal of free fatty acids by the liver, and increased clearance of apoB.",The molecular weight is 250.34.,Gemfibrozil has a topological polar surface area of 46.53.,The log p value of  is 3.94.,Gemfibrozil is approved.,Gemfibrozil is a solid.,True
14325,"Clomipramine, the 3-chloro analog of imipramine, is a dibenzazepine-derivative tricyclic antidepressant (TCA). TCAs are structurally similar to phenothiazines. They contain a tricyclic ring system with an alkyl amine substituent on the central ring. In non-depressed individuals, clomipramine does not affect mood or arousal, but may cause sedation. In depressed individuals, clomipramine exerts a positive effect on mood. TCAs are potent inhibitors of serotonin and norepinephrine reuptake. Tertiary amine TCAs, such as clomipramine, are more potent inhibitors of serotonin reuptake than secondary amine TCAs, such as nortriptyline and desipramine. TCAs also down-regulate cerebral cortical &beta;-adrenergic receptors and sensitize post-synaptic serotonergic receptors with chronic use. The antidepressant effects of TCAs are thought to be due to an overall increase in serotonergic neurotransmission. TCAs also block histamine-H<sub>1</sub> receptors, &alpha;<sub>1</sub>-adrenergic receptors and muscarinic receptors, which accounts for their sedative, hypotensive and anticholinergic effects (e.g. blurred vision, dry mouth, constipation, urinary retention), respectively. See toxicity section below for a complete listing of side effects. Clomipramine may be used to treat obsessive-compulsive disorder and disorders with an obsessive-compulsive component (e.g. depression, schizophrenia, Tourette’s disorder). Unlabeled indications include panic disorder, chronic pain (e.g. central pain, idiopathic pain disorder, tension headache, diabetic peripheral neuropathy, neuropathic pain), cataplexy and associated narcolepsy, autistic disorder, trichotillomania, onchophagia, stuttering, premature ejaculation, and premenstrual syndrome. Clomipramine is rapidly absorbed from the gastrointestinal tract and demethylated in the liver to its primary active metabolite, desmethylclomipramine. May be used to treat obsessive-compulsive disorder and disorders with an obsessive-compulsive component (e.g. depression, schizophrenia, Tourette’s disorder). Clomipramine, a tricyclic antidepressant, is the 3-chloro derivative of Imipramine. It was thought that tricyclic antidepressants work exclusively by inhibiting the re-uptake of the neurotransmitters norepinephrine and serotonin by nerve cells. However, this response occurs immediately, yet mood does not lift for around two weeks. It is now thought that changes occur in receptor sensitivity in the cerebral cortex and hippocampus. The hippocampus is part of the limbic system, a part of the brain involved in emotions. Presynaptic receptors are affected: &alpha;<sub>1</sub> and &beta;<sub>1</sub> receptors are sensitized, &alpha;<sub>2</sub> receptors are desensitized (leading to increased noradrenaline production). Tricyclics are also known as effective analgesics for different types of pain, especially neuropathic or neuralgic pain. Clomipramine is a strong, but not completely selective serotonin reuptake inhibitor (SRI), as the active main metabolite desmethyclomipramine acts preferably as an inhibitor of noradrenaline reuptake. &alpha;<sub>1</sub>-receptor blockage and &beta;-down-regulation have been noted and most likely play a role in the short term effects of clomipramine. A blockade of sodium-channels and NDMA-receptors might, as with other tricyclics, account for its effect in chronic pain, in particular the neuropathic type.",The molecular weight is 314.86.,Clomipramine has a topological polar surface area of 6.48.,The log p value of  is 5.92.,Clomipramine is approved and investigational and vet_approved.,Clomipramine is a solid.,True
14326,"Darunavir is a protease inhibitor used with other HIV protease inhibitor drugs as well as for the effective management of HIV-1 infection. As a second-generation protease inhibitor, darunavir is designed to combat resistance to standard HIV therapy. It was initially approved by the FDA in 2006. Darunavir, co-administered with ritonavir, and with other antiretroviral agents, is indicated for the treatment of human immunodeficiency virus (HIV) in children age 3 or above and adults with HIV-1 infection.  Darunavir is an inhibitor of the human immunodeficiency virus (HIV) protease, which prevents HIV viral replication. When administered with ritonavir in combination antiretroviral therapy, darunavir significantly decreases viral load and increases CD4 cell counts, decreasing the morbidity and mortality of HIV infection. The HIV-1 protease enzyme is necessary for viral precursor protein processing and viral maturation in preparation for infection, and is therefore a target for antiretroviral therapy for HIV. Protease inhibitors are used as a part of highly active antiretroviral therapy (HAART) in patients diagnosed with HIV infection. It has been shown to effectively suppress the virus, leading to significantly decreased morbidity and mortality rates.",The molecular weight is 547.67.,Darunavir has a topological polar surface area of 140.42.,The log p value of  is 2.89.,Darunavir is approved.,Darunavir is a solid.,True
14327,"Originally developed in the 1950s as a malaria treatment, hydralazine showed antihypertensive ability and was soon repurposed. Hydralazine is a hydrazine derivative vasodilator used alone or as adjunct therapy in the treatment of hypertension and only as adjunct therapy in the treatment of heart failure. Hydralazine is no longer a first line therapy for these indications since the development of newer antihypertensive medications. Hydralazine is indicated alone or adjunct to standard therapy to treat essential hypertension. A combination product with isosorbide dinitrate is indicated as an adjunct therapy in the treatment of heart failure. Hydralazine interferes with calcium transport to relax arteriolar smooth muscle and lower blood pressure. Hydralazine has a short duration of action of 2-6h. This drug has a wide therapeutic window, as patients can tolerate doses of up to 300mg. Patients should be cautioned regarding the risk of developing systemic lupus erythematosus syndrome. Hydralazine may interfere with calcium transport in vascular smooth muscle by an unknown mechanism to relax arteriolar smooth muscle and lower blood pressure. The interference with calcium transport may be by preventing influx of calcium into cells, preventing calcium release from intracellular compartments, directly acting on actin and myosin, or a combination of these actions. This decrease in vascular resistance leads to increased heart rate, stroke volume, and cardiac output.",The molecular weight is 160.18.,Hydralazine has a topological polar surface area of 63.83.,The log p value of  is 1.17.,Hydralazine is approved.,Hydralazine is a solid.,True
14328,"Exenatide is a glucagon-like peptide-1 (GLP-1) analog. It functions to activate the GLP-1 receptor and increases insulin secretion, decrease glucagon secretion, and slow gastric emptying to improve glycemic control. Exenatide was given FDA approval on April 28, 2005. Exenatide is indicated for improving glycemic control in adults with type 2 diabetes mellitus along with diet and exercise. When patients take exenatide the body's natural response to glucose is modulated. More insulin and less glucagon are released in response to glucose, though in cases of hypoglycemia a normal amount of glucagon is released. Exenatide also slows gastric emptying, leading to a slower and prolonged release of glucose into the systemic circulation. Together these effects prevent hyper and hypoglycemia. Exenatide is a human glucacon-like peptide-1(GLP-1) receptor agonist. By activating this receptor, insulin secretion is increased and glucagon secretion is decreased in a glucose dependant manner. Exenatide also slows gastric emptying and decreases food intake. These effects work synergistically to improve glycemic control by reducing the likelihood of hyper and hypoglycemia.",The molecular weight is 4186.63.,Exenatide has a topological polar surface area of 1749.75.,,Exenatide is approved and investigational.,Exenatide is a solid.,True
14329,"Insulin detemir is a long-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Insulin is typically prescribed for the management of diabetes mellitus to mimic the activity of endogenously produced human insulin, a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin detemir is indicated to improve glycemic control in adults and children with diabetes mellitus. Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, the pancreas produces a continuous supply of low levels of basal insulin along with spikes of insulin following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by the liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin detemir is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals. The onset of action of insulin detemir is 1 to 2 hours and its duration of action is up to 24 hours. Interestingly, it has a lower affinity (30%) for the insulin receptor than human insulin. Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signalling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism.",The molecular weight is 5916.89.,Insulin detemir has a topological polar surface area of 2252.82.,,Insulin detemir is approved.,Insulin detemir is a liquid.,True
14330,"Fosphenytoin is a water-soluble phenytoin prodrug used only in hospitals for the treatment of epileptic seizures. It works by slowing down impulses in the brain that cause seizures. Its main mechanism is to block frequency-dependent, use-dependent and voltage-dependent neuronal sodium channels, and therefore limit repetitive firing of action potentials. Fosphenytoin is indicated for the treatment of generalized tonic-clonic status epilepticus and for the prevention and treatment of seizures occurring during neurosurgery in adult patients. It can also be substituted, short-term, for oral phenytoin in patients aged two years and older when oral phenytoin administration is not possible. Fosphenytoin is a water-soluble phenytoin prodrug used for the treatment of epileptic seizures. Following parenteral administration of fosphenytoin, fosphenytoin is converted to the anticonvulsant phenytoin by endogenous phosphatases. Each 1.5 mg of fosphenytoin sodium is equivalent to 1.0mg of phenytoin sodium (PE equivalents); care should be taken to calculate the dose required in PE equivalents properly. Serious adverse effects such as Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS), Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis (SJS/TEN), and hematopoietic complications may occur and indicate an alternate antiepileptic should be used. Withdrawal of fosphenytoin sodium may precipitate seizures and should be done gradually. Fosphenytoin is a prodrug of phenytoin and accordingly, its anticonvulsant effects are attributable to phenytoin. Phenytoin acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. By promoting sodium efflux from neurons, phenytoin tends to stabilize the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient. This includes the reduction of post-tetanic potentiation at synapses. Loss of post-tetanic potentiation prevents cortical seizure foci from detonating adjacent cortical areas.",The molecular weight is 362.28.,Fosphenytoin has a topological polar surface area of 116.17.,The log p value of  is 0.55.,Fosphenytoin is approved and investigational.,Fosphenytoin is a solid.,True
14331,"A thiazide diuretic with actions and uses similar to those of hydrochlorothiazide. (From Martindale, The Extra Pharmacopoeia, 30th ed, p826) Polythiazide is a thiazide diuretic used to decrease edema and decrease blood pressure. As a thiazide diuretic, Polythiazide inhibits the sodium-chloride symporter which decreases solute reabsorption leading to a retention of water in the urine, as water normally follows solutes. More frequent urination is due to the increased loss of water that has not been retained from the body as a result of a concomitant relationship with sodium loss from the convoluted tubule. The short-term anti-hypertensive action is based on the fact that thiazides decrease preload, decreasing blood pressure As a diuretic, polythiazide inhibits active chloride reabsorption at the early distal tubule via the thiazide-sensitive Na-Cl cotransporter (TSC), resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like polythiazide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of polythiazide may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle.",The molecular weight is 439.87.,Polythiazide has a topological polar surface area of 109.57.,The log p value of  is 1.83.,Polythiazide is approved.,Polythiazide is a solid.,True
14332,"A semisynthetic cephalosporin analog with broad-spectrum antibiotic action due to inhibition of bacterial cell wall synthesis. It attains high serum levels and is excreted quickly via the urine. Mainly used to treat bacterial infections of the skin. It can also be used to treat moderately severe bacterial infections involving the lung, bone, joint, stomach, blood, heart valve, and urinary tract. It is clinically effective against infections caused by staphylococci and streptococci species of Gram positive bacteria. May be used for surgical prophylaxis; if required metronidazole may be added to cover B. fragilis. Cefazolin (also known as cefazoline or cephazolin) is a semi-synthetic first generation cephalosporin for parenteral administration. Cefazolin has broad-spectrum antibiotic action due to inhibition of bacterial cell wall synthesis. It attains high serum levels and is excreted quickly via the urine. In vitro tests demonstrate that the bactericidal action of cephalosporins results from inhibition of cell wall synthesis. By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, it inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins.",The molecular weight is 454.5.,Cefazolin has a topological polar surface area of 156.09.,The log p value of  is -1.09.,Cefazolin is approved.,Cefazolin is a solid.,True
14333,"A second-generation cephalosporin administered intravenously or intramuscularly. Its bactericidal action results from inhibition of cell wall synthesis. It is used for urinary tract infections, lower respiratory tract infections, and soft tissue and bone infections. For the treatment of bacterial infections caused by susceptible microorganisms. Cefonicid is a second-generation cephalosporin administered intravenously or intramuscularly. Its bactericidal action results from inhibition of cell wall synthesis. It is used for urinary tract infections, lower respiratory tract infections, and soft tissue and bone infections. Cefonicid, like the penicillins, is a beta-lactam antibiotic. By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, it inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins.",The molecular weight is 542.56.,Cefonicid has a topological polar surface area of 204.91.,The log p value of  is -1.92.,Cefonicid is approved and investigational.,Cefonicid is a solid.,True
14334,"Cefoperazone is a semisynthetic broad-spectrum cephalosporin proposed to be effective against <i>Pseudomonas</i> infections. It is a third-generation antiobiotic agent and it is used in the treatment of various bacterial infections caused by susceptible organisms in the body, including respiratory tract infections, peritonitis, skin infections, endometritis, and bacterial septicemia. While its clinical use has been discontinued in the U.S., cefoperazone is available in several European countries most commonly under the product name, Sulperazon. Indicated for the treatment of following infections caused by susceptible bacteria: Cefoperazone is a third generation cephalosporin antibiotic. Cefoperazone exerts its bactericidal effect by inhibiting the bacterial cell wall synthesis Like all beta-lactam antibiotics, cefoperazone binds to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, causing the inhibition of the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins.",The molecular weight is 645.67.,Cefoperazone has a topological polar surface area of 220.26.,The log p value of  is -0.56.,Cefoperazone is approved and investigational.,Cefoperazone is a solid.,True
14335,A semisynthetic cephamycin antibiotic that is administered intravenously or intramuscularly. The drug is highly resistant to a broad spectrum of beta-lactamases and is active against a wide range of both aerobic and anaerobic gram-positive and gram-negative microorganisms. For prophylaxis and treatment of bacterial infections. Cefotetan is a semisynthetic cephamycin antibiotic that is administered intravenously or intramuscularly. The drug is highly resistant to a broad spectrum of beta-lactamases and is active against a wide range of both aerobic and anaerobic gram-positive and gram-negative microorganisms.  The bactericidal action of cefotetan results from inhibition of cell wall synthesis by binding and inhibiting the bacterial penicillin binding proteins which help in the cell wall biosynthesis.,The molecular weight is 575.6.,Cefotetan has a topological polar surface area of 219.93.,The log p value of  is -1.54.,Cefotetan is approved.,Cefotetan is a solid.,True
14336,"Ephedrine was first described in western literature in 1888, as a naturally occurring component of the ephedra plant, along with. Ephedrine is an adrenergic receptor agonist used for its vasoconstrictive, positive chronotropic, and positive inotropic effects. Ephedrine and are still commonly used to treat hypotension but their use in other indications has decreased due to the development of more selective adrenergic agonists. Ephedrine intravenous injections are indicated to treat hypotension under anesthesia, ephedrine injections by multiple routes are indicated to treat allergic conditions such as bronchial asthma, ephedrine nasal spray is and OTC medication used as a decongestant. Ephedrine is a sympathomimetic amine that activates adrenergic receptors, increasing heart rate and blood pressure, and causing bronchodilation. The therapeutic window is wide as patients can be given doses of 5mg up to 50mg. Patients should be counselled regarding the pressor effects of sympathomimetic amines and the risk of tachyphylaxis. Ephedrine is a direct and indirect sympathomimetic amine. Ephedrine activates adrenergic α and β-receptors as well as inhibiting norepinephrine reuptake, and increasing the release of norepinephrine from vesicles in nerve cells. These actions combined lead to larger quantities of norepinephrine present in the synapse, for longer periods of time, increasing stimulation of the sympathetic nervous system. Ephedrine's stimulation of α-1 receptors causes constriction of veins and a rise in blood pressure, stimulation of β-1 adrenergic receptors increase cardiac chronotropy and inotropy, stimulation of β-2 adrenergic receptors causes bronchodilation.",The molecular weight is 165.24.,Ephedrine has a topological polar surface area of 32.26.,The log p value of  is 0.89.,Ephedrine is approved.,Ephedrine is a solid.,True
14337,"A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98. Aluminum Acetate is an astringent. An astrignent is a chemical that tends to shrink or constrict body tissues, usually locally after topical medicinal application. The shrinkage or constriction is through osmotic flow of water (or other fluids) away from the area where the astringent was applied. Astringent medicines cause shrinkage of mucous membranes or exposed tissues and are often used internally to check discharge of blood serum or mucous secretions. This can happen with a sore throat, hemorrhages, diarrhea, or with peptic ulcers. Externally applied astringents, which cause mild coagulation of skin proteins, dry, harden, and protect the skin. Acne sufferers are often advised to use astringents if they have oily skin. Astringents also help heal stretch marks and other scars. Mild astringent solutions are used in the relief of such minor skin irritations as those resulting from superficial cuts, allergies, insect bites, or fungal infections such as athlete's foot. ",,,,Aluminium is approved and investigational.,Aluminium is a solid.,True
14338,"First approved by the FDA in 1961, colchicine is an alkaloid drug commonly used in the management of gout, a condition associated with the painful deposition of urate crystals in the joints. It is derived from a plant belonging to the Lily family, known as Colchicum autumnale, or \autumn crocus\"". Other than its use in gout, colchicine has been approved for managing exacerbations of Familial Mediterranean Fever (FMF), a hereditary autoinflammatory condition."" Colchicine is indicated for the prophylaxis and treatment of gout flares. It is also indicated in Familial Mediterranean fever (FMF) in children and adults of 4 years of age and older. It is important to note that this medication is not a pain reliever to be used for other painful conditions. Consider analgesics for this purpose. Some off-label uses of colchicine include the treatment of the manifestations of Behcet's syndrome, pericarditis, and postpericardiotomy syndrome. Colchicine reduces the pain resulting from gout and reduces flares of Familial Mediterranean fever by interfering with inflammatory pathways. This drug has a narrow therapeutic index. The exact mechanism of action of colchicine has not been fully established, however likely occurs via the downstream inhibition of inflammation caused by tubulin disruption. Studies have implied that that colchicine causes disruption of the inflammasome complex that is present in both monocytes and neutrophils, which normally leads to the activation of interleukin-1, an important mediator of inflammation. In addition to the above actions, colchicine acts to interfere with pathways including neutrophil adhesion and recruitment, superoxide production, the RhoA/Rho effector kinase (ROCK) pathway, as well as a type of nuclear factor κΒ (NF-κΒ) pathway, reducing inflammation. ",The molecular weight is 399.44.,Colchicine has a topological polar surface area of 83.09.,The log p value of  is 1.2.,Colchicine is approved.,Colchicine is a solid.,True
14339,"A cardiac glycoside sometimes used in place of digoxin. It has a longer half-life than digoxin; toxic effects, which are similar to those of digoxin, are longer lasting. (From Martindale, The Extra Pharmacopoeia, 30th ed, p665) For the treatment and management of congestive cardiac insufficiency, arrhythmias and heart failure. Digitoxin is a cardiac glycoside sometimes used in place of DIGOXIN. It has a longer half-life than digoxin; toxic effects, which are similar to those of digoxin, are longer lasting (From Martindale, The Extra Pharmacopoeia, 30th ed, p665). It is eliminated hepatically making it useful in patients with poor or erratic kidney function, although it is now rarely used in practice. Digitoxin lacks the strength of evidence that digoxin has in the management of heart failure. Digitoxin inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium and calcium concentrations. Increased intracellular concentrations of calcium may promote activation of contractile proteins (e.g., actin, myosin). Digitoxin also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.",The molecular weight is 764.95.,Digitoxin has a topological polar surface area of 182.83.,The log p value of  is 2.85.,Digitoxin is approved and investigational.,Digitoxin is a solid.,True
14340,"Magnesium salicylate is a non-steroidal anti-inflammatory drug (NSAID) used to treat mild to moderate pain. It is available in several over-the-counter (OTC) formulations. Though the recommended doseage is 1160 mg every six hours, per package directions of the Doan's OTC brand (580 mg magnesium salicylate tetrahydrate, equivalent to 934.4 mg anhydrous magnesium salicylate), effective pain relief is often found with a half dosage, with reduced anti-inflammatory results. Magnesium salicylate is a common analgesic and non-steroidal anti-inflammatory drug (NSAID) used to treat mild to moderate muscular pain Most NSAIDs act as nonselective inhibitors of the enzyme cyclooxygenase (COX), inhibiting both the cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) isoenzymes. COX catalyzes the formation of prostaglandins and thromboxane from arachidonic acid (itself derived from the cellular phospholipid bilayer by phospholipase A2). Prostaglandins act (among other things) as messenger molecules in the process of inflammation.",The molecular weight is 298.53.,,,Magnesium salicylate is experimental.,Magnesium salicylate is a solid.,True
14341,"Acenocoumarol is a coumarin derivative used as an anticoagulant. Coumarin derivatives inhibit the reduction of vitamin K by vitamin K reductase. This prevents carboxylation of vitamin K-dependent clotting factors, II, VII, IX and X, and interferes with coagulation. Hematocrit, hemoglobin, international normalized ratio and liver panel should be monitored. Patients on acenocoumarol are prohibited from giving blood. For the treatment and prevention of thromboembolic diseases. More specifically, it is indicated for the prevention of cerebral embolism, deep vein thrombosis, pulmonary embolism, thromboembolism in infarction and transient ischemic attacks. It is used for the treatment of deep vein thrombosis and myocardial infarction. Acenocoumarol inhibits the reduction of vitamin K by vitamin K reductase. This prevents carboxylation of certain glutamic acid residues near the N-terminals of clotting factors II, VII, IX and X, the vitamin K-dependent clotting factors. Glutamic acid carboxylation is important for the interaction between these clotting factors and calcium. Without this interaction, clotting cannot occur. Both the extrinsic (via factors VII, X and II) and intrinsic (via factors IX, X and II) are affected by acenocoumarol. Acenocoumarol inhibits vitamin K reductase, resulting in depletion of the reduced form of vitamin K (vitamin KH2). As vitamin K is a cofactor for the carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent clotting factors, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited resulting in decreased prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots.",The molecular weight is 355.3.,Acenocoumarol has a topological polar surface area of 126.97.,The log p value of  is 2.66.,Acenocoumarol is approved and investigational.,Acenocoumarol is a solid.,True
14342,"Testosterone propionate is a slower releasing anabolic steroid with a short half-life. This characteristic allows the user to run short testosterone propionate cycles of 8-10 weeks as optimal peak blood plasma levels are achieved at 2-4 weeks. It is a synthetic androstane steroid derivative of testosterone in the form of 17β propionate ester of testosterone. Testosterone propionate was developed initially by Watson labs, and FDA approved on February 5, 1974. Currently, this drug has been discontinued in humans, but the vet application is still available as an OTC. Testosterone propionate is often used for muscle mass building. The original medical indication is for the treatment of androgen deficiency in male adults either in hypogonadism or andropause. Nowadays testosterone propionate is indicated for its use in heifers in order to stimulate maximal growth. The administration of testosterone propionate can induce production of proteins related to male sexual development. On the other hand, testosterone itself present an estrogenic activity due to interaction with aromatase enzyme, thus the continuous aministration of testosterone propionate may cause the elevation of plasma estrogen. Clinical trials showed as well, a decrease in plasma LH after testosterone propionate administration. The effects of testosterone in humans and other vertebrates occur by way of two main mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors. Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5alpha-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5alpha-reductase. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.",The molecular weight is 344.5.,Testosterone propionate has a topological polar surface area of 43.37.,The log p value of  is 4.88.,Testosterone propionate is approved and investigational and vet_approved and withdrawn.,Testosterone propionate is a solid.,True
14343,"A sulfanilamide that is used as an antibacterial agent. A sulfanilamide that is used as an antibacterial agent. It can be used to treat bronchitis, prostatitis and urinary tract infections. Sulfonamides act as competitive inhibitors of the enzyme dihydropteroate synthetase (DHPS), an enzyme involved in folate synthesis in bacteria. Sulfamerazine is a sulfonamide drug that inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid (PABA) for binding to dihydropteroate synthetase (dihydrofolate synthetase). Sulfamerazine is bacteriostatic in nature. Inhibition of dihydrofolic acid synthesis decreases the synthesis of bacterial nucleotides and DNA. ",The molecular weight is 264.3.,Sulfamerazine has a topological polar surface area of 97.97.,The log p value of  is 0.6.,Sulfamerazine is approved and vet_approved.,Sulfamerazine is a solid.,True
14344,"A sulfanilamide anti-infective agent. It has a spectrum of antimicrobial action similar to other sulfonamides. For the treatment bacterial infections causing bronchitis, prostatitis and urinary tract infections. Sulfamethazine is a sulfonamide drug that inhibits bacterial synthesis of dihydrofolic acid by competing with para-aminobenzoic acid (PABA) for binding to dihydropteroate synthetase (dihydrofolate synthetase). Sulfamethazine is bacteriostatic in nature. Inhibition of dihydrofolic acid synthesis decreases the synthesis of bacterial nucleotides and DNA.  Sulfonamides inhibit the enzymatic conversion of pteridine and p-aminobenzoic acid (PABA) to dihydropteroic acid by competing with PABA for binding to dihydrofolate synthetase, an intermediate of tetrahydrofolic acid (THF) synthesis. THF is required for the synthesis of purines and dTMP and inhibition of its synthesis inhibits bacterial growth. Pyrimethamine and trimethoprim inhibit dihydrofolate reductase, another step in THF synthesis, and therefore act synergistically with the sulfonamides.",The molecular weight is 278.33.,Sulfamethazine has a topological polar surface area of 97.97.,The log p value of  is 1.1.,Sulfamethazine is approved and investigational and vet_approved.,Sulfamethazine is a solid.,True
14345,"Ketazolam is a benzodiazepine derivative with anxiolytic, anticonvulsant, sedative and skeletal muscle relaxant activity. Ketazolam is not approved in Canada or America. Ketazolam could be used for the treatment of anxiety. In approved countries, it is indicated for the treatment of anxiety, tension, irritability and similar stress related symptoms. Benzodiazepines enhance the effect of the neurotransmitter gamma-aminobutyric acid (GABA), which results in sedative, hypnotic, anxiolytic, anticonvulsant, muscle relaxant and amnesic action. Benzodiazepines share a similar chemical structure and their effects in humans are mainly produced by the allosteric modification of a specific kind of neurotransmitter receptor, the GABAA receptor, which increases the conductance of this inhibitory channel; this results in the various therapeutic effects as well as adverse effects of benzodiazepines. Binding of benzodiazepines to this receptor complex promotes binding of GABA, which in turn increases the conduction of chloride ions across the neuronal cell membrane. This increased conductance raises the membrane potential of the neuron resulting in inhibition of neuronal firing. In addition, different GABAA receptor subtypes have varying distributions within different regions of the brain and therefore control distinct neuronal circuits. Hence, activation of different GABAA receptor subtypes by benzodiazepines may result in distinct pharmacological actions.",The molecular weight is 368.82.,Ketazolam has a topological polar surface area of 49.85.,The log p value of  is 3.71.,Ketazolam is approved.,Ketazolam is a solid.,True
14346,"Lopinavir is an antiretroviral protease inhibitor used in combination with other antiretrovirals in the treatment of HIV-1 infection. Lopinavir is marketed and administered exclusively in combination with - this combination, first marketed by Abbott under the brand name Kaletra in 2000, is necessary due to lopinavir's poor oral bioavailability and extensive biotransformation. Ritonavir is a potent inhibitor of the enzymes responsible for lopinavir metabolism, and its co-administration \boosts\"" lopinavir exposure and improves antiviral activity. Like many other protease inhibitors (e.g. , ), lopinavir is a peptidomimetic molecule - it contains a hydroxyethylene scaffold that mimics the peptide linkage typically targeted by the HIV-1 protease enzyme but which itself cannot be cleaved, thus preventing the activity of the HIV-1 protease."" The combination product lopinavir/ritonavir, marketed under the brand name Kaletra, is indicated in combination with other antiretrovirals for the treatment of HIV-1 infection in adults and pediatric patients ≥14 days old. Lopinavir inhibits the activity of an enzyme critical for the HIV viral lifecycle. It has a moderate duration of action necessitating once or twice daily dosing. Lopinavir, like other protease inhibitors, has a propensity for participating in drug interactions - use caution when administering lopinavir to patients maintained on other pharmaceutical agents as pharmacodynamic and pharmacokinetic interactions are common. Fatal hepatotoxicity and pancreatitis have been noted in patients undergoing therapy with lopinavir and patients with an increased baseline risk of these events should be monitored closely throughout therapy. The HIV lifecycle is comprised of 3 distinct stages: assembly, involving creation and packaging of essential viral components; budding, wherein the viral particle crosses the host cell plasma membrane and forms a lipid envelope; and maturation, wherein the viral particle alters its structure and becomes infectious. At the center of this lifecycle is the Gag polyprotein which, along with the products of its proteolysis, coordinate these stages and function as the major structural proteins of the virus. The HIV-1 protease enzyme, a dimeric aspartic protease, is the enzyme responsible for cleaving the Gag polyprotein and thus plays a critical role in many aspects of the HIV viral lifecycle.",The molecular weight is 628.81.,Lopinavir has a topological polar surface area of 120.0.,The log p value of  is 6.09.,Lopinavir is approved.,Lopinavir is a solid.,True
14347,"Hydroxychloroquine is a racemic mixture consisting of an R and S enantiomer. Hydroxychloroquine is an aminoquinoline like. It is a commonly prescribed medication in the treatment of uncomplicated malaria, rheumatoid arthritis, chronic discoid lupus erythematosus, and systemic lupus erythematosus. Hydroxychloroquine is also used for the prophylaxis of malaria in regions where chloroquine resistance is unlikely. It was developed during World War II as a derivative of with less severe side effects. Chloroquine and hydroxychloroquine are both being investigated for the treatment of SARS-CoV-2. Hydroxychloroquine is indicated for the prophylaxis of malaria where chloroquine resistance is not reported, treatment of uncomplicated malaria (caused by _P. falciparum_, _P. malariae_, _P. ovale_, or _P. vivax_), chronic discoid lupus erythematosus, systemic lupus erythematosus, acute rheumatoid arthritis, and chronic rheumatoid arthritis. Hydroxychloroquine affects the function of lysozomes in humans as well as plasmodia. Altering the pH of the lysozomes reduces low affinity self antigen presentation in autoimmue diseases and interferes with the ability of plasmodia to proteolyse hemoglobin for their energy requirements. Hydroxychloroquine has a long duration of action as it may be taken on a weekly basis for some indications. Hydroxychloroquine may lead to severe hypoglycemia and so diabetic patients are advised to monitor their blood glucose levels. Hydroxychloroquine is not effective against malaria in areas where chloroquine resistance has been reported. The exact mechanisms of hydroxychloroquine are unknown. It has been shown that hydroxychloroquine accumulates in the lysosomes of the malaria parasite, raising the pH of the vacuole. This activity interferes with the parasite's ability to proteolyse hemoglobin, preventing the normal growth and replication of the parasite. Hydroxychloroquine can also interfere with the action of parasitic heme polymerase, allowing for the accumulation of the toxic product beta-hematin.",The molecular weight is 335.88.,Hydroxychloroquine has a topological polar surface area of 48.39.,The log p value of  is 4.12.,Hydroxychloroquine is approved.,Hydroxychloroquine is a solid.,True
14348,"Acepromazine is one of the phenothiazine derivative psychotropic drugs, used little in humans, however frequently in animals as a sedative and antiemetic. Acepromazine was first used in humans in the 1950s as an antipsychotic agent. It is now rarely used in humans. Acepromazine is frequently used in animals as a sedative and antiemetic. Its principal value is in quietening and calming anxious animals. Acepromazine is one of the phenothiazine derivative psychotropic drugs. Acepromazine has actions at all levels of the central nervous system-primarily at subcortical levels-as well as on multiple organ systems. Acepromazine has strong antiadrenergic and weaker peripheral anticholinergic activity; ganglionic blocking action is relatively slight. It also possesses slight antihistaminic and antiserotonin activity. Acepromazine acts as an antagonist (blocking agent) on different postsysnaptic receptors -on dopaminergic-receptors (subtypes D1, D2, D3 and D4 - different antipsychotic properties on productive and unproductive symptoms), on serotonergic-receptors (5-HT1 and 5-HT2, with anxiolytic, antidepressive and antiaggressive properties as well as an attenuation of extrapypramidal side-effects, but also leading to weight gain, fall in blood pressure, sedation and ejaculation difficulties), on histaminergic-receptors (H1-receptors, sedation, antiemesis, vertigo, fall in blood pressure and weight gain), alpha1/alpha2-receptors (antisympathomimetic properties, lowering of blood pressure, reflex tachycardia, vertigo, sedation, hypersalivation and incontinence as well as sexual dysfunction, but may also attenuate pseudoparkinsonism - controversial) and finally on muscarinic (cholinergic) M1/M2-receptors (causing anticholinergic symptoms like dry mouth, blurred vision, obstipation, difficulty/inability to urinate, sinus tachycardia, ECG-changes and loss of memory, but the anticholinergic action may attenuate extrapyramidal side-effects).",The molecular weight is 326.46.,Acepromazine has a topological polar surface area of 23.55.,The log p value of  is 4.38.,Acepromazine is experimental and vet_approved.,Acepromazine is a liquid.,True
14349,"Pipotiazine has actions similar to those of other phenothiazines. Among the different phenothiazine derivatives, it appears to be less sedating and to have a weak propensity for causing hypotension or potentiating the effects of CNS depressants and anesthetics. However, it produces a high incidence of extra pyramidal reactions. It is used for the maintenance treatment of chronic non-agitated schizophrenic patients. Symptoms of overdose include severe extrapyramidal manifestations, hypotension, lethargy and sedation. For the maintenance treatment of chronic non-agitated schizophrenic patients. Pipotiazine has actions similar to those of other phenothiazines. Among the different phenothiazine derivatives, it appears to be less sedating and to have a weak propensity for causing hypotension or potentiating the effects of CNS depressants and anesthetics. However, it produces a high incidence of extra pyramidal reactions. It reduces activity of dopamine receptors in the limbic system. Its 5-HT antagonism helps normalize dopamine activity in the cortical regions. Pipotiazine acts as an antagonist (blocking agent) on different postsysnaptic receptors -on dopaminergic-receptors (subtypes D1, D2, D3 and D4 - different antipsychotic properties on productive and unproductive symptoms), on serotonergic-receptors (5-HT1 and 5-HT2, with anxiolytic, antidepressive and antiaggressive properties as well as an attenuation of extrapypramidal side-effects, but also leading to weight gain, fall in blood pressure, sedation and ejaculation difficulties), on histaminergic-receptors (H1-receptors, sedation, antiemesis, vertigo, fall in blood pressure and weight gain), alpha1/alpha2-receptors (antisympathomimetic properties, lowering of blood pressure, reflex tachycardia, vertigo, sedation, hypersalivation and incontinence as well as sexual dysfunction, but may also attenuate pseudoparkinsonism - controversial) and finally on muscarinic (cholinergic) M1/M2-receptors (causing anticholinergic symptoms like dry mouth, blurred vision, obstipation, difficulty/inability to urinate, sinus tachycardia, ECG-changes and loss of memory, but the anticholinergic action may attenuate extrapyramidal side-effects).",,,,Pipotiazine is approved and investigational.,Pipotiazine is a solid.,True
14350,"Thioproperazine is a potent neuroleptic with antipsychotic properties. Thioproperazine has a marked cataleptic and antiapomorphine activity associated with relatively slight sedative, hypothermic and spasmolytic effects. It is virtually without antiserotonin and hypotensive action and has no antihistaminic property. It is used for the treatment of all types of acute and chronic schizophrenia, including those which did not respond to the usual neuroleptics; manic syndromes. For the treatment of all types of acute and chronic schizophrenia, including those which did not respond to the usual neuroleptics; manic syndromes. Thioproperazine is a potent neuroleptic with antipsychotic properties. Thioproperazine has a marked cataleptic and antiapomorphine activity associated with relatively slight sedative, hypothermic and spasmolytic effects. It is virtually without antiserotonin and hypotensive action and has no antihistaminic property. Thioproperazine acts as an antagonist (blocking agent) on different postsysnaptic receptors -on dopaminergic-receptors (subtypes D1, D2, D3 and D4 - different antipsychotic properties on productive and unproductive symptoms), on serotonergic-receptors (5-HT1 and 5-HT2, with anxiolytic, antidepressive and antiaggressive properties as well as an attenuation of extrapypramidal side-effects, but also leading to weight gain, fall in blood pressure, sedation and ejaculation difficulties), on histaminergic-receptors (H1-receptors, sedation, antiemesis, vertigo, fall in blood pressure and weight gain), alpha1/alpha2-receptors (antisympathomimetic properties, lowering of blood pressure, reflex tachycardia, vertigo, sedation, hypersalivation and incontinence as well as sexual dysfunction, but may also attenuate pseudoparkinsonism - controversial) and finally on muscarinic (cholinergic) M1/M2-receptors (causing anticholinergic symptoms like dry mouth, blurred vision, obstipation, difficulty/inability to urinate, sinus tachycardia, ECG-changes and loss of memory, but the anticholinergic action may attenuate extrapyramidal side-effects).",The molecular weight is 446.63.,Thioproperazine has a topological polar surface area of 47.1.,The log p value of  is 3.21.,Thioproperazine is experimental.,Thioproperazine is a solid.,True
14351,"A thioxanthine used as an antipsychotic agent. Its effects are similar to the phenothiazine antipsychotics. For the management of schizophrenia. Thiothixene is an antipsychotic of the thioxanthene series. Navane possesses certain chemical and pharmacological similarities to the piperazine phenothiazines and differences from the aliphatic group of phenothiazines. Although widely used in the treatment of schizophrenia for several decades, thiothixene is seldom used today in favor of atypical antipsychotics such as risperidone. Thiothixene acts as an antagonist (blocking agent) on different postsysnaptic receptors -on dopaminergic-receptors (subtypes D1, D2, D3 and D4 - different antipsychotic properties on productive and unproductive symptoms), on serotonergic-receptors (5-HT1 and 5-HT2, with anxiolytic, antidepressive and antiaggressive properties as well as an attenuation of extrapypramidal side-effects, but also leading to weight gain, fall in blood pressure, sedation and ejaculation difficulties), on histaminergic-receptors (H1-receptors, sedation, antiemesis, vertigo, fall in blood pressure and weight gain), alpha1/alpha2-receptors (antisympathomimetic properties, lowering of blood pressure, reflex tachycardia, vertigo, sedation, hypersalivation and incontinence as well as sexual dysfunction, but may also attenuate pseudoparkinsonism - controversial) and finally on muscarinic (cholinergic) M1/M2-receptors (causing anticholinergic symptoms like dry mouth, blurred vision, obstipation, difficulty/inability to urinate, sinus tachycardia, ECG-changes and loss of memory, but the anticholinergic action may attenuate extrapyramidal side-effects).",The molecular weight is 443.62.,Thiothixene has a topological polar surface area of 43.86.,The log p value of  is 3.23.,Thiothixene is approved.,Thiothixene is a solid.,True
14352,"Topiroxostat is a selective xanthine oxidase inhibitor developed for treatment and management of hyperuricemia and gout. Xanthine oxidase, or xanthine oxidoreductase (XOR), regulates purine metabolism, and inhibition of the enzyme results in efficacious reduction of serum urate levels. Xanthine oxidase inhibitors are classified into two groups; purine analogs such as and , and non-purine agents which includes topiroxostat. While is considered a first-line therapy in treating hyperuricemic conditions, it is often associated with side effects and ineffective in reducing uric acid levels under recommended dosing regimens. Renal complications are major comorbidities that limit the therapy as dose reductions are recommended. Topiroxostat and its metabolites are shown to be unaffected by renal complications, thus may be effective in patients with chronic kidney diseases. Approved for therapeutic use in Japan since 2013, topiroxostat is marketed under the name Topiloric and Uriadec and is orally administered twice daily. Indicated for the treatment of gout and hyperurcemia in Japan. Topiroxostat reduces the synthesis of uric acid by competitively inhibiting xanthine oxidase in a selective and time-dependent manner. It serves to reduce the concentration of insoluble urates and uric acid in tissues, plasma and urine. Topiroxostat is not reported to cause QT prolongation.  Uric acid synthesis depends on the action of xanthine oxidase activity in the conversion of hypoxanthine to xanthine, followed by the conversion of xanthine to uric acid. Xanthine oxidase consists of a molybdenum ion as cofactor in the active center that has different redox states upon substrate binding. When a substrate such as hypoxanthine or xanthine binds, xanthine oxidase hydroxylates it and molybdenum ion is reduced from hexavalent, Mo(VI), to tetravalent form, Mo(IV). Molybdenum ion is reoxidized into hexavalent state once the hydroxylated substrate, xanthine or uric acid, dissociates from the active site. Topiroxostat is shown to interact with multiple amino acid residues of the solvent channel and additionally forms a reaction intermediate by covalent binding with molybdenum (IV) ion via an oxygen atom. It also forms hydrogen bonds with molybdenum (VI) ion, suggesting that it has multiple inhibition modes to xanthine oxidase. Enhanced binding interactions to xanthine oxidase achieves delayed dissociation of topiroxostat from the enzyme. 2-hydroxy-topiroxostat, the metabolite formed by primary hydroxylation of topiroxostat by xanthine oxidase, also causes time and concentration-dependent inhibition of the enzyme. ",The molecular weight is 248.25.,Topiroxostat has a topological polar surface area of 91.14.,The log p value of  is 0.92.,Topiroxostat is experimental.,Topiroxostat is a solid.,True
14353,"Glucose is a simple sugar (monosaccharide) generated during phosynthesis involving water, carbon and sunlight in plants. It is produced in humans via hepatic gluconeogenesis and breakdown of polymeric glucose forms (glycogenolysis). It circulates in human circulation as blood glucose and acts as an essential energy source for many organisms through aerobic or anaerobic respiration and fermentation. It is primarily stored as starch in plants and glycogen in animals to be used in various metabolic processes in the cellular level. Its aldohexose stereoisomer, dextrose or D-glucose, is the most commonly occurring isomer of glucose in nature. L-glucose is a synthesized enantiomer that is used as a low-calorie sweetener and laxative. The unspecified form of glucose is commonly supplied as an injection for nutritional supplementation or metabolic disorders where glucose levels are improperly regulated. Glucose is listed on the World Health Organization's List of Essential Medicines, the most important medications needed in a basic health system. Glucose pharmaceutical formulations (oral tablets, injections) are indicated for caloric supply and carbohydrate supplementation in case of nutrient deprivation. It is also used for metabolic disorders such as hypoglycemia. Blood glucose is an obligatory energy source for humans involved in various cellular activities, and it also acts as a signaling molecule for diverse glucose-sensing molecules and proteins. Glucose undergoes oxidation into carbon dioxide, water, and yields energy molecules in the process of glycolysis and subsequent citric cycle and oxidative phosphorylation. Glucose is readily converted into fat in the body which can be used as a source of energy as required. Under a similar conversion into storage of energy, glucose is stored in the liver and muscles as glycogen. Glucose stores are mobilized in a regulated manner, depending on the tissues' metabolic demands. Oral glucose tablets or injections serve to increase the supply of glucose and oral glucose administration is more effective in stimulating insulin secretion because it stimulates the incretin hormones from the gut, which promotes insulin secretion. Glucose supplies most of the energy to all tissues by generating energy molecules ATP and NADH during a series of metabolism reactions called glycolysis. Glycolysis can be divided into two main phases where the preparatory phase is initiated by the phosphorylation of glucose by hexokinase to form glucose 6-phosphate. The addition of the high-energy phosphate group activates glucose for the subsequent breakdown in later steps of glycolysis and is the rate-limiting step. Products end up as substrates for following reactions, to ultimately convert C6 glucose molecule into two C3 sugar molecules. These products enter the energy-releasing phase where the total of 4ATP and 2NADH molecules are generated per one glucose molecule. The total aerobic metabolism of glucose can produce up to 36 ATP molecules. These energy-producing reactions of glucose are limited to D-glucose as L-glucose cannot be phosphorylated by hexokinase. Glucose can act as precursors to generate other biomolecules such as vitamin C. It plays a role as a signaling molecule to control glucose and energy homeostasis. Glucose can regulate gene transcription, enzyme activity, hormone secretion, and the activity of glucoregulatory neurons. The types, number, and kinetics of glucose transporters expressed depends on the tissues and fine-tunes glucose uptake, metabolism, and signal generation to preserve cellular and whole body metabolic integrity.",,,,D-glucose is approved and investigational and vet_approved.,D-glucose is a solid.,True
14354,"Lauric acid is an inexpensive, non-toxic and safe to handle compound often used in laboratory investigations of melting-point depression. Lauric acid is a solid at room temperature but melts easily in boiling water, so liquid lauric acid can be treated with various solutes and used to determine their molecular masses.",The molecular weight is 200.32.,Lauric acid has a topological polar surface area of 37.3.,The log p value of  is 5.1.,Lauric acid is approved and experimental.,Lauric acid is a solid.,True
14355,Stearic acid (IUPAC systematic name: octadecanoic acid) is one of the useful types of saturated fatty acids that comes from many animal and vegetable fats and oils. It is a waxy solid.,The molecular weight is 284.48.,Stearic acid has a topological polar surface area of 37.3.,The log p value of  is 8.27.,Stearic acid is approved and experimental.,Stearic acid is a solid.,True
14356,Oxyphenbutazone was withdrawn from the Canadian market in March 1985 due to concerns regarding bone marrow suppression.,The molecular weight is 324.38.,Oxyphenbutazone has a topological polar surface area of 60.85.,The log p value of  is 2.72.,Oxyphenbutazone is approved and withdrawn.,Oxyphenbutazone is a solid.,True
14357,"Decanoic acid is a solid. This compound belongs to the straight chain fatty acids. These are fatty acids with a straight aliphatic chain. The proteins that decanoic acid targets include furin, octanoyltransferase, 3-oxoacyl- synthase 1, peptostreptococcal albumin-binding protein, and putative uncharacterized protein tcp14.",,,,Capric acid is experimental.,Capric acid is a solid.,True
14358,"A common saturated fatty acid found in fats and waxes including olive oil, palm oil, and body lipids. Palmitic acid is the first fatty acid produced during lipogenesis (fatty acid synthesis) and from which longer fatty acids can be produced. Palmitate negatively feeds back on acetyl-CoA carboxylase (ACC) which is responsible for converting acetyl-ACP to malonyl-ACP on the growing acyl chain, thus preventing further palmitate generation",,,,Palmitic Acid is approved.,Palmitic Acid is a solid.,True
14359,"Quercetin is a flavonol widely distributed in plants. It is an antioxidant, like many other phenolic heterocyclic compounds. Glycosylated forms include RUTIN and quercetrin. Quercetin is a specific quinone reductase 2 (QR2) inhibitor, an enzyme (along with the human QR1 homolog) which catalyzes metabolism of toxic quinolines. Inhibition of QR2 in plasmodium may potentially cause lethal oxidative stress. The inhibition of antioxidant activity in plasmodium may contribute to killing the malaria causing parasites. ",The molecular weight is 302.24.,Quercetin has a topological polar surface area of 127.45.,The log p value of  is 1.5.,Quercetin is experimental and investigational.,Quercetin is a solid.,True
14360,"An unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. (Stedman, 26th ed)",The molecular weight is 282.47.,Oleic Acid has a topological polar surface area of 37.3.,The log p value of  is 7.79.,Oleic Acid is approved and investigational and vet_approved.,Oleic Acid is a solid.,True
14361,,,,,Glyphosate is experimental.,Glyphosate is a solid.,False
14362,"An unsaturated, essential fatty acid. It is found in animal and human fat as well as in the liver, brain, and glandular organs, and is a constituent of animal phosphatides. It is formed by the synthesis from dietary linoleic acid and is a precursor in the biosynthesis of prostaglandins, thromboxanes, and leukotrienes. ",,,,Arachidonic Acid is experimental.,Arachidonic Acid is a solid.,True
14363,"Estrone sulfate (as estropipate) is a form of estrogen. It has several uses such as: alleviate symptoms of menopause as hormone replacement therapy, treatment some types of infertility, treatment of some conditions leading to underdevelopment of female sexual characteristics, treatment of vaginal atrophy, treatment of some types of breast cancer (particularly in men and postmenopausal women), treatment of prostate cancer and prevention of osteoporosis. Estropipate is used for the treatment of moderate to severe vasomotor symptoms associated with the monopause, and moderate to severe symptoms of vulval and vaginal atrophy associated with the menopause. It is also used to treat hypoestrogenism due to hypogonadism, castration or primary ovarian failure, and prevent postmenopausal osteoporosis. Estropipate is an estrogenic substance. It acts as naturally produced estrogen does. Estrogens act through binding to nuclear receptors in estrogen-responsive tissues. Circulating estrogens modulate the pituitary secretion of the gonadotropins, luteinizing hormone (LH) and follicle stimulating hormone (FSH), through a negative feedback mechanism. Estrogens act to reduce the elevated levels of these hormones seen in postmenopausal women. Estradiol enters target cells freely (e.g., female organs, breasts, hypothalamus, pituitary) and interacts with a target cell receptor. When the estrogen receptor has bound its ligand it can enter the nucleus of the target cell, and regulate gene transcription which leads to formation of messenger RNA. The mRNA interacts with ribosomes to produce specific proteins that express the effect of estradiol upon the target cell. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary.",,,,Estrone sulfate is approved.,Estrone sulfate is a solid.,True
14364,"Camptothecin is an alkaloid isolated from the stem wood of the Chinese tree, <i>Camptotheca acuminata</i>. This compound selectively inhibits the nuclear enzyme DNA topoisomerase, type I. Several semisynthetic analogs of camptothecin have demonstrated antitumor activity. Investigated for the treatment of cancer. Camptothecin demonstrated strong anticancer activity in preliminary clinical trials but also low solubility and adverse drug reaction. Camptothecin is believed to be a potent topoisomerase inhibitor that interferes with the essential function of topoisomerase in DNA replication. Camptothecin binds to the topoisomerase I and DNA complex resulting in a ternary complex, stabilizing it and preventing DNA re-ligation and therefore causes DNA damage which results in apoptosis.",,,,Camptothecin is experimental.,Camptothecin is a solid.,True
14365,"Iodipamide is a water-soluble radiographic contrast media for cholecystography and intravenous cholangiography. Iodipamide is used as a contrast agent for cholecystography and intravenous cholangiography. Following intravenous administration of Cholografin Meglumine, iodipamide is carried to the liver where it is rapidly secreted. The contrast medium appears in the bile within 10 to 15 minutes after injection, thus permitting visualization of the hepatic and common bile ducts, even in cholecystectomized patients. The biliary ducts are readily visualized within about 25 minutes after administration, except in patients with impaired liver function. The gallbladder begins to fill within an hour after injection; maximum filling is reached after two to two and one-half hours. The contrast medium is finally eliminated in the feces without passing through the enterohepatic circulation, except for approximately 10 percent of the intravenously administered dose which is excreted through the kidneys. Organic iodine compounds block x-rays as they pass through the body, thereby allowing body structures containing iodine to be delineated in contrast to those structures that do not contain iodine. The degree of opacity produced by these iodinated organic compounds is directly proportional to the total amount (concentration and volume) of the iodinated contrast agent in the path of the x-rays. Iodipamide's primary excretion through the hepato-biliary system and concentration in bile allows visualization of the gallbladder and biliary ducts.",The molecular weight is 1139.77.,Iodipamide has a topological polar surface area of 132.8.,The log p value of  is 4.19.,Iodipamide is approved.,Iodipamide is a solid.,True
14366,"Withdrawn from the Canadian, US, and UK markets in 1998 due to genotoxicity.",The molecular weight is 240.21.,Dantron has a topological polar surface area of 74.6.,The log p value of  is 3.74.,Dantron is approved and investigational and withdrawn.,Dantron is a solid.,True
14367,"Zomepirac, formerly marketed as Zomax tablets, was associated with fatal and near-fatal anaphylactoid reactions. The manufacturer voluntarily removed Zomax tablets from the Canadian, US, and UK markets in March 1983. Zomepirac was indicated for the management of mild to severe pain.",The molecular weight is 291.73.,Zomepirac has a topological polar surface area of 59.3.,The log p value of  is 2.95.,Zomepirac is withdrawn.,Zomepirac is a solid.,True
14368,"Dronedarone is a Class III antiarrhythmic drug that works to restore the normal sinus rhythm in patients with paroxysmal or persistent atrial fibrillation. Atrial fibrillation is a common sustained arrhythmia where the treatment primarily focuses on stroke prevention and symptom management. It is managed by rate control, rhythm control, prevention of thromboembolic events, and treatment of the underlying disease. Similar to , dronedarone is a multichannel blocker that works to control rhythm and rate in atrial fibrillation. It meets criteria of all four Vaughan Williams antiarrhythmic drug classes by blocking sodium, potassium, and calcium ion channels and inhibiting β-adrenergic receptors.  Dronedarone is indicated for the management of atrial fibrillation (AF) in patients in sinus rhythm with a history of paroxysmal or persistent AF to reduce the risk of hospitalization. Dronedarone is an antiarrhythmic agent that restores normal sinus rhythm and reduces heart rate in atrial fibrillation. In another model, it prevents ventricular tachycardia and ventricular fibrillation. Dronedarone moderately prolongs the QTc interval by about 10 ms on average. Dronedarone decreases arterial blood pressure and reduces oxygen consumption. It reduces myocardial contractility with no change in left ventricular ejection fraction. Dronedarone vasodilates coronary arteries through activation of the nitric oxide pathway. In clinical studies, dronedarone reduced incidence of hospitalizations for acute coronary syndromes and reduced incidence of stroke. Dronedarone exhibits antiadrenergic effects by reducing alpha-adrenergic blood pressure response to epinephrine and beta 1 and beta 2 responses to isoproterenol.  Atrial fibrillation is the most common type of arrhythmia that is caused by abnormal electrical activity in the atria. In atrial fibrillation, tachyarrhythmia, or fast heart rate, can either be paroxysmal (less than 7 days) or persistent (more than 7 days). Atrial fibrillation causes turbulent and abnormal blood flow through the heart chambers, leading to decreased the effectiveness of the heart to pump blood and an increased likelihood of thrombus formation within the atria which can ultimately dislodge and cause a stroke. ",The molecular weight is 556.76.,Dronedarone has a topological polar surface area of 88.85.,The log p value of  is 8.57.,Dronedarone is approved.,Dronedarone is a solid.,True
14369,"Nebivolol is a racemic mixture of 2 enantiomers where one is a beta adrenergic antagonist and the other acts as a cardiac stimulant without beta adrenergic activity. Treatment with nebivolol leads to a greater decrease in systolic and diastolic blood pressure than , , or. Nebivolol and other beta blockers are generally not first line therapies as many patients are first treated with thiazide diuretics. Nebivolol is indicated to treat hypertension. Nebivolol is a selective beta-1 adrenergic receptor antagonist that decreases vascular resistance, increases stroke volume and cardiac output, and does not negatively affect left ventricular function. It has a long duration of action as effects can be seen 48 hours after stopping the medication and a wide therapeutic window as patients generally take 5-40mg daily. Patients should not abruptly stop taking this medication as this may lead to exacerbation of coronary artery disease. Diabetic patients should monitor their blood glucose levels as beta blockers may mask signs of hypoglycemia. Nebivolol is a highly selective beta-1 adrenergic receptor antagonist with weak beta-2 adrenergic receptor antagonist activity. Blocking beta-1 adrenergic receptors by d-nebivolol leads to decreased resting heart rate, exercise heart rate, myocardial contracility, systolic blood pressure, and diastolic blood pressure. The selectivity of d-nebivolol limits the magnitude of beta blocker adverse effects in the airways or relating to insulin sensitivity. Nebivolol also inhibits aldosterone, and beta-1 antagonism in the juxtaglomerular apparatus also inhibits the release of renin. Decreased aldosterone leads to decreased blood volume, and decreased renin leads to reduced vasoconstriction. l-nebivolol is responsible for beta-3 adrenergic receptor agonist activity that stimulates endothelial nitric oxide synthase, increasing nitric oxide levels; leading to vasodilation, decreased peripheral vascular resistance, increased stroke volume, ejection fraction, and cardiac output. The vasodilation, reduced oxidative stress, and reduced platelet volume and aggregation of nebivolol may lead to benefits in heart failure patients.",The molecular weight is 405.44.,Nebivolol has a topological polar surface area of 70.95.,The log p value of  is 3.5.,Nebivolol is approved and investigational.,Nebivolol is a solid.,True
14370,"Oritavancin is a glycopeptide antibiotic used for the treatment of skin infections. It was developed by The Medicines Company (acquired by Novartis). Oritavancin was initially approved by the FDA in 2014 and formulated to combat resistant Staphylococcus, Streptococcus, and other gram-positive bacteria that cause skin infections. It boasts the option of single-dose administration that has been proven as non-inferior to a full course of therapy. Oritavancin is indicated for the treatment of adult patients with acute bacterial skin and skin structure (including subcutaneous) infection. It is used for confirmed/suspected infections with designated and susceptible gram-positive organisms. Oritavancin interferes with bacterial cell wall synthesis and integrity, treating susceptible skin and subcutaneous tissue infections with gram-positive bacteria. This drug is known to artifically increase INR and aPTT, interfering with coagulation testing. Cases of infusion reactions have also been reported. The cell wall is vital for the survival and replication of bacteria, making it a primary target for antibiotic therapy. Oritavancin works against susceptible gram-positive organisms via three separate mechanisms. Firstly, it binds to the stem peptide of peptidoglycan precursors, inhibiting transglycosylation (polymerization). This process normally occurs during cell wall synthesis. Secondly, oritavancin inhibits crosslinking during bacterial cell wall biosynthesis via binding to cell wall pentaglycyl peptide bridging segments. Finally, this drug also acts by disrupting the bacterial cell membrane, interfering with its integrity, which eventually leads to cell death by various mechanisms.",The molecular weight is 1793.12.,Oritavancin has a topological polar surface area of 560.98.,The log p value of  is 3.59.,Oritavancin is approved and investigational.,Oritavancin is a solid.,True
14371,"Pirfenidone is an orally active small molecule drug that may inhibit collagen synthesis, down regulate production of multiple cytokines and block fibroblast proliferation and stimulation in response to cytokines. Pirfenidone has demonstrated activity in multiple fibrotic conditions, including those of the lung, kidney and liver. It is being investigated by InterMune. For the treatment of idiopathic pulmonary fibrosis (IPF). Pirfenidone is a novel agent with anti-inflammatory, antioxidant, and antifibrotic properties. It may improve lung function and reduce the number of acute exacerbations in patients with idiopathic pulmonary fibrosis (IPF). Although the precise mechanism of action of pirfenidone and its specific molecular targets have yet to be elucidated, the molecule has demonstrated anti-fibrotic, anti-inflammatory, and antioxidant activity. One vital anti-fibrotic mechanism involves suppression of TGF-β1 (transforming growth factor-β1), a key cytokine involved in fibrogenesis and extracellular matrix production. ",The molecular weight is 185.23.,Pirfenidone has a topological polar surface area of 20.31.,The log p value of  is 2.4.,Pirfenidone is approved and investigational.,Pirfenidone is a solid.,True
14372,"Tanespimycin, manufactured by Conforma Therapeutics is under development as a small molecule inhibitor of heat shock protein 90 (HSP90). It is developed for the treatment of several types of cancer, solid tumors or chronic myelogenous leukemia. Investigated for use/treatment in leukemia (myeloid) and solid tumors. Tanespimycin is a small molecule inhibitor of heat shock protein 90 (HSP90). HSP90 is a molecular “chaperone” protein that controls protein shape or conformation, including that of key signaling molecules involved in the growth and survival of tumor cells.",,,,Tanespimycin is investigational.,Tanespimycin is a solid.,True
14373,"Vandetanib is an oral once-daily kinase inhibitor of tumour angiogenesis and tumour cell proliferation with the potential for use in a broad range of tumour types. Vandetanib is currently approved as an alternative to local therapies for both unresectable and disseminated disease. Because Vandetanib can prolong the Q-T interval, it is contraindicated for use in patients with serious cardiac complications such as congenital long QT syndrome and uncompensated heart failure.  Mean IC50 of approximately 2.1 μg/mL. ZD-6474 is a potent and selective inhibitor of VEGFR (vascular endothelial growth factor receptor), EGFR (epidermal growth factor receptor) and RET (REarranged during Transfection) tyrosine kinases. ",The molecular weight is 475.36.,Vandetanib has a topological polar surface area of 59.51.,The log p value of  is 5.69.,Vandetanib is approved.,Vandetanib is a solid.,True
14374,"Iodine is commonly used as an antiseptic for minor cuts and abrasions, preventing infections that may result from contaminated wounds. Additionally, iodine has been studied in the treatment of fibrocystic disease and breast cancer. Investigated for use/treatment in breast disorders (unspecified) and pain (acute or chronic). Molecular iodine is known to inhibit the induction and promotion of N-methyl-n-nitrosourea-induced mammary carcinogenesis, to regress 7,12-dimethylbenz(a)anthracene-induced breast tumors in rats.It has also been shown to have beneficial effects in fibrocystic human breast disease.",The molecular weight is 253.81.,,,Iodine is approved and investigational.,Iodine is a solid.,True
14375,"Telaprevir is a direct acting antiviral medication used as part of combination therapy to treat chronic Hepatitis C, an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Treatment options for chronic Hepatitis C have advanced significantly since 2011, with the development of Direct Acting Antivirals (DAAs) such as Telaprevir. Telaprevir is an inhibitor of NS3/4A, a serine protease enzyme, encoded by HCV genotype 1. These enzymes are essential for viral replication and serve to cleave the virally encoded polyprotein into mature proteins like NS4A, NS4B, NS5A and NS5B. The barrier for develoment of resistance to NS3/4A inhibitors is lower than that of NS5B inhibitors, another class of DAAs. Subtitutions at amino acid positions 155, 156, or 168 are known to confer resistance. The substitutions of the enzyme's catalytic triad consisting of H58, D82, and S139 are also likely to alter the affinity of the drug for NS3/4A or the activity of the enzyme itself. Despite this disadvantage Telaprevir is still effective against HCV when paired with , , and. Telaprevir, when used in combination with , , and is indicated for use in the treatment of chronic HCV genotype 1 infection in adults. Telaprevir is classified as a direct-acting antiviral (DAA) and prevents viral replication in HCV genotype 1.  Telaprevir is a NS3/4a protease inhibitor used to inhibit viral HCV replication. NS3/4a protease is an integral part of viral replication and mediates the cleavage the virally encoded polyprotein to mature proteins (NS4A, NS4B, NS5A and NS5B). Telaprevir inhibits NS3/4A with an IC50 of 10nM.",The molecular weight is 679.86.,Telaprevir has a topological polar surface area of 179.56.,The log p value of  is 5.35.,Telaprevir is approved and withdrawn.,Telaprevir is a solid.,True
14376,"Abiraterone is a derivative of steroidal progesterone and is an innovative drug that offers clinical benefit to patients with hormone refractory prostate cancer. Abiraterone is administered as an acetate salt prodrug because it has a higher bioavailability and less susceptible to hydrolysis than abiraterone itself. FDA approved on April 28, 2011. Used in combination with prednisone for the treatment of metastatic, castration-resistant prostate cancer.  Abiraterone is associated with decreases in PSA levels, tumor shrinkage (as evaluated by RECIST criteria), radiographic regression of bone metastases and improvement in pain. Levels of adrenocorticotropic hormones increased up to 6-fold but this can be suppressed by dexamethasone.  Abiraterone is an orally active inhibitor of the steroidal enzyme CYP17A1 (17 alpha-hydroxylase/C17,20 lyase). It inhibits CYP17A1 in a selective and irreversible manner via covalent binding mechanism. CYP17A1 is an enzyme that catalyzes the biosynthesis of androgen and is highly expressed in testicular, adrenal, and prostatic tumor tissue. More specifically, abiraterone inhibits the conversion of 17-hydroxyprognenolone to dehydroepiandrosterone (DHEA) by the enzyme CYP17A1 to decrease serum levels of testosterone and other androgens. ",,,,Abiraterone is approved.,Abiraterone is a solid.,True
14377,"Cenobamate, or YKP-3089, is an antiepileptic drug developed by SK Pharmaceuticals and used to treat partial onset seizures. The exact mechanism of action has not been described in the literature, though it positively modulates GABA<sub>A</sub> and inhibits voltage gated sodium channels. Cenobamate is indicated for the treatment of partial onset seizures in adults. The mechanism of cenobamate is unknown, however it modulates GABA<sub>A</sub> and inhibit voltage gated sodium channels. Cenobamate is given once daily and so it has a long duration of action. The therapeutic window is wide as doses of 750mg can be well tolerated. Patients should be counselled regarding the risk of DRESS syndrome, QT interval shortening, suicidal behavior, and neurological adverse effects. Cenobamate inhibits voltage gated sodium channels and is a positive GABA<sub>A</sub> modulator. However, the exact mechanism of action remains unknown. Inhibition of voltage gated sodium channels increases the threshold for generating action potentials and decreases the number of action potentials.",,,,Cenobamate is approved and investigational.,Cenobamate is a solid.,True
14378,"Rufinamide is a triazole derivative and an anticonvulsant medication to treat seizure disorders like Lennox-Gastuat syndrome, a form of childhood epilepsy. Clinical trials suggest its efficacy in the treatment of partial seizures. Adjunct therapy for treatment of seizures associated with Lennox-Gastaut syndrome.   At high concentrations will inhibit action of mGluR5 subtype receptors thus preventing the production of glutamate.  Rufinamide is a triazole derivative antiepileptic that prolongs the inactive state of voltage gated sodium channels thus stabilizing membranes, ultimately blocking the spread of partial seizure activity.",The molecular weight is 238.2.,Rufinamide has a topological polar surface area of 73.8.,The log p value of  is 0.51.,Rufinamide is approved.,Rufinamide is a solid.,True
14379,"Prasugrel, a thienopyridine derivative, is a platelet activation and aggregation inhibitor structurally and pharmacologically related to clopidogrel and ticlopidine. Similar to clopidogrel, prasugrel is a prodrug that requires enzymatic transformation in the liver to its active metabolite, R-138727. R-138727 irreversibly binds to P2Y12 type ADP receptors on platelets thus preventing activation of the GPIIb/IIIa receptor complex. As a result, inhibition of ADP-mediated platelet activation and aggregation occurs. Prasugrel was developed by Daiichi Sankyo Co. and is currently marketed in the United States and Canada in cooperation with Eli Lilly and Company for acute coronary syndromes planned for percutaneous coronary intervention (PCI). FDA approved in 2009. Indicated in combination with acetylsalicylic acid (ASA) to prevent atherothrombotic events in patients with acute coronary syndrome (ACS) who are to be managed with percutaneous coronary intervention (PCI). May be used in patients with unstable angina (UA), non-ST elevation myocardial infarction (NSTEMI), ST-elevation myocardial infarction (STEMI) who are to be managed with PCI. Prasugrel is not recommended in patients 75 years of age or greater, those that weigh<60kg, and patients with a history of stroke or transient ischemic attack due to increased risk of fatal and intracranial bleeding.  Prasugrel is a thienopyridine ADP receptor inhibitors which inhibits platelet aggregation by irreversibly binding to P2Y12 receptors. Prasugrel is an thienopyridine and a prodrug which inhibits ADP receptors by irreversibly acting on the P2Y12 receptor on platelets. The active metabolite of prasugrel prevents binding of adenosine diphosphate (ADP) to its platelet receptor, impairing the ADP-mediated activation of the glycoprotein GPIIb/IIIa complex. Prasugrel is proposed to have a similar mechanism of action to clopidogrel.",The molecular weight is 373.44.,Prasugrel has a topological polar surface area of 46.61.,The log p value of  is 3.43.,Prasugrel is approved.,Prasugrel is a solid.,True
14380,"Developed by Schering-Plough after its merger with Organon International, asenapine is a sublingually administered, atypical antipsychotic for treatment of schizophrenia and acute mania associated with bipolar disorder. Asenapine also belongs to the dibenzo-oxepino pyrrole class. It is also for severe post-traumatic stress disorder nightmares in soldiers as an off-label use. FDA approved on August 13, 2009. Used for treatment in psychosis, schizophrenia and schizoaffective disorders, manic disorders, and bipolar disorders as monotherapy or in combination. Asenapine is a serotonin, dopamine, noradrenaline, and histamine antagonist in which asenapine possess more potent activity with serotonin receptors than dopamine. Sedation in patients is associated with asenapine's antagonist activity at histamine receptors. Its lower incidence of extrapyramidal effects are associated with the upregulation of D1 receptors. This upregulation occurs due to asenapine's dose-dependent effects on glutamate transmission in the brain. It does not have any significant activity with muscarinic, cholinergic receptors therefore symptoms associated with anticholinergic drug activity like dry mouth or constipation are not expected to be observed. Asenapine has a higher affinity for all aforementioned receptors compared to first-generation and second-generation antipsychotics except for 5-HT1A and 5-HT1B receptors.  Asenapine is an atypical antipsychotic multireceptor neuroleptic drug which shows strong 5HT2A (serotonin) and D2 (dopamine) receptor antagonism, which has been shown to enhance dopamine (DA) and acetylcholine (Ach) efflux in rat brains. Asenapine may improve cognitive function and negative symptoms in patients with schizophrenia. ",The molecular weight is 285.77.,Asenapine has a topological polar surface area of 12.47.,The log p value of  is 4.58.,Asenapine is approved.,Asenapine is a solid.,True
14381,"Levocetirizine is a selective histamine H<sub>1</sub> antagonist used to treat a variety of allergic symptoms. It is the R enantiomer of. Levocetirizine has greater affinity for the histamine H<sub>1</sub> receptor than cetirizine. Levocetirizine is indicated to treat symptoms of perennial allergic rhinitis and uncomplicated skin manifestations of chronic idiopathic urticaria. It is also used over the counter for a variety of mild allergy symptoms. Levocetirizine is a second generation histamine H<sub>1</sub> antagonist used to treat various allergic symptoms. It has a long duration of action as it is generally taken once daily, and a wide therapeutic window as animal studies show the maximal nonlethal dose is over 100x a normal dose. Patients are cautioned to avoid tasks that require complete alertness, avoid alertness, and use caution in patients with factors predisposing urinary retention. Levocetirizine selectively inhibits histamine H<sub>1</sub> receptors. This action prevents histamine from activating this receptor and causing effects like smooth muscle contraction, increased permeability of vascular endothelium, histidine uptake in basophils, stimulation of cough receptors, and stimulation of flare responses in the nervous system.",The molecular weight is 388.89.,Levocetirizine has a topological polar surface area of 53.01.,The log p value of  is 2.08.,Levocetirizine is approved.,Levocetirizine is a solid.,True
14382,"Simeprevir is a hepatitis C virus (HCV) NS3/4A protease inhibitor indicated in patient's with HCV genotype 1 for the treatment of chronic hepatitis C virus (HCV) infection. HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Like all NS3/4A inhibitors, simeprevir is a serine protease inhibitor in similarity to and but is classified as a second generation protease inhibitor. This class of antiviral drugs were the first direct acting antivirals approved but are associated with lower cure rates than newer drugs. Broad use of simeprevir occurred when it was used in combination with a newer drug,. Inhibiting HCV NS3/4A protease in a potent and highly specific manner, simeprevir is a direct-acting antiviral agent against the hepatitis C virus. Since the viral protease NS3/4A complex is essential for cleaving the HCV encoded polyprotein into individual viral proteins facilitating replication , the drug blocks the viral replication process. It is shown to display synergistic effects with interferon-α and HCV NS5B inhibitor, and additive effects with ribavirin in HCV replicon cells. Unlike first generation serine protease inhibitors, simprevir has a sightly different resistance profile where limited therapeutic efficacy of the drug is observed with NS3 Q80K polymorphic variants and simeprevir-specific amino acid position of 168 also results in higher treatment failure rates. The observed prevalence of the N3 Q80K polymorphism was 30% in subjects infected with HCV genotype 1a and 0.5% in subjects infected with HCV genotype 1b.  Indicated for the treatment of adults with chronic hepatitis C virus (HCV) infection: typically in combination with sofosbuvir in patients with HCV genotype 1 without cirrhosis or with compensated cirrhosis and in combination with peginterferon alfa (Peg-IFN-alfa) and ribavirin (RBV) in patients with HCV genotype 1 or 4 without cirrhosis or with compensated cirrhosis.  Simeprevir is a direct-acting antiviral agent and inhibitor for HCV NS3/4A protease, which is an important enzyme required for viral replication. Unlike and , simeprevir is a competitive, reversible, macrocyclic, noncovalent inhibitor. The macromolecular cyclic portion of the molecule improves the affnity and selectivity characteristics, which allows rapid association and slow dissociation to the protein target through noncovalent binding.  Simeprevir is accumulated in the liver after uptake into hepatocytes via OATP1B1/3. NS3/4A heterodimeric complex is composed of the cofactor N4A subunit and N3 subunit which contains the proteolytic site. The NS3/4A protease cleaves the HCV polyprotein downstream of the NS3 site, generating non-structural viral proteins NS3, NS4A, NS4B, NS5A and NS5A and subsequently formation of mature proteins. Simeprevir exerts an inhibitory action on HCV polyprotein cleavage via induced-fit binding to an extended S2 subsite located in the NS3 catalytic site. NS3/4A inhibitors usually depend on few interactions located in the substrate binding groove of the viral serine protease, thus are susceptible to resistance and failed treatment from few critical mutations in these sites. ",The molecular weight is 749.94.,Simeprevir has a topological polar surface area of 156.89.,The log p value of  is 5.3.,Simeprevir is approved.,Simeprevir is a solid.,True
14383,"Oxymetholone is a synthetic anabolic steroid marketed under the brand name Anapolon by Hoffmann La Roche Limitedand used in the treatment of osteoporosis, anaemia, and as an agent to stimulate muscle growth in malnourished or underdeveloped patients. Anabolic-androgenic steroids (AAS), such as oxymetholone, have been abused by bodybuilders and athletes. The uncontrolled misuse of oxymetholone can lead to a large variety of detrimental effects, the most often reported of which are cardiovascular events. In 2009, no producers of oxymetholone were identified worldwide (SRI 2009), but it was available from 14 suppliers, including 8 U.S. suppliers (ChemSources 2009). Indicated in the treatment of anemias caused by deficient red cell production. Acquired aplastic anemia, congenital aplastic anemia, myelofibrosis and the hypoplastic anemias due to the administration of myelotoxic drugs often respond. Oxymetholone should not replace other supportive measures such as transfusion, correction of iron, folic acid, vitamin B12 or pyridoxine deficiency, antibacterial therapy and the appropriate use of corticosteroids.  Oxymethalone is a 17 alpha-alkylated anabolic-androgenic steroid and a synthetic derivative of testosterone, whose anabolic effects are used to treat muscle wasting in HIV patients. The effects of testosterone in humans and other vertebrates occur by way of two main mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors. Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5α-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5α-reductase. DHT binds to the same androgen receptor even more strongly than T, so that its androgenic potency is about 2.5 times that of T. The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.",The molecular weight is 332.48.,Oxymetholone has a topological polar surface area of 57.53.,The log p value of  is 4.14.,Oxymetholone is approved and illicit.,Oxymetholone is a solid.,True
14384,"Prucalopride is a dihydrobenzofurancarboxamide derivative from the benzofurane family that selectively stimulates 5-HT4 receptors and thus, it presents enterokinetic properties. The high selectivity of prucalopride allowed further development as it prevented the cardiac adverse reactions observed due to non-target effects of precedent therapies. Prucalopride was developed by Shire Development LLC and approved for use in Europe in 2009, in Canada on December 7, 2011 and by the FDA on December 17, 2018. Prucalopride is indicated for the treatment of chronic idiopathic constipation (CIC) in adults. In animal studies, prucalopride induced a dose-dependent stimulation of contractile activity in the proximal colon and inhibition of the contractility in the distal colon. As well it has been shown that prucalopride stimulates and amplifies giant migratory contraction which is the high-amplitude type of contraction that initiates the urge to defecate. Thus, prucalopride not only accelerates the colonic transit but also accelerates gastric emptying and small bowel transit.  Prucalopride acts as a selective stimulator of the 5-HT4 receptors while having no interaction with hERG channel or 5-HT1 receptors which reduces significantly the cardiovascular risk found in other similar drugs.",The molecular weight is 367.87.,Prucalopride has a topological polar surface area of 76.82.,The log p value of  is 1.41.,Prucalopride is approved.,Prucalopride is a solid.,True
14385,"Victoza contains liraglutide, a synthetic analog of human glucagon-like peptide-1(GLP-1) and acts as a GLP-1 receptor agonist. Liraglutide is 97% homologous to native human GLP-1 by substituting arginine for lysine at position 34. Liraglutide is made by attaching a C-16 fatty acid (palmitic acid) with a glutamic acid spacer on the remaining lysine residue at position 26 of the peptide precursor. Liraglutide was granted FDA approval on Januray 25, 2010. Liraglutide is indicated in combination with diet and exercise to improve glycemic control in patients 10 years and older with type 2 diabetes mellitus. It is also indicated to reduce the risk of major adverse cardiovascular events in patients with type 2 diabetes mellitus as well as cardiovascular disease. Liraglutide is a once-daily GLP-1 derivative for the treatment of type 2 diabetes. The prolonged action of liraglutide is achieved by attaching a fatty acid molecule at position 26 of the GLP-1 molecule, enabling it to bind reversibly to albumin within the subcutaneous tissue and bloodstream and be released slowly over time. Binding with albumin results in slower degradation and reduced elimination of liraglutide from the circulation by the kidneys compared to GLP-1. The effect of liraglutide is the increased secretion of insulin and decreased secretion of glucagon in response to glucose as well as slower gastric emptying. Liraglutide also does not adversely affect glucagon secretion in response to low blood sugar. Liraglutide is an acylated synthetic glucagon-like peptide-1 analog. Liraglutide is an agonist of the glucagon-like peptide-1 receptor which is coupled to adenylate cyclase. The increase in cyclic AMP stimulates the glucose dependant release of insulin, inhibits the glucose dependant release of glucagon, and slows gastric emptying to increase control of blood sugar.",The molecular weight is 3751.26.,Liraglutide has a topological polar surface area of 1513.76.,,Liraglutide is approved.,Liraglutide is a solid.,True
14386,"Gadofosveset trisodium is an intravenous contrast agent used with magnetic resonance angiography(MRA), which is a non-invasive way of imaging blood vessels. The agent allows for the vascular system to be imaged more clearly by the MRA. In this way, gadofosveset trisodium is used to help diagnose certain disorders of the heart and blood vessels. Gadofosveset trisodium is indicated for use as a contrast agent in magnetic resonance angiography (MRA) to evaluate aortoiliac occlusive disease (AIOD) in adults with known or suspected peripheral vascular disease. Gadofosveset causes signal enhancement by shortening the T1 of water molecules that interact with it. The contrast agent complex's rotation rate is the primary factor determining the magnitude of relaxation enhancement. This relaxation enhancement increase only occurs when bound to human serum albumin.  Gadofosveset binds reversibly to endogenous serum albumin resulting in longer vascular residence time than non-protein binding contrast agents. The binding to serum albumin also increases the magnetic resonance relaxivity of gadofosveset and decreases the relaxation time (Tl) of water protons resulting in an increase in signal intensity (brightness) of blood.",,,,Gadofosveset trisodium is approved.,Gadofosveset trisodium is a solid.,True
14387,"A synthetic anabolic steroid used for treating men with testosterone deficiency or similar androgen replacement therapies. Also, has antineoplastic properties and so has been used secondarily in women with advanced breast cancer. Methyltestosterone is a schedule III drug in the US. Methyltestosterone is an anabolic steroid hormone used to treat men with a testosterone deficiency. It is also used in women to treat breast cancer, breast pain, swelling due to pregnancy, and with the addition of estrogen it can treat symptoms of menopause. Testosterone is a steroid hormone from the androgen group. Testosterone is primarily secreted from the testes of males. In females, it is produced in the ovaries, adrenal glands and by conversion of adrostenedione in the periphery. It is the principal male sex hormone and an anabolic steroid. In both males and females, it plays key roles in health and well-being. Examples include enhanced libido, energy, immune function, and protection against osteoporosis. On average, the adult male body produces about twenty times the amount of testosterone than an adult female's body does. The effects of testosterone in humans and other vertebrates occur by way of two main mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors. Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5&alpha;-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5&alpha;-reductase. DHT binds to the same androgen receptor even more strongly than T, so that its androgenic potency is about 2.5 times that of T. The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.",The molecular weight is 302.46.,Methyltestosterone has a topological polar surface area of 37.3.,The log p value of  is 3.93.,Methyltestosterone is approved.,Methyltestosterone is a solid.,True
14388,"Fospropofol is a water soluble prodrug and is converted to propofol in the liver. Fospropofol is a short acting hypnotic/sedative/anesthetic agent. Unlike propofol, does not cause injection-site pain as it is unable to activate TRPA1. FDA approved in December 2008. For monitored anaesthesia care sedation in patients undergoing diagnostic procedures like bronchoscopy and colonscopy or minor surgical procedures like arthroscopy and bunionectomy.  Fospropofol is a prodrug of propofol, a sedative hypnotic drug. Unlike propofol, fospropofol is water soluble and can be administered in an aqueous solution. 1.86 mg of fospropofol is the molar equivalent for 1mg of propofol.  After in-vivo conversion of fospropofol into propofol by endothelial alkaline phosphatase, propofol crosses the blood-brain barrier, binds to GABA-A receptors and acts as an agonist. By binding to GABA-A receptor, it will cause an increase in chloride conductance, thus inhibiting the firing of new action potentials in the post-synaptic neuron. ",The molecular weight is 288.28.,Fospropofol has a topological polar surface area of 75.99.,The log p value of  is 2.13.,Fospropofol is approved and illicit and investigational.,Fospropofol is a solid.,True
14389,"Mangafodipir is a contrast agent used as a diagnostic tool administered intravenously to enhance contrast in magnetic resonance imaging (MRI) of the liver and pancreas. This drug is made up of paramagnetic manganese (II) ions combined with the chelating agent _fodipir_ (dipyridoxyl diphosphate, DPDP). Manganese absorption into the tissues that makes the normal tissue appear brighter in MRI is limited in abnormal or cancerous tissue. Enhanced contrast by mangafodipir improves visualization and detection of lesions of the liver formed from metastatic disease or hepatocellular carcinomas. The contrast agent is present as mangafodipir trisodium marketed under the name Teslascan. Teslascan has been removed from the Drug Product List by FDA in 2003, and withdrawn from the European market in 2012. Indicated for use as an organ-specific paramagnetic contrast agent developed for imaging of the hepatobiliary system and detecting lesions in liver and pancreas. Manganese (II) metals exhibit paramagnetic properties that increases contrast between normal liver parenchyma and metastatic liver lesions after uptake into the hepatic or pancreatic parencyma. They serve to increase the signal intensity of liver or pancreas tissue. Enhancement in both organs is near maximal for up to approximately 4 hours after the end of administration. Lesion-related enhancement of certain types of lesions, such as liver metastases and hepatocellular carcinomas, may be detectable for up to 24 hours. After intravenous administration, the chelate dissociates slowly to manganese and organic ligand fodipir (dipyridoxyl diphosphate), and manganese is taken up by the hepatocytes with high affinity and selectivity. The ligand fodipir is distributed to the extracellular fluid and later eliminated via urine. Mangafodipir shortens the longitudinal relaxation time (T1) of targeted tissues during MRI, where signal intensity or brightness is increased in normal liver parenchyma. Overall, there is increased contrast between normal tissue and abnormal tissue with lesions because there is a difference between cellular compositions , and manganese uptake in metastatic tissue or focal lesions is minimal or nearly absent.",The molecular weight is 691.38.,,,Mangafodipir is approved and investigational and withdrawn.,Mangafodipir is a solid.,True
14390,,The molecular weight is 300.36.,Azapropazone has a topological polar surface area of 56.22.,The log p value of  is 1.78.,Azapropazone is withdrawn.,Azapropazone is a solid.,False
14391,,,,,3-CARBOXY-4-METHYL-5-PROPYL-2-FURANPROPIONIC is experimental.,3-CARBOXY-4-METHYL-5-PROPYL-2-FURANPROPIONIC is a solid.,False
14392,"Chloramphenicol succinate is an ester prodrug of. Chloramphenicol is a bacteriostatic antibiotic. Use of chloramphenicol succinate and chloramphenicol has decreased due to the risk of potentially fatal blood dyscrasias. Chloramphenicol succinate is indicated to treat serious and susceptible bacterial infections where less dangerous drugs are ineffective or contraindicated. Chloramphenicol succinate is a prodrug of chloramphenicol, which binds to bacterial ribosomes and prevents translation. It has a narrow therapeutic index and a moderate duration of action. Patients should be counselled regarding the risk of serious fatal blood dyscrasias. Chloramphenicol succinate is hydrolyzed into the active chloramphenicol. Chloramphenicol resembles uridine-5'-phosphate. It binds to the residues A2451 and A2452 in the 23S rRNA of the 50S ribosomal subunit of _E. coli_, which prevents translation.",,,,Chloramphenicol succinate is approved.,Chloramphenicol succinate is a solid.,True
14393,,,,,Indoxyl sulfate is experimental.,Indoxyl sulfate is a solid.,False
14394,,,,,Myristic acid is experimental.,Myristic acid is a solid.,False
14395,Warfarin consists of a racemic mixture of two active enantiomers—R- and S- forms—each of which is cleared by different pathways. S-warfarin is 2-5 times more potent than the R-isomer in producing an anticoagulant response.,,,,(R)-warfarin is experimental.,(R)-warfarin is a solid.,True
14396,,,,,"R,S-Warfarin alcohol is experimental.","R,S-Warfarin alcohol is a solid.",False
14397,,,,,"S,R-Warfarin alcohol is experimental.","S,R-Warfarin alcohol is a solid.",False
14398,"Triflusal is a 2-acetoxy-4-trifluoromethylbenzoic acid and it is an aspirin chemically-related molecule but not a derivative. The benefits of this agent are the lack of action over the arachidonic acid pathway, the driven production of nitric oxide and the increase of cyclic nucleotide concentration on endothelial cells. The latest translates into the expansion of peripheral blood vessels. It is very important as a secondary prevention of ischemic stroke by offering a lower risk of bleeding. It was developed by J. Uriach and Company and even though it is commercialized in different countries it is not approved by the FDA, EMA or HealthCanada. Triflusal is indicated as prophylaxis of thromboembolic disorders. It has been registered in Spain and in other countries of Europe, South America and South Korea for the prevention of Stroke and myocardial infarction. Triflusal is an antithrombotic anticoagulant. It irreversibly inhibits the production of thromboxane-B2 in platelets by acetylating cycloxygenase-1. Triflusal affects many other targets such as NF kappa B, which is a gene expression regulatory factor for cycloxygenase-a and cytokines. Numerous studies comparing the efficacy and safety profile (i.e. systemic hemorrhage) between triflusal and acetylsalsylic acid has shown either no significant difference or a better effacy and safety profile for triflusal. Triflusal has been shown to protect cerebral tissue due to its inhibition of lipid peroxidation resulting from anoxia-reoxygenation. Triflusal is chemically related to acetylsalicylic acid (ASA) and irreversibly inhibits cycloxygenase-1 (COX-1) in platelets. Acetylation of the active group of COX-1 prevents the formation of thromboxane-B2 in platelets. However, it is unique because it spares the arachidonic acid metabolic pathway in endothelial cells. In addition, it favors the production of nitric oxide, a vasodilator.",The molecular weight is 248.16.,Triflusal has a topological polar surface area of 63.6.,The log p value of  is 2.06.,Triflusal is approved and investigational.,Triflusal is a solid.,True
14399,"Ticagrelor, or AZD6140, was first described in the literature in 2003. Ticagrelor is an ADP derivative developed for its P2Y<sub>12</sub> receptor antagonism. Unlike , ticagrelor is not a prodrug. It is marketed by Astra Zeneca as Brilinta in the US and Brilique or Possia in the EU,. Ticagrelor is indicated to reduce the risk of cardiovascular death, myocardial infarction, and stroke in patients with acute coronary syndrome or a history of myocardial infarction. Ticagrelor is also indicated to reduce the risk of a first myocardial infarction or stroke in high risk patients with coronary artery disease. Ticagrelor is a P2Y<sub>12</sub> receptor antagonist that inhibits the formation of thromboses to reduce the risk of myocardial infarction and ischemic stroke. It has a moderate duration of action as it is given twice daily, and a wide therapeutic index as high single doses are well tolerated. Patients should be counselled regarding the risk of bleeding, dyspnea, and bradyarrhythmias. Ticagrelor is a P2Y<sub>12</sub> receptor antagonist.",The molecular weight is 522.57.,Ticagrelor has a topological polar surface area of 138.44.,The log p value of  is 2.55.,Ticagrelor is approved.,Ticagrelor is a solid.,True
14400,"Ivacaftor (also known as Kalydeco or VX-770) is a drug used for the management of Cystic Fibrosis (CF). It is manufactured and distributed by Vertex Pharmaceuticals. It was approved by the Food and Drug Administration on January 31, 2012, and by Health Canada in late 2012. Ivacaftor is administered as a monotherapy and also administered in combination with other drugs for the management of CF. When used as monotherapy as the product Kalydeco, ivacaftor is indicated for the management of CF in patients age 2 years and older who have a mutation in the CFTR gene that is responsive to ivacaftor potentiation. Ivacaftor received expanded approval in May 2017 for the following 33 CFTR mutations: E56K, P67L, R74W, D110E, D110H, R117C, R117H, G178R, E193K, L206W, R347H, R352Q, A455E, S549N, S549R, G551D, G551S, D579G, S945L, S977F, F1052V, K1060T, A1067T, G1069R, R1070Q, R1070W, F1074L, D1152H, G1244E, S1251N, S1255P, D1270N, and G1349D. The use of Ivacaftor has been shown to both improve CF symptoms and modulate underlying disease pathology. This is achieved by potentiating the channel opening probability (or gating) of CFTR protein in patients with impaired gating mechanisms. This is in contrast to , another CF medication, that functions by preventing misfolding of the CFTR protein and thereby results in increased processing and trafficking of mature protein to the cell surface.  A wide variety of CFTR mutations correlate to the Cystic Fibrosis phenotype and are associated with differing levels of disease severity. The most common mutation, affecting approximately 70% of patients with CF worldwide, is known as F508del-CFTR or delta-F508 (ΔF508), in which a deletion in the amino acid phenylalanine at position 508 results in impaired production of the CFTR protein, thereby causing a significant reduction in the amount of ion transporter present on cell membranes. Ivacaftor as monotherapy has failed to show a benefit for patients with delta-F508 mutations, most likely due to an insufficient amount of protein available at the cell membrane for interaction and potentiation by the drug. The next most common mutation, G551D, affecting 4-5% of CF patients worldwide is characterized as a missense mutation, whereby there is sufficient amount of protein at the cell surface, but opening and closing mechanisms of the channel are altered. Ivacaftor is indicated for the management of CF in patients with this second type of mutation, as it binds to and potentiates the channel opening ability of CFTR proteins on the cell membrane.",The molecular weight is 392.5.,Ivacaftor has a topological polar surface area of 78.43.,The log p value of  is 3.82.,Ivacaftor is approved.,Ivacaftor is a solid.,True
14401,"Vismodegib inhibits the hedgehog signalling pathway and is indicated for treatment of adult basal cell carcinoma. FDA approved on Jan 30, 2012. Vismodegib is used for treating locally advanced or metastatic basal cell carcinoma in patients whose carcinoma has recurred after surgery, and in patients who are not candidates for surgery or radiation. Vismodegib selectively binds to and inhibits the transmembrane protein Smoothened homologue (SMO) to inhibit the Hedgehog signalling pathway.  Mutations of the Hedgehog pathway may results in uncontrolled proliferation of skin basal cells. Vismodegib binds to and inhibits the transmembrane protein Smoothened homologue (SMO) to inhibit the Hedgehog signalling pathway. ",The molecular weight is 421.29.,Vismodegib has a topological polar surface area of 76.13.,The log p value of  is 2.74.,Vismodegib is approved and investigational.,Vismodegib is a solid.,True
14402,"Pitavastatin, also known as the brand name product Livalo, is a lipid-lowering drug belonging to the statin class of medications. By inhibiting the endogenous production of cholesterol within the liver, statins lower abnormal cholesterol and lipid levels and ultimately reduce the risk of cardiovascular disease. More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) Reductase, which catalyzes the conversion of HMG-CoA to mevalonic acid. This is the third step in a sequence of metabolic reactions involved in the production of several compounds involved in lipid metabolism and transport including cholesterol, low-density lipoprotein (LDL) (sometimes referred to as \bad cholesterol\""), and very low-density lipoprotein (VLDL). Prescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD, such as those with Type 2 Diabetes. The clear evidence of the benefit of statin use coupled with very minimal side effects or long term effects has resulted in this class becoming one of the most widely prescribed medications in North America."" Pitavastatin is indicated for the treatment of adult patients with primary hyperlipidemia or mixed dyslipidemia to reduce elevated total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), apolipoprotein B (Apo B), triglycerides (TG), and to increase high-density lipoprotein cholesterol (HDL-C). It is also indicated for the treatment of pediatric patients aged 8 years and older with heterozygous familial hypercholesterolemia (HeFH) to reduce elevated TC, LDL-C, and Apo B. Pitavastatin is an oral antilipemic agent which inhibits HMG-CoA reductase. It is used to lower total cholesterol, low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apoB), non-high density lipoprotein-cholesterol (non-HDL-C), and trigleride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease and high ratios are associated with higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, rosuvastatin reduces the risk of cardiovascular morbidity and mortality. Pitavastatin is a statin medication and a competitive inhibitor of the enzyme HMG-CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis. Pitavastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low density lipoprotein (LDL) receptors which increase hepatic uptake of LDL, thereby reducing circulating LDL-C levels. ",The molecular weight is 421.47.,Pitavastatin has a topological polar surface area of 90.65.,The log p value of  is 3.59.,Pitavastatin is approved.,Pitavastatin is a solid.,True
14403,"Rilpivirine is non-nucleoside reverse transcriptase inhibitor (NNRTI) which is used for the treatment of HIV-1 infections in treatment-naive patients. It is a diarylpyrimidine derivative, a class of molecules that resemble pyrimidine nucleotides found in DNA. The internal conformational flexibility of rilpivirine and the plasticity of it interacting binding site gives it a very high potency and an unlikely generation of resistance compared to other NNRTI's. Rilpivirine was developed by Tilbotec, Inc. and FDA approved on May 20, 2011. On November 21, 2017, Rilpivirine, in combination with dolutegravir, was approved as part of the first complete treatment regimen with only two drugs for the treatment of adults with HIV-1 named Juluca. Rilpivirine, in combination with other agents, is indicated for the treatment of HIV-1 infections in antiretroviral treatment-naive patients with HIV-1 RNA ≤100,000 copies/mL and CD4+ cell count >200 cells/mm3. The FDA combination therapy approval of rilpivirine and dolutegravir is indicated for adults with HIV-1 infections whose virus is currently suppressed (< 50 copies/ml) on a stable regimen for at least six months, without history of treatment failure and no known substitutions associated to resistance to any of the two components of the therapy. Ripivirine treatment produces a significant and effective reduction in the viral load based on the study of HIV-1 RNA copies per ml or immunologic changes by the determination of counts of CD4+ and CD8+ cells. The combinantion therapy (ripivirine and dolutegravir) presented the same viral supression found in previous three-drug therapies without integrase strand transfer inhibitor mutations or rilpivirine resistance. Rilpivirine is a non-competitive NNRTI that binds to reverse transcriptase. Its binding results in the blockage of RNA and DNA- dependent DNA polymerase activities, like HIV-1 replication. It does not present activity against human DNA polymerases α, β and γ. Rilpivirine binds to the HIV-1 reverse transcriptase (RT) and its flexible structure around the aromatic rings allows the adaptation to changes in the non-nucleoside RT binding pocket.",The molecular weight is 366.43.,Rilpivirine has a topological polar surface area of 97.42.,The log p value of  is 5.45.,Rilpivirine is approved.,Rilpivirine is a solid.,True
14404,"Ulipristal is a selective progesterone receptor modulator used for the purposes of emergency contraception (Ella) and for the treatment of uterine fibroids (Fibristal). It is a derivative of 19-norprogesterone and has both antagonistic and partial agonist activity at the progesterone receptor. It also binds to glucocorticoid receptor, however compared to mifepristone (a progesterone receptor antagonist), ulipristal is more tolerable and has lower glucocorticoid activity and better binding affinity.  As the product Ella (available in Canada and the US), ulipristal is indicated for use as emergency contraception after unprotected intercourse or possible contraceptive failure when administered within 120 hours (5 days) after unprotected intercourse or a known or suspected contraceptive failure. As the product Fibristal (available in Canada), ulipristal is indicated for treatment of the signs and symptoms of uterine fibroids in adult women. Ulipristal is a selective, reversible progestin receptor modulator and its tissue targets include the uterus, cervix, ovaries, and hypothalamus. Ulipristal may act as an agonist or antagonist in the presence or absence of progesterone based on the tissue target. If given mid-follicular phase, development of the follicle growth is delayed and estradiol concentrations decrease. If given at the time when luteinizing hormone peaks, follicular rapture is delayed by several days. If given early-luteal phase, a decrease in endometrial thickness can be observed.  The exact mechanism of action of ulipristal has been heavily debated. On one hand, the majority of official prescribing information labels, monographs, and prior research studies for ulipristal indicated as an emergency contraceptive suggest that its primary mechanism of action revolves around inhibiting or delaying ovulation by suppressing surges in LH that result in the postponement of follicular rupture.",,,,Ulipristal is approved.,Ulipristal is a solid.,True
14405,"Vemurafenib is a competitive kinase inhibitor with activity against BRAF kinase with mutations like V600E. It exerts its function by binding to the ATP-binding domain of the mutant BRAF. Vemurafenib was co-developed by Roche and Plexxikon and it obtained its FDA approval on August 17, 2011, under the company Hoffmann La Roche. After approval, Roche in collaboration with Genentech launched a broad development program.  Vemurafenib is approved since 2011 for the treatment of metastatic melanoma with a mutation on BRAF in the valine located in the exon 15 at codon 600, this mutation is denominated as V600E. The V600E mutation, a substitution of glutamic acid for valine, accounts for 54% of the cases of cutaneous melanoma.  BRAF activation results in cell growth, proliferation, and metastasis. BRAF is an intermediary molecule in MAPK whose activation depends on ERK activation, elevation of cyclin D1 and cellular proliferation. The mutation V600E produces a constitutively form of BRAF. Vemurafenib has been shown to reduce all activation markers related to BRAF; in clinical trials, vemurafenib treatment showed a reduction of cytoplasmic phosphorylated ERK and a cell proliferation driven by Ki-67. Studies also reported decrease in MAPK-related metabolic activity. All the different reports indicate thet Vemurafenib generates an almost complete inhibition of the MAPK pathway.  Vemurafenib is an orally available inhibitor of mutated BRAF-serine-threonine kinase. Vemurafenif is a small molecule that interacts as a competitive inhibitor of the mutated species of BRAF. It is especially potent against the BRAF V600E mutation. Vemurafenib blocks downstream processes to inhibit tumour growth and eventually trigger apoptosis. Vemurafenib does not have antitumour effects against melanoma cell lines with the wild-type BRAF mutation.",The molecular weight is 489.92.,Vemurafenib has a topological polar surface area of 91.92.,The log p value of  is 4.17.,Vemurafenib is approved.,Vemurafenib is a solid.,True
14406,"Mirabegron is a beta-3 adrenergic receptor agonist for the management of overactive bladder. It is an alternative to antimuscarinic drugs for this indication. FDA approved on June 28, 2012. Mirabegron is a beta-3 adrenergic agonist indicated for the treatment of overactive bladder (OAB) with symptoms of urge urinary incontinence, urgency, and urinary frequency. Mirabegron has little effect on the mean maximum flow rate or mean detrusor pressure at maximum flow rate in patients with lower urinary tract symptoms and bladder outlet obstruction. Furthermore, mirabegron increases blood pressure in a dose dependent manner. However, this effect is reversible when mirabegron is discontinued. Mirabegron also increases heart rate in a dose dependent manner. The dose in which half-maximal efficacy is demonstrated is 25 mg. Comparatively, the dose in which maximal efficacy is demonstrated is 100 mg.  Mirabegron is a potent and selective agonist for beta-3 adrenergic receptors. Once beta-3 receptors are activated, the detrusor smooth muscle relaxes to allow for a larger bladder capacity. At higher doses (200 mg), there is a potential for mirabegron to activate beta-1 and beta-2 adrenergic receptors. ",The molecular weight is 396.51.,Mirabegron has a topological polar surface area of 100.27.,The log p value of  is 1.32.,Mirabegron is approved.,Mirabegron is a solid.,True
14407,"Tofacitinib is an inhibitor of Janus kinases, a group of intracellular enzymes involved in signalling pathways that affect hematopoiesis and immune cell function. It is approved by the FDA for treatment of moderate to severe rheumatoid arthritis that responds inadequately to methotrexate or in those who are intolerant to methotrexate.  For the treatment of moderate to severe rheumatoid arthritis which is resistant or intolerant to methotrexate therapy. It may also be used as an adjunct to methotrexate therapy, or other non-biologic disease-modifying antirheumatic drugs (DMARDS), when methotrexate alone is not sufficient.  Tofacitinib targets inflammation present in rheumatoid arthritis by inhibiting the janus kinases involved in the inflammatory response pathway.  Rheumatoid arthritis is an autoimmune disease characterized by a dysregulation of pro-inflammatory cytokines including IL7, IL15, IL21, IL6, IFN-alpha, and IFN-beta. (3) Cytokines signalling results in tissue inflammation and joint damage by stimulating the recruitment and activation of immune cells via the janus kinase signalling pathway.",The molecular weight is 312.38.,Tofacitinib has a topological polar surface area of 88.91.,The log p value of  is 1.55.,Tofacitinib is approved and investigational.,Tofacitinib is a solid.,True
14408,"Enzalutamide is an androgen receptor inhibitor for the treatment of castration-resistant prostate cancer. FDA approved on August 31, 2012. Enzalutamide is indicated for the treatment of patients with metastatic castration-resistant prostate cancer who have previously received docetaxel. Resitance to enzalutamide therapy has been observed. This may occurred due to an upregulation of NF-κB2/p52.  Enzalutamide is a competitive androgen receptor inhibitor that effects multiple stages of the signalling pathway. It is able to inhibit androgen binding to its receptor, androgen receptor nuclear translocation, and subsequent interaction with DNA. As a result, proliferation of prostate cancer cells decreases which ultimately leads to apoptosis and decreased tumour volume. ",The molecular weight is 464.44.,Enzalutamide has a topological polar surface area of 76.44.,The log p value of  is 3.35.,Enzalutamide is approved.,Enzalutamide is a solid.,True
14409,"Riociguat is a soluble guanylate cyclase (sGC) agonist approved in the USA, Europe and several other regions for patients with group I PAH (pulmonary arterial hypertension) in WHO FC II or III; and for the treatment of patients with inoperable CTEPH (chronic thromboembolic pulmonary hypertension), or persistent/recurrent PH (pulmonary hypertension) after pulmonary endarterectomy in WHO FC II or III. Riociguat is marketed under the brand Adempas® by Bayer HealthCare Pharmaceuticals. Treatment with riociguat costs USD $7,500 for 30 days of treatment. Riociguat is indicated for the treatment of adults with persistent/recurrent chronic thromboembolic pulmonary hypertension (CTEPH), (WHO Group 4) after surgical treatment, or inoperable CTEPH, to improve exercise capacity and WHO functional class. Riociguat is a stimulator of soluble guanylate cyclase (sGC), an enzyme in the cardiopulmonary system and the receptor for nitric oxide (NO). When NO binds to sGC, the enzyme catalyzes synthesis of the signaling molecule cyclic guanosine monophosphate (cGMP). Intracellular cGMP plays an important role in regulating processes that influence vascular tone, proliferation, fibrosis and inflammation. Pulmonary hypertension is associated with endothelial dysfunction, impaired synthesis of nitric oxide and insufficient stimulation of the NO-sGC-cGMP pathway. ",The molecular weight is 422.42.,Riociguat has a topological polar surface area of 138.07.,The log p value of  is 1.84.,Riociguat is approved.,Riociguat is a solid.,True
14410,"Macitentan was approved in October 2013. It is indicated for patients with pulmonary arterial hypertension, and is marketed under the brand name Opsumit. Macitentan is an antagonist/blocker of endothelin receptors on blood vessels and smooth muscle, and, thus, blocks the stimulation of vasculature hypertrophy, inflammation, fibrosis, proliferation, and vasoconstriction. Similar to all drugs acting on the renin-angiotensin system, macitentan is associated with embryo and fetal toxicity, so it should not be used in pregnancy and has special precautions that must be followed for all females of child-bearing age. Macitentan is indicated for patients with pulmonary arterial hypertension. Macitentan blocks simulators of hypertrophy, inflammation, fibrosis, proliferation, and vasoconstriction.  Macitentan is an antagonist/blocker of endothelin receptors. Endothelin receptors are found in the endothelial cells of blood vessels and smooth muscle. Macitentan binds to the receptors, endothelin A and B (ETA and ETB), which prevents the agonist endothelin -1 (ET-1) from binding and stimulating the ETA and ETB receptors.",The molecular weight is 588.28.,Macitentan has a topological polar surface area of 128.22.,The log p value of  is 4.3.,Macitentan is approved.,Macitentan is a solid.,True
14411,"Ibrutinib is a small molecule that acts as an irreversible potent inhibitor of Burton's tyrosine kinase. It is designated as a targeted covalent drug and it presents a very promising activity in B cell malignancies. Ibrutinib was developed by Pharmacyclics Inc and in November 2013 was FDA-approved for the treatment of mantle cell lymphoma. Later, in February 2014, ibrutinib was approved for the treatment of chronic lymphocytic leukemia and it is also indicated for the treatment of patients with Waldenström's Macroglobulinemia. Ibrutinib has also been approved by the EMA for the treatment of chronic lymphocytic leukemia and mantle cell lymphoma. Ibrutinib was approved for use in chronic graft versus host disease in August 2017. Ibrutinib acquired an accelerated approval for the treatment of mantle cell lymphoma who have received at least one prior therapy. Mantle cell lymphoma (MCL) is a B-cell non-Hodgkin lymphoma that develops in the outer edge of a lymph node. MCL is usually diagnosed at late stages and it is easily spread into bone marrow, spleen, liver and gastrointestinal tract. In vitro studies have shown an induction of CLL cell apoptosis even in presence of prosurvival factors. It has also been reported an inhibition of CLL cell survival and proliferation as well as an impaired in cell migration and a reduction in the secretion of chemokines such as CCL3 and CCL4. The latter effect has been shown to produce regression in xenograft mouse models. Ibrutinib is an inhibitor of Bruton’s tyrosine kinase (BTK). It forms a covalent bond with a cysteine residue in the active site of BTK (Cys481), leading to its inhibition. The inhibition of BTK plays a role in the B-cell receptor signaling and thus, the presence of ibrutinib prevents the phosphorylation of downstream substrates such as PLC-γ. ",The molecular weight is 440.51.,Ibrutinib has a topological polar surface area of 99.16.,The log p value of  is 4.07.,Ibrutinib is approved.,Ibrutinib is a solid.,True
14412,"Palbociclib is a piperazine pyridopyrimidine that acts in the cell cycle machinery. It is a second generation cyclin-dependent kinase inhibitor selected from a group of pyridopyrimidine compounds due to its favorable physical and pharmaceutical properties. Palbociclib is indicated in combination with as initial endocrine-based therapy for the treatment of human epidermal growth factor receptor type 2 (HER2)-negative and hormone receptor(HR)-positive tumors in adult patients with advanced/metastatic breast cancer. It is as well approved in combination with in patients with disease progression with prior endocrine therapy. Due to its mechanism of action, palbociclib inhibits cell growth and suppresses DNA replication in retinoblastoma tumor suppressor gene (RB) proficient cancer cells. As expected, these RB cells present a significant increase in the proportion of cells in G1 state and the presence of palbociclib produces effective dephosphorylation of RB, reduce proliferation and induce senescence causing cell-cycle arrest. Palbociclib is a cyclin-dependent kinase 4/6 (CDK4/6) inhibitor that acts by binding to the ATP pocket with an IC50 in the range of 9-15 nmol/L. It is important to consider that it presents low to absent activity against other kinases. ",The molecular weight is 447.54.,Palbociclib has a topological polar surface area of 103.35.,The log p value of  is 2.2.,Palbociclib is approved and investigational.,Palbociclib is a solid.,True
14413,"Nintedanib is a small molecule kinase inhibitor used in the treatment of pulmonary fibrosis, systemic sclerosis-associated interstitial lung disease, and non-small cell lung cancer (NSCLC). It was first approved for use in the United States in 2014. Within the spectrum of idiopathic pulmonary fibrosis treatment options, nintedanib is currently one of only two disease-modifying therapies available and indicated for the condition (the other being ) and as such is used as a first-line treatment following diagnosis to slow down the progressive loss of lung function. As a chemotherapeutic agent for NSCLC, nintedanib, in combination with , is reserved for patients who have tried and failed first-line chemotherapeutic options. In the US, nintedanib is indicated for the treatment of idiopathic pulmonary fibrosis (IPF) and to slow declining pulmonary function in patients with systemic sclerosis-associated interstitial lung disease. In the EU, nintedanib is indicated in combination with docetaxel for the treatment of adult patients with metastatic, locally advanced, or locally recurrent non-small cell lung cancer of adenocarcinoma histology who have already tried first-line therapy. Nintedanib is a small molecule kinase inhibitor that inhibits upstream kinase activity to ultimately inhibit lung fibroblast proliferation and migration, as well as signalling pathways that promote the proliferation and survival of endothelial and perivascular cells in tumour tissues. Nintedanib is a small molecule, competitive, triple angiokinase inhibitor that targets multiple receptor tyrosine kinases (RTKs) and non-receptor tyrosine kinases (nRTKs). Many of these RTKs are implicated in lung fibrosis and tumour angiogenesis, so nintedanib is therefore used in the treatment of proliferative diseases such as idiopathic pulmonary fibrosis, non-small cell lung cancer, and systemic sclerosis-associated interstitial lung disease. The specific RTKs that nintedanib inhibits are platelet-derived growth factor (PDGFR) α and β, fibroblast growth factor receptor (FGFR) 1-3, vascular endothelial growth factor receptor (VEGFR) 1-3, and Fns-Like tyrosine kinase-3 (FLT3). Nintedanib binds to the ATP-binding pocket of these receptors and inhibits their activity, thereby blocking signalling cascades that result in the proliferation and migration of lung fibroblasts. Nintedanib also inhibits kinase signalling pathways in various cells within tumour tissues, including endothelial cells, pericytes, smooth muscle cells, and cells contributing to angiogenesis, culminating in an inhibition of cell proliferation and apoptosis of affected tumour cells.",The molecular weight is 539.64.,Nintedanib has a topological polar surface area of 94.22.,The log p value of  is 3.08.,Nintedanib is approved.,Nintedanib is a solid.,True
14414,"Potassium alum is considered by the FDA as a generally recognized as safe (GRAS) substance. It is an inorganic salt, also called potassium aluminum sulfate with a formula of AlK(SO4)2 that is predominantly produced in the dodecahydrate form (AlK(SO4)2 * 12H2O). Potassium alum is formed by large, transparent crystals that are used in different products like food or drugs as a buffer, neutralizing or forming agent. Potassium alum is considered safe by the FDA and its use is in homepathic or OTC products. Due to its presence in several different drugs, the main indications for the use of potassium alum are: The presence of potassium alum reduces swollen mucous membranes that result from inflammation of the nasal, gastrointestinal and urinary passages as well as in the presence of excessive secretions. The induction of the coagulation cascade will also stop bleeding. The main functions of potassium alum in drugs are as an astringent, antiseptic or adjuvant agent. The astringent action is performed by the induction of coagulation in the superficial tissue layers until the formation of a crust. The formation of alum ions neutralize the charges on plasma proteins, causing the blood to coagulate. Similar effect is observed in disinfectants where these ions react with the free organic acid and thiol groups of proteins on microbes and free proteins, resulting in protein precipitation. This action will generate the contraction of the tissue and dry up secretions. Its adjuvant properties are mainly used in the production of vaccines where the presence of this chemical enhances the immune response.",,,,Potassium alum is approved.,Potassium alum is a solid.,True
14415,"Chlortetracycline is a _tetracycline_ antibiotic, and historically the first member of this class to be identified. It was discovered in 1945 by the scientist, Benjamin Minge Duggar, working at Lederle Laboratories under the supervision of Yellapragada Subbarow. He discovered that this antibiotic was the product of an actinomycete strain he cultured and obtained from a soil sample from a field in Missouri. The organism was named _Streptomyces aureofaciens_ due to its gold-hued color. Used in the manufacuring of medicated animal feeds. Tetracycline antibiotics are bacteriostatic agents which act to inhibit bacterial growth and reproduction. Chlortetracycline, like other tetracyclines, competes for the A site of the bacterial ribosome. This binding competes with tRNA carrying amino acids preventing the addition of more amino acids to the peptide chain. This inhibition of protein synthesis ultimately inhibits growth and reproduction of the bacterial cell as necessary proteins cannot be synthesized.",The molecular weight is 478.88.,Chlortetracycline has a topological polar surface area of 181.62.,The log p value of  is -0.06.,Chlortetracycline is approved and investigational and vet_approved.,Chlortetracycline is a solid.,True
14416,"Technetium Tc-99m oxidronate, also known as 99mTc-methylene diphosphonate, is a radiopharmaceutical agent. A radiopharmaceutical is defined as a medicinal formulation containing radioisotopes that are used in major clinical areas for diagnosis and/or therapy. The radiopharmaceuticals based on technetium-99m are widely used for diagnostic purposes because 99mTc has a versatile chemistry which allows it to produce an extense variety of complexes with specific characteristics. These complexes are formed by the binding of 99mTc to metal atoms of an organic molecule. The group oxidronate falls into the category of diphosphonates whose structure allows them to bind to calcium. Thus, technetium Tc-99m oxidronate is a powerful detection tool for abnormal osteogenesis by skeletal scintigraphy. It was developed by Mallinkrodt nuclear and FDA approved on February 18, 1981. Technetium Tc-99m oxidronate is indicated in adult and pediatric patients to be used in skeletal imaging for diagnosis of areas that can present altered osteogenesis. When administered intravenously, it is able to generate a clear image of the bones which allows the physician to diagnose any bone problem. It is important to point out that this drug has to be manipulated only under the service of a nuclear specialist. The approved indications for a bone scan are 1) visualization of tumor metastasis in bone, 2) osteomyelitis, 3) fracture, 4) stress fracture, 5) avascular necrosis, 6) osteoporosis and 7) prosthetic joint evaluation. From all the major indications, the detection of a metastatic disease is the most common because it presents a 95% of sensitivity and lesion detection can be done 6 months earlier than with X-ray studies. The technetium is generated in a molibdene generator. Technetium Tc-99m presents a reduction of gamma emission after 6 hours and it is considered a quasi-stable molecule. The visualization of bone lesions is possible since there is an altered uptake in areas of abnormal osteogenesis. The principal photon used for detection is the gamma-2 with an energy of 140.5 keV. Its use for bone examination should be performed 2 hours after initial injection with a recommended activity on the range of 370-740 MBq. The exact mechanism for bone uptake of technetium Tc-99m oxidronate is unknown. The most accepted mechanism is the localization of 99m-Tc on the surface of hydroxyapatite crystals of bone by chemisorption. Chemisorption is explained as a type of adsorption that involves a chemical reaction between the surface and the adsorbate in which new strong interactions form electronic bonds at the adsorbent surface. The presented chemisorption are regulated by the blood flow and blood concentration because it restrains the delivery of the agent in the uptake sites.",,,,Technetium Tc-99m oxidronate is approved.,Technetium Tc-99m oxidronate is a solid.,True
14417,"Lorpiprazole is a serotonin antagonist and reuptake inhibitor used for the treatment of major depressive disorder. It is a piperazinyl-triazole derivative. In 2016, lorpiprazole was classified in the \Chemical structure-related drug-like criteria of global approved drugs\"" as an antipsychotic and anxiolytic. An antipsychotic is a medication used to treat a state of delusion, hallucination, paranoia or disordered thought. On the other hand, an anxiolytic is a medication used for the treatment of severe, chronic or debilitating anxiety. The anxiety state can be defined as an unpleasant state of tension, apprehension or uneasiness."" Drugs like lorpiprazole that fit in the category of serotonin antagonists and reuptake inhibitors present a wide variety of effects when administered. They inhibit serotonin receptors like 5-HT2A as well as prevent the reuptake of serotonin, norepinephrine and dopamine. Additionally, they antagonize some adrenergic receptors. This diverse functional profile allows lorpiprazole to have a large therapeutic spectrum from symptom control as an adjuvant of other drugs to control of depressive syndromes as a monotherapy. Lorpiprazole is a serotonin antagonist and reuptake inhibitor thus, its activity is performed by antagonizing the 5-HT2A and the 5-HT2C serotoninergic receptors as well as the alpha1 and alpha2 adrenergic receptors, H1 histaminergic receptors and at high doses, inhibiting the SERT serotonin transporter.",The molecular weight is 405.47.,Lorpiprazole has a topological polar surface area of 37.19.,The log p value of  is 3.02.,Lorpiprazole is approved.,Lorpiprazole is a solid.,True
14418,"Arotinolol is an alpha- and beta-receptor blocker developed in Japan. It is a thiopropanolamine with a tertiary butyl moiety. It has been studied for its potential to be an antihypertensive therapy. Artinolol is being developed by Sumitomo Pharmaceutical Co., Ltd. and it is currently under clinical trials. Artinolol was introduced to be used as an antihypertensive agent since 1986. It has been studied for other functions like tremor control for patients with Parkinson disease and it is currently in clinical trials for its use in the control of blood pressure and heart rate. Preclinical studies showed a lack of intrinsic sympathomimetic activities or membrane-establishing properties. It is confirmed that arotinolol presents vasorelaxant activity. This characteristic is also proved to be mainly mediated by its α1-blocking property. In preclinical hypertension trials, there is a specific acute bradycardiac and antihypertensive activity with a pronounced reduction in heart rate. Some reports indicate a delayed development of hypertension when arotinolol is administered daily. Arotinolol has a dose-dependent decrease in cardiac contractility and coronary blood flow as well as an increase in total peripheral resistance. The effects of arotinolol have been confirmed in clinical trials where this drug was able to decrease cardiac index and thus, blood pressure. Arotinolol binds to the β1-, β2- and α1- adrenergic receptor sites with a very high affinity. Radioligand studies have shown that arotinolol presents a higher affinity to the β-receptor compared to the α-receptor. The elucidated mechanism of action seems to be the result of a reduction in the cardiac output via the β-blockade and an additional inhibition of the counter-regulatory increase in peripheral resistance mediated by the α-blockade.",The molecular weight is 371.53.,Arotinolol has a topological polar surface area of 88.24.,The log p value of  is 2.08.,Arotinolol is investigational.,Arotinolol is a solid.,True
14419,"Dexibuprofen, S(+)-ibuprofen, is a non-steroidal anti-inflammatory drug (NSAID). It is a pharmacologically effective enantiomer of racemic ibuprofen that differs in physicochemical properties. It is proposed to be more pharmacologically active and tolerable with a better safety profile than ibuprofen due to higher concentration of active S enantiomer. Dexibuprofen has a slower dissolution rate in the simulated gastric and enteric juices compared with the racemic ibuprofen and displays improved oral bioavilability. For Metabolism, Enzymes, Carriers, Transporters Sections, refer to. For more information, refer to. For more information, refer to. Like common NSAIDs, dexibuprofen is an active enantiomer of that suppresses the prostanoid synthesis in the inflammatory cells via inhibition of the COX-2 isoform of the arachidonic acid COX. For more information, refer to.",The molecular weight is 206.28.,Dexibuprofen has a topological polar surface area of 37.3.,The log p value of  is 3.68.,Dexibuprofen is approved and investigational.,Dexibuprofen is a solid.,True
14420,"Blonanserin is an atypical antipsychotic approved in Japan in January, 2008. It offers improved tolerability as it lacks side effects such as extrapyramidal symptoms, excessive sedation, or hypotension. As a second-generation (atypical) antipsychotic, it is significantly more efficacious in the treatment of the negative symptoms of schizophrenia compared to first-generation (typical) antipsychotics. Used for the treatment of schizophrenia. Blonanserin antagonizes dopamine and serotonin receptors to reduce symptoms of schizophrenia. Blonanserin binds to and inhibits dopamine receptors D2 and D3 as well as the serotonin receptor 5-HT2A with high affinity. Blonanserin has low affinity for other dopamine and serotonin receptors as well as muscarinic, adrenergic, and histamine receptors. This reduces dopaminergic and serotonergic neurotransmission which is thought to produce a reduction in positive and negative symptoms of schizophrenia respectively.",The molecular weight is 367.51.,Blonanserin has a topological polar surface area of 19.37.,The log p value of  is 6.48.,Blonanserin is investigational.,Blonanserin is a solid.,True
14421,"Aranidipine is a novel dihydropyridine derivative that gives rise to two active metabolites (M-1α and M-1β) that exhibit hypotensive activity. It is a calcium antagonist with the formula methyl 2-oxopropyl 1,4-dihydro-2,6-dimethyl-4-(2-nitrophenyl)-3,5-pyridinedicarboxylate. It was developed by Maruko Seiyaku, introduced by Taiho and launched in Japan in 1997. Aranidipine has been used for many years to treat angina pectoris and hypertension. Pre-clinical studies with aranidipine and its two metabolites have shown production of increases in femoral blood flow. It has been shown to present potent and long-lasting vasodilating actions. Aranidipine and its metabolites are shown to inhibit calcium-induced contraction in isolated rabbit arteries. Studies have shown that aranidipine is more potent to reduce blood pressure than other dihydropyridines. Aranidipine produce changes in renal blood flow, this effect may be explained by its effect on alpha-2-adrenoreceptor-mediated vasoconstriction. The high potential of aranidipine is thought to be related to the additional calcium antagonistic activity of its metabolite. The mechanism is thought to be related to the capacity of aranidipine and its metabolites to vasodilate afferent and efferent arterioles. this action is performed through the inhibition of voltage-dependent calcium channels. The typical mechanism of action of aranidipine, as all dihydropyridines, is based on the inhibition of L-type calcium channels, decreasing calcium concentration and inducing smooth muscle relaxation. It is a selective alpha2-adrenoreceptor antagonist which inhibits vasoconstrictive responses.",The molecular weight is 388.38.,Aranidipine has a topological polar surface area of 124.84.,The log p value of  is 2.56.,Aranidipine is experimental.,Aranidipine is a solid.,True
14422,"Lacidipine is a lipophilic dihydropyridine calcium antagonist with an intrinsically slow onset of activity. Due to its long duration of action, lacidipine does not lead to reflex tachycardia. It displays specificity in the vascular smooth muscle, where it acts as an antihypertensive agent to dilate peripheral arterioles and reduce blood pressure. Compared to other dihydropyridine calcium antagonists, lacidipine exhibits a greater antioxidant activity which may confer potentially beneficial antiatherosclerotic effects. Lacidipine is a highly lipophilic molecule that interacts with the biological membranes. Through radiotracer analysis, it was determined that lacidipine displays a high membrane partition coefficient leading to accumulation of the drug in the membrane and slow rate of membrane washout. When visualized by small-angle X-ray diffraction with angstrom resolution to examine its location within the membranes, lacidipine was found deep within the membrane's hydrocarbon core. These results may explain the long clinical half-life of lacidipine.  Indicated for the treatment of hypertension either alone or in combination with other antihypertensive agents, including β-adrenoceptor antagonists, diuretics, and ACE-inhibitors. acidipine is a specific and potent calcium antagonist with a predominant selectivity for calcium channels in the vascular smooth muscle. Its main action is to dilate predominantly peripheral and coronary arteries, reducing peripheral vascular resistance and lowering blood pressure.  By blocking the voltage-dependent L-type calcium channels, it prevents the transmembrane calcium influx. Normally, calcium ions serve as intracellular messengers or activators in exictable cells including vascular smooth muscles. The influx of calcium ultimately causes the excitation and depolarization of the tissues. Lacidipine inhibits the contractile function in the vascular smooth muscle and reduce blood pressure. Due to its high membrane partition coefficient, some studies suggest that lacidipine may reach the receptor via a two-step process; it first binds and accumulates in the membrane lipid bilayer and then diffuses within the membrane to the calcium channel receptor. It is proposed that lacidipine preferentially blocks the inactivated state of the calcium channel.",The molecular weight is 455.55.,Lacidipine has a topological polar surface area of 90.93.,The log p value of  is 5.93.,Lacidipine is approved and investigational.,Lacidipine is a solid.,True
14423,"Levamlodipine, also known as S-amlodipine, is a pharmacologically active enantiomer of , an antihypertensive medication. Levamlodipine belongs to the dihydropyridine group of calcium channel blockers. This medication was first marketed in Russia and India before being granted FDA approval. The names S-amlodipine and levamlodipine may be used interchangeably as both substances are the same, however. As a racemic mixture, amlodipine contains (R) and (S)-amlodipine isomers, but only (S)-amlodipine as the active moiety possesses therapeutic activity. Levamlodipine is indicated alone or in combination to treat hypertension in adults and children. Levamlodipine inhibits L-type calcium channels in vascular smooth muscle, reducing peripheral vascular resistance and blood pressure. It is given once daily in doses of 1.25-2.5mg in children and 2.5-5mg in adults. Patients should be counselled regarding the risk of symptomatic hypotension, worsening angina, and myocardial infarction. Levamlodipine blocks the transmembrane influx of calcium through L-type calcium channels into the vascular and cardiac smooth muscles resulting in vasodilation and a subsequent decrease in blood pressure. Levamlodipine inhibits calcium influx in vascular smooth muscle to a greater degree than in cardiac muscle, leading to decreased peripheral vascular resistance and lowered blood pressure. In vitro studies have shown a negative inotropic effect but this is unlikely to be clinically relevant.",The molecular weight is 408.88.,Levamlodipine has a topological polar surface area of 99.88.,The log p value of  is 3.43.,Levamlodipine is approved and investigational.,Levamlodipine is a solid.,True
14424,"Methylene blue is an oxidation-reduction agent. The intravenous form of methylene blue is approved by the FDA for the treatment of pediatric and adult patients with acquired methemoglobinemia. Historically, it has been widely used in Africa to treat malaria, but now it disappeared when chloroquine (CQ) and other drugs entered the market. Its use as an urinary tract antiseptic has also been investigated.  Indicated for the treatment of pediatric and adult patients with acquired methemoglobinemia.  * Main mechanism of action involves inhibition of nitric oxide synthase and guanylate cyclase. ",The molecular weight is 284.4.,Methylene blue has a topological polar surface area of 19.37.,The log p value of  is 0.95.,Methylene blue is approved and investigational.,Methylene blue is a solid.,True
14425,"Imidafenacin is an antispasmodic agent with anticholinergic effects. It antagonizes muscarinic receptors in the bladder to reduce the frequency of urination in the treatment of overactive bladder. It is marketed in Japan under the tradenames Staybla by Ono Pharmaceutical and Uritos by Kyojin Pharmaceutical. Used in the treatment of overactive bladder. Imidafenacin is an antimuscarinic agent which acts to reduce the frequency of urination in patients with overactive bladder. Imidafenacin binds to and antagonizes muscarinic M1 and M3 receptors with high affinity. It also antagonizes muscarinic M2 receptors but with lower affinity. M3 receptors stimulate contraction of the detrusor muscle in the bladder via release of calcium from the sarcoplasmic reticulum. M2 receptors are also present in the detrusor muscle but serve to inhibit adenylate cyclase which reduces the relaxation mediated by β adrenergic receptors. Finally, M1 receptors are present on the parasympathetic neurons which release acetylcholine in the bladder. They act as an autocrine positive feedback loop and further increase release of acetylcholine. Antagonism of these receptors by imidafenacin prevents contraction of the bladder's detrusor muscle, prevents inhibition of the relation produced by sympathetic tone, and reduces acetylcholine release. Together these reduce the frequency of urination.",The molecular weight is 319.41.,Imidafenacin has a topological polar surface area of 60.91.,The log p value of  is 2.22.,Imidafenacin is investigational.,Imidafenacin is a solid.,True
14426,"Artesunate is indicated for the initial treatment of severe malaria. The World Health Organization recommends artesunate as first line treatment for severe malaria. Artesunate was developed out of a need for a more hydrophilic derivative of. Artesunate is indicated for the initial treatment of severe malaria in adult and pediatric patients. Artesunate is an artemisinin derivative that is metabolized to DHA, which generates free radicals to inhibit normal function of _Plasmodium_ parasites. It has a short duration of action due to its short half life, and a moderate therapeutic index. Patients should be counselled regarding the risk of post treatment hemolytic anemia and hypersenstivity. Artesunate is metabolized to the active DHA. the endoperoxide bridge of DHA reacts with heme, generating free radicals which inhibit protein and nucleic acid synthesis of the _Plasmodium_ parasites during all erythrocytic stages. Reactions with these free radicals can also lead to alkylation of parasitic proteins such as a calcium adenosine triphosphatase and EXP1, a glutathione S-transferase.",The molecular weight is 384.42.,Artesunate has a topological polar surface area of 100.52.,The log p value of  is 2.93.,Artesunate is approved and investigational.,Artesunate is a solid.,True
14427,"Lumacaftor is a drug used in combination with as the fixed dose combination product Orkambi for the management of Cystic Fibrosis (CF) in patients aged 6 years and older. Cystic Fibrosis is an autosomal recessive disorder caused by one of several different mutations in the gene for the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) protein, a transmembrane ion channel involved in the transport of chloride and sodium ions across cell membranes of the lungs, pancreas, and other organs. Mutations in the CFTR gene result in altered production, misfolding, or function of the CFTR protein and consequently abnormal fluid and ion transport across cell membranes. As a result, CF patients produce thick, sticky mucus that clogs the ducts of organs where it is produced making patients more susceptible to infections, lung damage, pancreatic insufficiency, and malnutrition. Lumacaftor improves CF symptoms and underlying disease pathology by aiding the conformational stability of F508del-mutated CFTR proteins, preventing misfolding and resulting in increased processing and trafficking of mature protein to the cell surface.  When given in combination with as the fixed dose combination product Orkambi, lumacaftor is indicated for the treatment of cystic fibrosis (CF) in patients age 6 years and older who are homozygous for the F508del mutation in the CFTR gene.  Results from clinical trials indicated that treatment with Orkambi (lumacaftor/ ) results in improved lung function, reduced chance of experiencing a pulmonary exacerbation, reduced sweat chloride, increased weight gain, and improvements in CF symptoms and quality of life. Lumacaftor improves CF symptoms and underlying disease pathology by aiding the conformational stability of F508del-mutated CFTR, resulting in increased processing and trafficking of mature protein to the cell surface. More specifically, lumacaftor acts as a protein-folding chaperone, preventing misfolding of CFTR ion channels and consequent destruction during processing in the endoplasmic reticulum. ",The molecular weight is 452.41.,Lumacaftor has a topological polar surface area of 97.75.,The log p value of  is 6.05.,Lumacaftor is approved.,Lumacaftor is a solid.,True
14428,"Tenofovir alafenamide is a novel prodrug developed in order to improve renal safety when compared to the counterpart. Both of these prodrugs were first created to cover the polar phosphonic acid group on tenofovir by using a novel oxycarbonyloxymethyl linkers to improve the oral bioavailability and intestinal diffusion. Tenofovir alafenamide is an alanine ester form characterized for presenting low systemic levels but high intracellular concentration. It has been reported to produce a large antiviral efficacy at doses ten times lower than tenofovir disoproxil. Tenofovir alafenamide is indicated to treat chronic hepatitis B, treat HIV-1, and prevent HIV-1 infections. Tenofovir alafenamide is indicated for the treatment of chronic hepatitis B in adult patients with compensated liver disease. Tenofovir alafenamide has been shown to be a potent inhibitor of hepatitis B viral replication. Tenofovir alafenamide presents 91% lower plasma concentration with an intracellular presence of about 20-fold higher when compared to. This is due to its prolonged systemic exposure and its higher intracellular accumulation of the active metabolite tenofovir diphosphate.",The molecular weight is 476.47.,Tenofovir alafenamide has a topological polar surface area of 143.48.,The log p value of  is 2.18.,Tenofovir alafenamide is approved.,Tenofovir alafenamide is a solid.,True
14429,"Iopodic acid, also known by the name of ipodate, is classified as a cholecystographic agent formed by a weak organic acid that contains a tri-iodinated benzene ring with iodine at positions 2, 4 and 6. Due to its particular structure, it presents a high degree of lipid solubility and a radiopaque property. It was developed and filed to the FDA by the company BRACCO. This drug was approved on March 15, 1962 but it is nowadays discontinued from the FDA and Health Canada. On September 22, 1981, ipodate was submitted again by the company Schering AG but it is currently under an inactive status. Iopodic acid is available as a cholecystographic agent. This denomination indicates the iopodic acid is a radiopaque substance that can be used to visualize the gallbladder and biliary channels in abdominal X-ray. An abdominal X-ray uses a minimal amount of ionizing radiation to produce pictures of the inside of the abdominal cavity. It is commonly used to evaluate the stomach, liver, intestines, and spleen. The thyroid effects of iopodic acid are related to the blocking of the more potent form of the thyroid hormone. It also blocks thyroid hormone release and it can interfere with its synthesis in some patients. The effects of iopopdic acid on some diseases, such as Graves disease, have been shown not to be as effective and to present a relapse after discontinuation. The effects of iopodic acid on thyroid has been proven to produce an inactivation of approximately 80% of the type II deiodinase in pituitary and cerebral cortex. For cholecystography, iopodic acid blocks the X-rays as they pass through the body which allows delineating the body structures that do not contain this compound.",The molecular weight is 597.96.,Iopodic acid has a topological polar surface area of 52.9.,The log p value of  is 4.22.,Iopodic acid is approved and investigational and withdrawn.,Iopodic acid is a solid.,True
14430,"Acetrizoic acid presents the molecular formula of 3-acetamidol-2,4,6-triiodobenzoic acid and it is the first monomeric ionic compound used as an X-ray contrast agent. It was first synthesized by Wallingford in 1953 and it was filled in the FDA by the Johnson & Johnson subsidiary, Cilag Chemie AG, on February 8th, 1978. Acetrizoic acid presents, in the FDA records, a category of drug substance with an inactive status. Acetrizoic acid indication was to be used as a contrast agent for X-ray. Some information indicates its nephrotropic property as one of the characteristics for the utilization of acetrizoic acid. The X-ray imaging depends on the difference in tissue density which is provided by an X-ray attenuation between the area of interest and the surrounding tissue. The use of contrast agents will provoke a contrast enhancement or opacification and it will improve the differentiation of pathological processes from normal tissue. Iodine, a big component in acetrizoic acid, is an element with a high atomic density. This property causes attenuation of X-rays within the diagnostic energy spectrum. Thus, acetrizoic acid is a water-soluble and reasonably safe iodinated contrast agent that can be intravenously administered for clinical applications.",The molecular weight is 556.86.,Acetrizoic acid has a topological polar surface area of 66.4.,The log p value of  is 1.91.,Acetrizoic acid is withdrawn.,Acetrizoic acid is a solid.,True
14431,"Propiolactone is a lactone compound with a four-membered ring. It is a colorless liquid with a pungent slightly sweet odor. Propiolactone is a disinfectant used for the sterilization of blood plasma, vaccines, tissue grafts, surgical instruments, and enzymes. It has been used against bacteria, fungi, and virus. It is currently FDA approved for its use as an indirect additive used in food contact substances. Propiolactone was first commercially available in the United States in 1958. Propiolactone was used for vaccines, tissue grafts, surgical instruments, and enzymes, as a sterilant of blood plasma, water, milk and nutrient broth as a vapor-phase disinfectant in enclosed spaces. Its sporicidal action is used against vegetative bacteria, pathologic fungi, and viruses. It is no longer used in medical procedures or in food. When employed under conditions of maximum effectiveness, propiolactone is approximately 25 more active as a vapor phase disinfectant than formaldehyde, 4000 times more active than ethylene oxide and 50000 times more active than methyl bromide. It has been shown to be mutagenic by inducing cell transformation, chromosomal aberrations and chromatoid exchange. Propiolactone has been shown to be mutagenic in both somatic and germ cells. Propiolactone is an alkylating agent that acts through alkylation of carboxyl- and hydroxyl- groups. The lactone ring splits either at the first or third carbon. Propiolactone reacts with polynucleotides and DNA, mainly at N7 of guanine and N1 of adenine to form carboxyethyl derivatives. It also forms adducts with N3 of cytosine and thymine.",The molecular weight is 72.06.,Propiolactone has a topological polar surface area of 26.3.,The log p value of  is -1.36.,Propiolactone is approved and withdrawn.,Propiolactone is a liquid.,True
14432,,The molecular weight is 372.46.,Meprednisone has a topological polar surface area of 91.67.,The log p value of  is 2.18.,Meprednisone is approved and investigational.,,False
14433,"Potassium perchlorate is an inorganic salt with the chemical formula KClO4. It is a strong oxidizer with the lowest solubility of the alkali metal perchlorates. Potassium is most commonly used in flares and automobile airbags. The use of potassium perchlorate as a component in sealing gaskets for food containers has been revoked by the FDA following the use being abandoned by the industry. Potassium perchlorate acts as a competitive inhibitor of iodine uptake by the thyroid gland and attenuates the production of the thyroid hormone. Thus the use of potassium perchlorate has been extensive for hyperthyroidism during the last 50 years, particularly in the late 1950s and early 1960s. The therapeutic use of potassium perchlorate in thyroid disorders has been ceased due to a high risk for developing aplastic anemia and nephrotic syndrome. No current FDA- or EMA-approved therapeutic indications. Potassium perchlorate inhibits thyroid iodide transport. The clinical use of potassium perchlorate in hyperthyroidism, such as Graves' disease and amiodarone-induced hypothyroidism, have been investigated in various studies. Thyroid dysfunction occurs in about 15-20% of the patients receiving long-term amiodarone therapy. In patients with amiodarone-induced hypothyroidism, short-term administration of potassium perchlorate resulted in restoration of euthyroidism in most patients. Euthyroidism promoted by potassium perchlorate does not persist unless amiodarone treatment is withdrawn. Thyroxine (T4) and tri-iodothyronine (T3) are major thyroid hormones, or iodothyronines, that are synthesized and released from the thyroid. Iodine plays an essential role in the synthesis of these hormones. Via the sodium-iodide symporter (NIS), which is a protein located on the basolateral membrane of the thyroid follicular cell, iodine is transported from the blood into the thyroid gland where it is oxidized to. Perchlorate (ClO4−) is the dissociated anion of potassium perchlorate that exerts an inhibitory effect on iodide uptake by the thyroid gland in the cellular level. Due to its similarity in ionic size and charge to iodide, perchlorate inhibits the sodium-iodide symporter (NIS) without being translocated into the thyroid follicular cell. The inhibition constant, Ki, is estimated as 0.4 µmol to 24 µmol. At therapeutic dosage levels this competitive inhibition decreases the entrance of iodide into the thyroid, resulting in less available iodide for hormone synthesis and, therefore, a decrease in T3 and T4 synthesis. When ambient iodine intake is low or iodide uptake is sufficiently inhibited, perchlorate is capable in inducing goiter and hypothyroidism from inhibited iodide uptake. At high doses of potassium perchlorate, reduced T3 and T4 levels may be accompanied by increased TSH levels via a negative feedback loop, affecting the thyroid, pituitary and hypothalamus. ",The molecular weight is 138.54.,Potassium perchlorate has a topological polar surface area of 74.27.,,Potassium perchlorate is approved and investigational.,Potassium perchlorate is a solid.,True
14434,"Hydroquinone is a topical lightening product found in OTC products, and is used to correct skin discoloration associated with disorders of hyperpigmentation including melasma, post-inflammatory hyperpigmention, sunspots, and freckles. It can be used alone, but is more frequently found in combination with other agents such as alpha-hydroxy acids, corticosteroids, retinoids, or sunscreen.  Hydroquinone is used as an OTC topical lightening agent for disorders of hyperpigmentation including melasma, post-inflammatory hyperpigmention, sunspots and freckles.  Hydroquinone reduces melanin pigment production through inhibition of the tyrosinase enzyme, which is involved in the initial step of the melanin pigment biosynthesis pathway. Hydroquinone takes several months to take effect. ",The molecular weight is 110.11.,Hydroquinone has a topological polar surface area of 40.46.,The log p value of  is 0.81.,Hydroquinone is approved and investigational.,,True
14435,"Insulin degludec is an ultra-long-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Insulin is typically prescribed for the management of diabetes mellitus to mimic the activity of endogenously produced human insulin, a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin degludec is indicated to improve glycemic control in patients 1 year of age and older with diabetes mellitus. Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, the pancreas produces a continuous supply of low levels of basal insulin along with spikes of insulin following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by the liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin detemir is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals. The onset of action of insulin detemir is 1 to 2 hours and its duration of action is up to 24 hours. Interestingly, it has a lower affinity (30%) for the insulin receptor than human insulin. Insulin detemir binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signalling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism.",The molecular weight is 6104.04.,Insulin degludec has a topological polar surface area of 2356.52.,,Insulin degludec is approved.,Insulin degludec is a liquid.,True
14436,"Calcium citrate is a salt typically used as a source of calcium in a variety of over the counter supplements. For use as an over the counter calcium supplement. Increases plasma calcium levels leading to a decrease in calcium flux and increase in calcium deposition into bone  Calcium citrate increases plasma calcium levels. This reduces calcium flux from osteocyte activity by reducing the secretion of parathyroid hormone (PTH). Calcium does this by stimulating a G-protein coupled calcium receptor on the surface of parathyroid cells. The reduction in calcium flux increases the amount of calcium deposited in bone resulting in an increase in bone mineral density. The reduction in PTH secretion also reduces the amount of vitamin D metabolized to its active form, calcidiol. Since calcidiol increases the expression of calcium dependent ATPases and transient receptor potential cation channel subfamily V member 6 (TRPV6) both of which are involved in calcium uptake from the gut, a reduction in calcidiol results in less calcium absorption. Additionally, TRPV5, the channel responsible for calcium reabsorption in the kidney, is downregulated when PTH secretion is reduced thus increasing calcium excretion via the kidneys. Another hormone, calitonin, is likely involved in the reduction of bone resorption during periods of high plasma calcium.",,,,Calcium citrate is approved and investigational.,Calcium citrate is a solid.,True
14437,"Opium is the first substance of the diverse group of the opiates. It has been known for a long time, and the first evidence of a poppy culture dates from 5 thousand years by the Sumerians. During the years, opium was used as a sedative and hypnotic, but it was determined to be addictive.  Opium and its derivatives are the most commonly used medications for the treatment of acute and chronic pain. Opium and its alkaloid-derivatives can also be used as tranquilizers, antitussives and in the treatment of diarrhea. The direct use of opium is not common nowadays but the use of some of its derivatives such as morphine and codeine, as well as the use of a tincture of opium for severe diarrhea can be seen in medical practice. Opioids can reduce the intensity and unpleasant feeling of pain. The unspecific effect of opium to the different opioid receptors produce the generation of various effects such as sedation, euphoria, dysphoria, respiratory depression, constipation, pruritus, nausea, and vomiting. It is reported that the secondary effects tend to be diminished as long-term use tolerance is developed. Some reports have also shown an opioid-driven impairment of the hypothalamic function that can result in a loss of libido, impotence, and infertility. Patients have reported a sensation of stress relief even in presence of pain as well as the presence of sedation, hypoventilation, cough inhibition, prolonged apnea, myosis and respiratory obstruction. Opium produces its effects by activating specific G protein-coupled receptors in the brain, spinal cord, and peripheral nervous system. There are three major classes of opioid receptors being δ-opioid, κ-opioid and μ-opioid. Opium will generate an agonist activity which will later open the potassium channels and prevent the opening of voltage-gated calcium channels. This activity causes a reduction in neuronal excitability and inhibits the release of pain neurotransmitters.",,,,Opium is approved and illicit.,Opium is a liquid.,True
14438,"Cupric oxide, or copper (II) oxide, is an inorganic compound with the chemical formula CuO. Cupric oxide is used as a precursor in many copper-containing products such as wood preservatives and ceramics. Cupric oxide may be found in over-the-counter vitamin-mineral supplements as a source of. The mean daily dietary intake of copper in adults ranges between 0.9 and 2.2 mg. Common routes of cupric oxide exposure include ingestion, dermal exposure and inhalation. Copper(II) oxide nanoparticles (NPCuO) have industrial applications as antimicrobial agents in textiles and paints, and catalysts in organic synthesis. They may also be produced from electronic wastes. Cupric oxide poses potential health and environmental concern due to toxic and mutagenic particles generating reactive oxygen species. No FDA- or EMA-approved therapeutic indications.  For pharmacodynamic information of copper, refer to drug entry for. Copper(II) oxide nanoparticles are known to generate reactive oxygen species (ROS), leading to cytotoxicity. In a comparative toxicity assay, nanoparticles caused significant mitochondrial depolarization leading to DNA damage. In the human skin organ culture study, topical application of copper oxide (CuO) nanoparticles induced inflammatory cytokine secretion and necrosis _in vitro_, indicating that the nanoparticles may adhere to the skin surface and react with the local acidic environment.  For pharmacodynamic information of copper, refer to drug entry for. Copper(II) oxide nanoparticles generate DNA-damaging reactive oxygen species at the nanoparticle surface or in solution by copper dissolved from the nanoparticle surface via Fenton-like reactions. In presence of H2O2, ascorbate, or both, copper (II) oxide generates hydroxyl radical, ascorbyl radical, and superoxide anion that interact with DNA, proteins, and lipids cause oxidative damage and cell death. ",The molecular weight is 79.54.,Cupric oxide has a topological polar surface area of 17.07.,,Cupric oxide is approved.,Cupric oxide is a solid.,True
14439,"Butamben is a local anesthetic in the form of n-butyl-p-aminobenzoate. Its structure corresponds to the standard molecule of a hydrophilic and hydrophobic domain separated by an intermediate ester found in most of the local anesthetics. Due to its very low water solubility, butamben was considered of low usability as it is only suitable to be used as a topical anesthesia. This belief changed with the introduction of epidural suspensions of butamben. All butamben-containing products were removed from the market under the belief that it is unsafe or ineffective. Butamben was indicated for the treatment of chronic pain due to its long-duration effect. It is also indicated as a surface anesthetic for skin a mucous membrane and for the relief of pain and pruritus associated with anorectal disorders. Butamben has been shown to selectively inhibit dorsal root pain signal transmission for periods of months when administered as epidural suspensions. The effect of butamben is not related to any significant loss of motor function which indicates that it targets specifically the pain-sensing C fibers of the dorsal root. When administered topically, butamben produced anesthesia by accumulating in the nerve cell membrane causing it to expand and lose its ability to depolarize and blocking the impulse transmission. Butamben acts by inhibiting the voltage-gated calcium channels in dorsal root ganglion neurons. The modification in this channels is thought to cause a disturbance of the channel kinetics acceleration. It is reported as well that butamben is an inhibitor of the sodium channels and a delayed rectifier of potassium currents. All the effects of butamben are performed in the root ganglion neurons which suggests that the related anesthetic effect may be caused by the reduced electrical excitability.",The molecular weight is 193.25.,Butamben has a topological polar surface area of 52.32.,The log p value of  is 2.98.,Butamben is approved and withdrawn.,Butamben is a solid.,True
14440,"Extracted from the dried leaves of bearberry plant in the genus _Arctostaphylos_ and other plants commonly in the _Ericaceae_ family, arbutin is a beta-D-glucopyranoside of. It is found in foods, over-the-counter drugs, and herbal dietary supplements. Most commonly, it is an active ingredient in skincare and cosmetic products as a skin-lightening agent for the prevention of melanin formation in various skin conditions that involve cutaneous hyperpigmentation or hyperactive melanocyte function. It has also been used as an anti-infective for the urinary system as well as a diuretic. Arbutin is available in both natural and synthetic forms; it can be synthesized from acetobromglucose and. Arbutin is a competitive inhibitor of tyrosinase (E.C.1.14.18.1) in melanocytes , and the inhibition of melanin synthesis at non-toxic concentrations was observed _in vitro_. Arbutin was shown to be less cytotoxic to melanocytes in culture compared to. Indicated for over-the-counter use for epidermal hyperpigmentation in various skin conditions, such as melasma, freckles, and senile lentigines.  At non-toxic concentrations, arbutin inhibited the activity of tyrosinase in cultured human keratinocytes, while having minimal effect on the expression of tyrosinase mRNA or the synthesis of the enzyme. α-Arbutin produced a concentration-dependent inhibition of melanin synthesis of human melanoma cells, HMV-II. No inhibitory effect on HMV-II cell growth was seen at concentrations lower than 1.0 mM. At concentrations of 0.5 mM of arbutin, tyrosinase activity was reduced to 60% of that in non-treated cells. The addition of arbutin blocked and inhibited α-MSH-stimulated melanogenesis in B16 melanoma cells, brownish guinea pig, and human skin tissue. In a pilot study of healthy male adults exposed to UV B irradiation, topical administration of arbutin inhibited UV-induced nuclear factor-kappaB activation in human keratinocytes. In mouse skin, arbutin counteracted oxidative stress induced by 12-O-tetradecanoylphorbol-13-acetate. Arbutin is a hydroquinone glycoside, however the hydroquinone moiety is not solely responsible for the de-pigmentating actions of arbutin. It acts as a competitive inhibitor of tyrosinase enzyme by acting on the L-tyrosine binding site to suppress melanogenesis and mediate its de-pigmenting actions on human skin. Tyrosinase is an enzyme involved in the regulation of rate-limiting steps during the synthesis of melanin; it regulates the conversion of L-tyrosine into L-dopa, and subsequent conversion of L-dopa to L-dopaquinone. Via inhibition of tyrosinase activity in a concentration-dependent manner, arbutin attenuates the production of melanin in melanocytes. While most studies suggest that arbutin has negligible effect on the tyrosinase mRNA expression, a study assessing the effect of arbutin on melanocyte differentiation inducement system using ES cells propose that arbutin may also downregulate the expression of tyrosinase in addition to its inhibitory action on the enzyme. The contradictory findings across studies may be due to previous studies using terminally-differentiated melanocytes and melanoma cells. ",The molecular weight is 272.25.,Arbutin has a topological polar surface area of 119.61.,The log p value of  is -0.51.,Arbutin is approved.,Arbutin is a solid.,True
14441,"Calcium phosphate is typically available as an over the counter supplement, antacid, or as an added ingredient in some toothpastes. For use as an over the counter calcium and phosphate supplement, antacid, or a source of calcium and phosphate in toothpaste. Calcium phosphate reacts with acid in the stomach to raise the pH. In toothpaste it provides a source of calcium and phosphate ions to support remineralization of the teeth. As a supplement it provides a source of calcium and phospate, both of which are important ions in bone homeostasis. The phosphate ions in calcium phosphate likely react with hydrochloric acid in the stomach to neutralize the pH. In toothpaste and in systemic circulation, calcium phosphate provides a source of calcium and phosphate ions to support remineralization of the teeth and bone homeostasis respectively. The increase in plasma calcium reduces calcium flux from osteocyte activity by reducing the secretion of parathyroid hormone (PTH). Calcium does this by stimulating a G-protein coupled calcium receptor on the surface of parathyroid cells. The reduction in calcium flux increases the amount of calcium deposited in bone resulting in an increase in bone mineral density. The reduction in PTH secretion also reduces the amount of vitamin D metabolized to its active form, calcidiol. Since calcidiol increases the expression of calcium dependent ATPases and transient receptor potential cation channel subfamily V member 6 (TRPV6) both of which are involved in calcium uptake from the gut, a reduction in calcidiol results in less calcium absorption. Additionally, TRPV5, the channel responsible for calcium reabsorption in the kidney, is downregulated when PTH secretion is reduced thus increasing calcium excretion via the kidneys. Another hormone, calitonin, is likely involved in the reduction of bone resorption during periods of high plasma calcium.",,,,Calcium Phosphate is approved.,Calcium Phosphate is a solid.,True
14442,"Dichlorvos or 2,2-dichlorovinyl dimethyl phosphate is a drug of the _organophosphate_ class, frequently used as an insecticide for the control of indoor pests and for the protection of stored products from insect infestations. The compound has been available on the market since 1961 and its use is a controversial topic due to environmental and health concerns. Dichlorvos is found in urban waterways and its toxicity may impact humans, leading to poisoning, neurotoxicity, and cancer.",,,,Dichlorvos is vet_approved.,,True
14443,"Grazoprevir is a direct acting antiviral medication used as part of combination therapy to treat chronic Hepatitis C, an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Treatment options for chronic Hepatitis C have advanced significantly since 2011, with the development of Direct Acting Antivirals (DAAs) such as Grazoprevir. Grazoprevir is an inhibitor of NS3/4A, a serine protease enzyme, encoded by HCV genotypes 1 and 4. These enzymes are essential for viral replication and serve to cleave the virally encoded polyprotein into mature proteins like NS3, NS4A, NS4B, NS5A and NS5B. The barrier for develoment of resistance to NS3/4A inhibitors is lower than that of NS5B inhibitors, another class of DAAs. Subtitutions at amino acid positions 155, 156, or 168 are known to confer resistance. The substitutions of the enzyme's catalytic triad consisting of H58, D82, and S139 are also likely to alter the affinity of the drug for NS3/4A or the activity of the enzyme itself. Despite this disadvantage Grazoprevir is still effective against HCV particularly when paired with. Grazoprevir is indicated in combination with (as the fixed dose combination product Zepatier) with or without for treatment of chronic HCV genotypes 1a, 1b, or 4 infection in adults.  Grazoprevir is classified as a direct-acting antiviral (DAA) and prevents viral replication in HCV genotypes 1a, 1b, and 4. Grazoprevir is a second generation NS3/4a protease inhibitor used to inhibit viral HCV replication. NS3/4a protease is an integral part of viral replication and mediates the cleavage the virally encoded polyprotein to mature proteins (NS3, NS4A, NS4B, NS5A and NS5B). Grazoprevir inhibits the NS3/4protease enzymes of HCV genotype 1a, 1B, and 4 with IC50 values of 7pM, 4pM, and 62pM, respectively.",The molecular weight is 766.91.,Grazoprevir has a topological polar surface area of 195.22.,The log p value of  is 6.32.,Grazoprevir is approved.,Grazoprevir is a solid.,True
14444,"Thiomersal (INN), commonly known in the U.S. as thimerosal, is an organomercury compound. This compound is a well-established and widely used antiseptic and antifungal agent.  Used as preservative in some cosmetics, topical pharmaceuticals, and biological drug products, which includes vaccines. Thimerosal is an organomercurial compound and derivative of thiosalicyclic acid with antibacterial and antifungal properties. Thimerosal, which consists of approximately 50% mercury by weight, has been one of the most widely used preservatives in vaccines. It is metabolized/degraded to ethylmercury and thiosalicylate. Ethylmercury is an organomercurial that must be carefully distinguished from methylmercury, a closely related substance that has been the focus of many studies. Methylmercury is the type of mercury found in various species of fish.  Experimental data demonstrates that the toxicokinetics of thimerosal (ethylmercury) is vastly different from that of methyl-mercury. Thus, methyl-mercury is not a suitable reference for assessing the risk from exposure to thimerosal-derived mercury. Although its mechanism of action is not fully understood, thimerosal inhibits sulfhydryl-containing active site of various enzymes and binds to sulfhydryl compounds, including glutathione, cysteine, and sulfhydryl groups of proteins. In addition, thimerosal activates the InsP3 calcium channel on the endoplasmic reticular membrane, thereby triggering the release of intracellular calcium resulting in a calcium-induced calcium-influx of extracellular calcium. Therefore, thimerosal may induce or inhibit various cellular functions that are dependent on the signaling of calcium.",The molecular weight is 404.81.,,,Thimerosal is approved.,Thimerosal is a solid.,True
14445,"Delamanid is an anti-tuberculosis agent derived from the nitro-dihydro-imidazooxazole class of compounds that inhibits mycolic acid synthesis of bacterial cell wall. It is used in the treatment of multidrug-resistant and extensively drug-resistant tuberculosis (TB) in a combination regimen. Emergence of multidrug-resistant and extensively drug-resistant tuberculosis creates clinical challenges for patients, as the disease is associated with a higher mortality rate and insufficient therapeutic response to standardized antituberculosis treatments as and. Multidrug-resistant tuberculosis may also require more than 2 years of chemotherapy and second-line therapies with narrow therapeutic index. In a clinical study involving patients with pulmonary multidrug-resistant tuberculosis or extensively drug-resistant tuberculosis, treatment of delamanid in combination with WHO-recommended optimised background treatment regimen was associated with improved treatment outcomes and reduced mortality rate. Spontaneous resistance to delamanid was observed during treatment, where mutation in one of the 5 F420 coenzymes responsible for bioactivation of delamanid contributes to this effect. Delamanid is approved by the EMA and is marketed under the trade name Deltyba as oral tablets. It is marketed by Otsuka Pharmaceutical Co., Ltd (Tokyo, Japan). Indicated for use as part of an appropriate combination regimen for pulmonary multi-drug resistant tuberculosis (MDR-TB) in adult patients when an effective treatment regimen cannot otherwise be composed for reasons of resistance or tolerability. The minimum inhibitory concentrations (MIC) of delamanid against _Mycobacterium tuberculosis_ isolates ranges from 0.006 to 0.024 g/mL. Among non-tuberculosis mycobacteria, delamanid has _in vitro_ activity against _M. kansasii_ and _M. bovis_. Delamanid has no in vitro activity against Gram negative or positive bacterial species and does not display cross-resistance to other anti-tuberculosis drugs. In murine models of chronic tuberculosis, the reduction of _M. tuberculosis_ colony counts by delamanid was demonstrated in a dose-dependent manner. Repeated dosing of delamanid may cause QTc-prolongation via inhibition of cardiac potassium channel (hERG channel), and this effect is mostly contributed by the main metabolite of delamanid, DM-6705. Animal studies indicate that delamanid may attenuate vitamin K-dependent blood clotting, increase prothrombin time (PT), and activated partial thromboplastin time (APTT). Delamanid is a prodrug that requires biotransformation via via the mycobacterial F420 coenzyme system, including the deazaflavin dependent nitroreductase (Rv3547), to mediate its antimycobacterial activity against both growing and nongrowing mycobacteria. Mutations in one of five coenzyme F420 genes, _fgd, Rv3547, fbiA, fbiB, and fbiC_ has been proposed as the mechanism of resistance to delamanid. Upon activation, the radical intermediate formed between delamanid and desnitro-imidazooxazole derivative is thought to mediate antimycobacterial actions via inhibition of methoxy-mycolic and keto-mycolic acid synthesis, leading to depletion of mycobacterial cell wall components and destruction of the mycobacteria. Nitroimidazooxazole derivative is thought to generate reactive nitrogen species, including nitrogen oxide (NO). However unlike isoniazid, delamanid does not alpha-mycolic acid. ",The molecular weight is 534.49.,Delamanid has a topological polar surface area of 101.12.,The log p value of  is 5.25.,Delamanid is approved and investigational.,Delamanid is a solid.,True
14446,"Vinflunine is a third-generation member of the vinca alkaloid family with anti-tumour actions. It was first described in 1998 at the Pierre Fabre research center in France. Like other vinca agents, vinflunine is an anti-mitotic agent that induces a cell cycle arrest at the G2/M phase and promotes cell death via apoptosis. Vinflunine is a microtubule inhibitor that binds to tubulin at or near to the vinca binding sites to inhibits its polymerization into microtubules during cell proliferation. In murine tumors and human tumor xenografts, vinflunine exhibits an antitumor efficacy than , , and.  For use as a monotherapy in adults with advanced or transitional cell carcinoma of the urothelial tract after failure of a prior platinum-containing therapy.  The antitumour effects of vinflunine are dependent on concentration and exposure duration of the drug. Vinflunine mediates an anti-mitotic action by inhibiting the microtubule assembly at micromolar concentrations and reducing the rate and extent of microtubule growing events. _In vivo_, vinflunine displays a significant antitumor activity against a broad spectrum of human xenografts in mice both in terms of survival prolongation and tumour growth inhibition. Compared with other vinca alkaloids, vinflunine is a less-potent inductor of drug resistance _in vitro_.  Microtubules are a major component of the cytoskeleton that have a critical role in maintenance of cell shape, mobility, adhesion and intracellular integrity. They also play a role in the formation of the mitotic spindle and chromosomal segregation to the daughter cells at mitosis. Via GTP hydrolysis at the β-tubulin subunit and polymerization of tubulin into linear polymers, microtubules, or macromolecular filaments composed of tubulin heterodimers, are formed via a mechanism of nucleation-elongation. At the onset of mitosis, the interphase microtubule network disassembles into the tubulin. The tubulin reassembles into a new population of mitotic spindle microtubules that further undergo rapid successions of lengthening and shortening until they are attached to the newly duplicated sister chromatids at their centromeres. The dynamic behaviour of microtubules are characterized by two mechanical process: dynamic instability indicating repeated switches of growth and shortening at the ends, and microtubule treadmilling that involves the fast-growing (+) end of the microtubule accompanied by a net loss of the opposite slow-growing (-) end. Microtubule treadmilling plays a critical role in mitosis by generating the forces for separation of the chromosomes in the mitotic spindle from centrosome and kinetochores. ",The molecular weight is 816.94.,Vinflunine has a topological polar surface area of 133.87.,The log p value of  is 5.37.,Vinflunine is approved and investigational.,Vinflunine is a solid.,True
14447,"Pitolisant is a selective antagonist or inverse agonist of the histamine H3 receptor used to treat type 1 or 2 narcolepsy. Narcolepsy is a chronic neurological disorder that affects 1 in 2,000 individuals and is characterized by excessive daytime sleepiness, abnormal REM sleep manifestations, sleep paralysis and hypnagogic hallucinations. About 60-70% of patients with narcolepsy experience cataplexy, which is a sudden loss of muscle tone triggered by positive or negative emotions. Histaminergic neuron signalling in the brain plays a role in maintaining wakefulness; by blocking histamine autoreceptors, pitolisant enhances the activity of histaminergic neurons, as well as increasing the signalling of other neurotransmitters in the brain. Pitolisant is indicated for the treatment of narcolepsy with or without cataplexy and excessive daytime sleepiness in narcolepsy in adult patients. Pitolisant promotes wakefulness in narcolepsy by enhancing histaminergic signalling in the central nervous system. It does not significantly bind to H1, H2, or H4 receptors. In patients with narcolepsy in presence or absence of cataplexy, treatment of pitolisant was associated with an improvement in the level and duration of wakefulness and daytime alertness assessed by objective measures of ability to sustain wakefulness (e.g. Maintenance of Wakefulness Test (MWT) and Epworth Sleepiness Scale (ESS) Scores) and attention (e.g. Sustained Attention to Response Task (SART)). Pitolisant also improved the frequency and severity of narcolepsy-associated cataplexy. Pitolisant acts as a blocker at hERG channels. In two QT studies, supra-therapeutic doses of pitolisant (3-6-times the therapeutic dose, that is 108 mg to 216 mg) produced mild to moderate prolongation of QTc interval (10-13 ms). Signalling of histaminergic neurons plays a key role in activating the arousal system with widespread projections to the whole brain via activating orexin receptors. Narcolepsy is characterized by insufficient neurotransmission by orexins, or hypocretins, which are excitatory peptides released by neurons located from the lateral hypothalamus. These neurons project to aminergic neurons, such as histaminergic or noradrenergic neurons, that are responsible for the effects of orexin and control of wakefulness. Histamine H3 receptors are presynaptic inhibitory autoreceptors that are located in the cerebral cortex, hypothalamus, hippocampus, and basal ganglia. H3 receptors promote the re-uptake of histamine at synaptic terminals and attenuate further histamine release into the synapse. By blocking H3 autoreceptors and increasing the levels of histamine transmitters at the synapse, pitolisant enhances the activity of histaminergic neurons and promotes wakefulness. Inverse agonism of pitolisant at H3 receptors also leads to enhanced synthesis and release of endogenous histamine over the basal level.",The molecular weight is 295.85.,Pitolisant has a topological polar surface area of 12.47.,The log p value of  is 4.82.,Pitolisant is approved and investigational.,Pitolisant is a solid.,True
14448,"Triheptanoin is a source of heptanoate fatty acids, which can be metabolized without the enzymes of long chain fatty acid oxidation. In clinical trials, patients with long chain fatty acid oxidation disorders (lc-FAODs) treated with triheptanoin are less likely to develop hypoglycemia, cardiomyopathy, rhabdomyolysis, and hepatomegaly. Complications in lc-FAOD patients are reduced from approximately 60% to approximately 10% with the addition of triheptanoin. Triheptanoin is a medium chain triglyceride indicated to provide calories and fatty acids to treat long chain fatty acid oxidation disorders (lc-FAODs). Triheptanoin is a source of medium chain fatty acids for patients with lc-FAODs. It has a moderate duration of action and a wide therapeutic window. Patients should be counselled regarding the risk of feeding tube dysfunction and intestinal malabsorption due to pancreatic insufficiency. Triheptanoin is a source of heptanoate fatty acids, which can be metabolized without the enzymes of long chain fatty acid oxidation. In clinical trials, patients with lc-FAODs treated with triheptanoin experienced improvements in hypoglycemia, cardiomyopathy, and rhabdomyolysis.",,,,Triheptanoin is approved and investigational.,Triheptanoin is a liquid.,True
14449,"Activation of the Raf-MEK-ERK signaling pathway is known to be implemented in several types of malignancies, thus, mitogen-activated protein kinase kinase (MEK) inhibitors such as selumetinib are important tools that can target the problematic overactivity of this pathway. Although selumetinib has been investigated for the treatment of several types of cancer, it is currently only indicated for the treatment of neurofibromatosis type 1 (NF1) in patients ≥2 years who have symptomatic, inoperable plexiform neurofibromas (PN). Selumetinib is a non-ATP-competitive mitogen-activated protein kinase kinase 1 and 2 (MEK1 and MEK2) inhibitor. By selectively targeting MEK1 and MEK2, selumetinib is able to inhibit oncogenic downstream effects of the Raf-MEK-ERK signaling pathway, which is often overactive in certain types of cancer. Indeed, a study investigating the effects of selumetinib in children with NF-1 found that treatment with the anti-neoplastic resulted in reduced tumor size. Decreases in tumor-associated pain and improvements in overall function were also subjectively reported. The Ras-Raf-MEK-ERK signaling cascade is known to be activated in several types of cancer, and regulates the transcription of proteins involved in apoptosis. In addition, studies have shown that mutations of the Raf component of the pathway can contribute to chemotherapy drug resistance. ",,,,Selumetinib is approved and investigational.,,True
14450,"To date, acalabrutinib has been used in trials studying the treatment of B-All, Myelofibrosis, Ovarian Cancer, Multiple Myeloma, and Hodgkin Lymphoma, among others. Acalabrutinib is currently indicated for the treatment of adult patients with Mantle Cell Lymphoma (MCL) who have received at least one prior therapy. It has also been recently approved for chronic lymphocytic leukemia and small lymphocytic lymphoma. Acalabrutinib is a Bruton Tyrosine Kinase inhibitor that prevents the proliferation, trafficking, chemotaxis, and adhesion of B cells. It is taken every 12 hours and can cause other effects such as atrial fibrillation, other malignancies, cytopenia, hemorrhage, and infection. Mantle Cell Lymphoma (MCL) is a rare yet aggressive type of B-cell non-Hodgkin lymphoma (NHL) with poor prognosis. Subsequently, relapse is common in MCL patients and ultimately represents disease progression.",The molecular weight is 465.52.,Acalabrutinib has a topological polar surface area of 118.51.,The log p value of  is 1.58.,Acalabrutinib is approved and investigational.,Acalabrutinib is a solid.,True
14451,"Rifamycin is the prime member of the rifamycin family which are represented by drugs that are a product of fermentation from the gram-positive bacterium _Amycolatopsis mediterranei_, also known as _Streptomyces mediterranei_. The parent compound of rifamycin was rifamycin B which was originally obtained as a main product in the presence of diethylbarburitic acid. Some small modifications where performed in this inactive compound and with the creation of rifamycin SV there was the first antibiotic used intravenously for the treatment of tuberculosis. Rifamycin is indicated for the treatment of adult patients with travelers' diarrhea caused by noninvasive strains of _E. coli_. The status of the disease should not be complicated by fever or blood in the stool. To prevent drug-resistant bacteria, it is important to mention that the use of rifamycin for this indication should be only done in cases where the infection is proven or strongly suspected to be caused by bacteria. Rifamycin is known to be effective against Gram-positive and Gram-negative pathogens and mycobacteria. It is very effective against _E. coli_ reporting a MIC90 of 64-128 mcg/ml without showing cross-resistance with other antimicrobial agents. Rifamycins, as well as all the other members of this group, present an antibacterial mechanism of action related to the inhibition of RNA synthesis. This mechanism of action is done by the strong binding to the DNA-dependent RNA polymerase of prokaryotes. The inhibition of the RNA synthesis is thought to be related with the initiation phase of the process and to involve stacking interactions between the naphthalene ring and the aromatic moiety in the polymerase. As well, it has been suggested that the presence of zinc atoms in the polymerase allows for the binding of phenolic -OH groups of the naphthalene ring. ",The molecular weight is 697.78.,Rifamycin has a topological polar surface area of 201.31.,The log p value of  is 3.86.,Rifamycin is approved and investigational.,Rifamycin is a solid.,True
14452,"Istradefylline, or KW6002, was developed by Kyowa Hakko Kirin in Japan for the treatment of Parkinson's disease as an adjunct to standard therapy. Unlike standard dopaminergic therapies for Parkinson's, Istradefylline targets adenosine A<sub>2A</sub> receptors in the basal ganglia. This region of the brain is highly involved in motor control. Istradefylline is indicated in adjunct to levodopa and carbidopa in the treatment of Parkinson's disease. Istradefylline is a selective adenosine A<sub>2A</sub> receptor inhibitor. It has a long duration of action as it is given once daily and has a half life of 64-69 hours. Patients taking this medication should be monitored for dyskinesia, hallucinations, and lack of impulse control. Consider dose reductions for these patients. Istradefylline is a selective adenosine A<sub>2A</sub> receptor inhibitor. These receptors are found in the basal ganglia, a region of the brain that suffers degeneration in Parkinson's disease, and is also significantly involved in motor control. A<sub>2A</sub> receptors are also expressed on GABAergic medium spiny neurons within the indirect striato-pallidal pathway. The GABAergic action of this pathway is thereby reduced. Istradefylline has 56 times the affinity for A<sub>2A</sub> receptors than A<sub>1</sub> receptors.",The molecular weight is 384.44.,Istradefylline has a topological polar surface area of 76.9.,The log p value of  is 3.37.,Istradefylline is approved and investigational.,Istradefylline is a solid.,True
14453,"Fostemsavir is the phosphonooxymethyl prodrug of temsavir, a novel HIV-1 attachment inhibitor. It binds to and inhibits the activity of gp120, a subunit within the HIV-1 gp160 envelope glycoprotein that facilitates the attachment of HIV-1 to host cell CD4 receptors - in doing so, temsavir prevents the first step in the HIV-1 viral lifecycle. The discovery of gp120 as a potential target of interest in the treatment of HIV-1 infection is relatively recent, and was born out of a desire to find alternative target proteins (i.e. mechanistically orthogonal therapies) for the treatment of HIV-1 patients with resistant infections. Fostemavir is the first attachment inhibitor to receive FDA approval, granted in July 2020 for use in combination with other antiretrovirals in highly treatment-experienced patients with multidrug-resistant HIV-1 infection whom are failing their current therapy. Targeting gp120 subunits is a new and novel therapeutic approach to HIV-1 infection, and the addition of attachment inhibitors, like temsavir, to the armament of therapies targeted against HIV-1 fills a necessary niche for therapeutic options in patients left with few, if any, viable treatments. Fostemsavir is indicated, in combination with other antiretrovirals, for the treatment of multidrug-resistant HIV-1 infection in heavily treatment-experienced adults failing their current antiretroviral therapy due to resistance, intolerance, or safety concerns. Temsavir inhibits the first stage in the HIV-1 viral lifecycle: attachment. It has a moderate duration of action necessitating twice-daily dosing. Fostemsavir, administered at roughly 4x the recommended human dose, has been observed to significantly prolong the QTc-interval. Patients with a history of QTc-prolongation, those receiving other QTc-prolonging medications, and/or those with pre-existing cardiac disease should use fostemsavir with caution, and should be monitored at baseline and throughout therapy for signs or symptoms suggestive of QTc-prolongation. Fostemsavir should also be used with caution in patients with hepatitis B or C co-infection as elevations in hepatic transaminases were observed in greater proportions in these populations in clinical trials. The gp120 subunit within the gp160 envelope glycoprotein of HIV-1 is a new and novel target in the treatment of HIV-1 infection. These subunits are responsible for facilitating the first step in the viral life cycle, attachment, by mediating the interaction between the virus and host cell CD4 receptors. Following attachment, HIV-1 undergoes assembly, budding, and maturation within the host cell, after which mature viral particles are released to continue the viral life cycle.",,,,Fostemsavir is approved and investigational.,Fostemsavir is a solid.,True
14454,"Chagas disease, caused by a parasite known as Trypanosoma cruzi (T.cruzi), is a vector-transmitted disease affecting animals and humans in the Americas. It is commonly known as American Trypanosomiasis. Nifurtimox is indicated in pediatric patients under 18 weighing at least 2.5 kg. Continued approval of this drug for this indication is dependent upon confirmatory clinical trial results. Nifurtimox exerts trypanosomal activity against Trypanosoma cruzi, treating Chagas disease. One study reports that nifurtimox and other benzofuran derivatives reduce parasite dehydrogenase activity. Results of a recent phase III clinical trial have shown that a significant number of pediatric patients with acute or chronic Chagas disease treated with nifurtimox were immunoglobulin G (IgG) antibody negative and demonstrated at least a 20% decrease in optical density on two IgG antibody tests for T. cruzi antigens. The mechanism of action of nifurtimox has not been fully elucidated, however, is believed to occur by the activation of nitroreductase enzymes that produce reactive metabolites with a series of deleterious effects on Trypanosoma cruzi, the parasite causing Chagas disease. The antiprotozoal actions of nifurtimox occur both intracellularly and extracellularly. Inhibition of parasite dehydrogenase activity is another purported mode of action of nifurtimox that warrants further research.",The molecular weight is 287.29.,Nifurtimox has a topological polar surface area of 106.02.,The log p value of  is 0.02.,Nifurtimox is approved and investigational.,Nifurtimox is a solid.,True
14455,"Ertugliflozin belongs to the class of potent and selective inhibitors of the sodium-dependent glucose cotransporters (SGLT), more specifically the type 2 which is responsible for about 90% of the glucose reabsorption from glomerulus. This drug was developed under the collaboration of Merck and Pfizer. It was FDA approved as monotherapy and in combination with sitagliptin or metformin hydrochloride on December 22, 2017. Ertugliflozin as a monotherapy is indicated to improve the glycemic control in adult patients with type 2 diabetes. Ertugliflozin, in combination with metformin hydrochloride, is indicated to improve glycemic control in patients with diabetes type 2 who are not controlled on a regimen of ertugliflozin or metformin or in patients who are already treated with both ertugliflozin and metformin. The administration of ertugliflozin in combination with sitagliptin is indicated to improve glycemic control in adult patients with type 2 diabetes when treatment with ertugliflozin and sitagliptin is appropriate. It is pointed out that the use of ertugliflozin has to be an adjunct therapy to the use of diet and exercise. Administration of ertugliflozin increases urinary glucose excretion which leads to a negative balance and osmotic diuresis. Thus, this antidiabetic agent has been reported to significantly reduce the body weight and blood pressure of diabetic patients.  As part of a normal process, the glucose from the blood is filtered for excretion and reabsorbed in the glomerulus so less than one percent of this glucose is excreted in the urine. The reabsorption is mediated by the sodium-dependent glucose cotransporter (SGLT), mainly the type 2 which is responsible for 90% of the reabsorbed glucose. Ertugliflozin is a small inhibitor of the SGLT2 and its activity increases glucose excretion, reducing hyperglycemia without the requirement of excessive insulin secretion.",The molecular weight is 436.89.,Ertugliflozin has a topological polar surface area of 108.61.,The log p value of  is 3.19.,Ertugliflozin is approved and investigational.,Ertugliflozin is a solid.,True
14456,"Neratinib was approved in July 2017 for use as an extended adjuvant therapy in Human Epidermal Growth Factor Receptor 2 (HER2) positive breast cancer. Approval was granted to Puma Biotechnology Inc. for the tradename Nerlynx. Neratinib is currently under investigation for use in many other forms of cancer. For use as an extended adjuvant treatment in adult patients with early stage HER2-overexpressed/amplified breast cancer, to follow adjuvant trastuzumab-based therapy. Neratinib is a tyrosine kinase inhibitor which exhibits antitumor action against Epidermal Growth Factor Receptor (EGFR), HER2, and Human Epidermal Growth Factor Receptor 4 (HER4) postive carcinomas. Neratinib binds to and irreversibly inhibits EGFR, HER2, and HER4. This prevents auotphoshorylation of tyrosine residues on the receptor and reduces oncogenic signalling through the mitogen-activated protein kinase and Akt pathways.",The molecular weight is 557.05.,Neratinib has a topological polar surface area of 112.4.,The log p value of  is 5.0.,Neratinib is approved and investigational.,Neratinib is a solid.,True
14457,"Relugolix is a gonadotropin-releasing hormone (GnRH) receptor antagonist used in the treatment of several hormone-responsive conditions. It was first approved in Japan in 2019, under the brand name Relumina, for the symptomatic treatment of uterine fibroids, and more recently by the United States' FDA in 2020, under the brand name Orgovyx, for the treatment of advanced prostate cancer. Relugolix has also been studied in the symptomatic treatment of endometriosis.  Relugolix is indicated for the treatment of adult patients with advanced prostate cancer. Approximately 56% of patients achieved castrate-level testosterone concentrations (<50 ng/dL) by day 4 of therapy and 97% of patients maintain these levels through 48 weeks of therapy. Relugolix requires once-daily oral administration to maintain the desired testosterone concentrations. The pathogenesis and progression of prostate cancer appear driven, at least in part, by the effects of testosterone. Androgen deprivation has been demonstrated to result in cell death and tumor regression in many well-differentiated prostate cancer cell lines - for this reason, androgen deprivation therapy (ADT) has become a standard in the treatment of prostate cancer, particularly in advanced disease.",,,,Relugolix is approved and investigational.,Relugolix is a solid.,True
14458,"Revefenacin is a novel biphenyl carbamate tertiary amine agent that belongs to the family of the long-acting muscarinic antagonists (LABA). The labile primary amide in the structure produces a \soft-drug\"" site that allows rapid systemic clearance and minimizing of the systemically mediated adverse reactions. The LABA group falls into a parent category known as long-acting inhaled bronchodilators and this type of agents are recommended as a maintenance therapy for chronic obstructive pulmonary disease (COPD). From the LABA group, revefenacin is the first once-daily nebulized LAMA treatment. It was developed by Theravance Biopharma and FDA approved on November 9, 2018."" Revefenacin is indicated as an inhalation solution for the maintenance treatment of patients with chronic obstructive pulmonary disease (COPD). Revefenacin has been reported to produce a sustained, long-acting bronchodilation with lower anti-muscarinic-related side effects. In clinical trials, revefenacin demonstrated to be of a long duration of action and low systemic exposure in patients with COPD. Also, it was reported that a dose of 88 mcg can produce a clinically effective bronchodilation measured by through forced expiratory volume in 1s and serial spirometric assessments. Revefenacin is an inhaled bronchodilator muscarinic antagonist with a long-acting bronchodilation activity. It has been shown to present a high affinity and behaved as a competitive antagonist of the five muscarinic cholinergic receptors. Studies have indicated that revefenacin dissociates significantly slower from the muscarinic receptor M3 (hM3) when compared to the receptor M2 (hM2) which indicates a kinetic selectivity for this subtype. This competitive antagonism produces a suppressive action of the acetylcholine-evoked calcium mobilization and contractile responses in the airway tissue. Lastly, due to the duration of the bronchodilation, revefenacin is considered a long-acting muscarinic antagonist which allows it to be dosed once daily.",,,,Revefenacin is approved and investigational.,Revefenacin is a solid.,True
14459,"Delafloxacin is a fluoroquinolone antibiotic which has been used in trials studying the treatment and basic science of Gonorrhea, Hepatic Impairment, Bacterial Skin Diseases, Skin Structure Infections, and Community Acquired Pneumonia, among others. It was approved in June 2017 under the trade name Baxdela for use in the treatment of acute bacterial skin and skin structure infections. Delafloxacin is indicated for the treatment of acute bacterial skin and skin structure infections caused by the Gram-positive organisms Staphylococcus aureus (including methicillin-resistant and methicillin-susceptible isolates), Staphylococcus haemolyticus, Staphylococcus lugdunensis, Streptococcus agalactiae, Streptococcus anginosus Group (including Streptococcus anginosus, Streptococcus intermedius, and Streptococcus constellatus), Streptococcus pyogenes, and Enterococcus faecalis as well as the Gram-negative organisms Escherichia coli, Enterobacter cloacae, Klebsiella pneumoniae, and Pseudomonas aeruginosa. Delafloxacin is a fluoroquinolone antibacterial drug which kills bacterial cells. Delafloxacin inhibits the activity of bacterial DNA topoisomerase IV and DNA gyrase (topoisomerase II). This interferes with bacterial DNA replication by preventing the relaxation of positive supercoils introduced as part of the elongation process. The resultant strain inhibits further elongation. Delafloxacin exerts concentration-dependent bacteriocidal activity.",The molecular weight is 440.76.,Delafloxacin has a topological polar surface area of 119.99.,The log p value of  is 1.25.,Delafloxacin is approved and investigational.,Delafloxacin is a solid.,True
14460,"Dacomitinib, designed as (2E)-N-16-4-(piperidin-1-yl) but-2-enamide, is an oral highly selective quinazalone part of the second-generation tyrosine kinase inhibitors which are characterized by the irreversible binding at the ATP domain of the epidermal growth factor receptor family kinase domains. Dacomitinib is indicated as the first-line treatment of patients with metastatic non-small cell lung cancer (NSCLC) with epidermal growth factor receptor (EGFR) exon 19 deletion or exon 21 L858R substitution mutations as verified by an FDA-approved test. Preclinical data suggested that dacomitinib increases the inhibition of the epidermal growth factor receptor kinase domain as well as the activity in cell lines harboring resistance mutations such as T790M. This activity further produced a significant reduction of EGFR phosphorylation and cell viability. In these studies, non-small cell lymphoma cancer cell lines with L858R/T790M mutations where used and an IC50 of about 280 nmol/L was observed. Dacomitinib is an irreversible small molecule inhibitor of the activity of the human epidermal growth factor receptor (EGFR) family (EGFR/HER1, HER2, and HER4) tyrosine kinases. It achieves irreversible inhibition via covalent bonding to the cysteine residues in the catalytic domains of the HER receptors. The affinity of dacomitinib has been shown to have an IC50 of 6 nmol/L.",,,,Dacomitinib is approved and investigational.,Dacomitinib is a solid.,True
14461,"Glasdegib, also known as PF-04449913, is a small-molecule hedgehog signaling inhibitor selected under the group of the benzimidazoles. In early research, benzimidazoles attracted large interest as they represented a class of inhibitors with a low molecular weight, potent inhibitory activity and lacking unstable functionality. The great lipophilicity of this group of compounds brought interest to further modification. This analysis concluded that the presence of p-cyano ureas presented good physicochemical and pharmacokinetic properties from which glasdegib was developed.  Glasdegib, in combination with cytarabine, is indicated for the treatment of newly diagnosed acute myeloid leukemia in adult patients who are over 75 years old or that have co-morbidities that preclude intensive induction chemotherapy. In preclinical studies, glasdegib achieved a significant reduction in leukemic stem cell burden in xenograft models and a reduction in cell population expressing leukemic stem cell markers. Glasdegib is a potent and selective inhibitor of the hedgehog signaling pathway that acts by binding to the smoothened (SMO) receptor.",,,,Glasdegib is approved and investigational.,Glasdegib is a solid.,True
14462,"Abemaciclib is an antitumor agent and dual inhibitor of cyclin-dependent kinases 4 (CDK4) and 6 (CDK6) that are involved in the cell cycle and promotion of cancer cell growth in case of unregulated activity. On September 28, 2017, FDA granted approval of abemaciclib treatment under the market name Verzenio for the treatment of HR-positive and HER2-negative advanced or metastatic breast cancer that has progressed after unsuccessful endocrine therapy. It is either given alone in patients who has undergone endocrine therapy and chemotherapy after the metastasis of cancer, or in combination with. Following oral treatment in patients with HR-positive, HER2-negative breast cancer, abemaciclib demonstrated increased progression-free survival rates and objective response rates. Abemaciclib has been used in trials studying the treatment of melanoma, lymphoma, neoplasm, solid tumor, and glioblastoma. * Indicated in combination with fulvestrant for the treatment of women with hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative advanced or metastatic breast cancer with disease progression following endocrine therapy.  In combination with fulvestrant, the progression-free survival for patients with HR-positive, HER2-negative breast cancer was 16.4 months compared to 9.3 months for patients taking a placebo with fulvestrant. As a monotherapy, 19.7% of patients taking abemaciclib achieved complete or partial shrinkage of their tumors for a median 8.6 months after treatment. Abemaciclib induces cell cycle arrest and exerts an antitumor activity in human tumor xenograft models.  Regulation of cell cycle is crucial in maintaining proper cell growth; dysregulated cell cycle signalling pathway is a key component in inducing hyperproliferation of cells and tumor formation in various cancers. G1 to S phase cell cycle progression, or transition through the G1 restriction point (R), is promoted by the retinoblastoma tumor suppressor protein (Rb)-mediated pathway. Activation of Rb-mediated pathway requires the interaction of Cyclin-dependent kinases (CDK) 4 and 6 with D-type cyclins, which drives the formation of active CDK4/CDK6 and subsequent phosphorylation of Rb. ",The molecular weight is 506.61.,Abemaciclib has a topological polar surface area of 75.0.,The log p value of  is 4.76.,Abemaciclib is approved and investigational.,,True
14463,"Gilteritinib, also known as ASP2215, is a small molecule part of the FLT3 tyrosine kinase inhibitors that presented a greater selectivity and potency when compared with other agents from this group. It is a pyrazinecarboxamide derivative that showed high selectivity to FLT3 preventing the c-Kit -driven myelosuppression observed in other therapies. Gilteritinib was developed by Astellas Pharma and FDA approved on November 28, 2018. This drug was approved after being designed as an orphan drug with a fast track and priority review status. Gilteritinib is indicated for the treatment of adult patients who have relapsed or refractory acute myeloid leukemia with an FLT3 mutation detected by an FDA-approved test. This indication was expanded for a companion diagnostic to include use with gilteritinib such as the LeukoStrat CDx FLT3 Mutation Assay. In preclinical trials, gilteritinib demonstrate an IC50 for the wild-type receptor of 5 nM, 0.7-1.8 nM for ITD-mutated and comparable inhibition to other therapies in the TKD-mutated. As well, data showed a gilteritinib-driven inhibition of the receptor tyrosine kinase AXL which is known to modulate the activity of FLT3 in acute myeloid leukemia. Another important result _in vivo_ was the localization in high levels in xenografted tumors which indicated high selectivity. Gilteritinib is a potent selective inhibitor of both of the mutations, internal tandem duplication (ITD) and tyrosine kinase domain (TKD), of the FLT3 receptor. In the same note, gilteritinib also inhibits AXL and ALK tyrosine kinases. FLT3 and AXL are molecules involved in the growth of cancer cells. The activity of gilteritinib permits an inhibition of the phosphorylation of FLT3 and its downstream targets such as STAT5, ERK and AKT.",,,,Gilteritinib is approved and investigational.,Gilteritinib is a solid.,True
14464,"Remimazolam is an ultra short-acting benzodiazepine used in the induction and maintenance of sedation during short (<30 minute) procedures. Recent trends in anesthesia-related drug development have touted the benefits of so-called \soft drugs\"" - these agents, such as , are designed to be metabolically fragile and thus susceptible to rapid biotransformation and elimination as inactive metabolites. These \""soft drugs\"" are useful in the context of surgical procedures, wherein a rapid onset/offset is desirable, enabling anesthesiologists to manipulate drug concentrations as needed. Remimazolam was the first \""soft\"" benzodiazepine analog to be developed and was approved for use by the FDA in July 2020 under the brand name Byfavo."" Remimazolam is indicated for the induction and maintenance of procedural sedation in adults undergoing procedures lasting 30 minutes or less. Remimazolam modulates the effects of GABA(A) receptors in order to enhance the effects of GABA. It is considered an \ultra short-acting\"" benzodiazepine that achieves peak sedation within 3 to 3.5 minutes following intravenous administration, a property that makes it desirable for use during short procedures. Hepatic impairment can result in elevated serum levels of remimazolam - patients with severe hepatic impairment should be carefully titrated to effect. As of its approval date, remimazolam has not received a scheduling action by the DEA under the Controlled Substances Act. As benzodiazepines as a class have been implicated in the development of drug dependence and have a known potential for abuse, remimazolam should be used with caution in patients with a history of drug dependence or abuse."" Like other benzodiazepines, remimazolam exerts its therapeutic effects by potentiating the effect of gamma-aminobutyric acid (GABA) on GABA(A) receptors, the main inhibitory neurotransmitter receptors in the mammalian brain. GABA(A) receptors are a component of GABA-gated ionotropic chloride channels that produce inhibitory postsynaptic potentials - following activation by GABA, the channel undergoes a conformational change that allows the passage of chloride ions through the channel. The inhibitory potentials produced by GABA neurotransmission play an integral role in the suppression and control of epileptiform nerve firing such as that seen in epilepsy, which makes the GABA system a desirable target in the treatment of epilepsy.",,,,Remimazolam is approved and investigational.,Remimazolam is a solid.,True
14465,"Omadacycline has been used in trials studying the treatment of Bacterial Pneumonia, Bacterial Infections, Community-Acquired Infections, and Skin Structures and Soft Tissue Infections. Omadacycline represents a significant advance over the well-known tetracycline family, and has been shown to be highly effective in animal models at treating increasingly problematic, clinically prevalent infections caused by gram-positive bacteria, such as methicillin-resistant Staphylococcus aureus (MRSA), and by gram-negative, atypical and anaerobic bacteria, including those resistant to currently available classes of antibiotics and known to cause diseases such as pneumonias, urinary tract infections, skin diseases and blood-borne infections in both the hospital and community settings. Omadacycline is indicated for the treatment of community acquired bacterial pneumonia and acute bacterial skin and skin structure infections caused by omadacycline-susceptible organisms in adults. Omadacycline can be either bacteriostatic or bacteriocidal depending on the organism involved. It disrupts bacterial protein synthesis without affecting DNA, RNA, or peptidoglycan synthesis. Omadacycline represents an improvement over existing tetracycline agents as it has not been found to be subject to tetracycline resistance mediated by tetracycline efflux pumps encoded by the tet(K), tet(L), and tet(B) or to ribosomal protection proteins encoded by tet(O) and tet(M). Omadacycline is susceptible to RNA mutations which confer resistance to tetracyclines. Omadacycline binds to the primary tetracycline binding site on the bacterial 30s ribosomal subunit with high specificity. There it acts to block protein synthesis, disrupting many facets of cellular function and resulting in either cell death or stasis.",,,,Omadacycline is approved and investigational.,Omadacycline is a solid.,True
14466,"Discovered by Toyama Chemical Co., Ltd. in Japan, favipiravir is a modified pyrazine analog that was initially approved for therapeutic use in resistant cases of influenza. The antiviral targets RNA-dependent RNA polymerase (RdRp) enzymes, which are necessary for the transcription and replication of viral genomes. In 2014, favipiravir was approved in Japan to treat cases of influenza that were unresponsive to conventional treatment. Given its efficacy at targetting several strains of influenza, it has been investigated in other countries to treat novel viruses including Ebola and most recently, COVID-19. Favipiravir functions as a prodrug and undergoes ribosylation and phosphorylation intracellularly to become the active favipiravir-RTP. Favipiravir-RTP binds to and inhibits RNA dependent RNA polymerase (RdRp), which ultimately prevents viral transcription and replication. The mechanism of action of favipiravir is novel compared to existing influenza antivirals that primarily prevent entry and exit of the virus from cells. The active favipiravir-RTP selectively inhibits RNA polymerase and prevents replication of the viral genome. There are several hypotheses as to how favipiravir-RTP interacts with RNA dependent RNA polymerase (RdRp). Some studies have shown that when favipiravir-RTP is incorporated into a nascent RNA strand, it prevents RNA strand elongation and viral proliferation. Studies have also found that the presence of purine analogs can reduce favipiravir’s antiviral activity, suggesting competition between favipiravir-RTP and purine nucleosides for RdRp binding.",The molecular weight is 157.1.,Favipiravir has a topological polar surface area of 89.1.,The log p value of  is 0.72.,Favipiravir is approved and investigational.,Favipiravir is a solid.,True
14467,"Copanlisib is a selective pan-Class I phosphoinositide 3-kinase (PI3K/Phosphatidylinositol-4,5-bisphosphate 3-kinase/phosphatidylinositide 3-kinase) inhibitor that was first developed by Bayer Healthcare Pharmaceuticals, Inc. The drug targets the enzyme that plays a role in regulating cell growth and survival. Copanlisib was granted accelerated approval on September 14, 2017 under the market name Aliqopa for the treatment of adult patients with relapsed follicular lymphoma and a treatment history of at least two prior systemic therapies. Follicular lymphoma is a slow-growing type of non-Hodgkin lymphoma that is caused by unregulated proliferation and growth of lymphocytes. The active ingredient in Aliquopa intravenous therapy is copanlisib dihydrochloride. Indicated for the treatment of adult patients with relapsed follicular lymphoma (FL) who have received at least two prior systemic therapies. Copanlisib has demonstrated potent anti-tumor and pro-apoptotic activity in various tumor cell lines and xenograft models. In clinical trials, 59 percent of patients receiving copanlisib achieved complete or partial shrinkage of their tumors after a median of 12.2 months. Higher systemic levels of copanlisib is associated with elevated plasma glucose levels.  Follicular lymphoma is a B-cell lymphoma that is one of the most common type of non-Hodgkin lymphoma (NHL). It involves unregulated growth and proliferation of lymphocytes that eventually may travel to other organs including the lymph nodes, spleen, and the bone marrow, to form tumors. The phosphatidylinositol 3-kinase (PI3K)-mediated pathway is involved in promoting cell survival proliferation and differentiation however abberant activation of this pathway may lead to tumorigenesis. Copanlisib mediates an inhibitory action on p110α and p110δ isoforms of phosphatidylinositol-3-kinase (PI3K) expressed in malignant B cells. It induces tumor cell death via apoptosis and inhibits the proliferation of primary malignant B cell lines. Copanlisib inhibits several key cell-signaling pathways, including B-cell receptor (BCR) signaling, CXCR12 mediated chemotaxis of malignant B cells, and NFκB signaling in lymphoma cell lines. ",The molecular weight is 480.53.,Copanlisib has a topological polar surface area of 139.79.,The log p value of  is 1.11.,Copanlisib is approved and investigational.,Copanlisib is a solid.,True
14468,"Lurbinectedin is a DNA alkylating agent that has been investigated in the treatment of a variety of cancers, including mesothelioma, chronic lymphocytic leukemia (CLL), breast cancer, and small-cell lung cancer (SCLC). It is a derivative of the marine-derived agent ecteinascidin (), an anticancer agent found in extracts of the tunicate _Ecteinascidia turbinata_, with the primary difference being the substitution of the tetrahydroisoquinoline with a tetrahydro β‐carboline that results in increased antitumour activity of lurbinectedin as compared to its predecessor. Lurbinectedin is indicated for the treatment of adult patients with metastatic small-cell lung cancer (SCLC) with disease progression on or after platinum-based chemotherapy. Lurbinectedin exerts its chemotherapeutic activity by covalently binding to DNA, resulting in double-strand DNA breaks and subsequent cell death. Lurbinectedin has been associated with myelosuppression, and patients receiving therapy with this agent should be closely monitored for evidence of cytopenias. Prior to beginning therapy, ensure baseline neutrophil counts are >1,500 cells/mm<sup>3</sup> and platelet counts are >100,000/mm<sup>3</sup>. The supplementary use of granulocyte colony-stimulating factor (G-CSF) should be considered if the neutrophil count falls below 500 cells/mm<sup>3</sup>. Lurbinectedin has also been associated with hepatotoxicity. Monitor liver function tests at baseline and regular intervals throughout therapy, and consider holding, reducing, or permanently discontinuing therapy based on the severity of observed hepatotoxicity. Lurbinectedin is a DNA alkylating agent. It covalently binds to guanine residues in the DNA minor groove, forming adducts that bend the DNA helix towards the major groove. This process triggers a cascade of events that affect the activity of transcription factors and impairs DNA repair pathways, ultimately leading to double-strand DNA breaks and eventual cell death. Additional mechanism(s) of action include inhibition of RNA-polymerase-II activity, inactivation of Ewing Sarcoma Oncoprotein (EWS-FL11) via nuclear redistribution, and the inhibition of human monocyte activity and macrophage infiltration into tumor tissue.",,,,Lurbinectedin is approved and investigational.,Lurbinectedin is a solid.,True
14469,"Grapiprant, also known as AT-001 and CJ-023, is a drug from the piprant class. These molecules were derived from acylsulfonamide and are characterized to be a novel series of para-N-acylaminomethylbenzoic acid known to be prostaglandin receptor antagonists. This type of molecules is currently in development for veterinary patients. This class of drugs was defined in 2013 by the World Health Organization.  The effects of grapiprant have been investigated in the area of analgesia and anti-inflammation due to the effects that have been reported about this molecule. Preclinical studies have shown that grapiprant is very effective to reduce acute and chronic pain and inflammation. The effect of grapiprant seems to be dose-dependent and it is comparable to the effect of rofecoxib and piroxicam. Grapiprant is an EP4 prostaglandin receptor antagonist and thus the activity of this drug is thought to be completely related to the selective blockade of this receptor. It binds to human and other mammals EP4 prostaglandin receptor with high affinity without interfering with other prostaglandin pathways which are important for a variety of physiological functions. The binding of grapiprant blocks PGE2 binding and hence its biological effect related to the signaling pain and inflammation cascade.",,,,Grapiprant is investigational and vet_approved.,Grapiprant is a solid.,True
14470,"Darolutamide is a nonsteroidal androgen receptor antagonist for the treatment of castrate-resistant, non-metastatic prostate cancer (nmCRPC). This condition occurs in the majority of patients with advanced prostate cancer who have been treated with androgen receptor antagonists. Though prior treatment for prostate cancer has been successful for these patients, the cancer eventually progresses to become resistant to existing therapies. This warrants further treatment. This drug is indicated for the treatment of patients diagnosed with non-metastatic and castrate-resistant prostate cancer. Darolutamide, through its downstream effects on cancer cell growth, treats castrate-resistant prostate cancer. It inhibits cancer cell growth and markedly lowers prostate specific antigen (PSA) levels through potent androgen receptor antagonism. The actions of androgens on androgen receptors (AR) potentiate the growth and survival of prostate cancer cells. Darolutamide competitively inhibits androgens from binding to their receptors, inhibiting AR nuclear translocation, as well as AR-mediated transcription. The end result of these processes is a decrease in prostate cancer cell proliferation and tumor size. Its main metabolite, keto-darolutamide, shows similar pharmacological activity to the parent drug, darolutamide. Darolutamide has been found to bind more tightly to the AR receptor than and , which are other androgen receptor antagonists.",,,,Darolutamide is approved and investigational.,Darolutamide is a solid.,True
14471,"Pexidartinib is a selective tyrosine kinase inhibitor that works by inhibiting the colony-stimulating factor (CSF1)/CSF1 receptor pathway. Pexidartinib was originally developed by Daiichi Sankyo, Inc. and it was approved by the FDA in August 2019 as the first systemic therapy for adult patients with symptomatic tenosynovial giant cell tumor. Tenosynovial giant cell tumor is a rare form of non-malignant tumor that causes the synovium and tendon sheaths to thicken and overgrow, leading to damage in surrounding joint tissue. Debilitating symptoms often follow with tenosynovial giant cell tumors, along with a risk of significant functional limitations and a reduced quality of life in patients. Pexidartinib is indicated for the treatment of adult patients with symptomatic tenosynovial giant cell tumor (TGCT) associated with severe morbidity or functional limitations and not amenable to improvement with surgery. Pexidartinib works by suppressing the growth of tenosynovial giant cell tumors. In clinical trials comprising of patients with symptomatic tenosynovial giant cell tumor, pexidartinib had a higher overall response rate, characterized by improved patient symptoms and functional outcomes, compared to placebo. Pexidartinib works by inhibiting the activation and signaling of tumor-permissive cytokines and receptor tyrosine kinases that play a central role in tumor cell proliferation and survival. Tenosynovial giant cell tumor is a rare, non-malignant neoplasm that causes abnormal growth and damage to the synovium, bursae, or tendon sheaths. Recruitment of immune cells, specifically macrophages, is closely associated with the tumor mass formation in tenosynovial giant cell tumors. Macrophages drive tumor-promoting inflammation and play a central role in every stage of tumor progression. As the most abundant immune cells in the tumor microenvironment of solid tumors, macrophages promote processes that enhance tumor survival, such as angiogenesis, tumor cell invasion, and intravasation at the primary site. They also modulate the immune response to tumors to inhibit tumor clearance and directly engage with tumor cells to activate pro-survival signaling pathways.",,,,Pexidartinib is approved and investigational.,Pexidartinib is a solid.,True
14472,Hypericin is under investigation for the treatment of Cutaneous T-cell Lymphoma.,,,,Hypericin is investigational.,,True
14473,"Edoxudine is a deoxythymidine analog with activity against herpes simplex virus. It is a potent and selective inhibitor of herpes simplex virus type 1 and 2. The obtained product is an antiviral ointment. The activity of edoxudine against herpes simplex virus was first recognized in 1967. It was later recognized to be effective in vivo in a preclinical model of keratitis caused by herpes virus. It was developed by McNeil Pharmaceutical and approved by Health Canada on December 31, 1992. This medication was later discontinued from the market in 1998. Edoxudine was used in Europe, in the form of a topical antiviral, for the treatment of human herpes keratitis. Human herpes keratitis is an inflammation of the cornea in the eye caused by herpes simplex virus infection. This infection is a cause of significant morbidity whose incidence is significantly increased in the presence of recurrent infection and it can even produce corneal blindness. In reports, it has been indicated that at antivirally active doses, edoxudine is phosphorylated to a much greater extent by hepatitis-infected cells when compared to mock-infected cells. Once phosphorylated, edoxudine is more highly incorporated into viral DNA than cellular DNA. The level of incorporation into viral DNA highly seems to be correlated with the concentration of edoxudine. The suppression of viral DNA synthesis caused a shutoff of viral replication and the viral titration is significantly reduced.The effect of edoxudine is also proven to reduce significantly the lesion area produced by the viral activity to an even 44% reduction. Edoxudine is a potent inhibitor of the replication of herpes simplex virus type 1 and 2. For the activation of this drug, the action of viral thymidine kinase is required to phosphorylate this molecule in order to form the 5'-monophosphate derivative. Then, it is needed to be further phosphorylated by cellular enzymes until the formation of the 5'-triphosphate derivative which is a competitive inhibitor of the viral-coded DNA polymerase. The advantage of edoxudine is that it is highly selective, this characteristic can be seen by its preferential phosphorylation in herpes-infected cells and its preferential incorporation into viral DNA.",The molecular weight is 256.26.,Edoxudine has a topological polar surface area of 99.1.,The log p value of  is -0.86.,Edoxudine is approved and investigational and withdrawn.,Edoxudine is a solid.,True
14474,"Bismuth subgallate is a yellow colored substance that presents as an odorless powder that undergoes discoloration when exposed to sunlight. It is a heavy metal salt of gallic acid that is highly insoluble and poorly absorbed. Possessing protective effects on the gastric mucosa, strong astringent effects, and not as yet elucidated antimicrobial and hemostatic actions, bismuth subgallate is most commonly available as an over-the-counter internal deodorant where it is often employed as the primary active ingredient. The most common medical purpose for which bismuth subgallate is currently and formally indicated for is the use as a non-prescription internal deodorant product for the purpose of deodorizing flatulence and stools. Bismuth subgallate is a heavy metal salt that is relatively insoluble and poorly absorbed. As a result, systemic absorption is not necessary or possibly even desired when the agent is administered orally or onto specific otorhinolaryngology and/or dermatologic wound sites where it can execute its pharmacologic action directly within the gastrointestinal lumen to deodorize flatulence and stools or potentially elicit a hemostatic effect on wounds. Bismuth salts exert their action largely in the upper gastrointestinal tract by way of local activity from luminal bismuth in the stomach and duodenum.",The molecular weight is 394.09.,Bismuth subgallate has a topological polar surface area of 96.22.,The log p value of  is -0.25.,Bismuth subgallate is approved.,Bismuth subgallate is a solid.,True
14475,"Semaglutide is a glucagon-like peptide 1 (GLP-1) analog used to manage type 2 diabetes along with lifestyle changes Other members of this drug class include and. Semaglutide was developed by Novo Nordisk and approved by the FDA for subcutaneous injection in December 2017. The tablet formulation was approved for oral administration in September 2019. Semaglutide is indicated to improve glycemic control in adults diagnosed with type 2 diabetes mellitus, and is used as an adjunct to diet and exercise.  Semaglutide reduces HbA1c, systolic blood pressure, and body weight. After 12 weeks of treatment, semaglutide decreased fasting and postprandial glucose by increasing insulin production and decreasing glucagon secretion (which is normally associated with increases in blood sugar). Semaglutide also lowers fasting triglycerides and VLDL cholesterol, exerting beneficial effects on cardiovascular health. **Mechanism of glycemic control**",The molecular weight is 4113.64.,Semaglutide has a topological polar surface area of 1646.18.,,Semaglutide is approved and investigational.,Semaglutide is a solid.,True
14476,"Testosterone cypionate is a synthetic derivative of testosterone in the form of an oil-soluble 17 (beta)-cyclopentylpropionate ester. Its benefit compared to other testosterone derivatives is the slow rate of release after injection and longer half-life. The characteristics of testosterone cypionate and testosterone enanthate are very similar, therefore both of them tend to be interchangeable. It was developed by the company Pharmacia and Upjohn and FDA approved on July 25, 1979. Testosterone cypionate is used in males that present conditions derived from a deficiency or absence of endogenous testosterone. These conditions are 1) primary hypogonadism, defined as the testicular failure due to cryptorchidism, bilateral torsion, orchitis, vanishing testis syndrome or orchidectomy; and 2) hypogonadotropic hypogonadism characterized by idiopathic gonadotropin, LHRH deficiency or pituitary-hypothalamic injury from tumors, trauma or radiation. Testosterone cypionate presents the same properties than its analog testosterone with the advantage that this molecule has a longer release rate and half-life. Administration of ester derivatives of testosterone as testosterone cypionate generates an increase in serum testosterone to levels reaching 400% from the baseline within 24 hours of administration. These androgen levels remain elevated for 3-5 days after initial administration. The continuous variation in plasma testosterone after intramuscular administration of testosterone cypionate results in fluctuations in mood and libido as well as some local inflammation. The effects of testosterone in humans and other vertebrates occur by way of two main mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors. Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5&alpha;-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5&alpha;-reductase. DHT binds to the same androgen receptor even more strongly than T, so that its androgenic potency is about 2.5 times that of T. The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.",The molecular weight is 412.61.,Testosterone cypionate has a topological polar surface area of 43.37.,The log p value of  is 6.97.,Testosterone cypionate is approved.,Testosterone cypionate is a solid.,True
14477,"Testosterone enanthate is an esterified variant of testosterone that comes as an injectable compound with a slow release rate. It is the first injectable ester preparation of testosterone. This slow release is achieved by the presence of the enanthate ester functional group attached to the testosterone molecule. This testosterone derivative was first approved on December 24, 1953. Testosterone enanthate in males is indicated as a replacement therapy in conditions associated with a deficiency or absence of endogenous testosterone. Some of the treated conditions are 1) primary hypogonadism, defined as testicular failure due to cryptorchidism, bilateral torsion, orchitis, vanishing testis syndrome or orchidectomy; 2) hypogonadotropic hypogonadism due to an idiopathic gonadotropin or luteinizing hormone-releasing hormone deficiency or due to a pituitary-hypothalamic injury from tumors, trauma or radiation, in this case it is important to accompany the treatment with adrenal cortical and thyroid hormone replacement therapy; 3) to stimulate puberty in patients with delayed puberty not secondary to a pathological disorder. If the conditions 1 and 2 occur prior to puberty, the androgen replacement therapy will be needed during adolescent years for the development of secondary sexual characteristics and prolonged androgen treatment might be needed it to maintain sexual characteristics after puberty. Testosterone enanthate presents the same properties as its analog testosterone with the advantage that this molecule has a longer release rate and half-life. Administration of ester derivatives of testosterone as testosterone enanthate generates an increase in serum testosterone to levels reaching 400% from the baseline within 24 hours of administration. These androgen levels remain elevated for 3-5 days after initial administration. Continuous administration of testosterone enanthate shows a significant suppression of dihydrotestosterone, serum PSA, HDL and FSH, as well as a slight increase in serum estradiol. The levels of dihydrotestosterone and FSH can remain suppressed even 14 days after treatment termination. There are no changes in mood and sexual activity by the presence of testosterone enanthate. The effects of testosterone in humans and other vertebrates occur by way of two main mechanisms: by activation of the androgen receptor (directly or as DHT), and by conversion to estradiol and activation of certain estrogen receptors. Free testosterone (T) is transported into the cytoplasm of target tissue cells, where it can bind to the androgen receptor, or can be reduced to 5&alpha;-dihydrotestosterone (DHT) by the cytoplasmic enzyme 5&alpha;-reductase. DHT binds to the same androgen receptor even more strongly than T, so that its androgenic potency is about 2.5 times that of T. The T-receptor or DHT-receptor complex undergoes a structural change that allows it to move into the cell nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing androgen effects.",The molecular weight is 400.6.,Testosterone enanthate has a topological polar surface area of 43.37.,The log p value of  is 7.0.,Testosterone enanthate is approved.,Testosterone enanthate is a solid.,True
14478,"Testosterone undecanoate is the ester prodrug of testosterone and has a midchain fatty acid at the 17Beta position.  It is available as an intramuscular injection and as an oral capsule, and is indicated for treatment of testosterone deficiency.  It should be noted that testosterone undecanoate is only indicated for treatment of hypogonadal conditions with structural or genetic etiologies and should not be used to manage \age-related hypogonadism\"". "" Testosterone undecanoate is indicated for replacement therapy in adult males with conditions that are linked with an absence or deficiency in endogenous testosterone production.  Testosterone plays a key role in male sexual differentiation and is involved in regulation of hematopoiesis, body composition, and bone metabolism. As a result, testosterone replacement therapy in males with hypogonadism can result in improved sexual function, increased lean body mass, bone density, erythropoiesis, prostate size, and changes in lipid profiles.  Testosterone is produced by Leydig cells and exerts it's effects by binding to androgen receptors throughout the body.  Testosterone affects the voice, genitalia, mood, and influences muscle growth and protein expression.  Accordingly, males with low levels of testosterone often experience decreased libido, fatigue, mood changes and dysphoria.  Exogenous sources of testosterone are designed to mimic the effects of endogenous testosterone.",The molecular weight is 456.71.,Testosterone undecanoate has a topological polar surface area of 43.37.,The log p value of  is 9.12.,Testosterone undecanoate is approved and investigational.,Testosterone undecanoate is a solid.,True
14479,"Estradiol acetate is a pro-drug ester of , a naturally occurring hormone that circulates endogenously within the human body. Estradiol is the most potent form of all mammalian estrogenic steroids and acts as the major female sex hormone. As a pro-drug of estradiol, estradiol acetate therefore has the same downstream effects within the body through binding to the Estrogen Receptor (ER) including ERα and ERβ subtypes, which are located in various tissues including in the breasts, uterus, ovaries, skin, prostate, bone, fat, and brain. Femring is indicated for the treatment of vasomotor and urogenital symptoms associated with menopause. Use of Femring (estradiol acetate) has been shown to improve symptoms caused by atrophy of the vagina (such as dryness, burning, pruritus and dyspareunia) and/or the lower urinary tract (urinary urgency and dysuria). Estrogen mediates its effects across the body through potent agonism of the Estrogen Receptor (ER), which is located in various tissues including in the breasts, uterus, ovaries, skin, prostate, bone, fat, and brain. Estradiol binds to both subtypes of the Estrogen Receptor: Estrogen Receptor Alpha (ERα) and Estrogen Receptor Beta (ERβ). Estradiol also acts as a potent agonist of G Protein-coupled Estrogen Receptor (GPER), which has recently been recognized as a major mediator of estradiol's rapid cellular effects.  Estradiol enters target cells freely (e.g., female organs, breasts, hypothalamus, pituitary) and interacts with a target cell receptor. When the estrogen receptor has bound its ligand it can enter the nucleus of the target cell, and regulate gene transcription which leads to formation of messenger RNA. The mRNA interacts with ribosomes to produce specific proteins that express the effect of estradiol upon the target cell. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary.",The molecular weight is 314.42.,Estradiol acetate has a topological polar surface area of 46.53.,The log p value of  is 3.8.,Estradiol acetate is approved and investigational and vet_approved.,,True
14480,"Estradiol Benzoate is a pro-drug ester of , a naturally occurring hormone that circulates endogenously within the human body. Estradiol is the most potent form of all mammalian estrogenic steroids and acts as the major female sex hormone. As a pro-drug of estradiol, estradiol benzoate therefore has the same downstream effects within the body through binding to the Estrogen Receptor (ER) including ERα and ERβ subtypes, which are located in various tissues including in the breasts, uterus, ovaries, skin, prostate, bone, fat, and brain. Estradiol benzoate is not currently available in any FDA or Health Canada approved products. Estradiol, the principal intracellular human estrogen, is substantially more active than its metabolites, estrone and estriol, at the cellular level. Estradiol enters target cells freely (e.g., female organs, breasts, hypothalamus, pituitary) and interacts with a target cell receptor. When the estrogen receptor has bound its ligand it can enter the nucleus of the target cell, and regulate gene transcription which leads to formation of messenger RNA. The mRNA interacts with ribosomes to produce specific proteins that express the effect of estradiol upon the target cell. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary.",The molecular weight is 376.5.,Estradiol benzoate has a topological polar surface area of 46.53.,The log p value of  is 5.93.,Estradiol benzoate is approved and investigational and vet_approved.,,True
14481,"Estradiol Cypionate is a pro-drug ester of , a naturally occurring hormone that circulates endogenously within the human body. Estradiol is the most potent form of all mammalian estrogenic steroids and acts as the major female sex hormone. As a pro-drug of estradiol, estradiol cypionate therefore has the same downstream effects within the body through binding to the Estrogen Receptor (ER) including ERα and ERβ subtypes, which are located in various tissues and organs such as the breasts, uterus, ovaries, skin, prostate, bone, fat, and brain. Depo-Estradiol intramuscular depot injection is indicated for the treatment of moderate to severe vasomotor symptoms and hypoestrogenism due to hypogonadism. Estrogen mediates its effects across the body through potent agonism of the Estrogen Receptor (ER), which is located in various tissues including in the breasts, uterus, ovaries, skin, prostate, bone, fat, and brain. Estradiol binds to both subtypes of the Estrogen Receptor: Estrogen Receptor Alpha (ERα) and Estrogen Receptor Beta (ERβ). Estradiol also acts as a potent agonist of G Protein-coupled Estrogen Receptor (GPER), which has recently been recognized as a major mediator of estradiol's rapid cellular effects.  Estradiol enters target cells freely (e.g., female organs, breasts, hypothalamus, pituitary) and interacts with a target cell receptor. When the estrogen receptor has bound its ligand it can enter the nucleus of the target cell, and regulate gene transcription which leads to formation of messenger RNA. The mRNA interacts with ribosomes to produce specific proteins that express the effect of estradiol upon the target cell. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary.",The molecular weight is 396.57.,Estradiol cypionate has a topological polar surface area of 46.53.,The log p value of  is 7.35.,Estradiol cypionate is approved and investigational and vet_approved.,,True
14482,"Estradiol Dienanthate is a pro-drug ester of , a naturally occurring hormone that circulates endogenously within the human body. Estradiol is the most potent form of all mammalian estrogenic steroids and acts as the major female sex hormone. As a pro-drug of estradiol, estradiol benzoate therefore has the same downstream effects within the body through binding to the Estrogen Receptor (ER) including ERα and ERβ subtypes, which are located in various tissues including in the breasts, uterus, ovaries, skin, prostate, bone, fat, and brain. Estradiol dienanthate is not currently available in any FDA or Health Canada approved products. Estradiol, the principal intracellular human estrogen, is substantially more active than its metabolites, estrone and estriol, at the cellular level. Estradiol enters target cells freely (e.g., female organs, breasts, hypothalamus, pituitary) and interacts with a target cell receptor. When the estrogen receptor has bound its ligand it can enter the nucleus of the target cell, and regulate gene transcription which leads to formation of messenger RNA. The mRNA interacts with ribosomes to produce specific proteins that express the effect of estradiol upon the target cell. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary.",,,,Estradiol dienanthate is approved and investigational and vet_approved.,,True
14483,"Estradiol Valerate (also known as E2V) is a pro-drug ester of , a naturally occurring hormone that circulates endogenously within the human body. Estradiol is the most potent form of all mammalian estrogenic steroids and acts as the major female sex hormone. As a pro-drug of estradiol, estradiol acetate therefore has the same downstream effects within the body through binding to the Estrogen Receptor (ER) including ERα and ERβ subtypes, which are located in various tissues including in the breasts, uterus, ovaries, skin, prostate, bone, fat, and brain. Estradiol valerate is commercially available as an intramuscular injection as the product Delestrogen and is indicated for the treatment of moderate to severe vasomotor symptoms and vulvovaginal atrophy due to menopause, for the treatment of hypoestrogenism due to hypogonadism, castration or primary ovarian failure, and for the treatment of advanced androgen-dependent carcinoma of the prostate (for palliation only).  Estrogen mediates its effects across the body through potent agonism of the Estrogen Receptor (ER), which is located in various tissues including in the breasts, uterus, ovaries, skin, prostate, bone, fat, and brain. Estradiol binds to both subtypes of the Estrogen Receptor: Estrogen Receptor Alpha (ERα) and Estrogen Receptor Beta (ERβ). Estradiol also acts as a potent agonist of G Protein-coupled Estrogen Receptor (GPER), which has recently been recognized as a major mediator of estradiol's rapid cellular effects.  Estradiol enters target cells freely (e.g., female organs, breasts, hypothalamus, pituitary) and interacts with a target cell receptor. When the estrogen receptor has bound its ligand it can enter the nucleus of the target cell, and regulate gene transcription which leads to formation of messenger RNA. The mRNA interacts with ribosomes to produce specific proteins that express the effect of estradiol upon the target cell. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary.",The molecular weight is 356.51.,Estradiol valerate has a topological polar surface area of 46.53.,The log p value of  is 6.32.,Estradiol valerate is approved and investigational and vet_approved.,,True
14484,"Tenofovir is an acyclic nucleotide diester analog of adenosine monophosphate. In the most strict sense and due to the fact that it presents a phosphate group bound to the nitrogenous base, it is determined as an actual nucleotide analog. The antiviral activities of tenofovir were first reported in 1993 and this agent was commercially available since 2008 in the form of and in order to obtain oral bioavailability. Tenofovir has been shown to be effective against HIV, herpes simplex virus-2, and hepatitis B virus. Tenofovir has been shown to be highly effective in patients that have never had an antiretroviral therapy and it seemed to have lower toxicity than other antivirals such as. In phase 3 clinical trials, tenofovir presented a similar efficacy than in treatment-naive HIV patients. In hepatitis B infected patients, after one year of tenofovir treatment, the viral DNA levels were undetectable. Once tenofovir is activated by a bi-phosphorylation it acts as an antiviral acyclic nucleoside phosphonate. It is a potent inhibitor of the viral reverse transcriptase with an inhibitory constant of approximately 0.022 micromolar. ",The molecular weight is 287.22.,Tenofovir has a topological polar surface area of 136.38.,The log p value of  is -1.56.,Tenofovir is experimental and investigational.,Tenofovir is a solid.,True
14485,"Aripiprazole lauroxil is a long-acting injectable atypical antipsychotic drug used in the treatment of schizophrenia in adult patients. It is a prodrug of , which acts as a partial agonist at the D2 and 5-HT1A receptors, and as an antagonist at the 5-HT2A receptors.  Aripiprazole lauroxil is indicated for the treatment of schizophrenia and related psychotic disorders. Aripiprazole, which is a major pharmacological metabolite of aripiprazole lauroxil, serves to improve the positive and negative symptoms of schizophrenia by modulating dopaminergic signalling pathways. Aripiprazole lauroxil is reported to have minimal effects on sexual function or prolactin levels.  The pharmacological activity of aripiprazole lauroxil is thought to be mainly mediated by its metabolite aripiprazole, and to a lesser extent, dehydro-aripiprazole. Aripiprazole functions as a partial agonist at the dopamine D2 and the serotonin 5-HT1A receptors, and as an antagonist at the serotonin 5-HT2A receptor. The desired outcome of antipsuchotic agents in schizophrenia is to inhibit dopaminergic transmission in the limbic system and enhance dopaminergic transmission in the prefrontal cortex. As a partial agonist at D2 receptors in the mesolimbic dopaminergic pathway, aripiprazole acts as a functional antagonist in the mesolimbic dopamine pathway and reduces the extent of dopaminergic pathway activity. This results in reduced positive symptoms in schizophrenia and extrapyramidal motor side effects. In contrast, aripiprazole is thought to act as a functional agonist in the mesocortical pathway, where reduced dopamine activity is seen in association with negative symptoms and cognitive impairment. Antagonism at 5-HT2A receptors by aripiprazole alleviates the negative symptoms and cognitive impairment of schizophrenia. 5-HT2A receptors are Gi/Go-coupled that upon activation, produce neuronal inhibition via decreased neuronal excitability and decreased transmitter release at the nerve terminals. In the nigrostriatal pathway, 5-HT2A regulates the release of dopamine. Through antagonism of 5-HT2A receptors, aripiprazole disinhibits the release of dopamine in the striatum and enhance the levels of the transmitters at the nerve terminals. The combined effects of D2 and 5-HT2A antagonism are thought to counteract the increased dopamine function causing increased extrapyramidal side effects. Blocking 5-HT2A receptors may also lead to the modulation of glutamate release in the mesocortical circuit, which is a transmitter that plays a role in schizophrenia. 5-HT1A receptors are autoreceptors that inhibit 5-HT release upon activation. Aripiprazole is a partial agonist at theses receptors and reduces 5-HT release; this results in potentiated dopamine release in the striatum and prefrontal cortex. It is reported that therapeutic doses of aripiprazole occupies up to 90% of brain D2 receptors in a dose-dependent manner. ",The molecular weight is 660.72.,Aripiprazole lauroxil has a topological polar surface area of 62.32.,The log p value of  is 10.8.,Aripiprazole lauroxil is approved and investigational.,Aripiprazole lauroxil is a solid.,True
14486,"For use as an over the counter calcium and phosphate supplement, antacid, or a source of calcium and phosphate in toothpaste. Calcium phosphate reacts with acid in the stomach to raise the pH. In toothpaste it provides a source of calcium and phosphate ions to support remineralization of the teeth. As a supplement it provides a source of calcium and phospate, both of which are important ions in bone homeostasis. The phosphate ions in calcium phosphate likely react with hydrochloric acid in the stomach to neutralize the pH. In toothpaste and in systemic circulation, calcium phosphate provides a source of calcium and phosphate ions to support remineralization of the teeth and bone homeostasis respectively. The increase in plasma calcium reduces calcium flux from osteocyte activity by reducing the secretion of parathyroid hormone (PTH). Calcium does this by stimulating a G-protein coupled calcium receptor on the surface of parathyroid cells. The reduction in calcium flux increases the amount of calcium deposited in bone resulting in an increase in bone mineral density. The reduction in PTH secretion also reduces the amount of vitamin D metabolized to its active form, calcidiol. Since calcidiol increases the expression of calcium dependent ATPases and transient receptor potential cation channel subfamily V member 6 (TRPV6) both of which are involved in calcium uptake from the gut, a reduction in calcidiol results in less calcium absorption. Additionally, TRPV5, the channel responsible for calcium reabsorption in the kidney, is downregulated when PTH secretion is reduced thus increasing calcium excretion via the kidneys. Another hormone, calitonin, is likely involved in the reduction of bone resorption during periods of high plasma calcium.",The molecular weight is 172.09.,Calcium phosphate dihydrate has a topological polar surface area of 83.42.,,Calcium phosphate dihydrate is approved.,,True
14487,"Magnesium is classified as an alkaline earth metal and has 2 hydration shells. The element can be found in abundance in the hydrosphere and in mineral salts such as dolomite and magnesium carbonate.  Healthy levels of magnesium can be achieved through a well balanced diet, but if food sources are insufficient, magnesium supplements can be used to prevent and treat magnesium deficiencies. Magnesium is important for many biochemical processes and is therefore quite common in humans. The majority of magnesium is stored in the bones (>50%), while the remainder is stored in muscle, soft tissue, red blood cells and serum. This is functionally important since the bones behave as a magnesium exchange reservoir and help maintain healthy levels of magnesium. Magnesium is a cofactor for at least 300 enzymes and is important for several functions in the body with some key processes identified below. Enzymes that rely on magnesium to operate help produce energy through oxidative phosphorylation, glycolysis and ATP metabolism. They are also involved in nerve function, muscle contraction, blood glucose control, hormone receptor binding, protein synthesis, cardiac excitability, blood pressure control, gating of calcium channels and transmembrane ion flux.",,,,Magnesium is approved and experimental and investigational.,,True
14488,"Aluminum Acetate is an astringent. An astrignent is a chemical that tends to shrink or constrict body tissues, usually locally after topical medicinal application. The shrinkage or constriction is through osmotic flow of water (or other fluids) away from the area where the astringent was applied. Astringent medicines cause shrinkage of mucous membranes or exposed tissues and are often used internally to check discharge of blood serum or mucous secretions. This can happen with a sore throat, hemorrhages, diarrhea, or with peptic ulcers. Externally applied astringents, which cause mild coagulation of skin proteins, dry, harden, and protect the skin. Acne sufferers are often advised to use astringents if they have oily skin. Astringents also help heal stretch marks and other scars. Mild astringent solutions are used in the relief of such minor skin irritations as those resulting from superficial cuts, allergies, insect bites, or fungal infections such as athlete's foot. ",The molecular weight is 121.95.,Aluminium phosphate has a topological polar surface area of 86.25.,,Aluminium phosphate is approved and investigational.,,True
14489,"Aluminum Acetate is an astringent. An astrignent is a chemical that tends to shrink or constrict body tissues, usually locally after topical medicinal application. The shrinkage or constriction is through osmotic flow of water (or other fluids) away from the area where the astringent was applied. Astringent medicines cause shrinkage of mucous membranes or exposed tissues and are often used internally to check discharge of blood serum or mucous secretions. This can happen with a sore throat, hemorrhages, diarrhea, or with peptic ulcers. Externally applied astringents, which cause mild coagulation of skin proteins, dry, harden, and protect the skin. Acne sufferers are often advised to use astringents if they have oily skin. Astringents also help heal stretch marks and other scars. Mild astringent solutions are used in the relief of such minor skin irritations as those resulting from superficial cuts, allergies, insect bites, or fungal infections such as athlete's foot. ",The molecular weight is 204.11.,,,Aluminum acetate is approved and investigational.,,True
14490,"Zinc chloride is a solution of ions indicated for use in total parenteral nutrition to maintain zinc levels and prevent deficiency syndromes. Zinc chloride injections are indicated for use total parenteral nutrition to maintain zinc serum levels and prevent deficiency syndromes. Zinc is a cofactor in many enzymes and mediates a number of catalytic, structural, and regulatory roles in the body. It has a wide therapeutic index and long duration of action, as most zinc in the body is reabsorbed. Patients should be counselled regarding the risk of administration in patients with severe kidney dysfunction. Zinc performs catalytic, structural, and regulatory roles in the body. Zinc is a component of approximately 3000 human proteins.",The molecular weight is 136.28.,,,Zinc chloride is approved and investigational.,Zinc chloride is a solid.,True
14491,Zinc sulfate is a common zinc supplement in parenteral nutrition. Zinc sulfate is a common zinc supplement in parenteral nutrition.,,,,"Zinc sulfate, unspecified form is approved and experimental.",,True
14492,"Parisiran is a first in class short interfering RNA for the treatment of patients with polyneuropathy caused by hereditary transthyretin-mediated amyloidosis. It is marketed as Onpattro which is formulated as patisiran within a liposome envelope for better delivery to the liver, where transthyretin is produced. The approval for Onpattro was granted to Alnylam Pharmaceuticals, Inc. in August of 2018. Onpattro has been granted Fast Track, Priority Review and Breakthrough Therapy, and Orphan Drug designations. Patisirant is indicated for the treatment of hereditary transthyretin-mediated amyloidosis in adults. Transthyretin normally plays a role in the transport of vitamin A in conjunction with retinol binding protein. Mutant transthyretin of the ATTR genotype is capable of forming amyloid fibrils and creating protein deposits in a condition known as transthyretin-mediated amyloidosis. Patisirant is a double-stranded short interfering RNA (siRNA) targeting mRNA encoding both wild-type and mutant transthyretin. Patisiran enters the cell an is processed by the Dicer enzyme. This processing involved cleaving overhanging nucleotides on the edges of the RNA. Once processed the siRNA can bind to the RNA-induced silencing complex (RISC). RISC separates the strands of the RNA sequence. One strand is released and one remains bound. The bound strand then acts as a targeting sequence for a complimentary mRNA sequence. In this case, the bound strand of patisiran binds to the complimentary transthyretin mRNA and aligns the RISC complex with it. The transthyretin mRNA is then cleaved and rendered non-functional. One targeting sequence may be used to destroy many copies of complimentary mRNA.",,,,Patisiran is approved and investigational.,,True
14493,"Commonly known as decadron, dexamethasone acetate is a glucocorticosteroid previously marketed in the USA for the treatment of inflammatory respiratory, allergic, autoimmune, and other conditions. Developed in 1957, dexamethasone is structurally similar to other corticosteroids such as and. Dexamethasone acetate has largely been replaced by phosphate and continues to be administered for a large variety of inflammatory conditions.",The molecular weight is 434.5.,Dexamethasone acetate has a topological polar surface area of 100.9.,The log p value of  is 2.32.,Dexamethasone acetate is approved and investigational and vet_approved.,,True
14494,"Ripretinib is a kinase inhibitor used for the treatment of advanced gastrointestinal stromal tumor (GIST) that has not adequately responded to other kinase inhibitors such as and. Ripretinib, also known as Qinlock, is manufactured by Deciphera Pharmaceuticals and was initially approved by the FDA on May 15, 2020.  Ripretinib is indicated to treat adults diagnosed with advanced gastrointestinal stromal tumor (GIST) who have had prior therapy with at least 3 kinase inhibitors, including the imatinib. As a broad-spectrum kinase inhibitor, ripretinib inhibits various gene mutations, increasing progression-free survival in patients with advanced gastrointestinal stromal tumors (GIST). It is effective in treating mutations that are resistant to chemotherapy with other kinase inhibitors, such as imatinib. Protein kinases play important roles in cellular function, and their dysregulation can lead to carcinogenesis. Ripretinib inhibits protein kinases including wild type and mutant platelet-derived growth factor receptor A (PDGFRA) and KIT that cause the majority of gastrointestinal stromal tumor (GIST). In vitro, ripretinib has been shown to inhibit PDGFRB, BRAF, VEGF, and TIE2 genes. ",,,,Ripretinib is approved.,Ripretinib is a solid.,True
14495,"Cefiderocol is a cephalosporin antibacterial drug and exerts a mechanism of action similar to other β-lactam antibiotics. Unlike other agents in this category, cefiderocol is a siderophore able to undergo active transport into the bacterial cell through iron channels. It represents a significant addition to antibacterial treatment option as it has proven to be effective *in vitro* against multidrug resistant strains including extended spectrum β-lactamase producers and carbapenemase producing bacteria. Cefiderocol is indicated for the treatment of complicated urinary tract infections with or without pyelonephritis. Similarly to other cephalosporins, cefiderocol exerts bactericidal activity against a range of bacterial species. Cefiderocol has primarily shown efficacy against aerobic Gram negative bacteria including *Escherichia coli*, *Klebsiella pneumoniae*, and *Pseudomonas aeruginosa*. Cefiderocol acts by binding to and inhibiting penicillin-binding proteins (PBPs), preventing cell wall synthesis and ultimately causing death of the bacterial cell. Like other β-lactam antibiotics cefiderocol is able to enter bacterial cells via passive diffusion through porins. Unlike other β-lactams, cefiderocol contains a chlorocatechol group which allows it to chelate iron. Once bound to ferric iron cefiderocol is able to undergo active transport into bacterial cells through iron channels in the outer cell membrane such as those encoded by the *cirA* and *fiu* genes in *E. coli* or the *PiuA* gene in *P. aeruginosa*. Once inside the cell, cefiderocol binds to and inhibits PBP3 with high affinity thereby preventing the linking of peptodoglycan layers via the pentapeptide bridge. PBP1a, 1b, 2,and 4 are also bound and inhibited by cefiderocol but with a lesser potency than PBP3 and are therefore expected to contribute less to its antibacterial effect.",,,,Cefiderocol is approved and investigational.,Cefiderocol is a solid.,True
14496,"Human interferon beta is a polypeptide used in the management of relapsing forms of Multiple Sclerosis (MS), and was initially approved by the FDA in 1992. Multiple Sclerosis is a devastating neurodegenerative disease that is usually progressive and significantly debilitating with a profound impact on the quality of life.  This drug is indicated to treat relapsing forms of Multiple Sclerosis (MS) in adults, which includes clinically isolated syndrome, relapsing-remitting disease, as well as active secondary progressive disease. Interferon-beta has antiviral and immunomodulatory effects. It reduces demyelination, the main component of Multiple Sclerosis pathophysiology, reducing the clinical frequency of MS attacks and slowing disease progression. Part of the pathophysiology of MS is immune cell activation in addition to degradation of the blood–brain barrier (BBB), resulting in both neural demyelination and axon injury. Immunomodulating drugs such as interferon-beta decrease the inflammation that results in demyelination of nerves. Binding of interferon-beta to type 1 interferon receptors induces a series of beneficial transcriptional JAK/STAT pathway changes. This decreases antigen presentation as well as the proliferation of inflammatory T-cells, reducing the inflammation associated with MS. It also changes the expression of cytokine and matrix metalloproteinase (MMP). ",,,,Human interferon beta is approved and investigational.,Human interferon beta is a solid.,True
14497,"Somapacitan, also known as NNC0195-0092, is a growth hormone analog indicated to treat adults with growth hormone deficiency. This human growth hormone analog differs by the creation of an albumin binding site, and prolonging the effect so that it requires weekly dosing rather than daily. Somapacitan is indicated as a replacement for growth hormone in adult patients with growth hormone deficiency. Somapacitan stimulates the growth hormone receptor. Somapacitan has a long duration of action as it is given once weekly. It has a moderately wide therapeutic window as an acute overdose may cause hypoglycemia followed by hyperglycemia. Patients should be counselled regarding the risk of increased mortality in patients with critical illness, risk of neoplasms, glucose intolerance in diabetes mellitus, intracranial hypertension, hypersensitivity, fluid retention, hypoadrenalism, hypothyroidism, pancreatitis, lipohypertrophy, and lipoatrophy. Somapacitan binds to the growth hormone receptor and induces intracellular signalling to up-regulate insulin-like growth factor I (IGF-1). IGF-1 causes growth in bones and muscle tissue. Growth hormones more directly cause the fusion of myoblasts and myotubes to cause muscle fibre growth, activate neural stem cells, and induce chondrocyte proliferation.",,,,Somapacitan is approved and investigational.,Somapacitan is a solid.,True
14498,"Risdiplam is an orally bioavailable mRNA splicing modifier used for the treatment of spinal muscular atrophy (SMA). It increases systemic SMN protein concentrations by improving the efficiency of _SMN2_ gene transcription. This mechanism of action is similar to its predecessor , the biggest difference being their route of administration: nusinersen requires intrathecal administration, as does the one-time gene therapy , whereas risdiplam offers the ease of oral bioavailability. Risdiplam is indicated for the treatment of spinal muscular atrophy (SMA) in patients 2 months of age and older. Risdiplam helps to alleviate symptoms of spinal muscular atrophy by stimulating the production of a critical protein in which these patients are deficient. Early trials with risdiplam demonstrated up to a 2-fold increase in SMN protein concentration in SMA patients after 12 weeks of therapy. Spinal muscular atrophy (SMA) is a severe and progressive congenital neuromuscular disease resulting from mutations in the survival of motor neuron 1 (_SMN1_) gene responsible for making SMN proteins. Clinical features of SMA include degeneration of motor neurons in the spinal cord which ultimately leads to muscular atrophy and, in some cases, loss of physical strength. SMN proteins are expressed ubiquitously throughout the body and are thought to hold diverse intracellular roles in DNA repair, cell signaling, endocytosis, and autophagy. A secondary _SMN_ gene (_SMN2_) can also produce SMN proteins, but a small nucleotide substitution in its sequence results in the exclusion of exon 7 during splicing in approximately 85% of the transcripts - this means that only ~15% of the SMN proteins produced by _SMN2_ are functional, which is insufficient to compensate for the deficits caused by _SMN1_ mutations. Emerging evidence suggests that many cells and tissues are selectively vulnerable to reduced SMN concentrations, making this protein a desirable target in the treatment of SMA.",,,,Risdiplam is approved and investigational.,Risdiplam is a solid.,True
14499,"Elexacaftor (previously VX-445) is a small molecule, next-generation corrector of the cystic fibrosis transmembrane conductance regulator (CFTR) protein. It received FDA approval in October 2019 in combination with and as the combination product Trikafta<sup>TM</sup>. Elexacaftor is considered a next-generation CFTR corrector as it possesses both a different structure and mechanism as compared to first generation correctors like tezacaftor. While dual corrector/potentiator combination therapy has proven useful in the treatment of a subset of CF patients, their use is typically limited to patients who are homozygous for the _F508del-CFTR_ gene. Elexacaftor, along with , was designed to fill the need for an efficacious CF therapy for patients who are heterozygous for _F508del-CFTR_ and a gene that does not produce protein or produces proteins unresponsive to ivacaftor or tezacaftor. The triple combination product Trikafta<sup>TM</sup>, manufactured by Vertex Pharmaceuticals, is the first product approved for the treatment of CF in individuals who are either homo- _or_ heterozygous for the _F508del-CFTR_ gene - this represents approximately 70-90% of all CF patients. Elexacaftor, in combination with and as the combination product Trikafta<sup>TM</sup>, is indicated for the treatment of cystic fibrosis (CF) in patients 12 years of age and older who have at least one _F508del_ mutation in the CTFR gene. As a CFTR corrector, elexacaftor works to increase the amount of mature CFTR proteins present on the surface of cells. When used in combination with CFTR potentiators, which enhance the function of cell-surface CFTR proteins, drugs like elexacaftor help to improve a variety of multi-organ cystic fibrosis symptoms, including lung function, nutritional status, and overall quality of life. Trikafta<sup>TM</sup>, the triple combination product containing elexacaftor, may cause elevations in liver transaminases. Liver function testing should be conducted prior to beginning Trikafta, every 3 months for the first year of treatment, and annually thereafter. Cystic fibrosis (CF) is the result of a mutation in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. The CFTR proteins produced by this gene are transmembrane ion channels that move sodium and chloride across cell membranes - water follows the flow of chloride ions to the cell surface, which consequently helps to hydrate the surface of the cell and thin the secretions (i.e. mucous) around the cell. Mutations in the CFTR gene produce CFTR proteins of insufficient quantity and/or function, leading to defective ion transport and a build-up of thick mucous throughout the body that causes multi-organ disease involving the pulmonary, gastrointestinal, and pancreatic systems (amongst others). The most common CFTR mutation, the _F508del_ mutation, is estimated to account for 70 to 90% of all CFTR mutations and results in severe processing and trafficking defects of the CFTR protein.",,,,Elexacaftor is approved and investigational.,Elexacaftor is a solid.,True
14500,Colchiceine is one of several metabolites of the anti-gout medication.,,,,Colchiceine is approved and experimental.,,True
14501,"Fluoroestradiol F-18 is an imaging agent used with positron emission tomography (PET) to detect estrogen receptor-positive breast cancer lesions. The ability to image ER-positive tumors _in vivo_ is advantageous in that, while helping to visualize tumor progression/regression, it may also be used to assess for heterogeneity in ER expression across metastases (i.e. to identify sites that no longer express ER) without the need for multiple biopsies. Fluoroestradiol F-18 is a radioactive diagnostic agent indicated for use with positron emission tomography (PET) imaging for the detection of estrogen receptor-positive lesions as an adjunct to biopsy in patients with recurrent or metastatic breast cancer. Fluoroestradiol F-18 is an analog of estradiol that emits small amounts of radioactivity, allowing it to be detected using PET. Following intravenous administration, it accumulates in cancerous tissues expressing estrogen receptors, thus allowing for visualization of these lesions. Fluoroestradiol has a relatively short duration of action - at 2 hours post-injection circulating levels are <5% those at peak concentration. Estrogen receptor (ER)-positive breast cancers are a subset of breast cancers in which the cancerous tissue expresses estrogen receptors - these receptors provide a useful target for imaging and treatment agents. Fluoroestradiol F-18 is a fluorinated analog of estradiol that binds to estrogen receptors, allowing for PET imaging of lesions.",,,,Fluoroestradiol F-18 is approved.,Fluoroestradiol F-18 is a solid.,True
14502,"Asparaginase derived from _Escherichia coli_ (L-asparagine amidohydrolase, EC 3.5.1.1) is an enzyme responsible for the metabolism of L-asparagine, by catalyzing L-asparagine into L-aspartic acid and ammonia. It also facilitates the production of oxaloacetate which is needed for general cellular metabolism. Asparaginase from _E. coli_ has clinically shown to exhibit antitumor actions in models of leukaemias. L-asparaginase of _E. coli_ is marketed under several different trade names, including Elspar, for the treatment of acute lymphoblastic leukemia (ALL) as part of a multi-agent chemotherapeutic regimen. It is available as intramuscular or intravenous injections. Therapeutic L-asparaginase from _E. coli_ works by depleting the levels of non-essential amino acid, asparagine, in lymphoblastic leukemic cells thus promoting apoptotic cell death. For patients who develop hypersensitivity to _E. coli_-derived formulations of L-asparaginase, the use of PEGylated or non-PEGylated is recommended. Indicated as a component of a multi-agent chemotherapeutic regimen for the treatment of patients with acute lymphoblastic leukemia (ALL). In clinical trials of patients with previously untreated, standard-risk ALL, administration of asparaginase resulted in a decrease of plasma asparagine levels from average of 41 μM to less than 3 μM. The native asparaginase in whom plasma enzyme activity before treatment was greater than 0.1 International Units/mL. In this study, cerebrospinal fluid asparagine levels in patients treated with asparaginase decreased from 2.8 μM (pretreatment) to 1.0 μM and 0.3 μM at day 7 and day 28 of induction, respectively. Native E. coli asparaginase results in asparagine depletion in 14 to 23 days following administration. Asparagine is a non-essential amino acid that maintains DNA, RNA and protein synthesis and promotes cell growth. While healthy and normal cells are capable of obtaining asparagine via dietary intake or synthesizing the asparagine from aspartate via asparagine synthetase activity, lymphoblastic leukemic cells lack the asparagine synthetase enzyme and cannot produce asparagine _de novo_. Thus, leukemic cells rely on exogenous source of asparagine for protein synthesis and cell survival. L-asparagine from E. coli serves to deplete plasma levels of asparagine in leukemic cells by converting L-asparagine to L-aspartic acid and ammonia , leading to reduced reduced DNA, RNA and protein synthesis; inhibition of cell growth; and ultimately the activation of apoptotic cell-death mechanisms. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase.",,,,Asparaginase Escherichia coli is approved and investigational.,Asparaginase Escherichia coli is a liquid.,True
14503,"Pegylated L-asparagine amidohydrolase from E. coli. Pegylation substantially (by a factor of 4) extends the protein half life. For treatment of acute lymphoblastic leukemia In a significant number of patients with acute leukemia, the malignant cells are dependent on an exogenous source of asparagine for survival. Normal cells, however, are able to synthesize asparagine and thus are affected less by the rapid depletion produced by treatment with the enzyme asparaginase. Oncaspar exploits a metabolic defect in asparagine synthesis of some malignant cells. Pegaspargase, more effective than asparaginase, converts asparagine to aspartic acid and ammonia. It facilitates production of oxaloacetate which is needed for general cellular metabolism. Some malignant cells lose the ability to produce asparagine and so the loss of exogenous sources of asparagine leads to cell death.",,,,Pegaspargase is approved and investigational.,Pegaspargase is a liquid.,True
14504,"An antineoplastic antimetabolite that is metabolized to fluorouracil when administered by rapid injection. Floxuridine is available as a sterile, nonpyrogenic, lyophilized powder for reconstitution. When administered by slow, continuous, intra-arterial infusion, it is converted to floxuridine monophosphate. It has been used to treat hepatic metastases of gastrointestinal adenocarcinomas and for palliation in malignant neoplasms of the liver and gastrointestinal tract. For palliative management of gastrointestinal adenocarcinoma metastatic to the liver, when given by continuous regional intra-arterial infusion in carefully selected patients who are considered incurable by surgery or other means. Also for the palliative management of liver cancer (usually administered by hepatic intra-arterial infusion). Floxuridine is an anti-metabolite or a pyrimidine analog that works by disrupting the process S-phase of cell division, selectively targeting rapidly dividing cells. Due to the structural similarities, antimetabolites act as pyrimidine-like molecules and prevent normal pyrimidines from being incorporated into DNA. After successful biotransformation, floxuridine is converted into an active component, flurouracil, which blocks the enzyme which converts cytosine nucleosides into the deoxy derivative. Flurouracil also physically prevents the incorporation of thymidine nucleotides into the DNA strand by taking their place, further preventing DNA synthesis.  Floxuridine rapidly undergoes catabolism to form 5-fluorouracil, which is the active component of the drug. 5-Fluorouracil primarily works by interfering with DNA synthesis; however, it may also inhibit the formation of fraudulent RNA via physical incorporation into the RNA. It is also an inhibitor of riboside phophorylase, preventing the utilization of pre-formed uracil in RNA synthesis. Floxuridine can also form 5-fluoro-2'-deoxyuridine-5'-phosphate (FUDR-MP), which is the monophosphate of floxuridine that inhibits thymidylate synthetase that plays a role in the methylation of deoxyuridylic acid to thymidylic acid during DNA synthesis. FUDR-MP thus interferes with DNA synthesis.",The molecular weight is 246.19.,Floxuridine has a topological polar surface area of 99.1.,The log p value of  is -1.4.,Floxuridine is approved.,Floxuridine is a solid.,True
14505,"Mephenytoin is used for the treatment of refractory partial epilepsy. Mephenytoin is a solid. This compound belongs to the phenylhydantoins. These are heterocyclic aromatic compounds containing an imiazolidinedione moiety substituted by a phenyl group. Mephenytoin is known to target sodium channel protein type 5 subunit alpha. Cytochrome P450 2C19, Cytochrome P450 2C8, Cytochrome P450 2C9, Cytochrome P450 2B6, Cytochrome P450 1A2, and Cytochrome P450 2D6 are known to metabolize mephenytoin. Mephenytoin is a hydantoin-derivative anticonvulsant used to control various partial seizures. Mephenytoin and oxazolidinedione derivatives are associated with higher incidences of blood dyscrasias compared to other anticonvulsants. For the treatment of refractory partial epilepsy. Mephenytoin is an antiepileptic drug which can be useful in the treatment of epilepsy. The primary site of action appears to be the motor cortex where spread of seizure activity is inhibited. Possibly by promoting sodium efflux from neurons, mephenytoin tends to stabilize the threshold against hyperexcitability caused by excessive stimulation or environmental changes capable of reducing membrane sodium gradient. This includes the reduction of posttetanic potentiation at synapses. Loss of posttetanic potentiation prevents cortical seizure foci from detonating adjacent cortical areas. Mephenytoin reduces the maximal activity of brain stem centers responsible for the tonic phase of tonic-clonic (grand mal) seizures. The mechanism of action of mephenytoin is not definitely known, but extensive research strongly suggests that its main mechanism is to block frequency-, use- and voltage-dependent neuronal sodium channels, and therefore limit repetitive firing of action potentials.",The molecular weight is 218.26.,Mephenytoin has a topological polar surface area of 49.41.,The log p value of  is 2.0.,Mephenytoin is approved and investigational and withdrawn.,Mephenytoin is a solid.,True
14506,"Niacin is a B vitamin used to treat vitamin deficiencies as well as hyperlipidemia, dyslipidemia, hypertriglyceridemia, and to reduce the risk of myocardial infarctions. Niacin is indicated to prevent vitamin deficiencies in pediatric and adult patients receiving parenteral nutrition as part of multivitamin intravenous injections. Niacin oral tablets are indicated as a monotherapy or in combination with simvastatin or lovastatin to treat primary hyperlipidemia and mixed dyslipidemia. It can also be used to reduce the risk of nonfatal myocardial infarctions in patients with a history of myocardial infarction and hyperlipidemia. Niacin is also indicated with bile acid binding resins to treat atherosclerosis in patients with coronary artery disease and hyperlipidemia or to treat primary hyperlipidemia. Finally niacin is indicated to treat severe hypertriglyceridemia. Niacin is a B vitamin used to treat vitamin deficiencies as well as hyperlipidemia, dyslipidemia, hypertriglyceridemia, and to reduce the risk of myocardial infarctions. Niacin acts to decrease levels of very low density lipoproteins and low density lipoproteins, while increasing levels of high density lipoproteins. Niacin has a wide therapeutic window with usual oral doses between 500mg and 2000mg. Patients with diabetes, renal failure, uncontrolled hypothyroidism, and elderly patients taking niacin with simvastatin or lovastatin are at increased risk of myopathy and rhabdomyolysis. Niacin performs a number of functions in the body and so has many mechanisms, not all of which have been fully described. Niacin can decrease lipids and apolipoprotein B (apo B)-containing lipoproteins by modulating triglyceride synthesis in the liver, which degrades apo B, or by modulating lipolysis in adipose tissue.",The molecular weight is 123.11.,Niacin has a topological polar surface area of 50.19.,The log p value of  is 0.8.,Niacin is approved and investigational and nutraceutical.,Niacin is a solid.,True
14507,"A fibric acid derivative used in the treatment of hyperlipoproteinemia type III and severe hypertriglyceridemia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p986) For Primary Dysbetalipoproteinemia (Type III hyperlipidemia) that does not respond adequately to diet. This helps control high cholesterol and high triglyceride levels.  Clofibrate is an antilipidemic agent similar to gemfibrozil. It acts to lower elevated serum lipids by reducing the very low-density lipoprotein fraction (S<sub>f</sub> 20-400) rich in triglycerides. Serum cholesterol may be decreased, particularly in those patients whose cholesterol elevation is due to the presence of IDL as a result of Type III hyperlipoproteinemia. Several investigators have observed in their studies that clofibrate may produce a decrease in cholesterol linoleate but an increase in palmitoleate and oleate, the latter being considered atherogenic in experimental animals. The significance of this finding is unknown at this time. Reduction of triglycerides in some patients treated with clofibrate or certain of its chemically and clinically similar analogs may be associated with an increase in LDL cholesterol. Increase in LDL cholesterol has been observed in patients whose cholesterol is initially normal. Animal studies suggest that clofibrate interrupts cholesterol biosynthesis prior to mevalonate formation. Clofibrate increases the activity of extrahepatic lipoprotein lipase (LL), thereby increasing lipoprotein triglyceride lipolysis. Chylomicrons are degraded, VLDLs are converted to LDLs, and LDLs are converted to HDL. This is accompanied by a slight increase in secretion of lipids into the bile and ultimately the intestine. Clofibrate also inhibits the synthesis and increases the clearance of apolipoprotein B, a carrier molecule for VLDL. Also, as a fibrate, Clofibrate is an agonist of the PPAR-α receptor in muscle, liver, and other tissues. This agonism ultimately leads to modification in gene expression resulting in increased beta-oxidation, decreased triglyceride secretion, increased HDL, increased lipoprotein lipase activity.",The molecular weight is 242.7.,Clofibrate has a topological polar surface area of 35.53.,The log p value of  is 3.68.,Clofibrate is approved and investigational.,Clofibrate is a liquid.,True
14508,"Ethotoin is a hydantoin derivative and anticonvulsant. Ethotoin exerts an antiepileptic effect without causing general central nervous system depression. The mechanism of action is probably very similar to that of phenytoin. The latter drug appears to stabilize rather than to raise the normal seizure threshold, and to prevent the spread of seizure activity rather than to abolish the primary focus of seizure discharges. Ethotoin is no longer commonly used. For the control of tonic-clonic (grand mal) and complex partial (psychomotor) seizures. Ethotoin is a hydantoin derivative and anticonvulsant. Ethotoin exerts an antiepileptic effect without causing general central nervous system depression. The mechanism of action is probably very similar to that of phenytoin. The latter drug appears to stabilize rather than to raise the normal seizure threshold, and to prevent the spread of seizure activity rather than to abolish the primary focus of seizure discharges. The mechanism of action is probably very similar to that of phenytoin. The latter drug appears to stabilize rather than to raise the normal seizure threshold, and to prevent the spread of seizure activity rather than to abolish the primary focus of seizure discharges. Ethotoin inhibits nerve impulses in the motor cortex by lowering sodium ion influx, limiting tetanic stimulation.",The molecular weight is 204.23.,Ethotoin has a topological polar surface area of 49.41.,The log p value of  is 1.48.,Ethotoin is approved.,Ethotoin is a solid.,True
14509,"A non-steroidal anti-inflammatory agent with antipyretic and antigranulation activities. It also inhibits prostaglandin biosynthesis. For the relief of mild to moderate pain, for the treatment of primary dysmenorrhea and for the treatment of idiopathic heavy menstrual blood loss. Also for relief of the signs and symptoms of acute and chronic rheumatoid arthritis and osteoarthritis. Meclofenamic acid is a nonsteroidal agent which has demonstrated anti-inflammatory, analgesic, and antipyretic activity in laboratory animals. The mode of action, like that of other nonsteroidal anti-inflammatory agents, is not known. Therapeutic action does not result from pituitary-adrenal stimulation. In animal studies, meclofenamic acid was found to inhibit prostaglandin synthesis and to compete for binding at the prostaglandin receptor site. In vitro meclofenamic acid was found to be an inhibitor of human leukocyte 5-lipoxygenase activity. These properties may be responsible for the anti-inflammatory action of meclofenamic acid. There is no evidence that meclofenamic acid alters the course of the underlying disease.",The molecular weight is 296.15.,Meclofenamic acid has a topological polar surface area of 49.33.,The log p value of  is 6.26.,Meclofenamic acid is approved and vet_approved.,Meclofenamic acid is a solid.,True
14510,"Unfractionated heparin (UH) is a heterogenous preparation of anionic, sulfated glycosaminoglycan polymers with weights ranging from 3000 to 30,000 Da. It is a naturally occurring anticoagulant released from mast cells. It binds reversibly to antithrombin III (ATIII) and greatly accelerates the rate at which ATIII inactivates coagulation enzymes thrombin (factor IIa) and factor Xa. UH is different from low molecular weight heparin (LMWH) in the following ways: the average molecular weight of LMWH is about 4.5 kDa whereas it is 15 kDa for UH; UH requires continuous infusions; activated partial prothrombin time (aPTT) monitoring is required when using UH; and UH has a higher risk of bleeding and higher risk of osteoporosis in long term use. Unfractionated heparin is more specific than LMWH for thrombin. Furthermore, the effects of UH can typically be reversed by using protamine sulfate. Unfractionated heparin is indicated for prophylaxis and treatment of venous thrombosis and its extension, prevention of post-operative deep venous thrombosis and pulmonary embolism and prevention of clotting in arterial and cardiac surgery. In cardiology, it is used to prevent embolisms in patients with atrial fibrillation and as an adjunct antithrombin therapy in patients with unstable angina and/or non-Q wave myocardial infarctions (i.e. non-ST elevated acute coronary artery syndrome) who are on platelet glycoprotein (IIb/IIIa) receptor inhibitors. Additionally, it is used to prevent clotting during dialysis and surgical procedures, maintain the patency of intravenous injection devices and prevent in vitro coagulation of blood transfusions and in blood samples drawn for laboratory values. Unfractionated heparin is a highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from 3000 to 30,000 daltons. Heparin is obtained from liver, lung, mast cells, and other cells of vertebrates. Heparin is a well-known and commonly used anticoagulant which has antithrombotic properties. Heparin inhibits reactions that lead to the clotting of blood and the formation of fibrin clots both in vitro and in vivo. Small amounts of heparin in combination with antithrombin III, a heparin cofactor,) can inhibit thrombosis by inactivating Factor Xa and thrombin. Once active thrombosis has developed, larger amounts of heparin can inhibit further coagulation by inactivating thrombin and preventing the conversion of fibrinogen to fibrin. Heparin also prevents the formation of a stable fibrin clot by inhibiting the activation of the fibrin stabilizing factor. Heparin prolongs several coagulation tests. Of all the coagulation tests, activated partial prothrombin time (aPTT) is the most clinically important value. Under normal circumstances, antithrombin III (ATIII) inactivates thrombin (factor IIa) and factor Xa. This process occurs at a slow rate. Administered heparin binds reversibly to ATIII and leads to almost instantaneous inactivation of factors IIa and Xa The heparin-ATIII complex can also inactivate factors IX, XI, XII and plasmin. The mechanism of action of heparin is ATIII-dependent. It acts mainly by accelerating the rate of the neutralization of certain activated coagulation factors by antithrombin, but other mechanisms may also be involved. The antithrombotic effect of heparin is well correlated to the inhibition of factor Xa. Heparin is not a thrombolytic or fibrinolytic. It prevents progression of existing clots by inhibiting further clotting. The lysis of existing clots relies on endogenous thrombolytics.",,,,Heparin is approved and investigational.,Heparin is a solid.,True
14511,"Chemically, dantrolene is a hydantoin derivative, but does not exhibit antiepileptic activity like other hydantoin derivates such as phenytoin. For use, along with appropriate supportive measures, for the management of the fulminant hypermetabolism of skeletal muscle characteristic of malignant hyperthermia crises in patients of all ages. Also used preoperatively, and sometimes postoperatively, to prevent or attenuate the development of clinical and laboratory signs of malignant hyperthermia in individuals judged to be malignant hyperthermia susceptible. Dantrolene is classified as a direct-acting skeletal muscle relaxant. It is currently the only specific and effective treatment for malignant hyperthermia. In isolated nerve-muscle preparation, Dantrium has been shown to produce relaxation by affecting the contractile response of the muscle at a site beyond the myoneural junction. In skeletal muscle, Dantrium dissociates excitation-contraction coupling, probably by interfering with the release of Ca<sup>2+</sup> from the sarcoplasmic reticulum. In the anesthetic-induced malignant hyperthermia syndrome, evidence points to an intrinsic abnormality of skeletal muscle tissue. In selected humans, it has been postulated that &ldquo;triggering agents&rdquo; (e.g.,general anesthetics and depolarizing neuromuscular blocking agents) produce a change within the cell which results in an elevated myoplasmic calcium. This elevated myoplasmic calcium activates acute cellular catabolic processes that cascade to the malignant hyperthermia crisis. It is hypothesized that addition of Dantrium to the &ldquo;triggered&rdquo; malignant hyperthermic muscle cell reestablishes a normal level of ionized calcium in the myoplasm. Dantrolene depresses excitation-contraction coupling in skeletal muscle by binding to the ryanodine receptor 1, and decreasing intracellular calcium concentration. Ryanodine receptors mediate the release of calcium from the sarcoplasmic reticulum, an essential step in muscle contraction.",The molecular weight is 314.26.,Dantrolene has a topological polar surface area of 120.73.,The log p value of  is 1.63.,Dantrolene is approved and investigational.,Dantrolene is a solid.,True
14512,"Diamorphine (heroin) is a narcotic analgesic that may be habit-forming. It is a controlled substance (opium derivative) listed in the U.S. Code of Federal Regulations, Title 21 Parts 329.1, 1308.11 (1987). Sale is forbidden in the United States by Federal statute. (Merck Index, 11th ed) Internationally, diamorphine is controlled under Schedules I and IV of the Single Convention on Narcotic Drugs. As heroin, it is illegal to manufacture, possess, or sell in the United States and the UK. However, under the name diamorphine, heroin is a legal prescription drug in the United Kingdom. Diamorphine, as a prescription medication in the United Kingdom, is indicated for use in the treatment of severe pain associated with surgical procedures, myocardial infarction or pain in the terminally ill and for the relief of dyspnoea in acute pulmonary edema. The onset of heroin's effects is dependent on the method of administration. Taken orally, heroin is totally metabolized in vivo via extensive first-pass metabolism into morphine before crossing the blood-brain barrier; so the effects are the same as orally administered morphine. Take by injection, diamorphine's acetyl groups facilitate rapid crossing into the brain. Once in the brain, heroin is rapidly metabolized into morphine by removal of the acetyl groups, therefore making it a prodrug for the delivery of morphine. Subsequently, whether eliciting actions peripherally (on smooth muscle, skeletal muscle, kidney, lung, liver, or spleen tissue , for example) or on the central nervous system, it is ultimately the morphine metabolite of heroin that then binds with opioid receptors and produces the narcotic opioid effects commonly associated with the substance. When administered orally, diamorphine experiences extensive first-pass metabolism by way of deacetylation to generate the active metabolites 6-monoacetylmorphine (6-MAM) and morphine. Alternatively, when given as an injection the acetyl groups present in the diamorphine/diacetylmorphine compound confer the substance lipophilicity that facilitates diamorphine's rapid crossing of the blood-brain-barrier. Once in the brain, diamorphine is metabolised via deacetylation to the active 6-MAM and morphine metabolites as well. Despite diamorphine possessing little to no opioid agonist activity itself, its rapid transit across the blood-brain-barrier elicits a far faster onset of activity in comparison to the extensive first-pass metabolism of oral administration. Regardless, the metabolism of diamorphine to morphine makes heroin a prodrug for the delivery of morphine.",The molecular weight is 369.42.,Diamorphine has a topological polar surface area of 65.07.,The log p value of  is 1.48.,Diamorphine is approved and illicit and investigational.,Diamorphine is a solid.,True
14513,"5-fluorouridine is also known as FUrd, 5-Fluorouracil 1-beta-D-ribofuranoside, 5-Fur, or 5-Fluoro-uridine. 5-fluorouridine is a solid. This compound belongs to the pyrimidine nucleosides and analogues. These are compounds comprising a pyrimidine base attached to a sugar. 5-fluorouridine is known to target uridine phosphorylase. FUrd is often used in chemical and biochemical comparison studies with fluorouracil and thymine analogs.",,,,5-fluorouridine is experimental.,5-fluorouridine is a solid.,True
14514,"Erwinaze (asparaginase _Erwinia_ _chrysanthemi_) contains an asparaginase specific enzyme derived from _Erwinia_ _chrysanthemi_. Specifically, this L-asparaginase is a tetrameric enzyme consisting of four identical subunits, each having a molecular weight of about 35 kDa. The activity of Erwinaze is expressed in terms of International Units. It is an antineoplastic agent and was FDA approved in November 19, 2011. Asparaginase _Erwinia_ _chrysanthemi_ is for the treatment of patients with acute lymphoblastic leukemia (ALL) that have developed a hypersensitivity to E. coli-derivied asparaginase. It is a component of a multi-agent chemotherpeutic regimen for the treatment of the aforementioned disease and is considered second- or third- line treatment in European and American protocols.  Asparagine is ordinarily found incorporated into most endogenous proteins. In its absence however, protein synthesis is halted - which in turn also results in the inhibition of the RNA and DNA synthesis necessary for cellular proliferation.  Asparaginase _Erwinia_ _chrysanthemi_ catalyzes the deamidation of asparagine to aspartic acid and ammonia, resulting in a reduction in circulating levels of exogenous asparagine in the plasma. The mechanism of action of _Erwinia_ asparaginase is thought to be based on the inability of leukemic cells to synthesize asparagine due to lack of asparagine synthetase activity, resulting in cytotoxicity specific for leukemic cells that depend on an exogenous source of the amino acid asparagine for their protein metabolism and survival.",,,,Asparaginase Erwinia chrysanthemi is approved and investigational.,Asparaginase Erwinia chrysanthemi is a liquid.,True
14515,Etofenamate is used to treat muscle and joint paint. It is a non-steroidal anti-inflammatory drug (NSAID).,The molecular weight is 369.34.,Etofenamate has a topological polar surface area of 67.79.,The log p value of  is 4.74.,Etofenamate is experimental.,Etofenamate is a solid.,True
14516,"Tegafur (INN, BAN, USAN) is a prodrug of (5-FU), an antineoplastic agent used as the treatment of various cancers such as advanced gastric and colorectal cancers. It is a pyrimidine analogue used in combination therapies as an active chemotherapeutic agent in conjunction with and , or along with as. Tegafur is usually given in combination with other drugs that enhance the bioavailability of the 5-FU by blocking the enzyme responsible for its degradation, or serves to limit the toxicity of 5-FU by ensuring high concentrations of 5-FU at a lower dose of tegafur. When converted and bioactivated to 5-FU, the drug mediates an anticancer activity by inhibiting thymidylate synthase (TS) during the pyrimidine pathway involved in DNA synthesis. 5-FU is listed on the World Health Organization's List of Essential Medicines. Indicated for the treatment of cancer usually in combination with other biochemically modulating drugs. Tegafur is an antineoplastic agent that belongs in the class of pyrimidine analogues. It interferes with the 2'-deoxythymidylate (DTMP) synthesis in the pyrimidine pathway, resulting in inhibition of DNA synthesis. In a phase III trial investigating the clinical efficacy of S-1 (tegafur/gimeracil/oteracil) in patients with advanced or recurrent gastric cancer, treatment resulted in a high response rate and was associated with a longer overall survival and longer progression-free survival rate when used in combination with cisplatin. In a meta analysis, triple combination therapy consisting of tegafur, gimeracil and oteracil showed longer survival times and well tolerance in patients with advanced gastric cancer. Tegafur and its active metabolites are potent myleosuppressive agents.  The transformation of 2'-deoxyurindylate (dUMP) to 2'-deoxythymidylate (dTMP) is essential in driving the synthesis of DNA and purines in cells. Thymidylate synthase catalyzes the conversion of dUMP to dTMP, which is a precursor of thymidine triphosphate (TTP), one of the four deoxyribonucleotides required for DNA synthesis. After administration into the body, tegafur is converted into the active antineoplastic metabolite, fluorouracil (5-FU). In tumour cells, 5-FU undergoes phosphorylation to form the active anabolites, including 5-fluorodeoxyuridine monophosphate (FdUMP). FdUMP and reduced folate are bound to thymidylate synthase leading to formation of a ternary complex which inhibits DNA synthesis. In addition, 5-fluorouridine-triphosphate (FUTP) is incorporated into RNA causing disruption of RNA functions.",The molecular weight is 200.17.,Tegafur has a topological polar surface area of 58.64.,The log p value of  is -0.07.,Tegafur is approved and investigational.,Tegafur is a solid.,True
14517,"Synthetic conjugated estrogens A are composed of a blend of the following nine synthetic estrogenic substances: estrone sulfate, sodium equilin sulfate, sodium 17α-dihydroequilin sulfate, sodium 17α-estradiol sulfate, sodium 17β­ dihydroequilin sulfate, sodium 17α-dihydroequilenin sulfate, sodium 17β-dihydroequilenin sulfate, sodium equilenin sulfate, and sodium 17β-estradiol sulfate. This blend of nine estrogen derivatives are plant-derived forms of endogenous estrogens and contain many of the same compounds as the Conjugated Equine Estrogens (CEEs), although they are not considered to be equivalent. Available as the product Enjuvia (FDA), this combination of plant-derived estrogenic compounds is indicated for the treatment of moderate to severe vasomotor symptoms and vulvovaginal atrophy associated with menopause.  For the treatment of moderate to severe vasomotor symptoms due to menopause and for treatment of moderate to severe symptoms of vulvar and vaginal atrophy due to menopause. All estrogen products mimic the effects of endogenous estrogens in the body which are responsible for the development and maintenance of the female reproductive system and secondary sexual characteristics. Estrogens act by binding to estrogen receptors on a wide variety of tissues in the body and modulating the pituitary secretion of the gonadotropins, luteinizing hormone (LH) and follicle stimulating hormone (FSH) through a negative feedback mechanism. Prior to menopause, the primary source of estrogen is the ovarian follicle, which secretes 70-500 micrograms of estradiol daily, depending on the phase of the menstrual cycle. However, once a woman stops ovulating there is a sharp decline in the production of progesterone and estradiol by the ovaries and a consequent fluctuation in LH and FSH due to a lack of feedback control. This shift in hormone production is largely responsible for many of the symptoms experienced during and after menopause and includes hot flashes and other vasomotor symptoms, painful intercourse, vaginal dryness, and vulvovaginal atrophy. These symptoms are able to be reduced by replacing many of the hormones lost during and following menopause with synthetic or naturally occurring forms, in a therapy known as Hormone Replacement Therapy (HRT).",,,,"Synthetic Conjugated Estrogens, A is approved.","Synthetic Conjugated Estrogens, A is a solid.",True
14518,"Synthetic conjugated estrogens, B tablets contain a blend of ten synthetic estrogenic substances. The estrogenic substances are: sodium estrone sulfate, sodium equilin sulfate, sodium 17α-dihydroequilin sulfate, sodium 17α-estradiol sulfate, sodium 17β­ dihydroequilin sulfate, sodium 17α-dihydroequilenin sulfate, sodium 17β-dihydroequilenin sulfate, sodium equilenin sulfate, sodium 17β-estradiol sulfate, and sodium Δ8,9-dehydroestrone sulfate. This blend of ten estrogen derivatives are plant-derived forms of endogenous estrogens and contain many of the same compounds as the Conjugated Equine Estrogens (CEEs), although they are not considered to be equivalent. Available as the product Cenestin (FDA), this combination of plant-derived estrogenic compounds is indicated for the treatment of moderate to severe vasomotor symptoms, vulvovaginal atrophy, vaginal dryness, and paint with intercourse associated with menopause.  For the treatment of moderate to severe vasomotor symptoms due to menopause and for the treatment of moderate to severe vaginal dryness, pain with intercourse, and symptoms of vulvar and vaginal atrophy due to menopause. All estrogen products mimic the effects of endogenous estrogens in the body which are responsible for the development and maintenance of the female reproductive system and secondary sexual characteristics. Estrogens act by binding to estrogen receptors on a wide variety of tissues in the body and modulating the pituitary secretion of the gonadotropins, luteinizing hormone (LH) and follicle stimulating hormone (FSH) through a negative feedback mechanism. Prior to menopause, the primary source of estrogen is the ovarian follicle, which secretes 70-500 micrograms of estradiol daily, depending on the phase of the menstrual cycle. However, once a woman stops ovulating there is a sharp decline in the production of progesterone and estradiol by the ovaries and a consequent fluctuation in LH and FSH due to a lack of feedback control. This shift in hormone production is largely responsible for many of the symptoms experienced during and after menopause and includes hot flashes and other vasomotor symptoms, painful intercourse, vaginal dryness, and vulvovaginal atrophy. These symptoms are able to be reduced by replacing many of the hormones lost during and following menopause with synthetic or naturally occurring forms, in a therapy known as Hormone Replacement Therapy (HRT).",,,,"Synthetic Conjugated Estrogens, B is approved.","Synthetic Conjugated Estrogens, B is a solid.",True
14519,"Esterified estrogens contain a mixture of estrogenic substances; the principle component is estrone. Preparations contain 75% to 85% sodium estrone sulfate and 6% to 15% sodium equilin sulfate such that the total is not <90%. Esterified estrogens are a man-made mixture of estrogens that are used to treat symptoms of menopause such as hot flashes, vaginal dryness, vaginal burning or irritation, or other hormonal changes in the vagina. It is being also for the prevention and treatment of osteoporosis. Esterified estrogens are indicated to replace estrogen in women with ovarian failure or other conditions that cause a lack of natural estrogen in the body. Estrogens are responsible for the development and maintenance of the female reproductive system and secondary sexual characteristics. Estradiol is the principle intracellular human estrogen and is more potent than estrone and estriol at the receptor level; it is the primary estrogen secreted prior to menopause. Estrogens modulate the pituitary secretion of gonadotropins, luteinizing hormone, and follicle-stimulating hormone through a negative feedback system; estrogen replacement reduces elevated levels of these hormones.",,,,Esterified estrogens is approved.,,True
14520,"Allantoin is a substance that is endogenous to the human body and also found as a normal component of human diets. In healthy human volunteers, the mean plasma concentration of allantoin is about 2-3 mg/l. During exercise, the plasma allantoin concentration rapidly increases about two fold and remains elevated. In human muscle, urate is oxidized to allantoin during such exercise. The concentration of allantoin in muscles increases from a resting value of about 5000 ug/kg to about 16000 ug/kg immediately after short-term exhaustive cycling exercise.  Allantoin is commonly applied in a variety of topical vehicles or applications such as cosmetic creams, toothpastes, mouthwashes, shampoos, lipsticks, anti-acne products, and lotions for the purpose of moisturizing skin, enhancing the smoothness of skin, stimulating the healing of wounds, and soothing irritated skin. There is no well controlled and appropriate data that can formally substantiate the pharmacodynamic properties of allantoin. Nevertheless, ongoing studies suggest that allantoin possesses moisturizing and keratolytic effects, as well as abilities to increase the water content of the extracellular matrix and enhance the desquamation of upper layers of dead skin cells, all of which are activities that can promote cell proliferation and facilitate wound healing. There is no well controlled data that can formally substantiate the method of action. However, ongoing studies suggest that there may exist a histological wound healing profile induced by allantoin in rats that leads to the amelioration and fastening of the reestablishment of normal skin. This facilitation of wound healing is supported by observations that wounds inflicted to rat subjects to which topical allantoin preparations were applied histologically demonstrated increased vasodilation, presence of inflammatory exudates, number of inflammatory cells, angiogenesis, fibroblast proliferation, and increased collagen deposition when compared to rat subjects with wounds that did not receive any allantoin administration.",The molecular weight is 158.12.,Allantoin has a topological polar surface area of 113.32.,The log p value of  is -2.23.,Allantoin is approved.,,True
14521,"Liothyronine I-131 has been used in trials studying the treatment of Tricuspid Atresia and Heart Defects, Congenital.",,,,Liothyronine I-131 is investigational.,,True
14522,,The molecular weight is 367.4.,Neocitrullamon has a topological polar surface area of 112.73.,The log p value of  is 0.11.,Neocitrullamon is experimental.,,False
14523,,,,,"1-{2-Ethoxy}-4-(1,1,3,3-Tetramethylbutyl)Benzene is experimental.","1-{2-Ethoxy}-4-(1,1,3,3-Tetramethylbutyl)Benzene is a solid.",False
14524,"Alpha-tocopherol is the primary form of vitamin E that is preferentially used by the human body to meet appropriate dietary requirements. In particular, the RRR-alpha-tocopherol (or sometimes called the d-alpha-tocopherol stereoisomer) stereoisomer is considered the natural formation of alpha-tocopherol and generally exhibits the greatest bioavailability out of all of the alpha-tocopherol stereoisomers. Moreover, manufacturers typically convert the phenol component of the vitamin to esters using acetic or succinic acid, making a compound such as alpha-tocopherol succinate more stable and easier to use in vitamin supplements. The primary health-related use for which alpha-tocopherol succinate is formally indicated is as a dietary supplement for patients who demonstrate a genuine vitamin E deficiency. At the same time, vitamin E deficiency is generally quite rare but may occur in premature babies of very low birth weight (< 1500 grams), individuals with fat-malabsorption disorders (as fat is required for the digestive tract to absorb vitamin E), or individuals with abetalipoproteinemia - a rare, inherited disorder that causes poor absorption of dietary fat - who require extremely large doses of supplemental vitamin E daily (around 100 mg/kg or 5-10 g/day). In all such cases, alpha-tocopherol is largely the preferred form of vitamin E to be administered. Of the eight separate variants of vitamin E, alpha-tocopherol is the predominant form of vitamin E in human and animal tissues, and it has the highest bioavailability. This is because the liver preferentially resecretes only alpha-tocopherol by way of the hepatic alpha-tocopherol transfer protein (alpha-TTP); the liver metabolizes and excretes all the other vitamin E variants, which is why blood and cellular concentrations of other forms of vitamin E other than alpha-tocopherol are ultimately lower. Without further evidence to suggest otherwise, alpha-tocpherol succinate is generally believed to undergo a logical de-esterification in the gastrointestinal tract before being subsequently absorbed as free tocopherol. The free alpha-tocopherol is therefore available and capable of the following activities.",The molecular weight is 530.79.,alpha-Tocopherol succinate has a topological polar surface area of 72.83.,The log p value of  is 11.85.,alpha-Tocopherol succinate is approved and nutraceutical and vet_approved.,,True
14525,"Alpha-tocopherol is the primary form of vitamin E that is preferentially used by the human body to meet appropriate dietary requirements. In particular, the RRR-alpha-tocopherol (or sometimes called the d-alpha-tocopherol stereoisomer) stereoisomer is considered the natural formation of alpha-tocopherol and generally exhibits the greatest bioavailability out of all of the alpha-tocopherol stereoisomers. Moreover, RRR-alpha-tocopherol acetate is a relatively stabilized form of vitamin E that is most commonly used as a food additive when needed. _In addition to any following information, owing to d-alpha-Tocopherol acetate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data._ _In addition to any following information, owing to d-alpha-Tocopherol acetate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data._ _In addition to any following information, owing to d-alpha-Tocopherol acetate's closely related chemical nature with alpha-Tocopherol acetate, please also refer to the drug information page for alpha-Tocopherol acetate for further data._",The molecular weight is 472.75.,D-alpha-Tocopherol acetate has a topological polar surface area of 35.53.,The log p value of  is 12.15.,D-alpha-Tocopherol acetate is approved and nutraceutical and vet_approved.,,True
14526,"Drostanolone (also known as dromostanolone) is a potent synthetic androgenic anabolic steroid similar to testosterone. Drostanolone is indicated in postmenopausal women with recurrent breast cancer, in a combined hormone therapy.",,,,Drostanolone is illicit.,Drostanolone is a solid.,True
14527,"An anabolic steroid that has been used in the treatment of male hypogonadism, delayed puberty in males, and in the treatment of breast neoplasms in women. In males, used as replacement therapy in conditions associated with symptoms of deficiency or absence of endogenous testosterone. In females, for palliation of androgenresponsive recurrent mammary cancer in women who are more than one year but less than five years postmenopausal. Fluoxymesterone is a synthetic androgen, or male hormone, similar to testosterone. Fluoxymesterone works by attaching itself to androgen receptors; this causes it to interact with the parts of the cell involved in the making of proteins. It may cause an increase in the synthesis of some proteins or a decrease in the synthesis of others. These proteins have a variety of effects, including blocking the growth of some types of breast cancer cells, stimulating cells that cause male sexual characteristics, and stimulating the production of red blood cells. Fluoxymesterone is a synthetic androgenic anabolic steroid and is approximately 5 times as potent as natural methyltestosterone. Like testosterone and other androgenic hormones, fluoxymesterone binds to the androgen receptor. It produces retention of nitrogen, sodium, potassium, and phosphorus; increases protein anabolism; decreases amino acid catabolism and decreased urinary excretion of calcium. The antitumour activity of fluoxymesterone appears related to reduction or competitive inhibition of prolactin receptors or estrogen receptors or production.",The molecular weight is 336.45.,Fluoxymesterone has a topological polar surface area of 57.53.,The log p value of  is 2.84.,Fluoxymesterone is approved and illicit.,Fluoxymesterone is a solid.,True
14528,"A synthetic steroid with antigonadotropic and anti-estrogenic activities that acts as an anterior pituitary suppressant by inhibiting the pituitary output of gonadotropins. It possesses some androgenic properties. Danazol has been used in the treatment of endometriosis and some benign breast disorders. For the treatment of endometriosis and fibrocystic breast disease (in patients unresponsive to simple measures). Also used for the prophylactic treatment of all types of hereditary angioedema in males and females. Danazol is a derivative of the synthetic steroid ethisterone, a modified testosterone. It was approved by the U.S. Food and Drug Administration (FDA) as the first drug to specifically treat endometriosis, but its role as a treatment for endometriosis has been largely replaced by the gonadotropin-releasing hormone (GnRH) agonists. Danazol has antigonadotropic and anti-estrogenic activities. Danazol acts as an anterior pituitary suppressant by inhibiting the pituitary output of gonadotropins. It possesses some androgenic properties. As a gonadotropin inhibitor, danazol suppresses the pituitary-ovarian axis possibly by inhibiting the output of pituitary gonadotropins. Danazol also depresses the preovulatory surge in output of follicle-stimulating hormone (FSH) and luteinizing hormone (LH), thereby reducing ovarian estrogen production. Danazol may also directly inhibits ovarian steroidogenesis; bind to androgen, progesterone, and glucocorticoid receptors; bind to sex-hormone-binding globulin and corticosteroid-binding globulin; and increases the metabolic clearance rate of progesterone. Another mechanism of action by which danazol may use to facilitate regression of endometriosis is by decreasing IgG, IgM, and IgA concentrations, as well as phospholipid and IgG isotope autoantibodies. In the treatment of endometriosis, as a consequence of suppression of ovarian function, danazol causes both normal and ectopic endometrial tissues to become inactive and atrophic. This leads to anovulation and associated amenorrhea. In fibrocystic breast disease, the exact mechanism of action of danazol is unknown, but may be related to suppressed estrogenic stimulation as a result of decreased ovarian production of estrogen. A direct effect on steroid receptor sites in breast tissue is also possible. This leads to a disappearance of nodularity, relief of pain and tenderness, and possibly changes in the menstrual pattern. In terms of hereditary angioedema, danazol corrects the underlying biochemical deficiency by increasing serum concentrations of the deficient C1 esterase inhibitor, resulting in increased serum concentrations of the C4 component of the complement system. (Source: PharmGKB)",The molecular weight is 337.46.,Danazol has a topological polar surface area of 46.26.,The log p value of  is 3.75.,Danazol is approved.,Danazol is a solid.,True
14529,"2-Methoxyestradiol (2ME2) is a drug that prevents the formation of new blood vessels that tumors need in order to grow (angiogenesis). It has undergone Phase 1 clinical trials against breast cancers and preclinical studies suggest that 2ME2 could also be effective against inflammatory diseases such as rheumatoid arthritis. For the treatment of breast cancer and inflammatory diseases such as rheumatoid arthritis. 2-Methoxyestradiol belongs to the family of drugs called angiogenesis inhibitors. It also acts as a vasodilator. 2-Methoxyestradiol is an angiogenesis inhibitor, and has been shown to attack both tumor cells and their blood supply in preclinical testing. 2-methoxyestradiol is a naturally occurring estrogen metabolite but has no undesired estrogenic activity.",,,,2-Methoxyestradiol is investigational.,2-Methoxyestradiol is a solid.,True
14530,"A potent androgenic metabolite of testosterone. Dihydrotestosterone (DHT) is generated by a 5-alpha reduction of testosterone. Unlike testosterone, DHT cannot be aromatized to estradiol therefore DHT is considered a pure androgenic steroid.",The molecular weight is 290.45.,Stanolone has a topological polar surface area of 37.3.,The log p value of  is 3.55.,Stanolone is illicit and investigational.,Stanolone is a solid.,True
14531,,,,,"5-Alpha-Androstane-3-Beta,17beta-Diol is experimental.","5-Alpha-Androstane-3-Beta,17beta-Diol is a solid.",False
14532,"5alpha-androstane-3beta,17alpha-diol is the unspecified form of the steroid, normally a major metabolite of with androgenic activity. It has been implicated as a regulator of gonadotropin secretion.",,,,"5alpha-androstane-3beta,17alpha-diol is experimental.","5alpha-androstane-3beta,17alpha-diol is a solid.",True
14533,Stanolone acetate is a synthetic androgen and anabolic steroid and a dihydrotestosterone ester that was never marketed.,,,,Stanolone acetate is experimental.,,True
14534,,,,,"1,3,3-trimethyl-2-cyclohexene is experimental.","1,3,3-trimethyl-2-cyclohexene is a solid.",False
14535,,,,,Ro 12-7310 is experimental.,Ro 12-7310 is a solid.,False
14536,,,,,"6-(2,3,4,5,6,7-HEXAHYDRO-2,4,4-TRIMETHYL-1-METYLENEINDEN-2-YL)-3-METHYLHEXA-2,4-DIENOIC ACID is experimental.","6-(2,3,4,5,6,7-HEXAHYDRO-2,4,4-TRIMETHYL-1-METYLENEINDEN-2-YL)-3-METHYLHEXA-2,4-DIENOIC ACID is a solid.",False
14537,"Chronic angina is a common cardiovascular condition affecting millions worldwide and causes significant disability while interfering with daily activities. Ranolazine is a well-tolerated piperazine derivative used for the management of this condition, offering relief from uncomfortable and debilitating symptoms. With a mechanism of action different from drugs used to treat the same condition, ranolazine is a promising anti-anginal therapy. It was originally approved by the FDA in 2006. Ranolazine is indicated for the treatment of chronic angina. It can be used alone or in conjunction with nitrates, beta-blockers, angiotensin receptor blockers, anti-platelet drugs, calcium channel blockers, lipid-lowering drugs, and ACE inhibitors. Ranolazine exerts both antianginal and ischemic effects independent from lowering heart rate or blood pressure. It blocks IKr, the rapid portion of the delayed rectifier potassium current, and prolongs the QTc interval in a dose-dependent fashion. The Ikr is important for cardiac repolarization. Ranolazine exerts its therapeutic effects without negative chronotropic, dromotropic, or inotropic actions neither at rest, nor during exercise. Myocardial ischemia exerts effects on adenosine triphosphate flux, leading to a decrease in the energy available for contraction and relaxation of the heart muscle. Electrolyte balance of sodium and potassium is necessary for maintaining normal cardiac contraction and relaxation. Disruption of adequate sodium and potassium electrolyte balance leads to excessively high concentrations of sodium and calcium, which likely interferes with oxygen supply to the heart muscle. This imbalance eventually leads to angina symptoms of chest pain or pressure, nausea, and dizziness, among others.",The molecular weight is 427.54.,Ranolazine has a topological polar surface area of 74.27.,The log p value of  is 1.01.,Ranolazine is approved and investigational.,Ranolazine is a solid.,True
14538,"A class I anti-arrhythmic agent (one that interferes directly with the depolarization of the cardiac membrane and thus serves as a membrane-stabilizing agent) with a depressant action on the heart similar to that of guanidine. It also possesses some anticholinergic and local anesthetic properties. For the treatment of documented ventricular arrhythmias, such as sustained ventricular tachycardia, ventricular pre-excitation and cardiac dysrhythmias. It is a Class Ia antiarrhythmic drug. Disopyramide is an antiarrhythmic drug indicated for the treatment of documented ventricular arrhythmias, such as sustained ventricular tachycardia that are life-threatening. In man, Disopyramide at therapeutic plasma levels shortens the sinus node recovery time, lengthens the effective refractory period of the atrium, and has a minimal effect on the effective refractory period of the AV node. Little effect has been shown on AV-nodal and His-Purkinje conduction times or QRS duration. However, prolongation of conduction in accessory pathways occurs. Disopyramide is a Type 1A antiarrhythmic drug (ie, similar to procainamide and quinidine). It inhibits the fast sodium channels. In animal studies Disopyramide decreases the rate of diastolic depolarization (phase 4) in cells with augmented automaticity, decreases the upstroke velocity (phase 0) and increases the action potential duration of normal cardiac cells, decreases the disparity in refractoriness between infarcted and adjacent normally perfused myocardium, and has no effect on alpha- or beta-adrenergic receptors.",The molecular weight is 339.48.,Disopyramide has a topological polar surface area of 59.22.,The log p value of  is 2.58.,Disopyramide is approved.,Disopyramide is a solid.,True
14539,"Prazosin, also known as _Minipress_, is a drug used to treat hypertension. Prazosin is marketed by _Pfizer_ and was initially approved by the FDA in 1988. It belongs to the class of drugs known as alpha-1 antagonists ,.  This drug is indicated for the treatment of hypertension (high blood pressure). Prazosin can be given alone or given with other blood pressure-lowering drugs, including diuretics or beta-adrenergic blocking agents. **Effects on blood pressure** Alpha-adrenergic receptors are essential for the regulation of blood pressure in humans. Two types of alpha receptors, alpha 1 and alpha 2, both play a role in regulating blood pressure. Alpha-1 receptors are postsynaptic (located after the nerve junction, or space between a nerve fiber and target tissue). In this case, the target tissue is the vascular smooth muscle. These receptors, when activated, increase blood pressure. ",The molecular weight is 383.41.,Prazosin has a topological polar surface area of 106.95.,The log p value of  is 2.03.,Prazosin is approved.,Prazosin is a solid.,True
14540,"Amoxapine, the <i>N</i>-demethylated derivative of the antipsychotic agent loxapine, is a dibenzoxazepine-derivative tricyclic antidepressant (TCA). TCAs are structurally similar to phenothiazines. They contain a tricyclic ring system with an alkyl amine substituent on the central ring. In non-depressed individuals, amoxapine does not affect mood or arousal, but may cause sedation. In depressed individuals, amoxapine exerts a positive effect on mood. TCAs are potent inhibitors of serotonin and norepinephrine reuptake. In addition, TCAs down-regulate cerebral cortical &beta;-adrenergic receptors and sensitize post-synaptic serotonergic receptors with chronic use. The antidepressant effects of TCAs are thought to be due to an overall increase in serotonergic neurotransmission. TCAs also block histamine H<sub>1</sub> receptors, &alpha;<sub>1</sub>-adrenergic receptors and muscarinic receptors, which accounts for their sedative, hypotensive and anticholinergic effects (e.g. blurred vision, dry mouth, constipation, urinary retention), respectively. See toxicity section below for a complete listing of side effects. Amoxapine may be used to treat neurotic and reactive depressive disorders, endogenous and psychotic depression, and mixed symptoms of depression and anxiety or agitation. For the relief of symptoms of depression in patients with neurotic or reactive depressive disorders as well as endogenous and psychotic depressions. May also be used to treat depression accompanied by anxiety or agitation. Amoxapine is a tricyclic antidepressant of the dibenzoxazepine class, chemically distinct from the dibenzodiazepines, dibenzocycloheptenes, and dibenzoxepines. It has a mild sedative component to its action. The mechanism of its clinical action in man is not well understood. In animals, amoxapine reduced the uptake of nor-epinephirine and serotonin and blocked the response of dopamine receptors to dopamine. Amoxapine is not a monoamine oxidase inhibitor. Clinical studies have demonstrated that amoxapine has a more rapid onset of action than either amitriptyline or imipramine Amoxapine acts by decreasing the reuptake of norepinephrine and serotonin (5-HT).",The molecular weight is 313.79.,Amoxapine has a topological polar surface area of 36.86.,The log p value of  is 3.41.,Amoxapine is approved.,Amoxapine is a solid.,True
14541,"Tamsulosin is a selective alpha-1A and alpha-1B adrenoceptor antagonist that exerts its greatest effect in the prostate and bladder, where these receptors are most common. It is indicated for the treatment of signs and symptoms of benign prostatic hypertrophy. Antagonism of these receptors leads to relaxation of smooth muscle in the prostate and detrusor muscles in the bladder, allowing for better urinary flow. Other alpha-1 adrenoceptor antagonists developed in the 1980s were less selective and more likely to act on the smooth muscle of blood vessels, resulting in hypotension. Tamsulosin is indicated for the treatment of signs and symptoms of benign prostatic hyperplasia. Tamsulosin is an alpha adrenoceptor blocker with specificity for the alpha-1A and alpha-1D subtypes, which are more common in the prostate and submaxillary tissue. The final subtype, alpha-1B, are most common in the aorta and spleen. Tamsulosin binds to alpha-1A receptors 3.9-38 times more selectively than alpha-1B and 3-20 times more selectively than alpha-1D. This selectivity allows for a significant effect on urinary flow with a reduced incidence of adverse reactions like orthostatic hypotension. Tamsulosin is a blocker of alpha-1A and alpha-1D adrenoceptors. About 70% of the alpha-1 adrenoceptors in the prostate are of the alpha-1A subtype. By blocking these adrenoceptors, smooth muscle in the prostate is relaxed and urinary flow is improved. The blocking of alpha-1D adrenoceptors relaxes the detrusor muscles of the bladder which prevents storage symptoms. The specificity of tamsulosin focuses the effects to the target area while minimizing effects in other areas.",The molecular weight is 408.51.,Tamsulosin has a topological polar surface area of 99.88.,The log p value of  is 2.17.,Tamsulosin is approved and investigational.,Tamsulosin is a solid.,True
14542,"Maprotiline is a tetracyclic antidepressant with similar pharmacological properties to tricyclic antidepressants (TCAs). Similar to TCAs, maprotiline inhibits neuronal norepinephrine reuptake, possesses some anticholinergic activity, and does not affect monoamine oxidase activity. It differs from TCAs in that it does not appear to block serotonin reuptake. Maprotiline may be used to treat depressive affective disorders, including dysthymic disorder (depressive neurosis) and major depressive disorder. Maprotiline is effective at reducing symptoms of anxiety associated with depression. For treatment of depression, including the depressed phase of bipolar depression, psychotic depression, and involutional melancholia, and may also be helpful in treating certain patients suffering severe depressive neurosis. Maprotiline is a tetracyclic antidepressant. Although its main therapeutic use is in the treatment of depression, it has also been shown to exert a sedative effect on the anxiety component that often accompanies depression. In one sleep study, it was shown that maprotiline increases the duration of the REM sleep phase in depressed patients, compared to imipramine which reduced the REM sleep phase. Maprotiline is a strong inhibitor of noradrenaline reuptake in the brain and peripheral tissues, however it is worthy to note that it is a weak inhibitor of serotonergic uptake. In addition, it displays strong antihistaminic action (which may explain its sedative effects) as well as weak anticholinergic action. Maprotiline also has lower alpha adrenergic blocking activity than amitriptyline. Maprotiline exerts its antidepressant action by inhibition of presynaptic uptake of catecholamines, thereby increasing their concentration at the synaptic clefts of the brain. In single doses, the effect of maprotiline on the EEG revealed a rise in the alpha-wave density, a reduction of the alpha-wave frequency and an increase in the alpha-wave amplitude. However, as with other tricyclic antidepressants, maprotiline lowers the convulsive threshold. Maprotiline acts as an antagonist at central presynaptic &alpha;<sub>2</sub>-adrenergic inhibitory autoreceptors and hetero-receptors, an action that is postulated to result in an increase in central noradrenergic and serotonergic activity. Maprotiline is also a moderate peripheral &alpha;<sub>1</sub> adrenergic antagonist, which may explain the occasional orthostatic hypotension reported in association with its use. Maprotiline also inhibits the amine transporter, delaying the reuptake of noradrenaline and norepinephrine. Lastly, maprotiline is a strong inhibitor of the histamine H<sub>1</sub> receptor, which explains its sedative actions.",The molecular weight is 277.41.,Maprotiline has a topological polar surface area of 12.03.,The log p value of  is 4.52.,Maprotiline is approved and investigational.,Maprotiline is a solid.,True
14543,"Desipramine hydrochloride is a dibenzazepine-derivative tricyclic antidepressant (TCA). TCAs are structurally similar to phenothiazines. They contain a tricyclic ring system with an alkyl amine substituent on the central ring. In non-depressed individuals, desipramine does not affect mood or arousal, but may cause sedation. In depressed individuals, desipramine exerts a positive effect on mood. TCAs are potent inhibitors of serotonin and norepinephrine reuptake. Secondary amine TCAs, such as desipramine and nortriptyline, are more potent inhibitors of norepinephrine reuptake than tertiary amine TCAs, such as amitriptyline and doxepine. TCAs also down-regulate cerebral cortical &beta;-adrenergic receptors and sensitize post-synaptic serotonergic receptors with chronic use. The antidepressant effects of TCAs are thought to be due to an overall increase in serotonergic neurotransmission. TCAs also block histamine-H<sub>1</sub> receptors, &alpha;<sub>1</sub>-adrenergic receptors and muscarinic receptors, which accounts for their sedative, hypotensive and anticholinergic effects (e.g. blurred vision, dry mouth, constipation, urinary retention), respectively. See toxicity section below for a complete listing of side effects. Desipramine exerts less anticholinergic and sedative side effects compared to tertiary amine TCAs, such as amitriptyline and clomipramine. Desipramine may be used to treat depression, neuropathic pain (unlabeled use), agitation and insomnia (unlabeled use) and attention-deficit hyperactivity disorder (unlabeled use). For relief of symptoms in various depressive syndromes, especially endogenous depression. It has also been used to manage chronic peripheral neuropathic pain, as a second line agent for the management of anxiety disorders (e.g. panic disorder, generalized anxiety disorder), and as a second or third line agent in the ADHD management.  Desipramine, a secondary amine tricyclic antidepressant, is structurally related to both the skeletal muscle relaxant cyclobenzaprine and the thioxanthene antipsychotics such as thiothixene. It is the active metabolite of imipramine, a tertiary amine TCA. The acute effects of desipramine include inhibition of noradrenaline re-uptake at noradrenergic nerve endings and inhibition of serotonin (5-hydroxy tryptamine, 5HT) re-uptake at the serotoninergic nerve endings in the central nervous system. Desipramine exhibits greater noradrenergic re-uptake inhibition compared to the tertiary amine TCA imipramine. In addition to inhibiting neurotransmitter re-uptake, desipramine down-regulates beta-adrenergic receptors in the cerebral cortex and sensitizes serotonergic receptors with chronic use. The overall effect is increased serotonergic transmission. Antidepressant effects are typically observed 2 - 4 weeks following the onset of therapy though some patients may require up to 8 weeks of therapy prior to symptom improvement. Patients experiencing more severe depressive episodes may respond quicker than those with mild depressive symptoms. Desipramine is a tricyclic antidepressant (TCA) that selectively blocks reuptake of norepinephrine (noradrenaline) from the neuronal synapse. It also inhibits serotonin reuptake, but to a lesser extent compared to tertiary amine TCAs such as imipramine. Inhibition of neurotransmitter reuptake increases stimulation of the post-synaptic neuron. Chronic use of desipramine also leads to down-regulation of beta-adrenergic receptors in the cerebral cortex and sensitization of serotonergic receptors. An overall increase in serotonergic transmission likely confers desipramine its antidepressant effects. Desipramine also possesses minor anticholinergic activity, through its affinity for muscarinic receptors. TCAs are believed to act by restoring normal levels of neurotransmitters via synaptic reuptake inhibition and by increasing serotonergic neurotransmission via serotonergic receptor sensitization in the central nervous system.",The molecular weight is 266.39.,Desipramine has a topological polar surface area of 15.27.,The log p value of  is 4.47.,Desipramine is approved and investigational.,Desipramine is a solid.,True
14544,"Bupropion (also known as the brand name product Wellbutrin®) is a norepinephrine/dopamine-reuptake inhibitor (NDRI) used most commonly for the management of Major Depressive Disorder (MDD), Seasonal Affective Disorder (SAD), and as an aid for smoking cessation. Bupropion exerts its pharmacological effects by weakly inhibiting the enzymes involved in the uptake of the neurotransmitters norepinephrine and dopamine from the synaptic cleft, therefore prolonging their duration of action within the neuronal synapse and the downstream effects of these neurotransmitters. More specifically, bupropion binds to the norepinephrine transporter (NET) and the dopamine transporter (DAT). Bupropion is indicated for the treatment of major depressive disorder (MDD), seasonal affective disorder (SAD), and as an aid to smoking cessation.  Bupropion is chemically unrelated to tricyclic, tetracyclic, selective serotonin re-uptake inhibitors, or other known antidepressant agents. Compared to classical tricyclic antidepressants, Bupropion is a relatively weak inhibitor of the neuronal uptake of norepinephrine and dopamine. In addition, Bupropion does not inhibit monoamine oxidase. Bupropion has been found to be essentially inactive at the serotonin transporter (SERT)(IC50 >10 000 nM), however both bupropion and its primary metabolite hydroxybupropion have been found to block the function of cation-selective serotonin type 3A receptors (5-HT3ARs).  Bupropion is a norepinephrine/dopamine-reuptake inhibitor (NDRI) that exerts its pharmacological effects by weakly inhibiting the enzymes involved in the uptake of the neurotransmitters norepinephrine and dopamine from the synaptic cleft, therefore prolonging their duration of action within the neuronal synapse and the downstream effects of these neurotransmitters. More specifically, bupropion binds to the norepinephrine transporter (NET) and the dopamine transporter (DAT). ",The molecular weight is 239.74.,Bupropion has a topological polar surface area of 29.1.,The log p value of  is 3.21.,Bupropion is approved.,Bupropion is a solid.,True
14545,"Clindamycin is a semi-synthetic lincosamide antibiotic used in the treatment of a variety of serious infections due to susceptible microorganisms as well as topically for acne vulgaris. It has a relatively narrow spectrum of activity that includes anaerobic bacteria as well as gram-positive cocci and bacilli and gram-negative bacilli. Interestingly, clindamycin appears to carry some activity against protozoans, and has been used off-label in the treatment of toxoplasmosis, malaria, and babesiosis. In oral and parenteral formulations, clindamycin is indicated for the treatment of serious infections caused by susceptible anaerobic bacteria, as well as susceptible staphylococci, streptococci, and pneumococci. Used topically, it is indicated for the treatment of acne vulgaris and is available in combination with or for this purpose. Clindamycin is also indicated as a vaginal cream or suppository for the treatment of bacterial vaginosis in non-pregnant females. Clindamycin exerts its bacteriostatic effect via inhibition of microbial protein synthesis. Clindamycin has a relatively short T<sub>max</sub> and half-life necessitating administration every six hours to ensure adequate antibiotic concentrations.  Clindamycin inhibits bacterial protein synthesis by binding to 23S RNA of the 50S subunit of the bacterial ribosome. It impedes both the assembly of the ribosome and the translation process. The molecular mechanism through which this occurs is thought to be due to clindamycin's three-dimensional structure, which closely resembles the 3'-ends of L-Pro-Met-tRNA and deacylated-tRNA during the peptide elongation cycle - in acting as a structural analog of these tRNA molecules, clindamycin impairs peptide chain initiation and may stimulate dissociation of peptidyl-tRNA from bacterial ribosomes.",The molecular weight is 424.98.,Clindamycin has a topological polar surface area of 102.26.,The log p value of  is 2.57.,Clindamycin is approved and vet_approved.,Clindamycin is a solid.,True
14546,"Diabetic gastroparesis is a condition that causes frequent nausea and vomiting, which has a negative impact on quality of life and poses a significant burden on the healthcare system. Metoclopramide is a dopamine antagonist used to treat nausea and vomiting that may be associated with diabetic gastroparesis in addition to gastroesophageal reflux disease (GERD). It can also be used to prevent nausea or vomiting associated with chemotherapy or certain surgical or diagnostic procedures.  Metoclopramide in the oral tablet form is used for symptomatic treatment of both acute and recurrent diabetic gastroparesis, in addition to the treatment of gastroesophageal reflux disease (GERD) in patients who have failed to respond to traditional therapy. A nasal spray formulation is also indicated to treat adults with acute, recurrent diabetic gastroparesis. Metoclopramide increases gastric emptying by decreasing lower esophageal sphincter (LES) pressure. It also exerts effects on the area postrema of the brain, preventing and relieving the symptoms of nausea and vomiting. In addition, this drug increases gastrointestinal motility without increasing biliary, gastric, or pancreatic secretions. Metoclopramide causes antiemetic effects by inhibiting dopamine D2 and serotonin 5-HT3 receptors in the chemoreceptor trigger zone (CTZ) located in the area postrema of the brain. Administration of this drug leads to prokinetic effects via inhibitory actions on presynaptic and postsynaptic D2 receptors, agonism of serotonin 5-HT4 receptors, and antagonism of muscarinic receptor inhibition. This action enhances the release of acetylcholine, causing increased lower esophageal sphincter (LES) and gastric tone, accelerating gastric emptying and transit through the gut. Metoclopramide antagonizes the dopamine D2 receptors. Dopamine exerts relaxant effect on the gastrointestinal tract through binding to muscular D2 receptors.",The molecular weight is 299.8.,Metoclopramide has a topological polar surface area of 67.59.,The log p value of  is 2.23.,Metoclopramide is approved and investigational.,Metoclopramide is a solid.,True
14547,"Penbutolol is a drug in the beta-blocker class used to treat hypertension. Penbutolol binds both beta-1 and beta-2 adrenergic receptors, rendering it a non-selective beta-blocker. Penbutolol can act as a partial agonist at beta adrenergic receptors, since it is a sympathomimetric drug. Penbutolol also demonstrates high binding affinity to the 5-hydroxytryptamine receptor 1A with antagonistic effects. This binding characteristic of penbutolol is being investigated for its implications in Antidepressant Therapy. Penbutolol is contraindicated in patients with cardiogenic shock, sinus bradycardia, second and third degree atrioventricular conduction block, bronchial asthma, and those with known hypersensitivity. Penbutolol is indicated in the treatment of mild to moderate arterial hypertension. It may be used alone or in combination with other antihypertensive agents, especially thiazide-type diuretics.Penbutolol is contraindicated in patients with cardiogenic shock, sinus bradycardia, second and third degree atrioventricular conduction block, bronchial asthma, and those with known hypersensitivity. Penbutolol is a ß-1, ß-2 (nonselective) adrenergic receptor antagonist. Experimental studies showed a dose-dependent increase in heart rate in reserpinized (norepinephrine-depleted) rats given penbutolol intravenously at doses of 0.25 to 1.0 mg/kg, suggesting that penbutolol has some intrinsic sympathomimetic activity. In human studies, however, heart rate decreases have been similar to those seen with propranolol. Penbutolol acts on the β1 adrenergic receptors in both the heart and the kidney. When β1 receptors are activated by catecholamines, they stimulate a coupled G protein that leads to the conversion of adenosine triphosphate (ATP) to cyclic adenosine monophosphate (cAMP). The increase in cAMP leads to activation of protein kinase A (PKA), which alters the movement of calcium ions in heart muscle and increases the heart rate. Penbutolol blocks the catecholamine activation of β1 adrenergic receptors and decreases heart rate, which lowers blood pressure.",The molecular weight is 291.44.,Penbutolol has a topological polar surface area of 41.49.,The log p value of  is 3.64.,Penbutolol is approved and investigational.,Penbutolol is a solid.,True
14548,"An alkaloid found in the root of Rauwolfia serpentina, among other plant sources. It is a class Ia antiarrhythmic agent that apparently acts by changing the shape and threshold of cardiac action potentials. Ajmaline produces potent sodium channel blocking effects and a very short half-life which makes it a very useful drug for acute intravenous treatments. The drug has been very popular in some countries for the treatment of atrial fibrillation in patients with the Wolff–Parkinson–White syndrome and in well tolerated monomorphic ventricular tachycardias. It has also been used for many years as a drug to challenge the conduction system of the heart in cases of bundle branch block and syncope. In these cases, abnormal prolongation of the HV interval has been taken as a proof for infrahisian conduction defects tributary for permanent pacemaker implantation. For use as an antiarrhythmic agent. Ajmaline is a class 1A antiarrhythmic agent. By interfering with the sodium channels, this drug allows for improvement in abnormal rhythms of the heart The class I antiarrhythmic agents interfere with the sodium channel. A class IA agent lengthens the action potential (right shift) which brings about improvement in abnormal heart rhythms. This drug in particular has a high affinity for the Nav 1.5 sodium channel.",The molecular weight is 326.44.,Ajmaline has a topological polar surface area of 46.94.,The log p value of  is 2.17.,Ajmaline is approved and experimental.,Ajmaline is a solid.,True
14549,Aprindine is a cardiac depressant used in arrhythmias.,The molecular weight is 322.5.,Aprindine has a topological polar surface area of 6.48.,The log p value of  is 5.9.,Aprindine is experimental.,Aprindine is a solid.,True
14550,"Nomifensine, formerly marketed as Merital capsules, was associated with an increased incidence of hemolytic anemia. The approved application holder removed Merital capsules from the market on January 23, 1986. FDA published a notice of its determination that Merital capsules were removed from the market for safety reasons (see the Federal Register of June 17, 1986 (51 FR 21981)). Approval of the NDA for Merital capsules was withdrawn on March 20, 1992 (see the Federal Register of March 20, 1992 (57 FR 9729)). Also withdrawn from the Canadian and UK markets. Nomifensine is a dopamine reuptake inhibitor test-marketed in the United States by Hoechst AG (now Novartis) that increases the amount of synaptic dopamine available to receptors by blocking dopamine's re-uptake transporter. Nomifensine is now mainly used in scientific research, particularly in studies involving dopamine release in response to addiction.",The molecular weight is 238.33.,Nomifensine has a topological polar surface area of 29.26.,The log p value of  is 2.37.,Nomifensine is approved and withdrawn.,Nomifensine is a solid.,True
14551,"Canagliflozin, also known as _Invokana_, is a sodium-glucose cotransporter 2 (SGLT2) inhibitor used in the management of type 2 diabetes mellitus along with lifestyle changes including diet and exercise. This drug is used in conjunction with diet and exercise to increase glycemic control in adults diagnosed with type 2 diabetes mellitus. This drug increases urinary glucose excretion and decreases the renal threshold for glucose (RTG) in a dose-dependent manner. The renal threshold is defined as the lowest level of blood glucose associated with the appearance of detectable glucose in the urine. The end result of canagliflozin administration is increased urinary excretion of glucose and less renal absorption of glucose, decreasing glucose concentration in the blood and improving glycemic control.  The sodium-glucose co-transporter2 (SGLT2), is found in the proximal tubules of the kidney, and reabsorbs filtered glucose from the renal tubular lumen. Canagliflozin inhibits the SGLT2 co-transporter. This inhibition leads to lower reabsorption of filtered glucose into the body and decreases the renal threshold for glucose (RTG), leading to increased glucose excretion in the urine. ",The molecular weight is 444.52.,Canagliflozin has a topological polar surface area of 90.15.,The log p value of  is 4.55.,Canagliflozin is approved.,Canagliflozin is a solid.,True
14552,"The omega-3 carboxylic acid (OM3-CA) is a new formulation of omega-3 fatty acids that present an enhanced bioavailability in the treatment of dyslipidemia. The increased bioavailability is explained because OM3-CA is found in a form of polyunsaturated free fatty acids as opposed to other products whose form is as ethyl esters. It is a complex mixture of the free fatty acids form containing eicosapentaenoic acid and docosahexaenoic acid as the most abundant species found in a proportion of 55% and 20% respectively. The rest of the concentration is represented by docosapentaenoic acid and traces of some other components such as alpha-tocopherol, gelatin, glycerol, sorbitol and purified water. It was developed by AstraZeneca Pharmaceuticals and firstly approved by the FDA on May 05, 2014. OM3-CA is indicated as an adjunct to diet to reduce triglycerides levels in adults patients with severe hypertriglyceridemia (>500 mg/dL). The patients involved in this treatment should be laced with an appropriate lipid-lowering diet. OM3-CA is very effective in reducing triglyceride levels. After 14 days of treatment, it is possible to observe even a 21% reduction. The reduction of the triglycerides could reach even to 25% in cases with the maximal used concentration of 4 g. The reduction of the synthesis of triglycerides in the liver may be caused because the main components of OM3-CA, eicosapentaenoic acid, and docosahexaenoic acid, are poor substrates for the enzymes responsible for the synthesis of triglycerides. These two major components inhibit the esterification of other fatty acids. OM3-CA is also thought to enhance the clearance of triglycerides from the circulating very low-density lipoprotein particles by different potential effects such as inhibition of acyl-CoA:1,2-diacylglycerol acyltransferase, increase in mitochondrial and peroxisomal beta-oxidation in the liver, decrease lipogenesis in the liver and increase lipoprotein lipase activity.",,,,Omega-3-carboxylic acids is approved and investigational.,Omega-3-carboxylic acids is a liquid.,True
14553,"Pentetic acid, also known as diethylenetriaminepentaacetic acid (DTPA), is a synthetic polyamino carboxylic acid with eight coordinate bond forming sites that can sequester metal ions and form highly stable DTPA-metal ion complexes. DTPA, along with its calcium and zinc trisodium salts, are the only FDA approved agents for the treatment of internal contamination by transuranics. It is currently considered, in all the dosage forms, as a member of the list of approved inactive ingredients for drug products by the FDA. DPTA was developed by the pharmaceutical company CIS US and FDA approved on April 14, 2004. DTPA is widely used in industry and medicine. As a medical agent, it is approved for its use in medical imaging and for the decorporation of internally deposited radionuclides. It is FDA approved for the treatment of individuals with known or suspected internal contamination with plutonium, americium or curium to increase the rates of elimination. There are reports in vivo of low stability of complexes of DPTA with uranium and neptunium which is being reported to cause deposition of the radionuclides into the tissues. In the case of plutonium, some preclinical studies have shown a very high urine elimination efficacy 1 hour after initial contamination. This efficacy is conserved for approximately 24 hours while the radiocontaminant is circulating. When the radionuclide is inhaled, it has been reported a DPTA-induced reduction of even 98% of the lung deposits. It is important to consider that pentetic acid can bind directly to other trace metals in the body which can cause deficiencies. The calcium and zinc trisodium salts of DTPA achieve the therapeutical potential by exchanging calcium and zinc cations with transuranic radionuclides to form higher affinity complexes and then promote their elimination by glomerular filtration into the urine. DTPA as an acid acts in a very similar way by sequestering ions with its eight coordinate bond forming sites.",The molecular weight is 393.35.,Pentetic acid has a topological polar surface area of 196.22.,The log p value of  is -2.91.,Pentetic acid is approved.,Pentetic acid is a solid.,True
14554,"Mecasermin contains recombinant-DNA-engineered human insulin-like growth factor-1 (rhIGF-1). IGF-1 consists of 70 amino acids in a single chain with three intramolecular disulfide bridges and a molecular weight of 7649 daltons. The amino acid sequence of the product is identical to that of endogenous human IGF-1. The rhIGF-1 protein is synthesized in bacteria (E. coli) that have been modified by the addition of the gene for human IGF-1. For the long-term treatment of growth failure in pediatric patients with Primary IGFD or with GH gene deletion who have developed neutralizing antibodies to GH. It is not indicated to treat Secondary IGFD resulting from GH deficiency, malnutrition, hypothyroidism or other causes; it is not a substitute for GH therapy. Mecasermin is a biosynthetic (recombinant DNA origin) form of human insulin-like growth factor 1 (IGF-1) designed to replace natural IGF-1 in pediatric patients who are deficient, promoting normalized statural growth. Growth hormones (GH) bind to growth hormone receptors (GHR) in the liver and other tissues, which stimulates the synthesis of IGF-1. In target tissues, IGF-1 activates the IGF-1 receptor, resulting in intracellular signals that stimulate growth. Although many actions of the GH are mediated through IGF-1, the precise roles of GH and IGF-1 have not been fully elucidated. Patients with severe primary IGF-1 deficiency (Primary IGFD) fail to produce adequate levels of IGF-1, due to disruption of the GH pathway used to promote IGF-1 release (possible GH pathway disruptions include mutations in the GHR, post-GHR signaling pathway, and IGF-1 gene defects).  Mecasermin supplies recombinant-DNA-origin IGF-1, which binds to the Type I IGF-1 receptor. This receptor exerts intra-cellular signaling activity in a number of processes involved in statural growth, including mitogenesis in multiple tissue types, chondrocyte growth and division along cartilage growth plates, and increases in organ growth. ",The molecular weight is 7648.71.,Mecasermin has a topological polar surface area of 3126.93.,,Mecasermin is approved and investigational.,Mecasermin is a solid.,True
14555,"Technetium Tc-99m tetrofosmin is a drug used in nuclear myocardial perfusion imaging. The radioisotope, technetium-99m, is chelated by two 1,2-bisethane ligands which belong to the group of diphosphines and which are referred to as tetrofosmin. It is a lipophilic technetium phosphine dioxo cation that was formulated into a freeze-dried kit which yields an injection. Technetium Tc-99m tetrofosmin was developed by GE Healthcare and FDA approved on February 9, 1996. Technetium-99m tetrofosmin is indicated for the diagnosis of heart abnormalities by exercise myocardial scintigraphy. The exercise myocardial scintigraphy is an established method for the diagnosis of the severity of coronary artery disease. This method allows distinguishing regions of reversible myocardial ischemia in the presence or absence of infarcted myocardium following rest and stress conditions. The use of technetium-99m tetrofosmin is mainly used to assess myocardial perfusion in ischemia and infarction. Preclinical studies have reported that technetium-99m tetrofosmin presents a very good heart uptake and retention. The diagnosis based on the presence of technetium-99m is considered to have a principal photon gamma emissions at 140.5 keV. The imaging can be done at 15 minutes after stress and 30-60 minutes at rest but, due to its slow wash out from myocardium, it is possible to perform imaging for up to 4 hours post-injection. Administration of technetium-99m tetrofosmin generates a count elevation in white blood cell at 6-24 hours post-injection.  The mechanism for the uptake and retention of technetium-99m tetrofosmin is not well established. Nonetheless, it is known that technetium 99m tetrofosmin binds to the intracellular cytosol of myocytes. This uptake is thought to be because technetium-99m tetrofosmin is a lipophilic cationic agent which allows it to present a passive diffusion process. Once the uptake is done, the technetium-99m accumulates in viable myocardial tissue delineating the infarcts areas when administered at rest and delineating the ischemic areas when administered at stress.",The molecular weight is 895.83.,Technetium Tc-99m tetrofosmin has a topological polar surface area of 107.98.,,Technetium Tc-99m tetrofosmin is approved.,Technetium Tc-99m tetrofosmin is a solid.,True
14556,"Antihemophilic Factor (Recombinant), PEGylated, was approved by the FDA in December 2016 as the product _Adynovate_. For the management of hemophilia A (congenital factor VIII deficiency) ,. This drug temporarily replaces the missing coagulation factor VIII, required for effective hemostasis in patients with congenital hemophilia A. PEG with Factor VIII effectively increases the molecular weight and size of the protein by creating a hydrophilic cloud around the molecule. This molecular change may reduce the susceptibility of this molecule to proteolytic degradation. It is also believed that PEGylation alters the surface charge of the protein that inhibits receptor-mediated clearance. This drug reduces binding to the LRP1 receptor, which normally clears factor VIII from the circulation ,.",,,,"Antihemophilic Factor (Recombinant), PEGylated is approved and investigational.","Antihemophilic Factor (Recombinant), PEGylated is a solid.",True
14557,"Turoctocog alfa pegol is a pegylated version of. Novo Nordisk's brand name Esperoct (turoctocog alfa pegol, N8-GP) was approved by the US FDA on February 19, 2019. Turoctocog alfa pegol (N8-GP) is indicated for use in adults and children of all ages with hemophilia A (congenital factor VIII deficiency) for routine prophylaxis in reducing the frequency of bleeding episodes, on-demand treatment and control of bleeding episodes, and the perioperative management of bleeding. Based on results obtained from the Pathfinder clinical studies, turoctocog alfa pegol (N8-GP) was shown to provide effective routine prophylaxis in people with severe haemophilia A through a fixed dosing regimen of one injection every 4 days in adults and adolescents, or every 3-4 days (twice-weekly) in children. Furthermore, N8-GP provided effective prophylaxis and maintained a low median annualized bleeding rate (ABR) of 1.18 when administered at doses of 50 IU/kg every 4 days in adults and adolescents. Additionally, N8-GP was also found to be efficacious in the treatment and control of bleeding episodes and the perioperative management of bleeding. Across the clinical trials and age groups, N8-GP was shown to be well tolerated and no safety concerns were identified. The overall safety profile of N8-GP is similar to what has been reported for other long-action FVIII products. Moreover, in general, no FVIII inhibitor antibodies have been detected, and no thromboembolic events have occurred with the use of N8-GP. The principal characteristic that defines hemophilia A is the limited presence or complete deficiency of human clotting factor VIII in the body. Subsequently, because factor VIII is a critical component that is essential for the extrinsic tissue factor pathway of the blood coagulation cascade process to proceed, individuals with hemophilia A ultimately experience increased bleeding - in comparison to individuals without a factor VIII deficiency - after injury or any kind of medical procedure. Such increased bleeding can be heavy and/or fatal and may occur due to minimal injury or even when there is no injury whatsoever - in which case the bleeding is spontaneous. Furthermore, excessive bleeds that bleed into muscles, organs, and joints are also associated with dangerous complications and regular pain.",,,,Turoctocog alfa pegol is approved.,,True
14558,"Imidazole derivative anesthetic and hypnotic with little effect on blood gases, ventilation, or the cardiovascular system. It has been proposed as an induction anesthetic. Used in the induction of general anesthesia. Etomidate is a non-barbiturate hypnotic that acts at the level of the reticular-activating system to produce anesthesia. Etomidate is an imidazole compound that appears to depress CNS function via GABA. Duration of action is intermediate between thiopental and methohexital, and recovery from a single dose is rapid with little residual depression. Like the barbiturates and propofol, etomidate is does not induce analgesia. Etomidate induces unconsciousness within one circulation time. Recovery is rapid as a result of extensive redistribution and rapid metabolism. Etomidate binds at a distinct binding site associated with a Cl<sup>-</sup> ionopore at the GABA<sub>A</sub> receptor, increasing the duration of time for which the Cl<sup>-</sup> ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.",The molecular weight is 244.29.,Etomidate has a topological polar surface area of 44.12.,The log p value of  is 2.42.,Etomidate is approved.,Etomidate is a solid.,True
14559,"Calcitriol is an active metabolite of vitamin D with 3 hydroxyl (OH) groups and is commonly referred to as 1,25-dihydroxycholecalciferol, or 1alpha,25-dihydroxyvitamin D<sub>3</sub>, 1,25-dihydroxyvitamin D<sub>3</sub>. It is produced in the body after series of conversion steps of 7-dehydrocholesterol from exposure to UV light. 7-dehydrocholesterol is converted to (vitamin D3) in the skin, which is then converted to in the liver and kidneys. undergoes hydroxylation to form calcitriol via 1α-hydroxylase (CYP27B1) activity. Calcitriol is considered to be the most potent metabolite of vitamin D in humans. Renal production of calcitriol is stimulated in response to PTH, low calcium and low phosphate. Calcitriol plays a role in plasma calcium regulation in concert with parathyroid hormone (PTH) by enhancing absorption of dietary calcium and phosphate from the gastrointestinal tract, promoting renal tubular reabsorption of calcium in the kidneys, and stimulating the release of calcium stores from the skeletal system. In addition to promoting fatty acid synthesis and inhibiting lipolysis, calcitriol has been demonstrated to increase energy efficiency by suppressing UCP2 expression, which is modulated by signaling pathways of classical nuclear receptors (nVDR), where calcitriol acts as a natural ligand. There is also evidence that calcitriol modulates the action of cytokines and may regulate immune and inflammatory response, cell turnover, cell differentiation.  Used to treat vitamin D deficiency or insufficiency, refractory rickets (vitamin D resistant rickets), familial hypophosphatemia and hypoparathyroidism, and in the management of hypocalcemia and renal osteodystrophy in patients with chronic renal failure undergoing dialysis. Also used in conjunction with calcium in the management and prevention of primary or corticosteroid-induced osteoporosis. Calcitriol is a biologically active calcitrophic hormone with anti-osteoporotic, immunomodulatory, anticarcinogenic, antipsoriatic, antioxidant, and mood-modulatory activities. Its main sites of action are the intestine, bone, kidney and parathyroid hormone. Calcitriol is a ligand for the vitamin D nuclear receptor, which is expressed in, but not limited to, gastrointestinal (GI) tissues, bones, and kidneys. As an active form of vitamin D<sub>3</sub>, calcitriol elevates the plasma levels of calcium by stimulating intestinal calcium uptake, increasing reabsorption of calcium by the kidneys, and possibly increasing the release of calcium from skeletal stores. The duration of pharmacologic activity of a single dose of exogenous calcitriol is expected to be about 3 to 5 days.  The mechanism of action of calcitriol in the treatment of psoriasis is accounted for by their antiproliferative activity for keratinocytes and their stimulation of epidermal cell differentiation. The anticarcinogenic activity of the active form of Calcitriol appears to be correlated with cellular vitamin D receptor (VDR) levels. Vitamin D receptors belong to the superfamily of steroid-hormone zinc-finger receptors. VDRs selectively bind 1,25-(OH)<sub>2</sub>-D3 and retinoic acid X receptor (RXR) to form a heterodimeric complex that interacts with specific DNA sequences known as vitamin D-responsive elements. VDRs are ligand-activated transcription factors. The receptors activate or repress the transcription of target genes upon binding their respective ligands. It is thought that the anticarcinogenic effect of Calcitriol is mediated via VDRs in cancer cells. The immunomodulatory activity of calcitriol is thought to be mediated by vitamin D receptors (VDRs) which are expressed constitutively in monocytes but induced upon activation of T and B lymphocytes. 1,25-(OH)<sub>2</sub>-D3 has also been found to enhance the activity of some vitamin D-receptor positive immune cells and to enhance the sensitivity of certain target cells to various cytokines secreted by immune cells.",The molecular weight is 416.65.,Calcitriol has a topological polar surface area of 60.69.,The log p value of  is 6.04.,Calcitriol is approved and nutraceutical.,Calcitriol is a solid.,True
14560,"Ergocalciferol is an inactivated vitamin D analog. It is synthesized by some plants in the presence of UVB light. The production of ergocalciferol was prompted by the identification of dietary deficiency, more specifically vitamin D, as the main causative factor for the development of rickets. Ergocalciferol was isolated for the first time from yeast in 1931 and its structure was elucidated in 1932. Ergocalciferol is indicated for the treatment of hypoparathyroidism, refractory rickets, and familial hypophosphatemia. After the activation of the vitamin D receptor, some of the biological changes produced by ergocalciferol include mobilization and accretion of calcium and phosphorus in the bone, absorption of calcium and phosphorus in the intestine, and reabsorption of calcium and phosphorus in the kidney.  For its activity, ergocalciferol is required to be transformed to its major active circulating hydroxylated metabolite and transported to the target organs in order to bind to its target, the vitamin D receptor.",The molecular weight is 396.66.,Ergocalciferol has a topological polar surface area of 20.23.,The log p value of  is 9.39.,Ergocalciferol is approved and nutraceutical.,Ergocalciferol is a solid.,True
14561,"Vitamin D, in general, is a secosteroid generated in the skin when 7-dehydrocholesterol located there interacts with ultraviolet irradiation - like that commonly found in sunlight. Both the endogenous form of vitamin D (that results from 7-dehydrocholesterol transformation), vitamin D3 (cholecalciferol), and the plant-derived form, vitamin D2 (ergocalciferol), are considered the main forms of vitamin d and are found in various types of food for daily intake. Structurally, ergocalciferol differs from cholecalciferol in that it possesses a double bond between C22 and C23 and has an additional methyl group at C24. Finally, ergocalciferol is pharmacologically less potent than cholecalciferol, which makes vitamin D3 the preferred agent for medical use. Cholecalciferol use is indicated for the treatment of specific medical conditions like refractory rickets (or vitamin D resistant rickets), hypoparathyroidism, and familial hypophosphatemia. The in vivo synthesis of the predominant two biologically active metabolites of vitamin D occurs in two steps. The first hydroxylation of vitamin D3 cholecalciferol (or D2) occurs in the liver to yield 25-hydroxyvitamin D while the second hydroxylation happens in the kidneys to give 1, 25-dihydroxyvitamin D. These vitamin D metabolites subsequently facilitate the active absorption of calcium and phosphorus in the small intestine, serving to increase serum calcium and phosphate levels sufficiently to allow bone mineralization. Conversely, these vitamin D metabolites also assist in mobilizing calcium and phosphate from bone and likely increase the reabsorption of calcium and perhaps also of phosphate via the renal tubules. There exists a period of 10 to 24 hours between the administration of cholecalciferol and the initiation of its action in the body due to the necessity of synthesis of the active vitamin D metabolites in the liver and kidneys. It is parathyroid hormone that is responsible for the regulation of such metabolism at the level of the kidneys. Most individuals naturally generate adequate amounts of vitamin D through ordinary dietary intake of vitamin D (in some foods like eggs, fish, and cheese) and natural photochemical conversion of the vitamin D3 precursor 7-dehydrocholesterol in the skin via exposure to sunlight.",The molecular weight is 384.65.,Cholecalciferol has a topological polar surface area of 20.23.,The log p value of  is 9.48.,Cholecalciferol is approved and nutraceutical.,Cholecalciferol is a solid.,True
14562,"Alfacalcidol is an active metabolite of Vitamin D, which performs important functions in regulation of the calcium balance and the bone metabolism. Alfacalcidol is Vitamin D-hormone analog which is activated by the enzyme 25-hydroxylase in the liver for systemic and in osteoblasts for local D-hormone actions. It possesses a unique pattern of pleiotropic effects on, e.g. gut, bone, pararthyroids, muscle and brain. Alfacalcidol is superior to plain vitamin D (cholecalciferol) because the final kidney activation of the latter is regulated by a negative feedback mechanism.  Indicated for the management of hypocalcemia, secondary hyperparathyroidism, and osteodystrophy in patients with chronic renal failure. Alfacalcidol is Vitamin D-hormone analog which is activated by the enzyme 25-hydroxylase in the liver for systemic and in osteoblasts for local D-hormone actions. The first step involved in the activation of vitamin D3 is a 25-hydroxylation which is catalysed by the 25-hydroxylase in the liver and then by other enzymes. The mitochondrial sterol 27-hydroxylase catalyses the first reaction in the oxidation of the side chain of sterol intermediates. The active form of vitamin D3 (calcitriol) binds to intracellular receptors that then function as transcription factors to modulate gene expression. Like the receptors for other steroid hormones and thyroid hormones, the vitamin D receptor has hormone-binding and DNA-binding domains. The vitamin D receptor forms a complex with another intracellular receptor, the retinoid-X receptor, and that heterodimer is what binds to DNA. In most cases studied, the effect is to activate transcription, but situations are also known in which vitamin D suppresses transcription. Calcitriol increases the serum calcium concentrations by: increasing GI absorption of phosphorus and calcium, increasing osteoclastic resorption, and increasing distal renal tubular reabsorption of calcium. Calcitriol appears to promote intestinal absorption of calcium through binding to the vitamin D receptor in the mucosal cytoplasm of the intestine. Subsequently, calcium is absorbed through formation of a calcium-binding protein.",The molecular weight is 400.65.,Alfacalcidol has a topological polar surface area of 40.46.,The log p value of  is 8.24.,Alfacalcidol is approved and nutraceutical.,Alfacalcidol is a solid.,True
14563,,,,,3-sulfino-L-alanine is experimental.,3-sulfino-L-alanine is a solid.,False
14564,,,,,1-Hexadecanosulfonic Acid is experimental.,1-Hexadecanosulfonic Acid is a solid.,False
14565,,,,,2-{sulfanyl}-6-(trifluoromethyl)-4(1H)-pyrimidinone is experimental.,2-{sulfanyl}-6-(trifluoromethyl)-4(1H)-pyrimidinone is a solid.,False
14566,"Sodium propionate is the sodium salt of propionic acid that exists as colorless, transparent crystals or a granular crystalline powder. It is considered generally recognized as safe (GRAS) food ingredient by FDA, where it acts as an antimicrobial agent for food preservation and flavoring agent. Its use as a food additive is also approved in Europe. Sodium propionate is is prepared by neutralizing propionic acid with sodium hydroxide. Sodium propionate was previously approved in Canada as an active ingredient in Amino-Cerv (used to treat inflammation or injury of the cervix). Propanoic acid and various direct sodium or calcium salt formulations of the acid are currently most commonly approved and indicated by organizations like the FDA and EMA for use as an antibacterial food additive preservative in animal feed and food for human consumption. As a naturally occurring carboxylic acid, propionic acid typically undergoes metabolism via conversion to propionyl coenzyme A (propionyl-CoA), which is part of the usual metabolic pathway that carboxylic acids participate within in the human body. Most of propionic acid's antibacterial and preservative activities subsequently stem from this metabolic pathway as the metabolic fate of propionates varies in different microorganisms, resulting in antimicrobial mechanisms of action that may revolve around differing propionate metabolites causing competition, inhibition, and/or interference effects along other metabolic pathways in the various microorganisms affected. The metabolic fate of propionates varies in different microorganisms. Some have enzyme systems that can convert succinate to propionyl-coenzyme A and through various further steps to propionate, CO2, or propionyl phoshpate. Still others can convert propionic acid to B-alanine or directly to CO2. Whatever the case, the inhibiting effect for microbials is likely related to competition with acetate in the acetokinase system, to the blockage of pyruvate conversion to acetyl-coenzyme A and to interference with B-alanine in pantothenic acid syntheses.",,,,Propanoic acid is approved and vet_approved.,Propanoic acid is a solid.,True
14567,,,,,Carbazole Butanoic Acid is experimental.,Carbazole Butanoic Acid is a solid.,False
14568,,,,,"Cysteine-Methylene-Carbamoyl-1,10-Phenanthroline is experimental.","Cysteine-Methylene-Carbamoyl-1,10-Phenanthroline is a solid.",False
14569,,,,,"9-benzyl-2,3,4,9-tetrahydro-1H-carbazole-8-carboxylic acid is experimental.","9-benzyl-2,3,4,9-tetrahydro-1H-carbazole-8-carboxylic acid is a solid.",False
14570,,,,,"5-(3-carbamoylbenzyl)-5,6,7,8,9,10-hexahydrocycloheptaindole-4-carboxylic acid is experimental.","5-(3-carbamoylbenzyl)-5,6,7,8,9,10-hexahydrocycloheptaindole-4-carboxylic acid is a solid.",False
14571,,,,,"(5R)-5-(4-{METHOXY}BENZYL)-1,3-THIAZOLIDINE-2,4-DIONE is experimental.","(5R)-5-(4-{METHOXY}BENZYL)-1,3-THIAZOLIDINE-2,4-DIONE is a solid.",False
14572,"Alpha-linolenic acid (ALA) is a polyunsaturated omega-3 fatty acid. It is a component of many common vegetable oils and is important to human nutrition. For nutritional supplementation and for treating dietary shortage or imbalance. Alpha Linolenic Acid (ALA) is an 18-carbon polyunsaturated fatty acid with three double bonds. It is also called an omega-3 fatty acid, and is essential for all mammals. Alpha-linolenic acid (or omega 3 fatty acid) intake can decrease the risk of cardiovascular diseases by 1) preventing arrhythmias that can lead to sudden cardiac death, 2) decreasing the risk of thrombosis (blood clot formation) that can lead to heart attack or stroke, 3) decreasing serum triglyceride levels, 4) slowing the growth of atherosclerotic plaque, 5) improving vascular endothelial function, 6) lowering blood pressure slightly, and 7) decreasing inflammation. ALA deficiencies can lead to visual problems and sensory neuropathy. Scaly and hemorrhagic skin or scalp inflammations may also develop. Alpha Linolenic Acid or ALA is considered an essential fatty acid because it is required for human health, but cannot be synthesized by humans. It is in fact a plant-derived fatty acid. Humans can synthesize other omega-3 fatty acids from ALA, including eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). EPA is a precursor of the series-3 prostaglandins, the series-5 leukotrienes and the series-3 thromboxanes. These eicosanoids have anti-inflammatory and anti-atherogenic properties. ALA metabolites may also inhibit the production of the pro-inflammatory eicosanoids, prostaglandin E2 (PGE2) and leukotriene B4 (LTB4), as well as the pro-inflammatory cytokines, tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 beta (IL-1 beta). Omega-3 fatty acids like ALA and its byproducts can modulate the expression of a number of genes, including those involved with fatty acid metabolism and inflammation. They regulate gene expression through their effects on the activity of transcription factors including NF-kappa B and members of the peroxisome proliferator-activated receptor (PPAR) family. Incorporation of ALA and its metabolites in cell membranes can affect membrane fluidity and may play a role in anti-inflammatory activity, inhibition of platelet aggregation and possibly in anti-proliferative actions of ALA. ALA is first metabolized by delta6 desaturease into steridonic acid.",The molecular weight is 278.44.,alpha-Linolenic acid has a topological polar surface area of 37.3.,The log p value of  is 6.82.,alpha-Linolenic acid is approved and investigational and nutraceutical.,alpha-Linolenic acid is a liquid.,True
14573,"A 20-carbon-chain fatty acid, unsaturated at positions 8, 11, and 14. It differs from arachidonic acid, 5,8,11,14-eicosatetraenoic acid, only at position 5. For nutritional supplementation, also for treating dietary shortage or imbalance Dihomo gamma-linolenic acid or DHLA is an n-6 (omega-6) polyunsaturated fatty acid. It is comprised of 20 carbon atoms and three double bonds. DHLA is a byproduct of the 18 carbon gamma-linolenic acid (GLA). DHLA is then converted into prostaglandin E1 (PGE1). PGE1 inhibits platelet aggregation and also exerts a vasodilatory effect. DHLA (or DGLA) is a precursor in the synthesis of prostaglandin E1 (PGE1) as well as the series-3 prostaglandins. It also serves as a precursor in the synthesis of eicosapentaenoic acid (EPA). EPA is a precursor of the series-3 prostaglandins, the series-5 leukotrienes and the series-3 thromboxanes. These eicosanoids have anti-thrombogenic, anti-inflammatory and anti-atherogenic properties. PGE1 inhibits platelet aggregation and has a vasodilation action. DHLA has also been shown to reduce the production/activity of tumor necrosis factor alpha.",,,,Dihomo-gamma-linolenic acid is investigational and nutraceutical.,Dihomo-gamma-linolenic acid is a solid.,True
14574,"A uricosuric drug that is used to reduce the serum urate levels in gout therapy. It lacks anti-inflammatory, analgesic, and diuretic properties. For the treatment of gout and gouty arthritis. Sulfinpyrazone's pharmacologic activity is the potentiation of the urinary excretion of uric acid. It is useful for reducing the blood urate levels in patients with chronic tophaceous gout and acute intermittent gout, and for promoting the resorption of tophi. Sulfinpyrazone is an oral uricosuric agent (pyrazolone derivative) used to treat chronic or intermittent gouty arthritis. Sulfinpyrazone competitively inhibits the reabsorption of uric acid at the proximal convoluted tubule, thereby facilitating urinary excretion of uric acid and decreasing plasma urate concentrations. This is likely done through inhibition of the urate anion transporter (hURAT1) as well as the human organic anion transporter 4 (hOAT4). Sulfinpyrazone is not intended for the treatment of acute attacks because it lacks therapeutically useful analgesic and anti-inflammatory effects. Sulfinpyrazone and its sulfide metabolite possess COX inhibitory effects. Sulfinpyrazone has also been shown to be a UDP-glucuronsyltransferase inhibitor and a very potent CYP2C9 inhibitor. Sulfinpyrazone is also known to be a cystic fibrosis transmembrane conductance regulator (CFTR) inhibitor as well as an inhibitor of several multridrug resistance proteins (MRPs). ",The molecular weight is 404.48.,Sulfinpyrazone has a topological polar surface area of 57.69.,The log p value of  is 1.66.,Sulfinpyrazone is approved.,Sulfinpyrazone is a solid.,True
14575,"Dexchlorpheniramine is the S-enantiomer of chlorpheniramine which is a 1st generation anti-histamine. Dexchlorpheniramine has more pharmacological activity than the R and so is more potent than the racemic mixture. Dexchlorpheniramine can be used in the treatment of perennial and seasonal allergic rhinitis, vasomotor rhiniti, allergic conjunctivitis due to inhalant allergens and foods, mild uncomplicated allergic skin manifestations of urticaria and angioedema, amelioration of allergic reactions to blood or plasma, and dermographism. In allergic reactions, an allergen binds to IgE antibodies on mast cells and basophils. Once this occurs IgE receptors crosslink with each other triggering a series of events that eventually leads to cell-degranulation and the release of histamine (and other chemical mediators) from the mast cell or basophil. Histamine can react with local or widespread tissues through histamine receptors. Histamine, acting on H1-receptors, produces pruritis, vasodilatation, hypotension, flushing, headache, tachycardia, and bronchoconstriction. Histamine also increases vascular permeability and potentiates pain. Dexchlorpheniramine, is a histamine H1 antagonist of the alkylamine class. It competes with histamine for the normal H1-receptor sites on effector cells of the gastrointestinal tract, blood vessels and respiratory tract. It provides effective, temporary relief of sneezing, watery and itchy eyes, and runny nose due to hay fever and other upper respiratory allergies. Competes with histamine for H1-receptor sites on effector cells in the gastrointestinal tract, blood vessels, and respiratory tract. Dexchlorpheniramine is the predominant active isomer of chlorpheniramine and is approximately twice as active as the racemic compound. ",,,,Dexchlorpheniramine maleate is approved.,,True
14576,,,,,Butenoic Acid is experimental.,Butenoic Acid is a solid.,False
14577,,,,,S-Methylcysteine is experimental.,S-Methylcysteine is a solid.,False
14578,"A major primary bile acid produced in the liver and usually conjugated with glycine or taurine. It facilitates fat absorption and cholesterol excretion.  Oral cholic acid is indicated for: treatment of bile acid synthesis disorders due to single enzyme defects; and as adjunctive treatment of peroxisomal disorders including Zellweger spectrum disorders in patients who exhibit manifestations of liver disease, steatorrhea or complications from decreased fat soluble vitamin absorption. ",The molecular weight is 408.58.,Cholic Acid has a topological polar surface area of 97.99.,The log p value of  is 2.43.,Cholic Acid is approved.,Cholic Acid is a solid.,True
14579,"Nitazoxanide belongs to the class of drugs known as _thiazolides_. Nitazoxanide (NTZ) is a broad-spectrum anti-infective drug that markedly modulates the survival, growth, and proliferation of a range of extracellular and intracellular protozoa, helminths, anaerobic and microaerophilic bacteria, in addition to viruses. This drug is effective in the treatment of gastrointestinal infections including Cryptosporidium parvum or Giardia lamblia in healthy subjects. It is generally well tolerated. Nitazoxanide is a first-line, standard treatment for illness caused by C. parvum or G. lamblia infection in healthy (not immunosuppressed) adults and children and may also be considered in the treatment of illnesses caused by other protozoa or helminths. Recently, this drug has been studied as a broad-spectrum antiviral agent due to its ability to inhibit the replication of several RNA and DNA viruses. For the treatment of diarrhea in adults and children caused by the protozoa <i>Giardia lamblia</i>, and for the treatment of diarrhea in children caused by the protozoan, <i>Cryptosporidium parvum</i>. The general effect of this medication is the prevention of microbe activity through disruption of important energy pathways for survival and proliferation. Nitazoxanide exhibits antiprotozoal activity by interfering with the pyruvate ferredoxin/flavodoxin oxidoreductase dependent electron transfer reaction, an essential reaction need for anaerobic energy metabolism of various microorganisms. Sporozoites of Cryptosporidium parvum and trophozoites of Giardia lamblia are therefore inhibited, relieving symptoms of diahrrea. Interference with the PFOR enzyme-dependent electron transfer reaction may only be one of the many pathways by which nitazoxanide exhibits antiprotozoal activity.  The most widely accepted mechanism of NTZ is believed to be the disruption of the energy metabolism in anaerobic microbes by inhibition of the pyruvate: ferredoxin/flavodoxin oxidoreductase (PFOR) cycle. In parasitic-protozoa, Nitazoxanide also induces lesions in the cell membranes and depolarizes the mitochondrial membrane while inhibiting quinone oxidoreductase NQO1, nitroreductase-1 and protein disulphide isomerase enzymes. In addition, this drug also inhibits the glutathione-S-transferase (a major detoxifying enzyme) and modulates the Avr-14 gene, encoding for the alpha-type subunit of glutamate-gated chloride ion channel present in nematodes. Aside from its well understood non-competitive inhibition of the PFOR in anaerobic bacteria, NTZ also demonstrates various other antibacterial mechanisms. It inhibits pyruvate dehydrogenase in E Coli, disrupts the membrane potential and pH homeostasis in the Mycobacterium tuberculosis, suppresses the chaperone/usher (CU) pathway of the gram-negative bacteria, and stimulates host macrophage autophagy in tuberculosis patients. NTZ also suppresses viral replication by inhibiting the maturation of the viral hemagglutinin and the viral transcription factor immediate early 2 (IE2) as well as by activating the eukaryotic translation initiation factor 2α (an antiviral intracellular protein). Lastly, NTZ exhibits an inhibitory effect on tumor cell progression by altering drug detoxification (glutathione-S-transferase P1), unfolded protein response, autophagy, anti-cytokines activity, and c-Myc inhibition.",The molecular weight is 307.28.,Nitazoxanide has a topological polar surface area of 114.11.,The log p value of  is 1.24.,Nitazoxanide is approved and investigational and vet_approved.,Nitazoxanide is a solid.,True
14580,"Remoxipride is an atypical antipsychotic agent that is specific for dopamine D<sub>2</sub> receptors. It gained approval in the UK in 1989 but was withdrawn in 1993 after it was found to be associated with an increased incidence of aplastic anemia. Remoxipride is an atypical antipsychotic once used for the treatment of schizophrenia. Remoxipride is a weak selective dopamine D<sub>2</sub> receptor antagonist that was once used in the treatment of schizophrenia. It has a moderate therapeutic index and duration of action. Remoxipride was withdrawn due to deaths associated with aplastic anemia. Remoxipride is an atypical antipsychotic dopamine D<sub>2</sub> antagonist. Chronic use upregulates the expression of D<sub>2</sub> receptors, while downregulating the expression of D<sub>1</sub> and D<sub>5</sub> receptors in the prefrontal cortex. This activity may be related to the antipsychotic activity of remoxipride. Remoxipride displays weaker binding to D<sub>2</sub> dopaminergic receptors that dopamine. This weaker binding is thought to account for the reduced incidence of Parkinsonism. Remoxipride also increases expression of the protein _Fos_ in the nucleus accumbens but not the dorsolateral striatum, which may be responsible for a reduced incidence of extrapyramidal symptoms.",The molecular weight is 371.28.,Remoxipride has a topological polar surface area of 50.8.,The log p value of  is 3.25.,Remoxipride is approved and withdrawn.,Remoxipride is a solid.,True
14581,"An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake. For the introduction of local (topical) anesthesia of accessible mucous membranes of the oral, laryngeal and nasal cavities. Cocaine is a local anesthetic indicated for the introduction of local (topical) anesthesia of accessible mucous membranes of the oral, laryngeal and nasal cavities. Cocaine produces anesthesia by inhibiting excitation of nerve endings or by blocking conduction in peripheral nerves. This is achieved by reversibly binding to and inactivating sodium channels. Sodium influx through these channels is necessary for the depolarization of nerve cell membranes and subsequent propagation of impulses along the course of the nerve. Cocaine is the only local anesthetic with vasoconstrictive properties. This is a result of its blockade of norepinephrine reuptake in the autonomic nervous system. Cocaine binds differentially to the dopamine, serotonin, and norepinephrine transport proteins and directly prevents the re-uptake of dopamine, serotonin, and norepinephrine into pre-synaptic neurons. Its effect on dopamine levels is most responsible for the addictive property of cocaine.",The molecular weight is 303.36.,Cocaine has a topological polar surface area of 55.84.,The log p value of  is 2.57.,Cocaine is approved and illicit.,Cocaine is a solid.,True
14582,"Nadolol is a nonselective beta adrenal receptor blocker that is used to lower blood pressure. Nonselective beta adrenal receptor blockers may no longer be first line in the treatment of hypertension as newer generations of beta adrenal receptor blockers have higher selectivity and offer better rates of adverse effects. Nadolol is indicated to treat angina pectoris and hypertension. Another product formulated with is indicated to treat hypertension. Nadolol is a nonselective beta adrenal receptor blocker that is used to lower blood pressure. It has a long duration of action as it is usually taken once daily and a wide therapeutic index as patients start at doses of 40mg daily but may be increased to doses as high as 240mg daily. Patients taking nadolol should not aburptly stop taking it as this may lead to exacerbation of ischemic heart disease. Although nadolol is described as a non selective beta blocker, it does not interact with beta 3 adrenal receptors. Antagonism of beta-1 and beta-2 adrenoceptors in the heart inhibits cyclic AMP and its signalling pathway, decreasing the strength and speed of contractions as well as the speed of relaxation and conduction. Antagonism of beta-2 adrenoceptors in the smooth muscle cells of the vasculature inhibits their relaxation, leading to an increase in peripheral vascular resistance and reducing the risk of severe hypotension. The increase in peripheral vascular resistance may contribute to the decrease in insulin sensitivity associated with nadolol use. Antagonism of beta-1 adrenoceptors in the juxtaglomerular apparatus of the kidney inhibits the release of renin, and therefore angiotensin II mediated vasoconstriction, aldosterone mediated water retention, and the release of epinephrine. Antagonism of beta-2 adrenoceptors in the liver and skeletal muscle inhibits glycogenolysis, in the lungs prevents bronchodilation, and in the pancrease inhibits insulin release.",The molecular weight is 309.41.,Nadolol has a topological polar surface area of 81.95.,The log p value of  is 0.38.,Nadolol is approved.,Nadolol is a solid.,True
14583,"Solifenacin is a competitive muscarinic receptor antagonist indicated to treat an overactive bladder with urinary incontinence, urgency, and frequency. It has a long duration of action as it is usually taken once daily. Solifenacin tablets are indicated to treat an overactive bladder with urinary incontinence, urgency, and frequency. Solifenacin antagonizes the M2 and M3 muscarinic receptors in the bladder to treat an overactive bladder. It has a long duration of action as it is usually taken once daily. Patients taking solifenacin should be aware of the risks of angioedema and anaphylaxis. Solifenacin is a competitive muscarinic receptor antagonist. It has the highest affinity for M3, M1, and M2 muscarinic receptors. 80% of the muscarinic receptors in the bladder are M2, while 20% are M3. Solifenacin's antagonism of the M3 receptor prevents contraction of the detrusor muscle, while antagonism of the M2 receptor may prevent contraction of smooth muscle in the bladder.",The molecular weight is 362.47.,Solifenacin has a topological polar surface area of 32.78.,The log p value of  is 4.68.,Solifenacin is approved.,Solifenacin is a solid.,True
14584,"A non-essential amino acid present abundantly throughout the body and is involved in many metabolic processes. It is synthesized from glutamic acid and ammonia. It is the principal carrier of nitrogen in the body and is an important energy source for many cells. An oral formulation of L-glutamine was approved by the FDA in July 2017 for use in sickle cell disease. This oral formulation is marketed under the tradename Endari by Emmaus Medical. Used for nutritional supplementation, also for treating dietary shortage or imbalance. Like other amino acids, glutamine is biochemically important as a constituent of proteins. Glutamine is also crucial in nitrogen metabolism. Ammonia (formed by nitrogen fixation) is assimilated into organic compounds by converting glutamic acid to glutamine. The enzyme which accomplishes this is called glutamine synthetase. Glutamine can then be used as a nitrogen donor in the biosynthesis of many compounds, including other amino acids, purines, and pyrimidines. Supplemental L-glutamine's possible immunomodulatory role may be accounted for in a number of ways. L-glutamine appears to play a major role in protecting the integrity of the gastrointestinal tract and, in particular, the large intestine. During catabolic states, the integrity of the intestinal mucosa may be compromised with consequent increased intestinal permeability and translocation of Gram-negative bacteria from the large intestine into the body. The demand for L-glutamine by the intestine, as well as by cells such as lymphocytes, appears to be much greater than that supplied by skeletal muscle, the major storage tissue for L-glutamine. L-glutamine is the preferred respiratory fuel for enterocytes, colonocytes and lymphocytes. Therefore, supplying supplemental L-glutamine under these conditions may do a number of things. For one, it may reverse the catabolic state by sparing skeletal muscle L-glutamine. It also may inhibit translocation of Gram-negative bacteria from the large intestine. L-glutamine helps maintain secretory IgA, which functions primarily by preventing the attachment of bacteria to mucosal cells. L-glutamine appears to be required to support the proliferation of mitogen-stimulated lymphocytes, as well as the production of interleukin-2 (IL-2) and interferon-gamma (IFN-gamma). It is also required for the maintenance of lymphokine-activated killer cells (LAK). L-glutamine can enhance phagocytosis by neutrophils and monocytes. It can lead to an increased synthesis of glutathione in the intestine, which may also play a role in maintaining the integrity of the intestinal mucosa by ameliorating oxidative stress. The exact mechanism of the possible immunomodulatory action of supplemental L-glutamine, however, remains unclear. It is conceivable that the major effect of L-glutamine occurs at the level of the intestine. Perhaps enteral L-glutamine acts directly on intestine-associated lymphoid tissue and stimulates overall immune function by that mechanism, without passing beyond the splanchnic bed.",The molecular weight is 146.15.,L-Glutamine has a topological polar surface area of 106.41.,The log p value of  is -3.37.,L-Glutamine is approved and investigational and nutraceutical.,L-Glutamine is a solid.,True
14585,"Ammonia is a naturally-occurring compound with a chemical formula NH3 and structure of trigonal pyramidal geometry. It is a colorless gas with a pungent smell, and become NH4, or ammonium ion, when in water. Although ammonia is used as a food additive in the anhydrous form and serves as a starting material in pharmaceutical and commercial products, it is caustic and hazardous when concentrated. Ammonia gas has been used in the clinical setting as a respiratory stimulant to prevent fainting. The radiolabelled form of ammonia, ammonia N 13, is intravenously administered as a radioactive diagnostic agent for Positron Emission Tomography (PET) imaging of the myocardium to evaluate myocardial perfusion. Ammonia is a natural byproduct of biological and chemical reactions, including decomposition of organic matter, including plants, animals, and animal wastes. It is present in normally present in all tissues constituting a metabolic pool, where it is mostly taken up by glutamic acid and take part in transamination and other reactions, including the synthesis of protein by the Krebs-Hanseleit cycle in the liver. It is proposed that human adults produce about 1000 mmol of ammonia daily, most of which undergoes excretion in the urine. - Indicated for use as a smelling salt to treat or prevent fainting.  As a gas, ammonia is a natural byproduct and respiratory stimulant. Its renal metabolism plays a role in whole body acid-base balance. Renal excretion and metabolism of ammonia is critical in regulation of acid-base balance by generating bicarbonate ions and promoting renal net acid excretion, both under basal conditions and in response to acid-base disturbances. There is evidence that acute ammonia exposure activates NMDA receptor signalling pathways, and high concentrations of ammonia resulting from urea cycle enzyme deficiencies are associated with changes in astrocyte morphology due to glutamine accumulation, changes in the expression of key astrocyte proteins, and increased concentrations of neuroactive L-tryptophan metabolites. ",The molecular weight is 17.03.,Ammonia has a topological polar surface area of 13.59.,,Ammonia is approved.,Ammonia is a gas.,True
14586,"NADH is the reduced form of NAD+, and NAD+ is the oxidized form of NADH, a coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). It forms NADP with the addition of a phosphate group to the 2' position of the adenosyl nucleotide through an ester linkage. (Dorland, 27th ed) Some evidence suggests that NADH might be useful in treating Parkinson's disease, chronic fatigue syndrome, Alzheimer's disease and cardiovascular disease. A coenzyme composed of ribosylnicotinamide 5'-diphosphate coupled to adenosine 5'-phosphate by pyrophosphate linkage. It is found widely in nature and is involved in numerous enzymatic reactions in which it serves as an electron carrier by being alternately oxidized (NAD+) and reduced (NADH). The action of supplemental NADH is unclear. Oral NADH supplementation has been used to combat simple fatigue as well as such mysterious and energy-sapping disorders as chronic fatigue syndrome and fibromyalgia. Researchers are also studying the value of NADH supplements for improving mental function in people with Alzheimer's disease, and minimizing physical disability and relieving depression in people with Parkinson's disease. Some healthy individuals also take NADH supplements orally to improve concentration and memory capacity, as well as to increase athletic endurance. However, to date there have been no published studies to indicate that using NADH is in any way effective or safe for these purposes. NADH is synthesized by the body and thus is not an essential nutrient. It does require the essential nutrient nicotinamide for its synthesis, and its role in energy production is certainly an essential one. In addition to its role in the mitochondrial electron transport chain, NADH is produced in the cytosol. The mitochondrial membrane is impermeable to NADH, and this permeability barrier effectively separates the cytoplasmic from the mitochondrial NADH pools. However, cytoplasmic NADH can be used for biologic energy production. This occurs when the malate-aspartate shuttle introduces reducing equivalents from NADH in the cytosol to the electron transport chain of the mitochondria. This shuttle mainly occurs in the liver and heart.",,,,NADH is approved and nutraceutical.,NADH is a solid.,True
14587,"A clear, colorless liquid rapidly absorbed from the gastrointestinal tract and distributed throughout the body. It has bactericidal activity and is used often as a topical disinfectant. It is widely used as a solvent and preservative in pharmaceutical preparations as well as serving as the primary ingredient in alcoholic beverages. For therapeutic neurolysis of nerves or ganglia for the relief of intractable chronic pain in such conditions as inoperable cancer and trigeminal neuralgia (tic douloureux), in patients for whom neurosurgical procedures are contraindicated. Alcohol produces injury to cells by dehydration and precipitation of the cytoplasm or protoplasm. This accounts for its bacteriocidal and antifungal action. When alcohol is injected in close proximity to nerve tissues, it produces neuritis and nerve degeneration (neurolysis). Ninety to 98% of ethanol that enters the body is completely oxidized. Ethanol is also used as a cosolvent to dissolve many insoluble drugs and to serve as a mild sedative in some medicinal formulations. Ethanol also binds to GABA, glycine, NMDA receptors and modulates their effects. Ethanol is also metabolised by the hepatic enzyme alcohol dehydrogenase. Ethanol affects the brain’s neurons in several ways. It alters their membranes as well as their ion channels, enzymes, and receptors. Alcohol also binds directly to the receptors for acetylcholine, serotonin, GABA, and the NMDA receptors for glutamate. ",The molecular weight is 46.07.,Ethanol has a topological polar surface area of 20.23.,The log p value of  is -0.24.,Ethanol is approved.,Ethanol is a liquid.,True
14588,"Isosorbide mononitrate is an organic nitrate with vasodilating properties. It is an anti-anginal agent that works by relaxing the smooth muscles of both arteries and veins, but but predominantly veins to reduce cardiac preload. Isosorbide mononitrate is an active metabolite of. Like other organic nitrates, isosorbide mononitrate acts as a prodrug for its active metabolite, , which mediates the therapeutic action of isosorbide mononitrate. Isosorbide mononitrate has a longer duration of action than due to its slow onset of absorption and metabolism. Isosorbide mononitrate is indicated for the prevention and management of angina pectoris due to coronary artery disease. The onset of action of oral isosorbide mononitrate is not sufficiently rapid to be useful in aborting an acute anginal episode. Isosorbide mononitrate is an anti-anginal agent and vasodilator that relaxes vascular smooth muscle to prevent and manage angina pectoris. The pharmacological action is mediated by the active metabolite, , which is released when isosorbide mononitrate is metabolized. Nitric oxide works on both arteries and veins, but predominantly veins: by relaxing veins and reducing the central venous pressure, nitric oxide causes venous pooling and a decrease in the venous return to the heart, thus decreasing cardiac preload. In healthy subjects, the stroke volume is decreased and venous pooling can occur in the standing posture, leading to postural hypotension and dizziness.  Isosorbide mononitrate acts as a prodrug for nitric oxide (NO), which is a potent vasodilator gas that is released when the drug is metabolized. NO activates soluble guanylyl cyclase in vascular endothelial cells, which increases the intracellular concentrations of cyclic GMP (cGMP). cGMP activates cGMP-dependent protein kinases, such as protein kinase G and I, which activates the downstream intracellular cascades. The downstream cascade results in reduced intracellular concentrations of calcium, caused by processes including inhibition of IP<sub>3</sub>-mediated pathway, phosphorylation of big calcium-activated potassium channel leading to cell hyperpolarization and reduced calcium influx, and increased calcium efflux via the Ca2+-ATPase-pump. Reduced intracellular calcium concentrations lead to the dephosphorylation of myosin light chains and the relaxation of smooth muscle cells.",The molecular weight is 191.14.,Isosorbide mononitrate has a topological polar surface area of 93.74.,The log p value of  is -2.51.,Isosorbide mononitrate is approved.,Isosorbide mononitrate is a solid.,True
14589,"Polyethylene glycols (PEGs) are products made of condensed ethylene oxide and water that can contain various derivatives and have various functions. Because many PEG types are hydrophilic, they are favorably used as enhancers of penetration, and used heavily in topical dermatological preparations. PEGs, along with their many nonionic derivatives, are widely utilized in cosmetic products as surfactants, emulsifiers, cleansing agents, humectants, and skin conditioners. PEG-400 has been indicated for the temporary relief of burning and irritation due to dryness of the eye, and PEG, when used as PEG-400 for eye lubrication provides relief of dry eye symptoms and prevents further irritation, thus protecting the eye from injury.  PEG allows comfortable eye drop/natural tear instillation by offering improved spreading of the drop over the ocular surface with diminished blurring. PEG, depending on molecular weight, has various mechanisms of action , , ,. For the purpose of Peg-400, the mechanism of action on the eye tissues will be the primary focus of discussion. ",,,,Polyethylene glycol 400 is approved.,Polyethylene glycol 400 is a liquid.,True
14590,"Ozanimod is a once-daily sphingosine 1-phosphate receptor modulator for the treatment of relapsing Multiple Sclerosis (MS) and inflammatory bowel disease. It was developed by Celgene(now acquired by Bristol-Myers Squibb) and was approved by the FDA on March 26 2020. Ozanimod is indicated for adults in the treatment of relapsing forms of MS, which may include relapsing-remitting disease, clinically isolated syndrome, and active secondary progressive MS. Ozanimod reduces circulating lymphocytes that cause the neuroinflammation associated with MS, reducing debilitating symptoms and, possibly, disease progression. During clinical trials, ozanimod reduced MS-associated brain volume loss in several regions. Ozanimod causes the sequestration of peripheral lymphocytes, reducing circulating lymphocytes in the gastrointestinal tract. Sphingosine‐1‐phosphate (S1P) is an important phospholipid that binds to various G‐protein‐coupled receptor subtypes, which can be identified as S1P1–5R. S1P and the receptors it binds to perform regular functions in the immune, cardiovascular, pulmonary, and nervous system. S1P can be expressed ubiquitously, playing an important role in regulating inflammation. S1P1R, S1P2R, and S1P3R receptors can be found in the cardiovascular, immune, and central nervous systems. S1P4R is found on lymphocytic and hematopoietic cells, while S1P5R expression is found only on the spleen (on natural killer cells) or in the central nervous system.",,,,Ozanimod is approved and investigational.,Ozanimod is a solid.,True
14591,"A non-essential amino acid. It is found primarily in gelatin and silk fibroin and used therapeutically as a nutrient. It is also a fast inhibitory neurotransmitter. Supplemental glycine may have antispastic activity. Very early findings suggest it may also have antipsychotic activity as well as antioxidant and anti-inflammatory activities. Helps trigger the release of oxygen to the energy requiring cell-making process; Important in the manufacturing of hormones responsible for a strong immune system. In the CNS, there exist strychnine-sensitive glycine binding sites as well as strychnine-insensitive glycine binding sites. The strychnine-insensitive glycine-binding site is located on the NMDA receptor complex. The strychnine-sensitive glycine receptor complex is comprised of a chloride channel and is a member of the ligand-gated ion channel superfamily. The putative antispastic activity of supplemental glycine could be mediated by glycine's binding to strychnine-sensitive binding sites in the spinal cord. This would result in increased chloride conductance and consequent enhancement of inhibitory neurotransmission. The ability of glycine to potentiate NMDA receptor-mediated neurotransmission raised the possibility of its use in the management of neuroleptic-resistant negative symptoms in schizophrenia. <br/>Animal studies indicate that supplemental glycine protects against endotoxin-induced lethality, hypoxia-reperfusion injury after liver transplantation, and D-galactosamine-mediated liver injury. Neutrophils are thought to participate in these pathologic processes via invasion of tissue and releasing such reactive oxygen species as superoxide. In vitro studies have shown that neutrophils contain a glycine-gated chloride channel that can attenuate increases in intracellular calcium and diminsh neutrophil oxidant production. This research is ealy-stage, but suggests that supplementary glycine may turn out to be useful in processes where neutrophil infiltration contributes to toxicity, such as ARDS.",The molecular weight is 75.07.,Glycine has a topological polar surface area of 63.32.,The log p value of  is -3.21.,Glycine is approved and nutraceutical and vet_approved.,Glycine is a solid.,True
14592,"Magnesium gluconate is a magnesium salt of gluconate. It demonstrates the highest oral bioavailability of magnesium salts and is used as a mineral supplement. Magnesium is ubiquitous in the human body, and is naturally present in many foods, added to other food products, available as a dietary supplement and used as an ingredient in some medicines (such as antacids and laxatives). Magnesium gluconate is a mineral supplement which is used to prevent and treat low levels of magnesium. Magnesium is very important for the normal physiologic functioning of cells, nerves, muscles, bones, and the heart. Generally, a well-balanced diet provides the necessary amounts of magnesium for homeostasis. However, certain conditions causing chronic magnesium deficiency may decrease levels of magnesium. These conditions include treatment with diuretics, a poor diet, alcoholism, or other medical conditions (e.g., severe diarrhea/vomiting, stomach/intestinal absorption problems, poorly controlled diabetes). Magnesium is a cofactor in over 300 enzyme systems that regulate a variety of biochemical reactions in the body, including protein synthesis, muscle and nerve function, blood glucose control, and blood pressure regulation. Magnesium is necessary for energy production, oxidative phosphorylation, and glycolysis.  Replaces deficient circulating levels of magnesium.",,,,Magnesium gluconate is approved and investigational.,Magnesium gluconate is a solid.,True
14593,"Anti-inhibitor coagulant complex, also known as FEIBA (factor eight inhibitor bypassing activity), contains several proteins involved in the prothrombinase complex. It is used to control bleeding in hemophilia A and B patients with inhibitors. For use in the control of bleeding episodes, perioperative management, and routine prophylaxis against bleeding episodes in hemophilia A and B patients with inhibitors. It is not indicated in the absence of factor VIII or IX inhibitors. FEIBA contains several clotting factors which act at various points in the caogulation cascade to promote thrombosis. Factor VIIa present in FEIBA forms a complex with tissue factor and calcium which converts endogenous and FEIBA contained factor X to Xa. Endogenous and FEIBA contained factor Xa act as parrt of the prothrombinase complex to convert endogenous and FEIBA contained prothrombin to thrombin. Endogenous and FEIBA contained thrombin then cleave fibrinogen to insulouble fibrin and activate factor XIII which covalently cross-links fibrin to form a polymer mesh. FEIBA also contains factor IX and IXa which act as part of the tenase complex to convert factor X to Xa. Thrombin activates factor V, VII, and VIII as part of the amplification phase of the clotting cascade. These events promote the formation of blood clots to prevent or stop bleeding. ",,,,Anti-inhibitor coagulant complex is approved and investigational.,Anti-inhibitor coagulant complex is a solid.,True
14594,"Albutrepenonacog alfa (rIX-RFP) is a recombinant fusion protein that links a recombinant coagulation factor IX (rFIX) with a recombinant human albumin (rAlbumin). It was developed by CSL Behring Canada, Inc and approved by Health Canada on April 26, 2017. It was also approved by FDA and EMA in 2016. It is currently marketed in the forms of 250, 500, 1000 and 2000 IU/vial. Under the EMA and FDA, rIX-RFP is indicated in the treatment of hemophilia B. For Health Canada, rIX-FRP is also indicated to prevent or reduce bleeding episodes. Clinical trials with rIX-RFP in patients with moderately to severe hemophilia B demonstrated a lower annualized spontaneous, total and joint bleeding rates. It was also efficient against bleeding episodes and maintenance of hemostasis in the perioperative setting when compared with on-demand treatment. The administration of rIX-RFP presented no reports of inhibitor development. The current therapies against hemophilia B are hampered by the short half-life of the replacement FIX therapy. Thus, to solve this problem, in rIX-RFP there is the fusion of rFIX with rAlbumin which presents a much longer half-life and it does not present interactions with the immune system.",,,,Albutrepenonacog alfa is approved.,Albutrepenonacog alfa is a solid.,True
14595,"Desmopressin (dDAVP), a synthetic analogue of 8-arginine vasopressin (ADH), is an antidiuretic peptide drug modified by deamination of 1-cysteine and substitution of 8-L-arginine by 8-D-arginine. ADH is an endogenous pituitary hormone that has a crucial role in the control of the water content in the body. Upon release from the stimulation of increased plasma osmolarity or decreased circulating blood volume, ADH mainly acts on the cells of the distal part of the nephron and the collecting tubules in the kidney. The hormone interacts with V1, V2 or V3 receptors with differing signal cascade systems. - Indicated for the treatment of nocturia due to nocturnal polyuria in adults who awaken at least 2 times per night to void (intranasal).  By mimicking the actions of endogenous ADH, desmopressin acts as a selective agonist of V2 receptors expressed in the renal collecting duct (CD) to increase water re-absorption and reduce urine production. Desmopressin has been shown to be more potent than ADH in increasing plasma levels of factor VIII activity in patients with hemophilia and von Willebrand's disease Type I. Desmopressin demonstrates markedly diminished pressor activity. Desmopressin administered intranasally has an antidiuretic effect about one-tenth that of an equivalent dose administered by injection. Upon binding of desmopressin to V2 receptors in the basolateral membrane of the cells of the distal tubule and collecting ducts of the nephron, adenylyl cyclase is stimulated. The resulting intracellular cascades in the collecting duct lead to increased rate of insertion of water channels, called aquaporins, into the lumenal membrane and enhanced the permeability of the membrane to water. ",The molecular weight is 1069.22.,Desmopressin has a topological polar surface area of 435.41.,The log p value of  is -3.14.,Desmopressin is approved.,Desmopressin is a solid.,True
14596,"Eletriptan is a second generation triptan drug developed by Pfizer Inc for the treatment of migraine headaches. For the acute treatment of migraine with or without aura in adults. Eletriptan is a selective 5-hydroxytryptamine 1B/1D receptor agonist. In the anesthetized dog, eletriptan has been shown to reduce carotid arterial blood flow, with only a small increase in arterial blood pressure at high doses. While the effect on blood flow was selective for the carotid arterial bed, decreases in coronary artery diameter were observed. Eletriptan has also been shown to inhibit trigeminal nerve activity in the rat. Eletriptan binds with high affinity to 5-HT1B, 5-HT1D and 5-HT1F receptors, has modest affinity for 5-HT1A, 5-HT1E, 5-HT2B and 5-HT7 receptors, and little or no affinity for 5-HT2A, 5-HT2C, 5-HT3, 5-HT4, 5-HT5A and 5-HT6 receptors. In contrast, eletriptan displays insignificant pharmacological activity at adrenergic alpha1, alpha2, or beta; dopaminergic D1 or D2; muscarinic; or opioid receptors. While the full mechanism of action of 5-HT receptor agonists in relieving migrains is not fully elucidated, it is proposed that the activation of 5-HT1 receptors located on intracranial blood vessels leads to vasoconstriction that correlates with the relief of migraine headaches. It is also proposed that the activation of 5-HT1 receptors on sensory nerve endings in the trigeminal system leads to the inhibition of release of pro-inflammatory neuropeptides. ",The molecular weight is 382.52.,Eletriptan has a topological polar surface area of 53.17.,The log p value of  is 3.35.,Eletriptan is approved and investigational.,Eletriptan is a solid.,True
14597,"A sulfone active against a wide range of bacteria but mainly employed for its actions against mycobacterium leprae. Its mechanism of action is probably similar to that of the sulfonamides which involves inhibition of folic acid synthesis in susceptible organisms. It is also used with pyrimethamine in the treatment of malaria. (From Martindale, The Extra Pharmacopoeia, 30th ed, p157-8) For the treatment and management of leprosy and dermatitis herpetiformis. Dapsone is a sulfone with anti-inflammatory immunosuppressive properties as well as antibacterial and antibiotic properties. Dapsone is the principal drug in a multidrug regimen recommended by the World Health Organization for the treatment of leprosy. As an anti-infective agent, it is also used for treating malaria and, recently, for Pneumocystic carinii pneumonia in AIDS patients. Dapsone is absorbed rapidly and nearly completely from the gastrointestinal tract. Dapsone is distributed throughout total body water and is present in all tissues. However, it tends to be retained in skin and muscle and especially in the liver and kidney: traces of the drug are present in these organs up to 3 weeks after therapy cessation. Dapsone acts against bacteria and protozoa in the same way as sulphonamides, that is by inhibiting the synthesis of dihydrofolic acid through competition with para-amino-benzoate for the active site of dihydropteroate synthetase. The anti-inflammatory action of the drug is unrelated to its antibacterial action and is still not fully understood.",The molecular weight is 248.3.,Dapsone has a topological polar surface area of 86.18.,The log p value of  is 0.89.,Dapsone is approved and investigational.,Dapsone is a solid.,True
14598,"Dronabinol (marketed as Marinol) is a synthetic form of delta-9-tetrahydrocannabinol (Δ⁹-THC), the primary psychoactive component of cannabis (marijuana). THC demonstrates its effects through weak partial agonist activity at Cannabinoid-1 (CB1R) and Cannabinoid-2 (CB2R) receptors, which results in the well-known effects of smoking cannabis such as increased appetite, reduced pain, and changes in emotional and cognitive processes. Due to its evidence as an appetite stimulant and an anti-nauseant, Dronabinol is approved for use in anorexia associated with weight loss in patients with AIDS and for the treatment of nausea and vomiting associated with cancer chemotherapy in patients who have failed to respond adequately to conventional antiemetic treatments. For the treatment of anorexia associated with weight loss in patients with AIDS, and nausea and vomiting associated with cancer chemotherapy in patients who have failed to respond adequately to conventional antiemetic treatments Marinol may has complex effects on the central nervous system (CNS), including cannabinoid receptors. Dronabinol may inhibit endorphins in the emetic center, suppress prostaglandin synthesis, and/or inhibit medullary activity through an unspecified cortical action. Dronabinol is a synthetic form of delta-9-tetrahydrocannabinol (Δ⁹-THC), the primary psychoactive component of cannabis (marijuana). THC demonstrates its effects through weak partial agonist activity at Cannabinoid-1 (CB1R) and Cannabinoid-2 (CB2R) receptors, which results in the well-known effects of smoking cannabis such as increased appetite, reduced pain, and changes in emotional and cognitive processes.",The molecular weight is 314.47.,Dronabinol has a topological polar surface area of 29.46.,The log p value of  is 7.24.,Dronabinol is approved and illicit.,Dronabinol is a solid.,True
14599,"Montelukast was first approved for clinical use by the US FDA in 1998 as Merck's brand name Singulair. The medication is a member of the leukotriene receptor antagonist (LTRA) category of drugs. Although capable of demonstrating effectiveness, the use of such LTRAs like montelukast is typically in addition to or complementary with the use of inhaled corticosteroids or other agents in asthma step therapy. Regardless, in 2008-2009, there were FDA-led investigations into the possibility of montelukast to elicit neuropsychiatric effects like agitation, hallucinations, suicidal behaviour, and others in individuals who used the medication. And although these kinds of effects are currently included in the official prescribing information for montelukast, the drug still sees extensive use worldwide via millions of prescriptions annually and has since become available as a generic and as a brand name product. Montelukast is indicated for: Montelukast is a leukotriene receptor antagonist that demonstrates a marked affinity and selectivity to the cysteinyl leukotriene receptor type-1 in preference to many other crucial airway receptors like the prostanoid, cholinergic, or beta-adrenergic receptors. As a consequence, the agent can elicit substantial blockage of LTD4 leukotriene-mediated bronchoconstriction with doses as low as 5 mg. Moreover, a placebo-controlled, crossover study (n=12) demonstrated that montelukast is capable of inhibiting early and late phase bronchoconstriction caused by antigen challenge by 75% and 57% respectively. Cysteinyl leukotrienes (CysLT) like LTC4, LTD4, and LTE4, among others, are eicosanoids released by a variety of cells like mast cells and eosinophils. When such CysLT bind to corresponding CysLT receptors like CysLT type-1 receptors located on respiratory airway smooth muscle cells, airway macrophages, and on various pro-inflammatory cells like eosinophils and some specific myeloid stem cells activities that facilitate the pathophysiology of asthma and allergic rhinitis are stimulated.",The molecular weight is 586.19.,Montelukast has a topological polar surface area of 70.42.,The log p value of  is 8.47.,Montelukast is approved.,Montelukast is a solid.,True
14600,"Rofecoxib is used for the treatment of osteoarthritis, rheumatoid arthritis, acute pain in adults, and primary dysmenorrhea, as well as acute treatment of migraine attacks with or without auras. Rofecoxib is a solid. This compound belongs to the stilbenes. These are organic compounds containing a 1,2-diphenylethylene moiety. Stilbenes (C6-C2-C6 ) are derived from the common phenylpropene (C6-C3) skeleton building block. The introduction of one or more hydroxyl groups to a phenyl ring lead to stilbenoids. Rofecoxib has a half-life of 17 hours and its mean oral bioavailability at therapeutically recommended doses of 125, 25, and 50 mg is approximately 93%. The proteins that rofecoxib target include elastin and prostaglandin G/H synthase 2. Cytochrome P450 1A2, Cytochrome P450 3A4, Cytochrome P450 2C9, Cytochrome P450 2C8, and Prostaglandin G/H synthase 1 are known to metabolize rofecoxib. On September 30, 2004, Merck voluntarily withdrew rofecoxib from the market because of concerns about increased risk of heart attack and stroke associated with long-term, high-dosage use. For the treatment of osteoarthritis, rheumatoid arthritis, acute pain in adults, and primary dysmenorrhea, as well as acute treatment of migraine attacks with or without auras. Rofecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, is classified as a nonsteroidal anti-inflammatory drug (NSAID). Unlike celecoxib, rofecoxib lacks a sulfonamide chain and does not require CYP450 enzymes for metabolism. Like other NSAIDs, rofecoxib exhibits anti-inflammatory, analgesic, and antipyretic activity. NSAIDs appear to inhibit prostaglandin synthesis via the inhibition of cyclooxygenase (COX), which are responsible for catalyzing the formation of prostaglandins in the arachidonic acid pathyway. There are at least two isoenzymes, COX-1 and COX-2, that have been identified. Although the exact mechanisms have not been clearly established, NSAIDs exert their anti-inflammatory, analgesic, and antipyretic primarily through the inhibition of COX-2. The inhibition of COX-1 is principally responsible for the negative effects on the GI mucosa. As rofecoxib is selective for COX-2, it may be potentially associated with a decreased risk of certain adverse events, but more data is needed to fully evaulate the drug. The anti-inflammatory, analgesic, and antipyretic effects of NSAIDs appear to result from the inhibition of prostaglandin synthesis. Although the exact mechanism of action has not been determined, these effects appear to be mediated through the inhibition of the COX-2 isoenzyme at the sites of inflammation with subsequent reduction in the synthesis of certain prostaglandins from their arachidonic acid precursors. Rofecoxib selectively inhibits the cyclooxygenase-2 (COX-2) enzyme, which is important for the mediation of inflammation and pain. Unlike non-selective NSAIDs, rofecoxib does not inhibit platelet aggregation. It also has little to no affinity for COX-1.",The molecular weight is 314.36.,Rofecoxib has a topological polar surface area of 60.44.,The log p value of  is 1.8.,Rofecoxib is approved and investigational and withdrawn.,Rofecoxib is a solid.,True
14601,"Zafirlukast is an oral leukotriene receptor antagonist (LTRA) for the maintenance treatment of asthma, often used in conjunction with an inhaled steroid and/or long-acting bronchodilator. It is available as a tablet and is usually dosed twice daily. Another leukotriene receptor antagonist is montelukast (Singulair), which is usually taken just once daily. For the prophylaxis and chronic treatment of asthma. Zafirlukast is a synthetic, selective peptide leukotriene receptor antagonist (LTRA) indicated for the prophylaxis and chronic treatment of asthma. Patients with asthma were found in one study to be 25-100 times more sensitive to the bronchoconstricting activity of inhaled LTD<sub>4</sub> than nonasthmatic subjects. <i>In vitro</i> studies demonstrated that zafirlukast antagonized the contractile activity of three leukotrienes (LTC<sub>4</sub>, LTD<sub>4</sub> and LTE<sub>4</sub>) in conducting airway smooth muscle from laboratory animals and humans. Zafirlukast prevented intradermal LTD<sub>4</sub>-induced increases in cutaneous vascular permeability and inhibited inhaled LTD<sub>4</sub>-induced influx of eosinophils into animal lungs. Zafirlukast is a selective and competitive receptor antagonist of leukotriene D4 and E4 (LTD<sub>4</sub> and LTE4), components of slow-reacting substance of anaphylaxis (SRSA). Cysteinyl leukotriene production and receptor occupation have been correlated with the pathophysiology of asthma, including airway edema, smooth muscle constriction, and altered cellular activity associated with the inflammatory process, which contribute to the signs and symptoms of asthma.",The molecular weight is 575.68.,Zafirlukast has a topological polar surface area of 115.73.,The log p value of  is 7.09.,Zafirlukast is approved and investigational.,Zafirlukast is a solid.,True
14602,"Voriconazole (Vfend, Pfizer) is a triazole antifungal medication used to treat serious fungal infections. It is used to treat invasive fungal infections that are generally seen in patients who are immunocompromised. These include invasive candidiasis, invasive aspergillosis, and emerging fungal infections. For the treatment of esophageal candidiasis, invasive pulmonary aspergillosis, and serious fungal infections caused by <i>Scedosporium apiospermum</i> and <i>Fusarium</i> spp. Voriconazole is a triazole antifungal agent indicated for use in the treatment of fungal infections including invasive aspergillosis, esophageal candidiasis, and serious fungal infections caused by <i>Scedosporium apiospermum</i> (asexual form of <i>Pseudallescheria boydii</i>) and <i>Fusarium</i> spp. including <i>Fusarium solani</i>. Fungal plasma membranes are similar to mammalian plasma membranes, differing in having the nonpolar sterol ergosterol, rather than cholesterol, as the principal sterol. Membrane sterols such as ergosterol provide structure, modulation of membrane fluidity, and possibly control of some physiologic events. Voriconazole effects the formation of the fungal plasma membrane by indirectly inhibiting the biosynthesis of ergosterol. This results in plasma membrane permeability changes and inhibition of growth. Voriconazole binds and inhibits ergosterol synthesis by inhibiting CYP450-dependent 14-alpha sterol demethylase. The inhibition of 14-alpha sterol demethylase results in a depletion of ergosterol in fungal cell membrane.",The molecular weight is 349.32.,Voriconazole has a topological polar surface area of 76.72.,The log p value of  is 0.52.,Voriconazole is approved.,Voriconazole is a solid.,True
14603,"Chlorpropamide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It belongs to the sulfonylurea class of insulin secretagogues, which act by stimulating β cells of the pancreas to release insulin. Sulfonylureas increase both basal insulin secretion and meal-stimulated insulin release. Medications in this class differ in their dose, rate of absorption, duration of action, route of elimination and binding site on their target pancreatic β cell receptor. Sulfonylureas also increase peripheral glucose utilization, decrease hepatic gluconeogenesis and may increase the number and sensitivity of insulin receptors. Sulfonylureas are associated with weight gain, though less so than insulin. Due to their mechanism of action, sulfonylureas may cause hypoglycemia and require consistent food intake to decrease this risk. The risk of hypoglycemia is increased in elderly, debilitated and malnourished individuals. Chlorpropamide is not recommended for the treatment of NIDDM as it increases blood pressure and the risk of retinopathy (UKPDS-33). Up to 80% of the single oral dose of chlorpropramide is metabolized, likely in the liver; 80-90% of the dose is excreted in urine as unchanged drug and metabolites. Renal and hepatic dysfunction may increase the risk of hypoglycemia. For treatment of NIDDM in conjunction with diet and exercise.  Chlorpropamide, a second-generation sulfonylurea antidiabetic agent, is used with diet to lower blood glucose levels in patients with diabetes mellitus type II. Chlorpropamide is twice as potent as the related second-generation agent glipizide. Sulfonylureas such as chlorpropamide bind to ATP-sensitive potassium channels on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Depolarization stimulates calcium ion influx through voltage-sensitive calcium channels, raising intracellular concentrations of calcium ions, which induces the secretion, or exocytosis, of insulin.",The molecular weight is 276.74.,Chlorpropamide has a topological polar surface area of 75.27.,The log p value of  is 2.35.,Chlorpropamide is approved and investigational.,Chlorpropamide is a solid.,True
14604,"A semisynthetic derivative of podophyllotoxin that exhibits antitumor activity. Etoposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent entry into the mitotic phase of cell division, and lead to cell death. Etoposide acts primarily in the G2 and S phases of the cell cycle. For use in combination with other chemotherapeutic agents in the treatment of refractory testicular tumors and as first line treatment in patients with small cell lung cancer. Also used to treat other malignancies such as lymphoma, non-lymphocytic leukemia, and glioblastoma multiforme. Etoposide is an antineoplastic agent and an epipodophyllotoxin (a semisynthetic derivative of the podophyllotoxins). It inhibits DNA topoisomerase II, thereby ultimately inhibiting DNA synthesis. Etoposide is cell cycle dependent and phase specific, affecting mainly the S and G2 phases. Two different dose-dependent responses are seen. At high concentrations (10 &micro;g/mL or more), lysis of cells entering mitosis is observed. At low concentrations (0.3 to 10 &micro;g/mL), cells are inhibited from entering prophase. It does not interfere with microtubular assembly. The predominant macromolecular effect of etoposide appears to be the induction of DNA strand breaks by an interaction with DNA-topoisomerase II or the formation of free radicals. Etoposide inhibits DNA topoisomerase II, thereby inhibiting DNA re-ligation. This causes critical errors in DNA synthesis at the premitotic stage of cell division and can lead to apoptosis of the cancer cell. Etoposide is cell cycle dependent and phase specific, affecting mainly the S and G2 phases of cell division. Inhibition of the topoisomerase II alpha isoform results in the anti-tumour activity of etoposide. The drug is also capable of inhibiting the beta isoform but inhibition of this target is not associated with the anti-tumour activity. It is instead associated with the carcinogenic effect. ",The molecular weight is 588.56.,Etoposide has a topological polar surface area of 160.83.,The log p value of  is -0.11.,Etoposide is approved.,Etoposide is a solid.,True
14605,"Candesartan is an angiotensin-receptor blocker (ARB) that may be used alone or with other agents to treat hypertension. It is administered orally as the prodrug, candesartan cilexetil, which is rapidly converted to its active metabolite, candesartan, during absorption in the gastrointestinal tract. Candesartan lowers blood pressure by antagonizing the renin-angiotensin-aldosterone system (RAAS); it competes with angiotensin II for binding to the type-1 angiotensin II receptor (AT1) subtype and prevents the blood pressure increasing effects of angiotensin II. Unlike angiotensin-converting enzyme (ACE) inhibitors, ARBs do not have the adverse effect of dry cough. Candesartan may be used to treat hypertension, isolated systolic hypertension, left ventricular hypertrophy and diabetic nephropathy. It may also be used as an alternative agent for the treatment of heart failure, systolic dysfunction, myocardial infarction and coronary artery disease. May be used as a first line agent to treat uncomplicated hypertension, isolated systolic hypertension and left ventricular hypertrophy. May be used as a first line agent to delay progression of diabetic nephropathy. Candesartan may be also used as a second line agent in the treatment of congestive heart failure, systolic dysfunction, myocardial infarction and coronary artery disease in those intolerant of ACE inhibitors. Candesartan cilexetil is an ARB prodrug that is rapidly converted to candesartan, its active metabolite, during absorption from the gastrointestinal tract. Candesartan confers blood pressure lowering effects by antagonizing the hypertensive effects of angiotensin II via the RAAS. RAAS is a homeostatic mechanism for regulating hemodynamics, water and electrolyte balance. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from granular cells of the juxtaglomerular apparatus in the kidneys. Renin cleaves circulating angiotensinogen to angiotensin I, which is cleaved by angiotensin converting enzyme (ACE) to angiotensin II. Angiotensin II increases blood pressure by increasing total peripheral resistance, increasing sodium and water reabsorption in the kidneys via aldosterone secretion, and altering cardiovascular structure. Angiotensin II binds to two receptors: type-1 angiotensin II receptor (AT1) and type-2 angiotensin II receptor (AT2). AT1 is a G-protein coupled receptor (GPCR) that mediates the vasoconstrictive and aldosterone-secreting effects of angiotensin II. Studies performed in recent years suggest that AT2 antagonizes AT1-mediated effects and directly affects long-term blood pressure control by inducing vasorelaxation and increasing urinary sodium excretion. Angiotensin receptor blockers (ARBs) are non-peptide competitive inhibitors of AT1. ARBs block the ability of angiotensin II to stimulate pressor and cell proliferative effects. Unlike ACE inhibitors, ARBs do not affect bradykinin-induced vasodilation. The overall effect of ARBs is a decrease in blood pressure. Candesartan selectively blocks the binding of angiotensin II to AT1 in many tissues including vascular smooth muscle and the adrenal glands. This inhibits the AT1-mediated vasoconstrictive and aldosterone-secreting effects of angiotensin II and results in an overall decrease in blood pressure. Candesartan is greater than 10,000 times more selective for AT1 than AT2. Inhibition of aldosterone secretion may increase sodium and water excretion while decreasing potassium excretion.",The molecular weight is 610.67.,Candesartan cilexetil has a topological polar surface area of 143.34.,The log p value of  is 7.08.,Candesartan cilexetil is approved.,Candesartan cilexetil is a solid.,True
14606,"A piperidinyl isoindole originally introduced as a non-barbiturate hypnotic, but withdrawn from the market due to teratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppresive and anti-angiogenic activity. It inhibits release of tumor necrosis factor-alpha from monocytes, and modulates other cytokine action.  For the acute treatment of the cutaneous manifestations of moderate to severe erythema nodosum leprosum (ENL). Also for use as maintenance therapy for prevention and suppression of the cutaneous manifestations of ENL recurrence. Thalidomide is an immunomodulatory agent with a spectrum of activity that is not fully characterized. Thalidomide is racemic &mdash; it contains both left and right handed isomers in equal amounts: one enantiomer is effective against morning sickness, and the other is teratogenic. The enantiomers are converted to each other in vivo. That is, if a human is given D-thalidomide or L-thalidomide, both isomers can be found in the serum. Hence, administering only one enantiomer will not prevent the teratogenic effect in humans. In patients with erythema nodosum leprosum (ENL) the mechanism of action is not fully understood. Available data from in vitro studies and preliminary clinical trials suggest that the immunologic effects of this compound can vary substantially under different conditions, but may be related to suppression of excessive tumor necrosis factor-alpha (TNF-a) production and down-modulation of selected cell surface adhesion molecules involved in leukocyte migration. For example, administration of thalidomide has been reported to decrease circulating levels of TNF-a in patients with ENL, however, it has also been shown to increase plasma TNF-a levels in HIV-seropositive patients. As a cancer treatment, the drug may act as a VEGF inhibitor.",The molecular weight is 258.23.,Thalidomide has a topological polar surface area of 83.55.,The log p value of  is 0.53.,Thalidomide is approved and investigational and withdrawn.,Thalidomide is a solid.,True
14607,"Diphenhydramine - perhaps known most commonly as its brand name formulation Benadryl - is a first-generation H1 receptor antihistamine that is used extensively for the treatment of seasonal allergies, insect bites and stings, and rashes. However, it also has antiemetic, antitussive, hypnotic, and antiparkinson properties. As histamine receptors exist both peripherally and in the central nervous system, diphenhydramine has been shown to cause sedation due to its competitive antagonism of histamine H1 receptors within the central nervous system. While its use in allergy therapy can sometimes fall out of favor due to its sedative effect, diphenhydramine has been repurposed for use within many non-prescription over-the-counter sleep aids and cough-and-cold medications that have been marketed for \night time\"" use. "" Diphenhydramine is a first-generation histamine H1 receptor antagonist (H1 antihistamine) that is widely available as a non-prescription, over-the-counter (OTC) medication. As an OTC medication, diphenhydramine is typically formulated as tablets and creams indicated for use in treating sneezing, runny nose, itchy/watery eyes, itching of nose or throat, insomnia, pruritis, urticaria, insect bites/stings, allergic rashes, and nausea. Diphenhydramine has anti-histaminic (H1-receptor), anti-emetic, anti-vertigo and sedative and hypnotic properties. The anti-histamine action occurs by blocking the spasmogenic and congestive effects of histamine by competing with histamine for H1 receptor sites on effector cells, preventing but not reversing responses mediated by histamine alone. Such receptor sites may be found in the gut, uterus, large blood vessels, bronchial muscles, and elsewhere. Anti-emetic action is by inhibition at the medullary chemoreceptor trigger zone. Anti-vertigo action is by a central antimuscarinic effect on the vestibular apparatus and the integrative vomiting center and medullary chemoreceptor trigger zone of the midbrain. Diphenhydramine predominantly works via the antagonism of H1 (Histamine 1) receptors. Such H1 receptors are located on respiratory smooth muscles, vascular endothelial cells, the gastrointestinal tract (GIT), cardiac tissue, immune cells, the uterus, and the central nervous system (CNS) neurons. When the H1 receptor is stimulated in these tissues it produces a variety of actions including increased vascular permeability, promotion of vasodilation causing flushing, decreased atrioventricular (AV) node conduction time, stimulation of sensory nerves of airways producing coughing, smooth muscle contraction of bronchi and the GIT, and eosinophilic chemotaxis that promotes the allergic immune response.",The molecular weight is 255.36.,Diphenhydramine has a topological polar surface area of 12.47.,The log p value of  is 3.45.,Diphenhydramine is approved and investigational.,Diphenhydramine is a solid.,True
14608,"Ifosfamide is a chemotherapeutic agent chemically related to the nitrogen mustards and a synthetic analog of cyclophosphamide. It is active as an alkylating agent and an immunosuppressive agent. Used as a component of various chemotherapeutic regimens as third-line therapy for recurrent or refractory germ cell testicular cancer. Also used as a component of various chemotherapeutic regimens for the treatment of cervical cancer, as well as in conjunction with surgery and/or radiation therapy in the treatment of various soft tissue sarcomas. Other indications include treatment of osteosarcoma, bladder cancer, ovarian cancer. small cell lung cancer, and non-Hodgkin's lymphoma. Ifosfamide requires activation by microsomal liver enzymes to active metabolites in order to exert its cytotoxic effects. Activation occurs by hydroxylation at the ring carbon atom 4 to form the unstable intermediate 4-hydroxyifosfamide. This metabolite than rapidly degrades to the stable urinary metabolite 4-ketoifosfamide. The stable urinary metabolite, 4-carboxyifosfamide, is formed upon opening of the ring. These urinary metabolites have not been found to be cytotoxic. N, N-bis (2-chloroethyl)-phosphoric acid diamide (ifosphoramide) and acrolein are also found. The major urinary metabolites, dechloroethyl ifosfamide and dechloroethyl cyclophosphamide, are formed upon enzymatic oxidation of the chloroethyl side chains and subsequent dealkylation. It is the alkylated metabolites of ifosfamide that have been shown to interact with DNA. Ifosfamide is cycle-phase nonspecific. The exact mechanism of ifosfamide has not been determined, but appears to be similar to other alkylating agents. Ifosfamide requires biotransformation in the liver by mixed-function oxidases (cytochrome P450 system) before it becomes active. After metabolic activation, active metabolites of ifosfamide alkylate or bind with many intracellular molecular structures, including nucleic acids. The cytotoxic action is primarily through the alkylation of DNA, done by attaching the N-7 position of guanine to its reactive electrophilic groups. The formation of inter and intra strand cross-links in the DNA results in cell death.",The molecular weight is 261.08.,Ifosfamide has a topological polar surface area of 41.57.,The log p value of  is 0.92.,Ifosfamide is approved.,Ifosfamide is a solid.,True
14609,"Zopiclone is a novel hypnotic agent used in the treatment of insomnia. Its mechanism of action is based on modulating benzodiazepine receptors. In addition to zopiclone's benzodiazepine pharmacological properties it also has some barbiturate like properties. For the short-term treatment of insomnia. Zopiclone is a nonbenzodiazepine hypnotic from the pyrazolopyrimidine class and is indicated for the short-term treatment of insomnia. While Zopiclone is a hypnotic agent with a chemical structure unrelated to benzodiazepines, barbiturates, or other drugs with known hypnotic properties, it interacts with the gamma-aminobutyric acid-benzodiazepine (GABA<sub>B</sub>Z) receptor complex. Subunit modulation of the GABA<sub>B</sub>Z receptor chloride channel macromolecular complex is hypothesized to be responsible for some of the pharmacological properties of benzodiazepines, which include sedative, anxiolytic, muscle relaxant, and anticonvulsive effects in animal models. Zopiclone binds selectively to the brain alpha subunit of the GABA A omega-1 receptor. Zopiclone exerts its action by binding on the benzodiazepine receptor complex and modulation of the GABA<sub>B</sub>Z receptor chloride channel macromolecular complex. Both zopiclone and benzodiazepines act indiscriminately at the benzodiazepine binding site on α1, α2, α3 and α5 GABAA containing receptors as full agonists causing an enhancement of the inhibitory actions of GABA to produce the therapeutic (hypnotic and anxiolytic) and adverse effects of zopiclone.",The molecular weight is 388.81.,Zopiclone has a topological polar surface area of 91.76.,The log p value of  is 1.25.,Zopiclone is approved.,Zopiclone is a solid.,True
14610,"Ketamine is an NMDA receptor antagonist with a potent anesthetic effect. It was developed in 1963 as a replacement for phencyclidine (PCP) by Calvin Stevens at Parke Davis Laboratories. It started being used for veterinary purposes in Belgium and in 1964 was proven that compared to PCP, it produced minor hallucinogenic effects and shorter psychotomimetic effects. It was FDA approved in 1970, and from there, it has been used as an anesthetic for children or patients undergoing minor surgeries but mainly for veterinary purposes. Ketamine is indicated as an anesthetic agent for recommended diagnostic and surgical procedures. If skeletal muscle relaxation is needed, it should be combined with a muscle relaxant. If the surgical procedure involves visceral pain, it should be supplemented with an agent that obtunds visceral pain. Ketamine can be used for induction of anesthesia prior other general anesthetic agents and as a supplement of low potency agents. Ketamine is a rapid-acting general anesthetic producing an anesthetic state characterized by profound analgesia, normal pharyngeal-laryngeal reflexes, normal or slightly enhanced skeletal muscle tone, cardiovascular and respiratory stimulation, and occasionally a transient and minimal respiratory depression. The anesthetic state produced by Ketamine has been termed as \dissociative anesthesia\"" in that it appears to selectively interrupt association pathways of the brain before producing somesthetic sensory blockade. It may selectively depress the thalamoneocortical system before significantly obtunding the more ancient cerebral centers and pathways (reticular-activating and limbic systems)."" Ketamine interacts with N-methyl-D-aspartate (NMDA) receptors, opioid receptors, monoaminergic receptors, muscarinic receptors and voltage sensitive Ca ion channels. Unlike other general anaesthetic agents, ketamine does not interact with GABA receptors.",The molecular weight is 237.73.,Ketamine has a topological polar surface area of 29.1.,The log p value of  is 2.93.,Ketamine is approved and vet_approved.,Ketamine is a solid.,True
14611,"A barbiturate that is effective as a hypnotic and sedative. For the induction of anesthesia prior to the use of other general anesthetic agents and for induction of anesthesia for short surgical, diagnostic, or therapeutic procedures associated with minimal painful stimuli. Hexobarbital is a barbiturate derivative having hypnotic and sedative effects. It was subsequently used in the 1940s and 1950s as an anesthetic for surgery. Furthermore, the agent also demonstrates a fairly quick onset of action that also possesses a short duration of action. However it can be difficult to control the depth of anesthesia with hexobarbital which makes it quite dangerous, and it has now been replaced by safer drugs in human medicine, usually thiopental would be the barbiturate of choice for this application these days. Hexobarbital binds at a distinct binding site associated with a Cl- ionopore at the GABA-A receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.",The molecular weight is 236.27.,Hexobarbital has a topological polar surface area of 66.48.,The log p value of  is 1.63.,Hexobarbital is experimental.,Hexobarbital is a solid.,True
14612,"Trabectedin, also referred as ET-743 during its development, is a marine-derived antitumor agent discovered in the Carribean tunicate _Ecteinascidia turbinata_ and now produced synthetically. Trabectedin has a unique mechanism of action. It binds to the minor groove of DNA interfering with cell division and genetic transcription processes and DNA repair machinery. It is approved for use in Europe, Russia and South Korea for the treatment of advanced soft tissue sarcoma. It is currently under evaluation for the treatment of breast cancer, prostate cancer, in addition to pediatric sarcomas. Both the European Commission and the U.S. Food and Drug Administration (FDA) have approved trabectedin as an orphan drug in soft tissue sarcomas and ovarian cancer. On October 23, 2015, the FDA approved trabectedin, (as Yondelis), for the treatment of specific soft tissue sarcomas. Indicated for treatment of advanced soft tissue sarcoma in patients refractory to or unsuitable to receive anthracycline or ifosfamide chemotherapy in Europe, Russia and South Korea. Approved for orphan drug status by the U.S. FDA for treatment of soft tissue sarcomas and ovarian cancer. Investigated for use/treatment in cancer/tumors (unspecified), gastric cancer, ovarian cancer, pediatric indications, sarcoma, and solid tumors. Two of the rings in the drug's structure allows it to covalently bind to the minor groove of DNA. The third ring protrudes from the DNA which lets it interact with nearby nuclear proteins. This has the additive effect of blocking cell division at the G2 phase. Trabectedin interacts with the minor groove of DNA and alkylates guanine at the N2 position, which bends towards the major groove. In this manner, it is thought that the drug affects various transcription factors involved in cell proliferation, particularly via the transcription-coupled nucleotide excision repair system. Trabectedin blocks the cell cycle at the G2 phase, while cells at the G1 phase are most sensitive to the drug. It also inhibits overexpression of the multidrug resistance-1 gene (MDR-1) coding for the P-glycoprotein that is a major factor responsible for cells developing resistance to cancer drugs. The agent is also thought to interfere with the nucleotide excision repair pathways of cancer cells, suggesting that it could be effective in the treatment of many cancer types including melanoma and sarcoma, as well as lung, breast, ovarian, endometrial and prostate cancers; clinical evaluations are underway in these indications.",The molecular weight is 761.84.,Trabectedin has a topological polar surface area of 168.72.,The log p value of  is 2.76.,Trabectedin is approved and investigational.,Trabectedin is a solid.,True
14613,A non-steroidal anti-inflammatory drug approved for use in Japan in 1993.,The molecular weight is 298.36.,Zaltoprofen has a topological polar surface area of 54.37.,The log p value of  is 3.5.,Zaltoprofen is experimental.,Zaltoprofen is a solid.,True
14614,"Ketobemidone is a powerful opioid analgesic. It also has some NMDA-antagonist properties. This makes it useful for some types of pain that don't respond well to other opioids. The most commonly cited equalisation ratio for analgesic doses is 25 mg of ketobemidone hydrobromide to 60 mg of morphine hydrochloride or sulfate and circa 8 mg of ketobemidone by injection. For the treatment of all types of severe pain, such as postoperative, cancer, kidney stones and fractures. Ketobemidone (Cliradon, Ketogan, Ketodur, Cymidon, Ketorax, &amp;c.) is a powerful opioid analgesic. It also has some NMDA-antagonist properties. This makes it useful for some types of pain that don't respond well to other opioids. The most commonly cited equalisation ratio for analgesic doses is 25 mg of ketobemidone hydrobromide to 60 mg of morphine hydrochloride or sulfate and circa 8 mg of ketobemidone by injection.",The molecular weight is 247.34.,Ketobemidone has a topological polar surface area of 40.54.,The log p value of  is 1.17.,Ketobemidone is investigational.,Ketobemidone is a solid.,True
14615,Seratrodast (INN) is a thromboxane receptor antagonist used primarily in the treatment of asthma.,The molecular weight is 354.45.,Seratrodast has a topological polar surface area of 71.44.,The log p value of  is 4.95.,Seratrodast is experimental.,Seratrodast is a solid.,True
14616,"Dexketoprofen is a non-steroidal anti-inflammatory drug. It is available in the various countries in Europe, Asia and Latin America. It has analgesic, antipyretic and anti-inflammatory properties. For short-term treatment of mild to moderate pain, including dysmenorrhoea, musculoskeletal pain and toothache.  This drug is an isomer of ketoprofen.  Dexketoprofen a propionic acid derivative with analgesic, anti-inflammatory, and antipyretic properties.   It is a non-steroidal anti-inflammatory drug (NSAID) that reduces prostaglandin synthesis via inhibition of cyclooxygenase pathway (both COX-1 and COX-2) activity.",The molecular weight is 254.28.,Dexketoprofen has a topological polar surface area of 54.37.,The log p value of  is 2.76.,Dexketoprofen is approved and investigational.,Dexketoprofen is a solid.,True
14617,"Talniflumate, is an anti-inflammatory molecule studied and used as a mucin regulator in the treatment of cystic fibrosis, chronic obstructive pulmonary disease (COPD) and asthma. In addition, it is used in inflammatory conditions such as rheumatoid arthritis. Phase I trials with talniflumate for the treatment of cystic fibrosis and COPD were completed in August 2001, and phase II trials were performed in Ireland for the treatment of cystic fibrosis but this research has now been discontinued. Talniflumate has been approved for approximately 20 years in Argentina other countries (excluding the United States, Europe, and Japan). Talnifumate is a phthalidyl ester of nifumic acid, which has potent analgesic and anti-inflammatory effects and is widely used to treat inflammatory disorders, such as rheumatoid arthritis and osteoarthritis , and has also been studied for the management of cystic fibrosis. Talniflumate is metabolized to its prodrug, niflumic acid, which has several pharmacodynamic effects. Firstly, it blocks synthesis of mucin. Secondly, talniflumate blocks prostaglandin synthesis by cyclooxygenases, which aids in pain and inflammation management. Talniflumate is a strong and selective inhibitor of core mucin-synthesizing enzyme GCNT3 (core 2 b-1,6 N-acetylglucosaminyltransferase). Talniflumate decreases gene expression of GCNT3 and production of mucins in vivo and in vitro. Talniflumate improves response of pancreatic tumors to gefitinib (chemotherapy drug). Talniflumate is a strong calcium-activated chloride channel (CaCC) blocker.",The molecular weight is 414.34.,Talniflumate has a topological polar surface area of 77.52.,The log p value of  is 4.93.,Talniflumate is experimental.,Talniflumate is a solid.,True
14618,Candesartan is an angiotensin-receptor blocker (ARB) that may be used alone or with other agents to treat hypertension. It is available as a prodrug in the form of.,,,,Candesartan is experimental.,Candesartan is a solid.,True
14619,"Human recombinant antihemophilic factor (AHF) or Factor VIII, 2332 residues, glycosylated, produced by CHO cells For the treatment of hemophilia A, von Willebrand disease and Factor XIII deficiency. Antihemophilic Factor binds factor IXa along with calcium and phospholipid, This complex converts factor X to factor Xa to facilitate clotting cascade. Antihemophilic factor (AHF) is a protein found in normal plasma which is necessary for clot formation. The administration of AHF provides an increase in plasma levels of AHF and can temporarily correct the coagulation defect of patients with hemophilia A (classical hemophilia).",,,,"Antihemophilic factor, human recombinant is approved and investigational.","Antihemophilic factor, human recombinant is a solid.",True
14620,"Betrixaban is a non-vitamin K oral anticoagulant whose action is driven by the competitive and reversible inhibition of the factor Xa. It was selected among all lead compounds due to its low hERG channel affinity while sustaining its factor Xa inhibition capacity. Betrixaban, now developed by Portola Pharmaceuticals Inc., is prescribed as a venous thromboembolism (VTE) prophylactic for adult patients with moderate to severe restricted motility or with other risks for VTE. VTE can be manifested as deep vein thrombosis or pulmonary embolism and it is a leading cause of preventable death in hospitalized patients. Betrixaban is indicated for prophylaxis of venous thromboembolism (VTE) in conditions of moderate to severe restricted mobility or in patients that qualify as in risk of VTE.  Betrixaban is an oral anticoagulant that excerts its action by preventing thrombin generation without having a direct effect on platelet aggregation. Betrixaban is a cofactor-independent direct inhibitor of the Factor Xa and inhibits free and prothrombinase-bound Factor Xa.",The molecular weight is 451.91.,Betrixaban has a topological polar surface area of 107.41.,The log p value of  is 3.61.,Betrixaban is approved and investigational.,Betrixaban is a solid.,True
14621,"For the treatment of hemophilia A, von Willebrand disease and Factor XIII deficiency. Antihemophilic Factor binds factor IXa along with calcium and phospholipid, This complex converts factor X to factor Xa to facilitate clotting cascade. Antihemophilic factor (AHF) is a protein found in normal plasma which is necessary for clot formation. The administration of AHF provides an increase in plasma levels of AHF and can temporarily correct the coagulation defect of patients with hemophilia A (classical hemophilia).",,,,Lonoctocog alfa is approved and investigational.,,True
14622,"Moroctocog alfa, also known as BDDrFVIII (B domain deleted recombinant factor VIII), is a recombinant DNA-based drug with functional characteristics comparable to those of endogenous coagulation Factor VIII, the essential human blood clotting protein that is impaired in Hemophilia A. Moroctocog alfa is identical in sequence to endogenously produced Factor VIII, but does not contain the B-domain, which has no known biological function. Moroctocog alfa is produced through recombinant DNA technology and purification, resulting in a 1438 amino acid, 170 kDa protein. Clinical evaluation has shown that BDDrFVIII is pharmacokinetically equivalent to full-length recombinant FVIII. Moroctocog Alfa is approved by Health Canada for the control and prevention of hemorrhagic episodes and for routine and surgical prophylaxis in patients with hemophilia A (congenital factor VIII deficiency or classic hemophilia). Antihemophilic Factor binds factor IXa along with calcium and phospholipid, which converts factor X to factor Xa to facilitate the clotting cascade.  Antihemophilic factor (AHF) is a protein found in normal plasma which is necessary for clot formation. The administration of AHF provides an increase in plasma levels of AHF and can temporarily correct the coagulation defect of patients with hemophilia A (classical hemophilia). As factor VIII is the specific clotting factor deficient in patients with hemophilia A, replacement of clotting factor with Moroctocog alfa, also known as BDDrFVIII (B domain deleted recombinant factor VIII), is the cornerstone of the prevention and treatment of bleeding for this disorder. ",,,,Moroctocog alfa is approved.,Moroctocog alfa is a solid.,True
14623,"Prasterone, also known as dehydroepiandrosterone (DHEA) is a major C19 steroid produced by the adrenal cortex. It is also produced in small quantities in the testis and the ovary. Dehydroepiandrosterone (DHEA) can be converted to testosterone; androstenedione; estradiol; and estrone. Most of DHEA is sulfated (dehydroepiandrosterone sulfate) before secretion. DHEA is taken as a supplement for a variety of unsubstantiated indications. The following indications have shown promise and are backed up by some scientific evidence: schizophrenia (DHEA may be more effective in women than men); improving the appearance of older people’s skin (taking DHEA by mouth seems to increase skin thickness and moisture, and decrease facial “age spots” in elderly men and women); improving ability to achieve an erection in men with sexual dysfunction. Additionally, DHEA has shown promise in improving symptoms of lupus (SLE). Taking DHEA by mouth along with conventional treatment may help reduce the number of times symptoms flare up and may allow a reduction in the dose of prescription drugs needed. DHEA may also help SLE symptoms such as muscle ache and mouth ulcers. DHEA also seems to strengthen bones in SLE patients being treated with high-dose steroids (corticosteroids). DHEA is naturally produced from cholesterol through two cytochrome P450 enzymes. Cholesterol is converted to pregnenolone by the enzyme P450 scc (side chain cleavage); then another enzyme, CYP17A1, converts pregnenolone to 17α-Hydroxypregnenolone and then to DHEA. DHEA is increased by exercise and calorie restriction. Some theorize that the increase in endogenous DHEA brought about by calorie restriction is partially responsible for the longer life expectancy known to be associated with calorie restriction. DHEA can be understood as a prohormone for the sex steroids. DHEAS may be viewed as buffer and reservoir. As most DHEA is produced by the zona reticularis of the adrenal cortex, it is argued that there is a role in the immune and stress response. DHEAS/DHEA are useful to detect excess adrenal activity as seen in adrenal cancer or hyperplasia, including certain forms of congenital adrenal hyperplasia as it is produced nearly entirely by the adrenal glands. Women with polycystic ovary syndrome tend to have elevated levels of DHEAS.",The molecular weight is 288.43.,Prasterone has a topological polar surface area of 37.3.,The log p value of  is 3.07.,Prasterone is approved and investigational and nutraceutical.,Prasterone is a solid.,True
14624,"Tibolone is a synthetic steroid hormone drug, which is mainly non-selective in its binding profile, acting as an agonist primarily at estrogen receptors (ER), with a preference for ER alpha. For the relief of post-menopausal symptoms and for the prevention of osteoporosis. Tibolone prevents bone loss and treating post-menopausal symptoms without stimulating the endometrial tissues, which may lead to malignancy. Typical, drugs that treat post-menopausal symptoms such as estrogen, have a proliferative effect on the endometrium, increasing the risk of endometrial carcinoma. The effects on the bone, brain and vaginal tissues can be explained by the estrogenic activity of tibolone. It is important to note that activity is not expressed in the endometrium. Tibolone behaves differently from estrogen plus progesterone combinations on the breast. Therefore, tibolone can be characterized as a selective estrogen activity regulator. This drug's effects are owed to the activity of its metabolites in various tissues.",The molecular weight is 312.45.,Tibolone has a topological polar surface area of 37.3.,The log p value of  is 2.97.,Tibolone is approved and investigational.,Tibolone is a solid.,True
14625,"Corticotropin (ACTH or adrenocorticotropic hormone) is a polypeptide hormone produced and secreted by the pituitary gland. It is an important player in the hypothalamic-pituitary-adrenal axis. For use as a diagnostic agent in the screening of patients presumed to have adrenocortical insufficiency. Corticotropin acts through the stimulation of cell surface ACTH receptors, which are primarily located on the adrenocortical cells. Corticotropin stimulates the cortex of the adrenal gland and boosts the synthesis of corticosteroids, mainly glucocorticoids but also sex steroids (androgens). Corticotropin is also related to the circadian rhythm in many organisms. As a diagnostic aid (adrenocortical function), corticotropin combines with a specific receptor on the adrenal cell plasma membrane. In patients with normal adrenocortical function, it stimulates the initial reaction involved in the synthesis of adrenal steroids (including cortisol, cortisone, weak androgenic substances, and a limited quantity of aldosterone) from cholesterol by increasing the quantity of cholesterol within the mitochondria. Corticotropin does not significantly increase serum cortisol concentrations in patients with primary adrenocortical insufficiency (Addison's disease). The mechanism of action of corticotropin in the treatment of infantile myoclonic seizures is unknown.",,,,Corticotropin is approved and investigational and vet_approved.,Corticotropin is a solid.,True
14626,"Each year it is estimated there are 45,000 snakebites in the US and 300,000 to 400,000 bites worldwide. About 8000 of these snakebites involve venomous snake species. The majority of people bitten are males and about 50% occur in the age group of 18 to 28. CROFAB is indicated for the management of adult and pediatric patients with North American crotalid envenomation. The term crotalid is used to describe the Crotalinae subfamily (formerly known as Crotalidae) of venomous snakes which includes rattlesnakes, copperheads and cottonmouths/water moccasins. Crotalus atrox venom contains agents that render human fibrinogen and plasma incoagulable by thrombin.  CROFAB antivenom reverses these effects. CROFAB consists of venom-specific Fab fragments of immunoglobulin G (IgG) that work by binding to and neutralizing venom toxins, facilitating their redistribution away from target tissues and their elimination from the body.",,,,Crotalus atrox antivenin is approved and experimental.,,True
14627,"Each year it is estimated there are 45,000 snakebites in the US and 300,000 to 400,000 bites worldwide. About 8000 of these snakebites involve venomous snake species. The majority of people bitten are males and about 50% occur in the age group of 18 to 28. Indicated for North American crotalid envenomation by Crotalinae rattlesnakes (eg, cottonmouths/water moccasins, copperheads, rattlesnakes) ,. CROFAB consists of venom-specific Fab fragments of immunoglobulin G (IgG) that work by binding to and neutralizing venom toxins, facilitating their redistribution away from target tissues and their elimination from the body.",,,,Crotalus adamanteus antivenin is approved and experimental.,,True
14628,"An antineoplastic compound which also has antimetabolite action. The drug is used in the therapy of acute leukemia. For remission induction and remission consolidation treatment of acute nonlymphocytic leukemias. Thioguanine is an antineoplastic anti-metabolite used in the treatment of several forms of leukemia including acute nonlymphocytic leukemia. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA. They prevent these substances becoming incorporated in to DNA during the \S\"" phase (of the cell cycle), stopping normal development and division. Thioguanine was first synthesized and entered into clinical trial more than 30 years ago. It is a 6-thiopurine analogue of the naturally occurring purine bases hypoxanthine and guanine. Intracellular activation results in incorporation into DNA as a false purine base. An additional cytotoxic effect is related to its incorporation into RNA. Thioguanine is cross-resistant with mercaptopurine. Cytotoxicity is cell cycle phase-specific (S-phase)."" Thioguanine competes with hypoxanthine and guanine for the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRTase) and is itself converted to 6-thioguanilyic acid (TGMP), which reaches high intracellular concentrations at therapeutic doses. TGMP interferes with the synthesis of guanine nucleotides by its inhibition of purine biosynthesis by pseudofeedback inhibition of glutamine-5-phosphoribosylpyrophosphate amidotransferase, the first enzyme unique to the de novo pathway of purine ribonucleotide synthesis. TGMP also inhibits the conversion of inosinic acid (IMP) to xanthylic acid (XMP) by competition for the enzyme IMP dehydrogenase. Thioguanine nucleotides are incorporated into both the DNA and the RNA by phosphodiester linkages, and some studies have shown that incorporation of such false bases contributes to the cytotoxicity of thioguanine. Its tumor inhibitory properties may be due to one or more of its effects on feedback inhibition of de novo purine synthesis; inhibition of purine nucleotide interconversions; or incorporation into the DNA and RNA. The overall result of its action is a sequential blockade of the utilization and synthesis of the purine nucleotides.",The molecular weight is 167.19.,Tioguanine has a topological polar surface area of 79.09.,The log p value of  is -1.7.,Tioguanine is approved.,Tioguanine is a solid.,True
14629,"An essential amino acid that is necessary for normal growth in infants and for nitrogen balance in adults. It is a precursor of indole alkaloids in plants. It is a precursor of serotonin (hence its use as an antidepressant and sleep aid). It can be a precursor to niacin, albeit inefficiently, in mammals. Tryptophan may be useful in increasing serotonin production, promoting healthy sleep, managing depression by enhancing mental and emotional well-being, managing pain tolerance, and managing weight. Tryptophan is critical for the production of the body's proteins, enzymes and muscle tissue. It is also essential for the production of niacin, the synthesis of the neurotransmitter serotonin and melatonin. Tryptophan supplements can be used as natural relaxants to help relieve insomnia. Tryptophan can also reduce anxiety and depression and has been shown to reduce the intensity of migraine headaches. Other promising indications include the relief of chronic pain, reduction of impulsivity or mania and the treatment of obsessive or compulsive disorders. Tryptophan also appears to help the immune system and can reduce the risk of cardiac spasms. Tryptophan deficiencies may lead to coronary artery spasms. Tryptophan is used as an essential nutrient in infant formulas and intravenous feeding. Tryptophan is marketed as a prescription drug (Tryptan) for those who do not seem to respond well to conventional antidepressants. It may also be used to treat those afflicted with seasonal affective disorder (a winter-onset depression). Tryptopan serves as the precursor for the synthesis of serotonin (5-hydroxytryptamine, 5-HT) and melatonin (N-acetyl-5-methoxytryptamine). A number of important side reactions occur during the catabolism of tryptophan on the pathway to acetoacetate. The first enzyme of the catabolic pathway is an iron porphyrin oxygenase that opens the indole ring. The latter enzyme is highly inducible, its concentration rising almost 10-fold on a diet high in tryptophan. Kynurenine is the first key branch point intermediate in the pathway. Kynurenine undergoes deamniation in a standard transamination reaction yielding kynurenic acid. Kynurenic acid and metabolites have been shown to act as antiexcitotoxics and anticonvulsives. A second side branch reaction produces anthranilic acid plus alanine. Another equivalent of alanine is produced further along the main catabolic pathway, and it is the production of these alanine residues that allows tryptophan to be classified among the glucogenic and ketogenic amino acids. The second important branch point converts kynurenine into 2-amino-3-carboxymuconic semialdehyde, which has two fates. The main flow of carbon elements from this intermediate is to glutarate. An important side reaction in liver is a transamination and several rearrangements to produce limited amounts of nicotinic acid, which leads to production of a small amount of NAD<sup>+</sup> and NADP<sup>+</sup>.",The molecular weight is 204.23.,Tryptophan has a topological polar surface area of 79.11.,The log p value of  is -1.57.,Tryptophan is approved and nutraceutical and withdrawn.,Tryptophan is a solid.,True
14630,"Omega-3-acid ethyl esters are prescription drugs that contain eicosapentaenoic acid-ethyl ester (EPA) and docosahexaenoic acid-ethyl ester (DHA) that are used in combination with changes in diet to lower triglyceride levels in adults with severe (≥ 500 mg/dL) hypertriglyceridemia. Omega-3-acid ethyl esters are currently marketed in the US, EU, and many other regions under the brand name Lovaza. Omega-3-Acid Ethyl Esters capsules, USP are indicated as an adjunct to diet to reduce triglyceride (TG) levels in adult patients with severe (≥500 mg/dL) hypertriglyceridemia (HTG). Omega-3-acid ethyl esters reduce triglyceride production, increase fatty acid metabolism, inhibit the release of fatty acids, increase triglyceride clearance, and decrease production of very low density lipoprotein cholesterol(VLDL-C). Omega-3-acid ethyl esters reduce triglyceride production by the liver but this mechanism is not well understood. Omega-3-acid ethyl esters inhibit acyl-CoA:1,2-diacylglycerol acyltransferase, reducing triglyceride synthesis and increasing paroxysmal beta-oxidation, which increases fatty aside metabolism. Omega-3-acid ethyl esters also inhibit the release of fatty acids by competing for enzymes involved in the synthesis of triglycerides, increase triglyceride clearance by increasing the activity of lipoprotein lipase, and decrease production of VLDL-C.",,,,Omega-3-acid ethyl esters is approved and investigational.,Omega-3-acid ethyl esters is a liquid.,True
14631,"Spermine is a spermidine-derived biogenic polyamine found as a polycation at all pH values. Found in various tissues and organisms, it often acts as an essential growth factor in some bacterial species. Spermine is associated with nucleic acids, particularly in viruses, and is thought to stabilize the helical structure. For nutritional supplementation, also for treating dietary shortage or imbalance Spermine is a polyamine. It is an organic molecule that is involved in cellular metabolism. Spermine is derived from spermidine by spermine synthase. Spermine is a polyamine, a small organic cations that is absolutely required for eukaryotic cell growth. Spermine, is normally found in millimolar concentrations in the nucleus. Spermine functions directly as a free radical scavenger, and forms a variety of adducts that prevent oxidative damage to DNA. Oxidative damage to DNA by reactive oxygen species is a continual problem that cells must guard against to survive. Hence, spermine is a major natural intracellular compound capable of protecting DNA from free radical attack. Spermine is also implicated in the regulation of gene expression, the stabilization of chromatin, and the prevention of endonuclease-mediated DNA fragmentation.",,,,Spermine is experimental and nutraceutical.,Spermine is a solid.,True
14632,"Adenylic acid. Adenine nucleotide containing one phosphate group esterified to the sugar moiety in the 2&#39;-, 3&#39;-, or 5&#39;-position. For nutritional supplementation, also for treating dietary shortage or imbalance Adenosine monophosphate, also known as 5'-adenylic acid and abbreviated AMP, is a nucleotide that is found in RNA. It is an ester of phosphoric acid with the nucleoside adenosine. AMP consists of the phosphate group, the pentose sugar ribose, and the nucleobase adenine. AMP is used as a dietary supplement to boost immune activity, and is also used as a substitute sweetener to aid in the maintenance of a low-calorie diet. Nucleotides such as Adenosine-5'-Monophosphate affect a number of immune functions, including the reversal of malnutrition and starvation-induced immunosuppression, the enhancement of T-cell maturation and function, the enhancement of natural killer cell activity, the improvement of delayed cutaneous hypersensitivity, helping resistance to such infectious agents as Staphylococcus aureus and Candida albicans, and finally the modulation of T-cell responses toward type 1 CD4 helper lymphocytes or Th1 cells. Studies have shown that mice fed a nucleotide-free diet have both impaired humoral and cellular immune responses. The addition of dietary nucleotides normalizes both types of responses. RNA, a delivery form of nucleotides, and ribonucleotides were used in these studies. The mechanism of the immune-enhancing activity of nucleic acids/nucleotides is not clear.",The molecular weight is 347.22.,Adenosine phosphate has a topological polar surface area of 186.07.,The log p value of  is -4.08.,Adenosine phosphate is approved and investigational and nutraceutical.,Adenosine phosphate is a solid.,True
14633,"Schizophrenia is a complex mental illness and impacts approximately 1% of the population. Although there are several antipsychotics including , and available for clinical use, they are generally accompanied by significant metabolic and/or neurological adverse effects. Lumateperone is approved for the treatment of schizophrenia in adults. Lumateperone, also known as ITI-007, is an atypical antipsychotic that has proven to be effective in the treatment of schizophrenia. Lumateperone's receptor binding profile is unique, allowing it to target schizophrenia related symptoms while minimizing adverse effects. In contrast to other second generation antipsychotics such as and , lumateperone behaves as a partial agonist and as an antagonist at pre and postynaptic dopamine (D2) receptors respectively. There is much to learn about the pathophysiology of schizophrenia; however, dopamine abnormalities, specifically in the prefrontal and mesolimbic brain regions, are consistent in people with schizophrenia. In addition to dopamine, other neurotransmitters such as serotonin, glutamate, GABA and acetylcholine are thought to play a role. ",,,,Lumateperone is approved and investigational.,Lumateperone is a solid.,True
14634,"Nitric oxide or Nitrogen monoxide is a chemical compound with chemical formula NO. This gas is an important signaling molecule in the body of mammals including humans and is an extremely important intermediate in the chemical industry. It is also a toxic air pollutant produced by automobile engines and power plants. For the treatment of term and near-term (&gt;34 weeks) neonates with hypoxic respiratory failure Persistent pulmonary hypertension of the newborn (PPHN) occurs as a primary developmental defect or as a condition secondary to other diseases such as meconium aspiration syndrome (MAS), pneumonia, sepsis, hyaline membrane disease, congenital diaphragmatic hernia (CDH), and pulmonary hypoplasia. In these states, pulmonary vascular resistance (PVR) is high, which results in hypoxemia secondary to right-to-left shunting of blood through the patent ductus arteriosus and foramen ovale. In neonates with PPHN, Nitric oxide improves oxygenation (as indicated by significant increases in PaO2). Nitric oxide appears to increase the partial pressure of arterial oxygen (PaO2) by dilating pulmonary vessels in better entilated areas of the lung, redistributing pulmonary blood flow away from lung regions with low ventilation/perfusion (V/Q) ratios toward regions with normal ratios. Nitric oxide is a compound produced by many cells of the body. It relaxes vascular smooth muscle by binding to the heme moiety of cytosolic guanylate cyclase, activating guanylate cyclase and increasing intracellular levels of cyclic guanosine 3',5'-monophosphate, which then leads to vasodilation. When inhaled, nitric oxide produces pulmonary vasodilation.",The molecular weight is 30.01.,Nitric Oxide has a topological polar surface area of 34.14.,,Nitric Oxide is approved.,Nitric Oxide is a liquid.,True
14635,"Nitroglycerin is a vasodilator drug used for the treatment of chest pain and high blood pressure. It was first approved in 2000 and is currently marketed by Pfizer, and other companies, depending on the dosage form. Nitroglycerin is available in various forms, including a spray form, sublingual tablet form, intravenous form, extended-release tablet form, and transdermal form. A less commonly known fact is that in addition to treating angina, nitroglycerin is also used in an ointment to treat the pain that accompanies anal fissures. The rectal ointment form of nitroglycerin was approved by the FDA in 1955. Nitroglycerin is indicated for various purposes. It is indicated to prevent and treat angina or chest pain due to cardiovascular disease, as well as to treat peri-operative hypertension or induce intra-operative hypotension. It is also indicated to treat acute heart failure in patients with myocardial infarction. In the ointment form, nitroglycerin is indicated to treat pain caused by anal fissures. The transdermal form is applied directly to the skin to prevent acute anginal attacks.  Nitroglycerin causes the relaxation of vascular smooth muscles, causing arteriolar and venous dilatation. It reduces cardiac preload and afterload and reduces coronary artery spasm, decreasing systemic vascular resistance as well as systolic and diastolic blood pressure. The reduction of cardiac work by nitroglycerin is thought to cause the most relief of anginal symptoms, with some contributions from arteriolar dilatation effects. Nitroglycerin is converted by mitochondrial aldehyde dehydrogenase (mtALDH) to nitric oxide (NO), an active substance which then activates the enzyme guanylate cyclase. The activation of this enzyme is followed by the synthesis of cyclic guanosine 3',5'-monophosphate (cGMP), activating a cascade of protein kinase-dependent phosphorylation events in smooth muscles. This process eventually leads to the dephosphorylation of the myosin light chain of smooth muscles, causing relaxation and increased blood flow in veins, arteries and cardiac tissue.. The above processes lead to decreased work of the heart decreased blood pressure, relief of anginal symptoms, and increased blood flow to the myocardium.One in vitro study using mouse aorta suggests that nitric oxide (an activated metabolite of nitroglycerin) targets the natriuretic peptide receptors. ",The molecular weight is 227.08.,Nitroglycerin has a topological polar surface area of 165.15.,The log p value of  is -5.76.,Nitroglycerin is approved and investigational.,Nitroglycerin is a liquid.,True
14636,"Amyl Nitrite is an antihypertensive medicine. Amyl nitrite is employed medically to treat heart diseases such as angina and to treat cyanide poisoning. Its use as a prescription medicine comes from its ability to lower blood pressure. As an inhalant, it also has psychoactive effect which has led to illegal drug use. For the rapid relief of angina pectoris. Amyl nitrite, in common with other alkyl nitrites, is a potent vasodilator. It expands blood vessels, resulting in lowering of the blood pressure. Alkyl nitrite functions as a source of nitric oxide, which signals for relaxation of the involuntary muscles. Adverse effects are related to this pharmacological activity and include hypotension, headache, flushing of the face, tachycardia, dizziness, and relaxation of involuntary muscles, especially the blood vessel walls and the anal sphincter. Amyl nitrite's antianginal action is thought to be the result of a reduction in systemic and pulmonary arterial pressure (afterload) and decreased cardiac output because of peripheral vasodilation, rather than coronary artery dilation. Amyl nitrite is a source of nitric oxide, which accounts for the mechanism described above. As an antidote (to cyanide poisoning), amyl nitrite promotes formation of methemoglobin, which combines with cyanide to form nontoxic cyanmethemoglobin.",The molecular weight is 234.3.,Amyl Nitrite has a topological polar surface area of 38.66.,,Amyl Nitrite is approved.,Amyl Nitrite is a liquid.,True
14637,"Pentaerythritol tetranitrate is the nitrate ester of pentaerythritol that possesses explosive properties. When mixed with a plasticizer, this chemical forms a plastic explosive. It is recognized by the FDA to be a coronary vasodilator in the treatment of heart conditions such as angina. Used for the treatment of angina pectoris. Organic nitrate which causes systemic vasodilation, decreasing cardiovascular preload. Pentaerythritol tetranitrate is the lipid soluble polyol ester of nitric acid belonging to the family of _nitro-vasodilators_. Pentaerythritol tetranitrate releases free nitric oxide (NO) after the denitration reaction, which triggers NO-dependent signaling transduction involving soluble _guanylate cyclase (sGC_). Nitric oxide binds reversibly to the ferrous-heme center of sGC, causing conformational change and activating the enzyme. This enzyme activation results in increased cellular concentrations of _cyclic guanosine monophosphate _(cGMP) within the vascular smooth muscle, resulting in vasodilation mediated by cGMP-dependent protein kinases. Additionally, this agent causes dose-dependent arterial and venous bed.",The molecular weight is 316.14.,Pentaerythritol tetranitrate has a topological polar surface area of 220.2.,The log p value of  is -3.85.,Pentaerythritol tetranitrate is approved.,Pentaerythritol tetranitrate is a solid.,True
14638,"Ulesfia (benzyl alcohol) lotion is indicated for the topical treatment of head lice infestation in patients 6 months of age and older. Ulesfia Lotion does not have ovicidal activity. Benzyl alcohol inhibits lice from closing their respiratory spiracles, allowing the vehicle to obstruct the spiracles and causing the lice to asphyxiate.",The molecular weight is 108.14.,Benzyl alcohol has a topological polar surface area of 20.23.,The log p value of  is 1.1.,Benzyl alcohol is approved.,Benzyl alcohol is a liquid.,True
14639,"Paraldehyde was initially introduced into medical practice in the United Kingdom in 1882 by the Italian physician Vincenzo Cervello. It is classified as a central nervous system (CNS) depressant and has also been found to be an effective anticonvulsant, hypnotic and sedative agent due to its CNS depressant properties. Paraldehyde is used as an ingredient in some cough medicines as an expectorant, but its efficacy for this indication has not been confirmed and its use as an expectorant may possibly be due to a placebo effect. Paraldehyde was used historically as a sedative and hypnotic. It has been used in the treatment of seizures as an anticonvulsant. Paraldehyde blocks neuromuscular transmission. Paraldehyde is believed to reduce the release of acetylcholine in response to neuronal depolarization. The exact mechanism of this effect is unknown.",The molecular weight is 132.16.,Paraldehyde has a topological polar surface area of 27.69.,The log p value of  is 1.07.,Paraldehyde is approved and investigational.,Paraldehyde is a liquid.,True
14640,"A thiourea antithyroid agent. Propythiouracil inhibits the synthesis of thyroxine and inhibits the peripheral conversion of throxine to tri-iodothyronine. It is used in the treatment of hyperthyroidism. (From Martindale, The Extra Pharmacopeoia, 30th ed, p534) Used to manage hyperthyroidism which is due to an overactive thyroid gland (Grave's disease). Propylthiouracil is a thiourea antithyroid agent. Grave's disease is the most common cause of hyperthyroidism. It is an autoimmune disease where an individual's own antibodies attach to thyroid stimulating hormone receptors within cells of the thyroid gland and then trigger overproduction of thyroid hormone. The two thyroid hormones manufactured by the thyroid gland, thyroxine (T4) and triiodothyronine (T3), are formed by combining iodine and a protein called thyroglobulin with the assistance of an enzyme called peroxidase. PTU inhibits iodine and peroxidase from their normal interactions with thyroglobulin to form T4 and T3. This action decreases thyroid hormone production. PTU also interferes with the conversion of T4 to T3, and, since T3 is more potent than T4, this also reduces the activity of thyroid hormones. The actions and use of propylthiouracil are similar to those of methimazole. Propylthiouracil binds to thyroid peroxidase and thereby inhibits the conversion of iodide to iodine. Thyroid peroxidase normally converts iodide to iodine (via hydrogen peroxide as a cofactor) and also catalyzes the incorporation of the resulting iodide molecule onto both the 3 and/or 5 positions of the phenol rings of tyrosines found in thyroglobulin. Thyroglobulin is degraded to produce thyroxine (T4) and tri-iodothyronine (T3), which are the main hormones produced by the thyroid gland. Therefore propylthiouracil effectively inhibits the production of new thyroid hormones.",The molecular weight is 170.23.,Propylthiouracil has a topological polar surface area of 41.13.,The log p value of  is 0.97.,Propylthiouracil is approved and investigational.,Propylthiouracil is a solid.,True
14641,"One of the catecholamine neurotransmitters in the brain. It is derived from tyrosine and is the precursor to norepinephrine and epinephrine. Dopamine is a major transmitter in the extrapyramidal system of the brain, and important in regulating movement. A family of receptors (receptors, dopamine) mediate its action. For the correction of hemodynamic imbalances present in the shock syndrome due to myocardial infarction, trauma, endotoxic septicemia, open-heart surgery, renal failure, and chronic cardiac decompensation as in congestive failure Dopamine is a natural catecholamine formed by the decarboxylation of 3,4-dihydroxyphenylalanine (DOPA). It is a precursor to norepinephrine in noradrenergic nerves and is also a neurotransmitter in certain areas of the central nervous system, especially in the nigrostriatal tract, and in a few peripheral sympathetic nerves. Dopamine produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility. This is accomplished directly by exerting an agonist action on beta-adrenoceptors and indirectly by causing release of norepinephrine from storage sites in sympathetic nerve endings. Dopamine is a precursor to norepinephrine in noradrenergic nerves and is also a neurotransmitter in certain areas of the central nervous system. Dopamine produces positive chronotropic and inotropic effects on the myocardium, resulting in increased heart rate and cardiac contractility. This is accomplished directly by exerting an agonist action on beta-adrenoceptors and indirectly by causing release of norepinephrine from storage sites in sympathetic nerve endings. In the brain, dopamine actas as an agonist to the five dopamine receptor subtypes (D!, D2, D3, D4, D5).",The molecular weight is 153.18.,Dopamine has a topological polar surface area of 66.48.,The log p value of  is 0.17.,Dopamine is approved.,Dopamine is a solid.,True
14642,"Corticotropin-releasing factor is studied in the treatment of brain cancer. It is made naturally by the hypothalamus (a part of the brain) and can also be made in the laboratory. Human corticotropin-releasing factor may help reduce symptoms caused by edema (swelling) of the brain. It is a type of neurohormone, also called hCRF. Investigated for use/treatment in brain cancer and neurologic disorders. Corticotropin-releasing factor is produced by neuroendocrine cells in the paraventricular nucleus of the hypothalamus and is released from neurosecretory terminals of these neurons into the primary capillary plexus of the hypothalamo-hypophyseal portal system. The portal system carries the Corticotropin-releasing hormone(CRH) to the anterior lobe of the pituitary where it stimulates the secretion of corticotropin (ACTH) and other biologically active substances.",The molecular weight is 4757.52.,Corticorelin has a topological polar surface area of 1998.99.,,Corticorelin is investigational.,Corticorelin is a solid.,True
14643,"Capsaicin is most often used as a topical analgesic and exists in many formulations of cream, liquid, and patch preparations of various strengths; however, it may also be found in some dietary supplements. Capsaicin is a naturally-occurring botanical irritant in chili peppers, synthetically derived for pharmaceutical formulations. The most recent capsaicin FDA approval was Qutenza, an 8% capsaicin patch dermal-delivery system, indicated for neuropathic pain associated with post-herpetic neuralgia. The capsaicin 8% patch is indicated in the treatment of neuropathic pain associated with post-herpetic neuralgia. There are multiple topical capsaicin formulations available, including creams and solutions, indicated for temporary analgesia in muscle and join pain as well as neuropathic pain.  Capsaicin is a TRPV1 receptor agonist. TRPV1 is a trans-membrane receptor-ion channel complex activated by temperatures higher than 43 degrees Celsius, pH lower than 6, and endogenous lipids. When activated by a combination of these factors, the channel can transiently open and initiate depolarization due to the influx of calcium and sodium ions. Because TRPV1 is commonly expressed in A-delta and mostly C fibers, depolarization results in action potentials which send impulses to the brain and spinal cord. These impulses result in capsaicin effects of warming, tingling, itching, stinging, or burning. Capsaicin also causes more persistent activation of these receptors compared to the environmental agonists, resulting in a loss of response to many sensory stimuli, described as \defunctionalization\"". Capsaicin is associated with many enzymatic, cytoskeletal, and osmotic changes, as well as disruption of mitochondrial respiration, impairing nociceptor function for extended periods of time. "" Capsaicin has been shown to reduce the amount of substance P associated with inflammation - however this is not believed to be its main mechanism in the relief of pain. Capsaicin's mechanism of action is attributed to \defunctionalization\"" of nociceptor fibers by inducing a topical hypersensitivity reaction on the skin. This alteration in pain mechanisms is due to many of the following: temporary loss of membrane potential, inability to transport neurotrophic factors leading to altered phenotype, and reversible retraction of epidermal and dermal nerve fiber terminals. """,The molecular weight is 305.42.,Capsaicin has a topological polar surface area of 58.56.,The log p value of  is 3.75.,Capsaicin is approved.,Capsaicin is a solid.,True
14644,"Sodium oxybate (Xyrem) is a central nervous system depressant used for the treatment of cataplexy and extreme daytime sleepiness (EDS) associated with narcolepsy. It is the sodium salt of gamma hydroxybutyric acid (GHB) which is an endogenous compound and a metabolite of the neurotransmitter GABA. The exact mechanism of action for treating EDS and cataplexy is not known but is is hypothesised that its therapeutic effects are due to GABA(B) effects on noradrenergic, dopaminaergic and thalamocorticol neurons. The drug follows non-linear pharmacokinetics. As it has been associated with misuse/abuse it is strictly controlled and all patients and prescribers must enroll in the sodium oxybate REMs program in order to gain access to the medication. For the treatment of cataplexy and excessive daytime sleepiness (EDS) associated with narcolepsy. Sodium oxybate works through an unknown mechanism to treat narcolepsy by inducing sleep within about 5-15 minutes of administration.  The exact mechanism of action is unknown. It is the sodium salt of the endogenous compound gamma hydroxybutyrate which is a metabolite of the GABA neurotransmitter and it's thought that it's therapeutic effects are mediated via GABA B actions at noradrenergic, dopaminergic and thalamocortical neurons. ",The molecular weight is 126.09.,Sodium oxybate has a topological polar surface area of 60.36.,,Sodium oxybate is approved.,Sodium oxybate is a solid.,True
14645,"A sulfur containing essential amino acid that is important in many body functions. It is a chelating agent for heavy metals. Used for protein synthesis including the formation of SAMe, L-homocysteine, L-cysteine, taurine, and sulfate. L-Methionine is a principle supplier of sulfur which prevents disorders of the hair, skin and nails; helps lower cholesterol levels by increasing the liver's production of lecithin; reduces liver fat and protects the kidneys; a natural chelating agent for heavy metals; regulates the formation of ammonia and creates ammonia-free urine which reduces bladder irritation; influences hair follicles and promotes hair growth. L-methionine may protect against the toxic effects of hepatotoxins, such as acetaminophen. Methionine may have antioxidant activity. The mechanism of the possible anti-hepatotoxic activity of L-methionine is not entirely clear. It is thought that metabolism of high doses of acetaminophen in the liver lead to decreased levels of hepatic glutathione and increased oxidative stress. L-methionine is a precursor to L-cysteine. L-cysteine itself may have antioxidant activity. L-cysteine is also a precursor to the antioxidant glutathione. Antioxidant activity of L-methionine and metabolites of L-methionine appear to account for its possible anti-hepatotoxic activity. Recent research suggests that methionine itself has free-radical scavenging activity by virtue of its sulfur, as well as its chelating ability.",The molecular weight is 149.21.,Methionine has a topological polar surface area of 63.32.,The log p value of  is -1.73.,Methionine is approved and nutraceutical.,Methionine is a solid.,True
14646,"A water-soluble, colorless crystal with an acid taste that is used as a chemical intermediate, in medicine, the manufacture of lacquers, and to make perfume esters. It is also used in foods as a sequestrant, buffer, and a neutralizing agent. (Hawley's Condensed Chemical Dictionary, 12th ed, p1099; McGraw-Hill Dictionary of Scientific and Technical Terms, 4th ed, p1851) For nutritional supplementation, also for treating dietary shortage or imbalance Succinate is an essential component of the Krebs or citric acid cycle and serves an electron donor in the production of fumaric acid and FADH2. It also has been shown to be a good \natural\"" antibiotic because of its relative acidic or caustic nature (high concentrations can even cause burns). Succinate supplements have been shown to help reduce the effects of hangovers by activating the degradation of acetaldehyde - a toxic byproduct of alcohol metabolism - into CO2 and H2O through aerobic metabolism. Succinic acid has been shown to stimulate neural system recovery and bolster the immune system. Claims have also been made that it boosts awareness, concentration and reflexes.""",The molecular weight is 118.09.,Succinic acid has a topological polar surface area of 74.6.,The log p value of  is -0.53.,Succinic acid is approved and nutraceutical.,Succinic acid is a solid.,True
14647,,,,,Pyridoxine phosphate is experimental.,Pyridoxine phosphate is a solid.,False
14648,"Molsidomine is an orally active, long-acting vasodilator, which belongs to the class of medications known as syndnones. Interestingly, it is being studied as being a preventive measure in cerebral infarction. The indications for use of molsidomine include ischemic heart disease, angina, chronic heart failure, and pulmonary hypertension. Molsidomine leads to smooth muscle relaxation in the coronary blood vessels, relieving symptoms of angina and increasing blood flow to the coronary arteries.  Molsidomine, a cardiovascular drug, acts in a similar fashion to organic nitrates. The SIN-1A metabolite of molsidomine has a pharmacologically active group of nitric oxide, which increases levels of cyclic GMP, and decreases intracellular calcium ions in smooth muscle cells. This leads to relaxation of smooth muscle in the blood vessels, and inhibits platelet aggregation.",The molecular weight is 242.24.,Molsidomine has a topological polar surface area of 72.6.,The log p value of  is 1.33.,Molsidomine is approved and investigational.,Molsidomine is a solid.,True
14649,"Prothrombin Complex Concentrate (Human), is indicated for the urgent reversal of acquired coagulation factor deficiency induced by Vitamin K antagonist (VKA, e.g., warfarin) therapy in adult patients with acute major bleeding. For use in the emergency reversal of coagulation factor deficiency in patients receiving vitamin K antagonist therapy. Prothrombin is administered as part of a cocktail containing several coagulation factors.",,,,Prothrombin is approved.,Prothrombin is a liquid.,True
14650,"Dabigatran etexilate is an oral prodrug that is hydrolyzed to the competitive and reversible direct thrombin inhibitor. Dabigatran etexilate may be used to decrease the risk of venous thromboembolic events in patients in whom anticoagulation therapy is indicated. In contrast to warfarin, because its anticoagulant effects are predictable, lab monitoring is not necessary. Dabigatran etexilate was approved by the FDA in 2010. Dabigatran is indicated for the prevention of venous thromboembolic events in patients who have undergone elective hip or knee replacement surgery (based on RE-NOVATE, RE-MODEL, and RE-MOBILIZE trials). In 2010, it was approved in the US and Canada for prevention of stroke and systemic embolism in patients with atrial fibrillation (approval based on the RE-LY trial). Dabigatran directly inhibits thrombin in a concentration-dependent, reversible, specific, and competitive manner which results in a prolongation of aPTT (partial thromboplastin time), ECT (Ecarin clotting time), and TT (thrombin time). Dabigatran is hydrolysed to the active dabigatran by an esterase which induces hydrolysis. Dabigatran and it's glucuronidated metabolites all share equal pharmacological activity. Dabigatran and its metabolites inhibit thrombin, a serine protease. This inhibition prevents the thrombin mediated conversion of fibrinogen to fibrin, an early step in the coagulation cascade. With reduced conversion of fibrinogen to fibrin, clotting time increases.",The molecular weight is 627.75.,Dabigatran etexilate has a topological polar surface area of 151.53.,The log p value of  is 4.71.,Dabigatran etexilate is approved.,Dabigatran etexilate is a solid.,True
14651,"Valine is a branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway. Promotes mental vigor, muscle coordination, and calm emotions. May also be of use in a minority of patients with hepatic encephalopathy and in some with phenylketonuria. L-valine is a branched-chain essential amino acid (BCAA) that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway. Valine is one of three branched-chain amino acids (the others are leucine and isoleucine) that enhance energy, increase endurance, and aid in muscle tissue recovery and repair. This group also lowers elevated blood sugar levels and increases growth hormone production. Supplemental valine should always be combined with isoleucine and leucine at a respective milligram ratio of 2:1:2. It is an essential amino acid found in proteins; important for optimal growth in infants and for growth in children and nitrogen balance in adults. The lack of L-valine may influence the growth of body, cause neuropathic obstacle, anaemia. It has wide applications in the field of pharmaceutical and food industry. (Applies to Valine, Leucine and Isoleucine) <br/>This group of essential amino acids are identified as the branched-chain amino acids, BCAAs. Because this arrangement of carbon atoms cannot be made by humans, these amino acids are an essential element in the diet. The catabolism of all three compounds initiates in muscle and yields NADH and FADH2 which can be utilized for ATP generation. The catabolism of all three of these amino acids uses the same enzymes in the first two steps. The first step in each case is a transamination using a single BCAA aminotransferase, with a-ketoglutarate as amine acceptor. As a result, three different a-keto acids are produced and are oxidized using a common branched-chain a-keto acid dehydrogenase, yielding the three different CoA derivatives. Subsequently the metabolic pathways diverge, producing many intermediates. <br/>The principal product from valine is propionylCoA, the glucogenic precursor of succinyl-CoA. Isoleucine catabolism terminates with production of acetylCoA and propionylCoA; thus isoleucine is both glucogenic and ketogenic. Leucine gives rise to acetylCoA and acetoacetylCoA, and is thus classified as strictly ketogenic. <br/>There are a number of genetic diseases associated with faulty catabolism of the BCAAs. The most common defect is in the branched-chain a-keto acid dehydrogenase. Since there is only one dehydrogenase enzyme for all three amino acids, all three a-keto acids accumulate and are excreted in the urine. The disease is known as Maple syrup urine disease because of the characteristic odor of the urine in afflicted individuals. Mental retardation in these cases is extensive. Unfortunately, since these are essential amino acids, they cannot be heavily restricted in the diet; ultimately, the life of afflicted individuals is short and development is abnormal The main neurological problems are due to poor formation of myelin in the CNS.",The molecular weight is 117.15.,Valine has a topological polar surface area of 63.32.,The log p value of  is -2.29.,Valine is approved and nutraceutical.,Valine is a solid.,True
14652,"Potassium gluconate is a salt of and is classified as a food additive by the FDA. It is also used as a potassium supplement.  Because of potassium’s wide-ranging roles in the body, low intakes can increase the risk of illness. Potassium is an essential nutrient. It is the most abundant cation in intracellular fluid, where it plays a key role in maintaining cell function, especially in excitable cells such as skeletal muscles, the heart, and nerves. Potassium is the most abundant cation (approximately 150 to 160 mEq per liter) within human cells. Intracellular sodium content is relatively low. In the extracellular fluid, sodium predominates and the potassium content is low (3.5 to 5 mEq per liter). A membrane-bound enzyme, sodium-potassium–activated adenosinetriphosphatase (Na +K +ATPase), actively transports or pumps sodium out and potassium into cells to maintain the concentration gradients. The intracellular to extracellular potassium gradients are necessary for nerve impulse signaling in such specialized tissues as the heart, brain, and skeletal muscle, and for the maintenance of physiologic renal function and maintenance of acid-base balance. High intracellular potassium concentrations are necessary for numerous cellular metabolic processes.",The molecular weight is 234.24.,Potassium gluconate has a topological polar surface area of 141.28.,,Potassium gluconate is approved.,Potassium gluconate is a solid.,True
14653,"A basic constituent of lecithin that is found in many plants and animal organs. It is important as a precursor of acetylcholine, as a methyl donor in various metabolic processes, and in lipid metabolism. For nutritional supplementation, also for treating dietary shortage or imbalance This compound is needed for good nerve conduction throughout the CNS (central nervous system) as it is a precursor to acetylcholine (ACh). Choline is also needed for gallbladder regulation, liver function and lecithin (a key lipid) formation. Choline also aids in fat and cholesterol metabolism and prevents excessive fat build up in the liver. Choline has been used to mitigate the effects of Parkinsonism and tardive dyskinesia. Choline deficiencies may result in excessive build-up of fat in the liver, high blood pressure, gastric ulcers, kidney and liver dysfunction and stunted growth. Choline is a major part of the polar head group of phosphatidylcholine. Phosphatidylcholine's role in the maintenance of cell membrane integrity is vital to all of the basic biological processes: information flow, intracellular communication and bioenergetics. Inadequate choline intake would negatively affect all these processes. Choline is also a major part of another membrane phospholipid, sphingomyelin, also important for the maintenance of cell structure and function. It is noteworthy and not surprising that choline deficiency in cell culture causes apoptosis or programmed cell death. This appears to be due to abnormalities in cell membrane phosphatidylcholine content and an increase in ceramide, a precursor, as well as a metabolite, of sphingomyelin. Ceramide accumulation, which is caused by choline deficiency, appears to activate Caspase, a type of enzyme that mediates apoptosis. Betaine or trimethylglycine is derived from choline via an oxidation reaction. Betaine is one of the factors that maintains low levels of homocysteine by resynthesizing L-methionine from homocysteine. Elevated homocysteine levels are a significant risk factor for atherosclerosis, as well as other cardiovascular and neurological disorders. Acetylcholine is one of the major neurotransmitters and requires choline for its synthesis. Adequate acetylcholine levels in the brain are believed to be protective against certain types of dementia, including Alzheimer's disease.",The molecular weight is 104.17.,Choline has a topological polar surface area of 20.23.,The log p value of  is -4.36.,Choline is approved and nutraceutical.,Choline is a liquid.,True
14654,"Choline salicylate is an anti-inflammatory pain reliever agent that is related to aspirin. It is used to decrease swelling and to treat mild-moderate pain. It is used to treat arthritis in both children and adults. This medicine can also be used for fever. The oral gel is indicated for the relief of pain and discomfort of common mouth ulcers, cold sores, denture sore spots, infant teething and mouth ulcers, and sore spots due to orthodontic devices in children. This is an anti-inflammatory and antipyretic medication ,. Choline salicylate relieves pain by inhibition of prostaglandin synthesis and reduces fever by acting on the hypothalamus heat-regulating center. It also inhibits the generation of impulses through the inhibition of cyclooxygenase enzyme (COX) ,. ",,,,Choline salicylate is approved and nutraceutical.,Choline salicylate is a solid.,True
14655,"A potent lipoxygenase inhibitor that interferes with arachidonic acid metabolism. The compound also inhibits formyltetrahydrofolate synthetase, carboxylesterase, and cyclooxygenase to a lesser extent. It also serves as an antioxidant in fats and oils.  Used for the treatment of actinic keratoses (precancerous skin growths that can become malignant if left untreated). Masoprocol is a novel antineoplastic agent. It is not known exactly how masoprocol works. Laboratory experiments have shown that masoprocol prevents cells similar to the ones found in actinic keratoses from multiplying. Masoprocol was withdrawn from the U.S. market in June 1996. Although the exact mechanism of action is not known, studies have shown that masoprocol is a potent 5-lipoxygenase inhibitor and has antiproliferative activity against keratinocytes in tissue culture, but the relationship between this activity and its effectiveness in actinic keratoses is unknown. Masoprocol also inhibits prostaglandins but the significance of this action is not yet known.",The molecular weight is 302.37.,Masoprocol has a topological polar surface area of 80.92.,The log p value of  is 3.92.,Masoprocol is approved and investigational.,Masoprocol is a solid.,True
14656,"Cannabidiol, or CBD, is one of at least 85 active cannabinoids identified within the Cannabis plant. It is a major phytocannabinoid, accounting for up to 40% of the Cannabis plant's extract, that binds to a wide variety of physiological targets of the endocannabinoid system within the body. Although the exact medical implications are currently being investigated, CBD has shown promise as a therapeutic and pharmaceutical drug target. In particular, CBD has shown promise as an analgesic, anticonvulsant, muscle relaxant, anxiolytic, antipsychotic and has shown neuroprotective, anti-inflammatory, and antioxidant activity, among other currently investigated uses. CBD's exact place within medical practice is still currently hotly debated, however as the body of evidence grows and legislation changes to reflect its wide-spread use, public and medical opinion have changed significantly with regards to its usefulness in a number of medical conditions ranging from anxiety to epilepsy. When used in combination with delta-9-tetrahydrocannabinol as the product Sativex, cannabidiol was given a standard marketing authorization (ie. a Notice of Compliance (NOC)) by Health Canada for the following indications:  Although the exact mechanism and magnitude of effects of THC and CBD are not fully understood, CBD has been shown to have analgesic, anticonvulsant, muscle relaxant, anxiolytic, neuroprotective, anti-oxidant, and anti-psychotic activity. This wide variety of effects is likely due to it's complex pharmacological mechanisms. In addition to binding to CB1 and CB2 receptors of the endocannabinoid system, there is evidence that CBD activates 5-HT1A serotonergic and TRPV1–2 vanilloid receptors, antagonizes alpha-1 adrenergic and µ-opioid receptors, inhibits synaptosomal uptake of noradrenaline, dopamine, serotonin and gaminobutyric acid and cellular uptake of anandamide, acts on mitochondria Ca2 stores, blocks low-voltage-activated (T-type) Ca2 channels, stimulates activity of the inhibitory glycine-receptor, and inhibits activity of fatty amide hydrolase (FAAH). The exact mechanism of action of CBD and THC is not currently fully understood. However, it is known that CBD acts on cannabinoid (CB) receptors of the endocannabinoid system, which are found in numerous areas of the body, including the peripheral and central nervous systems, including the brain. The endocannabinoid system regulates many physiological responses of the body including pain, memory, appetite, and mood. More specifically, CB1 receptors can be found within the pain pathways of the brain and spinal cord where they may affect CBD-induced analgesia and anxiolysis, and CB2 receptors have an effect on immune cells, where they may affect CBD-induced anti-inflammatory processes. ",,,,Cannabidiol is approved and investigational.,Cannabidiol is a solid.,True
14657,"Morniflumate is a non-steroidal anti-inflammatory drug with antipyretic properties. It is the morpholinoethyl ester of niflumic acid. In one study, post morniflumate ingestion, physical examination and clinical symptoms of those with bronchitis showed improvement. Morniflumate, given at therapeutic dosages to healthy human volunteers, on leukotriene B4 (LTB4) and thromboxane (TXB2) synthesis, both in purified PMNs (polymorphnuclear neutrophils) and in whole blood. The primary mechanism of niflumic acid and its ester is action is inhibition of enzymes involved in the synthesis of inflammatory prostaglandins. This medication inhibits cyclooxygenase and 5-lipoxygenase pathways, which lead to fever and inflammation. ",The molecular weight is 395.38.,Morniflumate has a topological polar surface area of 63.69.,The log p value of  is 4.71.,Morniflumate is experimental.,Morniflumate is a solid.,True
14658,"Omega-3 fatty acids are polyunsaturated fatty acids (PUFAs) with a double bond at the third carbon atom from the end of the carbon chain. The three types of omega-3 fatty acids involved in human physiology are α-linolenic acid (ALA) (found in plant oils), eicosapentaenoic acid (EPA), and docosahexaenoic acid (DHA) (both commonly found in fish oil that originally come from microalgae that is further consumed by phytoplankton, a source of diet for fish). Omega-3 fatty acids play a critical role in metabolism and cellular function and they are available as daily supplements. On September 8, 2004, the U.S. Food and Drug Administration gave \qualified health claim\"" status to EPA and DHA omega-3 fatty acids. Therapeutic products containing omega-3 fatty acid and its derivatives for treatment of hypertriglyceridemia include Lovaza, Omtryg, Epanova, and Vascepa."" Provided as daily supplements. Aa preparation of omega-3-acid ethyl esters is licensed in UK for prevention of recurrent events after myocardial infarction in addition to treatment of hypertriglyceridaemia.  Omega-3 fatty acids are triglycerides that get broken down into smaller fatty acid units. They act to reduce plasma triglyceride levels however increase the cholesterol levels and are thought to possess potent antiarrythmic effects. Polyunsaturated fatty acids including eicosapentaenoic and docosahexaenoic acid mediate important cellular function such as inhibition of platelet function, prolongation of bleeding time, anti-inflammatory effects and reduction of plasma fibrinogen. Polyunsaturated fatty acids are components of the phospholipids that form the structures of the cell membranes and also serve as energy source. They form eicosanoids which are important signalling molecules with wide-ranging functions in the body's cardiovascular, pulmonary, immune and endocrine systems. DHA tends to exist in high concentrations in the retina, brain (via uptake by Mfsd2a as a transporter), and sperm. Omega-3 fatty acids mediate anti-inflammatory effects and increased levels of EPA or DHA has shown to decrease the levels of PGE2 and 4 series-LT. ",,,,Omega-3 fatty acids is approved and nutraceutical.,,True
14659,"Omega-6 fatty acids are polyunsaturated fatty acids with a final carbon-carbon double bond in the n-6 position, that is, the sixth bond, counting from the methyl end. They are a family of fatty acid molecules that act as precursors to potent lipid mediator signalling molecules with either pro-inflammatory and anti-inflammatory effects. Cells involved in the inflammatory response are typically rich in the n-6 fatty acid arachidonic acid, as generally, eicosanoids derived from n-6 PUFA are pro-inflammatory. Arachidonic acid, which is a main precursor of eicosanoids, is an example of omega-6 (n-6) polyunsaturated fatty acids. Vegetable oil is a major dietary sources of omega-6 fatty acids. There are no current pharmacotherapeutic products based on omega-6 fatty acids.  Omega-6 fatty acids mediate pro-inflammatory effects in the cellular level and compete for the same rate-limiting enzymes with omega-3 fatty acids. Arachidonic acid is converted to inflammatory mediators such as omega-6 prostaglandins and leukotriene eicosanoids during the inflammatory cascade. AA-derived eicosanoids are proinflammatory but they have important homeostatic functions in regulating both the promotion and resolution of inflammation in the immune response. It is reported that high intake of n-6 PUFA, along with low intakes of n-3 PUFA, shifts the physiological state to one that is proinflammatory and prothrombotic with increases in vasospasm, vasoconstriction, and blood viscosity and the development of diseases associated with these conditions. Thus maintaining the balance between 2 polyunsaturated fatty acids is critical in inflammatory cascade regulation.  Linoleic acid is the simplest omega-6 fatty acid that can generate longer n-6 polyunsaturated fatty acids such as eicosanoids, endocannabinoids and lipoxins by the insertion of additional double bonds during consecutive elongation and desaturation mechanisms. It gives rise to arachidonic acid (AA) via γ-linolenic acid (GLA, 18:3n-6) and dihomo-γ-linolenic acid (DGLA, 20:3n-6) and the same set of enzymes can also convert AA to EPA and DHA. The initial rate limiting desaturation of LA to GLA is catalysed by the enzyme delta-6-desaturase (FADS2) and elongation of GLA to DGLA by delta-5-desaturase (FADS1) generates AA. AA is also converted to 2-series prostaglandins (PGD2, PGE2, PGF2, PGI2) andthromboxanes (TXA2, TXB2) by COX-2 activity and 4-series leukotrienes (LTA4, LTB4, LTC4, LTD4, LTE4) by 5-LOX activity. Resulting lipid signalling molecules have various pro-inflammatory effects on target tissues and cells; bronchostriction, fever, pain, increased production of inflammatory cytokines such as TNF-alpha and IL-6, platelet aggregation, vasoconstriction, vascular permeability, chemotaxis of leukocytes, and release of reactive oxygen species by granulocytes. ",,,,Omega-6 fatty acids is nutraceutical.,Omega-6 fatty acids is a solid.,True
14660,"The use of the plant species _Cannabis sativa_ and _Cannabis indica_, popularly known as marijuana, has gained popularity in recent years for the management of a wide variety of medical conditions as a wave of legalization in North America has changed public and medical opinion on its use. Consequently, an expanding body of evidence has begun to emerge that has demonstrated its potential usefulness in the management of conditions such as chronic pain, spasticity, inflammation, epilepsy, and chemotherapy-induced nausea and vomiting among many others. This area of research is controversial and has been heavily debated, however, due to concerns over risks of addiction, long-term health effects, and Cannabis' association with schizophrenia. The primary psychoactive component of Cannabis, delta 9-tetrahydrocannabinol (Δ9-THC), demonstrates its effects through weak partial agonist activity at Cannabinoid-1 (CB1R) and Cannabinoid-2 (CB2R) receptors. This activity results in the well-known effects of smoking cannabis such as increased appetite, reduced pain, and changes in emotional and cognitive processes.",,,,Medical Cannabis is experimental and investigational.,Medical Cannabis is a solid.,True
14661,"Nabiximols (tradename Sativex®) is a whole plant extract from the Cannabis species _Cannabis sativa L._ that has been purified into the active components CBD (cannabidiol) and THC (delta-9-tetrahydrocannabinol). For trademark purposes, purified CBD is branded as Nabidiolex®, while THC is purified as the product Tetrabinex®. Sativex® is available in a 1:1 formulation of THC:CBD as an oro-mucosal pump spray used for treatment of neuropathic pain from Multiple Sclerosis (MS) and for intractable cancer pain. Although still largely debated, Cannabis has been shown to have analgesic, anticonvulsant, muscle relaxant, anxiolytic, neuroprotective, anti-oxidant, and anti-psychotic activity.  In Canada, Sativex has received a Notice of Compliance (NOC) for use as an as adjunctive treatment for symptomatic relief of spasticity in patients with multiple sclerosis (MS) who have not responded adequately to other therapy and who demonstrate meaningful improvement during an initial trial of therapy.  The principal pharmacological effects of THC include analgesic, muscle relaxant, antiemetic, appetite stimulant and psychoactive effects. CBD has analgesic, anticonvulsant, muscle relaxant, anxiolytic, neuroprotective, anti-oxidant and anti-psychotic activity.  The primary psychoactive component of Cannabis, delta 9-tetrahydrocannabinol (Δ9-THC), demonstrates its effects through weak partial agonist activity at Cannabinoid-1 (CB1R) and Cannabinoid-2 (CB2R) receptors. This activity results in the well-known effects of smoking cannabis such as increased appetite, reduced pain, and changes in emotional and cognitive processes. In contrast to THC's weak agonist activity, CBD has been shown to act as a negative allosteric modulator of the cannabinoid CB1 receptor, the most abundant G-Protein Coupled Receptor (GPCR) in the body. Allosteric regulation is achieved through the modulation of receptor activity on a functionally distinct site from the agonist or antagonist binding site. The negative allosteric modulatory effects of CBD are therapeutically important as direct agonists are limited by their psychomimetic effects while direct antagonists are limited by their depressant effects. ",The molecular weight is 628.94.,Nabiximols has a topological polar surface area of 29.46.,,Nabiximols is investigational.,Nabiximols is a solid.,True
14662,"Producing a broad-spectrum activity against several RNA and DNA viruses, Ribavirin is a synthetic guanosine nucleoside and antiviral agent that interferes with the synthesis of viral mRNA. It is primarily indicated for use in treating hepatitis C and viral hemorrhagic fevers. HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. It is reported that ribavirin might be only effective in early stages of viral hemorrhagic fevers including Lasser fever, Crimean-Congo hemorrhagic fever, Venezuelan hemorrhagic fever, and Hantavirus infection. Ribavirin is a prodrug that is metabolized into nucleoside analogs that blocks viral RNA synthesis and viral mRNA capping. Before the development of newer drugs, ribavirin and / dual therapy was considered the first-generation and standard antiviral treatment. The dual therapy was administered for 48 weeks in patients with genotype 1, 4, 5, and 6, and 24 weeks in patients with genotype 2 and 3. Newer drugs developed as Hepatitis C viral infection treatments can be used to reduce or eliminate the use of ribavirin, which are associated with serious adverse effects. They also improve therapeutic efficacy in patients with failed / and ribavirin-based therapy. The potential use of ribavirin as a treatment for acute myeloid leukemia is currently under investigation. Indicated for the treatment of chronic Hepatitis C virus (HCV) infection in combination with other antiviral agents with the intent to cure or achieve a sustained virologic response (SVR). Typically added to improve SVR and reduce relapse rates. Ribavirin mediates direct antiviral activity against a number of DNA and RNA viruses by increasing the mutation frequency in the genomes of several RNA viruses. It is a member of the nucleoside antimetabolite drugs that interfere with duplication of the viral genetic material. The drug inhibits the activity of the enzyme RNA dependent RNA polymerase, due to its resemblence to building blocks of the RNA molecules.  Ribavirin is reported to have several mechanism of actions that lead to inhibition of viral RNA and protein synthesis. ",The molecular weight is 244.21.,Ribavirin has a topological polar surface area of 143.72.,The log p value of  is -2.85.,Ribavirin is approved.,Ribavirin is a solid.,True
14663,"Aldesleukin, a lymphokine, is produced by recombinant DNA technology using a genetically engineered E. coli strain containing an analog of the human interleukin-2 gene. Genetic engineering techniques were used to modify the human IL-2 gene, and the resulting expression clone encodes a modified human interleukin-2. This recombinant form differs from native interleukin-2 in the following ways: a) Aldesleukin is not glycosylated because it is derived from E. coli; b) the molecule has no N-terminal alanine; the codon for this amino acid was deleted during the genetic engineering procedure; c) the molecule has serine substituted for cysteine at amino acid position 125. For treatment of adults with metastatic renal cell carcinoma. Used to treat renal cell carcinoma, Aldesleukin induces the enhancement of lymphocyte mitogenesis and stimulation of long-term growth of human interleukin-2 dependent cell lines, the enhancement of lymphocyte cytotoxicity, the induction of killer cell (lymphokine-activated (LAK) and natural (NK)) activity; and the induction of interferon-gamma production. IL-2 is normally produced by the body, secreted by T cells, and stimulates growth and differentiation of T cell response. It can be used in immunotherapy to treat cancer. It enhances the ability of the immune system to kill tumor cells and may interfere with blood flow to the tumor. Aldesleukin binds to the IL-2 receptor which leads to heterodimerization of the cytoplasmic domains of the IL-2R beta and gamma(c) chains, activation of the tyrosine kinase Jak3, and phosphorylation of tyrosine residues on the IL-2R beta chain. These events led to the creation of an activated receptor complex, to which various cytoplasmic signaling molecules are recruited and become substrates for regulatory enzymes (especially tyrosine kinases) that are associated with the receptor. These events stimulate growth and differentiation of T cells.",,,,Aldesleukin is approved.,Aldesleukin is a liquid.,True
14664,"Sapropterin (tetrahydrobiopterin or BH4) is a cofactor in the synthesis of nitric oxide. It is also essential in the conversion of phenylalanine to tyrosine by the enzyme phenylalanine-4-hydroxylase; the conversion of tyrosine to L-dopa by the enzyme tyrosine hydroxylase; and conversion of tryptophan to 5-hydroxytryptophan via tryptophan hydroxylase. For the treatment of tetrahydrobiopterin (BH4) deficiency. Tetrahydrobiopterin (BH4) is used to convert several amino acids, including phenylalanine, to other essential molecules in the body including neurotransmitters. Tetrahydrobiopterin deficiency can be caused by mutations in GTP cyclohydrolase 1 (GCH1), 6-pyruvoyl-tetrahydropterin synthase/dimerization cofactor of hepatocyte nuclear factor 1 alpha (PCBD1), 6-pyruvoyltetrahydropterin synthase (PTS), and quinoid dihydropteridine reductase (QDPR) genes. These genes make the enzymes that are critical for producing and recycling tetrahydrobiopterin. If one of the enzymes fails to function correctly because of a gene mutation, little or no tetrahydrobiopterin is produced. As a result, phenylalanine from the diet builds up in the bloodstream and other tissues and can damage nerve cells in the brain. High levels of phenylalanine can result in signs and symptoms ranging from temporary low muscle tone to mental retardation, movement disorders, difficulty swallowing, seizures, behavioral problems, progressive problems with development, and an inability to control body temperature. Tetrahydrobiopterin (BH4) is a natural co-factor or co-enzyme for phenylalanine-4-hydroxylase (PAH),Tetrahydrobiopterine, and tryptophan-5-hydroxylase. Tetrahydrobiopterin is also a natural co-factor for nitrate oxide synthase. Therefore BH4 is required for the conversion of phenylalanine to tyrosine, for the production of epinephrine (adrenaline) and the synthesis of the monoamine neuro-transmitters, serotonin, dopamine, and norepinephrine (noradrenaline). It is also involved in apoptosis and other cellular events mediated by nitric oxide production. As a coenzyme, BH4 reacts with molecular oxygen to form an active oxygen intermediate that can hydroxylate substrates. In the hydroxylation process, the co-enzyme loses two electrons and is regenerated in vivo in an NADH-dependent reaction. As a co-factor for PAH, tetrahydrobiopterin allows the conversion of phenylalanine to tyrosine and reduces the level of phenylalanine in the bloodstream, thereby reducing the toxic effects of of this amino acid. Normal serum concentrations of phenylalanine are 100 micomolar, while elevated (toxic) levels are typically >1200 micromolar. Individuals with a deficiency in tetrahydrobiopterin are not able to efficiently convert phenylalanine to tyrosine. The excess levels provided by tetrahydrobiopterin supplementation help improve enzyme efficiency. As a co-factor for tyrosine hydroxylase, BH4 facilitates the conversion of tyrosine to L-dopa while as a co-factor for tryptophan hydroxylase, BH4 allows the conversion of tryptophan to 5-hydroxytryptophan, which is then converted to serotonin.",The molecular weight is 241.25.,Sapropterin has a topological polar surface area of 132.0.,The log p value of  is -1.17.,Sapropterin is approved and investigational.,Sapropterin is a solid.,True
14665,"Clodronic acid is a first generation bisphosphonate similar to and. These drugs were developed to mimic the action of pyrophosphate, a regulator of calcification and decalcification. clodronate’s use has decreased over the years in favor of the third generation, nitrogen containing bisphosphonate , , , and. Clodronic acid is indicated as an adjunct in the management of osteolysis from bone metastases of malignant tumors and for management of hypercalcemia of malignancy. Clodronic acid is a first generation bisphosphonate that inhibits osteoclast mediated bone resorption. It has a wide therapeutic index as a large overdose is required for significant toxicity and a long duration of action due to the slow release from bone. Patients should be counselled regarding the risk of hypocalcemia, hypovolemia, renal insufficiency, transient hyperphosphatemia, and transient hyperparathyroidism. Bisphosphonates are taken into the bone where they bind to hydroxyapatite. Bone resorption by osteoclasts causes local acidification, releasing the bisphosphonate, which is taken into the osteoclast by fluid-phase endocytosis. Endocytic vesicles become acidified, releasing bisphosphonates into the cytosol of osteoclasts where they act.",The molecular weight is 244.88.,Clodronic acid has a topological polar surface area of 115.06.,The log p value of  is -0.14.,Clodronic acid is approved and investigational and vet_approved.,Clodronic acid is a solid.,True
14666,"Used, along with rest and physical therapy, to treat injuries and other painful muscular conditions. Investigated for use in trigeminal neuralgia (tic douloureux), a neuropathic disorder characterized by severe facial pain. Was investigated as a modulator of histamine release. Chlorphenesin is a muscle relaxant. It blocks nerve impulses (or pain sensations) that are sent to the brain.  The mechanism of action of chlorphenesin is not well defined, and its effects are measured mainly by subjective responses. It is known that chlorphenesin acts in the central nervous system (CNS) rather than directly on skeletal muscle.",,,,Chlorphenesin is approved and experimental.,Chlorphenesin is a solid.,True
14667,"Alendronic acid is a third generation bisphosphonate that is used for the treatment of some forms of osteoperosis and Paget's disease. It functions by preventing resorption of bone. Risedronic acid is indicated for the treatment of osteoperosis in men, treatment of Paget's disease, treatment and prevention of osteoperosis in postmenopausal women, and treatment and prevention of glucocorticoid-induced osteoperosis. Risedronate is a pyridine-based bisphosphonate that inhibits bone resorption caused by osteoclasts. Risedronatic acid binds to bone hydroxyapatite. Bone resorption causes local acidification, releasing risedronic acid which is that taken into osteoclasts by fluid-phase endocytosis. Endocytic vesicles are acidified, releasing risedronic acid to the cytosol of osteoclasts where they induce apoptosis through inhbition of farnesyl pyrophosphate synthase. Inhibition of osteoclasts results in decreased bone resorption.",The molecular weight is 283.11.,Risedronic acid has a topological polar surface area of 148.18.,The log p value of  is -2.62.,Risedronic acid is approved and investigational.,Risedronic acid is a solid.,True
14668,"Bumetanide is a sulfamyl diuretic. For the treatment of edema associated with congestive heart failure, hepatic and renal disease including the nephrotic syndrome. Bumetanide is a loop diuretic of the sulfamyl category to treat heart failure. It is often used in patients in whom high doses of furosemide are ineffective. There is however no reason not to use bumetanide as a first choice drug. The main difference between the two substances is in bioavailability. Bumetanide has more predictable pharmacokinetic properties as well as clinical effect. In patients with normal renal function, bumetanide is 40 times more effective than furosemide. Bumetanide interferes with renal cAMP and/or inhibits the sodium-potassium ATPase pump. Bumetanide appears to block the active reabsorption of chloride and possibly sodium in the ascending loop of Henle, altering electrolyte transfer in the proximal tubule. This results in excretion of sodium, chloride, and water and, hence, diuresis.",The molecular weight is 364.42.,Bumetanide has a topological polar surface area of 118.72.,The log p value of  is 3.37.,Bumetanide is approved.,Bumetanide is a solid.,True
14669,"Bromfenac is a nonsteroidal anti-inflammatory drug (NSAID) for ophthalmic use. Ophthalmic NSAIDs are becoming a cornerstone for the management of ocular pain and inflammation. Their well-characterized anti-inflammatory activity, analgesic property, and established safety record have also made NSAIDs an important tool to optimize surgical outcomes. For the treatment of postoperative inflammation in patients who have undergone cataract extraction. Bromfenac ophthalmic solution is a sterile, topical, nonsteroidal anti-inflammatory drug (NSAID) for ophthalmic use. The mechanism of its action is thought to be due to its ability to block prostaglandin synthesis by inhibiting cyclooxygenase 1 and 2. Prostaglandins have been shown in many animal models to be mediators of certain kinds of intraocular inflammation. In studies performed in animal eyes, prostaglandins have been shown to produce disruption of the blood-aqueous humor barrier, vasodilation, increased vascular permeability, leukocytosis, and increased intraocular pressure.",The molecular weight is 334.17.,Bromfenac has a topological polar surface area of 80.39.,The log p value of  is 3.28.,Bromfenac is approved.,Bromfenac is a solid.,True
14670,"Drospirenone is a synthetic progestin commonly found in the popular oral contraceptive, Yaz in combination with. Aside from its contraceptive effects, drospirenone is used with estrogens to control acne and premenstrual dysphoric disorder (PMDD).  Drospirenone, in combination with ethinyl estradiol, is indicated as an oral contraceptive for the prevention of pregnancy. In addition to its use for contraceptive effects, this combination is used to treat moderate acne vulgaris and the symptoms of premenstrual dysphoric disorder. The drug has approved indications for combination with estrogens for the treatment of menopause-associated symptoms, such as vasomotor symptoms and vulvovaginal atrophy. Drospirenone combined with estrogen may also may aid in the prevention of osteoporosis in women who have been post-menopausal for at least a year and are not candidates for other therapies.  It can sometimes be found in preparations containing estrogen and folic acid for folic acid replenishment during oral contraception. Drospirenone inhibits the maturation of follicles and inhibits ovulation, preventing pregnancy. It has antiandrogen effects, improving acne and hirsutism. When combined with ethinyl estradiol, it has been shown to have favorable effects on the plasma lipid profile. Due to its similarity to naturally occurring progesterone, drospirenone is thought to be associated with a lower incidence of progesterone contraceptive related adverse effects, such as breast tenderness and mood swings. Drospirenone and ethinyl estradiol in combination suppress the release of follicle stimulating hormone (FSH) and luteinizing hormone (LH), preventing ovulation. Other changes induced by this drug which may aid in the prevention of pregnancy include alterations in cervical mucus consistency, hindering sperm movement, and lowering the chance of embryo implantation.",The molecular weight is 366.5.,Drospirenone has a topological polar surface area of 43.37.,The log p value of  is 2.84.,Drospirenone is approved.,Drospirenone is a solid.,True
14671,"Cimicoxib is a selective COX-2 inhibitor being developed by Affectis as a treatment for depression and schizophrenia. If approved, Cimicoxib would be the first drug in decades to treat depression by a new mechanism of action. Investigated for use/treatment in depression. Depression and schizophrenia are inflammatory diseases. Increased levels of pro-inflammatory cytokines and prostaglandin E (PGE) have repeatedly been described in major depression. COX-2 inhibitors inhibit production of both. Cimicoxib is a selective COX-2 inhibitor. The mechanism by which some COX-2 inhibitors work in depression could be linked to their anti-inflammatory mechanisms.",,,,Cimicoxib is investigational.,Cimicoxib is a solid.,True
14672,"DHEA sulfate is the major steroid of the fetal adrenal. DHEA-S is the principal adrenal androgen and is secreted together with cortisol under the control of ACTH and prolactin. DHEA-S is elevated with hyperprolactinemia. Investigated for use/treatment in asthma and burns and burn infections. The low levels of dehydroepiandrosterone sulfate(DHEA-S)is associated with unfavorable levels of several strong cardiovascular disease risk factors, such as lipids and blood pleasure, which are components of the metabolic syndrome, and insulin levels. DHEA-S deficiency is risk factors of obesity and insulin resistance, but it is not clear, whether this possible influence is independent.",The molecular weight is 368.49.,Prasterone sulfate has a topological polar surface area of 80.67.,The log p value of  is 3.01.,Prasterone sulfate is investigational.,Prasterone sulfate is a solid.,True
14673,"Sar9, Met (O2)11-Substance P is a neurokinin-1 receptor agonist. It is an analog of the naturally occurring human neuropeptide Substance P, which can be found throughout the body, including in the airways of humans and many other species. Investigated for use/treatment in acute respiratory distress syndrome (ARDS) and viral infection. The endogenous receptor for Substance P is neurokinin 1 receptor (NK1-receptor, NK1R). Substance P has been shown to stimulate cellular growth in cell culture , and it was shown that Substance P could promote wound healing of non-healing ulcers in humans. It has also been shown to reverse diabetes in mice.",,,,"Sar9, Met (O2)11-Substance P is investigational.","Sar9, Met (O2)11-Substance P is a solid.",True
14674,"R-roscovitine (Seliciclib or CYC202) is a cyclin-dependent kinase (CDK) inhibitor that preferentially inhibits multiple enzyme targets including CDK2, CDK7 and CDK9, which alter the growth phase of treated cells. Developed by Cyclacel, seliciclib is being researched for the treatment of non-small cell lung cancer (NSCLC), leukemia, HIV infection, herpes simplex infection, and the mechanisms of chronic inflammation disorders. Investigated for use/treatment in breast cancer, lung cancer, lymphoma (unspecified), multiple myeloma, leukemia (lymphoid), and cancer/tumors (unspecified).",,,,Seliciclib is investigational.,Seliciclib is a solid.,True
14675,Investigated for use/treatment in colorectal cancer and lung cancer.,,,,Semaxanib is investigational.,Semaxanib is a solid.,True
14676,"Nonoxynol-9 (N-9) is a typical surfactant used as a vaginal spermicide. Spermicides are locally acting non-hormonal contraceptives. When present in the vagina during intercourse, they immobilize/inactivate/damage and/or kill sperms without eliciting systemic effects. N-9 has been in use for more than 30 years as an over-the-counter (OTC) drug in creams, gels, foams and condom lubricants. It is the most commonly used spermicidal contraceptive in the UK and the USA. In several European countries, spermicides are no longer on the market. Nonoxynol 9 is a surfactant spermicide used for contraception in spermicidal creams, jellies, foams, gel, and lubricants. It is also used in conjuction with other methods of contraception, including condoms, cervical caps and diaphragms. Nonoxynol-9 interacts with the lipids in the membranes of the acrosome and the midpiece of the sperm. The sperm membranes are lysed; the acrosome, neck and midpiece of the spermatozoa are loosened and then detached which results in their immobilization and death.",,,,Nonoxynol-9 is approved and withdrawn.,Nonoxynol-9 is a solid.,True
14677,"A prostaglandin analogue ester prodrug used topically (as eye drops) to control the progression of glaucoma and in the management of ocular hypertension. Chemically, tafluprost is a fluorinated analog of prostaglandin F2-alpha. Tafluprost was approved for use in the U.S. on February 10, 2012. Tafluprost is indicated for reducing elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension. Tafluprost is a novel prostaglandin analog with a high affinity for the fluoroprostaglandin (FP) receptor PGF2α. Tafluprost has an affinity for the FP receptor that is approximately 12 times higher than that of the carboxylic acid of latanoprost, but with almost no potential to bind to other receptors.  Tafluprost acid is a prostanoid selective FP receptor agonist that is believed to reduce the intraocular pressure (IOP) by increasing the outflow of aqueous humor. Studies in animals and humans suggest that the main mechanism of action is increased uveoscleral outflow.",The molecular weight is 452.54.,Tafluprost has a topological polar surface area of 75.99.,The log p value of  is 4.26.,Tafluprost is approved.,Tafluprost is a liquid.,True
14678,"Folic acid, also known as folate or Vitamin B9, is a member of the B vitamin family and an essential cofactor for enzymes involved in DNA and RNA synthesis. More specifically, folic acid is required by the body for the synthesis of purines, pyrimidines, and methionine before incorporation into DNA or protein. Folic acid is particularly important during phases of rapid cell division, such as infancy, pregnancy, and erythropoiesis, and plays a protective factor in the development of cancer. As humans are unable to synthesize folic acid endogenously, diet and supplementation is necessary to prevent deficiencies. For example, folic acid is present in green vegetables, beans, avocado, and some fruits. Folic acid is indicated for the treatment of folic acid deficiency, megaloblastic anemia, and in anemias of nutritional origins, pregnancy, infancy, or childhood. Folic acid is a water-soluble B-complex vitamin found in foods such as liver, kidney, yeast, and leafy, green vegetables. Also known as folate or Vitamin B9, folic acid is an essential cofactor for enzymes involved in DNA and RNA synthesis. More specifically, folic acid is required by the body for the synthesis of purines, pyrimidines, and methionine before incorporation into DNA or protein. Folic acid is the precursor of tetrahydrofolic acid, which is involved as a cofactor for transformylation reactions in the biosynthesis of purines and thymidylates of nucleic acids. Impairment of thymidylate synthesis in patients with folic acid deficiency is thought to account for the defective deoxyribonucleic acid (DNA) synthesis that leads to megaloblast formation and megaloblastic and macrocytic anemias. Folic acid is particularly important during phases of rapid cell division, such as infancy, pregnancy, and erythropoiesis, and plays a protective factor in the development of cancer. As humans are unable to synthesize folic acid endogenously, diet and supplementation is necessary to prevent deficiencies. In order to function properly within the body, folic acid must first be reduced by the enzyme dihydrofolate reductase (DHFR) into the cofactors dihydrofolate (DHF) and tetrahydrofolate (THF). This important pathway, which is required for de novo synthesis of nucleic acids and amino acids, is disrupted by anti-metabolite therapies such as as they function as DHFR inhibitors to prevent DNA synthesis in rapidly dividing cells, and therefore prevent the formation of DHF and THF.  Folic acid, as it is biochemically inactive, is converted to tetrahydrofolic acid and methyltetrahydrofolate by dihydrofolate reductase (DHFR). These folic acid congeners are transported across cells by receptor-mediated endocytosis where they are needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids, methylate tRNA, and generate and use formate. Using vitamin B12 as a cofactor, folic acid can normalize high homocysteine levels by remethylation of homocysteine to methionine via methionine synthetase.",The molecular weight is 441.4.,Folic acid has a topological polar surface area of 207.93.,The log p value of  is -2.04.,Folic acid is approved and nutraceutical and vet_approved.,Folic acid is a solid.,True
14679,"A metallic element of atomic number 30 and atomic weight 65.38. It is a necessary trace element in the diet, forming an essential part of many enzymes, and playing an important role in protein synthesis and in cell division. Zinc deficiency is associated with anemia, short stature, hypogonadism, impaired wound healing, and geophagia. It is identified by the symbol _Zn_. Zinc can be used for the treatment and prevention of zinc deficiency/its consequences, including stunted growth and acute diarrhea in children, and slowed wound healing. It is also utilized for boosting the immune system, treating the common cold and recurrent ear infections, as well as preventing lower respiratory tract infections.  Zinc is involved in various aspects of cellular metabolism. It has been estimated that approximately 10% of human proteins may bind zinc, in addition to hundreds of proteins that transport and traffic zinc. It is required for the catalytic activity of more than 200 enzymes, and it plays a role in immune function wound healing, protein synthesis, DNA synthesis, and cell division. Zinc is an essential element for a proper sense of taste and smell and supports normal growth and development during pregnancy, childhood, and adolescence. It is thought to have antioxidant properties, which may be protective against accelerated aging and helps to speed up the healing process after an injury; however, studies differ as to its effectiveness. Zinc ions are effective antimicrobial agents even if administered in low concentrations. **Zinc has three primary biological roles**: _catalytic_, _structural_, and _regulatory_. The catalytic and structural role of zinc is well established, and there are various noteworthy reviews on these functions. For example, zinc is a structural constituent in numerous proteins, inclusive of growth factors, cytokines, receptors, enzymes, and transcription factors for different cellular signaling pathways. It is implicated in numerous cellular processes as a cofactor for approximately 3000 human proteins including enzymes, nuclear factors, and hormones.",,,,Zinc is approved and investigational.,Zinc is a solid.,True
14680,"Zinc can be used for the treatment and prevention of zinc deficiency/its consequences, including stunted growth and acute diarrhea in children, and slowed wound healing. It is also utilized for boosting the immune system, treating the common cold and recurrent ear infections, as well as preventing lower respiratory tract infections.  Zinc is involved in various aspects of cellular metabolism. It has been estimated that approximately 10% of human proteins may bind zinc, in addition to hundreds of proteins that transport and traffic zinc. It is required for the catalytic activity of more than 200 enzymes, and it plays a role in immune function wound healing, protein synthesis, DNA synthesis, and cell division. Zinc is an essential element for a proper sense of taste and smell and supports normal growth and development during pregnancy, childhood, and adolescence. It is thought to have antioxidant properties, which may be protective against accelerated aging and helps to speed up the healing process after an injury; however, studies differ as to its effectiveness. Zinc ions are effective antimicrobial agents even if administered in low concentrations. **Zinc has three primary biological roles**: _catalytic_, _structural_, and _regulatory_. The catalytic and structural role of zinc is well established, and there are various noteworthy reviews on these functions. For example, zinc is a structural constituent in numerous proteins, inclusive of growth factors, cytokines, receptors, enzymes, and transcription factors for different cellular signaling pathways. It is implicated in numerous cellular processes as a cofactor for approximately 3000 human proteins including enzymes, nuclear factors, and hormones.",The molecular weight is 183.47.,Zinc acetate has a topological polar surface area of 40.13.,,Zinc acetate is approved and investigational.,,True
14681,"Physiologic methyl radical donor involved in enzymatic transmethylation reactions and present in all living organisms. It possesses anti-inflammatory activity and has been used in treatment of chronic liver disease. (From Merck, 11th ed) S-Adenosylmethionine (SAMe) is used as a drug in Europe for the treatment of depression, liver disorders, fibromyalgia, and osteoarthritis. It has also been introduced into the United States market as a dietary supplement for the support of bone and joint health, as well as mood and emotional well being. S-adenosylmethionine is an intermediate metabolite of methionine. Its involvement in methylation assists in cellular growth and repair, maintains the phospho-bilipid layer in cell membranes. It also helps in the maintenance of the action of several hormones and neurotransmitters that affect mood. Highest concentration are found in the brain and the liver. S-Adenosylmethionine (SAMe) is a natural substance present in the cells of the body. It is a direct metabolite of the essential amino acid L-methionine. SAMe plays a crucial biochemical role in the body by donating a one-carbon methyl group in a process called transmethylation. SAMe, formed from the reaction of L-methionine and adenosine triphosphate catalyzed by the enzyme S-adenosylmethionine synthetase, is the methyl-group donor in the biosynthesis of both DNA and RNA nucleic acids, phospholipids, proteins, epinephrine, melatonin, creatine and other molecules.",The molecular weight is 398.44.,Ademetionine has a topological polar surface area of 185.46.,The log p value of  is -5.08.,Ademetionine is approved and investigational and nutraceutical.,Ademetionine is a solid.,True
14682,"A nonclassical folic acid inhibitor through its inhibition of the enzyme dihydrofolate reductase. It is being tested for efficacy as an antineoplastic agent and as an antiparasitic agent against pneumocystis pneumonia in AIDS patients. Myelosuppression is its dose-limiting toxic effect. For use, with concurrent leucovorin administration (leucovorin protection), as an alternative therapy for the treatment of moderate-to-severe <i>Pneumocystis carinii</i> pneumonia (PCP) in immunocompromised patients, including patients with the acquired immunodeficiency syndrome (AIDS). Also used to treat several types of cancer including colon cancer. Trimetrexate, a non-classical folate antagonist, is a synthetic inhibitor of the enzyme dihydrofolate reductase (DHFR). During DNA synthesis and cellular reproduction, folic acid is reduced to tetrahydrofolic acid by the enzyme folic acid reductase. By interfering with the reduction of folic acid, trimetrexate interferes with tissue cell reproduction. Generally, the most sensitive cells to the antimetabolite effect of trimetrexate are those cells which are most actively proliferating such as malignant cells, dermal epithelium, buccal and intestinal mucosa, bone marrow, fetal cells, and cells of the urinary bladder. Because the proliferation of cells in malignant tissues is greater than in most normal tissues, trimetrexate may impair the growth of the malignant tissues without causing irreversible damage to normal tissues. Due to very serious and potentially life-threatening side-effects of this drug, leucovorin must be co-administered for at least 72 hours after the last dose. In vitro studies have shown that trimetrexate is a competitive inhibitor of dihydrofolate reductase (DHFR) from bacterial, protozoan, and mammalian sources. DHFR catalyzes the reduction of intracellular dihydrofolate to the active coenzyme tetrahydrofolate. Inhibition of DHFR results in the depletion of this coenzyme, leading directly to interference with thymidylate biosynthesis, as well as inhibition of folate-dependent formyltransferases, and indirectly to inhibition of p.r.n. biosynthesis. The end result is disruption of DNA, RNA, and protein synthesis, with consequent cell death.",The molecular weight is 369.42.,Trimetrexate has a topological polar surface area of 117.54.,The log p value of  is 1.84.,Trimetrexate is approved and investigational.,Trimetrexate is a solid.,True
14683,"Aminopterin is an amino derivative of folic acid, which was once used as an antineoplastic agent in the treatment of pediatric leukemia. In the 1950's its production was discontinued in favor of methotrexate, which is less potent but less toxic. Off label, aminopterin has also been used in the treatment of psoriasis. Clinicians need to be aware of the characteristic teratologic effects of aminopterin and methotrexate. Prior to its withdrawal, aminopterin was initially used in the treatment of childhood leukemia; specifically to induce remissions. Later, aminopterin was used off-label in the United States to treat psoriasis, yielding dramatic lesion clearing. Aminopterin was later supplanted by methotrexate for treating cancer because of its better therapeutic index. Aminopterin (as well as methotrexate) has also been explored for use as an abortifacient. However, their association with severe congenital malformations and teratogenic effects have become known as fetal aminopterin syndrome.  Aminopterin is an amino derivative of folic acid which binds competitively to the dihydrofolate reductase enzyme to block tetrahydrofolate synthesis. Tetrahydrofolate is essential in the production of purines and pyrimadines, thus it's deficiency results in a reduction of DNA, RNA and protein synthesis. ",The molecular weight is 440.42.,Aminopterin has a topological polar surface area of 219.33.,The log p value of  is -1.36.,Aminopterin is investigational and withdrawn.,Aminopterin is a solid.,True
14684,"Cupric sulfate is a salt created by treating cupric oxide with sulfuric acid. This forms as large, bright blue crystals containing five molecules of water (CuSO4∙5H2O) and is also known as _blue vitriol_. The anhydrous salt is created by heating the hydrate to 150 °C (300 °F). Cupric sulfate is used primarily for agricultural purposes, as a pesticide, germicide, feed additive, and soil additive. Some of its secondary uses are as a raw material in the preparation of other copper compounds, as a reagent in analytic chemistry, as an electrolyte for batteries and electroplating baths, and in medical practice as a locally applied fungicide, bactericide, and astringent. Elemental use in copper deficiency  Copper is an essential mineral that plays a key role in many physiological processes, including angiogenesis, skin generation and expression and stabilization of skin proteins. Copper is found naturally in many food sources including meats, vegetables, and grains. Copper has potent biocidal properties and is used to eliminate bacteria, viruses and parasites ,. This drug is an essential trace element for the functioning of many metalloenzymes including ceruloplasmin, ferroxidase II, lysyl oxidase, monoamine oxidase, Zn-copper superoxide dismutase, tyrosinase, dopamine-β-hydroxylase, and cytochrome-c-oxidase.",,,,Cupric sulfate is approved.,Cupric sulfate is a solid.,True
14685,"Progesterone is a hormone that occurs naturally in females, and is essential for endometrial receptivity, embryo implantation, and the successful establishment of pregnancy. A low progesterone concentration or an insufficient response to progesterone can cause infertility and pregnancy loss. Progesterone is used in various contraceptive preparations to prevent ovulation and fertilization , as well as in other formulations to promote and support pregnancy. Please see , , and entries for information on various other forms of progesterone. **Gelatinized capsules** Progesterone, depending on concentration and dosage form, and timing of exposure may have several pharmacodynamic effects. These actions, according, to various preparations, are listed below: Progesterone binds and activates its nuclear receptor, _PR_, which plays an important part in the signaling of stimuli that maintain the endometrium during its preparation for pregnancy.",The molecular weight is 314.47.,Progesterone has a topological polar surface area of 34.14.,The log p value of  is 3.96.,Progesterone is approved and vet_approved.,Progesterone is a solid.,True
14686,"A triphenyl ethylene stilbene derivative which is an estrogen agonist or antagonist depending on the target tissue. Used mainly in female infertility due to anovulation (e.g. due to polycystic ovary syndrome) to induce ovulation.  Clomifene (previously clomiphene) is an orally administered, non steroidal, ovulatory stimulant that acts as a selective estrogen receptor modulator (SERM). Clomifene can lead to multiple ovulation, and hence increase the risk of conceiving twins. In comparison to purified FSH, the rate of ovarian hyperstimulation syndrome is low. There may be an increased risk of ovarian cancer and weight gain. Clomifene is capable of interacting with estrogen-receptor-containing tissues, including the hypothalamus, pituitary, ovary, endometrium, vagina, and cervix. It may compete with estrogen for estrogen-receptor-binding sites and may delay replenishment of intracellular estrogen receptors. Clomifene initiates a series of endocrine events culminating in a preovulatory gonadotropin surge and subsequent follicular rupture. The first endocrine event, in response to a course of clomifene therapy, is an increase in the release of pituitary gonadotropins. This initiates steroidogenesis and folliculogenesis resulting in growth of the ovarian follicle and an increase in the circulating level of estradiol. Following ovulation, plasma progesterone and estradiol rise and fall as they would in a normal ovulatory cycle. Clomifene has both estrogenic and anti-estrogenic properties, but its precise mechanism of action has not been determined. Clomifene appears to stumulate the release of gonadotropins, follicle-stimulating hormone (FSH), and leuteinizing hormone (LH), which leads to the development and maturation of ovarian follicle, ovulation, and subsequent development and function of the coprus luteum, thus resulting in pregnancy. Gonadotropin release may result from direct stimulation of the hypothalamic-pituitary axis or from a decreased inhibitory influence of estrogens on the hypothalamic-pituitary axis by competing with the endogenous estrogens of the uterus, pituitary, or hypothalamus. Clomifene has no apparent progestational, androgenic, or antrandrogenic effects and does not appear to interfere with pituitary-adrenal or pituitary-thyroid function.",The molecular weight is 405.97.,Clomifene has a topological polar surface area of 12.47.,The log p value of  is 7.15.,Clomifene is approved and investigational.,Clomifene is a solid.,True
14687,"Aminophenazone is a pyrazolone with analgesic, anti-inflammatory, and antipyretic properties that carries a risk of agranulocytosis. In biomedical applications, radiolabelled (13C-labeled) aminophenazone has been used in breath tests to measure the cytochrome P-450 metabolic activity in liver function tests. Formerly widely used as an antipyretic and analgesic in rheumatism, neuritis, and common colds. Currently used to measure total body water. Aminophenazone exhibits analgesic, anti-inflammatory, and antipyretic properties. Aminophenazone is metabolized very slowly by normal newborn babies. In older infants, a higher amount of exhaled 13-CO2 is observed.",The molecular weight is 231.3.,Aminophenazone has a topological polar surface area of 26.79.,The log p value of  is 1.04.,Aminophenazone is approved and withdrawn.,Aminophenazone is a solid.,True
14688,"A hormone secreted by the adrenal cortex that regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium. At the late distal tubule and collecting duct, aldosterone has two main actions: 1) aldosterone acts on mineralocorticoid receptors (MR) on principal cells in the distal tubule of the kidney nephron, increasing the permeability of their apical (luminal) membrane to potassium and sodium and activates their basolateral Na+/K+ pumps, stimulating ATP hydrolysis leading to phosphorylation of the pump and a conformational change in the pump exposes the Na+ ions to the outside. The phosphorylated form of the pump has a low affinity for Na+ ions, hence reabsorbing sodium (Na+) ions and water into the blood, and secreting potassium (K+) ions into the urine; 2) aldosterone stimulates H+ secretion by intercalated cells in the collecting duct, regulating plasma bicarbonate (HCO3−) levels and its acid/base balance; and 3) aldosterone may act on the central nervous system via the posterior pituitary gland to release vasopressin (ADH) which serves to conserve water by direct actions on renal tubular resorption.",The molecular weight is 360.45.,Aldosterone has a topological polar surface area of 91.67.,The log p value of  is 1.76.,Aldosterone is experimental and investigational.,Aldosterone is a solid.,True
14689,"Sodium Acetate is chemically designated CH3COONa, a hygroscopic powder very soluble in water. Sodium acetate could be used as additives in food, industry, concrete manufacture, heating pads and in buffer solutions. Medically, sodium acetate is important component as an electrolyte replenisher when given intravenously. It is mainly indicated to correct sodium levels in hyponatremic patients. It can be used also in metabolic acidosis and for urine alkalinization. Injection, USP 40 mEq is indicated as a source of sodium, for addition to large volume intravenous fluids to prevent or correct hyponatremia in patients with restricted or no oral intake. It is also useful as an additive for preparing specific intravenous fluid formulas when the needs of the patient cannot be met by standard electrolyte or nutrient solutions. Sodium acetate and other bicarbonate precursors are alkalinising agents, and can be used to correct metabolic acidosis, or for alkalinisation of the urine. Sodium is the principal cation of extracellular fluid. It comprises more than 90% of total cations at its normal plasma concentration of approximately 140 mEq/liter. The sodium ion exerts a primary role in controlling total body water and its distribution. Acetate ions acts as hydrogen ion acceptor which is alternative to bicarbonate.  It works as a source of sodium ions especially in cases of hyponatremic patients. Sodium has a primary role in regulating extracellular fluid volume. It controls water distribution, fluid and electrolyte balance and the osmotic pressure of body fluids. Sodium is also involved in nerve conduction, muscle contraction, acid-base balance and cell nutrient uptake.",The molecular weight is 82.03.,,,Sodium acetate is approved and investigational.,,True
14690,"High levels of LDL cholesterol (LDL-C) are a major risk factor for cardiovascular events. Caused by genetic mutations or lifestyle factors, hypercholesterolemia can significantly reduce quality of life and increase the risk of mortality from cardiovascular disease. About 1 in 4 patients, or 15 million Americans with elevated LDL-C, are insufficiently managed with maximally tolerated statin therapy alone, requiring additional treatment for hypercholesterolemia. Bempedoic acid is indicated as an adjunct to diet and maximally tolerated statin therapy for adults with heterozygous familial hypercholesterolemia or existing atherosclerotic cardiovascular disease that warrants additional lowering of LDL-C. Bempedoic acid inhibits the synthesis of cholesterol in the liver, reducing LDL-C levels. This reduces the development of atherosclerotic plaques that may increase the risk of cardiovascular events. Earlier clinical trials studying the effects of bempedoic acid showed a dose‐dependent reduction of LDL‐C levels in addition to decreased LDL particle number, and reduced levels of apolipoprotein B, non–HDL cholesterol, and high‐sensitivity C‐reactive protein. Normally, LDL cholesterol is produced in the liver and circulates in the blood. When the blood becomes saturated, excess LDL deposits in blood vessels including the coronary arteries, increasing the risk of cardiovascular events.",,,,Bempedoic acid is approved and investigational.,Bempedoic acid is a solid.,True
14691,"A pyrazine compound inhibiting sodium reabsorption through sodium channels in renal epithelial cells. This inhibition creates a negative potential in the luminal membranes of principal cells, located in the distal convoluted tubule and collecting duct. Negative potential reduces secretion of potassium and hydrogen ions. Amiloride is used in conjunction with diuretics to spare potassium loss. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p705) For use as adjunctive treatment with thiazide diuretics or other kaliuretic-diuretic agents in congestive heart failure or hypertension. Amiloride, an antikaliuretic-diuretic agent, is a pyrazine-carbonyl-guanidine that is unrelated chemically to other known antikaliuretic or diuretic agents. It is an antihypertensive, potassium-sparing diuretic that was first approved for use in 1967 and helps to treat hypertension and congestive heart failure. The drug is often used in conjunction with thiazide or loop diuretics. Due to its potassium-sparing capacities, hyperkalemia (high blood potassium levels) are occasionally observed in patients taking amiloride. The risk is high in concurrent use of ACE inhibitors or spironolactone. Patients are also advised not to use potassium-containing salt replacements. Amiloride works by inhibiting sodium reabsorption in the distal convoluted tubules and collecting ducts in the kidneys by binding to the amiloride-sensitive sodium channels. This promotes the loss of sodium and water from the body, but without depleting potassium. Amiloride exerts its potassium sparing effect through the inhibition of sodium reabsorption at the distal convoluted tubule, cortical collecting tubule and collecting duct; this decreases the net negative potential of the tubular lumen and reduces both potassium and hydrogen secretion and their subsequent excretion. Amiloride is not an aldosterone antagonist and its effects are seen even in the absence of aldosterone.",The molecular weight is 229.63.,Amiloride has a topological polar surface area of 156.79.,The log p value of  is 0.11.,Amiloride is approved.,Amiloride is a solid.,True
14692,"Antihemophilic factor human, also known as Coagulation Factor VIII or Anti-Hemophilic Factor (AHF), is a non-recombinant, lyophilized concentrate of coagulation factor VIII, an endogenous protein and essential component of the coagulation cascade. Antihemophilic factor is manufactured with reduced amounts of von Willebrand Factor antigen (VWF:Ag) and purified from extraneous plasma-derived protein by affinity chromatography. The small amount of VWF:Ag is used to purify factor VIII complex and then removed from the final preparation. The final purified concentrate contains albumin as a stabilizer.. The complex was developed by CSL Behring or Baxter Healthcare Corporation and approved in the 90s. The human antihemophilic factor is indicated for the cases of hemophilia A, also known as classical hemophilia for the prevention and control of hemorrhagic episodes. If surgery is needed in patients with hemophilia A there is a need of correction of the clotting abnormality. In this cases, the human antihemophilic factor may be administered followed by intermittent maintenance doses. The hemophilia A is characterized by the deficiency of the coagulation factor VIII that results in prolonged blood flow after injury or surgery as well as recurrent bleeding. The human antihemophilic factor assists in the convertion of prothrombin to thrombin. Its administration generates the formation of a complex constituted by the Factor IXa, Factor X and the antihemophilic factor which triggers the normal coagulation cascade for the formation of blood clots. The human antihemophilic factor is increased in the plasma thus enabling temporary correction of the hemophilia A bleeding. Its effect is reported as the normalization of the partial thromboplastin time.  The human antihemophilic factor replaces the coagulation factor VIII. It acts as a co-factor for factor IX to activate factor X in the intrinsic pathway of blood coagulation.",,,,Antihemophilic factor human is approved.,Antihemophilic factor human is a solid.,True
14693,"Calcitonin was first discovered in isolated parathyroid tissue as a substance with a serum-calcium-lowering effect. It is constituted as a 32-amino acid single chain polypeptide structure that gets secreted as a regulatory agent in calcium-phosphorus metabolism. It is used as an alternative for people developing antibodies against salmon calcitonin. Human calcitonin is indicated for the treatment of Paget's disease in the cases where the use of salmon calcitonin may provoke the generation of high-titer of antibodies. Paget's disease is a metabolic bone disorder characterized by focal areas of increased and disorganized bone turnover coupled with an increased bone formation. The majority of the cases are asymptomatic but some clinical manifestations include pain, bone deformity and some complications such as pathological fractures and deafness. The increased activity in bone is associated with a rise in serum level of alkaline phosphatase and the increased urinary excretion of hydroxyproline which is a product of bone breakdown. Administration of human calcitonin has shown to increase bone calcium content and reduce the levels of serum calcium and serum phosphorus. This calcium inhibition leads to decreases in urinary calcium, magnesium and urine hydroxyproline. Some reports indicate a calcitonin-driven reduction of phosphate plasma concentration which is thought to be related to increased excretion of phosphate. Calcitonin can increase excretion of calcium, phosphate, and sodium. It also is proven to induce the appearance of normal lamellar bone against the diseased trabeculae and a striking decrease in the number of osteoclasts. Bone pain tends to be relieved within a few weeks, and it does not present an important effect on normal bone. It is important to point out that human calcitonin is less active than the salmon calcitonin. This characteristic happens because of a high tendency to aggregate, and thus, human calcitonin is used just in cases where the usage of salmon calcitonin generated the formation of antibodies. For this reason, the use of human calcitonin is only indicated when there is the appearance of a high-titer of antibodies anti-salmon calcitonin because these antibodies are suggested to cause a relapse. Calcitonin inhibits osteoclast-mediated bone resorption through the regulation of the number and activity of osteoclasts. The action of human calcitonin on osteoclasts is due to a disruption of cytoskeletal organization, by the distraction of actin rings, and due to a disappearance of the cellular polarity of osteoclasts. At the subcellular level, calcitonin is suggested to perform its activity by the modulation of the cAMP-PKA signaling pathway.",The molecular weight is 3417.88.,Human calcitonin has a topological polar surface area of 1359.6.,The log p value of  is -8.49.,Human calcitonin is approved and investigational.,Human calcitonin is a solid.,True
14694,"Pegfilgrastim is a PEGylated form of the recombinant human granulocyte colony-stimulating factor (G-CSF) analogue,. It is used to decrease the incidence of infection, as manifested by febrile neutropenia, in patients with with non-myeloid cancer receiving myelosuppressive anti-cancer treatment. Some patients with greater risk factors may develop febrile neutropenia from myelosuppressive therapy and are susceptible to an increased risk of developing infections. Although the risk of developing febrile neutropenia is less than 20% in many readily used chemotherapy regimens, infections pose risks of hospitalization and mortalities. Due to the relatively short circulating half-life of filgrastim, a 20 kDa PEG moiety was covalently conjugated to the N-terminus of filgrastim (at the methionine residue) to develop a longer acting version of the drug. Due to a longer half-life and slower elimination rate than filgrastim, pegfilgrastim requires less frequent dosing than filgrastim. However, pegfilgrastim retains the same biological activity as filgrastim and binds to the same G-CSF receptor to stimulate the proliferation, differentiation, and activation of neutrophils. Pegfilgrastim is indicated to decrease the incidence of infection, as manifested by febrile neutropenia, in patients with non­ myeloid malignancies receiving myelosuppressive anti-cancer drugs associated with a clinically significant incidence of febrile neutropenia. Pegfilgrastim is a recombinant human granulocyte colony-stimulating factor (G-CSF) that promotes the production, proliferation, and maturation of neutrophils, which are white blood cells involved in both innate and adaptive immune responses. The safety and efficacy of pegfilgrastim in reducing the risk of febrile neutropenia and infections have been demonstrated in various tumor types and settings.  Neutrophils are short-lived immune cells that are highly susceptible to cell death following myelosuppressive chemotherapy. This marked reduction in neutrophil numbers during chemotherapy increases the risk of hospitalization, infection, and infection-related mortality. It also directly impacts the clinical outcome of patients if cases of febrile neutropenia requires dose reductions or schedule delay of chemotherapy, thus reducing the clinical efficacy of chemotherapy and patient benefit from receiving appropriate treatment. ",,,,Pegfilgrastim is approved.,Pegfilgrastim is a liquid.,True
14695,"Pegvisomant is a highly selective growth hormone (GH) receptor antagonist. It is used to treat acromegaly. Unlike dopamine or somatostatin analogs (which inhibit growth hormone secretion), this drug actually blocks the hepatic (GH-mediated) production of insulin like growth factor (IGF-1), which is the main mediator of growth hormone activity. Pegvisomant is a growth hormone receptor antagonist used for the treatment of acromegaly. Somavert is used for the treatment of acromegaly, which arises from excessive IGF-1 levels. Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH, and thus interferes with GH signal transduction. Inhibition of GH action results in decreased serum concentrations of insulin-like growth factor-I (IGF-I), and IGF binding protein-3 (IGFBP-3). This reduces the symptoms of acromegaly. Somavert selectively binds to growth hormone (GH) receptors on cell surfaces, where it blocks the binding of endogenous GH. This leads to the normalization of serum IGF-1 levels.",,,,Pegvisomant is approved.,Pegvisomant is a liquid.,True
14696,"Antiprotozoal agent effective in trypanosomiasis, leishmaniasis, and some fungal infections; used in treatment of pneumocystis pneumonia in HIV-infected patients. It may cause diabetes mellitus, central nervous system damage, and other toxic effects. For the treatment of pneumonia due to <i>Pneumocystis carinii</i>. Pentamidine is an antiprotozoal agent. It is an aromatic diamidine, and is known to have activity against <i>Pneumocystis carinii</i>. The exact nature of its antiprotozoal action is unknown. <i>in vitro</i> studies with mammalian tissues and the protozoan <i>Crithidia oncopelti</i> indicate that the drug interferes with nuclear metabolism producing inhibition of the synthesis of DNA, RNA, phospholipids and proteins. Little is known about the drug's pharmacokinetics. The medication is also useful in Leishmaniasis and in prophylaxis against sleeping sickness caused by <i>Trypanosoma brucei gambiense</i>. Hydration before treatment lessens the incidence and severity of side effects, which include liver or kidney dysfunction, hypertension, hypotension, hypoglycemia, hypocalemia, leukopenia, thrombcytopenia, anemia, and allergic reaction. It is generally well-tolerated. The mode of action of pentamidine is not fully understood. It is thought that the drug interferes with nuclear metabolism producing inhibition of the synthesis of DNA, RNA, phospholipids, and proteins.",The molecular weight is 340.43.,Pentamidine has a topological polar surface area of 118.2.,The log p value of  is 2.31.,Pentamidine is approved and investigational.,Pentamidine is a solid.,True
14697,"Aplidine is a peptide found in tunicates which shows promise in shrinking tumors in pancreatic, stomach, bladder, and prostate cancers. The specific marine organism is _Aplidium albicans_. Aplidine is also of interest as a potential treatment for some leukemias. Intended for the treatment of various forms of cancer. Aplidine inhibits the growth and induces apoptosis in MOLT-4 cells through the indirect inhibition of VEGF secretion which blocks the VEGF/VEGFR-1 autocrine loop necessary for the growth of these cells.",,,,Plitidepsin is investigational.,Plitidepsin is a solid.,True
14698,"Pyrantel is a pyrimidine-derivative anthelmintic agent for the oral treatment of various parasitic worm infections including ascariasis, hookworm infections, enterobiasis (pinworm infection), trichostrongyliasis, and trichinellosis. For the treatment of enterobiasis including roundworm (ascariasis), pinworm (enterobius) and hookworm (strongyloides) and hookworm (ancylostoma) in the pyrantel pamoate form. It has similar properties to both competitive and depolarizing neuromuscular blocking agents, which leads to the understanding of the paralytic effect of the drug has on parasites, ultimately resulting in the death of the parasite ,.  By promoting the release of acetylcholine, inhibiting cholinesterase, and stimulating ganglionic neurons, pyrantel serves as a depolarizing neuromuscular blocking agent in helminths. This causes extensive depolarization of the helminth muscle membrane, resulting in tension to the helminth's muscles, leading to paralysis and release of their attachment to the host organism intestinal walls.",The molecular weight is 206.31.,Pyrantel has a topological polar surface area of 15.6.,The log p value of  is 3.03.,Pyrantel is approved and vet_approved.,Pyrantel is a solid.,True
14699,"Lusutrombopag is an orally bioavailable thrombopoietin receptor (TPOR) agonist developed by Shionogi & Company (Osaka, Japan). TPOR is a regulatory target site for endogenous thrombopoietin, which acts as a primary cytokine to promote megakaryocyte proliferation and differentiation, and affect other hematopoietic lineages as well, including erythroid, granulocytic and lymphoid lineages. Thrombocytopenia, which indicates abnormally low levels of platelets, is a common complication related to chronic liver disease. This hematological abnormality, especially in cases of severe thrombocytopenia (platelet count <50,000/μL), creates challenges to patients requiring invasive medical procedures where there is a significant risk for spontaneous bleeding. Lusutrombopag binds to the transmembrane domain of TPOR expressed on megakaryocytes, and causes the proliferation and differentiation of megakaryocytic progenitor cells from hematopoietic stem cells.  Lusutrombopag is indicated for the treatment of thrombocytopenia in adults with chronic liver disease who are scheduled to undergo a medical or dental procedure. The AUC of lusutrombopag was found to correlate the increased platelet counts. Following administration of 3 mg daily dose in patients with chronic liver disease and thrombocytopenia, the mean (standard deviation) maximum platelet count in patients (N=74) without platelet transfusion was 86.9 (27.2) × 10^9/L, and the median time to reach the maximum platelet count was 12.0 (5 to 35) days. Lusutrombopag was not shown to induce any clinically significant QTc prolongation at a dose 8 times the recommended dosage.  Lusutrombopag mimics the biological actions of endogenous thrombopoietin (TPO) by acting as an agonist for the thrombopoietin receptor (TPOR) expressed on megakaryocytes. It binds to the transmembrane domain of the receptor and induces thrombocytopoiesis by targeting the same signal transduction system as that of endogenous TPO, which involves the activation of JAK and STAT pathways. It stimulates the proliferation and differentiation of bone marrow progenitor cells into megakaryocytes, which undergoes maturation to act as precursor cells for platelets. A single megakaryocyte produces and releases thousands of platelets upon maturation and series of remodeling events. Lusutrombopag displays high specificity towards human TPORs when compared to murine TPORs. Lusutrombopag may affect other hematopoietic lineages as well, including erythroid, granulocytic and lymphoid lineages. One case of increased leukocyte and erythrocyte counts that prolonged for over 120 days was reported following administration in a patient with liver cirrhosis (LC) due to hepatitis C virus. ",The molecular weight is 591.54.,Lusutrombopag has a topological polar surface area of 97.75.,The log p value of  is 7.92.,Lusutrombopag is approved and investigational.,Lusutrombopag is a solid.,True
14700,"Tildrakizumab is a high-affinity, humanized, IgG1 κ antibody targeting interleukin 23 p19 that shows promise in the evolution of treatment strategy in chronic plaque psoriasis. Moderate-severe plaque psoriasis ,. Tildrakuzimab is a targeted immunomodulator that decreases inflammation by inhibiting the action of various cytokines associated with plaque psoriasis, thus relieving its symptom of scaly plaques ,. This drug selectively binds interleukin (IL)-23 p19 subunit of cytokine IL-23 and neutralizes its function IL-23 regulates Th17 cells and is a powerful activator of keratinocyte proliferation. Targeting IL-23p19 alone has been found to be a promising treatment approach in patients with moderate-to-severe chronic plaque psoriasis. Upon administration, downregulation of Th17 and Th22 cell responses occur.",,,,Tildrakizumab is approved and investigational.,Tildrakizumab is a liquid.,True
14701,"A phospholipid-interacting antimalarial drug (antimalarials). It is very effective against plasmodium falciparum with very few side effects.  For the treatment of mild to moderate acute malaria caused by Mefloquineuine-susceptible strains of <i>Plasmodium falciparum</i> (both chloroquine-susceptible and resistant strains) or by <i>Plasmodium vivax</i>. Also for the prophylaxis of <i>Plasmodium falciparum</i> and <i>Plasmodium vivax</i> malaria infections, including prophylaxis of chloroquine-resistant strains of <i>Plasmodium falciparum</i>. Mefloquine is an antimalarial agent which acts as a blood schizonticide. Mefloquine is active against the erythrocytic stages of Plasmodium species. However, the drug has no effect against the exoerythrocytic (hepatic) stages of the parasite. Mefloquine is effective against malaria parasites resistant to chloroquine. Mefloquine is a chiral molecule. It is reported that while the (+) enantiomer primarily mediates an antimalarial activity, the (-) enantiomer contribute to the psychotrophic effects by specifically binding to adenosine receptors in the central nervous system.  Mefloquine has been found to produce swelling of the <i>Plasmodium falciparum</i> food vacuoles. It may act by forming toxic complexes with free heme that damage membranes and interact with other plasmodial components.",The molecular weight is 378.32.,Mefloquine has a topological polar surface area of 45.15.,The log p value of  is 3.67.,Mefloquine is approved and investigational.,Mefloquine is a solid.,True
14702,"Ranitidine is a commonly used drug, classified as a histamine H2-receptor antagonist, and belongs to the same drug class as and. This drug helps to prevent and treat gastric-acid associated conditions, including ulcers, because of its ability to decrease gastric acid secretion. Ranitidine is often referred to as Zantac, and is available in various forms, including tablet, injection, and effervescent tablet preparations. This drug is used alone or with concomitant antacids for the following conditions: short-term treatment of active duodenal ulcer, treating gastric acid hypersecretion due to Zollinger-Ellison syndrome, systemic mastocytosis, and other conditions that may pathologically raise gastric acid levels. It also used in the short term treatment of active benign gastric ulcers and maintenance therapy of gastric ulcers at a reduced dose. In addition to the above, ranitidine can be used for the treatment of GERD symptoms, treatment of erosive esophagitis (endoscopically diagnosed) and the maintenance of gastric or duodenal ulcer healing. Ranitidine decreases the secretion of gastric acid stimulated by food and drugs. It also reduces the secretion of gastric acid in hypersecretory conditions such as Zollinger-Ellison syndrome. Marked improvements in the appearance of the esophageal tissues have been observed by endoscopic imaging after ranitidine therapy. After a meal, the hormone gastrin, produced by cells in the lining of the stomach, stimulates the release of histamine, which then binds to histamine H2 receptors, leading to the secretion of gastric acid. Ranitidine reduces the secretion of gastric acid by reversible binding to histamine (H2) receptors, which are found on gastric parietal cells. This process leads to the inhibition of histamine binding to this receptor, causing the reduction of gastric acid secretion. The relief of gastric-acid related symptoms can occur as soon as 60 minutes after administration of a single dose, and the effects can last from 4-10 hours, providing fast and effective symptomatic relief.",The molecular weight is 314.4.,Ranitidine has a topological polar surface area of 83.58.,The log p value of  is 0.67.,Ranitidine is approved and withdrawn.,Ranitidine is a solid.,True
14703,"Methantheline is a synthetic antispasmodic. Antispasmodics are used to relieve cramps or spasms of the stomach, intestines, and bladder. Methantheline is used to treat intestine or stomach ulcers (peptic ulcer disease), intestine problems (irritable bowel syndrome), pancreatitis, gastritis, biliary dyskinesia, pylorosplasm, or urinary problems (reflex neurogenic bladder in children). For the treatment of peptic ulcer disease, irritable bowel syndrome, pancreatitis, gastritis, biliary dyskinesia, pylorosplasm, and reflex neurogenic bladder in children. Methantheline is a synthetic quarternary ammonium antimuscarinic used to relieve cramps or spasms of the stomach, intestines, and bladder. It can be used together with antacids or other medicines, such as H2-receptor antagonists, in the treatment of peptic ulcer. Methantheline inhibits muscarinic actions at postganglionic parasympathetic neuroeffector sites. Methantheline inhibits the muscarinic actions of acetylcholine on structures innervated by postganglionic cholinergic nerves as well as on smooth muscles that respond to acetylcholine but lack cholinergic innervation. These postganglionic receptor sites are present in the autonomic effector cells of the smooth muscle, cardiac muscle, sinoatrial and atrioventricular nodes, and exocrine glands. Depending on the dose, anticholinergics may reduce the motility and secretory activity of the gastrointestinal system, and the tone of the ureter and urinary bladder and may have a slight relaxant action on the bile ducts and gallbladder.",The molecular weight is 340.44.,Methantheline has a topological polar surface area of 35.53.,The log p value of  is 0.87.,Methantheline is approved and investigational.,Methantheline is a solid.,True
14704,"The major circulating metabolite of vitamin D3 (cholecalciferol). It is produced in the liver and is the best indicator of the body's vitamin D stores. It is effective in the treatment of rickets and osteomalacia, both in azotemic and non-azotemic patients. Calcifediol also has mineralizing properties. Used to treat vitamin D deficiency or insufficiency, refractory rickets (vitamin D resistant rickets), familial hypophosphatemia and hypoparathyroidism, and in the management of hypocalcemia and renal osteodystrophy in patients with chronic renal failure undergoing dialysis. Also used in conjunction with calcium in the management and prevention of primary or corticosteroid-induced osteoporosis. Calcidiol is the precursor of vitamin D3. Vitamin D3 is a steroid hormone that has long been known for its important role in regulating body levels of calcium and phosphorus, in mineralization of bone, and for the assimilation of vitamin A. The classical manifestations of vitamin D deficiency is rickets, which is seen in children and results in bony deformaties including bowed long bones. Deficiency in adults leads to the disease osteomalacia. Both rickets and osteomalacia reflect impaired mineralization of newly synthesized bone matrix, and usually result from a combination of inadequate exposure to sunlight and decreased dietary intake of vitamin D. Common causes of vitamin D deficiency include genetic defects in the vitamin D receptor, severe liver or kidney disease, and insufficient exposure to sunlight. Vitamin D plays an important role in maintaining calcium balance and in the regulation of parathyroid hormone (PTH). It promotes renal reabsorption of calcium, increases intestinal absorption of calcium and phosphorus, and increases calcium and phosphorus mobilization from bone to plasma. Calcidiol is transformed in the kidney by 25-hydroxyvitamin D3-1-(alpha)-hydroxylase to calcitriol, the active form of vitamin D3. Calcitriol binds to intracellular receptors that then function as transcription factors to modulate gene expression. Like the receptors for other steroid hormones and thyroid hormones, the vitamin D receptor has hormone-binding and DNA-binding domains. The vitamin D receptor forms a complex with another intracellular receptor, the retinoid-X receptor, and that heterodimer is what binds to DNA. In most cases studied, the effect is to activate transcription, but situations are also known in which vitamin D suppresses transcription. Calcitriol increases the serum calcium concentrations by: increasing GI absorption of phosphorus and calcium, increasing osteoclastic resorption, and increasing distal renal tubular reabsorption of calcium. Calcitriol appears to promote intestinal absorption of calcium through binding to the vitamin D receptor in the mucosal cytoplasm of the intestine. Subsequently, calcium is absorbed through formation of a calcium-binding protein.",The molecular weight is 400.65.,Calcifediol has a topological polar surface area of 40.46.,The log p value of  is 7.27.,Calcifediol is approved and nutraceutical.,Calcifediol is a solid.,True
14705,"Vitamin D ultimately comprises a group of lipid-soluble secosteroids responsible for a variety of biological effects, some of which include increasing the intestinal absorption of calcium, magnesium, and phosphate. With reference to human use, there are 2 main forms of vitamin D - vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol). When non-specific references are made about 'vitamin d', the references are usually about the use of vitamin D3 and/or D2. Vitamin D is indicated for use in the treatment of hypoparathyroidism, refractory rickets (also known as vitamin D resistant rickets), and familial hypophosphatemia. The in vivo synthesis of the predominant two biologically active metabolites of vitamin D occurs in two steps. The first hydroxylation of vitamin D3 or D2 occurs in the liver to yield 25-hydroxyvitamin D while the second hydroxylation happens in the kidneys to give 1, 25-dihydroxyvitamin D. These vitamin D metabolites subsequently facilitate the active absorption of calcium and phosphorus in the small intestine, serving to increase serum calcium and phosphate levels sufficiently to allow bone mineralization. Conversely, these vitamin D metabolites also assist in mobilizing calcium and phosphate from bone and likely increase the reabsorption of calcium and perhaps also of phosphate via the renal tubules. There exists a period of 10 to 24 hours between the administration of vitamin D and the initiation of its action in the body due to the necessity of synthesis of the active vitamin D metabolites in the liver and kidneys. It is parathyroid hormone that is responsible for the regulation of such metabolism at the level of the kidneys. Most individuals naturally generate adequate amounts of vitamin D through ordinary dietary intake of vitamin D (in some foods like eggs, fish, and cheese) and natural photochemical conversion of the vitamin D3 precursor 7-dehydrocholesterol in the skin via exposure to sunlight.",,,,Vitamin D is approved and nutraceutical and vet_approved.,,True
14706,"Cyanocobalamin (commonly known as Vitamin B12) is a highly complex, essential vitamin, owing its name to the fact that it contains the mineral, cobalt. This vitamin is produced naturally by bacteria , and is necessary for DNA synthesis and cellular energy production. Vitamin B12 has many forms, including the cyano-, methyl-, deoxyadenosyl- and hydroxy-cobalamin forms. The _cyano_ form, is the most widely used form in supplements and prescription drugs ,. Several pharmaceutical forms of cyanocobalamin have been developed, including the tablet, injection, and nasal spray forms , ,. This drug was initially approved by the FDA in 1942. Vitamin B12 serves as a cofactor for _methionine synthase_ and _L-methylmalonyl-CoA mutase_ enzymes. Methionine synthase is essential for the synthesis of purines and pyrimidines that form DNA. L-methylmalonyl-CoA mutase converts L-methylmalonyl-CoA to _succinyl-CoA_ in the degradation of propionate , an important reaction required for both fat and protein metabolism. It is a lack of vitamin B12 cofactor in the above reaction and the resulting accumulation of methylmalonyl CoA that is believed to be responsible for the neurological manifestations of B12 deficiency. Succinyl-CoA is also necessary for the synthesis of hemoglobin. ",The molecular weight is 1355.39.,Cyanocobalamin has a topological polar surface area of 512.5.,,Cyanocobalamin is approved and nutraceutical.,Cyanocobalamin is a solid.,True
14707,"Iron deficiency anemia is a large public health concern worldwide, especially in young children, infants, and women of childbearing age. This type of anemia occurs when iron intake, iron stores, and iron loss do not adequately support the formation of erythrocytes, also known as red blood cells.  Ferrous sulfate is used for the prevention and treatment of iron deficiency anemia in adults and children. Ferrous sulfate replenishes iron, an essential component in hemoglobin, myoglobin, and various enzymes. It replaces the iron that is usually found in hemoglobin and myoglobin. Iron participates in oxygen transport and storage, electron transport and energy metabolism, antioxidant and beneficial pro-oxidant functions, oxygen sensing, tissue proliferation and growth, as well as DNA replication and repair. Iron is required to maintain optimal health, particularly for helping to form red blood cells (RBC) that carry oxygen around the body. A deficiency in iron indicates that the body cannot produce enough normal red blood cells. Iron deficiency anemia occurs when body stores of iron decrease to very low levels, and the stored iron is insufficient to support normal red blood cell (RBC) production. Insufficient dietary iron, impaired iron absorption, bleeding, pregnancy, or loss of iron through the urine can lead to iron deficiency. Symptoms of iron deficiency anemia include fatigue, breathlessness, palpitations, dizziness, and headache.",The molecular weight is 151.9.,Ferrous sulfate anhydrous has a topological polar surface area of 80.26.,,Ferrous sulfate anhydrous is approved.,Ferrous sulfate anhydrous is a solid.,True
14708,"Tucatinbib is a kinase inhibitor drug used with and in the treatment of unresectable or metastatic HER-2 positive breast cancer. It was developed by Seattle Genetics and approved by the FDA on April 17, 2020. Tucatinib is a promising new treatment for patients with metastatic breast cancer who have not responded adequately to other chemotherapy regimens. Tucatinib is indicated with trastuzumab and capecitabine for treatment of adults diagnosed with advanced unresectable or metastatic HER2-positive breast cancer. This includes patients with brain metastases and those  who have received one or more prior anti-HER2-based regimens in the metastatic setting.  By inhibiting tyrosine kinase, tucatinib exerts anti-tumor activity, reducing the size of HER-2 positive breast cancer tumors. In clinical trials, the regimen of tucatinib and showed enhanced activity both in vitro and in vivo when compared to either drug administered by itself. Mutations in the HER-2 gene are observed in some types of breast carcinoma. Tucatinib inhibits the tyrosine kinase enzyme of the HER-2 gene. Mutations of tyrosine kinase in the HER-2 gene lead to cascade effects of increased cell signaling and proliferation, resulting in malignancy. Results of in vitro studies show that tucatinib inhibits the phosphorylation of both HER-2 and HER-3, leading to downstream changes in MAPK and AKT signaling and cell proliferation. Anti-tumor activity occured in the cells that expressed HER-2. In vivo, tucatinib has been shown to inhibit HER-2 expressing tumors, likely by the same mechanism.",,,,Tucatinib is approved and investigational.,Tucatinib is a solid.,True
14709,"Gabapentin is a structural analogue of the inhibitory neurotransmitter gamma-aminobutyric acid () that was first approved for use in the United States in 1993. It was originally developed as a novel anti-epileptic for the treatment of certain types of seizures - today it is also widely used to treat neuropathic pain. Gabapentin has some stark advantages as compared with other anti-epileptics, such as a relatively benign adverse effect profile, wide therapeutic index, and lack of appreciable metabolism making it unlikely to participate in pharmacokinetic drug interactions.. It is structurally and functionally related to another GABA derivative,. In the United States, gabapentin is officially indicated for the treatment of postherpetic neuralgia in adults and for the adjunctive treatment of partial-onset seizures, with or without secondary generalization, in patients 3 years of age and older. In Europe, gabapentin is indicated for adjunctive therapy in the treatment of partial-onset seizures, with or without secondary generalization, in patients 6 years of age and older and as monotherapy in patients 12 years of age and older. It is also used in adults for the treatment of various types of peripheral neuropathic pain, such as painful diabetic neuropathy. Gabapentin is an anti-convulsant medication that inhibits the release of excitatory neurotransmitters, allowing for its use against pathologic neurotransmission such as that seen in neuropathic pain and seizure disorders. It has a wide therapeutic index, with doses in excess of 8000 mg/kg failing to cause a fatal reaction in rats. The precise mechanism through which gabapentin exerts its therapeutic effects is unclear. The primary mode of action appears to be at the auxillary α2δ-1 subunit of voltage-gated calcium channels (though a low affinity for the α2δ-2 subunit has also been reported). The major function of these subunits is to facilitate the movement of pore-forming α1 subunits of calcium channels from the endoplasmic reticulum to the cell membrane of pre-synaptic neurons. There is evidence that chronic pain states can cause an increase in the expression of α2δ subunits and that these changes correlate with hyperalgesia. Gabapentin appears to inhibit the action of α2δ-1 subunits, thus decreasing the density of pre-synaptic voltage-gated calcium channels and subsequent release of excitatory neurotransmitters. It is likely that this inhibition is also responsible for the anti-epileptic action of gabapentin.",The molecular weight is 171.24.,Gabapentin has a topological polar surface area of 63.32.,The log p value of  is -0.66.,Gabapentin is approved and investigational.,Gabapentin is a solid.,True
14710,"Doxercalciferol is a synthetic vitamin D2 analog that undergoes metabolic activation in vivo to form 1α,25-dihydroxyvitamin D2 (1α,25-(OH)2D2), a naturally occurring, biologically active form of vitamin D2. Doxercalciferol is indicated for the treatment of secondary hyperparathyroidism in patients with chronic kidney disease on dialysis, as well as for the treatment of secondary hyperparathyroidism in patients with Stage 3 or Stage 4 chronic kidney disease. Doxercalciferol is marketed under the brand name Hectoral by Genzyme Corporation, and is manufactured by Catalent Pharma Solutions, Inc. Doxercalciferol is indicated for the treatment of secondary hyperparathyroidism in patients with chronic kidney disease on dialysis, as well as for the treatment of secondary hyperparathyroidism in patients with Stage 3 or Stage 4 chronic kidney disease.  Calcitriol (1α,25-(OH)2D3) and 1α,25-(OH)2D2 regulate blood calcium at levels required for essential body functions. Specifically, the biologically active vitamin D metabolites control the intestinal absorption of dietary calcium, the tubular reabsorption of calcium by the kidney and, in conjunction with parathyroid hormone (PTH), the mobilization of calcium from the skeleton. They act directly on bone cells (osteoblasts) to stimulate skeletal growth, and on the parathyroid glands to suppress PTH (parathyroid hormone) synthesis and secretion. These functions are mediated by the interaction of these biologically active metabolites with specific receptor proteins in the various target tissues. In patients with chronic kidney disease (CKD), deficient production of biologically active vitamin D metabolites (due to lack of or insufficient 25-hydroxyvitamin D-1-alpha-hydroxylase activity) leads to secondary hyperparathyroidism, which contributes to the development of metabolic bone disease. ",The molecular weight is 412.66.,Doxercalciferol has a topological polar surface area of 40.46.,The log p value of  is 8.16.,Doxercalciferol is approved.,Doxercalciferol is a solid.,True
14711,"Chenodeoxycholic acid (or Chenodiol) is an epimer of ursodeoxycholic acid (DB01586). Chenodeoxycholic acid is a bile acid naturally found in the body. It works by dissolving the cholesterol that makes gallstones and inhibiting production of cholesterol in the liver and absorption in the intestines, which helps to decrease the formation of gallstones. It can also reduce the amount of other bile acids that can be harmful to liver cells when levels are elevated. Chenodiol is indicated for patients with radiolucent stones in well-opacifying gallbladders, in whom selective surgery would be undertaken except for the presence of increased surgical risk due to systemic disease or age. Chenodiol will not dissolve calcified (radiopaque) or radiolucent bile pigment stones. It acts by reducing levels of cholesterol in the bile, helping gallstones that are made predominantly of cholesterol to dissolve. Chenodeoxycholic acid is ineffective with stones of a high calcium or bile acid content. Chenodiol suppresses hepatic synthesis of both cholesterol and cholic acid, gradually replacing the latter and its metabolite, deoxycholic acid in an expanded bile acid pool. These actions contribute to biliary cholesterol desaturation and gradual dissolution of radiolucent cholesterol gallstones in the presence of a gall-bladder visualized by oral cholecystography. Bile acids may also bind the the bile acid receptor (FXR) which regulates the synthesis and transport of bile acids. ",The molecular weight is 392.58.,Chenodeoxycholic acid has a topological polar surface area of 77.76.,The log p value of  is 4.51.,Chenodeoxycholic acid is approved.,Chenodeoxycholic acid is a solid.,True
14712,"A trihydroxy sugar alcohol that is an intermediate in carbohydrate and lipid metabolism. It is used as a solvent, emollient, pharmaceutical agent, and sweetening agent. Glycerin is commonly classified as an osmotic laxative but may act additionally or alternatively through its local irritant effects; it may also have lubricating and fecal softening actions. Glycerin suppositories usually work within 15 to 30 minutes. When administered rectally, glycerin exerts a hygroscopic and/or local irritant action, drawing water from the tissues into the feces and reflexively stimulating evacuation. ",The molecular weight is 92.09.,Glycerin has a topological polar surface area of 60.69.,The log p value of  is -1.54.,Glycerin is approved and investigational.,,True
14713,"Myelodysplastic syndromes (MDS) are a heterogeneous group of hematopoietic neoplasms with variable underlying etiology and presentation, including neutropenia and thrombocytopenia. Further mutations leading to increased proliferation of cancerous cells can eventually lead to secondary acute myeloid leukemia, which has a poor prognosis. Among treatment options, nucleoside analogues such as decitabine and integrate into cellular DNA and inhibit the action of DNA methyltransferases, leading to global hypomethylation and related downstream therapeutic benefits. Decitabine is indicated for the treatment of patients with myelodysplastic syndromes (MDS) including all French-American-British subtypes (refractory anemia, refractory anemia with ringed sideroblasts, refractory anemia with excess blasts, refractory anemia with excess blasts in transformation, and chronic myelomonocytic leukemia), as well as for MDS scored as belonging to the intermediate-1, intermediate-2, or high-risk group in the International Prognostic Scoring System. Decitabine is a prodrug analogue of the natural nucleotide 2’-deoxycytidine, which, upon being phosphorylated intracellularly, is incorporated into DNA and exerts numerous effects on gene expression. The use of decitabine is associated with neutropenia and thrombocytopenia. In addition, decitabine can cause fetal harm in pregnant women; effective contraception and avoidance of pregnancy are recommended during treatment with decitabine. Myelodysplastic syndromes (MDS) are a group of hematopoietic neoplasms that manifest in peripheral cytopenias and may eventually progress to secondary acute myeloid leukemia (sAML). Included in the over 45 genes commonly mutated in MDS patients are those involved in DNA methylation and histone modification, and it is well-established that alteration of the epigenetic landscape is a feature of myeloid leukemias.",The molecular weight is 228.21.,Decitabine has a topological polar surface area of 120.74.,The log p value of  is -1.9.,Decitabine is approved and investigational.,Decitabine is a solid.,True
14714,"Sofosbuvir (tradename Sovaldi) is a direct acting antiviral medication used as part of combination therapy to treat chronic Hepatitis C, an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Treatment options for chronic Hepatitis C have advanced significantly since 2011, with the development of Direct Acting Antivirals (DAAs) such as sofosbuvir. As a prodrug nucleotide analog, Sofosbuvir is metabolized into its active form as the antiviral agent 2'-deoxy-2'-α-fluoro-β-C-methyluridine-5'-triphosphate (also known as GS-461203), which acts as a defective substrate for NS5B (non-structural protein 5B). NS5B, an RNA-dependent RNA polymerase, is essential for the transcription of Hepatitis C viral RNA and for its high replicative rate and genetic diversity. Sofosbuvir and other direct acting antivirals are therefore very potent options for the treatment of Hepatitis C, as they exhibit a high barrier to the development of resistance. This is an important advantage relative to HCV drugs that target other viral enzymes such as the protease, for which rapid development of resistance has proven to be an important cause of therapeutic failure.  Sofosbuvir is used in combination therapy with other antiviral medications to treat chronic hepatitis C virus (HCV) infected patients with HCV genoptypes 1-6, and to treat HCV and HIV co-infected patients. Depending on the level of cirrhosis or decompensation, combination therapy can also include either ribavirin alone or ribavirin and peg-interferon alfa. Sofosbuvir acts against HCV and is categorized as a direct-acting antiviral agent (DAA). Sofosbuvir is nucleotide analog inhibitor, which specifically inhibits HCV NS5B (non-structural protein 5B) RNA-dependent RNA polymerase. Following intracellular metabolism to form the pharmacologically active uridine analog triphosphate (GS-461203), sofosbuvir incorporates into HCV RNA by the NS5B polymerase and acts as a chain terminator. More specifically, Sofosbuvir prevents HCV viral replication by binding to the two Mg2+ ions present in HCV NS5B polymerase's GDD active site motif and preventing further replication of HCV genetic material.",The molecular weight is 529.46.,Sofosbuvir has a topological polar surface area of 152.73.,The log p value of  is 0.84.,Sofosbuvir is approved.,Sofosbuvir is a solid.,True
14715,"Coenzyme M (commonly known by its salt form, Mesna) is a synthetic sulfhydryl (thiol) compound and is used for prophylaxis of Ifosfamide and cyclophosphamide induced hemorrhagic cystitis. Mesna is a uroprotective agent and is used prophylactically to reduce ifosfamide and cyclophosphamide induced hemorrhagic cystitis. Mesna binds to and inactivates acrolein there by preventing or reducing bladder problems A metabolite called acrolein is produced when ifosfamide and cyclophosphamide are metabolized. This metabolite concentrates in the bladder and causes cell death via upregulation of reactive oxygen species (ROS), and activates inducible nitric oxide synthase (iNOS) which leads to production of nitric oxide (NO). Both ROS and NO produce products which are detrimental to lipids, proteins and DNA strands. Furthermore, ROS stimulate gene expression of pro-inflammatory cytokines such as TNF-α AND IL-1β. Acrolein may also lead to ulceration of the bladder urothelium. Mesna protects against cyclophosphamide and ifosfamide induced hemorrhagic cystitis by binding to their toxic metabolites. Mesna is metabolized to dimesna and excreted by the kidneys. Glutathione dihydrogenase acts on the reabsorbed portion and produces free sulfhydryl groups. These free sulfhydryl groups bind acrolein in the bladder, allowing effective excretion and prevention of toxic effects. In addition, Mesna binds to and detoxifies a urotoxic ifosfamide metabolite called 4-hydroxy-ifosfamide.",The molecular weight is 142.19.,Coenzyme M has a topological polar surface area of 54.37.,The log p value of  is -1.55.,Coenzyme M is approved and investigational.,Coenzyme M is a solid.,True
14716,"Selenium is a trace metal in the human body particularly important as a component of glutathione peroxidase, an important enzyme in the prevention of cellular damage by free radicals and reactive oxygen species  For the supplementation of total parenteral nutrition to prevent hyposelenemia. Selenium is incorporated into many different selenoproteins which serve various functions throughout the body. Selenium is first metabolized to selenophosphate and selenocysteine. Selenium incorporation is genetically encoded through the RNA sequence UGA. This sequence is recognized by RNA ste loop structures called selenocysteine inserting sequences (SECIS). These structures require the binding of SECIS binding proteins (SBP-2) to recognize selenocystiene. The specialized tRNA is first bound to a serine residue which is then enzymatically processed to a selylcysteyl-tRNA by selenocystiene sythase using selenophosphate as a selenium donor. Other unidentified proteins are required as part of the binding of this tRNA to the ribosome. Selenoproteins appear to be necessary for life as mice with the specialized tRNA gene knocked out exhibited early embryonic lethality.",,,,Selenium is approved and investigational and vet_approved.,Selenium is a solid.,True
14717,"Streptokinase, is a sterile, purified preparation of a bacterial protein elaborated by group C (beta) -hemolytic streptococci. For the treatment of acute evolving transmural myocardial infarction, pulmonary embolism, deep vein thrombosis, arterial thrombosis or emolism and occlusion of arteriovenous cannulae Streptokinase creates an active complex which promotes the cleavage of the Arg/Val bond in plasminogen to form the proteolytic enzyme plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. This helps eliminate blood clots or arterial blockages that cause myocardial infarction. Plasminogen is an inactive molecule that becomes activated to plasmin when the Arg/Val bond is cleaved. Plasmin breaks down fibrin clots created by the blood clotting cascade. Streptokinase forms a highly specific 1:1 enzymatic complex with plasminogen which converts inactive plasminogen molecules into active plasmin. Plasmin degrades fibrin clots as well as fibrinogen and other plasma proteins. This in turn leads to the degradation of blood clots.",,,,Streptokinase is approved and investigational.,Streptokinase is a liquid.,True
14718,"A slowly hydrolyzed cholinergic agonist that acts at both muscarinic and nicotinic receptors. Primarily used in the treatment of glaucoma, but is also used during ophthalmic surgery. Carbachol is a potent cholinergic (parasympathomimetic) agent which produces constriction of the iris and ciliary body resulting in reduction in intraocular pressure. The exact mechanism by which carbachol lowers intraocular pressure is not precisely known. In the cat and rat, carbachol is well-known for its ability to induce rapid eye movement (REM) sleep when microinjected into the pontine reticular formation by activating the postsynaptic muscarinic acetylcholine receptors (mAChRs).  Carbachol is a parasympathomimetic that stimulates both muscarinic and nicotinic receptors. In topical ocular and intraocular administration its principal effects are miosis and increased aqueous humour outflow.",,,,Carbamoylcholine is approved.,Carbamoylcholine is a solid.,True
14719,"An anthracycline which is the 4&#39;-epi-isomer of doxorubicin. The compound exerts its antitumor effects by interference with the synthesis and function of DNA. For use as a component of adjuvant therapy in patients with evidence of axillary node tumor involvement following resection of primary breast cancer. Epirubicin is an antineoplastic in the anthracycline class. General properties of drugs in this class include: interaction with DNA in a variety of different ways including intercalation (squeezing between the base pairs), DNA strand breakage and inhibition with the enzyme topoisomerase II. Most of these compounds have been isolated from natural sources and antibiotics. However, they lack the specificity of the antimicrobial antibiotics and thus produce significant toxicity. The anthracyclines are among the most important antitumor drugs available. Doxorubicin is widely used for the treatment of several solid tumors while daunorubicin and idarubicin are used exclusively for the treatment of leukemia. Epirubicin may also inhibit polymerase activity, affect regulation of gene expression, and produce free radical damage to DNA. Epirubicin possesses an antitumor effect against a wide spectrum of tumors, either grafted or spontaneous. The anthracyclines are cell cycle-nonspecific. Epirubicin has antimitotic and cytotoxic activity. It inhibits nucleic acid (DNA and RNA) and protein synthesis through a number of proposed mechanisms of action: Epirubicin forms complexes with DNA by intercalation between base pairs, and it inhibits topoisomerase II activity by stabilizing the DNA-topoisomerase II complex, preventing the religation portion of the ligation-religation reaction that topoisomerase II catalyzes. It also interferes with DNA replication and transcription by inhibiting DNA helicase activity.",The molecular weight is 543.52.,Epirubicin has a topological polar surface area of 206.07.,The log p value of  is 0.32.,Epirubicin is approved.,Epirubicin is a solid.,True
14720,"Broad-spectrum semisynthetic penicillin derivative used parenterally. It is susceptible to gastric juice and penicillinase and may damage platelet function. For the treatment of acute and chronic infections of the upper and lower urinary tract and in asymptomatic bacteriuria due to susceptible strains of bacteria. Carbenicillin is a semisynthetic penicillin. Though carbenicillin provides substantial <i>in vitro</i> activity against a variety of both gram-positive and gram-negative microorganisms, the most important aspect of its profile is in its antipseudomonal and antiproteal activity. Because of the high urine levels obtained following administration, carbenicillin has demonstrated clinical efficacy in urinary infections due to susceptible strains of: <i>Escherichia coli</i>, <i>Proteus mirabilis</i>, <i>Proteus vulgaris</i>, <i>Morganella morganii</i>, <i>Pseudomonas</i> species, <i>Providencia rettgeri</i>, <i>Enterobacter</i> species, and <i>Enterococci</i> (<i>S. faecalis</i>). Free carbenicillin is the predominant pharmacologically active fraction of the salt. Carbenicillin exerts its antibacterial activity by interference with final cell wall synthesis of susceptible bacteria. Penicillins acylate the penicillin-sensitive transpeptidase C-terminal domain by opening the lactam ring. This inactivation of the enzyme prevents the formation of a cross-link of two linear peptidoglycan strands, inhibiting the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that carbenicillin interferes with an autolysin inhibitor.",The molecular weight is 378.4.,Carbenicillin has a topological polar surface area of 124.01.,The log p value of  is 1.64.,Carbenicillin is approved and investigational.,Carbenicillin is a solid.,True
14721,"Orlistat is a drug used in the treatment of obesity. Its primary function is preventing the absorption of fats from the human diet, thereby reducing caloric intake. Orlistat works by inhibiting pancreatic lipase, an enzyme that breaks down triglycerides in the intestine. Without this enzyme, triglycerides from the diet are prevented from being hydrolyzed into absorbable free fatty acids and are excreted undigested. For obesity management including weight loss and weight maintenance when used in conjunction with a reduced-calorie diet. Also used to reduce the risk for weight regain after prior weight loss. Use of orlistat is pending revision due to reports of liver-related adverse events. Orlistat is a lipase inhibitor for obesity management that acts by Orlistat is a reversible inhibitor of lipases. It exerts its therapeutic activity in the lumen of the stomach and small intestine by forming a covalent bond with the active serine residue site of gastric and pancreatic lipases. The inactivated enzymes are thus unavailable to hydrolyze dietary fat in the form of triglycerides into absorbable free fatty acids and monoglycerides. As undigested triglycerides are not absorbed, the resulting caloric deficit may have a positive effect on weight control.",The molecular weight is 495.74.,Orlistat has a topological polar surface area of 81.7.,The log p value of  is 8.61.,Orlistat is approved and investigational.,Orlistat is a solid.,True
14722,"A polyanionic compound with an unknown mechanism of action. It is used parenterally in the treatment of African trypanosomiasis and it has been used clinically with diethylcarbamazine to kill the adult Onchocerca. (From AMA Drug Evaluations Annual, 1992, p1643) It has also been shown to have potent antineoplastic properties. Suramin is manufactured by Bayer in Germany as Germanin®. For treatment of human sleeping sickness, onchocerciasis and other diseases caused by trypanosomes and worms. The mechanism is unknown, but the trypanocidal activity may be due to the inhibition of enzymes involved with the oxidation of reduced nicotinamide-adenine dinucleotide (NADH), which functions as a co-enzyme in many cellular reactions, such as respiration and glycolysis, in the trypanosome parasite. Suramin's action in the treatment of onchocerciasis is macrofilaricidal and partially microfilaricidal. It may also act as an antagonist of P2 receptors and as an agonist of Ryanodine receptors. It also can inhibit follicle-stimulating hormone receptors.",The molecular weight is 1297.26.,Suramin has a topological polar surface area of 483.75.,The log p value of  is -8.58.,Suramin is investigational.,Suramin is a solid.,True
14723,"Urethane, formerly marketed as an inactive ingredient in Profenil injection, was determined to be carcinogenic and was removed from the Canadian, US, and UK markets in 1963.",,,,Urethane is approved and withdrawn.,Urethane is a solid.,True
14724,"Lancovutide, a peptide antibiotic, is in clinical development for the treatment of cystic fibrosis. Duramycin is a 19-amino-acid tetracyclic peptide produced by Streptoverticillium cinnamoneus and is closely related to cinnamycin (Ro09-0198). It belongs to the lantibiotics. Lantibiotics are bacteriocins that are characterized by the presence of a high proportion of unusual amino acids. Investigated for use/treatment in cystic fibrosis and eye disorders/infections. Duramycin becomes deposited in cellular membranes where it binds to phosphatidylethanolamine. It may thereby change biophysical membrane properties and perturb ion channel function.",,,,Lancovutide is investigational.,Lancovutide is a solid.,True
14725,"Glycerol phenylbutyrate is a nitrogen-binding agent. Chemically, it is a triglyceride in which three molecules of phenylbutyrate are linked to a glycerol backbone. FDA approved on February 1, 2013. Glycerol phenylbutyrate is a nitrogen-binding agent for the chronic management of adult and pediatric patients ≥2 years of age with urea cycle disorders (UCDs) who cannot be managed by dietary protein restriction and/or amino acid supplementation alone.  Glycerol phenylbutyrate prolongs the QTc interval.  The toxic accumulation of ammonia in the blood and brain arise from urea cycle disorders in which patients are deficient in critical enzymes or transporters that are involved in the synthesis of urea from ammonia. Glycerol phenylbutyrate is a prodrug - the major metabolite, phenylacetate (PAA) is the molecule that binds to nitrogen. PAA conjugates with glutamine (which contains 2 molecules of nitrogen) via acetylation in the liver and kidneys to form phenylacetylglutamine (PAGN), which is excreted by the kidneys. PAGN, like urea, contains 2 moles of nitrogen and provides an alternate vehicle for waste nitrogen excretion. ",The molecular weight is 530.66.,Glycerol phenylbutyrate has a topological polar surface area of 78.9.,The log p value of  is 7.87.,Glycerol phenylbutyrate is approved.,Glycerol phenylbutyrate is a solid.,True
14726,"Melatonin is a biogenic amine that is found in animals, plants and microbes. Aaron B. Lerner of Yale University is credited for naming the hormone and for defining its chemical structure in 1958. In mammals, melatonin is produced by the pineal gland. The pineal gland is small endocrine gland, about the size of a rice grain and shaped like a pine cone (hence the name), that is located in the center of the brain (rostro-dorsal to the superior colliculus) but outside the blood-brain barrier. The secretion of melatonin increases in darkness and decreases during exposure to light, thereby regulating the circadian rhythms of several biological functions, including the sleep-wake cycle. In particular, melatonin regulates the sleep-wake cycle by chemically causing drowsiness and lowering the body temperature. Melatonin is also implicated in the regulation of mood, learning and memory, immune activity, dreaming, fertility and reproduction. Melatonin is also an effective antioxidant. Most of the actions of melatonin are mediated through the binding and activation of melatonin receptors. Individuals with autism spectrum disorders (ASD) may have lower than normal levels of melatonin. A 2008 study found that unaffected parents of individuals with ASD also have lower melatonin levels, and that the deficits were associated with low activity of the ASMT gene, which encodes the last enzyme of melatonin synthesis. Reduced melatonin production has also been proposed as a likely factor in the significantly higher cancer rates in night workers. Used orally for jet lag, insomnia, shift-work disorder, circadian rhythm disorders in the blind (evidence for efficacy), and benzodiazepine and nicotine withdrawal. Evidence indicates that melatonin is likely effective for treating circadian rhythm sleep disorders in blind children and adults. It has received FDA orphan drug status as an oral medication for this use. A number of studies have shown that melatonin may be effective for treating sleep-wake cycle disturbances in children and adolescents with mental retardation, autism, and other central nervous system disorders. It appears to decrease the time to fall asleep in children with developmental disabilities, such as cerebral palsy, autism, and mental retardation. It may also improve secondary insomnia associated with various sleep-wake cycle disturbances. Other possible uses for which there is some evidence for include: benzodiazepine withdrawal, cluster headache, delayed sleep phase syndrome (DSPS), primary insomnia, jet lag, nicotine withdrawal, preoperative anxiety and sedation, prostate cancer, solid tumors (when combined with IL-2 therapy in certain cancers), sunburn prevention (topical use), tardive dyskinesia, thrombocytopenia associated with cancer, chemotherapy and other disorders.  Melatonin is a hormone normally produced in the pineal gland and released into the blood. The essential amino acid L-tryptophan is a precursor in the synthesis of melatonin. It helps regulate sleep-wake cycles or the circadian rhythm. Production of melatonin is stimulated by darkness and inhibited by light. High levels of melatonin induce sleep and so consumption of the drug can be used to combat insomnia and jet lag. Melatonin is a derivative of tryptophan. It binds to melatonin receptor type 1A, which then acts on adenylate cylcase and the inhibition of a cAMP signal transduction pathway. Melatonin not only inhibits adenylate cyclase, but it also activates phosphilpase C. This potentiates the release of arachidonate. By binding to melatonin receptors 1 and 2, the downstream signallling cascades have various effects in the body. The melatonin receptors are G protein-coupled receptors and are expressed in various tissues of the body. There are two subtypes of the receptor in humans, melatonin receptor 1 (MT1) and melatonin receptor 2 (MT2). Melatonin and melatonin receptor agonists, on market or in clinical trials, all bind to and activate both receptor types.The binding of the agonists to the receptors has been investigated for over two decades or since 1986. It is somewhat known, but still not fully understood. When melatonin receptor agonists bind to and activate their receptors it causes numerous physiological processes.",The molecular weight is 232.28.,Melatonin has a topological polar surface area of 54.12.,The log p value of  is 1.03.,Melatonin is approved and nutraceutical and vet_approved.,Melatonin is a solid.,True
14727,"Pralatrexate is an antimetabolite for the treatment of relapsed or refractory peripheral T-cell lymphoma. It is more efficiently retained in cancer cells than methotrexate. FDA approved on September 24, 2009. Treatment of relapsed or refractory peripheral T-cell lymphoma.  Pralatrexate is a 10-deazaaminopterin analogue of methotrexate. Compared to methotrexate, pralatrexate binds to RTC-1 with 10-times the affinity and is a more potent substrate for FPGS. As a result, pralatrexate is better internalized and retained in cancer cells and is more cytotoxic.  The selectivity of pralatrexate for cancer cells is based upon the observation that cancer cells generally have an overexpression of reduced folate carrier protein-1 (RTC-1) compared to normal somatic cells. This carrier protein allows the entrance of pralatrexate into the cell. Upon entering the cell, folypolyglutamate synthase FPGS catalyzes the polyglutamination of pralatrexate so that it is retained inside the cell. ",The molecular weight is 477.48.,Pralatrexate has a topological polar surface area of 207.3.,The log p value of  is -0.11.,Pralatrexate is approved and investigational.,Pralatrexate is a solid.,True
14728,"Kappadione is a Vitamin K derivative (chemically, it is menadiol sodium diphosphate), previously approved by FDA prior to 1982 and marketed by Lilly Marketing for this drug has been discontinued and is not available in North America. It has been found to have carcinogenic potential in mammalian cells as well as cytotoxic properties. Studies involving the active metabolite of this formulation, menadione, showed oocyte toxicity in a study of mice. Anticoagulant-induced prothrombin deficiency caused by coumadin or indanedione derivatives, Menadiol sodium diphosphate is a highly water-soluble vitamin K analog. The presence of vitamin K is necessary for the formation of prothrombin, factor VII, factor IX and factor X. Lack of vitamin K results in an increased risk of hemorrhage, which can be minor or life-threatening. Menadiol sodium phosphate (vitamin K3) is involved as a cofactor in the posttranslational gamma-carboxylation of glutamic acid residues of various proteins in the body, allowing for propagation of the clotting cascade that results in coagulation. These proteins are comprised of the vitamin K-dependent coagulation factors II (prothrombin), VII (proconvertin), IX (Christmas factor), X (Stuart factor), protein C, protein S, protein Zv and a growth-arrest-specific factor (Gas6). The two vitamin K-dependent proteins found in bone are osteocalcin, also known as bone G1a (gamma-carboxyglutamate) protein or BGP, and the matrix G1a protein or MGP. Gamma-carboxylation is catalyzed by the vitamin K-dependent gamma-carboxylases. The reduced form of vitamin K, vitamin K hydroquinone, is the actual cofactor for the gamma-carboxylases. Proteins containing gamma-carboxyglutamate are called G1a proteins. ",,,,Kappadione is approved.,Kappadione is a solid.,True
14729,"A histamine congener, it competitively inhibits histamine binding to histamine H2 receptors. Cimetidine has a range of pharmacological actions. It inhibits gastric acid secretion, as well as pepsin and gastrins output. It also blocks the activity of cytochrome P-450 which might explain proposals for use in neoadjuvant therapy. For the treatment and the management of acid-reflux disorders (GERD), peptic ulcer disease, heartburn, and acid indigestion. Cimetidine is a histamine H<sub>2</sub>-receptor antagonist. It reduces basal and nocturnal gastric acid secretion and a reduction in gastric volume, acidity, and amount of gastric acid released in response to stimuli including food, caffeine, insulin, betazole, or pentagastrin. It is used to treat gastrointestinal disorders such as gastric or duodenal ulcer, gastroesophageal reflux disease, and pathological hypersecretory conditions. Cimetidine inhibits many of the isoenzymes of the hepatic CYP450 enzyme system. Other actions of Cimetidine include an increase in gastric bacterial flora such as nitrate-reducing organisms. Cimetidine binds to an H<sub>2</sub>-receptor located on the basolateral membrane of the gastric parietal cell, blocking histamine effects. This competitive inhibition results in reduced gastric acid secretion and a reduction in gastric volume and acidity.",The molecular weight is 252.34.,Cimetidine has a topological polar surface area of 88.89.,The log p value of  is 0.38.,Cimetidine is approved and investigational.,Cimetidine is a solid.,True
14730,"An inhibitor of the enzyme steroid 11-beta-monooxygenase. It is used as a test of the feedback hypothalamic-pituitary mechanism in the diagnosis of cushing syndrome. Used as a diagnostic drug for testing hypothalamic-pituitary ACTH function. Occasionally used in Cushing's syndrome. Metopirone is an inhibitor of endogenous adrenal corticosteroid synthesis. The pharmacological effect of Metopirone is to reduce cortisol and corticosterone production by inhibiting the 11-&szlig;-hydroxylation reaction in the adrenal cortex. Removal of the strong inhibitory feedback mechanism exerted by cortisol results in an increase in adrenocorticotropic hormone (ACTH) production by the pituitary. With continued blockade of the enzymatic steps leading to production of cortisol and corticosterone, there is a marked increase in adrenocortical secretion of their immediate precursors, 11-desoxycortisol and desoxycorticosterone, which are weak suppressors of ACTH release, and a corresponding elevation of these steroids in the plasma and of their metabolites in the urine. These metabolites are readily determined by measuring urinary 17-hydroxycorticosteroids (17-OHCS) or 17-ketogenic steroids (17-KGS). Because of these actions, metopirone is used as a diagnostic test, with urinary 17-OHCS measured as an index of pituitary ACTH responsiveness. Metopirone may also suppress biosynthesis of aldosterone, resulting in a mild natriuresis.",The molecular weight is 226.28.,Metyrapone has a topological polar surface area of 42.85.,The log p value of  is 1.46.,Metyrapone is approved and investigational.,Metyrapone is a solid.,True
14731,"Mibefradil was withdrawn from the market in 1998 because of potentially harmful interactions with other drugs. For the treatment of angina and high blood pressure. Mibefradil belongs to a group of medicines called calcium channel blocking agents, or, more commonly, calcium channel blockers. Calcium channel blocking agents affect the movement of calcium into the cells of the heart and blood vessels. As a result, they relax blood vessels and increase the supply of blood and oxygen to the heart while reducing its workload. Mibefradil is a benzimidazoyl-substituted tetraline that selectively binds and inhibits T-type calcium channels. Mibefradil is a tetralol calcium channel blocking agent that inhibits the influx of calcium ions across both the T (low-voltage) and L (high-voltage) calcium channels of cardiac and vascular smooth muscle, with a greater selectivity for T channels. Vasodilation occurs in vascular smooth muscle, causing a decrease in peripheral vascular resistance and a resulting decrease in blood pressure. Mibefradil causes a slight increase in cardiac output during chronic dosing. Mibefradil slows sinus and atrioventricular (AV) node conduction, producing a slight reduction in heart rate and a slight increase in the PR interval. It has also been shown to slightly lengthen the corrected sinus node recovery time and AH interval and to raise the Wenckebach point. The mechanism by which mibefradil reduces angina is not known, but is thought to be attributed to a reduction in heart rate, total peripheral resistance (afterload), and the heart rate&ndash;systolic blood pressure product at any given level of exercise. The result of these effects is a decrease in cardiac workload and myocardial oxygen demand.",The molecular weight is 495.64.,Mibefradil has a topological polar surface area of 67.45.,The log p value of  is 6.36.,Mibefradil is investigational and withdrawn.,Mibefradil is a solid.,True
14732,,,,,Hydrocortisone succinate is approved.,,False
14733,"Levomefolic acid (INN) is the metabolite of folic acid (Vitamin B9) and it is a predominant active form of folate found in foods and in the blood circulation, accounting for 98% of folates in human plasma. It is transported across the membranes including the blood-brain barrier into various tissues where it plays an essential role in the DNA synthesis, cysteine cycle and regulation of homocysteine, where it methylates homocysteine and forms methionine and tetrahydrofolate (THF). Levomefolate is approved as a food additive and is designated a GRAS (generally regarded as safe) compound. It is available commercially as a crystalline form of the calcium salt (Metafolin(R)), which has the stability required for use as a supplement. Supplementation of levomefolic acid is desired over folic acid due to reduced potential for masking vitamin B12 deficiency symptoms. For the treatment and prevention of folate deficiency and for use as an antidote against folic acid antagonists. Contained in oral contraceptives to reduce the risk of neural tube defects arising from folic acid deficiency for pregnant women who conceived during use or shortly after the discontinuation of the product. Being studied for use as a treatment for cardiovascular diseases and adjunct therapy for patients undergoing antidepressant pharmacotherapy. Levomefolic acid is an active metabolite of folic acid and a methyl group donor in one-carbon metabolism reactions. It regulates important cellular functions such as DNA biosynthesis, gene expression regulation, amino acid synthesis and metabolism, and myelin synthesis and repair. As a only form of folate that can cross the blood-brain barrier, it acts as a cofactor in the production of monoamine neurotransmitters such as dopamine, serotonin and norepinephrine. Levomefolic acid is also involved in red blood cell formation. Levomefolic acid plays a critical role in methylating homocysteines into methionine by acting as a methyl donor in a reaction catalyzed by vitamine B12-dependent methionine synthase. Homocysteine must either be further metabolized via transulfuration to become cysteine, taurine, and glutathione via a B6-dependent process, or re-methylated to become methionine again. Methionine formed from remethylation of homocysteine by levomefolic acid forms the downstream metabolite S-adenosylmethionine (SAMe), which is involved in numerous biochemical methyl donation reactions, including reactions forming monoamine neurotransmitters. Studies suggest that high plasma levels of homocysteine is associated with increased incidences of arterial plaque formation. ",The molecular weight is 459.46.,Levomefolic acid has a topological polar surface area of 198.48.,The log p value of  is -2.25.,Levomefolic acid is approved and investigational.,Levomefolic acid is a solid.,True
14734,"Polaprezinc is a chelated form of zinc and L-carnosine. It is a zinc-related medicine approved for the first time in Japan, which has been clinically used to treat gastric ulcers. It was determined that polaprezinc may be effective in pressure ulcer treatment. A study in 2013 showed that CO-administration of polaprezinc may be effective against small intestine mucosal injury associated with long-term aspirin therapy. Peptic ulcer disease, dyspepsia. Used to treat/manage peptic ulcer disease or irritation of the gastrointestinal tract by promoting tissue healing by the elimination of free radicals. Polaprezinc increases the expression of various antioxidant enzymes, including superoxide dismutase 1 (SOD-1), SOD-2, heme oxygenase-1 (HO-1), glutathione S-transferase (GST), glutathione peroxidase (GSH-px), peroxidredoxin-1 (PRDX1; PRXI) and PRXD5 (PRXV). ",The molecular weight is 289.6.,,,Polaprezinc is experimental.,Polaprezinc is a solid.,True
14735,"As of March 2019, brexanolone - developed and made available commercially by Sage Therapeutics Inc. as the brand name product Zulresso - is the first drug to have ever been approved by the US FDA specifically for the treatment of postpartum depression (PPD) in adult females. Since PPD, like various other types of depression, is characterized by feelings of sadness, worthlessness or guilt, cognitive impairment, and/or possibly suicidal ideation, it is considered a life-threatening condition. Studies have consequently found that PPD can genuinely have profound negative effects on the maternal-infant bond and later infant development. The development and availability of brexanolone for the treatment of PPD in adult females subsequently provides a new and promising therapy where few existed before. Brexanolone is a synthetic neuroactive steroid gamma-aminobutyric acid A (GABA(a)) receptor positive modulator indicated for the treatment of postpartum depression (PPD) in adult women. Brexanolone potentiated GABA-mediated currents from recombinant human GABA(a) receptors in mammalian cells expressing α1β2γ2 receptor subunits, α4β3δ receptor subunits, and α6β3δ receptor subunits. Brexanolone is a neuroactive steroid that occurs naturally (referred to as natural allopregnanolone) in the body when the female sex hormone progesterone is metabolized. This steroid compound is also believed to exhibit activity as a barbiturate-like, positive allosteric modulator of both synaptic and extrasynaptic GABA(a) receptors. In doing so, brexanolone can enhance the activity of GABA at such receptors by having GABA(a) receptor calcium channels open more often and for longer periods of time. Furthermore, it is believed that brexanolone elicits such action on GABA(a) receptors at a binding site that is distinct from those associated with benzodiazepines.",,,,Brexanolone is approved and investigational.,Brexanolone is a solid.,True
14736,"Oxaliplatin is a platinum-based chemotherapy drug in the same family as cisplatin and carboplatin. It is typically administered in combination with fluorouracil and leucovorin in a combination known as Folfox for the treatment of colorectal cancer. Compared to cisplatin the two amine groups are replaced by cyclohexyldiamine for improved antitumour activity. The chlorine ligands are replaced by the oxalato bidentate derived from oxalic acid in order to improve water solubility. Oxaliplatin is marketed by Sanofi-Aventis under the trademark Eloxatin&reg;. Used in combination with infusional 5-FU/LV, is indicated for the treatment of advanced carcinoma of the colon or rectum and for adjuvant treatment of stage III colon cancer patients who have undergone complete resection of the primary tumor.  Oxaliplatin selectively inhibits the synthesis of deoxyribonucleic acid (DNA). The guanine and cytosine content correlates with the degree of Oxaliplatin-induced cross-linking. At high concentrations of the drug, cellular RNA and protein synthesis are also suppressed.  Oxaliplatin undergoes nonenzymatic conversion to active derivatives via displacement of the labile oxalate ligand. Several transient reactive species are formed, including monoaquo and diaquo DACH platinum, which covalently bind with macromolecules. After activation, oxaliplatin binds preferentially to the guanine and cytosine moieties of DNA, leading to cross-linking of DNA, thus inhibiting DNA synthesis and transcription. Cytotoxicity is cell-cycle nonspecific. ",The molecular weight is 397.29.,,,Oxaliplatin is approved and investigational.,Oxaliplatin is a solid.,True
14737,"An organoplatinum compound that possesses antineoplastic activity. For the initial treatment of advanced ovarian carcinoma in established combination with other approved chemotherapeutic agents. One established combination regimen consists of PARAPLATIN and cyclophosphamide. It is also indicated for the palliative treatment of patients with ovarian carcinoma recurrent after prior chemotherapy, including patients who have been previously treated with cisplatin.  Carboplatin is an antineoplastic in the class of alkylating agents and is used to treat various forms of cancer. Alkylating agents are so named because of their ability to add alkyl groups to many electronegative groups under conditions present in cells. They stop tumor growth by cross-linking guanine bases in DNA double-helix strands - directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. In addition, these drugs add methyl or other alkyl groups onto molecules where they do not belong which in turn inhibits their correct utilization by base pairing and causes a miscoding of DNA. Alkylating agents are cell cycle-nonspecific. Alkylating agents work by three different mechanisms all of which achieve the same end result - disruption of DNA function and cell death. Alkylating agents work by three different mechanisms: 1) attachment of alkyl groups to DNA bases, resulting in the DNA being fragmented by repair enzymes in their attempts to replace the alkylated bases, preventing DNA synthesis and RNA transcription from the affected DNA, 2) DNA damage via the formation of cross-links (bonds between atoms in the DNA) which prevents DNA from being separated for synthesis or transcription, and 3) the induction of mispairing of the nucleotides leading to mutations.",The molecular weight is 371.26.,Carboplatin has a topological polar surface area of 107.88.,,Carboplatin is approved.,Carboplatin is a solid.,True
14738,"Busulfan is a bifunctional alkylating agent, having a selective immunosuppressive effect on bone marrow. It is not a structural analog of the nitrogen mustards. It has been used in the palliative treatment of chronic myeloid leukemia (myeloid leukemia, chronic), but although symptomatic relief is provided, no permanent remission is brought about. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), busulfan is listed as a known carcinogen. For use in combination with cyclophosphamide as a conditioning regimen prior to allogeneic hematopoietic progenitor cell transplantation for chronic myelogenous (myeloid, myelocytic, granulocytic) leukemia (FDA has designated busulfan as an orphan drug for this use). It is also used as a component of pretransplant conditioning regimens in patients undergoing bone marrow transplantation for acute myeloid leukemia and nonmalignant diseases. Busulfan is an antineoplastic in the class of alkylating agents and is used to treat various forms of cancer. Alkylating agents are so named because of their ability to add alkyl groups to many electronegative groups under conditions present in cells. They stop tumor growth by cross-linking guanine bases in DNA double-helix strands - directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. In addition, these drugs add methyl or other alkyl groups onto molecules where they do not belong which in turn leads to a miscoding of DNA. Alkylating agents are cell cycle-nonspecific and work by three different mechanisms, all of which achieve the same end result - disruption of DNA function and cell death. Overexpression of MGST2, a glutathione s-transferase, is thought to confer resistance to busulfan. The role of MGST2 in the metabolism of busulfan is unknown however.  Busulfan is an alkylating agent that contains 2 labile methanesulfonate groups attached to opposite ends of a 4-carbon alkyl chain. Once busulfan is hydrolyzed, the methanesulfonate groups are released and carbonium ions are produced. These carbonium ions alkylate DNA, which results in the interference of DNA replication and RNA transcription, ultimately leading to the disruption of nucleic acid function. Specifically, its mechanism of action through alkylation produces guanine-adenine intrastrand crosslinks. These crosslinks occur through a SN2 reaction guanine N7 nucleophilically attacks the carbon adjacent to the mesylate leaving group. This kind of damage cannot be repaired by cellular machinery and thus the cell undergoes apoptosis.",The molecular weight is 246.29.,Busulfan has a topological polar surface area of 86.74.,The log p value of  is -0.59.,Busulfan is approved and investigational.,Busulfan is a solid.,True
14739,"Curcumin, also known as diferuloylmethane, is an active component in the golden spice turmeric (Curcuma longa) and in. It is a highly pleiotropic molecule that exhibits antibacterial, anti-inflammatory, hypoglycemic, antioxidant, wound-healing, and antimicrobial activities. Due to these properties, curcumin has been investigated for the treatment and supportive care of clinical conditions including proteinuria, breast cancer, multiple myeloma, depression, and Non Small Cell Lung Cancer (NSCLC). Despite proven efficacy against numerous experimental models, poor bioavailability due to poor absorption, rapid metabolism, and rapid systemic elimination have been shown to limit the therapeutic efficacy of curcumin. Curcumin is under investigation for the treatment and supportive care of various clinical conditions including mucositis, rectal cancer, prostate cancer, chronic schizophrenia, and Mild Cognitive Impairment (MCI). No approved therapeutic indications.  Intravenous application of 25 mg/kg bw curcumin to rats resulted in an increase in bile flow by 80 and 120%. In the rat model of inflammation, curcumin was shown to inhibit edema formation. In nude mouse that had been injected subcutaneously with prostate cancer cells, administration of curcumin caused a marked decrease in the extent of cell proliferation, a significant increase of apoptosis and micro-vessel density. Curcumin may exert choleretic effects by increasing biliary excretion of bile salts, cholesterol, and bilirubin, as well as increasing bile solubility. Curcumin inhibited arachidonic acid-induced platelet aggregation _in vitro_. Curcumin acts as a scavenger of oxygen species, such as hydroxyl radical, superoxide anion, and singlet oxygen and inhibit lipid peroxidation as well as peroxide-induced DNA damage. Curcumin mediates potent anti-inflammatory agent and anti-carcinogenic actions via modulating various signalling molecules. It suppresses a number of key elements in cellular signal transduction pathways pertinent to growth, differentiation, and malignant transformation; it was demonstrated _in vitro_ that curcumin inhibits protein kinases, c-Jun/AP-1 activation, prostaglandin biosynthesis, and the activity and expression of the enzyme cyclooxygenase (COX)-2.",,,,Curcumin is approved and experimental and investigational.,Curcumin is a solid.,True
14740,"A nitrogen mustard alkylating agent used as antineoplastic agent for the treatment of various malignant and nonmalignant diseases. Although it is less toxic than most other nitrogen mustards, it has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (Merck Index, 11th ed) For treatment of chronic lymphatic (lymphocytic) leukemia, childhood minimal-change nephrotic syndrome, and malignant lymphomas including lymphosarcoma, giant follicular lymphoma, Hodgkin's disease, non-Hodgkin's lymphomas, and Waldenström’s Macroglobulinemia. Chlorambucil is an antineoplastic in the class of alkylating agents that is used to treat various forms of cancer. Alkylating agents are so named because of their ability to add alkyl groups to many electronegative groups under conditions present in cells. They stop tumor growth by cross-linking guanine bases in DNA double-helix strands - directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. In addition, these drugs add methyl or other alkyl groups onto molecules where they do not belong which in turn inhibits their correct utilization by base pairing and causes a miscoding of DNA. Alkylating agents are cell cycle-nonspecific. Alkylating agents work by three different mechanisms all of which achieve the same end result - disruption of DNA function and cell death. Alkylating agents work by three different mechanisms: 1) attachment of alkyl groups to DNA bases, resulting in the DNA being fragmented by repair enzymes in their attempts to replace the alkylated bases, preventing DNA synthesis and RNA transcription from the affected DNA, 2) DNA damage via the formation of cross-links (bonds between atoms in the DNA) which prevents DNA from being separated for synthesis or transcription, and 3) the induction of mispairing of the nucleotides leading to mutations.",The molecular weight is 304.21.,Chlorambucil has a topological polar surface area of 40.54.,The log p value of  is 3.63.,Chlorambucil is approved.,Chlorambucil is a solid.,True
14741,"Hydrogen peroxide is the simplest peroxide with a chemical formula H2O2. Hydrogen peroxide is an unstable compound in the presence of a base or catalyst, and is typically stored with a stabilizer in a weakly acidic solution. If heated to its boiling point, it may undergo potentially explosive thermal decomposition. Hydrogen peroxide is formed in the body of mammals during reduction of oxygen either directly in a two-electron transfer reaction. As a natural product of metabolism, it readily undergoes decomposition by catalase in normal cells.  Indicated to be used as a disinfectant and sterilizer.  Hydrogen peroxide exhibits antimicrobial properties against most forms of microorganisms, including dormant forms with known high resistance profiles, such as bacterial spores and protozoal cysts. It acts as an oxidative biocide to generate free radical species to induce DNA, protein and membrane lipid damage via oxidation.  The production of free hydroxyl radicals in the Fenton reaction is thought to be the basis of biocidal actions of hydrogen peroxide. Free radicals eventually lead to oxidative damage proteins and membrane lipids _in vivo_. The oxidizing radical as the ferryl radical induces DNA oxidation.",The molecular weight is 34.01.,Hydrogen peroxide has a topological polar surface area of 40.46.,,Hydrogen peroxide is approved and vet_approved.,Hydrogen peroxide is a liquid.,True
14742,"Selenious acid is the acid form of sodium selenite, a form of selenium. Selenium is a component glutathione peroxidase, which protects cells from oxidative damage caused by peroxidases produced during cellular metabolism.",,,,Selenious acid is approved and investigational.,Selenious acid is a solid.,True
14743,"Indocyanine Green is a water soluble, tricarbocyanine dye with a peak spectral absorption at 800 nm. The chemical name for Indocyanine Green is 1 H-Benzindolium, 2- indol-2-ylidene]-1,3,5-heptatrienyl]-1,1-dimethyl-3-(4-sulfobutyl)-,hydroxide, inner salt, sodium salt. Indocyanine Green for Injection USP has a pH of approximately 6.5 when reconstituted. Each vial of Indocyanine Green for Injection USP contains 25 mg of Indocyanine Green as a sterile lyophilized powder with no more than 5% sodium iodide. For Determining Cardiac Output, Hepatic Function and Liver Blood Flow Indocyanine Green for Injection USP undergoes no significant extrahepatic or enterohepatic circulation; simultaneous arterial and venous blood estimations have shown negligible renal, peripheral, lung or cerebro-spinal uptake of the dye. Indocyanine Green for Injection USP is taken up from the plasma almost exclusively by the hepatic parenchymal cells and is secreted entirely into the bile. After biliary obstruction, the dye appears in the hepatic lymph, independently of the bile, suggesting that the biliary mucosa is sufficiently intact to prevent diffusion of the dye, though allowing diffusion of bilirubin. These characteristics make Indocyanine Green for Injection USP a helpful index of hepatic function.",,,,Indocyanine green acid form is approved and investigational.,,True
14744,"Esculin is found in barley. Vitamin C2 is generally considered a bioflavanoid, related to vitamin P esculin is a glucoside that naturally occurs in the horse chestnut (Aesculus hippocastanum), California Buckeye (Aesculus californica) and in daphnin (the dark green resin of Daphne mezereum). Esculin belongs to the family of Glycosyl Compounds. These are carbohydrate derivatives in which a sugar group is bonded through its anmoeric carbonA to another group via a C-, S-,N-,O-, or Se- glycosidic bond. As medication, esculin is sometimes used as a vasoprotective agent. Topically applied Esculine increases the “capillary density” (the number of capillaries open to flow per surface unit) and improves the morphological aspect of the smallest blood vessels. The main activities of Esculine focus on capillary protection, as it improves capillary permeability and fragility. It is reported to inhibit catabolic enzymes such as hyaluronidase and collagenase, thus preserving the integrity of the perivascular connective tissue. Esculine also showed good antioxidant properties, protecting triglycerides against auto-oxidation at high temperatures. The antioxidant property might as well explain some of the anti-inflammatory activity of the product, making it a suitable product for after sun treatments, for example.",,,,Esculin is approved.,Esculin is a solid.,True
14745,"Levomethamphetamine, the L-enantiomer of methamphetamine is a sympathomimetic vasoconstrictor used in some over-the-counter (OTC) nasal decongestant inhalers in the United States. Used over-the-counter for nasal congestion. Levomethamphetamine increases norepinephrine release resulting in increased vasocontriction. Levomethamphetamine crosses the blood-brain-barrier and acts as a TAAR1 agonist, functioning as a selective norepinephrine releasing agent in the central nervous system,",The molecular weight is 149.24.,Levmetamfetamine has a topological polar surface area of 12.03.,The log p value of  is 1.89.,Levmetamfetamine is approved.,Levmetamfetamine is a solid.,True
14746,"Trastuzumab deruxtecan is a HER-2 directed antibody attached to a topoisomerase inhibitor that is approved for use in certain types of metastatic, unresectable breast cancer. It is classified as an antibody-drug conjugate. The cleavable peptide linker used to bind the antibody and drug in this product distinguishes it from other members of its class. Trastuzumab deruxtecan has been granted FDA approval for specific patients with HER-2 positive breast cancer who have failed other treatments. Trastuzumab deruxtecan is indicated for the treatment of adult patients with HER-2 positive breast cancer that is unresectable or metastatic and was previously treated with at least 2 anti-HER2-based regimens while the cancer was metastatic. Trastuzumab demonstrates antitumor activity against certain types of HER2 positive breast cancer, however, clinical trials are still ongoing to confirm its efficacy. By exploiting both targeted antibody and cytotoxic effects, trastuzumab deruxtecan can effectively destroy tumors.  Trastuzumab deruxtecan is a humanized anti-HER2 IgG1 antibody, targeting cancer cause by mutation of the HER2 gene. In addition, the small molecule portion of this drug, deruxtecan (DXd), is a topoisomerase I inhibitor. It is attached to the antibody by a peptide linker. After trastuzumab deruxtecan binds to HER2 found on malignant cells, it is internalized and linker cleavage occurs through the actions of lysosomal enzymes. After it is released through cleavage, DXd causes targeted DNA damage and apoptosis in cancer cells, due to the ability to cross cell membranes.",,,,Trastuzumab deruxtecan is approved and investigational.,,True
14747,"Chondroitin sulfate is a glycosaminoglycan considered as a symptomatic slow-acting drug for osteoarthritis (SYSADOA). The SYSADOA status suggested a pain relief and increased joint mobility after a relative long regular administration, as well as a long-lasting effect after the end of the treatment. Chondroitin sulfate is composed of alternating 1,3-N-acetyl-β-d-galactosamine and 1,4-β-d-glucuronic acid units which bear 4-O- and/or 6-O-sulfations at the N-acetylgalactosamine units disposed of in specific patterns. Depending on the predominating disaccharide unit, it will present different biological activities. Chondroitin sulfate is sold as an OTC dietary supplement in North America and it is a prescription drug under the EMA in Europe. Chondroitin sulfate, used with glucosamine, is indicated to alleviate pain and inflammation from primary osteoarthritis. This supplement is reported to improve joint function and slow disease progression. Osteoarthritis is characterized by progressive structural and metabolic changes in joint tissues, mainly cartilage degradation, subchondral bone sclerosis and inflammation of synovial membrane. In clinical trials, chondroitin sulfate has been reported a significant pain relief. Some reports have shown no slow in joint damage. The effects of chondroitin sulfate have been very controversial. One of the characteristics of chondroitin is a slow onset of action with a maximal effect attained after several months. Chondroitin sulfate has been reported to have anti-inflammatory properties by reducing the synovitis and prevent proinflammatory cytokine up-regulation in arthritis models. Chondroitin sulfate functions as a major component of the intricate extracellular matrix. It is proposed that chondroitin sulfate supply can provide new building blocks for the synthesis of new matrix components.",,,,Chondroitin sulfate is approved and investigational and nutraceutical.,Chondroitin sulfate is a solid.,True
14748,"Propacetamol is a non-opioid analgesic devoid of the major contraindications. It is a derivative of , or paracetamol, with the molecular formula glycine, N, N-diethyl-,4-(acetylamino)phenyl ester. Propacetamol is a parenteral formulation of paracetamol and thus, it is a prodrug that is completely hydrolyzed to paracetamol. It is not available in the United States but this prodrug has been widely used in other countries such as France since 1985. Propacetamol is a paracetamol prodrug of intravenous administration used to control fever and pain of perioperative period in multimodal analgesia therapy. Propacetamol is hydrolyzed to paracetamol and then it presents a weak inhibition of COX-1 and COX-2 which is translated into a low anti-inflammatory activity. Therefore, in high inflammatory conditions, such as rheumatoid arthritis, these agents show limited in vivo suppression of inflammation and platelet activity. The formation of N-arachidonoylphenolamine, donates paracetamol with analgesic and antipyretic properties. As propacetamol is a prodrug, its mechanism of action is directly linked to the activity of paracetamol. The mechanism of action of paracetamol is described by the inhibition of prostaglandin synthesis. This inhibition is attained by inhibition of COX-1 and COX-2 in an environment where arachidonic acid and peroxides are kept low. It is considered that paracetamol presents a very complex mechanism of action involving effects in the peripheral system, described by direct COX inhibition; the central system, characterized by inhibition of COX, serotonergic descending neuronal pathway, L-arginine/NO pathway and cannabinoid system; and a redox mechanism. In the brain and spinal cord, paracetamol can combine with arachidonic acid to form N-arachidonoylphenolamine. This metabolite is an activator of capsaicin receptor (TRPV1) and cannabinoid CB1.",The molecular weight is 264.32.,Propacetamol has a topological polar surface area of 58.64.,The log p value of  is 1.66.,Propacetamol is experimental.,Propacetamol is a solid.,True
14749,"Vayarin is a prescription medical food for the clinical dietary management of certain lipid imbalances blamed to be associated with attention deficit hyperactivity disorder (ADHD) in children. Vayarin contains _Lipirinen_, a proprietary composition containing phosphatidylserine-omega 3, EPA (eicosapentaenoic acid), and docosahexaenoic acid (DHA). Vayarin is currently available only by prescription in the USA. This drug has also been used for management of hypertriglyceridemia. ADHD in children, hypertriglyceridemia. Compared to healthy children of the same age, children with ADHD have lower circulating concentrations of omega-3 long-chain polyunsaturated fatty acid. These lipids, found in the brain, play an essential role in central nervous system development and function. It has been reported that omega-3 fatty acid deficiency is directly associated with decreased brain phosphatidylserine, which is mainly in the form of phosphatidylserine-Omega-3 (Ps-Omega-3). Phosphatidylserine (PS) in the mammalian nervous system, containing high levels of omega-3 fatty acids, has been implicated in numerous membrane-associated functions, such as maintaining the integrity of cell membranes, cell excitability and cell-to-cell recognition and communication. While the exact mechanism by which this medical food exerts its effects is not fully understood, PS has been found to regulate important proteins in neuronal cell membranes, including sodium/calcium ATPase and protein kinase C, which perform crucial functions in many signal transduction pathways. Similarly, PS interacts with Raf-1 protein kinase to promote a cascade of reactions that are believed to be involved in the survival of cells. Additionally, PS has been found to influence neurotransmitter activity, such as the release of acetylcholine (Ach), dopamine, and noradrenaline. In addition, it is also thought to increase brain glucose concentrations. Administration of specially processed formulations consisting of PS conjugated to omega-3 fatty acids was found to significantly increase DHA levels in the brain tissue of rats. ",,,,Vayarin is approved and investigational.,Vayarin is a solid.,True
14750,"Evening primrose oil comes from the extraction from _Oenothera biennis_ seeds and it is commonly used as an alternative source for omega-6 essential fatty acids. In its composition it presents some fatty acids such as and. Evening primrose oil has been filled for the FDA by Humanetics Corporation on April 2000 to be a new dietary ingredient but its current status is \Inadequate basis for expectation of safety\"". By Health Canada, evening primrose oil is approved in over-the-counter combination dietary supplements. By the EMA, evening primrose oil is approved in herbal preparations."" Evening primrose oil is used as part of over-the-counter dietary supplements. The effectivity of evening primrose oil is debatable as the evidence is very limited. Evening primrose oil improves the essential fatty acid content in plasma, erythrocyte, and platelet lipids. It has also been registered to increase alpha-tocopherol levels in non-diabetic and type I diabetic patients. Evening primrose oil affects the fatty acid composition of serum lipids and adipose tissue as well as it helps maintain normal cellular structures and it serves as a prostaglandin precursor. Administration of evening primrose oil is part of long-term therapy and thus, immediate results are never expected. Evening primrose oil presents a content of 74% and 9% from which the later seems to be the key active ingredient of this oil. These major essential fatty acids are required for the normal structure of cell membranes and they are not synthesized endogenously. The therapeutic activity of evening primrose oil is attributed to the direct action of its essential fatty acids on immune cells as well as to an indirect effect on the synthesis of eicosanoids. The actions of highly unsaturated fatty acids in tissues and eicosanoids are thought to be implicated in inflammatory and immunologic pathogeneses.",,,,Evening primrose oil is investigational and nutraceutical.,Evening primrose oil is a liquid.,True
14751,"Zinc sulfate is the inorganic compound with the formula ZnSO4 and historically known as \white vitriol\"". It is on the World Health Organization's List of Essential Medicines, a list of the most important medication needed in a basic health system."" This medication is a mineral used to treat or prevent low levels of zinc alone and together with oral rehydration therapy (ORT). It is also used as a topical astringent. Zinc Sulfate Injection, USP is indicated for use as a supplement to intravenous solutions given for TPN.  Zinc has been identified as a cofactor for over 70 different enzymes, including alkaline phosphatase, lactic dehydrogenase and both RNA and DNA polymerase. Zinc facilitates wound healing, helps maintain normal growth rates, normal skin hydration and the senses of taste and smell. Zinc inhibits cAMP-induced, chloride-dependent fluid secretion by inhibiting basolateral potassium (K) channels, in in-vitro studies with rat ileum. This study has also shown the specificity of Zn to cAMP-activated K channels, because zinc did not block the calcium (Ca)-mediated K channels. As this study was not performed in Zn-deficient animals, it provides evidence that Zn is probably effective in the absence of Zn deficiency. Zinc also improves the absorption of water and electrolytes, improves regeneration of the intestinal epithelium, increases the levels of brush border enzymes, and enhances the immune response, allowing for a better clearance of the pathogens.",The molecular weight is 161.44.,,,Zinc sulfate is approved and investigational.,Zinc sulfate is a solid.,True
14752,"Strontium chloride (Sr-89), initially FDA-approved in 1993, is used as a paliative therapeutic option to help relieve the pain from bone metastases. Strontium chloride is mainly used in cases of metastatic castrate-resistant prostate cancer. Bone metastases is a common and severe complication presented in advanced stages of the disease. It is usually presented mainly in patients with prostatic and breast cancer, as well as in cancer of lung, bladder and thyroid. There has been some cases of apparent tumor regression which has given it a potential tumoricidal effect. Strontium-89 Chloride Injection is indicated as a paliative for the relief of bone pain in patients with skeletal metastases. It is impotant to confirm the presence of bone metastases prior the beginning of therapy. Metastatic bone lesions are zones of high bone mineral turnover. Thus, there is a constant need of calcium supply for the development of the malignancy. Strontium chloride 89 is a divalent ion, similar to calcium, therefore it is taken up by sites of active osteogenesis. This relieves bone metastatic-driven pain withouth generating important side effects and it also presents a very little radioprotection concern. Once combined with external beam radiotherapy, strontium chloride 89 can emit β particules with a maximum range in tissue of 6-8mm. This radiation is capable to reduce new bone metastases and produces an analgesic role. Strontium chloride 89, a similar to calcium divalent ion, concentrates in areas of increased osteogenesis, by being taken up into the inorganic matter of the bone. Strontium chloride 89 presents a 10-fold higher affinity for metastatic bone. Some reports indicate that after Strontium chloride 89 is incorporated into the osteoid matrix adjascently to the metastatic cells, it emits β-rays getting even to 1.3-64Gy. Thus, there is a possible tumoricidal effect driven by the radiation selectively emited by strontium chloride 89 into metastatic bones. ",,,,Strontium chloride Sr-89 is approved and investigational.,Strontium chloride Sr-89 is a liquid.,True
14753,"Mersalyl is the sodium salt form of mersalyl acid, a mercurial diuretic. It is an outdated drug, and its approval has been discontinued by the FDA. Mersalyl acid is currently replaced by less toxic non-mercury containing diuretics. The sodium salt of a mercury-containing derivative of salicylamide, was formerly used (often in combination with theophylline) to treat edema, due to its powerful diuretic properties. Interestingly, it has been found to have antiviral properties in mice. Elevated blood pressure, edema. Mersalyl acid is an organomercuric compound. It is used as a diuretic. Mercury is a heavy, silvery d-block metal and one of six elements that are liquid at or near room temperature and pressure. It is a naturally occuring substance, and combines with other elements such as chlorine, sulfur, or oxygen to form inorganic mercury compounds (salts). Mercury also combines with carbon to make organic mercury compounds. Mersalyl is a mercurial diuretic which acts on the renal tubules, increasing the excretion of sodium and chloride, in approximately equal amounts, and of water. As a result, blood pressure and edema is markedly decreased. ",,,,Mersalyl is experimental.,Mersalyl is a solid.,True
14754,"Loteprednol Etabonate (LE) is a topical corticoid anti-inflammatory. It is used in ophthalmic solution for the treatment of steroid responsive inflammatory conditions of the eye such as allergic conjunctivitis, uveitis, acne rosacea, superficial punctate keratitis, herpes zoster keratitis, iritis, cyclitis, and selected infective conjunctivitides. As a nasal spray, it can be used for the treatment and management of seasonal allergic rhinitis. A number of prescription loteprednol etabonate ophthalmic products are specifically indicated for the treatment of post-operative inflammation and pain following ocular surgery.  Loteprednol etabonate (LE) belongs to a unique class of corticosteroids with potent anti-inflammatory effects designed to be active at the site of action. Animal studies have shown that LE has a binding affinity to steroid receptors that is 4.3 times greater than dexamethasone. This particular class of steroids consists of bioactive molecules whose in-vivo transformation to non-toxic substances can be predicted from their chemistry and knowledge of enzymatic pathways in the body. Cortienic acid is an inactive metabolite of hydrocortisone and analogs of cortienic acid are also devoid of corticosteroid activity. Specifically, LE is an ester derivative of one of these analogs, cortienic acid etabonate. In particular, LE possesses a metabolically labile 17 beta-chloromethyl ester function which was designed in order to be hydrolyzed to an inactive carboxylic acid moiety. This inactive metabolite is more hydrophilic and is thus readily eliminated from the body. LE also exhibits good ocular permeation properties and good skin permeation properties. Corticosteroids like loteprednol etabonate inhibit the inflammatory response to a variety of inciting agents and likely delay or slow healing. They inhibit the edema, fibrin deposition, capillary dilation, leukocyte migration, capillary proliferation, fibroblast proliferation, deposition of collagen, and scar formation that are commonly associated with inflammation. While glucocorticoids are known to bind to and activate the glucocorticoid receptor, the molecular mechanisms involved in glucocorticoid/glucocorticoid receptor-dependent modulation of inflammation are not clearly established. Moreover, corticosteroids are thought to inhibit prostaglandin production through several independent mechanisms. In particular, corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2. ",The molecular weight is 466.96.,Loteprednol etabonate has a topological polar surface area of 99.13.,The log p value of  is 3.34.,Loteprednol etabonate is approved.,Loteprednol etabonate is a solid.,True
14755,"Edetate calcium disodium is a metal ion chelator used to reduce blood concentrations and depot stores of lead from the body. It is on the World Health Organization Model List of Essential Medicines. Edetate calcium disodium is indicated to reduce blood levels and depot stores of lead in acute and chronic lead poisoning. Edetate calcium disodium is a polyvalent ion chelator used to remove lead from the body after lead poisoning. It has a wide therapeutic index, as overdoses must be well in excess of the therapeutic dose to show symptoms. It has a long duration of action, as doses are given at least a day apart. Patients should be counselled regarding the risk of increased intracranial pressure with intravenous infusions. Edetate calcium disodium distributes into tissues, such as the kidney and bone, where it chelates lead ions. The lead ions are then eliminated in the normal urinary excretion of edetate. Lead in certain tissues such as the liver and bone, redistribute to other tissues after edetate calcium disodium treatment, but lead levels do not decrease to levels seen in unexposed patients.",,,,Edetate calcium disodium anhydrous is approved.,Edetate calcium disodium anhydrous is a solid.,True
14756,"Edetate disodium anhydrous is a polyvalent chelating agent used to treat hypercalcemia and digitalis toxicity associated ventricular arrhythmias. Edetate disodium is indicated for emergency treatment of hypercalcemia and digitalis toxicity associated ventricular arrhythmias. Edetate disodium anhydrous is a polyvalent ion chelator that reduces blood concentrations of calcium or digitalis. It has a long duration of action as patients are generally given 1 daily dose. The therapeutic index is wide, as high doses are generally well tolerated. Patients should be counselled regarding the risk of postural hypotension, effects of myocardial contractility, hypokalemia, hypomagnesemia, and hypoglycemia. Edetate disodium anhydrous chelates divalent and trivalent ions such as magnesium, zinc, and calcium. The chelate is excreted in the urine, reducing concentrations of these ions in the blood.",,,,Edetate disodium anhydrous is approved and vet_approved.,Edetate disodium anhydrous is a solid.,True
14757,"No approved therapeutic indications.  Intravenous application of 25 mg/kg bw curcumin to rats resulted in an increase in bile flow by 80 and 120%. In the rat model of inflammation, curcumin was shown to inhibit edema formation. In nude mouse that had been injected subcutaneously with prostate cancer cells, administration of curcumin caused a marked decrease in the extent of cell proliferation, a significant increase of apoptosis and micro-vessel density. Curcumin may exert choleretic effects by increasing biliary excretion of bile salts, cholesterol, and bilirubin, as well as increasing bile solubility. Curcumin inhibited arachidonic acid-induced platelet aggregation _in vitro_. Curcumin acts as a scavenger of oxygen species, such as hydroxyl radical, superoxide anion, and singlet oxygen and inhibit lipid peroxidation as well as peroxide-induced DNA damage. Curcumin mediates potent anti-inflammatory agent and anti-carcinogenic actions via modulating various signalling molecules. It suppresses a number of key elements in cellular signal transduction pathways pertinent to growth, differentiation, and malignant transformation; it was demonstrated _in vitro_ that curcumin inhibits protein kinases, c-Jun/AP-1 activation, prostaglandin biosynthesis, and the activity and expression of the enzyme cyclooxygenase (COX)-2.",,,,Curcumin sulfate is experimental.,,True
14758,"Capecitabine is an orally-administered chemotherapeutic agent used in the treatment of metastatic breast and colorectal cancers. Capecitabine is a prodrug, that is enzymatically converted to fluorouracil (antimetabolite) in the tumor, where it inhibits DNA synthesis and slows growth of tumor tissue. For the treatment of patients with metastatic breast cancer resistant to both paclitaxel and an anthracycline-containing chemotherapy regimen. May also be used in combination with docetaxel for the treatment of metastatic breast cancer in patients who have failed to respond to, or recurred or relasped during or following anthracycline-containing chemotherapy. Capecitabine is used alone as an adjuvant therapy following the complete resection of primary tumor in patients with stage III colon cancer when monotherapy with fluroprymidine is preferred. The use or capecitabine in combination regimens for advanced gastric cancer is currently being investigated. Capecitabine is a fluoropyrimidine carbamate with antineoplastic activity indicated for the treatment of metastatic breast cancer and colon cancer. It is an orally administered systemic prodrug that has little pharmacologic activity until it is converted to fluorouracil by enzymes that are expressed in higher concentrations in many tumors. Fluorouracil it then metabolized both normal and tumor cells to 5-fluoro-2′-deoxyuridine 5′-monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP). Capecitabine is a prodrug that is selectively tumour-activated to its cytotoxic moiety, fluorouracil, by thymidine phosphorylase, an enzyme found in higher concentrations in many tumors compared to normal tissues or plasma. Fluorouracil is further metabolized to two active metabolites, 5-fluoro-2'-deoxyuridine 5'-monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP), within normal and tumour cells. These metabolites cause cell injury by two different mechanisms. First, FdUMP and the folate cofactor, N5-10-methylenetetrahydrofolate, bind to thymidylate synthase (TS) to form a covalently bound ternary complex. This binding inhibits the formation of thymidylate from 2'-deaxyuridylate. Thymidylate is the necessary precursor of thymidine triphosphate, which is essential for the synthesis of DNA, therefore a deficiency of this compound can inhibit cell division. Secondly, nuclear transcriptional enzymes can mistakenly incorporate FUTP in place of uridine triphosphate (UTP) during the synthesis of RNA. This metabolic error can interfere with RNA processing and protein synthesis through the production of fraudulent RNA.",The molecular weight is 359.35.,Capecitabine has a topological polar surface area of 120.69.,The log p value of  is 0.84.,Capecitabine is approved and investigational.,Capecitabine is a solid.,True
14759,"Tegafur-uracil is an anti-tumor compound containing tegafur (1-(2-tetrahydrofuryl)-5-fluorouracil) and uracil in a molar ratio of 1:4. It was developed as an anti-cancer therapy by Taiho Pharmaceutical Co Ltd. It is approved in different countries but it is not yet approved by the FDA, Health Canada or EMA. Tegafur-uracil is indicated for the first line treatment of metastatic colorectal cancer with concomitant administration of calcium folinate. Colorectal cancer is the third most diagnosed cancer and 30% of the cases can present the metastatic state. The use of the combination of tegafur and uracil allows increasing the oral bioavailability, improving the pharmacokinetic behavior of the delivered 5-fluoruracil and increasing the half-life of tegafur. The effect of this combo drug can ameliorate the usage by reducing the dosage frequency which tends to be uncomfortable for the patients. The effect of tegafur's metabolites results in a decreased thymidine synthesis, DNA synthesis, disrupted RNA function and tumor cell cytotoxicity. The generation of this combo was conceived under the reported activation by the transformation of tegafur to 5-fluorouracil. These findings have convened with results that suggested that the degradation of 5-fluorouracil can be depressed by the addition of uracil. Uracil competitively inhibits the catabolic action of dihydropyrimidine dehydrogenase. This combined activity allows a significant increase in blood and tissue 5-fluorouracil levels by inhibiting its first-pass hepatic metabolism. The active metabolites of tegafur inhibit the enzyme thymidylate synthase (5-fluoro-deoxyuridine-monophosphate) and intercalate into RNA (5-fluorouridine-triphosphate).",The molecular weight is 312.26.,,,Tegafur-uracil is approved and investigational.,Tegafur-uracil is a solid.,True
14760,"Tyropanoic acid is a radiocontrast agent used in cholecystography, the X-ray diagnosis of gallstones under the trade names include Bilopaque, Lumopaque, Tyropaque, and Bilopac. The molecule contains three heavy iodine atoms which obstruct X-rays in the same way as the calcium in bones, which results in a visible image. For use in cholecystography (X-ray diagnosis/imaging of gallstones). Tyropanoate sodium, also known as sodium tyropanoate, is a radiocontrast agent used in cholecystography (X-ray imagining and diagnosis of gallstones). This molecule contains three heavy iodine atoms which obstruct X-rays to produce a visible image. After injection, it is rapidly excreted into the bile.",The molecular weight is 641.03.,Tyropanoic acid has a topological polar surface area of 66.4.,The log p value of  is 4.15.,Tyropanoic acid is approved.,Tyropanoic acid is a solid.,True
14761,"Niraparib is an orally active PARP inhibitor developed by Tesaro to treat ovarian cancer. FDA approval on March 2017. Niraparib is indicated for the maintenance treatment of adult patients with recurrent epithelial ovarian, fallopian tube, or primary peritoneal cancer who are in complete or partial response to platinum-based chemotherapy Cardiovascular Effects: Niraparib is an inhibitor of poly (ADP-ribose) polymerase (PARP) enzymes, PARP-1 and PARP-2, which play a role in DNA repair. In vitro studies have shown that niraparib-induced cytotoxicity may involve inhibition of PARP enzymatic activity and increased formation of PARP-DNA complexes resulting in DNA damage, apoptosis and cell death. Increased niraparib-induced cytotoxicity was observed in tumor cell lines with or without deficiencies in BRCA1/2. Niraparib decreased tumor growth in mouse xenograft models of human cancer cell lines with deficiencies in BRCA1/2 and in human patient-derived xenograft tumor models with homologous recombination deficiency that had either mutated or wild type BRCA1/2. ",The molecular weight is 320.4.,Niraparib has a topological polar surface area of 72.94.,The log p value of  is 2.72.,Niraparib is approved and investigational.,,True
14762,"A thiazide diuretic with actions and uses similar to those of hydrochlorothiazide. It has been used in the treatment of familial hyperkalemia, hypertension, edema, and urinary tract disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p810) For the treatment of high blood pressure and management of edema related to heart failure. Bendroflumethiazide, a thiazide diuretic, removes excess water from the body by increasing how often you urinate (pass water) and also widens the blood vessels which helps to reduce blood pressure. It inhibits Na<sup>+</sup>/Cl<sup>-</sup> reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue. As a diuretic, bendroflumethiazide inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like bendroflumethiazide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of bendroflumethiazide is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle.",The molecular weight is 421.41.,Bendroflumethiazide has a topological polar surface area of 118.36.,The log p value of  is 1.73.,Bendroflumethiazide is approved.,Bendroflumethiazide is a solid.,True
14763,"A thiazide diuretic with properties similar to those of hydrochlorothiazide. (From Martindale, The Extra Pharmacopoeia, 30th ed, p830) Used in the treatment of oedema (including that associated with heart failure) and hypertension. Trichloromethiazide is indicated as adjunctive therapy in edema associated with congestive heart failure, hepatic cirrhosis, and corticosteroid and estrogen therapy. Trichloromethiazide has also been found useful in edema due to various forms of renal dysfunction such as nephrotic syndrome, acute glomer-ulonephritis, and chronic renal failure. Trichloromethiazide is also indicated in the management of hypertension either as the sole therapeutic agent or to enhance the effectiveness of other antihypertensive drugs in the more severe forms of hypertension. Like other thiazides, Trichloromethiazide promotes water loss from the body (diuretics). They inhibit Na<sup>+</sup>/Cl<sup>-</sup> reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue. Trichlormethiazide seemingly appears to inhibit the active reabsorption of chloride in the ascending loop of Henle. Additionally, it may also do the same for sodium. These actions subsequently alter electrolyte transfer in the proximal tubule. This results in excretion of sodium, chloride, and water and, hence, diuresis. As a diuretic, Trichloromethiazide inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like Trichloromethiazide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of Trichloromethiazide is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle.",The molecular weight is 380.64.,Trichlormethiazide has a topological polar surface area of 118.36.,The log p value of  is 0.88.,Trichlormethiazide is approved and vet_approved.,Trichlormethiazide is a solid.,True
14764,"An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes with nucleic acid synthesis by inhibiting purine metabolism and is used, usually in combination with other drugs, in the treatment of or in remission maintenance programs for leukemia. For remission induction and maintenance therapy of acute lymphatic leukemia. Mercaptopurine is one of a large series of purine analogues which interfere with nucleic acid biosynthesis and has been found active against human leukemias. It is an analogue of the purine bases adenine and hypoxanthine. It is not known exactly which of any one or more of the biochemical effects of mercaptopurine and its metabolites are directly or predominantly responsible for cell death. Mercaptopurine competes with hypoxanthine and guanine for the enzyme hypoxanthine-guanine phosphoribosyltransferase (HGPRTase) and is itself converted to thioinosinic acid (TIMP). TIMP inhibits several reactions that involve inosinic acid (IMP), such as the conversion of IMP to xanthylic acid (XMP) and the conversion of IMP to adenylic acid (AMP) via adenylosuccinate (SAMP). Upon methylation, TIMP forms 6-methylthioinosinate (MTIMP) which inhibits glutamine-5-phosphoribosylpyrophosphate amidotransferase in addition to TIMP. Glutamine-5-phosphoribosylpyrophosphate amidotransferase is the first enzyme unique to the _de novo_ pathway for purine ribonucleotide synthesis. According to experimental findings using radiolabeled mercaptopurine, mercaptopurine may be recovered from the DNA in the form of deoxythioguanosine. In comparison, some mercaptopurine may be converted to nucleotide derivatives of 6-thioguanine (6-TG) via actions of inosinate (IMP) dehydrogenase and xanthylate (XMP) aminase that convert TIMP to thioguanylic acid (TGMP).",The molecular weight is 152.18.,Mercaptopurine has a topological polar surface area of 53.07.,The log p value of  is -1.33.,Mercaptopurine is approved.,Mercaptopurine is a solid.,True
14765,"Cobimetinib is an orally active, potent and highly selective small molecule inhibiting mitogen-activated protein kinase kinase 1 (MAP2K1 or MEK1), and central components of the RAS/RAF/MEK/ERK signal transduction pathway. It has been approved in Switzerland and the US, in combination with vemurafenib for the treatment of patients with unresectable or metastatic BRAF V600 mutation-positive melanoma. For the treatment of patients with unresectable or metastatic melanoma with a BRAF V600E or V600K mutation. Cobimetinib is used in combination with vemurafenib, a BRAF inhibitor. Cobimetinib is a reversible inhibitor of mitogen-activated protein kinase 1 (MAPK)/extracellular signal regulated kinase 1 (MEK1) and MEK2. Preclinical studies have demonstrated that this agent is effective in inhibiting the growth of tumor cells bearing a BRAF mutation, which has been found to be associated with many tumor types. A threonine-tyrosine kinase and a key component of the RAS/RAF/MEK/ERK signalling pathway that is frequently activated in human tumors, MEK1 is required for the transmission of growth-promoting signals from numerous receptor tyrosine kinases. Cobimetinib is used in combination with vemurafenib because the clinical benefit of a BRAF inhibitor is limited by intrinsic and acquired resistance. Reactivation of the MAPK pathway is a major contributor to treatment failure in BRAF-mutant melanomas, approximately ~80% of melanoma tumors becomes BRAF-inhibitor resistant due to reactivation of MAPK signalling. BRAF-inhibitor resistant tumor cells are sensitive to MEK inhibition, therefore cobimetinib and vemurafenib will result in dual inhibition of BRAF and its downstream target, MEK.  MEK inhibitor Cobimetinib specifically binds to and inhibits the catalytic activity of MEK1, resulting in inhibition of extracellular signal-related kinase 2 (ERK2) phosphorylation and activation and decreased tumor cell proliferation. Cobimetinib and vemurafenib target two different kinases in the RAS/RAF/MEK/ERK pathway. ",The molecular weight is 531.32.,Cobimetinib has a topological polar surface area of 64.6.,The log p value of  is 5.11.,Cobimetinib is approved and investigational.,Cobimetinib is a solid.,True
14766,"Glucose is a simple sugar (monosaccharide) generated during phosynthesis involving water, carbon and sunlight in plants. It is produced in humans via hepatic gluconeogenesis and breakdown of polymeric glucose forms (glycogenolysis). It circulates in human circulation as blood glucose and acts as an essential energy source for many organisms through aerobic or anaerobic respiration and fermentation. It is primarily stored as starch in plants and glycogen in animals to be used in various metabolic processes in the cellular level. Its aldohexose stereoisomer, dextrose or D-glucose, is the most commonly occurring isomer of glucose in nature. L-glucose is a synthesized enantiomer that is used as a low-calorie sweetener and laxative. The unspecified form of glucose is commonly supplied as an injection for nutritional supplementation or metabolic disorders where glucose levels are improperly regulated. Glucose is listed on the World Health Organization's List of Essential Medicines. Glucose pharmaceutical formulations (oral tablets, injections) are indicated for caloric supply and carbohydrate supplementation in case of nutrient deprivation. It is also used in metabolic disorders such as hypoglycemia. Blood glucose is an obligatory energy source in humans involved in various cellular activities, and it also acts as a signalling molecule for diverse glucose-sensing molecules and proteins. Glucose undergoes oxidation into carbon dioxide, water and yields energy molecules in the process of glycolysis and subsequent citric cycle and oxidative phosphorylation. Glucose is readily converted into fat in the body which can be used as a source of energy as required. Under a similar conversion into storage of energy, glucose is stored in the liver and muscles as glycogen. Glucose stores are mobilized in a regulated manner, depending on the tissues' metabolic demands. Oral glucose tablets or injections serve to increase the supply of glucose and oral glucose administration is more effective in stimulating insulin secretion because it stimulates the incretin hormones from the gut, which promotes insulin secretion.  Glucose supplies most of the energy to all tissues by generating energy molecules ATP and NADH during a series of metabolism reactions called glycolysis. Glycolysis can be divided into 2 main phases where the preparatory phase is initiated by the phosphorylation of glucose by a hexokinase to form glucose 6-phosphate. The addition of the high-energy phosphate group activates glucose for subsequent breakdown in later steps of glycolysis and is the rate-limiting step. Products end up as substrates for following reactions, to ultimately convert C6 glucose molecule into two C3 sugar molecules. These products enter the energy-releasing phase where total of 4ATP and 2NADH molecules are generated per one glucose molecule. The total aerobic metabolism of glucose can produce up to 36 ATP molecules. This energy-producing reactions of glucose is limited to D-glucose as L-glucose cannot be phosphorlyated by hexokinase. ",,,,"Dextrose, unspecified form is approved and vet_approved.","Dextrose, unspecified form is a solid.",True
14767,"Invert sugar is obtained from sugar cane when this is treated with dilute acid or with the invertase enzyme. It is formed by an equal amount of glucose and fructose. It differentiates from sugar cane in the rotation of the polarized light, which in the case of invert sugar it is to the left (levorotatory). Invert sugar is FDA approved since 1988 as a safe substance (GRAS). Invert sugar presents a large variety of uses. It can be used therapeutically for parenteral hyperalimentation or to be used as an excipient with a known effect. Invert sugar is also approved for its use in food products as a humectant, crystallization modifier, and liquid and nutritive sweetener. Intravenous administration of invert sugar has been proven to be favorable. These reports indicate a temporary rise, within physiological levels, of lactate, pyruvate, and insulin in the blood plasma whereas the level of free fatty acids was declined.",,,,Invert sugar is experimental.,Invert sugar is a liquid.,True
14768,"Dalteparin, a low molecular weight heparin (LMWH) prepared by nitrous acid degradation of unfractionated heparin of porcine intestinal mucosa origin, is an anticoagulant. It is composed of strongly acidic sulphated polysaccharide chains with an average molecular weight of 5000 and about 90% of the material within the range of 2000-9000. LMWHs have a more predictable response, a greater bioavailability, and a longer anti-Xa half life than unfractionated heparin. Dalteparin can also be safely used in most pregnant women. Low molecular weight heparins are less effective at inactivating factor IIa due to their shorter length compared to unfractionated heparin. Dalteparin is used as a prophylaxis for deep-vein thrombosis and pulmonary embolisms in patients undergoing general surgery (e.g., abdominal, gynecologic, urologic), and in patients with acute medical conditions (e.g. cancer, bed rest, heart failure, severe lung disease). It is also used in patients who have severely restricted mobility, which poses a risk for thromboembolic complications.  Dalteparin has an antithrombin binding site that is essential for high affinity binding to the plasma protein antithrombin (ATIII). Anti-Xa activity of plasma is used as both as an estimate of clotting activity, and as a basis to determine dosage. Its use should be avoided in patients with a creatinine clearance less than 20mL/min. In these patients, unfractionated heparin should only be used. As for monitoring, active partial thromboplastin time (aPTT) will only increase at high doses of low molecular weight heparins (LMWH). Therefore, monitoring aPTT is not recommended. However, anti-Xa activity can be measured to monitor the efficacy of the LMWH.  Dalteparin potentiates the activity of ATIII, inhibiting the formation of both factor Xa and thrombin. The main difference between dalteparin and unfractionated heparin (UH) is that dalteparin preferentially inactivates factor Xa. As a result, only a slight increase in clotting time is observed relative to UH. For this same reason, APTT is not used to monitor the effects of dalteparin except as an indicator for overdosage. ",,,,Dalteparin is approved.,Dalteparin is a solid.,True
14769,"Ataluren is a novel, orally administered drug that targets nonsense mutations. Ataluren is approved for use by the European Medicines Agency to treat Duchenne Muscular Dystrophy in patients aged 5 years and older who are able to walk. More specifically, ataluren is used in the small group of patients whose disease is caused by a specific genetic defect (called a ‘nonsense mutation’) in the dystrophin gene. Ataluren is approved for use by the European Medicines Agency to treat Duchenne Muscular Dystrophy in patients aged 5 years and older who are able to walk. More specifically, ataluren is used in the small group of patients whose disease is caused by a specific genetic defect (called a ‘nonsense mutation’) in the dystrophin gene. Ataluren enables ribosomal readthrough of mRNA containing premature stop codons that otherwise would result in premature termination of protein chains. Use of ataluren allows cellular machinery to bypass nonsense mutations in genetic material, continue the translation process, and thereby restore the production of a full-length, functional protein.",The molecular weight is 284.25.,Ataluren has a topological polar surface area of 76.22.,The log p value of  is 3.67.,Ataluren is approved and investigational.,Ataluren is a solid.,True
14770,"Bivalirudin is a synthetic 20 residue peptide (thrombin inhibitor) which reversibly inhibits thrombin. Once bound to the active site, thrombin cannot activate fibrinogen into fibrin, the crucial step in the formation of thrombus. It is administered intravenously. Because it can cause blood stagnation, it is important to monitor changes in hematocrit, activated partial thromboplastin time, international normalized ratio and blood pressure. For treatment of heparin-induced thrombocytopenia and for the prevention of thrombosis. Bivalirudin is indicated for use in patients undergoing percutaneous coronary intervention (PCI), in patients at moderate to high risk acute coronary syndromes due to unstable angina or non-ST segment elevation in whom a PCI is planned. Bivalirudin mediates an inhibitory action on thrombin by directly and specifically binding to both the catalytic site and anion-binding exosite of circulating and clot-bound thrombin. The action of bivalirudin is reversible because thrombin will slowly cleave the thrombin-bivalirudin bond which recovers the active site of thrombin.  Inhibits the action of thrombin by binding both to its catalytic site and to its anion-binding exosite. Thrombin is a serine proteinase that plays a central role in the thrombotic process, acting to cleave fibrinogen into fibrin monomers and to activate Factor XIII to Factor XIIIa, allowing fibrin to develop a covalently cross-linked framework which stabilizes the thrombus; thrombin also activates Factors V and VIII, promoting further thrombin generation, and activates platelets, stimulating aggregation and granule release.",The molecular weight is 2180.32.,Bivalirudin has a topological polar surface area of 901.57.,The log p value of  is 0.0.,Bivalirudin is approved and investigational.,Bivalirudin is a solid.,True
14771,"Ticlopidine is an effective inhibitor of platelet aggregation. It is a prodrug that is metabolised to an active form, which blocks the ADP receptor that is involved in GPIIb/IIIa receptor activation leading to platelet aggregation. Ticlopidine is marketed under the brand name Ticlid and is indicated for patients who cannot take aspirin or in whom aspirin has not worked to prevent a thrombotic stroke. The FDA label includes a black-box warning of neutropenia, aplastic anemia, thrombotic thrombocytopenia purpura, and agranulocytosis, so it is necessary to monitor patients' WBC and platelets when they are taking ticlopidine. Used in patients, who have had a stroke or stroke precursors and who cannot take aspirin or aspirin has not worked, to try to prevent another thrombotic stroke. Ticlopidine is a prodrug that is metabolised to an as yet undetermined metabolite that acts as a platelet aggregation inhibitor. Inhibition of platelet aggregation causes a prolongation of bleeding time. In its prodrug form, ticlopidine has no significant in vitro activity at the concentrations attained in vivo. The active metabolite of ticlopidine prevents binding of adenosine diphosphate (ADP) to its platelet receptor, impairing the ADP-mediated activation of the glycoprotein GPIIb/IIIa complex. It is proposed that the inhibition involves a defect in the mobilization from the storage sites of the platelet granules to the outer membrane. No direct interference occurs with the GPIIb/IIIa receptor. As the glycoprotein GPIIb/IIIa complex is the major receptor for fibrinogen, its impaired activation prevents fibrinogen binding to platelets and inhibits platelet aggregation. By blocking the amplification of platelet activation by released ADP, platelet aggregation induced by agonists other than ADP is also inhibited by the active metabolite of ticlopidine.",The molecular weight is 263.78.,Ticlopidine has a topological polar surface area of 3.24.,The log p value of  is 4.39.,Ticlopidine is approved.,Ticlopidine is a solid.,True
14772,"An antitubercular agent often administered in association with isoniazid. The sodium salt of the drug is better tolerated than the free acid. For the treatment of tuberculosis Aminosalicylic acid is an anti-mycobacterial agent used with other anti-tuberculosis drugs (most often isoniazid) for the treatment of all forms of active tuberculosis due to susceptible strains of tubercle bacilli. The two major considerations in the clinical pharmacology of aminosalicylic acid are the prompt production of a toxic inactive metabolite under acid conditions and the short serum half life of one hour for the free drug. Aminosalicylic acid is bacteriostatic against <i>Mycobacterium tuberculosis</i> (prevents the multiplying of bacteria without destroying them). It also inhibits the onset of bacterial resistance to streptomycin and isoniazid. There are two mechanisms responsible for aminosalicylic acid's bacteriostatic action against <i>Mycobacterium tuberculosis</i>. Firstly, aminosalicylic acid inhibits folic acid synthesis (without potentiation with antifolic compounds). The binding of para-aminobenzoic acid to pteridine synthetase acts as the first step in folic acid synthesis. Aminosalicylic acid binds pteridine synthetase with greater affinity than para-aminobenzoic acid, effectively inhibiting the synthesis of folic acid. As bacteria are unable to use external sources of folic acid, cell growth and multiplication slows. Secondly, aminosalicylic acid may inhibit the synthesis of the cell wall component, mycobactin, thus reducing iron uptake by <i>M. tuberculosis</i>.",The molecular weight is 153.14.,Aminosalicylic acid has a topological polar surface area of 83.55.,The log p value of  is 1.06.,Aminosalicylic acid is approved.,Aminosalicylic acid is a solid.,True
14773,"Semisynthetic, broad-spectrum antibiotic derivative of cephalexin. For the treatment of certain infections caused by bacteria such as pneumonia and ear, lung, skin, throat, and urinary tract infections. Cefaclor is a second generation cephalosporin antibiotic with a spectrum resembling first-generation cephalosporins. <i>In vitro</i> tests demonstrate that the bactericidal action of the cephalosporins results from inhibition of cell-wall synthesis. As indicated by _in vitro_ and _in vivo_ clinical studies, cefaclor was shown to be effective against most strains of Gram positive aerobes - Staphylococci (including coagulase-positive, coagulase-negative, and penicillinase-producing strains), <i>Streptococcus pneumoniae</i>, <i>Streptococcus pyogenes</i> (group A &szlig;-hemolytic streptococci), as well as Gram-negative aerobes - <i>Escherichia coli</i>, <i>Haemophilus influenzae</i> (including &szlig;-lactamase-producing ampicillin-resistant strains), <i>Klebsiella sp</i>, and <i>Proteus mirabilis</i>. Cefaclor, like the penicillins, is a beta-lactam antibiotic. By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, it inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins. It is possible that cefaclor interferes with an autolysin inhibitor.",The molecular weight is 367.8.,Cefaclor has a topological polar surface area of 112.73.,The log p value of  is -1.64.,Cefaclor is approved.,Cefaclor is a solid.,True
14774,"Enoxaparin is a low molecular weight heparin. Enoxaparin is used to prevent and treat deep vein thrombosis or pulmonary embolism, and is given as a subcutaneous injection. Enoxaparin binds to and accelerates the activity of antithrombin III. By activating antithrombin III, enoxaparin preferentially potentiates the inhibition of coagulation factors Xa and IIa. Factor Xa catalyzes the conversion of prothrombin to thrombin, so enoxaparin's inhibition of this process results in decreased thrombin and ultimately the prevention of fibrin clot formation. Low molecular weight heparins are less effective at inactivating factor IIa due to their shorter length compared to unfractionated heparin. For the prophylaxis of deep vein thrombosis, which may lead to pulmonary embolism, and also for the prophylaxis of ischemic complications of unstable angina and non-Q-wave myocardial infarction, when concurrently administered with aspirin. Enoxaparin is a highly acidic mucopolysaccharide formed of equal parts of sulfated D-glucosamine and D-glucuronic acid with sulfaminic bridges. The molecular weight ranges from 3800 to 5000 daltons. Enoxaparin occurs in and is obtained from liver, lung, mast cells, etc., of vertebrates. Enoxaparin is a well known and commonly used anticoagulant which has antithrombotic properties. Enoxaparin inhibits reactions that lead to the clotting of blood and the formation of fibrin clots both in vitro and in vivo. Enoxaparin acts at multiple sites in the normal coagulation system. Small amounts of enoxaparin in combination with antithrombin III (enoxaparin cofactor) can inhibit thrombosis by inactivating activated Factor X and inhibiting the conversion of prothrombin to thrombin. Once active thrombosis has developed, larger amounts of enoxaparin can inhibit further coagulation by inactivating thrombin and preventing the conversion of fibrinogen to fibrin. Enoxaparin also prevents the formation of a stable fibrin clot by inhibiting the activation of the fibrin stabilizing factor. Its use should be avoided in patients with a creatinine clearance less than 20mL/min. In these patients, unfractionated heparin should only be used. As for monitoring, active partial thromboplastin time (aPTT) will only increase at high doses of low molecular weight heparins (LMWH). Therefore, monitoring aPTT is not recommended. However, anti-Xa activity can be measured to monitor the efficacy of the LMWH.  The mechanism of action of enoxaparin is antithrombin-dependent. It acts mainly by accelerating the rate of the neutralization of certain activated coagulation factors by antithrombin, but other mechanisms may also be involved. The antithrombotic effect of enoxaparin is well correlated to the inhibition of factor Xa. Enoxaparin interacts with Antithrombin III, Prothrombin and Factor X. Enoxaparin binds to and accelerates the activity of antithrombin III. By activating antithrombin III, enoxaparin preferentially potentiates the inhibition of coagulation factors Xa and IIa.",,,,Enoxaparin is approved.,Enoxaparin is a solid.,True
14775,"Calcipotriol (INN) or calcipotriene (USAN) is a sythetic derivative of calcitriol or Vitamin D. For the treatment of moderate plaque psoriasis in adults. Calcipotriene is a synthetic analog of vitamin D. In humans, the natural supply of vitamin D depends mainly on exposure to the ultraviolet rays of the sun for conversion of 7-dehydrocholesterol to vitamin D3 (cholecalciferol) in the skin.  The precise mechanism of calcipotriol in remitting psoriasis is not well-understood, however, it has been shown to have comparable affinity with calcitriol for the Vitamin D receptor while being less than 1% the activity in regulating calcium metabolism. The Vitamin D receptor (VDR) belongs to the steroid/thyroid receptor superfamily, and is found on the cells of many different tissues including the thyroid, bone, kindney, and T cells of the immune system. T cells are known to play a role in psoriasis and are believed to undergo modulation of gene expression with binding of calcipotriol to the VDR. This modulation is thought to affect gene products related to cell differentiation and proliferation.",The molecular weight is 412.61.,Calcipotriol has a topological polar surface area of 60.69.,The log p value of  is 5.27.,Calcipotriol is approved.,Calcipotriol is a solid.,True
14776,"Elafin is a human protein that is produced naturally in the skin, lung and breast, protecting the respective tissue from destruction by the immune system. Elafin’s ability to block the activity of destructive enzymes that are involved in inflammatory reactions makes it a highly promising active compound for the treatment of inflammatory lung diseases or severe reperfusion injuries occurring after heart attacks, serious injuries and organ transplantation. The excellent tolerability of Elafin in human subjects was demonstrated in a Phase I clinical single dose escalating study. Investigated for use/treatment in inflammatory disorders (unspecified). Elafin is able to abrogate lipopolysaccharide-induced production of monocyte chemotactic protein 1 in monocytes by inhibiting AP-1 and NFkappaB activation. Due to its selective expression at mucosal surfaces as well as in alveolar macrophages, monocytes and neutrophils, the ability of Elafin to inhibit the lipopolysaccharide signaling pathway may be important in disease states such as cystic fibrosis, pneumonia, and acute respiratory distress syndrome. The inhibition of two key inflammatory pathways confirms the importance of Elafin as a mediator of the innate immune response.",,,,Elafin is investigational.,Elafin is a solid.,True
14777,AB192 is a DPP IV enzymatic activity inhibitor. Investigated for use/treatment in diabetes mellitus type 2.,,,,AB192 is experimental.,AB192 is a solid.,True
14778,"Investigated for use/treatment in cardiac surgery. Cariporide is a selective sodium-hydrogen antiporter inhibitor. The sodium-hydrogen exchanger is an importatn player in the pathophysiology of myocardial ischemia-referfusion injury. The accumulation of hydrogen ions in the myocyte cytoso; during ischemia creates a proton gradiant that promote the efflux of hydrogen ions in exchange for the influx of sodium ions. This sodium buildup can secondary activates the sodium-calcium exchanger to operate in the reverse mode, resulting in a net calcium accumulation in myocyte cytosol, which leads to dysfunction and cell death. By inhibiting sodium-hydrogen exchange, Cariporide can prevent the accumulation of calcium in cytosol, therefore reduce the infarct size.",,,,Cariporide is investigational.,Cariporide is a solid.,True
14779,"Tiopronin is a prescription thiol drug used primarily in the treatment of severe homozygous cystinuria. Patients with cystinuria excrete high levels of cystine in their urine and are at risk for kidney stone formation. Tiopronin is used as a second-line therapy to control the rate of cystine precipitation and excretion, and prevent kidney stone formation. It is used after a failure of the non-pharmacological first line treatment consisting of increased fluid intake, restriction of sodium and protein, and urinary alkalinization. As cystinuria is a relatively rare disease, tiopronin is classified as an orphan drug and is not patented in the United States. It is similar to d-penicillamine in use and efficacy, but offers the advantage of far less adverse effects. Tiopronin is dosed on an individual basis using close monitoring of urinary cystine concentrations and urinary output. Tiopronin is indicated for the prevention of kidney stone formation in patients with severe homozygous cystinuria consisting of a urinary cystine concentration greater than 500 mg/day, and who have failed treatment with non-pharmacological measures of increased fluid intake, decreased sodium and protein intake, and urine alkalinization. Kidney stones form when the solubility limit is exceeded and urine becomes supersaturated with endogenous cystine. Tiopronin is an active reducing agent which undergoes a thiol-disulfide exchange with cystine to form a water-soluble mixed disulfide complex. Thus, the amount of sparingly soluble cystine is reduced. By reducing urinary cystine concentrations below the solubility limit, tiopronin helps reduce cystine stone formation. ",The molecular weight is 163.19.,Tiopronin has a topological polar surface area of 66.4.,The log p value of  is -0.23.,Tiopronin is approved and investigational.,Tiopronin is a solid.,True
14780,"A pyrimidine nucleoside analog that is used mainly in the treatment of leukemia, especially acute non-lymphoblastic leukemia. Cytarabine is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. Its actions are specific for the S phase of the cell cycle. It also has antiviral and immunosuppressant properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p472) For the treatment of acute non-lymphocytic leukemia, acute lymphocytic leukemia and blast phase of chronic myelocytic leukemia. Cytarabine is an antineoplastic anti-metabolite used in the treatment of several forms of leukemia including acute myelogenous leukemia and meningeal leukemia. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA. They prevent these substances becoming incorporated in to DNA during the \S\"" phase (of the cell cycle), stopping normal development and division. Cytarabine is metabolized intracellularly into its active triphosphate form (cytosine arabinoside triphosphate). This metabolite then damages DNA by multiple mechanisms, including the inhibition of alpha-DNA polymerase, inhibition of DNA repair through an effect on beta-DNA polymerase, and incorporation into DNA. The latter mechanism is probably the most important. Cytotoxicity is highly specific for the S phase of the cell cycle."" Cytarabine acts through direct DNA damage and incorporation into DNA. Cytarabine is cytotoxic to a wide variety of proliferating mammalian cells in culture. It exhibits cell phase specificity, primarily killing cells undergoing DNA synthesis (S-phase) and under certain conditions blocking the progression of cells from the G1 phase to the S-phase. Although the mechanism of action is not completely understood, it appears that cytarabine acts through the inhibition of DNA polymerase. A limited, but significant, incorporation of cytarabine into both DNA and RNA has also been reported.",The molecular weight is 243.22.,Cytarabine has a topological polar surface area of 128.61.,The log p value of  is -2.2.,Cytarabine is approved and investigational.,Cytarabine is a solid.,True
14781,"Fludeoxyglucose F 18 Injection is a positron emitting radiopharmaceutical containing no-carrier added radioactive 2-deoxy-2-fluoro-D-g1ucose, which is used for diagnostic purposes in conjunction with Positron Emission Tomography (PET). It is administered by intravenous injection. The uptake of 18F-FDG by tissues is a marker for the tissue uptake of glucose, which in turn is closely correlated with certain types of tissue metabolism. Fludeoxyglucose F 18 Injection is rapidly distributed to all organs of the body after intravenous administration. After background clearance of Fludeoxyglucose F 18 Injection, optimal PET imaging is generally achieved between 30 to 40 minutes after administration. Fludeoxyglucose F 18 is a glucose analog that concentrates in cells that rely upon glucose as an energy source, or in cells whose dependence on glucose increases under pathophysiological conditions. Fludeoxyglucose F 18 is transported through the cell membrane by facilitative glucose transporter proteins and is phosphorylated within the cell to FDG-6- phosphate by the enzyme hexokinase. Once phosphorylated it cannot exit until it is dephosphorylated by glucose-6-phosphatase. Therefore, within a given tissue or pathophysiological process, the retention and clearance of Fludeoxyglucose F 18 reflect a balance involving glucose transporter, hexokinase and glucose-6- phosphatase activities. When allowance is made for the kinetic differences between glucose and Fludeoxyglucose F 18 transport and phosphorylation (expressed as the “lumped constant” ratio), Fludeoxyglucose F 18 is used to assess glucose metabolism.",,,,Fludeoxyglucose (18F) is approved and investigational.,,True
14782,"A water-soluble, enzyme co-factor present in minute amounts in every living cell. It occurs mainly bound to proteins or polypeptides and is abundant in liver, kidney, pancreas, yeast, and milk. For nutritional supplementation, also for treating dietary shortage or imbalance. Biotin is a water-soluble B-complex vitamin which is composed of an ureido ring fused with a tetrahydrothiophene ring, which attaches a valeric acid substituent at one of its carbon atoms. Biotin is used in cell growth, the production of fatty acids, metabolism of fats, and amino acids. It plays a role in the Kreb cycle, which is the process in which energy is released from food. Biotin not only assists in various metabolic chemical conversions, but also helps with the transfer of carbon dioxide. Biotin is also helpful in maintaining a steady blood sugar level. Biotin is often recommended for strengthening hair and nails. Consequenty, it is found in many cosmetic and health products for the hair and skin. Biotin deficiency is a rare nutritional disorder caused by a deficiency of biotin. Initial symptoms of biotin deficiency include: Dry skin, Seborrheic dermatitis, Fungal infections, rashes including erythematous periorofacial macular rash, fine and brittle hair, and hair loss or total alopecia. If left untreated, neurological symptoms can develop, including mild depression, which may progress to profound lassitude and, eventually, to somnolence; changes in mental status, generalized muscular pains (myalgias), hyperesthesias and paresthesias. The treatment for biotin deficiency is to simply start taking some biotin supplements. A lack of biotin in infants will lead to a condition called seborrheic dermatitis or \cradle cap\"". Biotin deficiencies are extremely rare in adults but if it does occur, it will lead to anemia, depression, hair loss, high blood sugar levels, muscle pain, nausea, loss of appetite and inflamed mucous membranes."" Biotin is necessary for the proper functioning of enzymes that transport carboxyl units and fix carbon dioxide, and is required for various metabolic functions, including gluconeogenesis, lipogenesis, fatty acid biosynthesis, propionate metabolism, and catabolism of branched-chain amino acids.",The molecular weight is 244.31.,Biotin has a topological polar surface area of 78.43.,The log p value of  is -0.08.,Biotin is approved and investigational and nutraceutical.,Biotin is a solid.,True
14783,"Caffeine is a drug of the methylxanthine class used for a variety of purposes, including certain respiratory conditions of the premature newborn, pain relief, and to combat drowsiness. Caffeine is similar in chemical structure to and. It can be sourced from coffee beans, but also occurs naturally in various teas and cacao beans, which are different than coffee beans. Caffeine is also used in a variety of cosmetic products and can be administered topically, orally, by inhalation, or by injection. Caffeine is indicated for the short term treatment of apnea of prematurity in infants and off label for the prevention and treatment of bronchopulmonary dysplasia caused by premature birth. In addition, it is indicated in combination with sodium benzoate to treat respiratory depression resulting from an overdose with CNS depressant drugs. Caffeine has a broad range of over the counter uses, and is found in energy supplements, athletic enhancement products, pain relief products, as well as cosmetic products. Caffeine stimulates the central nervous system (CNS), heightening alertness, and sometimes causing restlessness and agitation. It relaxes smooth muscle, stimulates the contraction of cardiac muscle, and enhances athletic performance. Caffeine promotes gastric acid secretion and increases gastrointestinal motility. It is often combined in products with analgesics and ergot alkaloids, relieving the symptoms of migraine and other types of headaches. Finally, caffeine acts as a mild diuretic. The mechanism of action of caffeine is complex, as it impacts several body systems, which are listed below. The effects as they relate to various body systems are described as follows:",The molecular weight is 194.19.,Caffeine has a topological polar surface area of 58.44.,The log p value of  is -0.04.,Caffeine is approved.,Caffeine is a solid.,True
14784,"A methylxanthine derivative from tea with diuretic, smooth muscle relaxant, bronchial dilation, cardiac and central nervous system stimulant activities. Mechanistically, theophylline acts as a phosphodiesterase inhibitor, adenosine receptor blocker, and histone deacetylase activator. Theophylline is marketed under several brand names such as Uniphyl and Theochron, and it is indicated mainly for asthma, bronchospasm, and COPD. For the treatment of the symptoms and reversible airflow obstruction associated with chronic asthma and other chronic lung diseases, such as emphysema and chronic bronchitis. Theophylline, an xanthine derivative chemically similar to caffeine and theobromine, is used to treat asthma and bronchospasm. Theophylline has two distinct actions in the airways of patients with reversible (asthmatic) obstruction; smooth muscle relaxation (i.e., bronchodilation) and suppression of the response of the airways to stimuli (i.e., non-bronchodilator prophylactic effects). Theophylline relaxes the smooth muscle of the bronchial airways and pulmonary blood vessels and reduces airway responsiveness to histamine, methacholine, adenosine, and allergen. Theophylline competitively inhibits type III and type IV phosphodiesterase (PDE), the enzyme responsible for breaking down cyclic AMP in smooth muscle cells, possibly resulting in bronchodilation. Theophylline also binds to the adenosine A2B receptor and blocks adenosine mediated bronchoconstriction. In inflammatory states, theophylline activates histone deacetylase to prevent transcription of inflammatory genes that require the acetylation of histones for transcription to begin.",The molecular weight is 180.17.,Theophylline has a topological polar surface area of 69.3.,The log p value of  is -0.03.,Theophylline is approved.,Theophylline is a solid.,True
14785,"Originally approved by the FDA in 1989, omeprazole is a _proton-pump inhibitor_, used to treat gastric acid-related disorders. These disorders may include gastroesophageal reflux disease (GERD), peptic ulcer disease, and other diseases characterized by the oversecretion of gastric acid. This drug was the first clinical useful drug in its class, and its approval was followed by the formulation of many other proton pump inhibitor drugs. Omeprazole is generally effective and well-tolerated, promoting its popular use in children and adults. Omeprazole, according to the FDA label is a proton pump inhibitor (PPI) used for the following purposes: **Effects on gastric acid secretion** Hydrochloric acid (HCl) secretion into the gastric lumen is a process regulated mainly by the H(+)/K(+)-ATPase of the proton pump , expressed in high quantities by the parietal cells of the stomach. ATPase is an enzyme on the parietal cell membrane that facilitates hydrogen and potassium exchange through the cell, which normally results in the extrusion of potassium and formation of HCl (gastric acid).",The molecular weight is 345.42.,Omeprazole has a topological polar surface area of 77.1.,The log p value of  is 2.57.,Omeprazole is approved and investigational and vet_approved.,Omeprazole is a solid.,True
14786,"Lansoprazole marketed under the brand Prevacid, is a proton pump inhibitor (PPI) and is structurally classified as a substituted benzimidazole. It reduces gastric acid secretion by targeting gastric H,K-ATPase pumps and is thus effective at promoting healing in ulcerative diseases, and treating gastroesophageal reflux disease (GERD) along with other pathologies caused by excessive acid secretion. Lansoprazole is used to reduce gastric acid secretion and is approved for short term treatment of active gastric ulcers, active duodenal ulcers, erosive reflux oesophagitis, symptomatic gastroesophageal reflux disease, and non-steroidal anti-inflammatory drug (NSAID) induced gastric and duodenal ulcers.  It may be used in the maintenance and healing of several gastric conditions including duodenal ulcers, NSAID related gastric ulcers, and erosive esophagitis. Lansoprazole prevents recurrence of gastric ulcers in patients who have a documented history of gastric ulcers who also use NSAIDs chronically.  Predictably, it is also useful in the management of hypersecretory conditions including Zollinger-Ellison syndrome.  Lansoprazole is effective at eradicating H. pylori when used in conjunction with amoxicillin and clarithromycin (triple therapy) or with amoxicillin alone (dual therapy).  Lansoprazole decreases gastric acid secretion by targeting H+,K+-ATPase, which is the enzyme that catalyzes the final step in the acid secretion pathway in parietal cells.  Conveniently, lansoprazole administered any time of day is able to inhibit both daytime and nocturnal acid secretion. The result is that lansoprazole is effective at healing duodenal ulcers, reduces ulcer-related pain, and offers relief from symptoms of heartburn  Lansoprazole also reduces pepsin secretion, making it a useful treatment option for hypersecretory conditions such as Zollinger-Ellison syndrome. As a PPI, lansoprazole is a prodrug and requires protonation via an acidic environment to become activated.  Once protonated, lansoprazole is able to react with cysteine residues, specifically Cys813 and Cys321, on parietal H+,K+-ATPase resulting in stable disulfides. PPI's in general are able to provide prolonged inhibition of acid secretion due to their ability to bind covalently to their targets.  ",The molecular weight is 369.36.,Lansoprazole has a topological polar surface area of 67.87.,The log p value of  is 2.6.,Lansoprazole is approved and investigational.,Lansoprazole is a solid.,True
14787,"An antiandrogen with about the same potency as cyproterone in rodent and canine species. For the management of locally confined Stage B2-C and Stage D2 metastatic carcinoma of the prostate Flutamide is a nonsteroidal antiandrogen. In animal studies, flutamide demonstrates potent antiandrogenic effects. It exerts its antiandrogenic action by inhibiting androgen uptake and/or by inhibiting nuclear binding of androgen in target tissues or both. Prostatic carcinoma is known to be androgen-sensitive and responds to treatment that counteracts the effect of androgen and/or removes the source of androgen, e.g. castration. Elevations of plasma testosterone and estradiol levels have been noted following flutamide administration. Flutamide is a nonsteroidal antiandrogen that blocks the action of both endogenous and exogenous testosterone by binding to the androgen receptor. In addition Flutamide is a potent inhibitor of testosterone-stimulated prostatic DNA synthesis. Moreover, it is capable of inhibiting prostatic nuclear uptake of androgen.",The molecular weight is 276.21.,Flutamide has a topological polar surface area of 74.92.,The log p value of  is 3.33.,Flutamide is approved and investigational.,Flutamide is a solid.,True
14788,"A 4-aminoquinoquinoline compound with anti-inflammatory properties. For treatment of acute malarial attacks in non-immune subjects. Amodiaquine, a 4-aminoquinoline similar to chloroquine in structure and activity, has been used as both an antimalarial and an anti-inflammatory agent for more than 40 years. Amodiaquine is at least as effective as chloroquine, and is effective against some chloroquine-resistant strains, although resistance to amodiaquine has been reported. The mode of action of amodiaquine has not yet been determined. 4-Aminoquinolines depress cardiac muscle, impair cardiac conductivity, and produce vasodilatation with resultant hypotension. They depress respiration and cause diplopia, dizziness and nausea. The mechanism of plasmodicidal action of amodiaquine is not completely certain. Like other quinoline derivatives, it is thought to inhibit heme polymerase activity. This results in accumulation of free heme, which is toxic to the parasites. The drug binds the free heme preventing the parasite from converting it to a form less toxic. This drug-heme complex is toxic and disrupts membrane function.",The molecular weight is 355.87.,Amodiaquine has a topological polar surface area of 48.39.,The log p value of  is 5.32.,Amodiaquine is approved and investigational.,Amodiaquine is a solid.,True
14789,"A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of leukemia and other neoplasms. For remission induction in acute nonlymphocytic leukemia (myelogenous, monocytic, erythroid) of adults and for remission induction in acute lymphocytic leukemia of children and adults. Daunorubicin is an antineoplastic in the anthracycline class. General properties of drugs in this class include: interaction with DNA in a variety of different ways including intercalation (squeezing between the base pairs), DNA strand breakage and inhibition with the enzyme topoisomerase II. Most of these compounds have been isolated from natural sources and antibiotics. However, they lack the specificity of the antimicrobial antibiotics and thus produce significant toxicity. The anthracyclines are among the most important antitumor drugs available. Doxorubicin is widely used for the treatment of several solid tumors while daunorubicin and idarubicin are used exclusively for the treatment of leukemia. Daunorubicin may also inhibit polymerase activity, affect regulation of gene expression, and produce free radical damage to DNA. Daunorubicin possesses an antitumor effect against a wide spectrum of tumors, either grafted or spontaneous. The anthracyclines are cell cycle-nonspecific. Daunorubicin has antimitotic and cytotoxic activity through a number of proposed mechanisms of action: Daunorubicin forms complexes with DNA by intercalation between base pairs, and it inhibits topoisomerase II activity by stabilizing the DNA-topoisomerase II complex, preventing the religation portion of the ligation-religation reaction that topoisomerase II catalyzes.",The molecular weight is 527.53.,Daunorubicin has a topological polar surface area of 185.84.,The log p value of  is 0.84.,Daunorubicin is approved.,Daunorubicin is a solid.,True
14790,"An aminoquinoline that is given by mouth to produce a radical cure and prevent relapse of vivax and ovale malarias following treatment with a blood schizontocide. It has also been used to prevent transmission of falciparum malaria by those returning to areas where there is a potential for re-introduction of malaria. Adverse effects include anemias and GI disturbances. (From Martindale, The Extra Pharmacopeia, 30th ed, p404) For the treatment of malaria. Primaquine is an antimalarial agent and is the essential co-drug with chloroquine in treating all cases of malaria. In the blood, malaria parasites break down a part of the red blood cells known as haemoglobin. When this happens haemoglobin is divided into two parts; haem and globin. Haem is toxic to the malaria parasite. To prevent it from being damaged, the malaria parasite produces an chemical which converts the toxic haem into a non-toxic product. Primaquine acts by interfering with a part of the parasite (mitochondria) that is responsible for supplying it with energy. Without energy the parasite dies. This stops the infection from continuing and allows the person to recover. Primaquine kills the intrahepatic form of <i>Plasmodium vivax</i> and <i>Plasmodium ovale</i>, and thereby prevents the development of the erythrocytic forms that are responsible for relapses (it also kills gametocytes). Primaquine is not used in the prevention of malaria, only in the treatment. It has insignificant activity against the asexual blood forms of the parasite and therefore it is always used in conjunction with a blood schizonticide and never as a single agent. Primaquine has gametocytocidal activity against all plasmodia, including <i>P. falciparum</i>. Primaquine's mechanism of action is not well understood. It may be acting by generating reactive oxygen species or by interfering with the electron transport in the parasite. Also, although its mechanism of action is unclear, primaquine may bind to and alter the properties of protozoal DNA.",The molecular weight is 259.35.,Primaquine has a topological polar surface area of 60.17.,The log p value of  is 2.6.,Primaquine is approved.,Primaquine is a solid.,True
14791,"An anthracenedione-derived antineoplastic agent. For the treatment of secondary (chronic) progressive, progressive relapsing, or worsening relapsing-remitting multiple sclerosis Mitoxantrone has been shown in vitro to inhibit B cell, T cell, and macrophage proliferation and impair antigen presentation, as well as the secretion of interferon gamma, TNFa, and IL-2. Mitoxantrone, a DNA-reactive agent that intercalates into deoxyribonucleic acid (DNA) through hydrogen bonding, causes crosslinks and strand breaks. Mitoxantrone also interferes with ribonucleic acid (RNA) and is a potent inhibitor of topoisomerase II, an enzyme responsible for uncoiling and repairing damaged DNA. It has a cytocidal effect on both proliferating and nonproliferating cultured human cells, suggesting lack of cell cycle phase specificity.",The molecular weight is 444.49.,Mitoxantrone has a topological polar surface area of 163.18.,The log p value of  is 2.3.,Mitoxantrone is approved and investigational.,Mitoxantrone is a liquid.,True
14792,"Paclitaxel is a chemotherapeutic agent marketed under the brand name Taxol among others. Used as a treatment for various cancers, paclitaxel is a mitotic inhibitor that was first isolated in 1971 from the bark of the Pacific yew tree which contains endophytic fungi that synthesize paclitaxel. It is available as an intravenous solution for injection and the newer formulation contains albumin-bound paclitaxel marketed under the brand name Abraxane. Used in the treatment of Kaposi's sarcoma and cancer of the lung, ovarian, and breast. Abraxane® is specfically indicated for the treatment of metastatic breast cancer and locally advanced or metastatic non-small cell lung cancer. Paclitaxel is a taxoid antineoplastic agent indicated as first-line and subsequent therapy for the treatment of advanced carcinoma of the ovary, and other various cancers including breast cancer. Paclitaxel is a novel antimicrotubule agent that promotes the assembly of microtubules from tubulin dimers and stabilizes microtubules by preventing depolymerization. This stability results in the inhibition of the normal dynamic reorganization of the microtubule network that is essential for vital interphase and mitotic cellular functions. In addition, paclitaxel induces abnormal arrays or \bundles\"" of microtubules throughout the cell cycle and multiple asters of microtubules during mitosis."" Paclitaxel interferes with the normal function of microtubule growth. Whereas drugs like colchicine cause the depolymerization of microtubules in vivo, paclitaxel arrests their function by having the opposite effect; it hyper-stabilizes their structure. This destroys the cell's ability to use its cytoskeleton in a flexible manner. Specifically, paclitaxel binds to the &beta; subunit of tubulin. Tubulin is the \building block\"" of mictotubules, and the binding of paclitaxel locks these building blocks in place. The resulting microtubule/paclitaxel complex does not have the ability to disassemble. This adversely affects cell function because the shortening and lengthening of microtubules (termed dynamic instability) is necessary for their function as a transportation highway for the cell. Chromosomes, for example, rely upon this property of microtubules during mitosis. Further research has indicated that paclitaxel induces programmed cell death (apoptosis) in cancer cells by binding to an apoptosis stopping protein called Bcl-2 (B-cell leukemia 2) and thus arresting its function.""",The molecular weight is 853.92.,Paclitaxel has a topological polar surface area of 221.29.,The log p value of  is 4.73.,Paclitaxel is approved and vet_approved.,Paclitaxel is a solid.,True
14793,"Docetaxel is a clinically well established anti-mitotic chemotherapy medication used mainly for the treatment of breast, ovarian, and non-small cell lung cancer. Docetaxel reversibly binds to tubulin with high affinity in a 1:1 stoichiometric ratio For the treatment of patients with locally advanced or metastatic breast cancer after failure of prior chemotherapy. Also used as a single agent in the treatment of patients with locally advanced or metastatic non-small cell lung cancer after failure of prior platinum-based chemotherapy. It is also used in combination with prednisone, in the treatment of patients with androgen independent (hormone refractory) metastatic prostate cancer. Furthermore, docetaxel has uses in the treatment of gastric adenocarinoma and head and neck cancer.  Docetaxel is a taxoid antineoplastic agent. It promotes the assembly of microtubules from tubulin dimers and stabilizes microtubules by preventing depolymerization. This stability results in the inhibition of the normal dynamic reorganization of the microtubule network that is essential for vital interphase and mitotic cellular functions. In addition, docetaxel induces abnormal arrays or \bundles\"" of microtubules throughout the cell cycle and multiple asters of microtubules during mitosis."" Docetaxel interferes with the normal function of microtubule growth. Whereas drugs like colchicine cause the depolymerization of microtubules in vivo, docetaxel arrests their function by having the opposite effect; it hyper-stabilizes their structure. This destroys the cell's ability to use its cytoskeleton in a flexible manner. Specifically, docetaxel binds to the &beta;-subunit of tubulin. Tubulin is the \building block\"" of microtubules, and the binding of docetaxel locks these building blocks in place. The resulting microtubule/docetaxel complex does not have the ability to disassemble. This adversely affects cell function because the shortening and lengthening of microtubules (termed dynamic instability) is necessary for their function as a transportation highway for the cell. Chromosomes, for example, rely upon this property of microtubules during mitosis. Further research has indicated that docetaxel induces programmed cell death (apoptosis) in cancer cells by binding to an apoptosis stopping protein called Bcl-2 (B-cell leukemia 2) and thus arresting its function.""",The molecular weight is 807.89.,Docetaxel has a topological polar surface area of 224.45.,The log p value of  is 4.08.,Docetaxel is approved and investigational.,Docetaxel is a solid.,True
14794,"Dasatinib is an oral dual BCR/ABL and Src family tyrosine kinase inhibitor approved for use in patients with chronic myelogenous leukemia (CML). The main targets of Dasatinib, are BCRABL, SRC, Ephrins and GFR. For the treatment of adults with chronic, accelerated, or myeloid or lymphoid blast phase chronic myeloid leukemia with resistance or intolerance to prior therapy. Also indicated for the treatment of adults with Philadelphia chromosome-positive acute lymphoblastic leukemia with resistance or intolerance to prior therapy. Dasatinib is an oral dual BCR/ABL and Src family tyrosine kinase inhibitor Dasatinib, at nanomolar concentrations, inhibits the following kinases: BCR-ABL, SRC family (SRC, LCK, YES, FYN), c-KIT, EPHA2, and PDGFR&beta;. Based on modeling studies, dasatinib is predicted to bind to multiple conformations of the ABL kinase. In vitro, dasatinib was active in leukemic cell lines representing variants of imatinib mesylate sensitive and resistant disease. Dasatinib inhibited the growth of chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL) cell lines overexpressing BCR-ABL. Under the conditions of the assays, dasatinib was able to overcome imatinib resistance resulting from BCR-ABL kinase domain mutations, activation of alternate signaling pathways involving the SRC family kinases (LYN, HCK), and multi-drug resistance gene overexpression. ",The molecular weight is 488.01.,Dasatinib has a topological polar surface area of 106.51.,The log p value of  is 2.38.,Dasatinib is approved and investigational.,Dasatinib is a solid.,True
14795,"Triclocarban, with the chemical formula C13H9Cl3N2O is an antibacterial agent that is particularly effective against Gram-positive bacteria such as *Staphylococcus aureus*. It is a bacteriostatic compound that has been found in antibacterial soaps and other personal care products. In 2017, the US FDA prohibited the marketing of over-the-counter (OTC) consumer antiseptic wash products containing triclocarban due to negative health effects such as bacterial resistance or hormonal effects ,. Triclocarban (TCC), or 3,4,4'-trichlorocarbanilide, is an antibacterial agent used in bar and liquid soaps and body washes. The antimicrobial mechanism underlying the bacteriostatic and bactericidal effects of triclocarban is believed to be an unspecific adsorption to cell membranes and interruption of their function. As a result, the growth of gram-positive as well as gram-negative bacteria is inhibited. Triclocarban is a triclosan analog with an antibacterial activity. Triclocarban exerts its effect by inhibiting the activity of _enoyl-(acyl-carrier protein) (ACP) reductase_, which is ubiquitously distributed in bacteria, fungi and various plants. ACP reductase catalyzes the last step in each cycle of fatty acid elongation in the type II fatty acid synthase systems. As a result, this agent interrupts cell membrane synthesis and leads to bacterial growth inhibition.",The molecular weight is 315.58.,Triclocarban has a topological polar surface area of 41.13.,The log p value of  is 5.47.,Triclocarban is approved.,Triclocarban is a solid.,True
14796,"Triclabendazole, manufactured by Novartis pharmaceuticals, is an antihelminthic drug that was approved by the FDA in February 2019 for the treatment of fascioliasis in humans.  Fascioliasis is a parasitic infection often caused by the helminth, _Fasciola hepatica_, which is also known as “the common liver fluke” or “the sheep liver fluke” or by _Fasciola gigantica_, another helminth. These parasites can infect humans following ingestion of larvae in contaminated water or food.  This drug is indicated for the treatment of fascioliasis in patients aged 6 years old and above. Triclabendazole is an anthelmintic agent against _Fasciola_ species.",The molecular weight is 359.65.,Triclabendazole has a topological polar surface area of 37.91.,The log p value of  is 6.44.,Triclabendazole is approved and investigational.,Triclabendazole is a solid.,True
14797,"Imipenem is a semisynthetic thienamycin that has a wide spectrum of antibacterial activity against gram-negative and gram-positive aerobic and anaerobic bacteria, including many multiresistant strains. It is stable to many beta-lactamases. Similar compounds include , known for having greater activity against Gram negative bacteria, and the newer which exhibits a longer half-life due to increased binding to plasma proteins. Imipenem is commonly used in combination with and is now available in a triple-drug product with cilastatin and which was recently approved by the FDA. Imipenem was first approved by the FDA in November 1985 as the combination product Primaxin marketed by Merck & Co. Imipenem is indicated, in combination with with or without , for the treatment of bacterial infections including respiratory, skin, bone, gynecologic, urinary tract, and intra-abdominal as well as septicemia and endocarditis. Imipenem is a beta-lactam antibiotic belongings to the subgroup of carbapenems. Imipenem is active against aerobic and anaerobic Gram positive as well as Gram negative bacteria including <i>Pseudomonas aeruginosa</i> and the <i>Enterococcus</i>. It exerts a bactericidal effects by disrupting cell wall synthesis. Imipenem acts as an antimicrobial through the inhibition of cell wall synthesis of various gram-positive and gram-negative bacteria. This inhibition of cell wall synthesis in gram-negative bateria is attained by binding to penicillin-binding proteins (PBPs). In E. coli and selected strains of P. aeruginosa, imipenem has shown to have the highest affinity to PBP-2, PBP-1a, and PBP-1b. This inhibition of PBPs prevents the bacterial cell from adding to the peptidoglycan polymer which forms the bacterial cell wall eventually leading to cell death.",The molecular weight is 299.35.,Imipenem has a topological polar surface area of 113.72.,The log p value of  is -1.35.,Imipenem is approved.,Imipenem is a solid.,True
14798,"Doripenem is a broad-spectrum, carbapenem antibiotic marketed under the brand name Doribax by Janssen. Doripenem injection was approved by the FDA in 2007 to treat complicated urinary tract and intra-abdominal infections. In a clinical trial of doripenem treatment in ventilator associated pneumonia (vs. imipenem and cilastatin), it was found that doripenem carried an increased risk of death and lower clinical cure rates, resulting in a premature termination of the trial. The FDA revised the doripenem label in 2014 to include a warning against use in ventilator-associated pneumonia and to reiterate its safety and efficacy for its approved indications. Doripenem is indicated in the treatment of complicated intra-abdominal infections and complicated urinary tract infections, including pyelonephritis, caused by designated susceptible bacteria. Similar to other beta-lactam antimicrobial agents, the time that unbound plasma concentration of doripenem exceeds the MIC (T>MIC) of the infecting organism has been shown to best correlate with efficacy in animal models of infection. Doripenem is a broad-spectrum carbapenem antibiotic with activity against many gram-positive and gram-negative aerobic bacteria, as well as a variety of anaerobes. Like other beta-lactam antibiotics, doripenem's bactericidal mechanism of action is mostly due to cell death after inhibition of bacterial enzymes called penicillin-bindng proteins (PBPs), which are responsible for peptidoglycan cross-linking during the synthesis of the bacterial cell wall. Carbapenems mainly have high affinity for PBPs 1a, 1b, 2 and 3. Inhibition of each PBP usually results in a different inactivating mechanism. Inhibition of PBPs 1a and 1b results in fast bacterial killing through the formation of spheroplasts, inhibition of PBP 2 results in rod-shaped bacteria to become spherical, and inhibition of PBP 3 results in filamentous-shaped organisms. The PBPs preferentially bound by different carbapenems depend on the organism. In E.coli and P.aeruginosa, doripenem binds to PBP",The molecular weight is 420.5.,Doripenem has a topological polar surface area of 162.06.,The log p value of  is -3.83.,Doripenem is approved and investigational.,Doripenem is a solid.,True
14799,"Human Insulin, also known as Regular Insulin, is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Human insulin is produced by recombinant DNA technology and is identical to endogenously produced insulin. Typically prescribed for the management of diabetes mellitus, insulin is a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Human insulin is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis).  The primary activity of insulin is the regulation of glucose metabolism. Insulin promotes glucose and amino acid uptake into muscle and adipose tissues, and other tissues except brain and liver. It also has an anabolic role in stimulating glycogen, fatty acid, and protein synthesis. Insulin inhibits gluconeogenesis in the liver.",The molecular weight is 5807.63.,Insulin human has a topological polar surface area of 2299.07.,,Insulin human is approved and investigational.,Insulin human is a liquid.,True
14800,"Norelgestromin is a drug used in contraception. Norelgestromin is the active progestin responsible for the progestational activity that occurs in women after application of ORTHO EVRA patch. Norelgestromin is used for contraception and menopausal hormonal therapy. Norelgestromin may potentially be used in breast cancer treatment due to its inhibitory effect on estrone sulfatase. They convert sulfated steroid precursors to estrogen during pregnancy.  Norelgestromin is used for contraception and menopausal hormonal therapy transdermally or in combination with ethinyl estradiol as a vaginal ring. Norelgestromin, in combination with ethinyl estradiol inhibits ovulation by suppressing gonadotropins.  Norelgestromin inhibits estrone sulfatase, which converts sulfated steroid precursors to estrogen during pregnancy. Norgelgestromin/ethinylestradiol suppresses follicular development, induces changes to the endometrium, which decreases chances of implantation and thickens the cervical mucus, impeding sperm swimming into the uterus. It also has similar agonisting binding affinities as its parent compound, Norgestimate, for progesterone and estrogen receptors.",The molecular weight is 327.47.,Norelgestromin has a topological polar surface area of 52.82.,The log p value of  is 3.92.,Norelgestromin is approved and investigational.,Norelgestromin is a solid.,True
14801,"Urokinase is an endogenous peptide that is cleaved in the presence of plasmin between lysine 158 and isoleucine 159 to yield active urokinase. Urokinase remains connected between these 2 chains by a sulfhydryl bond. In Canada, urokinase is indicated for lysis of acute massive pulmonary emboli, acute thrombi obstructing coronary arteries, occlusive thromboemboli in peripheral arteries and grafts, and restoration of patency to intravenous catheters. Urokinase is a serine protease that activates plasminogen to an active fibrinolytic protease. The duration of action is short due to the short half life. Patients should be counselled regarding the risk of bleeding, anaphylaxis, infusion reactions, and cholesterol embolization.[L12138 Urokinase is a serine protease. It cleaves plasminogen to form the active fibrinolytic protease, plasmin.",,,,Urokinase is approved and investigational and withdrawn.,Urokinase is a liquid.,True
14802,"Pemetrexed is a chemotherapy drug that is manufactured and marketed by Eli Lilly and Company under the brand name Alimta. It is indicated for use in combination with cisplatin for the treatment of patients with malignant pleural mesothelioma whose disease is either unresectable or who are otherwise not candidates for curative surgery. Its use in non-small cell lung cancer has also been investigated. Used in combination with cisplatin for the treatment of malignant pleural mesothelioma in adults whose disease is unresectable or who otherwise are not candidates for potentially curative surgery. Also used as a monotherapy for the treatment of locally advanced or metastatic non-small cell lung cancer (NSCLC) after prior chemotherapy Preclinical studies have shown that pemetrexed inhibits the in vitro growth of mesothelioma cell lines (MSTO-211H, NCI-H2052). Studies with the MSTO-211H mesothelioma cell line showed synergistic effects when pemetrexed was combined concurrently with cisplatin. Pemetrexed is an antifolate containing the pyrrolopyrimidine-based nucleus that exerts its antineoplastic activity by disrupting folate-dependent metabolic processes essential for cell replication. In vitro studies have shown that pemetrexed inhibits thymidylate synthase (TS), dihydrofolate reductase (DHFR), and glycinamide ribonucleotide formyltransferase (GARFT), all folate-dependent enzymes involved in the de novo biosynthesis of thymidine and purine nucleotides. Pemetrexed is transported into cells by both the reduced folate carrier and membrane folate binding protein transport systems. Once in the cell, pemetrexed is converted to polyglutamate forms by the enzyme folylpolyglutamate synthetase. The polyglutamate forms are retained in cells and are inhibitors of TS and GARFT. Polyglutamation is a time- and concentration-dependent process that occurs in tumor cells and, to a lesser extent, in normal tissues. Polyglutamated metabolites have an increased intracellular half-life resulting in prolonged drug action in malignant cells.",The molecular weight is 427.42.,Pemetrexed has a topological polar surface area of 186.97.,The log p value of  is -1.17.,Pemetrexed is approved and investigational.,Pemetrexed is a solid.,True
14803,"Calcium carbimide, sold as the citrate salt, is an alcohol-sensitizing agent. Its effects are similar to the drug disulfiram (Antabuse) in that it interferes with the normal metabolism of alcohol by preventing the breakdown of the metabolic product acetaldehyde. Calcium carbimide was conceived as an alternative for the treatment of alcoholism with a reduced side effect profile either when it is consumed accompanied by alcohol or without it. This drug was developed by Lederle Cyanamid Canada Inc and approved for marketing in Canada in 1959. The current status of calcium carbimide is cancelled post marketing. Calcium carbimide has not been approved by the FDA but the intended indication is for the treatment of alcoholism. This medication was marketed in Canada, United Kingdom and Europe under the trade name of Temposil for the sole use of alcoholism treatment. Administration of calcium carbimide causes a syndrome characterized by intense flushing, rapid pulse, panting respiration and perception of acetaldehyde in the exhaled breath. This syndrome remains for a few hours after alcohol consumption and it stops completeley after 24 hours. This syndrome is caused by the accumulation of acetaldehyde and altered vascular reaction. Therefore, the more the alcohol consumption the more the adverse effects caused by acetaldehyde accumulation. Calcium carbimide is a potent inhibitor of the aldehyde dehydrogenase. Ethanol is normally metabolized to acetaldehyde that is quickly metabolized because this molecule is toxic, thus it has to stay in very low quantities in the body. Carbimide performs its effect by being a competitive inhibitor of the hepatic aldehyde-NAD oxidoreductase dehydrogenase which is the enzyme responsible for the oxidation of acetaldehyde to water and acetate.",The molecular weight is 80.1.,Calcium carbimide has a topological polar surface area of 46.85.,,Calcium carbimide is approved and withdrawn.,Calcium carbimide is a solid.,True
14804,"Tartaric acid is a white crystalline organic acid that occurs naturally in many plants, most notably in grapes.Tartaric is an alpha-hydroxy-carboxylic acid, is diprotic and aldaric in acid characteristics, and is a dihydroxyl derivative of succinic acid. Tartaric Acid is primarily indicated in conditions like Antiscorbutic, Antiseptic.  Tartaric acid is used to generate carbon dioxide through interaction with sodium bicarbonate following oral administration. Carbon dioxide extends the stomach and provides a negative contrast medium during double contrast radiography. In high doses, this agent acts as a muscle toxin by inhibiting the production of malic acid, which could cause paralysis and maybe death.",The molecular weight is 150.09.,L-tartaric acid has a topological polar surface area of 115.06.,The log p value of  is -3.22.,L-tartaric acid is experimental.,,True
14805,"Gabexate is a synthetic serine protease inhibitor which has been used as an anticoagulant. It also known to decrease production of inflammatory cytokines. Gabexate has been investigated for use in cancer, ischemia-reperfusion injury, and pancreatitis. No approved indication. Gabexate bind and inhibits serine proteases in the coagulation cascade to prevent blood clotting. It also prevents proteolytic destruction of IkappaB resulting in suppression of the nuclear factor kappa-B signalling pathway. Ultimately this decreases the production of inflammatory cytokines such as tumor necrosis factor alpha which are produced as a result of NFkappaB activation. Gabexate inhibits kallikrein, plasmin, and thrombin by binding to their active sites. The inhibition of these components of the coagulation cascade ultimately prevents the formation of fibrin which must be present and polymerized to form a clot. Gabexate decreases the production of inflammatory cytokines by attenuating NFkappaB and c-Jun N-terminal kinase (JNK) pathway activity. The exact mechanism for this is unknown but it is thought that gabexate prevents the proteolyytic destruction of IkappaB which deactivates NFkappaB and interferes with activator protein 1 binding to DNA.",The molecular weight is 321.38.,Gabexate has a topological polar surface area of 114.5.,The log p value of  is 1.63.,Gabexate is investigational.,Gabexate is a solid.,True
14806,"Entacapone is a selective, reversible catechol-O-methyl transferase (COMT) inhibitor for the treatment of Parkinson's disease. It is a member of the class of nitrocatechols. When administered concomittantly with levodopa and a decarboxylase inhibitor (e.g., carbidopa), increased and more sustained plasma levodopa concentrations are reached as compared to the administration of levodopa and a decarboxylase inhibitor. Used as an adjunct to levodopa / carbidopa in the symptomatic treatment of patients with idiopathic Parkinson's Disease who experience the signs and symptoms of end-of-dose \wearing-off\""."" Entacapone is structurally and pharmacologically related to tolcapone, but unlike tolcapone, is not associated with hepatotoxicity. Entacapone is used in the treatment of Parkinson&rsquo;s disease as an adjunct to levodopa/carbidopa therapy. Entacapone selectively and reversiblly inhibits catechol-O-methyltransferase (COMT). In mammals, COMT is distributed throughout various organs with the highest activities in the liver and kidney. COMT also occurs in the heart, lung, smooth and skeletal muscles, intestinal tract, reproductive organs, various glands, adipose tissue, skin, blood cells and neuronal tissues, especially in glial cells. COMT catalyzes the transfer of the methyl group of S-adenosyl-L-methionine to the phenolic group of substrates that contain a catechol structure. Physiological substrates of COMT include dopa, catecholamines (dopamine, norepinephrine, and epinephrine) and their hydroxylated metabolites. The function of COMT is the elimination of biologically active catechols and some other hydroxylated metabolites. COMT is responsible for the elimination of biologically active catechols and some other hydroxylated metabolites. In the presence of a decarboxylase inhibitor, COMT becomes the major metabolizing enzyme for levodopa, catalyzing the it to 3-methoxy-4-hydroxy-L-phenylalanine (3-OMD) in the brain and periphery. The mechanism of action of entacapone is believed to be through its ability to inhibit COMT in peripheral tissues, altering the plasma pharmacokinetics of levodopa. When entacapone is given in conjunction with levodopa and an aromatic amino acid decarboxylase inhibitor, such as carbidopa, plasma levels of levodopa are greater and more sustained than after administration of levodopa and an aromatic amino acid decarboxylase inhibitor alone. It is believed that at a given frequency of levodopa administration, these more sustained plasma levels of levodopa result in more constant dopaminergic stimulation in the brain, leading to a greater reduction in the manifestations of parkinsonian syndrome.",The molecular weight is 305.29.,Entacapone has a topological polar surface area of 130.38.,The log p value of  is 1.76.,Entacapone is approved and investigational.,Entacapone is a solid.,True
14807,"Epinephrine, also known as _adrenaline_, is a hormone and neurotransmitter and produced by the adrenal glands that can also be used as a drug due to its various important functions. Though it has long been used in the treatment of hypersensitivity reactions, epinephrine in the auto-injector form (EpiPen) has been available since 1987 in the USA. Many new products/biosimilars and dosage routes have been approved under various names over the last several decades , ,. On August 16, 2018, Teva Pharmaceuticals USA gained approval to market its generic epinephrine auto-injector in 0.3 mg and 0.15 mg strengths. Dosage delivery routes for epinephrine include intravenous, inhalation, nebulization, intramuscular injection, and subcutaneous injection. Epinephrine injection is indicated in the emergency treatment of allergic reactions (Type I) including anaphylaxis to stinging insects (e.g., order Hymenoptera, which include bees, wasps, hornets, yellow jackets and fire ants) and biting insects (e.g., triatoma, mosquitos), allergen immunotherapy, foods, drugs, diagnostic testing substances (e.g., radiocontrast media) and other allergens, as well as idiopathic anaphylaxis or exercise-induced anaphylaxis. Injectable epinephrine is intended for immediate/urgent administration in patients, who are found to be at increased risk for anaphylaxis, including individuals with a history of anaphylaxis. Selection of the appropriate dosage strength is determined according to body weight.  Epinephrine is a sympathomimetic drug. It causes an adrenergic receptive mechanism on effector cells and mimics all actions of the sympathetic nervous system except those on the facial arteries and sweat glands.  Epinephrine acts on alpha and beta-adrenergic receptors. Epinephrine acts on alpha and beta receptors and is the strongest alpha receptor activator. Through its action on alpha-adrenergic receptors, epinephrine minimizes the vasodilation and increased the vascular permeability that occurs during anaphylaxis, which can cause the loss of intravascular fluid volume as well as hypotension. Epinephrine relaxes the smooth muscle of the bronchi and iris and is a histamine antagonist, rendering it useful in treating the manifestations of allergic reactions and associated conditions. This drug also produces an increase in blood sugar and increases glycogenolysis in the liver. Through its action on beta-adrenergic receptors, epinephrine leads to bronchial smooth muscle relaxation that helps to relieve bronchospasm, wheezing, and dyspnea that may occur during anaphylaxis.",The molecular weight is 183.21.,Epinephrine has a topological polar surface area of 72.72.,The log p value of  is -0.68.,Epinephrine is approved and vet_approved.,Epinephrine is a solid.,True
14808,"A beta-1 agonist catecholamine that has cardiac stimulant action without evoking vasoconstriction or tachycardia. It is proposed as a cardiotonic after myocardial infarction or open heart surgery. Indicated when parenteral therapy is necessary for inotropic support in the short-term treatment of patients with cardiac decompensation due to depressed contractility resulting either from organic heart disease or from cardiac surgical procedures. Dobutamine is a direct-acting inotropic agent whose primary activity results from stimulation of the beta-adrenoceptors of the heart while producing comparatively mild chronotropic, hypertensive, arrhythmogenic, and vasodilative effects. Dobutamine acts primarily on beta-1 adrenergic receptors, with negligible effects on beta-2 or alpha receptors. It does not cause the release of endogenous norepinephrine, as does dopamine.  Dobutamine directly stimulates beta-1 receptors of the heart to increase myocardial contractility and stroke volume, resulting in increased cardiac output.",The molecular weight is 301.39.,Dobutamine has a topological polar surface area of 72.72.,The log p value of  is 2.43.,Dobutamine is approved.,Dobutamine is a solid.,True
14809,"An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.  For use in the treatment of hypertension. Methyldopa is an aromatic-amino-acid decarboxylase inhibitor in animals and in man. Only methyldopa, the <i>L</i>-isomer of alpha-methyldopa, has the ability to inhibit dopa decarboxylase and to deplete animal tissues of norepinephrine. In man the antihypertensive activity appears to be due solely to the L-isomer. About twice the dose of the racemate (DL-alpha-methyldopa) is required for equal antihypertensive effect. Methyldopa has no direct effect on cardiac function and usually does not reduce glomerular filtration rate, renal blood flow, or filtration fraction. Cardiac output usually is maintained without cardiac acceleration. In some patients the heart rate is slowed. Normal or elevated plasma renin activity may decrease in the course of methyldopa therapy. Methyldopa reduces both supine and standing blood pressure. Methyldopa usually produces highly effective lowering of the supine pressure with infrequent symptomatic postural hypotension. Exercise hypotension and diurnal blood pressure variations rarely occur. Although the mechanism of action has yet to be conclusively demonstrated, the resultant hypotensive effect is most likely due to the drug's action on the CNS. Methyldopa is converted into the metabolite, alpha-methylnorepinephrine, in the CNS, where it stimulates the central inhibitory alpha-adrenergic receptors, leading to a reduction in sympathetic tone, total peripheral resistance, and blood pressure. Reduction in plasma renin activity, as well as the inhibition of both central and peripheral norepinephrine and serotonine production may also contribute to the drug's antihypertensive effect, although this is not a major mechanism of action. This is done through the inhibition of the decarboxylation of dihydroxyphenylalanine (dopa)—the precursor of norepinephrine—and of 5-hydroxytryptophan (5-HTP)—the precursor of serotonin—in the CNS and in most peripheral tissues.",The molecular weight is 211.22.,Methyldopa has a topological polar surface area of 103.78.,The log p value of  is -2.26.,Methyldopa is approved.,Methyldopa is a solid.,True
14810,"Micafungin is an antifungal drug. It belongs to the antifungal class of compounds known as echinocandins and exerts its effect by inhibiting the synthesis of 1,3-beta-D-glucan, an integral component of the fungal cell wall. Indicated for the treatment of candidemia, acute disseminated candidiasis, and certain other invasive <i>Candida</i> infections, as well as esophageal candidiasis, and prophylaxis of <i>Candida</i> infections in patients undergoing hematopoietic stem cell transplantation. Micafungin is also used as an alternative for the treatment of oropharyngeal candidiases and has been used with some success as primary or salvage therapy, alone or in combination with other antifungals, for the treatment of invasive aspergillosis. Formerly known as FK463, micafungin is a semisynthetic lipopeptide synthesized from a fermentation product of <i>Coleophoma empetri</i> that works as an antifungal agent. It is a glucan synthesis inhibitor of the echinocandin structural class. The U.S. Food and Drug Administration approved micafungin in March 2005. Micafungin inhibits an enzyme essential for fungal cell-wall synthesis. Depending on its concentration, micafungin may be fungicidal against some <i>Candida</i>, but is usually fungistatic against <i>Apergillus</i>. Micafungin can be used concomitantly with a variety of other drugs, including the HIV protease inhibitor ritonavir and the transplant medications cyclosporine and tacrolimus. Micafungin inhibits the synthesis of beta-1,3-D-glucan, an essential component of fungal cell walls which is not present in mammalian cells. It does this by inhibiting beta-1,3-D-glucan synthase.",The molecular weight is 1270.28.,Micafungin has a topological polar surface area of 510.14.,The log p value of  is -2.59.,Micafungin is approved and investigational.,Micafungin is a solid.,True
14811,"Nylidrin, also known as _buphenine_ belongs to the category of drugs called _vasodilators_, which relax blood vessels and increase blood flow. Nylidrin is a peripheral vasodilator. Some studies show the evidence of improving cognitive impairment in selected individuals, such as geriatric patients with mild to moderate symptoms of cognitive, emotional and physical impairment. Nylidrin is mainly indicated in conditions like arteriosclerosis, cerebrovascular disease, peripheral vascular disease, Raynaud's disease, thrombo-angitis obliterans, and thrombophlebitis. It may sometimes be used in the treatment of peripheral vascular disorders in addition premature labor (however, the drug is not approved for premature labor). This drug is classified as a beta receptor agonist.The β2-adrenergic receptor belongs to the widely expressed _7-transmembrane receptors superfamily_, which signals through heterotrimeric _G-proteins_. They are frequently referred to as G-protein-coupled receptors because they accomplish signal transduction to the interior of the cell by interactions with _guanine nucleotide regulatory binding proteins_. The receptor-coupled G-proteins work as “molecular switches” which alternate from an inactive guanosine-diphosphate to an active guanosine-triphosphate (GTP) state, which then act to modulate all downstream cell processes. Signaling by various hormones and neurotransmitters, as well as photons and odors, follows the same general pathway, (i.e., by binding of an extracellular ligand to the receptor, which then interacts with the membrane-bound G-protein). This complex, often referred to as the ternary complex, then acts through the activated G-protein to regulate an effector, such as _adenylyl cyclase_, _phospholipase C_, or ion channels. ",The molecular weight is 299.41.,Nylidrin has a topological polar surface area of 52.49.,The log p value of  is 3.01.,Nylidrin is approved.,Nylidrin is a solid.,True
14812,"Echinacoside is a phenylethanoid glycoside isolated from _Echinacea angustifolia_ in 1950, and currently being investigated for the treatment of Parkinson's, Alzheimer's, atherosclerosis, osteoporosis, acute colitis, wound treatment, and hepatitis. Echinacoside has demonstrated inhibition of apoptosis in neural cell lines, demonstrating potential for use in the treatment of neurological conditions. The neuroprotective effects are thought to be mediated via effects on mitogen-activated protein kinase, nuclear factor kappa-B, caspases 3 and 8, as well as CHOP pathways.",,,,Echinacoside is experimental.,Echinacoside is a solid.,True
14813,"Troglitazone was withdrawn in 2000 due to risk of hepatotoxicity. It was superseded by and. For the treatment of Type II diabetes mellitus. It is used alone or in combination with a sulfonylurea, metformin, or insulin as an adjunct to diet and exercise. Troglitazone is an oral antihyperglycemic agent which acts primarily by decreasing insulin resistance. Troglitazone is used in the management of type II diabetes (noninsulin-dependent diabetes mellitus (NIDDM) also known as adult-onset diabetes). It improves sensitivity to insulin in muscle and adipose tissue and inhibits hepatic gluconeogenesis. Troglitazone is not chemically or functionally related to either the sulfonylureas, the biguanides, or the g-glucosidase inhibitors. Troglitazone may be used concomitantly with a sulfonylurea or insulin to improve glycemic control. Troglitazone is a thiazolidinedione antidiabetic agent that lowers blood glucose by improving target cell response to insulin. It has a unique mechanism of action that is dependent on the presence of insulin for activity. Troglitazone decreases hepatic glucose output and increases insulin dependent glucose disposal in skeletal muscle. Its mechanism of action is thought to involve binding to nuclear receptors (PPAR) that regulate the transcription of a number of insulin responsive genes critical for the control of glucose and lipid metabolism. Troglitazone is a ligand to both PPARα and PPARγ, with a highter affinity for PPARγ. The drug also contains an α-tocopheroyl moiety, potentially giving it vitamin E-like activity. Troglitazone has been shown to reduce inflammation, and is associated with a decrase in nuclear factor kappa-B (NF-κB) and a concomitant increase in its inhibitor (IκB). Unlike sulfonylureas, troglitazone is not an insulin secretagogue.",The molecular weight is 441.54.,Troglitazone has a topological polar surface area of 84.86.,The log p value of  is 5.59.,Troglitazone is approved and investigational and withdrawn.,Troglitazone is a solid.,True
14814,"A powerful synthetic, non-steroidal estrogen.  Used to treat symptoms of menopause, deficiencies in ovary function (including underdevelopment of female sexual characteristics and some types of infertility), and in rare cases, prostate cancer. Chlorotrianisene may also be used to prevent breast engorgement following childbirth. Chlorotrianisene is a nonsteroidal synthetic estrogen. After menopause, when the body no longer produces estrogen, chlorotrianisene is used as a simple replacement of estrogen. The estrogen-stimulated endometrium may bleed within 48-72 hours after discontinuance of estrogen therapy. Paradoxically, prolonged estrogen therapy may cause shrinkage of the endometrium and an increase in size of the myometrium. Estrogens have a weak anabolic effect and may cause sodium retention with associated fluid retention and edema. Estrogens may also decrease elevated blood cholesterol and phospholipid concentrations. Estrogens affect bone by increasing calcium deposition and accelerating epiphyseal closure, following initial growth stimulation. During the preovulatory or nonovulatory phase of the menstrual cycle, estrogen is the principal determinant in the onset of menstruation. A decline of estrogenic activity at the end of the menstrual cycle also may induce menstruation; however, the cessation of progesterone secretion is the most important factor during the mature ovulatory phase of the menstrual cycle. The benefit derived from estrogen therapy in the prevention of postpartum breast engorgement must be carefully weighed against the potential&nbsp;increased risk of puerperal thromboembolism&nbsp;associated with the use of large doses of estrogens. Chlorotrianisene binds to the estrogen receptor on various estrogen receptor bearing cells. Target cells include cells in the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary.",The molecular weight is 380.87.,Chlorotrianisene has a topological polar surface area of 27.69.,The log p value of  is 5.83.,Chlorotrianisene is investigational and withdrawn.,Chlorotrianisene is a solid.,True
14815,"An imidazole antithyroid agent. Carbimazole is metabolized to methimazole, which is responsible for the antithyroid activity. For the treatment of hyperthyroidism and thyrotoxicosis. It is also used to prepare patients for thyroidectomy. Carbimazole is a carbethoxy derivative of methimazole. Its antithyroid action is due to its conversion to methimazole after absorption. It is used to treat hyperthyroidism and thyrotoxicosis. Carbimazole is an aitithyroid agent that decreases the uptake and concentration of inorganic iodine by thyroid, it also reduces the formation of di-iodotyrosine and thyroxine. Once converted to its active form of methimazole, it prevents the thyroid peroxidase enzyme from coupling and iodinating the tyrosine residues on thyroglobulin, hence reducing the production of the thyroid hormones T3 and T4.",The molecular weight is 186.23.,Carbimazole has a topological polar surface area of 32.78.,The log p value of  is 1.68.,Carbimazole is approved and investigational.,Carbimazole is a solid.,True
14816,"A chelating agent (chelating agents) that sequesters a variety of polyvalent cations. It is used in pharmaceutical manufacturing and as a food additive. For the reduction of blood levels and depot stores of lead in lead poisoning (acute and chronic) and lead encephalopathy, in both pediatric populations and adults. Edetate calcium is a heavy metal chelating agent. The calcium in edetate calcium can be displaced by divalent or trivalent metals to form a stable water soluble complex that can be excreted in the urine. In theory, 1 g of edetate calcium can theoretically bind 620 mg of lead, but in reality only about 5 mg per gram is actually excreted into the urine in lead poisoned patients. In addition to chelating lead, edetate calcium also chelates and eliminates zinc from the body. Edetate calcium also binds cadmium, copper, iron and manganese, but to a much lesser extent than either lead or zinc. Edetate calcium is relatively ineffective for use in treating mercury, gold or arsenic poisoning. The pharmacologic effects of edetate calcium disodium are due to the formation of chelates with divalent and trivalent metals. A stable chelate will form with any metal that has the ability to displace calcium from the molecule, a feature shared by lead, zinc, cadmium, manganese, iron and mercury. The amounts of manganese and iron metabolized are not significant. Copper is not mobilized and mercury is unavailable for chelation because it is too tightly bound to body ligands or it is stored in inaccessible body compartments. The excretion of calcium by the body is not increased following intravenous administration of edetate calcium disodium, but the excretion of zinc is considerably increased.",The molecular weight is 292.24.,Edetic acid has a topological polar surface area of 155.68.,The log p value of  is -1.93.,Edetic acid is approved and vet_approved.,Edetic acid is a solid.,True
14817,"Exemestane is an oral steroidal aromatase inhibitor used in the adjuvant treatment of hormonally-responsive (also called hormone-receptor-positive, estrogen-responsive) breast cancer in postmenopausal women. It irreversibly binds to the active site of the enzyme resulting in permanent inhibition. For the treatment of advanced breast cancer in postmenopausal women whose disease has progressed following tamoxifen therapy. Aromatase is an enzyme that converts hormones to estrogen in the body's adrenal glands. The aromatase inhibitors (AIs) are drugs that reduce estrogen levels by blocking the action of aromatase in the adrenal glands. The selective AIs (SAIs) selectively reduce levels of estrogen without interfering with levels of other steroid hormones that are produced by the adrenal gland. Drugs in this class include anastrozole (Arimidex &trade;), letrozole (Femara &trade;) and exemestane (Aromasin &trade;). Breast cancer cell growth may be estrogen-dependent. Aromatase (exemestane) is the principal enzyme that converts androgens to estrogens both in pre- and postmenopausal women. While the main source of estrogen (primarily estradiol) is the ovary in premenopausal women, the principal source of circulating estrogens in postmenopausal women is from conversion of adrenal and ovarian androgens (androstenedione and testosterone) to estrogens (estrone and estradiol) by the aromatase enzyme in peripheral tissues. Estrogen deprivation through aromatase inhibition is an effective and selective treatment for some postmenopausal patients with hormone-dependent breast cancer. Exemestane is an irreversible, steroidal aromatase inactivator, structurally related to the natural substrate androstenedione. It irreversibly binds to the active site causing permanent inhibition necessitating de novo synthesis to restore enzymatic function. Exemestane significantly lowers circulating estrogen concentrations in postmenopausal women, but has no detectable effect on the adrenal biosynthesis of corticosteroids or aldosterone. This reduction in serum and tumor concentrations of estrogen delays tumor growth and disease progression. Exemestane has no effect on other enzymes involved in the steroidogenic pathway up to a concentration at least 600 times higher than that inhibiting the aromatase enzyme.",The molecular weight is 296.41.,Exemestane has a topological polar surface area of 34.14.,The log p value of  is 3.28.,Exemestane is approved and investigational.,Exemestane is a solid.,True
14818,"Tioconazole is an imidazole antifungal used to treat fungal and yeast infections. Topical formulations are used for ringworm, jock itch, athlete's foot, and tinea versicolor or \sun fungus\"". Tioconazole interacts with 14-alpha demethylase, a cytochrome P-450 enzyme that converts lanosterol to ergosterol, an essential component of the yeast membrane. In this way, tioconazole inhibits ergosterol synthesis, resulting in increased cellular permeability."" For the local treatment of vulvovaginal candidiasis (moniliasis). Tioconazole is a broad-spectrum imidazole antifungal agent that inhibits the growth of human pathogenic yeasts. Tioconazole exhibits fungicidal activity in vitro against <i>Candida albicans</i>, other species of the genus Candida, and against <i>Torulopsis glabrata</i>. Tioconazole prevents the growth and function of some fungal organisms by interfering with the production of substances needed to preserve the cell membrane. This drug is effective only for infections caused by fungal organisms. It will not work for bacterial or viral infections. Tioconazole interacts with 14-&alpha; demethylase, a cytochrome P-450 enzyme that converts lanosterol to ergosterol, an essential component of the yeast membrane. In this way, tioconazole inhibits ergosterol synthesis, resulting in increased cellular permeability. Tioconazole may also inhibit endogenous respiration, interact with membrane phospholipids, inhibit the transformation of yeasts to mycelial forms and the uptake of purine, impair triglyceride and/or phospholipid biosynthesis, and inhibit the movement of calcium and potassium ions across the cell membrane by blocking the ion transport pathway known as the Gardos channel.",The molecular weight is 387.7.,Tioconazole has a topological polar surface area of 27.05.,The log p value of  is 4.79.,Tioconazole is approved.,Tioconazole is a solid.,True
14819,"A broad spectrum antimycotic with some action against Gram positive bacteria. It is used topically in dermatomycoses also orally and parenterally. For topical application in the treatment of tinea pedis, tinea cruris, and tinea corporis caused by <i>Trichophyton rubrum</i>, <i>Trichophyton mentagrophytes</i>, <i>Trichophyton tonsurans</i>, <i>Microsporum canis</i>, <i>Microsporum audouini</i>, <i>Microsporum gypseum</i>, and <i>Epidermophyton floccosum</i>, in the treatment of cutaneous candidiasis, and in the treatment of tinea versicolor. Econazole is an antifungal medication related to fluconazole (Diflucan), ketoconazole (Nizoral), itraconazole (Sporanox), and clotrimazole (Lotrimin, Mycelex). Econazole prevents fungal organisms from producing vital substances required for growth and function. This medication is effective only for infections caused by fungal organisms. It will not work for bacterial or viral infections. Econazole interacts with 14-&alpha; demethylase, a cytochrome P-450 enzyme necessary to convert lanosterol to ergosterol. As ergosterol is an essential component of the fungal cell membrane, inhibition of its synthesis results in increased cellular permeability causing leakage of cellular contents. Econazole may also inhibit endogenous respiration, interact with membrane phospholipids, inhibit the transformation of yeasts to mycelial forms, inhibit purine uptake, and impair triglyceride and/or phospholipid biosynthesis.",The molecular weight is 381.68.,Econazole has a topological polar surface area of 27.05.,The log p value of  is 5.1.,Econazole is approved.,Econazole is a solid.,True
14820,"Bifonazole is an azole antifungal drug. Used for the treatment of various topical fungal infections, including athlete's foot (tinea pedis). Bifonazole is a type of antifungal medicine known as an imidazole. It kills fungi and yeasts by interfering with their cell membranes. Bifonazole works by inhibiting the production of a substance called ergosterol, which is an essential component of fungal cell membranes.It acts to destabilize the fungal cyctochrome p450 51 enzyme (also known as Lanosterol 14-alpha demethylase). This is vital in the cell membrance structure of the fungus. Its inhibition leads to cell lysis. The disruption in production of ergosterol disrupts the cell membrane and causes holes to appear. The cell membranes of fungi are vital for their survival. They keep unwanted substances from entering the cells and stop the contents of the cells from leaking out. As bifonazole causes holes to appear in the cell membranes, essential constituents of the fungal cells can leak out. This kills the fungi.",The molecular weight is 310.4.,Bifonazole has a topological polar surface area of 17.82.,The log p value of  is 4.74.,Bifonazole is approved and investigational.,Bifonazole is a solid.,True
14821,"An anti-androgen that, in the form of its acetate (cyproterone acetate), also has progestational properties. It is used in the treatment of hypersexuality in males, as a palliative in prostatic carcinoma, and, in combination with estrogen, for the therapy of severe acne and hirsutism in females. For the palliative treatment of patients with advanced prostatic carcinoma. Cyproterone is an antiandrogen. It suppresses the actions of testosterone (and its metabolite dihydrotestosterone) on tissues. It acts by blocking androgen receptors which prevents androgens from binding to them and suppresses luteinizing hormone (which in turn reduces testosterone levels). The direct antiandrogenic effect of cyproterone is blockage of the binding of dihydrotestosterone to the specific receptors in the prostatic carcinoma cell. In addition, cyproterone exerts a negative feed-back on the hypothalamo-pituitary axis, by inhibiting the secretion of luteinizing hormone resulting in diminished production of testicular testosterone.",The molecular weight is 416.94.,Cyproterone acetate has a topological polar surface area of 60.44.,The log p value of  is 3.96.,Cyproterone acetate is approved and investigational.,Cyproterone acetate is a solid.,True
14822,"Sulfathiazole is a short-acting sulfa drug. It used to be a common oral and topical antimicrobial until less toxic alternatives were discovered. It is still occasionally used, sometimes in combination with sulfabenzamide and sulfacetamide. Sulfathiazole is effective against a wide range of gram positive and gram negative pathogenic microorganisms. Although no longer used in humans, it is used in cattle.",The molecular weight is 255.31.,Sulfathiazole has a topological polar surface area of 85.08.,The log p value of  is 0.73.,Sulfathiazole is approved and vet_approved.,Sulfathiazole is a solid.,True
14823,"Investigated for use/treatment in cancer/tumors (unspecified), macular degeneration, and diabetic retinopathy. Endostatin is an endogenous antitumor protein. Endostatin is a 20-kDa C-terminal fragment derived from type XVIII collagen which inhibits cell proliferation and migration, and induces endothelial cell apoptosis and cell cycle arrest. It is proposed that endostatin's effects are due to inhibition of vascular endothelial growth factor (VEGF) tyrosine phosphorylation of KDR/F1k-1 (VEGF receptor 2), the cell surface receptor for VEGF. VEGF is an important mediator of angiogensis. Endostatin additionally blocks activation of extracellular signal related kinases, or ERK, protein 38 mitogen activated protein kinase, or p38 MAPK (signal transduction pathways involving kinases that couple growth factors to cell surface receptors), as well as focal adhesion kinase (p125FAK). Studies are being done to determine if endostatin has possible impact on other pathways, and may also target E-selectin and block activity of metalloproteinases 2, 9 and 13. There is further research into a possible mechanistic link involving endostatin's angiogenic and zinc binding ability. ",,,,Endostatin is investigational.,Endostatin is a solid.,True
14824,"Buserelin is a synthetic peptide analog of the luteinizing hormone-releasing hormone (LHRH) agonist, which stimulates the pituitary gland's gonadotrophin-releasing hormone receptor (GnRHR). It is used in prostate cancer treatment. Buserelin may be used in the treatment of hormone-responsive cancers such as prostate cancer or breast cancer, estrogen-dependent conditions (such as endometriosis or uterine fibroids), and in assisted reproduction. The substitution of glycine in position 6 by D-serine, and that of glycinamide in position 10 by ethylamide, leads to a nonapeptide with a greatly enhanced LHRH effect. The effects of buserelin on FSH and LH release are 20 to 170 times greater than those of LHRH. Buserelin also has a longer duration of action than natural LHRH. Investigations in healthy adult males and females have demonstrated that the increase in plasma LH and FSH levels persist for at least 7 hours and that a return to basal values requires about 24 hours. Buserelin stimulates the pituitary gland's gonadotrophin-releasing hormone receptor (GnRHR). Buserelin desensitizes the GnRH receptor, reducing the amount of gonadotropin. In males, this results in a reduction in the synthesis and release of testosterone. In females, estrogen secretion is inhibited. While initially, there is a rise in FSH and LH levels, chronic administration of Buserelin results in a sustained suppression of these hormones.",The molecular weight is 1239.45.,Buserelin has a topological polar surface area of 438.27.,The log p value of  is -1.45.,Buserelin is approved and investigational.,Buserelin is a liquid.,True
14825,"C18 steroid with androgenic and anabolic properties. It is generally prepared from alkyl ethers of estradiol to resemble testosterone but less one carbon at the 19 position. It is a schedule III drug in the U.S. For the treatment of refractory deficient red cell production anemias, breast carcinoma, hereditary angioedema, antithrombin III deficiency, fibrinogen excess, growth failure and Turner's syndrome. It is also indicated in the prophylaxis of hereditary angioedema. Nandrolone is an anabolic steroid occurring naturally in the human body, albeit in small quantities. Nandrolone increases production and urinary excretion of erythropoietin. It may also have a direct action on bone marrow. Nandrolone binds to the androgen receptor to a greater degree than testosterone, but due to its inability to act on the muscle in ways unmediated by the receptor, has less overall effect on muscle growth. Nandrolone is an androgen receptor agonist. The drug bound to the receptor complexes which allows it to enter the nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.",The molecular weight is 428.66.,Nandrolone decanoate has a topological polar surface area of 43.37.,The log p value of  is 8.07.,Nandrolone decanoate is approved and illicit.,Nandrolone decanoate is a solid.,True
14826,"Norgestrel is synthetic steroidal progestin that is used in combination with ethinyl estradiol for oral contraception. Norgestrel is composed of a racemic mixture of two stereoisomers, dextronorgestrel and levonorgestrel. However, only the levorotary enantiomer () is biologically active. Norgestrel in combination with ethinyl estradiol is indicated for the prevention of pregnancy in women who elect to use this product as a method of contraception. Norgestrel (and more specifically the active stereoisomer levonorgestrel) binds to the progesterone and estrogen receptors within the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Once bound to the receptor, progestins like levonorgestrel will slow the frequency of release of gonadotropin releasing hormone (GnRH) from the hypothalamus and blunt the pre-ovulatory LH (luteinizing hormone) surge. Loss of the LH surge inhibits ovulation and thereby prevents pregnancy.",,,,Norgestrel is approved.,,True
14827,"Synthetic 9 residue cyclic peptide. The hormone is prepared synthetically to avoid possible contamination with vasopressin (ADH) and other small polypeptides with biologic activity. Used for labor induction, augmentation of labor, postpartum abbreviation of third stage of labor, postpartum control of uterine bleeding, termination of pregnancy and for the evaluation of fetal respiratory capability. Oxytocin cannot be used for elective induction of labor, there must be a clear medical requirement.  Indirectly stimulates contraction of uterine smooth muscle by increasing the sodium permeability of uterine myofibrils. Increases contraction amplitude and frequency, which tends to decrease cervical activity, produce dilation and effacement of the cervix, and transiently impede uterine blood flow; contractions produced by oxytocin at term are similar to those occurring during spontaneous labor. High estrogen concentrations lower the threshold for uterine response to oxytocin. Uterine response increases with the duration of pregnancy and is greater in labor than when not in labor; only very large doses elicit contractions in early pregnancy. Contracts myoepithelial cells surrounding the alveoli of the breasts, forcing milk from the alveoli into the larger ducts and facilitating milk ejection. Minimal antidiuretic activity relative to vasopressin; water intoxication possible at high doses and/or excessive electrolyte-free fluid.  Uterine motility depends on the formation of the contractile protein actomyosin under the influence of the Ca2+-dependent phosphorylating enzyme myosin light-chain kinase. Oxytocin promotes contractions by increasing the intracellular Ca2+, which in turn activates myosin's light chain kinase.. Oxytocin has specific receptors in the muscle lining of the uterus and the receptor concentration increases greatly during pregnancy, reaching a maximum in early labor at term.",The molecular weight is 1007.19.,Oxytocin has a topological polar surface area of 399.53.,The log p value of  is -0.65.,Oxytocin is approved and vet_approved.,Oxytocin is a liquid.,True
14828,"Antibiotic substance produced by Streptomyces garyphalus. Used in combination with up to 5 other drugs as a treatment for Mycobacterium avium complex (MAC) and is also used to treat tuberculosis (TB). Cycloserine, a broad-spectrum antibiotic, may be bactericidal or bacteriostatic, depending on its concentration at the site of infection and the susceptibility of the organism. Cycloserine works by blocking the formation of these peptidoglycans. By doing this the walls of the bacteria become weak and it results in the death of the bacteria Cycloserine is an analog of the amino acid D-alanine. It interferes with an early step in bacterial cell wall synthesis in the cytoplasm by competitive inhibition of two enzymes, L-alanine racemase, which forms D-alanine from L-alanine, and D-alanylalanine synthetase, which incorporates D-alanine into the pentapeptide necessary for peptidoglycan formation and bacterial cell wall synthesis.",The molecular weight is 102.09.,Cycloserine has a topological polar surface area of 64.35.,The log p value of  is -1.19.,Cycloserine is approved.,Cycloserine is a solid.,True
14829,"Flupentixol is an antipsychotic neuroleptic drug. It is a thioxanthene, and therefore closely related to the phenothiazines. Its primary use is as a long acting injection given two or three weekly to people with schizophrenia who have a poor compliance with medication and suffer frequent relapses of illness. It is a D1 and D2 receptor antagonist. It is not approved in the United States. For use in the treatment of schizophrenia and depression Flupenthixol is an anxiolytic, antidepressive agent and a mood stabilizer. It inhibits the central monoamine receptors, particularly the dopamine D1 and D2 receptors. Therefore, it increases the amount of serotonin and noradrenaline that control mood and thinking, and improves mood. Flupenthixol is a thioxanthene antipsychotic. The mechanism of action of Flupenthixol is not completely understood. Flupenthixol is a powerful antagonist of both D1 and D2 dopamine receptors, and an alpha-adrenergic receptor antagonist. It's antipsychotic activity is thought to be related to blocks postsynaptic dopamine receptors in the CNS.",The molecular weight is 434.52.,Flupentixol has a topological polar surface area of 26.71.,The log p value of  is 4.34.,Flupentixol is approved and investigational and withdrawn.,Flupentixol is a solid.,True
14830,"An antiviral that is used in the prophylactic or symptomatic treatment of influenza A. It is also used as an antiparkinsonian agent, to treat extrapyramidal reactions, and for postherpetic neuralgia. The mechanisms of its effects in movement disorders are not well understood but probably reflect an increase in synthesis and release of dopamine, with perhaps some inhibition of dopamine uptake. For the chemoprophylaxis, prophylaxis, and treatment of signs and symptoms of infection caused by various strains of influenza A virus. Also for the treatment of parkinsonism and drug-induced extrapyramidal reactions. Amantadine is an antiviral drug which also acts as an antiparkinson agent, for which it is usually combined with L-DOPA when L-DOPA responses decline (probably due to tolerance). It is a derivate of adamantane, like a similar drug rimantadine. The mechanism of action of amantadine in the treatment of Parkinson's disease and drug-induced extrapyramidal reactions is not known. It has been shown to cause an increase in dopamine release in the animal brain, and does not possess anticholinergic activity. The mechanism of its antiparkinsonic effect is not fully understood, but it appears to be releasing dopamine from the nerve endings of the brain cells, together with stimulation of norepinephrine response. It also has NMDA receptor antagonistic effects. The antiviral mechanism seems to be unrelated. The drug interferes with a viral protein, M2 (an ion channel), which is needed for the viral particle to become \uncoated\"" once it is taken inside the cell by endocytosis.""",The molecular weight is 151.25.,Amantadine has a topological polar surface area of 26.02.,The log p value of  is 2.0.,Amantadine is approved.,Amantadine is a solid.,True
14831,"Droxidopa is a precursor of noradrenaline that is used in the treatment of Parkinsonism. It is approved for use in Japan and is currently in trials in the U.S. The racaemic form (dl-threo-3,4-dihydroxyphenylserine) has also been used, and has been investigated in the treatment of orthostatic hypotension. There is a deficit of noradrenaline as well as of dopamine in Parkinson's disease and it has been proposed that this underlies the sudden transient freezing seen usually in advanced disease. For treatment of neurogenic orthostatic hypotension (NOH) associated with various disorders including Multiple System Atrophy, Familial Amyloid Polyneuropathy, hemodialysis induced hypotension and Parkinson's Disease. Also investigated for use/treatment in neurologic disorders, nephropathy, blood (blood forming organ disorders, unspecified), and dizzy/fainting spells. Droxidopa is an orally active synthetic precursor of norepinephrine that increases the deficient supply of norepinephrine in patients with NOH, thereby improving orthostatic blood pressure and alleviating associated symptoms of lightheadedness, dizziness, blurred vision, and syncope through the induction of tachycardia (increased heart rate) and hypertension. Droxidopa crosses the blood-brain barrier where it is converted to norepinephrine via decarboxylation by L-aromatic-amino-acid decarboxylase. Norephinephrine acts at alpha-adrenergic receptors as a vasoconstrictor and at beta-adrenergic receptors as a heart stimulator and artery dilator.",The molecular weight is 213.19.,Droxidopa has a topological polar surface area of 124.01.,The log p value of  is -2.48.,Droxidopa is approved and investigational.,Droxidopa is a solid.,True
14832,Fluorodopa F 18 is a fluorinated analog of used as a diagnostic agent for positron emission tomography (PET) in the evaluation of Parkinsonian syndromes. Fluorodopa F 18 PET is used adjunctly with other diagnostic investigations and serves primarily to visualize dopaminergic nerve terminals in the striatum. Fluorodopa F 18 is indicated for use with positron emission tomography (PET) to visualize dopaminergic nerve terminals in the striatum for the evaluation of adult patients with suspected Parkinsonian syndromes (PS).,The molecular weight is 214.18.,Fluorodopa (18F) has a topological polar surface area of 103.78.,The log p value of  is -2.29.,Fluorodopa (18F) is approved and experimental.,Fluorodopa (18F) is a solid.,True
14833,"Nutritional factor found in milk, eggs, malted barley, liver, kidney, heart, and leafy vegetables. The richest natural source is yeast. It occurs in the free form only in the retina of the eye, in whey, and in urine; its principal forms in tissues and cells are as flavin mononucleotide and flavin-adenine dinucleotide. For the treatment of ariboflavinosis (vitamin B2 deficiency). Riboflavin or vitamin B2 is an easily absorbed, water-soluble micronutrient with a key role in maintaining human health. Like the other B vitamins, it supports energy production by aiding in the metabolising of fats, carbohydrates, and proteins. Vitamin B2 is also required for red blood cell formation and respiration, antibody production, and for regulating human growth and reproduction. It is essential for healthy skin, nails, hair growth and general good health, including regulating thyroid activity. Riboflavin also helps in the prevention or treatment of many types of eye disorders, including some cases of cataracts. Binds to riboflavin hydrogenase, riboflavin kinase, and riboflavin synthase. Riboflavin is the precursor of flavin mononucleotide (FMN, riboflavin monophosphate) and flavin adenine dinucleotide (FAD). The antioxidant activity of riboflavin is principally derived from its role as a precursor of FAD and the role of this cofactor in the production of the antioxidant reduced glutathione. Reduced glutathione is the cofactor of the selenium-containing glutathione peroxidases among other things. The glutathione peroxidases are major antioxidant enzymes. Reduced glutathione is generated by the FAD-containing enzyme glutathione reductase.",The molecular weight is 376.37.,Riboflavin has a topological polar surface area of 155.05.,The log p value of  is -0.73.,Riboflavin is approved and investigational and nutraceutical and vet_approved.,Riboflavin is a solid.,True
14834,"A synthetic naphthoquinone without the isoprenoid side chain and biological activity, but can be converted to active vitamin K2, menaquinone, after alkylation in vivo. The primary known function of vitamin K is to assist in the normal clotting of blood, but it may also play a role in normal bone calcification. Menadione (Vitamin K3) is a fat-soluble vitamin precursor that is converted into menaquinone in the liver. Vitamin K1 and K2 are the naturally occurring types of vitamin K. The former, which is also known as phylloquinone, is synthesized by plants and can be found in such foods as spinach, broccoli, lettuce, and soybeans. The latter, sometimes alternatively referred to as menaquinone, is primarily produced by bacteria in the anterior part of the gut and the intestines. Vitamin K3, on the other hand, is one of the many manmade versions of vitamin K. Also called menadione, this yellowish, synthetic crystalline substance is converted into the active form of the K2 vitamin inside of the animal body. While a vitamin K deficiency can be dangerous, especially to infants that may easily suffer from extensive hemorrhaging, an overdose can be as equally detrimental. Newborns that are administered too great a dosage of vitamin K3 can suffer from kernicterus, a form of severe brain damage that may produce decreased movement, loss of appetite, seizures, deafness, mental retardation, and even death. This condition is associated with an abnormally high concentration of bilirubin, a bile pigment, in the tissues of the brain, which can be caused by the presence of K3. For this reason, K3 is less often utilized medically than it was in former times. Menadione (vitamin K3) is involved as a cofactor in the posttranslational gamma-carboxylation of glutamic acid residues of certain proteins in the body. These proteins include the vitamin K-dependent coagulation factors II (prothrombin), VII (proconvertin), IX (Christmas factor), X (Stuart factor), protein C, protein S, protein Zv and a growth-arrest-specific factor (Gas6). In contrast to the other vitamin K-dependent proteins in the blood coagulation cascade, protein C and protein S serve anticoagulant roles. The two vitamin K-dependent proteins found in bone are osteocalcin, also known as bone G1a (gamma-carboxyglutamate) protein or BGP, and the matrix G1a protein or MGP. Gamma-carboxylation is catalyzed by the vitamin K-dependent gamma-carboxylases. The reduced form of vitamin K, vitamin K hydroquinone, is the actual cofactor for the gamma-carboxylases. Proteins containing gamma-carboxyglutamate are called G1a proteins.",The molecular weight is 172.18.,Menadione has a topological polar surface area of 34.14.,The log p value of  is 2.45.,Menadione is approved and nutraceutical.,Menadione is a solid.,True
14835,"Benazepril, brand name Lotensin, is a medication used to treat high blood pressure (hypertension), congestive heart failure, and chronic renal failure. Upon cleavage of its ester group by the liver, benazepril is converted into its active form benazeprilat, a non-sulfhydryl angiotensin-converting enzyme (ACE) inhibitor. Benazepril is indicated for the treatment of hypertension. It may be used alone or in combination with thiazide diuretics. Benazepril, an angiotensin-converting enzyme (ACE) inhibitor, is a prodrug which, when hydrolyzed by esterases to its active Benazeprilat, is used to treat hypertension and heart failure, to reduce proteinuria and renal disease in patients with nephropathies, and to prevent stroke, myocardial infarction, and cardiac death in high-risk patients. Benazepril and Benazeprilat inhibit angiotensin-converting enzyme (ACE) in human subjects and animals. ACE is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex. Benazeprilat, the active metabolite of Benazepril, competes with angiotensin I for binding at the angiotensin-converting enzyme, blocking the conversion of angiotensin I to angiotensin II. Inhibition of ACE results in decreased plasma angiotensin II. As angiotensin II is a vasoconstrictor and a negative-feedback mediator for renin activity, lower concentrations result in a decrease in blood pressure and stimulation of baroreceptor reflex mechanisms, which leads to decreased vasopressor activity and to decreased aldosterone secretion.",The molecular weight is 424.5.,Benazepril has a topological polar surface area of 95.94.,The log p value of  is 1.82.,Benazepril is approved and investigational.,Benazepril is a solid.,True
14836,"Ramipril is a prodrug belonging to the angiotensin-converting enzyme (ACE) inhibitor class of medications. It is metabolized to ramiprilat in the liver and, to a lesser extent, kidneys. Ramiprilat is a potent, competitive inhibitor of ACE, the enzyme responsible for the conversion of angiotensin I (ATI) to angiotensin II (ATII). ATII regulates blood pressure and is a key component of the renin-angiotensin-aldosterone system (RAAS). Ramipril may be used in the treatment of hypertension, congestive heart failure, nephropathy, and to reduce the rate of death, myocardial infarction and stroke in individuals at high risk of cardiovascular events. For the management of mild to severe hypertension. May be used to reduce cardiovascular mortality following myocardial infarction in hemodynamically stable individuals who develop clinical signs of congestive heart failure within a few days following myocardial infarction. To reduce the rate of death, myocardial infarction and stroke in individuals at high risk of cardiovascular events. May be used to slow the progression of renal disease in individuals with hypertension, diabetes mellitus and microalubinuria or overt nephropathy.  Ramipril is an ACE inhibitor similar to benazepril, fosinopril and quinapril. It is an inactive prodrug that is converted to ramiprilat in the liver, the main site of activation, and kidneys. Ramiprilat confers blood pressure lowing effects by antagonizing the effect of the RAAS. The RAAS is a homeostatic mechanism for regulating hemodynamics, water and electrolyte balance. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from the granular cells of the juxtaglomerular apparatus in the kidneys. In the blood stream, renin cleaves circulating angiotensinogen to ATI, which is subsequently cleaved to ATII by ACE. ATII increases blood pressure using a number of mechanisms. First, it stimulates the secretion of aldosterone from the adrenal cortex. Aldosterone travels to the distal convoluted tubule (DCT) and collecting tubule of nephrons where it increases sodium and water reabsorption by increasing the number of sodium channels and sodium-potassium ATPases on cell membranes. Second, ATII stimulates the secretion of vasopressin (also known as antidiuretic hormone or ADH) from the posterior pituitary gland. ADH stimulates further water reabsorption from the kidneys via insertion of aquaporin-2 channels on the apical surface of cells of the DCT and collecting tubules. Third, ATII increases blood pressure through direct arterial vasoconstriction. Stimulation of the Type 1 ATII receptor on vascular smooth muscle cells leads to a cascade of events resulting in myocyte contraction and vasoconstriction. In addition to these major effects, ATII induces the thirst response via stimulation of hypothalamic neurons. ACE inhibitors inhibit the rapid conversion of ATI to ATII and antagonize RAAS-induced increases in blood pressure. ACE (also known as kininase II) is also involved in the enzymatic deactivation of bradykinin, a vasodilator. Inhibiting the deactivation of bradykinin increases bradykinin levels and may sustain the effects of ramiprilat by causing increased vasodilation and decreased blood pressure. Ramipril inhibits the RAAS system by binding to and inhibiting ACE thereby preventing the conversion of angiotensin I to angiotensin II. As plasma levels of angiotensin II fall, less activation of the G-protein coupled receptors angiotensin receptor I (AT<sub>1</sub>R) and angiotensin receptor II (AT<sub>2</sub>R) occurs. ",The molecular weight is 416.52.,Ramipril has a topological polar surface area of 95.94.,The log p value of  is 1.54.,Ramipril is approved.,Ramipril is a solid.,True
14837,"A synthetic pentapeptide that mimics the actions of endogenous gastrin when given parenterally. It works by stimulating the secretion of gastric acid, pepsin, and intrinsic factor. It has also been used as a diagnostic aid. Used as a diagnostic aid for evaluation of gastric acid secretory function Pentagastrin is indicated as a diagnostic aid for evaluation of gastric acid secretory function. It is effective in testing for anacidity (achlorhydria) in patients with suspected pernicious anemia, atrophic gastritis, or gastric carcinoma. It is also effective in determining the reduction in acid output after operations for peptic ulcer, such as vagotomy or gastric resection. The exact mechanism by which pentagastrin stimulates gastric acid, pepsin, and intrinsic factor secretion is unknown; however, since pentagastrin is an analogue of natural gastrin, it is believed that it excites the oxyntic cells of the stomach to secrete to their maximum capacity. Pentagastrin stimulates pancreatic secretion, especially when administered in large intramuscular doses. Pentagastrin also increases gastrointestinal motility by a direct effect on the intestinal smooth muscle. However, it delays gastric emptying time probably by stimulation of terminal antral contractions, which enhance retropulsion.",The molecular weight is 767.9.,Pentagastrin has a topological polar surface area of 250.91.,The log p value of  is 1.72.,Pentagastrin is approved.,Pentagastrin is a solid.,True
14838,"A quaternary skeletal muscle relaxant usually used in the form of its bromide, chloride, or iodide. It is a depolarizing relaxant, acting in about 30 seconds and with a duration of effect averaging three to five minutes. Succinylcholine is used in surgical, anesthetic, and other procedures in which a brief period of muscle relaxation is called for. Used in surgical procedures where a rapid onset and brief duration of muscle relaxation is needed (includes intubation, endoscopies, and ECT) Succinylcholine is indicated as an adjunct to general anesthesia, to facilitate tracheal intubation, and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Succinylcholine is a depolarizing skeletal muscle relaxant. As does acetylcholine, it combines with the cholinergic receptors of the motor end plate to produce depolarization. This depolarization may be observed as fasciculations. Subsequent neuromuscular transmission is inhibited so long as adequate concentration of succinylcholine remains at the receptor site. Succinylcholine has no direct action on the uterus or other smooth muscle structures. The mechanism of action of Succinylcholine involves what appears to be a \persistent\"" depolarization of the neuromuscular junction. This depolarization is caused by Succinylcholine mimicking the effect of acetylcholine but without being rapidly hydrolysed by acetylcholinesterase. This depolarization leads to desensitization.""",The molecular weight is 290.4.,Succinylcholine has a topological polar surface area of 52.6.,The log p value of  is -6.87.,Succinylcholine is approved.,Succinylcholine is a solid.,True
14839,"A dopamine D2-receptor antagonist. It has been used therapeutically as an antidepressant, antipsychotic, and as a digestive aid. (From Merck Index, 11th ed) Sulpiride is indicated for the treatment of schizophrenia. Sulpiride is a substituted benzamide derivative and a selective dopamine D2 antagonist with antipsychotic and antidepressant activity. Other benzamide derivatives include metoclopramide, tiapride, and sultopride. In contrast to most other neuroleptics which block both dopamine D1 and D2 receptors, Sulpiride is more selective and acts primarily as a dopamine D2 antagonist. Sulpiride appears to lack effects on norepinephrine, acetylcholine, serotonin, histamine, or gamma-aminobutyric acid (GABA) receptors.",The molecular weight is 341.43.,Sulpiride has a topological polar surface area of 101.73.,The log p value of  is 1.11.,Sulpiride is approved and investigational.,Sulpiride is a solid.,True
14840,"Profenamine is a medication derived from phenothiazine. It is primarily used as an antidyskinetic to treat parkinsonism. It is sold under the trade names Parsidol in the United States and Parsidan in Canada. For use in the treatment of Parkinson's disease and also used to control severe reactions to certain medicines such as reserpine. Ethopropazine, a phenothiazine and antidyskinetic, is used in the treatment of Parkinson's disease. By improving muscle control and reducing stiffness, this drug permits more normal movements of the body as the disease symptoms are reduced. It is also used to control severe reactions to certain medicines such as reserpine, phenothiazines, chlorprothixene, thiothixene, loxapine, and haloperidol. Unlike other NMDA antagonists, ethopropazine &mdash; because of its anticholinergic action &mdash; is largely devoid of neurotoxic side effects. Ethopropazine also has a slight antihistaminic and local anesthetic effect. Ethopropazine's antiparkinson action can be attributed to its anticholinergic properties. Ethopropazine partially blocks central (striatal) cholinergic receptors, thereby helping to balance cholinergic and dopaminergic activity in the basal ganglia; salivation may be decreased, and smooth muscle may be relaxed. Drug-induced extrapyramidal symptoms and those due to parkinsonism may be relieved, but tardive dyskinesia is not alleviated and may be aggravated by anticholinergic effects. Ethopropazine's local anesthetic effect is due to its antagonism of the NMDA glutamate receptor. Glutamate is recognized as an important transmitter in nociceptive pathways, and the N-methyl-D-aspartate (NMDA) subtype of the glutamate receptor, in particular, has been implicated in the mediation of neuropathic pain. Excessive release of glutamate at NMDA receptors on dorsal horn neurons of the spinal cord results in hyperactivation and hypersensitivity of these receptors (perceived as hyperalgesia), thought to be an integral feature of neuropathic pain.",The molecular weight is 312.48.,Profenamine has a topological polar surface area of 6.48.,The log p value of  is 5.66.,Profenamine is approved.,Profenamine is a solid.,True
14841,"A phenothiazine used as an antipsychotic agent and as an antiemetic. Used mainly in the management of psychoses. Also used to control nausea and vomiting. Triflupromazine is a member of a class of drugs called phenthiazines, which are dopamine D1/D2 receptor antagonists. Phenothiazines are used to treat serious mental and emotional disorders, including schizophrenia and other psychotic disorders. It reduces anxiety, emotional withdrawal, hallucinations, disorganized thoughts, blunted mood, and suspiciousness. Triflupromazine is used particularly to control violent behavior during acute episodes of psychotic disorders. It can also be used to control severe nausea and vomiting, severe hiccups, and moderate to severe pain in some hospitalized patients. Triflupromazine acts on the central nervous system. Triflupromazine binds to the dopamine D1 and dopamine D2 receptors and inhibits their activity. The mechanism of the anti-emetic effect is due predominantly to blockage of the dopamine D2 neurotransmitter receptors in the chemoreceptor trigger zone (CTZ) and vomiting centre. Triflupromazine blocks the neurotransmitter dopamine and the vagus nerve in the gastrointestinal tract. Triflupromazine also binds the muscarinic acetylcholine receptors (M1 and M2) and the tryptamine D receptors (5HT<sub>2B</sub>).",The molecular weight is 352.42.,Triflupromazine has a topological polar surface area of 6.48.,The log p value of  is 5.81.,Triflupromazine is approved and vet_approved.,Triflupromazine is a solid.,True
14842,"A local anesthetic of the amide type now generally used for surface anesthesia. It is one of the most potent and toxic of the long-acting local anesthetics and its parenteral use is restricted to spinal anesthesia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1006) For production of local or regional anesthesia by infiltration techniques such as percutaneous injection and intravenous regional anesthesia by peripheral nerve block techniques such as brachial plexus and intercostal and by central neural techniques such as lumbar and caudal epidural blocks. Dibucaine is an amide-type local anesthetic, similar to lidocaine. Local anesthetics block both the initiation and conduction of nerve impulses by decreasing the neuronal membrane's permeability to sodium ions through sodium channel inhibition. This reversibly stabilizes the membrane and inhibits depolarization, resulting in the failure of a propagated action potential and subsequent conduction blockade.",The molecular weight is 343.47.,Cinchocaine has a topological polar surface area of 54.46.,The log p value of  is 5.35.,Cinchocaine is approved and vet_approved.,Cinchocaine is a solid.,True
14843,"A histamine H2 receptor antagonist with low toxicity that inhibits gastric acid secretion. The drug is used for the treatment of duodenal ulcers. For the treatment of acid-reflux disorders (GERD), peptic ulcer disease, active benign gastric ulcer, and active duodenal ulcer. Nizatidine is a competitive, reversible inhibitor of histamine at the histamine H2-receptors, particularly those in the gastric parietal cells. By inhibiting the action of histamine on stomach cells, nizatidine reduces stomach acid production. Nizatidine had no demonstrable antiandrogenic action. Full-dose therapy for the problems treated by nizatidine lasts no longer than 8 weeks. It has been demonstrated that treatment with a reduced dose of nizatidine is effective as maintenance therapy following healing of active duodenal ulcers. Nizatidine competes with histamine for binding at the H<sub>2</sub>-receptors on the gastric basolateral membrane of parietal cells. Competitive inhibition results in reduction of basal and nocturnal gastric acid secretions. The drug also decreases the gastric acid response to stimuli such as food, caffeine, insulin, betazole, or pentagastrin.",The molecular weight is 331.45.,Nizatidine has a topological polar surface area of 83.33.,The log p value of  is -0.16.,Nizatidine is approved.,Nizatidine is a solid.,True
14844,"An anthelmintic used primarily as the citrate in the treatment of filariasis, particularly infestations with Wucheria bancrofti or Loa loa. Used for the treatment of certain filarial diseases, including tropical pulmonary eosinophilia, loiasis, and lymphatic filariasis caused by infection with <i>Wuchereria bancrofti</i>, <i>Brugia malayi</i>, or <i>Brugia timori</i>. Diethylcarbamazine is an anthelmintic drug that does not resemble other antiparasitic compounds. It is a synthetic organic compound which is highly specific for several parasites and does not contain any toxic metallic elements.  The mechanism of action of diethylcarbamazine is thought to involve sensitizing the microfilariae to phagocytosis. One study showed that diethylcarbamazine's activity against <i>Brugia malayi</i> microfilariae is dependent on inducible nitric-oxide synthase and the cyclooxygenase pathway. It confirmed the important role of the arachidonic acid metabolic pathway in diethylcarbamazine's mechanism of action <i>in vivo</i> and showes that in addition to its effects on the 5-lipoxygenase pathway, it targets the cyclooxygenase pathway and COX-1.",The molecular weight is 199.3.,Diethylcarbamazine has a topological polar surface area of 26.79.,The log p value of  is 1.62.,Diethylcarbamazine is approved and investigational and vet_approved.,Diethylcarbamazine is a solid.,True
14845,"A local anesthetic of the ester type that has a slow onset and a short duration of action. It is mainly used for infiltration anesthesia, peripheral nerve block, and spinal block. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1016). Procaine has also been investigated as an oral entry inhibitor in treatment-experienced HIV patients. Used as a local anesthetic primarily in oral surgery Procaine is an anesthetic agent indicated for production of local or regional anesthesia, particularly for oral surgery. Procaine (like cocaine) has the advantage of constricting blood vessels which reduces bleeding, unlike other local anesthetics like lidocaine. Procaine is an ester anesthetic. It is metabolized in the plasma by the enzyme pseudocholinesterase through hydrolysis into para-aminobenzoic acid (PABA), which is then excreted by the kidneys into the urine. Procaine acts mainly by inhibiting sodium influx through voltage gated sodium channels in the neuronal cell membrane of peripheral nerves. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is thus inhibited. The receptor site is thought to be located at the cytoplasmic (inner) portion of the sodium channel. Procaine has also been shown to bind or antagonize the function of N-methyl-D-aspartate (NMDA) receptors as well as nicotinic acetylcholine receptors and the serotonin receptor-ion channel complex.",The molecular weight is 236.32.,Procaine has a topological polar surface area of 55.56.,The log p value of  is 2.54.,Procaine is approved and investigational and vet_approved.,Procaine is a solid.,True
14846,"Perindopril is a nonsulfhydryl prodrug that belongs to the angiotensin-converting enzyme (ACE) inhibitor class of medications. It is rapidly metabolized in the liver to perindoprilat, its active metabolite, following oral administration. Perindoprilat is a potent, competitive inhibitor of ACE, the enzyme responsible for the conversion of angiotensin I (ATI) to angiotensin II (ATII). ATII regulates blood pressure and is a key component of the renin-angiotensin-aldosterone system (RAAS). Perindopril may be used to treat mild to moderate essential hypertension, mild to moderate congestive heart failure, and to reduce the cardiovascular risk of individuals with hypertension or post-myocardial infarction and stable coronary disease. For the treatment of mild to moderate essential hypertension, mild to moderate congestive heart failure, and to reduce the cardiovascular risk of individuals with hypertension or post-myocardial infarction and stable coronary disease.  Perindopril is a nonsulfhydryl prodrug that is metabolized via first pass effect (62%) and systemic hydrolysis (38%) to perindoprilat, its active metabolite, following oral administration. Perindoprilat lowers blood pressure by antagonizing the effect of the RAAS. The RAAS is a homeostatic mechanism for regulating hemodynamics, water and electrolyte balance. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from the granular cells of the juxtaglomerular apparatus in the kidneys. In the blood stream, renin cleaves circulating angiotensinogen to ATI, which is subsequently cleaved to ATII by ACE. ATII increases blood pressure using a number of mechanisms. First, it stimulates the secretion of aldosterone from the adrenal cortex. Aldosterone travels to the distal convoluted tubule (DCT) and collecting tubule of nephrons where it increases sodium and water reabsorption by increasing the number of sodium channels and sodium-potassium ATPases on cell membranes. Second, ATII stimulates the secretion of vasopressin (also known as antidiuretic hormone or ADH) from the posterior pituitary gland. ADH stimulates further water reabsorption from the kidneys via insertion of aquaporin-2 channels on the apical surface of cells of the DCT and collecting tubules. Third, ATII increases blood pressure through direct arterial vasoconstriction. Stimulation of the Type 1 ATII receptor on vascular smooth muscle cells leads to a cascade of events resulting in myocyte contraction and vasoconstriction. In addition to these major effects, ATII induces the thirst response via stimulation of hypothalamic neurons. ACE inhibitors inhibit the rapid conversion of ATI to ATII and antagonize RAAS-induced increases in blood pressure. ACE (also known as kininase II) is also involved in the enzymatic deactivation of bradykinin, a vasodilator. Inhibiting the deactivation of bradykinin increases bradykinin levels and may sustain the effects of perindoprilat by causing increased vasodilation and decreased blood pressure. There are two isoforms of ACE: the somatic isoform, which exists as a glycoprotein comprised of a single polypeptide chain of 1277; and the testicular isoform, which has a lower molecular mass and is thought to play a role in sperm maturation and binding of sperm to the oviduct epithelium. Somatic ACE has two functionally active domains, N and C, which arise from tandem gene duplication. Although the two domains have high sequence similarity, they play distinct physiological roles. The C-domain is predominantly involved in blood pressure regulation while the N-domain plays a role in hematopoietic stem cell differentiation and proliferation. ACE inhibitors bind to and inhibit the activity of both domains, but have much greater affinity for and inhibitory activity against the C-domain. Perindoprilat, the active metabolite of perindopril, competes with ATI for binding to ACE and inhibits and enzymatic proteolysis of ATI to ATII. Decreasing ATII levels in the body decreases blood pressure by inhibiting the pressor effects of ATII as described in the Pharmacology section above. Perindopril also causes an increase in plasma renin activity likely due to a loss of feedback inhibition mediated by ATII on the release of renin and/or stimulation of reflex mechanisms via baroreceptors. ",The molecular weight is 368.47.,Perindopril has a topological polar surface area of 95.94.,The log p value of  is 1.21.,Perindopril is approved.,Perindopril is a solid.,True
14847,"Benzonatate is an oral antitussive drug used in the relief and suppression of cough in patients older than ten years of age. Currently, benzonatate is the only non-narcotic antitussive available as a prescription drug. It works to reduce the activity of cough reflex by desensitizing the tissues of the lungs and pleura involved in the cough reflex. Benzonatate was approved by the FDA in 1958 under the market name Tessalon Perles. Because its chemical structure resembles that of the anesthetic agents in the para-amino-benzoic acid class (such as and ), benzonatate exhibits anesthetic or numbing action. Although it not prone to drug misuse or abuse, benzonatate is associated with a risk for severe toxicity and overdose, especially in children. Benzonatate is indicated for the symptomatic relief of cough. Benzonatate suppresses cough associated with both acute and chronic respiratory conditions. Its works by desensitizing the pulmonary stretch receptors involved in the cough reflex. There are limited clinical trials of benzonatate; however, earlier studies demonstrated inhibition of experimentally-induced cough and subjectively-measured pathological cough by benzonatate. Benzonatate is a local anesthetic drug that acts peripherally by anesthetizing and reducing the activity of vagal stretch receptors or nerve fibres located in the respiratory passages, lungs, and pleura. Once the stretch receptors are stimulated, they send impulses to the cough centre located in the medulla via an afferent pathway consisting of sensory nerve fibres or the vagus nerve. The efferent signal is then generated that sends impulses to the expiratory muscles to produce a cough. Anesthetizing these receptors by benzonatate results in the inhibition of the cough reflex activity and cough production. Benzonatate also inhibits the transmission of impulses of the cough reflex in the vagal nuclei of the medulla. There are several proposed mechanisms of benzonatate; it is also a potent voltage-gated sodium channel inhibitor.",,,,Benzonatate is approved.,Benzonatate is a liquid.,True
14848,"A selective beta-2 adrenergic agonist used as a bronchodilator and tocolytic. For the prevention and reversal of bronchospasm in patients 12 years of age and older with reversible, obstructive airway disease, as well as symptomatic management of reversible bronchospasm associated with bronchitis and emphysema. Also used acute IV and sub-Q therapy in selected women to inhibit uterine contractions in preterm labor (tocolysis) and prolong gestation when beneficial. Terbutaline is a relatively selective beta2-adrenergic bronchodilator that has little or no effect on alpha-adrenergic receptors. The drug has exerts a preferential effect on beta2-adrenergic receptors but stimulates beta-adrenergic receptors less selectively than relatively selective beta2-agonists. Terbutaline appears to have a greater stimulating effect on beta-receptors of the bronchial, vascular, and uterine smooth muscles (beta2 receptors) than on the beta-receptors of the heart (beta1 receptors). This drug relaxes smooth muscle and inhibits uterine contractions, but may also cause some cardiostimulatory effects and CNS stimulation. The pharmacologic effects of terbutaline are at least in part attributable to stimulation through beta-adrenergic receptors of intracellular adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic- 3',5'- adenosine monophosphate (c-AMP). Increased c-AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells.",The molecular weight is 225.29.,Terbutaline has a topological polar surface area of 72.72.,The log p value of  is 0.48.,Terbutaline is approved.,Terbutaline is a solid.,True
14849,"A vesicant and necrotizing irritant destructive to mucous membranes, mechlorethamine is an alkylating drug. It was formerly used as a war gas. The hydrochloride is used as an antineoplastic in Hodgkin's disease and lymphomas. It causes severe gastrointestinal and bone marrow damage. For the palliative treatment of Hodgkin's disease (Stages III and IV), lymphosarcoma, chronic myelocytic or chronic lymphocytic leukemia, polycythemia vera, mycosis fungoides, and bronchogenic carcinoma. Also for the palliative treatment of metastatic carcinoma resulting in effusion. Mechlorethamine also known as mustine, nitrogen mustard, and HN2, is the prototype anticancer chemotherapeutic drug. Successful clinical use of mechlorethamine gave birth to the field of anticancer chemotherapy. The drug is an analogue of mustard gas and was derived from toxic gas warfare research. Mechlorethamine is a nitrogen mustard alkylating agent. Alkylating agents work by three different mechanisms all of which achieve the same end result - disruption of DNA function and cell death. Alkylating agents work by three different mechanisms: 1) attachment of alkyl groups to DNA bases, resulting in the DNA being fragmented by repair enzymes in their attempts to replace the alkylated bases, preventing DNA synthesis and RNA transcription from the affected DNA, 2) DNA damage via the formation of cross-links (bonds between atoms in the DNA) which prevents DNA from being separated for synthesis or transcription, and 3) the induction of mispairing of the nucleotides leading to mutations. Mechlorethamine is cell cycle phase-nonspecific.",The molecular weight is 156.05.,Mechlorethamine has a topological polar surface area of 3.24.,The log p value of  is 1.2.,Mechlorethamine is approved and investigational.,Mechlorethamine is a solid.,True
14850,"Oxybuprocaine (also known as Benoxinate) is a local anesthetic, which is used especially in ophthalmology and otolaryngology. Oxybuprocaine binds to sodium channels and reversibly stabilizes the neuronal membrane which decreases its permeability to sodium ions. Used to temporarily numb the front surface of the eye so that the eye pressure can be measured or a foreign body removed. Oxybuprocaine is a local anaesthetic. It may be less irritating than tetracaine, and the onset and duration of action are similar to tetracaine. Oxybuprocaine binds to sodium channel and reversibly stabilizes the neuronal membrane which decreases its permeability to sodium ions. Depolarization of the neuronal membrane is inhibited thereby blocking the initiation and conduction of nerve impulses.",The molecular weight is 308.42.,Oxybuprocaine has a topological polar surface area of 64.79.,The log p value of  is 4.36.,Oxybuprocaine is approved and investigational.,Oxybuprocaine is a solid.,True
14851,"A parasympatholytic anticholinergic used solely to obtain mydriasis or cycloplegia. Used mainly to produce mydriasis and cycloplegia for diagnostic purposes. Cyclopentolate is an anti-muscarinic in the same class as atropine and scopolamine. Cyclopentolate blocks the receptors in the muscles of the eye (muscarinic receptors). These receptors are involved controlling the pupil size and the shape of the lens. Cyclopentolate thus induces relaxation of the sphincter of the iris and the ciliary muscles. When applied topically to the eyes, it causes a rapid, intense cycloplegic and mydriatic effect that is maximal in 15 to 60 minutes; recovery usually occurs within 24 hours. The cycloplegic and mydriatic effects are slower in onset and longer in duration in patients who have dark pigmented irises. By blocking muscarinic receptors, cyclopentolate produces dilatation of the pupil (mydriasis) and prevents the eye from accommodating for near vision (cycloplegia).",The molecular weight is 291.39.,Cyclopentolate has a topological polar surface area of 49.77.,The log p value of  is 2.69.,Cyclopentolate is approved.,Cyclopentolate is a solid.,True
14852,"A derivative of procaine with less CNS action. For the treatment of life-threatening ventricular arrhythmias. Procainamide is an agent indicated for production of local or regional anesthesia and in the treatment of ventricular tachycardia occurring during cardiac manipulation, such as surgery or catheterization, or which may occur during acute myocardial infarction, digitalis toxicity, or other cardiac diseases. The mode of action of the antiarrhythmic effect of Procainamide appears to be similar to that of procaine and quinidine. Ventricular excitability is depressed and the stimulation threshold of the ventricle is increased during diastole. The sinoatrial node is, however, unaffected. Procainamide is sodium channel blocker. It stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses thereby effecting local anesthetic action.",The molecular weight is 235.33.,Procainamide has a topological polar surface area of 58.36.,The log p value of  is 1.42.,Procainamide is approved.,Procainamide is a solid.,True
14853,"A nicotinic antagonist that has been used as a ganglionic blocker in hypertension, as an adjunct to anesthesia, and to induce hypotension during surgery. For the controlled reduction of blood pressure during surgery and in the treatment of hypertensive emergencies. Trimethaphan is indicated for production of controlled hypotension during surgery to reduce bleeding into the surgical field and also for rapid reduction of blood pressure in the treatment of hypertensive emergencies, especially in patients with acute dissecting aneurysm, and in the emergency treatment of pulmonary edema in patients with pulmonary hypertension associated with systemic hypertension. Trimethaphan is a ganglionic blocking agent prevents stimulation of postsynaptic receptors by competing with acetylcholine for these receptor sites. Additional effects may include direct peripheral vasodilation and release of histamine. Trimethaphan's hypotensive effect is due to reduction in sympathetic tone and vasodilation, and is primarily postural.",The molecular weight is 365.51.,Trimethaphan has a topological polar surface area of 23.55.,The log p value of  is 4.3.,Trimethaphan is approved and investigational.,Trimethaphan is a solid.,True
14854,"Ambenonium is a cholinesterase inhibitor. It is used in the management of myasthenia gravis. Ambenonium is used to treat muscle weakness due to muscle disease (myasthenia gravis). Ambenonium, similar to pyridostigmine and neostigmine, is used for the treatment of muscle weakness and fatigue in people with myasthenia gravis. It is postulated to exert its therapeutic effect by enhancing cholinergic function through the inhibition of the acetylcholine hydrolysis by acetylcholinesterase. Increased levels of acetylcholine has peripheral effects, as acetylcholine is also used in the brain, where it tends to cause excitatory actions. The glands that receive impulses from the parasympathetic part of the autonomic nervous system are also stimulated in the same way. This is why an increase in acetylcholine causes a decreased heart rate and increased production of saliva. Ambenonium is used less commonly than neostigmine or pyridostigmine but may be preferred in patients hypersensitive to the bromide ion. Ambenonium produces fewer muscarinic side effects than neostigmine, but more than pyridostigmine. Ambenonium exerts its actions against myasthenia gravis by competitive, reversible inhibition of acetylcholinesterase. The disease myasthenia gravis occurs when the body inappropriately produces antibodies against acetylcholine receptors, and thus inhibits proper acetylcholine signal transmission (when acetylcholine binds to acetylcholine receptors of striated muscle fibers, it stimulates those fibers to contract). Ambenonium reversibly binds acetylcholinesterase at the anionic site, which results in the blockage of the site of acetycholine binding, thereby inhibiting acetylcholine hydrolysis and enhancing cholinergic function through the accumulation of acetycholine at cholinergic synpases. Elevated acetylcholine levels lead to facilitates transmission of impulses across the myoneural junction. ",The molecular weight is 537.57.,Ambenonium has a topological polar surface area of 58.2.,The log p value of  is 0.18.,Ambenonium is approved.,Ambenonium is a solid.,True
14855,"Doxacurium chloride is a long-acting, nondepolarizing skeletal muscle relaxant for intravenous administration. Used to provide skeletal muscle relaxation as an adjunct to general anesthesia, for endotracheal intubation or to facilitate mechanical ventilation. Doxacurium chloride is a long-acting, nondepolarizing skeletal muscle relaxant. The neuromuscular block produced by doxacurium chloride may be antagonized by anticholinesterase agents. As with other nondepolarizing neuromuscular blocking agents, the more profound the neuromuscular block at reversal, the longer the time and the greater the dose of anticholinesterase required for recovery of neuromuscular function. Doxacurium chloride is approximately 2.5 to 3 times more potent than pancuronium and 10 to 12 times more potent than metocurine. Doxacurium chloride binds competitively to cholinergic receptors on the motor end-plate to antagonize the action of acetylcholine, resulting in a block of neuromuscular transmission (non-depolarizing). This action is antagonized by acetylcholinesterase inhibitors, such as neostigmine.",,,,Doxacurium is approved.,Doxacurium is a solid.,True
14856,"Chloroprocaine hydrochloride is a local anesthetic given by injection during surgical procedures and labor and delivery. Chloroprocaine, like other local anesthetics, blocks the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse and by reducing the rate of rise of the action potential. For the production of local anesthesia by infiltration and peripheral nerve block. They are not to be used for lumbar or caudal epidural anesthesia. Chloroprocaine is an ester type anesthetic agent indicated for production of local or regional anesthesia, particularly for oral surgery. Chloroprocaine (like cocaine) has the advantage of constricting blood vessels which reduces bleeding, unlike other local anesthetics like lidocaine. Chloroprocaine acts mainly by inhibiting sodium influx through voltage gated sodium channels in the neuronal cell membrane of peripheral nerves. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is thus inhibited. The receptor site is thought to be located at the cytoplasmic (inner) portion of the sodium channel. It is hypothesized that Chloroprocaine binds or antagonizes the function of N-methyl-D-aspartate (NMDA) receptors as well as nicotinic acetylcholine receptors and the serotonin receptor-ion channel complex.",The molecular weight is 270.76.,Chloroprocaine has a topological polar surface area of 55.56.,The log p value of  is 2.91.,Chloroprocaine is approved.,Chloroprocaine is a solid.,True
14857,"Tubocurarine is a non-depolarizing neuromuscular blocking agent and the first identified curare alkaloid. Curare is one of the names used to describe plant-derived poisons used by indigenous South Americans to coat the tips of hunting arrows and darts, which were typically derived from plants of the genera _Chondrodendron_ and _Strychnos_. Tubocurarine is a benzylisoquinoline derivative and shares this structural backbone with a number of plant-derived alkaloids, including and. It was first isolated by Harold King in 1935 and was used clinically to induce neuromuscular blockade during surgeries, particularly those involving the abdomen. Tubocurarine's clinical use was limited by its relatively long duration of action (30-60 minutes) and a number of significant side effects. Safer and more pharmacokinetically favorable non-depolarizing neuromuscular blockers, such as , have largely replaced the use of tubocurarine in the clinical setting. Tubocurarine exerts its neuromuscular blocking effects via inhibition of acetylcholine (ACh) activity. It exerts a sort of reversible competitive antagonistic effect at post-synaptic nicotinic receptors, reducing the probability of activation via ACh by repeatedly associating and dissociating from these receptors - in doing so, tubocurarine prevents depolarization of the affected nerves. This mechanism distinguishes tubocurarine and similars from other neuromuscular blocking agents and is the reason they are referred to as \non-depolarizing neuromuscular blockers\"".""",,,,Tubocurarine is approved.,Tubocurarine is a solid.,True
14858,"Decamethonium is used in anesthesia to cause paralysis. It is a short acting depolarizing muscle relaxant. It is similar to acetylcholine and acts as a partial agonist of the nicotinic acetylcholine receptor. For use as a skeletal muscle relaxant Decamethonium acts as a depolarizing muscle relaxant or neuromuscular blocking agent. It acts as an agonist of nicotinic acetycholine receptors in the motor endplate and causes depolarization. This class of drugs has its effect at the neuromuscular junction by preventing the effects of acetylcholine. Normally, when a nerve stimulus acts to contract a muscle, it releases acetylcholine. The binding of this acetylcholine to receptors causes the muscle to contract. Muscle relaxants play an important role in anesthesia even though they don't provide any pain relief or produce unconsciousness. Binds to the nicotinic acetycholine receptors (by virtue of its similarity to acetylcholine) in the motor endplate and blocks access to the receptors. In the process of binding, the receptor is actually activated - causing a process known as depolarization. Since it is not degraded in the neuromuscular junction, the depolarized membrance remains depolarized and unresponsive to any other impulse, causing muscle paralysis.",The molecular weight is 258.49.,,The log p value of  is -6.97.,Decamethonium is approved.,Decamethonium is a solid.,True
14859,"A bis-quaternary steroid that is a competitive nicotinic antagonist. As a neuromuscular blocking agent it is more potent than curare but has less effect on the circulatory system and on histamine release. Used as a muscle relaxant during anesthesia and surgical procedures. Pancuronium is a non-depolarising muscle relaxant similar to curare. It acts as a competitive acetylcholine antagonist on neuromuscular junctions, displacing acetylcholine (hence competitive) from its post-synaptic nicotinic acetylcholine receptors. It is, unlike suxamethonium, a non-depolarising agent, which means, that it causes no spontaneous depolarisations upon association with the nicotinic receptor in neuromuscular junction, thus producing no muscle fasciculations upon administration. Pancuronium has no hormonal activity. It exerts slight vagolytic activity (i.e. diminishing activity of the vagus nerve) and no ganglioplegic (i.e., blocking ganglions) activity. Nondepolarizing neuromuscular blocking agents inhibit neuromuscular transmission by competing with acetylcholine for the cholinergic receptors of the motor end plate, thereby reducing the response of the end plate to acetylcholine. This type of neuromuscular block is usually antagonized by anticholinesterase agents.",,,,Pancuronium is approved.,Pancuronium is a solid.,True
14860,"Pipecuronium is a piperazinyl androstane derivative which is a non-depolarizing neuromuscular blocking agent. Used as a muscle relaxant during anesthesia and surgical procedures. Pipecuronium is a nondepolarizing neuromuscular blocking agent. Neuromuscular blocking agents produce skeletal muscle paralysis by blocking neural transmission at the myoneural junction. The paralysis is selective initially and usually appears in the following muscles consecutively: levator muscles of eyelids, muscles of mastication, limb muscles, abdominal muscles, muscles of the glottis, and finally, the intercostal muscles and the diaphragm. Neuromuscular blocking agents have no clinically significant effect on consciousness or the pain threshold.  Nondepolarizing neuromuscular blocking agents inhibit neuromuscular transmission by competing with acetylcholine for the cholinergic receptors of the motor end plate, thereby reducing the response of the end plate to acetylcholine. This type of neuromuscular block is usually antagonized by anticholinesterase agents.",The molecular weight is 602.9.,Pipecuronium has a topological polar surface area of 59.08.,The log p value of  is 0.63.,Pipecuronium is approved.,Pipecuronium is a solid.,True
14861,"A cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike physostigmine, does not cross the blood-brain barrier. Neostigmine is used for the symptomatic treatment of myasthenia gravis by improving muscle tone. Neostigmine is a cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike physostigmine, does not cross the blood-brain barrier. By inhibiting acetylcholinesterase, more acetylcholine is available in the synapse, therefore, more of it can bind to the fewer receptors present in myasthenia gravis and can better trigger muscular contraction. Neostigmine is a parasympathomimetic, specifically, a reversible cholinesterase inhibitor. The drug inhibits acetylcholinesterase which is responsible for the degredation of acetylcholine. So, with acetylcholinesterase inhibited, more acetylcholine is present By interfering with the breakdown of acetylcholine, neostigmine indirectly stimulates both nicotinic and muscarinic receptors which are involved in muscle contraction.. It does not cross the blood-brain barrier.",The molecular weight is 223.3.,Neostigmine has a topological polar surface area of 29.54.,The log p value of  is -2.81.,Neostigmine is approved and vet_approved.,Neostigmine is a solid.,True
14862,"Bambuterol is a long acting beta-adrenoceptor agonist used in the treatment of asthma. It is a prodrug of terbutaline. For the prevention and reversal of bronchospasm in patients 12 years of age and older with asthma and reversible bronchospasm associated with bronchitis and emphysema. Bambuterol is a long acting beta2-adrenoceptor agonist used in the treatment of asthma. It is a prodrug of terbutaline. Bambuterol causes smooth muscle relaxation, resulting in dilation of bronchial passages. The pharmacologic effects of bambuterol are at least in part attributable to stimulation through beta-adrenergic receptors (beta 2 receptors) of intracellular adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic AMP. Increased cyclic AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells.",The molecular weight is 367.45.,Bambuterol has a topological polar surface area of 91.34.,The log p value of  is 0.56.,Bambuterol is investigational.,Bambuterol is a solid.,True
14863,,,,,Methylphosphinic Acid is experimental.,Methylphosphinic Acid is a solid.,False
14864,"A four carbon acid, CH3CH2CH2COOH, with an unpleasant odor that occurs in butter and animal fat as the glycerol ester.",,,,Butyric Acid is experimental and investigational.,Butyric Acid is a solid.,True
14865,,,,,Ethyl dihydrogen phosphate is experimental.,Ethyl dihydrogen phosphate is a solid.,False
14866,,,,,Phosphorylisopropane is experimental.,Phosphorylisopropane is a solid.,False
14867,A sulfur-containing analog of butyrylcholine which is hydrolyzed by butyrylcholinesterase to butyrate and thiocholine. It is used as a reagent in the determination of butyrylcholinesterase activity. ,,,,Butyrylthiocholine is experimental.,Butyrylthiocholine is a solid.,True
14868,"N,N'N'-triethylenethiophosphoramide (ThioTEPA) is a cancer chemotherapeutic member of the alkylating agent group, now in use for over 50 years. It is a stable derivative of N,N',N''- triethylenephosphoramide (TEPA). It is mostly used to treat breast cancer, ovarian cancer and bladder cancer. It is also used as conditioning for Bone marrow transplantation. Its main toxicity is myelosuppression. ThioTEPA is used a as conditioning treatment prior to allogeneic or autologous haematopoietic progenitor cell transplantation (HPCT) in haematological diseases in adult and paediatric patients. Also, when high dose chemotherapy with HPCT support it is appropriate for the treatment of solid tumours in adult and paediatric patients. The unstable nitrogen-carbon groups alkylate with DNA causing irrepairable DNA damage. They stop tumor growth by crosslinking guanine nucleobases in DNA double-helix strands, directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. These drugs act nonspecifically. The alkyl group is attached to the guanine base of DNA, at the number 7 nitrogen atom of the imidazole ring. They stop tumor growth by crosslinking guanine nucleobases in DNA double-helix strands, directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. These drugs act nonspecifically.",The molecular weight is 189.22.,Thiotepa has a topological polar surface area of 9.03.,The log p value of  is 0.52.,Thiotepa is approved and investigational.,Thiotepa is a solid.,True
14869,"Clevidipine is a dihydropyridine L-type calcium channel blocker that is selective for vascular smooth muscle and is indicated for blood pressure reduction when oral therapy is not an option. For the reduction of blood pressure when when oral antihypertensive therapy is not feasible or not desirable. Clevidipine belongs to a well-known class of drugs called dihydropyridine calcium channel antagonists. Clevidpine is the first third generation intravenous dihydropyridine calcium channel blocker. In vitro studies demonstrated that clevidipine acts by selectively relaxing the smooth muscle cells that line small arteries, resulting in arterial dilation, widening of the artery opening, and without reducing central venous pressure or reducing cardiac output. Possibly by deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum, clevidipine inhibits the influx of extracellular calcium across both the myocardial and vascular smooth muscle cell membranes. The resultant inhibition of the contractile processes of the myocardial smooth muscle cells leads to dilation of the coronary and systemic arteries and improved oxygen delivery to the myocardial tissue.",The molecular weight is 456.32.,Clevidipine has a topological polar surface area of 90.93.,The log p value of  is 5.53.,Clevidipine is approved and investigational.,Clevidipine is a solid.,True
14870,"Regramostim (GM-CSF) is a differentially glycosylated factor produced mainly by activated T cells and macrophages. Endothelial cells and fibroblasts can also produce GM-CSF after exposure to TNF-α, IL-1, IL-2 and IFN-γ. GM-CSF is found associated with extracellular matrix and in membrane-bound formats too. GM-CSF stimulates proliferation, activation and differentiation of macrophages and granulocytes and their progenitors. Investigated for use/treatment in adverse effects (chemotherapy) and bone marrow transplant. This drug activates mononuclear phagocytes, promotes migration of epithelial cells, and further regulates cytokine production. In 2 recent placebo-controlled studies involving venous leg ulceration, subcutaneous perilesional injections of recombinant human granulocyte-macrophage colony-stimulating factor were found to be significantly better than placebo in the time to complete wound healing. In other studies, recombinant human granulocyte-macrophage colony-stimulating factor was administered topically to wounds. Several case reports have also demonstrated the use of recombinant human granulocyte-macrophage colony-stimulating factor for postsurgical wounds, chronic leg ulcers of sickle cell anemia patients, and refract and refractory pyoderma gangrenosum. ",,,,Regramostim is investigational.,Regramostim is a solid.,True
14871,"Aprotinin is a protein-based drug that is also known as bovine pancreatic trypsin inhibitor (BPTI). Since it demonstrates the capacity to slow fibrinolysis, it has been employed to reduce bleeding during complex surgery such as heart and liver surgery. For this use, it is typically administered by injection. The goal of using of aprotinin was subsequently to minimize end-organ damage resulting from hypotension due to blood loss in surgery and to reduce the necessity for blood transfusions during surgery. Nevertheless, the drug was formally withdrawn worldwide in May of 2008 after studies confirmed that its use enhanced the risk of complications or death. The substance is consequently made available only for very restricted research use. For prophylactic use to reduce perioperative blood loss and the need for blood transfusion in patients undergoing cardiopulmonary bypass in the course of coronary artery bypass graft surgery who are at an increased risk for blood loss and blood transfusion. Aprotinin is a broad spectrum protease inhibitor which modulates the systemic inflammatory response (SIR) associated with cardiopulmonary bypass (CPB) surgery. SIR results in the interrelated activation of the hemostatic, fibrinolytic, cellular and humoral inflammatory systems. Aprotinin, through its inhibition of multiple mediators results in the attenuation of inflammatory responses, fibrinolysis, and thrombin generation. Aprotinin inhibits pro-inflammatory cytokine release and maintains glycoprotein homeostasis. In platelets, aprotinin reduces glycoprotein loss (e.g., GpIb, GpIIb/IIIa), while in granulocytes it prevents the expression of pro-inflammatory adhesive glycoproteins (e.g., CD11b). The effects of aprotinin use in CPB involves a reduction in inflammatory response which translates into a decreased need for allogeneic blood transfusions, reduced bleeding, and decreased mediastinal re-exploration for bleeding. Aprotinin inhibits serine proteases including trypsin, chymotrypsin and plasmin at a concentration of about 125,000 IU/mL, and kallikrein at 300,000 IU/mL. The inhibition of kallikrein inhibits formation of factor XIIa. This inhibits the intrinsic pathway of coagulation and fibrinolysis. Inhibition of plasmin also slows fibrinolysis.",The molecular weight is 6511.51.,Aprotinin has a topological polar surface area of 2645.74.,,Aprotinin is approved and investigational and withdrawn.,Aprotinin is a liquid.,True
14872,"Betaine is a methyl group donor that functions in the normal metabolic cycle of methionine and reduces homocystinuria in patients with inborn errors of methionine metabolism. In the United States, betaine is distributed under the brand name Cystadane® by Rare Disease Therapeutics. Many reports have shown that betaine's therapeutic effectiveness is limited, and does not lower tHcy levels or prevent clinical symptoms. Betaine is indicated for the treatment of homocystinuria to decrease elevated homocysteine blood levels. Included within the category of homocystinuria are deficiencies or defects in: 1. cystathionine beta-synthase (CBS), 2. 5,10-methylenetetrahydrofolate reductase (MTHFR), 3. cobalamin cofactor metabolism (cbl).  Betaine acts as a methyl group donor in the remethylation of homocysteine to methionine in patients with homocystinuria. ",,,,Glycine betaine is approved and nutraceutical.,Glycine betaine is a solid.,True
14873,"Aclidinium is an anticholinergic for the long-term management of chronic obstructive pulmonary disease (COPD). It has a much higher propensity to bind to muscarinic receptors than nicotinic receptors. FDA approved on July 24, 2012. Aclidinium bromide inhalation powder is indicated for the long-term, maintenance treatment of bronchospasm associated with chronic obstructive pulmonary disease (COPD), including chronic bronchitis and emphysema. Aclidinium does not prolong the QTc interval or have significant effects on cardiac rhythm.  Aclidinium is a long-acting, competitive, and reversible anticholinergic drug that is specific for the acetylcholine muscarinic receptors. It binds to all 5 muscarinic receptor subtypes to a similar affinity. Aclidinium's effects on the airways are mediated through the M3 receptor at the smooth muscle to cause bronchodilation. Prevention of acetylcholine-induced bronchoconstriction effects was dose-dependent and lasted longer than 24 hours.",,,,Aclidinium is approved.,Aclidinium is a solid.,True
14874,"Moxisylyte, denominated as thymoxamine in the UK, is a specific and orally active α1-adrenergic antagonist. According to the WHO, moxisylyte is approved since 1987 and in the same year, it acquired the denomination of orphan product by the FDA. This drug was developed by the Japanese company Fujirebio and also by the American company Iolab in the late 80s. By the WHO, moxisylyte is indicated for the symptomatic management of sequelae of cerebral infarction or hemorrhage. The cerebral infarction is characterized by the blockage of the artery either by the formation of a thrombus or an embolus.  Administration of moxisylyte has shown to improve peripheral flow in occlusive arterial disease with little effect in blood pressure. There are reports of increases in cutaneous blood flow and skin temperature after local application of moxisylyte. Moxisylyte is vasodilator that works as a specific alpha-adrenergic blocking agent. Its action is known to be competitive against norepinephrine without beta-receptor blocking, anti-angiotensin or anti-serotonin activity.",The molecular weight is 279.38.,Moxisylyte has a topological polar surface area of 38.77.,The log p value of  is 3.2.,Moxisylyte is approved and investigational.,Moxisylyte is a solid.,True
14875,Toxic alkylating agent used in industry; also as antineoplastic and research tool to produce chromosome aberrations and cancers.,The molecular weight is 204.24.,Tretamine has a topological polar surface area of 47.7.,The log p value of  is -1.35.,Tretamine is experimental.,Tretamine is a solid.,True
14876,"Miltefosine is a broad spectrum antimicrobial, anti-leishmanial, phospholipid drug that was originally developed in the 1980s as an anti-cancer agent. It is currently the only recognized oral agent used to treat visceral, cutaneous, and mucosal forms of leishmaniasis, a neglected tropical disease. It can be administered topically or orally and is only indicated in patients aged 12 years or older. The CDC has also recommended it as a first line treatment for free-living amebae (FLA) infections such as primary amebic meningoencephalitis and granulomatous amebic encephalitis. For the treatment of mucosal (caused by Leishmania braziliensis), cutaneous (caused by L. braziliensis, L. guyanensis, and L. panamensis), and visceral leishmaniasis (caused by L. donovani). In comparing Leishmania drug susceptibility, it has been found that L. donovani is the most susceptible to miltefosine while L. major is the least susceptible. Off-label use includes treatment of free-living amebae (FLA) infections (unlabeled use; CDC, 2013).  Little is known about the clinical pharmacodynamics of miltefosine and other antileishmanial drugs.  Miltefosine has demonstrated activity against Leishmania parasites and neoplastic cells primarily due to its effects on apoptosis and disturbance of lipid-dependent cell signalling pathways. Several potential antileishmanial mechanisms of action have been proposed, however no mechanism has been identified definitely. Within the mitochondria, miltefosine inhibits cytochrome-c oxidase leading to mitochondrial dysfunction and apoptosis-like cell death. Antineoplastic mechanisms of action are related to antileishmanial targets and include inhibition of phosphatidylcholine biosynthesis and inhibition of Akt (also known as protein kinase B), which is a crucial protein within the PI3K/Akt/mTOR intracellular signalling pathway involved in regulating the cell cycle. Animal studies also suggest it may be effective against Trypanosome cruzi (the organism responsible for Chagas' disease), metronidazole-resistant strains of Trichonomas vaginalis, and it may have broad-spectrum anti-fungal activity. ",The molecular weight is 407.58.,Miltefosine has a topological polar surface area of 58.59.,The log p value of  is -2.38.,Miltefosine is approved and investigational.,Miltefosine is a solid.,True
14877,"A tripeptide with many roles in cells. It conjugates to drugs to make them more soluble for excretion, is a cofactor for some enzymes, is involved in protein disulfide bond rearrangement and reduces peroxides. For nutritional supplementation, also for treating dietary shortage or imbalance Glutathione (GSH) participates in leukotriene synthesis and is a cofactor for the enzyme glutathione peroxidase. It also plays a role in the hepatic biotransformation and detoxification process; it acts as a hydrophilic molecule that is added to other lipophilic toxins or wastes prior to entering biliary excretion. It participates in the detoxification of methylglyoxal, a toxic by-product of metabolism, mediated by glyoxalase enzymes. Glyoxalase I catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II catalyzes the conversion of S-D-Lactoyl Glutathione to Reduced Glutathione and D-lactate. Glyoxalase I catalyzes the conversion of methylglyoxal and reduced glutathione to S-D-Lactoyl-glutathione. Glyoxalase II catalyzes the conversion of S-D-Lactoyl Glutathione to Reduced Glutathione and D-lactate. GSH is a cofactor of conjugation and reduction reactions that are catalyzed by glutathione S-transferase enzymes expressed in the cytosol, microsomes, and mitochondria. However, it is capable of participating in non-enzymatic conjugation with some chemicals, as it is hypothesized to do to a significant extent with n-acetyl-p-benzoquinone imine (NAPQI), the reactive cytochrome P450 reactive metabolite formed by toxic overdose of acetaminophen. Glutathione in this capacity binds to NAPQI as a suicide substrate and in the process detoxifies it, taking the place of cellular protein sulfhydryl groups which would otherwise be toxically adducted. The preferred medical treatment to an overdose of this nature, whose efficacy has been consistently supported in literature, is the administration (usually in atomized form) of N-acetylcysteine, which is used by cells to replace spent GSSG and allow a usable GSH pool.",The molecular weight is 307.32.,Glutathione has a topological polar surface area of 158.82.,The log p value of  is -3.05.,Glutathione is approved and investigational and nutraceutical.,Glutathione is a solid.,True
14878,"Cidofovir is an injectable antiviral medication employed in the treatment of cytomegalovirus (CMV) retinitis in patients diagnosed with AIDS. It suppresses CMV replication through selective inhibition of viral DNA synthesis. It was manufactured by _Gilead_ and initially approved by the FDA in 1996, but has since been discontinued. For the treatment of CMV retinitis in patients with acquired immunodeficiency syndrome (AIDS) Cidofovir is a new anti-viral drug. It is classified as a nucleotide analogue and is active against herpes cytomegalovirus (CMV) retinitis infection. Most adults are infected with CMV. Cidofovir suppresses cytomegalovirus (CMV) replication by selective inhibition of viral DNA synthesis.  Cidofovir acts through the selective inhibition of viral DNA polymerase.Biochemical data support selective inhibition of CMV DNA polymerase by cidofovir diphosphate, the active intracellular metabolite of cidofovir. Cidofovir diphosphate inhibits herpesvirus polymerases at concentrations that are 8- to 600-fold lower than those needed to inhibit human cellular DNA polymerase alpha, beta, and gamma(1,2,3). Incorporation of cidofovir into the growing viral DNA chain results in reductions in the rate of viral DNA synthesis.",The molecular weight is 279.19.,Cidofovir has a topological polar surface area of 145.68.,The log p value of  is -2.39.,Cidofovir is approved.,Cidofovir is a solid.,True
14879,"A synthetic purine nucleoside analogue with potential antineoplastic activity. Investigated for use/treatment in colorectal cancer, lung cancer, leukemia (unspecified), and gastric cancer. Phosphorylated by cellular kinases, tezacitabine is converted into its active diphosphate and triphosphate metabolites. Tezacitabine diphosphate binds to and irreversibly inhibits the activity of the enzyme ribonucleotide reductase (RNR), which may result in the inhibition of DNA synthesis in tumor cells and tumor cell apoptosis. Tezacitabine triphosphate acts as a substrate for DNA polymerase, further compromising DNA replication. This agent is relatively resistant to metabolic deactivation by cytidine deaminase. RNR catalyzes the conversion of ribonucleoside 5'-diphosphates to deoxyribonucleoside 5'-diphosphates necessary for DNA synthesis and is overexpressed in many tumor types.",,,,Tezacitabine is investigational.,Tezacitabine is a solid.,True
14880,"Nicotine is highly toxic alkaloid. It is the prototypical agonist at nicotinic cholinergic receptors where it dramatically stimulates neurons and ultimately blocks synaptic transmission. Nicotine is also important medically because of its presence in tobacco smoke. For the relief of nicotine withdrawal symptoms and as an aid to smoking cessation. Nicotine, the primary alkaloid in tobacco products binds stereo-selectively to nicotinic-cholinergic receptors on autonomic ganglia, the adrenal medulla, neuromuscular junctions and in the brain. Nicotine exerts two effects, a stimulant effect exerted at the locus ceruleus and a reward effect in the limbic system. Itranvenous administration of nicotine causes release of acetylcholine, norepinephrine, dopamine, serotonine, vasopressin, beta-endorphin and ACTH. Nicotine is a highly addictive substance. Nicotine also induces peripheral vasoconstriction, tachycardia and elevated blood pressure. Nicotine inhalers and patches are used to treat smoking withdrawl syndrome. Nicotine is classified as a stimulant of autonomic ganglia. Nicotine is a stimulant drug that acts as an agonist at nicotinic acetylcholine receptors. These are ionotropic receptors composed up of five homomeric or heteromeric subunits. In the brain, nicotine binds to nicotinic acetylcholine receptors on dopaminergic neurons in the cortico-limbic pathways. This causes the channel to open and allow conductance of multiple cations including sodium, calcium, and potassium. This leads to depolarization, which activates voltage-gated calcium channels and allows more calcium to enter the axon terminal. Calcium stimulates vesicle trafficking towards the plasma membrane and the release of dopamine into the synapse. Dopamine binding to its receptors is responsible the euphoric and addictive properties of nicotine.",The molecular weight is 162.24.,Nicotine has a topological polar surface area of 16.13.,The log p value of  is 0.88.,Nicotine is approved.,Nicotine is a liquid.,True
14881,"Phenylephrine is an alpha-1 adrenergic receptor agonist used to treat hypotension, dilate the pupil, and induce local vasoconstriction. The action of phenylephrine, or neo-synephrine, was first described in literature in the 1930s. Phenylephrine injections are indicated to treat hypotension caused by shock or anesthesia, an ophthalmic formulation is indicated to dilate pupils and induce vasoconstriction, an intranasal formulation is used to treat congestion, and a topical formulation is used to treat hemorrhoids. Off-label uses include situations that require local blood flow restriction such as the treatment of priapism. Phenylephrine is an alpha-1 adrenergic agonist that raises blood pressure, dilates the pupils, and causes local vasoconstriction. Ophthalmic formulations of phenylephrine act for 3-8 hours while intravenous solutions have an effective half life of 5 minutes and an elimination half life of 2.5 hours. Patients taking ophthalmic formulations of phenylephrine should be counselled about the risk of arrhythmia, hypertension, and rebound miosis. Patients taking an intravenous formulation should be counselled regarding the risk of bradycardia, allergic reactions, extravasation causing necrosis or tissue sloughing, and the concomitant use of oxytocic drugs. Phenylephrine is an alpha-1 adrenergic agonist that mediates vasoconstriction and mydriasis depending on the route and location of administration. Systemic exposure to phenylephrine also leads to agonism of alpha-1 adrenergic receptors, raising systolic and diastolic pressure as well as peripheral vascular resistance. Increased blood pressure stimulates the vagus nerve, causing reflex bradycardia.",The molecular weight is 167.21.,Phenylephrine has a topological polar surface area of 52.49.,The log p value of  is -0.09.,Phenylephrine is approved.,Phenylephrine is a solid.,True
14882,"Linezolid is a synthetic antibiotic, the first of the oxazolidinone class, used for the treatment of infections caused by multi-resistant bacteria including streptococcus and methicillin-resistant Staphylococcus aureus (MRSA). The drug works by inhibiting the initiation of bacterial protein synthesis. For the treatment of bacterial infections caused by susceptible strains of vancomycin resistant <i>Enterococcus faecium</i>, <i>Staphylococcal aureus</i> (methicillin resistant and susceptible strains), <i>Streptococcus pneumoniae</i>, <i>Streptococcus pyogenes</i>, <i>Streptococcus agalactiae</i>. Linezolid is a synthetic antibacterial agent of a new class of antibiotics, the oxazolidinones, which has clinical utility in the treatment of infections caused by aerobic Gram-positive bacteria. The in vitro spectrum of activity of linezolid also includes certain Gram-negative bacteria and anaerobic bacteria. Susceptible organisms include methicillin- and vancomycin-resistant staphylococci, vancomycin-resistant enterococci, penicillin-resistant pneumococci and anaerobes. Oxazolidinones inhibit protein synthesis by binding at the P site at the ribosomal 50S subunit. Resistance to other protein synthesis inhibitors does not affect oxazolidinone activity, however rare development of oxazolidinone resistance cases, associated with 23S rRNA alterations during treatment have been reported. Linezolid inhibits bacterial protein synthesis through a mechanism of action different from that of other antibacterial agents; therefore, cross-resistance between linezolid and other classes of antibiotics is unlikely. Linezolid is a synthetic antibacterial agent of the oxazolidinone class of antibiotics. It has in vitro activity against aerobic Gram positive bacteria, certain Gram negative bacteria and anaerobic microorganisms. It selectively inhibits bacterial protein synthesis through binding to sites on the bacterial ribosome and prevents the formation of a functional 70S-initiation complex. Specifically, linezolid binds to a site on the bacterial 23S ribosomal RNA of the 50S subunit and prevents the formation of a functional 70S initiation complex, which is an essential component of the bacterial translation process. The results of time-kill studies have shown linezolid to be bacteriostatic against enterococci and staphylococci. For streptococci, linezolid was found to be bactericidal for the majority of strains. Linezolid is also a reversible, nonselective inhibitor of monoamine oxidase. Therefore, linezolid has the potential for interaction with adrenergic and serotonergic agents.",The molecular weight is 337.35.,Linezolid has a topological polar surface area of 71.11.,The log p value of  is 0.17.,Linezolid is approved and investigational.,Linezolid is a solid.,True
14883,"A nitrofuran derivative with antiprotozoal and antibacterial activity. Furazolidone binds bacterial DNA which leads to the gradual inhibition of monoamine oxidase. (From Martindale, The Extra Pharmacopoeia, 30th ed, p514) For the specific and symptomatic treatment of bacterial or protozoal diarrhea and enteritis caused by susceptible organisms. Furoxone has a broad antibacterial spectrum covering the majority of gastrointestinal tract pathogens including E. coli, staphylococci, Salmonella, Shigella, Proteus, Aerobacter aerogenes, Vibrio cholerae and Giardia lamblia. Its bactericidal activity is based upon its interference with DNA replication and protein production; this antimicrobial action minimizes the development of resistant organisms. Furazolidone and its related free radical products are believed to bind DNA and induce cross-links. Bacterial DNA is particularly susceptible to this drug leading to high levels of mutations (transitions and transversions) in the bacterial chromosome.",The molecular weight is 225.16.,Furazolidone has a topological polar surface area of 98.18.,The log p value of  is -0.04.,Furazolidone is experimental and vet_approved.,Furazolidone is a solid.,True
14884,"Phenelzine, with the formula β-phenylethylhydrazine, is a monoamine oxidase inhibiting antidepressant that is effective in the treatment of panic disorder and social anxiety disorder. It was developed by Parke Davis and originally FDA approved on June 9th, 1961. It is currently approved under prescription by the name of Nardil. Phenelzine is indicated for the treatment of nonendogenous, neurotic or atypical depression for patients that do not tolerate other forms of therapy.  The elimination of monoamine oxidase by phenelzine results in the elevation of brain amines such as 2-phenylethylamine which is a metabolite of phenelzine. These amines have then marked effects on the uptake and release of catecholamines and serotonin in nerve endings. Phenelzine is shown to elevate brain levels of the gamma-aminobutyric acid (GABA) and alanine (ALA) as well as to inhibit the activity of the transaminases that normally metabolize these amino acids. In preclinical studies, it has been shown to be neuroprotective in cerebral ischemia. The basic mechanism of action of phenelzine acts as an inhibitor and substrate of monoamine oxidase which subsequently causes an elevation in brain levels of catecholamines and serotonin. It also presents a similar structure to amphetamine which explains the effect on the uptake and release of dopamine, noradrenaline, and serotonin. Phenelzine has been reported to inhibit tyrosine aminotransferase, aromatic amino acid decarboxylase, and dopamine B-hydroxylase.",The molecular weight is 136.2.,Phenelzine has a topological polar surface area of 38.05.,The log p value of  is 1.03.,Phenelzine is approved.,Phenelzine is a liquid.,True
14885,"A reversible monoamine oxidase inhibitor (MAOI) selective for isoform A (RIMA) used to treat major depressive disorder. Most meta-analyses and most studies indicate that in the acute management of depression, moclobemide is more efficacious than placebo medication and similarly efficacious as tricyclic antidepressants (TCA) or selective serotonin reuptake inhibitors (SSRIs). Due to negligible anticholinergic and antihistaminic actions, moclobemide has been better tolerated than tri- or heterocyclic antidepressants. For the treatment of major depressive disorder and bipolar disorder.  A selective, reversible inhibitor of monoamine oxidase (MAO) which increases the. Besides its presence in sympathetic nerves, there is an abundant evidence that MAO-A is localized in noradrenergic neurons in the locus coeruleus and MAO-B is closely associated with serotonergic neurons of the raphe nucleus. The mechanism of action of moclobemide involves the selective, reversible inhibition of MAO-A. This inhibition leads to a decrease in the metabolism and destruction of monoamines in the neurotransmitters. This results in an increase in the monoamines, relieving depressive symptoms.",The molecular weight is 268.74.,Moclobemide has a topological polar surface area of 41.57.,The log p value of  is 2.17.,Moclobemide is approved and investigational.,Moclobemide is a solid.,True
14886,Isatin is an indole derivative first obtained by Erdman and Laurent in 1841 as an oxidation product of Indigo dye with nitric acid and chromic acids. The compound is found in many plants and Schiff bases of Isatin are have been investigated for pharmaceutical applications.,,,,Isatin is experimental.,Isatin is a solid.,True
14887,,,,,(R)-N-methyl-N-2-propynyl-1-indanamine is experimental.,(R)-N-methyl-N-2-propynyl-1-indanamine is a solid.,False
14888,"A colorless liquid extracted from oils of plants such as citronella, neroli, cyclamen, and tuberose. It is an intermediate step in the biological synthesis of cholesterol from mevalonic acid in vertebrates. It has a delicate odor and is used in perfumery. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)",,,,Farnesol is experimental.,Farnesol is a solid.,True
14889,"A condensation product of riboflavin and adenosine diphosphate. The coenzyme of various aerobic dehydrogenases, e.g., D-amino acid oxidase and L-amino acid oxidase. (Lehninger, Principles of Biochemistry, 1982, p972) Used to treat eye diseases caused by vitamin B2 deficiency, such as keratitis and blepharitis.",,,,Flavin adenine dinucleotide is approved.,Flavin adenine dinucleotide is a solid.,True
14890,,,,,N-Propargyl-1(S)-Aminoindan is experimental.,N-Propargyl-1(S)-Aminoindan is a solid.,False
14891,,,,,Dodecyldimethylamine N-oxide is experimental.,Dodecyldimethylamine N-oxide is a solid.,False
14892,,,,,5-Hydroxy-N-Propargyl-1(R)-Aminoindan is experimental.,5-Hydroxy-N-Propargyl-1(R)-Aminoindan is a solid.,False
14893,Withdrawn from the Canadian market in July 1964 due to interactions with food products containing tyrosine. For the treatment of depression (originally intended to treat tuberculosis). Iproniazid is a monoamine oxidase inhibitor (MAOI) that was developed as the first anti-depressant.,The molecular weight is 179.22.,Iproniazid has a topological polar surface area of 54.02.,The log p value of  is 0.26.,Iproniazid is withdrawn.,Iproniazid is a solid.,True
14894,"Bicifadine (DOV-220075) is a nonopioid analgesic. It is an inhibitor of both the norepinephrine and serotonin transporters and an NMDA antagonist with a non-narcotic profile. Bicifadine was shown to have potent analgesic activity in vivo and was chosen for further development for the treatment of pain. For the treatment of pain. Bicifadine is a chemically distinct molecule with a unique profile of pharmacological activity. Its primary pharmacological action is to enhance and prolong the actions of norepinephrine and serotonin by inhibiting the transport proteins that terminate the physiological actions of the two biogenic amines. Bicifadine is not a narcotic and is well-tolerated and, in preclinical studies, has been shown not to act at any opiate receptor. Bicifadine does not exhibit any anti-inflammatory activity and does not inhibit prostaglandin synthetase in vitro. Preclinical studies and clinical trials indicate that bicifadine's analgesic properties result through the enhancement and prolongation of norepinephrine and serotonin actions, however other actions may be involved.",,,,Bicifadine is investigational.,Bicifadine is a solid.,True
14895,"Drug-resistant bacteria, such as methicillin-resistant _Staphylococcus aureus_, vancomycin-resistant _Enterococcus faecium_, and penicillin-resistant _Streptococcus penumoniae_, represent a massive public health threat. Tedizolid is a member of the oxazolidinone class of antibiotics, which includes the previously approved and is generally effective against multidrug-resistant Gram-positive bacteria. Tedizolid is indicated for the treatment of acute bacterial skin and skin structure infections (ABSSSI) and is generally more effective and more tolerable than. Tedizolid is indicated for the treatment of acute bacterial infections of the skin and skin structure (ABSSSI). To prevent drug resistance, tedizolid should only be used for infections that are caused by susceptible bacteria. Tedizolid is an oxazolidinone antibiotic that works by inhibiting protein synthesis by bacterial ribosomes. However, oxazolidinone antibiotics can also bind to human mitochondrial, but not cytoplasmic, ribosomes. Mitochondrial protein synthesis inhibition is associated with adverse patient effects such as neurological, hematological, and gastrointestinal toxicity, although tedizolid is tolerated better than the related. Alternative therapies should be considered when treating neutropenic patients with ABSSSI. _Clostridium difficile_-associated diarrhea has been reported in patients treated with tedizolid. Despite renewed efforts to combat the spread of antimicrobial resistance, multidrug-resistant organisms, including gram-positive bacteria such as methicillin-resistant _Staphylococcus aureus_, remain a threat. Oxazolidinones represent a relatively new class of antibacterials inhibiting protein synthesis that is generally capable of overcoming resistance to other bacterial protein synthesis inhibitors.",The molecular weight is 450.32.,Tedizolid phosphate has a topological polar surface area of 152.79.,The log p value of  is -0.5.,Tedizolid phosphate is approved.,Tedizolid phosphate is a solid.,True
14896,"Drug-resistant bacteria, such as methicillin-resistant _Staphylococcus aureus_, vancomycin-resistant _Enterococcus faecium_, and penicillin-resistant _Streptococcus penumoniae_, represent a massive public health threat. Tedizolid is a member of the oxazolidinone class of antibiotics, which includes the previously approved and is generally effective against multidrug-resistant Gram-positive bacteria. Tedizolid is indicated for the treatment of acute bacterial skin and skin structure infections (ABSSSI) and is generally more effective and more tolerable than. Tedizolid is indicated for the treatment of acute bacterial infections of the skin and skin structure (ABSSSI). To prevent drug resistance, tedizolid should only be used for infections that are caused by susceptible bacteria. Tedizolid is an oxazolidinone antibiotic that works by inhibiting protein synthesis by bacterial ribosomes. However, oxazolidinone antibiotics can also bind to human mitochondrial, but not cytoplasmic, ribosomes. Mitochondrial protein synthesis inhibition is associated with adverse patient effects such as neurological, hematological, and gastrointestinal toxicity, although tedizolid is tolerated better than the related. Alternative therapies should be considered when treating neutropenic patients with ABSSSI. _Clostridium difficile_-associated diarrhea has been reported in patients treated with tedizolid. Despite renewed efforts to combat the spread of antimicrobial resistance, multidrug-resistant organisms, including gram-positive bacteria such as methicillin-resistant _Staphylococcus aureus_, remain a threat. Oxazolidinones represent a relatively new class of antibacterials inhibiting protein synthesis that is generally capable of overcoming resistance to other bacterial protein synthesis inhibitors.",,,,Tedizolid is approved and investigational.,Tedizolid is a solid.,True
14897,"Zolmitriptan is a member of the triptan class of 5-hydroxytryptamine(5-HT)<sub>1B/1D/(1F)</sub> receptor agonists used to treat acute migraine. was the first triptan to be developed, but had poor oral bioavailability and lipophilicity. This led to the development of second-generation triptans, including , , , , , and zolmitriptan. Triptans can be administered alone or in combination with an NSAID like , and represent the current \gold standard\"" for acute migraine treatment."" Zolmitriptan is indicated for the acute treatment of migraine with or without auras in patients aged 18 and over. Zolmitriptan, like other triptans, is a serotonin (5-hydroxytryptamine; 5-HT) receptor agonist, with enhanced specificity for the 5-HT<sub>1B</sub> and 5-HT<sub>1D</sub> receptor subtypes. It is through the downstream effects of 5-HT<sub>1B/1D</sub> activation that triptans are proposed to provide acute relief of migraines. Zolmitriptan is also a vasoconstrictor, leading to possible adverse cardiovascular effects such as myocardial ischemia/infarction, arrhythmias, cerebral and subarachnoid hemorrhage, stroke, gastrointestinal ischemia, and peripheral vasospastic reactions. In addition, chest/throat/neck/jaw pain, tightness, and/or pressure has been reported, along with the possibility of medication overuse headaches and serotonin syndrome. Patients with phenylketonuria should be advised that ZOMIG-ZMT contains phenylalanine. Migraines are complex physiological events characterized by unilateral throbbing headaches combined with photophobia and other aversions to sensory input. Migraine attacks are generally divided into phases: the premonitory phase, which typically involves irritability, fatigue, yawning, and stiff neck; the headache phase, which lasts for between four and 72 hours; and the postdrome phase, which lasts for up to a day following resolution of pain and whose symptoms are similar to those of the premonitory phase. In addition, neurological deficits, collectively termed migraine aura, may precede the headache phase.",The molecular weight is 287.36.,Zolmitriptan has a topological polar surface area of 57.36.,The log p value of  is 1.29.,Zolmitriptan is approved and investigational.,Zolmitriptan is a solid.,True
14898,"Phenylpropanolamine is a sympathomimetic agent that acts as a nonselective adrenergic receptor agonist and norepinephrine reuptake inhibitor. It has been used as a decongestant and appetite suppressant. Currently, it is withdrawn from the market in Canada and the United States due to the risk for hemorrahgic strokes. For the treatment of nasal congestion, control of urinary incontinence, priapism and obesity. Phenylpropanolamine (PPA), a sympathomimetic agent structurally similar to pseudoephedrine, is used to treat nasal congestion. Phenylpropanolamine is found in appetite suppressant formulations and with guaifenesinin in cough-cold formulations. In 2000, the FDA requested that all drug companies discontinue marketing products containing phenylpropanolamine, due to an increased risk of hemorrhagic stroke in women who used phenylpropanolamine. Phenylpropanolamine acts directly on alpha- and, to a lesser degree, beta-adrenergic receptors in the mucosa of the respiratory tract. Stimulation of alpha-adrenergic receptors produces vasoconstriction, reduces tissue hyperemia, edema, and nasal congestion, and increases nasal airway patency. PPA indirectly stimulates beta-receptors, producing tachycardia and a positive inotropic effect.",The molecular weight is 151.21.,Phenylpropanolamine has a topological polar surface area of 46.25.,The log p value of  is 0.58.,Phenylpropanolamine is approved and vet_approved and withdrawn.,Phenylpropanolamine is a solid.,True
14899,"Sumatriptan is a serotonin receptor agonist commonly used to treat migraines and sometimes cluster headaches. Sumatriptan is the first of the triptans and was made available in Europe in 1991 to treat migraines. Sumatriptan was granted FDA approval on 28 December 1992. A combination sumatriptan and tablet is indicated for the treatment of migraines with or without auras in patients 12 years of age and older. Sumatriptan nasal powder, nasal spray, subcutaneous injection, and tablets are indicated to treat migraines with or without auras in adults. One of the subcutaneous formulations of sumatriptan is also indicated to treat cluster headaches in adults, while the other subcutaneous formulation is not. Sumatriptan constricts cranial blood vessels and prevents the release of vasoactive peptides. The dose of sumatriptan varies widely by route of administration and in most cases, no more than 2 doses should be given daily. Medication overuse headaches may occur in patients who use sumatriptan frequently. Sumatriptan is an agonist of 5-HT<sub>1B</sub> and 5-HT<sub>1D</sub>. This agonism leads to constriction of cranial blood vessels and inhibits the release of pro-inflammatory neuropeptides. Sumatriptan decreases carotid arterial blood flow, but increases blood flow velocity in the internal carotid artery and middle cerebral artery.",The molecular weight is 295.4.,Sumatriptan has a topological polar surface area of 65.2.,The log p value of  is 0.74.,Sumatriptan is approved and investigational.,Sumatriptan is a solid.,True
14900,"Almotriptan is a triptan drug for the treatment of migraine headaches. Almotriptan is in a class of medications called selective serotonin receptor agonists. It works by narrowing blood vessels in the brain, stopping pain signals from being sent to the brain, and stopping the release of certain natural substances that cause pain, nausea, and other symptoms of migraine. Almotriptan does not prevent migraine attacks. For the treatment of acute migraine headache in adults Almotriptan is a selective 5-hydroxytryptamine receptor subtype agonist indicated for the acute treatment of migraine attacks with or without aura in adults. Almotriptan is not intended for the prophylactic therapy of migraine or for use in the management of hemiplegic or basilar migraine. Almotriptan is an agonist for a vascular 5-hydroxytryptamine receptor subtype (probably a member of the 5-HT<sub>1D</sub> family) having only a weak affinity for 5-HT<sub>1A</sub>, 5-HT<sub>5A</sub>, and 5-HT<sub>7</sub> receptors and no significant affinity or pharmacological activity at 5-HT<sub>2</sub>, 5-HT<sub>3</sub> or 5-HT<sub>4</sub> receptor subtypes or at alpha1-, alpha2-, or beta-adrenergic, dopamine1,; dopamine2; muscarinic, or benzodiazepine receptors. This action in humans correlates with the relief of migraine headache. In addition to causing vasoconstriction, experimental data from animal studies show that Almotriptan also activates 5-HT<sub>1</sub> receptors on peripheral terminals of the trigeminal nerve innervating cranial blood vessels, which may also contribute to the antimigrainous effect of Almotriptan in humans. Almotriptan binds with high affinity to human 5-HT<sub>1B</sub> and 5-HT<sub>1D</sub> receptors leading to cranial blood vessel constriction.",The molecular weight is 335.47.,Almotriptan has a topological polar surface area of 56.41.,The log p value of  is 1.79.,Almotriptan is approved and investigational.,Almotriptan is a solid.,True
14901,"Naratriptan is a triptan drug that is selective for the 5-hydroxytryptamine1 receptor subtype. It is typically used for the treatment of migraine headaches. For the acute treatment of migraine attacks with or without aura in adults. Naratriptan is a selective agonist of serotonin (5-hydroxytryptamine; 5-HT) type 1B and 1D receptors. It is structurally and pharmacologically related to other selective 5-HT1B/1D receptor agonist. Naratriptan has only a weak affinity for 5-HT<sub>1A</sub>, 5-HT<sub>5A</sub>, and 5-HT<sub>7</sub> receptors and no significant affinity or pharmacological activity at 5-HT<sub>2</sub>, 5-HT<sub>3</sub> or 5-HT<sub>4</sub> receptor subtypes or at alpha1-, alpha2-, or beta-adrenergic, dopamine1,; dopamine2; muscarinic, or benzodiazepine receptors. This action in humans correlates with the relief of migraine headache. In addition to causing vasoconstriction, experimental data from animal studies show that Naratriptan also activates 5-HT<sub>1</sub> receptors on peripheral terminals of the trigeminal nerve innervating cranial blood vessels, which may also contribute to the antimigrainous effect of Naratriptan in humans. Three distinct pharmacological actions have been implicated in the antimigraine effect of the triptans: (1) stimulation of presynaptic 5-HT1D receptors, which serves to inhibit both dural vasodilation and inflammation; (2) direct inhibition of trigeminal nuclei cell excitability via 5-HT1B/1D receptor agonism in the brainstem and (3) vasoconstriction of meningeal, dural, cerebral or pial vessels as a result of vascular 5-HT1B receptor agonism.",The molecular weight is 335.47.,Naratriptan has a topological polar surface area of 65.2.,The log p value of  is 1.7.,Naratriptan is approved and investigational.,Naratriptan is a solid.,True
14902,"Rizatriptan is a triptan drug used for the treatment of migraine headaches. It is a selective 5-hydroxytryptamine1 receptor subtype agonist. For treatment of acute migraine attacks with or without aura. Rizatriptan is a selective agonist of serotonin (5-hydroxytryptamine; 5-HT) type 1B and 1D receptors. It is structurally and pharmacologically related to other selective 5-HT1B/1D receptor agonists and has only a weak affinity for 5-HT<sub>1A</sub>, 5-HT<sub>5A</sub>, and 5-HT<sub>7</sub> receptors and no significant affinity or pharmacological activity at 5-HT<sub>2</sub>, 5-HT<sub>3</sub> or 5-HT<sub>4</sub> receptor subtypes or at alpha1-, alpha2-, or beta-adrenergic, dopamine1,; dopamine2; muscarinic, or benzodiazepine receptors. This action in humans correlates with the relief of migraine headache. In addition to causing vasoconstriction, experimental data from animal studies show that Rizatriptan also activates 5-HT<sub>1</sub> receptors on peripheral terminals of the trigeminal nerve innervating cranial blood vessels, which may also contribute to the antimigrainous effect of Rizatriptan in humans. Three distinct pharmacological actions have been implicated in the antimigraine effect of the triptans: (1) stimulation of presynaptic 5-HT1D receptors, which serves to inhibit both dural vasodilation and inflammation; (2) direct inhibition of trigeminal nuclei cell excitability via 5-HT1B/1D receptor agonism in the brainstem and (3) vasoconstriction of meningeal, dural, cerebral or pial vessels as a result of vascular 5-HT1B receptor agonism.",The molecular weight is 269.35.,Rizatriptan has a topological polar surface area of 49.74.,The log p value of  is 1.18.,Rizatriptan is approved.,Rizatriptan is a solid.,True
14903,"A hallucinogenic serotonin analog found in frog or toad skins, mushrooms, higher plants, and mammals, especially in the brains, plasma, and urine of schizophrenics. Bufotenin has been used as a tool in CNS studies and misused as a psychedelic. Bufotenin is a tryptamine related to the neurotransmitter serotonin.",,,,Bufotenine is experimental and illicit.,Bufotenine is a solid.,True
14904,"Safinamide is for the treatment of parkinson's disease. It was approved in Europe in February 2015, and in the United States on March 21, 2017. Safinamide is indicated as an add-on treatment to levodopa with or without other medicines for Parkinson’s disease Safinamide is a unique molecule with multiple mechanisms of action and a very high therapeutic index. It combines potent, selective, and reversible inhibition of MAO-B with blockade of voltage-dependent Na+ and Ca2+ channels and inhibition of glutamate release. Safinamide has neuroprotective and neurorescuing effects in MPTP-treated mice, in the rat kainic acid, and in the gerbil ischemia model.",The molecular weight is 302.35.,Safinamide has a topological polar surface area of 64.35.,The log p value of  is 2.49.,Safinamide is approved and investigational.,Safinamide is a solid.,True
14905,"This drug is classified as a reversible inhibitor of monoamine oxidase A enzyme (also known as a RIMA drug). It was developed and is currently used as an antidepressant in Russia. Its chemical structure is similar to metralindole, and it also shares pharmacological properties with this drug. For the treatment of major depression. Pirlindole regulates that metabolism of norepinephrine and catecholamines, leading to relief of depressive symptoms. The prevention of breakdown of these neuromodulators is thought to elevate mood. This drug is a selective and reversible inhibitor of monoamine oxidase A (also known as MAO-A). Its main mechanism of action is selective and reversible inhibition of monoamine oxidase A. Its secondary mechanism of action is the inhibition effect of noradrenaline and 5-hydroxytryptamine reuptake.",The molecular weight is 226.32.,Pirlindole has a topological polar surface area of 16.96.,The log p value of  is 3.27.,Pirlindole is experimental.,Pirlindole is a solid.,True
14906,"Toloxatone is an antidepressant agent, the first ever use of which was in France, 1984. It acts as a selective and reversible inhibitor of monoamine oxidase-A (MOA). For the treatment of major depressive disorder.  This drug has been shown to help manage the symptoms of depression by maintaining neuro-synaptic levels of serotonin and catecholamines while regulating their metabolism, which leads to relief of depressive symptoms. This medication is a reversible inhibitor of monoamine oxidase type-A (also known as RIMA). ",The molecular weight is 205.26.,Toloxatone has a topological polar surface area of 29.54.,The log p value of  is 2.69.,Toloxatone is experimental.,Toloxatone is a solid.,True
14907,"Eravacycline, known as _Xerava_ by Tetraphase Pharmaceuticals, is a fully synthetic fluorocycline antibiotic of the tetracycline class with activity against clinically significant gram-negative, gram-positive aerobic, and facultative bacteria. This includes most of those bacteria resistant to cephalosporins, fluoroquinolones, β-lactam/β-lactamase inhibitors, multidrug-resistant strains, and carbapenem-resistant Enterobacteriaceae, and the majority of anaerobic pathogens. It was first approved by the FDA on August 27, 2018. Eravacycline has demonstrated superior potency to that of antibiotics that are currently being marketed for intraabdominal infections. This drug is a tetracycline class antibacterial indicated for the treatment of complicated intra-abdominal infections in patients 18 years of age and older. Eravacycline is an antibiotic that disrupts bacterial protein synthesis, treating complicated intraabdominal infections. Eravacycline is a fluorocycline antibacterial of the tetracycline class of antibacterial drugs. Eravacycline disrupts bacterial protein synthesis by binding to the 30S ribosomal subunit, preventing the incorporation of amino acid residues into elongating peptide chains.",,,,Eravacycline is approved and investigational.,Eravacycline is a solid.,True
14908,"Ubrogepant is indicated for the acute treatment of migraine headaches with or without aura in adults. It was approved by the FDA on December 23, 2019, and is the first oral calcitonin gene-related peptide (CGRP) receptor antagonist approved for the acute treatment of migraine. Several oral small molecule CGRP receptor antagonists, belonging to a class of medications referred to as \gepants\"", have been investigated for migraines, but only ubrogepant and remain in clinical development. Previous agents within this class were efficacious but limited by liver toxicity - this led to the development of ubrogepant, which was designed to be a hepatoxicity-free alternative to its predecessors. Several parenteral monoclonal antibodies acting against the CGRP pathway (e.g. , , ) have also been approved in recent years."" Ubrogepant is indicated for the acute treatment of migraine with or without aura in adults. Ubrogepant acutely treats migraine headache pain by blocking the activity of a key transmitter involved in migraine pathogenesis. Exposure to ubrogepant can be significantly increased in patients with severe hepatic or renal insufficiency - dose adjustments are required for these patients in order to avoid excessive exposure, and ubrogepant is not recommended in patients with end-stage renal disease. The currently accepted theory of migraine pathophysiology considers dysfunction of the central nervous system, in particular the trigeminal ganglion, to be the root cause behind the condition. Activation of the trigeminal ganglion triggers the stimulation of trigeminal afferents that project to the spinal cord and synapse on various pain-sensing intra- and extracranial structures, such as the dura mater. Pain signals are then further transmitted via second-order ascending neurons to the brainstem, hypothalamus, and thalamic nuclei, and from there to several cortical regions (e.g. auditory, visual, motor cortices). The trigeminal ganglion appears to amplify and perpetuate the migraine headache pain through the activation of perivascular fibers and the release of molecules involved in pain generation, such as calcitonin gene-related peptide (CGRP).",,,,Ubrogepant is approved and investigational.,Ubrogepant is a solid.,True
14909,"A topical anti-infective agent effective against gram-negative and gram-positive bacteria. It is used for superficial wounds, burns, ulcers, and skin infections. Nitrofurazone has also been administered orally in the treatment of trypanosomiasis. For the treatment of bacterial skin infections including pyodermas, infected dermatoses and infections of cuts, wounds, burns and ulcers due to susceptible organisms. Nitrofurazone is a topical antibacterial agent indicated as an adjunctive therapy for second and third degree burns when resistance to other agents is a real or potential problem. Nitrofurazone is also indicated in skin grafting when bacterial contamination may cause graft rejection or donor site infection, especially in hospitals with a history of resistant bacteria. The exact mechanism of action is unknown. Nitrofurazone inhibits several bacterial enzymes, especially those involved in the aerobic and anaerobic degradation of glucose and pyruvate. This activity is believed also to affect pyruvate dehydrogenase, citrate synthetase, malate dehydrogenase, glutathione reductase, and pyruvate decarboxylase.",The molecular weight is 198.14.,Nitrofural has a topological polar surface area of 126.44.,The log p value of  is 0.2.,Nitrofural is approved and investigational and vet_approved.,Nitrofural is a solid.,True
14910,"A pyrazine that is used therapeutically as an antitubercular agent. For the initial treatment of active tuberculosis in adults and children when combined with other antituberculous agents. Pyrazinamide kills or stops the growth of certain bacteria that cause tuberculosis (TB). It is used with other drugs to treat tuberculosis. It is a highly specific agent and is active only against <i>Mycobacterium tuberculosis</i>. In vitro and in vivo, the drug is active only at a slightly acid pH. Pyrazinamie gets activated to Pyrazinoic acid in the bacilli where it interferes with fatty acid synthase FAS I. This interferes with the bacteriums ability to synthesize new fatty acids, required for growth and replication. Pyrazinamide diffuses into active _M. tuberculosis_ that express pyrazinamidase enzyme that converts pyrazinamide to the active form pyrazinoic acid. Pyrazinoic acid can leak out under acidic conditions to be converted to the protonated conjugate acid, which is readily diffused back into the bacilli and accumulate intracellularly. The net effect is that more pyrazinoic acid accumulates inside the bacillus at acid pH than at neutral pH. Pyrazinoic acid was thought to inhibit the enzyme fatty acid synthase (FAS) I, which is required by the bacterium to synthesise fatty acids. However, this theory was thought to have been discounted. However, further studies reproduced the results of FAS I inhibition as the putative mechanism first in whole cell assay of replicating M. tuberculosis bacilli which have shown that pyrazinoic acid and its ester inhibit the synthesis of fatty acids. This study was followed by in vitro assay of tuberculous FAS I enzyme that tested the activity with pyrazinamide, pyrazinoic acid and several classes of pyrazinamide analogs. Pyrazinamide and its analogs inhibited the activity of purified FAS I. ",The molecular weight is 123.12.,Pyrazinamide has a topological polar surface area of 68.87.,The log p value of  is -0.68.,Pyrazinamide is approved and investigational.,Pyrazinamide is a solid.,True
14911,"Gout is a disease that occurs by the deposition of monosodium urate crystals (MSU) in body tissues, especially around joints. This disease has been well-documented in historical medical records and appears in the biographies of several prominent, historically recognized individuals. Allopurinol is indicated in : Allopurinol is a structural analog of the natural purine base, hypoxanthine. After ingestion, allopurinol is metabolized to its active metabolite, oxypurinol (_alloxanthine_) in the liver , which acts as an inhibitor of xanthine oxidase enzyme. ",The molecular weight is 136.11.,Allopurinol has a topological polar surface area of 74.69.,The log p value of  is 0.63.,Allopurinol is approved.,Allopurinol is a solid.,True
14912,"Natural product isolated from Streptomyces pilosus. It forms iron complexes and is used as a chelating agent, particularly in the mesylate form. Used to treat acute iron or aluminum toxicity (an excess of aluminum in the body) in certain patients. Also used in certain patients with anemia who must receive many blood transfusions. Deferoxamine, otherwise known as desferrioxamine or desferal, is a chelating agent used to remove excess iron or aluminum from the body. It acts by binding free iron or aluminum in the bloodstream and enhancing its elimination in the urine. By removing excess iron or aluminum, the agent reduces the damage done to various organs and tissues, such as the liver. Deferoxamine works in treating iron toxicity by binding trivalent (ferric) iron (for which it has a strong affinity), forming ferrioxamine, a stable complex which is eliminated via the kidneys. 100 mg of deferoxamine is capable of binding approximately 8.5 mg of trivalent (ferric) iron. Deferoxamine works in treating aluminum toxicity by binding to tissue-bound aluminum to form aluminoxamine, a stable, water-soluble complex. The formation of aluminoxamine increases blood concentrations of aluminum, resulting in an increased concentration gradient between the blood and dialysate, boosting the removal of aluminum during dialysis. 100 mg of deferoxamine is capable of binding approximately 4.1 mg of aluminum.",The molecular weight is 560.69.,Deferoxamine has a topological polar surface area of 205.84.,The log p value of  is -0.18.,Deferoxamine is approved and investigational.,Deferoxamine is a solid.,True
14913,"A phenothiazine with actions similar to chlorpromazine. It is used as an antipsychotic and an antiemetic. For the treatment of anxiety disorders, depressive symptoms secondary to anxiety and agitation. Trifluoperazine is a trifluoro-methyl phenothiazine derivative intended for the management of schizophrenia and other psychotic disorders. Trifluoperazine has not been shown effective in the management of behaviorial complications in patients with mental retardation. Trifluoperazine blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain; depresses the release of hypothalamic and hypophyseal hormones and is believed to depress the reticular activating system thus affecting basal metabolism, body temperature, wakefulness, vasomotor tone, and emesis.",The molecular weight is 407.5.,Trifluoperazine has a topological polar surface area of 9.72.,The log p value of  is 4.89.,Trifluoperazine is approved and investigational.,Trifluoperazine is a solid.,True
14914,"An antineoplastic agent used primarily in combination with mechlorethamine, vincristine, and prednisone (the MOPP protocol) in the treatment of Hodgkin's disease. For use with other anticancer drugs for the treatment of stage III and stage IV Hodgkin's disease. Procarbazine is an antineoplastic in the class of alkylating agents and is used to treat various forms of cancer. Alkylating agents are so named because of their ability to add alkyl groups to many electronegative groups under conditions present in cells. They stop tumor growth by cross-linking guanine bases in DNA double-helix strands - directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. In addition, these drugs add methyl or other alkyl groups onto molecules where they do not belong which in turn inhibits their correct utilization by base pairing and causes a miscoding of DNA. Procarbazine is cell-phase specific for the S phase of cell division. The precise mode of cytotoxic action of procarbazine has not been clearly defined. There is evidence that the drug may act by inhibition of protein, RNA and DNA synthesis. Studies have suggested that procarbazine may inhibit transmethylation of methyl groups of methionine into t-RNA. The absence of functional t-RNA could cause the cessation of protein synthesis and consequently DNA and RNA synthesis. In addition, procarbazine may directly damage DNA. Hydrogen peroxide, formed during the auto-oxidation of the drug, may attack protein sulfhydryl groups contained in residual protein which is tightly bound to DNA.",The molecular weight is 221.3.,Procarbazine has a topological polar surface area of 53.16.,The log p value of  is -0.08.,Procarbazine is approved and investigational.,Procarbazine is a solid.,True
14915,"A purine nucleoside that has hypoxanthine linked by the N9 nitrogen to the C1 carbon of ribose. It is an intermediate in the degradation of purines and purine nucleosides to uric acid and in pathways of purine salvage. It also occurs in the anticodon of certain transfer RNA molecules. (Dorland, 28th ed) The primary popular claim made for inosine, that it enhances exercise and athletic performance, is refuted by the available research data. There is some preliminary evidence that inosine may have some neurorestorative, anti-inflammatory, immunomodulatory and cardioprotective effects. Inosine may have neuroprotective, cardioprotective, anti-inflammatory and immunomodulatory activities. Inosine has been found to have potent axon-promoting effects in vivo following unilateral transection of the corticospinal tract of rats. The mechanism of this action is unclear. Possibilities include serving as an agonist of a nerve growth factor-activated protein kinase (N-Kinase), conversion to cyclic nucleotides that enable advancing nerve endings to overcome the inhibitory effects of myelin, stimulation of differentiation in rat sympathetic neurons, augmentation of nerve growth factor-induced neuritogenesis and promotion of the survival of astrocytes, among others. The mechanism of inosine's possible cardioprotective effect is similarly unclear. Inosine has been reported to have a positive inotropic effect and also to have mild coronary vasodilation activity. Exogenous inosine may contribute to the high-energy phosphate pool of cardiac muscle cells and favorably affect bioenergetics generally. Inosine has also been reported to enhance the myocardial uptake of carbohydrates relative to free fatty acids as well as glycolysis. In cell culture studies, inosine has been found to inhibit the production, in immunostimulated macrophages and spleen cells, of the proinflammatory cytokines, tumor necrosis factor (TNF)-alpha, interleukin (IL)-1, interleukin (IL)-12, macrophage-inflammatory protein-1 alpha and interferon (IFN)-gamma. It also suppressed proinflammatory cytokine production and mortality in a mouse endotoxemic model. These actions might account for the possible immunomodulatory, anti-inflammatory and anti-ischemic actions of inosine.",The molecular weight is 268.23.,Inosine has a topological polar surface area of 129.2.,The log p value of  is -3.11.,Inosine is experimental and investigational.,Inosine is a solid.,True
14916,Porfiromycin is a substance that is being studied in the treatment of cancer. It belongs to the family of drugs called anticancer antibiotics. Investigated for use/treatment in head and neck cancer.,,,,Porfiromycin is investigational.,Porfiromycin is a solid.,True
14917,"A nucleoside antibiotic isolated from Streptomyces antibioticus. It has some antineoplastic properties and has broad spectrum activity against DNA viruses in cell cultures and significant antiviral activity against infections caused by a variety of viruses such as the herpes viruses, the vaccinia VIRUS and varicella zoster virus. For treatment of chickenpox - varicella, herpes zoster and herpes simplex Vidarabine is a synthetic purine nucleoside analogue with <i>in vitro</i> and <i>in vivo</i> inhibitory activity against herpes simplex virus types 1 (HSV-1), 2 (HSV-2), and varicella-zoster virus (VZV). The inhibitory activity of Vidarabine is highly selective due to its affinity for the enzyme thymidine kinase (TK) encoded by HSV and VZV. This viral enzyme converts Vidarabine into Vidarabine monophosphate, a nucleotide analogue. The monophosphate is further converted into diphosphate by cellular guanylate kinase and into triphosphate by a number of cellular enzymes. <i>In vitro</i>, Vidarabine triphosphate stops the DNA replication of herpes virus by being incorporated into the DNA strand and preventing the formation of phosphodiester bridges between bases. This ultimately leads to destabilization of the viral DNA strands.  Vidarabine stops replication of herpes viral DNA in 2 ways: 1) competitive inhibition of viral DNA polymerase, and consequently 2) incorporation into and termination of the growing viral DNA chain.",,,,Vidarabine is approved and investigational.,Vidarabine is a solid.,True
14918,"A nucleoside that is composed of adenine and d-ribose. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter. Used as an initial treatment for the termination of paroxysmal supraventricular tachycardia (PVST), including that associated with accessory bypass tracts, and is a drug of choice for terminating stable, narrow-complex supraventricular tachycardias (SVT). Also used as an adjunct to thallous chloride TI 201 myocardial perfusion scintigraphy (thallium stress test) in patients who are unable to exercise adequately, as well as an adjunct to vagal maneuvers and clinical assessment to establish a specific diagnosis of undefined, stable, narrow-complex SVT. Adenosine is an endogenous nucleoside occurring in all cells of the body and is not chemically related to other antiarrhythmic drugs. Adenosine may exert its pharmacologic effects by activation of purine (cell surface A<sub>1</sub> and A<sub>2</sub> adenosine) receptors, as well as relax vascular smooth muscles through the reduction in calcium uptake by inhibition of slow inward calcium current and activation of adenylate cyclase in smooth muscle cells. Adenosine may reduce vascular tone by modulation of sympathetic neurotransmission. The drug also has negative chronotropic, dromotropic, and inotropic effects on the heart by slowing conduction time throught he AV node and interrupting AV nodal reentry pathways. Adenosine is a potent vasodilator in most vascular beds, but vasoconstriction is produced in renal afferent arterioles and hepatic veins. The drug produces a net mild to moderate reduction in systolic, diastolic, and mean arterial blood pressure and a reflex increase in heart rate. Adenosine is antagonized competitively by methylxanthines such as caffeine and theophylline, and potentiated by blockers of nucleoside transport such as dipyridamole. Adenosine is not blocked by atropine. Adenosine slows conduction time through the AV node and can interrupt the reentry pathways through the AV node, resulting in the restoration of normal sinus rhythm in patients with paroxysmal supraventricular tachycardia (PSVT), including PSVT associated with Wolff-Parkinson-White Syndrome. This effect may be mediated through the drug's activation of cell-surface A<sub>1</sub> and A<sub>2</sub> adenosine receptors. Adenosine also inhibits the slow inward calcium current and activation of adenylate cyclase in smooth muscle cells, thereby causing relaxation of vascular smooth muscle. By increasing blood flow in normal coronary arteries with little or no increase in stenotic arteries (with little to no increase in stenotic arteries), adenosine produces a relative difference in thallous (thallium) chloride TI 201 uptake in myocardium supplied by normal verus stenotic coronary arteries.",The molecular weight is 267.24.,Adenosine has a topological polar surface area of 139.54.,The log p value of  is -2.16.,Adenosine is approved and investigational.,Adenosine is a solid.,True
14919,"Nelarabine is an antineoplastic agent that is typically employed to treat acute T-cell lymphoblastic leukemia. Nelarabine is a purine nucleoside analog converted to its corresponding arabinosylguanine nucleotide triphosphate (araGTP), resulting in inhibition of DNA synthesis and cytotoxicity. For the treatment of pediatric and adult patients with acute T-cell lymphoblastic leukemia and T-cell lymphoblastic lymphoma whose disease has not responded to or has relapsed following treatment with at least two chemotherapy regimens. Nelarabine is a prodrug of the cytotoxic deoxyguanosine analogue 9-&szlig;-D-arabinofuranosylguanine (ara-G). Nelarabine is demethylated by adenosine deaminase (ADA) to ara-G. Ara-G is then transported into cells, where it undergoes three phosphorylation steps, resulting in the formation of ara-G triphosphate (ara-GTP). In the first phosphorylation step, ara-G is converted to ara-G monophosphate (ara-GMP). Ara-GMP is then monophosphorylated by deoxyguanosine kinase and deoxycytidine kinase to ara-G diphosphate, and then subsequently to the active ara-G triphosphate (ara-GTP). Ara-GTP is the one that exerts the pharmacological effect. Pre-clinical studies have demonstrated that targeted T-cells possess marked sensitivity to the agent. Once nelarabine is metabolized into ara-GTP, the metabolite accumulates in leukemic blasts and incorporates into DNA to exert its S phase-specific cytotoxic effects, leading to the induction of fragmentation and apoptosis. Ara-GTP competes with endogenous deoxyGTP (dGTP) for incorporation into DNA. Once ara-GTP is incorporated at the 3' end of DNA, further DNA elongation is inhibited, which signals apoptosis and leads to cellular destruction. Additional cytotoxic activities may exist, but these are not fully understood.",The molecular weight is 297.27.,Nelarabine has a topological polar surface area of 148.77.,The log p value of  is -1.19.,Nelarabine is approved and investigational.,Nelarabine is a solid.,True
14920,"Erdosteine is a drug that causes a breakdown of mucus, also known as a _mucolytic_ agent. It is a _thiol_ derivative produced for the clinical management of chronic obstructive bronchitis, in addition to infective exacerbations of chronic bronchitis. This drug contains sulfhydryl groups which are released after erdosteine undergoes hepatic first pass metabolism. Three active metabolites result and possess mucolytic activity in addition to free radical scavenging activity. Erdosteine acts to control mucus production and control its viscosity while increasing mucociliary transport. It also combats the effects of free radicals resulting from cigarette smoke. Erdosteine has been shown to be safe and well tolerated in clinical trials. Erdosteine 300mg twice daily reduced cough (both frequency and severity) and sputum viscosity more quickly and more effectively than placebo and reduced the adhesivity of sputum more effectively than ambroxol 30mg twice daily. Co-administration of erdosteine and amoxicillin in patients with acute infective exacerbation of chronic bronchitis resulted in higher concentrations of the antibiotic in the sputum, leading to earlier and more pronounced amelioration of clinical symptoms compared with placebo. Erdosteine is associated with a low incidence of adverse events, most of which are gastrointestinal and generally mild. Fro the treatment of chronic bronchitis in adults. Erdosteine, is an orally administered mucolytic agent. It is classified as a thiol derivative and produced for the management of symptoms caused by chronic obstructive bronchitis. Erdosteine contains sulfhydryl groups which are released after hepatic first-pass metabolism in the liver. Its active metabolites (3 in number) exert both mucolytic activity and scavenging activity against free radicals. Erdosteine acts to regulate the production of mucus in the airway and regulates its viscosity while enhancing mucociliary transport. This leads to an increase in expectoration. Erdosteine shows inhibition against the effects of free radicals from cigarette smoke. Clinical studies in patients with chronic obstructive lung disease (COPD) have shown that this drug is generally safe and well tolerated. Erdosteine 300mg twice daily reduced cough (both frequency and severity) and sputum viscosity more quickly and more effectively than placebo and reduced the adhesivity of sputum more effectively than ambroxol 30mg twice daily. Co-administration of erdosteine and amoxicillin in patients with acute infective exacerbation of chronic bronchitis resulted in higher concentrations of the antibiotic in the sputum, leading to earlier and more pronounced amelioration of clinical symptoms compared with placebo. Erdosteine is associated with a low incidence of adverse events, most of which are gastrointestinal and generally mild.",The molecular weight is 249.3.,Erdosteine has a topological polar surface area of 83.47.,The log p value of  is -0.39.,Erdosteine is approved and investigational.,Erdosteine is a solid.,True
14921,"One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter. There is no support for the claim that aspartates are exercise performance enhancers, i.e. ergogenic aids. L-aspartate is considered a non-essential amino acid, meaning that, under normal physiological conditions, sufficient amounts of the amino acid are synthesized in the body to meet the body's requirements. L-aspartate is formed by the transamination of the Krebs cycle intermediate oxaloacetate. The amino acid serves as a precursor for synthesis of proteins, oligopeptides, purines, pyrimidines, nucleic acids and L-arginine. L-aspartate is a glycogenic amino acid, and it can also promote energy production via its metabolism in the Krebs cycle. These latter activities were the rationale for the claim that supplemental aspartate has an anti-fatigue effect on skeletal muscle, a claim that was never confirmed. There are also claims that L-aspartate has ergogenic effects, that it enhances performance in both prolonged exercise and short intensive exercise. It is hypothesized that L-aspartate, especially the potassium magnesium aspartate salt, spares stores of muscle glycogen and/or promotes a faster rate of glycogen resynthesis during exercise. It has also been hypothesized that L-aspartate can enhance short intensive exercise by serving as a substrate for energy production in the Krebs cycle and for stimulating the purine nucleotide cycle.",The molecular weight is 133.1.,Aspartic acid has a topological polar surface area of 100.62.,The log p value of  is -2.41.,Aspartic acid is approved and nutraceutical.,Aspartic acid is a solid.,True
14922,"Taurine, whose chemical name is 2-aminoethanesulfonic acid, is one of the most abundant amino acids in several organs. It plays important role in essential biological processes. This conditional amino acid can be either be manufactured by the body or obtained in the diet mainly by the consumption of fish and meat. The supplements containing taurine were FDA approved by 1984 and they are hypertonic injections composed by cristalline amino acids. The use of diet supplements containing taurine is indicated for the nutritional support of infants and young pediatric patients requiring total parenteral nutrition via central or peripheral routes. The usage of diet supplements containing taurine prevents nitrogen and weight loss or to treat negative nitrogen balance in pediatric patients where the alimentary tract cannot be done through oral, gastrostomy or jejunostomy administration, there is impaired gastrointestinal absorption or protein requirements are substantially increased. The diet supplements containing taurine are formulated as a well-tolerated nitrogen source for nutritional support. Administration of diet supplements regulates the level of plasma amino acid concentration, nitrogen balance, weight and serum protein concentration to reach normal values, thus improving the nutritional status. The diet supplements containing taurine function by replacing the missing nutriments in the body. Taurine, as a single agent, presents different functions like substrate for formation of bile salts, cell volume regulation, modulation of intracellular calcium, cytoprotection of central nervous system, etc.",The molecular weight is 125.14.,Taurine has a topological polar surface area of 80.39.,The log p value of  is -4.79.,Taurine is approved and nutraceutical.,Taurine is a solid.,True
14923,"A noncompetitive antagonist at GABA-A receptors and thus a convulsant. Picrotoxin blocks the gamma-aminobutyric acid-activated chloride ionophore. Although it is most often used as a research tool, it has been used as a CNS stimulant and an antidote in poisoning by CNS depressants, especially the barbiturates.  Used internally for relieving respiratory distress. Also for use as an antidote in poisoning by CNS depressants, especially barbiturates. Picrotoxin is a toxin obtained from the seeds of the shrub <i>Anamirta cocculus</i>. It is used as a central nervous system stimulant, antidote, convulsant, and GABA (gamma aminobutyric acid) antagonist. It is a noncompetitive antagonist at GABA<sub>A</sub> receptors and thus a convulsant. Picrotoxin blocks the GABA<sub>A</sub>ctivated chloride ionophore. Although it is most often used as a research tool, it has been used as a CNS stimulant and an antidote in poisoning by CNS depressants, especially barbiturates. Picrotoxin antagonizes the GABA<sub>A</sub> receptor channel directly, which is a ligand-gated ion channel concerned chiefly with the passing of chloride ions across the cell membrane. Therefore picrotoxin prevents Cl<sup>-</sup> channel permeability and thus promtes an inhibitory influence on the target neuron. Picrotoxin reduces conductance through the channel by reducing not only the opening frequency but also the mean open time. Picrotoxin also antagonizes GABA<sub>C</sub> receptors (also called GABA<sub>A</sub>-rho receptors) but the result of this action is not known. The GABA<sub>C</sub> receptor is also linked to chloride channels, with distinct physiological and pharmacological properties. In contrast to the fast and transient responses elicited from GABA<sub>A</sub> receptors, GABA<sub>C</sub> receptors mediate slow and sustained responses.",The molecular weight is 602.59.,Picrotoxin has a topological polar surface area of 105.59.,,Picrotoxin is experimental.,Picrotoxin is a solid.,True
14924,"A benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group. Used parentally to treat hypertensive emergencies. Also used to treat hypoglycemia secondary to insulinoma. Diazoxide is a potassium channel activator. Its mechanism of action revolves around enhancing cell membrane permeability to potassium ions. This action consequently elicits the relaxation of local smooth muscles. This switches off voltage-gated calcium ion channels which inhibits the generation of an action potential. Diazoxide inhibits insulin release from the pancreas, by opening potassium channels in the beta cell membrane. Diazoxide is chemically related to thiazide diuretics but does not inhibit carbonic anhydrase and does not have chloriuretic or natriuretic activity. It also exhibits hypotensive activity by reducing arteriolar smooth muscle and vascular resistance.",The molecular weight is 230.67.,Diazoxide has a topological polar surface area of 58.53.,The log p value of  is 1.2.,Diazoxide is approved.,Diazoxide is a solid.,True
14925,"Ethyl biscoumacetate is a courmarin that is used as an anticoagulant. It has actions similar to those of Warfarin. (From Martindale, The Extra Pharmacopoeia, 30th ed, p226)",The molecular weight is 408.36.,Ethyl biscoumacetate has a topological polar surface area of 119.36.,The log p value of  is 3.15.,Ethyl biscoumacetate is withdrawn.,Ethyl biscoumacetate is a solid.,True
14926,"Paricalcitol is a synthetic vitamin D analog. Paricalcitol has been used to reduce parathyroid hormone levels. Paricalcitol is indicated for the prevention and treatment of secondary hyperparathyroidism associated with chronic renal failure. For treatment of secondary hyperparathyroidism associated with chronic kidney disease (CKD) Stage 3 and 4 Secondary hyperparathyroidism is characterized by an elevation in parathyroid hormone (PTH) associated with inadequate levels of active vitamin D hormone. The source of vitamin D in the body is from synthesis in the skin and from dietary intake. Vitamin D requires two sequential hydroxylations in the liver and the kidney to bind to and to activate the vitamin D receptor (VDR). The endogenous VDR activator, calcitriol , is a hormone that binds to VDRs that are present in the parathyroid gland, intestine, kidney, and bone to maintain parathyroid function and calcium and phosphorus homeostasis, and to VDRs found in many other tissues, including prostate, endothelium and immune cells. VDR activation is essential for the proper formation and maintenance of normal bone. In the diseased kidney, the activation of vitamin D is diminished, resulting in a rise of PTH, subsequently leading to secondary hyperparathyroidism and disturbances in the calcium and phosphorus homeostasis.1 Decreased levels of 1,25(OH)2 D3 have been observed in early stages of chronic kidney disease. The decreased levels of 1,25(OH)2 D3 and resultant elevated PTH levels, both of which often precede abnormalities in serum calcium and phosphorus, affect bone turnover rate and may result in renal osteodystrophy. An in vitro study indicates that paricalcitol is not an inhibitor of CYP1A2, CYP2A6, CYP2B6, CYP2C8, CYP2C9, CYP2C19, CYP2D6, CYP2E1 or CYP3A at concentrations up to 50 nM (21 ng/mL). Paricalcitol is a synthetic, biologically active vitamin D analog of calcitriol with modifications to the side chain (D2) and the A (19-nor) ring. Preclinical andin vitro studies have demonstrated that paricalcitol's biological actions are mediated through binding of the VDR, which results in the selective activation of vitamin D responsive pathways. Vitamin D and paricalcitol have been shown to reduce parathyroid hormone levels by inhibiting PTH synthesis and secretion.",The molecular weight is 416.65.,Paricalcitol has a topological polar surface area of 60.69.,The log p value of  is 5.69.,Paricalcitol is approved and investigational.,Paricalcitol is a solid.,True
14927,"Ammonia N 13 Injection, USP is a positron emitting radiopharmaceutical that is used for diagnostic purposes in conjunction with positron emission tomography (PET) imaging. The active ingredient, ammonia, has the molecular formula of 13NH3 with a molecular weight of 16.02. For diagnostic Positron Emission Tomography (PET) imaging of the myocardium under rest or pharmacologic stress conditions to evaluate myocardial perfusion in patients with suspected or existing coronary artery disease. Following intravenous injection, ammonia N 13 enters the myocardium through the coronary arteries. The PET technique measures myocardial blood flow based on the assumption of a three-compartmental disposition of intravenous ammonia N 13 in the myocardium. In this model, the value of the rate constant, which represents the delivery of blood to myocardium, and the fraction of ammonia N 13 extracted into the myocardial cells, is a measure of myocardial blood flow. Optimal PET imaging of the myocardium is generally achieved between 10 to 20 minutes after administration. Ammonia N 13 Injection is a radiolabeled analog of ammonia that is distributed to all organs of the body after intravenous administration. It is extracted from the blood in the coronary capillaries into the myocardial cells where it is metabolized to glutamine N 13 and retained in the cells. The presence of ammonia N 13 and glutamine N 13 in the myocardium allows for PET imaging of the myocardium.",The molecular weight is 16.03.,Ammonia N-13 has a topological polar surface area of 13.59.,,Ammonia N-13 is approved.,Ammonia N-13 is a solid.,True
14928,,,,,2-Hydroxyethyl Disulfide is experimental.,2-Hydroxyethyl Disulfide is a solid.,False
14929,,,,,N-(4-Aminobutanoyl)-S-(4-methoxybenzyl)-L-cysteinylglycine is experimental.,N-(4-Aminobutanoyl)-S-(4-methoxybenzyl)-L-cysteinylglycine is a solid.,False
14930,,,,,S-benzylglutathione is experimental.,S-benzylglutathione is a solid.,False
14931,,,,,S-Hexylglutathione is experimental.,S-Hexylglutathione is a solid.,False
14932,"Proline is one of the twenty amino acids used in living organisms as the building blocks of proteins. Proline is sometimes called an imino acid, although the IUPAC definition of an imine requires a carbon-nitrogen double bond. Proline is a non-essential amino acid that is synthesized from glutamic acid. It is an essential component of collagen and is important for proper functioning of joints and tendons. L-Proline is extremely important for the proper functioning of joints and tendons and also helps maintain and strengthen heart muscles. L-Proline is a major amino acid found in cartilage and is important for maintaining youthful skin as well as repair of muscle, connective tissue and skin damage. It is also essential for the immune system, and for necessary balance of this formula. It is an essential component of collagen and is important for proper functioning of joints and tendons. L-Proline is extremely important for the proper functioning of joints and tendons. Helps maintain and strengthen heart muscles. Glycogenic, by L-Proline oxidase in the kidney, it is ring-opened and is oxidized to form L-Glutamic acid. L-Ornithine and L-Glutamic acid are converted to L-Proline via L-Glutamic acid-gamma-semialdehyde. It is contained abundantly in collagen, and is intimately involved in the function of arthrosis and chordae.",The molecular weight is 115.13.,Proline has a topological polar surface area of 49.33.,The log p value of  is -2.41.,Proline is nutraceutical.,Proline is a solid.,True
14933,"Valaciclovir (valacyclovir), also known as _Valtrex_, is an antiviral drug that has been used to manage and treat various herpes infections for more than 2 decades. It was initially approved by the FDA in 1995 and marketed by GlaxoSmithKline. Valacyclovir is the L-valine ester of aciclovir. It is a member of the purine (guanine) nucleoside analog drug class. This class of drugs forms an important part of hepatitis, HIV, and cytomegalovirus drug regimens. Valacyclovir is a nucleoside analog DNA polymerase inhibitor indicated for :  **Antiviral effects** Valacyclovir is the L-valine ester of aciclovir. It is classified as a nucleoside analog DNA polymerase enzyme inhibitor. Aciclovir is a purine (guanine) nucleoside analog is a metabolite that heavily contributes to the pharmacological actions of valacyclovir. In fact, most of valacyclovir's activity is attributed to acyclovir.",,,,Valaciclovir is approved and investigational.,Valaciclovir is a solid.,True
14934,"Cyclosporine is a calcineurin inhibitor known for its immunomodulatory properties that prevent organ transplant rejection and treat various inflammatory and autoimmune conditions. It is isolated from the fungus _Beauveria nivea_. Initially manufactured by Sandoz and approved for use by the FDA in 1983, cyclosporine is now available in various products by Novartis (previously known as Sandoz). Cyclosporine is approved for a variety of conditions. Firstly, it is approved for the prophylaxis of organ rejection in allogeneic kidney, liver, and heart transplants. It is also used to prevent bone marrow transplant rejection. For the above indications, cyclosporine can be used in conjunction with azathioprine and corticosteroids. Finally, cyclosporine can be used in patients who have chronic transplant rejection and have received previous immunosuppressive therapy and to prevent or treat graft-versus-host disease (GVHD). Cyclosporine exerts potent immunosuppressive actions on T cells, thereby prolonging survival following organ and bone marrow transplants. This drug prevents and controls serious immune-mediated reactions including allograft rejection, graft versus host disease, and inflammatory autoimmune disease. Cyclosporine is a calcineurin inhibitor that inhibits T cell activation. Its binding to the receptor cyclophilin-1 inside cells produces a complex known as cyclosporine-cyclophilin. This complex subsequently inhibits calcineurin, which in turn stops the dephosphorylation as well as the activation of the nuclear factor of activated T cells (NF-AT) that normally cause inflammatory reactions. NF-AT is a transcription factor that promotes the production of cytokines such as IL-2, IL-4, interferon-gamma and TNF-alpha, all of which are involved in the inflammatory process. Specifically, the inhibition of IL-2, which is necessary for T cell activation or proliferation, is believed to be responsible for cyclosporine's immunosuppressive actions. In addition to the above, the inhibition of NF-AT leads to lower levels of other factors associated with T helper cell function and thymocyte development.",The molecular weight is 1202.64.,Cyclosporine has a topological polar surface area of 278.8.,The log p value of  is 14.36.,Cyclosporine is approved and investigational and vet_approved.,Cyclosporine is a solid.,True
14935,"Fluconazole, commonly known as _Diflucan_, is an antifungal drug used for the treatment of both systemic and superficial fungal infections in a variety of tissues. It was initially approved by the FDA in 1990. This drug is an _azole_ antifungal, in the same drug family as and. Fluconazole has many advantages over the other antifungal drugs including the option of oral administration. The side effect profile of this drug is minimal. It has been demonstrated as an efficacious treatment for vaginal yeast infections in one single dose. Fluconazole can be administered in the treatment of the following fungal infections: Fluconazole has been demonstrated to show fungistatic activity against the majority of strains of the following microorganisms, curing fungal infections: Fluconazole is a very selective inhibitor of fungal cytochrome P450 dependent enzyme _lanosterol 14-α-demethylase_. This enzyme normally works to convert _lanosterol_ to _ergosterol_, which is necessary for fungal cell wall synthesis. The free nitrogen atom located on the azole ring of fluconazole binds with a single iron atom located in the heme group of lanosterol 14-α-demethylase. This prevents oxygen activation and, as a result, inhibits the demethylation of lanosterol, halting the process of ergosterol biosynthesis. Methylated sterols are then found to accumulate in the fungal cellular membrane, leading to an arrest of fungal growth. These accumulated sterols negatively affect the structure and function of the fungal cell plasma membrane.",The molecular weight is 306.28.,Fluconazole has a topological polar surface area of 81.65.,The log p value of  is -0.44.,Fluconazole is approved and investigational.,Fluconazole is a solid.,True
14936,"Erythromycin is a bacteriostatic antibiotic drug produced by a strain of Saccharopolyspora erythraea (formerly Streptomyces erythraeus) and belongs to the macrolide group of antibiotics which consists of , , and others. It was originally discovered in 1952. Erythromycin is widely used for treating a variety of infections, including those caused by gram-positive and gram-negative bacteria. It is available for administration in various forms, including intravenous, topical, and eye drop preparations. Macrolides, such as erythromycin, stop bacterial growth by inhibiting protein synthesis and translation, treating bacterial infections. Erythromycin does not exert effects on nucleic acid synthesis. This drug has been shown to be active against most strains of the following microorganisms, effectively treating both in vitro and clinical infections. Despite this, it is important to perform bacterial susceptibility testing before administering this antibiotic, as resistance is a common issue that may affect treatment.  In order to replicate, bacteria require a specific process of protein synthesis, enabled by ribosomal proteins. Erythromycin acts by inhibition of protein synthesis by binding to the 23S ribosomal RNA molecule in the 50S subunit of ribosomes in susceptible bacterial organisms. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit. This results in the control of various bacterial infections. The strong affinity of macrolides, including erythromycin, for bacterial ribosomes, supports their broad‐spectrum antibacterial activities.",The molecular weight is 733.94.,Erythromycin has a topological polar surface area of 193.91.,The log p value of  is 1.61.,Erythromycin is approved and investigational and vet_approved.,Erythromycin is a solid.,True
14937,"In eliciting its mechanism of action, sildenafil ultimately prevents or minimizes the breakdown of cyclic guanosine monophosphate (cGMP) by inhibiting cGMP specific phosphodiesterase type 5 (PDE5). The result of doing so allows cGMP present in both the penis and pulmonary vasculature to elicit smooth muscle relaxation and vasodilation that subsequently facilitates relief in pulmonary arterial hypertension and the increased flow of blood into the spongy erectile tissue of the penis that consequently allows it to grow in size and become erect and rigid. Sildenafil is a phosphodiesterase-5 (PDE5) inhibitor that is predominantly employed for two primary indications: In vitro studies have shown that sildenafil is selective for phosphodiesterase-5 (PDE5). Its effect is more potent on PDE5 than on other known phosphodiesterases. In particular, there is a 10-times selectivity over PDE6 which is involved in the phototransduction pathway in the retina. There is an 80-times selectivity over PDE1, and over 700-times over PDE 2, 3, 4, 7, 8, 9, 10 and 11. And finally, sildenafil has greater than 4,000-times selectivity for PDE5 over PDE3, the cAMP-specific phosphodiesterase isoform involved in the control of cardiac contractility. Sildenafil is an oral therapy for erectile dysfunction. In the natural setting, i.e. with sexual stimulation, it restores impaired erectile function by increasing blood flow to the penis.",The molecular weight is 474.58.,Sildenafil has a topological polar surface area of 109.13.,The log p value of  is 1.98.,Sildenafil is approved and investigational.,Sildenafil is a solid.,True
14938,"An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria. Reserpine inhibits the uptake of norepinephrine into storage vesicles resulting in depletion of catecholamines and serotonin from central and peripheral axon terminals. It has been used as an antihypertensive and an antipsychotic as well as a research tool, but its adverse effects limit its clinical use. For the treatment of hypertension Reserpine is an adrenergic blocking agent used to treat mild to moderate hypertension via the disruption of norepinephrine vesicular storage. The antihypertensive actions of Reserpine are a result of its ability to deplete catecholamines from peripheral sympathetic nerve endings. These substances are normally involved in controlling heart rate, force of cardiac contraction and peripheral resistance. Reserpine's mechanism of action is through inhibition of the ATP/Mg<sup>2+</sup> pump responsible for the sequestering of neurotransmitters into storage vesicles located in the presynaptic neuron. The neurotransmitters that are not sequestered in the storage vesicle are readily metabolized by monoamine oxidase (MAO) causing a reduction in catecholamines.",The molecular weight is 608.69.,Reserpine has a topological polar surface area of 117.78.,The log p value of  is 3.86.,Reserpine is approved and investigational.,Reserpine is a solid.,True
14939,"A potent and specific HIV protease inhibitor that appears to have good oral bioavailability.  Indinavir is an antiretroviral drug for the treatment of HIV infection. Indinavir is a protease inhibitor with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Protease inhibitors block the part of HIV called protease. HIV-1 protease is an enzyme required for the proteolytic cleavage of the viral polyprotein precursors into the individual functional proteins found in infectious HIV-1. Indinavir binds to the protease active site and inhibits the activity of the enzyme. This inhibition prevents cleavage of the viral polyproteins resulting in the formation of immature non-infectious viral particles. Protease inhibitors are almost always used in combination with at least two other anti-HIV drugs. Indinavir inhibits the HIV viral protease enzyme which prevents cleavage of the gag-pol polyprotein, resulting in noninfectious, immature viral particles.",The molecular weight is 613.8.,Indinavir has a topological polar surface area of 118.03.,The log p value of  is 3.68.,Indinavir is approved.,Indinavir is a solid.,True
14940,"Ever since its discovery and availability for sale and use in the late 1940s, lidocaine has become an exceptionally commonly used medication. In particular, lidocaine's principal mode of action in acting as a local anesthetic that numbs the sensations of tissues means the agent is indicated for facilitating local anesthesia for a large variety of surgical procedures. It ultimately elicits its numbing activity by blocking sodium channels so that the neurons of local tissues that have the medication applied on are transiently incapable of signaling the brain regarding sensations. In doing so, however, it can block or decrease muscle contractile, resulting in effects like vasodilation, hypotension, and irregular heart rate, among others. As a result, lidocaine is also considered a class Ib anti-arrhythmic agent. Nevertheless, lidocaine's local anesthetic action sees its use in many medical situations or circumstances that may benefit from its action, including the treatment of premature ejaculation. Lidocaine is an anesthetic of the amide group indicated for production of local or regional anesthesia by infiltration techniques such as percutaneous injection and intravenous regional anesthesia by peripheral nerve block techniques such as brachial plexus and intercostal and by central neural techniques such as lumbar and caudal epidural blocks. Excessive blood levels of lidocaine can cause changes in cardiac output, total peripheral resistance, and mean arterial pressure. With central neural blockade these changes may be attributable to the block of autonomic fibers, a direct depressant effect of the local anesthetic agent on various components of the cardiovascular system, and/or the beta-adrenergic receptor stimulating action of epinephrine when present. The net effect is normally a modest hypotension when the recommended dosages are not exceeded. Lidocaine is a local anesthetic of the amide type. It is used to provide local anesthesia by nerve blockade at various sites in the body. It does so by stabilizing the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses, thereby effecting local anesthetic action. In particular, the lidocaine agent acts on sodium ion channels located on the internal surface of nerve cell membranes. At these channels, neutral uncharged lidocaine molecules diffuse through neural sheaths into the axoplasm where they are subsequently ionized by joining with hydrogen ions. The resultant lidocaine cations are then capable of reversibly binding the sodium channels from the inside, keeping them locked in an open state that prevents nerve depolarization. As a result, with sufficient blockage, the membrane of the postsynaptic neuron will ultimately not depolarize and will thus fail to transmit an action potential. This facilitates an anesthetic effect by not merely preventing pain signals from propagating to the brain but by aborting their generation in the first place.",The molecular weight is 234.34.,Lidocaine has a topological polar surface area of 32.34.,The log p value of  is 1.95.,Lidocaine is approved and vet_approved.,Lidocaine is a solid.,True
14941,"Amcinonide is a corticosteroid. For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Amcinonide is a topical corticosteroid. The topical corticosteroids constitute a class of primarily synthetic steroids used as anti-inflammatory and antipruritic agents. Amcinonide reduces or inhibits the actions of chemicals in the body that cause inflammation, redness, and swelling. The mechanism of anti-inflammatory activity of the topical corticosteroids is unclear. Various laboratory methods, including vasoconstrictor assays, are used to compare and predict potencies and/or clinical efficacies of the topical corticosteroids. There is some evidence to suggest that a recognizable correlation exists between vasoconstrictor potency and therapeutic efficacy in man. When in an ointment form, amcinonide also helps the skin maintain moisture. The mechanism of the anti-inflammatory activity of the topical steroids, in general, is unclear. However, corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor, arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2. Amcinonide has affinity for the glucocorticoid receptor. It has weak affinity for the progesterone receptor, and virtually no affinity for the mineralocorticoid, estrogen, or androgen receptors.",The molecular weight is 502.58.,Amcinonide has a topological polar surface area of 99.13.,The log p value of  is 2.88.,Amcinonide is approved.,Amcinonide is a solid.,True
14942,"In the U.S., Terfenadine was superseded by fexofenadine in the 1990s due to the risk of cardiac arrhythmia caused by QT interval prolongation. For the treatment of allergic rhinitis, hay fever, and allergic skin disorders. Terfenadine, an H1-receptor antagonist antihistamine, is similar in structure to astemizole and haloperidol, a butyrophenone antipsychotic. The active metabolite of terfenadine is fexofenadine. Terfenadine competes with histamine for binding at H1-receptor sites in the GI tract, uterus, large blood vessels, and bronchial muscle. This reversible binding of terfenadine to H1-receptors suppresses the formation of edema, flare, and pruritus resulting from histaminic activity. As the drug does not readily cross the blood-brain barrier, CNS depression is minimal.",The molecular weight is 471.68.,Terfenadine has a topological polar surface area of 43.7.,The log p value of  is 6.07.,Terfenadine is approved and withdrawn.,Terfenadine is a solid.,True
14943,"Levonorgestrel (LNG) is a synthetic progestogen similar to used in contraception and hormone therapy. Also known as Plan B, it is used as a single agent in emergency contraception, and as a hormonal contraceptive released from an intrauterine device, commonly referred to as an IUD. Some of these devices are known as Jaydess, Kyleena, and Mirena. A subdermal implant of levonorgestrel that slowly releases the hormone over a long-term period is also available. In addition to the above uses, levonorgestrel is used as a component of long-term combination contraceptives.  **Emergency contraception** Levonorgestrel prevents pregnancy by interfering with ovulation, fertilization, and implantation. The levonorgestrel-only containing emergency contraceptive tablet is 89% effective if it is used according to prescribing information within 72 hours after intercourse. The intrauterine and implantable devices releasing levonorgestrel are more than 99% in preventing pregnancy. Levonorgestrel utilized as a component of hormonal therapy helps to prevent endometrial carcinoma associated with unopposed estrogen administration. **Mechanism of action on ovulation**",The molecular weight is 312.45.,Levonorgestrel has a topological polar surface area of 37.3.,The log p value of  is 3.32.,Levonorgestrel is approved and investigational.,Levonorgestrel is a solid.,True
14944,"Amlodipine, initially approved by the FDA in 1987, is a popular antihypertensive drug belonging to the group of drugs called _dihydropyridine calcium channel blockers_. Due to their selectivity for the peripheral blood vessels, dihydropyridine calcium channel blockers are associated with a lower incidence of myocardial depression and cardiac conduction abnormalities than other calcium channel blockers. Amlodipine may be used alone or in combination with other antihypertensive and antianginal agents for the treatment of the following conditions : **General pharmacodynamic effects** **Mechanism of action on blood pressure**",The molecular weight is 408.88.,Amlodipine has a topological polar surface area of 99.88.,The log p value of  is 3.43.,Amlodipine is approved.,Amlodipine is a solid.,True
14945,"Sorafenib (rINN), marketed as Nexavar by Bayer, is a drug approved for the treatment of advanced renal cell carcinoma (primary kidney cancer). It has also received \Fast Track\"" designation by the FDA for the treatment of advanced hepatocellular carcinoma (primary liver cancer), and has since performed well in Phase III trials."" Sorafenib is indicated for the treatment of unresectable hepatocellular carcinoma and advanced renal cell carcinoma.  No large changes in QTc interval were observed. After one 28-day treatment cycle, the largest mean QTc interval change of 8.5 ms (upper bound of two-sided 90% confidence interval, 13.3 ms) was observed at 6 hours post-dose on day 1 of cycle 2.  Sorafenib interacts with multiple intracellular (CRAF, BRAF and mutant BRAF) and cell surface kinases (KIT, FLT-3, VEGFR-2, VEGFR-3, and PDGFR-&szlig;). Several of these kinases are thought to be involved in angiogenesis, thus sorafenib reduces blood flow to the tumor. Sorafenib is unique in targeting the Raf/Mek/Erk pathway. By inhibiting these kinases, genetic transcription involving cell proliferation and angiogenesis is inhibited.",The molecular weight is 464.83.,Sorafenib has a topological polar surface area of 92.35.,The log p value of  is 5.46.,Sorafenib is approved and investigational.,Sorafenib is a solid.,True
14946,"Nisoldipine is a 1,4-dihydropyridine calcium channel blocker. It acts primarily on vascular smooth muscle cells by stabilizing voltage-gated L-type calcium channels in their inactive conformation. By inhibiting the influx of calcium in smooth muscle cells, nisoldipine prevents calcium-dependent smooth muscle contraction and subsequent vasoconstriction. Nisoldipine may be used in alone or in combination with other agents in the management of hypertension. For the treatment of hypertension. It may be used alone or in combination with other antihypertensive agents. Nisoldipine, a dihydropyridine calcium-channel blocker, is used alone or with an angiotensin-converting enzyme inhibitor, to treat hypertension, chronic stable angina pectoris, and Prinzmetal's variant angina. Nisoldipine is similar to other peripheral vasodilators. Nisoldipine inhibits the influx of extra cellular calcium across the myocardial and vascular smooth muscle cell membranes possibly by deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum. The decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload. By deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum, Nisoldipine inhibits the influx of extracellular calcium across the myocardial and vascular smooth muscle cell membranes The decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload.",The molecular weight is 388.42.,Nisoldipine has a topological polar surface area of 107.77.,The log p value of  is 4.58.,Nisoldipine is approved.,Nisoldipine is a solid.,True
14947,"On August 8, 2001 the U.S. Food and Drug Administration (FDA) announced that Bayer Pharmaceutical Division voluntarily withdrew Baycol from the U.S. market, due to reports of fatal Rhabdomyolysis, a severe adverse reaction from this cholesterol-lowering (lipid-lowering) product. It has also been withdrawn from the Canadian market. Used as an adjunct to diet for the reduction of elevated total and LDL cholesterol levels in patients with primary hypercholesterolemia and mixed dyslipidemia (Fredrickson Types IIa and IIb) when the response to dietary restriction of saturated fat and cholesterol and other non-pharmacological measures alone has been inadequate. Cerivastatin, a competitive HMG-CoA reductase inhibitor effective in lowering LDL cholesterol and triglycerides, is used to treat primary hypercholesterolemia and mixed dyslipidemia (Fredrickson types IIa and IIb). Cerivastatin competitively inhibits hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase, the hepatic enzyme responsible for converting HMG-CoA to mevalonate. As mevalonate is a precursor of sterols such as cholesterol, this results in a decrease in cholesterol in hepatic cells, upregulation of LDL-receptors, and an increase in hepatic uptake of LDL-cholesterol from the circulation.",The molecular weight is 459.56.,Cerivastatin has a topological polar surface area of 99.88.,The log p value of  is 3.56.,Cerivastatin is approved and withdrawn.,Cerivastatin is a solid.,True
14948,"Teniposide is a semisynthetic derivative of podophyllotoxin that exhibits antitumor activity. Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent cells from entering into the mitotic phase of the cell cycle, and lead to cell death. Teniposide acts primarily in the G2 and S phases of the cycle. Teniposide is used for the treatment of refractory acute lymphoblastic leukaemia Teniposide is a phase-specific cytotoxic drug, acting in the late S or early G 2 phase of the cell cycle. Teniposide prevents cell mitosis by causing single and double stranded DNA breaks as well as cross linking between protein and DNA. The mechanism of action appears to be related to the inhibition of type II topoisomerase activity since teniposide does not intercalate into DNA or bind strongly to DNA. Teniposide binds to and inhibits DNA topoisomerase II. The cytotoxic effects of teniposide are related to the relative number of double-stranded DNA breaks produced in cells, which are a reflection of the stabilization of a topoisomerase II-DNA intermediate.",The molecular weight is 656.66.,Teniposide has a topological polar surface area of 160.83.,The log p value of  is 0.57.,Teniposide is approved.,Teniposide is a solid.,True
14949,"An antibiotic first isolated from cultures of _Streptomyces venequelae_ in 1947 but now produced synthetically. It has a relatively simple structure and was the first broad-spectrum antibiotic to be discovered. It acts by interfering with bacterial protein synthesis and is mainly bacteriostatic. (From Martindale, The Extra Pharmacopoeia, 29th ed, p106) Used in treatment of cholera, as it destroys the vibrios and decreases the diarrhea. It is effective against tetracycline-resistant vibrios. It is also used in eye drops or ointment to treat bacterial conjunctivitis. Chloramphenicol is a broad-spectrum antibiotic that was derived from the bacterium Streptomyces venezuelae and is now produced synthetically. Chloramphenicol is effective against a wide variety of microorganisms, but due to serious side-effects (e.g., damage to the bone marrow, including aplastic anemia) in humans, it is usually reserved for the treatment of serious and life-threatening infections (e.g., typhoid fever). Chloramphenicol is bacteriostatic but may be bactericidal in high concentrations or when used against highly susceptible organisms. Chloramphenicol stops bacterial growth by binding to the bacterial ribosome (blocking peptidyl transferase) and inhibiting protein synthesis. Chloramphenicol is lipid-soluble, allowing it to diffuse through the bacterial cell membrane. It then reversibly binds to the L16 protein of the 50S subunit of bacterial ribosomes, where transfer of amino acids to growing peptide chains is prevented (perhaps by suppression of peptidyl transferase activity), thus inhibiting peptide bond formation and subsequent protein synthesis.",The molecular weight is 323.13.,Chloramphenicol has a topological polar surface area of 115.38.,The log p value of  is 1.28.,Chloramphenicol is approved and vet_approved.,Chloramphenicol is a solid.,True
14950,"Loratadine is a second generation antihistamine used to manage symptoms of allergic rhinitis. A lack of sedative and CNS adverse effects make loratadine, along with other second generation antihistamines, preferable over their 1st generation counterparts in many clinical situations. Loratadine is a 2nd generation antihistamine and is used to manage symptoms of allergic rhinitis, wheal formation, urticaria, and other allergic dermatologic conditions.  Like other 2nd generation antihistamines, loratadine is selective for peripheral H1 receptors. Loratadine does not penetrate effectively into the central nervous system and has poor affinity for CNS H1-receptors. These qualities result in a lack of CNS depressant effects such as drowsiness, sedation, and impaired psychomotor function. Histamine release is a key mediator in allergic rhinitis and urticaria. As a result, loratadine exerts it's effect by targeting H1 histamine receptors.",The molecular weight is 382.89.,Loratadine has a topological polar surface area of 42.43.,The log p value of  is 5.05.,Loratadine is approved and investigational.,Loratadine is a solid.,True
14951,"An alkaloid derived from the bark of the cinchona tree. It is used as an antimalarial drug, and is the active ingredient in extracts of the cinchona that have been used for that purpose since before 1633. Quinine is also a mild antipyretic and analgesic and has been used in common cold preparations for that purpose. It was used commonly and as a bitter and flavoring agent, and is still useful for the treatment of babesiosis. Quinine is also useful in some muscular disorders, especially nocturnal leg cramps and myotonia congenita, because of its direct effects on muscle membrane and sodium channels. The mechanisms of its antimalarial effects are not well understood. For the treatment of malaria and leg cramps Quinine is used parenterally to treat life-threatening infections caused by chloroquine-resistant Plasmodium falciparum malaria. Quinine acts as a blood schizonticide although it also has gametocytocidal activity against P. vivax and P. malariae. Because it is a weak base, it is concentrated in the food vacuoles of P. falciparum. It is thought to act by inhibiting heme polymerase, thereby allowing accumulation of its cytotoxic substrate, heme. As a schizonticidal drug, it is less effective and more toxic than chloroquine. However, it has a special place in the management of severe falciparum malaria in areas with known resistance to chloroquine. The theorized mechanism of action for quinine and related anti-malarial drugs is that these drugs are toxic to the malaria parasite. Specifically, the drugs interfere with the parasite's ability to break down and digest hemoglobin. Consequently, the parasite starves and/or builds up toxic levels of partially degraded hemoglobin in itself. ",The molecular weight is 324.42.,Quinine has a topological polar surface area of 45.59.,The log p value of  is 2.79.,Quinine is approved.,Quinine is a solid.,True
14952,"Haloperidol is a high potency first-generation (typical) antipsychotic and one of the most frequently used antipsychotic medications used worldwide. While haloperidol has demonstrated pharmacologic activity at a number of receptors in the brain, it exerts its antipsychotic effect through its strong antagonism of the dopamine receptor (mainly D2), particularly within the mesolimbic and mesocortical systems of the brain. Haloperidol is indicated for the treatment of the manifestations of several psychotic disorders including schizophrenia, acute psychosis, Tourette syndrome, and other severe behavioural states. It is also used off-label for the management of chorea associated with Huntington's disease and for the treatment of intractable hiccups as it is a potent antiemetic. Dopamine-antagonizing medications such as haloperidol are though to improve psychotic symptoms and states that are caused by an over-production of dopamine, such as schizophrenia, which is theorized to be caused by a hyperdopaminergic state within the limbic system of the brain. Haloperidol is indicated for a number of conditions including for the treatment of schizophrenia, for the manifestations of psychotic disorders, for the control of tics and vocal utterances of Tourette’s Disorder in children and adults, for treatment of severe behavior problems in children of combative, explosive hyperexcitability (which cannot be accounted for by immediate provocation). Haloperidol is also indicated in the short-term treatment of hyperactive children who show excessive motor activity with accompanying conduct disorders consisting of some or all of the following symptoms: impulsivity, difficulty sustaining attention, aggressivity, mood lability, and poor frustration tolerance. Haloperidol should be reserved for these two groups of children only after failure to respond to psychotherapy or medications other than antipsychotics. Use of the first-generation antipsychotics (including haloperidol) is considered highly effective for the management of the \positive\"" symptoms of schizophrenia including hallucinations, hearing voices, aggression/hostility, disorganized speech, and psychomotor agitation. However, this class is limited by the development of movement disorders such as drug-induced parkinsonism, akathisia, dystonia, and tardive dyskinesia, and other side effects including sedation, weight gain, and prolactin changes. Compared to the lower-potency first-generation antipsychotics such as , , , and , haloperidol typically demonstrates the least amount of side effects within class, but demonstrates a stronger disposition for causing extrapyramidal symptoms (EPS). Low‐potency medications have a lower affinity for dopamine receptors so that a higher dose is required to effectively treat symptoms of schizophrenia. In addition, they block many receptors other than the primary target (dopamine receptors), such as cholinergic or histaminergic receptors, resulting in a higher incidence of side effects such as sedation, weight gain, and hypotension."" While haloperidol has demonstrated pharmacologic activity at a number of receptors in the brain, it exerts its antipsychotic effect through its strong antagonism of the dopamine receptor (mainly D2), particularly within the mesolimbic and mesocortical systems of the brain. Schizophrenia is theorized to be caused by a hyperdopaminergic state within the limbic system of the brain. Dopamine-antagonizing medications such as haloperidol, therefore, are thought to improve psychotic symptoms by halting this over-production of dopamine. The optimal clinical efficacy of antipsychotics is associated with the blockade of approximately 60 % - 80 % of D2 receptors in the brain.",The molecular weight is 375.87.,Haloperidol has a topological polar surface area of 40.54.,The log p value of  is 3.85.,Haloperidol is approved.,Haloperidol is a solid.,True
14953,"Lercanidipine is a calcium channel blocker of the dihydropyridine class. It is sold under various commercial names including Zanidip. For the treatment of Hypertension, management of angina pectoris and Raynaud's syndrome Lercanidipine, a dihydropyridine calcium-channel blocker, is used alone or with an angiotensin-converting enzyme inhibitor, to treat hypertension, chronic stable angina pectoris, and Prinzmetal's variant angina. Lercanidipine is similar to other peripheral vasodilators. Lercanidipine inhibits the influx of extra cellular calcium across the myocardial and vascular smooth muscle cell membranes possibly by deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum. The decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload. By deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum, Lercanidipine inhibits the influx of extracellular calcium across the myocardial and vascular smooth muscle cell membranes The decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload.",The molecular weight is 611.74.,Lercanidipine has a topological polar surface area of 111.01.,The log p value of  is 8.0.,Lercanidipine is approved and investigational.,Lercanidipine is a solid.,True
14954,"Precursor of an alkylating nitrogen mustard antineoplastic and immunosuppressive agent that must be activated in the liver to form the active aldophosphamide. It has been used in the treatment of lymphoma and leukemia. Its side effect, alopecia, has been used for defleecing sheep. Cyclophosphamide may also cause sterility, birth defects, mutations, and cancer. Cyclophosphamide is indicated for the treatment of malignant lymphomas, multiple myeloma, leukemias, mycosis fungoides (advanced disease), neuroblastoma (disseminated disease), adenocarcinoma of the ovary, retinoblastoma, and carcinoma of the breast. It is also indicated for the treatment of biopsy-proven minimal change nephrotic syndrome in pediatric patients.  Cyclophosphamide is an antineoplastic in the class of alkylating agents and is used to treat various forms of cancer. Alkylating agents are so named because of their ability to add alkyl groups to many electronegative groups under conditions present in cells. They stop tumor growth by cross-linking guanine bases in DNA double-helix strands - directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. In addition, these drugs add methyl or other alkyl groups onto molecules where they do not belong which in turn inhibits their correct utilization by base pairing and causes a miscoding of DNA. Alkylating agents are cell cycle-nonspecific. Alkylating agents work by three different mechanisms all of which achieve the same end result - disruption of DNA function and cell death. Alkylating agents work by three different mechanisms: 1) attachment of alkyl groups to DNA bases, resulting in the DNA being fragmented by repair enzymes in their attempts to replace the alkylated bases, preventing DNA synthesis and RNA transcription from the affected DNA, 2) DNA damage via the formation of cross-links (bonds between atoms in the DNA) which prevents DNA from being separated for synthesis or transcription, and 3) the induction of mispairing of the nucleotides leading to mutations.",The molecular weight is 261.08.,Cyclophosphamide has a topological polar surface area of 41.57.,The log p value of  is 0.8.,Cyclophosphamide is approved and investigational.,Cyclophosphamide is a solid.,True
14955,"Vincristine is an antitumor vinca alkaloid isolated from Vinca Rosea. It is marketed under several brand names, many of which have different formulations such as Marqibo (liposomal injection) and Vincasar. Vincristine is indicated for the treatment of acute leukaemia, malignant lymphoma, Hodgkin's disease, acute erythraemia, and acute panmyelosis. vincristine sulfate is often chosen as part of polychemotherapy because of lack of significant bone–marrow suppression (at recommended doses) and of unique clinical toxicity (neuropathy). Treatment of acute lymphocytic leukemia (ALL), Hodgkin lymphoma, non-Hodgkin lymphomas, Wilms' tumor, neuroblastoma, rhabdomyosarcoma. Liposomal vincristine is indicated for the treatment of relapsed Philadelphia chromosome-negative (Ph-) acute lymphoblastic leukemia (ALL).  Vincristine is a vinca alkaloid antineoplastic agent used as a treatment for various cancers including breast cancer, Hodgkin's disease, Kaposi's sarcoma, and testicular cancer. The vinca alkaloids are structurally similar compounds comprised of 2 multiringed units, vindoline and catharanthine. The vinca alkaloids have become clinically useful since the discovery of their antitumour properties in 1959. Initially, extracts of the periwinkle plant (Catharanthus roseus) were investigated because of putative hypoglycemic properties, but were noted to cause marrow suppression in rats and antileukemic effects <i>in vitro</i>. Vincristine binds to the microtubular proteins of the mitotic spindle, leading to crystallization of the microtubule and mitotic arrest or cell death. Vincristine has some immunosuppressant effect. The vinca alkaloids are considered to be cell cycle phase-specific. The antitumor activity of Vincristine is thought to be due primarily to inhibition of mitosis at metaphase through its interaction with tubulin. Like other vinca alkaloids, Vincristine may also interfere with: 1) amino acid, cyclic AMP, and glutathione metabolism, 2) calmodulin-dependent Ca<sup>2+</sup>-transport ATPase activity, 3) cellular respiration, and 4) nucleic acid and lipid biosynthesis.",The molecular weight is 824.97.,Vincristine has a topological polar surface area of 171.17.,The log p value of  is 4.04.,Vincristine is approved and investigational.,Vincristine is a solid.,True
14956,"Carbamazepine, also known as Tegretol, is an anticonvulsant drug and analgesic drug used to control seizures and to treat pain resulting from trigeminal neuralgia. It was initially approved by the FDA in 1965. Aside from the above uses, this drug is also given to control the symptoms of bipolar 1. Interestingly, carbamazepine was the first anticonvulsant used to treat individuals with bipolar disorder. Carbamazepine is indicated for the treatment of epilepsy and pain associated with true trigeminal neuralgia. In particular, carbamazepine has shown efficacy in treating mixed seizures, partial seizures with complex symptoms, and generalized tonic-clonic seizures. Carbamazepine is also indicated for the treatment of manic episodes and mixed manic-depressive episodes caused by bipolar I disorder. Some off-label, unapproved uses of carbamazepine include the treatment of alcohol withdrawal syndrome and restless leg syndrome. **General effects** Carbamazepine's mechanism of action is not fully elucidated and is widely debated. One major hypothesis is that carbamazepine inhibits sodium channel firing, treating seizure activity. Animal research studies have demonstrated that carbamazepine exerts its effects by lowering polysynaptic nerve response and inhibiting post-tetanic potentiation. In both cats and rats, carbamazepine was shown to decrease pain caused by infraorbital nerve stimulation. A decrease in the action potential in the nucleus ventralis of the thalamus in the brain and inhibition of the lingual mandibular reflex were observed in other studies after carbamazepine use. Carbamazepine causes the above effects by binding to voltage-dependent sodium channels and preventing action potentials, which normally lead to stimulatory effects on nerves. In bipolar disorder, carbamazepine is thought to increase dopamine turnover and increase GABA transmission, treating manic and depressive symptoms.",The molecular weight is 236.27.,Carbamazepine has a topological polar surface area of 46.33.,The log p value of  is 2.38.,Carbamazepine is approved and investigational.,Carbamazepine is a solid.,True
14957,"Dravet syndrome is a pediatric encephalopathy that typically manifests within the first year of life following exposure to elevated temperatures. It is characterized by recurrent pharmacoresistant seizures, which increase in frequency and severity with disease progression. Concomitantly with these seizures, patients typically display delayed development and neurocognitive impairment. Fenfluramine is a serotonergic phenethylamine originally used as an appetite suppressant until concerns regarding cardiotoxicity in obese patients lead to its withdrawal from the market in 1997. Through its ability to modulate neurotransmission, fenfluramine has reemerged as an effective therapy against pharmacoresistant seizures, such as those involved in Dravet syndrome. Fenfluramine is indicated for the treatment of seizures in Dravet syndrome patients aged two years and older. Fenfluramine increases extracellular serotonin levels, and also acts as both a serotonergic 5-HT<sub>2</sub> receptor agonist and σ1 receptor antagonist. These activities, through an incompletely understood mechanism, lead to anti-epileptiform activity and therapeutic benefit. This modulation has other effects such as decreased appetite, weight loss, sedation, lethargy, increased blood pressure, and mood alteration including possible suicidal ideation. There is a risk of glaucoma and potentially fatal serotonin syndrome. Fenfluramine should be gradually withdrawn following treatment alteration or cessation. Dravet syndrome is a complex pediatric encephalopathy characterized by recurrent pharmacoresistant seizures of variable type, delayed development, and in many cases, impairment in speech, language, gait, and other neurocognitive functions. Despite substantial variation in presentation and severity, roughly 80% of patients with Dravet syndrome have mutations in the _SCN1A_ gene, which encodes the alpha subunit of a voltage-gated sodium channel (Na<sub>v</sub>1.1). This channel is predominantly localized in inhibitory GABAergic interneurons as well as in excitatory pyramidal neurons; it is thought that dysfunction of neurotransmission regulation results in the seizures and other corresponding symptoms of Dravet syndrome.",The molecular weight is 231.26.,Fenfluramine has a topological polar surface area of 12.03.,The log p value of  is 3.3.,Fenfluramine is approved and illicit and investigational and withdrawn.,Fenfluramine is a solid.,True
14958,"In many countries (including Canada) cisapride has been either withdrawn or has had its indications limited due to reports about long QT syndrome due to cisapride, which predisposes to arrhythmias. The FDA issued a warning letter regarding this risk to health care professionals and patients. For the symptomatic treatment of adult patients with nocturnal heartburn due to gastroesophageal reflux disease. Cisapride is a parasympathomimetic which acts as a serotonin 5-HT<sub>4</sub> agonist; upon activation of the receptor signaling pathway, cisapride promotes the release of acetylcholine neurotransmitters in the enteric nervous system. Cisapride stimulates motility of the upper gastrointestinal tract without stimulating gastric, biliary, or pancreatic secretions. Cisapride increases the tone and amplitude of gastric (especially antral) contractions, relaxes the pyloric sphincter and the duodenal bulb, and increases peristalsis of the duodenum and jejunum resulting in accelerated gastric emptying and intestinal transit. It increases the resting tone of the lower esophageal sphincter. It has little, if any, effect on the motility of the colon or gallbladder. Cisapride does not induce muscarinic or nicotinic receptor stimulation, nor does it inhibit acetylcholinesterase activity. Cisapride acts through the stimulation of the serotonin 5-HT<sub>4</sub> receptors which increases acetylcholine release in the enteric nervous system (specifically the myenteric plexus). This results in increased tone and amplitude of gastric (especially antral) contractions, relaxation of the pyloric sphincter and the duodenal bulb, and increased peristalsis of the duodenum and jejunum resulting in accelerated gastric emptying and intestinal transit.",The molecular weight is 465.95.,Cisapride has a topological polar surface area of 86.05.,The log p value of  is 3.81.,Cisapride is approved and investigational and withdrawn.,Cisapride is a solid.,True
14959,"A potent calcium channel blockader with marked vasodilator action. It has antihypertensive properties and is effective in the treatment of angina and coronary spasms without showing cardiodepressant effects. It has also been used in the treatment of asthma and enhances the action of specific antineoplastic agents.  Used for the management of patients with chronic stable angina and for the treatment of hypertension. Nicardipine, a dihydropyridine calcium-channel blocker, is used alone or with an angiotensin-converting enzyme inhibitor, to treat hypertension, chronic stable angina pectoris, and Prinzmetal's variant angina. Nicardipine is similar to other peripheral vasodilators. Nicardipine inhibits the influx of extra cellular calcium across the myocardial and vascular smooth muscle cell membranes possibly by deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum. The decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload. By deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum, nicardipine inhibits the influx of extracellular calcium across the myocardial and vascular smooth muscle cell membranes The decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload.",The molecular weight is 479.53.,Nicardipine has a topological polar surface area of 111.01.,The log p value of  is 5.23.,Nicardipine is approved and investigational.,Nicardipine is a solid.,True
14960,"Astemizole is a long-acting, non-sedating second generation antihistamine used in the treatment of allergy symptoms. It was withdrawn from market by the manufacturer in 1999 due to the potential to cause arrhythmias at high doses, especially when when taken with CYP inhibitors or grapefruit juice. Astemizole was indicated for use in the relieving allergy symptoms, particularly rhinitis and conjunctivitis. It has been withdrawn from the market however due to concerns of arrhythmias. Astemizole is a second generation H<sub>1</sub>-receptor antagonist. It does not significantly cross the blood brain barrier and therefore does not cause drowsiness or CNS depression at normal doses. Astemizole competes with histamine for binding at H<sub>1</sub>-receptor sites in the GI tract, uterus, large blood vessels, and bronchial muscle. This reversible binding of astemizole to H<sub>1</sub>-receptors suppresses the formation of edema, flare, and pruritus resulting from histaminic activity. As the drug does not readily cross the blood-brain barrier and preferentially binds at H1 receptors in the peripehery rather than within the brain, CNS depression is minimal. Astemizole may also act on H<sub>3</sub>-receptors, producing adverse effects.",The molecular weight is 458.58.,Astemizole has a topological polar surface area of 42.32.,The log p value of  is 5.84.,Astemizole is approved and withdrawn.,Astemizole is a solid.,True
14961,"Simvastatin, also known as the brand name product Zocor, is a lipid-lowering drug derived synthetically from a fermentation product of _Aspergillus terreus_. It belongs to the statin class of medications, which are used to lower the risk of cardiovascular disease and manage abnormal lipid levels by inhibiting the endogenous production of cholesterol in the liver. More specifically, statin medications competitively inhibit the enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) Reductase, which catalyzes the conversion of HMG-CoA to mevalonic acid and is the third step in a sequence of metabolic reactions involved in the production of several compounds involved in lipid metabolism and transport including cholesterol, low-density lipoprotein (LDL) (sometimes referred to as \bad cholesterol\""), and very low-density lipoprotein (VLDL). Prescribing of statin medications is considered standard practice following any cardiovascular events and for people with a moderate to high risk of development of CVD, such as those with Type 2 Diabetes. The clear evidence of the benefit of statin use coupled with very minimal side effects or long term effects has resulted in this class becoming one of the most widely prescribed medications in North America."" Simvastatin is indicated for the treatment of hyperlipidemia to reduce elevated total cholesterol (total-C), low-density lipoprotein cholesterol (LDL‑C), apolipoprotein B (Apo B), and triglycerides (TG), and to increase high-density lipoprotein cholesterol (HDL-C). Simvastatin is an oral antilipemic agent which inhibits HMG-CoA reductase. It is used to lower total cholesterol, low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (apoB), non-high density lipoprotein-cholesterol (non-HDL-C), and trigleride (TG) plasma concentrations while increasing HDL-C concentrations. High LDL-C, low HDL-C and high TG concentrations in the plasma are associated with increased risk of atherosclerosis and cardiovascular disease. The total cholesterol to HDL-C ratio is a strong predictor of coronary artery disease and high ratios are associated with higher risk of disease. Increased levels of HDL-C are associated with lower cardiovascular risk. By decreasing LDL-C and TG and increasing HDL-C, rosuvastatin reduces the risk of cardiovascular morbidity and mortality. Simvastatin is a prodrug in which the 6-membered lactone ring of simvastatin is hydrolyzed <i>in vivo</i> to generate the beta,delta-dihydroxy acid, an active metabolite structurally similar to HMG-CoA (hydroxymethylglutaryl CoA). Once hydrolyzed, simvastatin competes with HMG-CoA for HMG-CoA reductase, a hepatic microsomal enzyme, which catalyzes the conversion of HMG-CoA to mevalonate, an early rate-limiting step in cholesterol biosynthesis. Simvastatin acts primarily in the liver, where decreased hepatic cholesterol concentrations stimulate the upregulation of hepatic low density lipoprotein (LDL) receptors which increases hepatic uptake of LDL. Simvastatin also inhibits hepatic synthesis of very low density lipoprotein (VLDL). The overall effect is a decrease in plasma LDL and VLDL. ",The molecular weight is 418.57.,Simvastatin has a topological polar surface area of 72.83.,The log p value of  is 4.48.,Simvastatin is approved.,Simvastatin is a solid.,True
14962,"Trazodone is triazolopyridine derivative from the serotonin receptor antagonists and reuptake inhibitors (SARIs) class of antidepressants. It is used in adults and has been shown to be comparable in efficacy to other drugs such as tricyclic antidepressants (TCAs), selective serotonin reuptake inhibitors (SSRIs), and serotonin-norepinephrine receptor inhibitor (SNRIs) in the treatment of depression. A unique feature of this drug is that it does not promote the anxiety symptoms, sexual symptoms, or insomnia, which are commonly associated with SSRI and SNRI therapy. Trazodone acts on various receptors, including certain histamine, serotonin, and adrenergic receptors, distinguishing it from other antidepressants that cover a narrow range of neurotransmitters. It was initially granted FDA approval in 1981. Trazodone is indicated for the treatment of major depressive disorder (MDD). It has been used off-label for adjunct therapy in alcohol dependence, and off-label to treat anxiety and insomnia. It may also be used off-label to treat symptoms of dementia, Alzheimer’s disease, schizophrenia, eating disorders, and fibromyalgia due to its effects on various neurotransmitter receptors. Trazodone treats depressed mood and other depression-related symptoms and shows benefit in the treatment of insomnia due to its sedating effects. It is known to prolong the cardiac QT-interval. Memory, alertness, and cognition may be decreased by trazodone, especially in elderly patients due to its central nervous system depressant effects. The mechanism of action of trazodone is not fully understood, however, it is known to inhibit the reuptake of serotonin and block both histamine and alpha-1-adrenergic receptors. Despite the fact that trazodone is frequently considered a selective serotonin reuptake inhibitor, several reports have shown that other mechanisms including antagonism at serotonin 5-HT1a, 5-HT1c, and 5-HT2 receptor subtypes may occur. The strongest antagonism of trazodone is reported to occur at the serotonin ",The molecular weight is 371.87.,Trazodone has a topological polar surface area of 42.39.,The log p value of  is 3.85.,Trazodone is approved and investigational.,Trazodone is a solid.,True
14963,"Midazolam is a short-acting hypnotic-sedative drug with anxiolytic, muscle relaxant, anticonvulsant, sedative, hypnotic, and amnesic properties. It belongs to a class of drugs called _benzodiazepines_. This drug is unique from others in this class due to its rapid onset of effects and short duration of action. Midazolam is available by oral, rectal, intranasal, intramuscular (IM), and intravenous (IV) routes and has been used in various biomedical applications, including dentistry, cardiac surgery, and endoscopic procedures as pre-anesthetic medication, and as an adjunct to local anesthesia. **Intravenous**  **General effects** The actions of benzodiazepines such as midazolam are mediated through the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), which is one of the major inhibitory neurotransmitters in the central nervous system. Benzodiazepines increase the activity of GABA, thereby producing a sedating effect, relaxing skeletal muscles, and inducing sleep, anesthesia, and amnesia. Benzodiazepines bind to the benzodiazepine site on GABA-A receptors, which potentiates the effects of GABA by increasing the frequency of chloride channel opening. These receptors have been identified in different body tissues including the heart and skeletal muscle, although mainly appear to be present in the central nervous system.",The molecular weight is 325.77.,Midazolam has a topological polar surface area of 30.18.,The log p value of  is 3.42.,Midazolam is approved and illicit.,Midazolam is a solid.,True
14964,"Mycophenolate mofetil, also known as MMF or CellCept, is a prodrug of mycophenolic acid, and classified as a reversible inhibitor of inosine monophosphate dehydrogenase (IMPDH). This drug is an immunosuppressant combined with drugs such as and corticosteroids to prevent organ rejection after hepatic, renal, and cardiac transplants. It is marketed by Roche Pharmaceuticals and was granted FDA approval for the prophylaxis of transplant rejection in 1995. In addition to the above uses, mycophenolate mofetil has also been studied for the treatment of nephritis and other complications of autoimmune diseases. Unlike another immunosuppressant class, the calcineurin inhibitors, MMF generally does not cause nephrotoxicity or fibrosis. Mycophenolate mofetil is indicated for the prophylaxis of organ rejection in patients undergoing allogeneic renal, hepatic, or cardiac transplants. It should be used with cyclosporine and corticosteroids. Mycophenolate mofetil may also be used off-label as a second-line treatment for autoimmune hepatitis that has not responded adequately to first-line therapy. Other off-label uses of this drug include lupus-associated nephritis and dermatitis in children. Mycophenolate mofetil is a prodrug of mycophenolic acid (MPA). The active form of mycophenolate, MPA, prevents the proliferation of immune cells and the formation of antibodies that cause transplant rejection. The above effects lead to higher rates of successful transplantation, avoiding the devastating effects of graft rejection. The active metabolite of mycophenolate, mycophenolic acid, prevents T-cell and B-cell proliferation and the production of cytotoxic T-cells and antibodies. Lymphocyte and monocyte adhesion to endothelial cells of blood vessels that normally part of inflammation is prevented via the glycosylation of cell adhesion molecules by MPA. MPA inhibits de novo purine biosynthesis (that promotes immune cell proliferation) by inhibiting inosine 5’-monophosphate dehydrogenase enzyme (IMPDH), with a preferential inhibition of IMPDH II. IMPDH normally transforms inosine monophosphate (IMP) to xanthine monophosphate (XMP), a metabolite contributing to the production of guanosine triphosphate (GTP). GTP is an important molecule for the synthesis of ribonucleic acid (RNA), deoxyribonucleic acid (DNA), and protein. As a result of the above cascade of effects, mycophenolate mofetil reduces de-novo production of guanosine nucleotides, interfering with the synthesis of DNA, RNA, and protein required for immune cell production. Further contributing to the above anti-inflammatory effects, MMF depletes tetrahydrobiopterin, causing the decreased function of inducible nitric oxide synthase enzyme, in turn decreasing the production of peroxynitrite, a molecule that promotes inflammation.",The molecular weight is 433.5.,Mycophenolate mofetil has a topological polar surface area of 94.53.,The log p value of  is 2.98.,Mycophenolate mofetil is approved and investigational.,Mycophenolate mofetil is a solid.,True
14965,"Eplerenone, an aldosterone receptor antagonist similar to spironolactone, has been shown to produce sustained increases in plasma renin and serum aldosterone, consistent with inhibition of the negative regulatory feedback of aldosterone on renin secretion. The resulting increased plasma renin activity and aldosterone circulating levels do not overcome the effects of eplerenone. Eplerenone selectively binds to recombinant human mineralocorticoid receptors relative to its binding to recombinant human glucocorticoid, progesterone and androgen receptors. For improvement of survival of stable patients with left ventricular systolic dysfunction (ejection fraction <40%) and clinical evidence of congestive heart failure after an acute myocardial infarction. Eplerenone, an aldosterone receptor antagonist similar to spironolactone, has been shown to produce sustained increases in plasma renin and serum aldosterone, consistent with inhibition of the negative regulatory feedback of aldosterone on renin secretion. The resulting increased plasma renin activity and aldosterone circulating levels do not overcome the effects of eplerenone. Eplerenone selectively binds to recombinant human mineralocorticoid receptors relative to its binding to recombinant human glucocorticoid, progesterone and androgen receptors. Eplerenone binds to the mineralocorticoid receptor and thereby blocks the binding of aldosterone (component of the renin-angiotensin-aldosterone-system, or RAAS). Aldosterone synthesis, which occurs primarily in the adrenal gland, is modulated by multiple factors, including angiotensin II and non-RAAS mediators such as adrenocorticotropic hormone (ACTH) and potassium. Aldosterone binds to mineralocorticoid receptors in both epithelial (e.g., kidney) and nonepithelial (e.g., heart, blood vessels, and brain) tissues and increases blood pressure through induction of sodium reabsorption and possibly other mechanisms.",The molecular weight is 414.5.,Eplerenone has a topological polar surface area of 82.2.,The log p value of  is 0.47.,Eplerenone is approved.,Eplerenone is a solid.,True
14966,"Amprenavir is a protease inhibitor used to treat HIV infection. For the treatment of HIV-1 infection in combination with other antiretroviral agents. Amprenavir is a protease inhibitor with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Protease inhibitors block the part of HIV called protease. HIV-1 protease is an enzyme required for the proteolytic cleavage of the viral polyprotein precursors into the individual functional proteins found in infectious HIV-1. Amprenavir binds to the protease active site and inhibits the activity of the enzyme. This inhibition prevents cleavage of the viral polyproteins resulting in the formation of immature non-infectious viral particles. Protease inhibitors are almost always used in combination with at least two other anti-HIV drugs. Amprenavir inhibits the HIV viral proteinase enzyme which prevents cleavage of the gag-pol polyprotein, resulting in noninfectious, immature viral particles.",The molecular weight is 505.63.,Amprenavir has a topological polar surface area of 131.19.,The log p value of  is 3.29.,Amprenavir is approved and investigational.,Amprenavir is a solid.,True
14967,"A potent, non-nucleoside reverse transcriptase inhibitor with activity specific for HIV-1. For the treatment of HIV-1 infection in combination with appropriate antiretroviral agents when therapy is warranted Delavirdine is a non-nucleoside reverse transcriptase inhibitor (nNRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Delavirdine binds directly to reverse transcriptase (RT) and blocks the RNA-dependent and DNA-dependent DNA polymerase activities by causing a disruption of the enzyme's catalytic site. The activity of Delavirdine does not compete with template or nucleoside triphosphates. HIV-2 RT and eukaryotic DNA polymerases (such as human DNA polymerases alpha, beta, or sigma) are not inhibited by Delavirdine. Delavirdine binds directly to viral reverse transcriptase (RT) and blocks the RNA-dependent and DNA-dependent DNA polymerase activities by disrupting the enzyme's catalytic site.",The molecular weight is 456.57.,Delavirdine has a topological polar surface area of 110.43.,The log p value of  is 2.41.,Delavirdine is approved.,Delavirdine is a solid.,True
14968,"Modafinil is a stimulant drug marketed as a 'wakefulness promoting agent' and is one of the stimulants used in the treatment of narcolepsy. Narcolepsy is caused by dysfunction of a family of wakefulness-promoting and sleep-suppressing peptides, the orexins, whose neurons are activated by modafinil. The prexin neuron activation is associated with psychoactivation and euphoria. The exact mechanism of action is unclear, although in vitro studies have shown it to inhibit the reuptake of dopamine by binding to the dopamine reuptake pump, and lead to an increase in extracellular dopamine. Modafinil activates glutamatergic circuits while inhibiting GABA. To improve wakefulness in patients with excessive daytime sleepiness (EDS) associated with narcolepsy. Modafinil is a stimulant drug marketed as a 'wakefulness promoting agent' and is one of the stimulants used in the treatment of narcolepsy. Narcolepsy is caused by dysfunction of a family of wakefulness-promoting and sleep-suppressing peptides, the orexins, whose neurons are activated by modafinil. The prexin neuron activation is associated with psychoactivation and euphoria. Modafinil is not indicated for complaints of lack of energy or fatigue; but it appears to be very helpful for some patients. Also, it has been used in the treatment of hypersomnia, a disorder in which patients lack the capacity for meaningful sleep and may require ten or more hours per day. Recent studies have have found that modafinil may help recovering cocaine addicts fight their addiction. The exact mechanism of action is unclear, although <i>in vitro</i> studies have shown it to inhibit the reuptake of dopamine by binding to the dopamine reuptake pump, and lead to an increase in extracellular dopamine. Modafinil activates glutamatergic circuits while inhibiting GABA. Modafinil is thought to have less potential for abuse than other stimulants due to the absence of any significant euphoric or pleasurable effects. It is possible that modafinil acts by a synergistic combination of mechanisms including direct inhibition of dopamine reuptake, indirect inhibition of noradrenalin reuptake in the VLPO and orexin activation. Modafinil has partial alpha 1B-adrenergic agonist effects by directly stimulating the receptors.",The molecular weight is 273.35.,Modafinil has a topological polar surface area of 60.16.,The log p value of  is 0.94.,Modafinil is approved and investigational.,Modafinil is a solid.,True
14969,"Clopidogrel is a prodrug of a platelet inhibitor used to reduce the risk of myocardial infarction and stroke. Clopidogrel is indicated to reduce the risk of myocardial infarction for patients with non-ST elevated acute coronary syndrome (ACS), patients with ST-elevated myocardial infarction, and in recent MI, stroke, or established peripheral arterial disease, Clopidogrel is indicated to reduce the risk of myocardial infarction for patients with non-ST elevated acute coronary syndrome (ACS), patients with ST-elevated myocardial infarction, and in recent MI, stroke, or established peripheral arterial disease, Clopidogrel is a prodrug of a platelet inhibitor used to reduce the risk of myocardial infarction and stroke. It has a long duration of action as it is taken once daily and a large therapeutic window as it is given in doses of 75-300mg daily. Clopidogrel is metabolized to its active form by carboxylesterase-1. The active form is a platelet inhibitor that irreversibly binds to P2Y<sub>12</sub> ADP receptors on platelets. This binding prevents ADP binding to P2Y<sub>12</sub> receptors, activation of the glycoprotein GPIIb/IIIa complex, and platelet aggregation.",The molecular weight is 321.82.,Clopidogrel has a topological polar surface area of 29.54.,The log p value of  is 4.21.,Clopidogrel is approved.,Clopidogrel is a solid.,True
14970,"Mometasone is a corticosteroid not currently used in medical products. however, is still in use. The inhaler is indicated for the maintenance treatment of asthma as prophylactic therapy. The nasal spray is indicated for the treatment of the nasal symptoms of seasonal allergic and perennial allergic rhinitis. Mometasone is a medium-potency synthetic corticosteroid with antiinflammatory, antipruritic, and vasoconstrictive properties. Studies in asthmatic patients have demonstrated that mometasone provides a favorable ratio of topical to systemic activity due to its primary local effect along with the extensive hepatic metabolism and the lack of active metabolites. Though effective for the treatment of asthma, glucocorticoids do not affect asthma symptoms immediately. Maximum improvement in symptoms following inhaled administration of mometasone furoate may not be achieved for 1 to 2 weeks or longer after starting treatment. When glucocorticoids are discontinued, asthma stability may persist for several days or longer. Mometasone has been shown in vitro to exhibit a binding affinity for the human glucocorticoid receptor which is approximately 12 times that of dexamethasone, 7 times that of triamcinolone acetonide, 5 times that of budesonide, and 1.5 times that of fluticasone. The clinical significance of these findings is unknown. Unbound corticosteroids cross cell membranes and bind with high affinity to specific cytoplasmic receptors. Inflammation is decreased by diminishing the release of leukocytic acid hydrolases, prevention of macrophage accumulation at inflamed sites, interference with leukocyte adhesion to the capillary wall, reduction of capillary membrane permeability, reduction of complement components, inhibition of histamine and kinin release, and interference with the formation of scar tissue. The antiinflammatory actions of corticosteroids are thought to involve phospholipase A<sub>2</sub> inhibitory proteins, lipocortins, which control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes. Mometasone furoate has been shown in vitro to exhibit a binding affinity for the human glucocorticoid receptor which is approximately 12 times that of dexamethasone, 7 times that of triamcinolone acetonide, 5 times that of budesonide, and 1.5 times that of fluticasone.",,,,Mometasone is experimental.,Mometasone is a solid.,True
14971,"Tadalafil is an orally administered drug used to treat male erectile dysfunction (impotence). It is marketed worldwide under the brand name Cialis. It is a phosphodiesterase 5 (PDE5) inhibitor. Tadalafil's distinguishing pharmacologic feature is its longer half-life (17.5 hours) compared with Viagra and Levitra (4-5 hours). This longer half-life results in a longer duration of action and is, in part, responsible for the Cialis nickname of the \weekend pill.\"" This longer half-life also is the basis of current investigation for tadalafil's use in pulmonary arterial hypertension as a once-daily therapy."" Used for the treatment of erectile dysfunction. Tadalafil is used to treat male erectile dysfunction (impotence) and pulmonary arterial hypertension (PAH). Part of the physiological process of erection involves the release of nitric oxide (NO) in the corpus cavernosum. This then activates the enzyme guanylate cyclase which results in increased levels of cyclic guanosine monophosphate (cGMP), leading to smooth muscle relaxation in the corpus cavernosum, resulting in increased inflow of blood and an erection. Tadalafil is a potent and selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5) which is responsible for degradation of cGMP in the corpus cavernosum. This means that, with tadalafil on board, normal sexual stimulation leads to increased levels of cGMP in the corpus cavernosum which leads to better erections. Without sexual stimulation and no activation of the NO/cGMP system, tadalafil should not cause an erection. Penile erection during sexual stimulation is achieved by the relaxation of penile arteries and corpus cavernosal smooth muscles, leading to increased blood flow to the organ. This response is mediated by the release of nitric oxide (NO) from nerve terminals and endothelial cells, which stimulates the synthesis of cGMP in smooth muscle cells. Cyclic GMP causes smooth muscle relaxation and increased blood flow into the corpus cavernosum, and is degraded by the cGMP specific phosphodiesterase type 5 (PDE5) in the corpus cavernosum located around the penis. Tadalafil inhibits PDE5 and thereby enhances erectile function by increasing the amount of cGMP available.",The molecular weight is 389.41.,Tadalafil has a topological polar surface area of 74.87.,The log p value of  is 2.58.,Tadalafil is approved and investigational.,Tadalafil is a solid.,True
14972,"A carbamate derivative used as an alcohol deterrent. It is a relatively nontoxic substance when administered alone, but markedly alters the intermediary metabolism of alcohol. When alcohol is ingested after administration of disulfiram, blood acetaldehyde concentrations are increased, followed by flushing, systemic vasodilation, respiratory difficulties, nausea, hypotension, and other symptoms (acetaldehyde syndrome). It acts by inhibiting aldehyde dehydrogenase. For the treatment and management of chronic alcoholism Disulfiram produces a sensitivity to alcohol which results in a highly unpleasant reaction when the patient under treatment ingests even small amounts of alcohol. Disulfiram blocks the oxidation of alcohol at the acetaldehyde stage during alcohol metabolism following disulfiram intake, the concentration of acetaldehyde occurring in the blood may be 5 to 10 times higher than that found during metabolism of the same amount of alcohol alone. Accumulation of acetaldehyde in the blood produces a complex of highly unpleasant symptoms referred to hereinafter as the disulfiram-alcohol reaction. This reaction, which is proportional to the dosage of both disulfiram and alcohol, will persist as long as alcohol is being metabolized. Disulfiram does not appear to influence the rate of alcohol elimination from the body. Prolonged administration of disulfiram does not produce tolerance; the longer a patient remains on therapy, the more exquisitely sensitive he becomes to alcohol. Disulfiram blocks the oxidation of alcohol at the acetaldehyde stage during alcohol metabolism following disulfiram intake causing an accumulation of acetaldehyde in the blood producing highly unpleasant symptoms. Disulfiram blocks the oxidation of alcohol through its irreversible inactivation of aldehyde dehydrogenase, which acts in the second step of ethanol utilization. In addition, disulfiram competitively binds and inhibits the peripheral benzodiazepine receptor, which may indicate some value in the treatment of the symptoms of alcohol withdrawal, however this activity has not been extensively studied.",The molecular weight is 296.52.,Disulfiram has a topological polar surface area of 6.48.,The log p value of  is 3.88.,Disulfiram is approved.,Disulfiram is a solid.,True
14973,"Mifepristone is a progestational and glucocorticoid hormone antagonist. Its inhibition of progesterone induces bleeding during the luteal phase and in early pregnancy by releasing endogenous prostaglandins from the endometrium or decidua. As a glucocorticoid receptor antagonist, the drug has been used to treat hypercortisolism in patients with nonpituitary cushing syndrome. The two marketed forms of mifepristone are Mifeprex® (mifepristone 200mg) and Korlym™ (mifepristone 300mg). Currently under investigation for use in psychotic depression (phase 3 trials). For the medical termination of intrauterine pregnancy through 49 days' pregnancy. Also indicated to control hyperglycemia secondary to hypercortisolism in adult patients with endogenous Cushing's syndrome who have type 2 diabetes mellitus or glucose intolerance and are not candidates for surgery or have had unsuccessful surgery. Mifepristone is a synthetic steroid with antiprogestational effects indicated for the medical termination of intrauterine pregnancy through 49 days' pregnancy. Doses of 1 mg/kg or greater of mifepristone have been shown to antagonize the endometrial and myometrial effects of progesterone in women. During pregnancy, the compound sensitizes the myometrium to the contraction-inducing activity of prostaglandins. Mifepristone also exhibits antiglucocorticoid and weak antiandrogenic activity. The activity of the glucocorticoid dexamethasone in rats was inhibited following doses of 10 to 25 mg/kg of mifepristone. Doses of 4.5 mg/kg or greater in human beings resulted in a compensatory elevation of adrenocorticotropic hormone (ACTH) and cortisol. The anti-progestational activity of mifepristone results from competitive interaction with progesterone at progesterone-receptor sites. Based on studies with various oral doses in several animal species (mouse, rat, rabbit and monkey), the compound inhibits the activity of endogenous or exogenous progesterone. The termination of pregnancy results.",The molecular weight is 429.6.,Mifepristone has a topological polar surface area of 40.54.,The log p value of  is 4.47.,Mifepristone is approved and investigational.,Mifepristone is a solid.,True
14974,"Vardenafil (Levitra) is an oral therapy for the treatment of erectile dysfunction. It is a selective inhibitor of cyclic guanosine monophosphate (cGMP)-specific phosphodiesterase type 5 (PDE5). Penile erection is a hemodynamic process initiated by the relaxation of smooth muscle in the corpus cavernosum and its associated arterioles. During sexual stimulation, nitric oxide is released from nerve endings and endothelial cells in the corpus cavernosum. Nitric oxide activates the enzyme guanylate cyclase resulting in increased synthesis of cyclic guanosine monophosphate (cGMP) in the smooth muscle cells of the corpus cavernosum. The cGMP in turn triggers smooth muscle relaxation, allowing increased blood flow into the penis, resulting in erection. The tissue concentration of cGMP is regulated by both the rates of synthesis and degradation via phosphodiesterases (PDEs). The most abundant PDE in the human corpus cavernosum is the cGMPspecific phosphodiesterase type 5 (PDE5); therefore, the inhibition of PDE5 enhances erectile function by increasing the amount of cGMP. Used for the treatment of erectile dysfunction Vardenafil is used to treat male erectile dysfunction (impotence) and pulmonary arterial hypertension (PAH). Part of the physiological process of erection involves the release of nitric oxide (NO) in the corpus cavernosum. This then activates the enzyme guanylate cyclase which results in increased levels of cyclic guanosine monophosphate (cGMP), leading to smooth muscle relaxation in the corpus cavernosum, resulting in increased inflow of blood and an erection. Vardenafil is a potent and selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5) which is responsible for degradation of cGMP in the corpus cavernosum. This means that, with vardenafil on board, normal sexual stimulation leads to increased levels of cGMP in the corpus cavernosum which leads to better erections. Without sexual stimulation and no activation of the NO/cGMP system, vardenafil should not cause an erection. Vardenafil inhibits the cGMP specific phosphodiesterase type 5 (PDE5) which is responsible for degradation of cGMP in the corpus cavernosum located around the penis. Penile erection during sexual stimulation is caused by increased penile blood flow resulting from the relaxation of penile arteries and corpus cavernosal smooth muscle. This response is mediated by the release of nitric oxide (NO) from nerve terminals and endothelial cells, which stimulates the synthesis of cGMP in smooth muscle cells. Cyclic GMP causes smooth muscle relaxation and increased blood flow into the corpus cavernosum. The inhibition of phosphodiesterase type 5 (PDE5) by vardenafil enhances erectile function by increasing the amount of cGMP.",The molecular weight is 488.61.,Vardenafil has a topological polar surface area of 109.13.,The log p value of  is 2.23.,Vardenafil is approved.,Vardenafil is a solid.,True
14975,"A macrolide compound obtained from Streptomyces hygroscopicus that acts by selectively blocking the transcriptional activation of cytokines thereby inhibiting cytokine production. It is bioactive only when bound to immunophilins. Sirolimus is a potent immunosuppressant and possesses both antifungal and antineoplastic properties. For the prophylaxis of organ rejection in patients receiving renal transplants. Sirolimus, a macrocyclic lactone produced by <i>Streptomyces hygroscopicus</i>, is an immunosuppressive agent indicated for the prophylaxis of organ rejection in patients receiving renal transplants. It is recommended that sirolimus be used in a regimen with cyclosporine and corticosteroids. Sirolimus inhibits T lymphocyte activation and proliferation that occurs in response to antigenic and cytokine (Interleukin IL-2, IL-4, and IL-15) stimulation by a mechanism that is distinct from that of other immunosuppressants. Sirolimus also inhibits antibody production. In cells, sirolimus binds to the immunophilin, FK Binding Protein-12 (FKBP-12), to generate an immunosuppressive complex. The sirolimus:FKBP-12 complex has no effect on calcineurin activity. This complex binds to and inhibits the activation of the mammalian Target Of Rapamycin (mTOR), a key regulatory kinase. This inhibition suppresses cytokine-driven T-cell proliferation, inhibiting the progression from the G1 to the S phase of the cell cycle.",The molecular weight is 914.19.,Sirolimus has a topological polar surface area of 195.43.,The log p value of  is 7.04.,Sirolimus is approved and investigational.,Sirolimus is a solid.,True
14976,"Withdrawn in the United Kingdom due to risk of psychiatric adverse drug reactions. This drug continues to be available in the U.S. Internationally, triazolam is a Schedule IV drug under the Convention on Psychotropic Substances. For the short-term treatment of insomnia. A short-acting benzodiazepine used as a hypnotic agent in the treatment of insomnia. Some countries temporarily withdrew triazolam from the market because of concerns about adverse reactions, mostly psychological, associated with higher dose ranges. Its use at lower doses with appropriate care and labeling has been reaffirmed by the FDA and most other countries. Triazolam has a shorter half-life than chlordiazepoxide, flurazepam, and prazepam and does not generate active metabolites. Benzodiazepines bind nonspecifically to bezodiazepine receptors BNZ1, which mediates sleep, and BNZ2, which affects affects muscle relaxation, anticonvulsant activity, motor coordination, and memory. As benzodiazepine receptors are thought to be coupled to gamma-aminobutyric acid-A (GABA<sub>A</sub>) receptors, this enhances the effects of GABA by increasing GABA affinity for the GABA receptor. Binding of GABA to the site opens the chloride channel, resulting in a hyperpolarized cell membrane that prevents further excitation of the cell.",The molecular weight is 343.21.,Triazolam has a topological polar surface area of 43.07.,The log p value of  is 2.62.,Triazolam is approved and investigational.,Triazolam is a solid.,True
14977,"A competitive serotonin type 3 receptor antagonist. It is effective in the treatment of nausea and vomiting caused by cytotoxic chemotherapy drugs, including cisplatin, and has reported anxiolytic and neuroleptic properties.  In the adult patient population: Ondansetron is a highly specific and selective serotonin 5-HT<sub>3</sub> receptor antagonist, not shown to have activity at other known serotonin receptors and with low affinity for dopamine receptors ,. The serotonin 5-HT<sub>3</sub> receptors are located on the nerve terminals of the vagus in the periphery, and centrally in the chemoreceptor trigger zone of the area postrema ,. The temporal relationship between the emetogenic action of emetogenic drugs and the release of serotonin, as well as the efficacy of antiemetic agents, suggest that chemotherapeutic agents release serotonin from the enterochromaffin cells of the small intestine by causing degenerative changes in the GI tract ,. The serotonin then stimulates the vagal and splanchnic nerve receptors that project to the medullary vomiting center, as well as the 5-HT<sub>3</sub> receptors in the area postrema, thus initiating the vomiting reflex, causing nausea and vomiting ,. Ondansetron is a selective antagonist of the serotonin receptor subtype, 5-HT3.",The molecular weight is 293.37.,Ondansetron has a topological polar surface area of 39.82.,The log p value of  is 2.72.,Ondansetron is approved.,Ondansetron is a solid.,True
14978,"Bimatoprost, also known as Latisse or Lumigan, belongs to a group of drugs called prostamides, which are synthetic structural analogs of prostaglandin. Bimatoprost, marketed by Allergan, is administered in both the ophthalmic solution and implant form. It has the ability to reduce ocular hypotension, proving effective in conditions such as ocular hypertension and glaucoma. Bimatoprost is also used to treat eyelash hypotrichosis, or sparse eyelash growth. It was initially approved by the FDA in 2001 for ocular hypertension and later approved for hypothrichosis in 2008, as eyelash growth became a desirable adverse effect for patients using this drug. Bimatoprost is used for the reduction of elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension. High intraocular pressure is a major risk factor for glaucoma-related visual field loss. A linear relationship exists between intraocular pressure and the risk of damaging the optic nerve, which can lead to considerable visual impairment. Therefore, conditions such as ocular hypertension and glaucoma can cause dangerous elevations of intraocular pressure. Bimatoprost rapidly decreases intraocular pressure and reduces the risk for visual field loss from ocular hypertension due to various causes. Bimatoprost imitates the effects of prostamides, specifically prostaglandin F2α. Bimatoprost mildly stimulates aqueous humor outflow, relieving elevated intraocular pressure and decreasing the risk of optic nerve damage. It is thought that bimatoprost reduces intraocular pressure (IOP) in humans by causing an increase in outflow of the aqueous humor via the trabecular meshwork and uveoscleral pathways. It achieves the above effects by decreasing tonographic resistance to aqueous humor outflow. Bimatoprost does not affect aqueous humor production.",The molecular weight is 415.57.,Bimatoprost has a topological polar surface area of 89.79.,The log p value of  is 1.75.,Bimatoprost is approved and investigational.,Bimatoprost is a solid.,True
14979,"Zonisamide is a sulfonamide anticonvulsant approved for use as an adjunctive therapy in adults with partial-onset seizures. Zonisamide may be a carbonic anhydrase inhibitor although this is not one of the primary mechanisms of action. Zonisamide may act by blocking repetitive firing of voltage-gated sodium channels leading to a reduction of T-type calcium channel currents, or by binding allosterically to GABA receptors. This latter action may inhibit the uptake of the inhibitory neurotransmitter GABA while enhancing the uptake of the excitatory neurotransmitter glutamate. For use as adjunctive treatment of partial seizures in adults with epilepsy. Zonisamide is a sulfonamide and therefore unrelated to other seizure medications. The mechanism is not know but it may block sodium and calcium channels. Blocking of these channels may prevent neuronal hypersynchronization. Sonisamide has also been found to potentiate dopaminergic and serotonergic neurotransmission but does not appear to potentiate syanptic activity by GABA (gamma amino butyric acid). Zonisamide binds to sodium channels and voltage sensitive calcium channels, which suppresses neuronal depolarization and hypersynchronization. Zonisamide also inhibits carbonic anhydrase to a weaker extent, but such an effect is not thought to contribute substantially to the drug's anticonvulsant activity.",The molecular weight is 212.22.,Zonisamide has a topological polar surface area of 86.19.,The log p value of  is -0.36.,Zonisamide is approved and investigational.,Zonisamide is a solid.,True
14980,"Metronidazole is a commonly used antibiotic, belonging to the nitroimidazole class of antibiotics. It is frequently used to treat gastrointestinal infections as well as trichomoniasis and giardiasis, and amebiasis which are parasitic infections. Metronidazole has been used as an antibiotic for several decades, with added antiparasitic properties that set it apart from many other antibacterial drugs, allowing it to treat a wide variety of infections. It is available in capsule form, tablet form, and topical form, and suppository preparations for the treatment of various infections. Metronidazole is indicated for the treatment of confirmed trichomoniasis caused by Trichomonas vaginalis (except for in the first trimester of pregnancy) and the patient's sexual partners, bacterial vaginosis, certain types of amebiasis, and various anaerobic infections. The above anaerobic infections may occur on the skin and skin structures, the abdomen, the heart, reproductive organs, central nervous system, and the respiratory system. Some may also be present in the bloodstream in cases of septicemia. Common infections treated by metronidazole are Bacteroides species infections, Clostridium infections, and Fusobacterium infections, as well as Peptococcus and Peptostreptococcus infections.  Metronidazole treats amebiasis, trichomoniasis, and giardiasis, exerting both antibacterial and antiprotozoal activities. Metronidazole is an effective treatment for some anaerobic bacterial infections. Metronidazole has shown antibacterial activity against the majority of obligate anaerobes, however, during in vitro studies, it does not demonstrate significant action against facultative anaerobes or obligate aerobes. The nitro group reduction of metronidazole by anaerobic organisms is likely responsible for the drug's antimicrobial cytotoxic effects, causing DNA strand damage to microbes. The exact mechanism of action of metronidazole has not been fully established, however, it is possible that an intermediate in the reduction of metronidazole which is only made by anaerobic bacteria and protozoa, binds deoxyribonucleic acid and electron-transport proteins of organisms, blocking nucleic acid synthesis.",The molecular weight is 171.16.,Metronidazole has a topological polar surface area of 81.19.,The log p value of  is -0.46.,Metronidazole is approved.,Metronidazole is a solid.,True
14981,"Buprenorphine is a weak partial mu-opioid receptor agonist and a weak kappa-opioid receptor antagonist used for the treatment of severe pain. It is also commonly used as an alternative to for the treatment of severe opioid addiction. Buprenorphine is commercially available as the brand name product Suboxone which is formulated in a 4:1 fixed-dose combination product along with , a non-selective competitive opioid receptor antagonist. Combination with naloxone is intended to reduce the abuse potential of Suboxone, as naloxone is poorly absorbed by the oral route (and has no effect when taken orally), but would reverse the opioid agonist effects of buprenorphine if injected intravenously. Buprenorphine has poor gastrointestinal absorption and is therefore formulated as a sublingual tablet. Buprenorphine is indicated for the management of pain severe enough to require an opioid analgesic and for which alternative treatments are inadequate. Buprenorphine is also used in combination with in a fixed-dose combination product for the treatment of moderate to severe opioid use disorder. Buprenorphine interacts predominately with the opioid mu-receptor. These mu-binding sites are discretely distributed in the human brain, spinal cord, and other tissues. In clinical settings, buprenorphine exerts its principal pharmacologic effects on the central nervous system. Its primary actions of therapeutic value are analgesia and sedation. In addition to analgesia, alterations in mood, euphoria and dysphoria, and drowsiness commonly occur. Buprenorphine depresses the respiratory centers, depresses the cough reflex, and constricts the pupils.  Buprenorphine is a partial agonist at the mu-opioid receptor and an antagonist at the kappa-opioid receptor. It demonstrates a high affinity for the mu-opioid receptor but has lower intrinsic activity compared to other full mu-opioid agonists such as , , or. This means that buprenorphine preferentially binds the opioid receptor and displaces lower affinity opioids without activating the receptor to a comparable degree. Clinically, this results in a slow onset of action and a clinical phenomenon known as the \ceiling effect\"" where once a certain dose is reached buprenorphine's effects plateau. This effect can be beneficial, however, as dose-related side effects such as respiratory depression, sedation, and intoxication also plateau at around 32mg, resulting in a lower risk of overdose compared to and other full agonist opioids. It also means that opioid-dependent patients do not experience sedation or euphoria at the same rate that they might experience with more potent opioids, improving quality of life for patients with severe pain and reducing the reinforcing effects of opioids which can lead to drug-seeking behaviours.""",The molecular weight is 467.65.,Buprenorphine has a topological polar surface area of 62.16.,The log p value of  is 3.99.,Buprenorphine is approved and illicit and investigational and vet_approved.,Buprenorphine is a solid.,True
14982,"Zaleplon is a sedative/hypnotic, mainly used for insomnia. It is known as a nonbenzodiazepine hypnotic. Zaleplon interacts with the GABA receptor complex and shares some of the pharmacological properties of the benzodiazepines. Zaleplon is a schedule IV drug in the United States. For the treatment of short-term treatment of insomnia in adults. Zaleplon is a nonbenzodiazepine hypnotic from the pyrazolopyrimidine class and is indicated for the short-term treatment of insomnia. While Zaleplon is a hypnotic agent with a chemical structure unrelated to benzodiazepines, barbiturates, or other drugs with known hypnotic properties, it interacts with the gamma-aminobutyric acid-benzodiazepine (GABA<sub>B</sub>Z) receptor complex. Subunit modulation of the GABA<sub>B</sub>Z receptor chloride channel macromolecular complex is hypothesized to be responsible for some of the pharmacological properties of benzodiazepines, which include sedative, anxiolytic, muscle relaxant, and anticonvulsive effects in animal models. Zaleplon also binds selectively to the CNS GABA<sub>A</sub>-receptor chloride ionophore complex at benzodiazepine(BZ) omega-1 (BZ1, ο1) receptors.  Zaleplon exerts its action through subunit modulation of the GABA<sub>B</sub>Z receptor chloride channel macromolecular complex. Zaleplon also binds selectively to the brain omega-1 receptor located on the alpha subunit of the GABA-A/chloride ion channel receptor complex and potentiates t-butyl-bicyclophosphorothionate (TBPS) binding.",The molecular weight is 305.34.,Zaleplon has a topological polar surface area of 74.29.,The log p value of  is 1.43.,Zaleplon is approved and illicit and investigational.,Zaleplon is a solid.,True
14983,"Azelastine, a phthalazine derivative, is an antihistamine available as an intranasal spray for the treatment of allergic and vasomotor rhinitis and as an ophthalmic solution for the treatment of allergic conjunctivitis. It is a racemic mixture, though there is no noted difference in pharmacologic activity between enantiomers, and was first granted FDA approval in 1996. Azelastine is also available in combination with fluticasone propionate as a nasal spray marketed under the trade name Dymista™, which is indicated for the symptomatic treatment of seasonal allergic rhinitis in patients 6 years of age and older. Intranasal azelastine is indicated for the symptomatic treatment of seasonal allergic rhinitis in patients 5 years and older and for the symptomatic treatment of vasomotor rhinitis in patients 12 years and older. Ophthalmic azelastine solution is indicated for the treatment of itchy eyes associated with allergic conjunctivitis. Azelastine antagonizes the actions of histamine, resulting in the relief of histamine-mediated allergy symptoms. Onset of action occurs within 15 minutes with intranasal formulations and as quickly as 3 minutes with ophthalmic solutions. Intranasal formulations have a relatively long-duration of action, with peak effects observed 4-6 hours after the initial dose and efficacy maintained over the entirety of the standard 12 hour dosing interval. Azelastine is primarily a selective antagonist of histamine H1-receptors, with a lesser affinity for H2-receptors, used for the symptomatic treatment of allergies. Histamine H1-receptors are G-protein-coupled receptors with 7 transmembrane spanning domains that are found on nerve endings, smooth muscle cells, and glandular cells. Following allergen exposure in sensitized individuals, IgE-receptor cross-linking on mast cells results in the release of histamine, which binds to H1-receptors and contributes to typical allergic symptoms such as itching, sneezing, and congestion. ",The molecular weight is 381.9.,Azelastine has a topological polar surface area of 35.91.,The log p value of  is 4.01.,Azelastine is approved.,Azelastine is a solid.,True
14984,"Felodipine is a long-acting 1,4-dihydropyridine calcium channel blocker (CCB)b. It acts primarily on vascular smooth muscle cells by stabilizing voltage-gated L-type calcium channels in their inactive conformation. By inhibiting the influx of calcium in smooth muscle cells, felodipine prevents calcium-dependent myocyte contraction and vasoconstriction. Felodipine is the most potent CCB in use and is unique in that it exhibits fluorescent activity. In addition to binding to L-type calcium channels, felodipine binds to a number of calcium-binding proteins, exhibits competitive antagonism of the mineralcorticoid receptor, inhibits the activity of calmodulin-dependent cyclic nucleotide phosphodiesterase, and blocks calcium influx through voltage-gated T-type calcium channels. Felodipine is used to treat mild to moderate essential hypertension. For the treatment of mild to moderate essential hypertension.  Felodipine belongs to the dihydropyridine (DHP) class of calcium channel blockers (CCBs), the most widely used class of CCBs. There are at least five different types of calcium channels in Homo sapiens: L-, N-, P/Q-, R- and T-type. It was widely accepted that CCBs target L-type calcium channels, the major channel in muscle cells that mediates contraction; however, some studies have shown that felodipine also binds to and inhibits T-type calcium channels. T-type calcium channels are most commonly found on neurons, cells with pacemaker activity and on osteocytes. The pharmacologic significance of T-type calcium channel blockade is unknown. Felodipine also binds to calmodulin and inhibits calmodulin-dependent calcium release from the sarcoplasmic reticulum. The effect of this interaction appears to be minor. Another study demonstrated that felodipine attenuates the activity of calmodulin-dependent cyclic nucleotide phosphodiesterase (CaMPDE) by binding to the PDE-1B1 and PDE-1A2 enzyme subunits. CaMPDE is one of the key enzymes involved in cyclic nucleotides and calcium second messenger systems. Felodipine also acts as an antagonist to the mineralcorticoid receptor by competing with aldosterone for binding and blocking aldosterone-induced coactivator recruitment of the mineralcorticoid receptor. Felodipine is able to bind to skeletal and cardiac muscle isoforms of troponin C, one of the key regulatory proteins in muscle contraction. Though felodipine exhibits binding to many endogenous molecules, its vasodilatory effects are still thought to be brought about primarily through inhibition of voltage-gated L-type calcium channels. Similar to other DHP CCBs, felodipine binds directly to inactive calcium channels stabilizing their inactive conformation. Since arterial smooth muscle depolarizations are longer in duration than cardiac muscle depolarizations, inactive channels are more prevalent in smooth muscle cells. Alternative splicing of the alpha-1 subunit of the channel gives felodipine additional arterial selectivity. At therapeutic sub-toxic concentrations, felodipine has little effect on cardiac myocytes and conduction cells. Felodipine decreases arterial smooth muscle contractility and subsequent vasoconstriction by inhibiting the influx of calcium ions through voltage-gated L-type calcium channels. It reversibly competes against nitrendipine and other DHP CCBs for DHP binding sites in vascular smooth muscle and cultured rabbit atrial cells. Calcium ions entering the cell through these channels bind to calmodulin. Calcium-bound calmodulin then binds to and activates myosin light chain kinase (MLCK). Activated MLCK catalyzes the phosphorylation of the regulatory light chain subunit of myosin, a key step in muscle contraction. Signal amplification is achieved by calcium-induced calcium release from the sarcoplasmic reticulum through ryanodine receptors. Inhibition of the initial influx of calcium decreases the contractile activity of arterial smooth muscle cells and results in vasodilation. The vasodilatory effects of felodipine result in an overall decrease in blood pressure. Felodipine may be used to treat mild to moderate essential hypertension.",The molecular weight is 384.25.,Felodipine has a topological polar surface area of 64.63.,The log p value of  is 5.3.,Felodipine is approved and investigational.,Felodipine is a solid.,True
14985,"Nitrendipine is a calcium channel blocker with marked vasodilator action. It is an effective antihypertensive agent and differs from other calcium channel blockers in that it does not reduce glomerular filtration rate and is mildly natriuretic, rather than sodium retentive. For the treatment of mild to moderate hypertension Nitrendipine, a dihydropyridine calcium-channel blocker, is used alone or with an angiotensin-converting enzyme inhibitor, to treat hypertension, chronic stable angina pectoris, and Prinzmetal's variant angina. Nitrendipine is similar to other peripheral vasodilators. Nitrendipine inhibits the influx of extra cellular calcium across the myocardial and vascular smooth muscle cell membranes possibly by deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum. The decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload. By deforming the channel, inhibiting ion-control gating mechanisms, and/or interfering with the release of calcium from the sarcoplasmic reticulum, Nitrendipine inhibits the influx of extracellular calcium across the myocardial and vascular smooth muscle cell membranes The decrease in intracellular calcium inhibits the contractile processes of the myocardial smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload.",The molecular weight is 360.37.,Nitrendipine has a topological polar surface area of 107.77.,The log p value of  is 3.73.,Nitrendipine is approved and investigational.,Nitrendipine is a solid.,True
14986,"An anthelmintic used in most schistosome and many cestode infestations. For the treatment of infections due to all species of schistosoma. Praziquantel is an anthelmintic used in most schistosome and many cestode infestations. Praziquantel effects the permeability of the cell membrane resulting in the contraction of schistosomes. The drug further causes vacuolization and disintegration of the schistosome tegument. The effect is more marked on adult worms compared to young worms. An increased calcium influx may play an important role. Secondary effects are inhibition of glucose uptake, lowering of glycogen levels and stimulation of lactate release. The action of praziquantel is limited very specifically to trematodes and cestodes; nematodes (including filariae) are not affected. Praziquantel works by causing severe spasms and paralysis of the worms' muscles. This paralysis is accompanied - and probably caused - by a rapid Ca 2+ influx inside the schistosome. Morphological alterations are another early effect of praziquantel. These morphological alterations are accompanied by an increased exposure of schistosome antigens at the parasite surface. The worms are then either completely destroyed in the intestine or passed in the stool. An interesting quirk of praziquantel is that it is relatively ineffective against juvenile schistosomes. While initially effective, effectiveness against schistosomes decreases until it reaches a minimum at 3-4 weeks. Effectiveness then increases again until it is once again fully effective at 6-7 weeks. Glutathione S-transferase (GST), an essential detoxification enzyme in parasitic helminths, is a major vaccine target and a drug target against schistosomiasis. Schistosome calcium ion channels are currently the only known target of praziquantel. ",The molecular weight is 312.41.,Praziquantel has a topological polar surface area of 40.62.,The log p value of  is 3.36.,Praziquantel is approved and investigational and vet_approved.,Praziquantel is a solid.,True
14987,"Fluvastatin is an antilipemic agent that competitively inhibits hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. HMG-CoA reductase catalyzes the conversion of HMG-CoA to mevalonic acid, the rate-limiting step in cholesterol biosynthesis. Fluvastatin belongs to a class of medications called statins and is used to reduce plasma cholesterol levels and prevent cardiovascular disease. It is also the first entirely synthetic HMG-CoA reductase inhibitor and is structurally distinct from the fungal derivatives of this therapeutic class. Fluvastatin is a racemate comprising equimolar amounts of (3R,5S)- and (3S,5R)-fluvastatin. To be used as an adjunct to dietary therapy to prevent cardiovascular events. May be used as secondary prevention in patients with coronary heart disease (CHD) to reduce the risk of requiring coronary revascularization procedures, for reducing progression of coronary atherosclerosis in hypercholesterolemic patients with CHD, and for the treatment of primary hypercholesterolemia and mixed dyslidipidemia.  Fluvastatin, the first synthetically-derived HMG-CoA reductase inhibitor, is a hydrophilic, acidic, antilipemic agent used to lower cholesterol and triglyceride levels associated with primary hypercholesterolemia and mixed dyslipidemia (Fredrickson types IIa and IIb), to slow the progression of coronary atherosclerosis in patients with CHD and as secondary prevention therapy in patients with CHD to reduce the risk of requiring coronary revascularization procedures. Although similar to lovastatin, simvastatin, and pravastatin, fluvastatin has a shorter half-life, no active metabolites, extensive protein binding, and minimal CSF penetration. Fluvastatin acts primarily in the liver. It is prepared as a racemate of two erythro enantiomers of which the 3R,5S enantiomer exerts the pharmacologic effect.  Fluvastatin selectively and competitively inhibits the hepatic enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. HMG-CoA reductase is responsible for converting HMG-CoA to mevalonate, the rate-limiting step in cholesterol biosynthesis. Inhibition results in a decrease in hepatic cholesterol levels which stimulates the synthesis of LDL receptors and increases hepatic uptake of LDL cholesterol. The end result is decreased levels of plasma total and LDL cholesterol. ",The molecular weight is 411.47.,Fluvastatin has a topological polar surface area of 82.69.,The log p value of  is 4.05.,Fluvastatin is approved.,Fluvastatin is a solid.,True
14988,"A diphenylbutylpiperidine that is effective as an antipsychotic agent and as an alternative to haloperidol for the suppression of vocal and motor tics in patients with Tourette syndrome. Although the precise mechanism of action is unknown, blockade of postsynaptic dopamine receptors has been postulated. (From AMA Drug Evaluations Annual, 1994, p403) Used for the suppression of motor and phonic tics in patients with Tourette's Disorder who have failed to respond satisfactorily to standard treatment. Pimozide is an orally active antipsychotic drug product which shares with other antipsychotics the ability to blockade dopaminergic receptors on neurons in the central nervous system. However, receptor blockade is often accompanied by a series of secondary alterations in central dopamine metabolism and function which may contribute to both pimozide's therapeutic and untoward effects. In addition, pimozide, in common with other antipsychotic drugs, has various effects on other central nervous system receptor systems which are not fully characterized. Pimozide also has less potential for inducing sedation and hypotension as it has more specific dopamine receptor blocking activity than other neuroleptic agents (and is therefore a suitable alternative to haloperidol). The ability of pimozide to suppress motor and phonic tics in Tourette's Disorder is thought to be primarily a function of its dopaminergic blocking activity. Pimozide binds and inhibits the dopamine D2 receptor in the CNS. ",The molecular weight is 461.56.,Pimozide has a topological polar surface area of 35.58.,The log p value of  is 6.4.,Pimozide is approved.,Pimozide is a solid.,True
14989,"An acridine derivative formerly widely used as an antimalarial but superseded by chloroquine in recent years. It has also been used as an anthelmintic and in the treatment of giardiasis and malignant effusions. It is used in cell biological experiments as an inhibitor of phospholipase A2. For the treatment of giardiasis and cutaneous leishmaniasis and the management of malignant effusions. Quinacrine has been used as an antimalarial drug and as an antibiotic. It is used to treat giardiasis, a protozoal infection of the intestinal tract, and certain types of lupus erythematosus, an inflammatory disease that affects the joints, tendons, and other connective tissues and organs. Quinacrine may be injected into the space surrounding the lungs to prevent reoccurrence of pneumothorax. The exact way in which quinacrine works is unknown. It appears to interfere with the parasite's metabolism. The exact mechanism of antiparasitic action is unknown; however, quinacrine binds to deoxyribonucleic acid (DNA) in vitro by intercalation between adjacent base pairs, inhibiting transcription and translation to ribonucleic acid (RNA). Quinacrine does not appear to localize to the nucleus of Giaridia trophozoites, suggesting that DNA binding may not be the primary mechanism of its antimicrobial action. Fluorescence studies using Giardia suggest that the outer membranes may be involved. Quinacrine inhibits succinate oxidation and interferes with electron transport. In addition, by binding to nucleoproteins, quinacrine suppress the lupus erythematous cell factor and acts as a strong inhibitor of cholinesterase.",The molecular weight is 399.96.,Quinacrine has a topological polar surface area of 37.39.,The log p value of  is 6.72.,Quinacrine is investigational.,Quinacrine is a solid.,True
14990,"A histamine H1 antagonist used in allergic reactions, hay fever, rhinitis, urticaria, and asthma. It has also been used in veterinary applications. One of the most widely used of the classical antihistaminics, it generally causes less drowsiness and sedation than promethazine. For the treatment of rhinitis, urticaria, allergy, common cold, asthma and hay fever. In allergic reactions an allergen interacts with and cross-links surface IgE antibodies on mast cells and basophils. Once the mast cell-antibody-antigen complex is formed, a complex series of events occurs that eventually leads to cell-degranulation and the release of histamine (and other chemical mediators) from the mast cell or basophil. Once released, histamine can react with local or widespread tissues through histamine receptors. Histamine, acting on H<sub>1</sub>-receptors, produces pruritis, vasodilatation, hypotension, flushing, headache, tachycardia, and bronchoconstriction. Histamine also increases vascular permeability and potentiates pain. Chlorpheniramine, is a histamine H1 antagonist (or more correctly, an inverse histamine agonist) of the alkylamine class. It competes with histamine for the normal H<sub>1</sub>-receptor sites on effector cells of the gastrointestinal tract, blood vessels and respiratory tract. It provides effective, temporary relief of sneezing, watery and itchy eyes, and runny nose due to hay fever and other upper respiratory allergies. Chlorpheniramine binds to the histamine H1 receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine.",The molecular weight is 274.79.,Chlorpheniramine has a topological polar surface area of 16.13.,The log p value of  is 3.15.,Chlorpheniramine is approved.,Chlorpheniramine is a liquid.,True
14991,"Cilostazol is a quinolinone derivative and antiplatelet agent with vasodilating properties that has been used in the symptomatic treatment of intermittent claudication in patients with peripheral ischaemia. It is marketed under the brand name Pletal by Otsuka Pharmaceutical Co.. Cilostazol works by inhibiting both primary and secondary aggregation and reducing calcium-induced contractions. Indicated for the alleviation of symptoms of intermittent claudication (pain in the legs that occurs with walking and disappears with rest). Cilostazol reduces the symptoms of intermittent claudication, as indicated by an increased walking distance. Intermittent claudication is pain in the legs that occurs with walking and disappears with rest. The pain occurs due to reduced blood flow to the legs. Cilostazol and several of its metabolites are cyclic AMP (cAMP) phosphodiesterase III inhibitors (PDE III inhibitors), inhibiting phosphodiesterase activity and suppressing cAMP degradation with a resultant increase in cAMP in platelets and blood vessels, leading to inhibition of platelet aggregation and vasodilation.",The molecular weight is 369.47.,Cilostazol has a topological polar surface area of 81.93.,The log p value of  is 3.53.,Cilostazol is approved and investigational.,Cilostazol is a solid.,True
14992,"One of the triazole antifungal agents that inhibits cytochrome P-450-dependent enzymes resulting in impairment of ergosterol synthesis. It has been used against histoplasmosis, blastomycosis, cryptococcal meningitis & aspergillosis. For the treatment of the following fungal infections in immunocompromised and non-immunocompromised patients: pulmonary and extrapulmonary blastomycosis, histoplasmosis, aspergillosis, and onychomycosis. Itraconazole is an imidazole/triazole type antifungal agent. Itraconazole is a highly selective inhibitor of fungal cytochrome P-450 sterol C-14 &alpha;-demethylation via the inhibition of the enzyme cytochrome P450 14&alpha;-demethylase. This enzyme converts lanosterol to ergosterol, and is required in fungal cell wall synthesis. The subsequent loss of normal sterols correlates with the accumulation of 14 &alpha;-methyl sterols in fungi and may be partly responsible for the fungistatic activity of fluconazole. Mammalian cell demethylation is much less sensitive to fluconazole inhibition. Itraconazole exhibits <i>in vitro</i> activity against <i>Cryptococcus neoformans</i> and <i>Candida spp.</i> Fungistatic activity has also been demonstrated in normal and immunocompromised animal models for systemic and intracranial fungal infections due to <i>Cryptococcus neoformans</i> and for systemic infections due to <i>Candida albicans</i>. Itraconazole interacts with 14-&alpha; demethylase, a cytochrome P-450 enzyme necessary to convert lanosterol to ergosterol. As ergosterol is an essential component of the fungal cell membrane, inhibition of its synthesis results in increased cellular permeability causing leakage of cellular contents. Itraconazole may also inhibit endogenous respiration, interact with membrane phospholipids, inhibit the transformation of yeasts to mycelial forms, inhibit purine uptake, and impair triglyceride and/or phospholipid biosynthesis.",The molecular weight is 705.64.,Itraconazole has a topological polar surface area of 100.79.,The log p value of  is 5.99.,Itraconazole is approved and investigational.,Itraconazole is a solid.,True
14993,"A barbituric acid derivative that acts as a nonselective central nervous system depressant. It promotes binding to inhibitory gamma-aminobutyric acid subtype receptors, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations. For the treatment of all types of seizures except absence seizures. Phenobarbital, the longest-acting barbiturate, is used for its anticonvulsant and sedative-hypnotic properties in the management of all seizure disorders except absence (petit mal). Phenobarbital acts on GABAA receptors, increasing synaptic inhibition. This has the effect of elevating seizure threshold and reducing the spread of seizure activity from a seizure focus. Phenobarbital may also inhibit calcium channels, resulting in a decrease in excitatory transmitter release. The sedative-hypnotic effects of phenobarbital are likely the result of its effect on the polysynaptic midbrain reticular formation, which controls CNS arousal.",The molecular weight is 232.24.,Phenobarbital has a topological polar surface area of 75.27.,The log p value of  is 1.37.,Phenobarbital is approved and investigational.,Phenobarbital is a solid.,True
14994,"A specific blocker of dopamine receptors. It speeds gastrointestinal peristalsis, causes prolactin release, and is used as antiemetic and tool in the study of dopaminergic mechanisms. For management of dyspepsia, heartburn, epigastric pain, nausea, and vomiting. Domperidone is a specific blocker of dopamine receptors. It speeds gastrointestinal peristalsis, causes prolactin release, and is used as antiemetic and tool in the study of dopaminergic mechanisms. Domperidone acts as a gastrointestinal emptying (delayed) adjunct and peristaltic stimulant. The gastroprokinetic properties of domperidone are related to its peripheral dopamine receptor blocking properties. Domperidone facilitates gastric emptying and decreases small bowel transit time by increasing esophageal and gastric peristalsis and by lowering esophageal sphincter pressure. Antiemetic: The antiemetic properties of domperidone are related to its dopamine receptor blocking activity at both the chemoreceptor trigger zone and at the gastric level. It has strong affinities for the D2 and D3 dopamine receptors, which are found in the chemoreceptor trigger zone, located just outside the blood brain barrier, which - among others - regulates nausea and vomiting",The molecular weight is 425.92.,Domperidone has a topological polar surface area of 67.92.,The log p value of  is 4.27.,Domperidone is approved and investigational and vet_approved.,Domperidone is a solid.,True
14995,"Clarithromycin, a semisynthetic macrolide antibiotic derived from erythromycin, inhibits bacterial protein synthesis by binding to the bacterial 50S ribosomal subunit. Binding inhibits peptidyl transferase activity and interferes with amino acid translocation during the translation and protein assembly process. Clarithromycin may be bacteriostatic or bactericidal depending on the organism and drug concentration. An alternative medication for the treatment of acute otitis media caused by <i>H. influenzae, M. catarrhalis, or S. pneumoniae</i> in patients with a history of type I penicillin hypersensitivity. Also for the treatment of pharyngitis and tonsillitis caused by susceptible <i>Streptococcus pyogenes</i>, as well as respiratory tract infections including acute maxillary sinusitis, acute bacterial exacerbations of chronic bronchitis, mild to moderate community-acquired pneuomia, Legionnaires' disease, and pertussis. Other indications include treatment of uncomplicated skin or skin structure infections, helicobacter pylori infection, duodenal ulcer disease, bartonella infections, early Lyme disease, and encephalitis caused by <i>Toxoplasma gondii</i> (in HIV infected patients in conjunction with pyrimethamine). Clarithromycin may also decrease the incidence of cryptosporidiosis, prevent the occurence of α-hemolytic (viridans group) streptococcal endocarditis, as well as serve as a primary prevention for <i>Mycobacterium avium</i> complex (MAC) bacteremia or disseminated infections (in adults, adolescents, and children with advanced HIV infection). Clarithromycin is a macrolide antibiotic whose spectrum of activity includes many gram-positive (<i>Staphylococcus aureus, S. pneumoniae, and S. pyogenes</i>) and gram-negative aerobic bacteria (<i>Haemophilus influenzae, H. parainfluenzae, and Moraxella catarrhalis</i>), many anaerobic bacteria, some mycobacteria, and some other organisms including <i>Mycoplasma, Ureaplasma, Chlamydia, Toxoplasma</i>, and <i>Borrelia</i>. Other aerobic bacteria that clarithromycin has activity against include <i>C. pneumoniae and M. pneumoniae</i>. Clarithromycin has an in-vitro activity that is similar or greater than that of erythromycin against erythromycin-susceptible organisms. Clarithromycin is usually bacteriostatic, but may be bactericidal depending on the organism and the drug concentration. Clarithromycin is first metabolized to 14-OH clarithromycin, which is active and works synergistically with its parent compound. Like other macrolides, it then penetrates bacteria cell wall and reversibly binds to domain V of the 23S ribosomal RNA of the 50S subunit of the bacterial ribosome, blocking translocation of aminoacyl transfer-RNA and polypeptide synthesis. Clarithromycin also inhibits the hepatic microsomal CYP3A4 isoenzyme and P-glycoprotein, an energy-dependent drug efflux pump.",The molecular weight is 747.96.,Clarithromycin has a topological polar surface area of 182.91.,The log p value of  is 2.37.,Clarithromycin is approved.,Clarithromycin is a solid.,True
14996,"Finasteride is a synthetic 4-azasteroid compound and specific inhibitor of steroid Type II 5α-reductase, which is an intracellular enzyme that converts the androgen testosterone into 5α-dihydrotestosterone (DHT). It works in a similar fashion as , which is another 5-alpha-reductase inhibitor, by exerting antiandrogenic effects. Finasteride is an orally active drug that was first approved by the FDA in 1992 for the treatment of benign prostatic hyperplasia to improve symptoms and reduce the risk for acute urinary retention or the need for surgical procedures. In 1998, it was approved by the FDA to treat male pattern hair loss. Finasteride is commonly marketed under the brand names Propecia and Proscar to be used aloneo or in combination with , an alpha-blocker. Indicated for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to improve symptoms, reduce the risk of acute urinary retention, and reduce the risk of the need for surgery including transurethral resection of the prostate (TURP) and prostatectomy. Finasteride is an antiandrogenic compound that works by suppressing the production of serum and intraprostatic dihydrotestosterone (DHT) in men via inhibiting the enzyme responsible for the biosynthesis of DHT. The maximum effect of a rapid reduction in serum DHT concentration is expected to be observed 8 hours following administration of the first dose. In a single man receiving a single oral dose of 5 mg finasteride for up to 4 years, there was a reduction in the serum DHT concentrations by approximately 70% and the median circulating level of testosterone increased by approximately 10-20% within the physiologic range. In a double-blind, placebo-controlled study, finasteride reduced intraprostatic DHT level by 91.4% but finasteride is not expected to decrease the DHT levels to castrate levels since circulating testosterone is also converted to DHT by the type 1 isoenzyme expressed in other tissues. It is expected that DHT levels return to normal within 14 days upon discontinuation of the drug. In a study of male patients with benign prostatic hyperplasia prior to prostatectomy, the treatment with finasteride resulted in an approximate 80% lower DHT content was measured in prostatic tissue removed at surgery compared to placebo. While finasteride reduces the size of the prostate gland by 20%, this may not correlate well with improvement in symptoms. The effects of finasteride are reported to be more pronounced in male patients with enlarged prostates (>25 mL) who are at the greatest risk of disease progression. Finasteride acts as a competitive and specific inhibitor of Type II 5α-reductase, a nuclear-bound steroid intracellular enzyme primarily located in the prostatic stromal cell that converts the androgen testosterone into the more active metabolite, 5α-dihydrotestosterone (DHT). DHT is considered to be the primary androgen playing a role in the development and enlargement of the prostate gland. It serves as the hormonal mediator for the hyperplasia upon accumulation within the prostate gland. DHT displays a higher affinity towards androgen receptors in the prostate gland compared to testosterone and by acting on the androgen receptors, DHT modulates genes that are responsible for cell proliferation. Responsible for the production of DHT together with type I 5α-reductase, the type II 5α-reductase isozyme is primarily found in the prostate, seminal vesicles, epididymides, and hair follicles as well as liver. Although finasteride is 100-fold more selective for type II 5α-reductase than for the type I isoenzyme, chronic treatment with this drug may have some effect on type I 5α-reductase, which is predominantly expressed in sebaceous glands of most regions of skin, including the scalp, and liver. It is proposed that the type I 5α-reductase and type II 5α-reductase is responsible for the production of one-third and two-thirds of circulating DHT, respectively. ",The molecular weight is 372.55.,Finasteride has a topological polar surface area of 58.2.,The log p value of  is 3.01.,Finasteride is approved.,Finasteride is a solid.,True
14997,"Anastrozole is a non-steroidal aromatase inhibitor (AI), similar to , used to decrease circulating estrogen levels in the treatment of postmenopausal women with estrogen-responsive breast cancer. Anastrozole is also related to , a steroidal AI, but its non-steroidal nature provides stark advantages including a lack of steroid-associated adverse effects such as weight gain and acne. Aromatase inhibitors, including anastrozole, have become endocrine drugs of choice in the treatment of postmenopausal breast cancer due to a more favourable efficacy and adverse effect profile as compared to earlier estrogen receptor modulators such as. Anastrozole is indicated as adjunct therapy in the treatment of hormone receptor-positive early breast cancer in postmenopausal women, and as a first-line treatment for hormone receptor-positive (or hormone receptor-unknown) locally advanced or metastatic breast cancer in postmenopausal women. It may also be used in the treatment of advanced breast cancer in postmenopausal women who experience disease progression despite treatment with.  Anastrozole prevents the conversion of adrenal androgens (e.g. ) to estrogen in peripheral and tumour tissues. As the growth of many breast cancers is stimulated and/or maintained by the presence of estrogen, anastrozole helps to treat these cancers by decreasing the levels of circulating estrogens. Anastrozole has a relatively long duration of action allowing for once daily dosing - serum estradiol is reduced by approximately 70% within 24 hours of beginning therapy with 1mg once daily, and levels remain suppressed for up to 6 days following cessation of therapy.  Anastrazole exerts its anti-estrogenic effects via selective and competitive inhibition of the aromatase enzyme found predominantly in the adrenal glands, liver, and fatty tissues. Many breast cancers are hormone receptor-positive, meaning their growth is stimulated and/or maintained by the presence of hormones such as estrogen or progesterone. In postmenopausal women, estrogen is primarily derived from the conversion of adrenally-produced androgens into estrogens by the aromatase enzyme - by competitively inhibiting the biosynthesis of estrogen at these enzymes, anastrozole effectively suppresses circulating estrogen levels and, subsequently, the growth of hormone receptor-positive tumours.",The molecular weight is 293.37.,Anastrozole has a topological polar surface area of 78.29.,The log p value of  is 1.48.,Anastrozole is approved and investigational.,Anastrozole is a solid.,True
14998,"Halofantrine is an antimalarial. It belongs to the phenanthrene class of compounds that includes quinine and lumefantrine. It appears to inhibit polymerisation of heme molecules (by the parasite enzyme \heme polymerase\""), resulting in the parasite being poisoned by its own waste. Halofantrine has been shown to preferentially block open and inactivated HERG channels leading to some degree of cardiotoxicity."" For treatment of Severe malaria Halofantrine is a synthetic antimalarial which acts as a blood schizonticide. It is effective against multi drug resistant (including mefloquine resistant) <i>P. falciparum</i> malaria. The mechanism of action of Halofantrine may be similar to that of chloroquine, quinine, and mefloquine; by forming toxic complexes with ferritoporphyrin IX that damage the membrane of the parasite.",The molecular weight is 500.43.,Halofantrine has a topological polar surface area of 23.47.,The log p value of  is 9.31.,Halofantrine is approved.,Halofantrine is a solid.,True
14999,"Initially approved by the FDA in 1997, quetiapine is a second-generation atypical antipsychotic used in schizophrenia, major depression, and bipolar disorder. Quetiapine demonstrates a high level of therapeutic efficacy and low risk of adverse effects during long-term treatment. It is well-tolerated and a suitable option for some patients with high sensitivity to other drugs, such as and. Quetiapine is used in the symptomatic treatment of schizophrenia. In addition, it may be used for the management of acute manic or mixed episodes in patients with bipolar I disorder, as a monotherapy or combined with other drugs. It may be used to manage depressive episodes in bipolar disorder. In addition to the above indications, quetiapine is used in combination with antidepressant drugs for the treatment of major depression. Quetiapine improves the positive and negative symptoms of schizophrenia and major depression by acting on various neurotransmitter receptors, such as the serotonin and dopamine receptors. In bipolar disorder, it improves both depressive and manic symptoms. Although the mechanism of action of quetiapine is not fully understood, several proposed mechanisms exist. In schizophrenia, its actions could occur from the antagonism of dopamine type 2 (D2) and serotonin 2A (5HT2A) receptors. In bipolar depression and major depression, quetiapine's actions may be attributed to the binding of this drug or its metabolite to the norepinephrine transporter. Additional effects of quetiapine, including somnolence, orthostatic hypotension, and anticholinergic effects, may result from the antagonism of H1 receptors, adrenergic α1 receptors, and muscarinic M1 receptors, respectively.",The molecular weight is 383.51.,Quetiapine has a topological polar surface area of 48.3.,The log p value of  is 2.99.,Quetiapine is approved.,Quetiapine is a solid.,True
15000,"Lapatinib is an anti-cancer drug developed by GlaxoSmithKline (GSK) as a treatment for solid tumours such as breast and lung cancer. It was approved by the FDA on March 13, 2007, for use in patients with advanced metastatic breast cancer in conjunction with the chemotherapy drug Capecitabine. Lapatinib is human epidermal growth factor receptor type 2 (HER2/ERBB2) and epidermal growth factor receptor (HER1/EGFR/ERBB1) tyrosine kinases inhibitor. It binds to the intracellular phosphorylation domain to prevent receptor autophosphorylation upon ligand binding. Indicated in combination with capecitabine for the treatment of patients with advanced or metastatic breast cancer whose tumors overexpress the human epidermal receptor type 2 (HER2) protein and who have received prior therapy including an anthracycline, a taxane, and trastuzuma. Lapatinib is a small molecule and a member of the 4-anilinoquinazoline class of kinase inhibitors. An anti-cancer drug, lapatinib was developed by GlaxoSmithKline (GSK) as a treatment for solid tumours such as breast and lung cancer. It was approved by the FDA on March 13, 2007, for use in patients with advanced metastatic breast cancer in conjunction with the chemotherapy drug capecitabine.  Lapatinib is a 4-anilinoquinazoline kinase inhibitor of the intracellular tyrosine kinase domains of both epidermal growth factor receptor (HER1/EGFR/ERBB1) and human epidermal growth factor receptor type 2 (HER2/ERBB2)with a dissociation half-life of &ge;300 minutes. Lapatinib inhibits ERBB-driven tumor cell growth in vitro and in various animal models. An additive effect was demonstrated in an in vitro study when lapatinib and 5-florouracil (the active metabolite of capecitabine) were used in combination in the 4 tumor cell lines tested. The growth inhibitory effects of lapatinib were evaluated in trastuzumab-conditioned cell lines. Lapatinib retained significant activity against breast cancer cell lines selected for long-term growth in trastuzumab-containing medium in vitro. These in vitro findings suggest non-cross-resistance between these two agents.",The molecular weight is 581.06.,Lapatinib has a topological polar surface area of 106.35.,The log p value of  is 5.82.,Lapatinib is approved and investigational.,Lapatinib is a solid.,True
15001,"Paliperidone is the primary active metabolite of risperidone. The mechanism of action is unknown but it is likely to act via a similar pathway to risperidone. It has been proposed that the drug's therapeutic activity in schizophrenia is mediated through a combination of central dopamine Type 2 (D2) and serotonin Type 2 (5HT2A) receptor antagonism. Paliperidone is also active as an antagonist at alpha 1 and alpha 2 adrenergic receptors and H1 histaminergic receptors, which may explain some of the other effects of the drug. Paliperidone was approved by the FDA for treatment of schizophrenia on December 20, 2006. For the treatment of schizophrenia. Paliperidone is an atypical antipsychotic developed by Janssen Pharmaceutica. Chemically, paliperidone is primary active metabolite of the older antipsychotic risperidone (paliperidone is 9-hydroxyrisperidone). The mechanism of action is unknown but it is likely to act via a similar pathway to risperidone. Paliperidone is the major active metabolite of risperidone. The mechanism of action of paliperidone, as with other drugs having efficacy in schizophrenia, is unknown, but it has been proposed that the drug's therapeutic activity in schizophrenia is mediated through a combination of central dopamine Type 2 (D2) and serotonin Type 2 (5HT2A) receptor antagonism.",The molecular weight is 426.49.,Paliperidone has a topological polar surface area of 82.17.,The log p value of  is 1.07.,Paliperidone is approved.,Paliperidone is a solid.,True
15002,"Sunitinib is a small-molecule multi-targeted receptor tyrosine kinase (RTK) inhibitor. On January 26, 2006, the agent was formally approved by the US FDA for the indications of treating renal cell carcinoma (RCC) and imatinib-resistant gastrointestinal stromal tumor (GIST). For these purposes, sunitinib is generally available as an orally administered formulation. Sunitinib inhibits cellular signaling by targeting multiple RTKs. These include all platelet-derived growth factor receptors (PDGF-R) and vascular endothelial growth factor receptors (VEGF-R). Sunitinib also inhibits KIT (CD117), the RTK that drives the majority of GISTs. In addition, sunitinib inhibits other RTKs including RET, CSF-1R, and flt3. For the treatment of advanced renal cell carcinoma as well as the treatment of gastrointestinal stromal tumor after disease progression on or intolerance to imatinib mesylate. Sunitinib is an oral, small-molecule, multi-targeted receptor tyrosine kinase (RTK) inhibitor that was approved by the FDA on January 26, 2006.  Sunitinib is a small molecule that inhibits multiple RTKs, some of which are implicated in tumor growth, pathologic angiogenesis, and metastatic progression of cancer. Sunitinib was evaluated for its inhibitory activity against a variety of kinases (>80 kinases) and was identified as an inhibitor of platelet-derived growth factor receptors (PDGFRa and PDGFRb), vascular endothelial growth factor receptors (VEGFR1, VEGFR2 and VEGFR3), stem cell factor receptor (KIT), Fms-like tyrosine kinase-3 (FLT3), colony stimulating factor receptor Type 1 (CSF-1R), and the glial cell-line derived neurotrophic factor receptor (RET). Sunitinib inhibition of the activity of these RTKs has been demonstrated in biochemical and cellular assays, and inhibition of function has been demonstrated in cell proliferation assays. The primary metabolite exhibits similar potency compared to sunitinib in biochemical and cellular assays.",The molecular weight is 398.48.,Sunitinib has a topological polar surface area of 77.23.,The log p value of  is 3.0.,Sunitinib is approved and investigational.,Sunitinib is a solid.,True
15003,"Cortisone acetate is a steroid hormone that has both glucocoriticoid and mineral corticoid activities. Corticosteroids are used to provide relief for inflamed areas of the body. They lessen swelling, redness, itching, and allergic reactions. They are often used as part of the treatment for a number of different diseases, such as severe allergies or skin problems, asthma, or arthritis. Endogenous glucocorticoids and some synthetic corticoids have high affinity to the protein transcortin (also called CBG, corticosteroid-binding protein), whereas all of them bind albumin. Glucocorticoids also bind to the cytosolic glucocorticoid receptor. For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Also used to treat endocrine (hormonal) disorders (adrenal insufficiency, Addisons disease). It is also used to treat many immune and allergic disorders. As a glucocorticoid agent, cortisone acetate changes genetic transcription levels causing varied metabolic effects and a modified immune response to varied stimuli. lucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated. Cortisone acetate binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes preventing the phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products in inflammation Prostaglandins and Leukotrienes are inhibited by the action of Glucocorticoids. Glucocorticoids also stimulate the lipocortin-1 escaping to the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines etc.) from neutrophils, macrophages and mastocytes. Additionally the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",The molecular weight is 402.49.,Cortisone acetate has a topological polar surface area of 97.74.,The log p value of  is 2.02.,Cortisone acetate is approved and investigational.,Cortisone acetate is a solid.,True
15004,A chelating agent that has been used to mobilize toxic metals from the tissues of man and experimental animals. It is the main metabolite of DISULFIRAM.,,,,Ditiocarb is experimental.,Ditiocarb is a solid.,True
15005,"Dexloxiglumide is a selective cholecystokinin type A (CCKA) receptor antagonist in phase III testing by Rottapharm in Europe only, as U.S. trials have been discontinued. As the D-isomer of loxiglumide, it retains all pharmacological properties of loxiglumide but is more potent. For the treatment of Irritable Bowel Syndrome (IBS) and Gastroesophageal Reflux Disease (GERD). Dexloxiglumide is a selective cholecystokinin type A (CCKA) receptor antagonist. In October 2003, following the completion of two phase III clinical studies involving dexloxiglumide in women with constipation-predominant irritable bowel syndrome (IBS), Forest Laboratories decided to discontinue development of the drug for this indication. The results of the studies showed that dexloxiglumide did not show statistically significant favorability over placebo. Rotta Research is continuing a phase III trial of a different design in Europe for the IBS indication and also for gastroesophogeal reflux disease. CCKA antagonists target receptors in the gastrointestinal system to increase gastric emptying and intestinal motility, as well as modulate intestinal sensitivity to distension.",The molecular weight is 461.38.,Dexloxiglumide has a topological polar surface area of 95.94.,The log p value of  is 4.34.,Dexloxiglumide is investigational.,Dexloxiglumide is a solid.,True
15006,"Iloperidone is an atypical antipsychotic for the treatment of schizophrenia symptoms. Hoechst Marion Roussel Inc. researched the drug until May 1996. In June 1997 they gave the research rights to Titan Pharmaceuticals, who gave the worldwide development, manufacturing, and marketing rights to Novartis in August 1998. On June 9, 2004, Titan Pharmaceuticals gave the Phase III development rights to Vanda Pharmaceuticals. FDA approved on May 9, 2009. Treatment of acute schizophrenia.  Iloperidone shows high affinity and maximal receptor occupancy for dopamine D2 receptors in the caudate nucleus and putamen of the brains of schizophrenic patients. The improvement in cognition is attributed to iloperidone's high affinity for α adrenergic receptors. Iloperidone also binds with high affinity to serotonin 5-HT2a and dopamine 3 receptors. Iloperidone binds with moderate affinity to dopamine D4, serotonin 5-HT6 and 5-HT7, and norepinephrine NEα1 receptors. Furthermore, iloperidone binds with weak affinity to serotonin 5-HT1A, dopamine D1, and histamine H1 receptors.  Iloperidone is a dopamine D2 and 5-HT2A receptor antagonist and acts as a neuroleptic agent. ",The molecular weight is 426.49.,Iloperidone has a topological polar surface area of 64.8.,The log p value of  is 3.92.,Iloperidone is approved.,Iloperidone is a solid.,True
15007,"Azimilide is an investigational class III anti-arrhythmic drug that blocks fast and slow components of the delayed rectifier cardiac potassium channels. It is not approved for use in any country, but is currently in clinical trials in the United States. Investigated for use/treatment in arrhythmia and atrial fibrillation. Azimilide is a new class III anti-arrhythmic agent. It is distinguished by a relative lack of reverse use-dependence, excellent oral absorption, no need for dose titration, an option for out-patient initiation, no need for adjustment associated with renal or liver failure and a lack of interaction with warfarin or digoxin. It carries some risk of torsade de pointes and rarely, neutropoenia. The mechanism of action of azimilide is to block both the slowly conducting (I(Ks)) and rapidly conducting (I(Kr)) rectifier potassium currents in cardiac cells. This differs from other class III agents that block I(Kr) exclusively or in combination with sodium, calcium, or transient outward (I(to)) potassium current channels. It also has blocking effects on sodium (I(Na)) and calcium currents (I(CaL)). Its effects on reentrant circuits in infarct border zones causing ventricular tachyarrhythmias are unknown. ",The molecular weight is 457.96.,Azimilide has a topological polar surface area of 72.6.,The log p value of  is 2.35.,Azimilide is investigational.,Azimilide is a solid.,True
15008,"Trastuzumab emtansine, formerly called Trastuzumab-DM1 (T-DM1) is a first-in-class HER2 antibody drug conjugate (ADC) comprised of Genentech's trastuzumab antibody linked to ImmunoGen's cell-killing agent, DM1. T-DM1 combines two strategies-- anti-HER2 activity and targeted intracellular delivery of the potent anti-microtubule agent, DM1 (a maytansine derivative)--to produce cell cycle arrest and apoptosis. Trastuzumab emtansine is marketed under the brand name Kadcyla and is indicated for use in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. The FDA label has two precautions. First that trastuzumab emtansine and trastuzumab cannot be interchanged. Second that there is a black box warning of serious side effects such as hepatotoxicity, embryo-fetal toxicity, and cardiac toxicity. Used in HER2-positive, metastatic breast cancer patients who have already used taxane and/or trastuzumab for metastatic disease or had their cancer recur within 6 months of adjuvant treatment. Trastuzumab emtansine was evaluated in two Herceptin-responsive and one Herceptin-resistant breast tumor models. In the Herceptin-responsive models, Trastuzumab-DM1 caused complete tumor regression in all mice, whereas Herceptin alone slowed tumor growth. In the Herceptin- resistant model, Herceptin alone had no effect on tumor growth. In contrast, Trastuzumab-DM1 caused >90% tumor reduction in all mice. In this Herceptin- resistant model, tumor regrowth was observed after cessation of Trastuzumab- DM1 treatment, yet regression re-occurred when dosing was resumed. The effect was specific for HER2-positive tumors. Thus the physiological effects of trastuzumab emtansine are cell cycle arrest and cell death by apoptosis.  Trastuzumab emtansine is a HER2 antibody drug conjugate. The antibody portion is trastuzumab, which is humanized anti-HER2 IgG1, and produced in the mammalian Chinese Hamster Ovary cells. The drug portion is DM1, which is a maytansine derivative that inhibits microtubules. These two portions are covalently connected by 4- cyclohexane-1-carboxylate (MCC), which is a stable thioether linker. Together MCC and DM1 are called emtansine and are produced by chemical synthesis.",,,,Trastuzumab emtansine is approved and investigational.,Trastuzumab emtansine is a solid.,True
15009,"Romidepsin is a selective inhibitor of histone deacetylase, approved in the US in 2009 for the treatment of cutaneous T-cell lymphoma (CTCL) or/and peripheral T-cell lymphoma (PTCL) in patients who have received at least one prior systemic therapy. These indications are based on response rate. Clinical benefit such as improvement in overall survival has not been demonstrated. For the treatment of cutaneous T-cell lymphoma (CTCL) or/and peripheral T-cell lymphoma (PTCL) in patients who have received at least one prior systemic therapy. These indications are based on response rate. Clinical benefit such as improvement in overall survival has not been demonstrated.  Romidepsin is a prodrug, where it becomes active once taken up into the cell. The active metabolite has a free thiol group, which interacts with zinc ions in the active site of class 1 and 2 HDAC enzymes, resulting in inhibition of its enzymatic activity. Certain tumors have over expressed HDACs and downregulated/mutated histone acetyltransferases. This imbalance of HDAC relative to histone acetyltransferase can lead to a decrease in regulatory genes, ensuing tumorigenesis. Inhibition of HDAC may restore normal gene expression in cancer cells and result in cell cycle arrest and apoptosis. ",The molecular weight is 540.69.,Romidepsin has a topological polar surface area of 142.7.,The log p value of  is 3.44.,Romidepsin is approved and investigational.,Romidepsin is a solid.,True
15010,"Rivaroxaban is an anticoagulant and the first orally active direct factor Xa inhibitor. Unlike warfarin, routine lab monitoring of INR is not necessary. However there is no antidote available in the event of a major bleed. Only the 10 mg tablet can be taken without regard to food. The 15 mg and 20 mg tablet should be taken with food. FDA approved on July 1, 2011. Rivaroxaban is indicated for the prevention of venous thromboembolic events (VTE) in patients who have undergone total hips replacements and total knee replacement surgery; prevention of stroke and systemic embolism in patients with nonvalvular atrial fibrillation; treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE); to reduce risk of recurrent DVT and/or PE. Rivaroxaban is also indicated, in combination with aspirin, for reducing the risk of major cardiovascular events in patients with chronic coronary artery disease or peripheral artery disease. Due to a lack of safety studies, it is not recommended for use in those under 18 years old. Its use is also not recommended in those with severe renal impairment (<30mL/min). Rivaroxaban is an anticoagulant which binds directly to factor Xa. Thereafter, it effectively blocks the amplification of the coagulation cascade, preventing the formation of thrombus. Rivaroxaban is a unqiue anticoagulant for two reasons. First of all, it is does not involve antithrombin III (ATIII) to exert its anticoagulant effects. Secondly, it is an oral agent whereas the widely used unfractionated heparin and low molecular weight heparins are for parenteral use only. Although the activated partial thromboplastin time (aPTT) and HepTest (a test developed to assay low molecular weight heparins) are prolonged in a dose-dependant manner, neither test is recommended for the assessment of the pharmacodynamic effects of rivaroxaban. Anti-Xa activity and inhibition of anti-Xa activity monitoring is also not recommended despite being influenced by rivaroxaban. Rivaroxaban competitively inhibits free and clot bound factor Xa. Factor Xa is needed to activate prothrombin (factor II) to thrombin (factor IIa). Thrombin is a serine protease that is required to activate fibrinogen to fibrin, which is the loose meshwork that completes the clotting process. Since one molecule of factor Xa can generate more than 1000 molecules of thrombin, selective inhibitors of factor Xa are profoundly useful in terminating the amplification of thrombin generation. The action of rivaroxaban is irreversible.",The molecular weight is 435.88.,Rivaroxaban has a topological polar surface area of 88.18.,The log p value of  is 2.39.,Rivaroxaban is approved.,Rivaroxaban is a solid.,True
15011,"Udenafil is a new phosphodiesterase type 5 (PDE5) inhibitor used to treat erectile dysfunction (ED). It has been approved in South Korea and will be marketed under the brand name Zydena. It is not yet approved for use in the U.S., E.U., or Canada. Investigated for use/treatment in erectile dysfunction and hypertension. Udenafil is a potent selective phosphodiesterase type 5 (PDE5) inhibitor. Udenafil inhibits the cGMP specific phosphodiesterase type 5 (PDE5) which is responsible for degradation of cGMP in the corpus cavernosum located around the penis. Penile erection during sexual stimulation is caused by increased penile blood flow resulting from the relaxation of penile arteries and corpus cavernosal smooth muscle. This response is mediated by the release of nitric oxide (NO) from nerve terminals and endothelial cells, which stimulates the synthesis of cGMP in smooth muscle cells. Cyclic GMP causes smooth muscle relaxation and increased blood flow into the corpus cavernosum. The inhibition of phosphodiesterase type 5 (PDE5) by udenafil enhances erectile function by increasing the amount of cGMP.",The molecular weight is 516.66.,Udenafil has a topological polar surface area of 117.92.,The log p value of  is 3.15.,Udenafil is approved and investigational.,Udenafil is a solid.,True
15012,"Temsirolimus is a derivative of sirolimus used in the treatment of renal cell carcinoma (RCC). It was developed by Wyeth Pharmaceuticals under the trade name Torisel. Temsirolimus was approved by the FDA in late May 2007 as well as the European Medicines Agency (EMEA) on November 2007. For the treatment of renal cell carcinoma (RCC). Also investigated for use/treatment in breast cancer, lymphoma (unspecified), rheumatoid arthritis, and multiple myeloma. Temsirolimus is an inhibitor of mTOR (mammalian target of rapamycin). Temsirolimus binds to an intracellular protein (FKBP-12), and the protein-drug complex inhibits the activity of mTOR that controls cell division. Inhibition of mTOR activity resulted in a G1 growth arrest in treated tumor cells. When mTOR was inhibited, its ability to phosphorylate p70S6k and S6 ribosomal protein, which are downstream of mTOR in the PI3 kinase/AKT pathway was blocked. In in vitro studies using renal cell carcinoma cell lines, temsirolimus inhibited the activity of mTOR and resulted in reduced levels of the hypoxia-inducible factors HIF-1 and HIF-2 alpha, and the vascular endothelial growth factor.",The molecular weight is 1030.3.,Temsirolimus has a topological polar surface area of 241.96.,The log p value of  is 7.46.,Temsirolimus is approved.,Temsirolimus is a solid.,True
15013,"Saxagliptin (rINN) is an orally active hypoglycemic (anti-diabetic drug) of the new dipeptidyl peptidase-4 (DPP-4) inhibitor class of drugs. FDA approved on July 31, 2009. Treatment of type 2 diabetes mellitus to improve glycemic control in combination with other agents or as monotherapy.  Post-administration of saxagliptin, GLP-1 and GIP levels rise up to 2- to 3- fold. Because it is very selective of DPP-4 inhibition, there are fewer systemic side effects. Saxagliptin inhibits DPP-4 enzyme activity for a 24-hour period. It also decreased glucagon concentrations and increased glucose-dependent insulin secretion from pancreatic beta cells. The half maximal inhibitory concentration (IC50) is 0.5 nmol/L. Saxagliptin did not prolong the QTc interval to a clinically significant degree.  Saxagliptin is a dipeptidyl peptidase-4 (DPP-4) inhibitor antidiabetic for the treatment of type 2 diabetes. DPP-4 inhibitors are a class of compounds that work by affecting the action of natural hormones in the body called incretins. Incretins decrease blood sugar by increasing consumption of sugar by the body, mainly through increasing insulin production in the pancreas, and by reducing production of sugar by the liver. ",The molecular weight is 315.42.,Saxagliptin has a topological polar surface area of 90.35.,The log p value of  is 0.01.,Saxagliptin is approved.,Saxagliptin is a solid.,True
15014,"Ambrisentan is an orally active selective type A endothelin receptor antagonist indicated for the treatment of pulmonary arterial hypertension. It is approved in Europe, Canada and the United States for use as a single agent to improve exercise ability and delay clinical worsening. In addition, it is approved in the United States for use in combination with tadalafil to reduce the risks of disease progression, hospitalization and to improve exercise ability. Studies establishing the efficacy of Ambrisentan included patients with both idiopathic or heritable pulmonary arterial hypertension and those with pulmonary arterial hypertension associated with connective tissue diseases. Patients studied displayed symptoms and etiologies predominantly of WHO Functional Class II-III. As an endothelin receptor antagonist, Ambrisentan prevents endogenous endothelin peptide from constricting the muscles in blood vessels, allowing them to relax and permit a reduction in blood pressure. Ambrisentan is indicated for treatment of idiopathic (‘primary’) pulmonary arterial hypertension (IPAH) and pulmonary arterial hypertension (PAH) associated with connective tissue disease in patients with WHO functional class II or III symptoms. In the United States of America, ambrisentan is also indicated in combination with tadalafil to reduce the risks of disease progression and hospitalization for worsening PAH, and to improve exercise ability. Ambrisentan 10 mg daily had no significant effect on the QTc interval, whereas a 40 mg daily dose of ambrisentan increased mean QTc at tmax by 5 ms with an upper 95% confidence limit of 9 ms. Significant QTc prolongation is not expected in patients taking ambrisentan without concomitant metabolic inhibitors.  Endothelin-1 (ET-1) is an endogenous peptide that acts on the endothelin type A (ETA) and endothelin type B (ETB) receptors in vascular smooth muscle and endothelium. ETA-mediated actions include vasoconstriction and cell proliferation, whereas ETB predominantly mediates vasodilation, anti-proliferation, and ET-1 clearance. In patients with pulmonary arterial hypertension, ET-1 levels are increased and correlate with increased right arterial pressure and severity of disease.",The molecular weight is 378.43.,Ambrisentan has a topological polar surface area of 81.54.,The log p value of  is 3.75.,Ambrisentan is approved and investigational.,Ambrisentan is a solid.,True
15015,"Armodafinil is the enantiopure of the wakefulness-promoting agent modafinil (Provigil), and is indicated to improve wakefulness in adult patients with excessive sleepiness associated with obstructive sleep apnea (OSA), narcolepsy, or shift work disorder (SWD). Research has shown that armodafinil significantly improves driving simulator performance in patients with SWD. Armodafinil consists of the (−)-R-enantiomer of the racemic modafinil. Armodafinil is produced by the pharmaceutical company Cephalon Inc. (a wholly owned subsidiary of Teva Pharmaceutical Industries Ltd.) and was approved by the U.S. Food and Drug Administration (FDA) in June 2007. Investigated for use/treatment in sleep disorders, obstructive sleep apnea, schizophrenia and schizoaffective disorders, depression, and bipolar disorders. Nuvigil (armodafinil) is a single-isomer of modafini. The exact mechanism of action is unknown. Armodafinil belongs to a class of drugs known as eugeroics, which are stimulants that provide long-lasting mental arousal. Pharmacologically, armodafinil does not bind to or inhibit several receptors and enzymes potentially relevant for sleep/wake regulation. Armodafinil is not a direct- or indirect-acting dopamine receptor agonist. However, in vitro, both armodafinil and modafinil bind to the dopamine transporter and inhibit dopamine reuptake. ",The molecular weight is 273.35.,Armodafinil has a topological polar surface area of 60.16.,The log p value of  is 0.94.,Armodafinil is approved and investigational.,Armodafinil is a solid.,True
15016,"Cethromycin is a 3-keto (ketolide) derivative of erythromycin A with an 11,12-carbamate group and an O-6-linked aromatic ring system. Cethromycin represents a joint development effort by Abbott Laboratories, Taisho Pharmaceuticals, and Advanced Life Sciences, intended to be marketed under the trade name Restanza for the treatment of community-acquired pneumonia. However, after completing phase III clinical trials, it was deemed safe but not sufficiently efficacious by the FDA. Cethromycin currently has no FDA-approved indications; it was granted orphan drug designation for the prophylactic treatment of inhalation anthrax in 2007 and for the prophylactic treatment of both plague due to _Yersinia pestis_ and tularemia due to _Francisella tularensis_ in 2009. Cethromycin binds to the 50S subunit of the bacterial ribosome to inhibit both ribosome assembly and bacterial protein synthesis. Adverse effects such as diarrhea, nausea, vomiting, and headache may be due to off-target inhibition of molecules within mammalian cells. Respiratory tract infections can be caused by numerous strains of bacteria, requiring careful consideration of treatment and antibiotics effective against a broad spectrum of potential pathogens. Cethromycin, like other macrolide antibiotics, binds to the 23S rRNA of the 50S subunit of the bacterial ribosome. This binding, primarily mediated through regions II and V of the rRNA, occludes the peptide exit tunnel and inhibits bacterial protein synthesis. In addition, cethromycin is capable of binding to ribosomal intermediates during ribosome biogenesis, inhibiting the formation of functional 70S bacterial ribosomes. Due to the sequence and structural similarity of ribosomes between species, cethromycin displays broad-spectrum activity against diverse Gram-positive, Gram-negative, and atypical bacteria.",,,,Cethromycin is investigational.,Cethromycin is a solid.,True
15017,"Hutchinson-Gilford progeria syndrome (HGPS) is a rare autosomal dominant disorder estimated to affect approximately one in 20 million individuals resulting in adverse symptoms associated with premature ageing: skeletal dysplasia, joint contractures, atherosclerosis, myocardial fibrosis/dysfunction, scleroderma-like cutaneous effects, lipoatrophy, alopecia, and a severe failure to thrive; HGPS is uniformly fatal. Mechanistically, HGPS is underpinned by a single heterozygous C-to-T mutation at position 1824 of the _LMNA_ gene, which results in the accumulation of an aberrant farnesylated form of lamin A called progerin in the inner nuclear membrane. Lonafarnib is a farnesyl transferase (FTase) inhibitor (FTI), which reduces the farnesylation of numerous cellular proteins, including progerin; as progerin farnesylation is important for localization to the nuclear membrane, lonafarnib inhibits progerin accumulation and improves symptoms in HGPS patients. Lonafarnib is a farnesyltransferase inhibitor indicated in patients aged 12 months and older with a body surface area of at least 0.39 m<sup>2</sup> to reduce the risk of mortality associated with Hutchinson-Gilford progeria syndrome (HGPS). It is also indicated in this same population for the treatment of processing-deficient progeroid laminopathies that either involve a heterozygous _LMNA_ mutation resulting in the accumulation of a progerin-like protein or homozygous/compound heterozygous mutations in _ZMPSTE24_. Lonafarnib is a direct farnesyl transferase inhibitor that reduces the farnesylation of numerous cellular proteins, including progerin, the aberrantly truncated form of lamin A that accumulates in progeroid laminopathies such as Hutchinson-Gilford progeria syndrome. Treatment with lonafarnib has been associated with electrolyte abnormalities, myelosuppression, and increased liver enzyme levels (AST/ALT), although causation remains unclear. Also, lonafarnib is known to cause nephrotoxicity in rats and rod-dependent low-light vision decline in monkeys at plasma levels similar to those achieved under recommended dosing guidelines in humans; patients taking lonafarnib should undergo regular monitoring for both renal and ophthalmological function. In addition, based on observations from animal studies with rats, monkeys, and rabbits with plasma drug concentrations approximately equal to those attained in humans, lonafarnib may cause both male and female fertility impairment and embryo-fetal toxicity. Hutchinson-Gilford progeria syndrome (HGPS) is a rare autosomal dominant disorder estimated to affect approximately one in 20 million individuals resulting in premature ageing, associated cardiovascular, cerebrovascular, and musculoskeletal effects and early death around 14 years of age. The _LMNA_ gene encodes lamin A and lamin C, two proteins involved in nuclear integrity and function at the inner nuclear membrane. Under normal conditions, the 12-exon _LMNA_ gene produces full-length prelamin A, which undergoes farnesylation of the C-terminal _CaaX_ motif, followed by proteolytic cleavage of the terminal three amino acids (_aaX_) by the metalloproteinase ZMPSTE24, subsequent carboxymethylation, and finally removal of the last 15 amino acids to yield mature, unfarnesylated, lamin A protein. In HGPS, a single heterozygous C-to-T mutation at position 1824 results in a cryptic splice site that removes the last 150 nucleotides of exon 11 and a concomitant 50-amino acid deletion in the C-terminus of the prelamin A protein. This aberrant prelamin A protein, often called progerin, is permanently farnesylated but unable to complete maturation due to the removal of the second endoproteolytic cleavage site.",,,,Lonafarnib is approved and investigational.,Lonafarnib is a solid.,True
15018,"Midostaurin (as Rydapt) is a multitarget kinase inhibitor for the treatment for adult patients with newly diagnosed acute myeloid leukemia (AML) who have a specific genetic mutation called FLT3. It was initially characterized as a potential broad-spectrum antineoplastic agent, with activity toward diverse solid and hematopoietic tumors. It was approved on April 28, 2017 and has shown to increase the overall survival rate in patients with AML as an adjunct therapy along with chemotherapeutic agents. Investigated for use/treatment in adult patients with high-risk acute myeloid leukemia (AML) who are FLT3 mutation-positive, agressive systemic mastocytosis (ASM), systemic mastocytosis with associated hematological neoplasm (SM-AHN), or mast cell leukemia (MCL).  It targets multiple WT and mutated kinases that, when activated, constitutively stimulate aberrant signalling cascades that lead to malignancies such as AML and ASM. Alternative pharmacodynamic effect of midostaurin in prolonging QTc intervals was not clinically significant in patients with advanced SM or AML when compared to placebo. Midostaurin is therapeutically beneficial as a combination therapy for patients undergoing chemotherapy.  It potently inhibits multiple receptor tyrosine kinases. Midostaurin and its major active metabolites CGP62221 and CGP52421 inhibit the activity of protein kinase C alpha (PKCalpha), VEGFR2, KIT, PDGFR and WT and/or mutant FLT3 tyrosine kinases. Inhibition of FLT3 receptor signalling cascades induces apoptosis of target leukemia cells expressing target receptors and mast cells, in addition to its antiproliferative activity toward multiple cancer cell lines. ",The molecular weight is 570.65.,Midostaurin has a topological polar surface area of 77.73.,The log p value of  is 5.49.,Midostaurin is approved and investigational.,Midostaurin is a solid.,True
15019,"Apixaban is an oral, direct, and highly selective factor Xa (FXa) inhibitor of both free and bound FXa, as well as prothrombinase, independent of antithrombin III for the prevention and treatment of thromboembolic diseases. It is marketed under the name Eliquis. Apixaban was approved by the FDA on December 28, 2012. Apixaban is indicated for reducing the risk of stroke and systemic embolism in patients who have nonvalvular atrial fibrillation, prophylaxis of deep vein thrombosis(DVT) leading to pulmonary embolism(PE) in patients after a hip or knee replacement surgery, and treatment of DVT and PE to reduce the risk of recurrence. Apixaban selectively inhibits factor Xa in its free and bound forms, independant of antithrombin III. Apixaban also inhibits prothrominase. These effects prevent the formation of a thrombus. Apixaban selectively inhibits factor Xa in its free and bound forms, independant of antithrombin III. Apixaban also inhibits prothrominase. These effects prevent the formation of a thrombus.",The molecular weight is 459.51.,Apixaban has a topological polar surface area of 110.76.,The log p value of  is 1.89.,Apixaban is approved.,Apixaban is a solid.,True
15020,"Axitinib is a second generation tyrosine kinase inhibitor that works by selectively inhibiting vascular endothelial growth factor receptors (VEGFR-1, VEGFR-2, VEGFR-3). Through this mechanism of action, axitinib blocks angiogenesis, tumour growth and metastases. It is reported to exhibit potency that is 50-450 times higher than that of the first generation VEGFR inhibitors. Axitinib is an indazole derivative. It is most commonly marketed under the name Inlyta® and is available in oral formulations. Used in kidney cell cancer and investigated for use/treatment in pancreatic and thyroid cancer. Axitinib prevents the progression of cancer by inhibiting angiogenesis and blocking tumor growth. Axitinib selectively blocks the tyrosine kinase receptors VEGFR-1 (vascular endothelial growth factor receptor), VEGFR-2, and VEGFR-3.",The molecular weight is 386.47.,Axitinib has a topological polar surface area of 70.67.,The log p value of  is 3.33.,Axitinib is approved and investigational.,Axitinib is a solid.,True
15021,"Vicriviroc, also known as SCH 417690 and SCH-D, is currently in clinical trials for the management of HIV-1. This pyrimidine based drug inhibits the interaction of HIV-1 with CCR5, preventing viral entry into cells. This drug was developed by Schering-Plough. Investigated for use/treatment in HIV infection and viral infection. Vicriviroc is a once daily oral inhibitor of CCR5. It noncompetitively binds to a hydrophobic pocket between transmembrance helices by the extracellular side of CCR5. This allosteric antagonism causes a conformational change in the protein preventing binding of gp120 to CCR5. This prevents the entry of HIV into the cell.",,,,Vicriviroc is investigational.,Vicriviroc is a solid.,True
15022,"Artemether is an antimalarial agent used to treat acute uncomplicated malaria. It is administered in combination with lumefantrine for improved efficacy. This combination therapy exerts its effects against the erythrocytic stages of <i>Plasmodium spp.</i> and may be used to treat infections caused by <i>P. falciparum</i> and unidentified <i>Plasmodium</i> species, including infections acquired in chloroquine-resistant areas. Artemether and lumefantrine combination therapy is indicated for the treatment of acute uncomplicated malaria caused by <i>Plasmodium falciparum</i>, including malaria acquired in chloroquine-resistant areas. May also be used to treat uncomplicated malaria when the <i>Plasmodium</i> species has not been identified. Indicated for use in adults and children greater than 5 kg.  In the body, artemether is metabolized into the active metabolite metabolite dihydroartemisinin. The drug works against the erythrocytic stages of <i>P. falciparum</i> by inhibiting nucleic acid and protein synthesis. Artemether is administered in combination with lumefantrine for improved efficacy. Artemether has a rapid onset of action and is rapidly cleared from the body. It is thought that artemether provides rapid symptomatic relief by reducing the number of malarial parasites. Lumefantrine has a much longer half life and is believed to clear residual parasites.  Involves an interaction with ferriprotoporphyrin IX (“heme”), or ferrous ions, in the acidic parasite food vacuole, which results in the generation of cytotoxic radical species. ",The molecular weight is 298.38.,Artemether has a topological polar surface area of 46.15.,The log p value of  is 3.05.,Artemether is approved.,Artemether is a solid.,True
15023,"Gestodene is a progestogen hormonal contraceptive. Products containing gestoden include Meliane, which contains 20 mcg of ethinylestradiol and 75 mcg of gestodene; and Gynera, which contains 30 mcg of ethinylestradiol and 75 mcg of gestodene.",The molecular weight is 310.44.,Gestodene has a topological polar surface area of 37.3.,The log p value of  is 3.04.,Gestodene is investigational.,Gestodene is a solid.,True
15024,Seproxetine is also known as (S)-norfluoxetine. It is a selective serotonin reuptake inhibitor (SSRI). It is an active metabolite of fluoxetine. Seproxetine was being investigated by Eli Lilly as an antidepressant but development was never completed and the drug was never marketed. Seproxetine is also known as (S)-norfluoxetine. It is a selective serotonin reuptake inhibitor (SSRI). It is an active metabolite of fluoxetine. Seproxetine was being investigated by Eli Lilly as an antidepressant but development was never completed and the drug was never marketed.,,,,Seproxetine is investigational.,Seproxetine is a solid.,True
15025,"Cabazitaxel is an anti-neoplastic used with the steroid medicine prednisone. Cabazitaxel is used to treat people with prostate cancer that has progressed despite treatment with docetaxel. Cabazitaxel is prepared by semi-synthesis with a precursor extracted from yew needles (10-deacetylbaccatin III). It was approved by the U.S. Food and Drug Administration (FDA) on June 17, 2010. For treatment of patients with hormone-refractory metastatic prostate cancer previously treated with a docetaxel-containing treatment regimen. Cabaitaxel has anti-tumour properties and is effective against docetaxel-sensitive and -insensitive tumours.  Cabazitaxel is a microtubule inhibitor. Cabazitaxel binds to tubulin and promotes its assembly into microtubules while simultaneously inhibiting disassembly. This leads to the stabilization of microtubules, which results in the interference of mitotic and interphase cellular functions. The cell is then unable to progress further into the cell cycle, being stalled at metaphase, thus triggering apoptosis of the cancer cell. ",The molecular weight is 835.94.,Cabazitaxel has a topological polar surface area of 202.45.,The log p value of  is 5.44.,Cabazitaxel is approved.,Cabazitaxel is a solid.,True
15026,"Hydroxyprogesterone caproate is a synthetic steroid hormone that is similar to medroxyprogesterone acetate and megestrol acetate. It is an ester derivative of 17α-hydroxyprogesterone formed from caproic acid (hexanoic acid). Hydroxyprogesterone caproate was previously marketed under the trade name Delalutin by Squibb, which was approved by the U.S. Food and Drug Administration (FDA) in 1956 and withdrawn from marketing in 1999. The U.S. FDA approved Makena from KV Pharmaceutical (previously named as Gestiva) on February 4, 2011 for prevention of preterm delivery in women with a history of preterm delivery, sparking a pricing controversy. Hydroxyprogesterone caproate is indicated for the prevention of spontaneous preterm births in singleton pregnancies in women who have previously had a spontaneous preterm birth. (1)  No specific pharmacodynamic studies have been performed to assess hydroxyprogesterone caproate injections. (4) However, the mechanism of action is likely related to increased interaction between progesterone and progesterone receptors. (5)  The mechanism by which progesterone prevents preterm birth is not well understood, but many pathways are likely involved. (1) Progesterone plays a vital role in regulation of the female reproductive system and is important for successful implantation of the embryo and maintenance of pregnancy. It acts by binding to progesterone receptors in the uterus, ovaries, breasts and in the central nervous system. These receptors exist in 2 isoforms, PR-A and PR-B. Progesterone binding to these receptors ultimately leads to regulation of gene transcription. (2) This results in an anti-inflammatory effect which blunts the proinflammatory state that occurs with initiation of labor, and maintains uterine queiscence by stabilizing progesterone acting on the myometrium. (2) ",The molecular weight is 428.61.,Hydroxyprogesterone caproate has a topological polar surface area of 60.44.,The log p value of  is 5.99.,Hydroxyprogesterone caproate is approved and investigational.,Hydroxyprogesterone caproate is a solid.,True
15027,"Crizotinib an inhibitor of receptor tyrosine kinase for the treatment of non-small cell lung cancer (NSCLC). Verification of the presence of ALK fusion gene is done by Abbott Molecular's Vysis ALK Break Apart FISH Probe Kit. This verification is used to select for patients suitable for treatment. FDA approved in August 26, 2011. Crizotinib is used for the treatment of locally advanced or metastatic non-small cell lung cancer (NSCLC) that is anaplastic-lymphoma kinase (ALK)-positive as detected by a FDA-approved test.  Crizotinib is a tyrosine kinase receptor inhibitor. More specifically, it inhibits anaplastic lymphoma kinase (ALK), hepatocyte growth factor receptor (HGFR, c-MET), and Recepteur d'Origine Nantais (RON). Abnormalities in the ALK gene caused by mutations or translocations may lead to expression of oncogenic fusion proteins. In patients with NSCLC, they have the EML4-ALK gene. Crizotinib inhibits ALK tyrosine kinase which ultimately results in decreased proliferation of cells that carry the genetic mutation and tumour survivability. ",The molecular weight is 450.34.,Crizotinib has a topological polar surface area of 77.99.,The log p value of  is 4.29.,Crizotinib is approved.,Crizotinib is a solid.,True
15028,"Boceprevir is a direct acting antiviral medication used as part of combination therapy to treat chronic Hepatitis C, an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Treatment options for chronic Hepatitis C have advanced significantly since 2011, with the development of Direct Acting Antivirals (DAAs) such as Boceprevir. Boceprevir is an inhibitor of NS3/4A, a serine protease enzyme, encoded by HCV genotypes 1 and 4. These enzymes are essential for viral replication and serve to cleave the virally encoded polyprotein into mature proteins like NS4A, NS4B, NS5A and NS5B. The barrier for develoment of resistance to NS3/4A inhibitors is lower than that of NS5B inhibitors, another class of DAAs. Subtitutions at amino acid positions 155, 156, or 168 are known to confer resistance. The substitutions of the enzyme's catalytic triad consisting of H58, D82, and S139 are also likely to alter the affinity of the drug for NS3/4A or the activity of the enzyme itself. Despite this disadvantage Boceprevir is still effective against HCV when paired with , , and. Boceprevir, when used in combination with , , and is indicated for use in the treatment of chronic HCV genotype 1 infection in adults. Boceprevir is classified as a direct-acting antiviral (DAA) and prevents viral replication in HCV genotype 1.  Boceprevir is a NS3/4a protease inhibitor used to inhibit viral HCV replication. NS3/4a protease is an integral part of viral replication and mediates the cleavage the virally encoded polyprotein to mature proteins (NS4A, NS4B, NS5A and NS5B). Boceprevir covalently but reversibly binds the serine (S139) resiude in the active site via a (α)-ketoamide functional group. This inhibits the proteolytic acitvity of the HCV 1a and 1b encoded enzyme.",The molecular weight is 519.69.,Boceprevir has a topological polar surface area of 150.7.,The log p value of  is 3.34.,Boceprevir is approved and withdrawn.,Boceprevir is a solid.,True
15029,"Perampanel is a noncompetitive AMPA glutamate receptor antagonist. It is marketed under the name Fycompa™ and is indicated as an adjunct in patients over 12 years old for the treatment of partial-onset seizures that may or may not occur with generalized seizures. The FDA label includes an important black-boxed warning of serious or life-threatening behavioral and psychiatric reactions in patients taking Fycompa™. Used in patients over 12 years old for the treatment of partial-onset seizures that may or may not occur with generalized seizures. Perampanel is involved in inhibiting neuronal excitation in the central nervous system leading to such effects as decreased pyschomotor performance. The exact mechanism of action of perampanel in seizures is not yet determined, but it is known that perampanel decreases neuronal excitation by non-competitive ihibition of the AMPA receptor.",The molecular weight is 349.39.,Perampanel has a topological polar surface area of 56.99.,The log p value of  is 4.17.,Perampanel is approved.,Perampanel is a solid.,True
15030,"Ponatinib is a novel Bcr-Abl tyrosine kinase inhibitor that is especially effective against the T315I mutation for the treatment of chronic myeloid leukemia. FDA approved on December 14, 2012. Ponatinib is indicated for the treatment of adult patients with chronic phase, accelerated phase, or blast phase chronic myeloid leukemia (CML) that is resistant or intolerant to prior tyrosine kinase inhibitor therapy or Philadelphia chromosome positive acute lymphoblastic leukemia (Ph+ALL) that is resistant or intolerant to prior tyrosine kinase inhibitor therapy. Ponatinib is a multi-target kinase inhibitor. Its primary cellular target is the Bcr-Abl tyrosine kinase protein which is constitutively active and promotes the progression of CML. This protein arises from the fused Bcr and Abl gene- what is commonly known as the Philadelphia chromosome. Ponatinib is unique in that it is especially useful in the treatment of resistant CML because it inhibits the tyrosine kinase activity of Abl and T315I mutant kinases. The T315I mutation confers resistance in cells as it prevents other Bcr-Abl inhibitors from binding to the Abl kinase. Other targets that ponatinib inhibits are members of the VEGFR, PDGFR, FGFR, EPH receptors and SRC families of kinases, and KIT, RET, TIE2, and FLT3. A decrease in tumour size expressing native or T315I mutant BCR-ABL have been observed in rats. ",The molecular weight is 532.57.,Ponatinib has a topological polar surface area of 65.77.,The log p value of  is 5.77.,Ponatinib is approved and investigational.,Ponatinib is a solid.,True
15031,Fluprednidene is a corticosteroid.,The molecular weight is 390.45.,Fluprednidene has a topological polar surface area of 94.83.,The log p value of  is 1.7.,Fluprednidene is experimental.,Fluprednidene is a solid.,True
15032,Fluocortolone is a glucocorticoid with anti-inflammatory activity used topically for various skin disorders.,The molecular weight is 376.47.,Fluocortolone has a topological polar surface area of 74.6.,The log p value of  is 2.61.,Fluocortolone is approved and withdrawn.,Fluocortolone is a solid.,True
15033,"Idelalisib is a phosphoinositide 3-kinase inhibitor indicated in the treatment of chronic lymphocytic leukemia (CLL), relapsed follicular B-cell non-Hodgkin lymphoma (FL), and relapsed small lymphocytic lymphoma (SLL). For the treatment of relapsed CLL, it is currently indicated as a second-line agent in combination with rituximab in patients for whom rituximab alone would be considered appropriate therapy due to other co-morbidities, while in the treatment of FL and SLL it is intended to be used in patients who have received at least two prior systemic therapies. More specifically, idelalisib targets P110δ, the delta isoform of the enzyme phosphatidylinositol-4,5-bisphosphate 3-kinase, also known as PI-3K. The PI-3Ks are a family of enzymes involved in cellular functions such as cell growth, proliferation, differentiation, motility, survival and intracellular trafficking, which in turn are involved in cancer. In contrast to the other class IA PI3Ks p110α and p110β, p110δ is principally expressed in leukocytes (white blood cells) and is important for the function of T cells, B cell, mast cells and neutrophils. By inhibiting this enzyme, idelalisib induces apoptosis of malignant cells and inhibits several cell signaling pathways, including B-cell receptor (BCR) signaling and C-X-C chemokine receptors type 5 and type 4 signalling, which are involved in trafficking and homing of B-cells to the lymph nodes and bone marrow. Treatment of lymphoma cells with idelalisib has been shown to result in inhibition of chemotaxis and adhesion, and reduced cell viability. Idelalisib is indicated in the treatment of chronic lymphocytic leukemia (CLL), relapsed follicular B-cell non-Hodgkin lymphoma (FL), and relapsed small lymphocytic lymphoma (SLL). For the treatment of relapsed CLL, it is currently indicated as a second-line agent in combination with rituximab in patients for whom rituximab alone would be considered appropriate therapy due to other co-morbidities, while in the treatment of FL and SLL it is intended to be used in patients who have received at least two prior systemic therapies. Idelalisib specifically inhibits P110δ, the delta isoform of the enzyme phosphatidylinositol-4,5-bisphosphate 3-kinase, also known as PI-3K. The PI-3Ks are a family of enzymes involved in cellular functions such as cell growth, proliferation, differentiation, motility, survival and intracellular trafficking, which in turn are involved in cancer. In contrast to the other class IA PI3Ks p110α and p110β, p110δ is principally expressed in leukocytes (white blood cells) and is important for the function of T cells, B cell, mast cells and neutrophils. By inhibiting this enzyme, idelalisib induces apoptosis of malignant cells and inhibits several cell signaling pathways, including B-cell receptor (BCR) signaling and C-X-C chemokine receptors type 5 and type 4 signalling, which are involved in trafficking and homing of B-cells to the lymph nodes and bone marrow. Treatment of lymphoma cells with idelalisib has been shown to result in inhibition of chemotaxis and adhesion, and reduced cell viability.",The molecular weight is 415.43.,Idelalisib has a topological polar surface area of 99.16.,The log p value of  is 3.62.,Idelalisib is approved.,Idelalisib is a solid.,True
15034,"Cobicistat, marketed under the name Tybost (formerly GS-9350), indicated for treating infection with human immunodeficiency virus (HIV). Although it does not have any anti-HIV activity, cobicistat acts as a pharmacokinetic enhancer by inhibiting cytochrome P450 3A isoforms (CYP3A) and therefore increases the systemic exposure of coadministered agents that are metabolized by CYP3A enzymes. More specifically, cobicistat is indicated to increase systemic exposure of atazanavir or darunavir (once daily dosing regimen) in combination with other antiretroviral agents in the treatment of HIV-1 infection. Increasing systemic exposure of anti-retrovirals (ARVs) without increasing dosage allows for better treatment outcomes and a decreased side effect profile. Cobicistat is a CYP3A inhibitor indicated to increase systemic exposure of atazanavir or darunavir (once daily dosing regimen) in combination with other antiretroviral agents in the treatment of HIV-1 infection. It is not interchangeable with ritonavir to increase systemic exposure of darunavir 600 mg twice daily, fosamprenavir, saquinavir, or tipranavir due to lack of exposure data. The use of cobicistat is not recommended with darunavir 600 mg twice daily, fosamprenavir, saquinavir or tipranavir. Complex or unknown mechanisms of drug interactions preclude extrapolation of ritonavir drug interactions to certain cobicistat interactions. Cobicistat and ritonavir when administered with either atazanavir or darunavir may result in different drug interactions when used with concomitant medications. Cobicistat is a mechanism-based inhibitor of cytochrome P450 3A (CYP3A) isoforms. Inhibition of CYP3A-mediated metabolism by cobicistat increases the systemic exposure of CYP3A substrates atazanavir and darunavir and therefore enables increased anti-viral activity at a lower dosage. Cobicistat does not have any anti-HIV activity on its own. ",The molecular weight is 776.03.,Cobicistat has a topological polar surface area of 138.02.,The log p value of  is 3.98.,Cobicistat is approved.,Cobicistat is a solid.,True
15035,"Vortioxetine is an atypical antipsychotic and antidepressant indicated for the treatment of major depressive disorder (MDD). It is classified as a serotonin modulator and simulator (SMS) as it has a multimodal mechanism of action towards the serotonin neurotransmitter system whereby it simultaneously modulates one or more serotonin receptors and inhibits the reuptake of serotonin. More specifically, vortioxetine acts via the following biological mechanisms: as a serotonin reuptake inhibitor (SRI) through inhibition of the serotonin transporter, as a partial agonist of the 5-HT1B receptor, an agonist of 5-HT1A, and an antagonist of the 5-HT3, 5-HT1D, and 5-HT7 receptors. SMSs were developed because there are many different subtypes of serotonin receptors, however, not all of these receptors appear to be involved in the antidepressant effects of SRIs. Some serotonin receptors seem to play a relatively neutral or insignificant role in the regulation of mood, but others, such as 5-HT1A autoreceptors and 5-HT7 receptors, appear to play an oppositional role in the efficacy of SRIs in treating depression. Vortioxetine is indicated for the treatment of major depressive disorder (MDD). Vortioxetine binds with high affinity to the human serotonin transporter (Ki=1.6 nM), but not to the norepinephrine (Ki=113 nM) or dopamine (Ki>1000 nM) transporters. Vortioxetine potently and selectively inhibits reuptake of serotonin by inhibition of the serotonin transporter (IC50=5.4 nM). Specifically, vortioxetine binds to 5­HT3 (Ki=3.7 nM), 5­HT1A (Ki=15 nM), 5­HT7 (Ki=19 nM), 5­HT1D (Ki=54 nM), and 5­HT1B (Ki=33 nM), receptors and is a 5­HT3, 5­HT1D, and 5­HT7 receptor antagonist, 5­HT1B receptor partial agonist, and 5­HT1A receptor agonist. Vortioxetine is classified as a serotonin modulator and simulator (SMS) as it has a multimodal mechanism of action towards the serotonin neurotransmitter system whereby it simultaneously modulates one or more serotonin receptors and inhibits the reuptake of serotonin. More specifically, vortioxetine acts via the following biological mechanisms: as a serotonin reuptake inhibitor (SRI) through inhibition of the serotonin transporter, while also acting as a partial agonist of the 5-HT1B receptor, an agonist of 5-HT1A, and antagonist of the 5-HT3, 5-HT1D, and 5-HT7 receptors.",The molecular weight is 298.45.,Vortioxetine has a topological polar surface area of 15.27.,The log p value of  is 4.92.,Vortioxetine is approved and investigational.,Vortioxetine is a solid.,True
15036,"Olaparib is an inhibitor of poly (ADP-ribose) polymerase (PARP) enzymes, including PARP1, PARP2, and PARP3. PARP enzymes are involved in normal cellular homeostasis, such as DNA transcription, cell cycle regulation, and DNA repair. Olaparib has been shown to inhibit growth of select tumor cell lines in vitro and decrease tumor growth in mouse xenograft models of human cancer both as monotherapy or following platinum-based chemotherapy. Increased cytotoxicity and anti-tumor activity following treatment with olaparib were noted in cell lines and mouse tumor models with deficiencies in BRCA. In vitro studies have shown that olaparib-induced cytotoxicity may involve inhibition of PARP enzymatic activity and increased formation of PARP-DNA complex, resulting in disruption of cellular homeostasis and cell death. Olaparib is a poly (ADP-ribose) polymerase (PARP) inhibitor indicated for the treatment of: The effect of olaparib on cardiac repolarization was assessed in 119 patients following a single dose of 300 mg and in 109 patients following multiple dosing of 300 mg twice daily. No clinically relevant effect of olaparib on QT interval was observed. Olaparib is an inhibitor of poly (ADP-ribose) polymerase (PARP) enzymes, including PARP1, PARP2, and PARP3. PARP enzymes are involved in normal cellular homeostasis, such as DNA transcription, cell cycle regulation, and DNA repair. Olaparib has been shown to inhibit growth of select tumor cell lines in vitro and decrease tumor growth in mouse xenograft models of human cancer both as monotherapy or following platinum-based chemotherapy. Increased cytotoxicity and anti-tumor activity following treatment with olaparib were noted in cell lines and mouse tumor models with deficiencies in BRCA. In vitro studies have shown that olaparib-induced cytotoxicity may involve inhibition of PARP enzymatic activity and increased formation of PARP-DNA complex, resulting in disruption of cellular homeostasis and cell death. ",The molecular weight is 434.47.,Olaparib has a topological polar surface area of 82.08.,The log p value of  is 1.24.,Olaparib is approved.,Olaparib is a solid.,True
15037,"Difluocortolone is a potent topical corticosteroid. It is commonly used in dermatology for the reduction of inflammation and itching. It was submited to the FDA in July 1984 by the pharmaceutical company Schering AG. Difluocortolone is used as a topical treatment of the symptoms of inflammatory skin disorders like eczema, seborrheic eczema, lichen planus and psoriasis. All these disorders present as a common characteristic the occurrence of symptoms as itching, swelling, redness and scaling. Diflucortolone is a steroid with the properties of being an anti-inflammatory, antipruritic and vasoconstrictive. Its activity causes the vasoconstriction of the blood vessels and thus a decrease in the release of inflammatory substances. These actions produce the effect of skin soothed and elimination of the symptoms. Diflucortolone performs its action by the induction of lipocortins which are phospholipase A2 inhibitory proteins and sequentially inhibiting the release of arachidonic acid. The absence of arachidonic acid translates to the inhibition of the formation, release and activity of endogenous chemical inflammatory mediators. Another mechanism of action is the transrepression in which diflucortolone binds to the glucocorticoid receptor which induces its migration to the nucleus where it stimulates the transcription of anti-inflammatory genes like tyrosine aminotransferase, phophoenolpyruvate carboxykinase, IL-10, etc. and suppress the expression of proinflammatory genes like cytokines, growth factors, adhesion molecules, etc.",The molecular weight is 394.46.,Difluocortolone has a topological polar surface area of 74.6.,The log p value of  is 2.45.,Difluocortolone is approved and investigational and withdrawn.,Difluocortolone is a solid.,True
15038,"Daclatasvir is a direct-acting antiviral agent against Hepatitis C Virus (HCV) used for the treatment of chronic HCV genotype 1 and 3 infection. It is marketed under the name DAKLINZA and is contained in daily oral tablets as the hydrochloride salt form. Hepatitis C is an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Daclatasvir was the first drug with demonstrated safety and therapeutic efficacy in treating HCV genotype 3 without the need for co-administration of interferon or. It exerts its antiviral action by preventing RNA replication and virion assembly via binding to NS5A, a nonstructural phosphoprotein encoded by HCV. Binding to the N-terminus of the D1 domain of NS5A prevents its interaction with host cell proteins and membranes required for virion replication complex assembly. Daclatasvir is shown to target both the cis- and trans-acting functions of NS5A and disrupts the function of new HCV replication complexes by modulating the NS5A phosphorylation status. The most common critical NS5A amino acid substitutions that led to reduced susceptibility to daclatasvir therapy occured at position Q30 (Q30H/K/R) and M28 in genotype 1a patients and Y93H in genotype 3 patients.  Indicated for use with sofosbuvir, with or without ribavirin, for the treatment of chronic HCV genotype 1a/b or 3 infection. The dosing regimen of 60mg daclatasvir 60 mg with 400mg sofosbuvir once a day is recommended for both genontypes.  Daclatasvir is a direct-acting antiviral agent that targets the NS5A and causes a decrease in serum HCV RNA levels. It disrupts HCV replication by specifically inhibiting the critical functions of an NS5A protein in the replication complex. It is shown to cause downregulation of the hyperphosphorylation of NS5A. It does not appear to prolong the QT interval even when given at 3 times the maximum recommended dose.  NS5A is a viral nonstructural phospoprotein that is part of a functional replication complex in charge of viral RNA genome amplification on endoplasmic reticulum membranes. It has the ability to bind to HCV RNA. It is shown to have two distinct functions in HCV RNA replication based on phosphorylated states. Maintaining the HCV replication complex is mediated by the cis-acting function of basally phosphorylated NS5A and the trans-acting function of hyperphosphorylated NS5A modulates HCV assembly and infectious particle formation. Daclatasvir is shown to disrupt hyperphosphorylated NS5A proteins thus interfere with the function of new HCV replication complexes. It is also reported that daclatasvir also blocks both intracellular viral RNA synthesis and virion assembly/secretion in vivo. ",The molecular weight is 738.89.,Daclatasvir has a topological polar surface area of 174.64.,The log p value of  is 4.72.,Daclatasvir is approved and investigational.,Daclatasvir is a solid.,True
15039,"Benidipine has the formula 1,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-3,5-pyridine-dicarboxylic acid methyl 1-(phenylmethyl)-3-piperidinyl ester hydrochloride. It is a synthetic dihydropyridine derivative that has anti-hypertensive and anti-anginal actions. It was originated in Japan by Kyowa Hakko, it is submitted for FDA approval and it is currently available in some Asian countries like India and Japan. Benidipine is a potent and long-lasting drug indicated for the treatment of cardiovascular diseases such as hypertension, renoparenchymal hypertension and angina pectoris. Benidipine reduces systolic and diastolic blood pressure as well as to present decreases in heart rate pulse after treatment. It is reported also a decrease urinary protein excretion and serum triglycerides. Different studies have shown benidipine anti-oxidative activity, stimulation of NO production, suppression of adhesion molecules expression, stimulation of osteoblast differentiation, suppression of the proliferation of vascular smooth muscle cells and mesangial cells, as well as myocardial protection. The enhancement of NO production is associated with the cardioprotective and antiartheriosclerotic effects of benidipine. Benidipine is a tripe calcium channel inhibitor by inhibiting L, N and T type calcium channel. It presents a very long-lasting activity that can be explained by its high affinity for cell membranes from the DHP binding site; this characteristic indicated a long-lasting pharmacological activity of benidipine. The additional property of benidipine is the vascular selectivity towards peripheral blood vessels.",The molecular weight is 505.57.,Benidipine has a topological polar surface area of 111.01.,The log p value of  is 5.71.,Benidipine is experimental.,Benidipine is a solid.,True
15040,"Paritaprevir is a direct acting antiviral medication used as part of combination therapy to treat chronic Hepatitis C, an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Treatment options for chronic Hepatitis C have advanced significantly since 2011, with the development of Direct Acting Antivirals (DAAs) such as paritaprevir. As a newer generation and directly acting HCV antiviral, paritaprevir products have better Sustained Virological Response (SVR) rates, higher barriers to resistance, fewer side effects, and a reduced pill burden compared to older agents such as , , , , and. By combining multiple antiretroviral medications into fixed dose products, the viral lifecycle can be targeted at multiple stages while simultaneously reducing the risk of developing resistant viral strains. Within Canada and the United States, paritaprevir is currently available in three fixed dose products: Viekira Pak (FDA), Technivie (FDA and Health Canada), and Holkira Pak (Health Canada). When used within the fixed-dose combination product with , , and as the FDA-approved product Viekira Pak, paritaprevir is indicated for the treatment of HCV genotype 1b without cirrhosis or with compensated cirrhosis, and when combined with for the treatment of HCV genotype 1a without cirrhosis or with compensated cirrhosis. At concentrations approximately 6 and 1.8 times the therapeutic concentrations of paritaprevir and ombitasvir, the combination did not prolong QTc to any clinically relevant extent. Paritaprevir is a potent inhibitor of the NS3/4A serine protease of Hepatitis C Virus (HCV). Following viral replication of HCV genetic material and translation into a single polypeptide, Nonstructural Protein 3 (NS3) and its activating cofactor Nonstructural Protein 4A (NS4A) are responsible for cleaving it into the following structural and nonstructural proteins required for assembly into mature virus: NS3, NS4A, NS4B, NS5A, and NS5B. By inhibiting viral protease NS3/4A, paritaprevir therefore prevents viral replication and function.",The molecular weight is 765.89.,Paritaprevir has a topological polar surface area of 189.65.,The log p value of  is 6.28.,Paritaprevir is approved and investigational.,Paritaprevir is a solid.,True
15041,"Dexamethasone isonicotinate is an anti-inflammatory, anti-allergic glucocorticoid that can be administered orally, by inhalation, topically, and parenterally. Its unintended mineralocorticoid action may cause salt and water retention.",,,,Dexamethasone isonicotinate is vet_approved.,Dexamethasone isonicotinate is a solid.,True
15042,"Elbasvir is a direct-acting antiviral medication used as part of combination therapy to treat chronic hepatitis C, an infectious liver disease caused by infection with hepatitis C virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, affecting 72% of all chronic HCV patients. Treatment options for chronic hepatitis C have advanced significantly since 2011, with the development of direct-acting antivirals (DAAs) such as elbasvir. Elbasvir is an inhibitor of NS5A, a protein essential for viral replication and virion assembly. The barrier to the development of resistance to NS5A inhibitors is lower than that of NS5B inhibitors, another class of DAAs. Substitutions at amino acid positions 28, 30, 31, or 93 are known to confer resistance to elbasvir. Despite this disadvantage elbasvir is still effective against HCV, particularly when paired with. Elbasvir, when used in combination with as the combination product Zepatier, is indicated for use with or without for the treatment of chronic HCV genotypes 1 or 4 infection in adults. Elbasvir is classified as a direct-acting antiviral (DAA) and prevents viral replication in HCV genotypes 1a, 1b, and 4. Elbasvir is an inhibitor of the HCV non-structural protein 5A. While the precise role of this protein is unknown, it is essential to viral replication and virion assembly. Potential modes of action of NS5A inhibitors like elbasvir include blocking signaling interactions, redistribution of NS5A from the endoplasmic reticulum to the surface of lipid droplets, and modification of the HCV replication complex.",The molecular weight is 882.04.,Elbasvir has a topological polar surface area of 188.8.,The log p value of  is 6.66.,Elbasvir is approved.,Elbasvir is a solid.,True
15043,"Asunaprevir, also named as BMS-650032, is a potent hepatitis C virus (HCV) NS3 protease inhibitor. It has been shown to have a very high efficacy in dual-combination regimens with daclatasvir in patients chronically infected with HCV genotype 1b. It was developed by Bristol-Myers Squibb Canada and approved by Health Canada on April 22, 2016. The commercialization of asunaprevir was canceled one year later on October 16, 2017. Asunaprevir is indicated in combination with other agents for the treatment of chronic hepatitis C in adult patients with hepatitis C virus genotypes 1 or 4 and compensated liver cirrhosis.  Studies in vitro demonstrated a significant antiviral activity in HCV replicon cell systems with an EC50 of 4nm and 1nm against the HCV genotype 1a and 1b respectively. These studies showed a limited activity against the genotypes 2 and 3. This property makes asunaprevir a highly selective anti-HCV agent that is not effective against HCV closely related virus. Asunaprevir produce robust declines in HCV RNA levels in patients with HCV genotype 1 infection.In clinical studies, it has been shown that asunaprevir is well-tolerated and the mean maximum HCV RNA level reduction from baseline was of approximately 2.87 log10 IU/ml. Asunaprevir is a highly active HCV NS3 protease inhibitor. The genome of HCV has a positive polarity which allows it to be translated into a protein in the host cell without further transformation steps. However, the resultant protein needs to be divided by the enzyme NS3 protease into single proteins in order to be able to exert its enzymatic activity or structural role. Therefore, due to NS3 vital importance for viral replication, the inhibiting action of asunaprevir causes a robust antiviral activity.",The molecular weight is 748.29.,Asunaprevir has a topological polar surface area of 182.33.,The log p value of  is 6.31.,Asunaprevir is approved and investigational and withdrawn.,Asunaprevir is a solid.,True
15044,"Isavuconazole is an triazole antifungal with broad spectrum of activity and good safety profile. It is approved by the FDA and EMA for the treatment of invasive aspergillosis and mucormycosis. It works by inhibiting fungal cell membrane synthesis. Invasive fungal infections pose significant clinical challenges for patients, especially those who are immunocompromised. In vitro, most of the _Candida_ species, most _Aspergillus_ species, Mucorales, _Cryptococcus_ spp., _Fusarium_ species, dermatophytes and dimorphic fungi displayed susceptibility to isavuconzaole. Resistance to isavuconazole has been associated with the mutation in the target gene CYP51. Cross-resistance between isavuconazole and other azoles was also proposed although the clinical relevance is unclear.  - Indicated for patients 18 years of age and older for the treatment of invasive aspergillosis. Isavucoanzole exhibits antifungal activity against most strains of _Aspergillus flavus, Aspergillus fumigatus, Aspergillus niger_, and Mucorales such as _Rhizopus oryzae_ and Mucormycetes species _in vivo_ and _in vitro_. In a cardiac electrophysiology study involving healthy subjects, isavuconazole induced dose-related shortening of the QTc interval but the additive effect of isavuconazole with other QTc-prolonging drug is unknown.  Isavuconazole displays fungicidal actions by disrupting the biosynthesis of ergosterol, which is a key component of fungal cell membrane. It inhibits cytochrome P-450 dependent enzyme lanosterol 14-alpha-demethylase that mediates the conversion of lanosterol to ergosterol. The side arm of of the active isavuconazole molecule allows for greater affinity for the binding pocket in the fungal CYP51 protein by orienting the triazole ring of the molecule to engage with the heme moiety at the bottom of the binding pocket. This explains the wide antifungal spectrum of isavuconazole and possible cross-resistance to other triazoles. As a result of lanosterol 14-alpha-demethylase inhibition, toxic methylated sterol precursors such as 14-α-methylated lanosterol, 4,14-dimethylzymosterol, and 24-methylenedihydrolanosterol alter the function of fungal membrane and accumulate within the fungal cytoplasm. Depletion of ergosterol within the fungal cell membrane leads to decreased structural integrity and function of the cell membrane, inhibited fungal cell growth and replication , and ultimately cell death. Mammalian cell demethylation is less sensitive to isavuconazole inhibition.",,,,Isavuconazole is approved and investigational.,,True
15045,"Tezacaftor is a drug of the cystic fibrosis transmembrane conductance regulator (CFTR) potentiator class. It was developed by Vertex Pharmaceuticals and FDA approved in combination with to manage cystic fibrosis. This drug was approved by the FDA on February 12, 2018. Tezacaftor is combined with ivacaftor in one product for the treatment of cystic fibrosis (CF) in patients aged 12 years or older with two copies of the _F508del_ gene mutation or at least one mutation in the CFTR gene that is responsive to this drug. Clinical studies have shown a significant decrease in sweat chloride and an increase in the forced expiratory volume (FEV), a measure of lung function, following Tevacaftor/Ivacaftor therapy. Phase 3 clinical studies have shown that a significant increase in forced expiratory volume was attained at 4 and 8 weeks after initiating this drug. The above effects lead to improvement of the respiratory symptoms of cystic fibrosis. Tezacaftor does not induce clinically significant QT prolongation. When given with ivacaftor, tezacaftor can lead to liver transaminase elevations. Testing of transaminases (ALT and AST) levels should occur before starting this combination every 3 months during the first year of treatment, and every year afterwards. Patients with a history of transaminase elevations should be monitored more frequently. The transport of charged ions across cell membranes is normally achieved through the actions of the cystic fibrosis transmembrane regulator (CFTR) protein. This protein acts as a channel and allows for the passage of chloride and sodium. This process affects the movement of water in and out of the tissues and impacts the production of mucus that lubricates and protects certain organs and body tissues, including the lungs. In the _F508del_ mutation of the CFTR gene, one amino acid is deleted at the position 508, therefore, the CFTR channel function is compromised, resulting in thickened mucus secretions. CFTR correctors such as tezacaftor aim to repair F508del cellular misprocessing. This is done by modulating the position of the CFTR protein on the cell surface to the correct position, allowing for adequate ion channel formation and increased in water and salt movement through the cell membrane. The concomitant use of ivacaftor is intended to maintain an open channel, increasing the transport of chloride, reducing thick mucus production.",The molecular weight is 520.5.,Tezacaftor has a topological polar surface area of 113.18.,The log p value of  is 3.68.,Tezacaftor is approved and investigational.,Tezacaftor is a solid.,True
15046,"Icotinib is a potent and specific epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) Icotinib hydrochloride is a novel epidermal growth factor receptor (EGFR)–tyrosine kinase inhibitor, exhibits encouraging efficacy and tolerability in patients with advanced non-small-cell lung cancer (NSCLC) who failed previous chemotherapy. In vitro: Icotinib inhibits EGFR activity in a dose-dependent manner, with an IC50 value of 5 nM and complete inhibition at 62.5 nM. Icotinib selectively solely inhibits the EGFR members including the wild type and mutants with inhibition efficacies of 61-99%. Icotinib blocks EGFR-mediated intracellular tyrosine phosphorylation in human epidermoid carcinoma A431 cells in a dose-dependent manner. Meanwhile, in the proliferation assay performed on A431, BGC-823, A549, H460, HCT8, KB and Bel-7402 cell lines, it was found that the relative sensitivity of cell lines to Icotinib is A431 > BGC-823 > A549 > H460 > KB > HCT8 and Bel-7402. Icotinib exhibits a broad spectrum of antitumor activity and it is especially effective against tumors expressing higher levels of EGFR. Icotinib is a highly selective, first generation epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) which binds reversibly to the ATP binding site of the EGFR protein, preventing completion of the signal transduction cascade. EGFR is an oncogenic receptor and patients with activating somatic mutations, such as an exon 19 deletion or exon 21 L858R mutation, within the tyrosine kinase domain display unchecked cell proliferation. ",The molecular weight is 391.43.,Icotinib has a topological polar surface area of 74.73.,The log p value of  is 4.16.,Icotinib is experimental and investigational.,,True
15047,Clobetasol is under investigation for the treatment of Scleroderma. Clobetasol has been investigated for the prevention of Psoriasis and Cutaneous Atrophy Due to Corticosteroids.,,,,Clobetasol is approved and experimental and investigational.,,True
15048,"Tenapanor is a novel, small molecule medication approved in September 2019 for the treatment of constipation-predominant irritable bowel-syndrome (IBS-C). It was first designed and synthesized in 2012. As an inhibitor of the sodium/hydrogen exchanger isoform 3 (NHE3) transporter, it is the first and currently only medication within its class and therefore exists as a novel alternative in the treatment of IBS-C. Tenapanor is indicated for the treatment of constipation-predominant irritable bowel syndrome (IBS-C) in adults. It is also currently being investigated as a treatment for hyperphosphatemia in chronic kidney disease patients undergoing dialysis (NCT02081534 and NCT02675998). Through the inhibition of dietary sodium absorption tenapanor causes an increase in water secretion into the intestines, thereby decreasing transit time and softening stool consistency. Tenapanor is a locally-acting small molecule inhibitor of the sodium/hydrogen exchanger isoform 3 (NHE3), an antiporter expressed on the apical surface of enterocytes in the small intestine and colon which is involved in sodium-fluid homeostasis. By inhibiting this antiporter tenapanor causes retention of sodium within the lumen of the intestine - this results in an osmotic gradient that draws water into the lumen and softens stool consistency.",,,,Tenapanor is approved and investigational.,Tenapanor is a solid.,True
15049,"Osilodrostat is an inhibitor of 11β-hydroxylase (also referred to as CYP11B1), the enzyme that catalyzes the final step in the biosynthesis of endogenous cortisol. It is used to lower circulating cortisol levels in the treatment of Cushing's disease, a disorder in which cortisol levels are chronically and supraphysiologically elevated. Cushing's disease is often the result of ACTH hypersecretion secondary to a pituitary tumor, and surgical resection of the tumour is generally the treatment of choice. As an orally bioavailable drug therapy, osilodrostat provides a novel treatment option for patients in whom removal of the causative tumor is not an option or for whom previous pituitary surgery has not been curative. Osilodrostat is indicated for the treatment of adult patients with Cushing's disease for whom pituitary surgery is not an option or has not been curative. Osilodrostat lowers endogenous cortisol levels by inhibiting the enzyme that catalyzes the final step in cortisol synthesis. As endogenous cortisol levels function as a surrogate marker for drug effect, 24-hour urine free cortisol levels should be assessed 1-2x weekly during the initial titration stage and every 1-2 months thereafter to ensure cortisol levels remain physiologically appropriate. Osilodrostat is highly metabolized and requires dose adjustments in patient with hepatic dysfunction. Cushing’s syndrome is an endocrinological disorder resulting from chronic and excessive exposure to glucocorticoids, the symptoms of which may include thinning of the skin and hair, weight gain, muscle weakness, and osteoporosis, as well a constellation of psychiatric, cardiovascular, and immunological deficiencies. Cushing’s syndrome is most commonly precipitated by exogenous treatment with supraphysiological doses of glucocorticoids such as those found in nasal sprays, skin creams, and inhalers. Cushing’s disease - another less common cause of Cushing’s syndrome - is generally the result of increased endogenous cortisol exposure due to excessive secretion of adrenocroticotrophic hormone (ACTH) from a pituitary adenoma.",,,,Osilodrostat is approved and investigational.,Osilodrostat is a solid.,True
15050,"Valbenazine (development name NBI-98854) has been used in trials studying the treatment and basic science of Tourette Syndrome and Tardive Dyskinesia. In April, 2017, valbenazine was approved by the FDA (as Ingrezza) as the first and only approved treatment for adults with Tardive Dyskinesia (TD). For the treatment of tardive dyskinesia in adults. Valbenazine decreases the availability of monoamine neurotransmitters by preventing their storage in synaptic vesicles. This is believed to be the reason behind its therapeutic effect in tardive dyskinesia although the exact mechanism is unknown. Valbenazine and its active meabolites bind to and inhibit vesicular monoamine transporter 2 (VMAT2)with high selectivity (valbenazine Ki = 150nM, -α-HTBZ Ki = 1.98nM, NBI136110 Ki = 160nM) with no significant binding to VMAT1 (Ki <10microM for each). This prevents the reuptake and storage of monoamine neurotransmitters noradrenaline, dopamine, and serotonin in synaptic vesicles making them vulnerable to metabolism by cytosolic enzymes. The presynaptic release of monoamine neurotransmitters is decreased due to the lack of vesicles with packaged neurotransmitter ready for release into the synapse. Neither valbenazine nor its active metabolite exhibit significant off target binding at dopamine, serotonin, or adrenaline receptors or uptake transporters at 10microM concentrations.",The molecular weight is 418.58.,Valbenazine has a topological polar surface area of 74.02.,The log p value of  is 3.97.,Valbenazine is approved and investigational.,Valbenazine is a solid.,True
15051,"Deflazacort, also known as Emflaza, is a corticosteroid prodrug used as an agent to manage Duchenne Muscular Dystrophy (DMD). It is marketed by Marathon Pharmaceuticals and was approved in February 2017 by the FDA. Deflazacort is indicated for the treatment of Duchenne Muscular Dystrophy (DMD) in patients 2 years of age and older. Deflazacort exerts anti-inflammatory activity in DMD, likely improving various symptoms, including muscle weakness and cardiorespiratory symptoms in addition to delaying their onset. This allows for an increased quality of life and prevents the necessity for surgical procedures, such as those for scoliosis, which is associated with DMD. Studies showed significant preservation of muscle mass in patients generally treated with 0.9 mg/kg/day of deflazacort compared to a control group. The following findings are based on clinical studies using deflazacort on a long term basis: Deflazacort is a corticosteroid prodrug with an active metabolite, 21-deflazacort, which binds to the glucocorticoid receptor to exert anti-inflammatory and immunosuppressive effects on the body. The exact mechanism by which deflazacort exerts its therapeutic effects in patients with DMD is unknown but likely occurs via its anti-inflammatory activities. ",The molecular weight is 441.52.,Deflazacort has a topological polar surface area of 102.26.,The log p value of  is 2.86.,Deflazacort is approved and investigational.,Deflazacort is a solid.,True
15052,"Lemborexant is a novel dual orexin receptor antagonist used in the treatment of insomnia characterized by difficulties with sleep onset and/or sleep maintenance. Recent research in the field of sleep disorders has revealed that insomnia is likely driven not by the inability of the brain to \switch on\"" sleep-related circuits, but rather an inability to \""switch-off\"" wake-promoting circuits. Whereas historically popular pharmacologic treatments for insomnia (e.g. , , benzodiazepines) focus on enhancing sleep drive via modulation of GABA and melatonin receptors, lemborexant and other orexin antagonists (e.g. ) act to counteract inappropriate wakefulness. This novel mechanism of action offers potential advantages over classic hypnotic agents, including a more favorable adverse effect profile and potentially greater efficacy, and may signal the beginning of a new wave of treatment options for patients suffering from insomnia."" Lemborexant is indicated for the treatment of adult patients with insomnia characterized by difficulties with sleep onset and/or sleep maintenance. Lemborexant promotes sleep by antagonizing the actions of wake-promoting chemicals in the brain. Episodes of complex sleep behaviors (e.g. eating food, having sex, making phone calls) have been reported in patients using lemborexant - these events may occur in hypnotic-naive and hyponotic-experienced patients, and patients are unlikely to remember these events. Patients exhibiting complex sleep behaviors should discontinue lemborexant immediately. Lemborexant may carry some risk of abuse, and should be used with caution in patients with a history of alcohol or drug addiction. Its controlled substance schedule is currently under review by the Drug Enforcement Administration. The orexin neuropeptide signaling system is involved in many physiologic functions, including sleep/wake control. Orexin-A and orexin-B activate post-synaptic G-protein coupled orexin-1 receptors (OX1R) and orexin-2 receptors (OX2R), which are found on neurons in the hypothalamus that project to numerous wake-controlling nuclei. Each receptor carries slightly different activity - activation of OX1R appears to suppress the onset of rapid eye movement (REM) sleep, whereas activation of OX2R appears to suppress non-REM sleep.",,,,Lemborexant is approved and investigational.,Lemborexant is a solid.,True
15053,"Letermovir recieved approval from the FDA on November 8th, 2017 for use in prophylaxis of cytomegalovirus (CMV) infection in allogeneic hematopoietic stem cell transplant patients. It represents the first entry into a new class of CMV anti-infectives, DNA terminase complex inhibitors. Letermovir has recieved both priority and orphan drug status from the FDA. It is currently marketed under the brand name Prevymis. For use in prophylaxis of cytomegalovirus (CMV) infection and disease in adult CMV-seropositive recipients of an allogeneic hematopoietic stem cell transplant (HSCT). Letermovir inhibits the activity of the DNA terminase complex of CMV thereby preventing the cutting of viral DNA into mature length genomes for packaging into viral particles. Letemovir inhibits the DNA terminase complex with an EC50 of 2.1nM. CMV relies on a DNA terminase complex consisting of multiple subunits (pUL51, pUL56, and pUL89) for processing of viral DNA. Viral DNA is produced in a single repeating strand which is then cut by the DNA terminase complex into individual viral genomes which can then be packaged into mature viral particles. Letemovir inhibits the activity of this complex to prevent production of mature viral genomes and the production of viable viral particles. The exact nature of Letemovir's binding to this complex is not currently known. Initially, the observation of resistance-causing mutations in pUL56 suggested this subunit was the location of Letemovir binding. However, resistance mutations have now been observed in pUL51, pUL56, and pUL89. It is possible that changes in amino acid sequence in one subunit could result in conformational changes to interacting subunits affecting Letemovir binding or that Letemovir interacts with multiple subunits of the complex but evidence towards either of these distinctions has not yet been seen. pUL89 is known to contain the endonuclease activity of the complex but because all members of the complex are necessary for targeting as well as protection from proteosomal degradation, it is difficult to discern if Letemovir inhibits pUL89's activity directly.",The molecular weight is 572.56.,Letermovir has a topological polar surface area of 77.84.,The log p value of  is 7.06.,Letermovir is approved and investigational.,Letermovir is a solid.,True
15054,"Lorlatinib has been used in trials studying the basic science and treatment of Non-small Cell Lung Cancer and anaplastic lymphoma kinase (ALK)-positive Non-Small Cell Lung Cancer (NSCLC) and ROS1-positive NSCLC. Despite initial responses from the use of various ALK inhibitors, however, it is virtually almost guaranteed that all patients with the condition in question will develop tumour progression or resistance to the current therapy in use. Lorlatinib is a third-generation anaplastic lymphoma kinase (ALK) tyrosine kinase inhibitor (TKI) indicated for the treatment of patients with ALK-positive metastatic non-small cell lung cancer (NSCLC) whose disease has progressed on a) the prior use of crizotinib and at least one other ALK inhibitor for metastatic disease, or b) the prior use of alectinib as the first ALK inhibitor therapy for metastatic disease, or c) the prior use of certinib as the first ALK inhibitor therapy for metastatic disease.  Based on data from Study B7461001, exposure-response relationships for Grade 3 or 4 hypercholesterolemia and for any Grade 3 or 4 adverse reaction were observed at steady-state exposures achieved at the recommended dosage, with higher probability of the occurrence of adverse reactions with increasing lorlatinib exposure. Non-small cell lung cancer (NSCLC) accounts for up to 85% of lung cancer cases worldwide and remains a particularly difficult to treat condition. The gene rearrangement of anaplastic lymphoma kinase (ALK) is a genetic alteration that drives the development of NSCLC in a number of patients. Ordinarily, ALK is a natural endogenous tyrosine kinase receptor that plays an important role in the development of the brain and elicits activity on various specific neurons in the nervous system.",,,,Lorlatinib is approved and investigational.,Lorlatinib is a solid.,True
15055,"Deutetrabenazine is a novel, highly selective vesicular monoamine transporter 2 (VMAT2) inhibitor indicated for the management of chorea associated with Huntington’s disease. It is a hexahydro-dimethoxybenzoquinolizine derivative and a deuterated. The presence of deuterium in deutetrabenazine increases the half-lives of the active metabolite and prolongs their pharmacological activity by attenuating CYP2D6 metabolism of the compound. This allows less frequent dosing and a lower daily dose with improvement in tolerability. Decreased plasma fluctuations of deutetrabenazine due to attenuated metabolism may explain a lower incidence of adverse reactions associated with deutetrabenazine. Deutetrabenazine is a racemic mixture containing RR-Deutetrabenazine and SS-Deutetrabenazine.  Indicated for the treatment of chorea associated with Huntington’s disease.  In clinical trials, there was an evidence of clinical effectiveness of deutetrabenazine in improving the symptoms of involuntary movements in patient with tardive dyskinesia by reducing the mean Abnormal Involuntary Movement Scale (AIMS) score. In a randomized, double-blind, placebo-controlled crossover study in healthy male and female subjects, single dose administration of 24 mg deutetrabenazine results in an approximately 4.5 msec mean increase in QTc. Effects at higher exposures to deutetrabenazine or its metabolites have not been evaluated. Deutetrabenazine and its metabolites were shown to bind to melanin-containing tissues including eyes, skin and fur in pigmented rats. After a single oral dose of radiolabeled deutetrabenazine, radioactivity was still detected in eye and fur at 35 days following dosing.  The precise mechanism of action of deutetrabenazine in mediating its anti-chorea effects is not fully elucidated. Deutetrabenazine reversibly depletes the levels of monoamines, such as dopamine, serotonin, norepinephrine, and histamine, from nerve terminals via its active metabolites. The major circulating metabolites are α-dihydrotetrabenazine and β-HTBZ that act as reversible inhibitors of VMAT2. Inhibition of VMAT2 results in decreased uptake of monoamines into synaptic terminal and depletion of monoamine stores from nerve terminals. ",The molecular weight is 323.47.,Deutetrabenazine has a topological polar surface area of 38.77.,The log p value of  is 3.46.,Deutetrabenazine is approved and investigational.,Deutetrabenazine is a solid.,True
15056,"Doravirine is an HIV-1 non-nucleoside reverse transcriptase inhibitor (NNRTI) intended to be administered in combination with other antiretroviral medicines. Doravirine is available by itself or as a combination product of doravirine (100 mg), lamivudine (300 mg), and tenofovir disoproxil fumarate (300 mg). Doravirine is indicated, in combination with other antiretroviral agents, for the treatment of HIV-1 infection in adult patients with no prior antiretroviral treatment history. It is also indicated to replace the current antiretroviral regimen in those who are virologically suppressed (HIV-1 RNA less than 50 copies per mL) on a stable antiretroviral regimen with no history of treatment failure and no known substitutions associated with resistance to doravirine. In a clinical phase 2 trial evaluating a dose range of 0.25-2x the recommended dose of doravirine (in combination with emtricitabine/tenofovir) in HIV-1 infected subjects with no antiretroviral treatment history, no exposure-response relationship for efficacy was identified for doravirine. Doravirine is a pyridinone non-nucleoside reverse transcriptase inhibitor of HIV-1. Reverse transcriptase is the enzyme with which HIV generates complementary DNA (cDNA) to its RNA genome - this cDNA is then inserted into the host cell genome, where it can be transcribed into viral RNA for the purposes of replication. Doravirine inhibits HIV-1 replication by non-competitively inhibiting HIV-1 reverse transcriptase. Doravirine does not, however, inhibit the human cellular DNA polymerases α, ß, and mitochondrial DNA polymerase γ.",,,,Doravirine is approved and investigational.,Doravirine is a solid.,True
15057,"Rucaparib is a potent mammalian poly(ADP-ribose) polymerase (PARP) 1, 2 and 3 inhibitor with anticancer properties. PPAR is an enzyme that plays an essential role in DNA repair by activating response pathways and facilitating repair , and defects in these repair mechanisms have been demonstrated in various malignancies, including cancer. Regulation of repair pathways is critical in promoting necessary cell death. BRCA genes are tumor suppressor genes mediate several cellular process including DNA replication, transcription regulation, cell cycle checkpoints, apoptosis, chromatin structuring and homologous recombination (HR). Homologous recombination deficiency (HRD), along with PPAR inhibition, is a vulnerability that enhances the cell death pathway when the single mutations alone would permit viability. Ovarian cancer commonly possesses defects in DNA repair pathways such as HRD due to BRCA mutations or otherwise.  Indicated as monotherapy for the treatment of patients with deleterious BRCA mutation (germline and/or somatic) associated advanced ovarian cancer who have been treated with two or more chemotherapies. Select patients for therapy based on an FDA-approved companion diagnostic for rucaparib. Rucaparib has been shown to decrease tumor growth in mouse xenograft models of human cancer with or without deficiencies in BRCA. Poly (ADP-ribose) polymerase (PARP) enzymes play a role in DNA repair. PPAR-1 is responsible in repairing single stranded breaks (SSBs) in base excision repair (BER). PARP1 also functions in nonhomologous end-joining (NHEJ) regulation, chromatin remodeling and homologous recombination (HR) DNA repair pathways. When PARP is inhibited, single-strand breaks become double-strand breaks, which are typically repaired via homologous recombination. Pre-existing homologous recombination deficiency (HRD) may occur through mutations in the BRCA1 or BRCA2 genes, which confers persistant cell repair and growth in cancer cells. ",The molecular weight is 323.37.,Rucaparib has a topological polar surface area of 56.92.,The log p value of  is 3.01.,Rucaparib is approved and investigational.,Rucaparib is a solid.,True
15058,Cortivazol is under investigation in clinical trial NCT00804895 (Cluster Headache Cortivazol Injection (CHCI)).,The molecular weight is 530.66.,Cortivazol has a topological polar surface area of 101.65.,The log p value of  is 5.32.,Cortivazol is investigational.,,True
15059,"A macrolide antibiotic that is similar to erythromycin. For the treatment of bacterial infection. Troleandomycin, like other macrolide antibiotics, inhibits bacterial protein synthesis to prevent growth. As a macrolide, troleandomycin binds to the 50S subunit of the bacterial ribosome. This binding inhibits translocation of tRNA along the A, P, and E sites of the ribosome. With tRNA unable to move from site to site, amino acids cannot be deposited onto the polypeptide chain leading to failure of protein synthesis. Bacterial cell growth and duplication is inhibited without the ability to generate the necessary proteins.",The molecular weight is 813.98.,Troleandomycin has a topological polar surface area of 184.19.,The log p value of  is 4.2.,Troleandomycin is approved.,Troleandomycin is a solid.,True
15060,Prednylidene is an experimental systemic glucocorticoid.,The molecular weight is 372.46.,Prednylidene has a topological polar surface area of 94.83.,The log p value of  is 1.86.,Prednylidene is experimental.,,True
15061,"Umifenovir is an indole-based, hydrophobic, dual-acting direct antiviral/host-targeting agent used for the treatment and prophylaxis of influenza and other respiratory infections. It has been in use in Russia for approximately 25 years and in China since 2006. Its invention is credited to a collaboration between Russian scientists from several research institutes 40-50 years ago, and reports of its chemical synthesis date back to 1993. Umifenovir's ability to exert antiviral effects through multiple pathways has resulted in considerable investigation into its use for a variety of enveloped and non-enveloped RNA and DNA viruses, including _Flavivirus_, Zika virus, foot-and-mouth disease, Lassa virus, Ebola virus, herpes simplex,, hepatitis B and C viruses, chikungunya virus, reovirus, Hantaan virus, and coxsackie virus B5. This dual activity may also confer additional protection against viral resistance, as the development of resistance to umifenovir does not appear to be significant. Umifenovir is currently licensed in China and Russia for the prophylaxis and treatment of influenza and other respiratory viral infections. It has demonstrated activity against a number of viruses and has been investigated in the treatment of _Flavivirus_, Zika virus, foot-and-mouth disease, Lassa virus, Ebola virus, and herpes simplex. In addition, it has shown _in vitro_ activity against hepatitis B and C viruses, chikungunya virus, reovirus, Hantaan virus, and coxsackie virus B5. Umifenovir exerts its antiviral effects via both direct-acting virucidal activity and by inhibiting one (or several) stage(s) of the viral life cycle. Its broad-spectrum of activity covers both enveloped and non-enveloped RNA and DNA viruses. It is relatively well-tolerated and possesses a large therapeutic window - weight-based doses up to 100-fold greater than those used in humans failed to produce any pathological changes in test animals. Umifenovir is considered both a direct-acting antiviral (DAA) due to direct virucidal effects and a host-targeting agent (HTA) due to effects on one or multiple stages of viral life cycle (e.g. attachment, internalization), and its broad-spectrum antiviral activity is thought to be due to this dual activity. It is a hydrophobic molecule capable of forming aromatic stacking interactions with certain amino acid residues (e.g. tyrosine, tryptophan), which contributes to its ability to directly act against viruses. Antiviral activity may also be due to interactions with aromatic residues within the viral glycoproteins involved in fusion and cellular recognition, with the plasma membrane to interfere with clathrin-mediated exocytosis and intracellular trafficking, or directly with the viral lipid envelope itself (in enveloped viruses). Interactions at the plasma membrane may also serve to stabilize it and prevent viral entry (e.g. stabilizing influenza hemagglutinin inhibits the fusion step necessary for viral entry).",The molecular weight is 477.42.,Umifenovir has a topological polar surface area of 54.7.,The log p value of  is 5.5.,Umifenovir is investigational.,Umifenovir is a solid.,True
15062,,The molecular weight is 444.9.,Halometasone has a topological polar surface area of 94.83.,The log p value of  is 2.6.,Halometasone is experimental.,,False
15063,Cloprednol is a synthetic glucocorticoid that has been investigated for use in the treatment of asthma. ,The molecular weight is 392.88.,Cloprednol has a topological polar surface area of 94.83.,The log p value of  is 1.52.,Cloprednol is experimental.,,True
15064,"Mometasone furoate is a corticosteroid drug that can be used for the treatment of asthma, rhinitis, and certain skin conditions. It has a glucocorticoid receptor binding affinity 22 times stronger than and higher than many other corticosteroids as well. Mometasone furoate is formulated as a dry powder inhaler, nasal spray, and ointment for its different indications. There are 3 formulations of mometasone furoate with various indications. The inhaler is indicated for prophylaxis of asthma in patients ≥4 years. The nasal spray is indicated for treating nasal symptoms of allergic rhinitis in patients ≥2 years, treating symptoms of nasal congestion from seasonal allergic rhinitis in patients ≥2 years, treating nasal polyps in patients ≥18 years, and prophylaxis of seasonal allergic rhinitis in patients ≥12 years. The ointment is indicated for symptomatic treatment of dermatitis and pruritis in patients ≥2 years. Mometasone is a synthetic corticosteroid with an affinity for glucocorticoid receptors 22 times higher than that of. Mometasone furoate also has a lower affinity to mineralocorticoid receptors than natural corticosteroids, making it more selective in its action. Mometasone furoate diffuses across cell membranes to activate pathways responsible for reducing inflammation. In asthma, mometasone is believed to inhibit mast cells, eosinophils, basophils, and lymphocytes. There is also evidence of inhibition of histamine, leukotrienes, and cytokines.",The molecular weight is 521.43.,Mometasone furoate has a topological polar surface area of 93.81.,The log p value of  is 4.12.,Mometasone furoate is approved and investigational and vet_approved.,Mometasone furoate is a solid.,True
15065,,The molecular weight is 460.52.,Prednisolone hemisuccinate has a topological polar surface area of 138.2.,The log p value of  is 1.73.,Prednisolone hemisuccinate is experimental.,,False
15066,Fluprednidene acetate is a corticosteroid. It has anti-inflammatory and anti-allergic properties.,The molecular weight is 432.49.,Fluprednidene acetate has a topological polar surface area of 100.9.,The log p value of  is 2.24.,Fluprednidene acetate is experimental.,,True
15067,"A water-soluble ester of methylprednisolone used for cardiac, allergic, and hypoxic emergencies. Methylprednisolone sodium succinate (the sodium salt of methylprednisolone hemisuccinate) has the same metabolic and anti-inflammatory actions as methylprednisolone. When given parenterally and in equimolar quantities, the two compounds are equivalent in biologic activity. ",The molecular weight is 474.55.,Methylprednisolone hemisuccinate has a topological polar surface area of 138.2.,The log p value of  is 2.05.,Methylprednisolone hemisuccinate is approved.,,True
15068,,,,,Prednisone acetate is approved and experimental and investigational.,,False
15069,,,,,Clocortolone acetate is experimental.,,False
15070,A 6-methyl progesterone acetate with reported glucocorticoid activity and effect on estrus.,,,,Melengestrol acetate is experimental.,,True
15071,"A naturally occurring glucocorticoid. It has been used in replacement therapy for adrenal insufficiency and as an anti-inflammatory agent. Cortisone itself is inactive. It is converted in the liver to the active metabolite hydrocortisone. (From Martindale, The Extra Pharmacopoeia, 30th ed, p726)",,,,Cortisone is experimental.,,True
15072,"Peginterferon alfa-2b is a form of recombinant interferon used as part of combination therapy to treat chronic Hepatitis C, an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Treatment options for chronic Hepatitis C have advanced significantly since 2011, with the development of Direct Acting Antivirals (DAAs) resulting in less use of Peginterferon alfa-2b. Peginterferon alfa-2b is derived from the alfa-2b moeity of recombinant human interferon and acts by binding to human type 1 interferon receptors. Activation and dimerization of this receptor induces the body's innate antiviral response by activating the janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. Use of Peginterferon alfa-2b is associated with a wide range of severe adverse effects including the aggravation and development of endocrine and autoimmune disorders, retinopathies, cardiovascular and neuropsychiatric complications, and increased risk of hepatic decompensation in patients with cirrhosis. The use of Peginterferon alfa-2b has largely declined since newer interferon-free antiviral therapies have been developed. Peginterferon alfa-2b is indicated for the treatment of HCV in combination with and a NS3/4A protease inhibitor for genotype 1 or without a NS3/4A protease inhibitor for genotypes 2-6. May be used as a monotherapy in patients with contraindications to or significant intolerance to other anti-viral therapies. Peginterferon alfa-2b inhibits viral replication in infected cells, suppresses cell proliferation, induces apoptosis, and exerts an anti-angiogenic effect. Exerts immunomodulatory effects such as enhancement of the phagocytic activity of macrophages, activation of NK cells, stimulation of cytotoxic T-lymphocytes, and the upregulation of the Th1 T-helper cell subset. Also increases concentrations of effector proteins such as serum neopterin and 2'5' oligoadenylate synthetase, raises body temperature, and causes reversible decreases in leukocyte and platelet counts. Peginterferon alfa-2b is derived from recombinant human interferon's alfa-2b moeity. It binds to and activates human type 1 interferon receptors causing them to dimerize. This activates the JAK/STAT pathway. Activation of the JAK/STAT pathway increases expression of multiple genes in multiple tissues involved in the innate antiviral response. Peginterferon alfa-2b may also acitvate the nuclear factor κB pathway.",,,,Peginterferon alfa-2b is approved.,Peginterferon alfa-2b is a liquid.,True
15073,"Fluvoxamine is an antidepressant which functions pharmacologically as a selective serotonin reuptake inhibitor. Though it is in the same class as other SSRI drugs, it is most often used to treat obsessive-compulsive disorder. Indicated predominantly for the management of depression and for Obsessive Compulsive Disorder (OCD). Has also been used in the management of bulimia nervosa. Fluvoxamine, an aralkylketone-derivative agent , is one of a class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs) that differs structurally from other SSRIs. It is used to treat the depression associated with mood disorders. It is also used on occassion in the treatment of body dysmorphic disorder and anxiety. The antidepressant, antiobsessive-compulsive, and antibulimic actions of Fluvoxamine are presumed to be linked to its inhibition of CNS neuronal uptake of serotonin. <i>In vitro</i> studies show that Fluvoxamine is a potent and selective inhibitor of neuronal serotonin reuptake and has only very weak effects on norepinephrine and dopamine neuronal reuptake. Moreover, apart from binding to σ1 receptors , fluvoxamine has no significant affinity for adrenergic (alpha1, alpha2, beta), cholinergic, GABA, dopaminergic, histaminergic, serotonergic (5HT<sub>1A</sub>, 5HT<sub>1B</sub>, 5HT<sub>2</sub>), or benzodiazepine receptors; antagonism of such receptors has been hypothesized to be associated with various anticholinergic, sedative, and cardiovascular effects for other psychotropic drugs. Furthermore, some studies have demonstrated that the chronic administration of Fluvoxamine was found to downregulate brain norepinephrine receptors (as has been observed with other drugs effective in the treatment of major depressive disorder), while others suggest the opposite. The exact mechanism of action of fluvoxamine has not been fully determined, but appears to be linked to its inhibition of CNS neuronal uptake of serotonin. Fluvoxamine blocks the reuptake of serotonin at the serotonin reuptake pump of the neuronal membrane, enhancing the actions of serotonin on 5HT<sub>1A</sub> autoreceptors. Studies have also demonstrated that fluvoxamine has virtually no affinity for α<sub>1</sub>- or α<sub>2</sub>-adrenergic, β-adrenergic, muscarinic, dopamine D<sub>2</sub>, histamine H<sub>1</sub>, GABA-benzodiazepine, opiate, 5-HT<sub>1</sub>, or 5-HT<sub>2</sub> receptors, despite having an affinity for binding to σ1 receptors.",The molecular weight is 318.34.,Fluvoxamine has a topological polar surface area of 56.84.,The log p value of  is 3.03.,Fluvoxamine is approved and investigational.,Fluvoxamine is a solid.,True
15074,"Amphetamine, a compound discovered over 100 years ago, is one of the more restricted controlled drugs. It was previously used for a large variety of conditions and this changed until this point where its use is highly restricted. Amphetamine, with the chemical formula alpha-methylphenethylamine, was discovered in 1910 and first synthesized by 1927. After being proven to reduce drug-induced anesthesia and produce arousal and insomnia, amphetamine racemic mix was registered by Smith, Kline and French in 1935. Amphetamine structure presents one chiral center and it exists in the form of dextro- and levo-isomers. The first product of Smith, Kline and French was approved by the FDA on 1976. Amphetamine is indicated for the treatment of attention-deficit/hyperactivity disorders (ADHD) as well as for the treatment of central nervous system disorders such as narcolepsy.  From its mechanism of action, it has been demonstrated that amphetamine augments the concentration of noradrenaline in the prefrontal cortex and dopamine in the striatum on a dose and time-dependent manner. The indistinct release of neurotransmitters which include adrenaline is known to produce cardiovascular side effects.  It is important to consider that amphetamine has a very similar structure to the catecholamine neurotransmitters mainly on the presence of a long planar conformation, the presence of an aromatic ring and nitrogen in the aryl side chain. Amphetamine, as well as other catecholamines, is taken into presynaptic nerve terminals by the association with two sodium ions and one chloride ion. The complex of the amphetamine with the ions is actively transported by monoamine reuptake transporters. As amphetamine acts competitively with the endogenous monoamines, the greater the number of amphetamines the more internalized amphetamine will be found.",The molecular weight is 135.21.,Amphetamine has a topological polar surface area of 26.02.,The log p value of  is 1.74.,Amphetamine is approved and illicit and investigational.,Amphetamine is a liquid.,True
15075,"Cevimeline is a parasympathomimetic agent that act as an agonist at the muscarinic acetylcholine receptors M1 and M3. It is indicated by the Food and Drug Administration for the treatment of dry mouth associated with Sjögren's syndrome. For the treatment of symptoms of dry mouth in patients with Sj&ouml;gren's Syndrome. Cevimeline is a cholinergic agonist which binds to muscarinic receptors. Muscarinic agonists in sufficient dosage can increase secretion of exocrine glands, such as salivary and sweat glands and increase tone of the smooth muscle in the gastrointestinal and urinary tracts. Muscarinic agonists such as cevimeline bind and activate the muscarinic M1 and M3 receptors. The M1 receptors are common in secretory glands (exocrine glands such as salivary and sweat glands), and their activation results in an increase in secretion from the secretory glands. The M3 receptors are found on smooth muscles and in many glands which help to stimulate secretion in salivary glands, and their activation generally results in smooth muscle contraction and increased glandular secretions. Therefore, as saliva excretion is increased, the symptoms of dry mouth are relieved.",The molecular weight is 199.31.,Cevimeline has a topological polar surface area of 12.47.,The log p value of  is 1.14.,Cevimeline is approved.,Cevimeline is a solid.,True
15076,"Esmolol, commonly marketed under the trade name Brevibloc, is a cardioselective beta-1 receptor blocker. It has a rapid onset but short duration of action without causing significant intrinsic sympathomimetic or membrane stabilizing activities at recommended therapeutic doses. It works by blocking beta-adrenergic receptors in the heart, which leads to decreased force and rate of heart contractions. Esmolol prevents the action of two naturally occurring substances: epinephrine and norepinephrine. For the rapid control of ventricular rate in patients with atrial fibrillation or atrial flutter in perioperative, postoperative, or other emergent circumstances where short term control of ventricular rate with a short-acting agent is desirable. Also used in noncompensatory sinus tachycardia where the rapid heart rate requires specific intervention. Similar to other beta-blockers, esmolol blocks the agonistic effect of the sympathetic neurotransmitters by competing for receptor binding sites. Because it predominantly blocks the beta-1 receptors in cardiac tissue, it is said to be cardioselective. In general, so-called cardioselective beta-blockers are relatively cardioselective; at lower doses they block beta-1 receptors only but begin to block beta-2 receptors as the dose increases. At therapeutic dosages, esmolol does not have intrinsic sympathomimetic activity (ISA) or membrane-stabilizing (quinidine-like) activity. Antiarrhythmic activity is due to blockade of adrenergic stimulation of cardiac pacemaker potentials. In the Vaughan Williams classification of antiarrhythmics, beta-blockers are considered to be class II agents.",The molecular weight is 295.38.,Esmolol has a topological polar surface area of 67.79.,The log p value of  is 1.72.,Esmolol is approved.,Esmolol is a solid.,True
15077,"Bortezomib is a dipeptide boronic acid derivative and proteasome inhibitor used to treat multiple myeloma and mantle cell lymphoma. It is a reversible inhibitor of the 26S proteasome, which is a protein complex that degrades ubiquitinated proteins in the ubiquitin-proteasome pathway. Inhibition of 26S proteasome leads to cell cycle arrest and apoptosis of cancer cells. While inhibition of the 26S proteasome is the main mechanism of action, multiple mechanisms may involved in the therapeutic action of bortezomib. Bortezomib is indicated for the treatment of adult patients with multiple myeloma or mantle cell lymphoma. Bortezomib works to target the ubiquitin-proteasome pathway, an essential molecular pathway that promotes protein degradation and maintains the homeostatic intracellular concentrations of proteins. However, there is strong evidence in the literature that the ubiquitin-proteasome pathway is often dysregulated, leading to aberrant pathway signalling. In one study, patient-derived chronic lymphocytic leukemia (CLL) cells contained 3-fold higher levels of chymotrypsin-like proteasome activity than normal lymphocytes, indicating that dysregulation of the ubiquitin-proteasome pathway is implicated in malignant cell transformation. By reversibly inhibiting an enzyme involved in the ubiquitin-proteasome pathway, bortezomib prevents the proteasome-mediated proteolysis. Bortezomib exerts a cytotoxic effect on various cancer cell types _in vitro_. In non-clinical tumour models, including multiple myeloma, bortezomib caused a delay in tumour growth. Bortezomib is a reversible inhibitor of the chymotrypsin-like activity of the 26S proteasome in mammalian cells. The 26S proteasome is a large protein complex that degrades ubiquitinated proteins. The active site of the proteasome has chymotrypsin-like, trypsin-like, and postglutamyl peptide hydrolysis activity. The 26S proteasome degrades various proteins critical to cancer cell survival, such as cyclins, tumor suppressors, BCL-2, and cyclin-dependent kinase inhibitors. Inhibition of these degradations sensitizes cells to apoptosis. Bortezomib is a potent inhibitor of 26S proteasome, which sensitizes activity in dividing multiple myeloma and leukemic cells, thus inducing apoptosis. In addition, bortezomib appears to increase the sensitivity of cancer cells to traditional anticancer agents (e.g., gemcitabine, cisplatin, paclitaxel, irinotecan, and radiation).",The molecular weight is 384.24.,Bortezomib has a topological polar surface area of 124.44.,The log p value of  is 0.78.,Bortezomib is approved and investigational.,Bortezomib is a solid.,True
15078,"Tramadol is a centrally acting synthetic opioid analgesic and SNRI (serotonin/norepinephrine reuptake-inhibitor) that is structurally related to and. Due to its good tolerability profile and multimodal mechanism of action, tramadol is generally considered a lower-risk opioid option for the treatment of moderate to severe pain. It is considered a Step 2 option on the World Health Organization's pain ladder and has about 1/10th of the potency of.  Tramadol is approved for the management of moderate to severe pain in adults. Tramadol modulates the descending pain pathways within the central nervous system through the binding of parent and M1 metabolite to μ-opioid receptors and the weak inhibition of the reuptake of norepinephrine and serotonin.  Tramadol is a centrally acting μ-opioid receptor agonist and SNRI (serotonin/norepinephrine reuptake-inhibitor) that is structurally related to and. Tramadol binds weakly to κ- and δ-opioid receptors and to the μ-opioid receptor with 6000-fold less affinity than morphine.",The molecular weight is 263.38.,Tramadol has a topological polar surface area of 32.7.,The log p value of  is 3.1.,Tramadol is approved and investigational.,Tramadol is a solid.,True
15079,"A cardioselective beta-1-adrenergic antagonist with no partial agonist activity. For the management of hypertension. Betaxolol is a competitive, beta(1)-selective (cardioselective) adrenergic antagonist. Betaxolol is used to treat hypertension, arrhythmias, coronary heart disease, glaucoma, and is also used to reduce non-fatal cardiac events in patients with heart failure. Activation of beta(1)-receptors (located mainly in the heart) by epinephrine increases the heart rate and the blood pressure, and the heart consumes more oxygen. Drugs such as betaxolol that block these receptors therefore have the reverse effect: they lower the heart rate and blood pressure and hence are used in conditions when the heart itself is deprived of oxygen. They are routinely prescribed in patients with ischemic heart disease. In addition, beta(1)-selective blockers prevent the release of renin, which is a hormone produced by the kidneys which leads to constriction of blood vessels. Betaxolol is lipophilic and exhibits no intrinsic sympathomimetic activity (ISA) or membrane stabilizing activity. Betaxolol selectively blocks catecholamine stimulation of beta(1)-adrenergic receptors in the heart and vascular smooth muscle. This results in a reduction of heart rate, cardiac output, systolic and diastolic blood pressure, and possibly reflex orthostatic hypotension. Betaxolol can also competitively block beta(2)-adrenergic responses in the bronchial and vascular smooth muscles, causing bronchospasm.",The molecular weight is 307.43.,Betaxolol has a topological polar surface area of 50.72.,The log p value of  is 2.32.,Betaxolol is approved and investigational.,Betaxolol is a solid.,True
15080,"Trospium is an antispasmodic agent used to treat the symptoms of overactive bladder, a condition that causes the bladder muscles to contract uncontrollably. An overactive bladder leads to an increased urge to urinate, frequent urination, and sometimes, loss of control over urination. Trospium is manufactured by _Indevus Pharmaceutical Inc._ and was granted FDA approval in 2007. For the treatment of overactive bladder with symptoms of urge urinary incontinence, urgency, and urinary frequency, detrusor instability and frequency of micturition. Trospium is an antispasmodic, antimuscarinic agent indicated for the treatment of overactive bladder with symptoms of urge urinary incontinence, urgency, and urinary frequency. According to receptor assays, it displays higher affinity towards muscarininc receptors compared to nicotinic receptors at therapeutic concentrations.  Trospium antagonizes the effect of acetylcholine on muscarinic receptors in cholinergically innervated organs. Its parasympatholytic action reduces the tonus of smooth muscle in the bladder.",,,,Trospium is approved.,Trospium is a solid.,True
15081,"An ethanolamine derivative that is an adrenergic alpha agonist. It is used as a vasoconstrictor agent in the treatment of hypotension. For the treatment of symptomatic orthostatic hypotension (OH). Midodrine is a prodrug, i.e., the therapeutic effect of orally administered midodrine is due to the major metabolite desglymidodrine formed by deglycination of midodrine. Administration of midodrine results in a rise in standing, sitting, and supine systolic and diastolic blood pressure in patients with orthostatic hypotension of various etiologies. Standing systolic blood pressure is elevated by approximately 15 to 30 mmHg at 1 hour after a 10-mg dose of midodrine, with some effect persisting for 2 to 3 hours. Midodrine has no clinically significant effect on standing or supine pulse rates in patients with autonomic failure. Midodrine undergoes metabolism to form its pharmacologically active metabolite, desglymidodrine. Desglymidodrine acts as an agonist at the alpha<sub>1</sub>-adrenergic receptors expressed in the arteriolar and venous vasculature. Activation of alpha<sub>1</sub>-adrenergic receptor signaling pathways lead to an increase in the vascular tone and elevation of blood pressure. Desglymidodrine is reported to have negligible effect on the cardiac beta-adrenergic receptors.",The molecular weight is 254.29.,Midodrine has a topological polar surface area of 93.81.,The log p value of  is -0.35.,Midodrine is approved.,Midodrine is a solid.,True
15082,"Citalopram belongs to a class of antidepressant agents known as selective _serotonin-reuptake inhibitors_ (SSRIs) and is widely used to treat the symptoms of depression. Its chemical structure is unrelated to that of other SSRIs or of tricyclic, tetracyclic, or other prescribed antidepressants. Citalopram is also known as _Celexa_, and available in tablet and solution forms. This drug was initially approved by the FDA in 1998. For the treatment of depression, as indicated by the FDA label. Off-label indications include but are not limited to: treatment of sexual dysfunction, post-stroke behavioural changes, ethanol abuse, obsessive-compulsive disorder (OCD) in children, and diabetic neuropathy , , , , , , ,. Citalopram belongs to a class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs). It has been found to relieve or manage symptoms of depression, anxiety, eating disorders and obsessive-compulsive disorder among other mood disorders. The antidepressant, anti-anxiety, and other actions of citalopram are linked to its inhibition of CNS central uptake of serotonin. Serotonergic abnormalities have been reported in patients with mood disorders. Behavioral and neuropsychological of effects of serotonin include the regulation of mood, perception, reward, anger, aggression, appetite, memory, sexuality, and attention, as examples. The onset of action for depression is approximately 1 to 4 weeks. The complete response may take 8-12 weeks after initiation of citalopram.",The molecular weight is 324.4.,Citalopram has a topological polar surface area of 36.26.,The log p value of  is 3.13.,Citalopram is approved.,Citalopram is a solid.,True
15083,"Reboxetine is an antidepressant drug used in the treatment of clinical depression, panic disorder and ADD/ADHD. Its mesylate (i.e. methanesulfonate) salt is sold under tradenames including Edronax, Norebox, Prolift, Solvex, Davedax or Vestra. Reboxetine has two chiral centers, but it only exists as two enantiomers, (R,R)-(-)- and (S,S)-(+)-reboxetine. For the treatment of clinical depression. Reboxetine is a selective noradrenaline reuptake inhibitor (NaRI), the first drug of new antidepressant class. Reboxetine is an a-ariloxybenzyl derivative of morpholine. Reboxetine is primarily used to treat depression but has also been found useful in the treatment of narcolepsy and panic disorders. Reboxetine is a selective inhibitor of noradrenaline reuptake. It inhibits noradrenaline reuptake <i>in vitro</i> to a similar extent to the tricyclic antidepressant desmethylimipramine. Reboxetine does not affect dopamine or serotonin reuptake and it has low <i>in vivo</i> and <i>in vitro</i> affinity for adrenergic, cholinergic, histaminergic, dopaminergic and serotonergic receptors.",The molecular weight is 313.4.,Reboxetine has a topological polar surface area of 39.72.,The log p value of  is 3.26.,Reboxetine is approved and experimental.,Reboxetine is a solid.,True
15084,"This drug is a broad spectrum antimycotic or antifungal agent. Clotrimazole's antimycotic properties were discovered in the late 1960s. Clotrimazole falls under the _imidazole_ category of _azole_ antifungals, possessing broad-spectrum antimycotic activity. It is available in various preparations, including creams, pessaries, and troche formulations (slowly dissolving tablets). As well as its antifungal activity, clotrimazole has become a drug of interest in treating several other diseases such as sickle cell disease, malaria and some cancers. The minimal side effect profile of this drug and its uncomplicated metabolic profile have led it to gain widespread acceptance for the treatment of mycotic outbreaks such as vaginal yeast infections as well as athlete's foot. **Topical preparations** Clotrimazole is a broad-spectrum antifungal agent that inhibits the growth of pathogenic yeasts by changing the permeability of cell membranes. The action of clotrimazole is fungistatic at concentrations of drug up to 20 mcg/mL and may be fungicidal _in vitro_ against Candida albicans and other species of the genus Candida at higher concentrations. Unfortunately, resistance to clotrimazole, which was rare in the past, is now common in various patient populations.  Clotrimazole acts primarily by damaging the permeability barrier in the cell membrane of fungi. Clotrimazole causes inhibition of ergosterol biosynthesis, an essential constituent of fungal cell membranes. If ergosterol synthesis is either completely or partially inhibited, the cell is no longer able to construct an intact and functional cell membrane ,. Because ergosterol directly promotes the growth of fungal cells in a hormone‐like fashion, rapid onset of the above events leads to dose-dependent inhibition of fungal growth.",The molecular weight is 344.84.,Clotrimazole has a topological polar surface area of 17.82.,The log p value of  is 5.0.,Clotrimazole is approved and vet_approved.,Clotrimazole is a solid.,True
15085,"Sulfanilamide is a molecule containing the sulfonamide functional group attached to an aniline. For the treatment of vulvovaginitis caused by <i>Candida albicans</i>. Sulfanilamide is a sulfonamide antibiotic. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of <i>p</i>-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus. Sulfanilamide is a competitive inhibitor of bacterial enzyme dihydropteroate synthetase. This enzyme normally uses para-aminobenzoic acid (PABA) for synthesizing the necessary folic acid. The inhibited reaction is normally necessary in these organisms for the synthesis of folic acid. Without it, bacteria cannot replicate.",The molecular weight is 172.2.,Sulfanilamide has a topological polar surface area of 86.18.,The log p value of  is -0.57.,Sulfanilamide is approved.,Sulfanilamide is a solid.,True
15086,"An ethanolamine-derivative, first generation histamine H1 antagonist used in hay fever, rhinitis, allergic skin conditions, and pruritus. It causes drowsiness. For the relief of symptoms associated with allergic rhinitis such as sneezing, rhinorrhea, pruritus and acrimation. Also for the management of mild, uncomplicated allergic skin manifestations of urticaria and angioedema. Used as self-medication for temporary relief of symptoms associated with the common cold. Clemastine is an antihistamine that also induces anticholinergic and sedative effects. Antihistamines competitively antagonize various physiological effects of histamine including increased capillary permeability and dilatation, the formation of edema, the \flare\"" and \""itch\"" response, and gastrointestinal and respiratory smooth muscle constriction. Within the vascular tree, H1- receptor antagonists inhibit both the vasoconstrictor and vasodilator effects of histamine. Depending on the dose, H1- receptor antagonists can produce CNS stimulation or depression. Most antihistamines exhibit central and/or peripheral anticholinergic activity. Antihistamines act by competitively blocking H1- receptor sites. Antihistamines do not pharmacologically antagonize or chemically inactivate histamine, nor do they prevent the release of histamine."" Clemastine is a selective histamine H1 antagonist and binds to the histamine H1 receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine.",The molecular weight is 343.9.,Clemastine has a topological polar surface area of 12.47.,The log p value of  is 5.45.,Clemastine is approved and investigational.,Clemastine is a solid.,True
15087,"Venlafaxine (Effexor) is an antidepressant within the serotonin-norepinephrine reuptake inhibitor (SNRI) class of medications. It exerts its effects primarily by blocking the transporters involved in the reuptake of the neurotransmitters serotonin and norepinephrine, therefore leaving more active neurotransmitter in the synapse. Venlafaxine is officially approved for use in the management of major depressive disorder (MDD), generalized anxiety disorder (GAD), social anxiety disorder, and panic disorder. As of 2014, Canadian clinical practice guidelines recommend venlafaxine as a first-line option for treatment of generalized anxiety, social anxiety, panic disorder, major depressive disorder (MDD), and consider it a second-line option for management of obsessive-compulsive disorder (OCD). Venlafaxine is also used off-label for prophylaxis of migraine headaches , for reduction of vasomotor symptoms associated with menopause , and for management of neuropathic pain (although there is only minimal evidence of efficacy for this condition). Venlafaxine is indicated in the management of major depressive disorder (MDD), generalized anxiety disorder (GAD), social anxiety disorder (social phobia), and panic disorder with or without agoraphobia. Venlafaxine is also used off-label for prophylaxis of migraine headaches , for reduction of vasomotor symptoms associated with menopause , and for management of neuropathic pain (although there is only minimal evidence of efficacy for this condition). It is also considered a second-line option for management of obsessive-compulsive disorder (OCD).  The mechanism of venlafaxine's (and its metabolite, O-desmethylvenlafaxine (ODV)) antidepressant effect is believed to be due to their potentiation of neurotransmitter activity in the central nervous system through the inhibition of the reuptake of serotonin and norepinephrine from within the synapse. Venlafaxine has also been shown to weakly inhibit dopamine reuptake. Neither venlafaxine nor ODV bind to muscarinic, histaminergic, or alpha-1 adrenergic receptors; pharmacologic activity at these receptors is hypothesized to be associated with the various anticholinergic, sedative, and cardiovascular effects seen with other psychotropic drugs. Hyponatremia has also been shown to occur as a result of treatment with SNRIs, and is associated with the development of the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Venlafaxine also demonstrates a clinically significant and dose-related effect on blood pressure, likely due to its potentiation of norepinephrine. The exact mechanism of action of venlafaxine is unknown, but appears to be associated with the potentiation of neurotransmitter activity in the CNS. Venlafaxine and its active metabolite, O-desmethylvenlafaxine (ODV), inhibit the reuptake of both serotonin and norepinephrine with a potency greater for the 5-HT than for the NE reuptake process. Both venlafaxine and the ODV metabolite have weak inhibitory effects on the reuptake of dopamine but, unlike the tricyclics and similar to SSRIs, they are not active at histaminergic, muscarinic, or alpha(1)-adrenergic receptors.",The molecular weight is 277.41.,Venlafaxine has a topological polar surface area of 32.7.,The log p value of  is 3.27.,Venlafaxine is approved.,Venlafaxine is a solid.,True
15088,"Bupivacaine is a widely used local anesthetic agent. For the production of local or regional anesthesia or analgesia for surgery, for oral surgery procedures, for diagnostic and therapeutic procedures, and for obstetrical procedures. Bupivacaine is a widely used local anesthetic agent. Bupivacaine is often administered by spinal injection prior to total hip arthroplasty. It is also commonly injected into surgical wound sites to reduce pain for up to 20 hours after surgery. In comparison to other local anesthetics it has a long duration of action. It is also the most toxic to the heart when administered in large doses. This problem has led to the use of other long-acting local anaesthetics:ropivacaine and levobupivacaine. Levobupivacaine is a derivative, specifically an enantiomer, of bupivacaine. Systemic absorption of local anesthetics produces effects on the cardiovascular and central nervous systems. At blood concentrations achieved with therapeutic doses, changes in cardiac conduction, excitability, refractoriness, contractility, and peripheral vascular resistance are minimal. However, toxic blood concentrations depress cardiac conduction and excitability, which may lead to atrioventricular block, ventricular arrhythmias and to cardiac arrest, sometimes resulting in fatalities. In addition, myocardial contractility is depressed and peripheral vasodilation occurs, leading to decreased cardiac output and arterial blood pressure. Following systemic absorption, local anesthetics can produce central nervous system stimulation, depression or both. Local anesthetics such as bupivacaine block the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. Bupivacaine prevents depolarization by bindng to the intracellular portion of sodium channels and blocking sodium ion influx into neurons. In general, the progression of anesthesia is related to the diameter, myelination and conduction velocity of affected nerve fibers. Clinically, the order of loss of nerve function is as follows: (1) pain, (2) temperature, (3) touch, (4) proprioception, and (5) skeletal muscle tone. The analgesic effects of Bupivicaine are thought to potentially be due to its binding to the prostaglandin E2 receptors, subtype EP1 (PGE2EP1), which inhibits the production of prostaglandins, thereby reducing fever, inflammation, and hyperalgesia.",The molecular weight is 288.44.,Bupivacaine has a topological polar surface area of 32.34.,The log p value of  is 3.69.,Bupivacaine is approved and investigational.,Bupivacaine is a solid.,True
15089,"The relief of pain (analgesia) is a primary goal for enhancing the quality of life of patients and for increasing the ability of patients to engage in day to day activities. Codeine, an opioid analgesic, was originally approved in the US in 1950 and is a drug used to decrease pain by increasing the threshold for pain without impairing consciousness or altering other sensory functions. Opiates such as codeine are derived from the poppy plant, _Papaver somniferum_ (Papaveraceae). Codeine sulfate is a form of this drug that is commonly used. It is available in tablet form and indicated for the relief of mild to moderately severe pain, where the use of an opioid analgesic is appropriate. **General effects** Codeine is a selective agonist for the mu opioid receptor, but with a much weaker affinity to this receptor than morphine, a more potent opioid drug. Codeine binds to mu-opioid receptors, which are involved in the transmission of pain throughout the body and central nervous system ,. The analgesic properties of codeine are thought to arise from its conversion to , although the exact mechanism of analgesic action is unknown at this time ,.",The molecular weight is 299.37.,Codeine has a topological polar surface area of 41.93.,The log p value of  is 0.98.,Codeine is approved and illicit.,Codeine is a solid.,True
15090,"Clobazam belongs to the 1,5-benzodiazepine class of drugs and is expected to have a better side-effect profile compared to older 1,4-benzodiazepines. It has been marketed as an anxiolytic since 1975 and an anticonvulsant since 1984. The oral preparation was FDA approved on October 21, 2011. An oral suspension is expected to be available in 2013. For treatment and management of epilepsy and seizures associated with Lennox-Gastaut syndrome, a difficult-to-treat form of childhood epilepsy.  Similar to other benzodiazepines, clobazam binds to the interface of the α and γ2-subunit of the GABA-A receptor. However, it is considered a partial agonist to GABA-A receptors which sets clobazam apart from 1,4-benzodiazepines which are full agonist. The significance of this difference is that one may experience less sedation with clobazam than with other benzodiazepines. Unlike the endogenous GABA ligand, clobazam binds allosterically to the GABA receptor to increase the frequency of the chloride channel opening and membrane permeability to chloride ions. Pharmacodynamic tolerance has been demonstrated in animal models.  Clobazam binds at distinct binding sites associated with the chloride ionopore at the post-synaptic GABA receptor. These GABA receptors are in various locations in the CNS (limbic, reticular formation) and clobazam increases the duration of time for which the chloride ionopore is open. As a result, hyper polarization and stabilization of the membrane occur as the post-synaptic inhibitory effect of GABA is enhanced. ",The molecular weight is 300.74.,Clobazam has a topological polar surface area of 40.62.,The log p value of  is 2.44.,Clobazam is approved and illicit.,Clobazam is a solid.,True
15091,"A centrally acting central muscle relaxant with sedative properties. It is claimed to inhibit muscle spasm by exerting an effect primarily at the level of the spinal cord and subcortical areas of the brain. (From Martindale, The Extra Pharmacopoea, 30th ed, p1202) For the relief of discomfort associated with acute painful musculoskeletal conditions. Chlorzoxazone is a centrally-acting agent for painful musculoskeletal conditions. Data available from animal experiments as well as human study indicate that chlorzoxazone acts primarily at the level of the spinal cord and subcortical areas of the brain where it inhibits multisynaptic reflex a.c. involved in producing and maintaining skeletal muscle spasm of varied etiology. The clinical result is a reduction of the skeletal muscle spasm with relief of pain and increased mobility of the involved muscles. Chlorzoxazone inhibits degranulation of mast cells, subsequently preventing the release of histamine and slow-reacting substance of anaphylaxis (SRS-A), mediators of type I allergic reactions. Chlorzoxazone also may reduce the release of inflammatory leukotrienes. Chlorzoxazone may act by inhibiting calcium and potassium influx which would lead to neuronal inhibition and muscle relaxation. Data available from animal experiments as well as human study indicate that chlorzoxazone acts primarily at the level of the spinal cord and subcortical areas of the brain where it inhibits multisynaptic reflex arcs involved in producing and maintaining skeletal muscle spasm",The molecular weight is 169.56.,Chlorzoxazone has a topological polar surface area of 38.33.,The log p value of  is 1.87.,Chlorzoxazone is approved.,Chlorzoxazone is a solid.,True
15092,"Vinorelbine is an anti-mitotic chemotherapy drug that is used in the treatment of several types of malignancies, including breast cancer and non-small cell lung cancer (NSCLC). It was initially approved in the USA in 1990's for the treatment of NSCLC. Vinca alkaloids are structurally similar compounds composed of two multi-ringed units, _vindoline_, and _catharanthine_. _Vinorelbine tartrate_ is a vinca alkaloid in which the catharanthine component is the target of structural modification ,.",The molecular weight is 778.95.,Vinorelbine has a topological polar surface area of 133.87.,The log p value of  is 5.94.,Vinorelbine is approved and investigational.,Vinorelbine is a solid.,True
15093,"A tricyclic dibenzodiazepine, classified as an atypical antipsychotic agent. It binds several types of central nervous system receptors, and displays a unique pharmacological profile. Clozapine is a serotonin antagonist, with strong binding to 5-HT 2A/2C receptor subtype. It also displays strong affinity to several dopaminergic receptors, but shows only weak antagonism at the dopamine D2 receptor, a receptor commonly thought to modulate neuroleptic activity. Agranulocytosis is a major adverse effect associated with administration of this agent. For use in patients with treatment-resistant schizophrenia. Clozapine is a psychotropic agent belonging to the chemical class of benzisoxazole derivatives and is indicated for the treatment of schizophrenia. Clozapine is a selective monoaminergic antagonist with high affinity for the serotonin Type 2 (5HT<sub>2</sub>), dopamine Type 2 (D2), 1 and 2 adrenergic, and H1 histaminergic receptors. Clozapine acts as an antagonist at other receptors, but with lower potency. Antagonism at receptors other than dopamine and 5HT<sub>2</sub> with similar receptor affinities may explain some of the other therapeutic and side effects of clozapine. Clozapine's antagonism of muscarinic M1-5 receptors may explain its anticholinergic effects. Clozapine's antagonism of histamine H1 receptors may explain the somnolence observed with this drug. Clozapine's antagonism of adrenergic a1 receptors may explain the orthostatic hypotension observed with this drug. Clozapine's antipsychotic action is likely mediated through a combination of antogistic effects at D2 receptors in the mesolimbic pathway and 5-HT2A receptors in the frontal cortex. D2 antagonism relieves positive symptoms while 5-HT2A antagonism alleviates negative symptoms.",The molecular weight is 326.83.,Clozapine has a topological polar surface area of 30.87.,The log p value of  is 3.56.,Clozapine is approved.,Clozapine is a solid.,True
15094,"Mirtazapine is a tetracyclic _piperazino-azepine_ antidepressant agent that was initially approved for the treatment of major depressive disorder (MDD) in the Netherlands in 1994. This drug was first manufactured by Organon Inc., and received FDA approval in 1997 for the treatment of major depressive disorder. The effects of this drug may be observed as early as 1 week after beginning therapy. This drug is indicated for the treatment of major depressive disorder and its associated symptoms. **General effects and a note on suicidality** **Summary**",The molecular weight is 265.36.,Mirtazapine has a topological polar surface area of 19.37.,The log p value of  is 2.81.,Mirtazapine is approved.,Mirtazapine is a solid.,True
15095,"Timolol is a nonselective beta-adrenergic antagonist given in an eye drop solution to reduce intraocular pressure, or pressure in the eyes. It is also used in tablet form as a drug to treat hypertension. Timolol was first approved by the FDA in 1978. This drug is marketed by several manufacturers and is an effective agent for the management of conditions such as open-angle glaucoma and hypertension.  Ophthalmic timolol is indicated for the treatment of increased intraocular pressure in patients with ocular hypertension or open-angle glaucoma. The oral form of this drug is used to treat high blood pressure. In certain cases, timolol is used in the prevention of migraine headaches.  Timolol, when administered by the ophthalmic route, rapidly reduces intraocular pressure. When administered in the tablet form, it reduces blood pressure, heart rate, and cardiac output, and decreases sympathetic activity.. This drug has a fast onset of action, usually occurring within 20 minutes of the administration of an ophthalmic dose. Timolol maleate can exert pharmacological actions for as long as 24 hours if given in the 0.5% or 0.25% doses. Timolol competes with adrenergic neurotransmitters for binding to beta(1)-adrenergic receptors in the heart and the beta(2)-receptors in the vascular and bronchial smooth muscle. This leads to diminished actions of catecholamines, which normally bind to adrenergic receptors and exert sympathetic effects leading to an increase in blood pressure and heart rate. Beta(1)-receptor blockade by timolol leads to a decrease in both heart rate and cardiac output during rest and exercise, and a decrease in both systolic and diastolic blood pressure. In addition to this, a reduction in reflex orthostatic hypotension may also occur. The blockade of beta(2) receptors by timolol in the blood vessels leads to a decrease in peripheral vascular resistance, reducing blood pressure.",The molecular weight is 316.42.,Timolol has a topological polar surface area of 79.74.,The log p value of  is 1.53.,Timolol is approved.,Timolol is a solid.,True
15096,"Palonosetron (INN, trade name Aloxi) is an antagonist of 5-HT3 receptors that is indicated for the prevention and treatment of chemotherapy-induced nausea and vomiting (CINV). It is the most effective of the 5-HT3 antagonists in controlling delayed CINV nausea and vomiting that appear more than 24 hours after the first dose of a course of chemotherapy and is the only drug of its class approved for this use by the U.S. Food and Drug Administration. As of 2008, it is the most recent 5-HT3 antagonist to enter clinical use. For the prevention of acute and delayed nausea and vomiting associated with initial and repeat courses of moderately emetogenic cancer chemotherapy, as well as prevention of acute nausea and vomiting associated with highly emetogenic cancer chemotherapy. Also used for the prevention of postoperative nausea and vomiting for up to 24 hours post operation. Palonosetron is an antinauseant and antiemetic agent indicated for the prevention of nausea and vomiting associated with moderately-emetogenic cancer chemotherapy and for the prevention of postoperative nausea and vomiting. Palonosetron is a highly specific and selective serotonin 5-HT<sub>3</sub> receptor antagonist that is pharmacologically related to other 5-HT<sub>3</sub> receptor antagonists, but differs structurally. Palonosetron has a high affinity for 5-HT<sub>3</sub> receptors, but has little to no affinity for other receptors. The serontonin 5-HT<sub>3</sub> receptors are located on the nerve terminals of the vagus in the periphery, and centrally in the chemoreceptor trigger zone of the area postrema. It is suggested that chemotherapeutic agents release serotonin from the enterochromaffin cells of the small intestine by causing degenerative changes in the GI tract. The serotonin then stimulates the vagal and splanchnic nerve receptors that project to the medullary vomiting center, as well as the 5-HT3 receptors in the area postrema, thus initiating the vomiting reflex, causing nausea and vomiting. Palonosetron is a selective serotonin 5-HT<sub>3</sub> receptor antagonist. The antiemetic activity of the drug is brought about through the inhibition of 5-HT<sub>3</sub> receptors present both centrally (medullary chemoreceptor zone) and peripherally (GI tract). This inhibition of 5-HT<sub>3</sub> receptors in turn inhibits the visceral afferent stimulation of the vomiting center, likely indirectly at the level of the area postrema, as well as through direct inhibition of serotonin activity within the area postrema and the chemoreceptor trigger zone. Alternative mechanisms appear to be primarily responsible for delayed nausea and vomiting induced by emetogenic chemotherapy, since similar temporal relationships between between serotonin and emesis beyond the first day after a dose have not been established, and 5-HT<sub>3</sub> receptor antagonists generally have not appeared to be effective alone in preventing or ameliorating delayed effects. It has been hypothesized that palonosetron's potency and long plasma half-life may contribute to its observed efficacy in preventing delayed nausea and vomiting caused by moderately emetogenic cancer chemotherapy.",,,,Palonosetron is approved and investigational.,Palonosetron is a solid.,True
15097,"Antiarrhythmic agent pharmacologically similar to lidocaine. It may have some anticonvulsant properties. For the treatment of ventricular tachycardia and symptomatic premature ventricular beats, and prevention of ventricular fibrillation. Mexiletine is a local anesthetic, antiarrhythmic agent (Class Ib), structurally similar to lidocaine, but orally active. Mexiletine has fast onset and offset kinetics, meaning that they have little or no effect at slower heart rates, and more effects at faster heart rates. It shortens the action potential duration, reduces refractoriness, and decreases Vmax in partially depolarized cells with fast response action potentials. Mexiletine either does not change the action potential duration, or decreases the action potential duration. Mexiletine, like lidocaine, inhibits the inward sodium current required for the initiation and conduction of impulses, thus reducing the rate of rise of the action potential, Phase 0. It achieves this reduced sodium current by inhibiting sodium channels. Mexiletine decreases the effective refractory period (ERP) in Purkinje fibers in the heart. The decrease in ERP is of lesser magnitude than the decrease in action potential duration (APD), which results in an increase in the ERP/APD ratio. It does not significantly affect resting membrane potential or sinus node automaticity, left ventricular function, systolic arterial blood pressure, atrioventricular (AV) conduction velocity, or QRS or QT intervals",The molecular weight is 179.26.,Mexiletine has a topological polar surface area of 35.25.,The log p value of  is 2.57.,Mexiletine is approved and investigational.,Mexiletine is a solid.,True
15098,"A phenothiazine with actions similar to chlorpromazine but with less antipsychotic activity. It is primarily used in short-term treatment of disturbed behavior and as an antiemetic. It is currently not approved for use in the United States. Used as an adjunct for short term treatment of moderate and severe psychomotor agitation. Also used to treat agitation or restlessness in the elderly. Promazine belongs to a group of medications known as the phenothiazine antipsychotics. It acts by blocking a variety of receptors in the brain, particularly dopamine receptors. Dopamine is involved in transmitting signals between brain cells. When there is an excess amount of dopamine in the brain it causes over-stimulation of dopamine receptors. These receptors normally act to modify behaviour and over-stimulation may result in psychotic illness. Promazine hydrochloride blocks these receptors and stops them becoming over-stimulated, thereby helping to control psychotic illness. Promazine has weak extrapyramidal and autonomic side effects which lead to its use in the elderly, for restless or psychotic patients. Its anti-psychotic effect is also weaker and it is not useful in general psychiatry. Promazine is an antagonist at types 1, 2, and 4 dopamine receptors, 5-HT receptor types 2A and 2C, muscarinic receptors 1 through 5, alpha(1)-receptors, and histamine H1-receptors. Promazine's antipsychotic effect is due to antagonism at dopamine and serotonin type 2 receptors, with greater activity at serotonin 5-HT2 receptors than at dopamine type-2 receptors. This may explain the lack of extrapyramidal effects. Promazine does not appear to block dopamine within the tubero-infundibular tract, explaining the lower incidence of hyperprolactinemia than with typical antipsychotic agents or risperidone. Antagonism at muscarinic receptors, H1-receptors, and alpha(1)-receptors also occurs with promazine.",The molecular weight is 284.42.,Promazine has a topological polar surface area of 6.48.,The log p value of  is 4.6.,Promazine is approved and vet_approved.,Promazine is a liquid.,True
15099,"Zolpidem, also known as _Ambien_, is a hypnotic drug that was initially approved by the FDA in 1992. Zolpidem improves sleep in patients with insomnia. It is aimed for use in patients with difficulties initiating sleep. This drug decreases the time to fall asleep (sleep latency), increases the duration of sleep, and decreases the number of awakenings during sleep in patients with temporary (transient) insomnia. It is available in both immediate acting and extended release forms ,.  This drug is indicated for the short-term treatment of insomnia in adults characterized by difficulties with sleep initiation.  **Effects on the central nervous system (CNS)**",The molecular weight is 307.4.,Zolpidem has a topological polar surface area of 37.61.,The log p value of  is 3.03.,Zolpidem is approved.,Zolpidem is a solid.,True
15100,"Prochlorperazine, also known as compazine, is a piperazine phenothiazine and first-generation antipsychotic drug that is used for the treatment of severe nausea and vomiting, as well as short-term management of psychotic disorders such as generalized non-psychotic anxiety and schizophrenia. It mainly works by depressing the chemoreceptor trigger zone and blocking D2 dopamine receptors in the brain. It was shown to also block histaminergic, cholinergic and noradrenergic receptors. Prochlorperazine was first developed in the 1950s and was first approved by the FDA in 1956. Although newer antiemetic agents such as 5-HT3 antagonists are more heavily promoted, prochlorperazine is still widely used in nausea and vomiting. Indicated for the symptomatic treatment of severe nausea and vomiting. Prochlorperazine is an antipsychotic agent that works to promote postsynaptic inhibition of dopaminergic neurons. It also exerts its anti-emetic actions via anti-dopaminergic effects, where it displays similar efficacy as ondansteron, a 5HT-3 receptor antagonist and anti-emetic, in preventing delayed nausea and vomiting. Prochlorperazine was shown to inhibit histaminergic, cholinergic and alpha-1 adrenergic receptors. The blockade of alpha-1 adrenergic receptors may result in sedation, muscle relaxation, and hypotension. It displays anti-anxiety effects as well. Compared to other phenothiazine derivatives, prochlorperazine is less sedating and has a weak propensity for causing hypotension or potentiating the effects of CNS depressants and anesthetics. Other than its primary action on D2 receptors, one study showed that prochlorperazine may inhibit the P2X7 receptor in human macrophages, leading to inhibition of calcium ion influx. The mechanism of action of prochlorperazine has not been fully determined, but may be primarily related to its anti-dopaminergic effects. Prochlorperazine blocks the D2 dopamine receptors in the brain, which are somatodendritic autoreceptors. Inhibition of D2 receptor signaling results in the blockade of postsynaptic dopamine receptors in the mesolimbic system and an increased dopamine turnover. Nausea and vomiting are proposed to arise from peripheral or central stimulation of serotonin type 3 (5-HT3) and dopamine type 2 receptors, the predominant receptors expressed at the chemoreceptor trigger zone (CTZ). Prochlorperazine exerts antiemetic effects and was shown to inhibit apomorphine-induced vomiting by blocking D2 dopamine receptors in the CTZ.. ",The molecular weight is 373.94.,Prochlorperazine has a topological polar surface area of 9.72.,The log p value of  is 4.58.,Prochlorperazine is approved and vet_approved.,Prochlorperazine is a solid.,True
15101,"Celecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, is a nonsteroidal anti-inflammatory drug (NSAID) which is known for its decreased risk of causing gastrointestinal bleeding compared to other NSAIDS. It is used to manage symptoms of various types of arthritis pain and in familial adenomatous polyposis (FAP) to reduce precancerous polyps in the colon. It is marketed by Pfizer under the brand name Celebrex, and was initially granted FDA approval in 1998.  Celecoxib is indicated for symptomatic treatment of adult osteoarthritis (OA) and adult rheumatoid arthritis (RA). Celecoxib is not a substitute for aspirin for cardiovascular event prophylaxis.  Unlike most NSAIDs, which inhibit both types of cyclooxygenases (COX-1 and COX-2), celecoxib is a selective noncompetitive inhibitor of cyclooxygenase-2 (COX-2) enzyme. COX-2 is expressed heavily in inflamed tissues where it is induced by inflammatory mediators. The inhibition of this enzyme reduces the synthesis of metabolites that include prostaglandin E2 (PGE2), prostacyclin (PGI2), thromboxane (TXA2), prostaglandin D2 (PGD2), and prostaglandin F2 (PGF2). Resultant inhibition of these mediators leads to the alleviation of pain and inflammation. ",The molecular weight is 381.37.,Celecoxib has a topological polar surface area of 77.98.,The log p value of  is 4.37.,Celecoxib is approved and investigational.,Celecoxib is a solid.,True
15102,"Sotalol is a methanesulfonanilide developed in 1960. It was the first of the class III anti arrhythmic drugs. Sotalol was first approved as an oral tablet on 30 October 1992. A racemic mixture of sotalol is currently formulated as a tablet, oral solution, and intravenous injection indicated for life threatening ventricular arrhythmias and maintaining normal sinus rhythm in atrial fibrillation or flutter. Sotalol is indicated to treat life threatening ventricular arrhytmias and maintain normal sinus rhythm in patients with atrial fibrillation or flutter. There are also oral solutions and intravenous injections indicated for patients requiring sotalol, but for whom a tablet would not be appropriate. Sotalol is a competitive inhibitor of the rapid potassium channel. This inhibition lengthens the duration of action potentials and the refractory period in the atria and ventricles. The inhibition of rapid potassium channels is increases as heart rate decreases, which is why adverse effects like torsades de points is more likely to be seen at lower heart rates. L-sotalol also has beta adrenergic receptor blocking activity seen above plasma concentrations of 800ng/L. The beta blocking ability of sotalol further prolongs action potentials. D-sotalol does not have beta blocking activity but also reduces a patient's heart rate while standing or exercising. These actions combine to produce a negative inotropic effect that reduces the strength of contractility of muscle cells in the heart. Extension of the QT interval is also adversely associated with the induction of arrhythmia in patients. Sotalol inhibits beta-1 adrenoceptors in the myocardium as well as rapid potassium channels to slow repolarization, lengthen the QT interval, and slow and shorten conduction of action potentials through the atria. The action of sotalol on beta adrenergic receptors lengthens the sinus node cycle, conduction time through the atrioventricular node, refractory period, and duration of action potentials.",The molecular weight is 272.36.,Sotalol has a topological polar surface area of 78.43.,The log p value of  is 0.23.,Sotalol is approved.,Sotalol is a solid.,True
15103,"Darifenacin (Enablex®, Novartis) is a medication used to treat urinary incontinence. For the treatment of overactive bladder with symptoms of urge urinary incontinence, urgency and frequency. Darifenacin is a competitive muscarinic receptor antagonist. <i>In vitro</i> studies using human recombinant muscarinic receptor subtypes show that darifenacin has greater affinity for the M3 receptor than for the other known muscarinic receptors (9 and 12-fold greater affinity for M3 compared to M1 and M5, respectively, and 59-fold greater affinity for M3 compared to both M2 and M4). Muscarinic receptors play an important role in several major cholinergically mediated functions, including contractions of the urinary bladder smooth muscle and stimulation of salivary secretion. Adverse drug effects such as dry mouth, constipation and abnormal vision may be mediated through effects on M3 receptors in these organs. Darifenacin selectively antagonizes the muscarinic M3 receptor. M3 receptors are involved in contraction of human bladder and gastrointestinal smooth muscle, saliva production, and iris sphincter function.",The molecular weight is 426.56.,Darifenacin has a topological polar surface area of 55.56.,The log p value of  is 3.62.,Darifenacin is approved and investigational.,Darifenacin is a solid.,True
15104,"Dextromethorphan is a levorphanol derivative and codeine analog commonly used as a cough suppressant and also a drug of abuse. Although similar in structure to other opioids, it has minimal interaction with opioid receptors. Dextromethorphan is indicated in combination with and in the treatment of coughs and upper respiratory symptoms associated with allergies or the common cold. Dextromethorphan is also used in combination with as an over the counter product to relieve a cough. Dextromethorpahn in combination with is indicated in the treatment of pseudobulbar affect. Dextromethorphan is an opioid-like molecule indicated in combination with other medication in the treatment of coughs and pseudobulbar affect. It has a moderate therapeutic window, as intoxication can occur at higher doses. Dextromethorphan has a moderate duration of action. Patients should be counselled regarding the risk of intoxication. Dextromethorphan is an agonist of NMDA and sigma-1 receptors. It is also an antagonist of α3/β4 nicotinic receptors. However, the mechanism by which dextromethorphan's receptor agonism and antagonism translates to a clinical effect is not well understood.",The molecular weight is 271.4.,Dextromethorphan has a topological polar surface area of 12.47.,The log p value of  is 3.95.,Dextromethorphan is approved.,Dextromethorphan is a solid.,True
15105,"A beta-adrenergic antagonist used as an anti-arrhythmia agent, an anti-angina agent, an antihypertensive agent, and an antiglaucoma agent. For the treatment of intraocular hypertension and chronic open-angle glaucoma Carteolol is a beta1 and beta2 (non-selective) adrenergic receptor-blocking agent that does not have significant intrinsic sympathomimetic, direct myocardial depressant, or local anesthetic (membrane-stabilizing) activity. Carteolol, when applied topically to the eye, has the action of reducing elevated, as well as normal, intraocular pressure, whether or not accompanied by glaucoma. Elevated intraocular pressure is a major risk factor in the pathogenesis of glaucomatous visual field loss and optic nerve damage. Carteolol reduces intraocular pressure with little or no effect on pupil size or accommodation in contrast to the miosis which cholinergic agents are known to produce. The primary mechanism of the ocular hypotensive action of carteolol in reducing intraocular pressure is most likely a decrease in aqueous humor production. This process is initiated by the non-selective beta1 and beta2 adrenergic receptor blockade.",The molecular weight is 292.38.,Carteolol has a topological polar surface area of 70.59.,The log p value of  is 1.29.,Carteolol is approved.,Carteolol is a solid.,True
15106,"First synthesized by Janssen Pharmaceuticals in 1955, cinnarizine is an anti-histaminic drug mainly used for the control of vestibular disorders and motion sickness. Cinnarizine is a specific calcium channel blocker that primarily works on the central vestibular system to interfere with the signal transmission between vestibular apparatus of the inner ear and the vomiting centre of the hypothalamus. Cinnarizine could be also viewed as a nootropic drug because of its vasorelaxating abilities (due to calcium channel blockage), which happen mostly in brain. Combination use of cinnarizine with other nootropics, such as resulted in enhanced effect of boosting brain oxygen supply. For the treatment of vertigo/meniere's disease, nausea and vomiting, motion sickness and also useful for vestibular symptoms of other origins. Cinnarizine is an antihistamine and a calcium channel blocker. Histamines mediate a number of activities such as contraction of smooth muscle of the airways and gastrointestinal tract, vasodilatation, cardiac stimulation, secretion of gastric acid, promotion of interleukin release and chemotaxis of eosinophils and mast cells. Competitive antagonists at histamine H1 receptors may be divided into first (sedating) and second (non-sedating) generation agents. Some, such as Cinnarizine also block muscarinic acetylcholine receptors and are used as anti-emetic agents. Cinnarizine through its calcium channel blocking ability also inhibits stimulation of the vestibular system. Cinnarizine inhibits contractions of vascular smooth muscle cells by blocking L-type and T-type voltage gated calcium channels. Cinnarizine has also been implicated in binding to dopamine D2 receptors, histamine H1 receptors, and muscarinic acetylcholine receptors. ",The molecular weight is 368.52.,Cinnarizine has a topological polar surface area of 6.48.,The log p value of  is 6.05.,Cinnarizine is approved and investigational.,Cinnarizine is a solid.,True
15107,"Antitumor alkaloid isolated from Vinca rosea. (Merck, 11th ed.) For treatment of breast cancer, testicular cancer, lymphomas, neuroblastoma, Hodgkin's and non-Hodgkin's lymphomas, mycosis fungoides, histiocytosis, and Kaposi's sarcoma. Vinblastine is a vinca alkaloid antineoplastic agent. The vinca alkaloids are structurally similar compounds comprised of 2 multiringed units: vindoline and catharanthine. The vinca alkaloids have become clinically useful since the discovery of their antitumour properties in 1959. Initially, extracts of the periwinkle plant (<i>Catharanthus roseus</i>) were investigated because of putative hypoglycemic properties, but were noted to cause marrow suppression in rats and antileukemic effects <i>in vitro</i>. Vinblastine has some immunosuppressant effect. The vinca alkaloids are considered to be cell cycle phase-specific. The antitumor activity of vinblastine is thought to be due primarily to inhibition of mitosis at metaphase through its interaction with tubulin. Vinblastine binds to the microtubular proteins of the mitotic spindle, leading to crystallization of the microtubule and mitotic arrest or cell death.",The molecular weight is 810.99.,Vinblastine has a topological polar surface area of 154.1.,The log p value of  is 5.23.,Vinblastine is approved.,Vinblastine is a solid.,True
15108,"Doxazosin is an alpha-1 antagonist used for the treatment of benign prostatic hypertrophy (BPH) symptoms and hypertension. Other members of this drug class include , , , and. Because of its long-lasting effects, doxazosin can be administered once a day. It is marketed by Pfizer and was initially approved by the FDA in 1990. Doxazosin is indicated to treat the symptoms of benign prostatic hypertrophy, which may include urinary frequency, urgency, and nocturia, among other symptoms. In addition, doxazosin is indicated alone or in combination with various antihypertensive agents for the management of hypertension. Off-label uses of doxazosin include the treatment of pediatric hypertension and the treatment of ureteric calculi. Doxazosin decreases standing and supine blood pressure and relieves the symptoms of benign prostatic hypertrophy through the inhibition of alpha-1 receptors. Doxazosin selectively inhibits the postsynaptic alpha-1 receptors on vascular smooth muscle by nonselectively blocking the alpha-1a, alpha-1b, and alpha-1d subtypes. This action on blood vessels decreases systemic peripheral vascular resistance, reducing blood pressure, exerting minimal effects on the heart rate due to its receptor selectivity. Norepinephrine-activated alpha-1 receptors located on the prostate gland and bladder neck normally cause contraction of regional muscular tissue, obstructing urinary flow and contributing to the symptoms of benign prostatic hypertrophy. Alpha-1 antagonism causes smooth muscle relaxation in the prostate and bladder, effectively relieving urinary frequency, urgency, weak urinary stream, and other unpleasant effects of BPH. Recently, doxazosin was found to cause apoptosis of hERG potassium channels in an in vitro setting, possibly contributing to a risk of heart failure with doxazosin use. ",The molecular weight is 451.48.,Doxazosin has a topological polar surface area of 112.27.,The log p value of  is 3.53.,Doxazosin is approved.,Doxazosin is a solid.,True
15109,"Piperazine is an organic compound that consists of a six-membered ring containing two opposing nitrogen atoms. First used as a solvent for uric acid, the use of piperazine as an anthelmintic agent was first introduced in 1953. Upon entry into the systemic circulation, the drug is partly oxidized and partly eliminated as an unchanged compound. Outside the body, piperazine has a remarkable power to dissolve uric acid and producing a soluble urate, but in clinical experience it has not proved equally successful. Piperazine was first introduced as an anthelmintic in 1953. Piperazine compounds mediate their anthelmintic action by generally paralyzing parasites, allowing the host body to easily remove or expel the invading organism. Used as alternative treatment for ascariasis caused by <i>Ascaris lumbricoides</i> (roundworm) and enterobiasis (oxyuriasis) caused by <i>Enterobius vermicularis</i> (pinworm). It is also used to treat partial intestinal obstruction by the common roundworm, a condition primarily occurring in children. Piperazine is an anthelminthic especially useful in the treatment of partial intestinal obstruction caused by Ascaris worms, which is a condition primarily seen in children. Piperazine hydrate and piperazine citrate are the main anthelminthic piperazines. Piperazine is a GABA receptor agonist. Piperzine binds directly and selectively to muscle membrane GABA receptors, presumably causing hyperpolarization of nerve endings, resulting in flaccid paralysis of the worm. While the worm is paralyzed, it is dislodged from the intestinal lumen and expelled live from the body by normal intestinal peristalsis.",The molecular weight is 86.14.,Piperazine has a topological polar surface area of 24.06.,The log p value of  is -1.48.,Piperazine is approved and vet_approved.,Piperazine is a solid.,True
15110,"A phenothiazine used in the treatment of psychoses. Its properties and uses are generally similar to those of chlorpromazine. For management of manifestations of psychotic disorders. Fluphenazine is a trifluoro-methyl phenothiazine derivative intended for the management of schizophrenia and other psychotic disorders. Fluphenazine has not been shown effective in the management of behaviorial complications in patients with mental retardation. Fluphenazine blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain; depresses the release of hypothalamic and hypophyseal hormones and is believed to depress the reticular activating system thus affecting basal metabolism, body temperature, wakefulness, vasomotor tone, and emesis.",The molecular weight is 437.53.,Fluphenazine has a topological polar surface area of 29.95.,The log p value of  is 4.32.,Fluphenazine is approved.,Fluphenazine is a liquid.,True
15111,"An agonist of receptors, adrenergic alpha-2 that is used in veterinary medicine for its analgesic and sedative properties. It is the racemate of dexmedetomidine. For sedation of initially intubated and mechanically ventilated patients during treatment in an intensive care setting, also used in pain relief; anxiety reduction and analgesia Dexmedetomidine activates 2-adrenoceptors, and causes the decrease of sympathetic tone, with attenuation of the neuroendocrine and hemodynamic responses to anesthesia and surgery; it reduces anesthetic and opioid requirements; and causes sedation and analgesia. Dexmedetomidine is a specific and selective alpha-2 adrenoceptor agonist. By binding to the presynaptic alpha-2 adrenoceptors, it inhibits the release if norepinephrine, therefore, terminate the propagation of pain signals. Activation of the postsynaptic alpha-2 adrenoceptors inhibits the sympathetic activity decreases blood pressure and heart rate.",The molecular weight is 200.28.,Dexmedetomidine has a topological polar surface area of 28.68.,The log p value of  is 3.11.,Dexmedetomidine is approved and vet_approved.,Dexmedetomidine is a solid.,True
15112,"Dextropropoxyphene is an opioid analgesic manufactured by Eli Lilly and Company. It is used in the symptomatic treatment of mild pain. It displays antitussive and local anaesthetic actions. Due to the risk of cardiac arrhythmias and overdose, possibly leading to death, dextropropoxyphene has been withdrawn from the market in Europe and the United States. The drug is often referred to as the general form, \propoxyphene\"", however only the dextro-isomer (dextropropoxyphene) has any analgesic effect. The levo-isomer appears to exhibit a very limited antitussive effect."" For the relief of mild to moderate pain. Propoxyphene, a synthetic opiate agonist, is structurally similar to methadone. Its general pharmacologic properties are those of the opiates as a group. The analgesic effect of propoxyphene is due to the d-isomer, dextropropoxyphene. It binds to the opiate receptors and leads to a decrease of the perception of pain stimuli. Propoxyphene possesses little to no antitussive activity and no antipyretic action. Propoxyphene acts as a weak agonist at OP1, OP2, and OP3 opiate receptors within the central nervous system (CNS). Propoxyphene primarily affects OP3 receptors, which are coupled with G-protein receptors and function as modulators, both positive and negative, of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine, and noradrenaline is inhibited. Opioids such as propoxyphene also inhibit the release of vasopressin, somatostatin, insulin, and glucagon. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability.",The molecular weight is 339.48.,Dextropropoxyphene has a topological polar surface area of 29.54.,The log p value of  is 5.21.,Dextropropoxyphene is approved and illicit and investigational and withdrawn.,Dextropropoxyphene is a solid.,True
15113,"Galantamine is a tertiary alkaloid and reversible, competitive inhibitor of the acetylcholinesterase (AChE) enzyme, which is a widely studied therapeutic target used in the treatment of Alzheimer's disease. First characterized in the early 1950s, galantamine is a tertiary alkaloid that was extracted from botanical sources, such as _Galanthus nivalis_. Galantamine was first studied in paralytic and neuropathic conditions, such as myopathies and postpolio paralytic conditions, and for reversal of neuromuscular blockade. Following the discovery of its AChE-inhibiting properties, the cognitive effects of galantamine were studied in a wide variety of psychiatric disorders such as mild cognitive impairment, cognitive impairment in schizophrenia and bipolar disorder, and autism; however, re-development of the drug for Alzheimer’s disease did not commence until the early 1990s due to difficulties in extraction and synthesis. Galantamine blocks the breakdown of acetylcholine in the synaptic cleft, thereby increasing acetylcholine neurotransmission. It also acts as an allosteric modulator of the nicotinic receptor, giving its dual mechanism of action clinical significance. Galantamine is indicated for the treatment of mild to moderate dementia of the Alzheimer’s type. Galantamine is a competitive and reversible inhibitor of acetylcholinesterase that works to increase acetylcholine levels. Galantamine acts both centrally and peripherally to inhibit both muscle and brain acetylcholinesterase, thereby increasing cholinergic tone. Galantamine is also a positive allosteric modulator of neuronal nicotinic acetylcholine receptors. As dementia is a progressive neurodegenerative disease, galatamine has a negligible effect in altering the course of the underlying process of dementia and may exert its therapeutic effectiveness for a short period of time. However, galantamine promoted improvements in cognition, global function, activities of daily living, and behavioural symptoms in clinical studies of Alzheimer’s disease. Alzheimer’s disease is characterized by progressive, irreversible degeneration of acetylcholine-producing neurons, cognitive impairment, and the accumulation of neurofibrillary tangles and amyloid plaques. The cholinergic system plays a critical role in memory, alongside other important neural functions such as attention, learning, stress response, wakefulness and sleep, and sensory information. Studies show that acetylcholine (ACh) is involved in the modulation of acquisition, encoding, consolidation, reconsolidation, extinction, and retrieval of memory. The gradual loss of cholinergic neurons in Alzheimer’s disease (AD) may, therefore, contribute to the memory loss exhibited by AD patients. ",The molecular weight is 287.36.,Galantamine has a topological polar surface area of 41.93.,The log p value of  is 1.02.,Galantamine is approved.,Galantamine is a solid.,True
15114,"A phenothiazine antipsychotic used in the management of psychoses, including schizophrenia, and in the control of severely disturbed or agitated behavior. It has little antiemetic activity. Thioridazine has a higher incidence of antimuscarinic effects, but a lower incidence of extrapyramidal symptoms, than chlorpromazine. (From Martindale, The Extra Pharmacopoeia, 30th ed, p618). For the treatment of schizophrenia and generalized anxiety disorder. Thioridazine is a trifluoro-methyl phenothiazine derivative intended for the management of schizophrenia and other psychotic disorders. Thioridazine has not been shown effective in the management of behaviorial complications in patients with mental retardation. Thioridazine blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain; blocks alpha-adrenergic effect, depresses the release of hypothalamic and hypophyseal hormones and is believed to depress the reticular activating system thus affecting basal metabolism, body temperature, wakefulness, vasomotor tone, and emesis.",The molecular weight is 370.57.,Thioridazine has a topological polar surface area of 6.48.,The log p value of  is 6.2.,Thioridazine is approved and withdrawn.,Thioridazine is a solid.,True
15115,"An ergot derivative that has been used as a cerebral vasodilator and in peripheral vascular disease. It has been suggested to ameliorate cognitive deficits in cerebrovascular disease. For the treatment of senile dementia, migraines of vascular origin, transient ischemia, platelet hyper-aggregability, and macular degeneration. Nicergoline is a potent vasodilator (improves brain blood flow). On the cerebral level it prompts a lowering of vascular resistance, an increase in arterial flow and stimulates the use of oxygen and glucose. Nicergoline also improves blood circulation in the lungs and limbs and has been shown to inhibit blood platelet aggregation. Nicergoline acts by inhibiting the postsynaptic alpha(1)-adrenoceptors on vascular smooth muscle. This inhibits the vasoconstrictor effect of circulating and locally released catecholamines (epinephrine and norepinephrine), resulting in peripheral vasodilation. Therefore the mechanism of Nicergoline is to increase vascular circulation in the brain, thereby enhancing the transmission of nerve signals across the nerve fibres, which secrete acetylcholine as a neural transmitter.",The molecular weight is 484.39.,Nicergoline has a topological polar surface area of 56.59.,The log p value of  is 4.07.,Nicergoline is approved and investigational.,Nicergoline is a solid.,True
15116,"Paroxetine is a selective serotonin reuptake inhibitor (SSRI) drug commonly known as Paxil. It has a variety of uses, including the treatment of anxiety disorders, major depression, posttraumatic stress disorder, and symptoms of menopause, among others. It was approved by the FDA in the early 1990s and marketed by SmithKline Beecham. A unique feature of this drug is that it is highly potent and selective in its inhibition of serotonin reuptake and has little effect on other neurotransmitters. Because of its potent inhibition of serotonin reuptake, paroxetine is more likely to cause withdrawal effects upon cessation. Paroxetine is well tolerated in most patients with a similar adverse effect profile to other members of its drug class. The controlled release formulation was designed to decrease the likelihood of nausea that is sometimes associated with paroxetine. Paroxetine is indicated for the management of depression, obsessive-compulsive disorder, panic disorder, social anxiety disorder, generalized anxiety disorder, posttraumatic stress disorder. One form of paroxetine, commercially known as Brisdelle, is used to manage mild to moderate vasomotor symptoms of menopause. Off-label, paroxetine may be used for the treatment of premature ejaculation or irritable bowel syndrome (IBS). Paroxetine treats the symptoms of depression, various anxiety disorders, posttraumatic stress disorder, obsessive-compulsive disorder, and the vasomotor symptoms of menopause via the inhibition of serotonin reuptake. The onset of action of paroxetine is reported to be approximately 6 weeks. Paroxetine enhances serotonergic activity via the inhibition presynaptic reuptake of serotonin by the serotonin (SERT) receptor. This inhibition raises the level of serotonin in the synaptic cleft, relieving various symptoms. This drug has been demonstrated to be a stronger inhibitor of serotonin reuptake than other members of the same drug class, including , , and. The mechanism of action of paroxetine in relieving the vasomotor symptoms of menopause is unknown, according to the Brisdelle prescribing information, but may occur due to its effects on thermoregulation.",The molecular weight is 329.37.,Paroxetine has a topological polar surface area of 39.72.,The log p value of  is 4.24.,Paroxetine is approved and investigational.,Paroxetine is a solid.,True
15117,"Tricyclic antidepressant similar to imipramine, but with more antihistaminic and sedative properties. For the treatment of depression and depression accompanied by anxiety, agitation or sleep disturbance Trimipramine is a tricyclic antidepressant. It was thought that tricyclic antidepressants work by inhibiting the re-uptake of the neurotransmitters norepinephrine and serotonin by nerve cells. However, this response occurs immediately, yet mood does not lift for around two weeks. It is now thought that changes occur in receptor sensitivity in the cerebral cortex and hippocampus. The hippocampus is part of the limbic system, a part of the brain involved in emotions. Presynaptic receptors are affected: a1 and b1 receptors are sensitized, a2 receptors are desensitised (leading to increased noradrenaline production). Tricyclics are also known as effective analgesics for different types of pain, especially neuropathic or neuralgic pain. A precise mechanism for their analgesic action is unknown, but it is thought that they modulate anti-pain opioid systems in the CNS via an indirect serotonergic route. They are also effective in migraine prophylaxis, but not in abortion of acute migraine attack. The mechanism of their anti-migraine action is also thought to be serotonergic. Trimipramine's mechanism of action differs from other tricyclic antidepressants. Trimipramine acts by decreasing the reuptake of norepinephrine and serotonin (5-HT).",The molecular weight is 294.44.,Trimipramine has a topological polar surface area of 6.48.,The log p value of  is 5.44.,Trimipramine is approved.,Trimipramine is a solid.,True
15118,"Epinastine is used for the prevention of itching associated with allergic conjunctivitis. It has a multi-action effect that inhibits the allergic response in 3 ways: 1. stabilizes mast cells by preventing mast cell degranulation to control the allergic response, 2. prevents histamine binding to both the H1- and H2-receptors to stop itching and provide lasting protection, and 3. prevents the release of proinflammatory chemical mediators from the blood vessel to halt progression of the allergic response. For the prevention of itching associated with allergic conjunctivitis. Epinastine is an antihistamine and an inhibitor of histamine release from the mast cell for topical administration to the eyes. Epinastine is indicated for the prevention of itching associated with allergic conjunctivitis. Epinastine is a topically active, direct H<sub>1</sub>-receptor antagonist and an inhibitor of the release of histamine from the mast cell. Epinastine is selective for the histamine H<sub>1</sub>-receptor and has affinity for the histamine H2 receptor. Epinastine also possesses affinity for the a1-, a2-, and 5-HT<sub>2</sub> -receptors. Epinastine does not penetrate the blood/brain barrier and, therefore, is not expected to induce side effects of the central nervous system. Epinastine has a multiaction effect that inhibits the allergic response in 3 ways: 1. stabilizes mast cells by preventing mast cell degranulation to control the allergic response, 2. prevents histamine binding to both the H1- and H<sub>2</sub>-receptors to stop itching and provide lasting protection, and 3. prevents the release of proinflammatory chemical mediators from the blood vessel to halt progression of the allergic response.",The molecular weight is 249.32.,Epinastine has a topological polar surface area of 41.62.,The log p value of  is 2.15.,Epinastine is approved and investigational.,Epinastine is a solid.,True
15119,"A propylamine formed from the cyclization of the side chain of amphetamine. This monoamine oxidase inhibitor is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in panic and phobic disorders (From AMA Drug Evaluations Annual, 1994, p311).  For the treatment of major depressive episode without melancholia. Tranylcypromine belongs to a class of antidepressants called monoamine oxidase inhibitors (MAOIs). Tranylcypromine is a non-hydrazine monoamine oxidase inhibitor with a rapid onset of activity. MAO is an enzyme that catalyzes the oxidative deamination of a number of amines, including serotonin, norepinephrine, epinephrine, and dopamine. Two isoforms of MAO, A and B, are found in the body. MAO-A is mainly found within cells located in the periphery and catalyzes the breakdown of serotonin, norepinephrine, epinephrine, dopamine and tyramine. MAO-B acts on phenylethylamine, norepinephrine, epinephrine, dopamine and tyramine, is localized extracellularly and is found predominantly in the brain. While the mechanism of MAOIs is still unclear, it is thought that they act by increasing free serotonin and norepinephrine concentrations and/or by altering the concentrations of other amines in the CNS. It has been postulated that depression is caused by low levels of serotonin and/or norepinephrine and that increasing serotonergic and norepinephrinergic neurotransmission results in relief of depressive symptoms. MAO A inhibition is thought to be more relevant to antidepressant activity than MAO B inhibition. Selective MAO B inhibitors, such as selegiline, have no antidepressant effects. Tranylcypromine irreversibly and nonselectively inhibits monoamine oxidase (MAO). Within neurons, MAO appears to regulate the levels of monoamines released upon synaptic firing. Since depression is associated with low levels of monoamines, the inhibition of MAO serves to ease depressive symptoms, as this results in an increase in the concentrations of these amines within the CNS.",The molecular weight is 133.19.,Tranylcypromine has a topological polar surface area of 26.02.,The log p value of  is 1.48.,Tranylcypromine is approved and investigational.,Tranylcypromine is a solid.,True
15120,"Dolasetron is an antinauseant and antiemetic agent indicated for the prevention of nausea and vomiting associated with moderately-emetogenic cancer chemotherapy and for the prevention of postoperative nausea and vomiting. Dolasetron is a highly specific and selective serotonin 5-HT3 receptor antagonist. This drug is not shown to have activity at other known serotonin receptors, and has low affinity for dopamine receptors. For the prevention of nausea and vomiting associated with emetogenic cancer chemotherapy, including initial and repeat courses of chemotherapy. Also used for the prevention of postoperative nausea and vomiting. This drug can be used intravenously for the treatment of postoperative nausea and vomiting. Dolasetron is a highly specific and selective serotonin 5-HT<sub>3</sub> receptor antagonist, not shown to have activity at other known serotonin receptors and with low affinity for dopamine receptors. It is structurally and pharmacologically related to other 5-HT<sub>3</sub> receptor agonists. The serontonin 5-HT<sub>3</sub> receptors are located on the nerve terminals of the vagus in the periphery, and centrally in the chemoreceptor trigger zone of the area postrema. It is suggested that chemotherapeutic agents release serotonin from the enterochromaffin cells of the small intestine by causing degenerative changes in the GI tract. The serotonin then stimulates the vagal and splanchnic nerve receptors that project to the medullary vomiting center, as well as the 5-HT<sub>3</sub> receptors in the area postrema, thus initiating the vomiting reflex, causing nausea and vomiting. Dolasetron is a selective serotonin 5-HT<sub>3</sub> receptor antagonist. In vivo, the drug is rapidly converted into its major active metabolite, hydrodolasetron, which seems to be largely responsible for the drug's pharmacological activity. The antiemetic activity of the drug is brought about through the inhibition of 5-HT<sub>3</sub> receptors present both centrally (medullary chemoreceptor zone) and peripherally (GI tract). This inhibition of 5-HT<sub>3</sub> receptors in turn inhibits the visceral afferent stimulation of the vomiting center, likely indirectly at the level of the area postrema, as well as through direct inhibition of serotonin activity within the area postrema and the chemoreceptor trigger zone.",The molecular weight is 324.38.,Dolasetron has a topological polar surface area of 62.4.,The log p value of  is 2.34.,Dolasetron is approved and investigational.,Dolasetron is a solid.,True
15121,"Methimazole is a thionamide antithyroid agent that inhibits the synthesis of thyroid hormones. It was first introduced as an antithyroid agent in 1949 and is now commonly used in the management of hyperthyroidism, particularly in those for whom more aggressive options such as surgery or radioactive iodine therapy are inappropriate. In the United States, methimazole is indicated for the treatment of hyperthyroidism in patients with Graves' disease or toxic multinodular goiter for whom thyroidectomy or radioactive iodine therapy are not appropriate treatment options. Methimazole is also indicated for the amelioration of hyperthyroid symptoms in preparation for thyroidectomy or radioactive iodine therapy. Methimazole inhibits the synthesis of thyroid hormones resulting in an alleviation of hyperthyroidism. Onset of action occurs within 12 to 18 hours, and its duration of action is 36 to 72 hours, likely due to concentration of methimazole and some metabolites within the thyroid gland after administration. Methimazole's primary mechanism of action appears to be interference in an early step in thyroid hormone synthesis involving thyroid peroxidase (TPO), however the exact method through which methimazole inhibits this step is unclear. TPO, along with hydrogen peroxide, normally catalyzes the conversion of iodide to iodine and then further catalyzes the incorporation of this iodine onto the 3 and/or 5 positions of the phenol rings of tyrosine residues in thyroglobulin. These thyroglobulin molecules then degrade within thyroid follicular cells to form either thyroxine (T<sub>4</sub>) or tri-iodothyronine (T<sub>3</sub>), which are the main hormones produced by the thyroid gland.",The molecular weight is 114.17.,Methimazole has a topological polar surface area of 15.27.,The log p value of  is -0.34.,Methimazole is approved.,Methimazole is a solid.,True
15122,"A histamine H1 antagonist with low sedative action but frequent gastrointestinal irritation. It is used to treat asthma; HAY fever; urticaria; and rhinitis; and also in veterinary applications. Tripelennamine is administered by various routes, including topically. Used for the symptomatic relief of hypersensitivity reactions, coughs, and the common cold. Used to treat the effects of colds and allergies. Tripelennamine is an antihistamine. Histamine, acting on H<sub>1</sub>-receptors, produces pruritis, vasodilatation, hypotension, flushing, headache, tachycardia, and bronchoconstriction. Histamine also increases vascular permeability and potentiates pain. Tripelennamine is a histamine H1 antagonist. It competes with histamine for the normal H<sub>1</sub>-receptor sites on effector cells of the gastrointestinal tract, blood vessels and respiratory tract. It provides effective, temporary relief of sneezing, watery and itchy eyes, and runny nose due to hay fever and other upper respiratory allergies. Tripelennamine binds to the histamine H1 receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine.",The molecular weight is 255.36.,Tripelennamine has a topological polar surface area of 19.37.,The log p value of  is 3.31.,Tripelennamine is approved and vet_approved.,Tripelennamine is a solid.,True
15123,"Minaprine is a psychotropic drug which has proved to be effective in the treatment of various depressive states. Like most antidepressants minaprine antagonizes behavioral despair. Minaprine is an amino-phenylpyridazine antidepressant reported to be relatively free of cardiotoxicity, drowsiness, and weight gain. For the treatment of depression Minaprine is an amino-phenylpyridazine antidepressant reported to be relatively free of cardiotoxicity, drowsiness, and weight gain. Similar to other antidepressant treatments, minaprine attenuates the beta-adrenergic receptor function. Studies have also shown that minaprine improves memory consolidation and that repeated drug administration leads to potentiation of this effect. Moreover, the effects of minaprine on memory consolidation are related to its dopaminergic action. Minaprine binds to serotonin type 2 receptors and to dopamine D1 and D2 type receptors. It also binds to the serotonin reuptake pump. Therefore, minaprine blocks the reuptake of both dopamine and serotonin. It is also, to a slight degree, cholinomimetic. Thus it may exhibit both mood-brightening and nootropic properties. It also acts as a reversible inhibitor of MAO-A (RIMA).It has also been found to inhibit acetylcholinesterase.",The molecular weight is 298.39.,Minaprine has a topological polar surface area of 50.28.,The log p value of  is 3.19.,Minaprine is approved.,Minaprine is a solid.,True
15124,"A muscarinic antagonist that has effects in both the central and peripheral nervous systems. It has been used in the treatment of arteriosclerotic, idiopathic, and postencephalitic parkinsonism. It has also been used to alleviate extrapyramidal symptoms induced by phenothiazine derivatives and reserpine. For use as an adjunct in the therapy of all forms of parkinsonism and control of extrapyramidal disorders secondary to neuroleptic drug therapy. Biperiden is a weak peripheral anticholinergic agent. It has, therefore, some antisecretory, antispasmodic and mydriatic effects. In addition, biperiden possesses nicotinolytic activity. The parenteral form of biperiden is an effective and reliable agent for the treatment of acute episodes of extrapyramidal disturbances sometimes seen during treatment with neuroleptic agents. Akathisia, akinesia, dyskinetic tremors, rigor, oculogyric crisis, spasmodic torticollis, and profuse sweating are markedly reduced or eliminated. With parenteral biperiden, these drug-induced disturbances are rapidly brought under control. Parkinsonism is thought to result from an imbalance between the excitatory (cholinergic) and inhibitory (dopaminergic) systems in the corpus striatum. The mechanism of action of centrally active anticholinergic drugs such as biperiden is considered to relate to competitive antagonism of acetylcholine at cholinergic receptors in the corpus striatum, which then restores the balance.",The molecular weight is 311.47.,Biperiden has a topological polar surface area of 23.47.,The log p value of  is 4.94.,Biperiden is approved and investigational.,Biperiden is a solid.,True
15125,"One of the long-acting synthetic antidiarrheals; it is not significantly absorbed from the gut, and has no effect on the adrenergic system or central nervous system, but may antagonize histamine and interfere with acetylcholine release locally. For the control and symptomatic relief of acute nonspecific diarrhea and of chronic diarrhea associated with inflammatory bowel disease or gastroenteritis. Also used for reducing the volume of discharge from ileostomies. Loperamide is a synthetic anti-diarrheal indicated for the control and symptomatic relief of acute nonspecific diarrhea and of chronic diarrhea associated with inflammatory bowel disease. Loperamide is also indicated for reducing the volume of discharge from ileostomies. In man, Loperamide prolongs the transit time of the intestinal contents. It reduces the daily fecal volume, increases the viscosity and bulk density, and diminishes the loss of fluid and electrolytes. Tolerance to the antidiarrheal effect has not been observed. Loperamide is an opioid receptor agonist and acts on the mu opioid receptors in the myenteric plexus large intestines; it does not affect the central nervous system like other opioids. It works specifically by decreasing the activity of the myenteric plexus which decreases the motility of the circular and longitudinal smooth muscles of the intestinal wall. This increases the amount of time substances stay in the intestine, allowing for more water to be absorbed out of the fecal matter. Loperamide also decreases colonic mass movements and suppresses the gastrocolic reflex. <i>In vitro</i> and animal studies show that Loperamide acts by slowing intestinal motility and by affecting water and electrolyte movement through the bowel. Loperamide inhibits peristaltic activity by a direct effect on the circular and longitudinal muscles of the intestinal wall. It is a non-selective calcium channel blocker and binds to opioid mu-receptors. Evidence also suggests that at higher concentrations it binds to calmodulin.",The molecular weight is 477.05.,Loperamide has a topological polar surface area of 43.78.,The log p value of  is 4.66.,Loperamide is approved.,Loperamide is a solid.,True
15126,"In 2016, the global burden of dementia was estimated to be 43.8 million, demonstrating a significant increase from a global prevalence of 20.2 million in 1990. Donepezil, also known as Aricept, is a piperidine derivative acetylcholinesterase inhibitor used in the management of the dementia of Alzheimer's Disease, and in some cases, is used to manage other types of dementia.  Donepezil is indicated for the management of mild to moderate Alzheimer’s Disease at doses of 5 mg or 10 mg. It is also indicated for the management of moderate to severe Alzheimer’s Disease in a higher dose of 10 mg or 23 mg administered once daily. Off-label uses include the management of vascular dementia, Parkinson's Disease-associated dementia, and Lewy body dementia, among others. When combined with memantine, the extended-release form of donepezil is indicated to treat the symptoms of moderate to severe dementia. By inhibiting the acetylcholinesterase enzyme, donepezil improves the cognitive and behavioral signs and symptoms of Alzheimer's Disease, which may include apathy, aggression, confusion, and psychosis.",The molecular weight is 379.5.,Donepezil has a topological polar surface area of 38.77.,The log p value of  is 4.6.,Donepezil is approved.,Donepezil is a solid.,True
15127,"An antipsychotic phenothiazine derivative with actions and uses similar to those of chlorpromazine. For use in the management of the manifestations of psychotic disorders and for the control of severe nausea and vomiting in adults. Perphenazine is a piperazinyl phenothiazine, acts on the central nervous system, and has a greater behavioral potency than other phenothiazine derivatives whose side chains do not contain a piperazine moiety. It is a member of a class of drugs called phenothiazines, which are dopamine D1/D2 receptor antagonists. Perphenazine is 10 to 15 times as potent as chlorpromazine; that means perphenazine is a highly potent antipsychotic. In equivalent doses it has approximately the same frequency and severity of early and late extrapypramidal side-effects compared to Haloperidol. Binds to the dopamine D1 and dopamine D2 receptors and inhibits their activity. The mechanism of the anti-emetic effect is due predominantly to blockage of the dopamine D2 neurotransmitter receptors in the chemoreceptor trigger zone and vomiting centre. Perphenazine also binds the alpha andrenergic receptor. This receptor's action is mediated by association with G proteins that activate a phosphatidylinositol-calcium second messenger system.",The molecular weight is 403.97.,Perphenazine has a topological polar surface area of 29.95.,The log p value of  is 4.01.,Perphenazine is approved.,Perphenazine is a solid.,True
15128,"One of the adrenergic beta-antagonists used as an antihypertensive, anti-anginal, and anti-arrhythmic agent. Alprenolol is no longer marketed by AstraZeneca, but may still be available in generic varieties. For the treatment of hypertension, angina, and arrhythmia Alprenolol is a non-selective beta-blocker used in the treatment of hypertension, edema, ventricular tachycardias, and atrial fibrillation. Alprenolol impairs AV node conduction and decreases sinus rate and may also increase plasma triglycerides and decrease HDL-cholesterol levels. Alprenolol is nonpolar and hydrophobic, with low to moderate lipid solubility. Alprenolol has little to no intrinsic sympathomimetic activity and, unlike some other beta-adrenergic blocking agents, alprenolol has little direct myocardial depressant activity and does not have an anesthetic-like membrane-stabilizing action. Alprenolol non-selectively blocks beta-1 adrenergic receptors mainly in the heart, inhibiting the effects of epinephrine and norepinephrine resulting in a decrease in heart rate and blood pressure. Also, with a more minor effect, by binding beta-2 receptors in the juxtaglomerular apparatus, alprenolol inhibits the production of renin, thereby inhibiting angiotensin II and aldosterone production and therefore inhibits the vasoconstriction and water retention due to angiotensin II and aldosterone, respectively.",The molecular weight is 249.35.,Alprenolol has a topological polar surface area of 41.49.,The log p value of  is 2.65.,Alprenolol is experimental and withdrawn.,Alprenolol is a solid.,True
15129,"A biguanide hypoglycemic agent with actions and uses similar to those of metformin. Although it is generally considered to be associated with an unacceptably high incidence of lactic acidosis, often fatal, it is still available in some countries. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290) For the reatment of type II diabetes mellitus. Used to treat diabetes, phenformin is a biguanide (contains 2 guanidino groups) hypoglycemic agent with actions and uses similar to those of metformin (Glucophage). Both drugs work by (1) decreasing the absorption of glucose by the intestines, (2) decreasing the production of glucose in the liver, and by (3) increasing the body's ability to use insulin more effectively. More specifically, phenformin improves glycemic control by improving insulin sensitivity. Phenformin is generally considered to be associated with an unacceptably high incidence of actic acidosis. In general biguanides should be used only in stable type II diabetics who are free of liver, kidney and cardiovascular problems and who cannot be controlled with diet. Phenformin binds to the AMP-activated protein kinase (AMPK). AMPK is an ultra-sensitive cellular energy sensor that monitors energy consumption and down-regulates ATP-consuming processes when activated. The biguanide phenformin has been shown to independently decrease ion transport processes, influence cellular metabolism and activate AMPK. Phenformin's hypoglycemic activity is related the effect it has in activating AMPK and fooling insulin sensitive cells into thinking that insulin levels are low and causing the body to use glucose as if in a state of low caloric consumption. This drug also seems to inhibit several varients of ATP-sensitive potassium channels (namely the receptor subtype Kir6.1).",The molecular weight is 205.26.,Phenformin has a topological polar surface area of 97.78.,The log p value of  is -1.03.,Phenformin is approved and investigational and withdrawn.,Phenformin is a solid.,True
15130,"Tipranavir is a sulfonamide-containing dyhydropyrone and a nonpeptidic protease inhibitor that targets the HIV protease. Tipranavir and ritonavir are coadministered to treat HIV. For combination antiretroviral treatment of HIV-1 infected adult patients with evidence of viral replication, who are highly treatment-experienced or have HIV-1 strains resistant to multiple protease inhibitors. Tipranavir is a non-peptidic protease inhibitor (PI) of HIV. Protease inhibitors block the part of HIV called protease. HIV-1 protease is an enzyme required for the proteolytic cleavage of the viral polyprotein precursors into the individual functional proteins found in infectious HIV-1. Nelfinavir binds to the protease active site and inhibits the activity of the enzyme. This inhibition prevents cleavage of the viral polyproteins resulting in the formation of immature non-infectious viral particles. Protease inhibitors are almost always used in combination with at least two other anti-HIV drugs. Tipranavir (TPV) is a non-peptidic HIV-1 protease inhibitor that inhibits the processing of the viral Gag and Gag-Pol polyproteins in HIV-1 infected cells, thus preventing formation of mature virions. Two mechanisms are suggested in regards to the potency of tipranavir: 1. Tipravanir may bind to the active site of the protease enzyme with fewer hydrogen bonds than peptidic protease inhibitors, which results in increased flexibility, allowing it to fit into the active site of the enzyme in viruses that have become resistance to other protease inhibitors. This also enables tipranavir to adjust to amino acid substitutions at the active site. 2. Tipranavir's strong hydrogen bonding interaction with the amide backbone of the protease active site Asp30 may lead to its activity against resistant viruses.",The molecular weight is 602.67.,Tipranavir has a topological polar surface area of 105.59.,The log p value of  is 7.76.,Tipranavir is approved and investigational.,Tipranavir is a solid.,True
15131,"A phenothiazine antipsychotic with effects similar to chlorpromazine. Used in the treatment of schizophrenia, organic brain disorders, alcoholism and psychoneuroses. Mesoridazine, the besylate salt of a metabolite of thioridazine, is a phenothiazine tranquilizer. Pharmacological studies in laboratory animals have established that mesoridazine has a spectrum of pharmacodynamic actions typical of a major tranquilizer. In common with other tranquilizers it inhibits spontaneous motor activity in mice, prolongs thiopental and hexobarbital sleeping time in mice and produces spindles and block of arousal reaction in the EEG of rabbits. It is effective in blocking spinal reflexes in the cut and antagonizes d-amphetamine excitation and toxicity in grouped mice. It shows a moderate adrenergic blocking activity in vitro and in vivo and antagonizes 5-hydroxytryptamine in vivo. Intravenously administered, it lowers the blood pressure of anesthetized dogs. It has a weak antiacetylcholine effect in vitro. Based upon animal studies, mesoridazine, as with other phenothiazines, acts indirectly on reticular formation, whereby neuronal activity into reticular formation is reduced without affecting its intrinsic ability to activate the cerebral cortex. In addition, the phenothiazines exhibit at least part of their activities through depression of hypothalamic centers. Neurochemically, the phenothiazines are thought to exert their effects by a central adrenergic blocking action.",The molecular weight is 386.57.,Mesoridazine has a topological polar surface area of 23.55.,The log p value of  is 4.64.,Mesoridazine is approved and investigational.,Mesoridazine is a solid.,True
15132,"Hydrocodone is a synthetic opioid derivative of codeine. It is commonly used in combination with to control moderate to severe pain. Historically, hydrocodone has been used as a cough suppressant although this has largely been replaced by in current cough and cold formulations. Hydrocodone's more potent metabolite, has also found wide use as an analgesic and is frequently used in cases of severe pain. The FDA first approved Hydrocodone for use as part of the cough suppressant syrup Hycodan in March of 1943. Hydrocodone is indicated for the management of acute pain, sometimes in combination with or , as well as the symptomatic treatment of the common cold and allergic rhinitis in combination with decongestants, antihistamines, and expectorants. Hydrocodone inhibits pain signaling in both the spinal cord and brain. Its actions in the brain also produce euphoria, respiratory depression, and sedation. Hydrocodone binds to the mu opioid receptor (MOR) with the highest affinity followed by the delta opioid receptors (DOR). Hydrocodone's agonist effect at the MOR is considered to contribute the most to its analgesic effects. Both MOR and DOR are Gi/o coupled and and produces its signal through activation of inward rectifier potassium (GIRK) channels, inhibition of voltage gated calcium channel opening, and decreased adenylyl cyclase activity. In the dorsal horn of the spinal cord, activation of pre-synaptic MOR on primary afferents the inhibition of calcium channel opening and increased activity of GIRK channels hyperpolarizes the neuron and prevents release of neurotransmitters. Post-synaptic MOR can also prevent activation of neurons by glutamate through the aforementioned mechanisms. ",The molecular weight is 299.37.,Hydrocodone has a topological polar surface area of 38.77.,The log p value of  is 1.13.,Hydrocodone is approved and illicit and investigational.,Hydrocodone is a solid.,True
15133,"A moderately lipophilic beta blocker (adrenergic beta-antagonists). It is non-cardioselective and has intrinsic sympathomimetic actions, but little membrane-stabilizing activity. (From Martindale, The Extra Pharmocopoeia, 30th ed, p638) For the management of hypertension, edema, ventricular tachycardias, and atrial fibrillation. Pindolol is a non-selective beta-adrenergic antagonist (beta-blocker) which possesses intrinsic sympathomimetic activity (ISA) in therapeutic dosage ranges but does not possess quinidine-like membrane stabilizing activity. Pindolol impairs AV node conduction and decreases sinus rate and may also increase plasma triglycerides and decrease HDL-cholesterol levels. Pindolol is nonpolar and hydrophobic, with low to moderate lipid solubility. Pindolol has little to no intrinsic sympathomimetic activity and, unlike some other beta-adrenergic blocking agents, pindolol has little direct myocardial depressant activity and does not have an anesthetic-like membrane-stabilizing action. Pindolol non-selectively blocks beta-1 adrenergic receptors mainly in the heart, inhibiting the effects of epinephrine and norepinephrine resulting in a decrease in heart rate and blood pressure. By binding beta-2 receptors in the juxtaglomerular apparatus, Pindolol inhibits the production of renin, thereby inhibiting angiotensin II and aldosterone production and therefore inhibits the vasoconstriction and water retention due to angiotensin II and aldosterone, respectively.",The molecular weight is 248.33.,Pindolol has a topological polar surface area of 57.28.,The log p value of  is 1.67.,Pindolol is approved and investigational.,Pindolol is a solid.,True
15134,"An antineoplastic agent that inhibits DNA synthesis through the inhibition of ribonucleoside diphosphate reductase. For management of melanoma, resistant chronic myelocytic leukemia, and recurrent, metastatic, or inoperable carcinoma of the ovary and Sickle-cell anemia. Hydroxyurea has dose-dependent synergistic activity with cisplatin <i>in vitro</i>. <i>In vivo</i> Hydroxyurea showed activity in combination with cisplatin against the LX-1 and CALU-6 human lung xenografts, but minimal activity was seen with the NCI-H460 or NCI-H520 xenografts. Hydroxyurea was synergistic with cisplatin in the Lewis lung murine xenograft. Sequential exposure to Hydroxyurea 4 hours before cisplatin produced the greatest interaction. Hydroxyurea is converted to a free radical nitroxide (NO) in vivo, and transported by diffusion into cells where it quenches the tyrosyl free radical at the active site of the M2 protein subunit of ribonucleotide reductase, inactivating the enzyme. The entire replicase complex, including ribonucleotide reductase, is inactivated and DNA synthesis is selectively inhibited, producing cell death in S phase and synchronization of the fraction of cells that survive. Repair of DNA damaged by chemicals or irradiation is also inhibited by hydroxyurea, offering potential synergy between hydroxyurea and radiation or alkylating agents. Hydroxyurea also increases the level of fetal hemoglobin, leading to a reduction in the incidence of vasoocclusive crises in sickle cell anemia. Levels of fetal hemoglobin increase in response to activation of soluble guanylyl cyclase (sGC) by hydroxyurea-derived NO.",The molecular weight is 76.06.,Hydroxyurea has a topological polar surface area of 75.35.,The log p value of  is -1.8.,Hydroxyurea is approved.,Hydroxyurea is a solid.,True
15135,"Cinacalcet is a calcimimetic sold by Amgen under the trade name Sensipar® in North America and Australia and as Mimpara® in Europe. It is used to treat hyperparathyroidism due to parathyroid tumours or renal failure. For the treatment of secondary hyperparathyroidism in patients with Chronic Kidney Disease who are on hemodialysis or peritoneal dialysis. Also for the treatment of hypercalcemia in patients with parathyroid carcinoma. Cinacalcet is a drug that acts as a calcimimetic (i.e. it mimics the action of calcium on tissues). Secondary hyperparathyroidism (HPT) in patients with chronic kidney disease (CKD) is a progressive disease, associated with increases in parathyroid hormone (PTH) levels and derangements in calcium and phosphorus metabolism. Increased PTH stimulates osteoclastic activity resulting in cortical bone resorption and marrow fibrosis. The goals of treatment of secondary hyperparathyroidism are to lower levels of PTH, calcium, and phosphorus in the blood, in order to prevent progressive bone disease and the systemic consequences of disordered mineral metabolism. In CKD patients on dialysis with uncontrolled secondary HPT, reductions in PTH are associated with a favorable impact on bone-specific alkaline phosphatase (BALP), bone turnover and bone fibrosis. Cinacalcet reduces calcium levels by increasing the sensitivity of the calcium sensing receptor to extracellular calcium. Cinacalcet directly lowers parathyroid hormone levels by increasing the sensitivity of the calcium sensing receptors to activation by extracellular calcium, resulting in the inhibition of PTH secretion. The reduction in PTH is associated with a concomitant decrease in serum calcium levels.",The molecular weight is 357.42.,Cinacalcet has a topological polar surface area of 12.03.,The log p value of  is 6.35.,Cinacalcet is approved.,Cinacalcet is a solid.,True
15136,"An inhalation anesthetic. Currently, methoxyflurane is rarely used for surgical, obstetric, or dental anesthesia. If so employed, it should be administered with nitrous oxide to achieve a relatively light level of anesthesia, and a neuromuscular blocking agent given concurrently to obtain the desired degree of muscular relaxation. (From AMA Drug Evaluations Annual, 1994, p180) For use in the induction and maintenance of general anesthesia Methoxyflurane is a general inhalation anesthetic used for induction and maintenance of general anesthesia. It induces muscle relaxation and reduces pains sensitivity by altering tissue excitability. It does so by decreasing the extent of gap junction mediated cell-cell coupling and altering the activity of the channels that underlie the action potential. Methoxyflurane induces a reduction in junctional conductance by decreasing gap junction channel opening times and increasing gap junction channel closing times. Methoxyflurane also activates calcium dependent ATPase in the sarcoplasmic reticulum by increasing the fluidity of the lipid membrane. It also appears to bind the D subunit of ATP synthase and NADH dehydogenase. Methoxyflurane also binds to the GABA receptor, the large conductance Ca<sup>2+</sup> activated potassium channel, the glutamate receptor and the glycine receptor.",The molecular weight is 164.96.,Methoxyflurane has a topological polar surface area of 9.23.,The log p value of  is 2.49.,Methoxyflurane is approved and investigational and vet_approved.,Methoxyflurane is a liquid.,True
15137,"Tolterodine is an antimuscarinic drug that is used to treat urinary incontinence. Tolterodine acts on M2 and M3 subtypes of muscarinic receptors. For the treatment of overactive bladder (with symptoms of urinary frequency, urgency, or urge incontinence). Tolterodine is a competitive muscarinic receptor antagonist. Both urinary bladder contraction and salivation are mediated via cholinergic muscarinic receptors. After oral administration, tolterodine is metabolized in the liver, resulting in the formation of the 5-hydroxymethyl derivative, a major pharmacologically active metabolite. The 5-hydroxymethyl metabolite, which exhibits an antimuscarinic activity similar to that of tolterodine, contributes significantly to the therapeutic effect. Both tolterodine and the 5-hydroxymethyl metabolite exhibit a high specificity for muscarinic receptors, since both show negligible activity or affinity for other neurotransmitter receptors and other potential cellular targets, such as calcium channels. Tolterodine has a pronounced effect on bladder function. The main effects of tolterodine are an increase in residual urine, reflecting an incomplete emptying of the bladder, and a decrease in detrusor pressure, consistent with an antimuscarinic action on the lower urinary tract. Both tolterodine and its active metabolite, 5-hydroxymethyltolterodine, act as competitive antagonists at muscarinic receptors. This antagonism results in inhibition of bladder contraction, decrease in detrusor pressure, and an incomplete emptying of the bladder.",The molecular weight is 325.5.,Tolterodine has a topological polar surface area of 23.47.,The log p value of  is 5.24.,Tolterodine is approved and investigational.,Tolterodine is a solid.,True
15138,"A selective, irreversible inhibitor of Type B monoamine oxidase. It is used in newly diagnosed patients with Parkinson's disease. It may slow progression of the clinical disease and delay the requirement for levodopa therapy. It also may be given with levodopa upon onset of disability. (From AMA Drug Evaluations Annual, 1994, p385) The compound without isomeric designation is Deprenyl. Monotherapy for initial treatment of Parkinson's disease, as well as an adjunct therapy in patients with a decreased response to levodopa/carbadopa. Also used for the palliative treatment of mild to moderate Alzheimer's disease and at higher doses, for the treatment of depression. Dopamine is an essential chemical that occurs in many parts of the body. It is the premature degradation of dopamine that results in the symptoms of Parkinson's disease. Monoamine oxidase (MAO) is an enzyme which accelerates the breakdown of dopamine. Selegiline can prolong the effects of dopamine in the brain by preventing its breakdown through seletively blocking MAO-B. It also may prevent the removal of dopamine between nerve endings and enhance release of dopamine from nerve cells. Although the mechanisms for selegiline's beneficial action in the treatment of Parkinson's disease are not fully understood, the selective, irreversible inhibition of monoamine oxidase type B (MAO-B) is thought to be of primary importance. MAO-B is involved in the oxidative deamination of dopamine in the brain. Selegiline binds to MAO-B within the nigrostriatal pathways in the central nervous system, thus blocking microsomal metabolism of dopamine and enhancing the dopaminergic activity in the substantial nigra. Selegiline may also increase dopaminergic activity through mechanisms other than inhibition of MAO-B. At higher doses, selegiline can also inhibit monozmine oxidase type A (MAO-A), allowing it to be used for the treatment of depression.",The molecular weight is 187.29.,Selegiline has a topological polar surface area of 3.24.,The log p value of  is 2.84.,Selegiline is approved and investigational and vet_approved.,Selegiline is a solid.,True
15139,"Mequitazine is a histamine H1 antagonist (antihistamine). It competes with histamine for the normal H1-receptor sites on effector cells of the gastrointestinal tract, blood vessels and respiratory tract. It provides effective, temporary relief of sneezing, watery and itchy eyes, and runny nose due to hay fever and other upper respiratory allergies. For the treatment of Hay fever, urticaria (hives) and allergic rhinitis In allergic reactions an allergen interacts with and cross-links surface IgE antibodies on mast cells and basophils. Once the mast cell-antibody-antigen complex is formed, a complex series of events occurs that eventually leads to cell-degranulation and the release of histamine (and other chemical mediators) from the mast cell or basophil. Once released, histamine can react with local or widespread tissues through histamine receptors. Histamine, acting on H<sub>1</sub>-receptors, produces pruritis, vasodilatation, hypotension, flushing, headache, tachycardia, and bronchoconstriction. Histamine also increases vascular permeability and potentiates pain. Mequitazine is a histamine H1 antagonist. It competes with histamine for the normal H<sub>1</sub>-receptor sites on effector cells of the gastrointestinal tract, blood vessels and respiratory tract. It provides effective, temporary relief of sneezing, watery and itchy eyes, and runny nose due to hay fever and other upper respiratory allergies. Mequitazine binds to the histamine H1 receptor sites on effector cells in the gastrointestinal tract, blood vessels, and respiratory tract. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine.",The molecular weight is 322.47.,Mequitazine has a topological polar surface area of 6.48.,The log p value of  is 4.91.,Mequitazine is experimental.,Mequitazine is a solid.,True
15140,"Perhexiline is a coronary vasodilator used especially for angina of effort. It may cause neuropathy and hepatitis. For the management of severe angina pectoris. Used in the treatment of unresponsive or refractory angina. Perhexiline increases glucose metabolism at the expense of free-fatty-acid metabolism, enhancing oxygen efficiency during myocardial ischaemia. Perhexiline also potentiates platelet responsiveness to nitric oxide both in patients with angina and patients with acute coronary syndrome. The predominant mechanism of this particular perhexiline effect is an increase in platelet cGMP responsiveness. Perhexiline also may reduce the potential for nitric oxide clearance by neutrophil-derived oxygen. Perhexiline relieves symptoms of angina, improves exercise tolerance, and increases the workload needed to induce ischaemia when used as monotherapy. The primary therapeutic roles for perhexiline are as short-term therapy (less than 3 months duration) in patients with severe ischaemia awaiting coronary revascularisation or long-term therapy in patients with ischaemic symptoms refractory to other therapeutic measures. Perhexiline binds to the mitochondrial enzyme carnitine palmitoyltransferase (CPT)-1 and CPT-2. It acts by shifting myocardial substrate utilisation from long chain fatty acids to carbohydrates through inhibition of CPT-1 and, to a lesser extent, CPT-2, resulting in increased glucose and lactate utilization. This results in increased ATP production for the same O2 consumption as before and consequently increases myocardial efficiency.",The molecular weight is 277.5.,Perhexiline has a topological polar surface area of 12.03.,The log p value of  is 7.15.,Perhexiline is approved and investigational.,Perhexiline is a solid.,True
15141,"Novartis' brand name Zelnorm (tegaserod) had originally received approval from the US FDA in 2002 for the treatment of irritable bowel syndrome with constipation (IBS-C). It was, however, voluntarily withdrawn from widespread use in the US market in 2007 after concerns arose over the possibility that tegaserod could potentially cause dangerous cardiovascular events in patients. Since then, closer evaluations of the original data suggesting such cardiovascular risk have resulted in the limited reintroduction or 're-approval' of tegaserod for treatment of IBS-C specifically in female patients less than 65 years of age and whom are considered to be at a lower risk of a cardiovascular event than the broader population. Zelnorm (tegaserod) by Sloan Pharma subsequently gained re-approval in April of 2019. Nevertheless, tegaserod remains un-approved in certain regions. Tegaserod is a serotonin-4 (5-HT4) receptor agonist indicated for the treatment of adult women less than 65 years of age with irritable bowel syndrome with constipation (IBS-C). The safety and effectiveness of tegaserod in men with IBS-C have not been established. In general, it has been determined that tegaserod is an agonist of serotonin type-4 (5-HT(4)) receptors, an antagonist at 5-HT(2B) receptors, but is expected to possess minimal binding to 5-HT(1) receptors, and virtually no affinity for 5-HT(3) or dopamine receptors. Irritable bowel syndrome (IBS) is a complex functional disorder comprised of various abnormal and discomforting effects on the gastrointestinal tract and bowel function. Although the cause of IBS has yet to be formally elucidated, patient experience has demonstrated that the disorder is typically associated with abdominal pain, abdominal distension, cramping or bloating, variations in urgency for bowel movements, feelings of incomplete evacuation, gastroesophageal reflux, and various other effects. In particular, IBS that features constipation as a predominant effect is categorized as constipation-predominant IBS, or IBS-C.",The molecular weight is 301.39.,Tegaserod has a topological polar surface area of 85.29.,The log p value of  is 2.81.,Tegaserod is approved and investigational and withdrawn.,Tegaserod is a solid.,True
15142,"An anthelmintic with schistosomicidal activity against Schistosoma mansoni, but not against other Schistosoma spp. Oxamniquine causes worms to shift from the mesenteric veins to the liver where the male worms are retained; the female worms return to the mesentery, but can no longer release eggs. (From Martidale, The Extra Pharmacopoeia, 31st ed, p121) For treatment of Schistosomiasis caused by <i>Schistosoma mansoni</i> Oxamniquine is an anthelmintic with schistosomicidal activity against <i>Schistosoma mansoni</i>, but not against other Schistosoma spp. Oxamniquine causes worms to shift from the mesenteric veins to the liver where the male worms are retained; the female worms return to the mesentery, but can no longer release egg. Oxamniquine may associate with an irreversible inhibition of the nucleic acid metabolism of the parasites. A hypothesis has been put forth that the drug is activated by a single step, in which a schistosome sulfotransferase enzyme converts oxamniquine into an ester (probably acetate, phosphate, or sulfate). Subsequently, the ester spontaneously dissociates, the resulting electrophilic reactant is capable of alkylation of schistosome DNA.",The molecular weight is 279.34.,Oxamniquine has a topological polar surface area of 87.43.,The log p value of  is 1.81.,Oxamniquine is approved.,Oxamniquine is a solid.,True
15143,"Bicalutamide is an oral non-steroidal anti-androgen for prostate cancer. It is comprised of a racemic mixture that is a 50:50 composition of the (R)-bicalutamide and (S)-bicalutamide enantionmers. Bicalutamide binds to the androgen receptor. For treatment (together with surgery or LHRH analogue) of advanced prostatic cancer. Bicalutamide is an antineoplastic hormonal agent primarily used in the treatment of prostate cancer. Bicalutamide is a pure, nonsteroidal anti-androgen with affinity for androgen receptors (but not for progestogen, estrogen, or glucocorticoid receptors). Consequently, Bicalutamide blocks the action of androgens of adrenal and testicular origin which stimulate the growth of normal and malignant prostatic tissue. Prostate cancer is mostly androgen-dependent and can be treated with surgical or chemical castration. To date, antiandrogen monotherapy has not consistently been shown to be equivalent to castration. Bicalutamide competes with androgen for the binding of androgen receptors, consequently blocking the action of androgens of adrenal and testicular origin which stimulate the growth of normal and malignant prostatic tissue.",The molecular weight is 430.37.,Bicalutamide has a topological polar surface area of 107.26.,The log p value of  is 2.71.,Bicalutamide is approved.,Bicalutamide is a solid.,True
15144,"Rabeprazole is an antiulcer drug in the class of proton pump inhibitors. It is a prodrug - in the acid environment of the parietal cells it turns into active sulphenamide form. Rabeprazole inhibits the H+, K+ATPase of the coating gastric cells and dose-dependent oppresses basal and stimulated gastric acid secretion. For the treatment of acid-reflux disorders (GERD), peptic ulcer disease, H. pylori eradication, and prevention of gastroinetestinal bleeds with NSAID use. Rabeprazole prevents the production of acid in the stomach. It reduces symptoms and prevents injury to the esophagus or stomach in patients with gastroesophageal reflux disease (GERD) or ulcers. Rabeprazole is also useful in conditions that produce too much stomach acid such as Zollinger-Ellison syndrome. Rabeprazole may also be used with antibiotics to get rid of bacteria that are associated with some ulcers. Rabeprazole is a selective and irreversible proton pump inhibitor, suppresses gastric acid secretion by specific inhibition of the H<sup>+</sup>, K<sup>+</sup> -ATPase, which is found at the secretory surface of parietal cells. In doing so, it inhibits the final transport of hydrogen ions (via exchange with potassium ions) into the gastric lumen. Rabeprazole belongs to a class of antisecretory compounds (substituted benzimidazole proton-pump inhibitors) that do not exhibit anticholinergic or histamine H2-receptor antagonist properties, but suppress gastric acid secretion by inhibiting the gastric H<sup>+</sup>/K<sup>+</sup>ATPase (hydrogen-potassium adenosine triphosphatase) at the secretory surface of the gastric parietal cell. Because this enzyme is regarded as the acid (proton) pump within the parietal cell, rabeprazole has been characterized as a gastric proton-pump inhibitor. Rabeprazole blocks the final step of gastric acid secretion. In gastric parietal cells, rabeprazole is protonated, accumulates, and is transformed to an active sulfenamide. When studied in vitro, rabeprazole is chemically activated at pH 1.2 with a half-life of 78 seconds.",The molecular weight is 359.44.,Rabeprazole has a topological polar surface area of 77.1.,The log p value of  is 2.08.,Rabeprazole is approved and investigational.,Rabeprazole is a solid.,True
15145,"Proguanil is a prophylactic antimalarial drug, which works by stopping the malaria parasite, _Plasmodium falciparum_ and _Plasmodium vivax_, from reproducing once it is in the red blood cells. It does this by inhibiting the enzyme, dihydrofolate reductase, which is involved in the reproduction of the parasite. For the causal prevention and suppression of malaria caused by susceptible strains of <i>P. falciparum</i> and other species of Plasmodium found in some geographical areas of the world. Proguanil is a biguanide derivative that is converted to an active metabolite called cycloguanil. It exerts its antimalarial action by inhibiting parasitic dihydrofolate reductase enzyme. It has causal prophylactic and suppressive activity against <i>P. falciparum</i> and cures the acute infection. It is also effective in suppressing the clinical attacks of vivax malaria. However it is slower compared to 4-aminoquinolines. Proguanil inhibits the dihydrofolate reductase of plasmodia and thereby blocks the biosynthesis of purines and pyrimidines, which are essential for DNA synthesis and cell multiplication. This leads to failure of nuclear division at the time of schizont formation in erythrocytes and liver.",The molecular weight is 253.73.,Proguanil has a topological polar surface area of 83.79.,The log p value of  is 2.53.,Proguanil is approved.,Proguanil is a solid.,True
15146,"Nefazodone hydrochloride (trade name Serzone) is an antidepressant drug marketed by Bristol-Myers Squibb. Its sale was discontinued in 2003 in some countries, due to the small possibility of hepatic (liver) injury. Drug-induced hepatic injuries were associated with an risk of elevated need for a liver transplant, or even death, with the incidence of severe liver damage was shown to be approximately 1 in 250,000 to 300,000 patient-years. On May 20, 2004, Bristol-Myers Squibb discontinued the sale of Serzone in the United States. For the treatment of depression. Nefazodone, an antidepressant synthetically derived phenylpiperazine, is used to treat major depression. Although it is structurally similar to trazodone, nefazodone has a mechanism of action different from other antidepressants and, hence, lacks the risk for major cardiovascular toxicity seen with tricyclics and insomnia and inhibition of REM sleep seen with the selective serotonin reuptake inhibitors. Within the serotonergic system, nefazodone acts as an antagonist at type 2 serotonin (5-HT<sub>2</sub>) post-synaptic receptors and, like fluoxetine-type antidepressants, inhibits pre-synaptic serotonin (5-HT) reuptake. These mechanisms increase the amount of serotonin available to interact with 5-HT receptors. Within the noradrenergic system, nefazodone inhibits norepinephrine uptake minimally. Nefazodone also antagonizes alpha(1)-adrenergic receptors, producing sedation, muscle relaxation, and a variety of cardiovascular effects. Nefazodone's affinity for benzodiazepine, cholinergic, dopaminergic, histaminic, and beta or alpha(2)-adrenergic receptors is not significant.",The molecular weight is 470.01.,Nefazodone has a topological polar surface area of 51.62.,The log p value of  is 5.73.,Nefazodone is approved and withdrawn.,Nefazodone is a solid.,True
15147,"A muscarinic antagonist used to treat drug-induced parkinsonism and to relieve pain from muscle spasm. Indicated as an adjunct to rest, physical therapy, and other measures for the relief of discomfort associated with acute painful musculo skeletal conditions. Orphenadrine is indicated as an adjunct to rest, physical therapy, and other measures for the relief of discomfort associated with acute painful musculoskeletal conditions. Orphenadrine is an anticholinergic with a predominantly central effect and only a weak peripheral effect. In addition, it has mild antihistaminic and local anaesthetic properties. Parkinson's syndrome is the consequence of a disturbed balance between cholinergic and dopaminergic neurotransmission in the basal ganglia caused by a decrease in dopamine. Orphenadrine restores the physiological equilibrium and has a favourable effect on the rigidity and tremor of Parkinson's disease and Parkinsonian syndromes. The effect is somewhat less on bradykinesia. Orphenadrine binds and inhibits both histamine H1 receptors and NMDA receptors. It restores the motor disturbances induced by neuroleptics, in particular the hyperkinesia. The dopamine deficiency in the striatum increases the stimulating effects of the cholinergic system. This stimulation is counteracted by the anticholinergic effect of orphenadrine. It may have a relaxing effect on skeletal muscle spasms and it has a mood elevating effect.",The molecular weight is 269.39.,Orphenadrine has a topological polar surface area of 12.47.,The log p value of  is 3.9.,Orphenadrine is approved.,Orphenadrine is a solid.,True
15148,"Escitalopram is a selective serotonin re-uptake inhibitor (SSRI) and the S-enantiomer of racemic. It is used to restore serotonergic function in the treatment of depression and anxiety. Escitalopram is approximately 150 times more potent than citalopram’s R-enantiomer and is responsible for the vast majority of citalopram’s clinical activity, with some evidence suggesting that the R-enantiomer of racemic citalopram actively dampens the activity of escitalopram rather than existing simply as an inactive enantiomer. Amongst SSRIs, escitalopram exerts the highest degree of selectivity for the serotonin transporter (SERT) relative to other off-targets which may explain its lower rates of adverse effects as compared to other agents in this class. Escitalopram also differentiates itself from other SSRIs via allosteric action on its target - this may be the mechanism responsible for its observed superior efficacy and faster onset compared to other SSRIs. Escitalopram is indicated for both acute and maintenance treatment of major depressive disorder (MDD) and for the acute treatment of generalized anxiety disorder (GAD). It is additionally indicated for symptomatic relief of obsessive-compulsive disorder (OCD) in Canada. Escitalopram belongs to a class of medications called selective serotonin re-uptake inhibitors (SSRIs). These agents cause an increase in serotonin levels in neuronal synapses by preventing the re-uptake of serotonin (5-HT) into the presynaptic terminals of serotonergic neurons. As compared to other SSRIs, it appears to have a relatively quick onset of effect due to its potency. Escitalopram, like other selective serotonin re-uptake inhibitors, enhances serotonergic activity by binding to the orthosteric (i.e. primary) binding site on the serotonin transporter (SERT), the same site to which endogenous 5-HT binds, and thus prevents the re-uptake of serotonin into the presynaptic neuron. Escitalopram, along with , is also considered an allosteric serotonin re-uptake inhibitor - it binds to a secondary allosteric site on the SERT molecule to more strongly inhibit 5-HT re-uptake. Its combination of orthosteric and allosteric activity on SERT allows for greater extracellular 5-HT levels, a faster onset of action, and greater efficacy as compared to other SSRIs. The sustained elevation of synaptic 5-HT eventually causes desensitization of 5-HT<sub>1A</sub> auto-receptors, which normally shut down endogenous 5-HT release in the presence of excess 5-HT - this desensitization may be necessary for the full clinical effect of SSRIs and may be responsible for their typically prolonged onset of action.",The molecular weight is 324.4.,Escitalopram has a topological polar surface area of 36.26.,The log p value of  is 3.13.,Escitalopram is approved.,Escitalopram is a solid.,True
15149,"An orally administered anthracycline antineoplastic. The compound has shown activity against breast cancer, lymphomas and leukemias, together with the potential for reduced cardiac toxicity. For the treatment of acute myeloid leukemia (AML) in adults. This includes French-American-British (FAB) classifications M1 through M7. Idarubicin is an antineoplastic in the anthracycline class. General properties of drugs in this class include: interaction with DNA in a variety of different ways including intercalation (squeezing between the base pairs), DNA strand breakage and inhibition with the enzyme topoisomerase II. Most of these compounds have been isolated from natural sources and antibiotics. However, they lack the specificity of the antimicrobial antibiotics and thus produce significant toxicity. The anthracyclines are among the most important antitumor drugs available. Doxorubicin is widely used for the treatment of several solid tumors while daunorubicin and idarubicin are used exclusively for the treatment of leukemia. Idarubicin may also inhibit polymerase activity, affect regulation of gene expression, and produce free radical damage to DNA. Idarubicin possesses an antitumor effect against a wide spectrum of tumors, either grafted or spontaneous. The anthracyclines are cell cycle-nonspecific. Idarubicin has antimitotic and cytotoxic activity through a number of proposed mechanisms of action: Idarubicin forms complexes with DNA by intercalation between base pairs, and it inhibits topoisomerase II activity by stabilizing the DNA-topoisomerase II complex, preventing the religation portion of the ligation-religation reaction that topoisomerase II catalyzes.",The molecular weight is 497.5.,Idarubicin has a topological polar surface area of 176.61.,The log p value of  is 0.9.,Idarubicin is approved.,Idarubicin is a solid.,True
15150,"An antiarrhythmia agent that is particularly effective in ventricular arrhythmias. It also has weak beta-blocking activity. The drug is generally well tolerated. Used to prolong the time to recurrence of paroxysmal atrial fibrillation/flutter (PAF) associated with disabling symptoms in patients without structural heart disease. Also used for the treatment of life-threatening documented ventricular arrhythmias, such as sustained ventricular tachycardia. Propafenone is a Class 1C antiarrhythmic drug with local anesthetic effects, and a direct stabilizing action on myocardial membranes. It is used in the treatment of atrial and ventricular arrhythmias. It acts by inhibiting sodium channels to restrict the entry of sodium into cardiac cells resulting in reduced excitation. Propafenone has local anesthetic activity approximately equal to procaine. The electrophysiological effect of propafenone manifests itself in a reduction of upstroke velocity (Phase 0) of the monophasic action potential. In Purkinje fibers, and to a lesser extent myocardial fibers, propafenone reduces the fast inward current carried by sodium ions, which is responsible for the drugs antiarrhythmic actions. Diastolic excitability threshold is increased and effective refractory period prolonged. Propafenone reduces spontaneous automaticity and depresses triggered activity. At very high concentrations in vitro, propafenone can inhibit the slow inward current carried by calcium but this calcium antagonist effect probably does not contribute to antiarrhythmic efficacy.",The molecular weight is 341.45.,Propafenone has a topological polar surface area of 58.56.,The log p value of  is 3.64.,Propafenone is approved.,Propafenone is a solid.,True
15151,"Dexfenfluramine, also marketed under the name Redux, is a serotoninergic anorectic drug. For a fairly limited time during the middle of the nineties, the US FDA had approved it for use in managing weight loss. However, following multiple concerns about the cardiovascular side-effects of the drug, such approval was withdrawn. For the management of obesity including weight loss and maintenance of weight loss in patients on a reduced calorie diet Used to treat diabetes and obesity, Dexfenfluramine decreases caloric intake by increasing serotonin levels in the brain&rsquo;s synapses. Dexfenfluramine acts as a serotonin reuptake inhibitor. It also causes release of serotonin from the synaptosomes. Dexfenfluramine binds to the serotonin reuptake pump. This causes inhbition of serotonin reuptake. The increased levels of serotonin lead to greater serotonin receptor activation which in turn lead to enhancement of serotoninergic transmission in the centres of feeding behavior located in the hypothalamus. This suppresses the appetite for carbohydrates.",The molecular weight is 231.26.,Dexfenfluramine has a topological polar surface area of 12.03.,The log p value of  is 3.3.,Dexfenfluramine is approved and illicit and investigational and withdrawn.,Dexfenfluramine is a solid.,True
15152,"An opioid analgesic with actions and uses similar to those of morphine, apart from an absence of cough suppressant activity. It is used in the treatment of moderate to severe pain, including pain in obstetrics. It may also be used as an adjunct to anesthesia (From Martindale, The Extra Pharmacopoeia, 30th ed, p1092). On June 8, 2017, FDA requested Endo Pharmaceuticals to remove the medication from the market due to opioid misuse and abuse risks associated with the product's injectable reformulation. For the treatment of moderate-to-severe pain. Oxymorphone is a semi-synthetic opioid substitute for morphine. It is a potent analgesic. Opioid analgesics exert their principal pharmacologic effects on the CNS and the gastrointestinal tract. The principal actions of therapeutic value are analgesia and sedation. Opioids produce respiratory depression by direct action on brain stem respiratory centers. The mechanism of respiratory depression involves a reduction in the responsiveness of the brain stem respiratory centers to increases in carbon dioxide tension and to electrical stimulation. Oxymorphone interacts predominantly with the opioid mu-receptor. These mu-binding sites are discretely distributed in the human brain, with high densities in the posterior amygdala, hypothalamus, thalamus, nucleus caudatus, putamen, and certain cortical areas. They are also found on the terminal axons of primary afferents within laminae I and II (substantia gelatinosa) of the spinal cord and in the spinal nucleus of the trigeminal nerve. Also, it has been shown that oxymorphone binds to and inhibits GABA inhibitory interneurons via mu-receptors. These interneurons normally inhibit the descending pain inhibition pathway. So, without the inhibitory signals, pain modulation can proceed downstream.",The molecular weight is 301.34.,Oxymorphone has a topological polar surface area of 70.0.,The log p value of  is -0.48.,Oxymorphone is approved and investigational and vet_approved.,Oxymorphone is a solid.,True
15153,"A cardioselective beta-adrenergic antagonist with little effect on the bronchial receptors. The drug has stabilizing and quinidine-like effects on cardiac rhythm as well as weak inherent sympathomimetic action. For the management of hypertension and ventricular premature beats in adults. Acebutolol is a cardioselective, beta-adrenoreceptor blocking agent, which possesses mild intrinsic sympathomimetic activity (ISA) in its therapeutically effective dose range. In general, beta-blockers reduce the work the heart has to do and allow it to beat more regularly. Acebutolol has less antagonistic effects on peripheral vascular &szlig;2-receptors at rest and after epinephrine stimulation than nonselective beta-antagonists. Low doses of acebutolol produce less evidence of bronchoconstriction than nonselective agents like propranolol but more than atenolol. Acebutolol is a selective &beta;1-receptor antagonist. Activation of &beta;1-receptors by epinephrine increases the heart rate and the blood pressure, and the heart consumes more oxygen. Acebutolol blocks these receptors, lowering the heart rate and blood pressure. This drug then has the reverse effect of epinephrine. In addition, beta blockers prevent the release of renin, which is a hormone produced by the kidneys which leads to constriction of blood vessels.",The molecular weight is 336.43.,Acebutolol has a topological polar surface area of 87.66.,The log p value of  is 1.71.,Acebutolol is approved and investigational.,Acebutolol is a solid.,True
15154,"An alkylating agent of value against both hematologic malignancies and solid tumors. For the treatment of primary and metastatic brain tumors as a component of combination chemotherapy in addition to appropriate surgical and/or radiotherapeutic procedures. Also used in combination with other agents as secondary therapy for the treatment of refractory or relapsed Hodgkin's disease. Lomustine is an alkylating agent of the nitrosourea type. Lomustine and its metabolites interferes with the function of DNA and RNA. It is cell cycle&ndash;phase nonspecific. Cancers form when some cells within the body multiply uncontrollably and abnormally. These cells then spread and destroy nearby tissues. Lomustine acts by slowing this process down. It kills cancer cells by damaging the DNA (the genetic material inside the cells) and stops them from dividing. Lomustine is a highly lipophilic nitrosourea compound which undergoes hydrolysis in vivo to form reactive metabolites. These metabolites cause alkylation and cross-linking of DNA (at the O6 position of guanine-containing bases) and RNA, thus inducing cytotoxicity. Other biologic effects include inhibition of DNA synthesis and some cell cycle phase specificity. Nitrosureas generally lack cross-resistance with other alkylating agents. As lomustine is a nitrosurea, it may also inhibit several key processes such as carbamoylation and modification of cellular proteins.",The molecular weight is 233.7.,Lomustine has a topological polar surface area of 61.77.,The log p value of  is 2.75.,Lomustine is approved and investigational.,Lomustine is a solid.,True
15155,"A nonselective beta-adrenoceptor antagonist used in the treatment of glaucoma. For lowering intraocular pressure (IOP) and may be used in patients with chronic open-angle glaucoma or ocular hypertension. Levobunolol is an ophthalmic beta-blocker, equally effective at &beta;(1)- and &beta;(2)-receptor sites. Levobunolol reduces both elevated and normal IOP in patients with or without glaucoma. In patients with elevated IOP, levobunolol reduces mean IOP by approximately 25-40% from baseline. As the drug is a nonselective &beta-adrenergic blocking agent, it can produce both systemic pulmonary and cardiovascular effects following topical application to the eye. These effects include adverse pulmonary effects (eg. bronchoconstriction, increased airway resistance), and a decrease in blood pressure and heart rate.  Levobunolol's mechanism of action in reducing IOP is not clearly defined, but is believed to be due to a reduction of the production of aqueous humor via blockage of endogenous catecholamine-stimulated increases in cyclic adenosine monophosphate (AMP) concentrations within the ciliary processes.",The molecular weight is 291.39.,Levobunolol has a topological polar surface area of 58.56.,The log p value of  is 2.26.,Levobunolol is approved.,Levobunolol is a solid.,True
15156,"A beta-adrenergic antagonist effective for both beta-1 and beta-2 receptors. It is used as an antiarrhythmic, antihypertensive, and antiglaucoma agent. Indicated in the treatment of elevated intraocular pressure in patients with ocular hypertension or open angle glaucoma. Metipranolol is a beta1 and beta2 (non-selective) adrenergic receptor-blocking agent that does not have significant intrinsic sympathomimetic, direct myocardial depressant, or local anesthetic (membrane-stabilizing) activity. Metipranolol is indicated in the treatment of elevated intraocular pressure in patients with ocular hypertension or open-angle glaucoma. Metipranolol, when applied topically to the eye, has the action of reducing elevated, as well as normal, intraocular pressure, whether or not accompanied by glaucoma. Elevated intraocular pressure is a major risk factor in the pathogenesis of glaucomatous visual field loss and optic nerve damage. Metipranolol reduces intraocular pressure with little or no effect on pupil size or accommodation in contrast to the miosis which cholinergic agents are known to produce. Although it is known that metipranolol binds the beta1 and beta2 adrenergic receptors, the mechanism of metipranolol's action is not known. It has no significant intrinsic sympathomimetic activity, and has only weak local anesthetic (membrane-stabilizing) and myocardial depressant activity. It appears that the ophthalmic beta-adrenergic blocking agents reduce aqueous humor production, as demonstrated by tonography and fluorophotometry. A slight increase in aqueous humor outflow may be an additional mechanism.",The molecular weight is 309.41.,Metipranolol has a topological polar surface area of 67.79.,The log p value of  is 2.55.,Metipranolol is approved.,Metipranolol is a solid.,True
15157,"All drug products containing encainide hydrochloride. Encainide hydrochloride, formerly marketed as Enkaid capsules, was associated with increased death rates in patients who had asymptomatic heart rhythm abnormalities after a recent heart attack. The manufacturer of Enkaid capsules voluntarily withdrew the product from the US market on December 16, 1991. Encainide is a class Ic antiarrhythmic agent which was used for management of irregular heartbeats, such as atrial fibrillation, atrial flutter, ventricular tachycardia, and ventricular fibrillation.  Used to treat irregular heartbeats, encainide decreases excitability, conduction velocity, and automaticity as a result of slowed atrial, atrioventricular (AV) nodal, His-Purkinje, and intraventricular conduction. It causes a slight but significant prolongation of refractory periods in these tissues. The greatest effect is on the His-Purkinje system. Encainide decreases the rate of rise of the action potential without markedly affecting its duration. Encainide is a sodium channel blocker, binding to voltage gated sodium channels. It stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses. Ventricular excitability is depressed and the stimulation threshold of the ventricle is increased during diastole.",The molecular weight is 352.48.,Encainide has a topological polar surface area of 41.57.,The log p value of  is 3.52.,Encainide is approved and investigational and withdrawn.,Encainide is a solid.,True
15158,"A long-acting, non selective, calcium channel blocker with significant anti-anginal activity. The drug produces significant coronary vasodilation and modest peripheral effects. It has antihypertensive and selective anti-arrhythmia activities and acts as a calmodulin antagonist. It is no longer marketed in the United States, as it has been implicated in causing ventricular arrhythmias (ie. Torsade de pointes). For the treatment of hypertension, and chronic stable angina (classic effort-associated angina). Bepridil is a calcium channel blocker that has well characterized anti-anginal properties and known but poorly characterized type 1 anti-arrhythmic and anti-hypertensive properties. It is not related chemically to other calcium channel blockers such as diltiazem hydrochloride, nifedipine and verapamil hydrochloride. Bepridil has inhibitory effects on both the slow calcium (L-type) and fast sodium inward currents in myocardial and vascular smooth muscle, interferes with calcium binding to calmodulin, and blocks both voltage and receptor operated calcium channels. Bepridil inhibits the transmembrane influx of calcium ions into cardiac and vascular smooth muscle. This has been demonstrated in isolated myocardial and vascular smooth muscle preparations in which both the slope of the calcium dose response curve and the maximum calcium-induced inotropic response were significantly reduced by bepridil. In cardiac myocytes <i>in vitro</i>, bepridil was shown to be tightly bound to actin. Bepridil regularly reduces heart rate and arterial pressure at rest and at a given level of exercise by dilating peripheral arterioles and reducing total peripheral resistance (afterload) against which the heart works.",The molecular weight is 366.55.,Bepridil has a topological polar surface area of 15.71.,The log p value of  is 6.2.,Bepridil is approved and withdrawn.,Bepridil is a solid.,True
15159,"Also known as _Vyvanse_, lisdexamfetamine (L-lysine-d-amphetamine) is a prodrug of the psychostimulant d-amphetamine. It is paired with the essential amino acid _L-lysine_. Lisdexamfetamine dimesylate increases attention span and decreases restlessness in children and adults who are overactive/hyperactive, cannot concentrate for long periods, or are easily distracted or impulsive. For the treatment of Attention-deficit/hyperactivity disorder (ADHD) and for moderate to severe binge eating disorder in adults ,. Lisdexamfetamine dimesylate is a prodrug of _d-amphetamine_. Amphetamines are non-catecholamine sympathomimetic amines with CNS stimulating properties. This agent works primarily by inducing the release of the neurotransmitters dopamine and norepinephrine from their storage areas in presynaptic nerve terminals. Both of these transmitters contribute to alertness, increased concentration, in addition to effort and motivation. Lisdexamfetamine is a prodrug of dextroamphetamine. The active form of this drug blocks the reuptake of norepinephrine and dopamine into the presynaptic neuron and increase the release of these monoamines into the extraneuronal space. The parent drug, lisdexamfetamine, does not bind to the sites for the reuptake of norepinephrine and dopamine in vitro. The mechanism of therapeutic action in attention deficit hyperactivity disorder (ADHD) is not fully understood ,. Amphetamines have been recently found to target the trace amine-associated receptor 1 (TAAR1), which was recently discovered. This may explain some of its effects on the extraneuronal space , ,.  Ultimately, the ability of this agent to increase synaptic concentrations of the catecholamine neurotransmitters noradrenaline and dopamine in the prefrontal cortex (PFC), and in the striatum, results in several behavioral changes ,. ",The molecular weight is 263.38.,Lisdexamfetamine has a topological polar surface area of 81.14.,The log p value of  is 0.81.,Lisdexamfetamine is approved and investigational.,Lisdexamfetamine is a liquid.,True
15160,"Arformoterol is a bronchodilator. It works by relaxing muscles in the airways to improve breathing. Arformoterol inhalation is used to prevent bronchoconstriction in people with chronic obstructive pulmonary disease, including chronic bronchitis and emphysema. The use of arformoterol is pending revision due to safety concerns in regards to an increased risk of severe exacerbation of asthma symptoms, leading to hospitalization as well as death in some patients using long acting beta agonists for the treatment of asthma. A bronchodilator used for the long term, symptomatic treatment of reversible bronchoconstriction in patients with chronic obstructive pulmonary disease (COPD), including chronic bronchitis and emphysema.  Arformoterol, the active (R,R)-enantiomer of formoterol, is a selective long-acting β2-adrenergic receptor agonist (beta2-agonist) that has two-fold greater potency than racemic formoterol (which contains both the (S,S) and (R,R)-enantiomers). The (S,S)-enantiomer is about 1,000-fold less potent as a β2-agonist than the (R,R)-enantiomer. Arformoterol seems to have little or no effect on β1-adrenergic receptors. While it is recognized that β2-receptors are the predominant adrenergic receptors in bronchial smooth muscle and β1-receptors are the predominant receptors in the heart, data indicate that there are also β2-receptors in the human heart comprising 10% to 50% of the total beta-adrenergic receptors. The precise function of these receptors has not been established, but they raise the possibility that even highly selective β2-agonists may have cardiac effects. The pharmacologic effects of β2-adrenoceptor agonist drugs, including arformoterol, are at least in part attributable to stimulation of intracellular adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3&prime;,5&prime;-adenosine monophosphate (cyclic AMP). Increased intracellular cyclic AMP levels cause relaxation of bronchial smooth muscle and inhibition of release of proinflammatory mediators from cells, especially from mast cells. In vitro tests show that arformoterol is an inhibitor of the release of mast cell mediators, such as histamine and leukotrienes, from the human lung. Arformoterol also inhibits histamine-induced plasma albumin extravasation in anesthetized guinea pigs and inhibits allergen-induced eosinophil influx in dogs with airway hyper-response.",The molecular weight is 344.41.,Arformoterol has a topological polar surface area of 90.82.,The log p value of  is 1.26.,Arformoterol is approved and investigational.,Arformoterol is a solid.,True
15161,"Bevantolol is a beta-1 adrenoceptor antagonist that has been shown to be as effective as other beta blockers for the treatment of angina pectoris and hypertension. Mechanism of Action Animal experiments confirm both agonist and antagonist effects on alpha-receptors, in addition to antagonist activity at beta-1 receptors. For the treatment of angina pectoris and hypertension. Bevantolol is a beta-1 adrenoceptor antagonist that has been shown to be as effective as other beta blockers for the treatment of angina pectoris and hypertension. Animal experiments confirm both agonist and antagonist effects on alpha-receptors, in addition to antagonist activity at beta-1 receptors. By binding and antagonizing beta-1 receptors Bevantolol inhibits the normal normal epinephrine-mediated sympathetic actions such as increased heart rate. This has the effect of decreasing preload and blood pressure.",The molecular weight is 345.44.,Bevantolol has a topological polar surface area of 59.95.,The log p value of  is 3.0.,Bevantolol is experimental.,Bevantolol is a solid.,True
15162,"A beta-adrenergic antagonist that has been used in the emergency treatment of cardiac arrhythmias. Used in the emergency treatment of cardiac arrhythmias. Practolol is a beta-adrenergic receptor antagonist that has been used in the emergency treatment of cardiac arrhythmias. Beta blockers inhibit normal epinephrine-mediated sympathetic actions, but have minimal effect on resting subjects. That is, they reduce the effect of excitement/physical exertion on heart rate and force of contraction and dilation of blood vessels. Like other beta-adrenergic antagonists, practolol competes with adrenergic neurotransmitters such as catecholamines for binding at sympathetic receptor sites. Like propranolol and timolol, practolol binds at beta(1)-adrenergic receptors in the heart and vascular smooth muscle, inhibiting the effects of the catecholamines epinephrine and norepinephrine and decreasing heart rate, cardiac output, and systolic and diastolic blood pressure.",The molecular weight is 266.34.,Practolol has a topological polar surface area of 70.59.,The log p value of  is 0.75.,Practolol is approved.,Practolol is a solid.,True
15163,,,,,St. John's Wort is approved and investigational and nutraceutical.,St. John's Wort is a solid.,False
15164,"A plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of impotence. It is also alleged to be an aphrodisiac. Indicated as a sympatholytic and mydriatic. Impotence has been successfully treated with yohimbine in male patients with vascular or diabetic origins and psychogenic origins. Yohimbine is an indolalkylamine alkaloid with chemical similarity to reserpine. Yohimbine blocks presynaptic alpha-2 adrenergic receptors. Its action on peripheral blood vessels resembles that of reserpine, though it is weaker and of short duration. Yohimbine's peripheral autonomic nervous system effect is to increase parasympathetic (cholinergic) and decrease sympathetic (adrenergic) activity. It is to be noted that in male sexual performance, erection is linked to cholinergic activity and to alpha-2 adrenergic blockade which may theoretically result in increased penile inflow, decreased penile outflow or both. Yohimbine exerts a stimulating action on the mood and may increase anxiety. Such actions have not been adequately studied or related to dosage although they appear to require high doses of the drug. Yohimbine has a mild anti-diuretic action, probably via stimulation of hypothalmic center and release of posterior pituitary hormone. Reportedly Yohimbine exerts no significant influence on cardiac stimulation and other effects mediated by (beta)-adrenergic receptors. Its effect on blood pressure, if any, would be to lower it; however, no adequate studies are at hand to quantitate this effect in terms of Yohimbine dosage. Yohimbine is a pre-synaptic alpha 2-adrenergic blocking agent. The exact mechanism for its use in impotence has not been fully elucidated. However, yohimbine may exert its beneficial effect on erectile ability through blockade of central alpha 2-adrenergic receptors producing an increase in sympathetic drive secondary to an increase in norepinephrine release and in firing rate of cells in the brain noradrenergic nuclei. Yohimbine-mediated norepinephrine release at the level of the corporeal tissues may also be involved. In addition, beneficial effects may involve other neurotransmitters such as dopamine and serotonin and cholinergic receptors.",The molecular weight is 354.45.,Yohimbine has a topological polar surface area of 65.56.,The log p value of  is 2.17.,Yohimbine is approved and investigational and vet_approved.,Yohimbine is a solid.,True
15165,"A phenothiazine with pharmacological activity similar to that of both chlorpromazine and promethazine. It has the histamine-antagonist properties of the antihistamines together with central nervous system effects resembling those of chlorpromazine. (From Martindale, The Extra Pharmacopoeia, 30th ed, p604) For the treatment of psychosis, particular those of schizophrenia, and manic phases of bipolar disorder. Methotrimeprazine is a phenothiazine with pharmacological activity similar to that of both chlorpromazine and promethazine. It has the histamine-antagonist properties of the antihistamines together with central nervous system effects resembling those of chlorpromazine. (From Martindale, The Extra Pharmacopoeia, 30th ed, p604) Methotrimeprazine's antipsychotic effect is largely due to its antagonism of dopamine receptors in the brain. In addition, its binding to 5HT2 receptors may also play a role. ",The molecular weight is 328.47.,Methotrimeprazine has a topological polar surface area of 15.71.,The log p value of  is 5.03.,Methotrimeprazine is approved and investigational.,Methotrimeprazine is a solid.,True
15166,"Tiotropium is a long-acting, antimuscarinic bronchodilator used in the management of chronic obstructive pulmonary disease (COPD) and asthma. Tiotropium acts mainly on M3 muscarinic receptors located in the airways to produce smooth muscle relaxation and bronchodilation. Tiotropium powder for inhalation is indicated for the maintenance of bronchospasm in COPD and to prevent exacerbations of COPD. A combination tiotropium and metered inhalation spray is indicated for maintenance of COPD. A tiotropium inhalation spray is indicated for the maintenance of bronchospasm in COPD, to prevent exacerbations of COPD, and to treat asthma in patients 12 or more years old. A tiotropium metered inhalation spray is indicated for the maintenance of bronchospasm in COPD, to prevent exacerbations of COPD, and to treat asthma in patients 6 or more years old. Tiotropium is a long acting antimuscarinic that causes bronchodilation. The effects of tiotropium last over 24 hours and there is a wide therapeutic index as overdoses are uncommon even at doses well above the recommended maximum. Tiotropium is an antagonist of muscarinic receptors M<sub>1</sub> to M<sub>5</sub>. Inhibition of the M<sub>3</sub> receptor in the smooth muscle of the lungs leads to relaxation of smooth muscle and bronchodilation.",The molecular weight is 392.51.,Tiotropium has a topological polar surface area of 59.06.,The log p value of  is -1.71.,Tiotropium is approved.,Tiotropium is a solid.,True
15167,"An analgesic and antipyretic that has been given by mouth and as ear drops. Antipyrine is often used in testing the effects of other drugs or diseases on drug-metabolizing enzymes in the liver. (From Martindale, The Extra Pharmacopoeia, 30th ed, p29) Antipyrine is an analgesic often used to test effects of other drugs on liver enzymes. Antipyrine is an analgesic and antipyretic that has been given by mouth and as ear drops. Antipyrine is often used in testing the effects of other drugs or diseases on drug-metabolizing enzymes in the liver. (From Martindale, The Extra Pharmacopoeia, 30th ed, p29) Antipyrine is thought to act primarily in the CNS, increasing the pain threshold by inhibiting both isoforms of cyclooxygenase, COX-1, COX-2, and COX-3 enzymes involved in prostaglandin (PG) synthesis.",The molecular weight is 188.23.,Antipyrine has a topological polar surface area of 23.55.,The log p value of  is 0.2.,Antipyrine is approved and investigational.,Antipyrine is a solid.,True
15168,"An N-substituted amphetamine analog. It is a widely abused drug classified as a hallucinogen and causes marked, long-lasting changes in brain serotonergic systems. It is commonly referred to as MDMA or ecstasy. It is a widely abused drug classified as a hallucinogen and causes marked, long-lasting changes in brain serotonergic systems. Clinical trials are now testing the therapeutic potential of MDMA for post-traumatic stress disorder (PTSD) and anxiety associated with terminal cancer. MDMA is one of the four most widely used illicit drugs in the U.S. MDMA acts as a releasing agent of serotonin, norepinephrine, and dopamine. It enters neurons via carriage by the monoamine transporters. Once inside, MDMA inhibits the vesicular monoamine transporter, which results in increased concentrations of serotonin, norepinephrine, and dopamine into the cytoplasm, and induces their release by reversing their respective transporters through a process known as phosphorylation. It also acts as a weak 5-HT1 and 5-HT2 receptor agonist.",,,,Midomafetamine is experimental and illicit and investigational.,Midomafetamine is a solid.,True
15169,"A narcotic analgesic and antitussive. It is metabolized in the liver by ethylmorphine-N-demethylase and used as an indicator of liver function. It is not marketed in the US but is approved for use in various countries around the world. In the US it is a schedule II drug (single-entity) and schedule III drug (in combination products). Ethylmorphine is an analgesic used for pain relief. Ethylmorphine is metabolized by the enzyme cytochrome P450 2D6 to morphine. Morphine is a narcotic pain management agent indicated for the relief of pain in patients who require opioid analgesics for more than a few days. Morphine interacts predominantly with the opioid mu-receptor. These mu-binding sites are discretely distributed in the human brain, with high densities in the posterior amygdala, hypothalamus, thalamus, nucleus caudatus, putamen, and certain cortical areas. They are also found on the terminal axons of primary afferents within laminae I and II (substantia gelatinosa) of the spinal cord and in the spinal nucleus of the trigeminal nerve. In clinical settings, morphine exerts its principal pharmacological effect on the central nervous system and gastrointestinal tract. Its primary actions of therapeutic value are analgesia and sedation. Morphine appears to increase the patient's tolerance for pain and to decrease discomfort, although the presence of the pain itself may still be recognized. In addition to analgesia, alterations in mood, euphoria and dysphoria, and drowsiness commonly occur. Opioids also produce respiratory depression by direct action on brain stem respiratory centers. Ethylmorphine is metabolized by the liver enzyme cytochrome P450 2D6 to morphine. The precise mechanism of the analgesic action of morphine is unknown. However, specific CNS opiate receptors have been identified and likely play a role in the expression of analgesic effects. Morphine first acts on the mu-opioid receptors. The mechanism of respiratory depression involves a reduction in the responsiveness of the brain stem respiratory centers to increases in carbon dioxide tension and to electrical stimulation.",The molecular weight is 313.4.,Ethylmorphine has a topological polar surface area of 41.93.,The log p value of  is 1.51.,Ethylmorphine is experimental and illicit.,Ethylmorphine is a solid.,True
15170,4-Methoxyamphetamine is a seratogenic drug of the amphetamine class. The drug acts as a potent and selective serotonin releasing agent. It binds to alpha receptors to mediate these effects.,,,,4-Methoxyamphetamine is experimental and illicit.,4-Methoxyamphetamine is a solid.,True
15171,"Dihydrocodeine is an opioid analgesic used as an alternative or adjunct to codeine to treat moderate to severe pain, severe dyspnea, and cough.  Dihydrocodeine is used for the treatment of moderate to severe pain, including post-operative and dental pain. It can also be used to treat chronic pain , breathlessness and coughing.  Possible opioid related side effects include, but are not limited to, drowsiness, nausea, headache, dry mouth, constipation, difficulty passing urine, and mild euphoria.  Dihydrocodeine is metabolized to dihydromorphine -- a highly active metabolite with a high affinity for mu opioid receptors. ",The molecular weight is 301.39.,Dihydrocodeine has a topological polar surface area of 41.93.,The log p value of  is 1.26.,Dihydrocodeine is approved and illicit.,Dihydrocodeine is a solid.,True
15172,"1-(2-Phenylethyl)-4-phenyl-4-acetoxypiperidine (PEPAP) is a synthetic analogue of meperidine. It is sold as a \synthetic heroin.\""""",,,,1-(2-Phenylethyl)-4-phenyl-4-acetoxypiperidine is experimental and illicit.,1-(2-Phenylethyl)-4-phenyl-4-acetoxypiperidine is a solid.,True
15173,"Dextroamphetamine is the dextrorotary enantiomer of amphetamine. Dextroamphetamine was approved by the FDA in 2001 for the treatment of attention deficit hyperactivity disorder. Dextroamphetamine is indicated for the treatment of attention deficit hyperactivity disorder (ADHD). Dextroamphetamine is a noncatecholamine, sympathomimetic amine that acts as a CNS stimulant. Dextroamphetamine raises systolic and diastolic blood pressure, acts as a weak bronchodilator, and also acts as a respiratory stimulant. The general mechanism of action of dextroamphetamine has not been well established. The exact mechanism of amphetamines as a class is not known. Dextroamphetamine acts by preventing reuptake, increasing release, and stimulating reverse-transport of dopamine in synaptic clefts in the striatum. Newer evidence shows amphetamines may also alter the number of dopamine transporters in synaptic clefts.",The molecular weight is 135.21.,Dextroamphetamine has a topological polar surface area of 26.02.,The log p value of  is 1.74.,Dextroamphetamine is approved and illicit.,Dextroamphetamine is a liquid.,True
15174,"Metamfetamine (methamphetamine) is a psychostimulant and sympathomimetic drug. It is a member of the amphetamine group of sympathomimetic amines. Methamphetamine can induce effects such as euphoria, increased alertness and energy, and enhanced self-esteem. It is a scheduled drug in most countries due to its high potential for addiction and abuse. For the treatment of Attention Deficit Disorder with Hyperactivity (ADHD) and exogenous obesity. Methamphetamine is a potent central nervous system stimulant which affects neurochemical mechanisms responsible for regulating heart rate, body temperature, blood pressure, appetite, attention, mood and responses associated with alertness or alarm conditions. The acute effects of the drug closely resemble the physiological and psychological effects of an epinephrine-provoked fight-or-flight response, including increased heart rate and blood pressure, vasoconstriction (constriction of the arterial walls), bronchodilation, and hyperglycemia (increased blood sugar). Users experience an increase in focus, increased mental alertness, and the elimination of fatigue, as well as a decrease in appetite.  Methamphetamine enters the brain and triggers a cascading release of norepinephrine, dopamine and serotonin. To a lesser extent methamphetamine acts as a dopaminergic and adrenergic reuptake inhibitor and in high concentrations as a monamine oxidase inhibitor (MAOI). The mechanism of action involved in producing the beneficial behavioral changes seen in hyperkinetic children receiving methamphetamine is unknown.",The molecular weight is 149.24.,Metamfetamine has a topological polar surface area of 12.03.,The log p value of  is 1.89.,Metamfetamine is approved and illicit.,Metamfetamine is a solid.,True
15175,"A beta-adrenergic antagonist used in the treatment of hypertension, angina pectoris, arrhythmias, and anxiety. Used in the treatment of hypertension, angina pectoris, arrhythmias, and anxiety. Oxprenolol is a non-selective beta blocker with some intrinsic sympathomimetic activity. Oxprenolol is a lipophilic molecule and hence, it is able to cross the blood-brain barrier. As such, it is associated with a higher incidence of CNS-related side effects than hydrophilic ligands such as atenolol, sotalol and nadolol. Oxprenolol is an potent beta-blocker and should not be administered to asthmatics because it can cause irreversible airway failure and inflammation. Like other beta-adrenergic antagonists, oxprenolol competes with adrenergic neurotransmitters such as catecholamines for binding at sympathetic receptor sites. Like propranolol and timolol, oxprenolol binds at beta(1)-adrenergic receptors in the heart and vascular smooth muscle, inhibiting the effects of the catecholamines epinephrine and norepinephrine and decreasing heart rate, cardiac output, and systolic and diastolic blood pressure. It also blocks beta-2 adrenergic receptors located in bronchiole smooth muscle, causing vasoconstriction. By binding beta-2 receptors in the juxtaglomerular apparatus, oxprenolol inhibits the production of renin, thereby inhibiting angiotensin II and aldosterone production. Oxprenolol therefore inhibits the vasoconstriction and water retention due to angiotensin II and aldosterone, respectively.",The molecular weight is 265.35.,Oxprenolol has a topological polar surface area of 50.72.,The log p value of  is 2.09.,Oxprenolol is approved.,Oxprenolol is a solid.,True
15176,"Everolimus is a derivative of Rapamycin (sirolimus), and works similarly to Rapamycin as an mTOR (mammalian target of rapamycin) inhibitor. It is currently used as an immunosuppressant to prevent rejection of organ transplants. In a similar fashion to other mTOR inhibitors Everolimus' effect is solely on the mTORC1 protein and not on the mTORC2 protein. Everolimus is indicated for the treatment of postmenopausal women with advanced hormone receptor-positive, HER2-negative breast cancer (advanced HR+ BC) in combination with exemestane, after failure of treatment with letrozole or anastrozole. Everolimus is a mTOR inhibitor that binds with high affinity to the FK506 binding protein-12 (FKBP-12), thereby forming a drug complex that inhibits the activation of mTOR. This inhibition reduces the activity of effectors downstream, which leads to a blockage in the progression of cells from G1 into S phase, and subsequently inducing cell growth arrest and apoptosis. Everolimus also inhibits the expression of hypoxia-inducible factor, leading to a decrease in the expression of vascular endothelial growth factor. The result of everolimus inhibition of mTOR is a reduction in cell proliferation, angiogenesis, and glucose uptake.",The molecular weight is 958.24.,Everolimus has a topological polar surface area of 204.66.,The log p value of  is 7.1.,Everolimus is approved.,Everolimus is a solid.,True
15177,"Zuclopenthixol, also known as Zuclopentixol or Zuclopenthixolum, is an antipsychotic agent. Zuclopenthixol is a thioxanthene-based neuroleptic with therapeutic actions similar to the phenothiazine antipsychotics. It is an antagonist at D1 and D2 dopamine receptors. Major brands of zuclopenthixol are Cisordinol, Acuphase, and Clopixol. This drug is a liquid. This compound belongs to the thioxanthenes. These are organic polycyclic compounds containing a thioxanthene moiety, which is an aromatic tricycle derived from xanthene by replacing the oxygen atom with a sulfur atom. Known drug targets of zuclopenthixol include 5-hydroxytryptamine receptor 2A, D(1B) dopamine receptor, D(2) dopamine receptor, D(1A) dopamine receptor, and alpha-1A adrenergic receptor. It is known that zuclopenthixol is metabolized by Cytochrome P450 2D6. Zuclopenthixol was approved for use in Canada in 2011, but is not approved for use in the United States. Used in the management of acute psychoses such as mania or schizophrenia. However, the use of zuclopenthixol acetate in psychiatric emergencies as an alternative to standard treatments (haloperidol, clotiapine, etc.) should be cautioned, since well executed and documented trials of zuclopenthixol acetate for this use have yet to be conducted. Zuclopenthixol acetate is not intended for long-term use. Zuclopenthixol is a thioxanthene with therapeutic actions similar to the phenothiazine antipsychotics. It is an antagonist at D1 and D2 dopamine receptors. Zuclopenthixol is a typical antipsychotic neuroleptic drug of the thioxanthene class. It mainly acts by antagonism of D1 and D2 dopamine receptors. Zuclopenthixol also has high affinity for alpha1-adrenergic and 5-HT2 receptors. It has weaker histamine H1 receptor blocking activity, and even lower affinity for muscarinic cholinergic and alpha2-adrenergic receptors.",The molecular weight is 400.97.,Zuclopenthixol has a topological polar surface area of 26.71.,The log p value of  is 4.13.,Zuclopenthixol is approved and investigational.,Zuclopenthixol is a liquid.,True
15178,"Etoricoxib is a new COX-2 selective inhibitor. Current therapeutic indications are: treatment of rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, chronic low back pain, acute pain and gout. Like any other COX-2 selective inhibitor, Etoricoxib selectively inhibits isoform 2 of cyclo-oxigenase enzyme (COX-2) to reduce the generation of prostaglandins (PGs) from arachidonic acid. It is approved in more than 60 countries worldwide but not in the US. For the treatment of rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, chronic low back pain, acute pain and gout. Etoricoxib is a COX-2 selective inhibitor (approximately 106 times more selective for COX-2 inhibition over COX-1). Like any other COX-2 selective inhibitor Etoricoxib selectively inhibits isoform 2 of cyclo-oxigenase enzyme (COX-2), preventing production of prostaglandins (PGs) from arachidonic acid.",The molecular weight is 358.84.,Etoricoxib has a topological polar surface area of 59.92.,The log p value of  is 2.35.,Etoricoxib is approved and investigational.,Etoricoxib is a solid.,True
15179,An important compound functioning as a component of the coenzyme NAD. Its primary significance is in the prevention and/or cure of blacktongue and pellagra. Most animals cannot manufacture this compound in amounts sufficient to prevent nutritional deficiency and it therefore must be supplemented through dietary intake.,The molecular weight is 122.13.,Nicotinamide has a topological polar surface area of 55.98.,The log p value of  is -0.21.,Nicotinamide is approved and investigational.,Nicotinamide is a solid.,True
15180,"An antibiotic isolated from the fermentation broth of Fusidium coccineum. (From Merck Index, 11th ed) It acts by inhibiting translocation during protein synthesis. It is often used topically in creams and eyedrops but is available in systemic formulations including tablets and injections. For the treatment of bacterial infections. Fusidic acid is a bacteriostatic antibiotic and helps prevent bacterial growth while the immune system clears the infection. Fusidic acid works by interfering with bacterial protein synthesis, specifically by preventing the translocation of the elongation factor G (EF-G) from the ribosome. It also can inhibit chloramphenicol acetyltransferase enzymes.",The molecular weight is 516.72.,Fusidic acid has a topological polar surface area of 104.06.,The log p value of  is 7.28.,Fusidic acid is approved and investigational.,Fusidic acid is a solid.,True
15181,"Phenacetin was withdrawn from the Canadian market in June 1973 due to concerns regarding nephropathy (damage to or disease of the kidney). Used principally as an analgesic. Phenacetin was the first NSAID and fever reducer to go on the market. It acts as an analgesic at the spinal cord as well as a negative inotrope at the heart. It can be used to treat subacute rheumatoid arthritis, intercostal neuralgia, and ataxias.",The molecular weight is 179.22.,Phenacetin has a topological polar surface area of 38.33.,The log p value of  is 1.77.,Phenacetin is withdrawn.,Phenacetin is a solid.,True
15182,"Debate continues over the nature and causes of chronic flashbacks. Explanations in terms of LSD physically remaining in the body for months or years after consumption have been discounted by experimental evidence. Some say HPPD is a manifestation of post-traumatic stress disorder, not related to the direct action of LSD on brain chemistry, and varies according to the susceptibility of the individual to the disorder. Many emotionally intense experiences can lead to flashbacks when a person is reminded acutely of the original experience. However, not all published case reports of chronic flashbacks appear to describe an anxious hyper-vigilant state reminiscent of post-traumatic stress disorder.",The molecular weight is 323.44.,Lysergic acid diethylamide has a topological polar surface area of 39.34.,The log p value of  is 2.69.,Lysergic acid diethylamide is illicit and investigational and withdrawn.,Lysergic acid diethylamide is a solid.,True
15183,"An adrenergic neuron-blocking drug similar in effects to guanethidine. It is also noteworthy in being a substrate for a polymorphic cytochrome P-450 enzyme. Persons with certain isoforms of this enzyme are unable to properly metabolize this and many other clinically important drugs. They are commonly referred to as having a debrisoquin 4-hydroxylase polymorphism. For the treatment of moderate and severe hypertension, either alone or as an adjunct, and for the treatment of renal hypertension. Debrisoquin is an adrenergic neuron-blocking drug similar in effects to guanethidine. It is a substrate for a polymorphic cytochrome P-450 enzyme. Persons with certain isoforms of this enzyme are unable to properly metabolize this and many other clinically important drugs. They are commonly referred to as having a debrisoquin 4-hydroxylase polymorphism. Debrisoquin acts at the sympathetic neuroeffector junction by inhibiting or interfering with the release and/or distribution of norepinephrine, rather than acting at the effector cell by inhibiting the association of norepinephrine with its receptors. It is taken up by norepinephrine transporters. It becomes concentrated in NE transmitter vesicles, replacing NE in these vesicles. This leads to a gradual depletion of NE stores in the nerve endings. Once inside the terminal it blocks the release of noradrenaline in response to arrival of an action potential. In contrast to ganglionic blocking agents, debrisoquin suppresses equally the responses mediated by alpha-and beta-adrenergic receptors but does not produce parasympathetic blockade. Since sympathetic blockade results in modest decreases in peripheral resistance and cardiac output, debrisoquin lowers blood pressure in the supine position. It further reduces blood pressure by decreasing the degree of vasoconstriction that normally results from reflex sympathetic nervous activity upon assumption of the upright posture, thus reducing venous return and cardiac output more.",The molecular weight is 175.24.,Debrisoquine has a topological polar surface area of 53.11.,The log p value of  is 0.89.,Debrisoquine is approved and investigational.,Debrisoquine is a solid.,True
15184,"Flunarizine is a selective calcium entry blocker with calmodulin binding properties and histamine H1 blocking activity. It is effective in the prophylaxis of migraine, occlusive peripheral vascular disease, vertigo of central and peripheral origin, and as an adjuvant in the therapy of epilepsy. Used in the prophylaxis of migraine, occlusive peripheral vascular disease, vertigo of central and peripheral origin, and as an adjuvant in the therapy of epilepsy. Flunarizine is a selective calcium entry blocker with calmodulin binding properties and histamine H1 blocking activity. Flunarizine inhibits the influx of extracellular calcium through myocardial and vascular membrane pores by physically plugging the channel. The decrease in intracellular calcium inhibits the contractile processes of smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload.",The molecular weight is 404.5.,Flunarizine has a topological polar surface area of 6.48.,The log p value of  is 6.34.,Flunarizine is approved.,Flunarizine is a solid.,True
15185,"A drug formerly used as an antipsychotic but now used primarily in the symptomatic treatment of various hyperkinetic disorders. It is a monoamine depletor and used as symptomatic treatment of chorea associated with Huntington's disease. FDA approved on August 15, 2008. Treatment of hyperkinetic movement disorders like chorea in Huntington's disease, hemiballismus, senile chorea, Tourette syndrome and other tic disorders, and tardive dyskinesia  Prolongation of the QTc interval has been observed at doses of 50 mg. In rats, it has been observed that tetrabenazine or its metabolites bind to melanin-containing tissues such as the eyes and skin. After a single oral dose of radiolabeled tetrabenazine, radioactivity was still detected in eye and fur at 21 days post dosing.  Tetrabenazine is a reversible human vesicular monoamine transporter type 2 inhibitor (Ki = 100 nM). It acts within the basal ganglia and promotes depletion of monoamine neurotransmitters serotonin, norepinephrine, and dopamine from stores. It also decreases uptake into synaptic vesicles. Dopamine is required for fine motor movement, so the inhibition of its transmission is efficacious for hyperkinetic movement. Tetrabenazine exhibits weak in vitro binding affinity at the dopamine D2 receptor (Ki = 2100 nM).",The molecular weight is 317.43.,Tetrabenazine has a topological polar surface area of 38.77.,The log p value of  is 3.46.,Tetrabenazine is approved and investigational.,Tetrabenazine is a solid.,True
15186,"Celiprolol is indicated for the management of mild to moderate hypertension and effort-induced angina pectoris. It is simultaneously a selective β1 receptor antagonist, a β2 receptor partial agonist and a weak α2 receptor antagonist. In 2010 a clinical trial has suggested a use for this medication in the prevention of vascular complications of a rare inherited disease called vascular Ehlers–Danlos syndrome. This study demonstrated decreased incidence of arterial rupture or dissection (a specific type of arterial rupture in which the layers of the vessel separate prior to complete failure of the artery wall). Celiprolol is not approved for use by the FDA in the treatment of vascular Ehlers–Danlos syndrome. Celiprolol is indicated for the management of mild to moderate hypertension and effort-induced angina pectoris.  Celiprolol is a vasoactive beta-1 selective adrenoceptor antagonist with partial beta-2 agonist activity. The beta-2 agonist activity is thought to account for its mild vasodilating properties. It lowers blood pressure in hypertensive patients at rest and on exercise. The effects on heart rate and cardiac output are dependent on the pre-existing background level of sympathetic tone.",The molecular weight is 379.5.,Celiprolol has a topological polar surface area of 90.9.,The log p value of  is 1.86.,Celiprolol is approved and investigational.,Celiprolol is a solid.,True
15187,"Nilotinib, also known as AMN107, is a tyrosine kinase inhibitor under investigation as a possible treatment for chronic myelogenous leukemia (CML). A Phase I clinical trial in 2006 showed that this drug was relatively safe and offered significant therapeutic benefits in cases of CML which were found to be resistant to treatment with imatinib (Gleevec), another tyrosine kinase inhibitor used as a first-line treatment for CML. For the potential treatment of various leukemias, including chronic myeloid leukemia (CML). Nilotinib is a transduction inhibitor that targets BCR-ABL, c-kit and PDGF, for the potential treatment of various leukemias, including chronic myeloid leukemia (CML). Chronic myelogenous leukaemia (CML) is caused by the BCR-ABL oncogene. Nilotinib inhibits the tyrosine kinase activity of the BCR-ABL protein. Nilotinib fits into the ATP-binding site of the BCR-ABL protein with higher affinity than imatinib, over-riding resistance caused by mutations. The ability of AMN107 to inhibit TEL-platelet-derived growth factor receptor-beta (TEL-PDGFRbeta), which causes chronic myelomonocytic leukaemia, and FIP1-like-1-PDGFRalpha, which causes hypereosinophilic syndrome, suggests potential use of AMN107 for myeloproliferative diseases characterised by these kinase fusions (Stover et al, 2005; Weisberg et al, 2005). AMN107 also inhibits the c-Kit receptor kinase, including the D816V-mutated variant of KIT, at pharmacologically achievable concentrations, supporting potential utility in the treatment of mastocytosis, and gastrointestinal stromal tumours (Weisberg et al, 2005; von Bubnoff et al, 2005; Gleixner et al, 2006).",The molecular weight is 529.53.,Nilotinib has a topological polar surface area of 97.62.,The log p value of  is 5.69.,Nilotinib is approved and investigational.,Nilotinib is a solid.,True
15188,"Lorcaserin (previously APD-356), a highly selective 5HT2C receptor agonist, is used for the treatment of obesity. It has been shown to reduce body weight and food intake in animal models of obesity, and it is thought that targeting the 5HT2C receptor may alter body weight by regulating satiety. Lorcaserin is marketed as a salt form called Belviq, which is lorcaserin hydrochloride. For the treatment of obesity, as an adjunct to a reduced-calorie diet and increased physical activity. Lorcaserin produced a dose-dependent weight loss over a 12-week period by promoting satiety and decreasing food consumption. Although the exact mechanism is unknown, it is believed to involve the selective activation of 5-HT2C receptors in the anorexigenic pro-opiomelanocortin neurons in the arcuate nucleus of the hypothalamus. This results in decreased food intake and satiety by promoting the release of alpha-melanocortin stimulating hormone, which acts on melanocortin-4 receptors.",The molecular weight is 195.69.,Lorcaserin has a topological polar surface area of 12.03.,The log p value of  is 3.24.,Lorcaserin is approved.,Lorcaserin is a solid.,True
15189,"Dapoxetine is a selective serotonin reuptake inhibitor, for the treatment of premature ejaculation. In a phase II proof-of-concept study conducted by PPD, dapoxetine demonstrated a statistically significant increase in ejaculatory latency when compared to placebo. Alza submitted a NDA to the FDA for dapoxetine for the treatment of premature ejaculation in December 2004. In October 2005, the company received a FDA Non-Approvable letter from the FDA, at which time they planned to work with regulators to address outstanding questions. For the treatment of premature ejaculation. Dapoxetine is a selective serotonin reuptake inhibitor currently undergoing trials through Alza (under license from GenuPro, a collaboration between Eli Lilly and PPD). Dapoxetine is a short-acting SSRI drug currently being considered for approval by the Food and Drug Administration (FDA) for the treatment of premature ejaculation in men, which would make it the first drug approved for such treatment. Despite two clinical trials finished in 2006, experts doubt it will be approved by the FDA soon because SSRIs come with undesirable side-effects after long-term use, such as psychiatric problems, dermatological reactions, increase in body weight, lower sex-drive, nausea, headache, upset stomach and weakness, thus not significantly outweighing the benefit of premature ejaculation medication versus the risks. By contrast with SSRIs approved for depression, which take 2 weeks or longer to reach steady-state concentration, dapoxetine has a unique pharmacokinetic profile, with a short time to maximum serum concentration (about 1 h) and rapid elimination (initial half-life of 1-2 h). The drug's mechanism of action is thought to be related to inhibition of neuronal reuptake of serotonin and subsequent potentiation of serotonin activity. The central ejaculatory neural circuit comprises spinal and cerebral areas that form a highly interconnected network. The sympathetic, parasympathetic, and somatic spinal centers, under the influence of sensory genital and cerebral stimuli integrated and processed at the spinal cord level, act in synergy to command physiologic events occurring during ejaculation. Experimental evidence indicates that serotonin (5-HT), throughout brain descending pathways, exerts an inhibitory role on ejaculation. To date, three 5-HT receptor subtypes (5-HT(1A), 5-HT(1B), and 5-HT(2C)) have been postulated to mediate 5-HT's modulating activity on ejaculation.",The molecular weight is 305.42.,Dapoxetine has a topological polar surface area of 12.47.,The log p value of  is 5.34.,Dapoxetine is investigational.,Dapoxetine is a solid.,True
15190,"Tesmilifene is a novel potentiator of chemotherapy which, when added to doxorubicin, achieved an unexpected and very large survival advantage over doxorubicin alone in a randomized trial in advanced breast cancer. Intended for the treatment of various forms of cancer. Although the exact mechanism of action is not known, one study (PMID: 16413681) proposes that tesmilifene may be an activating p-gp substrate, which enables the p-gp pump to extrude typical p-gp substrates (such as anthracyclines or taxanes) more efficiently. This process consumes ATP, since the p-gp is absolutely, and highly dependent on ATP hydrolysis. The mechanism of cell death is likely to result not from the presence of chemotherapy inside the cell (in fact the chemotherapy is extruded) but, directly or indirectly, from the enhanced consumption of ATP. The ATP may be consumed below a threshold necessary for survival, or, (more likely) the enhanced ATP production required to maintain ATP levels may result in the generation of reactive oxygen species (ROS) to an extent that overwhelms the cell’s ability to inactivate them. The result would be additional cell death, but only in the mdr+ population. The doxorubicin would continue to act on the drug sensitive remainder of the cell population, but without the help of tesmilifene.",,,,Tesmilifene is investigational.,Tesmilifene is a solid.,True
15191,"Ospemifene is a new selective non-hormonal estrogen receptor modulator (SERM) that is used for the treatment of moderate to severe dyspareunia, a symptom of vulvar and vaginal atrophy, due to menopause. FDA approved on February 26, 2013. Ospemifene is used for the treatment of moderate to dyspareunia, a symptom of vulvar and vaginal atrophy, due to menopause. The half maximal inhibitory concentration (IC50) for estrogen receptor (ER) alpha and beta are 0.8 μM and 1.7 μM, respectively. Ospemifene has potential uses in the management of osteoporosis in postmenopausal women. It interacts with osteoblasts and osteoclasts in such a way that it reduces bone turnover. It also has potential uses in the prevention of breast cancer. Studies suggest that ospemifene, in a dose-dependent manner, reduces the incidence of tumours.  Ospemifene is a next generation SERM (selective estrogen receptor modulator) that selectively binds to estrogen receptors and either stimulates or blocks estrogen's activity in different tissue types. It has an agonistic effect on the endometrium.",The molecular weight is 378.9.,Ospemifene has a topological polar surface area of 29.46.,The log p value of  is 5.56.,Ospemifene is approved and investigational.,Ospemifene is a solid.,True
15192,"Lofexidine is a non-opioid centrally acting alpha2-adrenergic receptor agonist that was first approved for the treatment of opioid withdrawal in the United Kingdom in 1992. It was first studied for use as an antihypertensive in 1980, but its researched was stopped as it was found less effective for the treatment of hypertension than clonidine. Lofexidine was then repurposed for the treatment of opioid withdrawal, as it was seen to be more economical and have fewer side effects than clonidine. Lofexidine was developed by US Woldmeds LLC and it was approved by the FDA on May 16, 2018. Lofexidine is indicated for mitigation of symptoms associated with acute withdrawal from opioids and for facilitation of the completion of opioid discontinuation treatment. It is the first non-opioid medication for the symptomatic management of opioid discontinuation. In clinical trials, lofexidine presented more severe opioid withdrawal effects than observed with methadone. On the other hand, in clinical trials of methadone withdrawal, lofexidine effectively reduced withdrawal symptoms, especially hypotension. The clinical reports have also indicated that lofexidine presents a better outcome when used briefly. In phase 3 clinical trials, lofexidine was shown to generate a significantly higher completion rate of opioid discontinuation. Some pharmacological studies were performed and there were no off-target effects reported. Lofexidine is a potent alpha2-adrenergic receptor agonist with some moderate agonistic affinity towards Alpha-1A adrenergic receptor and 5-HT1a, 5-HT7, 5HT2c and 5HT1d receptors.",The molecular weight is 259.13.,Lofexidine has a topological polar surface area of 33.62.,The log p value of  is 3.46.,Lofexidine is approved and investigational.,Lofexidine is a solid.,True
15193,"Rotigotine (Neupro) is a non-ergoline dopamine agonist indicated for the treatment of Parkinson's disease (PD) and restless legs syndrome (RLS) in Europe and the United States. It is formulated as a once-daily transdermal patch which provides a slow and constant supply of the drug over the course of 24 hours. For use/treatment in neurologic disorders and parkinson's disease as well as moderate-to-severe primary Restless Legs Syndrome. Rotigotine is an agonist at all 5 dopamine receptor subtypes (D1-D5) but binds to the D3 receptor with the highest affinity. It is also an antagonist at α-2-adrenergic receptors and an agonist at the 5HT1A receptors. Rotigotine also inhibits dopamine uptake and prolactin secretion. There is no indication of a QT/QTc prolonging effect of Neupro in doses up to 24 mg/24 hours. The effects of Neupro at doses up to 24 mg/24 hours (supratherapeutic doses) on the QT/QTc interval was evaluated in a double-blind, randomized, placebo- and positive-controlled (moxifloxacin 400 mg IV, single dose) parallel-group trial with an overall treatment period of 52 days in male and female patients with advanced-stage Parkinson's disease. Assay sensitivity was confirmed by significant QTc prolongation by moxifloxacin.  Rotigotine, a member of the dopamine agonist class of drugs, is delivered continuously through the skin (transdermal) using a silicone-based patch that is replaced every 24 hours. A dopamine agonist works by activating dopamine receptors in the body, mimicking the effect of the neurotransmitter dopamine. The precise mechanism of action of rotigotine as a treatment for Restless Legs Syndrome is unknown but is thought to be related to its ability to stimulate dopamine ",The molecular weight is 315.48.,Rotigotine has a topological polar surface area of 23.47.,The log p value of  is 4.54.,Rotigotine is approved.,Rotigotine is a solid.,True
15194,"Cariprazine is an antipsychotic drug developed by Gedeon Richter and marketed by Actavis under the trade name Vraylar. Cariprazine acts as a D2 and D3 receptor partial agonist, with high selectivity towards the D3 receptor. This mechanism is relatively unique, since many other antipsychotics are D2 and 5-HT2A agonists. Cariprazine was approved by the FDA in September 2015 and is indicated in the treatment of schizophrenia and bipolar disorder. Action on the dopaminergic systems makes it also potentially useful as an add-on therapy in major depressive disorder. Cariprazine is an atypical antipsychotic indicated for the treatment of schizophrenia and for the acute treatment of manic or mixed episodes associated with bipolar I Cariprazine acts as a partial agonist at the dopamine D3 and D2 receptors with high binding affinity. Cariprazine acts as an antagonist at 5-HT2B and 5-HT2A receptors with high and moderate binding affinity as well as it binds to the histamine H1 receptors. Cariprazine shows lower binding affinity to the serotonin 5­ HT2C and α1A- adrenergic receptors and has no appreciable affinity for cholinergic muscarinic receptors. The mechanism of action of cariprazine in schizophrenia and bipolar I disorder is unknown. However, the efficacy of cariprazine could be mediated through a combination of partial agonist activity at central dopamine D2 and serotonin 5-HT1A receptors and antagonist activity at serotonin 5-HT2A receptors. Cariprazine forms two major metabolites, desmethyl cariprazine (DCAR) and didesmethyl cariprazine (DDCAR), that have in vitro receptor binding profiles similar to the parent drug.",The molecular weight is 427.41.,Cariprazine has a topological polar surface area of 38.82.,The log p value of  is 4.98.,Cariprazine is approved and investigational.,Cariprazine is a solid.,True
15195,"Tirbanibulin (KX-O1 or KX2–391) is a dual inhibitor of Src Kinase and tubulin. On December 14, 2020, tirbanibulin was approved by the FDA for the topical treatment of actinic keratosis on the face or scalp. It is marketed under the brand name Klisyri. Actinic keratosis is a chronic condition characterized by lesions, which can potentially transform into invasive squamous cell carcinoma with a risk of 1% over 10 years. Tirbanibulin blocks the molecular pathways that promote the proliferation, survival, and metastasis of malignant cells. Tirbanibulin exhibits antitumour effects in vitro and in vivo and has been investigated for its antitumor efficacy in the management of various cancers, such as prostate cancer and breast cancer. Tirbanibulin is indicated for the topical treatment of actinic keratosis on the face or scalp. In clinical trials composed comprising patients with actinic keratosis of the face or scalp, tirbanibulin promoted complete clearance of actinic keratosis lesions at day 57 in treated areas in 44-54% of patients compared to 5-13% of patients who received the placebo. Actinic keratosis is a chronic, pre-malignant condition characterized by lesions and proliferation of neoplastic keratinocytes. Tirbanibulin mediates an anti-proliferative effect by inhibiting tubulin polymerization and Src kinase signalling.  Src tyrosine kinases regulate normal cell growth: the expression of Src kinase is upregulated during the normal hair cycle during the proliferative anagen phase. Additionally, Src tyrosine kinases act as key modulators of cancer cell proliferation, survival, angiogenesis, migration, invasion and metastasis. Src is frequently upregulated in various epithelial tumours including colon, breast and pancreas compared with the adjacent normal tissues. The expression and activity of Src are also enhanced in human actinic keratosis, which is characterized by hyperproliferative premalignant skin lesions. The pathogenesis of actinic keratosis commonly involves skin inflammation, oxidative stress, immunosuppression, impaired apoptosis, mutagenesis, dysregulation of keratinocyte growth and proliferation, and tissue remodelling. _In vitro_ studies suggest that Src plays a predominant role in the early stages of human skin tumour development, rather than at later stages of tumour progression. ",,,,KX-01 is approved and investigational.,KX-01 is a solid.,True
15196,"Sertindole, a neuroleptic, is one of the newer antipsychotic medications available. Serdolect is developed by the Danish pharmaceutical company H. Lundbeck. It is a phenylindole derivative used in the treatment of schizophrenia. It was first marketed in 1996 in several European countries before being withdrawn two years later because of numerous cardiac adverse effects. It has once again been approved and should soon be available on the French and Australian market. Used in the treatment of schizophrenia. Sertindole is an atypical antipsychotic at least as effective as haloperidol and risperidone in the treatment of neuroleptic-responsive schizophrenia. Sertindole improves negative symptoms, and is also effective for the treatment of neuroleptic-resistant schizophrenia. Sertindole is generally well tolerated and is associated with a low rate of extrapyramidal symptoms (EPS). Sertindole is an antipsychotic drug with affinity for dopamine D2, serotonin 5-HT2A and 5-HT2C, and alpha1-adrenoreceptors. Preclinical studies suggest that sertindole acts preferentially on limbic and cortical dopaminergic neurons and clinical trials have confirmed that sertindole is effective at a low dopamine D2 occupancy level. ",The molecular weight is 440.95.,Sertindole has a topological polar surface area of 40.51.,The log p value of  is 5.27.,Sertindole is approved and investigational and withdrawn.,Sertindole is a solid.,True
15197,"A tetracyclic compound with antidepressant effects. Mianserin was previously available internationally, however in most markets it has been phased out in favour of. For the treatment of depression. Mianserin is a tetracyclic antidepressant that has antihistaminic and hypnosedative, but almost no anticholinergic, effect. It is a weak inhibitor of norepinephrine reuptake and strongly stimulates the release of norepinephrine. Interactions with serotonin receptors in the central nervous system have also been found. Its effect is usually noticeable after one to three weeks. Mianserin may cause drowsiness and hematological problems. Mianserin's mechanism of therapeutic action is not well understood, although it apparently blocks alpha-adrenergic, histamine H1, and some types of serotonin receptors.",The molecular weight is 264.37.,Mianserin has a topological polar surface area of 6.48.,The log p value of  is 3.76.,Mianserin is approved and investigational.,Mianserin is a solid.,True
15198,"Alogliptin is a selective, orally-bioavailable inhibitor of enzymatic activity of dipeptidyl peptidase-4 (DPP-4). Chemically, alogliptin is prepared as a benzoate salt and exists predominantly as the R-enantiomer (>99%). It undergoes little or no chiral conversion in vivo to the (S)-enantiomer. FDA approved January 25, 2013. Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.  Peak inhibition of DPP-4 occurs within 2-3 hours after a single-dose administration to healthy subjects. The peak inhibition of DPP-4 exceeded 93% across doses of 12.5 mg to 800 mg. Inhibition of DPP-4 remained above 80% at 24 hours for doses greater than or equal to 25 mg. Alogliptin also demonstrated decreases in postprandial glucagon while increasing postprandial active GLP-1 levels compared to placebo over an 8-hour period following a standardized meal. Alogliptin does not affect the QTc interval.  Alogliptin inhibits dipeptidyl peptidase 4 (DPP-4), which normally degrades the incretins glucose-dependent insulinotropic polypeptide (GIP) and glucagon like peptide 1 ( GLP-1). The inhibition of DPP-4 increases the amount of active plasma incretins which helps with glycemic control. GIP and GLP-1 stimulate glucose dependent secretion of insulin in pancreatic beta cells. GLP-1 has the additional effects of suppressing glucose dependent glucagon secretion, inducing satiety, reducing food intake, and reducing gastric emptying.",The molecular weight is 339.4.,Alogliptin has a topological polar surface area of 93.67.,The log p value of  is 0.99.,Alogliptin is approved.,Alogliptin is a solid.,True
15199,"Opioid analgesic for treatment of moderate to severe pain. FDA approved on Nov 20, 2008. The immediate-release formulation of tapentadol is indicated for the relief of moderate to severe acute pain. The long-acting formulation serves as a continuous, around-the-clock analgesic that is indicated for the relief of moderate to severe chronic pain or neuropathic pain associated with diabetic peripheral neuropathy.  Tapentadol is a centrally-acting synthetic analgesic that is 18 times less potent than morphine in binding mu-opioid receptors. It also increases norepinephrine concentrations in the brains of rats via inhibition of norepinephrine reuptake. Selective mu-opioid antagonists like naloxone can block analgesia from tapentadol. It also has not effect on the QT interval.  Tapendadol causes large increases in levels of extracellular norepinephrine (NE) due to a dual mechanism of action involving mu opioid receptor (MOR) agonism as well as noradrenaline reuptake inhibition.",,,,Tapentadol is approved.,Tapentadol is a solid.,True
15200,"Vernakalant was developed by Cardiome Pharma as as an antiarrhythmic drug intended for rapid conversion of atrial fibrillation to sinus rhythm. It acts as an atypical class III antiarrhythmic drug that potentiates its effect in higher heart rates. Intravenous formulation was approved in Europe in September 2010 as Brinavess and in Canada in April 2017. It is an investigational drug under regulatory review by FDA. Indicated for the rapid conversion of recent onset of atrial fibrillation to sinus rhythm in adults for non-surgery patients that lasts for less than 7 days of duration and post-cardiac surgery patients with atrial fibrillation lasting less than 3 days of duration. Vernakalant blocks currents in all phases of atrial action potential including atria-specific potassium currents (the ultra-rapid delayed rectifier and the acetylcholine dependent potassium currents) and prolongs the refractory period. It dose-dependently prolongs atrial refractoriness, prolongs AV nodal conduction and refractoriness, and slightly prolongs QRS duration without significantly affecting ventricular refractory period. Vernakalant has a high affinity to ion channels specifically involved in repolarization of atrial tissue and is thought to have a low proarrhythmic potential. Vernakalant blocks atrial voltage-gated sodium channels in a dose and frequency-dependent manner and inhibits late sodium current (INa)which confers its effect on intra-atrial conduction. This current blockade enhance and onset of drug action accelerates in higher heart rate as the affinity of vernakalant for INa also increases. Its binding offset is quick once the heart rate slows. It also blocks Kv 1.5 channel and its early activating potassium channels (IKur) and inhibits acetylcholine-activated potassium channels (IKAch), which are specific to the atrium and cause prolongation of atrial refractoriness. Vernakalant also blocks Kv4.3 channel and its cardiac transient outward potassium current (Ito), which is involved more with atrial than ventricular refractoriness. ",The molecular weight is 349.47.,Vernakalant has a topological polar surface area of 51.16.,The log p value of  is 2.73.,Vernakalant is approved and investigational.,Vernakalant is a solid.,True
15201,"Dapagliflozin is a sodium-glucose cotransporter 2 inhibitor indicated for managing diabetes mellitus type 2. When combined with diet and exercise in adults, dapagliflozin helps to improve glycemic control by inhibiting glucose resorption in the proximal tubule of the nephron and causing glycosuria. Dapagliflozin was approved by the FDA on Jan 08, 2014. Dapagliflozin is indicated to improve glycemic control in adult patients with type 2 diabetes mellitus along with diet and exercise. Dapagliflozin inhibits the sodium-glucose contransporter 2(SGLT2) which is primarily located in the proximal tubule of the nephron. SGLT2 facilitates 90% of glucose resorption in the kidneys and so its inhibition allows for glucose to be excreted in the urine. This excretion allows for better glycemic control and potentially weight loss in patients with type 2 diabetes mellitus.  Dapagliflozin inhibits the sodium-glucose contransporter 2(SGLT2) which is primarily located in the proximal tubule of the nephron. SGLT2 facilitates 90% of glucose resorption in the kidneys and so its inhibition allows for glucose to be excreted in the urine. This excretion allows for better glycemic control and potentially weight loss in patients with type 2 diabetes mellitus. ",The molecular weight is 408.88.,Dapagliflozin has a topological polar surface area of 99.38.,The log p value of  is 3.37.,Dapagliflozin is approved.,Dapagliflozin is a solid.,True
15202,Investigated for use/treatment in lung cancer. E7070 is a novel sulfonamide antitumoragent that exhibits potent antitumoractivity in vitro and in vivo. This compound affects cell cycleprogression in human tumor cells,,,,Indisulam is investigational.,Indisulam is a solid.,True
15203,"Repinotan is a high-affinity, selective, full agonist of the 5HT1A-receptor subtype with neuroprotective properties. Investigated for use/treatment in strokes, cerebral ischemia, and depression. Repinotan is a 5-HT1A receptor agonist which inhibits glutamate induced depolarization. The effect of repinotan in neuronal cells has been reported to be mediated by a variety of mechanisms/signaling pathways, including activation of the anti-apoptotic phosphatidylinositol 3-kinase (PI-3K) pathway, inhibition of glutamate release (probably via opening of K+ channels leading to membrane hyperpolarization), extracellular-regulated kinase (Erk)-stimulated Bcl-2 expression or inhibition of caspase-3 activity, and increased release of the neurite extension factor S-100 beta.",,,,Repinotan is investigational.,Repinotan is a solid.,True
15204,"Deramciclane (EGIS-3886) is used for the treatment of a number of anxiety disorders. Deramciclane differs from other anti anxiety medications in that it is not a benzodiazepine and so has a different structure and target. It antagonizes 5-HT2A receptors, agonizes 5-HT2C receptors, and functions as a GABA reuptake inhibitor. Investigated for use/treatment in anxiety disorders. Deramciclane is a new putative non-benzodiazepine-type anxiolytic compound. It is a selective serotonin 5-HT(2A) and 5-HT(2C) receptor antagonist and has also inverse agonist properties.",,,,Deramciclane is investigational.,Deramciclane is a solid.,True
15205,"Pazopanib is a small molecule inhibitor of multiple protein tyrosine kinases with potential antineoplastic activity. It is developed by GlaxoSmithKline and was FDA approved on October 19, 2009. Treatment of advanced renal cell cancer and advanced soft tissue sarcoma (in patients previously treated with chemotherapy)  Pazopanib is a synthetic indazolylpyrimidine and reaches steady state concentrations of >15 μg/ml. This concentration is high enough to observe maximal inhibition of VEGFR2 phosphorylation and some anti-tumour activity (concentration required to inhibit receptors is 0.01 - 0.084 μmol/L). A reduction in tumour blood flow, increased tumour apoptosis, inhibition of tumour growth, reduction in tumour interstitial fluid pressure, and hypoxia in cancer cells can be observed in patients receiving treatment.  Pazopanib is a second-generation multitargeted tyrosine kinase inhibitor against vascular endothelial growth factor receptor-1, -2, and -3, platelet-derived growth factor receptor-alpha, platelet-derived growth factor receptor-beta, and c-kit. These receptor targets are part of the angiogenesis pathway that facilitates the formation of tumour blood vessel for tumour survival and growth. ",The molecular weight is 437.52.,Pazopanib has a topological polar surface area of 119.03.,The log p value of  is 3.5.,Pazopanib is approved.,Pazopanib is a solid.,True
15206,"Panobinostat is an oral deacetylace (DAC) inhibitor approved on February 23, 2015 by the FDA for the treatment of multiple myeloma. The approval was accelerated based on progression-free survival, therefore confirmatory trials by the sponsor to demonstrate clinical efficacy in multiple myeloma treatment are in progress of being conducted. Panobinostat is marketed by Novartis under the brand name Farydak. Panobinostat acts as a non-selective histone deacetylase inhibitor (pan-HDAC inhibitor) and it is the most potent DAC inhibiting agent available on the market. Panobinostat is indicated in the treatment of multiple myeloma in combination with dexamethasone and bortezomib in patients who have received 2 previous treatment regimens including bortezomib and an immunomodulatory agent. This indication is approved by accelerated approval based on progression free survival as of February 23, 2015.  Panobinostat is a deacetylase (DAC) inhibitor. DACs, also known as histone DACs (HDAC), are responsible for regulating the acetylation of about 1750 proteins in the body; their functions are involved in many biological processes including DNA replication and repair, chromatin remodelling, transcription of genes, progression of the cell-cycle, protein degradation and cytoskeletal reorganization. In multiple myeloma, there is an overexpression of DAC proteins. Panobinostat inhibits class I (HDACs 1, 2, 3, 8), class II (HDACs 4, 5, 6, 7, 9, 10) and class IV (HDAC 11) proteins. Panobinostat's antitumor activity is believed to be attributed to epigenetic modulation of gene expression and inhibition of protein metabolism. Panobinostat also exhibits cytotoxic synergy with bortezomib, a proteasome inhibitor concurrently used in treatment of multiple myeloma. ",The molecular weight is 349.43.,Panobinostat has a topological polar surface area of 77.15.,The log p value of  is 2.64.,Panobinostat is approved and investigational.,Panobinostat is a solid.,True
15207,"Tafenoquine is an 8-aminoquinoline analogue of primaquine which varies only on the presence of a 5-phenoxy group. It was discovered by the scientists at the Walter Reed Army Institute of Research in 1978 as a substitute for primaquine that would be more effective against relapsing vivax malaria. Tafenoquine was further developed collaboratively between GlaxoSmithKline and Medicines for Malaria Venture. It was FDA approved on July 20, 2018. Tafenoquine is used for the treatment and prevention of relapse of Vivax malaria in patients 16 years and older. Tafenoquine is not indicated to treat acute vivax malaria.  In vitro studies have shown that tafenoquine presents an average 50% inhibitory concentration of 0.436 mcg against blood stages of seven strains of _P. falciparum_. In chloroquine-resistant _P. falciparum_ strains the IC50 of tafenoquine was greater when compared with primaquine and it ranged from 0.5 to 33.1 mcg. In studies evaluating the transmission-blocking activity of tafenoquine against the sporogonic stage of _P. vivax_, it was showed a reduced transmission at doses higher than 25 mg/kg. The mechanism of action of tafenoquine is not well established but studies have reported a longer and more effective action when compared to primaquine. The active moiety of tafenoquine, 5,6 ortho quinone tafenoquine, seems to be redox cycled by _P. falciparum_ which are upregulated in gametocytes and liver stages. Once inside, the oxidated metabolite produces hydrogen peroxide and hydroxyl radicals. It is thought that these radicals produce leads to the parasite death.",The molecular weight is 463.5.,Tafenoquine has a topological polar surface area of 78.63.,The log p value of  is 6.52.,Tafenoquine is approved and investigational.,Tafenoquine is a solid.,True
15208,"Esmirtazapine, known by the standardized identifier SCH 900265, was under development by Organon to treat insomnia and vasomotor symptoms associated with menopause. Esmirtazapine is the (S)-(+)-enantiomer of mirtazapine and possesses similar overall pharmacology. This includes inverse agonist activity of H1 and 5-HT2 receptors and antagonism of α2-adrenergic receptors. Merck has terminated its internal clinical development program for esmirtazapine as of March 2010. Investigated for use/treatment in insomnia and sleep disorders.",,,,Esmirtazapine is investigational.,Esmirtazapine is a solid.,True
15209,"Vilazodone is a novel compound with combined high affinity and selectivity for the 5-hydroxytryptamine (5-HT) transporter and 5-HT(1A) receptors. Vilazodone may also be associated with less sexual dysfunction and weight gain. Vilazodone was given FDA approval on January 21, 2011. Vilazodone is approved for treatment of major depressive disorder. Vilazodone increases serotonin levels in the brain by inhibiting the reuptake of serotonin while acting as a partial agonist on serotonin-1A receptors. Due to this activity vilazodone has sometimes been referred to as a selective partial agonist and reuptake inhibitor (SPARI). Vilazodone selectively inhibits serotonin reuptake in the central nervous system as well as acting as a partial agonist of 5HT-1A receptors. The exact mechanism for how these effects translate to its antidepressant effects are not known, though there is an association between these effects and antidepressive activity.",The molecular weight is 441.54.,Vilazodone has a topological polar surface area of 102.29.,The log p value of  is 4.08.,Vilazodone is approved.,Vilazodone is a solid.,True
15210,"Mepyramine, or pyrilamine, targets the H1 receptor. It is a first generation antihistamine. However, it rapidly permeates the brain and so often causes drowsiness as a side effect. It has been found in over-the-counter combination products for colds and menstrual symptoms, but is considered to be an unapproved prescription medication used for cough, cold, or allergic conditions. Indicated for the treatment of allergic conditions, symptomatic relief of hypersensitivity reaction, and treatment of pruritic skin disorders. Mepyramine is a histamine H1 receptor inverse agonist. It binds to a G protein-coupled form of the receptor and promotes a G protein-coupled inactive state of the H1 receptor that interferes with the Gq/11-mediated signaling. Mepyramine competes with histamine for binding at H<sub>1</sub>-receptor sites on the effector cell surface, resulting in suppression of histaminic edema, flare, and pruritus. The sedative properties of Mepyramine occur at the subcortical level of the CNS.",The molecular weight is 285.39.,Mepyramine has a topological polar surface area of 28.6.,The log p value of  is 3.23.,Mepyramine is approved and vet_approved.,Mepyramine is a solid.,True
15211,"Desvenlafaxine (O-desmethylvenlafaxine) the major active metabolite of venlafaxine, is an antidepressant from the serotonin norepinephrine reuptake inhibitor (SNRI) class. Desvenlafaxine may be used to treat major depressive disorder. It is formulated as an extended release tablet. Desvenlafaxine was approved by the FDA in 2008. Desvenlafaxine is indicated for the treatment of major depressive disorder in adults. Desvenlafaxine is a selective serotonin and norepinephrine reuptake inhibitor. It lacks significant activity on muscarinic-cholinergic, H<sub>1</sub>-histaminergic, or &alpha;<sub>1</sub>-adrenergic receptors <i>in vitro</i>. Desvenlafaxine does not appear to exert activity against calcium, chloride, potassium and sodium ion channels and also lacks monoamine oxidase (MAO) inhibitory activity. It was also shown to lack significant activity again the cardiac potassium channel, hERG, <i>in vitro</i>. Compared to other SNRIs, desvenlafaxine undergoes simple metabolism, has a low risk of drug-drug interactions and does not have to be extensively titrated to reach a therapeutic dose.  Desvenlafaxine, the active metabolite of venlafaxine, is a selective serotonin and norepinephrine reuptake inhibitor. Desvenlafaxine inhibits neurotransmitter reuptake in serotonin, norepinephrine, and dopamine transporters. Desvenlafaxine inhibits serotonin transporters with 10 times the affinity of norepinephrine transporters, and dopamine transporters with the lowest affinity. In vitro, desvenlafaxine has no inhibition of monoamine oxidase, and almost no affinity for muscarinic, cholinergic, H1-histaminergic, and alpha1-adrenergic receptors.",The molecular weight is 263.38.,Desvenlafaxine has a topological polar surface area of 43.7.,The log p value of  is 2.68.,Desvenlafaxine is approved and investigational.,Desvenlafaxine is a solid.,True
15212,"Fesoterodine is an antimuscarinic prodrug for the treatment of overactive bladder syndrome. For the treatment of overactive bladder (with symptoms of urinary frequency, urgency, or urge incontinence). In-vivo the fesoteridine prodrug is broken down into its active metabolite, 5-hydroxymethyl tolterodine (5-HMT), by plasma esterases. The 5-hydroxymethyl metabolite, which exhibits an antimuscarinic activity. Both urinary bladder contraction and salivation are mediated via cholinergic muscarinic receptors. Therefore, acting as a competitive muscarinic receptor antagonist, fesoterodine ultimately acts to decrease the detrusor pressure by its muscarinic antagonism, thereby decreasing bladder contraction and consequently, the urge to urinate. Fesoterodine, once converted to its active metabolite, 5-hydroxymethyltolterodine, acts as a competitive antagonists at muscarinic receptors. This results in the inhibition of bladder contraction, decrease in detrusor pressure, and an incomplete emptying of the bladder.",The molecular weight is 411.59.,Fesoterodine has a topological polar surface area of 49.77.,The log p value of  is 4.36.,Fesoterodine is approved.,Fesoterodine is a solid.,True
15213,"Lumefantrine is an antimalarial agent used to treat acute uncomplicated malaria. It is administered in combination with artemether for improved efficacy. This combination therapy exerts its effects against the erythrocytic stages of <i>Plasmodium spp.</i> and may be used to treat infections caused by <i>P. falciparum</i> and unidentified <i>Plasmodium</i> species, including infections acquired in chloroquine-resistant areas. Lumefantrine and artemether combination therapy is indicated for the treatment of acute uncomplicated malaria caused by <i>Plasmodium falciparum</i>, including malaria acquired in chloroquine-resistant areas. May also be used to treat uncomplicated malaria when the <i>Plasmodium</i> species has not been identified. Indicated for use in adults and children greater than 5 kg.  Lumefantrine is a blood schizonticide active against erythrocytic stages of <i>Plasmodium falciparum</i>. It is thought that administration of lumefantrine with artemether results in cooperate antimalarial clearing effects. Artemether has a rapid onset of action and is rapidly cleared from the body. It is thus thought to provide rapid symptomatic relief by reducing the number of malarial parasites. Lumefantrine has a much longer half life and is believed to clear residual parasites.  The exact mechanism by which lumefantrine exerts its antimalarial effect is unknown. However, available data suggest that lumefantrine inhibits the formation of &beta;-hematin by forming a complex with hemin and inhibits nucleic acid and protein synthesis. ",The molecular weight is 528.94.,Lumefantrine has a topological polar surface area of 23.47.,The log p value of  is 10.2.,Lumefantrine is approved.,Lumefantrine is a solid.,True
15214,"Bufuralol is a new, non-selective -adrenoceptor blocking agent.",The molecular weight is 261.36.,Bufuralol has a topological polar surface area of 45.4.,The log p value of  is 3.4.,Bufuralol is experimental.,Bufuralol is a solid.,True
15215,Sparteine is a plant alkaloid derived from Cytisus scoparius and Lupinus mutabilis which may chelate calcium and magnesium. It is a sodium channel blocker so it falls under the category of class 1a antiarrhythmic agents. Sparteine is not currently FDA approved for human use.,The molecular weight is 234.39.,Sparteine has a topological polar surface area of 6.48.,The log p value of  is 2.6.,Sparteine is experimental.,Sparteine is a solid.,True
15216,"Sulfaphenazole is a sulfonamide antibacterial. For the treatment bacterial infections. Sulfaphenazole is a sulfonamide antibacterial. In bacteria, antibacterial sulfonamides act as competitive inhibitors of the enzyme dihydropteroate synthetase (DHPS), an enzyme involved in folate synthesis. As such, the microorganism will be \starved\"" of folate and die.""",The molecular weight is 314.36.,Sulfaphenazole has a topological polar surface area of 90.01.,The log p value of  is 2.07.,Sulfaphenazole is approved.,Sulfaphenazole is a solid.,True
15217,,,,,Enclomiphene is investigational.,Enclomiphene is a solid.,False
15218,"A monocarboxylic acid the structure of which is that of butyric acid substituted with a phenyl group at C-4. It is a histone deacetylase inhibitor that displays anticancer activity. It inhibits cell proliferation, invasion and migration and induces apoptosis in glioma cells. It also inhibits protein isoprenylation, depletes plasma glutamine, increases production of foetal haemoglobin through transcriptional activation of the γ-globin gene and affects hPPARγ activation. Adjunctive therapy for the management of chronic urea cycle disorders due to deficiencies in carbamylphosphate (CPS), ornithine transcarbamylase (OTC), or argininosuccinic acid synthetase. it is indicated in all neonatal- onset efficiency presenting within the first 28 days of life. Also indicated in patients with late-onset, presenting after the first month of life with a history of hyperammonemic encephalopathy.  Decreases elevated plasma ammonia glutamine levels Sodium phenylbutyrate is a pro-drug that is metabolized to the active compound phenylacetate. Phenylacetate conjuages with glutamine via acetylation reaction to form the product phenylacetylglutamine, which is excreted by the kidneys. This provides an alternative mechanism for waste nitrogen excretion. ",The molecular weight is 164.2.,Phenylbutyric acid has a topological polar surface area of 37.3.,The log p value of  is 2.28.,Phenylbutyric acid is approved and investigational.,Phenylbutyric acid is a solid.,True
15219,"Sulconazole, brand name Exelderm, is a broad-spectrum anti-fungal agent available as a topical cream and solution. Sulconazole nitrate, the active ingredient, is an imidazole derivative that inhibits the growth of common pathogenic dermatophytes making it an effective treatment for tinea cruris and tinea corporis infections. Sulconazole solution 1.0% is indicated for the treatment of tinea cruris and tinea corporis caused by Trichophyton rubrum, Trichophyton mentagrophytes, Epidermophyton floccosum, and Microsporum canis; and for the treatment of tinea versicolor. Effectiveness has not been proven in tinea pedis (athlete’s foot). The function of imidazole derivatives can be attributed to their structural resemblance to purines essential to metabolism. ",The molecular weight is 397.74.,Sulconazole has a topological polar surface area of 17.82.,The log p value of  is 6.27.,Sulconazole is approved.,Sulconazole is a solid.,True
15220,"Bopindolol (INN) is an ester prodrug for the beta blocker. For the management of hypertension, edema, ventricular tachycardias, and atrial fibrillation. Bopindolol is a prodrug of pindolol. Pindolol is a non-selective beta-adrenergic antagonist (beta-blocker) which possesses intrinsic sympathomimetic activity (ISA) in therapeutic dosage ranges but does not possess quinidine-like membrane stabilizing activity. Pindolol impairs AV node conduction and decreases sinus rate and may also increase plasma triglycerides and decrease HDL-cholesterol levels. Pindolol is nonpolar and hydrophobic, with low to moderate lipid solubility. Pindolol has little to no intrinsic sympathomimetic activity and, unlike some other beta-adrenergic blocking agents, pindolol has little direct myocardial depressant activity and does not have an anesthetic-like membrane-stabilizing action. Bopindolol (as pindolol) non-selectively blocks beta-1 adrenergic receptors mainly in the heart, inhibiting the effects of epinephrine and norepinephrine resulting in a decrease in heart rate and blood pressure. By binding beta-2 receptors in the juxtaglomerular apparatus, Pindolol inhibits the production of renin, thereby inhibiting angiotensin II and aldosterone production and therefore inhibits the vasoconstriction and water retention due to angiotensin II and aldosterone, respectively.",The molecular weight is 380.49.,Bopindolol has a topological polar surface area of 63.35.,The log p value of  is 4.98.,Bopindolol is experimental.,Bopindolol is a solid.,True
15221,"Bupranolol is a non-selective beta blocker with potency similar to. It does not have intrinsic sympathomimetic activity (ISA), but does have strong membrane stabilizing activity. Used to manage hypertension and tachycardia. Also used to treat glaucoma. Bupranolol is a competitive, nonselective beta-blocker similar to propanolol without intrinsic sympathomimetic activity. Bupranolol competes with sympathomimetic neurotransmitters such as catecholamines for binding at beta(1)-adrenergic receptors in the heart, inhibiting sympathetic stimulation. This results in a reduction in resting heart rate, cardiac output, systolic and diastolic blood pressure, and reflex orthostatic hypotension.",The molecular weight is 271.79.,Bupranolol has a topological polar surface area of 41.49.,The log p value of  is 3.1.,Bupranolol is experimental.,Bupranolol is a solid.,True
15222,"Levomilnacipran is a selective serotonin and norepinephrine reuptake inhibitor. Chemically, levomilnacipran is the 1S,2R-enantiomer of milnacipran. FDA approved on July 25, 2013. Levomilnacipran is a serotonin and norepinephrine reuptake inhibitor and is indicated for the treatment of major depressive disorder (MDD).  Levomilnacipran binds with high affinity to human serotonin (5-HT) and norepinephrine (NE) transporters (Ki = 11 and 91 nM, respectively). It potently inhibits 5-HT and NE reuptake (IC50 = 16 - 19 and 11 nM, respectively). Levomilnacipran does not bind to any other receptors, ion channels, or transporters, including serotonergic (5HT1-7), α- and β adrenergic, muscarinic, or histaminergic receptors and Ca2+, Na+, K+ or Cl- channels to a significant degree. Levomilnacipran did not inhibit monoamine oxidase (MAO). Furthermore, levomilnacipran does not prolong the QTc interval to a clinically relevant extent.  The exact mechanism of the antidepressant action of levomilnacipran is unknown but is thought to be related to the potentiation of serotonin and norephinephrine in the central nervous system through inhibition of reuptake at serotonin and norepinephrine transporters. ",The molecular weight is 246.35.,Levomilnacipran has a topological polar surface area of 46.33.,The log p value of  is 1.91.,Levomilnacipran is approved and investigational.,Levomilnacipran is a solid.,True
15223,"Perospirone is an atypical or second-generation antipsychotic of the azapirone family that antagonizes serotonin 5HT2A receptors and dopamine D2 receptors. It also displays affinity towards 5HT1A receptors as a partial agonist. Dainippon Sumitomo Pharma developed perospirone in Japan in 2001 for the treatment of acute schizophrenia and bipolar mania as well as chronic schizophrenia. It is commonly present as the hydrated hydrochloride salt form. Classified as a neuroleptic agent, perospirone is shown to be effective against positive, negative and general symptoms in patients with schizophrenia. It is also shown to be less associated with extrapyramidal symptoms as a side effect compared to. For the treatment of schizophrenia and acute cases of bipolar mania. Perospirone is a serotonin 5-HT2 receptor inverse agonist and dopamine D2 receptor antagonist based on receptor binding experiments that binds to both receptors with high affinity. Perospirone is also a partial agonist at 5-HT1A receptors which are autoreceptors that stimulate the uptake of 5-HT and inhibit 5-HT release. It also interacts with D4 receptors and α₁-adrenergic receptors as an antagonist, as well as histamine H1 receptor an inverse agonist. Binding to these receptors may explain sedative and hypotensive actions. Perospirone binds to D1 receptors with low affinity and minimal clinical significance.  Antagonism at D2 receptors is believed to relieve the positive symptoms of schizophrenia such as delusions, hallucinations, and thought disorders. Perospirone targets the mesolimbic patway to reverse the overactivity of the dopaminergic signalling via D2 receptors. 5-HT2A antagonism is thought to allevaite the negative symptoms and cognitive impairments of schizophrenia. These receptors are Gi/Go coupled receptors that lead to decreased neurotransmitter release and neuronal inhibition when activated, thus play a role in dopamine release regulation. Perospirone targets these receptors in the nigrostriatal pathway to reduce dopamine release and function. In contrast, 5-HT2A receptor antagonism may improve the negative symptoms by enhancing dopamine and glutamate release in the mesocortical pathway. 5-HT1A receptor activation further inhibits the release of 5-HT into the synaptic cleft. ",The molecular weight is 426.58.,Perospirone has a topological polar surface area of 56.75.,The log p value of  is 3.76.,Perospirone is experimental.,Perospirone is a solid.,True
15224,Indenolol is a drug of the beta-adrenergic blocker class.,The molecular weight is 494.68.,,,Indenolol is withdrawn.,Indenolol is a solid.,True
15225,"Befunolol is a beta blocker introduced in 1983 by Kakenyaku Kakko. It is currently in experimental status, and is being tested for the management of open angle glaucoma. Used in the management of open angle glaucoma. PMID: 12480285. ",The molecular weight is 291.35.,Befunolol has a topological polar surface area of 71.7.,The log p value of  is 1.8.,Befunolol is experimental.,Befunolol is a solid.,True
15226,"Eliglustat, marketed by Genzyme as CERDELGA, is a glucosylceramide synthase inhibitor indicated for the long-term treatment of type 1 Gaucher disease. Patients selected for treatment with Eliglustat undergo an FDA approved genotype test to establish if they are CYP2D6 EM (extensive metabolizers), IM (intermediate metabolizers), or PM (poor metabolizers), as the results of this test dictate the dosage of Eliglustat recommended. There are no recommended dosing guidelines for CYP2D6 ultra-rapid or indeterminate metabolizers. Eliglustat was approved for use by the FDA in August 2014. Eliglustat is indicated for the long-term treatment of type 1 Gaucher disease in adult patients who are CYP2D6 extensive metabolizers (EMs), intermediate metabolizers (IMs), or poor metabolizers (PMs) as detected by an FDA-cleared test. According to pharmacokinetic and pharmacodynamic modelling, plasma concentrations of 500ng/mL of eliglustat are predicted to increase mean concentration in the PR, QRS, and QTcF intervals of 22, 7, and 13 msec, respectively. (Taken from Cerdelga prescribing information).  Eliglustat is a glucosylceramide synthase (IC50 = 10 ng/mL) specific inhibitor that acts as a substrate inhibitor of glucosylceramide. ",The molecular weight is 404.55.,Eliglustat has a topological polar surface area of 71.03.,The log p value of  is 4.83.,Eliglustat is approved.,Eliglustat is a solid.,True
15227,"Netupitant is an antiemitic drug approved by the FDA in October 2014 for use in combination with palonosetron for the prevention of acute and delayed vomiting and nausea associated with cancer chemotherapy including highly emetogenic chemotherapy. Netupitant is a neurokinin 1 receptor antagonist. The combination drug is marketed by Eisai Inc. and Helsinn Therapeutics (U.S.) Inc. under the brand Akynzeo. Netupitant is an antiemitic drug approved by the FDA in October 2014 for use in combination with palonosetron for the prevention of acute and delayed vomiting and nausea associated with cancer chemotherapy including highly emetogenic chemotherapy. Delayed emesis (vomiting) has been largely associated with the activation of tachykinin family neurokinin 1 (NK1) receptors (broadly distributed in the central and peripheral nervous systems) by substance P. As shown in in vitro and in vivo studies, netupitant inhibits substance P mediated responses.",The molecular weight is 578.6.,Netupitant has a topological polar surface area of 39.68.,The log p value of  is 6.51.,Netupitant is approved and investigational.,Netupitant is a solid.,True
15228,"Naloxegol, for \PEGylated naloxol\"" is a peripherally-selective opioid antagonist developed by AstraZeneca. It was approved by the FDA in September 2014 and is indicated for the treatment of opioid-induced constipation (OIC) in adult patients with chronic non‑cancer pain. The advantage of naloxegol over the opioid antagonist naloxone is that its PEGylated structure allows for high selectivity for peripheral opioid receptors and lack of entry into the central nervous system through the blood-brain barrier."" Indicated for the treatment of opioid-induced constipation (OIC) in adult patients with chronic non-cancer pain. Use of opioids induces slowing of gastrointestinal motility and transit. Patients do not develop tolerance to these effects, unlike many other opioid side effects. Naloxegol antagonizes mu, delta, and kappa opioid receptors, having the highest affinity for mu. Antagonism of gastrointestinal mu-opioid receptors by naloxegol inhibits opioid-induced delay of gastrointestinal transit time. Naloxegol is an antagonist of opioid binding at the mu-opioid receptor. When administered at the recommended dose levels, naloxegol functions as a peripherally-acting mu-opioid receptor antagonist in tissues such as the gastrointestinal tract, thereby decreasing the constipating effects of opioids. Naloxegol has shown more than 6000 fold selectivity for the peripheral mu receptors, and its PEGylated form restricts its action only to the periphery, not affecting the pain-relieving mechanism of opioids in the central nervous system.",The molecular weight is 651.79.,Naloxegol has a topological polar surface area of 126.77.,The log p value of  is 0.16.,Naloxegol is approved.,Naloxegol is a solid.,True
15229,"Umeclidinium is a long-acting muscarinic antagonist (LAMA) used as maintenance treatment for symptoms of chronic obstructive pulmonary disease (COPD). It is available as a once-daily inhalation monotherapy or as a fixed-dose combination product with the long-acting beta2-agonist vilanterol. COPD is a progressive obstructive lung disease characterized by shortness of breath, cough, sputum production, and chronically poor airflow with a forced expiratory volume in 1 second (FEV1) of less than 80%. By blocking the M3 muscarinic receptor which is highly expressed in airway smooth muscle of the lungs, umeclidinium inhibits the binding of acetylcholine and thereby opens up the airways by preventing bronchoconstriction. Its use has been shown to provide clinically significant, sustained improvements in lung function. Indicated for the long-term, once-daily, maintenance treatment of airflow obstruction in patients with chronic obstructive pulmonary disease (COPD). Umeclidinium is a long-acting, antimuscarinic agent, which is often referred to as an anticholinergic. It has similar affinity to the subtypes of muscarinic receptors M1 to M5. In the airways, it exhibits pharmacological effects through the inhibition of M3 receptor at the smooth muscle leading to bronchodilation. ",,,,Umeclidinium is approved.,Umeclidinium is a solid.,True
15230,"Lenvatinib is a receptor tyrosine kinase (RTK) inhibitor that inhibits the kinase activities of vascular endothelial growth factor (VEGF) receptors VEGFR1 (FLT1), VEGFR2 (KDR), and VEGFR3 (FLT4). Lenvatinib also inhibits other RTKs that have been implicated in pathogenic angiogenesis, tumor growth, and cancer progression in addition to their normal cellular functions, including fibroblast growth factor (FGF) receptors FGFR1, 2, 3, and 4; the platelet derived growth factor receptor alpha (PDGFRα), KIT, and RET. These receptor tyrosine kinases (RTKs) located in the cell membrane play a central role in the activation of signal transduction pathways involved in the normal regulation of cellular processes, such as cell proliferation, migration, apoptosis and differentiation, and in pathogenic angiogenesis, lymphogenesis, tumour growth and cancer progression. In particular, VEGF has been identified as a crucial regulator of both physiologic and pathologic angiogenesis and increased expression of VEGF is associated with a poor prognosis in many types of cancers. Lenvatinib is indicated for the treatment of following conditions. Based on x-ray crystallography and kinetic interaction studies, lenvatinib binds to the adenosine 5'-triphosphate binding site of VEGFR2 and to a neighbouring region via a cyclopropane ring and thereby inhibits tyrosine kinase activity and associated signalling pathways.  Lenvatinib is a receptor tyrosine kinase (RTK) inhibitor that inhibits the kinase activities of vascular endothelial growth factor (VEGF) receptors VEGFR1 (FLT1), VEGFR2 (KDR), and VEGFR3 (FLT4). Lenvatinib also inhibits other RTKs that have been implicated in pathogenic angiogenesis, tumor growth, and cancer progression in addition to their normal cellular functions, including fibroblast growth factor (FGF) receptors FGFR1, 2, 3, and 4; the platelet derived growth factor receptor alpha (PDGFRα), KIT, and RET.",The molecular weight is 426.86.,Lenvatinib has a topological polar surface area of 115.57.,The log p value of  is 3.35.,Lenvatinib is approved and investigational.,Lenvatinib is a solid.,True
15231,"Stiripentol is an anticonvulsant drug used in the treatment of epilepsy as an adjunct therapy along with and. This drug is currently approved in the USA, Canada, and European countries as oral tablets marketed as Diacomit.  FDA approval of this drug was granted on August 20, 2018 ,. Unrelated to other anticonvulsants, stiripentol belongs to the group of aromatic allylic alcohols and may potentiate the effect of other antiepileptic drugs (AEDs) due to pharmacokinetic interactions. It elevates the levels of gamma-aminobutyric acid (GABA), a major inhibitory neurotransmitter that regulates electrical activity in the central nervous system. Indicated for use in conjunction with clobazam and valproate as adjunctive therapy of refractory generalized tonic-clonic seizures in patients with severe myoclonic epilepsy in infancy (SMEI, Dravet’s syndrome) whose seizures are not adequately controlled with clobazam and valproate. Stiripentol is an orphan drug that effectively reduces seizure frequency in infantile epilepsy as an adjunct therapy and also exhibits a therapeutic advantage in improving the efficacy of other antiepileptic drugs. It potentiates GABA transmission by elevating the levels of the inhibitory neurotransmitters in the brain. Stiripentol is a positive allosteric modulator of GABA-A receptors in the brain that enhances the opening duration of the channel by binding to a site different than the benzodiazepine binding site. Reduced synaptosomal uptake of GABA and/or inhibition of GABA transaminase may also explain the role of stiripentol in reducing the events of seizure. The anticonvulsant activity of stiripentol is age-dependent, with increased efficacy in younger patients.  Stiripentol enhances GABAergic inhibition and prolongs the open duration of GABA-A receptor chloride channels by a barbiturate-like mechanism. It binds to GABA-A receptors containing any of the α, β, γ, or δ-subunits but displays strongest potency when bound to receptors containing α3 or δ subunits. Stiripentol is an inhibitor of lactate dehydrogenase (LDH), which plays a physiological role in energy metabolism of neurons and regulation of neuronal excitation. It binds to the site separate from lactate and pyruvate binding sites of the enzyme and inhibits both pyruvate-to-lactate conversion and lactate-to-pyruvate conversion. LDH inhibitors including stiripentol as antiepileptic treatments mimic ketogenic diet, where the energy source in the brain is switched from glucose to mainly ketone bodies. The ketone bodies directly regulate neuronal excitation and seizures via ATP-sensitive potassium channels and vesicular glutamate transporters. As a potent inhibitor of hepatic cytochrome P450 enzymes, mainly CYP3A4 and CYP2C19, stiripentol co-administration with other antiepileptic drugs elevates the free unchanged active drugs (such as carbamazepine, sodium valproate, phenytoin, phenobarbital and many benzodiazepines) in the circulation to mediate their therapeutic actions. ",The molecular weight is 234.3.,Stiripentol has a topological polar surface area of 38.69.,The log p value of  is 3.21.,Stiripentol is approved.,Stiripentol is a solid.,True
15232,"Brexpiprazole is a novel D2 dopamine and serotonin 1A partial agonist, called serotonin-dopamine activity modulator (SDAM), and a potent antagonist of serotonin 2A receptors, noradrenergic alpha 1B and 2C receptors. Brexpiprazole is approved for the treatment of schizophrenia, and as an adjunctive treatment for major depressive disorder (MDD). Although it failed Phase II clinical trials for ADHD, it has been designed to provide improved efficacy and tolerability (e.g., less akathisia, restlessness and/or insomnia) over established adjunctive treatments for major depressive disorder (MDD). As an adjunctive treatment of major depressive disorder (MDD) and for treatment of schizophrenia.  Although the mechanism of action of brexpiprazole in the treatment of MDD and schizophrenia is unclear, the efficacy of brexpiprazole may be attributed to partial agonist activity at serotonin 1A and dopamine D2 receptors, and antagonist activity at serotonin 2A receptors. ",The molecular weight is 433.57.,Brexpiprazole has a topological polar surface area of 44.81.,The log p value of  is 4.65.,Brexpiprazole is approved and investigational.,Brexpiprazole is a solid.,True
15233,"Dosulepin (INN, BAN) formerly known as dothiepin (USAN), is a tricyclic antidepressant with anxiolytic properties that is used in several European and South Asian countries, as well as Australia, South Africa, and New Zealand. It is not FDA-approved due to low therpeutic index and significant toxicity in overdose. Dosulepin inhibits the reuptake of biogenic amines, increasing available neurotransmitter levels at the synaptic cleft. The use of dosulepsin is only recommended in patients who are intolerant or unresponsive to alternative antidepressant therapies. Dosulepsin is a thio derivative of with a similar efficacy to that of , and also exhibits anticholinergic, antihistamine and central sedative properties.  Indicated in the treatment of symptoms of depressive illness, especially where an anti-anxiety effect is required. Dosulepin is a tricyclic antidepressant that interacts with various receptors and transporters. It is a monoamine reuptake inhibitor with approximately equal potency for noradrenaline and 5-HT that increases the availability of these neurotransmitters at the central synapses. The metabolites of dosulepin are shown to inhibit 5HT uptake by the human blood platelet. By binding to noradrenaline transporter (NAT) and serotonin transporter (SERT) in an equipotent manner and inhibiting the reuptake activity, dosulepin increases the free levels of noradrenaline and 5HT at the synaptic cleft. It is shown that the main metabolite northiaden is a more potent inhibitor of noradrenaline uptake than the parent drug. ",The molecular weight is 295.44.,Dosulepin has a topological polar surface area of 3.24.,The log p value of  is 4.53.,Dosulepin is approved.,Dosulepin is a solid.,True
15234,Butyrfentanyl or butyrylfentanyl (not to be confused with 3-methylfentanyl) is a potent short-acting synthetic opioid analgesic drug. It is an analog of with roughly 1/30 the potency. Butyrfentanyl was first synthesized in 1961 by Janssen Pharmaceuticals as a new opioid analgesic. Butyrfentanyl was investigated as a potential opioid analgesic but is no longer used for this purpose. It is more often being used as a recreational drug. Data for the pharmacodynamics of butyrfentanyl are not readily available. Butyrfentanyl is a µ opioid receptor agonist similar to fentanyl.,,,,Butyrfentanyl is illicit.,Butyrfentanyl is a solid.,True
15235,"Dasabuvir is a direct acting antiviral medication used as part of combination therapy to treat chronic Hepatitis C, an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Treatment options for chronic Hepatitis C have advanced significantly since 2011, with the development of Direct Acting Antivirals (DAAs) such as Dasabuvir. Dasabuvir is a non-nucleoside NS5B inhibitor which binds to the palm domain of NS5B and induces a conformational change which renders the polymerase unable to elongate viral RNA. The binding sites for non-nucleoside NS5B inhibitors are poorly conserved across HCV genotypes leading to the restriction of Dasabuvir's use to genotype 1 only. Dasabuvir, in combination with , , and (as Viekira Pak) is indicated for the treatment of patients with HCV genotype 1a with or genotype 1b without including those with compensated cirrhosis. Dasabuvir is classified as a direct-acting antiviral (DAA) and prevents viral replication in HCV genotype 1. Dasabuvir is a non-nucleoside inhibitor of the HCV RNA-dependent RNA polymerase encoded by the NS5B gene, which is essential for replication of the viral genome. Based on drug resistance mapping studies of HCV genotypes 1a and 1b, dasabuvir targets the palm domain of the NS5B polymerase, and is therefore referred to as a non-nucleoside NS5B-palm polymerase inhibitor. The EC50 values of dasabuvir against genotype 1a-H77 and 1b-Con1 strains in HCV replicon cell culture assays were 7.7 nM and 1.8 nM, respectively.",The molecular weight is 493.58.,Dasabuvir has a topological polar surface area of 104.81.,The log p value of  is 4.07.,Dasabuvir is approved.,Dasabuvir is a solid.,True
15236,"Melperone is an atypical antipsychotic of the butyrophenone chemical class, making it structurally related to the typical antipsychotic haloperidol. Melperone has been used for a span of greater than 30 years in the European Union. It has been well established in the treatment of confusion, anxiety, restlessness (particularly in the elderly) and schizophrenia as It is known to be well-tolerated with an excellent safety profile. Recently, it has been studied as a treatment of psychosis related to Parkinson's disease. For the treatment of schizophrenia, sleep, disorders, agitation and mentally confused states.  Melperone has been demonstrated to produce an antipsychotic effect at doses that cause minimal extrapyramidal symptoms frequently associated with more traditional antipsychotics.  Melperone demonstrates antagonist activity at D2 dopaminergic and 5HT2A serotonergic receptors. It has a weak affinity to D2 receptors and possesses less risk of inducing dopamine receptor supersensitivity after both acute and chronic administration. In addition, the ratio of dopamine D4/D2 occupancy for melperone has been shown to resemble the binding profile of clozapine.",The molecular weight is 263.36.,Melperone has a topological polar surface area of 20.31.,The log p value of  is 3.88.,Melperone is investigational.,Melperone is a solid.,True
15237,"Manidipine (INN) is a calcium channel blocker (dihydropyridine type) that is used clinically as an antihypertensive. It is selective for vasculature and does not produce effects on the heart at clinically relevant dosages. For the treatment of hypertension. Manidipine produces vasodilation resulting in lower blood pressure. Contraction of vascular smooth muscle is stimulated by Gq coupled receptors which produce calcium release from the sarcoplasmic reticulum. This is followed by opening of voltage dependent calcium channels and an influx of calcium into the cell ultimately producing contraction. Manidipine binds to and dissociates slowly from L- and T-type voltage dependent calcium channels on smooth muscle cells, blocking the entrance of extracellular calcium into the cell and preventing this contraction. This produces vasodilation which decreases blood pressure. Manidipine produces renal vasodilation and an increase in natriuresis. This likely contributes to the antihypertensive effect by reducing blood volume. Manidipine is selective for the vasculature and does not produce significant effects on the heart or central nervous system at clinically relevant dosages.",The molecular weight is 610.71.,Manidipine has a topological polar surface area of 114.25.,The log p value of  is 7.02.,Manidipine is approved and investigational.,Manidipine is a solid.,True
15238,"Rolapitant is a potent, highly selective, long-acting Neurokinin-1 (NK-1) receptor antagonist approved for the prevention of delayed chemotherapy-induced nausea and vomiting (CINV) in adults. Delayed-phase CINV typically occurs >24 hours after chemotherapy treatment and is principally mediated by Neurokinin-1 and its ligand Substance P, which is released in the gut following chemotherapy administration. Neurokinin-1 is also known as Tachykinin Receptor 1 (TACR1), Neurokinin 1 Receptor (NK1R), and Substance P Receptor (SPR).  This drug is indicated in adults in combination with other antiemetics for the prevention of delayed nausea and vomiting associated with emetogenic chemotherapy. Rolapitant is an orally active, highly selective Neurokinin-1 Receptor (NK1R) antagonist. NK1 receptors are located primarily in the gut and central nervous system and are activated by Substance P following chemotherapy administration. By binding to the NK1 receptor, rolapitant prevents binding of its ligand Substance P, which is released in the gut following chemotherapy administration. ",The molecular weight is 500.48.,Rolapitant has a topological polar surface area of 50.36.,The log p value of  is 4.71.,Rolapitant is approved and investigational.,Rolapitant is a solid.,True
15239,"Levobetaxolol is a beta-blocker used to lower the pressure in the eye to treat conditions such as glaucoma. It was marketed as a 0.5% ophthalmic solution of levobetaxolol hydrochloride under the trade name Betaxon but has been discontinued. Used in the treatment of open-angle glaucoma and ocular hypertension. Levobetaxolol is a selective β1 adrenergic receptor antagonist. It acts to lower intraocular pressure. Levobataxolol is condsidered to be the more active component of the betaxolol racemate. The exact mechanism by which levobetaxolol lowers intraocular pressure is not known. It it thought that antagonism of β-adrenergic receptors may reduce the production of aqueous humour stimulated via the cyclic adenosine monophosphate-protein kinase A pathway. It is also thought that the vasoconstriction produced by antagonism of β adrenergic receptors reduces blood flow to the eye and therefore the ultrafiltration responsible for aqueous humour production. β1 selective antagonists are less effective than non-selective β adrenergic receptor antagonists because β2 receptors make up the bulk of the population in the eye. They do, however, come with the benefit of reduced respiratory complications.",The molecular weight is 307.43.,Levobetaxolol has a topological polar surface area of 50.72.,The log p value of  is 2.32.,Levobetaxolol is approved and investigational.,Levobetaxolol is a solid.,True
15240,"Ixazomib a second generation proteasome inhibitor (PI) and the first oral PI approved by the FDA in November 2015 for multiple myeloma treatment in combination with 2 other therapies (lenalidomide and dexamethasone) for patients who have received at least 1 prior therapy. It was found to have similar efficacy to bortezomib (the first PI approved for multiple myeloma therapy) in the control of myeloma growth and prevention of bone loss. Ixazomib citrate is marketed by Takeda Pharmaceuticals under the brand name Ninlaro, which is a prodrug that becomes quickly converted to its active metabolite, ixazomib, after administration. Ixazomib is indicated in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received at least one prior therapy.  In vitro studies have shown ixazomib to induce apoptosis in multiple myeloma cells sensitive or resistant to other conventional therapies. In mouse xenograft models, ixazomib induced tumor growth inhibition. Ixazomib is an N-capped dipeptidyl leucine boronic acid which reversibly inhibits the CT-L proteolytic (β5) site of the 20S proteasome. At higher concentrations, ixazomib also seems to inhibit the proteolytic β1 and β2 subunits and to induce accumulation of ubiquitinated proteins. ",The molecular weight is 361.03.,Ixazomib has a topological polar surface area of 98.66.,The log p value of  is 1.1.,Ixazomib is approved and investigational.,Ixazomib is a solid.,True
15241,"Rupatadine is a dual histamine H1 receptor and platelet activating factor receptor antagonist that is used for symptomatic relief in seasonal and perennial rhinitis as well as chronic spontaneous urticaria. It was approved for marketing in Canada under the tradename Rupall and comes in tablet formulation for adult use and liquid formulation for pediatric use. For the symptomatic relief of nasal and non-nasal symptoms of seasonal allergic rhinitis and perennial allergic rhinitis in patients 2 years of age and older. Also used for the symptomatic relief of chronic spontaneous urticaria in patients 2 years of age and older. Rupatadine is an anti allergenic and acts to reduce allergic symptoms like urticaria, rhinorrhea, sneezing and itching. Rupatadine is a dual histamine H1 receptor and platelet activating (PAF) receptor antagonist. During allergic response mast cells undergo degranulation, releasing histamine and other substances. Histamine acts on H1 receptors to produce symptoms of nasal blockage, rhinorhea, itching, and swelling. PAF is produced from phospholipids cleaved by phospholipase A2. It acts to produce vascular leakage which contributes to rhinorhea and nasal blockage. By blocking both the H1 receptor and PAF receptor, rupatidine prevents these mediators from exerting their effects and so reduces the severity of allergic symptoms.",The molecular weight is 415.97.,Rupatadine has a topological polar surface area of 29.02.,The log p value of  is 5.06.,Rupatadine is approved.,Rupatadine is a solid.,True
15242,"Artenimol is an artemisinin derivative and antimalarial agent used in the treatment of uncomplicated *Plasmodium falciparum* infections. It was first authorized for market by the European Medicines Agency in October 2011 in combination with as the product Eurartesim. Artemisinin combination therapy is highly effective against malaria and stongly recommended by the World Health Organization. For the treatment of uncomplicated *Plasmodium falciparum* infection in adults, children, and infants aged 6 months and up weighing over 5 kg. Used in combination with. Artenimol is thought to form a reactive carbon radical intermediate which kills *P. falciparum* through alkylation of a wide array of proteins. Artemisinins, including Artenimol which is a major active metabolite of many artemisinins, are thought to act via a common mechanism. While the exact mechanism of action is not certain, theories exist as to how artemisinins produce their antimalarial effect.",The molecular weight is 284.35.,Artenimol has a topological polar surface area of 57.15.,The log p value of  is 2.45.,Artenimol is experimental and investigational.,Artenimol is a solid.,True
15243,"Encorafenib, also known as _BRAFTOVI_, is a kinase inhibitor. Encorafenib inhibits BRAF gene, which encodes for B-raf protein, which is a proto-oncogene involved in various genetic mutations. This protein plays a role in regulating the MAP kinase/ERK signaling pathway, which impacts cell division, differentiation, and secretion. Mutations in this gene, most frequently the V600E mutation, are the most commonly identified cancer-causing mutations in melanoma, and have been isolated in various other cancers as well, including non-Hodgkin lymphoma, colorectal cancer, thyroid carcinoma, non-small cell lung carcinoma, hairy cell leukemia and adenocarcinoma of the lung. Used in combination with in metastatic melanoma with a BRAF V600E or V600K mutation, as detected by an FDA-approved test. Encorafenib has shown improved efficacy in the treatment of metastatic melanoma. Encorafenib is a kinase inhibitor that specifically targets BRAF V600E, as well as wild-type BRAF and CRAF while tested with in vitro cell-free assays with IC50 values of 0.35, 0.47, and 0.3 nM, respectively. Mutations in the BRAF gene, including BRAF V600E, result in activated BRAF kinases that mahy stimulate tumor cell growth. Encorafenib is able to bind to other kinases in vitro including JNK1, JNK2, JNK3, LIMK1, LIMK2, MEK4, and STK36 and significantly reduce ligand binding to these kinases at clinically achievable concentrations (≤ 0.9 μM).",,,,Encorafenib is approved and investigational.,Encorafenib is a solid.,True
15244,"Lasmiditan is an oral medication used in the termination of migraine headaches that was first approved for use in the United States in October 2019. Lasmiditan is indicated for the acute treatment of migraine with or without aura in adults. Lasmiditan belongs to a new and novel class of acute anti-migraine medications that exert their effects via inhibition of neuronal firing rather than vasoconstriction of cerebral arteries. Lasmiditan appears to have a relatively quick onset of action (an important characteristic in acute migraine treatment) with some patients reporting benefit within 20 minutes. Due to its ability to cause CNS depression (e.g. drowsiness, dizziness), lasmiditan may cause significant driving impairment and patients should be advised not to participate in activities requiring mental alertness for at least 8 hours after dosing. Lasmiditan may carry some potential for abuse and should be used with caution in patients who may be at risk of drug abuse - its controlled substance scheduling is currently under review in the United States by the Drug Enforcement Administration (DEA). The acute treatment of migraine headaches has, in the past, been achieved via constriction of cerebral blood vessels, as the acute dilation of these vessels observed during migraines was thought to be the cause of the associated pain. The neurogenic hypothesis of migraine pathophysiology, an alternative to the vascular hypothesis, suggests that cerebral vasodilation is a secondary mechanism in migraine pathogenesis, and that the main contributor to migraine headache pain is the increased pathogenic firing of trigeminal nerve pathways. ",,,,Lasmiditan is approved and investigational.,Lasmiditan is a solid.,True
15245,Talinolol has been investigated for the basic science of Gastrointestinal Motility Disorder.,The molecular weight is 363.5.,Talinolol has a topological polar surface area of 82.62.,The log p value of  is 3.15.,Talinolol is investigational.,,True
15246,Anisodamine has been investigated for the treatment of Intestinal Diseases.,,,,Anisodamine is investigational.,,True
15247,"Elagolix has been used in trials studying the basic science and treatment of Endometriosis, Folliculogenesis, Uterine Fibroids, Heavy Uterine Bleeding, and Heavy Menstrual Bleeding. As of 24 July 2018, however, the U.S. Food and Drug Administration (FDA) approved AbbVie's elagolix under the brand name Orilissa as the first and only oral gonadotropin-releasing hormone (GnRH) antagonist specifically developed for women with moderate to severe endometriosis pain. Elagolix is a gonadotropin-releasing hormone (GnRH) receptor antagonist indicated for the management of moderate to severe pain associated with endometriosis. During a three menstrual cycle study in healthy women, an elagolix 150 mg once daily regimen and a 200 mg twice daily regimen resulted in an ovulation rate of about 50% and 32%, respectively. In Phase 3 trials in women with endometriosis, elagolix caused a dose-dependent reduction in median estradiol concentrations to approximately 42 pg/mL for the 150 mg once daily regimen and 12 pg/mL for the 200 mg twice daily regimen. Endometriosis develops when tissue that is similar to the kind that is normally located in the uterus starts to grow outside of the uterus. Such growth leads to various symptoms like pain during periods, pelvic pain between periods, and pain during sexual intercourse. The growths themselves are referred to as lesions and frequently develop on the ovaries, fallopian tubes, and other areas around the uterus, including the bowel or bladder. The growth of these lesions is dependent upon the estrogen hormone.",,,,Elagolix is approved and investigational.,Elagolix is a solid.,True
15248,Landiolol has been used in trials studying the treatment of Pharmacokinetics/Dynamics Study.,The molecular weight is 509.6.,Landiolol has a topological polar surface area of 127.82.,The log p value of  is 2.03.,Landiolol is investigational.,,True
15249,"Clascoterone (cortexolone 17α-propionate, CB-03-01) is a novel antagonist of androgen receptors. It binds to androgen receptors with high affinity. By competing with androgens for binding to androgen receptors, clascoterone works by blocking the androgen receptor signalling cascades that promote acne pathogenesis, such as sebaceous gland proliferation, excess sebum production, and inflammatory pathways. In August 2020, FDA approved clascoterone for the first-in-class topical treatment of acne (acne vulgaris) in male and female patients 12 years and older. Clascoterone is also being investigated as a novel treatment for androgenetic alopecia. Clascoterone is indicated for the topical treatment of acne vulgaris in patients 12 years of age and older. Clascoterone exerts anti-androgenic effects by working as an antagonist at androgen receptors (ARs) expressed throughout the skin, including sebaceous glands, sebocytes, and dermal papilla cells. Clascoterone blocks the effects of testosterone and dihydrotestosterone (DHT), which are androgens that bind to the ARs and contribute to the development of androgen-dependent conditions such as acne and alopecia. _In vitro_, the antiandrogenic effects of clascoterone in human primary sebocytes occurred in a dose-dependent manner. Clascoterone mediates selective topical activity by mainly targeting androgen receptors at the site of application. It has limited systemic effects. Acne is a multifactorial skin condition characterized by excess sebum production, epithelial hyperkeratinization, proliferation of the skin commensal bacteria, and inflammation. Circulating and locally synthesized natural ligands, testosterone and dihydrotestosterone (DHT), serve as causative factors in both males and females. Upon binding of DHT, the DHT-androgen receptor complex dimerizes and translocates to the nucleus where it promotes the transcription of genes involved in acne pathogenesis, including proliferation and differentiation of sebocytes, excess sebum production, and inflammatory cytokine production. Clascoterone is a potent antagonist at ARs and competes for androgens in binding to the receptor, thereby inhibiting downstream signalling of ARs that promote acne.",,,,Clascoterone is approved and investigational.,Clascoterone is a solid.,True
15250,"Fedratinib, also known as SAR302503 and TG101348, is a tyrosine kinase inhibitor used to treat intermediate-2 and high risk primary and secondary myelofibrosis. It is an anilinopyrimidine derivative. Fedratinib is indicated to treat adults with primary or secondary myelofibrosis that is either intermediate-2 or high risk. Fedratinib is a kinase inhibitor that inhibits cell division and induces apoptosis. Patients taking fedratinib may experience anemia, thrombocytopenia, gastrointestinal toxicity, hepatic toxicity, or elevated amylase and lipase. These effects should be managed by reducing the dose, temporarily stopping the medication, or providing transfusions on a case by case basis. Fedratinib is an inhibitor of Janus Activated Kinase 2 (JAK2) and FMS-like tyrosine kinase 3. JAK2 is highly active in myeloproliferative neoplasms like myelofibrosis. Fedratinib's inhibition of JAK2 inhibits phosphorylation of signal transducer and activator of transcription (STAT) 3 and 5, which prevents cell division and induces apoptosis.",,,,Fedratinib is approved and investigational.,Fedratinib is a solid.,True
15251,Mizolastine is under investigation in clinical trial NCT01928316 (A Bioequivalence Study of Domestic (Made in China) and Imported Mizolastine Tablets in Healthy Volunteers).,The molecular weight is 432.5.,Mizolastine has a topological polar surface area of 65.76.,The log p value of  is 2.84.,Mizolastine is approved and investigational.,,True
15252,Ritanserin has been used in trials studying the treatment of Cocaine-Related Disorders.,,,,Ritanserin is investigational.,,True
15253,Bucindolol has been investigated in Heart Failure.,,,,Bucindolol is investigational.,,True
15254,"Levosalbutamol, or levalbuterol, is a short-acting β2 adrenergic receptor agonist used in the treatment of asthma and chronic obstructive pulmonary disease (COPD).  Indicated for the management of COPD (chronic obstructive pulmonary disease, also known as chronic obstructive lung disease) and asthma. It acts by relaxing smooth muscle in the bronchial tubes to increase air flow and relieve acute shortness of breath. β2 adrenergic receptors on airway smooth muscle are Gs coupled and their activation by levosalbutamol leads to activation of adenylate cyclase and to an increase in the intracellular concentration of 3',5'-cyclic adenosine monophosphate (cyclic AMP). Increased cyclic AMP activates protein kinase A which itself inhibits the phosphorylation of myosin produces lower intracellular ionic calcium concentrations, inducing muscle relaxation. Increased cyclic AMP concentrations are also associated with the inhibition of the release of mediators from mast cells in the airways, potentially contributing to its benefit in asthma attacks.",The molecular weight is 239.32.,Levosalbutamol has a topological polar surface area of 72.72.,The log p value of  is 0.06.,Levosalbutamol is approved and investigational.,Levosalbutamol is a solid.,True
15255,"Rhein is an anthraquinone metabolite of rheinanthrone and senna glycoside is present in many medicinal plants including Rheum palmatum, Cassia tora, Polygonum multiflorum, and Aloe barbadensis. It is known to have hepatoprotective, nephroprotective, anti-cancer, anti-inflammatory, and several other protective effects. No approved indication. **Liver: **Reverses animal models of non-alcoholic fatty liver disease by lowering liver lipids and reducing inflammation. Also reverses and prevents fibrosis in liver injury. **Liver: **The reversal of non-alcoholic fatty liver disease stems from rhien's lipid lowering and anti-obesity actions which result in an overall decrease in body weight, high density lipoprotein, and low density lipoprotein as well as its anti-inflammatory action. The reversal of hepatic fibrosis is thought to be due to rhien's anti-inflammatory and anti-oxidant action which suppresses the pro-fibrotic signalling from macrophages and further damage from reactive oxygen species respectively. Ultimately this results in reduced expression of alpha-smooth muscle actin (Alpha-SMA) which is indicative of decreased hepatic stellate cell and myofibroblast activation. Rhein also appears to suppress the expression of transforming growth factor-Beta (TGF-Beta) ",,,,Rhein is experimental.,Rhein is a solid.,True
15256,"Ipecac is obtained from the plant _Cephaelis ipecacuanha_ and contains a number of emetic alkaloids including emetine and cephaeline. Ipecac was approved by Health Canada as an OTC but all those products are now discontinued. The FDA does not have currently any approved product containing ipecac, however, ipecac as an ingredient is accepted to be sold over the counter in packages of 1 fluid ounce (30 ml) for the emergency use to cause vomiting in poisoning. Ipecac is indicated as an emetic agent for the induction of vomiting in poisoning victims who ingested systemic poison in order to prevent absorption of the chemicals through the gastrointestinal tract. In low doses, ipecac was also used as an expectorant. An effective and safe dose of ipecac may cause vomiting within 20 minutes of the administration. In prospective studies with children, the mean time to vomit was reported to be of 21.7 minutes. The emetic components of ipecac, emetine and cephaeline, act centrally and locally in the gastrointestinal tract to cause vomiting. The mechanism by which ipecac performs his effect is by irritating the stomach lining and chemically stimulating the chemoreceptor trigger zone.",,,,Ipecac is approved and withdrawn.,Ipecac is a liquid.,True
15257,Esatenolol is a beta blocker.,The molecular weight is 266.34.,Esatenolol has a topological polar surface area of 84.58.,The log p value of  is -0.11.,Esatenolol is experimental.,,True
15258,,The molecular weight is 292.2.,Cloranolol has a topological polar surface area of 41.49.,The log p value of  is 3.36.,Cloranolol is experimental.,,False
15259,Mepindolol is a 2-methyl derivative of pindolol. It is a beta blocker.,The molecular weight is 262.35.,Mepindolol has a topological polar surface area of 57.28.,The log p value of  is 2.17.,Mepindolol is experimental.,,True
15260,Dexchlorpheniramine is a potent S-enantiomer of chlorpheniramine. The salt form dexchlorpheniramine maleate as the active ingredient is available as a prescription drug indicated for adjunctive therapy for allergic and anaphylactic reactions. It is an antihistamine drug with anticholinergic (drying) and sedative actions. It disrupts histamine signaling by competing with histamine for cell receptor sites on effector cells.,The molecular weight is 274.79.,Dexchlorpheniramine has a topological polar surface area of 16.13.,The log p value of  is 3.15.,Dexchlorpheniramine is experimental and investigational.,,True
15261,Epanolol is an beta blocker.,The molecular weight is 369.42.,Epanolol has a topological polar surface area of 114.61.,The log p value of  is 1.04.,Epanolol is experimental.,,True
15262,Tertatolol is a beta blocker.,The molecular weight is 295.44.,Tertatolol has a topological polar surface area of 41.49.,The log p value of  is 3.12.,Tertatolol is experimental.,,True
15263,"Enasidenib is an orally available treatment for the treatment of adult patients with relapsed or refractory acute myeloid leukemia (AML) with specific mutations in the isocitrate dehydrogenase 2 (IDH2) gene, which is a recurrent mutation detected in 12-20% of adult patients with AML. Patients eligible for this treatment are selected by testing the presence of IDH2 mutations in the blood or bone marrow. This small molecule acts as an allosteric inhibitor of mutant IDH2 enzyme to prevent cell growth, and it also has shown to block several other enzymes that play a role in abnormal cell differentiation. First developed by Agios Pharmaceuticals and licensed to Celgene, enasidenib was approved by U.S. Food and Drug Administration on August 1, 2017. Indicated for the treatment of adult patients with relapsed or refractory acute myeloid leukemia (AML) with an isocitrate dehydrogenase-2 (IDH2) mutation. In a study involving adult patients with relapsed or refractory AML, overall response rate of 40.3% was achieved in enasidenib therapy which was associated with cellular differentiation and maturation, typically without evidence of aplasia. Enasidenib is not shown to cause QTc prolongation.  Enasidenib is a selective inhibitor of IDH2, a mitochondria-localized enzyme involved in diverse cellular processes, including adaptation to hypoxia, histone demethylation and DNA modification. Wild-type IDH proteins play a cruicial role in the Krebs/citric acid cycle where it catalyzes the oxidative decarboxylation of isocitrate to α-ketoglutarate. In comparison, mutant forms of IDH2 enzyme mediates a neomorphic activity and catalyze reduction of α-KG to the (R) enantiomer of 2-hydroxyglutarate, which is associated with DNA and histone hypermethylation, altered gene expression and blocked cellular differentiation of hematopoietic progenitor cells. Enasidenib primarily targets the mutant IDH2 variants R140Q, R172S, and R172K with higher potency than the wild type enzyme form. Inhibition of the enzyme leads to decreased levels of 2-hydroxyglutarate (2-HG) and promotion of proper differentiation and clonal proliferation of cells of the myeloid lineage. ",The molecular weight is 473.38.,Enasidenib has a topological polar surface area of 108.74.,The log p value of  is 3.76.,Enasidenib is approved and investigational.,Enasidenib is a solid.,True
15264,"Black cohosh (_Actaea racemosa_ or _Cimicifuga racemosa_), a member of the buttercup family, is a perennial plant which native to North America. Historical names for this plant include snakeroot, black bugbane, rattleweed, macrotys, and rheumatism weed. Black cohosh has a long history of use. Native Americans used it for its purported benefits in treating musculoskeletal pain, fever, cough, pneumonia, sluggish labor, and menstrual irregularities. European settlers were said to use black cohosh as a tonic to support female reproductive health. Treatment of menopausal symptoms and menstrual dysfunction. This agent is purported to relieve some of the vasomotor symptoms of menopause, including hot flashes and night sweats. Although the mechanism by which black cohosh relieves menopausal symptoms is unknown, several hypotheses have been made. It is believed to act through the following mechanisms/effects:",,,,Black cohosh is experimental.,Black cohosh is a liquid.,True
15265,"5-methoxy-N,N-dimethyltryptamine (5-MeO-DMT) is a tryptamine with psychedelic properties. It is found in a wide variety of plant species, and a single psychoactive toad species, the Colorado River toad. This drug, as well as and , have been registered to be used in South America in religious and spiritual rituals.",,,,"5-methoxy-N,N-dimethyltryptamine is experimental and illicit.","5-methoxy-N,N-dimethyltryptamine is a solid.",True
15266,"Clinafloxacin is a fluoroquinolone antibacterial currently under research. It has been proven to present good antibiotic properties. However, its approval and release have been halted due to the presence of serious side effects.",The molecular weight is 365.79.,Clinafloxacin has a topological polar surface area of 86.87.,The log p value of  is -0.42.,Clinafloxacin is investigational.,Clinafloxacin is a solid.,True
15267,"Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative agent of coronavirus disease 2019 (COVID-19), which is a respiratory disease that is capable of progressing to viral pneumonia and acute respiratory distress syndrome (ARDS); COVID-19 can be fatal. Like other RNA viruses, SARS-CoV-2 depends on an RNA-dependent RNA polymerase (RdRp) enzyme complex for genomic replication, which can be inhibited by a class of drugs known as nucleoside analogues. Remdesivir is indicated for the treatment of adult and pediatric patients aged 12 years and over weighing at least 40 kg for coronavirus disease 2019 (COVID-19) infection requiring hospitalization. Under this indication, remdesivir should only be administered in a hospital or other healthcare setting capable of providing acute care comparable to an inpatient hospital setting. Remdesivir is a nucleoside analog used to inhibit the action of RNA polymerase. The duration of action is moderate, as it is given once daily. Due to much higher selectivity of mammalian DNA and RNA polymerases, including human mitochondrial RNA polymerase, for ATP over remdesivir triphosphate, remdesivir is not a significant inhibitor of these enzymes, which contributes to its overall tolerability and safety profile. Despite this, remdesivir carries risks for hypersensitivity reactions, including anaphylaxis and other infusion-related reactions, elevated transaminase levels, and potential decreased efficacy when combined with or. COVID-19 is caused by the positive-sense RNA virus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Replication of the viral genome is a key step in the infectious cycle of RNA viruses, including those of the _Filoviridae_, _Paramyxoviridae_, _Pneumoviridae_, and _Coronaviridae_ families, and is carried out by viral RNA-dependent RNA polymerase (RdRp) enzymes or enzyme complexes. For both SARS-CoV and SARS-CoV-2, the RdRp comprises nsp7, nsp8, and nsp12 subunits under physiological conditions, although functional RdRp complexes can be reassembled _in vitro_ that incorporate only the nsp8 and nsp12 subunits, similar to the Middle East respiratory syndrome coronavirus (MERS-CoV).",,,,Remdesivir is approved and investigational.,Remdesivir is a solid.,True
15268,"Severe acute pain occurs through nociceptive signalling involving both ascending and descending spinal pathways, in which nerve conductance is mediated in part by the action of opioid receptors. Opioid receptors are seven-transmembrane G-protein-coupled receptors (GPCRs), of which the μ-opioid receptor subtype is predominantly targeted by and is responsible for the effects of opioid agonists. However, due to the ability of some opioid agonists to bind to other targets, as well as activation of additional downstream pathways from opioid receptors such as those involving β-arrestin, the beneficial analgesic effects of opioids are coupled with severe adverse effects such as constipation and respiratory depression. Oliceridine is indicated for the management of acute pain in adults severe enough to require intravenous opioid analgesics and for whom no acceptable alternative treatments exist. Oliceridine is a biased μ-opioid receptor agonist that acts through downstream signalling pathways to exert antinociceptive analgesia in patients experience severe acute pain. Results from multiple clinical studies and simulation data demonstrate that oliceridine exerts significant analgesic benefits within 5-20 minutes following administration but dissipates quickly with a half-life between one and three hours. Despite an improved adverse effect profile over conventional opioids, oliceridine carries important clinical warnings. Oliceridine has the potential to cause severe respiratory depression, especially in patients who are elderly, cachectic, debilitated, or who otherwise have chronically impaired pulmonary function. In addition, severe respiratory depression or sedation may occur in patients with increased intracranial pressure, head injury, brain tumour, or impaired consciousness. Patients with adrenal insufficiency or severe hypotension may require treatment alterations or discontinuation. Finally, oliceridine has been demonstrated to prolong the QTc interval and has not been properly evaluated beyond a maximum daily dose of 27 mg; it is recommended not to exceed 27 mg per day. Pain perception follows a complex pathway initiated in primary sensory neurons, subsequently transmitted to the spinal cord dorsal horn and through ascending axons to multiple regions within the thalamus, brainstem, and midbrain, and finally relayed through descending signals that either inhibit or facilitate the nociceptive signalling. Opioid receptors are seven-transmembrane G-protein-coupled receptors (GPCRs) that can be divided into μ, κ, δ, and opioid-like-1 (ORL1) subtypes,. However, the μ-opioid receptor is predominantly targeted by and is responsible for the effects of traditional opioids. GPCRs in the inactive state are bound intracellularly by a complex consisting of a G<sub>α</sub>, β, and γ subunit together with guanosine diphosphate (GDP). Activation of the GPCR through extracellular agonist binding catalyzes the replacement of GDP with guanosine triphosphate (GTP), dissociation of both G<sub>α</sub>-GTP and a βγ heterodimer, and subsequent downstream effects.",,,,Oliceridine is approved and investigational.,Oliceridine is a solid.,True
15269,"Upadacitinib is an oral Janus kinase (JAK)1-selective inhibitor and a disease-modifying antirheumatic drug (DMARD) used in the treatment of rheumatoid arthritis to slow down disease progression. Rheumatoid arthritis is a chronic autoimmune inflammatory disease affecting the peripheral joints. It is characterized by synovial inflammation and hyperplasia, autoantibody production, cartilage damage and bone destruction, leading to co-morbidities. Despite a variety of therapeutic agents available for treatment, up to 40% of the patients do not respond to current therapies, including biological therapies. The etiology of the disease is mostly unknown; however, the role of JAK as a driver of immune-mediated conditions was discovered, leading to the use of JAK as therapeutic targets for rheumatoid arthritis. To reduce dose-related toxicity (as seen with some pan-JAK inhibitors) without significantly affecting efficacy, more selective JAK1 inhibitors, upadacitinib and , were developed. Upadacitinib is indicated for the treatment of adults with moderately to severely active rheumatoid arthritis who have had an inadequate response or intolerance to methotrexate. Upadacitinib is a DMARD that works by inhibiting the Janus Kinases (JAKs), which are essential downstream cell signalling mediators of pro-inflammatory cytokines. It is believed that these pro-inflammatory cytokines play a role in many autoimmune inflammatory conditions, such as rheumatoid arthritis. In clinical trials, upadacitinib decreased the activity of pro-inflammatory interleukins, transiently increased the levels of lymphocytes, and insignificantly decreased the levels of immunoglobulins from the baseline. Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory disease that involves the interplay of several mediators, including the immune cells (mainly T- and B-lymphocytes) and pro-inflammatory cytokines, such as the tumour necrosis factor (TNF), transforming growth factor (TGF), and interleukin 6 (IL-6). The Janus Kinase (JAK) family plays an essential role in the normal physiological functions (such as erythropoiesis), but also the signalling of pro-inflammatory cytokines that are implicated in many immune-mediated diseases. The JAK family consists of four isoforms (JAK1, JAK2, JAK3, and Tyrosine Kinase 2) that each interacts with different cytokine receptors and uniquely associates with the intracellular domains of Type I/II cytokine receptors. JAK1 is primarily involved in the signalling transduction pathways of IL-6, IFN and the common γ -chain cytokines, including IL-2 and IL-15. IL-6 has been closely studied in particular, as it is a major cytokine involved in B- and T-cell differentiation and the acute phase response in inflammation.",,,,Upadacitinib is approved and investigational.,Upadacitinib is a liquid.,True
15270,"A vitamin-like antioxidant. For nutritional supplementation, also for treating dietary shortage or imbalance. Lipoic acid (or &alpha;-lipoic acid) is able to pass the blood-brain barrier and is putatively used for detoxification of mercury attached to the brain cells. It can mobilise bound mercury into the blood stream as it is a mercaptan (sulfur compound which readily binds to the mercury). In the blood stream, another chelator such as dimercaptosuccinic acid (DMSA) or methylsulfonylmethane (MSM) is used to transfer mercury safely into the urine for excretion. Neither DMSA nor MSM can cross the blood-brain barrier, which is why both lipoic acid and DMSA are used. It is hypothesized that this treatment-along with carnitine, dimethylglycine (DMG), Vitamin B6, folic acid, and magnesium&mdash;could be used to treat autism and amalgam poisoning. In this hypothesis, the reason why autism is difficult to treat is that mercury is attached to the brain cells and most medicines and vitamin supplements do not penetrate the blood-brain barrier. However, &alpha;-lipoic acid and perhaps vitamin B12 could making it possible for other chelators to remove mercury safely out of the body and could perhaps one day be used as a treatment for autism. Because lipoic acid is related to cellular uptake of glucose and it is both soluble in water and fat, it is being used for treatment in diabetes. It may be helpful for people with Alzheimer's disease or Parkinson's disease. Lipoic Acid is generally involved in oxidative decarboxylations of keto acids and is presented as a growth factor for some organisms. Lipoic acid exists as two enantiomers, the R-enantiomer and the S-enantiomer. Normally only the R-enantiomer of an amino acid is biologically active, but for lipoic acid the S-enantiomer assists in the reduction of the R-enantiomer when a racemic mixture is given. Some recent studies have suggested that the S-enantiomer in fact has an inhibiting effect on the R-enantiomer, reducing its biological activity substantially and actually adding to oxidative stress rather than reducing it. Furthermore, the S-enantiomer has been found to reduce the expression of GLUT-4s in cells, responsible for glucose uptake, and hence reduce insulin sensitivity.",,,,Lipoic acid is approved and investigational and nutraceutical.,Lipoic acid is a solid.,True
15271,"Mitomycin is an antineoplastic antibiotic first isolated by Japanese microbiologists in the 1950s from cultures of _Streptomyces caespitosus_. It is an alkylating agent that inhibits DNA synthesis (and, at higher concentrations, RNA and protein synthesis) by cross-linking the complementary strands of the DNA double helix. Few other antibiotics have been discovered that work via this alkylating mechanism, making mitomycin relatively unique in the space of microbiota-derived therapies. For treatment of malignant neoplasm of lip, oral cavity, pharynx, digestive organs, peritoneum, female breast, and urinary bladder. Also used as an adjunct to ab externo glaucoma surgery. Mitomycin is also indicated as a pyelocalyceal solution for the treatment of adults with low-grade upper tract urothelial cancer (LG-UTUC). Mitomycin is one of the older chemotherapy drugs, which has been around and in use for decades. It is an antibiotic which has been shown to have antitumor activity. Mitomycin selectively inhibits the synthesis of deoxyribonucleic acid (DNA). The guanine and cytosine content correlates with the degree of mitomycin-induced cross-linking. At high concentrations of the drug, cellular RNA and protein synthesis are also suppressed. Mitomycin has been shown <i>in vitro</i> to inhibit B cell, T cell, and macrophage proliferation and impair antigen presentation, as well as the secretion of interferon gamma, TNFa, and IL-2. Mitomycin is activated in vivo to a bifunctional and trifunctional alkylating agent. Binding to DNA leads to cross-linking and inhibition of DNA synthesis and function. Mitomycin is cell cycle phase-nonspecific.",The molecular weight is 334.33.,Mitomycin has a topological polar surface area of 146.89.,The log p value of  is -1.35.,Mitomycin is approved.,Mitomycin is a solid.,True
15272,"Nilutamide is an antineoplastic hormonal agent primarily used in the treatment of prostate cancer. Nilutamide is a pure, nonsteroidal anti-androgen with affinity for androgen receptors (but not for progestogen, estrogen, or glucocorticoid receptors). Consequently, Nilutamide blocks the action of androgens of adrenal and testicular origin that stimulate the growth of normal and malignant prostatic tissue. Prostate cancer is mostly androgen-dependent and can be treated with surgical or chemical castration. To date, antiandrogen monotherapy has not consistently been shown to be equivalent to castration. For use in combination with surgical castration for the treatment of metastatic prostate cancer involving distant lymph nodes, bone, or visceral organs (Stage D2). Nilutamide is an antineoplastic hormonal agent primarily used in the treatment of prostate cancer. Nilutamide is a pure, nonsteroidal anti-androgen with affinity for androgen receptors (but not for progestogen, estrogen, or glucocorticoid receptors). Consequently, Nilutamide blocks the action of androgens of adrenal and testicular origin that stimulate the growth of normal and malignant prostatic tissue. Prostate cancer is mostly androgen-dependent and can be treated with surgical or chemical castration. To date, antiandrogen monotherapy has not consistently been shown to be equivalent to castration. The relative binding affinity of nilutamide at the androgen receptor is less than that of bicalutamide, but similar to that of hydroxuflutamide. Nilutamide competes with androgen for the binding of androgen receptors, consequently blocking the action of androgens of adrenal and testicular origin that stimulate the growth of normal and malignant prostatic tissue. This blockade of androgen receptors may result in growth arrest or transient tumor regression through inhibition of androgen-dependent DNA and protein synthesis.",The molecular weight is 317.22.,Nilutamide has a topological polar surface area of 92.55.,The log p value of  is 1.71.,Nilutamide is approved and investigational.,Nilutamide is a solid.,True
15273,"Nitrofurantoin is a nitrofuran antibiotic used to treat uncomplicated urinary tract infections. Nitrofurantoin is converted by bacterial nitroreductases to electrophilic intermediates which inhibit the citric acid cycle as well as synthesis of DNA, RNA, and protein. This drug is more resistant to the development of bacterial resistance because it acts on many targets at once. Nitrofurantoin is a second line treatment to /. Nitrofurantoin is indicated to treat acute uncomplicated urinary tract infections. Nitrofurantoin interferes with vital processes in bacteria, which leads to their death. Nitrofurantoin rapidly reaches therapeutic concentrations in the urine and is also cleared rapidly. Nitrofurantoin is converted by bacterial nitroreductases to electrophilic intermediates which inhibit the citric acid cycle as well as synthesis of DNA, RNA, and protein.",The molecular weight is 238.16.,Nitrofurantoin has a topological polar surface area of 120.73.,The log p value of  is -0.47.,Nitrofurantoin is approved and vet_approved.,Nitrofurantoin is a solid.,True
15274,"A sympathomimetic agent with properties similar to dextroamphetamine. It is used in the treatment of obesity. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1222) For the management of exogenous obesity as a short term adjunct (a few weeks) in a regimen of weight reduction based on caloric restriction Benzphetamine, a phenylalkylamin, is related to amphetamine both chemically and pharmacologically. It is an anorectic agent indicated in the management of exogenous obesity as a short term adjunct (a few weeks) in a regimen of weight reduction based on caloric restriction. Benzphetamine is a sympathomimetic amine with pharmacologic activity similar to the prototype drugs of this class used in obesity, the amphetamines. Actions include central nervous system stimulation and elevation of blood pressure. Tachyphylaxis and tolerance have been demonstrated with all drugs of this class in which these phenomena have been looked for. The mechanism of action of these drugs is not fully understood, however it may be similar to that of amphetamines. Amphetamines stimulate noepinephrine and dopamine release in nerve endings in the lateral hypothalamic feeding centre, decreasing appetite. This release is mediated by the binding of benzphetamine to centrally located adrenergic receptors.",The molecular weight is 239.36.,Benzphetamine has a topological polar surface area of 3.24.,The log p value of  is 4.38.,Benzphetamine is approved and illicit.,Benzphetamine is a solid.,True
15275,A coenzyme for a number of oxidative enzymes including NADH DEHYDROGENASE. It is the principal form in which RIBOFLAVIN is found in cells and tissues.,,,,Flavin mononucleotide is approved and investigational.,Flavin mononucleotide is a solid.,True
15276,"Amrubicin is a third-generation synthetic anthracycline currently in development for the treatment of small cell lung cancer. Pharmion licensed the rights to Amrubicin in November 2006. In 2002, Amrubicin was approved and launched for sale in Japan based on Phase 2 efficacy data in both SCLC and NSCLC. Since January 2005, Amrubicin has been marketed by Nippon Kayaku, a Japanese pharmaceutical firm focused on oncology, which licensed Japanese marketing rights from Dainippon Sumitomo, the original developer of Amrubicin. Investigated for use/treatment in lung cancer. The _anthracycline glycoside_ group of antibiotics, which includes amrubicin, represent a group of potent anticancer agents with potent activity against both solid tumors and hematological malignancies. They are the principal subjects of a large number of studies for the treatment of adult and childhood neoplastic diseases. As an anthracycline, amrubicin has antimitotic and cytotoxic activity through a variety of mechanisms of action. Amrubicin is found to form complexes with DNA via intercalation between base pairs, and it inhibits topoisomerase II enzyme activity by stabilizing the DNA-topoisomerase II complex, which prevents the re-ligation portion of the ligation-religation reaction that topoisomerase II normally catalyzes.",The molecular weight is 483.47.,Amrubicin has a topological polar surface area of 176.61.,The log p value of  is 0.03.,Amrubicin is investigational.,Amrubicin is a solid.,True
15277,"Peginterferon alfa-2a is a form of recombinant interferon used as part of combination therapy to treat chronic Hepatitis C, an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Treatment options for chronic Hepatitis C have advanced significantly since 2011, with the development of Direct Acting Antivirals (DAAs) resulting in less use of Peginterferon alfa-2a. Peginterferon alfa-2a is derived from the alfa-2a moeity of recombinant human interferon and acts by binding to human type 1 interferon receptors. Activation and dimerization of this receptor induces the body's innate antiviral response by activating the janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway. Use of Peginterferon alfa-2a is associated with a wide range of severe adverse effects including the aggravation and development of endocrine and autoimmune disorders, retinopathies, cardiovascular and neuropsychiatric complications, and increased risk of hepatic decompensation in patients with cirrhosis. The use of Peginterferon alfa-2a has largely declined since newer interferon-free antiviral therapies have been developed. Peginterferon alfa-2a is indicated for the treatment of HCV in combination with other antiviral drugs in patients over 5 years of age with compensated liver disease. May be used as a monotherapy in patients with contraindications to or significant intolerance to other anti-viral therapies. Peginterferon alfa-2a induces the body's innate antiviral response. Peginterferon alfa-2a is derived from recombinant human interferon's alfa-2a moeity. It binds to and activates human type 1 interferon receptors causing them to dimerize. This activates the JAK/STAT pathway. Activation of the JAK/STAT pathway increases expression of multiple genes in multiple tissues involved in the innate antiviral response.",,,,Peginterferon alfa-2a is approved and investigational.,Peginterferon alfa-2a is a liquid.,True
15278,"Purified, natural (n is for natural) glycosylated human interferon alpha proteins 166 residues For treatment of venereal or genital warts caused by the Human Papiloma Virus Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta.",,,,Interferon alfa-n1 is approved and investigational.,Interferon alfa-n1 is a liquid.,True
15279,"Purified, natural (n is for natural) human interferon alpha proteins (consists of 3 forms or polymorphisms including 2a, 2b and 2c). 166 residues, some are glycosylated (MW range from 16 kD to 27 kD). For the intralesional treatment of refractory or recurring external condylomata acuminata. Interferon alfa-n3 upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin, neopterin and protein kinase R. Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta.",,,,Interferon alfa-n3 is approved and investigational.,Interferon alfa-n3 is a liquid.,True
15280,"Human Interferon gamma-1b (140 residues), produced from E. coli. Production of Actimmune is achieved by fermentation of a genetically engineered Escherichia coli bacterium containing the DNA which encodes for the human protein. Purification of the product is achieved by conventional column chromatography.  Interferon gamma-1b is used for the treatment of Chronic granulomatous disease and Osteopetrosis. IFN gamma stimulates expression of the immunoglobulin heavy chain C gamma 3 and C gamma 2a germline transcripts in B cells. Many components of the antigen presentation pathways are also up-regulated by interferon gamma. It is also a potent activator of macrophages, it has antiproliferative effects on transformed cells and it can potentiate the antiviral and antitumor effects of type I interferons. Interferon gamma may also help the body regulate the activity of fibroblasts. By directly blocking the multiplication of fibroblasts and inhibiting the production and action of TGF-b, a potent scar-inducing molecule, Interferon gamma-1b may prevent excessive scarring. Binds directly to the type II interferon gamma receptor IFNGR1, leading to a complex of IFNGR1 and IFNGR2. This activates JAK1 and JAK2 kinases which form a STAT1 docking site. This leads to STAT1 phosphorylation, nuclear translocation and initiation of gene transcription of multiple immune-related genes.",,,,Interferon gamma-1b is approved and investigational.,Interferon gamma-1b is a liquid.,True
15281,"Interferon a (human leukocyte protein moiety reduced). A type I interferon consisting of 165 amino acid residues with lysine in position 23. This protein is produced by recombinant DNA technology and resembles interferon secreted by leukocytes. It is used extensively as an antiviral or antineoplastic agent. An oral form is being developed by Amarillo Biosciences. For the treatment of chronic hepatitis C, hairy cell leukemia, AIDS-related Kaposi's sarcoma, and chronic myelogenous leukemia. Also for the treatment of oral warts arising from HIV infection. Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta.",,,,"Interferon alfa-2a, Recombinant is approved and investigational.","Interferon alfa-2a, Recombinant is a liquid.",True
15282,"Insulin lispro is a rapid-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Insulin is prescribed for the management of diabetes mellitus to mimic the activity of endogenously produced human insulin, a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin lispro is indicated to improve glycemic control in adults and children with diabetes mellitus.  Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin lispro is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin lispro is 10-15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 4-5 hours. Compared to regular human insulin, insulin lispro has a more rapid onset of action and a shorter duration of action. Insulin lispro is also shown to be equipotent to human insulin on a molar basis.  Insulin lispro binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Reversal of the proline and lysine residues at positions B28 and B29 of native insulin eliminates hydrophobic interactions and weakens some of the hydrogen bonds that contribute to the stability of the insulin dimers that comprise insulin hexamers. Hexamers of insulin lispro are produced in the presence of zinc and <i>m</i>-cresol. These weakly associated hexamers quickly dissociate upon subcutaneous injection and are absorbed as monomers through vascular endothelial cells. These properties give insulin lispro its fast-acting properties. ",The molecular weight is 5807.63.,Insulin lispro has a topological polar surface area of 2299.07.,,Insulin lispro is approved.,Insulin lispro is a liquid.,True
15283,"Insulin glargine is a long-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Insulin is typically prescribed for the management of diabetes mellitus to mimic the activity of endogenously produced human insulin, a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis. Insulin glargine is indicated to improve glycemic control in adults and pediatric patients with type 1 diabetes mellitus and in adults with type 2 diabetes mellitus. Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, the pancreas produces a continuous supply of low levels of basal insulin along with spikes of insulin following meals. Increased insulin secretion following meals is responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin glargine is a long-acting insulin analogue with a flat and predictable action profile. It is used to mimic the basal levels of insulin in diabetic individuals.  Insulin glargine binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signalling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism. Insulin glargine is completely soluble at pH 4, the pH of administered solution, and has low solubility at physiological pH 7.4. Upon subcuteous injection, the solution is neutralized resulting in the formation of microprecipitates. Small amounts of insulin glargine are released from microprecipitates giving the drug a relatively constant concentration over time profile over 24 hours with no pronounced peak. This release mechanism allows the drug to mimic basal insulin levels within the body. ",The molecular weight is 6062.96.,Insulin glargine has a topological polar surface area of 2437.98.,,Insulin glargine is approved.,Insulin glargine is a liquid.,True
15284,"Human interferon beta (166 residues), glycosylated, MW=22.5kD. It is produced by mammalian cells (Chinese Hamster Ovary cells) into which the human interferon beta gene has been introduced. The amino acid sequence is identical to that of natural human interferon beta. For treatment of relapsing/remitting multiple sclerosis, also for condyloma acuminatum Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin and neopterin. Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha.",,,,Interferon beta-1a is approved and investigational.,Interferon beta-1a is a liquid.,True
15285,"Human interferon beta (165 residues), cysteine 17 is substituted with serine. Produced in E. coli, no carbohydrates, MW=18.5kD Interferon beta-1b is a drug used for the treatment of relapsing/remitting multiple sclerosis. It has been shown to slow the advance of the disease as well as to decrease the frequency of attacks. Interferon beta upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Type I interferons also induce the synthesis of several key antiviral mediators including 2'-5' oligoadenylate synthetase (2'-5' A synthetase), beta-2 microglobulin, neopterin and protein kinase R. Interferon beta binds to type I interferon receptors (IFNAR1 and IFNAR2c) which activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon beta binds more stably to type I interferon receptors than interferon alpha.",,,,Interferon beta-1b is approved.,Interferon beta-1b is a liquid.,True
15286,"Interferon alfacon-1 is a recombinant non-naturally occurring type-I interferon. The 166-amino acid sequence of Interferon alfacon-1 was derived by scanning the sequences of several natural interferon alpha subtypes and assigning the most frequently observed amino acid in each corresponding position. Four additional amino acid changes were made to facilitate the molecular construction, and a corresponding synthetic DNA sequence was constructed using chemical synthesis methodology. Interferon alfacon-1 differs from interferon alfa-2b at 20/166 amino acids (88% homology), and comparison with interferon-beta shows identity at over 30% of the amino acid positions. Interferon alfacon-1 is produced in Escherichia coli (E. coli) cells that have been genetically altered by insertion of a synthetically constructed sequence that codes for Interferon alfacon-1. Prior to final purification, Interferon alfacon-1 is allowed to oxidize to its native state, and its final purity is achieved by sequential passage over a series of chromatography columns. This protein has a molecular weight of 19,434 daltons. For the treatment of hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which, upon dimerization, activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription) which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta. The resulting actions include gene transcription, inhibition of cellular growth, alteration of the state of cellular differentiation, interference with oncogene expression, alteration of cell surface antigen expression, increasing phagocytic activity of macrophages, and augmentation of the cytotoxicity of lymphocytes for target cells.",,,,Interferon alfacon-1 is approved and investigational.,Interferon alfacon-1 is a liquid.,True
15287,"Insulin isolated from pig pancreas. Composed of alpha and beta chains, processed from pro-insulin. Forms a hexameric structure. For the treatment of type I and II diabetes mellitus. Insulin is used in the treatment of type I and type II diabetes. The primary activity of insulin is the regulation of glucose metabolism. In muscle and other tissues (except the brain), insulin causes rapid transport of glucose and amino acids intracellularly. It also promotes anabolism, and inhibits protein catabolism. In the liver, insulin promotes the uptake and storage of glucose in the form of glycogen, inhibits gluconeogenesis, and promotes the conversion of excess glucose into fat. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism.",The molecular weight is 5777.6.,Insulin pork has a topological polar surface area of 2278.84.,,Insulin pork is approved.,Insulin pork is a liquid.,True
15288,"Interferon alpha 2b (human leukocyte clone hif-sn 206 protein moiety reduced). A type I interferon consisting of 165 amino acid residues with arginine in position 23. This protein is produced by recombinant DNA technology and resembles interferon secreted by leukocytes. It is used extensively as an antiviral or antineoplastic agent. For the treatment of hairy cell leukemia, malignant melanoma, and AIDS-related Kaposi's sarcoma. Upregulates the expression of MHC I proteins, allowing for increased presentation of peptides derived from viral antigens. This enhances the activation of CD8+ T cells that are the precursors for cytotoxic T lymphocytes (CTLs) and makes the macrophage a better target for CTL-mediated killing. Interferon alpha also induce the synthesis of several key antiviral mediators, including 2'-5' oligoadenylate synthetase (2'-5' A synthetase) and protein kinase R. Interferon alpha binds to type I interferon receptors (IFNAR1 and IFNAR2c) which upon dimerization activate two Jak (Janus kinase) tyrosine kinases (Jak1 and Tyk2). These transphosphorylate themselves and phosphorylate the receptors. The phosphorylated INFAR receptors then bind to Stat1 and Stat2 (signal transducers and activators of transcription)which dimerize and activate multiple (~100) immunomodulatory and antiviral proteins. Interferon alpha binds less stably to type I interferon receptors than interferon beta.",,,,Interferon alfa-2b is approved.,Interferon alfa-2b is a liquid.,True
15289,"Moxifloxacin is a synthetic fluoroquinolone antibiotic agent. Bayer AG developed the drug (initially called BAY 12-8039) and it is marketed worldwide (as the hydrochloride) under the brand name Avelox (in some countries also Avalox) for oral treatment. For the treatment of sinus and lung infections such as sinusitis, pneumonia, and secondary infections in chronic bronchitis. Also for the treatment of bacterial conjunctivitis (pinkeye). Moxifloxacin is a quinolone/fluoroquinolone antibiotic. Moxifloxacin can be used to treat infections caused by the following bacteria: Aerobic Gram-positive microorganisms: <i>Corynebacterium</i> species, <i>Micrococcus luteus</i>, <i>Staphylococcus aureus</i>, <i>Staphylococcus epidermidis</i>, <i>Staphylococcus haemolyticus</i>, <i>Staphylococcus hominis</i>, <i>Staphylococcus warneri</i>, <i>Streptococcus pneumoniae</i>, and <i>Streptococcus viridans</i> group. Aerobic Gram-negative microorganisms: <i>Acinetobacter lwoffii</i>, <i>Haemophilus influenzae</i>, and <i>Haemophilus parainfluenzae</i>. Other microorganisms: <i>Chlamydia trachomatis</i>.<br/>Moxifloxacin is bactericidal and its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Notably the drug has 100 times higher affinity for bacterial DNA gyrase than for mammalian. Moxifloxacin is a broad-spectrum antibiotic that is active against both Gram-positive and Gram-negative bacteria. The bactericidal action of moxifloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV. DNA gyrase is an essential enzyme that is involved in the replication, transcription and repair of bacterial DNA. Topoisomerase IV is an enzyme known to play a key role in the partitioning of the chromosomal DNA during bacterial cell division.",The molecular weight is 401.44.,Moxifloxacin has a topological polar surface area of 82.11.,The log p value of  is -0.08.,Moxifloxacin is approved and investigational.,Moxifloxacin is a solid.,True
15290,"Anagrelide is a platelet-reducing agent used to lower dangerously elevated platelet levels (i.e. to treat thrombocythemia) in patients with myeloproliferative neoplasms. It is an oral imidazoquinazoline that was first approved for use in the US in 1997. It appears to carry a better response rate than other thrombocythemia treatments (e.g. , ) and may be better tolerated. Anagrelide is indicated for the treatment of thrombocythemia, secondary to malignant neoplasms, to reduce platelet count and the associated risk of thrombosis. It is also beneficial in the amelioration of thrombocythemia symptoms including thrombo-hemorrhagic events. Anagrelide decreases platelet counts by suppressing transcription factors necessary for the synthesis and maturation of platelet-producing cells. The drug itself appears to have a relatively short residence time in the body necessitating twice or four times daily dosing. However, given that the pharmacological effect of anagrelide therapy is reliant on a gradual suppression of platelet-producing cells, it may take 7 to 14 days for its administration to be reflected in reduced platelet counts - for this reason any changes to anagrelide doses should not exceed 0.5 mg/day in any one week. The exact mechanism by which anagrelide lowers platelet count is unclear. Evidence from human trials suggests a dose-related suppression of megakaryocyte maturation, the cells responsible for platelet production - blood drawn from patients receiving anagrelide showed a disruption to the post-mitotic phase of megakaryocyte development and a subsequent reduction in their size and ploidy. This may be achieved via indirect suppression of certain transcription factors required for megakaryocytopoeisis, including GATA-1 and FOG-1.",The molecular weight is 256.09.,Anagrelide has a topological polar surface area of 44.7.,The log p value of  is 1.02.,Anagrelide is approved.,Anagrelide is a solid.,True
15291,"Ropinirole, also known as _ReQuip_, is a non-ergoline dopamine agonist used in Parkinson's disease and restless legs syndrome ,. It is manufactured by GlaxoSmithKline Pharmaceuticals.  Ropinirole was initially approved in 1997 by the FDA for the management of Parkinson's disease. In 2005, it was the first drug approved in the US for the management of primary moderate to severe restless legs syndrome. For the treatment of the signs and symptoms of Parkinson's disease and for the treatment of primary moderate-severe restless legs syndrome. **Effects on Parkinson's and restless leg syndrome** Ropinirole is a non-ergoline dopamine agonist. Ropinirole has the highest affinity at the D3 receptors, which are concentrated in the limbic areas of the brain and may be responsible for some of the neuropsychiatric effects. The exact mechanism of action of ropinirole as a treatment for Parkinson’s disease is unknown, however, it is believed to be related to its ability to selectively stimulate dopamine D2 receptors within the caudate-putamen system in the brain. This system affects body movement. Negligible affinity is seen for ropinirole at α2 adrenoreceptors in the periphery and 5HT-1 receptor. Ropinirole has no affinity at the D1-like receptors, benzodiazepine or GABA receptors.",The molecular weight is 260.38.,Ropinirole has a topological polar surface area of 32.34.,The log p value of  is 2.8.,Ropinirole is approved and investigational.,Ropinirole is a solid.,True
15292,"Ropivacaine is an aminoamide local anaesthetic drug commonly marketed by AstraZeneca under the trade name Naropin. It is present as a racemic mixture of the enantiomers containing equal proportions of the “S” and “R” forms. The marketed form contains the single S-enantiomer as the active ingredient. Used in obstetric anesthesia and regional anesthesia for surgery. Ropivacaine, a local anesthetic agent, is indicated for the production of local or regional anesthesia or analgesia for surgery, for oral surgery procedures, for diagnostic and therapeutic procedures, and for obstetrical procedures. Local anesthetics such as Ropivacaine block the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. Specifically, they block the sodium-channel and decrease chances of depolarization and consequent action potentials. In general, the progression of anesthesia is related to the diameter, myelination and conduction velocity of affected nerve fibers.",The molecular weight is 274.41.,Ropivacaine has a topological polar surface area of 32.34.,The log p value of  is 3.16.,Ropivacaine is approved.,Ropivacaine is a solid.,True
15293,"Grepafloxacin is an oral broad-spectrum quinoline antibacterial agent used to treat bacterial infections. Due to the QTc-prolonging potential, as indicated by the changes in the QT interval on the electrocardiogram, and the risk for cardiovascular adverse events, grepafloxacin was withdrawn in the United States. For treatment of adults with mild to moderate infections caused by susceptible strains of <i>Haemophilus influenzae</i>, <i>Streptococcus pneumoniae</i>, or <i>Moraxella catarrhalis</i>. Grepafloxacin has in vitro activity against a wide range of gram-positive and gram-negative aerobic microorganisms, as well as some atypical microorganisms. Grepafloxacin exerts its antibacterial activity by inhibiting bacterial topoisomerase II (DNA gyrase) and topoisomerase IV, essential enzymes for duplication, transcription, and repair of bacterial DNA.",The molecular weight is 359.4.,Grepafloxacin has a topological polar surface area of 72.88.,The log p value of  is 0.29.,Grepafloxacin is approved and investigational and withdrawn.,Grepafloxacin is a solid.,True
15294,"A centerally active cholinesterase inhibitor that has been used to counter the effects of muscle relaxants, as a respiratory stimulant, and in the treatment of Alzheimer's disease and other central nervous system disorders. Tacrine has been discontinued for the United States market. For the palliative treatment of mild to moderate dementia of the Alzheimer's type. Tacrine is a parasympathomimetic- a reversible cholinesterase inhibitor that is indicated for the treatment of mild to moderate dementia of the Alzheimer's type. An early pathophysiological feature of Alzheimer's disease that is associated with memory loss and cognitive deficits is a deficiency of acetylcholine as a result of selective loss of cholinergic neurons in the cerebral cortex, nucleus basalis, and hippocampus. Tacrine is postulated to exert its therapeutic effect by enhancing cholinergic function. This is accomplished by increasing the concentration of acetylcholine at cholinergic synapses through reversible inhibition of its hydrolysis by acetylcholinesterase. If this proposed mechanism of action is correct, tacrine's effect may lessen as the disease progresses and fewer cholinergic neurons remain functionally intact. There is no evidence that tacrine alters the course of the underlying dementing process. The mechanism of tacrine is not fully known, but it is suggested that the drug is an anticholinesterase agent which reversibly binds with and inactivates cholinesterases. This inhibits the hydrolysis of acetylcholine released from functioning cholinergic neurons, thus leading to an accumulation of acetylcholine at cholinergic synapses. The result is a prolonged effect of acetylcholine.",The molecular weight is 198.27.,Tacrine has a topological polar surface area of 38.91.,The log p value of  is 3.27.,Tacrine is approved and investigational and withdrawn.,Tacrine is a solid.,True
15295,"Triamterene (2,4,7-triamino-6-phenylpteridine) is a potassium-sparing diuretic that is used in the management of hypertension. It works by promoting the excretion of sodium ions and water while decreasing the potassium excretion in the distal part of the nephron in the kidneys by working on the lumenal side. Since it acts on the distal nephron where only a small fraction of sodium ion reabsorption occurs, triamterene is reported to have limited diuretic efficacy. Due to its effects on increased serum potassium levels, triamterene is associated with a risk of producing hyperkalemia. Triamterene is a weak antagonist of folic acid, and a photosensitizing drug.  Triamterene is indicated for the treatment of edema associated with congestive heart failure, cirrhosis of the liver, and the nephrotic syndrome; also in steroid-induced edema, idiopathic edema, and edema due to secondary hyperaldosteronism. Triamterene, a relatively weak, potassium-sparing diuretic and antihypertensive, is used in the management of hypertension and edema. It primarily works on the distal nephron in the kidneys; it acts from the late distal tubule to the collecting duct to inhibit Na+ reabsorption and decreasing K+ excretion. As triamterene tends to conserve potassium more strongly than promoting Na+ excretion, it can cause an increase in serum potassium, which may result in hyperkalemia potentially associated with cardiac irregularities. In healthy volunteers administered with oral triamterene, there was an increase in the renal clearnace of sodium and magnesium, and a decrease in the clearance of uric acid and creatinine due to its effect of reducing glomerular filtration renal plasma flow. Triamterene does not affect calcium excretion. In clinical trials, the use of triamterene in combination with hydrochlorothiazide resulted an enhanced blood pressure-lowering effects of hydrochlorothiazide.  Triamterene inhibits the epithelial sodium channels (ENaC) located on the lumenal side in the late distal convoluted tubule and collecting tubule , which are transmembrane channels that normally promotes sodium uptake and potassium secretion. In the late distal tubule to the collecting duct, sodium ions are actively reabsorbed via ENaC on the lumnial membrane and are extruded out of the cell into the peritubular medium by a sodium-potassium exchange pump, the Na-K-ATPase, with water following passively. Triamterene exerts a diuretic effect on the distal renal tubule to inhibit the reabsorption of sodium ions in exchange for potassium and hydrogen ions and its natriuretic activity is limited by the amount of sodium reaching its site of action. Its action is antagonistic to that of adrenal mineralocorticoids, such as aldosterone, but it is not an inhibitor or antagonist of aldosterone. Triamterene maintains or increases the sodium excretionm, thereby increasing the excretion of water, and reduces the excess loss of potassium, hydrogen and chloride ions by inhibiting the distal tubular exchange mechanism. Due to its diuretic effect, triamterene rapidly and reversibly reduces the lumen-negative transepithelial potential difference by almost complete abolition of Na+ conductance without altering K+ conductance. This reduces the driving force for potassium movement into the tubular lumen and thus decreases potassium excretion. Triamterene is similar in action to but, unlike amiloride, increases the urinary excretion of magnesium.",The molecular weight is 253.27.,Triamterene has a topological polar surface area of 129.62.,The log p value of  is 1.61.,Triamterene is approved.,Triamterene is a solid.,True
15296,"An antifungal antibiotic. Griseofulvin may be given by mouth in the treatment of tinea infections. For the treatment of ringworm infections of the skin, hair, and nails, namely: tinea corporis, tinea pedis, tinea cruris, tinea barbae, cradle cap or other conditions caused by <i>Trichophyton</i> or <i>Microsporum</i> fungi. Griseofulvin is a mycotoxic metabolic product of <i>Penicillium spp.</i> It was the first available oral agent for the treatment of dermatophytoses and has now been used for more than forty years. Griseofulvin is fungistatic with in vitro activity against various species of Microsporum Epidermophyton, and Trichophyton. It has no effect on bacteria or on other genera of fungi. Following oral administration, griseofulvin is deposited in the keratin precursor cells and has a greater affinity for diseased tissue. The drug is tightly bound to the new keratin which becomes highly resistant to fungal invasions. Once the keratin-Griseofulvin complex reaches the skin site of action, it binds to fungal microtubules (tubulin) thus altering fungal mitosis. Griseofulvin is fungistatic, however the exact mechanism by which it inhibits the growth of dermatophytes is not clear. It is thought to inhibit fungal cell mitosis and nuclear acid synthesis. It also binds to and interferes with the function of spindle and cytoplasmic microtubules by binding to alpha and beta tubulin. It binds to keratin in human cells, then once it reaches the fungal site of action, it binds to fungal microtubes thus altering the fungal process of mitosis.",The molecular weight is 352.77.,Griseofulvin has a topological polar surface area of 71.06.,The log p value of  is 2.05.,Griseofulvin is approved and investigational and vet_approved.,Griseofulvin is a solid.,True
15297,"Secobarbital (marketed by Eli Lilly and Company under the brand names Seconal and Tuinal) is a barbiturate derivative drug with anaesthetic, anticonvulsant, sedative and hypnotic properties. It is commonly known as quinalbarbitone in the United Kingdom. For the Short-term treatment of intractable insomnia for patients habituated to barbiturates Secobarbital, a barbiturate, is used for the induction of anesthesia prior to the use of other general anesthetic agents and for induction of anesthesia for short surgical, diagnostic, or therapeutic procedures associated with minimal painful stimuli. Little analgesia is conferred by barbiturates; their use in the presence of pain may result in excitation. Secobarbital binds at a distinct binding site associated with a Cl<sup>-</sup> ionopore at the GABA<sub>A</sub> receptor, increasing the duration of time for which the Cl<sup>-</sup> ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.",The molecular weight is 238.29.,Secobarbital has a topological polar surface area of 75.27.,The log p value of  is 2.16.,Secobarbital is approved and vet_approved.,Secobarbital is a solid.,True
15298,"An antibiotic that is produced by Stretomyces achromogenes. It is used as an antineoplastic agent and to induce diabetes in experimental animals. For the treatment of malignant neoplasms of pancreas (metastatic islet cell carcinoma). Streptozocin is an antitumour antibiotic consisting of a nitrosourea moiety interposed between a methyl group and a glucosamine. Streptozocin is indicated in the treatment of metastatic islet cell carcinoma of the pancreas. Streptozocin inhibits DNA synthesis in bacterial and mammalian cells. In bacterial cells, a specific interaction with cytosine moieties leads to degradation of DNA. The biochemical mechanism leading to mammalian cell death has not been definitely established; streptozocin inhibits cell proliferation at a considerably lower level than that needed to inhibit precursor incorporation into DNA or to inhibit several of the enzymes involved in DNA synthesis. Although streptozocin inhibits the progression of cells into mitosis, no specific phase of the cell cycle is particularly sensitive to its lethal effects. Although its mechanism of action is not completely clear, streptozocin is known to inhibit DNA synthesis, interfere with biochemical reactions of NAD and NADH, and inhibit some enzymes involved in gluconeogenesis. Its activity appears to occur as a result of formation of methylcarbonium ions, which alkylate or bind with many intracellular molecular structures including nucleic acids. Its cytotoxic action is probably due to cross-linking of strands of DNA, resulting in inhibition of DNA synthesis.",The molecular weight is 265.22.,Streptozocin has a topological polar surface area of 151.92.,The log p value of  is -1.42.,Streptozocin is approved and investigational.,Streptozocin is a solid.,True
15299,"Trimethoprim is an antifolate antibacterial agent that inhibits bacterial dihydrofolate reductase (DHFR), a critical enzyme that catalyzes the formation of tetrahydrofolic acid (THF) - in doing so, it prevents the synthesis of bacterial DNA and ultimately continued bacterial survival. Trimethoprim is often used in combination with due to their complementary and synergistic mechanisms but may be used as a monotherapy in the treatment and/or prophylaxis of urinary tract infections. It is structurally and chemically related to , another antifolate antimicrobial used in the treatment of plasmodial infections. As a monotherapy, trimethoprim is indicated for the treatment of acute episodes of uncomplicated urinary tract infections caused by susceptible bacteria, including _E. coli._, _K. pneumoniae_, _Enterobacter spp._, _P. mirabilis_, and coagulase-negative _Staphylococcus_ species. In various formulations in combination with , trimethoprim is indicated for the following infections caused by bacteria with documented susceptibility: urinary tract infections, acute otitis media in pediatric patients (when clinically indicated), acute exacerbations of chronic bronchitis in adults, enteritis caused by susceptible _Shigella_, prophylaxis and treatment of _Pneumocystis jiroveci_ pneumonia, and travelers' diarrhea caused by enterotoxigenic _E. coli_. Trimethoprim exerts its antimicrobial effects by inhibiting an essential step in the synthesis of bacterial nucleic acids and proteins. It has shown activity against several species of gram-negative bacteria, as well as coagulase-negative _Staphylococcus_ species. Resistance to trimethoprim may arise via a variety of mechanisms, including alterations to the bacterial cell wall, overproduction of dihydrofolate reductase, or production of resistant dihydrofolate reductase. Rarely, trimethoprim can precipitate the development of blood disorders (e.g. thrombocytopenia, leukopenia, etc.) which may be preceded by symptoms such as sore throat, fever, pallor, and or purpura - patients should be monitored closely for the development of these symptoms throught the course of therapy. Trimethoprim is a reversible inhibitor of dihydrofolate reductase, one of the principal enzymes catalyzing the formation of tetrahydrofolic acid (THF) from dihydrofolic acid (DHF). Tetrahydrofolic acid is necessary for the biosynthesis of bacterial nucleic acids and proteins and ultimately for continued bacterial survival - inhibiting its synthesis, then, results in bactericidal activity. Trimethoprim binds with a much stronger affinity to bacterial dihydrofolate reductase as compared to its mammalian counterpart, allowing trimethoprim to selectively interfere with bacterial biosynthetic processes. ",The molecular weight is 290.32.,Trimethoprim has a topological polar surface area of 105.51.,The log p value of  is 0.98.,Trimethoprim is approved and vet_approved.,Trimethoprim is a solid.,True
15300,"A broad-spectrum 6-fluoronaphthyridinone antibacterial agent (fluoroquinolones) structurally related to nalidixic acid. For the treatment of adults (&ge;18 years of age) with the following infections caused by susceptible strains of the designated microorganisms: (1) uncomplicated urethral or cervical gonorrhea due to <i>Neisseria gonorrhoeae</i>, (2) uncomplicated urinary tract infections (cystitis) due to <i>Escherichia coli</i>, <i>Staphylococcus epidermidis</i>, or <i>Staphylococcus saprophyticus</i>, and (3) complicated urinary tract infections due to <i>Escherichia coli</i>, <i>Klebsiella pneumoniae</i>, <i>Proteus mirabilis</i>, <i>Pseudomonas aeruginosa</i>, <i>Staphylococcus epidermidis</i>, or <i>Enterobacter cloacae</i>. Enoxacin is a quinolone/fluoroquinolone antibiotic. Enoxacin is bactericidal and its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Enoxacin is a broad-spectrum antibiotic that is active against both Gram-positive and Gram-negative bacteria. Enoxacin may be active against pathogens resistant to drugs that act by different mechanisms. Enoxacin exerts its bactericidal action via the inhibition of the essential bacterial enzyme DNA gyrase (DNA Topoisomerase II).",The molecular weight is 320.32.,Enoxacin has a topological polar surface area of 85.77.,The log p value of  is -1.6.,Enoxacin is approved and investigational.,Enoxacin is a solid.,True
15301,"A synthetic broad-spectrum fluoroquinolone antibacterial agent active against most gram-negative and gram-positive bacteria. For the treatment of uncomplicated gonococcal urethritis in males and for gram-negative-bacterial infections in the gastrointestinal system and the genitourinary tract. Pefloxacin is a fluoroquinolone antibiotic. Flouroquinolones such as pefloxacin possess excellent activity against gram-negative aerobic bacteria such as <i>E.coli</i> and <i>Neisseria gonorrhoea</i> as well as gram-positive bacteria including <i>S. pneumoniae</i> and <i>Staphylococcus aureus</i>. They also posses effective activity against shigella, salmonella, campylobacter, gonococcal organisms, and multi drug resistant pseudomonas and enterobacter. The bactericidal action of pefloxacin results from interference with the activity of the bacterial enzymes DNA gyrase and topoisomerase IV, which are needed for the transcription and replication of bacterial DNA. DNA gyrase appears to be the primary quinolone target for gram-negative bacteria. Topoisomerase IV appears to be the preferential target in gram-positive organisms. Interference with these two topoisomerases results in strand breakage of the bacterial chromosome, supercoiling, and resealing. As a result DNA replication and transcription is inhibited.",The molecular weight is 333.36.,Pefloxacin has a topological polar surface area of 64.09.,The log p value of  is -0.32.,Pefloxacin is approved.,Pefloxacin is a solid.,True
15302,"A benzimidazole broad-spectrum anthelmintic structurally related to mebendazole that is effective against many diseases. (From Martindale, The Extra Pharmacopoeia, 30th ed, p38) For the treatment of parenchymal neurocysticercosis due to active lesions caused by larval forms of the pork tapeworm, <i>Taenia solium</i> and for the treatment of cystic hydatid disease of the liver, lung, and peritoneum, caused by the larval form of the dog tapeworm, <i>Echinococcus granulosus</i>. Albendazole is a broad-spectrum anthelmintic. The principal mode of action for albendazole is by its inhibitory effect on tubulin polymerization which results in the loss of cytoplasmic microtubules. Albendazole causes degenerative alterations in the tegument and intestinal cells of the worm by diminishing its energy production, ultimately leading to immobilization and death of the parasite. It works by binding to the colchicine-sensitive site of tubulin, thus inhibiting its polymerization or assembly into microtubules. As cytoplasmic microtubules are critical in promoting glucose uptake in larval and adult stages of the susceptible parasites, the glycogen stores of the parasites are depleted. Degenerative changes in the endoplasmic reticulum, the mitochondria of the germinal layer, and the subsequent release of lysosomes result in decreased production of adenosine triphosphate (ATP), which is the energy required for the survival of the helminth. ",The molecular weight is 265.33.,Albendazole has a topological polar surface area of 67.01.,The log p value of  is 3.46.,Albendazole is approved and vet_approved.,Albendazole is a solid.,True
15303,"A naturally occurring furocoumarin compound found in several species of plants, including Psoralea corylifolia. It is a photoactive substance that forms DNA adducts in the presence of ultraviolet A irradiation. For the treatment of psoriasis and vitiligo Methoxsalen selectively inhibits the synthesis of deoxyribonucleic acid (DNA). The guanine and cytosine content correlates with the degree of Methoxsalen-induced cross-linking. At high concentrations of the drug, cellular RNA and protein synthesis are also suppressed. After activation it binds preferentially to the guanine and cytosine moieties of DNA, leading to cross-linking of DNA, thus inhibiting DNA synthesis and function.",The molecular weight is 216.19.,Methoxsalen has a topological polar surface area of 48.67.,The log p value of  is 2.31.,Methoxsalen is approved.,Methoxsalen is a solid.,True
15304,"An alpha-2 selective adrenergic agonist used as an antihypertensive agent.  For management of High blood pressure Guanabenz, a centrally acting &alpha;-2 adrenergic agonist, is indicated for treatment of hypertension. Guanabenz's antihypertensive effect is thought to be due to central alpha-adrenergic stimulation, which results in a decreased sympathetic outflow to the heart, kidneys, and peripheral vasculature in addition to a decreased systolic and diastolic blood pressure and a slight slowing of pulse rate. Chronic administration of guanabenz also causes a decrease in peripheral vascular resistance.",The molecular weight is 231.08.,Guanabenz has a topological polar surface area of 74.26.,The log p value of  is 2.98.,Guanabenz is approved and investigational.,Guanabenz is a solid.,True
15305,"Trovafloxacin is a broad spectrum antibiotic that has been commonly marketed under the brand name Trovan by Pfizer. It exerts its antibacterial activity by inhibiting the uncoiling of supercoiled DNA in various bacteria by blocking the activity of DNA gyrase and topoisomerase IV. It was shown to be more effective against Gram-positive bacteria than Gram-negative bacteria when compared to previous fluoroquinolones. Due to its hepatotoxic potential, trovafloxacin was withdrawn from the market. For treatment of infections caused by susceptible strains of the designated microorganisms in uncomplicated urethral gonorrhea in males and endocervical and rectal gonorrhea in females caused by <i>Neisseria gonorrhoeae</i> as well as non gonoccocal urethritis and cervicitis due to <i>Chlamydia trachomatis</i>. Trovafloxacin is a broad spectrum antibiotic that inhibits DNA supercoiling in various bacteria by blocking the activity of DNA gyrase and topoisomerase IV. It is not used widely due to the risk of hepatotoxicity. It tends to have better gram-positive bacterial coverage and less gram-negative coverage than the previous fluoroquinolones. Mechanism of action of fluoroquinolones including trovafloxacin is different from that of penicillins, cephalosporins, aminoglycosides, macrolides, and tetracyclines. Therefore fluoroquinolones may be active against pathogens that are resistant to these antibiotics. There is no cross-resistance between trovafloxacin and the mentioned classes of antibiotics. The overall results obtained from in vitro synergy studies, testing combinations of trovafloxacin with beta-lactams and aminoglycosides, indicate that synergy is strain specific and not commonly encountered. This agrees with results obtained previously with other fluoroquinolones. Resistance to trovafloxacin in vitro develops slowly via multiple-step mutation in a manner similar to other fluoroquinolones. Resistance to trovafloxacin in vitro occurs at a general frequency of between 1x10<sup>-7</sup> to 10<sup>-10</sup>. Although cross-resistance has been observed between trovafloxacin and some other fluoroquinolones, some microorganisms resistant to other fluoroquinolones may be susceptible to trovafloxacin. Trovafloxacin is a fluoronaphthyridone related to the fluoroquinolones with in vitro activity against a wide range of gram-negative and gram-positive aerobic and anaerobic microorganisms. The bactericidal action of trovafloxacin results from inhibition of DNA gyrase and topoisomerase IV. DNA gyrase is an essential enzyme that is involved in the replication, transcription, and repair of bacterial DNA. Topoisomerase IV is an enzyme known to play a key role in the partitioning of the chromosomal DNA during bacterial cell division.",The molecular weight is 416.36.,Trovafloxacin has a topological polar surface area of 99.76.,The log p value of  is -1.0.,Trovafloxacin is approved and investigational and withdrawn.,Trovafloxacin is a solid.,True
15306,"Tizanidine is a fast-acting drug used for the management of muscle spasm, which may result from the effects of multiple sclerosis, stroke, an acquired brain injury, or a spinal cord injury. It may also be caused by musculoskeletal injury. Regardless of the cause, muscle spasticity can be an extremely painful and debilitating condition.  Tizanidine is indicated for the relief of muscle spasticity, which can interfere with daily activities. The general recommendation is to reserve tizanidine use for periods of time when there is a particular need for relief, as it has a short duration of action.  **A note on spasticity** Tizanidine reduces spasticity by causing presynaptic inhibition of motor neurons via agonist actions at Alpha-2 adrenergic receptor sites.",The molecular weight is 253.71.,Tizanidine has a topological polar surface area of 62.2.,The log p value of  is 2.32.,Tizanidine is approved and investigational.,Tizanidine is a solid.,True
15307,"2-Substituted benzimidazole first introduced in 1962. It is active against a variety of nematodes and is the drug of choice for strongyloidiasis. It has CNS side effects and hepatototoxic potential. (From Smith and Reynard, Textbook of Pharmacology, 1992, p919) For the treatment of strongyloidiasis (threadworm), cutaneous larva migrans (creeping eruption), visceral larva migrans, and trichinosis. Thiabendazole is a fungicide and parasiticide. Thiabendazole is also a chelating agent, which means that it is used medicinally to bind metals in cases of metal poisoning, such as lead poisoning, mercury poisoning or antimony poisoning. Thiabendazole is vermicidal and/or vermifugal against <i>Ascaris lumbricoides</i> (\common roundworm\""), <i>Strongyloides stercoralis</i> (threadworm), <i>Necator americanus</i>, <i>Ancylostoma duodenale</i> (hookworm), <i>Trichuris trichiura</i> (whipworm), <i>Ancylostoma braziliense</i> (dog and cat hookworm), <i>Toxocara canis</i>, <i>Toxocara cati</i> (ascarids), and <i>Enterobius vermicularis</i> (pinworm). Thiabendazole also suppresses egg and/or larval production and may inhibit the subsequent development of those eggs or larvae which are passed in the feces."" The precise mode of action of thiabendazole on the parasite is unknown, but it most likely inhibits the helminth-specific enzyme fumarate reductase.",The molecular weight is 201.25.,Thiabendazole has a topological polar surface area of 41.57.,The log p value of  is 2.36.,Thiabendazole is approved and vet_approved.,Thiabendazole is a solid.,True
15308,"A glutamate antagonist (receptors, glutamate) used as an anticonvulsant (anticonvulsants) and to prolong the survival of patients with amyotrophic lateral sclerosis. Riluzole is marketed as Rilutek by Sanofi. For the treatment of amyotrophic lateral sclerosis (ALS, Lou Gehrig's Disease) Riluzole, a member of the benzothiazole class, is indicated for the treatment of patients with amyotrophic lateral sclerosis (ALS). Riluzole extends survival and/or time to tracheostomy. It is also neuroprotective in various <i>in vivo</i> experimental models of neuronal injury involving excitotoxic mechanisms. The etiology and pathogenesis of amyotrophic lateral sclerosis (ALS) are not known, although a number of hypotheses have been advanced. One hypothesis is that motor neurons, made vulnerable through either genetic predisposition or environmental factors, are injured by glutamate. In some cases of familial ALS the enzyme superoxide dismutase has been found to be defective. The mode of action of riluzole is unknown. Its pharmacological properties include the following, some of which may be related to its effect: 1) an inhibitory effect on glutamate release (activation of glutamate reuptake), 2) inactivation of voltage-dependent sodium channels, and 3) ability to interfere with intracellular events that follow transmitter binding at excitatory amino acid receptors.",The molecular weight is 234.2.,Riluzole has a topological polar surface area of 48.14.,The log p value of  is 3.23.,Riluzole is approved and investigational.,Riluzole is a solid.,True
15309,"Malathion is a parasympathomimetic organophosphate compound that is used as an insecticide for the treatment of head lice. Malathion is an irreversible cholinesterase inhibitor and has low human toxicity. For patients infected with Pediculus humanus capitis (head lice and their ova) of the scalp hair. Malathion is an organophosphate insecticide commonly used to control mosquitos and other flying insects. Pharmaceutically, malathion is used to eliminate head lice. The principal toxicological effect of malathion is cholinesterase inhibition, due primarily to malaoxon and to phosphorus thionate impurities. Malathion is a nonsystemic, wide-spectrum organophosphate insecticide. It inhibits acetylcholinesterase activity of most eukaryotes. Malathion is toxic to aquatic organisms, but has a relatively low toxicity for birds and mammals. The major metabolites of malathion are mono- and di-carboxylic acid derivatives, and malaoxon is a minor metabolite. However, it is malaoxon that is the strongest cholinesterase inhibitor. Cholinesterases catalyze the hydrolysis of the neurotransmitter acetylcholine into choline and acetic acid, a reaction necessary to allow a cholinergic neuron to return to its resting state after activation. Because of its essential function, chemicals that interfere with the action of cholinesterase are potent neurotoxins, causing muscle spasms and ultimately death.",The molecular weight is 330.35.,Malathion has a topological polar surface area of 71.06.,The log p value of  is 2.48.,Malathion is approved and investigational.,Malathion is a liquid.,True
15310,"Nalidixic acid is a synthetic 1,8-naphthyridine antimicrobial agent with a limited bacteriocidal spectrum. It is an inhibitor of the A subunit of bacterial DNA gyrase. For the treatment of urinary tract infections caused by susceptible gram-negative microorganisms, including the majority of <i>E. Coli</i>, <i>Enterobacter</i> species, <i>Klebsiella</i> species, and <i>Proteus</i> species. Nalidixic acid is a quinolone antibacterial agent for oral administration. Nalidixic acid has marked antibacterial activity against gram-negative bacteria including <i>Enterobacter</i> species, <i>Escherichia coli</i>, <i>Morganella Morganii</i>; <i>Proteus Mirabilis</i>, <i>Proteus vulgaris</i>, and <i>Providencia rettgeri</i>. <i>Pseudomonas</i> species are generally resistant to the drug. Nalidixic acid is bactericidal and is effective over the entire urinary pH range. Conventional chromosomal resistance to nalidixic acid taken in full dosage has been reported to emerge in approximately 2 to 14 percent of patients during treatment; however, bacterial resistance to nalidixic acid has not been shown to be transferable via R factor. Evidence exists for Nalidixic acid that its active metabolite, hydroxynalidixic acid, binds strongly, but reversibly, to DNA, interfering with synthesis of RNA and, consequently, with protein synthesis.",The molecular weight is 232.24.,Nalidixic acid has a topological polar surface area of 70.5.,The log p value of  is 1.02.,Nalidixic acid is approved and investigational.,Nalidixic acid is a solid.,True
15311,"Primidone is an anticonvulsant used to treat essential tremor as well as grand mal, psychomotor, and focal epileptic seizures. Primidone was developed by J Yule Bogue and H C Carrington in 1949. Primidone is commonly indicated for the management of grand mal, psychomotor, and focal epileptic seizures. In addition, it has also been studied and utilized as an effective management of essential tremor. Primidone alters sodium and calcium channel transport, reducing the frequency of nerve firing, which may be responsible for its effect on convulsions and essential tremor. Primidone has a wide therapeutic window as doses of 50-1000mg/day were effective. Patients should be counselled regarding the risk of status epilepticus with abrupt cessation of primidone. Primidone and its metabolites, phenobarbital and phenylethylmalonamide (PEMA), are active anticonvulsants. Primidone does not directly interact with GABA-A receptors or chloride channels but phenobarbital does. Primidone alters transmembrane sodium and calcium channel transport, reducing the frequency of nerve firing, which may be responsible for the primidone’s effect on convulsions and essential tremor.",The molecular weight is 218.26.,Primidone has a topological polar surface area of 58.2.,The log p value of  is 0.88.,Primidone is approved and vet_approved.,Primidone is a solid.,True
15312,"A methylxanthine derivative that inhibits phosphodiesterase and affects blood rheology. It improves blood flow by increasing erythrocyte and leukocyte flexibility. It also inhibits platelet aggregation. Pentoxifylline modulates immunologic activity by stimulating cytokine production.  For the treatment of patients with intermittent lameness or immobility arising from chronic occlusive arterial disease of the limbs. Pentoxifylline, a synthetic dimethylxanthine derivative structurally related to theophylline and caffeine, is used in the treatment of peripheral vascular diseases and in the management of cerebrovascular insufficiency, sickle cell disease, and diabetic neuropathy. Pentoxifylline inhibits erythrocyte phosphodiesterase, resulting in an increase in erythrocyte cAMP activity. Subsequently, the erythrocyte membrane becomes more resistant to deformity. Along with erythrocyte activity, pentoxifylline also decreases blood viscosity by reducing plasma fibrinogen concentrations and increasing fibrinolytic activity. It is also a non selective adenosine receptor antagonist.",The molecular weight is 278.31.,Pentoxifylline has a topological polar surface area of 75.51.,The log p value of  is 0.12.,Pentoxifylline is approved and investigational.,Pentoxifylline is a solid.,True
15313,"Rosoxacin is a quinolone derivative antibiotic for the treatment of bacterial infection of respiratory tract, urinary tract, GI, CNS and immuno compromised patients. Rosoxacin is known to be effective against penicillin resistant strains and is a single dose orally administered drug, which avoids all complications of parenteral administration seen with penicillin, especially anaphylactic shock. For the treatment of bacterial infection of respiratory tract, urinary tract, GI, CNS and immuno compromised patients. Rosoxacin is a nonfluorinated quinolone antibiotic. Its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Rosoxacin is a broad-spectrum antibiotic that is active against both Gram-positive and Gram-negative bacteria. Rosoxacin binds to and inhibits the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV, which are required for bacterial DNA replication, transcription, repair, and recombination.",The molecular weight is 294.31.,Rosoxacin has a topological polar surface area of 70.5.,The log p value of  is 2.17.,Rosoxacin is approved and investigational.,Rosoxacin is a solid.,True
15314,"Synthetic antimicrobial related to oxolinic acid and nalidixic acid and used in urinary tract infections. For the treatment of initial and recurrent urinary tract infections in adults caused by the following susceptible microorganisms: <i>Escherichia coli</i>, <i>Proteus mirabilis</i>, <i>Proteus vulgaris</i>, <i>Klebsiella</i> species (including <i>K. pneumoniae</i>), and <i>Enterobacter</i> species. Cinoxacin is a synthetic antibacterial agent with <i>in vitro</i> activity against many gram-negative aerobic bacteria, particularly strains of the Enterobacteriaceae family. Cinoxacin inhibits bacterial deoxyribonucleic acid (DNA) synthesis, is bactericidal, and is active over the entire urinary pH range. Cross resistance with nalidixic acid has been demonstrated. Evidence exists that cinoxacin binds strongly, but reversibly, to DNA, interfering with synthesis of RNA and, consequently, with protein synthesis. It appears to also inhibit DNA gyrase. This enzyme is necessary for proper replicated DNA separation. By inhibiting this enzyme, DNA replication and cell division is inhibited.",The molecular weight is 262.22.,Cinoxacin has a topological polar surface area of 88.43.,The log p value of  is 1.74.,Cinoxacin is approved and investigational and withdrawn.,Cinoxacin is a solid.,True
15315,"An antineoplastic agent. It has significant activity against melanomas. (from Martindale, The Extra Pharmacopoeia, 31st ed, p564). Dacarbazine with Oblimersen is in clinical trials for the treatment of malignant melanoma. For the treatment of metastatic malignant melanoma. In addition, dacarbazine is also indicated for Hodgkin's disease as a secondary-line therapy when used in combination with other antineoplastic agents. Dacarbazine is a synthetic analog of naturally occurring purine precursor 5-amino-1H-imidazole-4-carboxamide (AIC). After intravenous administration of dacarbazine, the volume of distribution exceeds total body water content suggesting localization in some body tissue, probably the liver. Its disappearance from the plasma is biphasic with initial half-life of 19 minutes and a terminal half-life of 5 hours. 1 In a patient with renal and hepatic dysfunctions, the half-lives were lengthened to 55 minutes and 7.2 hours. 1 The average cumulative excretion of unchanged DTIC in the urine is 40% of the injected dose in 6 hours. 1 DTIC is subject to renal tubular secretion rather than glomerular filtration. At therapeutic concentrations dacarbazine is not appreciably bound to human plasma protein. The mechanism of action is not known, but appears to exert cytotoxic effects via its action as an alkylating agent. Other theories include DNA synthesis inhibition by its action as a purine analog, and interaction with SH groups. Dacarbazine is not cell cycle-phase specific.",The molecular weight is 182.19.,Dacarbazine has a topological polar surface area of 99.73.,The log p value of  is 0.47.,Dacarbazine is approved and investigational.,Dacarbazine is a solid.,True
15316,"Famotidine is a competitive histamine-2 (H<sub>2</sub>) receptor antagonist that works to inhibit gastric acid secretion. It is commonly used in gastrointestinal conditions related to acid secretion, such as gastric ulcers and gastroesophageal reflux disease (GERD), in adults and children. Compared to other H<sub>2</sub> receptor antagonists, famotidine displays high selectivity towards this receptor; in a study consisting of healthy volunteers and patients with acid hypersecretory disease, famotidine was about 20 to 50 times more potent at inhibiting gastric acid secretion than and eight times more potent than on a weight basis. Famotidine is used in various over-the-counter and off-label uses. While oral formulations of famotidine are more commonly used, the intravenous solution of the drug is available for use in hospital settings. Famotidine is indicated in pediatric and adult patients (with the bodyweight of 40 kg and above) for the management of active duodenal ulcer (DU), active gastric ulcer, symptomatic non-erosive gastroesophageal reflux disease (GERD), and erosive esophagitis due to GERD, diagnosed by biopsy. Famotidine decreases the production of gastric acid, suppresses acid concentration and pepsin content, and decreases the volume of gastric secretion. Famotidine inhibits both basal and nocturnal gastric acid secretion, as well as acid secretion stimulated by food, caffeine, insulin, and pentagastrin. Histamine acts as a local hormone that stimulates the acid output by parietal cells via a paracrine mechanism. Neuroendocrine cells called enterochromaffin-like (ECL) cells lie close to the parietal cells and regulate the basal secretion of histamine. Histamine release is also promoted from stimulation by acetylcholine and gastrin, a peptide hormone. Gastrin (G) cells release gastrin, which works on CCK<sub>2</sub> receptors on ECL cells. This action promotes the release of histamine from ECL cells. Upon release, histamine acts on H<sub>2</sub> receptors expressed on the basolateral membrane of parietal cells, leading to increased intracellular cAMP levels and activated proton pumps on parietal cells. Proton pump releases more protons into the stomach, thereby increasing the secretion of acid. In conditions that are associated with acid hypersecretion such as ulcers, there is a loss of regulation of acid secretion. Famotidine works on H<sub>2</sub> receptors and blocks the actions of histamine.",The molecular weight is 337.44.,Famotidine has a topological polar surface area of 170.83.,The log p value of  is -0.86.,Famotidine is approved.,Famotidine is a solid.,True
15317,"Alosetron is a 5-HT3 antagonist used only for the management of severe diarrhoea-predominant irritable bowel syndrome (IBS) in women. Alosetron has an antagonist action on the 5-HT3 receptors and thus may modulate serotonin-sensitive gastrointestinal (GI) processes. Alosetron was voluntarily withdrawn from the US market in November 2000 by the manufacturer due to numerous reports of severe adverse effects including ischemic colitis, severely obstructed or ruptured bowel, and death. In June 2002, the FDA approved a supplemental new drug application allowing the remarketing of the drug under restricted conditions of use. Only for the treatment of symptoms of severe diarrhea-predominant irritable bowel syndrome (IBS) in women with chronic symptoms (generally lasting greater than 6 months) who does not present with anatomic or biochemical GI abnormalities and have not responded to conventional therapy. Alosetron is a potent and selective antagonist of the serotonin 5-HT<sub>3</sub> receptor type. Activation of these receptors and the resulting neuronal depolarization affects the regulation of visceral pain, colonic transit, and GI secretions processes that are related to IBS. By blocking these receptors, alosetron is able to effectively control IBS. Alosetron is a potent and selective 5-HT<sub>3</sub> receptor antagonist. 5-HT<sub>3</sub> receptors are nonselective cation channels that are extensively distributed on enteric neurons in the human gastrointestinal tract, as well as other peripheral and central locations. Activation of these channels and the resulting neuronal depolarization affect the regulation of visceral pain, colonic transit and gastrointestinal secretions, processes that relate to the pathophysiology of irritable bowel syndrome (IBS). 5-HT<sub>3</sub> receptor antagonists such as alosetron inhibit activation of non-selective cation channels which results in the modulation of serotonin-sensitive GI motor and sensory processes.",The molecular weight is 294.36.,Alosetron has a topological polar surface area of 53.92.,The log p value of  is 1.74.,Alosetron is approved and withdrawn.,Alosetron is a solid.,True
15318,"Lomefloxacin is a fluoroquinolone antibiotic, used to treat bacterial infections including bronchitis and urinary tract infections (UTIs). Additionally, it has been employed for the prophylaxis of UTIs prior to surgery as well. For the treatment of bacterial infections of the respiratory tract (chronic bronchitis) and urinary tract, and as a pre-operative prophylactic to prevent urinary tract infection caused by: <i>S.pneumoniae</i>, <i>H.influenzae</i>, <i>S.aureus</i>, <i>P.aeruginosa</i>, <i>E. cloacae</i>, <i>P. mirabilis</i>, <i>C. civersus</i>, <i>S. asprphyticus</i>, <i>E.coli</i>, and <i>K.pneumoniae</i>. Lomefloxacin is a fluoroquinolone antibiotic used to treat chronic bronchitis, as well as complicated and uncomplicated urinary tract infections. It is also used as a prophylactic or preventative treatment to prevent urinary tract infections in patients undergoing transrectal or transurethral surgical procedures. Flouroquinolones such as lomefloxacin possess excellent activity against gram-negative aerobic bacteria such as <i>E.coli</i> and <i>Neisseria gonorrhoea</i> as well as gram-positive bacteria including <i>S. pneumoniae</i> and <i>Staphylococcus aureus</i>. They also posses effective activity against shigella, salmonella, campylobacter, gonococcal organisms, and multi drug resistant pseudomonas and enterobacter. Lomefloxacin is a bactericidal fluoroquinolone agent with activity against a wide range of gram-negative and gram-positive organisms. The bactericidal action of lomefloxacin results from interference with the activity of the bacterial enzymes DNA gyrase and topoisomerase IV, which are needed for the transcription and replication of bacterial DNA. DNA gyrase appears to be the primary quinolone target for gram-negative bacteria. Topoisomerase IV appears to be the preferential target in gram-positive organisms. Interference with these two topoisomerases results in strand breakage of the bacterial chromosome, supercoiling, and resealing. As a result DNA replication and transcription is inhibited.",The molecular weight is 351.35.,Lomefloxacin has a topological polar surface area of 72.88.,The log p value of  is -0.11.,Lomefloxacin is approved and investigational.,Lomefloxacin is a solid.,True
15319,"Ramelteon is the first in a new class of sleep agents that selectively binds to the melatonin receptors in the suprachiasmatic nucleus (SCN). It is used for insomnia, particularly delayed sleep onset. Ramelteon has not been shown to produce dependence and has shown no potential for abuse. For the treatment of insomnia characterized by difficulty with sleep onset. Ramelteon is the first selective melatonin agonist. It works by mimicking melatonin (MT), a naturally occuring hormone that is produced during the sleep period and thought to be responsible for the regulation of circadian rhythm underlying the normal sleep-wake cycle. Ramelteon has a high affinity for the MT<sub>1</sub> and MT<sub>2</sub> receptors. The MT<sub>1</sub> and MT<sub>2</sub> receptors are located in the brain's suprachiasmatic nuclei (SCN),which is known as the body's \master clock\"" because it regulates the 24-hour sleep-wake cycle. Ramelteon has an active metabolite that is less potent but circulates in higher concentrations than the parent compound. The metabolite also has weak affinity for the 5HT2b receptor."" Ramelteon is a melatonin receptor agonist with both high affinity for melatonin MT<sub>1</sub> and MT<sub>2</sub> receptors, and lower selectivity for the MT<sub>3</sub> receptor. Melatonin production is concurrent with nocturnal sleep, meaning that an increase in melatonin levels is related to the onset of self-reported sleepiness and an increase in sleep propensity. MT<sub>1</sub> receptors are believed to be responsible for regulation of sleepiness and facilitation of sleep onset, and MT<sub>2</sub> receptors are believed to mediate phase-shifting effects of melatonin on the circadian rhythm. While MT<sub>1</sub> and MT<sub>2</sub> receptors are associated with the sleep-wake cycle, MT<sub>3</sub> has a completely different profile, and therefore is not likely to be involved in the sleep-wake cycle. Remelteon has no appreciable affinity for the gamma-aminobutyric acid (GABA) receptor complex or receptors that bind neuropeptides, cytokines, serotonin, dopamine, norepinephrine, acetylcholine, or opiates.",The molecular weight is 259.35.,Ramelteon has a topological polar surface area of 38.33.,The log p value of  is 2.48.,Ramelteon is approved and investigational.,Ramelteon is a solid.,True
15320,"Frovatriptan is a triptan drug developed by Vernalis for the treatment of migraine headaches, in particular those associated with menstruation. Frovatriptan causes vasoconstriction of arteries and veins that supply blood to the head. For the acute treatment of migraine attacks with or without aura in adults. Frovatriptan is a second generation triptan 5-HT receptor agonist that binds with high affinity for 5-HT<sub>1B</sub> and 5-HT<sub>1D</sub> receptors. It is structurally distinct from, but pharmacologically related to other selective 5-HT<sub>1B/1D</sub> receptor agonists. Frovatriptan has no significant effects on GABA<sub>A</sub> mediated channel activity and has no significant affinity for benzodiazepine binding sites. Frovatriptan is believed to act on extracerebral, intracranial arteries and to inhibit excessive dilation of these vessels in migraine. Research has shown that migraine can be caused by the swelling of blood vessels around the brain. Frovatriptan eases the pain associated with migraine by narrowing these blood vessels. Frovatriptan has one of the highest affinities for the 5-HT<sub>1B</sub> of the second-generation triptan agonists. Three distinct pharmacological actions have been implicated in the antimigraine effect of the triptans: (1) stimulation of presynaptic 5-HT<sub>1D</sub> receptors, which serves to inhibit both dural vasodilation and inflammation; (2) direct inhibition of trigeminal nuclei cell excitability via 5-HT<sub>1B/1D</sub> receptor agonism in the brainstem and (3) vasoconstriction of meningeal, dural, cerebral or pial vessels as a result of vascular 5-HT<sub>1B</sub> receptor agonism.",The molecular weight is 243.31.,Frovatriptan has a topological polar surface area of 70.91.,The log p value of  is 0.72.,Frovatriptan is approved and investigational.,Frovatriptan is a solid.,True
15321,"Levobupivacaine is an amino-amide local anaesthetic drug belonging to the family of n-alkylsubstituted For the production of local or regional anesthesia for surgery and obstetrics, and for post-operative pain management Levobupivacaine, a local anesthetic agent, is indicated for the production of local or regional anesthesia or analgesia for surgery, for oral surgery procedures, for diagnostic and therapeutic procedures, and for obstetrical procedures. Local anesthetics such as Levobupivacaine block the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. In general, the progression of anesthesia is related to the diameter, myelination and conduction velocity of affected nerve fibers. Specifically, the drug binds to the intracellular portion of sodium channels and blocks sodium influx into nerve cells, which prevents depolarization.",The molecular weight is 288.44.,Levobupivacaine has a topological polar surface area of 32.34.,The log p value of  is 3.69.,Levobupivacaine is approved and investigational.,Levobupivacaine is a solid.,True
15322,"A synthetic fluoroquinolone (fluoroquinolones) with broad-spectrum antibacterial activity against most gram-negative and gram-positive bacteria. Norfloxacin inhibits bacterial DNA gyrase. For the treatment of urinary tract infection Norfloxacin is a quinolone/fluoroquinolone antibiotic. Norfloxacin is bactericidal and its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Notably the drug has 100 times higher affinity for bacterial DNA gyrase than for mammalian. The bactericidal action of Norfloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV, which are required for bacterial DNA replication, transcription, repair, and recombination. Norfloxacin is a broad-spectrum antibiotic agent that is shown to be effective against various Gram-positive and Gram-negative bacterial species. The fluorine atom at the 6 position increases potency against gram-negative organisms, and the piperazine moiety at the 7 position is responsible for anti-pseudomonal activity",The molecular weight is 319.34.,Norfloxacin has a topological polar surface area of 72.88.,The log p value of  is -0.78.,Norfloxacin is approved.,Norfloxacin is a solid.,True
15323,"Hesperetin belongs to the flavanone class of flavonoids. Hesperetin, in the form of its glycoside , is the predominant flavonoid in lemons and oranges. For lowering cholesterol and, possibly, otherwise favorably affecting lipids. <i>In vitro</i> research also suggests the possibility that hesperetin might have some anticancer effects and that it might have some anti-aromatase activity, as well as activity again. Hesperetin is a cholesterol lowering flavanoid found in a number of citrus juices. It appears to reduce cholesteryl ester mass and inhibit apoB secretion by up to 80%. Hesperetin may have antioxidant, anti-inflammatory, anti-allergic, hypolipidemic, vasoprotective and anticarcinogenic actions. Hesperetin reduces or inhibits the activity of acyl-coenzyme A:cholesterol acyltransferase genes (ACAT<sub>1</sub> and ACAT<sub>2</sub>) and it reduces microsomal triglyceride transfer protein (MTP) activity. Hesperetin also seems to upregulate the LDL receptor. This leads to the reduced assembly and secretion of apoB-containing lipoproteins and enhanced reuptake of those lipoproteins, thereby lowering cholesterol levels.",The molecular weight is 302.28.,Hesperetin has a topological polar surface area of 96.22.,The log p value of  is 2.29.,Hesperetin is experimental.,Hesperetin is a solid.,True
15324,"Leflunomide is a pyrimidine synthesis inhibitor belonging to the DMARD (disease-modifying antirheumatic drug) class of drugs, which are chemically and pharmacologically very heterogeneous. Leflunomide was approved by FDA and in many other countries (e.g., Canada, Europe) in 1999. For the management of the signs and symptoms of active rheumatoid arthritis (RA) to improve physical function and to slow the progression of structural damage associated with the disease. Has also been used for the prevention of acute and chronic rejection in recipients of solid organ trasnplants and is designated by the FDA as an orphan drug for this use. Leflunomide is a pyrimidine synthesis inhibitor indicated in adults for the treatment of active rheumatoid arthritis (RA). RA is an auto-immune disease characterized by high T-cell activity. T cells have two pathways to synthesize pyrimidines: the salvage pathways and the de novo synthesis. At rest, T lymphocytes meet their metabolic requirements by the salvage pathway. Activated lymphocytes need to expand their pyrimidine pool 7- to 8-fold, while the purine pool is expanded only 2- to 3-fold. To meet the need for more pyrimidines, activated T cells use the de novo pathway for pyrimidine synthesis. Therefore, activated T cells, which are dependent on de novo pyrimidine synthesis, will be more affected by leflunomide's inhibition of dihydroorotate dehydrogenase than other cell types that use the salvage pathway of pyrimidine synthesis. Leflunomide is a prodrug that is rapidly and almost completely metabolized following oral administration to its pharmacologically active metabolite, A77 1726. This metabolite is responsible for essentially all of the drug's activity in-vivo. The mechanism of action of leflunomide has not been fully determined, but appears to primarily involve regulation of autoimmune lymphocytes. It has been suggested that leflunomide exerts its immunomodulating effects by preventing the expansion of activated autoimmune lymphocytes via interferences with cell cycle progression. In-vitro data indicates that leflunomide interferes with cell cycle progression by inhibiting dihydroorotate dehydrogenase (a mitochondrial enzyme involved in de novo pyrimidine ribonucleotide uridine monophosphate (rUMP)synthesis) and has antiproliferative activity. Human dihydroorotate dehydrogenase consists of 2 domains: an α/β-barrel domain containing the active site and an α-helical domain that forms a tunnel leading to the active site. A77 1726 binds to the hydrophobic tunnel at a site near the flavin mononucleotide. Inhibition of dihydroorotate dehydrogenase by A77 1726 prevents production of rUMP by the de novo pathway; such inhibition leads to decreased rUMP levels, decreased DNA and RNA synthesis, inhibition of cell proliferation, and G1 cell cycle arrest. It is through this action that leflunomide inhibits autoimmune T-cell proliferation and production of autoantibodies by B cells. Since salvage pathways are expected to sustain cells arrested in the G1 phase, the activity of leflunomide is cytostatic rather than cytotoxic. Other effects that result from reduced rUMP levels include interference with adhesion of activated lymphocytes to the synovial vascular endothelial cells, and increased synthesis of immunosuppressive cytokines such as transforming growth factor-β (TGF-β). Leflunomide is also a tyrosine kinase inhibitor. Tyrosine kinases activate signalling pathways leading to DNA repair, apoptosis and cell proliferation. Inhibition of tyrosine kinases can help to treating cancer by preventing repair of tumor cells. ",The molecular weight is 270.21.,Leflunomide has a topological polar surface area of 55.13.,The log p value of  is 2.32.,Leflunomide is approved and investigational.,Leflunomide is a solid.,True
15325,"Gemifloxacin is a quinolone antibacterial agent with a broad-spectrum activity that is used in the treatment of acute bacterial exacerbation of chronic bronchitis and mild-to-moderate pneumonia. It is available in oral formulations. Gemifloxacin acts by inhibiting DNA synthesis through the inhibition of both DNA gyrase and topoisomerase IV, which are essential for bacterial growth. For the treatment of bacterial infection caused by susceptible strains such as <i>S. pneumoniae</i>, <i>H. influenzae</i>, <i>H. parainfluenzae</i>, or <i>M. catarrhalis</i>, <i>S. pneumoniae</i> (including multi-drug resistant strains ), <i>M. pneumoniae</i>, <i>C. pneumoniae</i>, or <i>K. pneumoniae</i>. Gemifloxacin is a quinolone/fluoroquinolone antibiotic. Gemifloxacin is bactericidal and its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Notably the drug has 100 times higher affinity for bacterial DNA gyrase than for mammalian. Gemifloxacin is a broad-spectrum antibiotic that is active against both Gram-positive and Gram-negative bacteria. The bactericidal action of gemifloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV, which are required for bacterial DNA replication, transcription, repair, and recombination.",The molecular weight is 389.39.,Gemifloxacin has a topological polar surface area of 121.35.,The log p value of  is -1.25.,Gemifloxacin is approved and investigational.,Gemifloxacin is a solid.,True
15326,"A synthetic fluoroquinolone (fluoroquinolones) antibacterial agent that inhibits the supercoiling activity of bacterial DNA gyrase, halting DNA replication. For the treatment of infections (respiratory tract, kidney, skin, soft tissue, UTI), urethral and cervical gonorrhoea. Ofloxacin is a quinolone/fluoroquinolone antibiotic. Ofloxacin is bactericidal and its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase, which allows the untwisting required to replicate one DNA double helix into two. Notably the drug has 100 times higher affinity for bacterial DNA gyrase than for mammalian. Ofloxacin is a broad-spectrum antibiotic that is active against both Gram-positive and Gram-negative bacteria. Ofloxacin acts on DNA gyrase and toposiomerase IV, enzymes which, like human topoisomerase, prevents the excessive supercoiling of DNA during replication or transcription. By inhibiting their function, the drug thereby inhibits normal cell division.",The molecular weight is 361.37.,Ofloxacin has a topological polar surface area of 73.32.,The log p value of  is -0.51.,Ofloxacin is approved.,Ofloxacin is a solid.,True
15327,"Sparfloxacin is a fluoroquinolone antibiotic indicated for bacterial infections. Sparfloxacin exerts its antibacterial activity by inhibiting DNA gyrase, a bacterial topoisomerase. DNA gyrase is an essential enzyme which controls DNA topology and assists in DNA replication, repair, deactivation, and transcription. For the treatment of adults with the following infections caused by susceptible strains microorganisms: community-acquired pneumonia (caused by <i>Chlamydia pneumoniae</i>, <i>Haemophilus influenzae</i>, <i>Haemophilus parainfluenzae</i>, <i>Moraxella catarrhalis</i>, <i>Mycoplasma pneumoniae</i>, or <i>Streptococcus pneumoniae</i>) and acute bacterial exacerbations of chronic bronchitis (caused by <i>Chlamydia pneumoniae</i>, <i>Enterobacter cloacae</i>, <i>Haemophilus influenzae</i>, <i>Haemophilus parainfluenzae</i>, <i>Klebsiella pneumoniae</i>, <i>Moraxella catarrhalis</i>, <i>Staphylococcus aureus</i>, or <i>Streptococcus pneumoniae</i>). Sparfloxacin is a synthetic fluoroquinolone broad-spectrum antimicrobial agent in the same class as ofloxacin and norfloxacin. Sparfloxacin has in vitro activity against a wide range of gram-negative and gram-positive microorganisms. Sparfloxacin exerts its antibacterial activity by inhibiting DNA gyrase, a bacterial topoisomerase. DNA gyrase is an essential enzyme which controls DNA topology and assists in DNA replication, repair, deactivation, and transcription. Quinolones differ in chemical structure and mode of action from (beta)-lactam antibiotics. Quinolones may, therefore, be active against bacteria resistant to (beta)-lactam antibiotics. Although cross-resistance has been observed between sparfloxacin and other fluoroquinolones, some microorganisms resistant to other fluoroquinolones may be susceptible to sparfloxacin. In vitro tests show that the combination of sparfloxacin and rifampin is antagonistic against Staphylococcus aureus. The bactericidal action of sparfloxacin results from inhibition of the enzymes topoisomerase II (DNA gyrase) and topoisomerase IV, which are required for bacterial DNA replication, transcription, repair, and recombination.",The molecular weight is 392.41.,Sparfloxacin has a topological polar surface area of 98.9.,The log p value of  is -0.6.,Sparfloxacin is approved and investigational and withdrawn.,Sparfloxacin is a solid.,True
15328,"Aminophylline is a drug combination that contains theophylline and ethylenediamine in a 2:1 ratio. Once in the body, theophylline is released and acts as a phosphodiesterase inhibitor, adenosine receptor blocker, and histone deacetylase activator. Similar to other theophyllines, aminophylline is indicated for the treatment of lung diseases such as asthma, chronic bronchitis, and COPD. The majority of aminophylline medications are discontinued and the remaining medications on the market are in short supply. For the treatment of bronchospasm due to asthma, emphysema and chronic bronchitis. Aminophylline is the ethylenediamine salt of theophylline. Theophylline stimulates the CNS, skeletal muscles, and cardiac muscle. It relaxes certain smooth muscles in the bronchi, produces diuresis, and causes an increase in gastric secretion. Aminophylline is the ethylenediamine salt of theophylline. After ingestion, theophylline is released from aminophylline, and theophylline relaxes the smooth muscle of the bronchial airways and pulmonary blood vessels and reduces airway responsiveness to histamine, methacholine, adenosine, and allergen. Theophylline competitively inhibits type III and type IV phosphodiesterase (PDE), the enzyme responsible for breaking down cyclic AMP in smooth muscle cells, possibly resulting in bronchodilation. Theophylline also binds to the adenosine A2B receptor and blocks adenosine mediated bronchoconstriction. In inflammatory states, theophylline activates histone deacetylase to prevent transcription of inflammatory genes that require the acetylation of histones for transcription to begin.",,,,Aminophylline is approved.,Aminophylline is a solid.,True
15329,"Lumiracoxib is a COX-2 selective non-steroidal anti-inflammatory drug (NSAID). On August 11, 2007, Australia's Therapeutic Goods Administration (TGA, the Australian equivalent of the FDA) cancelled the registration of lumiracoxib in Australia due to concerns that it may cause liver failure. New Zealand and Canada have also followed suit in recalling the drug. For the acute and chronic treatment of the signs and symptoms of osteoarthritis of the knee in adults. Lumiracoxib has a different structure from the standard COX-2 inhibitors (e.g. celecoxib). It more closely resembles the structure of diclofenac (one chlorine substituted by fluorine, the phenylacetic acid has another methyl group in meta position), making it a member of the arylalkanoic acid family of NSAIDs. It binds to a different site on the COX-2 receptor than the standard COX-2 inhibitors. It displays extremely high COX-2 selectivity. The mechanism of action of lumiracoxib is due to inhibition of prostaglandin synthesis via inhibition of cyclooygenase-2 (COX-2). Lumiracoxib does not inhibit COX-1 at therapeutic concentrations.",The molecular weight is 293.72.,Lumiracoxib has a topological polar surface area of 49.33.,The log p value of  is 4.51.,Lumiracoxib is approved and investigational.,Lumiracoxib is a solid.,True
15330,"Oxtriphylline is the choline salt form of. Once in the body, theophylline is released and acts as a phosphodiesterase inhibitor, adenosine receptor blocker, and histone deacetylase activator. Its main physiological reponse is to dilate the bronchioles. As such, oxytriphylline is indicated mainly for asthma, bronchospasm, and COPD (i.e. all the same indications as the other theophyllines). It is marketed under the name Choledyl SA, and several forms of oxytriphylline have been discontinued. In the US, oxtriphylline is no longer available. Used to treat the symptoms of asthma, bronchitis, COPD, and emphysema. Oxtriphylline is a bronchodilator. Oxtriphylline works in several ways: it relaxes muscles in your lungs and chest to allow more air in, decreases the sensitivity of your lungs to allergens and other substances that cause inflammation, and increases the contractions of your diaphragm to draw more air into the lungs. Oxtriphylline is a choline salt of theophylline. After ingestion, theophylline is released from oxytriphylline, and theophylline relaxes the smooth muscle of the bronchial airways and pulmonary blood vessels and reduces airway responsiveness to histamine, methacholine, adenosine, and allergen. Theophylline competitively inhibits type III and type IV phosphodiesterase (PDE), the enzyme responsible for breaking down cyclic AMP in smooth muscle cells, possibly resulting in bronchodilation. Theophylline also binds to the adenosine A2B receptor and blocks adenosine mediated bronchoconstriction. In inflammatory states, theophylline activates histone deacetylase to prevent transcription of inflammatory genes that require the acetylation of histones for transcription to begin.",The molecular weight is 283.33.,Oxtriphylline has a topological polar surface area of 66.4.,,Oxtriphylline is approved.,Oxtriphylline is a solid.,True
15331,"Insulin aspart is a rapid-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Insulin is typically prescribed for the management of diabetes mellitus to mimic the activity of endogenously produced human insulin, a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin aspart is indicated to improve glycemic control in adults and children with diabetes mellitus. Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin aspart is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin aspart is 10-15 minutes. Its activity peaks 60-90 minutes following subcutaneous injection and its duration of action is 4-5 hours. Insulin aspart binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the proline residue at B28 with aspartic acid reduces the tendency to form hexamers and results in a faster rate of absorption and onset of action and shorter duration of action. ",The molecular weight is 5825.6.,Insulin aspart has a topological polar surface area of 2345.16.,,Insulin aspart is approved.,Insulin aspart is a liquid.,True
15332,"Insulin glulisine is a short-acting form of insulin used for the treatment of hyperglycemia caused by Type 1 and Type 2 Diabetes. Insulin is typically prescribed for the management of diabetes mellitus to mimic the activity of endogenously produced human insulin, a peptide hormone produced by beta cells of the pancreas that promotes glucose metabolism. Insulin is released from the pancreas following a meal to promote the uptake of glucose from the blood into internal organs and tissues such as the liver, fat cells, and skeletal muscle. Absorption of glucose into cells allows for its transformation into glycogen or fat for storage. Insulin also inhibits hepatic glucose production, enhances protein synthesis, and inhibits lipolysis and proteolysis among many other functions. Insulin glulisine is indicated to improve glycemic control in adults and pediatric patients with diabetes mellitus. Insulin is a natural hormone produced by beta cells of the pancreas. In non-diabetic individuals, a basal level of insulin is supplemented with insulin spikes following meals. Postprandial insulin spikes are responsible for the metabolic changes that occur as the body transitions from a postabsorptive to absorptive state. Insulin promotes cellular uptake of glucose, particularly in muscle and adipose tissues, promotes energy storage via glycogenesis, opposes catabolism of energy stores, increases DNA replication and protein synthesis by stimulating amino acid uptake by liver, muscle and adipose tissue, and modifies the activity of numerous enzymes involved in glycogen synthesis and glycolysis. Insulin also promotes growth and is required for the actions of growth hormone (e.g. protein synthesis, cell division, DNA synthesis). Insulin glulisine is a rapid-acting insulin analogue used to mimic postprandial insulin spikes in diabetic individuals. The onset of action of insulin glulisine is approximately 15 minutes. Its activity peaks 60 minutes following subcutaneous injection and its duration of action is 2-4 hours. Insulin glulisine binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor autophosphorylates and phosphorylates numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. Activation of these proteins leads to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC), both of which play critical roles in metabolism and catabolism. In humans, insulin is stored in the form of hexamers; however, only insulin monomers are able to interact with IR. Substitution of the arginine at position B3 for lysine and replacement of the B29 lysine with glutamic acid decreases the propensity to form hexamers, stabilizes the hormone in monomeric form and results in a rapid rate of absorption and short duration of action. ",The molecular weight is 5822.64.,Insulin glulisine has a topological polar surface area of 2293.28.,,Insulin glulisine is approved.,Insulin glulisine is a liquid.,True
15333,"Rasagiline is an irreversible inhibitor of monoamine oxidase and is used as a monotherapy in early Parkinson's disease or as an adjunct therapy in more advanced cases. For the treatment of the signs and symptoms of idiopathic Parkinsons disease as initial monotherapy and as adjunct therapy to levodopa. Rasagiline is a propargylamine and an irreversible inhibitor of monoamine oxidase (MAO). MAO, a flavin-containing enzyme, regulates the metabolic degradation of catecholamines and serotonin in the CNS and peripheral tissues. It is classified into two major molecular species, A and B, and is localized in mitochondrial membranes throughout the body in nerve terminals, brain, liver and intestinal mucosa. MAO-A is found predominantly in the GI tract and liver, and regulates the metabolic degradation of circulating catecholamines and dietary amines. MAO-B is the major form in the human brain and is responsible for the regulation of the metabolic degradation of dopamine and phenylethylamine. In ex vivo animal studies in brain, liver and intestinal tissues rasagiline was shown to be a potent,selective, and irreversible monoamine oxidase type B (MAO-B) inhibitor. At the recommended therapeutic doses, Rasagiline was also shown to be a potent and irreversible inhibitor of MAO-B in platelets. The selectivity of rasagiline for inhibiting only MAO-B (and not MAO-A) in humans and the sensitivity to tyramine during rasagiline treatment at any dose has not been sufficiently characterized to avoid restriction of dietary tyramine and amines contained in medications. The precise mechanisms of action of rasagiline is unknown. One mechanism is believed to be related to its MAO-B inhibitory activity, which causes an increase in extracellular levels of dopamine in the striatum. The elevated dopamine level and subsequent increased dopaminergic activity are likely to mediate rasagiline's beneficial effects seen in models of dopaminergic motor dysfunction.",The molecular weight is 171.24.,Rasagiline has a topological polar surface area of 12.03.,The log p value of  is 2.34.,Rasagiline is approved.,Rasagiline is a solid.,True
15334,"Temafloxacin is an antibiotic agent belonging to the fluoroquinolone drug class. It was first approved for use in the U.S. market in 1992, but was withdrawn shortly due to the reports of serious adverse reactions, such as allergic reactions and hemolyric anemia, resulting in three deaths. For the treatment of lower respiratory tract infections, genital and urinary infections like prostatitis, and skin infections. Temafloxacin is a fluoroquinolone antibiotic drug, marketed as Omniflox by Abbot Laboratories, which was withdrawn from the market in 1992 due to fatal adverse effects. Flouroquinolones such as lomefloxacin possess excellent activity against gram-negative aerobic bacteria such as <i>E.coli</i> and <i>Neisseria gonorrhoea</i> as well as gram-positive bacteria including <i>S. pneumoniae</i> and <i>Staphylococcus aureus</i>. They also posses effective activity against shigella, salmonella, campylobacter, gonococcal organisms, and multi drug resistant pseudomonas and enterobacter. The bactericidal action of temafloxacin results from interference with the activity of the bacterial enzymes DNA gyrase and topoisomerase IV, which are needed for the transcription and replication of bacterial DNA. DNA gyrase appears to be the primary quinolone target for gram-negative bacteria. Topoisomerase IV appears to be the preferential target in gram-positive organisms. Interference with these two topoisomerases results in strand breakage of the bacterial chromosome, supercoiling, and resealing. As a result DNA replication and transcription is inhibited.",The molecular weight is 417.39.,Temafloxacin has a topological polar surface area of 72.88.,The log p value of  is 0.67.,Temafloxacin is withdrawn.,Temafloxacin is a solid.,True
15335,"Theobromine (3,7-dimethylxanthine) is the principle alkaloid in Theobroma cacao (the cacao bean) and other plants. A xanthine alkaloid that is used as a bronchodilator and as a vasodilator. It has a weaker diuretic activity than theophylline and is also a less powerful stimulant of smooth muscle. It has practically no stimulant effect on the central nervous system. It was formerly used as a diuretic and in the treatment of angina pectoris and hypertension. (From Martindale, The Extra Pharmacopoeia, 30th ed, pp1318-9) theobromine is used as a vasodilator, a diuretic, and heart stimulant. And similar to caffeine, it may be useful in management of fatigue and orthostatic hypotension. Theobromine, a xanthine derivative like caffeine and the bronchodilator theophylline, is used as a CNS stimulant, mild diuretic, and respiratory stimulant (in neonates with apnea of prematurity).  Theobromine stimulates medullary, vagal, vasomotor, and respiratory centers, promoting bradycardia, vasoconstriction, and increased respiratory rate. This action was previously believed to be due primarily to increased intracellular cyclic 3&prime;,5&prime;-adenosine monophosphate (cyclic AMP) following inhibition of phosphodiesterase, the enzyme that degrades cyclic AMP. It is now thought that xanthines such as caffeine and theobromine act as antagonist at adenosine-receptors within the plasma membrane of virtually every cell. As adenosine acts as an autocoid, inhibiting the release of neurotransmitters from presynaptic sites but augmenting the actions of norepinephrine or angiotensin, antagonism of adenosine receptors promotes neurotransmitter release. This explains the stimulatory effects of xanthine derivatives such as theobromine and caffeine. Blockade of the adenosine A1 receptor in the heart leads to the accelerated, pronounced \pounding\"" of the heart upon caffeine intake.""",The molecular weight is 180.17.,Theobromine has a topological polar surface area of 67.23.,The log p value of  is -0.67.,Theobromine is investigational.,Theobromine is a solid.,True
15336,,The molecular weight is 341.42.,Fenethylline has a topological polar surface area of 70.47.,The log p value of  is 1.9.,Fenethylline is experimental.,Fenethylline is a solid.,False
15337,"One of the benzodiazepines that is used in the treatment of anxiety disorders. It is a Schedule IV drug in the U.S. and Canada and under the Convention on Psychotropic Substances. It is a intermediate-acting benzodiazepine. For the short-term treatment of insomnia, short-term treatment of anxiety or panic attacks, if a benzodiazepine is required, and the alleviation of the symptoms of alcohol- and opiate-withdrawal. Bromazepam is a lipophilic, long-acting benzodiazepine and with sedative, hypnotic, anxiolytic and skeletal muscle relaxant properties. It does not possess any antidepressant qualities. Bromazepam, like other benzodiazepines, presents a risk of abuse, misuse, and dependence. According to many psychiatric experts, Bromazepam has a greater abuse potential than other benzodiazepines because of fast resorption and rapid onset of action. Bromazepam binds to the GABA-A receptor producing a conformational change and potentiating its inhibitory effects. Other neurotransmitters are not influenced.",The molecular weight is 316.16.,Bromazepam has a topological polar surface area of 54.35.,The log p value of  is 1.7.,Bromazepam is approved and illicit and investigational.,Bromazepam is a solid.,True
15338,"Deferasirox is an iron chelator and the first oral medication FDA approved for chronic iron overload in patients receiving long term blood transfusions. For the treatment of chronic iron overload due to blood transfusions (transfusional hemosiderosis) in patients 2 years of age and older. Deferasirox is an orally active chelator that is selective for iron (as Fe3+). It is a tridentate ligand that binds iron with high affinity in a 2:1 ratio. Although deferasirox has very low affinity for zinc and copper there are variable decreases in the serum concentration of these trace metals after the administration of deferasirox. The clinical significance of these decreases is uncertain. Two molecules of deferasirox are capable of binding to 1 atom of iron. Deferasirox works in treating iron toxicity by binding trivalent (ferric) iron (for which it has a strong affinity), forming a stable complex which is eliminated via the kidneys.",The molecular weight is 373.37.,Deferasirox has a topological polar surface area of 108.47.,The log p value of  is 3.67.,Deferasirox is approved and investigational.,Deferasirox is a solid.,True
15339,8-azaguanine is one of the early purine analogs showing antineoplastic activity. It functions as an antimetabolite and is easily incorporated into ribonucleic acids.,,,,8-azaguanine is experimental.,8-azaguanine is a solid.,True
15340,"A purine base found in most body tissues and fluids, certain plants, and some urinary calculi. It is an intermediate in the degradation of adenosine monophosphate to uric acid, being formed by oxidation of hypoxanthine. The methylated xanthine compounds caffeine, theobromine, and theophylline and their derivatives are used in medicine for their bronchodilator effects. (Dorland, 28th ed)",,,,Xanthine is experimental.,Xanthine is a solid.,True
15341,,,,,9-Methylguanine is experimental.,9-Methylguanine is a solid.,False
15342,Hypoxanthine is a purine and a reaction intermediate in the metabolism of adenosine and in the formation of nucleic acids by the salvage pathway.,,,,Hypoxanthine is experimental.,Hypoxanthine is a solid.,True
15343,,,,,9-Deazaguanine is experimental.,9-Deazaguanine is a solid.,False
15344,"Belinostat is a novel agent that inhibits the enzyme histone deacetylase (HDAC) with a sulfonamide-hydroxamide structure. It was developed as an orphan drug to target hematological malignancies and solid tumors by TopoTarget. The safety and efficacy of belinostat is currently being evaluated for use in combination with traditional front-line therapies for the treatment of PTCL. Intravenous administration of the agent is available as Beleodaq as monotherapy and the dosing regimen involves a 21-day cycle. It was US-approved in July 2014 as a therapeutic agent for relapsed or refractory peripheral T-cell lymphoma. Belinostat is indicated for the treatment of patients with relapsed or refractory peripheral T-cell lymphoma (PTCL) with manageable safety profile. It is a potential alternative therapy for patients who did not experience adequate response to first-line drugs for PTCL. It can be used in patients with baseline thrombocytopenia.  Beleodaq is a histone deacetylase (HDAC) inhibitor that exhibits pan-HDAC inhibition and potent growth inhibitory and pro-apoptotic activities in a variety of tumor cells, including PTCL cells, at nanomolar concentrations. None of the trials show any clinically relevant changes caused by Beleodaq on heart rate, PR duration or QRS duration as measures of autonomic state, atrio-ventricular conduction or depolarization; there were no cases of Torsades de Pointes. Belinostat inhibits the activity of histone deacetylase (HDAC) thus prevents the removal of acetyl groups from the lysine residues of histones and some non-histone proteins. In vitro, belinostat caused the accumulation of acetylated histones and other proteins, increased the expression of tumor-suppressor genes. It ultimately induces cell cycle arrest, inhibition of angiogenesis and/or apoptosis of some transformed cells. ",,,,Belinostat is approved and investigational.,Belinostat is a solid.,True
15345,"NN344 is a neutral, soluble long-acting human insulin analogue with 24 hour coverage by once daily injection. NN344 has a very flat and predictable action profile. The product is intended for basal insulin treatment of diabetes mellitus. Investigated for use/treatment in diabetes mellitus type 1 and 2. NN344 binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of NN344 to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism.",,,,NN344 is investigational.,NN344 is a solid.,True
15346,"Natural interferon alpha or Multiferon is obtained from the leukocyte fraction of human blood following induction with Sendai virus. Interferon alfa contains several naturally occurring IFN-α subtypes and is purified by affinity chromatography. Interferon alpha proteins are mainly involved in innate immune response against viral infection. They come in 13 subtypes that are called IFNA1, IFNA2, IFNA4, IFNA5, IFNA6, IFNA7, IFNA8, IFNA10, IFNA13, IFNA14, IFNA16, IFNA17, IFNA21. Multiferon consists of the 6 major subtypes are IFN-α1, IFN-α2, IFN-α8, IFN-α10, IFN-α14 and IFN-α21. Of these, IFN-α2 and IFN-α14 are glycosylated. Investigated for use/treatment in hepatitis (viral, C), leukemia (lymphoid), leukemia (myeloid), leukemia (unspecified), and melanoma. Natural alpha interferon offers multiple subtypes of interferon which may work together as a 'cocktail-in-one', while recombinant versions only exhibit a single subtype.\ Viragen offers MultiferonT at a cost which is competitive with recombinant interferon regimens.""",,,,Interferon alfa is investigational.,Interferon alfa is a liquid.,True
15347,"Albumin-interferon alpha (Albuferon) is a novel, long-acting form of interferon alpha. Recombinant interferon alpha is approved for the treatment of hepatitis C, hepatitis B, and a broad range of cancers. Human Genome Sciences modified interferon alpha to improve its pharmacological properties by using the company's proprietary albumin fusion technology. Human Genome Sciences is developing Albuferon as a potential treatment for chronic hepatitis C. The drug was under investigation as an alternative to pegylated IFN-α-2a for the treatment of hepatitis C. In response to an FDA ruling, Novartis and Human Genome Sciences announced on October 5, 2010 that they ceased development of the drug. Investigated for use/treatment in hepatitis (viral, C). Interferons belong to a family of proteins known as cytokines that occur naturally in the human body. Cytokines control cellular processes, such as cell growth, activation, migration and aging. While the precise mechanism of action for interferon alpha is not known, research has demonstrated direct antiviral activity in patients with diseases like hepatitis C, as well as immune-modulating and direct antitumor effects in certain types of cancer.",,,,Albinterferon Alfa-2B is investigational.,Albinterferon Alfa-2B is a liquid.,True
15348,"99mTc-Ciprofloxacin is a new formulation of ciprofloxacin (INFECTON), being investigated as a radioimaging agent for the potential diagnosis of infection, including fever of unknown origin, osteomyelitis, wound infection, abdominal abscess, pneumonia, appendicitis and tuberculosis. INFECTON combines the widely used antibiotic, ciprofloxacin, with Technetium ((99m)Tc), the most commonly used radioisotope in nuclear medical imaging There is currently controversy around the drug's ability to discriminate between sterile inflammation and bacterial versus nonbacterial infections. Investigated for use/treatment in infectious and parasitic disease (unspecified). This radiopharmaceutical diagnostic imaging agent is being investigated for its ability to uniquely detect and determine the location of bacterial infection in patients with difficult-to-diagnose signs and symptoms. This may be of use with the potential diagnosis of infection, including fever of unknown origin, osteomyelitis, wound infection, abdominal abscess, pneumonia, appendicitis and tuberculosis. Ciprofloxacin is a fluoroquinolone antibiotic. The mechanism of action of these fluoroquinolones is not fully understood, but it has been postulated that the interaction of ciprofloxacin with bacterial DNA gyrase (a type II topoisomerase) prevents DNA uncoiling and subsequent DNA synthesis within bacteria. Ciprofloxacin demonstrates a significant antibiotic effect for both gram-negative and gram-positive bacteria in either stationary or growth phases of bacterial replication. However, the addition of the 99mTc atom likely affects the interaction of the ciprofloxacin molecule with the enzyme.",,,,Technetium Tc-99m ciprofloxacin is investigational.,Technetium Tc-99m ciprofloxacin is a solid.,True
15349,"Apremilast, also known as Otezla, is a phosphodiesterase 4 (PDE4) inhibitor used to treat various types of symptoms resulting from certain inflammatory autoimmune diseases. It belongs to the same drug class as and. Initially approved in 2014, it is marketed by Celgene. In July 2019, apremilast was granted a new FDA approval for the treatment of oral ulcers associated with Behcet's disease, an autoimmune condition that causes recurrent skin, blood vessel, and central nervous system inflammation. Apremilast is indicated for the treating of active psoriatic arthritis in adults, for the treating of active moderate to severe psoriatic arthritis in patients who are eligible for phototherapy and systemic treatment. In addition, apremilast is now indicated for the treatment of oral ulcers associated with Behcet's disease in adults. Apremilast reduces but does not completely inhibit various inflammatory cytokines such as IL-1α, IL-6, IL-8, IL-10 MCP-1, MIP-1β, MMP-3, and TNF-α, relieving the symptoms of psoriasis and Behcet's disease, which are caused by an increase in these inflammatory mediators. This drug has also been proven to be effective in relieving the pain associated with oral ulcers in Behcet's disease.  The full mechanism of action of this drug is not fully established, however, it is known that apremilast is an inhibitor of phosphodiesterase 4 (PDE4), which mediates the activity of cyclic adenosine monophosphate (cAMP), a second messenger. The inhibition of PDE4 by apremilast leads to increased intracellular cAMP levels. An increase in cAMP results in the suppression of inflammation by decreasing the expression of TNF-α, IL-17, IL-23, and other inflammatory mediators. The above inflammatory mediators have been implicated in various psoriatic conditions as well as Behcet's disease, leading to their undesirable inflammatory symptoms such as mouth ulcers, skin lesions, and arthritis. Apremilast administration leads to a cascade which eventually decreases the levels of the above mediators, relieving inflammatory symptoms.",The molecular weight is 460.5.,Apremilast has a topological polar surface area of 119.08.,The log p value of  is 1.46.,Apremilast is approved and investigational.,Apremilast is a solid.,True
15350,"GTS-21 (also known as DMBX-A), is a novel, small-molecule, orally active and selective alpha-7 nicotinic acetylcholine (nACh) receptor agonist that has demonstrated memory and cognition enhancement activity in human clinical trials. Athenagen licensed the exclusive rights to the compound and a related library of analogs as part of the acquisition of Osprey Pharmaceutical Company in April 2006. GTS-21 has been studied in multiple Phase I studies in healthy volunteers and one Phase I/II study in schizophrenic patients. In all studies, the compound was well tolerated. In a Phase I multi-dose, double-blind, placebo controlled study in healthy adults, GTS-21 also demonstrated cognitive enhancement across all doses, with a statistically significant improvement in attention related and memory related tasks (Kitagawa, et al. Neuropsychopharmacology (2003), 28, 542-551). Investigated for use/treatment in alzheimer's disease and schizophrenia and schizoaffective disorders. Auditory sensory gating, a biological measurement of the ability to suppress the evoked response to the second of two auditory stimuli, is diminished in people with schizophrenia. Deficits in sensory gating are associated with attentional impairment, and may contribute to cognitive symptoms and perceptual disturbances. This inhibitory process, which involves the alpha(7) nicotinic receptor mediated release of gamma-aminobutyric acid (GABA) by hippocampal interneurons, represents a potential new target for therapeutic intervention in schizophrenia. GTS-21 is an orally active alpha-7 nicotinic acetylcholine (nACh) receptor agonist.",,,,GTS-21 is investigational.,GTS-21 is a solid.,True
15351,"Dovitinib is an orally active small molecule that exhibits potent inhibitory activity against multiple RTKs involved in tumor growth and angiogenesis. Preclinical data show that dovitinib works to inhibit multiple kinases associated with different cancers, including acute myeloid leukemia (AML) and multiple myeloma. Chiron currently has three ongoing Phase I clinical trials for dovitinib. Investigated for use/treatment in multiple myeloma and solid tumors. Unlike many kinase inhibitors that only target vascular endothelial growth factor (VEGF), Dovitinib inhibits receptors in the fibroblast growth factor (FGF ) pathway, as well as VEGF and platelet-derived growth factor (PDGF). FGF receptor tyrosine kinase inhibition is potentially of therapeutic significance to a group of myeloma patients whose cancer cells express high levels of surface FGF receptors.",,,,Dovitinib is investigational.,Dovitinib is a solid.,True
15352,"Primary biliary cirrhosis, or PBC, is a progressive and chronic condition that leads to hepatic injury often resulting in end-stage liver failure that requires liver transplantation. Obeticholic acid is indicated for the treatment of primary biliary cholangitis in combination with ursodeoxycholic acid (UDCA) in adults with an inadequate response to UDCA. It is also used as a monotherapy in adults with PBC that are unable to tolerate UDCA. The activation of the FXR by obeticholic acid acts to reduce the synthesis of bile acids, inflammation, and the resulting hepatic fibrosis. This may increase the survival of patients with PBC, but to date, an association between obeticholic acid and survival in PBC has not been established. Primary biliary cirrhosis is an autoimmune process by which the bile ducts and liver are damaged progressively, leading to fibrosis and cirrhosis. Bile acids increase the risk of damage and fibrosis to the damaged bile ducts. ",The molecular weight is 420.63.,Obeticholic acid has a topological polar surface area of 77.76.,The log p value of  is 5.36.,Obeticholic acid is approved.,Obeticholic acid is a solid.,True
15353,"Garenoxacin, a quinolone antibiotic, is being investigated for the treatment of gram-positive and gram-negative bacterial infections. Investigated for use/treatment in bacterial infection.",The molecular weight is 426.42.,Garenoxacin has a topological polar surface area of 78.87.,The log p value of  is 0.73.,Garenoxacin is investigational.,Garenoxacin is a solid.,True
15354,"Eltrombopag is used to treat low blood platelet counts in adults with chronic immune (idiopathic) thrombocytopenia (ITP), when certain other medicines, or surgery to remove the spleen, have not worked well enough. ITP is a condition that may cause unusual bruising or bleeding due to an abnormally low number of platelets in the blood. Eltrombopag has also been recently approved (late 2012) for the treatment of thrombocytopenia (low blood platelet counts) in patients with chronic hepatitis C to allow them to initiate and maintain interferon-based therapy. Thrombopoietin receptor agonists are pharmaceutical agents that stimulate platelet production in the bone marrow. In this, they differ from the previously discussed agents that act by attempting to curtail platelet destruction.  Eltrombopag is an orally bioavailable, small-molecule TPO-receptor agonist that interacts with the transmembrane domain of the human TPO-receptor. Eltrombopag is a stimulator of STAT and JAK phosphorylation. Unlike recombinant TPO or romiplostim, Eltrombopag does not activate the AKT pathway in any way. It should be noted that when given to patients with aplastic anemia, other lineages besides platelet count were increased, suggesting that either eltrombopag enhanced the effect of TPO in vivo; or there is a yet uncovered mechanism of action at work. ",The molecular weight is 442.48.,Eltrombopag has a topological polar surface area of 114.59.,The log p value of  is 5.25.,Eltrombopag is approved.,Eltrombopag is a solid.,True
15355,"Investigated for use/treatment in solid tumors, lung cancer, ovarian cancer, and prostate cancer. ASA404 (DMXAA) is a small-molecule vascular disrupting agent which targets the blood vessels that nourish tumours. The proposed mechanism of action for ASA404 is directly increasing permeability of the tumor's endothelial cells. Vasoactive mediators such as tumor necrosis factor (TNF) may also be implicated. Increased permeability of tumor cell vasculature may allow increased permeation of anticancer treatments such as cytotoxic drugs, antibodies, drug conjugates and gene therapy.",,,,Vadimezan is investigational.,Vadimezan is a solid.,True
15356,"Tolperisone is an oral, centrally acting muscle relaxant. Its precise mechanism is not completely understood, though it blocks sodium and calcium channels. It possesses a high affinity for nervous system tissue, reaching highest concentrations in brain stem, spinal cord and peripheral nerves. Based on existing clinical data, Tolperisone is not sedating and does not interact with alcohol. Investigated for use/treatment in neurologic disorders, spinal cord injuries, muscle spasm, back pain, and multiple sclerosis.",The molecular weight is 245.37.,Tolperisone has a topological polar surface area of 20.31.,The log p value of  is 3.83.,Tolperisone is investigational.,Tolperisone is a solid.,True
15357,Investigated for use/treatment in peripheral vascular disease.,,,,Avasimibe is investigational.,Avasimibe is a solid.,True
15358,"Investigated for use/treatment in alzheimer's disease. Propentofylline is a xanthine derivative and phosphodiesterase inhibitor with purported neuroprotective effects. It inhibits both phosphodiesterase and adenosine uptake. Phosphodiesterase has shown to associated with age-related memory impairment and Alzheimer's disease. β-Amyloid protein 1–42 (β42) can induce apoptosis in the cultured hippocampal neurons, suggesting that it plays an important role in causing neurodegeneration in Alzheimer's disease. Propentofylline is also capable of activating a cAMP–PKA system, depressing the caspase cascade and modifying Bcl-2 family proteins. Propentofylline blocked both the apoptotic features induced by β42 and further induced an anti-apoptotic protein, Bcl-2. It suggests that the protection of propentofylline on the β42-induced neurotoxicity is caused by enhancing anti-apoptotic action through cAMP–PKA system. ",The molecular weight is 306.37.,Propentofylline has a topological polar surface area of 75.51.,The log p value of  is 1.17.,Propentofylline is investigational.,Propentofylline is a solid.,True
15359,"Muraglitazar (Bristol-Myers Squibb/Merck) is a new agent under investigation for the treatment of patients with type 2 diabetes. It belongs to a novel class of drugs that target the peroxisome proliferator-activated receptors, both alpha and gamma subtypes. In addition to improvements in blood glucose and hemoglobin A1c (HbA1c), muraglitazar treatment is associated with a substantial reduction in triglycerides (TGs), an increase in HDL-C, and a modest decrease in LDL-C levels. Investigated for use/treatment in diabetes mellitus type 2. Muraglitazar is one of the dual peroxisome proliferator-activated receptor (PPAR) agonists. It interacts with both PPAR alpha and gamma receptors. Working through the PPAR gamma receptor, muraglitazar has very potent insulin-sensitizing effects on liver and muscle to lower the blood sugar levels. working through the PPAR alpha receptor, muraglitazar is very potent in terms of lowering the triglycerides and raising the HDL cholesterol and converting small dense LDL particles to larger, more buoyant particles, so it promotes a very good lipid profile from the standpoint of prevention of atherosclerosis.",,,,Muraglitazar is investigational.,Muraglitazar is a solid.,True
15360,"Agomelatine is structurally closely related to melatonin. Agomelatine is a potent agonist at melatonin receptors and an antagonist at serotonin-2C (5-HT2C) receptors, tested in an animal model of depression. Agomelatine was developed in Europe by Servier Laboratories Ltd. and submitted to the European Medicines Agency (EMA) in 2005. The Committee for Medical Products for Human Use (CHMP) recommended refusal of marketing authorization on 27 July 2006. The major concern was that efficacy had not been sufficiently shown. In 2006 Servier sold the rights to develop Agomelatine in the US to Novartis. Agomelatine is indicated to treat major depressive episodes in adults. Agomelatine resynchronises circadian rhythms in animal models of delayed sleep phase syndrome and other circadian rhythm disruptions. It increases noradrenaline and dopamine release specifically in the frontal cortex and has no influence on the extracellular levels of serotonin. Agomelatine has shown an antidepressant-like effect in animal depression models, (learned helplessness test, despair test, and chronic mild stress) circadian rhythm desynchronisation, and in stress and anxiety models. In humans, agomelatine has positive phase shifting properties; it induces a phase advance of sleep, body temperature decline and melatonin onset. Controlled studies in humans have shown that agomelatine is as effective as the SSRI antidepressants paroxetine and sertraline in the treatment of major depression The novel antidepressant agent, agomelatine, behaves as an agonist at melatonin receptors (MT1 and MT2) and as an antagonist at serotonin (5-HT)(2C) receptors.",The molecular weight is 243.31.,Agomelatine has a topological polar surface area of 38.33.,The log p value of  is 2.11.,Agomelatine is approved and investigational.,Agomelatine is a solid.,True
15361,Investigated for use/treatment in bacterial infection and pneumonia.,The molecular weight is 371.44.,Nemonoxacin has a topological polar surface area of 96.1.,The log p value of  is -0.28.,Nemonoxacin is investigational.,Nemonoxacin is a solid.,True
15362,"β-Naphthoflavone, also known as 5,6-benzoflavone, is a potent agonist of the aryl hydrocarbon receptor and induces cytochromes P450 (CYPs) and uridine 5'-diphospho-glucuronosyltransferases (UGTs). It may be a chemopreventive agent.",,,,beta-Naphthoflavone is experimental.,beta-Naphthoflavone is a solid.,True
15363,"Bendamustine is a nitrogen mustard drug indicated for use in the treatment of chronic lymphocytic leukemia (CLL) and indolent B-cell non-Hodgkin lymphoma (NHL) that has progressed during or within six months of treatment with rituximab or a rituximab-containing regimen. Bendamustine is a bifunctional mechlorethamine derivative capable of forming electrophilic alkyl groups that covalently bond to other molecules. Through this function as an alkylating agent, bendamustine causes intra- and inter-strand crosslinks between DNA bases resulting in cell death. It is active against both active and quiescent cells, although the exact mechanism of action is unknown. Bendamustine is indicated for use in the treatment of chronic lymphocytic leukemia (CLL) and indolent B-cell non-Hodgkin lymphoma (NHL) that has progressed during or within six months of treatment with rituximab or a rituximab-containing regimen. No mean changes in QTc interval greater than 20 milliseconds were detected up to one hour post-infusion.  Bendamustine is a bifunctional mechlorethamine derivative capable of forming electrophilic alkyl groups that covalently bond to other molecules. Through this function as an alkylating agent, bendamustine causes intra- and inter-strand crosslinks between DNA bases resulting in cell death. It is active against both active and quiescent cells, although the exact mechanism of action is unknown. ",The molecular weight is 358.26.,Bendamustine has a topological polar surface area of 58.36.,The log p value of  is 3.24.,Bendamustine is approved and investigational.,Bendamustine is a solid.,True
15364,"Besifloxacin is a fourth generation fluoroquinolone-type opthalmic antibiotic for the treatment of bacterial conjunctivitis. FDA approved on May 28, 2009. Treatment of bacterial conjunctivitis. Bacterial isolates that are susceptible to besifloxacin include: CDC coryneform group G; Corynebacterium pseudodiphtheriticum; Corynebacterium striatum; Haemophilus influenzae; Moraxella lacunata; Staphylococcus aureus; Staphylococcus epidermidis; Staphylococcus hominis; Staphylococcus lugdunensis; Streptococcus mitis group; Streptococcus oralis; Streptococcus pneumoniae; Streptococcus salivarius*  Besifloxacin tear concentrations were higher than MIC90 (minimum inhibitory concentration) values for common bacterial pathogens and sustained for 24 hours or longer. Mean residence time in the conjunctiva was 4.7 hours.  Besifloxacin is a bactericidal fluroquinolone-type antibiotic that inhibits bacterial enzymes, DNA gyrase and topoisomerase IV. By inhibiting DNA gyrase, DNA replication, transcription, and repair is impaired. By inhibiting topoisomerase IV, decatenation during cell devision is impaired. Inhibiting these two targets also slows down development of resistance. ",The molecular weight is 393.84.,Besifloxacin has a topological polar surface area of 86.87.,The log p value of  is 0.69.,Besifloxacin is approved.,Besifloxacin is a liquid.,True
15365,"Niclosamide is an antihelminthic used for the treatment of tapeworm infections. Helminths (worms) are multicellular organisms that infect very large numbers of humans and cause a broad range of diseases. Over 1 billion people are infected with intestinal nematodes, and many millions are infected with filarial nematodes, flukes, and tapeworms. They are an even greater problem in domestic animals. For the treatment of tapeworm and intestinal fluke infections: Taenia saginata (Beef Tapeworm), Taenia solium (Pork Tapeworm), Diphyllobothrium latum (Fish Tapeworm), Fasciolopsis buski (large intestinal fluke). Niclosamide is also used as a molluscicide in the control of schistosomiasis. Niclosamide is an antihelminth used against tapeworm infections. It may act by the uncoupling of the electron transport chain to ATP synthase. The disturbance of this crucial metabolic pathway prevents creation of adenosine tri-phosphate (ATP), an essential molecule that supplies energy for metabolism.  Niclosamide works by killing tapeworms on contact. Adult worms (but not ova) are rapidly killed, presumably due to uncoupling of oxidative phosphorylation or stimulation of ATPase activity. The killed worms are then passed in the stool or sometimes destroyed in the intestine. Niclosamide may work as a molluscicide by binding to and damaging DNA.",The molecular weight is 327.12.,Niclosamide has a topological polar surface area of 95.15.,The log p value of  is 4.34.,Niclosamide is approved and investigational and vet_approved.,Niclosamide is a solid.,True
15366,"Teriflunomide is the active metabolite of leflunomide, and it acts as an immunomodulatory agent by inhibiting pyrimidine synthesis. It is marketed under the name Aubagio® and is indicated for the treatment of multiple sclerosis, specifically relapsing forms. The FDA label states an important warning about the risk of hepatoxicity and teratogenicity for patients using teriflunomide. Used in the treatment of relapsing forms of multiple sclerosis (MS). Teriflunomide is an immunomodulatory agent that decreases the amount of activated CNS lymphocytes, which results in anti-inflammatory and antiproliferative effects. The exact mechanism by which teriflunomide acts in MS is not known. What is known is that teriflunomide prevents pyrimidine synthesis by inhibiting the mitochondrial enzyme",The molecular weight is 270.21.,Teriflunomide has a topological polar surface area of 73.12.,The log p value of  is 2.13.,Teriflunomide is approved.,Teriflunomide is a solid.,True
15367,"Pomalidomide, an analogue of thalidomide, is an immunomodulatory antineoplastic agent. FDA approved on February 8, 2013. Pomalidomide is indicated for patients with multiple myeloma who have received at least two prior therapies including lenalidomide and bortezomib and have demonstrated disease progression on or within 60 days of completion of the last therapy. Pomalidomide is more potent than thalidomide (100-times) and lenalidomide (10-times).  Promalidomide is an immunomodulatory agent with antineoplastic activity. It is shown to inhibit the proliferation and induce apoptosis of various tumour cells. Furthermore, promalidomide enhances T cell and natural killer (NK) cell-mediated immunity and inhibited the production of pro-inflammatory cytokines, like TNF-alpha or IL-6, by monocytes. The primary target of promalidomide is thought to be the protein cereblon. It binds to this target and inhibits ubiquitin ligase activity. It is also a transcriptional inhibitor of COX2. ",The molecular weight is 273.25.,Pomalidomide has a topological polar surface area of 109.57.,The log p value of  is -0.19.,Pomalidomide is approved.,Pomalidomide is a solid.,True
15368,Flumequine is a synthetic chemotherapeutic antibiotic of the fluoroquinolone drug class used to treat bacterial infections.,The molecular weight is 261.25.,Flumequine has a topological polar surface area of 57.61.,The log p value of  is 2.43.,Flumequine is withdrawn.,Flumequine is a solid.,True
15369,"Tasimelteon is a selective dual melatonin receptor agonist indicated for the treatment of Non-24-Hour Sleep-Wake Disorder (N24HSWD). Occurring commonly in blind individuals without light perception, this condition is often characterized by periods of night-time insomnia and day-time sleepiness. In blind individuals, a lack of light stimulation causes an extension of the 24-hour circadian cycle and can lead to progressively delayed sleep onset. By activating melatonin receptors MT1 and MT2 in the suprachiasmatic nucleus of the brain, tasimelteon has been shown to improve sleep by resynchronizing the circadian rhythm through its \non-photic\"" mechanism. Tasimelteon is currently the only drug available for the treatment of N24HSWD and was granted orphan drug status by the FDA in 2010."" Tasimelteon is indicated for the treatment of Non-24-Hour Sleep-Wake Disorder (N24HSWD). Tasimelteon is a selective dual agonist of the melatonin receptors MT1 and MT2. ",The molecular weight is 245.32.,Tasimelteon has a topological polar surface area of 38.33.,The log p value of  is 1.89.,Tasimelteon is approved and investigational.,Tasimelteon is a solid.,True
15370,"Zucapsaicin, the cis-isomer of capsaicin, is a topical analgesic used to treat osteoarthritis of the knee and other neuropathic pain. It is a modulator of transient receptor potential cation channel subfamily V member 1 (TRPV-1), also known as the vanilloid or capsaicin receptor 1, that reduces pain and improves articular functions. Zucapsaicin has also been evaluated for the management of several conditions manifested by chronic nerve pain. These conditions include herpes simplex (HSV) infections, cluster headaches, migraine, and osteoarthritis of the knee. Zucapsaicin was approved by the Health Canada in 2010 as topical cream marketed under the brand name Zuacta but currently not FDA-approved. Indicated to be used in conjunction with oral COX-2 inhibitors or NSAIDs for the relief of severe pain in adult patients with osteoarthritis of the knee, not controlled with oral COX-2 inhibitors or NSAIDs alone, for a duration of no more than three months.  Zucapsaicin mediates an antinociceptive action via acting as an agonist at TRPV1. TRPV1 play an important physiological role of transducing chemical, mechanical and thermal stimuli as well as pain transduction, and participate in pain modulation and perception. They are mainly distributed in C sensory nerve fibers as well as Aẟ fibers to transmit sensory information involving inflammatory and neuropathic pain, and activation of these channels releasesomatostatin, calcitonin gene-related peptide (CGRP) and other neuropeptides (neurokinin A, kassinin), leading to neurogenic inflammation. Zucapsaicin is also reported to affect the peptidergic afferent neurons via a desensitization mechanism to decrease the levels of dorsal root ganglia and sciatic calcitonin gene-related peptide (CGRP) and substance P (SP).  Zucapsaicin excites and desensitizes C-fibers via agonist at TRPV1 on nociceptive neurons. It binds to intracellular sites and initially stimulates the channels, causing burning sensation. Activation of TRPV1 results in calcium influx and sodium, which leads to cell depolarization. Hypersensitization by zucapsaicin is then followed by reduced sensitivity and persistent desensitization (tachyphylaxis) of the channels via various pathways. Densentiziation is thought to be dependent on intraceullar levels of calcium. Decreased TRPV1 channel action and release of inflammatory neuropeptides induces an analgesic effect, and pain relief. Zucapsaicin activates calcineurin and calcium-dependent protein kinase C isoforms which results in phosphorylation of TRPV1. Phosphorylation of TRPV1 enhances reponsivity to zucapsaicin by potentiating capsaicin- or proton-evoked responses and reducing the temperature threshold for TRPV1 activation. Studies suggest that zucapsaicin is involved in activation of phospholipase C with the subsequent phosphatidylinositol 4,5-biphosphate (PIP2) hydrolysis, which results in TRPV1 inactivation. ",The molecular weight is 305.42.,Zucapsaicin has a topological polar surface area of 58.56.,The log p value of  is 3.75.,Zucapsaicin is approved and investigational.,Zucapsaicin is a solid.,True
15371,"Peginterferon beta-1a is an interferon beta-1a to which a single, linear 20,000 dalton (Da) methoxy poly(ethyleneglycol)-O-2-methylpropionaldehyde (PEG) molecule is covalently attached to the alpha amino group of the N-terminal amino acid residue. The amino acid sequence of the recombinant interferon beta-1a is identical to that of the human interferon beta counterpart. Although it's mechanism of action is unknown, peginterferon beta-1a is indicated for use in relapsing forms of Multiple Sclerosis (MS). For the treatment of patients with relapsing forms of multiple sclerosis. The mechanism by which peginterferon beta-1a exerts its effects in patients with multiple sclerosis is unknown.",,,,Peginterferon beta-1a is approved.,Peginterferon beta-1a is a solid.,True
15372,"Viloxazine is a selective norepinephrine reuptake inhibitor (NRI) that was used in some European countries as an antidepressant drug. It structurally differs from conventional tri- or tetra-cyclic antidepressants and it does not produce sedative anticholinergic or adrenergic effects in man. While displaying amphetamine-like CNS stimulant effects, there is little evidence of drug dependence from viloxazine therapy. Viloxazine hydrochloride is a common active ingredient in drug formulation. It was discovered and brought to market in 1976 by Imperial Chemical Industries and in early 2000's, it was withdrawn from the market. Indicated for the treatment of clinical depression. Viloxazine is a selective noradrenaline reuptake inhibitor (NRI) with minimal inhibitory effect on the reuptake of 5-HT. It is also shown to upregulate the levels of GABA-B receptors in the rat frontal cortex. It is shown to form a complex with the human norepinephrine transporter (hNET). Viloxazine inhibits noradrenaline uptake in rat and mouse heart tissue and has a weak effect on the uptake of 5-HT. In a docking study, the amino group of viloxazine points towards Asp75 in the drug binding pocket of the transporter and forms hydrogen bonds with Phe72, Asp75 and Phe317. The rest of the drug molecule forms hydrophobic interactions with other key residues in the binding pocket. ",The molecular weight is 237.3.,Viloxazine has a topological polar surface area of 39.72.,The log p value of  is 1.76.,Viloxazine is approved and investigational and withdrawn.,Viloxazine is a solid.,True
15373,"Lobeglitazone is an antidiabetic medication from the thiazolidinedione class of drugs. It primarily functions as an insulin sensitizer by binding and activating Peroxisome Proliferator-Activated Receptors (PPAR) gamma within fat cells. By activating PPAR-gamma and promoting the binding of insulin at fat cells, lobeglitazone thereby has been shown to reduce blood sugar levels, lower hemoglobain A1C (HbA1C) levels, and improve lipid and liver profiles. Unlike , which is a dual PPAR agonist at PPAR-alpha and PPAR-gamma, Lobeglitazone is a pure PPAR-alpha agonist.  Lobeglitazone was approved by the Ministry of Food and Drug Safety (South Korea) in 2013, and is being monitored by postmarketing surveillance until 2019. Lobeglitazone is not approved for use by either the Food and Drug Administration (USA), Health Canada, or by the European Medicines Agency for use in the management of diabetes. Lobeglitazone acts as an insulin sensitizer by binding and activating Peroxisome Proliferator-Activated Receptors (PPAR) gamma within fat cells. By promoting the binding of insulin at fat cells, lobeglitazone has been shown to reduce blood sugar levels, lower hemoglobain A1C (HbA1C) levels, and improve lipid and liver profiles. Unlike , which is a dual PPAR agonist at PPAR-alpha and PPAR-gamma, Lobeglitazone is a pure PPAR-alpha agonist. ",The molecular weight is 480.54.,Lobeglitazone has a topological polar surface area of 102.88.,The log p value of  is 4.27.,Lobeglitazone is experimental.,Lobeglitazone is a solid.,True
15374,"Zotepine, with the formula (2-chloro-11-(2-dimethyl-amino-ethoxy)-dibenzo thiepin, is a neuroleptic drug. It was designed and synthesized by Fujisawa Pharmaceutical Co Ltd. It has been used as an antipsychotic in Japan, India and some places in Europe like UK and Germany since 1980's. Zotepine was never approved by the FDA. In 1993, it was classified as inactive drug substance (Status I, Type II) and in 1995 the FDA studied the manufacturing procedures of Zotepine tablets in Germany, but the status remained inactive. When the analysis of antipsychotics was retaken in 2016 by the FDA, zotepine did not reach the threshold effect to be further studied.. In the EMA, by 2015 it was under pharmacovigilance studies for the potential treatment of acute renal failure. Zotepine, like other atypical antipsychotics, is considered as the first-line treatment in newly diagnosed schizophrenia. It is usually thought to be an option of choice for managing acute schizophrenic episodes when discussion with the patient is not possible. Zotepine, as an atypical antipsychotic, is used in patients who are suffering unacceptable side effects from conventional antipsychotics or in relapse patients that were inadequately controlled.  In preclinical studies, zotepine is characterized by the presence of a strong antiserotonergic activity when compared with other neuroleptic drugs. It has also been reported to present elevations in the seizure threshold in the amygdaloid nucleus. When zotepine's effects were analyzed by electroencephalography, it was noted a typical response of a low-potency neuroleptics of the sedative type. Administration of zotepine has shown improvements in numerical movements and complex reaction. These effects tend to be accompanied by increases in pulse rate, increase in prolactin levels and some typical neuroleptic side effects. Zotepine is a dopamine antagonist that has a high affinity for D1- and D2-like receptors. It presents a strong antagonism for several serotonin receptors, such as 5-HT2a, 5-HT2c, 5-HT6 and 5-HT7. Zotepine activities are also related to the inhibition of noradrenaline reuptake and serotonergic activity. All these effects allow zotepine to improve the negative and cognitive symptoms of schizophrenia.",The molecular weight is 331.86.,Zotepine has a topological polar surface area of 12.47.,The log p value of  is 5.11.,Zotepine is approved and investigational and withdrawn.,Zotepine is a solid.,True
15375,"Doxofylline is a methylxanthine derivative with the presence of a dioxolane group in position 7. As a drug used in the treatment of asthma, doxofylline has shown similar efficacy to theophylline but with significantly fewer side effects in animal and human studies. In contrast with other xanthine derivatives, doxofylline does not significantly bind to adenosine alpha-1 or alpha-2 receptors and lacks stimulating effects. Decreased affinity for adenosine receptors may account for the better safety profile of doxofylline compared to theophylline. Unlike theophylline, doxofylline does not affect calcium influx and does not antagonize the actions of calcium channel blockers which could explain reduced cardiac adverse reactions associated with the drug. The anti-asthmatic effects of doxophylline are mediated by other mechanisms, primarily through inhibiting the activities of the phosphodiesterase (PDE) enzyme. Indicated for the treatment of chronic obstructive pulmonary disease (COPD), bronchial asthma and pulmonary disease with spastic bronchial component. Doxofylline is a methylxanthine bronchodilator with potent bronchodilator activity comparable to that of theophylline. In animal studies, doxofylline demonstrated to attenuate bronchoconstriction, inflammatory actions and the release of thromboxane A2 (TXA2) when challenged with platelet-activating factor.  The main mechanism of action of doxofylline is unclear. One of the mechanisms of action of is thought to arise from the inhibition of phosphodiesterase activity thus increasing the levels of cAMP and promoting smooth muscle relaxation. ",The molecular weight is 266.26.,Doxofylline has a topological polar surface area of 76.9.,The log p value of  is -0.42.,Doxofylline is experimental.,Doxofylline is a solid.,True
15376,"Ramosetron is a _serotonin 5-HT3 receptor antagonist_ commonly employed to treat nausea and vomiting, in addition to certain diarrheal conditions. It is believed to have higher potency and longer antiemetic action than other 1st generation 5-HT3 antagonists such as ondansetron. Currently, ramosetron is only approved for use Japan and in certain Southeast Asian countries. For the treatment of nausea and vomiting and diarrhea-predominant irritable bowel syndrome in males.",The molecular weight is 279.34.,Ramosetron has a topological polar surface area of 50.68.,The log p value of  is 2.13.,Ramosetron is investigational.,Ramosetron is a solid.,True
15377,"Osimertinib is an oral, third-generation epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) drug developed by AstraZeneca Pharmaceuticals. Its use is indicated for the treatment of metastatic non-small cell lung cancer (NSCLC) in cases where tumour EGFR expression is positive for the T790M mutation as detected by FDA-approved testing and which has progressed following therapy with a first-generation EGFR tyrosine kinase inhibitor. Approximately 10% of patients with NSCLC have a rapid and clinically effective response to EGFR-TKIs due to the presence of specific activating EGFR mutations within the tumour cells. More specifically, deletions around the LREA motif in exon 19 and exon 21 L858R point mutations are correlated with response to therapy.  Osimertinib is indicated for the treatment of patients with metastatic epidermal growth factor receptor (EGFR) T790M mutation-positive non-small cell lung cancer (NSCLC), as detected by an FDA- approved test, who have progressed on or after EGFR-TKI therapy. A pharmacokinetic/pharmacodynamic analysis suggested a concentration-dependent QTc interval prolongation of 14 msec (upper bound of two-sided 90% CI: 16 msec) at a dose of osimertinib 80 mg. Osimertinib is an epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) that binds to certain mutant forms of EGFR (T790M, L858R, and exon 19 deletion) that predominate in non-small cell lung cancer (NSCLC) tumours following treatment with first-line EGFR-TKIs. As a third-generation tyrosine kinase inhibitor, osimertinib is specific for the gate-keeper T790M mutation which increases ATP binding activity to EGFR and results in poor prognosis for late-stage disease. Furthermore, osimertinib has been shown to spare wild-type EGFR during therapy, thereby reducing non-specific binding and limiting toxicity. ",The molecular weight is 499.62.,Osimertinib has a topological polar surface area of 87.55.,The log p value of  is 4.6.,Osimertinib is approved.,Osimertinib is a solid.,True
15378,Insulin beef has been discontinued in the US and Canada since 2017.,The molecular weight is 5733.55.,Insulin beef has a topological polar surface area of 2258.61.,,Insulin beef is approved.,,True
15379,"Extracted from the stem, leaves, and flowers of _Mentha piperita_ L. plant, peppermint oil (Mentha piperita) is a popular essential oil used in aromatherapy for both external and internal use. Mentha piperita is a hybrid of spearmint (Mentha spicata) and water mint (Mentha aquatica). Medicinal use of herbal ingredients such as peppermint oil has a long history of treating digestive disorders and upper respiratory symptoms and cough. There are various over-the-counter and commercial uses of peppermint oil due to its carminative, cholagogue, antibacterial, secretolytic, and choleretic actions. Peppermint oil contains pulegone, which is a naturally-occurring pesticide. Other active constituents of peppermint oil include , menthone, cineol, and several other volatile oils.  Indicated for the over-the-counter use for: Peppermint oil induces a dose-related antispasmodic effects on the gastrointestinal smooth muscles. A meta-analysis study and additional clinical studies of patients with IBS demonstrated that the treatment with peppermint oil improves abdominal symptoms compared to the placebo group, resulting in reduced severity of abdominal pain, decreased abdominal distension, reduced stool frequency, and reduced flatulence. The use of enteric-coated peppermint oil was shown to be effective in reducing gastrointestinal symptoms of non-ulcer dyspepsia. In rats, peppermint oil promoted a time-dependent choleretic effect in increasing bile production and biliary output. In randomized controlled trials, topical application of peppermint oil was associated with a significant analgesic effect and a reduction in headache intensity compared to placebo. In a study of C57BL/6 mice, topical application of peppermint oil for 4 weeks was associated with a prominent hair growth effects; a significant increase in dermal thickness, follicle number, and follicle depth.  Dose-dependent antispasmodic effect of peppermint oil is largely mediated by its menthol constituent. It is proposed that peppermint oil relaxes gastrointestinal smooth muscle and attenuates contractile responses by reducing the influx of extracellular calcium ions. In rabbit jejunum smooth muscle cells investigated via whole cell clamp configuration technique, peppermint oil was shown to inhibit the potential-dependent calcium currents in a concentration-dependent manner. Both a reduction in peak current amplitude and an increase in the rate of current decay were observed, indicating that the pharmacological activity peppermint oil resembles that of dihydropyridine calcium antagonists. In a rat small intestine study, peppermint oil in the intestinal lumen inhibited enterocyte glucose uptake via a direct action on the brush border membrane and inhibited intestinal secretion. There is also evidence that menthol is an antagonist of L-type Ca2+ channels via interacting with dihydropyridine binding sites and blocks the currents of low-voltage-activated calcium channels. Peppermint oil may facilitate hair growth by promoting the conservation of vascularization of hair dermal papilla, which may contribute to the induction of early anagen stage of active growth phase of hair follicles. ",,,,Peppermint oil is approved and investigational.,Peppermint oil is a liquid.,True
15380,"Enrofloxacin is an antibiotic agent from the fluoroquinolone family produced by the Bayer Corporation. Enrofloxacin is approved by the FDA for its veterinary use. Due to the identification of fluoroquinolone-resistant strains of _Campylobacter_, in September 2005, the FDA withdrew the approval of enrofloxacin for its use in water to treat flocks of poultry.",,,,Enrofloxacin is vet_approved.,,True
15381,Orbifloxacin is a fluoroquinolone antibiotic. It is marketed by Schering-Plough Animal Health and approved for certain infections in dogs.,,,,Orbifloxacin is vet_approved.,,True
15382,,The molecular weight is 334.38.,Pimobendan has a topological polar surface area of 79.37.,The log p value of  is 2.9.,Pimobendan is vet_approved.,,False
15383,"Sarafloxacin is a quinolone antibiotic drug, which was discontinued by its manufacturer, Abbott Laboratories, before receiving approval for use in the US or Canada.",,,,Sarafloxacin is vet_approved and withdrawn.,Sarafloxacin is a solid.,True
15384,"Difloxacin is a synthetic fluoroquinolone used in veterinary. As an antibacterial, it presents a broad bactericidal spectrum and its effects are dependent on its concentration. However, it presents a reduced efficacy when compared to other fluoroquinolone antibacterials.",,,,Difloxacin is vet_approved.,,True
15385,,,,,Insulin peglispro is investigational.,Insulin peglispro is a solid.,False
15386,`code text here`,,,,Insulin tregopil is investigational.,Insulin tregopil is a solid.,True
15387,Pazufloxacin is under investigation in clinical trial NCT02592096 (Pazufloxacin Mesilate Ear Drops Clinical Trial Protocol).,The molecular weight is 318.3.,Pazufloxacin has a topological polar surface area of 92.86.,The log p value of  is -1.19.,Pazufloxacin is investigational.,,True
15388,"Capmatinib is a small molecule kinase inhibitor targeted against c-Met (a.k.a. hepatocyte growth factor receptor ), a receptor tyrosine kinase that, in healthy humans, activates signaling cascades involved in organ regeneration and tissue repair. Aberrant c-Met activation - via mutations, amplification, and/or overexpression - is known to occur in many types of cancer, and leads to overactivation of multiple downstream signaling pathways such as STAT3, PI3K/ATK, and RAS/MAPK. Mutations in _MET_ have been detected in non-small cell lung cancer (NSCLC), and the prevalence of _MET_ amplification in epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI)-naive patients with NSCLC has been reported to be 1.4% - 21%. This co-occurrence has made c-Met a desirable target in the treatment of NSCLC. Capmatinib is indicated for the treatment of adult patients with metastatic non-small cell lung cancer (NSCLC) whose tumors have a mutation that leads to mesenchymal-epithelial transition (MET) exon 14 skipping as detected by an FDA-approved test. Capmatinib inhibits the overactivity of c-Met, a receptor tyrosine kinase encoded by the _MET_ proto-oncogene. Mutations in _MET_ are involved in the proliferation of many cancers, including non-small cell lung cancer (NSCLC).  Aberrant activation of c-Met has been documented in many cancers, including non-small cell lung cancer (NSCLC). Mutations that result in the skipping of _MET_ exon 14 lead to the formation of a mutant c-Met with a missing regulatory domain - these mutant proteins have a reduced ability to negatively regulate, leading to a pathological increase in their downstream activity.",,,,Capmatinib is approved and investigational.,Capmatinib is a solid.,True
15389,Prulifloxacin has been investigated for the treatment of Urinary Tract Infection.,The molecular weight is 461.46.,Prulifloxacin has a topological polar surface area of 99.62.,The log p value of  is -0.93.,Prulifloxacin is investigational.,,True
15390,"Abametapir is a novel pediculicidal metalloproteinase inhibitor used to treat infestations of head lice. The life cycle of head lice (_Pediculus capitis_) is approximately 30 days, seven to twelve of which are spent as eggs laid on hair shafts near the scalp. Topical pediculicides generally lack adequate ovicidal activity, including standard-of-care treatments such as , and many require a second administration 7-10 days following the first to kill newly hatched lice that resisted the initial treatment. The necessity for follow-up treatment may lead to challenges with patient adherence, and resistance to agents like permethrin and / may be significant in some areas.  Abametapir is indicated, in the context of an overall lice management program, for the topical treatment of head lice infestation in patients 6 months of age and older. Abametavir has been shown to inhibit all stages of embryo development in both head and body lice by interfering with enzymes critical to this process. It is relatively unique amongst lice treatments in that it requires only a single application, whereas many current therapies require two applications, due to its exceptional potency and unique mechanism. Its predominant metabolite, abametapir carboxyl, has a prolonged residence time in the body, with an estimated half-life of 71 ± 40 hours or longer in adults - as this metabolite has been shown to inhibit cytochrome P450 enzymes _in vitro_, the use of substrates of CYP3A4, CYP2B6, or CYP1A2 should be avoided for two weeks following the administration of abametapir.  There are several metalloproteinases (enzymes requiring metal co-factors to function) involved in the process of louse egg hatching and survival. _In vitro_ studies have demonstrated that metal-chelating agents can inhibit the activity of these proteins, and may therefore be valuable pediculicidal agents.",,,,Abametapir is approved and investigational.,Abametapir is a solid.,True
15391,"Binimetinib, also known as _Mektovi_, is a potent is a potent and selective oral mitogen-activated protein kinase 1/2  (MEK 1/2) inhibitor which is combined with ,. Binimetinib is a MEK inhibitor. MEK is an enzyme that regulates the biosynthesis of the inflammatory cytokines TNF, IL-6 and IL-1. MEK inhibitors interfere with these biosynthetic processes.  It is a chemotherapeutic agent that has anti-tumor activity ,.",,,,Binimetinib is approved and investigational.,Binimetinib is a solid.,True
15392,"Voxilaprevir is a Direct-Acting Antiviral (DAA) medication used as part of combination therapy to treat chronic Hepatitis C, an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients.  Vosevi (Voxilaprevir//) is approved for use in patients with genotypes 1-6 who have been previously treated with an NS5A inhibitor, or patients with genotypes 1a or 3 infection who have previously been treated with an HCV regimen containing without an NS5A inhibitor.  Voxilaprevir is a direct-acting antiviral agent that targets viral NS3/4A protein and causes a decrease in serum HCV RNA levels. It disrupts HCV replication by specifically inhibiting the critical functions of NS3/4A protein in the replication complex. It does not appear to prolong the QT interval even when given at 9 times the maximum recommended dose.  Voxilaprevir exerts its antiviral action by reversibley binding and inhibiting the NS3/4A serine protease of Hepatitis C Virus (HCV). Following viral replication of HCV genetic material and translation into a single polypeptide, Nonstructural Protein 3 (NS3) and its activating cofactor Nonstructural Protein 4A (NS4A) are responsible for cleaving genetic material into the following structural and nonstructural proteins required for assembly into mature virus: NS3, NS4A, NS4B, NS5A, and NS5B. By inhibiting viral protease NS3/4A, voxilaprevir therefore prevents viral replication and function. ",The molecular weight is 868.94.,Voxilaprevir has a topological polar surface area of 195.22.,The log p value of  is 6.69.,Voxilaprevir is approved and investigational.,,True
15393,Lisofylline has been investigated for the treatment of Type 1 Diabetes Mellitus.,,,,Lisofylline is investigational.,,True
15394,Cepeginterferon alfa-2B is under investigation in clinical trial NCT01889433 (An Open-label Comparative Efficacy and Safety Study of Algeron (Cepeginterferon Alfa-2b) in Treatment-naive Patients With Chronic Hepatitis C).,,,,Cepeginterferon alfa-2B is investigational.,,True
15395,Dihydralazine is under investigation in clinical trial NCT00311974 (The Effect of Dihydralazine on Kidney Function and Hormones in Healthy Individuals).,The molecular weight is 190.21.,Dihydralazine has a topological polar surface area of 100.82.,The log p value of  is -1.52.,Dihydralazine is approved and experimental.,,True
15396,Bamifylline is a selective A1 adenosine receptor antagonist.,The molecular weight is 385.47.,Bamifylline has a topological polar surface area of 81.91.,The log p value of  is 2.03.,Bamifylline is experimental.,,True
15397,,,,,Sitafloxacin is experimental and investigational.,,False
15398,,The molecular weight is 238.25.,Proxyphylline has a topological polar surface area of 78.67.,The log p value of  is -0.56.,Proxyphylline is experimental.,,False
15399,,The molecular weight is 238.2.,Acefylline has a topological polar surface area of 95.74.,The log p value of  is -0.66.,Acefylline is experimental.,,False
15400,,The molecular weight is 279.34.,Etamiphylline has a topological polar surface area of 61.68.,The log p value of  is 1.14.,Etamiphylline is experimental.,,False
15401,,The molecular weight is 261.23.,Oxolinic acid has a topological polar surface area of 76.07.,The log p value of  is 1.65.,Oxolinic acid is experimental.,,False
15402,,The molecular weight is 264.33.,Pentifylline has a topological polar surface area of 58.44.,The log p value of  is 2.6.,Pentifylline is experimental.,,False
15403,Rufloxacin is a quinolone antibiotic. ,The molecular weight is 363.41.,Rufloxacin has a topological polar surface area of 64.09.,The log p value of  is -0.29.,Rufloxacin is experimental.,,True
15404,,The molecular weight is 269.3.,Bufylline has a topological polar surface area of 69.3.,,Bufylline is experimental.,,False
15405,,The molecular weight is 303.32.,Pipemidic acid has a topological polar surface area of 98.66.,The log p value of  is -2.48.,Pipemidic acid is experimental.,,False
15406,"Bromotheophylline is the active moiety of pamabrom, a mixture of 2-amino-2-methyl-propanol and bromotheophylline. From this mixture, bromotheophylline acts as a weak diuretic that has been used along with some analgesics to relieve the symptoms of premenstrual syndrome. Bromotheophylline is categorized on the FDA as a drug substance with an inactive state since March, 1980. It is also approved by Health Canada to be used alone or in combination with in OTC products. Bromotheophylline is used as a diuretic and also, in combination with , it is used for the relief of temporary water weight gain, bloating, swelling and full feeling associated with the premenstrual and menstrual periods. Bromotheophylline diuretic action will produce an immediate increase in urination frequency. This effect aids in the relief of bloating and menstrual pain. This diuretic function is performed by the an increase in glomerular filtration and a potential effect in the tubular reabsorption as it is established that the administration of these agents produce a rise in the urinary concentration of sodium a chloride and thus, an increase in their rates of excretion. Bromotheophylline is part of the group of the xanthines. As part of this group, it is thought that bromotheophylline increases the permeability of the renal tubule, increases glomerular filtration rate and inhibits the sodium reabsorption in the proximal tubule. It is thought but not confirmed that pamabrom as a mixture seems to have an additional mechanism of action in which the presence of 2-amino-2-methyl-1-propanol produces the suppression of the antidiuretic hormone in the posterior pituitary gland.",The molecular weight is 259.06.,Bromotheophylline has a topological polar surface area of 69.3.,The log p value of  is 0.93.,Bromotheophylline is approved.,Bromotheophylline is a solid.,True
15407,Furafylline is a derivative of methylxanthine derivative. It was developed on the context of asthma as a long-acting alternative for.,,,,Furafylline is experimental.,Furafylline is a solid.,True
15408,"8-Chlorotheophylline is a stimulant drug of the xanthine chemical class, with physiological effects similar to caffeine. Its main use is in combination with as the antiemetic drug. The stimulant properties of 8-chlorotheophylline are thought to ward off the drowsiness caused by diphenhydramine's anti-histamine activity in the central nervous system.  When used in combination with as the antiemetic , 8-chlorotheophylline is indicated for the prevention and treatment of nausea, vomiting, or vertigo of motion sickness. 8-chlorotheophylline produces a number of effects including nervousness, restlessness, insomnia, headache, and nausea, which are primarily attributed to its ability to block the adenosine receptor. Because adenosine causes a decrease in neuronal firing, blockade of the adenosine receptor causes the reverse effect resulting in excitation.",,,,8-chlorotheophylline is experimental.,,True
15409,Ropeginterferon alfa-2b is under investigation in clinical trial NCT01949805 (Pegylated Interferon Alpha-2b Versus Hydroxyurea in Polycythemia Vera).,,,,Ropeginterferon alfa-2b is approved and investigational.,,True
15410,Interferon alfa-2c is under investigation in clinical trial NCT00485563 (A Phase II Study of EC17 (Folate-hapten Conjugate) in Patients With Progressive Metastatic Renal Cell Carcinoma).,,,,Interferon alfa-2c is investigational.,,True
15411,5'-S-(3-Amino-3-carboxypropyl)-5'-thioadenosine. Formed from S-adenosylmethionine after transmethylation reactions.,,,,S-adenosyl-L-homocysteine is experimental.,S-adenosyl-L-homocysteine is a solid.,True
15412,"A depressor amine derived by enzymatic decarboxylation of histidine. It is a powerful stimulant of gastric secretion, a constrictor of bronchial smooth muscle, a vasodilator, and also a centrally acting neurotransmitter. Histamine phosphate is indicated as a diagnostic aid for the evaluation of gastric acid secretory function. Histamine stimulates gastric gland secretion, causing an increased secretion of gastric juice of high acidity. This action is probably due mainly to a direct action on parietal and chief gland cells. Histamine acts directly on the blood vessels to dilate arteries and capillaries; this action is mediated by both H 1- and H 2-receptors. Capillary dilatation may produce flushing of the face, a decrease in systemic blood pressure, and gastric gland secretion, causing an increased secretion of gastric juice of high acidity. Increased capillary permeability accompanies capillary dilatation, producing an outward passage of plasma protein and fluid into the extracellular spaces, an increase in lymph flow and protein content, and the formation of edema. In addition, histamine has a direct stimulant action on smooth muscle, producing contraction if H 1-receptors are activated, or mostly relaxation if H 2-receptors are activated. Also in humans, the stimulant effect of histamine may cause contraction of the intestinal muscle. However, little effect is noticed on the uterus, bladder, or gallbladder. Histamine has some stimulant effect on duodenal, salivary, pancreatic, bronchial, and lacrimal glands. Histamine also can bind to H3 and H4 receptors which are involved in the CNS/PNS neurotransmitter release and immune system chemotaxis, respectively.",The molecular weight is 111.15.,Histamine has a topological polar surface area of 54.7.,The log p value of  is -0.97.,Histamine is approved and investigational.,Histamine is a solid.,True
15413,"Gemcitabine is a nucleoside analog used as chemotherapy. It is marketed as Gemzar® by Eli Lilly and Company. As with fluorouracil and other analogues of pyrimidines, the drug replaces one of the building blocks of nucleic acids, in this case cytidine, during DNA replication. The process arrests tumor growth, as new nucleosides cannot be attached to the \faulty\"" nucleoside, resulting in apoptosis (cellular \""suicide\"")."" Gemcitabine is indicated for the treatment of advanced ovarian cancer that has relapsed at least 6 months after completion of platinum-based therapy; metastatic ovarian cancer; inoperable, locally advanced (Stage IIIA or IIIB), or metastatic (Stage IV) non-small cell lung cancer; and locally advanced (nonresectable Stage II or Stage III) or metastatic (Stage IV) adenocarcinoma of the pancreas.  Gemcitabine is an antineoplastic anti-metabolite. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA. They prevent these substances becoming incorporated in to DNA during the \S\"" phase (or DNA synthesis phase of the cell cycle), stopping normal development and division. Gemcitabine blocks an enzyme which converts the cytosine nucleotide into the deoxy derivative. In addition, DNA synthesis is further inhibited because Gemcitabine blocks the incorporation of the thymidine nucleotide into the DNA strand. It demonstrates dose-dependent synergistic activity with cisplatin in vitro. In vivo, gemcitabine showed activity in combination with cisplatin against the LX-1 and CALU-6 human lung xenografts, but minimal activity was seen with the NCI-H460 or NCI-H520 xenografts. Gemcitabine was synergistic with cisplatin in the Lewis lung murine xenograft. Sequential exposure to gemcitabine 4 hours before cisplatin produced the greatest interaction."" Gemcitabine inhibits thymidylate synthetase, leading to inhibition of DNA synthesis and cell death. Gemcitabine is a prodrug so activity occurs as a result of intracellular conversion to two active metabolites, gemcitabine diphosphate and gemcitabine triphosphate by deoxycitidine kinase. Gemcitabine diphosphate also inhibits ribonucleotide reductase, the enzyme responsible for catalyzing synthesis of deoxynucleoside triphosphates required for DNA synthesis. Finally, Gemcitabine triphosphate (diflurorodeoxycytidine triphosphate) competes with endogenous deoxynucleoside triphosphates for incorporation into DNA.",The molecular weight is 263.2.,Gemcitabine has a topological polar surface area of 108.38.,The log p value of  is -0.71.,Gemcitabine is approved.,Gemcitabine is a solid.,True
15414,"A pyrimidine nucleoside analogue that inhibits DNA methyltransferase, impairing DNA methylation. It is also an antimetabolite of cytidine, incorporated primarily into RNA. Azacytidine has been used as an antineoplastic agent. For treatment of patients with the following French-American-British myelodysplastic syndrome subtypes: refractory anemia or refractory anemia with ringed sideroblasts (if accompanied by neutropenia or thrombocytopenia or requiring transfusions), refractory anemia with excess blasts, refractory anemia with excess blasts in transformation (now classified as acute myelogenous leukemia with multilineage dysplasia), and chronic myelomonocytic leukemia. Azacitidine is believed to exert its antineoplastic effects by causing hypomethylation of DNA and direct cytotoxicity on abnormal hematopoietic cells in the bone marrow. The concentration of azacitidine required for maximum inhibition of DNA methylation in vitro does not cause major suppression of DNA synthesis. Hypomethylation may restore normal function to genes that are critical for differentiation and proliferation. The cytotoxic effects of azacitidine cause the death of rapidly dividing cells, including cancer cells that are no longer responsive to normal growth control mechanisms. Non-proliferating cells are relatively insensitive to azacitidine. Upon uptake into cells, azacitidine is phosphorylated to 5-azacytidine monophosphate by uridine-cytidine kinase, then to diphosphate by pyrimidine monophosphate kinases and triphosphate by diphosphate kinases. 5-Azacitidine triphosphate is incorporated into RNA, leading to the disruption of nuclear and cytoplasmic RNA metabolism and inhibition of protein synthesis. 5-Azacytidine diphosphate is reduced to 5-aza-deoxycytidine diphosphate by ribonucleotide reductase. The resultant metabolite is phosphorylated to 5-azadeoxycitidine triphosphate by nucleoside diphosphate kinases. 5-azadeoxycitidine triphosphate is then incoporated into DNA, leading to inhibition of DNA synthesis. Azacitidine is most toxic during the S-phase of the cell cycle. Azacitidine (5-azacytidine) is a chemical analogue of the cytosine nucleoside used in DNA and RNA. Azacitidine may induce antineoplastic activity by inhibition of DNA methyltransferase at low doses and cytotoxicity through incorporation into RNA and DNA at high doses. Covalent binding to DNA methyltransferase results in hypomethylation of DNA and prevents DNA synthesis. As azacitidine is a ribonucleoside, it incoporates into RNA to a larger extent than into DNA. The incorporation into RNA leads to the dissembly of polyribosomes, defective methylation and acceptor function of transfer RNA, and inhibition of the production of protein, resulting in cell death.",The molecular weight is 244.21.,Azacitidine has a topological polar surface area of 140.97.,The log p value of  is -2.2.,Azacitidine is approved and investigational.,Azacitidine is a solid.,True
15415,,,,,"1-Beta-Ribofuranosyl-1,3-Diazepinone is experimental.","1-Beta-Ribofuranosyl-1,3-Diazepinone is a solid.",False
15416,"Lorazepam is a short-acting and rapidly cleared benzodiazepine used commonly as a sedative and anxiolytic. It was developed by DJ Richards, presented and marketed initially by Wyeth Pharmaceuticals in the USA in 1977. The first historic FDA label approval is reported in 1985 by the company Mutual Pharm. Lorazepam is FDA-approved for the short-term relief of anxiety symptoms related to anxiety disorders and anxiety associated with depressive symptoms such as anxiety-associated insomnia. It is as well used as an anesthesia premedication in adults to relieve anxiety or to produce sedation/amnesia and for the treatment of status epilepticus. The effect of lorazepam in GABA-A receptors produces an increase in the frequency of opening of the chloride ion channel. However, for its effect to generate, the neurotransmitter is required. The anticonvulsant properties of lorazepam are thought to be related to the binding to voltage-dependent sodium channels in which the sustained repetitive firing gets limited by the slow recovery of sodium channels due to the benzodiazepine effect. Lorazepam allosterically binds on the benzodiazepine receptors in the post-synaptic GABA-A ligand-gated chloride channel in different sites of the central nervous system (CNS). This binding will result in an increase on the GABA inhibitory effects which is translated as an increase in the flow of chloride ions into the cell causing hyperpolarization and stabilization of the cellular plasma membrane.",The molecular weight is 321.16.,Lorazepam has a topological polar surface area of 61.69.,The log p value of  is 2.37.,Lorazepam is approved.,Lorazepam is a solid.,True
15417,"Phentermine is a sympathomimetic amine anorectic agent and it was introduced in 1959 as part of an anti-obesity combination drug. It is chemically related to amphetamine and it is commonly referred to as an atypical amphetamine. Phentermine has not been reported an addictive potential which allows this agent to be classified under the Schedule IV drugs (low abuse potential). Phentermine is indicated, alone or in combination with topiramate, as a short-term adjunct, not pass a few weeks, in a regimen of weight reduction based on exercise, behavioral modifications and caloric restriction in the management of exogenous obesity for patients with an initial body mass index (BMI) greater than 30 kg/m2 or greater than 27 kg/m2 in presence of other risk factors such as controller hypertension, diabetes or hyperlipidemia. It is reported that the main mechanism of action of phentermine is the generation of appetite suppression, maybe due to the increase in leptin, but it is considered that other mechanisms should be involved. Some reports have indicated that the weight loss effect is mainly due to the increase in resting energy expenditure. Phentermine is an indirect-acting sympathomimetic agent that acts by releasing noradrenaline from the presynaptic vesicles in the lateral hypothalamus. This increase in noradrenaline concentration in the synaptic cleft results in the stimulation of beta2-adrenergic receptors. Phentermine is classified as an indirect sympathomimetic due to the increase in the level of norepinephrine, dopamine and its indirect effect towards serotonin. Some reports have indicated that phentermine inhibits the neuropeptide Y which is a principal signaling pathway for the induction of hunger. This combined effect produces a continuous flight-or-fight response in the body which reduces the hunger signal as this state is on the immediate need for energy.",The molecular weight is 149.24.,Phentermine has a topological polar surface area of 26.02.,The log p value of  is 2.14.,Phentermine is approved and illicit.,Phentermine is a solid.,True
15418,"Dofetilide is a class III antiarrhythmic agent that is approved by the Food and Drug Administration (FDA) for the maintenance of sinus rhythm in individuals prone to the formation of atrial fibrillation and flutter, and for the chemical cardioversion to sinus rhythm from atrial fibrillation and flutter. For the maintenance of normal sinus rhythm (delay in time to recurrence of atrial fibrillation/atrial flutter ) in patients with atrial fibrillation/atrial flutter of greater than one week duration who have been converted to normal sinus rhythm Dofetilide is an antiarrhythmic drug with Class III (cardiac action potential duration prolonging) properties and is indicated for the maintenance of normal sinus rhythm. Dofetilide increases the monophasic action potential duration in a predictable, concentration-dependent manner, primarily due to delayed repolarization. At concentrations covering several orders of magnitude, Dofetilide blocks only IKr with no relevant block of the other repolarizing potassium currents (e.g., IKs, IK1). At clinically relevant concentrations, Dofetilide has no effect on sodium channels (associated with Class I effect), adrenergic alpha-receptors, or adrenergic beta-receptors. The mechanism of action of Dofetilide is a blockade of the cardiac ion channel carrying the rapid component of the delayed rectifier potassium current, IKr. This inhibition of potassium channels results in a prolongation of action potential duration and the effective refractory period of accessory pathways (both anterograde and retrograde conduction in the accessory pathway).",The molecular weight is 441.56.,Dofetilide has a topological polar surface area of 104.81.,The log p value of  is 1.99.,Dofetilide is approved and investigational.,Dofetilide is a solid.,True
15419,"Azithromycin is a broad-spectrum macrolide antibiotic with a long half-life and a high degree of tissue penetration. It was initially approved by the FDA in 1991. Azithromycin should be used only to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria in order to prevent the development antimicrobial resistance and maintain the efficacy of azithromycin. Macrolides stop bacterial growth by inhibiting protein synthesis and translation, treating bacterial infections. In order to replicate, bacteria require a specific process of protein synthesis, enabled by ribosomal proteins. Azithromycin binds to the 23S rRNA of the bacterial 50S ribosomal subunit. It stops bacterial protein synthesis by inhibiting the transpeptidation/translocation step of protein synthesis and by inhibiting the assembly of the 50S ribosomal subunit ,. This results in the control of various bacterial infections ,.  The strong affinity of macrolides, including azithromycin, for bacterial ribosomes, is consistent with their broad‐spectrum antibacterial activities.",The molecular weight is 749.0.,Azithromycin has a topological polar surface area of 180.08.,The log p value of  is 2.64.,Azithromycin is approved.,Azithromycin is a solid.,True
15420,"Pantoprazole is a first-generation proton pump inhibitor (PPI) used for the management of gastroesophageal reflux disease (GERD), for gastric protection to prevent recurrence of stomach ulcers or gastric damage from chronic use of NSAIDs, and for the treatment of pathological hypersecretory conditions including Zollinger-Ellison (ZE) Syndrome. It can also be found in quadruple regimens for the treatment of _H. pylori_ infections along with other antibiotics including , , and , for example. Its efficacy is considered similar to other medications within the PPI class including , , , , and. This drug acts to decrease gastric acid secretion, which reduces stomach acidity. Pantoprazole administration leads to long-lasting inhibition of gastric acid secretion. Hydrochloric acid (HCl) secretion into the gastric lumen is a process regulated mainly by the H(+)/K(+)-ATPase of the proton pump, expressed in high quantities by the parietal cells of the stomach. ATPase is an enzyme on the parietal cell membrane that facilitates hydrogen and potassium exchange through the cell, which normally results in the extrusion of potassium and formation of HCl (gastric acid). ",The molecular weight is 383.37.,Pantoprazole has a topological polar surface area of 86.33.,The log p value of  is 2.11.,Pantoprazole is approved.,Pantoprazole is a solid.,True
15421,"Temazepam, like many other similar and related benzodiazepines, acts as a gamma-aminobutyric acid (GABA) modulator and is capable of eliciting a variety of actions including sedation, hypnosis, skeletal muscle relaxation, anticonvulsant activity, and anxiolytic action. Temazepam is specifically indicated only for the short-term management of insomnia ,. Furthermore, such management is generally predominantly associated with the symptomatic relief of transient and short-term insomnia characterized by difficulty in falling asleep, frequent nocturnal awakenings and/or early morning awakenings. In particular, the official prescribing information for temazepam typically specifies that the instructions issued for dispensed prescriptions of the medication should indicate specifically that patients are only expected to use the therapy for short periods of time - usually 7-10 days in general. Subsequently, treatment with temazepam should usually not exceed 7 to 10 consecutive days and nor should it be prescribed in quantities exceeding a one-month supply. Temazepam is a benzodiazepine used as a hypnotic agent in the management of insomnia. Temazepam produces CNS depression at limbic, thalamic, and hypothalamic levels of the CNS. Temazepam increases the affinity of the neurotransmitter gamma-aminobutyric acid (GABA) for GABA receptors by binding to benzodiazepine receptors. Results are sedation, hypnosis, skeletal muscle relaxation, anticonvulsant activity, and anxiolytic action. Gamma-Aminobutyric acid (GABA) is considered the principal inhibitory neurotransmitter in the human body. When GABA binds to GABA(a) receptors found in neuron synapses, chloride ions are conducted across neuron cell membranes via an ion channel in the receptors. With enough chloride ions conducted, the local, associated neuron membrane potentials are hyperpolarized - making it more difficult or less likely for action potentials to fire, ultimately resulting in less excitation of the neurons. ",The molecular weight is 300.74.,Temazepam has a topological polar surface area of 52.9.,The log p value of  is 2.34.,Temazepam is approved and investigational.,Temazepam is a solid.,True
15422,"Oxiconazole is an antifungal agent that is commonly found in topical formulations. It is marketed under the brand names Oxistat and Oxistat, and is used in the treatment of various skin infections such as athlete's foot, jock itch and ringworm. For treatment of dermal fungal infection. Oxiconazole is a broad-spectrum imidazole derivative whose antifungal activity is derived primarily from the inhibition of ergosterol biosynthesis, which is critical for cellular membrane integrity. It has fungicidal or fungistatic activity in vitro against a number of pathogenic fungi including the following dermatophytes, and yeasts: <i>T. rubrum</i>, <i>T. mentagrophytes</i>, <i>T. tonsurans</i>, <i>T. violaceum</i>, <i>E. floccosum</i>, <i>M. canis</i>, <i>M. audouini</i>, <i>M. gypseum</i>, <i>C. albicans</i>, and <i>M. furfur</i>. Oxiconazole inhibits ergosterol biosynthesis, which is required for cytoplasmic membrane integrity of fungi. It acts to destabilize the fungal cyctochrome P450 51 enzyme (also known as Lanosterol 14-alpha demethylase). This is vital in the cell membrance structure of the fungus. Its inhibition leads to cell lysis. Oxiconazole has also been shown in inhibit DNA synthesis and suppress intracellular concentrations of ATP. Like other imidazole antifungals, Oxiconazole can increase membrane permeability to zinc, augmenting its cytotoxicity.",The molecular weight is 429.12.,Oxiconazole has a topological polar surface area of 39.41.,The log p value of  is 6.47.,Oxiconazole is approved.,Oxiconazole is a solid.,True
15423,"An ergot derivative that is a congener of lysergic acid diethylamide. It antagonizes the effects of serotonin in blood vessels and gastrointestinal smooth muscle, but has few of the properties of other ergot alkaloids. Methysergide is used prophylactically in migraine and other vascular headaches and to antagonize serotonin in the carcinoid syndrome. For the treatment of vascular headache Methysergide has been shown, <i>in vitro</i> and <i>in vivo</i>, to inhibit or block the effects of serotonin, a substance which may be involved in the mechanism of vascular headaches. Serotonin has been variously described as a central neurohumoral agent or chemical mediator, as a \headache substance\"" acting directly or indirectly to lower pain threshold, as an intrinsic \""motor hormone\"" of the gastrointestinal tract, and as a \""hormone\"" involved in connective tissue reparative processes."" Methysergide is serotonin antagonists acts on central nervous system (CNS), which directly stimulates the smooth muscle leading to vasoconstriction. Some alpha-adrenergic blocking activity has been reported. Suggestions have been made by investigators as to the mechanism whereby Methysergide produces its clinical effects, but this has not been finally established, although it may be related to the antiserotonin effect.",The molecular weight is 353.47.,Methysergide has a topological polar surface area of 57.5.,The log p value of  is 2.22.,Methysergide is approved.,Methysergide is a solid.,True
15424,"Cabergoline, an ergot derivative, is a long-acting dopamine agonist and prolactin inhibitor. It is used to treat hyperprolactinemic disorders and Parkinsonian Syndrome. Cabergoline possesses potent agonist activity on dopamine D2 receptors. For the treatment of hyperprolactinemic disorders, either idiopathic or due to prolactinoma (prolactin-secreting adenomas). May also be used to manage symptoms of Parkinsonian Syndrome as monotherapy during initial symptomatic management or as an adjunct to levodopa therapy during advanced stages of disease.  Cabergoline stimulates centrally-located dopaminergic receptors resulting in a number of pharmacologic effects. Five dopamine receptor types from two dopaminergic subfamilies have been identified. The dopaminergic D1 receptor subfamily consists of D<sub>1</sub> and D<sub>5</sub> subreceptors, which are associated with dyskinesias. The dopaminergic D2 receptor subfamily consists of D<sub>2</sub>, D<sub>3</sub> and D<sub>4</sub> subreceptors, which are associated with improvement of symptoms of movement disorders. Thus, agonist activity specific for D2 subfamily receptors, primarily D<sub>2</sub> and D<sub>3</sub> receptor subtypes, are the primary targets of dopaminergic antiparkinsonian agents. It is thought that postsynaptic D2 stimulation is primarily responsible for the antiparkinsonian effect of dopamine agonists, while presynaptic D2 stimulation confers neuroprotective effects. This semisynthetic ergot derivative exhibits potent agonist activity on dopamine D<sub>2</sub>- and D<sub>3</sub>-receptors. It also exhibits: agonist activity (in order of decreasing binding affinities) on 5-hydroxytryptamine (5-HT)<sub>2B</sub>, 5-HT<sub>2A</sub>, 5-HT<sub>1D</sub>, dopamine D<sub>4</sub>, 5-HT<sub>1A</sub>, dopamine D<sub>1</sub>, 5-HT<sub>1B</sub> and 5-HT<sub>2C</sub> receptors and antagonist activity on &alpha;<sub>2B</sub>, &alpha;<sub>2A</sub>, and &alpha;<sub>2C</sub> receptors. Parkinsonian Syndrome manifests when approximately 80% of dopaminergic activity in the nigrostriatal pathway of the brain is lost. As this striatum is involved in modulating the intensity of coordinated muscle activity (e.g. movement, balance, walking), loss of activity may result in dystonia (acute muscle contraction), Parkinsonism (including symptoms of bradykinesia, tremor, rigidity, and flattened affect), akathesia (inner restlessness), tardive dyskinesia (involuntary muscle movements usually associated with long-term loss of dopaminergic activity), and neuroleptic malignant syndrome, which manifests when complete blockage of nigrostriatal dopamine occurs. High dopaminergic activity in the mesolimbic pathway of the brain causes hallucinations and delusions; these side effects of dopamine agonists are manifestations seen in patients with schizophrenia who have overractivity in this area of the brain. The hallucinogenic side effects of dopamine agonists may also be due to 5-HT<sub>2A</sub> agonism. The tuberoinfundibular pathway of the brain originates in the hypothalamus and terminates in the pituitary gland. In this pathway, dopamine inhibits lactotrophs in anterior pituitary from secreting prolactin. Increased dopaminergic activity in the tuberoinfundibular pathway inhibits prolactin secretion.  The dopamine D<sub>2</sub> receptor is a 7-transmembrane G-protein coupled receptor associated with G<sub>i</sub> proteins. In lactotrophs, stimulation of dopamine D<sub>2</sub> causes inhibition of adenylyl cyclase, which decreases intracellular cAMP concentrations and blocks IP3-dependent release of Ca<sup>2+</sup> from intracellular stores. Decreases in intracellular calcium levels may also be brought about via inhibition of calcium influx through voltage-gated calcium channels, rather than via inhibition of adenylyl cyclase. Additionally, receptor activation blocks phosphorylation of p42/p44 MAPK and decreases MAPK/ERK kinase phosphorylation. Inhibition of MAPK appears to be mediated by c-Raf and B-Raf-dependent inhibition of MAPK/ERK kinase. Dopamine-stimulated growth hormone release from the pituitary gland is mediated by a decrease in intracellular calcium influx through voltage-gated calcium channels rather than via adenylyl cyclase inhibition. Stimulation of dopamine D<sub>2</sub> receptors in the nigrostriatal pathway leads to improvements in coordinated muscle activity in those with movement disorders. Cabergoline is a long-acting dopamine receptor agonist with a high affinity for D2 receptors. Receptor-binding studies indicate that cabergoline has low affinity for dopamine D1, &alpha;<sub>1</sub>,- and &alpha;<sub>2</sub>- adrenergic, and 5-HT<sub>1</sub>- and 5-HT<sub>2</sub>-serotonin receptors.",The molecular weight is 451.62.,Cabergoline has a topological polar surface area of 71.68.,The log p value of  is 4.17.,Cabergoline is approved.,Cabergoline is a solid.,True
15425,"Doxycycline is a broad-spectrum antibiotic synthetically derived from oxytetracycline. This drug is a second-generation tetracycline, exhibiting lesser toxicity than first-generation tetracyclines. Doxycycline may be used to treat a wide range of bacterial infections, depending on the results of antibiotic susceptibility testing. Doxycycline is indicated for the treatment of various infections by gram-positive and gram-negative bacteria, aerobes and anaerobes, as well other types of bacteria. A complete list of organisms is available in the FDA label and in the \indications\"" section of this drug entry."" The tetracyclines, including doxycycline, are mainly bacteriostatic and are thought to exert antimicrobial effects by the inhibition of protein synthesis.  Bacteriostatic antibiotics suppress the growth of bacteria, or keep them in the stationary phase of growth. The tetracyclines, including doxycycline, have a similar antimicrobial spectrum of activity against a variety of gram-positive and gram-negative microorganisms, treating numerous infectious diseases. Cross-resistance of these microorganisms to tetracyclines is a common occurrence.  Doxycycline shows favorable intra-cellular penetration, with bacteriostatic activity on a wide range of bacteria. Doxycycline has antiparasitic effects , ,. In addition to the above effects, this drug has demonstrated anti-inflammatory actions, which may help to manage inflammatory conditions such as rosacea.  In bacterial replication, an interaction that is important for translation initiation of proteins occurs at the 3′ end of the 16S rRNA, found on the ribosome on the 30S subunit , ,. The 30S subunit is the smaller subunit of the ribosome of prokaryotes, including bacteria. ",The molecular weight is 444.44.,Doxycycline has a topological polar surface area of 181.62.,The log p value of  is -0.5.,Doxycycline is approved and investigational and vet_approved.,Doxycycline is a solid.,True
15426,"Isradipine belongs to the dihydropyridine (DHP) class of calcium channel blockers (CCBs), the most widely used class of CCBs. It is structurally related to felodipine, nifedipine, and nimodipine and is the most potent calcium-channel blocking agent of the DHP class. Isradipine binds to calcium channels with high affinity and specificity and inhibits calcium flux into cardiac and arterial smooth muscle cells. It exhibits greater selectivity towards arterial smooth muscle cells owing to alternative splicing of the alpha-1 subunit of the channel and increased prevalence of inactive channels in smooth muscle cells. Isradipine may be used to treat mild to moderate essential hypertension. For the management of mild to moderate essential hypertension. It may be used alone or concurrently with thiazide-type diuretics. Isradipine decreases arterial smooth muscle contractility and subsequent vasoconstriction by inhibiting the influx of calcium ions through L-type calcium channels. Calcium ions entering the cell through these channels bind to calmodulin. Calcium-bound calmodulin then binds to and activates myosin light chain kinase (MLCK). Activated MLCK catalyzes the phosphorylation of the regulatory light chain subunit of myosin, a key step in muscle contraction. Signal amplification is achieved by calcium-induced calcium release from the sarcoplasmic reticulum through ryanodine receptors. Inhibition of the initial influx of calcium decreases the contractile activity of arterial smooth muscle cells and results in vasodilation. The vasodilatory effects of isradipine result in an overall decrease in blood pressure.  Isradipine belongs to the dihydropyridine (DHP) class of calcium channel blockers (CCBs), the most widely used class of CCBs. There are at least five different types of calcium channels in <i>Homo sapiens</i>: L-, N-, P/Q-, R- and T-type. CCBs target L-type calcium channels, the major channel in muscle cells that mediates contraction. Similar to other DHP CCBs, isradipine binds directly to inactive calcium channels stabilizing their inactive conformation. Since arterial smooth muscle depolarizations are longer in duration than cardiac muscle depolarizations, inactive channels are more prevalent in smooth muscle cells. Alternative splicing of the alpha-1 subunit of the channel gives isradipine additional arterial selectivity. At therapeutic sub-toxic concentrations, isradipine has little effect on cardiac myocytes and conduction cells.",The molecular weight is 371.39.,Isradipine has a topological polar surface area of 103.55.,The log p value of  is 3.92.,Isradipine is approved and investigational.,Isradipine is a solid.,True
15427,"Antibiotic analog of. Used to treat bacterial infection by susceptible microorganisms. Flucloxacillin is a penicillin beta-lactam antibiotic used in the treatment of bacterial infections caused by susceptible, usually gram-positive, organisms. The name \penicillin\"" can either refer to several variants of penicillin available, or to the group of antibiotics derived from the penicillins. Flucloxacillin has <i>in vitro</i> activity against gram-positive and gram-negative aerobic and anaerobic bacteria. The bactericidal activity of Flucloxacillin results from the inhibition of cell wall synthesis and is mediated through flucloxacillin binding to penicillin binding proteins (PBPs). Flucloxacillin is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, and cephalosporinases and extended spectrum beta-lactamases."" By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, flucloxacillin inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that flucloxacillin interferes with an autolysin inhibitor.",The molecular weight is 453.87.,Flucloxacillin has a topological polar surface area of 112.74.,The log p value of  is 2.66.,Flucloxacillin is approved and investigational.,Flucloxacillin is a solid.,True
15428,"Bexarotene (Targretin) is an antineoplastic agent indicated by the FDA for Cutaneous T cell lymphoma. It has been used off-label for lung cancer, breast cancer, and Kaposi's sarcoma. Used orally for the treatment of skin manifestations of cutaneous T-cell lymphoma (CTCL) in patients who are refractory to at least one prior systemic therapy. Also used topically for the treatment of skin lesions in early (stage IA and IB) CTCL in patients who experience refractory or persistent disease with the use of other therapies or are intolerant of other therapies. Bexarotene is a member of a subclass of retinoids that selectively activate retinoid X receptors (RXRs). These retinoid receptors have biologic activity distinct from that of retinoic acid receptors (RARs). Bexarotene is indicated for the treatment of cutaneous manifestations of cutaneous T-cell lymphoma in patients who are refractory to at least one prior systemic therapy. Bexarotene selectively binds and activates retinoid X receptor subtypes (RXR<sub>α</sub>, RXR<sub>β</sub>, RXR<sub>γ</sub>). RXRs can form heterodimers with various receptor partners such as retinoic acid receptors (RARs), vitamin D receptor, thyroid receptor, and peroxisome proliferator activator receptors (PPARs). Once activated, these receptors function as transcription factors that regulate the expression of genes that control cellular differentiation and proliferation. Bexarotene inhibits the growth <i>in vitro</i> of some tumor cell lines of hematopoietic and squamous cell origin. It also induces tumor regression <i>in vivo</i> in some animal models. Bexarotene selectively binds with and activates retinoid X receptor subtypes. There are three subtypes in total: RXR<sub>α</sub>, RXR<sub>β</sub>, RXR<sub>γ</sub>. The exact mechanism of action of bexarotene in the treatment of CTCL is unknown but the drug has activity in all clinical stages of CTCL.",The molecular weight is 348.49.,Bexarotene has a topological polar surface area of 37.3.,The log p value of  is 8.19.,Bexarotene is approved and investigational.,Bexarotene is a solid.,True
15429,"Vinblastine derivative with antineoplastic activity against cancer. Major side effects are myelosuppression and neurotoxicity. Vindesine is used extensively in chemotherapy protocols (antineoplastic combined chemotherapy protocols). For the treatment of acute leukaemia, malignant lymphoma, Hodgkin's disease, acute erythraemia and acute panmyelosis Vindesine is indicated for the treatment of acute lymphocytic leukemia of childhood that is resistant to vincristine and non-oat cell lung cancer. Vindesine causes the arrest of cells in metaphase mitosis. It is three times more potent than vincristine and nearly 10 times more potent than vinblastine in causing mitotic arrest in <i>in vitro</i> studies at doses designed to arrest from 10 to 15% of the cells in mitosis. Vindesine and vincristine are approximately equipotent at dose levels that arrest 40 to 50% of the cells in mitosis. Unlike vinblastine, vindesine produces very few postmetaphase cells. Vindesine has demonstrated activity in patients who have relapsed while receiving multiple-agent treatment that included vincristine. Vindesine acts by causing the arrest of cells in metaphase mitosis through its inhibition tubulin mitotic funcitoning. The drug is cell-cycle specific for the S phase.",The molecular weight is 753.94.,Vindesine has a topological polar surface area of 164.82.,The log p value of  is 3.42.,Vindesine is approved and investigational.,Vindesine is a solid.,True
15430,"A short-acting barbiturate that is effective as a sedative and hypnotic (but not as an anti-anxiety) agent and is usually given orally. It is prescribed more frequently for sleep induction than for sedation but, like similar agents, may lose its effectiveness by the second week of continued administration. (From AMA Drug Evaluations Annual, 1994, p236) For the short-term treatment of insomnia. Pentobarbital, a barbiturate, is used for the treatment of short term insomnia. It belongs to a group of medicines called central nervous system (CNS) depressants that induce drowsiness and relieve tension or nervousness. Little analgesia is conferred by barbiturates; their use in the presence of pain may result in excitation. Pentobarbital binds at a distinct binding site associated with a Cl- ionopore at the GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged. All of these effects are associated with marked decreases in GABA-sensitive neuronal calcium conductance (gCa). The net result of barbiturate action is acute potentiation of inhibitory GABAergic tone. Barbiturates also act through potent (if less well characterized) and direct inhibition of excitatory AMPA-type glutamate receptors, resulting in a profound suppression of glutamatergic neurotransmission.",The molecular weight is 226.28.,Pentobarbital has a topological polar surface area of 75.27.,The log p value of  is 2.11.,Pentobarbital is approved and investigational and vet_approved.,Pentobarbital is a solid.,True
15431,"A 9,10alpha-dihydro derivative of ergotamine. It is used as a vasoconstrictor, specifically for the therapy of migraine disorders. For the acute treatment of migraine headaches with or without aura and the acute treatment of cluster headache episodes. Dihydroergotamine is indicated for the acute treatment of migraine headaches with or without aura and the acute treatment of cluster headache episodes. Dihydroergotamine binds with high affinity to 5-HT<sub>1D</sub>a and 5-HT<sub>1D</sub>b receptors. It also binds with high affinity to serotonin 5-HT<sub>1A</sub>, 5-HT<sub>2A</sub>, and 5-HT<sub>2C</sub> receptors, noradrenaline a2A, a2B and a receptors, and dopamine D2L and D3 receptors. The therapeutic activity of Dihydroergotamine in migraine is generally attributed to the agonist effect at 5-HT<sub>1D</sub> receptors. Two theories have been proposed to explain the efficacy of 5-HT<sub>1D</sub> receptor agonists in migraine: 1) activation of 5-HT<sub>1D</sub> receptors located on intracranial blood vessels, including those on arterio-venous anastomoses, leads to vasoconstriction, which correlates with the relief of migraine headache and 2) activation of 5-HT<sub>1D</sub> receptors on sensory nerve endings of the trigeminal system results in the inhibition of pro-inflammatory neuropeptide release.",The molecular weight is 583.69.,Dihydroergotamine has a topological polar surface area of 118.21.,The log p value of  is 4.77.,Dihydroergotamine is approved and investigational.,Dihydroergotamine is a solid.,True
15432,"Pimecrolimus is an immunomodulating agent that was first marketed by Novartis under the trade name Elidel. It is now promoted in Canada by Galderma since early 2007. It is currently available as a topic cream used in the treatment of atopic dermatitis (eczema). For treatment of mild to moderate atopic dermatitis. Pimecrolimus is a chemical that is used to treat atopic dermatitis (eczema). Atopic dermatitis is a skin condition characterized by redness, itching, scaling and inflammation of the skin. The cause of atopic dermatitis is not known; however, scientists believe that it may be due to activation of the immune system by various environmental or emotional triggers. Scientists do not know exactly how pimecrolimus reduces the manifestations of atopic dermatitis, but pimecrolimus reduces the action of T-cells and mast cells which are part of the immune system and contribute to responses of the immune system. Pimecrolimus prevents the activation of T-cells by blocking the effects of chemicals (cytokines) released by the body that stimulate T-cells. Pimecrolimus also reduces the ability of mast cells to release chemicals that promote inflammation. Pimecrolimus binds with high affinity to macrophilin-12 (FKBP-12) and inhibits the calcium-dependent phosphatase, calcineurin. As a consequence, it inhibits T cell activation by blocking the transcription of early cytokines. In particular, pimecrolimus inhibits at nanomolar concentrations Interleukin-2 and interferon gamma (Th1-type) and Interleukin-4 and Interleukin-10 (Th2-type) cytokine synthesis in human T cells. Also, pimecrolimus prevents the release of inflammatory cytokines and mediators from mast cells in vitro after stimulation by antigen/lgE.",The molecular weight is 810.46.,Pimecrolimus has a topological polar surface area of 158.13.,The log p value of  is 7.1.,Pimecrolimus is approved and investigational.,Pimecrolimus is a solid.,True
15433,"Alfuzosin (INN, provided as the hydrochloride salt) is an alpha-adrenergic blocker used to treat benign prostatic hyperplasia (BPH). It works by relaxing the muscles in the prostate and bladder neck, making it easier to urinate. For the reduction of urinary obstruction and relief of associated manifestations (eg. sensation of incomplete bladder emptying or straining, urgency, interrupted or weak stream) in patients with symptomatic beningn prostatic hyperplasia. Alfuzosin is a quinazoline-derivative alpha-adrenergic blocking agent used to treat hypertension and benign prostatic hyperplasia. Accordingly, alfuzosin is a selective inhibitor of the alpha(1) subtype of alpha adrenergic receptors. In the human prostate, alfuzosin antagonizes phenylephrine (alpha(1) agonist)-induced contractions, <i>in vitro</i>, and binds with high affinity to the alpha1a adrenoceptor, which is thought to be the predominant functional type in the prostate. Studies in normal human subjects have shown that alfuzosin competitively antagonized the pressor effects of phenylephrine (an alpha(1) agonist) and the systolic pressor effect of norepinephrine. The antihypertensive effect of alfuzosin results from a decrease in systemic vascular resistance and the parent compound alfuzosin is primarily responsible for the antihypertensive activity. Alfuzosin is a non-subtype specific alpha(1)-adrenergic blocking agent that exhibits selectivity for alpha(1)-adrenergic receptors in the lower urinary tract. Inhibition of these adrenoreceptors leads to the relaxation of smooth muscle in the bladder neck and prostate, resulting in the improvement in urine flow and a reduction in symptoms in benign prostate hyperplasia. Alfuzosin also inhibits the vasoconstrictor effect of circulating and locally released catecholamines (epinephrine and norepinephrine), resulting in peripheral vasodilation.",The molecular weight is 389.46.,Alfuzosin has a topological polar surface area of 111.83.,The log p value of  is 2.55.,Alfuzosin is approved and investigational.,Alfuzosin is a solid.,True
15434,"An anticonvulsant effective in absence seizures, but generally reserved for refractory cases because of its toxicity. (From AMA Drug Evaluations Annual, 1994, p378) Used in the control of absence (petit mal) seizures that are refractory to treatment with other medications. Paramethadione and trimethadione are anticonvulsants indicated in the control of absence (petit mal) seizures that are refractory to treatment with other medications. Dione anticonvulsants are used in the treatment of epilepsy. They act on the central nervous system (CNS) to reduce the number of seizures. Dione anticonvulsants reduce T-type calcium currents in thalamic neurons, including thalamic relay neurons. It does so via the inhibition of voltage dependent T-type calcium channels. This raises the threshold for repetitive activity in the thalamus, and inhibits corticothalamic transmission. Thus, the abnormal thalamocortical rhythmicity, which is thought to underlie the 3-Hz spike-and-wave discharge seen on electroencephalogram(EEG) with absence seizures, is dampened.",The molecular weight is 143.14.,Trimethadione has a topological polar surface area of 46.61.,The log p value of  is -0.12.,Trimethadione is approved.,Trimethadione is a solid.,True
15435,"17-Hydroxy-6-methylpregna-3,6-diene-3,20-dione. A progestational hormone used most commonly as the acetate ester. As the acetate, it is more potent than progesterone both as a progestagen and as an ovulation inhibitor. It has also been used in the palliative treatment of breast cancer. For the treatment of anorexia, cachexia, or an unexplained, significant weight loss in patients with a diagnosis of acquired immunodeficiency syndrome (AIDS). Also used for the palliative management of recurrent, inoperable, or metastatic breast cancer, endometrial cancer, and prostate cancer in Canada and some other countries. Megestrol is a synthetic progestin and has the same physiologic effects as natural progesterone. These effects include induction of secretory changes in the endometrium, increase in basal body temperature, pituitary inhibition, and production of withdrawal bleeding in the presence of estrogen. Mestrogel has slight glucocorticoid activity and very slight mineralocorticoid activity. This drug has no estrogenic, androgenic, or anabolic activity. The precise mechanism of megestrol&rsquo;s antianorexic and anticachetic effects is unknown. Initially developed as a contraceptive, it was first evaluated in breast cancer treatment in 1967. The precise mechanism by which megestrol acetate produces effects in anorexia and cachexia is unknown at the present time, but its progestin antitumour activity may involve suppression of luteinizing hormone by inhibition of pituitary function. Studies also suggest that the megestrol's weight gain effect is related to its appetite-stimulant or metabolic effects rather than its glucocorticoid-like effects or the production of edema. It has also been suggested that megestrol may alter metabolic pathyways via interferences with the production or action of mediators such as cachectin, a hormone that inhibits adipocyte lipogenic enzymes. ",The molecular weight is 384.52.,Megestrol acetate has a topological polar surface area of 60.44.,The log p value of  is 3.77.,Megestrol acetate is approved and investigational and vet_approved.,Megestrol acetate is a solid.,True
15436,"A homolog of ergonovine containing one more CH2 group. (Merck Index, 11th ed) For the prevention and control of excessive bleeding following vaginal childbirth Methylergometrine is a semisynthetic ergot alkaloid and a derivative of ergonovine and is used for the prevention and control of postpartum and post-abortion hemorrhage. In general, the effects of all the ergot alkaloids appear to results from their actions as partial agonists or antagonists at adrenergic, dopaminergic, and tryptaminergic receptors. The spectrum of effects depends on the agent, dosage, species, tissue, and experimental or physiological conditions. All of the alkaloids of ergot significantly increase the motor activity of the uterus. After small doses contractions are increased in force or frequency, or both, but are followed by a normal degree of relaxation. As the dose is increased, contractions become more forceful and prolonged, resting tonus is markedly increased, and sustained contracture can result. Methylergometrine acts directly on the smooth muscle of the uterus and increases the tone, rate, and amplitude of rhythmic contractions through binding and the resultant antagonism of the dopamine D1 receptor. Thus, it induces a rapid and sustained tetanic uterotonic effect which shortens the third stage of labor and reduces blood loss.",The molecular weight is 339.44.,Methylergometrine has a topological polar surface area of 68.36.,The log p value of  is 1.76.,Methylergometrine is approved.,Methylergometrine is a solid.,True
15437,"An aromatase inhibitor that produces a state of \medical\"" adrenalectomy by blocking the production of adrenal steroids. It also blocks the conversion of androgens to estrogens. Aminoglutethimide has been used in the treatment of advanced breast and prostate cancer. It was formerly used for its weak anticonvulsant properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p454)"" For the suppression of adrenal function in selected patients with Cushing's syndrome, malignant neoplasm of the female breast, and carcinoma in situ of the breast. Aminoglutethimide inhibits the enzymatic conversion of cholesterol to D5-pregnenolone, resulting in a decrease in the production of adrenal glucocorticoids, mineralocorticoids, estrogens, and androgens. Aminoglutethimide reduces the production of D5-pregnenolone and blocks several other steps in steroid synthesis, including the C-11, C-18, and C-21 hydroxylations and the hydroxylations required for the aromatization of androgens to estrogens, mediated through the binding of aminoglutethimide to cytochrome P-450 complexes. Specifically, the drug binds to and inhibits aromatase which is essential for the generation of estrogens from androstenedione and testosterone. A decrease in adrenal secretion of cortisol is followed by an increased secretion of pituitary adrenocorticotropic hormone (ACTH), which will overcome the blockade of adrenocortical steroid synthesis by aminoglutethimide. The compensatory increase in ACTH secretion can be suppressed by the simultaneous administration of hydrocortisone. Since aminoglutethimide increases the rate of metabolism of dexamethasone but not that of hydrocortisone, the latter is preferred as the adrenal glucocorticoid replacement. Although aminoglutethimide inhibits the synthesis of thyroxine by the thyroid gland, the compensatory increase in thyroid-stimulating hormone (TSH) is frequently of sufficient magnitude to overcome the inhibition of thyroid synthesis due to aminoglutethimide. In spite of an increase in TSH, aminoglutethimide has not been associated with increased prolactin secretion.",The molecular weight is 232.28.,Aminoglutethimide has a topological polar surface area of 72.19.,The log p value of  is 0.77.,Aminoglutethimide is approved and investigational.,Aminoglutethimide is a solid.,True
15438,"One of the short-acting sulfonamides used in combination with pyrimethamine to treat toxoplasmosis in patients with acquired immunodeficiency syndrome and in newborns with congenital infections. For the treatment of rheumatic fever and meningococcal meningitis Sulfadiazine is a sulfonamide antibiotic. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of <i>p</i>-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus. Sulfadiazine is a competitive inhibitor of the bacterial enzyme dihydropteroate synthetase. This enzyme is needed for the proper processing of para-aminobenzoic acid (PABA) which is essential for folic acid synthesis. The inhibited reaction is necessary in these organisms for the synthesis of folic acid.",The molecular weight is 250.28.,Sulfadiazine has a topological polar surface area of 97.97.,The log p value of  is 0.1.,Sulfadiazine is approved and investigational and vet_approved.,Sulfadiazine is a solid.,True
15439,"A synthetic progestational hormone with no androgenic or estrogenic properties. Unlike many other progestational compounds, dydrogesterone produces no increase in temperature and does not inhibit ovulation. Used to treat irregular duration of cycles and irregular occurrence and duration of periods caused by progesterone deficiency. Also used to prevent natural abortion in patients who have a history of habitual abortions. Dydrogesterone is an orally active progestogen which acts directly on the uterus, producing a complete secretory endometrium in an estrogen-primed uterus. At therapeutic levels, dydrogesterone has no contraceptive effect as it does not inhibit or interfere with ovulation or the corpus luteum. Furthermore, dydrogesterone is non-androgenic, non-estrogenic, non-corticoid, non-anabolic and is not excreted as pregnanediol. Dydrogesterone helps to regulate the healthy growth and normal shedding of the uterus lining. Therefore, it may be useful in the treatment of menstrual disorders such as absent, irregular or painful menstrual periods, infertility, premenstrual syndrome and endometriosis. Dydrogesterone is a progestogen that works by regulating the healthy growth and normal shedding of the womb lining by acting on progesterone receptors in the uterus.",The molecular weight is 312.45.,Dydrogesterone has a topological polar surface area of 34.14.,The log p value of  is 3.54.,Dydrogesterone is approved and investigational and withdrawn.,Dydrogesterone is a solid.,True
15440,"Nimodipine is a 1,4-dihydropyridine calcium channel blocker. It acts primarily on vascular smooth muscle cells by stabilizing voltage-gated L-type calcium channels in their inactive conformation. By inhibiting the influx of calcium in smooth muscle cells, nimodipine prevents calcium-dependent smooth muscle contraction and subsequent vasoconstriction. Compared to other calcium channel blocking agents, nimodipine exhibits greater effects on cerebral circulation than on peripheral circulation. Nimodipine is used to as an adjunct to improve the neurologic outcome following subarachnoid hemorrhage from ruptured intracranial aneurysm. For use as an adjunct to improve neurologic outcome following subarachnoid hemorrhage (SAH) from ruptured intracranial berry aneurysms by reducing the incidence and severity of ischemic deficits. Nimodipine belongs to the class of pharmacological agents known as calcium channel blockers. Nimodipine is indicated for the improvement of neurological outcome by reducing the incidence and severity of ischemic deficits in patients with subarachnoid hemorrhage from ruptured congenital aneurysms who are in good neurological condition post-ictus (e.g., Hunt and Hess Grades I-III). The contractile processes of smooth muscle cells are dependent upon calcium ions, which enter these cells during depolarization as slow ionic transmembrane currents. Nimodipine inhibits calcium ion transfer into these cells and thus inhibits contractions of vascular smooth muscle. In animal experiments, nimodipine had a greater effect on cerebral arteries than on arteries elsewhere in the body perhaps because it is highly lipophilic, allowing it to cross the blood brain barrier.  Although the precise mechanism of action is not known, nimodipine blocks intracellular influx of calcium through voltage-dependent and receptor-operated slow calcium channels across the membranes of myocardial, vascular smooth muscle, and neuronal cells. By specifically binding to L-type voltage-gated calcium channels, nimodipine inhibits the calcium ion transfer, resulting in the inhibition of vascular smooth muscle contraction. Evidence suggests that the dilation of small cerebral resistance vessels, with a resultant increase in collateral circulation, and/or a direct effect involving the prevention of calcium overload in neurons may be responsible for nimodipine's clinical effect in patients with subarachnoid hemorrhage.",The molecular weight is 418.45.,Nimodipine has a topological polar surface area of 117.0.,The log p value of  is 4.0.,Nimodipine is approved and investigational.,Nimodipine is a solid.,True
15441,"Eszopiclone, marketed by Sepracor under the brand-name Lunesta, is a nonbenzodiazepine hypnotic drug used to treat insomnia. It is the active stereoisomer of zopiclone, belonging to the class of drugs known as _cyclopyrrolones_. Cyclopyrrolone drugs demonstrate high efficacy and low toxicity, offering a safer alternative to other drugs used for insomnia. Eszopiclone is indicated for the treatment of insomnia. Eszopiclone rapidly induces sleep and decreases sleep latency. It also aids in the maintenance of sleep, preventing frequent awakenings. This drug has shown anticonvulsant and muscle relaxant properties in animals but is used in humans for its sedating effects. The exact mechanism of action of eszopiclone is unknown at this time but is thought to occur via binding with the GABA receptor complexes at binding sites located near benzodiazepine receptors, possibly explaining its hypnotic and sedative effects. It has particular affinity for GABA-A (or GABAA) receptor subunits 1, 3 and 5. Eszopiclone increases GABA-A channel currents significantly. GABA-A channels are major inhibitory channels that cause CNS depression when their receptors are activated.",The molecular weight is 388.81.,Eszopiclone has a topological polar surface area of 91.76.,The log p value of  is 1.25.,Eszopiclone is approved and investigational.,Eszopiclone is a solid.,True
15442,"One of the penicillins which is resistant to penicillinase. Used to treat infections caused by penicillinase-producing staphylococci which have demonstrated susceptibility to the drug. Dicloxacillin is a beta-lactamase resistant penicillin similar to oxacillin. Dicloxacillin has <i>in vitro</i> activity against gram-positive and gram-negative aerobic and anaerobic bacteria. The bactericidal activity of dicloxacillin results from the inhibition of cell wall synthesis and is mediated through dicloxacillin binding to penicillin binding proteins (PBPs). Dicloxacillin is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, and cephalosporinases and extended spectrum beta-lactamases. Dicloxacillin exerts a bactericidal action against penicillin-susceptible microorganisms during the state of active multiplication. All penicillins inhibit the biosynthesis of the bacterial cell wall. By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, dicloxacillin inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that dicloxacillin interferes with an autolysin inhibitor.",The molecular weight is 470.32.,Dicloxacillin has a topological polar surface area of 112.74.,The log p value of  is 2.98.,Dicloxacillin is approved and investigational and vet_approved.,Dicloxacillin is a solid.,True
15443,"Caspofungin (brand name Cancidas worldwide) is an antifungal drug and the first member of a new drug class called the echinocandins, as coined by Merck & Co., Inc. It is typically administered intravenously. It shows activity against infections with Aspergillus and Candida, and works by inhibiting β(1,3)-D-Glucan of the fungal cell wall. For the treatment of esophageal candidiasis and invasive aspergillosis in patients who are refractory to or intolerant of other therapies. Caspofungin is an antifungal drug, and belongs to a new class termed the echinocandins. It is used to treat <i>Aspergillus</i> and <i>Candida</i> infection, and works by inhibiting cell wall synthesis. Antifungals in the echinocandin class inhibit the synthesis of glucan in the cell wall, probably via the enzyme 1,3-beta glucan synthase. There is a potential for resistance development to occur, however <i>in vitro</i> resistance development to Caspofungin by Aspergillus species has not been studied. Caspofungin inhibits the synthesis of beta-(1,3)-D-glucan, an essential component of the cell wall of <i>Aspergillus</i> species and <i>Candida</i> species. beta-(1,3)-D-glucan is not present in mammalian cells. The primary target is beta-(1,3)-glucan synthase.",The molecular weight is 1093.33.,Caspofungin has a topological polar surface area of 412.03.,The log p value of  is -2.95.,Caspofungin is approved.,Caspofungin is a solid.,True
15444,"A first generation nonsteroidal selective estrogen receptor modulator (SERM) that is structurally related to tamoxifen. Like tamoxifen, it is an estrogen agonist for bone tissue and cholesterol metabolism but is antagonistic on mammary and uterine tissue. For the treatment of metastatic breast cancer in postmenopausal women with estrogen receptor-positive or receptor-unknown tumors. Toremifene is currently under investigation as a preventative agent for prostate cancer in men with high-grade prostatic intraepithelial neoplasia and no evidence of prostate cancer. Toremifene is an antineoplastic hormonal agent primarily used in the treatment of advanced breast cancer. Toremifene is a nonsteroidal agent that has demonstrated potent antiestrogenic properties in animal test systems. The antiestrogenic effects may be related to its ability to compete with estrogen for binding sites in target tissues such as breast. Toremifene inhibits the induction of rat mammary carcinoma induced by dimethylbenzanthracene (DMBA) and causes the regression of already established DMBA-induced tumors. In this rat model, Toremifene appears to exert its antitumor effects by binding the estrogen receptors. In cytosols derived from human breast adenocarcinomas, Toremifene competes with estradiol for estrogen receptor protein. Toremifene is a nonsteroidal triphenylethylene derivative. Toremifene binds to estrogen receptors and may exert estrogenic, antiestrogenic, or both activities, depending upon the duration of treatment, animal species, gender, target organ, or endpoint selected. The antitumor effect of toremifene in breast cancer is believed to be mainly due to its antiestrogenic effects, in other words, its ability to compete with estrogen for binding sites in the cancer, blocking the growth-stimulating effects of estrogen in the tumor. Toremifene may also inhibit tumor growth through other mechanisms, such as induction of apoptosis, regulation of oncogene expression, and growth factors.",The molecular weight is 405.97.,Toremifene has a topological polar surface area of 12.47.,The log p value of  is 6.53.,Toremifene is approved and investigational.,Toremifene is a solid.,True
15445,"Adinazolam (Deracyn®) is a benzodiazepine derivative with anxiolytic, anticonvulsant, sedative, and antidepressant properties. Adinazolam was first developed to enhance the antidepressant effects of. It has never been approved by the FDA for clinical use. For the treatment of anxiety and status epilepticus. Adinazolam is a benzodiazepine derivative used to treat anxiety, status epilepticus, and for sedation induction and anterograde amnesia. Adinazolam binds with high affinity to the GABA benzodiazepine receptor complex. Considerable evidence suggest that the central pharmacologic/therapeutic actions of alprazolam are mediated via interaction with this receptor complex. Adinazolam binds to peripheral-type benzodiazepine receptors which interact allosterically with GABA receptors. This potentiates the effects of the inhibitory neurotransmitter GABA, increasing the inhibition of the ascending reticular activating system and blocking the cortical and limbic arousal that occurs following stimulation of the reticular pathways.",The molecular weight is 351.84.,Adinazolam has a topological polar surface area of 46.31.,The log p value of  is 2.12.,Adinazolam is experimental.,Adinazolam is a solid.,True
15446,"Bosentan is a dual endothelin receptor antagonist marketed under the trade name Tracleer by Actelion Pharmaceuticals. Bosentan is used to treat pulmonary hypertension by blocking the action of endothelin molecules that would otherwise promote narrowing of the blood vessels and lead to high blood pressure. Used in the treatment of pulmonary arterial hypertension (PAH), to improve exercise ability and to decrease the rate of clinical worsening (in patients with WHO Class III or IV symptoms). Bosentan belongs to a class of drugs known as endothelin receptor antagonists (ERAs). Patients with PAH have elevated levels of endothelin, a potent blood vessel constrictor, in their plasma and lung tissue. Bosentan blocks the binding of endothelin to its receptors, thereby negating endothelin's deleterious effects. Endothelin-1 (ET-1) is a neurohormone, the effects of which are mediated by binding to ET<sub>A</sub> and ET<sub>B</sub> receptors in the endothelium and vascular smooth muscle. It displays a slightly higher affinity towards ET<sub>A</sub> receptors than ET<sub>B</sub> receptors. ET-1 concentrations are elevated in plasma and lung tissue of patients with pulmonary arterial hypertension, suggesting a pathogenic role for ET-1 in this disease. Bosentan is a specific and competitive antagonist at endothelin receptor types ET<sub>A</sub> and ET<sub>B</sub>.",The molecular weight is 551.62.,Bosentan has a topological polar surface area of 145.65.,The log p value of  is 4.17.,Bosentan is approved and investigational.,Bosentan is a solid.,True
15447,"Valdecoxib was removed from the Canadian, U.S., and E.U. markets in 2005 due to concerns about a possible increased risk of heart attack and stroke. For the treatment of osteoarthritis and dysmenorrhoea Valdecoxib, a selective cyclooxygenase-2 (COX-2) inhibitor, is classified as a nonsteroidal anti-inflammatory drug (NSAID). Valdecoxib is used for its anti-inflammatory, analgesic, and antipyretic activities in the management of osteoarthritis (OA) and for the treatment of dysmenorrhea or acute pain. Unlike celecoxib, valdecoxib lacks a sulfonamide chain and does not require CYP450 enzymes for metabolism. Both COX-1 and COX-2 catalyze the conversion of arachidonic acid to prostaglandin (PG) H2, the precursor of PGs and thromboxane. Valdecoxib selectively inhibits the cyclooxygenase-2 (COX-2) enzyme, important for the mediation of inflammation and pain. Unlike non-selective NSAIDs, valdecoxib does not inhibit platelet aggregation.",The molecular weight is 314.36.,Valdecoxib has a topological polar surface area of 86.19.,The log p value of  is 1.83.,Valdecoxib is approved and investigational and withdrawn.,Valdecoxib is a solid.,True
15448,"An ergot derivative that acts as an agonist at dopamine D2 receptors (dopamine agonists). It may also act as an antagonist at dopamine D1 receptors, and as an agonist at some serotonin receptors (serotonin agonists). For the management of Parkinson's Disease There is evidence that lisuride lowers prolactin levels and, in low doses, prevents migraine attacks.  Lisuride is an anti-Parkinson drug chemically related to the dopaminergic ergoline Parkinson's drugs. Lisuride binds to the 5-HT(1A) and 5-HT(2A/2C) receptors. It is also thought to bind to the dopamine receptor and to act as a dopamine agonist. Evidence has also emerged that Lisuride also binds to the Histamine H1 receptor. ",The molecular weight is 338.46.,Lisuride has a topological polar surface area of 51.37.,The log p value of  is 2.67.,Lisuride is approved and investigational.,Lisuride is a solid.,True
15449,"An anticonvulsant especially useful in the treatment of absence seizures unaccompanied by other types of seizures. For the treatment of petit mal epilepsy. Used in the treatment of epilepsy. Ethosuximide suppresses the paroxysmal three cycle per second spike and wave activity associated with lapses of consciousness which is common in absence (petit mal) seizures. The frequency of epileptiform attacks is reduced, apparently by depression of the motor cortex and elevation of the threshold of the central nervous system to convulsive stimuli. Binds to T-type voltage sensitive calcium channels. Voltage-sensitive calcium channels (VSCC) mediate the entry of calcium ions into excitable cells and are also involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division and cell death. The isoform alpha-1G gives rise to T-type calcium currents. T-type calcium channels belong to the \low-voltage activated (LVA)\"" group and are strongly blocked by mibefradil. A particularity of this type of channels is an opening at quite negative potentials and a voltage-dependent inactivation. T-type channels serve pacemaking functions in both central neurons and cardiac nodal cells and support calcium signaling in secretory cells and vascular smooth muscle. They may also be involved in the modulation of firing patterns of neurons which is important for information processing as well as in cell growth processes.""",The molecular weight is 141.17.,Ethosuximide has a topological polar surface area of 46.17.,The log p value of  is 0.39.,Ethosuximide is approved.,Ethosuximide is a solid.,True
15450,"Ivermectin is a broad-spectrum anti-parasite medication. It was first marketed under the name Stromectol® and used against worms (except tapeworms), but, in 2012, it was approved for the topical treatment of head lice infestations in patients 6 months of age and older, and marketed under the name Sklice™ as well. Ivermectin is mainly used in humans in the treatment of onchocerciasis, but is also effective against other worm infestations (such as strongyloidiasis, ascariasis, trichuriasis and enterobiasis). For the treatment of intestinal (i.e., nondisseminated) strongyloidiasis due to the nematode parasite <i>Strongyloides stercoralis</i>. Also for the treatment of onchocerciasis (river blindness) due to the nematode parasite <i>Onchocerca volvulus</i>. Can be used to treat scabies caused by <i>Sarcoptes scabiei</i>. Ivermectin is a semisynthetic, anthelminitic agent. It is an avermectin which a group of pentacyclic sixteen-membered lactone (i.e. a macrocyclic lactone disaccharide) derived from the soil bacterium Streptomyces avermitilis. Avermectins are potent anti-parasitic agents. Ivermectin is the most common avermectin. It is a broad spectrum antiparasitic drug for oral administration. It is sometimes used to treat human onchocerciasis (river blindness). It is the mixture of 22,23-dihydro-avermectin B1a (at least 90%) and 22,23-dihydro-avermectin B1b (less than 10%). Ivermectin binds selectively and with high affinity to glutamate-gated chloride ion channels in invertebrate muscle and nerve cells of the microfilaria. This binding causes an increase in the permeability of the cell membrane to chloride ions and results in hyperpolarization of the cell, leading to paralysis and death of the parasite. Ivermectin also is believed to act as an agonist of the neurotransmitter gamma-aminobutyric acid (GABA), thereby disrupting GABA-mediated central nervous system (CNS) neurosynaptic transmission. Ivermectin may also impair normal intrauterine development of O. volvulus microfilariae and may inhibit their release from the uteri of gravid female worms.",The molecular weight is 1736.18.,,,Ivermectin is approved and investigational and vet_approved.,Ivermectin is a solid.,True
15451,"Bisoprolol is a cardioselective β1-adrenergic blocking agent used to treat high blood pressure. It is considered a potent drug with a long-half life that can be used once daily to reduce the need for multiple doses of antihypertensive drugs. Bisoprolol is generally well tolerated, likely due to its β1-adrenergic receptor selectivity and is a useful alternative to non-selective β-blocker drugs in the treatment of hypertension such as and. It may be used alone or in combination with other drugs to manage hypertension and can be useful in patients with chronic obstructive pulmonary disease (COPD) due to its receptor selectivity. Bisoprolol is indicated for the treatment of mild to moderate hypertension. It may be used off-label to treat heart failure, atrial fibrillation, and angina pectoris. Bisoprolol decreases heart rate (chronotropy), decreases contractility (inotropy), and reduces blood pressure. The results of various clinical studies indicate that bisoprolol reduces cardiovascular mortality and all-cause mortality in patients with heart failure and decreased cardiac ejection fraction (EF).  Though the mechanism of action of bisoprolol has not been fully elucidated in hypertension, it is thought that therapeutic effects are achieved through the antagonism of β-1adrenoceptors to result in lower cardiac output. Bisoprolol is a competitive, cardioselective β1-adrenergic antagonist. When β1-receptors (located mainly in the heart) are activated by adrenergic neurotransmitters such as epinephrine, both the blood pressure and heart rate increase, leading to greater cardiovascular work, increasing the demand for oxygen. Bisoprolol reduces cardiac workload by decreasing contractility and the need for oxygen through competitive inhibition of β1-adrenergic receptors.",The molecular weight is 325.45.,Bisoprolol has a topological polar surface area of 59.95.,The log p value of  is 1.79.,Bisoprolol is approved.,Bisoprolol is a solid.,True
15452,"A broad-spectrum antibiotic that is being used as prophylaxis against disseminated Mycobacterium avium complex infection in HIV-positive patients. For the prevention of disseminated <i>Mycobacterium avium</i> complex (MAC) disease in patients with advanced HIV infection. Rifabutin is an antibiotic that inhibits DNA-dependent RNA polymerase activity in susceptible cells. Specifically, it interacts with bacterial RNA polymerase but does not inhibit the mammalian enzyme. It is bactericidal and has a very broad spectrum of activity against most gram-positive and gram-negative organisms (including <i>Pseudomonas aeruginosa</i>) and specifically <i>Mycobacterium tuberculosis</i>. Because of rapid emergence of resistant bacteria, use is restricted to treatment of mycobacterial infections and a few other indications. Rifabutin is well absorbed when taken orally and is distributed widely in body tissues and fluids, including the CSF. It is metabolized in the liver and eliminated in bile and, to a much lesser extent, in urine, but dose adjustments are unnecessary with renal insufficiency. Rifabutin acts via the inhibition of DNA-dependent RNA polymerase in gram-positive and some gram-negative bacteria, leading to a suppression of RNA synthesis and cell death.",The molecular weight is 847.02.,Rifabutin has a topological polar surface area of 205.55.,The log p value of  is 4.73.,Rifabutin is approved and investigational.,Rifabutin is a solid.,True
15453,"Paramethadione is an anticonvulsant in the oxazolidinedione class. It is associated with fetal trimethadione syndrome, which is also known as paramethadione syndrome. Used for the control of absence (petit mal) seizures that are refractory to treatment with other medications. Paramethadione is an oxazolidinedione anticonvulsant similar to trimethadione that acts on the central nervous system (CNS) to reduce the number of absence seizures (often seen in epileptics). Absence seizures involve an interruption to consciousness where the person experiencing the seizure seems to become vacant and unresponsive for a short period of time (usually up to 30 seconds). Paramethadione acts on thalamic neurons in the thalamic reticular nucleus (which studies have shown to be associated with absence seizures, von Krosigk et al., 1993). Dione anticonvulsants such as paramethadione reduce T-type calcium currents in thalamic neurons (including thalamic relay neurons). This inhibits corticothalamic transmission and raises the threshold for repetitive activity in the thalamus. This results in a dampening of the abnormal thalamocortical rhythmicity proposed to underlie the 3-Hz spike-and-wave discharge seen on electroencephalogram (EEG) during absence seizures.",The molecular weight is 157.17.,Paramethadione has a topological polar surface area of 46.61.,The log p value of  is 0.41.,Paramethadione is approved.,Paramethadione is a liquid.,True
15454,"A water-soluble benzodiazepine derivative effective in the treatment of anxiety. It has also muscle relaxant and anticonvulsant actions. For the management of anxiety disorders or for the short-term relief of the symptoms of anxiety. Also used as adjunctive therapy in the management of partial seizures and for the symptomatic relief of acute alcohol withdrawal. Clorazepate is a member of the group of drugs called benzodiazepines. Pharmacologically, clorazepate has the characteristics of the benzodiazepines. It has depressant effects on the central nervous system. The primary metabolite, nordiazepam, quickly appears in the blood stream. Studies in healthy men have shown that clorazenate has depressant effects on the central nervous system. Since orally administered clorazepate dipotassium is rapidly decarboxylated to form nordiazepam, there is essentially no circulating parent drug. Benzodiazepines bind nonspecifically to benzodiazepine receptors BNZ1, which mediates sleep, and BNZ2, which affects affects muscle relaxation, anticonvulsant activity, motor coordination, and memory. As benzodiazepine receptors are thought to be coupled to gamma-aminobutyric acid-A (GABA<sub>A</sub>) receptors, this enhances the effects of GABA by increasing GABA affinity for the GABA receptor. Binding of the inhibitory neurotransmitter GABA to the site opens the chloride channel, resulting in a hyperpolarized cell membrane that prevents further excitation of the cell.",,,,Clorazepic acid is approved and illicit.,Clorazepic acid is a solid.,True
15455,"Aprepitant, an antiemetic, is a substance P/neurokinin 1 (NK1) receptor antagonist which, in combination with other antiemetic agents, is indicated for the prevention of acute and delayed nausea and vomiting associated with initial and repeat courses of highly emetogenic cancer chemotherapy. Aprepitant is a selective high-affinity antagonist of human substance P/neurokinin 1 (NK1) receptors. Aprepitant has little or no affinity for serotonin (5-HT3), dopamine, and corticosteroid receptors, the targets of existing therapies for chemotherapy-induced nausea and vomiting (CI NV). For the prevention of nausea and vomiting associated with highly emetogenic cancer chemotherapy, including high-dose cisplatin (in combination with other antiemetic agents). Aprepitant, an antiemetic, is a substance P/neurokinin 1 (NK1) receptor antagonist which, in combination with other antiemetic agents, is indicated for the prevention of acute and delayed nausea and vomiting associated with initial and repeat courses of highly emetogenic cancer chemotherapy. Aprepitant is a selective high-affinity antagonist of human substance P/neurokinin 1 (NK1) receptors. Aprepitant has little or no affinity for serotonin (5-HT<sub>3</sub>), dopamine, and corticosteroid receptors, the targets of existing therapies for chemotherapy-induced nausea and vomiting (CI NV). Aprepitant has been shown in animal models to inhibit emesis induced by cytotoxic chemotherapeutic agents, such as cisplatin, via central actions. Animal and human Positron Emission Tomography (PET) studies with Aprepitant have shown that it crosses the blood brain barrier and occupies brain NK1 receptors. Animal and human studies show that Aprepitant augments the antiemetic activity of the 5-HT<sub>3</sub>-receptor antagonist ondansetron and the corticosteroid",The molecular weight is 534.43.,Aprepitant has a topological polar surface area of 75.19.,The log p value of  is 4.6.,Aprepitant is approved and investigational.,Aprepitant is a solid.,True
15456,"Amphotericin B shows a high order of in vitro activity against many species of fungi. Histoplasma capsulatum, Coccidioides immitis, Candida species, Blastomyces dermatitidis, Rhodotorula, Cryptococcus neoformans, Sporothrix schenckii, Mucor mucedo, and Aspergillus fumigatus are all inhibited by concentrations of amphotericin B ranging from 0.03 to 1.0 mcg/mL in vitro. While Candida albicans is generally quite susceptible to amphotericin B, non-albicans species may be less susceptible. Pseudallescheria boydii and Fusarium sp. are often resistant to amphotericin B. The antibiotic is without effect on bacteria, rickettsiae, and viruses. Used to treat potentially life threatening fungal infections. Amphotericin B shows a high order of <i>in vitro</i> activity against many species of fungi. <i>Histoplasma capsulatum</i>, <i>Coccidioides immitis</i>, <i>Candida species</i>, <i>Blastomyces dermatitidis</i>, <i>Rhodotorula</i>, <i>Cryptococcus neoformans</i>, <i>Sporothrix schenckii</i>, <i>Mucor mucedo</i>, and <i>Aspergillus fumigatus</i> are all inhibited by concentrations of amphotericin B ranging from 0.03 to 1.0 mcg/mL <i>in vitro</i>. While <i>Candida albicans</i> is generally quite susceptible to amphotericin B, non-<i>albicans</i> species may be less susceptible. <i>Pseudallescheria boydii</i> and <i>Fusarium</i> sp. are often resistant to amphotericin B. The antibiotic is without effect on bacteria, rickettsiae, and viruses. Amphotericin B is fungistatic or fungicidal depending on the concentration obtained in body fluids and the susceptibility of the fungus. The drug acts by binding to sterols (ergosterol) in the cell membrane of susceptible fungi. This creates a transmembrane channel, and the resultant change in membrane permeability allowing leakage of intracellular components. Ergosterol, the principal sterol in the fungal cytoplasmic membrane, is the target site of action of amphotericin B and the azoles. Amphotericin B, a polyene, binds irreversibly to ergosterol, resulting in disruption of membrane integrity and ultimately cell death.",The molecular weight is 924.09.,Amphotericin B has a topological polar surface area of 319.61.,The log p value of  is -3.65.,Amphotericin B is approved and investigational.,Amphotericin B is a solid.,True
15457,"A benzodiazepine derivative used mainly as a hypnotic. For short-term and intermittent use in patients with recurring insomnia and poor sleeping habits Flurazepam, a benzodiazepine derivative, is a hypnotic agent which does not appear to decrease dream time as measured by rapid eye movements (REM). Furthermore, it decreases sleep latency and number of awakenings for a consequent increase in total sleep time. Flurazepam binds to an allosteric site on GABA-A receptors. Binding potentiates the action of GABA on GABA-A receptors by opening the chloride channel within the receptor, causing chloride influx and hyperpolarization.",The molecular weight is 387.88.,Flurazepam has a topological polar surface area of 35.91.,The log p value of  is 4.22.,Flurazepam is approved and illicit and investigational.,Flurazepam is a solid.,True
15458,"A vasoconstrictor found in ergot of Central Europe. It is an alpha-1 selective adrenergic agonist and is commonly used in the treatment of migraine disorders. For use as therapy to abort or prevent vascular headache, e.g., migraine, migraine variants, or so called \histaminic cephalalgia\""."" Ergotamine is a vasoconstrictor and alpha adrenoreceptor antagonist. The pharmacological properties of ergotamine are extremely complex; some of its actions are unrelated to each other, and even mutually antagonistic. The drug has partial agonist and/or antagonist activity against tryptaminergic, dopaminergic and alpha adrenergic receptors depending upon their site, and it is a highly active uterine stimulant. It causes constriction of peripheral and cranial blood vessels and produces depression of central vasomotor centers. The pain of a migraine attack is believed to be due to greatly increased amplitude of pulsations in the cranial arteries, especially the meningeal branches of the external carotid artery. Ergotamine reduces extracranial blood flow, causes a decline in the amplitude of pulsation in the cranial arteries, and decreases hyperperfusion of the territory of the basilar artery. It does not reduce cerebral hemispheric blood flow. Ergotamine acts on migraine by one of two proposed mechanisms: 1) activation of 5-HT<sub>1D</sub> receptors located on intracranial blood vessels, including those on arterio-venous anastomoses, leads to vasoconstriction, which correlates with the relief of migraine headache, and 2) activation of 5-HT<sub>1D</sub> receptors on sensory nerve endings of the trigeminal system results in the inhibition of pro-inflammatory neuropeptide release.",The molecular weight is 581.67.,Ergotamine has a topological polar surface area of 118.21.,The log p value of  is 4.66.,Ergotamine is approved.,Ergotamine is a solid.,True
15459,"Sufentanil is an opioid analgesic that is used as an adjunct in anesthesia, in balanced anesthesia, and as a primary anesthetic agent. It is administered by the intravenous, epidural and sublingual routes.  The indications for this drug are as follows: **Effect on the Central Nervous System (CNS)** Sufentanil is a synthetic, potent opioid with highly selective binding to μ-opioid receptors. These receptors are widely distributed in the human brain, spinal cord, and other tissues ,.",The molecular weight is 386.55.,Sufentanil has a topological polar surface area of 32.78.,The log p value of  is 3.59.,Sufentanil is approved and investigational.,Sufentanil is a solid.,True
15460,"Antihistamines such as azatadine appear to compete with histamine for histamine H1- receptor sites on effector cells. The antihistamines antagonize those pharmacological effects of histamine which are mediated through activation of H1- receptor sites and thereby reduce the intensity of allergic reactions and tissue injury response involving histamine release. For the relief of the symptoms of upper respiratory mucosal congestion in perennial and allergic rhinitis, and for the relief of nasal congestion and eustachian t.b. congestion. Azatadine is an antihistamine, related to cyproheptadine, with anti-serotonin, anticholinergic (drying), and sedative effects. Azatadine is in the same class of drugs as chlorpromazine (Thorazine) and trifluoperazine (Stelazine); however, unlike the other drugs in this class, azatadine is not used clinically as an anti-psychotic. Antihistamines antagonize the vasodilator effect of endogenously released histamine, especially in small vessels, and mitigate the effect of histamine which results in increased capillary permeability and edema formation. As consequences of these actions, antihistamines antagonize the physiological manifestations of histamine release in the nose following antigen-antibody interaction, such as congestion related to vascular engorgement, mucosal edema, and profuse, watery secretion, and irritation and sneezing resulting from histamine action on afferent nerve terminals. Antihistamines such as azatadine appear to compete with histamine for histamine H1- receptor sites on effector cells. The antihistamines antagonize those pharmacological effects of histamine which are mediated through activation of H1- receptor sites and thereby reduce the intensity of allergic reactions and tissue injury response involving histamine release.",The molecular weight is 290.41.,Azatadine has a topological polar surface area of 16.13.,The log p value of  is 3.56.,Azatadine is approved.,Azatadine is a solid.,True
15461,"Imiquimod is an immune response modifier that acts as a toll-like receptor 7 agonist. Imiquimod is commonly used topically to treat warts on the skin of the genital and anal areas. Imiquimod does not cure warts, and new warts may appear during treatment. Imiquimod does not fight the viruses that cause warts directly, however, it does help to relieve and control wart production. Miquimod is also used to treat a skin condition of the face and scalp called actinic keratoses and certain types of skin cancer called superficial basal cell carcinoma. For the topical treatment of clinically typical, nonhyperkeratotic, nonhypertrophic actinic keratoses on the face or scalp in immunocompetent adults. Also indicated for the treatment of external genital and perianal warts/condyloma acuminata in individuals 12 years old and above. Imiquimod is an immune response modifier that acts as a toll-like receptor 7 agonist. Imiquimod is commonly used topically to treat warts on the skin of the genital and anal areas. Imiquimod does not cure warts, and new warts may appear during treatment. Imiquimod does not fight the viruses that cause warts directly, however, it does help to relieve and control wart production. It is not used on warts inside the vagina, penis, or rectum. Imiquimod is also used to treat a skin condition of the face and scalp called actinic keratoses. Imiquimod can also be used to treat certain types of skin cancer called superficial basal cell carcinoma. Imiquimod is particularly useful on areas where surgery or other treatments may be difficult, complicated or otherwise undesirable, especially the face and lower legs. Imiquimod's mechanism of action is via stimulation of innate and acquired immune responses, which ultimately leads to inflammatory cell infiltration within the field of drug application followed by apoptosis of diseased tissue. Imiquimod does not have direct antiviral activity. Studies of mice show that imiquimod may induce cytokines, including interferon-alpha (IFNA) as well as several IFNA genes (IFNA1, IFNA2, IFNA5, IFNA6, and IFNA8) as well as the IFNB gene. Imiquimod also induced the expression of interleukin (IL)-6, IL-8, and tumor necrosis factor alpha genes. In the treatment of basal cell carcinoma, Imiquimod appears to act as a toll-like receptor-7 agonist, and is thought to exert its anti-tumor effect via modification of the immune response and stimulation of apoptosis in BCC cells. In treating basal cell carcinoma it may increase the infiltration of lymphocytes, dendritic cells, and macrophages into the tumor lesion.",The molecular weight is 240.31.,Imiquimod has a topological polar surface area of 56.73.,The log p value of  is 3.24.,Imiquimod is approved and investigational.,Imiquimod is a solid.,True
15462,"Esomeprazole, sold under the brand name Nexium, is a proton pump inhibitor (PPI) medication used for the management of gastroesophageal reflux disease (GERD), for gastric protection to prevent recurrence of stomach ulcers or gastric damage from chronic use of NSAIDs, and for the treatment of pathological hypersecretory conditions including Zollinger-Ellison (ZE) Syndrome. It can also be found in quadruple regimens for the treatment of _H. pylori_ infections along with other antibiotics including , , and , for example. Its efficacy is considered similar to other medications within the PPI class including , , , , and. Esomeprazole is the s-isomer of , which is a racemate of the S- and R-enantiomer. Esomeprazole has been shown to inhibit acid secretion to a similar extent as , without any significant differences between the two compounds _in vitro_.  Esomeprazole is indicated for the treatment of acid-reflux disorders including healing and maintenance of erosive esophagitis, and symptomatic gastroesophageal reflux disease (GERD), peptic ulcer disease, H. pylori eradication, prevention of gastrointestinal bleeds with NSAID use, and for the long-term treatment of pathological hypersecretory conditions including Zollinger-Ellison Syndrome.  Esomeprazole is a compound that inhibits gastric acid secretion and is indicated in the treatment of gastroesophageal reflux disease (GERD), the healing of erosive esophagitis, and <i>H. pylori</i> eradication to reduce the risk of duodenal ulcer recurrence. Esomeprazole belongs to a new class of antisecretory compounds, the substituted benzimidazoles, that do not exhibit anticholinergic or H2 histamine antagonistic properties, but that suppress gastric acid secretion by specific inhibition of the H<sup>+</sup>/K<sup>+</sup> ATPase at the secretory surface of the gastric parietal cell. By doing so, it inhibits acid secretion into the gsatric lumen. This effect is dose-related and leads to inhibition of both basal and stimulated acid secretion irrespective of the stimulus. Esomeprazole exerts its stomach acid-suppressing effects by preventing the final step in gastric acid production by covalently binding to sulfhydryl groups of cysteines found on the (H+, K+)-ATPase enzyme at the secretory surface of gastric parietal cells. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. As the binding of esomeprazole to the (H+, K+)-ATPase enzyme is irreversible and new enzyme needs to be expressed in order to resume acid secretion, esomeprazole's duration of antisecretory effect that persists longer than 24 hours.",The molecular weight is 345.42.,Esomeprazole has a topological polar surface area of 77.1.,The log p value of  is 2.57.,Esomeprazole is approved and investigational.,Esomeprazole is a solid.,True
15463,"Hydrocortamate is a synthetic glucocorticoid used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Used topically as an antiinflammatory in the treatment of steroid-responsive dermatoses Hydrocortamate is a synthetic glucocorticoid used for its anti-inflammatory or immunosuppressive properties to treat inflammation due to corticosteroid-responsive dermatoses. Glucocorticoids are a class of steroid hormones characterised by an ability to bind with the cortisol receptor and trigger a variety of important cardiovascular, metabolic, immunologic and homeostatic effects. Glucocorticoids are distinguished from mineralocorticoids and sex steroids by having different receptors, target cells, and effects. Technically, the term corticosteroid refers to both glucocorticoids and mineralocorticoids, but is often used as a synonym for glucocorticoid. Glucocorticoids suppress cell-mediated immunity. They act by inhibiting genes that code for the cytokines IL-1, IL-2, IL-3, IL-4, IL-5, IL-6, IL-8 and TNF-alpha, the most important of which is the IL-2. Reduced cytokine production limits T cell proliferation. Glucocorticoids also suppress humoral immunity, causing B cells to express lower amounts of IL-2 and IL-2 receptors. This diminishes both B cell clonal expansion and antibody synthesis. The diminished amounts of IL-2 also leads to fewer T lymphocyte cells being activated. Hydrocortamate binds to the cytosolic glucocorticoid receptor. After binding the receptor the newly formed receptor-ligand complex translocates itself into the cell nucleus, where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. The immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.",The molecular weight is 475.63.,Hydrocortamate has a topological polar surface area of 104.14.,The log p value of  is 3.5.,Hydrocortamate is approved.,Hydrocortamate is a solid.,True
15464,"Roxithromycin is a semi-synthethic macrolide antibiotic that is structurally and pharmacologically similar to , , or. It was shown to be more effective against certain Gram-negative bacteria, particularly _Legionella pneumophila_. Roxithromycin exerts its antibacterial action by binding to the bacterial ribosome and interfering with bacterial protein synthesis. It is marketed in Australia as a treatment for respiratory tract, urinary and soft tissue infections. Used to treat respiratory tract, urinary and soft tissue infections. Roxithromycin has the following antibacterial spectrum <i>in vitro</i>: <i>Streptococcus agalactiae</i>, <i>Streptococcus pneumoniae</i> (Pneumococcus), <i>Neisseria meningitides</i> (Meningococcus), <i>Listeria monocytogenes</i>, <i>Mycoplasma pneumoniae</i>, <i>Chlamydia trachomatis</i>, <i>Ureaplasma urealyticum</i>, <i>Legionella pneumophila</i>, <i>Helicobacter</i> (Campylobacter), <i>Gardnerella vaginalis</i>, <i>Bordetella pertussis</i>, <i>Moraxella catarrhalis</i> (<i>Branhamella Catarrhalis</i>), and <i>Haemophilus ducreyi</i>. Roxithromycin is highly concentrated in polymorphonuclear leukocytes and macrophages, achieving intracellular concentrations greater than those outside the cell. Roxithromycin enhances the adhesive and chemotactic functions of these cells which in the presence of infection produce phagocytosis and bacterial lysis. Roxithromycin also possesses intracellular bactericidal activity. Roxithromycin prevents bacterial growth by interfering with their protein synthesis. It binds to the 50S subunit of bacterial ribosomes and inhibits the translocation of peptides.",The molecular weight is 837.06.,Roxithromycin has a topological polar surface area of 216.89.,The log p value of  is 2.25.,Roxithromycin is approved and investigational and withdrawn.,Roxithromycin is a solid.,True
15465,"A drug that has anti-inflammatory, antipyretic, and analgesic activities. It is especially effective in the treatment of ankylosing spondylitis. It also is useful in rheumatoid arthritis and Reiter&#39;s syndrome (investigational indication). Although phenylbutazone is effective in gouty arthritis, risk/benefit considerations indicate that this drug should not be employed for this disease. (From AMA Drug Evaluations Annual, 1994, p1822) For the treatment of backache and ankylosing spondylitis Phenylbutazone is a synthetic, pyrazolone derivative. It is a nonhormonal anti-inflammatory, antipyretic compound useful in the management of inflammatory conditions. The apparent analgesic effect is probably related mainly to the compound's anti-inflammatory properties and arise from its ability to reduce production of prostaglandin H and prostacyclin. Prostaglandins act on a variety of cells such as vascular smooth muscle cells causing constriction or dilation, on platelets causing aggregation or disaggregation and on spinal neurons causing pain. Prostacylcin causes vascular constriction platelet disaggregation Phenylbutazone binds to and inactivates prostaglandin H synthase and prostacyclin synthase through peroxide (H2O2) mediated deactivation. The reduced production of prostaglandin leads to reduced inflammation of the surrounding tissues.",The molecular weight is 308.38.,Phenylbutazone has a topological polar surface area of 40.62.,The log p value of  is 3.38.,Phenylbutazone is approved and vet_approved.,Phenylbutazone is a solid.,True
15466,"One of the carbonic anhydrase inhibitors that is sometimes effective against absence seizures. It is sometimes useful also as an adjunct in the treatment of tonic-clonic, myoclonic, and atonic seizures, particularly in women whose seizures occur or are exacerbated at specific times in the menstrual cycle. However, its usefulness is transient often because of rapid development of tolerance. Its antiepileptic effect may be due to its inhibitory effect on brain carbonic anhydrase, which leads to an increased transneuronal chloride gradient, increased chloride current, and increased inhibition. (From Smith and Reynard, Textbook of Pharmacology, 1991, p337) For adjunctive treatment of: edema due to congestive heart failure; drug-induced edema; centrencephalic epilepsies; chronic simple (open-angle) glaucoma Acetazolamide is a potent carbonic anhydrase inhibitor, effective in the control of fluid secretion, in the treatment of certain convulsive disorders and in the promotion of diuresis in instances of abnormal fluid retention. Acetazolamide is not a mercurial diuretic. Rather, it is a nonbacteriostatic sulfonamide possessing a chemical structure and pharmacological activity distinctly different from the bacteriostatic sulfonamides. The anticonvulsant activity of Acetazolamide may depend on a direct inhibition of carbonic anhydrase in the CNS, which decreases carbon dioxide tension in the pulmonary alveoli, thus increasing arterial oxygen tension. The diuretic effect depends on the inhibition of carbonic anhydrase, causing a reduction in the availability of hydrogen ions for active transport in the renal tubule lumen. This leads to alkaline urine and an increase in the excretion of bicarbonate, sodium, potassium, and water.",The molecular weight is 222.24.,Acetazolamide has a topological polar surface area of 115.04.,The log p value of  is -0.98.,Acetazolamide is approved and vet_approved.,Acetazolamide is a solid.,True
15467,"A synthetic progestational hormone used alone or in combination with estrogens as an oral contraceptive. Although etynodiol or ethynodiol are sometimes used as a synonym for ethynodiol diacetate, what is usually being referred to is actually ethynodiol diacetate and not ethynodiol (which is a separate drug that has never been marketed, see ). For the prevention of pregnancy in women who elect to use this product as a method of contraception. Ethynodiol Diacetate is used as a female contraceptive. Ethynodiol Diacetate is a progestin or a synthetic form of the naturally occurring female sex hormone, progesterone. In a woman's normal menstrual cycle, an egg matures and is released from the ovaries (ovulation). The ovary then produces progesterone, preventing the release of further eggs and priming the lining of the womb for a possible pregnancy. If pregnancy occurs, progesterone levels in the body remain high, maintaining the womb lining. If pregnancy does not occur, progesterone levels in the body fall, resulting in a menstrual period. Ethynodiol Diacetate tricks the body processes into thinking that ovulation has already occurred, by maintaining high levels of the synthetic progesterone. This prevents the release of eggs from the ovaries. Binds to the progesterone and estrogen receptors. Target cells include the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Once bound to the receptor, progestins like Ethynodiol Diacetate will slow the frequency of release of gonadotropin releasing hormone (GnRH) from the hypothalamus and blunt the pre-ovulatory LH (luteinizing hormone) surge.",The molecular weight is 384.52.,Ethynodiol diacetate has a topological polar surface area of 52.6.,The log p value of  is 5.13.,Ethynodiol diacetate is approved.,Ethynodiol diacetate is a solid.,True
15468,"Menthol is a covalent organic compound made synthetically or obtained from peppermint or other mint oils. Forming clear or white waxy, crystalline substance, menthol is typically solid at room temperature. (-)-Menthol is the naturally-occurring and main form of menthol, and is assigned the (1R,2S,5R) configuration. Menthol mediates anesthetic properties and anti-irritating properties locally, thus it is widely used to relieve minor throat irritations. Used to treat occasional minor irritation, pain, sore mouth, and sore throat as well as cough associated with a cold or inhaled irritants. Menthol is a covalent organic compound made synthetically or obtained from peppermint or other mint oils. Menthol induces a cooling sensation on the skin upon inhalation, oral ingestion, or topical application by stimulating the cold-sensitive receptors expressed on the skin, without actually causing a drop in the skin temperature.  Menthol primarily activates the cold-sensitive TRPM8 receptors in the skin. Menthol, after topical application, causes a feeling of coolness due to stimulation of 'cold' receptors by inhibiting Ca++ currents of neuronal membranes. It may also yield analgesic properties via kappa-opioid receptor agonism. ",,,,Levomenthol is approved.,Levomenthol is a solid.,True
15469,"Amphoteric macrolide antifungal antibiotic from Streptomyces natalensis or S. chattanoogensis. It is used for a variety of fungal infections, mainly topically.  For the treatment of fungal blepharitis, conjunctivitis, and keratitis caused by susceptible organisms including <i>Fusarium solani</i> keratitis. Natamycin is an antifungal drug for topical ophthalmic administration. It is a tetraene polyene antibiotic derived from <i>Streptomyces natalensis</i>. It possesses in vitro activity against a variety of yeast and filamentous fungi, including <i>Candida</i>, <i>Aspergillus</i>, <i>Cephalosporium</i>, <i>Fusarium</i> and <i>Penicillium</i>. Although the activity against fungi is dose-related, natamycin is predominantly fungicidal. Natamycin is not effective in vitro against gram-positive or gram-negative bacteria. Topical administration appears to produce effective concentrations of natamycin within the corneal stroma but not in intraocular fluid. LIke other polyene antibiotics, Natamycin inhibits fungal growth by binding to sterols. Specifically, Natamycin binds to ergosterol in the plasma membrane, preventing ergosterol-dependent fusion of vacuoles, as well as membrane fusion and fission. This differs from the mechanism of most other polyene antibiotics, which tend to work by altering fungal membrane permeability instead.",The molecular weight is 665.73.,Natamycin has a topological polar surface area of 230.99.,The log p value of  is -4.75.,Natamycin is approved.,Natamycin is a solid.,True
15470,"Conivaptan is a non-peptide inhibitor of antidiuretic hormone (vasopressin). It was approved in 2004 for hyponatremia (low blood sodium levels) caused by syndrome of inappropriate antidiuretic hormone (SIADH). Conivaptan inhibits both isotypes of the vasopressin receptor (V1a and V2). For the treatment of euvolemic or hypervolemic hyponatremia (e.g. the syndrome of inappropriate secretion of antidiuretic hormone, or in the setting of hypothyroidism, adrenal insufficiency, pulmonary disorders, etc.) in hospitalized patients. Conivaptan is a nonpeptide, dual antagonist of arginine vasopressin (AVP) V<sub>1A</sub> and V<sub>2</sub> receptors. The level of AVP in circulating blood is critical for the regulation of water and electrolyte balance and is usually elevated in both euvolemic and hypervolemic hyponatremia. The AVP effect is mediated through V<sub>2</sub> receptors, which are functionally coupled to aquaporin channels in the apical membrane of the collecting ducts of the kidney. These receptors help to maintain plasma osmolality within the normal range by increasing permeability of the renal collecting ducts to water. Vasopressin also causes vasoconstriction through its actions on vascular <sub>1A</sub> receptors. The predominant pharmacodynamic effect of conivaptan in the treatment of hyponatremia is through its V<sub>2</sub> antagonism of AVP in the renal collecting ducts, an effect that results in aquaresis, or excretion of free water. Conivaptan's antagonist activity on V<sub>1A</sub> receptors may also cause splanchnic vasodilation, resulting in possible hypotension or variceal bleeding in patients with cirrhosis. The pharmacodynamic effects of conivaptan include increased free water excretion (i.e., effective water clearance ) generally accompanied by increased net fluid loss, increased urine output, and decreased urine osmolality. Conivaptan is a dual AVP antagonist with nanomolar affinity for human arginine vasopressin V<sub>1A</sub> and V<sub>2</sub> receptors <i>in vitro</i>. This antagonism occurs in the renal collecting ducts, resulting in aquaresis, or excretion of free water. ",,,,Conivaptan is approved and investigational.,Conivaptan is a solid.,True
15471,"A serotonin receptor (5HT-3 selective) antagonist that has been used as an antiemetic and antinauseant for cancer chemotherapy patients. For the prevention of nausea and vomiting associated with initial and repeat courses of emetogenic cancer therapy (including high dose cisplatin), postoperation, and radiation (including total body irradiation and daily fractionated abdominal radiation). Granisetron is a selective inhibitor of type 3 serotonergic (5-HT<sub>3</sub>) receptors. Granisetron has little or no affinity for other serotonin receptors, including 5-HT 1 , 5-HT 1A , 5-HT 1B/C , or 5-HT 2 ; for alpha 1 -, alpha 2 -, or beta-adrenoreceptors; for dopamine D 2 receptors; for histamine H 1 receptors; for benzodiazepine receptors; for picrotoxin receptors; or for opioid receptors. In most human studies, granisetron has had little effect on blood pressure, heart rate, or electrocardiogram (ECG). The drug is structurally and pharmacologically related to ondansetron, another selective inhibitor of 5-HT<sub>3</sub> receptors. The serontonin 5-HT<sub>3</sub> receptors are located on the nerve terminals of the vagus in the periphery, and centrally in the chemoreceptor trigger zone of the area postrema. The temporal relationship between the emetogenic action of emetogenic drugs and the release of serotonin, as well as the efficacy of antiemetic agents suggest that chemotherapeutic agents release serotonin from the enterochromaffin cells of the small intestine by causing degenerative changes in the GI tract. The serotonin then stimulates the vagal and splanchnic nerve receptors that project to the medullary vomiting center, as well as the 5-HT3 receptors in the area postrema, thus initiating the vomiting reflex, causing nausea and vomiting. Granisetron is a potent, selective antagonist of 5-HT<sub>3</sub> receptors. The antiemetic activity of the drug is brought about through the inhibition of 5-HT3 receptors present both centrally (medullary chemoreceptor zone) and peripherally (GI tract). This inhibition of 5-HT3 receptors in turn inhibits the visceral afferent stimulation of the vomiting center, likely indirectly at the level of the area postrema, as well as through direct inhibition of serotonin activity within the area postrema and the chemoreceptor trigger zone.",The molecular weight is 312.42.,Granisetron has a topological polar surface area of 50.16.,The log p value of  is 1.72.,Granisetron is approved and investigational.,Granisetron is a solid.,True
15472,"Tiagabine is an anti-convulsive medication. It is also used in the treatment for panic disorder as are a few other anticonvulsants. Though the exact mechanism by which tiagabine exerts its effect on the human body is unknown, it does appear to operate as a selective GABA reuptake inhibitor. For the treatment of partial seizures Tiagabine is used primarily as an anticonvulsant for the adjunctive treatment of epilepsy. The precise mechanism by which Tiagabine exerts its antiseizure effect is unknown, although it is believed to be related to its ability to enhance the activity of gamma aminobutyric acid (GABA), the major inhibitory neurotransmitter in the central nervous system. Tiagabine binds to recognition sites associated with the GABA uptake carrier. It is thought that, by this action, Tiagabine blocks GABA uptake into presynaptic neurons, permitting more GABA to be available for receptor binding on the surfaces of post-synaptic cells. Though the exact mechanism by which Tiagabine exerts its effect on the human body is unknown, it does appear to operate as a selective GABA reuptake inhibitor.",The molecular weight is 375.55.,Tiagabine has a topological polar surface area of 40.54.,The log p value of  is 2.78.,Tiagabine is approved and investigational.,Tiagabine is a solid.,True
15473,"A nitroimidazole antitrichomonal agent effective against _Trichomonas vaginalis_, _Entamoeba histolytica_, and _Giardia lamblia_ infections. For the treatment of trichomoniasis caused by <i>T. vaginalis</i> in both female and male patients. Also for the treatment of giardiasis caused by <i>G. duodenalis</i> in both adults and pediatric patients older than three years of age and for the treatment of intestinal amebiasis and amebic liver abscess caused by <i>E. histolytica</i> in both adults and pediatric patients older than three years of age. Tinidazole is a synthetic antiprotozoal agent. Tinidazole demonstrates activity both in vitro and in clinical infections against the following protozoa: <i>Trichomonas vaginalis</i>, <i>Giardia duodenalis</i> (also termed <i>G. lamblia</i>), and <i>Entamoeba histolytica</i>. Tinidazole does not appear to have activity against most strains of vaginal lactobacilli. Tinidazole is a prodrug and antiprotozoal agent. The nitro group of tinidazole is reduced in <i>Trichomonas</i> by a ferredoxin-mediated electron transport system. The free nitro radical generated as a result of this reduction is believed to be responsible for the antiprotozoal activity. It is suggested that the toxic free radicals covalently bind to DNA, causing DNA damage and leading to cell death. The mechanism by which tinidazole exhibits activity against <i>Giardia</i> and <i>Entamoeba</i> species is not known, though it is probably similar.",The molecular weight is 247.27.,Tinidazole has a topological polar surface area of 97.78.,The log p value of  is -0.32.,Tinidazole is approved and investigational.,Tinidazole is a solid.,True
15474,"Fulvestrant is a drug treatment of hormone receptor (HR)-positive metastatic breast cancer in post-menopausal women with disease progression following anti-estrogen therapy. It is an estrogen receptor antagonist with no agonist effects, which works both by down-regulating and by degrading the estrogen receptor. While it is used as monotherapy for the treatment of breast cancers, it is also used in combination with for the treatment of HR-positive, human epidermal growth factor receptor 2 (HER2)-negative, PIK3CA-mutated, advanced or metastatic breast cancer For the treatment of hormone receptor positive metastatic breast cancer in postmenopausal women with disease progression following anti-estrogen therapy, as monotherapy or in combination with other antineoplastic agents. Fulvestrant for intramuscular administration is an estrogen receptor antagonist without known agonist effects. Fulvestrant competitively and reversibly binds to estrogen receptors present in cancer cells and achieves its anti-estrogen effects through two separate mechanisms. First, fulvestrant binds to the receptors and downregulates them so that estrogen is no longer able to bind to these receptors. Second, fulvestrant degrades the estrogen receptors to which it is bound. Both of these mechanisms inhibit the growth of tamoxifen-resistant as well as estrogen-sensitive human breast cancer cell lines.",The molecular weight is 606.78.,Fulvestrant has a topological polar surface area of 57.53.,The log p value of  is 7.35.,Fulvestrant is approved and investigational.,Fulvestrant is a solid.,True
15475,"Felbamate is an anticonvulsant drug used in the treatment of epilepsy. In particular, in the adult patient population, it can be employed to treat partial seizures (with and without generalization). Alternatively, it is used to treat partial and generalized seizures associated with Lennox-Gastaut syndrome in children. It has a weak inhibitory effect on GABA receptor binding sites. For use only in those patients who respond inadequately to alternative treatments and whose epilepsy is so severe that a substantial risk of aplastic anemia and/or liver failure is deemed acceptable in light of the benefits conferred by its use. Felbamate is an antiepileptic indicated as monotherapy or as an adjunct to other anticonvulsants for the treatment of partial seizures resulting from epilepsy. Receptor-binding studies <i>in vitro</i> indicate that felbamate has weak inhibitory effects on GABA-receptor binding, benzodiazepine receptor binding, and is devoid of activity at the MK-801 receptor binding site of the NMDA receptor-ionophore complex. However, felbamate does interact as an antagonist at the strychnine-insensitive glycine recognition site of the NMDA receptor-ionophore complex. The mechanism by which felbamate exerts its anticonvulsant activity is unknown, but in animal test systems designed to detect anticonvulsant activity, felbamate has properties in common with other marketed anticonvulsants. <i>In vitro</i> receptor binding studies suggest that felbamate may be an antagonist at the strychnine-insensitive glycine-recognition site of the N-methyl-D-aspartate (NMDA) receptor-ionophore complex. Antagonism of the NMDA receptor glycine binding site may block the effects of the excitatory amino acids and suppress seizure activity. Animal studies indicate that felbamate may increase the seizure threshold and may decrease seizure spread. It is also indicated that felbamate has weak inhibitory effects on GABA-receptor binding, benzodiazepine receptor binding.",The molecular weight is 238.24.,Felbamate has a topological polar surface area of 104.64.,The log p value of  is 0.5.,Felbamate is approved.,Felbamate is a solid.,True
15476,"Dirithromycin is a macrolide glycopeptide antibiotic used to treat many different types of bacterial infections, such as bronchitis, pneumonia, tonsillitis, and even skin infections. For the treatment of the following mild-to-moderate infections caused by susceptible strains of microorganisms: acute bacterial exacerbations of chronic bronchitis, secondary bacterial infection of acute bronchitis, community-acquired pneumonia, pharyngitis/tonsilitis, and uncomplicated skin and skin structure infections. Dirithromycin is a pro-drug which is converted non-enzymatically during intestinal absorption into the microbiologically active moiety erythromycylamine. Erythromycylamine exerts its activity by binding to the 50S ribosomal subunits of susceptible mircoorganisms resulting in inhibition of protein synthesis. Dirithromycin/erythromycylamine has been shown to be active against most strains of the following microorganisms both in vitro and in clinical infections: <i>Staphylococcus aureus</i> (methicillin-susceptible strains only), <i>Streptococcus pneumoniae</i>, <i>Streptococcus pyogenes</i>, <i>Haemophilus influenzae</i>, <i>Legionella pneumophila</i>, <i>Moraxella catarrhalis</i>, and <i>Mycoplasma pneumoniae</i>. Dirithromycin prevents bacteria from growing, by interfering with their protein synthesis. Dirithromycin binds to the 50S subunit of the 70S bacterial ribosome, and thus inhibits the translocation of peptides. Dirithromycin has over 10 times higher affinity to the subunit 50S than erythromycin. In addition, dirithromycin binds simultaneously in to two domains of 23S RNA of the ribosomal subunit 50S, where older macrolides bind only in one. Dirithromycin can also inhibit the formation of ribosomal subunits 50S and 30S.",The molecular weight is 835.09.,Dirithromycin has a topological polar surface area of 196.33.,The log p value of  is 2.74.,Dirithromycin is experimental.,Dirithromycin is a solid.,True
15477,"Ezetimibe is a lipid-lowering compound that inhibits intestinal cholesterol and phytosterol absorption. The discovery and research of this drug began in the early 1990s, after the intravenous administration of radiolabelled ezetimibe in rats revealed that it was being localized within enterocytes of the intestinal villi - this prompted studies investigating the effect of ezetimibe on intestinal cholesterol absorption. Ezetimibe is used as an adjunctive therapy to a healthy diet to lower cholesterol levels in primary hyperlipidemia, mixed hyperlipidemia, homozygous familial hypercholesterolemia (HoFH), and homozygous sitosterolemia (phytosterolemia). Ezetimibe is indicated to reduce elevated total-C, LDL-C, Apo B, and non-HDL-C in patients with primary hyperlipidemia, alone or in combination with an HMG-CoA reductase inhibitor (statin). It is also indicated to reduce elevated total-C, LDL-C, Apo B, and non-HDL-C in patients with mixed hyperlipidemia in combination with fenofibrate, and to reduce elevated total-C and LDL-C in patients with homozygous familial hypercholesterolemia (HoFH), in combination with atorvastatin or simvastatin. Ezetimibe may also be used to reduce elevated sitosterol and campesterol in patients with homozygous sitosterolemia (phytosterolemia). Ezetimibe was shown to reduce the levels of total cholesterol (total-C), low-density lipoprotein cholesterol (LDL-C), apoprotein B (Apo B), non-high-density lipoprotein cholesterol (non-HDL-C), and triglycerides (TG), and increase high-density lipoprotein cholesterol (HDL-C) in patients with hyperlipidemia. This therapeutic effect was more profound when ezetimibe was co-administered with a statin or fenofibrate compared to either treatment alone. In clinical trials involving patients with homozygous and heterozygous familial hypercholesterolemia and in those with sitosterolemia, a recommended therapeutic dose of ezetimibe was effective in reducing the LDL levels by 15-20% while increasing HDL-C by 2.5-5%. Ezetimibe mediates its blood cholesterol-lowering effect via selectively inhibiting the absorption of cholesterol and phytosterol by the small intestine without altering the absorption of fat-soluble vitamins and nutrients. The primary target of ezetimibe is the cholesterol transport protein Niemann-Pick C1-Like 1 (NPC1L1) protein. NPC1L1 is expressed on enterocytes/gut lumen (apical) as well as the hepatobiliary (canalicular) interface and plays a role in facilitating internalization of free cholesterol into the enterocyte in conjunction with the adaptor protein 2 (AP2) complex and clathrin. Once cholesterol in the gut lumen or bile is incorporated into the cell membrane of enterocytes, it binds to the sterol-sensing domain of NPC1L1 and forms a NPC1L1/cholesterol complex. The complex is then internalized or endocytosed by joining to AP2 clathrin, forming a vesicle complex that is translocated for storage in the endocytic recycling compartment.",The molecular weight is 409.43.,Ezetimibe has a topological polar surface area of 60.77.,The log p value of  is 3.96.,Ezetimibe is approved.,Ezetimibe is a solid.,True
15478,"Telithromycin, a semi-synthetic erythromycin derivative, belongs to a new chemical class of antibiotics called ketolides. Ketolides have been recently added to the macrolide-lincosamide-streptogramin class of antibiotics. Similar to the macrolide antibiotics, telithromycin prevents bacterial growth by interfering with bacterial protein synthesis. Telithromycin binds to the 50S subunit of the 70S bacterial ribosome and blocks further peptide elongation. Binding occurs simultaneously at to two domains of 23S RNA of the 50S ribosomal subunit, domain II and V, where older macrolides bind only to one. It is used to treat mild to moderate respiratory infections. For the treatment of <i>Pneumococcal</i> infection, acute sinusitis, acute bacterial tonsillitis, acute bronchitis and bronchiolitis, lower respiratory tract infection and lobar (pneumococcal) pneumonia. Telithromycin is a ketolide antibiotic which has an antimicrobial spectrum similar or slightly broader than that of penicillin. It is often used as an alternative in patients who have an allergy to penicillins. For respiratory tract infections, it has better coverage of atypical organisms, including mycoplasma. Telithromycin prevents bacterial growth by binding to bacterial 50S ribosomal subunits and interfering with bacterial peptide translocation and elongation. Telithromycin acts by binding to domains II and V of 23S rRNA of the 50S ribosomal subunit. By binding at domain II, telithromycin retains activity against gram-positive cocci (e.g. Streptococcus pneumoniae) in the presence of resistance mediated by methylases (erm genes) that alter the binding site at domain V. Telithromycin may also inhibit the assembly of nascent ribosomal units. Compared to erythromycin A, telithromycin binds to the 23S rRNA with 10 times greater affinity in erythromycin-susceptible organisms and 25 times greater affinity in macrolide-resistant strains. This increased binding affinity may be conferred by the C11-12 carbamate side chain of telithromycin. The side chain appears to maintain binding at domain II in the presence of resistance mediated by alterations in domain V. ",The molecular weight is 812.02.,Telithromycin has a topological polar surface area of 171.85.,The log p value of  is 3.75.,Telithromycin is approved.,Telithromycin is a solid.,True
15479,"Salbutamol is a short-acting, selective beta2-adrenergic receptor agonist used in the treatment of asthma and COPD. It is 29 times more selective for beta2 receptors than beta1 receptors giving it higher specificity for pulmonary beta receptors versus beta1-adrenergic receptors located in the heart. Salbutamol is formulated as a racemic mixture of the R- and S-isomers. The R-isomer has 150 times greater affinity for the beta2-receptor than the S-isomer and the S-isomer has been associated with toxicity. This lead to the development of levalbuterol, the single R-isomer of salbutamol. However, the high cost of levalbuterol compared to salbutamol has deterred wide-spread use of this enantiomerically pure version of the drug. Salbutamol is generally used for acute episodes of bronchospasm caused by bronchial asthma, chronic bronchitis and other chronic bronchopulmonary disorders such as chronic obstructive pulmonary disorder (COPD). It is also used prophylactically for exercise-induced asthma. Salbutamol is indicated for (i) the symptomatic relief and prevention of bronchospasm due to bronchial asthma, chronic bronchitis, reversible obstructive airway disease, and other chronic bronchopulmonary disorders in which bronchospasm is a complicating factor, and/or (ii) the acute prophylaxis against exercise-induced bronchospasm and other stimuli known to induce bronchospasm. Salbutamol (INN) or albuterol (USAN), a moderately selective beta(2)-receptor agonist similar in structure to terbutaline, is widely used as a bronchodilator to manage asthma and other chronic obstructive airway diseases. The R-isomer, levalbuterol, is responsible for bronchodilation while the S-isomer increases bronchial reactivity. The R-enantiomer is available and sold in its pure form as levalbuterol and subsequently may produce fewer side-effects with only the R-enantiomer present - although this has not been formally demonstrated. In vitro studies and in vivo pharmacologic studies have shown that salbutamol has a preferential effect on beta2-adrenergic receptors compared with isoproterenol. Although beta2­ adrenoceptors are the predominant adrenergic receptors in bronchial smooth muscle and beta1 adrenoceptors are the predominant receptors in the heart, there are also beta2-adrenoceptors in the human heart comprising 10% to 50% of the total beta-adrenoceptors. The precise function of these receptors has not been established, but their presence raises the possibility that even selective beta2-agonists may have cardiac effects.",The molecular weight is 239.32.,Salbutamol has a topological polar surface area of 72.72.,The log p value of  is 0.06.,Salbutamol is approved and vet_approved.,Salbutamol is a solid.,True
15480,"Guanfacine, or BS 100-141, is a selective alpha-A2 adrenergic receptor agonist initially indicated for the treatment of hypertension but is now indicated as an extended release tablet for the treatment of ADHD. Guanfacine was first described in the literature in 1974. Guanfacine is indicated alone or as an adjunct with stimulants to treat ADHD. Guanfacine is a selective alpha-2A adrenergic receptor agonist but it is unclear how this translates to the treatment of ADHD. It has a long duration of action as it is given once daily and a wide therapeutic window as fatal overdoses have not been described in literature. Patients should be counselled regarding the risk of hypotension, bradycardia, and syncope. Guanfacine is a selective alpha-2A adrenergic receptor agonist, which reduces the effects of the sympathetic nervous system on the heart and circulatory system. The link between guanfacine’s molecular mechanism and it’s effect on the treatment of ADHD has not been determined.",The molecular weight is 246.09.,Guanfacine has a topological polar surface area of 78.97.,The log p value of  is 1.37.,Guanfacine is approved and investigational.,Guanfacine is a solid.,True
15481,"An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA topoisomerases, type I. For the treatment of advanced ovarian cancer in patients with disease that has recurred or progressed following therapy with platinum-based regimens. Also used as a second-line therapy for treatment-sensitive small cell lung cancer, as well as in combination with cisplatin for the treatment of stage IV-B, recurrent, or persistent cervical cancer not amenable to curative treatment with surgery and/or radiation therapy. Topotecan, a semi-synthetic derivative of camptothecin (a plant alkaloid obtained from the <i>Camptotheca acuminata</i> tree), is an anti-tumor drug with topoisomerase I-inhibitory activity similar to irinotecan. DNA topoisomerases are enzymes in the cell nucleus that regulate DNA topology (3-dimensional conformation) and facilitate nuclear processes such as DNA replication, recombination, and repair. During these processes, DNA topoisomerase I creates reversible single-stranded breaks in double-stranded DNA, allowing intact single DNA strands to pass through the break and relieve the topologic constraints inherent in supercoiled DNA. The 3'-DNA terminus of the broken DNA strand binds covalently with the topoisomerase enzyme to form a catalytic intermediate called a cleavable complex. After DNA is sufficiently relaxed and the strand passage reaction is complete, DNA topoisomerase reattaches the broken DNA strands to form the unaltered topoisomers that allow transcription to proceed. Topotecan interferes with the growth of cancer cells, which are eventually destroyed. Since the growth of normal cells can be affected by the medicine, other effects may also occur. Unlike irinotecan, topotecan is found predominantly in the inactive carboxylate form at neutral pH and it is not a prodrug. Topotecan has the same mechanism of action as irinotecan and is believed to exert its cytotoxic effects during the S-phase of DNA synthesis. Topoisomerase I relieves torsional strain in DNA by inducing reversible single strand breaks. Topotecan binds to the topoisomerase I-DNA complex and prevents religation of these single strand breaks. This ternary complex interferes with the moving replication fork, which leads to the induction of replication arrest and lethal double-stranded breaks in DNA. As mammalian cells cannot efficiently repair these double strand breaks, the formation of this ternary complex eventually leads to apoptosis (programmed cell death).",The molecular weight is 421.45.,Topotecan has a topological polar surface area of 103.2.,The log p value of  is 0.43.,Topotecan is approved and investigational.,Topotecan is a solid.,True
15482,"Ergoloid Mesylate is an equiproportional preparation of three different ergotamantriones: dihydroergocornine, dihydroergocristine, and dihydroergocryptine. All these components are produced by the fungus _Claviceps purpurea_ and are all derivatives of the tetracyclic compound 6-methylergonovine. The derivatives of this fungus are identified to be about 350 different substances from which the components of the ergoloid mesylate mixture are composed of the dihydrogenated ergot alkaloid derivatives. The mixture of ergoloid mesylate was first developed by Novartis and FDA approved on November 5, 1953, but this specific formulation is now discontinued.Later in 1991, the mixture of ergoloid mesylates was retaken by Sun Pharmaceutical Industries and approved by the FDA. To know more about the individual components of the ergoloid mixture, please visit , , and. It was labeled by the FDA for the treatment of symptoms of an idiopathic decline in the mental capacity not related to a potentially reversible condition as well as for age-related cognitive impairment. The prescription of this drug is conditioned to the corroboration that the patient is not suffering from a potentially reversible and treatable condition especially delirium and dementiform illness secondary to systemic disease, primary neurological disease or primary mood disturbance. To know more about the individual components of the ergoloid mixture, please visit and  The mechanism of action of ergoloid mesylate is not completely established but it is thought that it increases both the blood flow and cerebral metabolism. Some studies have shown a significant improvement in alertness and memory, as well as a decline in confusion while some other benefits have shown a lack of effect. Its action produces a damper in the impulses from the vasomotor center which reduces the vascular tone which translates in the slow of pulse rate, prevention of compensatory tachycardia. To know more about the individual components of the ergoloid mixture, please visit , and. The general mechanism of action of ergoloid mesylate is the dual action of partial agonism/antagonism of adrenergic, dopaminergic and serotonergic receptors. The pharmacological activity is determined by the degree of activity of each component at the receptor site. To know more about the individual components of the ergoloid mixture, please visit , , and. ",,,,Ergoloid mesylate is approved.,Ergoloid mesylate is a solid.,True
15483,"A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma. For the treatment of radiation-induced dry mouth (xerostomia) and symptoms of dry mouth in patients with Sj&ouml;grens syndrome. Pilocarpine is a choline ester miotic and a positively charged quaternary ammonium compound. Pilocarpine, in appropriate dosage, can increase secretion by the exocrine glands. The sweat, salivary, lacrimal, gastric, pancreatic, and intestinal glands and the mucous cells of the respiratory tract may be stimulated. When applied topically to the eye as a single dose it causes miosis, spasm of accommodation, and may cause a transitory rise in intraocular pressure followed by a more persistent fall. Dose-related smooth muscle stimulation of the intestinal tract may cause increased tone, increased motility, spasm, and tenesmus. Bronchial smooth muscle tone may increase. The tone and motility of urinary tract, gallbladder, and biliary duct smooth muscle may be enhanced. Pilocarpine may have paradoxical effects on the cardiovascular system. The expected effect of a muscarinic agonist is vasodepression, but administration of pilocarpine may produce hypertension after a brief episode of hypotension. Bradycardia and tachycardia have both been reported with use of pilocarpine. Pilocarpine is a cholinergic parasympathomimetic agent. It increase secretion by the exocrine glands, and produces contraction of the iris sphincter muscle and ciliary muscle (when given topically to the eyes) by mainly stimulating muscarinic receptors.",The molecular weight is 208.26.,Pilocarpine has a topological polar surface area of 44.12.,The log p value of  is -0.2.,Pilocarpine is approved and investigational.,Pilocarpine is a solid.,True
15484,"Sibutramine (trade name Meridia in the USA, Reductil in Europe and other countries), usually as sibutramide hydrochloride monohydrate, is an orally administered agent for the treatment of obesity. It is a centrally acting stimulant chemically related to amphetamines thus it is classified as a Schedule IV controlled substance in the United States. In October 2010, Sibutramine was withdrawn from Canadian and U.S. markets due to concerns that the drug increases the risk of heart attack and stroke in patients with a history of heart disease. For the treatment of obesity. Sibutramine is an orally administered agent for the treatment of obesity. Sibutramine exerts its pharmacological actions predominantly via its secondary (M1) and primary (M2) amine metabolites. The parent compound, sibutramine, is a potent inhibitor of serotonin and norepinephrine reuptake <i>in vivo</i>, but not <i>in vitro</i>. However, metabolites M1 and M2 inhibit the reuptake of these neurotransmitters both <i>in vitro</i> and <i>in vivo</i>. In human brain tissue, M1 and M2 also inhibit dopamine reuptake <i>in vitro</i>, but with ~3-fold lower potency than for the reuptake inhibition of serotonin or norepinephrine. Sibutramine, M1 and M2 exhibit no evidence of anticholinergic or antihistaminergic actions. In addition, receptor binding profiles show that sibutramine, M1 and M2 have low affinity for serotonin (5-HT<sub>1</sub>, 5-HT<sub>1A</sub>, 5-HT<sub>1B</sub>, 5-HT<sub>2A</sub>, 5-HT<sub>2C</sub>), norepinephrine (b, b1, b3, a1 and a2), dopamine (D1 and D2), benzodiazepine, and glutamate (NMDA) receptors. These compounds also lack monoamine oxidase inhibitory activity <i>in vitro</i> and <i>in vivo</i>. Sibutramine produces its therapeutic effects by inhibition of norepinephrine (NE), serotonin (5-hydroxytryptamine, 5-HT), and to a lesser extent, dopamine reuptake at the neuronal synapse. By inhibiting the reuptake of these neurotransmitters, sibutramine promotes a sense of satiety and decrease in appetite, thereby reducing food intake. Data from animal studies also suggest that sibutramine may also increase energy expenditure through thermogenic effects in both the basal and fed states, but this has not been confirmed in humans. Sibutramine and its major pharmacologically active metabolites (M1 and M2) do not act via release of monoamines. ",The molecular weight is 279.85.,Sibutramine has a topological polar surface area of 3.24.,The log p value of  is 5.59.,Sibutramine is approved and illicit and investigational and withdrawn.,Sibutramine is a solid.,True
15485,"Atovaquone is a hydroxynaphthoquinone, or an analog of ubiquinone, that has antimicrobial and antipneumocystis activity. It is being used in antimalarial protocols. For the treatment or prevention of <i>Pneumocystis carinii</i> pneumonia in patients who are intolerant to trimethoprim-sulfamethoxazole (TMP-SMX). Also indicated for the acute oral treatment of mild to moderate PCP in patients who are intolerant to TMP-SMX. Atovaquone is a highly lipophilic drug that closely resembles the structure. Its inhibitory effect being comparable to ubiquinone, atovaquone can act by selectively affecting mitochondrial electron transport and parallel processes such as ATP and pyrimidine biosynthesis in atovaquone-responsive parasites. Cytochrome bc1 complex (complex III) seems to serve as a highly discriminating molecular target for atovaquone in Plasmodia. There is no significant risk for myelosuppression associated with atovaquone, making this drug a beneficial therapeutic agent for recipients of bone marrow transplantation. The mechanism of action against <i>Pneumocystis carinii</i> has not been fully elucidated. In Plasmodium species, the site of action appears to be the cytochrome bc1 complex (Complex III). Several metabolic enzymes are linked to the mitochondrial electron transport chain via ubiquinone. Inhibition of electron transport by atovaquone will result in indirect inhibition of these enzymes. The ultimate metabolic effects of such blockade may include inhibition of nucleic acid and ATP synthesis. Atovaquone also has been shown to have good <i>in vitro</i> activity against <i>Toxoplasma gondii</i>.",The molecular weight is 366.84.,Atovaquone has a topological polar surface area of 54.37.,The log p value of  is 6.35.,Atovaquone is approved.,Atovaquone is a solid.,True
15486,"Prednicarbate is a relatively new topical corticosteroid drug that displays a similar potency as. It is used in the treatment of inflammatory skin diseases, such as atopic dermatitis. It has a favorable benefit-risk ratio, with an inflammatory action similar to that of a medium potency corticosteroid, but with a low potential to cause skin atrophy. The anti-inflammation action of corticosteroids is associated with the inhibition of the interleukin 1-alpha cytokine within keratinocytes. IL-1a is also found in fibroblasts, where it is responsible for proliferation, collagenase induction and IL-6 synthesis, which are related to skin thickness. For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Corticosteroids diffuse across cell membranes and complex with specific cytoplasmic receptors. These complexes then enter the cell nucleus, bind to DNA (chromatin), and stimulate transcription of messenger RNA (mRNA) and subsequent protein synthesis of various inhibitory enzymes responsible for the anti-inflammatory effects of topical corticosteroids. These anti-inflammatory effects include inhibition of early processes such as edema, fibrin deposition, capillary dilatation, movement of phagocytes into the area, and phagocytic activities. Later processes, such as capillary production, collagen deposition, and keloid formation also are inhibited by corticosteroids. In common with other topical corticosteroids, prednicarbate has anti-inflammatory, antipruritic, and vasoconstrictive properties. In general, the mechanism of the anti-inflammatory activity of topical steroids is unclear. However, corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2.",The molecular weight is 488.58.,Prednicarbate has a topological polar surface area of 116.2.,The log p value of  is 3.5.,Prednicarbate is approved and investigational.,Prednicarbate is a solid.,True
15487,"Desoxycorticosterone pivalate is a mineralocorticoid hormone and an analog of desoxycorticosterone. It is white, odorless, and stable in air. It is practically insoluble in water, sparingly soluble in acetone, slightly soluble in methanol, ether and vegetable oils. Federal (U.S.A.) law restricts this drug to use by or on the order of a licensed veterinarian. Examined for treatment of adrenocortical insufficiency especially in multiple sclerosis, congenital cerebral palsy, polyarteritis nodosa, and rheumatoid arthritis. Currently only approved in treating cats and dogs for the treatment of Addison's disease. Used to treat adrenocortical insufficiency, desoxycorticosterone pivalate is a mineralocorticoid hormone and an analogue of desoxycorticosterone. It primarily acts on the metabolism of sodium, potassium and water. When the drug is given, there is decreased excretion of sodium accompanied by increased excretion of potassium; the concentration of sodium in the blood is thereby increased whereas that of potassium is decreased. There is a concomitant increase in the volume of blood and extracellular fluids, with a fall in hematocrit. It increases the rate of renal tubular absorption of sodium. Desoxycorticosterone Pivalate binds to the mineralocorticoid receptor. Mineralocorticoids are a family of steroids, secreted by the adrenal cortex, necessary for the regulation of a number of metabolic processes including electrolyte regulation. Desoxycorticosterone pivalate exerts its effect through its interaction with the mineralocorticoid receptor (MR), whereby it reacts with the receptor proteins to form a steroid-receptor complex. This complex moves into the nucleus, where it binds to chromatin which results in genetic transcription of cellular DNA to messenger RNA. The steroid hormones appear to induce transcription and synthesis of specific proteins, which produce the physiological effects seen after administration.",The molecular weight is 414.59.,Desoxycorticosterone pivalate has a topological polar surface area of 60.44.,The log p value of  is 5.21.,Desoxycorticosterone pivalate is experimental and vet_approved.,Desoxycorticosterone pivalate is a solid.,True
15488,"Candicidin is an antibiotic obtained from a streptomyces (Streptomyces griseus) and active against some fungi of the genus Candida (C. albicans). Candicidin is administered intravaginally in the treatment of vulvovaginal candidiasis. Used in the topical treatment of vulvovaginal candidiasis. Candicidin is a polyene antifungal antibiotic produced by a strain of <i>Streptomyces griseus</i>. It is especially effective against <i>Candida albicans</i> (more effective than amphotericin B), and is administered intravaginally in the treatment of vulvovaginal candidiasis. Ergosterol, the principal sterol in the fungal cytoplasmic membrane, is the target site of action of Candicidin. Candicidin binds irreversibly to ergosterol, resulting in disruption of membrane integrity and ultimately cell death. There is some evidence that the binding site in the cell wall may be to fatty acids or fatty acid esters and that this binding capacity must be satisfied before candicidin can bring about its lethal effect by binding to sterol in the cell membrane.",The molecular weight is 1109.32.,Candicidin has a topological polar surface area of 356.38.,The log p value of  is -1.46.,Candicidin is approved and withdrawn.,Candicidin is a solid.,True
15489,"A barbiturate that is administered intravenously for the production of complete anesthesia of short duration, for the induction of general anesthesia, or for inducing a hypnotic state. (From Martindale, The Extra Pharmacopoeia, 30th ed, p919) Used for the production of complete anaesthesia of short duration, for the induction of general anaesthesia, and for inducing a hypnotic state. Thiamylal, a barbiturate, is used in combination with acetaminophen or aspirin and caffeine for its sedative and relaxant effects in the treatment of tension headaches, migraines, and pain. Barbiturates act as nonselective depressants of the central nervous system (CNS), capable of producing all levels of CNS mood alteration from excitation to mild sedation, hypnosis, and deep coma. In sufficiently high therapeutic doses, barbiturates induce anesthesia. Thiamylal binds at a distinct binding site associated with a Cl<sup>-</sup> ionopore at the GABA<sub>A</sub> receptor, increasing the duration of time for which the Cl<sup>-</sup> ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.",The molecular weight is 254.35.,Thiamylal has a topological polar surface area of 58.2.,The log p value of  is 3.03.,Thiamylal is approved and vet_approved.,Thiamylal is a solid.,True
15490,"Pergolide is a long-acting dopamine agonist approved in 1982 for the treatment of Parkinson’s Disease. It is an ergot derivative that acts on the dopamine D2 and D3, alpha2- and alpha1-adrenergic, and 5-hydroxytryptamine (5-HT) receptors. It was indicated as adjunct therapy with levodopa/carbidopa in the symptomatic treatment of parkinsonian syndrome. It was later found that pergolide increased the risk of cardiac valvulopathy. The drug was withdrawn from the US market in March 2007 and from the Canadian market in August 2007. While the use of pergolide in humans is still approved in only some countries, pergolide is mainly used for veterinary purposes. Indicated as adjunctive treatment to levodopa/carbidopa in the management of the signs and symptoms of Parkinson's disease. It was withdrawn from the US and Canadian markets in 2007 due to an increased risk of cardiac valvulopathy.  Pergolide stimulates centrally-located dopaminergic receptors resulting in a number of pharmacologic effects. Five dopamine receptor types from two dopaminergic subfamilies have been identified. The dopaminergic D1 receptor subfamily consists of D<sub>1</sub> and D<sub>5</sub> subreceptors and are associated with dyskinesias. The dopaminergic D2 receptor subfamily consists of D<sub>2</sub>, D<sub>3</sub> and D<sub>4</sub> subreceptors and has been associated with improvement of symptoms of movement disorders. Thus, agonist activity specific for D2 subfamily receptors, primarily D<sub>2</sub> and D<sub>3</sub> receptor subtypes, are the primary targets of dopaminergic antiparkinsonian agents. It is thought that postsynaptic D2 stimulation is primarily responsible for the antiparkinsonian effect of dopamine agonists, while presynaptic D2 stimulation confers neuroprotective effects. This semisynthetic ergot derivative exhibits potent agonist activity on dopamine D<sub>2</sub>- and D<sub>3</sub>-receptors. It also exhibits agonist activity on dopamine D<sub>4</sub>, D<sub>1</sub>, and D<sub>5</sub>, 5-hydroxytryptamine (5-HT)<sub>1A</sub>, 5-HT<sub>1B</sub>, 5-HT<sub>1D</sub>, 5-HT<sub>2A</sub>, 5-HT<sub>2B</sub>, 5-HT<sub>2C</sub>, &alpha;<sub>2A</sub>-, &alpha;<sub>2B</sub>-, &alpha;<sub>2C</sub>-, &alpha;<sub>1A</sub>-, &alpha;<sub>1B</sub>-, and &alpha;<sub>1D</sub>-adrenergic receptors. Parkinsonian Syndrome manifests when approximately 80% of dopaminergic activity in the nigrostriatal pathway of the brain is lost. As this striatum is involved in modulating the intensity of coordinated muscle activity (e.g. movement, balance, walking), loss of activity may result in dystonia (acute muscle contraction), Parkinsonism (including symptoms of bradykinesia, tremor, rigidity, and flattened affect), akathesia (inner restlessness), tardive dyskinesia (involuntary muscle movements usually associated with long-term loss of dopaminergic activity), and neuroleptic malignant syndrome, which manifests when complete blockage of nigrostriatal dopamine occurs. High dopaminergic activity in the mesolimbic pathway of the brain causes hallucinations and delusions; these side effects of dopamine agonists are manifestations seen in patients with schizophrenia who have overractivity in this area of the brain. The hallucinogenic side effects of dopamine agonists may also be due to 5-HT<sub>2A</sub> agonism. The tuberoinfundibular pathway of the brain originates in the hypothalamus and terminates in the pituitary gland. In this pathway, dopamine inhibits lactotrophs in anterior pituitary from secreting prolactin. Increased dopaminergic activity in the tuberoinfundibular pathway inhibits prolactin secretion. Pergolide also causes transient increases in somatotropin (growth hormone) secretion and decreases in luteinizing hormone (LH) concentrations.  The dopamine D<sub>2</sub> receptor is a 7-transmembrane G-protein coupled receptor associated with G<sub>i</sub> proteins. In lactotrophs, stimulation of dopamine D<sub>2</sub> receptor causes inhibition of adenylyl cyclase, which decreases intracellular cAMP concentrations and blocks IP3-dependent release of Ca<sup>2+</sup> from intracellular stores. Decreases in intracellular calcium levels may also be brought about via inhibition of calcium influx through voltage-gated calcium channels, rather than via inhibition of adenylyl cyclase. Additionally, receptor activation blocks phosphorylation of p42/p44 MAPK and decreases MAPK/ERK kinase phosphorylation. Inhibition of MAPK appears to be mediated by c-Raf and B-Raf-dependent inhibition of MAPK/ERK kinase. Dopamine-stimulated growth hormone release from the pituitary gland is mediated by a decrease in intracellular calcium influx through voltage-gated calcium channels rather than via adenylyl cyclase inhibition. Stimulation of dopamine D<sub>2</sub> receptors in the nigrostriatal pathway leads to improvements in coordinated muscle activity in those with movement disorders. ",The molecular weight is 314.49.,Pergolide has a topological polar surface area of 19.03.,The log p value of  is 4.4.,Pergolide is approved and investigational and vet_approved and withdrawn.,Pergolide is a solid.,True
15491,"Brinzolamide is a highly specific, non-competitive, reversible carbonic anhydrase inhibitor. Carbonic anhydrase (CA) is an enzyme found in many tissues of the body including the eye. It catalyzes the reversible reaction involving the hydration of carbon dioxide and the dehydration of carbonic acid. In humans, carbonic anhydrase exists as a number of isoenzymes, the most active being carbonic anhydrase II (CA-II). Inhibition of carbonic anhydrase in the ciliary processes of the eye decreases aqueous humor secretion, presumably by slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport. The result is a reduction in intraocular pressure. Brinzolamide is indicated in the treatment of elevated intraocular pressure in patients with ocular hypertension or open-angle glaucoma. For the treatment of elevated intraocular pressure in patients with ocular hypertension or open-angle glaucoma. Used in the treatment of glaucoma, brinzolamide inhibits aqueous humor formation and reduces elevated intraocular pressure. Elevated intraocular pressure is a major risk factor in the pathogenesis of optic nerve damage and glaucomatous visual field loss. Brinzolamide can decrease intraocular pressure by approximately 16-19% in patients with elevated intraocular pressure. Brinzolamide is a highly specific inhibitor of CA-II, which is the main CA isoenzyme involved in the secretion of aqueous humor. Inhibition of CA in the ciliary process of the eye slows the formation of bicarbonate, and reduces sodium and fluid transport. This results in a reduction in the rate of aqueous humor secretion and the intraocular pressure. Brinzolamide is absorbed systemically following topical ocular administration. Since it has a high affinity for CA-II, brinzolamide binds extensively to red blood cells, where CA-II is primarily found. As sufficient CA-II activity remains, adverse effects resulting from the systemic inhibition of CA by brinzolamide are not observed. The metabolite N-desethyl brinzolamide is also formed. This metabolite binds to CA and accumulates in red blood cells as well. In the presence of brinzolamide, the metabolite binds mainly to carbonic anhydrase I (CA-I).",The molecular weight is 383.5.,Brinzolamide has a topological polar surface area of 118.8.,The log p value of  is 0.33.,Brinzolamide is approved.,Brinzolamide is a solid.,True
15492,"A nitrogen mustard linked to estradiol, usually as phosphate; used to treat prostatic neoplasms; also has radiation protective properties. For the palliative treatment of patients with metastatic and/or progressive carcinoma of the prostate Estramustine is an antineoplastic agent indicated in the palliative treatment of patients with metastatic and/or progressive carcinoma of the prostate. Estramustine is a combination of estradiol with nitrogen mustard. In vivo, the nitrogen-mustard moiety becomes active and participates in alkylation of DNA or other cellular components.. This causes DNA damage in rapidly dividing cancerous cells leading to cell death and ideally, tumor shrinkage. Estramustine is a derivative of estradiol with a nitrogen mustard moiety. This gives it alkylating properties. In vivo, the nitrogen mustard component is active and can alklyate DNA and other cellular components (such as tubulin components) of rapidly dividing cells. This causes DNA strandbreaks or misscoding events. This leads to apoptosis and cell death. Also, due to the drugs estrogen component, it can bind more selectively to active estrogen receptors.",The molecular weight is 440.41.,Estramustine has a topological polar surface area of 49.77.,The log p value of  is 4.92.,Estramustine is approved and investigational.,Estramustine is a solid.,True
15493,"Bromocriptine mesylate is a semisynthetic ergot alkaloid derivative with potent dopaminergic activity. It is indicated for the management of signs and symptoms of Parkinsonian Syndrome. Bromocriptine also inhibits prolactin secretion and may be used to treat dysfunctions associated with hyperprolactinemia. It also causes sustained suppression of somatotropin (growth hormone) secretion in some patients with acromegaly. Bromocriptine has been associated with pulmonary fibrosis. For the treatment of galactorrhea due to hyperprolactinemia, prolactin-dependent menstrual disorders and infertility, prolactin-secreting adenomas, prolactin-dependent male hypogonadism, as adjunct therapy to surgery or radiotherapy for acromegaly or as monotherapy is special cases, as monotherapy in early Parksinsonian Syndrome or as an adjunct with levodopa in advanced cases with motor complications. Bromocriptine has also been used off-label to treat restless legs syndrome and neuroleptic malignant syndrome. Bromocriptine stimulates centrally-located dopaminergic receptors resulting in a number of pharmacologic effects. Five dopamine receptor types from two dopaminergic subfamilies have been identified. The dopaminergic D1 receptor subfamily consists of D<sub>1</sub> and D<sub>5</sub> subreceptors, which are associated with dyskinesias. The dopaminergic D2 receptor subfamily consists of D<sub>2</sub>, D<sub>3</sub> and D<sub>4</sub> subreceptors, which are associated with improvement of symptoms of movement disorders. Thus, agonist activity specific for D2 subfamily receptors, primarily D<sub>2</sub> and D<sub>3</sub> receptor subtypes, are the primary targets of dopaminergic antiparkinsonian agents. It is thought that postsynaptic D<sub>2</sub> stimulation is primarily responsible for the antiparkinsonian effect of dopamine agonists, while presynaptic D<sub>2</sub> stimulation confers neuroprotective effects. This semisynthetic ergot derivative exhibits potent agonist activity on dopamine D<sub>2</sub>-receptors. It also exhibits agonist activity (in order of decreasing binding affinity) on 5-hydroxytryptamine (5-HT)<sub>1D</sub>, dopamine D<sub>3</sub>, 5-HT<sub>1A</sub>, 5-HT<sub>2A</sub>, 5-HT<sub>1B</sub>, and 5-HT<sub>2C</sub> receptors, antagonist activity on &alpha;<sub>2A</sub>-adrenergic, &alpha;<sub>2C</sub>, &alpha;<sub>2B</sub>, and dopamine D<sub>1</sub> receptors, partial agonist activity at receptor 5-HT<sub>2B</sub>, and inactivates dopamine D<sub>4</sub> and 5-HT<sub>7</sub> receptors. Parkinsonian Syndrome manifests when approximately 80% of dopaminergic activity in the nigrostriatal pathway of the brain is lost. As this striatum is involved in modulating the intensity of coordinated muscle activity (e.g. movement, balance, walking), loss of activity may result in dystonia (acute muscle contraction), Parkinsonism (including symptoms of bradykinesia, tremor, rigidity, and flattened affect), akathesia (inner restlessness), tardive dyskinesia (involuntary muscle movements usually associated with long-term loss of dopaminergic activity), and neuroleptic malignant syndrome, which manifests when complete blockage of nigrostriatal dopamine occurs. High dopaminergic activity in the mesolimbic pathway of the brain causes hallucinations and delusions; these side effects of dopamine agonists are manifestations seen in patients with schizophrenia who have overractivity in this area of the brain. The hallucinogenic side effects of dopamine agonists may also be due to 5-HT<sub>2A</sub> agonism. The tuberoinfundibular pathway of the brain originates in the hypothalamus and terminates in the pituitary gland. In this pathway, dopamine inhibits lactotrophs in anterior pituitary from secreting prolactin. Increased dopaminergic activity in the tuberoinfundibular pathway inhibits prolactin secretion making bromocriptine an effective agent for treating disorders associated with hypersecretion of prolactin. Pulmonary fibrosis may be associated bromocriptine’s agonist activity at 5-HT<sub>1B</sub> and 5-HT<sub>2B</sub> receptors.  The dopamine D<sub>2</sub> receptor is a 7-transmembrane G-protein coupled receptor associated with G<sub>i</sub> proteins. In lactotrophs, stimulation of dopamine D<sub>2</sub> receptor causes inhibition of adenylyl cyclase, which decreases intracellular cAMP concentrations and blocks IP3-dependent release of Ca<sup>2+</sup> from intracellular stores. Decreases in intracellular calcium levels may also be brought about via inhibition of calcium influx through voltage-gated calcium channels, rather than via inhibition of adenylyl cyclase. Additionally, receptor activation blocks phosphorylation of p42/p44 MAPK and decreases MAPK/ERK kinase phosphorylation. Inhibition of MAPK appears to be mediated by c-Raf and B-Raf-dependent inhibition of MAPK/ERK kinase. Dopamine-stimulated growth hormone release from the pituitary gland is mediated by a decrease in intracellular calcium influx through voltage-gated calcium channels rather than via adenylyl cyclase inhibition. Stimulation of dopamine D<sub>2</sub> receptors in the nigrostriatal pathway leads to improvements in coordinated muscle activity in those with movement disorders. ",The molecular weight is 654.61.,Bromocriptine has a topological polar surface area of 118.21.,The log p value of  is 6.58.,Bromocriptine is approved and investigational.,Bromocriptine is a solid.,True
15494,"Rifapentine is an antibiotic drug used in the treatment of tuberculosis. It inhibits DNA-dependent RNA polymerase activity in susceptible cells. Specifically, it interacts with bacterial RNA polymerase but does not inhibit the mammalian enzyme. For the treatment of pulmonary tuberculosis. Rifapentine is an antibiotic that inhibits DNA-dependent RNA polymerase activity in susceptible cells. Specifically, it interacts with bacterial RNA polymerase but does not inhibit the mammalian enzyme. It is bactericidal and has a very broad spectrum of activity against most gram-positive and gram-negative organisms (including Pseudomonas aeruginosa) and specifically Mycobacterium tuberculosis. Because of rapid emergence of resistant bacteria, use is restricted to treatment of mycobacterial infections and a few other indications. Rifampin is well absorbed when taken orally and is distributed widely in body tissues and fluids, including the CSF. It is metabolized in the liver and eliminated in bile and, to a much lesser extent, in urine, but dose adjustments are unnecessary with renal insufficiency. Rifapentine has shown higher bacteriostatic and bactericidal activities especially against intracellular bacteria growing in human monocyte-derived macrophages. Rifapentine inhibits DNA-dependent RNA polymerase in susceptible strains of M. tuberculosis. Rifapentine acts via the inhibition of DNA-dependent RNA polymerase, leading to a suppression of RNA synthesis and cell death.",The molecular weight is 877.04.,Rifapentine has a topological polar surface area of 220.15.,The log p value of  is 5.09.,Rifapentine is approved and investigational.,Rifapentine is a solid.,True
15495,"A benzodiazepine with anticonvulsant, hypnotic, and muscle relaxant properties. It has been shown in some cases to be more potent than diazepam or nitrazepam. For the short-term management of insomnia characterized by difficulty in falling asleep, frequent nocturnal awakenings, and/or early morning awakenings. Estazolam, a triazolobenzodiazepine derivative, is an oral hypnotic agent with anticonvulsant, hypnotic, and muscle relaxant properties. It has been shown in some cases to be more potent than diazepam or nitrazepam. Benzodiazepines bind nonspecifically to benzodiazepine receptors, which affects affects muscle relaxation, anticonvulsant activity, motor coordination, and memory. As benzodiazepine receptors are thought to be coupled to gamma-aminobutyric acid-A (GABA<sub>A</sub>) receptors, this enhances the effects GABA by increasing GABA affinity for the GABA receptor. Binding of the inhibitory neurotransmitter GABA to the site opens the chloride channel, resulting in a hyperpolarized cell membrane that prevents further excitation of the cell.",The molecular weight is 294.74.,Estazolam has a topological polar surface area of 43.07.,The log p value of  is 2.29.,Estazolam is approved and illicit.,Estazolam is a solid.,True
15496,"Rifaximin is a semisynthetic, rifamycin-based non-systemic antibiotic, meaning that the drug will not pass the gastrointestinal wall into the circulation as is common for other types of orally administered antibiotics. It has multiple indications and is used in treatment of traveller's diarrhea caused by E. coli; reduction in risk of overt hepatic encephalopathy recurrence; as well as diarrhea-predominant irritable bowel syndrome (IBS-D) in adult women and men. It is marketed under the brand name Xifaxan by Salix Pharmaceuticals. Rifaximin has multiple indications by the FDA: for the treatment of patients (≥12 years of age) with traveller's diarrhea caused by noninvasive strains of Escherichia coli; for the reduction of overt hepatic encephalopathy recurrence in patients ≥18 years of age; and in May 2015 it was approved for irritable bowel syndrome with diarrhea (IBS-D) treatment in adult men and women.  Rifaximin is a structural analog of rifampin and a non-systemic, gastrointestinal site-specific antibiotic. This non-systemic property of the drug is due to the addition of a pyridoimidazole ring, which renders it non-absorbable. Rifaximin acts by inhibiting bacterial ribonucleic acid (RNA) synthesis and contributes to restore intestinal microflora imbalance. Other studies have also shown rifaximin to be an pregnane X receptor (PXR) activator. As PXR is responsible for inhibiting the proinflammatory transcription factor NF-kappa B (NF-κB) and is inhibited in inflammatory bowel disease (IBD), rifaximin was proven to be effective for the treatment of IBS-D. Rifaximin acts by inhibiting RNA synthesis in susceptible bacteria by binding to the beta-subunit of bacterial deoxyribonucleic acid (DNA)-dependent ribonucleic acid (RNA) polymerase enzyme. This binding blocks translocation, which stops transcription.",The molecular weight is 785.89.,Rifaximin has a topological polar surface area of 198.38.,The log p value of  is 7.19.,Rifaximin is approved and investigational.,Rifaximin is a solid.,True
15497,"A narcotic analgesic with a long onset and duration of action. It is used mainly in the treatment of narcotic dependence. For the treatment and management of opiate dependence. It is sometimes used to treat severe pain in terminal patients. Levomethadyl acetate (also known as LAAM) is a synthetic synthetic opioid analgesic with multiple actions quantitatively similar to those as morphine, the most prominent of which involve the central nervous system and organs composed of smooth muscle. However, levomethadyl acetate is more active and more toxic than morphine. The principal actions of therapeutic value are analgesia and sedation and detoxification or temporary maintenance in narcotic addiction. In this respect, the drug is similar to Methadone and also has structural similarities to it. The levomethadyl acetate abstinence syndrome, although qualitatively similar to that of morphine, differs in that the onset is slower, the course is more prolonged, and the symptoms are less severe. Opiate receptors (Mu, Kappa, Delta) are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Levomethadyl acetate effectively opens calcium-dependent inwardly rectifying potassium channels (OP1 receptor agonist), resulting in hyperpolarization and reduced neuronal excitability.",The molecular weight is 353.51.,Levacetylmethadol has a topological polar surface area of 29.54.,The log p value of  is 4.59.,Levacetylmethadol is approved and investigational.,Levacetylmethadol is a solid.,True
15498,"An ergot alkaloid with uterine and vascular smooth muscle contractile properties. Used to treat postpartum haemorrhage and postabortion haemorrhage in patients with uterine atony.  Ergonovine belongs to the group of medicines known as ergot alkaloids. These medicines are usually given to stop excessive bleeding that sometimes occurs after abortion or a baby is delivered. They work by causing the muscle of the uterus to contract. Ergonovine directly stimulates the uterine muscle to increase force and frequency of contractions. With usual doses, these contractions precede periods of relaxation; with larger doses, basal uterine tone is elevated and these relaxation periods will be decreased. Contraction of the uterine wall around bleeding vessels at the placental site produces hemostasis. Ergonovine also induces cervical contractions. The sensitivity of the uterus to the oxytocic effect is much greater toward the end of pregnancy. The oxytocic actions of ergonovine are greater than its vascular effects. Ergonovine, like other ergot alkaloids, produces arterial vasoconstriction by stimulation of alpha-adrenergic and serotonin receptors and inhibition of endothelial-derived relaxation factor release. It is a less potent vasoconstrictor than ergotamine. As a diagnostic aid (coronary vasospasm), ergonovine causes vasoconstriction of coronary arteries.",The molecular weight is 325.41.,Ergometrine has a topological polar surface area of 68.36.,The log p value of  is 1.23.,Ergometrine is approved.,Ergometrine is a solid.,True
15499,"Retapamulin, marketed by GlaxoSmithKline as the ointment Altabax, is an antibiotic for skin infections like impetigo. It was approved by the FDA in April 2007. For use in adults and pediatric patients aged 9 months and older for the topical treatment of impetigo (up to 100 cm<sup>2</sup> in total area in adults or 2% total body surface area in pediatric patients aged 9 months or older) due to Staphylococcus aureus (methicillin-susceptible isolates only) or Streptococcus pyogenes. Retapamulin is a semisynthetic pleuromutilin antibiotic. This drug is usually bacteriostatic in action, but may become bactericidal at highed concentrations (when MBC is 1000 times higher than MIC). Retapamulin acts by selectively inhibiting the initiation of protein synthesis in bacteria at the level of bacterial 50S ribosome. Retapamulin is a bacterial protein synthesis inhibitor belonging to a class of compounds called pleuromutilins. These compounds inhibit the initiation of protein synthesis by binding to a specific site on the 50S subunit of bacterial ribosome (domain V of 23S rRNA). This binding site involves ribosomal protein L3 and is in the region of the ribosomal P site and peptidyl transferase center. By virtue of binding to this site, pleuromutilins inhibit peptidyl transfer, block P-site interactions, and prevent the normal formation of active 50S ribosomal subunits.",The molecular weight is 517.77.,Retapamulin has a topological polar surface area of 66.84.,The log p value of  is 5.21.,Retapamulin is approved.,Retapamulin is a solid.,True
15500,"A nonfluorinated corticosteroid anti-inflammatory agent used topically for dermatoses. For the relief of the inflammatory and pruritic manifestations of corticosteroid responsive dermatose. Desonide is a synthetic nonfluorinated corticosteroid for topical dermatologic use. The corticosteroids constitute a class of primarily synthetic steroids used topically as anti-inflammatory and antipruritic agents. Like other topical corticosteroids, desonide has anti-inflammatory, antipruritic and vasoconstrictive properties. The drug binds to cytosolic glucocorticoid receptors. This complex migrates to the nucleus and binds to genetic elements on the DNA. This activates and represses various genes. However corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2.",The molecular weight is 416.51.,Desonide has a topological polar surface area of 93.06.,The log p value of  is 2.37.,Desonide is approved and investigational.,Desonide is a solid.,True
15501,"Sitagliptin is an oral dipeptidyl peptidase-4 (DPP-4) inhibitor used in conjunction with diet and exercise to improve glycemic control in patients with type 2 diabetes mellitus. The effect of this medication leads to glucose dependent increases in insulin and decreases in glucagon to improve control of blood sugar. Sitagliptin was granted FDA approval on October 16, 2006. Sitagliptin is indicated for the management of glycemic control in type 2 diabetes mellitus along with diet and exercise. Sitagliptin inhibits DPP-4 which leads to increased levels of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide(GIP), decreased levels of glucagon, and a stronger insulin response to glucose. Inhibition of DPP-4 by sitagliptin slows DPP-4 mediated inactivation of incretins like GLP-1 and GIP. Incretins are released throughout the day and upregulated in response to meals as part of glucose homeostasis. Reduced inhibition of incretins increase insulin synthesis and decrease glucagon release in a manner dependant on glucose concentrations. These effects lead to an overall increase in blood glucose control which is demonstrated by reduced glycosylated hemoglobin (HbA1c).",The molecular weight is 407.32.,Sitagliptin has a topological polar surface area of 77.04.,The log p value of  is 0.69.,Sitagliptin is approved and investigational.,Sitagliptin is a solid.,True
15502,"Posaconazole is a triazole antifungal drug that is used to treat invasive infections by Candida species and Aspergillus species in severely immunocompromised patients. For prophylaxis of invasive <em>Aspergillus</em> and <em>Candida</em> infections in patients, 13 years of age and older, who are at high risk of developing these infections due to being severely immunocompromised as a result of procedures such as hematopoietic stem cell transplant (HSCT) recipients with graft-versus-host disease (GVHD), or due to hematologic malignancies with prolonged neutropenia from chemotherapy. Also for the treatment of oropharyngeal candidiasis, including oropharyngeal candidiasis refractory to itraconazole and/or fluconazole. Posaconazole is used as an alternative treatment for invasive aspergillosis, <em>Fusarium</em> infections, and zygomycosis in patients who are intolerant of, or whose disease is refractory to, other antifungals. Posaconazole is an antifungal agent structurally related to itraconazole. It is a drug derived from itraconzaole through the replacement of the chlorine substituents with flourine in the phenyl ring, as well as hydroxylation of the triazolone side chain. These modifications enhance the potency and spectrum of activity of the drug. Posaconazole can be either fungicial or fungistatic in action. As a triazole antifungal agent, posaconazole exerts its antifungal activity through blockage of the cytochrome P-450 dependent enzyme, sterol 14&alpha;-demethylase, in fungi by binding to the heme cofactor located on the enzyme. This leads to the inhibition of the synthesis of ergosterol, a key component of the fungal cell membrane, and accumulation of methylated sterol precursors. This results in inhibition of fungal cell growth and ultimately, cell death.",The molecular weight is 700.79.,Posaconazole has a topological polar surface area of 111.79.,The log p value of  is 4.11.,Posaconazole is approved and investigational and vet_approved.,Posaconazole is a solid.,True
15503,"Fosamprenavir is a prodrug of amprenavir, an inhibitor of human immunodeficiency virus (HIV) protease. Indicated in combination with other antiretroviral agents for the treatment of human immunodeficiency virus (HIV-1) infection, as well as postexposure prophylaxis of HIV infection in individuals who have had occupational or nonoccupational exposure to potentially infectious body fluids of a person known to be infected with HIV when that exposure represents a substantial risk for HIV transmission. The use of fosamprenavir is pending revision due to a potential association between the drug and myocardial infarction and dyslipidemia in HIV infected adults. Fosamprenavir is hydrolyzed by cellular phosphatases to the antiretroviral protease inhibitor amprenavir. This hydrolysis allows for the slow release of amprenavir, reducing the number of pills a patient must take. Fosamprenavir is a prodrug that is rapidly hydrolyzed to amprenavir by cellular phosphatases in the gut epithelium as it is absorbed. Amprenavir is an inhibitor of HIV-1 protease. During HIV replication, HIV protease cleaves viral polypeptide products of the Gag and Gag-Pol genes to form structural proteins of the virion core and essential viral enzymes. Amprenavir interferes with this process by binding to the active site of HIV-1 protease, thereby preventing the processing of viral Gag and Gag-Pol polyprotein precursors, resulting in the formation of immature non-infectious viral particles.",The molecular weight is 585.61.,Fosamprenavir has a topological polar surface area of 177.72.,The log p value of  is 2.5.,Fosamprenavir is approved.,Fosamprenavir is a solid.,True
15504,"A semi-synthetic cephalosporin antibiotic. Cefradine is a first generation cephalosporin antibiotic with a spectrum of activity similar to Cefalexin. Cefradine, like the penicillins, is a beta-lactam antibiotic. By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, it inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that Cefradine interferes with an autolysin inhibitor.",The molecular weight is 349.41.,Cefradine has a topological polar surface area of 112.73.,The log p value of  is -1.73.,Cefradine is approved.,Cefradine is a solid.,True
15505,"Tasosartan is a long-acting angiotensin II (AngII) receptor blocker. Its long duration of action has been attributed to its active metabolite enoltasosartan. It is used to treat patients with essential hypertension. Tasosartan is infrequently in the treatment of hypertension and heart failure. By blocking the angiotensin II (AT1) receptor, the drug ultimately causes vasodilation, reduced secretion of vasopressin (ADH), reduced production and secretion of aldosterone, amongst other actions leading to the combined effect of a reduction of blood pressure. Tasosartan is a selective, potent, orally active and long-acting nonpeptide Angiotensin II type 1 (AT1) receptor antagonist. Tasosartan blocks the renin-angiotensin-aldosterone system (RAAS) at the level of the AT1 receptor that mediates most, if not all, of the important actions of Ang II. Tasosartan binds reversibly to the AT1 receptors in vascular smooth muscle and the adrenal gland. As angiotensin II is a vasoconstrictor, which also stimulates the synthesis and release of aldosterone, blockage of its effects results in decreases in systemic vascular resistance. AT1 receptor antagonists avoid the nonspecificity of the Ang I converting enzyme (ACE) inhibitors. ",The molecular weight is 411.47.,Tasosartan has a topological polar surface area of 100.55.,The log p value of  is 2.45.,Tasosartan is experimental.,Tasosartan is a solid.,True
15506,"Aprobarbital is a barbiturate derivative synthesized in the 1920s by Ernst Preiswerk. It was determined that the substance was capable of demonstrating sedative, hypnotic, and anticonvulsant effects. A primary treatment indicated for the use of aprobarbital was subsequently insomnia. Aprobarbital was never as widely used as more common barbiturate derivatives such as phenobarbital and is now rarely prescribed. Aprobarbital (like all barbiturates) works by binding to the GABAA receptor at either the alpha or the beta sub unit. These are binding sites that are distinct from GABA itself and also distinct from the benzodiazepine binding site. Like benzodiazepines, barbiturates potentiate the effect of GABA at this receptor. This GABAA receptor binding decreases input resistance, depresses burst and tonic firing, especially in ventrobasal and intralaminar neurons, while at the same time increasing burst duration and mean conductance at individual chloride channels; this increases both the amplitude and decay time of inhibitory postsynaptic currents. In addition to this GABA-ergic effect, barbiturates also block the AMPA receptor, a subtype of glutamate receptor. Glutamate is the principal excitatory neurotransmitter in the mammalian CNS. Aprobarbital also appears to bind neuronal nicotinic acetylcholine receptors.",The molecular weight is 210.23.,Aprobarbital has a topological polar surface area of 75.27.,The log p value of  is 1.1.,Aprobarbital is experimental and illicit.,Aprobarbital is a solid.,True
15507,"The 3-methyl ether of ethinyl estradiol. It must be demethylated to be biologically active. It is used as the estrogen component of many combination ORAL contraceptives. Mestranol was used as one of the first oral contraceptives. Mestranol is the 3-methyl ether of ethinylestradiol. Ethinylestradiol, is a synthetic derivative of estradiol. Ethinylestradiol is orally bio-active and the estrogen used in almost all modern formulations of combined oral contraceptive pills. It binds to (and activates) the estrogen receptor. Mestranol is a biologically inactive prodrug of ethinylestradiol to which it is demethylated in the liver with a conversion efficiency of 70%.",The molecular weight is 310.44.,Mestranol has a topological polar surface area of 29.46.,The log p value of  is 4.27.,Mestranol is approved.,Mestranol is a solid.,True
15508,"Quinupristin/dalfopristin is a combination of two antibiotics used to treat infections by staphylococci and by vancomycin-resistant Enterococcus faecium. Dalfopristin inhibits the early phase of protein synthesis in the bacterial ribosome and quinupristin inhibits the late phase of protein synthesis. The combination of the two components acts synergistically and is more effective in vitro than each component alone. For the treatment of bacterial infections (usually in combination with dalfopristin). Quinupristin is a streptogramin antibiotic, derived from pristinamycin I. By inhibiting the bacterial ribosomal subunits, protein synthesis is inhibited thus leading to eventual bacterial cell death or stasis. Quinupristin inhibits the late phase of protein synthesis in the bacterial ribosome. Dalfopristin binds to the 23S portion of the 50S ribosomal subunit, and changes the conformation it, enhancing the binding of quinupristin by a factor of about 100. In addition, it inhibits peptidyl transferase. Quinupristin binds to a nearby site on the 50S ribosomal subunit and prevents elongation of the polypeptide as well as causing incomplete chains to be released.",The molecular weight is 1022.23.,Quinupristin has a topological polar surface area of 231.2.,The log p value of  is 7.21.,Quinupristin is approved.,Quinupristin is a solid.,True
15509,"The extract of the Ginkgo leaves contains flavonoid glycosides and terpenoids (ginkgolides, bilobalides) and has been used pharmaceutically for hundreds of years. It has many alleged nootropic properties, and is mainly used as memory and concentration enhancer, and anti-vertigo agent. Ginkgo extract seems to have three effects on the human body: it improves blood flow (including microcirculation in small capillaries) to most tissues and organs; it protects against oxidative cell damage from free radicals; and it blocks many of the effects of PAF (platelet aggregation, blood clotting) that have been related to the development of a number of cardiovascular, renal, respiratory and CNS (Central Nervous System) disorders. Appears to be effective in: alleviating age-related memory impairment in some elderly people with mild to moderate age-related memory or cognitive impairment; improving cognitive function in healthy young to middle-aged people; improving symptoms of Alzheimer's, vascular or mixed dementia; improving damage to the visual field in patients with normal tension glaucoma; decreasing the number of painful attacks in patients with Raynaud's syndrome; and may improve symptoms of vertigo and dizziness in some patients.  The mechanism by which ginkgo biloba is thought to be effective for these conditions appears to be in part through active \ginkgolides\"" terpenoids and flavinoids that appear to inhibit platelet aggregation, neutrophil degranulation, and the induction of oxygen-free radical production"" The compounds found in ginkgo may have a protective",,,,Ginkgo biloba is approved and investigational and nutraceutical.,Ginkgo biloba is a solid.,True
15510,"Antilipemic agent that lowers cholesterol and triglycerides. It decreases low density lipoproteins and increases high density lipoproteins. For the treatment of primary hyperlipidaemia types IIa, IIb, III, IV and V (Fredrickson classification) corresponding to groups I, II and III of the European Atherosclerosis Society guidelines - when diet alone or improvements in lifestyle such as increased exercise or weight reduction do not lead to an adequate response. Also for the treatment of secondary hyperlipidaemias, e.g. severe hypertriglyceridemias, when sufficient improvement does not occur after correction of the underlying disorder (e.g. diabetes mellitus). Bezafibrate is an antilipemic agent that lowers cholesterol and triglycerides. It decreases low density lipoproteins and increases high density lipoproteins. Bezafibrate lowers elevated blood lipids (triglycerides and cholesterol). Elevated VLDL and LDL are reduced by treatment with bezafibrate, whilst HDL-levels are increased. The activity of triglyceride lipases (lipoprotein lipase and hepatic lipoproteinlipase) involved in the catabolism of triglyceride-rich lipoproteins is increased by bezafibrate. In the course of the intensified degradation of triglyceride-rich lipoproteins (chylomicrons, VLDL) precursors for the formation of HDL are formed which explains an increase in HDL. Furthermore, cholesterol biosynthesis is reduced by bezafibrate, which is accompanied by a stimulation of the LDL-receptor-mediated lipoprotein catabolism. Elevated fibrinogen appears to be an important risk-factor, alongside the lipids, smoking and hypertension, in the development of atheroma. Fibrinogen plays an important role in viscosity, and therefore blood flow, and also appears to play an important role in thrombus development and lysability. Bezafibrate exerts an effect on thrombogenic factors. A significant decrease in elevated plasma fibrinogen levels can be achieved. This may lead, amongst other things, to a reduction in both blood and plasma viscosity. Inhibition of platelet aggregation has also been observed. A reduction in blood glucose concentration due to an increase in glucose tolerance has been reported in diabetic patients. In the same patients, the concentration of fasting and postprandial free fatty acids was reduced by bezafibrate. It is generally accepted that bezafibrate is likely an agonist of PPAR-alpha. However, certain other investigations have also suggested that the substance might also elicit some effects on PPAR-gamma and PPAR-delta too.",The molecular weight is 361.82.,Bezafibrate has a topological polar surface area of 75.63.,The log p value of  is 3.7.,Bezafibrate is approved and investigational.,Bezafibrate is a solid.,True
15511,"Pranlukast is a cysteinyl leukotriene receptor-1 antagonist. It antagonizes or reduces bronchospasm caused, principally in asthmatics, by an allergic reaction to accidentally or inadvertently encountered allergens. Used as an adjunct to the standard therapy of inhaled steroids with inhaled long- and/or short-acting beta-agonists.  Pranlukast is a cysteinyl leukotriene receptor-1 antagonist. Pranlukast selectively antagonizes leukotriene D<sub>4</sub> (LTD<sub>4</sub>) at the cysteinyl leukotriene receptor, CysLT<sub>1</sub>, in the human airway. Pranlukast inhibits the actions of LTD<sub>4</sub> at the CysLT<sub>1</sub> receptor, preventing airway edema, smooth muscle contraction, and enhanced secretion of thick, viscous mucus.",The molecular weight is 481.51.,Pranlukast has a topological polar surface area of 119.09.,The log p value of  is 5.06.,Pranlukast is investigational.,Pranlukast is a solid.,True
15512,"5-androstenedione is a prohormone of testosterone. In the United States, the Controlled Substance Act is inclusive to anabolic steroids and their precursors. Thus 5-androstenedione is a controlled substance, and its use in athletes is prohibited by The World Anti-Doping Agency. Apart from the positioning of a carbon-carbon double bond, its structure is similar to , which is a prohormone which is naturally produced in the body by the adrenal glands and gonads, and acts as precursor to testosterone, as well as estrone and estradiol.",,,,5-androstenedione is experimental and illicit.,5-androstenedione is a solid.,True
15513,A long-acting barbiturate that depresses most metabolic processes at high doses. It is used as a hypnotic and sedative and may induce dependence. Barbital is also used in veterinary practice for central nervous system depression. Barbital is a schedule IV controlled drug.,The molecular weight is 184.2.,Barbital has a topological polar surface area of 75.27.,The log p value of  is 0.66.,Barbital is illicit.,Barbital is a solid.,True
15514,"A delta-4 C19 steroid that is produced not only in the testis, but also in the ovary and the adrenal cortex. Depending on the tissue type, androstenedione can serve as a precursor to testosterone as well as estrone and estradiol. 4-androstenedione is a 19-carbon steroid hormone produced in the adrenal glands and the gonads as an intermediate step in the biochemical pathway that produces the androgen testosterone and the estrogens estrone and estradiol.",The molecular weight is 286.42.,Androstenedione has a topological polar surface area of 34.14.,The log p value of  is 3.01.,Androstenedione is experimental and illicit.,Androstenedione is a solid.,True
15515,"Flunitrazepam is a benzodiazepine with pharmacologic actions similar to those of diazepam that can cause anterograde amnesia. Some reports indicate that it is used as a date rape drug and suggest that it may precipitate violent behavior. The United States Government has banned the importation of this drug. For short-term treatment of severe insomnias, that are not responsive to other hypnotics. Flunitrazepam is a powerful hypnotic drug that is a benzodiazepine derivative. It has powerful hypnotic, sedative, anxiolytic, and skeletal muscle relaxant properties. The drug is sometimes used as a date rape drug. In the United States, the drug has not been approved by the Food and Drug Administration for medical use, and is considered to be an illegal drug. It has however been approved in the United Kingdom and other countries. Benzodiazepines bind nonspecifically to benzodiazepine receptors BNZ1, which mediates sleep, and BNZ2, which affects affects muscle relaxation, anticonvulsant activity, motor coordination, and memory. As benzodiazepine receptors are thought to be coupled to gamma-aminobutyric acid-A (GABAA) receptors, this enhances the effects of GABA by increasing GABA affinity for the GABA receptor. Binding of the inhibitory neurotransmitter GABA to the site opens the chloride channel, resulting in a hyperpolarized cell membrane that prevents further excitation of the cell.",The molecular weight is 313.29.,Flunitrazepam has a topological polar surface area of 78.49.,The log p value of  is 1.78.,Flunitrazepam is approved and illicit.,Flunitrazepam is a solid.,True
15516,"Clotiazepam is a benzodiazepine derivative, not approved for sale in the U.S. or Canada, but has been approved in the U.K. It is a schedule IV drug in Canada. For the treatment of anxiety disorders. Clotiazepam is a benzodiazepine derivative possessing anxiolytic, anticonvulsant, sedative and skeletal muscle relaxant properties. It increases the stage 2 non-rapid eye movement sleep. Clotiazepam acts at the benzodiazepine receptors (BZD). This agonizes the action of GABA, increasing the frequency of opening of the channel chlorinates and penetration of the ions chlorinates through the ionophore. Increase in membrane polarization decreases the probability of discharge of neurons.",The molecular weight is 318.82.,Clotiazepam has a topological polar surface area of 32.67.,The log p value of  is 3.03.,Clotiazepam is approved and illicit.,Clotiazepam is a solid.,True
15517,"Prazepam is a benzodiazepine that is used in the treatment of anxiety disorders. It is a schedule IV drug in the U.S. For the treatment of anxiety disorders. Prazepam is a benzodiazepine derivative with anxiolytic, anticonvulsant, sedative and skeletal muscle relaxant activity. Benzodiazepines may be habit-forming (causing mental or physical dependence), especially when taken for a long time or in high doses. Prazepam is believed to stimulate GABA receptors in the ascending reticular activating system. Since GABA is inhibitory, receptor stimulation increases inhibition and blocks both cortical and limbic arousal following stimulation of the brain stem reticular formation.",The molecular weight is 324.81.,Prazepam has a topological polar surface area of 32.67.,The log p value of  is 3.93.,Prazepam is approved and illicit.,Prazepam is a solid.,True
15518,Quazepam is a drug which is a benzodiazepine derivative. It induces impairment of motor function and has hypnotic properties. Quazepam is used to treat insomnia. Used to treat insomnia. Quazepam is a benzodiazepine derivative. The main pharmacological action of quazepam is the enhancement of the neurotransmitter GABA at the GABA<sub>A</sub> receptor.,The molecular weight is 386.79.,Quazepam has a topological polar surface area of 15.6.,The log p value of  is 3.7.,Quazepam is approved and illicit.,Quazepam is a solid.,True
15519,"A benzodiazepine derivative used as an anticonvulsant and hypnotic. Used to treat short-term sleeping problems (insomnia), such as difficulty falling asleep, frequent awakenings during the night, and early-morning awakening. Nitrazepam is a type of benzodiazepine drug. It is a powerful hypnotic drug which possesses strong sedative, anxiolytic, amnestic, anticonvulsant, and skeletal muscle relaxant properties. Nitrazepam shortens the time required to fall asleep and lengthens the duration of sleep. It is also useful for the management of myoclonic seizures. Nitrazepam belongs to a group of medicines called benzodiazepines. This drug affects central benzodiazepine receptors, which are associated with inhibitory GABA (gamma amino butyric acid)receptors, leading to enhanced GABA binding activity. GABA is a major neurotransmitter in the brain, which causes somnolence, relaxation of muscles, a decrease in anxiety and general central nervous system depression. Nitrazepam has anticonvulsant properties that may be attributed to its ability to bind to voltage-dependent sodium channels. Sustained repetitive firing seems to be limited by benzodiazepines effect of slowing recovery of sodium channels from inactivation.",The molecular weight is 281.27.,Nitrazepam has a topological polar surface area of 87.28.,The log p value of  is 2.32.,Nitrazepam is approved.,Nitrazepam is a solid.,True
15520,"Roflumilast is a phosphodiesterase-4 (PDE-4) inhibitor. Due to its selective inhibition of the PDE4 isoenzyme in lung cells, roflumilast is indicated for the management of chronic obstrtuctive pulmonary disease (COPD) exacerbations. Treatment with Roflumilast is associated with an increase in psychiatric adverse reactions, including suicide and suicidal attempts. Roflumilast is indicated as a treatment to reduce the risk of COPD exacerbations in patients with severe COPD associated with chronic bronchitis and a history of exacerbations. Roflumilast is not a bronchodilator and is not indicated for the relief of acute bronchospasm. Roflumilast (and its active metabolite, roflumilast N-oxide) increases cyclic adenosine-3′, 5′-monophosphate (cAMP) in lung cells by inhibiting PDE4. Increased cAMP activates PKA, which inactivates transcription factors involved in inflammation. Romflumilast also decreases the amount of sputum neutrophils and eosinophils in COPD patients. Roflumilast is a phosphodiesterase-4 (PDE-4) inhibitor which, due to its selective inhibition of the PDE4 isoenzyme, has potential antiinflammatory and antimodulatory effects in the pulmonary system. It is thought that the increased levels of intracellular cyclic AMP are responsible for the therapeutic actions of Roflumilast. ",The molecular weight is 403.21.,Roflumilast has a topological polar surface area of 60.45.,The log p value of  is 3.0.,Roflumilast is approved.,Roflumilast is a solid.,True
15521,"A flavonol glycoside found in many plants, including buckwheat; tobacco; forsythia; hydrangea; viola, etc. It has been used therapeutically to decrease capillary fragility.",The molecular weight is 610.52.,Rutin has a topological polar surface area of 265.52.,The log p value of  is -1.36.,Rutin is approved and experimental and investigational.,Rutin is a solid.,True
15522,"Dalfopristin is a combination of two antibiotics (Dalfopristin and quinupristin) used to treat infections by staphylococci and by vancomycin-resistant Enterococcus faecium. It is not effective against Enterococcus faecalis infections. Dalfopristin inhibits the early phase of protein synthesis in the bacterial ribosome and quinupristin inhibits the late phase of protein synthesis. For the treatment of bacterial infections (usually in combination with quinupristin). Dalfopristin is a streptogramin antibiotic, derived from pristinamycin IIA.  The site of action of dalfopristin is the bacterial ribosome. Dalfopristin ",The molecular weight is 690.85.,Dalfopristin has a topological polar surface area of 176.42.,The log p value of  is 1.35.,Dalfopristin is approved.,Dalfopristin is a solid.,True
15523,"Investigated for use/treatment in colorectal cancer, lung cancer, breast cancer, solid tumors, and prostate cancer. The principal mechanism of the epothilone class is inhibition of microtubule function. Microtubules are essential to cell division, and epothilones therefore stop cells from properly dividing. ",,,,Epothilone D is investigational.,Epothilone D is a solid.,True
15524,"An estrogenic steroid produced by horses. It has a total of four double bonds in the A- and B-ring. High concentration of equilin is found in the urine of pregnant mares. For the treatment of moderate to severe vasomotor symptoms associated with the menopause, atrophic vaginitis, osteoporosis, hypoestrogenism due to hypogonadism, castration, primary ovarian failure, breast cancer (for palliation only), and Advanced androgen-dependent carcinoma of the prostate (for palliation only) Equilin is a component of Premarin (conjugated estrogens), a mixture of the water soluble salts of sulfate esters from estrone, equilin, 17 alpha-dihydroequilin, and other related steroids, may be derived from pregnant equine urine or yam and soy plants. Estrogens are important in the development and maintenance of the female reproductive system and secondary sex characteristics. They promote growth and development of the vagina, uterus, and fallopian tubes, and enlargement of the breasts. Indirectly, they contribute to the shaping of the skeleton, maintenance of tone and elasticity of urogenital structures, changes in the epiphyses of the long bones that allow for the pubertal growth spurt and its termination, growth of axillary and pubic hair, and pigmentation of the nipples and genitals. Decline of estrogenic activity at the end of the menstrual cycle can bring on menstruation, although the cessation of progesterone secretion is the most important factor in the mature ovulatory cycle. However, in the preovulatory or nonovulatory cycle, estrogen is the primary determinant in the onset of menstruation. Estrogens also affect the release of pituitary gonadotropins. The pharmacologic effects of conjugated estrogens are similar to those of endogenous estrogens. Estrogens enter the cells of responsive tissues (e.g., female organs, breasts, hypothalamus, pituitary) where they interact with a protein receptor, subsequently increasing the rate of synthesis of DNA, RNA, and some proteins. Estrogens decrease the secretion of gonadotropin-releasing hormone by the hypothalamus, reducing the secretion of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) from the pituitary.",,,,Equilin is experimental.,Equilin is a solid.,True
15525,"A 21-carbon steroid, derived from cholesterol and found in steroid hormone-producing tissues. Pregnenolone is the precursor to gonadal steroid hormones and the adrenal corticosteroids.",,,,Pregnenolone is approved and experimental.,Pregnenolone is a solid.,True
15526,"Epothilone B is a 16-membered macrolide that mimics the biological effects of taxol. Investigated for use/treatment in ovarian cancer, lung cancer, brain cancer, breast cancer, and gastric cancer. The principal mechanism of the epothilone class is inhibition of microtubule function. Microtubules are essential to cell division, and epothilones therefore stop cells from properly dividing. Epothilone B possess the same biological effects as taxol both in vitro and in cultured cells. This is because they share the same binding site, as well as binding affinity to the microtubule. Like taxol, epothilone B binds to the αβ-tubulin heterodimer subunit. Once bound, the rate of αβ-tubulin dissociation decreases, thus stabilizing the microtubules. Furthermore, epothilone B has also been shown to induce tubulin polymerization into microtubules without the presence of GTP. This is caused by formation of microtubule bundles throughout the cytoplasm. Finally, epothilone B also causes cell cycle arrest at the G2-M transition phase, thus leading to cytotoxicity and eventually cell apoptosis.",,,,Patupilone is experimental and investigational.,Patupilone is a solid.,True
15527,Equilenin is an estrogenic steroid produced by horses. It has a total of five double bonds in the A- and B-ring. High concentration of equilenin is found in the urine of pregnant mares.,,,,Equilenin is experimental.,Equilenin is a solid.,True
15528,,,,,Vanoxerine is investigational.,Vanoxerine is a solid.,False
15529,,,,,6-Deoxyerythronolide B is experimental.,6-Deoxyerythronolide B is a solid.,False
15530,"An adrenocortical steroid that has modest but significant activities as a mineralocorticoid and a glucocorticoid. (From Goodman and Gilman&#39;s The Pharmacological Basis of Therapeutics, 8th ed, p1437)",,,,Corticosterone is experimental.,Corticosterone is a solid.,True
15531,"Nimesulide is a relatively COX-2 selective, non-steroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic properties. Its approved indications are the treatment of acute pain, the symptomatic treatment of osteoarthritis and primary dysmenorrhoea in adolescents and adults above 12 years old. Due to concerns about the risk of hepatotoxicity, nimesulide has been withdrawn from market in many countries. For the treatment of acute pain, the symptomatic treatment of osteoarthritis and primary dysmenorrhoea in adolescents and adults above 12 years old. Food, gender and advanced age have negligible effects on nimesulide pharmacokinetics. The therapeutic effects of Nimesulide are the result of its complete mode of action which targets a number of key mediators of the inflammatory process such as: COX-2 mediated prostaglandins, free radicals, proteolytic enzymes and histamine.",The molecular weight is 308.31.,Nimesulide has a topological polar surface area of 101.22.,The log p value of  is 3.21.,Nimesulide is approved and investigational and withdrawn.,Nimesulide is a solid.,True
15532,"Metamizole, formerly marketed as Dimethone tablets and injection, Protemp oral liquid, and other drug products, was associated with potentially fatal agranulocytosis. Approvals of the NDA's for dipyrone drug products were withdrawn on June 27, 1977 (see the Federal Register of June 17, 1977 (42 FR 30893)). Withdrawn from the Canadian market in 1963. Used in the past as a powerful painkiller and fever reducer. Dipyrone is a non-steroidal anti-inflammatory drug (NSAID), commonly used in the past as a powerful painkiller and fever reducer.",,,,Metamizole is approved and investigational and withdrawn.,Metamizole is a solid.,True
15533,"Prenylamine was withdrawn from the Canadian, US, and UK markets in 1988 due to concerns regarding cardiac arrhythmias.",The molecular weight is 329.49.,Prenylamine has a topological polar surface area of 12.03.,The log p value of  is 5.8.,Prenylamine is approved and withdrawn.,Prenylamine is a solid.,True
15534,"Zimelidine has been banned worldwide due to serious, sometimes fatal, cases of central and/or peripheral neuropathy known as Guillain-Barré syndrome and due to a peculiar hypersensitivity reaction involving many organs including skin exanthema, flu-like symptoms, arthralgias, and sometimes eosinophilia. Additionally, zimelidine was charged to cause an increase in suicidal ideation and/or attempts among depressive patients. For the treatment of depression. Zimelidine was the first marketed selective serotonin reuptake inhibitor (SSRI) antidepressant. It is a pyridylallylamine, structurally different from other antidepressants. The antidepressant actions of zimelidine are presumed to be linked to its inhibition of CNS neuronal uptake of serotonin. Zimelidine blocks the reuptake of serotonin at the serotonin reuptake pump of the neuronal membrane, enhancing the actions of serotonin on 5HT1A autoreceptors. SSRIs bind with significantly less affinity to histamine, acetylcholine, and norepinephrine receptors than tricyclic antidepressant drugs.",The molecular weight is 317.23.,Zimelidine has a topological polar surface area of 16.13.,The log p value of  is 3.19.,Zimelidine is approved and withdrawn.,Zimelidine is a solid.,True
15535,"Methaqualone is a sedative-hypnotic drug that is similar in effect to barbiturates, a general central nervous system depressant. The sedative-hypnotic activity was first noted by Indian researchers in the 1950s and in 1962 methaqualone itself was patented in the US by Wallace and Tiernan. Its use peaked in the early 1970s as a hypnotic, sedative, and muscle relaxant commonly used for insomnia. It has also been used illegally as a recreational drug, commonly known as Quaaludes, Sopors, Ludes or Mandrax (particularly in the 1970s in North America) depending on the manufacturer. Since at least 2001, it has been widely used in South Africa, where it is commonly referred to as \smarties\"" or \""geluk-tablette\"" (meaning happy tablets). Clandestinely produced methaqualone is still seized by government agencies and police forces around the world."" For the treatment of insomnia, and as a sedative and muscle relaxant.",The molecular weight is 250.3.,Methaqualone has a topological polar surface area of 32.67.,The log p value of  is 3.65.,Methaqualone is illicit and withdrawn.,Methaqualone is a solid.,True
15536,"Maraviroc (brand-named Selzentry, or Celsentri outside the U.S.) is a chemokine receptor antagonist drug developed by the drug company Pfizer that is designed to act against HIV by interfering with the interaction between HIV and CCR5. It was originally labelled as UK-427857 during development but was assigned the Maraviroc name as it entered trials. It was approved for use by the FDA in August, 2007. For treatment-experienced adult patients infected with only CCR5-tropic HIV-1 detectable, who have evidence of viral replication and HIV-1 strains resistant to multiple antiretroviral agents. Maraviroc is a chemokine receptor antagonist drug developed by the drug company Pfizer that is designed to act against HIV by interfering with the interaction between HIV and CCR5. Maraviroc is an entry inhibitor and works by blocking HIV from entering human cells. Specifically maraviroc is a selective, slowly reversible, small molecule antagonist of the interaction between human CCR5 and HIV-1 gp120. Maraviroc selectively binds to the human chemokine receptor CCR5 present on the membrane of CD4 cells (T-cells), preventing the interaction of HIV-1 gp120 and CCR5 necessary for CCR5-tropic HIV-1 to enter cells.",The molecular weight is 513.68.,Maraviroc has a topological polar surface area of 63.05.,The log p value of  is 3.26.,Maraviroc is approved and investigational.,Maraviroc is a solid.,True
15537,"A direct-acting smooth muscle relaxant used to dilate blood vessels. It may cause gastrointestinal distress and tachycardia. Cyclandelate is not approved for use in the U.S. or Canada, but is approved in various European countries. Used in the treatment of various blood vessel diseases (e.g., claudication, arteriosclerosis and Raynaud's disease) and nighttime leg cramps. Cyclandelate is in a class of drugs called vasodilators. Cyclandelate relaxes veins and arteries, which makes them wider and allows blood to pass through them more easily. Cyclandelate produces peripheral vasodilation by a direct effect on vascular smooth muscle. Pharmacological action may be due to calcium-channel antagonism.",The molecular weight is 276.38.,Cyclandelate has a topological polar surface area of 46.53.,The log p value of  is 4.64.,Cyclandelate is approved.,Cyclandelate is a solid.,True
15538,"A long-acting injectable antipsychotic agent used for chronic schizophrenia. Used for the treatment of schizophrenia. Fluspirilene is a relatively long-acting injectable depot antipsychotic drug used for schizophrenia. Fluspirilene does not differ greatly from other depot antipsychotics (fluphenazine decanoate, fluphenazine enathate, perphenazine onanthat, pipotiazine undecylenate) with respect to treatment efficacy, response or tolerability. Outcomes suggest that fluspirilene does not differ significantly from oral antipsychotics or in different weekly regimens, although much cannot be inferred because of the shortage of trials.",The molecular weight is 475.58.,Fluspirilene has a topological polar surface area of 35.58.,The log p value of  is 5.42.,Fluspirilene is approved and investigational.,Fluspirilene is a solid.,True
15539,"Ixabepilone is an epothilone B analog developed by Bristol-Myers Squibb as a cancer drug. It was FDA approved on October 16, 2007, for the treatment of unresponsive aggressive metastatic or locally advanced breast cancer. Ixabepilone is administered through injection, and will be marketed under the trade name Ixempra. Ixabepilone is a semisynthetic analogue of epothilone B. It has a lactone–lactam modification that minimizes susceptibility to esterase degradation. Investigated for use/treatment in breast cancer, head and neck cancer, melanoma, lung cancer, lymphoma (non-hodgkin's), prostate cancer, renal cell carcinoma, and cancer/tumors (unspecified). Binding of Ixabepilone to beta-tubulins (e.g. beta-III tubulin) stabilizes microtubules. Microtubules are essential to cell division, and epothilones therefore stop cells from properly dividing. Like taxol, Ixabepilone binds to the αβ-tubulin heterodimer subunit. Once bound, the rate of αβ-tubulin dissociation decreases, thus stabilizing the microtubules.",The molecular weight is 506.7.,Ixabepilone has a topological polar surface area of 112.05.,The log p value of  is 3.52.,Ixabepilone is approved and investigational.,Ixabepilone is a solid.,True
15540,"Calanolide A is a new non-nucleoside reverse transcriptase inhibitor (NNRTI) derived from a plant found in the Malaysian rain forest. A related compound, calanolide B, also has anti-HIV activity. Both drugs are being developed by Sarawak Pharmaceuticals. A preliminary dosing study among HIV-infected individuals showed a significant antiviral effect compared with placebo. For use in combination treatment of HIV infection (AIDS). Calanolide A is a new non-nucleoside reverse transcriptase inhibitor (NNRTI) derived from a plant found in the Malaysian rain forest. A related compound, calanolide B, also has anti-HIV activity. Both drugs are being developed by Sarawak Pharmaceuticals. The drug is metabolised by cytochrome P450 CYP3A, and its developers have suggested that drug levels may be enhanced if co-administered with ritonavir (Norvir). The drug is active in the test tube against HIV with the two most common NNRTI-related mutations, K103N and Y181C, and selects for a mutation which does not cause cross-resistance with any other NNRTIs currently under investigation. A substitution at codon Y188H of reverse transcriptase has been associated with 30-fold resistance to calanolide A in vitro (Quan 1999). The compound is essentially inactive against strains of the less common HIV type 2. Viral life-cycle studies indicate that calanolide A acts early in the infection process, similar to the known HIV reverse transcriptase (RT) inhibitor 2', 3'-dideoxycytidine. In enzyme inhibition assays, calanolide A potently and selectively inhibits recombinant HIV type 1 RT but not cellular DNA polymerases or HIV type 2 RT within the concentration range tested.",,,,Calanolide A is investigational.,Calanolide A is a solid.,True
15541,"Vapreotide is a synthetic octapeptide somatostatin analog. It was being studied for the treatment of cancer. For the treatment of esophageal variceal bleeding in patients with cirrhotic liver disease and has also shown efficacy in the treatment of patients with AIDS-related diarrhea. Vapreotide is a somatostatin analog with a higher metabolic stability than the parent hormone. Vapreotide reduces splanchnic blood flow; inhibits growth hormone release, and inhibits the release of peptides and vasoactive compounds from neuroendocrine tumors. The exact mechanism of action is unknown, although one study has provided in vitro and in vivo evidence for a tachykinin NK1 receptor antagonist effect in the analgesic effects of vapreotide (PMID: 7556407).",,,,Vapreotide is experimental and investigational.,Vapreotide is a solid.,True
15542,"Milnacipran is a selective serotonin and norepinephrine reuptake inhibitor (SNRI) and like many agents in this category was originally developed for and continues to be approved and indicated for the treatment of depression. Furthermore, in 2009 the US FDA approved milnacipran for the additional indication of treating fibromyalgia , although other regional regulatory authorities like the EMA, among others, have not yet approved the agent for such treatment, citing lack of robust evidence of efficacy, insufficient demonstration of maintenance of effect, and other concerns. Nevertheless, milnacipran demonstrates a somewhat unique characteristic among SNRIs to elicit a relatively balanced reuptake inhibition of both serotonin and noradrenaline, with a somewhat increased preference for noradrenaline reuptake inhibition - which is potentially a point of interest given the plausible proposal that noradrenaline plays an important role in the mitigation of pain signals in the descending inhibitory pain pathways in the brain and spinal cord. Milnacipran is a selective serotonin and norepinephrine reuptake inhibitor (SNRI) indicated for the management of fibromyalgia in patients that are 18 years old or above.  When utilized to treat fibromyalgia, the effect of milnacipran on the QTcF interval in patients was measured in a double-blind placebo-and positive-controlled parallel study in 88 healthy subjects using three to six times the recommended therapeutic dose for fibromyalgia at 600 mg/day. After baseline and placebo adjustment, the maximum mean QTcF change was 8 ms - an increase that is generally not considered to be clinically significant. The dual ability for milnacipran to inhibit the reuptake of both serotonin (5HT) and norepinephrine (NE) facilitates its treatment of both fibromyalgia and major depressive disorder (MDD).",The molecular weight is 246.35.,Milnacipran has a topological polar surface area of 46.33.,The log p value of  is 1.91.,Milnacipran is approved and investigational.,Milnacipran is a solid.,True
15543,"Flibanserin is the first drug to be approved for hypoactive sexual desire disorder (HSDD) in premenopausal women by the FDA in August 2015. It was originally developed as an antidepressant medication by Boehringer Ingelheim, but showed lack of efficacy in trials and was further developed as a hypoactive sexual disorder drug by Sprout Pharmaceuticals. Flibanserin's mechanism of action is attributed to its high affinity for 5-HTA1 and 5-HTA2 receptors, displaying agonist activity on 5-HTA1 and antagonist on 5-HTA2, resulting in lowering of serotonin in the brain as well as an effect on increasing norepinephrine and dopamine neurotransmitters. For the treatment of hypoactive sexual desire disorder (HSDD) in premenopausal women.  Flibansetrin has high affinity for serotonin receptors in the brain: it acts as an agonist on 5-HT1A and an antagonist on 5-HT2A. In vivo, flibanserin binds equally to 5-HT1A and 5-HT2A receptors. However, under higher levels of brain 5-HT (i.e., under stress), flibanserin may occupy 5-HT2A receptors in higher proportion than 5-HT(1A) receptors. It may also moderately antagonize D4 (dopamine) receptors and 5-HT2B and 5-HTB2C. Its action on neurotransmitter receptors may contribute to reduction in serotonin levels and increase in dopamine and norepinephrine levels, all of which may play part in reward processing. ",The molecular weight is 390.41.,Flibanserin has a topological polar surface area of 38.82.,The log p value of  is 4.73.,Flibanserin is approved and investigational.,Flibanserin is a solid.,True
15544,"Rifalazil is a derivative of the antibiotic rifamycin. It is being investigated by ActivBiotics for the treatment of various bacterial infections. Investigated for use/treatment in atherosclerosis, bacterial infection, and peripheral vascular disease. Rifalazil represents a new generation of ansamycins that contain a unique four-ring structure. Originally rifalazil was developed as a therapeutic agent to replace rifampin as part of a multiple drug regimen in the treatment of tuberculosis. As a result of its superior antimicrobial activity and high intracellular levels, rifalazil has potential to treat indications caused by the intracellular pathogen, <i>Chlamydia trachomatis</i>, which causes non-gonococcal urethritis and cervicitis, often leading to pelvic inflammatory disease. Rifalazil also has potential to treat the related microorganism, <i>Chlamydia pneumoniae</i>, which may be involved in chronic inflammatory processes thought to be partly responsible for atherosclerosis. Due to its favourable antimicrobial spectrum and other positive attributes, rifalazil may also prove valuable in the treatment of gastric ulcer disease, caused by <i>Helicobacter pylori</i>, and antibiotic-associated colitis, the result of toxin production following the growth of <i>Clostridium difficile</i> in the colon. The potential value of rifalazil in the treatment of these indications will be assessed in human clinical trials. The potent antimycobacterial activity of rifalazil is due to inhibition of bacterial RNA polymerase.",,,,Rifalazil is investigational.,Rifalazil is a solid.,True
15545,"Banoxantrone is a highly selective bioreductive drug that is activated in, and is preferentially toxic to, hypoxic cells in tumours. It has been shown to work synergistically with fractionated radiation to significantly delay growth of tumours compared to administration of either banoxantrone or radiation alone. Banoxantrone was also efficacious in tumour models when administered in combination with either cisplatin or chemoradiation.  For the treatment of various forms of cancer. AQ4N was rationally designed to have anti-tumor activity following bioreduction by tissue cytochrome P450 to AQ4, an active DNA topoisomerase II inhibitor. Preclinical studies demonstrated AQ4N selectively targets lymphoid tissues and hypoxic tumor tissues. Banoxantrone (formally known as AQ4N) is preferentially and irreversibly converted to AQ4, its cytotoxic form, in hypoxic tumour cells where it remains localised. When the surrounding oxygenated cells are killed by radiotherapy or chemotherapy bringing these AQ4-containing quiescent cells closer to the oxygen source, they become reoxygenated, attempt to resume replication and, in this state, are killed by AQ4 through potent DNA intercalation and topoisomerase II inhibition.",,,,Banoxantrone is investigational.,Banoxantrone is a solid.,True
15546,"Indacaterol is a novel, ultra-long-acting, rapid onset β(2)-adrenoceptor agonist developed for Novartis for the once-daily management of asthma and chronic obstructive pulmonary disease. It was approved by the European Medicines Agency (EMA) on 30 November 2009 and by the FDA on 1 July 2011. It is marketed in Europe as Onbrez and in America as Arcapta Neohaler. Indacaterol is provided as its maleate salt form. Indacaterol is also a chiral molecule but only the pure R-enantiomer is dispensed. For the long term, once-daily-dosing maintenance of airflow obstruction in patients with chronic obstructive pulmonary disease (COPD), including chronic bronchitis and/or emphysema. Bronchodilator drugs are the foundation for the treatment of chronic obstructive pulmonary disease. The principal inhaled bronchodilator treatments used are β(2) -agonists and anticholinergics, either alone or in combination. Currently available β(2) -agonists are of either short duration and used multiple times/day, or of long duration, which requires twice-daily administration. Indacaterol is considered an ultra-long-acting β(2) -agonist and was recently approved for use in the United States. Its duration of action is approximately 24 hours, allowing for once-daily administration. Furthermore, this chiral compound it is given as the R-enantiomer and acts as a full agonist. Cough was the most commonly reported adverse effect with use of indacaterol. Compared to salmeterol, it has 35% more agonist activity. Cough usually occurred within 15 seconds of inhalation of the drug, lasted around 6 seconds, was not associated with bronchospasm, and did not cause discontinuation of the drug. Otherwise, the drug's safety profile was similar to that of other bronchodilators.  Indacaterol works by stimulating adrenergic beta-2 receptors in the smooth muscle of the airways. This causes relaxation of the muscle, thereby increasing the diameter of the airways, which become constricted in asthma and COPD. It is also long acting due to its high affinity to the lipid raft domains in the airway membrane so it slowly dissociates from the receptors. Indacaterol also has a high intrinsic efficacy so it is also very rapid acting - onset of action occurs within 5 minutes. ",The molecular weight is 392.5.,Indacaterol has a topological polar surface area of 81.59.,The log p value of  is 2.97.,Indacaterol is approved.,Indacaterol is a solid.,True
15547,"Persistent forms of tuberculosis (TB) have proven to be a major cause of global morbidity and mortality and a cause for significant concern. Research in recent years has been geared toward the development of novel therapies that target persistent forms of this disease, which have shown resistance to standard therapy regimens. Pretomanid is an antimycobacterial agent that is administered with and to treat resistant forms of pulmonary TB. It was the first TB drug developed by a nonprofit organization, known as TB Alliance, and was granted FDA approval on August 14, 2019. Unlike other therapeutic regimens for the treatment of resistant TB, which may take 18 months or longer and may not be effective, the pretomanid-containing regimen allows for a more efficacious and shorter duration of treatment with fewer drugs. Pretomanid is indicated for adults in combination with bedaquiline and linezolid for the treatment of pulmonary forms of nonresponsive multidrug-resistant (MDR), extensively drug-resistant (XDR), and treatment-intolerant forms of pulmonary tuberculosis (TB). Pretomanid kills the actively replicating bacteria causing tuberculosis, known as Mycobacterium tuberculosis, and shortens the duration of treatment in patients who suffer from resistant forms of pulmonary TB by killing dormant bacteria. Pretomanid is a prodrug which is metabolically activated by a nitroreductase enzyme, known as Ddn, producing various active metabolites that are responsible for its other therapeutic actions, particularly the induction of nitric oxide. The nitroreductase enzyme which activates pretomanid is deazaflavin dependent and relies on reduced cofactor F420. Reduction of F420 occurs via the enzyme glucose-6-phosphate dehydrogenase. Reduction of pretomanid's imidazole ring at the C-3 position causes the formation of the metabolites, which include a des-nitro derivative. The formation of this derivative leads to increased levels of nitric oxide, leading to bactericidal activities under anaerobic conditions via its action as a bacterial respiratory poison. Bactericidal activity against anaerobes is reported to be associated with a shortened duration of antibiotic treatment. ",,,,Pretomanid is approved.,Pretomanid is a solid.,True
15548,"For the treatment of rheumatoid arthritis and type 2 diabetes. Potential mechanisms of action for HE3286 include regulation of NF-kB and increasing the production of regulatory T cells (Treg cells). NF-kB is a well-known transcription factor that controls the production of inflammatory cytokines such as TNF-a and interferon-g. Treg cells are referred to in the scientific literature as the peacekeepers of the body. Their role is to keep the immune system from attacking the body itself. Recent studies of Treg cells indicate that they may play a broader role than simply preventing autoimmune conditions. Manipulation of these cells may offer new treatments for conditions ranging from diabetes and organ rejection to cancer and infectious diseases. In type II diabetes, moderate inhibition of NF-kB improves glucose tolerance. ",,,,HE3286 is investigational.,HE3286 is a solid.,True
15549,"Dexlansoprazole is a new generation proton pump inhibitor (PPI) used for the management of symptoms associated with gastroesophageal reflux disease (GERD) and erosive esophagitis. Dexlansoprazole is the R-enantiomer of , which is composed of a racemic mixture of the R- and S-enantiomers. Compared to the older generation of PPIs (which includes , , and ) , dexlansoprazole MR has a unique pharmacokinetic profile due to its delayed-release and dual-delivery release system. The active ingredient is released in two phases at different pH values and at different time points, resulting in two peak concentrations in the blood; 25% of the dose is released at pH 5.5 in the proximal duodenum, while the remaining 75% is released at pH 6.75 in the distal small intestine. As a result, dexlansoprazole has a peak concentration within 1-2 hours after dosing and another within 4-5 hours. Dexlansoprazole's unique pharmacokinetics addresses limitations of the older generation PPIs including short plasma half-life, break-through symptoms, and need for meal-associated dosing. These characteristics make dexlansoprazole a good option for people who struggle with adherence and strict dosage timing before meals.  Dexlansoprazole is indicated for healing all grades of erosive esophagitis (EE), maintaining and healing of EE and relief of heartburn, and treating heartburn associated with symptomatic non-erosive gastroesophageal reflux disease (GERD).  Dexlansoprazole is a proton pump inhibitor (PPI) and is included in the drug class of antisecretory compounds. It blocks the final step of gastric acid secretion by specific inhibition of the (H+, K+)-ATPase at the secretory surface of the parietal cells on gastric mucosa.  Dexlansoprazole inhibits the H/K ATPase enzyme, which is involved in the secretion of hydrochloric acid, hydrolyzing ATP and exchanging H+ ions from the cytoplasm for K+ ions in the secretory canaliculus, which results in HCl secretion into the gastric lumen. Dexlansoprazole inhibits this effect of H/K ATPase by demonstrating a high degree of activation in the acidic environment. After passing through the liver and reaching the gastric parietal cells activated by a meal, PPIs undergo protonation in the acidic pH environment, followed by conversion to sulphenamide which represents the active form of the drug. Sulphenamide inhibits the activity of the proton pump and hence the transport of hydrogen ions into the gastric lumen via covalent binding to the SH groups of the cysteine residues of H/K ATPase. The delivery technology of dexlansoprazole MR is designed to release the drug in two separate pH-dependent phases, the first in the proximal duodenum (25% of total drug dose) and the second (75% of total drug dose) in the more distal small intestine. Dexlansoprazole reduces both basal and stimulated gastric acid secretion. ",The molecular weight is 369.36.,Dexlansoprazole has a topological polar surface area of 67.87.,The log p value of  is 2.6.,Dexlansoprazole is approved and investigational.,Dexlansoprazole is a solid.,True
15550,"7-ethyl-10-hydroxycamptothecin (SN 38) is a liposomal formulation of the active metabolite of Irinotecan , a chemotherapeutic pro-drug approved for the treatment of advanced colorectal cancer. SN 38 has been used in trials studying the treatment of Cancer, Advanced Solid Tumors, Small Cell Lung Cancer, Metastatic Colorectal Cancer, and Triple Negative Breast Cancer, among others. Investigated for use/treatment in colorectal cancer. SN-38 (7-ethyl-10-hydroxycamptothecin) is the active metabolite of Irinotecan (CPT-11). Irinotecan is a topoisomerase I inhibitor commercially available as Camptosar®. SN-38 has been found to be 200–2000 times more cytotoxic than CPT-11, but has not been used as an anticancer drug due to its poor solubility in pharmaceutically acceptable solvents and low affinity to lipid membranes. SN-38 also undergoes a reversible conversion to an inactive open lactone ring structure at physiological pH. LE-SN-38 is a novel lipsome based formulation containing liposomes of uniform size distribution (<200 nm). Drug entrapment efficiency of the formulation is>95%. The entrapment of SN-38 in lipsomes results in a more stable and more soluble form of the drug. This allows for increased affinity of SN-38 to lipid membranes and improved delivery of the drug to tumor sites. SN-38 is a highly effective cytotoxic topoisomerase I inhibitor. ",,,,7-ethyl-10-hydroxycamptothecin is investigational.,7-ethyl-10-hydroxycamptothecin is a solid.,True
15551,"Brivaracetam is a racetam derivative of levetiracetam used in the treatment of partial-onset seizures. Brivaracetam binds SV2A with 20 times higher affinity than levetiracetam. It is available under the brand name Briviact made by UCB. Briviact received FDA approval on February 19, 2016. Used as adjunctive therapy for partial-onset seizures in patients 16 years of age or older. Brivaracetam binds SV2A with high affinity. SV2A is known to play a role in epileptogenesis through modulation of synaptic GABA release. It is thought that brivaracetam exerts its anti-epileptogenic effects through its binding to SV2A. Brivaracetam is also known to inhibit Na+ channels which may also contribute to its anti-epileptogenic action. The precise mechanism of brivaracetam's anti-epileptogenic activity is unknown.",The molecular weight is 212.29.,Brivaracetam has a topological polar surface area of 63.4.,The log p value of  is 1.01.,Brivaracetam is approved and investigational.,Brivaracetam is a solid.,True
15552,GPI 1485 is a product candidate that belongs to a class of small molecule compounds called neuroimmunophilin ligands. Investigated for use/treatment in erectile dysfunction and parkinson's disease.,,,,GPI-1485 is investigational.,GPI-1485 is a solid.,True
15553,"Seletracetam is a pyrrolidone derivative and with a structural similarity to newer generation antiepileptic drug levetiracetam. It binds to the same target as levetiracetam but with higher affinity and has shown potent seizure suppression in models of acquired and genetic epilepsy with high CNS tolerability. It is predicted to have low drug-drug interactions and inhibition or induction of any major human metabolizing enzymes. Seletracetam was in Phase II clinical trials under the supervision of the U.S. Food and Drug Administration (FDA) investigated as treatment of epilepsy and partial epilepsy however its development had been put on hold in July 2007. As of 2010, its production was further halted due to the investigation of a newer antiepileptic agent, brivaracetam. Investigated for use/treatment in epilepsy. Seletracetam is an antiepileptic agent that targets the presynaptic mechanisms of epilepsy. It interferes with synaptic vesicle exocytosis and neurotransmitter release by binding to synaptic vesicle protein 2A (SV2A) which is involved in synaptic vesicle docking and fusion. It is also a N-type calcium channel blocker that inhibits the abnormal neuronal discharge by inhibiting the calcium channel function and associated calcium currents. Seletracetam markedly reduces epileptiform markers of both hyper-excitability and hyper-synchronization in an in vitro slice model of epilepsy and potently suppresses seizures in in vivo epilepsy models mimicking both partial and generalized epilepsy.  Seletracetam binds to SV2A in a stereospecific and selective manner. SV2A is a membrane glycoprotein present in synaptic vesicles of neurons that plays a role as calcium regulators in neurotransmitter release and modulate synaptic networks. Seletracetam is thought to reduce excessive neuronal activity by modulating SV2A function and restoring the ability of a neuron to regulate its neurotransmitter release.",,,,Seletracetam is investigational.,Seletracetam is a solid.,True
15554,"KOS-1584 is a second-generation epothilone. Epothilones are anticancer agents with a taxane-like mechanism of action that have demonstrated activity in taxane-resistant tumors. KOS-1584 is a second-generation compound with increased potency, favorable tissue distribution, and ease of formulation. Investigated for use/treatment in solid tumors. Epothilones are highly potent microtubulin stabilizing compounds with a similar mechanism of action to taxanes and broad applicability in a wide range of tumors. Epothilones are active in both taxane-sensitive and taxane-resistant cancers and have demonstrated low susceptibility to tumor resistance mechanisms.",,,,KOS-1584 is investigational.,KOS-1584 is a solid.,True
15555,"Rimonabant is an anorectic anti-obesity drug produced and marketed by Sanofi-Aventis. It is an inverse agonist for the cannabinoid receptor CB1. Its main avenue of effect is reduction in appetite. Rimonabant is the first selective CB1 receptor blocker to be approved for use anywhere in the world. Rimonabant is approved in 38 countries including the E.U., Mexico, and Brazil. It was rejected for approval for use in the United States. This decision was made after a U.S. advisory panel recommended the medicine not be approved because it may increase suicidal thinking and depression. For use in conjunction with diet and exercise for patients with a body mass index greater than 30 kg/m<sup>2</sup>, or patients wih a BMI greater than 27 kg/m<sup>2</sup> with associated risk factors, such as type 2 diabetes or dyslipidaemia. In the RIO-North America trial, 3040 patients were randomized to receive either placebo or one of two doses of rimonabant (5 mg or 20 mg per day). Patients taking 20 mg rimonabant had significant weigh loss, decrease in waist circumference, improved insulin sensitivity, and increases in HDL cholesterol, compared to patients on placebo. Rimonabant is a specific CB1 cannabinoid receptor antagonist. There is considerable evidence that the endocannabinoid (endogenous cannabinoid) system plays a significant role in appetitive drive and associated behaviours. It is therefore reasonable to hypothesize that the attenuation of the activity of this system would have therapeutic benefit in treating disorders that might have a component of excess appetitive drive or over-activity of the endocannabinoid system, such as obesity, ethanol and other drug abuse, and a variety of central nervous system and other disorders.",The molecular weight is 463.79.,Rimonabant has a topological polar surface area of 50.16.,The log p value of  is 6.47.,Rimonabant is approved and investigational.,Rimonabant is a solid.,True
15556,"Investigated for use/treatment in lymphoma (non-hodgkin's), leukemia (lymphoid), cancer/tumors (unspecified), and multiple myeloma. Noscapine's antitussive effects appear to be primarily mediated by its sigma receptor agonist activity. Evidence for this mechanism is suggested by experimental evidence in rats. Pretreatment with rimcazole, a sigma specific antagonist, causes a dose-dependent reduction in antitussive activity of noscapine.",The molecular weight is 413.43.,Noscapine has a topological polar surface area of 75.69.,The log p value of  is 2.27.,Noscapine is approved and investigational.,Noscapine is a solid.,True
15557,"Silodosin is an α1-adrenoceptor antagonist that is selective for the prostate. Silodosin is for symptomatic treatment of benign prostatic hyperplasia. FDA approved Oct 9, 2008. Treatment for symptomatic relief of benign prostatic hyperplasia  Silodosin is 583 times more selective for human alpha-1A receptors than alpha-1B receptors. It is also 56 times more selective for human alpha-1A receptors than alpha-1D. Silodosin does not prolong the QT interval.  Benign prostate hyperplasia (BPH), or an enlarged prostate, is a condition found only in men and is characterized by a non-cancerous enlargement of the prostate gland. Symptoms of BPH include urinary difficulty, urinary frequency and an inability to complete bladder emptying. Silodosin is highly uroselective for the alpha (1A) receptors located in the prostate,. Blocking these receptors relaxes the smooth muscles, resulting in an improvement in urine flow and a reduction in BPH symptoms. The selective binding of silodosin to the alpha (1A) receptors is substantially greater than the binding to the cardiovascular-associated alpha (1B) receptors and thereby maximizes target organ activity while minimizing the potential for blood pressure effects. Silodosin is alpha 1A-adrenoceptor selective antagonist which inhibits sympathetic nerve stimulation and relaxation of smooth muscle tone in the lower urinary tract which relieves the pressure from contraction of smooth muscle. The reduction of intraurethral pressure improves voiding and storage issues associated with BPH. ",The molecular weight is 495.54.,Silodosin has a topological polar surface area of 97.05.,The log p value of  is 2.97.,Silodosin is approved.,Silodosin is a solid.,True
15558,"Tolvaptan is used to treat low blood sodium levels (hyponatremia) associated with various conditions like congestive heart failure, cirrhosis, and syndrome of inappropriate antidiuretic hormones (SIADH). FDA approved on May 19, 2009. Treatment of symptomatic and resistant to fluid restriction euvolemic or hypervolemic hyponatremia associated with congestive heart failure, SIADH, and cirrhosis.  Urine volume and fluid intake increase in a dose dependent manner which results in overall negative fluid balance in patients taking tolvaptan. Increases in serum sodium and osmolality can be observed 4-8 hours post-administration and is maintained for 24 hours. The magnitude of serum sodium and osmolality change increases with escalating doses. Furthermore, a decrease in urine osmolality and increase in free water clearance can be observed 4 hours after post-administration of tolvaptan. The affinity for V2 receptors is 29x greater than that of V1a receptors and does not have any appreciable affinity for V2 receptors.  Tolvaptan is a selective and competitive arginine vasopressin receptor 2 antagonist. Vasopressin acts on the V2 receptors found in the walls of the vasculature and luminal membranes of renal collecting ducts. By blocking V2 receptors in the renal collecting ducts, aquaporins do not insert themselves into the walls thus preventing water absorption. This action ultimately results in an increase in urine volume, decrease urine osmolality, and increase electrolyte-free water clearance to reduce intravascular volume and an increase serum sodium levels. Tolvaptan is especially useful for heart failure patients as they have higher serum levels of vasopressin. ",The molecular weight is 448.95.,Tolvaptan has a topological polar surface area of 69.64.,The log p value of  is 4.31.,Tolvaptan is approved.,Tolvaptan is a solid.,True
15559,"Lacosamide is a functionalized amino acid that has activity in the maximal electroshock seizure test, and is indicated for the adjunctive treatment of partial-onset seizures and diabetic neuropathic pain. Recent studies indicate that Lacosamide only affects those neurons which are depolarized or active for long periods of time, typical of neurons at the focus of an epileptic seizure, as opposed to other antiepileptic drugs such as carbamazepine or lamotrigine which slow the recovery from inactivation and reduce the ability of neurons to fire action potentials. Lacosamide is indicated for adjunctive therapy for partial onset seizures in patients with epilepsy over 17 years old. Injection is indicated for short term use when oral therapy is not feasible.  Lacosamide therapy is correlated with a decrease in seizure frequency. It should be noted that in group analyses, dosages above 400 mg/day do not appear to result in additional benefit. It is proposed that lacosamide's inhibition of sodium channels is responsible for analgesia. Lacosamide may be selective for inhibiting depolarized neurons rather than neurons with normal resting potentials. Pain and nociceptor hyperexcitability are associated with neural membrane depolarization. Lacosamide binds to collapsin response mediator protein-2 (CRMP-2), a phosphoprotein which is expressed primarily in the nervous system and is involved in neuronal differentiation and control of axonal outgrowth. The role CRMP-2 of binding in seizure control is hasn't been elucidated. ",The molecular weight is 250.3.,Lacosamide has a topological polar surface area of 67.43.,The log p value of  is 0.39.,Lacosamide is approved.,Lacosamide is a solid.,True
15560,"Investigated for use/treatment in solid tumors, sarcoma, cancer/tumors (unspecified), endometrial cancer, prostate cancer, and bone metastases. Deforolimus inhibits the mammalian target of rapamycin (mTOR), a serine kinase of the phosphatidylinositol-3-kinase (PI3K) family that regulates protein synthesis, affecting cell growth and proliferation. mTOR is a downstream effector of the phosphatidylinositol 3-kinase/Akt and nutrient-sensing pathways which cancer cells need to proliferate.",The molecular weight is 990.22.,Ridaforolimus has a topological polar surface area of 201.5.,The log p value of  is 7.2.,Ridaforolimus is investigational.,Ridaforolimus is a solid.,True
15561,"Avanafil is a new phosphodiesterase-5 inhibitor that is faster acting and more selective than other drugs belonging to the same class. Chemically, it is a derivative of pyrimidine and is only available as the S-enantiomer. FDA approved on April 27, 2012. Treatment of erectile dysfunction in males.  Avanafil is a strong, competitive inhibitor of PDE5. It is also 100-times more potent for PDE5 than PDE6. The IC50 of avanafil is 5.2 nM. Compared to other PDE5 inhibitor like sildenafil and vardenafil, it is 16- and 21-fold more selective for PDE5 respectively. Avanafil does not bind to PDE6 and PDE11 to a considerable degree. The impact of this finding is that avanafil is less likely to cause side effects such as visual disturbances and myalgia. These are side effects that patients on sildenafil or tadalafil are more likely to experience. Furthermore, single oral doses of avanafil (200 mg) administered to healthy male volunteers resulted in mean changes from baseline in systolic/diastolic blood pressure of -5.3/-3.7 mmHg at 1 hour after dosing. Avanafil does not causes changes in QTc interval or ventricular repolarization.  Avanafil is a selective phosphodiesterase 5 (PDE5) enzyme inhibitor used for the treatment of erectile dysfunction caused by diabetes, age induced oxidative stress or other complications. Avanafil inhibits the cGMP specific phosphodiesterase type 5 (PDE5) which is responsible for degradation of cGMP in the corpus cavernosum located around the penis. Penile erection during sexual stimulation is caused by increased penile blood flow resulting from the relaxation of penile arteries and corpus cavernosal smooth muscle. This response is mediated by the release of nitric oxide (NO) from nerve terminals and endothelial cells, which stimulates the synthesis of cGMP in smooth muscle cells. Cyclic GMP causes smooth muscle relaxation and increased blood flow into the corpus cavernosum. The inhibition of phosphodiesterase type 5 (PDE5) by avanafil enhances erectile function by increasing the amount of cGMP.",The molecular weight is 483.96.,Avanafil has a topological polar surface area of 125.39.,The log p value of  is 2.36.,Avanafil is approved.,Avanafil is a solid.,True
15562,"Sitaxentan was marketed under the trade name Thelin for the treatment of pulmonary arterial hypertension (PAH) by Encysive Pharmaceuticals until Pfizer purchased Encysive in February 2008. In 2010, Pfizer voluntarily removed sitaxentan from the market over concerns of hepatotoxicity. Investigated for use/treatment in pulmonary hypertension, connective tissue diseases, hypertension, and congestive heart failure. Sitaxentan belongs to a class of drugs known as endothelin receptor antagonists (ERAs). Patients with PAH have elevated levels of endothelin, a potent blood vessel constrictor, in their plasma and lung tissue. Sitaxentan blocks the binding of endothelin to its receptors, thereby negating endothelin's deleterious effects. Sitaxentan is a competitive antagonist of endothelin-1 at the endothelin-A (ET-A) and endothelin-B (ET-B) receptors. Under normal conditions, endothelin-1 binding of ET-A or ET-B receptors causes pulmonary vasoconstriction. By blocking this interaction, Sitaxentan decreases pulmonary vascular resistance. Sitaxentan has a higher affinity for ET-A than ET-B.",,,,Sitaxentan is approved and investigational and withdrawn.,Sitaxentan is a solid.,True
15563,"Tocilizumab is a recombinant humanized monoclonal antibody IL-6 receptor inhibitor used to treat inflammatory and autoimmune conditions. It was first described in the literature in 2003 when Chugai, a subsidiary of Roche began developing IL-6 inhibiting monoclonal antibodies. It is currently being investigated to treat severely ill patients with COVID-19. Tocilizumab is indicated to treat moderate to severe rheumatoid arthritis, giant cell arteritis, polyarticular juvenile idiopathic arthritis, systemic juvenile idiopathic arthritis, and cytokine release syndrome. Tocilizumab is an IL-6 inhibiting monoclonal antibody used to treat autoimmune and inflammatory conditions. Tocilizumab has a long duration of action as it is generally given every 4 weeks and has a wide therapeutic index. Patients should be counselled regarding the risk of infections, GI perforation, and hepatotoxicity. Interleukin 6 (IL-6) is a pro-inflammatory cytokine produced by cells including T-cells, B-cells, lymphocytes, monocytes, fibroblasts. IL-6 rapidly induces C-reactive protein, serum amyloid A, fibrinogen, haptoglobin, and α-1-antichymotrypsin while inhibiting production of fibronectin, albumin, and transferrin. IL-6 also induces antibody production, induces cytotoxic T-cell differentiation, and inhibits regulatory T-cell differentiation. Tocilizumab binds soluble and membrane bound IL-6 receptors, preventing IL-6 mediated inflammation.",,,,Tocilizumab is approved.,Tocilizumab is a liquid.,True
15564,"AVE9633 is an anti-CD33 monoclonal antibody-DM4 conjugate. Investigated for use/treatment in leukemia (myeloid). An immunoconjugate consisting of the humanized monoclonal antibody huMy9-6 conjugated to the cytotoxic maytansinoid derivative DM4 with potential antineoplastic activity. The monoclonal antibody portion of anti-CD33 monoclonal antibody-DM4 conjugate AVE9633 specifically binds to the cell surface antigen CD33 expressed on myeloid leukemia cells; upon internalization, the DM4 moiety is released, binds tubulin, and disrupts microtubule assembly/disassembly dynamics, resulting in the inhibition of cell division and cell growth in myeloid leukemia cells that express CD33. CD33 is expressed on normal non-pluripotent hematopoietic stem cells as well as on myeloid leukemia cells. ",,,,AVE9633 is investigational.,AVE9633 is a solid.,True
15565,"Coltuximab ravtansine (SAR3419) targets CD19 and is being investigated for the treatment of acute lymphoblastic leukemia (ALL). Investigated for use/treatment in lymphoma (non-hodgkin's). SAR3419 is an anti-CD19-DM4 immunoconjugate consisting of an anti-CD19 monoclonal antibody conjugated to the maytansinoid DM4, a derivative of the cytotoxic agent maytansine (DM1), with potential antineoplastic activity. SAR3419 targets the cell surface antigen CD19, found on a number of B-cell-derived cancers. Upon antibody/antigen binding and internalization, the immunoconjugate releases DM4, which binds to tubulin and disrupts microtubule assembly/disassembly dynamics, resulting in inhibition of cell division and cell growth of CD19-expressing tumor cells. ",,,,Coltuximab ravtansine is investigational.,Coltuximab ravtansine is a solid.,True
15566,"Etravirine is an antiretroviral agent more specifically classified as a Non-Nucleoside Reverse Transcriptase Inhibitor(NNRTI). Etraverine is used clinically for the treatment of human immunodeficiency virus type 1 (HIV-1) infection.  Indicated as an adjunct therapy in the treatment of adult HIV-1 infections resistant to therapy with other NNRTIs and antiretroviral agents.  Clinical trials have shown no prolongation of QT intervals on electrocardiograms after 8 days of dosing.  Etravirine exerts its effects via direct inhibition of the reverse transcriptase enzyme of human immunodeficiency virus type 1 (HIV-1). It directly binds reverse transcriptase and consequently blocks DNA-dependent and RNA-dependent polymerase activity. Etravirine does not inhibit human DNA polymerase alpha, beta or gamma. ",The molecular weight is 435.28.,Etravirine has a topological polar surface area of 120.64.,The log p value of  is 5.07.,Etravirine is approved.,Etravirine is a solid.,True
15567,Investigated for use/treatment in migraine and cluster headaches.,,,,Dotarizine is investigational.,Dotarizine is a solid.,True
15568,"Investigated for use/treatment in epilepsy, huntington's disease, and parkinson's disease.",,,,Remacemide is investigational.,Remacemide is a solid.,True
15569,"Investigated for use/treatment in pancreatic cancer, prostate cancer, and leukemia (myeloid). Lestaurtinib inhibits autophosphorylation of FMS-like tyrosine kinase 3 (FLT3), resulting in inhibition of FLT3 activity and induction of apoptosis in tumor cells that overexpress FLT3.",,,,Lestaurtinib is investigational.,Lestaurtinib is a solid.,True
15570,"Clomethiazole is a well-established γ-aminobutyric acid (GABAA)-mimetic drug. It is a sedative and hypnotic that is widely used in treating and preventing symptoms of acute alcohol withdrawal. It is a drug which is structurally related to thiamine (vitamin B1) but acts like a sedative, hypnotic, muscle relaxant and anticonvulsant. It is also used for the management of agitation, restlessness, short-term insomnia and Parkinson's disease in the elderly. Investigated for use/treatment in strokes. clomethiazole interacts with the GABAA receptor complex. It inhibits the binding of butyl-bicyclophosphorothionate (TBPS), an effect indicative of GABAA receptor-channel activation, by increasing the rate of TBPS dissociation and decreasing the binding affinity. Gamma-aminobutyric acid (GABA), acting at GABAA receptors, is the main fast inhibitory neurotransmitter in mammalian central nervous system",The molecular weight is 161.65.,Clomethiazole has a topological polar surface area of 12.89.,The log p value of  is 1.68.,Clomethiazole is investigational.,Clomethiazole is a solid.,True
15571,"Mitemcinal (GM-611) is a novel erythromycin-derived prokinetic agent that acts as an agonist at the motilin receptor. Investigated for use/treatment in gastroparesis and irritable bowel syndrome (IBS). Mitemcinal, an oral motilin agonist, accelerates gastric emptying.",,,,Mitemcinal is investigational.,Mitemcinal is a solid.,True
15572,"Bosutinib is a Bcr-Abl kinase inhibitor for the treatment of Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML). Compared to other tyrosine kinase inhibitors, it has a more favourable hematologic toxicity profile. FDA approved on September 4, 2012. Treatment of chronic, accelerated, or blast phase Philadelphia chromosome-positive (Ph+) chronic myelogenous leukemia (CML) with resistance or intolerance to prior therapy in adult patients.  Bosutinib is a tyrosine kinase inhibitor. Although it is able to inhibit several tyrosine kinases such as Src, Lyn, and Hck, which are members of the Src-family of kinases, its primary target is the Bcr-Abl kinase. The Bcr-Abl gene is a chimeric oncogene created from the fusion of the breakpoint-cluster (Bcr) gene and Abelson (Abl) tyrosine gene. This chromosomal abnormality results in the formation of what is commonly known as the Philadelphia chromosome or Philadelphia translocation. The Bcr-Abl gene expresses a particular kinase that promotes the progression of CML. A decrease in the growth and size of the CML tumour has been observed following administration of bosutinib. Bosutinib did not inhibit the T315I and V299L mutant cells. ",The molecular weight is 530.45.,Bosutinib has a topological polar surface area of 82.88.,The log p value of  is 4.94.,Bosutinib is approved.,Bosutinib is a solid.,True
15573,"Isavuconazonium is a second-generation triazole antifungal approved on March 6, 2015 by the FDA for the treatment of invasive aspergillosis and invasive mucormycosis, marketed by Astellas under the brand Cresemba. It is the prodrug form of isavuconazole, the active moiety, and it is available in oral and parenteral formulations. Due to low solubility in water of isavuconazole on its own, the isovuconazonium formulation is favorable as it has high solubility in water and allows for intravenous administration. This formulation also avoids the use of a cyclodextrin vehicle for solubilization required for intravenous administration of other antifungals such as voriconazole and posaconazole, eliminating concerns of nephrotoxicity associated with cyclodextrin. Isovuconazonium has excellent oral bioavailability, predictable pharmacokinetics, and a good safety profile, making it a reasonable alternative to its few other competitors on the market. Indicated in the treatment of invasive aspergillosis and invasive mucormycosis. Antifungals in the triazole class, such as isavuconazonium, target and inhibit the sterol 14-α-demethylase (Erg11p) which is a key player in the demethylation step of the ergosterol biosynthetic pathway. This inhibition results in a halt in production of ergosterol, a molecule typically found in the membranes of fungi such as Aspergillus, Candida, and Mucorales that plays a role in regulation of membrane integrity, fluidity and permeability. The inhibition of Erg11p also causes the buildup of ergosterol precursors, which are toxic and cause cell death. ",The molecular weight is 717.77.,Isavuconazonium has a topological polar surface area of 159.37.,The log p value of  is -1.15.,Isavuconazonium is approved and investigational.,Isavuconazonium is a solid.,True
15574,"Pasireotide is a synthetic long-acting cyclic hexapeptide with somatostatin-like activity. It is marketed as a diaspartate salt called Signifor, which is used in the treatment of Cushing's disease. For the treatment of Cushing’s disease, specifically for those patients whom pituitary surgery has not been curative or is not an option. Signifor® is an analogue of somatostatin that promotes reduced levels of cortisol secretion in Cushing's disease patients. Pasireotide activates a broad spectrum of somatostatin receptors, exhbiting a much higher binding affinity for somatostatin receptors 1, 3, and 5 than octreotide in vitro, as well as a comparable binding affinity for somatostatin receptor 2. The binding and activation of the somatostatin receptors causes inhibition of ACTH secretion and results in reduced cortisol secretion in Cushing's disease patients. Also this agent is more potent than somatostatin in inhibiting the release of human growth hormone (HGH), glucagon, and insulin. ",The molecular weight is 1047.23.,Pasireotide has a topological polar surface area of 281.2.,The log p value of  is 6.72.,Pasireotide is approved.,Pasireotide is a solid.,True
15575,"Odanacatib is an inhibiter of cathepsin K which was originally developed be Merck & Co as a new treatment for osteoporosis. The drug made it to phase III trials before abandoned due to increased stroke. Investigated for use/treatment in osteoporosis. Increases bone mineral density and reduces risk of fractures in osteoporosis. Odanacatib inhibits cathepsin K, likely by binding to its active site. Cathepsin K is a cysteine protease enzyme which is secreted by osteoclasts. Cathepsin K is responsible for the breakdown of collagen in the bone matrix as part of bone resorption. The inhibition of this enzyme results in decreased bone resorption without affecting bone deposition resulting in increased bone mineral density. This increased bone mineral density strengthens the bone which leads to fewer fractures in osteoporosis.",,,,Odanacatib is investigational.,Odanacatib is a solid.,True
15576,"Laquinimod is an immunomodulator developed by Active Biotech and produced by Teva Pharmaceutical Industries. It is currently under development in phase III trials for treatment of multiple sclerosis as an oral therapy, like fingolimod. It has been shown to reduce disease activity on magnetic resonance imaging and to be well tolerated orally. Investigated for use/treatment in multiple sclerosis.",,,,Laquinimod is investigational.,Laquinimod is a solid.,True
15577,"Nilvadipine is a calcium channel blocker (CCB) for treatment of hypertension. For the management of vasospastic angina, chronic stable angina and hypertension. Nilvadipine is similar to other dihydropyridines including amlodipine, felodipine, isradipine, and nicardipine. Nilvadipine is used to treat Prinzmetal's angina, hypertension, and other vascular disorders such as Raynaud's phenomenon. By blocking the calcium channels, Nifedipine inhibits the spasm of the coronary artery and dilates the systemic arteries, results in a increase of myocardial oxygen supply and a decrease in systemic blood pressure. Nilvadipine inhibits the influx of extracellular calcium through myocardial and vascular membrane pores by physically plugging the channel. The decrease in intracellular calcium inhibits the contractile processes of smooth muscle cells, causing dilation of the coronary and systemic arteries, increased oxygen delivery to the myocardial tissue, decreased total peripheral resistance, decreased systemic blood pressure, and decreased afterload.",The molecular weight is 385.38.,Nilvadipine has a topological polar surface area of 131.56.,The log p value of  is 3.04.,Nilvadipine is approved and investigational.,Nilvadipine is a solid.,True
15578,"Fosaprepitant is an intravenously administered antiemetic drug. It is a prodrug of Aprepitant. It aids in the prevention of acute and delayed nausea and vomiting associated with chemotherapy treatment. For the prevention of nausea and vomiting associated with highly emetogenic cancer chemotherapy. Fosaprepitant is a prodrug of Aprepitant. Once biologically activated, the drug acts as a substance P/neurokinin 1 (NK1) receptor antagonist which, in combination with other antiemetic agents, is indicated for the prevention of acute and delayed nausea and vomiting associated with initial and repeat courses of highly emetogenic cancer chemotherapy. Aprepitant is a selective high-affinity antagonist of human substance P/neurokinin 1 (NK1) receptors. Aprepitant has little or no affinity for serotonin (5-HT<sub>3</sub>), dopamine, and corticosteroid receptors, the targets of existing therapies for chemotherapy-induced nausea and vomiting (CI NV). Aprepitant has been shown in animal models to inhibit emesis induced by cytotoxic chemotherapeutic agents, such as cisplatin, via central actions. Animal and human Positron Emission Tomography (PET) studies with Aprepitant have shown that it crosses the blood brain barrier and occupies brain NK1 receptors. Animal and human studies show that Aprepitant augments the antiemetic activity of the 5-HT<sub>3</sub>-receptor antagonist ondansetron and the corticosteroid",The molecular weight is 614.41.,Fosaprepitant has a topological polar surface area of 123.93.,The log p value of  is 2.38.,Fosaprepitant is approved.,Fosaprepitant is a solid.,True
15579,"Ambroxol is a secretolytic agent used in the treatment of respiratory diseases associated with viscid or excessive mucus. It is the active ingredient of Mucosolvan, Lasolvan or Mucoangin. The substance is a mucoactive drug with several properties including secretolytic and secretomotoric actions that restore the physiological clearance mechanisms of the respiratory tract which play an important role in the body’s natural defence mechanisms. It stimulates synthesis and release of surfactant by type II pneumocytes. Surfactants acts as an anti-glue factor by reducing the adhesion of mucus to the bronchial wall, in improving its transport and in providing protection against infection and irritating agents. Ambroxol is indicated for secretolytic therapy in bronchoplmonary diseaes with abnormal mucus secretion and transport. It allows the mucus to be more easily cleared and ease a patient's breathing. Ambroxol is a mucolytic agent. Excessive Nitric oxide (NO) is associated with inflammatory and some other disturbances of airways function. NO enhances the activation of soluble guanylate cyclase and cGMP accumulation. Ambroxol has been shown to inhibit the NO-dependent activation of soluble guanylate cyclase. It is also possible that the inhibition of NO-dependent activation of soluble guanylate cyclase can suppress the excessive mucus secretion, therefore it lowers the phlegm viscosity and improves the mucociliary transport of bronchial secretions.",The molecular weight is 378.11.,Ambroxol has a topological polar surface area of 58.28.,The log p value of  is 2.33.,Ambroxol is approved and investigational.,Ambroxol is a solid.,True
15580,"Pinacidil is a cyanoguanidine drug that acts by opening ATP-sensitive potassium channels, leading to peripheral vasodilatation of arterioles and decreasing peripheral vascular resistance. The above processes result in reduced blood pressure. This drug has been discontinued by the FDA.",The molecular weight is 245.33.,Pinacidil has a topological polar surface area of 73.1.,The log p value of  is 1.91.,Pinacidil is approved.,Pinacidil is a solid.,True
15581,,The molecular weight is 372.5.,Desoxycorticosterone acetate has a topological polar surface area of 60.44.,The log p value of  is 3.98.,Desoxycorticosterone acetate is approved.,Desoxycorticosterone acetate is a solid.,False
15582,"Difluprednate is a topical corticosteroid indicated for the treatment of infammation and pain associated with ocular surgery. It is a butyrate ester of 6(α), 9(α)-difluoro prednisolone acetate. Difluprednate is abbreviated DFBA, or difluoroprednisolone butyrate acetate. It is indicated for treatment of endogenous anterior uveiti. For the treatment of inflammation and pain associated with ocular surgery. Difluprednate is a corticosteroid used as an anti-inflammatory steroidal drug used primarily in ocular surgery. Corticosteroids are thought to act by the induction of phospholipase A2 inhibitory proteins (lipocortins). It is postulated that these proteins control the biosynthesis of potent mediators of infammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A2.",The molecular weight is 508.56.,Difluprednate has a topological polar surface area of 106.97.,The log p value of  is 3.44.,Difluprednate is approved.,Difluprednate is a solid.,True
15583,"Halcinonide is a corticosteroid indicated for the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses, and is distributed as a cream and ointment. Halcinonide is marketed under the brand name Halog® by Ranbaxy Laboratories Inc. Research suggests that clobetasol propionate demonstrates superior pharmacologic efficacy in the treatment of psoriasis when compared to halcinonide. Indicated for the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses.  The precise mechanism of action of topical corticosteroids is unclear. However they possess anti-inflammatory, antipruritic, and vasoconstrictive actions.",The molecular weight is 454.96.,Halcinonide has a topological polar surface area of 72.83.,The log p value of  is 3.31.,Halcinonide is approved and investigational and withdrawn.,Halcinonide is a liquid.,True
15584,"Lanreotide is a drug employed in the management of acromegaly (a hormonal condition caused by excess growth hormone) in addition to symptoms caused by neuroendocrine tumors, especially carcinoid syndrome. This drug is a long-acting analog of the drug somatostatin, a growth hormone inhibitor. Lanreotide is manufactured by the company, _Ipsen Pharmaceuticals_ as lanreotide acetate, and marketed as _Somatuline_. It is approved in several countries worldwide, including the United Kingdom, Australia, and Canada. Lanreotide was first approved for use in the United States by the FDA on August 30, 2007. Lanreotide is a somatostatin analog approved for treatment of neuroendocrine tumours and acromegaly. Lanreotide exhibits antisecretory effects through cAMP suppression, and activation of ion currents such as K+ and Ca2+ which leads to hyperpolarization of the membrane and inhibition of Ca2+ mediated depolarization.  Lanreotide is a somatostatin analogue (SSA) and has mainly inhibitory effects which are mediated via somatostatin receptors (SSTRs) 2 and 5 and include inhibition of growth hormone release in the brain. Tumor SSTR activation induces downstream cell cycle arrest and/or apoptosis, and also results in blunted production of substances that support tumor growth as well as tumor angiogenesis. This leads to the anti-proliferative effects of Lanreotide.",The molecular weight is 1096.33.,Lanreotide has a topological polar surface area of 355.08.,The log p value of  is 3.4.,Lanreotide is approved.,Lanreotide is a solid.,True
15585,A metabolite from Penicillium brefeldianum that exhibits a wide range of antibiotic activity.,,,,Brefeldin A is experimental.,Brefeldin A is a solid.,True
15586,"Tranilast is an antiallergic drug developed by Kissei Pharmaceuticals. In 1982, it was approved in Japan and South Korea for the management of bronchial asthma. Indications for keloid and hypertrophic scar were added in 1993. It has been used for the treatment of allergic disorders such as asthma, allergic rhinitis and atopic dermatitis. For the treatment of bronchial asthma, keloid and hypertrophic scar, and allergic disorders such as asthma, allergic rhinitis and atopic dermatitis.",The molecular weight is 327.34.,Tranilast has a topological polar surface area of 84.86.,The log p value of  is 3.99.,Tranilast is investigational.,Tranilast is a solid.,True
15587,"Parecoxib is a water-soluble and injectable prodrug of valdecoxib. It is marketed as Dynastat in the European Union. Parecoxib is a COX2 selective inhibitor in the same category as celecoxib (Celebrex) and rofecoxib (Vioxx). As it is injectable, it can be used perioperatively when patients are unable to take oral medications. It is approved through much of Europe for short term perioperative pain control much in the same way ketorolac (Toradol) is used in the United States. A letter of non-approval for parecoxib was issued by the FDA in 2005. Used for short term perioperative pain control.",The molecular weight is 370.42.,Parecoxib has a topological polar surface area of 89.27.,The log p value of  is 2.05.,Parecoxib is approved.,Parecoxib is a solid.,True
15588,Investigated for use/treatment in acquired immune deficiency syndrome (AIDS) and aids-related infections and HIV infection.,,,,Capravirine is investigational.,Capravirine is a solid.,True
15589,"Tofisopam (marketed under brand names Emandaxin and Grandaxin) is a 2,3-benzodiazepine drug which is a benzodiazepine derivative. In contrast to classical 1,4-benzodiazepines, the compound does not bind to the benzodiazepine binding site of the gamma-aminobutyric acid receptor and its psychopharmacological profile differs from such compounds. Although Tofisopam is not approved for sale in North America, it is approved for use in various countries worldwide, including parts of Europe. The D-enantiomer () is currently in phase II trials in the U.S. for the treatment of irritable bowel syndrome. For the treatment of anxiety and alcohol withdrawal. Like other benzodiazepines, tofisopam possesses anxiolytic properties but unlike other benzodiazepines it does not have anticonvulsant, sedative, skeletal muscle relaxant, motor skill-impairing or amnestic properties. It enhances the anticonvulsant activity of 1,4-benzodiazepines like diazepam but not sodium valproate, carbamazepine, phenobarbital, or phenytoin. Tofisopam does not bind to the benzodiazepine binding site of the gamma-aminobutyric acid receptor. One study (Rundfeldt C. et al.) has shown that tofisopam acts as an isoenzyme-selective inhibitor of phosphodiesterases (PDEs) with highest affinity to PDE-4A1 (0.42 μM) followed by PDE-10A1 (0.92 μM), PDE-3 (1.98 μM) and PDE-2A3 (2.11 μM).",The molecular weight is 382.46.,Tofisopam has a topological polar surface area of 61.64.,The log p value of  is 5.08.,Tofisopam is experimental.,Tofisopam is a solid.,True
15590,"Lurasidone is an atypical antipsychotic developed by Dainippon Sumitomo Pharma. It was approved by the U.S. Food and Drug Administration (FDA) for treatment of schizophrenia on October 29, 2010 and is currently pending approval for the treatment of bipolar disorder in the United States. Treatment of schizophrenia.  Lurasidone is a benzothiazol derivative that is an antagonist and binds with high affinity to Dopamine-2 (D2) (Ki = 0.994 nM), 5-HT2A (Ki = 0.47 nM) receptors, and 5-HT7 receptors (Ki = 0.495 nM). It also binds with moderate affinity to alpha-2C adrenergic receptors (Ki = 10.8 nM) and is a partial agonist at 5-HT1A receptors (Ki = 6.38 nM). Its actions on histaminergic and muscarinic receptors are negligible.  Lurasidone is an atypical antipsychotic that is a D2 and 5-HT2A (mixed serotonin and dopamine activity) to improve cognition. It is thought that antagonism of serotonin receptors can improve negative symptoms of psychoses and reduce the extrapyramidal side effects that are often associated with typical antipsychotics. ",The molecular weight is 492.68.,Lurasidone has a topological polar surface area of 56.75.,The log p value of  is 5.61.,Lurasidone is approved and investigational.,Lurasidone is a solid.,True
15591,"Lomitapide is a microsomal triglyceride transfer protein (MTP) inhibitor used in homozygous familial hypercholesterolemia (HoFH) patients. It is marketed under the name Juxtapid (R). Used in homozygous familial hypercholesterolemia (HoFH) patients to reduce low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), apolipoprotein B (apo B), and non-high-density lipoprotein cholesterol (non-HDL-C). Lomitapide directly inhibits microsomal triglyceride transfer protein (MTP). Within the lumen of the endoplasmic reticulum, lomitapide inhibits microsomal triglyceride transfer protein (MTP), which prevents the formation of apolipoprotein B, and, thus, the formation of VLDL and chylomicrons as well. Altogether, this leads to a reduction of low-density lipoprotein cholesterol.",The molecular weight is 693.73.,Lomitapide has a topological polar surface area of 61.44.,The log p value of  is 7.0.,Lomitapide is approved and investigational.,Lomitapide is a solid.,True
15592,"Taurochenodeoxycholic acid is an experimental drug that is normally produced in the liver. Its physiologic function is to emulsify lipids such as cholesterol in the bile. As a medication, taurochenodeoxycholic acid reduces cholesterol formation in the liver, and is likely used as a choleretic to increase the volume of bile secretion from the liver and as a cholagogue to increase bile discharge into the duodenum. It is also being investigated for its role in inflammation and cancer therapy. Taurochenodeoxycholic acid is likely indicated as a choleretic and cholagogue. It is also being investigated for its role in inflammation and cancer therapy. Chenodeoxycholic acid is a primary bile acid in the liver that combines with taurine to form the bile acid taurochenodeoxycholic acid. In the bile, taurochenodeoxycholic acid is either a sodium (most) or potassium salt. Taurochenodeoxycholic acid is normally produced in the liver, and its physiologic function as a bile salt is to emulsify lipids such as cholesterol in the bile. As a medication, taurochenodeoxycholic acid reduces cholesterol formation in the liver, and is likely used as a choleretic to increase the volume of bile secretion from the liver and as a cholagogue to increase bile discharge into the duodenum. The mechanism of action of taurochenodeoxycholic acid in inflammation and cancer has yet to be determined.",,,,Taurochenodeoxycholic acid is experimental.,Taurochenodeoxycholic acid is a solid.,True
15593,"Agmantine is a natural metabolite of the amino acid arginine. It is formed when arginine is decarboxylated by the enzyme arginine decarboxylase and is found naturally in ragweed pollen, ergot fungi, octopus muscle, herring sperm, sponges, and the mammalian brain. Agmatine is both an experimental and investigational drug. As an investigational drug, it is being studied in a non-blinded prospective case study in the United States looking at patients who have been diagnosed with small fiber peripheral neuropathy between the ages of 18 to 75 years. Up to now (July 2013), the results of this study have not yet been published. As an experimental drug, agmatine is being studied for several indications such as cardioprotection, diabetes, decreased kidney function, neuroprotection (stroke, severe CNS injuries, epilepsy, glaucoma, and neuropathic pain), and psychiatric conditions (depression, anxiety, schizophrenia, and cognition). The exact mechanism of action is still being investigated for all of the potential indications of agmatine. Agmatine is being studied experimentally for several indications such as cardioprotection, diabetes, decreased kidney function, neuroprotection (stroke, severe CNS injuries, epilepsy, glaucoma, and neuropathic pain), and psychiatric conditions (depression, anxiety, schizophrenia, and cognition). As an investigational drug, agamatine is being studied in a non-blinded prospective case study in the United States looking at patients who have been diagnosed with small fiber peripheral neuropathy. Agmatine has several physiological effects. Its cardiovascular effects include mildly reducing heart rate and blood pressure. Also it promotes a mild hypoglycemic state, reduces cellular oxidative stress, and enhances glomerular filtration rate. The exact mechanism of action is still being investigated for all of the potential indications of agmatine. Some of the biochemical mechanisms discovered so far concern agmatine's indication for diabetes, neuroprotection, and psychiatric conditions. In diabetes, agmatine produces hypoglycemia by increasing the release of insulin form pancreatic islet cells and increasing glucose uptake by the cells through increased endorphin release from the adrenal glands. Concerning neuroprotection, agmatine's effects are thought to involve modulation of receptors (NMDA, alpha 2, and imidazoline) and ion channels (ATP sensitive potassium channels and voltage-gated calcium channels) as well as blocking nitric oxide synthesis. Agmatine blocks nitric oxide synthesis by reducing the nitric oxide synthase -2 (NOS-2) protein in astroglial cells and macrophages. With respect to agmatine's benefit in psychiatric disorders, it is suggested that the mechanism involves neurotransmitter receptor modulation of the NMDA, alpha-2, serotonin, opioid, and imidazoline receptors. Specifically when agmatine binds to the imidazoline and alpha 2 receptors, it acts as a neurotransmitter and releases catecholamines from the adrenal gland. ",,,,Agmatine is experimental.,Agmatine is a solid.,True
15594,"Brentuximab vedotin, also known as Adcetris®, is an antibody-drug conjugate that combines an anti-CD30 antibody with the drug monomethyl auristatin E (MMAE). It is an anti-neoplastic agent used in the treatment of Hodgkin's lymphoma and systemic anaplastic large cell lymphoma. Brentuximab vedotin was initially approved in 2011. In January 2012, the drug label was revised with a boxed warning of a condition known as progressive multifocal leukoencephalopathy and death due to opportunistic JC virus infection post treatment.  Seattle Genetics Announced FDA Approval of ADCETRIS® (Brentuximab Vedotin) in combination with chemotherapy for adults with previously untreated stage III or IV Classical Hodgkin Lymphoma in March 2018. Brentuximab vedotin causes apoptosis of tumor cells by preventing cell cycle progression of the G2 to M phase through disruption of the cytosolic microtuble network, thus preventing tumor growth and proliferation. Brentuximab vedotin is composed of 3 parts: a chimeric human-murine IgG1 that selectively targets CD30, monomethyl auristatin E (MMAE), which is a microtubule-disrupting agent, and a protease-susceptible linker that links the antibody and MMAE. The IgG1 antibody enables Brentuximab vedotin to target tumor cells expressing CD30 on their surface. Following this Brentuximab vedotin enters the cell. Once inside, the linker is cleaved releasing MMAE which binds disrupts the microtubule network.",,,,Brentuximab vedotin is approved and investigational.,Brentuximab vedotin is a solid.,True
15595,"Fidaxomicin is a novel macrolide antibiotic used in the treatment of diarrhea caused by _Clostridioides_ (formerly _Clostridium_) _difficile_ in adult and pediatric patients over the age of 6 months. Fidaxomicin is a naturally-occurring 18-member macrocycle derived from fermentation. Because fidaxomicin contains an 18-membered lactone ring in its structure, it is referred to as a macrocyclic lactone antibiotic drug. The antibacterial activity of fidaxomicin is distinct from macrolides and rifamycins, as the bactericidal activity is time-dependent, and not concentration-dependent. Fidaxomicin was the first macrocyclic lactone antibiotic with activity against _C. difficile_, and it displays a narrow spectrum of activity against gram-positive anaerobes. It mediates its potent bactericidal action on the bacteria by inhibiting the bacterial RNA synthase, thereby disrupting bacterial transcription. The minimum inhibitory concentration (MIC<sub>90</sub>) for fidaxomicin is four times less than that of , which was the primary drug of choice for _C. difficile_ infection before the approval of fidaxomicin. Unlike vancomycin, however, fidaxomicin has a negligible effect on normal colonic microflora. Fidaxomicin is indicated for the treatment of _Clostridioides_ (formerly _Clostridium_) _difficile_-associated diarrhea in adult and pediatric patients 6 months of age and older. Fidaxomicin has a narrow-spectrum antibacterial profile, with potent bactericidal activity specifically against C. difficile. The minimum inhibitory concentration for 90% of organisms for fidaxomicin against _C. difficile_ ranged from 0.0078 to 2 μg/mL _in vitro_. The bactericidal activity of fidaxomicin is time-dependent. Other than _C. difficile_, fidaxomicin has moderate inhibitory activity against Gram-positive bacteria (_S. aureus_ and _Enterococcus spp._) and poor activity against normal colonic flora, including anaerobes and enteric Gram-negative bacilli. Isolates of _C. difficile_ that are resistant to rifamycins or other antimicrobial classes (such as cephalosporins, fluoroquinolones, clindamycin) were not shown to be cross-resistant to fidaxomicin. _Clostridium difficile_ is a Gram-positive bacterium that causes various gastrointestinal complications, such as antibiotic-associated diarrhea. _C. difficile_ infection can be caused by antibiotic therapy, resulting in the disruption of the human gut flora leads to an overgrowth of _C. difficile_. The consequences of _C. difficile_ infection can be mild to severe and sometimes fatal. ",The molecular weight is 1058.05.,Fidaxomicin has a topological polar surface area of 266.66.,The log p value of  is 7.19.,Fidaxomicin is approved.,Fidaxomicin is a solid.,True
15596,"Cabozantinib was first approved in 2012 and is a non-specific tyrosine kinase inhibitor. It was initially approved in the US under the brand name Cometriq, which is indicated for the treatment of metastatic medullary thyroid cancer. In 2016, a capsule formulation (Cabometyx) was approved for the treatment of advanced renal cell carcinoma, and this same formulation gained additional approval in both the US and Canada in 2019 for the treatment of hepatocellular carcinoma in previously treated patients. Cabozantinib is indicated for the treatment of progressive, metastatic medullary thyroid cancer. It is also indicated for the treatment of advanced renal cell carcinoma and for hepatocellular carcinoma in patients previously treated with sorafenib. Cabozantinib suppresses metastasis, angiogenesis, and oncognesis by inhibiting receptor tyrosine kinases. Cabozantinib inhibits specific receptor tyrosine kinases such as VEGFR-1, -2 and -3, KIT, TRKB, FLT-3, AXL, RET, MET, and TIE-2.",The molecular weight is 501.51.,Cabozantinib has a topological polar surface area of 98.78.,The log p value of  is 4.94.,Cabozantinib is approved and investigational.,Cabozantinib is a solid.,True
15597,"Ruxolitinib is a janus-associated kinase inhibitor indicated to treat bone marrow cancer, specifically intermediate or high-risk myelofibrosis. FDA approved on November 16, 2011. Treatment of intermediate or high-risk myelofibrosis, including primary myelofibrosis, post-polycythemia vera (post-PV) myelofibrosis and post-essential thrombocythemia (post-ET) myelofibrosis. Myeolofibrosis is the proliferation of abnormal bone marrow stem cells which cause fibrosis (the excessive formation of connective tissue). The mean half-maximal inhibitory concentration (IC50) for JAK 1 and JAK 2 are 2.8 nmol/L and 3.3 nmol/L respectively. After administration of ruxolitinib, a decrease in levels of phosphorylated STAT (marker for JAK activity) in a dose-dependent manner can be observed. Pharmacodynamic resistance has not been observed.  Ruxolitinib is a kinase inhibitor that is selective for the Janus Associated Kinases (JAK) 1 and 2. These kinases are responsible for the mediation of cytokine and growth factor signalling which in turn effect immune function and hematopoiesis. The signalling process involves signal transducers and transcription activators (STAT) which modulate gene expression. Patients with myelofibrosis have abnormal JAK1 and JAK2 activity thus ruxolitinib works to regulate this. ",The molecular weight is 306.37.,Ruxolitinib has a topological polar surface area of 83.18.,The log p value of  is 2.22.,Ruxolitinib is approved.,Ruxolitinib is a solid.,True
15598,"Linagliptin is a DPP-4 inhibitor developed by Boehringer Ingelheim for the treatment of type II diabetes. Linagliptin differs from other DPP-4 inhibitors in that it has a non-linear pharmacokinetic profile, is not primarily eliminated by the renal system, and obeys concentration dependant protein binding. Linagliptin was approved by the FDA on May 2, 2011. Linagliptin is indicated for the treatment of type II diabetes in addition to diet and exercise. It should not be used to treat type I diabetes or in diabetic ketoacidosis. An extended-release combination product containing empagliflozin, linagliptin, and metformin was approved by the FDA in January 2020 for the improvement of glycemic control in adults with type 2 diabetes mellitus when used adjunctively with diet and exercise. A 5mg oral dose of linagliptin results in >80% inhibition of dipeptidyl peptidase 4 (DPP-4) for ≥24 hours. Inhibition of DPP-4 increases the concentration of glucagon-like peptide 1 (GLP-1), leading to decreased glycosylated hemoglobin and fasting plasma glucose. Linagliptin is a competitive, reversible DPP-4 inhibitor. Inhibition of this enzyme slows the breakdown of GLP-1 and glucose-dependant insulinotropic polypeptide (GIP). GLP-1 and GIP stimulate the release of insulin from beta cells in the pancreas while inhibiting release of glucagon from pancreatic beta cells. These effects together reduce the breakdown of glycogen in the liver and increase insulin release in response to glucose.",The molecular weight is 472.55.,Linagliptin has a topological polar surface area of 113.48.,The log p value of  is 1.91.,Linagliptin is approved.,Linagliptin is a solid.,True
15599,"Regorafenib is an orally-administered inhibitor of multiple kinases. It is used for the treatment of metastatic colorectal cancer, advanced gastrointestinal stromal tumours, and hepatocellular carcinoma. FDA approved on September 27, 2012. Approved use of Regorafenib was expanded to treat Hepatocellular Carcinoma in April 2017. Regorafenib is indicated for the treatment of patients with metastatic colorectal cancer (CRC) who have been previously treated with fluoropyrimidine-, oxaliplatin- and irinotecan-based chemotherapy, an anti-VEGF therapy, and, if KRAS wild type, an anti-EGFR therapy. Regorafenib is also indicated for the treatment of patients with locally advanced, unresectable or metastatic gastrointestinal stromal tumour (GIST) who have been previously treated with imatinib mesylate and sunitinib malate. Regorafenib is also indicated for the treatment of patients with hepatocellular carcinoma (HCC) previously treated with sorafenib. Regorafenib is a small molecule inhibitor of multiple membrane-bound and intracellular kinases involved in normal cellular functions and in pathologic processes such as oncogenesis, tumor angiogenesis, and maintenance of the tumor microenvironment. In in vitro biochemical or cellular assays, regorafenib or its major human active metabolites M-2 and M-5 inhibited the activity of RET, VEGFR1, VEGFR2, VEGFR3, KIT, PDGFR-alpha, PDGFR-beta, FGFR1, FGFR2, TIE2, DDR2, TrkA, Eph2A, RAF-1, BRAF, BRAFV600E , SAPK2, PTK5, and Abl at concentrations of regorafenib that have been achieved clinically. In in vivo models, regorafenib demonstrated anti-angiogenic activity in a rat tumor model, and inhibition of tumor growth as well as anti-metastatic activity in several mouse xenograft models including some for human colorectal carcinoma.",The molecular weight is 482.82.,Regorafenib has a topological polar surface area of 92.35.,The log p value of  is 5.19.,Regorafenib is approved.,Regorafenib is a solid.,True
15600,"Bedaquiline is a bactericidal antimycobacterial drug. Chemically it is a diarylquinoline. FDA approved on December 28, 2012. Bedaquiline is indicated as part of combination therapy in adults (≥ 18 years) with pulmonary multi-drug resistant tuberculosis (MDR-TB).  Bedaquiline is primarily subjected to oxidative metabolism leading to the formation of N-monodesmethyl metabolite (M2). M2 is not thought to contribute significantly to clinical efficacy given its lower average exposure (23% to 31%) in humans and lower antimycobacterial activity (4 to 6-fold lower) compared to the parent compound. M2 concentrations appeared to correlate with QT prolongation. Bedaquiline inhibits mycobacterial TB at a minimal inhibitory concentration (MIC) from 0.002-0.06 μg/ml and with a MIC50 of 0.03 μg/ml. Furthermore, bacteria that have smaller ATP stores (usually in dormant, nonreplicating bacilli) are more susceptible to bedaquiline.  Bedaquiline is a diarylquinoline antimycobacterial drug that inhibits the proton pump of mycobacterial ATP (adenosine 5'-triphosphate) synthase, an enzyme that is essential for the generation of energy in Mycobacterium tuberculosis. Bacterial death occurs as a result of bedaquiline. ",The molecular weight is 555.52.,Bedaquiline has a topological polar surface area of 45.59.,The log p value of  is 7.25.,Bedaquiline is approved.,Bedaquiline is a solid.,True
15601,"Formestane was the first selective, type I, steroidal aromatase inhibitor used in the treatment of estrogen-receptor positive breast cancer in post-menopausal women. Formestane suppresses estrogen production from anabolic steroids or prohormones. Formestane is also a prohormone of 4-hydroxytestosterone, an active steroid with weak androgenic activity and mild aromatase inhibitor activity. It is listed as a prohibited substance by the World Anti-Doping Agency for use in athletes.  For the treatment of estrogen-receptor positive breast cancer in post-menopausal women. By significantly reducing estrogen levels in the bloodstream, formestane may exhibit antitumor activity.  Formestane is a second generation, irreversible, steroidal aromatase inhibitor. It inhibits the aromatase enzyme responsible for converting androgens to estrogens, thereby preventing estrogen production. ",The molecular weight is 302.41.,Formestane has a topological polar surface area of 54.37.,The log p value of  is 2.86.,Formestane is approved and investigational and withdrawn.,Formestane is a solid.,True
15602,"Trametinib dimethyl sulfoxide is a kinase inhibitor. Each 1-mg tablet contains 1.127 mg trametinib dimethyl sulfoxide equivalent to 1 mg of trametinib non-solvated parent. FDA approved on May 29, 2013. Trametinib is indicated for the treatment of unresectable or metastatic melanoma with BRAF V600E or V600K mutations, as detected by an FDA-approved test. Trametinib is an anticancer agent which causes apoptosis (or programmed cell death) and inhibits cell proliferation, which are both important in the treatment of malignancies. Trametinib is a reversible, allosteric inhibitor of mitogen-activated extracellular signal regulated kinase 1 _(MEK1)_ and _MEK2_ activation and of_ MEK1_ and _MEK2_ kinase activity. MEK proteins are upstream regulators of the extracellular signal-related kinase (ERK) pathway, which promotes cellular proliferation. Trametinib helps with melanoma with the BRAF V600E or V600K as the mutation results in the constitutive activation of the BRAF pathway which includes MEK1 and MEK2.",The molecular weight is 615.4.,Trametinib has a topological polar surface area of 102.06.,The log p value of  is 4.84.,Trametinib is approved.,Trametinib is a solid.,True
15603,"Dabrafenib mesylate (Tafinlar) is a reversible ATP-competitive kinase inhibitor and targets the MAPK pathway. It was approved on May 29, 2013 for the treatment of melanoma. Tafinlar is a kinase inhibitor that was initially indicated as a single agent for the treatment of patients with unresectable or metastatic melanoma with BRAF V600E mutation as detected by an FDA-approved test. Dabrafenib causes an inhibition of phosphorylated extracellular signal-regulated kinase (ERK). This indicates a decrease in cell proliferation. Furthermore, within 24 hours of administration, downstream mediators of the MAPK pathway were inhibited.",The molecular weight is 519.56.,Dabrafenib has a topological polar surface area of 110.86.,The log p value of  is 4.61.,Dabrafenib is approved and investigational.,Dabrafenib is a solid.,True
15604,"Luliconazole is a topical antifungal agent that acts by unknown mechanisms but is postulated to involve altering the synthesis of fungi cell membranes. It was approved by the FDA (USA) in November 2013 and is marketed under the brand name Luzu. Luliconazole is also approved in Japan. Luliconazole is indicated in adults aged 18 years and older for the topical treatment of fungal infections caused by Trichophyton rubrum and Epidermophyton floccosum, specifically tinea pedis, cruris, and corporis. Luliconazole kills the organisms Trichophyton rubrum and Epidermophyton floccosum, most likely by altering their fungal cell membranes. The exact mechanism of action for luliconazole's anti-fungal activity is still not known, but luliconazole is thought to inhibit the enzyme lanosterol demethylase. Lanosterol demethylase is needed for the synthesis of ergosterol, which is a major component of the fungus cell membranes. ",The molecular weight is 354.27.,Luliconazole has a topological polar surface area of 41.61.,The log p value of  is 3.49.,Luliconazole is approved.,Luliconazole is a solid.,True
15605,"Indalpine was one of the first selective serotonin reuptake inhibitors to reach the American market. It was initially marketed by Pharmuka. However, after the emergence of widespread concern regarding adverse effects caused by SSRIs, and reported hematological effects caused by Indalpine, it was abruptly withdrawn from the US market.",The molecular weight is 228.34.,Indalpine has a topological polar surface area of 27.82.,The log p value of  is 3.39.,Indalpine is investigational and withdrawn.,Indalpine is a solid.,True
15606,Fendiline is a coronary vasodilator which inhibits calcium function in muscle cells in excitation-contraction coupling. It has been proposed as an antiarrhythmic and antianginal agent. Fendiline is non-selective.,The molecular weight is 315.46.,Fendiline has a topological polar surface area of 12.03.,The log p value of  is 5.73.,Fendiline is withdrawn.,Fendiline is a solid.,True
15607,"Eperisone is an antispasmodic drug which relaxes both skeletal muscles and vascular smooth muscles, and demonstrates a variety of effects such as reduction of myotonia, improvement of circulation, and suppression of the pain reflex. It is not approved for use in the United States, but is available in other countries like India, South Korea, and Bangladesh.",The molecular weight is 259.39.,Eperisone has a topological polar surface area of 20.31.,The log p value of  is 4.36.,Eperisone is investigational.,Eperisone is a solid.,True
15608,"Brotizolam is a sedative-hypnotic thienodiazepine drug which is a benzodiazepine analog. It demonstrates anxiolytic, anticonvulsant, hypnotic, sedative and skeletal muscle relaxant effects. Brotizolam has similar effects to short-acting benzodiazepines such as triazolam. Brotizolam is indicated for 2-4 weeks of treatment for severe or debilitating insomnia. Brotizolam is an extremely potent drug and it is rapidly eliminated with an average half-life of 4.4 hours (range 3.6 - 7.9 hours). Brotizolam is indicated for 2-4 weeks in the treatment of severe or debilitating insomnia. ",The molecular weight is 393.69.,Brotizolam has a topological polar surface area of 43.07.,The log p value of  is 2.71.,Brotizolam is investigational and withdrawn.,Brotizolam is a solid.,True
15609,"Aliskiren is the first drug in the renin inhibitor drug class and is used for the treatment of hypertension. It was developed by Speedel and Novartis and initially approved by the FDA in early 2007. Aliskiren has been proven to efficacious in reducing blood pressure when used alone or in conjunction with other antihypertensive agents. Aliskiren is used for the treatment of hypertension in children above 6 years and adults. This drug may also be used in conjunction with antihypertensives such as calcium channel blockers and thiazides in products form to provide additional blood pressure control. Aliskiren reduces blood pressure by inhibiting renin. This leads to a cascade of events that decreases blood pressure, lowering the risk of fatal and nonfatal cardiovascular events including stroke and myocardial infarction. Aliskiren is a renin inhibitor. Renin is secreted by the kidneys when blood volume and renal perfusion decrease. It normally cleaves the protein angiotensinogen to form angiotensin I. Angiotensin I is then converted to angiotensin II, an active protein. Angiotensin II is a potent vasoconstrictor that causes the release of catecholamines into the circulation. It also promotes the secretion of aldosterone in addition to sodium reabsorption, increasing blood pressure. Additionally, angiotensin II acts on the adrenal cortex where it stimulates aldosterone release. Aldosterone increases sodium reabsorption and potassium excretion in the nephron. ",The molecular weight is 551.77.,Aliskiren has a topological polar surface area of 146.13.,The log p value of  is 3.51.,Aliskiren is approved and investigational.,Aliskiren is a solid.,True
15610,"Vorapaxar is a tricyclic himbacine-derived selective inhibitor of protease activated receptor (PAR-1) indicated for reducing the incidence of thrombotic cardiovascular events in patients with a history of myocardial infarction (MI) or with peripheral arterial disease (PAD). By inhibiting PAR-1, a thrombin receptor expressed on platelets, vorapaxar prevents thrombin-related platelet aggregation. Vorapaxar is indicated for the reduction of thrombotic cardiovascular events in patients with a history of myocardial infarction (MI) or peripheral arterial disease (PAD). It is usually co-administered with acetylsalicylic acid (ASA) and/or clopidogrel, and should therefore be administered as an addition to these medications as it has not been studied alone.  Vorapaxar inhibits platelet aggregation through the reversible antagonism of protease-activated receptor 1 (PAR-1), also known as thrombin receptor. PARs are a family of G-protein coupled receptors highly expressed on platelets and activated by serine protease activity of thrombin to mediate thrombotic response. By blocking PAR-1 activating, vorapaxar inhibits thrombin-induced platelet aggregation and thrombin receptor agonist peptide (TRAP)-induced platelet aggregation. Vorapaxar does not inhibit platelet aggregation induced by other agonists such as adenosine diphosphate (ADP), collagen or a thromboxane mimetic.",The molecular weight is 492.59.,Vorapaxar has a topological polar surface area of 77.52.,The log p value of  is 4.34.,Vorapaxar is approved.,Vorapaxar is a solid.,True
15611,"Suvorexant is a selective dual antagonist of orexin receptors OX1R and OX2R that promotes sleep by reducing wakefulness and arousal. It has been approved for the treatment of insomnia. Suvorexant is indicated for the treatment of insomnia characterized by difficulties with sleep onset and/or sleep maintenance. Suvorexant is a dual antagonist of orexin receptors OX1R and OX2R. It exerts its pharmacological effect by inhibiting binding of neuropeptides orexin A and B, also known as hypocretin 1 and 2, that are produced by neurons in the lateral hypothalamus. These neurons control the wake-promoting centers of the brain and are active during wakefulness, especially during motor activities, and stop firing during sleep. By inhibiting the reinforcement of arousal systems, suvorexant use causes a decrease in arousal and wakefulness, rather than having a direct sleep-promoting effect.",The molecular weight is 450.93.,Suvorexant has a topological polar surface area of 80.29.,The log p value of  is 4.79.,Suvorexant is approved and investigational.,Suvorexant is a solid.,True
15612,"Siltuximab is a chimeric (human-mouse) monoclonal immunoglobulin G1-kappa antibody produced in a Chinese hamster ovary (CHO) cell line by recombinant DNA technology. Siltuximab prevents the binding of IL-6 to soluble and membrane-bound IL-6 receptors by forming high affinity complexes with human interleukin-6 (IL-6). Its use is indicated for the treatment of adult patients with multicentric Castleman's disease (MCD) who are human immunodeficiency virus (HIV) negative and human herpesvirus-8 (HHV-8) negative. MCD is a rare blood disorder caused by dysregulated IL-6 production, proliferation of lymphocytes, and subsequent enlargement of the lymph nodes. It is administered as a 1 hour intravenous infusion every 3 weeks. Siltuximab is indicated for the treatment of patients with multicentric Castleman's disease (MCD) who are human immunodeficiency virus (HIV) negative and human herpesvirus-8 (HHV-8) negative. Siltuximab did not bind to virally produced IL-6 in a nonclinical study and was therefore not studied in patients with MCD who are HIV or HHV-8 positive. Siltuximab-neutralized antibody-IL-6 complexes interfere with current immunological-based IL-6 quantification methods, therefore measurement of serum or plasma IL-6 concentrations should not be used as a pharmacodynamic marker during treatment. As well, cytochrome P450 enzymes in the liver are down regulated by infection and inflammation stimuli, which includes cytokines such as IL-6. By preventing IL-6 signalling through treatment with siltuximab, CYP450 activity may be increased leading to faster metabolism of drugs that are CYP450 substrates.  Siltuximab complexes with human IL-6 and prevents binding to soluble and membrane-bound IL-6 receptors, thereby inhibiting the proliferation of lymphocytes. ",,,,Siltuximab is approved and investigational.,Siltuximab is a solid.,True
15613,"Ceritinib is used for the treatment of adults with anaplastic lymphoma kinase (ALK)-positive metastatic non-small cell lung cancer (NSCLC) following failure (secondary to resistance or intolerance) of prior crizotinib therapy. About 4% of patients with NSCLC have a chromosomal rearrangement that generates a fusion gene between EML4 (echinoderm microtubule-associated protein-like 4) and ALK (anaplastic lymphoma kinase), which results in constitutive kinase activity that contributes to carcinogenesis and seems to drive the malignant phenotype. Ceritinib exerts its therapeutic effect by inhibiting autophosphorylation of ALK, ALK-mediated phosphorylation of the downstream signaling protein STAT3, and proliferation of ALK-dependent cancer cells. Following treatment with crizotinib (a first-generation ALK inhibitor), most tumours develop drug resistance due to mutations in key \gatekeeper\"" residues of the enzyme. This occurrence led to development of novel second-generation ALK inhibitors such as ceritinib to overcome crizotinib resistance. The FDA approved ceritinib in April 2014 due to a surprisingly high response rate (56%) towards crizotinib-resistant tumours and has designated it with orphan drug status."" Ceritinib is a kinase inhibitor indicated for the treatment of patients with anaplastic lymphoma kinase (ALK)-positive metastatic non-small cell lung cancer (NSCLC) who have progressed on or are intolerant to crizotinib. This indication is approved under accelerated approval based on tumor response rate and duration of response. An improvement in survival or disease-related symptoms has not been established. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials. Ceritinib inhibits Anaplastic lymphoma kinase (ALK) also known as ALK tyrosine kinase receptor or CD246 (cluster of differentiation 246), which is an enzyme that in humans is encoded by the ALK gene. About 4-5% of NSCLCs have a chromosomal rearrangement that generates a fusion gene between EML4 (echinoderm microtubule-associated protein-like 4) and ALK (anaplastic lymphoma kinase), which results in constitutive kinase activity that contributes to carcinogenesis and seems to drive the malignant phenotype. Ceritinib exerts its therapeutic effect by inhibiting autophosphorylation of ALK, ALK-mediated phosphorylation of the downstream signaling protein STAT3, and proliferation of ALK-dependent cancer cells. Ceritinib has been shown to inhibit in vitro proliferation of cell lines expressing EML4-ALK and NPM-ALK fusion proteins and demonstrated dose-dependent inhibition of EML4-ALK-positive NSCLC xenograft growth in mice and rats.",The molecular weight is 558.14.,Ceritinib has a topological polar surface area of 105.24.,The log p value of  is 6.41.,Ceritinib is approved.,Ceritinib is a solid.,True
15614,"Vilanterol is a selective long-acting beta2-adrenergic agonist (LABA) with inherent 24-hour activity for once daily treatment of COPD and asthma. Its pharmacological effect is attributable to stimulation of intracellular adenylyl cyclase which catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3',5'-adenosine monophosphate (cAMP). Increases in cyclic AMP are associated with relaxation of bronchial smooth muscle and inhibition of release of hypersensitivity mediators from mast cells in the lungs.  Vilanterol is approved for use in several combination products such as with fluticasone furoate under the tradename Breo Ellipta and in combination with umeclidinium bromide as Anoro Ellipta. Approved by the FDA in 2013, use of Breo Ellipta is indicated for the long-term, once-daily maintenance treatment of airflow obstruction in patients with COPD, including chronic bronchitis and emphysema. It is also indicated for once-daily maintenance treatment of asthma in patients aged 18 or older with reversible obstructive airways disease. Vilanterol is a selective long-acting beta2-adrenergic agonist. Its pharmacological effect is attributable to stimulation of intracellular adenylyl cyclase which catalyzes the conversion of adenosine triphosphate (ATP) to cyclic-3',5'-adenosine monophosphate (cAMP). Increases in cyclic AMP are associated with relaxation of bronchial smooth muscle and inhibition of release of hypersensitivity mediators from mast cells in the lungs. ",The molecular weight is 486.43.,Vilanterol has a topological polar surface area of 91.18.,The log p value of  is 3.19.,Vilanterol is approved.,Vilanterol is a solid.,True
15615,"Ivabradine is a novel heart rate lowering medicine for the symptomatic management of stable angina pectoralis and symptomatic chronic heart failure. Ivabradine, brand name Corlanor, was approved by the FDA in April 2015 for the treatment of chronic heart failure in patients with an ejection fraction of ≤35%, in sinus rhythm with resting heart rate ≥70 beats per minute, who are not on beta-blockers due to contraindications or already receiving maximum beta-blocker dose. Recently a new indication was added to treat symptomatic heart failure from dilated cardiomyopathy for patients 6 months or more in age. Ivabradine acts by selectively inhibiting the \funny\"" channel pacemaker current (If) in the sinoatrial node in a dose-dependent fashion, resulting in a lower heart rate and thus more blood to flow to the myocardium. Although non-dihydropyridine calcium channel blockers and beta blockers also effectively lower heart rate, they exhibit adverse events due to their negative ionotropic effects. Therefore, as ivabradine is designed as a \""pure\"" heart rate-lowering drug by selectively acting on the If channels, it may offer a more favorable side effect profile due to its lower likelihood of causing serious adverse effects."" Ivabradine is indicated by the FDA to reduce the risk of hospitalization for worsening heart failure in adult patients with stable, symptomatic chronic heart failure with left ventricular ejection fraction ≤35%, who are in sinus rhythm with resting heart rate ≥70 beats per minute and either are on maximally tolerated doses of beta-blockers or have a contraindication to beta-blocker use. It is also indicated for treatment of stable symptomatic heart failure as a result of dilated cardiomyopathy for pediatric patients 6 months of age or more. The funny channels (If) open during repolarization and close during depolarization, making ivabradine's activity dependent on heart rate or the closing and opening of the channels. Therefore ivabradine exhibits use-dependence and is more pharmacologically active at higher heart rates. Ivabradine exhibits a linear dose-dependent heart-rate lowering activity (bradycardic effect) until a maximum dose of 30-40mg. At higher doses, the concentration of ivabradine tends to plateau, reducing risk of serious sinus bradycardia. It has been shown that the metabolite of ivabradine lowers heart rate as well, contributing to ivabradine's overall effect.  Ivabradine lowers heart rate by selectively inhibiting If channels (\funny channels\"") in the heart in a concentration-dependent manner without affecting any other cardiac ionic channels (including calcium or potassium). Ivabradine binds by entering and attaching to a site on the channel pore from the intracellular side and disrupts If ion current flow, which prolongs diastolic depolarization, lowering heart rate. The If currents are located in the sinoatrial node and are the home of all cardiac pacemaker activity. Ivabradine therefore lowers the pacemaker firing rate, consequently lowering heart rate and reducing myocardial oxygen demand. This allows for an improved oxygen supply and therefore mitigation of ischemia, allowing for a higher exercise capacity and reduction in angina episodes. """,The molecular weight is 468.59.,Ivabradine has a topological polar surface area of 60.47.,The log p value of  is 3.27.,Ivabradine is approved.,Ivabradine is a solid.,True
15616,"Trimebutine is a spasmolytic agent that regulates intestinal and colonic motility and relieves abdominal pain with antimuscarinic and weak mu opioid agonist effects. It is marketed for the treatment of irritable bowel syndrome (IBS) and lower gastrointestinal tract motility disorders, with IBS being one of the most common multifactorial GI disorders. It is used to restore normal bowel function and is commonly present in pharmaceutical mixtures as trimebutine maleate salt form. Trimebutine is not a FDA-approved drug, but it is available in Canada and several other international countries. Indicated for symptomatic treatment of irritable bowel syndrome (IBS) and treatment of postoperative paralytic ileus following abdominal surgery.  Trimebutine is a spasmolytic agent that acts directly on smooth muscle to modulate gastric motility. It shows a \dual function\"" that stimulates or inhibits spontaneous contractions depending on the concentration and prior contractile activity in the preparation. Targeting ion conductance that regulates GI motility, trimebutine inhibits the inward calcium currents and calcium-dependent potassium currents in a concentration-dependent manner. At lower concentrations (1-10uM), trimebutine depolarizes the resting membrane potential without affecting the amplitude of contractions, which is thought to be mediated by inhibition of outward potassium currents. It is also shown to activate T-type Ca2+ channel and increase gastric emptying, intestinal and colonic contractility. At higher concentrations (100-300uM), reduced amplitude of spontaneous contractions and action potentials is thought to be mediated by inhibition of L-type Ca2+ channels and inward calcium current. Trimebutine mediates a local anesthetic action by acting as a weak agonist at mu opioid receptors."" At high concentrations, trimebutine is shown to inhibit the extracellular Ca2+ influx in the smooth muscle cells through voltage dependent L-type Ca2+ channels and further Ca2+ release from intracellular Ca2+ stores. Trimebutine is suggested to bind to the inactivated state of the calcium channel with high affinity. Reduced calcium influx attenuates membrane depolarization and decrease colon peristalsis. It also inhibits outward K+ currents in response to membrane depolarization of the GI smooth muscle cells at resting conditions through inhibition of delayed rectifier K+ channels and Ca2+ dependent K+ channels, which results in induced muscle contractions. Trimebutine binds to mu opioid receptors with more selectivity compared to delta or kappa opioid receptors but with lower affinity than their natural ligands. Its metabolites (N-monodesmethyl-trimebutine or nor-trimebutine), are also shown to bind to opoid receptors on brain membranes and myenteric synaptosomes. ",The molecular weight is 387.48.,Trimebutine has a topological polar surface area of 57.23.,The log p value of  is 4.26.,Trimebutine is approved.,Trimebutine is a solid.,True
15617,"Pinaverium is a spasmolytic agent used for functional gastrointestinal disorders. It is a quaternary ammonium compound that acts as an atypical calcium antagonist to restore normal bowel function. It is shown to relieve GI spasm and pain, transit disturbances and other symptoms related to motility disorders and may be considered as effective first-lline therapy for patients with irritable bowel syndrome (IBS). Pinaverium bromide is the common ingredient in formulations, mostly as oral tablets. Although it is not a currently approved drug by the FDA, pinaverium is available in over 60 countries including Canada. Pinaverium is indicated for the symptomatic treatment of irritable bowel syndrome (IBS) and functional disorders of the biliary tract. Pinaverium is a selective and specific voltage-dependent calcium channel blocker located on intestinal smooth muscle cells to inhibit calcium influx. It mediates various effects on the GI tract: it causes oesophageal, gastric and duodenal relaxation, relaxes the colon and intestines, inhibits colonic motility in response to food, hormonal or pharmacological stimuli, accelerates gastric emptying, and reduces contractions of the gallbladder and phasic contractions of sphincter of Oddi. At higher concentrations, pinaverium also exhibits very weak anticholinergic effects but is not shown to display vasodilatory or anti-arrythmic actions.  Pinaverium interacts with the 1,4-dihydropyridine binding sites on voltage dependent L-type calcium channels located on GI smooth muscle cells in a competitve manner. The binding site is located in the alpha 1S subunit and pinaverium most likely antagonizes the action of calcium ions by stabilizing a non-conducting channel state. Pinaverium inhibits smooth muscle contractions of the GI tract by inhibiting inward calcium current and calcium influx. It is suggested that pinaverium may be able to bind to both closed or inactivates states of the calcium channel with similar affinity. ",The molecular weight is 511.52.,Pinaverium has a topological polar surface area of 36.92.,The log p value of  is 5.79.,Pinaverium is approved.,Pinaverium is a solid.,True
15618,"Somatostatin, also known as growth hormone-inhibiting hormone, is a naturally-occurring peptide hormone of 14 or 28 amino acid residues that regulates the endocrine system. It is secreted by the D cells of the islets to inhibit the release of insulin and glucagon, and is also generated in the hypothalamus, where it inhibits the release of growth hormone and thyroid-stimulating hormones from the anterior pituitary. Somatostatin is initially secreted as a 116 amino acid precursor, preprosomatostatin, which undergoes endoproteolytic cleavage to prosomastatin. Prosomastatin is further process into two active forms, somatostatin-14 (SST-14) and somatostatin-28 (SST-28), an extended SST-14 sequence to the N-terminus. The actions of somatostatin are mediated via signalling pathways of G protein-coupled somatostatin receptors.  For the symptomatic treatment of acute bleeding from esophageal varices. Other treatment options for long-term management of the condition may be considered if necessary, once initial control has been established. Somatostatin is an endogenous peptide hormone that is secreted by the central nervous system, gastrointestinal tract, retina, peripheral neurons and pancreatic D cells of the islets of Langerhans. It exhibits several biological roles but predominantly exerts an inhibitory effect on secretion of other hormones and transmitters. While distribution of two active isoforms of somatostatin is similar, SST-14 is more predominant in the enteric neurons and peripheral nerves whereas SST-28 is more prominent in the retina and intestinal mucosal cells. Somatostatin binds to 5 subtypes of somatostatin receptors (SSTRs), which are all Gi-protein-coupled transmembrane receptors that inhibits adenylyl cyclase upon activation. By inhibiting intracellular cyclic AMP and Ca2+ and by a receptor-linked distal effect on exocytosis, SSTRs block cell secretion. The common pathway shared by the receptors involve the activation of phosphotyrosine phosphatase (PTP), and modulation of mitogen-activated protein kinase (MAPK). With the exception of SSTR3, activation of SSTRs lead to activation of voltage-gated potassium channels accompanied by increased K+ currents. This result in membrane hyperpolarization and inhibits depolarization-induced Ca2+ influx through voltage-sensitive Ca2+ channels. Depending on the receptor subtype, signalling cascades involve activation of other downstream targets such as Na+/H+ exchanger, Rho GTPase, and nitric oxide synthase (NOS). SSTRs 1 to 4 bind both somatostatin isoforms with equal nanomolar binding affinity whereas SSTR5 exhibits a 5- to 10-fold higher binding affinity for SST-28. ",The molecular weight is 1637.9.,Somatostatin has a topological polar surface area of 613.23.,The log p value of  is -1.46.,Somatostatin is approved and investigational.,Somatostatin is a solid.,True
15619,"Elvitegravir is a human immunodeficiency virus type 1 (HIV-1) integrase strand transfer inhibitor (INSTI) used for the treatment of HIV-1 infection in antiretroviral treatment-experienced adults. Because integrase is necessary for viral replication, inhibition prevents the integration of HIV-1 DNA into the host genome and thereby blocks the formation of the HIV-1 provirus and resulting propagation of the viral infection. Although available as a single dose tablet, elvitegravir must be used in combination with an HIV protease inhibitor coadministered with ritonavir and another antiretroviral drug. Elvitegravir in combination with an HIV protease inhibitor coadministered with ritonavir and with other antiretroviral drug(s) is indicated for the treatment of HIV-1 infection in antiretroviral treatment-experienced adults. Elvitegravir is an HIV-1 integrase strand transfer inhibitor (INSTI). Integrase is an HIV-1 encoded enzyme that is required for viral replication. Inhibition of integrase prevents the integration of HIV-1 DNA into host genomic DNA, blocking the formation of the HIV-1 provirus and propagation of the viral infection. Elvitegravir does not inhibit human topoisomerases I or II.",The molecular weight is 447.89.,Elvitegravir has a topological polar surface area of 87.07.,The log p value of  is 4.56.,Elvitegravir is approved.,Elvitegravir is a solid.,True
15620,"Eslicarbazepine acetate (ESL) is an anticonvulsant medication approved for use in Europe, the United States and Canada as an adjunctive therapy for partial-onset seizures that are not adequately controlled with conventional therapy. Eslicarbazepine acetate is a prodrug that is rapidly converted to eslicarbazepine, the primary active metabolite in the body. Eslicarbazepine's mechanism of action is not well understood, but it is known that it does exert anticonvulsant activity by inhibiting repeated neuronal firing and stabilizing the inactivated state of voltage-gated sodium channels, thus preventing their return to the activated state during which seizure activity can occur. Eslicarbazepine acetate is indicated as adjunctive therapy in the treatment of partial-onset seizures that are not adequately controlled with conventional therapy in epileptic patients.  Eslicarbazepine acetate is associated with a dose- and concentration-dependant increase in heart rate and prolongation of PR interval. Eslicarbazepine acetate is converted to the active metabolite eslicarbazepine which carries out its anticonvulsant activity. The exact mechanism of action is unknown, but it is thought to involve the inhibition of voltage-gated sodium channels. In in vitro electrophysiological studies, eslicarbazepine was shown to inhibit repeated neuronal firing by stabilizing the inactivated state of voltage-gated sodium channels and preventing their return to the activated state. In vitro studies also showed eslicarbazepine inhibiting T-type calcium channels, which likely also has a role in anticonvulsant activity. ",The molecular weight is 296.33.,Eslicarbazepine acetate has a topological polar surface area of 72.63.,The log p value of  is 1.5.,Eslicarbazepine acetate is approved.,Eslicarbazepine acetate is a solid.,True
15621,"Dienogest is an orally-active semisynthetic progestogen which also possesses the properties of 17α-hydroxyprogesterone. It is a derivative of 19-nortestosterone and has antiandrogenic properties. It is primarily used as a contraceptive in combination with ethinylestradiol, or in other combination form pills approved in United States and Europe however it is not available in the US by itself. In Europe, Australia, Malaysia, Singapore and Japan, dienogest single therapy is an approved treatment for endometriosis to alleviate painful symptoms of endometriosis and reduce endometriotic lesions. Dienogest is commonly marketed as Visanne, Natazia and Qlaira. Indicated for use as the treatment of endometriosis alone and as a contraceptive in combination with ethinylestradiol.  Dienogest exhibits a very potent progestagenic effect in the endometrium, and causes endometrial atrophy after prolonged use. It also mediates an antiandrogenic effect that is equivalent to approximately one third that of cyproterone acetate. A dose of 2 mg inhibits the growth of ovarian follicles at 10 mm and maintains the concentration of progesterone at a low level, but has a weak inhibitory effect on FSH and LH. 1mg/kg of dienogest also directly inhibits ovulation. In clinical trials composing of patients with endometriosis, dienogest therapy effectively reduced painful symptoms and endometriotic lesions associated with the disorder. Dienogest acts as an agonist at the progesterone receptor (PR) with weak affinity that is comparable to that of progesterone but has a very potent progestagenic effect in the endometrium, causing endometrial atrophy after prolonged use. It promotes antiproliferative, immunologic and antiangiogenic effects on endometrial tissue. Dienogest reduces the level of endogenous production of oestradiol and thereby suppressing the trophic effects of oestradiol on both the eutopic and ectopic endometrium. Continous administration of dienogest results in hyperprogestogenic and moderately hypoestrogenic endocrine environment, which causes initial decidualization of endometrial tissue. ",The molecular weight is 311.42.,Dienogest has a topological polar surface area of 61.09.,The log p value of  is 2.16.,Dienogest is approved.,Dienogest is a solid.,True
15622,"Sonidegib is a Hedgehog signaling pathway inhibitor (via smoothened antagonism) developed as an anticancer agent by Novartis. It was FDA approved in 2015 for the treatment of basal cell carcinoma. Sonidegib is approved for use in the US and EU for treatment of adults with locally advanced basal cell carcinoma (BCC) that has recurred post surgery or radiation therapy. It is also approved for adult patients with BCC who are not eligible for surgery or radiation therapy. (2) Sonidegib has been shown to inhibit a transmembrane protein called SMO which plays a role in Hh signal transduction. This has resulted in inhibition of Hh signaling as well as antitumour activity in various animal models. In a transgenic mouse model of islet cell neoplasms, tumour volume was reduce by 95% in mice treated with sonidegib when compared with untreated mice. (2) The hedgehog pathway is involved in many human cancers. Sonidegib effectively inhibits the regulator called smoothened (Smo), preventing the hedgehog pathway from functioning. As a result, tumours that depend on the hedgehog pathway are unable to grow. (1)",The molecular weight is 485.51.,Sonidegib has a topological polar surface area of 63.69.,The log p value of  is 5.84.,Sonidegib is approved and investigational.,Sonidegib is a solid.,True
15623,"Etizolam is a thienodiazepine which is chemically related to benzodiazepine (BDZ) drug class; it differs from BDZs in having a benzene ring replaced with a thiophene ring. It is an agonist at GABA-A receptors and possesses amnesic, anxiolytic, anticonvulsant, hypnotic, sedative and skeletal muscle relaxant properties. Initially introduced in 1983 in Japan as treatment for neurological conditions such as anxiety and sleep disorders, etizolam is marketed in Japan, Italy and India. It is not approved for use by FDA in the US; however it remains unscheduled in several states and is legal for research purposes. Indicated for the treatment of generalized anxiety disorder with depression, panic disorder and insomnia. Etizolam is a CNS depressant with anxiolytic, anticonvulsant, sedative-hypnotic and muscle relaxant effects. It acts on the benzodiazepine site of the GABA-A receptor as an agonist to increase inhibitory GABAergic transmission throughout the central nervous system. Studies indicate that etizolam mediates its pharmacological actions with 6 to 10 times more potency than that of diazepam. Clinical human studies performed in Italy showed clinical effectiveness of etizolam in relieving symptoms in patients with generalized anxiety disorders with depressive symptoms. Etizolam also mediates imipramine-like neuropharmacological and behavioral effects, as well as minor effects on cognitive functioning. It is shown to substitute the actions of a short-acting barbiturate, pentobarbitol, in a drug discrimination study.  Etizolam is selectively a full agonist at GABA-A receptors to increase GABAergic transmission and enhance GABA-induced Cl- currents. It is reported to bind to the benzodiazepine binding site which is located across the interface between the alpha and gamma subunits. Benzodiazapines are reported to only bind to receptors that contain gamma 2 and alpha 1/2/3/5 subunits. Alpha-1-containing receptors mediate the sedative effects of etizolam whereas alpha-2 and alpha-3 subunit-containing receptors mediate the anxiolytic effect. Etizolam shows high potency and affinity towards GABA-A receptor with alpha 1 beta 2 gamma 2S subunit combination. By binding to the regulatory site of the receptor, etizolam potentiates GABA transmission by facilitating the opening of GABA-induced chloride channels.",The molecular weight is 342.85.,Etizolam has a topological polar surface area of 43.07.,The log p value of  is 2.87.,Etizolam is experimental.,Etizolam is a solid.,True
15624,Netoglitazone (MCC-555) is a hypoglycemic agent.,,,,Netoglitazone is experimental.,Netoglitazone is a solid.,True
15625,Rivoglitazone (INN) is a thiazolidinedione undergoing research for use in the treatment of type 2 diabetes. It is being developed by Daiichi Sankyo Co.,,,,Rivoglitazone is experimental and investigational.,Rivoglitazone is a solid.,True
15626,"Developed by Takeda Pharmaceuticals in the early 1980s, it is considered the prototypical compound for the thiazolidinedione class.",,,,Ciglitazone is experimental.,Ciglitazone is a solid.,True
15627,"Tolfenamic acid, with the formula N-(2-methyl-3-chlorphenyl)-anthranilic acid, is a nonsteroidal anti-inflammatory agent. It was discovered by scientists at Medica Pharmaceutical Company in Finland. It is used in the UK as a treatment for migraine under the name of Clotam. In the US, it presents a Status class I by the FDA. By the European Medicine Agency, it was granted in 2016 with the status of orphan for the treatment of supranuclear palsy. In the information for tolfenamic acid, it is stated that this drug, being an NSAID, is effective in treating the pain associated with the acute attack of migraines in adults. Studies have shown that tolfenamic acid presents a non-dose dependent partial inhibition of irritant-induced temperature rise as well as a dose-dependent inhibition of skin edema. By studying its NSAID properties more closely, it was noted a dose-related inhibition of serum thromboxane which indicated the inhibition of COX-1. In the same line, there was noted a inhibition of prostaglandin E2 synthesis which marks a related COX-2 inhibition. The maximal inhibition of thromboxane was greater than 80% as well as is proven to be a potent prostaglandin E inhibitor. Tolfenamic acid inhibits the biosynthesis of prostaglandins, and it also presents inhibitory actions on the prostaglandin receptors. As commonly thought, the mechanism of action of tolfenamic acid is based on the major mechanism of NSAIDs which consists of the inhibition of COX-1 and COX-2 pathways to inhibit prostaglandin secretion and action and thus, to exert its anti-inflammatory and pain-blocking action. Nonetheless, some report currently indicates that tolfenamic acid inhibits leukotriene B4 chemotaxis of human polymorphonuclear leukocytes leading to an inhibition of even 25% of the chemotactic response. This activity is a not ligand specific additional anti-inflammatory mechanism of tolfenamic acid.",The molecular weight is 261.71.,Tolfenamic acid has a topological polar surface area of 49.33.,The log p value of  is 5.51.,Tolfenamic acid is approved and investigational.,Tolfenamic acid is a solid.,True
15628,"Barnidipine is a long-acting novel calcium antagonist that belongs to the dihydropyridine (DHP) group of calcium channel blockers. Used in the treatment of hypertension, barnidipine displays high affinity for the calcium channels of the smooth muscle cells in the vascular wall and selectivity against cardiovascular L-type calcium channels. Barnidipine contains two chiral centres thus can have four possible enantiomers. The active component is composed of a single optical isomer (*3'S, 4S* configuration), which is the most potent and longest-acting of the four enantiomers. Compared to several other calcium antagonists which are racemates, the barnidipine compound consisting of a single enantiomer may offer a high degree of pharmacological selectivity. Indicated for the treatment of mild to moderate essential hypertension and management of chronic stable angina. Barnidipine reduces peripheral resistance and lowers blood pressure. The chronic use of the drug is not reported to lead to an increase in basic heart frequency. The antihypertensive effects of barnidipine are reported to remain during the entire 24-hour dose interval. Barnidipine does not exert any negative effect on serum lipids profile, glucose level or blood electrolytes.  Barnidipine is a lipophilic 1,4-dihydropyridine calcium antagonist that is characterized by a slow onset of action and a strong and long-lasting binding to the L-type calcium channels. It displays high affinity for the channels expressed in the smooth muscle cells in the vascular wall. Its main mechanism of action arises from the reduction of peripheral vascular resistance secondary to its vasodilatory actions. ",The molecular weight is 491.54.,Barnidipine has a topological polar surface area of 111.01.,The log p value of  is 5.15.,Barnidipine is experimental.,Barnidipine is a solid.,True
15629,"Azelnidipine is a dihydropyridine calcium channel blocker. It is marketed by Daiichi-Sankyo pharmaceuticals, Inc. in Japan. It has a gradual onset of action and produces a long-lasting decrease in blood pressure, with only a small increase in heart rate, unlike some other calcium channel blockers. It is currently being studied for post-ischemic stroke management. For the treatment of hypertension.  Azelnidipine is a vasodilator that induces a gradual decrease in blood pressure in hypertensive patients. Unlike other members of its drug class, azelnidipine does not induce reflex tachycardia due to vasodilation. This is likely due to the fact that it elicits a gradual fall in blood pressure Azelnidipine inhibits trans-membrane Ca2+ influx through the voltage-dependent channels of smooth muscles in vascular walls. Ca2+ channels are classified into various categories, including L-type, T-type, N-type, P/Q-type, and R-type Ca2+ channels. The L-type Ca2+ channels.  Normally, calcium induces smooth muscle contraction, contributing to hypertension. When calcium channels are blocked, the vascular smooth muscle does not contract, resulting in relaxation of vascular smooth muscle walls and decreased blood pressure.",The molecular weight is 582.66.,Azelnidipine has a topological polar surface area of 137.03.,The log p value of  is 6.96.,Azelnidipine is investigational.,Azelnidipine is a solid.,True
15630,"Cilnidipine is a dihydropyridine calcium antagonist. It was jointly developed by Fuji Viscera Pharmaceutical Company, Japan and Ajinomoto, Japan and approved in 1995. Compared with other calcium antagonists, cilnidipine can act on the N-type calcium channel that existing sympathetic nerve end besides acting on L-type calcium channel that similar to most of the calcium antagonists. This drug is approved in China, Japan, Korea, India, and several countries in the European Union. Cilnidipine is indicated for the management of hypertension for end-organ protection. It is reported to be useful in elderly patients and in those with diabetes and albuminuria. Cilnidipine has been increasingly used in patients with chronic kidney disease  Administration of cilnidipine has been shown to present an antisympathetic profile in vitro and in vivo. It decreases blood pressure safely and effectively without excessive blood pressure reduction or tachycardia. Cilnidipine acts on the L-type calcium channels of blood vessels by blocking the incoming calcium and suppressing the contraction of blood vessels, thereby reducing blood pressure. Cilnidipine also works on the N-type calcium channel located at the end of the sympathetic nerve, inhibiting the emission of norepinephrine and suppressing the increase in stress blood pressure.",The molecular weight is 492.53.,Cilnidipine has a topological polar surface area of 117.0.,The log p value of  is 5.54.,Cilnidipine is investigational.,Cilnidipine is a solid.,True
15631,Darodipine is a calcium channel blocker.,,,,Darodipine is experimental.,Darodipine is a solid.,True
15632,"Efonidipine is a calcium channel blocker of the _dihydropyridine class_, commercialized by Shionogi & Co. (Japan). Initially, it was marketed in 1995 under the trade name, _Landel_. The drug has been shown to block T-type in addition to L-type calcium channels. It has also been studied in atherosclerosis and acute renal failure. This drug is also known as NZ-105, and several studies have been done on its pharmacokinetics in animals. For the treatment of hypertension. Dihydropyridines (DHPs), act mainly on L-type calcium channels, essentially causing reflex tachycardia, which negatively affects cardiac function. This leads to a decrease in blood pressure and an increase in heart rate. Efonidipine acts on both L-type and T-type calcium channels. Because inhibition of T-type calcium channels in the sinoatrial (SA node) node attenuate reflex tachycardia, this drug favorably affects cardiac pacing. The effect of efonidipine on heart rate deserves special recognition with regard to reflex tachycardia, due to its unique effects in relation to other drugs in its class. This drug inhibits the L-type and T-type calcium channels, thereby leading to vasodilation and decreased automaticity of the heart. Efonidipine exerts negative chronotropic effects, decreasing heart rate. Acting on SA node cells by inhibiting T-type calcium channel activity, Efonidipine prolongs the late phase-4 depolarization of the sinoatrial node action potential, decreasing heart rate. This is associated with decreased myocardial oxygen demand and increases of blood flow to the coronary arteries and thereby attenuates myocardial ischemia. Efonidipine increases glomerular filtration rate (GFR) without increasing intra-glomerular pressure and filtration fraction. This increase leads to the prevention of renal damage that is normally associated with hypertension.",The molecular weight is 631.67.,Efonidipine has a topological polar surface area of 120.24.,The log p value of  is 6.54.,Efonidipine is experimental.,Efonidipine is a solid.,True
15633,Niguldipine is a calcium channel blocker drug (CCB) with a1-adrenergic antagonist properties.,,,,Niguldipine is experimental.,Niguldipine is a solid.,True
15634,Niludipine is a calcium channel blocker.,,,,Niludipine is experimental.,Niludipine is a solid.,True
15635,"Tianeptine is a drug used primarily in the treatment of major depressive disorder and has been studied in the treatment of irritable bowel syndrome (IBS). Structurally, it is classified as a tricyclic antidepressant (TCA), however, it possesses different pharmacological properties than typical tricyclic antidepressants. Used primarily in the treatment of major depressive disorder and anxiety. It is currently being studied for fibromyalgia pain treatment. Recent studies suggest that tianeptine acts as a full agonist at the mu-type opioid receptor (MOR) ,.  The mu opioid receptors are currently being studied as effective targets for antidepressant therapies. It is believed that the clinical effects of tianeptine are owed to its modulation of these receptors. In addition to its actions on the opioid receptor, previous studies have owed its action to its effect on the serotonin receptor , , dopamine (D2/3) receptors , and glutamate receptors , , as discussed below:",The molecular weight is 436.95.,Tianeptine has a topological polar surface area of 86.71.,The log p value of  is 1.52.,Tianeptine is investigational.,Tianeptine is a solid.,True
15636,Solithromycin is a ketolide antibiotic undergoing clinical development for the treatment of community-acquired pneumonia (CAP) and other infections. Investigated for the treatment of community-acquired pneumonia (CAP).,,,,Solithromycin is investigational.,Solithromycin is a solid.,True
15637,Kitasamycin is a macrolide antibiotic derived from <em>Streptomyces kitasatoensis</em>.,,,,Kitasamycin is experimental.,Kitasamycin is a solid.,True
15638,"A synthetic progestational hormone with actions and uses similar to those of PROGESTERONE. It has been used in the treatment of functional uterine bleeding and endometriosis. As a contraceptive, it has usually been administered in combination with MESTRANOL.",The molecular weight is 298.43.,Norethynodrel has a topological polar surface area of 37.3.,The log p value of  is 2.65.,Norethynodrel is approved.,,True
15639,A synthetic glucocorticoid with anti-inflammatory properties.,The molecular weight is 378.44.,Fluprednisolone has a topological polar surface area of 94.83.,The log p value of  is 1.47.,Fluprednisolone is approved.,,True
15640,"Dihydroergocornine is one of the dihydrogenated ergot compounds that present very large hypotensive effects. It is an artificial derivative of the crude extract of ergot and later purified, ergocornine. The formation of dihydroergocornine implies the hydrogenation of the double bonds in the lysergic acid. Dihydroergocornine presents a formula of 9,10 alpha-dihydro-12'-hydroxy-2',5'alpha-bis(1-methylethyl)-ergotaman-3',6',18-trione. It is found as one of the components in the ergoloid mesylate mixture. To know more about this mixture please refer to  To know more about the approved indications please visit  It is reported that dihydroergocornine administration, in non-toxic doses, presents sympatholytic and hypotensive properties which are observed as a significantly decreased mean arterial pressure. In the brain, the activity of dihydroergocornine was observed as a decrease in cerebral blood flow, cerebral vascular resistance and oxygen uptake. The effect in the brain seems to allow a cerebral metabolic homeostasis. To know more about the pharmacology please visit  The mechanism of action by which dihydroergocornine exerts its effects are not entirely defined. However, it is reported that dihydroergocornine has central and peripheral effects. The fall in blood pressure seems to be related to the stimulation of the vasodilator center. It has been demonstrated that dihydroergocornine possesses potent adrenolytic and sympathicolytic actions. The effect of dihydroergocornine is related to the inhibitory effect against the serotonin and noradrenaline receptors in which dihydroergocornine seems to be very potent against a stimulation-induced noradrenaline overflow. It also presents a stimulatory effect in arterial and venous smooth muscle when administered at slightly higher concentrations than the necessary for the inhibitory effect.",The molecular weight is 563.7.,Dihydroergocornine has a topological polar surface area of 118.21.,The log p value of  is 5.07.,Dihydroergocornine is approved.,Dihydroergocornine is a solid.,True
15641,"Alpha-dihydroergocryptine is usually referred to the mixture of the alpha and beta dihydroergocryptine. These two compounds are differentiated in the position of a methyl group. This structural difference is due to a proteinogenic amino acid replacement from leucine to isoleucine. Both compounds are hydrogenated ergot derivatives. Alpha-dihydroergocryptine approved drug product is as a part of an ergoloid mixture. To know more about this mixture, please visit  Alpha-dihydroergocryptine has been studied for the early treatment of Parkinson disease as well as for its use in migraine prophylaxis, treatment of low blood pressure and peripheral vascular disorder. To know more about the ergoloid mesylate mixture and its uses please visit. The effect of alpha-dihydroergocryptine in dopamine receptors was tested in PD patients and seem to generate a significant clinical improvement in the tested patients as well as to reduce motor complications and side effects. In long-term clinical trials with Parkinson disease patients, the administration of alpha-dihydroergocryptine and levodopa, the symptoms were reposted to improve or completely vanish in 80% of the tested individuals. All the registered effects of alpha-dihydroergocryptine suggest a potential neuroprotective effect of this drug and some reports have indicated that this activity may be related to the activation of NF-kB. The effect of alpha-dihydroergocryptine in the dopamine D2 receptor also reduces prolactin plasma levels and induce hypotension. To know more about the ergoloid mesylate mixture please visit. Alpha-dihydroergocryptine is an established high-affinity ligand to alpha 1 and alpha 2 adrenoreceptors in a number of tissues as well as a dopamine ligand in the brain. It is reported to be a potent agonist of the dopamine D2 receptor and a partial agonist of the dopamine receptors D1 and D3. To know more about the ergoloid mesylate mixture please visit and to know more about the isomer please visit.",The molecular weight is 577.73.,Dihydro-alpha-ergocryptine has a topological polar surface area of 118.21.,The log p value of  is 5.6.,Dihydro-alpha-ergocryptine is approved.,Dihydro-alpha-ergocryptine is a solid.,True
15642,"Selexipag was approved by the United States FDA on December 22, 2015 for the treatment of pulmonary arterial hypertension (PAH) to delay disease progression and reduce risk of hospitalization. PAH is a relatively rare disease with usually a poor prognosis requiring more treatment options to prolong long-term outcomes. Marketed by Actelion Pharmaceuticals under brand name Uptravi, selexipag and its active metabolite, ACT-333679 (MRE-269), act as agonists of the prostacyclin receptor to increase vasodilation in the pulmonary circulation and decrease elevated pressure in the blood vessels supplying blood to the lungs. Selexipag is indicated for the treatment of pulmonary arterial hypertension (PAH) to delay disease progression and reduce risk of hospitalization. At the maximum tolerated dose of 1600 mcg twice per day, selexipag was not found to prolong the QT interval to a clinically relevant extent. Both selexipag and its metabolite caused concentration-dependent inhibition of platelet aggregation in vitro with IC50 of 5.5 µM and 0.21 µM, respectively. However, at clinically relevant concentrations, there was no effect on platelet aggregation test parameters following multiple dose administration of selexipag in healthy patients.  Selexipag is a selective prostacyclin (IP, also called PGI2) receptor agonist. The key features of pulmonary arterial hypertension include a decrease in prostacyclin and prostacyclin synthase (enzyme that helps produce prostacyclin) in the lung. Prostacyclin is a potent vasodilator with anti-proliferative, anti-inflammatory, and anti-thrombotic effects; therefore, there is strong rationale for treatment with IP receptor agonists. Selexipag is chemically distinct as it is not PGI2 or a PGI2 analogue and has high selectivity for the IP receptor. It is metabolized by carboxylesterase 1 to yield an active metabolite (ACT-333679) that is approximately 37 times more potent than selexipag. Both selexipag and its metabolite are selective for the IP receptor over other prostanoid receptors. ",The molecular weight is 496.63.,Selexipag has a topological polar surface area of 101.49.,The log p value of  is 4.18.,Selexipag is approved.,Selexipag is a solid.,True
15643,"Carbomycin, also called magnamycin, is crystalline macrolide antibiotic. This antibacterial is obtained from _Streptomyces halstedii_ and it presents a large inhibitory effect against Gram-positive bacteria and some Mycoplasma strains. The structure of carbomycin was generated in 1957 by Robert Woodward and later modified in 1965.",,,,Carbomycin is vet_approved.,,True
15644,"Doramectin is a veterinary drug approved by the Food and Drug Administration for the treatment of parasites such as gastrointestinal roundworms, lungworms, eyeworms, grubs, sucking lice and mange mites in cattle.",,,,Doramectin is vet_approved.,,True
15645,,,,,Eprinomectin is vet_approved.,,False
15646,"Oleandomycin is a macrolide antibiotic, though it is less effective than erythromycin. It is synthesized from strains of _Streptomyces antibioticus_.",The molecular weight is 687.87.,Oleandomycin has a topological polar surface area of 165.98.,The log p value of  is 1.59.,Oleandomycin is vet_approved.,,True
15647,"Selamectin is a topical parasiticide and antihelminthic used on dogs and cats to treat and prevent infections of heartworms, fleas, ear mites, sarcoptic mange, and certain types of ticks in dogs as well as prevent heartworms, fleas, ear mites, hookworms, and roundworms in cats. It also removes 2 types of lungworm in cats and one type of lungworm in dogs. It is distributed by Zoetis, a former Pfizer subsidiary. It is structurally related to ivermectin and milbemycin. Selamectin is not approved for human use.",,,,Selamectin is vet_approved.,,True
15648,Tildipirosin is a veterinary antibiotic.,,,,Tildipirosin is vet_approved.,,True
15649,Tilmicosin is a macrolide antibiotic. It is used in veterinary medicine for the treatment of bovine respiratory disease and ovine respiratory disease associated with _Mannheimia haemolytica_.,,,,Tilmicosin is investigational and vet_approved.,,True
15650,Tylosin is a bacteriostatic macrolide antibiotic and feed additive used in veterinary medicine. It has a broad spectrum of activity against Gram-positive organisms and a limited range of Gram-negative organisms. Tylosin is produced as a fermentation product of Streptomyces fradiae.,,,,Tylosin is vet_approved.,,True
15651,"Melengestrol is a steroidal progestin and antineoplastic agent which was never marketed. An acylated derivative, melengestrol acetate, is used as a growth promoter in animals.",,,,Melengestrol is vet_approved.,,True
15652,,,,,Tylvalosin is vet_approved.,,False
15653,"Lesinurad is an oral uric acid transporter 1 (URAT1) inhibitor indicated for the treatment of hyperuricemia associated with gout. It reduces serum uric acid concentration through the inhibition of URAT1, an enzyme responsible for reuptake of uric acid from the renal tubule, and OAT4, another uric acid transporter associated with diuretic-induced hyperuricemia. For use, in combination with a xanthine oxidase inhibitor, for the treatment of hyperuricemia associated with gout in patients who have not achieved target serum uric acid levels with a xanthine oxidase inhibitor alone. Dose-dependent reductions in serum uric acid levels and increases in urinary uric acid excretion have been observed following single and multiple oral doses of lesinurad. Lesinurad inhibits the activity of uric acid transporter 1 (URAT1) and organic anion transporter 4 (OAT4). URAT1 is a major transporter enzyme responsible for reuptake of uric acid from the renal tubules; inhibition of URAT1 function thereby increases excretion of uric acid. ",The molecular weight is 404.28.,Lesinurad has a topological polar surface area of 68.01.,The log p value of  is 4.01.,Lesinurad is approved and investigational.,Lesinurad is a solid.,True
15654,"Venetoclax is a BCL-2 inhibitor that was initially approved by the FDA in April 2016. Proteins in the B cell CLL/lymphoma 2 (BCL-2) family are important regulators of the apoptotic (programmed cell death) process ,. Venetoclax is used to treat chronic lymphocytic leukemia (CLL) and certain types of small lymphocytic lymphoma. CLL is the most prevalent leukemia diagnosed in Western countries. Venetoclax was developed through reverse engineering of the BCL-2 protein family inhibitor, navitoclax. Venetoclax is approximately 10 times more potent than navitoclax with regard to induction of apoptosis in CLL cells. A new indication was approved in 2018 for the treatment patients with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL), with or without 17p deletion, who have received at least one prior therapy. Previously, this drug was indicated only for patients with 17p gene deletion. A BCL-2 inhibitor indicated for the treatment of patients with chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL), with or without 17p deletion, who have received at least one prior therapy. Venetoclax induces rapid and potent onset apoptosis of CLL cells, powerful enough to act within 24h and to lead to tumor lysis syndrome , ,. Selective targeting of BCL2 with venetoclax has demonstrated a manageable safety profile and has been shown to induce significant response in patients with relapsed CLL (chronic lymphocytic leukemia) or SLL (small lymphocytic leukemia), including patients with poor prognostic features. This drug is not expected to have a significant impact on the cardiac QT interval. Venetoclax has demonstrated efficacy in various types of lymphoid malignancies, including relapsed/ refractory CLL harboring deletion 17p, with an overall response rate of approximately 80%. Proteins in the B cell CLL/lymphoma 2 (BCL-2) family are necessary regulators of the apoptotic (anti-cell programmed death) process. This family comprises proapoptotic and prosurvival proteins for various cells. Cancer cells evade apoptosis by inhibiting programmed cell death (apoptosis). The therapeutic potential of directly inhibiting prosurvival proteins was unveiled with the development of navitoclax, a selective inhibitor of both BCL-2 and BCL-2-like 1 (BCL-X(L)), which has demonstrated clinical efficacy in some BCL-2-dependent hematological cancers. Selective inhibition of BCL-2 by venetoclax, sparing BCL-xL enables therapeutic induction of apoptosis without the negative effect of thrombocytopenia ,.  Venetoclax helps restore the process of apoptosis by binding directly to the BCL-2 protein, displacing pro-apoptotic proteins, leading to mitochondrial outer membrane permeabilization and the activation of caspase enzymes. In nonclinical studies, venetoclax has shown cytotoxic activity in tumor cells that overexpress BCL-2.",The molecular weight is 868.45.,Venetoclax has a topological polar surface area of 172.03.,The log p value of  is 10.31.,Venetoclax is approved and investigational.,Venetoclax is a solid.,True
15655,"Velpatasvir is a Direct-Acting Antiviral (DAA) medication used as part of combination therapy to treat chronic Hepatitis C, an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Velpatasvir acts as a defective substrate for NS5A (Non-Structural Protein 5A), a non-enzymatic viral protein that plays a key role in Hepatitis C Virus replication, assembly, and modulation of host immune responses. Treatment options for chronic Hepatitis C have advanced significantly since 2011, with the development of Direct Acting Antivirals (DAAs) such as velpatasvir. Notably, velpatasvir has a significantly higher barrier to resistance than the first generation NS5A inhibitors, such as and , making it a highly potent and reliable alternative for treatment of chronic Hepatitis C.  Velpatasvir is used in combination therapy with other antiviral medications to treat chronic hepatitis C virus (HCV) infected patients with HCV genoptypes 1-6, and to treat HCV and HIV co-infected patients. Depending on the level of cirrhosis or decompensation, combination therapy can also include therapy with. Velpatasvir is a small molecule direct-acting antiviral used in the treatment of hepatitis C in combination with sofosbuvir. Velpatasvir prevents viral replication by inhibiting non-structural protein 5A (NS5A).  Velpatasvir's mechanism of action is likely similar to other selective NS5A inhibitors which bind domain I of NS5A consisting of amino acids 33-202. NS5A inhibitors compete with RNA for binding at this site. It is also thought that NS5A inhibitors bind the target during its action in replication when the binding site is exposed. Inhibition of NS5A is also known to produce redistribution of the protein to lipid droplets. The exact role of NS5A in RNA replication is not yet understood although it is known to be an important component.",The molecular weight is 883.02.,Velpatasvir has a topological polar surface area of 193.1.,The log p value of  is 5.7.,Velpatasvir is approved and investigational.,Velpatasvir is a solid.,True
15656,"Gestrinone, also known as ethylnorgestrienone, is a synthetic steroid of the 19-nortestosterone group that is marketed in Europe, Australia, and Latin America, though not the United States or Canada, and is used primarily in the treatment of endometriosis. Endometriosis with or without accompanying sterility. Treatment is limited to a single course of 6 months duration per lifetime. Gestrinone is a synthetic steroidal hormone which has androgenic, anti-estrogenic and anti-progestogenic properties.  The findings of several studies suggest that gestrinone is as effective as danazol in the treatment of infertility associated with endometriosis and is better tolerated, in terms of adverse effects. ",The molecular weight is 308.42.,Gestrinone has a topological polar surface area of 37.3.,The log p value of  is 2.44.,Gestrinone is approved.,Gestrinone is a solid.,True
15657,"D-Alpha-tocopheryl polyethylene glycol 1000 succinate (Tocofersolan, Vedrop), has been developed in Europe as an orally bioavailable source of vitamin E in children suffering from cholestasis. Cholestasis is the reduction or stoppage of bile flow, either to impaired secretion by _hepatocytes_ (liver cells) or obstruction ,. Tocofersolan is indicated in vitamin E deficiency caused by digestive malabsorption in pediatric patients with congenital chronic cholestasis or hereditary chronic cholestasis from birth (full term newborns) up to 18 years of age. Vitamin E is a major lipo-soluble antioxidant in humans. It acts as a free radical chain breaking molecule, halting the peroxidation of polyunsaturated fatty acids and it plays an important role in maintaining both the stability and integrity of cell membranes.",,,,Tocofersolan is approved.,Tocofersolan is a solid.,True
15658,Nomegestrol is an ingredient in the EMA-authorised product Zoely.,The molecular weight is 328.45.,Nomegestrol has a topological polar surface area of 54.37.,The log p value of  is 2.72.,Nomegestrol is approved.,,True
15659,"Ribociclib is a selective cyclin-dependent kinase inhibitor, a class of drugs that help slow the progression of cancer by inhibiting two proteins called cyclin-dependent kinase 4 and 6 (CDK4/6). These proteins, when over-activated, can enable cancer cells to grow and divide too quickly. Targeting CDK4/6 with enhanced precision may play a role in ensuring that cancer cells do not continue to replicate uncontrollably. Ribociclib was approved by the U.S. FDA in March, 2017 as Kisqali. Kisqali (ribociclib) is a selective cyclin-dependent kinase inhibitor, a class of drugs that help slow the progression of cancer by inhibiting two proteins called cyclin-dependent kinase 4 and 6 (CDK4/6). These proteins, when over-activated, can enable cancer cells to grow and divide too quickly. Targeting CDK4/6 with enhanced precision may play a role in ensuring that cancer cells do not continue to replicate uncontrollably. Inhibition of cyclin-dependent kinase 4 and 6 (CDK4/6) may provide protection against oncogenic processes in specific tissue types. For example, CDK4 is not required for normal mammary tissue development based on knockout mouse studies, but it is needed for growth of Ras-induced mammary tumors, suggesting a potential therapeutic window for treatment with lower toxicity.",The molecular weight is 434.55.,Ribociclib has a topological polar surface area of 91.21.,The log p value of  is 1.8.,Ribociclib is approved and investigational.,,True
15660,Ebastine is under investigation for the treatment of Irritable Bowel Syndrome (IBS). Ebastine has been investigated for the treatment of Urticaria.,The molecular weight is 469.67.,Ebastine has a topological polar surface area of 29.54.,The log p value of  is 6.94.,Ebastine is approved and investigational.,,True
15661,Bryostatin 1 has been investigated for the treatment of HIV Infection and Alzheimer's Disease.,,,,Bryostatin 1 is investigational.,Bryostatin 1 is a solid.,True
15662,"Sarilumab is a fully human anti-IL-6R monoclonal IgG1 antibody that binds to both membrane bound and soluble interleukin 6 (IL-6) receptor forms, thus blocking the cis- and trans-inflammatory signalling cascades of IL-6. Sarilumab was developped by Sanofi and Regeneron Pharmaceuticals, Inc; it was US FDA-approved in May 2017 and followed by EU approval in June 2017 for the treatment of moderate to severe Rheumatoid Arthritis (RA) in combination with methotrexate. RA is a chronic inflammatory disease characterized by polyarthritis and its treatment has been challenged by the different response in every patient. Subcutaneous administration of Sarilumab has been shown to decrease acute-phase reactant levels and improve in clinical RA symptoms. Indicated for modere to severe reactive RA in adult patients who are irresponsive, respond inadequately or present intolerance to disease-modifying anti-rheumatic drugs (DMARDs) or tumor necrosis factor (TNF) antagonists. It is indicated to be used in combination with methotrexate (MTX) or as a monotherapy when there is intolerance to MTX or MTX administration is inappropriate. Single-dose subcutaneous administration of Sarilumab produced a rapid reduction of CRP levels, leading to normal levels after two weeks of treatment. Peak reduction in the absolute neutrophile count was observed after 3 to 4 days of treatment followed by a recovery to baseline levels. It is observed a decrease in fibrinogen and serum amyloid A as well as an increase in hemoglobin and serum albumin.  Sarilumab is a human recombinant IgG1 antibody that binds to both forms of interleukin 6 receptors (IL-6R), thus inhibiting the IL-6-mediated signaling. IL-6 is known to be a pleiotropic cytokine that activates immune cells (T and B cells), as well as hepatocytes for the release of acute phase proteins like CRP, serum amyloid A and fibrinogen which are biomarkers of RA activity. IL-6 is also found in synovial fluid and plays a major role in the pathological inflammation and joint destruction features of RA. Thus, it is used for the treatment of RA due to its ability to inhibit intra-articular and systemic IL-6 signaling.",,,,Sarilumab is approved and investigational.,Sarilumab is a solid.,True
15663,"Danoprevir has been used in trials studying the treatment of Hepatitis C, Chronic. Danoprevir is a NS3/4A protease inhibitor. The HCV NS3/4A protease is an attractive drug target because of its potential involvement in viral replication and suppressive effects on host response to viral infection. Inhibitors of the HCV protease, such as Danoprevir, represent a promising new class of drugs for HCV.",,,,Danoprevir is investigational.,,True
15664,"Bictegravir is a recently approved investigational drug that has been used in trials studying the treatment of HIV-1 and HIV-2 infection. It has been approved for HIV-1 monotherapy combined with 2 other antiretrovirals in a single tablet. Bictegravir is indicated in the management of HIV-1 infection in patients not previously treated with antiretroviral therapy. Additionally, Bictegravir is indicated in the management of HIV-1 infection in patients who are virologically suppressed (HIV-1 RNA <50 c/mL) on a regular antiretroviral regimen for a minimum of three months without a history of failure in treatment and no known factors associated with the resistance to the individual components of the medication. It is used in combination with tenofovir and emtricitabine. Bictegravir is an HIV-1 integrase strand transfer inhibitor (INSTI). Bictegravir (BIC) inhibits HIV-1 virus replication into the human genome. It can be taken once daily without additional dosing. Bictegravir (BIC) inhibits strand transfer of viral DNA into the host genome and thereby prevents HIV-1 replication.  This single dose medication inhibits the strand transfer of viral DNA into the human genome, preventing HIV-1 virus replication and propagation.",The molecular weight is 449.39.,Bictegravir has a topological polar surface area of 99.18.,The log p value of  is -0.01.,Bictegravir is approved and investigational.,Bictegravir is a solid.,True
15665,"Saracatinib has been investigated for the treatment of Cancer, Osteosarcoma, Ovarian Cancer, Fallopian Tube Cancer, and Primary Peritoneal Cancer.",,,,Saracatinib is investigational.,,True
15666,"Baricitinib is a selective and reversible Janus kinase 1 (JAK1) and 2 (JAK2) inhibitor. Janus kinases belong to the tyrosine protein kinase family and play an important role in the proinflammatory pathway signalling that is frequently over-activated in autoimmune disorders such as rheumatoid arthritis. By blocking the actions of JAK1/2, baricitinib disrupts the activation of downstream signalling molecules and proinflammatory mediators.  Indicated for the treatment of moderate to severe active rheumatoid arthritis in adult patients who have responded inadequately to, or who are intolerant to one or more disease-modifying anti-rheumatic drugs as monotherapy or in combination with methotrexate. JAK enzymes are part of the family of tyrosine kinases that constitutively bind to the intracellular domains of cytokine receptors and promote the signalling cascades of cytokines and growth factors involved in haematopoiesis, inflammation and immune function that are also implicated in the pathogenesis of rheumatoid arthritis. Circulating proinflammatory cytokines bind to these cell surface receptors. Upon binding of extracellular cytokines and growth factors, JAKs are phosphorylated and activate signal transducers and activators of transcription (STATs). Through the signalling cascades, inflammatory cytokine and chemokine transcription is induced to form inflammatory mediators including IL-2, IL-6, IL-12, IL-15, IL-23, IFN-γ and GM-CSF. ",The molecular weight is 371.42.,Baricitinib has a topological polar surface area of 120.56.,The log p value of  is 0.41.,Baricitinib is approved and investigational.,Baricitinib is a solid.,True
15667,"Major depressive disorder (MDD) is a significant cause of disability worldwide and the most common illness preceding suicide ,. On March 5, 2019, the nasal spray drug, _esketamine_, also known as _Spravato_ (by Janssen Pharmaceuticals), was approved by the FDA for treatment-resistant major depression.  This drug is indicated in conjunction with an oral antidepressant for the treatment of treatment-resistant depression (TRD) in adults. **General effects** Esketamine, the S-enantiomer of racemic ketamine, is a non-selective, non-competitive antagonist of the N-methyl-D-aspartate (NMDA) receptor, an ionotropic glutamate receptor. The exact mechanism by which esketamine acts as an antidepressant is unknown. The primary circulating metabolite of esketamine (_noresketamine_) shows activity at the same receptor with a weaker affinity. ",The molecular weight is 237.73.,Esketamine has a topological polar surface area of 29.1.,The log p value of  is 2.93.,Esketamine is approved and investigational.,Esketamine is a solid.,True
15668,"Apalutamide is a potent androgen receptor (AR) antagonist that selectively binds to the ligand-binding domain of AR and blocks AR nuclear translocation or binding to androgen response elements. It has been used in trials studying the treatment of Prostate Cancer, Hepatic Impairment, Prostatic Neoplasms, Castration-Resistant Prostate Cancer, and Prostatic Neoplasms, Castration-Resistant, among others. Exerting an antitumor action, apalutamide blocking the effect of androgens that promote tumor growth. It targets the AR ligand-binding domain and prevents AR nuclear translocation, DNA binding, and transcription of AR gene targets in prostate tumors. In mice bearing human CRPC xenograft models, apalutamide treatment produced tumor regressions in a dose-dependent manner that was more effective than that of or. Unlike bicalutamide, apalutamide antagonized AR-mediated signaling in AR overexpressing human CRPC cell lines. Indicated for the treatment of patients with non-metastatic, castration-resistant prostate cancer (NM-CRPC). In an open-label, uncontrolled, multi-center, single-arm dedicated QT study in 45 patients with CRPC, an exposure-QT analysis suggested a concentration-dependent increase in QTcF for apalutamide and its active metabolite. Apalutamide demonstrated an antitumor activity in the mouse xenograft models of prostate cancer, where it decreased tumor cell proliferation and reduced tumor volume. Persistent androgen receptor (AR) signaling is a common feature of castration-resistant prostate cancer (CRPC), attributed to AR gene-amplification, AR gene mutation, increased AR expression or increased androgen biosynthesis in prostate tumors. Apalutamide is an antagonist of AR that to the binding-site in the ligand-binding domain of the receptor with the IC50 of 16 nM. Upon binding, apalutamide disrupts AR signalling, inhibits DNA binding, and impedes AR-mediated gene transcription. Apalutamide impairs the translocation of AR from the cytoplasm to the nucleus thus reduces the concentrations of AR available to interact with the androgen response-elements (AREs). Upon treatment with apalutamide, AR was not recruited to the DNA promoter-regions. ",The molecular weight is 477.44.,Apalutamide has a topological polar surface area of 89.33.,The log p value of  is 2.14.,Apalutamide is approved and investigational.,Apalutamide is a solid.,True
15669,"6-O-benzylguanine has been used in trials studying the treatment of HIV Infection, Adult Gliosarcoma, Adult Glioblastoma, Stage I Adult Hodgkin Lymphoma, and Stage II Adult Hodgkin Lymphoma, among others.",,,,6-O-benzylguanine is investigational.,,True
15670,"Selinexor is a first-in-class selective inhibitor of nuclear transport (SINE) compound. It is currently approved for the treatment of multiple myeloma, a cancer which forms from antibody-producing plasma cells. This condition is typically treated with high dose and dexamethasone chemotherapy followed by autologous stem-cell transplant. Other chemotherapies for multiple myeloma include and , , and may include if the patient is not eligible for transplant. Selinexor was approved by the FDA in June 2019. It was granted fast track and orphan designation as well as accelerated approval based on single arm, open label trial data. The Bortezomib, Selinexor, and Dexamethasone in Patients With Multiple Myeloma (BOSTON) trial is planned to finish in 2020. Selinexor is indicated for the treatment of relapsed or refractory multiple myeloma in combination with dexamethasone. Patients must have received at least 4 prior therapies and have disease which is refractory to least two proteasome inhibitors, at least two immunomodulatory agents, and an anti‐CD38 monoclonal antibody. Selinexor causes cell cycle arrest and apoptosis in cancer cells. Selinexor binds to and inhibits exportin-1 (XPO1). XPO1 is a nuclear exporter protein which contains a pocket to which nuclear proteins can bind. When complexed with these proteins and Ran, activated through guanosine triphosphate (GTP) binding, the XPO1-protein-Ran-GTP complex is able to exit the nucleus through a nuclear pore. Once outside, GTP is hydrolyzed and the complex dissociates. The inhibition of this process in cancer cells allows the targets of XPO1, many of which are tumor suppressors, to collect in the nucleus and result in increased transcription of tumor suppressor genes. Tumor suppressor proteins known to be affected by XPO1 inhibition include p53, p73, adenomatous polyposis coli, retinoblastoma, forkhead box protein O, breast cancer 1, nucleophosmin, and merlin. Regulators of cell cycle progression are also affected, namely p21, p27, galectin-3, and Tob. Inhibitor of NFκB also collects in the nucleus as a result leading to reduced activity of NFκB, a known contributor to cancer. XPO1 participates in the formation of a complex with eukaryotic initiation factor 4E and contributes to the transport of messenger RNA for several oncegenes including cell cycle promotors, cyclin D1, cyclin E, and CDK2/4/6, as well as antiapoptotic proteins, Mcl-1 and Bcl-xL. These wide ranging changes in protein expression and gene transcription culminate in cell cycle arrest and the promotion of apoptosis in cancer cells.",,,,Selinexor is approved and investigational.,Selinexor is a solid.,True
15671,"Duvelisib, also known as IPI-145 and INK-1197, is a small-molecule inhibitor of phosphoinositide-3 kinases that was designed initially to prove that simultaneous inhibition of the isoforms delta and gamma can produce a broad adaptative and innate immune cell inhibitory activity. All the work around duvelisib showed that this agent is a potent inhibitor of both forms. Duvelisib was developed by Verastem, Inc and FDA approved on September 24, 2018. Duvelisib is indicated for the treatment of adult patients with relapsed or refractory chronic lymphocytic leukemia (CLL) or small lymphocytic lymphoma (SLL) after at least two prior therapies. Preclinical data showed that duvelisib presents cytotoxic actions at micromolar doses and antagonizes the activation of downstream signaling even in the presence of the mutation BTK C481S, which allows for the treatment of patients resistant to ibrutinib. Duvelisib acts as a strong reversible inhibitor of the isoform gamma and delta of the phosphoinositide3-kinase (PI3K). PI3K plays a very important role in innate and adaptative immunity and the inhibition of the form delta and gamma has been very important for the suppression of immunity.",,,,Duvelisib is approved and investigational.,Duvelisib is a solid.,True
15672,"Carboxyamidotriazole has been used in trials studying the treatment of Lymphoma, Lung Cancer, Breast Cancer, Kidney Cancer, and Ovarian Cancer, among others.",,,,Carboxyamidotriazole is investigational.,,True
15673,"Entrectinib is a tropomyosin receptor tyrosine kinase (TRK) TRKA, TRKB, TRKC, proto-oncogene tyrosine-protein kinase ROS1, and anaplastic lymphoma kinase (ALK) inhibitor. It was approved by the FDA in August 2019 for use in the treatment of ROS1-positive metastatic non-small cell lung cancer and NTRK gene fusion positive solid tumors. Entrectinib's approved use is meant as a last line of therapy due to its accelerated approval based on early trial data. This therapy offers benefit over similar ALK inhibitors such as , , and due to a wider range of targets. Entrectinib is indicated for the treatment of metastatic ROS1-positive non-small cell lung cancer in adults. Entrectinib is also indicated in adults and children over 12 years old for the treatment of NTRK gene fusion-positive solid tumors which have metastasized or for which surgical resection is likely to result in severe morbidity and for which has progressed on previous therapies or for which no comparable alternative therapies are available. Entrectinib and its active metabolite suppress several pathways which contribute to cell survival and proliferation. This suppression shifts the balance in favor of apoptosis thereby preventing cancer cell growth and shrinking tumors. Entrectinib is a tyrosine kinase inhibitor which acts on several receptors. It functions as an ATP competitor to inhibit tropomyosin receptor tyrosine kinases (TRK) TRKA, TRKB, TRKC, as well as proto-oncogene tyrosine-protein kinase ROS1 and anaplastic lymphoma kinase (ALK). TRK receptors produce cell proliferation via downstream signalling through the mitogen activated protein kinase, phosphoinositide 3-kinase, and phospholipase C-γ. ALK produces similar signalling with the addition of downstream JAK/STAT activation. Inhibition of these pathways suppresses cancer cell proliferation and shifts the balance in favor of apoptosis resulting in shrinking of tumor volume.",,,,Entrectinib is approved and investigational.,Entrectinib is a solid.,True
15674,"Fostamatinib has been investigated for the treatment and basic science of Rheumatoid Arthritis and Immune Thrombocytopenic Purpura (ITP). It was approved on April 17, 2018 under the trade name Tavalisse for use in ITP. Fostamatinib has also been granted orphan drug status by the FDA. Fostamatinib is indicated for use in the treatment of chronic immune thrombocytopenia (ITP) in patients who have had insufficient response to previous therapy. The active metabolite of fostamatinib, R406, inhibits signal transduction by Fcγ receptors involved in the antibody-mediated destruction of platelets by immune cells in chronic ITP. This results in increased platelet counts in this population. The active metabolite of fostamatinib, R406, is an inhibitor of spleen tyrosine kinase (Syk). It binds reversibly to the ATP binding pocket with high affinity (Ki = 30nM), inhibiting the kinase activity with an IC50 of 41nM.",,,,Fostamatinib is approved and investigational.,,True
15675,"Alpelisib is a phosphatidylinositol 3-kinase (PI3K) inhibitor with potent antitumor activity. It works by selectively inhibiting class I PI3K p110α , which is the catalytic subunit of PI3K, a lipid kinase that plays a role in various biological processes, including proliferation, survival, differentiation, and metabolism. Alpelisib was designed to target this enzyme that appears to be mutated at a rate of nearly 30% in human cancers, leading to hyperactivation.  Alpelisib is indicated in combination with fulvestrant to treat postmenopausal women, and men, with advanced or metastatic breast cancer. This cancer must be hormone receptor (HR)-positive, human epidermal growth factor receptor 2 (HER2)-negative, and PIK3CA­ mutated. The cancer must be detected by an FDA-approved test following progression on or after an endocrine-based regimen. Alpelisib does not prolong the QTcF interval. Patients taking alpelisib experience a dose dependent benefit from treatment with a 51% advantage of a 200mg daily dose over a 100mg dose and a 22% advantage of 300mg once daily over 150mg twice daily. This suggests patients requiring a lower dose may benefit from twice daily dosing. Phosphatidylinositol-3-kinase-α (PI3Kα) is responsible for cell proliferation in response to growth factor-tyrosine kinase pathway activation. In some cancers PI3Kα's p110α catalytic subunit is mutated making it hyperactive. Alpelisib inhibits (PI3K), with the highest specificity for PI3Kα.",,,,Alpelisib is approved and investigational.,Alpelisib is a solid.,True
15676,"Lorvotuzumab mertansine has been used in trials studying the treatment of SCLC, Leukemia, Ovarian Cancer, Multiple Myeloma, and Merkel Cell Carcinoma, among others.",,,,Lorvotuzumab mertansine is investigational.,,True
15677,Naftopidil has been investigated for the treatment of Disorder of Urinary Stent.,The molecular weight is 392.5.,Naftopidil has a topological polar surface area of 45.17.,The log p value of  is 4.43.,Naftopidil is investigational.,,True
15678,Tetrahydropalmatine is under investigation in clinical trial NCT02118610 (Treatment of Schizophrenia With L-tetrahydropalmatine (l-THP): a Novel Dopamine Antagonist With Anti-inflammatory and Antiprotozoal Activity).,,,,Tetrahydropalmatine is investigational.,,True
15679,Vinpocetine has been investigated for the treatment of Epilepsy.,The molecular weight is 350.46.,Vinpocetine has a topological polar surface area of 34.47.,The log p value of  is 4.83.,Vinpocetine is investigational.,,True
15680,"In early April of 2019, the US FDA approved Janssen Pharmaceutical Companies' brand name Balversa (erdafitinib) as the first-ever fibroblast growth factor receptor (FGFR) kinase inhibitor indicated for patients with locally advanced or metastatic urothelial carcinoma, with susceptible FGFR3 or FGFR2 genetic alterations, that has progressed during or following platinum-containing chemotherapy, including within 12 months of neoadjuvant or adjuvant platinum-containing chemotherapy. At the same time, the FDA also approved the therascreen FGFR RGQ RT-PCR Kit (Qiagen) for utilization as a companion diagnostic with erdafitinib for selecting patients for the indicated therapy. Erdafitinib is a pan-fibroblast growth factor receptor (FGFR) tyrosine kinase inhibitor that is indicated for the treatment of adult patients with locally advanced or metastatic urothelial carcinoma that has: Upon administration, it was observed that erdafitinib increased serum phosphate level as a consequence of FGFR inhibition. Erdafitinib should be increased to the maximum recommended dose to achieve target serum phosphate levels of 5.5– 7.0 mg/dL in early cycles with continuous daily dosing. Urothelial cancer is statistically the fourth most common kind of cancer in the world. In general, such urothelial cancers originate in the urothelium - or the transitional epithelium - a membrane that covers the renal pelvis to the ureter, the bladder, and the proximal two-thirds of the urethra. While 90 to 95% of urothelial cancers are bladder cancers and the other 5 to 10% are upper tract urothelial cancers, the bladder cancers can also be either superficial or invasive (either not having or having invaded the deeper layers of the bladder).",,,,Erdafitinib is approved and investigational.,Erdafitinib is a solid.,True
15681,"Polatuzumab vedotin is a CD79b specific antibody conjugated to the antineoplastic agent monomethyl auristatin E. This medication was granted accelerated FDA approval on 10 June 2019. This medication is indicated to treat adults with relapsed or refractory diffuse large B-cell lymphoma in combination with bendamustine and rituximab that has returned of progressed after 2 or more previous therapies. The binding of the unconjugated drug to microtubules in B cells leads to a number of immunosuppressant adverse effects including neutropenia and thrombocytopenia. Polatuzumab vedotin is an antibody targeted to CD79b conjugated to the antineoplastic agent monomethyl auristatin E (MMAE). The antibody binds to CD79b on the surface of B cells, causing the conjugate to be endocytosed. Once inside the cell, lysosomal proteases cleave the link between MMAE and the antibody allowing MMAE to bind to microtubules, inhibit cell division, and induce apoptosis.",,,,Polatuzumab vedotin is approved and investigational.,Polatuzumab vedotin is a solid.,True
15682,Epofolate has been used in trials studying the treatment of Advanced Solid Tumors.,,,,Epofolate is investigational.,,True
15683,"Brigatinib, originally named AP26113, is a reversible dual inhibitor of anaplastic lymphoma kinase (ALK) and epidermal growth factor receptor (EGFR). It presents selectivity against the mutant forms of EGFR compared to the wild-type. It also exhibits selectivity against 9 different Crizotinib-resistant mutants of the EML4-ALK fusion gene, which is a pivotal player in the transformation of susceptible lung parenchyma. Brigatinib was developed by Ariad Pharmaceuticals, a subsidiary of Takeda Pharmaceutical Company Limited, and FDA-approved on April 28, 2017. The anaplastic lymphoma kinase positive, metastatic non-small cell lung cancer (ALK+ NSCLC), represents only 3-5% of the NSCLC cancer cases, but the ALK mutation, overexpression and presence in several oncogenic fusion proteins in solid and hematologic tumors have pointed out the importance as well as its potential as a cancer therapy target. The ALK-related cases of NSCLC are associated with the presence of the fusion gene EML4-ALK which fused the ALK protein with the echinoderm microtubule-associated protein like-4 whose original function is the correct formation of microtubules. The presence of the aberrant fusion protein results in abnormal signaling that provokes increased cell growth, proliferation and survival. Crizotinib is indicated for the treatment of such cases but the presence of ALK kinase domain mutations confer resistance to the treatment. Thus, brigatinib is indicated for the treatment of patients with ALK+ NSCLC with intolerance to Crizotinib. Brigitanib inhibits proliferation and in vitro viability of cells expressing the fusion protein EML4-ALK as well as 17 crizotinib-resistant ALK mutants. Its action is expanded to cells expressing EGFR deletions, ROS1-L2026M, FLT3-F691L and FLT3-D835Y. Brigitanib presents a dose-dependent inhibition of tumor growth, tumor burden and prolonged survival in mice EML4-ALK xenograft models. Time course of Brigatinib and exposure-response studies are still unknown.  Brigitanib acts as a tyrosine kinase inhibitor with activity against multiple kinases including ALK, ROS1, insulin-like growth factor 1 receptor and against EGFR deletions and point mutations. It acts by inhibiting ALK phosphorylation and the activation of downstream signaling proteins.",The molecular weight is 584.1.,Brigatinib has a topological polar surface area of 85.86.,The log p value of  is 1.72.,Brigatinib is approved and investigational.,Brigatinib is a solid.,True
15684,"Propiverine is a widely used antimuscarinic drug with a mixed mode of action in the treatment of symptoms associated with overactive bladder (OAB). Indicated for symptomatic treatment of urinary incontinence and/or increased urinary frequency and urgency in patients with overactive bladder (OAB). Propiverine may also be used in patients with neurogenic bladder as a result of spinal cord injury. Propiverine demonstrates both anticholinergic and calcium-modulating properties. The efferent connection of the pelvic nerve is inhibited due to the anticholinergic action exerted by this drug, leading to relaxation of bladder smooth muscle. Propiverine blocks calcium ion influx and modulates the intracellular calcium in urinary bladder smooth muscle cells, resulting in the inhibition of muscle spasm. The bladder contains several muscarinic receptors. Acetylcholine is the main contractile neurotransmitter in the human bladder detrusor muscle, and antimuscarinics such as propiverine exert their effects by competitively inhibiting the binding of acetylcholine at muscarinic receptors on detrusor smooth muscle cells and other structures within the bladder wall. In one study, After oral treatment with propiverine, the bladder showed the highest concentration of M-2, indicating a targeted distribution of this metabolite into the bladder. Therefore, muscarinic receptor-2 may highly contribute to the relatively selective and long-lasting occupation of bladder muscarinic receptors after oral ingestion of propiverine.",The molecular weight is 367.49.,Propiverine has a topological polar surface area of 38.77.,The log p value of  is 3.79.,Propiverine is approved and investigational.,Propiverine is a solid.,True
15685,"Siponimod, also known as _Mayzent_, by Novartis, is a new drug formulated for the management of Multiple Sclerosis (MS). It was approved by the FDA on March 26, 2019 and by Health Canada on February 20, 2020. This drug is considered a _sphingosine-1-phosphate (S1P) receptor modulator_ and is thought to play a role in suppressing the central nervous system inflammation that is associated with MS. This drug is indicated for the treatment of relapsing forms of multiple sclerosis (MS), to include clinically isolated syndrome, relapsing-remitting disease, and active secondary progressive disease in adults. **Immune system effects** Inflammation of the white and gray matter tissues in the central nervous system caused by localized immune cell infiltration and their cytokines are the initial cause of damage in MS. B lymphocytes and their cytokines are other factors in the pathogenesis of MS. Lymphotoxin and TNF-α produced by these cells encourage inflammation. The S1P receptor is an important receptor related to the function of lymphocytes and can be found in the central nervous system. S1P receptor (S1PR) signaling is associated with a wide variety of physiological processes for lymphocytes, including their egress and recirculation. ",,,,Siponimod is approved and investigational.,Siponimod is a solid.,True
15686,"Sagopilone has been used in trials studying the treatment of Melanoma, Neoplasms, CNS Disease, Breast Cancer, and Breast Neoplasms, among others. It is a so-called fully synthetic epothilone and is the first such compound to be in clinical development to combat several forms of cancer. Epothilones are 16-member ring macrolides with antimicrotubule activity that share a similar mechanism of action to the taxanes but have demonstrated potent antiproliferative activity in several different multidrug-resistant and paclitaxel-resistant tumor cell lines in vitro and in vivo. Sagopilone is a highly potent, fully synthetic epothilone that was specifically designed to be safer and more effective than other chemotherapy drugs like paclitaxel and other epothilones for the treatment of solid tumor cancers. In early phase studies, Sagopilone appears to have greater antitumor activity relative to other epothilones, and appears to cross the blood-brain barrier which may help to treat brain tumors or metastases. Epothilones are a new class of cytotoxic agents that induce tubulin polymerization. Sagopilone, the only fully synthetic, third-generation analogue of epothilone B, is a highly potent tubulin stabilizer that has shown substantial preclinical antitumor activity, including against taxane-resistant models.",,,,Sagopilone is investigational.,,True
15687,"Rimegepant is an oral antagonist of the CGRP receptor developed by Biohaven Pharmaceuticals. It received FDA approval on February 27, 2020 for the acute treatment migraine headache. While several parenteral antagonists of CGRP and its receptor have been approved for migraine therapy (e.g. , , ), rimegepant and are the only members of the \gepants\"" family of medications remaining in development, and the only CGRP antagonists that possess oral bioavailability."" Rimegepant is indicated for the acute treatment of migraine with or without aura in adults. Rimegepant helps to abort migraine headaches by preventing the activity of a pronociceptive molecule that has been implicated in migraine pathophysiology. It is intended for use as an abortive migraine therapy and therefore has a relatively rapid onset of effect, with most efficacy trials evaluating for effect at the 2 hour mark.  The currently accepted theory of migraine pathophysiology considers dysfunction of the central nervous system, in particular the trigeminal ganglion, to be the root cause behind the condition. Activation of the trigeminal ganglion triggers the stimulation of trigeminal afferents that project to the spinal cord and synapse on various pain-sensing intra- and extracranial structures, such as the dura mater. Pain signals are then further transmitted via second-order ascending neurons to the brainstem, hypothalamus, and thalamic nuclei, and from there to several cortical regions (e.g. auditory, visual, motor cortices). The trigeminal ganglion appears to amplify and perpetuate the migraine headache pain through the activation of perivascular fibers and the release of molecules involved in pain generation, such as calcitonin gene-related peptide (CGRP).",,,,Rimegepant is approved and investigational.,Rimegepant is a solid.,True
15688,Lynestrenol has been used in trials studying the basic science of Transsexualism and Gender Dysphoria.,The molecular weight is 284.44.,Lynestrenol has a topological polar surface area of 20.23.,The log p value of  is 4.94.,Lynestrenol is approved and investigational.,,True
15689,"Mirvetuximab Soravtansine has been used in trials studying the treatment of Ovarian cancer, Endometrial Cancer, Fallopian tube cancer, Epithelial Ovarian Cancer, and Primary Peritoneal Cancer, among others.",,,,Mirvetuximab Soravtansine is investigational.,,True
15690,"Aminocamptothecin has been used in trials studying the treatment of Lymphoma, Gastric Cancer, Ovarian Cancer, Esophageal Cancer, and Ovarian Neoplasms, among others.",,,,9-aminocamptothecin is investigational.,,True
15691,"Oxetacaine, also called oxethazaince, is a potent surface analgesic with the molecular formula N, N-bis-(N-methyl-N-phenyl-t-butyl-acetamide)-beta-hydroxyethylamine that conserves its unionized form at low pH levels. Its actions have shown to relieve dysphagia, relieve pain due to reflux, chronic gastritis, and duodenal ulcer. Oxetacaine is approved by Health Canada since 1995 for its use as an antacid combination in over-the-counter preparations. It is also in the list of approved derivatives of herbal products by the EMA. Oxetacaine is available as an over-the-counter antacid and it is used to alleviate pain associated with gastritis, peptic ulcer disease, heartburn, esophagitis, hiatus hernia, and anorexia.  Oxetacaine improves common gastrointestinal symptoms. Oxetacaine is part of the anesthetic antacids which increase the gastric pH while providing relief from pain for a longer period of duration at a lower dosage. This property has been reported to relieve the symptoms of hyperacidity. Oxetacaine is reported to produce a reversible loss of sensation and to provide a prompt and prolonged relief of pain. In vitro, oxetacaine was showed to produce an antispasmodic action on the smooth muscle and block the action of serotonin. Oxetacaine inhibits gastric acid secretion by suppressing gastrin secretion.",The molecular weight is 467.65.,Oxetacaine has a topological polar surface area of 64.09.,The log p value of  is 4.72.,Oxetacaine is approved and investigational.,Oxetacaine is a solid.,True
15692,"Benzodiazepine is under investigation for the prevention of Delirium and C.Surgical Procedure; Cardiac. Benzodiazepine has been investigated for the treatment of Obesity, Sleep Apnea, Obstructive, and Disorders of Gallbladder, Biliary Tract and Pancrease.",,,,Benzodiazepine is approved and investigational.,,True
15693,Bioperine has been used in trials studying the treatment of Multiple Myeloma and Deglutition Disorders.,,,,Piperine is investigational.,,True
15694,DITPA has been investigated in Congestive Heart Failure.,,,,"3,5-diiodothyropropionic acid is investigational.",,True
15695,"Balaglitazone has been used in trials studying the treatment of Diabetes Mellitus, Type 2.",,,,Balaglitazone is investigational.,,True
15696,"Trifarotene is a topical retinoid cream used in the treatment of acne vulgaris that was first approved for use in the United States in October 2019. Retinoids are a class of medications structurally and functionally analogous to , though later generation retinoids such as trifarotene and bear little structural resemblance to vitamin A and are analogous only in function. Trifarotene is considered the first of the \fourth-generation\"" retinoids due to its uniquely selective activity - this selectivity appears to confer improved efficacy and reduced side effects as compared to older, less selective retinoids."" Trifarotene is indicated for the topical treatment of acne vulgaris in patients 9 years of age and older. Trifarotene exerts its effects via agonism at retinoid receptors - these receptors function to alter DNA transcription, resulting in downstream modulation of the expression of various genes involved in acne pathogenesis. It may be associated with skin irritation and should not be applied to cuts, abrasions, or otherwise damaged skin. As trifarotene may result in photosensitivity, patients should be cautioned to avoid excess sun exposure and to use sunscreen and/or protective clothing if exposure is unavoidable. Trifarotene is a potent and selective agonist of retinoic acid receptor-γ (RAR-γ). It has significantly less activity at RAR-β and RAR-α (16- and 65-fold lower than activity at RAR-γ, respectively), and has no activity at retinoid X receptors (RXRs). Agonism at retinoic acid receptors results in dimerization, and the resulting receptor-ligand dimer binds to specific DNA regulatory sequences (retinoic acid response elements, or RAREs) in the promotor regions of retinoid-responsible genes. Downstream alterations to gene expression induced by binding to these regions is the principle mechanism through which trifarotene exerts its comedolytic, anti-inflammatory, and depigmenting effects. ",,,,Trifarotene is approved and investigational.,Trifarotene is a solid.,True
15697,"Lefamulin is a pleuromutilin antibiotic used for the treatment of bacterial community-acquired pneumonia. A pleuromotilin is a more recently developed type of antibiotic that is derived from the fungus, Pleurotus mutilus. Lefamulin is available in intravenous and oral preparations and was granted FDA approval in August 2019. This drug is the first semi-synthetic pleuromutilin that has been designed for systemic administration. Lefamulin features a novel mechanism of action that shows benefit against resistant bacteria that cause pneumonia. The chemical structure of lefamulin contains a tricyclic mutilin core that is necessary for some of its antimicrobial activity. Lefamulin is indicated to treat adults diagnosed with community-acquired bacterial pneumonia (CABP) that is caused by susceptible bacteria. Its use should be reserved for confirmed susceptible organisms or a high probability of infection with susceptible organisms. The list of susceptible bacteria includes Streptococcus pneumoniae, Staphylococcus aureus (methicillin-susceptible), Legionella pneumophila, Haemophilus influenza, Chlamydophila pneumoniae, and Mycoplasma pneumoniae. Lefamulin demonstrates strong antibacterial activity against several microbes that are found to be common in both acute bacterial skin and skin structure infections as well as community-acquired bacterial pneumonia.  It shows antibacterial activity against gram-positive and atypical microbes (for example, Streptococcus pneumoniae, Legionella pneumophila, Mycoplasma pneumoniae, Haemophilus influenzae, and Chlamydophila pneumoniae). Lefamulin also exerts activity against Staphylococcus aureus, methicillin-resistant Staphylococcus aureus, and vancomycin-resistant Enterococcus faecium. It does not treat Pseudomonas aeruginosa infections. During in vitro studies, drug has also has demonstrated activity against Neisseria gonorrhoeae and Mycoplasma genitalium. Lefamulin inhibits prokaryotic ribosomal protein synthesis via its binding to the peptidyl transferase center (PTC) of the ribosomal bacterial 50S subunit. It inhibits protein translation through binding to both the A and P sites of the PTC via four hydrogen bonds, resulting in the interruption of peptide bond formation. Lefamulin's tricyclic mutilin core is the common moiety for binding of all members of its drug class, the pleuromutilins. Although the tricyclic motilin core doesn’t form any hydrogen bonds with the PTC nucleotides, it is stabilized or anchored by hydrophobic and Van der Waals interactions. Lefamulin exerts a selective inhibition of protein translation in eukaryotes, however, does not affect ribosomal translation of eukaryotes. Lefamulin demonstrates a unique induced-fit type of action that closes the binding pocket within a ribosome, conferring close contact of the drug to its target, therefore improving therapeutic efficacy. Because of its mechanism of action that differs from that of other antimicrobials, cross-resistance to other antibiotic classes is less likely.",,,,Lefamulin is approved and investigational.,Lefamulin is a solid.,True
15698,"Tazemetostat is a methyltransferase inhibitor used to treat metastatic or locally advanced epithelioid sarcoma not eligible for complete resection. Tazemetostat was first named in literature as EPZ-6438. Tazemetostat is indicated to treat adult and pediatric patients 16 years and older with metastatic or locally advanced epithelioid sarcoma that is not eligible for complete resection. Tazemetostat is a methyltransferase inhibitor that prevents hyper-trimethylation of histones and inhibits cancer cell de-differentiation. The duration of action is long as it is given twice daily. Patients should be counselled regarding the risk of secondary malignancies and embryo-fetal toxicity. EZH2 is a methyltransferase subunit of the polycomb repressive complex 2 (PRC2) which catalyzes multiple methylations of lysine 27 on histone H3 (H3K27). Trimethylation of this lysine inhibits the transcription of genes associated with cell cycle arrest. PRC2 is antagonized by the switch/sucrose non-fermentable (SWI/SNF) multiprotein complex. Abnormal activation of EZH2 or loss of function mutations in SWI/SNF lead to hyper-trimethylation of H3K27. Hyper-trimethylation of H3K27 leads to cancer cell de-differentiation, a gain of cancer stem cell-like properties. De-differentiation can allow for cancer cell proliferation.",,,,Tazemetostat is approved and investigational.,Tazemetostat is a solid.,True
15699,Gallopamil has been used in trials studying the treatment of Asthma.,The molecular weight is 484.64.,Gallopamil has a topological polar surface area of 73.18.,The log p value of  is 4.11.,Gallopamil is investigational.,,True
15700,"Methylprednisone has been used in trials studying the treatment of Leukemia, Rheumatoid Arthritis, Renal Transplantation, Kidney Transplantation, and Acute Lymphocytic Leukemia, among others.",,,,Methylprednisone is approved and investigational.,,True
15701,"Enfortumab vedotin is an antibody-drug conjugate used in the treatment of patients with advanced, treatment-resistant urothelial cancers. It is comprised of a fully human monoclonal antibody targeted against Nectin-4 and a microtubule-disrupting chemotherapeutic agent, monomethyl auristatin E (MMAE), joined by a protease-cleavable link. It is similar to , another antibody conjugated with MMAE that targets CD-30 instead of Nectin-4. Enfortumab vedotin is indicated for the treatment of adult patients with locally advanced or metastatic urothelial cancer who have previously received a programmed death receptor-1 (PD-1) or programmed death-ligand 1 (PD-L1) inhibitor, and a platinum-containing chemotherapy in the neoadjuvant/adjuvant, locally advanced, or metastatic setting. Enfortumab vedotin is an anti-cancer agent that destroys tumor cells by inhibiting their ability to replicate. Patients with moderate to severe hepatic impairment should not use enfortumab vedotin - although it has not been studied in this population, other MMAE-containing antibody-drug conjugates have demonstrated increased rates of adverse effects in patients with moderate-severe hepatic impairment. Enfortumab vedotin may also cause significant hyperglycemia leading, in some cases, to diabetic ketoacidosis, and should not be administered to patients with a blood glucose level >250 mg/dl. Enfortumab vedotin is an antibody-drug conjugate comprised of multiple components. It contains a fully human monoclonal antibody directed against Nectin-4, an extracellular adhesion protein which is highly expressed in urothelial cancers, attached to a chemotherapeutic microtubule-disrupting agent, monomethyl auristatin E (MMAE). These two components are joined via a protease-cleavable linker. Enfortumab vedotin binds to cells expressing Nectin-4 and the resulting enfortumab-Nectin-4 complex is internalized into the cell. Once inside the cell, MMAE is released from enfortumab vedotin via proteolytic cleavage and goes on to disrupt the microtubule network within the cell, arresting the cell cycle and ultimately inducing apoptosis.",,,,Enfortumab vedotin is approved and investigational.,Enfortumab vedotin is a solid.,True
15702,"Macimorelin, a novel and orally active ghrelin mimetic that stimulates GH secretion, is used in the diagnosis of adult GH deficiency (AGHD). More specifically, macimorelin is a peptidomimetic growth hormone secretagogue (GHS) that acts as an agonist of GH secretagogue receptor, or ghrelin receptor (GHS-R1a) to dose-dependently increase GH levels. Growth hormone secretagogues (GHS) represent a new class of pharmacological agents which have the potential to be used in numerous clinical applications. They include treatment for growth retardation in children and cachexia associated with chronic disease such as AIDS and cancer.  Indicated for the diagnosis of adult growth hormone deficiency (AGHD). Maximum GH levels from stimulation are observed between 30 to 90 minutes after administration of macimorelin. Increase in the QTcF interval may be observed from macimorelin administration. Ghrelin is an endogenous ligand for the GH secretagogue receptor that is also called the ghrelin receptor (GHS-R1a). Upon activation of the receptor, ghrelin serves to increase growth hormone (GH) secretion. Macimorelin mimics the actions of ghrelin by stimulating GH release. As a synthetic agonist, it activates growth hormone secretagogue receptors present in the pituitary and hypothalamus. ",The molecular weight is 474.56.,Macimorelin has a topological polar surface area of 144.9.,The log p value of  is 1.14.,Macimorelin is approved and investigational.,,True
15703,"Clobetasone is a corticosteroid that is often employed topically as a treatment for a variety of conditions such as eczema, psoriasis, various forms of dermatitis, and also for certain ophthalmologic conditions. Topical clobetasone butyrate has shown minimal suppression of the Hypothalamic-pituitary-adrenal axis. In dermatology, topical clobestasone butyrate helps to reduce the itchiness and erythema associated with eczema and dermatitis. Topical corticosteroid like clobetasone are synthetic derivatives of cortisone which produce anti-inflammatory, antiproliferative, immunosuppressive and vasoconstrictor effects when applied to the skin. Topically applied clobeyasone are thought to bind with cytoplasmic receptors in the dermal and intradermal cells and to induce inhibitory proteins, thus leading to decreased activity of prostaglandins, kinins, histamine, liposomal enzymes and other endogenous mediators of inflammation. Topical corticosteroids inhibit the migration of macrophages and leukocytes into areas of inflamed skin by reversing vascular dilation and permeability, resulting in decreased erythema, edema and pruritus.",,,,Clobetasone is approved.,Clobetasone is a solid.,True
15704,"Miocamycin is a macrolide type antimicrobial. This drug may be marketed in Japan for clinical use as it is listed in the Japanese pharmacopeia. It has shown to be effective against several gram-positive and gram-negative microbes and may be useful in the treatment of upper and lower respiratory tract infections, and urogenital tract infections or as an alternative to erythromycin treatment.",The molecular weight is 898.05.,Miocamycin has a topological polar surface area of 218.19.,The log p value of  is 5.11.,Miocamycin is approved.,,True
15705,,The molecular weight is 751.93.,Flurithromycin has a topological polar surface area of 193.91.,The log p value of  is 1.4.,Flurithromycin is experimental.,,False
15706,"Dihydroergocristine is part of the ergoloid mixture products. It is a semisynthetic ergot alkaloid and thus, it is characterized by a structural skeleton formed by an alkaloid ergoline. To know more about ergoloid mixtures, please visit. Dihydroergocristine is used in some countries such as Brasil as a single agent for the treatment of cerebral and peripheric vascular events. To know more about dihydroergocristine as part of the ergoloid mesylate mixture, please visit. Dihydroergocristine has been shown to present effect on memory and cognition. This activity in the brain is been reported by an increase in glutathione in age-related brain states. The reported effect on serotonin and adrenergic receptors has also been correlated to an inhibition of platelet aggregation. It has also been reported that individuals exposed to dihydroergocristine may present an amphoteric vasoregulating activity either hypotensive in hypertensive individuals or hypertensive in hypotensive individuals. This action is performed by promoting a dilating action in the contracted arteries and a tonic action in the dilated arteries and arterioles. The vasoregulating effect causes an increase in cerebral blood flow and oxygen consumption by the brain, which correlates with the brain protective function of dihydroergocristine. In Alzheimer studies, dihydroergocristine reduced the amyloid-beta levels in different cell types. To know more about dihydroergocristine as part of the ergoloid mesylate mixture, please visit. Dihydroergocristine mechanism of action seems to be related to a noncompetitive antagonistic activity in the serotonin receptors as well as a double partial agonist/antagonist activity in dopaminergic and adrenergic receptors. In Alzheimer studies, dihydroergocristine act as a direct inhibitor of γ-secretase.",The molecular weight is 611.74.,Dihydroergocristine has a topological polar surface area of 118.21.,The log p value of  is 5.56.,Dihydroergocristine is approved and experimental.,Dihydroergocristine is a solid.,True
15707,,The molecular weight is 340.38.,Diphenadione has a topological polar surface area of 51.21.,The log p value of  is 3.54.,Diphenadione is experimental.,,False
15708,,,,,Dihydroergocryptine is experimental.,,False
15709,,The molecular weight is 340.47.,Terguride has a topological polar surface area of 51.37.,The log p value of  is 2.78.,Terguride is experimental.,,False
15710,,The molecular weight is 828.01.,Rokitamycin has a topological polar surface area of 206.05.,The log p value of  is 3.84.,Rokitamycin is experimental.,,False
15711,"Midecamycin is a naturally occurring 16-membered macrolide that fits under the category of acetoxy-substituted macrolide antibiotics. In this molecule, an acetoxy group is substituted on the position 9 of the 16-member ring and on position 4 of the terminal sugar. Until 2017, midecamycin was still under the list of approved antimicrobial active pharmaceutical ingredients by Health Canada. Midecamycin was used for the treatment of infections in the oral cavity, upper and lower respiratory tracts and skin and soft tissue infections. The alone use of midecamycin was mainly used in Europe or Japan.  Reports have indicated that midecamycin is active against both erythromycin-susceptible and efflux-mediated erythromycin-resistant strains. The diacetate form of this product reduces gastrointestinal side effects and improves its pharmacokinetic profile. Studies have proved that midecamycin is highly active against Gram-positive organisms. The activity of midecamycin in the form of acetate salt presents a better activity, which seems to be potentiated at pH 7-8, as well as a longer half-life. Midecamycin, as part of the macrolides, act by inhibiting bacterial protein synthesis. More specifically, midecamycin inhibits bacterial growth by targetting the 50S ribosomal subunit preventing peptide bond formation and translocation during protein synthesis. The presence of mutations in the 50S RNA can prevent midecamycin binding. Midecamycin is a broad spectrum antibiotic and thus, it can interact with different bacteria.",The molecular weight is 813.98.,Midecamycin has a topological polar surface area of 206.05.,The log p value of  is 3.27.,Midecamycin is experimental.,Midecamycin is a solid.,True
15712,A vasodilator agent found to be effective in a variety of peripheral circulation disorders. It has various other potentially useful pharmacological effects. Its mechanism may involve block of calcium channels.,The molecular weight is 289.46.,Bencyclane has a topological polar surface area of 12.47.,The log p value of  is 5.18.,Bencyclane is experimental.,,True
15713,,,,,Otilonium is experimental and investigational.,,False
15714,,,,,Chlormadinone is experimental.,,False
15715,,The molecular weight is 326.48.,Promegestone has a topological polar surface area of 34.14.,The log p value of  is 4.07.,Promegestone is experimental.,,False
15716,,The molecular weight is 2268.69.,Mepartricin has a topological polar surface area of 354.78.,,Mepartricin is experimental.,,False
15717,,,,,Quingestanol is experimental.,,False
15718,,The molecular weight is 281.44.,Terodiline has a topological polar surface area of 12.03.,The log p value of  is 4.94.,Terodiline is experimental.,,False
15719,"Bioallethrin refers to a mixture of two of the allethrin isomers (1R,trans;1R and 1R,trans;1S) in an approximate ratio of 1:1, where both isomers are active ingredients. A mixture of the two same stereoisomers, but in an approximate ratio of R:S in 1:3, is called esbiothrin. A mixture containing only S-forms of allethrin is referred to as esbioallethrin or S-bioallethrin. Bioallethrin is a synthetic pyrethroid used as a pesticide against household pest insects such as mosquitoes, houseflies and cockroaches. It is claimed to have low mammalian toxicity. Bioallethrin was used for lice and scabies infestation. Other pyrethroids are now used in place of bioallethrin. Bioallethrin causes respiratory paralysis in lice and scabies parasites resulting in death. Bioallethrin, like other pyrethroids, binds to voltage gated sodium channels in their closed state and modifies the gating kinetics. Channel opening appears to increase affinity of the channel for pyrethroids like bioallethrin. Once bound pyrethroids slow both the opening and closing of the sodium channel resulting in a need for stronger excitatory potentials to produce an action potential and a delay in repolarization. The these changes make the neuron more susceptible to large action potentials and repeated firing by both increasing the initial threshold and reducing the input needed for after-potentials. When repeated firing does occur, the nerve terminal will release more neurotransmitter which can produce muscle paralysis through tetanus. This paralysis stops the breathing of lice and scabies parasites resulting in death.",,,,Bioallethrin is approved and experimental.,Bioallethrin is a liquid.,True
15720,,The molecular weight is 491.63.,Lidoflazine has a topological polar surface area of 35.58.,The log p value of  is 4.79.,Lidoflazine is approved and experimental.,,False
15721,,The molecular weight is 523.97.,Penfluridol has a topological polar surface area of 23.47.,The log p value of  is 7.11.,Penfluridol is experimental.,,False
15722,,The molecular weight is 365.48.,Caroverine has a topological polar surface area of 45.14.,The log p value of  is 4.11.,Caroverine is experimental.,,False
15723,"Demegestone is a progesterone receptor agonist that was previously used to treat luteal insufficiency. It was previously marketed in France as Lutionex, but has since been discontinued.",The molecular weight is 312.45.,Demegestone has a topological polar surface area of 34.14.,The log p value of  is 3.54.,Demegestone is experimental.,,True
15724,"Etynodiol (INN), or ethynodiol (BAN) is a steroidal progestin related to norethisterone which was never marketed. While etynodiol is sometimes used as a synonym for etynodiol diacetate, it usually refers to etynodiol diacetate (see ), not etynodiol.",,,,Etynodiol is experimental.,Etynodiol is a solid.,True
15725,"Glecaprevir is a direct acting antiviral agent and Hepatitis C virus (HCV) NS3/4A protease inhibitor that targets the the viral RNA replication. In combination with , glecaprevir is a useful therapy for patients who experienced therapeutic failure from other NS3/4A protease inhibitors. It demonstrates a high genetic barrier against resistance mutations of the virus. In cell cultures, the emergence of amino acid substitutions at NS3 resistance-associated positions A156 or D/Q168 in HCV genotype 1a, 2a or 3a replicons led to reduced susceptibility to glecaprevir. The combinations of amino acid substitutions at NS3 position Y65H and D/Q168 also results in greater reductions in glecaprevir susceptibility, and NS3 Q80R in genotype 3a patients also leads to glecaprevir resistance.  Indicated for the treatment of adult patients with chronic hepatitis C virus (HCV) genotype 1, 2, 3, 4, 5 or 6 infection without cirrhosis or with compensated cirrhosis (Child-Pugh In a biochemical assay studying clinical isolates of HCV genotypes 1a, 1b, 2a, 2b, 3a, 4a, 5a, and 6a, glecaprevir displayed IC50 values ranging from 3.5 to 11.3 nM that resulted in inhibition of the proteolytic activity of recombinant NS3/4A enzymes. In HCV replicon assays, glecaprevir had median EC50 values of 0.08-4.6 nM against laboratory and clinical isolates from subtypes 1a, 1b, 2a, 2b, 3a, 4a, 4d, 5a, and 6a. In a QT study, glecaprevir is not shown to prolong the QTc interval.  Glecaprevir is an inhibitor of the HCV NS3/4A protease, which is a viral enzyme necessary for the proteolytic cleavage of the HCV encoded polyprotein into mature forms of the NS3, NS4A, NS4B, NS5A, and NS5B proteins. These multifunctional proteins, including NS3, are essential for viral replication. The N-terminal of NS3 protein confers serine protease activity, whileThe C-terminus of NS3 encodes a DExH/D-box RNA helicase which hydyolyzes NTP as an energy source to unwind double-stranded RNA in a 3′ to 5′ direction during replication of viral genomic RNA. NS4A is a cofactor for NS3 that directs the localization of NS3 and modulates its enzymatic activities. Glecaprevir disrupts the intracellular processes of the viral life cycle through inhibiting the NS3/4A protease activity of cleaving downstream junctions of HCV polypeptide and proteolytic processing of mature structural proteins. ",The molecular weight is 838.87.,Glecaprevir has a topological polar surface area of 195.22.,The log p value of  is 4.0.,Glecaprevir is approved and investigational.,Glecaprevir is a solid.,True
15726,"Piperaquine is an antimalarial agent first synthesized in the 1960's and used throughout China. Its use declined in the 1980's as piperaquine resistant strains of *Plasmodium falciparum* appeared and artemisinin derivatives became available. It has come back into use in combination with the artemisinin derivative as part of the combination product Eurartesim. Eurartesim was first authorized for market by the European Medicines Agency in October 2011. For the treatment of uncomplicated *Plasmodium falciparum* infection in adults, children, and infants aged 6 months and up weighing over 5 kg. Used in combination with. Piperaquine inhibits the P. Falciparum parasite's haem detoxification pathway. The mechanism of piperaquine inhibition of the haem detoxification pathway is unknown but is expected to be similar to that of.",The molecular weight is 535.52.,Piperaquine has a topological polar surface area of 38.74.,The log p value of  is 6.46.,Piperaquine is experimental and investigational.,Piperaquine is a solid.,True
15727,"WIN 55,212-2 is a chemical described as an aminoalkylindole derivative, which produces effects similar to those of cannabinoids such as tetrahydrocannabinol (THC) but has an entirely different chemical structure. It is a potent cannabinoid receptor agonist that has been found to be a potent analgesic in a rat model of neuropathic pain. It activates p42 and p44 MAP kinase via receptor-mediated signaling.",,,,WIN 55212-2 is experimental.,WIN 55212-2 is a solid.,True
15728,"Fish oil is a component of SMOFLIPID, which was FDA approved in July 2016. It is indicated in adults as a source of calories and essential fatty acids for parenteral nutrition when oral or enteral nutrition is not possible, insufficient, or contraindicated. Under FDA approval, fish oil pharmaceuticals are typically products consisting of a combination of the omega-3-fatty acids eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) and are indicated primarily as an adjunct to diet to reduce triglyceride levels in adult patients with severe (>=500 mg/dL) hypertriglyceridemia. In general, the only practical method of obtaining and increasing the levels of eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) fish oil omega-3-fatty acids in the body is to consume them directly from foods and/or dietary supplements. Having EPA and DHA is important because they facilitate numerous important functions in the human body. As an example, such supplementation of fish oil EPA and DHA demonstrates a legitimate ability to decrease triglyceride levels as their presence in the body can act as poor substrates for the enzymes that are ordinarily responsible for triglyceride synthesis and also inhibit the esterification of other fatty acids, among other mechanisms. The specific mechanism of action by which the fish oil EPA and DHA acids are capable of reducing serum triglyceride levels is not yet fully understood. Nevertheless, it is proposed that such omega-3-fatty acids may not be the preferred substrates of the enzyme diacylglycerol O-acyltransferase that participates in the generation of triglycerides; that they might interact with nuclear transcription factors that manage lipogenesis; or that their presence and increase in levels can cause cellular metabolism to subsequently shift toward a decrease in triglyceride synthesis and an increase in fatty acid oxidation. Moreover, the EPA and DHA acids are also believed to be able to promote apolipoprotein B degradation in the liver through the stimulation of an autophagic process. It may also be possible that these fish oil acids can accelerate the clearance of very-low-density lipoprotein (VLDL) particles and chylomicron. The combination of all these actions results in fewer VLDL particles being assembled and secreted, which is of considerable importance as VLDL particles are the major endogenous source of triglycerides.",,,,Fish oil is approved and nutraceutical.,Fish oil is a liquid.,True
15729,"Nomegestrol acetate, also known as NOMAC, is a progestin used in oral contraceptives, menopausal hormone therapy, and for the treatment of gynecological disorders.",The molecular weight is 370.49.,Nomegestrol acetate has a topological polar surface area of 60.44.,The log p value of  is 3.25.,Nomegestrol acetate is approved and investigational.,Nomegestrol acetate is a solid.,True
15730,"Baloxavir marboxil is an antiviral drug developed by Shionogi Co., a Japanese pharmaceutical company and Roche for the treatment of influenza A and influenza B infections. The drug was initially approved for use in Japan in February 2018 and approved by the FDA on October 24, 2018 , for the treatment of acute uncomplicated influenza in patients 12 years of age and older who have been symptomatic for no more than 48 hours. Baloxavir marboxil, a cap-endonuclease inhibitor, has a unique mechanism of action when compared to the currently existing neuraminidase inhibitor drug class used to treat influenza infections. For the treatment of influenza A and B virus infection , in patients 12 and older who have been symptomatic for no more than 48 hours.  Baloxavir marboxil is a selective inhibitor of influenza cap-dependent endonuclease which prevents polymerase function and therefore influenza virus mRNA replication ,. It has shown therapeutic activity against influenza A and B virus infections, including strains resistant to current antiviral agents. This drug inhibits an enzyme required for viral replication, thus rapidly treating flu virus infection , and alleviating the symptoms associated with infection. A single dose of this agent was shown to be superior to placebo in relieving influenza symptoms and superior to both oseltamivir and placebo drug in virologic outcomes (marked by decreased viral load). The safety profile of Baloxavir marboxil compared favorably with that of oseltamivir, making it an effective treatment option for treatment of the flu virus, in one single dose ,. This drug is a CAP endonuclease inhibitor. The influenza endonuclease is an essential subdomain of the viral RNA polymerase enzyme.  CAP endonuclease processes host pre-mRNAs to serve as primers for viral mRNA and therefore has been a common target for studies of anti-influenza drugs. Inhibiting the activity of endonuclease can block the transcription of mRNA and inactivate the influenza virus.",,,,Baloxavir marboxil is approved and investigational.,Baloxavir marboxil is a solid.,True
15731,"In April 2018, the U.S. Food and Drug Administration (FDA) and the Swiss company Helsinn approved the intravenous formulation of AKYNZEO® (NEPA, a fixed antiemetic combination of fosnetupitant, 235mg, and palonosetron, 0.25mg) as an alternative treatment option for patients experiencing chemotherapy-induced nausea and vomiting. Fosnetupitant is the pro-drug form of netupitant. Indicated in combination palonosetron (as the drug Akynzeo) and dexamethasone in adults for the prevention of acute and delayed nausea and vomiting associated with initial and repeat courses of cancer chemotherapy, including, but not limited to, highly emetogenic chemotherapy. In the combination drug, Akynzeo, palonosetron prevents nausea and vomiting during the acute phase and fosnetupitant prevents nausea and vomiting during both the acute and delayed phase after cancer chemotherapy. The fosnetupitant in this drug combination is a selective P/neurokinin-1 (NK-1) receptor antagonist. ",,,,Fosnetupitant is approved.,Fosnetupitant is a solid.,True
15732,Warfarin consists of a racemic mixture of two active enantiomers—R- and S- forms—each of which is cleared by different pathways. S-warfarin is 2-5 times more potent than the R-isomer in producing an anticoagulant response.,,,,(S)-Warfarin is experimental and investigational.,(S)-Warfarin is a solid.,True
15733,,,,,Dexverapamil is experimental.,Dexverapamil is a solid.,False
15734,Prevents renal injury after warm & cold ischemia.,,,,Emopamil is experimental.,Emopamil is a solid.,True
15735,Used to treat migraines.,The molecular weight is 468.54.,Lomerizine has a topological polar surface area of 34.17.,The log p value of  is 5.11.,Lomerizine is experimental.,Lomerizine is a solid.,True
15736,,,,,Tetrandrine is experimental.,Tetrandrine is a solid.,False
15737,,The molecular weight is 609.72.,Dexniguldipine has a topological polar surface area of 111.01.,The log p value of  is 7.85.,Dexniguldipine is experimental.,Dexniguldipine is a solid.,False
15738,,,,,Echinacea is approved and experimental.,,False
15739,"Ivosidenib is a first in class isocitrate dehydrogenase-1 (IDH1) approved for use by the FDA in acute myeloid leukemia (AML) in July 2018. Ivosidenib is now available in the United States under the trade name Tibsovo marketed by Agios Pharmaceuticals, Inc. Ivosidenib has been granted fast track, priority review, and orphan drug designations by the FDA. Ivosidenib is approved for use in the treatment of relapsed or refractory AML with a susceptible IDH1 mutation as detected by an FDA-approved test. Many cancers undergo missense mutations of their IDH1 gene leading to substitution of arginine 132 residue of the IDH1 enzyme. Furthermore, methylation sensitive insulators can no longer regulate the activation of oncogenes when histones are hypermethylated. In AML this hypermethylation is known to disrupt hematopoietic differentiation. Ivosidenib is a reversible inhibitor of IDH1 which is non-competitive with respect to the cofactor NADH. It binds to many different 132-substituted IDH1 mutants as well as the wild type enzyme. It is considered to be a slow-binder of the wild type enzyme and binds to mutant enzymes at lower concentrations, both of which may contribute its selectivity. Ivosidenib has not been observed to inhibit any form of IDH2 at micromolar concentrations.",,,,Ivosidenib is approved and investigational.,Ivosidenib is a solid.,True
15740,,,,,Hydroxyprogesterone is experimental.,,False
15741,Adjunctive Therapy for Adults with Partial-Onset Seizures The precise mechanism(s) by which eslicarbazepine exerts anticonvulsant activity is unknown but is thought to involve inhibition of voltage-gated sodium channels.,,,,Eslicarbazepine is approved.,,True
15742,"Segesterone acetate is a steroidal progestin or synthetic progesterone and a 19-norprogesterone derivative with no CH3 group radical in position 6. In animal studies, segesterone acetate was shown to be one of the most potent progestins. It mediates progestational activity 100 times higher than that of. It is commonly sold under the brand names Nestorone and Elcometrine and serves as an active component in hormonal contraceptives. It is also used as a treatment for endometriosis in South American countries. Segesterone acetate binds selectively to progesterone receptors and not androgen receptors. Due to its rapid hepatic metabolism, segesterone acetate must be administered parenterally. Segesterone acetate is not an orally active compound, but it is proved to be a potent anti-ovulatory agent when given in implants, vaginal rings or percutaneous gel.  Segesterone acetate in combination with ethinyl estradiol is indicated for use by females of reproductive potential to prevent pregnancy as a combination hormonal contraceptive (CHC). It induces contraception for thirteen 28-day cycles (1 year) following vaginal administration. The vaginal system must remain in place continuously for 3 weeks (21 days) followed by a 1-week (7-day) vaginal system-free interval. The use in females with a body mass index of >29 kg/m^2 has not been adequately evaluated. Segesterone acetate suppresses ovulation. In a Phase I randomized, placebo-controlled, randomized crossover study involving healthy adult female subjects, there was no clinically significant QTc interval prolongation following a single intravenous bolus dose of segesterone acetate. Segesterone acetate shows no androgenic, anabolic, or estrogenic activity. It also did not show uterotropic activity in ovariectomized rats. In the endometrial transformation test to assess the progestational activity, dose-dependent increases in both uterine weight was observed following subcutaneous administration of segesterone acetate. Segesterone acetate selectively binds to the progesterone receptor (PR), a transcription factor belonging to the nuclear receptor superfamily, where it acts as an agonist and transactivator. According to the findings from docking experiments, it adopts the same docking position within the PR ligand-binding domain (LBD) as progesterone but due to additional stabilizing contacts between 17α-acetoxy and 16-methylene groups and PR LBD, segesterone acetate display higher potency than progesterone. As with other progestins, segesterone acetate prevents ovulation by blocking the midcycle surge in luteinizing hormone (LH) secretion, thereby inhibiting the development of ovarian follicles. When used in combination with segesterone acetate, ethinyl estradiol potentiates the antigonadotropic of the progestin and prevents irregular shedding of the endometrium. Segesterone acetate lacks androgenic activity, and displayed binding affinity to androgen receptors that was 500- to 600-fold less than that of testosterone. It does not display binding affinity toward estrogen receptors. When the relative binding affinities of segesterone acetate to human steroid receptors were investigated _in vitro_, it was demonstrated that segesterone acetate binds to the glucocorticoid receptor. However, segesterone acetate did not exert any glucocorticoid activity in the _in vivo_ assays showing no increase in liver glycogen and tyrosine transaminase TAT. ",The molecular weight is 370.49.,Segesterone acetate has a topological polar surface area of 60.44.,The log p value of  is 3.79.,Segesterone acetate is approved and experimental and investigational.,Segesterone acetate is a solid.,True
15743,,,,,Fluprednisolone acetate is experimental.,,False
15744,,The molecular weight is 410.6.,Norethindrone enanthate has a topological polar surface area of 43.37.,The log p value of  is 6.57.,Norethindrone enanthate is experimental.,,False
15745,"Larotrectinib is an orally administered tropomyosin receptor kinase (Trk) inhibitor with demonstrated antineoplastic activity. Upon administration, larotrectinib binds to Trk, thereby preventing neurotrophin-Trk interaction and Trk activation, which results in both the induction of cellular apoptosis and the inhibition of cell growth in tumors that overexpress Trk. Trk, a receptor tyrosine kinase activated by neurotrophins, is mutated in a variety of cancer cell types and plays an important role in tumor cell growth and survival. Larotrectinib is a tyrosine kinase inhibitor that is currently indicated for the treatment of adult and pediatric patients with solid tumors that either a) have a neurotrophic receptor tyrosine kinase (NTRK) gene fusion without a known acquired resistance mutation, b) are metastatic or where surgical resection is likely to result in severe morbidity, and c) have no satisfactory alternative treatments or that have progressed following treatment. At doses that are nine-fold greater than the recommended adult dose, larotrectinib does not elicit any QTc interval prolongation that is clinically relevant. Tropomysoin Receptor Kinases (TRK) like TRKA, TRKB, and TRKC elicit activities that regulate the natural growth, differentiation, and survival of neurons when they interact with endogenous neutrotrophin ligands. TRKA, TRKB, and TRKC are themselves encoded by the NTRK1, NTRK2, and NTRK3 genes, respectively. It has been discovered that chromosomal rearrangements involving in-frame fusions of these genes with various partners, translocations in the TRK kinase domains, mutations in the TRK ligand-binding site, amplifications of NTRK, or the expression of TRK splice variants can result in constitutively-activated chimeric TRK fusion proteins that can act as oncogenic drivers that promote cell proliferation and survival in tumor cell lines.",,,,Larotrectinib is approved and investigational.,Larotrectinib is a solid.,True
15746,"Vibegron is a potent, selective beta-3 adrenergic receptor (β3) agonist that relaxes the detrusor smooth muscle of the bladder, thereby increasing bladder capacity. Vibegron was first approved in Japan in September 2018 for the treatment of overactive bladder, a condition associated with distressing symptoms of urge urinary incontinence, urgency, and urinary frequency, and reduced quality of life of patients. On December 23, 2020, vibegron was approved for the same indication in adults. It is available as oral tablets under the market name GEMTESA.  Vibegron is indicated for the treatment of overactive bladder (OAB) with symptoms of urge urinary incontinence, urgency, and urinary frequency in adults. Vibegron selectivity for beta-3 adrenergic receptors is >9000 times higher than for β1AR or β2AR. Vibegron improves clinical symptoms of overactive bladder by increasing bladder capacity without affecting bladder contraction. It significantly increases the functional bladder volume in a dose-dependent manner, which results in prolongation of the interval between voids. In clinical studies, vibegron inhibited detrusor bladder contractions in a concentration-dependent manner, reduced voiding pressure, and increased bladder compliance. In Japanese clinical studies comprising patients with overactive bladder, vibegron significantly improved the frequency of micturition, urgency, and urgency incontinence episodes. Overactive bladder is characterized by symptoms of urge urinary incontinence, urgency, and urinary frequency. Bladder filling and emptying are regulated by the coordinated communication between sympathetic and parasympathetic systems. Bladder filling occurs via parasympathetic inhibition and the sympathetic hypogastric nerve releasing norepinephrine, which acts on beta-adrenergic receptors responsible for mediating detrusor muscle relaxation. Symptoms of overactive bladder are thought to be caused by the deterioration of the sensory connections between the bladder, spinal cord and brain, leading to changes in the lower urinary tract and abnormal bladder sensations of the urge to void at small bladder volumes.",,,,Vibegron is approved and investigational.,Vibegron is a solid.,True
15747,"Voxelotor is a novel hemoglobin S polymerization inhibitor for the treatment of sickle cell disease. This is a genetically inherited condition most prevalent in the Middle East, Africa, and certain parts of India. Sickle cell disease can lead to excruciating pain, stroke, infection, and various other complications arising from the blockage of blood vessels. Voxelotor is indicated to treat sickle cell disease in both adult and pediatric patients aged 12 years and above. Voxelotor modifies hemoglobin to prevent painful and dangerous sickle cell crises that normally lead to organ damage, hospitalization, and sometimes death. It prevents low hemoglobin, which is normally associated with the destruction of sickled blood cells in sickle cell disease. Voxelotor has led to up to a 40% increase in hemoglobin in clinical trials. Deoxygenated sickle hemoglobin (HbS) polymerization is the causal factor for sickle cell disease. The genetic mutation associated with this disease leads to the formation of abnormal, sickle shaped red blood cells that aggregate and block blood vessels throughout the body, causing vaso-occlusive crises. Voxelotor binds irreversibly with the N‐terminal valine of the α‐chain of hemoglobin, leading to an allosteric modification of Hb20, which increases the affinity for oxygen. Oxygenated HbS does not polymerize. By directly blocking HbS polymerization, voxelotor can successfully treat sickle cell disease by preventing the formation of abnormally shaped cells, which eventually cause lack of oxygenation and blood flow to organs.",,,,Voxelotor is approved and investigational.,Voxelotor is a solid.,True
15748,"Zanubrutinib is a novel Bruton's tyrosine kinase (BTK) inhibitor used for the treatment of adult patients with mantle cell lymphoma (MCL) who have received at least one prior therapy. Mantle cell lymphoma is an aggressive mature B-cell non-Hodgkin lymphoma that is associated with early relapse, poor clinical outcomes, and long-term survival. BTK is an enzyme that plays a role in oncogenic signalling pathways, where it promotes the survival and proliferation of malignant B cells. Compared to the first-generation BTK inhibitor , zanubrutinib displays higher potency and selectivity for BTK with fewer off-target effects. Due to this enhanced selectivity towards BTK, zanubrutinib belongs to the second-generation BTK inhibitor drug group that also includes , which was approved by the FDA in 2017. Zanubrutinib is indicated for the treatment of adult patients with mantle cell lymphoma (MCL) who have received at least one prior therapy. Zanubrutinib is an immunomodulating agent that decreases the survival of malignant B cells. It inhibits BTK by binding to its active site. It works to inhibit the proliferation and survival of malignant B cells to reduce the tumour size in mantle cell lymphoma. Bruton's tyrosine kinase (BTK) is a non-receptor kinase and a signalling molecule for the B cell receptors expressed on the peripheral B cell surface. The BCR signalling pathway plays a crucial role in normal B-cell development but also the proliferation and survival of malignant B cells in many B cell malignancies, including mantle-cell lymphoma (MCL). Once activated by upstream Src-family kinases, BTK phosphorylates phospholipase-Cγ (PLCγ), leading to Ca2+ mobilization and activation of NF-κB and MAP kinase pathways. These downstream cascades promote the expression of genes involved in B cell proliferation and survival. The BCR signalling pathway also induces the anti-apoptotic protein Bcl-xL and regulates the integrin α4β1 (VLA-4)-mediated adhesion of B cells to vascular cell adhesion molecule-1 (VCAM-1) and fibronectin via BTK. Apart from the direct downstream signal transduction pathway of B cells, BTK is also involved in chemokine receptor, Toll-like receptor (TLR) and Fc receptor signalling pathways. ",,,,Zanubrutinib is approved and investigational.,Zanubrutinib is a solid.,True
15749,"Pemigatinib is a small molecule kinase inhibitor with antitumour activity. It works by inhibiting fibroblast growth factor receptors (FGFRs), which are receptor tyrosine kinases that activate signalling pathways in tumour cells. FGFRs gained attention as potential therapeutic targets in selected cancers, as FGFR gene alterations were observed in a wide variety of cancers including those of the urinary bladder, breast, ovary, prostate, endometrium, lung, and stomach. Deregulated FGFR signalling pathway can lead the development of oncogenes and tumour-promoting physiological processes, such as cancer cell proliferation, enhanced angiogenesis, and evasion of cell death. Pemigatinib is indicated for the treatment of unresectable locally advanced or metastatic cholangiocarcinoma in previously-treated adult patients with a fibroblast growth factor receptor 2 (FGFR2) fusion or other rearrangement as detected by an FDA-approved test. Pemigatinib is a small molecule kinase inhibitor that exerts anti-tumour activity through inhibition of fibroblast growth factor receptors (FGFRs). With an IC<sub>50</sub> of less than 2 nM, pemigatinib displays potent inhibition of FGFR1, FGFR2, and FGFR3. In mouse xenograft models of human tumours with FGFR1, FGFR2, or FGFR3 alterations, pemigatinib exhibited potent anti-tumour activity by suppressing the growth of xenografted tumour models. It also showed efficacy against a patient-derived xenograft model of cholangiocarcinoma that expressed an oncogenic FGFR2­ Transformer-2 beta homolog (TRA2b) fusion protein. Pemigatinib also inhibited FGFR4 _in vitro_, however at a concentration approximately 100 times higher than those that inhibit FGFR1, 2, and 3. Fibroblast growth factor receptor (FGFR) is a receptor tyrosine kinase involved in activating signalling pathways that promote cell proliferation, survival, and migration, as well as growth arrest and cellular differentiation. The initiation of the FGFR signalling pathway requires the binding of its natural ligand, fibroblast growth factor (FGF). Once FGF binds to the extracellular ligand-binding domain of the receptor, FGFRs dimerize and autophosphorylate the tyrosine residue in the intracellular tyrosine-kinase domain, leading to the activation of the tyrosine kinase. Downstream cascades involve phosphorylation of multiple intracellular signalling proteins, such as phosphatidylinositol 3 kinase (PI3K)-AKT and RAS/mitogen-activated protein kinase (MAPK), and phospholipase Cγ, which activates the protein kinase C pathway. FGFR-mediated pathway ultimately promotes cell growth, differentiation, survival, angiogenesis, and organogenesis, depending on cell type. Expressed in different isoforms in various tissues and cell lines, FGFRs are not constitutively active in normal cells. However, FGFR1, FGFR2, or FGFR3 alterations in certain tumours can lead to constitutive FGFR activation and aberrant FGFR signalling, supporting the proliferation and survival of malignant cells.",,,,Pemigatinib is approved and investigational.,Pemigatinib is a solid.,True
15750,"Avapritinib, or BLU-285, is a selective tyrosine kinase inhibitor of KIT and platelet derived growth factor receptor alpha indicated for the treatment of unresectable, metastatic gastrointestinal stromal tumors. It is one of the first medications available for the treatment of multidrug resistant cancers. Avapritinib shares a similar mechanism with. Avapritinib is indicated for the treatment of unresectable, metastatic gastrointestinal stromal tumors with a platelet-derived growth factor receptor alpha exon 18 mutation. Avapritinib is a selective kinase inhibitor that negatively modulates the action of cell transporters to resensitize them to other chemotherapies. It has a long duration of action as it is given once daily. Patients should be counselled regarding the risk of intracranial hemorrhage, CNS effects, and embryo-fetal toxicity. Avapritinib has a negative modulating effect on the transporters ABCB1 and ABCG2, which mediate the multidrug resistance phenotype of some cancers. This modulation may be due to interactions of avapritinib with the drug binding pocket of these transporters. Negative modulation of these transporters, resensitizes cancerous cells to treatment with chemotherapeutic agents like.",,,,Avapritinib is approved and investigational.,Avapritinib is a solid.,True
15751,"Mexazolam (CS-386) is a benzodiazepine indicated for the treatment of anxiety with or without psychoneurotic conditions. Mexazolam's structure is similar to that of other benzodiazepines such as and. The use of benzodiazepines in the treatment of anxiety is generally a second line measure. Mexazolam is indicated for the treatment of anxiety with or without psychoneurotic conditions. Mexazolam is a benzodiazepine that binds to benzodiazepine-type receptors, inhibiting gamma-aminobutyric acid.",The molecular weight is 363.24.,Mexazolam has a topological polar surface area of 41.57.,The log p value of  is 4.82.,Mexazolam is experimental.,,True
15752,"Selpercatinib is a kinase inhibitor with enhanced specificity for RET tyrosine kinase receptors (RTKs) over other RTK classes. Enhanced RET (Rearranged during transfection) oncogene expression is a hallmark of many cancers. Although multikinase inhibitors, including , , , , and , have shown efficacy in RET-driven cancers, their lack of specificity is generally associated with substantial toxicity. Selpercatinib (LOXO-292) and pralsetinib (BLU-667) represent the first generation of specific RET RTK inhibitors for the treatment of RET-driven cancers. Selpercatinib is indicated for the treatment of _RET_ fusion-positive non-small cell lung cancer in adult patients. Selpercatinib is also indicated for the systemic treatment of advanced or metastatic _RET_-mutant medullary thyroid cancer and for the systemic treatment of _RET_ fusion-positive radioactive iodine-refractory thyroid cancer in both adult and pediatric patients aged 12 and over. Selpercatinib exerts anti-tumour activity in specific cancers through inhibition of mutated forms of RET tyrosine kinases. Due to its increased specificity for RET over other tyrosine kinases, selpercatinib is thought to have an improved safety profile compared to other multi-kinase inhibitors. Despite this, selpercatinib treatment is associated with hepatotoxicity, hypertension, QT interval prolongation, hemorrhagic events, risk of impaired wound healing, and embryo-fetal toxicity; some patients may also exhibit hypersensitivity to selpercatinib. Rearranged during transfection (RET) is a transmembrane receptor tyrosine kinase containing extracellular, transmembrane, and intracellular domains whose activity is required for normal kidney and nervous system development. Constitutive RET activation is primarily achieved through chromosomal rearrangements producing 5' fusions of dimerizable domains to the 3' _RET_ tyrosine kinase domain, such as _KIF5B-RET_ and _CCDC6-RET_, resulting in constitutive dimerization and subsequent autophosphorylation. Constitutive activation leads to increased downstream signalling and is associated with tumour invasion, migration, and proliferation.",,,,Selpercatinib is approved and investigational.,Selpercatinib is a solid.,True
15753,"Miglitol inhibits the breakdown complex carbohydrates into glucose. It is primarily used in diabetes mellitus type 2 for establishing greater glycemic control by preventing the digestion of carbohydrates (such as disaccharides, oligosaccharides, and polysaccharides) into monosaccharides which can be absorbed by the body. For use as an adjunct to diet to improve glycemic control in patients with non-insulin-dependent diabetes mellitus (NIDDM) whose hyperglycemia cannot be managed with diet alone. Miglitol, an oral alpha-glucosidase inhibitor, is a desoxynojirimycin derivative that delays the digestion of ingested carbohydrates, thereby resulting in a smaller rise in blood glucose concentration following meals. As a consequence of plasma glucose reduction, miglitol reduce levels of glycosylated hemoglobin in patients with Type II (non-insulin-dependent) diabetes mellitus. Systemic nonenzymatic protein glycosylation, as reflected by levels of glycosylated hemoglobin, is a function of average blood glucose concentration over time. Because its mechanism of action is different, the effect of miglitol to enhance glycemic control is additive to that of sulfonylureas when used in combination. In addition, miglitol diminishes the insulinotropic and weight-increasing effects of sulfonylureas. Miglitol has minor inhibitory activity against lactase and consequently, at the recommended doses, would not be expected to induce lactose intolerance. In contrast to sulfonylureas, miglitol does not enhance insulin secretion. The antihyperglycemic action of miglitol results from a reversible inhibition of membrane-bound intestinal a-glucoside hydrolase enzymes. Membrane-bound intestinal a-glucosidases hydrolyze oligosaccharides and disaccharides to glucose and other monosaccharides in the brush border of the small intestine. In diabetic patients, this enzyme inhibition results in delayed glucose absorption and lowering of postprandial hyperglycemia.",The molecular weight is 207.23.,Miglitol has a topological polar surface area of 104.39.,The log p value of  is -1.26.,Miglitol is approved.,Miglitol is a solid.,True
15754,"Icodextrin is an iso-osmotic peritoneal dialysis solution containing glucose polymers. It is used primarily for ambulatory peritoneal dialysis (CAPD) of diabetic patients and automated peritoneal dialysis (APD) for patients with end-stage renal disease. It is injected as a solution into the peritoneal cavity. The drug is absorbed via convective transport via peritoneal lymphatic pathways. Used for continuous ambulatory peritoneal dialysis (CAPD) of diabetic patients or automated peritoneal dialysis (APD) for the management of end-stage renal disease. Icodextrin is an iso-osmotic peritoneal dialysis solution containing glucose polymers. It is used primarily for ambulatory peritoneal dialysis (CAPD) of diabetic patients and automated peritoneal dialysis (APD) for patients with end-stage renal disease. It is injected as a solution into the peritoneal cavity. The drug is absorbed via convective transport via peritoneal lymphatic pathways. Icodextrin is a starch-derived, water-soluble glucose polymer linked by alpha (1-4) and alpha (1-6) glycosidic bonds with an average molecular weight between 13,000 and 19,000 daltons. It functions as a colloid osmotic agent to achieve ultrafiltration during long (12-16 hour) peritoneal dialysis dwells. In other words it helps clean waste out of the body when the kidneys are not functioning properly. Icodectrin acts in the peritoneal cavity by exerting osmotic pressure across small intercellular pores resulting in transcapillary ultrafiltration through the dwell. This is due to the fact that the polymer is minimially absorbed across the peritoneal membrane. Icodextrin achieves superior fluid removal compared with glucose-based dialysates.",,,,Icodextrin is approved and investigational.,Icodextrin is a solid.,True
15755,A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.,The molecular weight is 180.16.,Beta-D-Glucose has a topological polar surface area of 110.38.,The log p value of  is -2.9.,Beta-D-Glucose is experimental.,Beta-D-Glucose is a solid.,True
15756,"Pidolic acid is a naturally occurring but little-studied amino acid derivative that can be formed enzymatically or non-enzymatically and participates as a biological intermediate with unique pharmacodynamics in various chemical pathways. Elevations of the acid in blood levels may be associated with problems of glutamine or glutathione metabolism. Pidolic acid, in general, is found in large quantities in brain tissue and other tissues in bound form, like skin. There is currently no clinically approved and/or marketed medicine that relies upon pidolic acid as an active ingredient for any formal therapeutic indication. Pidolic acid is a naturally occurring but little-studied amino acid derivative that can be formed enzymatically or non-enzymatically and participates as a biological intermediate in various chemical pathways. Elevations of the acid in blood levels may be associated with problems of glutamine or glutathione metabolism. Pidolic acid, in general, is found in large quantities in brain tissue and other tissues in bound form, like skin. Pidolic acid is an endogenous amino acid derivative where the free amino group of glutamic acid or glutamine cyclizes to generate a lactam. Subsequently it is also a metabolite in the glutathione cycle that is converted to glutamate by the enzyme 5-oxoprolinase. Moreover, N-terminal glutamic acid and glutamine residues can either spontaneously cyclize to become pidolic acid, or be enzymatically transformed by glutaminyl cyclases. In particular, this is ultimately a form of N-termini that is a challenge for N-terminal sequencing using Edman chemistry, which necessitates a free primary amino group that is not present in pidolic acid. Pyroglutamate aminopeptidase can restore a free N-terminus by cleaving off the pyroglutamate residue, however.",,,,Pidolic acid is approved and investigational.,Pidolic acid is a solid.,True
15757,,,,,5-Hydroxymethyl-Chonduritol is experimental.,5-Hydroxymethyl-Chonduritol is a solid.,False
15758,,,,,"4,6-dideoxy-4-amino-alpha-D-glucose is experimental.","4,6-dideoxy-4-amino-alpha-D-glucose is a solid.",False
15759,,,,,Acarbose Derived Hexasaccharide is experimental.,Acarbose Derived Hexasaccharide is a solid.,False
15760,,,,,"4-O-(4,6-Dideoxy-4-{-5,6-Dihydroxy-3-(Hydroxymethyl)Cyclohex-2-En-1-Yl]Amino}Hexopyranosyl)Hexopyranose is experimental.","4-O-(4,6-Dideoxy-4-{-5,6-Dihydroxy-3-(Hydroxymethyl)Cyclohex-2-En-1-Yl]Amino}Hexopyranosyl)Hexopyranose is a solid.",False
15761,"Oseltamivir (marketed as the product TamifluⓇ), is an antiviral neuraminidase inhibitor used for the treatment and prophylaxis of infection with influenza viruses A (including pandemic H1N1) and B. Oseltamivir exerts its antiviral activity by inhibiting the activity of the viral neuraminidase enzyme found on the surface of the virus, which prevents budding from the host cell, viral replication, and infectivity. According to FDA prescribing information, oseltamivir is indicated for the treatment of acute, uncomplicated illness due to influenza A and B infection in patients 2 weeks of age and older who have been symptomatic for no more than 48 hours. In particular, this agent is indicated in adults and children including full-term neonates who present with symptoms typical of influenza when influenza virus is circulating in the community. Efficacy has been demonstrated when treatment is initiated within two days of the first onset of symptoms. There have been postmarketing reports of delirium and abnormal behavior leading to injury, and in some cases resulting in fatal outcomes, in patients with influenza who were receiving oseltamivir. Because these events were reported voluntarily during clinical practice, estimates of frequency cannot be made but they appear to be uncommon based on oseltamivir. These events were reported primarily among pediatric patients and often had an abrupt onset and rapid resolution. The contribution of oseltamivir to these events has not been established. Influenza can be associated with a variety of neurologic and behavioral symptoms that can include events such as hallucinations, delirium, and abnormal behavior, in some cases resulting in fatal outcomes. These events may occur in the setting of encephalitis or encephalopathy but can occur without obvious severe disease. Oseltamivir phosphate is a pro-drug of the active metabolite (oseltamivir carboxylate) which is a potent and selective inhibitor of influenza virus neuraminidase enzymes, which are glycoproteins found on the virion surface. Viral neuraminidase enzyme activity is important for viral entry into uninfected cells, for the release of recently formed virus particles from infected cells, and for the further spread of the infectious virus in the body. Oseltamivir activity reduces viral shedding and infectivity.",The molecular weight is 312.41.,Oseltamivir has a topological polar surface area of 90.65.,The log p value of  is 2.13.,Oseltamivir is approved.,Oseltamivir is a solid.,True
15762,"Trandolapril is a non-sulhydryl prodrug that belongs to the angiotensin-converting enzyme (ACE) inhibitor class of medications. It is metabolized to its biologically active diacid form, trandolaprilat, in the liver. Trandolaprilat inhibits ACE, the enzyme responsible for the conversion of angiotensin I (ATI) to angiotensin II (ATII). ATII regulates blood pressure and is a key component of the renin-angiotensin-aldosterone system (RAAS). Trandolapril may be used to treat mild to moderate hypertension, to improve survival following myocardial infarction in clinically stable patients with left ventricular dysfunction, as an adjunct treatment for congestive heart failure, and to slow the rate of progression of renal disease in hypertensive individuals with diabetes mellitus and microalbuminuria or overt nephropathy. For the treatment of mild to moderate hypertension, as an adjunct in the treatment of congestive heart failure (CHF), to improve survival following myocardial infarction (MI) in individuals who are hemodynamically stable and demonstrate symptoms of left ventricular systolic dysfunction or signs of CHF within a few days following acute MI, and to slow progression of renal disease in hypertensive patients with diabetes mellitus and microalbuminuria or overt nephropathy.  Trandolapril is the ethyl ester prodrug of a nonsulfhydryl ACE inhibitor, trandolaprilat. Trandolapril is deesterified in the liver to the diacid metabolite, trandolaprilat, which is approximately eight times more active as an inhibitor of ACE than its parent compound. ACE is a peptidyl dipeptidase that is part of the RAAS. The RAAS is a homeostatic mechanism for regulating hemodynamics, water and electrolyte balance. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from the granular cells of the juxtaglomerular apparatus in the kidneys. In the blood stream, renin cleaves circulating angiotensinogen to ATI, which is subsequently cleaved to ATII by ACE. ATII increases blood pressure via a number of mechanisms. First, it stimulates the secretion of aldosterone from the adrenal cortex. Aldosterone travels to the distal convoluted tubule (DCT) and collecting tubule of nephrons where it increases sodium and water reabsorption by increasing the number of sodium channels and sodium-potassium ATPases on cell membranes. Second, ATII stimulates the secretion of vasopressin (also known as antidiuretic hormone or ADH) from the posterior pituitary gland. ADH stimulates further water reabsorption from the kidneys via insertion of aquaporin-2 channels on the apical surface of cells of the DCT and collecting tubules. Third, ATII increases blood pressure through direct arterial vasoconstriction. Stimulation of the Type 1 ATII receptor on vascular smooth muscle cells leads to a cascade of events resulting in myocyte contraction and vasoconstriction. In addition to these major effects, ATII induces the thirst response via stimulation of hypothalamic neurons. ACE inhibitors inhibit the rapid conversion of ATI to ATII and antagonize RAAS-induced increases in blood pressure. ACE (also known as kininase II) is also involved in the enzymatic deactivation of bradykinin, a vasodilator. Inhibiting the deactivation of bradykinin increases bradykinin levels and may further sustain the effects of trandolaprilat by causing increased vasodilation and decreased blood pressure. The blood pressure lowering effect of trandolaprilat is due to a decrease in peripheral vascular resistance, which is not accompanied by significant changes in urinary excretion of chloride or potassium or water or sodium retention.  There are two isoforms of ACE: the somatic isoform, which exists as a glycoprotein comprised of a single polypeptide chain of 1277; and the testicular isoform, which has a lower molecular mass and is thought to play a role in sperm maturation and binding of sperm to the oviduct epithelium. Somatic ACE has two functionally active domains, N and C, which arise from tandem gene duplication. Although the two domains have high sequence similarity, they play distinct physiological roles. The C-domain is predominantly involved in blood pressure regulation while the N-domain plays a role in hematopoietic stem cell differentiation and proliferation. ACE inhibitors bind to and inhibit the activity of both domains, but have much greater affinity for and inhibitory activity against the C-domain. Trandolaprilat, the active metabolite of trandolapril, competes with ATI for binding to ACE and inhibits and enzymatic proteolysis of ATI to ATII. Decreasing ATII levels in the body decreases blood pressure by inhibiting the pressor effects of ATII as described in the Pharmacology section above. Trandolaprilat also causes an increase in plasma renin activity likely due to a loss of feedback inhibition mediated by ATII on the release of renin and/or stimulation of reflex mechanisms via baroreceptors. ",The molecular weight is 430.54.,Trandolapril has a topological polar surface area of 95.94.,The log p value of  is 2.1.,Trandolapril is approved.,Trandolapril is a solid.,True
15763,"A surface anesthetic that acts by preventing transmission of impulses along nerve fibers and at nerve endings. For general use as a lubricant and topical anesthetic on esophagus, larynx, mouth, nasal cavity, rectum, respiratory tract or trachea, urinary tract, vagina. It is also used to suppress gag reflex. Benzocaine is a local anesthetic commonly used as a topical pain reliever. It is the active ingredient in many over-the-counter analgesic ointments. It is also indicated for general use as a lubricant and topical anesthetic on intratracheal catheters and pharyngeal and nasal airways to obtund the pharyngeal and tracheal reflexes; on nasogastric and endoscopic tubes; urinary catheters; laryngoscopes; proctoscopes; sigmoidoscopes and vaginal specula. Benzocaine binds to sodium channels and reversibly stabilizes the neuronal membrane which decreases its permeability to sodium ions. Depolarization of the neuronal membrane is inhibited thereby blocking the initiation and conduction of nerve impulses.",The molecular weight is 165.19.,Benzocaine has a topological polar surface area of 52.32.,The log p value of  is 1.92.,Benzocaine is approved and investigational.,Benzocaine is a solid.,True
15764,"Mevastatin or compactin is a cholesterol-lowering agent isolated from <i>Penicillium citinium</i>. It was the first discovered agent belonging to the class of cholesterol-lowering medications known as statins. During a search for antibiotic compounds produced by fungi in 1971, Akira Endo at Sankyo Co. (Japan) discovered a class of compounds that appeared to lower plasma cholesterol levels. Two years later, the research group isolated a compound structurally similar to hydroxymethylglutarate (HMG) that inhibited the incorporation of acetate. The compound was proposed to bind to the reductase enzyme and was named compactin. Mevastatin is a competitive inhibitor of HMG-Coenzyme A (HMG-CoA) reductase with a binding affinity 10,000 times greater than the HMG-CoA substrate itself. Mevastatin is a pro-drug that is activated by <i>in vivo</i> hydrolysis of the lactone ring. It has served as one of the lead compounds for the development of the synthetic compounds used today. Not used therapeutically due to its many side effects.  The primary cause of cardiovascular disease is atherosclerotic plaque formation. Mevastatin lowers hepatic production of cholesterol to reduce the risk of cardiovascular disease. Mevastatin competitively inhibits HMG-CoA reductase. This inhibition prevents the rate limiting step in cholesterol synthesis. Decreased hepatic cholesterol levels causes increased uptake of low density lipoprotein (LDL) cholesterol and reduces cholesterol levels in the circulation.  Mevastatin is structurally similar to the HMG, a substituent of the endogenous substrate of HMG-CoA reductase. Mevastatin is a prodrug that is activated <i>in vivo</i> via hydrolysis of the lactone ring. The hydrolyzed lactone ring mimics the tetrahedral intermediate produced by the reductase allowing the agent to bind with 10,000 times greater affinity than its natural substrate. The bicyclic portion of mevastatin binds to the coenzyme A portion of the active site. ",,,,Mevastatin is experimental.,Mevastatin is a solid.,True
15765,"Phenylacetic acid is an organic compound containing a phenyl functional group and a carboxylic acid functional group. It is a white solid with a disagreeable odor. Because it is used in the illicit production of phenylacetone (used in the manufacture of substituted amphetamines), it is subject to controls in countries including the United States and China. For use as adjunctive therapy for the treatment of acute hyperammonemia and associated encephalopathy in patients with deficiencies in enzymes of the urea cycle.",The molecular weight is 136.15.,Phenylacetic acid has a topological polar surface area of 37.3.,The log p value of  is 1.41.,Phenylacetic acid is approved.,Phenylacetic acid is a solid.,True
15766,"Propoxycaine is a local anesthetic of the ester type that has a rapid onset of action and a longer duration of action than procaine hydrochloride. This drug was removed from the US market in 1996.  Although no longer available in the United States, this medication was used in combination with procaine to aid in anesthesia during dental procedures. Used in combination with procaine, it was the only dental local anesthetic available in cartridge form. Propoxycaine is a local anesthetic medication. It was used beginning in the 1950s during dental procedures. It has been combined with procaine to accelerate its onset of action and provide longer-lasting anesthetic effect. Propoxycaine is a local anesthetic which acts to decrease nerve impulses and therefore pain sensation during dental procedures. Propoxycaine is a para-aminobenzoic acid ester with local anesthetic activity. Propoxycaine binds to and blocks voltage-gated sodium channels, thereby inhibiting the ionic flux essential for the conduction of nerve impulses. This results in a loss of sensation.",The molecular weight is 294.4.,Propoxycaine has a topological polar surface area of 64.79.,The log p value of  is 3.41.,Propoxycaine is approved.,Propoxycaine is a solid.,True
15767,"Homatropine is an anticholinergic drug that acts as an antagonist at muscarinic acetylcholine receptors. It is present in antitussives, under the trade name Hycodan, in combination with hydrocodone (dihydrocodeinone) bitartrate indicated for the symptomatic relief of cough as oral tablets or solutions. Homatropine is included in subtherapeutic amounts as homatropine methylbromide to discourage deliberate overdosage. Homatropine hydrobromide has been administered as ophthalmic solutions as a cycloplegic to temporarily paralyze accomodation, and to induce mydriasis (the dilation of the pupil); however such therapeutic use has not been approved by the FDA to be safe and effective. Indicated as an overdose-rescuing agent in combination with hydrocodone antitussive. Homatropine is an anticholinergic drug that produces typical anticholinergic effects inducing mydriasis and cycloplegia. Other effects of structurally-related atropine that could also apply to homatropine include inhibition of secretions, tachycardia, relaxation of smooth muscle and central nervous effects including excitation. Homatropine is a competitive muscarinic receptor antagonist with a bulky aromatic group in place of the acetyl group of acetylcholine. It is expected to act in similar manner as atropine, producing similar parasympatholytic effects. By blocking muscarinic receptors and cholinergic signalling pathways, homatropine blocks the response of the iris sphincter muscle and cause the pupil to become unresponsive to light upon dilation or mydriasis. It also blocks the accommodative muscle of the ciliary body to cholinergic stimulation.",The molecular weight is 275.35.,Homatropine has a topological polar surface area of 49.77.,The log p value of  is 1.43.,Homatropine is approved.,Homatropine is a solid.,True
15768,"Rheumatoid arthritis (RA) is a chronic, autoimmune, systemic, and inflammatory disease that causes synovial joint symptoms and can limit range of motion in severe cases. The disease is associated with extra-articular manifestations, progressive disability, and comorbidities including cardiovascular disease and mental disorders. 50-70% of patients with RA are unable to achieve sustained clinical remission despite the availability of several treatments including disease-modifying anti-rheumatic drugs (DMARDS) like , interleukin-6 (IL-6) blockers, and tumor necrosis factor (TNF) inhibitors. New therapeutic developments target other inflammatory pathways implicated in RA including the Janus kinase (JAK) signaling pathway as seen with filgotinib.  Filgotinib is indicated for the treatment of active moderate to severe rheumatoid arthritis alone or in combination with methotrexate. Filgotinib is currently reserved for patients who are unable to tolerate or who have not responded adequately to one or more disease-modifying anti-rheumatic drugs (DMARDS). In addition to targeted Janus kinase (JAK) 1 inhibition, filgotinib targets pro-inflammatory cytokine signalling by inhibiting IL-6 induced STAT1 phosphorylation. Serum C-reactive protein levels are also reduced in response to filgotinib administration. There are four Janus kinase (JAK) enzymes including JAK1, JAK2, JAK3, and tyrosine kinase 2. JAK1 mediates inflammatory cytokine signaling, while JAK2 and JAK3 are important components of hematologic and immune functions. Filgotinib selectively inhibits JAK1 and is for example nearly 30-fold more selective for JAK1 compared to JAK2. ",,,,Filgotinib is approved and investigational.,,True
15769,"Valsartan belongs to the angiotensin II receptor blocker (ARB) family of drugs, which also includes , , , , and. ARBs selectively bind to angiotensin receptor 1 (AT1) and prevent the protein angiotensin II from binding and exerting its hypertensive effects, which include vasoconstriction, stimulation and synthesis of aldosterone and ADH, cardiac stimulation, and renal reabsorption of sodium, among others. Overall, valsartan's physiologic effects lead to reduced blood pressure, lower aldosterone levels, reduced cardiac activity, and increased excretion of sodium.  Valsartan is indicated for the treatment of hypertension to reduce the risk of fatal and nonfatal cardiovascular events, primarily strokes and myocardial infarctions. It is also indicated for the treatment of heart failure (NYHA class II-IV) and for left ventricular dysfunction or failure after myocardial infarction when the use of an angiotensin-converting enzyme inhibitor (ACEI) is not appropriate. Valsartan inhibits the pressor effects of angiotensin II with oral doses of 80 mg inhibiting the pressor effect by about 80% at peak with approximately 30% inhibition persisting for 24 hours. Removal of the negative feedback of angiotensin II causes a 2- to 3-fold rise in plasma renin and consequent rise in angiotensin II plasma concentration in hypertensive patients. Minimal decreases in plasma aldosterone were observed after administration of valsartan. Valsartan belongs to the angiotensin II receptor blocker (ARB) family of drugs, which selectively bind to angiotensin receptor 1 (AT1) and prevent angiotensin II from binding and exerting its hypertensive effects. These include vasoconstriction, stimulation and synthesis of aldosterone and ADH, cardiac stimulation, and renal reabsorption of sodium among others. Overall, valsartan's physiologic effects lead to reduced blood pressure, lower aldosterone levels, reduced cardiac activity, and increased excretion of sodium. ",The molecular weight is 435.53.,Valsartan has a topological polar surface area of 112.07.,The log p value of  is 4.86.,Valsartan is approved and investigational.,Valsartan is a solid.,True
15770,"First introduced in 1995, glimepiride is a member of the second-generation sulfonylurea (SU) drug class used for the management of type 2 diabetes mellitus (T2DM) to improve glycemic control. Type 2 diabetes is a metabolic disorder with increasing prevalences worldwide; it is characterized by insulin resistance in accordance with progressive β cell failure and long-term microvascular and macrovascular complications that lead to co-morbidities and mortalities. Sulfonylureas are one of the insulin secretagogues widely used for the management of type 2 diabetes to lower blood glucose levels. The main effect of SUs is thought to be effective when residual pancreatic β-cells are present, as they work by stimulating the release of insulin from the pancreatic beta cells and they are also thought to exert extra-pancreatic effects, such as increasing the insulin-mediated peripheral glucose uptake.  Glimepiride is indicated for the management of type 2 diabetes in adults as an adjunct to diet and exercise to improve glycemic control as monotherapy.  Glimepiride stimulates the secretion of insulin granules from the pancreatic beta cells and improves the sensitivity of peripheral tissues to insulin to increase peripheral glucose uptake, thus reducing plasma blood glucose levels and glycated hemoglobin (HbA1C) levels. A multi-center, randomized, placebo-controlled clinical trial evaluated the efficacy of glimepiride (1–8 mg) as monotherapy titrated over 10 weeks compared with placebo in T2DM subjects who were not controlled by diet alone. In this study, there was a reduction in fasting plasma glucose (FPG) by 46 mg/dL, post-prandial glucose (PPG) by 72 mg/dL, and HbA1c by 1.4% more than the placebo. In another randomized study comprising of patients with T2DM receiving either placebo or one of the three doses (1, 4, or 8 mg) of glimepiride during a 14-week study period, all glimepiride regimens significantly reduced FPG, PPG, and HbA1c values (P < 0.001) compared to placebo by the end of the study period. The 4- and 8-mg doses of glimepiride were more effective than the 1-mg dose; however, the 4-mg dose provided a nearly maximal antihyperglycemic effect. ATP-sensitive potassium channels on pancreatic beta cells that are gated by intracellular ATP and ADP. The hetero-octomeric complex of the channel is composed of four pore-forming Kir6.2 subunits and four regulatory sulfonylurea receptor (SUR) subunits. Alternative splicing allows the formation of channels composed of varying subunit isoforms expressed at different concentrations in different tissues. In pancreatic beta cells, ATP-sensitive potassium channels play a role as essential metabolic sensors and regulators that couple membrane excitability with glucose-stimulated insulin secretion (GSIS). When there is a decrease in the ATP:ADP ratio, the channels are activated and open, leading to K+ efflux from the cell, membrane hyperpolarization, and suppression of insulin secretion. In contrast, increased uptake of glucose into the cell leads to elevated intracellular ATP:ADP ratio, leading to the closure of channels and membrane depolarization. Depolarization leads to activation and opening of the voltage-dependent Ca2+ channels and consequently an influx of calcium ions into the cell. Elevated intracellular calcium levels causes the contraction of the filaments of actomyosin responsible for the exocytosis of insulin granules stored in vesicles. Glimepiride blocks the ATP-sensitive potassium channel by binding non-specifically to the B sites of both sulfonylurea receptor-1 (SUR1) and sulfonylurea receptor-2A (SUR2A) subunits as well as the A site of SUR1 subunit of the channel to promote insulin secretion from the beta cell. ",The molecular weight is 490.62.,Glimepiride has a topological polar surface area of 124.68.,The log p value of  is 3.96.,Glimepiride is approved.,Glimepiride is a solid.,True
15771,"A short-acting sulfonamide antibacterial with activity against a wide range of gram- negative and gram-positive organisms. For the treatment of severe, repeated, or long-lasting urinary tract infections, meningococcal meningitis, acute otitis media, trachoma, inclusion conjunctivitis, nocardiosis, chancroid, toxoplasmosis, malaria and other bacterial infections. Sulfisoxazole is a sulfonamide antibiotic. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of <i>p</i>-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus. Sulfisoxazole is a competitive inhibitor of the enzyme dihydropteroate synthetase. It inhibits bacterial synthesis of dihydrofolic acid by preventing the condensation of the pteridine with para-aminobenzoic acid (PABA), a substrate of the enzyme dihydropteroate synthetase. The inhibited reaction is necessary in these organisms for the synthesis of folic acid.",The molecular weight is 267.3.,Sulfisoxazole has a topological polar surface area of 98.22.,The log p value of  is 0.22.,Sulfisoxazole is approved and vet_approved.,Sulfisoxazole is a solid.,True
15772,"Tolcapone is a drug that inhibits the enzyme catechol-O-methyl transferase (COMT). It is used in the treatment of Parkinson's disease as an adjunct to levodopa/carbidopa medication. It is a yellow, odorless, non-hygroscopic, crystalline compound. Tolcapone is associated with a risk of hepatotoxicity. Used as an adjunct to levodopa/carbidopa therapy for the symptomatic treatment of Parkinson's Disease. This drug is generally reserved for patients with parkinsonian syndrome receiving levodopa/carbidopa who are experiencing symptom fluctuations and are not responding adequately to or are not candidates for other adjunctive therapies. Tolcapone is a potent, selective, and reversible inhibitor of catechol-O-methyltransferase (COMT). In humans, COMT is distributed throughout various organs. COMT catalyzes the transfer of the methyl group of S-adenosyl-L-methionine to the phenolic group of substrates that contain a catechol structure. Physiological substrates of COMT include dopa, catecholamines (dopamine, norepinephrine, epinephrine) and their hydroxylated metabolites. The function of COMT is the elimination of biologically active catechols and some other hydroxylated metabolites. COMT is responsible for the elimination of biologically active catechols and some other hydroxylated metabolites. In the presence of a decarboxylase inhibitor, COMT becomes the major metabolizing enzyme for levodopa catalyzing it to 3-methoxy-4-hydroxy-L-phenylalanine (3-OMD) in the brain and periphery. When tolcapone is given in conjunction with levodopa and an aromatic amino acid decarboxylase inhibitor, such as carbidopa, plasma levels of levodopa are more sustained than after administration of levodopa and an aromatic amino acid decarboxylase inhibitor alone. It is believed that these sustained plasma levels of levodopa result in more constant dopaminergic stimulation in the brain, leading to greater effects on the signs and symptoms of Parkinson's disease in patients as well as increased levodopa adverse effects, sometimes requiring a decrease in the dose of levodopa. The precise mechanism of action of tolcapone is unknown, but it is believed to be related to its ability to inhibit COMT and alter the plasma pharmacokinetics of levodopa, resulting in an increase in plasma levodopa concentrations. The inhibition of COMT also causes a reduction in circulating 3-OMD as a result of decreased peripheral metabolism of levodopa. This may lead to an increase distribution of levodopa into the CNS through the reduction of its competitive substrate, 3-OMD, for transport mechanisms. Sustained levodopa concentrations presumably result in more consistent dopaminergic stimulation, resulting in greater reduction in the manifestations of parkinsonian syndrome.",The molecular weight is 273.24.,Tolcapone has a topological polar surface area of 103.35.,The log p value of  is 3.25.,Tolcapone is approved and withdrawn.,Tolcapone is a solid.,True
15773,"Treprostinil is a synthetic analogue of prostacyclin, used to treat pulmonary hypertension. For use as a continuous subcutaneous infusion or intravenous infusion (for those not able to tolerate a subcutaneous infusion) for the treatment of pulmonary arterial hypertension in patients with NYHA Class II-IV symptoms to diminish symptoms associated with exercise. Pulmonary arterial hypertension (PAH) is a disease in which blood pressure is abnormally high in the arteries between the heart and lungs. PAH is characterized by symptoms of shortness of breath during physical exertion. The condition can ultimately lead to heart failure. Treprostinil is a potent oral antiplatelet agent. The major pharmacologic actions of treprostinil are direct vasodilation of pulmonary and systemic arterial vascular beds and inhibition of platelet aggregation. In animals, the vasodilatory effects reduce right and left ventricular afterload and increase cardiac output and stroke volume. Other studies have shown that treprostinil causes a dose-related negative inotropic and lusitropic effect. No major effects on cardiac conduction have been observed. The major pharmacological actions of treprostinil are direct vasodilation of pulmonary and systemic arterial vascular beds and inhibition of platelet aggregation. In addition to treprostinil's direct vasodilatory effects, it also inhibits inflammatory cytokine. As a synthetic analogue of prostacyclin, it binds to the prostacyclin receptor, which subsequently induces the aforementioned downstream effects.",The molecular weight is 390.52.,Treprostinil has a topological polar surface area of 86.99.,The log p value of  is 3.72.,Treprostinil is approved and investigational.,Treprostinil is a solid.,True
15774,"Ketorolac is a Non-steroidal anti-inflammatory drug (NSAID) and is commercially available as an oral tablet, injectable, nasal spray and as an ophthalmic solution.  Ketorolac is a Non-steroidal anti-inflammatory drug (NSAID) and has antipyretic, analgesic and anti-inflammatory properties.  It is indicated for short term management of acute pain that requires the caliber of pain management offered by opioids.  Clinicians may choose to initiate ketorolac to manage post-operative pain, spinal and soft tissue pain, rheumatoid arthritis, osteoarthritis, ankylosing spondylitis, menstrual disorders and headaches among other ailments.  Regardless of the etiology of pain, patients should use the lowest possible dose, and avoid using ketorolac for an extended period of time (ideally ≤ 5 days). A benefit of choosing ketorolac over other analgesics with similar potency is that that there does not appear to be a risk of dependence or tolerance with ketorolac use.    Ketorolac is a non-selective NSAID and acts by inhibiting both COX-1 and COX-2 enzymes which are normally responsible for converting arachidonic acid to prostaglandins. The COX-1 enzyme is constitutively active and can be found in platelets, gastric mucosa, and vascular endothelium. On the other hand, the COX-2 enzyme is inducible and mediates inflammation, pain and fever.  Ketorolac inhibits key pathways in prostaglandin synthesis which is crucial to it's mechanism of action. Although ketorolac is non-selective and inhibits both COX-1 and COX-2 enzymes, it's clinical efficacy is derived from it's COX-2 inhibition. The COX-2 enzyme is inducible and is responsible for converting arachidonic acid to prostaglandins that mediate inflammation and pain. By blocking this pathway, ketorolac achieves analgesia and reduces inflammation. Ketorolac is administered as a racemic mixture; however, the \S\"" enantiomer is largely responsible for it's pharmacological activity.""",The molecular weight is 255.27.,Ketorolac has a topological polar surface area of 59.3.,The log p value of  is 1.62.,Ketorolac is approved.,Ketorolac is a solid.,True
15775,"Tenoxicam, an antiinflammatory agent with analgesic and antipyretic properties, is used to treat osteoarthritis and control acute pain. For the treatment of rheumatoid arthritis, osteoarthritis, backache, and pain. Tenoxicam, an antiinflammatory agent with analgesic and antipyretic properties, is used to treat osteoarthritis and control acute pain. The antiinflammatory effects of tenoxicam may result from the inhibition of the enzyme cycooxygenase and the subsequent peripheral inhibition of prostaglandin synthesis. As prostaglandins sensitize pain receptors, their inhibition accounts for the peripheral analgesic effects of tenoxicam. Antipyresis may occur by central action on the hypothalamus, resulting in peripheral dilation, increased cutaneous blood flow, and subsequent heat loss.",The molecular weight is 337.37.,Tenoxicam has a topological polar surface area of 99.6.,The log p value of  is 1.61.,Tenoxicam is approved.,Tenoxicam is a solid.,True
15776,"Nabilone (marketed as Cesamet) is a synthetic form of delta-9-tetrahydrocannabinol (Δ⁹-THC), the primary psychoactive component of cannabis (marijuana). Although structurally distinct from THC, nabilone mimics THC's structure and pharmacological activity through weak partial agonist activity at Cannabinoid-1 (CB1R) and Cannabinoid-2 (CB2R) receptors, however it is considered to be twice as active as Δ⁹-THC. Nabilone is approved by the FDA for the treatment of nausea and vomiting associated with cancer chemotherapy in patients who have failed to respond adequately to conventional antiemetic treatments. Nabilone is indicated for the treatment of the nausea and vomiting associated with cancer chemotherapy in patients who have failed to respond adequately to conventional antiemetic treatments. This restriction is required because a substantial proportion of any group of patients treated with Nabilone can be expected to experience disturbing psychotomimetic reactions not observed with other antiemetic agents. Nabilone is a cannabinoid with therapeutic uses. It is an analog of dronabinol (also known as tetrahydrocannabinol or THC), the psychoactive ingredient in cannabis. Although structurally distinct from THC, nabilone mimics THC's structure and pharmacological activity through weak partial agonist activity at Cannabinoid-1 (CB1R) and Cannabinoid-2 (CB2R) receptors, however it is considered to be twice as active as Δ⁹-THC.  Nabilone is an orally active synthetic cannabinoid which, like other cannabinoids, has complex effects on the central nervous system (CNS). It has been suggested that the antiemetic effect of nabilone is caused by interaction with the cannabinoid receptor system, i.e., the CB (1) receptor, which is a component of the endocannabinoid system of the body. ",The molecular weight is 372.55.,Nabilone has a topological polar surface area of 46.53.,The log p value of  is 6.72.,Nabilone is approved and investigational.,Nabilone is a solid.,True
15777,"A synthetic hormone with anabolic and androgenic properties. Use to promote weight gain after weight loss following extensive surgery. Oxandrolone is an anabolic steroids indicated as adjunctive therapy to promote weight gain after weight loss following extensive surgery, chronic infections, or severe trauma, and in some patients who without definite pathophysiologic reasons fail to gain or to maintain normal weight, to offset the protein catabolism associated with prolonged administration of corticosteroids, and for the relief of the bone pain frequently accompanying osteoporosis. Anabolic steroids are synthetic derivatives of testosterone. Oxandrolones interact with androgen receptors in target tissues.",The molecular weight is 306.45.,Oxandrolone has a topological polar surface area of 46.53.,The log p value of  is 2.96.,Oxandrolone is approved and investigational.,Oxandrolone is a solid.,True
15778,"A sulphonylurea hypoglycemic agent with actions and uses similar to those of chlorpropamide. For use as an adjunct to diet to lower the blood glucose in patients with non-insulin dependent diabetes mellitus (Type II) whose hyperglycemia cannot be satisfactorily controlled by diet alone. Tolazamide is an oral blood glucose lowering drug of the sulfonylurea class. Tolazamide appears to lower the blood glucose acutely by stimulating the release of insulin from the pancreas, an effect dependent upon functioning beta cells in the pancreatic islets. The mechanism by which tolazamide lowers blood glucose during long-term administration has not been clearly established. With chronic administration in Type II diabetic patients, the blood glucose lowering effect persists despite a gradual decline in the insulin secretory response to the drug. Extrapancreatic effects may be involved in the mechanism of action of oral sulfonylurea hypoglycemic drugs. Some patients who are initially responsive to oral hypoglycemic drugs, including tolazamide, may become unresponsive or poorly responsive over time. Alternatively, tolazamide may be effective in some patients who have become unresponsive to one or more other sulfonylurea drugs. In addition to its blood glucose lowering actions, tolazamide produces a mild diuresis by enhancement of renal free water clearance. Sulfonylureas likely bind to ATP-sensitive potassium-channel receptors on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Depolarization stimulates calcium ion influx through voltage-sensitive calcium channels, raising intracellular concentrations of calcium ions, which induces the secretion, or exocytosis, of insulin.",The molecular weight is 311.4.,Tolazamide has a topological polar surface area of 78.51.,The log p value of  is 1.34.,Tolazamide is approved and investigational.,Tolazamide is a solid.,True
15779,"Dorzolamide is a non-bacteriostatic sulfonamide derivative and topical carbonic anhydrase (CA) inhibitor that treats elevated intraocular pressure (IOP) associated with open-angle glaucoma and ocular hypertension. It works by blocking an enzyme in the ciliary process that regulates ion balance and fluid pressure in the eyes. Unlike oral CA inhibitors, dorzolamide has negligible effects of acid-base or electrolyte disturbances and other systemic adverse effects. First marketed in 1995, dorzolamide is available in ophthalmic solutions as monotherapy marketed as Trusopt or in combination with as Cosopt PF. Dorzolamide is indicated for the management of elevated intraocular pressure in patients with ocular hypertension or open-angle glaucoma. It can also be used in combination with for the same indication in patients who are insufficiently responsive to ophthalmic beta-blockers. Dorzolamide is a carbonic anhydrase inhibitor that reduces elevated intraocular pressure in open-angle glaucoma or ocular hypertension. When used in combination with topic beta-adrenergic antagonists, dorzolamide has an additive effect of lowering intraocular pressure. The peak ocular hypotensive effect of dorzolamide is observed at about 2 hours following ophthalmic administration. Elevated intraocular pressure is a characteristic manifestation of ocular hypertension or open-angle glaucoma. The level of intraocular pressure (IOP) is governed by the balance between the production of aqueous humour (by ocular ciliary processes) and its outflow from the anterior segment of the eye via trabecular (conventional) or uveoscleral (unconventional) pathways. When there is an increase in the resistance to the trabecular outflow of aqueous humour, the intraocular pressure is elevated. Subsequently, optic nerve damage can occur from blood flow restrictions and mechanical distortion of ocular structures. Optic nerve damage can further result in optic disc cupping and progressive visual field loss (and blindness in some cases). ",The molecular weight is 324.43.,Dorzolamide has a topological polar surface area of 106.33.,The log p value of  is 0.15.,Dorzolamide is approved.,Dorzolamide is a solid.,True
15780,"Antibacterial, potentially toxic, and previously used to treat certain skin diseases. No longer prescribed. For the treatment of dermatitis herpetiformis, benign mucous membrane pemphigoid and pyoderma gangrenosum Sulfapyridine is a sulfonamide antibiotic. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of <i>p</i>-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus. Sulfapyridine is a competitive inhibitor of the bacterial enzyme dihydropteroate synthetase. The inhibited reaction is necessary in these organisms for the synthesis of folic acid by means of processing the substrate para-aminobenzoic acid (PABA). Dihydropteroate synthetase activity is vital in the synthesis of folate, and folate is required for cells to make nucleic acids, such as DNA or RNA. So if DNA molecules cannot be built, the cell cannot divide.",The molecular weight is 249.29.,Sulfapyridine has a topological polar surface area of 85.08.,The log p value of  is 0.84.,Sulfapyridine is approved.,Sulfapyridine is a solid.,True
15781,"Also known as _Aspirin_, acetylsalicylic acid (ASA) is a commonly used drug for the treatment of pain and fever due to various causes. Acetylsalicylic acid has both anti-inflammatory and antipyretic effects. This drug also inhibits platelet aggregation and is used in the prevention of blood clots stroke, and myocardial infarction (MI).  **Pain, fever, and inflammation** **Effects on pain and fever** Acetylsalicylic acid (ASA) blocks prostaglandin synthesis. It is non-selective for COX-1 and COX-2 enzymes. Inhibition of COX-1 results in the inhibition of platelet aggregation for about 7-10 days (average platelet lifespan). The acetyl group of acetylsalicylic acid binds with a serine residue of the cyclooxygenase-1 (COX-1) enzyme, leading to irreversible inhibition. This prevents the production of pain-causing prostaglandins. This process also stops the conversion of arachidonic acid to thromboxane A2 (TXA2), which is a potent inducer of platelet aggregation. Platelet aggregation can result in clots and harmful venous and arterial thromboembolism, leading to conditions such as pulmonary embolism and stroke. ",The molecular weight is 180.16.,Acetylsalicylic acid has a topological polar surface area of 63.6.,The log p value of  is 1.02.,Acetylsalicylic acid is approved and vet_approved.,Acetylsalicylic acid is a solid.,True
15782,"Vigabatrin is an analog of gamma-aminobutyric acid (), the main inhibitory neurotransmitter in the central nervous system, used in the treatment of refractory seizures and infantile spasms. It irreversibly inhibits the enzyme responsible for GABA metabolism, thereby increasing levels of circulating GABA. Although administered as a racemic mixture, only the S(+) enantiomer is pharmacologically active. Vigabatrin is indicated as adjunctive therapy in the treatment of refractory complex partial seizures in patients 2 years of age and older who have had inadequate responses to multiple previous treatments (i.e. not to be used for first-line therapy). It is also indicated as monotherapy in the treatment of infantile spasms in patients between 1 month and 2 years of age for whom the potential benefits outweigh the risk of vision loss. Vigabatrin is an antiepileptic agent chemically unrelated to other anticonvulsants. Vigabatrin prevents the metabolism of GABA by irreversibly inhibiting GABA transaminase (GABA-T). As vigabatrin is an irreversible inhibitor of gamma-aminobutyric acid transaminase (GABA-T), its duration of effect is thought to be dependent on the rate of GABA-T re-synthesis rather than on the rate of drug elimination. Gamma-aminobutyric acid (GABA) is the major inhibitory transmitter throughout the central nervous system, and the potentiation of GABAergic neurotransmission is therefore a crucial mechanism through which antiepileptic agents may combat the pathologic excitatory neurotransmission seen in epilepsy. Vigabatrin increases concentrations of GABA in the central nervous system by irreversibly inhibiting the enzymes responsible for its metabolism to succinic semialdehyde: gamma-aminobutyric acid transaminase (GABA-T). ",The molecular weight is 129.16.,Vigabatrin has a topological polar surface area of 63.32.,The log p value of  is -2.22.,Vigabatrin is approved.,Vigabatrin is a solid.,True
15783,"A histamine H1 antagonist given by mouth or parenterally for the control of postoperative and drug-induced vomiting and in motion sickness. (From Martindale, The Extra Pharmacopoeia, 30th ed, p935) For prevention and treatment of nausea, vomiting, and dizziness associated with motion sickness, and vertigo (dizziness caused by other medical problems). Cyclizine is a piperazine-derivative antihistamine used as an antivertigo/antiemetic agent. Cyclizine is used in the prevention and treatment of nausea, vomiting, and dizziness associated with motion sickness. Additionally, it has been used in the management of vertigo in diseases affecting the vestibular apparatus. Although the mechanism by which cyclizine exerts its antiemetic and antivertigo effects has not been fully elucidated, its central anticholinergic properties are partially responsible. The drug depresses labyrinth excitability and vestibular stimulation, and it may affect the medullary chemoreceptor trigger zone. It also possesses anticholinergic, antihistaminic, central nervous system depressant, and local anesthetic effects. Vomiting (emesis) is essentially a protective mechanism for removing irritant or otherwise harmful substances from the upper GI tract. Emesis or vomiting is controlled by the vomiting centre in the medulla region of the brain, an important part of which is the chemotrigger zone (CTZ). The vomiting centre possesses neurons which are rich in muscarinic cholinergic and histamine containing synapses. These types of neurons are especially involved in transmission from the vestibular apparatus to the vomiting centre. Motion sickness principally involves overstimulation of these pathways due to various sensory stimuli. Hence the action of cyclizine which acts to block the histamine receptors in the vomiting centre and thus reduce activity along these pathways. Furthermore since cyclizine possesses anti-cholinergic properties as well, the muscarinic receptors are similarly blocked.",The molecular weight is 266.39.,Cyclizine has a topological polar surface area of 6.48.,The log p value of  is 3.8.,Cyclizine is approved.,Cyclizine is a solid.,True
15784,"Gliquidone is a sulfonylurea drug used to treat diabetes mellitus type 2. It is an ATP-dependent K+ (KATP) channel blocker. This block causes a depolarization which leads to activation of voltage-dependent Ca channels and Ca2+ influx, and eventually increases insulin release. Used in the treatment of diabetes mellitus type 2. Gliquidone is an anti-diabetic drug in the sulfonylurea class. In patients with diabetes mellitus, there is a deficiency or absence of a hormone manufactured by the pancreas called insulin. Insulin is the main hormone responsible for the control of sugar in the blood. Gliquidone is an antidiabetic medication which is used in those patients with adult maturity onset or non-insulin dependent diabetes (NIDDM). It works by lowering blood sugar levels by stimulating the production and release of insulin from the pancreas. It also promotes the movement of sugar from the blood into the cells in the body which need it. The mechanism of action of gliquidone in lowering blood glucose appears to be dependent on stimulating the release of insulin from functioning pancreatic beta cells, and increasing sensitivity of peripheral tissues to insulin. Gliquidone likely binds to ATP-sensitive potassium channel receptors on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Membrane depolarization stimulates calcium ion influx through voltage-sensitive calcium channels. This increase in intracellular calcium ion concentration induces the secretion of insulin.",The molecular weight is 527.64.,Gliquidone has a topological polar surface area of 121.88.,The log p value of  is 5.06.,Gliquidone is approved and investigational.,Gliquidone is a solid.,True
15785,"Glisoxepide is one of the sulphonamide-derived oral antidiabetic drugs. It inhibits the uptake of bile acids into isolated rat hepatocytes. However it inhibits taurocholate uptake only in the absence of sodium ions. Glisoxepide uptake could be further inhibited by blockers of the hepatocellular monocarboxylate transporter, by the loop diuretic bumetanide, by 4,4'-diisothiocyano-2,2'-stilbenedisulfonate (DIDS) and by sulphate. These results are consistent with the transport of glisoxepide via the transport system for the unconjugated bile acid cholate.  For the treatment of diabetes mellitus type 2. Glisoxepide is a sulfonylurea agent. It stimulates beta cells of the islet of Langerhans in the pancreas to release insulin. It also enhances peripheral insulin sensitivity. Overall it potentiates insulin release and improves insulin dynamics. Glisoxepide is a hypoglycemic sulphonylurea agent. The sulphonylureas are a family of drugs based on a common sulphonylurea core. These drugs act via augmentation of secretion of insulin from pancreatic beta-cells. Sulphonylureas may also cause a reduction in serum glucagon and potentiate the action of insulin at the extrapancreatic tissues. Glisoxepide functions as a non-selective K(ATP) channel blocker. It is thought to stimulate insulin secretion by closing the ATP-sensitive K(+) (K(ATP)) channels (Kir6.2/SUR1 complex, KATP channels) in pancreatic beta-cells. This inhibits a tonic, hyperpolarizing efflux of potassium, thus causing the electric potential over the membrane to become more positive. This depolarization opens voltage-gated Ca2+ channels. The rise in intracellular calcium leads to increased fusion of insulin granulae with the cell membrane, and therefore increased secretion of (pro)insulin.",The molecular weight is 449.53.,Glisoxepide has a topological polar surface area of 133.64.,The log p value of  is 0.71.,Glisoxepide is investigational.,Glisoxepide is a solid.,True
15786,"A mixture of fish oil and primrose oil, doconexent is used as a high-docosahexaenoic acid (DHA) supplement. DHA is a 22 carbon chain with 6 cis double bonds with anti-inflammatory effects. It can be biosythesized from alpha-linolenic acid or commercially manufactured from microalgae. It is an omega-3 fatty acid and primary structural component of the human brain, cerebral cortex, skin, and retina thus plays an important role in their development and function. The amino-phospholipid DHA is found at a high concentration across several brain subcellular fractions, including nerve terminals, microsomes, synaptic vesicles, and synaptosomal plasma membranes. Used as a high-docosahexaenoic acid (DHA) oral supplement.  DHA in the central nervous system is found in the phospholipid bilayers where it modulates the physical environment and increase the free volume within the membrane bilayer. It influences the G-protein coupled receptor activity and affects transmembrane transport and cell interaction with the exterior world. It is also reported to promote apoptosis, neuronal differentiation and ion channel activity. Like other polyunsaturated fatty acids, DHA acts as a ligand at PPARs that plays an anti-inflammatory effect and regulate inflammatory gene expression and NFκB activation. DHA also gives rise to resolvins and related compounds (e.g., protectins) through pathways involving cyclooxygenase and lipoxygenase enzymes to resolve the inflammatory responses.  DHA and its conversion to other lipid signalling moleccules compete with the arachidonic acid cascade from endogenous phospholipids and shift the inflammatory state to being more anti-inflammatory. DHA inhibits endotoxin-stimulated production of IL-6 and IL-8 in human endothelial cells. Derivatives of DHA are anti-inflammatory lipid mediators. Lipid mediators resolvin D1 and protectin D1 all inhibit transendothelial migration of neutrophils, so preventing neutrophilic infiltration at sites of inflammation, resolvin D1 inhibits IL-1β production, and protectin D1 inhibits TNF and IL-1β production. Monoxydroxy derivative of DHA converted by LOX inhibit thromboxane-induced platelet aggregation. DHA supplementation has also shown to reduce the levels of serum C-reactive protein (CRP) and other circulating markers of inflammation such as neutrophils in hypertriglyceridemic men. ",The molecular weight is 328.5.,Doconexent has a topological polar surface area of 37.3.,The log p value of  is 7.48.,Doconexent is approved and investigational.,Doconexent is a liquid.,True
15787,,The molecular weight is 146.15.,Coumarin has a topological polar surface area of 26.3.,The log p value of  is 1.41.,Coumarin is experimental.,Coumarin is a solid.,False
15788,"Developed by the German pharmaceutical company, Merckle GmbH, together with EuroAlliance partners Alfa Wassermann and Lacer, licofelone (ML3000) is a dual COX/LOX inhibitor and the first member of this new class of analgesic and anti-inflammatory drugs. It is currently under evaluation as a treatment for osteoarthritis (OA), the most common form of arthritis. Although phase III trials have been successfully completed in OA patients no dates for regulatory submission have yet been given. For the management of osteoarthritis. Licofelone belongs to a novel class of dual-acting anti-inflammatory drugs called COX/LO inhibitors. This group of drugs simultaneously inhibits the enzymes cyclooxygenase (COX) and 5-lipoxygenase (LO). Licofelone, through combined 5-LOX/COX-inhibition, reduces levels of inflammatory prostaglandins and leukotrienes.",,,,Licofelone is investigational.,Licofelone is a solid.,True
15789,"Tienilic acid, or ticrynafen, is a diuretic drug with uric acid-lowering action which was marketed for the treatment of hypertension. It was withdrawn in 1982 after case reports in the United States suggested a link between ticrynafen and hepatitis. (Manier et al., 1982) For the treatment of hypertension.",The molecular weight is 331.16.,Tienilic acid has a topological polar surface area of 63.6.,The log p value of  is 3.23.,Tienilic acid is withdrawn.,Tienilic acid is a solid.,True
15790,"Ximelagatran is an anticoagulant intended to become a replacement for warfarin by overcoming the dietary restrictions, drug interaction, and monitoring issues associated with the former. In 2006, its manufacturer AstraZeneca announced that it would not attempt to market ximelagatran after reports of hepatotoxicity (liver damage) during trials, and to discontinue its distribution in countries where the drug had been approved. For the treatment of acute deep vein thrombosis. Ximelagatran was the first member of the drug class of direct thrombin inhibitors that can be taken orally. Its effect is solely related to the inhibition of thrombin. ",The molecular weight is 473.57.,Ximelagatran has a topological polar surface area of 143.85.,The log p value of  is 1.77.,Ximelagatran is approved and investigational and withdrawn.,Ximelagatran is a solid.,True
15791,"Crisaborole is a novel oxaborole approved by FDA on December 14, 2016 as Eucrisa, a topical treatment of for mild to moderate atopic dermatitis.  Intended for the topical treatment of mild to moderate atopic dermatitis in patients 2 years of age and older. Crisaborole has broad-spectrum anti-inflammatory activity by mainly targeting phosphodiesterase 4 (PDE4) enzyme that is a key regulator of inflammatory cytokine production. As this enzyme is expressed in keratinocytes and immune cells, crisaborole mediates an anti-inflammatory effect on almost all inflammatory cells. Topical application of this drug is useful as it potentiates the localization of this drug in the skin and this anti-inflammatory activity is in the low micromolar range. Inhibition of PDE4 by crisaborole leads to elevated levels of cyclic adenosine monophosphate (cAMP). Increased intracellular levels of cAMP inhibit the NF-kB pathway and suppress the release of pro-inflammatory mediators such as TNF-alfa and various interleukins that play a causative role in psoriasis and atopic dermatitis. Suppression of downstream effects in different cell types may explain the therapeutic role of crisaborole in immune-mediated skin diseases. ",The molecular weight is 251.05.,Crisaborole has a topological polar surface area of 62.48.,The log p value of  is 2.63.,Crisaborole is approved and investigational.,Crisaborole is a solid.,True
15792,"Sulfadimethoxine is a sulfonamide antibiotic. Sulfadimethoxine is used to treat many infections including treatment of respiratory, urinary tract, enteric, and soft tissue infections. It is most frequently used in veterinary medicine, although it is approved in some countries for use in humans. Sulfadimethoxine inhibits bacterial synthesis of folic acid (pteroylglutamic acid) from para-aminobenzoic acid. Sulfadimethoxine is approved in Russia for use in humans, including children, and has been successfully used there for more than 35 years. It is widely available in Russia as an over-the-counter drug manufactured by a number of Russian pharmaceutical companies. For use in the treatment of infections. Sulfadimethoxine has been shown to be effective against streptococci, klebsiella, proteus, shigella, staphylococci, escherichia, and salmonella.",The molecular weight is 310.33.,Sulfadimethoxine has a topological polar surface area of 116.43.,The log p value of  is 1.98.,Sulfadimethoxine is approved and vet_approved.,Sulfadimethoxine is a solid.,True
15793,"Lornoxicam (chlortenoxicam) is a new nonsteroidal anti-inflammatory drug (NSAID) of the oxicam class with analgesic, anti-inflammatory and antipyretic properties. Lornoxicam differs from other oxicam compounds in its potent inhibition of prostaglandin biosynthesis, a property that explains the particularly pronounced efficacy of the drug. Lornoxicam is approved for use in Japan. For the treatment of acute mild to moderate pain, as well as pain and inflammation of the joints caused by certain types of rheumatic diseases. Lornoxicam is a non-steroidal anti-inflammatory drug (NSAID) that belongs to the oxicam class. As with other NSAIDS, lornoxicam is a potent inhibitor of the cyclooxgenase enzymes, which are responsible for catalyzing the formation of prostaglandins (act as messenger molecules in the process of inflammation) and thromboxane from arachidonic acid. Unlike some NSAIDS, lornoxicam's inhibition of cyclooxygenase does not lead to an increase in leukotriene formation, meaning that arachidonic acid is not moved to the 5-lipoxygenase cascade, resulting in the minimization of the risk of adverse events. Like other NSAIDS, lornoxicam's anti-inflammatory and analgesic activity is related to its inhibitory action on prostaglandin and thromboxane synthesis through the inhibition of both COX-1 and COX-2. This leads to the reduction of inflammation, pain, fever, and swelling, which are mediated by prostaglandins. However, the exact mechanism of lornoxicam, like that of the other NSAIDs, has not been fully determined.",The molecular weight is 371.81.,Lornoxicam has a topological polar surface area of 99.6.,The log p value of  is 2.34.,Lornoxicam is approved and investigational.,Lornoxicam is a solid.,True
15794,"Aceclofenac is an oral non-steroidal anti-inflammatory drug (NSAID) with marked anti-inflammatory and analgesic properties used to treat osteoarthritis, rheumatoid arthritis and ankylosing spondylitis. It is reported to have a higher anti-inflammatory action or at least comparable effects than conventional NSAIDs in double-blind studies. Aceclofenac potently inhibits the cyclo-oxygenase enzyme (COX) that is involved in the synthesis of prostaglandins, which are inflammatory mediators that cause pain, swelling, inflammation, and fever. Aceclofenac belongs to BCS Class II as it possesses poor aqueous solubility. It displays high permeability to penetrate into synovial joints where in patients with osteoarthritis and related conditions, the loss of articular cartilage in the area causes joint pain, tenderness, stiffness, crepitus, and local inflammation. Aceclofenac is also reported to be effective in other painful conditions such as dental and gynaecological conditions. In 1991, aceclofenac was developed as an analog of a commonly prescribed NSAID, , via chemical modification in effort to improve the gastrointestinal tolerability of the drug. It is a more commonly prescribed drug in Europe. Aceclofenac is indicated for the relief of pain and inflammation in osteoarthritis, rheumatoid arthritis and ankylosing spondylitis.  Aceclofenac is a NSAID that inhibits both isoforms of COX enzyme, a key enzyme involved in the inflammatory cascade. COX-1 enzyme is a constitutive enzyme involved in prostacyclin production and protective functions of gastric mucosa whereas COX-2 is an inducible enzyme involved in the production of inflammatory mediators in response to inflammatory stimuli. Aceclofenac displays more selectivity towards COX-2 (IC50 of 0.77uM) than COX-1 (IC50 of >100uM), which promotes its gastric tolerance compared to other NSAIDs. The primary metabolite, 4'-hydroxyaceclofenac, also minimally inhibits COX-2 with IC50 value of 36uM. Although the mode of action of aceclofenac is thought to mainly arise from the inhibition of synthesis of prostaglandins (PGE2), aceclofenac also inhibits the production of inflammatory cytokines, interleukins (IL-1β, IL-6), and tumor necrosis factors (TNF). It is also reported that aceclofenac also affects the cell adhesion molecules from neutrophils. Aceclofenac also targets the synthesis of glycosaminoglycan and mediates chrondroprotective effects.  Through COX-2 inhibition, aceclofenac downregulates the production of various inflammatory mediators including prostaglandin E2 (PGE2), IL-1β, and TNF from the arachidonic acid (AA) pathway. Inhibition of IL-6 is thought to be mediated by diclofenac converted from aceclofenac. Suppressed action of inflammatory cytokines decreases the production of reactive oxygen species. Aceclofenac is shown to decreased production of nitrous oxide in human articular chondrocytes. In addition, aceclofenac interferes with neutrophil adhesion to endothelium by decreasing the expression of L-selectin (CD62L), which is a cell adhesion molecule expressed on lymphocytes. Aceclofenac is proposed to stimulate the synthesis of glycosaminoglycan in human osteoarthritic cartilage which may be mediated through its inhibitory action on IL-1 production and activity. The chrondroprotective effects are generated by 4'-hydroxyaceclofenac which suppresses IL-1 mediated production of promatrix metalloproteinase-1 and metalloproteinase-3 and interferes with the release of proteoglycan from chrondrocytes. ",The molecular weight is 354.18.,Aceclofenac has a topological polar surface area of 75.63.,The log p value of  is 4.59.,Aceclofenac is approved and investigational.,Aceclofenac is a solid.,True
15795,"Sulfamoxole is an antibacterial in the sulfonamide class. For the treatment of bacterial infection. Sulfamoxole is a sulfonamide antibiotic. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of <i>p</i>-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus. Sulfamoxole is a competitive inhibitor of the bacterial enzyme dihydropteroate synthetase. This enzyme is needed for the proper processing of para-aminobenzoic acid (PABA) which is essential for folic acid synthesis. The inhibited reaction is necessary in these organisms for the synthesis of folic acid.",The molecular weight is 267.3.,Sulfamoxole has a topological polar surface area of 98.22.,The log p value of  is 0.5.,Sulfamoxole is experimental.,Sulfamoxole is a solid.,True
15796,Glibornuride is a sulfonylurea-type anti-diabetic drug.,The molecular weight is 366.48.,Glibornuride has a topological polar surface area of 95.5.,The log p value of  is 3.7.,Glibornuride is investigational and withdrawn.,Glibornuride is a solid.,True
15797,"Olodaterol is a novel, long-acting beta2-adrenergic agonist (LABA) that exerts its pharmacological effect by binding and activating beta2-adrenergic receptors located primarily in the lungs. Beta2-adrenergic receptors are membrane-bound receptors that are normally activated by endogenous epinephrine whose signalling, via a downstream L-type calcium channel interaction, mediates smooth muscle relaxation and bronchodilation. Activation of the receptor stimulates an associated G protein which then activates adenylate cyclase, catalyzing the formation of cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA). Elevation of these two molecules induces bronchodilation by relaxation of airway smooth muscles. It is by this mechanism that olodaterol is used for the treatment of chronic obstructive pulmonary disease (COPD) and the progressive airflow obstruction that is characteristic of it. Treatment with bronchodilators helps to mitigate associated symptoms such as shortness of breath, cough, and sputum production. Single doses of olodaterol have been shown to improve forced expiratory volume in 1 sec (FEV1) for 24 h in patients with COPD, allowing once daily dosing. A once-a-day treatment with a LABA has several advantages over short-acting bronchodilators and twice-daily LABAs including improved convenience and compliance and improved airflow over a 24-hour period. Despite similarities in symptoms, olodaterol is not indicated for the treatment of acute exacerbations of COPD or for the treatment of asthma. Olodaterol is indicated for use in chronic obstructive pulmonary disease (COPD), including chronic bronchitis and/or emphysema. It is not indicated for the treatment of acute exacerbations of COPD or for the treatment of asthma. Olodaterol is a potent agonist of the human beta2-adrenergic receptor in vitro, and is highly selective for this receptor, with much lower levels of activity at the b1- and b3-adrenergic receptors that are commonly expressed on cardiac smooth muscle and adipose tissue, respectively. Binding to the receptor causes smooth muscle relaxation in the lungs and bronchodilation. It has also been shown to potently reverse active bronchoconstriction.  Olodaterol is a long-acting beta2-adrenergic agonist (LABA) that exerts its pharmacological effect by binding and activating beta2-adrenergic receptors located primarily in the lungs. Beta2-adrenergic receptors are membrane-bound receptors that are normally activated by endogenous epinephrine whose signalling, via a downstream L-type calcium channel interaction, mediates smooth muscle relaxation and bronchodilation. Activation of the receptor stimulates an associated G protein which then activates adenylate cyclase, catalyzing the formation of cyclic adenosine monophosphate (cAMP) and protein kinase A (PKA). Elevation of these two molecules induces bronchodilation by relaxation of airway smooth muscles.",The molecular weight is 386.45.,Olodaterol has a topological polar surface area of 100.05.,The log p value of  is 1.44.,Olodaterol is approved.,Olodaterol is a solid.,True
15798,"Lifitegrast is a FDA approved drug for the treatment of keratoconjunctivitis sicca (dry eye syndrome). It is a tetrahydroisoquinoline derivative and lymphocyte function-associated antigen-1 ( LFA-1) antagonist that was discovered through the rational design process. The ophthalmic solution was approved in July, 2016 under the trade name Xiidra. It has shown to protect the corneal surface and alleviate the symptoms of dry eye syndrome with fast onset of action and well tolerated profile in both local and systemic setting. For the treatment of signs and symptoms of keratoconjunctivitis sicca (dry eye syndrome). Lifitegrast addresses both the symptoms and the resulting ocular surface damage by interfering with ocular inflammatory cycle. Lifitegrast is a lymphocyte function–associated antigen-1 antagonist through direct competitive antagonism and sequentially inhibits the T-cell recruitment, activation, and proinflammatory cytokine release associated with dry eye syndrome.  Lifitegrast binds to the integrin lymphocyte function-associated antigen-1 (LFA-1), a cell surface protein found on leukocytes and blocks the interaction of LFA-1 with its cognate ligand intercellular adhesion molecule-1 (ICAM-1). ICAM-1 may be overexpressed in corneal and conjunctival tissues in dry eye disease. LFA-1/ICAM-1 interaction can contribute to the formation of an immunological synapse resulting in T-cell proliferation/activation and migration to target tissues. In vitro studies demonstrated that lifitegrast may inhibit T-cell adhesion to ICAM-1 in a human T-cell line and may inhibit secretion of inflammatory cytokines, inflammatory mediators, chemokines, TNF-α, and IL-1 in human peripheral blood mononuclear cells.",The molecular weight is 615.48.,Lifitegrast has a topological polar surface area of 133.99.,The log p value of  is 2.28.,Lifitegrast is approved.,Lifitegrast is a solid.,True
15799,"Avatrombopag (_Doptelet_), is an orally administered, small-molecule thrombopoietin receptor (c-Mpl) agonist which increases platelet number, but not platelet activation ,. This decreases the need for blood transfusions.  Indicated for the treatment of thrombocytopenia in adult patients with chronic liver disease who are scheduled to undergo a procedure. Avatrombopag is an orally bioavailable, small molecule thrombopoietin (TPO) receptor agonist that stimulates proliferation and differentiation of megakaryocytes from bone marrow progenitor cells resulting in an increased production of platelets. Avatrombopag is not competitive with thrombopoietin for binding to the TPO receptor and has an additive pharmacological effect with TPO on platelet production.",,,,Avatrombopag is approved and investigational.,Avatrombopag is a solid.,True
15800,"Fluindione is under investigation for the treatment of Venous Thrombosis, Pulmonary Embolism, Permanent Atrial Fibrillation, and Anticoagulating Treatment on a Duration at Least 12-month-old Superior. Fluindione has been investigated for the treatment of Blood Coagulation Disorders.",The molecular weight is 240.23.,Fluindione has a topological polar surface area of 34.14.,The log p value of  is 2.95.,Fluindione is approved and investigational.,,True
15801,,The molecular weight is 271.34.,Carbutamide has a topological polar surface area of 101.29.,The log p value of  is 1.02.,Carbutamide is experimental.,,False
15802,,The molecular weight is 311.4.,Metahexamide has a topological polar surface area of 101.29.,The log p value of  is 1.91.,Metahexamide is experimental.,,False
15803,"Sulfisoxazole acetyl is an ester of _sulfisoxazole_, a broad-spectrum sulfanilamide and a synthetic analog of para-aminobenzoic acid (PABA) with antibacterial activity. Sulfisoxazole acetyl competes with PABA for the bacterial enzyme, _dihydropteroate synthase_, preventing the incorporation of PABA into dihydrofolic acid, which is the precursor of folic acid. This process causes an inhibition of bacterial folic acid synthesis and de novo synthesis of purines and pyrimidines, resulting in cell growth arrest and cell death. Acute, recurrent or chronic urinary tract infections (primarily pyelonephritis, pyelitis and cystitis) due to susceptible organisms (usually Escherichia coli, Klebsiella-Enterobacter, staphylococcus, Proteus mirabilis and, less frequently, Proteus vulgaris) in the absence of obstructive uropathy or foreign bodies  Sulfisoxazole is a sulfonamide antibiotic. The sulfonamides are synthetic bacteriostatic antibiotics with action against most gram-positive and many gram-negative organisms. Many strains of an individual species may be resistant to this drugf. Sulfonamides inhibit the multiplication of bacteria by acting as competitive inhibitors of <i>p</i>-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus. Sulfisoxazole is a competitive inhibitor of the enzyme dihydropteroate synthetase. It inhibits bacterial synthesis of dihydrofolic acid by preventing the condensation of the pteridine with para-aminobenzoic acid (PABA), a substrate of the enzyme dihydropteroate synthetase. The inhibited reaction is necessary in these organisms for the synthesis of folic acid.",The molecular weight is 309.34.,Acetyl sulfisoxazole has a topological polar surface area of 106.5.,The log p value of  is 1.03.,Acetyl sulfisoxazole is approved and vet_approved.,Acetyl sulfisoxazole is a solid.,True
15804,"An antineoplastic agent used in the treatment of lymphoproliferative diseases including hairy-cell leukemia. For the treatment of active hairy cell leukemia (leukemic reticuloendotheliosis) as defined by clinically significant anemia, neutropenia, thrombocytopenia, or disease-related symptoms. Also used as an alternative agent for the treatment of chronic lymphocytic leukemia (CLL), low-grade non-Hodgkin's lymphoma, and cutaneous T-cell lymphoma. Cladribine is a synthetic purine nucleoside that acts as an antineoplastic agent with immunosuppressive effects. Cladribine differs structurally from deoxyadenosine only by the presence of a chlorine atom at position 2 of the purine ring, which results in resistance to enzymatic degradation by adenosine deaminase. Due to this resistance, cladribine exhibits a more prolonged cytotoxic effect than deoxyadenosine against resting and proliferating lymphocytes. Cladribine is one of a group of chemotherapy drugs known as the anti-metabolites.&nbsp;Anti-metabolites stop cells from making and repairing DNA, which are processes that are necessary for cancer cells to grow and multiply. Cladribine is structurally related to fludarabine and pentostatin but has a different mechanism of action. Although the exact mechanism of action has not been fully determined, evidence shows that cladribine is phosphorylated by deoxycytidine kinase to the nucleotidecladribine triphosphate (CdATP; 2-chloro-2′-deoxyadenosine 5′-triphosphate), which accumulates and is incorporated into DNA in cells such as lymphocytes that contain high levels of deoxycytidine kinase and low levels of deoxynucleotidase, resulting in DNA strand breakage and inhibition of DNA synthesis and repair. High levels of CdATP also appear to inhibit ribonucleotide reductase, which leads to an imbalance in triphosphorylated deoxynucleotide (dNTP) pools and subsequent DNA strand breaks, inhibition of DNA synthesis and repair, nicotinamide adenine dinucleotide (NAD) and ATP depletion, and cell death. Unlike other antimetabolite drugs, cladribine has cytotoxic effects on resting as well as proliferating lymphocytes. However, it does cause cells to accumulate at the G1/S phase junction, suggesting that cytotoxicity is associated with events critical to cell entry into S phase. It also binds purine nucleoside phosphorylase (PNP), however no relationship between this binding and a mechanism of action has been established.",The molecular weight is 285.69.,Cladribine has a topological polar surface area of 119.31.,The log p value of  is -0.91.,Cladribine is approved and investigational.,Cladribine is a solid.,True
15805,"Clofarabine is a purine nucleoside antimetabolite that is being studied in the treatment of cancer. It is marketed as Clolar in the U.S. and Canada, or Evoltra in Europe, Australia, and New Zealand. Clofarabine is used in paediatrics to treat a type of leukaemia called relapsed or refractory acute lymphoblastic leukaemia (ALL), only after at least two other types of treatment have failed. It is not known if the drug extends life expectancy. Its potential use in acute myeloid leukaemia (AML) and juvenile myelomonocytic leukaemia (JMML) has been investigated. For the treatment of pediatric patients 1 to 21 years old with relapsed or refractory acute lymphocytic (lymphoblastic) leukemia after at least two prior regimens. It is designated as an orphan drug by the FDA for this use. Clofarabine is a purine nucleoside antimetabolite that differs from other puring nucleoside analogs by the presence of a chlorine in the purine ring and a flourine in the ribose moiety. Clofarabine seems to interfere with the growth of cancer cells, which are eventually destroyed. Since the growth of normal body cells may also be affected by clofarabine, other effects also occur. Clofarabine prevents cells from making DNA and RNA by interfering with the synthesis of nucleic acids, thus stopping the growth of cancer cells. Clofarabine is metabolized intracellularly to the active 5'-monophosphate metabolite by deoxycytidine kinase and 5'-triphosphate metabolite by mono- and di-phospho-kinases. This metabolite inhibits DNA synthesis through an inhibitory action on ribonucleotide reductase, and by terminating DNA chain elongation and inhibiting repair through competitive inhibition of DNA polymerases. This leads to the depletion of the intracellular deoxynucleotide triphosphate pool and the self-potentiation of clofarabine triphosphate incorporation into DNA, thereby intensifying the effectiveness of DNA synthesis inhibition. The affinity of clofarabine triphosphate for these enzymes is similar to or greater than that of deoxyadenosine triphosphate. In preclinical models, clofarabine has demonstrated the ability to inhibit DNA repair by incorporation into the DNA chain during the repair process. Clofarabine 5'-triphosphate also disrupts the integrity of mitochondrial membrane, leading to the release of the pro-apoptotic mitochondrial proteins, cytochrome C and apoptosis-inducing factor, leading to programmed cell death.",The molecular weight is 303.68.,Clofarabine has a topological polar surface area of 119.31.,The log p value of  is -0.46.,Clofarabine is approved and investigational.,Clofarabine is a solid.,True
15806,,,,,2'-Deoxycytidine is experimental and investigational.,2'-Deoxycytidine is a solid.,False
15807,"Troxacitabine is a nucleoside analog with antineoplastic activity. There has been growing interest in its development for the treatment of patients with refractory lymphoproliferative conditions. Investigated for use/treatment in leukemia (myeloid). Troxacitabine is a beta-L-nucleoside analog, which has shown preclinical antitumor activity in human xenograft tumor models and antileukemic response in patients with relapsed myeloid leukemia. Troxacitabine is activated by cellular kinases and incorporated into DNA, inhibiting its replication. In contrast to other cytosine nucleoside analogs, troxacitabine is resistant to inactivation by cytidine deaminase (CD).",The molecular weight is 213.19.,Troxacitabine has a topological polar surface area of 97.38.,The log p value of  is -1.77.,Troxacitabine is investigational.,Troxacitabine is a solid.,True
15808,"One of the folic acid antagonists that is used as an antimalarial or with a sulfonamide to treat toxoplasmosis. For the treatment of toxoplasmosis and acute malaria; For the prevention of malaria in areas non-resistant to pyrimethamine Pyrimethamine is an antiparasitic compound commonly used as an adjunct in the treatment of uncomplicated, chloroquine resistant, P. falciparum malaria. Pyrimethamine is a folic acid antagonist and the rationale for its therapeutic action is based on the differential requirement between host and parasite for nucleic acid precursors involved in growth. This activity is highly selective against plasmodia and Toxoplasma gondii. Pyrimethamine possesses blood schizonticidal and some tissue schizonticidal activity against malaria parasites of humans. However, the 4-amino-quinoline compounds are more effective against the erythrocytic schizonts. It does not destroy gametocytes, but arrests sporogony in the mosquito. The action of pyrimethamine against Toxoplasma gondii is greatly enhanced when used in conjunction with sulfonamides. Pyrimethamine inhibits the dihydrofolate reductase of plasmodia and thereby blocks the biosynthesis of purines and pyrimidines, which are essential for DNA synthesis and cell multiplication. This leads to failure of nuclear division at the time of schizont formation in erythrocytes and liver.",The molecular weight is 248.71.,Pyrimethamine has a topological polar surface area of 77.82.,The log p value of  is 3.0.,Pyrimethamine is approved and investigational and vet_approved.,Pyrimethamine is a solid.,True
15809,"Tazarotene, commonly marketed as Tazorac®, Avage®, and Zorac®, is member of the acetylenic class of retinoids. It is a prodrug that is found in topical formulations used in the treatment of various conditons, such as psoriasis, acne, and sun damaged skin (photodamage). Used to treat psoriasis, acne and sun damaged skin (photodamage). Following topical application, tazarotene undergoes esterase hydrolysis to form its active metabolite, tazarotenic acid. When treating acne tazarotene may be taken in conjunction with an oral antibiotic. Tazarotene has been shown in peer-reviewed double blinded studies to reduce: mottling and hyperpigmentation, sallowness, fine wrinkling and coarse wrinkling in sun damaged skin. Histological studies have shown that long term (greater than 1 year) use of Tazarotene is associated with a significant reduction in atypical melanocytes and keratocytes - cells considered to be precursors of skin cancer. Some studies have shown long term use of Tazarotene to be associated with increased collagen production and better organization of skin collagen bundles. Although the exact mechanism of tazarotene action is not known, studies have shown that the active form of the drug (tazarotenic acid) binds to all three members of the retinoic acid receptor (RAR) family: RARa, RARb, and RARg, but shows relative selectivity for RARb, and RARg and may modify gene expression. It also has affinity for RXR receptors.",The molecular weight is 351.46.,Tazarotene has a topological polar surface area of 39.19.,The log p value of  is 6.07.,Tazarotene is approved and investigational.,Tazarotene is a solid.,True
15810,"Beraprost is a synthetic analogue of prostacyclin, under clinical trials for the treatment of pulmonary hypertension. It is also being studied for use in avoiding reperfusion injury. For the treatment of pulmonary hypertension. Beraprost is a stable, orally active prostacyclin analogue with vasodilatory, antiplatelet and cytoprotective effects. Beraprost is generally well tolerated and appears to be an effective agent in the treatment of patients with Buerger's disease and arteriosclerosis obliterans. Comparative data from a large randomised trial indicated that the drug appears as effective as ticlopidine in patients with these conditions. In patients with intermittent claudication, significant benefits of beraprost compared with placebo were reported in a randomised clinical trial; however, the use of beraprost in these patients is not supported by recent preliminary unpublished data from a large, phase III, placebo-controlled study. Limited data suggest some efficacy with long-term beraprost treatment of patients with PAH, where options are few and where oral administration of the drug could be a considerable advantage over intravenous prostacyclin (PGI2) therapy. Beraprost acts by binding to prostacyclin membrane receptors ultimately inhibiting the release of Ca<sup>2+</sup> from intracellular storage sites. This reduction in the influx of Ca<sup>2+</sup> has been postulated to cause relaxation of the smooth muscle cells and vasodilation.",The molecular weight is 398.5.,Beraprost has a topological polar surface area of 86.99.,The log p value of  is 2.04.,Beraprost is investigational.,Beraprost is a solid.,True
15811,"Ombitasvir is a direct acting antiviral medication used as part of combination therapy to treat chronic Hepatitis C, an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Treatment options for chronic Hepatitis C have advanced significantly since 2011, with the development of Direct Acting Antivirals (DAAs) such as Ombitasvir. Ombitasvir is an inhibitor of NS5A, a protein essential for viral replication and virion assembly. The barrier for develoment of resistance to NS5A inhibitors is lower than that of NS5B inhibitors, another class of DAAs.  When used in combination with and (as the fixed dose product Technivie), Ombitasvir is indicated in combination with for the treatment of patients with genotype 4 chronic hepatitis C virus (HCV) infection without cirrhosis. Ombitasvir is classified as a direct acting antiviral and acts against HCV to inhibit viral replication. Ombitasvir is an inhibitor of the HCV non-structural protein 5A. While the precise role of this protein is unknown, it is essential to viral replication and virion assembly. Potential modes of action of NS5A inhibitors like Elbasvir include blocking signaling interactions, redistribution of NS5A from the endoplasmic reticulum to the surface of lipid droplets, and modification of the HCV replication complex.",The molecular weight is 894.13.,Ombitasvir has a topological polar surface area of 178.72.,The log p value of  is 8.03.,Ombitasvir is approved and investigational.,Ombitasvir is a solid.,True
15812,"Opicapone is a potent, reversible, and peripherally-acting third-generation inhibitor of catechol-o-methyltransferase (COMT), an enzyme involved in the breakdown of various catecholamines including dopamine.  Opicapone is approved as an adjunctive therapy in adults with Parkinson’s disease and end-of-dose motor fluctuations whose symptoms cannot be stabilized on levodopa/dopa decarboxylase inhibitor combinations.  Opicapone (OPC) is a powerful, reversible, and strictly peripheral third-generation catechol-O-methyltransferase inhibitor (COMT) inhibitor, which improves levodopa (L-Dopa) availability. It serves as adjunct therapy for L-Dopa treated patients with Parkinson's disease and motor fluctuations. Opicapone is a peripheral, selective and reversible catechol-O-methyltransferase (COMT) inhibitor endowed with a high binding affinity (sub-picomolar) that results in a slow complex dissociation rate constant and long-term action (>24 hours) in vivo.",The molecular weight is 413.17.,Opicapone has a topological polar surface area of 149.46.,The log p value of  is 2.32.,Opicapone is approved and investigational.,Opicapone is a solid.,True
15813,"Lubiprostone is a medication used in the management of idiopathic chronic constipation. A prostaglandin E1 derivative, lubiprostone is a bicyclic fatty acid that activates ClC-2 chloride channels located on the apical side of the gastrointestinal epithelial cells. Activation of these channels promotes the secretion of a chloride-rich fluid that soften the stool, increase gastrointestinal motility, and induce spontaneous bowel movements (SBM). For the treatment of chronic idiopathic constipation in the adult population. Also used for the treatment of irritable bowel syndrome with constipation in women who are 18 years of age or older. Chronic idiopathic constipation is generally defined by infrequent or difficult passage of stool. The signs and symptoms associated with chronic idiopathic constipation (i.e., abdominal pain or discomfort, bloating, straining, and hard or lumpy stools) may be the result of abnormal colonic motility that can delay the transit of intestinal contents and impede the evacuation of rectal contents. One approach to the treatment of chronic idiopathic constipation is the secretion of fluid into the abdominal lumen through the activation of chloride channels in the apical membrane of the gastrointestinal epithelium. Lubiprostone is a locally acting chloride channel activator that increases intestinal chloride and fluid secretion without altering sodium and potassium concentrations in the serum. Lubiprostone acts by specifically activating ClC-2 chloride channels, which is a normal constituent of the apical membrane of the human intestine, in a protein kinase A action independent fashion. Activation of ClC-2 chloride channels causes an efflux of chloride ions into the lumen, which in turn leads to an efflux of sodium ions through a paracellular pathway to maintain isoelectric neutrality. As a result, water follows sodium into the lumen in order to maintain isotonic equilibrium, thereby increasing intestinal fluid secretion. By increasing intestinal fluid secretion, lubiprostone increases motility in the intestine, thereby increasing the passage of stool and alleviating symptoms associated with chronic idiopathic constipation. Activation of ClC-2 chloride channels may also stimulate the recovery of muscosal barrier function by restoring tight junction protein complexes in the intestine. Patch clamp cell studies in human cell lines have indicated that the majority of the beneficial biological activity of lubiprostone and its metabolites is observed only on the apical (luminal) portion of the gastrointestinal epithelium.",,,,Lubiprostone is approved and investigational.,Lubiprostone is a solid.,True
15814,,,,,3-(4-Amino-1-Tert-Butyl-1h-PyrazoloPyrimidin-3-Yl)Phenol is experimental.,3-(4-Amino-1-Tert-Butyl-1h-PyrazoloPyrimidin-3-Yl)Phenol is a solid.,False
15815,"Sofalcone is a mucosal protective agent that has been reported to inhibit growth of Helicobacter pylori. on adherence, production of vacuolating toxin (VT), and induction of interleukin-8 (IL-8) secretion by H. pylori. Investigated for use/treatment in gastroenteritis and ulcers. Sofalcone has been reported to have an anti-bacterial effect on H. pylori and the inhibitory effects against the pathogenic factor of H. pylori in addition to the mucosal protective effect due to the inhibition of prostaglandins degradation enzyme. Sofalcone has a direct bactericidal effect on H pylori, anti-urease activity and reduces the adhesion of this organism to gastric epithelial cells",The molecular weight is 450.53.,Sofalcone has a topological polar surface area of 82.06.,The log p value of  is 5.94.,Sofalcone is investigational.,Sofalcone is a solid.,True
15816,"Loxoprofen is a propionic acid derivative non-steroidal anti-inflammatory drug. It is marketed under the trade name Loxonin in Brazil, Mexico and Japan by Sankyo, as Loxomac in India, and as Oxeno in Argentina. A transdermal preparation was approved for use in Japan in January 2006. Loxoprofen is non-steroidal anti-inflammatory medication (NSAID) indicated for pain and inflammation related to musculoskeletal and joint disorders. In addition to its effects on pain, it is an antipyretic and anti-inflammatory medication. Loxoprofen is a non-selective inhibitor of cyclooxygenase enzymes, which are responsible for the formation of various biologically active pain, fever, and inflammatory mediators. These include prostaglandins, prostacyclin, thromboxane, and arachidonic acid. Loxoprofen itself is a prodrug and carries little-to-no pharmacological activity - it is rapidly metabolized to its trans-alcohol form, which is a potent and non-selective inhibitor of cyclooxygenase. Cyclooxygenase (COX) is present in 2 forms, COX-1 and COX-2, with each serving different functions. COX-1 is present in human cells and is constitutively released, performing cellular housekeeping functions such as mucus production and platelet aggregation. COX-2 is induced in human cells post-injury or due to other stimuli, is triggered to appear in large quantities at the sites of injury/stimuli, and is ultimately responsible for the mediation of inflammation and pain.",The molecular weight is 246.31.,Loxoprofen has a topological polar surface area of 54.37.,The log p value of  is 1.97.,Loxoprofen is approved.,Loxoprofen is a solid.,True
15817,"Adefovir dipivoxil, previously called bis-POM PMEA, with trade names Preveon and Hepsera, is an orally-administered acyclic nucleotide analog reverse transcriptase inhibitor (ntRTI) used for treatment of hepatitis B. It is ineffective against HIV-1. Adefovir dipivoxil is the diester prodrug of adefovir. Indicated for the treatment of chronic hepatitis B in adult patients with evidence of active viral replication and either evidence of persistent elevations in serum aminotransferases (ALT or AST) or histologically active disease; this is based on histological, virological, biochemical, and serological responses in adult patients with HBeAg+ and HBeAg- chronic hepatitis B with compensated liver function, and in adult patients with clinical evidence of lamivudine-resistant hepatitis B virus with either compensated or decompensated liver function. Adefovir dipivoxil a diester prodrug of adefovir. Adefovir is an acyclic nucleotide analog with activity against human hepatitis B virus (HBV). The concentration of adefovir that inhibited 50% of viral DNA synthesis (IC50) in vitro ranged from 0.2 to 2.5 &mu;M in HBV transfected human hepatoma cell lines. The combination of adefovir with lamivudine showed additive anti-HBV activity. Adefovir dipivoxil is a prodrug of adefovir. Adefovir is an acyclic nucleotide analog of adenosine monophosphate which is phosphorylated to the active metabolite adefovir diphosphate by cellular kinases. Adefovir diphosphate inhibits HBV DNA polymerase (reverse transcriptase) by competing with the natural substrate deoxyadenosine triphosphate and by causing DNA chain termination after its incorporation into viral DNA. The inhibition constant (Ki) for adefovir diphosphate for HBV DNA polymerase was 0.1 &mu;M. Adefovir diphosphate is a weak inhibitor of human DNA polymerases &alpha; and &gamma; with Ki values of 1.18 &mu;M and 0.97&mu;M, respectively.",The molecular weight is 501.48.,Adefovir dipivoxil has a topological polar surface area of 166.98.,The log p value of  is 1.4.,Adefovir dipivoxil is approved and investigational.,Adefovir dipivoxil is a solid.,True
15818,"Initially approved by the FDA in 2013, memantine is an N-methyl-D-aspartate (NMDA) receptor antagonist used in the management of Alzheimer's Disease (AD). It is different from many other Alzheimer's Disease medications, as it works by a different mechanism than the cholinesterase enzyme inhibitors normally employed in the management of Alzheimer's disease. Memantine blocks the effects of glutamate, a neurotransmitter in the brain that leads to neuronal excitability and excessive stimulation in Alzheimer's Disease. Memantine is used to manage moderate to severe Alzheimer's dementia.  **General effects** Continuous activation of the N-methyl-D-aspartate (NMDA) receptors in the central nervous system caused by _glutamate_ is thought to cause some of the Alzheimer's disease symptoms. This overactivation is thought to contribute to neurotoxicity due to the excitatory properties of glutamate. The pharmacological effect of memantine likely occurs via the drug's behavior as an uncompetitive (open-channel) NMDA receptor antagonist, preventing glutamate action on this receptor. Memantine has a preference for the NMDA receptor-operated cation channels. Despite these antagonist effects, memantine has not been proven to prevent or retard the neurodegeneration seen in patients diagnosed with Alzheimer’s disease.",The molecular weight is 179.31.,Memantine has a topological polar surface area of 26.02.,The log p value of  is 3.03.,Memantine is approved and investigational.,Memantine is a solid.,True
15819,"Fomepizole is used as an antidote in confirmed or suspected methanol or ethylene glycol poisoning. Fomepizole is a competitive inhibitor of alcohol dehydrogenase, the enzyme that catalyzes the initial steps in the metabolism of ethylene glycol and methanol to their toxic metabolites. Antizol is indicated as an antidote for ethylene glycol (such as antifreeze) or methanol poisoning, or for use in suspected ethylene glycol or methanol ingestion, either alone or in combination with hemodialysis Fomepizole is a competitive inhibitor of alcohol dehydrogenase, the enzyme that catalyzes the initial steps in the metabolism of ethylene glycol and methanol to their toxic metabolites. Ethylene glycol is first metabolized to glycoaldehyde which then undergoes further oxidation to glycolate, glyoxylate, and oxalate. Glycolate and oxalate are primarily responsible for metabolic acidosis and renal damage seen in ethylene glycol toxicity. {01}{03} Methanol is first metabolized to formaldehyde and then undergoes subsequent oxidation via formaldehyde dehydrogenase to become formic acid. It is formic acid that is primarily responsible for the metabolic acidosis and visual disturbances that are associated with methanol poisoning. Antizol (fomepizole) is a competitive inhibitor of alcohol dehydrogenase. Alcohol dehydrogenase catalyzes the oxidation of ethanol to acetaldehyde. Alcohol dehydrogenase also catalyzes the initial steps in the metabolism of ethylene glycol and methanol to their toxic metabolites.",The molecular weight is 82.11.,Fomepizole has a topological polar surface area of 28.68.,The log p value of  is 0.51.,Fomepizole is approved and vet_approved.,Fomepizole is a liquid.,True
15820,"Enfuvirtide is a 36 amino acid biomimetic peptide that is structurally similar to the HIV proteins that are responsible for the fusion of the virus to cell membranes and subsequent intracellular uptake. The first agent in the novel class of antiretroviral drugs called HIV fusion inhibitors, enfuvirtide works by inhibiting HIV-1 fusion with CD4 cells. Enfuvirtide is an antiretroviral drug used in combination therapy for the treatment of HIV-1/AIDS. Enfuvirtide binds to the first heptad-repeat (HR1) in the gp41 subunit of the viral envelope glycoprotein and prevents the conformational changes required for the fusion of viral and cellular membranes. By disrupting the HIV-1 molecular machinery during its final stage of fusion with the target cell, enfuvirtide limits the spread of further infection. Enfuvirtide is a biomimetic peptide that was rationally designed to mimic components of the HIV-1 fusion machinery and displace them, preventing normal fusion. ",The molecular weight is 4491.94.,Enfuvirtide has a topological polar surface area of 1902.89.,,Enfuvirtide is approved and investigational.,Enfuvirtide is a solid.,True
15821,"A vasodilator used in the treatment of angina pectoris. Its actions are similar to nitroglycerin but with a slower onset of action. For the prevention of angina pectoris due to coronary artery disease. Isosorbide Dinitrate is a moderate to long acting oral organic nitrate used for the relief and prophylactic management of angina pectoris. It relaxes the vascular smooth muscle and consequent dilatation of peripheral arteries and veins, especially the latter. Dilatation of the veins promotes peripheral pooling of blood and decreases venous return to the heart, thereby reducing left ventricular end- diastolic pressure and pulmonary capillary wedge pressure (preload). Arteriolar relaxation reduces systemic vascular resistance, systolic arterial pressure, and mean arterial pressure. Isosorbide dinitrate is converted to the active nitric oxide to activate guanylate cyclase. This activation increases levels of cyclic guanosine 3',5'-monophosphate (cGMP). cGMP activates protein kinases and causes a series of phosphorylation reactions which leads to dephosphorylation of myosin light chains of smooth muscle fibres. Finally there is a release of calcium ions which causes smooth muscle relaxation and vasodilation.",The molecular weight is 236.14.,Isosorbide dinitrate has a topological polar surface area of 128.56.,The log p value of  is -3.5.,Isosorbide dinitrate is approved and investigational.,Isosorbide dinitrate is a solid.,True
15822,"Ursodeoxycholic acid is an epimer of. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic. The drug decreases the absorption of cholesterol and is used to dissolve (cholesterol) gallstones in patients as an alternative to a surgical procedure to remove the gallstones. Ursodiol (commonly known as ursodeoxycholic acid) is a product of metabolism of bacteria in the intestine. It is considered a secondary bile acid. The other type of bile acid, primary bile acids, are produced hepatically and subsequently stored in the gallbladder. When primary bile acids are secreted into the large intestine, they can be broken down into secondary bile acids by bacteria present in the intestine. Both types of bile acids assist in the metabolism of dietary fat. Ursodeoxycholic acid regulates cholesterol levels by slowing the rate at which the intestine is able to absorb cholesterol and also acts to break down micelles, which contain cholesterol. Because of this property, ursodeoxycholic acid is used to treat gall stones non-surgically. Ursodeoxycholic acid reduces elevated liver enzyme levels by facilitating bile flow through the liver and protecting liver cells.",The molecular weight is 392.58.,Ursodeoxycholic acid has a topological polar surface area of 77.76.,The log p value of  is 4.51.,Ursodeoxycholic acid is approved and investigational.,Ursodeoxycholic acid is a solid.,True
15823,,,,,"N,N-dimethylformamide is experimental.","N,N-dimethylformamide is a solid.",False
15824,,,,,N-Methyl-N-(Methylbenzyl)Formamide is experimental.,N-Methyl-N-(Methylbenzyl)Formamide is a solid.,False
15825,"Tirapazamine, also known as SR-4233, is an experimental anticancer drug that is activated in hypoxic conditions. This activation is very useful as this hypoxic state is found in human solid tumors in a common phenomenon known as tumor hypoxia. Hence, tirapazamine is solely activated in those hypoxic areas of solid tumors. It is important to take into consideration that normally, the cells in these hypoxic regions are resistant to radiotherapy and most anticancer drugs. For all these reasons, the combination of tirapazamine with other anticancer treatments is highly recommended.  For the treatment of head and neck cancer. Tirapazamine is a anticancer drug that is inactive in normal tissues that are well oxygenated, but becomes active at the low oxygen levels found in solid tumors. As a result, the drug kills these poorly oxygenated or hypoxic cells while limiting toxicity in normal tissue. Tirapazamine may prove highly effective when used in combination with standard anticancer therapy, as these hypoxic cells are characteristically resistant to radiation and common anticancer agents. Extensive preclinical testing has established that the mechanism for the selective toxicity towards hypoxic cells is the result of a one-electron reduction of the parent molecule to a free radical species that interacts with DNA to produce single- and double-strand breaks and lethal chromosome aberrations. It has also shown activity when combined with fractionated irradiation and when combined with some chemotherapy agents, particularly cisplatin and carboplatin.",,,,Tirapazamine is investigational.,Tirapazamine is a solid.,True
15826,"Dalfampridine is a potassium channel blocker used to help multiple sclerosis patients walk. This is the first drug that was specifically approved to help with mobility in these patients. FDA approved on January 22, 2010. Dalfampridine is a neurofunctional modifier that helps improve walking speed in patients with multiple sclerosis (MS).  Dalfampridine is a board-spectrum lipophillic potassium channel blocker and binds favourably to the open state than closed state of the potassium channel in the CNS. Its pharmacological target are the potassium channels exposed in MS patients. Does not prolong the QTc interval.  In MS, axons are progressively demyelinated which exposes potassium channels. As a result, there is a leak of potassium ions which results in the repolarization of cells and a decrease in neuronal excitability. The overall impact is the impairment of neuromuscular transmission as it is harder to trigger an action potential. ",The molecular weight is 94.12.,Dalfampridine has a topological polar surface area of 38.91.,The log p value of  is 0.32.,Dalfampridine is approved.,Dalfampridine is a solid.,True
15827,"Aniline, phenylamine or aminobenzene is an organic compound with the formula C6H5NH2. Consisting of an amine attached to a benzene ring, aniline is the prototypical aromatic amine. Being a precursor to many industrial chemicals, its main use is in the manufacture of precursors to polyurethane. Like most volatile amines, it possesses the somewhat unpleasant odour of rotten fish. Aniline is colorless, but it slowly oxidizes and resinifies in air, giving a red-brown tint to aged samples.",,,,Aniline is experimental.,Aniline is a liquid.,True
15828,"Ellagic acid is present in several fruits such as cranberries, strawberries, raspberries, and pomegranates. In pomegranates, there are several therapeutic compounds but ellagic acid is the most active and abundant. Ellagic acid is also present in vegetables. Ellagic acid is an investigational drug studied for treatment of Follicular Lymphoma (phase 2 trial), protection from brain injury of intrauterine growth restricted babies (phase 1 and 2 trial), improvement of cardiovascular function in adolescents who are obese (phase 2 trial), and topical treatment of solar lentigines. Ellagic acid's therapeutic action mostly involves antioxidant and anti-proliferative effects. Ellagic acid is being investigated for use in follicular lymphoma, brain injury in intrauterine growth restricted babies, obese adolescents, and solar lentigines. Ellagic acid's therapeutic action mostly involves antioxidant and anti-proliferative/anti-cancer effects. The exact mechanism of action of ellagic acid in its different potential indications is still being investigated.",,,,Ellagic acid is investigational.,Ellagic acid is a solid.,True
15829,"Multiple sclerosis or MS is a devastating inflammatory disease that often progresses and causes severe neurological, physical, and cognitive effects. Fingolimod is a sphingosine 1-phosphate receptor modulator for the treatment of relapsing-remitting multiple sclerosis. It was developed by Novartis and initially approved by the FDA in 2010. Fingolimod is indicated for the treatment of patients aged 10 and above with relapsing forms of multiple sclerosis, which may include clinically isolated syndrome, relapsing-remitting disease, as well as active secondary progressive disease. In multiple sclerosis, fingolimod binds to sphingosine receptors, reducing its associated neuroinflammation.In COVID-19, it may reduce lung inflammation and improve the clinical outcomes of patients with this disease.  Sphingosine‐1‐phosphate (S1P) is an important phospholipid that binds to various G‐protein‐coupled receptor subtypes, which can be identified as S1P1–5R. S1P and the receptors it binds to perform regular functions in the immune, cardiovascular, pulmonary, and nervous system. S1P can be expressed ubiquitously, playing an important role in regulating inflammation. S1P1R, S1P2R, and S1P3R receptors can be found in the cardiovascular, immune, and central nervous systems. S1P4R is found on lymphocytic and hematopoietic cells, while S1P5R expression is found only on the spleen (on natural killer cells) or in the central nervous system.",The molecular weight is 307.48.,Fingolimod has a topological polar surface area of 66.48.,The log p value of  is 5.06.,Fingolimod is approved and investigational.,Fingolimod is a solid.,True
15830,"1,2-Dichlorobenzene, also named ortho-dichlorobenzene, is an organic compound. It is a non-polar colorless liquid that is miscible in most organic solvents. This derivative of benzene differs from the parent compound by the presence of two adjacent chlorine atoms. 1,2-dichlorobenzene is used as a precursor for agrochemicals, as a solvent for fullerenes, as an insecticide and as an agent to remove carbon-based contamination from metal.",,,,"1,2-dichlorobenzene is experimental.","1,2-dichlorobenzene is a solid.",True
15831,"Dichlorobenzene refers to any of, or a mixture of, three isomers consisting of benzene in which two of the hydrogen atoms are replaced by chlorine atoms: ortho-, meta-, and paradichlorobenzene. It is a constituent of the ear-wax removal product Cerumol.",,,,Dichlorobenzene is approved and experimental.,Dichlorobenzene is a solid.,True
15832,"Originally approved by the FDA in 1959 , carisoprodol is a centrally acting muscle relaxant used in painful musculoskeletal conditions in conjunction with physical therapy and other medications. This drug is available by itself in an oral tablet or combined with aspirin, or in a fixed-dose combination with both aspirin and codeine. Carisoprodol is indicated for the relief of discomfort related to acute, painful musculoskeletal conditions. Carisoprodol is a centrally acting skeletal muscle relaxant that does not act directly on skeletal muscle but acts directly on the central nervous system (CNS). This drug relieves the painful effects of muscle spasm. A metabolite of carisoprodol, _meprobamate_, possesses both anxiolytic and sedative properties. Clinical studies have shown that this drug causes impairment of psychomotor performance in neuropsychological tests. The mechanism of action of carisoprodol in relieving discomfort associated with acute painful musculoskeletal conditions has not been confirmed.",The molecular weight is 260.33.,Carisoprodol has a topological polar surface area of 90.65.,The log p value of  is 2.34.,Carisoprodol is approved.,Carisoprodol is a solid.,True
15833,"An intravenous anesthetic with a short duration of action that may be used for induction of anesthesia. Methohexital is indicated for use as an intravenous anaesthetic. It has also been commonly used to induce deep sedation. Methohexital, a barbiturate, is used for the induction of anesthesia prior to the use of other general anesthetic agents and for induction of anesthesia for short surgical, diagnostic, or therapeutic procedures associated with minimal painful stimuli. Little analgesia is conferred by barbiturates; their use in the presence of pain may result in excitation. Methohexital binds at a distinct binding site associated with a Cl<sup>-</sup> ionopore at the GABA<sub>A</sub> receptor, increasing the duration of time for which the Cl<sup>-</sup> ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.",The molecular weight is 262.31.,Methohexital has a topological polar surface area of 66.48.,The log p value of  is 1.81.,Methohexital is approved.,Methohexital is a solid.,True
15834,"A barbiturate that is administered intravenously for the induction of general anesthesia or for the production of complete anesthesia of short duration. It is also used for hypnosis and for the control of convulsive states. It has been used in neurosurgical patients to reduce increased intracranial pressure. It does not produce any excitation but has poor analgesic and muscle relaxant properties. Small doses have been shown to be anti-analgesic and lower the pain threshold. (From Martindale, The Extra Pharmacopoeia, 30th ed, p920) For use as the sole anesthetic agent for brief (15 minute) procedures, for induction of anesthesia prior to administration of other anesthetic agents, to supplement regional anesthesia, to provide hypnosis during balanced anesthesia with other agents for analgesia or muscle relaxation, for the control of convulsive states during or following inhalation anesthesia or local anesthesia, in neurosurgical patients with increased intracranial pressure, and for narcoanalysis and narcosynthesis in psychiatric disorders. Thiopental, a barbiturate, is used for the induction of anesthesia prior to the use of other general anesthetic agents and for induction of anesthesia for short surgical, diagnostic, or therapeutic procedures associated with minimal painful stimuli. Thiopental is an ultrashort-acting depressant of the central nervous system which induces hypnosis and anesthesia, but not analgesia. It produces hypnosis within 30 to 40 seconds of intravenous injection. Recovery after a small dose is rapid, with some somnolence and retrograde amnesia. Repeated intravenous doses lead to prolonged anesthesia because fatty tissues act as a reservoir; they accumulate Pentothal in concentrations 6 to 12 times greater than the plasma concentration, and then release the drug slowly to cause prolonged anesthesia Thiopental binds at a distinct binding site associated with a Cl<sup>-</sup> ionopore at the GABA<sub>A</sub> receptor, increasing the duration of time for which the Cl<sup>-</sup> ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.",The molecular weight is 242.34.,Thiopental has a topological polar surface area of 58.2.,The log p value of  is 2.98.,Thiopental is approved and vet_approved.,Thiopental is a solid.,True
15835,"A barbiturate that is metabolized to phenobarbital. It has been used for similar purposes, especially in epilepsy, but there is no evidence mephobarbital offers any advantage over phenobarbital. For the relief of anxiety, tension, and apprehension, also used as an anticonvulsant for the treatment of epilepsy. Methylphenobarbital, a barbiturate, is used in combination with acetaminophen or aspirin and caffeine for its sedative and relaxant effects in the treatment of tension headaches, migraines, and pain. Barbiturates act as nonselective depressants of the central nervous system (CNS), capable of producing all levels of CNS mood alteration from excitation to mild sedation, hypnosis, and deep coma. In sufficiently high therapeutic doses, barbiturates induce anesthesia. Methylphenobarbital binds at a distinct binding site associated with a Cl<sup>-</sup> ionopore at the GABA<sub>A</sub> receptor, increasing the duration of time for which the Cl<sup>-</sup> ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.",The molecular weight is 246.27.,Methylphenobarbital has a topological polar surface area of 66.48.,The log p value of  is 1.85.,Methylphenobarbital is approved.,Methylphenobarbital is a solid.,True
15836,"Telmisartan is an angiotensin II receptor antagonist (ARB) used in the management of hypertension. Generally, angiotensin II receptor blockers (ARBs) such as telmisartan bind to the angiotensin II type 1 (AT1) receptors with high affinity, causing inhibition of the action of angiotensin II on vascular smooth muscle, ultimately leading to a reduction in arterial blood pressure. Recent studies suggest that telmisartan may also have PPAR-gamma agonistic properties that could potentially confer beneficial metabolic effects. Used alone or in combination with other classes of antihypertensives for the treatment of hypertension. Also used in the treatment of diabetic nephropathy in hypertensive patients with type 2 diabetes mellitus, as well as the treatment of congestive heart failure (only in patients who cannot tolerate ACE inhibitors). Telmisartan is an orally active nonpeptide angiotensin II antagonist that acts on the AT<sub>1</sub> receptor subtype. It has the highest affinity for the AT<sub>1</sub> receptor among commercially available ARBS and has minimal affinity for the AT<sub>2</sub> receptor. New studies suggest that telmisartan may also have PPAR&gamma; agonistic properties that could potentially confer beneficial metabolic effects, as PPAR&gamma; is a nuclear receptor that regulates specific gene transcription, and whose target genes are involved in the regulation of glucose and lipid metabolism, as well as anti-inflammatory responses. This observation is currently being explored in clinical trials. Angiotensin II is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme (ACE, kininase II). Angiotensin II is the principal pressor agent of the renin-angiotensin system, with effects that include vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Telmisartan works by blocking the vasoconstrictor and aldosterone secretory effects of angiotensin II. Telmisartan interferes with the binding of angiotensin II to the angiotensin II AT<sub>1</sub>-receptor by binding reversibly and selectively to the receptors in vascular smooth muscle and the adrenal gland. As angiotensin II is a vasoconstrictor, which also stimulates the synthesis and release of aldosterone, blockage of its effects results in decreases in systemic vascular resistance. Telmisartan does not inhibit the angiotensin converting enzyme, other hormone receptors, or ion channels. Studies also suggest that telmisartan is a partial agonist of PPAR&gamma;, which is an established target for antidiabetic drugs. This suggests that telmisartan can improve carbohydrate and lipid metabolism, as well as control insulin resistance without causing the side effects that are associated with full PPAR&gamma; activators.",The molecular weight is 514.63.,Telmisartan has a topological polar surface area of 72.94.,The log p value of  is 7.29.,Telmisartan is approved and investigational.,Telmisartan is a solid.,True
15837,"Mesuximide (or methsuximide) is an anticonvulsant medication. It is sold by Pfizer under the name Petinutin. For the control of absence (petit mal) seizures that are refractory to other drugs. Used in the treatment of epilepsy. Methsuximide suppresses the paroxysmal three cycle per second spike and wave activity associated with lapses of consciousness which is common in absence (petit mal) seizures. The frequency of epileptiform attacks is reduced, apparently by depression of the motor cortex and elevation of the threshold of the central nervous system to convulsive stimuli. Binds to T-type voltage sensitive calcium channels. Voltage-sensitive calcium channels (VSCC) mediate the entry of calcium ions into excitable cells and are also involved in a variety of calcium-dependent processes, including muscle contraction, hormone or neurotransmitter release, gene expression, cell motility, cell division and cell death. The isoform alpha-1G gives rise to T-type calcium currents. T-type calcium channels belong to the \low-voltage activated (LVA)\"" group and are strongly blocked by mibefradil. A particularity of this type of channels is an opening at quite negative potentials and a voltage-dependent inactivation. T-type channels serve pacemaking functions in both central neurons and cardiac nodal cells and support calcium signaling in secretory cells and vascular smooth muscle. They may also be involved in the modulation of firing patterns of neurons which is important for information processing as well as in cell growth processes.""",The molecular weight is 203.24.,Methsuximide has a topological polar surface area of 37.38.,The log p value of  is 1.46.,Methsuximide is approved.,Methsuximide is a solid.,True
15838,"Benzbromarone has been used in trials studying the basic science and treatment of Heart Failure, Hyperuricemia, Chronic Kidney Disease, Abnormal Renal Function, and Gout and Asymptomatic Hyperuricemia.",The molecular weight is 424.09.,Benzbromarone has a topological polar surface area of 50.44.,The log p value of  is 5.98.,Benzbromarone is investigational and withdrawn.,,True
15839,,The molecular weight is 359.44.,Dexrabeprazole has a topological polar surface area of 77.1.,The log p value of  is 2.08.,Dexrabeprazole is experimental.,,False
15840,"Digoxin is one of the oldest cardiovascular medications used today. It is a common agent used to manage atrial fibrillation and the symptoms of heart failure. Digoxin is classified as a cardiac glycoside and was initially approved by the FDA in 1954. Digoxin is indicated in the following conditions: 1) For the treatment of mild to moderate heart failure in adult patients. 2) To increase myocardial contraction in children diagnosed with heart failure. 3) To maintain control ventricular rate in adult patients diagnosed with chronic atrial fibrillation. Digoxin is a positive inotropic and negative chronotropic drug, meaning that it increases the force of the heartbeat and decreases the heart rate. The decrease in heart rate is particularly useful in cases of atrial fibrillation, a condition characterized by a fast and irregular heartbeat. The relief of heart failure symptoms during digoxin therapy has been demonstrated in clinical studies by increased exercise capacity and reduced hospitalization due to heart failure and reduced heart failure-related emergency medical visits. Digoxin has a narrow therapeutic window. Digoxin exerts hemodynamic, electrophysiologic, and neurohormonal effects on the cardiovascular system. It reversibly inhibits the Na-K ATPase enzyme, leading to various beneficial effects. The Na-K ATPase enzyme functions to maintain the intracellular environment by regulating the entry and exit of sodium, potassium, and calcium (indirectly). Na-K ATPase is also known as the _sodium pump_. The inhibition of the sodium pump by digoxin increases intracellular sodium and increases the calcium level in the myocardial cells, causing an increased contractile force of the heart. This improves the left ventricular ejection fraction (EF), an important measure of cardiac function.",The molecular weight is 780.95.,Digoxin has a topological polar surface area of 203.06.,The log p value of  is 1.42.,Digoxin is approved.,Digoxin is a solid.,True
15841,"Glutethimide is a hypnotic and sedative. Its use has been largely superseded by other drugs. For the treatment of insomnia. Glutethimide, like the barbiturates, is a hypnotic sedative. It was introduced in 1954 as a safer alternative to barbiturates but was soon determined to be just as likely to cause addiction and withdrawal symptoms. Glutethimide seems to be a GABA agonist which helps induce sedation. It also induces CYP 2D6. When taken with codeine, it enables the body to convert higher amounts of codeine (higher than the average 5 - 10%) to morphine. This combination of effects enhances sedation.",The molecular weight is 217.27.,Glutethimide has a topological polar surface area of 46.17.,The log p value of  is 1.99.,Glutethimide is approved and illicit.,Glutethimide is a solid.,True
15842,"Mycophenolic acid is an an immunosuppresant drug and potent anti-proliferative, and can be used in place of the older anti-proliferative azathioprine. It is usually used as part of triple therapy including a calcineurin inhibitor (ciclosporin or tacrolimus) and prednisolone. It is also useful in research for the selection of animal cells that express the E. coli gene coding for XGPRT (xanthine guanine phosphoribosyltransferase). For the prophylaxis of organ rejection in patients receiving allogeneic renal transplants, administered in combination with cyclosporine and corticosteroids. Mycophenolic acid is an antibiotic substance derived from <i>Penicillium stoloniferum</i>. It blocks de novo biosynthesis of purine nucleotides by inhibition of the enzyme inosine monophosphate dehydrogenase. Mycophenolic acid is important because of its selective effects on the immune system. It prevents the proliferation of T-cells, lymphocytes, and the formation of antibodies from B-cells. It also may inhibit recruitment of leukocytes to inflammatory sites. Mycophenolic acid is a potent, selective, uncompetitive, and reversible inhibitor of inosine monophosphate dehydrogenase (IMPDH), and therefore inhibits the de novo pathway of guanosine nucleotide synthesis without incorporation into DNA. Because T- and B-lymphocytes are critically dependent for their proliferation on de novo synthesis of purines, whereas other cell types can utilize salvage pathways, mycophenolic acid has potent cytostatic effects on lymphocytes. Mycophenolic acid inhibits proliferative responses of T- and B-lymphocytes to both mitogenic and allospecific stimulation. Addition of guanosine or deoxyguanosine reverses the cytostatic effects of mycophenolic acid on lymphocytes. Mycophenolic acid also suppresses antibody formation by B-lymphocytes. Mycophenolic acid prevents the glycosylation of lymphocyte and monocyte glycoproteins that are involved in intercellular adhesion to endothelial cells and may inhibit recruitment of leukocytes into sites of inflammation and graft rejection.",,,,Mycophenolic acid is approved.,Mycophenolic acid is a solid.,True
15843,"Niflumic acid is an analgesic and anti-inflammatory agent used in the treatment of rheumatoid arthritis. Used in the treatment of rheumatoid arthritis. Niflumic acid, a nonsteroidal anti-inflammatory fenamate, is a Ca<sup>2+</sup>-activated Cl<sup>-</sup> channel blocker. Niflumic acid is able to inhibit both phospholipase A2 as well as COX-2, thereby acting as an antiinflamatory and pain reduction agent.",The molecular weight is 282.22.,Niflumic acid has a topological polar surface area of 62.22.,The log p value of  is 4.77.,Niflumic acid is experimental.,Niflumic acid is a solid.,True
15844,"Ezogabine (D23129) is a close structural analog of the centrally acting analgesic flupitrine. It is a neuronal potassium channel opener being developed as a first-in-class antiepileptic drug (AED) and is currently being studied in Phase 3 trials as an adjunctive treatment for partial-onset seizures in adult patients with refractory epilepsy. FDA approved in June 10, 2011 under the name of ezogabine. Adjuvant treatment of partial-onset seizures.  As compared to other antiepileptic agents, ezogabine is unique in that it selectively activates potassium ion channels Kv 7.2-Kv7.5 and not cardiac Kv 7.1, thereby avoiding cardiac side effects. The antiepileptics, as a drug class, are routinely used in the treatment of a number of disease states in addition to epilepsy. Ezogabine is highly efficacious in a broad-spectrum of in vivo epilepsy and seizure models. A comparison of antiepileptic form activity of ezogabine with that of conventional anticonvulsants in in vitro models suggests that retigabine is especially likely to be useful in the treatment of pharmacoresistant epilepsy. Retigabine clearly attenuates pain-like behaviors in various animal models of neuropathic pain; it may also prove to be useful in treatment of clinical anxiety disorders. Clinical data obtained thus far indicate that retigabine is well tolerated in humans when titrated up to its therapeutic dose range. No tolerance, drug dependence, or withdrawal liability has been reported. Thus, retigabine may prove to be useful in the treatment of a diverse range of disease states in which neuronal hyperexcitability is a common underlying factor. Ezogabine has a novel mechanism of action that involves opening of neuronal Kv7.2-7.5 (formerly KCNQ2-5) voltage activated potassium channels. These channels (primarily Kv7.2/7.3) enable generation of the M-current, a sub-threshold potassium current that serves to stabilize the membrane potential and control neuronal excitability. In addition to acting on potassium ion channels, retigabine also affects GABA neurotransmission in the GABA-A receptor, which is a key inhibitory receptor in the central nervous system and is implicated in epilepsy. Malfunctioning of the GABA-A receptor leads to hyperexcitability in the brain, which causes seizures, making this receptor an important target for antiepileptic therapeutics. Apart from increasing the concentration of GABA in the brain (by either enhancing GABA synthesis or blocking GABA metabolism), retigabine allosterically potentiates GABA-induced current in rat cortical neurons in a concentration-dependent manner. Numerous studies have demonstrated that retigabine is effective in a broad spectrum of in vivo epilepsy and seizure models.",The molecular weight is 303.34.,Ezogabine has a topological polar surface area of 76.38.,The log p value of  is 2.0.,Ezogabine is approved and investigational.,Ezogabine is a solid.,True
15845,"Highly potent and selective non-competitive antagonist acting at the strychnine-insensitive glycine binding site of the NMDA receptor-channel complex (Kd = 0.8 nM). Gavestinel displays > 1000-fold selectivity over NMDA, AMPA and kainate binding sites and is orally bioavailable and active in vivo.",,,,Gavestinel is investigational.,Gavestinel is a solid.,True
15846,"Dolutegravir is a HIV-1 intergrase inhibitor that blocks the strand transfer step of the integration of the viral genome into the host cell (INSTI). The effect of this drug has no homology in human host cells which gives it an excellent tolerability and minimal toxicity. Dolutegravir was developed by ViiV Healthcare and FDA approved on August 12, 2013. On November 21, 2017, dolutegravir, in combination with rilpivirine, was approved as part of the first complete treatment regimen with only two drugs for the treatment of adults with HIV-1 named Juluca. Dolutegravir is indicated in combination with other antiretroviral agents for the treatment of patients with HIV-1 infection that comply with the characteristics of being adults or children aged 12 years and older and present at least a weight of 40 kg. The FDA combination therapy approval of dolutegravir and rilpivirine is indicated for adults with HIV-1 infections whose virus is currently suppressed (< 50 copies/ml) on a stable regimen for at least six months, without history of treatment failure and no known substitutions associated to resistance to any of the two components of the therapy. HIV-1 infected subjects on dolutegravir monotherapy demonstrated rapid and dose-dependent reduction of antiviral activity with declines of HIV-1 RNA copies per ml. The antiviral response was maintained for 3 to 4 days after the last dose. The sustained response obtained in clinical trials indicates that dolutegravir has a tight binding and longer dissociative half-life providing it a high barrier to resistance. The combination therapy (ripivirine and dolutegravir) presented the same viral suppression found in previous three-drug therapies without integrase strand transfer inhibitor mutations or rilpivirine resistance. Dolutegravir is an HIV-1 antiviral agent. It inhibits HIV integrase by binding to the active site and blocking the strand transfer step of retroviral DNA integration in the host cell. The strand transfer step is essential in the HIV replication cycle and results in the inhibition of viral activity. Dolutegravir has a mean EC50 value of 0.5 nM (0.21 ng/mL) to 2.1 nM (0.85 ng/mL) in peripheral blood mononuclear cells (PBMCs) and MT-4 cells.",The molecular weight is 419.38.,Dolutegravir has a topological polar surface area of 99.18.,The log p value of  is 0.05.,Dolutegravir is approved.,Dolutegravir is a solid.,True
15847,"Empagliflozin is an inhibitor of sodium-glucose co-transporter-2 (SGLT2), the transporters primarily responsible for the reabsorption of glucose in the kidney. It is used clinically as an adjunct to diet and exercise, often in combination with other drug therapies, for the management of type 2 diabetes mellitus. Empagliflozin is indicated as an adjunct to diet and exercise to improve glycemic control in adult patients with type 2 diabetes. It is also indicated to reduce the risk of cardiovascular death in adult patients with both type 2 diabetes mellitus and established cardiovascular disease. Empagliflozin lowers blood glucose levels by preventing glucose reabsorption in the kidneys, thereby increasing the amount of glucose excreted in the urine. It has a relatively long duration of action requiring only once-daily dosing. Patients should be monitored closely for signs and symptoms of ketoacidosis regardless of blood glucose level as empagliflozin may precipitate diabetic ketoacidosis in the absence of hyperglycemia. As its mechanism of action is contingent on the renal excretion of glucose, empagliflozin may be held in cases of acute kidney injury and/or discontinued in patients who develop chronic renal disease.  The vast majority of glucose filtered through the glomerulus is reabsorbed within the proximal tubule, primarily via SGLT2 (sodium-glucose linked co-transporter-2) which is responsible for ~90% of the total glucose reabsorption within the kidneys. Na<sup>+</sup>/K<sup>+</sup>-ATPase on the basolateral membrane of proximal tubular cells utilize ATP to actively pump Na+ ions into the interstitium surrounding the tubule, establishing a Na<sup>+</sup> gradient within the tubular cell. SGLT2 on the apical membrane of these cells then utilize this gradient to facilitate secondary active co-transport of both Na+ and glucose out of the filtrate, thereby reabsorbing glucose back into the blood – inhibiting this co-transport, then, allows for a marked increase in glucosuria and decrease in blood glucose levels. Empagliflozin is a potent inhibitor of renal SGLT2 transporters located in the proximal tubules of the kidneys and works to lower blood glucose levels via an increase in glucosuria.",The molecular weight is 450.91.,Empagliflozin has a topological polar surface area of 108.61.,The log p value of  is 2.59.,Empagliflozin is approved.,Empagliflozin is a solid.,True
15848,"Famciclovir, marketed as Famvir by Novartis, is a guanine analogue used to treat herpes virus infections. It is most commonly used to treat herpes zoster (shingles). Famciclovir is a prodrug of penciclovir with higher oral bioavailability. For the treatment of acute herpes zoster (shingles). Also for the treatment or suppression of recurrent genital herpes in immunocompetent patients and treatment of recurrent mucocutaneous herpes simplex infections in HIV infected patients. Famciclovir is a prodrug that undergoes rapid biotransformation to the active antiviral compound penciclovir. Penciclovir is an anti-viral drug which has inhibitory activity against herpes simplex virus types 1 (HSV-1) and 2 (HSV-2) and varicella zoster virus (VZV). Therefore, herpes viral DNA synthesis and replication are selectively inhibited. Famciclovir undergoes rapid biotransformation to the active antiviral compound penciclovir, which has inhibitory activity against herpes simplex virus types 1 (HSV-1) and 2 (HSV-2) and varicella zoster virus (VZV). In cells infected with HSV-1, HSV-2 or VZV, viral thymidine kinase phosphorylates penciclovir to a monophosphate form that, in turn, is converted to penciclovir triphosphate by cellular kinases. In vitro studies demonstrate that penciclovir triphosphate inhibits HSV-2 DNA polymerase competitively with deoxyguanosine triphosphate. Consequently, herpes viral DNA synthesis and, therefore, replication are selectively inhibited.",The molecular weight is 321.34.,Famciclovir has a topological polar surface area of 122.22.,The log p value of  is 0.08.,Famciclovir is approved and investigational.,Famciclovir is a solid.,True
15849,"Brimonidine is an alpha-adrenergic agonist and 2-imidazoline derivative that was first introduced in 1996. It is considered to be a third generation alpha-2 aadrenergic receptor agonist, since it displays preferential binding at alpha-2 adrenoceptors over alpha-1 receptors. Brimonidine displays a higher selectivity toward the alpha-2 adrenergic receptors than or , which are also alpha-2 adrenergic agonists. Alpha-2 adrenergic agonists are members of the ocular hypotensive agent drug class that are used in the chronic treatment of glaucoma. Early treatment and management of glaucoma, which predominantly involves the lowering of intraocular pressure, is critical since glaucoma is considered to be a common cause of blindness worldwide.  **Opthalmic** Brimonidine is a highly selective alpha-2 adrenergic receptor agonist that is 1000-fold more selective for the alpha2-adrenergic receptor than the alpha1-adrenergic receptor. This characteristic gives the drug some therapeutic advantages, since it reduces the risk of systemic side effects, such as systemic hypotension, bradycardia, and sedation. In addition, there is a reduction in the risk for developing alpha-1 mediated ocular unwanted effects, such as conjunctival blanching, mydriasis, and eyelid retraction. However, despite high alpha-2 receptor specificity, brimonidine may still produce alpha-1 adrenoceptor-mediated ocular effects, such as conjunctival vasoconstriction. Brimonidine has a peak ocular hypotensive effect occurring at two hours post-dosing. In a randomized, double-blind clinical study, ocular administration of 0.2% brimonidine in healthy volunteers resulted in a 23% reduction of mean intraocular pressure from baseline at 3 hours following administration. In comparative studies consisting of patients with open-angle glaucoma or ocular hypertension, the ocular hypotensive effect of brimonidine was maintained during treatment periods of up to 1 year.  In the eye, alpha-1 adrenoceptors play a role in vasoconstriction, mydriasis, eyelid retraction, and elevation of intraocular pressure (IOP) whereas alpha-2 adrenoceptors are responsible for IOP reduction via a complex Gi-coupled signaling cascade pathway. Activation of alpha-2 receptors leads to inhibition of adenylyl cyclase and reduction of cyclic AMP levels. As a result, there is a decrease in norpinephrine (NE) release at the synaptic junction, NE-induced stimulation of beta-2 adrenoceptors, and production of aqueous humor by the ciliary epithelium. An elevated IOP is the most significant risk factor for developing glaucomatous optic neuropathy, which is associated with progressive visual field loss and functional disability if left untreated. Regardless of the etiology of the disease, the aim of current therapies for glaucoma is to reduce IOP, as reduction of IOP significantly reduces the risk of progression of vision loss even when IOP is already within the normal range. When administered ophthalmically, brimonidine is rapidly absorbed into the eye, acts as an agonist at ocular alpha-2 adrenoceptors and lowers IOP via a dual mechanism of action. It is proposed that initial dosing of the drug causes a reduction in aqueous humour production and chronic dosing leads to an increase in uveoscleral outflow. Brimonidine does not affect episcleral venous pressure. By reducing IOP, brimonidine aims to reduce the likelihood of glaucomatous visual field loss in ocular hypertension, and slow the progression of visual field defect in established open-angle glaucoma. When applied topically on skin, brimonidine reduces erythema through direct vasocontriction of small arteries and veins. As brimonidine mediates a potent peripheral vasoconstrictive activity by selectively working on the alpha-2 adrenoceptors, the use of brimonidine is thought to be efficacious for the treatment of facial erythema of rosacea, which is thought to arise from vasomotor instability and abnormal vasodilation of the superficial cutaneous vasculature of the face.",The molecular weight is 292.14.,Brimonidine has a topological polar surface area of 62.2.,The log p value of  is 1.49.,Brimonidine is approved.,Brimonidine is a solid.,True
15850,"An antifibrinolytic agent that acts by inhibiting plasminogen activators which have fibrinolytic properties. For use in the treatment of excessive postoperative bleeding. Aminocaproic acid works as an antifibrinolytic. It is a derivative of the amino acid lysine. The fibrinolysis-inhibitory effects of aminocaproic acid appear to be exerted principally via inhibition of plasminogen activators and to a lesser degree through antiplasmin activity. Aminocaproic acid may be a possible prophylactic for vascular disease, as it may prevent formation of lipoprotein (a), a risk factor for vascular disease.  Aminocaproic acid binds reversibly to the kringle domain of plasminogen and blocks the binding of plasminogen to fibrin and its activation to plasmin. With NO activation of plasmin, there is a reduction in fibrinolysis. This consequently will reduce the amount of bleeding post surgery. Elevated plasma levels of lipoprotein(a) have been shown to increase the risk of vascular disease. Lipoprotein 9a)a has two components, apolipoprotein B-100, linked to apolipoprotein (a). Aminocaproic acid may change the conformation of apoliprotein (a), changing its binding properties and potentially preventing the formation of lipoprotein (a).",The molecular weight is 131.18.,Aminocaproic acid has a topological polar surface area of 63.32.,The log p value of  is -2.24.,Aminocaproic acid is approved and investigational.,Aminocaproic acid is a solid.,True
15851,"N-methylnicotinamide is an experimental drug with no approved indication or marketed formulation. It is a metabolite of niacinamide/nicotinamide and niacin/nicotinic acid (vitamin B3), and as such N-methylnicotinamide is used to diagnose niacin deficiency by measuring N-methylnicotinamide in the urine. N-methylnicotinamide is an experimental drug with no approved indication.",The molecular weight is 136.15.,N-methylnicotinamide has a topological polar surface area of 41.99.,The log p value of  is 0.11.,N-methylnicotinamide is experimental.,N-methylnicotinamide is a solid.,True
15852,"An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter. For nutritional supplementation, also for treating dietary shortage or imbalance Adenosine triphosphate (ATP) is the nucleotide known in biochemistry as the \molecular currency\"" of intracellular energy transfer; that is, ATP is able to store and transport chemical energy within cells. ATP also plays an important role in the synthesis of nucleic acids. The total quantity of ATP in the human body is about 0.1 mole. The energy used by human cells requires the hydrolysis of 200 to 300 moles of ATP daily. This means that each ATP molecule is recycled 2000 to 3000 times during a single day. ATP cannot be stored, hence its consumption must closely follow its synthesis."" ATP is able to store and transport chemical energy within cells. ATP also plays an important role in the synthesis of nucleic acids. ATP can be produced by various cellular processes, most typically in mitochondria by oxidative phosphorylation under the catalytic influence of ATP synthase. The total quantity of ATP in the human body is about 0.1 mole. The energy used by human cells requires the hydrolysis of 200 to 300 moles of ATP daily. This means that each ATP molecule is recycled 2000 to 3000 times during a single day. ATP cannot be stored, hence its consumption must closely follow its synthesis.",The molecular weight is 507.18.,ATP has a topological polar surface area of 279.13.,The log p value of  is -4.55.,ATP is investigational and nutraceutical.,ATP is a solid.,True
15853,"Abacavir (ABC) is a powerful nucleoside analog reverse transcriptase inhibitor (NRTI) used to treat HIV and AIDS. Chemically, it is a synthetic carbocyclic nucleoside and is the enantiomer with 1S, 4R absolute configuration on the cyclopentene ring. In vivo, abacavir sulfate dissociates to its free base, abacavir. For the treatment of HIV-1 infection, in combination with other antiretroviral agents. Abacavir is a nucleoside reverse transcriptase inhibitor (NRTI) with activity against Human Immunodeficiency Virus Type 1 (HIV-1). Abacavir is phosphorylated to active metabolites that compete for incorporation into viral DNA. They inhibit the HIV reverse transcriptase enzyme competitively and act as a chain terminator of DNA synthesis. The concentration of drug necessary to effect viral replication by 50 percent (EC50) ranged from 3.7 to 5.8 μM (1 μM = 0.28 mcg/mL) and 0.07 to 1.0 μM against HIV-1IIIB and HIV-1BaL, respectively, and was 0.26 ± 0.18 μM against 8 clinical isolates. Abacavir had synergistic activity in cell culture in combination with the nucleoside reverse transcriptase inhibitor (NRTI) zidovudine, the non-nucleoside reverse transcriptase inhibitor (NNRTI) nevirapine, and the protease inhibitor (PI) amprenavir; and additive activity in combination with the NRTIs didanosine, emtricitabine, lamivudine, stavudine, tenofovir, and zalcitabine.  Abacavir is a carbocyclic synthetic nucleoside analogue and an antiviral agent. Intracellularly, abacavir is converted by cellular enzymes to the active metabolite carbovir triphosphate, an analogue of deoxyguanosine-5'-triphosphate (dGTP). Carbovir triphosphate inhibits the activity of HIV-1 reverse transcriptase (RT) both by competing with the natural substrate dGTP and by its incorporation into viral DNA. Viral DNA growth is terminated because the incorporated nucleotide lacks a 3'-OH group, which is needed to form the 5′ to 3′ phosphodiester linkage essential for DNA chain elongation. ",The molecular weight is 286.34.,Abacavir has a topological polar surface area of 101.88.,The log p value of  is 0.81.,Abacavir is approved and investigational.,Abacavir is a solid.,True
15854,"A purine base and a fundamental unit of adenine nucleotides. For nutritional supplementation, also for treating dietary shortage or imbalance Adenine (sometimes known as vitamin B4) combines with the sugar ribose to form adenosine, which in turn can be bonded with from one to three phosphoric acid units, yielding AMP, ADP and ATP. These adenine derivatives perform important functions in cellular metabolism. Adenine is one of four nitrogenous bases utilized in the synthesis of nucleic acids. A modified form of adenosine monophosphate (cyclic AMP) is an imporant secondary messenger in the propagation of many hormonal stimuli. Adenine is an integral part of the structure of many coenzymes. Adenosine (adenine with a ribose group) causes transient heart block in the AV node of the heart. In individuals suspected of suffering from a supraventricular tachycardia (SVT), adenosine is used to help identify the rhythm. Certain SVTs can be successfully terminated with adenosine. Adenine forms adenosine, a nucleoside, when attached to ribose, and deoxyadenosine when attached to deoxyribose, and it forms adenosine triphosphate (ATP), which drives many cellular metabolic processes by transferring chemical energy between reactions. ",The molecular weight is 135.13.,Adenine has a topological polar surface area of 80.48.,The log p value of  is -0.15.,Adenine is approved and nutraceutical.,Adenine is a solid.,True
15855,"A potent direct-acting peripheral vasodilator (vasodilator agents) that reduces peripheral resistance and produces a fall in blood pressure. For the treatment of severe hypertension and in the topical treatment (regrowth) of androgenic alopecia in males and females and stabilisation of hair loss in patients with androgenic alopecia. Minoxidil is an orally effective direct acting peripheral vasodilator that reduces elevated systolic and diastolic blood pressure by decreasing peripheral vascular resistance. Minoxidil is also used topically to treat androgenetic alopecia. Microcirculatory blood flow in animals is enhanced or maintained in all systemic vascular beds. In man, forearm and renal vascular resistance decline; forearm blood flow increases while renal blood flow and glomerular filtration rate are preserved. The predominant site of minoxidil action is arterial. Venodilation does not occur with minoxidil; thus, postural hypotension is unusual with its administration. The antihypertensive activity of minoxidil is due to its sulphate metabolite, minoxidil sulfate. Minoxidil is thought to promote the survival of human dermal papillary cells (DPCs) or hair cells by activating both extracellular signal-regulated kinase (ERK) and Akt and by preventing cell death by increasing the ratio of BCl<sup>-</sup>2/Bax. Minoxidil may stimulate the growth of human hairs by prolonging anagen through these proliferative and anti-apoptotic effects on DPCs. Minoxidil, when used as a vasodilator, acts by opening adenosine triphosphate-sensitive potassium channels in vascular smooth muscle cells. This vasodilation may also improve the viability of hair cells or hair follicles.",The molecular weight is 209.25.,Minoxidil has a topological polar surface area of 93.63.,The log p value of  is 0.02.,Minoxidil is approved and investigational.,Minoxidil is a solid.,True
15856,"Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of naloxone. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence. Used as an adjunct to a medically supervised behaviour modification program in the maintenance of opiate cessation in individuals who were formerly physically dependent on opiates and who have successfully undergone detoxification. Also used for the management of alcohol dependence in conjunction with a behavioural modification program. Naltrexone, a pure opioid antagonist, is a synthetic congener of oxymorphone with no opioid agonist properties. Naltrexone is indicated in the treatment of alcohol dependence and for the blockade of the effects of exogenously administered opioids. It markedly attenuates or completely blocks, reversibly, the subjective effects of intravenously administered opioids. When co-administered with morphine, on a chronic basis, naltrexone blocks the physical dependence to morphine, heroin and other opioids. In subjects physically dependent on opioids, naltrexone will precipitate withdrawal symptomatology. Naltrexone is a pure opiate antagonist and has little or no agonist activity. The mechanism of action of naltrexone in alcoholism is not understood; however, involvement of the endogenous opioid system is suggested by preclinical data. Naltrexone is thought to act as a competitive antagonist at mc, κ, and δ receptors in the CNS, with the highest affintiy for the μ receptor. Naltrexone competitively binds to such receptors and may block the effects of endogenous opioids. This leads to the antagonization of most of the subjective and objective effects of opiates, including respiratory depression, miosis, euphoria, and drug craving. The major metabolite of naltrexone, 6-β-naltrexol, is also an opiate antagonist and may contribute to the antagonistic activity of the drug.",The molecular weight is 341.41.,Naltrexone has a topological polar surface area of 70.0.,The log p value of  is 0.36.,Naltrexone is approved and investigational and vet_approved.,Naltrexone is a solid.,True
15857,"Alvocidib is a synthetic flavonoid based on an extract from an Indian plant for the potential treatment of cancer. It works by inhibiting cyclin-dependent kinases, arresting cell division and causing apoptosis in non-small lung cancer cells. Investigated for use/treatment in esophageal cancer, leukemia (lymphoid), lung cancer, liver cancer, and lymphoma (unspecified). Inhibits cyclin-dependent kinases, arresting cell division and causing apoptosis in non-small lung cancer cells.",,,,Alvocidib is experimental and investigational.,Alvocidib is a solid.,True
15858,"Fabry disease is a rare, progressive genetic disorder characterized by a defective GLA gene that causes a deficiency in the enzyme alpha-Galactosidase A (alpha-Gal A). This enzyme is responsible for breaking down glycosphingolipid substrate that, when deficient in patients with Fabry disease, builds up in the blood vessels, the kidneys, the nerves, the heart, and other organs. In the U.S., it is estimated that more than 3,000 people are living with Fabry disease, and an estimated more than 50 percent of these diagnosed patients are currently untreated. Migalastat is an alpha-galactosidase A (alpha-Gal A) pharmacological chaperone indicated for the long-term treatment of adults and adolescents aged 16 years and older with a confirmed diagnosis of Fabry disease (alpha-galactosidase A deficiency) and an amenable galactosidase alpha gene (GLA) mutation/variant based upon in vitro assay data.  In general, treatment in patients with migalastat in Phase 2 pharmacodynamic trials resulted in increases in endogenous alpha-galactosidase (alpha-Gal A) activity in white blood cells, as well as in skin and kidney for the majority of patients. In patients with amenable galactosidase alpha gene (GLA) mutations, globotriaosylceramide (GL-3) levels tended to decrease in the urine and in the kidney interstitial capillaries. Fabry disease is a progressive X-linked lysosomal storage disorder which affects males and females. Fabry disease-causing mutations occur in the galactosidase alpha (GLA) gene and result in a deficiency of the lysosomal enzyme alpha-galactosidase A (alpha-Gal A) that is required for glycosphingolipid substrate (GL-3 and lyso-Gb3) metabolism. Reduced alpha-Gal A activity is, therefore, associated with the progressive accumulation of glycosphingolipid substrate in vulnerable organs and tissues, which ultimately leads to the morbidity and mortality associated with Fabry disease.",The molecular weight is 163.17.,Migalastat has a topological polar surface area of 92.95.,The log p value of  is -1.42.,Migalastat is approved and investigational.,Migalastat is a solid.,True
15859,"Raltegravir is an antiretroviral drug produced by Merck & Co., used to treat HIV infection. It received approval by the U.S. Food and Drug Administration (FDA) on 12 October 2007, the first of a new class of HIV drugs, the integrase inhibitors, to receive such approval. For the treatment of HIV-1 infection in conjunction with other antiretrovirals. Raltegravir inhibits HIV integrase to prevent the viral genome being incorporated into the human genome. Raltegravir is primarily metabolized by glucuronidation.",The molecular weight is 444.42.,Raltegravir has a topological polar surface area of 150.02.,The log p value of  is 1.16.,Raltegravir is approved.,Raltegravir is a solid.,True
15860,"Sodium aurothiomalate is a gold compound that is used for its immunosuppressive anti-rheumatic effects. Gold Sodium Thiomalate is supplied as a solution for intramuscular injection containing 50 mg of Gold Sodium Thiomalate per mL. It is most effective in active progressive rheumatoid arthritis and of little or no value in the presence of extensive deformities or in the treatment of other forms of arthritis. A disease-modifying antirheumatic drug (DMARD) indicated for the symptomatic treatment of arthritis.  Unknown, may decrease prostaglandin synthesis or may alter cellular mechanisms by inhibiting sulfhydryl systems. The precise mechanism of action is unknown. It is known that sodium aurothiomalate inhibits the synthesis of prostaglandins. The predominant action appears to be a suppressive effect on the synovitis of active rheumatoid disease.",The molecular weight is 390.07.,Sodium aurothiomalate has a topological polar surface area of 80.26.,,Sodium aurothiomalate is approved and investigational.,Sodium aurothiomalate is a solid.,True
15861,"Silibinin is the major active constituent of silymarin, a standardized extract of the milk thistle seeds, containing a mixture of flavonolignans consisting of silibinin, isosilibinin, silicristin, silidianin and others. Silibinin is presented as a mixture of two diastereomers, silybin A and silybin B, which are found in an approximately equimolar ratio. Both in vitro and animal research suggest that silibinin has hepatoprotective (antihepatotoxic) properties that protect liver cells against toxins. Silibinin has also demonstrated in vitro anti-cancer effects against human prostate adenocarcinoma cells, estrogen-dependent and -independent human breast carcinoma cells, human ectocervical carcinoma cells, human colon cancer cells, and both small and nonsmall human lung carcinoma cells. Currently being tested as a treatment of severe intoxications with hepatotoxic substances, such as death cap (Amanita phalloides) poisoning.",,,,Silibinin is experimental and investigational.,Silibinin is a solid.,True
15862,"The World Health Organization declared smallpox, a contagious and sometimes fatal infectious disease, eradicated in 1980. However, there have been longstanding concerns that smallpox may be used as a bioweapon. Tecovirimat is indicated for the treatment of smallpox infection. It can be administered in children and adults with a minimum body weight of 13 kg. Tecovirimat is an inhibitor of the Orthopoxvirus VP37 envelope wrapping protein. Tecovirimat prevents viral spread throughout the body. Tecovirimat inhibits the production of extracellular viral forms, which are responsible for the systemic spread of infection, inhibiting virus-induced cytopathic effects. Tecovirimat does not inhibit the formation of intracellular forms of the virus (IMV); however, by inhibiting envelopment, and therefore preventing the exit of viral particles from an infected cell, the smallpox infection is slowed to a point where the immune system can eliminate the virus.",,,,Tecovirimat is approved and investigational.,Tecovirimat is a solid.,True
15863,"Metastatic triple-negative breast cancer (mTNBC) is an aggressive form of breast cancer with limited treatment options involving cytotoxic chemotherapy agents. Targeted chemotherapy through the application of antibody-conjugated agents (ADCs) is a recent advance in cancer treatment. One such ADC is sacituzumab govitecan, which combines a humanized anti-trophoblast cell-surface antigen 2 (TROP-2) antibody with the topoisomerase I inhibitor SN-38. Sacituzumab govitecan is indicated for adult patients with metastatic triple-negative breast cancer (mTNBC) who have undergone two or more prior therapies for metastatic disease. Sacituzumab govitecan is a humanized monoclonal antibody/topoisomerase inhibitor conjugate designed to induce DNA damage-mediated cell death preferentially in TROP-2-expressing cancer cells. Detailed pharmacodynamic studies have not been performed for sacituzumab govitecan, although as a therapeutic protein, there is potential for immunogenicity. In addition, sacituzumab govitecan has the potential to cause severe hypersensitivity, nausea and vomiting, and embryo-fetal toxicity. Patients who are homozygous for the uridine diphosphate-glucuronosyl transferase 1A1 (UGT1A1)*28 allele are at increased risk for neutropenia. Sacituzumab govitecan is an antibody-drug conjugate (ADC) targeting TROP-2-expressing cancer cells to induce DNA-damage-mediated cell death. The conjugate comprises a humanized anti-TROP-2 monoclonal antibody (RS7-3G11, also known as RS7) chemically linked by a hydrolyzable CL2A linker to the cytotoxic drug SN-38.",,,,Sacituzumab govitecan is approved and investigational.,,True
15864,"Pibrentasvir is a direct acting antiviral agent and Hepatitis C virus (HCV) NS5A inhibitor that targets the the viral RNA replication and viron assembly. In combination with , pibrentastiv is a useful therapy for patients who experienced therapeutic failure from other NS5A inhibitors. In cell cultures, the emergence of amino acid substitutions at known NS5A inhibitor resistance-associated positions in HCV genotype 1a, 2a or 3a replicons led to reduced susceptibility and resistance to pibrentasvir. These resistance-associated amino acid substitutions included Q30D/deletion, Y93D/H/N or H58D +Y93H in genotype 1a replicons, F28S + M31I or P29S + K30G in genotype 2a replicons, and Y93H in genotype 3a replicons. Individual NS5A amino acid substitutions that reduced susceptibility to pibrentasvir include M28G or Q30D in a genotype 1a replicon and P32-deletion in a genotype 1b replicon.  Indicated for the treatment of adult patients with chronic hepatitis C virus (HCV) genotype 1, 2, 3, 4, 5 or 6 infection without cirrhosis or with compensated cirrhosis (Child-Pugh Pibrentasvir is a pan-genotypic. According to HCV replicon assays, pibrentasvir has EC50 values ranging from 0.08-4.6 nM agaisnt laboratory and clinical isolates from subtypes 1a, 1b, 2a, 2b, 3a, 4a, 4d, 5a, and 6a, or EC50 values of 0.5-4.3 pM against laboratory and clinical isolates from subtypes 1a, 1b, 2a, 2b, 3a, 4a, 4b, 4d, 5a, 6a, 6e and 6p. It is active against common resistance-conferring substitutions in HCV genotypes 1 to 6 that confers resistance and decreased therapeutic response from other NS5A inhibitors, inluding positions 24, 28, 30, 31, 58, 92, or 93 in NS5A. In a QT study, pibrentasvir is not shown to prolong the QTc interval.  NS5A is a phosphoprotein that plays an essential role in replication, assembly and maturation of infectious viral proteins. The basal phosphorylated form of NS5A, which is maintained by C-terminal serine cluster, is key in ensuring its interaction with the viral capsid protein, or the core protein. By blocking this interaction, pibrentasvir inhibits the assembly of proteins and production of mature HCV particles. NS5A also interacts with viral and cellular proteins to form the HCV replicase complex, and supports the RNA replication of HCV.",The molecular weight is 1113.2.,Pibrentasvir has a topological polar surface area of 199.58.,The log p value of  is 7.2.,Pibrentasvir is approved and investigational.,Pibrentasvir is a solid.,True
15865,"Torcetrapib (CP-529414, Pfizer) was developed to treat hypercholesterolemia but its development was halted in 2006 when phase III studies showed excessive mortality in the treatment group receiving a combination of atorvastatin and the study drug. Investigated for use/treatment in peripheral vascular disease and hyperlipidemia. Torcetrapib is an inhibitor of cholesteryl ester-transfer protein (CETP) that increases high-density lipoprotein (HDL) cholesterol levels. The drug increases HDL-cholesterol and apolipoprotein A-I levels and decreases LDL-cholesterol and apolipoprotein B levels. The effect is showed in monotherapy and when administered in combination with statins.",,,,Torcetrapib is investigational.,Torcetrapib is a solid.,True
15866,"Nitroprusside serves as a source of nitric oxide, a potent peripheral vasodilator that affects both arterioles and venules (venules more than arterioles). Nitroprusside is often administered intravenously to patients who are experiencing a hypertensive emergency. For immediate reduction of blood pressure of patients in hypertensive crises, reduce bleeding during surgery, and for the treatment of acute congestive heart failure Nitroprusside a powerful vasodilator relaxes the vascular smooth muscle and produce consequent dilatation of peripheral arteries and veins. Other smooth muscle (e.g., uterus, duodenum) is not affected. Sodium nitroprusside is more active on veins than on arteries. One molecule of sodium nitroprusside is metabolized by combination with hemoglobin to produce one molecule of cyanmethemoglobin and four CN- ions; methemoglobin, obtained from hemoglobin, can sequester cyanide as cyanmethemoglobin; thiosulfate reacts with cyanide to produce thiocyanate; thiocyanate is eliminated in the urine; cyanide not otherwise removed binds to cytochromes. Cyanide ion is normally found in serum; it is derived from dietary substrates and from tobacco smoke. Cyanide binds avidly (but reversibly) to ferric ion (Fe+++), most body stores of which are found in erythrocyte methemoglobin (metHgb) and in mitochondrial cytochromes. When CN is infused or generated within the bloodstream, essentially all of it is bound to methemoglobin until intraerythrocytic methemoglobin has been saturated. ",,,,Nitroprusside is approved and investigational.,Nitroprusside is a solid.,True
15867,"A benzimidazole that acts by interfering with carbohydrate metabolism and inhibiting polymerization of microtubules.  For the treatment of <i>Enterobius vermicularis</i> (pinworm), <i>Trichuris trichiura</i> (whipworm), <i>Ascaris lumbricoides</i> (common roundworm), <i>Ancylostoma duodenale</i> (common hookworm), <i>Necator americanus</i> (American hookworm) in single or mixed infections. Mebendazole is a (synthetic) broad-spectrum anthelmintic. The principal mode of action for Mebendazole is by its inhibitory effect on tubulin polymerization which results in the loss of cytoplasmic microtubules. Mebendazole causes degenerative alterations in the tegument and intestinal cells of the worm by binding to the colchicine-sensitive site of tubulin, thus inhibiting its polymerization or assembly into microtubules. The loss of the cytoplasmic microtubules leads to impaired uptake of glucose by the larval and adult stages of the susceptible parasites, and depletes their glycogen stores. Degenerative changes in the endoplasmic reticulum, the mitochondria of the germinal layer, and the subsequent release of lysosomes result in decreased production of adenosine triphosphate (ATP), which is the energy required for the survival of the helminth. Due to diminished energy production, the parasite is immobilized and eventually dies.",The molecular weight is 295.3.,Mebendazole has a topological polar surface area of 84.08.,The log p value of  is 3.08.,Mebendazole is approved and vet_approved.,Mebendazole is a solid.,True
15868,"Isopropyl analog of epinephrine; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant. For the treatment of mild or transient episodes of heart block that do not require electric shock or pacemaker therapy also used in management of asthma and chronic bronchitis Isoproterenol is a relatively selective beta2-adrenergic bronchodilator. Isoproterenol is indicated for the relief of bronchospasm associated with chronic obstructive pulmonary disease. The pharmacologic effects of beta adrenergic agonist drugs, including Isoproterenol, are at least in part attributable to stimulation through beta adrenergic receptors of intracellular adenyl cyclase, the enzyme which catalyzes the conversion of adenosine triphosphate (ATP) to cyclic- 3',5'- adenosine monophosphate (c-AMP). Increased c-AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells. The pharmacologic effects of isoproterenol are at least in part attributable to stimulation through beta-adrenergic receptors of intracellular adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic AMP. Increased cyclic AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells.",The molecular weight is 211.26.,Isoprenaline has a topological polar surface area of 72.72.,The log p value of  is 0.15.,Isoprenaline is approved and investigational.,Isoprenaline is a solid.,True
15869,"A substituted phenylaminoethanol that has beta-2 adrenomimetic properties at very low doses. It is used as a bronchodilator in asthma. Used as a bronchodilator in the treatment of asthma patients.  Clenbuterol is a substituted phenylaminoethanol that has beta-2 adrenomimetic properties at very low doses. It is used as a bronchodilator in asthma. Although approved for use in some countries, as of fall, 2006, clenbuterol is not an ingredient of any therapeutic drug approved by the U.S. Food and Drug Administration. Clenbuterol is a Beta(2) agonist similar in some structural respects to salbutamol. Agonism of the beta(2) receptor stimulates adenylyl cyclase activity which ultimately leads to downstream effects of smooth muscle relaxation in the bronchioles.",The molecular weight is 277.19.,Clenbuterol has a topological polar surface area of 58.28.,The log p value of  is 2.39.,Clenbuterol is approved and investigational and vet_approved.,Clenbuterol is a solid.,True
15870,"A phosphorothioate proposed as a radiation-protective agent. It causes splenic vasodilation and may block autonomic ganglia. For reduction in the cumulative renal toxicity in patients with ovarian cancer (using cisplatin) and moderate to severe xerostomia in patients undergoing post-operative radiation treatment for head and neck cancer. Amifostine is an organic thiophosphate cytoprotective agent indicated to reduce the cumulative renal toxicity associated with repeated administration of cisplatin in patients with advanced ovarian cancer or non-small cell lung cancer and also to reduce the incidence of moderate to severe xerostomia in patients undergoing post-operative radiation treatment for head and neck cancer. Amifostine is a prodrug that is dephosphorylated by alkaline phosphatase in tissues to a pharmacologically active free thiol metabolite, believed to be responsible for the reduction of the cumulative renal toxicity of cisplatin and for the reduction of the toxic effects of radiation on normal oral tissues. Healthy cells are preferentially protected because amifostine and metabolites are present in healthy cells at 100-fold greater concentrations than in tumour cells. The thiol metabolite is responsible for most of the cytoprotective and radioprotective properties of amifostine. It is readily taken up by cells where it binds to and detoxifies reactive metabolites of platinum and alkylating agents as well as scavenges free radicals. Other possible effects include inhibition of apoptosis, alteration of gene expression and modification of enzyme activity.",The molecular weight is 214.22.,Amifostine has a topological polar surface area of 95.58.,The log p value of  is -1.85.,Amifostine is approved and investigational.,Amifostine is a solid.,True
15871,"A hallucinogen formerly used as a veterinary anesthetic, and briefly as a general anesthetic for humans. Phencyclidine is similar to ketamine in structure and in many of its effects. Like ketamine, it can produce a dissociative state. It exerts its pharmacological action through inhibition of NMDA receptors (receptors, N-methyl-D-aspartate). As a drug of abuse, it is known as PCP and Angel Dust. Phencyclidine works primarily as an NMDA receptor antagonist, which blocks the activity of the NMDA Receptor. The N-methyl-D-Aspartate (NMDA) receptor, a type of ionotropic receptor, is found on the dendrites of neurons and receives signals in the form of neurotransmitters. It is a major excitatory receptor in the brain. Normal physiological function requires that the activated receptor fluxes positive ions through the channel part of the receptor. PCP enters the ion channel from the outside of the neuron and binds, reversibly, to a site in the channel pore, blocking the flux of positive ions into the cell. PCP therefore inhibits depolarization of neurons and interferes with cognitive and other functions of the nervous system.",The molecular weight is 243.39.,Phencyclidine has a topological polar surface area of 3.24.,The log p value of  is 5.1.,Phencyclidine is illicit.,Phencyclidine is a solid.,True
15872,"A pyrethroid insecticide commonly used in the treatment of lice infestations and scabies. It is a yellow to light orange-brown, low melt-ing solid or viscous liquid. For the treatment of infestation with <i>Sarcoptes scabiei</i> (scabies). Permethrin, a pyrethroid, is active against a broad range of pests including lice, ticks, fleas, mites, and other arthropods. Permethrin acts on the nerve cell membrane to disrupt the sodium channel current by which the polarization of the membrane is regulated. Delayed repolarization and paralysis of the pests are the consequences of this disturbance.",The molecular weight is 391.29.,Permethrin has a topological polar surface area of 35.53.,The log p value of  is 7.61.,Permethrin is approved and investigational.,Permethrin is a solid.,True
15873,"Artemisinin has been used in trials studying the treatment of Schizophrenia, Malaria, Falciparum, and Plasmodium Falciparum.",The molecular weight is 282.34.,Artemisinin has a topological polar surface area of 53.99.,The log p value of  is 2.72.,Artemisinin is investigational.,,True
15874,"Adrenergic beta-agonist used to control premature labor. For the treatment and prophylaxis of premature labour Beta-2 adrenergic receptors are located at sympathetic neuroeffector junctions of many organs, including uterus. Ritodrine is beta-2 adrenergic agonist. It stimulates beta-2 adrenergic receptor, increases cAMP level and decreases intracellular calcium concentration. The decrease of calcium concentration leads to a relaxation of uterine smooth muscle and, therefore, a decrease in premature uterine contractions.  Ritodrine is beta-2 adrenergic agonist. It binds to beta-2 adrenergic receptors on outer membrane of myometrial cell, activates adenyl cyclase to increase the level of cAMP which decreases intracellular calcium and leads to a decrease of uterine contractions.",The molecular weight is 287.36.,Ritodrine has a topological polar surface area of 72.72.,The log p value of  is 1.65.,Ritodrine is approved and investigational.,Ritodrine is a solid.,True
15875,"Amifampridine, or 3,4-diaminopyridine (3,4-DAP), is a quaternary ammonium compound that blocks presynaptic potassium channels, and subsequently prolongs the action potential and increases presynaptic calcium concentrations. It was first discovered in Scotland in the 1970s and its clinical effectiveness for neuromuscular disorders, including Lambert–Eaton myasthenic syndrome (LEMS), has been investigated in the 1980s. Amifampridine phosphate is a more stable salt that serves as an active ingredient of EMA-approved Firdapse, which was previously marketed as Zenas. It is currently used as the first-line symptomatic treatment for LEMS in adult patients and is ideally given as oral tablets in divided doses, three or four times a day. Firdapse (amifampridine) was formally approved by the US FDA for the treatment of adults with LEMS as recently as November of 2018. Amifampridine is indicated for the symptomatic treatment of Lambert-Eaton myasthenic syndrome (LEMS) in adults and in patients aged 6 to less than 17 years of age. Nevertheless, it is important to note that at the current time only the Firdapse brand of amifampridine is indicated for the treatment of LEMS in adults and the Ruzurgi brand of amifampridine is indicated for the treatment of LEMS in patients aged 6 to less than 17 years. Administration of amifampridine to patients with LES in clinical trials resulted in improvement of the compound muscle action potential (CMAP), muscle function, and quantitative myasthenia gravis (QMG) score. One case of a slight prolongation of the QTc interval in male patient with LEMS and euthyroid Hashimoto’s disease treated with 90 mg of amifampridine in combination with 100 mg azathioprine was reported. I_n vitro_, amifampridine was shown to modulate cardiac conduction and induce phasic contractions in different arteries from several species. In addition, it stimulated potassium-evoked dopamine and noradrenaline release in rat hippocampal slices and upregulate acetylcholine release in the brain. It may also potentiate adrenergic and cholinergic neuromuscular transmission in the gatrointestinal tract. In a single pharmacokinetic study, no effect was observed of amifampridine phosphate on cardiac repolarization as assessed using the QTc interval. There were no changes in heart rate, atrioventricular conduction or cardiac depolarization as measured by the heart rate, PR and QRS interval durations. Amifampridine is a symptomatic treatment that increases acetylcholine concentrations at the neuromuscular junction. It selectively blocks presynaptic fast voltage-gated potassium channels, thereby prolonging cell membrane depolarization and action potential, and augmenting calcium transport into the nerve endings. Increased intracellular calcium enhances the exocytosis of acetylcholine-containing vesicles and enhances impulse transmission at central, autonomic, and neuromuscular synapses. Amifampridine improves muscle strength and resting compound muscle action potential (CMAP) amplitudes with an overall weighted mean difference of 1.69 mV. ",The molecular weight is 109.13.,Amifampridine has a topological polar surface area of 64.93.,The log p value of  is 0.39.,Amifampridine is approved and investigational.,Amifampridine is a solid.,True
15876,"An anti-inflammatory agent, structurally related to the salicylates and non-steroidal anti-inflammatory drugs like acetylsalicylic acid, which is active in inflammatory bowel disease. It is considered to be the active moiety of sulphasalazine. (From Martindale, The Extra Pharmacopoeia, 30th ed) Although demonstrably effective in treating and maintaining remission for ulcerative colitis, mesalazine has historically faced a number of issues regarding its lack of stability as a pharmaceutical agent. Throughout the late seventies and the eighties, important research initiatives developed stable mesalazine formulations like the eudragit-S coating of Asacol brand mesalazine and the Pentasa brand's encapsulation of mesalazine within microgranules. In the present day, contemporary research regarding novel methods to stabilize mesalazine continues and interest in the agent's capacity to decrease inflammatory activity and subsequently potentially reduce the risk of colorectal cancer in conditions like ulcerative colitis is maintained. Mesalazine is indicated for the induction of remission in patients with active or mild to moderate acute exacerbations of ulcerative colitis and for the maintenance of remission of ulcerative colitis ,. Prescribing information for mesalazine in the UK also indicates the medication for the maintenance of remission of Crohn's ileo-colitis. Mesalazine is one of the two components of sulphasalazine, the other being sulphapyridine. It is the latter which is responsible for the majority of the side effects associated with sulphasalazine therapy whilst mesalazine is known to be the active moiety in the treatment of ulcerative colitis. Although the mechanism of action of mesalazine is not fully understood, it is believed to possess a topical anti-inflammatory effect on colonic epithelial cells. Mucosal production of arachidonic acid metabolites, both through the cyclooxygenase pathways, i.e., prostanoids, and through the lipoxygenase pathways, i.e., leukotrienes and hydroxyeicosatetraenoic acids, is increased in patients with chronic inflammatory bowel disease, and it is possible that mesalazine diminishes inflammation by blocking cyclooxygenase and inhibiting prostaglandin production in the colon.",The molecular weight is 153.14.,Mesalazine has a topological polar surface area of 83.55.,The log p value of  is 1.06.,Mesalazine is approved.,Mesalazine is a solid.,True
15877,"A serotonin antagonist and a histamine H1 blocker used as antipruritic, appetite stimulant, antiallergic, and for the post-gastrectomy dumping syndrome, etc. For treatment of perennial and seasonal allergic rhinitis, vasomotor rhinitis, allergic conjunctivitis due to inhalant allergens and foods, mild uncomplicated allergic skin manifestations of urticaria and angioedema, amelioration of allergic reactions to blood or plasma, cold urticaria, dermatographism, and as therapy for anaphylactic reactions adjunctive to epinephrine. Cyproheptadine is a piperidine antihistamine. Unlike other antihistamines, this drug also antagonizes serotonin receptors. This action makes Cyproheptadine useful in conditions such as vascular headache and anorexia. Cyproheptadine does not prevent the release of histamine but rather competes with free histamine for binding at HA-receptor sites. Cyproheptadine competitively antagonizes the effects of histamine on HA-receptors in the GI tract, uterus, large blood vessels, and bronchial smooth muscle. Most antihistamines possess significant anticholinergic properties, but Cyproheptadine exerts only weak anticholinergic actions. Blockade of central muscarinic receptors appears to account for Cyproheptadine's antiemetic effects, although the exact mechanism is unknown. Cyproheptadine also competes with serotonin at receptor sites in smooth muscle in the intestines and other locations. Antagonism of serotonin on the appetite center of the hypothalamus may account for Cyproheptadine's ability to stimulate appetite. Cyproheptadine also has been used to counter vascular headaches, which many believe are caused by changes in serotonin activity, however it is unclear how Cyproheptadine exerts a beneficial effect on this condition. Cyproheptadine competes with free histamine for binding at HA-receptor sites. This antagonizes the effects of histamine on HA-receptors, leading to a reduction of the negative symptoms brought on by histamine HA-receptor binding. Cyproheptadine also competes with serotonin at receptor sites in smooth muscle in the intestines and other locations. Antagonism of serotonin on the appetite center of the hypothalamus may account for Cyproheptadine's ability to stimulate appetite.",The molecular weight is 287.41.,Cyproheptadine has a topological polar surface area of 3.24.,The log p value of  is 5.3.,Cyproheptadine is approved.,Cyproheptadine is a solid.,True
15878,"Mitiglinide is a drug for the treatment of type 2 diabetes. It may stimulate insulin secretion in beta-cells by closing off ATP dependant potassium ion channels. For the treatment of type 2 diabetes. Mitiglinide belongs to the meglitinide class of blood glucose-lowering drugs. It is approved for use in Japan but has not yet gained FDA approval. Mitiglinide is thought to stimulate insulin secretion by binding to and blocking ATP-sensitive K(+) (K(ATP)) channels (Kir6.2/SUR1 complex, KATP channels) in pancreatic beta-cells. Closure of potassium channels causes depolarization which stimulates calcium influx through voltage-gated calcium channels. High intracellular calcium subsequently triggers the exocytosis of insulin granules. ",The molecular weight is 315.41.,Mitiglinide has a topological polar surface area of 57.61.,The log p value of  is 3.06.,Mitiglinide is investigational.,Mitiglinide is a solid.,True
15879,"Nalmefene is a 6-methylene analogue of naltrexone and opioid system modulator but with no opioid activity. It mediates a partial agonist effect on kappa receptors. It is primarily used in the management of alcohol dependence in adult patients in conjunction with continuous psychosocial support focused on treatment adherence and reducing alcohol consumption when it is exists as the hydrochloride dihydrate form under the trade name Selincro. Selincro is orally administered as tablets. Nalmefene works to reduce alcohol consumption in individuals by positive reward effect of alcohol which involves the opioid system, as well as the sedative and dysphoric properties of alcohol.  Indicated for the reduction of alcohol consumption in adult patients with alcohol dependence who have a high drinking risk level (DRL), without physical withdrawal symptoms and who do not require immediate detoxification. Nalmefene has not been shown to produce tolerance, physical dependence, or abuse potential.  Nalmefene is an opioid system modulator with a distinct μ, δ, and κ receptor profile. It acts as a selective opioid receptor ligand with antagonist activity at the μ and δ receptors and partial agonist activity at the κ receptor. Animal studies suggest that the kappa receptor signalling responses lead to antagonism of acute reward and positive reinforcement effects of drugs by decreasing dopamine in the nucleus accumbens. Thus it is suggested that nalmefene may be more effective treatment for alcohol dependence than , which is a pure mu and delta receptor antagonist. In vivo studies and rat studies have demonstrated that nalmefene reduces self-administration of alcohol, possibly by modulating cortico-mesolimbic functions. ",The molecular weight is 339.44.,Nalmefene has a topological polar surface area of 52.93.,The log p value of  is 2.64.,Nalmefene is approved and investigational and withdrawn.,Nalmefene is a solid.,True
15880,"Naldemedine is an opioid receptor antagonist. It is a modified form of to which a side chain has been added to increase molecular weight and polar surface area resulting in restricted transport across the blood brain barrier. Naldemedine was approved in 2017 in both the US and Japan for the treatment of Opioid-induced Constipation. For the treatment of opioid-induced constipation. Naldemedine is an opioid receptor antagonist with restricted movement across the blood brain barrier. This allows it to antagonize the periperal effects of opioid drugs such as constipation without interfering with the effects on the central nervous system. Naldemedine binds to and antagonizes mu-, delta-, and kappa-opioid receptors. The binding of opioid agonists to peripheral mu-opioid receptors slows the transit of feces through the intestine resulting in constipation. By antagonizing mu-opioid receptors, naldemedine inhibits this effect.",The molecular weight is 570.65.,Naldemedine has a topological polar surface area of 141.18.,The log p value of  is 2.83.,Naldemedine is approved and investigational.,,True
15881,"Bazedoxifene is a third generation selective estrogen receptor modulator (SERM), developed by Pfizer following the completion of their takeover of Wyeth Pharmaceuticals. In late 2013, Pfizer received approval for bazedoxifene as part of the combination drug DUAVEE in the prevention (not treatment) of postmenopausal osteoporosis. It is approved in the European Union (marketed in Italy and Spain) and Japan as monotherapy. In 2013, the combination product containing conjugated estrogens and bazedoxifene was approved by the FDA for the treatment of moderate to severe vasomotor symptoms associated with menopause, as well as the prevention of postmenopausal osteoporosis in women. Indicated for following conditions alone or in combination with conjugated estrogens in women with a uterus: Bazedoxifene belongs to a class of compounds known as selective estrogen receptor modulators (SERMs). Bazedoxifene acts as both an oestrogen-receptor agonist and/or antagonist, depending upon the cell and tissue type and target genes. Bazedoxifene decreases bone resorption and reduces biochemical markers of bone turnover to the premenopausal range. These effects on bone remodelling lead to an increase in bone mineral density (BMD), which in turn contributes to a reduction in the risk of fractures. Bazedoxifene functions primarily as an oestrogen-receptor antagonist in uterine and breast tissues.",The molecular weight is 470.61.,Bazedoxifene has a topological polar surface area of 57.86.,The log p value of  is 7.15.,Bazedoxifene is approved and investigational.,Bazedoxifene is a solid.,True
15882,"Acemetacin is a carboxymethyl ester of indometacin. It is a potent non-steroidal anti-inflammatory drug, derived from the indol-3-acetic acid, whose activity is thought to be mainly through its active metabolite indomethacin. In clinical trials, acemetacin exhibits a better gastric tolerability compared to its active metabolite indometacin. It was developed by E. Merck and Company in Germany as an attempt to provide a safer drug but other than the amelioration on the gastrointestinal effects, the metabolism of acetamicin led to the formation of indomethacin and it kept the same side effects. Acemetacin is not FDA, Canada or EMA approved, but in the countries where it is marketed it is indicated for the symptomatic treatment of pain and swelling in acute inflammation of the joints in rheumathoid arthritis, osteoarthritis, low back pain and post-surgical pain. It is also indicated for the treatment of chronic inflammation of the joints in presence of rheumatoid arthritis, treatment of ankylosing spondylitis, treatment of irritation in the joints and spinal column caused by degenerative disorders, treatment of inflammatory soft-tissue rheumatism syndrome and painful swelling and inflammation caused by injury. The effect of acemetacin causes a weak reduction of prostaglandin synthesis which generates an anti-inflammatory and analgesic effect. The weak inhibition of prostaglandin reduces significantly the damage caused in the mucous membrane of the gastrointestinal tract. Studies have shown that acemetacin strongly inhibits the release of histamine from mast cells and the generation of hyperthermia. Acemetacin effect also causes changes in systolic and diastolic blood pressure as well as inhibition of platelet aggregation.  Acemetacin is a non-selective inhibitor of the production of pro-inflammatory mediators derived from the action of the enzyme COX. COX is essential for the synthesis of prostaglandin E2 and F2 which are molecules derived from fatty acids and stored in the cell membrane. Acetometacine is metabolized and forms its major metabolite indometacin which is also a non-selective inhibitor of COX and exhibits the capacity to inhibit the motility of polymorphonuclear leukocytes and decreased cerebral flow by modulating the nitric oxide pathway and vasoconstriction.",The molecular weight is 415.83.,Acemetacin has a topological polar surface area of 94.83.,The log p value of  is 4.2.,Acemetacin is approved and investigational.,Acemetacin is a solid.,True
15883,"Florbetaben is a fluorine-18 (18F)-labeled stilbene derivative used for Positron Emission Tomography (PET) imaging of the brain. It is used for the non-invasive detection of the density of ß-amyloid neuritic plaques in the brain of adult patients with cognitive impairment. Florbetaben is a radioactive diagnostic agent indicated for Positron Emission Tomography (PET) imaging of the brain to estimate β-amyloid neuritic plaque density in adult patients with cognitive impairment who are being evaluated for Alzheimer’s Disease (AD) and other causes of cognitive decline. Following intravenous administration, Neuraceq crosses the blood brain barrier and shows differential retention in brain regions that contain β-amyloid deposits. Differences in signal intensity between brain regions showing specific and non-specific Neuraceq uptake form the basis for the image interpretation method. Florbetaben F18 is a F18-labeled stilbene derivative, which binds to β-amyloid plaques in the brain. The F 18 isotope produces a positron signal that is detected by a PET scanner.",The molecular weight is 358.44.,Florbetaben (18F) has a topological polar surface area of 39.72.,The log p value of  is 4.08.,Florbetaben (18F) is approved.,Florbetaben (18F) is a solid.,True
15884,"Desirudin is a direct inhibitor of human thrombin. It has a protein structure that is similar to that of hirudin, the naturally occurring anticoagulant present in the peripharyngeal glands in the medicinal leech, Hirudo medicinalis. Hirudin is a single polypeptide chain of 65 amino acids residues and contains three disulfide bridges. Desirudin has a chemical formula of C287H440N80O110S6 with a molecular weight of 6963.52. Indicated as prophylaxis of deep vein thrombosis for patients undergoing hip replacement surgery.  Desirudin results in dose-dependent prolongation of the activated partial thromboplastin time (aPTT).  Desirudin is a direct, highly selective thrombin inhibitor. Reversibly binds to the active thrombin site of free and clot-associated thrombin. Inhibits fibrin formation, activation of coagulation factors V, VII, and XIII, and thrombin-induced platelet aggregation resulting in a dose-dependent prolongation of the activated partial thromboplastin time (aPTT). ",The molecular weight is 6963.49.,Desirudin has a topological polar surface area of 3086.89.,,Desirudin is approved.,,True
15885,"Inositol nicotinate, also known as Inositol hexaniacinate/hexanicotinate or \no-flush niacin\"", is a niacin ester and vasodilator. It is used in food supplements as a source of niacin (vitamin B3), where hydrolysis of 1 g (1.23 mmol) inositol hexanicotinate yields 0.91 g nicotinic acid and 0.22 g inositol. Niacin exists in different forms including nicotinic acid, nicotinamide and other derivatives such as inositol nicotinate. It is associated with reduced flushing compared to other vasodilators by being broken down into the metabolites and inositol at a slower rate. Nicotinic acid plays an essential role in many important metabolic processes and has been used as lipid-lowering agent. Inositol nicotinate is prescribed in Europe under the name Hexopal as a symptomatic treatment for severe intermittent claudication and Raynaud’s phenomenon."" Indicated as a dietary supplement for the source of niacin. Has been investigated for potential beneficial effects on serum lipids. In Europe, inositol hexanicotinate is indicated as a patented drug known as Hexopal, which is therapeutically indicated for the symptomatic relief of severe intermittent claudication and Raynaud’s phenomenon.  Inositol nicotinate mediates a vasodilatory, lipid-lowering and fibrinolytic effect on the cardiovascular system. Like other niacins, inositol nicotinate is a lipid-regulating agent that reduces the levels of plasma triglycerides, atherogenic apolipoprotein B (apoB)-containing lipoproteins (VLDL, LDL and lipoprotein a) while increasing antiatherogenic apoA-I-containing HDL levels.  Inositol nicotinate and other niacins directly and noncompetitively inhibit microsomal enzyme diacylglycerol acyltransferase 2 (DGAT2) responsible for esterification of fatty acids to form triglycerides, resulting in decreased triglyceride synthesis and hepatic atherogenic lipoprotein secretion. Inhibitied triglyceride synthesis results in accelerated intracellular hepatic apo B degradation and the decreased secretion of VLDL and LDL particles. Niacin also inhibits hepatic expression of beta-chain adenosine triphosphate synthase which inhibits the removal or uptake of HDL–apo A-I. It is also suggested that niacin increases vascular endothelial cell redox state, resulting in the inhibition of oxidative stress and vascular inflammatory genes or key cytokines involved in atherosclerosis. It acts as a ligand on G-protein coupled receptor 109A (HCAR2/HM74A) and 109B (HCAR3/HM74) which mediates the anti-lipolytic and lipid-lowering effects of nicotinic acid. Niacin-mediated signalling of GPR109A expressed on adipocytes and G(i)-mediated decrease in cAMP levels result in decreased lipolysis, fatty acid mobilization, and triglyceride synthesis. The action of inositol nicotinate on GPR109A expressed on skin and macrophages to cause increased prostaglandin D2/E2 activity is thought to be less significant compared to other niacin molecules as it involves sustained release that leads to less flushing. ",The molecular weight is 810.73.,Inositol nicotinate has a topological polar surface area of 235.14.,The log p value of  is 2.42.,Inositol nicotinate is approved and withdrawn.,Inositol nicotinate is a solid.,True
15886,"Sodium fluoride is an inorganic chemical compound that is a source of the fluoride ion in many applications, including dental care and radiographic imaging when it is used as. Sodium fluoride's benefits on dental health were first observed in the 1930s, when individuals in communities with fluoridated drinking water showed less tooth decay than those without fluoridated water. The use of fluoride in dental practice began in the 1940s. Now, sodium fluoride may be found in a variety of gels, varnishes, rinses, toothpaste products, and fluoride treatments provided in dental care. According to the American Dental Association (ADA), thorough evidence reviews have indicated that the use of fluoride to prevent and control dental caries is safe when used correctly and is highly effective in reducing the prevalence of caries. Sodium fluoride in the oral or topical form is indicated for the prevention and control of dental caries and for the maintenance of dental health. Fluoride supplements in the form of tablets and other formulas may be prescribed to prevent tooth decay in high-risk children aged 6 months to 16 years old whose drinking water source contains low fluoride concentrations. Sodium fluoride protects the teeth from acid demineralization while preventing tooth decay by bacteria while strengthening tooth enamel. It is important to note that excess fluoride exposure during tooth mineralization, especially in children 1-3 years old, may cause fluorosis. It is a condition manifested by white lines, pitting, or discoloration of teeth resulting from changes in tooth enamel. The risk of fluorosis can be decreased by the use of a rice-size amount of fluoridated toothpaste in children younger than 3 years old. It is recommended that no more than a pea-sized quantity of fluoridated toothpaste should be used for children from 3 to 6 years old. The American Dentistry Association (ADA) recommends that children should be closely supervised during toothpaste use to prevent excess fluoride ingestion. The prevention of dental caries by topical fluoride is achieved by various mechanisms. Sodium fluoride kills bacteria that cause caries, such a Streptococcus mutans and lactobacilli by interfering with their metabolic activities that result in the formation of lactic acid. Fluoride ions cause the inhibition of glycolytic and other enzymes involved in bacterial metabolism. It changes the permeability of cell membranes, lowering the pH in the cytoplasm of the cell, leading to a decrease in acidity, which is normally implicated in tooth decay. ",The molecular weight is 41.99.,,,Sodium fluoride is approved.,Sodium fluoride is a solid.,True
15887,"Certolizumab pegol is a pegylated monoclonal antibody against the tumor necrosis factor-alpha (TNF-alpha). It is formed with a humanized Fab fragment of 50 kDa, from an IgG 1 isotype, fused to a 40 kDa polyethylene glycol moiety replacing the Fc antibody region. The absence of the Fc region was ideated to prevent complement fixation and antibody-mediated cytotoxicity as well as to markedly increase its half-life.  Certolizumab pegol has been approved for several different conditions listed below: As part of the mechanism of action and nature of the drug, certolizumab does not induce apoptosis in cultured lymphocytes and monocytes. However, as a piece of the inhibition of inflammation, certolizumab pegol inhibits lipopolysaccharide-induced production of IL-1 beta and it induces nonapoptotic cell death via signaling transmembrane TNF-alpha.  Certolizumab targets the activation of TNF-alpha with high affinity (KD 90 pM and IC90 0.004 mcg/ml) which in order, inhibits the downstream inflammatory process. It acts by binding and neutralizing the soluble and membrane portions of TNF-alpha without inducing complement or antibody-dependent cytotoxicity due to the lack of the Fc region. The inhibition of TNF-alpha is achieved in a dose-dependent manner and it does not present activity against lymphotoxin alpha (TNF-beta).",,,,Certolizumab pegol is approved.,Certolizumab pegol is a solid.,True
15888,"Thiosulfuric acid (as sodium thiosulfate) has the chemical name thiosulfuric acid, disodium salt, pentahydrate. The chemical formula is Na2S2O3•5H2O and the molecular weight is 248.17. Sodium Thiosulfate Injection is a cyanide antidote which contains one 50 mL glass vial containing a 25% solution of Sodium Thiosulfate Injection. Indicated for sequential intravenous use with sodium nitrite for the treatment of acute cyanide poisoning that is judged to be life-threatening. In dogs, pretreatment with sodium thiosulfate to achieve a steady state level of 2 µmol/mL increased the rate of conversion of cyanide to thiocyanate over 30-fold. As antidote: Sodium thiosulfate acts as a sulfur donor for the endogenous sulfur transferase enzyme, rhodanese. It is used together with sodium nitrite for cyanide poisiong as antidote. Cyanide has a very high affinity for iron in the ferric state. It reacts with the trivalent (ferric) iron of mitochondrial cytochrome oxidase, thereby inhibiting cellular respiration, resulting in lactic acidosis and cytotoxic hypoxia. Sodium nitrite reacts with hemoglobin to form methemoglobin, which competes with cytochrome oxidase for the cyanide ion. Cyanide binds to methemoglobin to form cyanmethemoglobin and restore the activity of cytochrome oxidase. When cyanide dissociates from methemoglobin, sodium thiosulfate facilitates its conversion by rhodanese to thiocyanate, a less toxic ion. ",,,,Thiosulfuric acid is approved and investigational.,,True
15889,"Tenofovir disoproxil fumarate (a prodrug of tenofovir), marketed by Gilead Sciences under the trade name _Viread_, belongs to a class of antiretroviral drugs known as nucleotide analogue reverse transcriptase inhibitors (nRTIs). This drug is prescribed in combination with other drugs for the management of HIV infection as well as for Hepatitis B therapy. Tenofovir disoproxil was initially approved in 2001. Tenofovir is indicated in combination with other antiretroviral agents for the management of HIV-1 infection in adults and pediatric patients 2 years of age and older. It is also indicated for the treatment of chronic hepatitis B in adults and pediatric patients 12 years of age and older. This drug is also a component of multiple products used for the management of HIV-1 infection ,.  This drug prevents viral DNA chain elongation through inhibition of enzymes necessary for host cell infection viral replication in HIV-1 and Hepatitis B infections ,. Tenofovir belongs to a class of antiretroviral drugs known as nucleotide analog reverse transcriptase inhibitors (NtRTIs), which block reverse transcriptase, an enzyme necessary for viral production in HIV-infected individuals. This enables the management of HIV viral load through decreased viral replication.",The molecular weight is 519.45.,Tenofovir disoproxil has a topological polar surface area of 185.44.,The log p value of  is 0.8.,Tenofovir disoproxil is approved and investigational.,Tenofovir disoproxil is a solid.,True
15890,"Tinzaparin is a low molecular weight heparin (LMWH), produced by enzymatic depolymerization of unfractionated heparin from porcine intestinal mucosa. It is a heterogeneous mixture of with an average molecular weight between 5500 and 7500 daltons. Tinzaparin is composed of molecules with and without a special site for high affinity binding to antithrombin III (ATIII). This complex greatly accelerates the inhibition of factor Xa. It is an anticoagulant and considered an antithrombotic. Tinzaparin must be given either subcutaneously or parenterally. LMWHs are less effective at inactivating factor IIa due to their shorter length compared to unfractionated heparin. Tinzaparin is used for the prevention of postoperative venous thromboembolism in patients undergoing orthopedic surgery and in patients undergoing general surgery who are at high risk of developing postoperative venous thromboembolism. It is also used for the treatment of deep vein thrombosis and/or pulmonary embolism. It is indicated for use in preventing clot formation in indwelling intravenous lines for hemodialysis. Tinzaparin, like other LMWHs, have a higher anti-Xa activity than anti-IIa activity. The anti-Xa activity of tinzaparin is 2.0 +/- 0.5 times greater than its to anti-IIa activity. Heparin exhibits approximately equal inhibitory activity against Xa and IIa. Tinzaparin is an anticoagulant that blocks the formation of thrombi. Like all LMWHs, tinzaparin only causes activated partial thromboplastin time (aPTT) prolongation at higher doses and routine monitoring is not recommended. However, anti-factor Xa levels may be monitored in some conditions such as pregnancy and renal dysfunction. Its use should be avoided in patients with a creatinine clearance less than 20 mL/min. In these patients, unfractionated heparin should be used. Tinzaparin can be used in patients who have a creatinine clearance between 20-30 mL/min, giving it the highest safety threshold for use in renal failure patients compared to all the LMWHs. Tinzaparin binds to the plasma protein antithrombin III, forming a complex with then accelerates the inhibition of factor Xa. Its affinity for factor Xa is 2-4 times greater than that of unbound ATIII. The inactivation of factor Xa in turn will exponentially generation of thrombin (factor IIa) molecules, which is needed to activate fibrinogen to fibrin. The coagulation cascade is inhibited because fibrin cannot be formed in the presence of tinzaparin. Like all LMWH, it cannot be given intramuscularly due to increased risk of hematoma.",,,,Tinzaparin is approved.,Tinzaparin is a solid.,True
15891,"Deferiprone is an oral iron chelator used as a second line agent in thalassemia syndromes when iron overload from blood transfusions occurs. Thalassemias are a type of hereditary anaemia due a defect in the production of hemoglobin. As a result, erythropoiesis, the production of new red blood cells, is impaired. FDA approved on October 14, 2011. Deferiprone is indicated in thalassemia syndromes when first line chelation agents are not adequate to treat transfusional iron overload. Deferiprone is an iron chelator that binds to ferric ions (iron III) and forms a 3:1 (deferiprone:iron) stable complex and is then eliminated in the urine. Deferiprone is more selective for iron in which other metals such as zinc, copper, and aluminum have a lower affinity for deferiprone.",The molecular weight is 139.15.,Deferiprone has a topological polar surface area of 40.54.,The log p value of  is -0.9.,Deferiprone is approved.,Deferiprone is a solid.,True
15892,"Ferric maltol is an iron(III) atom complexed with 3 maltol molecules to increase the bioavailability compared to iron(II), without depositing it in the duodenum as insoluble ferric hydroxide and phosphate. Ferric maltol has been described in literature since at least the late 1980s as a potential treatment for iron deficiency. Ferric maltol is indicated to treat iron deficiency in adults. Ferric maltol is used to provide supplemental iron to patients with an iron deficiency. It has a wide therapeutic index as patients generally take 30mg twice daily, while concentrations of 20mg/kg may produce toxicity. Patients should be counselled regarding the risk of inflammatory bowel disease flares, iron overload, and accidental ingestion in children. Ferric maltol dissociates as the iron atom is donated to unknown iron uptake mechanisms, possibly beta 3 integrin or divalent metal transporter 1, in the ileum and duodenum. Once the iron is in circulation, it then associates with transferrin and ferritin.",The molecular weight is 431.15.,Ferric maltol has a topological polar surface area of 157.8.,,Ferric maltol is approved.,Ferric maltol is a solid.,True
15893,"A complex of related glycopeptide antibiotics from <i>Streptomyces verticillus</i> consisting of bleomycin A2 and B2 (B2 CAS # 9060-10-0). It inhibits DNA metabolism and is used as an antineoplastic, especially for solid tumors. Bleomycin A2 is used as the representative structure for Bleomycin. For palliative treatment in the management malignant neoplasm (trachea, bronchus, lung), squamous cell carcinoma, and lymphomas. Bleomycin is an antibiotic which has been shown to have antitumor activity. Bleomycin selectively inhibits the synthesis of deoxyribonucleic acid (DNA). The guanine and cytosine content correlates with the degree of mitomycin-induced cross-linking. At high concentrations of the drug, cellular RNA and protein synthesis are also suppressed. Bleomycin has been shown <i>in vitro</i> to inhibit B cell, T cell, and macrophage proliferation and impair antigen presentation, as well as the secretion of interferon gamma, TNFa, and IL-2. The antibiotic antitumor drugs are cell cycle-nonspecific except for Bleomycin (which has major effects in G2 and M phases). Although the exact mechanism of action of bleomycin is unknown, available evidence would seem to indicate that the main mode of action is the inhibition of DNA synthesis with some evidence of lesser inhibition of RNA and protein synthesis. As evident in _in vitro_ studies, the DNA-cleaving actions of bleomycin is dependent on oxygen and metal ions. It is believed that bleomycin chelates metal ions (primarily iron) producing a pseudoenzyme that reacts with oxygen to produce superoxide and hydroxide free radicals that cleave DNA.",The molecular weight is 2841.07.,Bleomycin has a topological polar surface area of 688.97.,,Bleomycin is approved and investigational.,Bleomycin is a solid.,True
15894,"Extractives and their physically modified derivatives such as tinctures, concretes, absolutes, essential oils, oleoresins, terpenes, terpene-free fractions, distillates, residues, obtained from Commiphora abyssinica, Burseraceae. FDA approved only for use in food. Historically used for indigestion, ulcers, colds, cough, asthma, bronchial congestion, arthritic pain, cancer, leprosy, and syphilis. It is also used orally as a stimulant, antispasmodic, and to increase menstrual flow. Topically, myrrh is used for mild inflammation of the oral and pharyngeal mucosa, aphthous ulcers, gingivitis, chapped lips, hemorrhoids, bedsores, wounds, abrasions, furunculosis, bad breath, and loose teeth. In foods and beverages, myrrh is used as a flavoring component. In manufacturing, myrrh is used as a fragrance and fixative in cosmetics. It is also used in embalming and as incense.  Myrrh reduces the production of cytokines and reduces the effects of inflammation. It is also suggested to produce an analgesic effect. Myrrh produces cell damage and death in various cancer cell types. Myrrh has been observed to exert anantibacterial, antiparasitic, and antifungal activities. Myrrh reduces liver injury in response to carbon tetrachloride insult, suggesting hepoprotective action. It also displays antioxidant properties. Myrrh reduces low density lipoprotein levels. Myrrh appears to be cardioprotective, producing a decrease in heart rate and restoring blood pressure in response to isoproteronol challenge. Myrrh lowers plasma glucose and insulin levels in type 2 diabetes mellitus models suggesting an improvement in insulin sensitivity. Myrrh has been observed to protect against both substance and stress induced gastric lesions. **Anti-inflammatory:** Myrrh is thought to mediate its anti-inflammatory activity through inducing haem oxygenase activity. Haem oxygenase then appears to prevent the degradation of IKBalpha in response to inflammatory receptor activation. This prevents translocation of nuclear factor kappaB (NFkappaB) to the nucleus and inhibits the expression of genes under its control like cyclooxygenase-2 and the inducible form of nitric oxide synthase. The suppression of the NFkappaB pathway likely also reduces the expression of inflammatory cytokines. Myrhh also inhibits the mitogen activated protein kinase (MAPK) pathway, specifically producing inhibition of p38 and c-jun N-terminal kinase (JNK). This is associated with a reduction in c-jun and c-fos expression which would likely result in a reduction in activator protein-1 and and inhibition of its associated inflammatory gene expression. Myrrh exibits inhibitory activity against 5-lipoxygenase helping to suppress the production of leukotrienes, another class of inflammatory cytokine. In addition to its effects on the NFkappaB system, myrrh also inhibits the signal transducer and activator of transcription (STAT) -1 and -3 resulting in a decrease in cytokine production by the janus kinase/STAT pathway. Myrrh also reduces the downregulation of suppresor of cytokine synthesis (SOCS) in response to interleukin-1beta and interferon-gamma. SOCS serves as an autoregulator of the JAK/STAT pathway under transcriptional control of STATs and inhibits activation of the pathway.",,,,Myrrh is approved.,Myrrh is a liquid.,True
15895,"Mirodenafil has been used in trials studying the treatment and supportive care of Kidney Diseases, Urologic Diseases, Renal Insufficiency, Erectile Dysfunction, and Male Erectile Dysfunction.",The molecular weight is 533.69.,Mirodenafil has a topological polar surface area of 114.78.,The log p value of  is 3.78.,Mirodenafil is investigational.,,True
15896,"Foretinib has been used in trials studying the treatment of Cancer, Breast Cancer, Carcinoma, Renal Cell, Recurrent Breast Cancer, and Neoplasms, Head and Neck, among others. Foretinib is an orally available small molecule compound designed to target multiple RTKs implicated in the development, progression and spread of cancer. It inhibits the activation of MET, RON, ERK and AKT, decreased proliferation and increased apoptosis. Activation of MET by mutation is the causative factor in an inherited kidney cancer syndrome, hereditary papilliary renal cell carcinaoma. Mutational activation of MET has also been found in sporadic kidney cancer, lung carcinomas and head and neck carcinomas. MET is a key driver of tumor cell growth, motility, invasion, metastasis and angiogenesis. Foretinib has attractive pharmaceutical properties with high solubility and oral bioavailability and demonstrates nanomolar potency against its targets, VEGFR, MET, which translates to potent activity in cellular assays. In preclinical studies, Foretinib, developed as a balanced inhibitor of these receptor tyrosine kinases, potently inhibited both MET and VEGFR, including mutant activated forms of MET found in hereditary papillary renal carcinomas. The compound also demonstrated dose-dependent growth inhibition in tumor models of breast, colorectal, non-small cell lung cancer and glioblastoma and has been shown to cause substantial tumor regression in all models tested.",,,,Foretinib is investigational.,,True
15897,,,,,Ambroxol acefyllinate is experimental and investigational.,Ambroxol acefyllinate is a solid.,False
15898,"Ménière's disease is a progressive disease of the inner ear characterized by vertigo, tinnitus, and hearing loss. It has a significant impact on both the physical and social functioning of affected individuals.  Betahistine is indicated for the reduction of recurrent vertigo episodes associated with Ménière's disease in patients 18 years old and above. Through its actions on the histamine receptors, betahistine provides relief from vertigo associated with Ménière's disease.  Vertigo is a disturbing sensation of movement caused by dysfunction of the labyrinth (inner ear), vestibular nerve, cerebellum, brainstem, or Central Nervous System (CNS). Vestibular forms of vertigo are often accompanied by auditory dysfunctions such as hyperacusis, hearing loss, and tinnitus. In most cases, adaptive mechanisms of the CNS lead to functional recovery after episodes of vertigo, however, syndromes such as Ménière's disease tend to cause the recurrence of vertigo symptoms. This significantly impacts the quality of life and the ability to carry out daily activities. ",The molecular weight is 136.2.,Betahistine has a topological polar surface area of 24.92.,The log p value of  is 0.08.,Betahistine is approved and investigational.,Betahistine is a solid.,True
15899,"Rauwolfia (Rauwolfia serpentina), also spelled _ravolphia_, is a medicinal plant in the milkweed family. The root of the plant is ground into a powder or sold in tablets or capsules. It is a compound commonly used in Asian medicine, which includes traditional Ayurvedic medicine native to India. The active ingredients in this drug are alkaloids and about 50 have been identified through various studies, although the primary psychoactive components appear to be reserpine, rescinnamine, and deserpidine. Rauwolfia alkaloids are indicated in the treatment of hypertension. Rauwolfia alkaloids have been used for relief of symptoms in agitated psychotic states such as schizophrenia; however, use as antipsychotics and sedatives have been replaced with the use of more effective, safer agents. Reserpine is used to treat high blood pressure. It also is used to treat severe agitation in patients with mental disorders. Reserpine is in a class of medications called rauwolfia alkaloids. It works by slowing the activity of the nervous system, causing the heart rate to slow and the blood vessels to dilate.",,,,Rauwolfia serpentina root is investigational.,,True
15900,"Manganese is a transition metal with a molar mass of 54.94g/mol. Manganese is considered critical for human health, and plays important roles in development, metabolism, and the antioxidant system. That said, excessive manganese intake is associated with manganism, a neurodegenerative disorder that causes dopaminergic neuronal death and parkinsonian-like symptoms. Indicated for use as a supplement to intravenous solutions given for Total Parenteral Nutrition (TPN). Administration helps to maintain plasma levels and to prevent depletion of endogenous stores and subsequent deficiency symptoms.",,,,Manganese is approved and nutraceutical.,Manganese is a solid.,True
15901,"Evolocumab is a monoclonal antibody designed for the treatment of hyperlipidemia by Amgen. It is a subcutaneous injection approved by the FDA for individuals on maximum statin therapy who still require additional LDL-cholesterol lowering. It is approved for both homozygous and heterozygous familial cholesterolemia as an adjunct to other first-line therapies. Evolocumab is a human IgG2 monoclonal antibody that targets the proprotein convertase subtilisin/kexin type 9 (PCSK9). PCSK9 is a protein that targets LDL receptors for degradation, therefore reducing the liver's ability to remove LDL-cholesterol (LDL-C), or \bad\"" cholesterol, from the blood. Evolocumab is designed to bind to PCSK9 and inhibit PCSK9 from binding to LDL receptors on the liver surface, resulting in more LDL receptors on the surface of the liver to remove LDL-C from the blood. Evolocumab is the second PCSK9 inhibitor on the market, first being alirocumab."" For the treatment of heterozygous/homozygous familial hypercholesterolemia or clinical atherosclerotic cardiovascular disease in patients on maximum tolerated statin therapy requiring additional LDL-cholesterol lowering.  Evolocumab is a human IgG monoclonal antibody which targets PCSK9 (proprotein convertase subtilisin/kexin type 9). PCSK9 is a serine protease produced by the liver which binds LDL receptors and creates a complex to be targeted for lysosomal degradation. LDL receptors typically bind LDL-cholesterol (\bad\"" cholesterol) for cellular reuptake, therefore the formation of these complexes with PCSK9 inhibits LDL receptor recycling to the cell surface, resulting in decreased cellular reuptake of LDL-C and increased levels of free LDL-C in the plasma. Individuals with familial hypercholesterolemia often may have \""gain of function\"" mutations in the PCSK9 molecules in their body, resulting in increased LDL-C plasma levels and a consequent cardiovascular risk. Evolocumab is able to bind both the normal PCSK9 and the \""gain of function\"" mutant, D374Y. The exact mechanism of the binding has not been published, however the precursor molecule, mAb1, is indicative of the interaction. The mAb1 molecule binds on the catalytic site of PCSK9 next to the binding site for the LDL receptor and creates hydrogen bonds and hydrophobic interactions, resulting in the steric inhibition of binding between PCSK9 and the LDL receptor. Because the formation of complexes between LDL receptor and PCSK9 are prevented, the internalized LDL receptors are less likely to be degrated by lysosomes and may recycle to the surface of the cell to serve their function of removing LDL from the blood. """,,,,Evolocumab is approved.,Evolocumab is a liquid.,True
15902,"Vonicog Alfa is a recombinant von Willebrand factor manufactured by Baxalta. It was FDA approved in December 2015. The gen of von Willebrand factor was first cloned in 1985 by Stuart Orkin and David Ginsburg. By the EMA, vonicog alfa is still under clinical analysis. Vonicog alfa is indicated for the on-demand treatment and control of bleeding episodes in adults previously diagnosed with von Willebrand disease. Vonicog alfa contains only the vWF and thus, its administration offers the flexibility to administer the coagulation factor VIII if needed. The von Willebrand disease is an inherited disorder characterized by the deficiency or misfunction of the von Willebrand factor (vWF). Due to this deficiency, the blood cannot clot properly and the patients that present this disease are prone to prolonged or excessive bleeding. There are three types of this disease, and type 3 is an autosomal recessive inherited disorder marked by very low or absent levels of vWF. Vonicog alfa does not present a risk of transmission of blood-borne pathogens as it is a recombinant, plasma- and albumin-free protein. The two first clinical trials showed an effective reduction of bleeding episodes in different sites of the body. This effect was observed even after the first infusion in 81% of the cases. Von Willebrand factor (vWF) is an important piece of the blood coagulation cascade and it acts by stabilizing the coagulation factor VIII. It also binds to collagen and platelets in blood vessel walls which helps with the formation of a platelet plug during clotting process. The presence of different mutations in vWF causes a common bleeding disorder named von Willebrand disease. The bleeding episodes were usually treated with plasma-derived vWF/factor VIII concentrates which required high doses and long treatment duration. The use of vonicog alfa allows a separate administration of vWF without the presence of the Factor VIII. This separate dosing allows the personalization of the dosage according to the patient's needs. On the same note, the plasma-derived vWF concentrates variably lack ULM due to an in vivo exposure to plasma ADAMTS13 and granulocyte elastases. Vonicog alfa can be delivered as an unaltered vWF and it functions as a replacement of vWF. Thus, it mediates platelet adhesion and aggregation as well as stabilization of the procoagulant factor VIII.",,,,Vonicog Alfa is approved and investigational.,Vonicog Alfa is a solid.,True
15903,"von Willebrand Factor (vWF) is a multimeric glycoprotein that consists of disulfide-bridge linked dimers. It is usually circulating in plasma as a stable complex with the coagulation factor VIII. The human vWF, as a drug product, is a complex that also contains the coagulation factor VIII. This complex was developed by Octapharma Pharmazeutika Produktionsges and FDA approved on August 21, 2015. The vWF and Factor VIII complex is indicated for the prevention of excessive bleeding during and after minor and major surgery in adult and pediatric von Willebrand disease patients. It is also indicated for the on-demand treatment and control of bleeding episodes. The von Willebrand disease is an inherited disorder characterized by the deficiency or misfunction of the von Willebrand factor (vWF). Due to this deficiency, the blood cannot clot properly and the patients that present this disease are prone to prolonged or excessive bleeding. There are three types of this disease, and type 3 is an autosomal recessive inherited disorder marked by very low or absent levels of vWF. The efficacy in clinical trials of vWF in surgical procedures is of 96.7% regardless the type of von Willebrand disease. In a perioperative setting, the hemostatic effects were rated as excellent in a dose of 848.6 IU/kg and no anti-factor VII or inhibitors were detected. These excellent results come from the re-establishment of platelet-adhesion to the subendothelium at sites of vascular damage and the aggregation of platelets. vWF allows the protection of factor VIII from the rapid degradation and thus it restores normal coagulation. The vWF is involved in primary and secondary homeostasis and it is also a carrier and stabilizing protein that protects the coagulation factor VIII from proteolysis and clearance. vWF also presents an adhesive function in which it mediates the binding between platelets and subendothelial tissues. The external human vWF acts as the endogenous vWF and thus, it presents all the functions abovementioned.",,,,Von Willebrand Factor Human is approved and investigational.,Von Willebrand Factor Human is a solid.,True
15904,"Pizotifen belongs to the class of antamines and is related to. It is a potent serotonin and tryptamine antagonist that has been used for migraine prevention for many years. It exhibits weak anticholinergic, antihistamine, and antikinin actions in addition to sedative and appetite-stimulating properties. Some patients receiving pizotifen treatment developed tolerance with the prolonged use of the drug. Numerous studies have revealed the potential antidepressant effects of pizotifen, which are independent of its antimigraine action. While it is suggested that pizotifen may act similarly to the classic tricyclic antidepressants , its full mechanism of antidepressant action is not fully elucidated. Pizotifen hydrochloride is an active ingredient in Sandomigran, which is used for the prophylactic management of migraines. Sandomigran is available in a number of countries but is not approved by the FDA nor EMA. Indicated for the prophylactic management of migraines.  Various studies have shown pizotifen to be effective in the prophylaxis of migraines in reducing the frequency and severity of vascular headaches. Evidence from studies _in vivo_ and _in vitro_ demonstrate antagonistic actions towards serotonin and histamine. Pizotifen blocks the postsynaptic 5-HT2 receptors, as supported by antagonism of several direct agonists of 5-HT receptors. It is an antagonist at histamine H1 receptors, and is weakly anticholinergic. It also binds to α1- and α2-adrenergic receptors, and dopamine receptors. Pizotifen elicits a minimal effect as an epinephrine or bradykinin antagonist. Pizotifen exhibits weak sedative properties in mouse and monkey studies, as indicated by inhibition of locomotion and potentiation of barbiturates, without changes in cardiac or respiratory rates. In dogs, intravenous administration of pizotifen cause rapid hypotension but was reversed to normal within 30 minutes. Pizotifen was shown to inhibit serotonin uptake in the isolated perfused cat spleen and, _in vivo_, inhibits serotonin-induced contractions in rat uterus and cat nictiating membrane. In contrast, pizotifen demonstrated a venoconstrictor activity _in vivo_ when orally or intravenously administered to saphenous veins in conscious dogs. Pizotifen has the potential to stimulate the appetite and may cause weight gain upon treatment.  While the mechanism of action is not fully understood, it is proposed that pizotifen works by inhibiting the peripheral actions of serotonin and histamine in increasing the membrane permeability of cranial vessels and transudation of plasmakinin, while altering pain thresholds in migraines. By blocking 5-HT receptors, pizotifen attenuates the signalling of serotonin in causing cranial vasoconstriction, as well as serotonin-enhanced platelet function and aggregation. There is evidence that it also inhibits the peripheral actions of bradykinin. Pizotifen may inhibit serotonin reuptake by blood platelets, which affects the tonicity and decreases passive distension of extracranial arteries. The effects of pizotifen leading to appetite stimulation may be due to the drug acting at the metabolic level rather than a direct stimulation of the appetite centre. ",The molecular weight is 295.44.,Pizotifen has a topological polar surface area of 3.24.,The log p value of  is 4.7.,Pizotifen is approved.,Pizotifen is a solid.,True
15905,"Metenkefalin is an endogenous opioid and beta-endorphin. It has been shown to reduce chromosomal abberations in patients with multiple sclerosis. Metenkefalin, along with , are under investigation as an immunomodulatory therapy for moderate to severe COVID-19. Metenkefalin is indicated in Bosnia for the treatment of relapsing-remitting multiple sclerosis. Metenkefalin is an agonist of µ and δ opioid receptors. It also causes immunostimulation at low doses and immunosuppression at higher doses. Metenkefalin can also inhibit the production of aldosterone, deoxycorticosterone, and corticosterone. Unfortuneately, the mechanisms by which these effects occur have not been well described in the literature.",,,,Metenkefalin is investigational.,,True
15906,"This is the active form of vitamin B6 serving as a coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, aminolevulinic acid. During transamination of amino acids, pyridoxal phosphate is transiently converted into pyridoxamine phosphate (pyridoxamine). For nutritional supplementation and for treating dietary shortage or imbalance. The two major forms of vitamin B6 are pyridoxine and pyridoxamine. In the liver they are converted to pyridoxal phosphate (PLP) which is a cofactor in many reactions of amino acid metabolism. PLP also is necessary for the enzymatic reaction governing the release of glucose from glycogen. Pyroluria is one potential cause of vitamin B6 deficiency. Pyridoxal Phosphate is a coenzyme of many enzymatic reactions. It is the active form of vitamin B6 which comprises three natural organic compounds, pyridoxal, pyridoxamine and pyridoxine. Pyridoxal phosphate acts as a coenzyme in all transamination reactions, and in some ",The molecular weight is 247.14.,Pyridoxal phosphate has a topological polar surface area of 116.95.,The log p value of  is -0.57.,Pyridoxal phosphate is approved and investigational and nutraceutical.,Pyridoxal phosphate is a solid.,True
15907,"An essential amino acid that is required for the production of histamine. The actions of supplemental L-histidine are entirely unclear. It may have some immunomodulatory as well as antioxidant activity. L-histidine may be indicated for use in some with rheumatoid arthritis. It is not indicated for treatment of anemia or uremia or for lowering serum cholesterol. Is found abundantly in hemoglobin; has been used in the treatment of rheumatoid arthritis, allergic diseases, ulcers and anemia. A deficiency can cause poor hearing. Since the actions of supplemental L-histidine are unclear, any postulated mechanism is entirely speculative. However, some facts are known about L-histidine and some of its metabolites, such as histamine and trans-urocanic acid, which suggest that supplemental L-histidine may one day be shown to have immunomodulatory and/or antioxidant activities. Low free histidine has been found in the serum of some rheumatoid arthritis patients. Serum concentrations of other amino acids have been found to be normal in these patients. L-histidine is an excellent chelating agent for such metals as copper, iron and zinc. Copper and iron participate in a reaction (Fenton reaction) that generates potent reactive oxygen species that could be destructive to tissues, including joints. <br/>L-histidine is the obligate precursor of histamine, which is produced via the decarboxylation of the amino acid. In experimental animals, tissue histamine levels increase as the amount of dietary L-histidine increases. It is likely that this would be the case in humans as well. Histamine is known to possess immunomodulatory and antioxidant activity. Suppressor T cells have H2 receptors, and histamine activates them. Promotion of suppressor T cell activity could be beneficial in rheumatoid arthritis. Further, histamine has been shown to down-regulate the production of reactive oxygen species in phagocytic cells, such as monocytes, by binding to the H2 receptors on these cells. Decreased reactive oxygen species production by phagocytes could play antioxidant, anti-inflammatory and immunomodulatory roles in such diseases as rheumatoid arthritis. <br/>This latter mechanism is the rationale for the use of histamine itself in several clinical trials studying histamine for the treatment of certain types of cancer and viral diseases. In these trials, down-regulation by histamine of reactive oxygen species formation appears to inhibit the suppression of natural killer (NK) cells and cytotoxic T lymphocytes, allowing these cells to be more effective in attacking cancer cells and virally infected cells.",The molecular weight is 155.16.,Histidine has a topological polar surface area of 92.0.,The log p value of  is -3.73.,Histidine is investigational and nutraceutical.,Histidine is a solid.,True
15908,"A peptide that is a homopolymer of glutamic acid. Considered to be nature's \Brain food\"" by improving mental capacities; helps speed the healing of ulcers; gives a \""lift\"" from fatigue; helps control alcoholism, schizophrenia and the craving for sugar."" In addition to being one of the building blocks in protein synthesis, it is the most widespread neurotransmitter in brain function, as an excitatory neurotransmitter and as a precursor for the synthesis of GABA in GABAergic neurons. Glutamate activates both ionotropic and metabotropic glutamate receptors. The ionotropic ones being non-NMDA (AMPA and kainate) and NMDA receptors. Free glutamic acid cannot cross the blood-brain barrier in appreciable quantities; instead it is converted into L-glutamine, which the brain uses for fuel and protein synthesis. It is conjectured that glutamate is involved in cognitive functions like learning and memory in the brain, though excessive amounts may cause neuronal damage associated in diseases like amyotrophic lateral sclerosis, lathyrism, and Alzheimer's disease. Also, the drug phencyclidine (more commonly known as PCP) antagonizes glutamate at the NMDA receptor, causing behavior reminiscent of schizophrenia. Glutamate in action is extremely difficult to study due to its transient nature.",The molecular weight is 147.13.,Glutamic acid has a topological polar surface area of 100.62.,The log p value of  is -2.69.,Glutamic acid is approved and nutraceutical.,Glutamic acid is a solid.,True
15909,,,,,N-Acetyl-Serine is experimental.,N-Acetyl-Serine is a solid.,False
15910,"Also known as coagulation factor II, thrombin is a serine protease that plays a physiological role in regulating hemostasis and maintaining blood coagulation. Once converted from prothrombin, thrombin converts fibrinogen to fibrin, which, in combination with platelets from the blood, forms a clot. Bovine thrombin is a topical thrombin indicated to aid hemostasis whenever oozing blood and minor bleeding from capillaries and small venules is accessible and control of bleeding by standard surgical techniques (like suture, ligature, or cautery) is ineffective or impractical. Additionally, topical bovine thrombin can also be used in combination with an absorbable gelatin sponge, USP. Little has been reported about the systemic pharmacodynamics and pharmacokinetics of bovine thrombin preparations , but it is expected that bovine thrombin elicits similar activities as endogenous thrombin. Subsequently, it is believed that bovine thrombin, like endogenous thrombin, functions as a coagulation factor that converts clotting factor XI to XIa, factor VIII to VIIIa, V to Va, fibrinogen to fibrin, and XIII to XIIIa. Specifically, factor XIIIa catalyzes covalent bonds between lysine and glutamine residues that are found in fibrin. These covalent bonds assist in increasing the stability of the fibrin clot. Additionally, thrombin also promotes the activation and aggregation of platelets by way of activating protease-activated receptors on the cell membranes of platelets. Bovine thrombin requires no intermediate physiological agent for its action. It activates platelets and catalyzes the conversion of fibrinogen to fibrin, which are essential steps for clot formation. Failure to clot blood occurs in the case where the primary clotting defect is the absence of fibrinogen itself. The speed with which the bovine thrombin clots blood is dependent upon the concentration of both the bovine thrombin and the fibrinogen present.",,,,Thrombin is approved and investigational.,Thrombin is a solid.,True
15911,"Human thrombin is a sterile solution, pH 6.8-7.2, containing highly purified human thrombin for the activation of clotting. Thrombin is a highly specific serine protease encoded by the F2 gene that transforms soluble fibrinogen into insoluble fibrin. This transformation mimics the final coagulation cascade step which involves the clotting mass that adheres to the wound surface and achieves hemostasis and sealing of open tissues. Human thrombin is indicated as an aid to hemostasis whenever oozing blood and minor bleeding from capillaries and small venules are accessible and control of bleeding by standard surgical techniques (such as suture, ligature, or cautery) is ineffective or impractical. Clinical pharmacodynamic studies with human thrombin have not been performed at this time. Human thrombin (coagulation factor IIa) is a highly specific protease that transforms plasma fibrinogen into fibrin which, in the presence of clotting factor XIII in the patient's plasma, is cross-linked to form a stable clot. When applied to a surgical wound where bleeding is present, thrombin activates fibrinogen in the patient's plasma to form fibrin, which results in clot formation and hemostasis. The fibrin clot is stabilized by cross-linking occurring as a result of activation of the patient's endogenous factor XIII, which requires the presence of calcium. ",,,,Human thrombin is approved.,Human thrombin is a solid.,True
15912,"An essential amino acid that is physiologically active in the L-form. Used for nutritional supplementation, also for treating dietary shortage or imbalance. Studies have shown that is has improved immune responses to bacteria, viruses and tumor cells; promotes wound healing and regeneration of the liver; causes the release of growth hormones; considered crucial for optimal muscle growth and tissue repair. Many of supplemental L-arginine's activities, including its possible anti-atherogenic actions, may be accounted for by its role as the precursor to nitric oxide or NO. NO is produced by all tissues of the body and plays very important roles in the cardiovascular system, immune system and nervous system. NO is formed from L-arginine via the enzyme nitric oxide synthase or synthetase (NOS), and the effects of NO are mainly mediated by 3,'5' -cyclic guanylate or cyclic GMP. NO activates the enzyme guanylate cyclase, which catalyzes the synthesis of cyclic GMP from guanosine triphosphate or GTP. Cyclic GMP is converted to guanylic acid via the enzyme cyclic GMP phosphodiesterase. NOS is a heme-containing enzyme with some sequences similar to cytochrome P-450 reductase. Several isoforms of NOS exist, two of which are constitutive and one of which is inducible by immunological stimuli. The constitutive NOS found in the vascular endothelium is designated eNOS and that present in the brain, spinal cord and peripheral nervous system is designated nNOS. The form of NOS induced by immunological or inflammatory stimuli is known as iNOS. iNOS may be expressed constitutively in select tissues such as lung epithelium. All the nitric oxide synthases use NADPH (reduced nicotinamide adenine dinucleotide phosphate) and oxygen (O2) as cosubstrates, as well as the cofactors FAD (flavin adenine dinucleotide), FMN (flavin mononucleotide), tetrahydrobiopterin and heme. Interestingly, ascorbic acid appears to enhance NOS activity by increasing intracellular tetrahydrobiopterin. eNOS and nNOS synthesize NO in response to an increased concentration of calcium ions or in some cases in response to calcium-independent stimuli, such as shear stress. In vitro studies of NOS indicate that the Km of the enzyme for L-arginine is in the micromolar range. The concentration of L-arginine in endothelial cells, as well as in other cells, and in plasma is in the millimolar range. What this means is that, under physiological conditions, NOS is saturated with its L-arginine substrate. In other words, L-arginine would not be expected to be rate-limiting for the enzyme, and it would not appear that supraphysiological levels of L-arginine which could occur with oral supplementation of the amino acid^would make any difference with regard to NO production. The reaction would appear to have reached its maximum level. However, in vivo studies have demonstrated that, under certain conditions, e.g. hypercholesterolemia, supplemental L-arginine could enhance endothelial-dependent vasodilation and NO production.",The molecular weight is 174.2.,Arginine has a topological polar surface area of 125.22.,The log p value of  is -3.52.,Arginine is investigational and nutraceutical.,Arginine is a solid.,True
15913,"Citrulline is an amino acid. It is made from ornithine and carbamoyl phosphate in one of the central reactions in the urea cycle. It is also produced from arginine as a by-product of the reaction catalyzed by NOS family. Its name is derived from citrullus, the Latin word for watermelon, from which it was first isolated. Used for nutritional supplementation, also for treating dietary shortage or imbalance. A non-essential amino acid and a precursor of arginine. Citrulline supplements have been claimed to promote energy levels, stimulate the immune system and help detoxify ammonia (a cell toxin). L-citrulline is made from L-ornithine and carbamoyl phosphate in one of the central reactions in the urea cycle. It is also produced from L-arginine as a by-product of the reaction catalyzed by the enzyme NO synthase. L-citrulline, while being an amino acid, is not involved in protein synthesis and is not one of the amino acids coded for by DNA. Although citrulline cannot be incorporated in proteins during protein synthesis, several proteins are known to contain citrulline as an amino acid. These citrulline residues are generated by a family of enzymes called peptidylarginine deiminases (PADs), which convert the amino acid arginine into citrulline. Proteins that contain citrulline residues include myelin basic protein (MBP), fillagrin and several histone proteins. L-citrulline is converted to L-arginine by argininosuccinate synthase. L-arginine is in turn responsible for citrulline's therapeutic affects. Many of L-arginine's activities, including its possible anti-atherogenic actions, may be accounted for by its role as the precursor to nitric oxide or NO. NO is produced by all tissues of the body and plays very important roles in the cardiovascular system, immune system and nervous system. NO is formed from L-arginine via the enzyme nitric oxide synthase or synthetase (NOS), and the effects of NO are mainly mediated by 3',5' -cyclic guanylate or cyclic GMP. NO activates the enzyme guanylate cyclase, which catalyzes the synthesis of cyclic GMP from guanosine triphosphate or GTP. Cyclic GMP is converted to guanylic acid via the enzyme cyclic GMP phosphodiesterase. <br/><br/>NOS is a heme-containing enzyme with some sequences similar to cytochrome P-450 reductase. Several isoforms of NOS exist, two of which are constitutive and one of which is inducible by immunological stimuli. The constitutive NOS found in the vascular endothelium is designated eNOS and that present in the brain, spinal cord and peripheral nervous system is designated nNOS. The form of NOS induced by immunological or inflammatory stimuli is known as iNOS. iNOS may be expressed constitutively in select tissues such as lung epithelium. <br/><br/>All the nitric oxide synthases use NADPH (reduced nicotinamide adenine dinucleotide phosphate) and oxygen (O<sub>2</sub>) as cosubstrates, as well as the cofactors FAD (flavin adenine dinucleotide), FMN (flavin mononucleotide), tetrahydrobiopterin and heme. Interestingly, ascorbic acid appears to enhance NOS activity by increasing intracellular tetrahydrobiopterin. eNOS and nNOS synthesize NO in response to an increased concentration of calcium ions or in some cases in response to calcium-independent stimuli, such as shear stress. <i>In vitro</i> studies of NOS indicate that the Km of the enzyme for L-arginine is in the micromolar range. The concentration of L-arginine in endothelial cells, as well as in other cells, and in plasma is in the millimolar range. What this means is that, under physiological conditions, NOS is saturated with its L-arginine substrate. In other words, L-arginine would not be expected to be rate-limiting for the enzyme, and it would not appear that supraphysiological levels of L-arginine which could occur with oral supplementation of the amino acid would make any difference with regard to NO production. The reaction would appear to have reached its maximum level. However, <i>in vivo</i> studies have demonstrated that, under certain conditions, e.g. hypercholesterolemia, L-arginine could enhance endothelial-dependent vasodilation and NO production.",The molecular weight is 175.19.,Citrulline has a topological polar surface area of 118.44.,The log p value of  is -3.36.,Citrulline is investigational and nutraceutical.,Citrulline is a solid.,True
15914,"Minocycline was first described in the literacture in 1966. It is a second generation tetracycline antibiotic that is active against gram-negative and gram-positive bacteria. Like other semisynthetic tetracyclines, minocycline has modifications to carbons 7-9 on the D ring to generate higher efficacy than previous tetracyclines. Oral and topical minocycline are indicated to treat inflammatory lesions of acne vulgaris. Subgingival microspheres are indicated as an adjunct treatment in the reduction of pocket depth in adults with periodontitis. Oral and intravenous formulations are indicated to treat infections of susceptible microorganisms. These include rickettsiae, _Mycoplasma pneumoniae_, _Chlamydia trachomatis_, _Chlamydophila psittaci_, _Chlamydia trachomatis_, _Ureaplasma urealyticum_, _Borrelia recurrentis_, _Haemophilus ducreyi_, _Yersinia pestis_, _Francisella tularensis_, _Vibrio cholerae_, _Campylobacter fetus_, _Brucella_ species, _Bartonella bacilliformis_, _Klebsiella granulomatis_, _Escherichia coli_, _Enterobacter aerogenes_, _Shigella_ species, _Acinetobacter_ species, _Haemophilus influenzae_, and _Kelbsiella_ species. Minocycline is a tetracycline antibiotic that binds to the bacterial 30S ribosomal subunit and interferes with protein synthesis. It is generally given 2-4 times daily, so the duration of action is short. Intravenous minocycline should not exceed 400mg in 24 hours. Patients should be counselled regarding the risks related to tooth and bone development, pseudomembranous colitis, central nervous system side effects, and pseudotumor cerebri. Tetracyclines enter bacterial cells through OmpF and OmpC porins by coordinating with cations like magnesium. This allows tetracyclines into the periplasm where they dissociate, allowing the lipophilic tetracycline to diffuse into the bacterial cytoplasm. Tetracyclines prevent aminoacyl-tRNA from binding to the 30S ribosome, inhibiting protein synthesis. ",The molecular weight is 457.48.,Minocycline has a topological polar surface area of 164.63.,The log p value of  is 0.21.,Minocycline is approved and investigational.,Minocycline is a solid.,True
15915,"Asymmetric dimethylarginine (ADMA) is a naturally occurring chemical found in blood plasma. It is a metabolic by-product of continual protein modification processes in the cytoplasm of all human cells which is closely related to L-arginine, a conditionally-essential amino acid. ADMA interferes with L-arginine in the production of nitric oxide, a key chemical to endothelial and hence cardiovascular health. Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, is formed by methylation of arginine residues in proteins and released after proteolysis. In this reaction, S-adenosylmethionine is methyldonor and S-adenosylhomocysteine the demethylated product. ADMA and homocysteine are thus biochemically linked. Both plasma homocysteine and ADMA concentrations are increased in patients with renal dysfunction, probably as a result of an impairment in their metabolic, but not urinary, clearance. Hyperhomocysteinemia has been associated with an increased risk of cardiovascular disease in end-stage renal disease, especially in patients without malnutrition and inflammation. Also, plasma ADMA levels have been associated with cardiovascular disease in renal failure patients. Both homocysteine and ADMA are thought to mediate their adverse vascular effects by impairing endothelial, nitric oxide-dependent function resulting in decreased vasodilatation, increased smooth muscle cell proliferation, platelet dysfunction and increased monocyte adhesion.",,,,"N,N-dimethylarginine is experimental.","N,N-dimethylarginine is a solid.",True
15916,,,,,4R-Fluoro-N6-ethanimidoyl-L-lysine is experimental.,4R-Fluoro-N6-ethanimidoyl-L-lysine is a solid.,False
15917,,,,,3-Bromo-7-Nitroindazole is experimental.,3-Bromo-7-Nitroindazole is a solid.,False
15918,,,,,N-acetamidine is experimental.,N-acetamidine is a solid.,False
15919,,,,,7-Nitroindazole is experimental.,7-Nitroindazole is a solid.,False
15920,S-Ethylisothiourea is a nitric oxide synthase inhibitor.,,,,S-Ethylisothiourea is experimental.,S-Ethylisothiourea is a solid.,True
15921,,,,,Thiocoumarin is experimental.,Thiocoumarin is a solid.,False
15922,,,,,N-omega-propyl-L-arginine is experimental.,N-omega-propyl-L-arginine is a solid.,False
15923,,,,,6-Nitroindazole is experimental.,6-Nitroindazole is a solid.,False
15924,,,,,N(5)--L-ornithine is experimental.,N(5)--L-ornithine is a solid.,False
15925,,,,,Imidazole is experimental and investigational.,Imidazole is a solid.,False
15926,,,,,N-(4-{2-ethyl}phenyl)thiophene-2-carboximidamide is experimental.,N-(4-{2-ethyl}phenyl)thiophene-2-carboximidamide is a solid.,False
15927,,,,,Thiocitrulline is experimental.,Thiocitrulline is a solid.,False
15928,"7,8-Dihydrobiopterin is an inhibitor of the enzyme dihydroneopterin aldolase (DHNA), which catalyzes the conversion of 7,8-Dihydrobiopterin to 6-hydroxymethyl-7,8-dihydropterin and glycolaldehyde.",,,,"L-erythro-7,8-dihydrobiopterin is experimental.","L-erythro-7,8-dihydrobiopterin is a solid.",True
15929,,,,,5-Nitroindazole is experimental.,5-Nitroindazole is a solid.,False
15930,"KD7040 is a topically-delivered inducible nitric oxide synthase (iNOS) inhibitor for the treatment of neuropathic pain. The KD7040 IND was filed in 4Q06, and a Phase Ib clinical trial began 2Q07. It is being developed by Kalypsys. For the treatment of pain. KD7040 demonstrates robust reduction of tactile allodynia in rodent models of pain, including the Chung model (peripheral neuropathy), the Bennet chronic constrictive injury model, and the capsaicin model of central sensitization. Preliminary data from GLP safety pharmacology and toxicology studies have defined a favorable safety profile for entry into the clinic. KD7040 is a potent, topically administered, inhibitor of inducible nitric oxide synthase (iNOS) with greater than 200-fold and 2000-fold selectivity over nNOS and eNOS respectively.",,,,KD7040 is investigational.,KD7040 is a solid.,True
15931,"Fenoxaprop-ethyl (organic nitrate combined with L-arginine), is an oral proprietary nitrate therapeutic shown to induce coronary vasodilation while overcoming the significant problem of drug tolerance. Fenoxaprop-ethyl has been investigated to treat chronic angina, the chest pain that occurs from inadequate blood flow to the coronary arteries around the heart. Chronic angina and Coronary Artery Disease  Fenoxaprop-ethyl is a proprietary combination of nitrate and L-arginine that provides the beneficial cardiovascular effects of nitrates. Combining L-arginine with organic nitrates prevents the endothelial cell's depletion of L-arginine and the associated problem of nitrate tolerance. By eliminating nitrate tolerance, Fenoxaprop-ethyl allows patients to receive the continuous, 24-hour benefit of a potent nitrate product, thus sustaining the desired vasodilation effect.",,,,Fenoxaprop-ethyl is investigational.,Fenoxaprop-ethyl is a solid.,True
15932,"Pimagedine has been developed by Synvista Therapeutics, Inc for the treatment of diabetic kidney disease. It is an advanced glycation end product inhibitor which manages diabetic nephropathy, either alone or in combination with other therapies. It is beneficial in treating patients with diabetic nephropathy. Investigated for use/treatment in diabetic kidney disease. Pimagedine reportedly inhibits the formation of glycosylated proteins (advanced glycosylation end-products) and has other actions including inhibition of aldose reductase.",,,,Pimagedine is investigational.,Pimagedine is a solid.,True
15933,,,,,"5-(4'-AMINO-1'-ETHYL-5',8'-DIFLUORO-1'H-SPIRO-1-YLCARBONYL)PICOLINONITRILE is experimental.","5-(4'-AMINO-1'-ETHYL-5',8'-DIFLUORO-1'H-SPIRO-1-YLCARBONYL)PICOLINONITRILE is a solid.",False
15934,,,,,N--1--D-PROLINAMIDE is experimental.,N--1--D-PROLINAMIDE is a solid.,False
15935,,,,,4-({4-piperidin-1-yl}carbonyl)benzonitrile is experimental.,4-({4-piperidin-1-yl}carbonyl)benzonitrile is a solid.,False
15936,,,,,"(2S)-2-methyl-2,3-dihydrothienooxazepin-5-amine is experimental.","(2S)-2-methyl-2,3-dihydrothienooxazepin-5-amine is a solid.",False
15937,,,,,"(3R)-3--2,3-dihydrothienooxazepin-5-amine is experimental.","(3R)-3--2,3-dihydrothienooxazepin-5-amine is a solid.",False
15938,,,,,"4-(1,3-BENZODIOXOL-5-YLOXY)-2-PYRIMIDINE is experimental.","4-(1,3-BENZODIOXOL-5-YLOXY)-2-PYRIMIDINE is a solid.",False
15939,,,,,"(3S)-1-(1,3-BENZODIOXOL-5-YLMETHYL)-3-PIPERIDINE is experimental.","(3S)-1-(1,3-BENZODIOXOL-5-YLMETHYL)-3-PIPERIDINE is a solid.",False
15940,,,,,"4-(1,3-BENZODIOXOL-5-YLOXY)-2--6-METHYLPYRIMIDINE is experimental.","4-(1,3-BENZODIOXOL-5-YLOXY)-2--6-METHYLPYRIMIDINE is a solid.",False
15941,,,,,ETHYL 4-PIPERIDINE-1-CARBOXYLATE is experimental.,ETHYL 4-PIPERIDINE-1-CARBOXYLATE is a solid.,False
15942,,,,,N--3-FURAMIDE is experimental.,N--3-FURAMIDE is a solid.,False
15943,,,,,ETHYL 4-PIPERIDINE-1-CARBOXYLATE is experimental.,ETHYL 4-PIPERIDINE-1-CARBOXYLATE is a solid.,False
15944,,,,,N--4-CYANOBENZAMIDE is experimental.,N--4-CYANOBENZAMIDE is a solid.,False
15945,,,,,"1-(6-CYANO-3-PYRIDYLCARBONYL)-5',8'-DIFLUOROSPIRO-4'-AMINE is experimental.","1-(6-CYANO-3-PYRIDYLCARBONYL)-5',8'-DIFLUOROSPIRO-4'-AMINE is a solid.",False
15946,,,,,4-(1H-IMIDAZOL-1-YL)PHENOL is experimental.,4-(1H-IMIDAZOL-1-YL)PHENOL is a solid.,False
15947,,,,,1--5'-FLUORO-1'H-SPIRO-4'-AMINE is experimental.,1--5'-FLUORO-1'H-SPIRO-4'-AMINE is a solid.,False
15948,"Dipyrithione is a pyrithione derivate used as bactericide and fungicide. The drug was marketed under the name Crimanex in the form of shampoo for the treatment of dandruff, however it is no longer available on the manufacturer website (Drossa Pharm. It is currently used as a pesticide. Scalp dandruff  This drug decreases or eliminates dandruff from the scalp, which is caused by various types of fungi ,. This drug is a fungicidal agent ,. ",The molecular weight is 252.31.,Dipyrithione has a topological polar surface area of 50.92.,The log p value of  is -1.57.,Dipyrithione is approved.,,True
15949,,,,,7-thionicotinamide-adenine-dinucleotide phosphate is experimental.,7-thionicotinamide-adenine-dinucleotide phosphate is a solid.,False
15950,"Nicotinamide adenine dinucleotide phosphate. A coenzyme composed of ribosylnicotinamide 5&#39;-phosphate (NMN) coupled by pyrophosphate linkage to the 5&#39;-phosphate adenosine 2&#39;,5&#39;-bisphosphate. It serves as an electron carrier in a number of reactions, being alternately oxidized (NADP+) and reduced (NADPH). (Dorland, 27th ed)",,,,Nicotinamide adenine dinucleotide phosphate is experimental.,Nicotinamide adenine dinucleotide phosphate is a solid.,True
15951,"Xanthinol is a very potent water-soluble derivative of niacin that can be found in diet supplements. It is also known as xanthinol nicotinate. Xaninthol is known to be a potent vasodilator that can easily pass through the cell membrane and once inside the cell it causes an increase in glucose metabolism resulting in an increased energy. It was approved as a drug in 1998 in Canada and nowadays its status is cancelled post marketing. Xanthinol is primarily used in diet supplements to increase the brain metabolism of glucose and obtain ATP. Xanthinol is also used as an agent to reduced cholesterol as it is a vasodilator. Its action allows having an elevated rate of blood flow in the brain which helps improve memory function, concentration and awareness. Thus, due to his actions, xanthinol is indicated to improve cerebrovascular and peripheral vascular disorders as well as hyperlipidaemias. Reports indicate that xanthinol increases blood flow in the vascular beds. The use of xanthinol in clinical trials have reported improvements in the performance of healthy elderly individuals in short- and long-term memory tests. The later effect is explained by the enhancing on the cell metabolism and oxygen supply in the brain by the rise of ATP in erythrocytes which allows penetration into capillaries easier and a higher oxygen pressure in the capillary blood which improves oxygenation of surrounding tissue. The positively charged xanthinol ion is thought to help the transportation of the nicotinic acid into the cell since the later cannot freely diffuse through the cell membrane. The mechanism of action is thought to be related to present influence in the cell metabolism through the nucleotides NAD and NADP. Also, the nicotinic acid is a coenzyme for a lot of proteins involved in tissue respiration (Embden-Meyerhof and citrate cycle). The effect of xanthinol nicotinate causes an increase in glucose metabolism and energy gain.",,,,Xanthinol is approved and withdrawn.,Xanthinol is a solid.,True
15952,,,,,12-Hydroxydodecanoic Acid is experimental.,12-Hydroxydodecanoic Acid is a solid.,False
15953,,,,,S-Hydroxymethyl Glutathione is experimental.,S-Hydroxymethyl Glutathione is a solid.,False
15954,"Tetrahydrofolic acid is a folic acid derivative that is produced from dihydrofolic acid after conversion by dihydrofolate reductase. It is converted into 5,10-methylenetetrahydrofolate by serine hydroxymethyltransferase. It is a soluble coenzyme in many reactions, especially in the metabolism of amino acids and nucleic acids. For nutritional supplementation, also for treating dietary shortage or imbalance. Tetrahydrofolate is the main active metabolite of dietary folate. It is vital as a coenzyme in reactions involving transfers of single carbon groups. Tetrahydrofolate has a role in nucleic and amino acid synthesis. As nucleic and amino acid synthesis is affected by a deficiency of tetrahydrofolate, actively dividing and growing cells tend to be the first affected. Tetrahydrofolate is used to treat topical sprue and megaloblastic and macrocytic anemias, hematologic complications resulting from a deficiency in folic acid. Tetrahydrofolate is transported across cells by receptor-mediated endocytosis where it is needed to maintain normal erythropoiesis, synthesize purine and thymidylate nucleic acids, interconvert amino acids, methylate tRNA, and generate and use formate.",,,,Tetrahydrofolic acid is nutraceutical.,Tetrahydrofolic acid is a solid.,True
15955,"5-methyltetrahydrofolic acid is a methylated derivate of tetrahydrofolate. It is generated by methylenetetrahydrofolate reductase from 5,10-methylenetetrahydrofolate and used to recycle homocysteine back to methionine by 5-methyltetrahydrofolate-homocysteine methyltransferases (also called methionine synthases).",,,,5-methyltetrahydrofolic acid is investigational and nutraceutical.,5-methyltetrahydrofolic acid is a solid.,True
15956,"Dyphylline is a theophylline derivative with broncho- and vasodilator properties. It is typically used in the management of asthma, cardiac dyspnea, and bronchitis. For relief of acute bronchial asthma and for reversible bronchospasm associated with chronic bronchitis and emphysema. Dyphylline, a xanthine derivative, is a bronchodilator used for relief of acute bronchial asthma and for reversible bronchospasm associated with chronic bronchitis and emphysema. Dyphylline is a xanthine derivative with pharmacologic actions similar to theophylline and other members of this class of drugs. Its primary action is that of bronchodilation, but it also exhibits peripheral vasodilatory and other smooth muscle relaxant activity to a lesser degree. The bronchodilatory action of dyphylline, as with other xanthines, is thought to be mediated through competitive inhibition of phosphodiesterase with a resulting increase in cyclic AMP producing relaxation of bronchial smooth muscle as well as antagonism of adenosine receptors.",The molecular weight is 254.25.,Dyphylline has a topological polar surface area of 98.9.,The log p value of  is -1.29.,Dyphylline is approved.,Dyphylline is a solid.,True
15957,"Enprofylline is a derivative of theophylline which shares bronchodilator properties. Enprofylline is used in asthma, chronic obstructive pulmonary disease, and in the management of cerebrovascular insufficiency, sickle cell disease, and diabetic neuropathy. Long-term enprofylline administration may be associated with elevation in liver enzyme levels and unpredictable blood levels. Used in the management of symptoms of asthma. Also used in the treatment of peripheral vascular diseases and in the management of cerebrovascular insufficiency, sickle cell disease, and diabetic neuropathy. Enprofylline is a synthetic dimethylxanthine derivative structurally related to theophylline and caffeine. It antagonizes erythrocyte phosphodiesterase, increasing cAMP activity. Enprofylline inhibits erythrocyte phosphodiesterase, resulting in an increase in erythrocyte cAMP activity. Subsequently, the erythrocyte membrane becomes more resistant to deformity. Along with erythrocyte activity, enprofylline also decreases blood viscosity by reducing plasma fibrinogen concentrations and increasing fibrinolytic activity.",The molecular weight is 194.19.,Enprofylline has a topological polar surface area of 78.09.,The log p value of  is 0.4.,Enprofylline is approved and experimental.,Enprofylline is a solid.,True
15958,"Defibrotide is the sodium salt of a mixture of single-stranded oligodeoxyribonucleotides derived from porcine mucosal DNA. It has been shown to have antithrombotic, anti-inflammatory and anti-ischemic properties (but without associated significant systemic anticoagulant effects). It is marketed under the brand names Dasovas (FM), Noravid, and Prociclide in a variety of countries. In the USA it is was approved in March, 2016 as Defitelio. Indicated for the treatment of severe hepatic veno-occlusive disease (VOD), also known as sinusoidal obstruction syndrome (SOS), with renal or pulmonary dysfunction following hematopoietic stem-cell transplantation (HSCT). Defibrotide is a deoxyribonucleic acid derivative extracted from mammalian organs, which has been developed for the treatment of a number of vascular disorders. It appears to increase fibrinolysis and may possess antithrombotic, antiatherosclerotic and anti-ischaemic actions, probably due to its ability to selectively increase prostaglandin I2 and E2 levels and to increase tissue plasminogen activator and decrease plasminogen activator inhibitor function. Defibrotide is available as an intravenous and intramuscular preparation, and also as an oral formulation for long term use. The drug appears to prevent the formation of blood clots and to help dissolve blood clots by increasing levels of prostaglandin I2, E2, and prostacyclin, altering platelet activity, increasing tissue plasminogen activator function, and decreasing activity of tissue plasminogen activator inhibitor. Prostaglandin I2 relaxes the smooth muscle of blood vessels and prevents platelets from adhering to each other. Prostaglandin E2 at certain concentrations also inhibits platelet aggregation. Moreover, the drug provides additional beneficial anti-inflammatory and antiischemic activities as recent sudies have shown. It is yet unclear, if the latter effects can be utilized clinically (e.g., treatment of ischemic stroke).",,,,Defibrotide is approved and investigational.,Defibrotide is a solid.,True
15959,"Tecadenoson is a novel selective A1 adenosine receptor agonist that is currently being evaluated for the conversion of paroxysmal supraventricular tachycardia (PSVT) to sinus rhythm. It is being developed by CV Therapeutics, Inc. Investigated for use/treatment in arrhythmia and atrial fibrillation. Tecadenoson is a novel A1 adenosine receptor stimulator. Adenosine is a naturally occurring compound that stimulates all adenosine receptor subtypes in the body, including the A2 adenosine receptor which lowers blood pressure. In non-clinical trials, tecadenoson selectively stimulated the A1 adenosine receptor in the AV node and slowed the speed of electrical conduction across the AV node, reducing the number of electrical impulses that reached the ventricle, without affecting blood pressure. Clinical studies to date with intravenous tecadenoson suggest that it may slow the speed of AV nodal conduction by selectively stimulating the A1 adenosine receptor, and may avoid blood pressure lowering by not stimulating the A2 adenosine receptor. Thus, it may be possible to use intravenous tecadenoson to convert patients from PSVT to normal sinus rhythm without lowering blood pressure or causing adverse events related to vasodilitation such as flushing, palpitations or headache. Tecadenoson selectively stimulates the A1 adenosine receptor. Stimulation of the A1 adenosine receptor slows the conduction of electrical impulses in the AV node of the heart, a region that controls the transmission of electrical impulses from the atria to the ventricles.",,,,Tecadenoson is investigational.,Tecadenoson is a solid.,True
15960,Investigated for use/treatment in congestive heart failure.,,,,Naxifylline is investigational.,Naxifylline is a solid.,True
15961,"Tonapofylline has been used in trials studying the treatment of Heart Failure, Renal Insufficiency, and Congestive Heart Failure. Stimulation of A1 adenosine receptors in the kidney reduces glomerular filtration rate (GFR) via tubuloglomerular feedback and increases sodium reabsorption. Blocking A1 adenosine receptors would therefore maintain GFR and cause natriuresis. Tonapofylline is a xanthine derivative that binds with high affinity to A1 adenosine receptors from several species including human and acts as a competitive antagonist at these receptors.",,,,Tonapofylline is investigational.,,True
15962,"Rolofylline is under clinical development by pharmaceutical company NovaCardia for the treatment of congestive heart failure. Rolofylline is an adenosine A1-receptor antagonist. Plasma adenosine levels are elevated in patients with heart failure and adenosine A1 receptors in the kidney mediate vasoconstriction of afferent arterioles, reabsorption of sodium and water in proximal tubules, and tubuloglomerular feedback in the juxtaglomerular apparatus. Accordingly, inhibition of these receptors would be expected to increase renal blood flow and enhance diuresis. The effects of Rolofylline on renal function are consistent with those obtained with another adenosine A1-receptor antagonist in both experimental and human heart failure.",,,,Rolofylline is investigational.,,True
15963,,,,,N-Amino]Phenyl]-3-Pyridinecarboxamide is experimental.,N-Amino]Phenyl]-3-Pyridinecarboxamide is a solid.,False
15964,"XL228 is a novel anticancer compound designed to inhibit the insulin-like growth factor type-1 receptor (IGF1R), Src and Abl tyrosine kinases – targets that play crucial roles in cancer cell proliferation, survival and metastasis. Investigated for use/treatment in leukemia (lymphoid) and leukemia (myeloid). XL228 potently inhibits the T315I mutant form of ABL, which is resistant to inhibition by other targeted therapies approved for chronic myelogenous leukemia. XL228 also targets IGF1R, which is a receptor tyrosine kinase that is highly expressed and activated in a broad range of human tumors and is thought to promote tumor growth, survival and resistance to chemotherapeutic agents. XL228 showed efficacy in a variety of solid tumor xenograft models.",,,,XL228 is investigational.,XL228 is a solid.,True
15965,,,,,2-{AMINO}-N-BENZAMIDE is experimental.,2-{AMINO}-N-BENZAMIDE is a solid.,False
15966,,,,,1--3-UREA is experimental.,1--3-UREA is a solid.,False
15967,,,,,PD-166326 is experimental.,PD-166326 is a solid.,False
15968,,,,,"5-PYRIDIN-5-YL]-N,N-DIMETHYLPYRIDINE-3-CARBOXAMIDE is experimental.","5-PYRIDIN-5-YL]-N,N-DIMETHYLPYRIDINE-3-CARBOXAMIDE is a solid.",False
15969,,,,,"2-amino-5-pyridin-5-yl]-N,N-dimethylbenzamide is experimental.","2-amino-5-pyridin-5-yl]-N,N-dimethylbenzamide is a solid.",False
15970,"Radotinib is under investigation for the treatment of Leukemia, Myelogenous, Chronic, BCR-ABL Positive. Radotinib is indicated for the treatment of different types of cancer, most notably Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia (CML) with resistance or intolerance of other Bcr-Abl tyrosine-kinase inhibitors, such as patients resistant or intolerant to imatinib. Philadelphia chromosome positive (Ph+) leukemia is driven by the constitutive enzymatic activity of the BCR-ABL1 fusion kinase. Tyrosine kinase inhibitors (TKIs) that block the activity of BCR-ABL1 are successfully used clinically to treat chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ ALL). ",The molecular weight is 530.52.,Radotinib has a topological polar surface area of 110.51.,The log p value of  is 4.94.,Radotinib is investigational.,,True
15971,"Omalizumab, manufactured by _Genentech_, was first FDA approved in 2003 to treat adults and children 12 years of age and older with moderate to severe persistent allergic asthma which is not controlled by inhaled steroids. Since its U.S. approval, more than 200,000 patients older than 12 with allergic asthma have been treated. In September 2018, a new prefilled syringe formulation of this drug was approved by the FDA. This drug is an anti-IgE antibody indicated for: Omalizumab is a recombinant, humanized, monoclonal antibody against human immunoglobulin E (IgE) which treats the symptoms of asthma and chronic idiopathic urticaria by limiting the allergic response ,. It inhibits the binding of IgE to receptors on mast cells and basophils, blocking the IgE-mediated secretion of inflammatory mediators from these cells. When an environmental allergen first enters the body, is taken up by antigen-presenting cells (APCs). It is then processed, and presented to T and B immune cells. This is followed by the activation of B-lymphocyte and production of allergen-specific IgE. This IgE is then released by plasma cells (converted B lymphocytes) and is therefore available to bind to IgE receptors on several other cells.",,,,Omalizumab is approved and investigational.,Omalizumab is a solid.,True
15972,"Benzylpenicilloyl polylysine is used as a skin-testing reagent to detect immunoglobulin E antibodies in people with a history of penicillin allergy. The quantitation of in vitro IgE antibodies to the benzylpenicilloyl determinant is a useful tool for evaluating allergic subjects. For use as a adjunct in assessing the risk of administering penicillin (benzylpenicillin or penicillin G). Benylpenicilloyl polylysine is penicilloyl bound to polylysine and is considered to be the major determinant of penicillin metabolism; it is used as a skin-testing reagent to detect immunoglobulin E antibodies in people with a history of penicillin allergy. If skin testing using benzylpenicilloyl and penicillin G (as the sole source of minor determinants) is negative, approximately 97% of patients with a negative skin test will tolerate penicillin. The skin test for penicillin demonstrates the presence or absence of specific IgE antibodies to major and minor penicillin determinants. IgE antibodies to major determinants can be detected by using benzylpenicilloyl polylysine. A penicillin skin test predicts only the presence of IgE antibodies for the major or minor penicillin determinants at the time of application and does not predict the future development of IgE-mediated reactions during subsequent courses of penicillin. Benzylpenicilloyl polylysine reacts specifically with penicilloyl skin sensitizing antibodies (reagins) to produce immediate wheal and flare reactions which may reflect increased risk of allergic reactions to subsequent penicillin therapy.",,,,Benzylpenicilloyl polylysine is approved.,Benzylpenicilloyl polylysine is a solid.,True
15973,"TNX-901 is a therapeutic monoclonal antibodies designed to address significant unmet medical needs in the areas of asthma, allergy, inflammation and other diseases affecting the human immune system. Investigated for use/treatment in allergic reaction. TNX-901 is an anti-IgE antibody. IgE antibody is the receptor responsible for allergic reactions and severe asthma attacks. An anti-IgE antibody binds IgE and prevents it from initiating an allergic reaction.",,,,TNX-901 is investigational.,TNX-901 is a solid.,True
15974,"Drotrecogin alfa is activated human protein C that is synthesized by recombinant DNA technology. It is a glycoprotein of approximately 55 kilodalton molecular weight, consisting of a heavy chain and a light chain linked by a disulfide bond. Drotrecogin alfa was withdrawn from the market after a major study indicated that it was not effective in improving outcomes in patients with sepsis. For reduction of mortality in patients with severe sepsis. Drotrecogin alfa is activated human protein C that is synthesized by recombinant DNA technology. It is a glycoprotein of approximately 55 kilodalton molecular weight, consisting of a heavy chain and a light chain linked by a disulfide bond. Activated protein C combines with protein S on platelet surfaces and then degrades factor Va and factor VIIIa, thereby reducing blood coagulability.",,,,Drotrecogin alfa is approved and investigational and withdrawn.,Drotrecogin alfa is a liquid.,True
15975,"Recombinant Coagulation Factor IX is a purified Factor IX glycoprotein produced by recombinant DNA technology. It has a primary amino acid sequence that is identical to the Ala148 allelic form of human factor IX, and has structural and functional characteristics similar to those of endogenous factor IX. It is not derived from human blood (unlike human Factor IX complex), and is instead produced by a genetically engineered Chinese hamster ovary (CHO) cell line that secretes recombinant Factor IX into cell medium that is then processed and purified for use as a pharmaceutical agent.  For treatment of hemophilia (Christmas disease). Binds vitamin K and factor VIIIa. Cleaves the Arg-Ile bond in factor X to form active factor Xa. Plays a key role in blood coagulation and clotting. Injections of factor IX are used to treat hemophilia B, which is sometimes called Christmas disease. AlphaNine is injected to increase plasma levels of Factor IX and can temporarily correct this coagulation defect. The activated partial thromboplastin time (aPTT) is prolonged in people with hemophilia B. Treatment with factor IX concentrate may normalize the aPTT by temporarily replacing the factor IX. The administration of BeneFIX increases plasma levels of factor IX, and can temporarily correct the coagulation defect in these patients. Coagulation Factor IX is an important protein in the process of hemostasis and normal blood clotting as it plays a key role within the coagulation cascade. It is located within the blood plasma as a zymogen, an antecedent to enzymatic function, in its inactivated state. Factor IX is dependent on the presence of Vitamin K, and is activated to a serine protease by the function of Coagulation Factor XIa. Factor XIa cleaves the peptide bond associated with protein activation in Factor IX, leaving Factor IX with two exposed chains, a light chain and a heavy chain. These two chains are held together by several disulfide bonds that reinforce the structure of Factor IX's activated form. After being activated, Factor IX forms a complex with calcium ions, membrane phospholipids and Coagulation Factor VIII to activate Coagulation Factor X. The activation of Factor X then performs a similarly integral step in the blood coagulation cascade. The ultimate result of phenotypically normal coagulation factors is the creation of platelets for normal blood clotting.",,,,Coagulation Factor IX (Recombinant) is approved and investigational.,Coagulation Factor IX (Recombinant) is a liquid.,True
15976,"TB-402 is a human antibody binding to Factor VIII, which plays a crucial role in the coagulation of the blood. It is expected to be developed as a potential treatment to prevent blood clot formation in connection with certain types of heart arrhythmia, such as atrial fibrillation. Investigated for use/treatment in atrial fibrillation and thrombosis. TB-402 is a human antibody binding to Factor VIII, which plays a crucial role in the coagulation of the blood. The antibody has shown a beneficial partial inhibition of Factor VIII,",,,,TB-402 is investigational.,TB-402 is a solid.,True
15977,"Protein C is an endogenously occurring plasma protein that plays a key role within the coagulation cascade. Protein C is a zymogen, or enzyme precursor, of a vitamin K-dependent anticoagulant glycoprotein (serine protease) that is synthesized in the liver. It is converted by the thrombin/thrombomodulin-complex on the endothelial cell surface to Activated Protein C (APC). Once in its activated form, APC functions as a serine protease with potent anticoagulant effects, especially in the presence of its cofactor protein S. APC exerts its effect by inactivating essential components of the coagulation cascade (specifically factors V and VIII), which leads to a decrease in thrombin formation, and therefore a reduction in clot formation.  Protein C concentrate is indicated for pediatric and adult patients with severe congenital protein C deficiency for the prevention and treatment of venous thrombosis and purpura fulminans. It is also found as a component of some prothrombin complex concentrate (i.e. ) formulations, such as Kcentra. In clinical studies, the intravenous administration of Protein C Concentrate demonstrated a temporary increase, within approximately half an hour of administration, in plasma levels of APC. Replacement of protein C in protein C-deficient patients is expected to control or, if given prophylactically, to prevent thrombotic complications. Protein C is an endogenously occurring plasma protein that plays a key role within the coagulation cascade. Also known as blood coagulation factor XIV, Protein C is a zymogen, or enzyme precursor, of a vitamin K-dependent anticoagulant glycoprotein (serine protease) that is synthesized in the liver. It is converted by the thrombin/thrombomodulin-complex on the endothelial cell surface to Activated Protein C (APC). Once in its activated form, APC functions as a serine protease with potent anticoagulant effects, especially in the presence of its cofactor protein S. APC exerts its effect by inactivating essential components of the coagulation cascade (specifically factors V and VIII), which leads to a decrease in thrombin formation, and therefore a reduction in clot formation. ",,,,Protein C is approved.,Protein C is a solid.,True
15978,"Thrombin Alfa is a human coagulation protein produced via recombinant DNA technology from a genetically modified CHO cell line. Thrombin Alfa is identical in amino acid sequence and structurally similar to naturally occurring human thrombin. Thrombin Alfa precursor is secreted to culture medium as single chain form that is proteolytically converted to a two-chain active form (using a protein derived from snakes) and is purified by a chromatographic process that yields a product having hemostatic activities similar to native human thrombin. The cell line used to manufacture Thrombin Alfa has been tested and shown to be free of known infectious agents. The cell culture process used in the manufacture of Thrombin Alfa employs no additives of human or animal origin. The purification process includes solvent-detergent treatment and nano-filtration steps dedicated to viral clearance. The thrombin alfa product ultimate comes from recombinant human prethrombin-1. Indicated to aid hemostasis whenever oozing blood and minor bleeding from capillaries and small venules is accessible and control of bleeding by standard surgical techniques (such as suture, ligature, or cautery) is ineffective or impractical in adults and pediatric populations greater than or equal to one month of age. As thrombin alfa, a recombinant thrombin, is considered to be identical in amino acid sequence and structural similarity to naturally occurring human thrombin, it is believed that thrombin alfa shares the same pharmacodynamics as endogenous or natural human thrombin coagulation factor. Specifically, thrombin alfa is a human serine protease that promotes hemostasis and acts locally when applied topically to a site of bleeding. In particular, thrombin alfa activates platelets and cleaves fibrinogen to fibrin, leading directly to clot formation. It also activates clotting factor XIII, leading to fibrin cross-linking and clot stability. The ability of thrombin alfa to bypass the initial enzymatic steps of the coagulation pathway provides a clear rationale as to why thrombin alfa may be used as a topical haemostatic agent.",,,,Thrombin alfa is approved.,Thrombin alfa is a solid.,True
15979,"Factor IX (or Christmas factor) is one of the serine proteases of the coagulation system; it belongs to peptidase family S1. Deficiency of this protein causes hemophilia B. Factor IX is used to treat Christmas disease. Factor IX deficiency is treated by injection factor IX produced from human plasma. Tranexamic acid may be of value in patients undergoing surgery who have inherited factor IX deficiency in order to reduce the perioperative risk of bleeding. Binds vitamin K and factor VIIIa. Cleaves the Arg-Ile bond in factor X to form active factor Xa. Plays a key role in blood coagulation and clotting. Injections of factor IX are used to treat hemophilia B, which is sometimes called Christmas disease. AlphaNine is injected to increase plasma levels of Factor IX and can temporarily correct this coagulation defect. The activated partial thromboplastin time (aPTT) is prolonged in people with hemophilia B. Treatment with factor IX concentrate may normalize the aPTT by temporarily replacing the factor IX. The administration of BeneFIX increases plasma levels of factor IX, and can temporarily correct the coagulation defect in these patients. Coagulation Factor IX is an important protein in the process of hemostasis and normal blood clotting as it plays a key role within the coagulation cascade. It is located within the blood plasma as a zymogen, an antecedent to enzymatic function, in its inactivated state. Factor IX is dependent on the presence of Vitamin K, and is activated to a serine protease by the function of Coagulation Factor XIa. Factor XIa cleaves the peptide bond associated with protein activation in Factor IX, leaving Factor IX with two exposed chains, a light chain and a heavy chain. These two chains are held together by several disulfide bonds that reinforce the structure of Factor IX's activated form. After being activated, Factor IX forms a complex with calcium ions, membrane phospholipids and Coagulation Factor VIII to activate Coagulation Factor X. The activation of Factor X then performs a similarly integral step in the blood coagulation cascade. The ultimate result of phenotypically normal coagulation factors is the creation of platelets for normal blood clotting.",,,,Coagulation Factor IX Human is approved.,Coagulation Factor IX Human is a liquid.,True
15980,"Nonacog beta pegol is a recombinant coagulation factor IX derivative. It is produced without animal-derived materials and with an attached 40kDa polyethylene glycol (PEG) molecule for peptide activation by a site-directed glycoPEGylation. Once activated, the activation molecule with PEG are cleaved to leave the activated factor IX (Factor IXa). Nonacog beta pegol was developed by Novo Nordisk, obtained EMA marketing authorisation in June 6, 2017. Nonacog beta pegol is indicated for the use in adults and children with hemophilia B for control and prevention of bleeding episodes, routine prophylaxis and perioperative management. In the EMA approval, it is also indicated for on-demand treatment of bleeding episodes. Hemophilia B is characterized by a deficiency in the coagulation factor IX which results in prolonged oozing after injuries and delayed or recurring bleeding prior wound healing. Hemophilia B patients present more frequent bleeding episodes during childhood and adolescence than in adulthood. After nonacog beta pegol is activated by the coagulation factor IXa and tissue-coagulation factor VIIa, the peptide is cleaved off. In preclinical studies, once the peptide is free, there was a restoration of whole blood clotting time activity and the activated-partial thromboplastin time was returned to normal limits. In clinical trials, the administration of nonacog beta pegol significantly increased the levels of factor IX in plasma and temporarily correct the level of activated partial thromboplastin time. The effect of nonacog beta pegol translated into good hemostasis when used to treat bleeds on-demand and in a reduction of annualized bleeding rates when used as prophylaxis without formation of factor IX inhibitors, allergic reactions or thromboembolic complications. The reports in clinical trials have also shown a significant prolongation in the duration of the hemostatic effect. Nonacog beta pegol is activated by the factor IXa and the tissue complex factor VII. When activated, the peptide including the 40kDa PEG moiety is cleaved off leaving an activated recombinant factor IX ready to be part of the coagulation cascade replacing the missing clotting factor IX. Thus, after activation, nonacog beta pegol will present the same mechanism of action than the endogenous coagulation factor IXa. The activated coagulation factor IX function is, in combination with the factor VIIIa, to activate the coagulation factor X to trigger the coagulation cascade that finalizes in the conversion of prothrombin into thrombin and the thrombin-driven conversion of fibrinogen into fibrin for the formation of a clot.",,,,Nonacog beta pegol is approved and investigational.,Nonacog beta pegol is a solid.,True
15981,"In recent years, various extended half-life factor VIII and factor IX preparations have been studied and gained approval. In order to extend half-lives, techniques such as fusion to protein conjugates (Fc part of IgG1 or albumin), chemical modification (PEGylation), and protein sequence modification have been utilized. Indicated for use in previously treated adults and adolescents (12 years of age and above) with hemophilia A (congenital Factor VIII deficiency) for: This agent is engineered to prolong blood FVIII activity while maintaining coagulation activity using PEGylation, where a PEG (Polyethylene glycol) molecule is continually attached to the factor VIII protein at a specific site ,. This prevents and controls bleeding episodes associated with hemophilia A. This drug is a site-specifically PEGylated recombinant antihemophilic factor, which temporarily replaces the missing coagulation Factor VIII. The site-specific PEGylation in the A3 domain reduces binding to the physiological Factor VIII clearance receptors resulting in a longer half-life and increased AUC (area under the curve).",,,,Damoctocog alfa pegol is approved and investigational.,Damoctocog alfa pegol is a solid.,True
15982,"A drug that is used in the management of inflammatory bowel diseases. Its activity is generally considered to lie in its metabolic breakdown product, 5-aminosalicylic acid (see mesalamine) released in the colon. (From Martindale, The Extra Pharmacopoeia, 30th ed, p907) For the treatment of Crohn's disease and rheumatoid arthritis as a second-line agent. Sulfasalazine is an anti-inflammatory indicated for the treatment of ulcerative colitis and rheumatoid arthritis. The mode of action of Sulfasalazine or its metabolites, 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP), is still under investigation, but may be related to the anti-inflammatory and/or immunomodulatory properties that have been observed in animal and <i>in vitro</i> models, to its affinity for connective tissue, and/or to the relatively high concentration it reaches in serous fluids, the liver and intestinal walls, as demonstrated in autoradiographic studies in animals. In ulcerative colitis, clinical studies utilizing rectal administration of Sulfasalazine, SP and 5-ASA have indicated that the major therapeutic action may reside in the 5-ASA moiety. The relative contribution of the parent drug and the major metabolites in rheumatoid arthritis is unknown.",The molecular weight is 398.39.,Sulfasalazine has a topological polar surface area of 141.31.,The log p value of  is 3.99.,Sulfasalazine is approved.,Sulfasalazine is a solid.,True
15983,"Carprofen is a non-steroidal anti-inflammatory drug (NSAID) that is used by veterinarians as a supportive treatment for the relief of arthritic symptoms in geriatric dogs. Carprofen was previously used in human medicine for over 10 years (1985-1995). It was generally well tolerated, with the majority of adverse effects being mild, such as gastro-intestinal pain and nausea, similar to those recorded with aspirin and other non-steroidal anti-inflammatory drugs. It is no longer marketed for human usage, after being withdrawn on commercial grounds. For use as a pain reliever in the treatment of joint pain and post-surgical pain. Carprofen is a non-steroidal anti-inflammatory drug (NSAID) of the propionic acid class that includes ibuprofen, naproxen, and ketoprofen. It is no longer used in the clinical setting, but is approved for use in dogs. Carprofen is non-narcotic and has characteristic analgesic and antipyretic activity approximately equipotent to indomethacin in animal models. The mechanism of action of carprofen, like that of other NSAIDs, is believed to be associated with the inhibition of cyclooxygenase activity. Two unique cyclooxygenases have been described in mammals. The constitutive cyclooxygenase, COX-1, synthesizes prostaglandins necessary for normal gastrointestinal and renal function. The inducible cyclooxygenase, COX-2, generates prostaglandins involved in inflammation. Inhibition of COX-1 is thought to be associated with gastrointestinal and renal toxicity while inhibition of COX-2 provides anti-inflammatory activity. In an <i>in vitro</i> study using canine cell cultures, carprofen demonstrated selective inhibition of COX-2 versus COX-1.",The molecular weight is 273.72.,Carprofen has a topological polar surface area of 53.09.,The log p value of  is 3.98.,Carprofen is approved and vet_approved and withdrawn.,Carprofen is a solid.,True
15984,"Oxaprozin is a non-narcotic, non-steroidal anti-inflammatory drug (NSAID), used to relieve the inflammation, swelling, stiffness, and joint pain associated with osteoarthritis and rheumatoid arthritis. Used to relieve the inflammation, swelling, stiffness, and joint pain associated with rheumatoid arthritis and osteoarthritis. Oxaprozin is a nonsteroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic properties. Oxaprozin is used to treat rheumatoid arthritis, osteoarthritis, dysmenorrhea, and to alleviate moderate pain. Anti-inflammatory effects of Oxaprozin are believed to be due to inhibition of cylooxygenase in platelets which leads to the blockage of prostaglandin synthesis. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation. Oxaprozin is a non-selective NSAID, with a cell assay system showing lower COX-2 selectivity implying higher COX-1 selectivity.  ",The molecular weight is 293.32.,Oxaprozin has a topological polar surface area of 63.33.,The log p value of  is 2.95.,Oxaprozin is approved.,Oxaprozin is a solid.,True
15985,"Balsalazide is an anti-inflammatory drug used in the treatment of Inflammatory Bowel Disease. It is sold under the name \Colazal\"" in the US and \""Colazide\"" in the UK."" For the treatment of mildly to moderately active ulcerative colitis. Balsalazide is a prodrug that has little or no pharmacologic activity until it is enzymatically cleaved in the colon to produce mesalamine (5-aminosalicylic acid), an anti inflammatory drug indicated for the treatment of mildly to moderately active ulcerative colitis. Balsalazide disodium is delivered intact to the colon where it is cleaved by bacterial azoreduction to release equimolar quantities of mesalamine, which is the therapeutically active portion of the molecule, and the intert 4-aminobenzoyl-(beta)-alanine. As a result, the spectrum of pharmacologic activity of balsalazide is similar to that of mesalamine. The mechanism of action of 5-aminosalicylic acid is unknown, but appears exert its anti-inflammatory effects locally (in the GI tract) rather than systemically. Mucosal production of arachidonic acid metabolites, both through the cyclooxygenase pathways (catalyzes the formation of prostaglandin precursors from arachidonic acid), and through the lipoxygenase pathways (catalyzes the formation of leukotrienes and hydroxyeicosatetraenoic acids from arachidonic acid and its metabolites), is increased in patients with chronic inflammatory bowel disease. Therefore, it is possible that 5-aminosalicylic acid diminishes inflammation by blocking production of arachidonic acid metabolites in the colon through both the inhibition of cyclooxygenase and lipoxygenase.",The molecular weight is 357.32.,Balsalazide has a topological polar surface area of 148.65.,The log p value of  is 3.32.,Balsalazide is approved and investigational.,Balsalazide is a solid.,True
15986,"Salsalate is a nonsteroidal anti-inflammatory agent for oral administration. Salsalate's mode of action as an anti-inflammatory and antirheumatic agent may be due to inhibition of synthesis and release of prostaglandins. The usefulness of salicylic acid, the active in vivo product of salsalate, in the treatment of arthritic disorders has been established. In contrast to aspirin, salsalate causes no greater fecal gastrointestinal blood loss than placebo. Salsalate is readily soluble in the small intestine where it is partially hydrolyzed to two molecules of salicylic acid. A significant portion of the parent compound is absorbed unchanged and undergoes rapid esterase hydrolysis in the body. The parent compound has an elimination half-life of about 1 hour. Salicylic acid (the active metabolite) biotransformation is saturated at anti-inflammatory doses of salsalate. Such capacity limited biotransformation results in an increase in the half-life of salicylic acid from 3.5 to 16 or more hours. For relief of the signs and symptoms of rheumatoid arthritis, osteoarthritis and related rheumatic disorders. Salsalate is a nonsteroidal anti-inflammatory agent for oral administration. Salsalate's mode of action as an anti-inflammatory and antirheumatic agent may be due to inhibition of synthesis and release of prostaglandins. The usefulness of salicylic acid, the active in vivo product of salsalate, in the treatment of arthritic disorders has been established. In contrast to aspirin, salsalate causes no greater fecal gastrointestinal blood loss than placebo. The mode of anti-inflammatory action of salsalate and other nonsteroidal anti-inflammatory drugs is not fully defined, but appears to be primarily associated with inhibition of prostaglandin synthesis. This inhibition of prostaglandin synthesis is done through the inactivation of cyclooxygenase-1 (COX-1) and COX-2, which are reponsible for catalyzing the formation of prostaglandins in the arachidonic acid pathway. Although salicylic acid (the primary metabolite of salsalate) is a weak inhibitor of prostaglandin synthesis in vitro, salsalate appears to selectively inhibit prostaglandin synthesis in vivo, providing anti-inflammatory activity equivalent to aspirin and indomethacin. Unlike aspirin, salsalate does not inhibit platelet aggregation.",The molecular weight is 258.23.,Salsalate has a topological polar surface area of 83.83.,The log p value of  is 3.33.,Salsalate is approved.,Salsalate is a solid.,True
15987,"Choline magnesium trisalicylate is a non-acetylated salicylate used widely as a nonsteroidal anti-inflammatory drug. Trisalicylate significantly reduces methotrexate renal clearance, displacing methotrexate from protein, increasing the fraction unbound by 28%. Choline magnesium trisalicylate is used to reduce pain and inflammation caused by conditions such as arthritis. This medication is also used to treat fever in adults. Trisalicylate-choline is a non-steroidal anti-inflammatory drug (NSAID) that contains a combination of choline salicylate and magnesium salicylate. Does not affect platelet aggregation. Inhibits prostaglandin synthesis; acts on the hypothalamus heat-regulating center to reduce fever; blocks the generation of pain impulses",The molecular weight is 539.82.,,,Choline magnesium trisalicylate is approved.,Choline magnesium trisalicylate is a solid.,True
15988,"Antrafenine is a piperazine derivative drug that acts as an analgesic and anti-inflammatory drug with similar efficacy to naproxen. It is not widely used as it has largely been replaced by newer drugs. Antrafenine is used as an anti-inflammatory and analgesic agent for the relief of mild to moderate pain. Its mode of action is not fully understood; however, its ability to inhibit prostaglandin synthesis may be involved in the anti-inflammatory effect. Antrafenine is believed to be associated with the inhibition of cyclooxygenase activity. Two unique cyclooxygenases have been described in mammals. The constitutive cyclooxygenase, COX-1, synthesizes prostaglandins necessary for normal gastrointestinal and renal function. The inducible cyclooxygenase, COX-2, generates prostaglandins involved in inflammation. Inhibition of COX-1 is thought to be associated with gastrointestinal and renal toxicity while inhibition of COX-2 provides anti-inflammatory activity.",The molecular weight is 588.55.,Antrafenine has a topological polar surface area of 57.7.,The log p value of  is 9.16.,Antrafenine is approved.,Antrafenine is a solid.,True
15989,"Tiaprofenic acid is a non-steroidal anti-inflammatory drug employed in the treatment of pain, particularly arthritis pain. It belongs to the _arylpropionic acid_ (profen) group of nonsteroidal anti-inflammatory drugs (NSAIDs). Tiaprofenic acid is used to treat pain, especially arthritic pain. Tiaprofenic acid is a non-steroidal anti-inflammatory drug of the arylpropionic acid (profen) class, used to treat pain, especially arthritic pain. The typical adult dose is 300mg twice daily. This drug is not recommended for use in the pediatric population. Tiaprofenic acid belongs to a group of medicines called non-steroidal anti-inflammatory drugs (NSAIDs). It works by blocking the production of a chemical (prostaglandin) which the body produces in response to injury or certain diseases. This prostaglandin would otherwise go on to cause swelling, pain and inflammation.",The molecular weight is 260.31.,Tiaprofenic acid has a topological polar surface area of 54.37.,The log p value of  is 2.54.,Tiaprofenic acid is approved.,Tiaprofenic acid is a solid.,True
15990,,,,,O-acetyl-L-serine is experimental.,O-acetyl-L-serine is a solid.,False
15991,"Hyperforin is a phytochemical generated by the plants of the Hypericum family. One of the most important members of this family, due to its medical properties, is _Hypericum perforatum_, also known as St John's wort. Hyperforin is believed to be the primary active constituent responsible for the antidepressant and anxiolytic properties of the extracts of St. John's wort. It acts as a reuptake inhibitor of monoamines, including serotonin, norepinephrine, dopamine, and of GABA and glutamate, with IC50 values of 0.05-0.10 mcg/ml for all compounds, with the exception of glutamate, which is in the 0.5 mcg/ml range. It appears to exert these effects by activating the transient receptor potential ion channel TRPC6. Activation of TRPC6 induces the entry of sodium and calcium into the cell which causes inhibition of monoamine reuptake. Hyperforin is also thought to be responsible for the induction of the cytochrome P450 enzymes CYP3A4 and CYP2C9 by binding to and activating the pregnane X receptor (PXR). Hyperforin is believed to be the primary active constituent responsible for the antidepressant and anxiolytic properties of the extracts of St. John's wort. It acts as a reuptake inhibitor of monoamines, including serotonin, norepinephrine, dopamine, and of GABA and glutamate, with IC50 values of 0.05-0.10 mcg/ml for all compounds, with the exception of glutamate, which is in the 0.5 mcg/ml range. It appears to exert these effects by activating the transient receptor potential ion channel TRPC6. Activation of TRPC6 induces the entry of sodium and calcium into the cell which causes inhibition of monoamine reuptake.",,,,Hyperforin is nutraceutical.,Hyperforin is a solid.,True
15992,,,,,(+)-2-(4-biphenyl)propionic acid is experimental.,(+)-2-(4-biphenyl)propionic acid is a solid.,False
15993,,,,,Protoporphyrin Ix Containing Co is experimental.,Protoporphyrin Ix Containing Co is a solid.,False
15994,,,,,2-Bromoacetyl Group is experimental.,2-Bromoacetyl Group is a solid.,False
15995,,,,,(3-Chloro-4-Propoxy-Phenyl)-Acetic Acid is experimental.,(3-Chloro-4-Propoxy-Phenyl)-Acetic Acid is a solid.,False
15996,,,,,Acetic Acid Salicyloyl-Amino-Ester is experimental.,Acetic Acid Salicyloyl-Amino-Ester is a solid.,False
15997,,,,,P-(2'-Iodo-5'-Thenoyl)Hydrotropic Acid is experimental.,P-(2'-Iodo-5'-Thenoyl)Hydrotropic Acid is a solid.,False
15998,,,,,Flurbiprofen Methyl Ester is experimental.,Flurbiprofen Methyl Ester is a solid.,False
15999,"Nepafenac is a non-steroidal anti-inflammatory prodrug (NSAID) usually sold as a prescription eye drop. It is used to treat pain and inflammation associated with cataract surgery. For the treatment of pain and inflammation associated with cataract surgery. Low but quantifiable plasma concentrations of nepafenac and amfenac were observed in the majority of subjects 2 and 3 hours postdose, respectively, following bilateral topical ocular TID dosing of nepafenac ophthalmic suspension, 0.1%. The mean steady-state Cmax for nepafenac and for amfenac were 0.310 ± 0.104 ng/ml and 0.422 ± 0.121 ng/ml, respectively, following ocular administration. Nepafenac is a prodrug. After penetrating the cornea, nepafenac undergoes rapid bioactivation to amfenac, which is a potent NSAID that uniformly inhibits the COX1 and COX2 activity.",The molecular weight is 254.29.,Nepafenac has a topological polar surface area of 86.18.,The log p value of  is 1.38.,Nepafenac is approved and investigational.,Nepafenac is a solid.,True
16000,,,,,2--n-acetamide is experimental.,2--n-acetamide is a solid.,False
16001,,,,,1-(4-IODOBENZOYL)-5-METHOXY-2-METHYL INDOLE-3-ACETIC ACID is experimental.,1-(4-IODOBENZOYL)-5-METHOXY-2-METHYL INDOLE-3-ACETIC ACID is a solid.,False
16002,,,,,2--n-acetamide is experimental.,2--n-acetamide is a solid.,False
16003,"Droxicam is an oxicam non-steroidal anti-inflammatory drug and a prodrug of. It is used to reduce pain and inflammation in musculoskeletal disorders such as rheumatoid arthritis and osteoarthritis. Droxicam is an NSAID previously used for the treatment of inflammation and rheumatoid arthritis. Droxicam is a prodrug of. Droxicam administration produces anti-inflammatory, antirheumatic, analgesic, and antipyretic effects similar to. Droxicam is converted to via hydrolysis of the ester group in the intestine. Droxicam administration inhibits the synthesis of prostaglandins by cyclooxygenase enzymes.",The molecular weight is 357.34.,Droxicam has a topological polar surface area of 96.88.,The log p value of  is 0.19.,Droxicam is withdrawn.,Droxicam is a solid.,True
16004,"Phenyl salicylate is a 2-hydroxybenzoic acid phenyl ester. It is utilized in some manufacturing processes of polymers, lacquers, adhesives, waxes, as well as polishes. It is an active ingredient in some pharmaceutical products as a mild analgesic for pain relief by releasing salicylate (found in ). Phenyl salicylate may also be found in some antiseptic agents. It is synthesized by heating salicylic acid with phenol ,. Pain and fever. Phenyl salicylate has several medical uses. It can be used as an analgesic to relieve pain, as an antiseptic with antibacterial effect as well as a kind of antipyretic for the treatment of fever. It is also used for the treatment of inflammation in the lower urinary tract. It is no longer commonly applied to human medical practice but is still used in veterinary medicine. Inhibits the activity of the enzyme known as cyclooxygenase (COX) which causes the formation of prostaglandins, substances which cause inflammation, swelling, pain, and fever. For more information, refer to the drug entry.",The molecular weight is 214.22.,Phenyl salicylate has a topological polar surface area of 46.53.,The log p value of  is 3.84.,Phenyl salicylate is approved.,Phenyl salicylate is a solid.,True
16005,"Trolamine salicylate is an organic compound or a salt formed between triethanolamine and salicylic acid. Triethanolamine neutralizes the acidity of the salicylic acid. It is a topical analgesic used for temporary relief of minor pain associated with arthritis, simple backache, muscle strains, sprains, and bruises. Unlike other topical analgesics, trolamine salicylate has no distinct odor which improves patient acceptability. It also displays low systemic absorption upon dermal or topical administration and has low skin irritant properties. As with other salicylates, trolamine salicylate is an inhibitor of cyclo-oxygenase (COX) enzymes with no reported selectivity towards a specific enzyme isoform. Trolamine salicylate serves as an active ingredient in topical over-the-counter products for temporary management of mild to moderate muscular and joint pains. Indicated for the temporary relief of aches, and pains of muscles and joints associated with backache, lumbago, strains, bruises, sprains and arthritic or rheumatic pain, pain of tendons and ligaments. Trolamine salicylate is a salicylate that inhibits cyclo-oxygenase (COX) enzymes responsible for generating pro-inflammatory factors such as to induce pain and inflammation. It is thought to mediate its analgesic effect through inhibition of COX-2 enzyme, which is an induced enzyme responsible for inflammatory responses and pain in muscle and joint disorders. By inhibiting fatty acid COX enzyme, trolamine salicylate inhibits the production of prostaglandins and thromboxanes in inflammatory cells involved in generating pain and inflammation. It thereby works to temporarily reduce mild to moderate pain. In subjects with muscle soreness from exercise, administration of topical trolamine salicylate was associated with reduced duration and severity of muscule soreness compared to placebo. In subjects with osteoarthritis in hands, trolamine salicylate cream was shown to be effective in achieving temporary relief of minor pain and stiffness. Inflammation and tissue damage in different conditions including arthritis, bursitis, joint disorder, bruises, and strains or sprains of muscle origin, induce mild to moderate pain and are associated with increase prostaglandin synthesis. This is thought to be a result of COX-2 enzyme induction. COX-2 is induced in inflammatory cells in case of cell injury, infection or activation from inflammatory cytokines such as interleukin (IL)-1 and tumor necrosis factor (TNF)-α. Upon activation, COX-2 produces prostanoid mediators of inflammation such as prostaglandins and thromboxanes. Trolamine salicylate mediates its analgesic effect by inhibiting the production of inflammatory mediators that sensitize nociceptive nerve endings and generate pain.",The molecular weight is 287.31.,Trolamine salicylate has a topological polar surface area of 60.36.,,Trolamine salicylate is approved.,,True
16006,"Menthyl salicylate is an ester of menthol and salicylic acid. Menthol and methyl salicylate are known as counterirritants. They work by causing the skin to feel cool and then warm. Used together, they provide symptomatic relief for mild to moderate muscular and joint aches and pains, muscle cramps, shoulder aches and stiff neck..",The molecular weight is 276.38.,Menthyl salicylate has a topological polar surface area of 46.53.,The log p value of  is 6.33.,Menthyl salicylate is approved.,Menthyl salicylate is a liquid.,True
16007,"Glycol salicylate, also known as _2-hydroxyethyl salicylate_, is a benzoate ester formed from the condensation of the carboxy group of salicylic acid with one of the hydroxy groups of ethylene glycol. It is found as an active ingredient and topical analgesic in patches used to provide relief for mild to moderate muscle and joint pain.  This drug is only recommended for topical usages for the relief of muscular and rheumatic pain in human and animals. Temporarily relieves minor to moderate aches and pains. Works with ingredients such as menthol, which has counter-irritant properties. Counter-irritants are externally applied, and lead to irritation or mild inflammation of the skin to relieve pain in muscles or joints by reducing inflammation in deeper adjacent structures. Counter-irritants relieve pain by disrupting the brain from receiving pain signals resulting from conditions such as osteoarthritis (OA) or injuries such as sprains or strains. These agents may cause vasodilatation or skin irritation, leading to a false sensation of heat or warmth. Similar to other salicylates. Salicylates and other analgesics and anti-inflammatory drugs, particularly the non-steroidal anti-inflammatory drugs (NSAID) mainly used in rheumatology, inhibit cyclooxygenase, therefore reducing prostaglandin synthesis. ",The molecular weight is 182.18.,Glycol salicylate has a topological polar surface area of 66.76.,The log p value of  is 1.45.,Glycol salicylate is approved.,Glycol salicylate is a liquid.,True
16008,Nitroaspirin has been investigated for the treatment of Intermittent Claudication.,,,,Nitroaspirin is investigational.,,True
16009,"Bufexamac is a non-steroidal anti-inflammatory drug (NSAID) under the market name Droxaryl, Malipuran, Paraderm and Parfenac. It is typically administered topically for the treatment of subacute and chronic eczema of the skin, including atopic eczema and other inflammatory dermatoses, as well as sunburn and other minor burns, and itching. It has also been used in suppositories in combination with local anaesthetics indicated for haemorrhoids. The use of bufexamac has been discontinued in Canada and the United States, which may be due to undetermined clinical efficacy and a high prevalence of contact sensitization. Bufexamac was also withdrawn by the EMA in April 2010. Indicated for the treatment of various skin conditions, such as atopic eczema and other inflammatory dermatoses.  Bufexamac is a topically-active anti-inflammatory agent that inhibits the cyclooxygenase enzyme. In cutaneous and deep experimental inflammation, topical administration of bufexamac exerted a dose-related anti-inflammatory effect. In guinea pigs, bufexamax was shown to be more active than topical acetylsalicylic acid 5% or phenylbutazone 5% in delaying the local increase in temperature resulting from UV exposure. Bufexamac is unlikely to have any effect on wound healing. The full mechanism of action is unclear. It is proposed that bufexamac acts similarly to other non-steroidal anti-inflammatory drugs to inhibit prostaglandin biosynthesis _in vitro_, via inhibiting cyclo-oxygenase (COX) enzymes. Systematically administered bufexamac may accumulate preferentially in the adrenal cortex of rats and may play a role in adrenal stimulation; however its topical anti-inflammatory action is likely to be independent of this effect. ",The molecular weight is 223.27.,Bufexamac has a topological polar surface area of 58.56.,The log p value of  is 1.85.,Bufexamac is approved and withdrawn.,Bufexamac is a solid.,True
16010,"Bendazac is an oxyacetic acid. Despite possessing anti-inflammatory, anti-necrotic, choleretic, and anti-lipidemic characteristics, most research has revolved around studying and demonstrating the agent's principal action in inhibiting the denaturation of proteins - an effect that has primarily proven useful in managing and delaying the progression of ocular cataracts. Bendazac, however, has since been withdrawn or discontinued in various international regions due to its capability or risk for eliciting hepatotoxicity in patients although a small handful of regions may continue to have the medication available for purchase and use either as a topical anti-inflammatory/analgesic cream or eye drop formulation. Prior to the withdrawal of bendazac from various international regions of use due to concerns for hepatotoxicity the chemical had demonstrated potential usefulness predominantly as the prescription medication bendazac lysine for the indication of managing the level of vision in patients with mild to moderate cataracts to facilitate delaying the need for surgical intervention. Bendazac principally demonstrates an antidenaturant action on proteins. This effect has been shown to inhibit the denaturation of various proteins like ocular lens proteins by heat, ultraviolet radiation, free radicals, and other chemicals. The medication may be administered to patients via a number of different formulations, including orally as the lysine salt, as eye drops, or even topical applications for the skin. Bendazac seems to elicit an anticataract action by inhibiting the denaturation of ocular lens proteins, although the precise mechanisms by which this action occurs has not yet been formally elucidated - despite there being many proposed mechanisms. In particular, the denaturation of lens proteins may in part be prevented by inhibiting the binding of certain chemicals like cyanates or sugars and 5-hydroxybendazac - the major metabolite of bendazac - has been shown to be capable of inhibiting the glycosylation of lens proteins by sugars like galactose or glucose-6-phosphate in a dose-dependent manner. Moreover, the apparent ability for administered bendazac to elicit free radical scavenger activities due to interactions with protein molecules suggests that the medication may also be able to prevent the oxidation of lens proteins by free radicals in the development of cataracts. Furthermore, bendazac may also be capable of reducing the sulfhydryl group oxidation of lens proteins by the saliva, serum, or urine from patients with cataracts following single dose administration and reduce biological liquid oxidant activity (BLOA) in doing so.",The molecular weight is 282.3.,Bendazac has a topological polar surface area of 64.35.,The log p value of  is 3.08.,Bendazac is approved and withdrawn.,,True
16011,"An antipsychotic agent used in schizophrenia.  For the management of the manifestations of psychotic disorders such as schizophrenia Loxapine, a dibenzoxazepine compound, represents a subclass of tricyclic antipsychotic agents, chemically distinct from the thioxanthenes, butyrophenones, and phenothiazines. Pharmacologically, Loxapine is a tranquilizer for which the exact mode of action has not been established, however, it is believed that by antagonising dopamine and serotonin receptors, there is a marked cortical inhibition which can manifest as tranquilization and suppression of aggression. Loxapine is a dopamine antagonist, and also a serotonin 5-HT2 blocker. The exact mode of action of Loxapine has not been established, however changes in the level of excitability of subcortical inhibitory areas have been observed in several animal species in association with such manifestations of tranquilization as calming effects and suppression of aggressive behavior.",The molecular weight is 327.81.,Loxapine has a topological polar surface area of 28.07.,The log p value of  is 3.98.,Loxapine is approved.,Loxapine is a solid.,True
16012,"A dopamine D1 receptor agonist that is used as an antihypertensive agent. It lowers blood pressure through arteriolar vasodilation. For the in-hospital, short-term (up to 48 hours) management of severe hypertension when rapid, but quickly reversible, emergency reduction of blood pressure is clinically indicated, including malignant hypertension with deteriorating end-organ function. Fenoldopam is an agonist at D<sub>1</sub>-like dopamine receptors, binds to &alpha;<sub>2</sub>-adrenoceptors, increasing renal blood flow. Fenoldopam is a rapid-acting vasodilator. It is an agonist for D<sub>1</sub>-like dopamine receptors and binds with moderate affinity to &alpha;<sub>2</sub>-adrenoceptors. It has no significant affinity for D<sub>2</sub>-like receptors, &alpha;<sub>1</sub> and &beta;-adrenoceptors, 5<sub>HT1</sub> and 5<sub>HT2</sub> receptors, or muscarinic receptors. Fenoldopam is a racemic mixture with the R-isomer responsible for the biological activity. The R-isomer has approximately 250-fold higher affinity for D<sub>1</sub>-like receptors than does the S-isomer. In non-clinical studies, fenoldopam had no agonist effect on presynaptic D<sub>2</sub>-like dopamine receptors, or &alpha; or &beta; -adrenoceptors, nor did it affect angiotensin-converting enzyme activity. Fenoldopam may increase norepinephrine plasma concentration.",The molecular weight is 305.76.,Fenoldopam has a topological polar surface area of 72.72.,The log p value of  is 2.4.,Fenoldopam is approved.,Fenoldopam is a solid.,True
16013,"Carphenazine is an antipsychotic drug, used in hospitalized patients in the management of chronic schizophrenic psychoses. Used in the treatment of acute or chronic schizophrenic reactions in hospitalized patients. Carphenazine is a phenothiazine antipsychotic agent with a piperazine side-chain. A yellow, powdered, phenothiazine antipsychotic agent used in the treatment of acute or chronic schizophrenia. The term \phenothiazines\"" is used to describe the largest of the five main classes of neuroleptic antipsychotic drugs. These drugs have antipsychotic and, often, antiemetic properties, although they may also cause severe side effects such as akathisia, tardive dyskinesia and extrapyramidal symptoms. Carphenazine blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain; depresses the release of hypothalamic and hypophyseal hormones and is believed to depress the reticular activating system thus affecting basal metabolism, body temperature, wakefulness, vasomotor tone, and emesis.""",The molecular weight is 425.59.,Carphenazine has a topological polar surface area of 47.02.,The log p value of  is 3.44.,Carphenazine is withdrawn.,Carphenazine is a solid.,True
16014,"Chlorprothixene is a typical antipsychotic drug of the thioxanthene (tricyclic) class. Chlorprothixene exerts strong blocking effects by blocking the 5-HT2 D1, D2, D3, histamine H1, muscarinic and alpha1 adrenergic receptors. For treatment of psychotic disorders (e.g. schizophrenia) and of acute mania occuring as part of bipolar disorders. Chlorprothixene is a typical antipsychotic drug of the thioxanthine class. It has a low antipsychotic potency (half to 2/3 of chlorpromazine). Chlorprothixene has not thoroughly demonstrated an antidepressant or analgesic effect but it has demonstrated antiemetic effects. It is used in the treatment of nervous, mental, and emotional conditions. Improvement in such conditions is thought to result from the effect of the medicine on nerve pathways in specific areas of the brain. Chlorprothixene has a similar side effect profile to chlorpromazine, though allergic side effects and liver damage are less frequent. Chlorprothixene blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain; depresses the release of hypothalamic and hypophyseal hormones and is believed to depress the reticular activating system thus affecting basal metabolism, body temperature, wakefulness, vasomotor tone, and emesis.",The molecular weight is 315.86.,Chlorprothixene has a topological polar surface area of 3.24.,The log p value of  is 5.48.,Chlorprothixene is approved and experimental and investigational and withdrawn.,Chlorprothixene is a solid.,True
16015,"Periciazine is a phenothiazine of the piperidine group. It has been shown to reduce pathologic arousal and affective tension in some psychotic patients, while the symptoms of abnormal mental integration are relatively unaffected. It is a sedative phenothiazine with weak antipsychotic properties. It also has adrenolytic, anticholinergic, metabolic and endocrine effects and an action on the extrapyramidal system. It is used as an adjunctive medication in some psychotic patients, for the control of residual prevailing hostility, impulsiveness and aggressiveness. Pericyazine, like other phenothiazines, is presumed to act principally in the subcortical areas, by producing what has been described as a central adrenergic blockade. For use as adjunctive medication in some psychotic patients. Propericiazine (Pericyazine)is used for the control of residual prevailing hostility, impulsiveness and aggressiveness.  Pericyazine is a phenothiazine of the piperidine group. It has been shown to reduce pathologic arousal and affective tension in some psychotic patients, while the symptoms of abnormal mental integration are relatively unaffected. It is a sedative phenothiazine with weak antipsychotic properties. It also has adrenolytic, anticholinergic, metabolic and endocrine effects, and an action on the extrapyramidal system. Pericyazine, like other phenothiazines, is presumed to act principally in the subcortical areas, by producing what has been described as a central adrenergic blockade of the alpha adrenergic receptors as well as antagonism of the D(1) dopamine receptor.",The molecular weight is 365.5.,Periciazine has a topological polar surface area of 50.5.,The log p value of  is 3.44.,Periciazine is approved and investigational.,Periciazine is a solid.,True
16016,"Pipamperone is a typical antipsychotic of the _butyrophenone_ family used in the treatment of schizophrenia. It was developed by Janssen Pharmaceutica in 1961 and started its first round of clinical trials in 1963. Treatment of chronic psychoses and states of aggressiveness of various origins. Pipamperone is an antipsychotic medication that has sedative effects, which may be beneficial in the management of agitation and disordered sleep. Pipamperone, showing antidopaminergic and anti-serotonergic properties, has been noted for its anti- Pipamperone binds mainly to 5-HT2A receptors, with a nearly equal affinity to D4 receptors and a moderate affinity for 5-HT2C, D2, D3, 1- and 2B-adrenoceptors.",The molecular weight is 375.49.,Pipamperone has a topological polar surface area of 66.64.,The log p value of  is 2.24.,Pipamperone is investigational.,Pipamperone is a solid.,True
16017,"Dihydrexidine has been used in trials studying the treatment of SPD, Cocaine-Related Disorders, and Schizotypal Personality Disorder.",,,,Dihydrexidine is investigational.,,True
16018,"Vatalanib (PTK787/ZK-222584) is a new oral antiangiogenic molecule that inhibits all known vascular endothelial growth factor receptors. Vatalanib is under investigation for the treatment of solid tumors. Used in combination with first- and second-line chemotherapy for the treatment of metastatic colorectal cancer and non-small cell lung cancer (NSCLC). Vatalanib is a novel oral angiogenesis inhibitor being developed by Schering (in collaboration with Novartis AG). Vatalanib selectively inhibits the tyrosine kinase domains of vascular endothelial growth factor (VEGF) receptors, platelet-derived growth factor (PDGF) receptor, and c-KIT. Vatalanib potently inhibits vascular endothelial growth factor (VEGF) receptor tyrosine kinases, important enzymes in the formation of new blood vessels that contribute to tumor growth and metastasis.",,,,Vatalanib is investigational.,Vatalanib is a solid.,True
16019,"TG100801 is a topically applied kinase inhibitor in macular degeneration patients. It is administered noninvasively as an eye drop and is designed to suppress VEGF mediated leakage and additional kinase targets associated with inflammation, edema, and angiogenesis which are the pathological hallmarks of AMD and other back of the eye diseases including diabetic macular edema and proliferative diabetic retinopathy. Investigated for use/treatment in macular degeneration. In cell based assays, following topical instillation, TG100572, the active drug produced by conversion of TG100801 as it penetrates the eye, was shown to induce apoptosis in proliferating endothelial cells responsible for neovasculariztion and to inhibit inflammatory-mediated processes as measured by endotoxin-induced nitric oxide release in vitro. TG100801 is the first topically applied, multitargeted vascular endothelial growth factor receptor (VEGFR)/Src kinase inhibitor to advance into the clinic. TG100801 significantly reduced VEGF mediated retinal leakage and choroidal neovascularization in relevant pre-clinical models of macular degeneration. In cell based assays, following topical instillation, TG100572, the active drug produced by conversion of TG100801 as it penetrates the eye, was shown to induce apoptosis in proliferating endothelial cells responsible for neovasculariztion and to inhibit inflammatory-mediated processes as measured by endotoxin-induced nitric oxide release in vitro.",,,,TG-100801 is investigational.,TG-100801 is a solid.,True
16020,"Denibulin is a novel small molecule Vascular Disrupting Agent under development by MediciNova for treatment of solid tumor cancers. Investigated for use/treatment in solid tumors. Denibulin selectively disrupts newly-formed tumor blood vessels, shutting down tumor blood flow and causing central necrosis of solid tumors. Consistent with its proposed mechanism of action, denibulin has been shown to reduce tumor blood flow resulting in tumor cell necrosis in rats bearing a human lung tumor xenograft. The present Phase I study now extends these findings (reductions in tumor blood flow) to cancer patients.",,,,Denibulin is investigational.,Denibulin is a solid.,True
16021,"ABT-869 is a small molecule vascular endothelial growth factor (VEGF) receptor-based kinase inhibitor that is designed to suppress tumor growth by preventing the formation of new blood vessels that supply the tumor with oxygen and nutrients and by inhibiting key angiogenic signaling pathways. ABT-869 is intended for the treatment of hematologic malignancies and the solid tumors. Investigated for use/treatment in leukemia (myeloid), myelodysplastic syndrome, and solid tumors. ABT-869 was effective in a broad range of cancers including small cell lung carcinoma, colon carcinoma, breast carcinoma and MV4-11 tumors in vitro and in vivo. ABT-869 induced significant apoptosis in cells with FLT3 mutation in vitro (IC50 value of 4 nM) and profound anti-leukemic effect in a mouse xenograft model. However, in vitro ABT-869 only shows minimal cytotoxic effect on AML cells with wild-type FLT3. Based on the preclinical studies suggesting the role of VEGF pathways in leukemogenesis, it is likely that the anti-leukemic effect of ABT-869 will be best evaluated in vivo. ABT-869, a multi-targeted receptor tyrosine kinase inhibitor, has been shown to inhibit of all members of the VEGF and PDGF receptor families (e.g., KDR IC50 value of 4 nM), and have less activity (IC50 values >1 µM) against unrelated receptor tyrosine kinases, soluble tyrosine kinases and serine/threonine kinases. In addition, it exhibits potent anti-proliferative and apoptotic effects on tumor cells dependent on mutant, constitutively active, FLT3 and KIT kinases.",,,,ABT-869 is investigational.,ABT-869 is a solid.,True
16022,"IMC-1C11 is an anti-angiogenesis agent. It is a chimeric anti-kinase insert domain-containing receptor (KDR) antibody that blocks VEGFR-KDR interaction and inhibits VEGFR-induced endothelial cell proliferation. IMC-1C11 is used for treatment of patients with liver metastases from colorectal carcinoma. Investigated for use/treatment in cancer/tumors (unspecified). IMC-1C11 is a chimerized antibody that targets the KDR receptor (also referred to as VEGFr) on vascular endothelial cells by inhibiting binding of the essential ligand, vascular endothelial growth factor (VEGF), to its receptor. KDR is a key receptor associated with tumor angiogenesis. As solid tumors cannot grow efficiently without new blood supply, use of IMC-1C11 results in the inhibition of tumor growth and death of tumor cells by apoptosis.",,,,IMC-1C11 is investigational.,IMC-1C11 is a solid.,True
16023,"Collagenase clostridium histolyticum is an enzyme produced by the bacterium Clostridium histolyticum. It is beneficial in the breakdown of collagen plaques for the treatment of Dupuytren's contracture and Peyronie's disease. The topical formulation is used for the debridement of necrotic tissue due to burns or chronic ulcers. Collagenase clostridium histolyticum is indicated for the treatment of adults with Dupuytren's contracture with a palpable cord. Additionally, it is used to treat men with Peyronie's disease diagnosed with a penile curvature deformity of at least a 30-degree angle at the beginning of therapy in addition to palpable plaques. Collagenase ointment is used for the tissue debridement of chronic dermal ulcers and severely burned tissues. Collagenase digests collagen, treating conditions such as Peyronie's disease, cellulite, chronic ulcers, burns, and contractures. Peyronie's disease is a fibrous lesion of the tunica albuginea in the penile tissues. Cellulite is a multifactorial condition resulting in the accumulation of fibrotic dermal septae and the expansion of subcutaneous fat. Dupuytren's contracture is a fibroproliferative disease that results in the fibrous deposition of collagen in the hands, limiting mobility and functionality of the hands. The collagen deposition in the abovementioned conditions is the target of collagenase enzyme therapy.",,,,Collagenase clostridium histolyticum is approved and investigational.,Collagenase clostridium histolyticum is a solid.,True
16024,"Halofuginone is a low molecular weight quinazolinone alkaloid, and a potent inhibitor of collagen alpha1(I) and matrix metalloproteinase 2 (MMP-2) gene expression. Halofuginone also effectively suppresses tumor progression and metastasis in mice. Collgard Biopharmaceuticals is developing halofuginone for the treatment of scleroderma and received orphan drug designation from the U.S. Food and Drug Administration in March, 2000. For the treatment of scleroderma, cancer, and restenosis. Halofuginone, a fully synthetic small molecule, is a potent and selective regulator of stromal cell activation, cell migration and Collagen type I synthesis, a process that has been identified as a 'master switch' in the body's tissue repair process. Halofuginone is a potent inhibitor of collagen a1(I) and matrix metalloproteinase 2 (MMP-2) gene expression. Halofuginone also suppresses extracellular matrix deposition and cell proliferation. The profound antitumoral effect of halofuginone is attributed to its combined inhibition of the tumor stromal support, vascularization, invasiveness, and cell proliferation.",,,,Halofuginone is investigational and vet_approved.,Halofuginone is a solid.,True
16025,"Clove oil is obtained by extraction from the dried flower buds of the clove plant. Traditionally, it has been used as a flavouring spice in foods, or as a fragrance. It is also found in topical analgesics. Clove oil has shown to exert some antimicrobial activities. The antioxidant and antimicrobial activity of clove is higher than that of many fruits, vegetables, and other spices. Clove oil is primarily indicated in conditions like colic, flatulence, and toothache. Clove (Eugenia caryophyllata Thunb. ) essential oil (CEO) has been demonstrated to possess antimicrobial, antifungal, antiviral, antioxidant, anti-inflammatory, anti-histamine, and anticancer properties. However, few studies have focused on its topical use ,. The chief constituent present in clove oil is the phenol \_eugenol_\"" which is present in amounts up to 85%. Clove oil acts as a germicide to Escherichia coli, Staphylococcus aureus and Pseudomonas aeruginosa. """,,,,Clove oil is approved and nutraceutical.,Clove oil is a liquid.,True
16026,"CYT997 is an orally available vascular argeting and cytotoxic agent that has proven effective in animal models of a wide range of tumour types including breast, prostate and colon, as well as some leukemias. Investigated for use/treatment in solid tumors. CYT997 is a vascular disrupting agent and a tubulin inhibitor for various cancers. The essential role of microtubules in cell division and the capacity of drugs that interact with the protein subunits of microtubules (α- and β-tubulin) to interfere with the cell cycle, have made tubulin a highly successful target for the development of therapeutic drugs, such as anti-cancer drugs and vascular disrupting agents.",,,,CYT997 is investigational.,CYT997 is a solid.,True
16027,"ZEN-012 is a novel small molecule and the first anti-cancer drug in development involving two mechanisms of action: tubulin and topoisomerase II inhibition. ZEN-012 also expresses additional modes of action such as pro-apoptotic and anti-angiogenic properties. It is developed for the treatment of solid tumors. Investigated for use/treatment in cancer/tumors (unspecified). In vitro: ZEN-012 has shown potent in vitro anti-proliferative activity at nanomolar concentrations against human tumor cell lines of different origin. ZEN-012 is active in tumor cell lines which are resistant to cisplatin and doxorubicin as well as to tubulin inhibitors such as vincristine and paclitaxel. Furthermore, it was shown thatZEN-012 is a catalytic inhibitor of the enzyme topoisomerase II with the same potency as amsacrine. Mode of action studies revealed that the compound ZEN-012 inhibits the polymerization of ß-tubulin in low micromolar concentrations. Competition studies suggest that ZEN-012 interacts with the same binding site on microtubules as colchicine. ZEN-012 destroys the mitotic spindles of the cancer cells, arrests the cancer cells in G2/M phase at low concentrations, mediates DNA fragmentation via inhibition of topoisomerase II and induces apoptosis via various mechanisms.",,,,ZEN-012 is investigational.,ZEN-012 is a solid.,True
16028,"Eribulin is a microtubule inhibitor indicated for the treatment of patients with metastatic breast cancer who have previously received at least two chemotherapeutic regimens for the treatment of metastatic disease. Eribulin was isolated from the marine sponge Halichondria okadai. Eribulin is also being investigated for use in the treatment of advanced solid tumors. For the treatment of patients with metastatic breast cancer who have previously received at least two chemotherapeutic regimens for the treatment of metastatic cancer.  Linear Eribulin inhibits the growth phase of microtubules without affecting the shortening phase and sequesters tubulin into nonproductive aggregates. Eribulin exerts its effects via a tubulin-based antimitotic mechanism leading to G2/M cell-cycle block, disruption of mitotic spindles, and, ultimately, apoptotic cell death after prolonged mitotic blockage. ",The molecular weight is 729.91.,Eribulin has a topological polar surface area of 146.39.,The log p value of  is 1.24.,Eribulin is approved and investigational.,Eribulin is a liquid.,True
16029,Milataxel has been used in trials studying the treatment of Mesothelioma. Milataxel enhances the rate of tubulin polymerization in vitro and causes the bundling of microtubules in cells.,,,,Milataxel is investigational.,,True
16030,"Phenethyl Isothiocyanate has been used in trials studying the prevention and treatment of Leukemia, Lung Cancer, Tobacco Use Disorder, and Lymphoproliferative Disorders.",,,,Phenethyl Isothiocyanate is investigational.,,True
16031,"Phenylalanine is an essential aromatic amino acid that is a precursor of melanin, , (norepinephrine), and. L-phenylalanine may be helpful in some with depression. It may also be useful in the treatment of vitiligo. There is some evidence that L-phenylalanine may exacerbate tardive dyskinesia in some schizophrenic patients and in some who have used neuroleptic drugs. Used by the brain to produce Norepinephrine, a chemical that transmits signals between nerve cells and the brain; keeps you awake and alert; reduces hunger pains; functions as an antidepressant and helps improve memory. The supposed antidepressant effects of L-phenylalanine may be due to its role as a precursor in the synthesis of the neurotransmitters norepinephrine and dopamine. Elevated brain norepinephrine and dopamine levels are thought to be associated with antidepressant effects. <br/>The mechanism of L-phenylalanine's possible antivitiligo activity is not well understood. It is thought that L-phenylalanine may stimulate the production of melanin in the affected skin",The molecular weight is 165.19.,Phenylalanine has a topological polar surface area of 63.32.,The log p value of  is -1.56.,Phenylalanine is approved and investigational and nutraceutical.,Phenylalanine is a solid.,True
16032,"OSI-930 is an orally active inhibitor of two clinically validated targets: c-Kit and the vascular endothelial growth factor receptor-2 (VEGFR-2). OSI-930 is designed to target both cancer cell proliferation and blood vessel growth (angiogenesis) in selected tumors. In preclinical studies, OSI-930 shows broad efficacy in tumor models representative of small cell lung cancer, glioblastoma, colorectal, renal, head and neck, non-small cell lung cancer and gastric cancers. Investigated for use/treatment in solid tumors. OSI-930 is a multi-targeted tyrosine kinase inhibitor that is designed to act as a potent co-inhibitor of the receptor tyrosine kinases c-Kit and VEGFR-2. The inhibition of the tyrosine kinase activity of Kit is expected to result in reduced cancer cell proliferation and increased cellular apoptosis in tumor types driven by Kit, resulting in inhibition of tumor growth. OSI-930 is also capable of inhibiting VEGFR-2. This receptor is present on endothelial cells and is a key mediator of blood vessel growth in response to the angiogenic growth factor VEGF. This pathway is believed to be the single most important mechanism for recruitment of new blood vessels in nearly all solid tumors. Inhibition of this pathway should therefore impact the growth and metastases of a wide range of angiogenesis-dependent malignancies. ",,,,OSI-930 is investigational.,OSI-930 is a solid.,True
16033,,,,,N-(4-chlorophenyl)-2-benzamide is experimental.,N-(4-chlorophenyl)-2-benzamide is a solid.,False
16034,"Foreskin fibroblast-like stromal cells (FDSCs) are progenitors isolated from human tissue that can differentiate into various cell types. This device is indicated for use for the treatment of full-thickness, diabetic foot ulcers greater than six weeks duration which extends through the dermis, but without tendon, muscle, joint capsule or bone exposure. This drug should be used in conjunction with standard wound care regimens and in patients with an adequate blood supply to the involved foot. This physiologically active dermal substitute is a scaffold upon which tissue can grow, allowing for effective healing of wounds. Dermagraft is a cryopreserved, human fibroblast-derived dermal substitute that contains fibroblasts, extracellular matrix, and a bioabsorbable polyglactin mesh scaffold. The fibroblasts are obtained from human newborn foreskin tissue. The fibroblasts are then placed on a scaffold and progress to proliferate and produce human dermal collagen, matrix proteins, growth factors, and cytokines. The above steps create a three-dimensional human dermal substitute with active human cells. Dermagraft does not contain macrophages, lymphocytes, blood vessels, nor hair follicles. It is available frozen as a single sheet (2 by 3 inches) for a single application.",,,,Foreskin fibroblast (neonatal) is approved.,Foreskin fibroblast (neonatal) is a solid.,True
16035,"A covalently linked dimeric nonessential amino acid formed by the oxidation of cysteine. Two molecules of cysteine are joined together by a disulfide bridge to form cystine. It has been claimed that L-cysteine has anti-inflammatory properties, that it can protect against various toxins, and that it might be helpful in osteoarthritis and rheumatoid arthritis. More research will have to be done before L-cysteine can be indicated for any of these conditions. Research to date has mostly been in animal models. L-Cystine is a covalently linked dimeric nonessential amino acid formed by the oxidation of cysteine. Two molecules of cysteine are joined together by a disulfide bridge to form cystine. Cystine is a chemical substance which naturally occurs as a deposit in the urine, and can form a calculus (hard mineral formation) when deposited in the kidney. The compound produced when two cysteine molecules linked by a disulfide (S-S) bond. Cystine is required for proper vitamin B6 utilization and is also helpful in the healing of burns and wounds, breaking down mucus deposits in illnesses such as bronchitis as well as cystic fibrosis. Cysteine also assists in the supply of insulin to the pancreas, which is needed for the assimilation of sugars and starches. It increases the level of glutathione in the lungs, liver, kidneys and bone marrow, and this may have an anti-aging effect on the body by reducing age-spots etc. Certain conditions, e.g. an acetaminophen overdose, deplete hepatic glutathione and subject the tissues to oxidative stress resulting in loss of cellular integrity. L-Cystine serves as a major precursor for synthesis of glutathione.",The molecular weight is 240.29.,Cystine has a topological polar surface area of 126.64.,The log p value of  is -4.46.,Cystine is approved and nutraceutical.,Cystine is a solid.,True
16036,"Acetylcysteine (also known as N-acetylcysteine or N-acetyl-L-cysteine or NAC) is primarily used as a mucolytic agent and in the management of acetaminophen poisoning. It is a derivative of cysteine with an acetyl group attached to the amino group of cysteine. NAC is essentially a prodrug that is converted to cysteine (in the intestine by the enzyme aminoacylase 1) and absorbed in the intestine into the blood stream. Cysteine is a key constituent to glutathione and hence administration of acetylcysteine replenishes glutathione stores. Acetylcysteine can also be used as a general antioxidant which can help mitigate symptoms for a variety of diseases exacerbated by reactive oxygen species (ROS). For instance, acetylcysteine is commonly used in individuals with renal impairment to prevent the precipitation of acute renal failure. Acetylcysteine has been shown to have efficacy in treating mild to moderate traumatic brain injury including ischemic brain injury, particularly in reducing neuronal losses, and also reducing cognitive and neurological symptoms when administered promptly after injury. N-acetylcysteine is now widely used in the treatment of HIV, and it has reported efficacy in chronic obstructive pulmonary disease and contrast-induced nephropathy. Acetylcysteine is also being successfully used to treat a variety of neuropsychiatric and neurodegenerative disorders including cocaine, cannabis, and smoking addictions, Alzheimer's and Parkinson's diseases, autism, compulsive and grooming disorders, schizophrenia, depression, and bipolar disorder. Recent data also shows that N-acetylcysteine inhibits muscle fatigue and can be used to enhance performance in endurance events and in exercise and endurance training. Acetylcysteine is used mainly as a mucolytic and in the management of paracetamol (acetaminophen) overdose. Acetylcysteine has been shown to reduce the extent of liver injury following acetaminophen overdose. It is most effective when given early, with benefit seen principally in patients treated within 8-10 hours of the overdose. Acetylcysteine likely protects the liver by maintaining or restoring the glutathione levels, or by acting as an alternate substrate for conjugation with, and thus detoxification of, the reactive metabolite. Acetylcysteine protects against acetaminophen overdose-induced hepatotoxicity by maintaining or restoring hepatic concentrations of glutathione. It does this by producing the glutathione precursor L-cysteine. Glutathione is required to inactivate an intermediate metabolite (N-acetyl-p-benzoquinoneimine or NAPQI) of acetaminophen that is thought to be hepatotoxic. In acetaminophen overdose cases, excessive quantities of this metabolite are formed because the primary metabolic (glucuronide and sulfate conjugation) pathways become saturated. Acetylcysteine may act by reducing the metabolite to the parent compound and/or by providing sulfhydryl for conjugation of the metabolite. Experimental evidence also suggests that a sulfhydryl-containing compound such as acetylcysteine may also directly inactivate the metabolite. The mechanisms of action for acetylcysteine’s well-known mucolytic effects are different. In particular, when inhaled, acetylcysteine (and its metabolic byproduct cysteine) exerts its mucolytic action through its free sulfhydryl group, which reduces the disulfide bonds in the mucus matrix and lowers mucus viscosity. This action increases with increasing pH and is most significant at pH 7 to 9. The mucolytic action of acetylcysteine is not affected by the presence of DNA. Acetylcysteine is also an antioxidant and reduces oxidative stress. Acetylcysteine serves as a prodrug to L-cysteine which is a precursor to the biologic antioxidant, glutathione and hence administration of acetylcysteine replenishes glutathione stores. L-cysteine also serves as a precursor to cystine which in turn serves as a substrate for the cystine-glutamate antiporter on astrocytes hence increasing glutamate release into the extracellular space. This glutamate in turn acts on mGluR2/3 receptors, and at higher doses of acetylcysteine, mGluR5. Glutathione also modulates the NMDA receptor by acting at the redox site. These effects on glutamate and NMDA signaling appear to explain some of the positive neuropsychotropic effects associated with NAC. Acetylcysteine also possesses some anti-inflammatory effects possibly via inhibiting NF-κB through redox activation of the nuclear factor kappa kinases thereby modulating cytokine synthesis.",The molecular weight is 163.19.,Acetylcysteine has a topological polar surface area of 66.4.,The log p value of  is -0.62.,Acetylcysteine is approved and investigational.,Acetylcysteine is a solid.,True
16037,,,,,Adenosine-5'-Triphosphate is experimental.,Adenosine-5'-Triphosphate is a solid.,False
16038,"AT1391 is a daily insulin skin patch designed to provide continuous basal levels of insulin for patients with diabetes. Investigated for use/treatment in diabetes mellitus type 1 and 2. Insulin binds to the insulin receptor (IR), a heterotetrameric protein consisting of two extracellular alpha units and two transmembrane beta units. The binding of insulin to the alpha subunit of IR stimulates the tyrosine kinase activity intrinsic to the beta subunit of the receptor. The bound receptor is able to autophosphorylate and phosphorylate numerous intracellular substrates such as insulin receptor substrates (IRS) proteins, Cbl, APS, Shc and Gab 1. These activated proteins, in turn, lead to the activation of downstream signaling molecules including PI3 kinase and Akt. Akt regulates the activity of glucose transporter 4 (GLUT4) and protein kinase C (PKC) which play a critical role in metabolism and catabolism.",,,,AT1391 is investigational.,AT1391 is a solid.,True
16039,,,,,PYRIMIDIN-2-YL}AMINO)PHENYL]ACETIC ACID is experimental.,PYRIMIDIN-2-YL}AMINO)PHENYL]ACETIC ACID is a solid.,False
16040,"Chromic chloride, for injection, is a sterile, nonpyrogenic solution intended for use as an additive to solutions for Total Parenteral Nutrition (TPN). For use as a supplement to intravenous solutions given for total parenteral nutrition (TPN). Trivalent chromium is part of glucose tolerance factor, an essential activator of insulin-mediated reactions. Chromium helps to maintain normal glucose metabolism and peripheral nerve function. Providing chromium during TPN helps prevent deficiency symptoms including impaired glucose tolerance, ataxia, peripheral neuropathy and a confusional state similar to mild/moderate hepatic encephalopathy. Metallic chromium has no biological activity. Chromium is referred as a glucose tolerance factor. This glucose tolerance factor is a complex of molecules. Glycine, cysteine, glutamic acid and nicotinic acid along with chromium form this complex.",The molecular weight is 158.35.,,,Chromic chloride is approved.,Chromic chloride is a solid.,True
16041,"Mecasermin rinfabate is approved for severe primary insulin-like growth factor (IGF) deficiency or in patients with GH gene deletion who have developed antibodies to growth hormone (GH). Mecasermin rinfabate is similar to in that both drugs contain recombinant DNA origin insulin-like growth factor 1 (IGF-1). Mecasermin rinfabate however, is already bound to recombinant DNA origin insulin-like growth factor binding protein 3 (IGFBP-3). The binding of IGF-1 to IGFBP-3 is said to extend the half life and reduce the clearance of IGF-1 in patients with growth hormone resistant syndromes and low levels of IGFBP-3 though this may represent <500 patients worldwide. Mecasermin rinfabate was approved for treatment of severe primary insulin-like growth factor (IGF) deficiency or in patients with GH gene deletion who have developed antibodies to growth hormone (GH). Mecasermin rinfabate promotes vertical growth in pediatric patients in a similar fashion to. Mecasermin rinfabate supplies recombinant-DNA-origin IGF-1 (rhIGF-1) bound to recombinant-DNA-origin IGFBP-3. 80% of IGF-1 is naturally bound to IGFBP-3 so the binding of rhIGF-1 to rhIGFBP-3 increases the half life of rhIGF-1 compared to. rhIGF-1 binds to the Type I IGF-1 receptor. This receptor exerts intra-cellular signaling activity in a number of processes involved in statural growth, including mitogenesis in multiple tissue types, chondrocyte growth and division along cartilage growth plates, and increases in organ growth.",The molecular weight is 36404.45.,Mecasermin rinfabate has a topological polar surface area of 12082.97.,,Mecasermin rinfabate is approved.,Mecasermin rinfabate is a solid.,True
16042,"NeoPharm is developing liposome-encapsulated, c-Raf antisense oligodeoxynucleotides (LErafAON) for the potential treatment of various solid tumors, including those that have become resistant to radiation or chemotherapy. Phase I/II trials commenced in March 2001 and were ongoing as of June 2003. Intended for the treatment of various forms of cancer. Raf-1 protein serine threonine kinase plays an important role in cell survival and proliferation. Antisense inhibition of Raf-1 expression by drugs such as LErafAON has been shown to enhance the cytotoxic effects of radiation and anticancer drugs.",,,,LErafAON is investigational.,LErafAON is a liquid.,True
16043,"XL281 is a novel anticancer compound designed to potently inhibit the RAS/RAF/MEK/ERK signaling pathway. Mutational activation of RAS occurs in about 30 percent of all human tumors, including non-small cell lung, pancreatic, and colon cancer. XL281 is a specific inhibitor of RAF kinases, including the mutant form of B-RAF, which is activated in 60 percent of melanomas, 24-44 percent of thyroid cancers, and 9 percent of colon cancers. Investigated for use/treatment in solid tumors. XL281 is a novel small molecule drug designed to specifically inhibit RAF kinases, which lie immediately downstream of RAS and are key components of the RAS/RAF/MEK/ERK kinase signaling pathway. Genetic lesions that activate this pathway are common in human tumors, with activating mutations in K-Ras occurring in 30 percent of tumors and activating mutations in B-RAF occurring in approximately 60 percent of melanomas. The RAS/RAF/MEK/ERK pathway also plays a key role in the transmission of growth-promoting signals downstream of receptor tyrosine kinases. This suggests that deregulation of this pathway plays a pivotal role in the progression of many human tumors, and that inhibition of the pathway may provide clinical benefit in the treatment of cancer. In preclinical studies, XL281 showed potent inhibition of B-RAF, mutationally activated B-RAF and C-RAF, and did not interact with kinases outside of the RAF family. XL281 displays high oral bioavailability and strongly inhibits RAS/RAF/MEK/ERK signaling in human tumor models.",,,,XL281 is investigational.,XL281 is a solid.,True
16044,"iCo-007 (formerly known as ISIS 13650) is a second generation antisense compound being developed by iCo for the treatment of various eye diseases caused by the formation of new blood vessels (angiogenesis) such as age-related macular degeneration (AMD) and diabetic retinopathy(DR). Various eye diseases iCo-007 is an antisense inhibitor of c-Raf kinase, an enzyme important in the signal transduction pathway triggered by VEGF as well as other important growth factors. In preclinical studies, antisense inhibition of c-Raf kinase was associated with a reduction in the formation of new blood vessels in the eye, suggesting c-Raf kinase inhibition could be valuable in the treatment of both AMD and diabetic retinopathy.",,,,iCo-007 is investigational.,iCo-007 is a solid.,True
16045,"Cholecystokinin ( also known as _CCK or CCK-PZ_) is a peptide hormone of the gastrointestinal system which is responsible for stimulating the digestion of fat and protein. Cholecystokinin, previously called _pancreozymin_, is synthesized and secreted by enteroendocrine cells in the duodenum (the first portion of the small intestine) and leads to the release of bile and digestive enzymes. CCK also acts as an appetite suppressant and has been studied for weight management regimens.  For use as a diagnostic aid for evaluation of gallbladder disorders. It is also used in conjunction with secretin in pancreatic insufficiency. Cholecystokinin (CCK) plays an imperative role in facilitating digestion within the small intestine. The activation of the CCK1 receptor by CCK has demonstrated to be responsible for a wide variety of important physiologic functions, including the stimulation of gallbladder, contraction and exocrine pancreatic enzyme secretion, delay of gastric emptying, relaxation of the sphincter of Oddi, inhibition of gastric acid secretion, and induction of satiety. Cholecystokinin is also produced by neurons in the enteric nervous system and is found to be widely distributed in the brain. An interesting function of CCK is the role it plays in stimulating the CCK receptor and subsequently regulating food consumption, which may prove to be a highly useful treatment for obesity.  Exogenous administration CCK has been widely studied.  Cholecystokinin (CCK) is a peptide hormone discovered in the small intestine. Together with secretin and gastrin, CCK constitutes the classical gut hormone triad. In addition to gallbladder contraction, CCK also regulates pancreatic enzyme secretion and growth, intestinal motility, satiety signaling and the inhibition of gastric acid secretion. CCK is, however, also a transmitter in central and intestinal neurons. Notably, CCK is the most ubiquitously found neuropeptide in the human brain. Owing to difficulties in developing accurate assays for the hormone, knowledge about CCK secretion in disease is limited. Available data indicate, however, that proCCK is expressed in certain malignant neuroendocrine tumors and sarcomas, whereas the secretion of CCK is affected in celiac disease and the eating disorder bulimia nervosa. Stimulation with exogenous CCK has proved this protein useful in diagnostic imaging of gallbladder and pancreatic diseases, as well as testing of medullary thyroid carcinomas.",,,,Cholecystokinin is approved and investigational.,Cholecystokinin is a solid.,True
16046,"Thrombomodulin Alfa is a novel, recombinant and soluble thrombomodulin (ART-123). It is a human protein with both thrombin inhibiting and protein C stimulating activities, for the potential treatment of thromboembolism and blood clotting disorders, such as disseminated intravascular thromboembolism.  Investigated for use/treatment in blood preservative, blood (blood forming organ disorders, unspecified), sepsis and septicemia, and thrombosis. Thrombomodulin (TM) alfa, a recombinant human soluble TM, enhances activation of pro-carboxypeptidase B2 (pro-CPB2) by thrombin. Activated pro-CPB2 (CPB2) exerts anti-inflammatory and anti-fibrinolytic activities. Thrombomodulin alfa is a soluble form of recombinant human thrombomodulin comprising all extracellular domains of thrombomodulin. Bound to thrombin, Thrombomodulin alfa inhibits its procoagulant activity and promotes activation of protein C. Thrombomodulin alfa inhibits thrombin generation by the activation of protein C and the subsequent inactivation of factor Va in the presence of protein S. Thrombomodulin alfa attenuates the extension of the clot by inhibiting further thrombin generation on clots, while other anticoagulants inhibit the initiation of clot formation. A higher concentration of Thrombomodulin alfa is needed to affect clotting time and platelet aggregation than thrombin generation. ",,,,Thrombomodulin Alfa is approved and investigational.,Thrombomodulin Alfa is a solid.,True
16047,Protein S human is a vitamin K-dependent plasma glycoprotein which has antcoagulant properties. It serves as a negative feedback mechanism in the coagulation cascade. For use in the emergency reversal of coagulation factor deficiency in patients recieving vitamin K antagonist therapy. Protein S is administered as part of a cocktail containing several other coagulation factors. Protein S acts as an anticoagulant serves as a negative feedback mechanism in the coagulation cascade. Thrombin converts protein C to activated protein C (APC). Protein S functions as a cofactor for APC and together they proteolytically cleave factor Va and VIIIa. This inhibits the activities of the prothrombinase and tenase complexes respectively and leads to a reduction in thrombin generation. The reduction in thrombin generation suppresses the coagulation cascade preventing additional clotting from occuring. Protein S is suggested to inhibit factors Va and Xa through protein-protein interactions. Protein S is also suggested to inhibit production of factor Xa by the tenase complex by competing for binding to phospholipids via its gamma-carboxyglutamic acid domain.,,,,Protein S human is approved.,Protein S human is a solid.,True
16048,"The 4-carboxyaldehyde form of vitamin B 6 which is converted to pyridoxal phosphate which is a coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, aminolevulinic acid.  Pyridoxal is one of the natural forms available of vitamin B6, therefore, it is used for nutritional supplementation and for treating dietary shortage or imbalances. Pyridoxal principally in the form of the coenzyme pyridoxal 5'-phosphate, is involved in a wide range of biochemical reactions, including the metabolism of amino acids and glycogen, the synthesis of nucleic acids, hemogloblin, sphingomyelin and other sphingolipids, and the synthesis of the neurotransmitters serotonin, dopamine, norepinephrine and gamma-aminobutyric acid (GABA). Pyridoxal is the precursor to pyridoxal phosphate. Pyridoxal 5'-phosphate is involved in a wide range of biochemical reactions, including the metabolism of amino acids and glycogen, the synthesis of nucleic acids, hemogloblin, sphingomyelin and other sphingolipids, and the synthesis of the neurotransmitters serotonin, dopamine, norepinephrine and gamma-aminobutyric acid (GABA).",,,,Pyridoxal is experimental and nutraceutical.,Pyridoxal is a solid.,True
16049,,,,,"O6-(R)-ROSCOVITINE, R-2-(6-BENZYLOXY-9-ISOPROPYL-9H-PURIN-2-YLAMINO)-BUTAN-1-OL is experimental.","O6-(R)-ROSCOVITINE, R-2-(6-BENZYLOXY-9-ISOPROPYL-9H-PURIN-2-YLAMINO)-BUTAN-1-OL is a solid.",False
16050,,,,,(2R)-2-({6--9-isopropyl-9H-purin-2-yl}amino)butan-1-ol is experimental.,(2R)-2-({6--9-isopropyl-9H-purin-2-yl}amino)butan-1-ol is a solid.,False
16051,"SPI-1620 is an endothelin B receptor agonist. In animal models SPI-1620 selectively and transiently increases tumor blood flow allowing increased delivery of anticancer agents to the tumor. It is being developed as an adjunct to chemotherapy. Investigated for use/treatment in cancer/tumors (unspecified). In animal models SPI-1620 selectively and transiently increases tumor blood flow allowing increased delivery of anticancer agents to the tumor. SPI-1620 is a highly selective peptide agonist of endothelin-B receptors, which can stimulate receptors on endothelial cells, the innermost layer of cells lining the blood vessels. The blood supply to tumors is different than the blood supply to healthy organs. Blood vessels in the growing part of tumors are relatively devoid of smooth muscle covering and are rich in endothelial cells. Therefore, by stimulating the endothelial-B receptors present on the endothelial cells, SPI-1620 should selectively increase tumor blood flow while sparing healthy tissue.",,,,IRL-1620 is investigational.,IRL-1620 is a solid.,True
16052,"Investigated for use/treatment in congestive heart failure, chronic obstructive pulmonary disease (COPD), and benign prostatic hyperplasia.",,,,Enrasentan is investigational.,Enrasentan is a solid.,True
16053,"Tezosentan is an intravenous endothelin receptor A/B antagonist. Tezosentan was initially developed for vasodilation in patients with acute heart failure but studies have shown that it does not assist in the treatment of dyspnea or prevent cardiovascular events. Investigated for use/treatment in congestive heart failure, liver disease, and heart disease.",,,,Tezosentan is investigational.,Tezosentan is a solid.,True
16054,"One of the centrally acting muscarinic antagonists used for treatment of parkinsonian disorders and drug-induced extrapyramidal movement disorders and as an antispasmodic. Indicated for the treatment of parkinson's disease and extrapyramidal reactions caused by drugs. Trihexyphenidyl is an anticholinergic used in the symptomatic treatment of all etiologic groups of parkinsonism and drug induced extrapyramidal reactions (except tardive dyskinesia). Trihexyphenidyl possesses both anticholinergic and antihistaminic effects, although only the former has been established as therapeutically significant in the management of parkinsonism. Trihexyphenidyl is a non-selective muscarinic acetylcholine receptor antagonist but binds with higher affinity to the M1 subtype. In vivo studies have shown that trihexyphenidyl demonstrates higher affinity for central muscarinic receptors located in the cerebral cortex and lower affinity for those located peripherally. Other studies suggest that trihexyphenidyl may modify nicotinic acetylcholine receptor neurotransmission, leading indirectly to enhanced dopamine release in the striatum. Although the anticholinergic has proven to be useful in the treatment of symptoms associated with Parkinson’s disease or other movement disorders, its mechanism of action has yet to be fully elucidated.",The molecular weight is 301.47.,Trihexyphenidyl has a topological polar surface area of 23.47.,The log p value of  is 5.15.,Trihexyphenidyl is approved.,Trihexyphenidyl is a solid.,True
16055,"Oxyphencyclimine is an anticholinergic drug (trade name Daricon) used in treating peptic ulcers. For the treatment of peptic ulcer disease and the relief of smooth muscle spasms in gastrointestinal disorders. Oxyphencyclimine is a synthetic anticholinergic agent which has been shown in experimental and clinical studies to have a pronounced antispasmodic and antisecretory effect on the gastrointestinal tract. Oxyphencyclimine is an antimuscarinic, anticholinergic drug. Oxyphencyclimine binds the muscarinic acetylcholine receptor. It may block all three types of muscarinic receptors including M-1 receptors in the CNS and ganglia, M-2 receptors in the heart (vagus) and M-3 receptors at the parasympathetic NEJ system. The muscarinic acetylcholine receptors mediate various cellular responses, including inhibition of adenylate cyclase, breakdown of phosphoinositides and modulation of potassium channels through the action of G proteins. Oxphencyclimine inhibits vagally mediated reflexes by antagonizing the action of acetylcholine. This in turn reduces the secretion of gastric acids in the stomach.",The molecular weight is 344.46.,Oxyphencyclimine has a topological polar surface area of 62.13.,The log p value of  is 4.44.,Oxyphencyclimine is approved.,Oxyphencyclimine is a solid.,True
16056,"A muscarinic antagonist that crosses the blood-brain barrier and is used in the treatment of drug-induced extrapyramidal disorders and in parkinsonism. For the treatment of all forms of Parkinson's Disease, as well as control of extrapyramidal reactions induced by antipsychotic agents. Procyclidine has an atropine-like action on parasympathetic-innervated peripheral structures including smooth muscle. It's antispasmodic effects are thought to be related to the blockage of central cholinergic receptors M1, M2 and M4. It is used to treat symptomatic Parkinsonism and extrapyramidal dysfunction caused by antipsychotic agents. The mechanism of action is unknown. It is thought that Procyclidine acts by blocking central cholinergic receptors, and thus balancing cholinergic and dopaminergic activity in the basal ganglia. Many of its effects are due to its pharmacologic similarities with atropine. Procyclidine exerts an antispasmodic effect on smooth muscle, and may produce mydriasis and reduction in salivation.",The molecular weight is 287.45.,Procyclidine has a topological polar surface area of 23.47.,The log p value of  is 4.59.,Procyclidine is approved.,Procyclidine is a solid.,True
16057,"Hyoscyamine is a chemical compound, a tropane alkaloid it is the levo-isomer to atropine. It is a secondary metabolite of some plants, particularly henbane (Hyoscamus niger.) For treatment of bladder spasms, peptic ulcer disease, diverticulitis, colic, irritable bowel syndrome, cystitis, and pancreatitis. Also used to treat certain heart conditions, to control the symptoms of Parkinson's disease and rhinitis. L-Hyoscyamine, the active optical isomer of atropine (dl-hyoscyamine), is a tertiary amine anticholinergic gastrointestinal agent. Hyoscyamine competes favorably with acetylcholine for binding at muscarinic receptors in the salivary, bronchial, and sweat glands as well as in the eye, heart, and gastrointestinal tract. The actions of hyoscyamine result in a reduction in salivary, bronchial, gastric and sweat gland secretions, mydriasis, cycloplegia, change in heart rate, contraction of the bladder detrusor muscle and of the gastrointestinal smooth muscle, and decreased gastrointestinal motility.",The molecular weight is 289.38.,Hyoscyamine has a topological polar surface area of 49.77.,The log p value of  is 1.3.,Hyoscyamine is approved.,Hyoscyamine is a solid.,True
16058,"A muscarinic antagonist used to study binding characteristics of muscarinic cholinergic receptors. Used as adjunctive therapy for the treatment of peptic ulcer. Also used to treat nausea and vomiting due to motion sickness. Methscopolamine is a muscarinic antagonist structurally similar to the neurotransmitter acetylcholine and acts by blocking the muscarinic acetylcholine receptors and is thus classified as an anticholinergic. Methscopolamine has many uses including the prevention of motion sickness. It is not clear how Methscopolamine prevents nausea and vomiting due to motion sickness. The vestibular part of the ear is very important for balance. When a person becomes disoriented due to motion, the vestibule sends a signal through nerves to the vomiting center in the brain, and vomiting occurs. Acetylcholine is a chemical that nerves use to transmit messages to each other. It is believe that Methscopolamine prevents communication between the nerves of the vestibule and the vomiting center in the brain by blocking the action of acetylcholine. Methscopolamine also may work directly on the vomiting center. Methscopolamine must be taken before the onset of motion sickness to be effective. Methscopolamine acts by interfering with the transmission of nerve impulses by acetylcholine in the parasympathetic nervous system (specifically the vomiting center). It does so by acting as a muscarinic antagonist.",,,,Methscopolamine bromide is approved.,Methscopolamine bromide is a solid.,True
16059,"Tridihexethyl is a synthetic anticholinergic agent which has been shown in experimental and clinical studies to have a pronounced antispasmodic and antisecretory effect on the gastrointestinal tract. Tridihexethyl is an antimuscarinic, anticholinergic drug. Tridihexethyl is no longer available in the US market.  Used as an adjunct in the treatment of peptic ulcer disease and in Acquired nystagmus Tridihexethyl is a synthetic anticholinergic agent which has been shown in experimental and clinical studies to have a pronounced antispasmodic and antisecretory effect on the gastrointestinal tract. Tridihexethyl is an antimuscarinic, anticholinergic drug. Tridihexethyl binds the muscarinic acetylcholine receptor. It may block all three types of muscarinic receptors including M-1 receptors in the CNS and ganglia, M-2 receptors in the heart (vagus) and M-3 receptors at the parasympathetic NEJ system. The muscarinic acetylcholine receptors mediate various cellular responses, including inhibition of adenylate cyclase, breakdown of phosphoinositides and modulation of potassium channels through the action of G proteins. Tridihexethyl inhibits vagally mediated reflexes by antagonizing the action of acetylcholine. This in turn reduces the secretion of gastric acids in the stomach.",The molecular weight is 318.52.,Tridihexethyl has a topological polar surface area of 20.23.,The log p value of  is 1.32.,Tridihexethyl is withdrawn.,Tridihexethyl is a solid.,True
16060,"Anisotropine methylbromide is a quaternary ammonium compound. Its use as treatment adjunct in peptic ulcer has been replaced by the use of more effective agents. Depending on the dose, anisotropine methylbromide may reduce the motility and secretory activity of the gastrointestinal system, and the tone of the ureter and urinary bladder and may have a slight relaxant action on the bile ducts and gallbladder. In general, smaller doses of anisotropine methylbromide inhibit salivary and bronchial secretions, sweating, and accommodation; cause dilatation of the pupil; and increase the heart rate. Larger doses are required to decrease motility of the gastrointestinal and urinary tracts and to inhibit gastric acid secretion. For use in conjunction with antacids or histamine H<sub>2</sub>-receptor antagonists in the treatment of peptic ulcer, to reduce further gastric acid secretion and delay gastric emptying. Anisotropine methylbromide is a quaternary ammonium compound. Its use as treatment adjunct in peptic ulcer has been replaced by the use of more effective agents. Depending on the dose, anisotropine methylbromide may reduce the motility and secretory activity of the gastrointestinal system, and the tone of the ureter and urinary bladder and may have a slight relaxant action on the bile ducts and gallbladder. In general, smaller doses of anisotropine methylbromide inhibit salivary and bronchial secretions, sweating, and accommodation; cause dilatation of the pupil; and increase the heart rate. Larger doses are required to decrease motility of the gastrointestinal and urinary tracts and to inhibit gastric acid secretion. Quaternary ammonium compounds such as anisotropine methylbromide inhibit the muscarinic actions of acetylcholine on structures innervated by postganglionic cholinergic nerves as well as on smooth muscles that respond to acetylcholine but lack cholinergic innervation. These postganglionic receptor sites are present in the autonomic effector cells of the smooth muscle, cardiac muscle, sinoatrial and atrioventricular nodes, and exocrine glands.",The molecular weight is 282.45.,Anisotropine methylbromide has a topological polar surface area of 26.3.,The log p value of  is -0.82.,Anisotropine methylbromide is approved.,Anisotropine methylbromide is a solid.,True
16061,"An alkaloid, originally from Atropa belladonna, but found in other plants, mainly solanaceae. For the treatment of poisoning by susceptible organophosphorous nerve agents having anti-cholinesterase activity (cholinesterase inhibitors) as well as organophosphorous or carbamate insecticides. Atropine, a naturally occurring belladonna alkaloid, is a racemic mixture of equal parts of d- and l-hyoscyamine, whose activity is due almost entirely to the levo isomer of the drug. Atropine is commonly classified as an anticholinergic or antiparasympathetic (parasympatholytic) drug. More precisely, however, it is termed an antimuscarinic agent since it antagonizes the muscarine-like actions of acetylcholine and other choline esters. Adequate doses of atropine abolish various types of reflex vagal cardiac slowing or asystole. The drug also prevents or abolishes bradycardia or asystole produced by injection of choline esters, anticholinesterase agents or other parasympathomimetic drugs, and cardiac arrest produced by stimulation of the vagus. Atropine may also lessen the degree of partial heart block when vagal activity is an etiologic factor. Atropine in clinical doses counteracts the peripheral dilatation and abrupt decrease in blood pressure produced by choline esters. However, when given by itself, atropine does not exert a striking or uniform effect on blood vessels or blood pressure. Atropine binds to and inhibit muscarinic acetylcholine receptors, producing a wide range of anticholinergic effects.",The molecular weight is 289.38.,Atropine has a topological polar surface area of 49.77.,The log p value of  is 1.3.,Atropine is approved and vet_approved.,Atropine is a solid.,True
16062,"Homatropine methylbromide is a quaternary ammonium muscarinic acetylcholine receptor antagonist belonging to the group of medicines called anti-muscarinics. Homatropine is used to treat duodenal or stomach ulcers or intestine problems. It can be used together with antacids or other medicine in the treatment of peptic ulcer. It may also be used to prevent nausea, vomiting, and motion sickness. Used in conjunction with antacids or histamine H2-receptor antagonists in the treatment of peptic ulcers, gastric ulcers and duodenal ulcers, to reduce further gastric acid secretion and delay gastric emptying. Homatropine methylbromide belongs to the group of medicines called anti-muscarinics. Homatropine is used to treat duodenal or stomach ulcers or intestine problems. It can be used together with antacids or other medicine in the treatment of peptic ulcer. It may also be used to prevent nausea, vomiting, and motion sickness. Homatropine is a quaternary ammonium muscarinic acetylcholine receptor antagonist. The muscarinic acetylcholine receptor mediates various cellular responses, including inhibition of adenylate cyclase, breakdown of phosphoinositides and modulation of potassium channels through the action of G proteins. Homatropine methylbromide inhibits the muscarinic actions of acetylcholine on structures innervated by postganglionic cholinergic nerves as well as on smooth muscles that respond to acetylcholine but lack cholinergic innervation. These postganglionic receptor sites are present in the autonomic effector cells of the smooth muscle, cardiac muscle, sinoatrial and atrioventricular nodes, and exocrine glands. Depending on the dose, anticholinergics may reduce the motility and secretory activity of the gastrointestinal system, and the tone of the ureter and urinary bladder and may have a slight relaxant action on the bile ducts and gallbladder.",The molecular weight is 290.38.,Homatropine methylbromide has a topological polar surface area of 46.53.,The log p value of  is -2.9.,Homatropine methylbromide is approved.,Homatropine methylbromide is a solid.,True
16063,"An alkaloid from Solanaceae, especially Datura metel L. and Scopola carniolica. Scopolamine and its quaternary derivatives act as antimuscarinics like atropine, but may have more central nervous system effects. Among the many uses are as an anesthetic premedication, in urinary incontinence, in motion sickness, as an antispasmodic, and as a mydriatic and cycloplegic. For the treatment of excessive salivation, colicky abdominal pain, bradycardia, sialorrhoea, diverticulitis, irritable bowel syndrome and motion sickness. Scopolamine is a muscarinic antagonist structurally similar to the neurotransmitter acetylcholine and acts by blocking the muscarinic acetylcholine receptors and is thus classified as an anticholinergic. Scopolamine has many uses including the prevention of motion sickness. It is not clear how Scopolamine prevents nausea and vomiting due to motion sickness. The vestibular part of the ear is very important for balance. When a person becomes disoriented due to motion, the vestibule sends a signal through nerves to the vomiting center in the brain, and vomiting occurs. Acetylcholine is a chemical that nerves use to transmit messages to each other. It is believe that Scopolamine prevents communication between the nerves of the vestibule and the vomiting center in the brain by blocking the action of acetylcholine. Scopolamine also may work directly on the vomiting center. Scopolamine must be taken before the onset of motion sickness to be effective. Scopolamine acts by interfering with the transmission of nerve impulses by acetylcholine in the parasympathetic nervous system (specifically the vomiting center).",The molecular weight is 303.36.,Scopolamine has a topological polar surface area of 62.3.,The log p value of  is 0.29.,Scopolamine is approved and investigational.,Scopolamine is a solid.,True
16064,"Benzquinamide is a discontinued antiemetic compound with antihistaminic, mild anticholinergic, and sedative properties. The mechanism of action is not known, but presumably benzquinamide works via antagonism of muscarinic acetycholine receptors and histamine H1 receptors.  Used to prevent and treat nausea and vomiting associated with anesthesia and surgery, administered intramuscularly or intravenously. Benzquinamide is an antiemetic compound with antihistaminic, mild anticholinergic, and sedative properties. The mechanism of action is not known, but presumably benzquinamide works via antagonism of muscarinic acetycholine receptors and histamine H1 receptors.",The molecular weight is 404.51.,Benzquinamide has a topological polar surface area of 68.31.,The log p value of  is 3.02.,Benzquinamide is withdrawn.,Benzquinamide is a solid.,True
16065,"One of the muscarinic antagonists with pharmacologic action similar to atropine and used mainly as an ophthalmic parasympatholytic or mydriatic.  Indicated to induce mydriasis (dilation of the pupil) and cycloplegia (paralysis of the ciliary muscle of the eye) in diagnostic procedures, such as measurement of refractive errors and examination of the fundus of the eye. Tropicamide belongs to the group of medicines called anti-muscarinics. Tropicamide blocks the receptors in the muscles of the eye (muscarinic receptors). These receptors are involved controlling the pupil size and the shape of the lens. By blocking these receptors, tropicamide produces dilatation of the pupil (mydriasis) and prevents the eye from accommodating for near vision (cycloplegia). Tropicamide is given as eye drops to dilate the pupil and relax the lens so that eye examinations can be carried out thoroughly. Tropicamide binds to and blocks the receptors in the muscles of the eye (muscarinic receptor M4). Tropicamide acts by blocking the responses of the iris sphincter muscle to the iris and ciliary muscles to cholinergic stimulation, producing dilation of the pupil and paralysis of the ciliary muscle.",The molecular weight is 284.36.,Tropicamide has a topological polar surface area of 53.43.,The log p value of  is 1.18.,Tropicamide is approved and investigational.,Tropicamide is a solid.,True
16066,"Histamine H1 antagonist used in treatment of allergies, rhinitis, and urticaria. For the treatment of the symptoms of the common cold and allergic rhinitis, such as runny nose, itchy eyes, watery eyes, and sneezing. Brompheniramine is an antihistaminergic medication of the propylamine class. It is a first-generation antihistamine. In allergic reactions an allergen interacts with and cross-links surface IgE antibodies on mast cells and basophils. Once the mast cell-antibody-antigen complex is formed, a complex series of events occurs that eventually leads to cell-degranulation and the release of histamine (and other chemical mediators) from the mast cell or basophil. Once released, histamine can react with local or widespread tissues through histamine receptors. Histamine, acting on H<sub>1</sub>-receptors, produces pruritis, vasodilatation, hypotension, flushing, headache, tachycardia, and bronchoconstriction. Histamine also increases vascular permeability and potentiates pain. Brompheniramine is a histamine H1 antagonist (or more correctly, an inverse histamine agonist) of the alkylamine class. It provides effective, temporary relief of sneezing, watery and itchy eyes, and runny nose due to hay fever and other upper respiratory allergies. Brompheniramine is an antagonist of the H1 histamine receptors with moderate antimuscarinic actions, as with other common antihistamines such as diphenhydramine. Due to its anticholindergic effects, brompheniramine may cause drowsiness, sedation, dry mouth, dry throat, blurred vision, and increased heart rate.",The molecular weight is 319.25.,Brompheniramine has a topological polar surface area of 16.13.,The log p value of  is 3.3.,Brompheniramine is approved.,Brompheniramine is a liquid.,True
16067,"Glycopyrronium (as the bromide salt glycopyrrolate) is a synthetic anticholinergic agent with a quaternary ammonium structure. A muscarinic competitive antagonist used as an antispasmodic, in some disorders of the gastrointestinal tract, and to reduce salivation with some anesthetics. In October 2015, glycopyrrolate was approved by the FDA for use as a standalone treatment for Chronic obstructive pulmonary disease (COPD), as Seebri Neohaler. For use as a preoperative antimuscarinic to reduce salivary, tracheobronchial, and pharyngeal secretions, to reduce the volume and free acidity of gastric secretions and to block cardiac vagal inhibitory reflexes during induction of anesthesia and intubation. Also used to treat chronic obstructive pulmonary disease (COPD). Glycopyrrolate decreases acid secretion in the stomach. Hence it can be used for treating ulcers in the stomach and small intestine, in combination with other medications. In anesthesia, glycopyrrolate injection serves as a preoperative antimuscarinic operation that reduces salivary, tracheobronchial, and pharyngeal secretions, as well as decreases the acidity of gastric secretions blocks cardiac vagal inhibitory reflexes during intubation Glycopyrrolate binds competitively to the muscarinic acetylcholine receptor. Like other anticholinergic (antimuscarinic) agents, it inhibits the action of acetylcholine on structures innervated by postganglionic cholinergic nerves and on smooth muscles that respond to acetylcholine but lack cholinergic innervation. These peripheral cholinergic receptors are present in the autonomic effector cells of smooth muscle, cardiac muscle, the sinoatrial node, the atrioventricular node, exocrine glands and, to a limited degree, in the autonomic ganglia. Thus, it diminishes the volume and free acidity of gastric secretions and controls excessive pharyngeal, tracheal, and bronchial secretions.",,,,Glycopyrronium is approved and investigational and vet_approved.,Glycopyrronium is a solid.,True
16068,"Bethanechol is a synthetic ester structurally and pharmacologically related to acetylcholine. A slowly hydrolyzed muscarinic agonist with no nicotinic effects, bethanechol is generally used to increase smooth muscle tone, as in the GI tract following abdominal surgery or in urinary retention in the absence of obstruction. It may cause hypotension, cardiac rate changes, and bronchial spasms. For the treatment of acute postoperative and postpartum nonobstructive (functional) urinary retention and for neurogenic atony of the urinary bladder with retention. Bethanechol is a parasympathomimetic (cholinergic) used for the treatment of acute postoperative and postpartum nonobstructive (functional) urinary retention and for neurogenic atony of the urinary bladder with retention. Bethanechol, a cholinergic agent, is a synthetic ester which is structurally and pharmacologically related to acetylcholine. It increases the tone of the detrusor urinae muscle, usually producing a contraction sufficiently strong to initiate micturition and empty the bladder. It stimulates gastric motility, increases gastric tone, and often restores impaired rhythmic peristalsis. Bethanechol chloride is not destroyed by cholinesterase and its effects are more prolonged than those of acetytcholine. Bethanechol directly stimulates cholinergic receptors in the parasympathetic nervous system while stimulating the ganglia to a lesser extent. Its effects are predominantly muscarinic, inducing little effect on nicotinic receptors and negligible effects on the cardiovascular system.",The molecular weight is 161.22.,Bethanechol has a topological polar surface area of 52.32.,The log p value of  is -4.01.,Bethanechol is approved.,Bethanechol is a solid.,True
16069,"Mivacurium is a bisbenzylisoquinolinium based neuromuscular blocker or muscle relaxant. It binds competitively to cholinergic receptors on the motor end-plate to antagonize the action of acetylcholine, resulting in a block of neuromuscular transmission. For inpatients and outpatients, as an adjunct to general anesthesia, to facilitate tracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Mivacurium is a short-acting, nondepolarizing skeletal neuromuscular blocking agent which is hydrolyzed by plasma cholinesterase. Mivacurium results in a blockade of neuromuscular transmission by binding competitively with cholinergic receptors on the motor end-plate to antagonize the action of acetylcholine. The neuromuscular block produced by mivacurium is readily antagonized by anticholinesterase agents. The deeper the level of neuromuscular block at reversal, the longer the time required for recovery of neuromuscular function and the greater the dose of anticholinesterase agent required. Because spontaneous recovery after mivacurium is rapid, routine reversal may not always result in a clinical benefit. Mivacurium binds competitively to cholinergic receptors on the motor end-plate to antagonize the action of acetylcholine, resulting in a block of neuromuscular transmission. This action is antagonized by acetylcholinesterase inhibitors, such as neostigmine.",The molecular weight is 1029.28.,Mivacurium has a topological polar surface area of 144.9.,The log p value of  is 2.64.,Mivacurium is approved.,Mivacurium is a liquid.,True
16070,"Diphenidol is an antiemetic agent used in the treatment of vomiting and vertigo. Diphenidol overdose may result in serious toxicity in children. For use in the prevention and symptomatic treatment of peripheral (labyrinthine) vertigo and associated nausea and vomiting that occur in such conditions as Meniere's disease and surgery of the middle and inner ear. Also for the control of nausea and vomiting associated with postoperative states, malignant neoplasms, labyrinthine disturbances, antineoplastic agent therapy, radiation sickness, and infectious diseases. Diphenidol is used for control of nausea and vomiting. It has an antivertigo effect on the vestibular apparatus, inhibiting the chemoreceptor trigger zone to control nausea and vomiting, thus preventing motion sickness. The mechanism by which diphenidol exerts its antiemetic and antivertigo effects is not precisely known. It is thought to diminish vestibular stimulation and depress labyrinthine function and as an antimuscarinic agent. An action on the medullary chemoreceptive trigger zone may also be involved in the antiemetic effect. Diphenidol has no significant sedative, tranquilizing, or antihistaminic action. It has a weak peripheral anticholinergic effect.",The molecular weight is 309.45.,Diphenidol has a topological polar surface area of 23.47.,The log p value of  is 4.07.,Diphenidol is approved and investigational and withdrawn.,Diphenidol is a solid.,True
16071,"Isopropamide iodide is a long-acting quaternary anticholinergic drug. It is used in the treatment of peptic ulcer and other gastrointestinal disorders marked by hyperacidity and hypermotility. For the treatment of a wide range of gastrointestinal disorders, including such conditions as peptic ulcer, gastritis, hyperchlorhydria, functional diarrhea, irritable or spastic colon, pyloroduodenal irritability, pylorospasm, acute nonspecific gastroenteritis, biliary dyskinesia and chronic cholelithiasis, duodenitis, gastrointestinal spasm; it may also be used to treat genitourinary spasm. Isopropamide is a long-acting quaternary anticholinergic drug. It is used in the treatment of peptic ulcer and other gastrointestinal disorders marked by hyperacidity and hypermotility. Anticholinergics are a class of medications that inhibit parasympathetic nerve impulses by selectively blocking the binding of the neurotransmitter acetylcholine to its receptor in nerve cells. The nerve fibers of the parasympathetic system are responsible for the involuntary movements of smooth muscles present in the gastrointestinal tract. Inhibition here decreases acidity and motility, aiding in the treatment of gastrointestinal disorders.",The molecular weight is 353.53.,Isopropamide has a topological polar surface area of 43.09.,The log p value of  is -0.2.,Isopropamide is approved and vet_approved.,Isopropamide is a solid.,True
16072,"A neurotransmitter. Acetylcholine in vertebrates is the major transmitter at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system. It is generally not used as an administered drug because it is broken down very rapidly by cholinesterases, but it is useful in some ophthalmological applications. Used to obtain miosis of the iris in seconds after delivery of the lens in cataract surgery, in penetrating keratoplasty, iridectomy and other anterior segment surgery where rapid miosis may be required.",The molecular weight is 146.21.,Acetylcholine has a topological polar surface area of 26.3.,The log p value of  is -3.47.,Acetylcholine is approved and investigational.,Acetylcholine is a solid.,True
16073,"An alkaloid obtained from the betel nut (Areca catechu), fruit of a palm tree. It is an agonist at both muscarinic and nicotinic acetylcholine receptors. It is used in the form of various salts as a ganglionic stimulant, a parasympathomimetic, and a vermifuge, especially in veterinary practice. It has been used as a euphoriant in the Pacific Islands.",,,,Arecoline is experimental.,Arecoline is a solid.,True
16074,"Mepenzolate is a post-ganglionic parasympathetic inhibitor. It decreases gastric acid and pepsin secretion and suppresses spontaneous contractions of the colon. Mepenzolate diminishes gastric acid and pepsin secretion. Mepenzolate also suppresses spontaneous contractions of the colon. Pharmacologically, it is a post-ganglionic parasympathetic inhibitor. It has not been shown to be effective in contributing to the healing of peptic ulcer, decreasing the rate of recurrence, or preventing complications. For use as adjunctive therapy in the treatment of peptic ulcer. It has not been  Mepenzolate diminishes gastric acid and pepsin secretion. Mepenzolate also suppresses spontaneous contractions of the colon. Pharmacologically, it is a post-ganglionic parasympathetic inhibitor. Mepenzolate is a post-ganglionic parasympathetic inhibitor. It specifically antagonizes muscarinic receptors. This leads to decreases in gastric acid and pepsin secretion and suppression of spontaneous contractions of the colon.",The molecular weight is 340.44.,Mepenzolate has a topological polar surface area of 46.53.,The log p value of  is 0.16.,Mepenzolate is approved.,Mepenzolate is a solid.,True
16075,"ALKS 27 is an inhaled formulation of trospium chloride for the treatment of chronic obstructive pulmonary disease (COPD). Study showed that ALKS 27 was well-tolerated over a wide dose range, with no dose-limited effects observed. Investigated for use/treatment in chronic obstructive pulmonary disease (COPD). ALKS 27 is a muscarinic receptor antagonist that relaxes smooth muscle tissue and has the potential to improve airflow in patients with chronic obstructive pulmonary disease (COPD).",,,,ALKS 27 is investigational.,ALKS 27 is a solid.,True
16076,"Methacholine acts as a non-selective muscarinic receptor agonist to stimulate the parasympathetic nervous system. It is most commonly used for diagnosing bronchial hyperreactivity, using the bronchial challenge test. Through this test, the drug causes bronchoconstriction and people with pre-existing airway hyperreactivity, such as asthmatics, will react to lower doses of drug. It is most commonly used for diagnosing bronchial hyperreactivity, using the bronchial challenge test. Methacholine acts as a non-selective muscarinic receptor agonist to stimulate the parasympathetic nervous system. It is highly active at all of the muscarinic receptors By agonizing the muscarinic receptors, this drug induces bronchoconstriction. This bronchoconstriction is used as a test in asthmatics and in bronchial hyperreactivity.",The molecular weight is 160.24.,Methacholine has a topological polar surface area of 26.3.,The log p value of  is -3.16.,Methacholine is approved and investigational.,Methacholine is a solid.,True
16077,"Hexocyclium is a muscarinic acetylcholine receptor antagonist which was presumably used in the treatment of gastric ulcer or diarrhea. It was once available under the tradename Tral marketed by Abbvie Inc. but has been discontinued. Proton pump inhibitors like and opiate anti-diarrheal agents like have largely replaced the use of anti-muscarinics in the treatment of gastric ulcers and diarrhea due to their more favorable side effect profiles. The World Health Organization classifies hexocyclium as a drug for functional gastrointestinal disorders. Like other anti-muscarinic agents, hexocyclium was likely used to treat peptic ulcers or diarrhea. Hexocyclium reduces gastrointesitinal motility and gastric acid secretion. Hexocyclium binds to and inhibits muscarinic acetylcholine receptors. This decreases gastric acid secretion by preventing the activation of M3 receptors on pareital cells and subsequent stimulation of gastric acid secretion. The antagonism of M3 receptors in the intestine inhibits smooth muscle contraction resulting in a decrease in motility. The binding of hexocyclium to other muscarinic receptor types produces typical anti-muscarinic side effects.",The molecular weight is 317.5.,Hexocyclium has a topological polar surface area of 23.47.,The log p value of  is 1.41.,Hexocyclium is approved.,Hexocyclium is a solid.,True
16078,"Butylscopolamine is a peripherally acting antimuscarinic, anticholinergic agent. It is used to treat pain and discomfort caused by abdominal cramps, menstrual cramps, or other spasmodic activity in the digestive system. It is also effective at preventing bladder spasms. It is not a pain medication in the normal sense, since it does not directly affect pain, but rather works to prevent painful cramps and spasms from occurring. It is on the WHO Model List of Essential Medicines, the most important medications needed in a basic health system. Used to treat abdmoninal cramping and pain. Scopolamine butylbromide is a muscarinic antagonist which acts to prevent acetylcholine-stimulated contraction of smooth muscle in the gastrointestinal tract. Scopolamine butylbromide binds to muscarinic M3 receptors in the gastrointestinal tract. This prevents acetycholine from binding to and activating the receptors which would result in contraction of the smooth muscle. The inhibition of contraction reduces spasms and their related pain during abdominal cramping.",The molecular weight is 360.47.,Butylscopolamine has a topological polar surface area of 59.06.,The log p value of  is -0.89.,Butylscopolamine is approved and investigational and vet_approved.,Butylscopolamine is a solid.,True
16079,"Thonzylamine is an antihistamine and anticholinergic drug. It is available as combination products with or for temporary relief of symptoms of common cold, hay fever (allergic rhinitis) or other upper respiratory allergies. Thozylamine is indicated for use in the symptomatic control of allergic rhinitis or other upper respiratory allergic symptoms. It is typically a part of combination over the counter products. Thonzylamine is a first-generation antihistamine. It antagonizes the action of histamine to relief allergic symptoms like nasal congestion, runny nose, itchy eyes, itchy nose and throat, and sneezing  Thonzylamine competes with histamine for binding to the H1 histamine receptor. Binding of histamine to this receptor stimulates vasodilation and increased vascular permeability leading to nasal congestion and runny nose. Histamine also produces itchiness by stimulating nerve endings which can result in sneezing. By blocking these effects, thonzylamine can reduce or eliminate symptoms of allergic rhinitis.",The molecular weight is 286.38.,Thonzylamine has a topological polar surface area of 41.49.,The log p value of  is 2.46.,Thonzylamine is approved.,Thonzylamine is a solid.,True
16080,,The molecular weight is 339.52.,Rociverine has a topological polar surface area of 49.77.,The log p value of  is 5.16.,Rociverine is experimental.,,False
16081,"Used in the treatment of peptic ulcer, gastric hyperacidity, and hypermotility in gastritis and pylorospasm, and in the treatment of hyperhidrosis (excessive perspiration). Diphemanil Methylsulfate is a quaternary ammonium anticholinergic. It binds muscarinic acetycholine receptors and thereby decreases secretory excretion of stomach acids as well as saliva and sweat. Diphemanil Methylsulfate exerts its action by primarily binding the muscarinic M3 receptor. M3 receptors are located in the smooth muscles of the blood vessels, as well as in the lungs. This means they cause vasodilation and bronchoconstriction. They are also in the smooth muscles of the gastrointestinal tract (GIT), which help in increasing intestinal motility and dilating sphincters. The M3 receptors are also located in many glands which help to stimulate secretion in salivary glands and other glands of the body.",,,,Diphemanil is approved and vet_approved and withdrawn.,,True
16082,"An intermediate compound in the metabolism of carbohydrates, proteins, and fats. In thiamine deficiency, its oxidation is retarded and it accumulates in the tissues, especially in nervous structures. (From Stedman, 26th ed) For nutritional supplementation, also for treating dietary shortage or imbalance Pyruvic acid or pyruvate is a key intermediate in the glycolytic and pyruvate dehydrogenase pathways, which are involved in biological energy production. Pyruvate is widely found in living organisms. It is not an essential nutrient since it can be synthesized in the cells of the body. Certain fruits and vegetables are rich in pyruvate. For example, an average-size red apple contains approximately 450 milligrams. Dark beer and red wine are also rich sources of pyruvate. Recent research suggests that pyruvate in high concentrations may have a role in cardiovascular therapy, as an inotropic agent. Supplements of this dietary substance may also have bariatric and ergogenic applications. Pyruvate serves as a biological fuel by being converted to acetyl coenzyme A, which enters the tricarboxylic acid or Krebs cycle where it is metabolized to produce ATP aerobically. Energy can also be obtained anaerobically from pyruvate via its conversion to lactate. Pyruvate injections or perfusions increase contractile function of hearts when metabolizing glucose or fatty acids. This inotropic effect is striking in hearts stunned by ischemia/reperfusion. The inotropic effect of pyruvate requires intracoronary infusion. Among possible mechanisms for this effect are increased generation of ATP and an increase in ATP phosphorylation potential. Another is activation of pyruvate dehydrogenase, promoting its own oxidation by inhibiting pyruvate dehydrogenase kinase. Pyruvate dehydrogenase is inactivated in ischemia myocardium. Yet another is reduction of cytosolic inorganic phosphate concentration. Pyruvate, as an antioxidant, is known to scavenge such reactive oxygen species as hydrogen peroxide and lipid peroxides. Indirectly, supraphysiological levels of pyruvate may increase cellular reduced glutathione.",,,,Pyruvic acid is approved and investigational and nutraceutical.,Pyruvic acid is a liquid.,True
16083,,,,,2-Phosphoglycolic Acid is experimental.,2-Phosphoglycolic Acid is a solid.,False
16084,,,,,"beta-D-fructofuranose 1,6-bisphosphate is experimental.","beta-D-fructofuranose 1,6-bisphosphate is a solid.",False
16085,"A white crystal or crystalline powder used as an electrolyte replenisher, in the treatment of hypokalemia, in buffer solutions, and in fertilizers and explosives. For use as an electrolyte replenisher and in the treatment of hypokalemia. The potassium ion is in the principle intracellular cation of most body tissues. Potassium ions participate in a number of essential physiological processes including the maintenance of intracellular tonicity, the transmission of nerve impulses, the contraction of cardiac, skeletal and smooth muscle, and the maintenance of normal renal function. The intracellular concentration of potassium is approximately 150 to 160 mEq per liter. The normal adult plasma concentration is 3.5 to 5 mEq per liter. An active ion transport system maintains this gradient across the plasma membrane. Potassium is a normal dietary constituent and under steady-state conditions the amount of potassium absorbed from the gastrointestinal tract is equal to the amount excreted in the urine. The usual dietary intake of potassium is 50 to 100 mEq per day. Potassium depletion will occur whenever the rate of potassium loss through renal excretion and/or loss from the gastrointestinal tract exceeds the rate of potassium intake. Such depletion usually develops as a consequence of therapy with diuretics, primarily or secondary hyperaldosteronism, diabetic ketoacidosis, or inadequate replacement of potassium in patients on prolonged parenteral nutrition. Depletion can develop rapidly with severe diarrhea, especially if associated with vomiting. Potassium depletion due to these causes is usually accompanied by concomitant loss of chloride and is manifested by hypokalemia and metabolic alkalosis. Potassium depletion may produce weakness, fatigue, disturbances of cardiac rhythm (primarily ectopic beats), prominent U-waves in the electrocardiogram, and, in advanced cases, flaccid paralysis and/or impaired ability to concentrate urine. If potassium depletion associated with metabolic alkalosis cannot be managed by correcting the fundamental cause of the deficiency, e.g., where the patient requires long-term diuretic therapy, supplemental potassium in the form of high potassium food or potassium chloride may be able to restore normal potassium levels. In rare circumstances (e.g., patients with renal tubular acidosis) potassium depletion may be associated with metabolic acidosis and hyperchloremia. In such patients, potassium replacement should be accomplished with potassium salts other than the chloride, such as potassium bicarbonate, potassium citrate, potassium acetate, or potassium gluconate. Supplemental potassium in the form of high potassium food or potassium chloride may be able to restore normal potassium levels.",The molecular weight is 74.55.,,,Potassium chloride is approved and withdrawn.,Potassium chloride is a solid.,True
16086,"Lepirudin is identical to natural hirudin except for substitution of leucine for isoleucine at the N-terminal end of the molecule and the absence of a sulfate group on the tyrosine at position 63. It is produced via yeast cells. Bayer ceased the production of lepirudin (Refludan) effective May 31, 2012. For the treatment of heparin-induced thrombocytopenia Lepirudin is used to break up clots and to reduce thrombocytopenia. It binds to thrombin and prevents thrombus or clot formation. It is a highly potent, selective, and essentially irreversible inhibitor of thrombin and clot-bond thrombin. Lepirudin requires no cofactor for its anticoagulant action. Lepirudin is a recombinant form of hirudin, an endogenous anticoagulant found in medicinal leeches. Lepirudin forms a stable non-covalent complex with alpha-thrombin, thereby abolishing its ability to cleave fibrinogen and initiate the clotting cascade. The inhibition of thrombin prevents the blood clotting cascade. ",The molecular weight is 6979.49.,Lepirudin has a topological polar surface area of 3107.12.,,Lepirudin is approved.,Lepirudin is a liquid.,True
16087,"3,6-Diaminoacridine. Topical antiseptic used mainly in wound dressings. Topical antiseptic used mainly in wound dressings. Proflavine is an acriflavine derivative which is a disinfectant bacteriostatic against many gram-positive bacteria. Proflavine is toxic and carcinogenic in mammals and so it is used only as a surface disinfectant or for treating superficial wounds. Proflavine acts by interchelating DNA (intercalation), thereby disrupting DNA synthesis and leading to high levels of mutation in the copied DNA strands. This prevents bacterial reproduction.",The molecular weight is 209.25.,Proflavine has a topological polar surface area of 64.93.,The log p value of  is 2.31.,Proflavine is approved.,Proflavine is a solid.,True
16088,,,,,"2-{2-hydroxy--3-yl}-1H-1,3-benzodiazole-5-carboximidamide is experimental.","2-{2-hydroxy--3-yl}-1H-1,3-benzodiazole-5-carboximidamide is a solid.",False
16089,,,,,Beta-(2-Naphthyl)-Alanine is experimental.,Beta-(2-Naphthyl)-Alanine is a solid.,False
16090,,,,,Hemi-Babim is experimental.,Hemi-Babim is a solid.,False
16091,,,,,2-(2-hydroxy-phenyl)-3H-benzoimidazole-5-carboxamidine is experimental.,2-(2-hydroxy-phenyl)-3H-benzoimidazole-5-carboxamidine is a solid.,False
16092,,,,,4-Oxo-2-Phenylmethanesulfonyl-Octahydro-PyrroloPyrazine-6-Carboxylic Acid -Amide is experimental.,4-Oxo-2-Phenylmethanesulfonyl-Octahydro-PyrroloPyrazine-6-Carboxylic Acid -Amide is a solid.,False
16093,,,,,4-IodobenzoThiophene-2-Carboxamidine is experimental.,4-IodobenzoThiophene-2-Carboxamidine is a solid.,False
16094,,,,,CRA_8696 is experimental.,CRA_8696 is a solid.,False
16095,,,,,gamma-carboxy-L-glutamic acid is experimental.,gamma-carboxy-L-glutamic acid is a solid.,False
16096,,,,,6-Chloro-2-(2-Hydroxy-Biphenyl-3-Yl)-1h-Indole-5-Carboxamidine is experimental.,6-Chloro-2-(2-Hydroxy-Biphenyl-3-Yl)-1h-Indole-5-Carboxamidine is a solid.,False
16097,,,,,Lysophosphotidylserine is experimental.,Lysophosphotidylserine is a solid.,False
16098,,,,,"N-{2,2-DIFLUORO-2-ETHYL}-2-OXAZOLOPYRIDIN-4-AMINE is experimental.","N-{2,2-DIFLUORO-2-ETHYL}-2-OXAZOLOPYRIDIN-4-AMINE is a solid.",False
16099,,,,,TRANS-4-(GUANIDINOMETHYL)-CYCLOHEXANE-L-YL-D-3-CYCLOHEXYLALANYL-L-AZETIDINE-2-YL-D-TYROSINYL-L-HOMOARGININAMIDE is experimental.,TRANS-4-(GUANIDINOMETHYL)-CYCLOHEXANE-L-YL-D-3-CYCLOHEXYLALANYL-L-AZETIDINE-2-YL-D-TYROSINYL-L-HOMOARGININAMIDE is a solid.,False
16100,,,,,2-imino-1-hydroxypyridin-2-yl]-N-acetamide is experimental.,2-imino-1-hydroxypyridin-2-yl]-N-acetamide is a solid.,False
16101,,,,,1-GUANIDINO-4-(N-NITRO-BENZOYLAMINO-L-LEUCYL-L-PROLYLAMINO)BUTANE is experimental.,1-GUANIDINO-4-(N-NITRO-BENZOYLAMINO-L-LEUCYL-L-PROLYLAMINO)BUTANE is a solid.,False
16102,,,,,1-GUANIDINO-4-(N-PHENYLMETHANESULFONYL-L-LEUCYL-L-PROLYLAMINO)BUTANE is experimental.,1-GUANIDINO-4-(N-PHENYLMETHANESULFONYL-L-LEUCYL-L-PROLYLAMINO)BUTANE is a solid.,False
16103,Investigated for use/treatment in thrombosis.,,,,Flovagatran is investigational.,Flovagatran is a solid.,True
16104,"C1 Esterase Inhibitor (Human) is composed of purified endogenous complement component-1 esterase inhibitor (hC1INH) isolated from human plasma. The primary function of endogenous C1INH is to regulate the activation of the complement and contact system pathways. C1 esterase inhibitors are indicated for the prophylaxis and treatment of acute attacks of hereditary angioedema in patients at least 6 years old. The C1 esterase inhibitor treats and prevents attacks of hereditary angioedema. It has a long duration of action as it is given every 3-4 days prophylactically. Patients should be counselled regarding the risk of hypersensitivity reactions as well as arterial and venous thromboemboli. The C1 esterase inhibitor binds to proteins such as C1s, kallikrein, factor XIIa, and XIa and irreversibly inactivates them. Patients with hereditary angioedema have low levels of C1 esterase inhibitors. By providing patients with C1 esterase inhibitors, this may prevent contact system activation, which prevents increases in vascular permeability. Manifestations of hereditary angioedema may be prevented by preventing increases in vascular permeability.",,,,Human C1-esterase inhibitor is approved.,Human C1-esterase inhibitor is a solid.,True
16105,,,,,methyl L-phenylalaninate is experimental.,methyl L-phenylalaninate is a solid.,False
16106,,,,,carbamoyl]pyrrolidin-1-yl]-1-oxo-3-phenylpropan-2-yl]azanium is experimental.,carbamoyl]pyrrolidin-1-yl]-1-oxo-3-phenylpropan-2-yl]azanium is a solid.,False
16107,,,,,(S)-N-(4-carbamimidoylbenzyl)-1-(2-(cyclopentylamino)ethanoyl)pyrrolidine-2-carboxamide is experimental.,(S)-N-(4-carbamimidoylbenzyl)-1-(2-(cyclopentylamino)ethanoyl)pyrrolidine-2-carboxamide is a solid.,False
16108,,,,,(S)-N-(4-carbamimidoylbenzyl)-1-(2-(cyclohexylamino)ethanoyl)pyrrolidine-2-carboxamide is experimental.,(S)-N-(4-carbamimidoylbenzyl)-1-(2-(cyclohexylamino)ethanoyl)pyrrolidine-2-carboxamide is a solid.,False
16109,,,,,N-cycloheptylglycyl-N-(4-carbamimidoylbenzyl)-L-prolinamide is experimental.,N-cycloheptylglycyl-N-(4-carbamimidoylbenzyl)-L-prolinamide is a solid.,False
16110,,,,,N-cyclooctylglycyl-N-(4-carbamimidoylbenzyl)-L-prolinamide is experimental.,N-cyclooctylglycyl-N-(4-carbamimidoylbenzyl)-L-prolinamide is a solid.,False
16111,,,,,N-ALLYL-5-AMIDINOAMINOOXY-PROPYLOXY-3-CHLORO-N-CYCLOPENTYLBENZAMIDE is experimental.,N-ALLYL-5-AMIDINOAMINOOXY-PROPYLOXY-3-CHLORO-N-CYCLOPENTYLBENZAMIDE is a solid.,False
16112,,,,,6-(2-HYDROXY-CYCLOPENTYL)-7-OXO-HEPTANAMIDINE is experimental.,6-(2-HYDROXY-CYCLOPENTYL)-7-OXO-HEPTANAMIDINE is a solid.,False
16113,,,,,6-CARBAMIMIDOYL-2--HEXANOIC ACID is experimental.,6-CARBAMIMIDOYL-2--HEXANOIC ACID is a solid.,False
16114,,,,,6-CARBAMIMIDOYL-2--HEXANOIC ACID is experimental.,6-CARBAMIMIDOYL-2--HEXANOIC ACID is a solid.,False
16115,,,,,N-(3-chlorobenzyl)-1-(4-methylpentanoyl)-L-prolinamide is experimental.,N-(3-chlorobenzyl)-1-(4-methylpentanoyl)-L-prolinamide is a solid.,False
16116,,,,,1--PYRROLIDINE-3-CARBOXYLIC ACID 5-CHLORO-2-(2-ETHYLCARBAMOYL-ETHOXY)-BENZYLAMIDE is experimental.,1--PYRROLIDINE-3-CARBOXYLIC ACID 5-CHLORO-2-(2-ETHYLCARBAMOYL-ETHOXY)-BENZYLAMIDE is a solid.,False
16117,,,,,1--N-(3-chlorobenzyl)-L-prolinamide is experimental.,1--N-(3-chlorobenzyl)-L-prolinamide is a solid.,False
16118,,,,,D-leucyl-N-(3-chlorobenzyl)-L-prolinamide is experimental.,D-leucyl-N-(3-chlorobenzyl)-L-prolinamide is a solid.,False
16119,,,,,D-phenylalanyl-N-(3-chlorobenzyl)-L-prolinamide is experimental.,D-phenylalanyl-N-(3-chlorobenzyl)-L-prolinamide is a solid.,False
16120,,,,,1-butanoyl-N-(4-carbamimidoylbenzyl)-L-prolinamide is experimental.,1-butanoyl-N-(4-carbamimidoylbenzyl)-L-prolinamide is a solid.,False
16121,,,,,N-(4-carbamimidoylbenzyl)-1-(4-methylpentanoyl)-L-prolinamide is experimental.,N-(4-carbamimidoylbenzyl)-1-(4-methylpentanoyl)-L-prolinamide is a solid.,False
16122,N-(4-carbamimidoylbenzyl)-1-(3-phenylpropanoyl)-l-prolinamide is a solid. This compound belongs to the alpha amino acid amides. These are amide derivatives of alpha amino acids. This medication targets the protein prothrombin.,,,,N-(4-carbamimidoylbenzyl)-1-(3-phenylpropanoyl)-L-prolinamide is experimental.,N-(4-carbamimidoylbenzyl)-1-(3-phenylpropanoyl)-L-prolinamide is a solid.,True
16123,,,,,1--N-(4-carbamimidoylbenzyl)-L-prolinamide is experimental.,1--N-(4-carbamimidoylbenzyl)-L-prolinamide is a solid.,False
16124,,,,,D-leucyl-N-(4-carbamimidoylbenzyl)-L-prolinamide is experimental.,D-leucyl-N-(4-carbamimidoylbenzyl)-L-prolinamide is a solid.,False
16125,,,,,D-phenylalanyl-N-{4-benzyl}-L-prolinamide is experimental.,D-phenylalanyl-N-{4-benzyl}-L-prolinamide is a solid.,False
16126,,,,,"(3R)-8-(dioxidosulfanyl)-3-methyl-1,2,3,4-tetrahydroquinoline is experimental.","(3R)-8-(dioxidosulfanyl)-3-methyl-1,2,3,4-tetrahydroquinoline is a solid.",False
16127,,,,,D-phenylalanyl-N-(3-fluorobenzyl)-L-prolinamide is experimental.,D-phenylalanyl-N-(3-fluorobenzyl)-L-prolinamide is a solid.,False
16128,,,,,beta-phenyl-D-phenylalanyl-N-propyl-L-prolinamide is experimental.,beta-phenyl-D-phenylalanyl-N-propyl-L-prolinamide is a solid.,False
16129,,,,,(S)-N-(4-carbamimidoylbenzyl)-1-(2-(cyclopentyloxy)ethanoyl)pyrrolidine-2-carboxamide is experimental.,(S)-N-(4-carbamimidoylbenzyl)-1-(2-(cyclopentyloxy)ethanoyl)pyrrolidine-2-carboxamide is a solid.,False
16130,,,,,(S)-N-(4-carbamimidoylbenzyl)-1-(2-(cyclohexyloxy)ethanoyl)pyrrolidine-2-carboxamide is experimental.,(S)-N-(4-carbamimidoylbenzyl)-1-(2-(cyclohexyloxy)ethanoyl)pyrrolidine-2-carboxamide is a solid.,False
16131,,,,,(S)-N-(4-carbamimidoylbenzyl)-1-(3-cyclopentylpropanoyl)pyrrolidine-2-carboxamide is experimental.,(S)-N-(4-carbamimidoylbenzyl)-1-(3-cyclopentylpropanoyl)pyrrolidine-2-carboxamide is a solid.,False
16132,,,,,2--3-(4-Guanidino-Phenyl)-Propionamide is experimental.,2--3-(4-Guanidino-Phenyl)-Propionamide is a solid.,False
16133,,,,,"3-Carbamimidamido-1,1-diphenylurea is experimental.","3-Carbamimidamido-1,1-diphenylurea is a solid.",False
16134,,,,,"N7-BUTYL-N2-(5-CHLORO-2-METHYLPHENYL)-5-METHYLTRIAZOLOPYRIMIDINE-2,7-DIAMINE is experimental.","N7-BUTYL-N2-(5-CHLORO-2-METHYLPHENYL)-5-METHYLTRIAZOLOPYRIMIDINE-2,7-DIAMINE is a solid.",False
16135,,,,,(S)-N-(4-carbamimidoylbenzyl)-1-(3-cyclohexylpropanoyl)pyrrolidine-2-carboxamide is experimental.,(S)-N-(4-carbamimidoylbenzyl)-1-(3-cyclohexylpropanoyl)pyrrolidine-2-carboxamide is a solid.,False
16136,,,,,D-phenylalanyl-N-(3-methylbenzyl)-L-prolinamide is experimental.,D-phenylalanyl-N-(3-methylbenzyl)-L-prolinamide is a solid.,False
16137,,,,,D-phenylalanyl-N-benzyl-L-prolinamide is experimental.,D-phenylalanyl-N-benzyl-L-prolinamide is a solid.,False
16138,,,,,N-(5-CHLORO-BENZOTHIOPHEN-3-YLMETHYL)-2--ACETAMIDE is experimental.,N-(5-CHLORO-BENZOTHIOPHEN-3-YLMETHYL)-2--ACETAMIDE is a solid.,False
16139,,,,,3-cyclohexyl-D-alanyl-N-(3-chlorobenzyl)-L-prolinamide is experimental.,3-cyclohexyl-D-alanyl-N-(3-chlorobenzyl)-L-prolinamide is a solid.,False
16140,,,,,(2R)-2-(5-CHLORO-2-THIENYL)-N-{(3S)-1--2-OXOPYRROLIDIN-3-YL}PROPENE-1-SULFONAMIDE is experimental.,(2R)-2-(5-CHLORO-2-THIENYL)-N-{(3S)-1--2-OXOPYRROLIDIN-3-YL}PROPENE-1-SULFONAMIDE is a solid.,False
16141,,,,,2-(5-CHLORO-2-THIENYL)-N-{(3S)-1--2-OXOPYRROLIDIN-3-YL}ETHANESULFONAMIDE is experimental.,2-(5-CHLORO-2-THIENYL)-N-{(3S)-1--2-OXOPYRROLIDIN-3-YL}ETHANESULFONAMIDE is a solid.,False
16142,,,,,GW-813893 is experimental.,GW-813893 is a solid.,False
16143,,,,,N-ETHYL-N-ISOPROPYL-3-METHYL-5-{OXY}BENZAMIDE is experimental.,N-ETHYL-N-ISOPROPYL-3-METHYL-5-{OXY}BENZAMIDE is a solid.,False
16144,,,,,"4-(2,5-DIAMINO-5-HYDROXY-PENTYL)-PHENOL is experimental.","4-(2,5-DIAMINO-5-HYDROXY-PENTYL)-PHENOL is a solid.",False
16145,,,,,2--PYRROLIDINE-1-CARBOXYLIC ACID BENZYL ESTER is experimental.,2--PYRROLIDINE-1-CARBOXYLIC ACID BENZYL ESTER is a solid.,False
16146,,,,,5-(DIMETHYLAMINO)-1-NAPHTHALENESULFONIC ACID(DANSYL ACID) is experimental.,5-(DIMETHYLAMINO)-1-NAPHTHALENESULFONIC ACID(DANSYL ACID) is a solid.,False
16147,,,,,1-ETHOXYCARBONYL-D-PHE-PRO-2(4-AMINOBUTYL)HYDRAZINE is experimental.,1-ETHOXYCARBONYL-D-PHE-PRO-2(4-AMINOBUTYL)HYDRAZINE is a solid.,False
16148,,,,,4-TERT-BUTYLBENZENESULFONIC ACID is experimental.,4-TERT-BUTYLBENZENESULFONIC ACID is a solid.,False
16149,,,,,"3-AMINO-3-BENZYL-9-CARBOXAMIDEBICYCLO-1,6-DIAZANONAN-2-ONE is experimental.","3-AMINO-3-BENZYL-9-CARBOXAMIDEBICYCLO-1,6-DIAZANONAN-2-ONE is a solid.",False
16150,,,,,4-(5-BENZENESULFONYLAMINO-1-METHYL-1H-BENZOIMIDAZOL-2-YLMETHYL)-BENZAMIDINE is experimental.,4-(5-BENZENESULFONYLAMINO-1-METHYL-1H-BENZOIMIDAZOL-2-YLMETHYL)-BENZAMIDINE is a solid.,False
16151,,,,,"1-(2-{amino}ethyl)-6-chloro-3--1,4-dihydropyrazin-2-ol is experimental.","1-(2-{amino}ethyl)-6-chloro-3--1,4-dihydropyrazin-2-ol is a solid.",False
16152,,,,,"(3Z,6S)-6-Chloro-1-(2-{amino}ethyl)-3-({2-ethyl}imino)-2-piperazinol is experimental.","(3Z,6S)-6-Chloro-1-(2-{amino}ethyl)-3-({2-ethyl}imino)-2-piperazinol is a solid.",False
16153,,,,,N-NAPHTHALENE-2-SULFONAMIDE is experimental.,N-NAPHTHALENE-2-SULFONAMIDE is a solid.,False
16154,,,,,"N--4-METHOXY-2,3,6-TRIMETHYLBENZENESULFONAMIDE is experimental.","N--4-METHOXY-2,3,6-TRIMETHYLBENZENESULFONAMIDE is a solid.",False
16155,,,,,2-(6-CHLORO-3-{AMINO}-2-OXO-1(2H)-PYRAZINYL)-N-ACETAMIDE is experimental.,2-(6-CHLORO-3-{AMINO}-2-OXO-1(2H)-PYRAZINYL)-N-ACETAMIDE is a solid.,False
16156,,,,,2-(6-CHLORO-3-{AMINO}-2-OXO-1(2H)-PYRAZINYL)-N-ACETAMIDE is experimental.,2-(6-CHLORO-3-{AMINO}-2-OXO-1(2H)-PYRAZINYL)-N-ACETAMIDE is a solid.,False
16157,,,,,2-(6-CHLORO-3-{AMINO}-2-OXO-1(2H)-PYRAZINYL)-N-ACETAMIDE is experimental.,2-(6-CHLORO-3-{AMINO}-2-OXO-1(2H)-PYRAZINYL)-N-ACETAMIDE is a solid.,False
16158,,,,,3-(7-DIAMINOMETHYL-NAPHTHALEN-2-YL)-PROPIONIC ACID ETHYL ESTER is experimental.,3-(7-DIAMINOMETHYL-NAPHTHALEN-2-YL)-PROPIONIC ACID ETHYL ESTER is a solid.,False
16159,,,,,AC-(D)Phe-pro-borolys-OH is experimental.,AC-(D)Phe-pro-borolys-OH is a solid.,False
16160,,,,,AC-(D)PHE-PRO-BOROHOMOLYS-OH is experimental.,AC-(D)PHE-PRO-BOROHOMOLYS-OH is a solid.,False
16161,,,,,AC-(D)PHE-PRO-BOROHOMOORNITHINE-OH is experimental.,AC-(D)PHE-PRO-BOROHOMOORNITHINE-OH is a solid.,False
16162,,,,,N--2-{6-cyano-3--2-fluorophenyl}acetamide is experimental.,N--2-{6-cyano-3--2-fluorophenyl}acetamide is a solid.,False
16163,,,,,4-Hydroxyphenylpyruvic acid is experimental.,4-Hydroxyphenylpyruvic acid is a solid.,False
16164,,,,,"4-(1R,3AS,4R,8AS,8BR)-PYRROLIZIN-4-YL]BENZAMIDINE is experimental.","4-(1R,3AS,4R,8AS,8BR)-PYRROLIZIN-4-YL]BENZAMIDINE is a solid.",False
16165,,,,,"(3ASR,4RS,8ASR,8BRS)-4-(2-(4-FLUOROBENZYL)-1,3-DIOXODEACAHYDROPYRROLO PYRROLIZIN-4-YL)BENZAMIDINE is experimental.","(3ASR,4RS,8ASR,8BRS)-4-(2-(4-FLUOROBENZYL)-1,3-DIOXODEACAHYDROPYRROLO PYRROLIZIN-4-YL)BENZAMIDINE is a solid.",False
16166,,,,,4-({AMINO}METHYL)BENZENECARBOXIMIDAMIDE is experimental.,4-({AMINO}METHYL)BENZENECARBOXIMIDAMIDE is a solid.,False
16167,,,,,1-(HYDROXYMETHYLENEAMINO)-8-HYDROXY-OCTANE is experimental.,1-(HYDROXYMETHYLENEAMINO)-8-HYDROXY-OCTANE is a solid.,False
16168,,,,,-3ALANYL]PIPERIDINE is experimental.,-3ALANYL]PIPERIDINE is a solid.,False
16169,,,,,N-{3-METHYL-5--PHENYL}-BENZENESULFONAMIDE is experimental.,N-{3-METHYL-5--PHENYL}-BENZENESULFONAMIDE is a solid.,False
16170,,,,,N-amino}oxy)ethyl]-2-{6-chloro-3--2-fluorophenyl}acetamide is experimental.,N-amino}oxy)ethyl]-2-{6-chloro-3--2-fluorophenyl}acetamide is a solid.,False
16171,,,,,4-PIPERIDINE is experimental.,4-PIPERIDINE is a solid.,False
16172,,,,,"3-(4-CHLOROPHENYL)-5-(METHYLTHIO)-4H-1,2,4-TRIAZOLE is experimental.","3-(4-CHLOROPHENYL)-5-(METHYLTHIO)-4H-1,2,4-TRIAZOLE is a solid.",False
16173,,,,,{(2S)-1-pyrrolidin-2-yl}methyl (3-chlorophenyl)acetate is experimental.,{(2S)-1-pyrrolidin-2-yl}methyl (3-chlorophenyl)acetate is a solid.,False
16174,,,,,N-Methylphenylalanyl-N--L-prolinamide is experimental.,N-Methylphenylalanyl-N--L-prolinamide is a solid.,False
16175,,,,,2-Naphthalenesulfonic acid is experimental.,2-Naphthalenesulfonic acid is a solid.,False
16176,,,,,--AMINE is experimental.,--AMINE is a solid.,False
16177,,,,,4-PYRROLIZIN-4-YL]BENZENECARBOXIMIDAMIDE is experimental.,4-PYRROLIZIN-4-YL]BENZENECARBOXIMIDAMIDE is a solid.,False
16178,,,,,1-guanidine is experimental.,1-guanidine is a solid.,False
16179,"Turoctocog alfa is a recombinant factor VIII (rFVIII) with a truncated B-domain made from the sequence coding for 10 amino acids from the N-terminus and 11 amino acids from the C-terminus of the naturally occurring B-domain. Turoctocog alfa is produced in Chinese hamster ovary (CHO) cells without addition of any human- or animal-derived materials. During secretion, some rFVIII molecules are cleaved at the C-terminal of the heavy chain (HC) at amino acid 720, and a monoclonal antibody binding C-terminal to this position is used in the purification process allowing isolation of the intact rFVIII. It was developped by Novo Nordisk and FDA approved in October 16, 2013. Turoctocog alfa is indicated for the treatment and prophylaxis of bleedings in patients presenting hemophilia A. The treatment with turoctocog alfa is related with its use to control bleeding episodes or as a perioperative management. Hemophilia A is a hereditary hemorrhagic disorder generated by the congenital deficit of the coagulation factor VIII. This disease is manifested as excessive spontaneous or trauma-driven bleeding. The coagulation factor VIII is a robust initiator of thrombin which is later required for the generation of fibrin to form a platelet plug and its gene is expressed in the X chromosome. After turoctocog alfa administration, it has been reported a significant improvement in hemostasis. This effect was observed by the amelioration on whole blood clotting time. In clinical trials, there were no reports of development of factor VIII inhibitors and even 90% of the ocurred bleeds were resolved with 1 or 2 infusions of turoctocog alfa. There are no reports of treatment failure. In vitro studies confirmed the ability of turoctocog alfa to improve clot formation and clot stability. All these studies prove that turoctocog alfa is fully functional and its activity is similar to the one showed by other recombinant factor VIII products. The B domain is known to perform the function of restrict the expression of the endogenous coagulation factor VIII but it has no direct relationship to the function of this factor. In normal conditions during hemostasis, the coagulation factor VIII will be activated by specific thrombin cleavages producing A1, A2 and A3-C1-C2 fragments of activated factor VIII (Factor VIIIa) which will form a complex with the factor IXa and activate the factor X leading to a stable haemostatic plug. Turoctocog contains all function-related domains with a considerably easier intact expression of the protein in mammalian cells by truncating the B domain. This recombinant structure allows it to replace the missing factor VIII and restore hemostasis.",,,,Turoctocog alfa is approved and investigational.,Turoctocog alfa is a liquid.,True
16180,"C1 Esterase Inhibitor (Recombinant) is a recombinant analogue of endogenous complement component-1 esterase inhibitor (rhC1INH), purified from the milk of transgenic rabbits. The primary function of endogenous C1INH is to regulate the activation of the complement and contact system pathways. It does this through inhibition of several target proteases within these pathways including activated C1s, kallikrein, factor XIIa and factor XIa. C1 esterase inhibitor has also been shown to inhibit the action of thrombin within the coagulation pathway, and tPA and plasmin within the fibrinolytic pathway. Deficiency of C1-inhibitor allows for increased plasma kallikrein activation and subsequent production of bradykinin. Additionally, C4 and C2 cleavage occurs resulting in auto-activation of the complement system. Down-stream effects of the lack of enzyme inhibition by C1 esterase inhibitor results in swelling due to leakage of fluid from blood vessels into connective tissue and consequently the presentation of hereditary angioedema (HAE).  For the treatment of acute attacks of hereditary angioedema (HAE) due to C1 esterase inhibitor deficiency in adults. A dose of 50 U/kg of Ruconest increases plasma C1INH activity levels to greater than 0.7 U/mL (the lower limit of normal) in HAE patients. The primary function of endogenous C1INH is to regulate the activation of the complement and contact system pathways. It does this through inhibition of several target proteases within these pathways including activated C1s, kallikrein, factor XIIa and factor XIa. C1 esterase inhibitor has also been shown to inhibit the action of thrombin within the coagulation pathway, and tPA and plasmin within the fibrinolytic pathway. Deficiency of C1-inhibitor allows increased plasma kallikrein activation and subsequent production of bradykinin. Additionally, C4 and C2 cleavage is no longer inhibited allowing auto-activation of the complement system. Down-stream effects of the lack of enzyme inhibition by C1 esterase inhibitor results in swelling due to leakage of fluid from blood vessels into connective tissue and consequently the presentation of hereditary angioedema (HAE). Replacement of C1 esterase inhibitor results in a reversal of these effects.",,,,Conestat alfa is approved and investigational.,Conestat alfa is a liquid.,True
16181,"Antithrombin Alfa is a recombinant antithrombin , an anticoagulant, that is used for the prevention of thromboembolic events in patients that have hereditary deficiency of antithrombin in high risk situations. Antithrombin alfa is a recombinant antithrombin it is indicated for the prevention of peri-operative and peri-partum thromboembolic events in patients with hereditary deficiency of antithrombin.  Hereditary antithrombin deficiency causes an increased risk of venous thromboembolism (VTE). In high risk situations, such as surgery or trauma or for pregnant women during the peri-partum period, the risk of development of VTEs is 10-50 times greater than the general population. In hereditary antithrombin deficient patients antithrombin alfa normalizes plasma antthrombin activity levels during peri-operative and peri-partum periods. Antithrombin is the main inhibitor of thrombin and Factor Xa , the serine proteases involved in blood coagulation. Antithrombin neutralizes the activity of thrombin and Factor Xa by forming a complex which is rapidly removed from the circulation. ",,,,Antithrombin Alfa is approved and investigational.,,True
16182,"Nafamostat is a synthetic serine protease inhibitor that is commonly formulated with hydrochloric acid due to its basic properties. It has been used in trials studying the prevention of Liver Transplantation and Postreperfusion Syndrome. The use of nafamostat in Asian countries is approved as an anticoagulant therapy for patients undergoing continuous renal replacement therapy due to acute kidney injury. Used as an anticoagulant in patients with disseminative blood vessel coagulation, hemorrhagic lesions, and hemorrhagic tendencies. It prevents blood clot formation during extracorporeal circulation in patients undergoing continuous renal replacement therapy and extra corporeal membrane oxygenation.  Nafamostat is a fast-acting proteolytic inhibitor used during hemodialysis to prevent the proteolysis of fibrinogen into fibrin by competitively inhibiting several serine proteases including thrombin. It improves acute pancreatitis and prevents blood clot formation during extracorporeal circulation and has an anti-inflammatory effect in vitro. A study suggets that nafamostat has a neuroprotective role during ischemia-induced brain injury from antithrombin activity.  Nafamostat mesilate inhibits various enzyme systems, such as coagulation and fibrinolytic systems (thrombin, Xa, and XIIa), the kallikrein–kinin system, the complement system, pancreatic proteases and activation of protease-activated receptors (PARs). Nafamostat inhibits lipopolysaccharide-induced nitric oxide production, apoptosis, and interleukin (IL)-6 and IL-8 levels in cultured human trophoblasts. It is shown to act as an antioxidant in TNF-α-induced ROS production. ",The molecular weight is 347.38.,Nafamostat has a topological polar surface area of 138.07.,The log p value of  is 2.28.,Nafamostat is investigational.,Nafamostat is a solid.,True
16183,"A compound produced from succinyl-CoA and glycine as an intermediate in heme synthesis. It is used as a photochemotherapy for actinic keratosis.  Aminolevulinic acid plus blue light illumination using a blue light photodynamic therapy illuminator is indicated for the treatment of minimally to moderately thick actinic keratoses of the face or scalp. The metabolism of aminolevulinic acid (ALA) is the first step in the biochemical pathway resulting in heme synthesis. Aminolevulinic acid is not a photosensitizer, but rather a metabolic precursor of protoporphyrin IX (PpIX), which is a photosensitizer. The synthesis of ALA is normally tightly controlled by feedback inhibition of the enzyme, ALA synthetase, presumably by intracellular heme levels. ALA, when provided to the cell, bypasses this control point and results in the accumulation of PpIX, which is converted into heme by ferrochelatase through the addition of iron to the PpIX nucleus. According to the presumed mechanism of action, photosensitization following application of aminolevulinic acid (ALA) topical solution occurs through the metabolic conversion of ALA to protoporphyrin IX (PpIX), which accumulates in the skin to which aminolevulinic acid has been applied. When exposed to light of appropriate wavelength and energy, the accumulated PpIX produces a photodynamic reaction, a cytotoxic process dependent upon the simultaneous presence of light and oxygen. The absorption of light results in an excited state of the porphyrin molecule, and subsequent spin transfer from PpIX to molecular oxygen generates singlet oxygen, which can further react to form superoxide and hydroxyl radicals. Photosensitization of actinic (solar) keratosis lesions using aminolevulinic acid, plus illumination with the BLU-UTM Blue Light Photodynamic Therapy Illuminator (BLU-U), is the basis for aminolevulinic acid photodynamic therapy (PDT).",The molecular weight is 131.13.,Aminolevulinic acid has a topological polar surface area of 80.39.,The log p value of  is -3.41.,Aminolevulinic acid is approved.,Aminolevulinic acid is a solid.,True
16184,,,,,Delta-Amino Valeric Acid is experimental.,Delta-Amino Valeric Acid is a solid.,False
16185,,,,,Laevulinic Acid is experimental.,Laevulinic Acid is a solid.,False
16186,,,,,4-Oxosebacic Acid is experimental.,4-Oxosebacic Acid is a solid.,False
16187,"Porphobilinogen is a pyrrole involved in porphyrin metabolism. It is generated by the enzyme ALA dehydratase, and converted into hydroxymethyl bilane by the enzyme porphobilinogen deaminase.",,,,Porphobilinogen is experimental.,Porphobilinogen is a solid.,True
16188,,,,,3-(2-Aminoethyl)-4-(Aminomethyl)Heptanedioic Acid is experimental.,3-(2-Aminoethyl)-4-(Aminomethyl)Heptanedioic Acid is a solid.,False
16189,,,,,"4,7-Dioxosebacic Acid is experimental.","4,7-Dioxosebacic Acid is a solid.",False
16190,,,,,5-hydroxyvaleric acid is experimental.,5-hydroxyvaleric acid is a solid.,False
16191,"Trilostane is an inhibitor of 3 beta-hydroxysteroid dehydrogenase used in the treatment of Cushing's syndrome. It was withdrawn from the United States market in April 1994. Used in the treatment of Cushing's syndrome. It is normally used in short-term treatment until permanent therapy is possible. Trilostane blocks an enzyme involved in the production of several steroids including cortisol. Inhibiting this enzyme inhibits the production of cortisol. In Cushing's syndrome, the adrenal gland overproduces steroids. Although steroids are important for various functions of the body, too much can cause problems. Trilostane reduces the amount of steroids produced by the adrenal gland. This product was withdrawn from the U.S. market in April 1994. Trilostane produces suppression of the adrenal cortex by inhibiting enzymatic conversion of steroids by 3-beta-hydroxysteroid dehydrogenase/delta 5,4 ketosteroid isomerase, thus blocking synthesis of adrenal steroids.",The molecular weight is 329.44.,Trilostane has a topological polar surface area of 76.78.,The log p value of  is 2.33.,Trilostane is approved and investigational and vet_approved and withdrawn.,Trilostane is a solid.,True
16192,"L-Lysine (abbreviated as Lys or K) is an α-amino acid with the chemical formula HO2CCH(NH2)(CH2)4NH2. This amino acid is an essential amino acid, which means that humans cannot synthesize it. Its codons are AAA and AAG. L-Lysine is a base, as are arginine and histidine. The ε-amino group acts as a site for hydrogen binding and a general base in catalysis. Common posttranslational modifications include methylation of the ε-amino group, giving methyl-, dimethyl-, and trimethyllysine. The latter occurs in calmodulin. Other posttranslational modifications include acetylation. Collagen contains hydroxylysine which is derived from lysine by lysyl hydroxylase. O-Glycosylation of lysine residues in the endoplasmic reticulum or Golgi apparatus is used to mark certain proteins for secretion from the cell. Supplemental L-lysine has putative anti-herpes simplex virus activity. There is preliminary research suggesting that it may have some anti-osteoporotic activity. Insures the adequate absorption of calcium; helps form collagen ( which makes up bone cartilage &amp; connective tissues); aids in the production of antibodies, hormones &amp; enzymes. Recent studies have shown that Lysine may be effective against herpes by improving the balance of nutrients that reduce viral growth. A deficiency may result in tiredness, inability to concentrate, irritability, bloodshot eyes, retarded growth, hair loss, anemia &amp; reproductive problems. Proteins of the herpes simplex virus are rich in L-arginine, and tissue culture studies indicate an enhancing effect on viral replication when the amino acid ratio of L-arginine to L-lysine is high in the tissue culture media. When the ratio of L-lysine to L-arginine is high, viral replication and the cytopathogenicity of herpes simplex virus have been found to be inhibited. L-lysine may facilitate the absorption of calcium from the small intestine.",The molecular weight is 146.19.,L-Lysine has a topological polar surface area of 89.34.,The log p value of  is -3.42.,L-Lysine is approved and nutraceutical.,L-Lysine is a solid.,True
16193,"An organochlorine insecticide that has been used as a pediculicide and a scabicide. Lindane has been banned in California, United Kingdom, Australia, and many western countries due to concerns about neurotoxicity and adverse effects on the environment. In Canada, Lindane is not recommmended as a first-line therapy due to reports of resistance, neurotoxicity, and bone marrow suppression, but has been approved by the FDA as a second-line therapy for topical treatment of pediculosis capitis (head lice), pediculosis pubis (pubic lice), or scabies in patients greater than two years of age who cannot tolerate or have failed first-line treatment. Lindane is still allowed for pharmaceutical use until 2015. For the treatment of patients infested with Sarcoptes scabiei or pediculosis capitis who have either failed to respond to adequate doses, or are intolerant of other approved therapies. Scabies is a common, highly pruritic infestation of the skin caused by Sarcoptes scabiei (lice). It is a very contagious condition with specific lesions, such as burrows, and nonspecific lesions, such as papules, vesicles and excoriations. The typical areas of the body it affects are finger webs, scalp (hair), wrists, axillary folds, abdomen, buttocks, inframammary folds and genitalia (males). It is characterized by intense night-time itching. Scabies is spread through close personal contact (relatives, sexual partners, schoolchildren, chronically ill patients and crowded communities). Scabies infestations and the corresponding symptoms can be eliminated by killing the scabies with topical insecticides or scabicides. Lindane is a scabicide that is essentially an organochloride insecticide. Lindane is an organochloride insecticide that has similar neurotoxic protperties to DDT. It exerts its parasiticidal action by being directly absorbed through the parasite's exoskeleton (primarily lice, or scabies) and their ova. The gamma-aminobutyric acid (GABA(1)) receptor/chloride ionophore complex is the primary site of action for lindane, and other insecticides such as endosulfan, and fipronil. Blockage of the GABA-gated chloride channel reduces neuronal inhibition, which leads to hyperexcitation of the central nervous system. This results in paralysis, convulsions, and death. Lindane has very low ovicidal activity.",The molecular weight is 290.81.,,The log p value of  is 3.75.,Lindane is approved and withdrawn.,Lindane is a liquid.,True
16194,"Used in the treatment of cancer, Marmiastat is an angiogenesis and metastasis inhibitor. As an angiogenesis inhibitor it limits the growth and production of blood vessels. As an antimetatstatic agent it prevents malignant cells from breaching the basement membranes. For the treatment of various cancers Used in the treatment of cancer, it is an angiogenesis and metastasis inhibitor. As an angiogenesis inhibitor it limits the growth and production of blood vessels. As an antimetatstatic agent it prevents malignant cells from breaching the basement membranes. Marimastat is a broad spectrum matrix metalloprotease inhibitor. It mimics the peptide structure of natural MMP substrates and binds to matrix metalloproteases, thereby preventing the degradation of the basement membrane by these proteases. This antiprotease action prevents the migration of endothelial cells needed to form new blood vessels. Inhibition of MMPs also prevents the entry and exit of tumor cells into existing blood cells, thereby preventing metastasis.",,,,Marimastat is investigational.,Marimastat is a solid.,True
16195,"Glucosamine is commonly used as a treatment for osteoarthritis, although its acceptance as a medical therapy varies. It is an amino sugar and precursor of glycosylated proteins and lipids. Since glucosamine is a precursor for glycosaminoglycans, and glycosaminoglycans are a major component of joint cartilage, supplemental glucosamine may help to rebuild cartilage and treat arthritis. Glucosamine is usually used in the treatment of osteoarthritis, although its efficacy is still in question. Osteoarthritis is characterized by the progressive degeneration of cartilage glycosaminoglycans. The formation of glucosamine is the rate limiting step in glycosaminoglycans synthesis thus the addition is glucosamine, would in theory provide a building block towards the synthesis of glycosaminoglycans and thus slow down the progression of osteoarthritis. Thus far however, the results have not been conclusive. Glucosamine is a precursor of glycosylated proteins and lipids. Oral glucosamine is commonly used for the treatment of osteoarthritis. Since glucosamine is a precursor for glycosaminoglycans, and glycosaminoglycans are a major component of joint cartilage, supplemental glucosamine may help to rebuild cartilage and treat arthritis. Its use as a therapy for osteoarthritis appears safe, but there is conflicting evidence as to its effectiveness with more recent studies showing limited to no clinical benefit of use. Glucosamine is not FDA approved for use in humans. Since glucosamine is classified as a dietary supplement, safety and formulation are solely the responsibility of the manufacturer; evidence of safety and efficacy is not required as long as it is not advertised as a treatment for a medical condition.",The molecular weight is 179.17.,Glucosamine has a topological polar surface area of 116.17.,The log p value of  is -2.18.,Glucosamine is approved and investigational.,Glucosamine is a solid.,True
16196,,,,,"2-Amino-N,3,3-Trimethylbutanamide is experimental.","2-Amino-N,3,3-Trimethylbutanamide is a solid.",False
16197,,,,,2-{Methyl}-4-Methylpentanoic Acid is experimental.,2-{Methyl}-4-Methylpentanoic Acid is a solid.,False
16198,"AE-941 is a naturally occurring anti-angiogenic compound, extracted from cartilage, with multiple anti-angiogenic mechanisms of action that provide broad therapeutic potential for a number of diseases. It is currently in international Phase III trials for renal cell carcinoma and non-small-cell lung cancer. Investigated for use/treatment in kidney cancer, lung cancer, macular degeneration, multiple myeloma, prostate cancer, and psoriasis and psoriatic disorders. AE-941(Neovastat) contains a component that specifically prevents the binding of VEGF (Vascular Endothelial Growth Factor) to its receptors. It inhibits gelatinolytic and elastinolytic activities for MMP-2, MMP-9, and MMP-12. The MMP's are often over expressed in tumors and play an important role in the degradation of the matrix that surrounds the cell (extracellular matrix), which allows tumor growth and invasion (metastasis). It also induces apoptosis (programmed cell death) which is an additional Anti angiogenic activity found in Neovastat.",,,,AE-941 is investigational.,AE-941 is a solid.,True
16199,"PG-530742 selectively inhibits certain matrix metalloproteinases that have been implicated in the cartilage degradation that occurs in osteoarthritis. By inhibiting these MMPs, it potentially limits cartilage degradation and disease progression. Studies are currently assessing the efficacy and safety of PG-530742 in the treatment of mild to moderate knee osteoarthritis. Investigated for use/treatment in osteoarthritis. PG-530742 selectively inhibits certain matrix metalloproteinases that have been implicated in the cartilage degradation that occurs in osteoarthritis. By inhibiting these MMPs, it potentially limits cartilage degradation and disease progression. Studies are currently assessing the efficacy and safety of PG-530742 in the treatment of mild to moderate knee osteoarthritis. PG-530742 selectively inhibits certain matrix metalloproteinases: In an independent research study, the drug-treated group showed decreased levels of MMP-2, -3, -9, and -13.",,,,PG-530742 is investigational.,PG-530742 is a solid.,True
16200,,,,,"5-(4-PHENOXYPHENYL)-5-(4-PYRIMIDIN-2-YLPIPERAZIN-1-YL)PYRIMIDINE-2,4,6(2H,3H)-TRIONE is experimental.","5-(4-PHENOXYPHENYL)-5-(4-PYRIMIDIN-2-YLPIPERAZIN-1-YL)PYRIMIDINE-2,4,6(2H,3H)-TRIONE is a solid.",False
16201,,,,,"(2R)-2-AMINO-3,3,3-TRIFLUORO-N-HYDROXY-2-{METHYL}PROPANAMIDE is experimental.","(2R)-2-AMINO-3,3,3-TRIFLUORO-N-HYDROXY-2-{METHYL}PROPANAMIDE is a solid.",False
16202,,,,,"(3R)-4,4-DIFLUORO-3-BUTANOIC ACID is experimental.","(3R)-4,4-DIFLUORO-3-BUTANOIC ACID is a solid.",False
16203,,The molecular weight is 298.47.,Ricinoleic Acid has a topological polar surface area of 57.53.,The log p value of  is 5.58.,Ricinoleic Acid is experimental.,Ricinoleic Acid is a solid.,False
16204,"SLV319 belongs to a novel class of agents called CB1 antagonists, which work by blocking the cannabinoid type 1 (CB1) receptor. It is developed for the treatment of obesity and other metabolic disorders. Investigated for use/treatment in obesity. SLV319 belongs to a novel class of agents called CB1 antagonists, which work by blocking the cannabinoid type 1 (CB1) receptor. Clinical and preclinical studies involving this class of drug have shown that blocking the cannabinoid type 1 (CB1) receptor results in reduced food intake..",,,,SLV319 is investigational.,SLV319 is a solid.,True
16205,"The anti-obesity drug, V24343, acts by targeting the CB1 receptor in the brain and suppressing a person's appetite. Obesity related disorders such as cardiovascular disease and type II diabetes About V24343 Scientists have long known that cannabis, which stimulates a receptor in the brain called the CB1 receptor, also stimulates appetite as evidenced by the hunger pangs or \munchies\"" often experienced by cannabis smokers. Blockade of these CB1 receptors by products like V24343 has been shown to cause weight loss and may reduce risk factors for obesity related disorders such as cardiovascular disease and type II diabetes.""",,,,V24343 is investigational.,V24343 is a solid.,True
16206,"AVE-1625 is an oral selective and potent antagonist of cannabinoid 1 (CB1) receptors having the same mechanism of action as rimonabant. It is currently developed in obesity and its associated comorbidities. AVE-1625 is also being developed for the treatment of Alzheimer disease. Investigated for use/treatment in alzheimer's disease, obesity, and schizophrenia and schizoaffective disorders. AVE-1625 is a selective and potent antagonist of cannabinoid 1 (CB1) receptors having the same mechanism of action as rimonabant.",,,,AVE-1625 is investigational.,AVE-1625 is a solid.,True
16207,Otenabant has been investigated for the treatment of Obesity. Pre-clinical and clinical trial data suggest that CB-1 antagonists may have favorable effects on glucose metabolism in patients with type 2 diabetes and may also be an effective therapy for the treatment of obesity.,,,,Otenabant is investigational.,,True
16208,"Tetrahydrocannabivarin (THCV) is a propyl analogue of tetrahydrocannabinol (Δ9-THC), one of the primary pharmacological components of. Δ9-THC is currently available in several synthetic forms, including , while purified or isolated THCV is not approved for any medical uses and is not available as any marketed products. As a major phytocannabinoid, however, THCV is accessible within along with other identified cannabinoids including (CBD), (CBN), (CBG), (CBC), (CBV), and (CBDV).  THCV does not currently have any FDA, Health Canada, or EMA approved indications. Compared to THC which demonstrates its effects through weak partial agonist activity at Cannabinoid-1 (CB1R) and Cannabinoid-2 (CB2R) receptors, THCV acts as a CB1 antagonist and a partial agonist of CB2. Further evidence has also shown that THCV acts as an agonist of GPR55 and l-α-lysophosphatidylinositol (LPI). Beyond the endocannabinoid system, THCV has also been reported to activate 5HT1A receptors to produce an antipsychotic effect that has therapeutic potential for ameliorating some of the negative, cognitive and positive symptoms of schizophrenia. Furthermore, THCV interacts with different transient receptor potential (TRP) channels including TRPV1, which may contribute to the analgesic, anti-inflammatory and anti-cancer effects of cannabinoids and Cannabis extracts.",,,,Tetrahydrocannabivarin is investigational.,,True
16209,"Olmesartan belongs to the angiotensin II receptor blocker (ARB) family of drugs, which also includes , , , , and. ARBs selectively bind to angiotensin receptor 1 (AT1) and prevent the protein angiotensin II from binding and exerting its hypertensive effects, which include vasoconstriction, stimulation and synthesis of aldosterone and ADH, cardiac stimulation, and renal reabsorption of sodium, among others. Overall, olmesartan's physiologic effects lead to reduced blood pressure, lower aldosterone levels, reduced cardiac activity, and increased excretion of sodium.  Olmesartan is indicated for the treatment of hypertension either alone or in combination with other antihypertensive agents.  Overall, olmesartan's physiologic effects lead to reduced blood pressure, lower aldosterone levels, reduced cardiac activity, and increased excretion of sodium.  Olmesartan belongs to the angiotensin II receptor blocker (ARB) family of drugs, which also includes , , , , and. ARBs selectively bind to angiotensin receptor 1 (AT1) and prevent the protein angiotensin II from binding and exerting its hypertensive effects. As the principal pressor agent of the renin-angiotensin system, Angiotensin II causes vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation and renal reabsorption of sodium. Olmesartan blocks the vasoconstrictor effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT1 receptor in vascular smooth muscle. Its action is, therefore, independent of the pathways for angiotensin II synthesis. Overall, olmesartan's physiologic effects lead to reduced blood pressure, lower aldosterone levels, reduced cardiac activity, and increased excretion of sodium. ",,,,Olmesartan is approved and investigational.,Olmesartan is a solid.,True
16210,"Eprosartan is an angiotensin II receptor antagonist used to treat hypertension. It performs 2 actions on the renin angiotensin system. By preventing the binding of angiotensin II to AT1, vascular smooth muscle relaxes and vasodilation occurs. By inhibiting norepinephrine production, blood pressure is further reduced. For the management of hypertension alone or in combination with other classes of antihypertensive agents. Also used as a first-line agent in the treatment of diabetic nephropathy, as well as a second-line agent in the treatment of congestive heart failure (only in those intolerant of ACE inhibitors). Angiotensin II, the principal pressor agent of the renin-angiotensin system, is formed from angiotensin I in a reaction catalyzed by angiotensin-converting enzyme. It is responsible for effects such as vasoconstriction, stimulation of synthesis and release of aldosterone, cardiac stimulation, and renal reabsorption of sodium. Eprosartan selectively blocks the binding of angiotensin II to the AT<sub>1</sub> receptor, which in turn leads to multiple effects including vasodilation, a reduction in the secretion of vasopressin, and reduction in the production and secretion of aldosterone. The resulting effect is a decrease in blood pressure. Eprosartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II by selectively blocking the binding of angiotensin II to the AT<sub>1</sub> receptor found in many tissues (e.g., vascular smooth muscle, adrenal gland). There is also an AT<sub>2</sub> receptor found in many tissues but it is not known to be associated with cardiovascular homeostasis. Eprosartan does not exhibit any partial agonist activity at the AT<sub>1</sub> receptor. Its affinity for the AT<sub>1</sub> receptor is 1,000 times greater than for the AT<sub>2</sub> receptor. In vitro binding studies indicate that eprosartan is a reversible, competitive inhibitor of the AT<sub>1</sub> receptor. Eprosartan has also been shown to bind to AT<sub>1</sub> receptors both presynaptically and synaptically. Its action on presynaptic AT<sub>1</sub> receptors results in the inhibition of sympathetically stimulated noradrenaline release. Unlike ACE inhibitors, eprosartan and other ARBs do not interfere with response to bradykinins and substance P, which allows for the absence of adverse effects that are present in ACE inhibitors (eg. dry cough).",The molecular weight is 424.52.,Eprosartan has a topological polar surface area of 92.42.,The log p value of  is 4.8.,Eprosartan is approved.,Eprosartan is a solid.,True
16211,"Forasartan, a specific angiotensin II antagonist, is used alone or with other antihypertensive agents to treat hypertension. Forasartan competes with angiotensin II for binding at the AT1 receptor subtype. As angiotensin II is a vasoconstrictor which also stimulates the synthesis and release of aldosterone, blockage of its effects results in a decreases in systemic vascular resistance. For the treatment of hypertension. Forasartan, a specific angiotensin II antagonist, is used alone or with other antihypertensive agents to treat hypertension. By inhibiting angiotensin II receptors, this drug leads to a decrease in sodium reabsorption (which decreases water content of blood) and a decrease in vasoconstriction. Combined, this has the effect of lowering blood pressure. Forasartan competes with angiotensin II for binding at the AT<sub>1</sub> receptor subtype. As angiotensin II is a vasoconstrictor which also stimulates the synthesis and release of aldosterone, blockage of its effects results in a decreases in systemic vascular resistance. Also, since angiotensin causes vasoconstriction, the inhibition of this receptor decreases vasoconstriction, which consequently also decreases vascular resistnace.",,,,Forasartan is experimental.,Forasartan is a solid.,True
16212,"Saprisartan is an AT1 receptor antagonist. It is based on medications of losartan's prototypical chemical structure. The mode of (functional) AT1 receptor antagonism has been characterized as insurmountable/noncompetitive for saprisartan. It is very likely that slow dissociation kinetics from the AT1 receptor underlie insurmountable antagonism. Saprisartan is used in the treatment of hypertension and heart failure. By inhibiting the angiotensin II receptor, this drug leades to a decrease in sodium reabsorption and a decrease in vasoconstriction. This has the combined effect of decreasing blood pressure. Saprisartan is a selective, potent, orally active and long-acting nonpeptide Angiotensin II type 1 (AT1) receptor antagonist. Saprisartan blocks the renin-angiotensin-aldosterone system (RAAS) at the level of the AT1 receptor that mediates most, if not all, of the important actions of Ang II. Saprisartan binds reversibly to the AT1 receptors in vascular smooth muscle and the adrenal gland. As angiotensin II is a vasoconstrictor, which also stimulates the synthesis and release of aldosterone, blockage of its effects results in decreases in systemic vascular resistance. AT1 receptor antagonists avoid the nonspecificity of the Ang I converting enzyme (ACE) inhibitors. ",,,,Saprisartan is experimental.,Saprisartan is a solid.,True
16213,"CYT006-AngQb is a therapeutic vaccine in development for treatment of hypertension. It is designed to instruct the patient’s immune system to produce an antibody response against angiotensin II, a small peptide that causes blood vessels to narrow and results in increased blood pressure. It is a unique treatment modality that aims to address the issue of patient compliance by offering convenient dosing schedules due to the long-lasting effect induced by vaccination. Investigated for use/treatment in hypertension. The so called renin-angiotensin system (RAS) is an important regulator of blood pressure and has already been successfully targeted by three major classes of",,,,CYT006-AngQb is investigational.,CYT006-AngQb is a solid.,True
16214,"Azilsartan medoxomil is an angiotensin II receptor antagonist indicated for the treatment of mild to moderate essential hypertension. Azilsartan medoxomil is a prodrug of Azilsartan marketed as \Edarbi\"" by Takeda. Azilsartan medoxomil has so far been shown to be superior to olmesartan and valsartan in lowering blood pressure."" Treatment of hypertension (alone or as an adjunct). Azilsartan medoxomil decreases the pressor effect of angiotensin II. In response, angiotensin I, angiotensin II, and renin are increased while aldosterone is decreased. Azilsartan medoxomil blocks the angiotensin II type 1 receptor preventing angiotensin II from binding and causing vasoconstriction. Azilsartan's ability to remain tightly bound to AT1 receptors for very long periods after drug washout is among its most unusual features. ",The molecular weight is 568.54.,Azilsartan medoxomil has a topological polar surface area of 139.57.,The log p value of  is 4.24.,Azilsartan medoxomil is approved and investigational.,Azilsartan medoxomil is a solid.,True
16215,"Fimasartan is an angiotensin II receptor antagonist (ARB) drug employed in the treatment of both hypertension and heart failure. It has been found to be safe when administered with hydrochlorothiazide (a diuretic) in clinical trials. Fimasartan was initially approved September 9th, 2010 in South Korea and is marketed under the brand name _Kanarb_ by Boryung Pharmaceuticals. Used for the treatment of hypertension and heart failure. Fimasartan is a selective angiotensin receptor 1 (AR1) inhibitor. It acts to lower blood pressure by inhibiting vasoconstriction Angiotensin II activates AR1 leading to vasoconstriction and increased noradrenaline release which further increases vasoconstriction via action at α1-adrenergic receptors. It also stimulates secretion of aldosterone which acts to increase sodium and water reabsorption in the renal tubules. Fimasartan bind to and antagonizes AR1 preventing vasoconstriction and reducing aldosterone secretion to increase natriuresis leading to a reduction in blood volume. Together these effects produce an anti-hypertensive effect.",The molecular weight is 501.65.,Fimasartan has a topological polar surface area of 90.37.,The log p value of  is 3.02.,Fimasartan is investigational.,Fimasartan is a solid.,True
16216,"Angiotensin II is under investigation for the treatment of Sepsis, Septic Shock, Diabetes Mellitus, and Acute Renal Failure. Angiotensin II has been investigated for the treatment, basic science, and diagnostic of Hypertension, Renin Angiotensin System, and Idiopathic Membranous Nephropathy. Angiotensin II is a vasoconstrictor indicated for increasing blood pressure in adults with septic or other distributive shock. Angiotensin II is a naturally occurring peptide hormone of the renin-angiotensin-aldosterone-system (RAAS) that has the capacity to cause vasoconstriction and an increase in blood pressure in the human body.  As part of the renin-angiotensin-aldosterone-system (RAAS), angiotensin II raises blood pressure by vasoconstriction, increased aldosterone release by the adrenal zona glomerulosa, sodium and water reabsorption in the proximal tubular cells, and vasopressin secretion ",The molecular weight is 1046.2.,Angiotensin II has a topological polar surface area of 406.34.,,Angiotensin II is approved and investigational.,Angiotensin II is a liquid.,True
16217,"A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from glycine or threonine. It is involved in the biosynthesis of purines; pyrimidines; and other amino acids. Used as a natural moisturizing agent in some cosmetics and skin care products. Serine is classified as a nutritionally non-essential amino acid. Serine is critical for the production of the body's proteins, enzymes and muscle tissue. Serine is needed for the proper metabolism of fats and fatty acids. It also helps in the production of antibodies. Serine is used as a natural moisturizing agent in some cosmetics and skin care products. The main source of essential amino acids is from the diet, non-essential amino acids are normally synthesize by humans and other mammals from common intermediates. L-Serine plays a role in cell growth and development (cellular proliferation). The conversion of L-serine to glycine by serine hydroxymethyltransferase results in the formation of the one-carbon units necessary for the synthesis of the purine bases, adenine and guanine. These bases when linked to the phosphate ester of pentose sugars are essential components of DNA and RNA and the end products of energy producing metabolic pathways, ATP and GTP. In addition, L-serine conversion to glycine via this same enzyme provides the one-carbon units necessary for production of the pyrimidine nucleotide, deoxythymidine monophosphate, also an essential component of DNA.",The molecular weight is 105.09.,Serine has a topological polar surface area of 83.55.,The log p value of  is -2.81.,Serine is investigational and nutraceutical.,Serine is a solid.,True
16218,"A nonsteroidal abortifacient agent that is effective in both the first and second trimesters of pregnancy. For aborting pregnancy between the 13th and 20th weeks of gestation as calculated from the first day of the last normal menstrual period and in the following conditions related to second trimester abortion: 1. Failure of expulsion of the fetus during the course of treatment by another method; 2. Premature rupture of membranes in intrauterine methods with loss of drug and insufficient or absent uterine activity; 3. Requirement of a repeat intrauterine instillation of drug for expulsion of the fetus; 4. Inadvertent or spontaneous rupture of membranes in the presence of a previable fetus and absence of adequate activity for expulsion. Also for the treatment of postpartum hemorrhage due to uterine atony which has not responded to conventional methods of management. Carboprost tromethamine administered intramuscularly stimulates in the gravid uterus myometrial contractions similar to labor contractions at the end of a full term pregnancy. Whether or not these contractions result from a direct effect of carboprost on the myome-trium has not been determined. Nonetheless, they evacuate the products of conception from the uterus in most cases. Postpartum, the resultant myometrial contractions provide hemostasis at the site of placentation. Carboprost tromethamine also stimulates the smooth muscle of the human gastrointestinal tract. This activity may produce the vomiting or diarrhea or both that is common when carbo-prost tromethamine is used to terminate pregnancy and for use postpartum. In laboratory animals and also in humans carboprost tromethamine can elevate body temperature. With the clinical doses of carboprost trometh-amine used for the termination of pregnancy, and for use postpartum, some patients do experience transient temperature increases. In laboratory animals and in humans large doses of carboprost tromethamine can raise blood pressure, probably by contracting the vascular smooth muscle. With the doses of carboprost tromethamine used for terminating pregnancy, this effect has not been clinically significant. In laboratory animals and also in humans carboprost tromethamine can elevate body temperature. With the clinical doses of carboprost tromethamine used for the termination of pregnancy, some patients do experience temperature increases. In some patients, carboprost tromethamine may cause transient bronchoconstriction. Carboprost is a synthetic prostaglandin. It binds the prostaglandin E2 receptor, causing myometrial contractions, casuing the induction of labour or the expulsion of the placenta. Prostaglandins occur naturally in the body and act at several sites in the body including the womb (uterus). They act on the muscles of the womb, causing them to contract.",,,,Carboprost tromethamine is approved.,Carboprost tromethamine is a solid.,True
16219,"Alprostadil is produced endogenously and causes vasodilation by means of a direct effect on vascular and ductus arteriosus (DA) smooth muscle, preventing or reversing the functional closure of the DA that occurs shortly after birth. This results in increased pulmonary or systemic blood flow in infants. In infants, it is used for palliative, not definitive, therapy to temporarily maintain the patency of the ductus arteriosus until corrective or palliative surgery can be performed in neonates who have congenital heart defects and who depend upon the patent ductus for survival. In adults, it is used for the treatment of erectile dysfunction due to neurogenic, vasculogenic, psychogenic, or mixed etiology. For palliative, not definitive, therapy to temporarily maintain the patency of the ductus arteriosus until corrective or palliative surgery can be performed in neonates who have congenital heart defects and who depend upon the patent ductus for survival. Also for the treatment of erectile dysfunction due to neurogenic, vasculogenic, psychogenic, or mixed etiology. Alprostadil (prostaglandin E1) is produced endogenously to relax vascular smooth muscle and cause vasodilation. In adult males, the vasodilatory effects of alprostadil on the cavernosal arteries and the trabecular smooth muscle of the corpora cavernosa result in rapid arteriolar inflow and expansion of the lacunar spaces within the corpora.&nbsp;As the expanded corporal sinusoids are compressed against the tunica albuginea, venous outflow through the subtunical vessels is impeded and penile rigidity develops.&nbsp;This is referred to as the corporal veno-occlusive mechanism. In infants, the vasodilatory effects of alprostadil increase pulmonary or systemic blood flow. Alprostadil causes vasodilation by means of a direct effect on vascular and ductus arteriosus (DA) smooth muscle, preventing or reversing the functional closure of the DA that occurs shortly after birth. This is because, as a form of prostaglandinE1 (PGE1) it has multiple effects on blood flow. This results in increased pulmonary or systemic blood flow in infants. In cyanotic congenital heart disease, alprostadil's actions result in an increased oxygen supply to the tissues. In infants with interrupted aortic arch or very severe aortic coarctation, alprostadil maintains distal aortic perfusion by permitting blood flow through the DA from the pulmonary artery to the aorta. In infants with aortic coarctation, alprostadil reduces aortic obstruction either by relaxing ductus tissue in the aortic wall or by increasing effective aortic diameter by dilating the DA. In infants with these aortic arch anomalies, systemic blood flow to the lower body is increased, improving tissue oxygen supply and renal perfusion. When administered by intracavernosal injection or as an intraurethral suppository, alprostadil acts locally to relax the trabecular smooth muscle of the corpora cavernosa and the cavernosal arteries. Swelling, elongation, and rigidity of the penis result when arterial blood rapidly flows into the corpus cavernosum to expand the lacunar spaces. The entrapped blood reduces the venous blood outflow as sinusoids compress against the tunica albuginea.",The molecular weight is 354.49.,Alprostadil has a topological polar surface area of 94.83.,The log p value of  is 2.5.,Alprostadil is approved and investigational.,Alprostadil is a solid.,True
16220,"Dinoprostone is a naturally occurring prostaglandin E2 (PGE2). It has important effects in labour. It also stimulates osteoblasts to release factors which stimualtes bone resorption by osteoclasts. As a prescription drug it is used as a vaginal suppository, to prepare the cervix for labour and to induce labour. For the termination of pregnancy during the second trimester (from the 12th through the 20th gestational week as calculated from the first day of the last normal menstrual period), as well as for evacuation of the uterine contents in the management of missed abortion or intrauterine fetal death up to 28 weeks of gestational age as calculated from the first day of the last normal menstrual period. Also used in the management of nonmetastatic gestational trophoblastic disease (benign hydatidiform mole). Other indications include improving the cervical inducibility (cervical \ripening\"") in pregnant women at or near term with a medical or obstetrical need for labor induction, and the management of postpartum hemorrhage."" Dinoprostone is equivalent to prostaglandin E2 (PGE2). It stimulates labor and delivery by stimulating the uterine, and thus terminates pregnancy. Dinoprostone is also capable of stimulating the smooth muscle of the gastrointestinal tract of man. This activity may be responsible for the vomiting and/or diarrhea that is not uncommon when dinoprostone is used to terminate pregnancy. Dinoprostone administered intravaginally stimulates the myometrium of the gravid uterus to contract in a manner that is similar to the contractions seen in the term uterus during labor, resulting in the evacuation of the products of conception from the uterus. It is believed that dinoprostone exerts its uterine effects via direct myometrial stimulation, but the exact mechanism of action is unkown. Other suggested mechanisms include the regulation of cellular membrane calcium transport and of intracellular concentrations of cyclic 3',5'-adenosine monophosphate. Dinoprostone also appears to produce local cervical effects including softening, effacement, and dilation. The exact mechanism of action for this effect is also unknown, but it has been suggested that this effect may be associated with collagen degradation caused by secretion of the enzyme collagenase as a partial response to locally administered dinoprostone.",The molecular weight is 352.47.,Dinoprostone has a topological polar surface area of 94.83.,The log p value of  is 2.01.,Dinoprostone is approved.,Dinoprostone is a solid.,True
16221,"Misoprostol is a prostaglandin analog used to reduce the risk of NSAID related ulcers, manage miscarriages, prevent post partum hemorrhage, and also for first trimester abortions. The stimulation of prostaglandin receptors in the stomach reduces gastric acid secretion, while stimulating these receptors in the uterus and cervix can increase the strength and frequency of contractions and decrease cervical tone. Misoprostol is indicated as a tablet to reduce the risk of NSAID induced gastric ulcers but not duodenal ulcers in high risk patients. Misoprostol is also formulated in combination with diclofenac to treat symptoms of osteoarthritis or rheumatoid arthritis in patients with a high risk of developing gastric ulcers. Misoprostol is used off label for the management of miscarriages, prevention of post partum hemorrhage, and is also used alone or in combination with mifepristone in other countries for first trimester abortions. Misoprostol is a prostaglandin E1 analog used to reduce the risk of NSAID induced gastric ulcers by reducing secretion of gastric acid from parietal cells. Misoprostol is also used to manage miscarriages and used alone or in combination with mifepristone for first trimester abortions. An oral dose of misoprostol has an 8 minute onset of action and a duration of action of approximately 2 hours, a sublingual dose has an 11 minute onset of action and a duration of action of approximately 3 hours, a vaginal dose has a 20 minute onset of action and a duration of action of approximately 4 hours, and a rectal dose has a 100 minute onset of action and a duration of action of approximately 4 hours. Misoprostol is a synthetic prostaglandin E1 analog that stimulates prostaglandin E1 receptors on parietal cells in the stomach to reduce gastric acid secretion. Mucus and bicarbonate secretion are also increased along with thickening of the mucosal bilayer so the mucosa can generate new cells. ",The molecular weight is 382.54.,Misoprostol has a topological polar surface area of 83.83.,The log p value of  is 3.07.,Misoprostol is approved.,Misoprostol is a liquid.,True
16222,"Iloprost is a synthetic analogue of prostacyclin PGI2 that dilates systemic and pulmonary arterial vascular beds. It is used to treat pulmonary arterial hypertension (PAH). Used for the treatment of pulmonary arterial hypertension. Iloprost is a synthetic analogue of prostacyclin PGI2 that dilates systemic and pulmonary arterial vascular beds. It was shown to affect platelet aggregation, but whether this effect contributes to its vasodilatory action has not been elucidated. There are two diastereoisomers of iloprost and the 4S isomer is reported to exhibit a higher potency in dilating blood vessels compared to the 4R isomer. Iloprost is a second generation structural analog of prostacyclin (PGI) with about ten-fold greater potency than the first generation stable analogs, such as carbaprostacyclin. Iloprost binds with equal affinity to human prostacyclin (Prostanoid IP) and prostaglandin EP1 receptors. Iloprost constricts the ilium and fundus circular smooth muscle as strongly as prostaglandin E2 (PGE2) itself. Iloprost inhibits the ADP, thrombin, and collagen-induced aggregation of human platelets. In whole animals, iloprost acts as a vasodilator, hypotensive, antidiuretic, and prolongs bleeding time. All of these properties help to antagonize the pathological changes that take place in the small pulmonary arteries of patients with pulmonary hypertension.",The molecular weight is 360.49.,Iloprost has a topological polar surface area of 77.76.,The log p value of  is 2.71.,Iloprost is approved and investigational.,Iloprost is a solid.,True
16223,"Limaprost (as Limaprost alfadex; CAS number 88852-12-4) is an oral prostaglandin E1 analog. Prostaglandins act on a variety of cells such as vascular smooth muscle cells causing constriction or dilation, on platelets causing aggregation or disaggregation and on spinal neurons causing pain. Prostaglandins have a wide variety of actions, including, but not limited to muscular constriction and mediation of inflammation. Limaprost alfadex has been shown to improve peripheral circulatory failure with a vasodilator action and an antithrombotic effect. It also improves poor blood flow in the nerve tissue in cervical spondylosis and normalizes nerve function. Limaprost alfadex was discovered from collaborative research between Ono Pharmaceutical (Ono) and Dainippon Sumitomo Pharma (DSP). It was approved for the treatment of ischemic symptoms such as skin ulcer, pain and coldness accompanying thromboangiitis obliterans in 1988; and for the treatment of subjective symptoms such as pain and numbness in the lower leg and walking disability associated with acquired lumbar spinal canal stenosis as an additional indication in 2001. The drug has been sold under the trade name of Opalmon® Tablets by Ono and Prorenal® Tablets by DSP. In 2011, Ono and DSP initiated Phase II clinical trials in Japan for the treatment of carpal tunnel syndrome. In 2013, these trials were discontinued because the study failed to demonstrate efficacy. Ono and DSP also discontinued the development of limaprost alfadex for the additional indication of cervical spondylosis in 2008 due to the failure to demonstrate the anticipated efficacy in a Phase II study in patients with the disease. However, it was verified by Seoul National University Hospital in November of 2014 that the study on the efficacy of oral limaprost alfadex after surgery for cervical myelopathy was still ongoing. Limaprost is used for the improvement of various ischemic symptoms such as ulcer, pain and feeling of coldness associated with thromboangiitis obliterans as well as improvement of subjective symptoms (pain and numbness of lower legs) and gait ability associated with acquired lumbar spinal canal stenosis (in patients with bilateral intermittent claudication showing normal SLR test result). Limaprost produces vasodilation to improve blood flow to the extremities and increase cutaneous temperature. As a prostglandin E1 analog, limaprost acts as an agonist at prostraglandin E2 receptors. It likely stimulates the adenylate cyclase coupled E2 subtype of these receptors to produce smooth muscle relaxation. ",The molecular weight is 380.52.,Limaprost has a topological polar surface area of 94.83.,The log p value of  is 3.44.,Limaprost is investigational.,Limaprost is a solid.,True
16224,,,,,Radicicol is experimental.,Radicicol is a solid.,False
16225,,,,,Dihydrolipoic Acid is experimental.,Dihydrolipoic Acid is a solid.,False
16226,"Rituximab is a genetically engineered chimeric murine/human monoclonal antibody directed against the CD20 antigen found on the surface of normal and malignant B lymphocytes. The antibody is an IgG1 kappa immunoglobulin containing murine light and heavy-chain variable region sequences and human constant region sequences ,. It was originally approved by the U.S. FDA in 1997 as a single agent to treat patients with B-cell Non-Hodgkin's Lymphoma (NHL) , however, has now been approved for a variety of conditions. On November 28, 2018, the US FDA approved _Truxima_, the first biosimilar to Rituxan (Rituximab). Rituximab is indicated in the following conditions : Rituximab binds to the CD20 antigen, which is predominantly expressed on mature B cells and on >90% of B-cell non-Hodgkin's lymphomas. The antibody leads to selective killing of B-cells. The following are the pharmacodynamic outcomes for various conditions, including non- Hodgkin's Lymphoma : Rituximab is a monoclonal antibody that targets the CD20 antigen, which is expressed on the surface of pre-B and mature B-lymphocytes , , ,. After binding to CD20, rituximab mediates B-cell lysis (or breakdown). The possible mechanisms of cell lysis include complement dependent cytotoxicity (CDC) and antibody dependent cell-mediated cytotoxicity (ADCC).",,,,Rituximab is approved.,Rituximab is a liquid.,True
16227,"Indium or yttrium conjugated murine IgG1 kappa monoclonal antibody directed against the CD20 antigen, which is found on the surface of normal and malignant B lymphocytes. Ibritumomab is produced in Chinese hamster ovary cells and is composed of two murine gamma 1 heavy chains of 445 amino acids each and two kappa light chains of 213 amino acids each. For treatment of non-Hodgkin's lymphoma Ibritumomab is a murine monoclonal antibody against CD20 that has been radiolabeled with yttrium-90. The Fab segment of the antibody targets the CD20 epitope on B-cells, allowing the radioactive yttrium to destroy the cell via production of beta particles.",,,,Ibritumomab tiuxetan is approved and investigational.,Ibritumomab tiuxetan is a liquid.,True
16228,"Murine IgG2a lambda monoclonal antibody against CD20 antigen (2 heavy chains of 451 residues, 2 lambda chains of 220 residues). It is produced in an antibiotic-free culture of mammalian cells. It can be covalently linked to Iodine 131 (a radioactive isotope of iodine). For treatment of non-Hodgkin's lymphoma (CD20 positive, follicular) Tositumomab binds to the CD20 antigen, which is predominantly expressed on mature B cells and on >90% of B-cell non-Hodgkin's lympohomas. The antibody leads to selective killing of B-cells. Binds to the CD20 antigen which is found on mature B lymphocytes. The antibody binding appears to induce apoptosis, complement-dependent cytotoxicity and cell death through ionizing radiation.",,,,Tositumomab is approved and investigational.,Tositumomab is a liquid.,True
16229,"Ofatumumab is a novel anti-CD20 monoclonal antibody that targets B-cells. It is an IgG1κ human monoclonal antibody produced from a recombinant murine cell line (NS0) via transgenic mouse and hybridoma technology. Ofatumumab works by recognizing antigens that are expressed on the tumour cells in certain cancers; however, the antigen is not tumour-specific and can also be found in normal B-cells. Ofatumumab was first approved by the FDA in 2009. It is used in the treatment of recurrent, progressive, or recurrent chronic lymphocytic leukemia (CLL) or CLL in treatment-naive patients in whom fludarabine-based therapy is considered inappropriate. Ofatumumab is used as monotherapy or in combination with other medications, depending on the patient profile and previous treatment history. Although it has a similar molecular mechanism of action as , another CD-20 monoclonal antibody used in the treatment of rheumatoid arthritis and B-cell non-Hodgkin's lymphoma, ofatumumab has a higher affinity towards CD20. Ofatumumab is indicated, in combination with , for the treatment of previously untreated patients with chronic lymphocytic leukemia (CLL) for whom fludarabine-based therapy is considered inappropriate. Ofatumumab works by binding to and blocking the action of CD-20, a molecule expressed on the surface of both healthy and leukemic B lymphocytes. In patients with previously untreated chronic lymphocytic leukemia (CLL), ofatumumab caused B-cell depletion in the peripheral blood after six months following the last dose. However, observable depletion of B cells in the peripheral blood does not directly correlate with the depletion of B-cells in solid organs or malignant tumours. In vitro, ofatumumab induces complement-dependent cytotoxicity (CDC) and antibody-dependent cellular cytotoxicity (ADCC). CD20 is expressed on normal pre-B lymphocytes and mature B lymphocytes, as well as malignant B lymphocytes. Numerous studies demonstrate that the depletion of B-cells can significantly alleviate symptoms of many forms of leukemia and lymphoma, which are malignancies associated with B-cell dysfunctions and high expression of CD20. ",,,,Ofatumumab is approved.,Ofatumumab is a liquid.,True
16230,"Obinutuzumab is a humanized monoclonal antibody used as a combination treatment with chlorambucil to treat patients with untreated chronic lymphocytic leukemia. It was approved by the FDA in November 2013 and is marketed under the brand name Gazyva. There is a black box warning of fatal Hepatitis B Virus (HBV) reactivation and fatal Progressive Multifocal Leukoencephalopathy (PML). Obinutuzumab is used as a combination treatment with chlorambucil to treat patients with untreated chronic lymphocytic leukemia. Obinutuzumab is more potent than rituximab in depleting B-cells, antitumor activity, and tumor regression. In contrast to rituximab, which is a classic type I CD20 antibody, obinutuzumab binds to type II CD20 antibodies. This allows obinutuzumab to have a much higher induction of antibody-dependant cytotoxicity and a higher direct cytotoxic effect than the classic CD20 antibodies.",,,,Obinutuzumab is approved and investigational.,Obinutuzumab is a liquid.,True
16231,"Technetium Tc-99m nofetumomab merpentan (Tc-99m nm) consists of a Fab fragment of an IgG2b of the pancarcinoma murine antibody NR-LU-10. The NR-LU-10 antibody is directed against a 40 kDa glycoprotein antigen expressed in a variety of cancers and some normal tissues. Tc-99m nm was developed by Boehringer Ingelheim Pharma KG and FDA approved on September 14, 1992. It was after discontinued on August 13, 2013, but in the 2018 FDA submission list, it can be found as a substance type II (Drug substance) with an active status. Tc-99m nm is one of the technetium-labeled antibodies and it is indicated for the detection of small-cell lung cancer. The small cell lung cancer is a syndrome characterized by the abnormal and uncontrolled cell growth and it is characterized by a shorter doubling time, higher growth fraction and earlier development of metastases. Studies have shown that the Fab fragment presents high immunoreactivity in small cell lung cancer tumors. The adenocarcinomas of the kidney and pancreas are not detected. This lack of diagnostic detection can be explained because some radioactivity gets accumulated in the excretion pathway, in nonspecific vascular locations and in non-tumor areas with traces of inflammation, increased vascular pool or recent surgical. Therefore, the detection rate may be reduced in those areas and its adjacent zones. The mechanism of action in Tc-99m nm is ruled by the presence of nofetumomab, which can recognize the pancarcinoma antigen EpCAM and/or CD20/MS4A1, and merpentan, that acts as a linker for the binding of technetium.",,,,Technetium Tc-99m nofetumomab merpentan is approved and withdrawn.,Technetium Tc-99m nofetumomab merpentan is a solid.,True
16232,"Ocrelizumab is a CD20-directed cytolytic antibody indicated for the treatment of patients with relapsing or primary progressive forms of multiple sclerosis. It is a second-generation recombinant humanized monoclonal IgG1 antibody that selectively targets the B lymphocytes that express the CD20 antigen. As a humanized molecule, ocrelizumab is expected to be less immunogenic with repeated infusions which improves the benefit-to-risk profile for patients with relapsing or progressive forms of MS.  Indicated for the treatment of adult patients with relapsing or primary progressive forms of multiple sclerosis. Since ocrelizumab interferes with the CD20 assay, CD19+B-cells were used to assess B-cell counts after ocrelizumab treatment. 14 days following infusion, a reduction in CD19+B-cell counts was observed. In clinical studies, B-cell counts rose to above the lower limit of normal (LLN) or above baseline counts between infusions of ocrelizumab at least one time in 0.3% to 4.1% of patients. In a clinical study involving 51 patients, the time for B-cell counts to return to baseline or LLN was ranged from 27 to 125 weeks, with the median time of 72 weeks, after the last infusion. Within 2.5 years after the last infusion, B-cell counts returned to either baseline or LNN in 90% of the patients. B lymphocytes are known to contribute to the pathogenesis of MS through activation of pro-inflammatory T cells and secretion of proinflammatory cytokines. B cells may differentiate into plasma cells that can produce autoantibodies directed against myelin and cause complement-mediated attack on the myelin sheath. CD20 is a cell-surface antigen found on pre-B cells, naïve and mature B cells and memory B cells. However, this activated glycosylated phosphoprotein is not expressed on haematopoietic stem cells, pro-B cells (precursors), or differentiated plasma cells. ",,,,Ocrelizumab is approved and investigational.,Ocrelizumab is a solid.,True
16233,,,,,"L-N(omega)-Nitroarginine-2,4-L-diaminobutyric amide is experimental.","L-N(omega)-Nitroarginine-2,4-L-diaminobutyric amide is a solid.",False
16234,"Formic acid (systematically called methanoic acid) is the simplest carboxylic acid. It is an important intermediate in chemical synthesis and occurs naturally, most famously in the venom of bee and ant stings. It is commonly used as a preservative and antibacterial agent in livestock feed.",,,,Formic acid is experimental and investigational.,Formic acid is a liquid.,True
16235,,,,,N-{(4S)-4-Amino-5-pentyl}-N'-nitroguanidine is experimental.,N-{(4S)-4-Amino-5-pentyl}-N'-nitroguanidine is a solid.,False
16236,,,,,L-N(omega)-nitroarginine-(4R)-amino-L-proline amide is experimental.,L-N(omega)-nitroarginine-(4R)-amino-L-proline amide is a solid.,False
16237,,,,,1-hydroxy-2-isopropylguanidine is experimental.,1-hydroxy-2-isopropylguanidine is a solid.,False
16238,,,,,2-butyl-1-hydroxyguanidine is experimental.,2-butyl-1-hydroxyguanidine is a solid.,False
16239,,,,,S-Ethyl-N-Isothiourea is experimental.,S-Ethyl-N-Isothiourea is a solid.,False
16240,,,,,S-Ethyl-N-Phenyl-Isothiourea is experimental.,S-Ethyl-N-Phenyl-Isothiourea is a solid.,False
16241,,,,,azanium is experimental.,azanium is a solid.,False
16242,,,,,5-N-Allyl-arginine is experimental.,5-N-Allyl-arginine is a solid.,False
16243,An inhibitor of nitric oxide synthetase which has been shown to prevent glutamate toxicity. Nitroarginine has been experimentally tested for its ability to prevent ammonia toxicity and ammonia-induced alterations in brain energy and ammonia metabolites. (Neurochem Res 1995:200(4):451-6),,,,Nitroarginine is experimental and investigational.,Nitroarginine is a solid.,True
16244,"NXN-188 is a first-in-class, dual-action small molecule incorporating both neuronal nitric oxide synthase (nNOS) inhibition and 5-HT agonism that is being developed for the treatment of acute migraine. Investigated for use/treatment in migraine and cluster headaches. NXN-188 is a first-in-class, dual-action, small molecule that is being developed for the treatment of acute migraine and which incorporates both 5-HT agonism (the mechanism of action of triptans, the current standard of care in migraine therapy) and nNOS inhibition. NOS is a validated target for migraine therapy as migraine models indicate that nNOS inhibition can relieve pain. Additionally, nitric oxide induces migraines in migraineurs, while the inhibition of NOS has been demonstrated to relieve migraine pain.",,,,NXN-188 is investigational.,NXN-188 is a solid.,True
16245,,,,,"N-{(3S,4S)-4-PYRROLIDIN-3-YL}-N'-(4-CHLOROBENZYL)ETHANE-1,2-DIAMINE is experimental.","N-{(3S,4S)-4-PYRROLIDIN-3-YL}-N'-(4-CHLOROBENZYL)ETHANE-1,2-DIAMINE is a solid.",False
16246,,,,,"N-{(3R,4S)-4-pyrrolidin-3-yl}-N'-(3-chlorobenzyl)ethane-1,2-diamine is experimental.","N-{(3R,4S)-4-pyrrolidin-3-yl}-N'-(3-chlorobenzyl)ethane-1,2-diamine is a solid.",False
16247,,,,,"4-Hydroxy-1,2,5-oxadiazole-3-carboxylic acid is experimental.","4-Hydroxy-1,2,5-oxadiazole-3-carboxylic acid is a solid.",False
16248,Amino-substituted glyoxylic acid derivative. ,,,,Oxamic Acid is experimental.,Oxamic Acid is a solid.,True
16249,Varespladib methyl has been investigated for the treatment of Acute Coronary Syndrome. Studies showed that Varespladib methyl treatment resulted in significant positive changes on lipoproteins and inflammation. Investigated for use/treatment in atherosclerosis and coronary artery disease. A–002 is an orally administered‚ potent inhibitor of secretory phospholipase spla2(spla2)‚ including groups IIA‚ V‚ and X. Atherosclerosis is a disease of the arteries that results from inflammation and the build-up of plaque under the lining of the blood vessel. This build-up can cause vascular swelling and eventual rupture. spla2 levels have been shown to be elevated in patients with both stable and unstable coronary artery disease. Higher levels of the enzyme have been shown to predict an increased risk for future cardiovascular events such as heart attacks and stroke.,,,,Varespladib methyl is investigational.,Varespladib methyl is a solid.,True
16250,"Agkistrodon piscivorus antivenin is derived and purified immunoglobulin fragments obtained from other domestic animals such as sheep previously immunized with Agkistrodon piscivorus (_Cottonmouth_ or _Water Moccasin snake_). The final purified antivenin product is obtained by mixing other different monospecific snake antivenins and isolating the antivenin of interest through fractionation and chromatography techniques. It is intravenously (IV) administered to limit/prevent systemic toxicity. CROFAB is a sheep-derived antivenin indicated for the management of adult and pediatric patients with North American crotalid envenomation. The Crotalidae family produces venoms which are generally necrolytic and hemolyzing to tissues. _Hemorrhagins_ in crotalid venom is toxic to the blood vessels and therefore cause hemorrhage and edema at the wound site, in addition to systemic hemorrhage and shock. Significant anemia is observed due to hemolysis and extravasation of blood due to damaged vessels. Disseminated intravascular coagulation (DIC) has been observed in some cases. The most frequent initial clinical pathological changes include echinocytosis, thrombocytopenia, leukocytosis and prolonged activated clotting time. In general, edema and erythema along with fang marks (_Crotalidae _family) may be seen at the site of bite although it is tough to identify due to thick hair coat in animals.  CROFAB is a mixture of 4 different monospecific antivenoms derived from serum of healthy sheep immunized with one of the following North American snake venoms: C. atrox (Western diamondback rattlesnake), C. adamanteus (Eastern diamondback rattlesnake), C. scutulatus (Mojave rattlesnake), or A. piscivorus (cottonmouth or water moccasin).",,,,Agkistrodon piscivorus antivenin is approved and experimental.,,True
16251,,,,,"N,N-Bis(3-(D-gluconamido)propyl)deoxycholamide is experimental.","N,N-Bis(3-(D-gluconamido)propyl)deoxycholamide is a solid.",False
16252,,,,,Phthalic Acid is experimental.,Phthalic Acid is a solid.,False
16253,"Caprylic acid is an eight-carbon chain fatty acid, also known systematically as octanoic acid. It is found naturally in coconuts and breast milk. It is an oily liquid with a slightly unpleasant rancid-like smell that is minimally soluble in water.",The molecular weight is 144.21.,Caprylic acid has a topological polar surface area of 37.3.,The log p value of  is 2.98.,Caprylic acid is investigational.,Caprylic acid is a liquid.,True
16254,"Reglitazar, an isoxazolidine-3,5-dione derivative, is being developed by Pfizer for the treatment of diabetes. It is the first non-thiazolidenedione to enter clinical trials. For the treatment of diabetes mellitus type 1 and 2. Reglixane shows a hypoglycemic effect and also a stronger triglyceride-lowering effect than the thiazolidine-2,4-diones. In preclinical studies, reglixane has been shown to prevent several diabetic complications, such as cataract, nephropathy, and neuropathy. Reglixane is an agonist of peroxisome proliferator-activated receptor (PPAR) gamma and alpha.",,,,Reglitazar is investigational.,Reglitazar is a solid.,True
16255,"Elafibranor (code name GFT505) is a multimodal and pluripotent medication for treatment of atherogenic dyslipidemia for an overweight patient with or without diabetes. It is an oral treatment that acts on the 3 sub-types of PPAR (PPARa, PPARg, PPARd) with a preferential action on PPARa. As of February 2016, elafibranor has completed 8 clinical trials and a phase III is in progress. Investigated for use/treatment in atherosclerosis and diabetes mellitus type 2. GFT505 is an oral treatment that acts on the 3 sub-types of PPAR (PPARa, PPARg, PPARd) with a preferential action on PPARa. It has a sophisticated mechanism of action. It is able to differentially recruit cofactors to the nuclear receptor, which subsequently lead to differential regulation of genes and biological effect. Therefore, the ability to identify and profile the activity of selective nuclear receptor modulator (SNuRMs) is a powerful approach to select innovative drug candidates with improved efficacy and diminished side effects. These pluripotent and multimodal molecules have significant positive effects on obesity, insulin-resistance and diabetes, atherosclerosis, inflammation, and the lipid triad (increasing of HDL cholesterol, lowering of triglycerides and LDL cholesterol).",,,,Elafibranor is investigational.,Elafibranor is a solid.,True
16256,"Cardarine (GW-501516) is a peroxisome proliferator-activator receptor-delta agonist for the potential treatment of dyslipidemia. Cardarine has been investigated for the treatment of Obesity, Lipid Disorders, and Cardiovascular Disease. Investigated for use/treatment in hyperlipidemia. This drug regulates fatty acid oxidation in several tissues, such as skeletal muscle and adipose tissue. Overexpression of PPARdelta using a transgenic murine model promotes an increase of muscle oxidative capability. It also plays a major role in the metabolic adaptations to western diet characterized by an excessive amount of saturated fat.",,,,Cardarine is investigational.,Cardarine is a solid.,True
16257,"Ertiprotafib belongs to a novel class of insulin sensitizers developed for treatment of type 2 diabetes. In insulin-resistant rodent models, ertiprotafib and a close analog lowered both fasting blood glucose and insulin levels and improved glycemic excursion during an oral glucose tolerance test. Investigated for use/treatment in diabetes mellitus type 2. The complete mechanism of action for ertiprotafib and related compounds in vivo may involve multiple independent mechanisms, including (but not necessarily limited to) PTP1b inhibition and dual PPARalpha/PPARgamma agonism.",,,,Ertiprotafib is investigational.,Ertiprotafib is a solid.,True
16258,Investigated for use/treatment in diabetes mellitus type 2.,,,,Ragaglitazar is investigational.,Ragaglitazar is a solid.,True
16259,"Tesaglitazar is a dual peroxisome proliferator-activated receptor alpha/gamma agonist which improves apolipoprotein levels in non-diabetic subjects with insulin resistance. Tesaglitazar is a proposed treatment for type 2 diabetes and has completed several phase III clinical trials, however in May 2006 AstraZeneca announced that they had discontinued further development. Investigated for use/treatment in diabetes mellitus type 2. Treatment with tesaglitazar lowered fasting plasma glucose, improved glucose tolerance, substantially reduced fasting and postload insulin levels, and markedly lowered fasting TG and improved lipid tolerance.",,,,Tesaglitazar is investigational.,Tesaglitazar is a solid.,True
16260,,,,,GW-590735 is investigational.,GW-590735 is a solid.,False
16261,,,,,Indeglitazar is experimental.,Indeglitazar is a solid.,False
16262,"Aleglitazar is an investigational drug from the company Hoffmann–La Roche and is currently in a phase III clinical trial called ALECARDIO. It is being investigated for use in patients with type II diabetes to reduce their risks of cardiovascular mortality and morbidity. Aleglitazar is an agonist at the peroxisome proliferator-activated receptor (PPAR) for both the PPARα and PPARγ receptor subtypes. In the phase II clinical trial called SYNCHRONY, with type II diabetic patients, aleglitazar was able to control both lipid and glucose levels in a synergistic manner while also having limited side effects and toxicity. Investigated for use in patients with type II diabetes to reduce their risks of cardiovascular mortality and morbidity. Aleglitazar was rationally designed to be an agonist at the peroxisome proliferator-activated receptor (PPAR) for both the PPARα and PPARγ receptor subtypes. Agonistic action at PPARα controls lipid levels, which improves dyslipidemia, and agonistic action at PPARγ controls glucose levels, which improves insulin sensitivity in diabetes.",,,,Aleglitazar is investigational.,Aleglitazar is a solid.,True
16263,Clinofibrate is a fibrate drug sold and marketed in Japan.,The molecular weight is 468.59.,Clinofibrate has a topological polar surface area of 93.06.,The log p value of  is 7.03.,Clinofibrate is experimental.,Clinofibrate is a solid.,True
16264,,The molecular weight is 289.15.,Ciprofibrate has a topological polar surface area of 46.53.,The log p value of  is 3.18.,Ciprofibrate is approved and investigational.,Ciprofibrate is a solid.,False
16265,"Derived from soybeans, soybean oil is a common vegetable oil and a source of polyunsaturated and saturated fatty acids. It is a complex mixture of triglycerides where per 100 g, soybean oil has 16 g of saturated fat, 23 g of monounsaturated fat, and 58 g of polyunsaturated fat. The major component fatty acids are linoleic (48% - 58%), oleic (17% - 30%), palmitic (9% -13%), linolenic (4% - 11%), and stearic (2.5% - 5.0%). It is used as a cooking oil and lipid emulsion for parenteral nutrition in clinical settings. Soybean oil-based lipid emulsion is the only FDA-approved lipid formulation for clinical use. Indicated for parenteral nutrition as a source of calories and essential fatty acids when oral or enteral nutrition is not possible, insufficient, or contraindicated.  Soybean oil is a nutrition source that provides a biologically utilizable source of calories and essential fatty acids. It prevents the biochemical lesions of essential fatty acid deficiency (EFAD), and correct the clinical manifestations of the EFAD syndrome by supplying energy and nutrients.  Fatty acids serve as an important substrate for energy production. The most common mechanism of action for energy production derived from fatty acid metabolism is beta oxidation. Fatty acids are also important for membrane structure and function, precursors for bioactive molecules (such as prostaglandins), and as regulators of gene expression. Soybean oil-based lipid emulsion may also cause an increase in heat production, decrease in respiratory quotient, and increase in oxygen consumption following its administration. Soybean oil contents prevent abnormally high triacylglycerol synthesis and its accumulation as lipid droplets in the liver by regulating hepatic lipogenesis and lipolysis. In vitro, soybean oil is shown to prevent downregulation of CYP2C2, CYP2C11 and CYP3A2 mRNA thus maintaining hepatic drug oxidation capabilities. Soybean oil is broken down into free fatty acids that activate PPAR-alpha, which regulate hepatic CYP4A1 that hydroxylate saturated and unsaturated fatty acids. Soybean oil is also shown to prevent up/downregulation of efflux transporters and maintain mRNA levels of hepatic antioxidant enzymes in vitro rat studies. ",,,,Soybean oil is approved.,,True
16266,"Isoflavone is a soy phytoestrogen and a biologically active component of several agriculturally important legumes such as soy, peanut, green peas, chick peas and alfalfa. Soybean is an exceptionally rich source of dietary isoflavones, where the average isoflavone content is 1-2 mg/gram. The main soy isoflavones are mostly present in glycosylated forms and include , , and glycitein, which accounts for approximately 50%, 40%, and 10%, respectively, of the total soybean isoflavone content. The clinical benefits of soy proteins have been studied and demonstrated for many years, with some evidence of soy products associated with a reduced incidences of coronary heart disease, atherosclerosis, type II diabetes mellitus, and breast and prostate cancer. While existing data are consistent or inadequate in supporting most of the suggested health benefits of consuming soy proteins and isoflavones , the trials investigating isoflavone as a potential treatment for atrophy, menopause, and postmenopausal symptoms are ongoing. Isoflavone is found as one of constituents in oral over-the-counter dietary supplements indicated for improved bone mass density and body fat regulation. Indicated for over-the-counter use as a dietary supplement for increasing bone density and regulating blood fat.  Isolated soy protein with isoflavones was shown to decrease LDL cholesterol levels in randomized trials assessed by the American Heart Association. In a study of postmenopausal women, daily dietary intake of 101 mg of aglycone isoflavones (indicating and ) was associated with lowered LDL cholesterol and apolipoprotein B levels by 8% and reduced systolic and diastolic blood pressure by 6.8% in hypertensive women. In a meta-analysis of randomized controlled trials of menopausal women, soy isoflavones attenuated bone loss of the spine and decreased the levels of deoxypyridinoline, a bone resorption marker, while increasing serum bone-specific alkaline phosphatase, a bone formation marker. The findings from studies investigating the effects of soy consumption on menopausal symptoms, breast cancer, and prostate cancer remain somewhat controversial and inconclusive. Consumption of soy isoflavones may decrease the markers of cancer development and progression in prostate cells, including prostate-specific antigen (PSA), testosterone, and androgen receptor in patients with prostate cancer but not in normal subjects. Although epidemiologic data in Asian women demonstrate that high soy food intake is associated with protection against breast cancer, soy foods have little effect on intermediary markers of breast cancer risk and postmenopausal soy intake may not reduce the risk of developing breast cancer. However, preliminary studies show that soy food intake reduces tumor recurrence in breast cancer patients. Soy isoflavones reported to interfere with thyroid peroxidase, which are involved in the production of thyroid hormones. Isoflavones are selective estrogen receptor modulators that exert estrogenic-like effects under certain experimental conditions , as they are structurally similar to mammalian 17β-estradiol. They may bind to both α and β isoforms of estrogen receptor (ER), but with binding affinities to ERβ approximately 20 times higher than that to ERα. The role of isoflavones on estrogen-dependent cancer has been studied, since they may mediate antiestrogenic actions by blocking the binding of endogenous estrogens and their receptor signalling. In cell culture, inhibited the proliferation of MDA-MB-231 human breast cancer cells, probably by arresting the cell cycle progression at the G2–M transition. In addition, genistein was shown to induce apoptosis, modify eicosanoid metabolism, and inhibit angiogenesis. There is an evidence that soy isoflavones may act on androgen receptors to inhibit tyrosine kinase activity, thereby blocking the growth and proliferation of cancer cells. ",,,,Isoflavone is experimental.,Isoflavone is a solid.,True
16267,Leukotriene B4 has been used in trials studying the treatment of HIV Infections.,,,,Leukotriene B4 is investigational.,,True
16268,"Fenofibric acid is a lipid-lowering agent that is used in severe hypertriglyceridemia, primary hyperlipidemia, and mixed dyslipidemia. It works to decrease elevated low-density lipoprotein cholesterol, total cholesterol, triglycerides, apolipoprotein B, while increasing high-density lipoprotein cholesterol. Due to its high hydrophilicity and poor absorption profile, prodrug ,, and other conjugated compounds of fenofibric acid, such as choline fenofibrate, have been developed for improved solubility, gastrointestinal absorption, and bioavailability, and more convenient administration. For use as an adjunctive therapy to diet to: (a) reduce triglyceride levels in adult patients with severe hypertriglyceridemia, and (b) reduce elevated total cholesterol, low-density-lipoprotein (LDL-C), triglycerides, and apolipoprotein B, and to increase high-density-lipoprotein (HDL-C) in adult patients with primary hypercholesterolemia or mixed dyslipidemia (Fredrickson Types IIa and IIb).  Various clinical studies have shown that elevated levels of total cholesterol, low-desnsity-lipoprotein (LDL-C), and apolipoprotein B (apo B) - an LDL membrane complex - are associated with human atherosclerosis. Concurrently, decreased levels of high-density-lioprotein (HDL-C) and its transport complex, apolipoproteins apo AI and apo AII, are associated with the development of atherosclerosis. Furthermore, epidemiological investigations demonstrate that cardiovascular morbidity and mortality vary directly with the levels of total cholesterol, LDL-C, and triglycerides, and inversely with the level of HDL-C. Having performed clinical studies with in vivo transgenic mice and in vitro human hepatocyte cultures, it is believed that the principal mechanism of action of fenofibric acid is demonstrated through its capability to activate peroxisome proliferator receptor alpha (PPAR-alpha).",The molecular weight is 318.75.,Fenofibric acid has a topological polar surface area of 63.6.,The log p value of  is 4.07.,Fenofibric acid is approved.,Fenofibric acid is a solid.,True
16269,,,,,NADPH is experimental.,NADPH is a solid.,False
16270,,,,,L-Saccharopine is experimental.,L-Saccharopine is a solid.,False
16271,"Recombinant human growth hormone (somatotropin) 191 residues, MW 22.1 kD, synthesized in E. coli For treatment of dwarfism, acromegaly and prevention of HIV-induced weight loss Used in the treatment of dwarfism and growth failure, growth hormone (hGH) stimulates skeletal growth in pediatric patients with growth failure due to a lack of adequate secretion of endogenous GH. Skeletal growth is accomplished at the epiphyseal plates at the ends of a growing bone. Growth and metabolism of epiphyseal plate cells are directly stimulated by GH and one of its mediators, IGF-I (insulin-like growth factor). hGH binds to the human growth hormone receptor (GHR). Upon binding, hGH causes dimerization of GHR, activation of the GHR-associated JAK2 tyrosine kinase, and tyrosyl phosphorylation of both JAK2 and GHR. These events recruit and/or activate a variety of signaling molecules, including MAP kinases, insulin receptor substrates, phosphatidylinositol 3' phosphate kinase, diacylglycerol, protein kinase C, intracellular calcium, and Stat transcription factors. These signaling molecules contribute to the GH-induced changes in enzymatic activity, transport function, and gene expression that ultimately culminate in changes in growth and metabolism.",The molecular weight is 22125.07.,Somatotropin has a topological polar surface area of 9147.67.,,Somatotropin is approved and investigational.,Somatotropin is a liquid.,True
16272,"Despite the ability of almost all contemporary recombinant growth hormones to cause definite and demonstrable increases in growth rate in patients who are administered the drug, the use of these agents continues to be mired in persistent bioethical debate. Such discussion revolves around whether patients' natural disposition of short stature should be considered a medical condition justifying medical treatment with such hormone therapy - especially when these hormone agents have been proven effective at increasing the height of children with or without growth hormone deficiency. Somatrem is a recombinant human growth hormone indicated for: (a) treatment of paediatric patients with growth failure due to growth hormone deficiency (GHD), (b) treatment of paediatric patients with growth failure due to idiopathic short stature (ISS), (c) treatment of paediatric patients with growth failure due to Turner syndrome (TS), (d) treatment of paediatric patients with growth failure due to chronic kidney disease (CKD) up to the time of renal transplantation, (e) treatment of adults with childhood-onset GHD, or (f) treatment of adults with adult-onset GHD. In vitro and in vivo preclinical and clinical testing have demonstrated that somatrem is therapeutically equivalent to pituitary derived human growth hormone (hGH). Paediatric patients who lack adequate endogenous growth hormone secretion, patients with chronic kidney disease, and patients with Turner syndrome that were treated with somatrem resulted in an increase in growth rate and an increase in insulin-like growth factor (IGF-1) levels similar to that seen with patients who possess endogenous pituitary derived hGH. With normalized levels of growth hormone and related mediator agents like IGF-1, patients demonstrate normalized skeletal, cell, organ, and overall tissue growth. Somatrem - as well as endogenous growth hormone - binds to dimeric growth hormone (GH) receptors located within the cell membranes of target tissue cells resulting in intracellular signal transduction and a host of pharmacodynamic effects. Some of these pharmacodynamic effects are primarily mediated by insulin like growth factor (IGF-1) produced in the liver and also locally (ie. skeletal growth, protein synthesis), while others are primarily a consequence of the direct effects of somatropin (ie. lipolysis).",,,,Somatrem is approved and investigational and withdrawn.,Somatrem is a liquid.,True
16273,"The key substance in the biosynthesis of histidine, tryptophan, and purine and pyrimidine nucleotides.",,,,5-O-phosphono-alpha-D-ribofuranosyl diphosphate is approved and experimental and investigational.,5-O-phosphono-alpha-D-ribofuranosyl diphosphate is a solid.,True
16274,,,,,5-monophosphate-9-beta-D-ribofuranosyl xanthine is experimental.,5-monophosphate-9-beta-D-ribofuranosyl xanthine is a solid.,False
16275,,,,,3H-pyrazolopyrimidin-7-ol is experimental.,3H-pyrazolopyrimidin-7-ol is a solid.,False
16276,"Acne vulgaris is a multifactorial disorder of the pilosebaceous unit involving increased sebum production, inflammation, and hyperproliferation/hyperkeratinization of the follicular infundibulum. It is also associated with _Cutibacterium acnes_ (also known as _Propionibacterium acnes_). Adapalene is a third-generation topical retinoid used for the treatment of acne vulgaris. Adapalene has similar efficacy but a superior safety profile compared to tretinoin. is more efficacious than adapalene but is designated as pregnancy category X and hence is contraindicated in pregnant women. Adapalene can also be combined with benzoyl peroxide (BPO), which possesses bactericidal properties, and either adapalene alone, or adapalene BPO combination products, are commonly used to treat mild-to-severe acne. Adapalene is indicated for the topical treatment of acne vulgaris in patients aged 12 and over. Adapalene is anticomedogenic, preventing the formation of new comedones and inflammatory lesions, and also acts to reduce inflammation by modulating the innate immune response. Like other retinoid compounds, adapalene is chemically stable but photosensitive; use with sunscreen is recommended. Minor skin irritations, including erythema, scaling, dryness, and stinging/burning, have been reported. Adapalene is used for the treatment/maintenance of mild-to-severe acne (acne vulgaris). Acne is a multifactorial condition, and evidence exists to support multiple mechanisms of action for adapalene. Adapalene binds to retinoic acid receptor (RAR)-beta and RAR-gamma; this complex subsequently binds to one of three retinoid X receptors (RXRs), which as a complex is capable of binding DNA to modulate transcriptional activity. Although the full extent of transcriptional modulation is not described, retinoid activation is generally known to affect cellular proliferation and differentiation, and adapalene has been shown to inhibit HeLa cell proliferation and human keratinocyte differentiation. These effects primarily account for adapalene's comedolytic and anticomedogenic properties.",The molecular weight is 412.53.,Adapalene has a topological polar surface area of 46.53.,The log p value of  is 9.15.,Adapalene is approved.,Adapalene is a solid.,True
16277,LG-100268 is a retinoid X receptor (RXR) selective compound.,,,,LG-100268 is experimental.,LG-100268 is a solid.,True
16278,TO-901317 is an LXRalpha and LXRbeta agonist.,,,,TO-901317 is experimental.,TO-901317 is a solid.,True
16279,,,,,"N-(TERT-BUTYL)-3,5-DIMETHYL-N'-BENZOHYDRAZIDE is experimental.","N-(TERT-BUTYL)-3,5-DIMETHYL-N'-BENZOHYDRAZIDE is a solid.",False
16280,,,,,"(2E,4E)-11-METHOXY-3,7,11-TRIMETHYLDODECA-2,4-DIENOIC ACID is experimental.","(2E,4E)-11-METHOXY-3,7,11-TRIMETHYLDODECA-2,4-DIENOIC ACID is a solid.",False
16281,"A thiol-containing non-essential amino acid that is oxidized to form cystine. For the prevention of liver damage and kidney damage associated with overdoses of acetaminophen Due to this ability to undergo redox reactions, cysteine has antioxidant properties. Cysteine is an important source of sulfur in human metabolism, and although it is classified as a non-essential amino acid, cysteine may be essential for infants, the elderly, and individuals with certain metabolic disease or who suffer from malabsorption syndromes. Cysteine may at some point be recognized as an essential or conditionally essential amino acid. Cysteine can usually be synthesized by the human body under normal physiological conditions if a sufficient quantity of methionine is available. Cysteine is typically synthesized in the human body when there is sufficient methionine available. Cysteine exhibits antioxidant properties and participates in redox reactions. Cysteine's antioxidant properties are typically expressed in the tripeptide glutathione, which occurs in humans as well as other organisms. Glutathione (GSH) typically requires biosynthesis from its constituent amino acids, cysteine, glycine, and glutamic acid, due to its limited systemic availability. Glutamic acid and glycine are readily available in the diets of most industrialized countries, but the availability of cysteine can be the limiting substrate. In human metabolism, cysteine is also involved in the generation of sulfide present in iron-sulfur clusters and nitrogenase by acting as a precursor. In a 1994 report released by five top cigarette companies, cysteine is one of the 599 additives to cigarettes. Its use or purpose, however, is unknown, like most cigarette additives. Its inclusion in cigarettes could offer two benefits: Acting as an expectorant, since smoking increases mucus production in the lungs; and increasing the beneficial antioxidant glutathione (which is diminished in smokers).",The molecular weight is 121.15.,Cysteine has a topological polar surface area of 63.32.,The log p value of  is -2.35.,Cysteine is approved and nutraceutical.,Cysteine is a solid.,True
16282,"Telotristat only approved oral therapy for carcinoid syndrome diarrhea. Telotristat was approved by the FDA in March, 2017 as Xermelo. As a serotonin synthesis inhibitor, telotristat etiprate, has the potential to reduce serotonin levels and address the key elements of carcinoid syndrome.   Activity is mainly in the gastrointestinal tract, with minimal effects reported on the brain and cardiovascular system, accompanied by an excellent safety profile. Telotristat etiprate is an ethyl ester prodrug which is hydrolyzed to its active moiety LP-778902 both in vivo and in vitro. Systemic exposure of telotristat etiprate is relatively low, as the hydrolysis to the active moiety is rapid. LP-778902 is a potent inhibitor of TPH with an in vivo IC50 of 0.028 μM. While existing treatments for carcinoid syndrome work to reduce the release of serotonin outside tumor cells, telotristat etiprate works at the source to reduce serotonin production within the tumor cells. By specifically inhibiting serotonin production, telotristat etiprate seeks to control this important driver of carcinoid syndrome and, in turn, provide patients with more control over their disease. ",The molecular weight is 574.99.,Telotristat ethyl has a topological polar surface area of 131.17.,The log p value of  is 5.36.,Telotristat ethyl is approved and investigational.,Telotristat ethyl is a solid.,True
16283,"An amino acid derivative that occurs in vertebrate tissues and in urine. In muscle tissue, creatine generally occurs as phosphocreatine. Creatine is excreted as creatinine in the urine. For nutritional supplementation, also for treating dietary shortage or imbalance. Creatine is a essential, non-proteinaceous amino acid derivative found in all animals. It is synthesized in the kidney, liver, and pancreas from L-arginine, glycine and L-methionine. Following its biosynthesis, creatine is transported to the skeletal muscle, heart, brain and other tissues. Most of the creatine is metabolized in these tissues to phosphocreatine (creatine phosphate). Phosphocreatine is a major energy storage form in the body. Supplemental creatine may have an energy-generating action during anaerobic exercise and may also have neuroprotective and cardioprotective actions. In the muscles, a fraction of the total creatine binds to phosphate - forming creatine phosphate. The reaction is catalysed by creatine kinase, and the result is phosphocreatine (PCr). Phosphocreatine binds with adenosine diphosphate to convert it back to ATP (adenosine triphosphate), an important cellular energy source for short term ATP needs prior to oxidative phosphorylation.",The molecular weight is 131.14.,Creatine has a topological polar surface area of 90.41.,The log p value of  is -1.51.,Creatine is approved and investigational and nutraceutical.,Creatine is a solid.,True
16284,"Phosphocreatine - or creatine phosphate - is the phosphorylated form of creatine. It is primarily found endogenously in the skeletal muscles of vertebrates where it serves a critical role as a rapidly acting energy buffer for muscle cell actions like contractions via its ability to regenerate adenosine triphosphate (ATP) from adenosine diphosphate (ADP). Phosphocreatine is a naturally occuring substance that is found predominantly in the skeletal muscles of vertebrates. Its primary utility within the body is to serve in the maintanence and recycling of adenosine triphosphate (ATP) for muscular activity like contractions. Creatine is a naturally occurring chemical within the body and is primarily stored in skeletal muscle in both free and phosphorylated forms. Phosphocreatine is the name given to the phosphorylated form of creatine. Additionally, phosphocreatine can also be found in other areas of the body like the kidneys, liver, and brain. In fact, most *in vivo* synthesis of creatine occurs in the liver where amidine groups from arginine are transfered to glycine with the help of the glycine transaminidase enzyme to form guanidinoacetic acid. This acid is then methylated with the methyl group of S-adenosylmethionine via guanidinoacetate methyltransferase to generate creatine. The synthesized creatine is transported to storage sites in skeletal muscle via the bloodstream. Adenosine triphosphate (ATP) is the primary source of chemical energy that body muscles use to perform contractions. During such contraction processes, ATP molecules are depleted as they undergo hydrolysis reactions and become adenosine diphosphate (ADP). To maintain homeostasis in muscle activity, the ATP supply of muscles must be regenerated regularly.",The molecular weight is 211.11.,Phosphocreatine has a topological polar surface area of 133.95.,The log p value of  is -1.73.,Phosphocreatine is nutraceutical.,Phosphocreatine is a solid.,True
16285,"Humanized monoclonal antibody specific to lymphocyte antigens. It is a recombinant DNA-derived humanized monoclonal antibody (Campath-1H) that is directed against the 21-28 kD cell surface glycoprotein,CD52. The Campath-1H antibody is an IgG1 kappa with human variable framework and constant regions, and complementarity-determining regions from a murine (rat) monoclonal antibody (Campath-1G). Campath is produced in mammalian cell (Chinese hamster ovary) suspension culture in a medium containing neomycin. Alemtuzumab (Campath) is a monoclonal antibody therapy used for treatment of B-cell chronic lymphocytic leukemia. Campath is used to treat leukemia by exploiting antibody mediated lysis of CD52 presenting cells. The CD52 antigen is a cell surface protein found on essentially all B and T lymphocytes, a majority of monocytes, macrophages and most granulocytes. The CD52 antigen is not present on erythrocytes or hematopoetic stem cells. In leukemia there is an excess of B and T cells, so Campath permits selective reduction of lymphocyte populations. Campath binds to the CD52 antigen present on most B and T lymphocytes. This binding leads to antibody-dependent lysis of leukemic cells.",,,,Alemtuzumab is approved and investigational.,Alemtuzumab is a liquid.,True
16286,"Piboserod (SB 207266) is a selective 5-HT(4) receptor antagonist. For the treatment of atrial fibrillation and irritable bowel syndrome (IBS). GlaxoSmithKline was investigating piboserod, a 5HT4 antagonist, for the treatment of atrial fibrillation. Phase II trials were ongoing in March 2004, but by December of that year, development had been discontinued. Piboserod had previously being investigated for the treatment of irritable bowel syndrome (IBS), but development for this indication was terminated in 1999. Piboserod appears to act as a specific antagonist of one of the receptors for 5-hydroxytryptamine, the 5-HT4 receptor. The 5-HT4 receptor antagonists are thought to antagonize both the ability of serotonin to sensitize the peristaltic reflex and 5-HT-induced defecation, at least in animal studies. As 5-HT4 receptors are present in human atrial cells and when stimulated may cause atrial arrhythmias, piboserod was under investigation in clinical trials for atrial fibrillation.",,,,Piboserod is investigational.,Piboserod is a solid.,True
16287,Renzapride is currently in Phase III clinical development in the United States for the treatment of constipation-predominant irritable bowel syndrome (IBS-C). It has been suggested that renzapride is effective in the treatment of irritable bowel syndrome with alternating stool pattern. It is being developed by Alizyme of the UK. For the treatment of constipation-predominant irritable bowel syndrome (IBS-C). Renzapride is a substituted benzamide which acts on the upper gastrointestinal tract. It has been shown to enhance stomach emptying in normal subjects; doses of 2 and 5 mg decreasing by 21 and 37% respectively the volume of gastric contents aspirated 80 min after a test meal. Renzapride was found to reduce the oro-caecal transit time as assessed by the lactulose/breath hydrogen method in a dose related manner from 0.2 to 5 mg; the later dose producing a 62% reduction. Renzapride is a full serotonin 5-HT4 receptor agonist and partial serotonin 5-HT3 receptor antagonist.,,,,Renzapride is investigational.,Renzapride is a solid.,True
16288,Investigated for use/treatment in gastroesophageal reflux disease (GERD) and gastroparesis.,,,,Naronapride is investigational.,Naronapride is a solid.,True
16289,"TD-2749 is selective 5-HT4 agonists discovered by Theravance through the application of multivalent drug design in a drug discovery program dedicated to finding new medicines for GI motility disorders such as chronic constipation, constipation-predominant irritable bowel syndrome (C-IBS), opioid-induced constipation, functional dyspepsia and diabetic gastroparesis. Investigated for use/treatment in constipation, gastrointestinal diseases and disorders (miscellaneous), gastroparesis, and irritable bowel syndrome (IBS).",,,,TD-2749 is investigational.,TD-2749 is a solid.,True
16290,"Investigated for use/treatment in gastroesophageal reflux disease (GERD) and gastroparesis. Ticalopride is an isomer of the active metabolite of cisapride. Cisapride acts through the stimulation of the serotonin 5-HT4 receptors which increases acetylcholine release in the enteric nervous system (specifically the myenteric plexus). This results in increased tone and amplitude of gastric (especially antral) contractions, relaxation of the pyloric sphincter and the duodenal bulb, and increased peristalsis of the duodenum and jejunum resulting in accelerated gastric emptying and intestinal transit. ",,,,Ticalopride is investigational.,Ticalopride is a solid.,True
16291,"Cinitapride is a gastroprokinetic agent and antiulcer benzamide with agonist activity at 5-HT1 and 5-HT4 receptors and antagonist activity at 5-HT2 receptors. It is marketed in Spain and Mexico. It is indicated to treat gastrointestinal disorders associated with motility disturbances like gastroesophageal reflux disease (GERD), non-ulcer dyspepsia and delayed gastric emptying. Cinitapride is a substituted benzamide with 5-HT receptor antagonist and agonist activity.",The molecular weight is 402.5.,Cinitapride has a topological polar surface area of 110.73.,The log p value of  is 3.27.,Cinitapride is investigational.,Cinitapride is a solid.,True
16292,"Velusetrag has been used in trials studying the treatment of Gastroparesis and Alzheimer's Disease. It is a highly selective serotonin receptor agonist effective in patients with chronic constipation. It is being developed by Theravance. Velusetrag was discovered by Theravance through the application of its multivalent drug design in a research program dedicated to finding new treatments for GI motility disorders. Studies demonstrating the in vivo preclinical profile of Velusetrag showed that the compound has potent 5-HT4 receptor agonist activity by several routes of administration, including oral, providing robust prokinetic activity in the digestive tract of three different animal species, consistent with its highly potent and selective 5-HT4 receptor agonist in vitro profile. Velusetrag is a potent, highly selective agonist with high intrinsic activity at the 5-HT4 receptor. Relative to other 5-HT receptor types, Velusetrag is > 500-fold selective for binding to the human 5-HT4 receptor. Theravance anticipates that the high degree of selectivity of Velusetrag provides the potential for it to be a better and safer medicine for the treatment of patients with severe constipation and possibly constipation predominant irritable bowel syndrome.",,,,Velusetrag is investigational.,,True
16293,,The molecular weight is 562.67.,Protoporphyrin has a topological polar surface area of 131.96.,The log p value of  is 8.36.,Protoporphyrin is experimental.,Protoporphyrin is a solid.,False
16294,"Ferric pyrophosphate is an iron replacement product. Free iron presents several side effects as it can catalyze free radical formation and lipid peroxidation as well as the presence of interactions of iron in plasma. The ferric ion is strongly complexed by pyrophosphate. It presents an increasing interest as this insoluble form can be milder in the gastrointestinal tract and present higher bioavailability. Ferric pyrophosphate is intended to be indicated for the treatment of iron loss or iron deficiency as a formulation with a milder gastrointestinal effect.  Iron supplementation typically results in increases in serum iron, transferrin-bound iron, and iron-stored in the form of ferritin in hepatocytes and macrophages. The available iron is usually used in bone marrow for the synthesis of hemoglobin. The usage of ferric pyrophosphate is based on the strong complex formation between these two species. Besides, the capacity of pyrophosphate to trigger iron removal from transferrin, enhance iron transfer from transferrin to ferritin and promote iron exchange between transferrin molecules. These properties make it a very suitable compound for parenteral administration, iron delivery into circulation and incorporation into hemoglobin.",,,,Ferric pyrophosphate is experimental.,Ferric pyrophosphate is a solid.,True
16295,"Sodium ferric gluconate complex is an iron replacement product for treatment of iron deficiency anemia. The stable macromolecular complex is negatively charged at alkaline pH with an apparent molecular weight of 289,000 – 440,000 daltons on gel chromatography. It is composed of iron (III) oxide hydrate directly bonded to sucrose with a chelating gluconate function in a molar ratio of two iron molecules to one gluconate. It is used in adult and in pediatric patients over the age of 6 years with chronic kidney disease (CKD) receiving hemodialysis and receiving supplemental epoetin therapy. Used to replete the total body content of iron during iron deficiency anemia in patients age 6 years and older with chronic kidney disease receiving hemodialysis and receiving supplemental epoetin therapy. Sodium ferric gluconate complex is an exogenous epoetin that acts to restore the body's content of iron, which is essential for normal hemoglobin synthesis, oxygen transport and enzymatic processes. The complex increases red blood cell production and increased iron utilization.  The complex is endocytosed by macrophages of the reticuloendothelial system. Within an endosome of the macrophage , lysosome fuses with the endosome creating an acidic environment leading to the cleavage of the complex from iron. Iron is then incorporated in ferritin, transferrin or hemoglobin. Sodium ferric gluconate also normalizes RBC production by binding with hemoglobin ",,,,Sodium ferric gluconate complex is approved.,Sodium ferric gluconate complex is a liquid.,True
16296,"Ferric pyrophosphate citrate is a soluble iron replacement product. Free iron presents several side effects as it can catalyze free radical formation and lipid peroxidation as well as the presence of interactions of iron in plasma. The ferric ion is strongly complexed by pyrophosphate and citrate. FPC is categorized in Japan as a second class OTC drug. This category is given to drugs with ingredients that in rare cases may cause health problems requiring hospitalization or worst. It is also FDA approved since 2015. Ferric pyrophosphate citrate is indicated for the treatment of iron loss or iron deficiency to maintain hemoglobin and to reduce the prescribed dose of erythropoiesis-stimulating agent (ESA) required to maintain desired hemoglobin levels.  Iron supplementation typically results in increases in serum iron, transferrin-bound iron, and iron-stored in the form of ferritin in hepatocytes and macrophages. The available iron is usually used in bone marrow for the synthesis of hemoglobin. The usage of ferric pyrophosphate is based on the strong complex formation between these two species. Besides, the capacity of pyrophosphate to trigger iron removal from transferrin, enhance iron transfer from transferrin to ferritin and promote iron exchange between transferrin molecules. These properties make it a very suitable compound for parenteral administration, iron delivery into circulation and incorporation into hemoglobin.",,,,Ferric pyrophosphate citrate is approved and investigational.,Ferric pyrophosphate citrate is a solid.,True
16297,,,,,L-Phospholactate is experimental.,L-Phospholactate is a solid.,False
16298,,,,,"6-(2-fluorobenzyl)-2,4-dimethyl-4,6-dihydro-5H-thienopyrrolopyridazin-5-one is experimental.","6-(2-fluorobenzyl)-2,4-dimethyl-4,6-dihydro-5H-thienopyrrolopyridazin-5-one is a solid.",False
16299,,,,,"1--4-(2,3-dihydro-1,4-benzodioxin-6-ylsulfonyl)piperazine is experimental.","1--4-(2,3-dihydro-1,4-benzodioxin-6-ylsulfonyl)piperazine is a solid.",False
16300,,,,,"1-(2,3-dihydro-1,4-benzodioxin-6-ylsulfonyl)-4-piperazine is experimental.","1-(2,3-dihydro-1,4-benzodioxin-6-ylsulfonyl)-4-piperazine is a solid.",False
16301,"Aminoacridine derivative that is a potent intercalating antineoplastic agent. It is effective in the treatment of acute leukemias and malignant lymphomas, but has poor activity in the treatment of solid tumors. It is frequently used in combination with other antineoplastic agents in chemotherapy protocols. It produces consistent but acceptable myelosuppression and cardiotoxic effects. For treatment of acute myeloid leukaemia. Amsacrine is an aminoacridine derivative that is a potent intercalating antineoplastic agent. It is effective in the treatment of acute leukemias and malignant lymphomas, but has poor activity in the treatment of solid tumors. It is frequently used in combination with other antineoplastic agents in chemotherapy protocols. It produces consistent but acceptable myelosuppression and cardiotoxic effects. Amsacrine binds to DNA through intercalation and external binding. It has a base specificity for A-T pairs. Rapidly dividing cells are two to four times more sensitive to amsacrine than are resting cells. Amsacrine appears to cleave DNA by inducing double stranded breaks. Amsacrine also targets and inhibits topoisomerase II. Cytotoxicity is greatest during the S phase of the cell cycle when topoisomerase levels are at a maximum.",The molecular weight is 393.46.,Amsacrine has a topological polar surface area of 80.32.,The log p value of  is 4.54.,Amsacrine is approved and investigational.,Amsacrine is a solid.,True
16302,"Ibutilide is a Class III antiarrhythmic agent available in intravenous formulations. It is indicated for the conversion of acute atrial flutter and recent onset atrial fibrillation to normal sinus rhythm (NSR). Indicated for the rapid conversion of atrial fibrillation or atrial flutter of recent onset to sinus rhythm. Ibutilide prolongs the action potential duration and increases both atrial and ventricular refractoriness in vivo, i.e., class III electrophysiologic effects. Voltage clamp studies indicate that ibutilide, at nanomolar concentrations, delays repolarization by activation of a slow, inward current (predominantly sodium), rather than by blocking outward potassium currents, which is the mechanism by which most other class III antiarrhythmics act. Ibutilide is a 'pure' class III antiarrhythmic drug, used intravenously against atrial flutter and fibrillation. At a cellular level it exerts two main actions: induction of a persistent Na+ current sensitive to dihydropyridine Ca<sup>2+</sup> channel blockers and potent inhibition of the cardiac rapid delayed rectifier K<sup>+</sup> current, by binding within potassium channel pores. In other words, Ibutilide binds to and alters the activity of hERG potassium channels, delayed inward rectifier potassium (IKr) channels and L-type (dihydropyridine sensitive) calcium channels",The molecular weight is 384.58.,Ibutilide has a topological polar surface area of 69.64.,The log p value of  is 3.78.,Ibutilide is approved.,Ibutilide is a solid.,True
16303,"Terazosin is a quinazoline derivative alpha-1-selective adrenergic blocking agent indicated for benign prostatic hyperplasia and hypertension. Terazosin blocks adrenaline's action on alpha-1 adrenergic receptors, causing relaxation of smooth muscle in blood vessels and the prostate. Terazosin is indicated for use in treating symptomatic benign prostatic hyperplasia and hypertension. Terazosin is a quinazoline derivative alpha-1-selective adrenergic blocker. Terazosin is selective for alpha-1-adrenoceptors but not their individual subtypes. Inhibition of these alpha-1-adrenoceptors results in relaxation of smooth muscle in blood vessels and the prostate, lowering blood pressure and improving urinary flow. Smooth muscle cells accounts for roughly 40% of the volume of the prostate and so their relaxation reduces pressure on the urethra.",The molecular weight is 387.44.,Terazosin has a topological polar surface area of 103.04.,The log p value of  is 2.18.,Terazosin is approved.,Terazosin is a solid.,True
16304,Investigated for use/treatment in allergic rhinitis.,,,,Tecastemizole is investigational.,Tecastemizole is a solid.,True
16305,"Potassium nitrate is an inorganic salt with a chemical formula of KNO3. It is a natural source of nitrate and has been used as a constituent for several different purposes, including food preservatives, fertilizers, tree stump removal, rocket propellants, and fireworks. Potassium nitrate is a common active ingredient in toothpaste, exerting an anti-sensitivity action. It provides increasing protection against painful sensitivity of the teeth to cold, heat, acids, sweets or contact. For the relief of tooth sensitivity, and is also used as a pesticide, insecticide, as a food additive, and a rodenticide. The potassium cation is an essential electrolyte that is important for the maintenance of intracellular osmotic pressure and for the maintenance of cell membrane potential, in particular, the potential of electrically excitable tissues. It is a regular component of the diet and is particularly abundant in fruit and vegetables. The recommended daily intake varies from 350-1275 mg in children to 1875 and 5625 mg in adults. In the United Kingdom, the recommended intake is 3.5 g/day for healthy adults. Potassium ions are believed to disturb the synapse between nerve cells, thus decreasing nerve excitation and the associated pain. Potassium (K+) is the principal cation modulating the osmotic balance of the body fluids. In animals, the maintenance of normal cell volume and pressure is dependent on Na+ and K+ pumping. Potassium transport through the hydrophobic interior of a cell membrane may be facilitated by several naturally occurring compounds that form lipid-soluble alkali metal cation complexes. Potassium has the critical role of a calcium counter-ion for numerous carboxylates, phosphates, and sulfates, and also acts to stabilize macromolecular structures.",The molecular weight is 101.1.,,,Potassium nitrate is approved.,Potassium nitrate is a solid.,True
16306,"Pentoxyverine, also referred to as carbetapentane, is a non-opioid central acting antitussive with antimuscarinic, anticonvulsant , and local anesthetic properties. It is an active ingredient in over-the-counter cough suppressants in combination with guaifenesin and H1-receptor antagonists. Pentoxyverine acts on sigma-1 receptors, as well as kappa and mu-opioid receptors. Indicated as a cough suppressant to relieve cough caused by the common cold, flu, bronchitis, and sinusitis.  Pentoxyverine induces an antitussive action. In animal studies, intraperitoneal administration of pentoxyverine inhibited citric-acid-induced cough in guinea-pigs _in vivo_. Some mice and rat studies suggest that pentoxyverine may also exert anticonvulsant activities without inducing a protective effect from NMDA-induced lethality. Protective effects against maximal electroshock-induced seizures in a dose-related fashion was also observed following either intraperitoneal or oral administration. In hERG-transfected cells, pentoxyverine inhibited the outward current of the hERG ion channel with half-maximal inhibition concentrations (IC50) of 3.0 µM. In rats receiving intrathecal administration, pentoxyverine exhibited dose-dependent spinal blockade with a more sensory-selective action over motor blockade. It induced a spinal blockade with a more sensory/nociceptive-selective action over motor blockade compared to lidocaine.  While the mechanism of antitussive action of pentoxyverine is not fully understood, it is thought to be mediated via sigma-1 receptors expressed in the central nervous system. Pentoxyverine acts as an agonist at sigma receptors with the Ki of 75±28 nM, as demonstrated in a competitive binding assay. The function of sigma receptors on cough suppressant activities is unclear, however these receptors are highly expressed in the nucleus tractus solitarius (NTS) of the brainstem where the afferent fibres first synapse. NTS is located very close to the cough centre in the brainstem thus may function as a ‘gate' for the cough reflex and allow sigma-1 receptor agonists to modulate afferent activity prior to reaching the cough center. It is suggested that highly lipophilic sigma-1 agonists may penetrate the CNS following systemic administration. When administered as aerosols, sigma-1 receptor agonists may temporarily act in the periphery to modulate cough by acting activate sigma receptors expressed in the lungs. However there is limited evidence of peripheral localization of the sigma agonists following aerosol administration and the ruling out of systemic exposure. The local anesthesia action of pentoxyverine may occur through inhibition of voltage-gated Na(+) currents. ",The molecular weight is 333.47.,Pentoxyverine has a topological polar surface area of 38.77.,The log p value of  is 4.7.,Pentoxyverine is approved and investigational.,Pentoxyverine is a solid.,True
16307,"Chlorobutanol, or chlorbutol, is an alcohol-based preservative with no surfactant activity. It also elicits sedative-hypnotic and weak local anesthetic actions in addition to antibacterial and antifungal properties. Similar in nature to chloral hydrate, it is formed by the simple nucleophilic addition of chloroform and acetone.  No approved therapeutic indications on its own.  Chlorobutanol is a detergent preservative with a broad spectrum of antimicrobial activity. _In vitro_, chlorobutanol demonstrated to inhibit platelet aggregation and release via unknown mechanisms. A study proposes that the antiplatelet effect of chlorobutanol may occur from inhibition of the arachidonic acid pathway. It attenuated thromboxane B2 formation, elevation of cytosolic free calcium, and ATP release, and additionally exhibited a significant inhibitory activity toward several aggregation inducers in a time- and concentration-dependent manner. Chlorobutanol may exert a direct negative inotropic effect on myocardial cells to isometric tension produced by the heart. Chlorobutanol was shown to induce conjunctival and corneal cell toxicity _in vitro_: at a concentration of 0.1%, Cbl caused near depletion of the squamous layer while degeneration of corneal epithelial cells, generation of conspicuous membranous blebs, cytoplasmic swelling, and occasional breaks in the external cell membrane were observed at a concentration of 0.5%.  As a detergent, chlorobutanol disrupts the lipid structure of the cell membrane and increases the cell permeability, leading to cell lysis. It induces conjunctival and corneal cell toxicity via causing cell retraction and cessation of normal cytokines, cell movement, and mitotic activity. It disrupts the barrier and transport properties of the corneal epithelium as well as inhibits the utilization of oxygen by the cornea. Chlorobutanol also inhibits oxygen use by the cornea, which increases susceptibility to infection.",The molecular weight is 177.45.,Chlorobutanol has a topological polar surface area of 20.23.,The log p value of  is 2.25.,Chlorobutanol is approved and investigational and vet_approved.,Chlorobutanol is a solid.,True
16308,"A quaternary ammonium anticholinergic agent with peripheral side effects similar to those of atropine. It is used as an adjunct in the treatment of gastric and duodenal ulcer, and to relieve visceral spasms. The drug has also been used in the form of eye drops for mydriatic effect.  For the treatment of visceral spasms Oxyphenonium is an anticholinergic drug, a medication that reduces the effect of acetylcholine, a chemical released from nerves that stimulates muscles, by blocking the receptors for acetylcholine on smooth muscle (a type of muscle). It also has a direct relaxing effect on smooth muscle. Oxyphenonium is used to treat or prevent spasm in the muscles of the gastrointestinal tract in the irritable bowel syndrome. In addition, Oxyphenonium inhibits gastrointestinal propulsive motility and decreases gastric acid secretion and controls excessive pharyngeal, tracheal and bronchial secretions. Action is achieved via a dual mechanism: (1) a specific anticholinergic effect (antimuscarinic) at the acetylcholine-receptor sites and (2) a direct effect upon smooth muscle (musculotropic).",The molecular weight is 348.51.,Oxyphenonium has a topological polar surface area of 46.53.,The log p value of  is 0.88.,Oxyphenonium is approved.,Oxyphenonium is a solid.,True
16309,"Buclizine is an antihistamine medication with both antiemetic and anticholinergic effects , belonging to the _piperazine derivative_ family of drugs. It was manufactured by Stuart Pharms and initially approved by the FDA in 1957. Following this, it was touted to be effective as an appetite stimulant in children when administered in the syrup form, however, this indication has not been validated. In addition to the above conditions, buclizine has been studied in the treatment of migraine attacks and in the treatment of nausea and vomiting during pregnancy.  For prevention and treatment of nausea, vomiting, and dizziness associated with motion sickness and vertigo (dizziness caused by other medical problems). Buclizine is a piperazine-derivative antihistamine used as an antivertigo/antiemetic agent. Buclizine is used in the prevention and treatment of nausea, vomiting, and dizziness associated with motion sickness. Additionally, it has been used in the management of vertigo in diseases affecting the vestibular apparatus. Although the mechanism by which buclizine exerts its antiemetic and antivertigo effects has not been fully elucidated, its central anticholinergic properties are partially responsible. The drug depresses labyrinth excitability and vestibular stimulation, and it may affect the medullary chemoreceptor trigger zone. It also possesses anticholinergic, antihistaminic, central nervous system depressant, and local anesthetic effects. Vomiting (emesis) is essentially a protective mechanism for removing irritant or otherwise harmful substances from the upper GI tract. Emesis or vomiting is controlled by the vomiting centre in the medulla region of the brain, an important part of which is the chemotrigger zone (CTZ). The vomiting centre possesses neurons which are rich in muscarinic cholinergic and histamine containing synapses. These types of neurons are especially involved in transmission from the vestibular apparatus to the vomiting centre. Motion sickness principally involves overstimulation of these pathways due to various sensory stimuli. Hence the action of buclizine which acts to block the histamine receptors in the vomiting centre and thus reduce activity along these pathways. Furthermore since buclizine possesses anti-cholinergic properties as well, the muscarinic receptors are similarly blocked.",The molecular weight is 433.04.,Buclizine has a topological polar surface area of 6.48.,The log p value of  is 8.06.,Buclizine is approved.,Buclizine is a liquid.,True
16310,"A synthetic nondepolarizing blocking drug. The actions of gallamine triethiodide are similar to those of tubocurarine, but this agent blocks the cardiac vagus and may cause sinus tachycardia and, occasionally, hypertension and increased cardiac output. It should be used cautiously in patients at risk from increased heart rate but may be preferred for patients with bradycardia. (From AMA Drug Evaluations Annual, 1992, p198) For use as adjuncts to anesthesia to induce skeletal muscle relaxation and to facilitate the management of patients undergoing mechanical ventilation Gallamine Triethiodide is a nondepolarizing neuromuscular blocking drug (NDMRD) used as an adjunct to anesthesia to induce skeletal muscle relaxation. The actions of gallamine triethiodide are similar to those of tubocurarine, but this agent blocks the cardiac vagus and may cause sinus tachycardia and, occasionally, hypertension and increased cardiac output. Muscle groups differ in their sensitivity to these types of relaxants with ocular muscles (controlling eyelids) being most sensitive, followed by the muscles of the neck, jaw, limbs and then abdomen. The diaphragm is the least sensitive muscle to NDMRDs. Although the nondepolarizing neuromuscular blocking drugs do not have the same adverse effects as succinylcholine, their onset of action is slower. They also have a longer duration of action, making them more suitable for maintaining neuromuscular relaxation during major surgical procedures. It competes with acetylcholine (ACh) molecules and binds to muscarinic acetylcholine receptors on the post-synaptic membrane of the motor endplate. It acts by combining with the cholinergic receptor sites in muscle and competitively blocking the transmitter action of acetylcholine. It blocks the action of ACh and prevents activation of the muscle contraction process. It can also act on nicotinic presynaptic acetylcholine receptors which inhibits the release of ACh.",,,,Gallamine triethiodide is approved.,Gallamine triethiodide is a solid.,True
16311,"An antimuscarinic agent that inhibits gastric secretion at lower doses than are required to affect gastrointestinal motility, salivary, central nervous system, cardiovascular, ocular, and urinary function. It promotes the healing of duodenal ulcers and due to its cytoprotective action is beneficial in the prevention of duodenal ulcer recurrence. It also potentiates the effect of other antiulcer agents such as cimetidine and ranitidine. It is generally well tolerated by patients. For the treatment of peptic ulcer, gastric ulcer, and duodenal ulcer. Pirenzepine belongs to a group of medications called antispasmodics/anticholinergics. These medications are used to relieve cramps or spasms of the stomach, intestines, and bladder. Pirenzepine is used to treat duodenal or stomach ulcers or intestine problems. It can be used together with antacids or other medicine in the treatment of peptic ulcer. It may also be used to prevent nausea, vomiting, and motion sickness. Pirenzepine is a muscarinic receptor antagonist and binds to the muscarinic acetylcholine receptor. The muscarinic acetylcholine receptor mediates various cellular responses, including inhibition of adenylate cyclase, breakdown of phosphoinositides and modulation of potassium channels through the action of G proteins.",The molecular weight is 351.41.,Pirenzepine has a topological polar surface area of 68.78.,The log p value of  is -0.35.,Pirenzepine is approved.,Pirenzepine is a solid.,True
16312,"Clidinium is a synthetic anticholinergic agent which has been shown in experimental and clinical studies to have a pronounced antispasmodic and antisecretory effect on the gastrointestinal tract. It inhibits muscarinic actions of acetylcholine at postganglionic parasympathetic neuroeffector sites. It is used for the treatment of peptic ulcer disease and also to help relieve abdominal or stomach spasms or cramps due to colicky abdominal pain, diverticulitis, and irritable bowel syndrome. For the treatment of peptic ulcer disease and also to help relieve abdominal or stomach spasms or cramps due to colicky abdominal pain, diverticulitis, and irritable bowel syndrome. Clidinium is a synthetic anticholinergic agent which has been shown in experimental and clinical studies to have a pronounced antispasmodic and antisecretory effect on the gastrointestinal tract. Inhibits muscarinic actions of acetylcholine at postganglionic parasympathetic neuroeffector sites primarily by inhibiting the M1 muscarinic receptors.",The molecular weight is 352.45.,Clidinium has a topological polar surface area of 46.53.,The log p value of  is -0.05.,Clidinium is approved.,Clidinium is a solid.,True
16313,"A muscarinic antagonist used as an antispasmodic, in rhinitis, in urinary incontinence, and in the treatment of ulcers. At high doses it has nicotinic effects resulting in neuromuscular blocking. For the treatment of enuresis. It has also been used for hyperhidrosis, and cramps or spasms of the stomach, intestines or bladder. Propantheline is an anticholinergic drug, a medication that reduces the effect of acetylcholine, a chemical released from nerves that stimulates muscles, by blocking the receptors for acetylcholine on smooth muscle (a type of muscle). It also has a direct relaxing effect on smooth muscle. Propantheline is used to treat or prevent spasm in the muscles of the gastrointestinal tract in the irritable bowel syndrome. In addition, Propantheline inhibits gastrointestinal propulsive motility and decreases gastric acid secretion and controls excessive pharyngeal, tracheal and bronchial secretions. Action is achieved via a dual mechanism: (1) a specific anticholinergic effect (antimuscarinic) at the acetylcholine-receptor sites and (2) a direct effect upon smooth muscle (musculotropic).",The molecular weight is 368.5.,Propantheline has a topological polar surface area of 35.53.,The log p value of  is 1.49.,Propantheline is approved.,Propantheline is a solid.,True
16314,"Dicyclomine is a muscarinic M1 and M2 receptor antagonist as well as a non-competitive inhibitor of histamine and bradykinin used to treat spasms of the intestines seen in functional bowel disorder and irritable bowel syndrome. Though it is commonly prescribed, its recommendation may have been based on a small amount of evidence and so its prescription is becoming less favourable. Dicyclomine is indicated for the treatment of functional bowel disorder and irritable bowel syndrome. Dicyclomine is an anticholinergic drug used to relax the smooth muscles of the intestines. It's duration of action is not especially long as it is usually taken 4 times daily with individual doses of 20-40mg orally or 10-20mg by intramuscular injection. Dicyclomine should not be administered intravenously. Dicyclomine achieves its action partially through direct antimuscarinic activity of the M1 and M2 receptors, and partially through antagonism of bradykinin and histamine. Dicyclomine non-competitively inhibits the action of bradykinin and histamine, resulting in direct action on the smooth muscle, and decreased strength of contractions seen in spasms of the ileum.",The molecular weight is 309.49.,Dicyclomine has a topological polar surface area of 29.54.,The log p value of  is 6.14.,Dicyclomine is approved.,Dicyclomine is a solid.,True
16315,"Cycrimine is a drug used to reduce levels of acetylcholine to return a balance with dopamine in the treatment and management of Parkinson's disease. For treatment and management of Parkinson's disease. Cycrimine is a central anticholenergic used in the treatment of the symptoms of Parkinson's disease. It is a drug used to reduce levels of acetylcholine. Acetylcholine is usually in balance with dopamine neurotransmitters, however lower levels of dopamine are present in the brain of patients suffering from Parkinson's disease. By lowering levels of acetylcholine, it is thought that this balance may be restored. Cycrimine binds the muscarinic acetylcholine receptor M1, effectively inhibiting acetylcholine. This decrease in acetylcholine restores the normal dopamine-acetylcholine balance and relieves the symptoms of Parkinson's disease.",The molecular weight is 287.45.,Cycrimine has a topological polar surface area of 23.47.,The log p value of  is 4.59.,Cycrimine is approved.,Cycrimine is a solid.,True
16316,"A drug that has been used in various urinary syndromes and as an antispasmodic. Its therapeutic usefulness and its mechanism of action are not clear. It may have local anesthetic activity and direct relaxing effects on smooth muscle as well as some activity as a muscarinic antagonist.  For symptomatic relief of dysuria, urgency, nocturia, suprapubic pain, frequency and incontinence as may occur in cystitis, prostatitis, urethritis, urethrocystitis/urethrotrigonitis. Flavoxate is a spasmolytic flavone derivative that acts by relaxing the smooth muscle in the urinary tract. Flavoxate is a competitive muscarinic receptor antagonist indicated for the treatment of overactive bladder with symptoms of urge urinary incontinence, urgency, and urinary frequency. Muscarinic receptors play an important role in several major cholin-ergically mediated functions, including contractions of urinary bladder smooth muscle and stimulation of salivary secretion. Flavoxate acts as a direct antagonist at muscarinic acetylcholine receptors in cholinergically innervated organs. Its anticholinergic-parasympatholytic action reduces the tonus of smooth muscle in the bladder, effectively reducing the number of required voids, urge incontinence episodes, urge severity and improving retention, facilitating increased volume per void.",The molecular weight is 391.47.,Flavoxate has a topological polar surface area of 55.84.,The log p value of  is 4.97.,Flavoxate is approved.,Flavoxate is a solid.,True
16317,"An indole derivative effective in schizophrenia and other psychoses and possibly useful in the treatment of the aggressive type of undersocialized conduct disorder. Molindone has much lower affinity for D2 receptors than most antipsychotic agents and has a relatively low affinity for D1 receptors. It has only low to moderate affinity for cholinergic and alpha-adrenergic receptors. Some electrophysiologic data from animals indicate that molindone has certain characteristics that resemble those of clozapine. (From AMA Drug Evaluations Annual, 1994, p283) Molindone is used for the management of the manifestations of psychotic disorders. Molindone is a dihydroindolone compound which is not structurally related to the phenothiazines, the butyrophenones, or the thioxanthenes. Molindone has a pharmacological profile in laboratory animals which predominantly resembles that of major tranquilizers causing reduction of spontaneous locomotion and aggressiveness, suppression of a conditioned response and antagonism of the bizarre stereotyped behavior and hyperactivity induced by amphetamines. In addition, molindone antagonizes the depression caused by the tranquilizing agent tetrabenazine. The exact mechanism has not been established, however, based on electroencephalogram (EEG) studies, molindone is thought to act by occupying (antagonizing) dopamine (D2) receptor sites in the reticular limbic systems in the brain, thus decreasing dopamine activity. Decreased dopamine activity results in decreased physiological effects normally induced by excessive dopamine stimulation, such as those typically seen in manifestations of psychotic disorders.",The molecular weight is 276.38.,Molindone has a topological polar surface area of 45.33.,The log p value of  is 2.57.,Molindone is approved.,Molindone is a solid.,True
16318,An indolocarbazole that is a potent protein kinase C inhibitor which enhances cAMP-mediated responses in human neuroblastoma cells. (Biochem Biophys Res Commun 1995;214(3):1114-20),,,,Staurosporine is experimental.,Staurosporine is a solid.,True
16319,"NGX267 is a muscarinic agonist. It is developed for the treatment of Alzheimer’s disease and has shown the potential to both reduce symptoms and slow disease progression. Investigated for use/treatment in alzheimer's disease and schizophrenia and schizoaffective disorders. Due to its mechanism of action, NGX267 may be simultaneously effective in treating the memory and cognitive disturbances experienced by Alzheimer's patients and in reducing the creation of neurotoxic proteins, thereby delaying disease progression. NGX267 has been shown to stimulate M1 receptors in a fashion analogous to acetylcholine, a neurotransmitter essential for memory and cognitive function that is depleted when neurons, or brain cells, degenerate. The M1 receptor plays an important role in memory and cognitive processing. Its activation has also been linked to decreases in two biochemical processes, AB production and tau protein phosphorylation, both of which are involved in the creation of the neurofibrillary tangles and amyloidplaques that are major histopathological hallmarks of Alzheimer's disease. By selectively enhancing M1 cholinergic neurotransmission in the brain, NGX267 may offer advantages over current therapies for Alzheimer's disease due to the relative preservation of this system in patients who are clinically symptomatic. ",,,,NGX267 is investigational.,NGX267 is a solid.,True
16320,"ACP-104, or N-desmethylclozapine, is the major metabolite of clozapine, and is being developed by ACADIA as a novel, stand-alone therapy for schizophrenia. It combines an atypical antipsychotic efficacy profile with the added potential benefit of enhanced cognition, thereby addressing one of the major challenges in treating schizophrenia today. Investigated for use/treatment in schizophrenia and schizoaffective disorders.  ACP-104 is a small molecule drug candidate we are developing as a novel therapy for schizophrenia. It is known that large amounts of ACP-104, or N-desmethylclozapine, are formed in the body after administration of clozapine. That is, clozapine is metabolized to ACP-104. We discovered that ACP-104 has a unique ability to stimulate m1 muscarinic receptors, a key muscarinic receptor. The m1 muscarinic receptors are widely known to play an important role in cognition. Since clozapine itself blocks the m1 muscarinic receptor, patients need to extensively metabolize clozapine into ACP-104 to stimulate this receptor and thereby overcome the blocking action of clozapine. Administration of ACP-104 will avoid the variability of this metabolic process and the competing action of clozapine. Like clozapine, ACP-104 is a dopamine antagonist and a 5-HT2A inverse agonist. We believe that ACP-104 represents a new approach to schizophrenia therapy that combines an atypical antipsychotic efficacy profile with the added advantage of beneficial cognitive effects. ACP-104 combines M1 muscarinic agonism, 5-HT2A inverse agonism, and D2 and D3 dopamine partial agonism in a single compound. ACP-104 uniquely stimulates brain cells known as M1 muscarinic receptors that play an important role in cognition. ACP-104 is a partial-agonist that causes weak activation of dopamine D2 and D3 receptors. These partial agonist properties of ACP-104 may lead to less motoric side effects than seen with most other antipsychotic drugs.",,,,ACP-104 is investigational.,ACP-104 is a solid.,True
16321,"Lasofoxifene is a non-steroidal 3rd generation selective estrogen receptor modulator (SERM) that selectively binds to both ERα and ERβ with high affinity. It is a naphthalene derivative marketed for prevention and treatment of osteoporosis and for the treatment of vaginal atrophy. It was initially developed as Oporia by Pfizer as a treatment for postmenopausal osteoporosis and vaginal atrophy, in which were both rejected for approval by FDA. Later Fablyn was developed as a result of a research collaboration between Pfizer and Ligand Pharmaceuticals with a newly submitted New Drug Application in 2008. It gained approval by European Commission in March 2009. Ligand Pharmaceuticals signed a license agreement with Sermonix Pharmaceuticals for the development and commercialization of oral lasofoxifene in the USA. Investigated for use/treatment in postmenopausal osteoporosis to reduce the risk of both vertebral and novertebral fractures, as well as address other postmenopausal conditions, including reduction in risk of breast cancer and treatment of vulvar and vaginal atrophy (VVA) Lasofoxifene exhibits both significant estrogenic and antiestrogenic activity both in vitro and in vivo, targeting any tissues that possess ERs, such as bone, uterus, breast, blood vessels, and liver. Binding assays demonstrated high affinity of the compound for both ERα and ERβ in a tissue-dependent manner. It mimics the effects of estradiol with varying agonist and antagonist effects.  Lasofoxifene mediates an agonist effect on estrogen receptors expressed on bone to mimic the positive effects of estrogen to reduce the production and lifespan of osteoclasts via altering the NF-kappaB ligand (RANKL)/RANK/osteoprotegerin system, stimulation of osteoblast (the bone forming cells) activity and additional effects on calcium homeostasis. It acts as an antagonist at uterus and mammary glands by suppressing the estrogen signaling in oncogenic pathways and inhibits the downstream gene transcription.",The molecular weight is 413.56.,Lasofoxifene has a topological polar surface area of 32.7.,The log p value of  is 6.71.,Lasofoxifene is approved and investigational.,Lasofoxifene is a solid.,True
16322,"Constituent of striated muscle and liver. It is used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias. For treatment of primary systemic carnitine deficiency, a genetic impairment of normal biosynthesis or utilization of levocarnitine from dietary sources, or for the treatment of secondary carnitine deficiency resulting from an inborn error of metabolism such as glutaric aciduria II, methyl malonic aciduria, propionic acidemia, and medium chain fatty acylCoA dehydrogenase deficiency. Used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias. Parenteral levocarnitine is indicated for the prevention and treatment of carnitine deficiency in patients with end-stage renal disease. Levocarnitine is a carrier molecule in the transport of long chain fatty acids across the inner mitochondrial membrane. It also exports acyl groups from subcellular organelles and from cells to urine before they accumulate to toxic concentrations. Lack of carnitine can lead to liver, heart, and muscle problems. Carnitine deficiency is defined biochemically as abnormally low plasma concentrations of free carnitine, less than 20 &micro;mol/L at one week post term and may be associated with low tissue and/or urine concentrations. Further, this condition may be associated with a plasma concentration ratio of acylcarnitine/levocarnitine greater than 0.4 or abnormally elevated concentrations of acylcarnitine in the urine. Only the L isomer of carnitine (sometimes called vitamin BT) affects lipid metabolism. The \vitamin BT\"" form actually contains D,L-carnitine, which competitively inhibits levocarnitine and can cause deficiency. Levocarnitine can be used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias."" Levocarnitine can be synthesised within the body from the amino acids lysine or methionine. Vitamin C (ascorbic acid) is essential to the synthesis of carnitine. Levocarnitine is a carrier molecule in the transport of long chain fatty acids across the inner mitochondrial membrane. It also exports acyl groups from subcellular organelles and from cells to urine before they accumulate to toxic concentrations. Only the L isomer of carnitine (sometimes called vitamin BT) affects lipid metabolism. Levocarnitine is handled by several proteins in different pathways including carnitine transporters, carnitine translocases, carnitine acetyltransferases and carnitine palmitoyltransferases.",The molecular weight is 161.2.,Levocarnitine has a topological polar surface area of 60.36.,The log p value of  is -7.73.,Levocarnitine is approved and investigational.,Levocarnitine is a solid.,True
16323,"A pyranoquinolone derivative that inhibits activation of inflammatory cells which are associated with asthma, including eosinophils, neutrophils, macrophages, mast cells, monocytes, and platelets. For the treatment of mild to moderate asthma Nedocromil is a anti-inflammatory agent and can be administered directly to the bronchial mucosa. It has significant inhibitory effect on allergen-induced early and late asthmatic reactions and on bronchial hyperresponsiveness. Nedocromil has been shown to inhibit the in vitro activation of, and mediator release from, a variety of inflammatory cell types associated with asthma, including eosinophils, neutrophils, macrophages, mast cells, monocytes, and platelets. Nedocromil inhibits activation and release of inflammatory mediators such as histamine, prostaglandin D2 and leukotrienes c4 from different types of cells in the lumen and mucosa of the bronchial tree. These mediators are derived from arachidonic acid metabolism through the lipoxygenase and cyclo-oxygenase pathways. The mechanism of action of nedocromil may be due partly to inhibition of axon reflexes and release of sensory neuropeptides, such as substance P, neurokinin A, and calcitonin-gene&ntilde;related peptides. The result is inhibition of bradykinin-induced bronchoconstriction. Nedocromil does not posess any bronchodilator, antihistamine, or corticosteroid activity.",The molecular weight is 371.34.,Nedocromil has a topological polar surface area of 121.21.,The log p value of  is 1.5.,Nedocromil is approved and investigational.,Nedocromil is a solid.,True
16324,"The conjugation product of LEUKOTRIENE A4 and glutathione. It is the major arachidonic acid metabolite in macrophages and human mast cells as well as in antigen-sensitized lung tissue. It stimulates mucus secretion in the lung, and produces contractions of nonvascular and some vascular smooth muscle. (From Dictionary of Prostaglandins and Related Compounds, 1990)",,,,Leukotriene C4 is experimental and investigational.,Leukotriene C4 is a solid.,True
16325,Leukotriene D4 has been used in trials studying the diagnostic of Asthma and Allergic Rhinitis.,,,,Leukotriene D4 is investigational.,,True
16326,"Putrescine is a toxic diamine formed by putrefaction from the decarboxylation of arginine and ornithine. Putrescine is a solid. This compound belongs to the polyamines. These are compounds containing more than one amine group. Known drug targets of putrescine include putrescine-binding periplasmic protein, ornithine decarboxylase, and S-adenosylmethionine decarboxylase proenzyme. ",,,,Putrescine is experimental.,Putrescine is a solid.,True
16327,,,,,5'-{(methyl)amino}-5'-deoxy-8-ethenyladenosine is experimental.,5'-{(methyl)amino}-5'-deoxy-8-ethenyladenosine is a solid.,False
16328,"Alanine is a non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system. Used for protein synthesis. Is an important source of energy for muscle tissue, the brain and central nervous system; strengthens the immune system by producing antibodies; helps in the metabolism of sugars and organic acids. L-Alanine is a non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases immunity, and provides energy for muscle tissue, brain, and the central nervous system. BCAAs are used as a source of energy for muscle cells. During prolonged exercise, BCAAs are released from skeletal muscles and their carbon backbones are used as fuel, while their nitrogen portion is used to form another amino acid, Alanine. Alanine is then converted to Glucose by the liver. This form of energy production is called the Alanine-Glucose cycle, and it plays a major role in maintaining the body's blood sugar balance.",The molecular weight is 89.09.,Alanine has a topological polar surface area of 63.32.,The log p value of  is -3.12.,Alanine is nutraceutical.,Alanine is a solid.,True
16329,"Reduced Fab fragment of the murine IgG1 monoclonal antibody IMMU-4 (also called NP-4) with specificity for carcinoembryonic antigen (CEA) covalently labeled with Technitium 99. The molecule has a molecular weight of ~54,000 Daltons. For imaging colorectal tumors Binds to the carcinoembryonic antigen, which is a cell surface protein generally overexpressed in colon (and other) cancers. The radioactive Tc99, which is covalently attached to the antibody, allows radiodiagnostic detection of CEA expressing cells and tumors Binds selectively to cell-surface carcinoembryonic antigen (CEA) expressed on colorectal tumors.",,,,Technetium Tc-99m arcitumomab is experimental.,Technetium Tc-99m arcitumomab is a liquid.,True
16330,"The N-acetyl derivative of glucosamine. For the treatment and prevention of osteoarthritis, by itself or in combination with chondroitin sulfate. The mechanism of action in relieving arthritic pain and in repair of cartilage is a matter of speculation. Biochemically, glucosamine is involved in glycoprotein metabolism. Glycoproteins, known as proteoglycans, form the ground substance in the extra-cellular matrix of connective tissue. Proteoglycans are polyanionic substances of high-molecular weight and contain many different types of heteropolysaccharide side-chains covalently linked to a polypeptide-chain backbone. These polysaccharides make up to 95% of the proteoglycan structure. In fact, chemically, proteoglycans resemble polysaccharides more than they do proteins. The polysaccharide groups in proteoglycans are called glycosaminoglycans (GAGs). GAGs include hyaluronic acid, chondroitin sulfate, dermatan sulfate, keratan sulfate, heparin and heparan sulfate. All of the GAGs contain derivatives of glucosamine or galactosamine. Glucosamine derivatives are found in hyaluronic acid, keratan sulfate and heparan sulfate. Chondroitin sulfate contains derivatives of galactosamine. The glucosamine-containing glycosaminoglycan hyaluronic acid is vital for the function of articular cartilage. GAG chains are fundamental components of aggrecan found in articular cartilage. Aggrecan confers upon articular cartilage shock-absorbing properties. It does this by providing cartilage with a swelling pressure that is restrained by the tensile forces of collagen fibers. This balance confers upon articular cartilage the deformable resilience vital to its function. In the early stages of degenerative joint disease, aggrecan biosynthesis is increased. However, in later stages, aggrecan synthesis is decreased, leading eventually to the loss of cartilage resiliency and to most of the symptoms that accompany osteoarthritis. During the progression of osteoarthritis, exogenous glucosamine may have a beneficial role. It is known that, in vitro, chondrocytes do synthesize more aggregan when the culture medium is supplemented with glucosamine. N-acetylglucosamine is found to be less effective in these in vitro studies. Glucosamine has also been found to have antioxidant activity and to be beneficial in animal models of experimental arthritis. The counter anion of the glucosamine salt (i.e. chloride or sulfate) is unlikely to play any role in the action or pharmacokinetics of glucosamine. Further, the sulfate in glucosamine sulfate supplements should not be confused with the glucosamine sulfate found in such GAGs as keratan sulfate and heparan sulfate. In the case of the supplement, sulfate is the anion of the salt. In the case of the above GAGs, sulfate is present as an ester. Also, there is no glucosamine sulfate in chondroitin sulfate (source: PDRhealth).",The molecular weight is 221.21.,N-Acetylglucosamine has a topological polar surface area of 119.25.,The log p value of  is -1.77.,N-Acetylglucosamine is approved and investigational and nutraceutical.,N-Acetylglucosamine is a solid.,True
16331,"A prostaglandin that is a powerful vasodilator and inhibits platelet aggregation. It is biosynthesized enzymatically from prostaglandin endoperoxides in human vascular tissue. The sodium salt has been also used to treat primary pulmonary hypertension. For the long-term intravenous treatment of primary pulmonary hypertension and pulmonary hypertension associated with the scleroderma spectrum of disease in NYHA Class III and Class IV patients who do not respond adequately to conventional therapy. Epoprostenol has two major pharmacological actions: (1) direct vasodilation of pulmonary and systemic arterial vascular beds, and (2) inhibition of platelet aggregation. In animals, the vasodilatory effects reduce right and left ventricular afterload and increase cardiac output and stroke volume. The effect of epoprostenol on heart rate in animals varies with dose. At low doses, there is vagally mediated brudycardia, but at higher doses, epoprostenol causes reflex tachycardia in response to direct vasodilation and hypotension. No major effects on cardiac conduction have been observed. Additional pharmacologic effects of epoprostenol in animals include bronchodilation, inhibition of gastric acid secretion, and decreased gastric emptying. No available chemical assay is sufficiently sensitive and specific to assess the in vivo human pharmacokinetics of epoprostenol. Prostaglandins are present in most body tissues and fluids and mediate many biological functions. Epoprostenol (PGI2) is a member of the family of prostaglandins that is derived from arachidonic acid. The major pharmacological actions of epoprostenol is ultimately inhibition of platelet aggregation. Prostacycline (PGI2) from endothelial cells activate G protein-coupled receptors on platelets and endothelial cells. This activation causes adenylate cyclase to produce cyclic AMP which inhibits further platelet activation and activates protein kinase A. Cyclic AMP also prevents coagulation by preventing an increase in intracellular calcium from thromboxane A2 binding. PKA then continues the cascade by phosphorylating and inhibiting myosin light-chain kinase which leads to smooth muscle relaxation and vasodilation. Notably, PGI2 and TXA2 work as physiological antagonists.",The molecular weight is 352.47.,Epoprostenol has a topological polar surface area of 86.99.,The log p value of  is 2.33.,Epoprostenol is approved.,Epoprostenol is a solid.,True
16332,"Investigated for use/treatment in cardiac surgery, coronary artery disease, thrombosis, and transfusion.",,,,Regrelor is investigational.,Regrelor is a solid.,True
16333,"A P2Y12 inhibitor and platelet aggregation inhibitor. Investigated for use/treatment in cardiovascular disorders and myocardial infarction. PRT060128 is a specific, reversible ADP receptor antagonist that binds to the P2Y12 receptor on platelets. PRT06128 prevents binding of adenosine diphosphate (ADP) to its platelet receptor, impairing the ADP-mediated activation of the glycoprotein GPIIb/IIIa complex, a key step in the coagulation cascade. PRT060128 likely has a similar mechanism of action to clopidogrel.",,,,Elinogrel is investigational.,Elinogrel is a solid.,True
16334,"Cangrelor is an intravenous, direct-acting, reversible P2Y12 inhibitor for patients undergoing percutaneous coronary intervention (PCI) who have not been yet treated by oral P2Y12 inhibitors. An advantage Cangrelor provides over oral P2Y12 inhibitors (such as prasugrel, ticagrelor, and clopidogrel) is that it is an active drug not requiring metabolic conversion therefore providing a rapid onset and offset of action. Cangrelor was approved by the FDA in June 2015 for intravenous application. For use as an adjunct to percutaneous coronary intervention (PCI) for reducing the risk of periprocedural myocardial infarction (MI), repeat coronary revascularization, and stent thrombosis (ST) in patients in who have not been treated with a P2Y12 platelet inhibitor and are not being given a glycoprotein IIb/IIIa inhibitor. Cangrelor is a selective, reversible, P2Y12 platelet receptor antagonist which inhibits ADP platelet aggregation. ADP is typically released by damaged blood vessels, red blood cells, and/or platelets due to agonists stimulating platelet activity. ADP binds to P2Y12 to stimulate and complete platelet aggregation by inhibiting adenylyl cyclase by a Gi protein, thus potentiating dense granule secretion and increasing coagulation activity. Cangrelor acts on the same target as oral irreversible inhibitors clopidogrel and ticlopidine and has a similar mechanism of action, but is reversible and provides a fast onset and offset of action. ",The molecular weight is 776.35.,Cangrelor has a topological polar surface area of 255.91.,The log p value of  is 1.56.,Cangrelor is approved.,Cangrelor is a solid.,True
16335,,,,,"N-ethyl-N-propane-1,3-diamine is experimental.","N-ethyl-N-propane-1,3-diamine is a solid.",False
16336,"A histamine H2 agonist used clinically to test gastric secretory function. For use clinically to test gastric secretory function. Betazole is a histamine H2 agonist used in a test for measuring maximal production of gastric acidity or anacidity. This measurement can be used to diagnose diseases such as Zollinger-Ellison syndrome, whereby the volume of gastric and basal secretions is measured following betazole administration (greater than 60% of the maximal acid secretion following betazole stimulation). In another test, gastritis can be diagnosed given late absence of gastric acid which is unresponsive to betazole stimulation. Betazole can be used as a gastric secretory stimulant instead of histamine with the advantage of not provoking side effects and thus not requiring the use of antihistaminic compounds. Betazole is a histamine analogue. It produces the same effects as histamine, binding the H2 receptor which is a mediator of gastric acid secretion. This agonist action thereby results in an increase in the volume of gastric acid produced.",The molecular weight is 111.15.,Betazole has a topological polar surface area of 54.7.,The log p value of  is -0.7.,Betazole is approved.,Betazole is a liquid.,True
16337,"A vasodilator that apparently has direct actions on blood vessels and also increases cardiac output. Tolazoline can interact to some degree with histamine, adrenergic, and cholinergic receptors, but the mechanisms of its therapeutic effects are not clear. It is used in treatment of persistent pulmonary hypertension of the newborn. For the treatment of pulmonary artery anomalies Tolazoline is a pulmonary vasodilator indicated used to decrease pulmonary vascular resistance (PVR) in persistent pulmonary hypertension of the newborn (PPHN). Vasodilation by means of a direct effect on peripheral vascular smooth muscle and indirect effects produced, in part, by release of endogenous histamine; tolazoline has moderate alpha-adrenergic blocking activity and has histamine agonist activity. Tolazoline usually reduces pulmonary arterial pressure and vascular resistance.",The molecular weight is 160.22.,Tolazoline has a topological polar surface area of 24.39.,The log p value of  is 2.65.,Tolazoline is approved and vet_approved.,Tolazoline is a solid.,True
16338,"HZT-501 is under investigation by Horizon Therapeutics, Inc., a privately held biopharmaceutical company. It has entered Phase 3 clinical trials in March 2007 for reduction of the risk of development of ibuprofen-associated upper gastrointestinal (i.e., gastric and/or duodenal) ulcers. HZT-501 is a combination product including ibuprofen and the acid reducing agent famotidine. Investigated for use/treatment in pain (acute or chronic). HZT-501 is a proprietary formulation of ibuprofen, the most prescribed NSAID in the United States, combined with famotidine, the most potent H2 receptor antagonist, in a single pill. HZT-501 is specifically designed to provide pain relief while reducing stomach acidity during the peak time of risk for gastric ulceration.",,,,HZT-501 is investigational.,HZT-501 is a solid.,True
16339,"Metiamide is an H-2 receptor antagonist derived from burimamide. It was an intermediate product on the path to developing cimetidine. Potential in the treatment and the management of acid-reflux disorders (GERD), peptic ulcer disease, heartburn, and acid indigestion. Metiamide is a histamine H<sub>2</sub>-receptor antagonist. It reduces basal and nocturnal gastric acid secretion and a reduction in gastric volume, acidity, and amount of gastric acid released in response to stimuli including food, caffeine, insulin, betazole, or pentagastrin. Metiamide inhibits many of the isoenzymes of the hepatic CYP450 enzyme system. Other actions of Metiamide include an increase in gastric bacterial flora such as nitrate-reducing organisms. Metiamide binds to an H<sub>2</sub>-receptor located on the basolateral membrane of the gastric parietal cell, blocking histamine effects. This competitive inhibition results in reduced gastric acid secretion and a reduction in gastric volume and acidity.",,,,Metiamide is experimental.,Metiamide is a solid.,True
16340,"Roxatidine acetate is a specific and competitive H2 receptor antagonist. It is currently approved in South Africa under the tradename Roxit. For the treatment of disorders of the upper gastro-intestinal region that are due to an excess of hydrochloric acid in the gastric juice, i.e. duodenal ulcers, benign gastric ulcers. Also for prophylaxis of recurrent gastric and duodenal ulcers Roxatidine acetate suppresses the effect of histamine on the parietal cells of the stomach (H2-receptor antagonist). This suppressive action is dose-dependent. As a result, the production and secretion, particularly of gastric acid, are reduced. Roxatidine acetate has no antiandrogenic effects and does not influence drug-metabolizing enzymes in the liver. The H2 antagonists are competitive inhibitors of histamine at the parietal cell H2 receptor. They suppress the normal secretion of acid by parietal cells and the meal-stimulated secretion of acid. They accomplish this by two mechanisms: histamine released by ECL cells in the stomach is blocked from binding on parietal cell H2 receptors which stimulate acid secretion, and other substances that promote acid secretion (such as gastrin and acetylcholine) have a reduced effect on parietal cells when the H2 receptors are blocked.",The molecular weight is 348.44.,Roxatidine acetate has a topological polar surface area of 67.87.,The log p value of  is 2.8.,Roxatidine acetate is experimental.,Roxatidine acetate is a solid.,True
16341,"A metallic element found in certain minerals, in nearly all soils, and in mineral waters. It is an essential constituent of hemoglobin, cytochrome, and other components of respiratory enzyme systems. Its chief functions are in the transport of oxygen to tissue (hemoglobin) and in cellular oxidation mechanisms. Depletion of iron stores may result in iron-deficiency anemia. Iron is used to build up the blood in anemia. Used in preventing and treating iron-deficiency anemia. The major activity of supplemental iron is in the prevention and treatment of iron deficiency anemia. Iron has putative immune-enhancing, anticarcinogenic and cognition-enhancing activities. Iron is necessary for the production of hemoglobin. Iron-deficiency can lead to decreased production of hemoglobin and a microcytic, hypochromic anemia.",The molecular weight is 55.84.,,,Iron is approved.,Iron is a solid.,True
16342,,,,,dATP is experimental.,dATP is a solid.,False
16343,,,,,"(1S)-1,2,3,4-TETRAHYDRO-BENZOPHENANTHRENE-2,3,4-TRIOL is experimental.","(1S)-1,2,3,4-TETRAHYDRO-BENZOPHENANTHRENE-2,3,4-TRIOL is a solid.",False
16344,"Used in preventing and treating iron-deficiency anemia. The major activity of supplemental iron is in the prevention and treatment of iron deficiency anemia. Iron has putative immune-enhancing, anticarcinogenic and cognition-enhancing activities. Iron is necessary for the production of hemoglobin. Iron-deficiency can lead to decreased production of hemoglobin and a microcytic, hypochromic anemia.",The molecular weight is 446.14.,Ferrous gluconate has a topological polar surface area of 265.04.,,Ferrous gluconate is approved.,,True
16345,"Used in preventing and treating iron-deficiency anemia. The major activity of supplemental iron is in the prevention and treatment of iron deficiency anemia. Iron has putative immune-enhancing, anticarcinogenic and cognition-enhancing activities. Iron is necessary for the production of hemoglobin. Iron-deficiency can lead to decreased production of hemoglobin and a microcytic, hypochromic anemia.",The molecular weight is 171.92.,Ferrous succinate has a topological polar surface area of 80.26.,,Ferrous succinate is approved.,,True
16346,"Used in preventing and treating iron-deficiency anemia. The major activity of supplemental iron is in the prevention and treatment of iron deficiency anemia. Iron has putative immune-enhancing, anticarcinogenic and cognition-enhancing activities. Iron is necessary for the production of hemoglobin. Iron-deficiency can lead to decreased production of hemoglobin and a microcytic, hypochromic anemia.",The molecular weight is 406.08.,,,Ferrous ascorbate is approved.,,True
16347,"Used in treatment of iron deficiency anemia. Used in preventing and treating iron-deficiency anemia. The major activity of supplemental iron is in the prevention and treatment of iron deficiency anemia. Iron has putative immune-enhancing, anticarcinogenic and cognition-enhancing activities. Iron is necessary for the production of hemoglobin. Iron-deficiency can lead to decreased production of hemoglobin and a microcytic, hypochromic anemia.",The molecular weight is 169.9.,,,Ferrous fumarate is approved.,,True
16348,"Used in preventing and treating iron-deficiency anemia. The major activity of supplemental iron is in the prevention and treatment of iron deficiency anemia. Iron has putative immune-enhancing, anticarcinogenic and cognition-enhancing activities. Iron is necessary for the production of hemoglobin. Iron-deficiency can lead to decreased production of hemoglobin and a microcytic, hypochromic anemia.",,,,Ferrous glycine sulfate is approved.,,True
16349,,,,,9-Deazaadenine is experimental.,9-Deazaadenine is a solid.,False
16350,A key intermediate in metabolism. It is an acid compound found in citrus fruits. The salts of citric acid (citrates) can be used as anticoagulants due to their calcium chelating ability.,The molecular weight is 192.12.,Citric acid has a topological polar surface area of 132.13.,The log p value of  is -2.0.,Citric acid is approved and nutraceutical and vet_approved.,Citric acid is a solid.,True
16351,,,,,"(5Z)-7-{(1R,4S,5R,6R)-6--2,3-diazabicyclohept-2-en-5-yl}-5-heptenoic acid is experimental.","(5Z)-7-{(1R,4S,5R,6R)-6--2,3-diazabicyclohept-2-en-5-yl}-5-heptenoic acid is a solid.",False
16352,Precursor of epinephrine that is secreted by the adrenal medulla and is a widespread central and autonomic neurotransmitter. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. It is also found in plants and is used pharmacologically as a sympathomimetic. Mainly used to treat patients in vasodilatory shock states such as septic shock and neurogenic shock and has shown a survival benefit over dopamine. Also used as a vasopressor medication for patients with critical hypotension. Noradrenaline acts on both alpha-1 and alpha-2 adrenergic receptors to cause vasoconstriction. Its effect in-vitro is often limited to the increasing of blood pressure through antagonising alpha-1 and alpha-2 receptors and causing a resultant increase in systemic vascular resistance. Norepinephrine functions as a peripheral vasoconstrictor by acting on alpha-adrenergic receptors. It is also an inotropic stimulator of the heart and dilator of coronary arteries as a result of it's activity at the beta-adrenergic receptors.,The molecular weight is 169.18.,Norepinephrine has a topological polar surface area of 86.71.,The log p value of  is -0.99.,Norepinephrine is approved.,Norepinephrine is a solid.,True
16353,"Mazindol is a tricyclic anorexigenic agent that is unrelated to and less toxic than , but with some similar side effects. It inhibits uptake of catecholamines and blocks the binding of cocaine to the dopamine uptake transporter. Mazindol is only approved in the United States for the treatment of Duchenne muscular dystrophy, and is not marketed or available in the United States for use in the treatment of obesity. Used in short-term (a few weeks) treatment of exogenous obesity in conjunction with a regimen of weight reduction based on caloric restriction, exercise, and behavior modification in patients with a body mass index of 30 kg of body weight per height in meters squared (kg/m<sup>2</sup>) or in patients with a body mass index of 27 kg/m<sup>2</sup> in the presence of risk factors such as hypertension, diabetes, or hyperlipidemia. Mazindol is a sympathomimetic amine that stimulates the central nervous system (nerves and brain), leading to increased your heart rate and blood pressure, and decreased appetite. Since the appetite-suppressing effect of the drug tends to decrease after few weeks of treatment, sympathomimetic appetite suppressants are typically used short-term weight-loss program.  Unlike other sympathomimetic appetite suppressants such as phentermine, mazindol is thought to inhibit the reuptake of norepinephrine rather than to cause its release.",The molecular weight is 284.74.,Mazindol has a topological polar surface area of 35.83.,The log p value of  is 3.39.,Mazindol is approved and investigational.,Mazindol is a solid.,True
16354,"Deserpidine is an ester alkaloid drug isolated from Rauwolfia canescens (family Apocynaceae) with antipsychotic and antihypertensive properties that has been used for the control of high blood pressure and for the relief of psychotic behavior. For the treatment of hypertension. Deserpidine, an alkaloid of <i>Rauwolfia canescens</i>, is used as an antihypertensive. Rauwolfia alkaloids work by controlling nerve impulses along certain nerve pathways. As a result, they act on the heart and blood vessels to lower blood pressure. Deserpidine's mechanism of action is through inhibition of the ATP/Mg<sup>2+</sup> pump responsible for the sequestering of neurotransmitters into storage vesicles located in the presynaptic neuron. The neurotransmitters that are not sequestered in the storage vesicle are readily metabolized by monoamine oxidase (MAO) causing a reduction in catecholamines.",The molecular weight is 578.66.,Deserpidine has a topological polar surface area of 108.55.,The log p value of  is 3.84.,Deserpidine is approved.,Deserpidine is a solid.,True
16355,"Ephedra is an alkaloid chemical compound traditionally obtained from the plant _Ephedra sinica_. The sale of ephedra-containing supplements intended to increase muscle weight or promote weight loss was banned in the United States in 2004 due to the risk for adverse effects and a lack of evidence for clinical effectiveness. The drug is still sold in Canada in OTC formulations for respiratory conditions associated with bronchial asthma. Ephedra is indicated for the temporary relief of shortness of breath, tightness of chest, and wheezing due to bronchial asthma. For the temporary relief of bronchial asthma in over-the-counter formulations.  The alkaloids ephedrine and pseudoephedrine are the active constituents of Ephedra. Pseudoephedrine is used in over-the-counter decongestants. Derivatives of ephedrine are used to treat low blood pressure, but alternatives with reduced cardiovascular risk have replaced it for treating asthma. Ephedrine is also considered a performance-enhancing drug and is prohibited in most competitive sports. Ephedrine is a sympathomimetic amine - that is, its principal mechanism of action relies on its direct and indirect actions on the adrenergic receptor system, which is part of the sympathetic nervous system. Ephedrine increases post-synaptic noradrenergic receptor activity by (weakly) directly activating post-synaptic α-receptors and β-receptors, but the bulk of its effect comes from the pre-synaptic neuron being unable to distinguish between real adrenaline or noradrenaline from ephedrine. The ephedrine, mixed with noradrenaline, is transported through the noradrenaline reuptake complex and packaged (along with real noradrenaline) into vesicles that reside at the terminal button of a nerve cell. Ephedrine's action as an agonist at most major noradrenaline receptors and its ability to increase the release of both dopamine and to a lesser extent, serotonin by the same mechanism is presumed to have a major role in its mechanism of action.",,,,Ephedra sinica root is nutraceutical.,Ephedra sinica root is a solid.,True
16356,"MMDA, or 3-methoxy-4,5-methylenedioxyamphetamine, is a member of the amphetamine drug class with stimulant and psychedelic properties. It also acts as an entheogen and an entactogen. MMDA bears resemblance to the psychopharmacologically active essential oils elemicin and myristicin found in nutmeg. The effects of MMDA includes feelings of euphoria and warmth, as well as realistic closed-eye visuals. MMDA is a recreational drug. It has no current medical uses and is a Schedule I controlled substance in the USA at present. The mechanism that produces the psychedelic activity of MMDA has not been definitively established. There are, as of the present time, no reported studies on the human pharmacokinetics or metabolism of MMDA. Based on its structural relationship with other similar drugs for which the pharmacology is known, it is likely that MMDA has multiple mechanisms of action, and probably acts both as a 5HT2A agonist in a similar manner to hallucinogenic amphetamines such as DOM, and also as a serotonin releaser by reversing the direction of the serotonin reuptake transporter in a similar manner to MDMA.",,,,MMDA is experimental and illicit.,MMDA is a solid.,True
16357,"Isometheptene is a sympathomimetic drug which causes vasoconstriction. It is used for treating migraines and tension headaches. Isometheptene is a sympathomimetic drug which causes vasoconstriction. It is used for treating migraines and tension headaches. Isometheptene Mucate is an indirect-acting sympathomimetic. Due to its vasoconstricting properties, Isometheptene Mucate is used for the treatment of acute migraine attacks, usually in combination with other analgeics. It can also displace catecholamines from vesicles inside the neuron leading to the sympathetic responses it is known for. Isometheptene's vasoconstricting properties arise through activation of the sympathetic nervous system via epinephrine and norepinephrine (or their molecular analogues as is the case with this drug). These compounds elicites smooth muscle activation leading to vasoconstriction. These compounds interact with cell surface adrenergic receptors. Such stimuli result in a signal transduction cascade that leads to increased intracellular calcium from the sarcoplasmic reticulum through IP3 mediated calcium release, as well as enhanced calcium entry across the sarcolemma through calcium channels. The rise in intracellular calcium complexes with calmodulin, which in turn activates myosin light chain kinase. This enzyme is responsible for phosphorylating the light chain of myosin to stimulate cross bridge cycling.",The molecular weight is 141.26.,Isometheptene has a topological polar surface area of 12.03.,The log p value of  is 2.35.,Isometheptene is approved.,Isometheptene is a solid.,True
16358,"Propylhexedrine is an alpha-adrenergic agonist often used in nasal decongestant inhalers. It is used to give temporary relief for nasal congestion from colds, allergic rhinitis, or allergies. It is used to provide temporary symptomatic relief of nasal congestion due to colds, allergies and allergic rhinitis. Like other monoamine releasing stimulants propylhexedrine is active as a norepinephrine and dopamine releaser in the central nervous system. The acute effects of the drug closely resemble the physiological and psychological effects of an epinephrine-provoked fight-or-flight response, including increased heart rate and blood pressure, vasoconstriction (constriction of the arterial walls), bronchodilation, and hyperglycemia (increased blood sugar). Propylhexidrine causes the norepinephrine, dopamine, and serotonin (5HT) transporters to reverse their direction of flow. This inversion leads to a release of these transmitters from the vesicles to the cytoplasm and from the cytoplasm to the synapse. It also antagonizes the action of VMAT2, causing the release of more neurotransmitters.",The molecular weight is 155.28.,Propylhexedrine has a topological polar surface area of 12.03.,The log p value of  is 2.97.,Propylhexedrine is approved.,Propylhexedrine is a solid.,True
16359,"For temporary relief of nervousness, anxiety, mood swings, joint pains, weakness, drowsiness, itching and lethargy. Not evaluated by the FDA, homeopathic product.",,,,Serotonin is investigational and nutraceutical.,Serotonin is a solid.,True
16360,"A drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. (From Martindale, The Extra Pharmacopoeia, 30th ed, p993). Used to lower LDL and HDL cholesterol. Probucol lowers cholesterol levels by increasing LDL (low-density lipoprotein) breakdown. Additionally, probucol may inhibit cholesterol synthesis and delay cholesterol absorption. Probucol is a powerful antioxidant drug normally used to prevent vascular disease caused by the free radicals in the body. Probucol lowers serum cholesterol by increasing the fractional rate of low-density lipoprotein (LDL) catabolism in the final metabolic pathway for cholesterol elimination from the body. This drug may also act to inhibit the initial stages of cholesterol synthesis and act to inhibit the absorption of cholesterol from the diet. Recent information suggests that probucol may inhibit the oxidation and tissue deposition of LDL cholesterol, thereby inhibiting atherogenesis. It appears to inhibits ABCA1-mediated cellular lipid efflux.",The molecular weight is 516.84.,Probucol has a topological polar surface area of 40.46.,The log p value of  is 10.97.,Probucol is approved and investigational.,Probucol is a solid.,True
16361,"LX1031 is an orally-dosed drug candidate for irritable bowel syndrome and other gastrointestinal disorders. LX1031 was generated by Lexicon medicinal chemists, and its target was internally identified as a key control point for the regulation of peripheral serotonin levels. LX1031 is designed to act locally in the gastrointestinal tract by reducing the serotonin available for receptor activation, without affecting serotonin levels in the brain or its central nervous system functions. Irritable bowel syndrome (IBS) and other gastrointestinal disorders LX1031 is designed to act locally in the gastrointestinal tract by reducing the serotonin available for receptor activation, without affecting serotonin levels in the brain or its central nervous system functions.",,,,LX1031 is investigational.,LX1031 is a solid.,True
16362,"A chlorinated bisphenol antiseptic with a bacteriostatic action against Gram-positive organisms, but much less effective against Gram-negative organisms. It is mainly used in soaps and creams and is an ingredient of various preparations used for skin disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p797) For use as a surgical scrub and a bacteriostatic skin cleanser. It may also be used to control an outbreak of gram-positive infection where other infection control procedures have been unsuccessful. Hexachlorophene, a detergent cleanser, is an antibacterial sudsing emulsion for topical administration. It is a bacteriostatic cleansing agent. It cleanses the skin thoroughly and has bacteriostatic action against staphylococci and other gram-positive bacteria. Cumulative antibacterial action develops with repeated use. Cleansing with alcohol or soaps containing alcohol removes the antibacterial residue. The primary mechanism of action of hexachlorophene, based on studies with <i>Bacillus megatherium</i>, is to inhibit the membrane-bound part of the electron transport chain, respiratory D-lactate dehydrogenase. It induces leakage, causes protoplast lysis, and inhibits respiration.",The molecular weight is 406.89.,Hexachlorophene has a topological polar surface area of 40.46.,The log p value of  is 7.03.,Hexachlorophene is approved and withdrawn.,Hexachlorophene is a liquid.,True
16363,"Dienestrol is a synthetic, non-steroidal estrogen. It is an estrogen receptor agonist. Estrogens work partly by increasing a normal clear discharge from the vagina and making the vulva and urethra healthy. Using or applying an estrogen relieves or lessens: dryness and soreness in the vagina, itching, redness, or soreness of the vulva. Conditions that are treated with vaginal estrogens include a genital skin condition (vulvar atrophy), inflammation of the vagina (atrophic vaginitis), and inflammation of the urethra (atrophic urethritis). For use in the treatment of atrophic vaginitis and kraurosis vulvae. Estrogens diffuse into their target cells and interact with a protein receptor. Target cells include the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary. The combination of an estrogen with a progestin suppresses the hypothalamic-pituitary system, decreasing the secretion of gonadotropin-releasing hormone (GnRH). Dienestrol is a synthetic, non-steroidal estrogen. Estrogens passively diffuse into target cells of responsive tissues, complex with the estrogen receptors, and enter the cell's nucleus to initiate or enhance gene transcription of protein synthesis after binding to DNA.",,,,Dienestrol is approved and investigational.,Dienestrol is a solid.,True
16364,"Oxybenzone is an organic compound used in sunscreens. It is a derivative of benzophenone. It forms colorless crystals that are readily soluble in most organic solvents. It is used as an ingredient in sunscreen and other cosmetics because it absorbs UV-A ultraviolet rays. Used as an ingredient in sunscreen and other cosmetics. Oxybenzone is an organic compound used in sunscreens. It is a derivative of benzophenone. Oxybenzone absorbs UV-A ultraviolet rays, preventing them from reaching the skin.",The molecular weight is 228.25.,Oxybenzone has a topological polar surface area of 46.53.,The log p value of  is 3.59.,Oxybenzone is approved and investigational.,Oxybenzone is a solid.,True
16365,"A synthetic steroid with progestational activity. It is widely marketed throughout Europe, including Russia and many other European countries, and is also available in Japan, Hong Kong, India, Bangladesh, Indonesia, and much of Southeast Asia, though notably not in the United States or Canada. Allylestrenol was designed to be used for miscarriage prevention, prevention of premature labour and has been investigated for possible use in men for treatment for benign prostatic hyperplasia. Allylestrenol is a progestogen structurally related to progesterone that has been given in threatened and recurrent miscarriage, and to prevent premature labour. However, with the exception of proven progesterone deficiency, such use is no longer recommended. In threatened miscarriage in progesterone-deficient women a suggested dose is 5 mg three times daily by mouth for 5 to 7 days. Allylestrenol is similar in structure and function to progesterone. Progesterone shares the pharmacological actions of the progestins. Progesterone binds to the progesterone and estrogen receptors. Target cells include the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Once bound to the receptor, progestins like Progesterone will slow the frequency of release of gonadotropin releasing hormone (GnRH) from the hypothalamus and blunt the pre-ovulatory LH (luteinizing hormone) surge. In women who have adequate endogenous estrogen, progesterone transforms a proliferative endometrium into a secretory one. Progesterone is essential for the development of decidual tissue and is necessary to increase endometrial receptivity for implantation of an embryo. Once an embryo has been implanted, progesterone acts to maintain the pregnancy. Progesterone also stimulates the growth of mammary alveolar tissue and relaxes uterine smooth muscle. It has little estrogenic and androgenic activity.",The molecular weight is 300.49.,Allylestrenol has a topological polar surface area of 20.23.,The log p value of  is 6.13.,Allylestrenol is experimental.,Allylestrenol is a solid.,True
16366,Benzophenone is the organic compound. Substituted benzophenones such as oxybenzone and dioxybenzone are used in sunscreen.,,,,Benzophenone is experimental.,Benzophenone is a solid.,True
16367,,,,,Compound 19 is experimental.,Compound 19 is a solid.,False
16368,,,,,Compound 18 is experimental.,Compound 18 is a solid.,False
16369,,,,,Pyrazole is experimental.,Pyrazole is a solid.,False
16370,,,,,Naringenin is experimental.,Naringenin is a solid.,False
16371,,,,,Compound 4-D is experimental.,Compound 4-D is a solid.,False
16372,,,,,"1-Pyrazin-2-Yl)-Phenyl]-2-Phenyl-1,2,3,4-Tetrahydro-Isoquinolin-6-Ol is experimental.","1-Pyrazin-2-Yl)-Phenyl]-2-Phenyl-1,2,3,4-Tetrahydro-Isoquinolin-6-Ol is a solid.",False
16373,"Afimoxifene (4-Hydroxytamoxifen, trade name TamoGel) is a new estrogen inhibitor under investigation for a variety of estrogen-dependent conditions, including cyclic breast pain and gynecomastia. TamoGel is formulated using Enhanced Hydroalcoholic Gel (EHG) Technology. This technology enables percutaneous delivery of drugs that cannot be delivered orally. It is being developed by Ascent Therapeutics. For the potential treatment of menstrual-cycle related mastalgia, fibrocystic breast disease, breast disease, gynecomastia and Keloid scarring. Afimoxifene binds to estrogen receptors (ER), inducing a conformational change in the receptor. This results in a blockage or change in the expression of estrogen dependent genes. ",,,,Afimoxifene is investigational.,Afimoxifene is a solid.,True
16374,,,,,"2-Phenyl-1--1,2,3,4-Tetrahydro-Isoquinolin-6-Ol is experimental.","2-Phenyl-1--1,2,3,4-Tetrahydro-Isoquinolin-6-Ol is a solid.",False
16375,"A hydroxylated metabolite of estradiol or estrone that has a hydroxyl group at C3-beta, 16-alpha, and 17-beta position. Estriol is a major urinary estrogen. During pregnancy, large amount of estriol is produced by the placenta. Isomers with inversion of the hydroxyl group or groups are called epiestriol. Though estriol is used as part of the primarily North American phenomenon of bioidentical hormone replacement therapy, it is not approved for use by the FDA or Health Canada. It is however available in the United States by prescription filled only by compounding pharmacies. It has also been approved and marketed throughout Europe and Asia for approximately 40 years for the treatment of post-menopausal hot flashes. Used as a test to determine the general health of an unborn fetus. Estriol (also oestriol) is one of the three main estrogens produced by the human body. It is only produced in significant amounts during pregnancy as it is made by the placenta. In pregnant women with multiple sclerosis (MS), estriol reduces the disease's symptoms noticeably, according to researchers at UCLA's Geffen Medical School. Estriol levels can be measured to give an indication of the general health of the fetus. DHEA-S is produced by the adrenal cortex of the fetus. This is converted to estriol by the placenta. If levels of \unconjugated estriol\"" are abnormally low in a pregnant woman, this may indicate a problem with the development of the child. The drug interacts with a target cell receptor. When the estrogen receptor has bound its ligand it can enter the nucleus of the target cell, and regulate gene transcription which leads to formation of messenger RNA. The mRNA interacts with ribosomes to produce specific proteins that express the effect of estriol upon the target cell. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary.""",The molecular weight is 288.39.,Estriol has a topological polar surface area of 60.69.,The log p value of  is 3.2.,Estriol is approved and investigational and vet_approved.,Estriol is a solid.,True
16376,"The 3-cyclopentyl ether of ethinyl estradiol. Used in hormone replacement therapy, treating symptoms of menopause such as hot flashes. Also used to treat breast and prostate cancer. Quinestrol is the 3-cyclopentyl ether of ethinyl estradiol (the active metabolite). After gastrointestinal absorption, it is stored in adipose tissue where it is slowly released and metabolized principally to the parent compound, ethinyl estradiol. Ethinyl estradiol is a synthetic derivative of the natural estrogen estradiol. Estrogens diffuse into their target cells and interact with a protein receptor (the estrogen receptor). Estrogen interacts with a target cell receptor. When the estrogen receptor has bound its ligand it can enter the nucleus of the target cell, and regulate gene transcription which leads to formation of messenger RNA. The mRNA interacts with ribosomes to produce specific proteins that express the effect of estradiol upon the target cell. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary. Target cells include the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary. The combination of an estrogen with a progestin suppresses the hypothalamic-pituitary system, decreasing the secretion of gonadotropin-releasing hormone (GnRH).",The molecular weight is 364.53.,Quinestrol has a topological polar surface area of 29.46.,The log p value of  is 5.74.,Quinestrol is approved.,Quinestrol is a solid.,True
16377,Phenolphthalein was withdrawn in Canada due to concerns with carcinogenicity in 1997. Used for over a century as a laxative.,The molecular weight is 318.33.,Phenolphthalein has a topological polar surface area of 66.76.,The log p value of  is 2.58.,Phenolphthalein is approved and withdrawn.,Phenolphthalein is a solid.,True
16378,"A transdermal gel containing ethinyl estradiol and norelgestromin being investigated by Antares Pharma for use as a female contraceptive. For use as a female contraceptive. Estrogens diffuse into their target cells and interact with a protein receptor. Target cells include the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Estrogens increase the hepatic synthesis of sex hormone binding globulin (SHBG), thyroid-binding globulin (TBG), and other serum proteins and suppress follicle-stimulating hormone (FSH) from the anterior pituitary. The combination of an estrogen with a progestin suppresses the hypothalamic-pituitary system, decreasing the secretion of gonadotropin-releasing hormone (GnRH).",,,,AP1081 is investigational.,AP1081 is a solid.,True
16379,"Custirsen is a benzopyran with potential antineoplastic activity. Custirsen acts as a selective estrogen receptor modulator (SERM), inhibiting the proliferation of estrogen-sensitive breast cancer cells. This agent also inhibits growth and induces apoptosis of glioblastoma cells via a mechanism independent of estrogen receptor-related mechanisms. Custirsen is also being investigated in the treatment of primary brain tumors. Investigated for use/treatment in brain cancer and breast cancer. CC-8490, a new anti-cancer compound from Celgene's proprietary class of benzopyrans, being evaluated as a potential therapy for brain cancer. The National Cancer Institute also reports applications in breast cancer related to potential antineoplastic activity. CC-8490 acts as a selective estrogen receptor modulator (SERM), inhibiting the proliferation of estrogen-sensitive breast cancer cells. This agent also inhibits growth and induces apoptosis of glioblastoma cells via a mechanism independent of estrogen receptor-related mechanisms. CC-8490 acts as a selective estrogen receptor modulator (SERM), inhibiting the proliferation of estrogen-sensitive breast cancer cells. This agent also inhibits growth and induces apoptosis of glioblastoma cells via a mechanism independent of estrogen receptor-related mechanisms.",,,,Custirsen is investigational.,Custirsen is a solid.,True
16380,"NP-50301 is an ophthalmic therapeutic eye drop treating post-menopausal Dry Eye Syndrome (DES). It is being developed by Nascent Pharmaceuticals. It is estimated that about 30% of postmenopausal women suffer symptoms of DES, which accounts for over 12 million women in the U.S. The majority of sufferers of DES are postmenopausal women; and clinical research around the world has suggested the benefits of both topical and systemic estrogen therapy in the treatment of DES in this population. Investigated for use/treatment in eye disorders/infections. Trial results indicate that NP50301 therapy provides a benefit in relieving the signs and symptoms presented by DES in postmenopausal women. Importantly, there were no drug-related serious adverse events in the study. NP50301 is an estrogen ester compound believed to act by multiple mechanisms, including influencing the health of the cornea, the meibomian glands and the conjunctiva.",,,,NP-50301 is investigational.,NP-50301 is a solid.,True
16381,"CHF 4227 is a new selective estrogen receptor modulator (SERM). The compound has a high receptor affinity and has shown promising efficacy in the prevention of bone loss in animal models of osteoporosis. Additionally, the compound has shown no uterotrophic activity suggesting a potential therapeutic advantage over drugs normally used in postmenopausal therapy. Investigated for use/treatment in osteoporosis. CHF 4227 binds with high affinity to the human estrogen receptor-alpha and beta. It compares favorably in efficacy and potency with raloxifene in preventing bone loss and in antagonizing EE2 stimulation of the uterus. This attribute along with the minimal uterine stimulation suggests a therapeutic advantage to CHF 4227 over EE2 or raloxifene for the treatment of postmenopausal women.",,,,CHF 4227 is investigational.,CHF 4227 is a solid.,True
16382,"Investigated for use/treatment in breast cancer. TAS-108 binds to and inhibits estrogenic receptor alpha (ERa), mainly expressed in the mammary gland and uterus and upregulated in estrogen-dependent tumors. Blockage of ERa by TAS-108 prevents the binding and effects of estrogen and may lead to an inhibition of estrogen-dependent cancer cell proliferation. TAS-108 also is a partial agonist of the estrogenic receptor beta (ERb), expressed in many tissues including the central nervous system, urogenital tract, bone and cardiovascular system, thereby exerting a positive effect on these tissues. In addition, TAS-108 activates the co-repressor Silencing Mediator for Retinoid and Thyroid hormone receptor (SMRT), a protein that inhibits the activities of the estrogen receptors, which may contribute to the antitumor activity of TAS-108.",,,,TAS-108 is investigational.,TAS-108 is a solid.,True
16383,"Investigated for use/treatment in breast cancer, osteoporosis, and endometrial cancer. Arzoxifene is a selective estrogen receptor modulator (SERM) ",,,,Arzoxifene is approved and investigational.,Arzoxifene is a solid.,True
16384,"Investigated for use/treatment in menopause and female hormonal deficiencies/abnormalities. RAD1901 is a novel selective estrogen receptor modulator(SERM). SERMs are small molecules that bind to and selectively modulate estrogen receptors. These molecules have the ability to stimulate or block estrogen's activity in different types of tissue, functioning as estrogen receptor agonists in some tissues and as estrogen receptor antagonists in others.",,,,Elacestrant is investigational.,Elacestrant is a solid.,True
16385,,,,,17-METHYL-17-ALPHA-DIHYDROEQUILENIN is experimental.,17-METHYL-17-ALPHA-DIHYDROEQUILENIN is a solid.,False
16386,,,,,4-(2-amino-1-methyl-1H-imidazopyridin-6-yl)phenol is experimental.,4-(2-amino-1-methyl-1H-imidazopyridin-6-yl)phenol is a solid.,False
16387,,,,,ACETONITRILE is experimental.,ACETONITRILE is a solid.,False
16388,,,,,4-NON-7-EN-2-YL]PHENOL is experimental.,4-NON-7-EN-2-YL]PHENOL is a solid.,False
16389,,,,,4-NON-7-EN-2-YL]PHENOL is experimental.,4-NON-7-EN-2-YL]PHENOL is a solid.,False
16390,,,,,4-NON-7-EN-2-YL]PHENOL is experimental.,4-NON-7-EN-2-YL]PHENOL is a solid.,False
16391,,,,,"(2R,3R,4S)-3-(4-HYDROXYPHENYL)-4-METHYL-2-CHROMAN-6-OL is experimental.","(2R,3R,4S)-3-(4-HYDROXYPHENYL)-4-METHYL-2-CHROMAN-6-OL is a solid.",False
16392,,,,,"(3AS,4R,9BR)-2,2-DIFLUORO-4-(4-HYDROXYPHENYL)-1,2,3,3A,4,9B-HEXAHYDROCYCLOPENTACHROMEN-8-OL is experimental.","(3AS,4R,9BR)-2,2-DIFLUORO-4-(4-HYDROXYPHENYL)-1,2,3,3A,4,9B-HEXAHYDROCYCLOPENTACHROMEN-8-OL is a solid.",False
16393,,,,,"(9ALPHA,13BETA,17BETA)-2-ESTRA-1,3,5(10)-TRIENE-3,17-DIOL is experimental.","(9ALPHA,13BETA,17BETA)-2-ESTRA-1,3,5(10)-TRIENE-3,17-DIOL is a solid.",False
16394,,,,,"(9BETA,11ALPHA,13ALPHA,14BETA,17ALPHA)-11-(METHOXYMETHYL)ESTRA-1(10),2,4-TRIENE-3,17-DIOL is experimental.","(9BETA,11ALPHA,13ALPHA,14BETA,17ALPHA)-11-(METHOXYMETHYL)ESTRA-1(10),2,4-TRIENE-3,17-DIOL is a solid.",False
16395,,,,,3-CHLORO-2-(4-HYDROXYPHENYL)-2H-INDAZOL-5-OL is experimental.,3-CHLORO-2-(4-HYDROXYPHENYL)-2H-INDAZOL-5-OL is a solid.,False
16396,,,,,3-ETHYL-2-(4-HYDROXYPHENYL)-2H-INDAZOL-5-OL is experimental.,3-ETHYL-2-(4-HYDROXYPHENYL)-2H-INDAZOL-5-OL is a solid.,False
16397,A synthetic estrogen that has been used as a hormonal antineoplastic agent.,The molecular weight is 270.37.,Hexestrol has a topological polar surface area of 40.46.,The log p value of  is 5.11.,Hexestrol is withdrawn.,Hexestrol is a solid.,True
16398,,,,,"dimethyl (1R,4S)-5,6-bis(4-hydroxyphenyl)-7-oxabicyclohepta-2,5-diene-2,3-dicarboxylate is experimental.","dimethyl (1R,4S)-5,6-bis(4-hydroxyphenyl)-7-oxabicyclohepta-2,5-diene-2,3-dicarboxylate is a solid.",False
16399,Erteberel is an estrogen receptor beta agonist that has been used in trials studying the treatment of Benign Prostatic Hyperplasia.,,,,Erteberel is experimental and investigational.,Erteberel is a solid.,True
16400,,,,,N--2-(2-PHENYL-1H-INDOL-3-YL)ACETAMIDE is experimental.,N--2-(2-PHENYL-1H-INDOL-3-YL)ACETAMIDE is a solid.,False
16401,,,,,"(3AS,4R,9BR)-4-(4-HYDROXYPHENYL)-6-(METHOXYMETHYL)-1,2,3,3A,4,9B-HEXAHYDROCYCLOPENTACHROMEN-8-OL is experimental.","(3AS,4R,9BR)-4-(4-HYDROXYPHENYL)-6-(METHOXYMETHYL)-1,2,3,3A,4,9B-HEXAHYDROCYCLOPENTACHROMEN-8-OL is a solid.",False
16402,,,,,"4-benzene-1,3-diol is experimental.","4-benzene-1,3-diol is a solid.",False
16403,,,,,"4-(6-HYDROXY-1H-INDAZOL-3-YL)BENZENE-1,3-DIOL is experimental.","4-(6-HYDROXY-1H-INDAZOL-3-YL)BENZENE-1,3-DIOL is a solid.",False
16404,,,,,"DIETHYL (1R,2S,3R,4S)-5,6-BIS(4-HYDROXYPHENYL)-7-OXABICYCLOHEPT-5-ENE-2,3-DICARBOXYLATE is experimental.","DIETHYL (1R,2S,3R,4S)-5,6-BIS(4-HYDROXYPHENYL)-7-OXABICYCLOHEPT-5-ENE-2,3-DICARBOXYLATE is a solid.",False
16405,"PhIP (2-Amino-1-methyl-6-phenylimidazo(4,5-b)pyridine) has been used in trials studying the basic science of Pancreas Cancer.",,,,"2-Amino-1-methyl-6-phenylimidazo(4,5-b)pyridine is investigational.","2-Amino-1-methyl-6-phenylimidazo(4,5-b)pyridine is a solid.",True
16406,,,,,4-NON-7-EN-2-YL]PHENOL is experimental.,4-NON-7-EN-2-YL]PHENOL is a solid.,False
16407,,,,,"(3AS,4R,9BR)-4-(4-HYDROXYPHENYL)-1,2,3,3A,4,9B-HEXAHYDROCYCLOPENTACHROMEN-9-OL is experimental.","(3AS,4R,9BR)-4-(4-HYDROXYPHENYL)-1,2,3,3A,4,9B-HEXAHYDROCYCLOPENTACHROMEN-9-OL is a solid.",False
16408,,,,,2-(4-hydroxyphenyl)benzothiophen-6-ol is experimental.,2-(4-hydroxyphenyl)benzothiophen-6-ol is a solid.,False
16409,"Eugenol is a naturally occurring phenolic molecule found in several plants such as cinnamon, clove, and bay leaves. It has been used as a topical antiseptic as a counter-irritant and in dental preparations with zinc oxide for root canal sealing and pain control. Although not currently available in any FDA-approved products (including OTC), eugenol has been found to have anti-inflammatory, neuroprotective, antipyretic, antioxidant, antifungal and analgesic properties. Its exact mechanism of action is unknown, however, it has been shown to interfere with action potential conduction.  Eugenol is not currently available in any FDA-approved drug products. There are a number of unapproved OTC products that advertise it for the use of toothache. Eugenol is is also commonly used in combination with zinc oxide in dental procedures for the cementation of temporary prostheses and the temporary restoration of teeth and cavities. The exact mechanism of action of eugenol is unknown. However, eugenol has been shown to interrupt action potentials, which may be involved in its anti-pain activity. Research has also shown eugenol to have anti-inflammatory, neuroprotective, antipyretic, antioxidant, antifungal and analgesic properties.",The molecular weight is 164.2.,Eugenol has a topological polar surface area of 29.46.,The log p value of  is 2.4.,Eugenol is approved.,Eugenol is a solid.,True
16410,Polymeric phosphoric acid ester of estradiol.,,,,Polyestradiol phosphate is approved.,,True
16411,"Octocrylene is an organic compound used as an ingredient in sunscreens and cosmetics. In the US, Octocrylene has been evaluated by the FDA and is considered safe for use up to 10% in the formula. Similarly, the EU allows its use up to 10% in a formula while Health Canada allows a maximum use level of 12%.  Octocrylene is an effective oil soluble liquid UV‐B filter. It has excellent dissolving properties for crystalline UV filters. Due to its outstanding photostability it is used as photostabilizer. Conjugated acrylate portion absorbs UVB and short-wave UVA (ultraviolet) rays with wavelengths in the range of 280-320 nm which protects the skin from direct DNA damage. The ethylhexanol portion is a fatty alcohol, which functions as an emollient due to it's hydrophobicity.",The molecular weight is 361.48.,Octocrylene has a topological polar surface area of 50.09.,The log p value of  is 6.8.,Octocrylene is approved and investigational.,,True
16412,"Homosalate is an organic compound that belongs to salicylates. It is an ester formed from salicylic acid and 3,3,5-trimethylcyclohexanol, a derivative of cyclohexanol. Salicylates prevent direct skin exposure to the sun’s harmful rays by absorbing ultraviolet (UV) light. Homosalate specifically absorbs short-wave UVB rays, which are associated with DNA damage and increased risk of skin cancer.  As ingredient in many sunscreen for protection against sunburn, skin aging and skin cancer.  Acts as UV filters.  Homosalate has the ability to convert incident ultraviolet radiation into less damaging infrared radiation (heat). ",The molecular weight is 262.35.,Homosalate has a topological polar surface area of 46.53.,The log p value of  is 5.92.,Homosalate is approved and investigational.,,True
16413,"Commonly known as 4-methylbenzylidene-camphor (4-MBC), enzacamene is a camphor derivative and an organic chemical UV-B filter. It is used in cosmetic products such as sunscreen to provide skin protection against UV rays. While its effects on the human reproductive system as an endocrine disruptor are being investigated, its use in over-the-counter and cosmetic products is approved by Health Canada. Its tradenames include Eusolex 6300 (Merck) and Parsol 5000 (DSM). Indicated for use as an active sunscreen agent.  Several studies suggest that enzacamene elicit estrogen-like effects. In prepubertal male rats exposed to enzacamene during embryonic and fetal development, decrease in testicular weight with decreased levels of LH, GnRH, and glutamate were observed; in comparison, there was an increase in LH, GnRH, and aspartate levels in peripubertal rats. These findings suggest that high concentrations of enzacamene during embryonic and fetal stage inhibits the testicular axis in male rats during the prepubertal stage and stimulates it during peripubertad stage. In a study of zebrafish (Danio rerio) embryo, exposure to enzacamene during early vertebrate development was associated with muscular and neuronal defects that may result in developmental defects, including a reduction in AChE activity, disorganized pattern of slow muscle fibers, and axon pathfinding errors during motor neuron innervation. Enzacamene displays a weak binding activity in receptors binding assays using the mammalian estrogen receptor (ER).  Enzacamene absorbs UV-B rays. It is proposed that enzacamene exerts estrogen-like activities in the same direction as endogenous estrogens via nonclassical estrogen signaling mechanisms that do not involve gene regulation by the nuclear ER. It binds to cytosolic estradiol binding sites of estrogen receptors with low to moderate affinity compared to that of the endogenous agonist. Based on the findings of a study with _Xenopus_ hepatocytes in culture, enzacamene has a potential to induce the ER gene only at higher concentrations (10–100 μmol/L). While enzacamene was not shown to activate estrogen-dependent gene transcription when tested in an ER reporter gene assay in yeast cells, it was demonstrated in _Xenopus_ hepatocytes cultures that activate ER-dependent signaling mechanisms leading to altered gene expression. In micromolar concentrations, enzacamene accelerates cell proliferation rate in MCF-7 human breast cancer cells. ",The molecular weight is 254.37.,Enzacamene has a topological polar surface area of 17.07.,The log p value of  is 5.02.,Enzacamene is approved.,Enzacamene is a solid.,True
16414,"Zeranol is a non-steroidal estrogen agonist. It is a mycotoxin, derived from fungi in the Fusarium family, and may be found as a contaminant in fungus-infected crops. It is 3-4x more potent as an estrogen agonist than the related compound zearalenone.",The molecular weight is 322.4.,Zeranol has a topological polar surface area of 86.99.,The log p value of  is 4.37.,Zeranol is experimental and vet_approved.,,True
16415,,,,,Ractopamine is vet_approved.,,False
16416,Propyl Gallate is under investigation in clinical trial NCT01450098 (A Study of LY2484595 in Healthy Subjects).,,,,Propyl Gallate is investigational.,,True
16417,TIMBD is an azaresveratrol analog.,,,,2-Methoxy-6-{(E)-methyl}phenol is experimental.,2-Methoxy-6-{(E)-methyl}phenol is a solid.,True
16418,,,,,Estriol tripropionate is experimental.,,False
16419,"Amlexanox is an antiallergic drug, clinically effective for atopic diseases, especially allergic asthma and rhinitis. Amlexanox as a topical paste is a well tolerated treatment of recurrent aphthous ulcers. Recurrent aphthous ulcer (RAU) is the most prevalent oral mucosal disease in humans, estimated to affect between 5% and 50% of the general population. Used as a paste in the mouth to treat aphthous ulcers (canker sores).  Amlexanox is a mucoadhesive oral paste which has been clinically proven to abort the onset, accelerate healing and resolve the pain of aphthous ulcers (canker sores). It decreases the time ulcers take to heal. Because amlexanox decreases the healing time, it also decreases the pain you feel. Recent studies have also shown that the majority of ulcers can be prevented by application of the paste during the prodromal (pre-ulcerative) phase of the disease. Recurrent Aphthous Ulcers (RAU) also known as Recurrent Aphthous Stomatitis (RAS) is recognized as the most common oral mucosal disease known to man. Estimates suggest that 20% - 25% of the general population suffer at least one incidence of aphthous ulcers each year. Amlexanox is also being investigated for its anti-allergenic and anti-inflammatory properties. As a benzopyrano-bipyridine carboxylic acid derivative, amlexanox has anti-inflammatory and antiallergic properties. It inhibits chemical mediatory release of the slow-reacting substance of anaphylaxis (SRS-A) and may have antagonistic effects on interleukin-3. When cells are under stress, they release an inactive form of human fibroblast growth factor 1 (FGF-1), a potent mitogen (entity that causes mitosis). Amlexanox binds to FGF1, increasing its conformational stability, sterically blocking Cu(2+) induced oxidation which normally leads to activation of FGF-1. ",The molecular weight is 298.3.,Amlexanox has a topological polar surface area of 102.51.,The log p value of  is 3.07.,Amlexanox is approved and investigational and withdrawn.,Amlexanox is a solid.,True
16420,"Epitestosterone is the 17-alpha isomer of testosterone, derived from pregnenolone via the delta5-steroid pathway, and via 5-androstene-3-beta,17-alpha-diol. Epitestosterone acts as an antiandrogen in various target tissues. The ratio between testosterone/epitestosterone is used to monitor anabolic drug abuse.",,,,Epitestosterone is experimental.,Epitestosterone is a solid.,True
16421,"Fludiazepam is a drug which is a benzodiazepine derivative. It possesses anxiolytic, anticonvulsant, sedative and skeletal muscle relaxant properties. It is a scheduled drug in the U.S., but is approved for use in Japan. Used for the short-term treatment of anxiety disorders. Fludiazepam is a benzodiazepine derivative. It possesses anxiolytic, anticonvulsant, sedative and skeletal muscle relaxant properties. Fludiazepam accumulates primarily in the cortex and thalamus.  Fludiazepam has similar action to diazepam, but binds with four times more affinity to benzodiazepine receptors than diazepam. ",The molecular weight is 302.73.,Fludiazepam has a topological polar surface area of 32.67.,The log p value of  is 2.75.,Fludiazepam is experimental and illicit.,Fludiazepam is a solid.,True
16422,,,,,4-Carboxycinnamic Acid is experimental.,4-Carboxycinnamic Acid is a solid.,False
16423,,,,,2-pyridine is experimental.,2-pyridine is a solid.,False
16424,,,,,4-pyridine is experimental.,4-pyridine is a solid.,False
16425,,,,,Sebacic acid is experimental.,Sebacic acid is a solid.,False
16426,,,,,2-CARBONYL}AMINO)PHENOXY]-2-METHYLPROPANOIC ACID is experimental.,2-CARBONYL}AMINO)PHENOXY]-2-METHYLPROPANOIC ACID is a solid.,False
16427,"2,6-dicarboxynaphthalene is a solid. This compound belongs to the naphthalenecarboxylic acids. These are compounds containing a napthalene moiety with a ring carbon which bears a carboxylic acid group. This drug targets the proteins hemoglobin subunit alpha and hemoglobin subunit beta.",,,,"2,6-dicarboxynaphthalene is experimental.","2,6-dicarboxynaphthalene is a solid.",True
16428,,The molecular weight is 341.41.,Efaproxiral has a topological polar surface area of 75.63.,The log p value of  is 3.52.,Efaproxiral is investigational.,Efaproxiral is a solid.,False
16429,,,,,Trimesic acid is experimental.,Trimesic acid is a solid.,False
16430,"Nitrous acid (as sodium nitrite) is used as part of an intravenous mixture with sodium thiosulfate to treat cyanide poisoning. It is on the World Health Organization's List of Essential Medicines, a list of the most important medications needed in a basic health system. There is also research to investigate its applicability towards treatments for heart attacks, brain aneurysms, pulmonary hypertension in infants, and Pseudomonas aeruginosa infections. For sequential use with sodium thiosulfate for the treatment of acute cyanide poisoning that is judged to be life-threatening. Sodium nitrite reverses cyanide toxicity and produces blood vessel dilation. Cyanide has a high affinity for the oxidized form of iron (Fe3+) such as that found in cytochrome oxidase a3. Cyanide binds to and inhibits cytochrome oxidase a3, preventing oxidative phophorylation from occuring. The resultant lack of ATP cannot support normal cellular processes, particularly in the brain. Compensatory increases in anaerobic respiration result in rising levels of lactic acid and subsequent acidosis. ",,,,Nitrous acid is approved and investigational.,Nitrous acid is a solid.,True
16431,"Iron deficiency is an extremely common condition and is the most frequent cause of anemia worldwide. Iron deficiency results when iron intake, iron stores, and loss of iron from the body do not adequately support production of erythrocytes, also known as red blood cells. Though it is generally considered non life-threatening, iron deficiency may considerably affect quality of life. This drug is indicated for the treatment of iron deficiency anemia in adult patients who have experienced intolerance to oral iron preparations or insufficient clinical response to orally administered iron. Ferric derisomaltase is also indicated for patients with non-hemodialysis dependent chronic kidney disease. In Australia and United Kingdom, ferric derisomaltase is indicated for cases in which rapid delivery of iron is required. Ferric derisomaltase increases the reticulocyte count and ultimately increases hemoglobin, treating iron deficiency anemia and its various symptoms. Parenteral iron, such as ferric derisomaltose, may cause false elevations in serum bilirubin levels and falsely reduced serum calcium. This drug is a complex made of iron (III) hydroxide and derisomaltose, which is an iron carbohydrate oligosaccharide that works to releases iron. The released iron then binds to the transport protein, transferrin, and is taken to erythroid precursor cells for incorporation into the hemoglobin molecule.",,,,Ferric derisomaltose is approved.,Ferric derisomaltose is a solid.,True
16432,"Formebolone, a derivative of androstane, is an anabolic androgenic steroid. It is on the list of substances prohibited by the Word Anti-Doping Agency, and is regularly screened for in athletes. It is also classified by the US Drug Enforcement Administration as Schedule III drug in the Controlled Substances Act. It has been used experimentally in the treatment of growth retardation, and has been noted to increase bone mass. Additionally, it has been patented for use in development of novel transdermal delivery systems for enhanced drug delivery. No approved indications. Studied experimentally as a treatment for non-pituitary growth retardation.",The molecular weight is 344.45.,Formebolone has a topological polar surface area of 74.6.,The log p value of  is 2.06.,Formebolone is experimental and illicit.,Formebolone is a solid.,True
16433,"C18 steroid with androgenic and anabolic properties. It is generally prepared from alkyl ethers of estradiol to resemble testosterone but less one carbon at the 19 position. It is a schedule III drug in the U.S. For the treatment of refractory deficient red cell production anemias, breast carcinoma, hereditary angioedema, antithrombin III deficiency, fibrinogen excess, growth failure and Turner's syndrome. It is also indicated in the prophylaxis of hereditary angioedema. Nandrolone is an anabolic steroid occurring naturally in the human body, albeit in small quantities. Nandrolone increases production and urinary excretion of erythropoietin. It may also have a direct action on bone marrow. Nandrolone binds to the androgen receptor to a greater degree than testosterone, but due to its inability to act on the muscle in ways unmediated by the receptor, has less overall effect on muscle growth. Nandrolone is an androgen receptor agonist. The drug bound to the receptor complexes which allows it to enter the nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects.",The molecular weight is 406.57.,Nandrolone phenpropionate has a topological polar surface area of 43.37.,The log p value of  is 5.93.,Nandrolone phenpropionate is approved and illicit and investigational.,Nandrolone phenpropionate is a solid.,True
16434,"Acetophenazine is an antipsychotic drug of moderate-potency. It is used in the treatment of disorganized and psychotic thinking. It is also used to help treat false perceptions (e.g. hallucinations or delusions). It primarily targets the dopamine D2 receptor. For the treatment of disorganized and psychotic thinking. Also used to help treat false perceptions (e.g. hallucinations or delusions.) Acetophenzine is a phenothiazine antipsychotic intended for the management of schizophrenia and other psychotic disorders. Acetophenazine blocks postsynaptic mesolimbic dopaminergic D1 and D2 receptors in the brain; depresses the release of hypothalamic and hypophyseal hormones and is believed to depress the reticular activating system thus affecting basal metabolism, body temperature, wakefulness, vasomotor tone, and emesis.",The molecular weight is 411.56.,Acetophenazine has a topological polar surface area of 47.02.,The log p value of  is 2.91.,Acetophenazine is approved.,Acetophenazine is a solid.,True
16435,"1-Testosterone is an anabolic steroid that differs from testosterone by having a 1,2-double bond instead of 4,5-double bond in its A ring. Delta1-dihydrotestosterone binds to the androgen receptor, a nuclear receptor which binds the androgenic hormones testosterone and dihydrotestosterone. Once bound, the receptor/ligand complex localizes to the nucleus and acts as a DNA binding transcription factor, regulating gene expression. In animals, Delta1-dihydrotestosterone stimulates the growth of the prostate as well as the seminal vesicles.  Delta1-dihydrotestosterone binds to the androgen receptor, a nuclear receptor which binds the androgenic hormones testosterone and dihydrotestosterone. Once bound, the receptor/ligand complex localizes to the nucleus and acts as a DNA binding transcription factor, regulating gene expression. ",,,,1-Testosterone is experimental and illicit and investigational.,1-Testosterone is a solid.,True
16436,"Boldenone is an anabolic steroid developed for veterinary use, mostly for treatment of horses. It is not indicated for use in humans in the US and is only available through veterinary clinics. Boldenone has primarily anabolic activity with low androgenic potency. The drug is commonly used in doping within bodybuilding, even though this use is illegal. If intended to assist in bodybuilding, the drug is taken as part of a steroid stack of other anabolic steroids, usually with a potent androgen like testosterone as the 'base' of the stack. Boldenone is an androgen that differs from 17b-testosterone (17b-T) by only one double bond at the 1-position, and the removal of the methyl group protecting the 17-OH group allows it to be orally active. Boldenone is a steroid hormone which has androgenic activity. Androgens bind to the androgen receptor, which regulates gene transcription. ",,,,Boldenone is illicit and vet_approved.,Boldenone is a solid.,True
16437,"A 17-alkylated orally active androgenic steroid. A Schedule IV drug in Canada. An anabolic steroid which can theoretically aid in restauration and buildup of certain tissues, especially muscle. It is similar to synthetic testosterone and is still in early investigation. It was also investigated for use as a treatment for metastatic breast cancer. Calusterone is a 17-alkylated orally active androgenic steroid. Calusterone may alter the metabolism of estradiol and reduce estrogen production. Calusterone has been investigated for possible antitumor properties. The effects of calusterone in humans most likely occur by way of two main mechanisms: by activation of the androgen receptor, and by conversion to estradiol and activation of certain estrogen receptors.",The molecular weight is 316.48.,Calusterone has a topological polar surface area of 37.3.,The log p value of  is 4.25.,Calusterone is experimental and illicit.,Calusterone is a solid.,True
16438,,,,,(R)-Bicalutamide is experimental.,(R)-Bicalutamide is a solid.,False
16439,A synthetic non-aromatizable androgen and anabolic steroid. It binds strongly to the androgen receptor and has therefore also been used as an affinity label for this receptor in the prostate and in prostatic tumors.,,,,Metribolone is experimental.,Metribolone is a solid.,True
16440,,,,,"(3AALPHA,4ALPHA,7ALPHA,7AALPHA)- 3A,4,7,7A-TETRAHYDRO-2-(4-NITRO-1-NAPHTHALENYL)-4,7-ETHANO-1H-ISOINDOLE-1,3(2H)-DIONE is experimental.","(3AALPHA,4ALPHA,7ALPHA,7AALPHA)- 3A,4,7,7A-TETRAHYDRO-2-(4-NITRO-1-NAPHTHALENYL)-4,7-ETHANO-1H-ISOINDOLE-1,3(2H)-DIONE is a solid.",False
16441,"LGD2941 is a non-steroidal, selective androgen receptor modulator (SARM) developed jointly by Ligand and TAP. For the treatment and prevention of osteoporosis. LGD2941 is a non-steroidal, selective androgen receptor modulator (SARM). SARMs are a novel class of non-steroidal, orally active molecules that selectively modulate the activity of the androgen receptor (AR) in different tissues, providing a wide range of opportunities for the treatment of many diseases and disorders with large patient populations in both men and women. Tissue-selective AR agonists or antagonists may provide utility in male hormone therapy and the treatment of patients with male hypogonadism, female and male osteoporosis, male and female sexual dysfunction, frailty, prostate cancer, hirsutism, acne, androgenetic alopecia and other diseases. LGD2941 selectively modulates the activity of the androgen receptor (AR) in different tissues.",,,,LGD2941 is investigational.,LGD2941 is a solid.,True
16442,Dimethylcurcumin is a synthetic chemical compound that is loosely based on a compound found in curcumin. It is a novel anti-androgen that enhances androgen receptor degradation. Investigated for use/treatment in acne and alopecia.,,,,Dimethylcurcumin is investigational.,Dimethylcurcumin is a solid.,True
16443,"Stanozolol is a synthetic anabolic steroid with therapeutic uses in treating hereditary angioedema. Stanozolol is derived from testosterone, and has been abused by several high profile professional athletes. Stanozolol is a synthetic anabolic steroid with therapeutic uses in treating C1-inhibitor deficient hereditary angioedema. C1-inhibitor is a protease that inhibits the complement system (part of the innate immune system), a biochemical chain of reactions which assists the body in removing pathogens from the body. Stanozolol may help control attacks of hereditary angioedema. Stanozolol can be administered orally or intramuscularly.  Stanozolol is a synthetic anabolic-androgenic steroid (AAS), which promotes cell growth (anabolism) and development/maintenance of masculine characteristics (androgenism).  Stanozolol binds to androgen receptors, such as membrane bound receptor proteins LAGS and stanozolol-binding protein (STBP). ",The molecular weight is 328.5.,Stanozolol has a topological polar surface area of 48.91.,The log p value of  is 4.56.,Stanozolol is approved and vet_approved.,Stanozolol is a solid.,True
16444,,,,,Tetrahydrogestrinone is experimental.,Tetrahydrogestrinone is a solid.,False
16445,,,,,(2S)-N-(4-cyano-3-iodophenyl)-3-(4-cyanophenoxy)-2-hydroxy-2-methylpropanamide is experimental.,(2S)-N-(4-cyano-3-iodophenyl)-3-(4-cyanophenoxy)-2-hydroxy-2-methylpropanamide is a solid.,False
16446,"BMS-564929 is an investigational therapeutic agent built to be a selective androgen receptor modulator (SARM). So far, it has been developed by Bristol-Myers Squibb for the symptomatic treatment of andropause.",,,,BMS-564929 is experimental.,BMS-564929 is a solid.,True
16447,An androgen receptor modulator.,,,,S-23 is experimental.,S-23 is a solid.,True
16448,,,,,4-{amino}-2-(trifluoromethyl)benzonitrile is experimental.,4-{amino}-2-(trifluoromethyl)benzonitrile is a solid.,False
16449,,,,,(2S)-2-hydroxy-2-methyl-N--3-(pentafluorophenoxy)propanamide is experimental.,(2S)-2-hydroxy-2-methyl-N--3-(pentafluorophenoxy)propanamide is a solid.,False
16450,Andarine is a non-steroidal selective androgen receptor modulator.,,,,Andarine is experimental.,Andarine is a solid.,True
16451,,,,,(R)-3-BROMO-2-HYDROXY-2-METHYL-N-PROPANAMIDE is experimental.,(R)-3-BROMO-2-HYDROXY-2-METHYL-N-PROPANAMIDE is a solid.,False
16452,,,,,"(5S,8R,9S,10S,13R,14S,17S)-13-{2-ETHYL}-17-HYDROXY-10-METHYLHEXADECAHYDRO-3H-CYCLOPENTAPHENANTHREN-3-ONE is experimental.","(5S,8R,9S,10S,13R,14S,17S)-13-{2-ETHYL}-17-HYDROXY-10-METHYLHEXADECAHYDRO-3H-CYCLOPENTAPHENANTHREN-3-ONE is a solid.",False
16453,,,,,S-3-(4-FLUOROPHENOXY)-2-HYDROXY-2-METHYL-N-PROPANAMIDE is experimental.,S-3-(4-FLUOROPHENOXY)-2-HYDROXY-2-METHYL-N-PROPANAMIDE is a solid.,False
16454,,,,,"1-TERT-BUTYL-3-(2,5-DIMETHYLBENZYL)-1H-PYRAZOLOPYRIMIDIN-4-AMINE is experimental.","1-TERT-BUTYL-3-(2,5-DIMETHYLBENZYL)-1H-PYRAZOLOPYRIMIDIN-4-AMINE is a solid.",False
16455,,,,,4-IMIDAZOL-2(3H)-YL]-1-NAPHTHONITRILE is experimental.,4-IMIDAZOL-2(3H)-YL]-1-NAPHTHONITRILE is a solid.,False
16456,,,,,2-chloro-4-{oxazol-3-ylidene]amino}-3-methylbenzonitrile is experimental.,2-chloro-4-{oxazol-3-ylidene]amino}-3-methylbenzonitrile is a solid.,False
16457,An androgen receptor modulator.,,,,LGD-2226 is experimental.,LGD-2226 is a solid.,True
16458,,,,,3-PYRIMIDIN-3-YL)METHYL]PHENOL is experimental.,3-PYRIMIDIN-3-YL)METHYL]PHENOL is a solid.,False
16459,"An aromatic ether that is phenol which is substituted at C-5 by a chloro group and at C-2 by a 2,4-dichlorophenoxy group. It is widely used as a preservative and antimicrobial agent in personal care products such as soaps, skin creams, toothpaste and deodorants as well as in household items such as plastic chopping boards, sports equipment and shoes. Triclosan is used in a variety of common household products, including soaps, mouthwashes, dish detergents, toothpastes, deodorants, and hand sanitizers. It is also used in health care settings in surgical scrubs and personnel hand washes. Triclosan is a biocidal compound with multiple targets in the cytoplasm and membrane. At lower concentrations, however, triclosan appears bacteriostatic and is seen to target bacteria mainly by inhibiting fatty acid synthesis. Triclosan binds to enoyl-acyl carrier protein reductase enzyme (ENR). This complex has increased affinity for NAD+ and forms a ternary complex. This complex is unable to participate in fatty acid synthesis, weakening the cell membrane and causing cell death. Humans do not have an ENR enzyme, and thus are not affected.",The molecular weight is 289.54.,Triclosan has a topological polar surface area of 29.46.,The log p value of  is 5.53.,Triclosan is approved and investigational.,Triclosan is a solid.,True
16460,Mibolerone is a potent anabolic steroid which is both higher affinity and more selective for the androgen receptor than metribolone.,,,,Mibolerone is vet_approved.,,True
16461,Phenothiazine (PTZ) is an organic thiazine compound.,,,,Phenothiazine is experimental and vet_approved.,,True
16462,Ligandrol is an investigational selective androgen receptor modulator (SARM) for treatment of conditions such as muscle wasting and osteoporosis.,,,,Ligandrol is investigational.,Ligandrol is a solid.,True
16463,"The activity of boldenone is mainly anabolic, with a low androgenic potency. The drug is commonly used in doping within bodybuilding, even though this use is illegal. If intended to assist in bodybuilding, the drug is taken as part of a steroid stack of other anabolic steroids, usually with a potent androgen like testosterone as the 'base' of the stack. Boldenone is an androgen that differs from 17b-testosterone (17b-T) by only one double bond at the 1-position, and the removal of the methyl group protecting the 17-OH group allows it to be orally active. Boldenone is a steroid hormone which has androgenic activity. Androgens bind to the androgen receptor, which regulates gene transcription. ",,,,Boldenone undecylenate is illicit and vet_approved.,,True
16464,"Ketodarolutamide, a nonsteroidal antiandrogen (NSAA), is the major active metabolite of.",,,,Ketodarolutamide is experimental.,Ketodarolutamide is a solid.,True
16465,"A strong organic base existing primarily as guanidium ions at physiological pH. It is found in the urine as a normal product of protein metabolism. It is also used in laboratory research as a protein denaturant. (From Martindale, the Extra Pharmacopoeia, 30th ed and Merck Index, 12th ed) It is also used in the treatment of myasthenia and as a fluorescent probe in HPLC. For the reduction of the symptoms of muscle weakness and easy fatigability associated with the myasthenic syndrome of Eaton-Lambert. It is not indicated for treating myasthenia gravis. Guanidine apparently acts by enhancing the release of acetylcholine following a nerve impulse. It also appears to slow the rates of depolarization and repolarization of muscle cell membranes.",The molecular weight is 59.07.,Guanidine has a topological polar surface area of 75.89.,The log p value of  is -2.39.,Guanidine is approved.,Guanidine is a solid.,True
16466,,,,,Daidzin is experimental.,Daidzin is a solid.,False
16467,,,,,Crotonaldehyde is experimental.,Crotonaldehyde is a solid.,False
16468,"Goserelin is a synthetic hormone. In men, it stops the production of the hormone testosterone, which may stimulate the growth of cancer cells. In women, goserelin decreases the production of the hormone estradiol (which may stimulate the growth of cancer cells) to levels similar to a postmenopausal state. When the medication is stopped, hormone levels return to normal. Goserelin is indicated for: The pharmacokinetics of goserelin have been determined in both male and female healthy volunteers and patients. In these studies, goserelin was administered as a single 250µg (aqueous solution) dose and as a single or multiple 3.6 mg depot dose by subcutaneous route. Goserelin is a synthetic decapeptide analogue of LHRH. Goserelin acts as a potent inhibitor of pituitary gonadotropin secretion when administered in the biodegradable formulation. The result is sustained suppression of LH and serum testosterone levels.",The molecular weight is 1269.43.,Goserelin has a topological polar surface area of 493.39.,The log p value of  is -2.86.,Goserelin is approved.,Goserelin is a solid.,True
16469,"Menotropins contains follicle stimulating hormone (FSH) and luteinizing hormone (LH) purified from the urine of postmenopausal women. It is used as a fertility medication that is injected either subcutaneously or intramuscularly. It is composed of LH with 2 subunits, alpha = 92 residues, beta = 121 residues and FSH with 2 subunits, alpha = 92 residues, beta=111 residues. For the treatment of female infertility Used to treat female infertility, Menotropins stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Menotropins bind to the LH/hCG/FSH receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. Being a combination drug, Menotropins bind to the follicle stimulating hormone receptor (FSH), which results in ovulation in the absence of sufficient endogenous luteinizing hormone (LH). It also binds the LH receptor, thereby stimulating proper hormone release. The drug contains both FSH and LH, therefore, it induces ovarian follicular growth and development as well as gonadal steroid production in women who do not have ovarian failure. FSH is the primary driver of follicular recruitment and growth in early folliculogenesis, while LH is important for ovarian steroidogenesis and is involved in the physiological events leading to development of a competent pre-ovulatory follicle.",,,,Menotropins is approved.,Menotropins is a liquid.,True
16470,"Lutropin alfa is a recombinant human luteinizing hormone produced in yeast with 2 subunits, alpha = 92 residues, beta = 121 residues. It is a heterodimeric glycoprotein made up of monomeric units. Lutropin alfa was the first and only recombinant human form of luteinizing hormone (LH) developed for use in the stimulation of follicular development. Its pharmacological action mimics the biological activity of endogenous LH; an acute rise of LH, or LH surge, in females triggers ovulation and the development of the corpous luteum. In males, LH stimulates Leydig cell to produce testosterone. For treatment of infertility in women with hypothalamic or pituitary insufficiency (hypogonadotropic hypogonadism) and profound LH deficiency (LH <1.2 international units /L) Used to facilitate female conception, lutropin alfa performs the same actions as luteinizing hormone (LH), which is normally produced in the pituitary gland. Lutropin is usually given in combination with follitropin alfa. Together they stimulate the development of a follicle to prepare the reproductive tract for implementation and pregnancy. Lutropin alfa also stimulates the theca cells to produce androgens and the secretion of estradiol by the follicles. Lutropin alfa and follitropin alfa are discontinued once ultrasound assessment and serum estradiol concentrations show sufficient follicular maturation. hCG is then administered to complete follicular maturation and induce ovulation. In females, a LH surge about halfway through the menstrual cycle triggers the onset of ovulation. Lutropin alfa substitutes for endogenous LH and induces rupture of the preovulatory ovarian follicle and oocyte expulsion. Lutropin alfa induces and maintains the corpus luteum, which then secretes progesterone. Luteinizing hormone binds to a receptor shared with the human chorionic gonadotropin hormone (hCG) on the ovarian theca (and granulosa) cells and testicular Leydig cells. This LH/CG transmembrane receptor is a member of the super-family of G protein-coupled receptors. Adenylate cyclase then activates many other pathways leading to steroid hormone production and other follicle maturation processes. ",,,,Lutropin alfa is approved.,Lutropin alfa is a liquid.,True
16471,"Cetrorelix is a man-made hormone that blocks the effects of Gonadotropin Releasing Hormone (GnRH). GnRH controls another hormone that is called luteinizing hormone (LH), which is the hormone that starts ovulation during the menstrual cycle. When undergoing hormone treatment sometimes premature ovulation can occur, leading to eggs that are not ready for fertilization to be released. Cetrorelix does not allow the premature release of these eggs to occur. For the inhibition of premature LH surges in women undergoing controlled ovarian stimulation Cetrorelix is a synthetic decapeptide with gonadotropin-releasing hormone (GnRH) antagonistic activity. GnRH induces the production and release of luteinizing hormone (LH) and follicle stimulating hormone (FSH) from the gonadotrophic cells of the anterior pituitary. Due to a positive estradiol (E2) feedback at midcycle, GnRH liberation is enhanced resulting in an LH-surge. This LH-surge induces the ovulation of the dominant follicle, resumption of oocyte meiosis and subsequently luteinization as indicated by rising progesterone levels. Cetrorelix competes with natural GnRH for binding to membrane receptors on pituitary cells and thus controls the release of LH and FSH in a dose-dependent manner. Cetrorelix binds to the gonadotropin releasing hormone receptor and acts as a potent inhibitor of gonadotropin secretion. It competes with natural GnRH for binding to membrane receptors on pituitary cells and thus controls the release of LH and FSH in a dose-dependent manner.",The molecular weight is 1431.06.,Cetrorelix has a topological polar surface area of 495.67.,The log p value of  is -0.4.,Cetrorelix is approved and investigational.,Cetrorelix is a solid.,True
16472,"Recombinant human chorionic gonadotropin with 2 subunits, alpha = 92 residues, beta = 145 residues, each with N-and O-linked carbohydrate moieties linked to ASN-52 and ASN-78 (on alpha subunit) and ASN-13, ASN-30, SER-121, SER-127, SER-132 and SER-138 (on beta subunit). The primary structure of the alpha-chain of r-hCG is identical to that of the alpha-chain of hCG, FSH and LH. For the treatment of female infertility Choriogonadotropin alfa is used to treat female infertility, Choriogonadotropin alfa stimulates late follicular maturation and resumption of oocyte meiosis, and initiates rupture of the pre-ovulatory ovarian follicle. Ovidrel is an analogue of Luteinizing Hormone (LH) and binds to the LH/hCG receptor of the granulosa and theca cells of the ovary to effect these changes in the absence of an endogenous LH surge. Choriogonadotropin alfa binds to the Follicle stimulating hormone receptor which results in ovulation in the absence of sufficient endogenous Luteinizing hormone.",,,,Choriogonadotropin alfa is approved.,Choriogonadotropin alfa is a solid.,True
16473,"Human chorionic gonadotropin (HCG), a polypeptide hormone produced by the human placenta. Endogenously produced HCG interacts with the LHCG receptor of the ovary and promotes the maintenance of the corpus luteum during the beginning of pregnancy. This allows the corpus luteum to continuously secrete the hormone progesterone during the first trimester, which is required for maintenance of the uterus and prevents menstruation. In males, HCG also stimulates the production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testis to produce androgens.  For the treatment of prepubertal cryptorchidism (not due to anatomical obstruction), for the treatment of selected cases of hypogonadotropic hypogonadism (hypogonadism secondary to a pituitary deficiency) in males and for the induction of ovulation and pregnancy in the anovulatory, infertile woman in whom the cause of anovulation is secondary and not due to primary ovarian failure, and who has been appropriately pretreated with human menotropins. The action of HCG is virtually identical to that of pituitary LH, although HCG appears to have a small degree of FSH activity as well. It stimulates production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testis to produce androgens and the corpus luteum of the ovary to produce progesterone.",,,,Chorionic Gonadotropin (Human) is approved and vet_approved.,Chorionic Gonadotropin (Human) is a solid.,True
16474,"Fluciclovine is a -tagged synthetic analog of the amino acid L-leucine. It presents excellent diagnostic properties to be used in positron emission tomography (PET) imaging. The structure of fluciclovine allows it to be uptaken by the tumoral cells by its amino acid transporter without incorporating in the metabolism within the body. Fluciclovine was developed by Blue Earth Diagnostics, Ltd. and FDA approved in May 27, 2016. Fluciclovine is indicated as a detection agent for positron emission tomography (PET) in men with suspected prostate cancer recurrence based on elevated blood prostate specific antigen (PSA) levels following prior treatment. The overexpression of L-type amino acid transporters such as LAT1 and LAT3 that mediate the uptake of essential amino acids has been extensively reported as a tumoral mechanism of cell growth. Following intravenous administration, the tumor-to-normal tissue contrast is highest between 2 and 10 minutes after injection, with a 63% reduction in mean tumor uptake at 90 minutes after injection. The scanning time point should be evaluated carefully as an early scanning can present an increased blood pool and a late scanning will translate into an increased muscle uptake. These variations should always be considered in the image interpretation. Fluciclovine is transported into the prostate cancer cells via ASCT2 and LAT1 transporters. The activity of LAT1 gets increased in acidic pH, condition that is developed intra-tumorally at certain size. The uptake of fluciclovine presents an androgen-dependent dynamic in hormone sensitive cells.",The molecular weight is 132.12.,Fluciclovine (18F) has a topological polar surface area of 63.32.,,Fluciclovine (18F) is approved.,Fluciclovine (18F) is a liquid.,True
16475,"Phenacemide is used to control certain seizures in the treatment of epilepsy. This medicine acts on the central nervous system (CNS) to reduce the number and severity of seizures. Used to control certain seizures in the treatment of epilepsy. Phenacemide is a ureal anticonvulsant indicated for control of severe epilepsy, particularly mixed forms of complex partial (psychomotor or temporal lobe) seizures, refractory to other anticonvulsants. Phenacemide elevates the threshold for minimal electroshock convulsions and abolishes the tonic phase of maximal electroshock seizures. It also prevents or modifies seizures induced by pentylenetetrazol or other convulsants. Phenacemide binds to and blocks neuronal sodium channels or voltage sensitive calcium channels. This blocks or suppresses neuronal depolarization and hypersynchronization. Hypersynchronization is what often causes seizures.",The molecular weight is 178.19.,Phenacemide has a topological polar surface area of 72.19.,The log p value of  is 0.87.,Phenacemide is approved.,Phenacemide is a solid.,True
16476,"Phenazopyridine, also known as Pyridium, is a urinary tract analgesic used for the short-term management of urinary tract irritation and its associated unpleasant symptoms such as burning and pain during urination. In the USA, this drug was previously marked by Roche but has been discontinued by the FDA. It is still used in various parts of the world. Ingestion of phenazopyridine is found to change the appearance of the urine by imparting an orange or red color, as it is considered an azo dye. Phenazopyridine hydrochloride is indicated to relieve uncomfortable symptoms that occur as a consequence of mucosal irritation of the lower urinary tract in adults. The irritation may be a result of trauma, surgery, endoscopic procedures, infection, or the insertion of instruments or urinary catheters. Phenazopyridine may be used in combination with antimicrobial therapy but is not used as an antimicrobial agent. It contributes to the relief of discomfort and pain before antimicrobial therapy begins to take effect. It is important to note that the duration of treatment with this drug should last a maximum of 2 days. Phenazopyridine is available in many countries as an over the counter drug. Phenazopyridine acts as a local anesthetic offering relief from irritating conditions of the urinary tract. It relieves urinary urgency frequency, burning, pain, and discomfort.  The full mechanism of action of phenazopyridine is not fully elucidated, however, it is reported to exert a direct topical analgesic effect on the mucosal lining of the urinary tract via the inhibition of voltage-gated sodium channels and possibly group A nerve fibers, as suggested by the results of a study in rats. The above actions likely lead to the relief of unpleasant urinary symptoms.",The molecular weight is 213.24.,Phenazopyridine has a topological polar surface area of 89.65.,The log p value of  is 2.32.,Phenazopyridine is approved.,Phenazopyridine is a solid.,True
16477,"An aminoperhydroquinazoline poison found mainly in the liver and ovaries of fishes in the order tetraodontiformes, which are eaten. The toxin causes paresthesia and paralysis through interference with neuromuscular conduction. Tetrodotoxin is being investigated by Wex Pharmaceuticals for the treatment of chronic and breakthrough pain in advanced cancer patients as well as for the treatment of opioid dependence. For the treatment of chronic and breakthrough pain in advanced cancer patients as well as for the treatment of opioid dependence. Tetrodotoxin binds to site 1 of the fast voltage-gated sodium channel located at the extracellular pore opening. The binding of any molecules to this site will temporarily disable the function of the ion channel. Saxitoxin and several of the conotoxins also bind the same site.",,,,Tetrodotoxin is investigational.,Tetrodotoxin is a solid.,True
16478,"A lignan found in podophyllin resin from the roots of podophyllum plants. It is a potent spindle poison, toxic if taken internally, and has been used as a cathartic. It is very irritating to skin and mucous membranes, has keratolytic actions, has been used to treat warts and keratoses, and may have antineoplastic properties, as do some of its congeners and derivatives. For treatment of external genital warts (<i>Condyloma acuminatum</i>). Podofilox, also called podophyllotoxin, is a purer and more stable form of podophyllin in which only the biologically active portion of the compound is present. Podofilox is used to remove certain types of warts on the outside skin of the genital areas. The exact mechanism of action is not well understood. It does appear, however, that it and its derivatives may bind and inhibit topoisomerase II during the late S and early G2 stage. The drug may bind and stabilize the temporary break caused by the enzyme. This disrupts the reparation of the break through which the double-stranded DNA passes, and consequently stops DNA unwinding and replication",The molecular weight is 414.41.,Podofilox has a topological polar surface area of 92.68.,The log p value of  is 1.3.,Podofilox is approved.,Podofilox is a solid.,True
16479,"CA4P (Combretastatin)has been shown in the laboratory to shut down the blood supply to tumours. It is one of the first vascular targeting drugs to be tested in patients. This drug was originally isolated from the African Bush Willow. The first studies in patients with this drug were aimed at finding out whether it can be safely given to patients, what side effects it produces and whether it can actually shut down the blood supply to human tumours.  CA4P binds tubulin with a higher efficacy than colchicines, and was therefore initially investigated as an anti-mitotic agent. However, it was later observed to also induce vascular shutdown and necrosis in tumours. Clinical trials have revealed its positive effects, either as a single agent or in combination with chemotherapy, in patients with ovarian, lung or anaplastic thyroid cancer.",,,,CA4P is investigational.,CA4P is a solid.,True
16480,"Depatuxizumab/Denintuzumab mafodotin has been used in trials studying the treatment of Lymphoma, Gliosarcoma, Glioblastoma, Malignant Glioma, Squamous Cell Tumors, and Glioblastoma Multiforme. No approved indication. Selectively targets cancer cells expressing mutant epidermal growth factor receptor (EGFR) vIII or over expressing wild type EGFR. Depatuxizumab mafodotin acts on these cells to inhibit microtuble polymerization thus disrupting mitosis and vesicular trafficking  Depatuxizumab is a chimeric monoclonal antibody for EGFR which is linked to monomethyl aurastatin F via a maleimidocaproyl linker (mafodotin). Once delivered to the cancer cell, the mafodotin component is able to bind to tubulin and inhibit the exchange of GDP for GTP necessary for the polymerization of tubulin subunits to form microtubules. The inhibition of microtubule polymerization disrupts mitosis and interferes with vesicle trafficking in the cancer cell.",,,,Depatuxizumab mafodotin is investigational.,,True
16481,,,,,SR11254 is experimental.,SR11254 is a solid.,False
16482,,,,,BMS-181156 is experimental.,BMS-181156 is a solid.,False
16483,,,,,CD564 is experimental.,CD564 is a solid.,False
16484,,,,,Dodecyl-Alpha-D-Maltoside is experimental.,Dodecyl-Alpha-D-Maltoside is a solid.,False
16485,,,,,BMS184394 is experimental.,BMS184394 is a solid.,False
16486,"R667 is an orally active, gamma selective retinoid agonist that shows promise as a treatment for emhysema, as it has, in animal models, promoted structural lung repair and functional improvement with fewer side effects. It is currently in Phase II Trials for emphysema secondary to alpha-1 antitrypsin Investigated for use/treatment in emphysema. R667 is an orally active, gamma selective retinoid agonist that shows promise as a treatment for emhysema. Gamma-selective retinoic acid receptor agonist.",,,,R667 is investigational.,R667 is a solid.,True
16487,"LGD-1550 is an orally-active synthetic aromatic retinoic acid agent with potential antineoplastic and chemopreventive activities. Investigated for use/treatment in cancer/tumors (unspecified). LGD 1550 selectively binds to all three retinoic acid receptors (RAR-alpha, RAR-beta, and RAR-gamma), resulting in alterations in the expression of genes responsible for cell differentiation and proliferation. This agent also acts as an inhibitor of activator protein 1 (AP-1), a protein that mediates trophic responses and malignant transformation.",,,,LGD-1550 is investigational.,LGD-1550 is a solid.,True
16488,,,,,3-Fluoro-4-{amino}benzoic acid is experimental.,3-Fluoro-4-{amino}benzoic acid is a solid.,False
16489,,,,,3-fluoro-4--benzoic acid is experimental.,3-fluoro-4--benzoic acid is a solid.,False
16490,"Pheniramine is a first generation antihistamine in the alkylamine class, similar to and. It is used in  Pheniramine is commonly used in over-the-counter products to treat seasonal allergies or cold and flu symptoms. Pheniramine acts as an antagonist to allergic symptoms stemming from inappropriate histamine release to reduce edema, itching, and redness. The same antihistamine effect also produces sedation by acting in the central nervous system. Pheniramine competes with histamine for the histamine H1 receptor, acting as an inverse agonist once bound. The reduction in H1 receptor activity is responsible for reduced itching as well as reduced vasodilation and capillary leakage leading to less redness and edema. This can be seen in the suppression of the histamine-induced wheal (swelling) and flare (vasodilation) response. Inverse agonism of the H1 receptor in the CNS is also responsible for the sedation produced by first-generation antihistamines like pheniramine. The binding of pheniramine to H4 receptors, and subsequent inverse agonism, may also contribute to reduced itching by antagonizing inflammation.",The molecular weight is 240.35.,Pheniramine has a topological polar surface area of 16.13.,The log p value of  is 2.43.,Pheniramine is approved.,Pheniramine is a solid.,True
16491,"rEV131 is in development for allergic rhinitis, asthma and several inflammatory eye diseases. It is a topically delivered small protein that acts as an anti-inflammatory agent. Investigated for use/treatment in allergic reaction, allergic rhinitis, and cataracts. rEV131 is smaller than therapeutic antibodies and its compact structure gives good bioavailablity by a number of routes including: injected, inhaled, intraperitoneal, topical (ocular and nasal). The molecule is thermo-stable and can be stored in solution for more than 18 months at room temperature without significant loss of activity. This is an attractive feature for a protein drug candidate.",,,,REV131 is investigational.,REV131 is a solid.,True
16492,"XL999 has the potential to provide benefit to patients with lung cancer and acute myelogenous leukemia. XL999 is a new chemical entity that inhibits a spectrum of receptor tyrosine kinases (RTKs) with growth promoting and angiogenic properties, including FGFR 1/3, PDGFRα/β, VEGFR2/KDR, KIT, and FLT3. XL999 also inhibits FLT4 and SRC. XL999 has the potential to prevent tumor growth — both directly by a novel effect on tumor cell proliferation and indirectly through inhibition of the host angiogenic response. XL999 induces a cell-cycle block by a mechanism distinct from those previously identified and exhibits broad antitumor activity in xenograft models. Investigated for use/treatment in cancer/tumors (unspecified), lung cancer, and solid tumors. XL999 is a potent inhibitor of key receptor tyrosine kinases implicated in the development and maintenance of tumor vasculature and in the proliferation of some tumor cells. It inhibits FGFR1, FGFR3, RET, VEGFR2 and PDGFR, and is also a potent inhibitor of FLT3, an important driver of leukemia cell proliferation in some patients with acute myelogenous leukemia (AML). XL999 exhibited excellent activity in target-specific cellular functional assays.",,,,XL999 is investigational.,XL999 is a solid.,True
16493,"MLN518 is a novel, oral, small molecule designed to inhibit type III receptor tyrosine kinases, including FLT3, (platelet-derived growth-factor receptor) PDGFR and c-KIT. Tyrosine kinases are enzymes involved in several cellular processes and are known to be activated in cancer cells to drive tumor growth. AML patients with FLT3 mutations experience earlier disease relapse and shorter survival rates compared to patients without these mutations. Approximately 25 to 30 percent of all adult AML patients have a mutation of the FLT3 gene. The use of MLN518 to treat AML has been granted fast-track status by the U.S. Food and Drug Administration. Phase I/II trials are underway. Investigated for use/treatment in leukemia (myeloid). MLN518 is a novel quinazoline-based small molecule inhibitor of the FLT3, KIT, and platelet-derived growth-factor receptor (PDGFR) tyrosine kinases with that has been shown to have great efficacy in murine models of FLT3 ITD-positive leukemia. Experiments with mice demonstrate that at effective concentrations, MLN518 has mild toxicity toward normal hematopoiesis for FLT3 ITD-positive leukemia. MLN518 has also been shown to preferentially inhibit the growth of blast colonies from FLT3 ITD-positive as compared to ITD-negative patients with AML, without significantly affecting colony formation by normal human progenitor cells.  MLN518 inhibits tyrosine kinases; Specifically, it is selective for FLT3, KIT, and platelet-derived growth-factor receptor (PDGFR).",,,,Tandutinib is investigational.,Tandutinib is a solid.,True
16494,"Amuvatinib has been used in trials studying the treatment of Solid Tumors and Small Cell Lung Carcinoma. Amuvatinib is an oral, selective multi-targeted tyrosine kinase inhibitor that suppresses c-MET, c-RET and the mutant forms of c-KIT, PDGFR and FLT3. Amuvatinib also suppresses Rad51 protein, a critical component of double-stranded DNA repair in cancer cells. Amuvatinib is a selective multi-targeted tyrosine kinase inhibitor that suppresses c-MET, c-RET and the mutant forms of c-KIT, PDGFR and FLT3. Amuvatinib also suppresses Rad51 protein, a critical component of double-stranded DNA repair in cancer cells.",,,,Amuvatinib is investigational.,,True
16495,"Quizartinib is under investigation in Childhood Acute Myeloid Leukemia/Other Myeloid Malignancies. It is a potent inhibitor of FLT3. In preclinical studies, Quizartinib demonstrated dose-dependent activity and favorable drug-like profiles in bioavailability, pharmacokinetics, cytochrome P450 (CYP) liability, and absorption, distribution, metabolism, excretion (ADME). Quizartinib potently inhibits FLT3, a kinase that is mutated in approximately one-third of acute myeloid leukemia cases, and patients with FLT3 mutations are less responsive to traditional therapies.",,,,Quizartinib is investigational.,,True
16496,,The molecular weight is 116.07.,Fumaric Acid has a topological polar surface area of 74.6.,The log p value of  is -0.17.,Fumaric Acid is experimental and investigational.,Fumaric Acid is a solid.,False
16497,,,,,D-Malic acid is experimental.,D-Malic acid is a solid.,False
16498,,,,,Mesoxalic acid is experimental.,Mesoxalic acid is a solid.,False
16499,,,,,Tartronate is experimental.,Tartronate is a solid.,False
16500,"Chlormerodrin is a mercurial compound with toxic side effects that was previously used as a diuretic. The radiolabeled form has been used as a diagnostic and research tool. It is no longer used and has been replaced with new classes of diuretic drugs. Previously used as a diuretic. The radiolabeled form has been used as a diagnostic and research tool. Chlormerodrin is a mercurial compound with toxic side effects. It is no longer used and has been replaced with new classes of diuretic drugs. Chlormerodrin most likely acts by a direct renal action. Mercurial diuresis is presumed to occur through inhibition of reabsorption of water and electrolytes in the convoluted tubules, although the problem of whether the locus of action is primarily on the proximal or distal portion has not yet been settled. There is also evidence that mercurials interfere with the permeability of the membrane of tubular cells by increasing passive influx of Na<sup>+</sup> ion, Cl<sup>-</sup> ion and water into the cells, without interfering with the active extrusion of Na<sup>+</sup> ion. Lastly, there is some evidence that chlormerodrin inhibits succinic dehydrogenase, but the clinical significance of this binding is not known.",The molecular weight is 367.2.,Chlormerodrin has a topological polar surface area of 81.42.,,Chlormerodrin is approved and withdrawn.,Chlormerodrin is a solid.,True
16501,"The administration of quinidine derivatives helps to observe various skin and mucosal reactions. A papulopurpuric eruption in a patient (without thrombopenia) can be developed who is taking quinidine phenylethyl barbiturate intermittently and at reintroduction.(PMID: 9739909) Barbiturates work by binding to the GABAA receptor at either the alpha or the beta sub unit. These are binding sites that are distinct from GABA itself and also distinct from the benzodiazepine binding site. Like benzodiazepines, barbiturates potentiate the effect of GABA at this receptor. This GABAA receptor binding decreases input resistance, depresses burst and tonic firing, especially in ventrobasal and intralaminar neurons, while at the same time increasing burst duration and mean conductance at individual chloride channels; this increases both the amplitude and decay time of inhibitory postsynaptic currents. In addition to this GABA-ergic effect, barbiturates also block the AMPA receptor, a subtype of glutamate receptor. Glutamate is the principal excitatory neurotransmitter in the mammalian CNS.",,,,Quinidine barbiturate is approved.,Quinidine barbiturate is a solid.,True
16502,"Isatoribine is a selective agonist of TLR7. For the treatment of Hepatitis C. Isatoribine is a compound that elevates levels of interferon-alpha and provides antiviral and antimetastatic activity in a variety of murine systems. Isatoribine interacts with a specific receptor, Toll-like receptor 7, or TLR7, that is present on certain immune system cells. The compound also has a promising toxicity profile in multiple species. As of February 2007 this drug was no longer listed on Anadys development pipeline. Isatoribine is believed to act by a mechanism of action involving interaction with Toll-like receptor 7 (TLR7) and stimulation of the patient's own immune system, but the precise mechanism by which isatoribine reduced viral load is unknown (possible mechanisms include an antiviral effect, modulation of innate immunity, or enhancement of cellular responses).",,,,Isatoribine is investigational.,Isatoribine is a solid.,True
16503,"ANA971, an orally administered prodrug of isatoribine. Isatoribine is a nucleoside analog in development for the treatment of chronic hepatitis C virus (HCV) infection. ANA971 is a prodrug designed to improve the oral bioavailability of isatoribine. ANA971 resulted in higher levels of isatoribine in the blood than were present after oral administration of isatoribine itself. Investigated for use/treatment in hepatitis (viral, C). The mechanism of action is the same as for isatoribine. Isatoribine is believed to act by a mechanism of action involving interaction with Toll-like receptor 7 (TLR7) and stimulation of the patient's own immune system, but the precise mechanism by which isatoribine reduced viral load is unknown (possible mechanisms include an antiviral effect, modulation of innate immunity, or enhancement of cellular responses).",,,,ANA971 is investigational.,ANA971 is a solid.,True
16504,"SCV-07 (g -D-glutamyl-L-tryptophan) is a novel synthetic dipeptide that acts broadly on the Toll-like receptor pathway. It has been shown to stimulate T-lymphocyte differentiation, macrocytic phagocytosis, and specific immune responses, and enhance IL-2 and INF-g production. Due to this preferential activation of Th1 cytokine production, SCV-07 may show utility in treatment of tuberculosis. It can be administered orally or subcutaneously. In independent studies, treatment of tuberculosis with SCV-07 improved clearance of mycobacteria, improved cavity healing, improvements in immune parameters and reduced symptoms (fever, weakness, sweating, dry cough, productive cough, dyspnea, chest pain, tachycardia) without any adverse local or general effects. SCV-07 has shown efficacy in treating various viral and bacterial infections. Investigated for use/treatment in hepatitis (viral, C), infectious and parasitic disease (unspecified), and tuberculosis. SCV-07 (g -D-glutamyl-L-tryptophan) is a novel synthetic dipeptide that acts broadly on the Toll-like receptor pathway. It has been shown to stimulate T-lymphocyte differentiation, macrocytic phagocytosis, and specific immune responses, and enhance IL-2 and INF-g production.  SCV-07 (g -D-glutamyl-L-tryptophan) has broad effects on the Toll-like receptor (TLR) pathway. ",,,,Golotimod is investigational.,Golotimod is a solid.,True
16505,"A substance being studied in the treatment of some types of skin cancer. When put on the skin, resiquimod causes some immune cells to make certain chemicals that may help them kill tumor cells. It is also being studied to find out if adding it to a tumor vaccine improves the antitumor immune response. It is a type of imidazoquinoline and a type of immunomodulator. Investigated for use/treatment in genital herpes. Resiquimod is a Toll-like receptor 7 (TLR7) and TLR8 agonist that is a potent inducer of alpha interferon (IFN-alpha) and other cytokines.",,,,Resiquimod is investigational.,Resiquimod is a solid.,True
16506,"The first mixed agonist-antagonist analgesic to be marketed. It is an agonist at the kappa and sigma opioid receptors and has a weak antagonist action at the mu receptor. (From AMA Drug Evaluations Annual, 1991, p97) For the relief of moderate to severe pain. Pentazocine is a potent analgesic which when administered orally in a 50 mg dose appears equivalent in analgesic effect to 60 mg (1 grain) of codeine. Onset of significant analgesia usually occurs between 15 and 30 minutes after oral administration, and duration of action is usually three hours or longer. Onset and duration of action and the degree of pain relief are related both to dose and the severity of pretreatment pain. Pentazocine weakly antagonizes the analgesic effects of morphine and meperidine; in addition, it produces incomplete reversal of cardiovascular, respiratory, and behavioral depression induced by morphine and meperidine. Pentazocine has about 1/50 the antagonistic activity of nalorphine. It also has sedative activity. The preponderance of evidence suggests that pentazocine antagonizes the opioid effects by competing for the same receptor sites, especially the opioid mu receptor.",The molecular weight is 285.43.,Pentazocine has a topological polar surface area of 23.47.,The log p value of  is 4.67.,Pentazocine is approved and vet_approved.,Pentazocine is a solid.,True
16507,"An N-methylated indoleamine derivative, a serotonergic hallucinogen found in several plants, especially Prestonia amazonica (Apocynaceae) and in mammalian brain, blood, and urine. It apparently acts as an agonist at some types of serotonin receptors and an antagonist at others. Some people use this compound as a psychedelic inducing agent. DMT acts as a non-selective agonist at most or all of the serotonin receptors.",,,,Dimethyltryptamine is experimental and illicit.,Dimethyltryptamine is a solid.,True
16508,"Captodiame, also known as captodiamine, is an antihistamine which is used as a sedative and anxiolytic. It is a derivative of diphenhydramine. Captodiame has been suggested for use in preventing benzodiazepine withdrawal syndrome. Captodiame is indicated for the treatment of anxiety. ",The molecular weight is 359.59.,Captodiame has a topological polar surface area of 3.24.,The log p value of  is 6.4.,Captodiame is experimental.,Captodiame is a solid.,True
16509,,,,,Pyrithiamine Pyrophosphate is experimental.,Pyrithiamine Pyrophosphate is a solid.,False
16510,"There is a great deal of evidence indicating that vascular endothelial growth factor (VEGF) is important for the survival and proliferation of cancer cells. VEGF plays an important role in angiogenesis, lymphangiogenesis, and tumor growth, which are all factors that contribute to its attractiveness as a therapeutic target for anti-cancer therapies.  As a vascular endothelial growth factor (VEGF) inhibitor, bevacizumab is used in several chemotherapy regimens to treat metastatic colorectal cancer; metastatic, unresectable, locally advanced or recurrent non-squamous non-small cell lung cancer; metastatic renal cell carcinoma; metastatic, persistent, or recurrent cervical cancer; primary peritoneal cancer; epithelial ovarian cancer; and fallopian tube cancer. It can also be used to treat recurrent glioblastoma. Bevacizumab binds circulating vascular endothelial-derived growth factor (VEGF) and blocks it from binding to its associated receptors, effectively blunting downstream signaling. The effects of bevacizumab have been shown to re-establish normal vasculature at the tumor site resulting in increased nutrient and oxygen supply, while also improving the delivery of chemotherapeutic drugs to the target area. On the other hand, VEGF signaling is a vital component of several processes including angiogenesis, lymphangiogenesis, blood pressure regulation, wound healing, coagulation, and renal filtration. Although blocking VEGF may inhibit metastatic disease progression, it may also result in unintended effects due to the role of VEGF in several other physiologic processes. Transcription of the VEGF protein is induced by 'hypoxia inducible factor' (HIF) in a hypoxic environment. When circulating VEGF binds to VEGF receptors (VEGFR-1 and VEGFR-2) located on endothelial cells, various downstream effects are initiated. It should be noted that VEGF also binds to the neuropilin co-receptors (NRP-1 and NRP-1), leading to enhanced signaling. ",,,,Bevacizumab is approved and investigational.,Bevacizumab is a liquid.,True
16511,"Ranibizumab is a recombinant humanized IgG1 kappa isotype monoclonal antibody fragment designed for intraocular use. Ranibizumab binds to and inhibits the biologic activity of human vascular endothelial growth factor A (VEGF-A). Ranibizumab has a molecular weight of approximately 48 kilodaltons and is produced by an E. coli expression system in a nutrient medium containing the antibiotic tetracycline (tetracycline is not detectable in the final product). Ranibizumab is marketed under the name Lucentis®. It is indicated for the treatment of macular edema after retinal vein occlusion, age-related macular degeneration (wet), and diabetic macular edema. For the treatment of patients with macular edema after retinal vein occlusion, age-related macular degeneration (wet), and diabetic macular edema. Ranibizumab is a recombinant humanized IgG1 kappa isotype monoclonal antibody fragment designed for intraocular use. Ranibizumab is a VEGF-A antagonist that binds to and inhibits the biologic activity of active forms of human VEGF-A, including the cleaved form (VEGF<sub>110</sub>). VEGF-A has been shown to cause neovascularization (angiogenesis) and an increase in vascular permeability, which is thought to contribute to the progression of the neovascular form of age-related macular degeneration (AMD).  Ranibizumab binds to the receptor binding site of active forms of VEGF-A, including the biologically active, cleaved form of this molecule, VEGF<sub>110</sub>. The binding of ranibizumab to VEGF-A prevents the interaction of VEGF-A with its receptors (VEGFR1 and VEGFR2) on the surface of endothelial cells, reducing endothelial cell proliferation, vascular leakage, and new blood vessel formation.",,,,Ranibizumab is approved.,Ranibizumab is a liquid.,True
16512,"Pegaptanib is a polynucleotide aptamer. Pegatinib aids neovascular age-related macular degeneration by binding to VEGF which in order reduces angiogenesis and vessel permeability. For the treatment of neovascular (wet) age-related macular degeneration. Pegaptanib is a selective vascular endothelial growth factor (VEGF) antagonist. VEGF is a secreted protein that selectively binds and activates its receptors located primarily on the surface of vascular endothelial cells. VEGF induces angiogenesis, and increases vascular permeability and inflammation, all of which are thought to contribute to the progression of the neovascular (wet) form of age-related macular degeneration (AMD), a leading cause of blindness. VEGF has been implicated in blood retinal barrier breakdown and pathological ocular neovascularization. VEGF-A promotes angiogenesis. Patients with certain ocular conditions, such as the wet form of age related macular degeneration (AMD), have increased levels of VEGF-A. VEGF-A, in patients with wet AMD, also increases vascular permeability and inflammation in the eye, leading to progression of the condition. Pegaptanib is a pegylated oligonucleotide that selectively binds VEGF165, the isoform most responsible for VEGF-A's pathological action in wet AMD. This binding prevents VEGF165 from binding to its receptors, slowing or preventing further progression of wet AMD. Pegaptanib does not inhibit VEGF121, the physiological isoform.",,,,Pegaptanib is approved and investigational.,Pegaptanib is a liquid.,True
16513,"ABT-510 is peptide mimetics of thrombospondin-1 (TSP-1), block angiogenesis in vitro and in vivo and slow tumor growth. It is developed by Abbott Laboratories for the treatment of Solid Tumors, Lymphoma and Melanoma. Investigated for use/treatment in lymphoma (unspecified), melanoma, and solid tumors. ABT-510 is a synthetic peptide that mimics the anti-angiogenic activity of the naturally occurring protein, thrombospondin-1 (TSP-1). Angiogenesis is the process of new blood vessel formation. ABT-510 blocks the actions of multiple pro-angiogenic growth factors known to play a role in cancer related blood vessel growth, such as VEGF, bFGF, HGF, and IL-8. ABT-510 is the first compound with this mechanism of action to be studied.",,,,ABT-510 is investigational.,ABT-510 is a solid.,True
16514,"VEGF-AS (Veglin) is an anti-angiogenesis non-chemotherapy drug (angiogenesis inhibitor) that was developed by VasGene Therapeutics, Inc. for the treatment of a variety of malignancies including mesothelioma. Veglin is one of several newly developed non-chemotherapy drugs being tested for possible utilization in the ongoing struggle to combat malignant mesothelioma. Investigated for use/treatment in cancer/tumors (unspecified) and solid tumors. (VEGF-AS)Veglin is an antisense oligonucleotide that binds with DNA genes that are responsible for the production of proteins called Vascular Endothelial Growth Factors (VEGF), with the intention of inhibiting their production. VEGF (Vascular Endothelial Growth Factor) is an essential family of naturally-occurring growth factors found in humans and other animals that stimulates growth and supports survival of cells of the vascular system. VEGF is necessary for production of the blood vessels that transport nutrients and oxygen to cells and organs (angiogenesis). Without these vessels, tumors have limited capacity to grow. In addition, certain tumor cells themselves express the receptors for VEGF, and use VEGF as a growth stimulus.",,,,Veglin is investigational.,Veglin is a solid.,True
16515,"Investigated for use/treatment in cancer/tumors (unspecified), leukemia (unspecified), lymphoma (unspecified), multiple myeloma, and solid tumors. SNS-032 is a potent and selective inhibitor of CDKs 2, 7 and 9, which are critical in the communication and relay of signals to promote cellular growth and function. CDK2 is involved in cellular proliferation by regulating the initiation of and progression through the DNA-synthesis phase of the cell cycle. CDK7 and CDK9 are involved in transcriptional regulation of certain proteins involved in cell survival. Inappropriate activity by these CDKs can lead to unregulated proliferation, avoidance of apoptosis and increased cell survival, all of which are hallmarks of cancer. By selectively targeting these CDKs, SNS-032 may halt both aberrant cell proliferation and induce apoptosis.",,,,SNS-032 is investigational.,SNS-032 is a solid.,True
16516,"Bevasiranib is a small interfering RNA (siRNA) targeting vascular endothelial growth factor A (VEGF-A). Investigated for use/treatment in macular degeneration and diabetic retinopathy. Bevasiranib represents the first drug in a promising new class of experimental medical treatments. It is a small interfering RNA (siRNA) drug, which silences the genes that produce Vascular Endothelial Growth Factor (VEGF), a protein that promotes blood vessel growth. The treatment slows the growth and leakage of abnormal blood vessels that are associated with the wet form of macular degeneration. The drug is injected directly into the eye.",,,,Bevasiranib is investigational.,Bevasiranib is a solid.,True
16517,"Aflibercept is a recombinant protein composed of the binding domains of two human vascular endothelial growth factor (VEGF) receptors fused with the Fc region of human immunoglobulin gamma 1 (IgG1). Structurally, Aflibercept is a dimeric glycoprotein with a protein molecular weight of 96.9 kilo Daltons (kDa). It contains approximately 15% glycosylation to give a total molecular weight of 115 kDa. All five putative N-glycosylation sites on each polypeptide chain predicted by the primary sequence can be occupied with carbohydrate and exhibit some degree of chain heterogeneity, including heterogeneity in terminal sialic acid residues, except at the single unsialylated site associated with the Fc domain. Aflibercept, as an ophthalmic agent, is used in the treatment of macular edema following Central Retinal Vein Occlusion (CRVO) and neovascular Age-Related Macular Degeneration (AMD). Ziv-aflibercept, under the brand name Zaltrap, was developed as an injection for treatment of metastatic colorectal cancer. FDA approved in November 18, 2011 and EMA approved in November 2012. The opthalmic agent is used for the treatment of neovascular (wet) age-related mascular degeneration (AMD) and macular edema following central retinal vein occulsion (CRVO). The systemic injection, known as ziv-aflibercept, in combination with 5-fluorouracil, leucovorin, irinotecan-(FOLFIRI), is for the treatment of metastatic colorectal cancer that is resistant to or progressed following treatment with oxaliplatin.  Compared to other anti-VEGF drugs like bevacizumab and ranibizumab, aflibercept has a higher binding affinity to VEGF-A (Kd = 0.5 pM).  Ablibercept is a recombinant fusion protein that acts as a decoy receptor for the ligands, vascular endothelial growth factor-A (VEGF-A) and placental growth factor (PIGF). It prevents these ligands to binding to endothelial receptors, VEGFR-1 and VEGFR-2, to suppress neovascularization and decrease vascular permeability. This ultimately will slow vision loss or the progression of metastatic colorectal cancer. ",,,,Aflibercept is approved.,Aflibercept is a liquid.,True
16518,"Skin, the largest organ of the human body, plays the main role in protecting the body from mechanical damage. It is composed of epidermal, dermal and hypodermal layers. The barrier function of the skin owed to its avascular epidermal layer, which is made mainly of keratinocytes. The keratinocytes form a stratified epithelium, with growing basal cells at the innermost layer and the keratinized, and mostly impermeable outer stratum corneum layer on the surface. For chronic leg ulcers and diabetic foot.  Foreskin keratinocyte grafts lead to the re‐epithelialization of partial deep severe burns, thus allowing complete wound closure, and improves the condition of scars. Foreskin keratinocytes promote the proliferation of epithelial (skin) cells. ",,,,Foreskin keratinocyte (neonatal) is approved.,,True
16519,"Brolucizumab, also known as RTH258 or ESBA1008, is a monoclonal antibody indicated to treat neovascular age related macular degeneration. Brolucizumab is a monoclonal antibody indicated to treat neovascular age related macular degeneration. Brolucizumab is a vascular endothelial growth factor (VEGF) inhibitor which reduces proliferation of endothelial cells, vascularization of the tissue, and permeability of the vasculature. It has a long duration of action as it is given monthly. Patients should be counselled regarding the risk of endophthalmitis, retinal detachment, and arterial thromboembolic events following administration of this medication. Brolucizumab is a vascular endothelial growth factor (VEGF) inhibitor which targets the major VEGF-A isoforms: VEGF<sub>110</sub>, VEGF<sub>121</sub>, and VEGF<sub>165</sub>. Inhibition of these VEGF-A isoforms reduce proliferation of endothelial cells, vascularization of the tissue, and permeability of the vasculature.",,,,Brolucizumab is approved and investigational.,Brolucizumab is a solid.,True
16520,"Retinal vascular diseases (RVDs) such as diabetic macular edema (DME), age-related macular degeneration (AMD), and retinal vein occlusion (RVO) are typically caused by retinal ischemia and subsequent neovascularization (NV). Vascular endothelial growth factor A (VEGF-A) is a well-known mediator of retinal NV, and many currently approved RVD therapies such as and solely target VEGF-A. However, another set of factors, the Tie/Ang axis, comprising the transmembrane Tie-2 receptor and its soluble ligands Ang-1 and Ang-2, has been shown to play critical roles in mediating VEGF-A-induced NV. Faricimab is an IgG<sub>1</sub>-derived bispecific antibody capable of simultaneously binding to and depleting VEGF-A and Ang-2, which has been developed to improve therapeutic efficacy, especially in patients that respond poorly to anti-VEGF-A monotherapy. The retina is largely avascular to facilitate effective photoreceptor function; rather, the retina is fed by both retinal and choroidal capillary networks, pathologies of which result in retinal and choroidal vascular diseases such as diabetic macular edema (DME), age-related macular degeneration (AMD), and retinal vein occlusion (RVO). One of the underlying causes of retinal vascular diseases (RVDs) is retinal neovascularization (NV), the aberrant growth of new vasculature, usually due to sustained retinal ischemia and mediated primarily by vascular endothelial growth factor A (VEGF-A). VEGF-A is a VEGF family member, which also includes VEGF-B, -C, and -D, whose members signal through the VEGF receptors (VEGFRs) VEGFR-1, -2, and -3 to mediate endothelial and lymphatic growth. Extensive work in animal models of RVD has demonstrated that VEGF-A is necessary but not sufficient in many cases to mediate NV, suggesting that additional factors may be required in deep retinal capillary beds. One such factor has been identified as the angiopoietins Ang-1 and Ang-2 and their cellular receptor Tie-2; Ang-1 is a full Tie-2 agonist whose binding results in Tie-2 phosphorylation and downstream signalling, whereas Ang-2 is a Tie-2 partial agonist/antagonist that inhibits Tie-2 phosphorylation. Ang-1 generally has a protective effect, making endothelial cells less responsive to VEGF-A, while Ang-2 increases VEGF-A-dependent NV and stimulates pericyte apoptosis and breakdown of both the blood-brain and blood-retinal barriers; Ang-2 is upregulated in retinal vascular development and retinal ischemia.",,,,Faricimab is investigational.,,True
16521,"Antidiuretic hormone, also known as vasopressin, is a nine amino acid peptide secreted from the posterior pituitary. Antidiuretic hormone binds to receptors in the distal or collecting tubules of the kidney and promotes reabsorbtion of water back into the circulation For the treatment of enuresis, polyuria, diabetes insipidus, polydipsia and oesophageal varices with bleeding Vasopressin is an antidiuretic hormone indicated for the prevention and treatment of postoperative abdominal distention, in abdominal roentgenography to dispel interfering gas shadows, and in diabetes insipidus. Vasopressin can cause contraction of smooth muscle of the gastrointestinal tract and of all parts of the vascular bed, especially the capillaries, small arterioles and venules. It has less effect on the smooth musculature of the large veins. Vasopressin may also be used to control bleeding in some forms of von Willebrand disease and to treat extreme cases of bed wetting in children. It may also play a role in memory formation although the mechanism is unknown. Vasopressin acts on three different receptors, vasopressin receptor V1a (which initiates vasoconstriction, liver gluconeogenesis, platelet aggregation and release of factor VIII), vasopressin receptor V1b (which mediates corticotrophin secretion from the pituitary) and vasopressin receptor V2 which controls free water reabsorption in the renal medullar. The binding of vasopressin to the V2 receptor activates adenylate cyclase which causes the release of aquaporin 2 channels into the cells lining the renal medullar duct. This allows water to be reabsorbed down an osmotic gradient so the urine is more concentrated.",,,,Vasopressin is approved.,Vasopressin is a solid.,True
16522,"A synthetic nonapeptide comprising cysteinyl, phenylalanyl, phenylalanyl, glutaminyl, asparaginyl, cysteinyl, prolyl, lysyl, and glycinamide residues in sequence, with a disulfide bridge joining the two cysteine residues. Its antidiuretic effects are less than those of vasopressin. It is a non-catecholamine vasoconstrictor used in local anaesthetic injections for dental use, and is an ingredient of preparations that have been used for treatment of pain and inflammation of the mouth. For use as an alternative to adrenaline as a localising agent, provided that local ischaemia is not essential. Felypressin is a synthetic analog of lypressin or vasopressin with a greater vasoconstrictor activity than antidiuretic action. It is used primarily as a hemostatic.  Felypressin binds to the vasopressin receptor V1a. This causes contraction of the smooth muscle in the vascular bed, especially capillaries, small arterioles and venules.",The molecular weight is 1040.23.,Felypressin has a topological polar surface area of 405.32.,The log p value of  is -1.78.,Felypressin is experimental.,Felypressin is a solid.,True
16523,"Terlipressin is an analogue of vasopressin used as a vasoactive drug in the management of hypotension which has been found to be effective when norepinephrine fails. Commonly used to stop bleeding of varices in the food pipe (oesophagus). Terlipressin is a medicine similar to a naturally occurring hormone present in the body, known as antidiuretic hormone (ADH) or vasopressin. ADH has two main effects in the body. Firstly, it causes narrowing of blood vessels (vasoconstriction), thereby limiting blood flow to a particular area of the body. It also acts on receptors in the kidney to retain water in the body, which helps to prevent excessive loss of water in the urine.  Terlipressin, an analogue of vasopressin, acts on three different receptors, vasopressin receptor V1a (which initiates vasoconstriction, liver gluconeogenesis, platelet aggregation and release of factor VIII), vasopressin receptor V1b (which mediates corticotrophin secretion from the pituitary) and vasopressin receptor V2 which controls free water reabsorption in the renal medullar. The binding of terlipressin to the V2 receptor activates adenylate cyclase which causes the release of aquaporin 2 channels into the cells lining the renal medullar duct. This allows water to be reabsorbed down an osmotic gradient so the urine is more concentrated.",The molecular weight is 1227.38.,Terlipressin has a topological polar surface area of 512.85.,The log p value of  is -4.07.,Terlipressin is approved and investigational.,Terlipressin is a solid.,True
16524,"PH-284 belongs to a new family of new chemical entities called vomeropherins. Vomeropherins are self-administered by the patient with a metered nasal spray, or nasal aerosol device so that they can bind to peripheral chemosensory receptors in the nasal passages. This binding produces neural impulses that are transmitted by specific pathways to the hypothalamic centre that directly and rapidly affect brain function. PH-284 is under investigation by Pherin and Organon for the treatment of anorexia nervosa, and loss of appetite and cachexia in cancer and AIDS patients. Investigated for use/treatment in anorexia and other conditions causing harmful weight loss. The manufacturer suggests it could be relevant for treatment of weight loss and the associated symptoms-- i.e., lack of energy, decrease in appetite, physical wasting, vulnerability to toxicity, and sometimes reduced life expectancy-- in patients with eating disorders, patients with advanced cancer, patients with AIDS, and patients experiencing loss of appetite due to aging, acute illness, or pregnancy. Vomeropherins are self-administered by the patient with a metered nasal spray, or nasal aerosol device so that they can bind to peripheral chemosensory receptors in the nasal passages. This binding produces neural impulses that are transmitted by specific pathways to the hypothalamic centre that directly and rapidly affect brain function. Vomeropherins bind to peripheral chemosensory receptors in the vomeronasal organ.",,,,PH-284 is investigational.,PH-284 is a solid.,True
16525,"Atosiban is an inhibitor of the hormones oxytocin and vasopressin. It is used intravenously to halt premature labor. Although initial studies suggested it could be used as a nasal spray and hence would not require hospital admission, it is not used in that form. Atobisan was developed by the Swedish company Ferring Pharmaceuticals. It was first reported in the literature in 1985. Atosiban is licensed in proprietary and generic forms for the delay of imminent pre-term birth in pregnant adult women. Atosiban is indicated for use in delaying imminent pre-term birth in pregnant adult women with:  Atosiban reduces the frequency of uterine contractions to delay pre-term birth in adult females and induces uterine quiescence. Atosiban is a synthetic peptide oxytocin antagonist. It resembles oxytocin with has modifications at the 1, 2, 4, and 8 positions. The N-terminus of the cysteine residue is deaminated to form 3-mercaptopropanic acid at position 1, at position 2 L-tyrosine is modified to D-tyrosine with an ethoxy group replacing the phenol , threonine replaces glutamine at postion 4, and ornithine replaces leucine at position 8.",The molecular weight is 994.19.,Atosiban has a topological polar surface area of 365.67.,The log p value of  is -0.05.,Atosiban is approved and investigational.,Atosiban is a solid.,True
16526,,,,,Relcovaptan is investigational.,Relcovaptan is a solid.,False
16527,,The molecular weight is 1056.23.,Lypressin has a topological polar surface area of 425.55.,The log p value of  is -2.45.,Lypressin is approved.,,False
16528,A reagent commonly used in biochemical studies as a protective agent to prevent the oxidation of SH (thiol) groups and for reducing disulphides to dithiols. ,,,,"1,4-Dithiothreitol is experimental.","1,4-Dithiothreitol is a solid.",True
16529,"Isoetharine is a selective adrenergic beta-2 agonist used as fast acting bronchodilator for emphysema, bronchitis and asthma. For the treatment of asthma, wheezing, and chronic asthmatic bronchitis. Isoetharine is a relatively selective beta2-adrenergic bronchodilator. Isoetharine is indicated for the relief of bronchospasm associated with chronic obstructive pulmonary disease. Adrenergic bronchodilators are breathed in through the mouth to open up the bronchial tubes (air passages) of the lungs. The pharmacologic effects of isoetharine are attributable to stimulation through beta-adrenergic receptors of intracellular adenyl cyclase, the enzyme that catalyzes the conversion of adenosine triphosphate (ATP) to cyclic AMP. Increased cyclic AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells.",,,,Isoetharine is approved.,Isoetharine is a solid.,True
16530,"Arbutamine, administered through a closed-loop, computer-controlled drug-delivery system, is indicated to elicit acute cardiovascular responses, similar to those produced by exercise, in order to aid in diagnosing the presence or absence of coronary artery disease in patients who cannot exercise adequately. Used to elicit acute cardiovascular responses (cardiac stumulant), similar to those produced by exercise, in order to aid in diagnosing the presence or absence of coronary artery disease (CAD) in patients who cannot exercise adequately. Arbutamine is a synthetic catecholamine with positive chronotropic and inotropic properties. The chronotropic (increase in heart rate) and inotropic (increase in force of contraction) effects of arbutamine serve to mimic exercise by increasing cardiac work (producing stress) and provoke myocardial ischemia in patients with compromised coronary arteries. The increase in heart rate caused by arbutamine is thought to limit regional subendocardial perfusion, thereby limiting tissue oxygenation. In functional assays, arbutamine is more selective for beta-adrenergic receptors than for alpha-adrenergic receptors. The beta-agonist activity of arbutamine provides cardiac stress by increasing heart rate, cardiac contractility, and systolic blood pressure. The degree of hypotension that occurs for a given chronotropic activity is less with arbutamine than, for example, with isoproterenol because alpha receptor activity is retained.",The molecular weight is 317.38.,Arbutamine has a topological polar surface area of 92.95.,The log p value of  is 1.65.,Arbutamine is approved.,Arbutamine is a solid.,True
16531,"Fenoterol is an adrenergic beta-2 agonist that is used as a bronchodilator and tocolytic. Fenoterol is used for the treatment of asthma. Fenoterol is a beta agonist designed to open up the airways to the lungs by decreasing bronchconstriction. Beta(2)-receptor stimulation in the lung causes relaxation of bronchial smooth muscle, bronchodilation, and increased bronchial airflow.",The molecular weight is 303.36.,Fenoterol has a topological polar surface area of 92.95.,The log p value of  is 0.98.,Fenoterol is approved and investigational.,Fenoterol is a solid.,True
16532,"Pirbuterol is a beta-2 adrenergic bronchodilator. In vitro studies and in vivo pharmacologic studies have demonstrated that pirbuterol has a preferential effect on beta-2 Adrenergic receptors compared with isoproterenol. While it is recognized that beta-2 adrenergic receptors are the predominant receptors in bronchial smooth muscle, data indicate that there is a population of beta-2 receptors in the human heart, existing in a concentration between 10-50%. The precise function of these receptors has not been established. For the prevention and reversal of bronchospasm in patients 12 years of age and older with reversible bronchospasm including asthma. Pirbuterol is a beta-2 adrenergic bronchodilator. In vitro studies and in vivo pharmacologic studies have demonstrated that pirbuterol has a preferential effect on beta-2 adrenergic receptors compared with isoproterenol. While it is recognized that beta-2 adrenergic receptors are the predominant receptors in bronchial smooth muscle, data indicate that there is a population of beta-2 receptors in the human heart, existing in a concentration between 10-50%. The precise function of these receptors has not been established. The pharmacologic effects of beta adrenergic agonist drugs, including pirbuterol, are at least in proof attributable to stimulation through beta adrenergic receptors of intracellular adenyl cyclase, the enzyme which catalyzes the conversion of adenosine triphosphate (AlP) to cyclic-3&#8224; ,5&#8224;-adenosine monophosphate (c-AMP). Increased c-AMP levels are associated with relaxation of bronchial smooth muscle and inhibition of release of mediators of immediate hypersensitivity from cells, especially from mast cells.",The molecular weight is 240.3.,Pirbuterol has a topological polar surface area of 85.61.,The log p value of  is -0.03.,Pirbuterol is approved.,Pirbuterol is a solid.,True
16533,"Spermidine is a polyamine formed from putrescine. It is found in almost all tissues in association with nucleic acids. It is found as a cation at all pH values, and is thought to help stabilize some membranes and nucleic acid structures. It is a precursor of spermine.",,,,Spermidine is experimental.,Spermidine is a solid.,True
16534,,,,,4-{oxy}-3H-indole-2-carbonitrile is experimental.,4-{oxy}-3H-indole-2-carbonitrile is a solid.,False
16535,,,,,"2-HYDROXYMETHYL-6-OCTYLSULFANYL-TETRAHYDRO-PYRAN-3,4,5-TRIOL is experimental.","2-HYDROXYMETHYL-6-OCTYLSULFANYL-TETRAHYDRO-PYRAN-3,4,5-TRIOL is a solid.",False
16536,"Racepinephrine is a racemic mixture consisting of d- and l- enantiomers. Epinephrine is a non-selective α- and β-adrenergic receptor agonist. It is a bronchodilator used in the temporary relief of mild symptoms of intermittent asthma including wheezing, tightness of chest and shortness of breath. It is an active ingredient in oral inhalation over-the-counter products as racepinephrine hydrochloride. Indicated for temporary relief of mild symptoms of intermittent asthma. Epinephrine acts on α- and β-adrenergic receptors. When given subcutaneously or intramuscularly, epinephrine has a rapid onset and short duration of action. Epinephrine induces bronchial smooth muscle relaxation to relieve respiratory distress in asthma. In a clinical trial of paediatric patients with bronchiolitis, administration of aerosolized racemic epinephrine via inhalation resulted in improved clinical symptoms such as wheezing and retractions. The clinical efficacy of racemic epinephrine was comparable to that of salbutamol or albuterol, which are commonly used bronchodilators.  Epinephrine is a non-selective agonist at α- and β-adrenergic receptors, which are all G-protein-coupled receptors. The main therapeutic effect of epinephrine arises from its agonist action on β2-adrenergic receptors, which activate adenylyl cyclase and increase intracellular cyclic AMP production. Epinephrine causes smooth muscle relaxation on various tissues, including bronchial smooth muscles. As a result, epinephrine serves to alleviate bronchospasm, wheezing and tightness of chest that may occur during asthmatic attacks. Via its relaxer effects on the smooth muscle of the stomach, intestine, uterus and urinary bladder, epinephrine may also alleviate pruritus, urticaria, and angioedema and may relieve gastrointestinal and genitourinary symptoms associated with anaphylaxis. ",The molecular weight is 183.21.,Racepinephrine has a topological polar surface area of 72.72.,The log p value of  is -0.68.,Racepinephrine is approved.,,True
16537,"Methylephedrine is a sympathomimetic amine that appears in various over-the-counter cough and cold medications throughout the world , ,. The abuse of methylephedrine-containing medications has been reported in Japan. Methylephedrine is not legally available in the United States, but has been identified in cases of drug abuse. Used as an antitussive and decongestant. This drugs acts as an antitussive, bronchodilator, and adrenergic receptor agonist. It stimulates the alpha and beta adrenergic receptors, relieving cough and congestion. The pharmacology of methylephedrine is similar to that of other members of the ephedra alkaloid class of drugs. These compounds are sympathomimetic amines because they mimic the effects of the catecholamines on the sympathetic nervous system. These alkaloids permeate the blood-brain barrier and have a direct central nervous system stimulant effect with peripheral effects; the peripheral effects are indirect and primarily mediated by norepinephrine release. ",,,,DL-Methylephedrine is approved.,DL-Methylephedrine is a solid.,True
16538,Xamoterol is a β1-adrenoceptor partial agonist that has shown to improve systolic and diastolic function in studies with heart failure patients. It modulates the sympathetic control of the heart but has no agonist action on β2-adrenoceptors.,The molecular weight is 339.39.,Xamoterol has a topological polar surface area of 103.29.,The log p value of  is 0.43.,Xamoterol is approved.,,True
16539,,,,,"2-Hexyloxy-6-Hydroxymethyl-Tetrahydro-Pyran-3,4,5-Triol is experimental.","2-Hexyloxy-6-Hydroxymethyl-Tetrahydro-Pyran-3,4,5-Triol is a solid.",False
16540,A systemic agricultural fungicide and seed treatment agent.,,,,Carboxin is approved and experimental.,Carboxin is a solid.,True
16541,"Thenoyltrifluoroacetone is a chelating agent and inhibitor of cellular respiration. Studies indicate that thenoyltrifluoroacetone is a potent inhibitor of carboxylesterase activity, in addition to its ability to inhibit mitochondrial complex II activity. ",,,,Thenoyltrifluoroacetone is experimental.,Thenoyltrifluoroacetone is a solid.,True
16542,,,,,Ubiquinone Q1 is experimental.,Ubiquinone Q1 is a solid.,False
16543,"Hexylcaine hydrochloride is also known as cyclaine and osmocaine. It is a short acting local anesthetic that acts through inhibition of sodium channels. Patients experience an overdose may present with headache, tinnitus, numbness and tingling around the mouth and tongue, convulsions, inability to breathe, and decreased heart function. Hexylcaine has been discontinued in the US market. Used as a local anesthetic for surface application, infiltration or nerve block Hexylcaine is a local ester-class anesthetic. Local anesthetics produce a transient block of nerve conduction by interfering with sodium channels. This effect of the anesthetic interferes with the development of an action potential across the nerve. Hexyl caine acts mainly by inhibiting sodium influx through voltage gated sodium channels in the neuronal cell membrane of peripheral nerves. When the influx of sodium is interrupted, an action potential cannot arise and signal conduction is thus inhibited. The receptor site is thought to be located at the cytoplasmic (inner) portion of the sodium channel.",The molecular weight is 261.36.,Hexylcaine has a topological polar surface area of 38.33.,The log p value of  is 3.94.,Hexylcaine is approved and withdrawn.,Hexylcaine is a solid.,True
16544,"Dyclonine is an oral anaesthetic found in Sucrets, an over the counter throat lozenge. It may also be found in some Cepacol sore throat spray products. Used to provide topical anesthesia of accessible mucous membranes prior to examination, endoscopy or instrumentation, or other procedures involving the esophagus, larynx, mouth, pharynx or throat, respiratory tract or trachea, urinary tract, or vagina. Also used to suppress the gag reflex and/or other laryngeal and esophageal reflexes to facilitate dental examination or procedures (including oral surgery), endoscopy, or intubation. Also used for relief of canker sores, cold sores or fever blister. Dyclonine is an oral anasthetic. If substantial quantities of local anesthetics are absorbed through the mucosa, actions on the central nervous system (CNS) may cause CNS stimulation and/or CNS depression. Actions on the cardiovascular system may cause depression of cardiac conduction and excitability and, with some of these agents, peripheral vasodilation. Local anesthetics block both the initiation and conduction of nerve impulses by decreasing the neuronal membrane's permeability to sodium ions. This reversibly stabilizes the membrane and inhibits depolarization, resulting in the failure of a propagated action potential and subsequent conduction blockade.",The molecular weight is 289.42.,Dyclonine has a topological polar surface area of 29.54.,The log p value of  is 4.83.,Dyclonine is approved.,Dyclonine is a solid.,True
16545,"Proparacaine is a topical anesthetic drug of the amino ester group. It is found in ophthalmic solutions at a concentration of 0.5% as the hydrochloride salt. Used as a local (ophthalmic) anesthetic. Proparacaine stabilizes the neuronal membrane by inhibiting the ionic fluxes required for the initiation and conduction of impulses thereby effecting local anesthetic action. More specifically, proparacaine appears to bind or antagonize the function of voltage gated sodium channels. The exact mechanism whereby proparacaine and other local anesthetics influence the permeability of the cell membrane is unknown; however, several studies indicate that local anesthetics may limit sodium ion permeability through the lipid layer of the nerve cell membrane. Proparacaine may alter epithelial sodium channels through interaction with channel protein residues. This limitation prevents the fundamental change necessary for the generation of the action potential.",The molecular weight is 294.4.,Proparacaine has a topological polar surface area of 64.79.,The log p value of  is 3.83.,Proparacaine is approved and vet_approved.,Proparacaine is a solid.,True
16546,"A local anesthetic that is chemically related to bupivacaine but pharmacologically related to lidocaine. It is indicated for infiltration, nerve block, and epidural anesthesia. Mepivacaine is effective topically only in large doses and therefore should not be used by this route. (From AMA Drug Evaluations, 1994, p168) For production of local or regional analgesia and anesthesia by local infiltration, peripheral nerve block techniques, and central neural techniques including epidural and caudal blocks. Mepivicaine is an amide local anesthetic. Mepivicaine as a reasonably rapid onset and medium duration and is known by the proprietary names as Carbocaine and Polocaine. Mepivicaine is used in local infiltration and regional anesthesia. Systemic absorption of local anesthetics produces effects on the cardiovascular and central nervous systems. At blood concentrations achieved with normal therapeutic doses, changes in cardiac conduction, excitability, refractoriness, contractility, and peripheral vascular resistance are minimal. Local anesthetics block the generation and the conduction of nerve impulses, presumably by increasing the threshold for electrical excitation in the nerve, by slowing the propagation of the nerve impulse, and by reducing the rate of rise of the action potential. In general, the progression of anesthesia is related to the diameter, myelination, and conduction velocity of affected nerve fibers. Clinically, the order of loss of nerve function is as follows: pain, temperature, touch, proprioception, and skeletal muscle tone.",The molecular weight is 246.35.,Mepivacaine has a topological polar surface area of 32.34.,The log p value of  is 2.1.,Mepivacaine is approved and vet_approved.,Mepivacaine is a solid.,True
16547,Guanosine 5&#39;-(tetrahydrogen triphosphate). A guanine nucleotide containing three phosphate groups esterified to the sugar moiety. ,,,,Guanosine-5'-Triphosphate is experimental.,Guanosine-5'-Triphosphate is a solid.,True
16548,"Aluminum chloride is a chemical compound with the chemical formula AlCl3. When contaminated with iron chloride, it often displays a yellow color compared to the white pure compound. It is used in various chemical applications as a Lewis base, with anhydrous aluminium trichloride being the most commonly used Lewis acid. It may also be found in over-the-counter as an antiperspirant or prescription products as an antihemorrhagic agent. In antiperspirant products, FDA approves the use of aluminum chloride as an active ingredient up to 15%, calculated on the hexahydrate form, in an aqueous solution nonaerosol dosage form. - Indicated for the control of minor hemorrhage during dental restorative procedures. Aluminum chloride is a hemostatic and antiperspirant agent. Aluminum chloride is commonly used topical antiperspirant. It is proposed that aluminum chloride works by causing an obstruction of the distal sweat gland ducts, where the metal ions precipitate with mucopolysaccharides, damaging epithelial cells along the lumen of the duct and forming a plug that blocks sweat output. Aluminum chloride is also an astringent that promotes hemostasis; it precipitates proteins on the superficial layer of mucosa and make it mechanically stronger. It creates superficial and local coagulation in minor hemorrhages. ",The molecular weight is 133.33.,,,Aluminum chloride is approved and investigational.,Aluminum chloride is a solid.,True
16549,,,,,Mercaptoethanol is experimental.,Mercaptoethanol is a solid.,False
16550,"A phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells. Dipyridamole also potentiates the antiaggregating action of prostacyclin. (From AMA Drug Evaluations Annual, 1994, p752) For as an adjunct to coumarin anticoagulants in the prevention of postoperative thromboembolic complications of cardiac valve replacement and also used in prevention of angina. Dipyridamole, a non-nitrate coronary vasodilator that also inhibits platelet aggregation, is combined with other anticoagulant drugs, such as warfarin, to prevent thrombosis in patients with valvular or vascular disorders. Dipyridamole is also used in myocardial perfusion imaging, as an antiplatelet agent, and in combination with aspirin for stroke prophylaxis. Dipyridamole likely inhibits both adenosine deaminase and phosphodiesterase, preventing the degradation of cAMP, an inhibitor of platelet function. This elevation in cAMP blocks the release of arachidonic acid from membrane phospholipids and reduces thromboxane A2 activity. Dipyridamole also directly stimulates the release of prostacyclin, which induces adenylate cyclase activity, thereby raising the intraplatelet concentration of cAMP and further inhibiting platelet aggregation.",The molecular weight is 504.64.,Dipyridamole has a topological polar surface area of 145.44.,The log p value of  is 1.49.,Dipyridamole is approved.,Dipyridamole is a solid.,True
16551,Guanosine 5&#39;-monophosphate. A guanine nucleotide containing one phosphate group esterified to the sugar moiety and found widely in nature. ,,,,Guanosine-5'-Monophosphate is experimental.,Guanosine-5'-Monophosphate is a solid.,True
16552,,,,,gamma-Glutamylglycine is experimental.,gamma-Glutamylglycine is a solid.,False
16553,"OSI-461 is a second-generation molecule belonging to a new class of drugs termed selective apoptotic anti-neoplastic drugs (SAANDs). Investigated for use/treatment in crohn's disease, inflammatory bowel disease, kidney cancer, leukemia (lymphoid), and prostate cancer. OSI-461 is cGMP phosphodiesterase (cGMP-PDEs) inhibitors which is designed to lead to sustained activation of the intracellular signaling protein, Protein Kinase G (PKG), and subsequent stimulation of apoptosis through the c-Jun kinase pathway. Broad spectrum inhibition of cGMP-PDEs have been shown to lead to elevation in cGMP levels and the sustained activation of PKG. This in turn directly phosphorylates MEKK1 leading to activation of the N-terminal c-Jun kinase (JNK-1) pathway, a known pro-apoptotic signaling pathway.",,,,OSI-461 is investigational.,OSI-461 is a solid.,True
16554,"Investigated for use/treatment in adenomatous polyposis coli, lung cancer, prostate cancer, colon polyps, Barrett's esophagus disease, and pediatric indications. Exisulind is a sulindac derivative of a class of compounds called selective apoptotic anti-neoplastic drugs (SAANDs), which inhibit the enzyme cyclic guanosine monophosphodiesterase (cGMP - PDE). Exisulind is specific for apoptotic effects in precancerous and cancerous colorectal cells due to their overexpression of cGMP. Sustained elevation of cGMP and protein kinase G (PKG) activation may be also implicated in the induction of apoptosis by Exisulind.",The molecular weight is 372.41.,Exisulind has a topological polar surface area of 71.44.,The log p value of  is 3.11.,Exisulind is investigational.,Exisulind is a solid.,True
16555,,,,,3-isobutyl-1-methyl-7H-xanthine is experimental.,3-isobutyl-1-methyl-7H-xanthine is a solid.,False
16556,,,,,"5-ethoxy-4-(1-methyl-7-oxo-3-propyl-6,7-dihydro-1H-pyrazolopyrimidin-5-yl)thiophene-2-sulfonamide is experimental.","5-ethoxy-4-(1-methyl-7-oxo-3-propyl-6,7-dihydro-1H-pyrazolopyrimidin-5-yl)thiophene-2-sulfonamide is a solid.",False
16557,"Epratuzumab is a humanized monoclonal antibody derived from the murine IG2a monoclonal antibody, LL2 (EPB-2). This agent may subsequently be well matched for use in oncology and the treatment of inflammatory autoimmune disorders, such as lupus. Investigated for use/treatment in leukemia (lymphoid), lymphoma (non-hodgkin's), and systemic lupus erythematosus. Epratuzumab is a recombinant, humanized monoclonal antibody directed against CD22, a cell surface glycoprotein present on mature B-cells and on many types of malignant B-cells. It binds with high specificity to normal B-cells and B-cell tumors at the third Ig-like domain of CD22. After binding to CD22, epratuzumab's predominant antitumor activity appears to be mediated through antibody-dependent cellular cytotoxicity (ADCC). ",,,,Epratuzumab is investigational.,Epratuzumab is a solid.,True
16558,"Inotuzumab ozogamicin is an antibody-drug conjugate using linker and cytotoxic drug technology similar to that developed for the ground-breaking treatment Mylotarg (), which was approved by the US FDA in 2000 for the treatment of acute myeloid leukaemia. Inotuzumab ozogamicin consists of a recombinant humanised IgG4 kappa CD22-targeting monoclonal antibody covalently attached to calicheamicin derivative, N-acetyl-gamma-calicheamicin dimethylhydrazide, which is a potent DNA-binding cytotoxic agent. Developed by Pfizer and UCB, inotuzumab ozogamicin was granted approval by EU in June 2017 followed by FDA on August 17th, 2017 for the treatment of adults with relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). ALL is a rapidly progressing cancer of the bone marrow that is associated with high mortality rates and low therapeutic response from standard chemotherapies in relasping conditions. In a randomized trial, inotuzumab ozogamicin displayed higher percentages of patients undergoing longer periods of complete remission with no evidence of disease in comparison to patients receiving alternative chemotherapy. Indicated as monotherapy for the treatment of adults with relapsed or refractory CD22-positive B cell precursor acute lymphoblastic leukaemia (ALL).  Inotuzumab ozogamicin is an antineoplastic agent that targets CD22 antigen expressed on immature B-cell lymphocytes and blocks further growth of tumor cells. The drug aims to restore normal blood counts and achieve complete remission from the disease. QT interval prolongation was observed in patients receiving inotuzumab ozogamicin.  Inotuzumab ozogamicin is comprised of cytotoxic antibiotic N-acetyl-gamma-calicheamicin dimethylhydrazide attached to a humanized monoclonal IgG4 antibody via 4-(4 acetylphenoxy) butanoic acid (acetyl butyrate) linker. The drug exerts a potent cytotoxic effect against CD22+ B-cell lymphoma when the antibody binds to the CD22 receptor on the surface of B cells. The drug-CD22 complex is rapidly internalized into the cell, forming an endosome which subsequently fuses with lysosomes. N-acetyl-gamma-calicheamicin dimethylhydrazide is then intracellularly released into the acidic environment. N-acetyl-gamma-calicheamicin dimethylhydrazide is a calicheamicin derivative, which is naturally produced by the bacterium Micromonospora echinospora, and is toxic to the body when not bound to the antibody. It mediates apoptosis of the cell by binding to the minor groove of DNA in a sequence-specific manner and undergoing a structural change to generate diradicals. These changes abstract hydrogen ions from the phosphodiester bonds of double-stranded DNA, resulting in breaks and cell apoptosis. ",,,,Inotuzumab ozogamicin is approved and investigational.,Inotuzumab ozogamicin is a solid.,True
16559,"CD22 is a lineage-restricted B-cell antigen that is expressed solely in on B-chronic lymphocytic leukemia, hairy cell leukemia, acute lymphocytic leukemiathe and Burkitt's lymphoma. The predecessor of Moxetumab pasudotox (MxP), named BL22, was first created based on the antibody RFB4 which specifically binds to CD22. This antibody was used to generate a recombinant immunotoxin in which a stabilized Fv segment by a disulfide bond is fused to the _Pseudomonas_ exotoxin A (PE38) which does not have the cell-binding portion.  MxP is indicated for the treatment of adult patients with relapsed or refractory hairy cell leukemia (HCL) who received at least two prior systemic therapies including treatment with a purine nucleoside analog. The use of this drug is not recommended in patients with severe renal impairment (CrCl < 29 ml/min). Compared with its predecessor, MxP is even 50-fold more active on lymphoma cell lines and leukemic cells. In phase I clinical trial, MxP showed no dose-limiting toxicity and the overall response rate was of 79%. From pediatric patients with acute lymphoblastic leukemia, the complete response was observed in 12 individuals which is a result that has never been seen before. MxP is a CD22-directed cytotoxin. It is stated as an immunotoxin which is defined as the class of agents that combine the selectivity of antibodies towards the target and the potency of toxins to perform the pharmacological anticancer function. CD22 is a B-lymphocyte restricted transmembrane protein with a high density in HCL cells when compared with normal B cells. After binding to CD22, MxP is internalized and processed, which allows the release of the modified toxin. This toxin inhibits protein translation which induces an apoptotic state of the high CD22-expressed cancer cell.",,,,Moxetumomab Pasudotox is approved and investigational.,Moxetumomab Pasudotox is a solid.,True
16560,,,,,gamma-Glutamylcysteine is experimental.,gamma-Glutamylcysteine is a solid.,False
16561,"5&#39;-Adenylic acid, monoanhydride with imidodiphosphoric acid. An analog of ATP, in which the oxygen atom bridging the beta to the gamma phosphate is replaced by a nitrogen atom. It is a potent competitive inhibitor of soluble and membrane-bound mitochondrial ATPase and also inhibits ATP-dependent reactions of oxidative phosphorylation. ",,,,Phosphoaminophosphonic Acid-Adenylate Ester is experimental.,Phosphoaminophosphonic Acid-Adenylate Ester is a solid.,True
16562,,,,,5'-O-(L-Prolylsulfamoyl)adenosine is experimental.,5'-O-(L-Prolylsulfamoyl)adenosine is a solid.,False
16563,,,,,5'-O-(L-Cysteinylsulfamoyl)adenosine is experimental.,5'-O-(L-Cysteinylsulfamoyl)adenosine is a solid.,False
16564,,,,,5'-O-(N-(Alanyl)sulfamoyl)adenosine is experimental.,5'-O-(N-(Alanyl)sulfamoyl)adenosine is a solid.,False
16565,"Phosphatidyl serine (PS) is a phospholipid nutrient found in fish, green leafy vegetables, soybeans and rice, and is essential for the normal functioning of neuronal cell membranes and activates Protein kinase C (PKC) which has been shown to be involved in memory function. In apoptosis, phosphatidyl serine is transferred to the outer leaflet of the plasma membrane. This is part of the process by which the cell is targeted for phagocytosis. PS has been shown to slow cognitive decline in animal models. PS has been investigated in a small number of double-blind placebo trials and has been shown to increase memory performance in the elderly. Because of the potentail cognitive benefits of phosphatidylserine, the substance is sold as a dietary supplement to people who believe they can benefit from an increased intake. Phosphatidylserine has demonstrated some usefulness in treating cognitive impairment, including Alzheimer's disease, age-associated memory impairment and some non-Alzheimer's dementias. More research is needed before phosphatidylserine can be indicated for immune enhancement or for reduction of exercise stress. Phosphatidylserine is indicated in the treatment of cognitive impairment, including Alzheimer's disease, age-associated memory impairment and some non-Alzheimer's dementias. Further research is required before phosphatidylserine can be indicated for immune enhancement or for reduction of exercise stress. Phosphatidylserine was first isolated from brain lipids called cephalins. The major cephalins are phosphatidylserine and phophatidylethanolamine. Phosphatidylserine is involved in signal transduction activity as well as being a basic structural component of biologic membranes. Cholinergic hypofunction is thought to account in part for the cognitive deficits found in Alzheimer's disease. The most commonly used drugs for the treatment of Alzheimer's disease are reversible acetylcholinesterase inhibitors. The rationale of these drugs is to increase acetylcholine levels in the brains of Alzheimer's patients, and they may be somewhat effective in some cases. Phosphatidylserine restores acetylcholine release in aging humans by maintaining an adequate supply of the molecule and is able to increase the availability of endogenous choline for de novo acetylcholine synthesis. The hippocampus of the brain is believed to be important for cognitive processes and is affected in those with Alzheimer's disease. The dendritic spines of pyramidal cells, the post-synaptic target of the excitatory input to the hippocampus, have been proposed as a substrate for information storage. Age-dependent dendritic spine loss in pyramidal neurons has been reported in the human brain, and the extent of synaptic loss appears to correlate with the degree of cognitive impairment. Phosphatidylserine treatment prevents the age-related reduction in dendritic spine density in rat hippocampus. Protein kinase C facilitation of acetylcholine release has been reported in rats. Phosphatidylserine was found to restore protein kinase C activity in aging rats. Stimulation of calcium uptake by brain synaptosomes and activation of protein kinase C are yet other speculative mechanisms of phosphatidylserine's putative cognition-enhancing action.",,,,Phosphatidyl serine is investigational and nutraceutical.,Phosphatidyl serine is a solid.,True
16566,,,,,Androstanedione is experimental and illicit.,Androstanedione is a solid.,False
16567,,,,,EM-1745 is experimental.,EM-1745 is a solid.,False
16568,"Indecainide is a rarely used antidysrhythmic. Indecainide has local anesthetic activity and belongs to the membrane stabilizing (Class 1) group of antiarrhythmic agents; it has electrophysiologic effects characteristic of the IC class of antiarrhythmics. For the treatment of life-threatening dysrhythmias and sustained ventricular tachycardia. Indecainide is a rarely used antidysrhythmic. Indecainide has local anesthetic activity and belongs to the membrane stabilizing (Class 1) group of antiarrhythmic agents; it has electrophysiologic effects characteristic of the IC class of antiarrhythmics. Indecainide acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. The antiarrhythmic actions are mediated through effects on sodium channels in Purkinje fibers.",The molecular weight is 308.42.,Indecainide has a topological polar surface area of 55.12.,The log p value of  is 2.46.,Indecainide is approved.,Indecainide is a solid.,True
16569,"An antiarrhythmia agent used primarily for ventricular rhythm disturbances. Used to treat irregular heartbeats (arrhythmias) and maintain a normal heart rate. Moricizine is used to treat irregular heartbeats (arrhythmias) and to maintain a normal heart rate. It acts on the heart muscle to improve the heart's rhythm. Moricizine has potent local anesthetic activity and membrane stabilizing effect. Decreases excitability, conduction velocity, and automaticity as a result of slowed atrioventricular (AV) nodal and His-Purkinje conduction. Decreases the action potential duration (APD) in Purkinje fibers; also decreases the effective refractory period (ERP) but to a lesser extent than the APD, so the ERP/APD ratio is increased. Decreases the maxiumum rate of Phase 0 depolarization (V max ), but does not affect action potential amplitude or maximum diastolic potential. Does not affect atrial, AV nodal, or left ventricular refractory periods and has minimal effect on ventricular repolarization (evidenced by the overall decrease in JT interval). Has no effect on sinoatrial (SA) nodal or intra-atrial conduction and only minimal effect on sinus cycle length and sinus node recovery time. In the Vaughan Williams classification of antiarrhythmics, moricizine is considered to be a class I agent. It has properties of class IA, IB, and IC agents but does not clearly belong to any of the three subclasses. It has less effect on the slope of phase 0 and a greater effect on action potential duration and effective refractory period than class IC agents. Moricizine works by inhibiting the rapid inward sodium current across myocardial cell membranes.",The molecular weight is 427.52.,Moricizine has a topological polar surface area of 71.11.,The log p value of  is 2.84.,Moricizine is approved and investigational and withdrawn.,Moricizine is a solid.,True
16570,"A local anesthetic that is similar pharmacologically to lidocaine. Currently, it is used most often for infiltration anesthesia in dentistry. (From AMA Drug Evaluations Annual, 1992, p165) Used as a local anaesthetic and is often used in dentistry. Prilocaine binds to the intracellular surface of sodium channels which blocks the subsequent influx of sodium into the cell. Action potential propagation and never function is, therefore, prevented. This block is reversible and when the drug diffuses away from the cell, sodium channel function is restored and nerve propagation returns. Prilocaine acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. The antiarrhythmic actions are mediated through effects on sodium channels in Purkinje fibers.",The molecular weight is 220.32.,Prilocaine has a topological polar surface area of 41.13.,The log p value of  is 1.81.,Prilocaine is approved.,Prilocaine is a solid.,True
16571,"Produced during the urea cycle, ornithine is an amino acid produced from the splitting off of urea from arginine. L-Ornithine allows for the disposal of excess nitrogen and acts as a precursor of citrulline and arginine. Used for nutritional supplementation, also for treating dietary shortage or imbalance. It has been claimed that ornithine improves athletic performance, has anabolic effects, has wound-healing effects, and is immuno-enhancing. A non-essential and nonprotein amino acid, ornithine is critical for the production of the body's proteins, enzymes and muscle tissue. Ornithine plays a central role in the urea cycle and is important for the disposal of excess nitrogen (ammonia). Ornithine is the starting point for the synthesis of many polyamines such as putrescine and spermine. Ornithine supplements are claimed to enhance the release of growth hormone and to burn excess body fat. Ornithine is necessary for proper immune function and good liver function. L-Ornithine is metabolised to L-arginine. L-arginine stimulates the pituitary release of growth hormone. Burns or other injuries affect the state of L-arginine in tissues throughout the body. As De novo synthesis of L-arginine during these conditions is usually not sufficient for normal immune function, nor for normal protein synthesis, L-ornithine may have immunomodulatory and wound-healing activities under these conditions (by virtue of its metabolism to L-arginine).",The molecular weight is 132.16.,Ornithine has a topological polar surface area of 89.34.,The log p value of  is -2.84.,Ornithine is approved and nutraceutical.,Ornithine is a solid.,True
16572,"Leuprolide is a synthetic 9-residue peptide analogue of gonadotropin-releasing hormone (GnRH). Unlike the endogenous decapeptide GnRH, leuprolide contains a single D-amino acid (D-leucyl) residue, which helps to increase its circulating half-life from three to four minutes to approximately three hours. As a GnRH mimic, leuprolide is capable of binding to the GnRH receptor (GnRHR) and inducing downstream modulation of both gonadotropin hormone and sex steroid levels. Prolonged activation of GnRHR results in significant downregulation of sex steroid levels, which is primarily responsible for the clinical efficacy of leuprolide in diverse conditions, including advanced prostate cancer, endometriosis, and central precocious puberty. Leuprolide is indicated for the palliative treatment of advanced prostate cancer as well as for the treatment of pediatric patients with central precocious puberty (CPP). In combination with oral (also known as norethindrone), leuprolide is also indicated for the initial treatment of the symptoms of endometriosis. Finally, in combination with iron supplementation, leuprolide is indicated for the preoperative hematological improvement of anemic patients with uterine leiomyomata (uterine fibroids). Leuprolide is a gonadotropin-releasing hormone (GnRH) analogue that functions as a GnRH receptor superagonist. After an initial spike in GnRH-mediated steroidal production, including testosterone and estradiol, prolonged use results in a significant drop in circulating steroid levels, in line with those produced through other forms of androgen-deprivation therapy (ADT). The corresponding hormonal/steroidal changes produce specific adverse effects in different patient populations. Gonadotropin-releasing hormone (GnRH) is a naturally occurring decapeptide that modulates the hypothalamic-pituitary-gonadal (HPG) axis. GnRH binds to corresponding receptors (GnRHRs) on the anterior pituitary gonadotropes, which in turn release luteinizing hormone (LH) and follicle-stimulating hormone (FSH); these, in turn, affect the downstream synthesis and release of the sex hormones testosterone, dihydrotestosterone, estrone, and estradiol.",The molecular weight is 1209.42.,Leuprolide has a topological polar surface area of 429.04.,The log p value of  is -0.99.,Leuprolide is approved and investigational.,Leuprolide is a solid.,True
16573,Synthetic decapeptide antagonist to gonadotropin releasing hormone (GnRH). It is marketed by Praecis Pharmaceuticals as Plenaxis. Praecis announced in June 2006 that it was voluntarily withdrawing the drug from the market. For palliative treatment of advanced prostate cancer. Used in the palliative treatment of advanced prostate cancer. Abarelix is a luteinizing hormone agonist that results in suppression of testicular or follicular steroidogenesis. Abarelix binds to the gonadotropin releasing hormone receptor and acts as a potent inhibitor of gonadotropin secretion.,The molecular weight is 1416.09.,Abarelix has a topological polar surface area of 424.98.,The log p value of  is 2.95.,Abarelix is approved and investigational and withdrawn.,Abarelix is a solid.,True
16574,"Gonadorelin is another name for gonadotropin-releasing hormone (GnRH). It is a synthetic decapeptide prepared using solid phase peptide synthesis. GnRH is responsible for the release of follicle stimulating hormone and leutinizing hormone from the anterior pituitary. For evaluating the functional capacity and response of the gonadotropes of the anterior pituitary also for evaluating residual gonadotropic function of the pituitary following removal of a pituitary tumor by surgery and/or irradiation. Gonadorelin is responsible for the release of follicle stimulating hormone and leutinizing hormone from the anterior pitutitary. In the pituitary GnRH stimulates synthesis and release of FSH and LH, a process that is controlled by the frequency and amplitude of GnRH pulses, as well as the feedback of androgens and estrogens. The pulsatility of GnRH secretion has been seen in all vertebrates, and it is necessary to ensure a correct reproductive function. Thus a single hormone, GnRH, controls a complex process of follicular growth, ovulation, and corpus luteum maintenance in the female, and spermatogenesis in the male. Its short half life requires infusion pumps for its clinical use Systemic - Like naturally occurring gonadotropin-releasing hormone (GnRH), gonadorelin primarily stimulates the synthesis and release of luteinizing hormone (LH) from the anterior pituitary gland. Follicle-stimulating hormone (FSH) production and release is also increased by gonadorelin, but to a lesser degree. In prepubertal females and some gonadal function disorders, the FSH response may be greater than the LH response. For the treatment of amenorrhea, delayed puberty, and infertility the administration of gonadorelin is used to simulate the physiologic release of GnRH from the hypothalamus in treatment of delayed puberty, treatment of infertility caused by hypogonadotropic hypogonadism, and induction of ovulation in those women with hypothalamic amenorrhea. This results in increased levels of pituitary gonadotropins LH and FSH, which subsequently stimulate the gonads to produce reproductive steroids.",The molecular weight is 1182.31.,Gonadorelin has a topological polar surface area of 472.13.,The log p value of  is -4.12.,Gonadorelin is approved and investigational and vet_approved.,Gonadorelin is a liquid.,True
16575,"Nafarelin is a potent synthetic agonist of gonadotropin-releasing hormone with 3-(2-naphthyl)-D-alanine substitution at residue 6. Nafarelin has been used in the treatments of central precocious puberty and endometriosis. For treatment of central precocious puberty (true precocious puberty, GnRH-dependent precocious precocity, complete isosexual precocity) in children of both sexes and for the treatment of endometriosis. Nafarelin is a potent agonistic analog of gonadotropin-releasing hormone (GnRH). At the onset of administration, nafarelin stimulates the release of the pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), resulting in a temporary increase of gonadal steroidogenesis. Repeated dosing abolishes the stimulatory effect on the pituitary gland. Twice daily administration leads to decreased secretion of gonadal steroids by about 4 weeks; consequently, tissues and functions that depend on gonadal steroids for their maintenance become quiescent. After nafarelin therapy is discontinued, pituitary and ovarian function normalize and estradiol serum concentrations increase to pretreatment levels. Recurrences of endometriosis are frequent after cessation of any hormonal therapy, or surgery that leaves the ovaries and/or uterus intact. Like GnRH, initial or intermittent administration of nafarelin stimulates release of the gonadotropins luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the pituitary gland, which in turn transiently increases production of estradiol in females and testosterone in both sexes. However, with continuous daily administration, nafarelin continuously occupies the GnRH receptor, leading to a reversible down-regulation of the GnRH receptors in the pituitary gland and desensitization of the pituitary gonadotropes. This causes a significant and sustained decline in the production of LH and FSH. A decline in gonadotropin production and release causes a dramatic reversible decrease in synthesis of estradiol, progesterone, and testosterone by the ovaries or testes. Like normal endometrium, endometriotic implants contain estrogen receptors. Estrogen stimulates the growth of endometrium. Use of nafarelin induces anovulation and amenorrhea and decreases serum concentrations of estradiol to the postmenopausal range, which induces atrophy of endometriotic implants. However, nafarelin does not abolish the underlying pathophysiology of endometriosis. In children with central precocious puberty receiving nafarelin, serum LH, testosterone, and estradiol concentrations return to prepubertal levels. This results in the supression of secondary sexual characteristics and decrased rate of linear growth and skeletal maturation. Following disconinuation of nafarelin, the effects of the drug is reversed, meaning FSH and LH concentrations usually return to pretreatment levels.",The molecular weight is 1322.5.,Nafarelin has a topological polar surface area of 472.13.,The log p value of  is -1.22.,Nafarelin is approved.,Nafarelin is a solid.,True
16576,"A synthetic decapeptide, water-soluble Gonadotropin-releasing hormone antagonist. It has reached phase II clinical trials. Investigated for use/treatment in benign prostatic hyperplasia, endometriosis, and prostate cancer. Teverelix is a GnRH (Gonadotropin releasing hormone) antagonist.",,,,Teverelix is investigational.,Teverelix is a solid.,True
16577,"Investigated for use/treatment in endometriosis and uterine fibroids. Endometriosis is a painful, fertility threatening condition that is a result of tissue similar to that found in the womb lining growing elsewhere in the pelvis. The condition is sex hormone dependent, with gonadotropin releasing hormone (GnRH), a hypothalamic decapeptide amide that plays an important part in the regulation of reproductive processes, being implicated.",,,,Sufugolix is investigational.,Sufugolix is a solid.,True
16578,"Degarelix is used for the treatment of advanced prostate cancer. Degarelix is a synthetic peptide derivative drug which binds to gonadotropin-releasing hormone (GnRH) receptors in the pituitary gland and blocks interaction with GnRH. This antagonism reduces luteinising hormone (LH) and follicle-stimulating hormone (FSH) which ultimately causes testosterone suppression. Reduction in testosterone is important in treating men with advanced prostate cancer. Chemically, it is a synthetic linear decapeptide amide with seven unnatural amino acids, five of which are D-amino acids. FDA approved on December 24, 2008. Degaralix is used for the management of advanced prostate cancer.  Degarelix is a synthetic derivative of GnRH decapeptide, the ligand of the GnRH receptor. Gonadotropin and androgen production result from the binding of endogenous GnRH to the GnRH receptor. Degarelix antagonizes the GnRH receptor which in turn blocks the release of LH and FSH from the pituitary. LF and FSH decreases in a concentration-dependent manner. The reduction in LH leads to a decrease in testosterone release from the testes.  Degarelix competitively inhibits GnRH receptors in the pituitary gland, preventing the release of luteinizing hormone (LH) and follicle stimulating hormone. Reduced LH suppresses testosterone release, which slows the growth and reduces the size of prostate cancers.",The molecular weight is 1632.29.,Degarelix has a topological polar surface area of 512.87.,The log p value of  is 2.75.,Degarelix is approved.,Degarelix is a solid.,True
16579,"Ganirelix is an injectable competitive gonadotropin-releasing hormone antagonist (GnRH antagonist). It is utilized frequently in assisted reproduction therapy to control the occurrence of ovulation. The drug exerts its effects by inhibiting the action of GnRH in the pituitary gland, leading to fast suppression of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). Ganirelix is used in fertility treatment to prevent premature ovulation that could result in the harvesting of eggs that are too immature to be used in procedures such as in vitro fertilization. Ganirelix is marketed by Merck & Co., Inc. as Orgalutran®. For the inhibition of premature LH surges in women undergoing controlled ovarian hyperstimulation. Ganirelix acts by competitively blocking the GnRH receptors on the pituitary gonadotroph and subsequent transduction pathway. It induces a rapid, reversible suppression of gonadotropin secretion. The suppression of pituitary LH secretion by ganirelix is more pronounced than that of FSH. An initial release of endogenous gonadotropins has not been detected with ganirelix, which is consistent with an antagonist effect. Upon discontinuation of ganirelix, pituitary LH and FSH levels are fully recovered within 48 hours.",The molecular weight is 1570.35.,Ganirelix has a topological polar surface area of 451.49.,The log p value of  is 5.04.,Ganirelix is approved.,Ganirelix is a solid.,True
16580,"Histrelin is a gonadotropin releasing hormone (GnRH) agonist that acts as a potent inhibitor of gonadotropin when administered as an implant that delivers continuous therapeutic doses. Following an initial stimulatory phase with increased circulating levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), leading to a transient increase in concentration of gonadal steroids (testosterone and dihydrotestosterone in males), continuous administration of histrelin acetate results in decreased levels of LH and FSH due to a reversible down-regulation of the GnRH receptors in the pituitary gland and desensitization of the pituitary gonadotropes.  As the product Supprelin LA (FDA), histrelin is indicated for the treatment of children with central precocious puberty (CPP). As the product Vantas (FDA), histrelin is indicated for the palliative treatment of advanced prostate cancer.  Long-term treatment with histrelin acetate suppresses the LH response to GnRH causing LH levels to decrease to prepubertal levels within 1 month of treatment. As a result, serum concentrations of sex steroids (estrogen or testosterone) also decrease. In the treatment of Central Precocious Puberty, this is relevant as secondary sexual development ceases to progress in most patients. Additionally, linear growth velocity is slowed which improves the chance of attaining predicted adult height. Histrelin is a gonadotropin releasing hormone (GnRH) agonist that acts as a potent inhibitor of gonadotropin when administered as an implant that delivers continuous therapeutic doses. Following an initial stimulatory phase with increased circulating levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), leading to a transient increase in concentration of gonadal steroids (testosterone and dihydrotestosterone in males), continuous administration of histrelin acetate results in decreased levels of LH and FSH due to a reversible down-regulation of the GnRH receptors in the pituitary gland and desensitization of the pituitary gonadotropes. ",The molecular weight is 1323.53.,Histrelin has a topological polar surface area of 446.86.,The log p value of  is -1.9.,Histrelin is approved.,Histrelin is a solid.,True
16581,"Triptorelin is a synthetic decapeptide agonist analog of luteinizing hormone releasing hormone (LHRH). Possessing greater potency than endogenous LHRH, triptorelin reversibly represses gonadotropin secretion. After chronic, continuous administration, this agent effects sustained decreases in LH and FSH production and testicular and ovarian steroidogenesis. Serum testosterone concentrations may fall to levels typically observed in surgically castrated men. Triptorelin is indicated for the palliative treatment of advanced prostate cancer. The first administration of triptorelin is followed by a transient surge of follicle stimulating hormone (FSH), luteinizing hormone (LH), estradiol,and testosterone. The time, peak and decline of testosterone in the body varies depending on the dose administered. This initial surge is often responsible for worsening of prostate cancer symptoms such as urethral or bladder outlet obstruction, bone pain, spinal cord injury and hematuria in the early stages. A sustained decrease in FSH and LH, and significant reduction of testicular steroidogenesis is usually seen 2-4 weeks post-initiation of therapy. This result is a reduction of serum testosterone to levels which are typically seen in surgically castrated men. Ultimately, tissues and functions that require these hormones become inactive. The effects of triptorelin can usually be reversed once the drug is discontinued. Triptorelin is a synthetic agonist analog of gonadotropin releasing hormone (GnRH). Animal studies comparing triptorelin to native GnRH found that triptorelin had 13 fold higher releasing activity for luteinizing hormone, and 21-fold higher releasing activity for follicle-stimulating hormone.",The molecular weight is 1311.47.,Triptorelin has a topological polar surface area of 487.92.,The log p value of  is -2.4.,Triptorelin is approved and vet_approved.,Triptorelin is a solid.,True
16582,"An essential branched-chain amino acid important for hemoglobin formation. Indicated to assist in the prevention of the breakdown of muscle proteins that sometimes occur after trauma or severe stress. An essential amino acid. (Claim) Leucine helps with the regulation of blood-sugar levels, the growth and repair of muscle tissue (such as bones, skin and muscles), growth hormone production, wound healing as well as energy regulation. It can assist to prevent the breakdown of muscle proteins that sometimes occur after trauma or severe stress. It may also be beneficial for individuals with phenylketonuria - a condition in which the body cannot metabolize the amino acid phenylalanine This group of essential amino acids are identified as the branched-chain amino acids, BCAAs. Because this arrangement of carbon atoms cannot be made by humans, these amino acids are an essential element in the diet. The catabolism of all three compounds initiates in muscle and yields NADH and FADH2 which can be utilized for ATP generation. The catabolism of all three of these amino acids uses the same enzymes in the first two steps. The first step in each case is a transamination using a single BCAA aminotransferase, with a-ketoglutarate as amine acceptor. As a result, three different a-keto acids are produced and are oxidized using a common branched-chain a-keto acid dehydrogenase, yielding the three different CoA derivatives. Subsequently the metabolic pathways diverge, producing many intermediates. The principal product from valine is propionylCoA, the glucogenic precursor of succinyl-CoA. Isoleucine catabolism terminates with production of acetylCoA and propionylCoA; thus isoleucine is both glucogenic and ketogenic. Leucine gives rise to acetylCoA and acetoacetylCoA, and is thus classified as strictly ketogenic. There are a number of genetic diseases associated with faulty catabolism of the BCAAs. The most common defect is in the branched-chain a-keto acid dehydrogenase. Since there is only one dehydrogenase enzyme for all three amino acids, all three a-keto acids accumulate and are excreted in the urine. The disease is known as Maple syrup urine disease because of the characteristic odor of the urine in afflicted individuals. Mental retardation in these cases is extensive. Unfortunately, since these are essential amino acids, they cannot be heavily restricted in the diet; ultimately, the life of afflicted individuals is short and development is abnormal The main neurological problems are due to poor formation of myelin in the CNS.",The molecular weight is 131.18.,Leucine has a topological polar surface area of 63.32.,The log p value of  is -1.67.,Leucine is investigational and nutraceutical.,Leucine is a solid.,True
16583,"Becaplermin is produced by recombinant DNA technology by insertion of the gene for the B chain of platelet derived growth factor (PDGF) into the yeast, Saccharomyces cerevisiae. Becaplermin has a molecular weight of approximately 25 KD and is a homodimer composed of two identical polypeptide chains that are bound together by disulfide bonds. For topical treatment of skin ulcers (from diabetes) Used for the topical treatment of skin ulcers, Regranex has a biological activity similar to that of endogenous platelet-derived growth factor, which includes promoting the chemotactic recruitment and proliferation of cells involved in wound repair and enhancing the formation of granulation tissue. Binds to the beta platelet-derived growth factor (PDGF) receptor, a tyrosine kinase receptor. PDGF is known to exist as a dimer, and activates its signaling pathway by a ligand induced receptor dimerization and autophosphorylation. PDGF receptors also contain many auto-phosphorylation sites, which serve to mediate binding of SH2 sites and subsequently signal corresponding pathways. There are five different isoforms of PDGF that activate through two different receptors (alpha and beta).",,,,Becaplermin is approved and investigational.,Becaplermin is a liquid.,True
16584,"XL820 is investigated for use/treatment in solid tumors. XL820 is a solid. The proteins that XL820 inhibit include platelet-derived growth factor receptor beta (PDGFR), mast/stem cell growth factor receptor KIT, vascular endothelial growth factor receptor 2, and platelet-derived growth factor receptor alpha, clinically validated targets implicated in a variety of human cancers. XL820 exhibits dose-dependent growth inhibition in models of breast carcinoma, gliomas and leukemia. Investigated for use/treatment in solid tumors. XL820 inhibits KIT as well as VEGFR2 and PDGFR, clinically validated targets implicated in a variety of human cancers. In tumor models of breast carcinoma, glioma and leukemia, the compound exhibited dose-dependent growth inhibition and has been shown to cause tumor regression. XL820 demonstrated excellent activity in target-specific cellular functional assays. In biochemical and cellular assays, XL820 potently inhibits mutant forms of KIT that confer resistance to approved KIT inhibitors. XL820 has good oral bioavailability and has shown sustained inhibition of target RTKs in vivo following a single oral dose.",,,,XL820 is investigational.,XL820 is a solid.,True
16585,"Trapidil, a platelet-derived growth factor antagonist, was originally developed as a vasodilator and anti-platelet agent and has been used to treat patients with ischemic coronary heart, liver, and kidney disease. Used in the treatment of chronic stable angina. Trapidil exerts vasodilatory and antiplatelet effects. It also inhibits the activity of platelet derived growth factor (PDGF). Trapidil is thought to inhibit cyclic adenosine monophosphate (cAMP) phosphodiesterase enzymes. The resultant increase in cAMP potentiates the inhibition of platelets by adenosine. The reduction in platelet activation is likely responsible for the decrease in thromboxane A2 generation seen with trapidil. The increase in cAMP is also likely responsible for the vasdilatory action of trapidil. The increase in protein kinase A activity due to increased cAMP activated L-type calcium channels in the heart leading to increased depolarization and a positive inotropic effect. Lastly, PKA inactivates Raf-1, an activator of mitogen activated protein kinase (MAPK), which leads to a reduction in MAPK activation. This reduction in MAPK prevents mitogenesis due to PDGF binding to PDGF receptors. ",The molecular weight is 205.26.,Trapidil has a topological polar surface area of 46.32.,The log p value of  is 1.75.,Trapidil is experimental.,Trapidil is a solid.,True
16586,Arotinoid acid is a retinoic acid analog which acts as a selective RAR agonist.,,,,Arotinoid acid is experimental.,Arotinoid acid is a solid.,True
16587,"Glycodiazine is used with diet to lower blood glucose by increasing the secretion of insulin from pancreas and increasing the sensitivity of peripheral tissues to insulin. The mechanism of action of glycodiazine in lowering blood glucose appears to be dependent on stimulating the release of insulin from functioning pancreatic beta cells, and increasing sensitivity of peripheral tissues to insulin. Glycodiazine likely binds to ATP-sensitive potassium channel receptors on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Membrane depolarization stimulates calcium ion influx through voltage-sensitive calcium channels. This increase in intracellular calcium ion concentration induces the secretion of insulin. It is used for the concomitant use with insulin for the treatment of noninsulin-dependent (type 2) diabetes mellitus. Glycodiazine is used concomitantly with insulin for the treatment of noninsulin-dependent (type 2) diabetes mellitus.  Glycodiazine is used with diet to lower blood glucose by increasing the secretion of insulin from pancreas and increasing the sensitivity of peripheral tissues to insulin. The mechanism of action of glycodiazine in lowering blood glucose appears to be dependent on stimulating the release of insulin from functioning pancreatic beta cells, and increasing sensitivity of peripheral tissues to insulin. Glycodiazine likely binds to ATP-sensitive potassium channel receptors on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Membrane depolarization stimulates calcium ion influx through voltage-sensitive calcium channels. The rise in intracellular calcium leads to increased fusion of insulin granulae with the cell membrane, and therefore increased secretion of (pro)insulin.",,,,Glymidine is approved and investigational.,Glymidine is a solid.,True
16588,"Metformin is an antihyperglycemic agent of the _biguanide_ class, used for the management of type II diabetes). Currently, metformin is the first drug of choice for the management of type II diabetes and is prescribed to at least 120 million people worldwide.  **Metformin tablet** **General effects** Metformin's mechanisms of action are unique from other classes of oral antihyperglycemic drugs. Metformin decreases blood glucose levels by decreasing hepatic glucose production (gluconeogenesis), decreasing the intestinal absorption of glucose, and increasing insulin sensitivity by increasing peripheral glucose uptake and utilization. It is well established that metformin inhibits mitochondrial complex I activity, and it has since been generally postulated that its potent antidiabetic effects occur through this mechanism.  The above processes lead to a decrease in blood glucose, managing type II diabetes and exerting positive effects on glycemic control.",The molecular weight is 129.17.,Metformin has a topological polar surface area of 88.99.,The log p value of  is -1.43.,Metformin is approved.,Metformin is a solid.,True
16589,"Human tissue plasminogen activator, purified, glycosylated, 527 residues purified from CHO cells For management of acute myocardial infarction, acute ischemic strok and for lysis of acute pulmonary emboli Alteplase binds to fibrin in a thrombus and converts the entrapped plasminogen to plasmin. It also produces limited conversion of plasminogen in the absence of fibrin. Alteplase binds to fibrin rich clots via the fibronectin finger-like domain and the Kringle 2 domain. The protease domain then cleaves the Arg/Val bond in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. ",,,,Alteplase is approved.,Alteplase is a liquid.,True
16590,"Human tissue plasminogen activator, purified, glycosylated, 355 residues purified from CHO cells. Retavase is considered a \third-generation\"" thrombolytic agent, genetically engineered to retain and delete certain portions of human tPA. Retavase is a deletion mutein of human tPA formed by deleting various amino acids present in endogenous human tPA. Retavase contains 355 of the 527 amino acids of native human tPA (amino acids 1-3 and 176-527), and retains the activity-related kringle-2 and serine protease domains of human tPA. Three domains are deleted from retavase - kringle-1, finger, and epidermal growth factor (EGF)."" For lysis of acute pulmonary emboli, intracoronary emboli, and management of myocardial infarction. Reteplase cleaves the Arg/Val bond in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. This helps eliminate blood clots or arterial blockages that cause myocardial infarction. Reteplase binds to fibrin rich clots via the fibronectin finger-like domain and the Kringle 2 domain. The protease domain then cleaves the Arg/Val bond in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. ",,,,Reteplase is approved and investigational.,Reteplase is a liquid.,True
16591,"Human tissue plasminogen activator, purified, glycosylated, 527 residues purified from CHO cells. Eminase is a lyophilized (freeze-dried) formulation of anistreplase, the p-anisoyl derivative of the primary Lys-plasminogen-streptokinase activator complex (a complex of Lys-plasminogen and streptokinase). A p-anisoyl group is chemically conjugated to a complex of bacterial-derived streptokinase and human Plasma-derived Lys-plasminogen proteins. For lysis of acute pulmonary emboli, intracoronary emboli and management of myocardial infarction Anistreplase cleaves the Arg/Val bond in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. This helps eliminate blood clots or arterial blockages that cause myocardial infarction. Anistreplase cleaves the Arg/Val bond in plasminogen to form plasmin. This in turn leads to the degradation of blood clots.",,,,Anistreplase is approved.,Anistreplase is a liquid.,True
16592,"Tenecteplase is a tissue plasminogen activator (tPA) developed from modifications of natural human tPA complementary DNA (cDNA). It is a 527 amino acid with a substitution of threonine 103 with asparagine and substitution of asparagine 117 with glutamine within the kringle 1 domain, and a tetra-alanine substitution at amino acids 296-299 in the protease domain. For treatment of myocardial infarction and lysis of intracoronary emboli Tenecteplase is a fibrin-specific tissue-plasminogen activator. It binds to fibrin rich clots and cleaves the Arg/Val bond in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. This helps eliminate blood clots or arterial blockages that cause myocardial infarction. Tenecteplase binds to fibrin rich clots via the fibronectin finger-like domain and the Kringle 2 domain. The protease domain then cleaves the Arg/Val bond in plasminogen to form plasmin. Plasmin in turn degrades the fibrin matrix of the thrombus, thereby exerting its thrombolytic action. ",,,,Tenecteplase is approved.,Tenecteplase is a liquid.,True
16593,"Antifibrinolytic hemostatic used in severe hemorrhage. For use in patients with hemophilia for short term use (two to eight days) to reduce or prevent hemorrhage and reduce the need for replacement therapy during and following tooth extraction. It can also be used for excessive bleeding in menstruation, surgery, or trauma cases. Tranexamic acid is an antifibrinolytic that competitively inhibits the activation of plasminogen to plasmin. Tranexamic acid is a competitive inhibitor of plasminogen activation, and at much higher concentrations, a noncompetitive inhibitor of plasmin, i.e., actions similar to aminocaproic acid. Tranexamic acid is about 10 times more potent in vitro than aminocaproic acid. Tranexamic acid binds more strongly than aminocaproic acid to both the strong and weak receptor sites of the plasminogen molecule in a ratio corresponding to the difference in potency between the compounds. Tranexamic acid in a concentration of 1 mg per mL does not aggregate platelets in vitro. In patients with hereditary angioedema, inhibition of the formation and activity of plasmin by tranexamic acid may prevent attacks of angioedema by decreasing plasmin-induced activation of the first complement protein (C1). Tranexamic acid competitively inhibits activation of plasminogen (via binding to the kringle domain), thereby reducing conversion of plasminogen to plasmin (fibrinolysin), an enzyme that degrades fibrin clots, fibrinogen, and other plasma proteins, including the procoagulant factors V and VIII. Tranexamic acid also directly inhibits plasmin activity, but higher doses are required than are needed to reduce plasmin formation.",The molecular weight is 157.21.,Tranexamic acid has a topological polar surface area of 63.32.,The log p value of  is -1.8.,Tranexamic acid is approved.,Tranexamic acid is a solid.,True
16594,,,,,Bicine is experimental.,Bicine is a solid.,False
16595,"Desmoteplase is a chemical in the saliva of vampire bats. It activates plasminogen to the serine protease, plasmin. Plasmin acts by breaking down fibrin blood clots. When a vampire bat bites its victim, it secretes an enzyme that prevents the blood from clotting. The enzyme is called DSPA (Desmodus rotundus salivary plasminogen activator) and scientists are using DSPA as stroke and heart attack medication. Desmoteplase is a recombinant form of vampire bat DSPA (Salivary plasminogen activator alpha 1). Investigated for use/treatment in cerebral ischemia and strokes. Desmoteplase is a novel thrombolytic agent derived from vampire-bat saliva. It is genetically related to the clot buster tissue plasminogen activator (t-PA) but is more potent and demonstrates a safer toxicity profile (desmoteplase does not promote kainate- or NMDA-mediated neurotoxicity in vivo). Plasminogen activators are enzymes found in all vertebrate species investigated so far. Their physiological function is the generation of localized proteolysis in the context of tissue remodeling, wound healing and neuronal plasticity.  Desmoteplase targets and destroys fibrin, the structural scaffold of blood clots.",,,,Desmoteplase is investigational.,Desmoteplase is a liquid.,True
16596,,,,,Uridine-Diphosphate-N-Acetylgalactosamine is experimental.,Uridine-Diphosphate-N-Acetylgalactosamine is a solid.,False
16597,A uracil nucleotide containing a pyrophosphate group esterified to C5 of the sugar moiety. ,,,,Uridine-5'-Diphosphate is experimental.,Uridine-5'-Diphosphate is a solid.,True
16598,"A nucleoside diphosphate sugar which can be epimerized into UDPglucose for entry into the mainstream of carbohydrate metabolism. Serves as a source of galactose in the synthesis of lipopolysaccharides, cerebrosides, and lactose.",,,,Galactose-uridine-5'-diphosphate is experimental.,Galactose-uridine-5'-diphosphate is a solid.,True
16599,,,,,"2-Hexyloxy-6-Hydroxymethyl-Tetrahydro-Pyran-3,5-Diol is experimental.","2-Hexyloxy-6-Hydroxymethyl-Tetrahydro-Pyran-3,5-Diol is a solid.",False
16600,,,,,H TYPE II TRISACCHARIDE is experimental.,H TYPE II TRISACCHARIDE is a solid.,False
16601,,,,,Human blood group H type 1 trisaccharide is experimental.,Human blood group H type 1 trisaccharide is a solid.,False
16602,,,,,GALACTOSE GREASE is experimental.,GALACTOSE GREASE is a solid.,False
16603,,,,,BETA-METHYLLACTOSIDE is experimental.,BETA-METHYLLACTOSIDE is a solid.,False
16604,,,,,"octyl 3-amino-3-deoxy-2-O-(2,6-dideoxy-alpha-L-lyxo-hexopyranosyl)-beta-D-galactopyranoside is experimental.","octyl 3-amino-3-deoxy-2-O-(2,6-dideoxy-alpha-L-lyxo-hexopyranosyl)-beta-D-galactopyranoside is a solid.",False
16605,,,,,"4-AMINO-2-HEXYLOXY-6-HYDROXYMETHYL-TETRAHYDRO-PYRAN-3,5-DIOL is experimental.","4-AMINO-2-HEXYLOXY-6-HYDROXYMETHYL-TETRAHYDRO-PYRAN-3,5-DIOL is a solid.",False
16606,,,,,"4-AMINO-2-OCTYLOXY-6-HYDROXYMETHYL-TETRAHYDRO-PYRAN-3,5-DIOL is experimental.","4-AMINO-2-OCTYLOXY-6-HYDROXYMETHYL-TETRAHYDRO-PYRAN-3,5-DIOL is a solid.",False
16607,,,,,octyl 3-deoxy-2-O-(6-deoxy-alpha-L-galactopyranosyl)-beta-D-xylo-hexopyranoside is experimental.,octyl 3-deoxy-2-O-(6-deoxy-alpha-L-galactopyranosyl)-beta-D-xylo-hexopyranoside is a solid.,False
16608,,,,,(S)-3-(4-(2-Carbazol-9-Yl-Ethoxy)-Phenyl)-2-Ethoxy-Propionic Acid is experimental.,(S)-3-(4-(2-Carbazol-9-Yl-Ethoxy)-Phenyl)-2-Ethoxy-Propionic Acid is a solid.,False
16609,,,,,2-{5-INDOL-1-YL}ETHANOIC ACID is experimental.,2-{5-INDOL-1-YL}ETHANOIC ACID is a solid.,False
16610,"AMG-131 (T131), an orally-administered therapy, is expected to lower blood glucose in type II diabetic patients by improving the body’s ability to respond to insulin. T131 is a selective modulator of PPARg (peroxisome proliferator activated receptor gamma), a receptor involved in regulating the body’s ability to respond to insulin. T131 is not structurally related to the thiazolidinedione class of PPARg agonists, which includes Actos and Avandia. Investigated for use/treatment in diabetes mellitus type 2. T131, an orally-administered therapy, is expected to lower blood glucose in type II diabetic patients by improving the body’s ability to respond to insulin. T131 is not structurally related to the thiazolidinedione class of PPARg agonists, which includes Actos and Avandia T131 is a selective modulator of PPARg (peroxisome proliferator activated receptor gamma), a receptor involved in regulating the body’s ability to respond to insulin. T131 is not structurally related to the thiazolidinedione class of PPARg agonists, which includes Actos and Avandia",,,,AMG-131 is investigational.,AMG-131 is a solid.,True
16611,"CLX-0921 is investigated for use/treatment in diabetes mellitus type 2. CLX-0921 is a solid. CLX-0921 has a spectrum of activity that differs from commercially available thiazolidinediones. This substance targets the protein peroxisome proliferator-activated receptor gamma. It is a pharmacologically active antihyperglycemic agent that acts by increasing peripheral tissue sensitivity to insulin. Investigated for use/treatment in diabetes mellitus type 2. CLX-0921 has a spectrum of activity that differs from commercially available TZDs. It also increases glycogen synthesis, an activity not typically associated with rosiglitazone or pioglitazone. Thus it appears to have a distinct spectrum of activity relative to other TZDs.",,,,CLX-0921 is investigational.,CLX-0921 is a solid.,True
16612,,,,,(2S)-3-(1-{METHYL}-1H-INDOL-5-YL)-2-ETHOXYPROPANOIC ACID is experimental.,(2S)-3-(1-{METHYL}-1H-INDOL-5-YL)-2-ETHOXYPROPANOIC ACID is a solid.,False
16613,,,,,"(9Z,11E,13S)-13-hydroxyoctadeca-9,11-dienoic acid is experimental.","(9Z,11E,13S)-13-hydroxyoctadeca-9,11-dienoic acid is a solid.",False
16614,,,,,2-{5-ISOXAZOL-6-YLOXY)PROPOXY]INDOL-1-YL}ETHANOIC ACID is experimental.,2-{5-ISOXAZOL-6-YLOXY)PROPOXY]INDOL-1-YL}ETHANOIC ACID is a solid.,False
16615,,,,,"(4S,5E,7Z,10Z,13Z,16Z,19Z)-4-hydroxydocosa-5,7,10,13,16,19-hexaenoic acid is experimental.","(4S,5E,7Z,10Z,13Z,16Z,19Z)-4-hydroxydocosa-5,7,10,13,16,19-hexaenoic acid is a solid.",False
16616,,,,,"(5R,6E,8Z,11Z,14Z,17Z)-5-hydroxyicosa-6,8,11,14,17-pentaenoic acid is experimental.","(5R,6E,8Z,11Z,14Z,17Z)-5-hydroxyicosa-6,8,11,14,17-pentaenoic acid is a solid.",False
16617,,,,,"(8E,10S,12Z)-10-hydroxy-6-oxooctadeca-8,12-dienoic acid is experimental.","(8E,10S,12Z)-10-hydroxy-6-oxooctadeca-8,12-dienoic acid is a solid.",False
16618,,,,,"(8R,9Z,12Z)-8-hydroxy-6-oxooctadeca-9,12-dienoic acid is experimental.","(8R,9Z,12Z)-8-hydroxy-6-oxooctadeca-9,12-dienoic acid is a solid.",False
16619,,,,,9(S)-HODE is experimental.,9(S)-HODE is a solid.,False
16620,,,,,difluoro(5-{2--2H-pyrrol-5-yl-kappaN}pentanoato)boron is experimental.,difluoro(5-{2--2H-pyrrol-5-yl-kappaN}pentanoato)boron is a solid.,False
16621,,,,,(2S)-2-ETHOXY-3-{4-PHENYL}PROPANOIC ACID is experimental.,(2S)-2-ETHOXY-3-{4-PHENYL}PROPANOIC ACID is a solid.,False
16622,,,,,3-(5-methoxy-1H-indol-3-yl)propanoic acid is experimental.,3-(5-methoxy-1H-indol-3-yl)propanoic acid is a solid.,False
16623,,,,,(2S)-2-(4-ethylphenoxy)-3-phenylpropanoic acid is experimental.,(2S)-2-(4-ethylphenoxy)-3-phenylpropanoic acid is a solid.,False
16624,,,,,2-chloro-5-nitro-N-phenylbenzamide is experimental.,2-chloro-5-nitro-N-phenylbenzamide is a solid.,False
16625,,,,,(2S)-2-(biphenyl-4-yloxy)-3-phenylpropanoic acid is experimental.,(2S)-2-(biphenyl-4-yloxy)-3-phenylpropanoic acid is a solid.,False
16626,,,,,3-benzoic acid is experimental.,3-benzoic acid is a solid.,False
16627,,,,,2--5-(PYRIMIDIN-2-YLOXY)BENZOIC ACID is experimental.,2--5-(PYRIMIDIN-2-YLOXY)BENZOIC ACID is a solid.,False
16628,,,,,"(5E,14E)-11-oxoprosta-5,9,12,14-tetraen-1-oic acid is experimental.","(5E,14E)-11-oxoprosta-5,9,12,14-tetraen-1-oic acid is a solid.",False
16629,,,,,3-FLUORO-N-BENZENESULFONAMIDE is experimental.,3-FLUORO-N-BENZENESULFONAMIDE is a solid.,False
16630,,,,,(2S)-2-(4-chlorophenoxy)-3-phenylpropanoic acid is experimental.,(2S)-2-(4-chlorophenoxy)-3-phenylpropanoic acid is a solid.,False
16631,"Arhalofenate has been investigated for the treatment of Gout and Hyperuricemia. Partial agonist of peroxisome proliferator-activated receptor (PPAR) gamma; results in improved glucose, lipid, and weight management.",,,,Arhalofenate is investigational.,,True
16632,"Naveglitazar has been used in trials studying the treatment of Diabetes Mellitus, Non-Insulin-Dependent.",,,,Naveglitazar is investigational.,,True
16633,,,,,Darglitazone is experimental.,Darglitazone is a solid.,False
16634,"Recombinant human coagulation Factor VIIa (rFVIIa), intended for promoting hemostasis by activating the extrinsic pathway of the coagulation cascade. NovoSeven is a vitamin K-dependent glycoprotein consisting of 406 amino acid residues. Cloned and expressed in hamster kidney cells, the protein is catalytically active in a two-chain form. For treatment of hemorrhagic complications in hemophilia A and B. Used in the treatment of bleeding episodes in hemophilia A or B. NovoSeven is recombinant Factor VIIa and, when complexed with tissue factor can activate coagulation Factor X to Factor Xa, as well as coagulation Factor IX to Factor IXa. Factor Xa, in complex with other factors, then converts prothrombin to thrombin, which leads to the formation of a hemostatic plug by converting fibrinogen to fibrin and thereby inducing local clotting. NovoSeven activates the coagulation or clotting cascade by cleaving Factor IX and Factor X, which activates them and then leads to activation of thrombin and fibrin.",,,,Coagulation factor VIIa Recombinant Human is approved.,Coagulation factor VIIa Recombinant Human is a liquid.,True
16635,"Fondaparinux (Arixtra) is a synthetic anticoagulant agent consisting of five monomeric sugar units and a O-methyl group at the reducing end of the molecule. It is structurally similar to polymeric glycosaminoglycan heparin and heparan sulfate (HS) when they are cleaved into monomeric units. The monomeric sequence in heparin and HS is thought to form the high affinity binding site for the natural anti-coagulant factor, antithrombin III (ATIII). Once bound to heparin or HS, the anticoagulant activity of ATIII is potentiated by 1000-fold. Fondaparinux potentiates the neutralizing action of ATIII on activated Factor X 300-fold. Fondaparinux may be used: to prevent venous thromboembolism in patients who have undergone orthopedic surgery of the lower limbs (e.g. hip fracture, hip replacement and knee surgery); to prevent VTE in patients undergoing abdominal surgery who are are at high risk of thromboembolic complications; in the treatment of deep vein thrombosis (DVT) and pumonary embolism (PE); in the management of unstable angina (UA) and non-ST segment elevation myocardial infarction (NSTEMI); and in the management of ST segment elevation myocardial infarction (STEMI). Approved for: (1) prophylaxis of VTE for up to one month post surgery in patients undergoing orthopedic surgery of the lower limbs such as hip fracture, hip replacement and knee surgery; (2) prophylaxis of VTE patients undergoing abdominal surgery who are at high risk of thromboembolic complications (e.g. patients undergoing abdominal cancer surgery); (3) treatment of acute DVT and PE; (4) management of UA and NSTEMI for the prevention of death and subsequent myocardial infarction (MI); and (5) management of STEMI for the prevention of death and myocardial reinfarction in patients who are managed with thrombolytics or who are initially to receive no form of reperfusion therapy. Fondaparinux should not be used as the sole anticoagulant during percutaneous coronary intervention (PCI) due to an increased risk of guiding catheter thrombosis.  Fondaparinux binds specifically to the natural anticoagulant factor, ATIII. Binding to ATIII potentiates the neutralizing action of ATIII on Factor Xa 300-times. Neutralization of Factor Xa decreases the conversion of prothrombin to thrombin, which subsequently decreases the conversion of fibrinogen to fibrin (loose meshwork). The decrease in thrombin also decreases the activation of Factor XIII, which decreases the conversion of fibrin in its loose meshwork form to its stabilized meshwork form. Disruption of the coagulation cascade effectively decreases the formation of blood clots. Fondaparinux does not inactivate thrombin (activated Factor II). According to the manufacturer, fondaparinux has no known effect on platelet function. In studies comparing fondaparinux to enoxaparin, decreases in platelet levels were observed in similar numbers of patients from both groups (2-5%). At the recommended dose, Fondaparinux does not affect fibrinolytic activity or bleeding time. There is no antidote for fondaparinux. Monitoring of the anticoagulant activity of fondaparinux is not generally required. The anti-factor Xa assay may be used to monitor therapy in special populations such as those with renal impairment or who are pregnant. Complete blood count (CBC) and kidney function should be monitored during treatment.  The antithrombotic activity of fondaparinux is the result of ATIII-mediated selective inhibition of Factor Xa. By selectively binding to ATIII, Fondaparinux potentiates (about 300 times) the neutralization of Factor Xa by ATIII. Neutralization of Factor Xa interrupts the blood coagulation cascade and thus inhibits thrombin formation and thrombus development. It is thought that fondaparinux is unlikely to induce thrombocytopenia via a heparin-induced thrombocytopenia (HIT)-like mechanism given its chemical structure. As a result, fondaparinux has been used as an alternative anticoagulant in heparin-induced thrombocytopenia (HIT) patients. However, it is important to note that rare cases of HIT have been reported in patients treated with fondaparinux.",The molecular weight is 1508.22.,Fondaparinux has a topological polar surface area of 805.48.,The log p value of  is -10.96.,Fondaparinux is approved and investigational.,Fondaparinux is a solid.,True
16636,,,,,4--2-(2-METHYLPROPYL)-1-CARBONYL]PIPERAZINE is experimental.,4--2-(2-METHYLPROPYL)-1-CARBONYL]PIPERAZINE is a solid.,False
16637,"SSR-126517E is a second generation synthetic pentasaccharide that binds antithrombin with such high affinity that it assumes a plasma half-life of 80 hours.  Investigated for use/treatment in thrombosis and venous thromboembolism. SSR126517E is a biotinylated form of idraparinux. It can be neutralized with intravenous recombinant avidin. Avidin binds biotinylated fondaparinux with high affinity, and the complex is then rapidly cleared.",,,,SSR-126517E is investigational.,SSR-126517E is a solid.,True
16638,"LY517717 is an investigational oral direct inhibitor of activated Factor Xa. It is believed to be Lilly's PMD-3112 (licensed from Amgen). Investigated for use/treatment in thrombosis and venous thromboembolism. LY517717 has been well tolerated in healthy subjects. LY517717 is a blood thinner that may prevent blood clots from forming in the legs and may prevent those blood clots from traveling to the lungs. Leg and lung blood clots occur commonly after patients have surgery to replace a hip or knee joint. These clots often occur while patients are in bed in the hospital after hip or knee joint surgery. LY517717, an investigational oral direct inhibitor of activated Factor Xa, appears to interrupt thrombus formation without impairing platelet hemostatic function.",,,,LY-517717 is investigational.,LY-517717 is a solid.,True
16639,"Investigated for use/treatment in myocardial infarction. Lanoteplase is a second generation derivative of alteplase, and a third generation recombinant plasminogen activator made from a deletion and point mutant of tissue type-plasminogen activator (t-PA). Lanoteplase has a longer half life than alteplase. Lanoteplase is a serine protease that binds to fibrin in a thrombus (blood clot)and cleaves the Arg-Val bond in plasminogen, producing active plasmin. Plasmin is an enzyme that degrades plasma proteins such as fibrin clots to clear blocked blood vessels that cause myocardial infarction (heart attack) or stroke. ",,,,Lanoteplase is investigational.,Lanoteplase is a solid.,True
16640,"Investigated for use/treatment in thrombosis, venous thromboembolism, strokes, heart disease, and atrial fibrillation. Idraparinux sodium is a novel long-acting synthetic highly potent synthetic and specific indirect inhibitor of coagulation factor Xa, injectable subcutaneously.",,,,Idraparinux is investigational.,Idraparinux is a solid.,True
16641,"Recombinant nematode anticoagulant protein c2 (rNAPc2) is a specific inhibitor of tissue factor (TF)/factor VIIa complex with novel antithrombotic activity.  Investigated for use/treatment in thrombosis (deep vein), angina, coronary artery disease, and colorectal cancer. Recombinant Nematode Anticoagulant Protein c2 (rNAPc2) is a potent (K(i) =10 pM), inhibitor of the factor VIIa/tissue factor (fVIIa/TF) complex that requires the prerequisite binding to zymogen or activated factor X (fX). This has been shown to attenuate the activation of coagulation and to prevent death in a primate model of sepsis caused by gram-negative bacteria.",,,,rNAPc2 is investigational.,rNAPc2 is a solid.,True
16642,Otamixaban is a novel direct Factor Xa (FXa) inhibitor. It is currently being developed by the French pharmaceutical company Sanofi-Aventis as a treatment for acute coronary syndrome. Investigated for use/treatment in thrombosis.,,,,Otamixaban is investigational.,Otamixaban is a solid.,True
16643,,,,,Eribaxaban is experimental.,Eribaxaban is a solid.,False
16644,,,,,THIENOPYRIDINE-2-SULFONIC ACID -AMIDE is experimental.,THIENOPYRIDINE-2-SULFONIC ACID -AMIDE is a solid.,False
16645,,,,,2-({4-PIPERAZIN-1-YL}CARBONYL)THIENOPYRIDINE 4-OXIDE is experimental.,2-({4-PIPERAZIN-1-YL}CARBONYL)THIENOPYRIDINE 4-OXIDE is a solid.,False
16646,,,,,"N-((1R,2S)-2-(5-CHLORO-1H-INDOLE-2-CARBOXAMIDO)CYCLOHEXYL)-5-METHYL-4,5,6,7-TETRAHYDROTHIAZOLOPYRIDINE-2-CARBOXAMIDE is experimental.","N-((1R,2S)-2-(5-CHLORO-1H-INDOLE-2-CARBOXAMIDO)CYCLOHEXYL)-5-METHYL-4,5,6,7-TETRAHYDROTHIAZOLOPYRIDINE-2-CARBOXAMIDE is a solid.",False
16647,,,,,"N-((1R,2R)-2-(5-CHLORO-1H-INDOLE-2-CARBOXAMIDO)CYCLOHEXYL)-5-METHYL-4,5,6,7-TETRAHYDROTHIAZOLOPYRIDINE-2-CARBOXAMIDE is experimental.","N-((1R,2R)-2-(5-CHLORO-1H-INDOLE-2-CARBOXAMIDO)CYCLOHEXYL)-5-METHYL-4,5,6,7-TETRAHYDROTHIAZOLOPYRIDINE-2-CARBOXAMIDE is a solid.",False
16648,,,,,N-(2-(((5-CHLORO-2-PYRIDINYL)AMINO)SULFONYL)PHENYL)-4-(2-OXO-1(2H)-PYRIDINYL)BENZAMIDE is experimental.,N-(2-(((5-CHLORO-2-PYRIDINYL)AMINO)SULFONYL)PHENYL)-4-(2-OXO-1(2H)-PYRIDINYL)BENZAMIDE is a solid.,False
16649,,,,,"5-(5-CHLORO-2-THIENYL)-N-{(3S)-1--2-OXOPYRROLIDIN-3-YL}-1H-1,2,4-TRIAZOLE-3-SULFONAMIDE is experimental.","5-(5-CHLORO-2-THIENYL)-N-{(3S)-1--2-OXOPYRROLIDIN-3-YL}-1H-1,2,4-TRIAZOLE-3-SULFONAMIDE is a solid.",False
16650,,,,,5-CHLORO-N-{(3S)-1--2-OXOPYRROLIDIN-3-YL}-1-BENZOTHIOPHENE-2-SULFONAMIDE is experimental.,5-CHLORO-N-{(3S)-1--2-OXOPYRROLIDIN-3-YL}-1-BENZOTHIOPHENE-2-SULFONAMIDE is a solid.,False
16651,,,,,6-CHLORO-N-{(3S)-1--2-OXOPYRROLIDIN-3-YL}-1-BENZOTHIOPHENE-2-SULFONAMIDE is experimental.,6-CHLORO-N-{(3S)-1--2-OXOPYRROLIDIN-3-YL}-1-BENZOTHIOPHENE-2-SULFONAMIDE is a solid.,False
16652,,,,,6-CHLORO-N-{(3S)-1--2-OXO-3-PYRROLIDINYL}-2-NAPHTHALENESULFONAMIDE is experimental.,6-CHLORO-N-{(3S)-1--2-OXO-3-PYRROLIDINYL}-2-NAPHTHALENESULFONAMIDE is a solid.,False
16653,,,,,5-Chloro-N-{(3S)-1--2-oxo-3-pyrrolidinyl}-1H-indole-2-sulfonamide is experimental.,5-Chloro-N-{(3S)-1--2-oxo-3-pyrrolidinyl}-1H-indole-2-sulfonamide is a solid.,False
16654,,,,,5-chloro-N-amino}-2-oxoethyl)pyrrolidin-3-yl]thiophene-2-carboxamide is experimental.,5-chloro-N-amino}-2-oxoethyl)pyrrolidin-3-yl]thiophene-2-carboxamide is a solid.,False
16655,,,,,"5-Chloro-thiophene-2-carboxylic acid ((3S,4S)-1-{-methyl}-4-hydroxy-pyrrolidin-3-yl)-amide is experimental.","5-Chloro-thiophene-2-carboxylic acid ((3S,4S)-1-{-methyl}-4-hydroxy-pyrrolidin-3-yl)-amide is a solid.",False
16656,,,,,N-(1-ISOPROPYLPIPERIDIN-4-YL)-1-(3-METHOXYBENZYL)-1H-INDOLE-2-CARBOXAMIDE is experimental.,N-(1-ISOPROPYLPIPERIDIN-4-YL)-1-(3-METHOXYBENZYL)-1H-INDOLE-2-CARBOXAMIDE is a solid.,False
16657,,,,,1-{2--2-OXOETHYL}-N-(1-ISOPROPYLPIPERIDIN-4-YL)-1H-INDOLE-2-CARBOXAMIDE is experimental.,1-{2--2-OXOETHYL}-N-(1-ISOPROPYLPIPERIDIN-4-YL)-1H-INDOLE-2-CARBOXAMIDE is a solid.,False
16658,,,,,"5-CHLORO-THIOPHENE-2-CARBOXYLIC ACID ((3S,4S)-4-FLUORO- 1-{-METHYL}-PYRROLIDIN-3-YL)-AMIDE is experimental.","5-CHLORO-THIOPHENE-2-CARBOXYLIC ACID ((3S,4S)-4-FLUORO- 1-{-METHYL}-PYRROLIDIN-3-YL)-AMIDE is a solid.",False
16659,,,,,5-CHLORO-N-(2-(4-(2-OXOPYRIDIN-1(2H)-YL)BENZAMIDO)ETHYL)THIOPHENE-2-CARBOXAMIDE is experimental.,5-CHLORO-N-(2-(4-(2-OXOPYRIDIN-1(2H)-YL)BENZAMIDO)ETHYL)THIOPHENE-2-CARBOXAMIDE is a solid.,False
16660,,,,,"5-CHLORO-N-((1R,2S)-2-(4-(2-OXOPYRIDIN-1(2H)-YL)BENZAMIDO) CYCLOPENTYL)THIOPHENE-2-CARBOXAMIDE is experimental.","5-CHLORO-N-((1R,2S)-2-(4-(2-OXOPYRIDIN-1(2H)-YL)BENZAMIDO) CYCLOPENTYL)THIOPHENE-2-CARBOXAMIDE is a solid.",False
16661,,,,,THIENOPYRIDINE-2-SULFONIC ACID PYRIDIN-2-YLMETHYL)-PYRROLIDIN-3-YL]-AMIDE is experimental.,THIENOPYRIDINE-2-SULFONIC ACID PYRIDIN-2-YLMETHYL)-PYRROLIDIN-3-YL]-AMIDE is a solid.,False
16662,,,,,3-({4--2-OXOPIPERAZIN-1-YL}METHYL)BENZENECARBOXIMIDAMIDE is experimental.,3-({4--2-OXOPIPERAZIN-1-YL}METHYL)BENZENECARBOXIMIDAMIDE is a solid.,False
16663,,,,,4-{SULFONYL}-1-(1H-PYRROLOPYRIDIN-2-YLMETHYL)PIPERAZIN-2-ONE is experimental.,4-{SULFONYL}-1-(1H-PYRROLOPYRIDIN-2-YLMETHYL)PIPERAZIN-2-ONE is a solid.,False
16664,,,,,4-({4--2-OXOPIPERAZIN-1-YL}METHYL)BENZENECARBOXIMIDAMIDE is experimental.,4-({4--2-OXOPIPERAZIN-1-YL}METHYL)BENZENECARBOXIMIDAMIDE is a solid.,False
16665,,,,,4-SULFONYL]-1-METHYL]PIPERAZINONE is experimental.,4-SULFONYL]-1-METHYL]PIPERAZINONE is a solid.,False
16666,,,,,1-SULFONYL]-4-METHYL]PIPERAZINE is experimental.,1-SULFONYL]-4-METHYL]PIPERAZINE is a solid.,False
16667,"Edoxaban is a member of the Novel Oral Anti-Coagulants (NOACs) class of drugs, and is a rapidly acting, oral, selective factor Xa inhibitor. By inhibiting factor Xa, a key protein in the coagulation cascade, edoxaban prevents the stepwise amplification of protein factors needed to form blood clots. It is indicated to reduce the risk of stroke and systemic embolism (SE) in patients with nonvalvular atrial fibrillation (NVAF) and for the treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE) following 5-10 days of initial therapy with a parenteral anticoagulant. Traditionally, warfarin, a vitamin K antagonist, was used for stroke prevention in these individuals but effective use of this drug is limited by it's delayed onset, narrow therapeutic window, need for regular monitoring and INR testing, and numerous drug-drug and drug-food interactions. This has prompted enthusiasm for newer agents such as dabigatran, apixaban, and rivaroxaban for effective clot prevention. In addition to once daily dosing, the benefits over warfarin also include significant reductions in hemorrhagic stroke and GI bleeding, and improved compliance, which is beneficial as many patients will be on lifelong therapy. Edoxaban is indicated for reducing the risk of stroke and systemic embolism (SE) in patients with nonvalvular atrial fibrillation (NVAF). However, it should not be used in patients with creatinine clearance (CrCL) > 95 mL/min because of increased risk of ischemic stroke compared to warfarin at the highest dose studied (60 mg). It is also indicated for the treatment of deep vein thrombosis (DVT) and pulmonary embolism (PE) following 5-10 days of initial therapy with a parenteral anticoagulant. Administration of edoxaban results in prolongation of clotting time tests such as aPTT (activated partial thromboplastin time), PT (prothrombin time), and INR (international normalized ratio). Edoxaban is a selective inhibitor of factor Xa, a serine endopeptidase of the clotting cascade required for cleavage of prothrombin into thrombin.",The molecular weight is 548.06.,Edoxaban has a topological polar surface area of 136.63.,The log p value of  is 0.15.,Edoxaban is approved.,Edoxaban is a solid.,True
16668,"Since it's earliest discovery in salmon rine sperm heads in the late 1800's to its formal introduction via US FDA approval in 1939, protamine sulfate has occupied an important therapeutic niche as perhaps the only viable option for reversing the anticoagulant effect of heparin use for over 77 years. Subsequently, because most invasive surgical procedures involve the routine use of heparin to prevent potentially surgery-complicating blood clotting, most cases of major bleeding in these frequent procedures are managed with the use of protamine sulfate. The agent elicits this heparin reversal predominantly via the formation of an inactive complex between the anionic nature of heparin and its own cationic state. Protamine sulfate is indicated for counteracting or reversing the anticoagulant effect of heparin as necessary. Such reversal may, for example, be required often before surgery; after renal hemodialysis; post open heart surgery; whenever excessive bleeding results from heparin use; and/or for the treatment of heparin overdosage, among other similar or related circumstances. When not complexed with heparin, protamine sulfate by itself demonstrates a weak anticoagulant effect and also evidently prolongs the euglycaemic phase of the human body when used as an excipient in certain injectable insulin formulations. Furthermore, some animal studies have suggested that the long-term oral administration of protamine sulfate may favourably decrease serum lipid concentrations, presumably by enhancing the actions of the carnitine palmitoyltransferase-2 and acyl-CoA oxidase enzymes. Related studies have also shown that protamine sulfate may be able to decrease intestinal fat absorption and might possess certain antibacterial effects. It is generally understood that, when administered as an antidote to heparin, protamine sulfate is a fairly strong basic protein that subsequently binds with strongly acidic heparin to produce a stable and inactive complex (salt). This inactive complex between protamine sulfate and heparin neutralizes the anticoagulant effect of both solitary protamine and heparin. In this way, protamine sulfate is used as an effective antidote to reverse the activity of heparin, and is useful for treating hemorrhage as a result of severe heparin or low-molecular weight heparin overdosage. Moreover, protamine sulfate is also frequently used in the same manner to neutralize the effect of heparin given before surgery and during extracorporeal circulation procedures like those performed in hemodialysis or cardiac surgery. ",,,,Protamine sulfate is approved.,Protamine sulfate is a solid.,True
16669,"Bemiparin is an antithrombotic and belongs to the group of drugs known as the low molecular weight heparins (LMWH). Like semuloparin, bemiparin is classified as an ultra-LMH because of its low mean molecular mass of 3600 daltons, which is a unique property of this class. These heparins have lower anti-thrombin activity than the traditional low molecular weight heparins and act mainly on factor-Xa, reducing the risk of bleeding due to selectivity for this specific clotting factor. Interestingly, current research is underway for the potential benefit of bemiparin in the treatment of tumors and diabetic foot ulcers. Bemiparin is indicated in the following cases: To prevent blood clots in the veins after general abdominal surgery in patients with a moderate risk of venous thromboembolism; in the prevention of the thromboembolic disease in non-surgical patients; prevention of clotting in the extracorporeal circuit during hemodialysis; to prevent blood clots in the veins after a major orthopedic surgery in patients with high risk of venous thromboembolism; secondary prevention of venous thromboembolism; recurrence in patients with deep vein thrombosis; transient prevention and treatment of deep vein thrombosis (DVT). Bemiparin is an anticoagulant classified under the broad category of low molecular weight heparins.  This drug is a second-generation low molecular weight heparin (LMWH). It has a very low mean molecular weight (3600 Dalton), a long half-life (5.3 hrs) and a large anti-Xa: anti-IIa ratio (8:1). The mechanism of action of bemiparin is inhibition of factor Xa, which is a necessary step in the clotting cascade. Factor-Xa is necessary for the propagation of a thrombus.",,,,Bemiparin is approved and investigational.,Bemiparin is a solid.,True
16670,"Coagulation factor VII is human serine protease type enzyme that is involved in the extrinsic coagulation cascade which results in blood clotting. May be administered in cases of uncontrolled bleeding. Factor VII alone can be used in the treatment of congenital hemophilia A or B, acquired hemophilia, congenital factor VII deficiency, and Glanzmann's thrombasthenia. Off label use in the treatment of refractory bleeding after cardiac surgery and warfarin related intracerebral hemorrhage. Brands for human factor VII are currently only in combination with other vitamin K coagulation factors and can be used to reverse vitamin K antagonist activity in patients with acute major bleeds or for urgent surgery/invasive procedures.  Human Factor VII complexes with tissue factor resulting in its activation to VIIa. It is the activated Factor VIIa that then binds to Factor X activating it to Factor Xa, as well as coagulation Factor IX is activated to Factor IXa. Factor Xa continues the coagulation cascade to eventually convert prothrombin to thrombin, which leads to the formation of a clot by converting fibrinogen to fibrin. Factor VII is required in the extrinsic clotting cascade. When there is vascular damage tissue factor (TF) is released which then interacts with Factor VII resulting in the formation of the activated complex VIIa. Factor VIIa then continues to activate coagulation factors in the cascade until a clot is formed.",,,,Coagulation factor VII human is approved and investigational.,Coagulation factor VII human is a solid.,True
16671,"Emicizumab is a humanized recombinant monoclonal antibody that mimics the function of the coagulation Factor VIII and it has the capacity to bind simultaneously to activated Factor IX and Factor X. The ability of Emicizumab to bind to all these three different factors allows it to overcome immunogenicity and unstable hemostatic efficacy produced by previous Factor VII agents. Emicizumab was originated as an improved form of hBS23 and it was approved on November 16, 2017. It was created by Chugai Pharmaceuticals Co. Ltd. and co-developed with Roche and Genentech. The main function of Emicizumab is the prevention of bleeding episodes. Thus, Emicizumab is approved for the routine prophylaxis to prevent or reduce the frequency of bleeding episodes of adult and pediatric patients with hemophilia A with or without Factor VIII inhibitors. Emicizumab mimics the function of coagulation factor VIII, therefore it binds to the activated form of Factor IX (Factor IXa). This binding forms a complex that will later bind to the X factor of the coagulation factor. The ability of Emicizumab to interact with both factors (Factor IXa and Factor X) activates the coagulation cascade that will subsequently lead to the segmentation of fibrinogen into fibrin and the formation of blood clots. The effect of Emicizumab is translated into the restoration of the blood coagulation process and, therefore, in the reduction of hemorrhagic episodes. The activity of emicizumab can also produce changes in activated clotting time (ACT), activated partial thromboplastin time (aPTT) and one-step Factor VIII activity. In addition, the unique bispecific structure of Emicizumab prevents the formation of Factor VIII inhibitors or their effect.  Emicizumab exerts its action by performing the function of the coagulation Factor VIII without presenting a structural homology. It presents a dual specificity which allows it to bind to both the Factor IXa and Factor X, performing the required bridging activity for the launch of the coagulation cascade. ",,,,Emicizumab is approved and investigational.,Emicizumab is a liquid.,True
16672,"Baclofen is a gamma-aminobutyric acid (GABA) agonist used as a skeletal muscle relaxant used for the relief of painful and uncomfortable muscle spasms caused by a variety of conditions. It is known to be particularly useful in treating muscle spasticity associated with spinal cord injury.  Baclofen is administered for the relief of signs and symptoms of spasticity resulting from multiple sclerosis, particularly for the relief of flexor spasms and associated pain and clonus, in addition to muscular rigidity. In neurological diseases associated with spasm of the skeletal muscles, the clinical effects of baclofen occur due to baclofen action on reflex muscle contractions and of significant relief from painful spasm, automatism, as well as clonus. Baclofen, when used as indicated, improves mobility, increasing levels of independence, and facilitates both passive and active physiotherapy. Baclofen also stimulates gastric acid secretion. The exact mechanism of action of baclofen is not fully understood at this time ,. Many studies indicate that baclofen is a GABA-B receptor agonist , , , ,. Despite this, there is no conclusive evidence that the effects of baclofen on GABA systems are involved in the production of its clinical effects.  ",The molecular weight is 213.66.,Baclofen has a topological polar surface area of 63.32.,The log p value of  is -0.62.,Baclofen is approved.,Baclofen is a solid.,True
16673,"Progabide is an analog and prodrug of gamma-aminobutyric acid. It is commonly used in the treatment of epilepsy. It has agonistic activity for both the GABAA and GABAB receptors. In clinical trials, progabide has been investigated for Parkinson's disease, schizophrenia, clinical depression and anxiety disorder; its therapeutic effectiveness in these conditions is not fully elucidated. Indicated for the treatment of epilepsy. Progabide, a fatty acid derivative, is a GABA receptor agonist used to treat the symptoms of epilepsy. Progabide binds to both GABA<sub>A</sub> and GABA<sub>B</sub> receptors located on the terminals of primary afferent fibers. Binding to GABA<sub>A</sub> results in an increased affinity of the GABA receptor for the amino acid, an augmented flux of chloride ions across the terminal membrane, and an increase in the amount of presynaptic inhibition. Activation of the GABA<sub>B</sub> receptors retards the influx of calcium ions into the terminals, thereby reducing the evoked release of excitatory amino acids and possibly other transmitters.",The molecular weight is 334.78.,Progabide has a topological polar surface area of 75.68.,The log p value of  is 2.9.,Progabide is experimental.,Progabide is a solid.,True
16674,The most common inhibitory neurotransmitter in the central nervous system.,The molecular weight is 103.12.,gamma-Aminobutyric acid has a topological polar surface area of 63.32.,The log p value of  is -2.77.,gamma-Aminobutyric acid is approved and investigational.,gamma-Aminobutyric acid is a solid.,True
16675,"SGS-742 has been used in trials studying the treatment of Seizures and Metabolic Disease. Investigated for use/treatment in alzheimer's disease, attention deficit/hyperactivity disorder (ADHD), memory loss, and schizophrenia and schizoaffective disorders. SGS742 blocks the late inhibitory postsynaptic potential and the paired-pulse inhibition of population spikes recorded from CA1 pyramidal neurons of the hippocampus of rats in vitro and in vivo. SGS742 significantly enhances the release of glutamate, aspartate, glycine and somatostatin in vivo. Chronic administration of SGS742 causes an up-regulation of GABA(B) receptors in the frontal cortex of rats. Single doses cause a significant enhancement of the mRNA and protein levels of NGF and BDNF in the cortex and hippocampus of rats.",,,,SGS-742 is investigational.,SGS-742 is a solid.,True
16676,"Tezampanel is an AMPA receptor antagonist. Investigated for use/treatment in pain (acute or chronic) and migraine and cluster headaches. NGX426 is a prodrug of tezampanel (NGX424). Tezampanel is an antagonist that binds to glutamate kainate (Glu K5) receptors, inhibiting excitatory synapases the brain. ",,,,Tezampanel is investigational.,Tezampanel is a solid.,True
16677,"Arbaclofen, or STX209, is the R-enantiomer of baclofen. It is believed to be a selective gamma-amino butyric acid type B receptor agonist, and has been investigated as a treatment for autism spectrum disorder and fragile X syndrome in randomized, double blind, placebo controlled trials. It has also been investigated as a treatment for spasticity due to multiple sclerosis and spinal cord injury. Arbaclofen was investigated as a treatment for gastroesophageal reflux disease (GERD); however, with disappointing results. Investigated in clinical trials as a potential treatment for spasticity in multiple sclerosis, autism spectrum disorder, and social withdrawal in fragile X syndrome. Arbaclofen, or R-baclofen, acts upstream of the mGluR5 receptor to increase inhibitory neurotransmission. It is the isomer of baclofen which harbors antispastic activity. ",,,,Arbaclofen is investigational.,Arbaclofen is a solid.,True
16678,"Arbaclofen Placerbil is a prodrug of Arbaclofen, which is a selective gamma-amino-butyric acid type B receptor agonist and the R-enantiomer of baclofen. It was discovered, and has been patented by XenoPort as a new chemical entity with an improved pharmacokinetic profile compared to baclofen, which allows for sustained release properties.  Investigated for the treatment of spasticity in multiple sclerosis, acute back spasms, and GERD.  R-baclofen is postulated to aid in spasticity by acting as an agonist of the inhibitory gamma aminobutyric acid neurotransmission pathway. ",,,,Arbaclofen Placarbil is investigational.,Arbaclofen Placarbil is a solid.,True
16679,"Calcium plays a vital role in the anatomy, physiology and biochemistry of organisms and of the cell, particularly in signal transduction pathways. The skeleton acts as a major mineral storage site for the element and releases Ca2+ ions into the bloodstream under controlled conditions. Circulating calcium is either in the free, ionized form or bound to blood proteins such as serum albumin. Although calcium flow to and from the bone is neutral, about 5 mmol is turned over a day. Bone serves as an important storage point for calcium, as it contains 99% of the total body calcium. Low calcium intake may also be a risk factor in the development of osteoporosis. The best-absorbed form of calcium from a pill is a calcium salt like carbonate or phosphate. Calcium gluconate and calcium lactate are absorbed well by pregnant women. Seniors absorb calcium lactate, gluconate and citrate better unless they take their calcium supplement with a full breakfast. Calcium plays a vital role in the anatomy, physiology and biochemistry of organisms and of the cell, particularly in signal transduction pathways. It is vital in cell signaling, muscular contractions, bone health, and signalling cascades. Calcium (Ca2+) plays a pivotal role in the physiology and biochemistry of organisms and the cell. It plays an important role in signal transduction pathways, where it acts as a second messenger, in neurotransmitter release from neurons, contraction of all muscle cell types, and fertilization. Many enzymes require calcium ions as a cofactor, those of the blood-clotting cascade being notable examples. Extracellular calcium is also important for maintaining the potential difference across excitable cell membranes, as well as proper bone formation. Calcium plays a vital role in the anatomy, physiology and biochemistry of organisms and of the cell, particularly in signal transduction pathways. More than 500 human proteins are known to bind or transport calcium.  The skeleton acts as a major mineral storage site for the element and releases Ca2+ ions into the bloodstream under controlled conditions. Circulating calcium is either in the free, ionized form or bound to blood proteins such as serum albumin. Parathyroid hormone (secreted from the parathyroid gland) regulates the resorption of Ca2+ from bone. Calcitonin stimulates incorporation of calcium in bone, although this process is largely independent of calcitonin. Although calcium flow to and from the bone is neutral, about 5 mmol is turned over a day. Bone serves as an important storage point for calcium, as it contains 99% of the total body calcium. Low calcium intake may also be a risk factor in the development of osteoporosis. The best-absorbed form of calcium from a pill is a calcium salt like carbonate or phosphate. Calcium gluconate and calcium lactate are absorbed well by pregnant women. Seniors absorb calcium lactate, gluconate and citrate better unless they take their calcium supplement with a full breakfast. The currently recommended calcium intake is 1,500 milligrams per day for women not taking estrogen and 800 milligrams per day for women on estrogen. There is close to 300 milligrams of calcium in one cup of fluid milk. Calcium carbonate is currently the best and least expensive form of calcium supplement available.",,,,Calcium is nutraceutical.,Calcium is a solid.,True
16680,"A non-essential amino acid that is involved in the metabolic control of cell functions in nerve and brain tissue. It is biosynthesized from aspartic acid and ammonia by asparagine synthetase. (From Concise Encyclopedia Biochemistry and Molecular Biology, 3rd ed) Used for nutritional supplementation, also for treating dietary shortage or imbalance. A non-essential amino acid. Asparagine is critical for the production of the body's proteins, enzymes and muscle tissue. Supplements of this amino acid are claimed to balance nervous system function. Asparagine, a non-essential amino acid is important in the metabolism of toxic ammonia in the body through the action of asparagine synthase which attaches ammonia to aspartic acid in an amidation reaction. Asparagine is also used as a structural component in many proteins.",The molecular weight is 132.12.,Asparagine has a topological polar surface area of 106.41.,The log p value of  is -3.54.,Asparagine is approved and investigational and nutraceutical.,Asparagine is a solid.,True
16681,,,,,"10-Propargyl-5,8-Dideazafolic Acid is experimental.","10-Propargyl-5,8-Dideazafolic Acid is a solid.",False
16682,Tretazicar is under investigation in clinical trial NCT00746590 (Study of Anti-tumour Effects and Safety of Prolarix™ in Hepatocellular Carcinoma).,,,,Tretazicar is investigational.,Tretazicar is a solid.,True
16683,,,,,"(3S)-3-hydroxy-1-methyl-2,3-dihydro-1H-indole-5,6-dione is experimental.","(3S)-3-hydroxy-1-methyl-2,3-dihydro-1H-indole-5,6-dione is a solid.",False
16684,,,,,N-acetamide is experimental.,N-acetamide is a solid.,False
16685,,,,,"5,8-dimethoxy-1,4-dimethylquinolin-2(1H)-one is experimental.","5,8-dimethoxy-1,4-dimethylquinolin-2(1H)-one is a solid.",False
16686,Casimiroin is a quinone reductase 2 inhibitor isolated from _Casimiroa edulis_.,,,,Casimiroin is experimental.,Casimiroin is a solid.,True
16687,"Fosinopril is a phosphinic acid-containing ester prodrug that belongs to the angiotensin-converting enzyme (ACE) inhibitor class of medications. It is rapidly hydrolyzed to fosinoprilat, its principle active metabolite. Fosinoprilat inhibits ACE, the enzyme responsible for the conversion of angiotensin I (ATI) to angiotensin II (ATII). ATII regulates blood pressure and is a key component of the renin-angiotensin-aldosterone system (RAAS). Fosinopril may be used to treat mild to moderate hypertension, as an adjunct in the treatment of congestive heart failure, and to slow the rate of progression of renal disease in hypertensive individuals with diabetes mellitus and microalbuminuria or overt nephropathy. For treating mild to moderate hypertension, use as an adjunct in treating congestive heart failure, and may be used to slow the rate of progression of renal disease in hypertensive individuals with diabetes mellitus and microalbuminuria or overt nephropathy.  Following oral administration, fosinopril is rapidly and completely hydrolyzed to its principle active metabolite, fosinoprilat. Hydrolysis is thought to occur in the gastrointestinal mucosa and liver. Fosinoprilat is a competitive inhibitor of ACE, a peptidyl dipeptidase that is part of the RAAS. The RAAS is a homeostatic mechanism for regulating hemodynamics, water and electrolyte balance. During sympathetic stimulation or when renal blood pressure or blood flow is reduced, renin is released from the granular cells of the juxtaglomerular apparatus in the kidneys. In the blood stream, renin cleaves circulating angiotensinogen to ATI, which is subsequently cleaved to ATII by ACE. ATII increases blood pressure using a number of mechanisms. First, it stimulates the secretion of aldosterone from the adrenal cortex. Aldosterone travels to the distal convoluted tubule (DCT) and collecting tubule of nephrons where it increases sodium and water reabsorption by increasing the number of sodium channels and sodium-potassium ATPases on cell membranes. Second, ATII stimulates the secretion of vasopressin (also known as antidiuretic hormone or ADH) from the posterior pituitary gland. ADH stimulates further water reabsorption from the kidneys via insertion of aquaporin-2 channels on the apical surface of cells of the DCT and collecting tubules. Third, ATII increases blood pressure through direct arterial vasoconstriction. Stimulation of the Type 1 ATII receptor on vascular smooth muscle cells leads to a cascade of events resulting in myocyte contraction and vasoconstriction. In addition to these major effects, ATII induces the thirst response via stimulation of hypothalamic neurons. ACE inhibitors inhibit the rapid conversion of ATI to ATII and antagonize RAAS-induced increases in blood pressure. ACE (also known as kininase II) is also involved in the enzymatic deactivation of bradykinin, a vasodilator. Inhibiting the deactivation of bradykinin increases bradykinin levels and may further sustain the effects of fosinoprilat by causing increased vasodilation and decreased blood pressure.  There are two isoforms of ACE: the somatic isoform, which exists as a glycoprotein comprised of a single polypeptide chain of 1277; and the testicular isoform, which has a lower molecular mass and is thought to play a role in sperm maturation and binding of sperm to the oviduct epithelium. Somatic ACE has two functionally active domains, N and C, which arise from tandem gene duplication. Although the two domains have high sequence similarity, they play distinct physiological roles. The C-domain is predominantly involved in blood pressure regulation while the N-domain plays a role in hematopoietic stem cell differentiation and proliferation. ACE inhibitors bind to and inhibit the activity of both domains, but have much greater affinity for and inhibitory activity against the C-domain. Fosinoprilat, the active metabolite of fosinopril, competes with ATI for binding to ACE and inhibits and enzymatic proteolysis of ATI to ATII. Decreasing ATII levels in the body decreases blood pressure by inhibiting the pressor effects of ATII as described in the Pharmacology section above. Fosinoprilat also causes an increase in plasma renin activity likely due to a loss of feedback inhibition mediated by ATII on the release of renin and/or stimulation of reflex mechanisms via baroreceptors. ",The molecular weight is 563.67.,Fosinopril has a topological polar surface area of 110.21.,The log p value of  is 7.44.,Fosinopril is approved.,Fosinopril is a solid.,True
16688,"Candoxatril is the orally-active prodrug of candoxatrilat (UK-73967), a potent neutral endopeptidase (NEP) inhibitor. Neutral endopeptidase inhibitors such as Candoxatril have a dual mechanism of action. They inhibit two metalloprotease enzymes, neutral endopeptidase and ACE, resulting in an increased availability of natriuretic peptides that exhibit vasodilatory effects and, possibly, tissue protective effects.",,,,Candoxatril is experimental.,Candoxatril is a solid.,True
16689,"Moexipril is a non-sulfhydryl containing precursor of the active angiotensin-converting enzyme (ACE) inhibitor moexiprilat. It is used to treat high blood pressure (hypertension). It works by relaxing blood vessels, causing them to widen. Lowering high blood pressure helps prevent strokes, heart attacks and kidney problems. For the treatment of hypertension. Moexipril is a non-sulfhydryl containing precursor of the active angiotensin-converting enzyme (ACE) inhibitor moexiprilat. It is used to treat high blood pressure (hypertension). It works by relaxing blood vessels, causing them to widen. Lowering high blood pressure helps prevent strokes, heart attacks and kidney problems. Moexipril is a prodrug for moexiprilat, which inhibits ACE in humans and animals. The mechanism through which moexiprilat lowers blood pressure is believed to be primarily inhibition of ACE activity. ACE is a peptidyl dipeptidase that catalyzes the conversion of the inactive decapeptide angiotensin I to the vasoconstrictor substance angiotensin II. Angiotensin II is a potent peripheral vasoconstrictor that also stimulates aldosterone secretion by the adrenal cortex and provides negative feedback on renin secretion. ACE is identical to kininase II, an enzyme that degrades bradykinin, an endothelium-dependent vasodilator. Moexiprilat is about 1000 times as potent as moexipril in inhibiting ACE and kininase II. Inhibition of ACE results in decreased angiotensin II formation, leading to decreased vasoconstriction, increased plasma renin activity, and decreased aldosterone secretion. The latter results in diuresis and natriuresis and a small increase in serum potassium concentration (mean increases of about 0.25 mEq/L were seen when moexipril was used alone). Whether increased levels of bradykinin, a potent vasodepressor peptide, play a role in the therapeutic effects of moexipril remains to be elucidated. Although the principal mechanism of moexipril in blood pressure reduction is believed to be through the renin-angiotensin-aldosterone system, ACE inhibitors have some effect on blood pressure even in apparent low-renin hypertension.",The molecular weight is 498.58.,Moexipril has a topological polar surface area of 114.4.,The log p value of  is 1.39.,Moexipril is approved.,Moexipril is a solid.,True
16690,"Lisinopril is an angiotensin converting enzyme inhibitor (ACEI) used to treat hypertension, heart failure, and myocardial infarction. Lisinopril and are the only ACEIs that are not prodrugs. It functions by inhibition of angiotensin converting enzyme as well as the renin angiotensin aldosterone system. ACEIs are commonly used as a first line therapy in the treatment of hypertension, along with thiazide diuretics or beta blockers. Lisinopril is indicated for the treatment of acute myocardial infarction, hypertension in patients ≥6 years, and as an adjunct therapy for heart failure. A combination product with hydrochlorothiazide is indicated for the treatment of hypertension. Lisinopril is an angiotensin converting enzyme inhibitor used to treat hypertension, heart failure, and myocardial infarction. Lisinopril is not a prodrug, and functions by inhibition of angiotensin converting enzyme as well as the renin angiotensin aldosterone system. It has a wide therapeutic index and a long duration of action as patients are generally given 10-80mg daily. Angiotensin II constricts coronary blood vessels and is positively inotropic, which under normal circumstances, would increase vascular resistance and oxygen consumption. This action can eventually lead to myocyte hypertrophy and vascular smooth muscle cell proliferation.",The molecular weight is 405.5.,Lisinopril has a topological polar surface area of 132.96.,The log p value of  is -1.82.,Lisinopril is approved and investigational.,Lisinopril is a solid.,True
16691,"Omapatrilat is an investigational drug that inhibits both neutral endopeptidase (NEP) and angiotensin converting enzyme (ACE). The inhibition of NEP elevates natriuretic peptide levels, increasing excretion of sodium in urine, dilating blood vessels, and reducing preload and ventricular remodeling. This drug from BMS was not approved by the FDA due to angioedema safety concerns. For the treatment of hypertension. Omapatrilat is used to treat hypertension. Vasopeptidase inhibitor that simultaneously inhibits angiotensin-converting enzyme (ACE) and neutral endopeptidase (NEP). Omapatrilat lowers blood pressure by inhibiting the action of the angiotensin converting enzyme (ACE), which causes blood vessels to constrict. But unlike other drugs, omapatrilat also inhibits another enzyme known as neutral endopeptidase (NEP), which helps blood vessels relax. Omapatrilat demonstrated greater reduction in blood pressure than the ACE inhibitor lisinopril in individuals with salt-sensitive hypertension who typically do not respond well to ACE inhibitors. Omapatrilat binds to both angiotensin converting enzyme and neutral endopeptidase. This results in a decrease renin-angiotensin-aldosterone production and increase natriuretic peptidase circulation.",The molecular weight is 408.53.,Omapatrilat has a topological polar surface area of 86.71.,The log p value of  is 2.84.,Omapatrilat is investigational.,Omapatrilat is a solid.,True
16692,"Rescinnamine is an angiotensin-converting enzyme inhibitor used as an antihypertensive drug. It is an alkaloid obtained from _Rauwolfia serpentina_ and other species of _Rauwolfia_. For the treatment of hypertension. Used to treat hypertension. Rescinnamine inhibits angiotensin-converting enzyme. ACE is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. Angiotensin II also stimulates aldosterone secretion by the adrenal cortex and general vasoconstriction, both of which lead to increases vascular resistance. By inhibiting angiotensin II, aldosterone reabsorption is decreased as well as vasoconstriction. This combined effect serves to decrease blood pressure. Rescinnamine Binds to and inhibits the angiotensin converting enzyme. Rescinnamine competes with angiotensin I for binding at the angiotensin-converting enzyme, blocking the conversion of angiotensin I to angiotensin II. Inhibition of ACE results in decreased plasma angiotensin II. As angiotensin II is a vasoconstrictor and a negative-feedback mediator for renin activity, lower concentrations result in a decrease in blood pressure and stimulation of baroreceptor reflex mechanisms, which leads to decreased vasopressor activity and to decreased aldosterone secretion.",The molecular weight is 634.73.,Rescinnamine has a topological polar surface area of 117.78.,The log p value of  is 4.12.,Rescinnamine is approved.,Rescinnamine is a solid.,True
16693,"Cilazapril is an ACE inhibtor class drug used in the treatment of hypertension and heart failure. It belongs to the angiotensin-converting enzyme inhibitors (ACE inhibitors) class of drugs. It is a prodrug that is hydrolyzed after absorption to its main metabolite cilazaprilat. It is branded as Inhibace in Canada and other countries, Vascace and Dynorm in a number of European countries, among many other names. None of these varieties are available in the United States. Cilazapril is an ACE inhibtor class drug used in the treatment of hypertension and heart failure. Cilazapril inhibits the production angiotensin II. By doing so, it decreases sodium and water reabsorption (via aldosterone) and it decreases vasoconstriction. The combined effect of this is a decrease in vascular resistance, and therefore, blood pressure. The absolute bioavailability of cilazaprilat after oral administration of cilazapril is 57% based on urinary recovery data. (The absolute bioavailability of cilazaprilat after oral administration of cilazaprilat is 19%.) Ingestion of food immediately before the administration of cilazapril reduces the average peak plasma concentration of cilazaprilat by 29%, delays the peak by one hour and reduces the bioavailability of cilazaprilat by 14%. These pharmacokinetic changes have little influence on plasma ACE inhibition.  Cilazapril is a pyridazine ACE inhibitor. It competes with angiotensin I for binding at the angiotensin-converting enzyme, blocking the conversion of angiotensin I to angiotensin II. As angiotensin II is a vasoconstrictor and a negative feedback mediator for renin activity, lower angiotensin II levels results in a decrease in blood pressure, an increase in renin activity, and stimulation of baroreceptor reflex mechanisms. Kininase II, an enzyme which degrades the vasodilator bradykinin, is identical to ACE and may also be inhibited.",The molecular weight is 417.51.,Cilazapril has a topological polar surface area of 99.18.,The log p value of  is 1.47.,Cilazapril is approved.,Cilazapril is a solid.,True
16694,"Spirapril is an ACE inhibitor antihypertensive drug used to treat hypertension. Spirapril is converted to the active spiraprilat after administration. ACE inhibitors are used primarily in treatment of hypertension and congestive heart failure. Spirapril is an ACE inhibitor class drug used to treat hypertension. Spirapril is an angiotensin-converting enzyme (ACE) inhibitor. ACE is a peptidyl dipeptidase that catalyzes the conversion of angiotensin I to the vasoconstrictor substance, angiotensin II. By blocking ACE, spirapril decreases angiotensin II which is a vasoconstrictor and inducer of aldosterone. So by inhibiting the enzymes, aldosterone secreation is decreased (so less sodium is reabsorbed) and there is a decrease in vasoconstriction. Combined, this leades to a decrease in blood pressure. Spiraprilat, the active metabolite of spirapril, competes with angiotensin I for binding at the angiotensin-converting enzyme, blocking the conversion of angiotensin I to angiotensin II. Inhibition of ACE results in decreased plasma angiotensin II. As angiotensin II is a vasoconstrictor and a negative-feedback mediator for renin activity, lower concentrations result in a decrease in blood pressure and stimulation of baroreceptor reflex mechanisms, which leads to decreased vasopressor activity and to decreased aldosterone secretion. Spiraprilat may also act on kininase II, an enzyme identical to ACE that degrades the vasodilator bradykinin.",The molecular weight is 466.61.,Spirapril has a topological polar surface area of 95.94.,The log p value of  is 1.05.,Spirapril is approved.,Spirapril is a solid.,True
16695,,,,,Epicaptopril is experimental.,Epicaptopril is a solid.,False
16696,The N-acetyl derivative of glucosamine.,,,,N-acetyl-alpha-D-glucosamine is experimental.,N-acetyl-alpha-D-glucosamine is a solid.,True
16697,"Temocapril is a prodrug-type angiotensin-I converting enzyme (ACE) inhibitor not approved for use in the United States, but is approved in Japan and South Korea. Temocapril can also be used in hemodialysis patients without risk of serious accumulation.  Temocapril is an ACE inhibitor primarily indicated in the treatment of hypertension and congestive heart failure, diabetic nephropathy, and improvement of prognosis for coronary artery diseases (including acute myocardial infarction).  Temocapril is a prodrug of its active metabolite (and diacid form) temocaprilat which contains a thiazepine ring. Temocaprilat has slightly higher potency than enalaprilat in ACE inhibition isolated from rabbit lung. ACE inhibitors exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility.). When compared with other Angiotensin-converting Enzyme Inhibitors, temocapril's advantages include a rapid onset of action and what research suggests is tighter vascular ACE binding than enalaprilat. ",The molecular weight is 476.61.,Temocapril has a topological polar surface area of 95.94.,The log p value of  is 2.1.,Temocapril is experimental and investigational.,Temocapril is a solid.,True
16698,"Enalaprilat is the active metabolite of the orally available pro-drug,. Used in the treatment of hypertension, enalapril is an ACE inhibitor that prevents Angiotensin Converting Enzyme (ACE) from transforming angiotensin I into angiotensin II. As angiotensin II is responsible for vasoconstriction and sodium reabsorption in the proximal tubule of the kidney, down-regulation of this protein results in reduced blood pressure and blood fluid volume. Enalaprilat was originally created to overcome the limitations of the first ACE inhibitor, captopril, which had numerous side effects and left a metallic taste in the mouth. Removal of the problematic thiol group from captopril resulted in enalaprilat, which was then modified further with an ester to create the orally available pro-drug enalapril. Enalaprilat injection is indicated for the treatment of hypertension when oral therapy is not practical. Enalaprilat injection results in the reduction of both supine and standing systolic and diastolic blood pressure, usually with no orthostatic component. Symptomatic postural hypotension is therefore infrequent, although it might be anticipated in volume-depleted patients. The onset of action usually occurs within fifteen minutes of administration with the maximum effect occurring within one to four hours. The abrupt withdrawal of enalaprilat has not been associated with a rapid increase in blood pressure. Enalaprilat is the active metabolite of the orally available pro-drug, enalapril. Used in the treatment of hypertension, enalapril is an ACE inhibitor that prevents Angiotensin Converting Enzyme (ACE) from transforming angiotensin I into angiotensin II. As angiotensin II is responsible for vasoconstriction and sodium reabsorption in the proximal tubule of the kidney, down-regulation of this protein results in reduced blood pressure and blood fluid volume",The molecular weight is 348.4.,Enalaprilat has a topological polar surface area of 106.94.,The log p value of  is 0.75.,Enalaprilat is approved.,,True
16699,Zofenopril is employed as both a cardioprotective and anti-hypertensive agent. It is an angiotensin-converting enzyme (ACE) inhibitor.,The molecular weight is 429.55.,Zofenopril has a topological polar surface area of 74.68.,The log p value of  is 4.68.,Zofenopril is approved.,Zofenopril is a solid.,True
16700,,,,,Cilazaprilat is experimental.,,False
16701,,,,,4-Iodopyrazole is experimental.,4-Iodopyrazole is a solid.,False
16702,,,,,N-Cyclopentyl-N-Cyclobutylformamide is experimental.,N-Cyclopentyl-N-Cyclobutylformamide is a solid.,False
16703,,,,,Tryptophanyl-5'amp is experimental.,Tryptophanyl-5'amp is a solid.,False
16704,,,,,Tryptophanamide is experimental.,Tryptophanamide is a solid.,False
16705,"As a diuretic, cyclothiazide inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like cyclothiazide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of cyclothiazide is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle. Cyclothiazide is indicated as adjunctive therapy in edema associated with congestive heart failure, hepatic cirrhosis, and corticosteroid and estrogen therapy. It is also indicated in the management of hypertension either as the sole therapeutic agent or to enhance the effectiveness of other antihypertensive drugs in the more severe forms of hypertension. Cyclothiazide is indicated as adjunctive therapy in edema associated with congestive heart failure, hepatic cirrhosis, and corticosteroid and estrogen therapy. It is also indicated in the management of hypertension either as the sole therapeutic agent or to enhance the effectiveness of other antihypertensive drugs in the more severe forms of hypertension. Like other thiazides, cyclothiazide promotes water loss from the body (diuretics). It inhibits Na<sup>+</sup>/Cl<sup>-</sup> reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue. Cyclothiazide affects the distal renal tubular mechanism of electrolyte reabsorption. At maximal therapeutic dosages, all thiazides are approximately equal in their diuretic efficacy. Cyclothiazide increases excretion of sodium and chloride in approximately equivalent amounts. Natriuresis may be accompanied by some loss of potassium and bicarbonate. Hydrochlorothiazide, a thiazide diuretic, inhibits water reabsorption in the nephron by inhibiting the sodium-chloride symporter (SLC12A3) in the distal convoluted tubule, which is responsible for 5% of total sodium reabsorption. Normally, the sodium-chloride symporter transports sodium and chloride from the lumen into the epithelial cell lining the distal convoluted tubule. The energy for this is provided by a sodium gradient established by sodium-potassium ATPases on the basolateral membrane. Once sodium has entered the cell, it is transported out into the basolateral interstitium via the sodium-potassium ATPase, causing an increase in the osmolarity of the interstitium, thereby establishing an osmotic gradient for water reabsorption. By blocking the sodium-chloride symporter, hydrochlorothiazide effectively reduces the osmotic gradient and water reabsorption throughout the nephron.Hydrochlorothiazide, a thiazide diuretic, inhibits water reabsorption in the nephron by inhibiting the sodium-chloride symporter (SLC12A3) in the distal convoluted tubule, which is responsible for 5% of total sodium reabsorption. Normally, the sodium-chloride symporter transports sodium and chloride from the lumen into the epithelial cell lining the distal convoluted tubule. The energy for this is provided by a sodium gradient established by sodium-potassium ATPases on the basolateral membrane. Once sodium has entered the cell, it is transported out into the basolateral interstitium via the sodium-potassium ATPase, causing an increase in the osmolarity of the interstitium, thereby establishing an osmotic gradient for water reabsorption. By blocking the sodium-chloride symporter, hydrochlorothiazide effectively reduces the osmotic gradient and water reabsorption throughout the nephron.",The molecular weight is 389.87.,Cyclothiazide has a topological polar surface area of 118.36.,The log p value of  is 1.98.,Cyclothiazide is approved.,Cyclothiazide is a solid.,True
16706,"Tyrosine is a non-essential amino acid. In animals it is synthesized from. It is also the precursor of , thyroid hormones, and melanin. Tyrosine is claimed to act as an effective antidepressant, however results are mixed. Tyrosine has also been claimed to reduce stress and combat narcolepsy and chronic fatigue, however these claims have been refuted by some studies. Tyrosine is a nonessential amino acid synthesized in the body from phenylalanine. Tyrosine is critical for the production of the body's proteins, enzymes and muscle tissue. Tyrosine is a precursor to the neurotransmitters norepinephrine and dopamine. It can act as a mood elevator and an anti-depressant. It may improve memory and increase mental alertness. Tyrosine aids in the production of melanin and plays a critical role in the production of thyroxin (thyroid hormones). Tyrosine deficiencies are manifested by hypothyroidism, low blood pressure and low body temperature. Supplemental tyrosine has been used to reduce stress and combat narcolepsy and chronic fatigue. Tyrosine is produced in cells by hydroxylating the essential amino acid phenylalanine. This relationship is much like that between cysteine and methionine. Half of the phenylalanine required goes into the production of tyrosine; if the diet is rich in tyrosine itself, the requirements for phenylalanine are reduced by about 50%. The mechanism of L-tyrosine's antidepressant activity can be accounted for by the precursor role of L-tyrosine in the synthesis of the neurotransmitters norepinephrine and dopamine. Elevated brain norepinephrine and dopamine levels are thought to be associated with antidepressant effects.",The molecular weight is 181.19.,Tyrosine has a topological polar surface area of 83.55.,The log p value of  is -2.22.,Tyrosine is approved and investigational and nutraceutical.,Tyrosine is a solid.,True
16707,,,,,Tyrosinal is experimental.,Tyrosinal is a solid.,False
16708,,,,,N6-ISOPENTENYL-ADENOSINE-5'-MONOPHOSPHATE is experimental.,N6-ISOPENTENYL-ADENOSINE-5'-MONOPHOSPHATE is a solid.,False
16709,,,,,p-Benzoyl-L-phenylalanine is experimental.,p-Benzoyl-L-phenylalanine is a solid.,False
16710,,,,,"4-(2,2,2-TRIFLUOROETHYL)-L-PHENYLALANINE is experimental.","4-(2,2,2-TRIFLUOROETHYL)-L-PHENYLALANINE is a solid.",False
16711,"Implitapide is a microsomal triglyceride transfer protein (MTP)-inhibitor. For the treatment of atherosclerosis. Implitapide is an inhibitor of microsomal triglyceride transfer protein (MTP), a key enzyme involved in the assembly and release of cholesterol and triglyceride from the liver and intestinal tract. It is being investigated for the treatment of atherosclerosis. MTP mediates triglyceride absorption and chylomicron secretion from the intestine and very-low-density lipoprotein (VLDL) secretion from the liver by linking lipid molecules with apolipoprotein B (apoB). Inhibition of MTP reduces the level of all apoB-containing lipoproteins, including LDL.",,,,Implitapide is investigational.,Implitapide is a solid.,True
16712,"SLx-4090 is a microsomal triglyceride transfer protein (MTTP) inhibitor potentially for the treatment of type 2 diabetes.  Investigated for use/treatment in hyperlipidemia. SLx-4090 inhibits Microsomal Triglyceride Transfer Protein (MTP). It acts selectively in the enterocytes lining the gastrointestinal tract, preventing the formation of chylomicrons which are used to transport triglyceride (TG) and cholesterol into the systemic circulation.",,,,SLx-4090 is investigational.,SLx-4090 is a solid.,True
16713,"An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. L-Threonine makes up collagen, elastin, and enamel protein. It aids proper fat metabolism in the liver, helps the digestive and intestinal tracts function more smoothly, and assists in metabolism and assimilation. L-Threonine is an essential amino acid that helps to maintain the proper protein balance in the body. It is important for the formation of collagen, elastin, and tooth enamel, and aids liver and lipotropic function when combined with aspartic acid and methionine. L-Threonine is a precursor to the amino acids glycine and serine. It acts as a lipotropic in controlling fat build-up in the liver. May help combat mental illness and may be very useful in indigestion and intestinal malfunctions. Also, threonine prevents excessive liver fat. Nutrients are more readily absorbed when threonine is present.",The molecular weight is 119.12.,Threonine has a topological polar surface area of 83.55.,The log p value of  is -2.5.,Threonine is approved and nutraceutical.,Threonine is a solid.,True
16714,"Tyloxapol is a non-ionic detergent often used as a surfactant. Tyloxapol is an inhaled surfactant that assists in removing and liquefying and removing bronchopulmonary secretions with mucus and pus. Tyloxapol is administered either through nebulized solution or a stream of oxygen. Also investigated for use/treatment in cystic fibrosis and pediatric indications. It is used as a surfactant to aid liquefaction and removal of mucopurulent (containing mucus and pus) bronchopulmonary secretions. Tyloxapol also blocks plasma lipolytic activity, and thus the breakdown of triglyceride-rich lipoproteins. Tyloxapol, when injected IP, blocks plasma lipolytic activity, and thus the breakdown of triglyceride-rich lipoproteins. It has also been shown to be inhibitor of lipoprotein lipase, thus preventing triglyceride uptake.",,,,Tyloxapol is approved and investigational.,Tyloxapol is a liquid.,True
16715,"Fibrinolysin (also known as bovine plasmin) is a bovine enzyme derived from bovine plasma or extracted from bacterial cultures. It is a globular protein with a molecular weight of ~90,000 daltons. Fibrinolysin consists of two polypeptide chains, one light and one heavy, linked by a disulfide bond. The light chain has a molecular weight of approximately 27,000 Da and contains the active center of Fibrinolysin; the heavy chain has a molecular weight of approximately 57,000 Da. Fibrinolysin is used as a local healing ointment when combined together with the enzyme deoxyribonuclease I (extracted from bovine pancreas). Fibrinolysin and deoxyribonuclease both act as lytic enzymes. The combination is available as ointment containing 1 BU (Biological Unit) Fibrinolysin and 666 BUs desoxyribonuclease per gram. The ointment is marketed by Pfizer under the brand name Fibrolan in a variety of countries (e.g. Switzerland). It is currently not approved in the USA. Fibrinolysin assists with the healing of minor burns, superficial wounds, ulcers, surgical wounds, and superficial hematomas. Fibrinolysin attacks and inactivates fibrin molecules occurring in undesirable exudates on the surface of the human body and on human mucosa, e.g., in superficial wounds and burns, while desoxyribonuclease targets and destroys (human) DNA. The combination of the two enzymes has a synergistic effect on necrotic but not on living tissue.",,,,Fibrinolysin is investigational.,Fibrinolysin is a liquid.,True
16716,"CVT-6883 is a selective, potent and orally available A2B-adenosine receptor antagonist which CV Therapeutics is investigating for the potential treatment of asthma and other conditions related to inflammation and fibrosis. Investigated for use/treatment in asthma.",,,,CVT-6883 is investigational.,CVT-6883 is a solid.,True
16717,"A combination of DHA (a natural fatty acid) and paclitaxel (an anticancer drug) being studied in the treatment of cancer. It is a type of mitotic inhibitor. Investigated for use/treatment in breast cancer, colorectal cancer, gastric cancer, kidney cancer, lung cancer, pancreatic cancer, prostate cancer, and skin cancer. A prodrug comprised of the naturally occurring omega-3 fatty acid docosahexaenoic acid (DHA) covalently conjugated to the anti-microtubule agent paclitaxel. Because tumor cells take up DHA, DHA-paclitaxel is delivered directly to tumor tissue, where the paclitaxel moiety binds to tubulin and inhibits the disassembly of microtubules, thereby resulting in the inhibition of cell division. Paclitaxel also induces apoptosis by binding to and blocking the function of the apoptosis inhibitor protein Bcl-2 (B-cell Leukemia 2). DHA-paclitaxel exhibits improved pharmacokinetic and toxicity profiles when compared to conventional paclitaxel and has demonstrated antineoplastic activity in animal models of cancer.",,,,Paclitaxel docosahexaenoic acid is investigational.,Paclitaxel docosahexaenoic acid is a solid.,True
16718,Investigated for use/treatment in cancer/tumors (unspecified). HE3235 is a second generation antitumor agent that causes apoptosis (cell death). HE3235 inhibits the BCL2 gene which translates proteins that prevent apoptosis and stimulates the expression proteins that induce apoptosis. HE3235 also downregulates the gene that codes for the multi-drug resistant protein ABCG2 (BCRP1 – Breast Cancer Resistance Protein1).,,,,Apoptone is investigational.,Apoptone is a solid.,True
16719,Isosorbide is an organic nitrate with vasodilatory properties on both arteries and veins. Indicated for the prevention and treatment of angina pectoris due to coronary artery disease. The onset of action of oral isosorbide mononitrate is not sufficiently rapid for this product to be useful in aborting an acute anginal episode.,The molecular weight is 146.14.,Isosorbide has a topological polar surface area of 58.92.,The log p value of  is -1.53.,Isosorbide is approved and investigational.,,True
16720,"Obatoclax has been used in trials studying the treatment of AML, Leukemia, Myelofibrosis, Hodgkin's Lymphoma, and Mantle-Cell Lymphoma, among others. Obatoclax binds anti-apoptotic Bcl-2 proteins and interferes with their ability to interact with pro-apoptotic proteins.",,,,Obatoclax is investigational.,,True
16721,"Navitoclax has been used in trials studying the treatment and basic science of Solid Tumors, Non-Hodgkin's Lymphoma, EGFR Activating Mutation, Chronic Lymphoid Leukemia, and Hematological Malignancies, among others. Navitoclax targets the Bcl-2 family of proteins, the major negative regulators of apoptosis. The Bcl-2 proteins, including Bcl-2, Bcl-xL, and Bcl-w, work by binding to two other groups of proteins-the executioners (Bax, Bak) that actually start the destruction pathway, and the sentinel proteins. Cancer cells frequently overexpress the Bcl-2-like proteins, and thus, when they sustain DNA damage-from radiation, for example-they continue growing. Preventing the Bcl-2-like proteins from binding to the executioners might be able to trigger cell death in the tumor.",,,,Navitoclax is investigational.,,True
16722,"MLN-977 is a small molecule compound that inhibits the production of leukotrienes, especially 5-lipoxygenase. It is developed by PharmaEngine to treat asthma and chronic obstructive pulmonary disease. Investigated for use/treatment in asthma and chronic obstructive pulmonary disease (COPD). MLN977 is a second generation compound in the class of asthma therapies known as 5-LO inhibitors, which block the production of leukotrienes. Leukotrienes are major mediators of the inflammatory response.",,,,MLN-977 is investigational.,MLN-977 is a solid.,True
16723,"Diacerein is a prodrug which is metabolized to rhein. It is currently approved in France for the treatment of osteoarthritis although the use of diacerein is restricted due to the side effects including sevre diarrhea. Diacerein is under investigation for the treatment of Insulin Resistance, Diabetes Mellitus (Type 2), and Diabetes-Related Complications. For the treatment of osteoarthritis affecting the hip or knee. Decreases inflammation and cartilage destruction and also corrects altered osteoblast acitivity . Diacerein's active metabolite rhein reduces cartilage destruction by decreasing expression of matrix metalloproteinase (MMP)-1 and -3 as well as upregulating tissue inhibitor of matrix metalloproteinases which serve to reduce the activity of several MMPs. The anti-inflammatory action of rhein reduces the level of interleukin-1beta activity which plays a large role in reduction of extracellular matrix production, MMP activity, and continued inflammation. Rhein reduces abnormal osteoblast synthetic activity through an unknown mechanism.",The molecular weight is 368.3.,Diacerein has a topological polar surface area of 124.04.,The log p value of  is 2.13.,Diacerein is approved and investigational.,,True
16724,"Guvacine is a pyridine alkaloid found in the Areca nut (also known as the Betel nut). It is an experimental drug with no approved indication. Experimental studies are still being investigated to determine all of the physiological effects and mechanisms of action of guvacine. Currently it has been determined that guvacine is a specific GABA reuptake inhibitor with no significant affinity at GABA receptors.  There is no approved indication for guvacine. Experimental studies are still being investigated to determine all of the physiological effects of guvacine. Experimental studies are still being investigated to determine the exact mechanisms of action of guvacine. What is known is that guvacine binds selectively to presynaptic GABA reuptake transporters and prevents the reuptake of GABA, but has no affinity for GABA postsynaptic receptors.",,,,Guvacine is experimental.,Guvacine is a solid.,True
16725,,,,,"2,6-Diamino-(S)-9-Purine is experimental.","2,6-Diamino-(S)-9-Purine is a solid.",False
16726,,,,,Immucillin-G is experimental.,Immucillin-G is a solid.,False
16727,,,,,Guanine is experimental.,Guanine is a solid.,False
16728,,,,,"2-Amino-7--1,7-Dihydro-Purin-6-One is experimental.","2-Amino-7--1,7-Dihydro-Purin-6-One is a solid.",False
16729,Peldesine is a potent inhibitor of human CCRF-CEM T-cell proliferation. It has undergone phase I trials for the treatment of Human Immunodeficiency Virus (HIV) infections.,,,,Peldesine is investigational.,Peldesine is a solid.,True
16730,,,,,9-deazainosine is experimental.,9-deazainosine is a solid.,False
16731,"Guanosine is a nucleoside comprising guanine attached to a ribose (ribofuranose) ring via a β-N9-glycosidic bond. Guanosine can be phosphorylated to become GMP (guanosine monophosphate), cGMP (cyclic guanosine monophosphate), GDP (guanosine diphosphate) and GTP (guanosine triphosphate) which are factors in signal transduction pathways.",,,,Guanosine is experimental and investigational.,Guanosine is a solid.,True
16732,,,,,Ribose-1-Phosphate is experimental.,Ribose-1-Phosphate is a solid.,False
16733,,,,,"(3R,4R)-3-Hydroxy-4-(hydroxymethyl)-1-pyrimidin-7-yl)methyl]pyrrolidinium is experimental.","(3R,4R)-3-Hydroxy-4-(hydroxymethyl)-1-pyrimidin-7-yl)methyl]pyrrolidinium is a solid.",False
16734,3'-deoxyguanosine is a solid. This compound belongs to the purine nucleosides and analogues. These are compounds comprising a purine base attached to a sugar. This medication targets the protein purine nucleoside phosphorylase.,,,,3'-deoxyguanosine is experimental.,3'-deoxyguanosine is a solid.,True
16735,,,,,"(2S,3R,4S,5S)-3,4-Dihydroxy-2--5-(4-oxo-4,5-dihydro-1H-pyrrolopyrimidin-7-yl)pyrrolidinium is experimental.","(2S,3R,4S,5S)-3,4-Dihydroxy-2--5-(4-oxo-4,5-dihydro-1H-pyrrolopyrimidin-7-yl)pyrrolidinium is a solid.",False
16736,,,,,"9-(5,5-Difluoro-5-Phosphonopentyl)Guanine is experimental.","9-(5,5-Difluoro-5-Phosphonopentyl)Guanine is a solid.",False
16737,,,,,"9-DEAZAINOSINE-2',3'-O-ETHYLIDENEPHOSPHONATE is experimental.","9-DEAZAINOSINE-2',3'-O-ETHYLIDENEPHOSPHONATE is a solid.",False
16738,,,,,"GUANOSINE-2',3'-O-ETHYLIDENEPHOSPHONATE is experimental.","GUANOSINE-2',3'-O-ETHYLIDENEPHOSPHONATE is a solid.",False
16739,,,,,"GUANOSINE-2',3'-O-METHYLIDENEPHOSPHONATE is experimental.","GUANOSINE-2',3'-O-METHYLIDENEPHOSPHONATE is a solid.",False
16740,"Forodesine is a highly potent, orally active, rationally designed PNP inhibitor that has shown activity in preclinical studies with malignant cells and clinical utility against T-cell acute lymphoblastic leukemia and cutaneous T-cell lymphoma. Additional preliminary findings support its use for the management of some B-cell malignancies. Investigated for use/treatment in lymphoma (non-hodgkin's) and leukemia (lymphoid).",The molecular weight is 266.26.,Forodesine has a topological polar surface area of 129.97.,The log p value of  is -2.47.,Forodesine is investigational.,Forodesine is a solid.,True
16741,"Azelaic acid is a saturated dicarboxylic acid found naturally in wheat, rye, and barley. It is also produced by _Malassezia furfur_, also known as _Pityrosporum ovale_, which is a species of fungus that is normally found on human skin. Azelaic acid is effective against a number of skin conditions, such as mild to moderate acne, when applied topically in a cream formulation of 20%. It works in part by stopping the growth of skin bacteria that cause acne, and by keeping skin pores clear. Azelaic acid's antimicrobial action may be attributable to inhibition of microbial cellular protein synthesis. For the topical treatment of mild-to-moderate inflammatory acne vulgaris. Azelaic acid is a saturated dicarboxylic acid found naturally in wheat, rye, and barley. It is a natural substance that is produced by <i>Malassezia furfur</i> (also known as <i>Pityrosporum ovale</i>), a yeast that lives on normal skin. It is effective against a number of skin conditions, such as mild to moderate acne, when applied topically in a cream formulation of 20%. It works in part by stopping the growth of skin bacteria that cause acne, and by keeping skin pores clear. Azelaic acid's antimicrobial action may be attributable to inhibition of microbial cellular protein synthesis. The exact mechanism of action of azelaic acid is not known. It is thought that azelaic acid manifests its antibacterial effects by inhibiting the synthesis of cellular protein in anaerobic and aerobic bacteria, especially <i>Staphylococcus epidermidis</i> and <i>Propionibacterium acnes</i>. In aerobic bacteria, azelaic acid reversibly inhibits several oxidoreductive enzymes including tyrosinase, mitochondrial enzymes of the respiratory chain, thioredoxin reductase, 5-alpha-reductase, and DNA polymerases. In anaerobic bacteria, azelaic acid impedes glycolysis. Along with these actions, azelaic acid also improves acne vulgaris by normalizing the keratin process and decreasing microcomedo formation. Azelaic acid may be effective against both inflamed and noninflamed lesions. Specifically, azelaic acid reduces the thickness of the stratum corneum, shrinks keratohyalin granules by reducing the amount and distribution of filaggrin (a component of keratohyalin) in epidermal layers, and lowers the number of keratohyalin granules.",The molecular weight is 188.22.,Azelaic acid has a topological polar surface area of 74.6.,The log p value of  is 1.56.,Azelaic acid is approved.,Azelaic acid is a solid.,True
16742,"Monobenzone is the monobenzyl ether of hydroquinone used medically for depigmentation. Monobenzone occurs as a white, almost tasteless crystalline powder, soluble in alcohol and practically insoluble in water. It exerts a depigmenting effect on skin of mammals by increasing the excretion of melanin from the melanocytes. It may also cause destruction of melanocytes and permanent depigmentation. Used topically to treat the loss of skin color (vitiligo). Monobenzone is the monobenzyl ether of hydroquinone. Monobenzone, applied topically to the skin, is used as a depigmenting agent inhibitting melanin&nbsp;produced by polymerization of oxidation products of tyrosine and dihydroxyphenyl compounds. Monobenzone works by permanently removing color from normal skin located around skin with vitiligo. Monobenzone is a depigmenting agent whose mechanism of action is not fully understood. It is proposed that it increases the excretion of melanin from the melanocytes. This effect is erratic and may take one to four months to occur while existing melanin is lost with normal sloughing of the stratum corneum. Hyperpigmented skin appears to fade more rapidly than does normal skin, and exposure to sunlight reduces the depigmenting effect of the drug. Following skin depigmentation after topical application of monobenzone, the histological studies indicate similar results as that seen in vitiligo, where the epidermis is intact but with the absence of identifiable melanocytes. ",The molecular weight is 200.24.,Monobenzone has a topological polar surface area of 29.46.,The log p value of  is 3.34.,Monobenzone is approved.,Monobenzone is a solid.,True
16743,"Mimosine is an antineoplastic alanine-substituted pyridine derivative isolated from _Leucena glauca_. Mimosine inhibits DNA synthesis at the level of elongation of nascent chains by altering deoxyribonucleotide metabolism. It arrests the cell cycle in the late G(1) phase. Mimosine causes inhibition of DNA replication, changes in the progression of the cells in the cell cycle, and apoptosis. Mimosine appears to introduce breaks into DNA. Mimosine is an iron/zinc chelator. Iron depletion induces DNA double-strand breaks in treated cells, and activates a DNA damage response that results in focal phosphorylation of histones. This leads to inhibition of DNA replication and/or DNA elongation. Some studies indicate that mimosine prevents the initiation of DNA replication, whereas other studies indicate that mimosine disrupts elongation of the replication fork by impairing deoxyribonucleotide synthesis by inhibiting the activity of the iron-dependent enzyme ribonucleotide reductase and the transcription of the cytoplasmic serine hydroxymethyltransferase gene (SHMT). Inhibition of serine hydroxymethyltransferase is moderated by a zinc responsive unit located in front of the SHMT gene.",The molecular weight is 198.18.,Mimosine has a topological polar surface area of 103.86.,The log p value of  is -4.07.,Mimosine is experimental.,Mimosine is a solid.,True
16744,"Hexylresorcinol is a substituted dihydroxybenzene. It exhibits antiseptic, anthelmintic, and local anesthetic properties. It can be found in topical applications for minor skin infections and in oral solutions or throat lozenges for pain relief and first aid antiseptic. Hexylresorcinol is predominantly employed as the active ingredient in lotions, sprays, or lozenges indicated as a (a) topical antiseptic to help prevent skin infection in minor cuts, scrapes, or burns, or (b) as an antiseptic and local anesthetic for the relief of a sore throat and its associated pain. Hexylresorcinol is a phenol derivative, and in typical therapeutic usage is primarily a local anesthetic for topical use on the mucous membranes of the mouth and throat. The local anesthetic like properties of hexylresorcinol is likely due to its sodium channel blocking effects. The agent also demonstrates mild antiseptic activity as well as an apparent anti-inflammatory, demulcent action. When acting as an oral anesthetic for relieving sore throats, it is generally believed that hexylresorcinol is possibly capable of blocking voltage-gated neuronal sodium channels, which in turn would inhibit the initiation and conduction of nerve impulses for feeling or transmitting pain signals in the local area to which the hexylresorcinol is applied.",The molecular weight is 194.27.,Hexylresorcinol has a topological polar surface area of 40.46.,The log p value of  is 3.9.,Hexylresorcinol is approved.,,True
16745,,,,,(4e)-4-Aminohex-4-Enoic Acid is experimental.,(4e)-4-Aminohex-4-Enoic Acid is a solid.,False
16746,,,,,4-Amino Hexanoic Acid is experimental.,4-Amino Hexanoic Acid is a solid.,False
16747,"Lapachone has been used in trials studying the treatment of Cancer, Carcinoma, Advanced Solid Tumors, Head and Neck Neoplasms, and Carcinoma, Squamous Cell.",,,,Lapachone is investigational.,,True
16748,,,,,"6-Aminohexyl-uridine-C1,5'-diphosphate is experimental.","6-Aminohexyl-uridine-C1,5'-diphosphate is a solid.",False
16749,,,,,N-acetyl-beta-D-glucosaminyl-(1->4)-N-acetyl-beta-D-glucosamine is experimental.,N-acetyl-beta-D-glucosaminyl-(1->4)-N-acetyl-beta-D-glucosamine is a solid.,False
16750,"5'-Uridylic acid. A uracil nucleotide containing one phosphate group esterified to the sugar moiety in the 2', 3' or 5' position.",,,,Uridine monophosphate is experimental.,Uridine monophosphate is a solid.,True
16751,,,,,2-(N-morpholino)ethanesulfonic acid is experimental.,2-(N-morpholino)ethanesulfonic acid is a solid.,False
16752,"Investigated for use/treatment in hepatitis (viral, C). The prodrug taribavirin (1-b-D-ribofuranosyl-1H-1, 2, 4-triazole-3-carboxamidine) is a synthetic nucleoside (guanosine) analog under development for the treatment of patients with chronic hepatitis C. Taribavirin is metabolized by the liver and converted into its active metabolite, ribavirin. This pathway reduces exposure to red blood cells (RBCs) and increases exposure to the liver, the site of HCV replication. Ribavirin is readily phosphorylated intracellularly by adenosine kinase to ribavirin mono-, di-, and triphosphate metabolites. Ribavirin triphosphate (RTP) is a potent competitive inhibitor of inosine monophosphate (IMP) dehydrogenase, viral RNA polymerase and messenger RNA (mRNA) guanylyltransferase (viral). Guanylyltranserase inhibition stops the capping of mRNA. These diverse effects result in a marked reduction of intracellular guanosine triphosphate (GTP) pools and inhibition of viral RNA and protein synthesis. Ribavirin is also incorporated into the viral genome causing lethal mutagenesis and a subsequent decrease in specific viral infectivity.",The molecular weight is 243.22.,Taribavirin has a topological polar surface area of 150.5.,The log p value of  is -3.27.,Taribavirin is investigational.,Taribavirin is a solid.,True
16753,"Lenalidomide (initially known as CC-5013 and marketed as Revlimid® by Celgene) is a derivative of thalidomide introduced in 2004. It was initially intended as a treatment for multiple myeloma, for which thalidomide is an accepted therapeutic modality, but has also shown efficacy in the hematological disorders known as the myelodysplastic syndromes. FDA approved on December 27, 2005. Lenalidomide is indicated for the treatment of multiple myeloma in combination with dexamethasone. It is also indicated for the treatment of patients with transfusion-dependent anemia due to low- or intermediate- risk myelodysplastic syndromes (MDS) associated with a deletion 5q cytogenetic abnormality with or without additional cytogenetic abnormalities. Lenalidomide, a thalidomide analogue, is an immunomodulatory agent possessing immunomodulatory and antiangiogenic properties. Lenalidomide inhibits the secretion of pro-inflammatory cytokines and increases the secretion of anti-inflammatory cytokines from peripheral blood mononuclear cells. Lenalidomide inhibits cell proliferation with varying effectiveness (IC50s) in some but not all cell lines. Lenalidomide is effective in inhibiting growth of Namalwa cells (a human B cell lymphoma cell line with a deletion of one chromosome 5) but is much less effective in inhibiting growth of KG-1 cells (human myeloblastic cell line, also with a deletion of one chromosome 5) and other cell lines without chromosome 5 deletions. Lenalidomide does not prolong the QTc interval.  The mechanism of action of lenalidomide remains to be fully characterized, however it has been demonstrated that lenalidomide inhibits the expression of cyclooxygenase-2 (COX-2), but not COX-1, in vitro. In vivo it induces tumor cell apoptosis directly and indirectly by inhibition of bone marrow stromal cell support, by anti-angiogenic and anti-osteoclastogenic effects, and by immunomodulatory activity",The molecular weight is 259.26.,Lenalidomide has a topological polar surface area of 92.5.,The log p value of  is -0.41.,Lenalidomide is approved.,Lenalidomide is a solid.,True
16754,"Ginseng is promoted as an adaptogen (a product that increases the body's resistance to stress), one which can to a certain extent be supported with reference to its anticarcinogenic and antioxidant properties. Ginseng is also known to contain phytoestrogens.",,,,Ginseng is approved and investigational and nutraceutical.,Ginseng is a solid.,True
16755,,,,,1-Phenylsulfonamide-3-Trifluoromethyl-5-Parabromophenylpyrazole is experimental.,1-Phenylsulfonamide-3-Trifluoromethyl-5-Parabromophenylpyrazole is a solid.,False
16756,A cyclic endoperoxide intermediate produced by the action of CYCLOOXYGENASE on ARACHIDONIC ACID. It is further converted by a series of specific enzymes to the series 2 prostaglandins. ,,,,Prostaglandin G2 is experimental.,Prostaglandin G2 is a solid.,True
16757,Firocoxib is a cycooxygenase-2 (COX-2) selective non-steroidal anti-inflammatory drug. It currently approved for veterinary use in dogs and horses under the brand names Equioxx and Previcox. Firocoxib was the first COX-2 inhibitor approved by the U.S. Food and Drug Administration for horses. Firocoxib is not intended or approved for use in human medicine. Used for the treatment of pain inflammation and fever in horses and dogs.,,,,Firocoxib is experimental and vet_approved.,Firocoxib is a solid.,True
16758,"Alclofenac is a non-steroidal anti-inflammatory drug. It was withdrawn from the market in the United Kingdom in 1979. Alclofenac is indicated in rheumatology, in particular for the treatment of rheumatoid arthritis, ankylosing spondylitis and, as an analgesic, in painful arthritic pathologies. Alclofenac is an inhibitor of prostaglandin H2 synthase. The inhibition of the enzyme occurs through the reversible block of cyclooxygenase enzyme. Therefore, it prevents the production of inflammatory mediators (and pain) as prostacyclins and prostaglandins. Aclofenac has the ability to inhibit the biosynthesis of prostaglandins which may be an important factor in the action of these drugs, but in addition,  the effect of these agents in displacing endogenous anti-inflammatory substances from plasma protein binding sites is thought to be an equally important effect in their mechanism of action",The molecular weight is 226.66.,Alclofenac has a topological polar surface area of 46.53.,The log p value of  is 2.73.,Alclofenac is approved and withdrawn.,Alclofenac is a solid.,True
16759,,,,,Canavanine is experimental.,Canavanine is a solid.,False
16760,,,,,"1,2,4-Triazole-Carboxamidine is experimental.","1,2,4-Triazole-Carboxamidine is a solid.",False
16761,,,,,"S,S'-(1,4-Phenylene-Bis(1,2-Ethanediyl))Bis-Isothiourea is experimental.","S,S'-(1,4-Phenylene-Bis(1,2-Ethanediyl))Bis-Isothiourea is a solid.",False
16762,,,,,2-Aminothiazoline is experimental.,2-Aminothiazoline is a solid.,False
16763,,,,,Se-Ethyl-Isoselenourea is experimental.,Se-Ethyl-Isoselenourea is a solid.,False
16764,,,,,"2,4-Diamino-6-Phenyl-5,6,7,8,-Tetrahydropteridine is experimental.","2,4-Diamino-6-Phenyl-5,6,7,8,-Tetrahydropteridine is a solid.",False
16765,,,,,"N1,N14-Bis((S-Methyl)Isothioureido)Tetradecane is experimental.","N1,N14-Bis((S-Methyl)Isothioureido)Tetradecane is a solid.",False
16766,,The molecular weight is 138.0.,Cacodylic acid has a topological polar surface area of 37.3.,The log p value of  is -0.54.,Cacodylic acid is experimental.,Cacodylic acid is a solid.,False
16767,,,,,7-Nitroindazole-2-Carboxamidine is experimental.,7-Nitroindazole-2-Carboxamidine is a solid.,False
16768,,,,,N(G)-Iminoethylornithine is experimental.,N(G)-Iminoethylornithine is a solid.,False
16769,,,,,"5,6-Cyclic-Tetrahydropteridine is experimental.","5,6-Cyclic-Tetrahydropteridine is a solid.",False
16770,,,,,"S,S'-(1,3-Phenylene-Bis(1,2-Ethanediyl))Bis-Isothiourea is experimental.","S,S'-(1,3-Phenylene-Bis(1,2-Ethanediyl))Bis-Isothiourea is a solid.",False
16771,,,,,"6S-5,6,7,8-Tetrahydrobiopterin is experimental.","6S-5,6,7,8-Tetrahydrobiopterin is a solid.",False
16772,,,,,S-(Dimethylarsenic)Cysteine is experimental.,S-(Dimethylarsenic)Cysteine is a solid.,False
16773,,,,,L-homoarginine is experimental.,L-homoarginine is a solid.,False
16774,,,,,S-Isopropyl-Isothiourea is experimental.,S-Isopropyl-Isothiourea is a solid.,False
16775,,,,,N-(Chlorophenyl)-N'-hydroxyguanidine is experimental.,N-(Chlorophenyl)-N'-hydroxyguanidine is a solid.,False
16776,,,,,"(3S,5E)-3-propyl-3,4-dihydrothienooxazepin-5(2H)-imine is experimental.","(3S,5E)-3-propyl-3,4-dihydrothienooxazepin-5(2H)-imine is a solid.",False
16777,,,,,"5-{4-PHENYL}-6-ETHYLPYRIMIDINE-2,4-DIAMINE is experimental.","5-{4-PHENYL}-6-ETHYLPYRIMIDINE-2,4-DIAMINE is a solid.",False
16778,,,,,Dorsomorphin is experimental.,Dorsomorphin is a solid.,False
16779,,,,,"N--2-(1,1'-Biphenyl-4-Ylmethyl)Propanoyl]Alanine is experimental.","N--2-(1,1'-Biphenyl-4-Ylmethyl)Propanoyl]Alanine is a solid.",False
16780,,,,,Phosphoramidon is experimental.,Phosphoramidon is a solid.,False
16781,,,,,N-(3-Phenyl-2-Sulfanylpropanoyl)Phenylalanylalanine is experimental.,N-(3-Phenyl-2-Sulfanylpropanoyl)Phenylalanylalanine is a solid.,False
16782,,,,,-Phe-Ala is experimental.,-Phe-Ala is a solid.,False
16783,"Daglutril is an orally active, mixed neutral endopeptidase/endothelin converting enzyme inhibitor under development for the treatment of essential hypertension and congestive heart failure. Investigated for use/treatment in congestive heart failure and hypertension. SLV306 increased plasma natriuretic peptides and big endothelin-1 levels in a dose-dependent manner, confirming neutral endopeptidase and endothelin-converting enzyme inhibition. The combined inhibition of neutral endopeptidase and endothelin-converting enzyme may be useful in heart failure by reducing right and left cardiac filling pressures",,,,Daglutril is investigational.,Daglutril is a solid.,True
16784,,,,,2--1H-IMIDAZOPYRIDIN-5-IUM is experimental.,2--1H-IMIDAZOPYRIDIN-5-IUM is a solid.,False
16785,A potent inhibitor of membrane metalloendopeptidase (enkephalinase). Thiorphan potentiates morphine-induced analgesia and attenuates naloxone-precipitated withdrawal symptoms.,,,,Thiorphan is experimental.,Thiorphan is a solid.,True
16786,"Sacubitril is a prodrug neprilysin inhibitor used in combination with valsartan to reduce the risk of cardiovascular events in patients with chronic heart failure (NYHA Class II-IV) and reduced ejection fraction. It was approved by the FDA after being given the status of priority review for on July 7, 2015. Used in combination with valsartan to reduce the risk of cardiovascular events in patients with chronic heart failure (NYHA Class II-IV) and reduced ejection fraction. It is usually administered in conjunction with other heart failure therapies, in place of an ACE inhibitor or other ARB. n a 7-day valsartan-controlled study in patients with reduced ejection fraction (HFrEF), administration of sacubitril + valsartan (Entresto) resulted in a significant non-sustained increase in natriuresis, increased urine cGMP, and decreased plasma MR-proANP and NT-proBNP compared to valsartan. In a 21-day study in HFrEF patients, it significantly increased urine ANP and cGMP and plasma cGMP, and decreased plasma NT-proBNP, aldosterone and endothelin-1. In clinical studies, this combination had no effect on QTc interval. Sacubitril's active metabolite, LBQ657 inhibits neprilysin, a neutral endopeptidase that would typically cleave natiuretic peptides, which includes: atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP), and c-type natriuretic peptide (CNP). ANP and BNP are released under atrial and ventricle stress, which activate downstream receptors leading to vasodilation, natriuresis and diuresis. Under normal conditions, neprilysin breaks down other vasodilating peptides and also vasoconstrictors such as angiotensin I and II, endothelin-1 and peptide amyloid beta-protein. Therefore, the inhibition of neprilysin leads to reduced breakdown and increased concentration of endogenous natriuretic peptides in addition to increased levels of vasoconstricting hormones such as angiotensin II. (However, when combined with valsartan, would result in blocking of angiotensin II to its receptor, preventing the vasoconstrictive effects and resulting in a decrease in vascular resistance and blood pressure.) Cardiovascular and renal effects of sacubitril is a result of the increased levels of peptides that are normally degraded by neprilysin. ",The molecular weight is 411.5.,Sacubitril has a topological polar surface area of 92.7.,The log p value of  is 4.47.,Sacubitril is approved.,Sacubitril is a solid.,True
16787,"A dicarboxylic acid monoamide obtained by formal condensation between the amino group of cis-4-aminocyclohexanecarboxylic acid and the cyclopentanecarboxylic acid group of 1-cyclopentanecarboxylic acid. A potent inhibitor of neutral endopeptidase (NEP, neprilysin, EC 3.4.24.11), it is used as its 2,3-dihydro-1H-inden-5-yl ester prodrug in the treatment of chronic heart failure.",,,,Candoxatrilat is experimental.,Candoxatrilat is a solid.,True
16788,"A thiazide diuretic with properties similar to those of hydrochlorothiazide. (From Martindale, The Extra Pharmacopoeia, 30th ed, p825) For use in the management of hypertension either as the sole therapeutic agent or to enhance the effect of other antihypertensive drugs in the more severe forms of hypertension. Also used as adjunctive therapy in edema associated with congestive heart failure, hepatic cirrhosis, and corticosteroid and estrogen therapy. Methyclothiazide, a diuretic-antihypertensive agent, is a member of the benzothiadiazine (thiazide) class of drugs. Methyclothiazide has a per mg natriuretic activity approximately 100 times that of the prototype thiazide, chlorothiazide. At maximal therapeutic dosages, all thiazides are approximately equal in their diuretic/natriuretic effects. Like other benzothiadiazines, methyclothiazide also has antihypertensive properties, and may be used for this purpose either alone or to enhance the antihypertensive action of other drugs. Methyclothiazide appears to block the active reabsorption of chloride and possibly sodium in the ascending loop of Henle, altering electrolyte transfer in the proximal tubule. This results in excretion of sodium, chloride, and water and, hence, diuresis. As a diuretic, methyclothiazide inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like methyclothiazide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of methyclothiazide is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle.",The molecular weight is 360.22.,Methyclothiazide has a topological polar surface area of 109.57.,The log p value of  is 0.94.,Methyclothiazide is withdrawn.,Methyclothiazide is a solid.,True
16789,"Ethoxzolamide is a sulfonamide used as diuretic and in glaucoma. It inhibits carbonic anhydrase activity in proximal renal tubules to decrease reabsorption of water, sodium, potassium, bicarbonate. Its pharmacological activity thus confers the risk for hypokalemia. For use in the treatment of duodenal ulcers, as a diuretic, and in the treatment of glaucoma, and may also be useful in the treatment of seizures associated with epilepsy. Ethoxzolamide is an inhibitor of the carbonic anhydrase enzyme in proximal renal tubules that works by decreasing the reabsorption of water, sodium, potassium, bicarbonate. It also decreases the activity of carbonic anhydrase expressed in the CNS, which leads to increased seizure threshold. Inhibition of carbonic anhydrase in the eye contributes to its effect of reducing intraocular pressure and decreasing aqueous humor.  Ethoxzolamide binds to and inhibits carbonic anhydrase I, which plays an essential role in facilitating the transport of CO2 and H+ in the intracellular space, across biological membranes, and in the layers of the extracellular space. Through inhibition of the enzyme, the balance of applicable membrane equilibrium systems are affected. ",The molecular weight is 258.31.,Ethoxzolamide has a topological polar surface area of 82.28.,The log p value of  is 2.05.,Ethoxzolamide is withdrawn.,Ethoxzolamide is a solid.,True
16790,"Methocarbamol was developed in the early 1950s as a treatment for muscle spasticity and the associated pain. It is a guaiacol glyceryl ether. Methocarbamol tablets and intramuscular injections are indicated in the United States as an adjunct to rest, physical therapy, and other measures for the relief of discomforts associated with acute, painful musculoskeletal conditions. Oral methocarbamol in America may be given up to 1500mg 4 times daily for 2-3 days. Methacarbamol is a skeletal muscle relaxant with an unknown mechanism of action. Methacarbamol has been shown to block spinal polysynaptic reflexes, decrease nerve transmission in spinal and supraspinal polysynaptic pathways, and prolong the refractory period of muscle cells. Methocarbamol does not act as a local anesthetic upon injection. In animal studies, methocarbamol also prevents convulsions after electric shock. The mechanism of action of methocarbamol is thought to be dependant on its central nervous system depressant activity. This action may be mediated through blocking spinal polysynaptic reflexes, decreasing nerve transmission in spinal and supraspinal polysynaptic pathways, and prolonging the refractory period of muscle cells. Methocarbamol has been found to have no effect on contraction of muscle fibres, motor end plates, or nerve fibres.",The molecular weight is 241.24.,Methocarbamol has a topological polar surface area of 91.01.,The log p value of  is 0.15.,Methocarbamol is approved and vet_approved.,Methocarbamol is a solid.,True
16791,"Benzthiazide is used to treat hypertension and edema. Like other thiazides, benzthiazide promotes water loss from the body (diuretics). They inhibit Na+/Cl- reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue. For the treatment of high blood pressure and management of edema. Benzthiazide is used to treat hypertension and edema. Like other thiazides, benzthiazide promotes water loss from the body (diuretics). They inhibit Na<sup>+</sup>/Cl<sup>-</sup> reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue. As a diuretic, benzthiazide inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like benzthiazide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of benzthiazide is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle.",The molecular weight is 431.92.,Benzthiazide has a topological polar surface area of 118.69.,The log p value of  is 2.17.,Benzthiazide is approved.,Benzthiazide is a solid.,True
16792,"A carbonic anhydrase inhibitor that is used as a diuretic and in the treatment of glaucoma. For treatment of chronic open-angle glaucoma and acute angle-closure glaucoma Methazolamide is topical carbonic anhydrase inhibitor. Methazolamide is indicated for the reduction of elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension who are insufficiently responsive to beta-blockers. Methazolamide is a sulfonamide derivative; however, it does not have any clinically significant antimicrobial properties. Although methazolamide achieves a high concentration in the cerebrospinal fluid, it is not-considered an effective anticonvulsant. Methazolamide has a weak and transient diuretic effect, therefore use results in an increase in urinary volume, with excretion of sodium, potassium and chloride. Methazolamide is a potent inhibitor of carbonic anhydrase. Inhibition of carbonic anhydrase in the ciliary processes of the eye decreases aqueous humor secretion, presumably by slowing the formation of bicarbonate ions with subsequent reduction in sodium and fluid transport.",The molecular weight is 236.26.,Methazolamide has a topological polar surface area of 105.19.,The log p value of  is 0.09.,Methazolamide is approved.,Methazolamide is a solid.,True
16793,"A thiazide diuretic with actions and uses similar to those of hydrochlorothiazide. (From Martindale, The Extra Pharmacopoeia, 30th ed, p812) Chlorothiazide is indicated as adjunctive therapy in edema associated with congestive heart failure, hepatic cirrhosis, and corticosteroid and estrogen therapy. It is also indicated in the management of hypertension either as the sole therapeutic agent or to enhance the effectiveness of other antihypertensive drugs in the more severe forms of hypertension. Like other thiazides, chlorothiazide promotes water loss from the body (diuretics). It inhibits Na<sup>+</sup>/Cl<sup>-</sup> reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue. Chlorothiazide affects the distal renal tubular mechanism of electrolyte reabsorption. At maximal therapeutic dosages, all thiazides are approximately equal in their diuretic efficacy. Chlorothiazide increases excretion of sodium and chloride in approximately equivalent amounts. Natriuresis may be accompanied by some loss of potassium and bicarbonate. After oral doses, 10-15 percent of the dose is excreted unchanged in the urine. Chlorothiazide crosses the placental but not the blood-brain barrier and is excreted in breast milk. As a diuretic, chlorothiazide inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like chlorothiazide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of chlorothiazide is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle.",The molecular weight is 295.71.,Chlorothiazide has a topological polar surface area of 118.69.,The log p value of  is -0.29.,Chlorothiazide is approved and vet_approved.,Chlorothiazide is a solid.,True
16794,"Ethinamate is a short-acting sedative-hypnotic medication used to treat insomnia. Like many such similar medications, the regular use of ethinamate can result in the development of drug tolerance in a patient. Nevertheless, the medication itself is generally no longer effective after using it for greater than 7 days. Structurally, it does not resemble the barbituates, but it shares many effects with this class of drugs; the depressant effects of ethinamate are, however, generally milder than those of most barbiturates. Used for the short-term treatment of insomnia, however, it generally has been replaced by other sedative-hypnotic agents. Ethinamate is used to treat insomnia (trouble in sleeping). However, it has generally been replaced by other medicines for the treatment of insomnia. If ethinamate is used regularly (for example, every day) to help produce sleep, it is usually not effective for more than 7 days. Structurally, it does not resemble the barbiturates, but it shares many effects with this class of drugs; the depressant effects of ethinamate are, however, generally milder than those of most barbiturates. Continued and inappropriate use of ethinamate can lead to tolerance and physical dependence, with withdrawal symptoms very similar to those of the barbiturates. The mechanism of action is not known. However, studies have shown that ethinamate inhibits carbonic anhydrases I and II (J Biol Chem. 1992 Dec 15;267(35):25044-50). This inhibition by ethinamate is not sufficiently strong, however, to implicate carbonic anhydrases I and II in the mechanism of action.",The molecular weight is 167.21.,Ethinamate has a topological polar surface area of 52.32.,The log p value of  is 1.74.,Ethinamate is approved and illicit and withdrawn.,Ethinamate is a solid.,True
16795,"A carbonic anhydrase inhibitor that is used in the treatment of glaucoma. For adjunctive treatment of: chronic simple (open-angle) glaucoma, secondary glaucoma, and preoperatively in acute angle-closure glaucoma where delay of surgery is desired in order to lower intraocular pressure Dichlorphenamide is an oral carbonic anhydrase inhibitor indicated for adjunctive treatment of: chronic simple (open-angle) glaucoma, secondary glaucoma, and preoperatively in acute angle-closure glaucoma where delay of surgery is desired in order to lower intraocular pressure. Carbonic anhydrase inhibitors reduce intraocular pressure by partially suppressing the secretion of aqueous humor (inflow). Carbonic anhydrase inhibitors reduce intraocular pressure by partially suppressing the secretion of aqueous humor (inflow), although the mechanism by which they do this is not fully understood. Evidence suggests that HCO<sup>3-</sup> ions are produced in the ciliary body by hydration of carbon dioxide under the influence of carbonic anhydrase and diffuse into the posterior chamber which contains more Na<sup>+</sup> and HCO<sup>3-</sup> ions than does plasma and consequently is hypertonic. Water is then attracted to the posterior chamber by osmosis, resulting in a drop in pressure.",The molecular weight is 305.14.,Diclofenamide has a topological polar surface area of 120.32.,The log p value of  is 0.24.,Diclofenamide is approved and investigational.,Diclofenamide is a solid.,True
16796,"Quinethazone, marketed as Hydromox, is a thiazide diuretic indicated for hypertension. Patients may experience adverse reactions such as dizziness, dry mouth, nausea, and hypokalemia. Used to treat hypertension. Quinethazone is a thiazide diuretic used to treat hypertension. It inhibits Na<sup>+</sup>/Cl<sup>-</sup> reabsorption from the distal convoluted tubules in the kidneys. Thiazides also cause loss of potassium and an increase in serum uric acid. Thiazides are often used to treat hypertension, but their hypotensive effects are not necessarily due to their diuretic activity. Thiazides have been shown to prevent hypertension-related morbidity and mortality although the mechanism is not fully understood. Thiazides cause vasodilation by activating calcium-activated potassium channels (large conductance) in vascular smooth muscles and inhibiting various carbonic anhydrases in vascular tissue. As a diuretic, quinethazone inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like quinethazone also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of quinethazone is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle.",The molecular weight is 289.73.,Quinethazone has a topological polar surface area of 101.29.,The log p value of  is 0.58.,Quinethazone is approved.,Quinethazone is a solid.,True
16797,,,,,N-{2-ETHYL}ACETAMIDE is experimental.,N-{2-ETHYL}ACETAMIDE is a solid.,False
16798,,,,,3-PROPANOIC ACID is experimental.,3-PROPANOIC ACID is a solid.,False
16799,,,,,ETHYL 3-PROPANOATE is experimental.,ETHYL 3-PROPANOATE is a solid.,False
16800,"Sodium Carbonate is the disodium salt of carbonic acid with alkalinizing property. When dissolved in water, sodium carbonate forms carbonic acid and sodium hydroxide. As a strong base, sodium hydroxide neutralizes gastric acid thereby acting as an antacid. Used topically for dermatitides, mouthwash, vaginal douche; veterinary use as emergency emetic.Occasionally, for dermatitides topically as a lotion. Medication (Vet): In solution to cleanse skin, in eczema, to soften scabs of ringworm. Alkalizing buffering action: Sodium bicarbonate is an alkalinizing agent that dissociates to provide bicarbonate ion. Bicarbonate in excess of that needed to buffer hydrogen ions causes systemic alkalinization and, when excreted, urine alkalinization as well.  Carbon dioxide from the tissues diffuses rapidly into red blood cells, where it is hydrated with water to form carbonic acid. This reaction is accelerated by carbonic anhydrase, an enzyme present in high concentrations in red blood cells. The carbonic acid formed dissociates into bicarbonate and hydrogen ions. Most of the bicarbonate ions diffuse into the plasma. Since the ratio of H2CO3 to dissolved CO2 is constant at equilibrium, pH may be expressed in terms of bicarbonate ion concentration and partial pressure of CO2 by means of the Henderson-Hasselbach equation:",The molecular weight is 105.99.,Sodium carbonate has a topological polar surface area of 63.19.,,Sodium carbonate is approved.,,True
16801,"Sodium Sulfate Anhydrous is the anhydrous, sodium salt form of sulfuric acid. Sodium sulfate anhydrous disassociates in water to provide sodium ions and sulfate ions. Sodium ion is the principal cation of the extracellular fluid and plays a large part in the therapy of fluid and electrolyte disturbances. Sodium sulfate anhydrous is an electrolyte replenisher and is used in isosmotic solutions so that administration does not disturb normal electrolyte balance and does not lead to absorption or excretion of water and ions. indicated for bowel cleansing prior to colonoscopy or barium enema X-ray examination. Induces catharsis by the osmotic effects of the unabsorbed sulfate salts and polyethylene glycol (PEG) in the GI tract. Specifically, sulfate salts provide sulfate anions, which are poorly absorbed, and PEG, which is primarily unabsorbed, causes water to be retained in the GI tract resulting in watery diarrhea. MoviPrep produces a watery stool leading to cleansing of the colon. The osmotic activity of polyethylene glycol 3350, sodium sulfate, sodium chloride, potassium chloride, sodium ascorbate, and ascorbic acid, when taken with 1 liter of additional clear fluid, usually results in no net absorption or excretion of ions or water.",The molecular weight is 142.04.,Sodium sulfate has a topological polar surface area of 80.26.,,Sodium sulfate is approved and vet_approved.,,True
16802,"Aurothioglucose, also known as gold thioglucose, was formerly used to treat rheumatoid arthritis. Aurothioglucose is indicated for the adjunctive treatment of early active adult and juvenile type rheumatoid arthritis that is not adequately controlled by other anti-inflammatory agents and conservative measures like salicylate, glucocorticoids, etc.. In chronic, advanced cases of rheumatoid arthritis, such gold therapy is not demonstrated to be as valuable. After administration, patient serum levels of gold rise sharply but decline over the following week. Peak levels with aqueous preparations are higher and decline faster than those with oily preparations. Regular weekly administration produces a continuous rise in the basal value for several months, after which the serum level becomes relatively stable. After a standard weekly dose, considerable individual variation in the levels of gold can be observed. A steady decline in gold levels occurs when the interval between injections is lengthened, and small amounts may be found in the serum for months after discontinuation of therapy. The incidence of toxic reactions is seemingly unrelated to the plasma level of gold, but may perhaps be more associated with the total cumulative content of gold in the body. Rheumatoid arthritis is an autoimmune disease in which the body's immune system mistakenly attacks the lining of various skeletal bone joints of the body. These attacks are facilitated by various pro-inflammatory immune cells and agents like cytokines, histamines, mast cells, macrophages, monocytes, lymphocytes, leukocytes, and many others. The longterm result of this unwanted immune response is chronic inflammation and painful tissue damage. The cause of the malfunctioning immune system in rheumatoid arthritis is unknown and there is no definitive cure for the condition.",The molecular weight is 392.18.,,,Aurothioglucose is approved and withdrawn.,Aurothioglucose is a liquid.,True
16803,"Remikiren is an orally active, high specificity renin inhibitor. For the treatment of hypertension and heart failure Remikiren is an orally available renin inhibitor with an established blood pressure-lowering effect in patients with essential hypertension. No data are available on the renal effects of remikiren in humans. In patients with essential hypertension, a single oral dose of remikiren can induce a renal vasodilation, without affecting the GFR and despite a significant decrease in blood pressure. This systemic and renal hemodynamic response is more pronounced in case of a more activated renin-angiotensin system. Several in vivo experiments have shown that remikiren is specific for renin and does not decrease arterial pressure by an unrelated mechanism.",The molecular weight is 630.85.,Remikiren has a topological polar surface area of 161.48.,The log p value of  is 3.55.,Remikiren is experimental.,Remikiren is a solid.,True
16804,,,,,Isoamyl alcohol is experimental.,Isoamyl alcohol is a solid.,False
16805,,,,,"3-Phenyl-1,2-Propandiol is experimental.","3-Phenyl-1,2-Propandiol is a solid.",False
16806,,,,,2-Methyl-3-(2-Aminothiazolo)Propanal is experimental.,2-Methyl-3-(2-Aminothiazolo)Propanal is a solid.,False
16807,,,,,Enalkiren is experimental.,Enalkiren is a solid.,False
16808,,,,,2-Cyclopropylmethylenepropanal is experimental.,2-Cyclopropylmethylenepropanal is a solid.,False
16809,,,,,"1-Methyl-2-Oxy-5,5-Dimethyl Pyrrolidine is experimental.","1-Methyl-2-Oxy-5,5-Dimethyl Pyrrolidine is a solid.",False
16810,,,,,1-Hydroxy-2-Amino-3-Cyclohexylpropane is experimental.,1-Hydroxy-2-Amino-3-Cyclohexylpropane is a solid.,False
16811,"SPP1148, the most promising compound from a new series of renin inhibitors for the treatment of hypertension and related end-organ disease. Investigated for use/treatment in hypertension.",,,,SPP1148 is investigational.,SPP1148 is a solid.,True
16812,,,,,N-{2-ETHYL}ACETAMIDE is experimental.,N-{2-ETHYL}ACETAMIDE is a solid.,False
16813,,,,,"6-ETHYL-5-PYRIMIDINE-2,4-DIAMINE is experimental.","6-ETHYL-5-PYRIMIDINE-2,4-DIAMINE is a solid.",False
16814,,,,,N-{2-ETHYL}ACETAMIDE is experimental.,N-{2-ETHYL}ACETAMIDE is a solid.,False
16815,,,,,"(2S)-6-(2,4-DIAMINO-6-ETHYLPYRIMIDIN-5-YL)-2-(3,5-DIFLUOROPHENYL)-4-(3-METHOXYPROPYL)-2H-1,4-BENZOXAZIN-3(4H)-ONE is experimental.","(2S)-6-(2,4-DIAMINO-6-ETHYLPYRIMIDIN-5-YL)-2-(3,5-DIFLUOROPHENYL)-4-(3-METHOXYPROPYL)-2H-1,4-BENZOXAZIN-3(4H)-ONE is a solid.",False
16816,,,,,"6-(2,4-DIAMINO-6-ETHYLPYRIMIDIN-5-YL)-4-(3-METHOXYPROPYL)-2,2-DIMETHYL-2H-1,4-BENZOXAZIN-3(4H)-ONE is experimental.","6-(2,4-DIAMINO-6-ETHYLPYRIMIDIN-5-YL)-4-(3-METHOXYPROPYL)-2,2-DIMETHYL-2H-1,4-BENZOXAZIN-3(4H)-ONE is a solid.",False
16817,"6-ethyl-5-pyrimidine-2,4-diamine is a solid. This compound belongs to the phenylquinolines. These are heterocyclic compounds containing a quinoline moiety substituted with a phenyl group. This substance targets the protein renin.",,,,"6-ethyl-5-pyrimidine-2,4-diamine is experimental.","6-ethyl-5-pyrimidine-2,4-diamine is a solid.",True
16818,"Vintafolide is a folate-targeted chemotherapeutic conjugate (folate vitamin + vinca alkaloid) in clinical stage development as a treatment for folate-receptor positive cancers. Investigated for use/treatment in solid tumors. Vintafolide minimizes the off-target toxicity by delivering the vinca molecule directly and specifically to cancer cells that over-express the folate-receptor. Once delivered to the cancer cell surface, Vintafolide is internalized into the cancer cell via endocytosis, a natural cellular process. Once inside the cell, Endocyte’s proprietary linker technology releases the chemotherapy to eliminate the cancer cell.",The molecular weight is 1917.06.,Vintafolide has a topological polar surface area of 716.39.,The log p value of  is 0.0.,Vintafolide is investigational.,Vintafolide is a solid.,True
16819,,,,,Pyridoxamine-5'-Phosphate is experimental.,Pyridoxamine-5'-Phosphate is a solid.,False
16820,"An essential aromatic amino acid that is a precursor of melanin; dopamine; noradrenalin (norepinephrine), and thyroxine. ",,,,D-Phenylalanine is experimental.,D-Phenylalanine is a solid.,True
16821,,,,,N(6)-(pyridoxal phosphate)-L-lysine is experimental.,N(6)-(pyridoxal phosphate)-L-lysine is a solid.,False
16822,,,,,Indoleacetic acid is experimental.,Indoleacetic acid is a solid.,False
16823,"Murine monoclonal antibody specific to CD3 T-cell lymphocyte antigens. More specifically it is a purified murine (mouse) monoclonal antibody, directed against the CD3 (T3) receptor on the surface of human T-cells (T-lymphocytes) cultured using the murine ascites method. Muromonab is 93% monomeric immune globulin G type 2a (IgG2a). For treatment of organ transplant recipients, prevention of organ rejection Used in organ transplant prophylaxis, Muromonab or OKT-3 binds specifically to the CD-3 complex, which is involved in antigen recognition and cell stimulation, on the surface of T lymphocytes. Immediately after administration CD-3-positive T lymphocytes are abruptly removed from circulation. It has been effective in reversing corticosteroid-resistant acute rejection in renal, liver, and cardiac transplant recipients. Muromonab binds to the T-cell surface glycoprotein CD3 epsilon chain. It appears to kill CD-3 positive cells by inducing Fc mediated apoptosis, antibody mediated cytotoxicity and complement-dependent cytotoxicity.",,,,Muromonab is approved and investigational.,Muromonab is a liquid.,True
16824,"Catumaxumab is a trifunctional monoclonal antibody developed for use in cancer treatment. It has affinity for T-cells, accessory immune cells, and cancer cells. Catumaxumab was initially authorized for market by the European Medicines Agency in April 2009 for the treatment of malignant ascites. Its market authorization was withdrawn in the EU in June 2017 at the manufacturer's request due to the company's insolvency. Catumaxumab was approved for market in Canada in May 2012 for the same condition. It is currently available under the brand name Removab. For use in the management of malignant ascites tumours via intraperitoneal infusion where standard therapy is not available or feasible. Catumaxomab brings cancer cells, T cells, and accessory immune cells into close proximity and stimulates activation and of immune cells. This facilitates immune system-mediated destruction of the cancer cells. Catumaxomab contains epitopes for human CD3 and human epithelial cell adehesion molecule. It also has an intact immunoglobulin gamma constant region allowing it to bind to Fcγ I, IIa, and III receptors. By binding to CD3 on killer T cells, EpCAM on cancer cells, and Fcγ receptors on accessory immune cells like macrophages and NK cells, Catumaxomab brings immune cells into close proximity to EpCAM positive cancer cells. As a functional antibody, Catumaxomab also stimulates bound NK cells to release cytotoxic mediators like granzyme or bound macrophages to phagocytose the cancer cell. Phagocytosed cancer cells can be processed and have their antigens presented on major histocompatibililty complex II to activate helper T cells and contribute to humoural immunity and activation of killer T cells against EpCAM postive cancer cells. These macrophages also release inflammatory cytokines to attract additional immune cells to EpCAM positive tissues. When antibodies reach higher concentrations, they can stimulate complement-mediated cytotoxicity against EpCAM positive cancer cells. Bound killer T cells are activated resulting in proliferation and release of cytotoxic mediators resulting in antibody-dependent cell-mediated cytotoxicity against the cancer cell.",,,,Catumaxomab is approved and investigational and withdrawn.,Catumaxomab is a solid.,True
16825,"Ardeparin, marketed under the US trade name Normiflo, is a low molecular weight heparin (LMWH) anticoagulant used for the prevention of postoperative venous thrombosis. Ardeparin is derived via peroxide degradation of heparin extracted from porcine intestinal mucosa. Its molecular weight ranges from 2000 to 15,000 with an average molecular weight of 5500 to 6500. Normiflo was withdrawn from the US market in March 2000. For prevention of deep vein thrombosis, which may result in pulmonary embolism, following knee surgery. Ardeparin, an anticoagulant, is a fractionated heparin. It acts at multiple sites in the normal coagulation system to inhibit reactions that lead to the clotting of blood and the formation of fibrin clots both <i>in vitro</i> and <i>in vivo</i>. Ardeparin binds to antithrombin III, accelerating its activity in inactivating factor Xa and thrombin, thereby inhibiting thrombosis. Ardeparin also binds to heparin cofactor II, inhibiting thrombin. Ardeparin does not effect prothrombin time (PT) assays and may prolong activated partial thromboplastin time (APTT). Ardeparin has double the anti-factor Xa activity versus anti-factor IIa activity, compared to unfractionated heparin which has approximately equal anti-factor Xa activity and anti-factor IIa activity.",,,,Ardeparin is approved and investigational and withdrawn.,Ardeparin is a solid.,True
16826,N-Formylmethionine is effective in the initiation of protein synthesis. The initiating methionine residue enters the ribosome as N-formylmethionyl tRNA. This process occurs in Escherichia coli and other bacteria as well as in the mitochondria of eucaryotic cells.,,,,N-Formylmethionine is experimental.,N-Formylmethionine is a solid.,True
16827,"SR-123781A is a synthetic hexadecasaccharide Factor IIa and Xa antagonist. It is under investigation by Sanofi-Aventis and Organon for the treatment of thrombosis and acute coronary syndromes (ACS). Investigated for use/treatment in cardiovascular disorders, thrombosis, and venous thromboembolism. SR123781A is a synthetic hexadecasaccharide comprising an antithrombin (AT) binding domain, a thrombin binding domain, and a neutral methylated hexasaccharide sequence, was obtained from glucose through a convergent synthesis. SR123781A showed high affinity for human AT and was a potent catalyst of its inhibitory effect with regard to factor Xa and thrombin. ",,,,SR-123781A is investigational.,SR-123781A is a solid.,True
16828,"Sulodexide is a mixture of glycosaminoglycans (GAGs) composed of dermatan sulfate (DS) and fast moving heparin (FMH). Sulodexide has been used clinically for the prophylaxis and treatment of vascular diseases with increased risk of thrombosis, including intermittent claudication, peripheral arterial occlusive disease and post-myocardial infarc-tion. Also investigated in the treatment of diabetic kidney disease and diabetic neuropathy. New anti-inflammatory properties have also extended its use in venous disease. Sulodexide is extensively absorbed owing to its low molecular weight compared to unfractionated heparin. It offers the potential advantages of a longer half-life and reduced global anticoagulation effects, properties which differ from other glycosaminoglycans. Sulodexide potentiates antithrombin III and heparin cofactor II due to the presence of both glycoaminoglycan fractions. It is capable of inhibiting both anti-IIa and anti-Xa. It promotes fibrinolytic activity by releasing tissue plasminogen activator and reduces plasminogen activator inhibitor. The drug also blocks platelet adhesion and platelet function induced by cathepsin G and thrombin. Research has also shown that Sulodexide had endothelial protective properties by inducing the overexpression of growth factors important for the protection of organs. It has anti-inflammatory properties via its effect on the release of inflammatory mediators from macrophages. This results in anti-proliferative effects such as the regulation of growth factors like VEGF and FGF.  Thrombin inhibition produced by sulodexide is due to the additive effect of its components, namely, heparin cofactor II (HCII) catalysis by dermatan sulfate and antithrombin-III catalysis by fast moving heparin (FMH).",,,,Sulodexide is approved and investigational.,Sulodexide is a solid.,True
16829,"Danaparoid is a low-molecular-weight heparinoid with an average molecular weight of 5500 Daltons consisting of a mixture of glycosaminoglycans. The active constituents are heparan, dermatan and , and they are isolated from the porcine intestinal mucosa. Danaparoid possesses a potent antithrombic activity that works by inhibiting activated factor X (Factor Xa) and activated factor II (Factor IIa). It is chemically distinct from heparin by containing different protein binding properties, thus has lower cross-reactivity in heparin-intolerant patients. Danaproid is used in the treatment of heparin-induced thrombocytopenia (HIT) as an off-label indication and prevention of post-operative deep venous thrombosis (DVT). While it was initially approved by the FDA as Orgaran™, danaparoid was withdrawn by Organon International on August 14, 2002, due to a shortage in drug substance by the manufacturer. The use of Orgaran™ was discontinued in the United States however it is available in several other countries including European countries and Japan. Danaparoid sodium is the common salt form in therapeutic preparations and is typically administered subcutaneously. Indicated for the prophylaxis of post-operative deep venous thrombosis (DVT), which may lead to pulmonary embolism (PE), in patients undergoing elective hip replacement surgery. Danaparoid contains a mixture of heparan sulfate, dermatan sulfate and chondroitin sulfate in amounts of approximately 84%, 12% and 4%, respectively. Danaparoid is as an antithrombotic agent that prevents the formation of fibrin in the coagulation pathway. It has a high antifactor Xa to antifactor IIa (thrombin) activity that primarily works via antithrombin III-mediated inhibition of factor Xa. The ratio of antifactor Xa to antifactor II activity is ≥ 20:1. Danaparoid has a minor effect on platelet function and aggregation. In a worldwide compassionate-use programme involving a total of 667 patients with heparin-induced thrombocytopenia (HIT), treatment with danaparoid resulted in 93% of successful outcomes in resolving HIT.  In the coagulation cascade leading to clot formation, factor X and factor II requires activation to promote subsequent conversion of fibrinogen to fibrin. The mechanism of action of danaparoid resulting in anticoagulant and antithrombic effects involves a complex interaction between 2 components, factor IIa and in particular, factor Xa. Via binding to antithrombin and inducing a conformational change , danaparoid enhances and catalyzes the the binding of factor Xa to antithrombin, which induces antithrombin-mediated inactivation of factor Xa. This leads to inhibition of thrombin generation and subsequently, thrombus formation. Danaparoid also weakly enhances antithrombin III and heparin cofactor II inactivation of factor IIa. There is evidence that danaparoid also suppresses the activation of factor IX which, in conjunction with simultaneous inhibition of factor X, may lead to antithrombic effects. ",,,,Danaparoid is approved and withdrawn.,Danaparoid is a solid.,True
16830,"Nadroparin is a low molecular weight heparin (LMWH) which, when bound to antithrombin III (ATIII), accelerates the inactivation of factor II and factor Xa. Nadroparin halts the coagulation pathway by inhibiting the activation of thrombin (factor IIa) by factor Xa. The amplification of the fibrin clotting cascade is stopped once factors Xa and IIa are inactivated. It is derived from porcine sources and has a mean molecular size of 5000 daltons. Low molecular weight heparins are less effective at inactivating factor IIa due to their shorter length compared to unfractionated heparin. Nadroparin is used for prophylaxis of thromboembolic disorders and general surgery in orthopedic surgery, treatment of deep vein thrombosis, prevention of clotting during hemodialysis and treatment of unstable angina and non-Q wave myocardial infarction. Nadroparin is a low molecular weight heparin that is composed of a heterogeneous mixture of sulfated polysaccaride glycosaminoglycan chains. Th mean molecular weight is approximately 4300 daltons. The ratio of anti-Xa activity to anti-IIa is 3.5:1 whereas it is about 1:1 for heparin. Its use should be avoided in patients with a creatinine clearance less than 40mL/min. In these patients, unfractionated heparin should only be used. As for monitoring, active partial thromboplastin time (aPTT) will only increase at high doses of low molecular weight heparins (LMWH). Therefore, monitoring aPTT is not recommended. However, anti-Xa activity can be measured to monitor the efficacy of the LMWH.  The mechanism of action for nadroparin is similar to all other LMWHs. Like all LMWHs, nadroparin has a pentasaccharide sequence which binds to ATIII, which potentiates the action of ATIII. This complex greatly accelerates the inactivation of factor Xa and factor IIa. As a result, the coagulation cascade is inhibited.",,,,Nadroparin is approved and investigational.,Nadroparin is a solid.,True
16831,"A plasma alpha 2 glycoprotein that accounts for the major antithrombin activity of normal plasma and also inhibits several other enzymes. It is a member of the serpin superfamily. Antithrombin III human is a human antithrombin (AT) indicated in patients with hereditary antithrombin deficiency for the treatment and prevention of thromboembolism and prevention of peri-operative and peri-partum thromboembolism Hereditary AT deficiency causes an increased risk of venous thromboembolism (VTE). During high-risk situations such as surgery or trauma or for pregnant women, during the peri-partum period, the risk of development of VTEs as compared to the normal population in these situations is increased by a factor 10 to 50. In hereditary antithrombin deficient patients ATryn restores (normalize) plasma AT activity levels during peri-operative and peri-partum periods.  Antithrombin, an alpha2-glycoprotein of molecular weight 58,000, is normally present in human plasma at a concentration of approximately 12.5 mg/dL and is the major plasma inhibitor of thrombin. Inactivation of thrombin by AT occurs by formation of a covalent bond resulting in an inactive 1:1 stoichiometric complex between the two, involving an interaction of the active serine of thrombin and an arginine reactive site on AT. AT is also capable of inactivating other components of the coagulation cascade including factors IXa, Xa, XIa, and XIIa, as well as plasmin. The neutralization rate of serine proteases by AT proceeds slowly in the absence of heparin, but is greatly accelerated in the presence of heparin. As the therapeutic antithrombotic effect of heparin is mediated by AT, heparin in vivo is ineffective in the absence or near absence of AT.",,,,Antithrombin III human is approved.,Antithrombin III human is a solid.,True
16832,,,,,2(S)-Amino-6-Boronohexanoic Acid is experimental.,2(S)-Amino-6-Boronohexanoic Acid is a solid.,False
16833,N-Hydroxy-nor-L-arginine (nor-NOHA) is under investigation in clinical trial NCT02009527 (Arginase Inhibition in Ischemia-reperfusion Injury).,,,,nor-NOHA is investigational.,nor-NOHA is a solid.,True
16834,,,,,Dinor-N(Omega)-Hydroxy-L-Arginine is experimental.,Dinor-N(Omega)-Hydroxy-L-Arginine is a solid.,False
16835,,,,,S-{2-Ethyl}-D-Cysteine is experimental.,S-{2-Ethyl}-D-Cysteine is a solid.,False
16836,,,,,S-2-(Boronoethyl)-L-Cysteine is experimental.,S-2-(Boronoethyl)-L-Cysteine is a solid.,False
16837,"A compound formed in the liver from ammonia produced by the deamination of amino acids. It is the principal end product of protein catabolism and constitutes about one half of the total urinary solids. <ul> As a humectant, urea draws water into the striatum corneum.",The molecular weight is 60.06.,Urea has a topological polar surface area of 69.11.,The log p value of  is -1.66.,Urea is approved and investigational.,Urea is a solid.,True
16838,,,,,Descarboxy-nor-N(Omega)-Hydroxy-L-Arginine is experimental.,Descarboxy-nor-N(Omega)-Hydroxy-L-Arginine is a solid.,False
16839,,,,,"S,S-(2-Hydroxyethyl)Thiocysteine is experimental.","S,S-(2-Hydroxyethyl)Thiocysteine is a solid.",False
16840,,,,,DEHYDRO-2(S)-AMINO-6-BORONOHEXANOIC ACID is experimental.,DEHYDRO-2(S)-AMINO-6-BORONOHEXANOIC ACID is a solid.,False
16841,,,,,S-propylamine-L-cysteine is experimental.,S-propylamine-L-cysteine is a solid.,False
16842,"Pramipexole is a drug used to treat the symptoms of Parkinson's Disease (PD). It is a _non-ergot dopamine agonist_ drug that is efficacious in treating various Parkinson's symptoms such as tremor, rigidity, and bradykinesia (slow movement). It was first approved by the FDA in 1997. Parkinson's Disease is one of the most common neurodegenerative disorders and causes a high level of disability in patients , leading to increased difficulty in performing activities of daily living due to symptoms that progress over time. The prevalence of Parkinson's Disease worldwide has increased from approximately 2.5 million in 1990 to about 6.1 million in 2016. This increase may be attributed to an aging population along with other contributing factors. This drug is indicated for the symptomatic treatment of Parkinson’s disease. This drug can be administered as monotherapy or in conjunction with levodopa. It is also indicated for symptomatic treatment of moderate to severe primary Restless Legs Syndrome (RLS).  **Parkinson's Disease** The exact mechanism of action of pramipexole as a treatment for Parkinson's disease is unknown at this time. It is thought, however, that the ability of pramipexole to cause stimulation of the dopamine receptors in the striatum of the brain, a region that receives a vast array of neurological input and is responsible for a wide variety of functions, may be involved. Studies performed in animals show that pramipexole influences striatal neuronal transmission rates following activation of dopamine receptors. ",The molecular weight is 211.33.,Pramipexole has a topological polar surface area of 50.94.,The log p value of  is 1.17.,Pramipexole is approved and investigational.,Pramipexole is a solid.,True
16843,"Dipivefrin is a prodrug of adrenaline, which is used to treat glaucoma. It is available as ophthalmic solution (eye drops). Dipivefrin is a prodrug which is used as initial therapy for the control of intraocular pressure in chronic open-angle glaucoma. Dipivefrin is a member of a class of drugs known as prodrugs. Prodrugs are usually not active in themselves and require biotransformation to the parent compound before therapeutic activity is seen. These modifications are undertaken to enhance absorption, decrease side effects and enhance stability and comfort, thus making the parent compound a more useful drug. Enhanced absorption makes the prodrug a more efficient delivery system for the parent drug because less drug will be needed to produce the desired therapeutic response. Dipivefrin is a prodrug of epinephrine formed by the diesterification of epinephrine and pivalic acid. The addition of pivaloyl groups to the epinephrine molecule enhances its lipophilic character and, as a consequence, its penetration into the anterior chamber. Dipivefrin is a prodrug with little or no pharmacologically activity until it is hydrolyzed into epinephrine inside the human eye. The liberated epinephrine, an adrenergic agonist, appears to exert its action by stimulating α -and/or β<sub>2</sub>-adrenergic receptors, leading to a decrease in aqueous production and an enhancement of outflow facility. The dipivefrin prodrug delivery system is a more efficient way of delivering the therapeutic effects of epinephrine, with fewer side effects than are associated with conventional epinephrine therapy.",The molecular weight is 351.44.,Dipivefrin has a topological polar surface area of 84.86.,The log p value of  is 1.57.,Dipivefrin is approved.,Dipivefrin is a solid.,True
16844,"A nonselective alpha-adrenergic antagonist. It is used in the treatment of hypertension and hypertensive emergencies, pheochromocytoma, vasospasm of raynaud disease and frostbite, clonidine withdrawal syndrome, impotence, and peripheral vascular disease. Used as an aid for the diagnosis of pheochromocytoma, and may be administered immediately prior to or during pheochromocytomectomy to prevent or control paroxysmal hypertension resulting from anesthesia, stress, or operative manipulation of the tumor. Phentolamine has also been used to treat hypertensive crisis caused by sympathomimetic amines or catecholamine excess by certain foods or drugs in patients taking MAO inhibitors, or by clonidine withdrawal syndrome. Other indications include the prevention of dermal necrosis and sloughing following IV administration or extravasation of norepinephrine, decrease in impedance to left ventricular ejection and the infarct size in patients with MI associated with left ventricular failure, treatment of erectile dysfunction through self-injection of small doses combined with papaverine hydrochloride into the corpus cavernosum, and as an adjunct to the management of cocaine overdose to reverse coronary vasoconstriction following use of oxygen, benzodiazepines,and nitroglycerin.  Phentolamine is indicated for the control of episodes of hypertension and sweating that occur with a disease called pheochromocytoma. If tachycardia is excessive, it may be necessary to use a beta-blocking agent concomitantly. Phentolamine is a long-acting, adrenergic, alpha-receptor blocking agent which can produce and maintain \chemical sympathectomy\"" by oral administration. It increases blood flow to the skin, mucosa and abdominal viscera, and lowers both supine and erect blood pressures. It has no effect on the parasympathetic system. Phentolamine works by blocking alpha receptors in certain parts of the body. Alpha receptors are present in the muscle that lines the walls of blood vessels. When the receptors are blocked by Phentolamine, the muscle relaxes and the blood vessels widen. This widening of the blood vessels results in a lowering of blood pressure."" Phentolamine produces its therapeutic actions by competitively blocking alpha-adrenergic receptors (primarily excitatory responses of smooth muscle and exocrine glands), leading to a muscle relaxation and a widening of the blood vessels. This widening of the blood vessels results in a lowering of blood pressure. The action of phentolamine on the alpha adrenergic receptors is relatively transient and the blocking effect is incomplete. The drug is more effective in antagonizing responses to circulating epinephrine and/or norepinephrine than in antagonizing responses to mediator released at the adrenergic nerve ending. Phentolamine also stimulates β-adrenergic receptors and produces a positive inotropic and chronotropic effect on the heart and increases cardiac output.",The molecular weight is 281.36.,Phentolamine has a topological polar surface area of 47.86.,The log p value of  is 3.81.,Phentolamine is approved.,Phentolamine is a solid.,True
16845,"An alpha-adrenergic antagonist with long duration of action. It has been used to treat hypertension and as a peripheral vasodilator.  For the treatment of phaeochromocytoma (malignant), benign prostatic hypertrophy and malignant essential hypertension. Phenoxybenzamine is indicated for the control of episodes of hypertension and sweating that occur with a disease called pheochromocytoma. If tachycardia is excessive, it may be necessary to use a beta-blocking agent concomitantly. Phenoxybenzamine is a long-acting, adrenergic, alpha-receptor blocking agent which can produce and maintain \chemical sympathectomy\"" by oral administration. It increases blood flow to the skin, mucosa and abdominal viscera, and lowers both supine and erect blood pressures. It has no effect on the parasympathetic system. Phenoxybenzamine works by blocking alpha receptors in certain parts of the body. Alpha receptors are present in the muscle that lines the walls of blood vessels. When the receptors are blocked by Phenoxybenzamine, the muscle relaxes and the blood vessels widen. This widening of the blood vessels results in a lowering of blood pressure."" Phenoxybenzamine produces its therapeutic actions by blocking alpha receptors, leading to a muscle relaxation and a widening of the blood vessels. This widening of the blood vessels results in a lowering of blood pressure.",The molecular weight is 303.83.,Phenoxybenzamine has a topological polar surface area of 12.47.,The log p value of  is 4.92.,Phenoxybenzamine is approved.,Phenoxybenzamine is a solid.,True
16846,"Oxymetazoline is an imidazole derivative and alpha (α)-adrenergic agonist with greater affinity for the α2-adrenergic receptor than the α1-adrenergic receptor. Due to its vasoconstricting activity, oxymetazoline is used as a decongestant and topical hemostatic agent.  Oxymetazoline is indicated for the topical treatment of persistent facial erythema associated with rosacea in adults. Oxymetazoline a adrenergic alpha-agonists, direct acting sympathomimetic used as a vasoconstrictor to relieve nasal congestion The sympathomimetic action of oxymetazoline constricts the smaller arterioles of the nasal passages, producing a prolonged (up to 12 hours), gentle and decongesting effect. Oxymetazoline elicits relief of conjunctival hyperemia by causing vasoconstriction of superficial conjunctival blood vessels. The drug's action has been demonstrated in acute allergic conjunctivitis and in chemical (chloride) conjunctivitis.  Oxymetazoline is a direct acting sympathomimetic amine, which acts on alpha-adrenergic receptors in the arterioles of the conjunctiva and nasal mucosa. It produces vasoconstriction, resulting in decreased conjunctival congestion in ophthalmic. In nasal it produces constriction, resulting in decreased blood flow and decreased nasal congestion.",The molecular weight is 260.38.,Oxymetazoline has a topological polar surface area of 44.62.,The log p value of  is 4.61.,Oxymetazoline is approved and investigational.,Oxymetazoline is a solid.,True
16847,"Apraclonidine, also known as iopidine, is a sympathomimetic used in glaucoma therapy. It is an alpha2-adrenergic agonist. For prevention or reduction of intraoperative and postoperative increases in intraocular pressure (IOP) before and after ocular laser surgery when used prophylactically. Also used as a short-term adjunctive therapy in patients with open-angle glaucoma who are on maximally tolerated medical therapy requiring additional IOP reduction. Apraclonidine significantly lowers intraocular pressure with minimal effects on cardiovascular and pulmonary parameters. It lowers intraocular pressure by reducing aqueous humor production and increasing uveoscleral outflow. Apraclonidine is a relatively selective alpha2 adrenergic receptor agonist that stimulates alpha1 receptors to a lesser extent. It has a peak ocular hypotensive effect occurring at two hours post-dosing. The exact mechanism of action is unknown, but fluorophotometric studies in animals and humans suggest that Apraclonidine has a dual mechanism of action by reducing aqueous humor production through the constriction of afferent ciliary process vessels, and increasing uveoscleral outflow.",The molecular weight is 245.11.,Apraclonidine has a topological polar surface area of 62.44.,The log p value of  is 0.61.,Apraclonidine is approved.,Apraclonidine is a solid.,True
16848,"EpiCept NP-1 is a prescription topical analgesic cream designed to provide effective, long-term relief from the pain of peripheral neuropathies. Peripheral neuropathies are medical conditions caused by damage to the nerves in the peripheral nervous system. The peripheral nervous system includes nerves that run from the brain and spinal cord to the rest of the body. EpiCept NP-1 Cream is a patented formulation containing two FDA-approved drugs, amitriptyline (a widely-used antidepressant) and ketamine (an NMDA antagonist that is used as an anesthetic). Investigated for use/treatment in neuropathy (diabetic) and pain (acute or chronic). EpiCept NP-1 is a prescription topical analgesic cream designed to provide effective, long-term relief from the pain of peripheral neuropathies. Peripheral neuropathies are medical conditions caused by damage to the nerves in the peripheral nervous system. The peripheral nervous system includes nerves that run from the brain and spinal cord to the rest of the body. It is estimated that these conditions affect more than 15 million people in the U.S. and is associated with conditions that injure peripheral nerves, including herpes zoster, or shingles, diabetes, chemotherapy, HIV and other diseases. Peripheral neuropathies can also be caused by trauma or may result from surgical procedures. EpiCept NP-1 Cream is a patented formulation containing two FDA-approved drugs, amitriptyline (a widely-used antidepressant) and ketamine (an NMDA antagonist that is used as an anesthetic). The mechanism(s) of action are unclear for Epicept. Both ketamine and amitriptyline inhibit N-methyl-D-aspartate receptors in neuronal preparations and may be involved in sensitization of tetrodotoxin-resistant Na+ currents in nociceptors by blocking Na+ channels. In producing antihyperalgesia with pretreatment, but not posttreatment, regimens, ketamine and amitriptyline resemble the profile of a µ-opioid receptor agonist. In addition to the above effects, amitriptyline also inhibits noradrenaline, 5-HT, and adenosine uptake; inter-acts with opioid mechanisms; blocks Ca2+ channels; and blocks cholinergic, histamine H1, 5-HT2, and {alpha}-adrenergic receptors. Accordingly there are many possible mechanisms at work.",,,,Epicept NP-1 is investigational.,Epicept NP-1 is a solid.,True
16849,"Investigated for use/treatment in schizophrenia and schizoaffective disorders. Ocaperidone is a benzisoxazol piperidine antipsychotic primarily binds and with high affinity to 5-HT2 (serotonin) receptors, alpha1 and alpha 2 adrenergic receptors, dopamine D2 receptors and histamine H1 receptors. Ocaperidone is an antagonist primarily at the 5HT and D2 receptors. A proposed mechanism of action is the central D2 receptor blockade which is common to all neuroleptics that are used to treat positive symptoms of schizophrenia. ",,,,Ocaperidone is investigational.,Ocaperidone is a solid.,True
16850,"Flupirtine is a pyridine derivative that is in clinical use as a nonopioid analgesic. It was approved for the treatment of pain in 1984 in Europe. It is not approved for use in the U.S. or Canada, but is currently in phase II trials for the treatment of fibromyalgia. Investigated for use/treatment in fibromyalgia. Flupirtine upregulates Bcl-2, increases glutathione levels, activates an inwardly rectifying potassium channel, and delays loss of intermitochondrial membrane calcium retention capacity. Flupirtine acts like a NMDA receptor antagonists, but does not bind to the receptor. One study concluded that the discriminative effects of flupirtine are neither of opioid nor of alpha-1 adrenergic type, but are primarily mediated through alpha-2 adrenergic mechanisms.",The molecular weight is 304.32.,Flupirtine has a topological polar surface area of 89.27.,The log p value of  is 3.05.,Flupirtine is investigational.,Flupirtine is a solid.,True
16851,"A nasal vasoconstricting decongestant drug which acts by binding to the same receptors as adrenaline. It is applied as a spray or as drops into the nose to ease inflammation and congestion of the nasal passageways. It binds alpha-adrenergic receptors to activate the adrenal system which causes systemic vasoconstriction, thereby easing nasal congestion. It is used for treating nasal congestion and minor inflammation due to allergies or colds. Xylometazoline is a direct acting sympathomimetic adrenergic alpha-agonist used to induce systemic vasoconstriction, thereby decreasing nasal congestion. The sympathomimetic action of xylometazoline constricts the smaller arterioles of the nasal passages, producing a prolonged (8-12 hours) decongesting effect. Xylometazoline is a direct acting sympathomimetic drug, which acts on alpha-adrenergic receptors in the arterioles of the nasal mucosa. This activates the adrenal system to yield systemic vasoconstrction. In producing vasoconstriction, the result is a decrease in blood flow in the nasal passages and consequently decreased nasal congestion. ",The molecular weight is 244.38.,Xylometazoline has a topological polar surface area of 24.39.,The log p value of  is 5.38.,Xylometazoline is approved and investigational.,Xylometazoline is a solid.,True
16852,"Naphazoline is a rapid acting imidazoline sympathomimetic vasoconstrictor of ocular or nasal artierioles. It acts to decrease congestion and is found in many over the counter (OTC) eye drops and nasal preparations. Naphazoline is indicated for use as OTC eyedrops for ocular vasoconstriction or as a nasal preparation for nasal congestion. Naphazoline is a sympathomimetic alpha adrenergic agonist that acts to vasoconstrict nasal or ocular arterioles, resulting in reduced congestion at the site of administration. Naphazoline is a vasoconstrictor that functions by stimulating alpha adrenergic receptors in arterioles leading to decreased congestion at the site of administration.",The molecular weight is 210.28.,Naphazoline has a topological polar surface area of 24.39.,The log p value of  is 3.83.,Naphazoline is approved and investigational.,Naphazoline is a solid.,True
16853,"Moxonidine is a new-generation centrally acting antihypertensive drug approved for the treatment of mild to moderate essential hypertension. It is suggested to be effective in cases where other agents such as thiazides, beta-blockers, ACE inhibitors, and calcium channel blockers are not appropriate or irresponsive. As well, moxonidine has been shown to present blood pressure-independent beneficial effects on insulin resistance syndrome. For the treatment of mild to moderate essential or primary hypertension. Effective as most first-line antihypertensives when used as monotherapy. Antihypertensive agent whose site of action is the Central Nervous System (CNS), specifically involving interactions with I1- imidazoline and alpha-2-adrenergic rececptors within the rostral ventrolateral medulla (RSV).  Stimulation of central alpha 2-adrenergic receptors is associated with sympathoadrenal suppression and subsequent reduction of blood pressure. As this class was further explored it was discovered that sympathoadrenal activity can also be suppressed by a second pathway with a newly discovered drug target specific to imidazolines. Specifically, moxonidine binds the imidazoline receptor subtype 1 (I1) and to a lesser extent αlpha-2-adrenoreceptors in the RSV causing a reduction of sympathetic activity, reducing systemic vascular resistance and thus arterial blood pressure. ",The molecular weight is 241.68.,Moxonidine has a topological polar surface area of 71.43.,The log p value of  is 1.51.,Moxonidine is approved and investigational.,Moxonidine is a solid.,True
16854,Rilmenidine has been used in trials studying the treatment of Hypertension and Chronic Kidney Disease.,The molecular weight is 180.25.,Rilmenidine has a topological polar surface area of 33.62.,The log p value of  is 1.42.,Rilmenidine is approved and investigational.,,True
16855,"Methylphenidate is a central nervous system stimulant used most commonly in the treatment of Attention-Deficit/Hyperactivity Disorder (ADHD) and for narcolepsy. Also known as the marketed products Ritalin, Concerta, or Biphentin, methylphenidate is used with other treatment modalities (psychological, educational, cognitive behaviour therapy, etc) to improve the following group of developmentally inappropriate symptoms associated with ADHD: moderate-to-severe distractibility, short attention span, hyperactivity, emotional lability, and impulsivity. Long-acting formulations of psychostimulants such as methylphenidate, , and are considered the most effective and widely used treatment for ADHD, and are considered first-line options for children, adolescents, and adults as recommended by CADDRA (Canadian ADHD Resource Alliance). CADDRA recommends the use of methylphenidate due to long term studies, of over twenty years in duration, which show methylphenidate is safe and effective.  Methylphenidate is indicated for the treatment of Attention Deficit Hyperactivity Disorder (ADHD) in patients 6 years of age and older and for the treatment of narcolepsy. Methylphenidate is a racemic mixture comprised of the d- and l-isomers. The d-isomer is more pharmacologically active than the l-isomer. Radioligand binding studies demonstrate that binding of methylphenidate in the brain is localized to dopamine-rich areas, in particular in the prefrontal cortex which has been demonstrated to play a prominent role in ADHD pathophysiology. In a number of animal models, methylphenidate enhances locomotor activity and induces stereotypic behaviours.  While its exact mechanism is unclear, methylphenidate (MPH) has been shown to act as a norepinephrine and dopamine reuptake inhibitor (NDRI), thereby increasing the presence of these neurotransmitters in the extraneuronal space and prolonging their action. There is a dose-related effect of psychostimulants on receptor stimulation, where higher doses are shown to increase norepinephrine (NE) and dopamine (DA) efflux throughout the brain which can result in impaired cognition and locomotor-activating effects. In contrast, low doses are found to selectively activate NE and DE neurotransmission within the prefrontal cortex which is an area of the brain thought to play a prominent role in ADHD pathophysiology, thereby improving clinical efficacy and preventing side effects. The lower doses used to treat ADHD are not associated with the locomotor-activating effects associated with higher doses and instead reduce movement, impulsivity, and increase cognitive function including sustained attention and working memory. Methylphenidate's beneficial effects in sustaining attention have also been shown to be mediated by alpha-1 adrenergic receptor activity..",The molecular weight is 233.31.,Methylphenidate has a topological polar surface area of 38.33.,The log p value of  is 2.56.,Methylphenidate is approved and investigational.,Methylphenidate is a solid.,True
16856,"Alverine is a smooth muscle relaxant used to relieve cramps or spasms of the stomach and intestines. It is therefore useful in treating irritable bowel syndrome (IBS) and similar conditions. It can also be used to help relieve period pain. Used to relieve cramps or spasms of the stomach and intestines. It is also useful in treating irritable bowel syndrome (IBS) and similar conditions. It can also be used to help relieve period pain. Alverine citrate is also under investigation to increase the cytotoxic effects of the proteasome inhibitor MG132 on breast cancer cells.  Alverine is a smooth muscle relaxant. Smooth muscle is a type of muscle that is not under voluntary control; it is the muscle present in places such as the gut and uterus. Alverine acts directly on the muscle in the gut, causing it to relax. This prevents the muscle spasms which occur in the gut in conditions such as irritable bowel syndrome and diverticular disease. Diverticular disease is a condition in which small pouches form in the gut lining. These pouches can trap particles of food and become inflamed and painful. In irritable bowel syndrome the normal activity of the gut muscle is lost. The muscle spasms result in symptoms such as heartburn, abdominal pain and bloating, constipation or diarrhoea. By relaxing the gut muscle, alverine citrate relieves the symptoms of this condition. Alverine also relaxes the smooth muscle in the womb (uterus). It is therefore also used to treat painful menstruation, which is caused by muscle spasms in the uterus (dysmenorrhea).",The molecular weight is 281.44.,Alverine has a topological polar surface area of 3.24.,The log p value of  is 5.5.,Alverine is approved and investigational.,Alverine is a solid.,True
16857,"Bifeprunox is a novel atypical antipsychotic agent which, along with SLV313, and SSR-181507 combines minimal D2 receptor agonism with 5-HT receptor agonism. Bifeprunox is being evaluated for the treatment of schizophrenia, psychosis, and Parkinson's disease. Bifeprunox is an atypical antipsychotic drug with mixed (agonist/antagonist) receptor activity with the neurotransmitters dopamine (D2/3/4) and serotonin. Bifeprunox differs from first-generation atypical antipsychotics in that it acts as a partial D2 agonist. This property is shared by aripiprazole, a drug already marketed in Europe and the US for treatment of schizophrenia. A placebo-controlled, dose-finding phase II trial in patients with schizophrenia showed that bifeprunox was both efficacious and well tolerated. Importantly, treatment with bifeprunox did not appear to cause some of the side effects seen with other atypicals agents in routine use, such as weight gain, hyperprolactinaemia and cardiotoxicity. In contrast to D2 receptor antagonism, partial D2 agonism is believed to decrease dopamine activity in an overactive dopamine system while simultaneously increasing dopamine activity in regions of the brain where dopaminergic activity is too low. By blocking overstimulated receptors and stimulating underactive ones, partial D2 agonists act as dopamine stabilisers. In common with aripiprazole, bifeprunox also acts as a serotonin, 5-HT1A agonist. This property may contribute to efficacy against the negative symptoms of schizophrenia and reduce the likelihood of extrapyramidal symptoms (EPS).",,,,Bifeprunox is investigational.,Bifeprunox is a solid.,True
16858,"Lesopitron is an anxiolytic with pre- and post-synaptic 5-HT1A agonist activity, which is under development by Esteve. Intended for the treatment of anxiety disorders. In phase I trials in healthy volunteers, lesopitron was well tolerated in single doses up to 50 mg, and up to 45 mg/day in repeated doses. Lesopitron has negligible effects on alpha-adrenergic and dopaminergic receptors, and was more potent than structurally-related 5-HT1A agonists in rat social interaction and marmoset anxiety models. It also countered benzodiazepine withdrawal-induced anxiety in rodents. The acute toxicity of lesopitron is low and it does not potentiate the effects of alcohol or barbiturates. Long-term usage led to reductions in plasma glucose, triglycerides, phospholipids and cholesterol. Lesopitron acts as a ligand for central serotonin 5-HT1A receptors. Lesopitron inhibits haloperidol-induced catalepsy that is the consequence of its action on 5-HT1A autoreceptors. The ability of lesopitron to induce 5-HT syndrome reflects post-synaptic 5-HT1A receptor activation and the reversion of 8-OHDPAT-induced 5-HT syndrome by lesopitron suggests a partial agonist effect on this receptor-type. Lesopitron induced a hypothermic effect due to the enhanced activation of post-synaptic 5-HT1A receptors. The agonist effect of lesopitron on 5-HT1A receptors and its marked hypothermic effect is an added value for this drug and a stimulus to the study of its possible neuroprotective action.",,,,Lesopitron is investigational.,Lesopitron is a solid.,True
16859,"MN-305 is a novel, potent and highly selective serotonin 5-HT1A receptor agonist under development by MediciNova for the treatment of anxiety disorders beginning with Generalized Anxiety Disorder (GAD). Investigated for use/treatment in anxiety disorders, depression, insomnia, and neurologic disorders. MN-305 is a potent and highly-selective full agonist at the serotonin 5-HT1A receptor under development by MediciNova both for the treatment of insomnia, as well as for anxiety disorders such as Generalized Anxiety Disorder (GAD). MN-305 has been evaluated in an extensive preclinical toxicology program which showed no evidence of inducing genetic mutations, immune response or cancer. MN-305 has also proved to be consistently well-tolerated in clinical safety, efficacy and pharmacokinetic studies in over 1,200 subjects.",,,,MN-305 is investigational.,MN-305 is a solid.,True
16860,"LI 301 is an orally bio-available compound delivered in a fast melt mechanism with taste masking enabling it to be taken anytime without water. It has a novel mode of action combining both the light effect of a Selective Serotonin Reuptake Inhibitor (\SSRI\"")(most likely antagonistic at 5HT1a receptors) and antagonism at mu-opioid receptors. This results in a slight dulling of sensation that can be used to treat premature ejaculation without interfering with normal sexual pleasure or orgasm. "" Investigated for use/treatment in premature ejaculation. LI 301 is an orally bio-available compound delivered in a fast melt mechanism  with taste masking enabling it to be taken anytime without water. LI 301 is active in the system for up to seven hours once administered, enabling patients to relax and partners to feel unpressured by time limitation. LI 301 has a novel mode of action combining both the light effect of a Selective Serotonin Reuptake Inhibitor (\SSRI\"") and u-opioid. This results in a slight dulling of sensation that can be used to treat premature ejaculation without interfering with normal sexual pleasure or orgasm. "" LI 301 has a novel mode of action combining both the light effect of a Selective Serotonin Reuptake Inhibitor (\SSRI\"")(most likely antagonistic at 5HT1a receptors) and antagonism at mu-opioid receptors.""",,,,LI-301 is investigational.,LI-301 is a solid.,True
16861,Investigated for use/treatment in anxiety disorders and depression.,,,,Naluzotan is investigational.,Naluzotan is a solid.,True
16862,"Investigated for use/treatment in amyotrophic lateral sclerosis (ALS) and alzheimer's disease. Xaliproden is an orally-active, synthetic, non-peptidic 5-hydroxytryptamine (5-HT) 1A receptor agonist with neurotrophic and neuroprotective activities. Although its mechanism of action is not fully understood, xaliproden appears to either mimic the effects of neurotrophins or stimulate their synthesis, thereby stimulating neuronal cell differentiation and proliferation and inhibiting neuronal cell death. The neuroprotective effect of this agent involves the activation of MAP kinase pathways via stimulation of the 5-HT1A receptor.",,,,Xaliproden is investigational.,Xaliproden is a solid.,True
16863,Investigated for use/treatment in schizophrenia and schizoaffective disorders and parkinson's disease.,,,,Sarizotan is investigational.,Sarizotan is a solid.,True
16864,Investigated for use/treatment in anxiety disorders and depression.,,,,Robalzotan is investigational.,Robalzotan is a solid.,True
16865,"Pardoprunox has been used in trials studying the treatment of Early Stage Parkinson's Disease and Advanced Stage Parkinson's Disease. Pardoprunox is a partial dopamine D2 agonist and noradrenergic agonist with serotonin 5-HT1A agonist properties. Pardoprunox binds to dopamine D(2), D(3), and D(4) receptors and 5-HT(1) (A) receptors and is a partial agonist at dopamine D(2) and D(3) receptors and a full agonist at serotonin 5-HT(1) (A) receptors. Pardoprunox combines high potency partial agonism at dopamine D(2) and D(3) receptors with full efficacy low potency serotonin 5-HT(1) (A) receptor agonism and is worthy of profiling in in vivo models of Parkinson's disease.",,,,Pardoprunox is investigational.,,True
16866,"SEP-363856 is a novel psychotropic drug being investigated for the treatment of schizophrenia. Unlike other drugs used for this condition, SEP-363856 does not bind to the dopamine D2 receptors, but exerts actions on the trace amine–associated receptor 1 (TAAR1) and 5-hydroxytryptamine type 1A (5-HT1A). ",,,,SEP-363856 is investigational.,,True
16867,"A tetracycline analog having a 7-chloro and a 6-methyl. Because it is excreted more slowly than tetracycline, it maintains effective blood levels for longer periods of time. Used primarily to treat Lyme disease, acne, and bronchitis. Also indicated (but rarely used) to treat urinary tract infections, gum disease, malaria, and other bacterial infections such as gonorrhea and chlamydia. One of its other registered uses is the treatment of hyponatremia (low blood sodium concentration) due to the syndrome of inappropriate antidiuretic hormone (SIADH) where fluid restriction alone has been ineffective.  Demeclocycline is a tetracycline antibiotic active against the following microorganisms: <i>Rickettsiae</i> (Rocky Mountain spotted fever, typhus fever and the typhus group, Q fever, rickettsial pox, tick fevers), <i>Mycoplasma pneumoniae</i> (PPLO, Eaton agent), agents of psittacosis and ornithosis, agents of lymphogranulomavenereum and granuloma inguinale, the spirochetal agent of relapsing fever (<i>Borrelia recurrentis</i>), <i>Haemophilus ducreyi</i> (chancroid), <i>Yersinia pestis</i>, <i>Pasteurella pestis</i> and <i>Pasteurella tularensis</i>, <i>Bartonella bacilliformis</i>, <i>Bacteroides species</i>, <i>Vibrio comma</i> and <i>Vibrio fetus</i>, and <i>Brucella species</i> (in conjunction with streptomycin). Demeclocycline inhibits cell growth by inhibiting translation. Demeclocycline is lipophilic and can easily pass through the cell membrane or passively diffuses through porin channels in the bacterial membrane. Demeclocycline is not a direct bactericidal agent; rather, it is a bacteriostatic drug that impairs bacterial growth. Because it is excreted more slowly than tetracycline, it maintains effective blood levels for longer periods of time. Demeclocycline inhibits cell growth by inhibiting translation. It binds (reversibly) to the 30S and 50S ribosomal subunit and prevents the amino-acyl tRNA from binding to the A site of the ribosome, which impairs protein synthesis by bacteria. The binding is reversible in nature. The use in SIADH actually relies on a side-effect of tetracycline antibiotics; many may cause diabetes insipidus (dehydration due to the inability to concentrate urine). It is not completely understood why demeclocycline impairs the action of antidiuretic hormone, but it is thought that it blocks the binding of the hormone to its receptor.",The molecular weight is 464.86.,Demeclocycline has a topological polar surface area of 181.62.,The log p value of  is -0.58.,Demeclocycline is approved.,Demeclocycline is a solid.,True
16868,M0002 is an orally-active selective vasopressin antagonist that inhibits water re-absorption from the kidneys. It is a vasopressin 2 antagonist and represents a new class of compounds – aquaretics – that produce profound diuresis without loss of electrolytes. It will be of major benefit to those patients not responding satisfactorily to diuretics alone. Vasopressin regulates renal water resorption through the V2 receptor. Inhibition of vasopressin’s effects on V2 receptors enhances water excretion and increases urinary output. M0002 is a Vasopressin 2 antagonis. It is an electrolyte-sparing aquaretic and causes much lower levels of salt excretion. ,,,,M0002 is investigational.,M0002 is a solid.,True
16869,"OPC-51803 is the first nonpeptide vasopressin (AVP) V(2)-receptor-selective agonist. It is a V(2)-selective agonist that produces a significant antidiuretic action after single and multiple oral dosing in AVP-deficient and normal AVP states. It is useful therapeutic drug in the treatment of hypothalamic diabetes insipidus, nocturnal enuresis, and some kinds of urinary incontinence. Investigated for use/treatment in nocturia (frequent nighttime urination) and urinary incontinence.",,,,OPC-51803 is investigational.,OPC-51803 is a solid.,True
16870,,,,,"Cp-166572, 2-Hydroxymethyl-4-(4-N,N-Dimethylaminosulfonyl-1-Piperazino)-Pyrimidine is experimental.","Cp-166572, 2-Hydroxymethyl-4-(4-N,N-Dimethylaminosulfonyl-1-Piperazino)-Pyrimidine is a solid.",False
16871,,,,,N-(Phosphonoacetyl)-L-Ornithine is experimental.,N-(Phosphonoacetyl)-L-Ornithine is a solid.,False
16872,Norvaline is an isomer of the more common amino acid valine.,,,,Norvaline is experimental.,Norvaline is a solid.,True
16873,,,,,(2E)-3-(2-OCT-1-YN-1-YLPHENYL)ACRYLIC ACID is experimental.,(2E)-3-(2-OCT-1-YN-1-YLPHENYL)ACRYLIC ACID is a solid.,False
16874,"Rocuronium (rapid onset-curonium) is a desacetoxy analogue of vecuronium with a more rapid onset of action. It is an aminosteroid non-depolarizing neuromuscular blocker or muscle relaxant used in modern anaesthesia, to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Introduced in 1994, rocuronium has rapid onset, and intermediate duration of action. It is commonly marketed under the trade names Zemuron and Esmeron. The drug is associated with the risk of developing allergic reactions in some high-risk patients, such as those with asthma. However, there was a similar incidence of allergic reactions associated with other non-depolarizing neuromuscular blocking agents. is a γ-cyclodextrin derivative that has been introduced as a novel agent to reverse the action of rocuronium. For inpatients and outpatients as an adjunct to general anesthesia to facilitate both rapid sequence and routine tracheal intubation, and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Neuromuscular blocking agents are drugs that cause skeletal muscle relaxation primarily by causing a decreased response to the neurotransmitter acetylcholine (ACh) at the myoneural (neuromuscular) junction of skeletal muscle. At that site, ACh normally produces electrical depolarization of the postjunctional membrane of motor end-plate, which leads to conduction of muscle action potential and subsequently induces skeletal muscle contraction. Neuromuscular agents are classified as depolarizing or nondepolarizing. Rocuronium is a nondepolarizing neuromuscular blocking agent with a rapid to intermediate onset depending on dose and intermediate duration. Rocuronium, like vecuronium is longer acting in infants than in children. However, unlike vecuronium, rocuronium retains the characteristics of an intermediate-acting NMBD in infants. Rocuronium acts by competing for cholinergic receptors at the motor end-plate. This action is antagonized by acetylcholinesterase inhibitors, such as neostigmine and edrophonium. Rocuronium acts by competitively binding to nicotinic cholinergic receptors. The binding of vecuronium decreases the opportunity for acetylcholine to bind to the nicotinic receptor at the postjunctional membrane of the myoneural junction. As a result, depolarization is prevented, calcium ions are not released and muscle contraction does not occur. Evidence also suggests that nondepolarizing agents can affect ACh release. It has been hypothesized that nondepolarzing agents bind to postjunctional (\curare\"") receptors and may therefore interfere with the sodium and potassium flux, which is responsible for depolarization and repolarization of the membranes involved in muscle contraction. """,,,,Rocuronium is approved.,Rocuronium is a solid.,True
16875,"Cilansetron is a 5HT-3 antagonist made by Solvay Pharmaceuticals that is currently under trial phase in the EU and US. For the treatment of symptoms associated with irritable bowel syndrome. Cilansetron is an orally formulated medication that blocks the action of 5-hydroxy-tryptamine 3 (5-HT3) receptors. Phase III studies of cilansetron had been suspended by Solvay in order to assess whether the drug possesses safety concerns similar to alosetron. Alosetron, also a 5-HT3 antagonist, was withdrawn from the market due to questions regarding its safety. Phase III testing with cilansetron has since resumed. In June 2005 the company announced that they were reviewing the priority of the cilansetron program. Cilansetron is a potent and selective 5-HT<sub>3</sub> receptor antagonist. 5-HT<sub>3</sub> receptors are nonselective cation channels that are extensively distributed on enteric neurons in the human gastrointestinal tract, as well as other peripheral and central locations. Activation of these channels and the resulting neuronal depolarization affect the regulation of visceral pain, colonic transit and gastrointestinal secretions, processes that relate to the pathophysiology of irritable bowel syndrome (IBS). 5-HT<sub>3</sub> receptor antagonists such as cilansetron inhibit activation of non-selective cation channels which results in the modulation of the enteric nervous system.",,,,Cilansetron is investigational.,Cilansetron is a solid.,True
16876,"DDP733 is an oral prokinetic drug which Dynogen is developing as a treatment for both Irritable Bowel Syndrome with constipation (IBS-c) and nocturnal gastroesophageal reflux disease (NGERD). It is a partial agonist of the serotonin type 3 receptor (5-HT3). Serotonin is a neurotransmitter that is known to be involved in the control of the gastrointestinal (GI) system. Preclinical studies of DDP733 established the compound’s prokinetic properties (the ability to promote the motility of the GI tract). Investigated for use/treatment in constipation, gastroesophageal reflux disease (GERD), gastrointestinal diseases and disorders (miscellaneous), and irritable bowel syndrome (IBS). DDP733 is an agonist of 5-HT3 receptors, a specific sub-type of serotonin receptor. Serotonin, a neurotransmitter, is believed to play an important role in the regulation of gastrointestinal motility.",,,,DDP733 is investigational.,DDP733 is a solid.,True
16877,"DDP225 is both a noradrenaline reuptake inhibitor and a serotonin type 3 receptor (5-HT3) antagonist. Noradrenaline and serotonin are neurotransmitters that are known to be involved in the control of the gastrointestinal system. The unique combination of noradrenaline reuptake inhibition and 5-HT3 antagonism in one orally delivered compound represents a novel approach to treating IBS-d and other functional GI diseases. Dynogen licensed preclinical and clinical data related to DDP225 from Mitsubishi Pharma in October 2003. Investigated for use/treatment in alzheimer's disease, depression, diarrhea, gastrointestinal diseases and disorders (miscellaneous), and irritable bowel syndrome (IBS). DDP225 is an orally-active compound that targets two key pathways that control the gastrointestinal (GI) system, thus giving it the potential to address multiple symptoms associated with IBS-d. DDP225 has a dual mechanism of action. It possesses both noradrenaline reuptake inhibition and 5-HT3 receptor antagonist properties.",,,,DDP-225 is investigational.,DDP-225 is a solid.,True
16878,"Tropisetron is an indole derivative with antiemetic activity. As a selective serotonin receptor antagonist, tropisetron competitively blocks the action of serotonin at 5HT3 receptors, resulting in suppression of chemotherapy-and radiotherapy-induced nausea and vomiting. For the prevention of nausea and vomiting induced by cytotoxic therapy and postoperative.  Tropisetron competitively binds to and blocks the action of serotonin at 5HT3 receptors peripherally on vagus nerve terminals located in the gastrointestinal (GI) tract as well as centrally in the chemoreceptor trigger zone (CTZ) of the area postrema of the central nervous system (CNS). This results in the suppression of chemotherapy- and radiotherapy-induced nausea and vomiting.",The molecular weight is 284.36.,Tropisetron has a topological polar surface area of 45.33.,The log p value of  is 2.88.,Tropisetron is approved and investigational.,,True
16879,"The major hormone derived from the thyroid gland. Thyroxine is synthesized via the iodination of tyrosines (monoiodotyrosine) and the coupling of iodotyrosines (diiodotyrosine) in the thyroglobulin. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form triiodothyronine which exerts a broad spectrum of stimulatory effects on cell metabolism. Used to lower high cholesterol levels in the blood. Dextrothyroxine, the dextrorotary isomer of the synthetic thyroxine, is a antihyperlipidemic. Dextrothyroxine is a antihyperlipidemic. The mechanism of action is not completely understood, but dextrothyroxine apparently acts in the liver to stimulate formation of low-density lipoprotein (LDL) and, to a much greater extent, to increase catabolism of LDL. This leads to increased excretion of cholesterol and bile acids via the biliary route into the feces, with a resulting reduction in serum cholesterol and LDL. Dextrothyroxine has no significant effect on high-density lipoproteins (HDL).",The molecular weight is 776.87.,Dextrothyroxine has a topological polar surface area of 92.78.,The log p value of  is 3.51.,Dextrothyroxine is approved and investigational.,Dextrothyroxine is a solid.,True
16880,,,,,-Acetic Acid is experimental.,-Acetic Acid is a solid.,False
16881,An anticholesteremic agent.,,,,KB-141 is experimental.,KB-141 is a solid.,True
16882,,,,,"2--2h-Triazine-3,5-Dione is experimental.","2--2h-Triazine-3,5-Dione is a solid.",False
16883,"A metabolite of T3 and T4 thyroid hormones; promoted for hyperlipidemia, localized lipodystrophy, and obesity. Tiratricol has been used in trials studying the treatment of Allan-Herndon-Dudley Syndrome.",The molecular weight is 621.93.,Tiratricol has a topological polar surface area of 66.76.,The log p value of  is 5.6.,Tiratricol is investigational.,Tiratricol is a solid.,True
16884,,,,,GC-24 is experimental.,GC-24 is a solid.,False
16885,"Eprotirome which is a compound with promising properties for treatment of obesity and dyslipidemia. Eprotirome increases the body’s energy consumption and reduces body weight and markedly reduces blood lipids and blood glucose. Investigated for use/treatment in hyperlipidemia, metabolic disease, and obesity. KB2115 is liver selectuve TR agonist that can induce pharmacological effects in the liver. It increases energy consumption, reduces body weight and also markedly reduces blood lipids and blood glucose levels at doses not affecting heart rate, bone density or TSH levels. KB2115 works by selectively stimulating the thyroid hormone",,,,Eprotirome is investigational.,Eprotirome is a solid.,True
16886,"MB07811 is the first of a novel class of product candidates discovered by Metabasis designed to lower serum cholesterol and triglycerides. MB07811, a small molecule that is administered orally, has been extensively studied preclinically and is currently undergoing clinical testing. MB07811 combines a novel thyroid hormone receptor agonist with the Company's novel HepDirect liver targeting prodrug technology. The combination of selectivity for the beta form of the receptor, liver targeting and other structural characteristics that limit extra-hepatic activity is designed to provide significant efficacy while avoiding side effects associated with activation of thyroid hormone receptors outside the liver. Investigated for use/treatment in hyperlipidemia. MB07811's TR beta receptor selectivity and liver targeting could harness the efficacy of the approach, while avoiding extra-hepatic activation of TR alpha and TR beta receptors that may lead to therapy limiting side effects. These benefits may include: reduction of LDL and total cholesterol, Reduced liver and serum triglycerides, reduced Lp(a) and enhanced clearance of liver fat. Studies indicate that targeting TR agonists to the liver has the potential to lower both LDL-cholesterol (the \bad\"" cholesterol) and both hepatic and plasma triglyceride levels.""",,,,MB07811 is investigational.,MB07811 is a solid.,True
16887,,,,,Sobetirome is investigational.,Sobetirome is a solid.,False
16888,,,,,1-(4-HEXYLPHENYL)PROP-2-EN-1-ONE is experimental.,1-(4-HEXYLPHENYL)PROP-2-EN-1-ONE is a solid.,False
16889,"A compound that inhibits aminobutyrate aminotransferase activity in vivo, thereby raising the level of gamma-aminobutyric acid in tissues. ",,,,Aminooxyacetic acid is experimental.,Aminooxyacetic acid is a solid.,True
16890,,,,,4-(2-AMINOPHENYL)-4-OXOBUTANOIC ACID is experimental.,4-(2-AMINOPHENYL)-4-OXOBUTANOIC ACID is a solid.,False
16891,,,,,"1-Azepan-1-Yl-2-Phenyl-2-(4-Thioxo-1,4-Dihydro-PyrazoloPyrimidin-5-Yl)Ethanone Adduct is experimental.","1-Azepan-1-Yl-2-Phenyl-2-(4-Thioxo-1,4-Dihydro-PyrazoloPyrimidin-5-Yl)Ethanone Adduct is a solid.",False
16892,"Human secretin is a gastrointestinal peptide hormone that regulates secretions in the stomach, pancreas, and liver. The hormone is produced from the enterochromaffin cells in the duodenum in response to the duodenal content with the pH less than 4.5. The main action of secretin is to stimulate the pancreas to secrete pancreatic juice for pH regulation in the small intestines. Secretin is also responsible in body fluid homeostasis and bile production. Although it is a gastrointestinal hormone, secretin is also considered as a neuropeptide hormone since it is also expressed in the central nervous system. Indicated for the stimulation of: In clinical trials, intravenous administration of synthetic human secretin stimulated the exocrine pancreas to promote juice and bicarbonate secretion, with variable responses depending on the pancreatic function of the individual. Having an identical amino acid sequence to the biologically-derived secretin, synthetic human secretin exhibits an equivalent biological activity as the natural hormone. The biological activity of synthetic human secretin was approximately 5.0 CU per mcg. In patients with suspected or known exocrine pancreatic dysfunction, a volume response of less than 2 mL/kg/hr, peak bicarbonate concentration of less than 80 mEq/L, and a bicarbonate output of less than 0.2 mEq/kg/hr following intravenous synthetic human secretin. Administration in healthy subjects in three crossover studies led to overall pancreatic secretory response of a mean peak bicarbonate concentration of 100 mEq/L, a mean total volume over one hour of 260.7 mL, and a peak bicarbonate concentrations ≥ 80 mEq/L.  Synthetic human secretin mediates the same biological effects as the naturally-occurring gastrointestinal peptide hormone. Secretin is normally released from enterochromaffin cells and S cells in the intestinal mucosa of duodenum upon exposure of proximal intestinal lumen to the acidic gastric content, or fatty acids and amino acids. Secretin mediates an inhibitory effect on acid secretion by parietal cells of the stomach, and causes alkalinazation of the duodenal content by stimulating the release of pancreatic juice, which has high amounts of water and bicarbonate ions. Bicarbonate ions are released into the duodenum from the centroacinar cells, and epithelia lining the pancreatic and biliary ducts. Human secretin is a ligand at G-protein coupled secretin receptors which are expressed in the basolateral domain of several tissue cell types , including pancreas, stomach, liver, colon and other tissues. Upon interaction, levels of cAMP increase and initiates the cAMP-mediated signalling cascade that results in phosphorylation of protein kinase A (PKA) and activation of cystic fibrosis transmembrane conductance regulator (CFTR). Activation of CFTR activates Cl-/HCO3- anion exchanger 2 and leads to secretion of bicarbonate-rich-pancreatic fluid. Via the same cAMP signalling pathway, secretin promotes the secretion of water and electrolytes in cholangiocytes. Secretin may work through vagal-vagal neural pathways since stimulation of the efferent vagus nerve stimulates bicarbonate secretion and atropine blocks secretin-stimulated pancreatic secretion. Additionally, secretin acts as a diuretic to increase urinary volume and bicarbonate excretion. ",The molecular weight is 3039.46.,Secretin human has a topological polar surface area of 1401.22.,The log p value of  is 0.0.,Secretin human is approved.,Secretin human is a liquid.,True
16893,,,,,p-Hydroxymercuribenzoic acid is experimental.,p-Hydroxymercuribenzoic acid is a solid.,False
16894,,,,,N-Benzyl-4-Sulfamoyl-Benzamide is experimental.,N-Benzyl-4-Sulfamoyl-Benzamide is a solid.,False
16895,,,,,4-Flourobenzenesulfonamide is experimental.,4-Flourobenzenesulfonamide is a solid.,False
16896,,,,,AL5424 is experimental.,AL5424 is a solid.,False
16897,,,,,N-(2-Flouro-Benzyl)-4-Sulfamoyl-Benzamide is experimental.,N-(2-Flouro-Benzyl)-4-Sulfamoyl-Benzamide is a solid.,False
16898,,,,,"3,5-Difluorobenzenesulfonamide is experimental.","3,5-Difluorobenzenesulfonamide is a solid.",False
16899,,,,,AL7089A is experimental.,AL7089A is a solid.,False
16900,,,,,4-(Aminosulfonyl)-N--Benzamide is experimental.,4-(Aminosulfonyl)-N--Benzamide is a solid.,False
16901,Irosustat has been investigated for the treatment of Metastatic Breast Cancer and Locally Advanced Breast Cancer.,,,,Irosustat is investigational.,Irosustat is a solid.,True
16902,,,,,4-(Aminosulfonyl)-N--Benzamide is experimental.,4-(Aminosulfonyl)-N--Benzamide is a solid.,False
16903,,,,,(R)-N-(3-Indol-1-Yl-2-Methyl-Propyl)-4-Sulfamoyl-Benzamide is experimental.,(R)-N-(3-Indol-1-Yl-2-Methyl-Propyl)-4-Sulfamoyl-Benzamide is a solid.,False
16904,,,,,Aminodi(Ethyloxy)Ethylaminocarbonylbenzenesulfonamide is experimental.,Aminodi(Ethyloxy)Ethylaminocarbonylbenzenesulfonamide is a solid.,False
16905,,,,,AL7182 is experimental.,AL7182 is a solid.,False
16906,,,,,"N-(2,3,4,5,6-Pentaflouro-Benzyl)-4-Sulfamoyl-Benzamide is experimental.","N-(2,3,4,5,6-Pentaflouro-Benzyl)-4-Sulfamoyl-Benzamide is a solid.",False
16907,"A cyanide compound which has been used as a fertilizer, defoliant and in many manufacturing processes. It often occurs as the calcium salt, sometimes also referred to as cyanamide. The citrated calcium salt is used in the treatment of alcoholism. ",,,,Cyanamide is experimental.,Cyanamide is a solid.,True
16908,,,,,4-(Aminosulfonyl)-N--Benzamide is experimental.,4-(Aminosulfonyl)-N--Benzamide is a solid.,False
16909,,,,,Dansylamide is experimental.,Dansylamide is a solid.,False
16910,,,,,"Sulfamic Acid 2,3-O-(1-Methylethylidene)-4,5-O-Sulfonyl-Beta-Fructopyranose Ester is experimental.","Sulfamic Acid 2,3-O-(1-Methylethylidene)-4,5-O-Sulfonyl-Beta-Fructopyranose Ester is a solid.",False
16911,,,,,"N-(2-Thienylmethyl)-2,5-Thiophenedisulfonamide is experimental.","N-(2-Thienylmethyl)-2,5-Thiophenedisulfonamide is a solid.",False
16912,,,,,4-(Aminosulfonyl)-N--Benzamide is experimental.,4-(Aminosulfonyl)-N--Benzamide is a solid.,False
16913,,,,,AL7099A is experimental.,AL7099A is a solid.,False
16914,,,,,"Al-6619, -1,2-Thiazine-6-Sulfonamide,2-(3-Hydroxyphenyl)-3-(4-Morpholinyl)-, 1,1-Dioxide] is experimental.","Al-6619, -1,2-Thiazine-6-Sulfonamide,2-(3-Hydroxyphenyl)-3-(4-Morpholinyl)-, 1,1-Dioxide] is a solid.",False
16915,,,,,"2,6-Difluorobenzenesulfonamide is experimental.","2,6-Difluorobenzenesulfonamide is a solid.",False
16916,,,,,"1-Methyl-3-Oxo-1,3-Dihydro-BenzoIsothiazole-5-Sulfonic Acid Amide is experimental.","1-Methyl-3-Oxo-1,3-Dihydro-BenzoIsothiazole-5-Sulfonic Acid Amide is a solid.",False
16917,,,,,(4-sulfamoyl-phenyl)-thiocarbamic acid O-(2-thiophen-3-yl-ethyl) ester is experimental.,(4-sulfamoyl-phenyl)-thiocarbamic acid O-(2-thiophen-3-yl-ethyl) ester is a solid.,False
16918,,,,,4-Methylimidazole is experimental.,4-Methylimidazole is a solid.,False
16919,,,,,AL5927 is experimental.,AL5927 is a solid.,False
16920,,,,,"1,2,4-Triazole is experimental.","1,2,4-Triazole is a solid.",False
16921,,,,,N--4-Sulfamoyl-Benzamide is experimental.,N--4-Sulfamoyl-Benzamide is a solid.,False
16922,,,,,"Al-6629, -1,2-Thiazine-6-Sulfonamide,2-(3-Methoxyphenyl)-3-(4-Morpholinyl)-, 1,1-Dioxide] is experimental.","Al-6629, -1,2-Thiazine-6-Sulfonamide,2-(3-Methoxyphenyl)-3-(4-Morpholinyl)-, 1,1-Dioxide] is a solid.",False
16923,,,,,4-Sulfonamide-Benzamide is experimental.,4-Sulfonamide-Benzamide is a solid.,False
16924,,,,,"N-(2,6-Diflouro-Benzyl)-4-Sulfamoyl-Benzamide is experimental.","N-(2,6-Diflouro-Benzyl)-4-Sulfamoyl-Benzamide is a solid.",False
16925,,,,,AL-4623 is experimental.,AL-4623 is a solid.,False
16926,,,,,(S)-N-(3-Indol-1-Yl-2-Methyl-Propyl)-4-Sulfamoyl-Benzamide is experimental.,(S)-N-(3-Indol-1-Yl-2-Methyl-Propyl)-4-Sulfamoyl-Benzamide is a solid.,False
16927,,,,,Mercuribenzoic Acid is experimental.,Mercuribenzoic Acid is a solid.,False
16928,,,,,4-Sulfonamide-Benzamide is experimental.,4-Sulfonamide-Benzamide is a solid.,False
16929,,,,,"(4s-Trans)-4-(Methylamino)-5,6-Dihydro-6-Methyl-4h-Thieno(2,3-B)Thiopyran-2-Sulfonamide-7,7-Dioxide is experimental.","(4s-Trans)-4-(Methylamino)-5,6-Dihydro-6-Methyl-4h-Thieno(2,3-B)Thiopyran-2-Sulfonamide-7,7-Dioxide is a solid.",False
16930,,,,,AL5300 is experimental.,AL5300 is a solid.,False
16931,,,,,4-(Aminosulfonyl)-N--Benzamide is experimental.,4-(Aminosulfonyl)-N--Benzamide is a solid.,False
16932,,,,,3-Mercuri-4-Aminobenzenesulfonamide is experimental.,3-Mercuri-4-Aminobenzenesulfonamide is a solid.,False
16933,,,,,AL6528 is experimental.,AL6528 is a solid.,False
16934,,,,,3-Nitro-4-(2-Oxo-Pyrrolidin-1-Yl)-Benzenesulfonamide is experimental.,3-Nitro-4-(2-Oxo-Pyrrolidin-1-Yl)-Benzenesulfonamide is a solid.,False
16935,,,,,4-(Aminosulfonyl)-N--Benzamide is experimental.,4-(Aminosulfonyl)-N--Benzamide is a solid.,False
16936,,,,,4--4H--TRIAZOLE is experimental.,4--4H--TRIAZOLE is a solid.,False
16937,,,,,4--4H--TRIAZOLE is experimental.,4--4H--TRIAZOLE is a solid.,False
16938,,,,,"1-N-(4-SULFAMOYLPHENYL-ETHYL)-2,4,6-TRIMETHYLPYRIDINIUM is experimental.","1-N-(4-SULFAMOYLPHENYL-ETHYL)-2,4,6-TRIMETHYLPYRIDINIUM is a solid.",False
16939,,,,,"5-{AMINO}-1,3,4-THIADIAZOLE-2-SULFONAMIDE is experimental.","5-{AMINO}-1,3,4-THIADIAZOLE-2-SULFONAMIDE is a solid.",False
16940,,,,,"2-(cycloheptylmethyl)-1,1-dioxido-1-benzothiophen-6-yl sulfamate is experimental.","2-(cycloheptylmethyl)-1,1-dioxido-1-benzothiophen-6-yl sulfamate is a solid.",False
16941,,,,,N--2-propylpentanamide is experimental.,N--2-propylpentanamide is a solid.,False
16942,,,,,"5--1,3,4-thiadiazole-2-sulfonamide is experimental.","5--1,3,4-thiadiazole-2-sulfonamide is a solid.",False
16943,,,,,"THIOPHENE-2,5-DISULFONIC ACID 2-AMIDE-5-(4-METHYL-BENZYLAMIDE) is experimental.","THIOPHENE-2,5-DISULFONIC ACID 2-AMIDE-5-(4-METHYL-BENZYLAMIDE) is a solid.",False
16944,,,,,(S)-Indapamide is experimental.,(S)-Indapamide is a solid.,False
16945,,,,,N--2-MERCAPTOBENZAMIDE is experimental.,N--2-MERCAPTOBENZAMIDE is a solid.,False
16946,,,,,"(17beta)-17-(cyanomethyl)-2-methoxyestra-1(10),2,4-trien-3-yl sulfamate is experimental.","(17beta)-17-(cyanomethyl)-2-methoxyestra-1(10),2,4-trien-3-yl sulfamate is a solid.",False
16947,,,,,"5-(2-chlorophenyl)-1,3,4-thiadiazole-2-sulfonamide is experimental.","5-(2-chlorophenyl)-1,3,4-thiadiazole-2-sulfonamide is a solid.",False
16948,,,,,PHENYLALANYLAMINODI(ETHYLOXY)ETHYL BENZENESULFONAMIDEAMINOCARBONYLBENZENESULFONAMIDE is experimental.,PHENYLALANYLAMINODI(ETHYLOXY)ETHYL BENZENESULFONAMIDEAMINOCARBONYLBENZENESULFONAMIDE is a solid.,False
16949,,,,,"N-(2,3-DIFLUORO-BENZYL)-4-SULFAMOYL-BENZAMIDE is experimental.","N-(2,3-DIFLUORO-BENZYL)-4-SULFAMOYL-BENZAMIDE is a solid.",False
16950,,,,,2-chloro-5-benzenesulfonamide is experimental.,2-chloro-5-benzenesulfonamide is a solid.,False
16951,,,,,"2-(1,3-thiazol-4-yl)-1H-benzimidazole-5-sulfonamide is experimental.","2-(1,3-thiazol-4-yl)-1H-benzimidazole-5-sulfonamide is a solid.",False
16952,,,,,indane-5-sulfonamide is experimental.,indane-5-sulfonamide is a solid.,False
16953,,,,,4-({CARBONOTHIOYL}AMINO)BENZENESULFONAMIDE is experimental.,4-({CARBONOTHIOYL}AMINO)BENZENESULFONAMIDE is a solid.,False
16954,,,,,N-({AMINO}CARBONYL)-4-METHYLBENZENESULFONAMIDE is experimental.,N-({AMINO}CARBONYL)-4-METHYLBENZENESULFONAMIDE is a solid.,False
16955,,The molecular weight is 290.35.,Sulthiame has a topological polar surface area of 97.54.,The log p value of  is 0.03.,Sulthiame is approved.,Sulthiame is a solid.,False
16956,,,,,"(9BETA,13ALPHA,14BETA,17ALPHA)-2-METHOXYESTRA-1,3,5(10)-TRIENE-3,17-DIYL DISULFAMATE is experimental.","(9BETA,13ALPHA,14BETA,17ALPHA)-2-METHOXYESTRA-1,3,5(10)-TRIENE-3,17-DIYL DISULFAMATE is a solid.",False
16957,,,,,"(4aS,4bR,10bS,12aS)-12a-methyl-1,3-dioxo-2-(pyridin-3-ylmethyl)-1,2,3,4,4a,4b,5,6,10b,11,12,12a-dodecahydronaphthoisoquinolin-8-yl sulfamate is experimental.","(4aS,4bR,10bS,12aS)-12a-methyl-1,3-dioxo-2-(pyridin-3-ylmethyl)-1,2,3,4,4a,4b,5,6,10b,11,12,12a-dodecahydronaphthoisoquinolin-8-yl sulfamate is a solid.",False
16958,,,,,"6-CHLORO-3-(DICHLOROMETHYL)-3,4-DIHYDRO-2H-1,2,4-BENZOTHIADIAZINE-7-SULFONAMIDE 1,1-DIOXIDE is experimental.","6-CHLORO-3-(DICHLOROMETHYL)-3,4-DIHYDRO-2H-1,2,4-BENZOTHIADIAZINE-7-SULFONAMIDE 1,1-DIOXIDE is a solid.",False
16959,,,,,2-(hydrazinocarbonyl)-3-phenyl-1H-indole-5-sulfonamide is experimental.,2-(hydrazinocarbonyl)-3-phenyl-1H-indole-5-sulfonamide is a solid.,False
16960,,,,,"6-HYDROXY-1,3-BENZOTHIAZOLE-2-SULFONAMIDE is experimental.","6-HYDROXY-1,3-BENZOTHIAZOLE-2-SULFONAMIDE is a solid.",False
16961,,,,,4-(2-AMINOETHYL)BENZENESULFONAMIDE is experimental.,4-(2-AMINOETHYL)BENZENESULFONAMIDE is a solid.,False
16962,"Raltitrexed (brand name Tomudex&reg;) is a chemotherapy drug manufactured AstraZeneca Company, is an antimetabolite used in chemotherapy. It is an inhibitor of thymidylate synthase. For the treatment of malignant neoplasm of colon and rectum Raltitrexed belongs to a group of medicines known as antimetabolites. It is used to treat cancer of the colon and rectum. It may also be used to treat other kinds of cancer, as determined by your doctor. Raltitrexed blocks an enzyme needed by the cell to live. This interferes with the growth of cancer cells, which are eventually destroyed. Since the growth of normal body cells may also be affected by raltitrexed, other effects will also occur. Some of these may be serious and must be reported to your doctor. Other effects, like hair loss, may not be serious but may cause concern. Raltitrexed is an antineoplastic Agents and folic acid antagonists. Raltitrexed inhibits thymidylate synthase (TS) leading to DNA fragmentation and cell death. It is transported into cells via a reduced folate carrier. Inside the cell Raltitrexed is extensively polyglutamated, which enhances thymidylate synthase inhibitory power and duration. Inhibition of this enzyme results in decreased synthesis of thymidine triphosphate which is required for DNA synthesis. ",The molecular weight is 458.49.,Raltitrexed has a topological polar surface area of 148.4.,The log p value of  is 0.71.,Raltitrexed is approved and investigational.,Raltitrexed is a solid.,True
16963,5-Thymidylic acid. A thymine nucleotide containing one phosphate group esterified to the deoxyribose moiety.,,,,Thymidine monophosphate is experimental.,Thymidine monophosphate is a solid.,True
16964,,,,,Deoxyuridine monophosphate is experimental.,Deoxyuridine monophosphate is a solid.,False
16965,"Thymectacin, a phosphoramidate derivative of (E)-5-(2-bromovinyl)-2'-deoxyuridine, is a novel small molecule anticancer agent. Thymectacin is selectively active against tumor cells expressing high levels of thymidylate synthase (TS), a critical enzyme in DNA biosynthesis. Thymectacin was as efficacious as irinotecan, a drug recently approved for the treatment of 5-fluorouracil-resistant colon cancer. Investigated for use/treatment in colorectal cancer. NB1011 targets thymidylate synthase (TS), which catalyzes the transformation of E-5-(2-bromovinyl)-2'-deoxyuridine-5'-monophosphate (BVdUMP) into cytotoxic reaction products. Due to the elevated levels of TS expression in tumor cells compared to normal cells, these cytotoxic products are preferentially generated inside tumor cells, and, as expected, NB1011 is more toxic to cells with higher levels of TS expression. Therefore, NB1011 therapy should kill tumor cells without severely damaging normal cells.",,,,Thymectacin is investigational.,Thymectacin is a solid.,True
16966,"ANX-510 (CoFactor) is a folate-based biomodulator drug being developed to enhance the activity and reduce associated toxicity of the widely used cancer chemotherapy, 5-fluorouracil (5-FU). CoFactor use with 5-FU is being evaluated in clinical trials in first line treatment of metastatic colorectal cancer. Investigated for use/treatment in breast cancer, colorectal cancer, gall bladder cancer, and pancreatic cancer. ANX-510(CoFactor) enhances 5-FU activity to inhibit cancer growth by creating more stable binding of a metabolite of 5-FU, called 5-fluorodeoxyuracil monophosphate (FdUMP) to the target enzyme, thymidylate synthase (TS). Numerous preclinical and two clinical studies suggest that CoFactor provides a greater clinical benefit compared with the approved 5-FU biomodulator, leucovorin, which must undergo chemical conversion to become the active form of folate. As CoFactor is the active metabolite of leucovorin, CoFactor circumvents the chemical pathway that is required by leucovorin. CoFactor is able to directly deliver the active form of folate improving 5-FU performance with lower toxicity.",,,,ANX-510 is investigational.,ANX-510 is a solid.,True
16967,"OSI-7904L is a liposome encapsulated thymidylate synthase inhibitor, which is indicated for use in advanced gastric and/or gastroesophageal adenocarcinoma (A-G/GEJA). Current treatments also inhibit thymidylate synthase but the innovative lipid coating of OSI-7904L allows for more enduring results with administration of the TS inhibitor. Investigated for use/treatment in gastric cancer. OSI-7904L is a liposome encapsulated thymidylate synthase inhibitor, which is indicated for use in advanced gastric and/or gastroesophageal adenocarcinoma (A-G/GEJA). Current treatments also inhibit thymidylate synthase but the innovative lipid coating of OSI-7904L allows for more enduring results with administration of the TS inhibitor. Inhibits thymidylate synthase.",,,,OSI-7904L is investigational.,OSI-7904L is a solid.,True
16968,,,,,"2,4-Diamino-5-phenyl-6-ethylpyrimidine is experimental.","2,4-Diamino-5-phenyl-6-ethylpyrimidine is a solid.",False
16969,,,,,N-imidodicarbonimidic diamide is experimental.,N-imidodicarbonimidic diamide is a solid.,False
16970,,,,,"N-(3,5-dimethoxyphenyl)imidodicarbonimidic diamide is experimental.","N-(3,5-dimethoxyphenyl)imidodicarbonimidic diamide is a solid.",False
16971,,,,,"6,6-DIMETHYL-1--1,6-DIHYDRO-1,3,5-TRIAZINE-2,4-DIAMINE is experimental.","6,6-DIMETHYL-1--1,6-DIHYDRO-1,3,5-TRIAZINE-2,4-DIAMINE is a solid.",False
16972,"Fludarabine is a chemotherapeutic agent used in the treatment of hematological malignancies. It is commonly marketed under the brand name Fludara. For the treatment of adult patients with B-cell chronic lymphocytic leukemia (CLL) who have not responded to or whose disease has progressed during treatment with at least one standard alkylating-agent containing regimen Fludarabine is a chemotherapy drug used in the treatment of chronic lymphocytic leukemia. It acts at DNA polymerase alpha, ribonucleotide reductase and DNA primase, results in the inhibition of DNA synthesis, and destroys the cancer cells. Fludarabine phosphate is rapidly dephosphorylated to 2-fluoro-ara-A and then phosphorylated intracellularly by deoxycytidine kinase to the active triphosphate, 2-fluoro-ara-ATP. This metabolite appears to act by inhibiting DNA polymerase alpha, ribonucleotide reductase and DNA primase, thus inhibiting DNA synthesis. The mechanism of action of this antimetabolite is not completely characterized and may be multi-faceted.",,,,Fludarabine is approved.,Fludarabine is a solid.,True
16973,"Imexon is currently being studied for the treatment of pancreatic, lung, breast, prostate, melanoma, and multiple myeloma cancers. It belongs to the family of drugs called cyanoaziridine derivatives. Also called Amplimexon. Imexon is a cyanoaziridine derivative. Investigated for use/treatment in melanoma, multiple myeloma, ovarian cancer, pancreatic cancer, and solid tumors. Imexon enters the cell and binds to glutathione and other sulfhydryl compounds, effectively preventing them from scavenging the toxic free radicals. So, particularly in the rapidly dividing cancer cell, free radical build-up in the presence of imexon leads to changes in mitochondrial membrane potential and ultimately to the mitochondria swelling and bursting. Mitochondrial proteins, in particular cytochrome c, are released into the cytoplasm and this activates caspase-mediated apoptosis resulting in cancer cell death. This sequence of events has been well characterized and published in several papers in leading cancer journals. Imexon is probably the only cancer drug under development at this time which exploits this mechanism of action.",,,,Imexon is investigational.,Imexon is a solid.,True
16974,"Gallium maltolate is Titan’s novel oral agent in development for the potential treatment of chronic bacterial infections, bone disease and cancer. Investigated for use/treatment in bladder cancer, lymphoma (unspecified), multiple myeloma, paget's disease, and prostate cancer. Gallium maltolate is a novel orally active formulation of gallium, a semi-metallic element that is a potent inhibitor of ribonucleotide reductase, an enzyme that promotes tumor growth.Gallium is also known to concentrate in malignant tumors and sites of infection, and appears to favorably impact calcium deposition, making bones more resistant to degradation caused by cancer metastasis. Titan's novel product, gallium maltolate, may significantly expand the therapeutic potential of gallium by providing the advantages of enhanced bioavailablity, a potentially improved therapeutic profile and ease of administration.",,,,Gallium maltolate is investigational.,Gallium maltolate is a solid.,True
16975,Pentosan polysulfate is a sulfated pentosyl polysaccharide with heparin-like properties. For the relief of bladder pain or discomfort associated with interstitial cystitis. Pentosan polysulfate sodium is a low molecular weight heparin-like compound. It has anticoagulant and fibrinolytic effects. Pentosan polysulfate is a polymer of xylose hydrogen sulfate and contains two sulfate groups per carbohydrate monomer. It binds Fibroblast growth factors (FGFs) as well as other heparin-binding growth factors. It has been shown to interact also with the heparin-binding site of FGFR-1. It inhibits the growth of SW13 adrenocortical cells transfected with FGF-4 and tumorigenicity of MCF-7 breast carcinoma cells transfected with FGF-1 or FGF-4.,,,,Pentosan polysulfate is approved.,Pentosan polysulfate is a solid.,True
16976,"TP508 is a non-proteolytic synthetic peptide representing the portion of human thrombin originally identified as the fibroblast high-affinity receptor binding domain.  Investigated for use/treatment in bone fractures, diabetic foot ulcers, and wounds. TP508 is a 23-amino-acid peptide representing the receptor-binding domain of thrombin, and is thought to work by mimicking the ability of thrombin to activate platelets and a cascade of growth factors and enzymes that initiate and regulate the healing process. Although not tested with allografts, TP508/Chrysalin has been shown to improve fracture healing in experimental models and its application is associated with upregulation of angiogenic genes.",,,,TP-508 is investigational.,TP-508 is a solid.,True
16977,"An agent derived from licorice root. It is used for the treatment of digestive tract ulcers, especially in the stomach. Antidiuretic side effects are frequent, but otherwise the drug is low in toxicity. ",The molecular weight is 570.77.,Carbenoxolone has a topological polar surface area of 117.97.,The log p value of  is 7.19.,Carbenoxolone is experimental.,Carbenoxolone is a solid.,True
16978,"INCB13739 is developed as a new treatment for type 2 diabetes.  Investigated for use/treatment in diabetes mellitus type 2 and diabetes prevention. 11beta-HSD1 is an enzyme that converts cortisone into the potent biologically active hormone cortisol. This conversion occurs intra-cellularly within several key metabolic tissues including the liver, adipose, muscle and pancreas. Cortisol acts as an antagonist of insulin action, and 11beta-HSD1 mediated production of cortisol has been hypothesized to contribute to human insulin resistance and type 2 diabetes. INCB13739 inhibits 11beta-HSD1 and has the potential to provide a broad spectrum impact on the multiple components seen in patients with type 2 diabetes. INCB13739 is an inhibitor of 11beta-HSD1 (11-beta hydroxysteroid dehydrogenase type 1). 11beta-HSD1 is an enzyme that appears to be critical to the development of type 2 diabetes. INCB13739 completely inhibits the production of intra-adipose and intra-hepatic cortisol by 11beta-HSD1, while maintaining normal systemic cortisol levels, which are essential for immune function and response to stress.",,,,INCB13739 is investigational.,INCB13739 is a solid.,True
16979,,,,,"(3,3-dimethylpiperidin-1-yl)(6-(3-fluoro-4-methylphenyl)pyridin-2-yl)methanone is experimental.","(3,3-dimethylpiperidin-1-yl)(6-(3-fluoro-4-methylphenyl)pyridin-2-yl)methanone is a solid.",False
16980,,,,,"(5S)-2-{amino}-5-(2-hydroxy-2-propanyl)-5-methyl-1,3-thiazol-4(5H)-one is experimental.","(5S)-2-{amino}-5-(2-hydroxy-2-propanyl)-5-methyl-1,3-thiazol-4(5H)-one is a solid.",False
16981,,,,,(2R)-1--2-methyl-4-(4-nitrophenyl)piperazine is experimental.,(2R)-1--2-methyl-4-(4-nitrophenyl)piperazine is a solid.,False
16982,,,,,"2-(6-{amino}pyridin-2-yl)-N,N-diethylacetamide is experimental.","2-(6-{amino}pyridin-2-yl)-N,N-diethylacetamide is a solid.",False
16983,,,,,"(5S)-2-{amino}-5-methyl-5-(trifluoromethyl)-1,3-thiazol-4(5H)-one is experimental.","(5S)-2-{amino}-5-methyl-5-(trifluoromethyl)-1,3-thiazol-4(5H)-one is a solid.",False
16984,,,,,N-{1-piperidin-4-yl}-N-cyclopropyl-4-benzamide is experimental.,N-{1-piperidin-4-yl}-N-cyclopropyl-4-benzamide is a solid.,False
16985,,,,,N-cyclopropyl-N-(trans-4-pyridin-3-ylcyclohexyl)-4-benzamide is experimental.,N-cyclopropyl-N-(trans-4-pyridin-3-ylcyclohexyl)-4-benzamide is a solid.,False
16986,,,,,1-{phenyl}sulfonyl)piperazin-1-yl]methyl}cyclopropanecarboxamide is experimental.,1-{phenyl}sulfonyl)piperazin-1-yl]methyl}cyclopropanecarboxamide is a solid.,False
16987,,,,,"(5S)-2-(Cyclooctylamino)-5-methyl-5-propyl-1,3-thiazol-4(5H)-one is experimental.","(5S)-2-(Cyclooctylamino)-5-methyl-5-propyl-1,3-thiazol-4(5H)-one is a solid.",False
16988,,,,,2-(2-CHLORO-4-FLUOROPHENOXY)-2-METHYL-N-PROPANAMIDE is experimental.,2-(2-CHLORO-4-FLUOROPHENOXY)-2-METHYL-N-PROPANAMIDE is a solid.,False
16989,,,,,"(1S,3R,4S,5S,7S)-4-{AMINO}ADAMANTANE-1-CARBOXAMIDE is experimental.","(1S,3R,4S,5S,7S)-4-{AMINO}ADAMANTANE-1-CARBOXAMIDE is a solid.",False
16990,,,,,"(5R)-2--5-isopropyl-1,3-thiazol-4(5H)-one is experimental.","(5R)-2--5-isopropyl-1,3-thiazol-4(5H)-one is a solid.",False
16991,"A complex of three different closely related aminoglycoside sulfates, Gentamicins C1, C2, and C1a, obtained from Micromonospora purpurea and related species. They are broad-spectrum antibiotics, but may cause ear and kidney damage. They act to inhibit protein synthesis (genetic translation). For treatment of serious infections caused by susceptible strains of the following microorganisms: <i>P. aeruginosa</i>, <i>Proteus</i> species (indole-positive and indole-negative), <i>E. coli</i>, <i>Klebsiella-Enterobactor-Serratia</i> species, <i>Citrobacter</i> species and <i>Staphylococcus</i> species (coagulase-positive and coagulase-negative). Gentamicin is a broad spectrum aminoglycoside antibiotic. Aminoglycosides work by binding to the bacterial 30S ribosomal subunit, causing misreading of t-RNA, leaving the bacterium unable to synthesize proteins vital to its growth. Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. In addition, some mycobacteria, including the bacteria that cause tuberculosis, are susceptible to aminoglycosides. Infections caused by Gram-positive bacteria can also be treated with aminoglycosides, but other types of antibiotics are more potent and less damaging to the host. In the past the aminoglycosides have been used in conjunction with penicillin-related antibiotics in streptococcal infections for their synergistic effects, particularly in endocarditis. Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses. Aminoglycosides like gentamicin \irreversibly\"" bind to specific 30S-subunit proteins and 16S rRNA. Specifically gentamicin binds to four nucleotides of 16S rRNA and a single amino acid of protein S12. This interferes with decoding site in the vicinity of nucleotide 1400 in 16S rRNA of 30S subunit. This region interacts with the wobble base in the anticodon of tRNA. This leads to interference with the initiation complex, misreading of mRNA so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes.""",,,,Gentamicin is approved and vet_approved.,Gentamicin is a solid.,True
16992,,,,,"2,4-Diamino-5-Methyl-6-PyridoPyrimidine is experimental.","2,4-Diamino-5-Methyl-6-PyridoPyrimidine is a solid.",False
16993,,,,,"2,4-Diamino-6-Quinazoline is experimental.","2,4-Diamino-6-Quinazoline is a solid.",False
16994,,,,,"6-(Octahydro-1h-Indol-1-Ylmethyl)Decahydroquinazoline-2,4-Diamine is experimental.","6-(Octahydro-1h-Indol-1-Ylmethyl)Decahydroquinazoline-2,4-Diamine is a solid.",False
16995,,,,,"N6-(2,5-Dimethoxy-Benzyl)-N6-Methyl-PyridoPyrimidine-2,4,6-Triamine is experimental.","N6-(2,5-Dimethoxy-Benzyl)-N6-Methyl-PyridoPyrimidine-2,4,6-Triamine is a solid.",False
16996,,,,,"2,4-Diamino-6-PyridoPyrimidine is experimental.","2,4-Diamino-6-PyridoPyrimidine is a solid.",False
16997,,,,,Sri-9662 is experimental.,Sri-9662 is a solid.,False
16998,,,,,"2,4-Diamino-5-(3,4,5-Trimethoxy-Benzyl)-Pyrimidin-1-Ium is experimental.","2,4-Diamino-5-(3,4,5-Trimethoxy-Benzyl)-Pyrimidin-1-Ium is a solid.",False
16999,,,,,Sri-9439 is experimental.,Sri-9439 is a solid.,False
17000,"Piritrexim has been used in trials studying the treatment of Bladder Cancer, Urethral Cancer, and Transitional Cell Cancer of the Renal Pelvis and Ureter.",,,,Piritrexim is investigational.,Piritrexim is a solid.,True
17001,A natural product that has been considered as a growth factor for some insects. ,,,,Biopterin is experimental.,Biopterin is a solid.,True
17002,,,,,"2,4-Diamino-6-PyridoPyrimidine is experimental.","2,4-Diamino-6-PyridoPyrimidine is a solid.",False
17003,"Investigated for use/treatment in bacterial infection, skin infections/disorders, obesity, liver disease, kidney disease, and pneumonia. Iclaprim is a novel diaminopyrimidine, and an inhibitor of dihydrofolate reductase, which has shown potent, extended-spectrum in vitro activity against Gram-positive bacteria, including methicillin-resistant Staphylococcus aureus, vancomycin-intermediate and vancomycin-resistant S. aureus and macrolide-, quinolone- and trimethoprim-resistant strains. In addition, iclaprim has demonstrated activity against Streptococcus pneumoniae including penicillin-, erythromycin-, levofloxacin- and trimethoprim/sulfamethoxazole-resistant strains.",The molecular weight is 354.41.,Iclaprim has a topological polar surface area of 105.51.,The log p value of  is 2.64.,Iclaprim is investigational.,Iclaprim is a solid.,True
17004,,,,,"5--6-methylpyrimidine-2,4-diamine is experimental.","5--6-methylpyrimidine-2,4-diamine is a solid.",False
17005,,,,,"5--6-methylpyrimidine-2,4-diamine is experimental.","5--6-methylpyrimidine-2,4-diamine is a solid.",False
17006,,,,,"5--6-methylpyrimidine-2,4-diamine is experimental.","5--6-methylpyrimidine-2,4-diamine is a solid.",False
17007,,,,,"5--6-methylpyrimidine-2,4-diamine is experimental.","5--6-methylpyrimidine-2,4-diamine is a solid.",False
17008,,,,,"5--6-ethylpyrimidine-2,4-diamine is experimental.","5--6-ethylpyrimidine-2,4-diamine is a solid.",False
17009,,,,,-DIBENZAZEPINE is experimental.,-DIBENZAZEPINE is a solid.,False
17010,,,,,"(4aS)-5--4a,5-dihydro-2H-dibenzoazepin-8-ol is experimental.","(4aS)-5--4a,5-dihydro-2H-dibenzoazepin-8-ol is a solid.",False
17011,,,,,"(2R,6S)-6-{methyl}-1,2,5,6,7,8-hexahydroquinazoline-2,4-diamine is experimental.","(2R,6S)-6-{methyl}-1,2,5,6,7,8-hexahydroquinazoline-2,4-diamine is a solid.",False
17012,,,,,Triglu-5-formyl-tetrahydrofolate is experimental.,Triglu-5-formyl-tetrahydrofolate is a solid.,False
17013,,,,,"5-hydroxymethyl-5,6-dihydrofolic acid is experimental.","5-hydroxymethyl-5,6-dihydrofolic acid is a solid.",False
17014,,,,,N-Pyridoxyl-Glycine-5-Monophosphate is experimental.,N-Pyridoxyl-Glycine-5-Monophosphate is a solid.,False
17015,,,,,(2R)-({4-PHENYL}AMINO){5-ETHOXY-2-FLUORO-3-PHENYL}ACETICACID is experimental.,(2R)-({4-PHENYL}AMINO){5-ETHOXY-2-FLUORO-3-PHENYL}ACETICACID is a solid.,False
17016,,,,,3-({1--2-METHYL-BUTYLSULFAMOYL}-METHYL)-BENZOIC ACID is experimental.,3-({1--2-METHYL-BUTYLSULFAMOYL}-METHYL)-BENZOIC ACID is a solid.,False
17017,,,,,2--PENTANEDIOIC ACID 5-AMIDE 1-(4-CARBAMIMIDOYL-BENZYLAMIDE) is experimental.,2--PENTANEDIOIC ACID 5-AMIDE 1-(4-CARBAMIMIDOYL-BENZYLAMIDE) is a solid.,False
17018,,,,,2--PENTANEDIOIC ACID 5-AMIDE 1-(4-CARBAMIM IDOYL-BENZYLAMIDE) is experimental.,2--PENTANEDIOIC ACID 5-AMIDE 1-(4-CARBAMIM IDOYL-BENZYLAMIDE) is a solid.,False
17019,,,,,N--3-HYDROXY-2-PROPOXYAMINO-BUTYRAMID is experimental.,N--3-HYDROXY-2-PROPOXYAMINO-BUTYRAMID is a solid.,False
17020,,,,,2-(4-HYDROXY-5-PHENYL-1H-PYRAZOL-3-YL)-1H-BENZOIMIDAZOLE-5-CARBOXAMIDINE is experimental.,2-(4-HYDROXY-5-PHENYL-1H-PYRAZOL-3-YL)-1H-BENZOIMIDAZOLE-5-CARBOXAMIDINE is a solid.,False
17021,,,,,PYRIDIN-2-YL)-BIPHENYL-3-YLMETHYL]-UREA is experimental.,PYRIDIN-2-YL)-BIPHENYL-3-YLMETHYL]-UREA is a solid.,False
17022,,,,,pyridin-2-yl)-6-hydroxy-3'-nitro-3-biphenylyl]acetic acid is experimental.,pyridin-2-yl)-6-hydroxy-3'-nitro-3-biphenylyl]acetic acid is a solid.,False
17023,"Tafamidis and tafamidis meglumine (FX-1006A) are benzoxazole derivatives developed by FoldRX. Tafamidis is structurally similar to diflusinal. Tafamidis is indicated to treat cardiomyopathy of wild type or hereditary transthyretin-mediated amyloidosis in adults. Tafamidis stabilizes transthyretin tetramers, reducing the amount of monomers available for amyloidogenesis. It has a long duration of action as it is given once daily, and a wide therapeutic window. Genetic mutations or natural misfolding of transthyretin destabalizes transthyretin tetramers, leading to their dissociation and aggregation in tissues, and disrupting the normal function of these tissues. Tafamidis binds to transthyretin tetramers at the thyroxin binding sites, stabilizing the tetramer, reducing the availability of monomers for amyloidogenesis.",The molecular weight is 308.11.,Tafamidis has a topological polar surface area of 63.33.,The log p value of  is 5.0.,Tafamidis is approved and investigational.,Tafamidis is a solid.,True
17024,"At low doses, OPC 28326 selectively vasodilates the femoral arterial bed due to its inhibitory action at alpha-2-adrenoceptors while having minimal action on systemic blood pressure, heart rate and coronary, carotid, vertebral, renal, and mesenteric blood flows. It is the only clinical compound with this profile. It is currently being investigated in the treatment of peripheral vascular diseases and Raynaud's syndrome. Investigated for use/treatment in peripheral vascular disease and raynaud's disease. At low doses, OPC 28326 selectively vasodilates the femoral arterial bed due to its inhibitory action at alpha-2-adrenoceptors while having minimal action on systemic blood pressure, heart rate and coronary, carotid, vertebral, renal, and mesenteric blood flows. At low doses, OPC 28326 selectively vasodilates the femoral arterial bed due to its inhibitory action at alpha-2C-adrenoceptors. Other studies have also reported selectivity for a-2B-adrenoceptors.",,,,OPC-28326 is investigational.,OPC-28326 is a solid.,True
17025,,,,,Alpha-Aminobutyric Acid is experimental.,Alpha-Aminobutyric Acid is a solid.,False
17026,"Diminazene, also known as Diminazine, 4,4'-(Diazoamino)benzamidine, 4,4'-(1-triazene-1,3-diyl)bis-benzenecarboximidamide, diminazine aceturate, or Diminazene aceturate, is a trypanocidal agent. Major brands of Diminazene are Berenil, Pirocide, Ganasag, and Azidin. This substance is a solid. This compound belongs to the phenylhydrazines. These are compounds containing a phenylhydrazide moiety, which consists of a hydrazide substituent attached to a phenyl group. Known drug targets of diminazene include HTH-type transcriptional regulator QacR, trypsin-1, amiloride-sensitive amine oxidase , and mitochondrial peroxiredoxin-5.",,,,Diminazene is experimental.,Diminazene is a solid.,True
17027,"CF 101 (known generically as IB-MECA) is an anti-inflammatory drug for rheumatoid arthritis patients. Its novel mechanism of action relies on antagonism of adenoside A3 receptors.  Investigated for use/treatment in cancer/tumors (unspecified), eye disorders/infections, psoriasis and psoriatic disorders, and rheumatoid arthritis. CF-101 is an adenoside A3 agonist for the treatment of a variety of autoimmune-inflammatory disorders, particularly rhematoid arthritis. In clinical trials, it was found to be safe, well tolerated and showed strong evidence of an anti-inflammatory effect in rheumatoid arthritis patients. In this trial, a statistically significant correlation was found between A(3)AR expression level and response to the drug, so A(3)AR expression may serve as a biopredictor of patient response. CF 101 is an A(3)AR agonist. A(3)AR is highly expressed in inflammatory cells and overexpressed in peripheral blood mononuclear cells, reflecting its role in the remote inflammatory process. In normal tissues, there is low adenoside A3 receptor expression. A(3)AR activation with a specific agonist deregulates the NF-kappaB signaling pathway in inflammatory cells and initiates immunomodulatory effects.",,,,Piclidenoson is investigational.,Piclidenoson is a solid.,True
17028,"Ziconotide (also known as SNX-111) is a neurotoxic peptide derived from the cone snail _Conus magus_ comprising 25 amino acids with three disulphide bonds. Other such peptides, collectively termed conotoxins, exist, and some have shown efficacy in binding specific subsets of calcium channels; ziconotide is used in part because it can be synthesized without loss of proper bond formation or structural elements. Ziconotide is used to manage severe chronic pain refractory to other methods, through its ability to inhibit N-type calcium channels involved in nociceptive signalling. Ziconotide is indicated for the management of severe chronic pain in patients refractory to other treatments, and for whom intrathecal therapy is warranted. Ziconotide inhibits N-type calcium channels involved in nociceptive signalling, primarily in the dorsal horn of the spinal cord. Although binding is reversible, careful dosing is required to ensure therapeutic effects while minimizing adverse effects, and ziconotide has been described as possessing a narrow therapeutic window. Patients taking ziconontide may experience cognitive and neuropsychiatric symptoms, reduced levels of consciousness, and elevated serum creatine kinase levels. In addition, ziconotide may increase the risk of infection, including serious cases of meningitis. Patients who withdraw from opiates for ziconotide initiation are advised to taper off the dose. Nociceptive pain signalling is a complex processing pathway involving peripheral nociceptors, primary afferent nerve fibres, and downstream CNS neurons located in the spinal cord. Voltage-gated calcium channels (VGCCs) are important regulatory components of neural signalling and include the N-type (Cav2.2) heteromultimeric high-voltage type calcium channels. Chronic pain conditions, including inflammatory and neuropathic pain, often involve the aberrant upregulation of VGCC activity through various cellular mechanisms, which can lead to allodynia and hyperalgesia.",The molecular weight is 2639.14.,Ziconotide has a topological polar surface area of 1133.84.,The log p value of  is 0.0.,Ziconotide is approved.,Ziconotide is a solid.,True
17029,"Voclosporin is a novel cyclosporine analog and immunosuppressive compound currently being investigated for the treatment of psoriasis and for the prevention of organ rejection in kidney transplant patients. All studies to date suggest that Voclosporin is more potent and less toxic than currently available treatments within the drug class of calcineurin inhibitors. Voclosporin inhibits calcineurin. As a consequence, it inhibits T cell activation by blocking the transcription of early cytokines.",The molecular weight is 1214.65.,Voclosporin has a topological polar surface area of 278.8.,The log p value of  is 14.47.,Voclosporin is investigational.,,True
17030,"Alectinib is a second generation oral drug that selectively inhibits the activity of anaplastic lymphoma kinase (ALK) tyrosine kinase. It is specifically used in the treatment of non-small cell lung cancer (NSCLC) expressing the ALK-EML4 (echinoderm microtubule-associated protein-like 4) fusion protein that causes proliferation of NSCLC cells. Inhibition of ALK prevents phosphorylation and subsequent downstream activation of STAT3 and AKT resulting in reduced tumour cell viability.  Alectinib is a kinase inhibitor indicated for the treatment of patients with anaplastic lymphoma kinase (ALK)-positive, metastatic non-small cell lung cancer (NSCLC) who have progressed on or are intolerant to crizotinib. This indication is approved under accelerated approval based on tumor response rate and duration of response. Continued approval for this indication may be contingent upon verification and description of clinical benefit in confirmatory trials. Alectinib is a second generation oral drug that selectively inhibits the activity of anaplastic lymphoma kinase (ALK) tyrosine kinase. It is specifically used in the treatment of non-small cell lung cancer (NSCLC) expressing the ALK-EML4 (echinoderm microtubule-associated protein-like 4) fusion protein that causes proliferation of NSCLC cells. Inhibition of ALK prevents phosphorylation and subsequent downstream activation of STAT3 and AKT resulting in reduced tumour cell viability. Both alectinib and its major active metabolite M4 demonstrate similar in vivo and in vitro activity against multiple mutant forms of ALK. ",The molecular weight is 482.63.,Alectinib has a topological polar surface area of 72.36.,The log p value of  is 5.53.,Alectinib is approved and investigational.,Alectinib is a solid.,True
17031,,,,,Cyclohexylformamide is experimental.,Cyclohexylformamide is a solid.,False
17032,"TTP889, an orally bioavailable selective inhibitor of the intrinsic coagulation pathway, is being developed as an anticoagulant for the treatment of thromboembolic disorders. TTP889 is the only known selective small molecule inhibitor of Factor IX, a key enzyme of the intrinsic pathway of the blood coagulation system. TTP889 has proven to be effective in preventing clot formation in several animal models of human disease, without any signs of the bleeding associated with traditional anticoagulants.  Investigated for use/treatment in blood (blood forming organ disorders, unspecified), cardiac surgery, and venous thromboembolism. TTP889 is a factor IXa inhibitor with little or no activity against factors VIIIa, Xa, XIa, or XIIa. It is the only molecule in development that is an inhibitor of the intrinsic pathway in vitro and in vivo via FIX/IXa. TTP889 inhibits the ability of FIXa to form a fully functional tenase complex with FVIIIa. FIXa plays an integral role in the intrinsic coagulation pathway and a lesser role in the extrinsic pathway.",,,,TTP889 is investigational.,TTP889 is a solid.,True
17033,,,,,"5,7-Dichlorokynurenic acid is experimental.","5,7-Dichlorokynurenic acid is a solid.",False
17034,A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from GLYCINE or THREONINE. It is involved in the biosynthesis of PURINES; PYRIMIDINES; and other amino acids. ,,,,D-Serine is approved and experimental.,D-Serine is a solid.,True
17035,"Cycloleucine is non-metabolisable amino acid formed by cyclization of leucine. It is also a specific and reversible inhibitor of nucleic acid methylation and widely used in biochemical experiments. Cycloleucine has cytostatic, immunosuppressive and antineoplastic activities.",,,,Cycloleucine is experimental.,Cycloleucine is a solid.,True
17036,"CNS 5161 is a blocker of the NMDA ion channel and has completed Phase IIa proof of concept clinical trials as a novel compound for the treatment of neuropathic pain. Investigated for use/treatment in migraine and cluster headaches, neuropathy (diabetic), and pain (acute or chronic). CNS 5161 is a selective and high affinity N-methyl-D-aspartate (NMDA) receptor antagonist with preferential binding to the activated form of the receptor. CNS 5161 also penetrates the brain well and can be used to label selectively brain NMDA receptors in vivo. A radioactive form of CNS 5161 may be used as an agent to monitor NMDA receptors in the human brain using Positron Emission Tomography (\PET\"") and \""the significance of a selective, validated radiopharmaceutical agent suitable for detecting widespread as well as highly localized changes in the NMDA receptor in the living brain cannot be exaggerated\"".""",,,,CNS-5161 is investigational.,CNS-5161 is a solid.,True
17037,"N-methyl-D-aspartate (NMDA) receptors (NMDARs) are members of the ionotropic glutamate receptor family, with key roles in brain development and neurological function. NMDARs are heterotetramers that typically involve a dimer of dimers of both GluN1 and GluN2A-D subunits, with each subunit itself composed of an N-terminal domain (NTD), a ligand-binding domain (LBD), a transmembrane domain, and a C-terminal cytoplasmic domain. Binding at the LBD of the agonists glycine (or D-serine) to the GluN1 subunits and of glutamate to the GluN2 subunits is a regulatory mechanism for channel activation. In addition, allosteric modulators are known to bind at the NTDs and form another layer of regulation. One such allosteric regulator is ifenprodil, which was first shown to bind the NMDARs in the 1990s, and specifically to those NMDARs containing the GluN2B subunit. Further studies elucidated that ifenprodil binds strongly at the inter-subunit interface of adjacent GluN1 and GluN2B NTDs, where it acts as a non-competitive antagonist.",The molecular weight is 325.45.,Ifenprodil has a topological polar surface area of 43.7.,The log p value of  is 3.96.,Ifenprodil is investigational and withdrawn.,Ifenprodil is a solid.,True
17038,"Gemeprost is a prostaglandin E1 (PGE1) analog and antiprogestogen used for preoperative dilation of the cervix before surgical abortion. It is available as vaginal suppositories and also used in combination with the antiprogestin and mifepristone for termination of 1st- and 2nd-trimester pregnancy. It is not FDA-approved but available in Japan marketed as Preglandin. Indicated for the softening and dilatation of the cervix uteri prior to transcervical, intrauterine operative procedures in the first trimester of pregnancy or facilitating therapeutic termination of pregnancy in patients in the second trimester of gestation. Gemeprost softens and dilates of the cervix prior to transcervical intrauterine operative procedures. It is a prostaglandin E1 analog that potently stimulates uterine contractions and causes cervical ripening and relaxation. As a prostaglandin analog, gemeprost binds to prostaglandin E2 and E3 receptors as an agonist to cause myometrial contractions and progressive cervical dilation via tissue sensitization to oxytocin. ",The molecular weight is 394.55.,Gemeprost has a topological polar surface area of 83.83.,The log p value of  is 3.76.,Gemeprost is approved and withdrawn.,Gemeprost is a liquid.,True
17039,,,,,1-{4-pyrimidin-5-yl]phenyl}-3-urea is experimental.,1-{4-pyrimidin-5-yl]phenyl}-3-urea is a solid.,False
17040,"The novel indole-ether quinazoline Cediranib is a highly potent (IC<sub>50</sub> &lt; 1 nmol/L) ATP-competitive inhibitor of recombinant KDR tyrosine kinase in vitro. It is being developed clinically as a once-daily oral therapy for the treatment of cancer. For the treatment of liver cancer, advanced non-small cell lung cancer (NSCLC), advanced colorectal cancer (CRC) and other solid tumors. Cediranib is a once-daily, orally available, highly potent and selective VEGF signalling inhibitor that inhibits all three VEGF receptors. The preclinical profile of Cediranib indicates that it has the potential to be the 'best in class' VEGF signalling inhibitor. Phase I data indicate that Cediranib is generally well tolerated, with the most common dose related adverse events being diarrhoea, hoarseness, headache and hypertension. Cediranib inhibits vacular endothelial growth factor (VEGF) receptor tyrosine kinase (RTK). By forming a blockade at the VEGF receptors, Cediranib limits the growth of new blood vessels, which are essential to supporting tumor growth. Thus, lacking sufficient blood supply, tumor cells become starved for nutrients, slowing or halting growth and potentially improving the efficacy of other treatments. Preclinical evidence indicated that the drug had a high affinity at these sites, and was well tolerated and efficacious in animal studies.",,,,Cediranib is investigational.,Cediranib is a solid.,True
17041,"CYC116 is a novel anticancer compound with a unique target profile involving both cell cycle and angiogenesis inhibition mechanisms. In preclinical studies, CYC116 has demonstrated antitumor activity in both solid tumors and hematological cancers. Advanced solid tumors Aurora kinases are enzymes that help dividing cells share their materials between two daughter cells. In many people with cancer Aurora kinase malfunctions and normal control of cell division is lost resulting in abnormal growth.",,,,CYC116 is investigational.,CYC116 is a solid.,True
17042,"Ramucirumab is a human monoclonal antibody (IgG1) against vascular endothelial growth factor receptor 2 (VEGFR2), a type II trans-membrane tyrosine kinase receptor expressed on endothelial cells. By binding to VEGFR2, ramucirumab prevents binding of its ligands (VEGF-A, VEGF-C, and VEGF-D), thereby preventing VEGF-stimulated receptor phosphorylation and downstream ligand-induced proliferation, permeability, and migration of human endothelial cells. VEGFR stimulation also mediates downstream signalling required for angiogenesis and is postulated to be heavily involved in cancer progression, making it a highly likely drug target. In contrast to other agents directed against VEGFR-2, ramucirumab binds a specific epitope on the extracellular domain of VEGFR-2, thereby blocking all VEGF ligands from binding to it. Ramucirumab is indicated for us in advanced gastric or gastro-esophageal junction adenocarcinoma as a single agent or in combination with paclitaxel after prior fluoropyrimidine- or platinum-containing chemotherapy. For use in advanced gastric or gastro-esophageal junction adenocarcinoma as a single agent or in combination with paclitaxel after prior fluoropyrimidine- or platinum-containing chemotherapy. Ramucirumab is a human monoclonal antibody (IgG1) against vascular endothelial growth factor receptor 2 (VEGFR2), a type II trans-membrane tyrosine kinase receptor expressed on endothelial cells. By binding to VEGFR2, ramucirumab prevents binding of its ligands (VEGF-A, VEGF-C, and VEGF-D), thereby preventing VEGF-stimulated receptor phosphorylation and downstream ligand-induced proliferation, permeability, and migration of human endothelial cells.",,,,Ramucirumab is approved and investigational.,Ramucirumab is a solid.,True
17043,"CT-322 is a proprietary Adnectin(TM) protein therapeutic that, in preclinical studies, specifically binds to vascular endothelial growth factor receptor 2 (VEGFR-2), which regulates the primary tumor angiogenesis pathway. As a result, CT-322 blocks all known ligands for VEGFR-2. Investigated for use/treatment in cancer/tumors (unspecified) and macular degeneration. CT-322 specifically inhibits VEGFR-2 activation by its ligands VEGF-A, VEGF-C, and VEGF-D. In preclinical studies, this cell-surface receptor drives angiogenesis (growth of new blood vessels) in solid tumors, and CT-322 inhibits the tumorgenic effect of VEGFR-2 in preclinical models. CT-322 was designed using the PROfusion(TM) System, Adnexus' patented product design engine.",,,,Pegdinetanib is investigational.,Pegdinetanib is a solid.,True
17044,"Investigated for use/treatment in melanoma. CHIR-265 binds and inhibits Raf kinases, which may result in a reduction of tumor cell growth and proliferation, and tumor cell death. In addition, this agent inhibits vascular endothelial growth factor receptor type 2 (VEGFR-2), thereby disrupting tumor angiogenesis. Raf kinases are critical enzymes in the Ras/Raf/MEK/ERK signaling pathway and are frequently upregulated in neoplasms.",,,,RAF-265 is investigational.,RAF-265 is a solid.,True
17045,,,,,4-amino]-3H-benzimidazol-5-yl]oxy]-N-methyl-pyridine-2-carboxamide is experimental.,4-amino]-3H-benzimidazol-5-yl]oxy]-N-methyl-pyridine-2-carboxamide is a solid.,False
17046,,,,,N-(4-phenoxyphenyl)-2-nicotinamide is experimental.,N-(4-phenoxyphenyl)-2-nicotinamide is a solid.,False
17047,,,,,N-cyclopropyl-6-naphthalene-1-carboxamide is experimental.,N-cyclopropyl-6-naphthalene-1-carboxamide is a solid.,False
17048,,,,,"6-chloro-N-pyrimidin-5-yl-3-{amino}-1,2-benzisoxazole-7-carboxamide is experimental.","6-chloro-N-pyrimidin-5-yl-3-{amino}-1,2-benzisoxazole-7-carboxamide is a solid.",False
17049,,,,,"N-(CYCLOPROPYLMETHYL)-4-(METHYLOXY)-3-({5--1,3-OXAZOL-2-YL}AMINO)BENZENESULFONAMIDE is experimental.","N-(CYCLOPROPYLMETHYL)-4-(METHYLOXY)-3-({5--1,3-OXAZOL-2-YL}AMINO)BENZENESULFONAMIDE is a solid.",False
17050,,,,,"N--5--1,3-OXAZOL-2-AMINE is experimental.","N--5--1,3-OXAZOL-2-AMINE is a solid.",False
17051,,,,,"3-(2-aminoquinazolin-6-yl)-1-(3,3-dimethylindolin-6-yl)-4-methylpyridin-2(1H)-one is experimental.","3-(2-aminoquinazolin-6-yl)-1-(3,3-dimethylindolin-6-yl)-4-methylpyridin-2(1H)-one is a solid.",False
17052,,,,,3-(2-aminoquinazolin-6-yl)-4-methyl-1-pyridin-2(1H)-one is experimental.,3-(2-aminoquinazolin-6-yl)-4-methyl-1-pyridin-2(1H)-one is a solid.,False
17053,,,,,"N'-(6-aminopyridin-3-yl)-N-(2-cyclopentylethyl)-4-methyl-benzene-1,3-dicarboxamide is experimental.","N'-(6-aminopyridin-3-yl)-N-(2-cyclopentylethyl)-4-methyl-benzene-1,3-dicarboxamide is a solid.",False
17054,,,,,"N~4~-methyl-N~4~-(3-methyl-1H-indazol-6-yl)-N~2~-(3,4,5-trimethoxyphenyl)pyrimidine-2,4-diamine is experimental.","N~4~-methyl-N~4~-(3-methyl-1H-indazol-6-yl)-N~2~-(3,4,5-trimethoxyphenyl)pyrimidine-2,4-diamine is a solid.",False
17055,,,,,"N~4~-(3-methyl-1H-indazol-6-yl)-N~2~-(3,4,5-trimethoxyphenyl)pyrimidine-2,4-diamine is experimental.","N~4~-(3-methyl-1H-indazol-6-yl)-N~2~-(3,4,5-trimethoxyphenyl)pyrimidine-2,4-diamine is a solid.",False
17056,Constituent of striated muscle and liver. It is used therapeutically to stimulate gastric and pancreatic secretions and in the treatment of hyperlipoproteinemias. ,,,,(3-Carboxy-2-(R)-Hydroxy-Propyl)-Trimethyl-Ammonium is experimental.,(3-Carboxy-2-(R)-Hydroxy-Propyl)-Trimethyl-Ammonium is a solid.,True
17057,,,,,"3-Carboxy-N,N,N-Trimethyl-2-(Octanoyloxy)Propan-1-Aminium is experimental.","3-Carboxy-N,N,N-Trimethyl-2-(Octanoyloxy)Propan-1-Aminium is a solid.",False
17058,,,,,Acetoacetyl-CoA is experimental.,Acetoacetyl-CoA is a solid.,False
17059,,,,,3-Hydroxybutyryl-Coenzyme A is experimental.,3-Hydroxybutyryl-Coenzyme A is a solid.,False
17060,"An anionic surface-active agent used for its wetting properties in industry and used in medicine as an irritant and sclerosing agent for hemorrhoids and varicose veins. For the treatment of small uncomplicated varicose veins of the lower extremities that show simple dilation with competent valves. Sodium tetradecyl sulfate is an anionic surfactant which occurs as a white, waxy solid. It is used as a sclerosing agent in sclerotherapy. Sclerotherapy is an injection of a sclerosing agent directly through the skin into a lesion and is used primarily for slow-flow vascular anomalies, particularly for venous malformation and lymphatic malformation. Intravenous injection causes intima inflammation and thrombus formation. This usually occludes the injected vein. Subsequent formation of fibrous tissue results in partial or complete vein obliteration that may or may not be permanent. Sodium tetradecyl sulfate is a potent toxin for endothelial cells in that brief exposure to even low concentrations are effective in stripping endothelium over a considerable distance and exposing highly thrombogenic endothelium in the process. Diluted sodium tetradecyl sulfate is also able to induce a hypercoagulable state, possibly by selective inhibition of protein C, and can also promote platelet aggregation.",The molecular weight is 294.45.,Sodium tetradecyl sulfate has a topological polar surface area of 63.6.,The log p value of  is 5.57.,Sodium tetradecyl sulfate is approved and investigational.,Sodium tetradecyl sulfate is a solid.,True
17061,"Cupric chloride, for injection, is a sterile, nonpyrogenic solution intended for use as an additive to solutions for Total Parenteral Nutrition (TPN). For use as a supplement to intravenous solutions given for total parenteral nutrition (TPN). Copper is an essential nutrient which serves as a co factor for serum ceruloplasmin, an oxidase necessary for proper formation of the iron carrier protein, transferrin. Copper also helps maintain normal rates of red and white blood cell formation. Providing copper during Total Parenteral Nutrition helps prevent development of the following deficiency symptoms: Leukopenia, neutropenia, anemia, depressed ceruloplasmin levels, impaired transferrin formation, secondary iron deficiency and osteoporosis. The in vitro interaction of organic copper compounds with rat liver glutathione S-transferases was studied with reduced glutathione and 1-chloro-2,4-dinitrobenzene as substrates. Both organic and inorganic copper are spontaneously conjugated with glutathione, but interact with glutathione S-transferase by direct binding to these proteins. ",The molecular weight is 134.45.,,,Cupric Chloride is approved and investigational.,Cupric Chloride is a solid.,True
17062,"Butalbital, or 5-allyl-5-isobutylbarbituric acid, is a derivative of barbituric acid which the hydrogens at position 5 are substituted by an allyl group and an isobutyl group. It is a short-to-intermediate acting member of barbiturates that exhibit muscle-relaxing and anti-anxiety properties that produce central nervous system (CNS) depression that ranges from mild sedation to general anesthesia. Butalbital has a low degree of selectivity and a narrow therapeutic index. Typically indicated to manage tension (or muscle contraction) headaches, butalbital is often combined with one or more therapeutic agents, such as acetylsalicylic acid, acetaminophen, aspirin, and caffeine. There have not been clinical trials that evaluate the clinical efficacy of butalbital in migraines thus it is not indicated for such condition. As with other barbiturates, butalbital carries a risk of abuse or misuse potential, intoxication, hangover, tolerance, dependence, and overdosage possibly leading to death. Butalbital‐containing analgesics can also produce a drug‐induced headache in addition to tolerance and dependence. Due to these risks, the use of butalbital-containing combination products is typically limited for use only in cases where other medications are deemed ineffective and such usage is advised to be carefully monitored. Indicated for the management of the symptom complex of tension (or muscle contraction) headache, when other non-opioid analgesics and alternative treatments are inadequate, in various combinations with acetaminophen, aspirin, caffeine, and codeine. Butalbital is a short to intermediate-acting barbiturate that reversibly depresses the activity of excitable tissues, including the central nervous system in a nonselective manner. Barbiturates exhibit muscle-relaxing and anti-anxiety properties and they are capable of producing all levels of CNS mood alteration from excitation to mild sedation, hypnosis, and deep coma. The sedative dose of butalbital in nontolerant individuals is 5-100 mg and the hypnotic dose is 100-200 mg. Pain perception and reaction are relatively unimpaired until the moment of unconsciousness. In some cases, an unwanted paradoxical response of excitement may be observed instead of sedation with barbiturate treatment, which may be due to their depressant effects on inhibitory centers of the CNS. At sufficiently high therapeutic doses, barbiturates induce anesthesia; however, barbiturates are reported to lose their effectiveness for sleep induction and sleep maintenance after 2 weeks. Barbiturates are habit-forming; they can produce tolerance and both dependence and addiction, which is partly explained by decreased drug concentration at the site of action due to enhanced drug metabolism by induced enzymes, or to cellular adaptive changes. In addition, butalbital may lead to analgesic overuse headache.  Butalbital is a CNS depressant that suppresses neuronal excitability, impulse conduction, and the release of neurotransmitters, similar to actions of other barbiturates. Barbiturates primarily mediate suppressive actions on polysynaptic neuronal responses by diminishing facilitation while enhancing inhibition. Inhibition occurs at GABAergic synapses that express GABA-A receptors, which are transmembrane chloride ion channels that bind an inhibitory neurotransmitter GABA, barbiturates, benzodiazepines, neurosteroids, and ethanol. Upon activation, GABA-A receptors allow Cl- influx and K+ efflux into the postjunctional terminal, resulting in inhibition of the postsynaptic neuron. It is suggested that barbiturates, including butalbital, enhances GABA binding to the GABA-A receptors by binding to the α+/β− interface in the intracellular domain (ICD) as an allosteric modulator. Additionally, barbiturates promote benzodiazepine binding to the receptor. Barbiturates potentiate GABA-induced increases in chloride conductance and depress voltage-activated calcium currents while prolonging the duration of GABA-induced chloride channel opening. Butalbital may also inhibit the excitatory effects mediated by AMPA receptors by reducing glutamate-induced depolarizations of the receptor. It is also proposed that barbiturates and opioids may potentiate the analgesic effects of each other when co-administered, although there are inconsistencies across preclinical data.",The molecular weight is 224.26.,Butalbital has a topological polar surface area of 75.27.,The log p value of  is 1.63.,Butalbital is approved and illicit.,Butalbital is a solid.,True
17063,"Talbutal, also called 5-allyl-5-sec-butylbarbituric acid, is a barbiturate with a short to intermediate duration of action. Talbutal is a schedule III drug in the U.S. For use as a sedative and hypnotic. Talbutal is a short to intermediate-acting barbiturate that is a nonselective central nervous system (CNS) depressant. As with other barbiturates, talbutal is capable of producing all levels of CNS mood alteration from excitation to mild sedation, hypnosis, and deep coma. Barbiturates may also induce anesthesia at sufficiently high therapeutic doses.  Talbutal binds to GABA<sub>A</sub> receptors at a distinct binding site associated with a Cl<sup>-</sup> ionopore of the receptor. Upon binding, talbutal increases the duration of time for which the Cl<sup>-</sup> ionopore is open, leading to prolonged inhibitory effect of GABA at the postsynaptic thalamic neuron. ",The molecular weight is 224.26.,Talbutal has a topological polar surface area of 75.27.,The log p value of  is 1.63.,Talbutal is approved and illicit.,Talbutal is a solid.,True
17064,"A carbamate with hypnotic, sedative, and some muscle relaxant properties, although in therapeutic doses reduction of anxiety rather than a direct effect may be responsible for muscle relaxation. Meprobamate has been reported to have anticonvulsant actions against petit mal seizures, but not against grand mal seizures (which may be exacerbated). It is used in the treatment of anxiety disorders, and also for the short-term management of insomnia but has largely been superseded by the benzodiazepines. (From Martindale, The Extra Pharmacopoeia, 30th ed, p603) Meprobamate is a controlled substance in the U.S. For the management of anxiety disorders or for the short-term relief of the symptoms of anxiety. Meprobamate is an anxiolytic drug. It was the best selling minor tranquilizer for a time but has largely been replaced by benzodiazepines. Meprobamate has most of the pharmacological effects and dangers of the barbiturates (though it was marketed as being safer) but it is less sedating at effective doses. Meprobamate exhibits some anticonvulsant effects in absence seizures; however, it is reported to potentially exacerbate generalized tonic-clonic seizures. It has also been used as a hypnotic (sleeping pill). However, its is currently only licensed as an anxiolytic and it is a third or fourth-order choice. Meprobamate's mechanism of action is not fully understood; in animal studies, meprobamate is reported to act at multiple sites in the central nervous system, such as the thalamus and limbic system. It binds to the GABA<sub>A</sub> receptors, leading to inhibitory effects on the neurons transmitting signals in the reticular formation and spinal cord. Consequently, effects such as sedation and altered perception of pain are observed. ",The molecular weight is 218.25.,Meprobamate has a topological polar surface area of 104.64.,The log p value of  is 0.91.,Meprobamate is approved and illicit.,Meprobamate is a solid.,True
17065,"Metharbital is a barbiturate anticonvulsant, similar to phenobarbital, marketed as Gemonil by Abbott Laboratories. It was patented in 1905 by Emil Fischer of Merck. Metharbital is used for the treatment of epilepsy. Metharbital, a barbiturate, is used for the treatment of short term insomnia. It belongs to a group of medicines called central nervous system (CNS) depressants that induce drowsiness and relieve tension or nervousness. Little analgesia is conferred by barbiturates; their use in the presence of pain may result in excitation. Metharbital binds at a distinct binding site associated with a Cl<sup>-</sup> ionopore at the GABA<sub>A</sub> receptor, increasing the duration of time for which the Cl<sup>-</sup> ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged. All of these effects are associated with marked decreases in GABA-sensitive neuronal calcium conductance (gCa). The net result of barbiturate action is acute potentiation of inhibitory GABAergic tone. Barbiturates also act through potent (if less well characterized) and direct inhibition of excitatory AMPA-type glutamate receptors, resulting in a profound suppression of glutamatergic neurotransmission.",The molecular weight is 198.22.,Metharbital has a topological polar surface area of 66.48.,The log p value of  is 1.14.,Metharbital is withdrawn.,Metharbital is a solid.,True
17066,"A barbiturate with hypnotic and sedative properties (but not antianxiety). Adverse effects are mainly a consequence of dose-related CNS depression and the risk of dependence with continued use is high. (From Martindale, The Extra Pharmacopoeia, 30th ed, p565) Amobarbital (like all barbiturates) works by binding to the GABAA receptor at either the alpha or the beta sub unit. These are binding sites that are distinct from GABA itself and also distinct from the benzodiazepine binding site. Like benzodiazepines, barbiturates potentiate the effect of GABA at this receptor. This GABAA receptor binding decreases input resistance, depresses burst and tonic firing, especially in ventrobasal and intralaminar neurons, while at the same time increasing burst duration and mean conductance at individual chloride channels; this increases both the amplitude and decay time of inhibitory postsynaptic currents. In addition to this GABA-ergic effect, barbiturates also block the AMPA receptor, a subtype of glutamate receptor. Glutamate is the principal excitatory neurotransmitter in the mammalian CNS. Amobarbital also appears to bind neuronal nicotinic acetylcholine receptors. ",The molecular weight is 226.28.,Amobarbital has a topological polar surface area of 75.27.,The log p value of  is 2.11.,Amobarbital is approved and illicit.,Amobarbital is a solid.,True
17067,"Butobarbital is a sedative and a hypnotic drug. For the treatment of insomnia. Butethal (also known as butobarbitone and butobarbital) belongs to a group of medicines called the barbiturates. It is thought to act on receptors in the brain (GABA receptors) causing the release of the chemical GABA. This chemical inhibits certain areas of the brain resulting in sleepiness.  Butethal binds at a distinct binding site associated with a Cl<sup>-</sup> ionopore at the GABA<sub>A</sub> receptor, increasing the duration of time for which the Cl<sup>-</sup> ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged. All of these effects are associated with marked decreases in GABA-sensitive neuronal calcium conductance (gCa). The net result of barbiturate action is acute potentiation of inhibitory GABAergic tone. Barbiturates also act through potent (if less well characterized) and direct inhibition of excitatory AMPA-type glutamate receptors, resulting in a profound suppression of glutamatergic neurotransmission.",The molecular weight is 212.25.,Butobarbital has a topological polar surface area of 75.27.,The log p value of  is 1.71.,Butobarbital is approved and illicit.,Butobarbital is a solid.,True
17068,"Heptabarbital is an intermediate or short term barbiturate used mainly for sedation and hypnosis. Used mainly for sedation and hypnosis. Heptabarbital (like all barbiturates) works by binding to the GABAA receptor at either the alpha or the beta sub unit. These are binding sites that are distinct from GABA itself and also distinct from the benzodiazepine binding site. Like benzodiazepines, barbiturates potentiate the effect of GABA at this receptor. This GABAA receptor binding decreases input resistance, depresses burst and tonic firing, especially in ventrobasal and intralaminar neurons, while at the same time increasing burst duration and mean conductance at individual chloride channels; this increases both the amplitude and decay time of inhibitory postsynaptic currents. In addition to this GABA-ergic effect, barbiturates also block the AMPA receptor, a subtype of glutamate receptor. Glutamate is the principal excitatory neurotransmitter in the mammalian CNS. Heptabarbital also appears to bind neuronal nicotinic acetylcholine receptors.",The molecular weight is 250.3.,Heptabarbital has a topological polar surface area of 75.27.,The log p value of  is 2.43.,Heptabarbital is experimental.,Heptabarbital is a solid.,True
17069,,,,,"Dihydro-2-thioxo-5-((5-(2-(trifluoromethyl)phenyl)-2-furanyl)methyl)-4,6(1H,5H)-pyrimidinedione is experimental and illicit.","Dihydro-2-thioxo-5-((5-(2-(trifluoromethyl)phenyl)-2-furanyl)methyl)-4,6(1H,5H)-pyrimidinedione is a solid.",False
17070,"Pagoclone is an anxiolytic drug from the cyclopyrrolone family, which is related to other more well known drugs such as the sleeping medication zopiclone. It is one of a relatively recently developed class of medicines known as the nonbenzodiazepines, which have similar effects to the older benzodiazepine group, but with quite different chemical structures. For the potential treatment of panic and anxiety disorders. Pagoclone was originally developed as an anti-anxiety drug, but never commercialised. It is a partial agonist acting at GABAA receptors in the brain. In contrast to zopiclone, pagoclone produces anxiolytic effects with little or no sedative or amnestic actions at low doses. Pagoclone is a subtype-selective drug which binds primarily to the alpha2/alpha3 subtypes of the GABAA receptor which are responsible for the anti-anxiety effects of these kind of drugs, but has relatively little efficacy at the alpha1 subtype which produces the sedative and memory loss effects.",,,,Pagoclone is investigational.,Pagoclone is a solid.,True
17071,"Ganaxolone is the 3β-methylated synthetic analog of allopregnanolone; it belongs to a class of compounds referred to as neurosteroids. Ganaxolone is an allosteric modulator of GABAA receptors acting through binding sites which are distinct from the benzodiazepine binding site. It has activity in a broad range of animal models of epilepsy. Ganaxolone has been shown to be well tolerated in adults and children. In early phase II studies, Ganaxolone has been shown to have activity in adult patients with partial-onset seizures and epileptic children with history of infantile spasms. It is currently undergoing further development in infants with newly diagnosed infantile spasms, in women with catamenial epilepsy, and in adults with refractory partial-onset seizures. Investigated for use/treatment in pediatric indications and seizure disorders. Ganaxolone is a powerful positive allosteric modulator of GABAA receptors with potency and efficacy comparable to its endogenous analog 3a,5a-P (Carter et al., 1997). As with 3a,5a-P, Ganaxolone potentiation of the GABAA receptor occurs at a site distinct from the benzodiazepine site. Ganaxolone has protective activity in diverse rodent seizure models, including clonic seizures induced by pentylenetetrazol (PTZ) and bicuculline (BIC), limbic seizures in the 6 Hz model, and amygdala kindled seizures (Carter et al., 1997; Rogawski and Reddy, 2004; Kaminski et al., 2004). Ganaxolone belongs to a novel class of neuroactive steroids called epalons, which specifically modulate the γ-aminobutyric acid type A (GABAA) receptor in the central nervous system (CNS). Chemically related to progesterone but devoid of any hormonal activity, the epalons have potent antiepileptic, anxiolytic, sedative, and hypnotic activities in animals.",,,,Ganaxolone is investigational.,Ganaxolone is a solid.,True
17072,"AZD7325 is a high affinity, selective modulator of the GABAA receptor system. ",,,,AZD-7325 is investigational.,AZD-7325 is a solid.,True
17073,,The molecular weight is 156.1.,Orotic acid has a topological polar surface area of 95.5.,The log p value of  is -0.75.,Orotic acid is investigational.,Orotic acid is a solid.,False
17074,,,,,Capric dimethyl amine oxide is experimental.,Capric dimethyl amine oxide is a solid.,False
17075,,,,,Brequinar Analog is experimental.,Brequinar Analog is a solid.,False
17076,,,,,Brequinar is experimental.,Brequinar is a solid.,False
17077,,,,,"2--3,4-Dihydroxy-1(2h)-Naphthalenone is experimental.","2--3,4-Dihydroxy-1(2h)-Naphthalenone is a solid.",False
17078,,,,,"5-Carbamoyl-1,1':4',1''-terphenyl-3-carboxylic acid is experimental.","5-Carbamoyl-1,1':4',1''-terphenyl-3-carboxylic acid is a solid.",False
17079,"SC12267 is a novel, small molecule agent from the class of DMARDs (disease modifying anti-rheumatic drug) for the therapy of autoimmune diseases such as rheumatoid arthritis or multiple sclerosis. Through highly selective inhibition of pyrimidine biosynthesis, it controls the growth of rapidly proliferating cells, especially of lymphocytes, which are important for the immune response. Investigated for use/treatment in multiple sclerosis and rheumatoid arthritis. SC12267, a novel, selective and orally available, small molecule inhibitor of dihydroorotate dehydrogenase",,,,SC12267 is investigational.,SC12267 is a solid.,True
17080,"FK778, a novel compound with multiple mechanisms of action, is efficacious, well tolerated and safe in kidney transplant patients, potentially offering a breakthrough in immunosuppressive therapy. Investigated for use/treatment in immunosuppressive and transplant (rejection). FK778 exerts its immunosuppressive activity at the molecular level via the suppression of de-novo pyrimidine biosynthesis, inhibiting the action of dihydroorotate dehydrogenase, an enzyme critical in the process, and consequently inhibiting cell proliferation.",,,,Manitimus is investigational.,Manitimus is a solid.,True
17081,,,,,(2Z)-N-biphenyl-4-yl-2-cyano-3-hydroxybut-2-enamide is experimental.,(2Z)-N-biphenyl-4-yl-2-cyano-3-hydroxybut-2-enamide is a solid.,False
17082,,,,,"(2Z)-2-cyano-N-(2,2'-dichlorobiphenyl-4-yl)-3-hydroxybut-2-enamide is experimental.","(2Z)-2-cyano-N-(2,2'-dichlorobiphenyl-4-yl)-3-hydroxybut-2-enamide is a solid.",False
17083,,,,,(2Z)-2-cyano-N-(3'-ethoxybiphenyl-4-yl)-3-hydroxybut-2-enamide is experimental.,(2Z)-2-cyano-N-(3'-ethoxybiphenyl-4-yl)-3-hydroxybut-2-enamide is a solid.,False
17084,,,,,"UNDECYLAMINE-N,N-DIMETHYL-N-OXIDE is experimental.","UNDECYLAMINE-N,N-DIMETHYL-N-OXIDE is a solid.",False
17085,,,,,2-({AMINO}CARBONYL)CYCLOPENT-1-ENE-1-CARBOXYLIC ACID is experimental.,2-({AMINO}CARBONYL)CYCLOPENT-1-ENE-1-CARBOXYLIC ACID is a solid.,False
17086,,,,,3-{CARBONYL}THIOPHENE-2-CARBOXYLIC ACID is experimental.,3-{CARBONYL}THIOPHENE-2-CARBOXYLIC ACID is a solid.,False
17087,,,,,3-({AMINO}CARBONYL)THIOPHENE-2-CARBOXYLIC ACID is experimental.,3-({AMINO}CARBONYL)THIOPHENE-2-CARBOXYLIC ACID is a solid.,False
17088,,,,,"2-({AMINO}CARBONYL)CYCLOPENTA-1,3-DIENE-1-CARBOXYLIC ACID is experimental.","2-({AMINO}CARBONYL)CYCLOPENTA-1,3-DIENE-1-CARBOXYLIC ACID is a solid.",False
17089,,,,,N-anthracen-2-yl-5-methyltriazolopyrimidin-7-amine is experimental.,N-anthracen-2-yl-5-methyltriazolopyrimidin-7-amine is a solid.,False
17090,,,,,5-methyl-N-triazolopyrimidin-7-amine is experimental.,5-methyl-N-triazolopyrimidin-7-amine is a solid.,False
17091,,,,,(2Z)-N-biphenyl-4-yl-2-cyano-3-cyclopropyl-3-hydroxyprop-2-enamide is experimental.,(2Z)-N-biphenyl-4-yl-2-cyano-3-cyclopropyl-3-hydroxyprop-2-enamide is a solid.,False
17092,,,,,(2Z)-N-(3-chloro-2'-methoxybiphenyl-4-yl)-2-cyano-3-hydroxybut-2-enamide is experimental.,(2Z)-N-(3-chloro-2'-methoxybiphenyl-4-yl)-2-cyano-3-hydroxybut-2-enamide is a solid.,False
17093,,,,,"3,6,9,12,15-PENTAOXATRICOSAN-1-OL is experimental.","3,6,9,12,15-PENTAOXATRICOSAN-1-OL is a solid.",False
17094,,,,,4'-Deoxy-4'-Acetylyamino-Pyridoxal-5'-Phosphate is experimental.,4'-Deoxy-4'-Acetylyamino-Pyridoxal-5'-Phosphate is a solid.,False
17095,"AV608 is a NK-1 antagonist. It is developed for the treatment of Social anxiety disorder (SAD), irritable bowel syndrome (IBS) and overactive bladder (OAB). Investigated for use/treatment in anxiety disorders, irritable bowel syndrome (IBS), and urinary incontinence.  An extensive body of scientific literature supports the potential therapeutic application of NK-1 antagonists to the treatment of anxiety disorders. At a biological level, there is a close anatomical association between Substance P, NK-1 receptors and monoamines. More specifically, ~50% of ascending serotonin neurons in the brain also co-express substance P, and norepinephrine cell bodies in the locus coeruleus express NK-1 receptors. In addition, it has been demonstrated that NK-1 receptor blockade can alter the firing pattern of both serotonin and norepinephrine neurons and increase hippocampal neurogenesis. At a functional level, NK-1 antagonists (including AV608) have broadly demonstrated activity in nearly all of the traditionally used preclinical assays to identify anxiolytic agents, including those assays that are predictive for both benzodiazepines and selective serotonin reuptake inhibitors (SSRIs). Clinically, anxiety remains a high priority target for Industry, as evidenced by recent development activity in this area.",,,,AV608 is investigational.,AV608 is a solid.,True
17096,"GW 597599, a neurokinin-1 (NK1) receptor antagonist is currently in phase II trials for chemotherapy-induced vomiting; functional dyspepsia; depression and anxiety. Investigated for use/treatment in adverse effects (chemotherapy), anxiety disorders, depression, and gastrointestinal diseases and disorders (miscellaneous).",,,,GW 597599 is investigational.,GW 597599 is a solid.,True
17097,"CP-122721, neurokinin 1 (NK1) antagonist is developed by Pfizer to treat depression, emesis, and inflammatory diseases including asthma and irritable bowel syndrome. Investigated for use/treatment in asthma, depression, and irritable bowel syndrome (IBS). CP-122721 interacts with high affinity at the human NK1 receptor expressed in IM-9 cells. ",,,,CP-122721 is investigational.,CP-122721 is a solid.,True
17098,"R673 is a novel NK1 antagonist that penetrates the blood-brain barrier, has excellent safety and tolerability and shows low P450-based drug interaction potential. The phase II program for treatment of depression and anxiety is ongoing in the US and EU.It is not clear how tachykinin antagonists exert their effect, but SP levels have been commonly linked to the functioning of limbic system with respect to anxiety and depression. Investigated for use/treatment in depression and anxiety. R673 is a novel NK1 antagonist that penetrates the blood-brain barrier, has excellent safety and tolerability and shows low P450-based drug interaction potential. It is not clear how tachykinin antagonists exert their effect, but SP levels have been commonly linked to the functioning of limbic system with respect to anxiety and depression. R673 is a novel NK1 antagonist that penetrates the blood-brain barrier, has excellent safety and tolerability and shows low P450-based drug interaction potential. It is not clear how tachykinin antagonists exert their effect, but SP levels have been commonly linked to the functioning of limbic system with respect to anxiety and depression.",,,,R673 is investigational.,R673 is a solid.,True
17099,SR 140333 is tachykinin antagonist which has potential to treat diarrhoea due to food allergy or inflammatory bowel disease.  Investigated for use/treatment in asthma and inflammatory bowel disease.,,,,SR 140333 is investigational.,SR 140333 is a solid.,True
17100,Investigated for use/treatment in urinary incontinence and adverse effects (chemotherapy).,The molecular weight is 616.62.,Casopitant has a topological polar surface area of 47.1.,The log p value of  is 5.62.,Casopitant is investigational.,Casopitant is a solid.,True
17101,Vestipitant has been investigated for the treatment of Tinnitus.,,,,Vestipitant is investigational.,,True
17102,"Vofopitant has been used in trials studying the treatment of PTSD, Primary Insomnia, and Sleep Initiation and Maintenance Disorders.",,,,Vofopitant is investigational.,,True
17103,"Human interferon omega 1 (IFN-omega 1 = IFN-alpha II1) is a recently discovered protein structurally related to IFN-alpha and -beta. It occurs naturally in the human body and is currently being manufactured by Intarcia through genetic engineering. There are multiple routes for administration of omega interferon: injection, an implantable subcutaneous drug delivery system, and an oral formulation. It has been investigated both in single and combination treatment. The biological activities of IFN-omega 1 and its physiological role are not known to date. Investigated for use/treatment in hepatitis (viral, C). Human interferon omega 1 (IFN-omega 1 = IFN-alpha II1) is a recently discovered protein structurally related to IFN-alpha and -beta. It occurs naturally in the human body and is currently being manufactured by Intarcia through genetic engineering. The biological activities of IFN-omega 1 and its physiological role are not known to date.  Independent studies demonstrate that interferon omega binds to the alpha/beta receptor, but not the interferon gamma receptor.",,,,omega interferon is investigational.,omega interferon is a solid.,True
17104,"Follitropin is a human follicle stimulating hormone (FSH) preparation of recombinant DNA origin, which consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Follitropin beta is produced in genetically engineered Chinese hamster cell lines (CHO). The nomenclature “beta” differentiates it from another recombinant human FSH product that was marketed earlier as follitropin alpha. Follitropin is important in the development of follicles produced by the ovaries. Given by subcutaneous injection, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Numerous physio-chemical tests and bioassays indicate that follitropin beta and follitropin alpha are indistinguishable. However, a more recent study showed there is may be a slight clinical difference, with the alpha form tending towards a higher pregnancy rate and the beta form tending towards a lower pregnancy rate, but with significantly higher estradiol (E2) levels. Structural analysis shows that the amino acid sequence of follitropin beta is identical to that of natural human follicle stimulating hormone (FSH). Further, the ogliosaccharide side chains are very similar, but not completely identical to that of natural FSH. However, these small differences do not affect the bioactivity compared to natural FSH. In women having been diagnosed with primary ovarian failure, it is used in combination with human chorionic gonadotropin (hCG) to assist in ovulation and fertility. In men with hypogonadotrophic hypogonadism, it is used to induce spermatogenesis. Follitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). Used for the treatment of female infertility, Follitropin beta or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of Follitropin beta is the primary hormone responsible for follicular recruitment and development. Follitropin is a recombinant form of endogenous follicle stimulating hormone (FSH). FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells.",The molecular weight is 22668.79.,Follitropin has a topological polar surface area of 5077.47.,,Follitropin is approved.,Follitropin is a liquid.,True
17105,"Urofollitropin is a urinary-derived follicle-stimulating hormone (FSH) that is extracted and purified from human urine samples. It consists of two non-covalently linked, non-identical glycoproteins designated as the alpha- and beta- subunits. The alpha- and beta- subunits have 92 and 111 amino acids. The alpha subunit is glycosylated at Asn 51 and Asn 78 while the beta subunit is glycosylated at Asn 7 and Asn 24. Urofollitropin is typically used injected subcutaneously in combination with human chorionic gonadotropin (hCG) to induce ovulation. Urofollitropin may also be used to cause the ovary to produce several follicles, which can then be harvested for use in gamete intrafallopian transfer (GIFT) or in vitro fertilization (IVF). For treatment of female infertility Used for the treatment of female infertility, urofollitropin or follicle stimulating hormone (FSH) stimulates ovarian follicular growth in women who do not have primary ovarian failure. FSH, the active component of urofollitropin is the primary hormone responsible for follicular recruitment and development. FSH binds to the follicle stimulating hormone receptor which is a G-coupled transmembrane receptor. Binding of the FSH to its receptor seems to induce phosphorylation and activation of the PI3K (Phosphatidylinositol-3-kinase) and Akt signaling pathway, which is known to regulate many other metabolic and related survival/maturation functions in cells.",,,,Urofollitropin is approved and vet_approved.,Urofollitropin is a liquid.,True
17106,"Corifollitropin alfa, also known as _Elonva_ is used in women undergoing fertility treatment to stimulate the development of more than one mature egg (oocyte) at a time in the ovaries. This drug used together with _a gonadotropin-releasing hormone (GnRH) antagonist_, a type of medicine also used in fertility treatments. Elonva is available only by prescription. Controlled ovarian stimulation in cases of women who are undergoing fertility treatment to stimulate the development of more than one mature egg simultaneously in the ovaries in combination with a gonadotrophin-releasing hormone (GnRH) antagonist (a type of medicine also used in fertility treatments). A single dose of corifollitropin alfa could initiate and sustain multi-follicular growth in patients undergoing controlled ovarian stimulation, such as during in vitro fertilization or intracytoplasmic sperm injection. Corifollitropin alfa is a long-lasting single injection fusion protein which lacks luteinizing hormone (LH) activity. Only one injection is needed for the first 7 days, which replaces the first 7 daily injections of traditional follicle stimulating hormone (FSH). It is a follicle-stimulation hormone (human α-subunit reduced), a combination of follicle stimulation hormone (human β-subunit reduced) fusion protein with 118-145-chorionic gonadotropin (human β-subunit). Frequent, repetitive injections increase stress and error rates, and are often a burden for women, leading to therapy noncompliance.",The molecular weight is 25471.11.,Corifollitropin alfa has a topological polar surface area of 6163.54.,,Corifollitropin alfa is approved and investigational.,Corifollitropin alfa is a liquid.,True
17107,Investigated for use/treatment in parkinson's disease. Parkinson's disease results from degeneration of the dopaminergic cells in the substantia nigra. Several dopamine receptor agonists have been used as antiparkinsonian therapy. Sumanirole is a dopamine receptor agonist with a high selectivity for the D2 receptor subtype over the other closely related D3 and D4 receptor subtypes.,,,,Sumanirole is investigational.,Sumanirole is a solid.,True
17108,"Purified botulinum toxin from Clostridium botulinum, purified from culture via dialysis and acid precipitation. For the treatment of cervical dystonia in adults to decrease the severity of abnormal head position and neck pain associated with cervical dystonia. Also for the treatment of severe primary axillary hyperhidrosis that is inadequately managed with topical agents and for the treatment of strabismus and blepharospasm associated with dystonia, including benign essential blepharospasm or VII nerve disorders in patients 12 years of age and above. Also used cosmetically to temporarily improve the appearance of moderate-to-severe frown lines between the eyebrows (glabellar lines) as well as for the treatment of excessive underarm sweating. A 150 kDa neurotoxic protein produced from fermentation of Hall strain Clostridium botulinum type A grown in a medium containing casein hydrolysate, glucose and yeast extract. It is purified from the culture solution by dialysis and a series of acid precipitations to a complex consisting of the neurotoxin, and several accessory proteins. Botulinum Toxin Type A is not expected to be present in the peripheral blood at measurable levels following IM or intradermal injection at the recommended doses. The recommended quantities of neurotoxin administered at each treatment session are not expected to result in systemic, overt distant clinical effects, i.e. muscle weakness, in patients without other neuromuscular dysfunction. However, sub-clinical systemic effects have been shown by single-fiber electromyography after IM doses of botulinum toxins appropriate to produce clinically observable local muscle weakness. Botulinum Toxin Type A blocks neuromuscular transmission by binding to acceptor sites on motor or sympathetic nerve terminals, entering the nerve terminals, and inhibiting the release of acetylcholine. This inhibition occurs as the neurotoxin cleaves SNAP-25, a protein integral to the successful docking and release of acetylcholine from vesicles situated within nerve endings.",,,,Botulinum toxin type A is approved and investigational.,Botulinum toxin type A is a solid.,True
17109,,,,,m-Hydroxyhippuric acid is experimental.,m-Hydroxyhippuric acid is a solid.,False
17110,Investigated for use/treatment in chronic obstructive pulmonary disease (COPD) and pulmonary hypertension.,,,,PRX-08066 is investigational.,PRX-08066 is a solid.,True
17111,"Human alpha-1 proteinase inhibitor or alpha-1-antitrypsin, prepared from human plasma via Cohn alcohol fractionation followed by PEG and zinc chloride fractionation. For chronic augmentation and maintenance therapy in individuals with alpha1-proteinase inhibitor (A1-PI) deficiency and clinical evidence of emphysema. Prevents excessive accumulation of active neutrophil elastase and consequent proteolysis of elastin tissues in alveolar lung structures. This prevents the development of emphysema. Alpha-1 proteinase inhibitor is a serine protease inhibitor (Serpin). Its primary mechanism is inhibiting the action of the serine protease called elastase (also plasmin and thrombin) in the lungs. The reactive center loop (RCL) of alpha-1 proteinase inhibitor extends out from the body of the protein and directs binding to the target protease. The protease cleaves the serpin at the reactive site, establishing a covalent linkage between the carboxyl group of the serpin reactive site and the serine hydroxyl of the protease. The resulting inactive serpin-protease complex is highly stable.",,,,Alpha-1-proteinase inhibitor is approved.,Alpha-1-proteinase inhibitor is a liquid.,True
17112,"Chemotherapy-induced neutropenia (CIN) is a common and serious complication of myelosuppressive chemotherapy. It is associated with significant morbidity and mortality and can increase the cost of cancer therapy. In these cases, colony stimulating factor is necessary to restore important cells for immune function. This drug is a leucocyte growth factor indicated to: Filgrastim binds to the G-CSF receptor and stimulates the production of neutrophils in the bone marrow. As a G-CSF analog, this drug controls the proliferation of committed progenitor cells and influences their maturation into mature neutrophils. Filgrastim also stimulates the release of neutrophils from bone marrow storage pools and decreases their time to maturation. Filgrastim acts to increase the phagocytic activity of mature neutrophils, thus allowing them to prevent infection. In patients receiving cytotoxic chemotherapy, filgrastim may accelerate neutrophil recovery, leading to a reduction in the duration of the neutropenic phase post chemotherapy.",,,,Filgrastim is approved.,Filgrastim is a liquid.,True
17113,,,,,"Mdl 101,146 is experimental.","Mdl 101,146 is a solid.",False
17114,"Investigated for use/treatment in chronic obstructive pulmonary disease (COPD). ONO-6818 inhibits neutrophil elastase activity, reducing interleukin 8 production and the formation of the complement membrane attack complex. Consequently, neutrophil elastase levels are reduced during stimulated extracorporeal circulation.",,,,Freselestat is experimental and investigational.,Freselestat is a solid.,True
17115,"Flavoring agent sweeter than sugar, metabolized as phenylalanine and aspartic acid. Used as a diet supplement and sugar substitute. Aspartame (L-alpha-aspartyl-L-phenylalanine methyl ester) is a low-calorie sweetener used to sweeten a wide variety of low- and reduced-calorie foods and beverages, including low-calorie tabletop sweeteners. Aspartame is composed of two amino acids, aspartic acid and phenylalanine, as the methyl ester. Aspartic acid and phenylalanine are also found naturally in protein containing foods, including meats, grains and dairy products. Methyl esters are also found naturally in many foods such as fruits and vegetable and their juices. Upon digestion, aspartame breaks down into three components (aspartic acid, phenylalanine and methanol), which are then absorbed into the blood and used in normal body processes. Neither aspartame nor its components accumulates in the body. These components are used in the body in the same ways as when they are derived from common foods. 180 to 200 times sweeter than sucrose, it is metabolized as a protein and its subsequent amino-acids used up in there respective mechanisms.",,,,Aspartame is investigational and nutraceutical.,Aspartame is a solid.,True
17116,"A nonreducing disaccharide composed of glucose and fructose linked via their anomeric carbons. It is obtained commercially from sugarcane, sugar beet (beta vulgaris), and other plants and used extensively as a food and a sweetener.",The molecular weight is 342.3.,Sucrose has a topological polar surface area of 189.53.,The log p value of  is -3.09.,Sucrose is approved and experimental and investigational.,Sucrose is a solid.,True
17117,"Tenocyclidine (TCP, thienyl cyclohexylpiperidine) is a dissociative anesthetic drug with stimulant and hallucinogenic effects. It is more potent than phencyclidine and hence, this drug was classified under the schedule 1 in 1970. Because of its high affinity for the phencyclidine binding site on the NMDA receptor, the 3H radiolabelled form of tenocyclidine is widely used in research into NMDA receptors. When compared to phencyclidine, tenocyclidine presents more affinity for NMDA receptors and less affinity for sigma receptors. The primary interactions are as a non-competitive antagonist at the 3A-subunit of the NMDAR in Homo sapiens. TCP is known to bind, with relatively high affinity, to the D1 subunit of the human DAT, in addition to displaying a positive antagonistic effect at the α7-subunit of the Nicotinic Acetylcholine Receptor (nAChR). It also binds to the mu-opioid receptor, which seems to be a central part of the mechanism of action of drugs in this class. (For example, Dizocilpine shows little appreciable analgesic effect despite having a high specificity for the NMDA-3A and NMDA-3B subunits - this may well be mediated by the lack of related efficacy at the mu-opioid receptor, though the NMDAR certainly does play a role in transmission of pain signals).",,,,Tenocyclidine is experimental and illicit and investigational.,Tenocyclidine is a solid.,True
17118,Coenzyme A persulfide is a possible in vivo inhibitor of mammalian short chain acyl-CoA dehydrogenase.,,,,Coenzyme A persulfide is experimental.,Coenzyme A persulfide is a solid.,True
17119,,,,,N-Benzylformamide is experimental.,N-Benzylformamide is a solid.,False
17120,"Monohydroxy derivatives of cyclohexanes that contain the general formula R-C6H11O. They have a camphorlike odor and are used in making soaps, insecticides, germicides, dry cleaning, and plasticizers. ",,,,Cyclohexanol is experimental.,Cyclohexanol is a solid.,True
17121,,,,,N-Heptylformamide is experimental.,N-Heptylformamide is a solid.,False
17122,"Caerulein is a specific decapeptide similar in action and composition to the natural gastrointestinal peptide hormone cholecystokinin. It exerts stimulatory effects on the gastric, biliary, and pancreatic secretion, as well as on certain smooth muscles. Caerulein is used in the treatment of paralytic ileus and as diagnostic aid in pancreatic malfunction. Caerulein is a specific decapeptide similar in action and composition to the natural gastrointestinal peptide hormone cholecystokinin that stimulates gastric, biliary, and pancreatic secretion. It also exerts stimulatory actions on certain smooth muscles.  Caerulein acts according to its similarity to the natural gastrointestinal peptide hormone cholecystokinin. Cholecystokinin is a peptide hormone of the gastrointestinal system responsible for stimulating the digestion of fat and protein. Cholecystokinin is secreted by the duodenum, the first segment of the small intestine. There it binds to CCK receptors, activating them and causing downstream effects. Specifically, it results in the release of digestive enzymes and bile from the pancreas and gall bladder, respectively. It also acts as a hunger suppresant. Cholecystokinin is secreted by the duodenum when fat- or protein-rich chyme leaves the stomach and enters the duodenum. The hormone acts on the pancreas to stimulate the secretion of the enzymes lipase, amylase, trypsin, and chymotrypsin. Together these pancreatic enzymes catalyze the digestion of fat and protein. Cholecystokinin also stimulates both the contraction of the gall bladder, and the relaxtion of the Sphincter of Oddi (Glisson's Sphinctor), which delivers, (not secretes) bile into the small intestine. Bile salts serve to emulsify fats, thereby increasing the effectiveness with which enzymes can digest them.",The molecular weight is 1352.41.,Ceruletide has a topological polar surface area of 551.4.,The log p value of  is -5.64.,Ceruletide is approved.,Ceruletide is a solid.,True
17123,"Lintitript is a new, highly specific and potent CCK-A receptor antagonist. For the treatment of pancreatic cancer and appetite disorders. Lintitript SR 27897 is a selective cholecystokinin type A (CCK-A) receptor antagonist. In February 2000, Sanofi announced that it was halting development of the drug for appetite disorders, and in September 2002, Sanofi announced that it had stopped investigation all together. Cholecystokinin (CCK) modulates feeding and dopamine-induced behavior in the central and peripheral nervous system. Lintitript antagonizes the effect of cholecystokinin by binding to the cholecystokinin type A (CCK-A) receptor. This action presumably alters feeding habits, however the exact mechanism of action is not known.",,,,Lintitript is investigational.,Lintitript is a solid.,True
17124,"Phylloquinone is often called vitamin K1. Phylloquinone is fat soluble and stable in air and moisture. However, it degrades in sunlight. It is found naturally in a wide variety of green plants. Phylloquinone is also an antidote for coumatetralyl. Vitamin K is needed for the posttranslational modification of certain proteins, mostly required for blood coagulation. For the treatment of haemorrhagic conditions in infants, antidote for coumarin anticoagulants in hypoprothrombinaemia. Phylloquinone is a vitamin, indicated in the treatment of coagulation disorders which are due to faulty formation of factors II, VII, IX and X when caused by vitamin K deficiency or interference with vitamin K activity. Phylloquinone aqueous colloidal solution of vitamin K1 for parenteral injection, possesses the same type and degree of activity as does naturally-occurring vitamin K, which is necessary for the production via the liver of active prothrombin (factor II), proconvertin (factor VII), plasma thromboplastin component (factor IX), and Stuart factor (factor X). Vitamin K is an essential cofactor for the gamma-carboxylase enzymes which catalyze the posttranslational gamma-carboxylation of glutamic acid residues in inactive hepatic precursors of coagulation factors II (prothrombin), VII, IX and X. Gamma-carboxylation converts these inactive precursors into active coagulation factors which are secreted by hepatocytes into the blood. Supplementing with Phylloquinone results in a relief of vitamin K deficiency symptoms which include easy bruisability, epistaxis, gastrointestinal bleeding, menorrhagia and hematuria.",The molecular weight is 450.71.,Phylloquinone has a topological polar surface area of 34.14.,The log p value of  is 12.01.,Phylloquinone is approved and investigational.,Phylloquinone is a liquid.,True
17125,"Anisindione is a synthetic anticoagulant and an indanedione derivative. Its anticoagulant action is mediated through the inhibition of the vitamin K-mediated gamma-carboxylation of precursor proteins that are critical in forming the formation of active procoagulation factors II, VII, IX, and X, as well as the anticoagulant proteins C and S, in the liver. For the prophylaxis and treatment of venous thrombosis and its extension, the treatment of atrial fibrillation with embolization, the prophylaxis and treatment of pulmonary embolism, and as an adjunct in the treatment of coronary occlusion. Anisindione is a synthetic anticoagulant and an indanedione derivative. It is prescribed only if you cannot take coumarin-type anticoagulants such as coumadin as anisindione is a powerful drug with serious potential side effects. Anticoagulants decrease the clotting ability of the blood and therefore help to prevent harmful clots from forming in the blood vessels. These medicines are sometimes called blood thinners, although they do not actually thin the blood. They also will not dissolve clots that already have formed, but they may prevent the clots from becoming larger and causing more serious problems. Like phenindione, to which it is related chemically, anisindione exercises its therapeutic action by reducing the prothrombin activity of the blood. By inhibiting the vitamin K&ndash;mediated gamma-carboxylation of precursor proteins, the formation of active procoagulation factors II, VII, IX, and X, as well as the anticoagulant proteins C and S is prevented. Anisindione has no direct thrombolytic effect and does not reverse ischemic tissue damage, although it may limit extension of existing thrombi and prevent secondary thromboembolic complications.",The molecular weight is 252.27.,Anisindione has a topological polar surface area of 43.37.,The log p value of  is 2.73.,Anisindione is approved.,Anisindione is a solid.,True
17126,,,,,L-Eflornithine is experimental and investigational.,L-Eflornithine is a solid.,False
17127,"Geneticin (also known as G418) is an aminoglycoside antibiotic similar in structure to gentamicin B1, produced by Micromonospora rhodorangea. Geneticin blocks polypeptide synthesis by inhibiting the elongation step in both prokaryotic and eukaryotic cells and is commonly used in laboratory research to select genetically engineered cells. Resistance to Geneticin is conferred by the neo gene from Tn5 encoding an aminoglycoside 3‘-phosphotransferase, APH 3‘ II.",,,,Geneticin is experimental.,Geneticin is a solid.,True
17128,"Eflornithine is a prescription drug indicated in the treatment of facial hirsutism (excessive hair growth). Eflornithine hydrochloride cream for topical application is intended for use in women suffering from facial hirsutism and is sold by Allergan, Inc. under the brand name Vaniqa. Eflornithine for injection against sleeping sickness was manufactured by Sanofi Aventis and sold under the brand name Ornidyl in the USA. It is now discontinued. Eflornithine is on the World Health Organization's List of Essential Medicines. Eflornithine is indicated in the treatment of facial hirsutism (excessive hair growth). Eflornithine prevents hair growth by inhibiting the anagen phase of hair production. This occurs by eflornithine irreversibly binding (also called suicide inhibition) to ornithine decarboxylase (ODC) and physically preventing the natural substrate ornithine from accessing the active site. ",The molecular weight is 182.17.,Eflornithine has a topological polar surface area of 89.34.,The log p value of  is -1.84.,Eflornithine is approved and withdrawn.,Eflornithine is a solid.,True
17129,,,,,3-Oxiran-2ylalanine is experimental.,3-Oxiran-2ylalanine is a solid.,False
17130,,,,,L-2-amino-4-methoxy-cis-but-3-enoic acid is experimental.,L-2-amino-4-methoxy-cis-but-3-enoic acid is a solid.,False
17131,,,,,(R)-3-hydroxydecanoyl-CoA is experimental.,(R)-3-hydroxydecanoyl-CoA is a solid.,False
17132,"Pentolinium is a nicotinic antagonist that has been used as a ganglionic blocking agent in hypertension. Used to produce controlled hypotension during surgical procedures and in hypertensive crises. Pentolinium acts as a ganglionic blocking agent. Pentolinium inhibits release of adrenaline and noradrenaline from adrenergic nerves. It is used as an antihypertensive, and can be administered orally, intramuscularly, and subcutaneously. Pentolinium binds to the nicotinic (ganglion) acetylcholine receptor. This receptor/channel is permeable to a range of divalent cations including calcium, the influx of which may activate a potassium current which hyperpolarizes the cell membrane. Blockage of the receptor leads to smooth muscle relaxation and vasodilaton.",The molecular weight is 240.43.,,The log p value of  is -6.11.,Pentolinium is approved.,Pentolinium is a solid.,True
17133,"ATG003, a novel anti-angiogenic drug candidate and a formulation of mecamylamine, is currently in clinical development for neovascular age-related macular degeneration. Investigated for use/treatment in macular degeneration. ATG003 acts by inhibiting the angiogenic pathway mediated by the nicotinic acetylcholine receptors found on endothelial cells (EC-NAChR). Inhibiting this pathway also inhibits the synthesis and cellular responses mediated by growth factors such as VEGF and bFGF.",,,,ATG003 is investigational.,ATG003 is a solid.,True
17134,"An alkaloid that has actions similar to nicotine on nicotinic cholinergic receptors but is less potent. It has been proposed for a variety of therapeutic uses including in respiratory disorders, peripheral vascular disorders, insomnia, and smoking cessation.  Investigated for use/treatment in addictions. Lobeline inhibits nicotine-evoked dopamine release and nicotine binding, thus acting as a potent antagonist at both alpha3beta2(*) and alpha4beta2(*) neuronal nicotinic receptor subtypes. However, lobeline does not release dopamine from its presynaptic terminal, but appears to induce the metabolism of dopamine intraneuronally. Reevaluation of the mechanism by which lobeline alters dopamine function reveals that its primary mechanism is inhibition of dopamine uptake and promotion of dopamine release from the storage vesicles within the presynaptic terminal, via an interaction with the tetrabenazine-binding site on the vesicular monoamine transporter (VMAT2). Thus, lobeline appears to perturb the fundamental mechanisms of dopamine storage and release. Based on its neurochemical mechanism, the ability of lobeline to functionally antagonize the neurochemical and behavioral effects of the psychostimulants amphetamine and methamphetamine was examined. Lobeline was found to inhibit the amphetamine-induced release of dopamine in vitro, and amphetamine-induced hyperactivity, drug discrimination, and self-administration.",,,,Lobeline is investigational.,Lobeline is a solid.,True
17135,"RPI-78M is being developed for the treatment of multiple sclerosis (MS). Other neurological disorders that may be served by RPI-78M include myasthenia gravis (MG), muscular dystrophy (MD) and amyotrophic lateral sclerosis (ALS). Investigated for use/treatment in multiple sclerosis, neurologic disorders, and pain (acute or chronic). RPI-78M contains anticholinergic peptides that recognize the same receptors as nicotine (acetylcholine receptors) but have the opposite effect.",,,,RPI-78M is investigational.,RPI-78M is a solid.,True
17136,"Multiple Sclerosis (MS) is a chronic, debilitating neurological disease that can lead to profound cognitive and physical symptoms, severely affecting quality of life. It is the main cause of neurological disability not caused by trauma in the young adult population of both North America and Europe. Relapsing-remitting forms of MS lead to neurological symptoms that resolve and recur periodically. More than 80% of patients suffering from this disease have relapsing-remitting MS. Diroximel fumarate is indicated for the treatment of relapsing forms of multiple sclerosis (MS) in adults; specifically active secondary progressive disease and clinically isolated syndrome, as well as relapsing-remitting MS. Diroximel fumarate relieves the neurological symptoms of relapsing MS with less gastrointestinal effects than its bioequivalent counterpart, dimethyl fumarate. It is important to note that diroximel fumarate can cause angioedema, anaphylaxis, hepatotoxicity, flushing, lymphopenia, and Progressive Multifocal Leukoencephalopathy (PML).  Currently, the mechanism of action of this drug in MS is not fully understood. Diroximel fumarate is hypothesized to regulate cell signaling pathways, causing beneficial immune and neuroprotective effects. Monomethyl fumarate (MMF) is the active metabolite of diroximel fumarate, and activates the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathway in humans. This pathway occurs as a response to oxidative stress in cells.",,,,Diroximel fumarate is approved and investigational.,Diroximel fumarate is a solid.,True
17137,"Investigated for use/treatment in alzheimer's disease, neurologic disorders, pain (acute or chronic), and parkinson's disease. EVT 101 penetrates the brain at doses that are well tolerated in man and expected to be clinically relevant, shows activity in areas relevant to pain and, importantly, modulates the activity of specific brain regions during the performance of cognitive tasks relevant to Alzheimer's disease.",,,,EVT-101 is investigational.,EVT-101 is a solid.,True
17138,,,,,"3,20-Pregnanedione is experimental.","3,20-Pregnanedione is a solid.",False
17139,,,,,"1-BENZYL-3-(4-METHOXYPHENYLAMINO)-4-PHENYLPYRROLE-2,5-DIONE is experimental.","1-BENZYL-3-(4-METHOXYPHENYLAMINO)-4-PHENYLPYRROLE-2,5-DIONE is a solid.",False
17140,,,,,Tributyltin is experimental.,Tributyltin is a solid.,False
17141,"Oprelvekin, the active ingredient in Neumega®, is recombinant Interleukin-11 (IL-11), which is produced in Escherichia coli (E. coli) by recombinant DNA technology. With a molecular mass of approximately 19,000 daltons, the non-glycosylated protein is 177 amino acids in length in comparison to the natural IL-11, which is 178 amino acid long. However, it displays comparable biological activity compared to the natural IL-11 _in vitro_ and _in vivo_. Oprelvekin works by stimulating megakaryocytopoiesis and thrombopoiesis. In mice and nonhuman primate studies of animals with moderate and severe myelosuppression, in addition to compromised hematopoiesis, oprelvekin was shown to potently induce thrombopoiesis and improve platelet nadirs and accelerated platelet recoveries compared to controls. In animal studies, oprelvekin was also shown to regulate intestinal epithelium growth by enhancing healing of gastrointestinal lesions, inhibit adiopegenesis and macrophageal released pro-inflammatory cytokines, and induce acute phase protein synthesis. Indicated for the prevention of severe thrombocytopenia and the reduction of the need for platelet transfusions following myelosuppressive chemotherapy in adult patients with nonmyeloid malignancies who are at high risk of severe thrombocytopenia. Oprelvekin promotes hematopoiesis by stimulating megakaryocytopoiesis and thrombopoiesis. It is used in adult patients with nonmyeloid malignancies to prevent severe thrombocytopenia and reduce the need for platelet transfusions following therapies that cause myelosuppression. Its use is prioritized in patients who are at an elevated risk for developing severe thrombocytopenia. In clinical trials, oprelvekin has shown potent thrombopoietic activity in individuals with compromised hematopoiesis.  Oprelvekin binds to the interleukin 11 receptor which leads to a cascade of signal transduction events. Its pharmacological action mimics the biological activity of endogenous IL-11, which is a thrombopoietic growth factor that directly stimulates the proliferation of hematopoietic stem cells and megakaryocyte progenitor cells and induces megakaryocyte maturation resulting in increased platelet production.",,,,Oprelvekin is approved and investigational.,Oprelvekin is a liquid.,True
17142,,,,,Deacetoxyvinzolidine is experimental.,Deacetoxyvinzolidine is a solid.,False
17143,,,,,tert-butanol is experimental.,tert-butanol is a solid.,False
17144,,,,,Trimethyllysine is experimental.,Trimethyllysine is a solid.,False
17145,,,,,N-(6-Aminohexyl)-5-Chloro-1-Naphthalenesulfonamide is experimental.,N-(6-Aminohexyl)-5-Chloro-1-Naphthalenesulfonamide is a solid.,False
17146,,,,,"(3Z)-N,N-DIMETHYL-2-OXO-3-(4,5,6,7-TETRAHYDRO-1H-INDOL-2-YLMETHYLIDENE)-2,3-DIHYDRO-1H-INDOLE-5-SULFONAMIDE is experimental.","(3Z)-N,N-DIMETHYL-2-OXO-3-(4,5,6,7-TETRAHYDRO-1H-INDOL-2-YLMETHYLIDENE)-2,3-DIHYDRO-1H-INDOLE-5-SULFONAMIDE is a solid.",False
17147,"The relatively new calcium levulinate is produced from a direct reaction between L- or levulinic acid levulose and calcium hydroxide. The resultant calcium levulinate formulation, when used as a calcium supplement, possesses a high calcium content that is observed to be 14.8% higher than the content typically found in calcium lactate. This formulation is considered a low molecular weight organic calcium ion type that is easily absorbed through the intestinal wall. This new application of calcium is intended for use as a food fortifier, to fortify foods like sauces, condiments, beer, beverages, soft drinks, milk and milk products, soy milk and soy products with calcium nutrition. Calcium levulinate can be used alone, or with calcium lactate, calcium chloride, and other compounds, either for pharmaceutical tablets, capsules, or injections preparation. In essence, calcium levulinate is ultimately a relatively new calcium supplementation option. The relatively new calcium levulinate is produced from a direct reaction between L- or levulinic acid levulose and calcium hydroxide. The resultant calcium levulinate formulation, when used as a calcium supplement, possesses a high calcium content that is observed to be 14.8% higher than the content typically found in calcium lactate. Moreover, this formulation also demonstrates a high solubility of more than 30% at 25℃. Furthermore, the calcium levulinate is believed to be non-toxic and non-allergic, making it especially suitable for injection or infusion administrations. Additionally, this levulinate formulation is reported as having a good taste, little irritation with a pH value of 7, and good stability such that no precipitation or deterioration occurs during use. Finally, this calcium levulinate formulation is also believed to have good compatibility with calcium lactate, calcium chloride, and other material complexes which allows the formulation to also complex effectively with a diverse variety of foodstuffs and pharmaceutical dosage forms. Much like most calcium supplements, once calcium levulinate dissociates in the body after administration, absorption of the supplemental calcium ions across the intestinal wall serves to enhance calcium stores in the body.",,,,Calcium levulinate is approved and experimental.,,True
17148,"A quinazoline-sulfonamide that is considered a thiazide-like diuretic which is long-acting so useful in chronic renal failure. It also tends to lower blood pressure and increase potassium loss. For the treatment of hypertension, alone or in combination with other antihypertensive drugs of a different class. Metolazone is a quinazoline diuretic, with properties generally similar to the thiazide diuretics. A proximal action of metolazone has been shown in humans by increased excretion of phosphate and magnesium ions and by a markedly increased fractional excretion of sodium in patients with severely compromised glomerular filtration. This action has been demonstrated in animals by micropuncture studies. The actions of metolazone result from interference with the renal tubular mechanism of electrolyte reabsorption. Metolazone acts primarily to inhibit sodium reabsorption at the cortical diluting site and to a lesser extent in the proximal convoluted tubule. Sodium and chloride ions are excreted in approximately equivalent amounts. The increased delivery of sodium to the distal tubular exchange site results in increased potassium excretion. Metolazone does not inhibit carbonic anhydrase. The antihypertensive mechanism of action of metolazone is not fully understood but is presumed to be related to its saluretic and diuretic properties.",The molecular weight is 365.83.,Metolazone has a topological polar surface area of 92.5.,The log p value of  is 2.06.,Metolazone is approved.,Metolazone is a solid.,True
17149,"A synthetic morphinan analgesic with narcotic antagonist action. It is used in the management of severe pain. For the relief of moderate to severe pain. Butorphanol is a synthetic opioid agonist-antagonist analgesic with a pharmacological and therapeutic profile that has been well established since its launch as a parenteral formulation in 1978. The introduction of a transnasal formulation of butorphanol represents a new and noninvasive presentation of an analgesic for moderate to severe pain. This route of administration bypasses the gastrointestinal tract, and this is an advantage for a drug such as butorphanol that undergoes significant first-pass metabolism after oral administration. The onset of action and systemic bioavailability of butorphanol following transnasal delivery are similar to those after parenteral administration. Butorphanol blocks pain impulses at specific sites in the brain and spinal cord. The exact mechanism of action is unknown, but is believed to interact with an opiate receptor site in the CNS (probably in or associated with the limbic system). The opiate antagonistic effect may result from competitive inhibition at the opiate receptor, but may also be a result of other mechanisms. Butorphanol is a mixed agonist-antagonist that exerts antagonistic or partially antagonistic effects at mu opiate receptor sites, but is thought to exert its agonistic effects principally at the kappa and sigma opiate receptors.",The molecular weight is 327.47.,Butorphanol has a topological polar surface area of 43.7.,The log p value of  is 3.73.,Butorphanol is approved and illicit and vet_approved.,Butorphanol is a solid.,True
17150,"A narcotic used as a pain medication. It appears to be an agonist at kappa opioid receptors and an antagonist or partial agonist at mu opioid receptors. Nalbuphine is the only opioid analgesic that is not a controlled substance in the United States. For the relief of moderate to severe pain. Nalbuphine is a synthetic opioid agonist-antagonist analgesic of the phenanthrene series. Nalbuphine's analgesic potency is essentially equivalent to that of on a milligram basis. The opoioid antagonist activity of nalbuphine is about one-fourth to that of and 10 times to that of. Nalbuphine by itself has potent opioid antagonist activity at doses equal to or lower than its analgesic dose. When administered following or concurrent with mu agonist opioid analgesics (e.g., morphine, oxymorphone, fentanyl), nalbuphine may partially reverse or block opioid-induced respiratory depression from the mu agonist analgesic. Nalbuphine may precipitate withdrawal in patients dependent on opioid drugs. Nalbuphine should be used with caution in patients who have been receiving mu opioid analgesics on a regular basis. The exact mechanism of action is unknown, but is believed to interact with an opiate receptor site in the CNS (probably in or associated with the limbic system). The opiate antagonistic effect may result from competitive inhibition at the opiate receptor, but may also be a result of other mechanisms. Nalbuphine is thought primarily to be a kappa agonist. It is also a partial mu antagonist analgesic, with some binding to the delta receptor and minimal agonist activity at the sigma receptor.",The molecular weight is 357.45.,Nalbuphine has a topological polar surface area of 73.16.,The log p value of  is 1.39.,Nalbuphine is approved.,Nalbuphine is a solid.,True
17151,"A narcotic analgesic that may be habit-forming. It is nearly as effective orally as by injection. For the management of moderate to severe pain or as a preoperative medication where an opioid analgesic is appropriate. Levorphanol is a potent synthetic opioid analgesic indicated for the management of moderate to severe pain or as a preoperative medication where an opioid analgesic is appropriate. Levorphanol is similar to morphine in its actions, however it is up to 8 times more potent than morphine. Levorphanol produces a degree of respiratory depression similar to that produced by morphine at equianalgesic doses, and like many mu-opioid drugs, levorphanol produces euphoria or has a positive effect on mood in many individuals. Like other mu-agonist opioids it is believed to act at receptors in the periventricular and periaqueductal gray matter in both the brain and spinal cord to alter the transmission and perception of pain.",The molecular weight is 257.38.,Levorphanol has a topological polar surface area of 23.47.,The log p value of  is 3.53.,Levorphanol is approved.,Levorphanol is a solid.,True
17152,"Remifentanil (marketed by Abbott as Ultiva) is a potent ultra short-acting synthetic opioid given to patients during surgery for pain relief and adjunctive to an anaesthetic. Remifentanil is a specific mu-type-opioid receptor agonist which means it reduces sympathetic nervous system tone, and causes respiratory depression and analgesia. For use during the induction and maintenance of general anesthesia. Remifentanil is an opioid agonist with rapid onset and peak effect and ultra-short duration of action. The opioid activity of remifentanil is antagonized by opioid antagonists such as naloxone. The analgesic effects of remifentanil are rapid in onset and offset. Its effects and side effects are dose dependent and similar to other opioids. Remifentanil in humans has a rapid blood-brain equilibration half-time of 1 &plusmn; 1 minutes (mean &plusmn; SD) and a rapid onset of action. Remifentanil is a &micro;-opioid agonist with rapid onset and peak effect, and short duration of action. The &micro;-opioid activity of remifentanil is antagonized by opioid antagonists such as naloxone.",The molecular weight is 376.45.,Remifentanil has a topological polar surface area of 76.15.,The log p value of  is 1.96.,Remifentanil is approved.,Remifentanil is a solid.,True
17153,"A meperidine congener used as an antidiarrheal, usually in combination with atropine. At high doses, it acts like morphine. Its unesterified metabolite difenoxin has similar properties and is used similarly. It has little or no analgesic activity. This medication is classified as a Schedule V under the Controlled Substances Act by the Food and Drug Administration (FDA) and the DEA in the United States when used in preparations. When diphenoxylate is used alone, it is classified as a Schedule II. For as adjunctive therapy in the management of diarrhea Diphenoxylate, an antidiarrheal, is effective as adjunctive therapy in the management of diarrhea. Diphenoxylate is rapidly and extensively metabolized in man by ester hydrolysis to diphenoxylic acid (difenoxine), which is biologically active and the major metabolite in the blood. Diphenoxylate is an opiate receptor agonists that stimulate mu receptors in GI to decrease the peristalsis and constrict the sphincters. Diphenoxylate has a direct effect on circular smooth muscle of the bowel, that conceivably results in segmentation and prolongation of gastrointestinal transit time. The clinical antidiarrheal action of diphenoxylate may thus be a consequence of enhanced segmentation that allows increased contact of the intraluminal contents with the intestinal mucosa.",The molecular weight is 452.6.,Diphenoxylate has a topological polar surface area of 53.33.,The log p value of  is 5.33.,Diphenoxylate is approved and illicit.,Diphenoxylate is a solid.,True
17154,"3-Methyl-thiofentanyl is a analog and an opioid analgesic that works by inducing central nervous system (CNS) depression. 3-Methylthiofentanyl binds to the mu, delta, and kappa opioid receptors. These ultimately lead to decreased pain sensation as well as a number of side effects, such as euphoria, sedation, depressed breathing.",,,,3-Methylthiofentanyl is experimental and illicit.,3-Methylthiofentanyl is a solid.,True
17155,"Dimethylthiambutene (N,N-Dimethyl-1-methyl-3,3-di-2-thienylallylamine, Dimethibutin, Ohton) is an opioid analgesic drug. It is now under international control under Schedule I of the UN Single Convention On Narcotic Drugs 1961, presumably due to high abuse potential, although little more information is available. Dimethylthiambutene is an opioid analgesic previously used in moderate pain relief.",The molecular weight is 263.42.,Dimethylthiambutene has a topological polar surface area of 3.24.,The log p value of  is 3.43.,Dimethylthiambutene is experimental and illicit.,Dimethylthiambutene is a liquid.,True
17156,"A narcotic analgesic morphinan used as a sedative in veterinary practice. In certain countries, etorphine is classified as a Schedule 1 drug and hence, in these countries, it can be used legally only by health professionals and for research purposes. Etorphine is only available to the patients under an official prescription. In the US, Etorphine is listed as a Schedule I drug, although Etorphine hydrochloride is classified as Schedule II. Etorphine is only available for its use in veterinary. This main usage is related to the immobilization of large mammals. Etorphine is a synthetic cousin of morphine and 40,000 times more powerful.  Etorphine is an agonist at mu, delta, and kappa opioid receptors. It also has a weak affinity for the ORL1 nociceptin/orphanin FQ receptor.",,,,Etorphine is illicit and vet_approved.,Etorphine is a solid.,True
17157,"Carfentanil or carfentanyl (Wildnil) is an analogue of the popular synthetic opioid analgesic fentanyl, and is one of the most potent opioids known (also the most potent opioid used commercially). Carfentanil was first synthesized in 1974 by a team of chemists at Janssen Pharmaceutica which included Paul Janssen. It has a quantitative potency approximately 10,000 times that of morphine and 100 times that of fentanyl, with activity in humans starting at about 1 microgram. It is marketed under the trade name Wildnil as a general anaesthetic agent for large animals. Carfentanil is intended for large-animal use only as its extreme potency makes it inappropriate for use in humans. Currently sufentanil, approximately 10–20 times less potent (500 to 1000 times the efficacy of morphine per weight) than carfentanil, is the maximum strength fentanyl analog for use in humans. Carfentanil is similar (but more potent) to the opioid analgesic fentanyl. It is used as a tranquilizer for large animals. Carfentanil acts primarily on the mu (some kappa and delta) opioid receptors as an agonist. It will induce similar effects of analgesia as other opioids, however, due to its potency, it will also induce strong side effects such as sedation. Consequently, that is why it is used as a tranquilizer for large animals. Carfentanil binds very strongly to mu opioid receptors and acts as a competitive agonist. ",,,,Carfentanil is illicit and investigational and vet_approved.,Carfentanil is a solid.,True
17158,"A narcotic antagonist similar in action to naloxone. It is used to remobilize animals after etorphine neuroleptanalgesia and is considered a specific antagonist to etorphine.  Diprenorphine is indicated to reverse the effects of powerful opioids including etorphine and carfentanil, often used for tranquilizing large animals. This drug is not approved for use in humans. Diprenorphine binds approximately equally to the three subtypes of opioid receptorsand antagonizes them.",,,,Diprenorphine is illicit and vet_approved.,Diprenorphine is a solid.,True
17159,A semisynthetic analgesic used in the study of narcotic receptors. It has abuse potential.  Dihydromorphine is an opioid analgesic used for moderate to severe pain relief.,,,,Dihydromorphine is experimental and illicit.,Dihydromorphine is a solid.,True
17160,"3-Methylfentanyl is an opioid analgesic and is an analog of the potent opioid, fentanyl. 3-Methylfentanyl is one of the most powerful opioid drugs sold illegally and is estimated to be between 400-6000 times more potent than morphine in certain cases. 3-Methylfentanyl was initially discovered in 1974 and widespread illegal use of this drug has occurred since this time. 3-Methylfentanyl exhibits similar pharmacodynamic effects to fentanyl but has been proven to be significantly stronger in these effects due to increased binding affinity to the opioid receptor. Fentanyl, administered alone, has a strong affinity for opioid receptors. 3-methylfentanyl has the potential to be extremely hazardous when used without the prescription and supervision of a medical professional. Ingestion of this drug has resulted in numerous deaths among individuals using the drug recreationally. Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Fentanyl's analgesic activity is, most likely, due to its conversion to morphine. Opioids close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability.",,,,3-Methylfentanyl is illicit.,3-Methylfentanyl is a solid.,True
17161,"ADL5859 is a novel, oral compound that targets the Delta opioid receptor. Delta receptor agonists are thought to offer benefits over other approaches to the management of pain. Investigated for use/treatment in pain (acute or chronic). ADL5859 is a novel, oral compound that targets the Delta opioid receptor. Delta receptor agonists are thought to offer benefits over other approaches to the management of pain.",,,,ADL5859 is investigational.,ADL5859 is a solid.,True
17162,"Alvimopan is a peripherally acting μ opioid antagonist. It is used to avoid postoperative ileus following small or large bowel resection and accelerates the gastrointestinal recovery period. Used to accelerate the time to upper and lower gastrointestinal recovery following partial large or small bowel resection surgery with primary anastomosis. Also investigated for use in the treatment of pain (acute or chronic). Alvimopan competitively binds to mu-opioid receptor in the gastrointestinal tract but, unlike methylnaltrexone which relies upon it ionic charge, alvimopan owes its selectivity for peripheral receptors to its pharmacokinetics. Alvimopan binds to peripheral mu-receptors with a Ki of 0.2 ng/mL.",The molecular weight is 424.54.,Alvimopan has a topological polar surface area of 89.87.,The log p value of  is 2.16.,Alvimopan is approved and investigational.,Alvimopan is a solid.,True
17163,"Investigated for use/treatment in pain (acute or chronic). M6G, morphine-6-glucuronide, is an active metabolite from liver metabolism of morphine. M6G has a similar mechanism of action to morphine, primarily acting on the mu opioid receptor, with slightly higher affinity to the delta receptor than and lower affinity for the kappa receptor than morphine. It is proposed that M6G has a lower affinity than morphine at the mu2 receptor but equal affinity to the u1 receptor, but these results are uncertain and are undergoing further investigation. The precise mechanism of the analgesic action of morphine is unknown. However, specific CNS opiate receptors have been identified and likely play a role in the expression of analgesic effects. The mechanism of respiratory depression involves a reduction in the responsiveness of the brain stem respiratory centers to increases in carbon dioxide tension and to electrical stimulation.",,,,Morphine glucuronide is investigational.,Morphine glucuronide is a solid.,True
17164,"Pholcodine formula is 3-o-morpholinoethylmorphine and it is classified as an antitussive which is defined as an opioid cough suppressant. It belongs to the opioid family of compounds and it is widely used. Pholcodine activity is the suppression of unproductive cough and it also has a mild sedative effect with little or no analgesic effects. Pholcodine is not prescribed in the United States where it is classed as a Schedule I drug. It is categorized as Class B drug in the UK and officially taken out of the shelves in 2008. Pholcodine is not approved in Canada. Pholcodine is indicated as a cough suppressant for the temporary relief of non-productive dry cough. It is stated to present a required label indication of \temporary relief of dry cough.\"" Cough is the respiratory movement that occurs after an irritation signal is transmitted to the central nervous system and further stimulates the medulla oblongata. This stimulation causes a motor output that is sent through motoneurons to the respiratory muscles. A non-productive cough is a type of cough characterized by the absence of sputum, and it has a large inspiration that will cause continuous coughing."" The therapeutic doses of pholcodine have been shown not to cause depression of respiration, CNS excitation or other side effects associated with narcotics. It is thought that the impact of pholcodine is selective on the cough center without affecting the respiratory center. Pholcodine is not euphorigenic, and thus, psychological dependence is unlikely. Clinical trials have not shown any evidence of addiction after prolonged administration of pholcodine. It is well reported that pholcodine presents a more considerable respiratory depression effect than codeine and it causes hypotension in the same degree than codeine. Some other noted impacts of pholcodine in preclinical trials are: 1) the induction of histamine release, 2) anti-histaminic effect, 3) anti-acetylcholinic action, 4) anti-convulsant action and 5) mild tranquilizing action. The mechanism of action of pholcodine is directly performed in the medulla oblongata. In this site, it exerts analgesic properties on the peripheric reflexogenic receptors. This site is commonly known as the \cough center.\""""",The molecular weight is 398.5.,Pholcodine has a topological polar surface area of 54.4.,The log p value of  is 1.27.,Pholcodine is approved and illicit.,Pholcodine is a solid.,True
17165,"Eluxadoline is a mixed mu-opioid receptor agonist, kappa-opioid receptor agonist, and a-delta opioid receptor antagonist indicated for use in diarrhea-predominant irritable bowel syndrome (IBS-D). The mu-, kappa-, and delta-opioid receptors mediate endogenous and exogenous opioid response in the central nervous system and peripherally in the gastrointestinal system. Agonism of peripheral mu-opioid receptors results in reduced colonic motility, while antagonism of central delta-opioid receptors results in improved analgesia, making eluxadoline usable for the symptoms of both pain and diarrhea characteristic of IBS-D.  For the treatment of irritable bowel syndrome with diarrhea (IBS-D). Eluxadoline is a mu-opioid receptor agonis, kappa opioid receptor agonist and a delta opioid receptor antagonist. Eluxadoline is used for diarrhea predominant IBS because it reduces intestinal contractility and normalizes stress-induced acceleration of upper GI transit. Antagonistic activity at the delta receptor minimizes the constipating effect usually seen by mu-opioid receptor agonists alone. Because of it's limited systemic bioavailability, there may be less side effects associated with the use of eluxadoline in comparison with other therapies used to treat diarrhea predominant IBS. ",The molecular weight is 569.66.,Eluxadoline has a topological polar surface area of 164.63.,The log p value of  is 0.72.,Eluxadoline is approved and investigational.,Eluxadoline is a solid.,True
17166,"Loxicodegol was developed by Nektar Therapeutics as an opioid analgesic with low abuse potential for the treatment of chronic pain. The lack of abuse potential is believed to be due to the drug's slow rate of entry into brain, a unique characteristic compared to others in the opioid class. This is also thought to be the reason behind the reduced frequency of CNS-mediated adverse effects, like sedation, seen with Loxicodegol. Nektar Therapeutics has filed an application for FDA approval of Loxicodegol for use in the treatment of chronic lower back pain  Loxicodegol was developed as an opioid analgesic with low abuse potential for use in treating chronic pain. An application has been filed for FDA approval of Loxicodegol for use in treating chronic lower back pain. Loxicodegol displays full analgesic activity comparable to that of oxycodone, producing similar acetone-writhing test responses in mice and hot-plate test maximal latencies in rats. Loxicodegol is a full agonist at the μ-opioid receptor. It also displays selectivity towards this subtype with an affinity of 237 nM compared to 4150 nM and >100000 nM for the δ- and κ-opioid receptors. The μ-opioid receptor is activated with an EC₅₀ of 12.5 μM. Activation of this receptor produces an inhibitory effect on neurotransmission through Gi/Go coupling. Opioid medications like Loxicodegol inhibit voltage gated Ca²⁺ channel opening presynaptically on C fibres and activate inward-rectifying K⁺ channels post-synaptically on 2nd order neurons, leading to hyperpolarization. Together, these prevent the nociceptive signal from traveling up the spinal cord to the brain. In the brain, opioids work through a mechanism of inhibition of inhibition to allow regulatory neurons to suppress nociception. ",,,,Loxicodegol is investigational.,Loxicodegol is a solid.,True
17167,,,,,Gabaculine is experimental.,Gabaculine is a solid.,False
17168,,,,,Canaline is experimental.,Canaline is a solid.,False
17169,,,,,Etheno-NAD is experimental.,Etheno-NAD is a solid.,False
17170,"A cholinesterase inhibitor with a slightly longer duration of action than neostigmine. It is used in the treatment of myasthenia gravis and to reverse the actions of muscle relaxants. For the treatment of myasthenia gravis. Pyridostigmine is a parasympathomimetic and a reversible cholinesterase inhibitor. Since it is a quaternary amine, it is poorly absorbed in the gut and doesn't cross the blood-brain barrier. Pyridostigmine has a slightly longer duration of action than NEOSTIGMINE. It is used in the treatment of myasthenia gravis and to reverse the actions of muscle relaxants. Pyridostigmine inhibits acetylcholinesterase in the synaptic cleft by competing with acetylcholine for attachment to acetylcholinesterase, thus slowing down the hydrolysis of acetylcholine, and thereby increases efficiency of cholinergic transmission in the neuromuscular junction and prolonges the effects of acetylcholine.",The molecular weight is 181.21.,Pyridostigmine has a topological polar surface area of 33.42.,The log p value of  is -4.26.,Pyridostigmine is approved and investigational.,Pyridostigmine is a solid.,True
17171,"Pralidoxime is an antidote to organophosphate pesticides and chemicals. Organophosphates bind to the esteratic site of acetylcholinesterase, which results initially in reversible inactivation of the enzyme. If given within 24 hours,after organophosphate exposure, pralidoxime reactivates the enzyme cholinesterase by cleaving the phosphate-ester bond formed between the organophosphate and acetylcholinesterase. For the treatment of poisoning due to those pesticides and chemicals of the organophosphate class which have anticholinesterase activity and in the control of overdosage by anticholinesterase drugs used in the treatment of myasthenia gravis. Pralidoxime is to reactivate cholinesterase (mainly outside of the central nervous system) which has been inactivated by phosphorylation due to an organophosphate pesticide or related compound. The destruction of accumulated acetylcholine can then proceed, and neuromuscular junctions will again function normally. Pralidoxime also slows the process of \aging\"" of phosphorylated cholinesterase to a nonreactivatable form, and detoxifies certain organophosphates by direct chemical reaction. The drug has its most critical effect in relieving paralysis of the muscles of respiration. Because pralidoxime is less effective in relieving depression of the respiratory center, atropine is always required concomitantly to block the effect of accumulated acetylcholine at this site. Pralidoxime relieves muscarinic signs and symptoms, salivation, bronchospasm, etc., but this action is relatively unimportant since atropine is adequate for this purpose."" Pralidoxime is an antidote to organophosphate pesticides and chemicals. Organophosphates bind to the esteratic site of acetylcholinesterase, which results initially in reversible inactivation of the enzyme. Acetylcholinesterase inhibition causes acetylcholine to accumulate in synapses, producing continuous stimulation of cholinergic fibers throughout the nervous systems. If given within 24 hours after organophosphate exposure, pralidoxime reactivates the acetylcholinesterase by cleaving the phosphate-ester bond formed between the organophosphate and acetylcholinesterase.",,,,Pralidoxime is approved and vet_approved.,Pralidoxime is a solid.,True
17172,"Demecarium is an indirect-acting parasympathomimetic agent that is used to treat glaucoma. It is a cholinesterase inhibitor or an anticholinesterase. Cholinesterase inhibitors prolong the effect of acetylcholine, which is released at the neuroeffector junction of parasympathetic postganglion nerves, by inactivating the cholinesterases that break it down. Demecarium inactivates both pseudocholinesterase and acetylcholinesterase. In the eye, this causes constriction of the iris sphincter muscle (causing miosis) and the ciliary muscle. The outflow of the aqueous humor is facilitated, which leads to a reduction in intraocular pressure. For the topical treatment of chronic open-angle glaucoma. Demecarium is a long-acting cholinesterase inhibitor and potent miotic. Because of its toxicity, it should be reserved for use in patients with open-angle glaucoma or other chronic glaucomas not satisfactorily controlled with the short-acting miotics and other agents. Application of demecarium to the eye produces intense miosis and ciliary muscle contraction due to inhibition of cholinesterase, allowing acetylcholine to accumulate at sites of cholinergic transmission. These effects are accompanied by increased capillary permeability of the ciliary body and iris, increased permeability of the blood-aqueous barrier, and vasodilation. Myopia may be induced or, if present, may be augmented by the increased refractive power of the lens that results from the accommodative effect of the drug. Demecarium is an indirect-acting parasympathomimetic agent, also known as a cholinesterase inhibitor and anticholinesterase. Cholinesterase inhibitors prolong the effect of acetylcholine, which is released at the neuroeffector junction of parasympathetic postganglion nerves, by inactivating the cholinesterases that break it down. Demecarium inactivates both pseudocholinesterase and acetylcholinesterase. In the eye, this causes constriction of the iris sphincter muscle (causing miosis) and the ciliary muscle (affecting the accommodation reflex and causing a spasm of the focus to near vision). The outflow of the aqueous humor is facilitated, which leads to a reduction in intraocular pressure. Of the two actions, the effect on the accommodation reflex is the more transient and generally disappears before termination of the miosis.",,,,Demecarium is approved.,Demecarium is a solid.,True
17173,"A cholinesterase inhibitor that is rapidly absorbed through membranes. It can be applied topically to the conjunctiva. It also can cross the blood-brain barrier and is used when central nervous system effects are desired, as in the treatment of severe anticholinergic toxicity. For the treatment of glaucoma, and in the treatment of severe anticholinergic toxicity. Physostigmine is a parasympathomimetic, specifically, a reversible cholinesterase inhibitor which effectively increases the concentration of acetylcholine at the sites of cholinergic transmission. Physostigmine is used to treat glaucoma. Because it crosses the blood-brain barrier, it is also used to treat the central nervous system effects of atropine overdose and other anticholinergic drug overdoses. Physostigmine can reverse both central and peripheral anticholinergia. Physostigmine inhibits acetylcholinesterase, the enzyme responsible for the breakdown of used acetylcholine. By interfering with the metabolism of acetylcholine, physostigmine indirectly stimulates both nicotinic and muscarinic receptors due to the consequential increase in available acetylcholine at the synapse.",The molecular weight is 275.35.,Physostigmine has a topological polar surface area of 44.81.,The log p value of  is 1.95.,Physostigmine is approved and investigational.,Physostigmine is a solid.,True
17174,"Rivastigmine is a parasympathomimetic or cholinergic agent for the treatment of mild to moderate dementia of the Alzheimer's type. Rivastigmine is a cholinesterase inhibitor that inhibits both butyrylcholinesterase and acetylcholinesterase. For the treatment of mild to moderate dementia associated with Parkinson's disease or of the Alzheimer's type. Rivastigmine is a parasympathomimetic and a reversible cholinesterase inhibitor. An early pathophysiological feature of Alzheimer's disease that is associated with memory loss and cognitive deficits is a deficiency of acetylcholine as a result of selective loss of cholinergic neurons in the cerebral cortex, nucleus basalis, and hippocampus. Tacrine is postulated to exert its therapeutic effect by enhancing cholinergic function. While the precise mechanism of rivastigmine's action is unknown, it is postulated to exert its therapeutic effect by enhancing cholinergic function. This is accomplished by increasing the concentration of acetylcholine through reversible inhibition of its hydrolysis by cholinesterase. If this proposed mechanism is correct, rivastigmine's effect may lessen as the disease progresses and fewer cholinergic neurons remain functionally intact. Rivastigmine is a carbamate derivative that is structurally related to physostigmine, but not to donepezil and tacrine. The precise mechanism of rivastigmine has not been fully determined, but it is suggested that rivastigmine binds reversibly with and inactivates chlolinesterase (eg. acetylcholinesterase, butyrylcholinesterase), preventing the hydrolysis of acetycholine, and thus leading to an increased concentration of acetylcholine at cholinergic synapses. The anticholinesterase activity of rivastigmine is relatively specific for brain acetylcholinesterase and butyrylcholinesterase compared with those in peripheral tissues.",The molecular weight is 250.34.,Rivastigmine has a topological polar surface area of 32.78.,The log p value of  is 2.1.,Rivastigmine is approved and investigational.,Rivastigmine is a solid.,True
17175,"A rapid-onset, short-acting cholinesterase inhibitor used in cardiac arrhythmias and in the diagnosis of myasthenia gravis. It has also been used as an antidote to curare principles. For the differential diagnosis of myasthenia gravis and as an adjunct in the evaluation of treatment requirements in this disease. It may also be used for evaluating emergency treatment in myasthenic crises. Edrophonium is a short and rapid-acting anticholinesterase drug. Its effect is manifest within 30 to 60 seconds after injection and lasts an average of 10 minutes. Edrophonium's pharmacologic action is due primarily to the inhibition or inactivation of acetylcholinesterase at sites of cholinergic transmission. Nicotinic acetylcholine (nAChR)receptors are found throughout the body, especially on muscle. Stimulation of these receptors causes to muscle contraction. In myasthenia gravis the body's immune system destroys many of the nicotinic acetylcholine receptors, so that the muscle becomes less responsive to nervous stimulation. Edrophonium chloride increases the amount of acetylcholine at the nerve endings. Increased levels of acetylcholine allow the remaining receptors to function more efficiently. Edrophonium works by prolonging the action acetylcholine, which is found naturally in the body. It does this by inhibiting the action of the enzyme acetylcholinesterase. Acetylcholine stimulates nicotinic and muscarinic receptors. When stimulated, these receptors have a range of effects.",The molecular weight is 166.24.,Edrophonium has a topological polar surface area of 20.23.,The log p value of  is -2.44.,Edrophonium is approved.,Edrophonium is a liquid.,True
17176,,,,,Monoisopropylphosphorylserine is experimental.,Monoisopropylphosphorylserine is a solid.,False
17177,"Quaternary ammonium analog of ethidium; an intercalating dye with a specific affinity to certain forms of DNA and, used as diiodide, to separate them in density gradients; also forms fluorescent complexes with cholinesterase which it inhibits. ",,,,Propidium is experimental.,Propidium is a solid.,True
17178,,,,,"3,8-Diamino-6-Phenyl-5-Ethyl]-1h-1,2,3-Triazol-4-Yl]Hexyl]-Phenanthridinium is experimental.","3,8-Diamino-6-Phenyl-5-Ethyl]-1h-1,2,3-Triazol-4-Yl]Hexyl]-Phenanthridinium is a solid.",False
17179,,,,,"3,6,9,12,15-Pentaoxaheptadecane is experimental.","3,6,9,12,15-Pentaoxaheptadecane is a solid.",False
17180,,,,,1-Deoxy-1-Thio-Heptaethylene Glycol is experimental.,1-Deoxy-1-Thio-Heptaethylene Glycol is a solid.,False
17181,,,,,"(4aS,6R,8aS)-11--6-hydroxy-3-methoxy-5,6,9,10-tetrahydro-4aH-benzofurobenzazepin-11-ium is experimental.","(4aS,6R,8aS)-11--6-hydroxy-3-methoxy-5,6,9,10-tetrahydro-4aH-benzofurobenzazepin-11-ium is a solid.",False
17182,,,,,Methylphosphinate is experimental.,Methylphosphinate is a solid.,False
17183,,,,,"3,8-Diamino-6-Phenyl-5-Ethyl]-1h-1,2,3-Triazol-5-Yl]Hexyl]-Phenanthridinium is experimental.","3,8-Diamino-6-Phenyl-5-Ethyl]-1h-1,2,3-Triazol-5-Yl]Hexyl]-Phenanthridinium is a solid.",False
17184,,,,,beta-L-fucose is experimental.,beta-L-fucose is a solid.,False
17185,"Huperzine B is a novel acetylcholinesterase inhibitor. Under investigation for the treatment of Alzheimer's disease. Huperzine B is an alkaloid derived from <i>Huperzia serrata</i> (which is available as an herbal product in the US). It is under investigation as an acetylcholinesterase inhibitor. Clinical trials in China have shown that huperzine B is comparably effective to the drugs currently on the market, and may even be somewhat safer in terms of side effects. Huperzine B has been found to be an inhibitor of the enzyme acetylcholinesterase. This is the same mechanism of action of pharmaceutical drugs such as galantamine and donepezil used to treat Alzheimer's disease.",,,,Huperzine B is investigational.,Huperzine B is a solid.,True
17186,,,,,"M-(N,N,N-Trimethylammonio)-2,2,2-Trifluoro-1,1-Dihydroxyethylbenzene is experimental.","M-(N,N,N-Trimethylammonio)-2,2,2-Trifluoro-1,1-Dihydroxyethylbenzene is a solid.",False
17187,,,,,MF268 is experimental.,MF268 is a solid.,False
17188,,,,,"3-Chloro-9-Ethyl-6,7,8,9,10,11-Hexahydro-7,11-MethanocyclooctaQuinolin-12-Amine is experimental.","3-Chloro-9-Ethyl-6,7,8,9,10,11-Hexahydro-7,11-MethanocyclooctaQuinolin-12-Amine is a solid.",False
17189,,,,,NAP-226-90 is experimental.,NAP-226-90 is a solid.,False
17190,,,,,(R)-tacrine(10)-hupyridone is experimental.,(R)-tacrine(10)-hupyridone is a solid.,False
17191,,,,,(S)-tacrine(10)-hupyridone is experimental.,(S)-tacrine(10)-hupyridone is a solid.,False
17192,,,,,TACRINE(8)-4-AMINOQUINOLINE is experimental.,TACRINE(8)-4-AMINOQUINOLINE is a solid.,False
17193,,,,,"(9S)-9--1,2,3,4,9,10-HEXAHYDROACRIDINIUM is experimental.","(9S)-9--1,2,3,4,9,10-HEXAHYDROACRIDINIUM is a solid.",False
17194,"Zanapezil (TAK-147) is a selective acetylcholine (ACh) esterase inhibitor under investigation as a drug for Alzheimer's disease (AD) treatment. For the treatment of dementia in subjects with Alzheimer’s disease. Zanapezil is an acetylcholinesterase inhibitor being developed by Takeda for the treatment of dementia in subjects with Alzheimer’s disease. In May 2003, the company discontinued development of the compound due to a lack of a dose-dependent effect in the trials. Zanapezil inhibits the degradation of acetylcholine, a neurotransmitter, to prevent the reduction of cerebral acetylcholine levels and to enhance the mental function of patients with dementia. It is expected to act selectively on the central nervous system, resulting in fewer peripheral adverse reactions.",,,,Zanapezil is investigational.,Zanapezil is a solid.,True
17195,"Huperzine A, is a naturally occurring sesquiterpene alkaloid found in the extracts of the firmoss <i>Huperzia serrata</i>. The botanical has been used in China for centuries for the treatment of swelling, fever and blood disorders. Recently in clinical trials in China, it has demonstrated neuroprotective effects. It is currently being investigated as a possible treatment for diseases characterized by neurodegeneration – particularly Alzheimer’s disease. Investigated for use/treatment in alzheimer's disease. Huperzine A is an alkaloid derived from <i>Huperzia serrata</i> (which is available as an herbal product in the US). It is under investigation as an acetylcholinesterase inhibitor. Clinical trials in China have shown that huperzine A is comparably effective to the drugs currently on the market, and may even be somewhat safer in terms of side effects. Huperzine A has been found to be an inhibitor of the enzyme acetylcholinesterase. This is the same mechanism of action of pharmaceutical drugs such as and used to treat Alzheimer's disease.",,,,Huperzine A is approved and experimental.,Huperzine A is a solid.,True
17196,"Phenserine is under development by Axonyx, a US biopharmaceutical company that focuses on treatments for dementia. Phenserine is a next generation acetylcholinesterase (AChE) inhibitor indicated for the treatment of AD. Unlike currently marketed AChE inhibitors, it has a dual mechanism of action that also includes anti-amyloid activity, which may confer disease-modifying effects in patients with AD. If this is substantiated in an ongoing clinical trial then phenserine may open the door to an entirely new type of treatment for AD. Axonyx announced on 20 September 2005 that phenserine was ineffective in two curtailed phase 3 trials. For the treatment of Alzheimer's disease (AD). Phenserine, a phenylcarbamate of physostigmine, is a reversible acetyl-selective cholinesterase inhibitor. In studies of rats with lesions of the forebrain cholinergic system, injections of phenserine was found to significantly decrease the levels of secreted beta-APP in the CSF of the rats. A study on cultured human brain cells found that phenserine reduces Abeta levels by regulating beta-APP translation. Phenserine is a highly selective, reversible acetylcholinesterase inhibitor, a mechanism of action known to improve memory and cognition in Alzheimer’s subjects. Phenserine may prove to concentrate in the brain rapidly which would reduce the incidence of drug toxicity and side effects.",,,,Phenserine is investigational.,Phenserine is a solid.,True
17197,"Itopride is a dopamine D2 antagonist with acetylcholinesterase inhibitory actions. Investigated for use/treatment in gastrointestinal diseases and disorders (miscellaneous). Itopride has anticholinesterase (AchE) activity as well as dopamine D2 receptor antagonistic activity. It is well established that M3 receptors exist on the smooth muscle layer throughout the gut and acetylcholine (ACh) released from enteric nerve endings stimulates the contraction of smooth muscle through M3 receptors. The enzyme AChE hydrolyses the released ACh, inactivates it and thus inhibits the gastric motility leading to various digestive disorders. Besides ACh, dopamine is present in significant amounts in the gastrointestinal tract and has several inhibitory effects on gastrointestinal motility, including reduction of lower esophageal sphincter and intragastric pressure. These effects appear to result from suppression of ACh release from the myenteric motor neurons and are mediated by the D2 subtype of dopamine receptors. Itopride, by virtue of its dopamine D2 receptor antagonism, removes the inhibitory effects on Ach release. It also inhibits the enzyme AchE which prevents the degradation of ACh. The net effect is an increase in ACh concentration, which in turn, promotes gastric motility, increases the lower esophageal sphincter pressure, accelerates gastric emptying and improves gastro-duodenal coordination. This dual mode of action of Itopride is unique and different from the actions of other prokinetic agents available in the market.",The molecular weight is 358.44.,Itopride has a topological polar surface area of 60.03.,The log p value of  is 2.73.,Itopride is investigational.,Itopride is a solid.,True
17198,"Ganstigmine is an orally active, geneserine derived, carbamate-based acetylcholinesterase inhibitor developed for the treatment of Alzheimer's disease. Investigated for use/treatment in alzheimer's disease.",,,,Ganstigmine is investigational.,Ganstigmine is a solid.,True
17199,,,,,"Hydroxy(oxo)(2-{(1S)-2,2,2-trifluoro-1-ethyl}phenyl)ammonium is experimental.","Hydroxy(oxo)(2-{(1S)-2,2,2-trifluoro-1-ethyl}phenyl)ammonium is a solid.",False
17200,,,,,1-BENZYL-4-PIPERIDINE is experimental.,1-BENZYL-4-PIPERIDINE is a solid.,False
17201,,,,,"1-THIO}METHYL)PHENYL]-2,2,2-TRIFLUOROETHANE-1,1-DIOL is experimental.","1-THIO}METHYL)PHENYL]-2,2,2-TRIFLUOROETHANE-1,1-DIOL is a solid.",False
17202,,,,,"(3,4,8b-Trimethyl-3-oxido-2,3a-dihydro-1H-pyrroloindol-3-ium-7-yl) N-(2-ethylphenyl)carbamate is experimental.","(3,4,8b-Trimethyl-3-oxido-2,3a-dihydro-1H-pyrroloindol-3-ium-7-yl) N-(2-ethylphenyl)carbamate is a solid.",False
17203,,,,,Methylthioninium is experimental and investigational.,Methylthioninium is a solid.,False
17204,,,,,Diethylene glycol diethyl ether is experimental.,Diethylene glycol diethyl ether is a solid.,False
17205,,,,,"2--6-HYDROXY-3-METHYL-1,3-BENZOTHIAZOL-3-IUM is experimental.","2--6-HYDROXY-3-METHYL-1,3-BENZOTHIAZOL-3-IUM is a solid.",False
17206,"Dimetacrine is also known as dimethacrine or acripamine. It is marketed under the names Istonil, Istonyl, Linostil, and Miroistonil. Dimetacrine is a tricyclic antidepressant (TCA) with imipramine-like effects used in Europe for the treatment of depression. Dimetacrine is no longer used in Japan. Little is known about the pharmacology of dimetacrine. ",The molecular weight is 294.44.,Dimetacrine has a topological polar surface area of 6.48.,The log p value of  is 5.67.,Dimetacrine is experimental and withdrawn.,Dimetacrine is a solid.,True
17207,"Tyrothricin is an antibiotic peptide complex produced and extracted from the aerobic Gram-positive bacillus Brevibacillus parabrevis which was previously categorized as Bacillus brevis and Bacillus aneurinolyticus. This complex is a mixture comprised of 60% tyrocidine cationic cyclic decapeptides (consisting largely of the six predominant tyrocidines, TrcA/A1, TrcB/B1, TrcC/C1, and other more minor contributors) and 40% neutral linear gramicidins (where valine-gramicidin A is often the major gramicidin present, although the mixture composition can vary). Moreover, tyrothricin possesses broad spectrum Gram-positive antibacterial and antifungal activity that has not seen many - if any - significant reportings of microbial resistance during the over 60 years of therapeutic use the complex has provided. Nevertheless, as tyrothricin is both cytolytic and hemolytic, it does demonstrate systemic toxicity , although certain formulations that are safe for human use like throat lozenges do exist. Tyrothricin is used as an over the counter topical antibiotic. Tyrothricin consists of a mix of tyrocidines and gramcidins which exert a bacteriocidal effect. This clears the area of pathogenic bacteria to allow the body to heal wounds or other damage to the skin. Tyrocidines have a β-sheet structure containing both L and D amino acids. These structural features contribute to the formation of a curved dimer in which most amino acid side chains are located on the convex surface. The dimer orients itself at the membrane-water interface on bacterial cells with the relatively hydrophilic back-bone on the concave side facing the external environment and the many hydrophobic side chains on the convex side facing into the cell's lipid bilayer. The tyrocidine dimer is able to disrupt the cell membrane producing leakage of cell contents but the exact mechanism of this permeabilization is unclear.",,,,Tyrothricin is approved.,Tyrothricin is a solid.,True
17208,,,,,"Inositol 1,3,4,5-Tetrakisphosphate is experimental.","Inositol 1,3,4,5-Tetrakisphosphate is a solid.",False
17209,"Investigated for use/treatment in solid tumors. RX-0201 is a first-in-class signal inhibitor that directly represses the production of Akt, a protein kinase that plays a key role in cancer progression. A less toxic therapeutic approach to cancer treatment, RX-0201 blocks the growth of tumor cells and promotes cell death (apoptosis).",,,,Archexin is investigational.,Archexin is a solid.,True
17210,"Enzastaurin, an investigational, targeted, oral agent, will be evaluated at more than 100 sites worldwide for the treatment of relapsed glioblastoma multiforme (GBM), an aggressive and malignant form of brain cancer. Investigated for use/treatment in brain cancer, lymphoma (non-hodgkin's), and lung cancer. Enzastaurin is an oral serine-threonine kinase inhibitor that is designed to suppress tumor growth through multiple mechanisms. Preclinical data indicate it may reduce the cell's ability to reproduce (cell proliferation), increase the natural death of the tumor cells (apoptosis), and inhibit tumor- induced blood supply (angiogenesis). Enzastaurin has been shown to inhibit signaling through the PKC-B and PI3K/AKT pathways. These pathways have been shown to be activated in a wide variety of cancers. In addition to glioblastoma, enzastaurin is also being studied in multiple other tumor types, including non-Hodgkin's lymphoma, colorectal cancer, non-small cell lung cancer, pancreatic cancer, and mantle cell lymphoma.",,,,Enzastaurin is investigational.,Enzastaurin is a solid.,True
17211,"Perifosine is a novel alkylphospholipid with antiproliferative properties attributed to protein kinase B inhibition. Investigated for use/treatment in solid tumors, multiple myeloma, leukemia (unspecified), lung cancer, and brain cancer. Targeting cellular membranes, perifosine modulates membrane permeability, membrane lipid composition, phospholipid metabolism, and mitogenic signal transduction, resulting in cell differentiation and inhibition of cell growth. This agent also inhibits the anti-apoptotic mitogen-activated protein kinase (MAPK) pathway and modulates the balance between the MAPK and pro-apoptotic stress-activated protein kinase (SAPK/JNK) pathways, thereby inducing apoptosis.",,,,Perifosine is investigational.,Perifosine is a solid.,True
17212,,,,,N--7H-pyrrolopyrimidin-4-amine is experimental.,N--7H-pyrrolopyrimidin-4-amine is a solid.,False
17213,,,,,"5-(5-chloro-7H-pyrrolopyrimidin-4-yl)-4,5,6,7-tetrahydro-1H-imidazopyridine is experimental.","5-(5-chloro-7H-pyrrolopyrimidin-4-yl)-4,5,6,7-tetrahydro-1H-imidazopyridine is a solid.",False
17214,"Drotaverine (INN, also known as drotaverin) is an antispasmodic drug, structurally related to papaverine. Drotaverine is a selective inhibitor of phosphodiesterase 4, and has no anticholinergic effects. Drotaverine has been shown to possess dose-dependant analgesic effects in animal models. One small study has shown drotaverine to be eliminated mainly non-renally. Used in the treatment of functional bowel disorders and alleviating pain in renal colic. Drotaverine is a spasmolytic agent by inhibiting PDE4 in smooth muscle cells.  Drotaverine inhibits phosphodiesterases hydrolysing cAMP, thereby increasing cAMP concentration, decreasing Ca uptake of the cells and changing the distribution of calcium among the cells. It may also have minor allosteric calcium channel blocking properties.",The molecular weight is 397.52.,Drotaverine has a topological polar surface area of 48.95.,The log p value of  is 5.23.,Drotaverine is approved and investigational.,Drotaverine is a solid.,True
17215,"Synthetic peptide, 32 residues long formulated as a nasal spray. Used in the treatment of symptomatic Paget's disease for patients unresponsive to alternate treatments or intolerant to such treatments. In addition, it is used in emergency situations when serum calcium levels must be decreased quickly until the underlying condition is identified. It can also be added to existing therapeutic regimens for hypercalcemia such as intravenous fluids and furosemide, oral phosphate or corticosteroids, or other agents. Calcitonin can be used in patients with azotemia and cases where intravenous fluids would be contraindicated due to limited cardiac reserves. Also for the treatment of post-menopausal osteoporosis in women more than 5 years post-menopause.  Calcitonin inhibits bone resorption by osteoclasts (bone remodeling cells) and promotes bone formation by osteoblasts. This leads to a net increase in bone mass and a reduction in plasma calcium levels. It also promotes the renal excretion of ions such as calcium, phosphate, sodium, magnesium, and potassium by decreasing tubular reabsorption. In consequence, there is an increase in the jejunal secretion of water, sodium, potassium, and chloride. Calcitonin binds to the calcitonin receptor (found primarily in osteoclasts) which then enhances the production of vitamin D producing enzymes (25-hydroxyvitamine D-24-hydroxylase), leading to greater calcium retention and enhanced bone density. Binding of calcitonin to its receptor also activates adenylyl cyclase and the phosphatidyl-inositol-calcium pathway.",The molecular weight is 3431.9.,Salmon calcitonin has a topological polar surface area of 1508.21.,The log p value of  is 0.0.,Salmon calcitonin is approved and investigational.,Salmon calcitonin is a liquid.,True
17216,"Pramlintide is a relatively new adjunct treatment for diabetes (both type 1 and 2), developed by Amylin Pharmaceuticals. It is derived from amylin, a hormone that is released into the bloodstream, in a similar pattern as insulin, after a meal. Like insulin, amylin is deficient in individuals with diabetes. For the treatment of type 1 and type 2 diabetes mellitus as an adjunct to preprandial insulin therapy in patients without adequate glycemic control of insulin therapy. Pramlintide is a synthetic analog of amylin, a glucoregulatory hormone that is synthesized by pancreatic β-cells and released into the bloodstream, in a similar pattern as insulin, after a meal. Like insulin, amylin is deficient in individuals with diabetes. It is provided as an acetate salt. Pramlintide is a 37-amino acid polypeptide that differs structurally from human amylin by the replacement of alanine, serine, and serine at positions 25, 28, and 29 respectively with proline. Pramlintide is an amlyinomimetic, a functional analog of the naturally occurring pancreatic hormone amylin. Amylin has activity in a number of gastrointestinal and glucodynamic systems, and by mimicking its activity, pramlintide acts to improve glycemic control through modulation of the rate of gastric emptying, prevention of post-prandial rise in glucagon levels, and by increasing sensations of satiety, thereby reducing caloric intake and potentiating weight loss. There appears to be at least three distinct receptor complexes that bind with high affinity to amylin. All three complexes contain the calcitonin receptor at the core, plus one of three Receptor activity-modifying proteins, RAMP1, RAMP2, or RAMP3.",The molecular weight is 3949.44.,Pramlintide has a topological polar surface area of 1690.64.,,Pramlintide is approved and investigational.,Pramlintide is a liquid.,True
17217,"GW 468816 is glycine receptor antagonist. It is designed to aid abstinence in people who have just quit smoking, delaying the time to relapse. It was undergoing phase II trials since December 2003. Investigated for use/treatment in tobacco dependence.",,,,GW 468816 is investigational.,GW 468816 is a solid.,True
17218,"Thiocolchicoside is a semi-synthetic derivative of the colchicine, a natural anti-inflammatory glycoside which originates from the flower seeds of _superba gloriosa_. It is a muscle relaxant with anti-inflammatory and analgesic effects. It has potent convulsant activity and should not be administered to individuals prone to seizures. Thiocholchicoside is a muscle relaxing agent that works through selective binding to the GABA-A receptor. It prevents muscle contractions by activating the GABA inhibitory motor pathway. Thiocolchicoside, is a synthetic sulfur derivative of colchicoside, a naturally occurring glucoside contained in the Colchicum autumnale plant. Thiocolchicoside has a selective and potent affinity for g-aminobutyric acid A (GABA-A) receptors and acts on muscular contractures by activating the GABA inhibitory pathways thereby behaving as a potent muscle relaxant. Gamma-aminobutyric acid (GABA) is the main inhibitory neurotransmitter in the human cortex. GABAergic neurons are involved in myorelaxation, anxiolytic treatment, sedation, and anesthetics. GABA can also modulate heart rate and blood pressure.",The molecular weight is 563.62.,Thiocolchicoside has a topological polar surface area of 164.01.,The log p value of  is -0.4.,Thiocolchicoside is experimental.,Thiocolchicoside is a solid.,True
17219,,,,,K-00546 is experimental.,K-00546 is a solid.,False
17220,"A positive inotropic cardiotonic agent with vasodilator properties. It inhibits cAMP phosphodiesterase activity in myocardium and vascular smooth muscle. Milrinone is a derivative of amrinone and has 20-30 times the ionotropic potency of amrinone. Indicated for the treatment of congestive heart failure. Milrinone, a synthetic dimethylxanthine derivative structurally related to theophylline and caffeine, is used in the treatment of peripheral vascular diseases and in the management of cerebrovascular insufficiency, sickle cell disease, and diabetic neuropathy. Milrinone inhibits erythrocyte phosphodiesterase, resulting in an increase in erythrocyte cAMP activity. Subsequently, the erythrocyte membrane becomes more resistant to deformity. Along with erythrocyte activity, Milrinone also decreases blood viscosity by reducing plasma fibrinogen concentrations and increasing fibrinolytic activity.",The molecular weight is 211.22.,Milrinone has a topological polar surface area of 65.78.,The log p value of  is -0.03.,Milrinone is approved.,Milrinone is a solid.,True
17221,"Levosimendan increases calcium sensitivity to myocytes by binding to troponin C in a calcium dependent manner. This increases contractility without raising calcium levels. It also relaxes vascular smooth muscle by opening adenosine triphosphate sensitive potassium channels. Levosimendan is used to manage acutely decompensated congestive heart failure. For short term treatment of acutely decompensated severe chronic heart failure (CHF). Also being investigated for use/treatment in heart disease. Levosimendan is a new Ca<sup>2+</sup>-sensitizing inotropic agent. Ca<sup>2+</sup> sensitizers represent a new class of inotropic agents, which overcome the disadvantages associated with currently available inotropic agents in as they are not associated with an increased risk of arrhythmias, cell injury and death due to Ca<sup>2+</sup> overload in myocardial cells; they do not increase the activation energy; and they have the potential to reverse contractile dysfunction under pathophysiologic conditions, such as acidosis or myocardial stunning. Levosimendan has not been approved for use in the U.S. or Canada. Levosimendan appears to increase myofilament calcium sensitivity by binding to cardiac troponin C in a calcium-dependent manner. This stabilizes the calcium-induced conformational change of troponin C, thereby (1) changing actin-myosin cross-bridge kinetics apparently without increasing the cycling rate of the cross-bridges or myocardial ATP consumption, (2) increasing the effects of calcium on cardiac myofilaments during systole and (3) improving contraction at low energy cost (inotropic effect). Calcium concentration and, therefore, sensitization decline during diastole, allowing normal or improved diastolic relaxation. Levosimendan also leads to vasodilation through the opening of ATP-sensitive potassium channels. By these inotropic and vasodilatory actions, levosimendan increases cardiac output without increasing myocardial oxygen demand. Levosimendan also has a selective phosphodiesterase (PDE)-III inhibitory action that may contribute to the inotropic effect of this compound under certain experimental conditions. It has been reported that levosimendan may act preferentially as a Ca<sup>2+</sup> sensitizer at lower concentrations, whereas at higher concentrations its action as a PDE-III inhibitor becomes more prominent in experimental animals and humans.",The molecular weight is 280.29.,Levosimendan has a topological polar surface area of 113.43.,The log p value of  is 1.9.,Levosimendan is approved and investigational.,Levosimendan is a solid.,True
17222,"Amrinone (or inamrinone) is a type 3 pyridine phosphodiesterase inhibitor. It is used in the treatment of congestive heart failure. Used in the treatment of congestive heart failure. Amrinone is a positive inotropic cardiotonic with vasodilator properties, phosphodiesterase inhibitory activity, and the ability to stimulate calcium ion influx into the cardiac cell. Amrinone is a phosphodiesterase inhibitor (PDE3), resulting in increased cAMP and cGMP which leads to an increase in the calcium influx like that caused by beta-agonists resulting in increased inotropic effect.",The molecular weight is 187.2.,Amrinone has a topological polar surface area of 68.01.,The log p value of  is -0.69.,Amrinone is approved.,Amrinone is a solid.,True
17223,"Enoximone is a selective phosphodiesterase inhibitor with vasodilating and positive inotropic activity that does not cause changes in myocardial oxygen consumption. It is used in patients with congestive heart failure. Trials were halted in the U.S., but the drug is used in various countries. For the treatment of congestive heart failure. Enoximone is a phosphodiesterase inhibitor (type III) that increases the force of contraction of the heart and dilates blood vessels. In June 2005, Myogen announced that they were discontinuing development of enoximone due to negative results. The drug is approved for use in the UK. Further research is required to determine accurately the mechanism of action of drugs with phosphodiesterase inhibitory activity, however, inhibition of PDE3 inhibits degredation of cGMP. This allows for increased NO release and vascular relaxation.",The molecular weight is 248.3.,Enoximone has a topological polar surface area of 58.2.,The log p value of  is 2.25.,Enoximone is approved and investigational.,Enoximone is a solid.,True
17224,"Ibudilast is an anti-inflammatory and neuroprotective oral agent which shows an excellent safety profile at 60 mg/day and provides significantly prolonged time-to-first relapse and attenuated brain volume shrinkage in patients with relapsing-remitting (RR) and/or secondary progressive (SP) multiple sclerosis (MS). Ibudilast is currently in development in the U.S. (codes: AV-411 or MN-166), but is approved for use as an antiinflammatory in Japan. For the treatment of multiple sclerosis, asthma, and cerebrovascular disease. Ibudilast has mechanisms that include anti-inflammatory effects, such as phosphodiesterase inhibition, and neuroprotective effects, such as inhibition of synthesis and reduction in reactive oxygen species.",The molecular weight is 230.31.,Ibudilast has a topological polar surface area of 34.37.,The log p value of  is 3.25.,Ibudilast is investigational.,Ibudilast is a solid.,True
17225,"Abciximab is a Fab fragment of the chimeric human-murine monoclonal antibody 7E3. Abciximab binds to the glycoprotein (GP) IIb/IIIa receptor of human platelets and inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules. It also binds to vitronectin (αvβ3) receptor found on platelets and vessel wall endothelial and smooth muscle cells. Abciximab is indicated as an adjunct to percutaneous coronary intervention for the prevention of cardiac ischemic complications in patients undergoing percutaneous coronary intervention and in patients with unstable angina not responding to conventional medical therapy when percutaneous coronary intervention is planned within 24 hours. Abciximab is intended for use with aspirin and heparin and has been studied only in that setting. Abciximab inhibits platelet aggregation by preventing the binding of fibrinogen, von Willebrand factor, and other adhesive molecules to GPIIb/IIIa receptor sites on activated platelets. A single intravenous bolus dose from 0.15 mg/kg to 0.30 mg/kg produced rapid dose-dependent inhibition of platelet function. After two hours post-injection with a dose of 0.25 - 0.30 mg/kg, 80% of the GPIIb/IIIa receptors were blocked and platelet aggregation was prevented. GPIIb/IIIa is the major surface receptor involved in the final pathway of platelet aggregation. Bleeding time increases to over 30 minutes at the aforementioned doses. To compare, baseline values were five minutes.  Abciximab binds to the intact platelet GPIIb/IIIa receptor, which is a member of the integrin family of adhesion receptors and the major platelet surface receptor involved in platelet aggregation. This binding is thought to involve steric hindrance and/or conformational alterations which block access of large molecules to the receptor rather than direct interaction with the RGD (arginine-glycine-aspartic acid) binding site of GPIIb/IIIa. By binding to the vitronectin receptor (also known as the αvβ3 integrin), abciximab blocks effects mediated by this integrin which include cell adhesion. Furthermore, abciximab blocks Mac-1 receptor on monocytes and neutrophils thus inhibiting monocyte adhesion.",,,,Abciximab is approved.,Abciximab is a liquid.,True
17226,"Tirofiban prevents the blood from clotting during episodes of chest pain or a heart attack, or while the patient is undergoing a procedure to treat a blocked coronary artery. It is a non-peptide reversible antagonist of the platelet glycoprotein (GP) IIb/IIIa receptor, and inhibits platelet aggregation. For treatment, in combination with heparin, of acute coronary syndrome, including patients who are to be managed medically and those undergoing PTCA or atherectomy. Tirofiban prevents the blood from clotting during episodes of chest pain or a heart attack, or while the patient is undergoing a procedure to treat a blocked coronary artery. It is a non-peptide antagonist of the platelet glycoprotein (GP) IIb/IIIa receptor, and inhibits platelet aggregation. When administered intravenously, tirofiban inhibits ex vivo platelet aggregation in a dose- and concentration-dependent manner. When given according to the recommended regimen, >90% inhibition is attained by the end of the 30-minute infusion. Tirofiban has been recently shown in patients with unstable angina to reduce ischemic events at 48 hours following infusion when compared to standard heparin therapy. Tirofiban is a reversible antagonist of fibrinogen binding to the GP IIb/IIIa receptor, the major platelet surface receptor involved in platelet aggregation. Platelet aggregation inhibition is reversible following cessation of the infusion of tirofiban.",The molecular weight is 440.6.,Tirofiban has a topological polar surface area of 104.73.,The log p value of  is 2.0.,Tirofiban is approved.,Tirofiban is a solid.,True
17227,"Lefradafiban is an oral platelet glycoprotein IIb/IIIa receptor antagonist being investigated in the treatment of angina. For the treatment of unstable angina. Lefradafiban, an orally active prodrug of fradafiban, is a novel glycoprotein (IIb/IIIa) inhibitor for the treatment of unstable angina. Development was discontinued in 2000 due to lack of efficacy. GPIIb/IIIa inhibitors, such as lefradafiban, block the final common pathway of platelet aggregation.",,,,Lefradafiban is investigational.,Lefradafiban is a solid.,True
17228,"Investigated for use/treatment in angina. Fradafiban is a glycoprotein IIb/IIIa receptor antagonist. Activation of the platelet glycoprotein (GP IIb/IIIa) receptor on the platelet surface is the final pathway of platelet aggregation that may lead to embolism, which is one on the cause of angina.",,,,Fradafiban is investigational.,Fradafiban is a solid.,True
17229,"Cetirizine, also commonly known as _Zyrtec_, is an orally active second-generation histamine H1 antagonist proven effective in the treatment of various allergic symptoms, such as sneezing, coughing, nasal congestion, hives, and other symptoms ,.  **Seasonal Allergic Rhinitis**: Indicated for the relief of symptoms associated with seasonal allergic rhinitis caused by allergens such as ragweed, grass and tree pollens in adults and children 2 years of age and above. Symptoms treated effectively include sneezing, rhinorrhea, nasal pruritus, ocular pruritus, tearing, and redness of the eyes.  **General effects and respiratory effects** Cetirizine, a metabolite of _hydroxyzine_, is an antihistamine drug. Its main effects are achieved through selective inhibition of peripheral H1 receptors. The antihistamine activity of cetirizine has been shown in a variety of animal and human models. _In vivo_ and _ex vivo_ animal models have shown insignificant anticholinergic and antiserotonergic effects. In clinical studies, however, dry mouth was found to be more frequent with cetirizine than with a placebo. In vitro receptor binding studies have demonstrated no detectable affinity of cetirizine for histamine receptors other than the H1 receptors. Studies with radiolabeled cetirizine administration in the rat have demonstrated insignificant penetration into the brain. _Ex vivo_ studies in the mouse have shown that systemically administered cetirizine does not occupy cerebral H1 receptors significantly.",The molecular weight is 388.89.,Cetirizine has a topological polar surface area of 53.01.,The log p value of  is 2.08.,Cetirizine is approved.,Cetirizine is a solid.,True
17230,"Histamine H1 antagonist with pronounced sedative properties. It is used in allergies and as an antitussive, antiemetic, and hypnotic. Doxylamine has also been administered in veterinary applications and was formerly used in parkinsonism. Used alone as a short-term sleep aid, in combination with other drugs as a night-time cold and allergy relief drug. Also used in combination with Vitamin B6 (pyridoxine) to prevent morning sickness in pregnant women. Doxylamine is an antihistamine commonly used as a sleep aid. This drug is also used to relieve symptoms of hay fever (allergic rhinitis), hives (rash or itching), and other allergic reactions. Doxylamine is a member of the ethanolamine class of antihistamines and has anti-allergy power far superior to virtually every other antihistamine on the market, with the exception of diphenhydramine (Benadryl). It is also the most powerful over-the-counter sedative available in the United States, and more sedating than many prescription hypnotics. In a study, it was found to be superior to even the barbiturate, phenobarbital for use as a sedative. Doxylamine is also a potent anticholinergic. Like other antihistamines, doxylamine acts by competitively inhibiting histamine at H1&nbsp;receptors. It also has substantial sedative and anticholinergic effects.",The molecular weight is 270.38.,Doxylamine has a topological polar surface area of 25.36.,The log p value of  is 2.35.,Doxylamine is approved and vet_approved.,Doxylamine is a liquid.,True
17231,"Dexbrompheniramine maleate is an antihistamine agent that is used for the treatment of allergic conditions, such as hay fever or urticaria. For treatment and relief of symptoms of allergies, hay fever, and colds In allergic reactions an allergen interacts with and cross-links surface IgE antibodies on mast cells and basophils. Once the mast cell-antibody-antigen complex is formed, a complex series of events occurs that eventually leads to cell-degranulation and the release of histamine (and other chemical mediators) from the mast cell or basophil. Once released, histamine can react with local or widespread tissues through histamine receptors. Histamine, acting on H<sub>1</sub>-receptors, produces pruritis, vasodilatation, hypotension, flushing, headache, tachycardia, and bronchoconstriction. Histamine also increases vascular permeability and potentiates pain. Dexbrompheniramine is a histamine H1 antagonist (or more correctly, an inverse histamine agonist) of the alkylamine class. It provides effective, temporary relief of sneezing, watery and itchy eyes, and runny nose due to hay fever and other upper respiratory allergies. Dexbrompheniramine competitively binds to the histamine H<sub>1</sub>-receptor. It competes with histamine for the normal H<sub>1</sub>-receptor sites on effector cells of the gastrointestinal tract, blood vessels and respiratory tract. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine.",The molecular weight is 319.25.,Dexbrompheniramine has a topological polar surface area of 16.13.,The log p value of  is 3.3.,Dexbrompheniramine is approved.,Dexbrompheniramine is a solid.,True
17232,"First generation histamine H1 antagonist used in allergic rhinitis; asthma; and urticaria. It is a component of cough and cold medicines. It may cause drowsiness. For the symptomatic relief of seasonal or perennial allergic rhinitis or nonallergic rhinitis; allergic conjunctivitis; and mild, uncomplicated allergic skin manifestations of urticaria and angioedema. Also used in combination with other agents for the symptomatic relief of symptoms associated with the common cold. In allergic reactions an allergen interacts with and cross-links surface IgE antibodies on mast cells and basophils. Once the mast cell-antibody-antigen complex is formed, a complex series of events occurs that eventually leads to cell-degranulation and the release of histamine (and other chemical mediators) from the mast cell or basophil. Once released, histamine can react with local or widespread tissues through histamine receptors. Histamine, acting on H1-receptors, produces pruritis, vasodilatation, hypotension, flushing, headache, tachycardia, and bronchoconstriction. Histamine also increases vascular permeability and potentiates pain. Triprolidine, is a histamine H1 antagonist that competes with histamine for the normal H1-receptor sites on effector cells of the gastrointestinal tract, blood vessels and respiratory tract. It provides effective, temporary relief of sneezing, watery and itchy eyes, and runny nose due to hay fever and other upper respiratory allergies. Triprolidine has anticholinergic and sedative effects. Triprolidine binds to the histamine H1 receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine.",The molecular weight is 278.4.,Triprolidine has a topological polar surface area of 16.13.,The log p value of  is 3.63.,Triprolidine is approved.,Triprolidine is a solid.,True
17233,"Carbinoxamine is a first generation antihistamine that competes with free histamine for binding at HA-receptor sites. This antagonizes the effects of histamine on HA-receptors, leading to a reduction of the negative symptoms brought on by histamine HA-receptor binding. The product label for carbinoxamine as an over the counter cough and cold medicine is being modified to state \do not use\"" in children under 4 years of age in order to prevent and reduce misuse, as many unapproved carbinoxamine-containing preparations contained inappropriate labeling, which promoted unapproved uses (including management of congestion, cough, the common cold, and the use in children under 2 years of age), which can potentially cause serious health risks."" For symptomatic relief of seasonal and perennial allergic rhinitis and vasomotor rhinitis, as well as allergic conjunctivitis caused by foods and inhaled allergens. Also for the relief of allergic reactions to blood or plasma, and the symptomatic management of mild, uncomplicated allergic skin manifestations of urticaria and angioedema. Carbinoxamine is a first generation antihistamine of the ethanolamine class. Ethanolamine antihistamines have significant antimuscarinic activity and produce marked sedation in most patients. In addition to the usual allergic symptoms, the drug also treats irritant cough and nausea, vomiting, and vertigo associated with motion sickness. It also is used commonly to treat drug-induced extrapyramidal symptoms as well as to treat mild cases of Parkinson's disease. Rather than preventing the release of histamine, as do cromolyn and nedocromil, carbinoxamine competes with free histamine for binding at HA-receptor sites. Carbinoxamine competitively antagonizes the effects of histamine on HA-receptors in the GI tract, uterus, large blood vessels, and bronchial muscle. Ethanolamine derivatives have greater anticholinergic activity than do other antihistamines, which probably accounts for the antidyskinetic action of carbinoxamine. Carbinoxamine competes with free histamine for binding at HA-receptor sites. This antagonizes the effects of histamine on HA-receptors, leading to a reduction of the negative symptoms brought on by histamine HA-receptor binding. Carbinoxamine's anticholinergic action appears to be due to a central antimuscarinic effect, which also may be responsible for its antiemetic effects, although the exact mechanism is unknown.",The molecular weight is 290.79.,Carbinoxamine has a topological polar surface area of 25.36.,The log p value of  is 2.67.,Carbinoxamine is approved.,Carbinoxamine is a liquid.,True
17234,"Propiomazine, an atypical antipsychotic agent, is used to treat both negative and positive symptoms of schizophrenia, acute mania with bipolar disorder, agitation, and psychotic symptoms in dementia. Future uses may include the treatment of obsessive-compulsive disorder and severe behavioral disorders in autism. Structurally and pharmacologically similar to clozapine, propiomazine binds to alpha(1), dopamine, histamine H1, muscarinic, and serotonin type 2 (5-HT2) receptors. Propiomazine is largely used for its antihistamininc sleep inducing effects in treating insomnia. Although propiomazine is a phenothiazine, it is not used as an antipsychotic. It posesses antihistamine effects and is mostly used as a sedative in treating insomnia. Propiomazine acts as an antagonist of dopamine 1, 2, and 4 receptors, serotonin (5-HT) receptor types 2A and 2C, muscarinic receptors 1 through 5, alpha(1)-receptors, and histamine H1-receptors. Its main use as a sedative is due to its antihistamine effect.",The molecular weight is 340.49.,Propiomazine has a topological polar surface area of 23.55.,The log p value of  is 4.91.,Propiomazine is approved.,Propiomazine is a solid.,True
17235,"Methdilazine is a phenothiazine compound with antihistaminic activity. It is used in the treatment of various dermatoses to relieve pruritus. Used for the symptomatic relief of hypersensitivity reactions and particularly for the control of pruritic skin disorders In allergic reactions an allergen interacts with and cross-links surface IgE antibodies on mast cells and basophils. Once the mast cell-antibody-antigen complex is formed, a complex series of events occurs that eventually leads to cell-degranulation and the release of histamine (and other chemical mediators) from the mast cell or basophil. Once released, histamine can react with local or widespread tissues through histamine receptors. Histamine, acting on H<sub>1</sub>-receptors, produces pruritis, vasodilatation, hypotension, flushing, headache, tachycardia, and bronchoconstriction. Histamine also increases vascular permeability and potentiates pain. Methdilazine is a histamine H<sub>1</sub> antagonist. It competes with histamine for the normal H<sub>1</sub>-receptor sites on effector cells of the gastrointestinal tract, blood vessels and respiratory tract. It provides effective, temporary relief of sneezing, watery and itchy eyes, and runny nose due to hay fever and other upper respiratory allergies. Methdilazine binds to the histamine H<sub>1</sub> receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine.",The molecular weight is 296.43.,Methdilazine has a topological polar surface area of 6.48.,The log p value of  is 4.71.,Methdilazine is approved.,Methdilazine is a solid.,True
17236,"A cycloheptathiophene blocker of histamine H1 receptors and release of inflammatory mediators. It has been proposed for the treatment of asthma, rhinitis, skin allergies, and anaphylaxis. Indicated as an add-on or prophylactic oral medication in the chronic treatment of mild atopic asthmatic children. Also used as self-medication for the temporary relief of itching of the eye due to allergic conjunctivitis (ophthalmic). Ketotifen is a fast acting non-competitive histamine antagonist. It inhibits the release of mediators from mast cells. It is a non-bronchodilator antiasthmatic drug (when taken orally). Ketotifen is a relatively selective, non-competitive histamine antagonist (H1-receptor) and mast cell stabilizer. Ketotifen inhibits the release of mediators from mast cells involved in hypersensitivity reactions. Decreased chemotaxis and activation of eosinophils have also been demonstrated. Ketotifen also inhibits cAMP phosphodiesterase. Properties of ketotifen which may contribute to its antiallergic activity and its ability to affect the underlying pathology of asthma include inhibition of the development of airway hyper-reactivity associated with activation of platelets by PAF (Platelet Activating Factor), inhibition of PAF-induced accumulation of eosinophils and platelets in the airways, suppression of the priming of eosinophils by human recombinant cytokines and antagonism of bronchoconstriction due to leukotrienes. Ketotifen inhibits of the release of allergic mediators such as histamine, leukotrienes C4 and D4(SRS-A) and PAF.",The molecular weight is 309.43.,Ketotifen has a topological polar surface area of 20.31.,The log p value of  is 3.59.,Ketotifen is approved.,Ketotifen is a solid.,True
17237,"Desloratadine is a second generation, tricyclic antihistamine that which has a selective and peripheral H1-antagonist action. It is the active descarboethoxy metabolite of loratidine (a second generation histamine). Desloratidine has a long-lasting effect and does not cause drowsiness because it does not readily enter the central nervous system. For the relief of symptoms of seasonal allergic rhinitis, perennial (non-seasonal) allergic rhinitis. Desloratidine is also used for the sympomatic treatment of pruritus and urticaria (hives) associated with chronic idiopathic urticaria. Desloratadine is a long-acting second-generation H<sub>1</sub>-receptor antagonist which has a selective and peripheral H1-antagonist action. Histamine is a chemical that causes many of the signs that are part of allergic reactions, such as the swelling of tissues. Histamine is released from histamine-storing cells (mast cells) and attaches to other cells that have receptors for histamine. The attachment of the histamine to the receptors causes the cell to be \activated,\"" releasing other chemicals which produce the effects that we associate with allergies. Desloratadine blocks one type of receptor for histamine (the H1 receptor) and thus prevents activation of cells by histamine. Unlike most other antihistamines, Desloratadine does not enter the brain from the blood and, therefore, does not cause drowsiness."" Like other H1-blockers, Desloratadine competes with free histamine for binding at H<sub>1</sub>-receptors in the GI tract, uterus, large blood vessels, and bronchial smooth muscle. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms (eg. nasal congestion, watery eyes) brought on by histamine.",The molecular weight is 310.83.,Desloratadine has a topological polar surface area of 24.92.,The log p value of  is 3.83.,Desloratadine is approved and investigational.,Desloratadine is a solid.,True
17238,"Dimenhydrinate, also known as Dramamine or Gravol, is an over-the-counter drug used to prevent nausea, vomiting, and dizziness caused by motion sickness. Dimenhydrinate is a combination drug composed of and in a salt form, with 53%-55.5% of diphenhydramine, and not less than 44%-47% of 8-chlorotheophylline, calculated on the dried basis.  Dimenhydrinate is indicated for the prevention and treatment of nausea, vomiting, or vertigo of motion sickness. Dimenhydrinate is an antiemetics drug combination that contains diphenhydramine and theophylline. It is not effective in the treatment of nausea associated with cancer chemotherapy. Dimenhydrinate directly inhibits the stimulation of certain nerves in the brain and inner ear to suppress nausea, vomiting, dizziness, and vertigo. Diphenhydramine and dimenhydinate both reduce vestibular neuronal excitation due to angular or linear acceleration motions.  The mechanism by which some antihistamines exert their antiemetic, anti-motion sickness, and anti-vertigo effects is not precisely known but may be related to their central anticholinergic actions. They diminish vestibular stimulation and depress labyrinthine function. An action on the medullary chemoreceptive trigger zone may also be involved in the antiemetic effect. Dimenhydrinate is a competitive antagonist at the histamine H1 receptor, which is widely distributed in the human brain. Dimenhydrinate's anti-emetic effect is probably due to H1 antagonism in the vestibular system in the brain. ",The molecular weight is 469.97.,,,Dimenhydrinate is approved.,Dimenhydrinate is a solid.,True
17239,"Emedastine is an antihistamine used in eye drops to treat allergic conjunctivitis. For the temporary relief of the signs and symptoms of allergic conjunctivitis. Emedastine is a relatively selective H<sub>1</sub>-receptor antagonist. Emedastine is a relatively selective, histamine H<sub>1</sub> antagonist. In vitro examinations of emedastine's affinity for histamine receptors demonstrate relative selectivity for the H<sub>1</sub> histamine receptor. In vivo studies have shown concentration-dependent inhibition of histamine-stimulated vascular permeability in the conjunctiva following topical ocular administration. Emedastine appears exert negligible effects on adrenergic, dopaminergic and serotonin receptors.",The molecular weight is 302.42.,Emedastine has a topological polar surface area of 33.53.,The log p value of  is 2.3.,Emedastine is approved.,Emedastine is a solid.,True
17240,"Levocabastine is a selective second-generation H1-receptor antagonist used for allergic conjunctivitis. Levocabastine was discovered at Janssen Pharmaceutica in 1979. As an ophthalmic for the temporary relief of the signs and symptoms of seasonal allergic conjunctivitis. Also used as a nasal spray for allergic rhinitis. Levocabastine is a selective histamine H1-receptor antagonist exerting inhibitory effects on the release of chemical mediators from mast cells and on the chemotaxis of polymorphonuclear leukocytes and eosinophils. Both histamine and antigens induced conjunctivitis can be inhibited by levocabastine. Levocabastine can also reduce symptoms of allergic rhinitis by preventing an increase in vascular permeability of nasal mucosa. Levocabastine is a potent, selective histamine H1-receptor antagonist. It works by competing with histamine for H1-receptor sites on effector cells. It thereby prevents, but does not reverse, responses mediated by histamine alone. Levocabastine does not block histamine release but, rather, prevents histamine binding and activity. Levocabastine also binds neurotensin 2 receptors and serves as a neurotensin agonist. This can induce some degree of analgesia.",The molecular weight is 420.53.,Levocabastine has a topological polar surface area of 64.33.,The log p value of  is 1.86.,Levocabastine is approved and investigational.,Levocabastine is a solid.,True
17241,"Diphenylpyraline is an antihistamine. Antihistamines used in the treatment of allergy act by competing with histamine for H 1-receptor sites on effector cells. Antihistamines prevent, but do not reverse, responses mediated by histamine alone. Antihistamines antagonize, in varying degrees, most of the pharmacological effects of histamine, including urticaria and pruritus. For use in the treatment of allergic rhinitis, hay fever, and allergic skin disorders. Diphenylpyraline is an antihistamine that prevents, but does not reverse, responses mediated by histamine alone. Diphenylpyraline antagonizes most of the pharmacological effects of histamine, including urticaria and pruritus. Also, diphenylpyraline may exhibit anticholinergic actions (as do most of the antihistamines) and may thus provide a drying effect on the nasal mucosa. Antihistamines such as diphenylpyraline used in the treatment of allergy act by competing with histamine for H1-receptor sites on effector cells. This reduces the effects of histamine, leading to a temporary reduction of allergy symptoms.",The molecular weight is 281.4.,Diphenylpyraline has a topological polar surface area of 12.47.,The log p value of  is 3.21.,Diphenylpyraline is approved and investigational.,Diphenylpyraline is a solid.,True
17242,"Bromodiphenhydramine is an ethanolamine antihistamine with antimicrobial property. Bromodiphenhydramine is used in the control of cutaneous allergies. Ethanolamine antihistamines produce marked sedation in most patients. For management of symptoms related to hay fever and other types of allergy and used to help bring up phlegm, thin secretions, and make a cough productive. Bromodiphenhydramine is an antihistamine of the ethanolamine class. Ethanolamine antihistamines have significant antimuscarinic activity and produce marked sedation in most patients. In addition to the usual allergic symptoms, the drug also treats irritant cough and nausea, vomiting, and vertigo associated with motion sickness. It also is used commonly to treat drug-induced extrapyramidal symptoms as well as to treat mild cases of Parkinson's disease. Rather than preventing the release of histamine, as do cromolyn and nedocromil, Bromodiphenhydramine competes with free histamine for binding at HA-receptor sites. Bromodiphenhydramine competitively antagonizes the effects of histamine on HA-receptors in the GI tract, uterus, large blood vessels, and bronchial muscle. Ethanolamine derivatives have greater anticholinergic activity than do other antihistamines, which probably accounts for the antidyskinetic action of Bromodiphenhydramine. This anticholinergic action appears to be due to a central antimuscarinic effect, which also may be responsible for its antiemetic effects, although the exact mechanism is unknown. Bromodiphenhydramine competes with free histamine for binding at HA-receptor sites. This antagonizes the effects of histamine on HA-receptors, leading to a reduction of the negative symptoms brought on by histamine HA-receptor binding.",The molecular weight is 334.26.,Bromodiphenhydramine has a topological polar surface area of 12.47.,The log p value of  is 4.32.,Bromodiphenhydramine is approved.,Bromodiphenhydramine is a solid.,True
17243,"A phenothiazine derivative that is used as an antipruritic. Used to prevent and relieve allergic conditions which cause pruritus (itching) and urticaria (some allergic skin reactions). Trimeprazine (also known as Alimemazine) is a tricyclic antihistamine, similar in structure to the phenothiazine antipsychotics, but differing in the ring-substitution and chain characteristics. Trimeprazine is in the same class of drugs as chlorpromazine (Thorazine) and trifluoperazine (Stelazine); however, unlike the other drugs in this class, trimeprazine is not used clinically as an anti-psychotic. It acts as an anti-histamine, a sedative, and an anti-emetic (anti-nausea). Trimeprazine is used principally as an anti-emetic, to prevent motion sickness or as an anti-histamine in combination with other medications in cough and cold preparations. Tricyclic antihistamines are also structurally-related to the tricyclic antidepressants, explaining the antihistaminergic adverse effects of these two drug classes and also the poor tolerability profile of tricyclic H<sub>1</sub>-antihistamines. Trimeprazine competes with free histamine for binding at HA-receptor sites. This antagonizes the effects of histamine on HA-receptors, leading to a reduction of the negative symptoms brought on by histamine HA-receptor binding.",The molecular weight is 298.45.,Alimemazine has a topological polar surface area of 6.48.,The log p value of  is 5.0.,Alimemazine is approved and vet_approved.,Alimemazine is a solid.,True
17244,"Aceprometazine is a is a drug with neuroleptic and anti-histamine properties. Although not widely prescribed, it is used in combination with meprobamate for the treatment of sleep disorders in France under the trade name Mepronizine. Aceprometazine is often used in combination with meprobamate for the treatment of sleep disorders. Aceprometazine is a drug with neuroleptic and anti-histamine properties. It is not widely prescribed. Aceprometazine, acting as an H1-receptor antagonist can induce sedation by being able to cross the blood-brain-barrier and binding to H1-receptors in the central nervous system.",The molecular weight is 326.46.,Aceprometazine has a topological polar surface area of 23.55.,The log p value of  is 4.38.,Aceprometazine is experimental.,Aceprometazine is a solid.,True
17245,"Phenindamine is an antihistamine. Phenindamine blocks the effects of the naturally occurring chemical histamine in your body. Antihistamines such as phenindamine appear to compete with histamine for histamine H1- receptor sites on effector cells. The antihistamines antagonize those pharmacological effects of histamine which are mediated through activation of H1- receptor sites and thereby reduce the intensity of allergic reactions and tissue injury response involving histamine release. It is used to treat sneezing, runny nose, itching, watery eyes, hives, rashes, itching, and other symptoms of allergies and the common cold. Used to treat sneezing, runny nose, itching, watery eyes, hives, rashes, itching, and other symptoms of allergies and the common cold. Phenindamine is an antihistamine. Phenindamine blocks the effects of the naturally occurring chemical histamine in your body. Allergies are caused by an excessive type 1 hypersensitivity response of the body to allergens, mediated by inappropriate histamine signalling. By inhibiting the binding of histamine, antihistamines decrease the normal histamine response from cells, consequently decreasing allergic symptoms. Antihistamines such as phenindamine appear to compete with histamine for histamine H1- receptor sites on effector cells. The antihistamines antagonize those pharmacological effects of histamine which are mediated through activation of H1- receptor sites and thereby reduce the intensity of allergic reactions and tissue injury response involving histamine release.",The molecular weight is 261.37.,Phenindamine has a topological polar surface area of 3.24.,The log p value of  is 4.07.,Phenindamine is approved.,Phenindamine is a solid.,True
17246,"Clofedanol is a centrally-acting cough suppressant available in Canada under the trade name Ulone. It is not available in the United States. Used in the treatment of dry cough. Chlophedianol (or Clofedanol) is a centrally-acting cough suppressant. It has local anesthetic and antihistamine properties, and may have anticholinergic effects at high doses. Suppresses the cough reflex by a direct effect on the cough center in the medulla of the brain.",The molecular weight is 289.8.,Clofedanol has a topological polar surface area of 23.47.,The log p value of  is 3.63.,Clofedanol is approved and withdrawn.,Clofedanol is a solid.,True
17247,"Bepotastine is a non-sedating, selective antagonist of the histamine 1 (H1) receptor. Bepotastine was approved in Japan for use in the treatment of allergic rhinitis and uriticaria/puritus in July 2000 and January 2002, respectively, and is marketed by Tanabe Seiyaku Co., Ltd. under the brand name Talion. It is available in oral and opthalmic dosage forms in Japan. The opthalmic solution is FDA approved since Sept 8, 2009 and is under the brand name Bepreve. For the symptomatic treatment of itchy eyes (caused by IgE-induced mast cell degranulation) due to allergic conjunctivitis. Bepotastine is a non-sedating, selective antagonist of the histamine 1 (H1) receptor. It belongs to the second-generation piperidine chemical class. It is a mast cell stabilizer and suppresses the migration of eosinophils into inflamed tissues. Furthermore, bepotastine does not interact with serotonin, muscarinic, benzodiazepine, and beta-adrenergic receptor that would otherwise result in adverse reactions such as dry mouth or sonmolence.  Because of a type 1 hypersensitivity reaction cascade that is triggered by antigen exposure, allergic conjunctivitis occurs. Allergen exposure is followed by conjunctival mast cell degranulation and histamine released as a result of the formation of complementary IgE cross-links on the conjunctiva. Due to the release of histamine, symptoms such as itching can be observed. Bepotastine works to relieve itchy eyes by three primary mechanisms of action. It is a non-sedating, selective antagonist of the histamine 1 (H1) receptor, a mast cell stabilizer, and it suppresses the migration of eosinophils into inflamed tissues to prevent tissue damage and worsening of allergic inflammation of the conjunctiva. ",The molecular weight is 388.89.,Bepotastine has a topological polar surface area of 62.66.,The log p value of  is 0.28.,Bepotastine is approved.,Bepotastine is a liquid.,True
17248,"HY10275 is a novel compound specifically designed to modulate two key neurobiological mechanisms that interfere with the sleeping process. HY10275 is highly selective for histamine H1 and serotonin 5HT2a, two chemical receptors that are known to impact the ability to fall asleep and stay asleep. HY10275 was rationally designed to \let you sleep\"" rather than depress the entire brain to \""make you sleep.\"" This dual-acting receptor activity and the lack of affinity for undesired off- target receptors are thought to account for the compounds excellent efficacy and tolerability profile."" Investigated for use/treatment in insomnia. HY10275 is specifically designed to modulate two key neurobiological mechanisms that interfere with the sleeping process. The drug is highly selective for histamine H1 and serotonin 5HT2a, two chemical receptors that are known to impact the ability to fall asleep and stay asleep. This dual-acting receptor activity and the lack of affinity for undesired off-target receptors are thought to account for the compounds excellent efficacy and tolerability profile.",,,,HY10275 is investigational.,HY10275 is a solid.,True
17249,"OBE101 is a new weight loss drug developed by Obecure Ltd. It is a new formulation that is based on the vertigo medication, Betahistine. Obecure is repurposing betahistine, which is an H1 receptor agonist and partial H3 receptor antagonist for the treatment of obese individuals and for other weight management indications.  Investigated for use/treatment in adverse effects (drug), hyperlipidemia, and obesity. OBE101 is a H1 receptor agonist and partial H3 receptor antagonist. Because inhibition of H1 receptors increases feeding, agonism of H1 receptors by OBE101 should reduce feeding. By also partially antagonizing H3, OBE101 impedes a negative feedback loop that essentially prolongs stimulation of the H1 receptors.",,,,OBE101 is investigational.,OBE101 is a solid.,True
17250,"SO-101(Silenor) is a low-dose oral tablet formulation of doxepin hydrochloride that is patent protected for its use in insomnia. Doxepin has been prescribed for more than 40 years for the treatment of depression and anxiety at dosages typically ranging from 75 mg to 300 mg per day.  Investigated for use/treatment in insomnia. The mechanism of action for the sleep-promoting effects of is not definitively known, it differs from the currently available sleep-promoting agents in that the effects are mediated through the histaminergic system. The active ingredient in SO-101, doxepin HCl, is known to be a highly potent histamine antagonist. Histamine blocking has been demonstrated to reduce wakefulness and is thought to promote the initiation and maintenance of sleep.",,,,SO-101 is investigational.,SO-101 is a solid.,True
17251,"Alcaftadine is a H1 histamine receptor antagonist indicated for the prevention of itching associated with allergic conjunctivitis. This drug was approved in July 2010. For the prevention of itching associated with allergic conjunctivitis. Following bilateral topical ocular administration of alcaftadine ophthalmic solution, 0.25%, the mean plasma Cmax of alcaftadine was approximately 60 pg/mL and the median Tmax occurred at 15 minutes. Plasma concentrations of alcaftadine were below the lower limit of quantification (10 pg/mL) by 3 hours after dosing. The mean Cmax of the active carboxylic acid metabolite was approximately 3 ng/mL and occurred at 1 hour after dosing. Plasma concentrations of the carboxylic acid metabolite were below the lower limit of quantification (100 pg/mL) by 12 hours after dosing. Alcaftadine is a H1 histamine receptor antagonist and inhibitor of the release of histamine from mast cells. Decreased chemotaxis and inhibition of eosinophil activation has also been demonstrated.",The molecular weight is 307.4.,Alcaftadine has a topological polar surface area of 38.13.,The log p value of  is 2.45.,Alcaftadine is approved.,Alcaftadine is a solid.,True
17252,"Antazoline is a 1st generation antihistamine with anticholinergic activity. It is used to relieve nasal congestion. It is also formulated as eye drops with naphazoline to relieve allergic conjunctivitis. Used to relieve nasal congestion and in eye drops, usually in combination with naphazoline, to relieve the symptoms of allergic conjunctivitis. Antazoline is a histamine H1 receptor antagonist. It selectively bind to but does not activate histamine H1 receptors, thereby blocking the actions of endogenous histamine. Antazoline binds to the histamine H1 receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine.",The molecular weight is 265.36.,Antazoline has a topological polar surface area of 27.63.,The log p value of  is 4.11.,Antazoline is approved.,Antazoline is a solid.,True
17253,"Chlorpyramine is a first generation antihistamine used in Eastern European countries to treat bronchial asthma as well as allergice rhinitis, allergic conjunctivitis, and other allergic reactions. It is also indicated for Quincke's edema, allergic reactions to insect bites, food and drug allergies, and anaphylactic shock. For the treatment of allergic conjunctivitis, allergic rhinitis, bronchial asthma, and other atopic (allergic) conditions. Chlorpyramine is a competitive reversible H1 receptor antagonist. This inhibits vasodilation, increases in vascular permeability, and tissue edema associated with histamine release. In addition, chloropyramine has some anticholinergic properties. These effects, along with its ability to pass through the blood-brain barrier lead to side effects such as drowsiness, weakness, vertigo, fatigue, dryness in the mouth, constipation, and rarely - visual disturbances and increase of intraocular pressure. Chloropyramine binds to the histamine H1 receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine.",The molecular weight is 289.81.,Chloropyramine has a topological polar surface area of 19.37.,The log p value of  is 4.02.,Chloropyramine is experimental.,Chloropyramine is a solid.,True
17254,"Dimetindene (Fenistil) is an antihistamine/anticholinergic used orally and locally as an antipruritic. Indicated as symptomatic treatment of allergic reactions: urticaria, allergies of the upper respiratory tract such as hey fever and perennial rhinitis, food and drug allergies; pruritus of various origins, except pruritus due to cholestasis; insect bites. Dimethindene is also indicated for pruritus in eruptive skin diseases such as chicken-pox. Dimethindene can also be used as an adjuvant in eczema and other pruriginous dermatoses of allergic origin.  Dimethindene occurs as a racemic mixture. The (S)-(+)-dimethindene is a potent M2-selective muscarinic receptor antagonist (with lower affinity for M1, M3, and M4 muscarinic receptors). The (R)-(-)-enantiomer is the eutomer (responsible for bioactivity) for histamine H1 receptor binding. Dimethindene is a selective histamine H1 antagonist and binds to the histamine H1 receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine.",The molecular weight is 292.43.,Dimetindene has a topological polar surface area of 16.13.,The log p value of  is 3.53.,Dimetindene is approved and investigational.,Dimetindene is a solid.,True
17255,"Isothipendyl is an antihistamine and anticholinergic used as an antipruritic. For the topical treatment of itching associated with allergic reactions. Isothipendyl, an azaphenothiazine derivative, competitively binds to histamine (H1) receptors, resulting in inhibition of the pharmacological effects of histamines. It also has some sedative, anticholinergic and antiserotoninergic effects. Isothipendyl is a selective histamine H1 antagonist and binds to the histamine H1 receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine.",The molecular weight is 285.41.,Isothipendyl has a topological polar surface area of 19.37.,The log p value of  is 3.83.,Isothipendyl is experimental.,Isothipendyl is a solid.,True
17256,"Chlorcyclizine is a first generation phenylpiperazine class antihistamine used to treat urticaria, rhinitis, pruritus, and other allergy symptoms. Chlorcyclizine also has some local anesthetic, anticholinergic, and antiserotonergic properties, and can be used as an antiemetic.",The molecular weight is 300.83.,Chlorcyclizine has a topological polar surface area of 6.48.,The log p value of  is 4.51.,Chlorcyclizine is approved.,Chlorcyclizine is a solid.,True
17257,Butriptyline is a tricyclic antidepressant which has been used in Europe since 1974. It is the isobutyl side chain homologue of amitriptyline.,The molecular weight is 293.45.,Butriptyline has a topological polar surface area of 3.24.,The log p value of  is 5.55.,Butriptyline is approved.,Butriptyline is a solid.,True
17258,"Acrivastine is a triprolidine analog antihistamine indicated for the treatment of allergies and hay fever. As an H1 receptor antagonist, it functions by blocking the action of histamine at this receptor thereby preventing the symptoms associated with histamine release such as pruritis, vasodilation, hypotension, edema, bronchoconstriction, and tachycardia.  For the relief of symptoms associated with seasonal allergic rhinitis such as sneezing, rhinorrhea, pruritus, lacrimation, and nasal congestion.",The molecular weight is 348.45.,Acrivastine has a topological polar surface area of 53.43.,The log p value of  is 1.46.,Acrivastine is approved.,,True
17259,"Bilastine is a novel new-generation antihistamine that is highly selective for the H1 histamine receptor, has a rapid onset and prolonged duration of action. For symptomatic relief of nasal and non-nasal symptoms of seasonal rhinitis in patients 12 years of age and older and for symptomatic relief in chronic spontaneous urticaria in patients 18 years of age and older. Bilastine is an antiallergenic and acts to reduce allergic symptoms such as nasal congestion and urticaria. Bilastine is a selective histamine H1 receptor antagonist (Ki = 64nM). During allergic response mast cells undergo degranulation which releases histamine and other subastances. By binding to and preventing activation of the H1 receptor, bilastine reduces the development of allergic symptoms due to the release of histamine from mast cells.",The molecular weight is 463.62.,Bilastine has a topological polar surface area of 67.59.,The log p value of  is 1.95.,Bilastine is approved and investigational.,Bilastine is a solid.,True
17260,"Pralnacasan is an orally bioavailable pro-drug of a potent, non-peptide inhibitor of interleukin-1beta converting enzyme (ICE). For the treatment of rheumatoid arthritis (RA). Pralnacasan is a potent, non-peptide inhibitor of interleukin-1beta converting enzyme (ICE). Pralnacasan is an oral, anti-cytokine drug candidate licensed for development by Aventis Pharma from Vertex Pharmaceuticals. In November 2003, Aventis and Vertex Pharmaceuticals announced that they had voluntarily suspended the phase II clinical trials of pralnacasan due to results from an animal toxicity study that demonstrated liver abnormalities after a nine-month exposure to pralnacasan at high doses. While no similar liver toxicity has been seen to date in human trials, the companies will evaluate the animal toxicity results before proceeding with the phase II clinical program. Pralnacasan inhibits interleukin-1beta converting enzyme (ICE), an enzyme that regulates the production of IL-1 and IFN gamma - intercellular mediators that initiate and sustain the process of inflammation. Inhibiting ICE may be an effective strategy for curtailing damaging inflammatory processes common to a number of acute and chronic conditions, such as rheumatoid arthritis (RA) and osteoarthritis.",,,,Pralnacasan is investigational.,Pralnacasan is a solid.,True
17261,"LAX-101 treats hungtington’s disease, not just the symptoms but the disease itself. The active molecule in LAX-101 is Eicosapentaenoic Acid (EPA). All molecules of EPA are identical. The molecules of EPA found in LAX-101 are identical to the molecules of EPA found in fish oil food supplements. Investigated for use/treatment in depression and huntington's disease. LAX-101, a novel and proprietary compound that inhibits certain harmful enzymes including phospholipases and caspases, represents a new class of drugs sometimes referred to as NPLs. This class may function as \neuroprotectants\"" and appears to inhibit degradation of brain tissue by a variety of proposed mechanisms, including stabilization of the phospholipid components of cell membranes and mitochondria, cell structures that are important in cell regulation and brain function. """,,,,LAX-101 is investigational.,LAX-101 is a solid.,True
17262,"Emricasan is the first caspase inhibitor tested in human which has received orphan drug status by FDA. It is developed by Pfizer and made in such a way that it protects liver cells from excessive apoptosis. Investigated for use/treatment in hepatitis (viral, C), liver disease, and transplantation (organ or tissue). IDN-6556 significantly improves markers of liver damage in patients infected with the Hepatitis C virus (HCV), an infection that affects up to 170m patients worldwide. IDN-6556 represents a new class of drugs that protect the liver from inflammation and cellular damage induced by viral infections and other causes. Various studies have also shown that it significantly lowers aminotransferase activity in HCV patients and appeared to be well tolerated.",,,,Emricasan is investigational.,Emricasan is a solid.,True
17263,"VX-765 is the orally available prodrug of a potent and selective competitive inhibitor of ICE/caspase-1 (VRT-043198). VX-765 is currently under clinical development for the treatment of inflammatory and autoimmune conditions, as it blocks the hypersensitive response to an inflammatory stimulus. Investigated for use/treatment in inflammatory disorders (unspecified) and psoriasis and psoriatic disorders. VX-765 is an orally-absorbed pro-drug of VRT-043198, a potent and selective inhibitor of ICE/caspase-1 sub-family caspases.  It has been shown to reduce disease severity and the expression of inflammatory mediators in models of rheumatoid arthritis and skin inflammation, suggesting that it may be useful for treatment of inflammatory diseases. VX-765 is a potent and selective inhibitor of ICE/caspase-1 sub-family caspases. In preclinical trials, VX-765 was efficiently converted to VRT-043198 when administered orally to mice and inhibited LPS-induced cytokine secretion. The result was a blocking of IL-1beta and IL-18 secretion, with out much effect on the release of several other cytokines, including IL-1{alpha}, tumor necrosis factor-{alpha}, IL-6 and IL-8. There was also no demonstrable activity in cellular models of apoptosis and it did not affect the proliferation of activated primary T-cells or T-cell lines. ",,,,VX-765 is investigational.,VX-765 is a solid.,True
17264,,,,,1-METHYL-3-TRIFLUOROMETHYL-1H-THIENOPYRAZOLE-5-CARBOXYLIC ACID (2-MERCAPTO-ETHYL)-AMIDE is experimental.,1-METHYL-3-TRIFLUOROMETHYL-1H-THIENOPYRAZOLE-5-CARBOXYLIC ACID (2-MERCAPTO-ETHYL)-AMIDE is a solid.,False
17265,"Non-methylated, competitive, and irreversible inhibitor of caspase 1, as well as other caspases,1 which can be used directly with purified enzymes. It does not require an esterase to hydrolyze the O-methyl ester like the cell-permeable form, Z-Val-Ala-Asp(O-Me) fluoromethyl ketone.",,,,Z-Val-Ala-Asp fluoromethyl ketone is experimental.,Z-Val-Ala-Asp fluoromethyl ketone is a solid.,True
17266,,,,,3-{6--2-THIOPHEN-2-YL-HEXANOYLAMINO}-4-OXO-BUTYRI ACID is experimental.,3-{6--2-THIOPHEN-2-YL-HEXANOYLAMINO}-4-OXO-BUTYRI ACID is a solid.,False
17267,,,,,"4-Bromo-2,5-dimethoxyphenethylamine is experimental and illicit.","4-Bromo-2,5-dimethoxyphenethylamine is a solid.",False
17268,"Compound with anti-depressive properties used as a mental performance enhancer. Aniracetam possesses a wide range of anxiolytic properties, which may be mediated by an interaction between cholinergic, dopaminergic and serotonergic systems.",The molecular weight is 219.24.,Aniracetam has a topological polar surface area of 46.61.,The log p value of  is 0.72.,Aniracetam is experimental.,Aniracetam is a solid.,True
17269,"APD791 is an oral anti-thrombotic drug candidate being evaluated in a Phase 1 clinical trial by Arena. APD791 is intended to lower the risk of arterial thrombosis by reducing the amplification of platelet aggregation, arterial constriction and intimal hyperplasia mediated by serotonin. For the treatment and prophylaxis of arterial thrombosis. APD791 is intended to lower the risk of arterial thrombosis by reducing the amplification of platelet aggregation, arterial constriction and intimal hyperplasia mediated by serotonin. Preclinical testing suggests that APD791 could have a unique risk-benefit profile because its anti-thrombotic activity may be less likely to cause the increased bleeding seen with anti-thrombotic agents that are members of other classes of drugs. APD791 targets the 5-HT2A serotonin receptor, blocking the signal of serotonin, which facilitates thrombosis.",,,,APD791 is investigational.,APD791 is a solid.,True
17270,"Pimavanserin (ACP-103), marketed under the trade name Nuplazid, is a drug developed by Acadia Pharmaceuticals which acts as an inverse agonist on the serotonin receptor subtype 5-HT2A, with 40x selectivity over 5-HT2C, and no significant affinity or activity at 5-HT2B or dopamine receptors. As of September 3, 2009, pimavanserin has not met expectations for Phase III clinical trials for the treatment of Parkinson's disease psychosis. It is in Phase II trials for adjunctive treatment of schizophrenia alongside an antipsychotic medication and is expected to improve the effectiveness and side effect profile of antipsychotics. The results of a clinical trial examining the efficacy, tolerability and safety of adjunctive pimavanserin to risperidone and haloperidol were published in November 2012 and the results showed that pimavanserin potentiated the antipsychotic effects of subtherapeutic doses of risperidone and improve the tolerability of haloperidol treatment by reducing the incidence of extrapyramidal symptoms. On September 2, 2014, the United States Food and Drug administration granted Breakthrough Therapy status to Acadia's New Drug Application for pimavanserin. Investigated for use/treatment in neurologic disorders, parkinson's disease, psychosis, schizophrenia and schizoaffective disorders, and sleep disorders. ACP-103 reduces haloperidol-induced akathisia, a debilitating extrapyramidal side effect (EPS), in patients with schizophrenia. ACP-103 is a 5-HT2A inverse agonist, to reduce the side effects associated with antipsychotic drug treatment with haloperidol. ACP-103 reduced both the motor disturbances and hyperprolactinemia, a condition of elevated prolactin secretion, caused by haloperidol treatment.",The molecular weight is 427.56.,Pimavanserin has a topological polar surface area of 44.81.,The log p value of  is 4.11.,Pimavanserin is approved and investigational.,Pimavanserin is a solid.,True
17271,"BL-1020 is a first in class novel compound for the treatment of schizophrenia. It is being developed by BioLineRx (BioLine). Investigated for use/treatment in schizophrenia and schizoaffective disorders. Extensive preclinical testing of BL-1020 has shown it to have a positive safety and pharmacokinetic profile. BL-1020 reduces dopamine activity while avoiding the side affects associated with unmitigated dopamine blockade. In animal models of schizophrenia, BL-1020 reduces behaviors characteristic of psychosis and causes minimal or no impairment of movement, the most severe side effect of classic antipsychotic drugs. Biochemical testing confirms that BL-1020 works via the mechanism previously established for classic antipsychotics. BL-1020 is structurally and mechanistically distinct from the atypical antipsychotics and is not anticipated to trigger diabetes or elevated cholesterol. Preliminary studies do not reveal toxicity. In radioligand binding studies, BL-1020 displayed strong interaction with dopamine receptors especially D<sub>2L</sub> and D<sub>2S</sub> (K<sub>i</sub> of 0.27 nM and 0.17 nM respectively), the serotonin receptor 5-HY<sub>2a</sub> (K<sub>i</sub> 0.25 nM) as well as moderate interaction with the GABAA receptor (K<sub>i</sub> 3.29 microK).",,,,BL-1020 is investigational.,BL-1020 is a solid.,True
17272,"YKP1358 is a novel serotonin (5-HT2A) and dopamine (D2) antagonist that has demonstrated potent activity in animals that relates to both positive and negative symptoms of schizophrenia. In addition, the YKP1358 pharmacological profile suggests a very low potential for extrapyramidal side effects. Investigated for use/treatment in schizophrenia and schizoaffective disorders. serotonin (5-HT2A) and dopamine (D2) antagonist.",,,,YKP-1358 is investigational.,YKP-1358 is a solid.,True
17273,"Amisulpride (trade name Solian) is an antipsychotic drug sold by Sanofi-Aventis. It is not approved for use in the United States, but is approved for use in Europe and Australia for the treatment of psychoses and schizophrenia. Additionally, it is approved in Italy for the treatment of dysthymia (under the brand name Deniban). Amisulpride is a selective dopamine antagonist. Investigated for use/treatment in schizophrenia and schizoaffective disorders, mania in bipolar disorder, and depression. Amisulpride binds selectively to dopamine D(2) and D(3) receptors in the limbic system. Low doses of amisulpride preferentially block presynaptic D(2)/D(3)-dopamine autoreceptors, thereby enhancing dopaminergic transmission, whereas higher doses block postsynaptic receptors, thus inhibiting dopaminergic hyperactivity. It may also have 5-ht7 antagonistic effect, useful in depression treatment.",The molecular weight is 369.48.,Amisulpride has a topological polar surface area of 101.73.,The log p value of  is 1.8.,Amisulpride is approved and investigational.,Amisulpride is a solid.,True
17274,"Amperozide is a diphenylbutylpiperazine atypical antipsychotic which antagonizes 5-HT2A receptors. It inhibits dopamine release and alters the firing of dopaminergic neurons. Investigations regarding the use of the agent revolved primarily around its capability for treating schizophrenia in humans even though the drug was ultimately never clinically adopted for this indication. Alternatively, amperozide's main use lies in veterinary medicine, where it is typically employed to minimize aggression and stress in intensively farmed pigs.",The molecular weight is 401.5.,Amperozide has a topological polar surface area of 35.58.,The log p value of  is 5.37.,Amperozide is experimental.,Amperozide is a solid.,True
17275,"Etoperidone is an atypical antidepressant introduced in Europe in 1977. It is a phenylpiperazine-substituted triazole derivative with a composition that classifies it as an analog of tradozone and presents a similar pharmacological profile. Etoperidone was developed by Angelini Francesco ACRAF and even nowadays, there is uncertanty if this drug ever reached the market. Etoperidone has been studied for the treatment of depression, tremors in Parkinson, extrapyramidal symptoms and male impotence. It is not certain if it was ever approved and marketed but its current status is withdrawn. Etoperidone has a biphasic effect on the central transmission of serotonin. It presents the capacity to inhibit serotonin receptor but also to inhibit the reuptake of serotonin, norepinephrine and dopamine. As part of its actions, etoperidone also inhibits the α-adrenergic receptors which directly corresponds to the sedative and cardiovascular effects. The presence of both effects caused that the effective dose of etoperidone was poorly tolerated thus, efforts have been made to separate the serotonergic and adrenergic functions in order to generate etoperidone-derivatives like nefazodone. The activity of etoperidone is made mainly by its major metabolite 1-(3'-chlorophenyl)piperazine (mCPP). mCPP binds with different affinity to most of the serotonergic receptors and adrenergic receptors. This metabolite is an agonist of 5-HT2c and an antagonist of 5-HT2a. Part of etoperidone structure contibutes to the activity in the α-adrenergic receptors. ",The molecular weight is 377.92.,Etoperidone has a topological polar surface area of 42.39.,The log p value of  is 4.13.,Etoperidone is withdrawn.,Etoperidone is a solid.,True
17276,"Sarpogrelate has been investigated for the treatment of Diabetes Mellitus, Diabetic Nephropathy, Coronary Artery Disease, and Renal Insufficiency, Chronic.",The molecular weight is 429.51.,Sarpogrelate has a topological polar surface area of 85.3.,The log p value of  is 2.04.,Sarpogrelate is investigational.,,True
17277,"Eplivanserin has been used in trials studying the treatment of Sleep, Insomnia, Chronic Pain, Fibromyalgia, and Primary Insomnia, among others.",,,,Eplivanserin is investigational.,,True
17278,"Ketanserin has been investigated for the treatment of Septic Shock, Severe Sepsis, and Diabetic Foot Ulcer.",The molecular weight is 395.43.,Ketanserin has a topological polar surface area of 69.72.,The log p value of  is 3.0.,Ketanserin is investigational.,,True
17279,"Nelotanserin has been used in trials studying the treatment of Lewy Body Dementia, Visual Hallucinations, Dementia With Lewy Bodies, and REM Sleep Behavior Disorder. It is a highly selective antagonist at the 5-HT2A serotonin receptor. It increases non-REM sleep, the most restorative phase of the sleep cycle, without sacrificing REM or dream sleep. Nelotanserin works through a mechanism of action that is different from currently marketed drugs. Nelotanserin potently and selectively targets the 5-HT2A serotonin receptor, blocking a stimulatory pathway of the central nervous system. This mechanism is not expected to have the side effects of the GABA-A treatments.",,,,Nelotanserin is investigational.,,True
17280,"2,5-Dimethoxy-4-ethylthioamphetamine (ALEPH-2) is a phenylisopropylamine derivative with alleged anxiolytic and hallucinogenic properties.",,,,"2,5-Dimethoxy-4-ethylthioamphetamine is experimental.","2,5-Dimethoxy-4-ethylthioamphetamine is a solid.",True
17281,"25CN-NBOH (N-(2-hydroxybenzyl)-2,5-dimethoxy-4-cyanophenylethylamine) is a newly developed selective 5-HT2A agonist. It has been tested with regard to the head-twitch-response (HTR) model of 5-HT2A activity and effects on locomotion. It was discovered in 2014 at the University of Copenhagen. 25CN-NBOH is one of the most selective agonist ligands for the 5-HT2A receptor discovered. It has a pKi of 8.88 at the human 5-HT2A receptor and is 100x more selective for 5-HT2A over 5-HT2C, and 46x more selective for 5-HT2A over 5-HT2B.",,,,"N-(2-hydroxybenzyl)-2,5-dimethoxy-4-cyanophenylethylamine is experimental.","N-(2-hydroxybenzyl)-2,5-dimethoxy-4-cyanophenylethylamine is a solid.",True
17282,"A 177Lu-labeled somatostatin analog peptide, Lutetium Lu 177 dotatate belongs to an emerging form of treatments called Peptide Receptor Radionuclide Therapy (PRRT), which involves targeting tumours with molecules carrying radioactive particles that bind to specific receptors expressed by the tumour. Lutetium Lu 177 dotatate may also be referred to as 177Lu-DOTA-Tyr3-octreotate. Compared to the alternative somatostatin analogue DOTA-Tyr3-octreotide (dotatoc), Lutetium Lu 177 dotatate displays higher uptake of radioactivity in tumors and better residence times. In terms of biodistribution, Lutetium Lu 177 dotatate demonstrated a lower whole-body retention, indicating potentially lower risk for bone marrow toxicity. The presence of a radioligand allows monitoring of treatment response post therapy and prior to next fraction of the dose delivery which may be clinically beneficial in estimating the intensity of lesion uptakes or deciding the dose for subsequent administrations. Indicated for the treatment of somatostatin receptor-positive gastroenteropancreatic neuroendocrine tumors (GEP-NETs), including foregut, midgut, and hindgut neuroendocrine tumors in adults. Clinically significant myelosuppression occurred in less than 10% of patients in the Lutetium Lu 177 dotatate (177Lu-Dotatate) group in one clinical trial. According to an open label study involving 20 patients with somatostatin receptor-positive midgut carcinoid tumors, the treatment with did not result in any large changes in the mean QTc interval (i.e., >20 ms). Due to high expression of SSTR2, pancreas was the primary target in animal studies using a non-radioactive form of lutetium Lu 177 dotatate (lutetium Lu 175 dotatate).  Somatostatin receptors (SSRT) are inhibitory G-protein coupled receptors that are ubiquitously expressed in normal and cancer cells. The natural ligand of SSRTs, somatostatin, is a potent inhibitory regulator of pituitary and gastrointestinal hormone release and proliferation. Advanced and well-differentiated neuroendocrine tumors express high levels of somatostatin receptors, especially somatostatin recetor type 2 (SSRT2), and have the ability to incorporate amines intracellularly and decarboxylate them. ",The molecular weight is 1612.58.,Lutetium Lu 177 dotatate has a topological polar surface area of 484.5.,,Lutetium Lu 177 dotatate is approved and investigational.,Lutetium Lu 177 dotatate is a solid.,True
17283,"Edotreotide gallium Ga-68 is an 8 amino acid peptide bound to the chelator 1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid (DOTA). Edotreotide gallium Ga-68 is indicated for localizing somatostatin receptor positive neuroendocrine tumors by positron emission tomography. is used for a similar indication. Dotatate gallium Ga-68 has lower tumor uptake but this data is highly variable between patients. Edotreotide gallium Ga-68 is a radioactive diagnostic compound used in positron emission tomography (PET) for diagnose somatostatin receptor positive neuroendocrine tumors in pediatrics and adults. Edotreotide gallium Ga-68 binds to somatostatin receptors where it emits beta particle radiation for detection by positron emission tomography. The duration of action is short as it has short radioactive and biological half lives. Patients should hydrate before and after the administration of this medication to encourage frequent urination and rapid clearance. Edotreotide gallium Ga-68 binds to somatostatin receptors, with higher affinity for somatostatin receptor type 2, where it emits beta particle radiation for detection by positron emission tomography (PET).",,,,Edotreotide gallium Ga-68 is approved.,Edotreotide gallium Ga-68 is a solid.,True
17284,An amino acid that occurs in endogenous proteins. Tyrosine phosphorylation and dephosphorylation plays a role in cellular signal transduction and possibly in cell growth control and carcinogenesis. ,,,,Phosphonotyrosine is experimental.,Phosphonotyrosine is a solid.,True
17285,"Ancestim is a non-glycosylated recombinant methionyl human stem cell factor. It is a 166 amino acid protein produced by E. coli with an amino acid sequence that is identical to the natural sequence predicted from human DNA sequence analysis, except for the addition of an N-terminal methionine. Ancestim was developed by Amgen and sold to Biovitrium in December 2008. It was submitted to the FDA under the status of recommendation for approval with a 10 to 1 votes. It was also approved by Health Canada in 1999 but it is currently under the status of canceled post-market. Ancestim, in combination with filgrastim, is indicated for the setting of autologous peripheral blood progenitor cell transplantation in patients at risk of poor peripheral blood progenitor cell mobilisation. The use of ancestim with filgrastim will generate a sustained increase in the number of peripheral blood progenitor cells capable of engraftment. It is used for mobilization of progenitor cells from the bone marrow to the peripheral blood with or withouth mobilizing chemotherapy. The harvested progenitor cells can be used for transplant following myelosuppressive or myeloablative therapies. Ancestim action on hemotopeitic progenitor cells stimulates its proliferation, differentiation, commitment and functional activation. This stimulation results in an increase on circulating peripheral blood progenitor cells like CD34, granulocyte macrophage colony-forming units and erythroid burst-forming units.  Ancestim alone is unable to increase peripheral blood progenitor cells so it has to be administered with filgastrim, a granulocyte colony-stimulating factor. Ancestrim will bind to the c-KIT expressed in hemocytoblasts, myeloid progenitors, megakaryocytes, immature mast cells, myeloblasts and lymphoid progenitors. Ancestim binding will cause receptor homodimerization and autophosphorylation at tyrosine residues. The activation of this receptor leads to the activation of a signaling cascade that contains the RAS/ERK, PI3-Kinase, Src kinase and JAK/STAT pathways which will later stimulate proliferation, differentiation and activation of the cell lines.",,,,Ancestim is approved and investigational and withdrawn.,Ancestim is a solid.,True
17286,"Nitisinone is a synthetic reversible inhibitor of 4-hydroxyphenylpyruvate dioxygenase. It is used in the treatment of hereditary tyrosinemia type 1. It is sold under the brand name Orfadin. Used as an adjunct to dietary restriction of tyrosine and phenylalanine in the treatment of hereditary tyrosinemia type 1. Hereditary tyrosinemia type 1 occurs due to a deficiency in fumarylacetoacetase (FAH), the final enzyme in the tyrosine catabolic pathway. Nitisinone inhibits catabolism of tyrosine by preventing the catabolic intermediates. In patients with HT-1, these catabolic intermediates are converted to the toxic metabolites succinylacetone and succinylacetoacetate, which are responsible for the observed liver and kidney toxicity. Succinylacetone can also inhibit the porphyrin synthesis pathway leading to the accumulation of 5-aminolevulinate, a neurotoxin responsible for the porphyric crises characteristic of HT-1. Nitisinone is a competitive inhibitor of 4-hydroxyphenyl-pyruvate dioxygenase, an enzyme upstream of fumarylacetoacetate hydrolyase (FAH) in the tyrosine catabolic pathway. By inhibiting the normal catabolism of tyrosine in patients with hereditary tyrosinemia type 1 (HT-1), nitisinone prevents the accumulation of the catabolic intermediates maleylacetoacetate and fumarylacetoacetate.",The molecular weight is 329.23.,Nitisinone has a topological polar surface area of 94.35.,The log p value of  is 1.38.,Nitisinone is approved and investigational.,Nitisinone is a solid.,True
17287,,,,,DAS869 is experimental.,DAS869 is a solid.,False
17288,,,,,"2,3,4,5,6-Pentafluorobenzyl Alcohol is experimental.","2,3,4,5,6-Pentafluorobenzyl Alcohol is a solid.",False
17289,,,,,N-1-methylheptylformamide is experimental.,N-1-methylheptylformamide is a solid.,False
17290,,,,,2-Ethoxyethanol is experimental.,2-Ethoxyethanol is a solid.,False
17291,,,,,Para-Bromobenzyl Alcohol is experimental.,Para-Bromobenzyl Alcohol is a solid.,False
17292,,,,,3-Butylthiolane 1-Oxide is experimental.,3-Butylthiolane 1-Oxide is a solid.,False
17293,,,,,5-beta-D-ribofuranosylnicotinamide adenine dinucleotide is experimental.,5-beta-D-ribofuranosylnicotinamide adenine dinucleotide is a solid.,False
17294,,,,,(R)-N-(1-Methyl-Hexyl)-Formamide is experimental.,(R)-N-(1-Methyl-Hexyl)-Formamide is a solid.,False
17295,"A non-aqueous co-solvent that serves as tool to study protein folding. It is also used in various pharmaceutical, chemical and engineering applications.",,,,Trifluoroethanol is experimental.,Trifluoroethanol is a solid.,True
17296,,,,,Cpad is experimental.,Cpad is a solid.,False
17297,,,,,N-Formylpiperidine is experimental.,N-Formylpiperidine is a solid.,False
17298,,,,,"2,3-Difluorobenzyl Alcohol is experimental.","2,3-Difluorobenzyl Alcohol is a solid.",False
17299,,,,,"2,4-Difluorobenzyl Alcohol 2,4-Difluoro-1-(Hydroxymethyl)Benzene is experimental.","2,4-Difluorobenzyl Alcohol 2,4-Difluoro-1-(Hydroxymethyl)Benzene is a solid.",False
17300,"Nicorandil is an orally efficacious vasodilatory drug and antianginal agent marketed in the UK, Australia, most of Europe, India, Philippines, Japan, South Korea, and Taiwan. It is not an approved drug by FDA. It is a niacinamide derivative that induces vasodilation of arterioles and large coronary arteries by activating potassium channels. It is often used for patients with angina who remain symptomatic despite optimal treatment ith other antianginal drugs. Nicorandil is a dual-action potassium channel opener that relaxes vascular smooth muscle through membrane hyperpolarization via increased transmembrane potassium conductance and increased intracellular concentration of cyclic GMP. It is shown to dilate normal and stenotic coronary arteries and reduces both ventricular preload and afterload. Indicated for the prevention and treatment of chronic stable angina pectoris and reduction in the risk of acute coronary syndromes.  Nicorandil is a potassium channel opener with nitrovasodilator (NO donor) actions, making it both an arterial and a venous dilator. It causes sustained dilation of both the arterial resistance and conductive vessels that increases coronary blood flow, however the effect of the drug on coronary arteries does not involve the coronary steal phenomenon. Activation of potassium channels lead to hyperpolarization of the smooth muscle cells, followed by arterial dilation and afterload reduction. Nicorandil is shown to increase pooling in the capacitance vessels with a decrease in preload through relaxing the venous vascular system. Overall, improved blood flow and reduced infarct size are achieved through reduction of end-diastolix pressure and decreased extravascular component of vascular resistance. Open studies showed the effectiveness of nicorandil treatment on various types of angina pectoris.  Nicorandil mediates its therapeutic efficacy via two main mechanisms. Nicorandil is an activator and opener of ATP-sensitive (ATP-dependent) potassium channels (KATP channels) that are composed of Kir6.x-type subunits and sulfonylurea receptor (SUR) subunits. Nicorandil binding sites are located in the sulfonylurea receptor 2 (SUR2) in the ATP-sensitive potassium channel , which are regulatory subunits of the channel that exhibit an ATPase activitiy. There are 2 types of SUR2 subunits (2A/2B) that have identical nucleotide binding domains (NBD), where SUR2A is more predominantly expressed in skeletal and cardiac myocytes and SUR2B in smooth muscle cells. Nicorandil more potently activates SUR2B/Kir6.2 than SUR2A/Kir6.2 channels to cause hyperpolarization. ATP-NBD1 interaction influences the channel signalling by nicorandil, and the response of the channel to nicorandil is also facilitated and heightened by the interaction of ATP or ADP with NBD2. Potentiated activity of ATP-sensitive channels have cardioprotective role by limiting the duration of action potentials and preventing intraceullar calcium overload. This attenuates cellular injury by preserving cellular energetics and ultimately cell survival. KATP channel-dependent membrane hyperpolarization can also lead to vasodilation via reduction in Ca2+ influx through the voltage-gated Ca2+ channels and regulation of intracellular Ca2+ mobilization in smooth muscle cells. ",The molecular weight is 211.18.,Nicorandil has a topological polar surface area of 97.04.,The log p value of  is -1.8.,Nicorandil is approved and investigational.,Nicorandil is a solid.,True
17301,"Fumazenil is an imidazobenzodiazepine derivative and a potent benzodiazepine receptor antagonist that competitively inhibits the activity at the benzodiazepine recognition site on the GABA/benzodiazepine receptor complex, thereby reversing the effects of benzodiazepine on the central nervous system. For the complete or partial reversal of the sedative effects of benzodiazepines in cases where general anesthesia has been induced and/or maintained with benzodiazepines, and where sedation has been produced with benzodiazepines for diagnostic and therapeutic procedures. Also for the management of benzodiazepine overdose as an adjunct for appropriate supportive and symptomatic measures. Flumazenil antagonizes the CNS effects produced by benzodiazepines, but does not antagonize the central nervous system effects of drugs affecting GABA-ergic neurons by means other than the benzodiazepine receptor (including ethanol, barbiturates, or general anesthetics) and does not reverse the effects of opioids. Flumazenil, an imidazobenzodiazepine derivative, is a benzodiazepine antagonist. It competitively inhibits the benzodiazepine binding site on the GABA/benzodiazepine receptor complex. Flumazenil is a weak partial agonist in some animal models of activity, but has little or no agonist activity in man.",The molecular weight is 303.29.,Flumazenil has a topological polar surface area of 64.43.,The log p value of  is 1.29.,Flumazenil is approved.,Flumazenil is a solid.,True
17302,"The tromethamine (THAM) salt of the naturally occurring prostaglandin F2 alpha, dinoprost tromethamine occurs as a white to off-white, very hygroscopic, crystalline powder. Dinoprost tromethamine may also be known as dinoprost trometamol, PGF2 alpha THAM, or prostaglandin F2 alpha tromethamine. Used for aborting second-trimester pregnancy (between the twelfth to eighteenth week of gestation) and in incomplete abortion or for therapeutic abortion in cases of intrauterine fetal death and congenital abnormalities incompatible with life. Also used at low-doses for medically indicated induction of labor at term. Also injected intra-arterially for use as a vasodilator to assist in angiography. Dinoprost tromethamine is the tromethamine (THAM) salt of the naturally occurring prostaglandin F2<sub>alpha</sub>. Prostaglandin F2<sub>alpha</sub>&nbsp;has several pharmacologic effects on the female reproductive system, including stimulation of myometrial activity, relaxation of the cervix, inhibition of steroidogenesis by corpora lutea, and can potentially lyse corpora lutea. Dinoprost tromethamine appears to act directly on the myometrium, but this has not been completely established. Dinoprost stimulates myometrial contractions (via its interaction with the prostaglandin receptors) in the gravid uterus that are similar to the contractions that occur in the term uterus during labor. These contractions are usually sufficient to cause abortion. Uterine response to prostaglandins increases gradually throughout pregnancy. Dinoprost also facilitates cervical dilatation and softening.",,,,Dinoprost tromethamine is approved and vet_approved.,Dinoprost tromethamine is a solid.,True
17303,"Miglustat, commonly marketed under the trade name Zavesca, is a drug used to treat Gaucher disease. It inhibits the enzyme glucosylceramide synthase, an essential enzyme for the synthesis of most glycosphingolipids. It is only used for patients who cannot be treated with enzyme replacement therapy with imiglucerase. Miglustat is now the first and only approved therapy for patients with Niemann-Pick disease type C (NP-C). It has recently been approved for treatment of progressive neurological symptoms in adult and pediatric patients in the European Union, Brazil, and South Korea. Miglustat was first developed as an anti-HIV agent in the 1990s. However, clinical experience with miglustat showed that therapeutic levels of the drug could not be achieved in patients without a high incidence of adverse effect. For the treatment of adult patients with mild to moderate type 1 (nonneuropathic) Gaucher's disease for whom enzyme replacement therapy is not a therapeutic option (e.g. due to constraints such as allergy, hypersensitivity, or poor venous access). Now approved in some countries for the treatment of progressive neurological symptoms in adult and pediatric patients with Niemann-Pick disease type C (NP-C).  Miglustat, an N-alkylated imino sugar, is a synthetic analogue of D-glucose. Miglustat is an inhibitor of the enzyme glucosylceramide synthase, which is a glucosyl transferase enzyme responsible for catalyzing the formation of glucosylceramide (glucocerebroside). Glucosylceramide is a substrate for the endogenous glucocerebrosidase, an enzyme that is deficient in Gaucher's disease. The accumulation of glucosylceramide due to the absence of glucocerebrosidase results in the storage of this material in the lysosomes of tissue macrophages, leading to widespread pathology due to infiltration of lipid-engorged macrophages in the viscera, lymph nodes, and bone marrow. This results in secondary hematologic consequences including sever anemia and thrombocytopenia, in addition to the characteristic progressive hepatosplenomegaly, as well as skeletal complications including osteonecrosis and osteopenia with secondary pathological fractures. Miglustat functions as a competitive and reversible inhibitor of the enzyme glucosylceramide synthase, the initial enzyme in a series of reactions which results in the synthesis of most glycosphingolipids. The goal of treatment with miglustat is to reduce the rate of glycosphingolipid biosynthesis so that the amount of glycosphingolipid substrate is reduced to a level which allows the residual activity of the deficient glucocerebrosidase enzyme to be more effective (substrate reduction therapy), reducing the accumulation of glucocerebroside in macrophages. In vitro and in vivo studies have shown that miglustat can reduce the synthesis of glucosylceramide-based glycosphingolipids. In clinical trials, miglustat improved liver and spleen volume, as well as hemoglobin concentration and platelet count. Inhibition of glycosphingolipid synthesis has also shown to reduce intracellular lipid storage, improve fluid-phase endosomal uptake and normalize lipid transport in peripheral blood B lymphocytes of NP-C patients, which results in a decrease in the potentially neurotoxic accumulation of gnagliosides G<sub>M2</sub> and G<sub>M3</sub>, lactosylceramide and glucosylceramide, possibly preventing further neuronal damage. Other studies have also suggested that miglustat may indirectly modulate intracellular calcium homeostasis through its effects on glucosylceramide levels, and evidence has shown that an initiating factor in the pathogenesis of NP-C may be impaired calcium homeostasis related to sphingosine storage. Therefore, the effect that miglustat exerts on intracellular calcium levels may influence an important underlying pathogenic mechanism of NP-C.",The molecular weight is 219.28.,Miglustat has a topological polar surface area of 84.16.,The log p value of  is 0.91.,Miglustat is approved.,Miglustat is a solid.,True
17304,"Guanadrel is an antihypertensive agent and postganglionic adrenergic blocking agent. Used to treat and control hypertension. High blood pressure adds to the work load of the heart and arteries. If it continues for a long time, the heart and arteries may not function properly. This can damage the blood vessels of the brain, heart, and kidneys resulting in a stroke, heart failure, or kidney failure. High blood pressure may also increase the risk of heart attacks. These problems may be less likely to occur if blood pressure is controlled. Guanadrel works by controlling nerve impulses along certain nerve pathways. As a result, it relaxes the blood vessels so that blood passes through them more easily. This helps to lower blood pressure. Guanadrel is an adrenergic neuron inhibitor that slowly displaces norepinephrine from its storage in nerve endings. It blocks the release of norepinephrine in response to the sympathetic nerve stimulation, leading to reduced arteriolar vasoconstriction, especially the reflex increase in sympathetic tone that occurs with a change in position.",The molecular weight is 213.28.,Guanadrel has a topological polar surface area of 80.36.,The log p value of  is 0.63.,Guanadrel is approved.,Guanadrel is a solid.,True
17305,"Protriptyline hydrochloride is a dibenzocycloheptene-derivative tricyclic antidepressant (TCA). TCAs are structurally similar to phenothiazines. They contain a tricyclic ring system with an alkyl amine substituent on the central ring. In non-depressed individuals, protriptyline does not affect mood or arousal, but may cause sedation. In depressed individuals, protriptyline exerts a positive effect on mood. TCAs are potent inhibitors of serotonin and norepinephrine reuptake. In addition, TCAs down-regulate cerebral cortical &beta;-adrenergic receptors and sensitize post-synaptic serotonergic receptors with chronic use. The antidepressant effects of TCAs are thought to be due to an overall increase in serotonergic neurotransmission. TCAs also block histamine H<sub>1</sub> receptors, alpha<sub>1</sub>-adrenergic receptors and muscarinic receptors, which accounts for their sedative, hypotensive and anticholinergic effects (e.g. blurred vision, dry mouth, constipation, urinary retention), respectively. See toxicity section below for a complete listing of side effects. Protriptyline may be used for the treatment of depression. For the treatment of depression.  Protriptyline is a tricyclic antidepressant. It was thought that tricyclic antidepressants work by inhibiting the reuptake of the neurotransmitters norepinephrine and serotonin by nerve cells. The effectiveness of antidepressants appear after approximately two weeks following recommended adminsitration schedule. Gradual changes are thought to occur in the cerebral cortex and hippocampus, involved in emotion regulation as part of the limbic system, as receptor sensitivity is enhanced. While &alpha;<sub>1</sub> and &beta;<sub>1</sub> receptors are sensitized, &alpha;<sub>2</sub> receptors are desensitized (leading to increased noradrenaline production). Tricyclics are also reported to alter the perceptions of pain, including neuropathic or neuralgic pain, so they may exhibit analgesic properties. The mechanism of action behind this analgesic property is not fully understood; however, it is thought to involve modulation of endogenous opioid systems in the CNS via an indirect serotonergic route. Tricyclic antidepressants are also effective in relieving migraine prophylaxis, but not in abortion of acute migraine attack, potentially via their serotonergic effects.  Protriptyline acts by decreasing the reuptake of norepinephrine and serotonin (5-HT).",The molecular weight is 263.38.,Protriptyline has a topological polar surface area of 12.03.,The log p value of  is 4.86.,Protriptyline is approved.,Protriptyline is a solid.,True
17306,"A sympathomimetic drug used primarily as an appetite depressant. Its actions and mechanisms are similar to dextroamphetamine. Used as an anorectic in the treatment of obesity. Phenmetrazine is a sympathomimetic drug used primarily as an appetite depressant. Its actions and mechanisms are similar to dextroamphetamine. Amphetamines are non-catecholamine sympathomimetic amines with CNS stimulant activity. Phenmetrazine was originally sold under the tradename Preludin as an anorectic. It has since been removed from the market. It is by some considered to have a greater potential for addiction than the amphetamines, and has been abused in many countries, for example Sweden. Phenmetrazine is thought to block the reuptake of norepinephrine and dopamine into the presynaptic neuron leading to an increase in the release of these monoamines into the extraneuronal space. Dopamine integrates incoming sensory stimuli, initiates and controls fine movement (nigro-neostriatal pathway), controls emotional behavior (midbrain mesolimbic-forebrain system) and controls hypothalamic-pituitary endocrine system (tubero-infundibular system). It is this latter effect on the tubero-infundibular systm that seems to lead to reduced food intake. Phenmetrazine also acts as a monoamine oxidase inhibitor.",The molecular weight is 177.25.,Phenmetrazine has a topological polar surface area of 21.26.,The log p value of  is 1.67.,Phenmetrazine is approved and illicit.,Phenmetrazine is a solid.,True
17307,"A appetite depressant considered to produce less central nervous system disturbance than most drugs in this therapeutic category. It is also considered to be among the safest for patients with hypertension. (From AMA Drug Evaluations Annual, 1994, p2290) Used in the management of exogenous obesity as a short-term adjunct (a few weeks) in a regimen of weight reduction based on caloric restriction. Diethylpropion is a sympathomimetic stimulant drug marketed as an appetite suppressant. Chemically, it is the N,N-diethyl analog of cathinone. Its mechanism of action is similar to other appetite suppressants such as sibutramine, phentermine and dextroamphetamine. Diethylpropion is an amphetamine that stimulates neurons to release or maintain high levels of a particular group of neurotransmitters known as catecholamines; these include dopamine and norepinephrine. High levels of these catecholamines tend to suppress hunger signals and appetite. Diethylpropion (through catecholamine elevation) may also indirectly affect leptin levels in the brain. It is theorized that diethylpropion can raise levels of leptin which signal satiety. It is also theorized that increased levels of the catecholamines are partially responsible for halting another chemical messenger known as neuropeptide Y. This peptide initiates eating, decreases energy expenditure, and increases fat storage.",The molecular weight is 205.3.,Diethylpropion has a topological polar surface area of 20.31.,The log p value of  is 2.85.,Diethylpropion is approved and illicit.,Diethylpropion is a solid.,True
17308,"An antihypertensive agent that acts by inhibiting selectively transmission in post-ganglionic adrenergic nerves. It is believed to act mainly by preventing the release of norepinephrine at nerve endings and causes depletion of norepinephrine in peripheral sympathetic nerve terminals as well as in tissues.  For the treatment of moderate and severe hypertension, either alone or as an adjunct, and for the treatment of renal hypertension. High blood pressure can cause the heart and arteries to not function properly. This can damage the blood vessels of the brain, heart, and kidneys, resulting in a stroke, heart failure, or kidney failure. High blood pressure may also increase the risk of heart attacks. These problems may be less likely to occur if blood pressure is controlled. Guanethidine works by decreasing the heart rate and relaxing the blood vessels so that blood can flow more easily through the body, thereby reducing these risks. It is a postganglionic sympathetic nerve terminal blocker that prevents the release of norepinephrine from nerve terminals. Guanethidine acts at the sympathetic neuroeffector junction by inhibiting or interfering with the release and/or distribution of norepinephrine (NE), rather than acting at the effector cell by inhibiting the association of norepinephrine with its receptors. It is taken up by norepinephrine transporters to be concentrated within the transmitter vesicles in place of NE, leading to gradual depletion of NE stores in the nerve endings. Guanethidine at the nerve terminal blocks the release of noradrenaline in response to an action potential. In contrast to ganglionic blocking agents, Guanethidine suppresses equally the responses mediated by alpha-and beta-adrenergic receptors but does not produce parasympathetic blockade. Since sympathetic blockade results in modest decreases in peripheral resistance and cardiac output, Guanethidine lowers blood pressure in the supine position. It further reduces blood pressure by decreasing the degree of vasoconstriction that normally results from reflex sympathetic nervous activity upon assumption of the upright posture, thus reducing venous return and cardiac output more.",The molecular weight is 198.31.,Guanethidine has a topological polar surface area of 65.14.,The log p value of  is 1.35.,Guanethidine is approved.,Guanethidine is a solid.,True
17309,"Phendimetrazine is a weight loss medication. Phendimetrazine is chemically related to amphetamines and is a Schedule III drug under the Convention on Psychotropic Substances and in the US since 1970. Used in the management of exogenous obesity as a short term adjunct (a few weeks) in a regimen of weight reduction based on caloric restriction. Phendimetrazine is a phenylalkylamine sympathomimetic amine with pharmacological activity similar to the prototype drugs of this class used in obesity, the amphetamines. Actions include central nervous system stimulation and elevation of blood pressure. Tachyphylaxis and tolerance has been demonstrated with all drugs of this class in which these phenomena have been looked for. Drugs of this class used in obesity are commonly known as ''anorectics or anorexigenics.\ It has not been established, however, that the action of such drugs in treating obesity is primarily one of appetite suppression. Other central nervous system actions or metabolic effects, may be involved."" Phendimetrazine may act in a similar way to amphetamines in that it activates the alpha-adrenergic system to induce an appetite suppressive and metabolic increase effect. The drug also acts as a norepinephrine-dopamine releasing agent (NDRA). It can bind to and reverse the NET.",The molecular weight is 191.27.,Phendimetrazine has a topological polar surface area of 12.47.,The log p value of  is 2.13.,Phendimetrazine is approved and illicit.,Phendimetrazine is a solid.,True
17310,"The Food and Drug Administration suspended the marketing authorisation for Survector in 1999 and France withdrew it from the market, however several developing countries continued to produce it up until 2005. For the treatment of depression. Amineptine is an atypical tricyclic antidepressant. Amineptine selectively inhibits the reuptake of dopamine and to a lesser extent norepinephrine, thus exerting a powerful and fast-acting antidepressant effect.",The molecular weight is 337.46.,Amineptine has a topological polar surface area of 49.33.,The log p value of  is 2.51.,Amineptine is illicit and withdrawn.,Amineptine is a solid.,True
17311,"Xen2174 is a synthetic drug modeled on a peptide from the venom of a cone shell found on Australia's Great Barrier Reef. Xen2174 represents a new class of molecules, called the chi conopeptides that selectively inhibit the Norepinephrine Transporter (NET). NET is the primary mechanism regulating the biological effects of norepinephrine (NE) on the body. In episodes of pain, inhibition of NET by Xen2174 elevates the levels of NE leading to the activation of inhibitory pathways preventing pain signals from reaching the brain.  For the treatment of chronic cancer pain. Xen2174 targets the Norepinephrine Transporter (NET). Inhibition of this transporter elevates the levels of norepinephrine (NE) in the spinal cord preventing pain signals from reaching the brain. Xen2174 acts to restore the balance by promoting the activation of inhibitory pain pathways to relieve the sensation of pain.",,,,XEN2174 is investigational.,XEN2174 is a solid.,True
17312,"Investigated for use/treatment in depression. DOV 21947 exhibits antidepressant-like properties as well as potent analgesic activity. It inhibits reuptake of the three neurotransmitters most closely linked to depression - serotonin, norepinephrine and dopamine - can produce greater overall efficacy than currently marketed antidepressants. ",,,,Amitifadine is investigational.,Amitifadine is a solid.,True
17313,"Investigated for use/treatment in alzheimer's disease, parkinson's disease, and obesity. Tesofensine is a Serotonin-norepinephrine-dopamine-reuptake-inhibitor (SNDRI). SNDRIs are a class of psychoactive antidepressants. They act upon neurotransmitters in the brain, namely, serotonin, norepinephrine and dopamine. These three biogenic monoamines are associated with depression and increasing the availability in the brain is one method used to treat the condition.",,,,Tesofensine is investigational.,Tesofensine is a solid.,True
17314,"Trodusquemine, a spermine metabolite of cholesterol, is a naturally occurring aminosterol that inhibits protein tyrosine phosphatase 1B. It has demonstrated the ability to stimulate regeneration of heart and multiple other tissues in animal models. Investigated for use/treatment in obesity and diabetes mellitus type 2. Trodusquemine is a spermine metabolite of cholesterol which possibly acts on the paraventricular nucleus in the hypothalamus. Trodusquemine suppresses feeding, prevents reduction in energy expenditure, causes hormonal changes, and induces patterns of neuropeptide expression normally associated with weight loss. Trosdusquemine enhances insulin sensitivity through inhibition of protein tyrosine phostphatase 1B centrally and peripherally (PTP-1B), dopamine and norepinephrine reuptake, an ion transport modulator and a downregulator of Agouti-related peptide (AgRP) and neuropeptide Y (NPY) expression.",,,,Trodusquemine is investigational.,Trodusquemine is a solid.,True
17315,"Dexmethylphenidate is the dextrorotary form of methylphenidate introduced in 2002. It is a norepinephrine-dopamine reuptake inhibitor (NDRI) and thus a psychostimulant. It is used for treatment of Attention Deficit Hyperactivity Disorder (ADHD). The d-isomer is thought to have greater effect with fewer side effects than the l-isomer or the racemic mixture. Dexmethylphenidate is used as a treatment for ADHD, ideally in conjunction with psychological, educational, behavioral or other forms of treatment. Dexmethylphenidate is the d-enantiomer of methylphenidate. This enantiomer is more pharmacologically active than the racemic mixture and may block norepinephrine and dopamine reuptake in synapses. Methylphenidate inhibits dopamine and norepinephrine reuptake transporters in synapses, especially in the thalamus and striatum. One study shows no detectable difference in the caudal prefrontal cortex of treated or untreated monkeys, though multiple rat studies show activity on the prefrontal cortex. Imaging of human brains after administration of methylphenidate shows changes to blood flow of various regions of the brain including the striatum, supplementary motor area, and posterior parietal cortex.",The molecular weight is 233.31.,Dexmethylphenidate has a topological polar surface area of 38.33.,The log p value of  is 2.56.,Dexmethylphenidate is approved and investigational.,Dexmethylphenidate is a solid.,True
17316,"Dasotraline is a serotonin, norepinephrine and dopamine reuptake inhibitor (SNDRI) that is under investigation for the treatment of Binge Eating Disorder, Adult Attention Hyperactivity Disorder, Attention Deficit Hyperactivity Disorder, and Adult Attention Deficit Hyperactivity Disorder. Dasotraline has been shown in preclinical studies to be a potent and balanced reuptake inhibitor of serotonin, norepinephrine and dopamine (SNDRI). Serotonin, norepinephrine and dopamine are neurotransmitters associated with depression. There are currently no marketed treatments for depression that inhibit reuptake of all three neurotransmitters.",,,,Dasotraline is investigational.,,True
17317,"A Rho kinase inhibitor with norepinephrine transport inhibitory activity that reduces production of aqueous Netarsudil is indicated for the reduction of elevated intraocular pressure (IOP) in patients with open-angle glaucoma or ocular hypertension. Aqueous humour flows out of the eye via two pathways: 1) the conventional trabecular pathway and 2) the unconventional uveoscleral pathway. And, although it has been shown that the conventional trabecular pathway accounts for most aqueous outflow due to various pathologies, most medications available for treating glaucoma target the uveoscleral pathway for treatment and leave the diseased trabecular pathway untreated and unhindered in its progressive deterioration and dysfunction. The medical condition glaucoma is a leading cause of progressive visual impairment and blindness across the world with primary open-angle glaucoma (POAG) being the major type of glaucoma.",The molecular weight is 453.54.,Netarsudil has a topological polar surface area of 94.31.,The log p value of  is 5.01.,Netarsudil is approved.,Netarsudil is a liquid.,True
17318,"Solriamfetol marketed under the brand name Sunosi by Jazz Pharmaceuticals in the United States is a dopamine and norepinephrine reuptake inhibitor (DNRI) indicated in treating daytime sleepiness associated with narcolepsy or obstructive sleep apnea. Solriamfetol was given FDA approval in 2019. Solriamfetol is indicated for treatment of daytime sleepiness associated with obstructive sleep apnea and narcolepsy, but is not a treatment for the underlying airway obstruction in apnea patients. Solriamfetol weakly binds to dopamine and norepinephrine transporters but not serotonin transporters. Solriamfetol does not bind to dopamine, serotonin, norepinephrine, GABA, adenosine, histamine, orexin, benzodiazepines, or muscarinic and nicotinic receptors. The specific mechanism of action is unknown but it may be through its activity as a dopamine and norepinephrine reuptake inhibitor.",,,,Solriamfetol is approved.,,True
17319,"An alkaloid found in opium but not closely related to the other opium alkaloids in its structure or pharmacological actions. It is a direct-acting smooth muscle relaxant used in the treatment of impotence and as a vasodilator, especially for cerebral vasodilation. The mechanism of its pharmacological actions is not clear, but it apparently can inhibit phosphodiesterases and it may have direct actions on calcium channels. For the treatment of impotence and vasospasms. Papaverine is a nonxanthine phosphodiesterase inhibitor for the relief of cerebral and peripheral ischemia associated with arterial spasm and myocardial ischemia complicated by arrhythmias. The main actions of Papaverine are exerted on cardiac and smooth muscle. Like qathidine, Papaverine acts directly on the heart muscle to depress conduction and prolong the refractory period. Papaverine relaxes various smooth muscles. This relaxation may be prominent if spasm exists. The muscle cell is not paralyzed by Papaverine and still responds to drugs and other stimuli causing contraction. The antispasmodic effect is a direct one, and unrelated to muscle innervation. Papaverine is practically devoid of effects on the central nervous system. Papaverine relaxes the smooth musculature of the larger blood vessels, especially coronary, systemic peripheral, and pulmonary arteries. Perhaps by its direct vasodilating action on cerebral blood vessels, Papaverine increases cerebral blood flow and decreases cerebral vascular resistance in normal subjects; oxygen consumption is unaltered. These effects may explain the benefit reported from the drug in cerebral vascular encephalopathy.",The molecular weight is 339.39.,Papaverine has a topological polar surface area of 49.81.,The log p value of  is 3.78.,Papaverine is approved and investigational.,Papaverine is a solid.,True
17320,,,,,Daxalipram is experimental.,Daxalipram is a solid.,False
17321,"Piclamilast (RP-73,401), is a selective PDE4 inhibitor comparable to other PDE4 inhibitors for its anti-inflammatory effects. It has been investigated for its applications to the treatment of conditions such as chronic obstructive pulmonary disease, bronchopulmonary dysplasia and asthma. The structure for piclamilast was first elucidated in a 1995 European patent application and exhibits the structural functionalities of cilomilast and roflumilast.",,,,Piclamilast is experimental.,Piclamilast is a solid.,True
17322,A phosphodiesterase inhibitor with antidepressant properties.,,,,Rolipram is investigational.,Rolipram is a solid.,True
17323,,,,,"3,5-Dimethyl-1-(3-Nitrophenyl)-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester is experimental.","3,5-Dimethyl-1-(3-Nitrophenyl)-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester is a solid.",False
17324,"Filaminast is a phosphodiesterase 4 inhibitor (PDE4 inhibitor). As such, has potential in the treatment of asthma and chronic obstructive pulmonary disease (COPD).",,,,Filaminast is experimental.,Filaminast is a solid.,True
17325,,,,,8-Bromo-Adenosine-5'-Monophosphate is experimental.,8-Bromo-Adenosine-5'-Monophosphate is a solid.,False
17326,A phosphodiesterase inhibitor with antidepressant properties. ,,,,(S)-Rolipram is experimental.,(S)-Rolipram is a solid.,True
17327,,,,,"1-(2-Chlorophenyl)-3,5-Dimethyl-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester is experimental.","1-(2-Chlorophenyl)-3,5-Dimethyl-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester is a solid.",False
17328,"Cilomilast (Ariflo, SB-207,499) is a drug which was developed for the treatment of respiratory disorders such as asthma and Chronic Obstructive Pulmonary Disease (COPD). It is orally active and acts as a selective Phosphodiesterase-4 inhibitor. Following four clinical trials, the drug proved to be effective in treating COPD, however it has never been marketed due to a poor side effect profile. Investigated for use/treatment in chronic obstructive pulmonary disease (COPD). Cilomilast shows high selectivity for cAMP-specific PDE4, an isoenzyme that predominates in pro-inflammatory and immune cells and that is 10-fold more selective for PDE4D than for PDE4A, -B or -C. In vitro, cilomilast suppresses the activity of several pro-inflammatory and immune cells that have been implicated in the pathogenesis of asthma and COPD. Moreover, it is highly active in animal models of these diseases. Cilomilast has been shown to exert potent anti-inflammatory effects both in vitro and in vivo.",,,,Cilomilast is investigational.,Cilomilast is a solid.,True
17329,"The (R)-enantiomer of rolipram, it is a phosphodiesterase inhibitor with antidepressant properties.",,,,(R)-Rolipram is experimental.,(R)-Rolipram is a solid.,True
17330,,,,,1-ethyl-N-(phenylmethyl)-4-(tetrahydro-2H-pyran-4-ylamino)-1H-pyrazolopyridine-5-carboxamide is experimental.,1-ethyl-N-(phenylmethyl)-4-(tetrahydro-2H-pyran-4-ylamino)-1H-pyrazolopyridine-5-carboxamide is a solid.,False
17331,,,,,4-benzoic acid is experimental.,4-benzoic acid is a solid.,False
17332,"Thyrotropin alfa is a recombinant form of thyroid stimulating hormone used in performing certain tests in patients who have or have had thyroid cancer. It is also used along with a radioactive agent to destroy remaining thyroid tissue in certain patients who have had their thyroid gland removed because of thyroid cancer. It is a heterodimeric glycoprotein comprised of two non-covalently linked subunits, an alpha subunit of 92 amino acid residues containing two N-linked glycosylation sites and a beta subunit of 112 residues containing one N-linked glycosylation site. The alpha subunit of thyrotropin alfa, which is the effector region responsible for the stimulation of adenylate cyclase, displays close structural similarity with the alpha subunit of human chorionic gonadotropin (hCG), luteinizing hormone (LH), and follicle-stimulating hormone (FSH). The beta subunit (TSHB) bestows its receptor specificity due to the uniqueness to TSH. The amino acid sequence of thyrotropin alfa is identical to that of human pituitary thyroid stimulating hormone. For detection of residueal or recurrent thyroid cancer Binding of thyrotropin alfa to TSH receptors on normal thyroid epithelial cells or on well-differentiated thyroid cancer tissue stimulates iodine uptake and organification. Thyrogen is an exogenous source of human TSH that offers an additional diagnostic tool in the follow-up of patients with a history of well-differentiated thyroid cancer. Thyrotropin Alfa binds to the thyrotropin receptors found on any residual thyroid cells or tissues. This stimulates radioactive iodine uptake for better radiodiagnostic imaging.",,,,Thyrotropin alfa is approved and vet_approved.,Thyrotropin alfa is a liquid.,True
17333,"An essential branched-chain aliphatic amino acid found in many proteins. It is an isomer of leucine. It is important in hemoglobin synthesis and regulation of blood sugar and energy levels. The branched-chain amino acids may have antihepatic encephalopathy activity in some. They may also have anticatabolic and antitardive dyskinesia activity. They provide ingredients for the manufacturing of other essential biochemical components in the body, some of which are utilized for the production of energy, stimulants to the upper brain and helping you to be more alert. (Applies to Valine, Leucine and Isoleucine) <br/>This group of essential amino acids are identified as the branched-chain amino acids, BCAAs. Because this arrangement of carbon atoms cannot be made by humans, these amino acids are an essential element in the diet. The catabolism of all three compounds initiates in muscle and yields NADH and FADH2 which can be utilized for ATP generation. The catabolism of all three of these amino acids uses the same enzymes in the first two steps. The first step in each case is a transamination using a single BCAA aminotransferase, with a-ketoglutarate as amine acceptor. As a result, three different a-keto acids are produced and are oxidized using a common branched-chain a-keto acid dehydrogenase, yielding the three different CoA derivatives. Subsequently the metabolic pathways diverge, producing many intermediates. <br/>The principal product from valine is propionylCoA, the glucogenic precursor of succinyl-CoA. Isoleucine catabolism terminates with production of acetylCoA and propionylCoA; thus isoleucine is both glucogenic and ketogenic. Leucine gives rise to acetylCoA and acetoacetylCoA, and is thus classified as strictly ketogenic. <br/>There are a number of genetic diseases associated with faulty catabolism of the BCAAs. The most common defect is in the branched-chain a-keto acid dehydrogenase. Since there is only one dehydrogenase enzyme for all three amino acids, all three a-keto acids accumulate and are excreted in the urine. The disease is known as Maple syrup urine disease because of the characteristic odor of the urine in afflicted individuals. Mental retardation in these cases is extensive. Unfortunately, since these are essential amino acids, they cannot be heavily restricted in the diet; ultimately, the life of afflicted individuals is short and development is abnormal The main neurological problems are due to poor formation of myelin in the CNS.",The molecular weight is 131.18.,Isoleucine has a topological polar surface area of 63.32.,The log p value of  is -1.76.,Isoleucine is investigational and nutraceutical.,Isoleucine is a solid.,True
17334,"Coenzyme A (CoA, CoASH, or HSCoA) is a coenzyme, well known for it's role in the synthesis and oxidation of fatty acids, and the oxidation of pyruvate in the citric acid cycle. All genomes sequenced to date encode enzymes that use coenzyme A as a substrate, and around 4% of cellular enzymes use it, or a thioester form of it, as a substrate. It is used as a supplement for the hypothetical treatment of acne.",,,,Coenzyme A is investigational and nutraceutical.,Coenzyme A is a solid.,True
17335,"The purified component of hematoporphyrin derivative, it consists of a mixture of oligomeric porphyrins. It is used in photodynamic therapy (hematoporphyrin photoradiation); to treat malignant lesions with visible light and experimentally as an antiviral agent. It is the first drug to be approved in the use of photodynamic therapy in the United States. Indicated in the treatment of esophageal cancer. Porfimer is a photosensitizing agent used in the photodynamic therapy (PDT) of tumors. Porfimer is indicated for the palliation of patients with completely obstructing esophageal cancer, or of patients with partially obstructing esophageal cancer who cannot be satisfactorily treated with Nd:YAG laser therapy, reduction of obstruction and palliation of symptoms in patients with completely or partially obstructing endobronchial nonsmall cell lung cancer (NSCLC), and the treatment of microinvasive endobronchial NSCLC in patients for whom surgery and radiotherapy are not indicated. The cytotoxic and antitumor actions of porfimer are light and oxygen dependent. Tumor selectivity in treatment occurs through a combination of selective retention of porfimer and selective delivery of light. Cellular damage caused by porfimer is a consequence of the propagation of radical reactions. Radical initiation may occur after porfimer absorbs light to form a porphyrin excited state. Spin transfer from porfimer to molecular oxygen may then generate singlet oxygen. Subsequent radical reactions can form superoxide and hydroxyl radicals. Tumor death also occurs through ischemic necrosis secondary to vascular occlusion that appears to be partly mediated by thromboxane A2 release.",,,,Porfimer sodium is approved and investigational.,Porfimer sodium is a solid.,True
17336,"Dapiprazole (U.S. trade name Rev-Eyes) is an alpha blocker. It is found in ophthalmic solutions used to reverse mydriasis after an eye examination. Used in the treatment of iatrogenically induced mydriasis produced by adrenergic (phenylephrine) or parasympatholytic (tropicamide) agents used in certain eye examinations. Dapiprazole is an alpha-adrenergic blocking agent. It produces miosis by blocking the alpha-adrenergic receptors on the dilator muscle of the iris. Dapiprazole produces no significant action on ciliary muscle contraction and thus, there are no changes in the depth of the anterior chamber of the thickness of the lens. It does not alter the IOP either in normal eyes or in eyes with elevated IOP. The rate of pupillary constriction may be slightly slower in clients with brown irises than in clients with blue or green irises. Dapiprazole acts through blocking the alpha1-adrenergic receptors in smooth muscle. It produces miosis through an effect on the dilator muscle of the iris and does not have any significant activity on ciliary muscle contraction and, therefore does not induce a significant change in the anterior chamber depth or the thickness of the lens.",The molecular weight is 325.46.,Dapiprazole has a topological polar surface area of 37.19.,The log p value of  is 2.03.,Dapiprazole is approved.,Dapiprazole is a solid.,True
17337,"A butyrophenone with general properties similar to those of haloperidol. It is used in conjunction with an opioid analgesic such as fentanyl to maintain the patient in a calm state of neuroleptanalgesia with indifference to surroundings but still able to cooperate with the surgeon. It is also used as a premedicant, as an antiemetic, and for the control of agitation in acute psychoses. (From Martindale, The Extra Pharmacopoeia, 29th ed, p593) Droperidol is ssed to produce tranquilization and to reduce the incidence of nausea and vomiting in surgical and diagnostic procedures. Droperidol produces marked tranquilization and sedation. It allays apprehension and provides a state of mental detachment and indifference while maintaining a state of reflex alertness. Droperidol produces an antiemetic effect as evidenced by the antagonism of apomorphine in dogs. It lowers the incidence of nausea and vomiting during surgical procedures and provides antiemetic protection in the postoperative period. Droperidol potentiates other CNS depressants. It produces mild alpha-adrenergic blockade, peripheral vascular dilatation and reduction of the pressor effect of epinephrine. It can produce hypotension and decreased peripheral vascular resistance and may decrease pulmonary arterial pressure (particularly if it is abnormally high). It may reduce the incidence of epinephrine-induced arrhythmias, but it does not prevent other cardiac arrhythmias. The exact mechanism of action is unknown, however, droperidol causes a CNS depression at subcortical levels of the brain, midbrain, and brainstem reticular formation. It may antagonize the actions of glutamic acid within the extrapyramidal system. It may also inhibit cathecolamine receptors and the reuptake of neurotransmiters and has strong central antidopaminergic action and weak central anticholinergic action. It can also produce ganglionic blockade and reduced affective response. The main actions seem to stem from its potent Dopamine(2) receptor antagonism with minor antagonistic effects on alpha-1 adrenergic receptors as well.",The molecular weight is 379.44.,Droperidol has a topological polar surface area of 52.65.,The log p value of  is 3.06.,Droperidol is approved and vet_approved.,Droperidol is a solid.,True
17338,"An adrenergic agonist that acts predominantly at alpha adrenergic receptors and also stimulates the release of norepinephrine. It has been used primarily as a vasoconstrictor in the treatment of hypotension. For the treatment and prevention of hypotension due to hemorrhage, spinal anesthesia, and shock associated with brain damage Metaraminol is a potent sympathomimetic amine that increases both systolic and diastolic blood pressure. Metaraminol is indicated for prevention and treatment of the acute hypotensive state occurring with spinal anesthesia. It is also indicated as adjunctive treatment of hypotension due to hemorrhage, reactions to medications, surgical complications, and shock associated with brain damage due to trauma or tumor. Metaraminol acts on both &alpha;1-adrenergic receptors but appears to have no effect on &beta;-adrenergic receptors. It acts by increasing the force of the heart's pumping action as well as constricting peripheral blood vessels. Metaraminol acts through peripheral vasoconstriction by acting as a pure alpha-1 adrenergic receptor agonist, consequently increasing systemic blood pressure (both systolic &amp; diastolic). Its effect is thought to be associated with the inhibition of adenyl cyclase which leads to an inhibition of the production of cAMP. Another effect of Metaraminol is that it releases norepinephrine from its storage sites indirectly.",The molecular weight is 167.21.,Metaraminol has a topological polar surface area of 66.48.,The log p value of  is -0.08.,Metaraminol is approved and investigational.,Metaraminol is a solid.,True
17339,"An alpha-adrenergic agonist that causes prolonged peripheral vasoconstriction. It has little if any direct effect on the central nervous system. Indicated for the treatment and management of hypotension. Methoxamine is a potent sympathomimetic amine that increases both systolic and diastolic blood pressure. Methoxamine is indicated for prevention and treatment of the acute hypotensive state occurring with spinal anesthesia. It is also indicated as adjunctive treatment of hypotension due to hemorrhage, reactions to medications, surgical complications, and shock associated with brain damage due to trauma or tumor. Methoxamine acts on both &alpha;1-adrenergic receptors but appears to have no effect on &beta;-adrenergic receptors. It acts by increasing the force of the heart's pumping action as well as constricting peripheral blood vessels. Methoxamine acts through peripheral vasoconstriction by acting as a pure alpha-1 adrenergic receptor agonist, consequently increasing systemic blood pressure (both systolic and diastolic).",The molecular weight is 211.26.,Methoxamine has a topological polar surface area of 64.71.,The log p value of  is 0.59.,Methoxamine is approved and investigational.,Methoxamine is a solid.,True
17340,"R450 is an alpha 1 antagonist that acts to tighten the muscle tone in the bladder. It is being considered for treatment of stress-related urinary incontinence. Phase IIa data for the drug show it reduced the number of incontinent episodes compared to placebo with minimal cardiovascular effects. Investigated for use/treatment in urinary incontinence. R450 is an alpha 1 adrenoreceptor antagonist that acts to tighten the muscle tone in the bladder.  R450 is a selective alpha 1 adrenoreceptor antagonist. Research on the management of urinary incontinence suggests that it is most likely an antagonist at alpha-1B and alpha-1D, while it acts as an agonist on alpha-1a.",,,,R450 is investigational.,R450 is a solid.,True
17341,"Tetryzoline (also known as Tetrahydrozoline), a derivative of imidazoline, is found in over-the-counter eye drops and nasal sprays. Other derivatives include naphazoline, oxymetazoline, and xylometazoline. Johnson and Johnson manufactures tetryzoline eye drops under the brand Visine ®. For temporary relief of discomfort and redness of the eye due to minor eye irritations. Tetryzoline is an alpha-adrenergic agonist. Its primary action is the constriction of conjunctival blood vessels, which serves to decrease eye redness caused by minor ocular irritants. ",The molecular weight is 200.28.,Tetryzoline has a topological polar surface area of 24.39.,The log p value of  is 3.53.,Tetryzoline is approved.,Tetryzoline is a solid.,True
17342,Indoramin is a discontinued piperidine antiadrenergic drug with the trade names Baratol and Doralese. It is a selective alpha-1 adrenergic antagonist with no reflex tachycardia and direct myocardial depression action.,The molecular weight is 347.46.,Indoramin has a topological polar surface area of 48.13.,The log p value of  is 2.84.,Indoramin is approved and withdrawn.,Indoramin is a solid.,True
17343,"Cirazoline acts on a number of α adrenergic receptors. It is an agonist of α1A, partial agonist of α1B and α1D, and a nonselective antagonist of α2. It is believed that this combination of properties could make cirazoline an effective vasoconstricting agent. ",,,,Cirazoline is experimental.,Cirazoline is a solid.,True
17344,"Piretanide (INN, trade names Arelix, Eurelix, Tauliz) has been synthesized in 1973 at Hoechst AG (Germany) as a loop diuretic compound by using a then-new method for introducing cyclic amine residues in an aromatic nucleus in the presence of other aromatically bonded functional groups.",The molecular weight is 362.4.,Piretanide has a topological polar surface area of 109.93.,The log p value of  is 2.5.,Piretanide is approved.,Piretanide is a solid.,True
17345,"Resorcinol is a 1,3-isomer (or meta-isomer) of benzenediol with the formula C6H4(OH)2. It is used as an antiseptic and disinfectant in topical pharmaceutical products in the treatment of skin disorders and infections such as acne, seborrheic dermatitis, eczema, psoriasis, corns, calluses, and warts. It exerts a keratolytic activity. Resorcinol works by helping to remove hard, scaly, or roughened skin. Contemporary therapeutic uses for resorcinol primarily revolve around the use of the phenol derivative as an active ingredient in topical antiseptics or as topical antibacterial skin treatment products for conditions like acne, seborrheic dermatitis, eczema, and others. In vitro and in vivo studies have demonstrated that resorcinol can inhibit peroxidases in the thyroid and subsequently block the synthesis of thyroid hormones and cause goiter. Resorcinol interferes with the iodination of tyrosine and the oxidation of iodide. In an in vitro study involving lactoperoxidase (LPO) and thyroid peroxidase (TPO), it was shown that the mechanism of these two enzymes can become irreversibly inhibited by way of a suicide inactivation by resorcinol. Data regarding the specific mechanisms of action of resorcinol does not appear to be readily accessible in the literature. Nevertheless, the effectiveness of the agent in treating various topical, dermatological conditions by eliciting antibacterial and keratolytic actions appears to stem from resorcinol's propensity for protein precipitation. In particular, it appears that resorcinol indicated for treating acne, dermatitis, or eczema in various skin care topical applications and peels revolves around the compound's ability to precipitate cutaneous proteins from the treated skin.",The molecular weight is 110.11.,Resorcinol has a topological polar surface area of 40.46.,The log p value of  is 0.81.,Resorcinol is approved.,,True
17346,,,,,2-mercaptobenzothiazole is approved and experimental and vet_approved.,,False
17347,"Neomycin is a broad-spectrum aminoglycoside antibiotic drug that is derived from the metabolic products of _Streptomyces fradiae_. Neomycin is a complex comprised of three components, neomycin A, B, and C. Neomycin B, also known as , is the most active component of the complex and neomycin C is the isomer of neomycin B, making these two stereoisomers the active components of neomycin. Neomycin A, or , is a moiety that conjoins two molecules of neomycin B and C together. Neomycin is active against both gram-positive and gram-negative organisms and mediates its pharmacological action by binding to bacterial ribosomes and inhibiting protein synthesis, which is crucial for the survival of bacteria.  Oral neomycin sulfate is indicated as an adjunctive therapy in hepatic coma (portal-system encephalopathy) by reducing ammonia-forming bacteria in the intestinal tract. It is strongly recommended that oral neomycin is only used in infections that are proven or strongly suspected to be caused by susceptible bacteria to reduce the risk of the development of drug-resistant bacteria. Neomycin mediates its bactericidal action by inhibiting bacterial protein synthesis, thereby suppressing the growth and survival of susceptible bacteria. Following oral administration, the duration of bactericidal activity of neomycin ranged from 48 to 72 hours. By decreasing colonic bacteria that produce ammonia, neomycin was shown to be effective as an adjunctive therapy in hepatic coma to improve neurologic symptoms.  Like other aminoglycoside antibiotic drugs, neomycin inhibits bacterial ribosomes by binding to the 30S ribosomal subunit of susceptible bacteria and disrupting the translational machinery of bacterial protein synthesis. Bacterial translation is normally initiated by the mRNA binding to the 30S ribosomal subunit and subsequent binding with 50S subunit for elongation.",,,,Neomycin is approved and vet_approved.,Neomycin is a solid.,True
17348,"Ronacaleret is a calcium-sensing receptor antagonist. Post-menopausal women with osteoporosis 751689 is novel small molecules that work by antagonizing calcium-sensing receptors on the surface of the parathyroid gland, thereby triggering a transient release of the body's own stores of parathyroid hormone (PTH). This release of PTH may have the potential to rebuild the bone mass lost as a result of osteoporosis and improve overall bone microarchitecture in these patients. ",,,,Ronacaleret is investigational.,Ronacaleret is a solid.,True
17349,"Investigated for use/treatment in osteoporosis. NPS-2143 is the prototype calcilytic drug, designed to act on calcium receptors on the surface of parathyroid glands, stimulating the release of the body's own stores of native parathyroid hormone (PTH).",,,,NPS-2143 is investigational.,NPS-2143 is a solid.,True
17350,"Etelcalcetide is a calcimimetic drug for the treatment of secondary hyperparathyroidism in patients undergoing hemodialysis. Etelcalcetide was approved (trade name Parsabiv) for the treatment of secondary hyperparathyroidism (HPT) in adult patients with chronic kidney disease (CKD) on hemodialysis in February, 2017. Etelcalcetide is a calcium-sensing receptor agonist indicated for:  Following a single intravenous bolus administration of etelcalcetide, PTH levels decreased within 30 minutes post dose. In the single-dose study, the extent and duration of the reduction in PTH increased with increasing dose. Reduction in PTH levels correlated with plasma etelcalcetide concentrations in hemodialysis patients. The reduction in PTH resulted in reductions in calcium and attenuation of post-dialytic phosphate elevation. The effect of reducing PTH levels was maintained throughout the 6-month dosing period when etelcalcetide was administered by intravenous bolus three times a week.  Etelcalcetide is a calcimimetic agent that allosterically modulates the calcium-sensing receptor (CaSR). Etelcalcetide binds to the CaSR and enhances activation of the receptor by extracellular calcium. Activation of the CaSR on parathyroid chief cells decreases PTH secretion.  ",The molecular weight is 1048.26.,Etelcalcetide has a topological polar surface area of 557.71.,The log p value of  is -11.73.,Etelcalcetide is approved and investigational.,,True
17351,"Produced in CHO cell cultures, trastuzumab is a recombinant IgG1 kappa, humanized monoclonal antibody that selectively binds with high affinity in a cell-based assay (Kd = 5 nM) to the extracellular domain of the human epidermal growth factor receptor protein (HER2). It is used as a treatment of human epidermal growth factor receptor (HER)-2+ metastatic breast cancer, where there is a proven amplification of the HER-2 oncogene or over-expression of the HER-2 protein in tumours. It is suggested that the overexpression or gene amplification of HER2 has been found in about 20–30% of breast cancers and elevated activation of HER2 triggers multiple downstream pathways leading to abnormal proliferation of cancer cells. Trastuzumab binds to HER2 and suppresses cancer cells growth, proliferation, and survival directly and indirectly. For the adjuvant treatment of HER2-overexpressing breast cancer, trastuzumab is indicated in several clinical settings: as part of a treatment regimen consisting of doxorubicin, cyclophosphamide, and either paclitaxel or docetaxel; as part of a treatment regimen with docetaxel and carboplatin; or as monotherapy following multi-modality anthracycline-based therapy. Trastuzumab exerts an antitumour activity and is used in the treatment of HER2-positive breast cancer. HER2 protein overexpression is observed in 20%-30% of primary breast cancers thus HER2 presents as a useful therapeutic target for the treatment of breast cancers. Trastuzumab has been shown, in both _in vitro_ assays and in animals, to inhibit the proliferation of human tumour cells that overexpress HER2. It works as a mediator of antibody-dependent cellular cytotoxicity, where it binds as an antibody to cells over-expressing HER2, leading to preferential cell death. Trastuzumab was also shown to inhibit angiogenesis of tumor cells _in vivo_. Higher doses and longer dosing intervals show no significant benefit over standard dose schedules. In patients with HER2 positive solid tumours, trastuzumab did not exert any clinically significant QTc interval duration. Trastuzumab is a recombinant humanized IgG1 monoclonal antibody against the HER-2 receptor, a member of the epidermal growth factor receptors which is a photo-oncogene. Over-expressed in breast tumour cells, HER-2 overamplifies the signal provided by other receptors of the HER family by forming heterodimers. The HER-2 receptor is a transmembrane tyrosine kinase receptor that consists of an extracellular ligand-binding domain, a transmembrane region, and an intracellular or cytoplasmic tyrosine kinase domain. It is activated by the formation of homodimers or heterodimers with other EGFR proteins, leading to dimerization and autophosphorylation and/or transphosphorylation of specific tyrosine residues in EGFR intracellular domains. Further downstream molecular signaling cascades are activated, such as the Ras/Raf/mitogen-activated protein kinase (MAPK), the phosphoinositide 3-kinase/Akt, and the phospholipase Cγ (PLCγ)/protein kinase C (PKC) pathways that promote cell growth and survival and cell cycle progression. Due to upregulation of HER-2 in tumour cells, hyperactivation of these signaling pathways and abnormal cell proliferation is observed. Trastuzumab binds to the extracellular ligand-binding domain and blocks the cleavage of the extracellular domain of HER-2 to induce its antibody-induced receptor downmodulation , and subsequently inhibits HER-2-mediated intracellular signaling cascades. Inhibition of MAPK and PI3K/Akt pathways lead to an increase in cell cycle arrest, and the suppression of cell growth and proliferation. Trastuzumab also mediates the activation of antibody-dependent cell-mediated cytotoxicity (ADCC) by attracting the immune cells, such as natural killer (NK) cells, to tumor sites that overexpress HER-2. While the drug alone has a minimal potential to induce complement-dependent cytotoxicity (CDC), one study demonstrated increased therapeutic effectiveness and a synergistic effect on uterine serous carcinoma cells _in vitro_ when used in combination with , which also has minor effects on CDC alone. This study showed that only the combination of both cell-bound antibodies would be sufficient to bind and activate the complement component 1q (C1q) required to initiate the complement cascade reaction.",,,,Trastuzumab is approved and investigational.,Trastuzumab is a solid.,True
17352,"IGN311 is a humanized monoclonal antibody (mab) against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. Intended for the treatment of various forms of cancer. IGN311 is a fully humanized IgG1 variant 1 of the parent murine IgG3 mab ABL 364. It is an antibody against the Lewis-Y carbohydrate antigen and Igeneon's next-generation antibody, IGN312. IGN311 is a humanized monoclonal antibody against the Lewis Y carbohydrate antigen, a blood-group-related oligosaccharide. Lewis Y is over-expressed in up to 90% of all epithelial cancers and its expression on adult normal tissues is very restricted; hence IGN311 has the potential to target a broad range of carcinomas. IGN311 is designed to exert clinical effects by destruction of tumor cells by activation of effector functions and by selective growth inhibition via functional receptors.",,,,IGN311 is investigational.,IGN311 is a solid.,True
17353,"Varlitinib is an oral, selective, reversible, small molecule tyrosine kinase inhibitor of both ErbB-2 (Her-2/neu) and EGFR. Over-expression of ErbB-2 and EGFR receptors in tumors is predictive of poor prognosis in cancer patients. Varlitinib has shown significant anti-tumor activity in preclinical models of human breast, lung, and epidermal carcinoma tumors. Investigated for use/treatment in cancer/tumors (unspecified). Varlitinib is an orally active, reversible, enzymatic and cellular inhibitor, with nanomolar potency, of the key growth factor receptor tyrosine kinases ErbB-2 and EGFR. The compound possesses improved physiochemical properties relative to compounds directed at these targets currently in clinical development, and provides superior exposure and equivalent or greater efficacy in animal models of human cancer. Currently, there is no single drug on the market that selectively inhibits both ErbB-2 and EGFR. Varlitinib, which concurrently inhibits the molecular targets of the drugs Herceptin(R) (ErbB-2) and Erbitux(R) (EGFR), may provide enhanced efficacy in the treatment of cancer patients.",,,,Varlitinib is investigational.,Varlitinib is a solid.,True
17354,"Investigated for use/treatment in cancer/tumors (unspecified). AV-412 shows potent inhibition of the EGFR L858R mutations and, in two well-established animal models, demonstrated dose-dependant tumor regression in both small and large lung tumors and complete regression of lung tumors at a dose where erlotinib is inactive. AV-412's mechanism of action has the potential to benefit patients with Non-Small Cell Lung Cancer, Metastatic Breast Cancer, Pancreatic Cancer, Head & Neck Cancer and Hormone Refractory Prostate Cancer.",,,,AV-412 is investigational.,AV-412 is a solid.,True
17355,"Pertuzumab is a recombinant humanized monoclonal antibody that targets the extracellular dimerization domain (subdomain II) of the human epidermal growth factor receptor 2 protein (HER2). It consists of two heavy chains and two lights chains that have 448 and 214 residues respectively. It was first approved by the FDA in 2012 for use with and another HER2-targeted monoclonal antibody, , in the treatment of metastatic HER2-positive breast cancer. Its indicated conditions have since expanded to include use as both a neoadjuvant therapy and an adjuvant therapy in the treatment of HER2-positive breast cancers at high risk of recurrence. Pertuzumab is indicated for intravenous administration in combination with and for the treatment of patients with HER2-positive metastatic breast cancer who have not received prior anti-HER2 therapy or chemotherapy for metastatic disease. It is also indicated in combination with trastuzumab and other chemotherapies for the neoadjuvant treatment of HER2-positive locally advanced, inflammatory, or early-stage breast cancer as part of a complete treatment regimen and as adjuvant treatment in patients with HER2-positive early-stage breast cancer at high risk of recurrence. Pertuzumab exerts its antineoplastic effects by binding to and inhibiting the activity of HER2, an oncogene that has been implicated in the formation of numerous cancers. As with other therapeutic monoclonal antibodies, pertuzumab has a relatively long duration of action necessitating dosing every 3 weeks. Drugs that block HER2 activity, including pertuzumab, have been implicated in the development of cardiotoxicity (specifically left ventricular dysfunction) - a baseline assessment of left ventricular ejection fraction (LVEF) should be conducted prior to beginning therapy with pertuzumab and at regular intervals throughout therapy to ensure LVEF remains within normal limits. Consider indefinite suspension of therapy if LVEF declines and does not improve. Human epidermal growth factor receptor-2 (HER2) is a tyrosine kinase receptor that plays an integral role in cell proliferation, differentiation, and survival. HER2 becomes active following dimerization with another HER2 receptor, another member of the HER protein family (e.g. HER3), or with a ligand - this dimer then phosphorylates and activates numerous intracellular signaling proteins, initiating signal transduction via pathways that include the Ras/mitogen-activated protein kinase pathway, the phosphatidylinositol 3' kinase (PI3K)/Akt pathway, and then Janus kinases/signal transducer and activator transcription pathway. HER2 is also a known oncogene - it is overexpressed or gene-amplified (i.e. HER2-positive) in approximately 20% of breast cancers and these cancers carry a generally poorer prognosis than HER2-negative breast cancers.",,,,Pertuzumab is approved.,Pertuzumab is a solid.,True
17356,"Afatinib is a 4-anilinoquinazoline tyrosine kinase inhibitor in the form of a dimaleate salt available as Boehringer Ingelheim's brand name Gilotrif. For oral use, afatinib tablets are a first-line (initial) treatment for patients with metastatic non-small cell lung cancer (NSCLC) with common epidermal growth factor receptor (EGFR) mutations as detected by an FDA-approved test. Gilotrif (afatinib) is the first FDA-approved oncology product from Boehringer Ingelheim. Afatinib is a kinase inhibitor indicated as monotherapy for the first-line treatment of (a) Epidermal Growth Factor Receptor (EGFR) TKI (tyrosine kinase inhibitor)-naive adult patients with locally advanced or metastatic non-small cell lung cancer (NSCLC) whose tumours have non-resistant EGFR mutations as detected by an FDA-approved test , and (b) adult patients with locally advanced or metastatic NSCLC of squamous histology progressing on or after platinum-based chemotherapy. Aberrant ErbB signaling triggered by receptor mutations, and/or amplification, and/or receptor ligand overexpression contributes to the malignant phenotype. Mutation in EGFR defines a distinct molecular subtype of lung cancer. Afatinib is a potent and selective, irreversible ErbB family blocker. Afatinib covalently binds to and irreversibly blocks signaling from all homo and heterodimers formed by the ErbB family members EGFR (ErbB1), HER2 (ErbB2), ErbB3 and ErbB4.",The molecular weight is 485.94.,Afatinib has a topological polar surface area of 88.61.,The log p value of  is 4.34.,Afatinib is approved.,Afatinib is a solid.,True
17357,"Tesevatinib has been used in trials studying the treatment of Cancer, Stomach Cancer, Brain Metastases, Esophageal Cancer, and Leptomeningeal Metastases, among others. Tesevatinib inhibits the EGF, HER2, and VEGF RTKs, each of which is a target of currently approved cancer therapies. In addition, tesevatinib inhibits EphB4, an RTK that is highly expressed in many human tumors and plays a role in promoting angiogenesis. In a broad array of preclinical tumor models including breast, lung, colon and prostate cancer, XL647 demonstrated potent inhibition of tumor growth and causes tumor regression. In cell culture models, tesevatinib retains significant potency against mutant EGFRs that are resistant to current EGFR inhibitors.",,,,Tesevatinib is investigational.,,True
17358,"The HER2 oncoprotein, the product of the human _ERBB2_/mouse _neu_ genes, is a member of the HER family of receptor tyrosine kinases that includes the epidermal growth factor receptor (EGFR). Of the various subtypes of breast cancer, HER2-positive breast cancer is characterized by _ERBB2_ overexpression, a higher grade, a more aggressive phenotype, and a worse prognosis compared to HER2-negative cancer. The introduction of improved patient outcomes in HER2-positive breast cancer, but notably depended substantially on polymorphisms in the FcγRIIIA/CD16A receptor, whereby low affinity 158F CD16A variants are associated with shorter progression-free survival and worse patient outcomes. Margetuximab is an anti-HER2 monoclonal antibody indicated, in combination with chemotherapy, for the treatment of metastatic HER2-positive breast cancer in adult patients who have received two or more prior anti-HER2 regimens with at least one prior regimen for metastatic disease. Margetuximab is a chimeric IgG1κ monoclonal antibody (mAb) directed against the extracellular domain of the human epidermal growth factor receptor 2 (HER2) cell-surface protein. Also, margetuximab has an engineered Fc region that alters its affinity for the CD16A and CD32B effector cell receptors resulting in increased antibody-dependent cell-mediated cytotoxicity (ADCC). To date, the exposure-response and time course pharmacodynamic relationships of margetuximab remain incompletely characterized. Although generally well-tolerated, margetuximab carries a risk of infusion-related reactions, including symptoms such as fever, fatigue, nausea, vomiting, headache, tachycardia, hypotension, and cutaneous manifestations such as a rash or urticaria; infusion reactions may require alterations to the infusion or, in serious reactions, discontinuation. The HER family of transmembrane receptor tyrosine kinases (RTKs) includes the epidermal growth factor receptor (EGFR/HER1), HER2, HER3, and HER4 proteins; HER family members are generally involved in cell proliferation, angiogenesis, cell motility and invasiveness, and resistance to apoptosis. HER2 is an oncoprotein whose overexpression is observed in breast, gastric, and other cancers. HER2 undergoes both ligand-independent homodimerization and ligand-dependent heterodimerization with other HER family members, followed by RTK phosphorylation and induction of downstream oncogenic signalling pathways. EGFR/HER2 dimerization promotes EGFR recycling and prolonged signalling while HER2/HER3 dimerization potently stimulates the downstream PI3K/AKT pathway; HER2 homodimerization directly activates the RAS/MAPK pathway and indirectly activates the PI3K/AKT pathway.",,,,Margetuximab is investigational.,Margetuximab is a liquid.,True
17359,"Humanized IgG1 kappa isotype monoclonal antibody that binds to human CD11a. Efalizumab has a molecular weight of approximately 150 kilodaltons and is produced in a Chinese hamster ovary mammalian cell expression system in a nutrient medium containing the antibiotic gentamicin. For the treatment of adult patients with moderate to severe chronic plaque psoriasis, who are candidates for phototherapy or systemic therapy. Lymphocyte activation and trafficking to skin play a role in the pathophysiology of chronic plaque psoriasis. In psoriatic skin, ICAM-1 cell surface expression is upregulated on endothelium and keratinocytes. Raptiva inhibits the binding of LFA-1 to the intercellular adhesion molecule-1 (ICAM-1), thereby inhibiting the adhesion of leukocytes to other cell types. Efalizumab binds to CD11a, a subunit of leukocyte function antigen-1 (LFA-1), which is expressed on all leukocytes. As a result efalizumab decreases cell surface expression of CD11a.",,,,Efalizumab is approved and investigational.,Efalizumab is a liquid.,True
17360,"Rabbit anti-thymocyte globulin. Thymoglobulin is a polyclonal antibody that suppresses certain types of immune cells responsible for acute organ rejection in transplant patients. Thymoglobulin is a mixture of antibodies intended to bind to various cell surface antigens. The most common mode of action of Thymoglobulin is via selective depletion of T-cells. For prevention of renal transplant rejection Antithymocyte Globulin (ATG) is a concentrated anti-human T-lymphocyte immunoglobulin preparation derived from rabbits after immunization with a T-lympoblast cell line. ATG is an immunosuppressive product for the prevention and treatment of acute rejection following organ transplantation. ATG reduces the host immune response against tissue transplants or organ allografts. Binds to multiple, T-cell specific antigens leading to T-lymphocyte cell death via complement mediated cytotoxicity or apoptosis.",,,,Antithymocyte immunoglobulin (rabbit) is approved.,Antithymocyte immunoglobulin (rabbit) is a liquid.,True
17361,,,,,1-Acetyl-4-(4-{4--3-Nitrophenyl}Pyridin-2-Yl)Piperazine is experimental.,1-Acetyl-4-(4-{4--3-Nitrophenyl}Pyridin-2-Yl)Piperazine is a solid.,False
17362,,,,,LFA703 is experimental.,LFA703 is a solid.,False
17363,,,,,"(S)-2-((S)-3-isobutyl-2,5-dioxo-4-quinolin-3-ylmethyl-diazepan-1yl)-N-methyl-3-naphtalen-2-yl-propionamide is experimental.","(S)-2-((S)-3-isobutyl-2,5-dioxo-4-quinolin-3-ylmethyl-diazepan-1yl)-N-methyl-3-naphtalen-2-yl-propionamide is a solid.",False
17364,,,,,"7A--6-(3,5-dichlorophenyl)-5-oxo-2,3,5,7A-tetrahydro-1H-pyrrolopyrrole-7-carbonitrile is experimental.","7A--6-(3,5-dichlorophenyl)-5-oxo-2,3,5,7A-tetrahydro-1H-pyrrolopyrrole-7-carbonitrile is a solid.",False
17365,,,,,"3-({4--2,3-bis(trifluoromethyl)phenyl}sulfanyl)aniline is experimental.","3-({4--2,3-bis(trifluoromethyl)phenyl}sulfanyl)aniline is a solid.",False
17366,,,,,N'-(5-CHLOROBENZOFURAN-2-CARBONYL)-2-(TRIFLUOROMETHYL)BENZENESULFONOHYDRAZIDE is experimental.,N'-(5-CHLOROBENZOFURAN-2-CARBONYL)-2-(TRIFLUOROMETHYL)BENZENESULFONOHYDRAZIDE is a solid.,False
17367,,,,,Argininosuccinate is experimental.,Argininosuccinate is a solid.,False
17368,"Darusentan is a selective endothelin ETA receptor antagonist. It is being evaluated as a treatment for congestive heart failure and hypertension. For the treatment of congestive heart failure and hypertension. Darusentan is a selective endothelin ETA receptor antagonist. The mode of action by which the endothelin receptor antagonists cause a decrease of the BP is not yet totally elucidated; however, peripheral vasodilatation due to blockade of the vasoconstrictor effects of endothelin is the most likely explanation. A reduction of cardiac contractility is considered unlikely. Several studies have been published that investigated the effects of either selective or nonselective endothelin receptor blockade in patients with heart failure. In these studies, application of endothelin antagonists, while decreasing both systemic and pulmonary BP increased cardiac index and did not alter cardiac contractility or heart rate.",,,,Darusentan is investigational.,Darusentan is a solid.,True
17369,SPP301 (Avosentan) is a potent and highly selective ET receptor blocker and is clinically investigated in diabetic nephropathy. This study was designed to evaluate whether avosentan influences the pharmacokinetics of steroid oral contraceptives. Investigated for use/treatment in cardiovascular disorders and neuropathy (diabetic). Avosentan has effect on the concentration levels of ethinylestradiol and progesterone. That’s why it is possible that the contraceptive efficacy of low-dose combination oral contraceptives may be adversely affected during avosentan treatment.,,,,SPP 301 is investigational.,SPP 301 is a solid.,True
17370,"Actelion-1 is a tissue-targeting Endothelin Receptor Antagonist that has been discovered by Actelion Pharmaceuticals. Investigated for use/treatment in cardiovascular disorders, hypertension, and pulmonary hypertension. Through complete blockade of tissular endothelin, Actelion-1 is expected to protect tissue from the damaging effect of elevated endothelin, specifically in the cardiovascular system. In pre-clinical studies, Actelion-1 also exhibited effects suggesting that it maintains the integrity of the vascular wall and improves long-term outcome. Accordingly, Actelion-1 may provide therapeutic benefit in a wide range of cardiovascular indications.",,,,Actelion-1 is investigational.,Actelion-1 is a solid.,True
17371,"Atrasentan is a substance that is being studied in the treatment of cancer. It belongs to the family of drugs called endothelin-1 protein receptor antagonists. It is a novel, selective endothelin A receptor antagonist (SERA). Investigated for use/treatment in prostate cancer and cancer/tumors (unspecified).",,,,Atrasentan is investigational.,Atrasentan is a solid.,True
17372,Investigated for use/treatment in strokes.,,,,Clazosentan is investigational.,Clazosentan is a solid.,True
17373,"Sparsentan has been used in trials studying the treatment of Focal Segmental Glomerulosclerosis. Sparsentan is the first and only dual-acting angiotensin and endothelin receptor antagonist (DARA) in development. Sparsentan, which possesses two clinically validated mechanisms of action in a single molecule, works by selectively blocking the action of two potent vasoconstrictor and mitogenic agents, angiotensin II (AII) and endothelin 1 (ET1), at their respective receptors. Sparsentan is highly selective (10,000-fold) for the AII receptor sub-type 1 and the ET receptor sub-type A. As such, Sparsentan combines the properties of an angiotensin receptor blocker (ARB) and an endothelin receptor antagonist (ERA) in the same molecule.",,,,Sparsentan is investigational.,,True
17374,"Glucagon is a 29 amino acid hormone used as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia. Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose. Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and to treat severe hypoglycemia. Glucagon is indicated as a diagnostic aid in radiologic exams to temporarily inhibit the movement of the gastrointestinal tract and severe hypoglycemia. Glucagon raises blood sugar through activation of hepatic glucagon receptors, stimulating glycogenolysis and the release of glucose. Glucagon has a short duration of action. Glucagon may cause hyperglycemia in diabetic patients. Glucagon binds to the glucagon receptor activating G<sub>s</sub>α and G<sub>q</sub>. This activation activates adenylate cyclase, which increases intracellular cyclic AMP and activates protein kinase A. Activating G<sub>q</sub> activates phospholipase C, increases production of inositol 1,4,5-triphosphate, and releases intracellular calcium. Protein kinase A phosphorylates glycogen phosphorylase kinase, which phosphorylates glycogen phosphorylase, which phosphorylates glycogen, causing its breakdown.",,,,Glucagon is approved.,Glucagon is a liquid.,True
17375,,,,,Maleic Acid is experimental.,Maleic Acid is a solid.,False
17376,"Cefotaxime is a third-generation cephalosporin antibiotic. Like other third-generation cephalosporins, it has broad spectrum activity against Gram positive and Gram negative bacteria. In most cases, it is considered to be equivalent to ceftriaxone in terms of safety and efficacy. Cefotaxime sodium is marketed under various trade names including Claforan (Sanofi-Aventis). Used to treat gonorrhoea, meningitis, and severe infections including infections of the kidney (pyelonephritis) and urinary system. Also used before an operation to prevent infection after surgery. Cefotaxime is a third generation intravenous cephalosporin antibiotic. It has broad spectrum activity against Gram positive and Gram negative bacteria. It does not have activity against <i>Pseudomonas aeruginosa</i>. Cefotaxime works by inhibiting bacterial cell wall biosynthesis. A positive feature of cefotaxime is that it display a resistance to penicillinases and is useful to treat infections that are resistant to penicillin derivatives. The bactericidal activity of cefotaxime results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs). Cefotaxime shows high affinity for penicillin-binding proteins in the cell wall including PBP Ib and PBP III.",The molecular weight is 455.46.,Cefotaxime has a topological polar surface area of 173.51.,The log p value of  is 0.14.,Cefotaxime is approved.,Cefotaxime is a solid.,True
17377,"Phenol is an antiseptic and disinfectant. It is active against a wide range of micro-organisms including some fungi and viruses, but is only slowly effective against spores. Phenol has been used to disinfect skin and to relieve itching. Phenol is also used as an oral analgesic or anesthetic in products such as Chloraseptic to treat pharyngitis. Additionally, phenol and its related compounds are used in surgical ingrown toenail treatment, a process termed phenolization. Research indicates that parental exposure to phenol and its related compounds are positively associated with spontaneous abortion. During the second world war, phenol injections were used as a means of execution by the Nazis. Phenol is a toxic compound whose vapours are corrosive to the skin, eyes, and respiratory tract. Phenol is primarily indicated for minor sore throat pain, sore mouth, minor mouth irritation, and pain associated with canker sores. Additionally, phenol is indicated in the treatment of focal spasticity.  Phenol is a potent proteolytic agent. Concentrations in the 5% to 7% range dissolve tissue on contact via proteolysis. In high concentrations when injected next to a nerve, phenol produces a chemical neurolysis which is nonselective across nerve fiber size and most prominent on its outer aspect. Local anesthetic effects occur within 5-10 minutes. ",The molecular weight is 94.11.,Phenol has a topological polar surface area of 20.23.,The log p value of  is 1.47.,Phenol is approved and experimental.,Phenol is a solid.,True
17378,"Guaiacol is an agent thought to have disinfectant properties and used as an expectorant. Guaiacol is a phenolic natural product first isolated from Guaiac resin and the oxidation of lignin. Guaiacol is also present in wood smoke, as a product of pyrolysis of lignin. Guaiacol has been found in the urine of patients with neuroblastoma and pheochromocytoma. It is used medicinally as an expectorant, antiseptic, and local anesthetic. Guaiacol is used in traditional dental pulp sedation, and has the property of inducing cell proliferation; guaiacol is a potent scavenger of reactive oxygen radicals and its radical scavenging activity may be associated with its effect on cell proliferation. ",The molecular weight is 124.14.,Guaiacol has a topological polar surface area of 29.46.,The log p value of  is 1.32.,Guaiacol is approved.,,True
17379,"Silver (Ag) is a chemical element that belongs in the family of transition metals in the periodic table. It has a high electrical conductivity, thermal conductivity, and reflectivity. Silver exists as a pure elemental form, alloy with other metals, and mineral. Having critical roles in various applications inducing chemical and industrial fields, silver compounds have also been used in the field of medicine for centuries due to their broad-spectrum biological actions. Silver nanoparticles especially have been widely used in industrial, household, and healthcare-related products due to their potent antimicrobial activity. and have been used as topical antibacterial agents for the treatment of skin infections, while has also been valued for topical burn treatment. Silver and its compounds have been used in trials studying the management of dental caries since the 1800s, and they may be found in dental pastes as an active ingredients. However, some drawbacks of dental use of silver compounds include tooth discolouration and pulp irritation. Indicated for the treatment of acne for topical use or the management of dental caries for dental use.  Silver exhibits a broad-spectrum antimicrobial activity. Silver ions were shown to mediate an effective antibacterial action against _Streptococcus mutans_, one of major bacteria present in the human oral cavity and one of etiological microorganism of dental caries. A study reported a dose-dependent antimicrobial activity of silver nanoparticles against MRSA and non-MRSA bacteria. Silver nanoparticles were also shown to mediate antibacterial activity against Gram-positive _S. aureus_ and Gram-negative _E. coli_ by inhibiting the growth.  The majority of released silver ions precipitate with chloride or phosphate anions or bind to albumins, macroglobulins, or tissue debris. While bound silver ions do not exert antibacterial actions, they may potentially play a role in silver toxicity in case of chronic exposure. Silver ions mediate antibacterial effects via disrupting the bacterial, fungal, and protozoal cell membranes; they bind to disulphide in membrane proteins, readily allowing penetration through the membranes and intracellular absorption via pinocytosis. They may also bind to negatively-charged peptidoglycans in the cell wall via electrostatic interactions, leading to disruption of membrane transport function and loss of structural integrity. Silver ions also bind to and oxidize sulphydryl groups (SH) in bacterial cytoplasmic enzymes to aberrate their function in metabolic processes. Silver nanoparticles may cause an increase in reactive oxygen species (ROS) inside the microbial cells leading to metal-induced oxidative stress and cell damage. They also modulate cellular signal system via inhibition of phosphorylation of essential bacterial proteins to eventually cause cell death. It is also reported that silver ions also attach to guanine in bacterial DNA, which inhibits DNA replication. While it is not fully understood, the mode of action of silver compounds in preventing and arresting dental caries is thought to involve inhibition of the demineralization process in addition to cytoplasmic and membrane function perturbation mentioned above. Silver compounds may directly interact with hydroxyapatite, a major tooth component.",,,,Silver is approved and investigational.,Silver is a solid.,True
17380,"Patent blue is aniline dye and it is one of the most common dyes used. It is a sodium or calcium salt of diethylammonium hydroxide inner salt. It has the chemical designation of (4-(alpha-(p-(diethylamino)phenyl)-2,4-disulfobenzylidene)-2,5-cyclohexadiene-1-ylidene)diethylammonium hydroxide. Patent blue was developed by Guerbet and approved by Health Canada on December 31, 1979. The isomer isosulphan is used in the United States for the same indications than patent blue. Patent blue is used for marking lymphatic vessels and arterial territories as well as for sentinel lymph node prior to biopsy in patients with operable breast cancer and clinically negative lymph nodes in combination with a radiotracer. Administration of patent blue has been reported to cause hypersensitivity reactions in approximately 1% of the patients. It also presents a localized blue coloration which has made patent blue a sensitive and specific option for the detection of micrometastatic cancer in lymph nodes. The specific binding of patent blue allows it to freely travel in the breast lymphatics and allows staging with a less invasive alternative. Patent blue will form a complex with albumin which will be picked up by regional afferent lymphatics to identify sentinel lymph nodes. A sentinel lymph node is the first lymph node in a chain or group of lymph nodes that cancer is most likely to spread to. The determination of the sentinel lymph node allows the physician to stage cancer by observing if cancer has spread to the near lymph nodes.",,,,Patent Blue is approved.,Patent Blue is a solid.,True
17381,m-Chlorophenylpiperazine has been used in trials studying the treatment of Alcoholism.,,,,m-Chlorophenylpiperazine is investigational.,,True
17382,"Alfimeprase is a recombinant analog of fibrolase. Fibrolase is a zinc-containing metalloproteinase isolated from the venom of the southern copperhead snake (<i>Agkistrodon contortrix contortrix</i>). It is a small protein that contains 203 residues (Randolph et al. 1992). Alfimeprase is being developed by Nuvelo. Alfimeprase is being evaluated as a potential treatment for acute ischemic stroke, catheter occlusion (CO) and acute peripheral arterial occlusion (PAO). Alfimeprase is a recombinant direct acting fibrinolytic (rDAF), or blood clot dissolver, that has the potential to rapidly and directly degrade fibrin, a protein that provides the scaffolding for blood clots, when delivered through a catheter to the site of a blood clot. When delivered locally at the site of a blood clot, alfimeprase has the potential, through a unique mechanism of action, to directly and rapidly degrade fibrin, a protein that provides the scaffolding for blood clots. In addition, alfimeprase's thrombolytic activity appears to be localized to the site of delivery because it is rapidly inactivated by alpha-2 macroglobulin, a naturally occurring protein in the blood, as it moves away from the site of delivery and into the general blood circulation.",,,,Alfimeprase is investigational.,Alfimeprase is a liquid.,True
17383,"Ancrod, marketed as Viprinex, is a defibrinogenating agent derived from Malayan pit viper venom. The defribrinogenation of blood results in an anticoagulant effect. Currently, Viprinex®/ancrod is not approved or marketed in any country, but is being investigated as a stroke treatment in worldwide clinical trials. In January 2005, the U.S. FDA granted a 'fast-track status' for investigation of ancrod use in patients suffering from acute ischemic stroke, a life threatening condition caused by the blockage of blood vessels supplying blood and oxygen to portions of the brain, for which phase III trials are currently being conducted. Ancrod is indicated for the treatment of deep vein thrombosis (DVT), central retinal branch vein thrombosis, pripaism, pulmonary hypertension of embolic origin, embolism after insertion of prosthetic cardiac valves, rethrombosis after thrombolytic therapy, rethrombosis after vascular surgery, and prevention of DVT after repair of a fractured neck of a femur. The decreased viscosity is directly attributable to lowered fibrinogen levels and leads to important improvements in blood flow and perfusion of the microcirculation. Ancrod decreases the blood viscosity in affected arteries, leads to less intense pain, improves physical limb mobility, facilitates physical and ergo therapy, and decreases the likelihood of local thrombotic events. Ancrod's anticoagulant effects are through the rapid removal of fibrinogen from the blood within hours following ancrod administration. Ancrod specifically cleaves only the alpha chain of fibrinogen, producing the characteristic fibrinopeptides A, AP and AY, not the B-fibrinopeptide. The resulting fibrin polymers are imperfectly formed and much smaller in size (1 to 2 µm long) than the fibrin polymers produced by the action of thrombin. These ancrod-induced microthrombi are friable, unstable, urea-soluble and have significantly degraded a-chains. They do not cross-link to form thrombi. They are markedly susceptible to digestion by plasmin and are rapidly removed from circulation by either reticuloendothelial phagocytosis or normal fibrinolysis, or both. Blood viscosity is reduced by 30-40%.",,,,Ancrod is approved and investigational.,Ancrod is a solid.,True
17384,"EP-2104R is an imaging pharmaceutical under development for the detection of blood clots. It is the first targeted high-resolution technique designed to visualize blood clots directly. It is being developed by EPIX Pharmaceuticals, Inc. Investigated for use/treatment in cardiovascular disorders and thrombosis. EP-2104R is a gadolinium-based small peptide with high affinity and specificity for human fibrin. Molecular MR imaging with the fibrin-targeted contrast-agent EP-2104R allows selective visualization of acute coronary, cardiac, and pulmonary thrombi. EP-2104R binds specifically to fibrin, a protein present in all blood clots. When bound, it can be detected using a magnetic resonance imaging (MRI) scan.",,,,EP-2104R is investigational.,EP-2104R is a solid.,True
17385,,,,,Adenosine-5-Diphosphoribose is experimental.,Adenosine-5-Diphosphoribose is a solid.,False
17386,,,,,Thionicotinamide-Adenine-Dinucleotide is experimental.,Thionicotinamide-Adenine-Dinucleotide is a solid.,False
17387,,,,,4-(2-Aminoethyl)Benzenesulfonyl Fluoride is experimental.,4-(2-Aminoethyl)Benzenesulfonyl Fluoride is a solid.,False
17388,"Dequalinium is a quaternary ammonium cation that contains two quaternary quinolinium units linked by an N-decylene chain. It is an antiseptic and disinfectant agent with a broad bactericidal and fungicidal activity. It is most commonly available as a dichloride salt but is available as other various salts as well. It is used in wound dressings and mouth infections and may also have antifungal action, but may associate with skin ulceration. Dequalinium chloride is used as an active ingredient in tablets as Fluomizin for vaginal bacterial infections and in topical bacteriostat formulation as Dequadin. It has been studied for use in treatment of malaria and acute promyelocytic leukemia. Its multiple mode of action is thought to reduce the risk of resistance of pathogens. Effective local treatment as vaginal tablets for infections such as fluor vaginalis, bacterial vaginosis, aerobic vaginitis, vulvo-vaginal candidiasis and trichomoniasis. Used as a topical antimicrobial agent.  Dequalinium is an antimicrobial against Gram negative and positive bacteria, yeast and protozoa. It primarily mediates this action by increasing the cell permeability with subsequent loss of enzyme activity under a rapid bactericidal and fungicidal action. The enzymatic inactivation initially might be reversible but becomes irreversible after a longer contact time between the drug and bacteria. The bactericidal and fungicidal effect of dequalinium chloride has been demonstrated to occur within 30–60 min. Dequalinium targets a broad spectrum of microorganisms including aerobic and anaerobic bacteria, as well as Candida species.  Dequalinium has a multiple mode of action. It disrupts the cell permeability of the bacteria by absorbing onto the bacterial cell surface and diffusing across the membrane. It also binds to the cytoplasmic membrane with subsequent formation of complexes and protein precipitation and lyses the membrane in adequate concentrations, perturbing osmotic exchange. Loss of normal enzymatic activity is achieved through several different processes. Denaturation of proteins results in inhibition of bacterial cell metabolism. Disruption of bacterial energy production is mediated through inhibition of glucose metabolism and inhibition of mitochondrial ATP synthesis via inhibition of bacterial F1-ATPase. Protein synthesis is also terminated at the level of ribosomes. Bacterial nucleic acids are also affected through direct binding of the drug to DNA in vitro, and precipitation of cytoplasmic material with nucleic acids being the most sensitive. ",The molecular weight is 456.68.,Dequalinium has a topological polar surface area of 59.8.,The log p value of  is -2.95.,Dequalinium is approved and investigational.,Dequalinium is a solid.,True
17389,"A vasodilator with general properties similar to nitroglycerin. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1020) For the prevention of angina. Erythrityl Tetranitrate is a vasodilator with general properties similar to nitroglycerin. Similar to other nitrites and organic nitrates, erythrityl tetranitrate is converted to an active intermediate compound which activates the enzyme guanylate cyclase. This stimulates the synthesis of cyclic guanosine 3',5'-monophosphate (cGMP) which then activates a series of protein kinase-dependent phosphorylations in the smooth muscle cells, eventually resulting in the dephosphorylation of the myosin light chain of the smooth muscle fiber. The subsequent release of calcium ions results in the relaxation of the smooth muscle cells and vasodilation.",The molecular weight is 302.11.,Erythrityl tetranitrate has a topological polar surface area of 220.2.,The log p value of  is -7.46.,Erythrityl tetranitrate is approved and experimental and investigational.,Erythrityl tetranitrate is a solid.,True
17390,"Nesiritide is a medication used to treat acutely decompensated congestive heart failure with dyspnea at rest or with minimal exertion (such as talk, eating or bathing). Nesiritide is a 32 amino acid recombinant human B-type natriuretic peptide. For the intravenous treatment of patients with acutely decompensated congestive heart failure who have dyspnea at rest or with minimal activity. Nesiritide works by facilitating cardiovascular homeostasis through the negative regulation of the renin-angiotensin-aldosterone system. This regulation will in order stimulate cyclic guanosine monophosphate and smooth muscle cell relaxation. In simpler terms, it promotes vasodilation, natriuresis, and diuresis. Human BNP binds to the particulate guanylate cyclase receptor of vascular smooth muscle and endothelial cells, leading to increased intracellular concentrations of guanosine 3'5'-cyclic monophosphate (cGMP) and smooth muscle cell relaxation. Cyclic GMP serves as a second messenger to dilate veins and arteries. Nesiritide has been shown to relax isolated human arterial and venous tissue preparations that were precontracted with either endothelin-1 or the alpha-adrenergic agonist, phenylephrine. In human studies, nesiritide produced dose-dependent reductions in pulmonary capillary wedge pressure (PCWP) and systemic arterial pressure in patients with heart failure. In animals, nesiritide had no effects on cardiac contractility or on measures of cardiac electrophysiology such as atrial and ventricular effective refractory times or atrioventricular node conduction. Naturally occurring atrial natriuretic peptide (ANP), a related peptide, increases vascular permeability in animals and humans and may reduce intravascular volume. The effect of nesiritide on vascular permeability has not been studied.",The molecular weight is 3464.07.,Nesiritide has a topological polar surface area of 1512.74.,The log p value of  is 0.0.,Nesiritide is approved and investigational.,Nesiritide is a solid.,True
17391,"Ularitide is a synthetic form of urodilatin, a naturally occurring human natriuretic peptide that is involved in regulating blood pressure and the excretion of water and sodium from the kidneys. Urodilatin is produced in the kidney and excreted into the urine, and thus exists in low levels naturally in the systemic blood circulation. When injected into the blood, ularitide appears to cause diuresis (urine output) and natriuresis (sodium excretion), as well as vasodilation.  Investigated for use/treatment in congestive heart failure. Ularitide, a synthetic form of urodilatin, belongs to the family of natriuretic peptides. Urodilatin stimulates the intracellular guanylyl cyclase as the intracellular domain of the natriuretic peptide receptor A (NPR-A), the enzyme that catalyzes the conversion of GTP to cGMP. Activation of cGMP-dependent protein kinase inhibits sodium reabsorption via an amiloride-sensitive channel and furthermore results in smooth muscle relaxation via a decrease in intracellular Ca2+ concentration. Thus, ularitide is an intrarenal paracrine regulator of sodium and water homeostasis.",,,,Ularitide is investigational.,Ularitide is a solid.,True
17392,"Tanaproget (NSP-989) is an investigational non-steroidal progestin. It is a high affinity, high efficacy agonist of the progesterone receptor (PR) with a much more selective binding profile relative to most conventional progestins. Because of this tanaproget may prove to produce fewer side effects in comparison. It is currently in the process of being developed for clinical use as a contraceptive by Ligand Pharmaceuticals. An analog of tanaproget, 4-fluoropropyltanaproget (18F), has been developed as a radiotracer for imaging of the PR in positron emission tomography.",,,,Tanaproget is investigational.,Tanaproget is a solid.,True
17393,"Telapristone acetate, an orally-available, selective progesterone receptor modulator, is in development to alleviate symptoms associated with both uterine fibroids and endometriosis. For the treatment of uterine fibroids and endometriosis. Patients receiving Proellex saw improvements in key symptoms associated with uterine fibroids, namely reduced pain and bleeding, as well as effects on bone retention. Proellex selectively blocks the progesterone receptor thus avoiding the adverse effects of GnRH agonists associated with the induction of a low estrogen, menopausal-like state in women.",,,,Telapristone acetate is investigational.,Telapristone acetate is a solid.,True
17394,Asoprisnil (J867) is a selective progesterone receptor modulator. It can be used to treat progesterone sensitive myomata. Investigated for use/treatment in uterine fibroids.,,,,Asoprisnil is investigational.,Asoprisnil is a solid.,True
17395,"Cryptenamine is a mixture of closely related hypotensive alkaloids from Veratrum album (Liliaceae). It has been used in the treatment of hypertension but has largely been replaced by drugs with fewer adverse effects. Cryptenamine has a marked and re-producible depressor effect when given intravenously to hypertensive patients, however the mechanism of action is not known. For the treatment of hypertension. Cryptenamine is a mixture of closely related hypotensive alkaloids from <i>Veratrum album</i> (Liliaceae). It has been used in the treatment of hypertension but has largely been replaced by drugs with fewer adverse effects. Cryptenamine has a marked and re-producible depressor effect when given intravenously to hypertensive patients, however the mechanism of action is not known. Some evidence has suggested that cryptenamine acts in a similar fashion to atropine, which lowers the \rest and digest\"" activity of all muscles and glands regulated by the parasympathetic nervous system. This occurs because atropine is a competitive inhibitor of the muscarinic acetylcholine receptors (acetylcholine is the neurotransmitter used by the parasympathetic nervous system). Therefore muscarinic acetylcholine receptors will be listed as experimental targets for cryptenamine.""",,,,Cryptenamine is approved.,Cryptenamine is a solid.,True
17396,"Dimethyltubocurarinium (INN) or metocurine (USAN), also known as dimethyltubocurarine, is a non-depolarizing muscle relaxant. Patients on chronic anticonvulsant drugs are relatively resistant to metocurine.  Metocurine is a muscle relaxant. Metocurine antagonizes the neurotransmitter action of acetylcholine by binding competitively with cholinergic receptor sites on the motor end-plate. This antagonism is inhibited, and neuromuscular block reversed, by acetylcholinesterase inhibitors such as neostigmine, edrophonium, and pyridostigmine.",The molecular weight is 652.83.,Metocurine has a topological polar surface area of 55.38.,The log p value of  is 1.12.,Metocurine is approved.,Metocurine is a solid.,True
17397,"Rapacuronium was withdrawn in 2001 in many countries due to risk of fatal bronchospasm. Used in anaesthesia, to aid and enable endotracheal intubation. Rapacuronium is a rapidly acting, non-depolarizing neuromuscular blocker.",,,,Rapacuronium is approved and withdrawn.,Rapacuronium is a solid.,True
17398,"Anakinra is a recombinant, nonglycosylated human interleukin-1 receptor antagonist (IL-1Ra). The difference between anakinra and the native human IL-1Ra is that anakinra has an extra methionine residue at the amino terminus. It is manufactured by using the E. coli expression system. Anakinra is composed of 153 amino acid residues. FDA approved on November 14, 2001. For the treatment of adult rheumatoid arthritis and treatment of Neonatal-Onset Multisystem Inflammatory Disease (NOMID).  Used to treat rheumatoid arthritis, Anakinra blocks the biologic activity of IL-1 by competitively inhibiting IL-1 binding to the interleukin-1 type I receptor (IL-1RI), which is expressed in a wide variety of tissues and organs. IL-1 production is induced in response to inflammatory stimuli and mediates various physiologic responses including inflammatory and immunological responses. Patients with rheumatoid arthritis have elevated levels of IL-1. The levels of the naturally occurring IL-1Ra in synovium and synovial fluid from rheumatoid arthritis (RA) patients are not sufficient to compete with the elevated amount of locally produced IL-1. Increasing the levels of IL-1Ra by artificial means reduces the negative effects (cartilage degradation, bone resorption) of IL-1. Anakinra binds competitively to the Interleukin-1 type I receptor (IL-1RI), thereby inhibiting the action of elevated levels IL-1 which normally can lead to cartilage degradation and bone resorption.",The molecular weight is 17257.66.,Anakinra has a topological polar surface area of 7115.02.,,Anakinra is approved.,Anakinra is a liquid.,True
17399,"SD118 was previously under investigation in Japan for a different indication and now, following re-profiling and evaluation in experimental animal models, has demonstrated its potential as a new oral therapy for neuropathic pain. Central Nervous System - Neuropathic pain  Immune system modulator",,,,SD118 is investigational.,SD118 is a solid.,True
17400,"OMS103HP is the first drug being developed to improve joint function following arthroscopic surgery, one of the most common procedures performed today by orthopedic surgeons. Investigated for use/treatment in inflammatory disorders (unspecified), knee replacement, orthopedic surgery, and pain (acute or chronic). OMS-103HP is used to inhibit inflammation and pain associated with arthroscopy, provided statistically significant improvement in postoperative pain reduction, joint motion and recovery of function. It is a unique product that is added to standard irrigation solutions and perfused through the joint during arthroscopic surgery.",,,,OMS-103HP is investigational.,OMS-103HP is a solid.,True
17401,,,,,MDL72527 is experimental.,MDL72527 is a solid.,False
17402,,,,,Glycocyamine is experimental.,Glycocyamine is a solid.,False
17403,"Capromab is a Murine IgG1 monoclonal 7E11-C5.3 antibody that recognizes prostate specific membrane antigen (PSMA – also known as glutamate carboxypeptidase 2) from prostate cancer cells and normal prostate tissue. When linked to pendetide, capromab is used as a chelating agent for the radionuclide during imaging to evaluate the extent of prostate cancer. For diagnosis of prostate cancer and detection of intra-pelvic metastases. Binds to the prostate-specific membrane antigen, which is a cell surface protein generally overexpressed in prostate tissues and prostate cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of PSMA expressing cells and tumors. Binds selectively to cell-surface prostate-specific membrane antigen (PSMA) expressed on prostate tissues and tumors.",,,,Capromab pendetide is approved.,Capromab pendetide is a liquid.,True
17404,,,,,(2S)-2-{METHYL}PENTANEDIOIC ACID is experimental.,(2S)-2-{METHYL}PENTANEDIOIC ACID is a solid.,False
17405,,,,,DCFBC is experimental.,DCFBC is a solid.,False
17406,"Spaglumic acid is the β-aspartyl isoform of N-Acetyl-l-aspartylglutamate (isospaglumic Acid is N-(N-Acetyl-l-α-aspartyl)-l-glutamic acid). In eye drops, spaglumic acid is either a magnesium or sodium salt of N-Acetyl-l-aspartylglutamate. Spaglumic acid is a mast cell stabilizer. Thus it is used in allergic conditions such as allergic conjunctivitis. Specifically spaglumic acid is approved in Portugal under the brand name Naabak and in Greece under the brand name Naaxia for use in patients with allergic conjunctivitis. Used in patients with allergic conjunctivitis. Spaglumic acid is a mast cell stabilizer. Mast cells are involved in producing an allergic response by releasing inflammatory mediators such as histamine. Mast cell stablizers block the release of histamine and other mediators by inhibiting mast cell degranulation, which is the process of releasing these mediators. Inhibition occurs through inhibition of specific calcium channels to stabilize the mast cell and prevent degranulation. ",The molecular weight is 304.26.,Spaglumic Acid has a topological polar surface area of 170.1.,The log p value of  is -2.11.,Spaglumic Acid is experimental.,Spaglumic Acid is a solid.,True
17407,"Pravastatin is the 6-alpha-hydroxy acid form of. Pravastatin was firstly approved in 1991 becoming the second available statin in the United States. It was the first statin administered as the active form and not as a prodrug. This drug was developed by Sankyo Co. Ltd.; however, the first approved pravastatin product was developed by Bristol Myers Squibb and FDA approved in 1991. Pravastatin is indicated for primary prevention of coronary events hypercholesterolemic patients without clinical evidence of coronary heart disease. Its use includes the reduction of risk on myocardial infarction, undergoing myocardial revascularization procedures and cardiovascular mortality. The action of pravastatin on the 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase produces an increase in the expression of hepatic LDL receptors which in order decreases the plasma levels of LDL cholesterol. Pravastatin is a specific inhibitor of the hepatic HMG-CoA reductase in humans. The inhibition of this enzyme produces a reduction in cholesterol biosynthesis as HMG-CoA reductase activity is an early-limiting step in cholesterol biosynthesis.",The molecular weight is 424.53.,Pravastatin has a topological polar surface area of 124.29.,The log p value of  is 2.05.,Pravastatin is approved.,Pravastatin is a solid.,True
17408,,,,,(S)-Hmg-Coa is experimental.,(S)-Hmg-Coa is a solid.,False
17409,"An antilipemic agent which lowers cholesterol, triglycerides, serum beta-lipoproteins and phospholipids. It acts by interfering with the enzymatic steps involved in the conversion of acetate to hydroxymethylglutaryl coenzyme A as well as inhibiting the activity of HYDROXYMETHYLGLUTARYL COA REDUCTASES which is the rate limiting enzyme in the biosynthesis of cholesterol.",The molecular weight is 162.14.,Meglutol has a topological polar surface area of 94.83.,The log p value of  is -0.95.,Meglutol is experimental.,Meglutol is a solid.,True
17410,"TAK-475 is a \squalene synthase inhibitor\"", a type of cholesterol-lowering drug that has not yet been brought to market. "" Investigated for use/treatment in hyperlipidemia. Squalene synthase inhibitors are believed to have potential advantages over statins, which inhibit 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase. HMG-CoA catalyzes the conversion of HMG-CoA to mevalonate and thus serves as the primary rate-limiting enzyme in the hepatic biosynthesis of cholesterol. Squalene synthase acts downstream of mevalonate, catalyzing the dimerization of farnesyl-pyrophosphate to squalene. This is the first step in the cholesterol biosynthetic pathway that is solely committed to the production of cholesterol, and researchers believe that blockade at this site may avoid the effects associated with decreased formation of isoprenolated intermediates and metabolites in the pathway beyond HMG-CoA reductase.",,,,TAK-475 is investigational.,TAK-475 is a solid.,True
17411,"Naftifine is a synthetic, broad spectrum, antifungal agent and allylamine derivative for the topical treatment of tinea pedis, tinea cruris, and tinea corporis caused by the organisms Trichophyton rubrum, Trichophyton mentagrophytes, Trichophyton tonsurans and Epidermophyton floccosum. For the topical treatment of tinea pedis, tinea cruris, and tinea corporis caused by the organisms <i>Trichophyton rubrum</i>, <i>Trichophyton mentagrophytes</i>, <i>Trichophyton tonsurans</i> and <i>Epidermophyton floccosum</i>. Naftifine is a synthetic, broad spectrum, antifungal agent and allylamine derivative. The following in vitro data are available, but their clinical significance is unknown. Naftifine has been shown to exhibit fungicidal activity in vitro against a broad spectrum of organisms including <i>Trichophyton rubrum</i>, <i>Trichophyton mentagrophytes</i>, <i>Trichophyton tonsurans</i>, <i>Epidermophyton floccosum</i>, and <i>Microsporum canis</i>, <i>Microsporum audouini</i>, and <i>Microsporum gypseum</i>; and fungistatic activity against <i>Candida</i> species including <i>Candida albicans</i>. However it is only used to treat the organisms listed in the indications. Although the exact mechanism of action against fungi is not known, naftifine appears to interfere with sterol biosynthesis by inhibiting the enzyme squalene 2,3-epoxidase. This inhibition of enzyme activity results in decreased amounts of sterols, especially ergosterol, and a corresponding accumulation of squalene in the cells.",The molecular weight is 287.41.,Naftifine has a topological polar surface area of 3.24.,The log p value of  is 5.52.,Naftifine is approved.,Naftifine is a solid.,True
17412,"Butenafine hydrochloride is a synthetic benzylamine antifungal agent. Butenafine's mechanism of action is believed to involve the synthesis inhibition of sterols. In particular, butenafine acts to inhibit the activity of the squalene epoxidase enzyme that is essential in the formation of sterols necessary for fungal cell membranes. For the topical treatment of the following dermatologic infections: tinea (pityriasis) versicolor due to <i>M. furfur</i>, interdigital tinea pedis (athlete&rsquo;s foot), tinea corporis (ringworm) and tinea cruris (jock itch) due to <i>E. floccosum</i>, <i>T. mentagrophytes</i>, <i>T. rubrum</i>, and <i>T. tonsurans</i>. Butenafine is a synthetic antifungal agent that is structurally and pharmacologically related to allylamine antifungals. The exact mechanism of action has not been established, but it is suggested that butenafine's antifungal activity is exerted through the alteration of cellular membranes, which results in increased membrane permeability, and growth inhibition. Butenafine is mainly active against dermatophytes and has superior fungicidal activity against this group of fungi when compared to that of terbinafine, naftifine, tolnaftate, clotrimazole, and bifonazole. It is also active against <i>Candida albicans</i> and this activity is superior to that of terbinafine and naftifine. Butenafine also generates low MICs for <i>Cryptococcus neoformans</i> and <i>Aspergillus spp.</i> as well. Although the mechanism of action has not been fully established, it has been suggested that butenafine, like allylamines, interferes with sterol biosynthesis (especially ergosterol) by inhibiting squalene monooxygenase, an enzyme responsible for converting squalene to 2,3-oxydo squalene. As ergosterol is an essential component of the fungal cell membrane, inhibition of its synthesis results in increased cellular permeability causing leakage of cellular contents. Blockage of squalene monooxygenase also leads to a subsequent accumulation of squalene. When a high concentration of squalene is reached, it is thought to have an effect of directly kill fungal cells.",The molecular weight is 317.48.,Butenafine has a topological polar surface area of 3.24.,The log p value of  is 6.74.,Butenafine is approved.,Butenafine is a solid.,True
17413,"AS-8112 is a synthetic compound that acts as a selective antagonist at the dopamine receptor subtypes D2 and D3, and the serotonin receptor 5-HT3. It has been shown to exert potent antiemetic effects in animal studies and has been investigated for potential medical use.",,,,AS-8112 is experimental.,AS-8112 is a solid.,True
17414,Piribedil has been investigated in Parkinson's Disease.,The molecular weight is 298.35.,Piribedil has a topological polar surface area of 50.72.,The log p value of  is 2.13.,Piribedil is investigational.,,True
17415,"Tiapride is a selective D2 and D3 dopamine receptor blocker in the brain. Tiapride is indicated for the treatment of a variety of neurological and psychiatric disorders including dyskinesia, alcohol withdrawal syndrome, negative symptoms of psychosis, and agitation and aggression in the elderly. Tiapride has a high degree of regional selectivity for limbic areas. One study found that tiapride shows over three times as much affinity for limbic areas than striatal areas as opposed to the near equal selectivity for limbic and striatal regions shown by haloperidol. Tiapride is a selective dopamine D2 and D3 receptor antagonist, offering an advantage over other neuroleptic drugs, such as haloperidol and risperidone, which bind a range of targets including four of the five known dopamine receptor subtypes (D1-4), serotonin (5-HT2A, 2C), α1- and α2-adrenergic, and histamine H1 receptors. Compared to these drugs, tiapride has a relatively moderate affinity for its target receptors, displacing 50 percent of 3H-raclopride binding at a concentration of 320 nM at D2 receptors and a concentration of 180 nM at D3 receptors.",The molecular weight is 328.43.,Tiapride has a topological polar surface area of 75.71.,The log p value of  is 1.3.,Tiapride is investigational.,,True
17416,"Stannsoporfin is a competitive heme oxygenase (HO) inhibitor being developed by InfaCare, a subsidiary of WellSpring Pharmaceuticals, for the prevention of hyperbilirubinemia in infants at risk of developing jaundice. Investigated for use/treatment in liver disease, metabolic disease, and pediatric indications. Stannsoporfin is a chemical compound being investigated for use as a medicament in the treatment of infant jaundice. Stannsoporfin is also known to inhibit heme metabolism in mammals, to control the rate of tryptophan metabolism in mammals, and to increase the rate at which heme is excreted by mammals. Kernicterus is attributed to high levels of bilirubin, a by-product of heme metabolism. Bilirubin is a bile pigment, which is normally eliminated from the body after conversion into a water-soluble form by the liver. Stannsoporfin's mechanism of action specifically inhibits the enzyme that blocks the conversion of heme into bilirubin.",,,,Stannsoporfin is investigational.,Stannsoporfin is a solid.,True
17417,"Humanized IgG4k monoclonal antibody produced in murine myeloma cells. Natalizumab contains human framework regions and the complementarity-determining regions of a murine antibody that binds to a4-integrin. Natalizumab was voluntarily withdrawn from U.S. market because of risk of Progressive multifocal leukoencephalopathy (PML). It was returned to market July, 2006. For treatment of multiple sclerosis. In multiple sclerosis, lesions are believed to occur when activated inflammatory cells, including T-lymphocytes, cross the blood-brain barrier (BBB). Leukocyte migration across the BBB involves interaction between adhesion molecules on inflammatory cells, and their counter-receptors present on endothelial cells of the vessel wall. The clinical effect of natalizumab in multiple sclerosis may be a secondary result of its blockade of the molecular interaction of a 4b 1-integrin expressed by inflammatory cells with VCAM-1 on vascular endothelial cells, and with CS-1 and/or osteopontin expressed by parenchymal cells in the brain. α4-integrin is required for white blood cells to move into organs, therefore, natalizumab prevents these immune cells from crossing blood vessel walls to reach affected organs thereby decreasing inflamation. Binds to the &alpha;4-subunit of &alpha;4b 1 and &alpha;4b 7 integrins expressed on the surface of all leukocytes except neutrophils, and inhibits the &alpha;4-mediated adhesion of leukocytes to their counter-receptor(s).",,,,Natalizumab is approved and investigational.,Natalizumab is a liquid.,True
17418,"ATL1102 is a second-generation antisense inhibitor of CD49d, an immunesystem protein known as VLA-4, an immune cell molecule. It works by entering cells and targeting genes. Investigated for use/treatment in asthma and multiple sclerosis. With Multiple Sclerosis, excessive amounts of VLA-4 are believed to mediate the inappropriate migration of lymphocytes into the central nervous system, contributing to the pathogenesis of the disease. The inhibition of VLA-4 may prevent white blood cells from entering sites of inflammation, thereby halting progression of the disease. The mechanism of action of ATL1102 in blocking VLA-4 isdifferent to other drugs in development that target this same protein,including the monoclonal antibody Tysabri(R).",,,,ATL1102 is investigational.,ATL1102 is a solid.,True
17419,"CDP323 is an antagonist of the _vascular cell adhesion molecule 1_ (VCAM-1) binding to alpha4-integrins (other adhesion molecules), a process thought to be implicated in the pathophysiology of Multiple Sclerosis (MS). It is considered a small-molecule prodrug. CDP323 was originally developed by the British biopharmaceutical company Celltech plc. (now UCB S.A.) and is a putative new drug for oral treatment of multiple sclerosis. Investigated for use/treatment in multiple sclerosis. CDP323 is believed to stop immune cells from migrating from blood vessels walls to reach other tissues, including tissues in the central nervous system, where they can cause encephalomyelitis (or inflammation of the white matter in the brain and spinal cord). This inhibition of cell migration prevents immunogenic reactions that lead to tissue damage, which is often a consequence of uncontrolled cell migration.",,,,CDP323 is investigational.,CDP323 is a solid.,True
17420,"R1295 is an integrin antagonist currently in clinical trials for the treatment of rheumatoid arthritis. Integrins are associated to the pathology seen in some of the autoimmune diseases such as rheumatoid arthritis.  Investigated for use/treatment in rheumatoid arthritis. R1295 is an integrin antagonist. As leukocyte integrins are key molecules in immune-mediated and inflammatory processes,  R1295 may treat human inflammatory diseases such as rheumatoid arthritis. ",,,,R1295 is investigational.,R1295 is a solid.,True
17421,"R411 is a non-steroid oral medicine for the treatment of asthma. It is not immunosuppressive, but blocks the activation and recruitment of cells involved in respiratory inflammation. It is a dual-acting competitive integrin antagonist (as compared to previously developed single integrin antagonists or SIAs) that prevents binding of V-CAM1 to either a4b1 or a4b7.  Investigated for use/treatment in asthma. R411 is a non-steroid oral medicine for the treatment of asthma. It is not immunosuppressive, but blocks the activation and recruitment of cells involved in respiratory inflammation. It is a dual-acting competitive integrin antagonist (as compared to previously developed single integrin antagonists or SIAs) that prevents binding of V-CAM1 to either a4b1 or a4b7.  R411 prevents binding of V-CAM1 to either a4b1 or a4b7. ",,,,R411 is investigational.,R411 is a solid.,True
17422,"Vedolizumab is a recombinant humanized IgG1 monoclonal antibody directed against the human lymphocyte α4β7 integrin, a key mediator of gastrointestinal inflammation. It is used in the treatment of moderate to severe active ulcerative colitis and Crohn's disease for patients who have had an inadequate response with, lost response to, or were intolerant to inhibitors of tumor necrosis factor-alpha (TNF-alpha) or other conventional therapies. By blocking its primary target, α4β7 integrin, vedolizumab reduces inflammation in the gut. Vedolizumab is administered by IV infusion over a period of 30 minutes; after the first dose, it is given again at two and six weeks and then every 8 weeks thereafter. Vedolizumab is indicated for adult patients with moderately to severely active UC or CD who have had an inadequate response with, lost response to, or were intolerant to a tumor necrosis factor (TNF) blocker or immunomodulator; or had an inadequate response with, were intolerant to, or demonstrated dependence on corticosteroids.  Non-clinical studies have shown that the pharmacodynamic effects of vedolizumab are reversible upon removal of the antibody: pharmacologic activity of cells inhibited by vedolizumab could be partially restored within 24 hours after removal, with near complete restoration within 4 days. There are no known drug interactions as vedolizumab is a humanized antibody and does not modulate production of cytokines, which is known to affect drug metabolism.  Vedolizumab binds to α4β7 integrin, a key mediator of gastrointestinal inflammation expressed on the surfaces of T and B lymphocytes. By selectively inhibiting the α4β7 integrin, vedolizumab inhibits adhesion of lymphocytes to its natural ligand, mucosal addressin cell adhesion molecule-1 (MAdCAM-1), thereby preventing lymphocytic cells from entering the gut lamina propria and gut-associated lymphoid tissue (GALT). Specifically inhibiting this pathway alleviates GI inflammation without impairing systemic immune responses. ",,,,Vedolizumab is approved.,Vedolizumab is a solid.,True
17423,"The principal cyclooxygenase metabolite of arachidonic acid. It is released upon activation of mast cells and is also synthesized by alveolar macrophages. Among its many biological actions, the most important are its bronchoconstrictor, platelet-activating-factor-inhibitory, and cytotoxic effects.",,,,Prostaglandin D2 is investigational.,Prostaglandin D2 is a solid.,True
17424,,,,,"3-carboxamido-1,3,5(10)-estratrien-17(R)-spiro-2'(5',5'-dimethyl-6'oxo)tetrahydropyran is experimental.","3-carboxamido-1,3,5(10)-estratrien-17(R)-spiro-2'(5',5'-dimethyl-6'oxo)tetrahydropyran is a solid.",False
17425,,,,,Biliverdine IX Alpha is experimental.,Biliverdine IX Alpha is a solid.,False
17426,,,,,Lumichrome is experimental.,Lumichrome is a solid.,False
17427,,,,,Mesobiliverdin IV alpha is experimental.,Mesobiliverdin IV alpha is a solid.,False
17428,"Etidronic acid is a first generation bisphosphonate similar to and. These drugs were developed to mimic the action of pyrophosphate, a regulator of calcification and decalcification. Etidronate’s use has decreased over the years in favor of the third generation, nitrogen containing bisphosphonate , , , and. Etidronate is indicated to treat Paget's disease of bone, as well as the treatment and prevention of heterotropic ossification after total hip replacement of spinal cord injury. Etidronic acid is a first generation bisphosphonate that inhibits the action of osteoclasts, preventing bone resporption. It has a wide therapeutic index as overdoses are not associated with severe toxicity and a long duration of action as it slowly releases from the bone. Patients should be counselled regarding the risk of upper gastrointestinal adverse reactions. Bisphosphonates are taken into the bone where they bind to hydroxyapatite. Bone resorption by osteoclasts causes local acidification, releasing the bisphosphonate, which is taken into the osteoclast by fluid-phase endocytosis. Endocytic vesicles become acidified, releasing bisphosphonates into the cytosol of osteoclasts where they act.",The molecular weight is 206.03.,Etidronic acid has a topological polar surface area of 135.29.,The log p value of  is -2.54.,Etidronic acid is approved.,Etidronic acid is a solid.,True
17429,,,,,(Hydroxy)Dimethylammonium is experimental.,(Hydroxy)Dimethylammonium is a solid.,False
17430,,,,,Carboxyatractyloside is experimental.,Carboxyatractyloside is a solid.,False
17431,,,,,Tetrastearoyl cardiolipin is experimental.,Tetrastearoyl cardiolipin is a solid.,False
17432,,,,,Di-Stearoyl-3-Sn-Phosphatidylcholine is experimental.,Di-Stearoyl-3-Sn-Phosphatidylcholine is a solid.,False
17433,,,,,Methacrylyl-Coenzyme A is experimental.,Methacrylyl-Coenzyme A is a solid.,False
17434,"Travoprost ophthalmic solution is a topical medication used for controlling the progression of glaucoma or ocular hypertension, by reducing intraocular pressure. It is a synthetic prostaglandin F2alpha analog. Having been a well-received therapeutic agent with demonstrated efficacy and safety, travoprost is currently approved by the US FDA as a first-line treatment for lowering intraocular pressure in patients with open-angle glaucoma or ocular hypotension. Furthermore, this approval also solidifies the medication as the first and only prostaglandin analog approved by the FDA for first-line treatment of glaucoma patients that does not contain the preservative benzalkonium chloride. Moreover, travoprost is also currently approved in the EU for the decrease of elevated intraocular pressure in paediatric patients aged 2 months to < 18 years with ocular hypertension or paediatric glaucoma. Travoprost ophthalmic solution is indicated for the reduction of elevated intraocular pressure in patients with open-angle glaucoma or ocular hypertension. Travoprost, an isopropyl ester prodrug, is a synthetic prostaglandin F2 alpha analog that is rapidly hydrolyzed by esterases in the cornea to its biologically active free acid. The travoprost free acid is potent and highly selective for the FP prostanoid receptor.  Travoprost, a prostaglandin F2α analogue, is a highly selective full agonist which has a high affinity for the prostaglandin FP receptor, and facilitates reductions in intraocular pressure by increasing the outflow of aqueous humour via trabecular meshwork and uveoscleral pathways. Reduction of the intraocular pressure in man starts about 2 hours after administration and maximum effect is reached after 12 hours. Significant lowering of intraocular pressure can be maintained for periods exceeding 24 hours with a single dose.",The molecular weight is 500.56.,Travoprost has a topological polar surface area of 96.22.,The log p value of  is 3.92.,Travoprost is approved.,Travoprost is a liquid.,True
17435,"Latanoprost is a prodrug analog of prostaglandin F2 alpha that is used to treat elevated intraocular pressure (IOP). It was initially approved by the FDA in 1998. Latanoprost is the first topical prostaglandin F2 alpha analog used for glaucoma treatment. It has been found to be well-tolerated and its use does not normally result in systemic adverse effects like other drugs used to treat elevated intraocular pressure, such as. Another benefit latanoprost is that it can be administered once a day. Latanoprost is indicated for the reduction of elevated intraocular pressure in patients who have been diagnosed with open-angle glaucoma or ocular hypertension. Latanoprost may be combined in a product with , a rho kinase inhibitor, for the same indications. In addition to the above indications, the Canadian monograph for this drug also approves latanoprost for the treatment of elevated intraocular pressure as a result of angle-closure glaucoma that has been treated with peripheral iridotomy or laser iridoplasty. Latanoprost effectively decreases intraocular pressure by increasing uveoscleral outflow. A decrease in intraocular pressure has been measured within 3–4 hours post-administration, reaches a maximum decrease at 8–12 hours, and can be maintained for a period of 24 hours.   Elevated intraocular pressure leads to an increased risk of glaucomatous visual field loss. The higher the intraocular pressure, the higher the risk of damage to the optic nerve and loss of visual field. Latanoprost selectively stimulates the prostaglandin F2 alpha receptor and this results in a decreased intraocular pressure (IOP) via the increased outflow of aqueous humor, which is often implicated in cases of elevated intraocular pressure. Possible specific mechanisms of the abovementioned increased aqueous outflow are the remodeling of the extracellular matrix and regulation of matrix metalloproteinases. These actions result in higher tissue permeability related to humor outflow pathways, which likely change outflow resistance and/or outflow rates.",The molecular weight is 432.6.,Latanoprost has a topological polar surface area of 86.99.,The log p value of  is 3.6.,Latanoprost is approved and investigational.,Latanoprost is a liquid.,True
17436,"Latanoprostene Bunod has been used in trials studying the treatment of Glaucoma, Ocular Hypertension, Open-Angle Glaucoma, Open Angle Glaucoma, and Intraocular Pressure. Latanoprostene bunod opthalmic solution is indicated for the reduction of intraocular pressure in patients with open-angle glaucoma or ocular hypertension. Upon applying an appropriate dose of latanoprost bunod, reduction in intraocular pressure begins approximately 1 to 3 hours later with a maximum intraocular pressure reduction effect demonstrated after 11 to 13 hours. Open-angle glaucoma (OAG) is a medical condition that is associated with progressive visual field damage and the loss of vision.",The molecular weight is 507.62.,Latanoprostene bunod has a topological polar surface area of 139.36.,The log p value of  is 0.54.,Latanoprostene bunod is approved and investigational.,Latanoprostene bunod is a liquid.,True
17437,"An inhibitor of the enzyme tyrosine 3-monooxygenase, and consequently of the synthesis of catecholamines. It is used to control the symptoms of excessive sympathetic stimulation in patients with pheochromocytoma. (Martindale, The Extra Pharmacopoeia, 30th ed) For use in the treatment of patients with pheochromocytoma, for preoperative preparation of patients for surgery, management of patients when surgery is contraindicated, and chronic treatment of patients with malignant pheochromocytoma. In patients with pheochromocytoma, who produce excessive amounts of norepinephrine and epinephrine, administration of one to four grams of metyrosine per day has reduced catecholamine biosynthesis from about 35 to 80 percent as measured by the total excretion of catecholamines and their metabolites (metanephrine and vanillylmandelic acid). The maximum biochemical effect usually occurs within two to three days, and the urinary concentration of catecholamines and their metabolites usually returns to pretreatment levels within three to four days after metyrosine is discontinued. Most patients with pheochromocytoma treated with metyrosine experience decreased frequency and severity of hypertensive attacks with their associated headache, nausea, sweating, and tachycardia. In patients who respond, blood pressure decreases progressively during the first two days of therapy with metyrosine; after withdrawal, blood pressure usually increases gradually to pretreatment values within two to three days. Metyrosine inhibits tyrosine hydroxylase, which catalyzes the first transformation in catecholamine biosynthesis, i.e., the conversion of tyrosine to dihydroxyphenylalanine (DOPA). Because the first step is also the rate-limiting step, blockade of tyrosine hydroxylase activity results in decreased endogenous levels of catecholamines and their synthesis. This consequently, depletes the levels of the catecholamines dopamine, adrenaline and noradrenaline in the body,usually measured as decreased urinary excretion of catecholamines and their metabolites. One main end result of the catecholamine depletion is a decrease in blood presure.",The molecular weight is 195.22.,Metyrosine has a topological polar surface area of 83.55.,The log p value of  is -1.67.,Metyrosine is approved.,Metyrosine is a solid.,True
17438,,,,,3-Tyrosine is experimental.,3-Tyrosine is a solid.,False
17439,,,,,LY374571 is experimental.,LY374571 is a solid.,False
17440,,,,,LY249543 is experimental.,LY249543 is a solid.,False
17441,,,,,3-(Oxalyl-Amino)-Naphthalene-2-Carboxylic Acid is experimental.,3-(Oxalyl-Amino)-Naphthalene-2-Carboxylic Acid is a solid.,False
17442,,,,,2-{-oxalyl-amino}-benzoic acid is experimental.,2-{-oxalyl-amino}-benzoic acid is a solid.,False
17443,,,,,"5-(2-Fluoro-5-{(1E)-3--1-propen-1-yl}phenyl)-1,2-oxazole-3-carboxylic acid is experimental.","5-(2-Fluoro-5-{(1E)-3--1-propen-1-yl}phenyl)-1,2-oxazole-3-carboxylic acid is a solid.",False
17444,,,,,"2-(Oxalyl-Amino)-4,7-Dihydro-5h-ThienoThiopyran-3-Carboxylic Acid is experimental.","2-(Oxalyl-Amino)-4,7-Dihydro-5h-ThienoThiopyran-3-Carboxylic Acid is a solid.",False
17445,,,,,"3-(3,5-Dibromo-4-Hydroxy-Benzoyl)-2-Ethyl-Benzofuran-6-Sulfonic Acid (4-Sulfamoyl-Phenyl)-Amide is experimental.","3-(3,5-Dibromo-4-Hydroxy-Benzoyl)-2-Ethyl-Benzofuran-6-Sulfonic Acid (4-Sulfamoyl-Phenyl)-Amide is a solid.",False
17446,,,,,"Amino]Oxo-Acetic Acid, is experimental.","Amino]Oxo-Acetic Acid, is a solid.",False
17447,,,,,{4-carbamoyl}amino)-3-oxo-3-(pentylamino)propyl]phenoxy}malonic acid is experimental.,{4-carbamoyl}amino)-3-oxo-3-(pentylamino)propyl]phenoxy}malonic acid is a solid.,False
17448,,,,,3-(4-{2--ethylcarbamoyl}-cyclohexylcarbamoyl)-pyrazine-2-carboxylic acid is experimental.,3-(4-{2--ethylcarbamoyl}-cyclohexylcarbamoyl)-pyrazine-2-carboxylic acid is a solid.,False
17449,,,,,2-(Oxalyl-Amino)-Benzoic Acid is experimental.,2-(Oxalyl-Amino)-Benzoic Acid is a solid.,False
17450,,,,,{Bis}Bis(Phosphonic Acid) is experimental.,{Bis}Bis(Phosphonic Acid) is a solid.,False
17451,,,,,Novo Nordisk a/S Compound is experimental.,Novo Nordisk a/S Compound is a solid.,False
17452,,,,,N-(Bromoacetyl)-beta-alanyl-N-(2-{4-phenyl}ethyl)-L-serinamide is experimental.,N-(Bromoacetyl)-beta-alanyl-N-(2-{4-phenyl}ethyl)-L-serinamide is a solid.,False
17453,,,,,"7-(1,1-Dioxo-1h-BenzoIsothiazol-3-Yloxymethyl)-2-(Oxalyl-Amino)-4,7-Dihydro-5h-ThienoPyran-3-Carboxylic Acid is experimental.","7-(1,1-Dioxo-1h-BenzoIsothiazol-3-Yloxymethyl)-2-(Oxalyl-Amino)-4,7-Dihydro-5h-ThienoPyran-3-Carboxylic Acid is a solid.",False
17454,,,,,PNU177836 is experimental.,PNU177836 is a solid.,False
17455,,,,,"2-(Oxalyl-Amino)-4,7-Dihydro-5h-ThienoPyran-3-Carboxylic Acid is experimental.","2-(Oxalyl-Amino)-4,7-Dihydro-5h-ThienoPyran-3-Carboxylic Acid is a solid.",False
17456,,,,,{-Difluoro-Methyl}-Phosphonic Acid is experimental.,{-Difluoro-Methyl}-Phosphonic Acid is a solid.,False
17457,,,,,"3-(3,5-Dibromo-4-Hydroxy-Benzoyl)-2-Ethyl-Benzofuran-6-Sulfonic Acid -Amide is experimental.","3-(3,5-Dibromo-4-Hydroxy-Benzoyl)-2-Ethyl-Benzofuran-6-Sulfonic Acid -Amide is a solid.",False
17458,,,,,(4S)-5-phenyl]-1-oxopropan-2-yl]amino]-3-phenyl]-1-oxopropan-2-yl]amino]-4-benzamido-5-oxopentanoic acid is experimental.,(4S)-5-phenyl]-1-oxopropan-2-yl]amino]-3-phenyl]-1-oxopropan-2-yl]amino]-4-benzamido-5-oxopentanoic acid is a solid.,False
17459,,,,,4--6-oxohexyl]amino]-3-phenyl]-1-oxopropan-2-yl]amino]-3-phenyl]acetyl]amino]-4-oxobutanoic acid is experimental.,4--6-oxohexyl]amino]-3-phenyl]-1-oxopropan-2-yl]amino]-3-phenyl]acetyl]amino]-4-oxobutanoic acid is a solid.,False
17460,"L-cysteic acid is a beta-sulfoalanine. It is an amino acid with a C-terminal sulfonic acid group which has been isolated from human hair oxidized with permanganate. It occurs normally in the outer part of the sheep's fleece, where the wool is exposed to light and weather.",,,,L-cysteic acid is experimental.,L-cysteic acid is a solid.,True
17461,,,,,"2-(Oxalyl-Amino)-4,5,6,7-Tetrahydro-ThienoPyridine-3-Carboxylic Acid is experimental.","2-(Oxalyl-Amino)-4,5,6,7-Tetrahydro-ThienoPyridine-3-Carboxylic Acid is a solid.",False
17462,,,,,4-Carbamoyl-4-{-Amino}-Butyric Acid is experimental.,4-Carbamoyl-4-{-Amino}-Butyric Acid is a solid.,False
17463,,,,,"Compound 5, 2-(Naphthalen-1-Yl-Oxalyl-Amino)-Benzoicacid is experimental.","Compound 5, 2-(Naphthalen-1-Yl-Oxalyl-Amino)-Benzoicacid is a solid.",False
17464,,,,,6-(Oxalyl-Amino)-1h-Indole-5-Carboxylic Acid is experimental.,6-(Oxalyl-Amino)-1h-Indole-5-Carboxylic Acid is a solid.,False
17465,,,,,2-amino}-3-({4-butyl}amino)-3-oxopropyl]phenyl}(carboxycarbonyl)amino]benzoic acid is experimental.,2-amino}-3-({4-butyl}amino)-3-oxopropyl]phenyl}(carboxycarbonyl)amino]benzoic acid is a solid.,False
17466,,,,,"3-(3,5-Dibromo-4-Hydroxy-Benzoyl)-2-Ethyl-Benzofuran-6-Sulfonic Acid Dimethylamide is experimental.","3-(3,5-Dibromo-4-Hydroxy-Benzoyl)-2-Ethyl-Benzofuran-6-Sulfonic Acid Dimethylamide is a solid.",False
17467,,,,,-Butyl}-Phenyl)-Difluoro-Methyl]-Phosphonic Acid is experimental.,-Butyl}-Phenyl)-Difluoro-Methyl]-Phosphonic Acid is a solid.,False
17468,,,,,{4-Phenyl}(Difluoro)Methylphosphonic Acid is experimental.,{4-Phenyl}(Difluoro)Methylphosphonic Acid is a solid.,False
17469,,,,,N-(3-Carboxypropanoyl)-L-phenylalanyl-3-carboxy-O-(carboxymethyl)-N-pentyl-L-tyrosinamide is experimental.,N-(3-Carboxypropanoyl)-L-phenylalanyl-3-carboxy-O-(carboxymethyl)-N-pentyl-L-tyrosinamide is a solid.,False
17470,,,,,1-METHYL-3-PHENYL-1H-PYRAZOL-5-YLSULFAMIC ACID is experimental.,1-METHYL-3-PHENYL-1H-PYRAZOL-5-YLSULFAMIC ACID is a solid.,False
17471,"ISIS 113715 is our second-generation antisense inhibitor of protein tyrosine phosphatase 1b, or PTP‑1b, for the treatment of type 2 diabetes. In early trials, ISIS 113715 induced statistically significant improvements in multiple measures of glucose control along with statistically significant Investigated for use/treatment in diabetes mellitus type 2. Because ISIS 113715 is an insulin sensitizer that acts by increasing the activity of the insulin receptor in response to insulin, the most logical place for this drug in the diabetes treatment regimen is as an adjunct to insulin therapy. ISIS 113715 has a novel mechanism of PTP-1b inhibiting action, and acts as an insulin signal enhancer with anti-obesity and lipid lowering potential. PTP‑1b has long been recognized as an attractive target for treatment of diabetes, but due to structural similarities among closely related proteins, it has been difficult to identify small molecule drugs with sufficient specificity to be ISIS 113715 is our second-generation antisense inhibitor of protein tyrosine phosphatase 1b, or PTP‑1b, for the treatment of type 2 diabetes. PTP‑1b is responsible for turning off the activated insulin receptor, so by reducing levels of PTP‑1b, ISIS 113715 enhances the activity of insulin. Antisense technology allows us to design very specific drugs that inhibit PTP‑1b and that do not inhibit other family members, making it possible to reduce PTP‑1b activity without having other effects on closely related proteins that would likely lead to unwanted side effects.",,,,ISIS 113715 is investigational.,ISIS 113715 is a solid.,True
17472,,,,,4-BROMO-3-(CARBOXYMETHOXY)-5-THIOPHENE-2-CARBOXYLIC ACID is experimental.,4-BROMO-3-(CARBOXYMETHOXY)-5-THIOPHENE-2-CARBOXYLIC ACID is a solid.,False
17473,,,,,"carbonyl}-1,2,3,4-tetrahydro-7-isoquinolinyl]sulfamic acid is experimental.","carbonyl}-1,2,3,4-tetrahydro-7-isoquinolinyl]sulfamic acid is a solid.",False
17474,,,,,4-BROMO-3-(CARBOXYMETHOXY)-5-PHENYLTHIOPHENE-2-CARBOXYLIC ACID is experimental.,4-BROMO-3-(CARBOXYMETHOXY)-5-PHENYLTHIOPHENE-2-CARBOXYLIC ACID is a solid.,False
17475,,,,,"5-(4-CHLORO-5-PHENYL-3-THIENYL)-1,2,5-THIADIAZOLIDIN-3-ONE 1,1-DIOXIDE is experimental.","5-(4-CHLORO-5-PHENYL-3-THIENYL)-1,2,5-THIADIAZOLIDIN-3-ONE 1,1-DIOXIDE is a solid.",False
17476,,,,,4-BROMO-3-(CARBOXYMETHOXY)-5-(4-HYDROXYPHENYL)THIOPHENE-2-CARBOXYLIC ACID is experimental.,4-BROMO-3-(CARBOXYMETHOXY)-5-(4-HYDROXYPHENYL)THIOPHENE-2-CARBOXYLIC ACID is a solid.,False
17477,,,,,phenyl}(difluoro)methyl]phosphonic acid is experimental.,phenyl}(difluoro)methyl]phosphonic acid is a solid.,False
17478,,,,,5--4-BROMO-3-(CARBOXYMETHOXY)THIOPHENE-2-CARBOXYLIC ACID is experimental.,5--4-BROMO-3-(CARBOXYMETHOXY)THIOPHENE-2-CARBOXYLIC ACID is a solid.,False
17479,,,,,2--BENZOIC ACID is experimental.,2--BENZOIC ACID is a solid.,False
17480,,,,,3-(CARBOXYMETHOXY)THIENOPYRIDINE-2-CARBOXYLIC ACID is experimental.,3-(CARBOXYMETHOXY)THIENOPYRIDINE-2-CARBOXYLIC ACID is a solid.,False
17481,,,,,4-PHOSPHONOOXY-PHENYL-METHYL-BENZEN is experimental.,4-PHOSPHONOOXY-PHENYL-METHYL-BENZEN is a solid.,False
17482,,,,,N-ACETYL-L-PHENYLALANYL-4--L-PHENYLALANINAMIDE is experimental.,N-ACETYL-L-PHENYLALANYL-4--L-PHENYLALANINAMIDE is a solid.,False
17483,,,,,"carbonyl}-1,2,3,4-tetrahydro-7-isoquinolinyl]sulfamic acid is experimental.","carbonyl}-1,2,3,4-tetrahydro-7-isoquinolinyl]sulfamic acid is a solid.",False
17484,,,,,"5-(3-HYDROXYPHENYL)ISOTHIAZOL-3(2H)-ONE 1,1-DIOXIDE is experimental.","5-(3-HYDROXYPHENYL)ISOTHIAZOL-3(2H)-ONE 1,1-DIOXIDE is a solid.",False
17485,,,,,5-(3-{3-PROPENYL}PHENYL)-4-(HYDROXYMETHYL)ISOXAZOLE-3-CARBOXYLIC ACID is experimental.,5-(3-{3-PROPENYL}PHENYL)-4-(HYDROXYMETHYL)ISOXAZOLE-3-CARBOXYLIC ACID is a solid.,False
17486,,,,,ISOTHIAZOLIDINONE ANALOG is experimental.,ISOTHIAZOLIDINONE ANALOG is a solid.,False
17487,,,,,"4--2,4-dioxobutanoic acid is experimental.","4--2,4-dioxobutanoic acid is a solid.",False
17488,,,,,6-(DIFLUORO-PHOSPHONO-METHYL)-NAPHTHALENE-2-CARBOXYLIC ACID is experimental.,6-(DIFLUORO-PHOSPHONO-METHYL)-NAPHTHALENE-2-CARBOXYLIC ACID is a solid.,False
17489,,,,,"(3R)-METHYLCARBAMOYL-7-SULFOAMINO-3,4-DIHYDRO-1H-ISOQUINOLINE-2-CARBOXYLIC ACID BENZYL ESTER is experimental.","(3R)-METHYLCARBAMOYL-7-SULFOAMINO-3,4-DIHYDRO-1H-ISOQUINOLINE-2-CARBOXYLIC ACID BENZYL ESTER is a solid.",False
17490,,,,,"5-(4-METHOXYBIPHENYL-3-YL)-1,2,5-THIADIAZOLIDIN-3-ONE 1,1-DIOXIDE is experimental.","5-(4-METHOXYBIPHENYL-3-YL)-1,2,5-THIADIAZOLIDIN-3-ONE 1,1-DIOXIDE is a solid.",False
17491,,,,,"1,2,5-THIADIAZOLIDIN-3-ONE-1,1-DIOXIDE is experimental.","1,2,5-THIADIAZOLIDIN-3-ONE-1,1-DIOXIDE is a solid.",False
17492,,,,,(4-{(2S)-2--3-methoxy-3-oxopropyl}phenyl)methaneseleninic acid is experimental.,(4-{(2S)-2--3-methoxy-3-oxopropyl}phenyl)methaneseleninic acid is a solid.,False
17493,"Sermorelin acetate is the acetate salt of an amidated synthetic 29-amino acid peptide (GRF 1-29 NH 2 ) that corresponds to the amino-terminal segment of the naturally occurring human growth hormone-releasing hormone (GHRH or GRF) consisting of 44 amino acid residues For the treatment of dwarfism, prevention of HIV-induced weight loss Sermorelin is used in the treatment of children with growth hormone deficiency or growth failure. Geref increases plasma growth hormone (GH) concentration by stimulating the pituitary gland to release GH. Geref is similar to the full-length native hormone (44 residues) in its ability to stimulate GH secretion in humans. Sermorelin binds to the growth hormone releasing hormone receptor and mimics native GRF in its ability to stimulate growth hormone secretion.",The molecular weight is 3357.93.,Sermorelin has a topological polar surface area of 1446.9.,The log p value of  is 0.0.,Sermorelin is approved and withdrawn.,Sermorelin is a liquid.,True
17494,"Tesamorelin is a stabilized synthetic peptide analogue of the hypothalamic peptide, Growth Hormone Releasing Hormone (GHRH) indicated for the reduction of excess abdominal fat in HIV-infected patients with lipodystrophy. Lipodystrophy is a metabolic condition characterized by insulin resistance, fat redistribution, and hyperlipidemia associated with antiretroviral therapy for HIV infection. Tesamorelin acetate is a synthetic analogue of human hypothalamic Growth Hormone Releasing Factor (hGRF) indicated to induce and maintain a reduction of excess abdominal fat in HIV-infected patients with lipodystrophy.  Tesamorelin stimulates growth hormone secretion, and subsequently increases IGF-1 and IGFBP-3 levels. By acting on the pituitary cells in the brain, tesamorelin stimulates production and release of the endogenous hormone (hGRF). Tesamorelin therapy predisposes the patient to glucose intolerance and can also increase the risk of type 2 diabetes, so the drug is contraindicated in pregnancy. ",The molecular weight is 5040.71.,Tesamorelin has a topological polar surface area of 2330.5.,,Tesamorelin is approved and investigational.,Tesamorelin is a solid.,True
17495,"Sargramostim is a human recombinant granulocyte macrophage colony-stimulating factor (GM-CSF) expressed in yeast. It is a glycoprotein that is 127 residues. Substitution of Leu23 leads to a difference from native protein. For the treatment of cancer and bone marrow transplant Sargramostim is used in the treatment of bone marrow transplant recipients or those exposed to chemotherapy an recovering from acut myelogenous leukemia, Leukine or GM-CSF is a hematopoietic growth factor which stimulates the survival, clonal expansion (proliferation) and differentiation of hematopoietic progenitor cells. GM-CSF is also capable of activating mature granulocytes and macrophages. After a bone marrow transplant or chemotherapy, patients have a reduced capacity to produce red and white blood cells. Supplementing them with external sources of GM-CSF helps bring the level of neutrophils back to normal so that they can better fight infections. Sargramostim binds to the Granulocyte-macrophage colony stimulating factor receptor (GM-CSF-R-alpha or CSF2R) which stimulates a JAK2 STAT1/STAT3 signal transduction pathway. This leads to the production of hemopoietic cells and neutrophils",,,,Sargramostim is approved and investigational.,Sargramostim is a liquid.,True
17496,"KB002 is an engineered human IgG1k antibody engineered human. It is developed for the treatment of autoimmune diseases, initially rheumatoid arthritis. Investigated for use/treatment in rheumatoid arthritis. KB002 is an engineered human monoclonal antibody. The drug targets and neutralizes the activity of granulocyte macrophage colony-stimulating factor, (GM-CSF), a pro-inflammatory cytokine/growth factor that stimulates the survival, proliferation, differentiation and function of several types of white blood cells, including the monocytes/macrophages that play a key role in the tissue damage associated with many autoimmune diseases.",,,,KB002 is investigational.,KB002 is a solid.,True
17497,,,,,"4,5-bis(4-methoxyphenyl)-2-thiophen-2-yl-1H-imidazole is experimental.","4,5-bis(4-methoxyphenyl)-2-thiophen-2-yl-1H-imidazole is a solid.",False
17498,,,,,2-({4-phenoxy}methyl)quinoline is experimental.,2-({4-phenoxy}methyl)quinoline is a solid.,False
17499,,,,,2-{methyl}quinoline is experimental.,2-{methyl}quinoline is a solid.,False
17500,,,,,Mardepodect is investigational.,Mardepodect is a solid.,False
17501,,,,,"6,7-DIMETHOXY-4-QUINAZOLINE is experimental.","6,7-DIMETHOXY-4-QUINAZOLINE is a solid.",False
17502,,,,,PQ-10 is experimental.,PQ-10 is a solid.,False
17503,"Dezocine is a partial opiate drug and is used for pain management. Dezocine is a very effective alternative to fentanyl when administered during outpatient laparoscopy, although is associated with an increased incidence of postoperative nausea. Indicated in the treatment of moderate to severe pain. Dezocine is a parenteral narcotic analgesic possessing both agonist and antagonist activity. It is similar to morphine with respect to analgesic potency and onset and duration of action. The narcotic antagonist activity is greater than that of pentazocine. Dezocine is a opioid analgesic drug of mixed agonist-antagonist type. It binds with stereospecific receptors at many sites within the central nervous system (CNS) to alter processes affecting both the perception of pain and the emotional response to pain. At least 2 of these types of receptors (mu and kappa) mediate analgesia. Mu receptors are widely distributed throughout the CNS, especially in the limbic system (frontal cortex, temporal cortex, amygdala, and hippocampus), thalamus, striatum, hypothalamus, and midbrain as well as laminae I, II, IV, and V of the dorsal horn in the spinal cord. Kappa receptors are localized primarily in the spinal cord and in the cerebral cortex.",The molecular weight is 245.37.,Dezocine has a topological polar surface area of 46.25.,The log p value of  is 3.72.,Dezocine is approved and investigational.,Dezocine is a solid.,True
17504,"V1003 is an intranasal formulation of buprenorphine, an opiate analgesic, for the management of post-operative pain in hospital and home settings. Buprenorphine is a well-known analgesic and the intranasal formulation has the potential to provide a convenient alternative to other treatments, allowing patients to manage their post-operative pain both prior to discharge from hospital and at home during their recovery period. Investigated for use/treatment in pain (acute or chronic). V1003 is an intranasal formulation of buprenorphine. Buprenorphine's analgesic effect is due to partial agonist activity at mu-opioid receptors. Buprenorphine is also a kappa-opioid receptor antagonist. The partial agonist activity means that opioid receptor antagonists (e.g., an antidote such as naloxone) only partially reverse the effects of buprenorphine. The binding to the mu and kappa receptors results in hyperpolarization and reduced neuronal excitability.",,,,V1003 is investigational.,V1003 is a solid.,True
17505,"Asimadoline is a proprietary small molecule therapeutic, originally discovered by Merck KGaA of Darmstadt, Germany. Asimadoline was originally developed to treat peripheral pain such as arthritis. Asimadoline is an orally administered agent that acts as a kappa opioid receptor agonist. It has shown encouraging clinical efficacy for the treatment of IBS in a barostat study in IBS patients and has the potential for treating other gastrointestinal diseases. Investigated for use/treatment in irritable bowel syndrome (IBS). Asimadoline is an orally administered agent that acts as a kappa opioid receptor agonist. Kappa opioid receptors are found mostly in the digestive tract and are believed to play an important role in control of visceral pain and bowel motility. As such, kappa opioid agonists are ideal candidates to relieve the pain, discomfort an impaired motility common to IBS and other gastrointestinal disorders.",,,,Asimadoline is investigational.,Asimadoline is a solid.,True
17506,"CR665 is the lead clinical development candidate from a series of highly selective peripheral kappa opioid receptor agonists. In preclinical studies, CR665 was highly selective for the peripheral kappa opioid receptor. Preclinical animal studies suggest that CR665 is a potent analgesic compound. In addition, unlike currently marketed opioids, CR665 does not produce inhibition of intestinal transit (ileus), induce respiratory depression, or elicit signs of euphoria or addiction in animal models. Preclinical studies also indicate that CR665 possesses anti-inflammatory activities. Investigated for use/treatment in pain (acute or chronic). CR665 was highly selective for the peripheral kappa opioid receptor. It is intrinsically poor at penetrating the blood-brain barrier, which decreases the likelihood of CNS-mediated side effects. By acting with unprecedented selectivity at pain relieving receptors on peripheral nerves, and avoiding receptors in the central nervous system and gastrointestinal tract, CR665 has the potential to provide pain relief with minimal side effects.",,,,CR665 is investigational.,CR665 is a solid.,True
17507,"ADL 10-0101 is a peripheral kappa opioid agonist analgesic product candidate. Preclinical trials of ADL 10-0101 have suggested that the compound may be effective for the treatment of inflammatory pain, itch and visceral pain. Because ADL 10-0101 does not cross the blood-brain barrier and enter the brain when administered at therapeutic doses, it is expected to avoid central nervous system side effects. Investigated for use/treatment in pain (acute or chronic) and rheumatoid arthritis. Trials are also being conducted for relieving burn pain and dermal itch. ADL 10-0101 is a peripheral kappa opioid agonist. It cannot cross the blood-brain barrier. Agonist at peripheral kappa opioid receptors",,,,ADL 10-0101 is investigational.,ADL 10-0101 is a solid.,True
17508,"Methylnaltrexone is a pheriphally-acting μ-opioid antagonist that acts on the gastrointestinal tract to decrease opioid-induced constipation without producing analgesic effects or withdrawal symptoms. It is also a weak CYP2D6 inhibitor. FDA approved in 2008. Treatment of opioids induced constipation in palliative patients that are inadequately responding to laxative therapy.  Use of opioids induces slowing of gastrointestinal motility and transit. Following remifentanil administration, the methylnaltrexone and placebo groups showed no change in pupiliary constriction while the naloxone group showed a marked change over the time interval tested.  Methylnaltrexone is a pheriphally-acting μ-opioid antagonists that acts on the gastrointestinal tract inhibit opioid-induced decrease in gastric motility and transit time. Because methylnaltrexone is a quaternary derivative of naltrexone, it produces its gastrointestinal effects without producing analgesic effects or withdrawal symptoms as it does not cross the blood-brain-barrier. ",,,,Methylnaltrexone is approved.,Methylnaltrexone is a solid.,True
17509,,,,,PLX-4720 is experimental.,PLX-4720 is a solid.,False
17510,,,,,"N-{2,4-difluoro-3-pyridin-3-yl)carbonyl]phenyl}ethanesulfonamide is experimental.","N-{2,4-difluoro-3-pyridin-3-yl)carbonyl]phenyl}ethanesulfonamide is a solid.",False
17511,"(1E)-5-(1-piperidin-4-yl-3-pyridin-4-yl-1h-pyrazol-4-yl)-2,3-dihydro-1h-inden-1-one oxime is a solid. This compound belongs to the phenylpyrazoles. These are compounds containing a phenylpyrazole skeleton, which consists of a pyrazole bound to a phenyl group. It targets the protein serine/threonine-protein kinase B-raf.",,,,"(1E)-5-(1-piperidin-4-yl-3-pyridin-4-yl-1H-pyrazol-4-yl)-2,3-dihydro-1H-inden-1-one oxime is experimental.","(1E)-5-(1-piperidin-4-yl-3-pyridin-4-yl-1H-pyrazol-4-yl)-2,3-dihydro-1H-inden-1-one oxime is a solid.",True
17512,A pyrimidine ribonucleoside 5'-monophosphate having cytosine as the nucleobase.,,,,Cytidine-5'-Monophosphate is experimental.,Cytidine-5'-Monophosphate is a solid.,True
17513,,,,,P1-(adenosine-5'-P5-(uridine-5')pentaphosphate is experimental.,P1-(adenosine-5'-P5-(uridine-5')pentaphosphate is a solid.,False
17514,,,,,Tetrafluoroaluminate Ion is experimental.,Tetrafluoroaluminate Ion is a solid.,False
17515,"Talampanel is a substance that is being studied in the treatment of brain tumors and other brain disorders, such as epilepsy and Parkinson disease. It is a type of AMPA receptor antagonist. For the treatment of epilepsy. Talampanel, a potent and selective alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA)-receptor antagonist, is a potential new antiepileptic drug (AED). Talampanel dosing strategies may be reliant on concomitant AED medication, as enzyme-inducing AEDs enhance, whereas VPA inhibits its metabolism. Talampanel was well tolerated, although adverse events occurred at lower doses compared with those in healthy subjects, probably because of the additive effect of concomitant AEDs. Talampanel is a potent noncompetitive and selective antagonist of the glutamine AMPA receptors. Studies in primates have shown that the administration of talampanel to parkinsonian monkeys significantly decreased levodopa-induced dyskinesias by 40%. When given alone, talampanel did not modify the severity of parkinsonian symptoms. However, in combination with levodopa, talampanel potentiated the antiparkinsonian action of levodopa by increasing motor activity.",,,,Talampanel is investigational.,Talampanel is a solid.,True
17516,"CX-717 is an ampakine compound previously investigated for the treatment of Attention-Deficit/Hyperactivity Disorder (ADHD) and Alzheimer's disease. Investigated for the treatment of Attention-Deficit/Hyperactivity Disorder (ADHD) and Alzheimer's disease. CX-717 is an ampakine compound. It is a positive allosteric modulator of AMPA receptors. Its action is theorized to be due to the facilitation of transmission at cortical synapses that use glutamate as a neurotransmitter. This in turn may promote plasticity at the synapse, which could translate into better cognitive performance.",,,,CX717 is illicit and investigational.,CX717 is a solid.,True
17517,"Investigated for use/treatment in alzheimer's disease, memory loss, autism, neurologic disorders, dementia, schizophrenia and schizoaffective disorders, attention deficit/hyperactivity disorder (ADHD), and sleep disorders. CX 516 is a benzylpiperidine AMPAkine, an AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) modulator, that enhances the function of glutamate when it binds allosterically to the AMPA receptor channel complex. CX 516 slows receptor deactivation with a longer open time, slower excitatory postsynaptic potential (EPSP) decay and improvement of hippocampal long term potentiation (LTP).",,,,CX516 is investigational.,CX516 is a solid.,True
17518,"Rolicyclidine (PCPy) is classified as a dissociative anesthetic agent. It also has hallucinogenic and sedative properties. Because of its pharmacodynamic similarity to the drug phencyclidine (PCP), rolicyclidine was added to the Schedule I list of illegal drugs in the USA in the 1970s. Rolicyclidine has anesthetic properties and can induce a sedative effect.  Rolicyclidine is similar in effects to phencyclidine but is slightly less potent and has less stimulant effects. Instead it acts by inducing a sedative effect described as being somewhat similar to a barbiturate, but with additional PCP-like dissociative, anaesthetic and hallucinogenic effects. Rolicyclidine works primarily as an NMDA receptor antagonist, which blocks the activity of the NMDA Receptor.",,,,Rolicyclidine is experimental and illicit.,Rolicyclidine is a solid.,True
17519,"Neramexane is a low-to-moderate affinity uncompetitive NMDA receptor antagonist. Investigated for use/treatment in alzheimer's disease, hearing loss, and pain (acute or chronic). Neramexane is similar to memantine and acetylcholinesterase inhibitors in that neramexane targets the cognitive decline in Alzheimer’s Disease by altering neurotransmitter signaling, but not the underlying pathological mechanisms that cause the disease (amyloid production or neurofibrillary tangle accumulation). Neramexane is an uncompetitive NMDA receptor channel blocker.",,,,Neramexane is investigational.,Neramexane is a solid.,True
17520,,,,,SC-74020 is experimental.,SC-74020 is a solid.,False
17521,"A guanidinium antihypertensive agent that acts by blocking adrenergic transmission. For the treatment of hypertension. Bethanidine is a guanidinium antihypertensive agent that acts by blocking adrenergic transmission. The precise mode of action is not clear. Although bethanidine may produce adverse effects, they are beneficial in severe hypertension and produce fewer side effects than guanethidine. Bethanidine, a guanidine derivative, is a peripherally acting antiadrenergic agent which primarily acts as an alpha2a adrenergic agonist. Bethanidine effectively decreases blood pressure by suppressing renin secretion or interfering with function of the sympathetic nervous system.",The molecular weight is 177.25.,Bethanidine has a topological polar surface area of 36.42.,The log p value of  is 0.97.,Bethanidine is approved.,Bethanidine is a solid.,True
17522,"Fencamfamin (Glucoenergan, Reactivan) is a stimulant which was developed in the 1960s as an appetite suppressant, but was later withdrawn for this application due to problems with dependence and abuse. It is around half the potency of , and is prescribed at a dose of 10-60mg, although abusers of the drug tend to rapidly develop tolerance and escalate their dose. Fencamfamin is used for treating depressive day-time fatigue, lack of concentration and lethargy. It is especially useful in patients with chronic conditions due to its favourable safety profile. For the the treatment of depressive fatigue in convalescence and other debilitated states as well as in the treatment of depressive day-time fatigue, lack of concentration and lethargy. Fencamfamine increases drive and mental alertness and an elevation of mood and a general feeling of well-being. It is a central nervous system stimulant, which increases locomotor activity. Fencamfamine acts as an indirect dopamine agonist. It releases dopamine by a similar mechanism to amphetamines, but is 10x less potent than dexamphetamine at producing this effect. The drug seems to inhibit the dopamine transporter (DAT) that removes dopamine from the synapses. This inhibition of DAT blocks the reuptake of dopamine and norepinephrine into the presynaptic neuron, increasing the amount of dopamine in the synapse. It also stimulates the release of dopamine and norepinephrine into the synapse. Finally, it increases the magnitude of dopamine release after a stimulus, increasing the salience of stimulus. Also unlike amphetamines, fencamfamine does not inhibit the action of monoamine oxidase enzymes and so is somewhat safer. Some experiments also suggest a role for opioid receptors in the activity of fencamfamine, as low doses can cause paradoxical sedation, and some effects of the drug are blocked by naloxone.",The molecular weight is 215.34.,Fencamfamin has a topological polar surface area of 12.03.,The log p value of  is 3.87.,Fencamfamin is experimental and illicit and withdrawn.,Fencamfamin is a solid.,True
17523,"Boston Life Sciences (BLS) is developing Altropane as a potential radio-imaging agent to be used with single photon emission tomography (SPECT), for the early diagnosis of Parkinson's disease (PD) and attention deficit hyperactivity disorder (ADHD). Investigated for use/treatment in attention deficit/hyperactivity disorder (ADHD), parkinson's disease, and pediatric indications. Altropane is a molecular-imaging agent that specifically binds to the dopamine transporter (DAT) protein found on the surface of dopamine-producing neurons, making it visible during SPECT imaging. Since most forms of Parkinsonian Syndromes result in a decreased number of dopamine-producing cells, it would be expected that these patients also have fewer DATs than do patients without PS. Thus, it is believed that altropane used in conjunction with SPECT imaging could be a useful test to distinguish Parkinsonian Syndrome tremors from non-Parkinsonian tremor: non-Parkinsonian patients would have more altropane-binding visible in the SPECT image, while Parkinsonian patients would have less. Positron emission tomography (PET) cameras are expensive and scarce, and the tests are non-reimbursable. A less costly and more available test such as a single photon emission computed tomography (SPECT) may be helpful in the diagnosis of early or atypical Parkinson's disease (PD) if its sensitivity is comparable to a PET scan. Altropane is an iodinated form of the N-allyl analog of WIN 35,428 which acts as a dopamine transport inhibitor. When radiolabeled with the gamma emitting isotope , altropane serves as a SPECT ligand with high affinity and selectivity for the dopamine transporter. It is a good marker for dopamine neurons and is useful in detecting PD.",The molecular weight is 429.27.,Altropane has a topological polar surface area of 29.54.,The log p value of  is 4.51.,Altropane is investigational.,Altropane is a solid.,True
17524,"A cell-cycle phase nonspecific alkylating antineoplastic agent. It is used in the treatment of brain tumors and various other malignant neoplasms. (From Martindale, The Extra Pharmacopoeia, 30th ed, p462) This substance may reasonably be anticipated to be a carcinogen according to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (From Merck Index, 11th ed) For the treatment of brain tumors, multiple myeloma, Hodgkin's disease and Non-Hodgkin's lymphomas. Carmustine is one of the nitrosoureas indicated as palliative therapy as a single agent or in established combination therapy with other approved chemotherapeutic agents in treatment of brain tumors, multiple myeloma, Hodgkin's disease, and non-Hodgkin's lymphomas. Although it is generally agreed that carmustine alkylates DNA and RNA, it is not cross resistant with other alkylators. As with other nitrosoureas, it may also inhibit several key enzymatic processes by carbamoylation of amino acids in proteins. Carmustine causes cross-links in DNA and RNA, leading to the inhibition of DNA synthesis, RNA production and RNA translation (protein synthesis). Carmustine also binds to and modifies (carbamoylates) glutathione reductase. This leads to cell death.",The molecular weight is 214.05.,Carmustine has a topological polar surface area of 61.77.,The log p value of  is 1.32.,Carmustine is approved and investigational.,Carmustine is a solid.,True
17525,,,,,"3,6-dihydroxy-xanthene-9-propionic acid is experimental.","3,6-dihydroxy-xanthene-9-propionic acid is a solid.",False
17526,,,,,Glutathionylspermidine disulfide is experimental.,Glutathionylspermidine disulfide is a solid.,False
17527,,,,,3-(Prop-2-Ene-1-Sulfinyl)-Propene-1-Thiol is experimental.,3-(Prop-2-Ene-1-Sulfinyl)-Propene-1-Thiol is a solid.,False
17528,A GLUTATHIONE dimer formed by a disulfide bond between the cysteine sulfhydryl side chains during the course of being oxidized.,The molecular weight is 612.63.,Glutathione disulfide has a topological polar surface area of 317.64.,The log p value of  is -5.83.,Glutathione disulfide is approved and experimental and investigational.,Glutathione disulfide is a solid.,True
17529,,,,,3-nitro-L-tyrosine is experimental.,3-nitro-L-tyrosine is a solid.,False
17530,,,,,"2-(2-PHENYL-3-PYRIDIN-2-YL-4,5,6,7-TETRAHYDRO-2H-ISOPHOSPHINDOL-1-YL)PYRIDINE is experimental.","2-(2-PHENYL-3-PYRIDIN-2-YL-4,5,6,7-TETRAHYDRO-2H-ISOPHOSPHINDOL-1-YL)PYRIDINE is a solid.",False
17531,,,,,"6-(3-METHYL-1,4-DIOXO-1,4-DIHYDRONAPHTHALEN-2-YL)HEXANOIC ACID is experimental.","6-(3-METHYL-1,4-DIOXO-1,4-DIHYDRONAPHTHALEN-2-YL)HEXANOIC ACID is a solid.",False
17532,"SB-269970 is an experimental drug developed by GlaxoSmithKline. In the studies performed with this agent, it has been suggested that SB-269970 acts either as a selective antagonist or inverse agonist of the serotonin receptor 7 (5-HT7).",,,,SB-269970 is investigational.,SB-269970 is a solid.,True
17533,"A recombinant DNA-derived cytotoxic protein composed of the amino acid sequences for diphtheria toxin fragments A and B (Met 1-Thr 387)-His followed by the sequences for interleukin-2 (IL-2; Ala 1-Thr 133). It is produced in an E. coli expression system. For treatment of cutaneous T-cell lymphoma Denileukin diftitox (Ontak) directs the cytocidal action of diphtheria toxin to cells which express the IL-2 receptor. The human IL-2 receptor exists in three forms, low (CD25), intermediate (CD122/CD132) and high (CD25/CD122/CD132) affinity. Malignant cells expressing one or more of the subunits of the IL-2 receptor are found in certain leukemias and lymphomas including cutaneous T-cell lymphoma (CTCL). Ontak interacts with the high affinity IL-2 receptor on the cell surface and inhibits cellular protein synthesis, resulting in cell death within hours. Denileukin diftitox binds to the high-affinity IL-2 receptor complex. The IL-2 receptor (Tac) subunit is expressed on activated but not resting lymphocytes. The diphtheria toxin associated with Ontak then selectively kills the IL-2 bearing cells.",,,,Denileukin diftitox is approved and investigational.,Denileukin diftitox is a liquid.,True
17534,"A recombinant chimeric (murine/human) monoclonal antibody (IgG1k) that functions as an immunosuppressive agent, specifically binding to and blocking the interleukin-2 receptor a-chain (IL-2R alpha, also known as CD25 antigen) on the surface of activated T-lymphocytes. It is a 144 kDa glycoprotein obtained from fermentation of an established mouse myeloma cell line genetically engineered to express plasmids containing the human heavy and light chain constant region genes and mouse heavy and light chain variable region genes encoding the RFT5 antibody that binds selectively to the IL-2R alpha. For prophylactic treatment of kidney transplant rejection Basiliximab functions as an IL-2 receptor antagonist. Specifically it inhibits IL-2-mediated activation of lymphocytes, a critical pathway in the cellular immune response involved in allograft rejection. Basiliximab binds with high-affinity to the alpha-subunit (CD25) of the high-affinity IL-2 receptor. This inhibits IL-2 binding, which inhibits T-cell activation and prevents the body from mounting an immune response against the foreign kidney.",,,,Basiliximab is approved and investigational.,Basiliximab is a liquid.,True
17535,"Humanized IgG1 Mab that binds to the human interleukin-2 receptor (anti-Tac or anti-CD25). Daclizumab is a composite of human (90%) and murine (10%) antibody sequences. The human sequences were derived from the constant domains of human IgG1 and the variable framework regions of the Eu myeloma antibody. The murine sequences were derived from the complementarity-determining regions of a murine anti-Tac antibody. Zenapax is a humanized monoclonal antibody used for prevention of renal transplant rejection Zenapax functions as an IL-2 receptor antagonist. Specifically it inhibits IL-2-mediated activation of lymphocytes, a critical pathway in the cellular immune response involved in allograft rejection. Zenepax binds with high-affinity to the Tac subunit of the high-affinity IL-2 receptor complex and inhibits IL-2 binding. The IL-2 receptor (Tac) subunit is expressed on activated but not resting lymphocytes.",,,,Daclizumab is investigational and withdrawn.,Daclizumab is a liquid.,True
17536,"Human erythropoietin with 2 aa substitutions to enhance glycosylation (5 N-linked chains), 165 residues (MW=37 kD). Produced in Chinese hamster ovary (CHO) cells by recombinant DNA technology. For the treatment of anemia (from renal transplants or certain HIV treatment) Darbepoetin alfa is used in the treatment of anemia. It is involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. Darbepoetin alfa stimulates erythropoiesis by the same mechanism as endogenous erythropoietin. Erythropoietin interacts with",,,,Darbepoetin alfa is approved and investigational.,Darbepoetin alfa is a liquid.,True
17537,"Erythropoietin (EPO) is a growth factor produced in the kidneys that stimulates the production of red blood cells. It works by promoting the division and differentiation of committed erythroid progenitors in the bone marrow. Epoetin alfa (Epoge) was developed by Amgen Inc. in 1983 as the first rhEPO commercialized in the United States, followed by other alfa and beta formulations. Epoetin alfa is a 165-amino acid erythropoiesis-stimulating glycoprotein produced in cell culture using recombinant DNA technology and is used for the treatment of patients with anemia associated with various clinical conditions, such as chronic renal failure, antiviral drug therapy, chemotherapy, or a high risk for perioperative blood loss from surgical procedures. It has a molecular weight of approximately 30,400 daltons and is produced by mammalian cells into which the human erythropoietin gene has been introduced. The product contains the identical amino acid sequence of isolated natural erythropoietin and has the same biological activity as the endogenous erythropoietin. Epoetin alfa biosimilar, such as Retacrit (epoetin alfa-epbx or epoetin zeta), has been formulated to allow more access to treatment options for patients in the market. The biosimilar is approved by the FDA and EMA as a safe, effective and affordable biological product and displays equivalent clinical efficacy, potency, and purity to the reference product. Epoetin alfa formulations can be administered intravenously or subcutaneously. Indicated in adult and paediatric patients for the:  Erythropoietin and epoetin alfa are involved in the regulation of erythrocyte differentiation and the maintenance of a physiological level of circulating erythrocyte mass. It is reported to increase the reticulocyte count within 10 days of initiation, followed by increases in the RBC count, hemoglobin, and hematocrit, usually within 2 to 6 weeks. Depending on the dose administered, the rate of hemoglobin increase may vary. In patients receiving hemodialysis, a greater biologic response is not observed at doses exceeding 300 Units/kg 3 times weekly.  Erythropoietin or exogenous epoetin alfa binds to the erythropoietin receptor (EPO-R) and activates intracellular signal transduction pathways. The affinity (Kd) of EPO for its receptor on human cells is ∼100 to 200 pM. Upon binding to EPO-R on the surface of erythroid progenitor cells, a conformational change is induced which brings EPO-R-associated Janus family tyrosine protein kinase 2 (JAK2) molecules into close proximity. JAK2 molecules are subsequently activated via phosphorylation, then phosphorylate tyrosine residues in the cytoplasmic domain of the EPO-R that serve as docking sites for Src homology 2-domain-containing intracellular signaling proteins. The signalling proteins include STAT5 that once phosphorylated by JAK2, dissociates from the EPO-R, dimerizes, and translocates to the nucleus where they serve as transcription factors to activate target genes involved in cell division or differentiation, including the apoptosis inhibitor Bcl-x. The inhibition of apoptosis by the EPO-activated JAK2/STAT5/Bcl-x pathway is critical in erythroid differentiation. Via JAK2-mediated tyrosine phosphorylation, erythropoietin and epoetin alfa also activates other intracellular proteins involved in erythroid cell proliferation and survival, such as Shc , phosphatidylinositol 3-kinase (PI3K), and phospholipase C-γ1. ",,,,Erythropoietin is approved.,Erythropoietin is a liquid.,True
17538,,The molecular weight is 338.98.,Dibromotyrosine has a topological polar surface area of 83.55.,The log p value of  is -0.66.,Dibromotyrosine is experimental.,Dibromotyrosine is a solid.,False
17539,"Peginesatide is a synthetic peptide attached to polyethylene glycol for the treatment of anemia. The polyethylene glycol moiety helps make the drug less immunogenic and prolongs its plasma half-life. Chemically, peginesatide is designed to mimic the pharmacological activity of erythropoietin, but is not a replica of the structure itself. Peginesatide consists of two 21-amino acid chains that are covalently bonded by a linker derived from iminodiacetic acid and β-alanine. FDA approved March 27, 2012. Peginesatide is used for the treatment of anemia due to chronic kidney disease (CKD) in adult patients on dialysis  Peginesatide increases the reticulocyte count and levels of hemoglobin. It also increases RBC count, hematocrit, and soluble transferrin receptor protein in a dose-dependent manner.  Peginesatide binds to and activates the human erythropoietin receptor and stimulates erythropoiesis in human red cell precursors in vitro.",,,,Peginesatide is approved and investigational.,Peginesatide is a liquid.,True
17540,"Methoxy polyethylene glycol-epoetin beta is a chemically synthesised Erythropoiesis Stimulating Agent (ESA) with a longer half-life than erythropoietin. ESA is used to increase synthesis of red blood cells to treat chronic kidney disease associated anemia. For the treatment of patients with anaemia associated with chronic kidney disease. Not a substitute for RBC transfusion if immediate correction of anemia is required. Stimulates hemoglobin production by stimulating the erythropoetin receptor of erythroid progenitor cells in the bone marrow. Hemoglobin increase, following a single initial dose, occurs 7 to 15 days after. Erythropoietin is a growth factor for erythroid development. It is produced in the kidney and released into the bloodstream in response to hypoxia, interacting with erythroid progenitor cells to increase red blood cell production. Production of endogenous erythropoietin is impaired in patients with chronic kidney disease (CKD), and erythropoietin deficiency is the primary cause of their anaemia. Administration of methoxy polyethylene glycol-epoetin beta acts like endogenous erythropoetin and stimulates erythropoetin receptor of the erythroid progenitor cells in the bone marrow.",,,,Methoxy polyethylene glycol-epoetin beta is approved.,Methoxy polyethylene glycol-epoetin beta is a solid.,True
17541,Investigated for use/treatment in atherosclerosis. Darapladib is a selective lipoprotein-associated phospholipase A2 (Lp-PLA2) inhibitor. Lp-PLA2 is an enzymatic upstream mediator of inflammatory processes.,,,,Darapladib is investigational.,Darapladib is a solid.,True
17542,"ADX10061 is a potent, selective antagonist of the dopamine D1 receptor. It is developed by Addex Pharmaceuticals for the treatment of nicotine dependence. Investigated for use/treatment in sleep disorders, smoking cessation, and substance abuse. Activation of dopamine D1 receptor in the brain is implicated in reward-seeking behaviours and cue-induced craving, and is the fundamental mechanism by which nicotine causes addiction. Both reward (the “feel good” sensation a smoker gets from a cigarette) and cue (the habitual situations that trigger the craving to smoke) are important drivers of the desire to smoke. Blocking the D1 receptor will, it is hoped, reduce the association with the stimuli specific to reward-seeking behaviour that lead smokers who are trying to quit starting smoking again.",,,,ADX-10061 is investigational.,ADX-10061 is a solid.,True
17543,"DAS-431 IV is a dopamine D1 receptor agonist developed by DrugAbuse Sciences for the treatment of Addictions, Schizophrenia, Schizoaffective Disorders, Dementia, Parkinson's Disease, Strokes etc.  Investigated for use/treatment in addictions, dementia, parkinson's disease, schizophrenia and schizoaffective disorders, and strokes. DAS-431 IV is a dopamine D1 receptor agonist which is in Phase II evaluation for the treatment of cognitive impairment in the elderly and cocaine addiction and is in development for a broad range of CNS diseases, including schizophrenia. Dopamine D1 receptors are thought to play a role in mediating cognitive processes in the prefrontal cortex, particularly working memory. The number of D1 receptors appears to be decreased in the elderly, chronic addicts, patients with schizophrenia and, possibly, patients with Parkinson's disease and those who have experienced a stroke. DAS-431 directly activates D1 receptors in the prefrontal cortex and may be useful in treating these conditions. ",,,,DAS-431 IV is investigational.,DAS-431 IV is a solid.,True
17544,"ICA-105665 is a novel small molecule compound for the treatment of epilepsy. It is a novel opener of the KCNQ ion channel which in preclinical studies has demonstrated a broad spectrum of activity in models of epilepsy. In addition, ICA-105665 has also demonstrated activity in certain models of neuropathic pain. Investigated for use/treatment in epilepsy. ICA-105665 is an activator of subtypes of KCNQ ion channels, which are attractive targets for the treatment of epilepsy based on their function and genetic linkage to a seizure disorder.",,,,ICA-105665 is investigational.,ICA-105665 is a solid.,True
17545,"Gemtuzumab ozogamicin is a recombinant humanized IgG4 kappa antibody which is conjugated with calicheamicin derivative, a cytotoxic antitumor antibiotic isolated from fermentation of Micromonospora echinospora ssp. calichensis. Gemtuzumab ozogamicin has approximately 50% of the antibody loaded with 4-6 moles calicheamicin per mole of antibody. The antibody is specifically directed against the CD33 antigen present on leukemic myeloblasts in most patients with acute myeloid leukemia (AML). By binding to the CD33 antigen on tumors, the cytotoxic agent blocks the growth of cancerous cells and causes cell death.  Indicated for the treatment of patients with CD33 positive acute myeloid leukemia in first relapse who are 60 years of age or older and who are not considered candidates for other cytotoxic chemotherapy. Indicated for the treatment of patients aged 2 years and older with CD33-positive AML who have experienced a relapse or who have not responded to initial treatment (refractory).  Used for the treatment of acute myeloid leukemia (AML), mylotarg binds to the CD33 antigen, which is expressed on the surface of leukemic cells in more than 80% of patients with AML. The CD33 antigen is not expressed on pluripotent hematopoietic stem cells or nonhematopoietic cells. This gives mylotarg the selectivity needed to target leukemic cells. Mylotarg is directed against the CD33 antigen expressed by hematopoietic cells. Binding of the anti-CD33 antibody portion of Mylotarg with the CD33 antigen results in the formation of a complex that is internalized. Upon internalization, the calicheamicin derivative is released inside the lysosomes of the myeloid cell. The released calicheamicin derivative binds to DNA in the minor groove resulting in site-specific DNA double strand breaks via formation of a p-benzene diradical. Eventually, cell death is induced.",,,,Gemtuzumab ozogamicin is approved and investigational.,Gemtuzumab ozogamicin is a liquid.,True
17546,,,,,B-nonylglucoside is experimental.,B-nonylglucoside is a solid.,False
17547,,,,,(Hydroxyethyloxy)Tri(Ethyloxy)Octane is experimental.,(Hydroxyethyloxy)Tri(Ethyloxy)Octane is a solid.,False
17548,"Cetilistat is a novel inhibitor of pancreatic lipase being developed by Alizyme for the treatment of obesity and associated co-morbidities, including type 2 diabetes. Investigated for use/treatment in obesity. Cetilistat is a gastrointestinal lipase inhibitor that blocks fat digestion and absorption, leading to reduced energy intake, and thus weight loss. It is distinct from most other anti-obesity agents as it does not act on the brain to reduce appetite, but acts peripherally. The compound remains in the gastrointestinal tract with no significant absorption into the body.",The molecular weight is 401.59.,Cetilistat has a topological polar surface area of 47.89.,The log p value of  is 9.52.,Cetilistat is investigational.,Cetilistat is a solid.,True
17549,,,,,METHOXYUNDECYLPHOSPHINIC ACID is experimental.,METHOXYUNDECYLPHOSPHINIC ACID is a solid.,False
17550,,,,,4'-Hydroxyflavanone is experimental.,4'-Hydroxyflavanone is a solid.,False
17551,"Dioxybenzone, or benzophenone-8, is an organic compound derived from that is used as a sunscreen agent. It absorbed UV-B and UV-AII rays. Dioxybenzone is an approved sunscreen ingredient in concentrations up to 3%. Indicated for use as an active sunscreen agent.  Dioxybenzone is a sunscreen agent and chemical UV filter that absorbs UV-B rays and UV-AII rays to limit their penetration into human skin. In a screening protocol consisting of the _in vitro_ EBV-EA activation assay followed by the _in vivo_ confirmation test in the two-stage mouse skin cancer model utilizing NOR-1 as inducer and TPA as promoter of tumour, dioxybenzone exhibited a significant chemopreventive activity against mouse skin carcinogenesis which correlated with their antioxidant potency. There is some evidence that suggests some benzophenones and their hydroxylated metabolites act as weak estrogens in the environment; however similar effect of dioxybenzone has not been established.  Emitted by the sun, UVA-II rays, which range at 320–400 nm and are not absorbed by the ozone layer, and UVB rays, which range 290–320 nm and are partially absorbed by the ozone layer and exert a damaging effect on human skin, including basal cell carcinoma and melanoma. As a chemical filter, dioxybenzone absorb these rays to prevent their penetration into the skin and attenuate long-term skin damage caused by UV radiation from the sun. In a rat uterine cytosolic estrogen receptor (ER) competitive binding assay, dioxybenzone was not found to be a ER-binder. ",The molecular weight is 244.25.,Dioxybenzone has a topological polar surface area of 66.76.,The log p value of  is 3.49.,Dioxybenzone is approved.,Dioxybenzone is a solid.,True
17552,Equol has been used in trials studying the treatment of Breast Cancer.,,,,Equol is investigational.,,True
17553,,,,,Sucrosofate is experimental.,Sucrosofate is a solid.,False
17554,,,,,O2-Sulfo-Glucuronic Acid is experimental.,O2-Sulfo-Glucuronic Acid is a solid.,False
17555,,,,,"N,O6-Disulfo-Glucosamine is experimental.","N,O6-Disulfo-Glucosamine is a solid.",False
17556,,,,,Naphthalene Trisulfonate is experimental.,Naphthalene Trisulfonate is a solid.,False
17557,,,,,5-aminonaphthalene-2-sulfonic acid is experimental.,5-aminonaphthalene-2-sulfonic acid is a solid.,False
17558,"Pregabalin is structurally similar to gamma-aminobutyric acid (GABA) - an inhibitory neurotransmitter. It may be used to manage neuropathic pain, postherpetic neuralgia, and fibromyalgia among other conditions. Although as per the FDA Label the mechanism of action has not been definitively defined, there is evidence that pregabalin exerts its effects by binding to the α2δ subunit of voltage-dependent calcium channels. Pregabalin is marketed by Pfizer under the trade name Lyrica and Lyrica Cr (extended release). It may have dependence liability if misused but the risk appears to be highest in patients with current or past substance use disorders. Pregabalin is indicated for the management of neuropathic pain associated with diabetic peripheral neuropathy, postherpetic neuralgia, fibromyalgia, neuropathic pain associated with spinal cord injury, and as adjunctive therapy for the treatment of partial-onset seizures in patients 1 month of age and older. Although the structure of pregabalin is similar to gamma-aminobutyric acid (GABA), it does not bind to GABA receptors. Instead, it binds the alpha2-delta subunit of presynaptic voltage-gated calcium channels in the central nervous system. Pregabalin does not modulate dopamine receptors, serotonin receptors, opiate receptors, sodium channels or cyclooxygenase activity.  Although the mechanism of action has not been fully elucidated, studies involving structurally related drugs suggest that presynaptic binding of pregabalin to voltage-gated calcium channels is key to the antiseizure and antinociceptive effects observed in animal models. ",The molecular weight is 159.23.,Pregabalin has a topological polar surface area of 63.32.,The log p value of  is -0.92.,Pregabalin is approved and investigational.,Pregabalin is a solid.,True
17559,"Gabapentin enacarbil is marketed under the name Horizant. It is a prodrug of gabapentin, and indicated in adults for the treatment of Restless Legs Syndrome (RLS) and postherpetic neuralgia (PHN). For the treatment of adult Restless Legs Syndrome (RLS) and postherpetic neuralgia (PHN). Since gabapentin enacarbil is a prodrug of gabapentin, it's physiological effects are the same as gabapentin. Concerning PHN, gabapentin prevents allodynia and hyperalgesia. Although the exact mechanism of action of gabapentin in RLS and PHN is unknown, it is presumed to involve the descending noradrenergic system, resulting in the activation of spinal alpha2-adrenergic receptors. ",The molecular weight is 329.39.,Gabapentin enacarbil has a topological polar surface area of 101.93.,The log p value of  is 3.31.,Gabapentin enacarbil is approved and investigational.,Gabapentin enacarbil is a solid.,True
17560,"A beta-adrenergic agonist used in the treatment of asthma and bronchospasms.  For the treatment of bronchospasm, chronic bronchitis, asthma, and emphysema. Orciprenaline (also known as metaproterenol), a synthetic amine, is structurally and pharmacologically similar to isoproterenol. Orciprenaline is used exclusively as a bronchodilator. The pharmacological effects of beta adrenergic agonist drugs, such as orciprenaline, are at least in part attributable to stimulation through beta adrenergic receptors of intracellular adenyl cyclase, the enzyme which catalyzes the conversion of adenosine triphosphate (ATP) to cyclic- 3',5'- adenosine monophosphate (c-AMP). Increased cAMP levels lead to relaxation of bronchial smooth muscles and inhibition of the release of inalammatory mediators from mast cells that are involved in promoting immediate hypersensitivity. Orciprenaline stimulates the β2-adrenergic receptor expressed in the lungs, uterus, and vasculature supplying skeletal muscles by acting as a moderately selective agonist. It exerts minimal or no effect on alpha-adrenergic receptors. Intracellularly, the actions of orciprenaline are mediated by cAMP, the production of which is augmented by beta stimulation. The drug is believed to work by activating adenylate cyclase, the enzyme responsible for producing the cellular mediator cAMP.",The molecular weight is 211.26.,Orciprenaline has a topological polar surface area of 72.72.,The log p value of  is 0.08.,Orciprenaline is approved.,Orciprenaline is a solid.,True
17561,"Bitolterol mesylate was used to treat bronchospasms in asthma and COPD. It is a beta-2-adrenergic receptor agonist. Bitolterol was withdrawn from the market by Elan Pharmaceuticals in 2001. Used to dilate air passages in the lungs that have become narrowed as a result of disease or inflammation. It is used in the treatment of asthma and chronic obstructive pulmonary disease (COPD). Bitolterol, an adrenergic bronchodilator, is a prodrug that widens constricted airways in the lungs by relaxing the smooth muscles that surround the bronchial passages. Bitolterol probably does not affect the inflammation in the lung, such as in bronchitis. Bitolterol is unique in that it is a prodrug because it must first be metabolized by the body before it becomes active. Bitolterol is an adrenergic beta-2 agonist. Asthma results from a narrowing of the bronchial tubes. This narrowing is caused by muscle spasm and inflammation within the bronchial tubes. Agonism of the beta-2 adrenergic receptors by bitolterol leads to a relaxation of the smooth muscles surrounding these airway tubes which then increases the diameter and ease of air flow through the tubes.",The molecular weight is 461.56.,Bitolterol has a topological polar surface area of 84.86.,The log p value of  is 5.59.,Bitolterol is withdrawn.,Bitolterol is a solid.,True
17562,"A long-acting beta-2-adrenergic receptor agonist. It is a potent bronchodilator that may be administered orally or by aerosol inhalation.  For the treatment of asthma and chronic obstructive pulmonary disease (COPD). Procaterol is a long-acting beta-2-adrenergic receptor agonist. It is a potent bronchodilator that may be administered orally or by aerosol inhalation. Beta(2)-receptor stimulation in the lung causes relaxation of bronchial smooth muscle, bronchodilation, and increased bronchial airflow.",The molecular weight is 290.36.,Procaterol has a topological polar surface area of 81.59.,The log p value of  is 0.66.,Procaterol is approved and investigational.,Procaterol is a solid.,True
17563,Investigated for use/treatment in asthma and labor and delivery.,,,,Bedoradrine is investigational.,Bedoradrine is a solid.,True
17564,"NCX 950, beta2-adrenoceptor agonists is widely used in the treatment of pulmonary diseases. Investigated for use/treatment in asthma and chronic obstructive pulmonary disease (COPD). NCX-950 elicits potent relaxant and anti-inflammatory activities compared with salbutamol, and these effects may be mainly due to the activation of the beta2-adrenoceptor rather than the cGMP pathway.",,,,NCX 950 is investigational.,NCX 950 is a solid.,True
17565,Protokylol is a β-adrenergic receptor agonist used as a bronchodilator in Europe and the United States.,The molecular weight is 331.37.,Protokylol has a topological polar surface area of 91.18.,The log p value of  is 1.69.,Protokylol is approved and vet_approved.,Protokylol is a solid.,True
17566,,,,,(S)-carazolol is experimental.,(S)-carazolol is a solid.,False
17567,"Etafedrine (INN) or ethylephedrine is a long-acting bronchodilator and has been an ingredient combined with other drugs in the brand names Nethaprin and Dalmacol. It was previously available as both the free base and as the hydrochloride salt manufactured by Sanofi-Aventis (now Sanofi) has been discontinued. Conditions characterized by bronchial congestion and bronchospasm when an expectorant or bronchodilator action is required, such as acute bronchitis, acute episodes of chronic bronchitis and bronchial asthma ,.  A sympathomimetic agent, etafedrine acts on the sympathetic receptors of the bronchial tree, relieving spasm in a manner similar to that of ephedrine.",,,,Etafedrine is approved.,Etafedrine is a solid.,True
17568,Tulobuterol has been used in trials studying the treatment of Chronic Obstructive Pulmonary Disease.,The molecular weight is 227.73.,Tulobuterol has a topological polar surface area of 32.26.,The log p value of  is 2.53.,Tulobuterol is investigational.,,True
17569,,,,,"(3R)-4-(p-toluenesulfonyl)-1,4-thiazane-3-carboxylicacid-L-phenylalanine ethyl ester is experimental.","(3R)-4-(p-toluenesulfonyl)-1,4-thiazane-3-carboxylicacid-L-phenylalanine ethyl ester is a solid.",False
17570,,,,,{3--Piperidin-2yl}-Vinyloxy)-Propyl]-Phenoxy}-Acetic Acid is experimental.,{3--Piperidin-2yl}-Vinyloxy)-Propyl]-Phenoxy}-Acetic Acid is a solid.,False
17571,,,,,Gpi-1046 is experimental.,Gpi-1046 is a solid.,False
17572,,,,,Methyl Methylsulfinylmethyl Sulfide is experimental.,Methyl Methylsulfinylmethyl Sulfide is a solid.,False
17573,,,,,FKB-001 is experimental.,FKB-001 is a solid.,False
17574,,,,,Heptyl glucoside is experimental.,Heptyl glucoside is a solid.,False
17575,,,,,"L-709,587 is experimental.","L-709,587 is a solid.",False
17576,,,,,"(3r)-4-(P-Toluenesulfonyl)-1,4-Thiazane-3-Carboxylicacid-L-Leucine is experimental.","(3r)-4-(P-Toluenesulfonyl)-1,4-Thiazane-3-Carboxylicacid-L-Leucine is a solid.",False
17577,,,,,4-hydroxybutan-2-one is experimental.,4-hydroxybutan-2-one is a solid.,False
17578,,,,,"(21S)-1AZA-4,4-DIMETHYL-6,19-DIOXA-2,3,7,20-TETRAOXOBICYCLO PENTACOSANE is experimental.","(21S)-1AZA-4,4-DIMETHYL-6,19-DIOXA-2,3,7,20-TETRAOXOBICYCLO PENTACOSANE is a solid.",False
17579,,,,,5-(HEXAHYDRO-2-OXO-1H-THIENOIMIDAZOL-6-YL)PENTANAL is experimental.,5-(HEXAHYDRO-2-OXO-1H-THIENOIMIDAZOL-6-YL)PENTANAL is a solid.,False
17580,,,,,Soraphen A is experimental.,Soraphen A is a solid.,False
17581,,,,,2-Propanoic Acid is experimental.,2-Propanoic Acid is a solid.,False
17582,,,,,Haloxyfop-P is experimental.,Haloxyfop-P is a solid.,False
17583,"Dimeric fusion protein consisting of the extracellular ligand-binding portion of the human 75 kilodalton (p75) tumor necrosis factor receptor (TNFR) linked to the Fc portion of human IgG1. The Fc component of etanercept contains the CH2 domain, the CH3 domain and hinge region, but not the CH1 domain of IgG1. Etanercept is produced by recombinant DNA technology in a Chinese hamster ovary (CHO) mammalian cell expression system. It consists of 934 amino acids. It is used to treat or manage a variety of inflammatory conditions including rheumatoid arthritis (RA), ankylosing spondylitis (AS), and juvenile idiopathic poly-articular arthritis (JIA). Etanercept is indicated for the treatment of moderately to severely active rheumatoid arthritis in adults and in chronic moderate to severe plaque psoriasis in patients 4 years of age and older. It is also used to manage signs and symptoms of polyarticular idiopathic arthritis in those aged 2 years and older. Etanercept is also used to manage the symptoms of psoriatic arthritis and ankylosing spondylitis.  Etanercept binds specifically to tumor necrosis factor (TNF) and thereby modulates biological processes that are induced or regulated by TNF. Such processes or molecules affected include the level of adhesion molecules expressed, as well as serum levels of cytokines and matrix metalloproteinases. There are two distinct receptors for TNF (TNFRs), a 55 kilodalton protein (p55) and a 75 kilodalton protein (p75). The biological activity of TNF is dependent upon binding to either cell surface receptor (p75 or p55). Etanercept is a dimeric soluble form of the p75 TNF receptor that can bind to two TNF molecules, thereby effectively removing them from circulation. Notably, etancerpt is only capable of binding to the active trimeric form of TNF as its binding site is located in the cleft between subunits.TNF is a naturally occurring cytokine that is involved in normal inflammatory and immune responses. Increased levels of TNF are found in tissues and fluids of those with rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, and plaque psoriasis. ",,,,Etanercept is approved and investigational.,Etanercept is a liquid.,True
17584,"Adalimumab is a subcutaneously administered biological disease modifier for the treatment of rheumatoid arthritis and other chronic debilitating diseases mediated by tumor necrosis factor ,. It was originally launched by Abbvie in the U.S. and approved in 2002 by the FDA. This drug is frequently known as _Humira_. It is produced by recombinant DNA technology using a mammalian cell expression system. This drug is available in a prefilled syringe form and convenient pen form for subcutaneous self-administered doses. A new biosimilar to adalimumab, named _adalimumab-adaz_, was approved by the FDA on October 31, 2018. This biosimilar is known as _Hyrimoz_, and is a trademark of Novartis AG. The following are conditions for which adalimumab has been indicated , , , , ,.  After treatment with adalimumab, a decrease in levels of acute phase reactant proteins of inflammation (C­ reactive protein and erythrocyte sedimentation rate ) and serum cytokines (IL-6) was measured compared to baseline in patients diagnosed with rheumatoid arthritis. A decrease in CRP levels was also observed in patients diagnosed with Crohn’s disease. Serum levels of matrix metalloproteinases (MMP-1 and MMP-3) that lead to the tissue remodeling responsible for cartilage destruction were also found to be decreased after administration of adalimumab ,. A reduction in signs and symptoms of disease, the induction of a clinical response, an inhibition of structural damage, and improvements in physical function in adult and pediatric patients with various inflammatory conditions have been demonstrated , ,. Adalimumab binds with specificity to tumor necrosis factor-alpha (TNF-alpha) , and inhibits its interaction with the p55 and p75 cell surface TNF receptors. Adalimumab also lyses surface tumor necrosis factor expressing cells in vitro when in the presence of complement. Adalimumab does not bind or inactivate lymphotoxin (Tumor necrosis factor-beta). TNF is a naturally occurring cytokine that plays a role in normal inflammatory and immune responses. Increased levels of TNF are found in the joint synovial fluid of rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis patients, and play an imperative role in pathologic inflammation and the joint destruction that are major complications of these diseases. Increased levels of TNF are also measured in psoriasis plaques. In plaque psoriasis, treatment with adalimumab may decrease the epidermal thickness and inflammatory cell infiltration. The relationship between these pharmacodynamics and the mechanism(s) by which adalimumab achieves its clinical effects is not known. Additionally, adalimumab alters biological responses that are induced/regulated by TNF, including changes in the levels of adhesion molecules responsible for leukocyte migration during inflammation (ELAM-1, VCAM-1, and ICAM-1 with an IC50 of 1-2 X 10-10M).",,,,Adalimumab is approved and experimental.,Adalimumab is a liquid.,True
17585,"Infliximab is a tumor necrosis factor (TNF-alpha or TNF-α) blocker and a chimeric monoclonal IgG1 antibody composed of human constant (75%) and murine variable (25%) regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion. Tumor necrosis factor-alpha (TNF-α) is a key proinflammatory cytokine involved in chronic inflammatory diseases. Its hyperactivity and enhanced signalling pathways can be observed in inflammatory diseases where it activates further pro-inflammatory cascades. By binding to both the soluble subunit and the membrane-bound precursor of TNF-α , infliximab disrupts the interaction of TNF-α with its receptors and may also cause lysis of cells that produce TNF-α. * Indicated for reducing signs and symptoms and inducing and maintaining clinical remission in adult or pediatric (≥ 6 years of age) patients with moderately to severely active **Crohn’s disease** who have had an inadequate response to conventional therapy Infliximab disrupts the activation of pro-inflammaory cascade signalling. Infliximab has shown to reduce infiltration of inflammatory cells into sites of inflammation. It also attenautes the expression of molecules mediating cellular adhesion {including E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1)}, chemoattraction {. Infliximab is a IgG1κ monoclonal antibody that binds to soluble and transmembrane forms of TNF-α with high affinity to disrupt the pro-inflammatory cascade signalling. Binding of the antibody to TNF-α prevents TNF-α from interacting with its receptors. Infliximab does not neutralize TNF-β (lymphotoxin-α), a related cytokine that utilizes the same receptors as TNF-α. Blocked actions of TNF-α further leads to downregulation of local and systemic pro-inflammatory cytokines (i.e. IL-1, IL-6), reduction of lymphocyte and leukocyte migration to sites of inflammation, induction of apoptosis of TNF-producing cells (i.e. activated monocytes and T lymphocytes), increased levels of nuclear factor-κB inhibitor, and reduction of reduction of endothelial adhesion molecules and acute phase proteins. Its inhibitory actions on TNF-α was demonstrated in human fibroblasts, endothelial cells, neutrophils, B and Tlymphocytes and epithelial cells. Infliximab also atteunates the production of tissue degrading enzymes synthesized by synoviocytes and/or chondrocytes. According to a transgenic mice study that developed polyarthritis due to consitutive levels of human TNF-α, infliximab decreased synovitis and joint erosions in collagen-induced arthritis and allows eroded joints to heal. ",,,,Infliximab is approved.,Infliximab is a liquid.,True
17586,"Afelimomab (also known as Fab 2 or MAK 195F) is an anti-TNF-α monoclonal antibody. Administration of 195F reduces the concentration of interleukin-6 in patients with sepsis. Investigated for use/treatment in sepsis and septicemia. Afelimomab is the F(ab')2 fragment of a murine anti-TNF-alpha antibody, and has been evaluated in clinical trials in septic patients. The results suggest that the drug is well tolerated, and may be of benefit in certain groups of patients with sepsis. Afelimomab is safe, biologically active, and well tolerated in patients with severe sepsis, reduces 28-day all-cause mortality, and attenuates the severity of organ dysfunction in patients with elevated interleukin-6 levels.",,,,Afelimomab is investigational.,Afelimomab is a solid.,True
17587,"YSIL6 is a small-molecule drug in development for the treatment of inflammatory diseases, including rheumatoid arthritis and psoriasis. The molecule works by inhibiting TNF-alpha and IL-6 production in T-cells and macrophages, and by inhibiting T-cell proliferation and migration. Investigated for use/treatment in crohn's disease, psoriasis and psoriatic disorders, and rheumatoid arthritis. The molecule works by inhibiting TNF-alpha and IL-6 production in T-cells and macrophages, and by inhibiting T-cell proliferation and migration.",,,,YSIL6 is investigational.,YSIL6 is a solid.,True
17588,"PN0621 is an anti-TNF, domain antibody (dAb) based therapeutic. It targets tumour necrosis factor (TNF) to treat auto-immune inflammatory diseases such as rheumatoid arthritis. It is being developed by Peptech. Intended for the treatment of auto-immune diseases such as rheumatoid arthritis, psoriasis and Crohn's disease. PN0621 is an anti-TNF, a name given to a class of drugs being developed for the treatment of auto-immune diseases such as rheumatoid arthritis, psoriasis and Crohn's disease. Auto-immune diseases are indicated where an individual's immune system mistakenly attacks the body's own tissues. PN0621 works by blocking the action of TNF (tumour necrosis factor) which is involved in this attack.",,,,PN0621 is investigational.,PN0621 is a liquid.,True
17589,"Talmapimod is the first-generation oral p38 MAP kinase inhibitor developed by Scios. It has shown to be effective to cure inflammatory diseases such as Rheumatoid Arthritis. Investigated for use/treatment in pain (acute or chronic) and rheumatoid arthritis. SCIO-469 inhibits p38 kinase, a stimulatory modulator of pro-inflammatory factors including tumor necrosis factor-alpha (TNFa), interleukin-1 (IL-1), and cyclooxygenase-2 (COX-2), all of which are known to contribute to both symptoms and disease progression in patients with Rheumatoid Arthritis (RA). Existing protein-based products that antagonize TNFa have been shown to markedly relieve the symptoms and retard the progression of RA. It also has the potential for additional benefits associated with its inhibition of IL-1 and COX-2.",,,,Talmapimod is investigational.,Talmapimod is a solid.,True
17590,"VX-702 is a small molecule investigational oral anti-cytokine therapy for treatment of inflammatory diseases, specifically rheumatoid arthritis (RA). It acts as a p38 MAP kinase inhibitor. In the future, VX-702 may be investigated for combination with methotrexate, a commonly used therapy for RA. Investigated for use/treatment in coronary artery disease, inflammatory disorders (unspecified), and rheumatoid arthritis. VX-703 is an anti-cytokine therapy in which p38 MAP kinase inhibitor effectively inhibits LPS-stimulated TNF||, IL-6 and IL-1|| production. This p38 MAP kinase inhibitor effectively inhibits LPS-stimulated TNF||, IL-6 and IL-1|| production.",,,,VX-702 is investigational.,VX-702 is a solid.,True
17591,"Investigated for use/treatment in cancer/tumors (unspecified), multiple myeloma, and rheumatoid arthritis.",,,,Atiprimod is investigational.,Atiprimod is a solid.,True
17592,"CRx-139 is an oral synergistic combination drug candidates with novel mechanisms of action targeting multiple biological pathways simultaneously. It is a dissociated steroid designed to enhance the immuno-modulatory activity of a low-dose glucocorticoid steroid without a comparable increase in steroid-related side effects. The synergistic combination containing low doses of the glucocorticoid steroid prednisolone and the antidepressant paroxetine. This novel synergistic combination is developed for the treatment of immuno-inflammatory diseases. Investigated for use/treatment in rheumatoid arthritis. CRx-139 inhibits certain pro-inflammatory biomarkers, such as TNF-alpha, IL-6 and CRP and increases the anti-inflammatory cytokine IL-10.",,,,CRx-139 is investigational.,CRx-139 is a solid.,True
17593,"CYT007-TNFQb is an active immunization therapy that aims at Investigated for use/treatment in psoriasis and psoriatic disorders. CYT007-TNFQb is designed to instruct the patient’s immune system to produce an anti-TNF-α antibody response. The induced antibodies aim to bind and neutrolize soluble TNF-α in order to inhibit its inflammatory activity. That way, the subsequent inflammatory process should be slowed down and the deterioration of skin or other tissues reduced.",,,,CYT007-TNFQb is investigational.,CYT007-TNFQb is a solid.,True
17594,"Andrographolide (HMPL-004) is a botanical product extracted from a herb that occurs naturally in China. The herb has an extensive history of use in TCM for the treatment of upper respiratory tract infections and other inflammatory and infectious diseases. Investigated for use/treatment in ulcerative colitis. HMPL-004 acts on multiple cellular targets in the inflammatory signal transduction pathways resulting in suppressed inflammation cytokine expression including TNF-α, IL-1β and IL-6. HMPL-004 was demonstrated to inhibit TNF-α and IL-1β production in cell-based assays. HMPL-004 is also able to inhibit NF-kB activation. NF-kB is a family of transcriptional factors that regulate a wide spectrum of genes critically involved in host defence and inflammation. The mechanism of action of HMPL-004 was further supported in laboratory IBD animal models. Treatment of IBD rats with HMPL-004 caused a significant drop in plasma cytokine concentrations, including TNF-α and IL-1β.",,,,Andrographolide is investigational.,Andrographolide is a solid.,True
17595,"CTI-01 (ethyl pyruvate) is a novel anti-inflammatory agent for the treatment of critical inflammatory conditions. CTI-01 shows a potent anti-inflammatory and tissue protection activity in multiple animal models of disease including pancreatitis, ischemia-reperfusion injury, sepsis, renal injury and endotoxemia. Investigated for use/treatment in burns and burn infections, cardiac surgery, inflammatory disorders (unspecified), ischemic reperfusion injury, and sepsis and septicemia. CTI-01 inhibits the systemic release of cytokines, such as TNF-alpha and HMGB1, which promote the body's inflammatory response. The over-expression of these cytokines has been linked to diseases that occur in critical care settings, such as severe organ damage following cardiopulmonary bypass (CPB) and post-operative ileus following abdominal surgery.",,,,Ethyl pyruvate is investigational.,Ethyl pyruvate is a solid.,True
17596,"AME-527 is a humanized monoclonal antibody that recognizes human TNF-alpha (hTNF-alpha) with high affinity and specificity. AME-527 was generated by protein engineering and identified from a library of antibody variants based on its improved binding properties.  Investigated for use/treatment in rheumatoid arthritis. AME-527 is approximately ten-fold more potent than Remicade(R) in binding to and neutralizing the hTNF-alpha molecule, and 6 to 8-fold more potent than Humira(TM). Tumor necrosis factor-alpha (TNF-alpha) has a key role in rheumatoid synovitis, as an inflammatory cytokine at the top of the inflammatory cascade. Blocking TNF-alpha with AME-527 or fusion proteins is an important and established disease intervention, validating the role of the cytokine in disease activity and progression.",,,,AME-527 is investigational.,AME-527 is a solid.,True
17597,"Investigated for use/treatment in cancer/tumors (unspecified) and solid tumors. PR-104 is a novel hypoxia-activated DNA cross-linking agent with marked activity against human tumor xenografts, both as monotherapy and combined with radiotherapy and chemotherapy. Upon intravenous administration, PR-104 is converted by systemic phosphatases to the alcohol intermediate PR-104A, which is reduced to form the active DNA-crosslinking mustard species hydroxylamine PR-104H intracellularly under hypoxic conditions. PR-104H specifically crosslinks hypoxic tumor cell DNA, resulting in the inhibition of DNA repair and synthesis, cell-cycle arrest, and apoptosis in susceptible hypoxic tumor cell populations while sparing normoxic tissues.",,,,PR-104 is investigational.,PR-104 is a solid.,True
17598,"Investigated for use/treatment in cancer/tumors (unspecified). NPI-2358 is a vascular disrupting agent currently in clinical development for the treatment of cancer by Nereus. NPI-2358 is one of over 200 synthetic analogues that were prepared following the discovery of the compound Halimide isolated from a marine fungus. In preclinical models of cancer, including lung, breast, sarcoma, colon and prostate, NPI-2358 demonstrated potent and selective anti-tumor effects in combination with docetaxel and other oncology therapies, as well as single-agent efficacy in a number of orthotopic models. NPI-2358 interacts with soluble beta-tubulin and prevents the polymerization of tubulin without altering dynamic microtubule function of formed microtubules. As demonstrated in preclinical testing, this target profile results in a highly specific nanomolar cytotoxicity while reducing the side effects seen in first-generation VDAs due to cardiotoxicity, hemodynamic changes and neuropathies.",,,,Plinabulin is investigational.,Plinabulin is a solid.,True
17599,Investigated for use/treatment in traumatic brain injuries and neurologic disorders.,,,,Dexanabinol is investigational.,Dexanabinol is a solid.,True
17600,Investigated for use/treatment in psoriasis and psoriatic disorders and crohn's disease. Tumor necrosis factor (TNF) is a proinflammatory cytokine that plays a pivotal part in the pathogenesis of Crohn’s disease (CD).1 A number of anti-TNF therapies have been developed for the treatment of CD. Onercept is a recombinant form of the soluble human p55 TNF-greek small letter alpha receptor (also known as TNF-binding protein 1) produced by recombinant DNA technology. Its putative mechanism of action involves neutralizing the effects of TNF by the formation of high-affinity complexes.,,,,Onercept is investigational.,Onercept is a solid.,True
17601,"Golimumab is a human IgG1қ monoclonal antibody derived from immunizing genetically engineered mice with human TNFα. Golimumab binds and inhibits soluble and transmembrane human TNFα. Increased TNFα is associated with chronic inflammation. Thus golimumab is indicated for use in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) alone or as an adjunct to methotrexate treatment in patients with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS), and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. In the U.S. and Canada, golimumab is marketed under the brand name Simponi®. The FDA label includes a black box warning of serious infections and malignancy. Additionally in children and adolescents taking golimumab, there have been lymphoma and other malignancies observed. Used in adults (i) as an adjunct to methotrexate treatment in patients with moderate to severe active rheumatoid arthritis (RA), (ii) in patients 2 years old and above with active psoriatic arthritis (PsA), (iii) as a single agent in patients with active ankylosing spondylitis (AS) or in combination with methotrexate, and (iv) as a single agent in patients with moderate to severe ulcerative colitis (UC) who require chronic steroids or have experienced intolerance or only a partial response to previous medications. It is also indicated (v) for the treatment of active polyarticular juvenile idiopathic arthritis (pJIA) in patients 2 years of age and older. Golimumab inhibits the activity of the cytokine, tumor necrosis factor alpha (TNFα). In areas such as the joints and blood, increased TNFα is associated with chronic inflammation seen in patients with rheumatoid arthritis, psoriatic arthritis, and ankylosing spondylitis. Thus golimumab decreases the inflammation in these conditions. Concerning ulcerative colitis, the physiological effects of golimumab has yet to be determined. As a human monoclonal antibody, golimumab binds and inhibits soluble and transmembrane human TNFα. Inhibition of TNFα prevents it binding to its receptors, which prevents both leukocyte infiltration through prevention of cell adhesion proteins such as E-selectin, ICAM-1 and VCAM-1, and pro-inflammatory cytokine secretion such as IL-6, IL-8, G-CSF and GM-CSF in vitro. Consequently, in patients with chronic inflammatory conditions, decreases in ICAM-1 and IL-6 as well as C-reactive protein (CRP), matrix metalloproteinase 3 (MMP-3), and vascular endothelial growth factor (VEGF) were observed.",,,,Golimumab is approved.,Golimumab is a liquid.,True
17602,"Dilmapimod has been used in trials studying the treatment and diagnostic of Nerve Trauma, Inflammation, Pain, Neuropathic, Arthritis, Rheumatoid, and Coronary Heart Disease, among others. Dilmapimod (SB-681323) is a p38 MAP-kinase inhibitor that has potential uses in inflammatory conditions such as RA (Rheumatoid Arthritis). Previous p38 MAP-kinase inhibitors have been hindered in development by liver toxicity. Methotrexate (common treatment for RA patients) also has potential liver toxicity.} Dilmapimod has been used in trials studying the treatment and diagnostic of Nerve Trauma, Inflammation, Pain, Neuropathic, Arthritis, Rheumatoid, and Coronary Heart Disease, among others. Dilmapimod reduces the levels of proinflammatory cytokines and chemokines and reduce cellular infiltration to sites of inflammation, thereby reducing local damage. ",,,,Dilmapimod is investigational.,,True
17603,"Used in the treatment of asthma, cinalukast selectively antagonizes leukotriene D4 (LTD4) at the cysteinyl leukotriene receptor, CysLT1, in the human airway. Cinalukast inhibits the actions of LTD4 at the CysLT1 receptor, preventing airway edema, smooth muscle contraction, and enhanced secretion of thick, viscous mucus. For Protection against second- phase inflamation in exercise-induced bronchoconstriction and Asthma. Used in the treatment of asthma, cinalukast selectively antagonizes leukotriene D4 (LTD<sub>4</sub>) at the cysteinyl leukotriene receptor, CysLT1, in the human airway. Cinalukast inhibits the actions of LTD<sub>4</sub> at the CysLT1 receptor, preventing airway edema, smooth muscle contraction, and enhanced secretion of thick, viscous mucus. Binds to the cysteinyl leukotriene receptor. The cysteinyl leukotrienes (LTC4, LTD<sub>4</sub>, LTE4) are products of arachidonic acid metabolism and are released from various cells, including mast cells and eosinophils. These eicosanoids bind to cysteinyl leukotriene receptors (CysLT) found in the human airway. Cysteinyl leukotrienes and leukotriene receptor occupation have been correlated with the pathophysiology of asthma, including airway edema, smooth muscle contraction, and altered cellular activity associated with the inflammatory process, which contribute to the signs and symptoms of asthma.",The molecular weight is 412.55.,Cinalukast has a topological polar surface area of 79.29.,The log p value of  is 5.25.,Cinalukast is experimental.,Cinalukast is a solid.,True
17604,,,,,"3-(2,6-difluorophenyl)-2-(methylthio)quinazolin-4(3H)-one is experimental.","3-(2,6-difluorophenyl)-2-(methylthio)quinazolin-4(3H)-one is a solid.",False
17605,"Cetuximab is an epidermal growth factor receptor binding FAB. Cetuximab is composed of the Fv (variable; antigen-binding) regions of the 225 murine EGFr monoclonal antibody specific for the N-terminal portion of human EGFr with human IgG1 heavy and kappa light chain constant (framework) regions. Cetuximab is marketed under the brand Erbitux® by Eli Lilly and Company. In the United States, a regimen of cetuximab costs approximately $30,790 for an eight-week course. Cetuximab, used in combination with irinotecan, is indicated for the treatment of EGFR-expressing, metastatic colorectal carcinoma in patients who are refractory to irinotecan-based chemotherapy. Cetuximab administered as a single agent is indicated for the treatment of EGFR-expressing, metastatic colorectal carcinoma in patients who are intolerant to irinotecan-based chemotherapy. Used in the treatment of colorectal cancer, cetuximab binds specifically to the epidermal growth factor receptor (EGFr, HER1, c-ErbB-1) on both normal and tumor cells. EGFr is over-expressed in many colorectal cancers. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and other ligands, such as transforming growth factor–alpha. Binding of cetuximab to the EGFr blocks phosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased matrix metalloproteinase secretion and reduced vascular endothelial growth factor production. Cetuximab binds to the epidermal growth factor receptor (EGFr) on both normal and tumor cells. EGFr is over-expressed in many colorectal cancers. Cetuximab competitively inhibits the binding of epidermal growth factor (EGF) and TGF alpha, thereby reducing their effects on cell growth and metastatic spread.",,,,Cetuximab is approved.,Cetuximab is a liquid.,True
17606,"Intravenous immunoglobulin (IVIg) is a mixture of IgG1 and other antibodies derived from healthy human plasma via Cohn fractionation. The purification process includes cold alcohol fractionation, polyethylene glycol precipitation, and ion exchange chromatography. IVIg contains the same distribution of IgG antibody subclasses as is found in the general human population. IgG subclasses are fully represented in the following proportions: 70.3% IgG1, 24.7% IgG2, 3.1% IgG3, and 1.9% IgG4. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. IVIg is used in the treatment of immunodeficiencies, as well as autoimmune and inflammatory disorders. These indications includes idiopathic thrombocytopenic purpura, Kawasaki disease, hypogammaglobulinemia, B cell chronic lymphocytic leukemia, bone marrow transplant complications, Guillain-Barré syndrome, chronic inflammatory demyelinating polyneuropathy (CIDP), multiple sclerosis, rheumatoid arthritis, myesthenia gravis, Wiskott–Aldrich syndrome and inflammatory skin diseases. Used as a replacement therapy in inherited humoral immunodeficiency disorders such as severe combined immunodeficiency syndrome, x-linked agammaglobulinemia, and Wiskott-Aldrich Syndrome. The immunoglobulins target, bind and kill bacterial cells as well as viral particles. IgG is the monomeric immunoglobulin of which there are four subclasses (IgG1, IgG2, IgG3 and IgG4) in differing abundances (66%, 23%, 7% and 4%). IgAs represent about 15% of the immunoglobulins in the blood. These target inhaled or ingested pathogens. IVIg interacts with a number of different components of the immune system, including cytokines, complement, Fc receptors and several cell surface immunocompetent molecules. IVIg also impacts different effector cells of the immune system (B and T lymphocytes, dendritic cells, etc.) and regulates a wide range of genes. Its main mechanism of actions are believed to be Fc-dependent and F(ab')2-dependent. IVIg competitively blocks gamma Fc receptors, preventing the binding and ingestion of phagocytes and suppressing platelet depletion. IVIg contains a number of different antobodies, which prevent infection by attaching to the surface of invading pathogens and aiding in their disposal before they can infect cells. Antibodies remove pathogens via complement activation, agglutination or precipitation, pathogen receptor blocking, macrophage “tagging” or neutralization (via binding) of pathogen toxins. Intact IVIg and F(ab′)2 fragments of IVIg can also neutralize the activity of various autoantibodies. By triggering the production of interleukin-1 receptor antagonist, IVIg modulates of the production of cytokines and cytokine antagonists. It also prevents the generation of the C5b-9 membrane attack complex and subsequent complement-mediated tissue damage by binding active complement components.",,,,Human immunoglobulin G is approved and investigational.,Human immunoglobulin G is a liquid.,True
17607,"Humanized monoclonal antibody (IgG1k) produced by recombinant DNA technology, directed to an epitope in the A antigenic site of the F protein of respiratory syncytial virus (RSV). Synagis is a composite of human (95%) and murine (5%) antibody sequences. The human heavy chain sequence was derived from the constant domains of human IgG1 and the variable framework regions of the VH genes Cor (1) and Cess (2). The human lightchain sequence was derived from the constant domain of Ck and the variable framework regions of the VL gene K104 withJk-4. Palivizumab is expressed from a stable murine (mouse) myeloma cell line (NS0). Palivizumab is composed of to heavy chains (50.6 kDa each) and two light chains (27.6 kDa each), contains 1-2% carbohydrate by weight and has a molecular weight of 147.7 kDa +/- 1 kDa (MALDI-TOF) For prophylaxis of respiratory diseases casued by respiratory syncytial virus. Synagis exhibits neutralizing and fusion-inhibitory activity against Respiratory syncytial virus (RSV). These activities inhibit RSV replication or spread. Synagis is given to prevent the development of lower respiratory tract disease in pediatric patients. Palivizumab binds to the fusion glycoprotein of RSV. This prevents its binding and uptake by host cellular receptors.",,,,Palivizumab is approved and investigational.,Palivizumab is a liquid.,True
17608,"An indandione that has been used as an anticoagulant. Phenindione has actions similar to warfarin, but it is now rarely employed because of its higher incidence of severe adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p234) For the treatment of pulmonary embolism, cardiomyopathy, atrial fibrillation and flutter, cerebral embolism, mural thrombosis, and thrombophili. Also used for anticoagulant prophylaxis. Phenindione thins the blood by antagonizing vitamin K which is required for the production of clotting factors in the liver. Anticoagulants such as Phenindione have no direct effect on an established thrombus, nor do they reverse ischemic tissue damage (damage caused by an inadequate blood supply to an organ or part of the body). However, once a thrombus has occurred, the goal of anticoagulant treatment is to prevent further extension of the formed clot and prevent secondary thromboembolic complications which may result in serious and possibly fatal sequelae. Phenindione has actions similar to warfarin, but it is now rarely employed because of its higer incidence of severe adverse effects. Phenindione inhibits vitamin K reductase, resulting in depletion of the reduced form of vitamin K (vitamin KH2). As vitamin K is a cofactor for the carboxylation of glutamate residues on the N-terminal regions of vitamin K-dependent proteins, this limits the gamma-carboxylation and subsequent activation of the vitamin K-dependent coagulant proteins. The synthesis of vitamin K-dependent coagulation factors II, VII, IX, and X and anticoagulant proteins C and S is inhibited. Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decreased prothrombin levels and a decrease in the amount of thrombin generated and bound to fibrin. This reduces the thrombogenicity of clots.",The molecular weight is 222.24.,Phenindione has a topological polar surface area of 34.14.,The log p value of  is 2.81.,Phenindione is approved and investigational.,Phenindione is a solid.,True
17609,,,,,(Diaminomethyl-Methyl-Amino)-Acetic Acid is experimental.,(Diaminomethyl-Methyl-Amino)-Acetic Acid is a solid.,False
17610,A D-α-amino acid that is the D-isomer of arginine (only the L-form is physiologically active).,,,,D-arginine is experimental.,D-arginine is a solid.,True
17611,"WX-UK1 is a 3-amidinophenylalanine-based non-cytotoxic small molecule that belongs to a new class of drugs. In animal models, WX-UK1 blocks tumor cell invasion, metastasis and primary tumor growth by inhibiting serine proteases and the urokinase Plasminogen Activator (uPA) system, which have been shown to play a key role in metastasis and primary tumor growth of breast, gastric, colon cancer, and various other solid tumors. Independent studies show that administration of Wx-UK1 resulted in a decrease of tumor cell invasion, suggesting its efficacy as a an adjuvant antimetastatic therapy of carcinomas. Investigated for use/treatment in solid tumors. WX-UK1 is a 3-amidinophenylalanine-based non-cytotoxic small molecule that belongs to a new class of drugs. In animal models, WX-UK1 blocks tumor cell invasion, metastasis and primary tumor growth by inhibiting serine proteases and the urokinase Plasminogen Activator (uPA) system, which have been shown to play a key role in metastasis and primary tumor growth of breast, gastric, colon cancer, and various other solid tumors.  Activity at urokinase plasminogen activator receptors (uPAR) results in inhibition of uPA system. ",,,,WX-UK1 is investigational.,WX-UK1 is a solid.,True
17612,"Immunosuppressive dimeric fusion protein that consists of the extracellular CD2-binding portion of the human leukocyte function antigen-3 (LFA-3) linked to the Fc (hinge, CH2 and CH3 domains) portion of human IgG1. Produced by CHO cells, mW is 91.4 kD. As an immunosuppressive drug, Alefacept can be used for treatment of moderate to severe chronic plaque psoriasis Interferes with lymphocyte activation by specifically binding to the lymphocyte antigen, CD2, and inhibiting LFA-3/CD2 interaction. Activation of T lymphocytes involving the interaction between LFA-3 on antigen-presenting cells and CD2 on T lymphocytes plays a role in the pathophysiology of chronic plaque psoriasis. Also causes a reduction in subsets of CD2+ T lymphocytes as well as CD4+ and CD8+ T lymphocytes. Inhibits T-lymphocyte activation and production by binding to the CD2 lymphocyte antigen.",,,,Alefacept is approved and investigational and withdrawn.,Alefacept is a liquid.,True
17613,"Investigated for use/treatment in psoriasis and psoriatic disorders, transplant (rejection), graft versus host disease, lymphoma (unspecified), and leukemia (unspecified). Siplizumab has been shown to cause depletion of T-cells. It is therefore considered to be an immunomodulator in clinical settings where the depletion of T-cells may have clinical benefits, such as certain autoimmune diseases and T-cell cancers. In addition, preclinical studies have also suggested that siplizumab, by binding to the CD2 receptor, may selectively produce cell death and reduce cancerous cells.",,,,Siplizumab is investigational.,Siplizumab is a solid.,True
17614,,,,,(+)-Rutamarin alcohol is experimental.,(+)-Rutamarin alcohol is a solid.,False
17615,,,,,N-naphthalen-1-ylmethyl-2'--2'-deoxy-adenosine is experimental.,N-naphthalen-1-ylmethyl-2'--2'-deoxy-adenosine is a solid.,False
17616,,,,,2'-Deoxy-2'--N-adenosine is experimental.,2'-Deoxy-2'--N-adenosine is a solid.,False
17617,,,,,N--Isoleucine is experimental.,N--Isoleucine is a solid.,False
17618,,,,,alpha-Ketoisovalerate is experimental.,alpha-Ketoisovalerate is a solid.,False
17619,,,,,Selenazole-4-carboxyamide-adenine dinucleotide is experimental.,Selenazole-4-carboxyamide-adenine dinucleotide is a solid.,False
17620,,,,,"6-Chloropurine Riboside, 5'-Monophosphate is experimental.","6-Chloropurine Riboside, 5'-Monophosphate is a solid.",False
17621,Inosine 5'-Monophosphate. A purine nucleotide which has hypoxanthine as the base and one phosphate group esterified to the sugar moiety.,,,,Inosinic Acid is experimental.,Inosinic Acid is a solid.,True
17622,"VX-148 is a second-generation, orally administered inhibitor of inosine monophosphate dehydrogenase (IMPDH). The IMPDH enzyme plays a key role in regulating immune response and proliferation of specific cell types, including lymphocytes. VX-148 is a developed for the treatment of autoimmune diseases. Investigated for use/treatment in autoimmune diseases, psoriasis and psoriatic disorders, and viral infection. VX-148 is a potent inhibitor of inosine monophosphate dehydrogenase (IMPDH), a cellular enzyme that is essential for production of guanine nucleotides, one of the building blocks of RNA and DNA.",,,,VX-148 is investigational.,VX-148 is a solid.,True
17623,"Levoketoconazole is a cortisol synthesis inhibitor that is being developed as a therapy for glucose and cholesterol control in patients with type 2 diabetes mellitus. Investigated for use/treatment in diabetes mellitus type 2. Preliminary data suggests that DIO-902 increases insulin sensitivity by lowering cortisol levels. The primary mechanism of action is via inhibition of the 11-β-hydroxylase enzyme, the terminal step in cortisol synthesis in the adrenal gland. DIO-902 has also been shown to lower total and LDL-cholesterol by inhibiting 14-α-demethylase, a key enzyme in cholesterol synthesis. In combination with a typical glucose-lowering agent, such as metformin, DIO-902 may enhance glucose control and improve total and LDL-cholesterol. ",,,,Levoketoconazole is investigational.,Levoketoconazole is a solid.,True
17624,"Cardioactive derivative of lanatoside A or of digitoxin used for fast digitalization in congestive heart failure. Used for fast digitalization in congestive heart failure. The main pharmacological effects of acetyldigitoxin are on the heart. Extracardiac effects are responsible for many of the adverse effects. Its main cardiac effects are 1) a decrease of conduction of electrical impulses through the AV node, making it a commonly used drug in controlling the heart rate during atrial fibrillation or atrial flutter, and 2) an increase of force of contraction via inhibition of the Na<sup>+</sup>/K<sup>+</sup> ATPase pump. Acetyldigitoxin binds to a site on the extracellular aspect of the &alpha;-subunit of the Na<sup>+</sup>/K<sup>+</sup> ATPase pump in the membranes of heart cells (myocytes). This causes an increase in the level of sodium ions in the myocytes, which then leads to a rise in the level of calcium ions. The proposed mechanism is the following: inhibition of the Na<sup>+</sup>/K<sup>+</sup> pump leads to increased Na<sup>+</sup> levels, which in turn slows down the extrusion of Ca<sup>2+</sup> via the Na<sup>+</sup>/Ca<sup>2+</sup> exchange pump. Increased amounts of Ca<sup>2+</sup> are then stored in the sarcoplasmic reticulum and released by each action potential, which is unchanged by acetyldigitoxin. This is a different mechanism from that of catecholamines. Acetyldigitoxin also increases vagal activity via its central action on the central nervous system, thus decreasing the conduction of electrical impulses through the AV node. This is important for its clinical use in different arrhythmias.",The molecular weight is 806.99.,Acetyldigitoxin has a topological polar surface area of 188.9.,The log p value of  is 3.46.,Acetyldigitoxin is approved.,Acetyldigitoxin is a solid.,True
17625,"Deacetyllanatoside C. A cardiotonic glycoside from the leaves of Digitalis lanata. For the treatment and management of Congestive cardiac insufficiency, arrhythmias and heart failure. Deslanoside is a cardiac glycoside used to treat congestive heart failure and supraventricular arrhythmias due to reentry mechanisms, and to control ventricular rate in the treatment of chronic atrial fibrillation. Deslanoside inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium and calcium concentrations. Increased intracellular concentrations of calcium may promote activation of contractile proteins (e.g., actin, myosin). Deslanoside also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.",The molecular weight is 943.09.,Deslanoside has a topological polar surface area of 282.21.,The log p value of  is 0.32.,Deslanoside is approved.,Deslanoside is a solid.,True
17626,"A cardioactive glycoside consisting of rhamnose and ouabagenin, obtained from the seeds of Strophanthus gratus and other plants of the Apocynaceae; used like digitalis. It is commonly used in cell biological studies as an inhibitor of the NA(+)-K(+)-exchanging ATPase. For the treatment of atrial fibrillation and flutter and heart failure Ouabain, a cardiac glycoside similar to digitoxin, is used to treat congestive heart failure and supraventricular arrhythmias due to reentry mechanisms, and to control ventricular rate in the treatment of chronic atrial fibrillation. Ouabain inhibits the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium and calcium concentrations. Increased intracellular concentrations of calcium may promote activation of contractile proteins (e.g., actin, myosin). Ouabain also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.",The molecular weight is 584.66.,Ouabain has a topological polar surface area of 206.6.,The log p value of  is -1.66.,Ouabain is approved.,Ouabain is a solid.,True
17627,"Bretylium blocks the release of noradrenaline from the peripheral sympathetic nervous system, and is used in emergency medicine, cardiology, and other specialties for the acute management of ventricular tachycardia and ventricular fibrillation. The primary mode of action for bretylium is thought to be inhibition of voltage-gated K(+) channels. Recent evidence has shown that bretylium may also inhibit the Na,K-ATPase by binding to the extracellular K-site. For use in the prophylaxis and therapy of ventricular fibrillation. Also used in the treatment of life-threatening ventricular arrhythmias, such as ventricular tachycardia, that have failed to respond to adequate doses of a first-line antiarrhythmic agent, such as lidocaine. Bretylium is a bromobenzyl quaternary ammonium compound which selectively accumulates in sympathetic ganglia and their postganglionic adrenergic neurons where it inhibits norepinephrine release by depressing adrenergic nerve terminal excitability. Bretylium also suppresses ventricular fibrillation and ventricular arrhythmias. Bretylium inhibits norepinephrine release by depressing adrenergic nerve terminal excitability. The mechanisms of the antifibrillatory and antiarrhythmic actions of bretylium are not established. In efforts to define these mechanisms, the following electrophysiologic actions of bretylium have been demonstrated in animal experiments: increase in ventricular fibrillation threshold, increase in action potential duration and effective refractory period without changes in heart rate, little effect on the rate of rise or amplitude of the cardiac action potential (Phase 0) or in resting membrane potential (Phase 4) in normal myocardium, decrease in the disparity in action potential duration between normal and infarcted regions, and increase in impulse formation and spontaneous firing rate of pacemaker tissue as well as increase ventricular conduction velocity.",,,,Bretylium is approved.,Bretylium is a solid.,True
17628,"Ciclopirox olamine (used in preparations called Batrafen, Loprox, Mycoster, Penlac and Stieprox) is a synthetic antifungal agent for topical dermatologic treatment of superficial mycoses. In particular, the agent is especially effective in treating Tinea versicolor. Used as a topical treatment in immunocompetent patients with mild to moderate onychomycosis of fingernails and toenails without lunula involvement, due to <i>Trichophyton rubrum</i>. Ciclopirox is a broad-spectrum antifungal medication that also has antibacterial and anti-inflammatory properties. Its main mode of action is thought to be its high affinity for trivalent cations, which inhibit essential co-factors in enzymes. Ciclopirox exhibits either fungistatic or fungicidal activity in vitro against a broad spectrum of fungal organisms, such as dermatophytes, yeasts, dimorphic fungi, eumycetes, and actinomycetes. In addition to its broad spectrum of action, ciclopirox also exerts antibacterial activity against many Gram-positive and Gram-negative bacteria. Furthermore, the anti-inflammatory effects of ciclopirox have been demonstrated in human polymorphonuclear cells, where ciclopirox has inhibited the synthesis of prostaglandin and leukotriene. Ciclopirox can also exhibit its anti-inflammatory effects by inhibiting the formation of 5-lipoxygenase and cyclooxygenase. Unlike antifungals such as itraconazole and terbinafine, which affect sterol synthesis, ciclopirox is thought to act through the chelation of polyvalent metal cations, such as Fe<sup>3+</sup> and Al<sup>3+</sup>. These cations inhibit many enzymes, including cytochromes, thus disrupting cellular activities such as mitochondrial electron transport processes and energy production. Ciclopirox also appears to modify the plasma membrane of fungi, resulting in the disorganization of internal structures. The anti-inflammatory action of ciclopirox is most likely due to inhibition of 5-lipoxygenase and cyclooxygenase.",The molecular weight is 207.27.,Ciclopirox has a topological polar surface area of 40.54.,The log p value of  is 2.03.,Ciclopirox is approved and investigational.,Ciclopirox is a solid.,True
17629,"Potassium is the major cation (positive ion) inside animal cells, while sodium is the major cation outside animal cells. The concentration differences of these charged particles causes a difference in electric potential between the inside and outside of cells, known as the membrane potential. The balance between potassium and sodium is maintained by ion pumps in the cell membrane. The cell membrane potential created by potassium and sodium ions allows the cell generate an action potential—a \spike\"" of electrical discharge. The ability of cells to produce electrical discharge is critical for body functions such as neurotransmission, muscle contraction, and heart function. Potassium is also an essential mineral needed to regulate water balance, blood pressure and levels of acidity."" Potassium is used to regulate hypokalemia as a primary condition or secondary to other medical conditions.  Potassium is the major cation (positive ion) inside animal cells, while sodium is the major cation outside animal cells. The concentration differences of these charged particles causes a difference in electric potential between the inside and outside of cells, known as the membrane potential. The balance between potassium and sodium is maintained by ion pumps in the cell membrane. The cell membrane potential created by potassium and sodium ions allows the cell generate an action potential—a \spike\"" of electrical discharge. The ability of cells to produce electrical discharge is critical for body functions such as neurotransmission, muscle contraction, and heart function. Potassium is also an essential mineral needed to regulate water balance, blood pressure and levels of acidity.""",,,,Potassium cation is approved and investigational.,Potassium cation is a solid.,True
17630,"Magnesium hydroxide is used primarily in \Milk of Magnesia\"", a white aqueous, mildly alkaline suspension of magnesium hydroxide formulated at about 8%w/v. Milk of magnesia is primarily used to alleviate constipation, but can also be used to relieve indigestion and heartburn. When taken internally by mouth as a laxative, the osmotic force of the magnesia suspension acts to draw fluids from the body and to retain those already within the lumen of the intestine, serving to distend the bowel, thus stimulating nerves within the colon wall, inducing peristalsis and resulting in evacuation of colonic contents.""",,,,Magnesium cation is approved and nutraceutical.,Magnesium cation is a solid.,True
17631,Almitrine is a respiratory stimulant that enhances respiration by acting as an agonist of peripheral chemoreceptors located on the carotid bodies. It is used in the treatment of chronic obstructive pulmonary disease. It is also reported to have a potentially beneficial effect in treating the noctural oxygen desaturation without impairing the quality of sleep. For the treatment of chronic obstructive pulmonary disease. Almitrine is a respiratory stimulant that enhances respiration by acting as an agonist of peripheral chemoreceptors located on the carotid bodies.  Almitrine is an agonist at the peripheral chemoreceptors expressed on carotid bodies. It enhances respiration in patients with chronic obstructive pulmonary disease by increasing the arterial oxygen tension while decreasing the arterial carbon dioxide tension. ,The molecular weight is 477.56.,Almitrine has a topological polar surface area of 69.21.,The log p value of  is 6.33.,Almitrine is approved.,Almitrine is a solid.,True
17632,Investigated for use/treatment in heart disease. Reduces the sodium-potassium adenosine triphosphatase (ATPase) activity and stimulates the sarcoplasmic calcium ATPase isoform 2 reuptake function.,,,,Istaroxime is investigational.,Istaroxime is a solid.,True
17633,,The molecular weight is 142.39.,Magnesium acetate has a topological polar surface area of 40.13.,,Magnesium acetate is approved.,,False
17634,"Potassium is used to regulate hypokalemia as a primary condition or secondary to other medical conditions.  Potassium is the major cation (positive ion) inside animal cells, while sodium is the major cation outside animal cells. The concentration differences of these charged particles causes a difference in electric potential between the inside and outside of cells, known as the membrane potential. The balance between potassium and sodium is maintained by ion pumps in the cell membrane. The cell membrane potential created by potassium and sodium ions allows the cell generate an action potential—a \spike\"" of electrical discharge. The ability of cells to produce electrical discharge is critical for body functions such as neurotransmission, muscle contraction, and heart function. Potassium is also an essential mineral needed to regulate water balance, blood pressure and levels of acidity.""",The molecular weight is 98.14.,,,Potassium acetate is approved and investigational.,,True
17635,"Potassium is used to regulate hypokalemia as a primary condition or secondary to other medical conditions.  Potassium is the major cation (positive ion) inside animal cells, while sodium is the major cation outside animal cells. The concentration differences of these charged particles causes a difference in electric potential between the inside and outside of cells, known as the membrane potential. The balance between potassium and sodium is maintained by ion pumps in the cell membrane. The cell membrane potential created by potassium and sodium ions allows the cell generate an action potential—a \spike\"" of electrical discharge. The ability of cells to produce electrical discharge is critical for body functions such as neurotransmission, muscle contraction, and heart function. Potassium is also an essential mineral needed to regulate water balance, blood pressure and levels of acidity.""",,,,Potassium sulfate is approved and investigational.,,True
17636,"Potassium is an essential nutrient, like and. It was identified as a shortfall nutrient by the 2015-2020 Advisory Committee of Dietary Guidelines for Americans. Many conditions and diseases interfere with normal body potassium balance, and underconsumption of potassium is one example. Hypokalemia (low potassium) or hyperkalemia (high potassium) may result, manifesting as various signs and symptoms. Some examples of potassium-related complications include life-threatening arrhythmia, neuromuscular dysfunction, diarrhea, nausea, and vomiting. **General uses of potassium** Potassium maintains an electrolyte gradient on cell surfaces, keeping at specific concentrations inside and outside of the cell; this impacts fluid and electrolyte balance, nerve transmission, muscle contraction, as well as cardiac and kidney function. Clinical evidence has associated potassium intake with lower blood pressure in adults, reducing the risk stroke and heart disease. Dietary potassium may exert beneficial effects on bone loss in the elderly and kidney stones. Consumption of white vegetables, which are normally high in potassium, is associated with a lower risk of stroke. Potassium ion is the primary intracellular cation found in virtually all body tissues. The total amount of body potassium in adults is estimated at 45 millimole (mmol)/kg body weight (about 140 g for an adult weighing 175 pounds; 1 mmol = 1 milliequivalent or 39.1 mg of potassium). Potassium mainly stays in cells, and a small amount can be found in the extracellular fluid. The amount of potassium that stays in the cell (intracellular) is 30 times that of extracellular concentration, creating a transmembrane gradient, regulated by the sodium-potassium (Na+/K+) ATPase transporter. This is an important gradient for nerve conduction, muscle contractions, and renal function. Vomiting, diarrhea, renal disease, medications, and other conditions that alter potassium excretion or shift it inside or outside of cells. In healthy patients individuals with normal renal function, markedly high or low potassium levels are rare.",,,,Potassium is approved and experimental.,Potassium is a solid.,True
17637,,The molecular weight is 254.52.,Magnesium levulinate has a topological polar surface area of 57.2.,,Magnesium levulinate is nutraceutical.,,False
17638,,The molecular weight is 202.44.,,,Magnesium lactate is nutraceutical.,,False
17639,,The molecular weight is 1344.4.,Mecobalamin has a topological polar surface area of 488.71.,,Mecobalamin is approved and investigational.,Mecobalamin is a solid.,False
17640,,,,,12-Phenylheme is experimental.,12-Phenylheme is a solid.,False
17641,,,,,2-Phenylheme is experimental.,2-Phenylheme is a solid.,False
17642,,,,,Verdoheme is experimental.,Verdoheme is a solid.,False
17643,,,,,"1-({2--1,3-DIOXOLAN-2-YL}METHYL)-1H-IMIDAZOLE is experimental.","1-({2--1,3-DIOXOLAN-2-YL}METHYL)-1H-IMIDAZOLE is a solid.",False
17644,,,,,1-(adamantan-1-yl)-2-(1H-imidazol-1-yl)ethanone is experimental.,1-(adamantan-1-yl)-2-(1H-imidazol-1-yl)ethanone is a solid.,False
17645,"Metocurine iodide is a benzylisoquinolinium competitive nondepolarizing neuromuscular blocking agent. It is used as an anesthesia adjunct to induce skeletal muscle relaxation and to reduce the intensity of muscle contractions in convulsive therapy Metocurine iodide has a moderate risk of inducing histamine release and has some ganglion blocking activity. Metocurine iodide can be used most advantageously if muscle twitch response to peripheral nerve stimulation is monitored to assess degree of muscle relaxation. Metocurine Iodide is no longer available on the US market. For use as an anesthesia adjunct to induce skeletal muscle relaxation and to reduce the intensity of muscle contractions in convulsive therapy. Metocurine iodide is a benzylisoquinolinium competitive nondepolarizing neuromuscular blocking agent. Metocurine iodide has a moderate risk of inducing histamine release and has some ganglion blocking activity. Metocurine iodide can be used most advantageously if muscle twitch response to peripheral nerve stimulation is monitored to assess degree of muscle relaxation. As with other nondepolarizing neuromuscular blockers, the time to onset of paralysis decreases and the duration of maximum effect increases with increasing doses of metocurine iodide. Repeated administration of maintenance doses of metocurine iodide has no cumulative effect on the duration of neuromuscular block if recovery is allowed to begin prior to repeat dosing. Moreover, the time needed to recover from repeat doses does not change with additional doses. Repeat doses can therefore be administered at relatively regular intervals with predictable results. Metocurine iodide antagonizes the neurotransmitter action of acetylcholine by binding competitively with cholinergic receptor sites on the motor end-plate. This antagonism is inhibited, and neuromuscular block reversed, by acetylcholinesterase inhibitors such as neostigmine, edrophonium, and pyridostigmine.",,,,Metocurine iodide is approved and withdrawn.,Metocurine iodide is a solid.,True
17646,"Cisatracurium is a nondepolarizing skeletal muscle relaxant for intravenous administration. Cisatracurium acts on cholinergic receptors, blocking neuromuscular transmission. This action is antagonized by acetylcholinesterase inhibitors such as neostigmine. The neuromuscular block produced by cisatracurium besylate is readily antagonized by anticholinesterase agents once recovery has started. As with other nondepolarizing neuromuscular blocking agents, the more profound the neuromuscular block at the time of reversal, the longer the time required for recovery of neuromuscular function. Compared to other neuromuscular blocking agents, it is intermediate in its onset and duration of action. For inpatients and outpatients as an adjunct to general anesthesia, to facilitate tracheal intubation, and to provide skeletal muscle relaxation during surgery or mechanical ventilation in the ICU. Cisatracurium Besylate is a nondepolarizing skeletal muscle relaxant for intravenous administration. Cisatracurium Besylate acts on cholinergic receptors, blocking neuromuscular transmission. This action is antagonized by acetylcholinesterase inhibitors such as neostigmine. The neuromuscular block produced by cisatracurium besylate is readily antagonized by anticholinesterase agents once recovery has started. As with other nondepolarizing neuromuscular blocking agents, the more profound the neuromuscular block at the time of reversal, the longer the time required for recovery of neuromuscular function. Compared to other neuromuscular blocking agents, it is intermediate in its onset and duration of action. Cisatracurium Besylate binds to the nicotinic acetycholine (cholinergic) receptors in the motor endplate and blocks access to the receptors. In the process of binding, the receptor is actually activated - causing a process known as depolarization. Since it is not degraded in the neuromuscular junction, the depolarized membrane remains depolarized and unresponsive to any other impulse, causing muscle paralysis.",,,,Cisatracurium is approved.,Cisatracurium is a solid.,True
17647,"A nicotinic antagonist that is well absorbed from the gastrointestinal tract and crosses the blood-brain barrier. Mecamylamine has been used as a ganglionic blocker in treating hypertension, but, like most ganglionic blockers, is more often used now as a research tool. For the treatment of moderately severe to severe essential hypertension and in uncomplicated cases of malignant hypertension Mecamylamine is a potent, oral antihypertensive agent and ganglion blocker, and is a secondary amine. Mecamylamine is indicated for the management of moderately severe to severe essential hypertension and in uncomplicated cases of malignant hypertension. Mecamylamine reduces blood pressure in both normotensive and hypertensive individuals. A small oral dosage often produces a smooth and predictable reduction of blood pressure. Although this antihypertensive effect is predominantly orthostatic, the supine blood pressure is also significantly reduced. Mecamylamine crosses the blood-brain and placental barriers. Mecamylamine is a ganglionic blocker which prevents stimulation of postsynaptic receptors by acetylcholine released from presynaptic nerve endings. The hypotensive effect of Mecamylamine is attributed to reduction in sympathetic tone, vasodilation, and reduced cardiac output, and is primarily postural.",The molecular weight is 167.3.,Mecamylamine has a topological polar surface area of 12.03.,The log p value of  is 2.82.,Mecamylamine is approved and investigational.,Mecamylamine is a liquid.,True
17648,"A non-depolarizing neuromuscular blocking agent with short duration of action. Its lack of significant cardiovascular effects and its lack of dependence on good kidney function for elimination provide clinical advantage over alternate non-depolarizing neuromuscular blocking agents. For use, as an adjunct to general anesthesia, to facilitate endotracheal intubation and to provide skeletal muscle relaxation during surgery or mechanical ventilation. Atracurium is a nondepolarizing skeletal muscle relaxant. Atracurium can be used most advantageously if muscle twitch response to peripheral nerve stimulation is monitored to assess degree of muscle relaxation. The duration of neuromuscular block produced by Atracurium is approximately one third to one half the duration of block by d-tubocurarine, metocurine, and pancuronium at initially equipotent doses. As with other nondepolarizing neuromuscular blockers, the time to onset of paralysis decreases and the duration of maximum effect increases with increasing doses of Atracurium. Repeated administration of maintenance doses of Atracurium has no cumulative effect on the duration of neuromuscular block if recovery is allowed to begin prior to repeat dosing. Moreover, the time needed to recover from repeat doses does not change with additional doses. Repeat doses can therefore be administered at relatively regular intervals with predictable results. Atracurium antagonizes the neurotransmitter action of acetylcholine by binding competitively with cholinergic receptor sites on the motor end-plate. This antagonism is inhibited, and neuromuscular block reversed, by acetylcholinesterase inhibitors such as neostigmine, edrophonium, and pyridostigmine.",,,,Atracurium besylate is approved.,Atracurium besylate is a solid.,True
17649,"Monoquaternary homolog of pancuronium. A non-depolarizing neuromuscular blocking agent with shorter duration of action than pancuronium. Its lack of significant cardiovascular effects and lack of dependence on good kidney function for elimination as well as its short duration of action and easy reversibility provide advantages over, or alternatives to, other established neuromuscular blocking agents. Vecuronium is a muscle relaxing agent and is used as an adjunct in general anesthesia. The principal pharmacologic effects demonstrated by vecuronium revolve around its competitive binding of cholinergic receptors located at motor end plates. This competitive binding results in muscle relaxant effects that are typically employed as an adjunct to general anesthesia.  Vecuronium is a bisquaternary nitrogen compound that acts by competitively binding to nicotinic cholinergic receptors. The binding of vecuronium decreases the opportunity for acetylcholine to bind to the nicotinic receptor at the postjunctional membrane of the myoneural junction. As a result, depolarization is prevented, calcium ions are not released and muscle contraction does not occur.",,,,Vecuronium is approved and investigational.,Vecuronium is a solid.,True
17650,,,,,Epibatidine is experimental.,Epibatidine is a solid.,False
17651,"A nicotinic cholinergic antagonist often referred to as the prototypical ganglionic blocker. It is poorly absorbed from the gastrointestinal tract and does not cross the blood-brain barrier. It has been used for a variety of therapeutic purposes including hypertension but, like the other ganglionic blockers, it has been replaced by more specific drugs for most purposes, although it is widely used a research tool.",The molecular weight is 202.38.,,The log p value of  is -9.09.,Hexamethonium is experimental.,Hexamethonium is a solid.,True
17652,Tetracaine is an ester local anaesthetic currently available in combination with lidocaine as a cream and patch. Ophthalmic tetracaine is indicated for the for procedures requiring a rapid and short- acting topical ophthalmic anesthetic. Tetracaine is an ester-type anesthetic and produces local anesthesia by blocking the sodium ion channels involved in initiation and conduction of neuronal impulses.,The molecular weight is 264.37.,Tetracaine has a topological polar surface area of 41.57.,The log p value of  is 3.83.,Tetracaine is approved and vet_approved.,Tetracaine is a solid.,True
17653,"An antimitotic agent with immunosuppressive properties. Dexrazoxane, the (+)-enantiomorph of razoxane, provides cardioprotection against anthracycline toxicity. It appears to inhibit formation of a toxic iron-anthracycline complex.  For reducing the incidence and severity of cardiomyopathy associated with doxorubicin administration in women with metastatic breast cancer who have received a cumulative doxorubicin hydrochloride dose of 300 mg/m^2 and would benefit from continued doxorubicin therapy. Also approved for the treatment of extravasation from intravenous anthracyclines. Dexrazoxane is a cardioprotective agent for use in conjunction with doxorubicin indicated for reducing the incidence and severity of cardiomyopathy associated with doxorubicin administration in women with metastatic breast cancer who have received a cumulative doxorubicin dose. Patients receiving anthracycline-derivative antineoplastic agents may experience three types of cardiotoxicity: acute transient type; chronic, subacute type (related to cumulative dose and has a more indolent onset later on); and a late-onset type that manifests years after therapy, mainly in patients that have been exposed to the drug as a child. Although the exact mechanism of anthracycline-induced cardiotoxicity is not known, it has shown to exert a variety of actions that may result in the development of cardiotoxicity. In animals, anthracyclines cause a selective inhibition of cardiac muscle gene expression for α-actin, troponin, myosin light-chain 2, and the M isoform of creatine kinase. This may lead to myofibrillar loss associated with anthracycline-induced cardiotoxicity. Anthracyclines may also cause myocyte damage via calcium overload, altered myocardial adrenergic function, release of vasoactive amines, and proinflammatory cytokines. Furthermore, it has been suggested that the main cause of anthracycline-induced cardiotoxicity is associated with free-radical damage to DNA. The drugs intercalate DNA, chelate metal ions to produce drug-metal complexes, and generate superoxide radicals via oxidation-reduction reactions. Anthracyclines also contain a quinone structure that can undergo reduction via NADPH-dependent reactions to produce a semiquinone free radical that initiates a cascade of superoxide and hydroxide radical generation. Chelation of metal ions, particularly iron, by anthracyclines results in an anthracycline-metal complex that catalyzes the generation of reactive oxygen free radicals. This complex is a powerful oxidant that can initiate lipid peroxidation in the absence of oxygen free radicals. The toxicity induced by antrhacyclines may be exacerbated in cardiac cells, as these cells do not possess sufficient amounts of certain enzymes (e.g., superoxide dismutase, catalase, glutathione peroxidase) involved in detoxifying free radicals and protecting the cells from subsequent damage. The mechanism by which dexrazoxane exerts its cardioprotective activity is not fully understood. Dexrazoxane is a cyclic derivative of EDTA that readily penetrates cell membranes. Results of laboratory studies suggest that dexrazoxane (a prodrug) is converted intracellularly to a ring-opened bidentate chelating agent that chelates to free iron and interferes with iron-mediated free radical generation thought to be responsible, in part, for anthracycline-induced cardiomyopathy. It should be noted that dexrazoxane may also be protective through its inhibitory effect on topoisomerase II.",The molecular weight is 268.27.,Dexrazoxane has a topological polar surface area of 98.82.,The log p value of  is -1.33.,Dexrazoxane is approved and withdrawn.,Dexrazoxane is a solid.,True
17654,"Valrubicin (N-trifluoroacetyladriamycin-14-valerate) is a chemotherapy drug commonly marketed under the trade name VALSTAR. It is a semisynthetic analog of the , which is an anthracycline drug. Used in the treatment of the bladder cancer, valrubicin is administered by direct infusion into the bladder. For the treatment of cancer of the bladder. Valrubicin is an anticancer agent.  Valrubicin is an anthracycline that affects a variety of inter-related biological functions, most of which involve nucleic acid metabolism. It readily penetrates into cells, where after DNA intercalation, it inhibits the incorporation of nucleosides into nucleic acids, causes extensive chromosomal damage, and arrests cell cycle in G2. Although valrubicin does not bind strongly to DNA, a principal mechanism of its action, mediated by valrubicin metabolites, is interference with the normal DNA breaking-resealing action of DNA topoisomerase II.",The molecular weight is 723.65.,Valrubicin has a topological polar surface area of 215.22.,The log p value of  is 3.44.,Valrubicin is approved.,Valrubicin is a solid.,True
17655,"Fleroxacin is a broad-spectrum antimicrobial fluoroquinolone. It strongly inhibits the DNA-supercoiling activity of DNA gyrase. Fleroxacin is not an inhibitor of CYP1A2. Fleroxacin is a broad-spectrum antimicrobial fluoroquinolone. Fleroxacin is a broad-spectrum antimicrobial fluoroquinolone. It strongly inhibits the DNA-supercoiling activity of DNA gyrase. The inhibition of DNA gyrase and DNA topoisomerase 2 leads ultimately to cell death as these enzymes are required for bacterial DNA replication, transcription, repair, strand supercoiling repair, and recombination.",The molecular weight is 369.34.,Fleroxacin has a topological polar surface area of 64.09.,The log p value of  is -0.33.,Fleroxacin is experimental.,Fleroxacin is a solid.,True
17656,"One of the schistosomicides, it has been replaced largely by hycanthone and more recently praziquantel. (From Martindale The Extrapharmacopoeia, 30th ed., p46). It is currently being tested as a radiation sensitizer. Intended for use as a radiation sensitizer in the treatment of brain cancer. Although lucanthone has structural and biochemical similarities to Actinomycin D, it has no hematological or gastro-intestinal toxicity at clinically tolerated doses. In trials, Lucanthone was found to be safe, practical and effective and was proposed for use in clinical protocols for the treatment of cancer. The specificity of lucanthone in combination with radiation for the treatment of brain tumors arises from the fact that lucanthone acts preferentially on cycling cells (most of the normal brain cells are non-cycling) and the fact that lucanthone crosses the blood brain barrier efficiently. Recent data suggests that lucanthone inhibits post-radiation DNA repair in tumor cells. The ability of lucanthone to inhibit AP endonuclease and topoisomerase II probably account for the specific DNA repair inhibition in irradiated cells.",The molecular weight is 340.49.,Lucanthone has a topological polar surface area of 32.34.,The log p value of  is 5.19.,Lucanthone is investigational.,Lucanthone is a solid.,True
17657,"SP1049C is a novel anthracycline chemotherapeutic agent designed to overcome drug resistance in a number of cancers. It has successfully completed Phase 1 trials. Phase 2 results are currently under final review. Preliminary data, in its first clinically tested indication, shows that SP1049C is active in Stage IV non-resectable adenocarcinoma of the oesophagus. Median survival is encouraging and correlates strongly with dose levels. Intended for the treatment of carcinoma of the oesophagus. SP1049C is a novel anticancer agent containing doxorubicin and two nonionic pluronic block copolymers. Doxorubicin has antimitotic and cytotoxic activity through a number of proposed mechanisms of action: Doxorubicin forms complexes with DNA by intercalation between base pairs, and it inhibits topoisomerase II activity by stabilizing the DNA-topoisomerase II complex, preventing the religation portion of the ligation-religation reaction that topoisomerase II catalyzes.",,,,SP1049C is investigational.,SP1049C is a solid.,True
17658,"Amonafide is a substance that is being studied in the treatment of cancer. It belongs to the families of drugs called topoisomerase inhibitors and intercalating agents. Investigated for use/treatment in breast cancer, ovarian cancer, and prostate cancer. Amonafide is a DNA intercalating agent and inhibitor of topoisomerase II that has been extensively studied in patients with malignant solid tumors. Amonafide has also been studied in patients with AML.",,,,Amonafide is investigational.,Amonafide is a solid.,True
17659,"The cytostatic agent Elsamitrucin is a new fermentation product active in a variety of in vivo tumor models of murine and human origin. (PMID: 8150873) Investigated for use/treatment in lymphoma (non-hodgkin's). Elsamitrucin induces single strand breaks in DNA and inhibits topoisomerase I and II, enzymes that play an important role in DNA replication.",,,,Elsamitrucin is investigational.,Elsamitrucin is a solid.,True
17660,"GPX-100 is an anthracycline anticancer drug that belongs to the family of drugs called antitumor antibiotics. Investigated for use/treatment in breast cancer and cancer/tumors (unspecified). As an anthracycline, GPX-100 has antimitotic and cytotoxic activity through a number of proposed mechanisms of action: GPX-100 forms complexes with DNA by intercalation between base pairs, and it inhibits topoisomerase II activity by stabilizing the DNA-topoisomerase II complex, preventing the religation portion of the ligation-religation reaction that topoisomerase II catalyzes.",,,,13-deoxydoxorubicin is investigational.,13-deoxydoxorubicin is a solid.,True
17661,"RTA 744 is a novel anthracycline derivative that crosses the blood-brain barrier and shows significant potential for the treatment of primary and metastatic brain cancers. Anthracyclines are one of the most broadly used and effective classes of cancer therapies; however, they are not used to treat brain cancers because current therapies do not cross the blood-brain barrier. Investigated for use/treatment in brain cancer. RTA 744 is a substance being studied in the treatment of adult brain tumors. RTA 744 crosses the blood-brain barrier and blocks an enzyme needed for cancer growth. RTA 744 is a type of topoisomerase inhibitor. Also called topoisomerase II inhibitor RTA 744.",,,,RTA 744 is investigational.,RTA 744 is a solid.,True
17662,"Aldoxorubicin, an antineoplastic agents, is an albumin-binding prodrug of doxorubicin. Investigated for use/treatment in solid tumors. INNO-206 is the (6-Maleimidocaproyl) hydrazone of doxorubicin. INNO-206 is a prodrug of doxorubicin that binds endogenous albumin after administration. The bound doxorubicin is released in the acidic environment of the tumor cell through cleavage of an acid sensitive linker. In preclinical models, INNO-206 was superior to doxorubicin with regard to antitumor efficacy and toxicity.",,,,Aldoxorubicin is investigational.,Aldoxorubicin is a solid.,True
17663,"Becatecarin is a derivative of. Investigated for use/treatment in cancer/tumors (unspecified), liver cancer, gastric cancer, and leukemia (unspecified). Becatecarin is a small molecule, anticancer compound for the treatment of hepatobiliary duct tumors, a rare and aggressive form of cancer with a high medical need and very limited survival. Becatecarin intercalates into DNA and stabilizes the DNA-topoisomerase I complex, thereby interfering with the topoisomerase I-catalyzed DNA breakage-reunion reaction and initiating DNA cleavage and apoptosis.",,,,Becatecarin is investigational.,Becatecarin is a solid.,True
17664,"Investigated for use/treatment in breast cancer and leukemia (unspecified). Annamycin belongs to the anthracycline class of drugs, and has a pleiotropic mechanism of action where it targets topoisomerase II, causing strand breaks in DNA. Annamycin forms complexes with DNA by intercalation between base pairs, and it inhibits topoisomerase II activity by stabilizing the DNA-topoisomerase II complex, preventing the religation portion of the ligation-religation reaction that topoisomerase II catalyzes.",,,,Annamycin is investigational.,Annamycin is a solid.,True
17665,"Investigated for use/treatment in colorectal cancer and inflammatory bowel disease. Declopramide is a member of the N-substituted benzamide class of DNA repair inhibitors. There are two possible mechanisms of action of declopramide, with one involving (nuclear localizing factor kappaB) NFkB and the other involving the activation of the caspase cascade via the mitochondrial pathway, both of which lead to cell death (apoptosis). Declopramide may also increase the susceptibility of cancer cells to traditional radiation and/or chemotherapy treatment. It is proposed that G2/M cell cycle block is induced by pathways other than the protein 53 (p53) pathway. ",,,,Declopramide is investigational.,Declopramide is a solid.,True
17666,"Finafloxacin is a fluoroquinolone antibiotic indicated in the treatment of acute otitis externa (swimmer's ear) caused by the bacteria Pseudomonas aeruginosa and Staphylococcus aureus. Finafloxacin is marketed by Novartis under the brand Xtoro™, and was approved by the FDA in December 2014.  Finafloxacin is indicated for the treatment of acute otitis externa (AOE) with or without an otowick, caused by susceptible strains of <i>Pseudomonas aeruginosa</i> and <i>Staphylococcus aureus</i> in patients age 1 year and older.  Finafloxacin is a fluoroquinolone antibiotic, which selectively inhibit bacterial type II topoisomerase enzymes, DNA gyrase and topoisomerase IV, which are required for bacterial DNA replication, transcription, repair and recombination.",The molecular weight is 398.39.,Finafloxacin has a topological polar surface area of 105.9.,The log p value of  is -1.56.,Finafloxacin is approved and investigational.,Finafloxacin is a liquid.,True
17667,,,,,Inhibitor Idd 384 is experimental.,Inhibitor Idd 384 is a solid.,False
17668,,,,,alpha-D-glucose 6-phosphate is experimental.,alpha-D-glucose 6-phosphate is a solid.,False
17669,,,,,Alrestatin is experimental.,Alrestatin is a solid.,False
17670,,,,,Fidarestat is experimental.,Fidarestat is a solid.,False
17671,,,,,"(S,R)-fidarestat is experimental.","(S,R)-fidarestat is a solid.",False
17672,"Investigated for use/treatment in neuropathy (diabetic). Polyneuropathy, damage of peripheral neurons, is common in diabetes mellitus patients and causes pain, sensory and motor deficits in the limbs. Zenarestat is an aldose reductase inhibitor which inhibits the metabolism of glucose by the polyol pathway, which possibly slows or reduces progression of polyneuropathy. Chronic hyperglycemia affects peripheral nerves by an extracellular mechanism with many types of glycation reactions and chemical rearrangements, and an intracellular route involving increased amounts of glucose passing through the polyol pathway. The polyol pathway allows cells to produce fructose from glucose, and has two steps, which require energy and enzymes. Aldose reductase catalyzes the conversion of glucose to sorbitol in the first step, while the second involves the oxidation of nicotinamide adenine dicnucleotide phosphate (conversion of NADPH to NADP). Chronic hyperglycemia causes damage by overactivity of the polyol pathway, causing a decrease in cellular NADPH levels, reducing the amount of glutathione (a free radical scavenger), and nitric oxide (a vasodilator), as well as increasing cellular sorbital levels, causing decreased levels of myo-inositol (necessary for Na-K ATPase function) and increased fructose, thus increasing AGE (advanced glycosylation end products), the byproduct of the polyol pathway. The suppression of the first step in the polyol pathway by zenarestat prevents these deleterious processes from occuring.",,,,Zenarestat is experimental.,Zenarestat is a solid.,True
17673,"Tolrestat (INN) (AY-27773) is an aldose reductase inhibitor which was approved for the control of certain diabetic complications. While it was approved for marketed in several countries, it failed a Phase III trial in the U.S. due to toxicity and never received FDA approval. It was sold under the tradename Alredase but was discontinued by Wyeth in 1997 because of the risk of severe liver toxicity and death. For the pharmacological control of certain diabetic complications.",The molecular weight is 357.35.,Tolrestat has a topological polar surface area of 49.77.,The log p value of  is 3.43.,Tolrestat is withdrawn.,Tolrestat is a solid.,True
17674,,,,,N-Acetylalanine is experimental.,N-Acetylalanine is a solid.,False
17675,,,,,Sorbinil is experimental and investigational.,Sorbinil is a solid.,False
17676,,,,,IDD552 is experimental.,IDD552 is a solid.,False
17677,"Ranirestat is a structurally novel and stereospecifically potent aldose reductase (AKR1B; EC 1.1.1.21) inhibitor, which contains a succinimide ring that undergoes ring-opening at physiological pH levels. It has been used in trials studying the treatment of Mild to Moderate Diabetic Sensorimotor Polyneuropathy. Investigated for use/treatment in neuropathy (diabetic). Ranirestat alleviates diabetic neuropathy, a complication of diabetes, by inhibiting aldose reductase and thereby inhibiting the accumulation of intracellular sorbitol that causes diabetic neuropathy. This drug has a stronger inhibitory effect and is longer acting compared to other drugs in this therapeutic area. Ranirestat showed good penetration into the nerve tissue, resulting in dose-dependent inhibition of intraneural accumulation of sorbitol and fructose in a clinical study. ",,,,Ranirestat is investigational.,Ranirestat is a solid.,True
17678,"QR-333 has been investigated as a treatment for diabetic peripheral neuropathy. QR-333 is a concentrated and standardized nutrient based active compounds dosed in a topical cream designed to reduce oxidative stress and treat symptoms of Diabetic Peripheral Neuropathy, a nerve disorder that can lead to numbness, skin ulcers, constant pain or extreme sensitivity to a stimulus. Investigated for use/treatment in neuropathy (diabetic). QR-333, a topical compound that contains quercetin, a flavonoid with aldose reductase inhibitor effects, ascorbyl palmitate, and vitamin D(3), was formulated to decrease the oxidative stress that contributes to peripheral diabetic neuropathy and thus alleviate its symptoms.",,,,QR-333 is investigational.,QR-333 is a solid.,True
17679,,,,,(2-{CARBONYL}-5-CHLOROPHENOXY)ACETIC ACID is experimental.,(2-{CARBONYL}-5-CHLOROPHENOXY)ACETIC ACID is a solid.,False
17680,,,,,(5-CHLORO-2-{CARBONYL}PHENOXY)ACETIC ACID is experimental.,(5-CHLORO-2-{CARBONYL}PHENOXY)ACETIC ACID is a solid.,False
17681,,,,,Lidorestat is investigational.,Lidorestat is a solid.,False
17682,,,,,"{3--2,4-DIOXO-3,4-DIHYDROPYRIMIDIN-1(2H)-YL}ACETIC ACID is experimental.","{3--2,4-DIOXO-3,4-DIHYDROPYRIMIDIN-1(2H)-YL}ACETIC ACID is a solid.",False
17683,,,,,3-propanoic acid is experimental.,3-propanoic acid is a solid.,False
17684,,,,,CP-744809 is experimental.,CP-744809 is a solid.,False
17685,,,,,(R)-minalrestat is experimental.,(R)-minalrestat is a solid.,False
17686,,,,,4-BUTANOIC ACID is experimental.,4-BUTANOIC ACID is a solid.,False
17687,,,,,"{4--3,3-DIOXIDO-1-OXONAPHTHOISOTHIAZOL-2(1H)-YL}ACETIC ACID is experimental.","{4--3,3-DIOXIDO-1-OXONAPHTHOISOTHIAZOL-2(1H)-YL}ACETIC ACID is a solid.",False
17688,,,,,"2-(CARBOXYMETHYL)-1-OXO-1,2-DIHYDRONAPHTHOISOTHIAZOLE-4-CARBOXYLIC ACID 3,3-DIOXIDE is experimental.","2-(CARBOXYMETHYL)-1-OXO-1,2-DIHYDRONAPHTHOISOTHIAZOLE-4-CARBOXYLIC ACID 3,3-DIOXIDE is a solid.",False
17689,,,,,IDD594 is experimental.,IDD594 is a solid.,False
17690,This compound belongs to the nitrofurans. These are compounds containing a furan ring which bears a nitro group. It targets the protein aldose reductase.,,,,{thio}acetic acid is experimental.,{thio}acetic acid is a solid.,True
17691,,,,,"2-(3-((4,5,7-trifluorobenzothiazol-2-yl)methyl)-1H-pyrrolopyridin-1-yl)acetic acid is experimental.","2-(3-((4,5,7-trifluorobenzothiazol-2-yl)methyl)-1H-pyrrolopyridin-1-yl)acetic acid is a solid.",False
17692,,,,,Zopolrestat is experimental.,Zopolrestat is a solid.,False
17693,"Palifermin is a recombinant human keratinocyte growth factor (KGF). It is 140 residues long, and is produced using E. coli. For treatment of oral mucositis associated with chemotherapy and radiation therapy. Used in the prevention or treatment of oral mucoscitis (mouth ulcers arising from chemotherapy), Kepivance binds to the human keratinocyte growth factor (KGF) receptor on buccal cell surfaces. Kepivance acts as both a cell growth and survival factor by stimulating epithelial cell proliferation, differentiation, and migration around the tongue and mouth. The KGF receptor is found on many tissues particularly around the tongue, esophagus, salivary gland and other gastro-intestinal tract organs. Palifermin has been shown to protect oral and intestinal epithelia from the effects of radiation and chemotherapy, though the exact mechanism is not well understood. As a recombinant keratinocyte growth factor (KGF), palifermin may promote cell proliferation, reducing the severity of oral mucositis in patients in the relevant treatment groups. Agonism of fibroblast growth factor 2 may be predominantly responsible for this effect. The endogenous form if palifermin is expressed in the kidney of rats.",The molecular weight is 16279.9.,Palifermin has a topological polar surface area of 6730.23.,,Palifermin is approved.,Palifermin is a liquid.,True
17694,,,,,3--2-indolinone is experimental.,3--2-indolinone is a solid.,False
17695,,,,,4--5-Chloro-N-Pyrimidin-2-Amine is experimental.,4--5-Chloro-N-Pyrimidin-2-Amine is a solid.,False
17696,"OPC-14523 is an antidepressant drug developed by Otsuka America Pharmaceutical. Investigated for use/treatment in bulimia, depression, and obsessive-compulsive disorders. OPC-14523 is a serotonin reuptake inhibitor. It treats depression, especially refractory depression, in a mammal, including a human, by administering to the mammal a sigma receptor ligand in combination with an antidepressant agent. It also relates to pharmaceutical compositions containing a pharmaceutically acceptable carrier, a sigma receptor ligand and a serotonin reuptake inhibitor.",,,,OPC-14523 is investigational.,OPC-14523 is a solid.,True
17697,"Nisoxetine is a selective norepinephrine reuptake inhibitor (SNRI) developed in the 1970s. It was originally investigated as an antidepressant but has no current clinical applications aside from being a research standard SNRI. It has been used to research obesity and energy balance, and exerts some local analgesia effects.",,,,Nisoxetine is experimental.,Nisoxetine is a solid.,True
17698,,,,,Homoserine Lactone is experimental.,Homoserine Lactone is a solid.,False
17699,,,,,"Quinonoid 7,8-Tetrahydrobiopterin is experimental.","Quinonoid 7,8-Tetrahydrobiopterin is a solid.",False
17700,,,,,beta-2-Thienyl-L-alanine is experimental.,beta-2-Thienyl-L-alanine is a solid.,False
17701,"An unnatural amino acid that is used experimentally to study protein structure and function. It is structurally similar to METHIONINE, however it does not contain SULFUR.",,,,D-norleucine is experimental.,D-norleucine is a solid.,True
17702,"A dopamine antagonist that is particularly useful in treating the nausea and vomiting associated with anesthesia, mildly emetic cancer chemotherapy agents, radiation therapy, and toxins. This piperazine phenothiazine does not prevent vertigo or motion sickness. (From AMA Drug Evaluations Annual, 1994, p457) For the treatment or relief of nausea and vomiting. Thiethylperazine, an atypical antipsychotic agent, is used to treat both negative and positive symptoms of schizophrenia, acute mania with bipolar disorder, agitation, and psychotic symptoms in dementia. Future uses may include the treatment of obsessive-compulsive disorder and severe behavioral disorders in autism. Structurally and pharmacologically similar to clozapine, Thiethylperazine binds to alpha(1), dopamine, histamine H1, muscarinic, and serotonin type 2 (5-HT2) receptors. Thiethylperazine is an antagonist at types 1, 2, and 4 dopamine receptors, 5-HT receptor types 2A and 2C, muscarinic receptors 1 through 5, alpha(1)-receptors, and histamine H1-receptors. Thiethylperazine's antipsychotic effect is due to antagonism at dopamine and serotonin type 2 receptors, with greater activity at serotonin 5-HT2 receptors than at dopamine type-2 receptors. This may explain the lack of extrapyramidal effects. Thiethylperazine does not appear to block dopamine within the tubero-infundibular tract, explaining the lower incidence of hyperprolactinemia than with typical antipsychotic agents or risperidone. Antagonism at muscarinic receptors, H1-receptors, and alpha(1)-receptors also occurs with thiethylperazine.",The molecular weight is 399.62.,Thiethylperazine has a topological polar surface area of 9.72.,The log p value of  is 4.75.,Thiethylperazine is approved and withdrawn.,Thiethylperazine is a liquid.,True
17703,"Alizapride is a dopamine antagonist that is capable of demonstrating both prokinetic and antiemetic effects. This kind of pharmacological activity makes it effective for use in the treatment of various kinds of nausea and vomiting, including that which may occur postoperatively. Alizapride is used in the treatment of nausea and vomiting, including postoperative nausea and vomiting.  Alizapride is a dopamine antagonist. The anti-emetic action of Alizapride is due to its antagonist activity at D2 receptors in the chemoreceptor trigger zone (CTZ) in the central nervous system (CNS)—this action prevents nausea and vomiting triggered by most stimuli. Structurally similar to metoclopramide and, therefore, shares similar other atributres related to emesis and prokinetics.",The molecular weight is 315.38.,Alizapride has a topological polar surface area of 83.14.,The log p value of  is 2.53.,Alizapride is investigational.,Alizapride is a solid.,True
17704,"Brasofensine is an orally administered dopamine reuptake inhibitor being developed for the treatment of Parkinson's Disease. Phase I/II trials for brasofensine have been completed in the U.K. In November 2001, NeuroSearch confirmed that the drug's development was discontinued in favor of NS 2230. For the treatment of Parkinson's Disease. Brasofensine is an inhibitor of the synaptic dopamine transporter. It is a geometric isomer of the E-form; the Z-isomer is denoted as BMS-205912. When the neurotransmitter dopamine is released into the synaptic cleft, brasofensine prevents it from entering back into the source nerve cell, thereby allowing a longer period of synaptic activity.",,,,Brasofensine is investigational.,Brasofensine is a solid.,True
17705,"Bromopride is a dopamine antagonist used as an antiemetic. Its prokinetic properties are similar to those of metoclopramide. It is unavailable in America or the United Kingdom. Bromopride in indicated in the treatment of nausea and vomiting, including PONV (post-operative nausea and vomiting), gastroesophageal reflux disease (GERD/GORD), as well as endoscopy preparation and radiographic studies of the GI tract. ",The molecular weight is 344.25.,Bromopride has a topological polar surface area of 67.59.,The log p value of  is 2.43.,Bromopride is investigational.,Bromopride is a solid.,True
17706,"Quinagolide is a non-ergot-derived selective dopamine D2 receptor agonist used for the treatment of elevated levels of prolactin or hyperprolactinaemia. Hyperprolalctinaemia is associated with gonadal dysfunction, including infertility and reduced libido, as well as long-term complications such as osteoporosis. Newer dopamine receptor agonists such as quinagolide and are shown to effectively inhibit prolactin secretion with improved efficacy over. These drugs are effective in patients who are intolerant or resistant to. Quinagolide exists as a racemate and its relevant clinical activity is mediated predominantly by the (-) enantiomer. It is typically present in the hydrochloride salt form and is marketed as oral tablets under the brand name Norprolac contained as a racemate. Quinagolide is currently available in several countries including Canada, but not approved for treatment in the United States. Indicated for the treatment of hyperprolactinemia (idiopathic or originating from a prolactin-secreting pituitary microadenoma or macroadenoma). Quinagolide achieves long-lasting reduction in prolactin levels in a dose-proportional effect via selectively targeting D2 receptors as an agonist. It potently suppresses both basal and stimulated serum prolactin levels by exerting a strong inhibitory effect on the secretion of the anterior pituitary hormone prolactin. Prolactin secretion from the lactotroph cells present in the anterior pituiatry gland is under tonic inhibitory control mediated by dopaminergic signalling via D2 receptors. Quinagolide selectively binds to D2 receptors expressed on the surface of lactotroph cells with high affinity which results in reduced adenylyl cyclase activity, reduced intracellular cyclic adenosine monophosphate and inhibited prolactin secretion. It also binds to D1 receptors but with low affinity and little clinical relevance.",The molecular weight is 395.56.,Quinagolide has a topological polar surface area of 72.88.,The log p value of  is 3.72.,Quinagolide is approved and investigational.,Quinagolide is a solid.,True
17707,Raclopride has been used in trials studying Parkinson Disease.,,,,Raclopride is investigational.,,True
17708,JNJ-37822681 has been used in trials studying the treatment of Schizophrenia.,,,,JNJ-37822681 is investigational.,,True
17709,"Ridogrel is a dual action drug useful for the prevention of systemic thrombo-embolism and as an adjunctive agent to thrombolytic therapy in acute myocardial infarction. However, there currently are no clinical indications for preferential use of ridogrel over aspirin. Used as an adjunctive therapy to induce thrombolysis in patients suffering acute myocardial infarction. Ridogrel, a combined thromboxane synthase inhibitor and receptor antagonist, is used with streptokinase as an adjunctive therapy to reduce the formation and size of blood clots. Blood clots can cause ischemic cardiac events (heart attacks). Ridogrel has the dual property of inhibiting the synthesis of thromboxane and blocking the receptors of thromboxane/prostaglandin/endoperoxides. It has been shown to accelerate the speed of recanalization and to delay or prevent reocclusion during systemic thrombolysis with tissue plasminogen activator (streptokinase). Ridogrel is a more potent antiplatelet agent than aspirin and might offer an advantage over aspirin as an adjunct to thrombolysis in patients suffering from acute myocardial infarction. While aspirin inhibits cyclooxygenase, the enzyme responsible for producing thromboxane, ridogrel inhibits thromboxane synthesis directly. A recent comparison between aspirin and ridogrel in as adjunct to thrombolysis in patients with acute myocardial infarction demonstrated that ridogrel is not superior to aspirin in enhancing the fibrinolytic efficacy of streptokinase but might be more effective in preventing new ischemic events. Clinical experience with this drug is still relatively limited. Ridogrel inhibits thromboxane A2 synthase and also blocks the thromboxane A2/prostaglandin endoperoxide receptors.",,,,Ridogrel is experimental.,Ridogrel is a solid.,True
17710,Investigated for use/treatment in cystic fibrosis.,,,,Cobiprostone is investigational.,Cobiprostone is a solid.,True
17711,"Panitumumab (ABX-EGF) is a recombinant human IgG2 monoclonal antibody that binds specifically to the human epidermal growth factor receptor (EGFR). This drug is an antineoplastic agent. For the treatment of EGFR-expressing, metastatic colorectal carcinoma that is refractory to fluoropyrimidine-, oxaliplatin-, and irinotecan- containing chemotherapy regimens. Panitumumab is a recombinant, human IgG2 kappa monoclonal antibody that binds specifically to the human Epidermal Growth Factor Receptor (EGFR). EGFR is a transmembrane glycoprotein that belongs to the subfamily of type I receptor tyrosine kinases. Although EGFR is expressed in normal cells, the overexpression of EGFR is detected in many human cancers, including those of the colon and rectum. Interaction of EGFR with its normal ligands causes phosphorylation and activation of a series of intracellular proteins that will in turn regulate the transcription of genes involved with cellular growth and survival, motility, and prolieration. Signal transduction through EGFR leads to the activation of the wild type KRAS gene, but the presence of an activating somatic mutation of the KRAS gene within a cancer cell can result in the dysregulation of signaling pathways and resistance to EGFR inhibitor therapy.  Panitumumab binds specifically to EGFR on both normal and tumor cells, and competitively inhibits the binding of ligands for EGFR. Nonclinical studies show that binding of panitumumab to the EGFR prevents ligand-induced receptor autophosphorylation and activation of receptor-associated kinases, resulting in inhibition of cell growth, induction of apoptosis, decreased pro-inflammatory cytokine and vascular growth factor production, and internalization of the EGFR.",,,,Panitumumab is approved and investigational.,Panitumumab is a solid.,True
17712,"Matuzumab (formerly known as the experimental drug, EMD 72000) is a humanized monoclonal antibody used in cancer treatment. It has a high affinity for EGFR (epithelial growth factor receptor), frequently associated with the growth of blood vessels in malignancy, facilitating tumor growth and survival. Investigated for use/treatment in cervical dysplasia/cancer, colorectal cancer, gastric cancer, and lung cancer. Matuzumab binds the epidermal growth factor receptor (EGFR) with high affinity, competitively blocking natural ligand binding and blocking receptor-mediated downstream signalling, resulting in impaired tumor cell proliferation. Matuzumab (EMD-72000) is a humanized IgG1 MAb that not only binds with high specificity and affinity to EGFR, but also modulates antibody-dependent cellular cytotoxicity (ADCC).",,,,Matuzumab is investigational.,Matuzumab is a solid.,True
17713,"Rindopepimut (CDX-110) is an injectable peptide cancer vaccine which targets a mutant protein called EGFRvIII present in about 25% to 30% of glioblastoma cases. The vaccine consists of the EGFRv3-specific peptide (a 13-amino acid mutant vIII epitope) conjugated to the non-specific immunomodulator keyhole limpet hemocyanin (KLH). The US FDA granted it Breakthrough Therapy Designation for glioblastoma in Feb 2015. Investigated for use/treatment in brain cancer. CDX-110 is an investigational immunotherapy that targets the tumor specific molecule EGFRvIII, a functional variant of the epidermal growth factor receptor (EGFR), which is a protein that has been well validated as a target for cancer therapy. This particular variant, EGFRvIII occurs in about 40 percent of Glioblastoma Multiforme (GBM) patients. It was discovered in a collaborative effort between Dr. Bert Vogelstein and Dr Albert Wong at Johns Hopkins University and Dr. Darell Bigner at Duke University. Unlike EGFR, EGFRvIII is not present in normal tissues, suggesting this target will enable the development of a tumor-specific therapy for cancer patients. Furthermore, EGFRvIII is a transforming oncogene that can directly contribute to cancer cell growth. While originally discovered in GBM, the most common and aggressive form of brain cancer, the expression of EGFRvIII has also been observed in various other cancers such as breast, ovarian, metastatic prostate, colorectal, and head & neck cancers. Celldex has exclusive rights to EGFRvIII vaccines and is pursuing the development of CDX-110 for GBM therapy, as well as in other cancers through additional clinical studies.",,,,Rindopepimut is investigational.,Rindopepimut is a solid.,True
17714,"Canertinib is a pan-erbB tyrosine kinase inhibitor which work against esophageal squamous cell carcinoma in vitro and in vivo. Canertinib treatment significantly affects tumour metabolism, proliferation and hypoxia as determined by PET. Investigated for use/treatment in breast cancer and lung cancer. CI-1033 effectively inhibits the growth of esophageal squamous cell carcinoma which co-expresses both EGFR and HER2 with the inhibition of phosphorylation of both MAPK and AKT. Some studies suggest that CI-1033 holds significant clinical potential in esophageal cancer.",,,,Canertinib is investigational.,Canertinib is a solid.,True
17715,"Pelitinib (EKB-569) is a potent, low molecular weight, selective, and irreversible inhibitor of epidermal growth factor receptor (EGFR) that is being developed as an anticancer agent. Investigated for use/treatment in colorectal cancer and lung cancer.",,,,Pelitinib is investigational.,Pelitinib is a solid.,True
17716,,,,,S-{3--3-OXOPROPYL}-L-CYSTEINE is experimental.,S-{3--3-OXOPROPYL}-L-CYSTEINE is a solid.,False
17717,PD-168393 is an epidermal growth factor receptor inhibitor.,,,,PD-168393 is experimental.,PD-168393 is a solid.,True
17718,"Necitumumab is an intravenously administered recombinant monoclonal IgG1 antibody used in the treatment of non-small cell lung cancer (NSCLC) as an EGFR antagonist. It functions by binding to epidermal growth factor receptor (EGFR) and prevents binding of its ligands, a process that is involved in cell proliferation, metastasis, angiogenesis, and malignant progression. Binding of necitumumab to EGFR induces receptor internalization and degradation, thereby preventing further activation of EGFR which is beneficial in NSCLC as many patients have increased protein expression of EGFR. Necitumumab is approved for use in combination with cisplatin and gemcitabine as a first-line treatment for metastatic squamous non-small cell lung cancer (NSCLC). Necitumumab is approved for use in combination with cisplatin and gemcitabine as a first-line treatment for metastatic squamous non-small cell lung cancer (NSCLC). It is not indicated for treatment of non-squamous NSCLC.  Necitumumab is an EGFR antagonist that functions by binding to epidermal growth factor receptor (EGFR) and preventing binding of its ligands, a process that is involved in cell proliferation, metastasis, angiogenesis, and malignant progression. Binding of necitumumab to EGFR induces receptor internalization and degradation.",,,,Necitumumab is approved and investigational.,,True
17719,Zalutumumab is a fully human IgG1 monoclonal antibody designed to bind with selectivity to the epidermal growth factor receptor (EGFR). Zalutumumab has been investigated for the treatment of Squamous Cell Cancer and Head and Neck Cancer.,,,,Zalutumumab is investigational.,Zalutumumab is a liquid.,True
17720,"Olmutinib is an orally active epidermal growth factor receptor inhibitor used in the treatment of T790M mutation positive non-small cell lung cancer. It is available under the brand name Olita made by Hanmi Pharmaceuticals. Olmutinib was developed by Hanmi Pharmaceuticals and Boehringer Ingelheim. Olmutinib recieved breakthrough therapy designation in the United States in December 2015 and was approved for use in Korea in May 2016. For use in treatment of metastatic T790M mutation positive non-small cell lung cancer. Olmutinib selectively and irreversibly binds and inhibits epidermal growth factor receptors (EGFR) with the T790M activating mutation. EGFRs are frequently over-expressed in lung cancer and contribute to activation of the phosphoinositide 3-kinase and mitogen activated protein kinase pathways which both promote cell survival and proliferation. By inhibiting EGFR activation, olmutinib attenuates the activation of these tumor promoting pathways.  Olmutinib covalently binds a cysteine residue near the kinase domain of mutant EGFRs to prevent phosphorylation of the receptor. This inhibits receptor signalling as phosphorylation is necessary for recruitment of signalling cascade proteins.",The molecular weight is 486.59.,Olmutinib has a topological polar surface area of 82.62.,The log p value of  is 5.14.,Olmutinib is investigational.,Olmutinib is a solid.,True
17721,"Abivertinib is a tyrosine kinase inhibitor targeted against mutant forms of both human epidermal growth factor receptor (EGFR) and Bruton's tyrosine kinase (BTK). It has been investigated for use in the treatment of non-small cell lung cancer (NSCLC) and B-cell malignancies. In binding to and inhibiting EGFR and BTK receptors, abivertinib exerts immunomodulatory effects by preventing the production and release of pro-inflammatory cytokines (e.g. TNF-alpha, interleukins).",,,,Abivertinib is investigational.,,True
17722,"An opioid antagonist with properties similar to those of naloxone; in addition it also possesses some agonist properties. It should be used cautiously; levallorphan reverses severe opioid-induced respiratory depression but may exacerbate respiratory depression such as that induced by alcohol or other non-opioid central depressants. (From Martindale, The Extra Pharmacopoeia, 30th ed, p683) For the complete or partial reversal of narcotic depression, including respiratory depression, induced by opioids. Levallorphan, an opioid antagonist similar to naloxone, is used to treat drug overdoses. Levallorphan differs from naloxone in that it also possesses some agonist properties. It is an analogue of levelorphanol that counteracts the actions of narcotic analgesics such as morphine. It is used especially in the treatment of respiratory depression due to narcotic overdoses. Levallorphan prevents or reverses the effects of opioids including respiratory depression, sedation and hypotension. Also, it can reverse the psychotomimetic and dysphoric effects of agonist-antagonists such as pentazocine. Levallorphan antagonizes opioid effects by competing for the same receptor sites. It binds to the opioid mu receptor and the nicotinic acetylcholine receptor alpha2/alpha3.",The molecular weight is 283.42.,Levallorphan has a topological polar surface area of 23.47.,The log p value of  is 4.13.,Levallorphan is approved.,Levallorphan is a solid.,True
17723,"Anileridine is a synthetic opioid and strong analgesic medication. It is a narcotic pain reliever used to treat moderate to severe pain. Narcotic analgesics act in the central nervous system (CNS) to relieve pain. Some of their side effects are also caused by actions in the CNS. For treatment and management of pain (systemic) and for use as an anesthesia adjunct. Anileridine, a potent analgesic, is an analog of pethidine. Anileridine is useful for the relief of moderate to severe pain. It may also be used as an analgesic adjunct in general anesthesia in the same manner as meperidine to reduce the amount of anesthetic needed, to facilitate relaxation, and to reduce laryngospasm. In addition, anileridine exerts mild antihistaminic, spasmolytic and antitussive effects. Anileridine's main pharmacologic action is exerted on the CNS. Respiratory depression, when it occurs, is of shorter duration than that seen with morphine or meperidine when equipotent analgesic doses are used. Opiate receptors are coupled with G-protein receptors and function as both positive and negative regulators of synaptic transmission via G-proteins that activate effector proteins. Binding of the opiate stimulates the exchange of GTP for GDP on the G-protein complex. As the effector system is adenylate cyclase and cAMP located at the inner surface of the plasma membrane, opioids decrease intracellular cAMP by inhibiting adenylate cyclase. Subsequently, the release of nociceptive neurotransmitters such as substance P, GABA, dopamine, acetylcholine and noradrenaline is inhibited. Opioids also inhibit the release of vasopressin, somatostatin, insulin and glucagon. Opioids such as anileridine close N-type voltage-operated calcium channels (OP2-receptor agonist) and open calcium-dependent inwardly rectifying potassium channels (OP3 and OP1 receptor agonist). This results in hyperpolarization and reduced neuronal excitability.",The molecular weight is 352.48.,Anileridine has a topological polar surface area of 55.56.,The log p value of  is 3.1.,Anileridine is approved and illicit.,Anileridine is a solid.,True
17724,A narcotic analgesic with a long onset and duration of action. It is used mainly in the treatment of narcotic dependence. Used mainly in the treatment of narcotic dependence. Methadyl Acetate is a narcotic analgesic with a long onset and duration of action. The drug decreases a patients opioid use by preventing opioid withdrawal and in how it can mimic some of the effects of opioids. Methadyl Acetate is primarily a mu-type opioid receptor agonist. It functions similarily to methadone.,The molecular weight is 353.51.,Methadyl acetate has a topological polar surface area of 29.54.,The log p value of  is 4.59.,Methadyl acetate is experimental and illicit.,Methadyl acetate is a solid.,True
17725,,,,,Debromohymenialdisine is experimental.,Debromohymenialdisine is a solid.,False
17726,"SR 121463 is a nonpeptide aquaretic compound with potent selective antagonism of the vasopressin V2 (V1b) receptor subtype. It is a candidate for control of hyponatremia and in the treatment of syndrome of inappropriate secretion of anti-diuretic hormone (SIADH). Investigated for use/treatment in cardiovascular disorders, in the treatment of syndrome of inappropriate secretion of anti-diuretic hormone (SIADH) and in hyponatremia.  Increases urine volume through selective antagonism of V1b/V2 receptors.  Selectively antagonizes v1b receptors. ",,,,SR 121463 is investigational.,SR 121463 is a solid.,True
17727,"Pamidronic acid is a second generation, nitrogen containing bisphosphonate similar to and. Pamidronic acid was first described in the literature in 1977. The second generation bisphosphonates are less common as third generation bisphosphonates, such as , , , and are becoming more popular. Pamidronate is indicated to treat moderate to severe hypercalcemia of malignancy, moderate to severe Paget's disease of bone, osteolytic bone metastases of breast cancer, and osteolytic lesions of multiple myeloma. Pamidronic acid is a second generation, nitrogen containing bisphosphonate that inhibits osteoclast mediated bone loss It has a wide therapeutic index and a long duration of action as it can be given every 3-4 weeks for certain indications. Patients should be counselled regarding the risk of elevated blood urea nitrogen, renal tubular necrosis, and nephrotoxicity. Bisphosphonates are taken into the bone where they bind to hydroxyapatite. Bone resorption by osteoclasts causes local acidification, releasing the bisphosphonate, which is taken into the osteoclast by fluid-phase endocytosis. Endocytic vesicles become acidified, releasing bisphosphonates into the cytosol of osteoclasts where they act.",The molecular weight is 235.07.,Pamidronic acid has a topological polar surface area of 161.31.,The log p value of  is -6.17.,Pamidronic acid is approved.,Pamidronic acid is a solid.,True
17728,"Zoledronic acid, or CGP 42'446, is a third generation, nitrogen containing bisphosphonate similar to , , and. Zoledronic acid is used to treat and prevent multiple forms of osteoporosis, hypercalcemia of malignancy, multiple myeloma, bone metastases from solid tumors, and Paget’s disease of bone. Zoledronic acid was first described in the literature in 1994. Zoledronic acid is indicated to treat hypercalcemia of malignancy, multiple myeloma, bone metastases from solid tumors, osteoporosis in men and postmenopausal women, glucocorticoid induced osteoporosis, and Paget's disease of bone in men and women. Zoledronic acid is also indicated for the prevention of osteoporosis in post menopausal women and glucocorticoid induced osteoporosis. Zoledronic acid is a third generation, nitrogen containing bisphosphonate that inhibits osteoclast function and prevents bone resorption. The therapeutic window is wide as patients are unlikely to suffer severe effects from overdoses and the duration of action is long. Patients should be counselled regarding the risk of electrolyte deficiencies, renal impairment, osteonecrosis of the jaw, atypical femoral fractures, bronchoconstriction, hepatic impairment, hypocalcemia, and embryo-fetal toxicity. Bisphosphonates are taken into the bone where they bind to hydroxyapatite. Bone resorption by osteoclasts causes local acidification, releasing the bisphosphonate, which is taken into the osteoclast by fluid-phase endocytosis. Endocytic vesicles become acidified, releasing bisphosphonates into the cytosol of osteoclasts where they act.",The molecular weight is 272.09.,Zoledronic acid has a topological polar surface area of 153.11.,The log p value of  is -3.07.,Zoledronic acid is approved.,Zoledronic acid is a solid.,True
17729,"Alendronic acid is a second generation bisphosphonate that is used for the treatment of some forms of osteoperosis and Paget's disease. It functions by preventing resorption of bone. Alendronic acid is indicated for the treatment and prevention of osteoporosis in men and postmenopausal women, treatment of glucocorticoid-induced osteoporosis, and Paget's disease of bone. However, alendronic acid is not indicated for use in pediatric populations or patients with a creatinine clearance <35mL/min. Alendronic acid tablets have a very low oral bioavialability. After administration it distributes into soft tissue and bone or is excreted in the urine. Alendronic acid does not undergo metabolism. Alendronic acid binds to bone hydroxyapatite. Bone resorption causes local acidification, releasing alendronic acid which is that taken into osteoclasts by fluid-phase endocytosis. Endocytic vesicles are acidified, releasing alendronic acid to the cytosol of osteoclasts where they induce apoptosis. Inhibition of osteoclasts results in decreased bone resorption which is shown through decreased urinary calcium, deoxypyridinoline and cross-linked N-telopeptidases of type I collagen.",The molecular weight is 249.1.,Alendronic acid has a topological polar surface area of 161.31.,The log p value of  is -5.64.,Alendronic acid is approved.,Alendronic acid is a solid.,True
17730,"Ibandronate, or BM 21.0955, is a third generation, nitrogen containing bisphosphonate similar to , , and. It is used to prevent and treat postmenopausal osteoporosis. Ibandronate was first described in the literature in 1993 as a treatment for bone loss in dogs. For the treatment and prevention of osteoporosis in postmenopausal women. Ibandronate is a nitrogen containing bisphosphonate used to treat and prevent osteoporosis in postmenopausal women. The therapeutic index is wide as overdoses are not especially toxic, and the duration of action is long as the half life can be up to 157 hours. Patients should be counselled regarding the risk of upper GI adverse reactions, hypocalcemia, musculoskeletal pain, osteonecrosis of the jaw, atypical fractures of the femur, and severe renal impairment. Bisphosphonates are taken into the bone where they bind to hydroxyapatite. Bone resorption by osteoclasts causes local acidification, releasing the bisphosphonate, which is taken into the osteoclast by fluid-phase endocytosis. Endocytic vesicles become acidified, releasing bisphosphonates into the cytosol of osteoclasts where they act.",The molecular weight is 319.23.,Ibandronate has a topological polar surface area of 138.53.,The log p value of  is -3.37.,Ibandronate is approved and investigational.,Ibandronate is a solid.,True
17731,,,,,Dimethylallyl Diphosphate is experimental.,Dimethylallyl Diphosphate is a solid.,False
17732,,,,,Isopentyl Pyrophosphate is experimental.,Isopentyl Pyrophosphate is a solid.,False
17733,,,,,Geranyl Diphosphate is experimental.,Geranyl Diphosphate is a solid.,False
17734,,,,,ISOPENTENYL PYROPHOSPHATE is experimental.,ISOPENTENYL PYROPHOSPHATE is a solid.,False
17735,"Incadronate, or YM-175, is a nitrogen containing bisphosphonate. Along with being investigated to treat hypercalcemia of malignancy, it has also been investigated in the treatment of myeloma, leukemia, and other cancers. Incadronate has been investigated in the treatment of myeloma, leukemia, and other cancers. It has also been investigated in patients with hypercalcemia of malignancy. Bisphosphonates are taken into the bone where they bind to hydroxyapatite. Bone resorption by osteoclasts causes local acidification, releasing the bisphosphonate, which is taken into the osteoclast by fluid-phase endocytosis. Endocytic vesicles become acidified, releasing bisphosphonates into the cytosol of osteoclasts where they act.",The molecular weight is 287.19.,Incadronic acid has a topological polar surface area of 127.09.,The log p value of  is 0.25.,Incadronic acid is experimental.,Incadronic acid is a solid.,True
17736,"Investigated for use/treatment in multiple myeloma, breast cancer, osteoporosis, and lung cancer.",The molecular weight is 322.15.,Minodronic acid has a topological polar surface area of 152.59.,The log p value of  is -2.09.,Minodronic acid is investigational.,Minodronic acid is a solid.,True
17737,,,,,Farnesyl diphosphate is experimental.,Farnesyl diphosphate is a solid.,False
17738,,,,,Geranylgeranyl diphosphate is experimental.,Geranylgeranyl diphosphate is a solid.,False
17739,"A vitamin D that can be regarded as a reduction product of vitamin D2. Used for the prevention and treatment of rickets or osteomalacia, and to manage hypocalcemia associated with hypoparathyroidism or pseudohypoparathyroidism. Also used for the treatment of vitamin D dependent rickets, rickets or osteomalacia secondary to long-term high dose anticonvulsant therapy, early renal osteodystrophy, osteoporosis (in conjunction with calcium), and hypophosphatemia associated with Fanconi syndrome (with treatment of acidosis). Dihydrotachysterol is hydroxylated in the liver to 25-hydroxydihydrotachysterol, which is the major circulating active form of the drug. It does not undergo further hydroxylation by the kidney and therefore is the analogue of 1, 25-dihydroxyvitamin D. Dihydrotachysterol is effective in the elevation of serum calcium by stimulating intestinal calcium absorption and mobilizing bone calcium in the absence of parathyroid hormone and of functioning renal tissue. Dihydrotachysterol also increases renal phosphate excretion. Once hydroxylated to 25-hydroxydihydrotachysterol, the modified drug binds to the vitamin D receptor. The bound form of the vitamin D receptor serves as a transcriptional regulator of bone matrix proteins, inducing the expression of osteocalcin and suppressing synthesis of type I collagen. Vitamin D (when bound to the vitamin D receptor)stimulates the expression of a number of proteins involved in transporting calcium from the lumen of the intestine, across the epithelial cells and into blood. This stimulates intestinal calcium absorption and increases renal phosphate excretion. These are functions that are normally carried out by the parathyroid hormone. ",The molecular weight is 398.68.,Dihydrotachysterol has a topological polar surface area of 20.23.,The log p value of  is 9.85.,Dihydrotachysterol is approved.,Dihydrotachysterol is a solid.,True
17740,"Lexacalcitol is a solid. This compound belongs to the vitamin D and derivatives class of chemicals. These are compounds containing a secosteroid backbone, usually secoergostane or secocholestane. It is known to target the vitamin D3 receptor.",,,,Lexacalcitol is experimental.,Lexacalcitol is a solid.,True
17741,,,,,Seocalcitol is investigational.,Seocalcitol is a solid.,False
17742,"The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.",,,,Cholesterol is approved and investigational.,Cholesterol is a solid.,True
17743,"Investigated for use/treatment in prostate cancer, psoriasis and hyperparathyroidism. Inecalcitol is an analogue of calcitriol, the naturally active metabolite of vitamin D. Calcitriol and their analogues activate the vitamin D receptor (VDR). Vitamin D has a major role in regulating calcium absorption from the gut, storage in mineral form in the bones, and excretion by the kidney and effectively prevents rickets in infants. Vitamin D and calcitriol can cause hypercalcemia at high or frequently repeated doses; in turn, hypercalcemia can cause kidney toxicity by accumulation of calcium-containing micro-crystals and heart and muscle dysfunction by impairing contractions. The mechanism of action is currently unknown, but it is proposed that inecalcitol exerts its superagonistic action through enhancing coactivator binding by the VDR.",,,,Inecalcitol is investigational.,Inecalcitol is a solid.,True
17744,"Becocalcidiol is a vitamin D(3) analogue which has not caused hypercalcaemia or significant irritation in preclinical trials. For topical treatment of psoriasis and psoriatic disorders. Becocalcidiol (formerly QRX-101) is a novel vitamin D analogue for the treatment of mild to moderate psoriasis. In clinical and preclinical studies, becocalcidiol has been well tolerated with a low incidence of skin irritation. Based on the completed Phase IIb study, becocalcidiol was statistically superior to placebo in reducing plaque and did not result in excessive blood calcium levels, a side effect of existing calcitriol topical treatments for psoriasis. The mechanism of action of becocalcidiol in the treatment of psoriasis is accounted for by an antiproliferative activity for keratinocytes and the stimulation of epidermal cell differentiation.",,,,Becocalcidiol is investigational.,Becocalcidiol is a solid.,True
17745,"CTA018 is a member of a new class of vitamin D analogues with a dual mechanism of action, called Vitamin D Signal Amplifiers. This proprietary new drug is both a potent inhibitor of CYP24 (the enzyme responsible for the breakdown of vitamin D) and a potent activator of vitamin D signaling pathways. CTA018 will be the first drug with this novel dual mechanism of action to enter clinical development. Preclinical studies have shown that CTA018 inhibits the proliferation of rapidly dividing cells such as human epidermal keratinocytes (skin cells) and is also effective in inhibiting pro-inflammatory cytokine secretion which may be involved in the etiology of psoriasis. Cytochroma anticipates that CTA018 will be more potent than currently marketed vitamin D analogues such as calcitriol and calcipotriol and it is expected to have a greater safety index. Investigated for use/treatment in kidney disease and psoriasis and psoriatic disorders. CTA018 is a rationally designed Vitamin D hormone analog that acts as both a potent VDR agonist and CYP24 inhibitor. The Company believes this dual mechanism of action will provide efficacy and safety advantages over existing Vitamin D hormone replacement therapies for SHPT. CTA018 binds to the VDR located in parathyroid cells and triggers a genomic cascade of events resulting in suppression of PTH secretion. It also binds to the substrate binding pocket of CYP24, a cytochrome P450 enzyme that specifically and efficiently catabolizes Vitamin D hormones. By binding to CYP24 and blocking its activity, CTA018 levels in cells are more readily raised to therapeutic levels. Unlike common cytochrome P450 inhibitors (such as ketoconazole) which act non-specifically on all cytochromes, CTA018 specifically targets CYP24, making drug-drug interactions far less likely. The Company believes the novel dual activity of CTA018 will reduce the incidence of clinically-acquired resistance to Vitamin D hormone replacement therapy, allowing greatly improved efficacy at well tolerated dosages.",,,,CTA018 is investigational.,CTA018 is a solid.,True
17746,"Eldecalcitol (ED-71), a vitamin D analog, is a more potent inhibitor of bone resorption than alfacalcidol in an estrogen-deficient rat model of osteoporosis. Eldecalcitol, effectively and safely increased lumbar and hip bone mineral density (BMD) in osteoporotic patients who also received vitamin D3 supplementation. Investigated for use/treatment in osteoporosis. Eldecalcitol is an analog of 1a,25-dihydroxyvitamin D3 , bearing a hydroxypropoxy residue at the 2b position. Eldecalcitol is also effective in increasing bone mass and was able to enhance bone strength in rodents. It binds to the vitamin D receptor (VDR) with less affinity but binds to vitamin D-binding protein with higher affinity than 1,25(OH)2D, showing a long half-life in plasma.",The molecular weight is 490.72.,Eldecalcitol has a topological polar surface area of 90.15.,The log p value of  is 6.09.,Eldecalcitol is investigational.,Eldecalcitol is a solid.,True
17747,"Elocalcitol is a calcitriol analog for inhibition of prostate cell growth; in phase II clinical trial in patients with benign prostate hyperplasia (4/2004). Investigated for use/treatment in benign prostatic hyperplasia, urinary incontinence, prostate disorders, and infertility.",,,,Elocalcitol is investigational.,Elocalcitol is a solid.,True
17748,,,,,"(1R,3R)-5-cyclopentyl}prop-2-en-1-ylidene]cyclohexane-1,3-diol is experimental.","(1R,3R)-5-cyclopentyl}prop-2-en-1-ylidene]cyclohexane-1,3-diol is a solid.",False
17749,,,,,"1,3-CYCLOHEXANEDIOL, 4-METHYLENE-5-ETHYLIDENE]-, (1R,3S,5Z) is experimental.","1,3-CYCLOHEXANEDIOL, 4-METHYLENE-5-ETHYLIDENE]-, (1R,3S,5Z) is a solid.",False
17750,"Tetraethylammonium is an experimental drug with no approved indication or marketed formulation. The only marketed drug containing tetraethylammonium was a combination drug called Fosglutamina B6, but this drug has now been discontinued. As an experimental agent, tetraethylammonium is used in its salt forms such as tetraethylammonium chloride and tetraethylammonium bromide. Its mechanism of action is still being investigated, but it is known that tetraethylammonium blocks autonomic ganglia, calcium- and voltage- activated potassium channels, and nicotinic acetylcholine receptors. Because of its inhibitory actions at the autonomic ganglia, tetraethylammonium was thought to be a potential therapeutic vasodilator but serious toxic effects were found. The most common use of tetraethylammonium presently is as a pharmacological research agent that blocks selective potassium channels. Structurally, tetraethylammonium is positively charged due to its central quaternary ammonium. Tetraethylammonium is an experimental drug with no approved indication. Tetraethylammonium is a vasodilator because it blocks autonomic ganglia and prevents signals carrying vasoconstrictor impulses from proceeding. Tetraethylammonium's mechanism of action is still being investigated, but it is known that it blocks autonomic ganglia, calcium- and voltage- activated potassium channels, and nicotinic acetylcholine receptors.",,,,Tetraethylammonium is experimental and investigational.,Tetraethylammonium is a solid.,True
17751,"The pipecolinate derivative biricodar (VX-710) is a clinically applicable modulator of P-glycoprotein (Pgp) and multidrug resistance protein (MRP-1). Administered intravenously, biricodar dicitrate is to be used in combination with cancer chemotherapy agents. Biricodar dicitrate blocks two major multi-drug resistance mechanisms: P-glycoprotein (MDR-1) and multi-drug resistance-associated protein (MRP). Vertex&rsquo;s research shows that biricodar dicitrate can enhance the accumulation of chemotherapy agents in tumor cells by blocking the drug pumps P-gp and MRP, and that it is capable of restoring the sensitivity of tumors to treatment with chemotherapeutic agents.",,,,Biricodar is investigational.,Biricodar is a solid.,True
17752,,,,,2--5-Phosphono-Pent-3-Enoic Acid is experimental.,2--5-Phosphono-Pent-3-Enoic Acid is a solid.,False
17753,,,,,"Carboxymethylthio-3-(3-Chlorophenyl)-1,2,4-Oxadiazol is experimental.","Carboxymethylthio-3-(3-Chlorophenyl)-1,2,4-Oxadiazol is a solid.",False
17754,,,,,L-2-amino-3-butynoic acid is experimental.,L-2-amino-3-butynoic acid is a solid.,False
17755,,,,,Para-Mercury-Benzenesulfonic Acid is experimental.,Para-Mercury-Benzenesulfonic Acid is a solid.,False
17756,,,,,ICI-164384 is experimental.,ICI-164384 is a solid.,False
17757,,,,,"4-(2-{Sulfanyl}-6-(1-Piperazinyl)-1,3,5-Triazin-2-Yl]Amino}Ethyl)Phenol is experimental.","4-(2-{Sulfanyl}-6-(1-Piperazinyl)-1,3,5-Triazin-2-Yl]Amino}Ethyl)Phenol is a solid.",False
17758,"MF101 is a novel estrogen receptor beta (ERβ) selective agonist and unlike currently available hormone therapies, does not activate the estrogen receptor alpha (ERα), known to be implicated in tumor formation. MF101 is an oral drug designed for the treatment of hot flashes and night sweats in peri-menopausal and menopausal women. Investigated for use/treatment in hormone replacement therapy: menopause and menopause. MF101 promoted ERbeta, but not ERalpha, activation of an estrogen response element (ERE) upstream of the luciferase reporter gene. MF101 also selectively regulates transcription of endogenous genes through ERbeta. The ERbeta-selectivity was not due to differential binding, since MF101 binds equally to ERalpha and ERbeta. Fluorescence resonance energy transfer and protease digestion studies showed that MF101 produces a different conformation in ERalpha from ERbeta, when compared with the conformations produced by estradiol. The specific conformational change induced by MF101 allows ERbeta to bind to an ERE and recruit coregulatory proteins that are required for gene activation. MF101 did not activate the ERalpha-regulated proliferative genes, c-myc and cyclin D1, or stimulate MCF-7 breast cancer cell proliferation or tumor formation in a mouse xenograft model.",,,,MF101 is investigational.,MF101 is a solid.,True
17759,Prinaberel is an estrogen receptor beta agonist.,,,,Prinaberel is investigational.,Prinaberel is a solid.,True
17760,,,,,ERB-196 is experimental.,ERB-196 is a solid.,False
17761,,,,,"4-(6-HYDROXY-BENZOISOXAZOL-3-YL)BENZENE-1,3-DIOL is experimental.","4-(6-HYDROXY-BENZOISOXAZOL-3-YL)BENZENE-1,3-DIOL is a solid.",False
17762,,,,,"2-(5-HYDROXY-NAPHTHALEN-1-YL)-1,3-BENZOOXAZOL-6-OL is experimental.","2-(5-HYDROXY-NAPHTHALEN-1-YL)-1,3-BENZOOXAZOL-6-OL is a solid.",False
17763,,,,,2-(4-HYDROXY-PHENYL)BENZOFURAN-5-OL is experimental.,2-(4-HYDROXY-PHENYL)BENZOFURAN-5-OL is a solid.,False
17764,,,,,"(3aS,4R,9bR)-2,2-difluoro-4-(4-hydroxyphenyl)-6-(methoxymethyl)-1,2,3,3a,4,9b-hexahydrocyclopentachromen-8-ol is experimental.","(3aS,4R,9bR)-2,2-difluoro-4-(4-hydroxyphenyl)-6-(methoxymethyl)-1,2,3,3a,4,9b-hexahydrocyclopentachromen-8-ol is a solid.",False
17765,,,,,1-CHLORO-6-(4-HYDROXYPHENYL)-2-NAPHTHOL is experimental.,1-CHLORO-6-(4-HYDROXYPHENYL)-2-NAPHTHOL is a solid.,False
17766,,,,,4-(4-HYDROXYPHENYL)-1-NAPHTHALDEHYDE OXIME is experimental.,4-(4-HYDROXYPHENYL)-1-NAPHTHALDEHYDE OXIME is a solid.,False
17767,,,,,5-HYDROXY-2-(4-HYDROXYPHENYL)-1-BENZOFURAN-7-CARBONITRILE is experimental.,5-HYDROXY-2-(4-HYDROXYPHENYL)-1-BENZOFURAN-7-CARBONITRILE is a solid.,False
17768,,,,,3-BROMO-6-HYDROXY-2-(4-HYDROXYPHENYL)-1H-INDEN-1-ONE is experimental.,3-BROMO-6-HYDROXY-2-(4-HYDROXYPHENYL)-1H-INDEN-1-ONE is a solid.,False
17769,,,,,3-(6-HYDROXY-NAPHTHALEN-2-YL)-BENZOISOOXAZOL-6-OL is experimental.,3-(6-HYDROXY-NAPHTHALEN-2-YL)-BENZOISOOXAZOL-6-OL is a solid.,False
17770,,,,,17alpha-Estriol is experimental.,17alpha-Estriol is a solid.,False
17771,,,,,"(9aS)-4-bromo-9a-butyl-7-hydroxy-1,2,9,9a-tetrahydro-3H-fluoren-3-one is experimental.","(9aS)-4-bromo-9a-butyl-7-hydroxy-1,2,9,9a-tetrahydro-3H-fluoren-3-one is a solid.",False
17772,"FavId, is an active immunotherapy that is based upon unique genetic information extracted from a patient's tumor. B-cell non-Hodgkin's lymphoma It is designed to stimulate a patient's immune system to mount a specific and sustained response to disease. FavId is currently being developed for use following treatment with existing standards of care to extend time to disease progression in patients with B-cell non-Hodgkin's lymphoma",,,,FavId is investigational.,FavId is a solid.,True
17773,"Lenograstim is a recombinant granulocyte colony-stimulating factor used as an immunostimulating agent. The drug is used to reduce the risk of life-threatening infection in patients with neutropenia, particularly after cytotoxic chemotherapy.  Lenograstim has been confirmed as a valuable adjunct to minimise the haematological toxicity of myelosuppressive chemotherapy in patients with malignant disease. The drug also enhances neutrophil recovery in patients undergoing stem cell rescue, and assists peripheral blood progenitor cells mobilisation. Lenograstim is the glycosylated recombinant form of human granulocyte colony stimulating factor. Lenograstim accelerates neutrophil recovery significantly after chemotherapy, with beneficial effects on clinical end-points such as incidence of laboratory-confirmed infection and length of hospital stay. Chemotherapy dose intensity has also been increased in patients receiving lenograstim, notably those with breast or small cell lung cancer, although improvements in tumour response and survival have not been demonstrated. Lenograstim also assists neutrophil recovery in patients undergoing bone marrow transplantation, and stimulates the production of peripheral blood stem cells (PBSCs) for autologous transfusion after aggressive chemotherapy.",,,,Lenograstim is approved and investigational.,Lenograstim is a solid.,True
17774,"Lipegfilgrastim, previously known as XM22, is a pegylated, recombinant granulocyte colony-stimulating factor (G-CSF) that was synthetized using a highly site-specific glycoPEGylation technology. It is used as an alternate to for prophylactic use in cancer patients receiving chemotherapy and at risk for developing chemotherapy-induced neutropenia. Since July 2013, lipegfilgrastim is marketed by the EMA as Lonquex for subcutaneously injection, where it is administered once following cytotoxic chemotherapy for each chemotherapy cycle in adult patients being treated with cytotoxic chemotherapy for malignancy. It aims to reduce the duration of neutropenia and the incidence of febrile neutropenia. Indicated for the reduction in the duration of neutropenia and the incidence of febrile neutropenia in adult patients treated with cytotoxic chemotherapy for malignancy (with the exception of chronic myeloid leukaemia and myelodysplastic syndromes).  Mimicking endogenous granulocyte colony-stimulating factors, lipegfilgrastim enhances the number and function of circulating neutrophils by binding to endogenous G-CSF receptors. A small increase in monocyte and/or lymphocyte counts may also be observed. Following a single subcutaneous dose administration of 100 μg/kg, lipegfilgrastim resulted in a significant increase in neutrophilic granulocyte and large unstained cell counts. G-CSF also increases the antibacterial activities of neutrophils including the phagocytosis. Due to structural similarity between lipegfilgrastim and pegfilgrastim, G-CSF receptor binding was equivalent between two molecules. However, lipegfilgrastim showed greater time-dependent resistance to neutrophil elastase degradation and greater retention of activity than pegfilgrastim. Endogenous granulocyte colony-stimulating factor (G-CSF) is a glycoprotein that stimulates neutrophil progenitors. It is produced mainly by monocytes, fibroblasts and endothelial cells to promote the development of neutrophils and increase their proliferation and maturation. Subsequently, G-SCF stimulates the release of matured neutrophils from the bone marrow storage pools into the peripheral blood to enhance their function. Via binding to to the human G-CSF receptors, lipegfilgrastim activates the receptor signalling pathway as a growth factor to stimulate proliferation of haematopoietic progenitor cells and their differentiation into mature cells, and promote subsequent release into the peripheral blood. This stimulatory effect of lipegfilgrastim may extend to other single lineage and multilineage progenitors and pluripotent haematopoietic stem cells. The presence of the PEG moiety in lipegfilgrastim decreases the plasma clearance and extends the drug's terminal elimination half-life, allowing for less frequent dosing.",,,,Lipegfilgrastim is approved and investigational.,Lipegfilgrastim is a liquid.,True
17775,"Diflorasone is a topical corticosteroid used to treat itching and inflammation of the skin. For relief of the inflammatory and pruritic manifestations of corticosteroid responsive dermatoses. Like other topical corticosteroids, diflorasone has anti-inflammatory, antipruritic, and vasoconstrictive properties. Once absorbed through the skin, topical corticosteroids are handled through pharmacokinetic pathways similar to systemically administered corticosteroids. Diflorasone is a potent topical corticosteroid that should not be used with occlusive dressings. It is recommended that treatment should be limited to 2 consecutive weeks and therapy should be discontinued when adequate results have been achieved. The precise mechanism of the antiinflammatory activity of topical steroids in the treatment of steroid-responsive dermatoses, in general, is uncertain. However, corticosteroids are thought to act by the induction of phospholipase A<sub>2</sub> inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A<sub>2</sub>.",,,,Diflorasone is approved.,Diflorasone is a solid.,True
17776,"A topical anti-inflammatory glucocorticoid used in dermatoses, skin allergies, psoriasis, etc. For the relief of the inflammatory and pruritic manifestations of corticosteroid-responsive dermatoses. Like other topical corticosteroids, desoximetasone has anti-inflammatory, antipruritic, and vasoconstrictive properties. Once absorbed through the skin, topical corticosteroids are handled through pharmacokinetic pathways similar to systemically administered corticosteroids. Desoximetasone is a potent topical corticosteroid that should not be used with occlusive dressings. It is recommended that treatment should be limited to 2 consecutive weeks and therapy should be discontinued when adequate results have been achieved. The precise mechanism of the antiinflammatory activity of topical steroids in the treatment of steroid-responsive dermatoses, in general, is uncertain. However, corticosteroids are thought to act by the induction of phospholipase A<sub>2</sub> inhibitory proteins, collectively called lipocortins. This is achieved first by the drug binding to the glucocorticoid receptors which then translocates into the nucleus and binds to DNA causing various activations and repressions of genes. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A<sub>2</sub>.",The molecular weight is 376.47.,Desoximetasone has a topological polar surface area of 74.6.,The log p value of  is 2.41.,Desoximetasone is approved.,Desoximetasone is a solid.,True
17777,"Clocortolone is a medium potency corticosteroid that is often used as a topical cream for the relief of inflammatory oand pruritic (itching) arising from steroid-responsive dermatoses of the scalp. For short-term topical treatment of the inflammatory and pruritic manifestations of moderate to severe corticosteroid-responsive dermatoses of the scalp. Like other topical corticosteroids, clocortolone has anti-inflammatory, antipruritic, and vasoconstrictive properties. Once absorbed through the skin, topical corticosteroids are handled through pharmacokinetic pathways similar to systemically administered corticosteroids. Clocortolone is a moderate potency topical corticosteroid that should not be used with occlusive dressings. It is recommended that treatment should be limited to 2 consecutive weeks and therapy should be discontinued when adequate results have been achieved. The precise mechanism of the antiinflammatory activity of topical steroids in the treatment of steroid-responsive dermatoses, in general, is uncertain. However, corticosteroids are thought to act by the induction of phospholipase A<sub>2</sub> inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A<sub>2</sub>. These enzyme transcriptional changes are mediated by the drug binding first to the glucocorticoid receptor. This complex can migrate to the cell nucleus which then binds to DNA initiating genetic activation and repression of various genes.",,,,Clocortolone is approved.,Clocortolone is a solid.,True
17778,,,,,"Hexane-1,6-Diol is experimental.","Hexane-1,6-Diol is a solid.",False
17779,"ORG-34517 is currently under investigation by Organon for the treatment of depression. It has potential to treat a number of diseases such as Cushing’s disease, hypertension, diabetes, glaucoma etc, in which the activity of metabolites corticosterone and cortisol is high. Investigated for use/treatment in depression. Org-34517 is a glucocorticoid antagonist which may have a potential in a number of diseases where there is excess corticosterone/cortisol activity. The drug acts by normalizing hyperactivity in the hypothalamus-pituitary-adrenal (HPA) axis.",,,,ORG-34517 is investigational.,ORG-34517 is a solid.,True
17780,"Tixocortol is a 21-thiol derivative of hydrocortisone classified as a class A corticosteroid. It is a synthetic steroid with topical anti-inflammatory properties without the systemic glucocorticoid and mineralocorticoid activities and toxicity. Tixocortol is indicated for the treatment of rhinitis as a nasal suspension or aerosol. It is also used in the form of lozenges for the treatment of pharyngitis and in the form of enemas or rectal solution for the treatment of ulcerative colitis. Tixocortol can be used orally in a suspension or powder for the treatment of inflammatory conditions. It is also the substance used for the screening of contact allergies to class A steroids. Tixocortol presents the characteristic of local action which reduces significantly the side effects of systemic glucocorticoids. Reports have demonstrated that gastrointestinal administration of tixocortol generates a decrease in abdominal pain, bleeding, and frequency of stools which resulted in an amelioration in the malabsorption laboratory tests. All the effects were independent of suppression of the pituitary-adrenal axis, which was shown by the absence of significant depression of cortisol. Administration of tixocortol as a nasal spray has been shown to respect nasal drainage by the ciliary beats of the pituitary mucosa. The actions of tixocortol have no effect on leukocyte count, blood glucose level, sodium urinary excretion, and immunosupressive activity on lymphocytes. The mechanism of action of tixocortol is similar to other corticosteroids regarding the binding sites and prostaglandin synthesis but the local properties of tixocortol are given by the immediate liver metabolism and transformation withing red blood cells. All the immediate transformations of tixocortol classified it as part of the nonsystemic steroids.",,,,Tixocortol is approved and withdrawn.,Tixocortol is a solid.,True
17781,"Onapristone has been used in trials studying the treatment of Prostate Cancer, Recurrent Prostate Cancer, Metastatic Prostate Cancer, Androgen-independent Prostate Cancer, and Progesterone Receptor Positive Tumor: Max 1 Line of Prior Chemotherapy, no Prior Hormone Therapy.",,,,Onapristone is investigational.,,True
17782,"Methyprylon is a sedative of the piperidinedione derivative family that was previously used for the treatment of insomnia. However, with the introduction of newer drugs with fewer side effects, such as benzodiazepines, the clinical use of methyprylon is now limited. Methyprylon was withdrawn from the U.S. market in June 1965 and the Canadian market in September 1990 due to adverse events. For the treatment of insomnia. Methyprylon, a piperidinedione CNS depressant, is close to barbituric acid in structure, but different enough to be called a \non-barbiturate\"" sedative-hynotic. Methyprylon is used for insomnia and daytime tension. Methyprylon depresses the activity of muscle tissues, the heart, and the respiratory system."" Methyprylon binds at a distinct binding site associated with a Cl<sup>-</sup> ionopore at the GABA<sub>A</sub> receptor, increasing the duration of time for which the Cl<sup>-</sup> ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.",The molecular weight is 183.25.,Methyprylon has a topological polar surface area of 46.17.,The log p value of  is 1.78.,Methyprylon is approved and illicit and withdrawn.,Methyprylon is a solid.,True
17783,"Barbiturates work by binding to the GABAA receptor at either the alpha or the beta sub unit. These are binding sites that are distinct from GABA itself and also distinct from the benzodiazepine binding site. Like benzodiazepines, barbiturates potentiate the effect of GABA at this receptor. This GABAA receptor binding decreases input resistance, depresses burst and tonic firing, especially in ventrobasal and intralaminar neurons, while at the same time increasing burst duration and mean conductance at individual chloride channels; this increases both the amplitude and decay time of inhibitory postsynaptic currents. In addition to this GABA-ergic effect, barbiturates also block the AMPA receptor, a subtype of glutamate receptor. Glutamate is the principal excitatory neurotransmitter in the mammalian CNS.",,,,Dihydroquinidine barbiturate is experimental.,Dihydroquinidine barbiturate is a solid.,True
17784,Muscimol has been used in trials studying the treatment of Epilepsy and Parkinson's Disease.,,,,Muscimol is investigational.,,True
17785,,,,,"(9R,10R)-9-(S-glutathionyl)-10-hydroxy-9,10-dihydrophenanthrene is experimental.","(9R,10R)-9-(S-glutathionyl)-10-hydroxy-9,10-dihydrophenanthrene is a solid.",False
17786,,,,,Zinc trihydroxide is experimental.,Zinc trihydroxide is a solid.,False
17787,,,,,"S-(2,4-dinitrophenyl)glutathione is experimental.","S-(2,4-dinitrophenyl)glutathione is a solid.",False
17788,5-fluorotryptophan can be used as substrate analogue to study enzyme mechanisms by NMR spectroscopy.,,,,5-fluorotryptophan is experimental.,5-fluorotryptophan is a solid.,True
17789,,,,,"(9S,10S)-9-(S-glutathionyl)-10-hydroxy-9,10-dihydrophenanthrene is experimental.","(9S,10S)-9-(S-glutathionyl)-10-hydroxy-9,10-dihydrophenanthrene is a solid.",False
17790,,,,,GLUTATHIONE SULFINATE is experimental.,GLUTATHIONE SULFINATE is a solid.,False
17791,,,,,4-S-Glutathionyl-5-pentyl-tetrahydro-furan-2-ol is experimental.,4-S-Glutathionyl-5-pentyl-tetrahydro-furan-2-ol is a solid.,False
17792,,,,,Glutathione sulfonic acid is experimental.,Glutathione sulfonic acid is a solid.,False
17793,,,,,S-octylglutathione is experimental.,S-octylglutathione is a solid.,False
17794,,,,,1-Hydroxy-2-S-glutathionyl-3-para-nitrophenoxy-propane is experimental.,1-Hydroxy-2-S-glutathionyl-3-para-nitrophenoxy-propane is a solid.,False
17795,"S-hydroxycysteine is a solid. This compound belongs to the alpha amino acids and derivatives. These are amino acids in which the amino group is attached to the carbon atom immediately adjacent to the carboxylate group (alpha carbon), or a derivative thereof. It targets the proteins subtilisin BPN', glutathione S-transferase A1, glutathione S-transferase p, myelin P2 protein, and complement c3.",,,,S-Hydroxycysteine is experimental.,S-Hydroxycysteine is a solid.,True
17796,,,,,Cibacron Blue is experimental.,Cibacron Blue is a solid.,False
17797,"Deoxycholic acid is a a bile acid which emulsifies and solubilizes dietary fats in the intestine, and when injected subcutaneously, it disrupts cell membranes in adipocytes and destroys fat cells in that tissue. In April 2015, deoxycholic acid was approved by the FDA for the treatment submental fat to improve aesthetic appearance and reduce facial fullness or convexity. It is marketed under the brand name Kybella by Kythera Biopharma and is the first pharmacological agent available for submental fat reduction, allowing for a safer and less invasive alternative than surgical procedures. For improvement in appearance of moderate to severe fullness associated with submental fat in adults.  As a bile acid, deoxycholic acid emulsifies fat in the gut. Synthetically derived deoxycholic acid, when injected, stimulates a targeted breakdown of adipose cells by disrupting the cell membrane and causing adipocytolysis. This results in an inflammatory reaction and clearing of the adipose tissue remnants by macrophages. Deoxycholic acid's actions are reduced by albumin and tissue-associated proteins, therefore its effect is limited to protein-poor subcutaneous fat tissue. Protein-rich tissues like muscle and skin are unaffected by deoxycholic acid, contributing to its safety profile. ",The molecular weight is 392.58.,Deoxycholic acid has a topological polar surface area of 77.76.,The log p value of  is 4.51.,Deoxycholic acid is approved.,Deoxycholic acid is a solid.,True
17798,,,,,S-(4-nitrobenzyl)glutathione is experimental.,S-(4-nitrobenzyl)glutathione is a solid.,False
17799,Carbocisteine is a mucolytic that reduces the viscosity of sputum to relieve the symptoms of chronic obstructive pulmonary disorder (COPD) and bronchiectasis through easier expulsion of mucus. Carbocisteine should not be used with antitussives (cough suppressants) or medicines that dry up bronchial secretions as they are functional antagonists. Carbocisteine is produced by alkylation of cysteine with chloroacetic acid. Used to help relieve the symptoms of chronic obstructive pulmonary disorder (COPD) and bronchiectasis.,The molecular weight is 179.19.,Carbocisteine has a topological polar surface area of 100.62.,The log p value of  is -2.61.,Carbocisteine is approved and investigational.,Carbocisteine is a solid.,True
17800,"Canfosfamide is an active agent in chemotherapy-resistant ovarian cancer. Intended for the treatment of various forms of cancer. S-transferase P1-1 (GST P1-1) is an enzyme overexpressed in many human cancer cells. High levels of GST P1-1 are associated with a poor prognosis and resistance to certain chemotherapeutics. The activation of canfosfamide occurs when GST P1-1 splits canfosfamide into two active fragments: a glutathione analog fragment and an active cytotoxic fragment. The cytotoxic fragment reacts with important cell components, including RNA, DNA and proteins, leading to cell death. The glutathione analog fragment of canfosfamide may remain bound to GST P1-1, which may limit the ability of GST P1-1 to inactivate other cancer drugs. ",The molecular weight is 787.46.,Canfosfamide has a topological polar surface area of 225.74.,The log p value of  is -0.2.,Canfosfamide is investigational.,Canfosfamide is a solid.,True
17801,"Ezatiostat is investigated in clinical trials for treating myelodysplastic syndrome. This compound belongs to the peptides. These are compounds containing an amide derived from two or more amino carboxylic acid molecules (the same or different) by formation of a covalent bond from the carbonyl carbon of one to the nitrogen atom of another. This medication is known to target Glutathione S-transferase P. Ezatiostat is a small molecule drug that is an analog inhibitor of glutathione S-transferase P1-1. It acts intracellularly on the MAPK signaling pathway by activating ERK2. Ezatiostat has myelostimulant activity in preclinical rodent models and human bone marrow cultures, and differentiates granulocytes and monocytes in HL60 cells. Ezatiostat is a candidate designed to stimulate the formation of bone marrow cells that are precursors to granulocytes and monocytes (white blood cells), erythrocytes (red blood cells) and platelets. Many conditions are characterized by depleted bone marrow, including myelodysplastic syndrome (MDS), a form of pre-leukemia in which the bone marrow produces insufficient levels of one or more of the 3 major blood elements (white blood cells, red blood cells and platelets). It might also be relevant as an adjunct therapy since a reduction in blood cell levels is also a common, toxic effect of many standard chemotherapeutic drugs. Investigated for use/treatment in myelodysplastic syndrome.",,,,Ezatiostat is investigational.,Ezatiostat is a solid.,True
17802,,,,,S-NONYL-CYSTEINE is experimental.,S-NONYL-CYSTEINE is a solid.,False
17803,,,,,S-(4-BROMOBENZYL)CYSTEINE is experimental.,S-(4-BROMOBENZYL)CYSTEINE is a solid.,False
17804,Dinitrochlorobenzene has been used in trials studying the treatment of HIV Infections.,,,,Dinitrochlorobenzene is investigational.,,True
17805,"Dichloroacetic acid, often abbreviated DCA, is an acid analogue of acetic acid in which two of the three hydrogen atoms of the methyl group have been replaced by chlorine atoms. Salts of DCA are used as drugs since they inhibit the enzyme pyruvate dehydrogenase kinase. Early reports of its activity against brain cancer cells led patients to treat themselves with DCA, which is commercially available in non-pharmaceutical grade. A phase 1 study in 5 patients concluded that DCA was safe, but wasn't designed to establish effectiveness.",,,,Dichloroacetic acid is approved and investigational.,Dichloroacetic acid is a liquid.,True
17806,,,,,(6R)-Folinic acid is experimental.,(6R)-Folinic acid is a solid.,False
17807,,,,,(S)-alpha-methyl-4-carboxyphenylglycine is experimental.,(S)-alpha-methyl-4-carboxyphenylglycine is a solid.,False
17808,,,,,Domoic Acid is experimental.,Domoic Acid is a solid.,False
17809,"Quisqualic acid is an agonist at two subsets of excitatory amino acid receptors, ionotropic receptors that directly control membrane channels and metabotropic receptors that indirectly mediate calcium mobilization from intracellular stores. The compound is obtained from the seeds and fruit of _Quisqualis chinensis_.",,,,Quisqualic acid is experimental.,Quisqualic acid is a solid.,True
17810,,,,,"2s,4r-4-Methylglutamate is experimental.","2s,4r-4-Methylglutamate is a solid.",False
17811,,,,,(S)-DES-ME-AMPA is experimental.,(S)-DES-ME-AMPA is a solid.,False
17812,AMPA is a specific agonist for the AMPA receptor.,,,,(S)-AMPA is experimental.,(S)-AMPA is a solid.,True
17813,,,,,2-Amino-3-(5-Tert-Butyl-3-(Phosphonomethoxy)-4-Isoxazolyl)Propionic Acid is experimental.,2-Amino-3-(5-Tert-Butyl-3-(Phosphonomethoxy)-4-Isoxazolyl)Propionic Acid is a solid.,False
17814,,,,,Iodo-Willardiine is experimental.,Iodo-Willardiine is a solid.,False
17815,,,,,Fluoro-Willardiine is experimental.,Fluoro-Willardiine is a solid.,False
17816,,,,,"(S)-2-Amino-3-(1,3,5,7-Pentahydro-2,4-Dioxo-CyclopentaPyrimidin-1-Yl) Proionic Acid is experimental.","(S)-2-Amino-3-(1,3,5,7-Pentahydro-2,4-Dioxo-CyclopentaPyrimidin-1-Yl) Proionic Acid is a solid.",False
17817,,,,,(2S)-2-Ammonio-3-propanoate is experimental.,(2S)-2-Ammonio-3-propanoate is a solid.,False
17818,,,,,FG-9041 is experimental.,FG-9041 is a solid.,False
17819,,,,,Bromo-Willardiine is experimental.,Bromo-Willardiine is a solid.,False
17820,Willardiine is a compound isolated from seeds of _Acacia willariana_.,,,,Willardiine is experimental.,Willardiine is a solid.,True
17821,,,,,"2-Amino-3-(3-Hydroxy-7,8-Dihydro-6h-Cyclohepta-4-Isoxazolyl)Propionic Acid is experimental.","2-Amino-3-(3-Hydroxy-7,8-Dihydro-6h-Cyclohepta-4-Isoxazolyl)Propionic Acid is a solid.",False
17822,,,,,THIO-ATPA is experimental.,THIO-ATPA is a solid.,False
17823,,,,,"N,N'-dimethanesulfonamide is experimental.","N,N'-dimethanesulfonamide is a solid.",False
17824,,,,,"2,3,6A,7,8,9-HEXAHYDRO-11H-DIOXINOPYRROLOBENZOXAZIN-11-ONE is experimental.","2,3,6A,7,8,9-HEXAHYDRO-11H-DIOXINOPYRROLOBENZOXAZIN-11-ONE is a solid.",False
17825,,,,,"(3S)-3-cyclopentyl-6-methyl-7--3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide is experimental.","(3S)-3-cyclopentyl-6-methyl-7--3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide is a solid.",False
17826,,,,,"(3R)-3-cyclopentyl-7--3,4-dihydro-2H-1,2-benzothiazine 1,1-dioxide is experimental.","(3R)-3-cyclopentyl-7--3,4-dihydro-2H-1,2-benzothiazine 1,1-dioxide is a solid.",False
17827,,,,,"(3R)-3-cyclopentyl-6-methyl-7--3,4-dihydro-2H-1,2-benzothiazine 1,1-dioxide is experimental.","(3R)-3-cyclopentyl-6-methyl-7--3,4-dihydro-2H-1,2-benzothiazine 1,1-dioxide is a solid.",False
17828,"Lithium was used during the 19th century to treat gout. Lithium salts such as lithium carbonate (Li2CO3), lithium citrate, and lithium orotate are mood stabilizers. They are used in the treatment of bipolar disorder, since unlike most other mood altering drugs, they counteract both mania and depression. Lithium can also be used to augment other antidepressant drugs. It is also sometimes prescribed as a preventive treatment for migraine disease and cluster headaches. The active principle in these salts is the lithium ion Li+, which having a smaller diameter, can easily displace K+ and Na+ and even Ca+2, in spite of its greater charge, occupying their sites in several critical neuronal enzymes and neurotransmitter receptors. Lithium, in its salt forms, is used as a mood stabilizer and for the treatment of depression and mania. It is most frequently prescribed in the treatment of bipolar disorder. Although lithium has been used for over 50 years in treatment of bipolar disorder, the mechanism of action is still unknown. Lithium's therapeutic action may be due to a number of effects, ranging from inhibition of enzymes such as glycogen synthase kinase 3, inositol phosphatases, or modulation of glutamate receptors.  The precise mechanism of action of Li+ as a mood-stabilizing agent is currently unknown. It is possible that Li+ produces its effects by interacting with the transport of monovalent or divalent cations in neurons. An increasing number of scientists have come to the conclusion that the excitatory neurotransmitter glutamate is the key factor in understanding how lithium works. Lithium has been shown to change the inward and outward currents of glutamate receptors (especially GluR3), without a shift in reversal potential. Lithium has been found to exert a dual effect on glutamate receptors, acting to keep the amount of glutamate active between cells at a stable, healthy level, neither too much nor too little. It is postulated that too much glutamate in the space between neurons causes mania, and too little, depression. Another mechanism by which lithium might help to regulate mood include the non-competitive inhibition of an enzyme called inositol monophosphatase. Alternately lithium's action may be enhanced through the deactivation of the GSK-3B enzyme. The regulation of GSK-3B by lithium may affect the circadian clock. GSK-3 is known for phosphorylating and thus inactivating glycogen synthase. GSK-3B has also been implicated in the control of cellular response to damaged DNA. GSK-3 normally phosphorylates beta catenin, which leads to beta catenin degratation. When GSK-3 is inhibited, beta catenin increases and transgenic mice with overexpression of beta catenin express similar behaviour to mice treated with lithium. These results suggest that increase of beta catenin may be a possible pathway for the therapeutic action of lithium. ",,,,Lithium cation is experimental.,Lithium cation is a solid.,True
17829,"Lithium is used as a mood stabilizer, and is used for treatment of depression and mania. It is often used in bipolar disorder treatment. Although lithium has been used for over 50 years in treatment of bipolar disorder, the mechanism of action is still unknown. Lithium's therapeutic action may be due to a number of effects, ranging from inhibition of enzymes such as glycogen synthase kinase 3, inositol phosphatases, or modulation of glutamate receptors.  The precise mechanism of action of Li+ as a mood-stabilizing agent is currently unknown. It is possible that Li+ produces its effects by interacting with the transport of monovalent or divalent cations in neurons. An increasing number of scientists have come to the conclusion that the excitatory neurotransmitter glutamate is the key factor in understanding how lithium works. Lithium has been shown to change the inward and outward currents of glutamate receptors (especially GluR3), without a shift in reversal potential. Lithium has been found to exert a dual effect on glutamate receptors, acting to keep the amount of glutamate active between cells at a stable, healthy level, neither too much nor too little. It is postulated that too much glutamate in the space between neurons causes mania, and too little, depression. Another mechanism by which lithium might help to regulate mood include the non-competitive inhibition of an enzyme called inositol monophosphatase. Alternately lithium's action may be enhanced through the deactivation of the GSK-3B enzyme. The regulation of GSK-3B by lithium may affect the circadian clock. GSK-3 is known for phosphorylating and thus inactivating glycogen synthase. GSK-3B has also been implicated in the control of cellular response to damaged DNA. GSK-3 normally phosphorylates beta catenin, which leads to beta catenin degratation. When GSK-3 is inhibited, beta catenin increases and transgenic mice with overexpression of beta catenin express similar behaviour to mice treated with lithium. These results suggest that increase of beta catenin may be a possible pathway for the therapeutic action of lithium. ",The molecular weight is 209.92.,Lithium citrate has a topological polar surface area of 140.62.,,Lithium citrate is approved.,,True
17830,,,,,Lithium succinate is experimental.,,False
17831,"Lithium has been used to treat manic episodes since the 19th century. Though it is widely used, its mechanism of action is still unknown. Lithium carbonate has a narrow therapeutic range and so careful monitoring is required to avoid adverse effects. Lithium is used as a mood stabilizer, and is indicated for the treatment of manic episodes and maintenance of bipolar disorder. Lithium's mechanism of action is still unknown. Lithium's therapeutic action may be due to a number of effects, ranging from inhibition of enzymes such as glycogen synthase kinase 3, inositol phosphatases, or modulation of glutamate receptors. Lithium's mechanism of action is still unknown. However, the “inositol depletion theory” suggests 3 main potential targets. These targets are inositol monophosphatase, inositol polyphosphatase, and glycogen synthase kinase 3(GSK-3).",The molecular weight is 73.89.,Lithium carbonate has a topological polar surface area of 63.19.,,Lithium carbonate is approved.,,True
17832,"An inhibitor of alpha glucosidase that retards the digestion and absorption of carbohydrates in the small intestine and hence reduces the increase in blood-glucose concentrations after a carbohydrate load. It is given orally to non-insulin dependent diabetes mellitus patients where diet modification or oral hypoglycemic agents do not control their condition. (From Martindale The Extra Pharmacopoeia, 31st ed) For treatment and management of diabetes type II (used in combination therapy as a second or third line agent) Used to reduce blood gluose in patients with type 2 diabetes. Acarbose is a complex oligosaccharide that delays the digestion of ingested carbohydrates, thereby resulting in a smaller rise in blood glucose concentration following meals. Acarbose binds to and inhibits alpha amylase and alpha-gluocside hydrolases. In diabetic patients, this enzyme inhibition results in a delayed glucose absorption and a lowering of postprandial hyperglycemia. Acarbose reversibly bind to pancreatic alpha-amylase and membrane-bound intestinal alpha-glucoside hydrolases. These enzymes inhibit hydrolysis of complex starches to oligosaccharides in the lumen of the small intestine and hydrolysis of oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the brush border of the small intestine.",The molecular weight is 645.61.,Acarbose has a topological polar surface area of 321.17.,The log p value of  is -6.66.,Acarbose is approved and investigational.,Acarbose is a solid.,True
17833,"Voglibose is an alpha-glucosidase inhibitor used for lowering post-prandial blood glucose levels in people with diabetes mellitus. It is made in India by Ranbaxy Labs and sold under the trade name Volix. For the treatment of diabetes. It is specifically used for lowering post-prandial blood glucose levels thereby reducing the risk of macrovascular complications. Voglibose, an alpha-glucosidase inhibitor, is a synthetic compound with potent and enduring therapeutic efficacies against disorders of sensory, motor and autonomic nerve systems due to diabetes mellitus. The drug was approved in Japan in 1994 for the treatment of diabetes, and it is under further investigation by Takeda for the treatment of impaired glucose tolerance. Alpha-glucosidase inhibitors are oral anti-diabetic drugs used for diabetes mellitus type 2 that work by preventing the digestion of complex carbohydrates (such as starch). Complex carbohydrates are normally converted into simple sugars (monosaccharides) which can be absorbed through the intestine. Hence, alpha-glucosidase inhibitors reduce the impact of complex carbohydrates on blood sugar. Alpha-glucosidase inhibitors are saccharides that act as competitive inhibitors of enzymes needed to digest carbohydrates: specifically alpha-glucosidase enzymes in the brush border of the small intestines. The membrane-bound intestinal alpha-glucosidases hydrolyze oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the small intestine. Acarbose also blocks pancreatic alpha-amylase in addition to inhibiting membrane-bound alpha-glucosidases. Pancreatic alpha-amylase hydrolyzes complex starches to oligosaccharides in the lumen of the small intestine. Inhibition of these enzyme systems reduces the rate of digestion of complex carbohydrates. Less glucose is absorbed because the carbohydrates are not broken down into glucose molecules. In diabetic patients, the short-term effect of these drugs therapies is to decrease current blood glucose levels: the long term effect is a small reduction in hemoglobin-A1c level. (From Drug Therapy in Nursing, 2nd ed)",The molecular weight is 267.28.,Voglibose has a topological polar surface area of 153.64.,The log p value of  is -0.93.,Voglibose is investigational.,Voglibose is a solid.,True
17834,RU84687 is a subnanomolar and Src SH2 selective binder.,,,,RU84687 is experimental.,RU84687 is a solid.,True
17835,,,,,RU79256 is experimental.,RU79256 is a solid.,False
17836,,,,,N6-Benzyl Adenosine-5'-Diphosphate is experimental.,N6-Benzyl Adenosine-5'-Diphosphate is a solid.,False
17837,,,,,RU85493 is experimental.,RU85493 is a solid.,False
17838,,,,,RU78262 is experimental.,RU78262 is a solid.,False
17839,,,,,Malonic acid is experimental.,Malonic acid is a solid.,False
17840,,,,,RU83876 is experimental.,RU83876 is a solid.,False
17841,,,,,RU90395 is experimental.,RU90395 is a solid.,False
17842,,,,,RU79072 is experimental.,RU79072 is a solid.,False
17843,,,,,RU78783 is experimental.,RU78783 is a solid.,False
17844,,,,,1-Tert-Butyl-3-(4-Chloro-Phenyl)-1h-PyrazoloPyrimidin-4-Ylamine is experimental.,1-Tert-Butyl-3-(4-Chloro-Phenyl)-1h-PyrazoloPyrimidin-4-Ylamine is a solid.,False
17845,,,,,PASBN is experimental.,PASBN is a solid.,False
17846,,,,,2-azepan-3-yl]amino]prop-1-enyl]-2-formylphenyl]acetic acid is experimental.,2-azepan-3-yl]amino]prop-1-enyl]-2-formylphenyl]acetic acid is a solid.,False
17847,,,,,PAS219 is experimental.,PAS219 is a solid.,False
17848,,,,,DPI59 is experimental.,DPI59 is a solid.,False
17849,,,,,RU82197 is experimental.,RU82197 is a solid.,False
17850,,,,,Phenylphosphate is experimental.,Phenylphosphate is a solid.,False
17851,,,,,RU78300 is experimental.,RU78300 is a solid.,False
17852,,,,,RU79073 is experimental.,RU79073 is a solid.,False
17853,,,,,RU82209 is experimental.,RU82209 is a solid.,False
17854,,,,,ISO24 is experimental.,ISO24 is a solid.,False
17855,,,,,RU85053 is experimental.,RU85053 is a solid.,False
17856,,,,,RU78299 is experimental.,RU78299 is a solid.,False
17857,A strong dicarboxylic acid occurring in many plants and vegetables. It is produced in the body by metabolism of glyoxylic acid or ascorbic acid. It is not metabolized but excreted in the urine. It is used as an analytical reagent and general reducing agent. ,,,,Oxalic Acid is experimental.,Oxalic Acid is a solid.,True
17858,,,,,RU78191 is experimental.,RU78191 is a solid.,False
17859,,,,,Paratoulene phosphate is experimental.,Paratoulene phosphate is a solid.,False
17860,,,,,4--N-AMINO]PHENYL]-BENZAMIDE is experimental.,4--N-AMINO]PHENYL]-BENZAMIDE is a solid.,False
17861,,,,,Purvalanol A is experimental.,Purvalanol A is a solid.,False
17862,,,,,1--3-naphthalen-1-ylurea is experimental.,1--3-naphthalen-1-ylurea is a solid.,False
17863,,,,,1--3-phenylurea is experimental.,1--3-phenylurea is a solid.,False
17864,,,,,3-PYRIMIDIN-3-YL]PHENOL is experimental.,3-PYRIMIDIN-3-YL]PHENOL is a solid.,False
17865,,,,,quinazolin-2-yl}amino)phenyl]acetonitrile is experimental.,quinazolin-2-yl}amino)phenyl]acetonitrile is a solid.,False
17866,,,,,PP-121 is experimental.,PP-121 is a solid.,False
17867,,,,,"1-cyclobutyl-3-(3,4-dimethoxyphenyl)-1H-pyrazolopyrimidin-4-amine is experimental.","1-cyclobutyl-3-(3,4-dimethoxyphenyl)-1H-pyrazolopyrimidin-4-amine is a solid.",False
17868,,,,,1-(1-methylethyl)-3-quinolin-6-yl-1H-pyrazolopyrimidin-4-amine is experimental.,1-(1-methylethyl)-3-quinolin-6-yl-1H-pyrazolopyrimidin-4-amine is a solid.,False
17869,,,,,2-(4-CARCOXY-5-ISOPROPYLTHIAZOLYL)BENZOPIPERIDINE is experimental.,2-(4-CARCOXY-5-ISOPROPYLTHIAZOLYL)BENZOPIPERIDINE is a solid.,False
17870,,,,,N-(4-PHENYLAMINO-QUINAZOLIN-6-YL)-ACRYLAMIDE is experimental.,N-(4-PHENYLAMINO-QUINAZOLIN-6-YL)-ACRYLAMIDE is a solid.,False
17871,,,,,(2E)-N-{4-quinazolin-6-yl}-4-(dimethylamino)but-2-enamide is experimental.,(2E)-N-{4-quinazolin-6-yl}-4-(dimethylamino)but-2-enamide is a solid.,False
17872,Triethylene glycol dimethyl ether (also called triglyme) is a glycol ether used as a solvent.,,,,Triglyme is experimental.,Triglyme is a solid.,True
17873,,,,,AP-22408 is experimental.,AP-22408 is a solid.,False
17874,,,,,{4-ethyl}amino)-3-oxopropyl]-2-phosphonophenoxy}acetic acid is experimental.,{4-ethyl}amino)-3-oxopropyl]-2-phosphonophenoxy}acetic acid is a solid.,False
17875,,,,,3-(2-AMINOQUINAZOLIN-6-YL)-4-METHYL-N-BENZAMIDE is experimental.,3-(2-AMINOQUINAZOLIN-6-YL)-4-METHYL-N-BENZAMIDE is a solid.,False
17876,,,,,"2,3-DIPHENYL-N-(2-PIPERAZIN-1-YLETHYL)FUROPYRIDIN-4-AMINE is experimental.","2,3-DIPHENYL-N-(2-PIPERAZIN-1-YLETHYL)FUROPYRIDIN-4-AMINE is a solid.",False
17877,,,,,"5,6-DIPHENYL-N-(2-PIPERAZIN-1-YLETHYL)FUROPYRIMIDIN-4-AMINE is experimental.","5,6-DIPHENYL-N-(2-PIPERAZIN-1-YLETHYL)FUROPYRIMIDIN-4-AMINE is a solid.",False
17878,,,,,N-(2-chlorophenyl)-5-phenylimidazopyrazin-8-amine is experimental.,N-(2-chlorophenyl)-5-phenylimidazopyrazin-8-amine is a solid.,False
17879,,,,,"N-(2,6-dimethylphenyl)-5-phenylimidazopyrazin-8-amine is experimental.","N-(2,6-dimethylphenyl)-5-phenylimidazopyrazin-8-amine is a solid.",False
17880,,,,,N-(2-chloro-6-methylphenyl)-8-imidazoquinoxalin-4-amine is experimental.,N-(2-chloro-6-methylphenyl)-8-imidazoquinoxalin-4-amine is a solid.,False
17881,"Carbetocin is a drug used to control postpartum hemorrhage, bleeding after giving birth. It is an analogue of oxytocin, and its action is similar to that of oxytocin -- it causes contraction of the uterus. Used to control postpartum hemorrhage and bleeding after giving birth. Carbetocin is a drug used to control postpartum hemorrhage, bleeding after giving birth. It is sold under the trade name Duratocin. It is an analogue of oxytocin, and its action is similar to that of oxytocin; it causes contraction of the uterus. Carbetocin binds to oxytocin receptors present on the smooth musculature of the uterus, resulting in rhythmic contractions of the uterus, increased frequency of existing contractions, and increased uterine tone. The oxytocin receptor content of the uterus is very low in the non-pregnant state, and increases during pregnancy, reaching a peak at the time of delivery.",The molecular weight is 988.17.,Carbetocin has a topological polar surface area of 362.51.,The log p value of  is 0.11.,Carbetocin is approved and investigational.,Carbetocin is a solid.,True
17882,,,,,S-(D-Carboxybutyl)-L-Homocysteine is experimental.,S-(D-Carboxybutyl)-L-Homocysteine is a solid.,False
17883,"Abatacept is a soluble fusion protein, which links the extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) to the modified Fc (hinge, CH2, and CH3 domains) portion of human immunoglobulin G1 (IgG1). Structurally, abatacept is a glycosylated fusion protein with a MALDI-MS molecular weight of 92,300 Da and it is a homodimer of two homologous polypeptide chains of 357 amino acids each. It is produced through recombinant DNA technology in mammalian CHO cells. The drug has activity as a selective co-stimulation modulator with inhibitory activity on T lymphocytes. Although approved for the treatment of rheumatoid arthritis, Repligen has entered a slightly different formulation of CTLA4-Ig into clinical trials (RG2077). For the management of the signs and symptoms of moderate-to-severe active rheumatoid arthritis, inducing major clinical response, slowing the progression of structural damage, and improving physical function in adult patients. It is indicated both as a monotherapy and for use in combination with a continued regimen of DMARDs (not including TNF antagonists). Also used for the management of the signs and symptoms of moderately to severely active polyarticular juvenile idiopathic arthritis in children. Abatacept is the first in a new class of drugs known as Selective Co-stimulation Modulators. Known as a recombinant fusion protein, the drug consists of the extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) linked to a modified Fc portion of human immunoglobulin G<sub>1</sub> (IgG<sub>1</sub>. The Fc portion of the drug consists of the hinge region, the C<sub>H</sub>2 domain, and the C<sub>H</sub>3 domain of IgG<sub>1</sub>. Although there are multiple pathways and cell types involved in the pathogenesis of rheumatoid arthritis, evidence suggests that T-cell activation may play an important role in the immunopathology of the disease. Ordinarily, full T-cell activation requires binding of the T-cell receptor to an antigen-MHC complex on the antigen-presenting cell as well as a co-stimulatory signal provided by the binding of the CD28 protein on the surface of the T-cell with the CD80/86 proteins on the surface of the antigen-presenting cell. CTLA4 is a naturally occurring protein which is expressed on the surface of T-cells some hours or days after full T-cell activation and is capable of binding to CD80/86 on antigen-presenting cells with much greater affinity than CD28. Binding of CTLA4-Ig to CD80/86 provides a negative feedback mechanism which results in T-cell deactivation. Abatacept was developed by Bristol-Myers-Squibb and is licensed in the US for the treatment of Rheumatoid Arthritis in the case of inadequate response to anti-TNF-alpha therapy. Abatacept is a selective costimulation modulator, like CTLA-4, the drug has shown to inhibit T-cell (T lymphocyte) activation by binding to CD80 and CD86, thereby blocking interaction with CD28. Blockade of this interaction has been shown to inhibit the delivery of the second co-stimulatory signal required for optimal activation of T-cells. This results in the inhibition of autoimmune T-Cell activation that has been implcated in the pathogenesis of rheumatoid arthritis.",,,,Abatacept is approved.,Abatacept is a liquid.,True
17884,"Belatacept is a soluble fusion protein, which links the extracellular domain of human cytotoxic T-lymphocyte-associated antigen 4 (CTLA-4) to the modified Fc (hinge, CH2, and CH3 domains) portion of human immunoglobulin G1 (IgG1). Structurally, abatacept is a glycosylated fusion protein with a MALDI-MS molecular weight of 92,300 Da and it is a homodimer of two homologous polypeptide chains of 357 amino acids each. It is produced through recombinant DNA technology in mammalian CHO cells. The drug has activity as a selective co-stimulation modulator with inhibitory activity on T lymphocytes. It is approved for the treatment of rheumatoid arthritis. Belatacept selectively blocks the process of T-cell activation. It was developed by Bristol-Myers-Squibb. Belatacept is only 2 amino acids different from abatacept (Orencia). FDA approved on June 15, 2011. For prophylaxis of organ rejection. It is also used concomitantly with basiliximumab for induction therapy, mycophenolate, and corticosteriods in kidney transplant recepients that are seropositive for the Epstein-Barr virus.  Belatacept binds to CD86 with a 4-fold higher affinity than abatacept. It also binds to CD80 with a 2-fold higher affinity than abatacept. It was observed in non-human primates that belatacept prolongs graft survival due to a decrease in antibody production against the donor organ. Furthermore, belatacept also inhibits the primary humoral immune response which is indicated by the decrease in post-transplant levels of IgG, IgM, and IgA. The magnitude of this effect is more significant in belatacept than it is in cyclosporine.  Belatacept is a fusion protein in which the Fc portion of human IgG1 is attached onto the extracellular portion of human CTLA-4 (CD152). Belatacept specifically binds to CD80 and CD86 receptors that are found on the antigen-presenting cell (B cells, macrophages, dendritic cells) to block selective T-cell lymphocyte costimulation. CD80 and CD86 would normally act as the ligands to the CD28 receptor T-cells in which this interaction triggers the activation of T lymphocytes. However in the presence of belatacept, because the extracellular CTLA-4 component binds to CD28 with higher affinity than CD80 or CD86, T lymphyocyte anergy, a state of antigen specific tolerance, occurs instead. The T cell is also no longer able to respond to their antigen. ",,,,Belatacept is approved and investigational.,Belatacept is a liquid.,True
17885,"Galiximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. Investigated for use/treatment in lymphoma (non-hodgkin's), psoriasis and psoriatic disorders, bone metastases, multiple myeloma, prostate cancer, and rheumatoid arthritis. Galiximab is a monoclonal antibody that is being studied in the treatment of follicular non-Hodgkin lymphoma. Monoclonal antibodies are made in the laboratory and can locate and bind to cancer cells. Galiximab binds to the protein CD80, which is found on certain normal and cancerous white blood cells. Galiximab, an IgG(1) anti-CD80 antibody, binds to CD80, a costimulatory molecule involved in T-cell activation. Reduction in lesional, activated T cells induces improvement in psoriatic plaques.",,,,Galiximab is investigational.,Galiximab is a liquid.,True
17886,"Tetracosactide (also known as Cosyntropin) is a synthetic peptide that is identical to the 24-amino acid segment (sequence: SYSMEHFRWGKPVGKKRRPVKVYP) at the N-terminal of adrenocorticotropic hormone. ACTH (1-24), a segment similar in all species, contains the biological activity that stimulates production of corticosteroids in the adrenal cortex. Tetracosactide exhibits the same activity as natural ACTH with regard to all its biological activities. The complex results in a product whose absorption in man is effected over a longer period of time as compared to corticotropin. Therefore, therapy may be maintained with less frequent administration. For use as a diagnostic agent in the screening of patients presumed to have adrenocortical insufficiency. Cosyntropin exhibits the full corticosteroidogenic activity of natural ACTH. Various studies have shown that the biologic activity of ACTH resides in the N- terminal portion of the molecule and that the 1-20 amino acid residue is the minimal sequence retaining full activity. Partial or complete loss of activity is noted with progressive shortening of the chain beyond 20 amino acid residue. For example, the decrement from 20 to 19 results in a 70% loss of potency. The pharmacologic profile of Cosyntropin is similar to that of purified natural ACTH. It has been established that 0.25 mg of Cosyntropin will stimulate the adrenal cortex maximally and to the same extent as 25 units of natural ACTH. Cosyntropin has less immunogenic activity than ACTH because the amino acid sequence having most of the antigenic activity of ACTH, i.e., amino acids 25-39, is not present in cosyntropin. The extra-adrenal effects which natural ACTH and Cosyntropin have in common include increased melanotropic activity, increased growth hormone secretion and an adipokinetic effect. These are considered to be without physiological or clinical significance. Cosyntropin combines with a specific receptor in the adrenal cell plasma membrane and, in patients with normal adrenocortical function, stimulates the initial reaction involved in the synthesis of adrenal steroids (including cortisol, cortisone, weak androgenic substances, and a limited quantity of aldosterone) from cholesterol by increasing the quantity of the substrate within the mitochondria. Cosyntropin does not significantly increase plasma cortisol concentration in patients with primary or secondary adrenocortical insufficiency. ",The molecular weight is 2933.49.,Tetracosactide has a topological polar surface area of 1158.72.,The log p value of  is 0.0.,Tetracosactide is approved.,Tetracosactide is a solid.,True
17887,Seractide acetate is the acetate salt of full length human corticotropin.,The molecular weight is 4541.14.,Seractide acetate has a topological polar surface area of 1836.25.,,Seractide acetate is approved.,Seractide acetate is a solid.,True
17888,"Bremelanotide is a 7 amino acid peptide used to treat hypoactive sexual desire disorder in premenopausal women. Bremelanotide does not interact with alcohol. The mechanism by which bremelanotide's action on receptors translates to a clinical effect is still unknown. Bremelanotide is indicated to treat premenopausal women with hypoactive sexual desire disorder that is not due to a medical or psychiatric condition, problems with the relationship, or the effects of a medication or drug. Bremelanotide is a melanocortin receptor agonist injected 45 minutes before anticipated sexual activity. Agonism of the melanocortin receptor MC1R also leads to increased melanin expression. Patients taking bremelanotide may also experience nausea, headache, and vomiting. Bremelanotide is an agonist of many melanocortin receptors which in order of potency are MC1R, MC4R, MC3R, MC5R, and MC2R. The mechanism by which agonism of these receptors translates to an improvement in hypoactive sexual desire disorder is currently unknown, however MC4R receptors are present in many areas of the central nervous system. MC3R and MC4R are found in the hypothalamus and are involved in food intake and energy homeostasis.",,,,Bremelanotide is approved and investigational.,Bremelanotide is a solid.,True
17889,"Varenicline is a prescription medication used to treat smoking addiction. This medication is the first approved nicotinic receptor partial agonist. Specifically, varenicline is a partial agonist of the alpha4/beta2 subtype of the nicotinic acetylcholine receptor. In addition it acts on alpha3/beta4 and weakly on alpha3beta2 and alpha6-containing receptors. A full agonism was displayed on alpha7-receptors. For use as an aid in smoking cessation. Varenicline is a partial nicotinic acetylcholine receptor agonist, designed to partially activate this system while displacing nicotine at its sites of action in the brain. Varenicline is an alpha-4 beta-2 neuronal nicotinic acetylcholine receptor partial agonist. The drug shows high selectivity for this receptor subclass, relative to other nicotinic receptors (>500-fold alpha-3 beta-4, >3500-fold alpha-7, >20,000-fold alpha-1 beta gamma delta) or non-nicotinic receptors and transporters (>2000-fold). The drug competitively inhibits the ability of nicotine to bind to and activate the alpha-4 beta-2 receptor. The drug exerts mild agonistic activity at this site, though at a level much lower than nicotine; it is presumed that this activation eases withdrawal symptoms.",The molecular weight is 211.27.,Varenicline has a topological polar surface area of 37.81.,The log p value of  is 0.9.,Varenicline is approved and investigational.,Varenicline is a solid.,True
17890,"ABT-089 is a neuronal nicotinic acetylcholine receptor agonist that may have therapeutic utility for the treatment of several neurological disorders including Alzheimer, Attention Deficit Hyperactivity Disorder and Schizophrenia/Schizoaffective disorders. In radioligand binding studies, ABT-089 has shown selectivity toward the alpha4beta2 nAChR subtype as compared to the alpha7 and alpha1beta1deltagamma nAChR subtypes. Neuronal nicotinic acetylcholine receptors (nAChRs) modulate the release of several important neurotransmitters, such as acetylcholine and dopamine. Investigated for use/treatment in Alzheimer's disease, Attention Deficit/Hyperactivity Disorder (ADHD), and Schizophrenia and schizoaffective disorders. ABT-089 is a neuronal nicotinic acetylcholine receptor agonist. Neuronal nicotinic acetylcholine receptors (nAChRs) modulate the release of several important neurotransmitters, such as acetylcholine and dopamine. ABT-089 is a neuronal nicotinic acetylcholine receptor agonist. In radioligand binding studies, ABT-089 has shown selectivity toward the alpha4beta2 nAChR subtype as compared to the alpha7 and alpha1beta1deltagamma nAChR subtypes. ",,,,Pozanicline is investigational.,Pozanicline is a solid.,True
17891,"Cytisine is an alkaloid naturally derived from the Fabaceae family of plants including the genera Laburnum and Cytisus. Recent studies have shown it to be a more effective and significantly more affordable smoking cessation treatment than nicotine replacement therapy. Also known as baptitoxine or sophorine, cytisine has been used as a smoking cessation treatment since 1964, and is relatively unknown in regions outside of central and Eastern Europe. Cytisine is a partial nicotinic acetylcholine agonist with a half-life of 4.8 hours. Recent Phase III clinical trials using Tabex (a brand of Cytisine marketed by Sopharma AD) have shown similar efficacy to varenicline, but at a fraction of the cost. Indicated for use in smoking cessation.  Various models have been run where the affinity of nAChR agonists to the receptor subtype are tested to help identify the molecules, groups and steric conformation that are vital to greater affinity. By using a nAChR muscle receptor subtype (α1)2β1δγ model the following results were obtained: Cytisine is a low efficacy partial agonist of ⍺4-β2 nicotinic acetylcholine receptors. These which are believed to be central to the effect of nicotine (NIC) on the reward pathway and facilitate addiction. Cytisine reduces the effects of NIC on dopamine release in the mesolimbic system when given alone, while simultaneously attenuating NIC withdrawal symptoms that accompany cessation attempts.",The molecular weight is 190.25.,Cytisine has a topological polar surface area of 32.34.,The log p value of  is 0.01.,Cytisine is experimental.,Cytisine is a solid.,True
17892,"Rivanicline (TC-2403, RJR-2403, (E)-metanicotine) is a partial agonist at neuronal nicotinic acetylcholine receptors, binding primarily to the α4β2 subtype. It was originally developed as a potential treatment for Alzheimer's disease for its nootropic effects but has also been found to inhibit the production of Interleukin-8. It has subsequently been developed as a potential anti-inflammatory treatment for ulcerative colitis. Rivanicline also has stimulant and analgesic actions which are thought due to increased noradrenaline release. Investigated for use/treatment in ulcerative colitis. Rivanicline is a (E)-metanicotine hemigalactarate. It effectively inhibits TNF- and LPS-induced IL-8 production in different cell types. ",,,,Rivanicline is investigational.,Rivanicline is a solid.,True
17893,"Olaratumab (IMC-3G3) is a fully human IgG1 monoclonal antibody with antitumor activity that selectively binds the external domain of human platelet-derived growth factor receptor (PDGFR)-α with high affinity and blocks ligand binding. It is composed of two heavy chain molecule fragments and 2 light chain fragments. Studies show that the treatment of olaratumab in combination with doxorubicin resulted in significant reduction of cancer cell proliferation and tumor growth. Olaratumab was granted accelerated approval (as Lartruvo) as initial therapy to treat adults with certain types of soft tissue sarcoma (STS) in October, 2016. Olaratumab is indicated, in combination with doxorubicin, for the treatment of adult patients with advanced or mestastatic soft tissue sarcoma (STS) with a histologic subtype for which an anthracycline-containing regimen is appropriate and which is not amenable to curative treatment with radiotherapy or surgery.  It exerts an anti-tumor activity in vivo and in vitro against selected sarcoma cells by inhibiting tumor growth by binding to PDGFR-alpha that is present on several types of cancer on transformed cells and in tumor stroma. Olaratumab antibody binding leads to inhibition of ligand-dependent signaling in PDGFR(alpha)-expressing tumor cells, as well as stromal cells in the tumor microenviroment that are dependent on PDGFR(alpha) signaling. When used in a combination therapy with doxorubicin, olaratumab improves progression-free survival in patients with advanced soft-tissue sarcoma.  Olaratumab blocks ligand-induced tumor cell proliferation, and inhibits receptor autophosphorylation and ligand-induced phosphorylation of the downstream signaling molecules protein kinase B (Akt) and mitogen-activated protein kinase. PDGFR signalling is a type of tyrosine kinase-mediated pathway that normally regulates cell growth, chemotaxis, and mesenchymal stem cell differentiation. It also promotes internalization of PDGFR thus alters the surface levels of PDGFR. ",,,,Olaratumab is approved and investigational.,Olaratumab is a liquid.,True
17894,,,,,5-CYANO-FURAN-2-CARBOXYLIC ACID -AMIDE is experimental.,5-CYANO-FURAN-2-CARBOXYLIC ACID -AMIDE is a solid.,False
17895,,,,,6-CHLORO-3-(3-METHYLISOXAZOL-5-YL)-4-PHENYLQUINOLIN-2(1H)-ONE is experimental.,6-CHLORO-3-(3-METHYLISOXAZOL-5-YL)-4-PHENYLQUINOLIN-2(1H)-ONE is a solid.,False
17896,,,,,2-Amino-3-Methyl-1-Pyrrolidin-1-Yl-Butan-1-One is experimental.,2-Amino-3-Methyl-1-Pyrrolidin-1-Yl-Butan-1-One is a solid.,False
17897,,,,,"5-(Aminomethyl)-6-(2,4-Dichlorophenyl)-2-(3,5-Dimethoxyphenyl)Pyrimidin-4-Amine is experimental.","5-(Aminomethyl)-6-(2,4-Dichlorophenyl)-2-(3,5-Dimethoxyphenyl)Pyrimidin-4-Amine is a solid.",False
17898,,,,,(2s)-Pyrrolidin-2-Ylmethylamine is experimental.,(2s)-Pyrrolidin-2-Ylmethylamine is a solid.,False
17899,,,,,4-Iodo-L-phenylalanine is experimental.,4-Iodo-L-phenylalanine is a solid.,False
17900,,,,,Diisopropylphosphono Group is experimental.,Diisopropylphosphono Group is a solid.,False
17901,,,,,1-(1-phenylcyclopentyl)methylamine is experimental.,1-(1-phenylcyclopentyl)methylamine is a solid.,False
17902,,,,,"(S)-2--1,2,3,4-tetrahydroisoquinoline-3-carboxamide is experimental.","(S)-2--1,2,3,4-tetrahydroisoquinoline-3-carboxamide is a solid.",False
17903,"Vildagliptin, previously identified as LAF237, is a new oral anti-hyperglycemic agent (anti-diabetic drug) of the new dipeptidyl peptidase-4 (DPP-4) inhibitor class of drugs. Vidagliptin subsequently acts by inhibiting the inactivation of glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) by DPP-4. This inhibitory activity ultimately results in a two-fold action where GLP-1 and GIP are present to potentiate the secretion of insulin by beta cells and suppress glucagon secretion by alpha cells in the islets of Langerhans in the pancreas. It is currently in clinical trials in the U.S. and has been shown to reduce hyperglycemia in type 2 diabetes mellitus. While the drug is still not approved for use in the US, it was approved in Feb 2008 by European Medicines Agency for use within the EU and is listed on the Australian PBS with certain restrictions. Used to reduce hyperglycemia in type 2 diabetes mellitus. Vildagliptin belongs to a class of orally active antidiabetic drugs (DPP-IV inhibitors) that appear to have multiple functional benefits beyond simple blood-glucose control. One of these is a potential protective effect on pancreatic beta cells, which deteriorate in diabetes. Vildagliptin appears to be safe, very well tolerated, and efficacious. Following a meal, gut incretin hormones are released. The most important incretin hormones are GLP-1 and glucose-dependent insulinotropic polypeptide (GIP). These hormones, secreted in the human small intestine, are responsible for insulin release due to increased glucose levels. In contrast to agents that promote insulin secretion via glucose-independent mechanisms, GLP-1's dependence on glucose concentration is considered beneficial due to a lower risk of hypoglycemia. GLP-1 also inhibits glucagon secretion and increases beta cell mass by stimulating proliferation and neogenesis. However, the clinical utility of GLP-1 is limited by its short half-life (2 minutes). GLP-1 is rapidly degraded by the proteolytic enzyme DPP-IV. To enhance GLP-1 activity, inhibition of the DPP-IV enzyme is emerging as a novel therapeutic approach in the treatment of diabetes. Administration of vildagliptin enhances GLP-1's ability to produce insulin in response to elevated concentrations of blood glucose, inhibit the release of glucagon following meals, slow the rate of nutrient absorption into the bloodstream, slow the rate of gastric emptying, and reduce food intake. Vildagliptin inhibits dipeptidyl peptidase-4 (DPP-4). This in turn inhibits the inactivation of GLP-1 by DPP-4, allowing GLP-1 to potentiate the secretion of insulin in the beta cells. Dipeptidyl peptidase-4's role in blood glucose regulation is thought to be through degradation of GIP and the degradation of GLP-1.",The molecular weight is 303.41.,Vildagliptin has a topological polar surface area of 76.36.,The log p value of  is 0.73.,Vildagliptin is approved and investigational.,Vildagliptin is a solid.,True
17904,"PSN9301 is an oral small molecule inhibitor of Dipeptidyl Peptidase IV (DP-IV), being developed for the treatment of type 2 diabetes. PSN9301 has a very rapid onset and a relatively short duration of action, and available pre-clinical and clinical data indicate that it may be an ideal product candidate for meal-related dosing. Investigated for use/treatment in diabetes mellitus type 1 and 2. PSN9301 is an oral small molecule inhibitor of Dipeptidyl Peptidase IV (DP-IV), an enzyme involved in the inactivation of the gut hormone glucagon-like peptide-1 (GLP-1). GLP-1 plays an important role in regulating meal-related blood glucose by increasing the amount of insulin secreted in response to meals. PSN9301 increases GLP-1 activity and causes significant lowering of blood glucose levels. The increase in insulin secretion in response to GLP-1 is glucose-dependent, providing a built in safety mechanism against low blood glucose levels (hypoglycaemia) in response to treatment with DP-IV inhibitors.",,,,PSN9301 is investigational.,PSN9301 is a solid.,True
17905,"Investigated for use/treatment in diabetes mellitus type 2. AMG-222 is an orally active, small molecule inhibitor of Dipeptidyl Peptidase IV (DPP-IV). DPP-IV inactivates glucagon-like peptide-1 (GLP-1), an important mediator of blood glucose levels following meals. DPP-IV inhibitors have been clinically shown to provide long term improvement of glucose control without the risk of hypoglycemia, and to improve the function of pancreatic beta cells, the cells responsible for the production of insulin. DPP-IV inhibitors represent a novel approach to the treatment of type II diabetes.",,,,AMG-222 is investigational.,AMG-222 is a solid.,True
17906,"Bisegliptin is a compound for the treatment of type 2 diabetes. It is an orally active, dipeptidyl peptidase-IV (DPPIV) inhibitor which lowers blood glucose levels by blocking the degradation of the hormone GLP-1 thereby stimulating glucose-dependent insulin secretion and lowering blood glucose levels without hypoglycemic effects. Investigated for use/treatment in diabetes mellitus type 2. Bisegliptin is an orally active, dipeptidyl peptidase-IV (DPPIV) inhibitor which lowers blood glucose levels by blocking the degradation of the hormone GLP-1 thereby stimulating glucose-dependent insulin secretion and lowering blood glucose levels without hypoglycemic effects.",,,,Bisegliptin is investigational.,Bisegliptin is a solid.,True
17907,,,,,(1S)-2--1-CYCLOPENTYL-2-OXOETHANAMINE is experimental.,(1S)-2--1-CYCLOPENTYL-2-OXOETHANAMINE is a solid.,False
17908,,,,,"N-(TRANS-4-{(1S,2S)-2-AMINO-3--1-METHYL-3-OXOPROPYL}CYCLOHEXYL)-N-METHYLACETAMIDE is experimental.","N-(TRANS-4-{(1S,2S)-2-AMINO-3--1-METHYL-3-OXOPROPYL}CYCLOHEXYL)-N-METHYLACETAMIDE is a solid.",False
17909,,,,,"(2S,3S)-4-cyclopropyl-3-{(3R,5R)-3--1,2,4-oxadiazolidin-5-yl}-1--1-oxobutan-2-amine is experimental.","(2S,3S)-4-cyclopropyl-3-{(3R,5R)-3--1,2,4-oxadiazolidin-5-yl}-1--1-oxobutan-2-amine is a solid.",False
17910,,,,,"(2S,3S)-3-{3--1,2,4-oxadiazol-5-yl}-1-cyclopentylidene-4-cyclopropyl-1-fluorobutan-2-amine is experimental.","(2S,3S)-3-{3--1,2,4-oxadiazol-5-yl}-1-cyclopentylidene-4-cyclopropyl-1-fluorobutan-2-amine is a solid.",False
17911,,,,,"(3R,4R)-4-(pyrrolidin-1-ylcarbonyl)-1-(quinoxalin-2-ylcarbonyl)pyrrolidin-3-amine is experimental.","(3R,4R)-4-(pyrrolidin-1-ylcarbonyl)-1-(quinoxalin-2-ylcarbonyl)pyrrolidin-3-amine is a solid.",False
17912,,,,,"(7R,8R)-8-(2,4,5-trifluorophenyl)-6,7,8,9-tetrahydroimidazodipyridin-7-amine is experimental.","(7R,8R)-8-(2,4,5-trifluorophenyl)-6,7,8,9-tetrahydroimidazodipyridin-7-amine is a solid.",False
17913,,,,,"(2S,3S)-3-{3--1,2,4-OXADIAZOL-5-YL}-1-OXO-1-PYRROLIDIN-1-YLBUTAN-2-AMINE is experimental.","(2S,3S)-3-{3--1,2,4-OXADIAZOL-5-YL}-1-OXO-1-PYRROLIDIN-1-YLBUTAN-2-AMINE is a solid.",False
17914,,,,,"(1S,2R,5S)-5-TRIAZOLOPYRAZIN-7(8H)-YL]-2-(2,4,5-TRIFLUOROPHENYL)CYCLOHEXANAMINE is experimental.","(1S,2R,5S)-5-TRIAZOLOPYRAZIN-7(8H)-YL]-2-(2,4,5-TRIFLUOROPHENYL)CYCLOHEXANAMINE is a solid.",False
17915,,,,,"(2R)-4-TRIAZOLOPYRAZIN-7(8H)-YL]-4-OXO-1-(2,4,5-TRIFLUOROPHENYL)BUTAN-2-AMINE is experimental.","(2R)-4-TRIAZOLOPYRAZIN-7(8H)-YL]-4-OXO-1-(2,4,5-TRIFLUOROPHENYL)BUTAN-2-AMINE is a solid.",False
17916,,,,,"(2S,3S)-3-AMINO-4-(3,3-DIFLUOROPYRROLIDIN-1-YL)-N,N-DIMETHYL-4-OXO-2-(TRANS-4-TRIAZOLOPYRIDIN-6-YLCYCLOHEXYL)BUTANAMIDE is experimental.","(2S,3S)-3-AMINO-4-(3,3-DIFLUOROPYRROLIDIN-1-YL)-N,N-DIMETHYL-4-OXO-2-(TRANS-4-TRIAZOLOPYRIDIN-6-YLCYCLOHEXYL)BUTANAMIDE is a solid.",False
17917,,,,,"(2S,3S)-3-AMINO-4--N,N-DIMETHYL-4-OXO-2-(TRANS-4-TRIAZOLOPYRIDIN-5-YLCYCLOHEXYL)BUTANAMIDE is experimental.","(2S,3S)-3-AMINO-4--N,N-DIMETHYL-4-OXO-2-(TRANS-4-TRIAZOLOPYRIDIN-5-YLCYCLOHEXYL)BUTANAMIDE is a solid.",False
17918,,,,,"(3R)-4--3-METHYL-1,4-DIAZEPAN-2-ONE is experimental.","(3R)-4--3-METHYL-1,4-DIAZEPAN-2-ONE is a solid.",False
17919,,,,,4'-biphenyl-3-carboxamide is experimental.,4'-biphenyl-3-carboxamide is a solid.,False
17920,,,,,"(2R,3R)-7-(methylsulfonyl)-3-(2,4,5-trifluorophenyl)-1,2,3,4-tetrahydropyridobenzimidazol-2-amine is experimental.","(2R,3R)-7-(methylsulfonyl)-3-(2,4,5-trifluorophenyl)-1,2,3,4-tetrahydropyridobenzimidazol-2-amine is a solid.",False
17921,,,,,7-(aminomethyl)-6-(2-chlorophenyl)-1-methyl-1H-benzimidazole-5-carbonitrile is experimental.,7-(aminomethyl)-6-(2-chlorophenyl)-1-methyl-1H-benzimidazole-5-carbonitrile is a solid.,False
17922,,,,,"4--3-(2,2,2-trifluoroethyl)-1,4-diazepan-2-one is experimental.","4--3-(2,2,2-trifluoroethyl)-1,4-diazepan-2-one is a solid.",False
17923,,,,,METHYL 4-{CARBONYL}PYRROLIDIN-2-YL]METHYL}AMINO)CARBONYL]AMINO}BENZOATE is experimental.,METHYL 4-{CARBONYL}PYRROLIDIN-2-YL]METHYL}AMINO)CARBONYL]AMINO}BENZOATE is a solid.,False
17924,,,,,(1S)-2--1-CYCLOPENTYL-2-OXOETHANAMINE is experimental.,(1S)-2--1-CYCLOPENTYL-2-OXOETHANAMINE is a solid.,False
17925,,,,,1-biphenyl-2-ylmethanamine is experimental.,1-biphenyl-2-ylmethanamine is a solid.,False
17926,,,,,"(1S,3S,5S)-2-{(2S)-2-amino-2-dec-1-yl]acetyl}-2-azabicyclohexane-3-carbonitrile is experimental.","(1S,3S,5S)-2-{(2S)-2-amino-2-dec-1-yl]acetyl}-2-azabicyclohexane-3-carbonitrile is a solid.",False
17927,,,,,(2R)-N--N--L-PROLINAMIDE is experimental.,(2R)-N--N--L-PROLINAMIDE is a solid.,False
17928,,,,,"(3R,4S)-1-{6-PYRIMIDIN-4-YL}-4-(2,4,5-TRIFLUOROPHENYL)PYRROLIDIN-3-AMINE is experimental.","(3R,4S)-1-{6-PYRIMIDIN-4-YL}-4-(2,4,5-TRIFLUOROPHENYL)PYRROLIDIN-3-AMINE is a solid.",False
17929,,,,,N-({(2S)-1-PYRROLIDIN-2-YL}METHYL)BENZAMIDE is experimental.,N-({(2S)-1-PYRROLIDIN-2-YL}METHYL)BENZAMIDE is a solid.,False
17930,,,,,"(4R,5R)-5-AMINO-1--4-(2,4,5-TRIFLUOROPHENYL)PIPERIDIN-2-ONE is experimental.","(4R,5R)-5-AMINO-1--4-(2,4,5-TRIFLUOROPHENYL)PIPERIDIN-2-ONE is a solid.",False
17931,,,,,"(3R,4S)-1-(3,4-DIMETHOXYPHENYL)-3-(3-METHYLPHENYL)PIPERIDIN-4-AMINE is experimental.","(3R,4S)-1-(3,4-DIMETHOXYPHENYL)-3-(3-METHYLPHENYL)PIPERIDIN-4-AMINE is a solid.",False
17932,,,,,1--PYRROLIDINE-2-(S)-CARBONITRILE is experimental.,1--PYRROLIDINE-2-(S)-CARBONITRILE is a solid.,False
17933,ABT-341 is a potent and selective DPP-4 inhibitor with a structure very similar to sitagliptin (in 2D; the 3D structure is significantly different). ,,,,ABT-341 is experimental.,ABT-341 is a solid.,True
17934,,,,,"(2R)-4-(2-BENZOYL-1,2-DIAZEPAN-1-YL)-4-OXO-1-(2,4,5-TRIFLUOROPHENYL)BUTAN-2-AMINE is experimental.","(2R)-4-(2-BENZOYL-1,2-DIAZEPAN-1-YL)-4-OXO-1-(2,4,5-TRIFLUOROPHENYL)BUTAN-2-AMINE is a solid.",False
17935,,,,,"(3R,4R)-1-{6-PYRIMIDIN-4-YL}-4-(2,4,5-TRIFLUOROPHENYL)PIPERIDIN-3-AMINE is experimental.","(3R,4R)-1-{6-PYRIMIDIN-4-YL}-4-(2,4,5-TRIFLUOROPHENYL)PIPERIDIN-3-AMINE is a solid.",False
17936,"Gosogliptin has been used in trials studying the treatment of Renal Insufficiency, Chronic.",,,,Gosogliptin is investigational.,Gosogliptin is a solid.,True
17937,,,,,N-({(2S)-1-pyrrolidin-2-yl}methyl)-3-(methylsulfonyl)benzamide is experimental.,N-({(2S)-1-pyrrolidin-2-yl}methyl)-3-(methylsulfonyl)benzamide is a solid.,False
17938,,,,,"(3R,4S)-1--4-(2,4,5-TRIFLUOROPHENYL)PYRROLIDIN-3-AMINE is experimental.","(3R,4S)-1--4-(2,4,5-TRIFLUOROPHENYL)PYRROLIDIN-3-AMINE is a solid.",False
17939,,,,,"6-(4-{(1S,2S)-2-AMINO-1--3--3-OXOPROPYL}PHENYL)-1H-TRIAZOLOPYRIDIN-4-IUM is experimental.","6-(4-{(1S,2S)-2-AMINO-1--3--3-OXOPROPYL}PHENYL)-1H-TRIAZOLOPYRIDIN-4-IUM is a solid.",False
17940,,,,,"7-BENZYL-1,3-DIMETHYL-8-PIPERAZIN-1-YL-3,7-DIHYDRO-PURINE-2,6-DIONE is experimental.","7-BENZYL-1,3-DIMETHYL-8-PIPERAZIN-1-YL-3,7-DIHYDRO-PURINE-2,6-DIONE is a solid.",False
17941,,,,,2-({2--4-OXOQUINAZOLIN-3(4H)-YL}METHYL)BENZONITRILE is experimental.,2-({2--4-OXOQUINAZOLIN-3(4H)-YL}METHYL)BENZONITRILE is a solid.,False
17942,,,,,4-AMINO}BUTYL]BENZAMIDE is experimental.,4-AMINO}BUTYL]BENZAMIDE is a solid.,False
17943,,,,,"2-({8--1,3-DIMETHYL-2,6-DIOXO-1,2,3,6-TETRAHYDRO-7H-PURIN-7-YL}METHYL)BENZONITRILE is experimental.","2-({8--1,3-DIMETHYL-2,6-DIOXO-1,2,3,6-TETRAHYDRO-7H-PURIN-7-YL}METHYL)BENZONITRILE is a solid.",False
17944,"Dutogliptin has been investigated for the treatment of Diabetes Mellitus, Type II. Dutogliptin is a potent and selective inhibitor of DPP4, a serine protease that has emerged as an important target for the treatment of type 2 diabetes. Inhibiting DPP4 increases the physiological levels of regulatory peptides, such as GLP-1, an important modulator of insulin response and digestion.",,,,Dutogliptin is investigational.,,True
17945,"Eculizumab is a monoclonal antibody that targets complement protein C5. Binding to this protein prevents the activation of a complement terminal complex, which is used to treat a number of autoimmune conditions. Eculizumab is indicated to treat paroxysmal nocturnal hemoglobinuria (PNH) to reduce hemolysis, atypical hemolytic uremic syndrome to inhibit complement-mediated thrombotic microangiopathy, and neuromyelitis optica spectrum disorder (NMOSD). Eculizumab is a monoclonal antibody that prevents the activation of terminal complement in some autoimmune conditions. Eculizumab has a long duration of action. Patients taking this medication should be vaccinated against _Neisseria meningiditis_ as serious meningococcal infections have occurred in the past. Eculizumab is a monoclonal antibody that targets complement protein C5, preventing cleavage to C5a and C5b, and the formation of the terminal complement complex C5b-9. Inhibition of this complex prevents complement mediated intravascular hemolysis in paroxysmal nocturnal hemoglobunuria, complement mediated microangiopathy in atypical hemolytic uremic syndrome, and immune mediated inflammation and damage of the central nervous system in neuromyelitis optica spectrum disorder.",,,,Eculizumab is approved and investigational.,Eculizumab is a liquid.,True
17946,"Ravulizumab is considered a long-acting complement 5 (C5) inhibitor that has been undergoing clinical trials for the treatment of paroxysmal nocturnal haemoglobinuria (PNH) as of 4 February, 2016. A drug similar to ravulizumab (ALXN1210), called eculizumab, is currently approved for the treatment of PNH in 46 countries under the brand name Soliris®. Ravulizumab is considered by Alexion Pharmaceuticals Inc. to be a \next-generation\"" eculizumab molecule. Ravulizumab was subsequently approved by the US FDA in December of 2018 for a variety of beneficial characteristics that make it an advanced, next-generation agent in comparison to eculizumab. In particular, ravulizumab is currently the first and only long-acting C5 complement inhibitor that can be administered every eight weeks for the treatment of adult patients with PNH whereas eculizumab is a bi-weekly treatment. Moreover, virtually all of the phase 3 trial results for ravulizumab have demonstrated the equivalent efficacy and safety established by eculizumab and that patients transition safely and effectively from using eculizumab to ravulizumab. Subsequently, whereas PNH patients may have needed to previously plan their lives rather strictly around the bi-weekly infusion administrations of eculizumab, with ravulizumab such patients can find a more relaxed dosing schedule of only six or seven infusions over an entire year."" Ravulizumab is indicated for the treatment of adult patients with paroxysmal nocturnal hemoglobinuria (PNH). Immediate and complete inhibition of serum-free complement protein C5 (concentration of less than 0.5 mcg/mL) was observed by the end of the first ravulizumab infusion and sustained throughout the entire 26-week treatment period in all patients, both complement-inhibitor naïve and previously treated with eculizumab. Paroxysmal nocturnal hemoglobinuria (PNH) is a chronic, progressive, debilitating and life-threatening ultra-rare blood disorder characterized by hemolysis (destruction of red blood cells) that is mediated by the uncontrolled activation of the complement system, a component of the body’s immune system.",,,,Ravulizumab is approved and investigational.,Ravulizumab is a solid.,True
17947,"Idursulfase is a purified form of human iduronate-2-sulfatase, a lysosomal enzyme. Idursulfase is produced by recombinant DNA technology in a human cell line. Idursulfase is an enzyme that hydrolyzes the 2-sulfate esters of terminal iduronate sulfate residues from the glycosaminoglycans dermatan sulfate and heparan sulfate in the lysosomes of various cell types. Idursulfase is a 525-amino acid glycoprotein with a molecular weight of approximately 76 kilodaltons. The enzyme contains eight asparagine-linked glycosylation sites occupied by complex oligosaccharide structures. The enzyme activity of idursulfase is dependent on the post-translational modification of a specific cysteine to formylglycine. For the treatment of Hunter syndrome in adults and children ages 5 and older. Idursulfase is a purified form of the lysosomal enzyme human iduronate-2-sulfatase of recombinant DNA origin. It is designed to replace the natural enzyme, increasing catabolism of certain accumulated glycosaminoglycans (GAG), which abnormally accumulate in multiple tissue types in patients with mucopolysaccharidosis II (MPS-II, or Hunter syndrome). Hunter's Syndrome is an X-linked recessive disease caused by insufficient levels of the lysosomal enzyme iduronate-2-sulfatase. This enzyme cleaves the terminal 2-O-sulfate moieties from the glycosaminoglycans (GAG) dermatan sulfate and heparan sulfate. Due to the missing or defective iduronate-2-sulfatase enzyme in patients with Hunter's Syndrome, GAG progressively accumulate in the lysosomes of a variety of cells, leading to cellular engorgement, organomegaly, tissue destruction and organ system dysfunction. Treatment of Hunter's Syndrome patients with idursulfase provides exogenous enzyme for uptake into cellular lysosomes. Targeting of idursulfase to the lysosome occurs by endocytosis from the cell surface. Mannose-6-phosphate (M6P) residues on the oligosaccharide chains allow specific binding of the enzymes to the M6P receptors on the cell surface, leading to cellular internalization of the enzyme, targeting to intracellular lysosomes and subsequent catabolism of accumulated GAG.",,,,Idursulfase is approved.,Idursulfase is a solid.,True
17948,"Galsufase is a variant form of the polymorphic human enzyme N-acetylgalactosamine 4-sulfatase of recombinant DNA origin. Galsulfase is a glycoprotein with a molecular weight of approximately 56 kD. The recombinant protein is comprised of 495 amino acids and contains six asparagine-linked glycosylation sites, four of which carry a bis mannose-6-phosphate manose7 oligosaccharide for specific cellular recognition. Post-translational modification of Cys53 produces the catalytic amino acid residue Ca-formylglycine, which is required for enzyme activity and is conserved in all members of the sulfatase enzyme family. For the treatment of adults and children with Mucopolysaccharidosis VI. Mucopolysaccharide storage disorders are caused by the deficiency of specific lysosomal enzymes required for the catabolism of GAG. Mucopolysaccharidosis VI (MPS VI, Maroteaux-Lamy syndrome) is characterized by the absence or marked reduction in N-acetylgalactosamine 4-sulfatase. The sulfatase activity deficiency results in the accumulation of the GAG substrate dermatan sulfate, throughout the body. This accumulation leads to widespread cellular, tissue, and organ dysfunction. Galsulfase is intended to provide an exogenous enzyme that will be taken up into lysosomes and increase the catabolism of GAG. Galsulfase uptake by cells into lysosomes is most likely mediated by the binding of mannose-6-phosphate-terminated oligosaccharide chains of galsulfase to specific mannose-6-phosphate receptors. Galsulfase supplies recombinant-engineered galsulfase, a normal variant form of the polymorphic human enzyme, N-acetylgalactosamine 4-sulfatase. It is a lysosomal hydrolase that catalyzes the cleavage of the sulfate ester from terminal N-acetylgalactosamine 4-sulfate residues of GAG chondroitin 4-sulfate and dermatan sulfate. Increased catabolism of GAG in turn reduces systemic dermatan sulfate accumulation, thereby reducing the primary symptoms of MPS VI.",,,,Galsulfase is approved and investigational.,Galsulfase is a solid.,True
17949,"Albiglutide is a glucagon-like peptide-1 agonist (GLP-1) biologic drug indicated in the treatment of type 2 diabetes. It is marketed under the brands Eperzan and Tanzeum by GSK (GlaxoSmithKline). It is a dipeptidyl peptidase-4-resistant glucagon-like peptide-1 dimer fused to human albumin. Albiglutide was approved on April 15, 2014 by the FDA. Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. Albiglutide is an agonist of the GLP-1 (glucagon-like peptide 1) receptor and augments glucose-dependent insulin secretion. Albiglutide also slows gastric emptying. ",The molecular weight is 3284.64.,Albiglutide has a topological polar surface area of 1379.3.,,Albiglutide is approved.,Albiglutide is a solid.,True
17950,"Dulaglutide is a novel glucagon-like peptide-1 agonist (GLP-1) biologic drug consisting of a dipeptidyl peptidase-IV-protected GLP-1 analogue covalently linked to a human IgG4-Fc heavy chain by a small peptide linker. Dulaglutide is indicated in the treatment of type 2 diabetes and can be used once a week. It was approved by the FDA in September 2014. Dulaglutide is manufactured and marketed by Eli Lily under the brand Trulicity™. It is not known if dulaglutide can increase the risk of medullary thyroid carcinoma or multiple endocrine neoplasia syndrome type 2, and is thus not recommended for use in populations with a personal or family history of these conditions. Indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus. Dulaglutide activates human glucagon-like peptide-1 receptors, thus increasing intracellular cyclic AMP in beta cells. This, in turn, increases glucose-dependent insulin release. Dulaglutide also reduces glucagon secretion and slows gastric emptying. Dulaglutide is a human GLP-1 receptor agonist with 90% amino acid sequence homology to endogenous human GLP-1 (7-37). Dulaglutide activates the GLP-1 receptor, a membrane-bound cell-surface receptor coupled to adenylyl cyclase in pancreatic beta cells. Dulaglutide increases intracellular cyclic AMP (cAMP) in beta cells leading to glucose-dependent insulin release. Dulaglutide also decreases glucagon secretion and slows gastric emptying.",,,,Dulaglutide is approved and investigational.,Dulaglutide is a liquid.,True
17951,"Lixisenatide is a glucagon-like peptide-1 (GLP-1) receptor agonist used in the treatment of type 2 diabetes mellitus (T2DM). It is sold under the brand name Adlyxin by Sanofi-Aventis. Adlyxin recieved FDA approval July 28, 2016. For use as an antihyperglycemic agent in the treatment of T2DM. Lixisenatide acts as an agonist at the GLP-1 receptor. In the pancreas, this agonism results in increased glucose-stimulated insulin exocytosis by beta islet cells. This produces a reduction in blood glucose due to increased glucose uptake by tissues. GLP-1 receptor activation in the GI tract results in delayed gastric emptying which is thought to mediate the effects of lixisenatide on postprandial blood glucose. The activation of the GLP-1 receptor by lixisenatide results in the activation of adenylyl cyclase. This increases the concentration of cyclic adenosine monophosphate in the cell leading to the activation of protein kinase A (PKA) as well as Epac1 and Epac2. PKA, Epac1, and Epac2 are involved the in release of Ca2+ from the endoplasmic reticulum which is known as the \amplification\"" pathway which increases insulin release when the triggering pathway is activated. By activating this amplification pathway lixisenatide increases glucose stimulated insulin secretion.""",The molecular weight is 4858.56.,Lixisenatide has a topological polar surface area of 2060.16.,,Lixisenatide is approved.,Lixisenatide is a solid.,True
17952,"ATL1101 is a second-generation antisense drug designed to block the synthesis of the IGF-1 receptor, a protein involved in the regulation of cell overgrowth in psoriasis. ATL1101 is being developed as a cream for the topical treatment of mild to moderate cases of psoriasis. Investigated for use/treatment in psoriasis and psoriatic disorders. ATL1101 is an antisense compound targeting Insulin-like Growth Factor-I Receptor, or IGF-1R. Researchers believe that IGF-1R plays a pivotal role in the regulation of cell growth in psoriasis. Study shows that antisense molecules successfully inhibit production of IGF-1R and normalize the skin architecture in human psoriasis skin samples grafted onto mice.",,,,ATL1101 is investigational.,ATL1101 is a solid.,True
17953,rhIGFBP-3 (recombinant human insulin-like growth factor binding protein-3) is Insmed’s proprietary anti-cancer compound that has demonstrated significant decreases in cancerous growth in several models of human. It is developed by Insmed and is currently under phase I of the clinical trail. Investigated for use/treatment in cancer/tumors (unspecified). rhIGFBP-3 is a protein that is normally found in our bloodstream that has been shown to induce cancer cell death in a variety of experimental systems. Several studies have demonstrated that cancer risk increases with decreasing levels of circulating IGFBP-3. IGFBP-3 can induce cell cycle arrest and enhance the efficacy of chemotherapeutic agents. ,,,,rhIGFBP-3 is investigational.,rhIGFBP-3 is a solid.,True
17954,"An orally bioavailable small molecule inhibitor of the insulin-like growth factor 1 receptor (IGF-1R) with potential antineoplastic activity. IGF-1R inhibitor OSI-906 selectively inhibits IGF-1R, which may result in the inhibition of tumor cell proliferation and the induction of tumor cell apoptosis. Investigated for use/treatment in cancer/tumors (unspecified) and solid tumors. In laboratory studies of 28 human tumor cell lines, OSI-906 reduced growth of 15 cell lines representative of colorectal, lung, breast, pancreatic, and pediatric tumors and in mouse models. OSI-906 was particularly effective against tumors that are highly IGF-dependent such as colorectal cancers. According to the researchers, OSI-906 not only slowed tumor growth in mice, but decreased the size of some pre-existing tumors. IGF-1R stimulates proliferation, enables onogenic transformation, and suppresses apoptosis. Inhibitors of IGF-1R are expected to have broad utility in oncology since the over-expression of IGF-1R and/or its ligands or the down-regulation of ligand binding proteins occurs in numerous human malignancies including lung, colon, breast, prostate, brain and skin cancers. In addition, signaling through the IGF system has been implicated in protecting tumor cells from apoptosis induced by anti-cancer treatments such as cytotoxic agents and EGFR inhibitors.",,,,Linsitinib is investigational.,Linsitinib is a solid.,True
17955,"Teprotumumab is a fully human IgG1 monoclonal antibody directed against the human insulin-like growth factor-1 receptor. Following a clinical trial in which its efficacy in the treatment of thyroid eye disease (TED) was assessed, it received \breakthrough therapy\"" designation from the FDA in 2016 and was approved by the FDA in January 2020 for the treatment of TED. Thyroid eye disease is a potentially debilitating complication of Graves' Disease involving inflammation and tissue remodeling behind the eye, and previous treatment options typically involved multiple invasive surgeries - teprotumumab is the first drug ever approved for the treatment of TED and therefore represents a significant step forward in the treatment this disease."" Teprotumumab is indicated for the treatment of thyroid eye disease. Teprotumumab inhibits the downstream effects of IGF-1R signaling, namely tissue inflammation and remodeling, which are responsible for the various symptoms of thyroid eye disease. Teprotumumab may cause disease flares in patients with pre-existing inflammatory bowel disease (IBD) - patients experiencing an exacerbation should discontinue therapy with teprotumumab. Significant hyperglycemia has been observed in patients receiving treatment with teprotumumab which may require antihyperglycemic medications. Based on its mechanism of action, it is likely that teprotumumab will cause fetal harm in pregnant woman - for this reason, females of child-bearing age should use effective contraception prior to initiation, during therapy, and for 6 months following the last dose of teprotumumab. Graves’ Disease is an autoimmune syndrome involving the thyroid, orbital connective tissues, and some regions of the skin. One manifestation of Graves’ Disease is thyroid-associated ophthalmopathy, or thyroid eye disease, which is characterized by orbital inflammation, tissue remodeling, and fibrosis. As the disease progresses, patients may develop proptosis, strabismus, corneal ulceration, and optic neuropathy. It has been demonstrated that insulin-like growth factor-1 receptors (IGF-1R) are overexpressed by orbital fibroblasts in patients with thyroid eye disease, in addition to being overexpressed on T-cells and B-cells in these patients. It was found that Graves’ Disease IgG molecules could mimic the principal ligand of IGF-1R, insulin-like growth factor-1 (IGF-1), and their binding of IGF-1R induces the expression of chemokines that play roles in tissue remodeling and inflammation. For these reasons, IGF-1R was sought after as a potential therapeutic target for the treatment of thyroid eye disease.",,,,Teprotumumab is approved and investigational.,Teprotumumab is a solid.,True
17956,,,,,"(4Z)-6-bromo-4-({amino}methylidene)isoquinoline-1,3(2H,4H)-dione is experimental.","(4Z)-6-bromo-4-({amino}methylidene)isoquinoline-1,3(2H,4H)-dione is a solid.",False
17957,,,,,3--4-PYRIDIN-2(1H)-ONE is experimental.,3--4-PYRIDIN-2(1H)-ONE is a solid.,False
17958,"Cixutumumab has been used in trials studying the treatment of Lung Cancer, Malignant Neoplasm, Leukemia, Mast-Cell, Non-Small-Cell Lung Carcinoma, and Adenocarcinoma of the Prostate. Cixutumumab is a fully human monoclonal antibody that specifically targets the type 1 human insulin-like growth factor receptor (IGF-IR). Tumors have receptors for the insulin-like growth factor-1 (IGF-I), and it is thought that the presence of these receptors cause tumors to grow. Cixutumumab attaches to the receptors and may inhibit the growth of cancer cells.",,,,Cixutumumab is investigational.,,True
17959,,,,,"1,2,3,4-Tetrahydro-Isoquinoline-7-Sulfonic Acid Amide is experimental.","1,2,3,4-Tetrahydro-Isoquinoline-7-Sulfonic Acid Amide is a solid.",False
17960,,,,,"7-Iodo-1,2,3,4-Tetrahydro-Isoquinoline is experimental.","7-Iodo-1,2,3,4-Tetrahydro-Isoquinoline is a solid.",False
17961,,,,,"8,9-Dichloro-2,3,4,5-Tetrahydro-1h-BenzoAzepine is experimental.","8,9-Dichloro-2,3,4,5-Tetrahydro-1h-BenzoAzepine is a solid.",False
17962,,,,,"CIS-(1R,2S)-2-AMINO-1,2,3,4-TETRAHYDRONAPHTHALEN-1-OL is experimental.","CIS-(1R,2S)-2-AMINO-1,2,3,4-TETRAHYDRONAPHTHALEN-1-OL is a solid.",False
17963,,,,,"(3R)-3-(FLUOROMETHYL)-7-(THIOMORPHOLIN-4-YLSULFONYL)-1,2,3,4-TETRAHYDROISOQUINOLINE is experimental.","(3R)-3-(FLUOROMETHYL)-7-(THIOMORPHOLIN-4-YLSULFONYL)-1,2,3,4-TETRAHYDROISOQUINOLINE is a solid.",False
17964,,,,,"(3R)-N-(4-CHLOROPHENYL)-3-(HYDROXYMETHYL)-1,2,3,4-TETRAHYDROISOQUINOLINE-7-SULFONAMIDE is experimental.","(3R)-N-(4-CHLOROPHENYL)-3-(HYDROXYMETHYL)-1,2,3,4-TETRAHYDROISOQUINOLINE-7-SULFONAMIDE is a solid.",False
17965,,,,,"(3R)-3-(FLUOROMETHYL)-N-(3,3,3-TRIFLUOROPROPYL)-1,2,3,4-TETRAHYDROISOQUINOLINE-7-SULFONAMIDE is experimental.","(3R)-3-(FLUOROMETHYL)-N-(3,3,3-TRIFLUOROPROPYL)-1,2,3,4-TETRAHYDROISOQUINOLINE-7-SULFONAMIDE is a solid.",False
17966,,,,,METHANOL is experimental.,METHANOL is a solid.,False
17967,,,,,"(1S,4R,9S)-5-(trifluoromethyl)-1,2,3,4-tetrahydro-1,4-methanonaphthalen-9-amine is experimental.","(1S,4R,9S)-5-(trifluoromethyl)-1,2,3,4-tetrahydro-1,4-methanonaphthalen-9-amine is a solid.",False
17968,,,,,(1R)-2-amino-1-ethanol is experimental.,(1R)-2-amino-1-ethanol is a solid.,False
17969,Potent reversible inhibitor of phenylethanolamine N-methyltransferase.,,,,"7,8-Dichloro-1,2,3,4-tetrahydroisoquinoline is experimental.","7,8-Dichloro-1,2,3,4-tetrahydroisoquinoline is a solid.",True
17970,,,,,"N-(4-CHLOROPHENYL)-1,2,3,4-TETRAHYDROISOQUINOLINE-7-SULFONAMIDE is experimental.","N-(4-CHLOROPHENYL)-1,2,3,4-TETRAHYDROISOQUINOLINE-7-SULFONAMIDE is a solid.",False
17971,,,,,"TRANS-(1S,2S)-2-AMINO-1,2,3,4-TETRAHYDRONAPHTHALEN-1-OL is experimental.","TRANS-(1S,2S)-2-AMINO-1,2,3,4-TETRAHYDRONAPHTHALEN-1-OL is a solid.",False
17972,,,,,Dihydrogenphosphate is experimental.,Dihydrogenphosphate is a solid.,False
17973,,,,,K-252a is experimental.,K-252a is a solid.,False
17974,,,,,"5-Bromo-N--3,4-difluoro-2-benzamide is experimental.","5-Bromo-N--3,4-difluoro-2-benzamide is a solid.",False
17975,,,,,"(5S)-4,5-difluoro-6--N-(2-hydroxyethoxy)cyclohexa-1,3-diene-1-carboxamide is experimental.","(5S)-4,5-difluoro-6--N-(2-hydroxyethoxy)cyclohexa-1,3-diene-1-carboxamide is a solid.",False
17976,,,,,"2--N-{oxy}-3,4-difluorobenzamide is experimental.","2--N-{oxy}-3,4-difluorobenzamide is a solid.",False
17977,"PD-0325901 has been used in trials studying the treatment and basic science of Melanoma, Solid Tumour, Solid Tumors, Advanced Cancer, and Breast Neoplasms, among others.",,,,PD-0325901 is investigational.,PD-0325901 is a solid.,True
17978,,,,,"N-(5-{3,4-difluoro-2-phenyl}-1,3,4-oxadiazol-2-yl)ethane-1,2-diamine is experimental.","N-(5-{3,4-difluoro-2-phenyl}-1,3,4-oxadiazol-2-yl)ethane-1,2-diamine is a solid.",False
17979,,,,,"2--3,4-DIFLUORO-N-(2-HYDROXYETHOXY)BENZAMIDE is experimental.","2--3,4-DIFLUORO-N-(2-HYDROXYETHOXY)BENZAMIDE is a solid.",False
17980,,,,,4-{amino}-5-(trifluoromethyl)pyrimidin-2-yl]amino}-N-methylbenzenesulfonamide is experimental.,4-{amino}-5-(trifluoromethyl)pyrimidin-2-yl]amino}-N-methylbenzenesulfonamide is a solid.,False
17981,,,,,Phosphorylcolamine is experimental.,Phosphorylcolamine is a solid.,False
17982,,,,,(S)-econazole is experimental.,(S)-econazole is a solid.,False
17983,"AT2220 is an experimental, oral therapy for the treatment of Pompe disease and belongs to a class of molecules known as pharmacological chaperones. It is a small molecule designed to act as a pharmacological chaperone that specifically binds, stabilizes, and facilitates the proper folding and trafficking of α-glucosidase (GAA). GAA to the lysosome, where it can perform its normal function. AT2220 has been shown to increase GAA activity in cell lines derived from Pompe patients and in transfected cells expressing misfolded forms of GAA. Pompe disease, also known as glycogen storage disease type II or acid maltase deficiency, is a relatively rare neuromuscular and lysosomal storage disorder caused by inherited genetic mutations in a key enzyme called α-glucosidase (Gaa). AT2220 is designed to act as a pharmacological chaperone by selectively binding to the misfolded enzyme responsible for Pompe disease, Gaa. After binding to the enzyme, it is thought that AT2220 promotes the proper folding, processing, and trafficking of the enzyme from the endoplasmic reticulum to its final destination, the lysosome, the area of the cell where the enzyme does its work. Once it reaches the lysosome, the pharmacological chaperone is displaced, and the enzyme can perform its normal function, which is the breakdown of its natural substrate, glycogen.",,,,AT2220 is investigational.,AT2220 is a solid.,True
17984,Calcium and magnesium salts used therapeutically in hepatobiliary dysfunction.,,,,"N,N,N-Trimethyl-2-(phosphonooxy)ethanaminium is experimental.","N,N,N-Trimethyl-2-(phosphonooxy)ethanaminium is a solid.",True
17985,,,,,Glycinamide Ribonucleotide is experimental.,Glycinamide Ribonucleotide is a solid.,False
17986,,,,,"N-({4--1-(2,2,2-trifluoro-1,1-dihydroxyethyl)butyl]phenyl}carbonyl)-L-glutamic acid is experimental.","N-({4--1-(2,2,2-trifluoro-1,1-dihydroxyethyl)butyl]phenyl}carbonyl)-L-glutamic acid is a solid.",False
17987,"Calcium chloride is an ionic compound of calcium and chlorine. It is highly soluble in water and it is deliquescent. It is a salt that is solid at room temperature, and it behaves as a typical ionic halide. It has several common applications such as brine for refrigeration plants, ice and dust control on roads, and in cement. It can be produced directly from limestone, but large amounts are also produced as a by-product of the Solvay process. Because of its hygroscopic nature, it must be kept in tightly-sealed containers. For the treatment of hypocalcemia in those conditions requiring a prompt increase in blood plasma calcium levels, for the treatment of magnesium intoxication due to overdosage of magnesium sulfate, and used to combat the deleterious effects of hyperkalemia as measured by electrocardiographic (ECG), pending correction of the increased potassium level in the extracellular fluid. Calcium is the fifth most abundant element in the body and the major fraction is in the bony structure. Calcium plays important physiological roles, many of which are poorly understood. It is essential for the functional integrity of the nervous and muscular systems. It is necessary for normal cardiac function and is one of the factors that operates in the mechanisms involved in the coagulation of blood. Calcium chloride in water dissociates to provide calcium (Ca<sup>2+</sup>) and chloride (Cl<sup>-</sup>) ions. They are normal constituents of the body fluids and are dependent on various physiological mechanisms for maintenance of balance between intake and output. For hyperkalemia, the influx of calcium helps restore the normal gradient between threshold potential and resting membrane potential.",The molecular weight is 110.98.,,,Calcium chloride is approved.,Calcium chloride is a solid.,True
17988,,,,,"Adenosine 3',5'-diphosphate is experimental.","Adenosine 3',5'-diphosphate is a solid.",False
17989,The 5-beta-reduced isomer of androsterone. Etiocholanolone is a major metabolite of testosterone and androstenedione in many mammalian species including humans. It is excreted in the urine. ,,,,Aetiocholanolone is experimental.,Aetiocholanolone is a solid.,True
17990,,The molecular weight is 454.4.,,,Mercuric iodide is experimental.,Mercuric iodide is a solid.,False
17991,"Ipilimumab is a fully humanized IgG1 monoclonal antibody that blocks cytotoxic T lymphocyte antigen-4 (CTLA-4). Blocking CTLA-4 removes an inhibitory signal from reducing the activity of T lymphocytes. Ipilimumab was developed by Bristol-Myers Squibb and Medarex. Ipilimumab is indicated to treat unresectable or metastatic melanoma, as an adjuvant in the treatment of cutaneous melanoma, to treat microsatellite-high or mismatch repair deficient metastatic colorectal cancer, or to treat hepatocellular carcinoma. Ipilimumab with is indicated to treat advanced renal cell carcinoma. Ipilimumab is a human IgG1 that binds CTLA-4, preventing 1 T-cell inhibition signal pathway. It has a long duration of action as it is given every 3 to 4 weeks. Patients should be counselled regarding the risk of immune-mediated adverse effects, infusion related reactions, and embryo-fetal toxicity. Cytotoxic T-lymphocyte antigen-4 (CTLA-4) is an inhibitory molecule that competes with the stimulatory CD28 for binding to B7 on antigen presenting cells. CTLA-4 and CD28 are both presented on the surface of T-cells. Ipilimumab is a human IgG1 that binds CTLA-4, preventing the inhibition of T-cell mediated immune responses to tumors.",,,,Ipilimumab is approved.,Ipilimumab is a liquid.,True
17992,"Tremelimumab is under investigation for the treatment of Mesothelioma, Liver Cancer, Liver Neoplasms, Liver Cell Caricinoma, and HepatoCellular Carcinoma. Tremelimumab has been investigated in Part C: Malignant Mesothelioma and Part A and B: Advanced Solid Malignancies.",,,,Tremelimumab is investigational.,,True
17993,,,,,Indirubin-3'-monoxime is experimental.,Indirubin-3'-monoxime is a solid.,False
17994,,,,,Olomoucine is experimental.,Olomoucine is a solid.,False
17995,,,,,Hymenialdisine is experimental.,Hymenialdisine is a solid.,False
17996,,,,,SU9516 is experimental.,SU9516 is a solid.,False
17997,,,,,Alsterpaullone is experimental.,Alsterpaullone is a solid.,False
17998,,,,,6-PHENYLPYRROLOPYRAZINE is experimental.,6-PHENYLPYRROLOPYRAZINE is a solid.,False
17999,"A fluorinated cytosine analog that is used as an antifungal agent. For the treatment (in combination with amphotericin B) of serious infections caused by susceptible strains of Candida (septicemia, endocarditis and urinary system infections) and/or Cryptococcus (meningitis and pulmonary infections). Flucytosine is an antimetabolite that acts as an antifungal agent with <i>in vitro</i> and <i>in vivo</i> activity against Candida and Cryptococcus. Flucytosine enters the fungal cell via cytosine permease; thus, flucytosine is metabolized to 5-fluorouracil within fungal organisms. The 5-fluorouracil is extensively incorporated into fungal RNA and inhibits synthesis of both DNA and RNA. The result is unbalanced growth and death of the fungal organism. Antifungal synergism between Ancobon and polyene antibiotics, particularly amphotericin B, has been reported. Although the exact mode of action is unknown, it has been proposed that flucytosine acts directly on fungal organisms by competitive inhibition of purine and pyrimidine uptake and indirectly by intracellular metabolism to 5-fluorouracil. Flucytosine enters the fungal cell via cytosine permease; thus, flucytosine is metabolized to 5-fluorouracil within fungal organisms. The 5-fluorouracil is extensively incorporated into fungal RNA and inhibits synthesis of both DNA and RNA. The result is unbalanced growth and death of the fungal organism. It also appears to be an inhibitor of fungal thymidylate synthase.",The molecular weight is 129.09.,Flucytosine has a topological polar surface area of 67.48.,The log p value of  is -1.63.,Flucytosine is approved and investigational.,Flucytosine is a solid.,True
18000,"Palifosfamide (ZIO-201) is a proprietary stabilized metabolite of ifosfamide. Ifosfamide has been shown to be effective in high doses in treating testicular cancer, sarcoma and lymphoma. Investigated for use/treatment in cancer/tumors (unspecified), lymphoma (unspecified), and sarcoma. After metabolic activation, palifosfamide alkylates or binds with many intracellular molecular structures, including nucleic acids. The cytotoxic action is primarily due to cross-linking of strands of DNA and RNA, as well as inhibition of protein synthesis.",,,,Palifosfamide is investigational.,Palifosfamide is a solid.,True
18001,Epigallocatechin gallate has been investigated for the treatment of Hypertension and Diabetic Nephropathy.,,,,Epigallocatechin gallate is investigational.,,True
18002,,,,,2-(2-Hydroxy-5-Methoxy-Phenyl)-1h-Benzoimidazole-5-Carboxamidine is experimental.,2-(2-Hydroxy-5-Methoxy-Phenyl)-1h-Benzoimidazole-5-Carboxamidine is a solid.,False
18003,,,,,6-(N-Phenylcarbamyl)-2-Naphthalenecarboxamidine is experimental.,6-(N-Phenylcarbamyl)-2-Naphthalenecarboxamidine is a solid.,False
18004,,,,,6--2-Naphthalenecarboxamidine is experimental.,6--2-Naphthalenecarboxamidine is a solid.,False
18005,,,,,6--2-Naphthalenecarboxamidine is experimental.,6--2-Naphthalenecarboxamidine is a solid.,False
18006,,,,,CRA_10655 is experimental.,CRA_10655 is a solid.,False
18007,,,,,6--2-Naphthalenecarboxamidine is experimental.,6--2-Naphthalenecarboxamidine is a solid.,False
18008,,,,,6--2-Naphthalenecarboxamidine is experimental.,6--2-Naphthalenecarboxamidine is a solid.,False
18009,,,,,7-Methoxy-8-Naphthalene-2-Carboximidamide is experimental.,7-Methoxy-8-Naphthalene-2-Carboximidamide is a solid.,False
18010,,,,,6--N--4-(Pyrimidin-2-Ylamino)-2-Naphthamide is experimental.,6--N--4-(Pyrimidin-2-Ylamino)-2-Naphthamide is a solid.,False
18011,,,,,Benzamidine is experimental.,Benzamidine is a solid.,False
18012,,,,,Trans-6-(2-Phenylcyclopropyl)-Naphthalene-2-Carboxamidine is experimental.,Trans-6-(2-Phenylcyclopropyl)-Naphthalene-2-Carboxamidine is a solid.,False
18013,,,,,2-Amino-1H-benzimidazol-5-ol is experimental.,2-Amino-1H-benzimidazol-5-ol is a solid.,False
18014,,,,,N-(1-adamantyl)-N'-(4-guanidinobenzyl)urea is experimental.,N-(1-adamantyl)-N'-(4-guanidinobenzyl)urea is a solid.,False
18015,,,,,ThienoPyridine-2-Carboxamidine is experimental.,ThienoPyridine-2-Carboxamidine is a solid.,False
18016,,,,,8-(Pyrimidin-2-Ylamino)Naphthalene-2-Carboximidamide is experimental.,8-(Pyrimidin-2-Ylamino)Naphthalene-2-Carboximidamide is a solid.,False
18017,,,,,]-Piperazine-N'-Beta-Alanine is experimental.,]-Piperazine-N'-Beta-Alanine is a solid.,False
18018,,,,,6-fluoro-2-(2-hydroxy-3-isobutoxy-phenyl)-1H-benzoimidazole-5-carboxamidine is experimental.,6-fluoro-2-(2-hydroxy-3-isobutoxy-phenyl)-1H-benzoimidazole-5-carboxamidine is a solid.,False
18019,,,,,6-FLUORO-2--1H-INDOLE-5-CARBOXAMIDINE is experimental.,6-FLUORO-2--1H-INDOLE-5-CARBOXAMIDINE is a solid.,False
18020,,,,,N-(4-CARBAMIMIDOYL-3-CHORO-PHENYL)-2-HYDROXY-3-IODO-5-METHYL-BENZAMIDE is experimental.,N-(4-CARBAMIMIDOYL-3-CHORO-PHENYL)-2-HYDROXY-3-IODO-5-METHYL-BENZAMIDE is a solid.,False
18021,,,,,6--N--2-NAPHTHAMIDE is experimental.,6--N--2-NAPHTHAMIDE is a solid.,False
18022,,,,,1-guanidine is experimental.,1-guanidine is a solid.,False
18023,,,,,"(2R)-1-(2,6-dimethylphenoxy)propan-2-amine is experimental.","(2R)-1-(2,6-dimethylphenoxy)propan-2-amine is a solid.",False
18024,,,,,"4-(2-aminoethoxy)-N-(2,5-diethoxyphenyl)-3,5-dimethylbenzamide is experimental.","4-(2-aminoethoxy)-N-(2,5-diethoxyphenyl)-3,5-dimethylbenzamide is a solid.",False
18025,,,,,"4-(2-aminoethoxy)-N-(3-chloro-2-ethoxy-5-piperidin-1-ylphenyl)-3,5-dimethylbenzamide is experimental.","4-(2-aminoethoxy)-N-(3-chloro-2-ethoxy-5-piperidin-1-ylphenyl)-3,5-dimethylbenzamide is a solid.",False
18026,,,,,"4-(2-AMINOETHOXY)-3,5-DICHLORO-N-BENZAMIDE is experimental.","4-(2-AMINOETHOXY)-3,5-DICHLORO-N-BENZAMIDE is a solid.",False
18027,,,,,"4-(2-aminoethoxy)-N-(3-chloro-5-piperidin-1-ylphenyl)-3,5-dimethylbenzamide is experimental.","4-(2-aminoethoxy)-N-(3-chloro-5-piperidin-1-ylphenyl)-3,5-dimethylbenzamide is a solid.",False
18028,"Levamisole is an antihelminthic drug that was commonly used for the treatment of parasitic, viral, and bacterial infections. It was manufactured by _Janssen_ and first used in 1969 as an agent to treat worm infestations Levamisole was approved by the FDA in 1990 as an adjuvant treatment for colon cancer. Prior to this, levamisole was used as an antirheumatic therapy in the 1970s and 1980s for patients with rheumatoid arthritis.  For adjuvant treatment in combination with fluorouracil after surgical resection in patients with Dukes' stage C colon cancer. Also used to treat malignant melanoma and head/neck cancer. Levamisole is a synthetic imidazothiazole derivative that has been widely used in treatment of worm infestations in both humans and animals. As an anthelmintic, it probably works by targeting the nematode nicotinergic acetylcholine receptor. As an immunomodulator, it appears that Levamisole is an immunostimulant which has been shown to increase NK cells and activated T-cells in patients receiving this adjuvantly along with 5FU for Stage III colon cancer. The mechanism of action of levamisole as an antiparasitic agent appears to be tied to its agnositic activity towards the L-subtype nicotinic acetylcholine receptors in nematode muscles. This agonistic action reduces the capacity of the males to control their reproductive muscles and limits their ability to copulate. The mechanism of action of Levamisole as an anticancer drug in combination with fluorouracil is unknown. The effects of levamisole on the immune system are complex. The drug appears to restore depressed immune function rather than to stimulate response to above-normal levels. Levamisole can stimulate formation of antibodies to various antigens, enhance T-cell responses by stimulating T-cell activation and proliferation, potentiate monocyte and macrophage functions including phagocytosis and chemotaxis, and increase neutrophil mobility, adherence, and chemotaxis.",The molecular weight is 204.29.,Levamisole has a topological polar surface area of 15.6.,The log p value of  is 1.84.,Levamisole is approved and investigational and vet_approved and withdrawn.,Levamisole is a solid.,True
18029,,,,,Phosphoenolpyruvate is experimental.,Phosphoenolpyruvate is a solid.,False
18030,,,,,1-(2-Fluorobenzyl)-3-Butyl-8-(N-Acetyl-4-Aminobenzyl)-Xanthine is experimental.,1-(2-Fluorobenzyl)-3-Butyl-8-(N-Acetyl-4-Aminobenzyl)-Xanthine is a solid.,False
18031,,,,,1-Allyl-3-Butyl-8-(N-Acetyl-4-Aminobenzyl)-Xanthine is experimental.,1-Allyl-3-Butyl-8-(N-Acetyl-4-Aminobenzyl)-Xanthine is a solid.,False
18032,,,,,5'-Guanylylmethylenebisphosphonate is experimental.,5'-Guanylylmethylenebisphosphonate is a solid.,False
18033,,,,,Adenosine-2'-5'-Diphosphate is experimental.,Adenosine-2'-5'-Diphosphate is a solid.,False
18034,,,,,Oxaloacetate Ion is experimental.,Oxaloacetate Ion is a solid.,False
18035,,,,,N-acetylserotonin is experimental.,N-acetylserotonin is a solid.,False
18036,"Bacitracin is a combination of at least 9 bacitracins. 60-80% of commercially prepared bacitracin is bacitracin A. The bacillus that produces bacitracin was first isolated from a knee scrape in 1945 from the knee wound of a child named Margaret Tracy. Bacitracin is indicated in topical formulations for acute and chronic localized skin infections. Occasionally, it is also used intramuscularly for infantile streptococcal pneumonia and empyema. Bacitracin is also formulated as an ointment with neomycin and polymyxin B for over the counter use. A bacitracin ointment formulated with neomycin and polymyxin B along with hydrocortisone is indicated for the treatment of corticosteroid responsive dermatoses with secondary infection. Bacitracin is a mixture of polypeptides that prevent the formation of the bacterial cell wall and oxidatively cleave DNA. It has a short duration of action as it must be given every 3 to 4 hours topically. Bacitracin is nephrotoxic when given intramuscularly and may lead to renal failure. Bacitracin binds to a divalent metal ion such as Mn(II), Co(II), Ni(II), Cu(II), or Zn(II). These complexes bind C<sub>55</sub>-isoprenyl pyrophosphate, preventing the hydrolysis of a lipid dolichol pyrophosphate, which finally inhibits cell wall synthesis. Bacitracin metal complexes also bind and oxidatively cleave DNA.",The molecular weight is 5648.77.,Bacitracin has a topological polar surface area of 530.87.,,Bacitracin is approved and vet_approved.,Bacitracin is a solid.,True
18037,"Ocriplasmin is a recombinant truncated form of human plasmin with a molecular weight of 27.2 kDa produced by recombinant DNA technology in a Pichia pastoris expression system. Ocriplasmin is a protein made up of 249 amino acids and has two peptide chains. Agent for pharmacologic vitreolysis; thrombolytic agent. FDA approved in October 17, 2012. Ocriplasmin is a proteolytic enzyme indicated for the treatment for symptomatic vitreomacular adhesion.  Ocriplasmin has proteolytic activity against protein components of the vitreous body and the vitreoretinal interface (VRI) (e.g. laminin, fibronectin and collagen), thereby dissolving the protein matrix responsible for the vitreomacular adhesion (VMA).",,,,Ocriplasmin is approved.,Ocriplasmin is a solid.,True
18038,"AMD-070 is a small molecule drug candidate that belongs to a new investigational class of anti-HIV drugs known as entry (fusion) inhibitors. Currently there is only one FDA-approved entry inhibitor, enfuvirtide (Fuzeon), that is available for the treatment of HIV infection. Several experimental entry inhibitors are now in early stage testing, including AMD-070, which targets the CXCR4 receptor on HIV and prevents the virus from entering and infecting healthy cells. Other entry inhibitors target the CCR5 receptor of HIV.These new agents are widely viewed as next generation anti-HIV drugs with the potential to significantly advance HIV therapeutics. Investigated for use/treatment in HIV infection. AMD-070 is a small molecule drug candidate that belongs to a new investigational class of anti-HIV drugs known as entry (fusion) inhibitors. Approximately 76% of HIV-patients with measurable viral load are infected with a strain of virus that is resistant to one or more classes of antiretroviral agents, thus reducing treatment options. Unlike many existing HIV drugs that target the virus after it has infected a healthy cell, AMD-070 blocks the virus from entering a healthy cell, thus preventing the replication process. AMD-070 targets the CXCR4 receptor on HIV and prevents the virus from entering and infecting healthy cells.  Chemokine receptors expressed on the surface of immune cells are known to play a critical role in virus infection and transmission. CXCR4, and another chemokine receptor CCR5, are involved in HIV infection.",,,,AMD-070 is investigational.,AMD-070 is a solid.,True
18039,"CCR5 mAb is a fully human monoclonal antibody that specifically recognizes and binds the chemokine receptor CCR5, which is known to be a key facilitator of infection with human immunodeficiency virus (HIV-1). It was generated by HGS using the Abgenix XenoMouse technology. Investigated for use/treatment in HIV infection. The chemokine receptor CCR5 provides a portal of entry for HIV-1 and serves a target for potential new antiretroviral therapies. CCR5 monoclonal antibodies (mAb) and small-molecule CCR5 antagonists potently block HIV-1 entry in vitro, and controlled clinical trials have provided initial proof-of-concept for this mode of therapy.",,,,CCR5 mAb is investigational.,CCR5 mAb is a solid.,True
18040,"Leronlimab, or PRO-140, is a human monoclonal antibody developed by CytoDyn. It was first described in the literature in 2001. This antibody binds to CCR5, which may be useful in treating HIV, cancers, and severely ill COVID-19 patients. Leronlimab is currently being investigated for the treatment of a number of cancers and HIV. Leronlimab is a humanized monoclonal antibody that binds CCR5 being investigated for it's anti-HIV, immunomodulatory, and anti-cancer effects. CCR5 is a helical protein with multiple extracellular regions with adjacent G proteins. When a chemokine binds CCR5, the Gαβγ trimer phosphorylates GDP to GTP and Gα dissociates. Activated Gα activates adenylate cyclase, and increasing levels of cyclic AMP activate cytosolic protein kinase A. Further downstream effects of CCR5 signalling include activation of NF-κB and IL-6, as well as effects on cell proliferation, migration, and survival.",,,,Leronlimab is investigational.,Leronlimab is a solid.,True
18041,"A spiro-diketo-piperazine; a potent noncompetitive allosteric antagonist of the CCR5 receptor with concomitantly potent antiviral effects for HIV-1. Investigated for use/treatment in HIV infection. GW873140 is a novel CCR5 receptor antagonist that binds specifically to human CCR5. It binds to human CCR5 with a unique profile as evidenced by the selective inhibition of monoclonal antibody binding. One of the many ways in which CCR5 inhibitors differ from the currently available classes of HIV drugs is that they bind to the host (CCR5 receptor), the cell, target rather than to the viral enzymes in cells like the CD4 cell.",,,,Aplaviroc is investigational.,Aplaviroc is a solid.,True
18042,"Ibalizumab (also known as _ibalizumab-uiyk_ and formerly known as TNX-355) is a monoclonal antibody that binds to CD4 receptors on the surface of CD4-positive cells, preventing HIV particle entry into the lymphocytes. It is an advanced and current antibody in development for the treatment of HIV/AIDS. It has been developed by Taimed biologics and Theratechnologies. Indicated for the treatment of human immunodeficiency virus type 1 (HIV-1) infection in highly treatment-experienced adults with multidrug-resistant HIV-1 infection failing their current antiretroviral regimen. Trogarzo safety and effectiveness have been confirmed in a clinical trial of 40 patients who suffer multidrug-resistant HIV. The majority of these patients experienced a substantial decrease in their HIV-RNA levels within 7 days after receiving the drug. Approximately 43 percent of patients continued to experience HIV-RNA inhibition after 24 weeks of taking Trogarzo. Ibalizumab is a monoclonal antibody and viral-entry inhibitor that coats CD4-positive cells, the main target of HIV infection. By blocking viral entry into CD4 cells, ibalizumab creates a barrier for HIV, which is a different mechanism from those of entry inhibitors that target viral proteins or chemokine co-receptors.",,,,Ibalizumab is approved and investigational.,,True
18043,"INCB-9471 is a novel, orally available CCR5 antagonist that is part of a new class of drugs to treat HIV/AIDS. It is a potent, selective inhibitor of the HIV-1 virus. INCB-9471 is an antagonist of CCR5. It works through a different mechanism of action than currently marketed oral antiviral drugs. Rather than fighting HIV inside a patient's white blood cells, it prevents the virus from entering uninfected cells by blocking its predominant entry route, the CCR5 co-receptor.",,,,INCB-9471 is investigational.,,True
18044,"An N-acyl derivative of neuraminic acid. N-acetylneuraminic acid occurs in many polysaccharides, glycoproteins, and glycolipids in animals and bacteria. (From Dorland, 28th ed, p1518)",,,,N-acetyl-alpha-neuraminic acid is experimental.,N-acetyl-alpha-neuraminic acid is a solid.,True
18045,The phosphoric acid ester of serine.,The molecular weight is 185.07.,Dexfosfoserine has a topological polar surface area of 130.08.,The log p value of  is -4.46.,Dexfosfoserine is experimental.,Dexfosfoserine is a solid.,True
18046,"A MET receptor tyrosine kinase inhibitor. Investigated for use/treatment in solid tumors and cancer/tumors (unspecified). SGX523 is selective inhibitor of the receptor tyrosine kinase MET. MET is implicated in development and progression of cancer. SGX523 ihibits MET autophosphorylation and signalling, as well as activates cysteine-aspartic acid protease 3 (caspase 3), an enzyme which is part of the apoptosis signalling cascade. ",,,,SGX-523 is investigational.,SGX-523 is a solid.,True
18047,,,,,"1-(4-fluorophenyl)-N-pyridin-4-yloxy)phenyl]-2-oxo-1,2-dihydropyridine-3-carboxamide is experimental.","1-(4-fluorophenyl)-N-pyridin-4-yloxy)phenyl]-2-oxo-1,2-dihydropyridine-3-carboxamide is a solid.",False
18048,,,,,N-({4--3-fluorophenyl}carbamoyl)-2-(4-fluorophenyl)acetamide is experimental.,N-({4--3-fluorophenyl}carbamoyl)-2-(4-fluorophenyl)acetamide is a solid.,False
18049,,,,,2-(4-fluorophenyl)-N-{pyridin-4-yloxy)phenyl]carbamoyl}acetamide is experimental.,2-(4-fluorophenyl)-N-{pyridin-4-yloxy)phenyl]carbamoyl}acetamide is a solid.,False
18050,,,,,N-(3-chlorophenyl)-N-methyl-2-oxo-3--2H-indole-5-sulfonamide is experimental.,N-(3-chlorophenyl)-N-methyl-2-oxo-3--2H-indole-5-sulfonamide is a solid.,False
18051,,,,,3-phenol is experimental.,3-phenol is a solid.,False
18052,"AMG-208 has been used in trials studying the treatment of Cancer, Tumors, Oncology, Prostate Cancer, and Oncology Patients, among others.",,,,AMG-208 is investigational.,AMG-208 is a solid.,True
18053,,,,,1--1H-PYRROLOPYRIDINE-6-CARBOXAMIDE is experimental.,1--1H-PYRROLOPYRIDINE-6-CARBOXAMIDE is a solid.,False
18054,"Tivantinib has been investigated in Solid Tumors. Tivantinib mediates its effects by inhibiting the activity of c-Met, a receptor tyrosine kinase that plays multiple key roles in human cancer, including cancer cell growth, survival, angiogenesis, invasion and metastasis. C-Met is abnormally activated in most cancers and is believed to control multiple signal transduction pathways involved in tumor growth and metastasis.",,,,Tivantinib is investigational.,,True
18055,,,,,Beta-D-Glucopyranose Spirohydantoin is experimental.,Beta-D-Glucopyranose Spirohydantoin is a solid.,False
18056,,,,,"(5S,7R,8S,9S,10R)-3-Amino-8,9,10-trihydroxy-7-(hydroxymethyl)-6-oxa-1,3-diazaspirodecane-2,4-dione is experimental.","(5S,7R,8S,9S,10R)-3-Amino-8,9,10-trihydroxy-7-(hydroxymethyl)-6-oxa-1,3-diazaspirodecane-2,4-dione is a solid.",False
18057,,,,,N-beta-D-glucopyranosylacetamide is experimental.,N-beta-D-glucopyranosylacetamide is a solid.,False
18058,,,,,Monofluorophosphate ion is experimental.,Monofluorophosphate ion is a solid.,False
18059,,,,,"3,8,9,10-tetrahydroxy-7-hydroxymethyl-6-oxa-1,3-diaza-spirodecane-2,4-dione is experimental.","3,8,9,10-tetrahydroxy-7-hydroxymethyl-6-oxa-1,3-diaza-spirodecane-2,4-dione is a solid.",False
18060,,,,,Nojirimycine Tetrazole is experimental.,Nojirimycine Tetrazole is a solid.,False
18061,,,,,Indirubin-5-sulphonate is experimental.,Indirubin-5-sulphonate is a solid.,False
18062,,,,,2-Deoxy-Glucose-6-Phosphate is experimental.,2-Deoxy-Glucose-6-Phosphate is a solid.,False
18063,,,,,C-(1-hydrogyl-beta-D-glucopyranosyl) formamide is experimental.,C-(1-hydrogyl-beta-D-glucopyranosyl) formamide is a solid.,False
18064,,,,,alpha-D-glucopyranosyl-2-carboxylic acid amide is experimental.,alpha-D-glucopyranosyl-2-carboxylic acid amide is a solid.,False
18065,,The molecular weight is 260.14.,alpha-D-glucose-1-phosphate has a topological polar surface area of 156.91.,The log p value of  is -3.29.,alpha-D-glucose-1-phosphate is experimental.,alpha-D-glucose-1-phosphate is a solid.,False
18066,,,,,"8,9,10-Trihydroxy-7-hydroxymethyl-2-thioxo-6-oxa-1,3-diaza-spirodecan-4-one is experimental.","8,9,10-Trihydroxy-7-hydroxymethyl-2-thioxo-6-oxa-1,3-diaza-spirodecan-4-one is a solid.",False
18067,,,,,"4-{2,4-BisPhenoxy}Phthalic Acid is experimental.","4-{2,4-BisPhenoxy}Phthalic Acid is a solid.",False
18068,,,,,"2-(Beta-D-Glucopyranosyl)-5-Methyl-1,2,3-Benzimidazole is experimental.","2-(Beta-D-Glucopyranosyl)-5-Methyl-1,2,3-Benzimidazole is a solid.",False
18069,,,,,N-acetyl-N'-beta-D-glucopyranosyl urea is experimental.,N-acetyl-N'-beta-D-glucopyranosyl urea is a solid.,False
18070,,,,,"2-(Beta-D-Glucopyranosyl)-5-Methyl-1,3,4-Benzothiazole is experimental.","2-(Beta-D-Glucopyranosyl)-5-Methyl-1,3,4-Benzothiazole is a solid.",False
18071,,,,,C-(1-Azido-Alpha-D-Glucopyranosyl) Formamide is experimental.,C-(1-Azido-Alpha-D-Glucopyranosyl) Formamide is a solid.,False
18072,,,,,"2-(Beta-D-Glucopyranosyl)-5-Methyl-1,3,4-Oxadiazole is experimental.","2-(Beta-D-Glucopyranosyl)-5-Methyl-1,3,4-Oxadiazole is a solid.",False
18073,,,,,CP-320626 is experimental.,CP-320626 is a solid.,False
18074,,,,,"(3,4,5-Trihydroxy-6-Hydroxymethyl-Tetrahydro-Pyran-2-Yl)-Phosphoramidic Acid Dimethyl Ester is experimental.","(3,4,5-Trihydroxy-6-Hydroxymethyl-Tetrahydro-Pyran-2-Yl)-Phosphoramidic Acid Dimethyl Ester is a solid.",False
18075,,,,,"8,9,10-trihydroxy-7-hydroxymethyl-3-methyl-6-oxa-1,3-diaza-spirodecane-2,4-dione is experimental.","8,9,10-trihydroxy-7-hydroxymethyl-3-methyl-6-oxa-1,3-diaza-spirodecane-2,4-dione is a solid.",False
18076,,,,,1-deoxy-1-methoxycarbamido-beta-D-glucopyranose is experimental.,1-deoxy-1-methoxycarbamido-beta-D-glucopyranose is a solid.,False
18077,,,,,N-dec-3-yl]acetamide is experimental.,N-dec-3-yl]acetamide is a solid.,False
18078,,,,,1-Deoxy-1-methoxycarbamido-beta-D-gluco-2-heptulopyranosonamide is experimental.,1-Deoxy-1-methoxycarbamido-beta-D-gluco-2-heptulopyranosonamide is a solid.,False
18079,,,,,4-{2-Phenoxy}Phthalic Acid is experimental.,4-{2-Phenoxy}Phthalic Acid is a solid.,False
18080,,,,,"2,3-Dicarboxy-4-(2-Chloro-Phenyl)-1-Ethyl-5-Isopropoxycarbonyl-6-Methyl-Pyridinium is experimental.","2,3-Dicarboxy-4-(2-Chloro-Phenyl)-1-Ethyl-5-Isopropoxycarbonyl-6-Methyl-Pyridinium is a solid.",False
18081,,,,,Heptulose-2-Phosphate is experimental.,Heptulose-2-Phosphate is a solid.,False
18082,,,,,N-(Benzoylcarbamoyl)-beta-D-glucopyranosylamine is experimental.,N-(Benzoylcarbamoyl)-beta-D-glucopyranosylamine is a solid.,False
18083,,,,,1-Deoxy-1-acetylamino-beta-D-gluco-2-heptulopyranosonamide is experimental.,1-Deoxy-1-acetylamino-beta-D-gluco-2-heptulopyranosonamide is a solid.,False
18084,,,,,"7-{2,6-DICHLORO-4--PHENOXY}-HEPTANOIC ACID is experimental.","7-{2,6-DICHLORO-4--PHENOXY}-HEPTANOIC ACID is a solid.",False
18085,,,,,4-{3-CHLORO-4--PHENOXY}-BUTYRIC ACID is experimental.,4-{3-CHLORO-4--PHENOXY}-BUTYRIC ACID is a solid.,False
18086,,,,,"4-{4--2,3-DIMETHYL-PHENOXY}-BUTYRIC ACID is experimental.","4-{4--2,3-DIMETHYL-PHENOXY}-BUTYRIC ACID is a solid.",False
18087,,,,,5-{3--2-METHYL-PHENOXY}-PENTANOIC ACID is experimental.,5-{3--2-METHYL-PHENOXY}-PENTANOIC ACID is a solid.,False
18088,,,,,2-CHLORO-N--6H-THIENOPYRROLE-5-CARBOXAMIDE is experimental.,2-CHLORO-N--6H-THIENOPYRROLE-5-CARBOXAMIDE is a solid.,False
18089,,,,,2-CHLORO-N--6H-THIENOPYRROLE-5-CARBOXAMIDE is experimental.,2-CHLORO-N--6H-THIENOPYRROLE-5-CARBOXAMIDE is a solid.,False
18090,,,,,"(S)-2-CHLORO-N-(1-(2-(2-HYDROXYETHYLAMINO)-2-OXOETHYL)-2-OXO-1,2,3,4-TETRAHYDROQUINOLIN-3-YL)-6H-THIENOPYRROLE-5-CARBOXAMIDE is experimental.","(S)-2-CHLORO-N-(1-(2-(2-HYDROXYETHYLAMINO)-2-OXOETHYL)-2-OXO-1,2,3,4-TETRAHYDROQUINOLIN-3-YL)-6H-THIENOPYRROLE-5-CARBOXAMIDE is a solid.",False
18091,,,,,(2S)-N--2-CHLORO-2H-THIENOPYRROLE-5-CARBOXAMIDE is experimental.,(2S)-N--2-CHLORO-2H-THIENOPYRROLE-5-CARBOXAMIDE is a solid.,False
18092,,,,,"(3R,4R,5R)-5-(HYDROXYMETHYL)-1-(3-PHENYLPROPYL)PIPERIDINE-3,4-DIOL is experimental.","(3R,4R,5R)-5-(HYDROXYMETHYL)-1-(3-PHENYLPROPYL)PIPERIDINE-3,4-DIOL is a solid.",False
18093,,,,,({amino}oxy)acetic acid is experimental.,({amino}oxy)acetic acid is a solid.,False
18094,,,,,"(5R,7R,8S,9S,10R)-7-(hydroxymethyl)-3-phenyl-1,6-dioxa-2-azaspirodec-2-ene-8,9,10-triol is experimental.","(5R,7R,8S,9S,10R)-7-(hydroxymethyl)-3-phenyl-1,6-dioxa-2-azaspirodec-2-ene-8,9,10-triol is a solid.",False
18095,,,,,"2-DEOXY-3,4-BIS-O--L-THREO-PENTARIC ACID is experimental.","2-DEOXY-3,4-BIS-O--L-THREO-PENTARIC ACID is a solid.",False
18096,,,,,"(3S,5R,7R,8S,9S,10R)-7-(hydroxymethyl)-3-(2-naphthyl)-1,6-dioxa-2-azaspirodecane-8,9,10-triol is experimental.","(3S,5R,7R,8S,9S,10R)-7-(hydroxymethyl)-3-(2-naphthyl)-1,6-dioxa-2-azaspirodecane-8,9,10-triol is a solid.",False
18097,,,,,"(3S,5R,7R,8S,9S,10R)-7-(hydroxymethyl)-3-(4-methylphenyl)-1,6-dioxa-2-azaspirodecane-8,9,10-triol is experimental.","(3S,5R,7R,8S,9S,10R)-7-(hydroxymethyl)-3-(4-methylphenyl)-1,6-dioxa-2-azaspirodecane-8,9,10-triol is a solid.",False
18098,"Bovine adenosine deaminase derived from bovine intestine that has been extensively pegylated for extended serum half life. For treatment of adenosine deaminase deficiency Used to replace deficient or inactive adenosine deaminase which leads to severe combined immunodeficiency disease (SCID). The enzyme is responsible for converting adenosine to inosine. In the absence of adenosine deaminase, the purine substrates adenosine, 2'-deoxyadenosine and their metabolites are actually toxic to lymphocytes thereby leading to diminished immune function. Pegademase converts adenosine (toxic) to inosine (less toxic) by deamination. It also converts 2'-deoxyadenosine to 2'-deoxyinosine via deamination.",,,,Pegademase is approved.,Pegademase is a liquid.,True
18099,,,,,4-Icos-11-En-10-Yl]Benzylphosphonic Acid is experimental.,4-Icos-11-En-10-Yl]Benzylphosphonic Acid is a solid.,False
18100,"Tapinarof is targeted as a topical cream treatment for psoriasis, a chronic autoimmune skin disease. Investigated for use/treatment in psoriasis and psoriatic disorders. WBI-1001 selectively modulates the cytokine cascade deep under the skin, a process that rapidly decreases inflammations and skin plague. It targets the four major mechanisms involved in the disease.",,,,Tapinarof is investigational.,Tapinarof is a solid.,True
18101,"A component of neomycin that is produced by Streptomyces fradiae. On hydrolysis it yields neamine and neobiosamine B. (From Merck Index, 11th ed) For the treatment of bacterial blepharitis, bacterial bonjunctivitis, corneal injuries, corneal ulcers and meibomianitis. For the prophylaxis of ocular infections following foreign body removal Framycetin is used for the treatment of bacterial eye infections such as conjunctivitis. Framycetin is an antibiotic. It is not active against fungi, viruses and most kinds of anaerobic bacteria. Framycetin works by binding to the bacterial 30S ribosomal subunit, causing misreading of t-RNA, leaving the bacterium unable to synthesize proteins vital to its growth. Framycetin is useful primarily in infections involving aerobic bacteria bacteria. Framycetin binds to specific 30S-subunit proteins and 16S rRNA, four nucleotides of 16S rRNA and a single amino acid of protein S12. This interferes with decoding site in the vicinity of nucleotide 1400 in 16S rRNA of 30S subunit. This region interacts with the wobble base in the anticodon of tRNA. This leads to interference with the initiation complex, misreading of mRNA so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes.",The molecular weight is 614.65.,Framycetin has a topological polar surface area of 353.11.,The log p value of  is -6.47.,Framycetin is approved.,Framycetin is a solid.,True
18102,"Plerixafor is a hematopoietic stem cell mobilizer. It is used to stimulate the release of stem cells from the bone marrow into the blood in patients with non-Hodgkin lymphoma and multiple myeloma for the purpose of stimulating the immune system. These stem cells are then collected and used in autologous stem cell transplantation to replace blood-forming cells that were destroyed by chemotherapy. Plerixafor has orphan drug status in the United States and European Union; it was approved by the U.S. Food and Drug Administration on December 15, 2008. Used in combination with granulocyte-colony stimulating factor (G-CSF, filgrastim) to mobilize hematopoietic stem cells to the peripheral blood for collection and subsequent autologous transplantation in patients with non-Hodgkin’s lymphoma (NHL) and multiple myeloma (MM). Plerixafor is a bicyclam derivative that antagonizes CXCR4 by binding to three acidic residues in the ligand-binding pocket: Asp171, Asp262, and Glu288. Blood levels of CD34+ cells peaked at 9 hours after administration of 0.24 mg/kg plerixafor in healthy subjects. In patients that have non-Hodgkin’s lymphoma or multiple myeloma, blood levels of CD34+ peaked at 6 hours. In combination with a G-CSF, circulating CD34+ cells in the peripheral blood peaked at 9-14 hours.  Plerixafor inhibits the CXCR4 chemokine receptors on CD34+ cells and reversibly blocks binding of the ligand, stromal cell-derived factor-1-alpha (SDF-1α). By blocking the interaction between SDF-1α and CXCR4 with plerixafor, mobilization of progenitor cells is triggered. Filgrastim, a granulocyte-colony stimulating factor, is added to enhance CD34+ cell mobilization, thus increasing the yield of stem cells- an important determinant of graft adequacy. ",The molecular weight is 502.8.,Plerixafor has a topological polar surface area of 78.66.,The log p value of  is -0.25.,Plerixafor is approved.,Plerixafor is a liquid.,True
18103,,,,,CGS-27023 is experimental.,CGS-27023 is a solid.,False
18104,,,,,N--O-TYROSINE-N-METHYLAMIDE is experimental.,N--O-TYROSINE-N-METHYLAMIDE is a solid.,False
18105,,,,,METHYLAMINO-PHENYLALANYL-LEUCYL-HYDROXAMIC ACID is experimental.,METHYLAMINO-PHENYLALANYL-LEUCYL-HYDROXAMIC ACID is a solid.,False
18106,,,,,-3-METHYL-BUTYL]-CARBONYL-LEUCINYL]-ALANINE ETHYL ESTER is experimental.,-3-METHYL-BUTYL]-CARBONYL-LEUCINYL]-ALANINE ETHYL ESTER is a solid.,False
18107,,,,,N-HYDROXY-2--ACETAMIDE is experimental.,N-HYDROXY-2--ACETAMIDE is a solid.,False
18108,"The phosphoric acid ester of threonine. Used as an identifier in the analysis of peptides, proteins, and enzymes. ",,,,Phosphonothreonine is experimental.,Phosphonothreonine is a solid.,True
18109,,,,,Purvalanol is experimental.,Purvalanol is a solid.,False
18110,,,,,SB220025 is experimental.,SB220025 is a solid.,False
18111,,,,,"N,N-DIMETHYL-4-(4-PHENYL-1H-PYRAZOL-3-YL)-1H-PYRROLE-2-CARBOXAMIDE is experimental.","N,N-DIMETHYL-4-(4-PHENYL-1H-PYRAZOL-3-YL)-1H-PYRROLE-2-CARBOXAMIDE is a solid.",False
18112,,,,,N-BENZYL-4--1H-PYRROLE-2-CARBOXAMIDE is experimental.,N-BENZYL-4--1H-PYRROLE-2-CARBOXAMIDE is a solid.,False
18113,,,,,(S)-N-(1-(3-CHLORO-4-FLUOROPHENYL)-2-HYDROXYETHYL)-4-(4-(3-CHLOROPHENYL)-1H-PYRAZOL-3-YL)-1H-PYRROLE-2-CARBOXAMIDE is experimental.,(S)-N-(1-(3-CHLORO-4-FLUOROPHENYL)-2-HYDROXYETHYL)-4-(4-(3-CHLOROPHENYL)-1H-PYRAZOL-3-YL)-1H-PYRROLE-2-CARBOXAMIDE is a solid.,False
18114,,,,,"(3R,5Z,8S,9S,11E)-8,9,16-TRIHYDROXY-14-METHOXY-3-METHYL-3,4,9,10-TETRAHYDRO-1H-2-BENZOXACYCLOTETRADECINE-1,7(8H)-DIONE is experimental.","(3R,5Z,8S,9S,11E)-8,9,16-TRIHYDROXY-14-METHOXY-3-METHYL-3,4,9,10-TETRAHYDRO-1H-2-BENZOXACYCLOTETRADECINE-1,7(8H)-DIONE is a solid.",False
18115,,,,,5-(2-PHENYLPYRAZOLOPYRIDIN-3-YL)-1H-PYRAZOLOPYRIDAZIN-3-AMINE is experimental.,5-(2-PHENYLPYRAZOLOPYRIDIN-3-YL)-1H-PYRAZOLOPYRIDAZIN-3-AMINE is a solid.,False
18116,,,,,"(1aR,8S,13S,14S,15aR)-5,13,14-trihydroxy-3-methoxy-8-methyl-8,9,13,14,15,15a-hexahydro-6H-oxirenobenzoxacyclotetradecine-6,12(1aH)-dione is experimental.","(1aR,8S,13S,14S,15aR)-5,13,14-trihydroxy-3-methoxy-8-methyl-8,9,13,14,15,15a-hexahydro-6H-oxirenobenzoxacyclotetradecine-6,12(1aH)-dione is a solid.",False
18117,,,,,4-phenyl]-1H-imidazol-5-yl]pyridine is experimental.,4-phenyl]-1H-imidazol-5-yl]pyridine is a solid.,False
18118,"Turpentine, also known as spirit of turpentine, oil of turpentine, and wood turpentine, is a liquid extracted from live trees, mainly pine, through distillation of resin. It is used as a solvent and base material in organic synthesis reactions. Turpentine is composed of terpenes, mainly the monoterpenes alpha-pinene and beta-pinene with lesser amounts of carene, camphene, dipentene, and terpinolene. Turpentine has been used experimentally in a bath for the treatment of disseminated sclerosis and sexual dysfunction. It also has been studied for its antibacterial activity and inhibition of osteoclast activity. Turpentine is utilized in experimental models of inflammation to induce a systemic inflammatory immune response in animals. Turpentine oil, when inhaled, may help reduce congestion. When used on the skin, turpentine oil may cause warmth and redness that can help relieve pain in the tissue underneath. Binding of turpentine oil or inflammatory cytokines e.g. interleukin-1 (IL-1) activate signalling through the IL-1 Type 1 receptor (IL-1 R1). Initiation occurs by binding of Toll-interleukin 1 receptor adaptor protein (TIRAP) and Myeloid differentiation primary response gene 88 (mD88) which then dissociates and interacts with IRAK (Interleukin 1 receptor associated kinase) and the tumour necrosis factor receptor associated factor 6 (TRAF6). This activates the MAPK pathway leading to transcription of the nuclear factor κB transcription factor and production of inflammatory mediators. ",,,,Turpentine is approved and experimental.,,True
18119,"Ulixertinib is a a novel, reversible, ATP-competitive ERK1/2 inhibitor with high potency and ERK1/2 selectivity. It is currently in clinical trials for the treatment of a wide range of tumors.",,,,Ulixertinib is investigational.,Ulixertinib is a solid.,True
18120,"Binodenoson is a pharmacologic stress agent specific to the only adenosine receptor necessary for increased cardiac blood flow, the A<sub>2A</sub> receptor. This specificity allows Binodenoson to deliver - in a single injection - a more effective dose of medication with fewer side effects than current treatments, which typically require a 15-20 minute infusion. For cardiac pharmacologic stress SPECT imaging, which is used to diagnose coronary artery disease. Binodenoson, a novel cardiovascular disease diagnostic, is a adenosine A2A receptor agonist in development for cardiac pharmacologic stress SPECT imaging, which is used to diagnose coronary artery disease. Binodenoson is a highly selective adenosine A2A receptor agonist. The adenosine A2A receptor is necessary for increased cardiac blood flow, and specificity to this particular receptor allows binodenoson to deliver, in a single injection, a more effective dose of medication with fewer side effects than current treatments, which typically require a 15-20 minute infusion. Cardiac stress tests allow physicians to identify the presence of cardiovascular disease by examining the flow of blood through the heart.",,,,Binodenoson is investigational.,Binodenoson is a solid.,True
18121,Apadenoson is a selective A2a adenosine receptor agonist designed for use as a pharmacologic stress agent in cardiac perfusion imaging studies. It is developed by Bristol-Myers Squibb and is in phase II of clinical trials. Investigated for use/treatment in cardiovascular disorders and inflammatory disorders (unspecified). BMS068645 is designed to selectively stimulate the A2a adenosine receptor responsible for coronary vasodilation. Research to date suggests that this compound could potentially reduce or eliminate side effects associated with currently available pharmacologic stress agents that are not selective for the A2a adenosine receptor.,,,,Apadenoson is investigational.,Apadenoson is a solid.,True
18122,"ATL146e is an anti-inflammatory compounds which is an agonist of A2A adenosine receptors.  Investigated for use/treatment in inflammatory disorders (unspecified). ATL146e can inhibit neutrophil, macrophage and T cell activation and thereby reduce inflammation caused autoimmune responses. It also inhibits TNF-α and IL-1/3 production, neutrophil accumulation in gastric injury induced by NSAIDS (such as aspirin) without affecting mucosal prostaglandin E2 (PGE2) concentration. The effects of adenosine A2A agonists can be enhanced by type IV phosphodiesterase inhibitors, such as rolipram.",,,,Atl146e is investigational.,Atl146e is a solid.,True
18123,"Regadenoson is an A2A adenosine receptor agonist that causes coronary vasodilation and used for myocardial perfusion imagining. Manufactured by Astellas and FDA approved April 10, 2008. Diagnostic agent for radionuclide myocardial perfusion imaging (MPI)  Regadenoson rapidly increases coronary blood flow (CBF) which is sustained for a short duration. Mean average peak velocity increased to greater than twice baseline by 30 seconds and decreased to less than twice the baseline level within 10 minutes. Myocardial uptake of the radiopharmaceutical is proportional to (CBF). Regadenoson increases blood flow in normal coronary arteries but not in stenotic (blocked) arteries. The significance of this finding is that stenotic arteries will take up less of the radiopharmaceutical than normal coronary arteries, resulting in a signal that is less intense in these areas.  Regadenoson is an selective low-affinity (Ki= 1.3 µM) A2A receptor agonist that mimics the effects of adenosine in causing coronary vasodilatation and increasing myocardial blood flow. It is a very weak agonist of the A1 adenosine receptor (Ki > 16.5 µM). Furthermore, it has negligible affinity to A2B and A3 adenosine receptors. Regadenoson is undergoing trials for use in pharmacological stress tests. Adenosine slows conduction time through the A-V node, can interrupt the reentry pathways through the A-V node, and can restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardia (PSVT), including PSVT associated with Wolff-Parkinson-White Syndrome.",The molecular weight is 390.36.,Regadenoson has a topological polar surface area of 186.46.,The log p value of  is -2.86.,Regadenoson is approved and investigational.,Regadenoson is a liquid.,True
18124,,,,,4-{2-triazolotriazin-5-yl)amino]ethyl}phenol is experimental.,4-{2-triazolotriazin-5-yl)amino]ethyl}phenol is a solid.,False
18125,,,,,P-Nitrophenol is experimental.,P-Nitrophenol is a solid.,False
18126,,,,,5-Bromonicotinamide is experimental.,5-Bromonicotinamide is a solid.,False
18127,,,,,N-Methylleucine is experimental.,N-Methylleucine is a solid.,False
18128,"MDX-1100, a fully human antibody that targets IP10 (also known as CXCL10), a chemokine expressed in association with multiple inflammatory disease indications, such as rheumatoid arthritis, inflammatory bowel disease and multiple sclerosis. Investigated for use/treatment in ulcerative colitis. MDX-1100 binds selectively to CXCL10 and blocks CXCL10 induced calcium flux and cell migration.",,,,Eldelumab is investigational.,Eldelumab is a solid.,True
18129,,,,,Palmitoyl-Linoleoyl Phosphatidylcholine is experimental.,Palmitoyl-Linoleoyl Phosphatidylcholine is a solid.,False
18130,,,,,L-Dilinoleoyllecithin is experimental.,L-Dilinoleoyllecithin is a solid.,False
18131,,,,,"6-Hydroxy-5-undecyl-4,7-benzothiazoledione is experimental.","6-Hydroxy-5-undecyl-4,7-benzothiazoledione is a solid.",False
18132,Azoxystrobin is a methoxyacrylate analog and a strobilurin fungicide.,,,,Azoxystrobin is experimental.,Azoxystrobin is a solid.,True
18133,,,,,"5-Heptyl-6-hydroxy-1,3-benzothiazole-4,7-dione is experimental.","5-Heptyl-6-hydroxy-1,3-benzothiazole-4,7-dione is a solid.",False
18134,,,,,"(5S)-3-ANILINO-5-(2,4-DIFLUOROPHENYL)-5-METHYL-1,3-OXAZOLIDINE-2,4-DIONE is experimental.","(5S)-3-ANILINO-5-(2,4-DIFLUOROPHENYL)-5-METHYL-1,3-OXAZOLIDINE-2,4-DIONE is a solid.",False
18135,,,,,(S)-famoxadone is experimental.,(S)-famoxadone is a solid.,False
18136,,,,,METHYL (2Z)-3-METHOXY-2-{2-PHENYL}ACRYLATE is experimental.,METHYL (2Z)-3-METHOXY-2-{2-PHENYL}ACRYLATE is a solid.,False
18137,,,,,2-Nonyl-4-quinolinol 1-oxide is experimental.,2-Nonyl-4-quinolinol 1-oxide is a solid.,False
18138,,,,,Ubiquinone Q2 is experimental.,Ubiquinone Q2 is a solid.,False
18139,,,,,2-Aminoethanimidic Acid is experimental.,2-Aminoethanimidic Acid is a solid.,False
18140,,,,,3-Amino-4-Oxybenzyl-2-Butanone is experimental.,3-Amino-4-Oxybenzyl-2-Butanone is a solid.,False
18141,,,,,3-Methylphenylalanine is experimental.,3-Methylphenylalanine is a solid.,False
18142,,,,,N-(3-Propylcarbamoyloxirane-2-Carbonyl)-Isoleucyl-Proline is experimental.,N-(3-Propylcarbamoyloxirane-2-Carbonyl)-Isoleucyl-Proline is a solid.,False
18143,,,,,2-Pyridinethiol is experimental.,2-Pyridinethiol is a solid.,False
18144,,,,,Diphenylacetic acid is experimental.,Diphenylacetic acid is a solid.,False
18145,,,,,N-Leucylamino-2-Methyl-Butane is experimental.,N-Leucylamino-2-Methyl-Butane is a solid.,False
18146,,,,,N-{carbonyl}-L-threonyl-L-isoleucine is experimental.,N-{carbonyl}-L-threonyl-L-isoleucine is a solid.,False
18147,,,,,N-{CARBONYL}-L-ISOLEUCINE is experimental.,N-{CARBONYL}-L-ISOLEUCINE is a solid.,False
18148,,,,,"BENZYL N-({(2S,3S)-3-OXIRAN-2-YL}CARBONYL)-L-ISOLEUCYL-L-PROLINATE is experimental.","BENZYL N-({(2S,3S)-3-OXIRAN-2-YL}CARBONYL)-L-ISOLEUCYL-L-PROLINATE is a solid.",False
18149,,,,,"METHYL N-({(2S,3S)-3-OXIRAN-2-YL}CARBONYL)-L-ISOLEUCYL-L-PROLINATE is experimental.","METHYL N-({(2S,3S)-3-OXIRAN-2-YL}CARBONYL)-L-ISOLEUCYL-L-PROLINATE is a solid.",False
18150,,,,,N-{CARBONYL}-L-ISOLEUCYL-L-ALANINE is experimental.,N-{CARBONYL}-L-ISOLEUCYL-L-ALANINE is a solid.,False
18151,,,,,N-{CARBONYL}-L-ISOLEUCYL-L-ISOLEUCINE is experimental.,N-{CARBONYL}-L-ISOLEUCYL-L-ISOLEUCINE is a solid.,False
18152,,,,,"N-({(2S,3S)-3-OXIRAN-2-YL}CARBONYL)-L-ISOLEUCYL-L-PROLINE is experimental.","N-({(2S,3S)-3-OXIRAN-2-YL}CARBONYL)-L-ISOLEUCYL-L-PROLINE is a solid.",False
18153,,,,,1h-Benoximidazole-2-Carboxylic Acid is experimental.,1h-Benoximidazole-2-Carboxylic Acid is a solid.,False
18154,,,,,2-Morpholinoethylamine is experimental.,2-Morpholinoethylamine is a solid.,False
18155,,,,,5-AMINO-6-CYCLOHEXYL-4-HYDROXY-2-ISOBUTYL-HEXANOIC ACID is experimental.,5-AMINO-6-CYCLOHEXYL-4-HYDROXY-2-ISOBUTYL-HEXANOIC ACID is a solid.,False
18156,,,,,"CYCLOHEXYLMETHYL-2,3-DIHYDROXY-5-METHYL-HEXYLAMIDE is experimental.","CYCLOHEXYLMETHYL-2,3-DIHYDROXY-5-METHYL-HEXYLAMIDE is a solid.",False
18157,"Olsalazine is an anti-inflammatory drug used in the treatment of Inflammatory Bowel Disease and Ulcerative Colitis. Olsalazine is a derivative of salicylic acid. Inactive by itself (it is a prodrug), it is converted by the bacteria in the colon to mesalamine. Mesalamine works as an anti-inflammatory agent in treating inflammatory diseases of the intestines. For the treatment of Inflammatory Bowel Disease and Ulcerative Colitis. Olsalazine is an anti-inflammatory drug used in the treatment of Inflammatory Bowel Disease and Ulcerative Colitis. Olsalazine reduces the bowel inflammation, diarrhea (stool frequency), rectal bleeding, and abdominal pain. Olsalazine is thought to work like balsalazide, delivering mesalazine or 5-aminosalicylic acid past the small intestine to the large intestine to act on the site of disease. Orally administered olsalazine is converted to mesalamine which is thought to be the therapeutically active agent in the treatment of ulcerative colitis. The mechanism of action of mesalamine (and sulfasalazine) is unknown, but appears to be topical rather than systemic. Mucosal production of arachidonic acid (AA) metabolites, both through the cyclooxygenase pathways, i.e., prostanoids, and through the lipoxygenase pathways, i.e., leukotrienes (LTs) and hydroxyelcosatetraenoic acids (HETEs) is increased in patients with chronic inflammatory bowel disease, and it is possible that mesalamine diminishes inflammation by blocking cyclooxygenase and inhibiting prostaglandin (PG) production in the colon.",,,,Olsalazine is approved.,Olsalazine is a solid.,True
18158, is an experimental therapeutic vaccine currently in clinical trial. The aim of therapeutic vaccines is to augment the body's immune response to HIV and to delay or prevent progression to AIDS. Investigated for use/treatment in HIV infection. VIR201 uses DNA vaccine technology called Co-X-Gene in which HIV and human genetic material have been grafted on to a harmless fowlpox virus. This fowlpox vector carries genetic material for HIV proteins gag and pol. The aim of this component of the vaccine is to stimulate HIV-specific immune responses in people who have very low levels of HIV in their blood due to antiretroviral therapy. The vaccine also carries genetic material to stimulate the cytokine or immune system messenger called interferon gamma which is associated with delayed disease progression. The aim of this second component of the vaccine is to boost levels of interferon gamma and improve immune functioning.,,,,VIR201 is investigational.,VIR201 is a solid.,True
18159,Fontolizumab (marketed under the trade name HuZAF™) is a humanized monoclonal antibody which is used as an immunosuppressive drug to treat Crohn's disease. Investigated for use/treatment in crohn's disease and psoriasis and psoriatic disorders. Fontolizumab is a humanised antibody directed against recombinant human IFN-{gamma}. The antibody binds to natural human IFN-{gamma} and inhibits expression of IFN-{gamma} regulated genes known to be upregulated in Crohn’s disease.,,,,Fontolizumab is investigational.,Fontolizumab is a solid.,True
18160,"Emapalumab, also known as NI-0501, is a fully human monoclonal antibody that targets interferon gamma. Emapalumab development was sponsored by NovImmune SA, further developed by Sobi and FDA approved on November 20, 2018. The approval of emapalumab was followed by the designation of orphan drug, priority review and breakthrough therapy. As well, emapalumab was given the status of PRIME by the EMA. Emapalumab is indicated for the treatment of pediatric and adult patients with primary hemophagocytic lymphohistiocytosis (HLH) with refractory, recurrent or progressive disease or intolerance to conventional HLH therapy. In phase 2/3 clinical trials, emapalumab administered concomitantly with dexamethasone reported an overall response in 63% of the patients. The overall response was defined as achievement of a complete or partial response or HLH improvement. In this trial and as a proof of interferon-gamma neutralization, there was registered a sharp decrease in serum CXCL9 and to avoid QT prolongation in the presence of low doses of emapalumab. Emapalumab acts by binding and neutralizing interferon-gamma. The specific interaction between emapalumab and interferon-gamma produces an inhibition in the interaction between interferon-gamma and its cognate receptor on T-cells which produces the neutralizing activity. It is important to consider that emapalumab inhibits both free and IFNGR1-bound interferon-gamma as well as the interaction with IFNGR1 and IFNGR2 at the cell surface.",,,,Emapalumab is approved and investigational.,Emapalumab is a solid.,True
18161,"SGS518, a novel antagonist for the 5HT6 subtype of the serotonin receptor, is being developed as a treatment for Cognitive Impairment Associated with Schizophrenia (CIAS). Investigated for use/treatment in neurologic disorders and schizophrenia and schizoaffective disorders. SGS518 is a selective antagonist of the 5-Hydroxytryptamine-6 (5-HT6) serotonin receptor believed to act by enhancing transmission of chemicals in the brain. ",,,,SGS518 is investigational.,SGS518 is a solid.,True
18162,"Investigated for use/treatment in alzheimer's disease, obesity, and schizophrenia and schizoaffective disorders. PRX-07034 is a novel, highly selective, small-molecule antagonist of a specific G-protein coupled receptor (GPCR) known as 5-HT6 being developed for the treatment of obesity, Alzheimer's disease and cognitive impairment associated with schizophrenia.",,,,PRX-07034 is investigational.,PRX-07034 is a solid.,True
18163,"SUVN-502 is a novel, potent, safe, highly selective and orally active antagonist at a central nervous system serotonin receptor site 5-HT6 intended for treatment of cognitive disorders such as Alzheimer’s and Schizophrenia, an unmet medical need. Investigated for use/treatment in neurologic disorders.",,,,SUVN-502 is investigational.,SUVN-502 is a solid.,True
18164,,,,,Ethanesulfonic acid is experimental.,Ethanesulfonic acid is a solid.,False
18165,"Tasonermin is recombinant soluble form tumor necrosis factor &alpha; produced via _Escherichia coli_ cell culture. It was approved for use by the European Medicines Agency in April of 1999 for use as an adjunt to surgery for the subsequent removal of the tumor and in palliative care for irresectable soft tissue sarcoma of the limbs as the product Beromun. It is administered with via mild hyperthermic isolated limb perfusion. For use in adults as an adjunct to surgery for subsequent removal of the tumour so as to prevent or delay amputation, or in palliative care, for irresectable soft tissue sarcoma of the limbs. Used in combination with melphalan via mild hyperthermic isolated limb perfusion. Tasonermin is thought to contribute to the destruction of tumor tissue via several direct and indirect effects.  Since tasonermin is recombinant TNF-&alpha;, it functions exactly as endogenous TNF-&alpha; does. The direct cytotoxic effect of TNF-&alpha; is mediated by TNF-&alpha; receptor 1. The bound receptor activates the well-reviewed death receptor pathway involving the activation of initiator caspases 8 and 9 then ultimately ending in the activation of effector caspase 3 which begins the process of apoptosis.",The molecular weight is 17350.75.,Tasonermin has a topological polar surface area of 7163.87.,,Tasonermin is approved.,Tasonermin is a solid.,True
18166,,,,,N-Cyclohexyl-N'-(4-Iodophenyl)Urea is experimental.,N-Cyclohexyl-N'-(4-Iodophenyl)Urea is a solid.,False
18167,,,,,N-Cyclohexyl-N'-Decylurea is experimental.,N-Cyclohexyl-N'-Decylurea is a solid.,False
18168,,,,,N-Cyclohexyl-N'-(Propyl)Phenyl Urea is experimental.,N-Cyclohexyl-N'-(Propyl)Phenyl Urea is a solid.,False
18169,"AR-9281 inhibits soluble epoxide hydrolase. Investigated for use/treatment in hypertension. AR9281 inhibits soluble epoxide hydrolase (s-EH), an enzyme that plays a key role in the cytochrome P450 pathway of arachidonic acid metabolism. Nuclear factor alpha B (NF-alphaB) is a transcription factor implicated in cardiac hypertrophy, and can be anti or pro apoptotic under different conditions. Epoxyeicosatrienoic acids (EETs), a product of cytochrome P450 epoxygenase enzyme action, have a variety of anti-hypertensive and anti-inflammatory effects. EETs have a vasodilatory action similar to endothelium derived hyperpolarizing factor and may inhibit NF-alphaB through a currently unknown mechanism. The enzyme s-EH catalyzes the breakdown of EETs to dihydroxyeicosatrienoic acids. AR9281's inhibition of s-EH enhances EETs anti-hypertensive and anti-inflammatory activities by preventing their breakdown by s-EH, as well as inhibiting NF-alphaB. ",,,,AR-9281 is investigational.,AR-9281 is a solid.,True
18170,,,,,N-GLYCINE is experimental.,N-GLYCINE is a solid.,False
18171,,,,,4-{AMINO}BUTANOIC ACID is experimental.,4-{AMINO}BUTANOIC ACID is a solid.,False
18172,,,,,6-{AMINO}HEXANOIC ACID is experimental.,6-{AMINO}HEXANOIC ACID is a solid.,False
18173,,,,,7-{AMINO}HEPTANOIC ACID is experimental.,7-{AMINO}HEPTANOIC ACID is a solid.,False
18174,"Ebselen has been investigated for the treatment and basic science of Meniere's Disease, Type 2 Diabetes Mellitus, and Type 1 Diabetes Mellitus.",,,,Ebselen is investigational.,,True
18175,"3'-phospho-5'-adenylyl sulfate is a key intermediate in the formation by living cells of sulfate esters of phenols, alcohols, steroids, sulfated polysaccharides, and simple esters, such as choline sulfate. It is formed from sulfate ion and ATP in a two-step process. This compound also is an important step in the process of sulfur fixation in plants and microorganisms.",,,,3'-phospho-5'-adenylyl sulfate is experimental.,3'-phospho-5'-adenylyl sulfate is a solid.,True
18176,,,,,"2--6-Hydroxymethyl-Tetra Hydro-Pyran-3,4,5-Triol is experimental.","2--6-Hydroxymethyl-Tetra Hydro-Pyran-3,4,5-Triol is a solid.",False
18177,"Alpha 1-antitrypsin is a glycoprotein primarily produced by hepatocytes, and to a lesser extent, immune system cells. Recombinant alpha 1-antitrypsin (rAAT) is produced from yeast, which unlike commercially available forms of plasma-derived AAT, eliminates the risk associated with blood-borne infectious agents and allows for a increased manufacturing. rAAT belongs to a family of structurally-related proteins classified as serine protease inhibitors or SERPINS, which are known to inhibit several proteases including trypsin, cathepsin G, thrombin, tissue kallikrein, as well as neutrophil elastase. The proteinase/antiproteinase balance is believed to be important for maintaining healthy skin. The rAAT topical gel (Dermolastin™) is indicated for patients with atopic dermatitis and psoriasis. The company has indicated that other formulations for gastroenterological and urological indications will also be developed. Investigated for use/treatment in alpha 1 antitrypsin deficiency, atopic dermatitis, and chronic obstructive pulmonary disease (COPD). Alpha 1-antitrypsin is a glycoprotein primarily produced by hepatocytes, and to a lesser extent, immune system cells. Recombinant alpha 1-antitrypsin (rAAT) is produced from yeast, which unlike commercially available forms of plasma-derived AAT, eliminates the risk associated with blood-borne infectious agents and allows for a increased manufacturing. rAAT belongs to a family of structurally-related proteins classified as serine protease inhibitors or SERPINS, which are known to inhibit several proteases including trypsin, cathepsin G, thrombin, tissue kallikrein, as well as neutrophil elastase. The proteinase/antiproteinase balance is believed to be important for maintaining healthy skin.  rAAT belongs to a family of structurally-related proteins classified as serine protease inhibitors or SERPINS, which are known to inhibit several proteases including trypsin, cathepsin G, thrombin, tissue kallikrein, as well as neutrophil elastase.",,,,Recombinant alpha 1-antitrypsin is investigational.,Recombinant alpha 1-antitrypsin is a solid.,True
18178,Investigated for use/treatment in HIV infection. PPL-100 is a promising protease inhibitor which binds specifically to HIV-1 protease. It has been shown activity against several HIV-1 strains specifically selected for key mutations that render these strains resistant to currently marketed protease inhibitors,,,,PPL-100 is investigational.,PPL-100 is a solid.,True
18179,"Sucralfate is a medication that is widely used to prevent and treat a number of diseases in the gastrointestinal tract such as duodenal ulcers , gastro-esophageal reflux disease (GERD), gastritis, peptic ulcer disease, stress ulcer, in addition to dyspepsia. It is considered a _cytoprotective agent_, protecting cells in the gastrointestinal tract from damage caused by agents such as gastric acid, bile salts, alcohol, and acetylsalicylic acid (aspirin), among other substances. The sucralfate suspension and tablet are used for the treatment of active duodenal ulcer for up to 8 weeks. The tablet form may be used at a lower dose for healed duodenal ulcers, for the purpose of maintaining healing and preventing recurrence.  This drug aids in the healing of duodenal ulcers, relieving painful inflammation by creating a protective mechanical barrier between the lining or skin of the gastrointestinal tract and damaging substances. In addition, sucralfate acts to increase levels of growth factors locally, and also causes an increase in prostaglandins which are important in the healing of the mucosa (lining) of the gastrointestinal tract.  The mechanism of action of this drug in the healing duodenal ulcers is not yet completely defined, however, there are several probable mechanisms that adequately describe the healing activity of sucralfate. There is evidence that sucralfate acts locally to aid in tissue healing, and not systemically. ",,,,Sucralfate is approved.,Sucralfate is a solid.,True
18180,"SF1126 is an integrin-targeted PI3 kinase inhibitor. For the treatment of various forms of cancer. SF1126 is a covalent conjugate of LY294002 that contains a peptide-based targeting group to help increase the localization of the drug in the neovascular component supporting tumor growth. SF1126 is a highly water soluble solid which aids its administration via i.v. or s.c. injections. In vivo it converts spontaneously at physiological pH to LY294002 in a way that is well tolerated in mice, rats, and dogs. SF1126 has been evaluated in numerous animal tumor models showing good tumor inhibition or tumor regression. SF1126 is a small molecule conjugate containing a pan-PI3K inhibitor that selectively inhibits all PI3K class IA isoforms and other key members of the PI3K superfamily, including DNA-PK and mTOR. A major factor in tumor resistance to approved chemotherapy agents is thought to be the activation of the PI3K/PTEN pathway. As a result, it is thought that inhibiting this pathway, via SF1126, could cause the resetting of sensitivity to approved agents and exhibit synergistic anticancer effects.",,,,SF1126 is investigational.,SF1126 is a solid.,True
18181,"Wortmannin is a steroid metabolite of _Penicillium funiculosum_ and _Talaromyces wortmannii_ fungi. This drug acts as a nonspecific, covalent inhibitor of phosphoinositide 3-kinase enzymes (PI3Ks).",,,,Wortmannin is experimental.,Wortmannin is a solid.,True
18182,,,,,SR12813 is experimental.,SR12813 is a solid.,False
18183,"Pyrethrum is the crude extract form obtained from flowers of the plant Chrysanthemum cinerariifolium. Pyrethrin refers to a more refined extract of pyrethrum. While pyrethrum extract is composed of 6 esters, both organic compounds mediate insecticidal activities. Pyrethrum-containing mixtures are used as a common insecticide to control specific pest species. Pyrethrum extract is also used used to treat head, body, and pubic lice infections. The active compound is absorbed by the lice and destroys them by acting on their nervous systems but is thought to exert minimal effect on humans.",The molecular weight is 1377.8.,Pyrethrum extract has a topological polar surface area of 69.67.,,Pyrethrum extract is approved.,,True
18184,,,,,7-methyl-GpppA is experimental.,7-methyl-GpppA is a solid.,False
18185,,,,,"7-methyl-7,8-dihydroguanosine-5'-diphosphate is experimental.","7-methyl-7,8-dihydroguanosine-5'-diphosphate is a solid.",False
18186,,,,,7-methyl-guanosine-5'-triphosphate is experimental.,7-methyl-guanosine-5'-triphosphate is a solid.,False
18187,"LY2275796 is a second-generation antisense anti-cancer drug candidate for clinical development. LY2275796 targets eukaryotic initiation factor- 4E (eIF-4E), a protein involved in the translation of key growth and survival factors that drive tumor progression, angiogenesis and metastases. Investigated for use/treatment in cancer/tumors (unspecified) and solid tumors. LY2275796 targets eIF-4E, a protein that is upregulated or overexpressed in a variety of cancers, including breast, head and neck, prostate, lung, bladder, colon, thyroid and non-Hodgkin's lymphomas. The molecule facilitates the synthesis of tumor angiogenic factors (factors that facilitate the growth of new blood vessels to support the development and progression of tumors), growth factors and survival factors by selectively enhancing their translation. Based on scientific literature, there is a strong indication that eIF-4E may act as a critical \switch\"" in cancer progression.""",,,,LY2275796 is investigational.,LY2275796 is a solid.,True
18188,,,,,S- methanesulfonothioate is experimental.,S- methanesulfonothioate is a solid.,False
18189,"Cerulenin is an antifungal agent whose activity interferes with or otherwise acts to prevent the formation of fatty acids and sterols. In fatty acid synthesis, reported to bind in equimolar ratio to b-keto-acyl-ACP synthase. In sterol synthesis, inhibits HMG-CoA synthetase activity. It is also shown to inhibit feeding and induce dramatic weight loss in mice. It is found naturally in the Cephalosporium caerulensfungus. For use as a biochemical tool, Cerulenin is shown to cause dramatic weight loss in animals Cerulenin is an antifungal antibiotic isolated from <i>Cephalosporium caerulens</i>. It interrupts fungal growth by inhibiting the biosynthesis of sterols and fatty acids (inhibits bacterial fatty acid synthesis). It also inhibits HMG-CoA synthetase activity. Cerulenin produces metabolic effects similar to effects of leptin, but through mechanisms that are independent of, or down-stream from, both leptin and melanocortin receptors. Irreversibly binds to fatty acid synthase, specifically b-ketoacyl-acyl carrier protein synthase (FabH, FabB and FabF condensation enzymes). A number of tumor cells and cell lines have been observed to have highly upregulated expression and activity of fatty acid synthase (FAS). Inhibition of FAS by cerulenin leads to cytotoxicity and apoptosis in human cancer cell lines, an effect believed to be mediated by the accumulation of malonyl-coenzyme A in cells with an upregulated FAS pathway.",The molecular weight is 223.27.,Cerulenin has a topological polar surface area of 72.69.,The log p value of  is 0.84.,Cerulenin is experimental.,Cerulenin is a solid.,True
18190,,,,,"(5S)-5-Iododihydro-2,4(1H,3H)-pyrimidinedione is experimental.","(5S)-5-Iododihydro-2,4(1H,3H)-pyrimidinedione is a solid.",False
18191,,,,,6-Carboxymethyluracil is experimental.,6-Carboxymethyluracil is a solid.,False
18192,,,,,Uracil is experimental and investigational.,Uracil is a solid.,False
18193,"Eniluracil, which was previously under development by GlaxoSmithKline (GSK), is being developed by Adherex to enhance the therapeutic value and effectiveness of 5-fluorouracil (5-FU), one of the world’s most widely-used oncology agents. 5-FU is widely used in the U.S. and is often first or second line therapy for a variety of cancers including colorectal, breast, gastric, head and neck, ovarian and basal cell cancer of the skin. Eniluracil could improve 5-FU by increasing its effectiveness, reducing its side effects and/or making it orally available. Eniluracil has received Orphan Drug status from the FDA for the treatment of hepatocellular cancer in combination with fluoropyrimidines (including 5-FU). For the treatment of cancer in combination with 5-fluorouracil. Eniluracil is an orally active dihydropyrimidine dehydrogenase (DPD) inhibitor, designed to enhance activity of chemotaxic agents. It is under investigation by Adherex, under license from GlaxoSmithKline, for the treatment of cancer in combination with 5-fluorouracil (5-FU). Normally, 5-FU is rapidly broken down in the body by an enzyme known as dihydropyrimidine dehydrogenase (DPD). Eniluracil irreversibly inhibits DPD, thereby substantially slowing the breakdown of 5-FU and prolonging exposure of the tumor cells to the drug.",,,,Eniluracil is investigational.,Eniluracil is a solid.,True
18194,,,,,5-Iodouracil is experimental.,5-Iodouracil is a solid.,False
18195,"Gimeracil is an adjunct to antineoplastic therapy, used to increase the concentration and effect of the main active componets within chemotherapy regimens. Approved by the European Medicines Agency (EMA) in March 2011, Gimeracil is available in combination with and within the commercially available product \Teysuno\"". The main active ingredient in Teysuno is , a pro-drug of (5-FU), which is a cytotoxic anti-metabolite drug that acts on rapidly dividing cancer cells. By mimicking a class of compounds called \""pyrimidines\"" that are essential components of RNA and DNA, 5-FU is able to insert itself into strands of DNA and RNA, thereby halting the replication process necessary for continued cancer growth. "" Gimeracil is used as an adjunct to antineoplastic therapy. When used within the product Teysuno, gimeracil is indicated for the treatment of adults with advanced gastric (stomach) cancer when given in combination with cisplatin. Gimeracil's main role within Teysuno is to prevent the breakdown of (5-FU), which helps to maintin high enough concentrations for sustained effect against cancer cells. It functions by reversibly blocking the enzyme dihydropyrimidine dehydrogenase (DPD), which is involved in the degradation of 5-FU.",The molecular weight is 145.54.,Gimeracil has a topological polar surface area of 49.33.,The log p value of  is -0.16.,Gimeracil is approved.,Gimeracil is a solid.,True
18196,"MDX-018, also known as HuMax-Inflam, is a fully human antibody that is directed to IL-8 (interleukin-8) and may have potential application in oncology and inflammation. Trials will initially focus on studies to treat glioblastoma, a cancer of the central nervous system. Other possible indications include chronic obstructive pulmonary disease (COPD) and pustular dermatoses. In pre-clinical studies, HuMax-Inflam has been shown to inhibit tumor growth in tumor models using primary human tumors in immunodeficient mice. HuMax-Inflam was also effective in reducing disease activity in palmoplantar pustulosis patients in a clinical study. Investigated for use/treatment in autoimmune diseases and inflammatory disorders (unspecified). MDX-018 is a fully human anti-inflammatory antibody for the treatment of Autoimmune Disease. The drug inhibits tumour growth by targetting interleukin-8 (IL-8), a major inflammation mediator. It reduces disease activity in palmoplantar pustulosis patients and is also effective in the treatment of glioblastoma, which has a very low survival rate. he drug inhibits tumour growth by targetting interleukin-8 (IL-8), a major inflammation mediator.",,,,MDX-018 is investigational.,MDX-018 is a solid.,True
18197,,,,,S-P-Nitrobenzyloxycarbonylglutathione is experimental.,S-P-Nitrobenzyloxycarbonylglutathione is a solid.,False
18198,,,,,S-(N-hydroxy-N-iodophenylcarbamoyl)glutathione is experimental.,S-(N-hydroxy-N-iodophenylcarbamoyl)glutathione is a solid.,False
18199,,,,,"methyl 4-(2,3-dihydroxy-5-methylphenoxy)-2-hydroxy-6-methylbenzoate is experimental.","methyl 4-(2,3-dihydroxy-5-methylphenoxy)-2-hydroxy-6-methylbenzoate is a solid.",False
18200,"Mycobacterial Cell Wall-DNA Complex (MCC) is formulated from Mycobacterium phlei, a non-pathogenic strain of mycobacteria. MCC has been shown to have immune stimulatory and apoptosis (programmed cell death) activity against cancer cells. The product is a sterile biological composition in a sub-micron suspension. It is produced at the Bioniche manufacturing facility in Pointe-Claire, Quebec. Bladder cancer MCC has a therapeutic potential in high grade transitional cell carcinomas of the bladder, including refractory CIS. The combination of MCC with hyaluronic acid (HA) enhances both the apoptosis-inducing activity of MCC against prostate cancer cell lines, and the immune stimulatory activity of MCC (stimulation of anticancer cytokine synthesis by human immune effector cells). ",,,,MCC is investigational.,MCC is a solid.,True
18201,,,,,3-Methylpyridine is experimental.,3-Methylpyridine is a solid.,False
18202,,,,,2-{4--Tetrahydro-Pyran-4-Yl}-N-Hydroxy-Acetamide is experimental.,2-{4--Tetrahydro-Pyran-4-Yl}-N-Hydroxy-Acetamide is a solid.,False
18203,,,,,WAY-151693 is experimental.,WAY-151693 is a solid.,False
18204,,,,,Hydroxyaminovaline is experimental.,Hydroxyaminovaline is a solid.,False
18205,,,,,4-methoxybenzenesulfinate is experimental.,4-methoxybenzenesulfinate is a solid.,False
18206,,,,,"PYRIMIDINE-4,6-DICARBOXYLIC ACID BIS-(3-METHYL-BENZYLAMIDE) is experimental.","PYRIMIDINE-4,6-DICARBOXYLIC ACID BIS-(3-METHYL-BENZYLAMIDE) is a solid.",False
18207,,,,,"PYRIMIDINE-4,6-DICARBOXYLIC ACID BIS-(4-FLUORO-3-METHYL-BENZYLAMIDE) is experimental.","PYRIMIDINE-4,6-DICARBOXYLIC ACID BIS-(4-FLUORO-3-METHYL-BENZYLAMIDE) is a solid.",False
18208,,,,,"PYRIMIDINE-4,6-DICARBOXYLIC ACID BIS- is experimental.","PYRIMIDINE-4,6-DICARBOXYLIC ACID BIS- is a solid.",False
18209,,,,,TERT-BUTYL 4-({SULFONYL}METHYL)-4-PIPERIDINE-1-CARBOXYLATE is experimental.,TERT-BUTYL 4-({SULFONYL}METHYL)-4-PIPERIDINE-1-CARBOXYLATE is a solid.,False
18210,,,,,4-{METHYL}BENZOIC ACID is experimental.,4-{METHYL}BENZOIC ACID is a solid.,False
18211,,,,,"5-(2-ETHOXYETHYL)-5-PYRIMIDINE-2,4,6(1H,3H,5H)-TRIONE is experimental.","5-(2-ETHOXYETHYL)-5-PYRIMIDINE-2,4,6(1H,3H,5H)-TRIONE is a solid.",False
18212,CTS-1027 has been used in trials studying the treatment of Hepatitis C and Chronic Hepatitis C Virus Infection.,,,,CTS-1027 is experimental and investigational.,CTS-1027 is a solid.,True
18213,,,,,"BENZYL 6-BENZYL-5,7-DIOXO-6,7-DIHYDRO-5H-THIAZOLOPYRIMIDINE-2-CARBOXYLATE is experimental.","BENZYL 6-BENZYL-5,7-DIOXO-6,7-DIHYDRO-5H-THIAZOLOPYRIMIDINE-2-CARBOXYLATE is a solid.",False
18214,"Andexanet alfa is a recombinant human coagulation Factor Xa that promotes blood coagulation. It was developed by Portola Pharmaceuticals and was approved in in May 2018. It is marketed as Andexxa for intravenous injection or infusion and is indicated for the reversal of anticoagulation in combination with and in cases of life-threatening or uncontrolled bleeding. Rivaroxaban and apixaban are Factor Xa inhibitors that promote anticoagulation in situations where blood clotting is unfavourable, such as in deep vein thrombosis and pulmonary embolism. However, the use of these agents is associated with a risk for uncontrollable bleeding episodes that can lead to can cause serious or fatal bleeding. Andexanet alfa is currently under regulatory review by the European Union and is undergoing clinical development in Japan. Andexanet alfa is indicated for patients treated with and , when reversal of anticoagulation is needed due to life-threatening or uncontrolled bleeding. Andexxa has not been shown to be effective for, and is not indicated for, the treatment of bleeding related to any Factor Xa inhibitors other than apixaban and rivaroxaban. _In vitro_, andexanet alfa was shown to dose-dependently reverse the activity of apixaban, betrixaban, edoxaban, rivaroxaban, enoxaparin and fondaparinux on Factor Xa in human and rat plasma.  Factor Xa inhibitors promote anticoagulation by binding to both free Factor Xa in plasma and Factor Xa attached to the prothrombinase complex. This ultimately leads to the blockade of thrombin generation or clot formation. Andexanet alfa is a factor Xa decoy that binds to factor Xa inhibitors such as apixaban and rivaroxaban with high affinity and prevents them from binding to endogenous factor Xa. It was also shown to sequester factor Xa inhibitors, leading to reversing their anticoagulant effects and restoring the activity of endogenous factor Xa. Andexanet alfa may also achieve procoagulation via binding and inhibiting the activity of Tissue Factor Pathway Inhibitor (TFPI), which is an endogenous inhibitor of Factor Xa. Inhibition of TFPI by andexanet alfa resulted in a transient increase in the level of prothrombin fragments 1 and 2, thrombin-antithrombin complex and D-dimer. Subsequently, this may result in increased tissue factor-initiated thrombin generation. Since it is a genetically modified variant of human factor Xa, andexanet alfa is not able to cleave and activate prothrombin nor assemble into the prothrombinase complex. ",,,,Andexanet alfa is approved and investigational.,Andexanet alfa is a solid.,True
18215,"Edotecarin is a novel, non-camptothecin, DNA topoisomerase I inhibitor. It is member of the class of compounds called indolocarbazoles. Clinical studies with edotecarin have shown activity in subjects with colorectal cancer, esophageal cancer and other solid tumors. Edotecarin, formerly J-107088 is a novel, non-camptothecin, DNA topoisomerase-1 inhibitor. It is part of the class of compounds called indolocarbazoles. It is a novel inhibitor of topoisomerase I that induces single-strand DNA cleavage more effectively than NB-506 or camptothecin (CPT) and at different DNA sequences. The DNA-topoisomerase I complexes induced by edotecarin are more stable than those occurring after exposure to CPT or NB-506. The antitumor activity of edotecarin is less cell cycle dependent than other topoisomerase I inhibitors. Being an indolocarbazole, it is structurally related to staurosporine but does not possess protein kinase inhibitory properties. The antitumor activity of edotecarin has been tested in vitro and in vivo, and inhibition of tumor growth has been observed in breast, cervix, pharynx, lung, prostate, colon, gastric, and hepatic cancer models. Edotecarin is effective on cells that have acquired resistance related to P-glycoprotein. In vitro synergy has been demonstrated when edotecarin was tested in combination with cisplatin, 5-fluorouracil, etoposide, paclitaxel, doxorubicin, vincristine, CPT, and gemcitabine. Edotecarin inhibits the enzyme topoisomerase I through stabilization of the DNA-enzyme complex and enhanced single-strand DNA cleavage, resulting in inhibition of DNA replication and decreased tumor cell proliferation.",,,,Edotecarin is investigational.,Edotecarin is a solid.,True
18216,"Sodium stibogluconate is a medicine used to treat leishmaniasis and is only available for administration by injection. It belongs to the class of medicines known as the pentavalent antimonials. Sodium stibogluconate is sold in the UK as Pentostam (manufactured by GlaxoSmithKline). Widespread resistance has limited the utility of sodium stibogluconate, and in many parts of the world, amphotericin or miltefosine are used instead. It is also being investigated as an anti-tumor agent. For the treatment of various types of a protozoal infection called leishmaniasis, which may result from sandfly bites in tropical and temperate parts of the world. Also investigated for use/treatment in cancer/tumors (unspecified) and solid tumors. The mode of action of sodium stibogluconate is not clearly understood. In vitro exposure of amastigotes to 500 mg pentavalent antimony/ml results in a greater than 50% decrease in parasite DNA, RNA protein and purine nucleoside triphosphate levels. It has been postulated that the reduction in ATP (adenosine triphosphate) and GTP (guanosine triphosphate) synthesis contributes to decreased macromolecular synthesis. Sodium stibogluconate directly inhibits DNA topoisomerase I leading to inhibition of both DNA replication and transcription.",The molecular weight is 679.8.,Sodium stibogluconate has a topological polar surface area of 276.27.,The log p value of  is -0.4.,Sodium stibogluconate is approved and investigational.,Sodium stibogluconate is a solid.,True
18217,"Cositecan is the novel camptothecin derivative which is also known as Karenitecin. It has been developed for superior oral bioavailability and increased lactone stability. It is used to treat cancer. Investigated for use/treatment in brain cancer, lung cancer, and melanoma. BNP1350, 7--20(S)-camptothecin, is a novel semi-synthetic, highly lipophilic, silicon-containing camptothecin and an inhibitor of topoisomerase I. It has been supercomputer engineered for superior oral bioavailability, superior lactone stability, broad anti-tumor activity, increased potency and insensitivity to Pgp/MRP/LRP drug resistance.",,,,Cositecan is investigational.,Cositecan is a solid.,True
18218,"XMT-1001 is a polymer-based prodrug of camptothecin (CPT), a well-characterized topoisomerase I inhibitor with potent anti-tumor activity. It is a water-soluble macromolecular conjugate of camptothecin (CPT). In this novel CPT pro-drug, CPT is conjugated with a 70 kDa biodegradable hydrophilic polyacetal, poly (1-hydroxymethylene hydroxylmethylformal). XMT-1001 has demonstrated an improved therapeutic window as compared with CPT and irinotecan in human tumor xenografts models Investigated for use/treatment in solid tumors. In preclinical studies, XMT-1001 was better tolerated and more efficacious than either camptothecin or irinotecan in models of human cancer, showing extended plasma half-life and high concentrations in tumor tissue. The Phase I results show that, in humans, camptothecin, the active agent in XMT-1001, is released gradually from the Fleximer carrier as a pro-drug in a manner that will potentially avoid common safety problems associated with drugs in this class. XMT-1001 is Mersana’s most advanced Fleximer®-based product candidate. It utilizes a novel, dual release mechanism to liberate a camptothecin prodrug, which is then converted within cells into camptothecin, a DNA topoisomerase I inhibitor. It is a potent inhibitor of LS174 and A2780 human tumor xenografts in a mouse model.",,,,XMT-1001 is investigational.,XMT-1001 is a solid.,True
18219,"Investigated for use/treatment in pancreatic cancer, leukemia (unspecified), melanoma, ovarian cancer, and cancer/tumors (unspecified). Rubitecan prevents DNA from unwinding during replication via DNA topoisomerase 1, therefore interfering with tumor growth.",The molecular weight is 393.36.,Rubitecan has a topological polar surface area of 125.55.,The log p value of  is 0.46.,Rubitecan is investigational.,Rubitecan is a solid.,True
18220,,,,,"2,3-DIMETHOXY-12H-DIOXOLOINDENOISOQUINOLIN-6-IUM is experimental.","2,3-DIMETHOXY-12H-DIOXOLOINDENOISOQUINOLIN-6-IUM is a solid.",False
18221,,,,,"4-(5,11-DIOXO-5H-INDENOISOQUINOLIN-6(11H)-YL)BUTANOATE is experimental.","4-(5,11-DIOXO-5H-INDENOISOQUINOLIN-6(11H)-YL)BUTANOATE is a solid.",False
18222,"LY2140023 is an investigational drug from Lilly, which is being developed as a new treatment option for schizophrenia. LY2140023 is an oral \prodrug,\"" meaning it is devoid of intrinsic biological activity and, once administered, is metabolized to provide the active mGlu2/3 receptor agonist called LY404039. Most currently approved antipsychotic medications work by affecting the neurotransmitters dopamine or serotonin. For LY2140023, the active substance, LY404039, is thought to work by reducing the presynaptic release of another neurotransmitter, glutamate, in brain regions where mGlu2/3 receptors are expressed. Further studies are planned or are ongoing to learn more about the safety and effectiveness, including determining an optimal therapeutic dose for LY2140023."" Investigated for use/treatment in psychosis and schizophrenia and schizoaffective disorders. LY2140023 is an antipsychotic agent that is a metabotropic glutamate 2/3 receptor agonist. This agent has a new mechanism of action that is efficacious in treating schizophrenia and potentially other neuropsychiatric conditions. Once absorbed, LY2140023 is efficiently hydrolyzed to produce the active mGlu2/3 receptor agonist LY404039. LY404039 and other mGlu2/3 agonists do not directly interact with dopamine or serotonin (5-HT2A) receptors. However, 'functional' 5-HT2A receptor antagonism in the prefrontal cortex may represent a common mechanism shared by clinically effective atypical antipsychotics and mGlu2/3 receptor agonists, and may contribute to the antipsychotic actions of LY2140023.",,,,LY2140023 is investigational.,LY2140023 is a solid.,True
18223,,,,,Heparin Disaccharide I-S is experimental.,Heparin Disaccharide I-S is a solid.,False
18224,,,,,Heparin Disaccharide Iii-S is experimental.,Heparin Disaccharide Iii-S is a solid.,False
18225,"An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction. Scyllitol has been investigated for the treatment of Alzheimer Disease.",,,,scyllo-inositol is investigational.,scyllo-inositol is a solid.,True
18226,"Velaglucerase alfa is a gene-activated human recombinant glucocerebrosidase used for the treatment of Type 1 Gaucher disease, caused by a deficiency of the lysosomal enzyme glucocerebrosidase. Additionally, Velaglucerase alfa has also been investigated for use in Type 3 Gaucher disease. Velaglucerase alfa is a hydrolytic lysosomal glucocerebroside-specific enzyme indicated for long-term enzyme replacement therapy for pediatric and adult patients with type 1 Gaucher disease. Velaglucerase alfa catalyzes the hydrolysis of glucocerebroside, reducing the amount of accumulated glucocerebroside.",,,,Velaglucerase alfa is approved and investigational.,Velaglucerase alfa is a solid.,True
18227,,,,,"(2R,3R,4R,5S)-2-(HYDROXYMETHYL)-1-NONYLPIPERIDINE-3,4,5-TRIOL is experimental.","(2R,3R,4R,5S)-2-(HYDROXYMETHYL)-1-NONYLPIPERIDINE-3,4,5-TRIOL is a solid.",False
18228,,,,,5-Mercapto-2-Nitro-Benzoic Acid is experimental.,5-Mercapto-2-Nitro-Benzoic Acid is a solid.,False
18229,"Briakinumab is a human anti-IL-12 monoclonal antibody being developed for the treatment of a number of T-cell driven autoimmune diseases. It targets and neutralize interleukin-12 and interleukin-23, two proteins associated with inflammation, such as pro-inflammatory interleukins or tumor necrosis factor- alpha. Briakinumab represents a novel approach to treating psoriasis, Multiple Sclerosis, Crohn’s Disease and other autoimmune and inflammatory disorders. As of 2011 drug development for psoriasis has been discontinued in the U.S. and Europe. Investigated for use/treatment in autoimmune diseases, crohn's disease, multiple sclerosis, psoriasis and psoriatic disorders, and rheumatoid arthritis. Briakinumab is a human anti-IL-12 monoclonal antibody being developed for the treatment of a number of T-cell driven autoimmune diseases. It targets and neutralizes interleukin-12 and interleukin-23, two proteins associated with inflammation. Briakinumab targets and neutralizes interleukin-12 and interleukin-23.",,,,Briakinumab is investigational.,Briakinumab is a solid.,True
18230,"Ustekinumab is a human immunoglobulin (Ig) G1 kappa monoclonal antibody directed against interleukin(IL)-12 and IL-23, which are cytokines that are involved in immune and inflammatory responses. It was generated via recombinant human IL-12 immunization of human Ig (hu-Ig) transgenic mice. It is a targeted biologic disease-modifying anti-rheumatic drug (bDMARDs) that is used in the management of various inflammatory conditions that involve the activation of IL-12 and IL-23 signalling pathways. Ustekinumab is indicated for the management of moderate to severe plaque psoriasis in children aged 6 and above, adolescents, and adults who are candidates for phototherapy or systemic therapy. Ustekinumab is a targeted antibody therapy that suppresses immune responses. It acts by reducing the signaling pathways of pro-inflammatory cytokines IL-12 and IL-23, which play a role in various inflammatory conditions. It downregulates the gene expression of inflammatory cytokines and chemokines such as MCP-1, TNF-alpha, IP-10, and IL-8. The formation of cytochrome P-450 enzymes may be altered by elevated levels of certain cytokines during chronic inflammation. Research shows that there is an inverse relationship between plasma levels of inflammatory cytokines and CYP450 enzyme formation and activity. While ustekinumab may potentially normalize the formation of CYP enzymes and enhance the CYP-mediated metabolism of drugs, there were no clinically significant effects on human CYP enzyme activities. The steady-state was achieved by 28 weeks after multiple subcutaneous dose administration in adult patients with psoriasis. Interleukin (IL)-12 and IL-23 are heterodimeric cytokines that evoke immune and inflammatory responses, such as natural killer cell activation and CD4+ T-cell differentiation and activation. The role of IL-12 and IL-23 were implicated in a variety of chronic inflammatory conditions, such as psoriasis and inflammatory bowel diseases. They modulate lymphocyte function, including T-helper (Th) 1 and Th17 cell subsets, as CD4+ T cells can differentiate into T-helper (Th) effector lineages based on the environment. Th cells can further activate the downstream pro-inflammatory mediators and transcription factors such as TNFα and IFNγ that drive innate and adaptive immunity. ",,,,Ustekinumab is approved and investigational.,Ustekinumab is a liquid.,True
18231,"The humanized anti-IL-12 antibody is an important addition to PDL's already strong pipeline of humanized antibodies being developed for the treatment of autoimmune diseases. SMART Anti-IL-12 Antibody was humanized at PDL from a murine anti-IL-12 antibody that was licensed, together with certain intellectual property related to anti-IL-12 therapy, from Hoffmann-La Roche Inc. IL-12 is a cytokine that may have considerable potential as a target in the therapy of autoimmune diseases. Investigated for use/treatment in autoimmune diseases and inflammatory disorders (unspecified).",,,,humanized SMART Anti-IL-12 Antibody is investigational.,humanized SMART Anti-IL-12 Antibody is a solid.,True
18232,"First described in the literature in 2004, N-(2-Aminoethyl)-1-aziridineethanamine is an experimental angiotensin converting enzyme 2 inhibitor investigated for its use in treating cardiovascular disease and its activity against Severe Acute Respiratory Syndrome (SARS). This experimental drug was being researched for its use in the treatment of cardiovascular disease and SARS-CoV infections. Angiotensin II constricts coronary blood vessels and is positively inotropic, which under normal circumstances, would increase vascular resistance and oxygen consumption. This action can eventually lead to myocyte hypertrophy and vascular smooth muscle cell proliferation. N-(2-Aminoethyl)-1-aziridineethanamine may inhibit ACE2, preventing these actions from occurring.",,,,N-(2-Aminoethyl)-1-aziridineethanamine is experimental.,N-(2-Aminoethyl)-1-aziridineethanamine is a solid.,True
18233,"A purified preparation of the enzyme recombinant human hyaluronidase. Hyaluronidase (human recombinant) (INN Vorhyaluronidase alfa) is produced by genetically engineered Chinese Hamster Ovary (CHO) cells containing a DNA plasmid encoding for a soluble fragment of human hyaluronidase (PH20). Hyaluronidase is an enzyme used to improve the absorption and dispersion of parenterally administered fluids, drugs, and contrast agents. The action of hyaluronidase was first described in 1936, and named in 1939. Early research into hyaluronidase identified it as a \spreading factor\"" which allowed for increased permeability of the connective tissue. Hyaluronidase has been used in surgical settings for at least the past 60 years to improve the diffusion of local anesthetics."" Hyaluronidase is indicated for subcutaneous fluid administration for hydration, and increasing resorption of radiopaque agents in subcutaneous urography. Hyaluronidase is also indicated by multiple routes to increase the dispersion of other injectable drugs. Hyaluronidase cleaves hyaluronic acid in the extracellular matrix to improve the dispersion of injectable drugs. Hyaluronidase has a long duration of action and a wide therapeutic window. Patients should be counselled regarding the risk of spread of localized infection, ocular corneal damage, and inactivation by intravenous administration. Hyaluronidase cleaves hyaluronic acid at the glucosaminidic bond between C1 of glucosamine and C4 of glucuronic acid. Hyaluronic acid is a key component of the extracellular matrix. Injection of hyaluronidase with other fluids, drugs, or radiopaque agents improves the ability of these other compounds to permeate the extracellular space more easily.",,,,Hyaluronidase (human recombinant) is approved and investigational.,Hyaluronidase (human recombinant) is a solid.,True
18234,"Hyaluronidase is an enzyme used to improve the absorption and dispersion of parenterally administered fluids, drugs, and contrast agents. The action of hyaluronidase was first described in 1936, and named in 1939. Early research into hyaluronidase identified it as a \spreading factor\"" which allowed for increased permeability of the connective tissue. Hyaluronidase has been used in surgical settings for at least the past 60 years to improve the diffusion of local anesthetics."" Hyaluronidase is indicated for subcutaneous fluid administration for hydration, and increasing resorption of radiopaque agents in subcutaneous urography. Hyaluronidase is also indicated by multiple routes to increase the dispersion of other injectable drugs.  Hyaluronidase cleaves hyaluronic acid at the glucosaminidic bond between C1 of glucosamine and C4 of glucuronic acid. Hyaluronic acid is a key component of the extracellular matrix. Injection of hyaluronidase with other fluids, drugs, or radiopaque agents improves the ability of these other compounds to permeate the extracellular space more easily.",,,,Hyaluronidase is approved.,Hyaluronidase is a solid.,True
18235,Investigated for use/treatment in heart disease and myocardial infarction. Cardiac damage due to the buildup of sodium (Na+) ischemia and early reperfusion leads to increased calcium (Ca2+) through the reverse mode Na+/Ca2+(NCX) ion exchanger. Caldaret is an intracardiac calcium (Ca2+) handling modulator whose cardioprotective actions are presumed to be due to inhibition of the NCX exhanger and increasing the uptake of Ca2+ via the sarcoplasmic reticulum (SR).,,,,Caldaret is investigational.,Caldaret is a solid.,True
18236,,,,,MMI-175 is experimental.,MMI-175 is a solid.,False
18237,"CTS-21166 is a small-molecule beta-secretase inhibitor, which is being developed as a disease-modifying treatment for Alzheimer's disease. CTS-21166 is the only BACE1 inhibitor that has passed Phase I clinical trial thus far. In 2008, CoMentis revealed this small compound as a transition-state analog inhibitor (structure is currently undisclosed) with excellent properties in brain penetration, selectivity, metabolic stability, and oral availability; all of these have met the requirements of an ideal oral drug candidate. Investigated for use/treatment in alzheimer's disease. CTS-21166 produced a rapid and significant reduction of plasma amyloid beta, a key biomarker that is believed to be involved in the pathogenesis of Alzheimer's disease. CTS-21166 demonstrated excellent pharmacokinetic properties including dose proportional exposure and very low inter-subject pharmacokinetic variability. Beta secretase is the enzyme thought responsible for causing Alzheimer’s. CTS-21166 is a highly selective, potent and orally active beta-secretase inhibitor.",,,,CTS-21166 is investigational.,CTS-21166 is a solid.,True
18238,,,,,"N--2-(2,5-diphenyl-1H-pyrrol-1-yl)acetamide is experimental.","N--2-(2,5-diphenyl-1H-pyrrol-1-yl)acetamide is a solid.",False
18239,,,,,"N-DOCOSA-1(21),7(22),8,10,17,19-HEXAEN-19-YL]-N-METHYLMETHANESULFONAMIDE is experimental.","N-DOCOSA-1(21),7(22),8,10,17,19-HEXAEN-19-YL]-N-METHYLMETHANESULFONAMIDE is a solid.",False
18240,,,,,N--2-acetamide is experimental.,N--2-acetamide is a solid.,False
18241,,,,,4-(4-FLUOROBENZYL)PIPERIDINE is experimental.,4-(4-FLUOROBENZYL)PIPERIDINE is a solid.,False
18242,,,,,N-{2-methyl-5-phenyl}methanesulfonamide is experimental.,N-{2-methyl-5-phenyl}methanesulfonamide is a solid.,False
18243,,,,,6-PYRIDIN-2-AMINE is experimental.,6-PYRIDIN-2-AMINE is a solid.,False
18244,,,,,6-PYRIDIN-2-AMINE is experimental.,6-PYRIDIN-2-AMINE is a solid.,False
18245,,,,,"N~3~-BENZYLPYRIDINE-2,3-DIAMINE is experimental.","N~3~-BENZYLPYRIDINE-2,3-DIAMINE is a solid.",False
18246,,,,,"N~3~-(3-PYRIDIN-3-YLBENZYL)PYRIDINE-2,3-DIAMINE is experimental.","N~3~-(3-PYRIDIN-3-YLBENZYL)PYRIDINE-2,3-DIAMINE is a solid.",False
18247,,,,,"N~3~-PYRIDINE-2,3-DIAMINE is experimental.","N~3~-PYRIDINE-2,3-DIAMINE is a solid.",False
18248,,,,,4-(2-aminoethyl)-2-cyclohexylphenol is experimental.,4-(2-aminoethyl)-2-cyclohexylphenol is a solid.,False
18249,,,,,4-(2-aminoethyl)-2-ethylphenol is experimental.,4-(2-aminoethyl)-2-ethylphenol is a solid.,False
18250,,,,,4--1H-imidazol-2-amine is experimental.,4--1H-imidazol-2-amine is a solid.,False
18251,,,,,"(6R)-2-amino-6--3,6-dimethyl-5,6-dihydropyrimidin-4(3H)-one is experimental.","(6R)-2-amino-6--3,6-dimethyl-5,6-dihydropyrimidin-4(3H)-one is a solid.",False
18252,,,,,2-amino-6-pyrimidin-4(3H)-one is experimental.,2-amino-6-pyrimidin-4(3H)-one is a solid.,False
18253,,,,,"(2S)-1-(2,5-dimethylphenoxy)-3-morpholin-4-ylpropan-2-ol is experimental.","(2S)-1-(2,5-dimethylphenoxy)-3-morpholin-4-ylpropan-2-ol is a solid.",False
18254,,,,,N-(1-benzylpiperidin-4-yl)-4-sulfanylbutanamide is experimental.,N-(1-benzylpiperidin-4-yl)-4-sulfanylbutanamide is a solid.,False
18255,,,,,N--4-sulfanylbutanamide is experimental.,N--4-sulfanylbutanamide is a solid.,False
18256,,,,,(2S)-4-(4-fluorobenzyl)-N-(2-sulfanylethyl)piperazine-2-carboxamide is experimental.,(2S)-4-(4-fluorobenzyl)-N-(2-sulfanylethyl)piperazine-2-carboxamide is a solid.,False
18257,,,,,(2S)-4-(4-fluorobenzyl)-N-(3-sulfanylpropyl)piperazine-2-carboxamide is experimental.,(2S)-4-(4-fluorobenzyl)-N-(3-sulfanylpropyl)piperazine-2-carboxamide is a solid.,False
18258,,,,,N--4-sulfanylbutanamide is experimental.,N--4-sulfanylbutanamide is a solid.,False
18259,,,,,"(6S)-2-amino-6-(3'-methoxybiphenyl-3-yl)-3,6-dimethyl-5,6-dihydropyrimidin-4(3H)-one is experimental.","(6S)-2-amino-6-(3'-methoxybiphenyl-3-yl)-3,6-dimethyl-5,6-dihydropyrimidin-4(3H)-one is a solid.",False
18260,,,,,"N~3~-PYRIDINE-2,3-DIAMINE is experimental.","N~3~-PYRIDINE-2,3-DIAMINE is a solid.",False
18261,,,,,"N~3~-PYRIDINE-2,3-DIAMINE is experimental.","N~3~-PYRIDINE-2,3-DIAMINE is a solid.",False
18262,,,,,3-(2-AMINO-6-BENZOYLQUINAZOLIN-3(4H)-YL)-N-CYCLOHEXYL-N-METHYLPROPANAMIDE is experimental.,3-(2-AMINO-6-BENZOYLQUINAZOLIN-3(4H)-YL)-N-CYCLOHEXYL-N-METHYLPROPANAMIDE is a solid.,False
18263,"Verubecestat is under investigation for the treatment of Alzheimer's Disease, Prodromal Alzheimer's disease, and Amnestic Mild Cognitive Impairment.  The amyloid hypothesis asserts that the formation of amyloid peptides that lead to amyloid plaque deposits in the brain is a primary contributor to the underlying cause of Alzheimer's disease. BACE is believed to be a key enzyme in the production of amyloid β peptide. Evidence suggests that inhibiting BACE decreases the production of amyloid β peptide and may therefore reduce amyloid plaque formation and modify disease progression.",,,,Verubecestat is investigational.,,True
18264,"AT9283 is an aurora Kinase inhibitor developed by Astex Therapeutics for the treatment of cancer. It was discovered and developed internally using Astex’s fragment-based drug discovery platform, Pyramid. Investigated for use/treatment in cancer/tumors (unspecified), leukemia (myeloid), and solid tumors. AT9283 is an inhibitor of mitosis (cell division) and is the second most progressed drug candidate in the Astex portfolio of novel molecularly targeted cancer drugs. All of Astex’s current products have been discovered internally using its proprietary drug discovery approach. AT9283 is a potent inhibitor of the Aurora A and B kinases and has been shown to arrest tumour growth in a range of tumour models. Aurora kinases play a key role in mitotic checkpoint control in cell division. Both Aurora A and B are over-expressed in many human tumours and are believed to be excellent targets for anti-cancer therapy.",,,,AT9283 is investigational.,AT9283 is a solid.,True
18265,Alisertib is a novel aurora A kinase inhibitor under investigation for the treatment of various forms of cancer. For the treatment of various forms of cancer.,,,,Alisertib is investigational.,Alisertib is a solid.,True
18266,"SNS-314 is a potent and selective inhibitor of Aurora kinases A, B, and C. Proliferating cells treated with SNS-314 bypass the mitotic spindle checkpoint and fail to undergo cytokinesis, leading to multiple rounds of endoreduplication and eventually cell death. SNS-314 inhibits tumor growth in a variety of preclinical models, and it is now being tested in single agent Phase 1 studies in patients with advanced solid tumours. Investigated for use/treatment in solid tumors. SNS-314 inhibits Aurora kinases A, B, and C. Stopping Aurora kinases halts cellular division at the mitotoic phase of the cell cycle and proliferation in tumor cells that overexpress Aurora kinases. The process of cell division, or mitosis, plays a critical role in the uncontrolled proliferation that is a hallmark of cancer. During mitosis, a cell aligns duplicate copies of its DNA along a mitotic spindle and subdivides itself through a process called cytokinesis, creating two identical daughter cells. This process is often poorly regulated in cancer, leading to rapid proliferation and tissue growth. Aurora kinases (A, B, and C) play important, though differentiated, roles in mitosis. Aurora A controls the formation of the spindle assembly, while Aurora B ensures that the DNA is appropriately aligned and that cytokinesis proceeds successfully. Less is known about Aurora C, though it is thought to serve many of the same functions as Aurora B. Elevated expression of Aurora A has been detected in a high percentage of colon, breast, ovarian, gastric, and pancreatic tumors. Aurora B and C are also expressed at high levels in primary tumors.",,,,SNS-314 is investigational.,SNS-314 is a solid.,True
18267,"Cenisertib is an aurora kinase inhibitor. Investigated for use/treatment in solid tumors, leukemia (myeloid), myelodysplastic syndrome, and cancer/tumors (unspecified). R763 is a highly potent and specific inhibitor of Aurora kinase, which has been shown to block proliferation and trigger apoptosis (cell death) in several tumor cell lines including cervical, colon, lung, pancreas and prostate. The over-expression of Aurora kinase can cause cells to rapidly develop an abnormal number of chromosomes. Elevated levels of Aurora kinase are frequently associated with various human cancers and inhibition of this enzyme disrupts cell division and promotes apoptosis. A probable target for R763 is Aurora kinase A (serine/threonine protein kinase 6).",,,,Cenisertib is investigational.,Cenisertib is a solid.,True
18268,,,,,4-(4-METHYLPIPERAZIN-1-YL)-N-PYRAZOL-3-YL]BENZAMIDE is experimental.,4-(4-METHYLPIPERAZIN-1-YL)-N-PYRAZOL-3-YL]BENZAMIDE is a solid.,False
18269,AKI-001 is an aurora kinase inhibitor.,,,,AKI-001 is experimental.,AKI-001 is a solid.,True
18270,,,,,"1-{5-pyrimidin-4-ylamino)ethyl]-1,3-thiazol-2-yl}-3-urea is experimental.","1-{5-pyrimidin-4-ylamino)ethyl]-1,3-thiazol-2-yl}-3-urea is a solid.",False
18271,,,,,"1-(5-{2-pyrimidin-7-yl)amino]ethyl}-1,3-thiazol-2-yl)-3-urea is experimental.","1-(5-{2-pyrimidin-7-yl)amino]ethyl}-1,3-thiazol-2-yl)-3-urea is a solid.",False
18272,,,,,N-{3-AMINO}PYRIMIDIN-2-YL)AMINO]PHENYL}CYCLOPROPANECARBOXAMIDE is experimental.,N-{3-AMINO}PYRIMIDIN-2-YL)AMINO]PHENYL}CYCLOPROPANECARBOXAMIDE is a solid.,False
18273,,,,,N-butyl-3-{amino}benzamide is experimental.,N-butyl-3-{amino}benzamide is a solid.,False
18274,,,,,2-(1H-pyrazol-3-yl)-1H-benzimidazole is experimental.,2-(1H-pyrazol-3-yl)-1H-benzimidazole is a solid.,False
18275,,,,,N-BENZAMIDE is experimental.,N-BENZAMIDE is a solid.,False
18276,"MLN8054 has been used in trials studying the treatment of Colon Neoplasm, Breast Neoplasm, Bladder Neoplasm, Pancreatic Neoplasm, and Advanced Malignancies. MLN8054 is a selective small-molecule Aurora A kinase inhibitor that has entered Phase I clinical trials for advanced solid tumors. MLN8054 inhibits recombinant Aurora A kinase activity in vitro and is selective for Aurora A over the family member Aurora B in cultured cells. MLN8054 treatment results in G2/M accumulation and spindle defects and inhibits proliferation in multiple cultured human tumor cells lines.",,,,MLN8054 is investigational.,,True
18277,"Levetiracetam is a drug within the pyrrolidine class that is used to treat various types of seizures stemming from epileptic disorders. It was first approved for use in the United States in 1999 and is structurally and mechanistically unrelated to other anti-epileptic drugs (AEDs). Levetiracetam possesses a wide therapeutic index and little-to-no potential to produce, or be subject to, pharmacokinetic interactions - these characteristics make it a desirable choice over other AEDs, a class of drugs notorious for having generally narrow therapeutic indexes and a propensity for involvement in drug interactions. Levetiracetam is indicated as an adjunctive therapy in the treatment of partial onset seizures in epileptic patients who are one month of age and older. Additionally, it is indicated as an adjunct in the treatment of myoclonic seizures in patients with juvenile myoclonic epilepsy who are 12 years of age and older, and in primary generalized tonic-clonic seizures in patients with idiopathic generalized epilepsy who are 6 years of age and older. Levetiracetam appears to prevent seizure activity via the selective inhibition of hypersynchronized epileptiform burst firing without affecting normal neuronal transmission, though the exact mechanism through which this occurs is unclear. The therapeutic index of levetiracetam is wide, making it relatively unique amongst other anti-epileptic medications. The exact mechanism through which levetiracetam exerts its anti-epileptic effects is unclear, but is thought to be unique amongst other anti-epileptic medications. Current knowledge suggests that levetiracetam’s binding to synaptic vesicle protein 2A (SV2A) is a key driver of its action. SV2A is a membrane-bound protein that is found on synaptic vesicles and is ubiquitous throughout the CNS - it appears to play a role in vesicle exocytosis and in the modulation of synaptic transmission by increasing the available amount of secretory vesicles available for neurotransmission. Stimulation of pre-synaptic SV2A by levetiracetam may inhibit neurotransmitter release, but this action does not appear to affect normal neurotransmission. This has led to the suggestion that levetiracetam exclusively modulates the function of SV2A only under pathophysiological conditions. Levetiracetam and related analogues showed a correlation between affinity for SV2A and anti-epileptic potency, further suggesting that action at this site contributes to the anti-epileptic activity of the drug.",The molecular weight is 170.21.,Levetiracetam has a topological polar surface area of 63.4.,The log p value of  is -0.34.,Levetiracetam is approved.,Levetiracetam is a solid.,True
18278,,,,,"3h-Indole-5,6-Diol is experimental.","3h-Indole-5,6-Diol is a solid.",False
18279,"Nitrilotriacetic acid is a derivative of acetic acid, N(CH2COOH)3. It is a complexing (sequestering) agent that forms stable complexes with Zn2+. (From Miall's Dictionary of Chemistry, 5th ed.)",,,,Nitrilotriacetic acid is experimental.,Nitrilotriacetic acid is a solid.,True
18280,,,,,alpha-D-Fucopyranose is experimental.,alpha-D-Fucopyranose is a solid.,False
18281,,,,,(R)-Atenolol is experimental.,(R)-Atenolol is a solid.,False
18282,,,,,"1,4-Dioxane is experimental.","1,4-Dioxane is a solid.",False
18283,"Belimumab is an intravenous immunosupressant for the adjunctive treatment of systemic lupus erythematosus (SLE). More specifically, it is a fully human recombinant IgG1λ monoclonal antibody produced from a recombinant NS0 cell line stably transfected with the belimumab heavy chain and light chain genes. It is the first biological treatment approved for the indication of SLE. Concomitant use with live or inactivated vaccines must be avoided. Belimumab was FDA approved on March 9, 2011. Belimumab consists of 2 heavy chains, and 2 light chains of the lambda subclass. Each heavy chain contains 452 amino acid residues and each light chain contains 214 amino acid residues. There are 3 post-translational modifications: a conserved N-linked glycosylation on the CH2 domain at Asn 303 of the heavy chain, the conversion of the N-terminal glutamine residue of the heavy chain into pyroglutamate, and loss of C-terminal lysine residue of the heavy chain. Adjunct treatment for auto-antibody-positive active systemic lupus erythematosus (SLE). The intravenous injectable form is the only FDA approved treatment for pediatric patients with SLE. By the 52nd week of treatment with belimumab, a reduction in CD19+, CD20+, naive and activated B cells, plasma cells, plasmacytoid cells, and SLE B-cell subset can be observed. Reductions in plasma cells and SLE B-cell subset can be seen by the eighth week and these levels were maintained to week 52. Belimumab also reduced levels of IgG and anti-dsDNA. Belimumab selectively binds to soluble human B lymphocyte stimulator protein (BLyS) so that BLyS is unable to bind to receptors on B lymphocytes. The binding of BLyS to its receptor is essential for the survival of B lymphocytes. Consequently, belimumab reduces B-cell mediated immunity and the autoimmune response.",,,,Belimumab is approved.,Belimumab is a liquid.,True
18284,,,,,6-hydroxydopa quinone is experimental.,6-hydroxydopa quinone is a solid.,False
18285,,,,,Cis--Methanone is experimental.,Cis--Methanone is a solid.,False
18286,,,,,Cis--Piperazin-1-Yl-Methanone is experimental.,Cis--Piperazin-1-Yl-Methanone is a solid.,False
18287,,,,,Myxothiazol is experimental.,Myxothiazol is a solid.,False
18288,"Ruplizumab is a humanized monoclonal antibody used as an immunosuppressive drug and is a component of Antova. Investigated for use/treatment in thrombocytopenia, systemic lupus erythematosus, transplant (rejection), blood (blood forming organ disorders, unspecified), and multiple sclerosis. Ruplizumab is an anti-CD40L monoclonal antibody. The binding of CD40 to its ligand, CD40L, is a critical element in T cell activation. In systemic lupus erythematosus, CD40L is over-expressed on T cells, B cells, and monocytes.",,,,Ruplizumab is investigational.,Ruplizumab is a solid.,True
18289,,,,,cis-Vaccenic acid is experimental.,cis-Vaccenic acid is a solid.,False
18290,"KD3010 is a small molecule peroxisome proliferator-activator receptor delta (PPAR Delta) agonist for the treatment of metabolic disorders, including obesity. Investigated for use/treatment in metabolic disease and obesity. By activating PPAR Delta, which regulates lipid catabolism and energy utilization in peripheral tissues, KD3010 is designed to address the underlying metabolic derangement of these disorders. KD3010 results in significant reduction of central adiposity, atherogenic lipid profiles, and improved glucose utilization/insulin sensitivity. KD3010 is a potent, orally administered, peroxisome proliferator-activated receptor-delta (PPARδ) agonist that exhibits ~1000-fold selectivity over PPARγ and PPARα. PPARδ regulates lipid catabolism and energy utilization in peripheral tissues. Activation of PPARδ reduces central adiposity, improves atherogenic lipid profiles, and increases glucose utilization/insulin sensitivity.",,,,KD3010 is investigational.,KD3010 is a solid.,True
18291,,,,,(2S)-2-{3-carbonyl}amino)methyl]-4-methoxybenzyl}butanoic acid is experimental.,(2S)-2-{3-carbonyl}amino)methyl]-4-methoxybenzyl}butanoic acid is a solid.,False
18292,,,,,2-({carbonyl}amino)benzoic acid is experimental.,2-({carbonyl}amino)benzoic acid is a solid.,False
18293,,,,,{4-phenoxy}acetic acid is experimental.,{4-phenoxy}acetic acid is a solid.,False
18294,,,,,beta-D-Galactosamine is experimental.,beta-D-Galactosamine is a solid.,False
18295,,,,,Ferroheme C is experimental.,Ferroheme C is a solid.,False
18296,,,,,Protoporphyrin Ix Containing Zn is experimental.,Protoporphyrin Ix Containing Zn is a solid.,False
18297,,,,,Zinc Substituted Heme C is experimental.,Zinc Substituted Heme C is a solid.,False
18298,,,,,Bis-Napthyl Beta-Ketophosphonic Acid is experimental.,Bis-Napthyl Beta-Ketophosphonic Acid is a solid.,False
18299,,,,,2-Amino}Carbonyl)-2-Naphthyl]-1-(1-Naphthyl)-2-Oxoethylphosphonic Acid is experimental.,2-Amino}Carbonyl)-2-Naphthyl]-1-(1-Naphthyl)-2-Oxoethylphosphonic Acid is a solid.,False
18300,"Amibegron is an agonist for atypical beta3-adrenoceptors which inhibits intestinal motility. Investigated for use/treatment in depression, irritable bowel syndrome (IBS), and obesity. SR 58611 has positive chronotropic effect which is mainly of peripheral origin and can be attributed to a baroreceptor-mediated reflex due to the beta3-adrenoceptor mediated vasodilation with an increase in sympathetic tone and a reduction in vagal tone to the heart.",,,,Amibegron is investigational.,Amibegron is a solid.,True
18301,"Solabegron (GW-427,353) is a selective β3 adrenoceptor agonist being developed for the treatment of overactive bladder and irritable bowel syndrome. Investigated for use/treatment in diabetes mellitus type 2, irritable bowel syndrome (IBS), and urinary incontinence.",,,,Solabegron is investigational.,Solabegron is a solid.,True
18302,,,,,(3r)-1-Acetyl-3-Methylpiperidine is experimental.,(3r)-1-Acetyl-3-Methylpiperidine is a solid.,False
18303,,,,,Ethyl Oxo(Piperidin-1-Yl)Acetate is experimental.,Ethyl Oxo(Piperidin-1-Yl)Acetate is a solid.,False
18304,,,,,Sanglifehrin A is experimental.,Sanglifehrin A is a solid.,False
18305,,,,,"1,4-Dideoxy-O2-Sulfo-Glucuronic Acid is experimental.","1,4-Dideoxy-O2-Sulfo-Glucuronic Acid is a solid.",False
18306,,,,,"1,4-Dideoxy-5-Dehydro-O2-Sulfo-Glucuronic Acid is experimental.","1,4-Dideoxy-5-Dehydro-O2-Sulfo-Glucuronic Acid is a solid.",False
18307,,,,,Hydroxyfasudil is experimental.,Hydroxyfasudil is a solid.,False
18308,,,,,(S)-2-METHYL-1--HOMOPIPERAZINE is experimental.,(S)-2-METHYL-1--HOMOPIPERAZINE is a solid.,False
18309,Fasudil has been investigated in Carotid Stenosis.,The molecular weight is 291.37.,Fasudil has a topological polar surface area of 62.3.,The log p value of  is 1.04.,Fasudil is investigational.,Fasudil is a solid.,True
18310,Y-27632 is an inhibitor of Rho-associated protein kinase. It inhibits calcium sensitization to affect smooth muscle relaxation.,,,,Y-27632 is experimental.,Y-27632 is a solid.,True
18311,"Ripasudil, as hydrochloride hydrate (K-115), is a specifc Rho-associated coiled-coil containing protein kinase (ROCK) inhibitor used for the treatment of glaucoma and ocular hypertension. It was first approved for treatment in Japan in September 2014. This medication is available in the form of a 0.4% eye drop solution under the brand name Glanatec. Ripasudil is a well tolerated medication that is used when other drugs have been proven to be non-effective or cannot be administered. Ripasudil has been proven to be effective in the twice daily treatment of glaucoma and ocular hypertension. It is currently in studies to be approved for both diabetic retinopathy and diabetic macular oedema.  Ripasudil has high intraocular permeability and works by decreasing intraocular pressure (IOP) in a dose-dependent manner and increasing flow facility. The maximum reduction of IOP occurs after 1 to 2 hours. Ripasudil is a highly selective and potent Rho-associated coiled/coil-containing kinase protein (ROCK) inhibitor. Rho-kinase (ROCK) is an effector protein of Rho which binds with Rho to form a Rho/Rho-kinase complex. This complex then regulates many physiological functions including smooth muscle contractions, chemotaxis, neural growth and gene expression. ROCK comes in 2 isoforms: ROCK-1 and ROCK-2 and these two isoforms are distributed widely in our tissues including ocular tissues such as the iris, retina, trabecular meshwork and ciliary muscles. Atypical regulation of ROCK levels is involved in the pathogenesis of diseases such as glaucoma, ocular hypertension, cataracts and other retinal disorders.",The molecular weight is 323.39.,Ripasudil has a topological polar surface area of 62.3.,The log p value of  is 1.73.,Ripasudil is experimental.,Ripasudil is a solid.,True
18312,"Phenoxymethylpenicillin is a narrow spectrum antibiotic also commonly referred to as Penicillin V or Penicillin VK. It is a phenoxymethyl analog of Penicillin G, or. An orally active naturally penicillin, phenoxymethylpenicillin is used to treat mild to moderate infections in the respiratory tract, skin, and soft tissues caused by penicillin G­-sensitive microorganisms. Phenoxymethylpenicillin has also be used in some cases as prophylaxis against susceptible organisms. While there have been no controlled clinical efficacy studies that were conducted, phenoxymethylpenicillin has been suggested by the American Heart Association and the American Dental Association for use as an oral regimen for prophylaxis against bacterial endocarditis in patients with congenital heart disease or rheumatic or other acquired valvular heart disease when they undergo dental procedures and surgical procedures of the upper respiratory tract, except for those who are at an elevated risk for endocarditis. Indicated for the treatment of mild to moderately severe infections due to penicillin G­-sensitive microorganisms, with the use of bacteriological studies (including sensitivity tests) and clinical response.  Phenoxymethylpenicillin works against penicillin-sensitive microorganisms with bactericidal effects. It targets the bacteria during its active multiplication stage by interfering with bacterial cell wall peptidoglycan synthesis. _In vitro_, phenoxymethylpenicillin was shown to be active against staphylococci (except penicillinase-producing strains), streptococci (groups A, C, G, H, L and M), and pneumococci, as well as _Corynebacterium diphtheriae_, _Bacillus anthracis_, Clostridia, _Actinomyces bovis_, _Streptobacillus moniliformis_, _Listeria monocytogenes_, _Leptospira_, _Neisseria gonorrhoeae_, and _Treponema pallidum_. Phenoxymethylpenicillin inhibits the biosynthesis of cell wall mucopeptide by binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, which are critical in the cell wall synthesis and maintenance, as well as cell division. This disrupts the third and last stage of bacterial cell wall synthesis. This subsequently leads to cell lysis.",The molecular weight is 350.39.,Phenoxymethylpenicillin has a topological polar surface area of 95.94.,The log p value of  is 1.94.,Phenoxymethylpenicillin is approved and vet_approved.,Phenoxymethylpenicillin is a solid.,True
18313,"An antibiotic similar to used in resistant staphylococci infections. Used in the treatment of resistant staphylococci infections. Oxacillin is a penicillin beta-lactam antibiotic used in the treatment of bacterial infections caused by susceptible, usually gram-positive, organisms. The name \penicillin\"" can either refer to several variants of penicillin available, or to the group of antibiotics derived from the penicillins. Oxacillin has in vitro activity against gram-positive and gram-negative aerobic and anaerobic bacteria. The bactericidal activity of Oxacillin results from the inhibition of cell wall synthesis and is mediated through Oxacillin binding to penicillin binding proteins (PBPs). Oxacillin is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, and cephalosporinases and extended spectrum beta-lactamases."" By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, Oxacillin inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that Oxacillin interferes with an autolysin inhibitor.",The molecular weight is 401.44.,Oxacillin has a topological polar surface area of 112.74.,The log p value of  is 2.05.,Oxacillin is approved and investigational.,Oxacillin is a solid.,True
18314,"A fungistatic compound that is widely used as a food preservative. It is conjugated to GLYCINE in the liver and excreted as hippuric acid. As the sodium salt form, sodium benzoate is used as a treatment for urea cycle disorders due to its ability to bind amino acids. This leads to excretion of these amino acids and a decrease in ammonia levels. Recent research shows that sodium benzoate may be beneficial as an add-on therapy (1 gram/day) in schizophrenia. Total Positive and Negative Syndrome Scale scores dropped by 21% compared to placebo.",The molecular weight is 122.12.,Benzoic acid has a topological polar surface area of 37.3.,The log p value of  is 1.88.,Benzoic acid is approved and investigational.,Benzoic acid is a solid.,True
18315,,,,,4--1-methyl-4-(3-trifluoromethylphenyl)-1H-imidazol-2-yl]-piperidine is experimental.,4--1-methyl-4-(3-trifluoromethylphenyl)-1H-imidazol-2-yl]-piperidine is a solid.,False
18316,,,,,N--N'-(4-chlorophenyl)urea is experimental.,N--N'-(4-chlorophenyl)urea is a solid.,False
18317,,,,,"1-(2,6-Dichlorophenyl)-5-(2,4-Difluorophenyl)-7-Piperidin-4-Yl-3,4-Dihydroquinolin-2(1h)-One is experimental.","1-(2,6-Dichlorophenyl)-5-(2,4-Difluorophenyl)-7-Piperidin-4-Yl-3,4-Dihydroquinolin-2(1h)-One is a solid.",False
18318,"Inhibitor of P38 Kinase is a solid. This compound belongs to the indoles. These are compounds containing an indole moiety, which consists of a pyrrole ring fused to benzene to form 2,3-benzopyrrole. This drug is known to target mitogen-activated protein kinase 14.",,,,Inhibitor of P38 Kinase is experimental.,Inhibitor of P38 Kinase is a solid.,True
18319,,,,,6((S)-3-Benzylpiperazin-1-Yl)-3-(Naphthalen-2-Yl)-4-(Pyridin-4-Yl)Pyrazine is experimental.,6((S)-3-Benzylpiperazin-1-Yl)-3-(Naphthalen-2-Yl)-4-(Pyridin-4-Yl)Pyrazine is a solid.,False
18320,,,,,3-(4-Fluorophenyl)-1-Hydroxy-2-(Pyridin-4-Yl)-1h-PyrroloPyridine is experimental.,3-(4-Fluorophenyl)-1-Hydroxy-2-(Pyridin-4-Yl)-1h-PyrroloPyridine is a solid.,False
18321,,,,,1-(5-Tert-Butyl-2-Methyl-2h-Pyrazol-3-Yl)-3-(4-Chloro-Phenyl)-Urea is experimental.,1-(5-Tert-Butyl-2-Methyl-2h-Pyrazol-3-Yl)-3-(4-Chloro-Phenyl)-Urea is a solid.,False
18322,,,,,3-(Benzyloxy)Pyridin-2-Amine is experimental.,3-(Benzyloxy)Pyridin-2-Amine is a solid.,False
18323,,,,,"1-(2,6-Dichlorophenyl)-5-(2,4-Difluorophenyl)-7-Piperazin-1-Yl-3,4-Dihydroquinazolin-2(1h)-One is experimental.","1-(2,6-Dichlorophenyl)-5-(2,4-Difluorophenyl)-7-Piperazin-1-Yl-3,4-Dihydroquinazolin-2(1h)-One is a solid.",False
18324,,,,,"4--6,7-Dimethoxyquinazoline is experimental.","4--6,7-Dimethoxyquinazoline is a solid.",False
18325,Doramapimod is a P38 MAP kinase inhibitor.,,,,Doramapimod is investigational.,Doramapimod is a solid.,True
18326,,,,,2-Chlorophenol is experimental.,2-Chlorophenol is a solid.,False
18327,,,,,4-(Fluorophenyl)-1-Cyclopropylmethyl-5-(2-Amino-4-Pyrimidinyl)Imidazole is experimental.,4-(Fluorophenyl)-1-Cyclopropylmethyl-5-(2-Amino-4-Pyrimidinyl)Imidazole is a solid.,False
18328,,,,,4-(2-HYDROXYBENZYLAMINO)-N-(3-(4-FLUOROPHENOXY)PHENYL)PIPERIDINE-1-SULFONAMIDE is experimental.,4-(2-HYDROXYBENZYLAMINO)-N-(3-(4-FLUOROPHENOXY)PHENYL)PIPERIDINE-1-SULFONAMIDE is a solid.,False
18329,,,,,Triazolopyridine is experimental.,Triazolopyridine is a solid.,False
18330,"KC706 is a novel anti-inflammatory drug that works by inhibiting the activity of p38 MAP kinase. KC706 holds potential to treat inflammatory conditions such as rheumatoid arthritis, psoriasis, inflammatory bowel disease and cardiovascular disease. Investigated for use/treatment in cardiovascular disorders, inflammatory bowel disease, inflammatory disorders (unspecified), psoriasis and psoriatic disorders, and rheumatoid arthritis. KC706 has been demonstrated to be truly disease-modifying: it stops the destruction of joint tissue that is the underlying disease pathology in rheumatoid arthritis. KC706 is a novel anti-inflammatory drug that works by inhibiting the activity of p38 MAP kinase. p38 MAP kinase is a key component of the signaling pathway that regulates the body's production of inflammatory mediators, including TNFα and IL-1 beta. It has been demonstrated to be truly disease-modifying: it stops the destruction of joint tissue that is the underlying disease pathology in rheumatoid arthritis.",,,,KC706 is investigational.,KC706 is a solid.,True
18331,Investigated for use/treatment in rheumatoid arthritis.,,,,R-1487 is investigational.,R-1487 is a solid.,True
18332,"N-ethyl-4-{amino}-5-methylpyrrolotriazine-6-carboxamide is a solid. This compound belongs to the pyrrolotriazines. These are compounds containing a pyrrolotriazine moiety, which consists of a pyrrole ring fused to a triazine ring. N-ethyl-4-{amino}-5-methylpyrrolotriazine-6-carboxamide is known to target mitogen-activated protein kinase 14.",,,,N-ethyl-4-{amino}-5-methylpyrrolotriazine-6-carboxamide is experimental.,N-ethyl-4-{amino}-5-methylpyrrolotriazine-6-carboxamide is a solid.,True
18333,,,,,"N--2-{amino}-1,3-thiazole-5-carboxamide is experimental.","N--2-{amino}-1,3-thiazole-5-carboxamide is a solid.",False
18334,Neflamapimod has been used in trials studying the treatment of Alzheimer's Disease and Mild Cognitive Impairment.,,,,Neflamapimod is investigational.,Neflamapimod is a solid.,True
18335,,,,,N-cyclopropyl-4-methyl-3-benzamide is experimental.,N-cyclopropyl-4-methyl-3-benzamide is a solid.,False
18336,,,,,4-PHENOXY-N-(PYRIDIN-2-YLMETHYL)BENZAMIDE is experimental.,4-PHENOXY-N-(PYRIDIN-2-YLMETHYL)BENZAMIDE is a solid.,False
18337,,,,,4--PYRIDINE is experimental.,4--PYRIDINE is a solid.,False
18338,,,,,"N-cyclopropyl-2',6-dimethyl-4'-(5-methyl-1,3,4-oxadiazol-2-yl)biphenyl-3-carboxamide is experimental.","N-cyclopropyl-2',6-dimethyl-4'-(5-methyl-1,3,4-oxadiazol-2-yl)biphenyl-3-carboxamide is a solid.",False
18339,,,,,4-PYRIDINE is experimental.,4-PYRIDINE is a solid.,False
18340,,,,,"4-{4-quinolin-7-yl}-1,3-thiazole-2-carbaldehyde is experimental.","4-{4-quinolin-7-yl}-1,3-thiazole-2-carbaldehyde is a solid.",False
18341,,,,,"N-(3-cyanophenyl)-2'-methyl-5'-(5-methyl-1,3,4-oxadiazol-2-yl)-4-biphenylcarboxamide is experimental.","N-(3-cyanophenyl)-2'-methyl-5'-(5-methyl-1,3,4-oxadiazol-2-yl)-4-biphenylcarboxamide is a solid.",False
18342,,,,,"N-(cyclopropylmethyl)-2'-methyl-5'-(5-methyl-1,3,4-oxadiazol-2-yl)biphenyl-4-carboxamide is experimental.","N-(cyclopropylmethyl)-2'-methyl-5'-(5-methyl-1,3,4-oxadiazol-2-yl)biphenyl-4-carboxamide is a solid.",False
18343,,,,,"N~3~-cyclopropyl-N~4~'-(cyclopropylmethyl)-6-methylbiphenyl-3,4'-dicarboxamide is experimental.","N~3~-cyclopropyl-N~4~'-(cyclopropylmethyl)-6-methylbiphenyl-3,4'-dicarboxamide is a solid.",False
18344,PH-797804 has been investigated for the treatment of Osteoarthritis.,,,,PH-797804 is investigational.,PH-797804 is a solid.,True
18345,,,,,2-fluoro-4-pyridine is experimental.,2-fluoro-4-pyridine is a solid.,False
18346,,,,,SD-0006 is investigational.,SD-0006 is a solid.,False
18347,,,,,N-(3-TERT-BUTYL-1H-PYRAZOL-5-YL)-N'-{4-CHLORO-3-PHENYL}UREA is experimental.,N-(3-TERT-BUTYL-1H-PYRAZOL-5-YL)-N'-{4-CHLORO-3-PHENYL}UREA is a solid.,False
18348,,,,,N--3-FLUORO- is experimental.,N--3-FLUORO- is a solid.,False
18349,,,,,3-FLUORO-5-MORPHOLIN-4-YL-N-BENZAMIDE is experimental.,3-FLUORO-5-MORPHOLIN-4-YL-N-BENZAMIDE is a solid.,False
18350,3-fluoro-N-1H-indol-5-yl-5-morpholin-4-ylbenzamide is a solid. This compound belongs to the phenylmorpholines. These are aromatic compounds containing a morpholine ring and a benzene ring linked to each other through a CC or a CN bond. This drug targets mitogen-activated protein kinase 14.,,,,3-fluoro-N-1H-indol-5-yl-5-morpholin-4-ylbenzamide is experimental.,3-fluoro-N-1H-indol-5-yl-5-morpholin-4-ylbenzamide is a solid.,True
18351,,,,,3-(1-NAPHTHYLMETHOXY)PYRIDIN-2-AMINE is experimental.,3-(1-NAPHTHYLMETHOXY)PYRIDIN-2-AMINE is a solid.,False
18352,,,,,3-(2-CHLOROPHENYL)-1-(2-{AMINO}PYRIMIDIN-4-YL)-1-(4-METHOXYPHENYL)UREA is experimental.,3-(2-CHLOROPHENYL)-1-(2-{AMINO}PYRIMIDIN-4-YL)-1-(4-METHOXYPHENYL)UREA is a solid.,False
18353,,,,,"8-(2-CHLOROPHENYLAMINO)-2-(2,6-DIFLUOROPHENYLAMINO)-9-ETHYL-9H-PURINE-1,7-DIIUM is experimental.","8-(2-CHLOROPHENYLAMINO)-2-(2,6-DIFLUOROPHENYLAMINO)-9-ETHYL-9H-PURINE-1,7-DIIUM is a solid.",False
18354,,,,,"2-(2,6-DIFLUOROPHENOXY)-N-(2-FLUOROPHENYL)-9-ISOPROPYL-9H-PURIN-8-AMINE is experimental.","2-(2,6-DIFLUOROPHENOXY)-N-(2-FLUOROPHENYL)-9-ISOPROPYL-9H-PURIN-8-AMINE is a solid.",False
18355,,,,,"N,4-dimethyl-3-pyrimidin-4-yl)amino]benzamide is experimental.","N,4-dimethyl-3-pyrimidin-4-yl)amino]benzamide is a solid.",False
18356,,,,,N-cyclopropyl-3-{pyridin-4-yl]amino}-4-methylbenzamide is experimental.,N-cyclopropyl-3-{pyridin-4-yl]amino}-4-methylbenzamide is a solid.,False
18357,,,,,N-cyclopropyl-4-methyl-3-{2-quinazolin-6-yl}benzamide is experimental.,N-cyclopropyl-4-methyl-3-{2-quinazolin-6-yl}benzamide is a solid.,False
18358,,,,,"6--N-(1-methylethyl)-1,3-benzothiazol-2-amine is experimental.","6--N-(1-methylethyl)-1,3-benzothiazol-2-amine is a solid.",False
18359,,,,,2-(ETHOXYMETHYL)-4-(4-FLUOROPHENYL)-3-ISOXAZOL-5(2H)-ONE is experimental.,2-(ETHOXYMETHYL)-4-(4-FLUOROPHENYL)-3-ISOXAZOL-5(2H)-ONE is a solid.,False
18360,,,,,METHANONE is experimental.,METHANONE is a solid.,False
18361,,,,,(3-{OXY}PHENYL)METHANONE is experimental.,(3-{OXY}PHENYL)METHANONE is a solid.,False
18362,,,,,4-(4-FLUOROPHENYL)-1-CYCLOROPROPYLMETHYL-5-(4-PYRIDYL)-IMIDAZOLE is experimental.,4-(4-FLUOROPHENYL)-1-CYCLOROPROPYLMETHYL-5-(4-PYRIDYL)-IMIDAZOLE is a solid.,False
18363,,,,,3-FLUORO-5-MORPHOLIN-4-YL-N-BENZAMIDE is experimental.,3-FLUORO-5-MORPHOLIN-4-YL-N-BENZAMIDE is a solid.,False
18364,,,,,3-Hydroxypropyl 3-benzenesulfonate is experimental.,3-Hydroxypropyl 3-benzenesulfonate is a solid.,False
18365,,,,,(1R)-2--1-{4-phenyl}ethyl nicotinate is experimental.,(1R)-2--1-{4-phenyl}ethyl nicotinate is a solid.,False
18366,,,,,"(R)-1-(4-(4-(Hydroxymethyl)-1,3,2-dioxaborolan-2-YL)phenethyl)guanidine is experimental.","(R)-1-(4-(4-(Hydroxymethyl)-1,3,2-dioxaborolan-2-YL)phenethyl)guanidine is a solid.",False
18367,,,,,6-CARBAMIMIDOYL-4-(3-HYDROXY-2-METHYL-BENZOYLAMINO)-NAPHTHALENE-2-CARBOXYLIC ACID METHYL ESTER is experimental.,6-CARBAMIMIDOYL-4-(3-HYDROXY-2-METHYL-BENZOYLAMINO)-NAPHTHALENE-2-CARBOXYLIC ACID METHYL ESTER is a solid.,False
18368,,,,,"(R)-1-(4-(4-(Hydroxymethyl)-1,3,2-dioxaborolan-2-YL)phenyl)guanidine is experimental.","(R)-1-(4-(4-(Hydroxymethyl)-1,3,2-dioxaborolan-2-YL)phenyl)guanidine is a solid.",False
18369,,,,,N-(7-CARBAMIMIDOYL-NAPHTHALEN-1-YL)-3-HYDROXY-2-METHYL-BENZAMIDE is experimental.,N-(7-CARBAMIMIDOYL-NAPHTHALEN-1-YL)-3-HYDROXY-2-METHYL-BENZAMIDE is a solid.,False
18370,,,,,4-METHYL-PENTANOIC ACID {1--2-METHYL-PROPYL}-AMIDE is experimental.,4-METHYL-PENTANOIC ACID {1--2-METHYL-PROPYL}-AMIDE is a solid.,False
18371,,,,,"(R)-1-(4-(4-(hydroxymethyl)-1,3,2-dioxaborolan-2-yl)benzyl)guanidine is experimental.","(R)-1-(4-(4-(hydroxymethyl)-1,3,2-dioxaborolan-2-yl)benzyl)guanidine is a solid.",False
18372,"A bicyclic monoterpene ketone found widely in plants, especially cinnamomum camphora. It is used topically as a skin antipruritic and as an anti-infective agent.",,,,Camphor is approved.,Camphor is a solid.,True
18373,"Resiniferatoxin (RTX) is a naturally occurring, ultrapotent capsaicin analog that activates the vanilloid receptor in a subpopulation of primary afferent sensory neurons involved in nociception (the transmission of physiological pain). Investigated for use/treatment in interstitial cystitis and urinary incontinence.",,,,Resiniferatoxin is investigational.,Resiniferatoxin is a solid.,True
18374,"Capsicum oleoresin is an oily organic resin derived from the fruit of plants in the Capsicum genus, such as chilli peppers. When the plants are finely ground, capsicum oleoresin is formed after the extraction process of capsaicin using oragnic solvents such as ethanol. It is commonly used as a culinary spice. The intensity of biological actions and toxicological effects of capsicum oleoresin are a direct function of the amount of capsaicinoids, or capsaicin, present in the compound. Capsaicinoids comprise of a group of fat-soluble pungent chemical phenols and include , dihydrocapsaicin, nordihydrocapsaicin, homocapsaicin, and homodihydrocapsaicin. and dihydrocapsaicin are the most pungent capsaicinoid analogues. Indicated for the temporary relief of minor aches and pains of muscles and joints associated with simple backache, arthritis, strains and sprains.  Capsicum oleoresin is a topical analgesic and inflammatory agent. Capsaicin, an active ingredient in capsicum oleoresin, causes pain and sensitization of both peripheral and central nerves. It induces primary and secondary hyperalgesia and mimics the symptoms associated with neuropathic pain, such as allodynia, secondary hyperalgesia, referred pain area, and viscerovisceral hyperalgesia. In opposition, capsaicin also mediates analgesic actions via desensitization and withdrawal of epidermal nerve fibers. Systemic reviews of capsaicin-containing topical formulations demonstrate clinical effectiveness for pain reduction in postherpetic neuralgia, postsurgical neuropathies, and diabetic neuropathy, compared to placebo. Capsaicin is the active ingredient in capsicum oleoresin that confers the molecule its biological actions. It induces central sensitization to cause pain and depolarizes nociceptors to increases their cytosolic free Ca2+ concentration. It is a highly selective agonist and activator at the transient receptor potential vanilloid subfamily member 1 (TRPV1) receptors expressed in afferent neuronal C fibers and some Aδ fibers. The aliphatic tail of capsaicin interacts with the channel via nonspecific Van der Waals forces, while hydrogen bonds between its vanillyl “head” and amide “neck” with residues of glutamic acid E571 and T551 of the channel, respectively, confers specificity for ligand binding. Binding and local activation of these receptors lead to increased influx of calcium ions and nerve depolarization. Signal propagation to the central nervous system causes local heat, stinging, and/or itching sensations. Prolonged activation of TRPV1 receptors results in loss of receptor functionality, causing impaired local nociception for extended periods due to desensitization and inactivation of sensory neurons. It is thought that the activation of TRPV1 receptors is the main mechanism of action of capsaicin. Capsaicin also induces a local depletion of substance P, which is a neuropeptide involved in visceral pain signalling ; however this effect in the relief of pain remains controversial. ",,,,Capsicum oleoresin is approved.,Capsicum oleoresin is a liquid.,True
18375,"Nonivamide is found in herbs and spices. It is an alkaloid from the Capsicum species. The structures of and nonivamide differ only slightly with respect to the fatty acid moiety of the side chain (8-methyl nonenoic acid versus nonanoic acid).  Nonivamide is used as a topical analgesic and is also used as a flavoring ingredient , ,.  Relieves minor aches and pains of muscles and joints ,. Nonivamide is a naturally occurring analog of , isolated from peppers, described to produce effects similar to. It is an agonist of the VR1 (vanilloid/TRPV1 receptor). It serves as a transient agonist of these receptors, which are potentiated by pro-inflammatory drugs, a phenomenon that leads to thermal hyperalgesia, or increased heat sensation.",,,,Nonivamide is investigational.,,True
18376,"(S)-camphor, or L(-)-Camphor, is a stereoisomer of , a bicyclic monoterpene known to potentiate both heat and cold sensations. (S)-camphor is not the naturally-occurring stereoisomer but displays similar TRPV channel affinity and current inhibition. is isolated from the wood of the camphor laurel tree, _Cinnamomum camphora_, and had a long history of medicinal use. It has been used as a nasal decongestant and cough suppressant, and has been topically applied due to its antipruritic, analgesic, and counterirritant properties. Camphor is a major active ingredient in over-the-counter balms and liniments supplied as topical analgesics by causing sensitization to heat and coolness to relieve minor muscle and joint pain. Indicated for the temporary symptomatic relief of minor aches and pains of muscles and joints in topical analgesics.  Camphor exerts an analgesic action when applied topically by producing a warm sensation. It excites and desensitizes sensory nerves by activating heat-sensitive TRP vanilloid subtype 1 (TRPV1) and TRPV3 receptors. (S)-camphor is reported to exert a weaker action on TRPV1 channels, which is thought to be a result of tachyphylaxis, which is the reduction of the response to multiple stimulations.  TRPV3 cation channels are molecular sensors that play a role in nociception and thermosensation by inducing thermal sensation and heat-induced hyperalgesia. Camphor interacts with TRPV3 channels via pore-region cysteine residues , leading to channel activation and a rise in intracellular calcium levels. Camphor also activates TRPV1 and a TRPV1-like current in dorsal root ganglion (DRG) neurons but inhibits the ankyrin-repeat TRP 1 (TRPA1) channel expressed in most nociceptive DRG neurons, which is responsible for the detection of temperature. The precise role of TRPA1 current inhibition on the analgesic properties of camphor is unclear. Repeated stimulation by camphor leads to sensitization of the TRPV1 and TRPV3 channels, resulting in desensitization, or reduced channel response that likely leads to the analgesic effects of camphor. Camphor also activates cold-sensitive transient receptor potential melastatin 8 (TRPM8) and sensitizes cold-induced calcium transients, which explains the cooling effect of camphor following dermal application. Additionally, camphor was shown to inhibit the TRPM8 receptor response to menthol.",,,,(S)-camphor is experimental.,(S)-camphor is a solid.,True
18377,"Cannabidivarin, also known as cannabidivarol or CBDV, is a non-psychoactive cannabinoid found within. It is one of over 100 cannabinoids identified from the Cannabis plant that can modulate the physiological activity of cannabis, or marijuana. Compared to its homolog, , CBDV is shortened by two methyl (CH2) groups on its side chain. Notably, both and CBDV have demonstrated anticonvulsant activity in animal and human models and are demonstrating promising clinical trial results. Other cannabinoids with some evidence of anti-epileptic activity include (THCV) and Δ9-tetrahydrocannabinolic acid. Cannabidivarin does not currently have any FDA or Health Canada approved indications, however in October 2017 CBDV was given orphan designation by the European Medicines Agency for use in Rett Syndrome and again in February 2018 for treatment of Fragile X Syndrome. The anti-epileptic activity of CBD and CBDV is thought to be modulated by their effects on transient receptor potential cation channel subfamily V member 1 (TRPV1), also known as the capsaicin receptor, which is part of a large family of ion channels that are involved in the onset and progression of several types of epilepsy. CBD and CBDV have been shown to dose-dependently activate and then desensitize TRPV1 as well as TRPV2 and TRPA1 channels. Desensitization of these ion channels is a potential mechanism by which these molecules cause a reduction of neuronal hyperexcitability that contributes to epileptic activity and seizures. ",,,,Cannabidivarin is investigational.,Cannabidivarin is a solid.,True
18378,"Aluminium monostearate is a salt of stearic acid and aluminium with the molecular formula Al(OH)2C18H35O2. Also known as dihydroxyaluminium or dihydroxy(stearato)aluminium, it is used to form gels in the packaging of pharmaceuticals and in the preparation of colors for cosmetics. While considered safe for use, extensive usage may result in aluminum accumulation. Antacids perform a neutralization reaction, ie. they buffer gastric acid, raising the pH to reduce acidity in the stomach. When gastric hydrochloric acid reaches the nerves in the gasitrointestinal mucosa, they signal pain to the central nervous system. This happens when these nerves are exposed, as in peptic ulcers. The gastric acid may also reach ulcers in the esophagus or the duodenum. Other mechanisms may contribute, such as the effect of aluminum ions inhibiting smooth muscle cell contraction and delaying gastric emptying. Aluminum is known to bind troponin C (a muscle protein) and to interfere with voltage-dependent calcium transport. Aluminum also binds to and inhibits the activity of mitochondrial voltage gated channels (VDAC).",,,,Aluminium monostearate is experimental.,Aluminium monostearate is a solid.,True
18379,,,,,"5--6-Methyl-3,6-Dihydro-Thiadiazin-2-One is experimental.","5--6-Methyl-3,6-Dihydro-Thiadiazin-2-One is a solid.",False
18380,"ARC1779 is a therapeutic aptamer antagonist of the A1 domain of von Willebrand Factor (vWF), the ligand for receptor glycoprotein 1b on platelets. ARC1779 is being developed as a novel antithrombotic agent for use in patients with acute coronary syndromes. ARC1779 is a therapeutic oligonucleotide (\aptamer\"") which blocks the binding of the A1 domain of vWF to the platelet GPIb receptor, and thereby modulates platelet adhesion, activation, and aggregation under the high shear conditions of coronary arterial stenosis and plaque rupture."" Platelet aggregation, thrombosis and acute coronary syndromes ARC1779 can inhibit vWF activation and platelet function, which are both widely recognized as playing critical roles in clot formation which can critically impede blood flow to the heart. ",,,,Egaptivon pegol is investigational.,Egaptivon pegol is a solid.,True
18381,"Liposome-encapsulated form of prostaglandin E1 (Liprostin) is known to be a potent vasodilator and platelet inhibitor as well as an anti-inflammatory and anti-thrombotic agent. The liposomal formulation of PGE-1 changes the drug’s dynamics and improve its therapeutic index in ways that PGE-1 alone could not achieve. Investigated for use/treatment in neuropathy (diabetic) and peripheral vascular disease. The encapsulated formulation (Liprostin) has been shown to improve the therapeutic index of PGE-1, positively impacting many areas of treatment, such as heart attacks, occlusive disease, ischemic ulcers, critical limb salvage, claudicants, and arthritis.",,,,liposomal prostaglandin E1 is investigational.,liposomal prostaglandin E1 is a solid.,True
18382,,,,,2-aminoisobutyric acid is experimental.,2-aminoisobutyric acid is a solid.,False
18383,,,,,SP4160 is experimental.,SP4160 is a solid.,False
18384,,,,,"N(2)-carbamimidoyl-N-{2--2,3-dichlorophenyl}-1-methyl-1H-pyrazol-5-yl)piperidin-1-yl]-2-oxoethyl}-D-leucinamide is experimental.","N(2)-carbamimidoyl-N-{2--2,3-dichlorophenyl}-1-methyl-1H-pyrazol-5-yl)piperidin-1-yl]-2-oxoethyl}-D-leucinamide is a solid.",False
18385,,,,,"3-Mercapto-1-(1,3,4,9-Tetrahydro-B-Carbolin-2-Yl)-Propan-1-One is experimental.","3-Mercapto-1-(1,3,4,9-Tetrahydro-B-Carbolin-2-Yl)-Propan-1-One is a solid.",False
18386,"This solid compound belongs to the stilbenes. These are organic compounds containing a 1,2-diphenylethylene moiety. Stilbenes (C6-C2-C6 ) are derived from the common phenylpropene (C6-C3) skeleton building block. The introduction of one or more hydroxyl groups to a phenyl ring lead to stilbenoids. This substance targets the protein interleukin-2.",,,,Methyl (2S)-2-acetyl]amino]-3-propanoate is experimental.,Methyl (2S)-2-acetyl]amino]-3-propanoate is a solid.,True
18387,(1H-indol-3-yl)-(2-mercapto-ethoxyimino)-acetic acid is a solid. This compound belongs to the indole-3-acetic acid derivatives. These are compounds containing an acetic acid (or a derivative) linked to the C3 carbon atom of an indole. (1H-indol-3-yl)-(2-mercapto-ethoxyimino)-acetic acid is known to target interleukin-2.,,,,(1H-indol-3-yl)-(2-mercapto-ethoxyimino)-acetic acid is experimental.,(1H-indol-3-yl)-(2-mercapto-ethoxyimino)-acetic acid is a solid.,True
18388,,,,,SP2456 is experimental.,SP2456 is a solid.,False
18389,,,,,2--N-(3-mercapto-propyl)-propionamide is experimental.,2--N-(3-mercapto-propyl)-propionamide is a solid.,False
18390,"keyhole limpet hemocyanin is an immune modulators, given as a vaccine to help the body respond to cancer. A natural protein isolated from the marine mollusc keyhole limpet. Keyhole limpet hemocyanin is an immunogenic carrier protein that, in vivo, increases antigenic immune responses to haptens and other weak antigens such as idiotype proteins. Investigated for use/treatment in bladder cancer and solid tumors. Keyhole Limpet Hemocyanin (KLH) is generally a very efficient coupling agent. It is the most common carrier protein used in the preparation of hapten conjugates. KLH is composed of five subunits. It is lysine rich with a large number of available primary amines to facilitate conjugation, antibody production and promote peptide attachment after dissociation.",,,,keyhole limpet hemocyanin is approved and investigational.,keyhole limpet hemocyanin is a liquid.,True
18391,"Girentuximab is a monoclonal chimeric (mouse/human) antibody directed against carbonic anhydrase IX, an antigen expressed in 95% of clear cell renal cell carcinomas (RCC). Investigated for use/treatment in gall bladder cancer and renal cell carcinoma. Mechanism of action of girentuximab is antibody dependent cellular cytotoxicity (ADCC). As a monotherapy in metastatic renal cell carcinomas(RCC), girentuximab demonstrated minimal clinical activity with a 3% partial response rate and a median survival of 16 months. In vitro data suggest that the number of activated ADCC effector cells can be upregulated by low dose interleukin 2 (IL2) administered in a pulsatile fashion.",,,,Girentuximab is investigational.,Girentuximab is a solid.,True
18392,"A bivalent cancer vaccine comprised of a modified vaccinia virus Ankara (MVA) strain encoding human mucin 1 (MUC1) and interleukin-2 (IL-2) with potential immunostimulating and antineoplastic activities. Originally developed for the eradication of smallpox, MVA is a highly attenuated and replication-defective strain incapable of virion assembly and exerts potent immunostimulatory activity against antigens. Vaccination with MVA-MUC1-IL2 vaccine may stimulate the host immune system to mount a humoral and cytotoxic T lymphocyte (CTL) responses against tumor cells expressing MUC1, a tumor associated antigen, resulting in tumor cell lysis. Expression of IL-2 augments the specific CTL response against MUC1 expressing cells.  Investigated for use/treatment in breast cancer, renal cell carcinoma, prostate cancer, and lung cancer.",,,,TG4010 is investigational.,TG4010 is a solid.,True
18393,"Voacamine is an alkaloid isolated from the bark of the _Pescheria fuchsiae folia_ tree. It is an antimalarial drug approved for use in several African countries. Voacamine is also under investigation for use in modulating multidrug-resistance in tumor cells. For the treatment of malaria. Also under investigation for the modulation of multidrug resistance in cancer cells. Voacamine is an anti-malarial extracted from the Brazilian tree <i>Peschiera fuchsiaefolia</i>. In one study (PMID: 11180519), the in vivo antiplasmodial activity of voacamine was assessed in a 4-day test. It was shown to exhibit in vivo activity with 25.4% and 43.4% inhibition of parasitaemia with 2.5 and 10 mg/kg, respectively. In synchronized cultures, it was found to act on trophozoite and schizont stages of <i>Plasmodium falciparum</i>. Voacamine is possibly a substrate for P-glycoprotein (P-gp), an efflux pump responsible for multidrug resistance in tumor cells. Voacamine may compete with anticancer drugs such as doxorubicin for P-gp transport, decreasing removal of doxorubicin. ",The molecular weight is 704.91.,Voacamine has a topological polar surface area of 99.89.,The log p value of  is 7.17.,Voacamine is experimental.,Voacamine is a solid.,True
18394,"Elacridar (GW120918) is an oral bioenhancer that targets multiple drug resistance in tumors. In many cases, the appearance of multidrug resistance in cancer is due to a change in expression of protein inhibitors. As of August 2007 elacridar was not listed on GSK's product pipeline. Development is assumed to have been discontinued. For the treatment of solid tumors. Elacridar is an oral bioenhancer that targets multiple drug resistance in tumors. In many cases, the appearance of multidrug resistance in cancer is due to a change in expression of protein inhibitors. P-glycoprotein is a well characterized human ABC-transporter of the MDR/TAP subfamily. It is an ATP-dependent efflux pump with broad substrate specificity. It likely evolved as a defence mechanism against harmful substances. Increased intestinal expression of P-glycoprotein can reduce the absorption of drugs that are substrates for P-glycoprotein. Thus, there is a reduced bioavailability, therapeutic plasma concentrations are not attained. Elacridar functions by inhibiting P-glycoprotein, resulting in an increased bioavailability of coadminstered drugs.",,,,Elacridar is investigational.,Elacridar is a solid.,True
18395,"FM-VP4, is a novel hydrophilic phytostanol analogue representing a new class in cholesterol-lowering drugs called cholesterol absorption inhibitors. FM-VP4 has been shown to inhibit cholesterol absorption and to lower plasma LDL-cholesterol and total cholesterol in a broad range of animal species. Additional experiments suggest that FM-VP4 can reduce plasma LDL cholesterol levels and triglyceride levels, reduce weight gain and exert a anti-atherosclerosis effect. Investigated for use/treatment in hyperlipidemia and cancer/tumors (unspecified). FM VP4 is thought to bind competitively with cholesterol to MDR1 resulting in a synergistic decrease in cholesterol accumlation. Others have suggested that FM VP4 may act by inhibiting a transporter that mediates intestinal absorption of cholesterol.  FM VP4 is thought to bind competitively with cholesterol to MDR1 resulting in a synergistic decrease in cholesterol accumlation. Others have suggested that FM VP4 may act by inhibiting a transporter that mediates intestinal absorption of cholesterol.",,,,FM-VP4 is investigational.,FM-VP4 is a solid.,True
18396,"Zosuquidar is a compound of antineoplastic drug candidates currently under development. It is now in \Phase 3\"" of clinical tests in the United States. Its action mechanism consists of the inhibition of P-glycoproteins; other drugs with this mechanism include tariquidar and laniquidar."" Investigated for use/treatment in leukemia (myeloid) and myelodysplastic syndrome. P-glycoproteins are proteins which convert the energy derived from the hydrolysis of ATP to structural changes in protein molecules, in order to perform coupling, thus discharging medicine from cells. If P-glycoprotein coded with the MDR1 gene manifests itself in cancer cells, it discharges much of the antineoplastic drugs from the cells, making cancer cells medicine tolerant, and rendering antineoplastic drugs ineffective. This protein also manifests itself in normal organs not affected by the cancer (such as the liver, small intestine, and skin cells in blood vessels of the brain), and participates in the transportation of medicine. The compound Zosuquidar inhibits this P-glycoprotein, causing the cancer cells to lose their medicine tolerance, and making antineoplastic drugs effective.",,,,Zosuquidar is investigational.,Zosuquidar is a solid.,True
18397,"Investigated for use/treatment in ovarian cancer, lung cancer, and breast cancer. Tariquidar is an anthranilic acid derivative third generation P-glycoprotein (P-gp) inhibitors. P-gp is a transport protein found in normal cells that has many trasport and modulatory functions, from affecting the distribution and bioavailability of drugs to mediating the migration of dendritic cells. P-gp is responsible for multidrug resistance through transport of anti-cancer drugs out of their target cells. It is proposed that tariquidar's  and its derivatives may bind to the H-binding site of P-gp through multiple mechanisms of binding.",,,,Tariquidar is investigational.,Tariquidar is a solid.,True
18398,"Potentially toxic, but effective antischistosomal agent, it is a metabolite of LUCANTHONE. Hycanthone was approved by the FDA in 1975 but is no longer used.",The molecular weight is 356.48.,Hycanthone has a topological polar surface area of 52.57.,The log p value of  is 3.66.,Hycanthone is experimental.,Hycanthone is a solid.,True
18399,Concanamycin A is an H+-ATPase (vacuolar) inhibitor.,,,,Concanamycin A is experimental.,Concanamycin A is a solid.,True
18400,Dofequidar is an antineoplastic agent.,,,,Dofequidar is experimental and investigational.,Dofequidar is a solid.,True
18401,"ONT-093 is an orally bioavailable inhibitor of P-glycoprotein (P-gp). In pre-clinical studies, ONT-093 could inhibit P-gp and reverse multidrug resistance at nM concentrations with no effect on paclitaxel pharmacokinetics.",,,,ONT-093 is investigational.,ONT-093 is a solid.,True
18402,,,,,HM-30181 is experimental.,HM-30181 is a solid.,False
18403,Desmethylsertraline is a metabolite of sertraline.,,,,Desmethylsertraline is experimental.,Desmethylsertraline is a solid.,True
18404,Reversin 121 is a hydrophobic peptide chemosensitizer that can reverse P-glycoprotein-mediated multidrug resistance.,,,,Reversin 121 is experimental.,Reversin 121 is a solid.,True
18405,A guanine nucleotide containing two phosphate groups esterified to the sugar moiety. ,,,,Guanosine-5'-Diphosphate is experimental.,Guanosine-5'-Diphosphate is a solid.,True
18406,"Tagraxofusp is an IL-3 conjugated truncated diphtheria toxin. It is composed by the catalytic and translocation domains of diphtheria toxin fused via Met-His linker to a full-length human IL-3. Tagraxofusp was developed by Stemline Therapeutics Inc and FDA approved on December 21, 2018, as the first therapy for blastic plasmacytoid dendritic cell neoplasm. This drug achieved approval after being designated with the title of breakthrough therapy, priority review, and orphan drug status. Tagraxofusp has been designated as an orphan drug in the EU since November 2015. Tagraxofusp is indicated for the treatment of blastic plasmacytoid dendritic cell neoplasm (BPDCN) in adults and pediatric patients over 2 years old. This treatment allows an alternative for the previous intense treatment which consisted of intensive chemotherapy followed by bone marrow transplantation. In vitro studies showed that BPDCN blasts are ultrasensitive to tagraxofusp by presenting IC50 values in the femtomolar scale. One of the main physiological changes of BPDCN is the presence of elevated interferon alpha and to produce an inflammatory response. In trials with tagraxofusp and following cell depletion, there was observed a significant reduction in the levels of interferon alpha and interleukin 6. Tagraxofusp binds to cells expressing the IL-3 receptor and delivers in them the diphtheria toxin after binding. This is very useful as the malignant cells in BPDCN present a particularly high expression of IL-3 receptor (CD123+ pDC). To be more specific, tagraxofusp gets internalized to the IL-3 receptor-expressing cell allowing for diphtheria toxin translocation to the cytosol and followed by the binding to ADP-ribosylation elongation factor 2 which is a key factor for protein translation. Once the protein synthesis is inhibited, the cell goes under a process of apoptosis.",,,,Tagraxofusp is approved and investigational.,Tagraxofusp is a solid.,True
18407,,,,,Benzylsulfonic acid is experimental.,Benzylsulfonic acid is a solid.,False
18408,,,,,PHOSPHONIC ACID is experimental.,PHOSPHONIC ACID is a solid.,False
18409,"Cenegermin is a human beta-nerve growth factor (beta-ngf)-(1-118)- peptide (non-covalent dimer) produced in escherichia coli. It received European Union Approval in July, 2017 for the treatment of moderate to severe neurotrophic keratitis. Cenegermin received approval from the US FDA a year later in August of 2018. Cenegermin is indicated for the treatment of moderate (persistent epithelial defect) or severe (corneal ulcer) neurotrophic keratitis in adults.  Little to no pharmacodynamic studies have yet been conducted in humans.  Cenegermin is a recombinant form of human nerve growth factor.",The molecular weight is 13261.1.,Cenegermin has a topological polar surface area of 5485.74.,,Cenegermin is approved and investigational.,Cenegermin is a solid.,True
18410,"Caplacizumab, firstly called ALX-0081, is a humanized single-variable-domain immunoglobulin consisting of two identical humanized building blocks genetically linked by a three-alanine linker. Caplacizumab was developed by Ablynx, a Sanofi company and FDA approved on February 6, 2019, and approved previously by the EU in October 2018 as a combination therapy with plasma exchange and immunosuppression. Capacizumab is approved for the treatment of adults experiencing an episode of acquired thrombotic thrombocytopenic purpura (aTTP) in conjunction with plasma exchange and immunosuppression in patients 18 years or older. _In vitro_ studies have shown a caplacizumab-driven complete inhibition of platelet aggregation and in phase II clinical trials, it was shown to reduce the activity of the von Willebrand factor by 20% from treatment day 1 until treatment day 30. The level of von Willebrand factor in the plasma was also significantly reduced due to the clearance of the von Willebrand-caplacizumab complex. Caplacizumab acts by targetting the A1 domain of the ultra-large von Willebrand factor which in order inhibits the interaction with the glycoprotein Ib-IX-V receptor in the platelets. Caplacizumab binds to von Willebrand factor with an affinity of 8.5 nM, thus it is very target specific. The blockage of the von Willebrand factor prevents the interaction between the von Willebrand factor and the platelets, hence, preventing platelet aggregation.",,,,Caplacizumab is approved and investigational.,Caplacizumab is a solid.,True
18411,"Simoctocog alfa is a recombinant B-domain deleted (BDD) rFVIII produced in genetically modified human embryonic kidney (HEK) 293F cells. The harvested product is concentrated and purified by a series of chromatography steps. It is an antihemorrhagic agent used as a replacement therapy in individuals with Haemophilia A who lack the factor VIII in the intrinsic pathway of blood coagulation system. As patients with haemophilia A are predisposed to episodes of recurrent bleeding , simoctocog alfa can be administered for the treatment or prevention of bleeding such as prior to surgical procedures. Indicated for the treatment and prophylaxis of bleeding in patients of all ages with haemophilia A (congenital factor VIII deficiency). Simoctocog alfa is an antihemorrhagic agent that displays comparable hemostatic efficacy as the endogenous coagulation factor VIII. Following administration of simoctocog alfa, an increase plasma levels of factor VIII is observed to temporarily correct factor VIII deficiency and bleeding tendencies.  Haemophilia A is a sex-linked hereditary disorder of blood coagulation due to decreased levels of factor VIII:C. The disorder is associated with episodes of recurrent bleeding and profuse bleeding into joints, muscles or internal organs, either spontaneously or as results of accidental or surgical trauma. ",,,,Simoctocog alfa is approved.,Simoctocog alfa is a solid.,True
18412,"Intravenous susoctocog alfa is a recombinant, B-domain deleted, porcine sequence antihaemophilic factor VIII (FVIII) product that has recently been approved for the treatment of bleeding episodes in adults with acquired haemophilia A (AHA). AHA is a rare bleeding disorder that results in a prolonged clotting time as measured by the activated partial thromboplastin time (aPTT) assay, a conventional in vitro test for biological activity of factor VIII. Patients with AHA have normal Factor VIII genes for coagulation pathways but develop inhibitory autoantibodies directed against Factor VIII. These autoantibodies neutralize circulating human factor VIII and create a functional deficiency of this procoagulant protein. Susoctocog alfa serves to temporarily restore the inhibited endogenous Factor VIII for effective hemostasis.  Indicated for the treatment of bleeding episodes in adults with acquired hemophilia A. Following susoctocog alfa administration, the activated partial thromboplastin time (aPTT) is expected to normalize indicating restored biological activity of factor VIII and normal clotting time. In a prospective, open-label clinical trail involving 28 subjects with acquired haemophilia A, all subjects had a positive response to treatment for the initial bleeding episodes at 24 hours after dosing where bleeding was either stopped or substantially reduced.  Factor VIII circulates in the plasma as a hemostatically active protein complex that consists of factor VIII and a large carrier protein von Willebrand factor via a non-covalent binding interaction. This protein complex remains inactive until the coagulation cascade is activated which in turn activates factor VIII to be released from factor VIII/von Willebrand factor complex. Activated factor VIII acts as a cofactor for factor IX-mediated conversion of factor X to activated factor X. Activated factor X is critical in converting prothrombin into thrombin and sequentially, thrombin converts fibrinogen to fibrin for the formation of a blood clot.",,,,Susoctocog alfa is approved and investigational.,Susoctocog alfa is a solid.,True
18413,"Efmoroctocog alfa is a fully recombinant factor VIII-Fc fusion protein (rFVIIIFc) with an extended half-life compared with conventional factor VIII (FVIII) preparations, including recombinant FVIII (rFVIII) products such as. It is an antihemorrhagic agent used in replacement therapy for patients with haemophilia A (congenital factor VIII deficiency). It is suitable for all age groups. Haemophilia A is a rare bleeding disorder associated with a slow clotting process caused by the deficiency of factor VIII. Patients with this disorder are more susceptible to recurrent bleeding episodes and excessive bleeding following minor traumatic injuries or surgical procedures. Prophylactic treatment may dramatically improve the management of severe haemophilia A in the future by reducing joint bleeding and other hemorrhages that cause chronic pain and disability to patients. Prophylaxis has also shown to reduce the formation of neutralizing anti-FVIII antibodies, or inhibitors.  Indicated for the treatment and prophylaxis of bleeding in patients with haemophilia A (congenital factor VIII deficiency). In two multinational, open-label, noncomparative phase III trials involving previously treated pediatric and adult patients with severe haemophilia A, the clinical efficacy and safety of efmoroctocog alfa have been studied. The bleeding episodes were adequately controlled and bleeding rates were substantially reduced when efmoroctocog alfa has been used for individualized prophylaxis or treatment of bleeding. In adult patients receiving a single preoperative dose to maintain haemostasis during surgical procedures, the total dose on the day of surgery needed to maintain haemostasis ranged from 50.8 to 126.6 IU/kg. Factor VIII exists in a circulating protein complex consisting of two molecules via a non-covalent binding interaction; Factor VIII and von Willebrand factor. This complex remains inactive until the coagulation cascade is initiated, which activated factor VIII. Factor VIII is released from the protein complex upon activation and acts as a cofactor for factor IX-mediated conversion of factor X to activated factor X on phospholipid surfaces. Activated factor X is critical in converting prothrombin into thrombin and sequentially, thrombin converts fibrinogen to fibrin for the formation of a blood clot.",,,,Efmoroctocog alfa is approved and investigational.,Efmoroctocog alfa is a solid.,True
18414,"VP025, a novel drug formulation based on phospholipid microparticles incorporating phosphatidylglycerol, can inhibit neuroinflammation. VP025 may inhibit immune system activation and protect motoneurons from injury. It also shows the ability to reduce inflammation across the blood-brain barrier and improve correlates of memory and learning function. It is being developed to target the chronic inflammation within the central nervous system that is associated with a number of neurological diseases, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (Lou Gehrig’s disease). It is considered to be a systemic anti-inflammatory and neuroprotective agent. Investigated for use/treatment in alzheimer's disease and inflammatory disorders (unspecified). VP025 may invoke the body's response ti cell surface phospholipid components, the result of which is an up-regulation of regulatory T cells promoting a suppression of inflammation. VP025 cross the blood-brain barrier, demonstrating potent anti-inflammatory activity and preserving the function of neural pathways necessary for memory and learning. VP025 is being developed to exert its anti-inflammatory effects using an cell clearance mechanism. VP025, a preparation of phospholipid microparticles containing",,,,VP025 is investigational.,VP025 is a solid.,True
18415,Etiprednol dicloacetate (BNP-166) is a soft corticosteroid with anti-inflammatory properties that has been indicated in the treatment of asthma and Chron's disease. Anti-asthmatic effects were associated with decreased cytokine production in lipopolysaccharide-stimulated lymphocytes and attenuated lectin-induced proliferation of blood mononuclear cells in tissue culture. Investigated for use/treatment in asthma and crohn's disease.,The molecular weight is 485.4.,Etiprednol dicloacetate has a topological polar surface area of 89.9.,The log p value of  is 4.46.,Etiprednol dicloacetate is investigational.,Etiprednol dicloacetate is a solid.,True
18416,"Canakinumab is a recombinant, human anti-human-IL-1β monoclonal antibody that belongs to the IgG1/κ isotype subclass. It is expressed in a murine Sp2/0-Ag14 cell line and comprised of two 447- (or 448-) residue heavy chains and two 214-residue light chains, with a molecular mass of 145157 Daltons when deglycosylated. Both heavy chains of canakinumab contain oligosaccharide chains linked to the protein backbone at asparagine 298 (Asn 298). Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1alpha or IL-1 receptor antagonist (IL-1ra). Canakinumab is marketed under the brand name Ilaris and indicated for patients 4 years of age and older to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS) as well as for patients 2 years of age and older to treat systemic juvenile idiopathic arthritis (SJIA). Clinical trials have established the administration of canakinumab every 2 weeks to be safe and effective, offering a considerable advantage over the existing treatment with the human IL-1 receptor antagonist, anakinra, which must be injected daily and which is often poorly tolerated by patients. Used in patients 4 years of age and older to treat Familial Cold Autoinflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS), which are both part of the Cryopyrin-Associated Periodic Syndromes (CAPS) as well as for patients 2 years of age and older to treat systemic juvenile idiopathic arthritis (SJIA).  Novartis AG has developed canakinumab as a subcutaneous injection and fully human mAb that neutralizes the bioactivity of human IL-1beta, which is involved in several inflammatory disorders. Canakinumab has promising clinical safety and pharmacokinetic properties, and demonstrated potential for the treatment of cryopyrin-associated periodic syndromes (CAPS), systemic juvenile idiopathic arthritis (SJIA), and possibly for other complex inflammatory diseases, such as rheumatoid arthritis, COPD disease and ocular diseases.  In inflammatory diseases involving Cryopyrin-Associated Periodic Syndromes (CAPS), interleukin-1 beta (IL-1β) is excessively activated and drives inflammation. The protein cryopyrin controls the activation of IL-1β, and mutations in cryopyrin's gene, NLRP-3, up-regulate IL-1β activation. Canakinumab is a human monoclonal anti-human IL-1β antibody of the IgG1/κ isotype. Canakinumab binds to human IL-1β and neutralizes its inflammatory activity by blocking its interaction with IL-1 receptors, but it does not bind IL-1α or IL-1 receptor antagonist (IL-1ra).",,,,Canakinumab is approved and investigational.,Canakinumab is a liquid.,True
18417,"Rilonacept is a dimeric fusion protein consisting of portions of IL-1R and the IL-1R accessory protein linked to the Fc portion of immunoglobulin G1. Rilonacept functions as an interleukin 1 inhibitor and is used in the treatment of CAPS, also known as cryopyrin-associated periodic syndromes, including familial cold auto-inflammatory syndrome (FCAS) and Muckle-Wells Syndrome (MWS), in adults and children greater than 12 years old. Rilonacept is currently used in the treatment of cryopyrin-associated periodic syndrome. In May 2012, an advisory panel for the FDA voted 11-0 against the use of Rilonacept for the treatment of gout.  Treatment with Rilonacept resulted in decreased levels of mean C-Reactive Protein (CRP) and Serum Amyloid A (SAA). Higher levels of CRP and SAA are associated with inflammatory disease activity found in patients with Cryopyrin-Associated Periodic Syndromes.  CAPS refer to rare genetic syndromes generally caused by mutations in the NLRP-3 gene (also known as Cold-Induced Auto-inflammatory Syndtrome-1 ). CAPS disorders are inherited in an autosomal dominant pattern with male and female offspring equally affected. Fever, urticaria-like rash, arthralgia, myalgia, fatigue, and conjunctivitis are features common to all disorders. In most cases, inflammation in CAPS is associated with mutations in the NLRP-3 gene which encodes the protein cryopyrin, an important component of the inflammasome. Cryopyrin regulates the protease caspase-1 and controls the activation of interleukin-1 beta (IL-1β). Mutations in NLRP-3 result in an overactive inflammasome resulting in excessive release of activated IL-1β that drives inflammation. Rilonacept blocks IL-1β signaling by acting as a soluble decoy receptor that binds IL-1β and prevents its interaction with cell surface receptors. Rilonacept also binds IL-1α and IL-1 receptor antagonist (IL-1ra) with reduced affinity. By binding IL-1, rilonacept prevents the activation of IL-1 receptors, thus reducing inflammatory responses and other effects related to an excess of IL-1.",,,,Rilonacept is approved and investigational.,Rilonacept is a solid.,True
18418,"Gevokizumab has been used in trials studying the treatment of Acne Vulgaris, Osteoarthritis, Behcet's Uveitis, Pyoderma Gangrenosum, and Behcet's Disease Uveitis, among others. Gevokizumab acts as a modulator of cytokine imbalance in IL-1 mediated disease states. It has a very high binding affinity of 300fM and blocks the activation of IL-1 receptors.",,,,Gevokizumab is investigational.,,True
18419,,,,,"2-amino-N-(4-methyl-1,3-thiazol-2-yl)-5-benzamide is experimental.","2-amino-N-(4-methyl-1,3-thiazol-2-yl)-5-benzamide is a solid.",False
18420,,,,,"3--N-(4-methyl-1,3-thiazol-2-yl)-6-pyridine-2-carboxamide is experimental.","3--N-(4-methyl-1,3-thiazol-2-yl)-6-pyridine-2-carboxamide is a solid.",False
18421,,,,,"2-(methylamino)-N-(4-methyl-1,3-thiazol-2-yl)-5-benzamide is experimental.","2-(methylamino)-N-(4-methyl-1,3-thiazol-2-yl)-5-benzamide is a solid.",False
18422,,,,,"2-AMINO-4-FLUORO-5--N-(1,3-THIAZOL-2-YL)BENZAMIDE is experimental.","2-AMINO-4-FLUORO-5--N-(1,3-THIAZOL-2-YL)BENZAMIDE is a solid.",False
18423,"Carboxymethylcellulose is a cellulose derivative that consists of the cellulose backbone made up of glucopyranose monomers and their hydroxyl groups bound to carboxymethyl groups. It is added in food products as a viscosity modifier or thickener and emulsifier. It is also one of the most common viscous polymers used in artificial tears, and has shown to be effective in the treatment of aqueous tear-deficient dry eye symptoms and ocular surface staining. The viscous and mucoadhesive properties as well as its anionic charge allow prolonged retention time in the ocular surface. Sodium carboxymethylcellulose is the most commonly used salt. Indicated for the symptomatic relief of burning, irritation and discomfort of the eyes due to dryness or exposure to wind or sun. In a randomized clinical study of patients with mild or moderate forms of eye dryness, ophthalmic treatment with sodium carboxymethylcellulose resulted in a diminished frequency of symptoms compared to the placebo group. Carboxymethylcellulose interacts with human corneal epithelial cells to facilitate corneal epithelial wound healing and attenuate eye irritation in a dose-dependent manner. It exhibits protective actions on the ocular surface in various applications; it mediates cytoprotective effects on the ocular surface when applied prior to contact lenses and reduces the incidence of epithelial defects during LASIK. Carboxymethylcellulose binds to the surface of corneal epithelial cells via its glucopyranose subunits binding to glucose receptors GLUT-1. The residence time of carboxymethylcellulose bound to corneal cells is approximately 2 hours as indicated by a short-term binding assay. Binding of carboxymethylcellulose to the matrix proteins stimulated corneal epithelial cell attachment, migration, and re-epithelialization of corneal wounds.",,,,Carboxymethylcellulose is approved and investigational.,Carboxymethylcellulose is a solid.,True
18424,,,,,2-acetylamino-2-deoxy-b-D-allopyranose is experimental.,2-acetylamino-2-deoxy-b-D-allopyranose is a solid.,False
18425,,,,,2-(Acetylamino)-2-Deoxy-6-O-Methyl-Alpha-D-Allopyranose is experimental.,2-(Acetylamino)-2-Deoxy-6-O-Methyl-Alpha-D-Allopyranose is a solid.,False
18426,,,,,Argifin is experimental.,Argifin is a solid.,False
18427,,,,,Argadin is experimental.,Argadin is a solid.,False
18428,,,,,Allosamizoline is experimental.,Allosamizoline is a solid.,False
18429,,,,,5-iodotubercidin is experimental.,5-iodotubercidin is a solid.,False
18430,,,,,"3--4-(5-Fluoro-1-Methyl-1h-Indol-3-Yl)-Pyrrole-2,5-Dione is experimental.","3--4-(5-Fluoro-1-Methyl-1h-Indol-3-Yl)-Pyrrole-2,5-Dione is a solid.",False
18431,,,,,SB-409513 is experimental.,SB-409513 is a solid.,False
18432,,,,,AR-AO-14418 is experimental.,AR-AO-14418 is a solid.,False
18433,,,,,6-bromoindirubin-3'-oxime is experimental.,6-bromoindirubin-3'-oxime is a solid.,False
18434,,,,,"2-(1,3-benzodioxol-5-yl)-5--1,3,4-oxadiazole is experimental.","2-(1,3-benzodioxol-5-yl)-5--1,3,4-oxadiazole is a solid.",False
18435,,,,,"5--1,3,4-oxadiazole-2(3H)-thione is experimental.","5--1,3,4-oxadiazole-2(3H)-thione is a solid.",False
18436,,,,,"(7S)-2-(2-aminopyrimidin-4-yl)-7-(2-fluoroethyl)-1,5,6,7-tetrahydro-4H-pyrrolopyridin-4-one is experimental.","(7S)-2-(2-aminopyrimidin-4-yl)-7-(2-fluoroethyl)-1,5,6,7-tetrahydro-4H-pyrrolopyridin-4-one is a solid.",False
18437,,,,,"3-({oxy}amino)-1H,2'H-2,3'-biindol-2'-one is experimental.","3-({oxy}amino)-1H,2'H-2,3'-biindol-2'-one is a solid.",False
18438,,,,,N--5-(1H-pyrrolopyridin-4-yl)thiophene-2-carboxamide is experimental.,N--5-(1H-pyrrolopyridin-4-yl)thiophene-2-carboxamide is a solid.,False
18439,,,,,4-(4-CHLOROPHENYL)-4-PIPERIDINE is experimental.,4-(4-CHLOROPHENYL)-4-PIPERIDINE is a solid.,False
18440,,,,,ISOQUINOLINE-5-SULFONIC ACID (2-(2-(4-CHLOROBENZYLOXY)ETHYLAMINO)ETHYL)AMIDE is experimental.,ISOQUINOLINE-5-SULFONIC ACID (2-(2-(4-CHLOROBENZYLOXY)ETHYLAMINO)ETHYL)AMIDE is a solid.,False
18441,,,,,(2S)-1-(1H-INDOL-3-YL)-3-{OXY}PROPAN-2-AMINE is experimental.,(2S)-1-(1H-INDOL-3-YL)-3-{OXY}PROPAN-2-AMINE is a solid.,False
18442,"Tideglusib is under the investigation for the development of treatments for Alzheimer's disease and for progressive supranuclear palsy. It is reported to be a potent anti-inflammatory and neuroprotective that is a non-ATP competitive inhibitor of glycogen synthase kinase 3 (GSK-3). Tideglusib is being developed by the Spanish pharmaceutic company Zeltia group and its current status is withdrawn for the treatment of Alzheimer's disease as of 2012. Tideglusib was initially formulated for the treatment of Alzheimer and progressive supranuclear palsy. The raising interest for the use of tideglusib comes from the significant upregulation of GSK-3 in the brain in patients with Alzheimer disease. Its function as a degradant of β-catenin, was also important, as it prevents the transcription of cell survival genes. All these factors have directed current research towards this kinase as a potential target. Alzheimer disease is the most prevalent form of dementia. The most accepted hypothesis to explain this disease is related to the presence of amyloid β, which triggers a cascade that will alter the Tau protein and provoke synaptic dysfunction and neuronal death.  It is reported that tideglusib administration inhibits the activation of astrocytes and microglial cells, thus it presented a neuroprotective effect. It is known as well that the inactivation of GSK-3 protects against excitotoxicity. In pre-clinical trials, there have been reports of decrease Tau hyperphosphorylation, lower brain amyloid plaque load, learning and memory enhancement, prevention of neuronal loss and significant increases of the insulin growth factor 1 which is a potent neurotrophic peptide with therapeutic value.The reports in clinical trials have shown a trend in cognition increase of Alzheimer patients treated for 24 weeks.  GSK-3 is a proline/serine protein kinase that is ubiquitously expressed and involved in many cellular signaling pathways. From all its diverse functions, it plays a key role in Alzheimer's disease. This role is related to its link with β-amyloid and tau pathology. It has been suggested that aberrant Wnt or insulin signaling results in increased GSK-3 function. This kinase acts on γ-secretase producing the hyperphosphorylation of tau, the formation of neurofibrillary tangles and senile plaques. Tideglusib inhibits GSK-3 irreversibly by presenting a non-competitive inhibition pattern with respect to ATP. The binding of tideglusib seems to directly relate to the motif containing Cys199.",,,,Tideglusib is investigational and withdrawn.,Tideglusib is a solid.,True
18443,,,,,Dodecyltrimethylammonium is experimental.,Dodecyltrimethylammonium is a solid.,False
18444,,,,,"4-Pyrimidin-7-Ylamino]-N,N-Dimethylbenzenesulfonamide is experimental.","4-Pyrimidin-7-Ylamino]-N,N-Dimethylbenzenesulfonamide is a solid.",False
18445,,,,,"4-(2,4-Dimethyl-Thiazol-5-Yl)-Pyrimidin-2-Ylamine is experimental.","4-(2,4-Dimethyl-Thiazol-5-Yl)-Pyrimidin-2-Ylamine is a solid.",False
18446,,,,,4-Pyridin-3-Ylpyrimidin-2-Yl)Amino]Benzenesulfonamide is experimental.,4-Pyridin-3-Ylpyrimidin-2-Yl)Amino]Benzenesulfonamide is a solid.,False
18447,,,,,2-Amino-6-Chloropyrazine is experimental.,2-Amino-6-Chloropyrazine is a solid.,False
18448,,,,,6-O-Cyclohexylmethyl Guanine is experimental.,6-O-Cyclohexylmethyl Guanine is a solid.,False
18449,,,,,N-Pyridin-3-Yl)-2-Pyrimidinyl]Acetamide is experimental.,N-Pyridin-3-Yl)-2-Pyrimidinyl]Acetamide is a solid.,False
18450,,,,,1-Amino-6-Cyclohex-3-Enylmethyloxypurine is experimental.,1-Amino-6-Cyclohex-3-Enylmethyloxypurine is a solid.,False
18451,,,,,N-(5-Cyclopropyl-1h-Pyrazol-3-Yl)Benzamide is experimental.,N-(5-Cyclopropyl-1h-Pyrazol-3-Yl)Benzamide is a solid.,False
18452,,,,,-(3-Nitro-Phenyl)-Amine is experimental.,-(3-Nitro-Phenyl)-Amine is a solid.,False
18453,,,,,(5R)-5-{methyl}-2-pyrrolidinone is experimental.,(5R)-5-{methyl}-2-pyrrolidinone is a solid.,False
18454,,,,,"4-(2,4-Dimethyl-1,3-thiazol-5-yl)-N--2-pyrimidinamine is experimental.","4-(2,4-Dimethyl-1,3-thiazol-5-yl)-N--2-pyrimidinamine is a solid.",False
18455,,,,,(5-ChloropyrazoloPyrimidin-7-Yl)-(4-Methanesulfonylphenyl)Amine is experimental.,(5-ChloropyrazoloPyrimidin-7-Yl)-(4-Methanesulfonylphenyl)Amine is a solid.,False
18456,,,,,4-(5-Bromo-2-Oxo-2h-Indol-3-Ylazo)-Benzenesulfonamide is experimental.,4-(5-Bromo-2-Oxo-2h-Indol-3-Ylazo)-Benzenesulfonamide is a solid.,False
18457,,,,,"4-(2,5-Dichloro-Thiophen-3-Yl)-Pyrimidin-2-Ylamine is experimental.","4-(2,5-Dichloro-Thiophen-3-Yl)-Pyrimidin-2-Ylamine is a solid.",False
18458,,,,,4-Benzenesulfonamide is experimental.,4-Benzenesulfonamide is a solid.,False
18459,,,,,"4--6,7-Dimethoxyquinazoline is experimental.","4--6,7-Dimethoxyquinazoline is a solid.",False
18460,,,,,"3-Pyridin-4-Yl-2,4-Dihydro-IndenoPyrazole is experimental.","3-Pyridin-4-Yl-2,4-Dihydro-IndenoPyrazole is a solid.",False
18461,,,,,"(2E,3S)-3-hydroxy-5'--3-methyl-1,3-dihydro-2,3'-biindol-2'(1'H)-one is experimental.","(2E,3S)-3-hydroxy-5'--3-methyl-1,3-dihydro-2,3'-biindol-2'(1'H)-one is a solid.",False
18462,,,,,1--3-Methyl-2-Butanol is experimental.,1--3-Methyl-2-Butanol is a solid.,False
18463,,,,,"4-((3r,4s,5r)-4-Amino-3,5-Dihydroxy-Hex-1-Ynyl)-5-Fluoro-3--1,3-Dihydro-Indol-2-One is experimental.","4-((3r,4s,5r)-4-Amino-3,5-Dihydroxy-Hex-1-Ynyl)-5-Fluoro-3--1,3-Dihydro-Indol-2-One is a solid.",False
18464,,,,,Lysine Nz-Carboxylic Acid is experimental.,Lysine Nz-Carboxylic Acid is a solid.,False
18465,,,,,Pyridin-3-Yl]-Phenyl-Methanone is experimental.,Pyridin-3-Yl]-Phenyl-Methanone is a solid.,False
18466,,,,,N'--N-hydroxyimidoformamide is experimental.,N'--N-hydroxyimidoformamide is a solid.,False
18467,,,,,N'-(PyrrolidinoIsoindolin-4-On-8-Yl)-N-(Pyridin-2-Yl)Urea is experimental.,N'-(PyrrolidinoIsoindolin-4-On-8-Yl)-N-(Pyridin-2-Yl)Urea is a solid.,False
18468,,,,,2--6-(Benzyl-Amino)-9-Cyclopentylpurine is experimental.,2--6-(Benzyl-Amino)-9-Cyclopentylpurine is a solid.,False
18469,,,,,4--Phenol is experimental.,4--Phenol is a solid.,False
18470,,,,,3--Phenol is experimental.,3--Phenol is a solid.,False
18471,,,,,"PHENYLAMINOIMIDAZO(1,2-ALPHA)PYRIDINE is experimental.","PHENYLAMINOIMIDAZO(1,2-ALPHA)PYRIDINE is a solid.",False
18472,,,,,OLOMOUCINE II is experimental.,OLOMOUCINE II is a solid.,False
18473,,,,,TRIAZOLOPYRIMIDINE is experimental.,TRIAZOLOPYRIMIDINE is a solid.,False
18474,,,,,4-INDOL-8-YLMETHYL)-AMINO]-N-PYRIDIN-2-YL-BENZENESULFONAMIDE is experimental.,4-INDOL-8-YLMETHYL)-AMINO]-N-PYRIDIN-2-YL-BENZENESULFONAMIDE is a solid.,False
18475,,,,,"(13R,15S)-13-METHYL-16-OXA-8,9,12,22,24-PENTAAZAHEXACYCLOHEPTACOSA-1(24),2,4,6,17(25),18,20-HEPTAENE-23,26-DIONE is experimental.","(13R,15S)-13-METHYL-16-OXA-8,9,12,22,24-PENTAAZAHEXACYCLOHEPTACOSA-1(24),2,4,6,17(25),18,20-HEPTAENE-23,26-DIONE is a solid.",False
18476,"N-(3-cyclopropyl-1H-pyrazol-5-yl)-2-(2-naphthyl)acetamide is a solid. This compound belongs to the naphthalenes. These are compounds containing a naphthalene moiety, which consists of two fused benzene rings. The proteins that N-(3-cyclopropyl-1H-pyrazol-5-yl)-2-(2-naphthyl)acetamide targets include cyclin-A2 and cyclin-dependent kinase 2.",,,,N-(3-cyclopropyl-1H-pyrazol-5-yl)-2-(2-naphthyl)acetamide is experimental.,N-(3-cyclopropyl-1H-pyrazol-5-yl)-2-(2-naphthyl)acetamide is a solid.,True
18477,,,,,2-ANILINO-6-CYCLOHEXYLMETHOXYPURINE is experimental.,2-ANILINO-6-CYCLOHEXYLMETHOXYPURINE is a solid.,False
18478,,,,,"1-(5-OXO-2,3,5,9B-TETRAHYDRO-1H-PYRROLOISOINDOL-9-YL)-3-(5-PYRROLIDIN-2-YL-1H-PYRAZOL-3-YL)-UREA is experimental.","1-(5-OXO-2,3,5,9B-TETRAHYDRO-1H-PYRROLOISOINDOL-9-YL)-3-(5-PYRROLIDIN-2-YL-1H-PYRAZOL-3-YL)-UREA is a solid.",False
18479,,,,,(5-phenyl-7-(pyridin-3-ylmethylamino)pyrazolopyrimidin-3-yl)methanol is experimental.,(5-phenyl-7-(pyridin-3-ylmethylamino)pyrazolopyrimidin-3-yl)methanol is a solid.,False
18480,,,,,"2-(3,4-DIHYDROXYPHENYL)-8-(1,1-DIOXIDOISOTHIAZOLIDIN-2-YL)-3-HYDROXY-6-METHYL-4H-CHROMEN-4-ONE is experimental.","2-(3,4-DIHYDROXYPHENYL)-8-(1,1-DIOXIDOISOTHIAZOLIDIN-2-YL)-3-HYDROXY-6-METHYL-4H-CHROMEN-4-ONE is a solid.",False
18481,,,,,(2R)-1-(DIMETHYLAMINO)-3-{4-AMINO}PYRIMIDIN-4-YL)AMINO]PHENOXY}PROPAN-2-OL is experimental.,(2R)-1-(DIMETHYLAMINO)-3-{4-AMINO}PYRIMIDIN-4-YL)AMINO]PHENOXY}PROPAN-2-OL is a solid.,False
18482,,,,,"5-(2,3-dichlorophenyl)-N-(pyridin-4-ylmethyl)-3-thiocyanatopyrazolopyrimidin-7-amine is experimental.","5-(2,3-dichlorophenyl)-N-(pyridin-4-ylmethyl)-3-thiocyanatopyrazolopyrimidin-7-amine is a solid.",False
18483,,,,,O6-CYCLOHEXYLMETHOXY-2-(4'-SULPHAMOYLANILINO) PURINE is experimental.,O6-CYCLOHEXYLMETHOXY-2-(4'-SULPHAMOYLANILINO) PURINE is a solid.,False
18484,,,,,(2S)-N--2-propanamide is experimental.,(2S)-N--2-propanamide is a solid.,False
18485,,,,,5--6-FLUORO-3-(1H-PYRROL-2-YL)BENZOINDOL-2(1H)-ONE is experimental.,5--6-FLUORO-3-(1H-PYRROL-2-YL)BENZOINDOL-2(1H)-ONE is a solid.,False
18486,,,,,N-cyclopropyl-4-pyrazolopyridazin-3-ylpyrimidin-2-amine is experimental.,N-cyclopropyl-4-pyrazolopyridazin-3-ylpyrimidin-2-amine is a solid.,False
18487,,,,,3-((3-bromo-5-o-tolylpyrazolopyrimidin-7-ylamino)methyl)pyridine 1-oxide is experimental.,3-((3-bromo-5-o-tolylpyrazolopyrimidin-7-ylamino)methyl)pyridine 1-oxide is a solid.,False
18488,,,,,6-CYCLOHEXYLMETHOXY-2-(3'-CHLOROANILINO) PURINE is experimental.,6-CYCLOHEXYLMETHOXY-2-(3'-CHLOROANILINO) PURINE is a solid.,False
18489,,,,,3-bromo-5-phenyl-N-(pyridin-4-ylmethyl)pyrazolopyrimidin-7-amine is experimental.,3-bromo-5-phenyl-N-(pyridin-4-ylmethyl)pyrazolopyrimidin-7-amine is a solid.,False
18490,,,,,N--2-(4-PIPERIDIN-1-YLPHENYL)ACETAMIDE is experimental.,N--2-(4-PIPERIDIN-1-YLPHENYL)ACETAMIDE is a solid.,False
18491,,,,,"(3R)-3-(aminomethyl)-9-methoxy-1,2,3,4-tetrahydro-5H-benzothienodiazepin-5-one is experimental.","(3R)-3-(aminomethyl)-9-methoxy-1,2,3,4-tetrahydro-5H-benzothienodiazepin-5-one is a solid.",False
18492,,,,,5--3-{OXY}-2-THIOPHENECARBOXAMIDE is experimental.,5--3-{OXY}-2-THIOPHENECARBOXAMIDE is a solid.,False
18493,,,,,5-Bromoindirubin is experimental.,5-Bromoindirubin is a solid.,False
18494,,,,,(2S)-1-{4-phenoxy}-3-(dimethylamino)-2-propanol is experimental.,(2S)-1-{4-phenoxy}-3-(dimethylamino)-2-propanol is a solid.,False
18495,,,,,(2R)-1-{4-phenoxy}-3-(dimethylamino)-2-propanol is experimental.,(2R)-1-{4-phenoxy}-3-(dimethylamino)-2-propanol is a solid.,False
18496,,,,,"(5E)-2-Amino-5-(2-pyridinylmethylene)-1,3-thiazol-4(5H)-one is experimental.","(5E)-2-Amino-5-(2-pyridinylmethylene)-1,3-thiazol-4(5H)-one is a solid.",False
18497,,,,,4-{5-FURAN-2-YL}BENZENESULFONAMIDE is experimental.,4-{5-FURAN-2-YL}BENZENESULFONAMIDE is a solid.,False
18498,,,,,4-{5--2-FURYL}-N-METHYLBENZENESULFONAMIDE is experimental.,4-{5--2-FURYL}-N-METHYLBENZENESULFONAMIDE is a solid.,False
18499,,,,,4-{5-FURAN-2-YL}BENZENESULFONAMIDE is experimental.,4-{5-FURAN-2-YL}BENZENESULFONAMIDE is a solid.,False
18500,,,,,4-{5-FURAN-2-YL}-2-(TRIFLUOROMETHYL)BENZENESULFONAMIDE is experimental.,4-{5-FURAN-2-YL}-2-(TRIFLUOROMETHYL)BENZENESULFONAMIDE is a solid.,False
18501,,,,,4-{5-FURAN-2-YL}BENZOIC ACID is experimental.,4-{5-FURAN-2-YL}BENZOIC ACID is a solid.,False
18502,,,,,4-{5--2-FURYL}BENZENESULFONAMIDE is experimental.,4-{5--2-FURYL}BENZENESULFONAMIDE is a solid.,False
18503,,,,,"N--N',N'-DIMETHYL-BENZENE-1,4-DIAMINE is experimental.","N--N',N'-DIMETHYL-BENZENE-1,4-DIAMINE is a solid.",False
18504,,,,,"(5Z)-5-(3-BROMOCYCLOHEXA-2,5-DIEN-1-YLIDENE)-N-(PYRIDIN-4-YLMETHYL)-1,5-DIHYDROPYRAZOLOPYRIMIDIN-7-AMINE is experimental.","(5Z)-5-(3-BROMOCYCLOHEXA-2,5-DIEN-1-YLIDENE)-N-(PYRIDIN-4-YLMETHYL)-1,5-DIHYDROPYRAZOLOPYRIMIDIN-7-AMINE is a solid.",False
18505,,,,,"6-(3,4-DIHYDROXYBENZYL)-3-ETHYL-1-(2,4,6-TRICHLOROPHENYL)-1H-PYRAZOLOPYRIMIDIN-4(5H)-ONE is experimental.","6-(3,4-DIHYDROXYBENZYL)-3-ETHYL-1-(2,4,6-TRICHLOROPHENYL)-1H-PYRAZOLOPYRIMIDIN-4(5H)-ONE is a solid.",False
18506,,,,,6-(3-AMINOPHENYL)-N-(TERT-BUTYL)-2-(TRIFLUOROMETHYL)QUINAZOLIN-4-AMINE is experimental.,6-(3-AMINOPHENYL)-N-(TERT-BUTYL)-2-(TRIFLUOROMETHYL)QUINAZOLIN-4-AMINE is a solid.,False
18507,,,,,"2-(4-(AMINOMETHYL)PIPERIDIN-1-YL)-N-(3_CYCLOHEXYL-4-OXO-2,4-DIHYDROINDENOPYRAZOL-5-YL)ACETAMIDE is experimental.","2-(4-(AMINOMETHYL)PIPERIDIN-1-YL)-N-(3_CYCLOHEXYL-4-OXO-2,4-DIHYDROINDENOPYRAZOL-5-YL)ACETAMIDE is a solid.",False
18508,,,,,"1-(3-(2,4-DIMETHYLTHIAZOL-5-YL)-4-OXO-2,4-DIHYDROINDENOPYRAZOL-5-YL)-3-(4-METHYLPIPERAZIN-1-YL)UREA is experimental.","1-(3-(2,4-DIMETHYLTHIAZOL-5-YL)-4-OXO-2,4-DIHYDROINDENOPYRAZOL-5-YL)-3-(4-METHYLPIPERAZIN-1-YL)UREA is a solid.",False
18509,,,,,4-{TRIAZOLOPYRIMIDIN-7-YL]AMINO}BENZENESULFONAMIDE is experimental.,4-{TRIAZOLOPYRIMIDIN-7-YL]AMINO}BENZENESULFONAMIDE is a solid.,False
18510,,,,,4-{TRIAZOLOPYRIMIDIN-7-YL]AMINO}BENZENESULFONAMIDE is experimental.,4-{TRIAZOLOPYRIMIDIN-7-YL]AMINO}BENZENESULFONAMIDE is a solid.,False
18511,,,,,4-({5-TRIAZOLOPYRIMIDIN-7-YL}AMINO)BENZENESULFONAMIDE is experimental.,4-({5-TRIAZOLOPYRIMIDIN-7-YL}AMINO)BENZENESULFONAMIDE is a solid.,False
18512,,,,,4-{TRIAZOLOPYRIMIDIN-7-YL]AMINO}BENZENESULFONAMIDE is experimental.,4-{TRIAZOLOPYRIMIDIN-7-YL]AMINO}BENZENESULFONAMIDE is a solid.,False
18513,,,,,CAN-508 is experimental.,CAN-508 is a solid.,False
18514,,,,,(2R)-1--2-pyrimidinyl}amino)phenoxy]-3-(dimethylamino)-2-propanol is experimental.,(2R)-1--2-pyrimidinyl}amino)phenoxy]-3-(dimethylamino)-2-propanol is a solid.,False
18515,,,,,(2S)-1--4-pyrimidinyl}amino)phenoxy]-3-(dimethylamino)-2-propanol is experimental.,(2S)-1--4-pyrimidinyl}amino)phenoxy]-3-(dimethylamino)-2-propanol is a solid.,False
18516,,,,,(2S)-1--2-pyrimidinyl}amino)phenoxy]-3-(dimethylamino)-2-propanol is experimental.,(2S)-1--2-pyrimidinyl}amino)phenoxy]-3-(dimethylamino)-2-propanol is a solid.,False
18517,,,,,(2R)-1--4-pyrimidinyl}amino)phenoxy]-3-(dimethylamino)-2-propanol is experimental.,(2R)-1--4-pyrimidinyl}amino)phenoxy]-3-(dimethylamino)-2-propanol is a solid.,False
18518,,,,,N-(2-METHOXYETHYL)-4-({4-PYRIMIDIN-2-YL}AMINO)BENZENESULFONAMIDE is experimental.,N-(2-METHOXYETHYL)-4-({4-PYRIMIDIN-2-YL}AMINO)BENZENESULFONAMIDE is a solid.,False
18519,,,,,4-{AMINO}-N-METHYLBENZENESULFONAMIDE is experimental.,4-{AMINO}-N-METHYLBENZENESULFONAMIDE is a solid.,False
18520,,,,,"1-(3,5-DICHLOROPHENYL)-5-METHYL-1H-1,2,4-TRIAZOLE-3-CARBOXYLIC ACID is experimental.","1-(3,5-DICHLOROPHENYL)-5-METHYL-1H-1,2,4-TRIAZOLE-3-CARBOXYLIC ACID is a solid.",False
18521,,,,,(2S)-1-(Dimethylamino)-3-(4-{pyridin-3-yl)-2-pyrimidinyl]amino}phenoxy)-2-propanol is experimental.,(2S)-1-(Dimethylamino)-3-(4-{pyridin-3-yl)-2-pyrimidinyl]amino}phenoxy)-2-propanol is a solid.,False
18522,,,,,N-(4-{carbonyl}phenyl)-5-fluoro-4-pyrimidin-2-amine is experimental.,N-(4-{carbonyl}phenyl)-5-fluoro-4-pyrimidin-2-amine is a solid.,False
18523,,,,,2-{4-pyrimidin-2-yl}amino)phenyl]piperazin-1-yl}-2-oxoethanol is experimental.,2-{4-pyrimidin-2-yl}amino)phenyl]piperazin-1-yl}-2-oxoethanol is a solid.,False
18524,,,,,RO-4584820 is investigational.,RO-4584820 is a solid.,False
18525,,,,,N-Methyl-4-{amino}benzenesulfonamide is experimental.,N-Methyl-4-{amino}benzenesulfonamide is a solid.,False
18526,,,,,N-methyl-{4-thiazoloindol-8-ylidene)hydrazino]phenyl}methanesulfonamide is experimental.,N-methyl-{4-thiazoloindol-8-ylidene)hydrazino]phenyl}methanesulfonamide is a solid.,False
18527,,,,,"3-{methylene}-5-(1,3-oxazol-5-yl)-1,3-dihydro-2H-indol-2-one is experimental.","3-{methylene}-5-(1,3-oxazol-5-yl)-1,3-dihydro-2H-indol-2-one is a solid.",False
18528,,,,,"4-{amino}-N-(1,3-thiazol-2-yl)benzenesulfonamide is experimental.","4-{amino}-N-(1,3-thiazol-2-yl)benzenesulfonamide is a solid.",False
18529,,,,,"3-{aminosulfonyl)anilino]methylene}-2-oxo-2,3-dihydro-1H-indole is experimental.","3-{aminosulfonyl)anilino]methylene}-2-oxo-2,3-dihydro-1H-indole is a solid.",False
18530,,,,,5-hydroxynaphthalene-1-sulfonamide is experimental.,5-hydroxynaphthalene-1-sulfonamide is a solid.,False
18531,,,,,N-(4-sulfamoylphenyl)-1H-indazole-3-carboxamide is experimental.,N-(4-sulfamoylphenyl)-1H-indazole-3-carboxamide is a solid.,False
18532,,,,,4-benzenesulfonamide is experimental.,4-benzenesulfonamide is a solid.,False
18533,,,,,N-phenyl-1H-pyrazole-3-carboxamide is experimental.,N-phenyl-1H-pyrazole-3-carboxamide is a solid.,False
18534,,,,,4-(acetylamino)-N-(4-fluorophenyl)-1H-pyrazole-3-carboxamide is experimental.,4-(acetylamino)-N-(4-fluorophenyl)-1H-pyrazole-3-carboxamide is a solid.,False
18535,,,,,(4E)-N-(4-fluorophenyl)-4--4H-pyrazole-3-carboxamide is experimental.,(4E)-N-(4-fluorophenyl)-4--4H-pyrazole-3-carboxamide is a solid.,False
18536,,,,,{amino}-N-(4-fluorophenyl)-1H-pyrazole-3-carboxamide is experimental.,{amino}-N-(4-fluorophenyl)-1H-pyrazole-3-carboxamide is a solid.,False
18537,,,,,5-chloro-7-pyrazolopyrimidine-3-carbonitrile is experimental.,5-chloro-7-pyrazolopyrimidine-3-carbonitrile is a solid.,False
18538,,,,,5--7-(PROPAN-2-YLAMINO)PYRAZOLOPYRIMIDINE-3-CARBONITRILE is experimental.,5--7-(PROPAN-2-YLAMINO)PYRAZOLOPYRIMIDINE-3-CARBONITRILE is a solid.,False
18539,,,,,4-{amino}-N--1H-pyrazole-3-carboxamide is experimental.,4-{amino}-N--1H-pyrazole-3-carboxamide is a solid.,False
18540,"AT7519 is a selective inhibitor of certain Cyclin Dependent Kinases (CDKs) leading to tumour regression. It is developed by Astex for the treatment of solid tumours and haematological malignancies. Investigated for use/treatment in leukemia (unspecified), lymphoma (unspecified), myelodysplastic syndrome, and solid tumors. AT7519 is a selective inhibitor of certain Cyclin Dependent Kinases (CDKs) leading to tumour regression.",,,,AT-7519 is investigational.,AT-7519 is a solid.,True
18541,,,,,4-(4-methoxy-1H-pyrrolopyridin-3-yl)pyrimidin-2-amine is experimental.,4-(4-methoxy-1H-pyrrolopyridin-3-yl)pyrimidin-2-amine is a solid.,False
18542,,,,,4-(4-propoxy-1H-pyrrolopyridin-3-yl)pyrimidin-2-amine is experimental.,4-(4-propoxy-1H-pyrrolopyridin-3-yl)pyrimidin-2-amine is a solid.,False
18543,,,,,HYDROXY(OXO)(3-{PYRIMIDIN-2(5H)-YLIDENE]AMINO}PHENYL)AMMONIUM is experimental.,HYDROXY(OXO)(3-{PYRIMIDIN-2(5H)-YLIDENE]AMINO}PHENYL)AMMONIUM is a solid.,False
18544,,,,,"4-Methyl-5-imino}-2,5-dihydro-4-pyrimidinyl]-1,3-thiazol-2-amine is experimental.","4-Methyl-5-imino}-2,5-dihydro-4-pyrimidinyl]-1,3-thiazol-2-amine is a solid.",False
18545,,,,,6-CYCLOHEXYLMETHYLOXY-2-(4'-HYDROXYANILINO)PURINE is experimental.,6-CYCLOHEXYLMETHYLOXY-2-(4'-HYDROXYANILINO)PURINE is a solid.,False
18546,,,,,4-(6-CYCLOHEXYLMETHOXY-9H-PURIN-2-YLAMINO)--BENZAMIDE is experimental.,4-(6-CYCLOHEXYLMETHOXY-9H-PURIN-2-YLAMINO)--BENZAMIDE is a solid.,False
18547,,,,,6-(CYCLOHEXYLMETHOXY)-8-ISOPROPYL-9H-PURIN-2-AMINE is experimental.,6-(CYCLOHEXYLMETHOXY)-8-ISOPROPYL-9H-PURIN-2-AMINE is a solid.,False
18548,,,,,3-(6-CYCLOHEXYLMETHOXY-9H-PURIN-2-YLAMINO)-BENZENESULFONAMIDE is experimental.,3-(6-CYCLOHEXYLMETHOXY-9H-PURIN-2-YLAMINO)-BENZENESULFONAMIDE is a solid.,False
18549,,,,,(2R)-2-{triazin-2-yl]amino}butan-1-ol is experimental.,(2R)-2-{triazin-2-yl]amino}butan-1-ol is a solid.,False
18550,,,,,3-({2-AMINO}PHENYL)SULFONYL]ETHYL}AMINO)PROPAN-1-OL is experimental.,3-({2-AMINO}PHENYL)SULFONYL]ETHYL}AMINO)PROPAN-1-OL is a solid.,False
18551,,,,,"6-CYCLOHEXYLMETHYLOXY-5-NITROSO-PYRIMIDINE-2,4-DIAMINE is experimental.","6-CYCLOHEXYLMETHYLOXY-5-NITROSO-PYRIMIDINE-2,4-DIAMINE is a solid.",False
18552,,,,,"1-methyl-8-(phenylamino)-4,5-dihydro-1H-pyrazoloquinazoline-3-carboxylic acid is experimental.","1-methyl-8-(phenylamino)-4,5-dihydro-1H-pyrazoloquinazoline-3-carboxylic acid is a solid.",False
18553,,,,,"6-BROMO-13-THIA-2,4,8,12,19-PENTAAZATRICYCLONONADECA-1(18),3(19),4,6,14,16-HEXAENE 13,13-DIOXIDE is experimental.","6-BROMO-13-THIA-2,4,8,12,19-PENTAAZATRICYCLONONADECA-1(18),3(19),4,6,14,16-HEXAENE 13,13-DIOXIDE is a solid.",False
18554,,,,,(2R)-2-({9-(1-methylethyl)-6--9H-purin-2-yl}amino)butan-1-ol is experimental.,(2R)-2-({9-(1-methylethyl)-6--9H-purin-2-yl}amino)butan-1-ol is a solid.,False
18555,,,,,"1--1,6-DIHYDROPYRAZOLOINDAZOLE-3-CARBOXAMIDE is experimental.","1--1,6-DIHYDROPYRAZOLOINDAZOLE-3-CARBOXAMIDE is a solid.",False
18556,,,,,"5-(2,3-dichlorophenyl)-N-(pyridin-4-ylmethyl)pyrazolopyrimidin-7-amine is experimental.","5-(2,3-dichlorophenyl)-N-(pyridin-4-ylmethyl)pyrazolopyrimidin-7-amine is a solid.",False
18557,,,,,6-(2-fluorophenyl)-N-(pyridin-3-ylmethyl)imidazopyrazin-8-amine is experimental.,6-(2-fluorophenyl)-N-(pyridin-3-ylmethyl)imidazopyrazin-8-amine is a solid.,False
18558,,,,,3-methyl-N-(pyridin-4-ylmethyl)imidazopyrazin-8-amine is experimental.,3-methyl-N-(pyridin-4-ylmethyl)imidazopyrazin-8-amine is a solid.,False
18559,,,,,5-(2-fluorophenyl)-N-(pyridin-4-ylmethyl)pyrazolopyrimidin-7-amine is experimental.,5-(2-fluorophenyl)-N-(pyridin-4-ylmethyl)pyrazolopyrimidin-7-amine is a solid.,False
18560,,,,,3-bromo-5-phenyl-N-(pyridin-3-ylmethyl)pyrazolopyrimidin-7-amine is experimental.,3-bromo-5-phenyl-N-(pyridin-3-ylmethyl)pyrazolopyrimidin-7-amine is a solid.,False
18561,,,,,3-bromo-5-phenyl-N-(pyrimidin-5-ylmethyl)pyrazolopyridin-7-amine is experimental.,3-bromo-5-phenyl-N-(pyrimidin-5-ylmethyl)pyrazolopyridin-7-amine is a solid.,False
18562,,,,,3-bromo-6-phenyl-N-(pyrimidin-5-ylmethyl)imidazopyridin-8-amine is experimental.,3-bromo-6-phenyl-N-(pyrimidin-5-ylmethyl)imidazopyridin-8-amine is a solid.,False
18563,,,,,"N-((2-aminopyrimidin-5-yl)methyl)-5-(2,6-difluorophenyl)-3-ethylpyrazolopyrimidin-7-amine is experimental.","N-((2-aminopyrimidin-5-yl)methyl)-5-(2,6-difluorophenyl)-3-ethylpyrazolopyrimidin-7-amine is a solid.",False
18564,,,,,3-cyclopropyl-5-phenyl-N-(pyridin-3-ylmethyl)pyrazolopyrimidin-7-amine is experimental.,3-cyclopropyl-5-phenyl-N-(pyridin-3-ylmethyl)pyrazolopyrimidin-7-amine is a solid.,False
18565,,,,,4-{AMINO}BENZAMIDE is experimental.,4-{AMINO}BENZAMIDE is a solid.,False
18566,,,,,4-BENZENESULFONAMIDE is experimental.,4-BENZENESULFONAMIDE is a solid.,False
18567,,,,,N-(5-Isopropyl-thiazol-2-YL)-2-pyridin-3-YL-acetamide is experimental.,N-(5-Isopropyl-thiazol-2-YL)-2-pyridin-3-YL-acetamide is a solid.,False
18568,,,,,Variolin B is experimental.,Variolin B is a solid.,False
18569,,,,,N(6)-dimethylallyladenine is experimental.,N(6)-dimethylallyladenine is a solid.,False
18570,,,,,"D-Gluco-2,5-Anhydro-1-Deoxy-1-Phosphonohexitol-6-Phosphate is experimental.","D-Gluco-2,5-Anhydro-1-Deoxy-1-Phosphonohexitol-6-Phosphate is a solid.",False
18571,,,,,sn-glycerol 3-phosphate is experimental.,sn-glycerol 3-phosphate is a solid.,False
18572,A nucleoside triphosphate analogue that is ATP in which one of the oxygens attached to 3-phosphate group is replaced by sulfur.,,,,Adenosine 5'-triphosphate is experimental.,Adenosine 5'-triphosphate is a solid.,True
18573,,,,,Fructose-6-phosphate is experimental.,Fructose-6-phosphate is a solid.,False
18574,"Cefdinir, also known as Omnicef, is a semi-synthetic, broad-spectrum antibiotic belonging to the third generation of the cephalosporin class. It has been proven to be effective for the treatment of common bacterial infections in the ear, sinus, throat, lungs, and skin. Cefdinir was approved by the FDA in 1997 to treat a variety of mild to moderate infections and was initially marketed by Abbvie. Because of its chemical structure, it is effective against organisms that are resistant to first-line cephalosporin therapy due to the production of beta-lactamase enzymes. Cefdinir is indicated to treat acute bacterial otitis media, acute maxillary sinusitis, community-acquired (CA) pneumonia, acute bacterial exacerbations of chronic bronchitis, pharyngitis/tonsillitis, and uncomplicated skin and skin structure infections in children and adults. Cefdinir is a bactericidal agent that treats bacterial infections by interfering with cell wall synthesis. Five-member thiazolidine rings that make up penicillins are replaced in cephalosporins by a six-member dihydrothiazine ring, conferring greater bactericidal activity. This This 6-member ring enables cefdinir and other cephalosporins to resist inactivation by certain bacterial enzymes.",The molecular weight is 395.41.,Cefdinir has a topological polar surface area of 158.21.,The log p value of  is -0.48.,Cefdinir is approved.,Cefdinir is a solid.,True
18575,,,,,"N,N'-DIMETHYL-N-(ACETYL)-N'-(7-NITROBENZ-2-OXA-1,3-DIAZOL-4-YL)ETHYLENEDIAMINE is experimental.","N,N'-DIMETHYL-N-(ACETYL)-N'-(7-NITROBENZ-2-OXA-1,3-DIAZOL-4-YL)ETHYLENEDIAMINE is a solid.",False
18576,"Icatibant (Firazyr) is a synthetic peptidomimetic drug consisting of ten amino acids, and acts as an effective and specific antagonist of bradykinin B2 receptors. It has been approved in the EU for use in hereditary angioedema, and is under investigation for a number of other conditions in which bradykinin is thought to play a significant role. Icatibant currently has orphan drug status in the United States and FDA approved on August 25, 2011. Approved for use in acute attacks of hereditary angioedema (HAE). Investigated for use/treatment in angioedema, liver disease, and burns and burn infections. Icatibant is a potent, specific, competitive, and selective peptidomimetic bradykinin beta2-receptor antagonist (pA2 = 9.04). It has a modified peptide structure, and is the first bradykinin receptor antagonist to act on the guinea-pig trachea without demonstrating agonist effects. It also inhibits aminopeptidase N (Ki = 9.1 μM). If an IV dose of 0.4 and 0.8 mg/kg was infused over 4 hours, one may observe an inhibited response to bradykinin challenge for 6 - 8 hours following completion of infusion.  Bradykinin is a peptide-based hormone that is formed locally in tissues in response to a trauma and acts to increases vessel permeability, dilates blood vessels and causes smooth muscle cells to contract. Bradykinin plays an important role in the mediation of pain as surplus bradykinin is partly responsible for producing signs of inflammation by activating bradykinin B2 receptors. In patients with HAE, they have an absent or dysfunctional C1-esterase inhibitor. This inhibitor is responsible for the production of bradykinin in which displacement of bradykinin from B2 receptors by icatibant has an inhibitory effect on the receptor for a relatively long time.",The molecular weight is 1304.54.,Icatibant has a topological polar surface area of 516.22.,The log p value of  is -5.89.,Icatibant is approved and investigational.,Icatibant is a solid.,True
18577,,,,,Methyl nonanoate is experimental.,Methyl nonanoate is a solid.,False
18578,,,,,"2,3-Dihydroxy-Benzoic Acid is experimental.","2,3-Dihydroxy-Benzoic Acid is a solid.",False
18579,,,,,Carboxymycobactin S is experimental.,Carboxymycobactin S is a solid.,False
18580,,,,,"2,3,-Dihydroxybenzoylserine is experimental.","2,3,-Dihydroxybenzoylserine is a solid.",False
18581,,,,,Carboxymycobactin T is experimental.,Carboxymycobactin T is a solid.,False
18582,,,,,"Trencam-3,2-Hopo is experimental.","Trencam-3,2-Hopo is a solid.",False
18583,"Hyaluronic acid (HA) is an anionic, nonsulfated glycosaminoglycan distributed widely throughout connective, epithelial, and neural tissues. It is unique among glycosaminoglycans in that it is nonsulfated, forms in the plasma membrane instead of the Golgi, and can be very large, with its molecular weight often reaching the millions. One of the chief components of the extracellular matrix, hyaluronic acid contributes significantly to cell proliferation and migration, and may also be involved in the progression of some malignant tumors. Used to treat knee pain in patients with joint inflammation (osteoarthritis). It is usually used in patients who have not responded to other treatments such as acetaminophen, exercise, or physical therapy. Hyaluronic acid may also be used in plastic surgery to reduce wrinkles on the face or as a filler in other parts of the body. May be used in ophthalmology to assist in the extraction of cataracts, the implantation of intraocular lenses, corneal transplants, glaucoma filtration, retinal attachment and in the treatment of dry eyes. Finally, hyaluronic acid is also used to coat the bladder lining in treating interstitial cystitis. Hyaluronic acid is similar to a substance that occurs naturally in the joints. It may work by acting as a lubricant and shock absorber in the joint, helping the knee to move smoothly, thereby lessening pain. Hyaluronic acid performs its activities as a tissue lubricant and hence, it is thought to be key in the modulation of interactions between adjacent tissues. Hyaluronic acid is a polysaccharide which is distributed widely in the extracellular matrix of connective tissue in man. It forms a viscoelastic solution in water which makes it suitable for aqueous and vitreous humor in ophthalmic surgery. It is suggested to provide mechanical protection for ocular tissues and cell layers due to its high viscosity. The elasticity of the solutions of hyaluronic acid can assist in the absorption of mechanical stress and the generation of a protective buffer for the tissues. This viscoelasticity enables maintenance of a deep chamber during surgical manipulation since the solution does not flow out of the open anterior chamber. ",,,,Hyaluronic acid is approved and vet_approved.,Hyaluronic acid is a solid.,True
18584,"P54 reduces the inflammation associated with cancer/tumors, Crohn's disease, inflammatory bowel disease, osteoarthritis, and ulcerative colitis. It inhibits the induction of the enzyme NFkB, thereby inhibiting downstream inflammatory genes such as COX II and iNOS. Investigated for use/treatment in cancer/tumors (unspecified), crohn's disease, inflammatory bowel disease, osteoarthritis, and ulcerative colitis. P54 inhibits the induction of the enzyme NFkB, thereby inhibiting downstream inflammatory genes such as COX II and iNOS. P54 inhibits the induction of the enzyme NFkB, thereby inhibiting downstream inflammatory genes such as COX II and iNOS.",,,,P54 is investigational.,P54 is a solid.,True
18585,"NOX-700, an new orally active dithiocarbamate-based nitric oxide (NO) blocking agent that is in development for the treatment of diabetes mellitus (type 2 diabetes). In animal studies, NOX-700 lowered serum glucose, improved glucose tolerance, and reduced the percentage of total glycated hemoglobin. Immunohistochemical studies on Investigated for use/treatment in diabetes mellitus (type 2). NOX-700 is an orally active nitric oxide (NO) blocking agent in development for the treatment of diabetes mellitus (type 2). In animal studies, NOX-700 lowered serum glucose, improved glucose tolerance, and reduced the percentage of total glycated hemoglobin. Immunohistochemical studies on It has been found that oxidative signaling of the redox-sensitive transcription factor, NF-κB, and inhibiting protein glycation are responsible for the drug's therapeutic effects.",,,,NOX-700 is investigational.,NOX-700 is a solid.,True
18586,"SGN-30 is an engineered monoclonal antibody (mAb) that reacts with significant affinity to the CD30 antigen, which is highly expressed on a variety of hematologic malignancies as compared to on normal cells. SGN-30 has been shown to induce direct anti-cancer activity towards tumor cells expressing CD30 and is undergoing phase II trials for cancer therapy. SGN-30 has demonstrated objective antitumor responses as a single agent in phase II clinical trials. We are collaborating with the National Cancer Institute (NCI) on three clinical trials of SGN-30 in combination with chemotherapy for the treatment of relapsed Hodgkin lymphoma, front-line ALCL and pediatric ALCL. Investigated for use/treatment in autoimmune diseases, cancer/tumors (unspecified), lymphoma (non-hodgkin's), and lymphoma (unspecified). SGN-30, a monoclonal antibody with activity against CD30+ malignancies. Through investigation of the mechanisms underlying SGN-30's antitumor activity, SGN-30 treatment was found to activate NF-kappaB and modulation of several messages including the growth regulator p21WAF1/CIP1 (p21) and cellular adhesion marker ICAM-1. p21 protein level changes are believed to be associated with arresting cell growth.  Through investigation of the mechanisms underlying SGN-30's antitumor activity, SGN-30 treatment was found to activate NF-kappaB and modulation of several messages including the growth regulator p21WAF1/CIP1 (p21) and cellular adhesion marker ICAM-1. p21 protein level changes are believed to be associated with arresting cell growth. ",,,,SGN-30 is investigational.,SGN-30 is a solid.,True
18587,,,,,5-(DIMETHYLAMINO)-2-NAPHTHALENESULFONIC ACID is experimental.,5-(DIMETHYLAMINO)-2-NAPHTHALENESULFONIC ACID is a solid.,False
18588,,The molecular weight is 76.05.,Glycolic acid has a topological polar surface area of 57.53.,The log p value of  is -1.04.,Glycolic acid is approved and investigational.,Glycolic acid is a solid.,False
18589,"16-Bromoepiandrosterone is an injectable formulation of a compound called alpha-epi-bromide. It is a chemical relative of DHEA which was selected for development after it showed antiretroviral activity in laboratory tests. Investigated for use/treatment in cystic fibrosis, HIV infection, hepatitis (viral, B), and malaria. HE2000 interacts with certain enzymes, including G6PDH (glucose 6 phosphate dehydrogenase); these enzymes could be involved in the mechanism. Also, the compound is in the steroid hormone series, and involved in control mechanisms in our cells that are much more complex, interacting with receptors and therefore changing the biochemistry of cells. This compound may have many modes of action; we are trying to understand what they may be.",,,,16-Bromoepiandrosterone is investigational.,16-Bromoepiandrosterone is a solid.,True
18590,"Streptomycin is an aminoglycoside antibiotic produced by the soil actinomycete Streptomyces griseus. It acts by binding to the 30S ribosomal subunit of susceptible organisms and disrupting the initiation and elongation steps in protein synthesis. It is bactericidal due to effects that are not fully understood. For the treatment of tuberculosis. May also be used in combination with other drugs to treat tularemia (Francisella tularensis), plague (Yersia pestis), severe M. avium complex, brucellosis, and enterococcal endocarditis (e.g. E. faecalis, E. faecium). Streptomycin is an aminoglycoside antibiotic that works by binding to the bacterial 30S ribosomal subunit, causing misreading of t-RNA, leaving the bacterium unable to synthesize proteins vital to its growth. Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. In addition, some mycobacteria, including the bacteria that cause tuberculosis, are susceptible to aminoglycosides. Infections caused by Gram-positive bacteria can also be treated with aminoglycosides, but other types of antibiotics are more potent and less damaging to the host. In the past the aminoglycosides have been used in conjunction with penicillin-related antibiotics in streptococcal infections for their synergistic effects, particularly in endocarditis. Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses. Aminoglycosides like Streptomycin \irreversibly\"" bind to specific 30S-subunit proteins and 16S rRNA. Specifically Streptomycin binds to four nucleotides of 16S rRNA and a single amino acid of protein S12. This interferes with decoding site in the vicinity of nucleotide 1400 in 16S rRNA of 30S subunit. This region interacts with the wobble base in the anticodon of tRNA. This leads to interference with the initiation complex, misreading of mRNA so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes.""",The molecular weight is 581.58.,Streptomycin has a topological polar surface area of 331.43.,The log p value of  is -3.46.,Streptomycin is approved and vet_approved.,Streptomycin is a solid.,True
18591,,,,,N-benzamide is experimental.,N-benzamide is a solid.,False
18592,"RI 624 is a novel humanized monoclonal antibody that blocks nerve growth factor (NGF), a key mediator of acute and chronic pain. RI 624 is being developed by Rinat and is currently in Phase I clinical trials. Investigated for use/treatment in pain (acute or chronic). RI 624 works very differently from all currently approved drugs for the treatment of pain. Unlike the other pain relievers, RI 624 primarily works to inhibit the production of NGF, rather than COX-2 for instance. NGF is a member of a family of proteins known as neurotrophins that plays a role in the growth of certain sensory neurons, an activity that appears to end at birth or shortly afterward. Pain-causing injury or inflammation induces the synthesis and stimulates the release of NGF in later stages of life. Scientific observation has shown that the up-regulation of NGF is a common component of the inflammatory response that initiates and sustains the pain sensation. NGF therefore appears to have profound direct and indirect stimulatory effects on the primary sensory neurons that mediate pain. RI 624 essentially blocks NGF from binding to its target area and thus impedes an imflammatory response.",,,,RI 624 is investigational.,RI 624 is a solid.,True
18593,,,,,Pyrazolanthrone is experimental.,Pyrazolanthrone is a solid.,False
18594,,,,,Cyclohexyl-{4--Pyrimidin-2-Yl}Amine is experimental.,Cyclohexyl-{4--Pyrimidin-2-Yl}Amine is a solid.,False
18595,,,,,Cyclopropyl-{4--4-Yl-3-Propyl-3h-Imidazol-4-Yl]-Pyrimidin-2-Yl}Amine is experimental.,Cyclopropyl-{4--4-Yl-3-Propyl-3h-Imidazol-4-Yl]-Pyrimidin-2-Yl}Amine is a solid.,False
18596,,,,,"9-(4-Hydroxyphenyl)-2,7-Phenanthroline is experimental.","9-(4-Hydroxyphenyl)-2,7-Phenanthroline is a solid.",False
18597,,,,,N-(tert-butyl)-4-benzenesulfonamide is experimental.,N-(tert-butyl)-4-benzenesulfonamide is a solid.,False
18598,,,,,"N-(3-cyano-4,5,6,7-tetrahydro-1-benzothien-2-yl)-2-fluorobenzamide is experimental.","N-(3-cyano-4,5,6,7-tetrahydro-1-benzothien-2-yl)-2-fluorobenzamide is a solid.",False
18599,,,,,4-{amino}-N-ethylpiperidine-1-carboxamide is experimental.,4-{amino}-N-ethylpiperidine-1-carboxamide is a solid.,False
18600,,,,,"(3Z)-1--4--1H-indole-2,3-dione 3-oxime is experimental.","(3Z)-1--4--1H-indole-2,3-dione 3-oxime is a solid.",False
18601,,,,,"(3E)-5-fluoro-1--1H-indole-2,3-dione 3-oxime is experimental.","(3E)-5-fluoro-1--1H-indole-2,3-dione 3-oxime is a solid.",False
18602,,,,,"(3Z)-1--4-phenyl-1H-indole-2,3-dione 3-oxime is experimental.","(3Z)-1--4-phenyl-1H-indole-2,3-dione 3-oxime is a solid.",False
18603,,,,,5-bromo-N-(3-chloro-2-(4-(prop-2-ynyl)piperazin-1-yl)phenyl)furan-2-carboxamide is experimental.,5-bromo-N-(3-chloro-2-(4-(prop-2-ynyl)piperazin-1-yl)phenyl)furan-2-carboxamide is a solid.,False
18604,,,,,N-cyclohexyl-4-imidazopyridin-3-yl-N-methylpyrimidin-2-amine is experimental.,N-cyclohexyl-4-imidazopyridin-3-yl-N-methylpyrimidin-2-amine is a solid.,False
18605,,,,,"N-{2'--4,4'-BIPYRIDIN-2-YL}-4-METHOXYCYCLOHEXANECARBOXAMIDE is experimental.","N-{2'--4,4'-BIPYRIDIN-2-YL}-4-METHOXYCYCLOHEXANECARBOXAMIDE is a solid.",False
18606,,,,,2-{4-pyridin-3-ylpyrimidin-2-yl)amino]piperidin-1-yl}-N-methylacetamide is experimental.,2-{4-pyridin-3-ylpyrimidin-2-yl)amino]piperidin-1-yl}-N-methylacetamide is a solid.,False
18607,"1-(3-bromophenyl)-7-chloro-6-methoxy-3,4-dihydroisoquinoline is a solid. This compound belongs to the isoquinolines and derivatives. These are aromatic polycyclic compounds containing an isoquinoline moiety, which consists of a benzene ring fused to a pyridine ring and forming benzopyridine. This medication is known to target mitogen-activated protein kinase 10.",,,,"1-(3-bromophenyl)-7-chloro-6-methoxy-3,4-dihydroisoquinoline is experimental.","1-(3-bromophenyl)-7-chloro-6-methoxy-3,4-dihydroisoquinoline is a solid.",True
18608,,,,,"(2R,3R)-2,3-Dihydroxy-4-oxo-4-(propylamino)butanoic acid is experimental.","(2R,3R)-2,3-Dihydroxy-4-oxo-4-(propylamino)butanoic acid is a solid.",False
18609,,,,,Alpha-Benzyl-Aminobenzyl-Phosphonic Acid is experimental.,Alpha-Benzyl-Aminobenzyl-Phosphonic Acid is a solid.,False
18610,"Sipuleucel-T is a personalized, autologous, cellular immunotherapy. Sipuleucel-T is a therapeutic cancer vaccine for prostate cancer. Sipuleucel-T selectively targets the prostate-specific antigen (PSA) known as prostatic acid phosphatase (PAP) that is expressed in around 95% of prostate cancers. It must be prepared specifically for each patient. In metastatic prostate cancer, it has extended survival by median 4.1 months (IMPACT Phase III trial data). Sipuleucel-T is marketed under the brand name Provenge by Dendreon Corporation. Sipuleucel-T was approved by the U.S. Food and Drug Administration (FDA) on April 29, 2010, to treat asymptomatic or minimally symptomatic metastatic Hormone-Refractory Prostate Cancer (HRPC). The treatment initially cost $93,000 at the time of FDA approval, but rose to over $100,000 in 2014. Sipuleucel-T is an autologous cellular immunotherapy indicated for the treatment of asymptomatic or minimally symptomatic metastatic castrate resistant (hormone refractory) prostate cancer.  Sipuleucel-T is designed to induce an immune response targeted against PAP, an antigen expressed in most prostate cancers. During ex vivo culture with PAP-GM-CSF, APCs take up and process the recombinant target antigen into small peptides that are then displayed on the APC surface. This process is done indirectly by the activation of T-cells against PAP which is upregulated by the metastatic cancer cells. The precise mechanism remains unknown, however. ",,,,Sipuleucel-T is approved and investigational.,,True
18611,"Lonidamine (LND) is a drug that interferes with energy metabolism of cancer cells, principally inhibiting aerobic glycolytic activity, by its effect on mitochondrially-bound hexokinase (HK). In such way LND could impair energy-requiring processes, as recovery from potentially lethal damage, induced by radiation treatment and by some cytotoxic drugs. Investigated for use/treatment in benign prostatic hyperplasia, prostate disorders, and cancer/tumors (unspecified). Lonidamine is an orally administered small molecule that inhibits glycolysis by the inactivation of hexokinase. Hexokinase is an enzyme that catalyzes glucose, the first step in glycolysis. The inhibition of hexokinase by lonidamine is well established. In addition, there is evidence that lonidamine may increase programmed cell death. This stems from the observation that mitochondria and mitochondria-bound hexokinase are crucial for induction of apoptosis; agents that directly effect mitochondria may, therefore, trigger apoptosis. Indeed, in vitro models with lonidamine exhibit the hallmarks of apoptosis, including mitochondrial membrane depolarization, release of cytochrome C, phosphatidylserine externalization, and DNA fragmentation. ",The molecular weight is 321.16.,Lonidamine has a topological polar surface area of 55.12.,The log p value of  is 5.03.,Lonidamine is investigational.,Lonidamine is a solid.,True
18612,,,,,Flavone is approved and experimental.,Flavone is a solid.,False
18613,Bivatuzumab (previously BIWA 4) is a humanized monoclonal antibody against CD44 v6.  Investigated for use/treatment in cancer/tumors (unspecified) and head and neck cancer.,,,,Bivatuzumab is investigational.,Bivatuzumab is a solid.,True
18614,"AGI-1067, is a novel small molecule with anti-oxidant and anti-inflammatory properties that was discovered by AtheroGenics and designed to treat atherosclerosis of the blood vessels of the heart, or coronary artery disease. Investigated for use/treatment in atherosclerosis, coronary artery disease, diabetes mellitus type 2, and in-stent restenosis. AGI-1067 works by inhibiting key oxidant signals within cells of blood vessel walls that generate inflammatory processes that are key to the pathogenesis of atherosclerosis. This includes inhibition of inflammatory cytokines, chemokines and vascular adhesion molecules that participate in the initiation, growth and eventual destabilization of the plaque. Its anti-oxidant properties also play a role in its ability to inhibit the formation of oxidized LDL, a critical component in the formation of atherosclerotic plaque.",,,,Succinobucol is investigational.,Succinobucol is a solid.,True
18615,,,,,"N-Hydroxy 1n(4-Methoxyphenyl)Sulfonyl-4-(Z,E-N-Methoxyimino)Pyrrolidine-2r-Carboxamide is experimental.","N-Hydroxy 1n(4-Methoxyphenyl)Sulfonyl-4-(Z,E-N-Methoxyimino)Pyrrolidine-2r-Carboxamide is a solid.",False
18616,,,,,A Disubstituted Succinyl Caprolactam Hydroxymate Mmp3inhibitor is experimental.,A Disubstituted Succinyl Caprolactam Hydroxymate Mmp3inhibitor is a solid.,False
18617,,,,,"N-Hydroxy-4--2,2-Dimethyl-Hexahydro-1,4-Thiazepine-3(S)-Carboxamide is experimental.","N-Hydroxy-4--2,2-Dimethyl-Hexahydro-1,4-Thiazepine-3(S)-Carboxamide is a solid.",False
18618,,,,,(1n)-4-N-Butoxyphenylsulfonyl-(2r)-N-Hydroxycarboxamido-(4s)-Methanesulfonylamino-Pyrrolidine is experimental.,(1n)-4-N-Butoxyphenylsulfonyl-(2r)-N-Hydroxycarboxamido-(4s)-Methanesulfonylamino-Pyrrolidine is a solid.,False
18619,,,,,3-(1h-Indol-3-Yl)-2--Propionic Acid is experimental.,3-(1h-Indol-3-Yl)-2--Propionic Acid is a solid.,False
18620,,,,,"5-Methyl-5-(4-Phenoxy-Phenyl)-Pyrimidine-2,4,6-Trione is experimental.","5-Methyl-5-(4-Phenoxy-Phenyl)-Pyrimidine-2,4,6-Trione is a solid.",False
18621,,,,,1-Benzyl-3-(4-Methoxy-Benzenesulfonyl)-6-Oxo-Hexahydro-Pyrimidine-4-Carboxylic Acid Hydroxyamide is experimental.,1-Benzyl-3-(4-Methoxy-Benzenesulfonyl)-6-Oxo-Hexahydro-Pyrimidine-4-Carboxylic Acid Hydroxyamide is a solid.,False
18622,,,,,N-Hydroxy-1-(4-Methoxyphenyl)Sulfonyl-4-Benzyloxycarbonyl-Piperazine-2-Carboxamide is experimental.,N-Hydroxy-1-(4-Methoxyphenyl)Sulfonyl-4-Benzyloxycarbonyl-Piperazine-2-Carboxamide is a solid.,False
18623,,,,,R-2-{-Sulfonyl}-Amino-6-Methoxy-Hex-4-Ynoic Acid is experimental.,R-2-{-Sulfonyl}-Amino-6-Methoxy-Hex-4-Ynoic Acid is a solid.,False
18624,,,,,2-thiadiazol-2-yl)-ureido]-N-methyl-3-phenyl-propionamide is experimental.,2-thiadiazol-2-yl)-ureido]-N-methyl-3-phenyl-propionamide is a solid.,False
18625,,,,,-ACETIC ACID is experimental.,-ACETIC ACID is a solid.,False
18626,,,,,thiadiazol-2-ylcarbamoyl)-1-phenyl-ethyl]-carbamic acid benzyl ester is experimental.,thiadiazol-2-ylcarbamoyl)-1-phenyl-ethyl]-carbamic acid benzyl ester is a solid.,False
18627,,,,,2-thiadiazol-2yl)-ureido]-N-methyl-3-pentafluorophenyl-propionamide is experimental.,2-thiadiazol-2yl)-ureido]-N-methyl-3-pentafluorophenyl-propionamide is a solid.,False
18628,,,,,N~2~-(biphenyl-4-ylsulfonyl)-N-hydroxy-N~2~-(2-hydroxyethyl)glycinamide is experimental.,N~2~-(biphenyl-4-ylsulfonyl)-N-hydroxy-N~2~-(2-hydroxyethyl)glycinamide is a solid.,False
18629,,,,,3--N-hydroxypropanamide is experimental.,3--N-hydroxypropanamide is a solid.,False
18630,,,,,N-ISOBUTYL-N-GLYCYL HYDROXAMIC ACID is experimental.,N-ISOBUTYL-N-GLYCYL HYDROXAMIC ACID is a solid.,False
18631,,,,,N-BUT-4-YL-N]-BENZYL-P--P-PHOSPHINAMID is experimental.,N-BUT-4-YL-N]-BENZYL-P--P-PHOSPHINAMID is a solid.,False
18632,,,,,2-(2-{2--3-MERCAPTO-PENTANOYLAMINO}-ACETYLAMINO)-3-METHYL-BUTYRIC ACID METHYL ESTER is experimental.,2-(2-{2--3-MERCAPTO-PENTANOYLAMINO}-ACETYLAMINO)-3-METHYL-BUTYRIC ACID METHYL ESTER is a solid.,False
18633,,,,,"9-Butyl-8-(2,5-Dimethoxy-Benzyl)-9h-Purin-6-Ylamine is experimental.","9-Butyl-8-(2,5-Dimethoxy-Benzyl)-9h-Purin-6-Ylamine is a solid.",False
18634,,,,,Geldanamycin is experimental and investigational.,Geldanamycin is a solid.,False
18635,,,,,"8-(2-Chloro-3,4,5-Trimethoxy-Benzyl)-2-Fluoro-9-Pent-4-Ylnyl-9h-Purin-6-Ylamine is experimental.","8-(2-Chloro-3,4,5-Trimethoxy-Benzyl)-2-Fluoro-9-Pent-4-Ylnyl-9h-Purin-6-Ylamine is a solid.",False
18636,,,,,"9-Butyl-8-(3,4,5-Trimethoxybenzyl)-9h-Purin-6-Amine is experimental.","9-Butyl-8-(3,4,5-Trimethoxybenzyl)-9h-Purin-6-Amine is a solid.",False
18637,,,,,"4-(1,3-Benzodioxol-5-Yl)-5-(5-Ethyl-2,4-Dihydroxyphenyl)-2h-Pyrazole-3-Carboxylic Acid is experimental.","4-(1,3-Benzodioxol-5-Yl)-5-(5-Ethyl-2,4-Dihydroxyphenyl)-2h-Pyrazole-3-Carboxylic Acid is a solid.",False
18638,,,,,"8-(2,5-Dimethoxy-Benzyl)-2-Fluoro-9h-Purin-6-Ylamine is experimental.","8-(2,5-Dimethoxy-Benzyl)-2-Fluoro-9h-Purin-6-Ylamine is a solid.",False
18639,,,,,"8-(2,5-Dimethoxy-Benzyl)-2-Fluoro-9-Pent-9h-Purin-6-Ylamine is experimental.","8-(2,5-Dimethoxy-Benzyl)-2-Fluoro-9-Pent-9h-Purin-6-Ylamine is a solid.",False
18640,,,,,"9-Butyl-8-(2-Chloro-3,4,5-Trimethoxy-Benzyl)-9h-Purin-6-Ylamine is experimental.","9-Butyl-8-(2-Chloro-3,4,5-Trimethoxy-Benzyl)-9h-Purin-6-Ylamine is a solid.",False
18641,,,,,"4-(1h-Imidazol-4-Yl)-3-(5-Ethyl-2,4-Dihydroxy-Phenyl)-1h-Pyrazole is experimental.","4-(1h-Imidazol-4-Yl)-3-(5-Ethyl-2,4-Dihydroxy-Phenyl)-1h-Pyrazole is a solid.",False
18642,,,,,9-Butyl-8-(3-Methoxybenzyl)-9h-Purin-6-Amine is experimental.,9-Butyl-8-(3-Methoxybenzyl)-9h-Purin-6-Amine is a solid.,False
18643,,,,,9-Butyl-8-(4-Methoxybenzyl)-9h-Purin-6-Amine is experimental.,9-Butyl-8-(4-Methoxybenzyl)-9h-Purin-6-Amine is a solid.,False
18644,,,,,"9-Butyl-8-(2,5-Dimethoxy-Benzyl)-2-Fluoro-9h-Purin-6-Ylamine is experimental.","9-Butyl-8-(2,5-Dimethoxy-Benzyl)-2-Fluoro-9h-Purin-6-Ylamine is a solid.",False
18645,,,,,"8-BenzoDioxol-,5-Ylmethyl-9-Butyl-2-Fluoro-9h-Purin-6-Ylamine is experimental.","8-BenzoDioxol-,5-Ylmethyl-9-Butyl-2-Fluoro-9h-Purin-6-Ylamine is a solid.",False
18646,,,,,"8-(2-Chloro-3,4,5-Trimethoxy-Benzyl)-9-Pent-4-Ylnyl-9h-Purin-6-Ylamine is experimental.","8-(2-Chloro-3,4,5-Trimethoxy-Benzyl)-9-Pent-4-Ylnyl-9h-Purin-6-Ylamine is a solid.",False
18647,,,,,"N--5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-1H-PYRAZOLE-4-CARBOXAMIDE is experimental.","N--5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-1H-PYRAZOLE-4-CARBOXAMIDE is a solid.",False
18648,"SNX-5422 is a synthetic, novel, small molecule Hsp90 Inhibitor. As an oral formulation that demonstrates strong efficacy and tolerability, SNX-5422 is positioned as a breakthrough therapy with broad applicability across a wide range of cancers. Investigated for use/treatment in cancer/tumors (unspecified). SNX-5422 is under development by Serenex. It is orally administered (pill form). Once in the body, SNX-5422 is converted to SNX-2122; that is, SNX-5422 is a prodrug of SNX-2112, which is the active form. SNX-5422 is a direct, potent inhibitor of Hsp90 across a broad range of human cancer cell lines and causes degradation of important Hsp90 client proteins including HER2, AKT and ERK.",,,,SNX-5422 is investigational.,SNX-5422 is a solid.,True
18649,,,,,"N-(4-ACETYLPHENYL)-5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-1H-PYRAZOLE-4-CARBOXAMIDE is experimental.","N-(4-ACETYLPHENYL)-5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-1H-PYRAZOLE-4-CARBOXAMIDE is a solid.",False
18650,,,,,"4-CHLORO-6-(4-{4-PIPERAZIN-1-YL}-1H-PYRAZOL-5-YL)BENZENE-1,3-DIOL is experimental.","4-CHLORO-6-(4-{4-PIPERAZIN-1-YL}-1H-PYRAZOL-5-YL)BENZENE-1,3-DIOL is a solid.",False
18651,,,,,"5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-N-ETHYL-4-PIPERAZIN-1-YL-1H-PYRAZOLE-3-CARBOXAMIDE is experimental.","5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-N-ETHYL-4-PIPERAZIN-1-YL-1H-PYRAZOLE-3-CARBOXAMIDE is a solid.",False
18652,,,,,"5-(5-chloro-2,4-dihydroxyphenyl)-N-ethyl-4-isoxazole-3-carboxamide is experimental.","5-(5-chloro-2,4-dihydroxyphenyl)-N-ethyl-4-isoxazole-3-carboxamide is a solid.",False
18653,,,,,"5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-N-ETHYL-4-(4-METHOXYPHENYL)ISOXAZOLE-3-CARBOXAMIDE is experimental.","5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-N-ETHYL-4-(4-METHOXYPHENYL)ISOXAZOLE-3-CARBOXAMIDE is a solid.",False
18654,,,,,2-amino-4--N-ethylthienopyrimidine-6-carboxamide is experimental.,2-amino-4--N-ethylthienopyrimidine-6-carboxamide is a solid.,False
18655,,,,,"4-CHLORO-6-(4-PIPERAZIN-1-YL-1H-PYRAZOL-5-YL)BENZENE-1,3-DIOL is experimental.","4-CHLORO-6-(4-PIPERAZIN-1-YL-1H-PYRAZOL-5-YL)BENZENE-1,3-DIOL is a solid.",False
18656,,,,,(3E)-3-dihydrofuran-2(3H)-one is experimental.,(3E)-3-dihydrofuran-2(3H)-one is a solid.,False
18657,,,,,"6-(3-BROMO-2-NAPHTHYL)-1,3,5-TRIAZINE-2,4-DIAMINE is experimental.","6-(3-BROMO-2-NAPHTHYL)-1,3,5-TRIAZINE-2,4-DIAMINE is a solid.",False
18658,,,,,"3-({2-BENZYL}AMINO)-1,3-OXAZOL-2(3H)-ONE is experimental.","3-({2-BENZYL}AMINO)-1,3-OXAZOL-2(3H)-ONE is a solid.",False
18659,,,,,N--3-{AMINO}BENZENESULFONAMIDE is experimental.,N--3-{AMINO}BENZENESULFONAMIDE is a solid.,False
18660,,,,,"5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-N-ETHYL-4-(4-METHOXYPHENYL)-1H-PYRAZOLE-3-CARBOXAMIDE is experimental.","5-(5-CHLORO-2,4-DIHYDROXYPHENYL)-N-ETHYL-4-(4-METHOXYPHENYL)-1H-PYRAZOLE-3-CARBOXAMIDE is a solid.",False
18661,,,,,"4-bromo-6-(6-hydroxy-1,2-benzisoxazol-3-yl)benzene-1,3-diol is experimental.","4-bromo-6-(6-hydroxy-1,2-benzisoxazol-3-yl)benzene-1,3-diol is a solid.",False
18662,,,,,CCT-018159 is experimental.,CCT-018159 is a solid.,False
18663,,,,,"4-chloro-6-{5--1,2-benzisoxazol-3-yl}benzene-1,3-diol is experimental.","4-chloro-6-{5--1,2-benzisoxazol-3-yl}benzene-1,3-diol is a solid.",False
18664,,,,,8-(6-BROMO-BENZODIOXOL-5-YLSULFANYL)-9-(3-ISOPROPYLAMINO-PROPYL)-ADENINE is experimental.,8-(6-BROMO-BENZODIOXOL-5-YLSULFANYL)-9-(3-ISOPROPYLAMINO-PROPYL)-ADENINE is a solid.,False
18665,,,,,"4-methyl-7,8-dihydro-5H-thiopyranopyrimidin-2-amine is experimental.","4-methyl-7,8-dihydro-5H-thiopyranopyrimidin-2-amine is a solid.",False
18666,,,,,"(5E,7S)-2-amino-7-(4-fluoro-2-pyridin-3-ylphenyl)-4-methyl-7,8-dihydroquinazolin-5(6H)-one oxime is experimental.","(5E,7S)-2-amino-7-(4-fluoro-2-pyridin-3-ylphenyl)-4-methyl-7,8-dihydroquinazolin-5(6H)-one oxime is a solid.",False
18667,,,,,"8-BENZODIOXOL-,5-YLMETHYL-9-BUTYL-9H- is experimental.","8-BENZODIOXOL-,5-YLMETHYL-9-BUTYL-9H- is a solid.",False
18668,,,,,"4-{carbonyl}benzene-1,3-diol is experimental.","4-{carbonyl}benzene-1,3-diol is a solid.",False
18669,,,,,"2-(1H-pyrrol-1-ylcarbonyl)benzene-1,3,5-triol is experimental.","2-(1H-pyrrol-1-ylcarbonyl)benzene-1,3,5-triol is a solid.",False
18670,,,,,"2--4-(4-oxo-1,2,3,4-tetrahydro-9H-carbazol-9-yl)benzamide is experimental.","2--4-(4-oxo-1,2,3,4-tetrahydro-9H-carbazol-9-yl)benzamide is a solid.",False
18671,,,,,4-(2-methoxyethoxy)-6-methylpyrimidin-2-amine is experimental.,4-(2-methoxyethoxy)-6-methylpyrimidin-2-amine is a solid.,False
18672,,,,,"4-(2,4-dichlorophenyl)-5-phenyldiazenyl-pyrimidin-2-amine is experimental.","4-(2,4-dichlorophenyl)-5-phenyldiazenyl-pyrimidin-2-amine is a solid.",False
18673,,,,,"3,6-DIAMINO-5-CYANO-4-(4-ETHOXYPHENYL)THIENOPYRIDINE-2-CARBOXAMIDE is experimental.","3,6-DIAMINO-5-CYANO-4-(4-ETHOXYPHENYL)THIENOPYRIDINE-2-CARBOXAMIDE is a solid.",False
18674,,,,,"2-AMINO-4-(2,4-DICHLOROPHENYL)-N-ETHYLTHIENOPYRIMIDINE-6-CARBOXAMIDE is experimental.","2-AMINO-4-(2,4-DICHLOROPHENYL)-N-ETHYLTHIENOPYRIMIDINE-6-CARBOXAMIDE is a solid.",False
18675,"Alvespimycin is a derivative of geldanamycin and heat shock protein (HSP) 90 inhibitor. It has been used in trials studying the treatment of solid tumor in various cancer as an antitumor agent. In comparison to the first HSP90 inhibitor tanespimycin, it exhibits some pharmacologically desirable properties such as reduced metabolic liability, lower plasma protein binding, increased water solubility, higher oral bioavailability, reduced hepatotoxicity and superior antitumor activity. Investigated for use as an antineoplastic agent for solid tumors, advanced solid tumours or acute myeloid leukaemia.  Alvespimycin mediates an antitumor activity through HSP90 inhibition that targets client proteins for proteasomal destruction, including oncogenic kinases such as BRAF. The administration of the drug is shown to result in the depletion of client proteins that have oncogenic activity and potential induction of HSP70 (HSP72). It is more selective for tumors over normal tissue. A study also reports that alvespimycin enhances the potency of telomerase inhibition by imetelstat in pre-clinical models of human osteosarcoma. Alvespimycin inhibits HSP90 and its regulation of correct folding and function of many cellular signalling proteins, which are referred to as Hsp90 client proteins. These client proteins are also referred to as oncoproteins and include Her-2, EGFR, Akt, Raf-1, p53, Bcr-Abl, Cdk4, Cdk6 and steroid receptors that are involved in cellular signalling pathways that drive cellular proliferation and counteract apoptosis. They are often over-expressed or mutated in tumors, and contribute to cancer progression and therapy resistance. Alvespimycin promotes an anticancer activity by disrupting Hsp90's chaperone function and inducing the proteasomal degradation of oncoproteins. It is shown to reduce the levels of CDK4 and ERBB2. ",,,,Alvespimycin is investigational.,Alvespimycin is a solid.,True
18676,,,,,"(2S,3S,4R,5S)-2-(4-Amino-4,5-dihydro-1H-pyrrolopyrimidin-7-yl)-5--3,4-pyrrolidinediol is experimental.","(2S,3S,4R,5S)-2-(4-Amino-4,5-dihydro-1H-pyrrolopyrimidin-7-yl)-5--3,4-pyrrolidinediol is a solid.",False
18677,,,,,Formycin is experimental.,Formycin is a solid.,False
18678,,,,,5'-S-methyl-5'-thioadenosine is experimental.,5'-S-methyl-5'-thioadenosine is a solid.,False
18679,,,,,5'-Deoxy-5'-(Methylthio)-Tubercidin is experimental.,5'-Deoxy-5'-(Methylthio)-Tubercidin is a solid.,False
18680,"Ingenol mebutate was approved by the FDA in January 2012, and it is marketed under the name Picato®. Picato gel is indicated for the topical treatment of actinic keratosis. Before approval, ingenol mebutate was called PEP005 as an investigational drug. PEP005 is a selective small molecule activator of protein kinase C (PKC) extracted from the plant Euphorbia peplus, whose sap has been used as a traditional medicine for the treatment of skin conditions including warts and cancer. PEP005 also has potent anti-leukemic effects, inducing apoptosis in myeloid leukemia cell lines and primary AML cells at nanomolar concentrations. For the topical treatment of actinic keratosis. The pharmacodynamics of ingenol mebutate in producing cell death in actinic keratosis is unknown. The exact mechanism of action of ingenol mebutate in actinic keratosis is unknown. It is presumed to involve primary necrosis then neutrophil-mediated inflammation and antibody-dependent cell death of residual disease cells. Additionally in early studies, PEP005 was shown to be an effective activator of PKC-delta and PKC-delta translocation into nucleus and membranes. PEP005 also downregulates the expression and activity of PKC-alpha. PEP005 induced modulation of PKCs leads to Ras/Raf/MAPK and p38 activation and AKT/PKB inhibition.",The molecular weight is 430.54.,Ingenol mebutate has a topological polar surface area of 104.06.,The log p value of  is 3.41.,Ingenol mebutate is approved.,Ingenol mebutate is a solid.,True
18681,Aprinocarsen is a specific antisense oligonucleotide inhibitor of protein kinase C-alpha. Investigated for use/treatment in lung cancer.,,,,Aprinocarsen is investigational.,Aprinocarsen is a solid.,True
18682,,,,,(4R)-4-(3-butoxy-4-methoxybenzyl)imidazolidin-2-one is experimental.,(4R)-4-(3-butoxy-4-methoxybenzyl)imidazolidin-2-one is a solid.,False
18683,,,,,"6--2-(3-Nitrophenyl)-5-Thioxo-5,6,-Dihydro-7h-ThienolPyrroloImidazol-7-One is experimental.","6--2-(3-Nitrophenyl)-5-Thioxo-5,6,-Dihydro-7h-ThienolPyrroloImidazol-7-One is a solid.",False
18684,,,,,L-778123 is experimental.,L-778123 is a solid.,False
18685,,,,,2--ETHYL-DIPHOSPHATE is experimental.,2--ETHYL-DIPHOSPHATE is a solid.,False
18686,,,,,S-Benzylcysteine is experimental.,S-Benzylcysteine is a solid.,False
18687,"Cilastatin is an inhibitor of renal dehydropeptidase, an enzyme responsible for both the metabolism of thienamycin beta-lactam antibiotics as well as conversion of leukotriene D4 to leukotriene E4. Since the antibiotic, , is one such antibiotic that is hydrolyzed by dehydropeptidase, cilastatin is used in combination with imipenem to prevent its metabolism. The first combination product containing both drugs was approved by the FDA in November of 1985 under the trade name Primaxin, marketed by Merck & Co. A newer triple-drug product was approved in July 2019 under the trade name Recarbrio which also contains. Cilastatin is indicated, in combination with with or without , for the treatment of bacterial infections including respiratory, skin, bone, gynecologic, urinary tract, and intra-abdominal as well as septicemia and endocarditis. Cilastatin is a chemical compound which inhibits the human enzyme dehydropeptidase. Renal Dehydropeptidase degrades the antibiotic. Cilastatin is therefore combined intravenously with imipenem in order to protect it from dehydropeptidase and prolong its antibacterial effect. However, cilastatin in and of itself does not have any antibacterial activity. The increased renal excretion of unchanged imipenem appears to prevent proximal tubular necrosis associated with high doses of imipenem. Cilastatin is a renal dehydropeptidase-I inhibitor. Since the antibiotic, imipenem, is hydrolyzed by dehydropeptidase-I, which resides in the brush border of the renal tubule, cilastatin is administered with imipenem to block the metabolism of imipenem.",The molecular weight is 358.45.,Cilastatin has a topological polar surface area of 129.72.,The log p value of  is 0.47.,Cilastatin is approved and investigational.,Cilastatin is a solid.,True
18688,,,,,1-Guanidinium-7-Aminoheptane is experimental.,1-Guanidinium-7-Aminoheptane is a solid.,False
18689,"CTCE-0214 is a stable peptide agonist of stromal cell-derived factor-1 (SDF-1), a key signaling molecule in the proliferation, homing, engraftment and expansion of hematopoietic stem cells and white blood cells. Investigated for use/treatment in adverse effects (chemotherapy), blood (blood forming organ disorders, unspecified), cancer/tumors (unspecified), neutropenics, and vascular diseases. CTCE-0214 mimics the activity of the natural chemokine SDF-1 by increasing the level of white blood cells (neutrophils), bleeding prevention cells (platelets) and stem cells (primitive blood forming cells) in the blood. SDF-1 is also believed to work as a traffic controller for infection-fighting white blood cells and progenitor cell migration providing an essential function to combat immunosuppression.",,,,CTCE-0214 is investigational.,CTCE-0214 is a solid.,True
18690,,,,,L-Myo-Inositol-1-Phosphate is experimental.,L-Myo-Inositol-1-Phosphate is a solid.,False
18691,,,,,"2-Acetamido-2-Deoxy-D-Glucono-1,5-Lactone is experimental.","2-Acetamido-2-Deoxy-D-Glucono-1,5-Lactone is a solid.",False
18692,"N-Acetyl-glucosamine thiazoline (NAG-thiazoline) is an analog of the oxazolinium bicyclic intermediate leading from N-acetylglucosamine to 1,6-anhydro-N-acetylmuramic acid.",,,,N-Acetyl-glucosamine thiazoline is experimental.,N-Acetyl-glucosamine thiazoline is a solid.,True
18693,,,,,"(2R,3R,4S,5R)-2-acetamido-3,4-dihydroxy-5-hydroxymethyl-piperidine is experimental.","(2R,3R,4S,5R)-2-acetamido-3,4-dihydroxy-5-hydroxymethyl-piperidine is a solid.",False
18694,"MLN0415 is a novel, small molecule IKK2 inhibitor, discovered by Millennium scientists. In preclinical studies, MLN0415 was shown to decrease NF-kB activation and down-regulate the expression of a number of inflammatory proteins. Because inflammatory proteins play a critical role in inflammation and drive the inflammatory response to disease, controlling these proteins may prevent or slow disease progression.  Investigated for use/treatment in inflammatory disorders (unspecified). MLN0415 is an oral, highly selective, small molecule",,,,MLN0415 is investigational.,MLN0415 is a solid.,True
18695,"Synthetic cyclic hexapeptide that binds to platelet receptor glycoprotein and inhibits platelet aggregation. Derived from venom of the Southeastern pygmy rattlesnake (Sistrurus miliarus barbouri), eptifibatide is a cyclic heptapeptide that belongs to the class of arginin-glycin-aspartat-mimetics. For treatment of myocardial infarction and acute coronary syndrome. Eptifibatide is an anti-coagulant that selectively and reversibly blocks the platelet glycoprotein IIb/IIIa receptor.  Eptifibatide inhibits platelet aggregation by reversibly binding to the platelet receptor glycoprotein (GP) IIb/IIIa of human platelets, thus preventing the binding of fibrinogen, von Willebrand factor, and other adhesive ligands. Inhibition of platelet aggregation occurs in a dose- and concentration-dependent manner.",The molecular weight is 831.97.,Eptifibatide has a topological polar surface area of 323.89.,The log p value of  is -2.86.,Eptifibatide is approved and investigational.,Eptifibatide is a liquid.,True
18696,"LM-609 (Vitaxin) is an artificial antibody that targets a protein on the surface of newly forming blood vessels, as well as on certain tumors. In addition to cancer, the protein has been implicated in bone destruction in rheumatoid arthritis and the inflammatory process in psoriasis. Investigated for use/treatment in colorectal cancer, melanoma, prostate cancer, psoriasis and psoriatic disorders, rheumatoid arthritis, and solid tumors. LM-609 targets the alpha-v beta-3 integrin, which is a protein complex expressed on the surface of newly forming blood vessels, certain tumor types, and on a number of other cell types, including macrophages and osteoclasts. As such, alpha-v beta-3 integrin is implicated in a number of disease processes, including the growth and metastasis of tumors, the bone destruction in RA and the inflammatory process in psoriasis.",,,,LM-609 is investigational.,LM-609 is a solid.,True
18697,,,,,"1--Pyrrolidine-2-Carboxylic Acid(1,2,3,4-Tetrahydro-Naphthalen-1-Yl)-Amide is experimental.","1--Pyrrolidine-2-Carboxylic Acid(1,2,3,4-Tetrahydro-Naphthalen-1-Yl)-Amide is a solid.",False
18698,,,,,"N-METHYLALANYL-3-METHYLVALYL-4-PHENOXY-N-(1,2,3,4-TETRAHYDRONAPHTHALEN-1-YL)PROLINAMIDE is experimental.","N-METHYLALANYL-3-METHYLVALYL-4-PHENOXY-N-(1,2,3,4-TETRAHYDRONAPHTHALEN-1-YL)PROLINAMIDE is a solid.",False
18699,"A second-generation synthetic antisense oligonucleotide with potential antineoplastic activity. AEG35156 selectively blocks the cellular expression of X-linked inhibitor of apoptosis protein (XIAP), a pivotal inhibitor of apoptosis that is overexpressed in many tumors. This agent reduces total levels of XIAP in tumor cells, working synergistically with cytotoxic drugs to overcome tumor cell resistance to apoptosis. XIAP interferes with both the intrinsic and extrinsic program-death signaling pathways, which may render tumor cells resistant to apoptosis. Investigated for use/treatment in cancer/tumors (unspecified) and leukemia (myeloid).",,,,AEG35156 is investigational.,AEG35156 is a solid.,True
18700,"Crizanlizumab is a humanized IgG2 monoclonal antibody used to reduce the frequency of vaso-occlusive crises in patients with sickle cell disease. Sickle cell disease is a genetically inherited condition prevalent in the Middle East, Africa, and certain parts of India. The genetic mutation associated with this disease leads to the formation of abnormal, sickle shaped red blood cells that aggregate and block blood vessels throughout the body, causing vaso-occlusive crises. Sickle cell disease can lead to excruciating pain, stroke, infection, and various other complications arising from the blockage of blood vessels. Crizanlizumab is indicated to reduce the frequency of vaso-occlusive crisis in patients with sickle cell diseases who are ≥16 years old. Crizanlizumab is a P-selectin inhibitor that prevents interactions between endothelial cells, platelets, red blood cells, and leukocytes. It has a long duration of action as it is given every 4 weeks. Patients should be counselled regarding the risk of infusion reactions as well as crizanlizumab's interference with platelet counts using EDTA tubes. Crizanlizumab binds to P-selectin on endothelial cells and platelets, preventing their interaction with P-selectin glycoprotein ligand 1 on endothelial cells, platelets, red blood cells, and leukocytes. By preventing this interaction, components of the blood are less likely to come together, causing a vaso-occlusive crisis in patients with sickle cell diseases. The median per year incidence of vaso-occlusive crises was 1.04 in the high-dose crizanlizumab group, 2.00 in the low-dose crizanlizumab group, and 2.08 in the placebo group.",,,,Crizanlizumab is approved and investigational.,Crizanlizumab is a solid.,True
18701,,,,,Phosphatidylethanolamine is experimental.,Phosphatidylethanolamine is a solid.,False
18702,"Sodium tetradecyl sulfate is an anionic surface-active agent which is used for its wetting properties in the industry and is also used in medicine as a blood vessel irritant and sclerosing agent for hemorrhoids and varicose veins. Sotradecol (sodium tetradecyl sulfate injection) is indicated in the treatment of small, uncomplicated varicose veins of the legs showing simple dilation, with competent valves. Telangiectasias or varicose veins occur in about 33% of adult women and about 15% of adult men. Sclerotherapy with sotradecol is widely used in the treatment of varicose veins. When injected directly into a vein, sodium tetradecyl sulfate causes intimal inflammation and venous thrombus formation, which then results in occlusion of the vein. Following this sequence of events, fibrous tissue forms and causes partial to complete obliteration of the vein, which may be temporary or permanent. An important role of this drug, as well as other sclerosing agents, is to control active hemorrhage and encourage hemostasis. This may be due to the esophageal and vascular smooth muscle spasm induced by the sclerosing agent. ",,,,Tetradecyl hydrogen sulfate (ester) is approved.,,True
18703,,,,,5--2-Hydroxy-Benzoic Acid is experimental.,5--2-Hydroxy-Benzoic Acid is a solid.,False
18704,,,,,2-HYDROXY-5-(2-MERCAPTO-ETHYLSULFAMOYL)-BENZOIC ACID is experimental.,2-HYDROXY-5-(2-MERCAPTO-ETHYLSULFAMOYL)-BENZOIC ACID is a solid.,False
18705,,,,,methyl (3S)-3--4-oxopentanoate is experimental.,methyl (3S)-3--4-oxopentanoate is a solid.,False
18706,,,,,"1-METHYL-5-(2-PHENOXYMETHYL-PYRROLIDINE-1-SULFONYL)-1H-INDOLE-2,3-DIONE is experimental.","1-METHYL-5-(2-PHENOXYMETHYL-PYRROLIDINE-1-SULFONYL)-1H-INDOLE-2,3-DIONE is a solid.",False
18707,,,,,-acetic acid is experimental.,-acetic acid is a solid.,False
18708,,,,,4--BENZOIC ACID is experimental.,4--BENZOIC ACID is a solid.,False
18709,,,,,(1S)-2-oxo-1-phenyl-2-ethyl acetate is experimental.,(1S)-2-oxo-1-phenyl-2-ethyl acetate is a solid.,False
18710,,,,,(1S)-1-(3-chlorophenyl)-2-oxo-2-ethyl acetate is experimental.,(1S)-1-(3-chlorophenyl)-2-oxo-2-ethyl acetate is a solid.,False
18711,,,,,"N--N'-(1,3,4-trioxo-1,2,3,4-tetrahydroisoquinolin-6-yl)butanediamide is experimental.","N--N'-(1,3,4-trioxo-1,2,3,4-tetrahydroisoquinolin-6-yl)butanediamide is a solid.",False
18712,"Vaccine against Lyme disease that contains lipoprotein OspA, an outer surface protein of Borrelia burgdorferi sensu stricto ZS7, as expressed by Escherichia coli. Lipoprotein OspA is a single polypeptide chain of 257 amino acids with lipids covalently bonded to the N terminus. It is conjugated with alum (aluminum hydroxide) as an adjuvant. For prophylactic treatment of Lyme Disease OspA lipoprotein is a single polypeptide chain of 270 amino acids. It is a vaccination used to prevent Lyme Disease. OspA lipoprotein, an outer surface protein of the bacteria Borrelia burgdorferi sensu stricto ZS7, is used to stimulate the production of specific antibodies against B. burgdorferi. It is used as a vaccination against Lyme Disease, a disease carried by ticks.",,,,Lyme disease vaccine (recombinant OspA) is approved and withdrawn.,Lyme disease vaccine (recombinant OspA) is a liquid.,True
18713,"Tuberculin Purified Protein Derivative (PPD) is a sterile aqueous solution of a purified protein fraction for intradermal administration as an aid in the diagnosis of tuberculosis. The diagnostic test is commonly referred to as the Mantoux test which serves to minimize the risk of transmission of infection with *Mycobacterium tuberculosis* through early diagnosis and appropriate therapeutic intervention. The purified protein fraction is isolated from culture media filtrates of a human strain of Mycobacterium tuberculosis. It is included in the World Health Organization's List of Essential Medicines. Indicated as a diagnostic agent in Mantoux Test used to detect infection with *Mycobacterium tuberculosis*.  It is intradermally administered to facilitate detection of active tuberculosis caused by *Mycobacterium tuberculosis*. Tuberculin PPD is an inactivated purified protein fraction obtained from human strain of *Mycobacterium tuberculosis*and antigen that induces a delayed hypersensitivity response after few hours following administration. When the person has already acquired the tuberculin antigen, the immune response is stimulated to produce antigen-specific T cells that circulate in the bloodstream for up to several months and years. Clinically, a delayed hypersensitivity reaction to tuberculin is a manifestation of previous infection with M tuberculosis or a variety of non-tuberculosis bacteria. In most cases sensitization is induced by natural mycobacterial infection or by vaccination with BCG Vaccine. The antigen causes, pain, edema and infiltration of immune cells in the injection area.  When exposed to *M. tuberculosis* antigen, the sensitization initiates in the regional lymph nodes where T lymphocytes proliferate in response to the antigenic stimulus to give rise to specifically sensitized lymphocytes which may exist in the circulation up to many years. Antigen is presented to T cells by being ingested by antigen presenting cells (APC), which then present it on their surface to lymphocytes in combination with various MHC molecules once they reach local lymph nodes. Tuberculin PPD most likely interacts with toll-like receptor 2 expressed on APCs that initiates an inflammatory response. Subsequent restimulation of these sensitized lymphocytes with the same or a similar antigen, such as the intradermal injection of tuberculin PPD, evokes a local reaction mediated by these cells. This reaction is referred to as a delayed-type hypersensitivity response that includes vasodilation, edema, and the infiltration of lymphocytes, basophils, monocytes, and neutrophils into the site of antigen injection. The sensitized antigen-specific T lymphocytes proliferate and release lymphokines, which mediate the accumulation of other cells at the site. In vitro studies show that Tuberculin PPD promotes the upregulation of vascular endothelial growth factor (VEGF) expression in T lymphocytes through major histocompatibility (MHC) class II interaction with CD4+ T lymphocyte interaction. The reactions are evident after 5-6 hours following administration. ",,,,Tuberculin purified protein derivative is approved.,Tuberculin purified protein derivative is a liquid.,True
18714,,,,,2-Chlorodideoxyadenosine is experimental.,2-Chlorodideoxyadenosine is a solid.,False
18715,,,,,Diglyme is experimental.,Diglyme is a solid.,False
18716,"A stable adenosine A1 and A2 receptor agonist. Experimentally, it inhibits cAMP and cGMP phosphodiesterase activity. ",,,,N-Ethyl-5'-Carboxamido Adenosine is experimental.,N-Ethyl-5'-Carboxamido Adenosine is a solid.,True
18717,,,,,"METHYL 3-CHLORO-2-{3--3-OXOPROPYL}-4,6-DIHYDROXYBENZOATE is experimental.","METHYL 3-CHLORO-2-{3--3-OXOPROPYL}-4,6-DIHYDROXYBENZOATE is a solid.",False
18718,,,,,"2-(3-AMINO-2,5,6-TRIMETHOXYPHENYL)ETHYL 5-CHLORO-2,4-DIHYDROXYBENZOATE is experimental.","2-(3-AMINO-2,5,6-TRIMETHOXYPHENYL)ETHYL 5-CHLORO-2,4-DIHYDROXYBENZOATE is a solid.",False
18719,,,,,2-(2f-Benzothiazolyl)-5-Styryl-3-(4f-Phthalhydrazidyl)Tetrazolium Chloride is experimental.,2-(2f-Benzothiazolyl)-5-Styryl-3-(4f-Phthalhydrazidyl)Tetrazolium Chloride is a solid.,False
18720,,,,,3-phenyl-5-(1H-pyrazol-3-yl)isoxazole is experimental.,3-phenyl-5-(1H-pyrazol-3-yl)isoxazole is a solid.,False
18721,,,,,"PHENYL-5-(1H-PYRAZOL-3-YL)-1,3-THIAZOLE is experimental.","PHENYL-5-(1H-PYRAZOL-3-YL)-1,3-THIAZOLE is a solid.",False
18722,,,,,4-{amino}-2-hydroxybenzoic acid is experimental.,4-{amino}-2-hydroxybenzoic acid is a solid.,False
18723,,,,,4-(BENZHYDRYLOXY)-1-PIPERIDINE is experimental.,4-(BENZHYDRYLOXY)-1-PIPERIDINE is a solid.,False
18724,Nocodazole is an antineoplastic agent which exerts its effect by depolymerizing microtubules.,,,,Nocodazole is experimental.,Nocodazole is a solid.,True
18725,,,,,3-(4-nitrophenyl)-1H-pyrazole is experimental.,3-(4-nitrophenyl)-1H-pyrazole is a solid.,False
18726,,,,,1-PHENYL-1H-PYRAZOLE-4-CARBOXYLIC ACID is experimental.,1-PHENYL-1H-PYRAZOLE-4-CARBOXYLIC ACID is a solid.,False
18727,"ISS 1018 is a short, synthetic, unmethylated CpG oligodeoxynucleotide (CpG ODN) with immunostimulatory activity. ISS 1018 signals through Toll-like receptor 9 (TLR9) to induce the production of immunoglobulin by B cells and interferon (IFN) -alpha, IFN-beta, interleukin-12 (IL-12), and tumor necrosis factor - alpha (TNF-alpha) by plasmacytoid dendritic cells (pDC). ISS 1018 CpG ODN promotes antigen presentation and co-stimulatory molecule expression. ISS 1018 is currently being investigated in combination with HBsAg vaccine as a prophylactic treatment for to prevent Hepatitis B in adults. It is also being investigated in combination with rituximab for treatment of b-cell or non-hodgkin's lymphoma. Investigated for use/treatment in colorectal cancer, hepatitis (viral, B), and lymphoma (non-hodgkin's). ISS 1018 is a short, synthetic CpG oligodeoxynucleotide (CpG ODN) with immunostimulatory activity. ISS 1018 is an unmethylated CpG motifs in which regions of genomic DNA containing the cytosine-guanine dinucleotide does not show methylation of cytosine. ISS 1018 signals through Toll-like receptor 9 (TLR9) to induce the production of immunoglobulin by B cells and interferon (IFN) -alpha, IFN-beta, interleukin-12 (IL-12), and tumor necrosis factor - alpha (TNF-alpha) by plasmacytoid dendritic cells (pDC). ISS 1018 CpG ODN also promotes antigen presentation and co-stimulatory molecule expression.  ISS 1018 signals through Toll-like receptor 9 (TLR9) to induce the production of immunoglobulin by B cells and interferon (IFN) -alpha, IFN-beta, interleukin-12 (IL-12), and tumor necrosis factor - alpha (TNF-alpha) by plasmacytoid dendritic cells (pDC). pDC and IFN-alpha and -beta then induce natural killer (NK) cell proliferation, NK cell production of IFN-gamma, and NK cell-mediated cytotoxicity. Secreted IFNs also stimulate bystander T cell activation and differentiation of naive CD4+ T cells into T-helper 1 cells on specific antigen challenge.",,,,ISS-1018 is investigational.,ISS-1018 is a solid.,True
18728,"CPG 10101 is a synthetic oligodeoxynucleotide (ODN) in clinical trials. It is a toll-like receptor 9 (TLR9) agonist with antiviral and immunomodulatory properties that could potentially influence chronic infection with HCV. Investigated for use/treatment in hepatitis (viral, C) and viral infection.",,,,CPG 10101 is investigational.,CPG 10101 is a solid.,True
18729,,,,,Dimethyl Propionate Ester Heme is experimental.,Dimethyl Propionate Ester Heme is a solid.,False
18730,,,,,Di-Stearoyl-3-Sn-Phosphatidylethanolamine is experimental.,Di-Stearoyl-3-Sn-Phosphatidylethanolamine is a solid.,False
18731,Arundic acid has been investigated for the treatment of Amyotrophic Lateral Sclerosis (ALS). Investigated for use/treatment in cerebral ischemia. ONO-256 is a neuroprotective because of its actions on glia cells. It has inhibitory effects on the synthesis of a calcium-binding protein S100B. ONO-2506 is undergoing clinical trials for the treatment of patients with stroke and Alzheimer's disease.,,,,Arundic acid is investigational.,Arundic acid is a solid.,True
18732,"(Z)-2-diazenecarbothioamide is a solid. This compound belongs to the phenylpiperazines. These are compounds containing a phenylpiperazine skeleton, which consists of a piperazine bound to a phenyl group. This drug targets the protein S100B.",,,,(Z)-2-diazenecarbothioamide is experimental.,(Z)-2-diazenecarbothioamide is a solid.,True
18733,,,,,2--N-methylhydrazinecarbothioamide is experimental.,2--N-methylhydrazinecarbothioamide is a solid.,False
18734,,,,,1-Hydroxyamine-2-Isobutylmalonic Acid is experimental.,1-Hydroxyamine-2-Isobutylmalonic Acid is a solid.,False
18735,,,,,2-Thiomethyl-3-Phenylpropanoic Acid is experimental.,2-Thiomethyl-3-Phenylpropanoic Acid is a solid.,False
18736,,,,,"2-(Biphenyl-4-Sulfonyl)-1,2,3,4-Tetrahydro-Isoquinoline-3-Carboxylic Acid is experimental.","2-(Biphenyl-4-Sulfonyl)-1,2,3,4-Tetrahydro-Isoquinoline-3-Carboxylic Acid is a solid.",False
18737,,,,,"5--5-phenyl-2,4,6(1H,3H,5H)-pyrimidinetrione is experimental.","5--5-phenyl-2,4,6(1H,3H,5H)-pyrimidinetrione is a solid.",False
18738,,,,,Glycinamide is experimental.,Glycinamide is a solid.,False
18739,An anticancer drug that belongs to the family of drugs called angiogenesis inhibitors. Batimastat is a matrix metalloproteinase inhibitor.,,,,Batimastat is experimental.,Batimastat is a solid.,True
18740,,,,,N-{2-ETHYL}-N'-HYDROXY-N-METHYLUREA is experimental.,N-{2-ETHYL}-N'-HYDROXY-N-METHYLUREA is a solid.,False
18741,,,,,"(5S)-5-(2-amino-2-oxoethyl)-4-oxo-N--3,4,5,6,7,8-hexahydrobenzothienopyrimidine-2-carboxamide is experimental.","(5S)-5-(2-amino-2-oxoethyl)-4-oxo-N--3,4,5,6,7,8-hexahydrobenzothienopyrimidine-2-carboxamide is a solid.",False
18742,,,,,(1S)-1-{amino}-2-methylpropylphosphonic acid is experimental.,(1S)-1-{amino}-2-methylpropylphosphonic acid is a solid.,False
18743,,,,,(1R)-1-{amino}-2-methylpropylphosphonic acid is experimental.,(1R)-1-{amino}-2-methylpropylphosphonic acid is a solid.,False
18744,,,,,3-FORMYL-2-HYDROXY-5-METHYL-HEXANOIC ACID HYDROXYAMIDE is experimental.,3-FORMYL-2-HYDROXY-5-METHYL-HEXANOIC ACID HYDROXYAMIDE is a solid.,False
18745,,,,,BUT-3-ENYL-THIADIAZIN-2-YLIDENE]-AMINE is experimental.,BUT-3-ENYL-THIADIAZIN-2-YLIDENE]-AMINE is a solid.,False
18746,,,,,3-AMINO-AZACYCLOTRIDECAN-2-ONE is experimental.,3-AMINO-AZACYCLOTRIDECAN-2-ONE is a solid.,False
18747,,,,,Duroquinone is experimental.,Duroquinone is a solid.,False
18748,,,,,3-Hydroxymethyl-5-Aziridinyl-1methyl-2--Propanol is experimental.,3-Hydroxymethyl-5-Aziridinyl-1methyl-2--Propanol is a solid.,False
18749,,,,,ES-936 is experimental.,ES-936 is a solid.,False
18750,,,,,"5-Methoxy-1,2-Dimethyl-3-(Phenoxymethyl)Indole-4,7-Dione is experimental.","5-Methoxy-1,2-Dimethyl-3-(Phenoxymethyl)Indole-4,7-Dione is a solid.",False
18751,RH-1 has been used in trials studying the treatment of Advanced Solid Tumors and Non-Hodgkin's Lymphoma.,,,,RH-1 is experimental and investigational.,RH-1 is a solid.,True
18752,,,,,Bishydroxy is experimental.,Bishydroxy is a solid.,False
18753,,,,,"3-(HYDROXYMETHYL)-1-METHYL-5-(2-METHYLAZIRIDIN-1-YL)-2-PHENYL-1H-INDOLE-4,7-DIONE is experimental.","3-(HYDROXYMETHYL)-1-METHYL-5-(2-METHYLAZIRIDIN-1-YL)-2-PHENYL-1H-INDOLE-4,7-DIONE is a solid.",False
18754,,,,,S-Methyl glutathione is experimental.,S-Methyl glutathione is a solid.,False
18755,"A chromone complex that acts by inhibiting the release of chemical mediators from sensitized mast cells. It is used in the prophylactic treatment of both allergic and exercise-induced asthma, but does not affect an established asthmatic attack. For the management of patients with bronchial asthma. Also used in the treatment of vernal keratoconjunctivitis, vernal conjunctivitis, and vernal keratitis. Cromoglicate or cromolyn (USAN), a synthetic compound, inhibits antigen-induced bronchospasms and, hence, is used to treat asthma and allergic rhinitis. Cromoglicate is used as an ophthalmic solution to treat conjunctivitis and is taken orally to treat systemic mastocytosis and ulcerative colitis. Cromoglicate inhibits degranulation of mast cells, subsequently preventing the release of histamine and slow-reacting substance of anaphylaxis (SRS-A), mediators of type I allergic reactions. Cromoglicate also may reduce the release of inflammatory leukotrienes. Cromoglicate may act by inhibiting calcium influx.",The molecular weight is 468.37.,Cromoglicic acid has a topological polar surface area of 165.89.,The log p value of  is 1.48.,Cromoglicic acid is approved.,Cromoglicic acid is a solid.,True
18756,"Acamprosate, also known by the brand name Campral&trade;, is a drug used for treating alcohol dependence. Acamprosate is thought to stabilize the chemical balance in the brain that would otherwise be disrupted by alcoholism, possibly by blocking glutaminergic N-methyl-D-aspartate receptors, while gamma-aminobutyric acid type A receptors are activated. Reports indicate that acamprosate only works with a combination of attending support groups and abstinence from alcohol. Certain serious side effects include allergic reactions, irregular heartbeats, and low or high blood pressure, while less serious side effects include headaches, insomnia, and impotence. Acamprosate should not be taken by people with kidney problems or allergies to the drug. For the maintenance of abstinence from alcohol in patients with alcohol dependence who are abstinent at treatment initiation Pharmacodynamic studies have shown that acamprosate calcium reduces alcohol intake in alcohol-dependent animals in a dose-dependent manner and that this effect appears to be specific to alcohol and the mechanisms of alcohol dependence. Acamprosate calcium has negligible observable central nervous system (CNS) activity in animals outside of its effects on alcohol dependence, exhibiting no anticonvulsant, antidepressant, or anxiolytic activity. The mechanism of action of acamprosate in maintenance of alcohol abstinence is not completely understood. Chronic alcohol exposure is hypothesized to alter the normal balance between neuronal excitation and inhibition. <i>in vitro</i> and <i>in vivo</i> studies in animals have provided evidence to suggest acamprosate may interact with glutamate and GABA neurotransmitter systems centrally, and has led to the hypothesis that acamprosate restores this balance. It seems to inhibit NMDA receptors while activating GABA receptors.",The molecular weight is 181.21.,Acamprosate has a topological polar surface area of 83.47.,The log p value of  is -2.47.,Acamprosate is approved and investigational.,Acamprosate is a solid.,True
18757,"ADX10059 is a metabotropic glutamate receptor 5 (mGluR5) negative allosteric modulator (NAM). The orally available small molecule drug candidate, which is highly specific for mGluR5, was discovered at Addex in 2003. It is developed for the treatment of GERD, migraine and anxiety. Investigated for use/treatment in anxiety disorders, gastroesophageal reflux disease (GERD), and migraine and cluster headaches. ADX10059 is a selective mGluR5 negative allosteric modulator, it may have the possibility to reduce inappropriate esophageal sphincter relaxations and prevent reflux in man.",,,,ADX10059 is investigational.,ADX10059 is a solid.,True
18758,Dipraglurant has been used in trials studying the treatment of Parkinson's Disease. It is a metabotropic glutamate receptor 5 (mGluR5) negative allosteric modulator (NAM).,,,,Dipraglurant is investigational.,,True
18759,,,,,7-Hydroxystaurosporine is experimental and investigational.,7-Hydroxystaurosporine is a solid.,False
18760,,,,,Bisindolylmaleimide VIII is experimental.,Bisindolylmaleimide VIII is a solid.,False
18761,,,,,Bisindolylmaleimide I is experimental.,Bisindolylmaleimide I is a solid.,False
18762,,,,,"10,11-dimethoxy-4-methyldibenzo-2,7-naphthyridine-3,6-diamine is experimental.","10,11-dimethoxy-4-methyldibenzo-2,7-naphthyridine-3,6-diamine is a solid.",False
18763,,,,,5-HYDROXY-3--2H-INDOL-2-ONE is experimental.,5-HYDROXY-3--2H-INDOL-2-ONE is a solid.,False
18764,,,,,1-{2-OXO-3--2H-INDOL-5-YL}UREA is experimental.,1-{2-OXO-3--2H-INDOL-5-YL}UREA is a solid.,False
18765,,,,,2-(1H-imidazol-1-yl)-9-methoxy-8-(2-methoxyethoxy)benzonaphthyridin-4-amine is experimental.,2-(1H-imidazol-1-yl)-9-methoxy-8-(2-methoxyethoxy)benzonaphthyridin-4-amine is a solid.,False
18766,,,,,"3-(1H-indol-3-yl)-4-(1-{2-ethyl}-1H-indol-3-yl)-1H-pyrrole-2,5-dione is experimental.","3-(1H-indol-3-yl)-4-(1-{2-ethyl}-1H-indol-3-yl)-1H-pyrrole-2,5-dione is a solid.",False
18767,,,,,"3--4-(1H-INDOL-3-YL)-1H-PYRROLE-2,5-DIONE is experimental.","3--4-(1H-INDOL-3-YL)-1H-PYRROLE-2,5-DIONE is a solid.",False
18768,"Potent activator of the adenylate cyclase system and the biosynthesis of cyclic AMP. From the plant Coleus forskohlii. Has antihypertensive, positive inotropic, platelet aggregation inhibitory, and smooth muscle relaxant activities; also lowers intraocular pressure and promotes release of hormones from the pituitary gland.",,,,Colforsin is experimental and investigational.,Colforsin is a solid.,True
18769,"Crofelemer, previously known as the investigational drug SP-303, is a novel proanthocyanidin purified from the bark latex of the Amazonian Croton tree <i>Croton lechleri</i>. It is marketed under the brand name Fulyzaq and indicated for the symptomatic treatment of non-infectious diarrhea in adult patients with HIV/AIDS who are taking antiretroviral therapy. For the symptomatic treatment of non-infectious diarrhea in adult patients with HIV/AIDS who are taking antiretroviral therapy. Crofelemer is an inhibitor of secretory diarrhea via inhibition of the CFTR chloride transporter. Crofelemer is not an antimicrobial, and therefore does not drive the emergence of resistance; it does not inhibit motility, and therefore does not cause constipation or rebound diarrhea; and it is not systemically absorbed, reducing the potential for adverse drug interactions and toxicity. Crofelemer is an inhibitor of the cystic fibrosis transmembrane regulator chloride channel (CFTR), as evidenced by its activity on cell cultures, single cell patch clamps, single CFTR channels, and elaboration of mouse intestinal fluid secretion. Crofelemer also inhibits calcium activated chloride channels (CaCC), which in combination with CFTR, are expressed on the luminal side of intestinal cells. Crofelemer inhibition of both of these channels prevents water loss from diarrhea by inhibiting chloride secretion.",,,,Crofelemer is approved.,Crofelemer is a solid.,True
18770,"Investigated for use/treatment in leukemia (lymphoid), multiple myeloma, and lymphoma (unspecified). HCD122 is a fully human, antagonist antibody that targets the CD40 antigen. HCD122 binds to tumor cells that express CD40 and antagonizes (prevents) CD40 ligand-mediated growth and survival of malignant B cells. Based on preclinical data, HCD122 also induces antibody-dependent cellular cytotoxicity (ADCC), killing CD40 expressing tumor cells by immune effector cells. This dual mechanism of action makes HCD122 a drug candidate with potential for the treatment of B-cell malignancies. ",,,,Lucatumumab is investigational.,Lucatumumab is a solid.,True
18771,"Dacetuzumab has been used in trials studying the treatment of Multiple Myeloma, Non-Hodgkin Lymphoma, Leukemia, Lymphocytic, Chronic, and Lymphoma, Large B-Cell, Diffuse. It is a humanized anti-CD40 antibody and induces cytotoxicity in human multiple myeloma cells. Investigated for use/treatment in lymphoma (non-hodgkin's) and multiple myeloma.",,,,Dacetuzumab is investigational.,,True
18772,,,,,2-Amino-3-Oxo-4-Sulfo-Butyric Acid is experimental.,2-Amino-3-Oxo-4-Sulfo-Butyric Acid is a solid.,False
18773,"Acetohydroxamic Acid, a synthetic drug derived from hydroxylamine and ethyl acetate, is similar in structure to urea. In the urine, it acts as an antagonist of the bacterial enzyme urease. Acetohydroxamic Acid has no direct antimicrobial action and does not acidify urine directly. It is used, in addition to antibiotics or medical procedures, to treat chronic urea-splitting urinary infections. Used, in addition to antibiotics or medical procedures, to treat chronic urea-splitting urinary infections. Acetohydroxamic Acid, a synthetic drug derived from hydroxylamine and ethyl acetate, is similar in structure to urea. In the urine, it acts as an antagonist of the bacterial enzyme urease. Acetohydroxamic Acid has no direct antimicrobial action and does not acidify urine directly. Acetohydroxamic Acid reversibly inhibits the bacterial enzyme urease. This inhibits the hydrolysis of urea and production of ammonia in urine infected with urea-splitting organisms, leading to a decrease in pH and ammonia levels. As antimicrobial agents are more effective in such conditions, the effectiveness of these agents is amplified, resulting in a higher cure rate.",The molecular weight is 75.07.,Acetohydroxamic acid has a topological polar surface area of 49.33.,The log p value of  is -1.59.,Acetohydroxamic acid is approved.,Acetohydroxamic acid is a solid.,True
18774,,,,,CP-271485 is experimental.,CP-271485 is a solid.,False
18775,,,,,PF-00356231 is experimental.,PF-00356231 is a solid.,False
18776,,,,,"2--4-(4'-Ethoxy-1,1'-Biphenyl-4-Yl)-4-Oxobutanoic Acid is experimental.","2--4-(4'-Ethoxy-1,1'-Biphenyl-4-Yl)-4-Oxobutanoic Acid is a solid.",False
18777,,,,,"(1S,5S,7R)-N~7~-(BIPHENYL-4-YLMETHYL)-N~3~-HYDROXY-6,8-DIOXA-3-AZABICYCLOOCTANE-3,7-DICARBOXAMIDE is experimental.","(1S,5S,7R)-N~7~-(BIPHENYL-4-YLMETHYL)-N~3~-HYDROXY-6,8-DIOXA-3-AZABICYCLOOCTANE-3,7-DICARBOXAMIDE is a solid.",False
18778,,,,,N-(biphenyl-4-ylsulfonyl)-D-leucine is experimental.,N-(biphenyl-4-ylsulfonyl)-D-leucine is a solid.,False
18779,,,,,N-(dibenzothiophen-3-ylsulfonyl)-L-valine is experimental.,N-(dibenzothiophen-3-ylsulfonyl)-L-valine is a solid.,False
18780,,,,,N-oxo-2-ethanamide is experimental.,N-oxo-2-ethanamide is a solid.,False
18781,,,,,2--N-oxo-ethanamide is experimental.,2--N-oxo-ethanamide is a solid.,False
18782,,,,,N-oxo-2-(phenylsulfonylamino)ethanamide is experimental.,N-oxo-2-(phenylsulfonylamino)ethanamide is a solid.,False
18783,,,,,N--D-alanine is experimental.,N--D-alanine is a solid.,False
18784,,,,,6-phospho-D-gluconic acid is experimental.,6-phospho-D-gluconic acid is a solid.,False
18785,,,,,5-phospho-D-arabinohydroxamic acid is experimental.,5-phospho-D-arabinohydroxamic acid is a solid.,False
18786,,,,,D-glucitol 6-phosphate is experimental.,D-glucitol 6-phosphate is a solid.,False
18787,,,,,5-Phosphoarabinonic Acid is experimental.,5-Phosphoarabinonic Acid is a solid.,False
18788,"An ester of glucose with phosphoric acid, made in the course of glucose metabolism by mammalian and other cells. It is a normal constituent of resting muscle and probably is in constant equilibrium with fructose-6-phosphate. (Stedman, 26th ed)",,,,Glucose-6-Phosphate is experimental.,Glucose-6-Phosphate is a solid.,True
18789,,,,,D-erythrose 4-phosphate is experimental.,D-erythrose 4-phosphate is a solid.,False
18790,,,,,N-Acetylmethionine is experimental.,N-Acetylmethionine is a solid.,False
18791,,,,,"1,2-dihexadecanoyl-sn-glycero-3-phosphoethanolamine is experimental.","1,2-dihexadecanoyl-sn-glycero-3-phosphoethanolamine is a solid.",False
18792,,,,,B-2-Octylglucoside is experimental.,B-2-Octylglucoside is a solid.,False
18793,,,,,Hexadecanal is experimental.,Hexadecanal is a solid.,False
18794,,,,,"Heptane-1,2,3-Triol is experimental.","Heptane-1,2,3-Triol is a solid.",False
18795,,,,,Heptyl 1-Thiohexopyranoside is experimental.,Heptyl 1-Thiohexopyranoside is a solid.,False
18796,,,,,Deoxyuridine-5'-Diphosphate is experimental.,Deoxyuridine-5'-Diphosphate is a solid.,False
18797,,,,,"1-{(2S,5S)-4-FLUORO-5-TETRAHYDROFURAN-2-YL}PYRIMIDINE-2,4(1H,3H)-DIONE is experimental.","1-{(2S,5S)-4-FLUORO-5-TETRAHYDROFURAN-2-YL}PYRIMIDINE-2,4(1H,3H)-DIONE is a solid.",False
18798,"Reslizumab is a humanized interleukin-5 (IL-5) antagonist monoclonal antibody (IgG4 kappa) that is produced by recombinant DNA technology in murine myeloma non-secreting 0 (NS0) cells. IL-5 is a pro-inflammatory cytokine that is responsible for the growth and differentiation, recruitment, activation, and survival of eosinophils. Elevated levels of eosinophils increase the risk for asthma exacerbations, including both allergic forms and nonallergic forms of asthma where eosinophilia is prominent. By targeting the IL-5 and disrupting its signalling pathways, reslizumab aims to inhibit eosinophil maturation and promote programmed cell death. Indicated for the add-on maintenance treatment of patients with severe asthma aged 18 years and older with an eosinophilic phenotype. A reduction in blood eosinophil counts was observed in clinical studies following an initial infusion of 3 mg/kg reslizumab and was maintained through 52 weeks of treatment with no signs of tachyphylaxis. Greater reductions of blood eosinophils were observed in subjects with higher reslizumab serum concentrations. This effect was independent of the presence of treatment-emergent anti-reslizumab antibodies.  Reslizumab an interleukin-5 (IL-5) antagonist (IgG4, kappa) that binds to IL-5 with a dissociation constant of 81 pM. IL-5 is a proinflammatory cytokine responsible for the terminal maturation of eosinophils and increases chemotaxis, endothelial adhesion, activation and survival of eosinophils. Eosinophils are known to play a central role in the pathophysiology of many patients with asthma; upon activation, eosinophils release leukotrienes, platelet activation factor, major basic protein, eosinophil cationic protein, eosinophil peroxidase, eosinophil-derived neurotoxin, and other cytokines that are cytotoxic to the bronchial epithelium and lead to airway inflammation and bronchospasm. IL-5 production is increased by upon activation of TH2 lymphocytes after antigen exposure and IL-5 stimulates the production and maturation of eosinophil precursors in the bone marrow. IL-5 promotes the growth and differentiation, recruitment, activation, and survival of eosinophils via interacting with the IL-5 receptor expressed on the eosinophil surface. Increased production and activation of eosinophils is especially prominent in nonallergic forms of asthma.",,,,Reslizumab is approved and investigational.,Reslizumab is a solid.,True
18799,"Eosinophils are involved in inflammatory immune responses, and prolonged hypereosinophilia (typically defined as absolute eosinophil levels of 1500/mm<sup>3</sup> or more) is associated with a spectrum of diseases, including severe asthma, eosinophilic granulomatosis with polyangiitis (EGPA), and hypereosinophilic syndrome (HES). The pathogenesis of eosinophilia is complex, but IL-5 is recognized as a key cytokine involved in the differentiation, recruitment, activation, and prolonged survival of eosinophils in peripheral tissue. Activated eosinophils further stimulate an inflammatory response and also induce tissue lesions and promote fibrosis, all of which contribute to the multifactorial symptomatology of hypereosinophilic diseases. Mepolizumab is an anti-IL-5 IgG1 kappa monoclonal antibody indicated as an add-on maintenance treatment in patients aged six years and older with severe eosinophilic asthma and as a treatment in adult patients for eosinophilic granulomatosis with polyangiitis (EGPA). Mepolizumab is also indicated for the treatment of hypereosinophilic syndrome (HES) in patients aged 12 and older in whom eosinophilia is present for at least six months without an identifiable non-hematologic secondary cause. Mepolizumab is a monoclonal antibody that acts through interleukin-5 (IL-5) antagonism to reduce blood eosinophil levels, generally in the range of 60-90% of baseline depending on dose, which in turn offers therapeutic benefit in the specific conditions for which mepolizumab is indicated. Mepolizumab has a relatively long half-life of between 16 and 22 days, which allows for long-lasting therapeutic benefit and a four-week dosing schedule. Despite a good demonstrated safety profile, mepolizumab use does act to depress part of the immune system and may be associated with increased infections, such as with herpes zoster virus; pre-existing helminth infections should be treated before starting mepolizumab therapy. Inhaled and oral corticosteroids should not be discontinued after starting mepolizumab but may be tapered as appropriate. Mepolizumab should not be used to treat acute bronchospasms or status asthmatics. Finally, hypersensitivity reactions, including anaphylaxis, have been reported in patients; mepolizumab should be discontinued in patients with suspected or confirmed hypersensitivity. Hypereosinophilia is typically considered as an absolute eosinophil count of 1500/mm<sup>3</sup> or higher and is associated with aberrant immune responses in several conditions, including severe asthma, eosinophilic granulomatosis with polyangiitis, and the variable spectrum of hypereosinophilic syndrome (HES). Eosinophils are involved in the inflammatory response by secretion of molecules such as MBP, leukotrienes, matrix metalloproteinases, transforming growth factor-β, nitric oxide, and other reactive oxygen species. Interleukin-5 (IL-5) is the primary cytokine associated with the differentiation of bone marrow progenitor cells into mature inflammatory neutrophils and the subsequent migration, activation, and prolonged survival of activated neutrophils. In concert with other cells, including lymphocytes, neutrophils, mast cells, and macrophages, which themselves can secrete additional pro-inflammatory molecules, high concentrations of neutrophils are associated with tissue damage and fibrosis, leading to the symptoms of eosinophilic diseases.",,,,Mepolizumab is approved and investigational.,Mepolizumab is a solid.,True
18800,,,,,(5-hydroxyindoloquinazolin-7-yl)acetic acid is experimental.,(5-hydroxyindoloquinazolin-7-yl)acetic acid is a solid.,False
18801,,,,,"1,8-Di-Hydroxy-4-Nitro-Xanthen-9-One is experimental.","1,8-Di-Hydroxy-4-Nitro-Xanthen-9-One is a solid.",False
18802,,,,,"1,8-Di-Hydroxy-4-Nitro-Anthraquinone is experimental.","1,8-Di-Hydroxy-4-Nitro-Anthraquinone is a solid.",False
18803,,,,,"5,8-Di-Amino-1,4-Dihydroxy-Anthraquinone is experimental.","5,8-Di-Amino-1,4-Dihydroxy-Anthraquinone is a solid.",False
18804,,,,,Tetrabromo-2-Benzotriazole is experimental.,Tetrabromo-2-Benzotriazole is a solid.,False
18805,,,,,"DIMETHYL-(4,5,6,7-TETRABROMO-1H-BENZOIMIDAZOL-2-YL)-AMINE is experimental.","DIMETHYL-(4,5,6,7-TETRABROMO-1H-BENZOIMIDAZOL-2-YL)-AMINE is a solid.",False
18806,,,,,"S-METHYL-4,5,6,7-TETRABROMO-BENZIMIDAZOLE is experimental.","S-METHYL-4,5,6,7-TETRABROMO-BENZIMIDAZOLE is a solid.",False
18807,,,,,"N1,N2-ETHYLENE-2-METHYLAMINO-4,5,6,7-TETRABROMO-BENZIMIDAZOLE is experimental.","N1,N2-ETHYLENE-2-METHYLAMINO-4,5,6,7-TETRABROMO-BENZIMIDAZOLE is a solid.",False
18808,Emodin has been investigated for the treatment of Polycystic Kidney.,,,,Emodin is investigational.,Emodin is a solid.,True
18809,,,,,"3,8-DIBROMO-7-HYDROXY-4-METHYL-2H-CHROMEN-2-ONE is experimental.","3,8-DIBROMO-7-HYDROXY-4-METHYL-2H-CHROMEN-2-ONE is a solid.",False
18810,,,,,"19-(cyclopropylamino)-4,6,7,15-tetrahydro-5H-16,1-(azenometheno)-10,14-(metheno)pyrazolotriazacyclohexadecin-8(9H)-one is experimental.","19-(cyclopropylamino)-4,6,7,15-tetrahydro-5H-16,1-(azenometheno)-10,14-(metheno)pyrazolotriazacyclohexadecin-8(9H)-one is a solid.",False
18811,,,,,"N,N'-DIPHENYLPYRAZOLOTRIAZINE-2,4-DIAMINE is experimental.","N,N'-DIPHENYLPYRAZOLOTRIAZINE-2,4-DIAMINE is a solid.",False
18812,,,,,4-(2-(1H-IMIDAZOL-4-YL)ETHYLAMINO)-2-(PHENYLAMINO)PYRAZOLOTRIAZINE-8-CARBONITRILE is experimental.,4-(2-(1H-IMIDAZOL-4-YL)ETHYLAMINO)-2-(PHENYLAMINO)PYRAZOLOTRIAZINE-8-CARBONITRILE is a solid.,False
18813,,,,,2-(CYCLOHEXYLMETHYLAMINO)-4-(PHENYLAMINO)PYRAZOLOTRIAZINE-8-CARBONITRILE is experimental.,2-(CYCLOHEXYLMETHYLAMINO)-4-(PHENYLAMINO)PYRAZOLOTRIAZINE-8-CARBONITRILE is a solid.,False
18814,,,,,2-(4-CHLOROBENZYLAMINO)-4-(PHENYLAMINO)PYRAZOLOTRIAZINE-8-CARBONITRILE is experimental.,2-(4-CHLOROBENZYLAMINO)-4-(PHENYLAMINO)PYRAZOLOTRIAZINE-8-CARBONITRILE is a solid.,False
18815,,,,,2-(4-ETHYLPIPERAZIN-1-YL)-4-(PHENYLAMINO)PYRAZOLOTRIAZINE-8-CARBONITRILE is experimental.,2-(4-ETHYLPIPERAZIN-1-YL)-4-(PHENYLAMINO)PYRAZOLOTRIAZINE-8-CARBONITRILE is a solid.,False
18816,,,,,N-(3-(8-CYANO-4-(PHENYLAMINO)PYRAZOLOTRIAZIN-2-YLAMINO)PHENYL)ACETAMIDE is experimental.,N-(3-(8-CYANO-4-(PHENYLAMINO)PYRAZOLOTRIAZIN-2-YLAMINO)PHENYL)ACETAMIDE is a solid.,False
18817,,,,,Dichlororibofuranosylbenzimidazole is experimental.,Dichlororibofuranosylbenzimidazole is a solid.,False
18818,,,,,Quinalizarin is experimental.,Quinalizarin is a solid.,False
18819,,,,,"Methyl 4,6-O--beta-D-galactopyranoside is experimental.","Methyl 4,6-O--beta-D-galactopyranoside is a solid.",False
18820,,,,,"Bis-1,2-{-5-yloxycarbamoyl}-ethane is experimental.","Bis-1,2-{-5-yloxycarbamoyl}-ethane is a solid.",False
18821,,,,,"BIS-1,2-{-5-YLOXYCARBONYL}-PIPERAZINE is experimental.","BIS-1,2-{-5-YLOXYCARBONYL}-PIPERAZINE is a solid.",False
18822,,,,,7-methyl-5'-guanylic acid is experimental.,7-methyl-5'-guanylic acid is a solid.,False
18823,,,,,7-methyl-guanosine-5'-triphosphate-5'-guanosine is experimental.,7-methyl-guanosine-5'-triphosphate-5'-guanosine is a solid.,False
18824,,,,,"5-{methoxy}quinazoline-2,4-diamine is experimental.","5-{methoxy}quinazoline-2,4-diamine is a solid.",False
18825,,,,,"5-{methoxy}quinazoline-2,4-diamine is experimental.","5-{methoxy}quinazoline-2,4-diamine is a solid.",False
18826,,,,,"5-quinazoline-2,4-diamine is experimental.","5-quinazoline-2,4-diamine is a solid.",False
18827,,,,,"2',3'-Dideoxythymidine-5'-Monophosphate is experimental.","2',3'-Dideoxythymidine-5'-Monophosphate is a solid.",False
18828,,,,,3'-Fluoro-3'-deoxythymidine 5'-monophosphate is experimental.,3'-Fluoro-3'-deoxythymidine 5'-monophosphate is a solid.,False
18829,,,,,3'-deoxy-3'-aminothymidine monophosphate is experimental.,3'-deoxy-3'-aminothymidine monophosphate is a solid.,False
18830,,,,,p1-(5'-adenosyl)p5-(5'-thymidyl)pentaphosphate is experimental.,p1-(5'-adenosyl)p5-(5'-thymidyl)pentaphosphate is a solid.,False
18831,,,,,Zidovudine monophosphate is experimental.,Zidovudine monophosphate is a solid.,False
18832,,,,,P1-(5'-Adenosyl)P5-(5'-(3'azido-3'-Deoxythymidyl))Pentaphosphate is experimental.,P1-(5'-Adenosyl)P5-(5'-(3'azido-3'-Deoxythymidyl))Pentaphosphate is a solid.,False
18833,,,,,"6-(4-{amino}phenyl)-5-methyl-4,5-dihydropyridazin-3(2H)-one is experimental.","6-(4-{amino}phenyl)-5-methyl-4,5-dihydropyridazin-3(2H)-one is a solid.",False
18834,,,,,"Hg9a-9, Nonanoyl-N-Hydroxyethylglucamide is experimental.","Hg9a-9, Nonanoyl-N-Hydroxyethylglucamide is a solid.",False
18835,5-Aminoimidazole-4-carboxamide ribonucleotide (AICAR) is an intermediate in the generation of inosine monophosphate and analog of adenosine monophosphate (AMP) that is capable of stimulating AMP-dependent protein kinase (AMPK) activity. AICAR has been used clinically to treat and protect against cardiac ischemic injury. The drug was first used in the 1980s as a method to preserve blood flow to the heart during surgery and is currently of interest as a potential treatment for diabetes by increasing the metabolic activity of tissues by changing the physical composition of muscle.,,,,AICA ribonucleotide is experimental and investigational.,AICA ribonucleotide is a solid.,True
18836,,,,,Acid yellow 54 free acid is experimental.,Acid yellow 54 free acid is a solid.,False
18837,,,,,N-pyrimidin-6-yl)methyl]{(2E)-3--2-propenoyl}amino)benzoyl]-L-glutamic acid is experimental.,N-pyrimidin-6-yl)methyl]{(2E)-3--2-propenoyl}amino)benzoyl]-L-glutamic acid is a solid.,False
18838,"3-Carbamoyl-1-beta-D-ribofuranosyl pyridinium hydroxide-5&#39;phosphate, inner salt. A nucleotide in which the nitrogenous base, nicotinamide, is in beta-N-glycosidic linkage with the C-1 position of D-ribose. Synonyms: Nicotinamide Ribonucleotide; NMN. ",,,,Nicotinamide Mononucleotide is experimental.,Nicotinamide Mononucleotide is a solid.,True
18839,,,,,Etheno-Nadp is experimental.,Etheno-Nadp is a solid.,False
18840,,,,,D-tartaric acid is experimental.,D-tartaric acid is a solid.,False
18841,,,,,Isocitric Acid is experimental.,Isocitric Acid is a solid.,False
18842,"A compound that, along with its isomer, Cleland's reagent (dithiothreitol), is used for the protection of sulfhydryl groups against oxidation to disulfides and for the reduction of disulfides to sulfhydryl groups. ",,,,Dithioerythritol is experimental.,Dithioerythritol is a solid.,True
18843,,,,,Thymidine 5'-triphosphate is experimental.,Thymidine 5'-triphosphate is a solid.,False
18844,,,,,Bis(Adenosine)-5'-Pentaphosphate is experimental.,Bis(Adenosine)-5'-Pentaphosphate is a solid.,False
18845,,,,,N-cyclohexyltaurine is experimental.,N-cyclohexyltaurine is a solid.,False
18846,"Guanosine 5&#39;-(trihydrogen diphosphate), monoanhydride with phosphorothioic acid. A stable GTP analog which enjoys a variety of physiological actions such as stimulation of guanine nucleotide-binding proteins, phosphoinositide hydrolysis, cyclic AMP accumulation, and activation of specific proto-oncogenes.",,,,5'-Guanosine-Diphosphate-Monothiophosphate is experimental.,5'-Guanosine-Diphosphate-Monothiophosphate is a solid.,True
18847,,,,,2-MERCAPTO-N-HEPTALEN-7-YL]ACETAMIDE is experimental.,2-MERCAPTO-N-HEPTALEN-7-YL]ACETAMIDE is a solid.,False
18848,,,,,"3,4-Dihydroxy-1-Methylquinolin-2(1h)-One is experimental.","3,4-Dihydroxy-1-Methylquinolin-2(1h)-One is a solid.",False
18849,Specific inhibitor of phosphatidylinositol 3-kinase.,,,,LY-294002 is experimental.,LY-294002 is a solid.,True
18850,,,,,(3e)-3--1h-Indol-2(3h)-One is experimental.,(3e)-3--1h-Indol-2(3h)-One is a solid.,False
18851,,,,,IMIDAZOPYRIDAZIN 1 is experimental.,IMIDAZOPYRIDAZIN 1 is a solid.,False
18852,,,,,4-(4-hydroxy-3-methylphenyl)-6-phenylpyrimidin-2(5H)-one is experimental.,4-(4-hydroxy-3-methylphenyl)-6-phenylpyrimidin-2(5H)-one is a solid.,False
18853,,,,,"(4R)-7,8-dichloro-1',9-dimethyl-1-oxo-1,2,4,9-tetrahydrospiro-4-carbonitrile is experimental.","(4R)-7,8-dichloro-1',9-dimethyl-1-oxo-1,2,4,9-tetrahydrospiro-4-carbonitrile is a solid.",False
18854,,,,,N-phenyl-1H-pyrrolopyridin-3-amine is experimental.,N-phenyl-1H-pyrrolopyridin-3-amine is a solid.,False
18855,,,,,"(2S)-1,3-benzothiazol-2-yl{2-pyrimidin-4-yl}ethanenitrile is experimental.","(2S)-1,3-benzothiazol-2-yl{2-pyrimidin-4-yl}ethanenitrile is a solid.",False
18856,,,,,"(4R)-7-chloro-9-methyl-1-oxo-1,2,4,9-tetrahydrospiro-4-carbonitrile is experimental.","(4R)-7-chloro-9-methyl-1-oxo-1,2,4,9-tetrahydrospiro-4-carbonitrile is a solid.",False
18857,,,,,Tricetin is experimental.,Tricetin is a solid.,False
18858,,,,,"6-(5-BROMO-2-HYDROXYPHENYL)-2-OXO-4-PHENYL-1,2-DIHYDROPYRIDINE-3-CARBONITRILE is experimental.","6-(5-BROMO-2-HYDROXYPHENYL)-2-OXO-4-PHENYL-1,2-DIHYDROPYRIDINE-3-CARBONITRILE is a solid.",False
18859,,,,,4-pyrimidin-2-amine is experimental.,4-pyrimidin-2-amine is a solid.,False
18860,,,,,N-cyclohexyl-3-triazolopyridazin-6-amine is experimental.,N-cyclohexyl-3-triazolopyridazin-6-amine is a solid.,False
18861,,,,,"2,3-diphenyl-1H-indole-7-carboxylic acid is experimental.","2,3-diphenyl-1H-indole-7-carboxylic acid is a solid.",False
18862,"XL418 is a novel anticancer compound. Cancer XL418 is a small molecule that inhibits the activity of protein kinase B (PKB or AKT) and S6 Kinase (S6K), which act downstream of phosphoinosotide-3 kinase (PI3K). Activation of these kinases is a frequent event in human tumors, promoting cell growth, survival, and resistance to chemotherapy and radiotherapy. Inactivation of the pathway through inhibition of AKT is expected to induce apoptosis (programmed cell death) in tumor cells. AKT inhibitors may also sensitize tumor cells to a wide range of chemotherapy.",,,,XL418 is investigational.,XL418 is a solid.,True
18863,,,,,"2--2-Hydroxymethyl-Propane-1,3-Diol is experimental.","2--2-Hydroxymethyl-Propane-1,3-Diol is a solid.",False
18864,,,,,Zardaverine is experimental.,Zardaverine is a solid.,False
18865,,,,,"1-(4-Aminophenyl)-3,5-Dimethyl-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester is experimental.","1-(4-Aminophenyl)-3,5-Dimethyl-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester is a solid.",False
18866,,,,,"3,5-Dimethyl-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester is experimental.","3,5-Dimethyl-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester is a solid.",False
18867,,,,,"1-(4-Methoxyphenyl)-3,5-Dimethyl-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester is experimental.","1-(4-Methoxyphenyl)-3,5-Dimethyl-1h-Pyrazole-4-Carboxylic Acid Ethyl Ester is a solid.",False
18868,"Tetomilast has been used in trials studying the treatment of Crohn Disease, Colitis, Ulcerative, and Chronic Obstructive Pulmonary Disease. Investigated for use/treatment in ulcerative colitis.",,,,Tetomilast is investigational.,Tetomilast is a solid.,True
18869,,,,,"3,5-DIMETHYL-1-PHENYL-1H-PYRAZOLE-4-CARBOXYLIC ACID ETHYL ESTER is experimental.","3,5-DIMETHYL-1-PHENYL-1H-PYRAZOLE-4-CARBOXYLIC ACID ETHYL ESTER is a solid.",False
18870,,,,,Myricetin is experimental.,Myricetin is a solid.,False
18871,,,,,"5-QUINOXALIN-6-YLMETHYLENE-THIAZOLIDINE-2,4-DIONE is experimental.","5-QUINOXALIN-6-YLMETHYLENE-THIAZOLIDINE-2,4-DIONE is a solid.",False
18872,"XL765 is an orally available small molecule that has been shown in preclinical studies to selectively inhibit the activity of phosphoinositide-3 kinase (PI3K) and mammalian target of rapamycin (mTOR). It is being developed by Exelixis, Inc. For the treatment of various forms of cancer. XL765 is an orally available small molecule that has been shown in preclinical studies to selectively inhibit the activity of phosphoinositide-3 kinase (PI3K) and mammalian target of rapamycin (mTOR). Activation of PI3K is a frequent event in human tumors, promoting tumor cell growth, survival, and resistance to chemotherapy and radiotherapy. mTOR is also frequently activated in human tumors and plays a central role in tumor cell growth. mTOR can be activated via upregulation of PI3K, or via PI3K-independent mechanisms. Inactivation of PI3K has been shown to inhibit growth and induce apoptosis (programmed cell death) in tumor cells, whereas inactivation of mTOR has been shown to inhibit the growth of tumor cells. In preclinical studies, XL765 slowed tumor growth or caused tumor shrinkage in multiple preclinical cancer models, including breast, lung, ovarian, and prostate cancers, and gliomas. XL765 has also been shown to enhance the anti-tumor effects of several chemotherapeutic agents in preclinical cancer models. XL765 has at least a 24-hour duration of action against both PI3K and mTOR readouts in tumors in vivo following a single oral (PO) dose of 30-100 mg/kg. XL765 inhibits the activity of phosphoinositide-3 kinase (PI3K), which is frequently activated in tumors and promotes cell growth, survival and resistance to chemotherapy and radiotherapy. XL765 also inhibits mammalian target of rapamycin (mTOR), which also is activated frequently in human tumors and plays a central role in tumor cell growth. XL765 potently inhibits Class I PI3K isoforms and mTOR.",,,,XL765 is investigational.,XL765 is a solid.,True
18873,An NSAID that inhibits PI-3K gamma and delta. Investigated for use/treatment in angioedema and myocardial infarction.,,,,TG100-115 is investigational.,TG100-115 is a solid.,True
18874,,,,,2-((9H-PURIN-6-YLTHIO)METHYL)-5-CHLORO-3-(2-METHOXYPHENYL)QUINAZOLIN-4(3H)-ONE is experimental.,2-((9H-PURIN-6-YLTHIO)METHYL)-5-CHLORO-3-(2-METHOXYPHENYL)QUINAZOLIN-4(3H)-ONE is a solid.,False
18875,,,,,"N-(5-{4-Chloro-3-phenyl}-4-methyl-1,3-thiazol-2-yl)acetamide is experimental.","N-(5-{4-Chloro-3-phenyl}-4-methyl-1,3-thiazol-2-yl)acetamide is a solid.",False
18876,,,,,"5,5-dimethyl-2-morpholin-4-yl-5,6-dihydro-1,3-benzothiazol-7(4H)-one is experimental.","5,5-dimethyl-2-morpholin-4-yl-5,6-dihydro-1,3-benzothiazol-7(4H)-one is a solid.",False
18877,,,,,"(5E)-5--1,3-THIAZOLIDINE-2,4-DIONE is experimental.","(5E)-5--1,3-THIAZOLIDINE-2,4-DIONE is a solid.",False
18878,,,,,1-methyl-3-naphthalen-2-yl-1H-pyrazolopyrimidin-4-amine is experimental.,1-methyl-3-naphthalen-2-yl-1H-pyrazolopyrimidin-4-amine is a solid.,False
18879,,,,,"N-(2-hydroxy-1,1-dimethylethyl)-1-methyl-3-(1H-pyrrolopyridin-2-yl)-1H-indole-5-carboxamide is experimental.","N-(2-hydroxy-1,1-dimethylethyl)-1-methyl-3-(1H-pyrrolopyridin-2-yl)-1H-indole-5-carboxamide is a solid.",False
18880,,,,,Tamatinib is experimental and investigational.,Tamatinib is a solid.,False
18881,,,,,"2-{2-pyrimidin-4-yl}-N--4-methyl-1,3-thiazole-5-carboxamide is experimental.","2-{2-pyrimidin-4-yl}-N--4-methyl-1,3-thiazole-5-carboxamide is a solid.",False
18882,,,,,2-{amino}-4-pyrimidine-5-carboxamide is experimental.,2-{amino}-4-pyrimidine-5-carboxamide is a solid.,False
18883,,,,,"2,3,5,6-Tetrafluoro-4-Methoxy-Benzamide is experimental.","2,3,5,6-Tetrafluoro-4-Methoxy-Benzamide is a solid.",False
18884,"A disaccharide of glucose and galactose in human and cow milk. It is used in pharmacy for tablets, in medicine as a nutrient, and in industry.",The molecular weight is 342.3.,Lactose has a topological polar surface area of 189.53.,The log p value of  is -4.4.,Lactose is approved and experimental and investigational.,Lactose is a solid.,True
18885,"Oxibendazole is a polymerase inhibitor in phase III trials for the treatment of helminth intestinal infections. Investigated for use/treatment in infectious and parasitic disease (unspecified) and pediatric indications. Oxibendazole causes degenerative alterations in the tegument and intestinal cells of the worm by binding to the colchicine-sensitive site of tubulin, thus inhibiting its polymerization or assembly into microtubules. The loss of the cytoplasmic microtubules leads to impaired uptake of glucose by the larval and adult stages of the susceptible parasites, and depletes their glycogen stores. Degenerative changes in the endoplasmic reticulum, the mitochondria of the germinal layer, and the subsequent release of lysosomes result in decreased production of adenosine triphosphate (ATP), which is the energy required for the survival of the helminth. Due to diminished energy production, the parasite is immobilized and eventually dies.",,,,Oxibendazole is investigational and vet_approved.,Oxibendazole is a solid.,True
18886,,,,,"3-{amino}-4-(pyridin-4-ylamino)cyclobut-3-ene-1,2-dione is experimental.","3-{amino}-4-(pyridin-4-ylamino)cyclobut-3-ene-1,2-dione is a solid.",False
18887,,,,,"(4R)-N-AMINO}CARBONYL)-1,3-THIAZOL-2-YL]-4-METHYL-1-OXO-2,3,4,9-TETRAHYDRO-1H-BETA-CARBOLINE-6-CARBOXAMIDE is experimental.","(4R)-N-AMINO}CARBONYL)-1,3-THIAZOL-2-YL]-4-METHYL-1-OXO-2,3,4,9-TETRAHYDRO-1H-BETA-CARBOLINE-6-CARBOXAMIDE is a solid.",False
18888,,,,,"(10R)-10-methyl-3-(6-methylpyridin-3-yl)-9,10,11,12-tetrahydro-8H-diazepinothienoquinolin-8-one is experimental.","(10R)-10-methyl-3-(6-methylpyridin-3-yl)-9,10,11,12-tetrahydro-8H-diazepinothienoquinolin-8-one is a solid.",False
18889,,,,,"2--1,5,6,7-TETRAHYDRO-4H-PYRROLOPYRIDIN-4-ONE is experimental.","2--1,5,6,7-TETRAHYDRO-4H-PYRROLOPYRIDIN-4-ONE is a solid.",False
18890,,,,,"2-(2-QUINOLIN-3-YLPYRIDIN-4-YL)-1,5,6,7-TETRAHYDRO-4H-PYRROLOPYRIDIN-4-ONE is experimental.","2-(2-QUINOLIN-3-YLPYRIDIN-4-YL)-1,5,6,7-TETRAHYDRO-4H-PYRROLOPYRIDIN-4-ONE is a solid.",False
18891,,,,,Coumarin 120 is experimental.,Coumarin 120 is a solid.,False
18892,,,,,"1,4-Butanediol is experimental.","1,4-Butanediol is a solid.",False
18893,,,,,Methyl-2-S-(Alpha-D-Mannopyranosyl)-2-Thio-Alpha-D-Mannopyranoside is experimental.,Methyl-2-S-(Alpha-D-Mannopyranosyl)-2-Thio-Alpha-D-Mannopyranoside is a solid.,False
18894,,,,,Kifunensine is experimental.,Kifunensine is a solid.,False
18895,An alpha-glucosidase inhibitor with antiviral action. Derivatives of deoxynojirimycin may have anti-HIV activity.,,,,Duvoglustat is investigational.,Duvoglustat is a solid.,True
18896,,,,,1-Ter-Butyl-3-P-Tolyl-1h-PyrazoloPyrimidin-4-Ylamine is experimental.,1-Ter-Butyl-3-P-Tolyl-1h-PyrazoloPyrimidin-4-Ylamine is a solid.,False
18897,,,,,Uridine-Diphosphate-N-Acetylglucosamine is experimental.,Uridine-Diphosphate-N-Acetylglucosamine is a solid.,False
18898,,,,,Platelet Activating Factor is experimental.,Platelet Activating Factor is a solid.,False
18899,,,,,Lpc-Ether is experimental.,Lpc-Ether is a solid.,False
18900,"A component of phosphatidylcholines (lecithins), in which the two hydroxy groups of glycerol are esterified with fatty acids. (From Stedman, 26th ed) It counteracts the effects of urea on enzymes and other macromolecules. ",The molecular weight is 257.22.,Choline alfoscerate has a topological polar surface area of 99.05.,The log p value of  is -12.6.,Choline alfoscerate is experimental and investigational.,Choline alfoscerate is a solid.,True
18901,A specific inhibitor of phosphoserine/threonine protein phosphatase 1 and 2a. It is also a potent tumor promoter. (Thromb Res 1992;67(4):345-54 & Cancer Res 1993;53(2):239-41),,,,"9,10-Deepithio-9,10-Didehydroacanthifolicin is experimental.","9,10-Deepithio-9,10-Didehydroacanthifolicin is a solid.",True
18902,,,,,Calyculin A is experimental.,Calyculin A is a solid.,False
18903,Motuporin is a toxin isolated from the marine sponge Thenonella swinhoie grey.,,,,Motuporin is experimental.,Motuporin is a solid.,True
18904,,,,,R048-8071 is experimental.,R048-8071 is a solid.,False
18905,,,,,Lanosterol is experimental.,Lanosterol is a solid.,False
18906,,,,,5'-O-(N-Ethyl-Sulfamoyl)Adenosine is experimental.,5'-O-(N-Ethyl-Sulfamoyl)Adenosine is a solid.,False
18907,,,,,Adenosine-5'-ditungstate is experimental.,Adenosine-5'-ditungstate is a solid.,False
18908,,,,,Amido Phenyl Pyruvic Acid is experimental.,Amido Phenyl Pyruvic Acid is a solid.,False
18909,,,,,4-PIPERIDIN-4-YLBUTANAL is experimental.,4-PIPERIDIN-4-YLBUTANAL is a solid.,False
18910,,,,,-(5-PHENETHYL- PYRIDIN-3-YL)-METHANONE is experimental.,-(5-PHENETHYL- PYRIDIN-3-YL)-METHANONE is a solid.,False
18911,"JNJ-27390467 is a potent, nonpeptide inhibitor of human mast cell tryptase.",,,,JNJ-27390467 is experimental.,JNJ-27390467 is a solid.,True
18912,,,,,Cytidine is experimental.,Cytidine is a solid.,False
18913,Cytidine 5&#39;-(tetrahydrogen triphosphate). A cytosine nucleotide containing three phosphate groups esterified to the sugar moiety. ,,,,Cytidine-5'-Triphosphate is experimental.,Cytidine-5'-Triphosphate is a solid.,True
18914,Uridine 5&#39;-(tetrahydrogen triphosphate). A uracil nucleotide containing three phosphate groups esterified to the sugar moiety.,The molecular weight is 484.14.,Uridine 5'-triphosphate has a topological polar surface area of 258.92.,The log p value of  is -4.61.,Uridine 5'-triphosphate is experimental and investigational.,Uridine 5'-triphosphate is a solid.,True
18915,,,,,-Carbamic Acid Benzyl Ester is experimental.,-Carbamic Acid Benzyl Ester is a solid.,False
18916,,,,,-Carbamic Acid Benzyl Ester is experimental.,-Carbamic Acid Benzyl Ester is a solid.,False
18917,,,,,4-Morpholin-4-Yl-Piperidine-1-Carboxylic Acid -Amide is experimental.,4-Morpholin-4-Yl-Piperidine-1-Carboxylic Acid -Amide is a solid.,False
18918,,,,,Benzyl N-amino]-1-oxopentan-2-yl]carbamate is experimental.,Benzyl N-amino]-1-oxopentan-2-yl]carbamate is a solid.,False
18919,,,,,WRR-99 is experimental.,WRR-99 is a solid.,False
18920,,,,,WRR-112 is experimental.,WRR-112 is a solid.,False
18921,,,,,HOMOPHENYLALANINYLMETHANE is experimental.,HOMOPHENYLALANINYLMETHANE is a solid.,False
18922,,,,,Benzoyl-tyrosine-alanine-fluoro-methyl ketone is experimental.,Benzoyl-tyrosine-alanine-fluoro-methyl ketone is a solid.,False
18923,,,,,"1,2-diacyl-sn-glycero-3-phosphoinositol is experimental.","1,2-diacyl-sn-glycero-3-phosphoinositol is a solid.",False
18924,,,,,"(Z,Z)-4-Hydroxy-N,N,N-Trimethyl-10-Oxo-7--3,5,9-Trioxa-4-Phosphaheptacos-18-En-1-Aminium-4-Oxide is experimental.","(Z,Z)-4-Hydroxy-N,N,N-Trimethyl-10-Oxo-7--3,5,9-Trioxa-4-Phosphaheptacos-18-En-1-Aminium-4-Oxide is a solid.",False
18925,,,,,Dpb-T is experimental.,Dpb-T is a solid.,False
18926,,,,,"Cyclic 3',5'-thymidine monophosphate is experimental.","Cyclic 3',5'-thymidine monophosphate is a solid.",False
18927,"A key intermediate in carbohydrate metabolism. Serves as a precursor of glycogen, can be metabolized into UDPgalactose and UDPglucuronic acid which can then be incorporated into polysaccharides as galactose and glucuronic acid. Also serves as a precursor of sucrose lipopolysaccharides, and glycosphingolipids.",,,,Uridine diphosphate glucose is experimental.,Uridine diphosphate glucose is a solid.,True
18928,"A nucleoside diphosphate sugar which serves as a source of glucuronic acid for polysaccharide biosynthesis. It may also be epimerized to UDP iduronic acid, which donates iduronic acid to polysaccharides. In animals, UDP glucuronic acid is used for formation of many glucosiduronides with various aglycones. ",,,,UDP-alpha-D-glucuronic acid is experimental.,UDP-alpha-D-glucuronic acid is a solid.,True
18929,,,,,Tetramethylammonium is experimental.,Tetramethylammonium is a solid.,False
18930,,,,,"2-(2-Hydroxy-1,1-Dihydroxymethyl-Ethylamino)-Ethanesulfonic Acid is experimental.","2-(2-Hydroxy-1,1-Dihydroxymethyl-Ethylamino)-Ethanesulfonic Acid is a solid.",False
18931,Nitroxoline is a urinary antibacterial agent active against susceptible gram-positive and gram-negative organisms commonly found in urinary tract infections. It is a hydroxyquinoline derivative unrelated to other classes of drugs. Nitroxoline is active against bacterial gyrases. Nitroxoline is an antibiotic agent. This drug may also have antitumor activity by inhibition of type 2 methionine aminopeptidase (MetAP2) protein which is involved in angiogenesis. Its antibacterial activity may stem from the metal ion complexation vital for bacterial growth.,The molecular weight is 190.16.,Nitroxoline has a topological polar surface area of 78.94.,The log p value of  is 2.08.,Nitroxoline is experimental.,Nitroxoline is a solid.,True
18932,,,,,"3,5,6,8-Tetramethyl-N-Methyl Phenanthrolinium is experimental.","3,5,6,8-Tetramethyl-N-Methyl Phenanthrolinium is a solid.",False
18933,,The molecular weight is 458.55.,Fumagillin has a topological polar surface area of 97.89.,The log p value of  is 2.91.,Fumagillin is experimental.,Fumagillin is a solid.,False
18934,,,,,D-Methionine is approved and experimental and investigational.,D-Methionine is a solid.,False
18935,,,,,"N'-(2s,3r)-3-Amino-4-Cyclohexyl-2-Hydroxy-Butano-N-(4-Methylphenyl)Hydrazide is experimental.","N'-(2s,3r)-3-Amino-4-Cyclohexyl-2-Hydroxy-Butano-N-(4-Methylphenyl)Hydrazide is a solid.",False
18936,,,,,"(2R,3R,4S,5R,6E)-3,4,5-Trihydroxy-N--2-methoxy-8,8-dimethyl-6-nonenamide is experimental.","(2R,3R,4S,5R,6E)-3,4,5-Trihydroxy-N--2-methoxy-8,8-dimethyl-6-nonenamide is a solid.",False
18937,,,,,"(2s,3r)-3-Amino-2-Hydroxy-5-(Ethylsulfanyl)Pentanoyl-((S)-(-)-(1-Naphthyl)Ethyl)Amide is experimental.","(2s,3r)-3-Amino-2-Hydroxy-5-(Ethylsulfanyl)Pentanoyl-((S)-(-)-(1-Naphthyl)Ethyl)Amide is a solid.",False
18938,,,,,Ovalicin is experimental.,Ovalicin is a solid.,False
18939,"PPI-2458 represents a potentially new and important addition to the growing list of therapeutics aimed at specific molecular oncology targets. PPI-2458 is a novel, proprietary molecule belonging to the fumagillin class of compounds that specifically targets the MetAP-2 enzyme. This class of compounds has been shown to prevent both abnormal cell growth and the formation of new blood vessels (known as angiogenesis), which contribute to the growth of aberrant tissues in diseases such as cancer and rheumatoid arthritis. Clinical development with previous fumagillin derivatives has been limited by their toxicity profile. In preclinical studies to date, PPI-2458 has demonstrated the potent pharmacologic activity of this class of compounds while displaying an improved pharmacokinetic and toxicity profile. Investigated for use/treatment in lymphoma (non-hodgkin's) and solid tumors. PPI-2458's potent inhibition of MetAP-2 presents the potential for use as a new therapy for non-Hodgkin's lymphoma (NHL). MetAP-2 is highly expressed in human germinal center B cells. The neoplastic counterparts of these cells are the cell types observed in certain NHL subtypes, such as diffuse large B cell lymphoma and follicular lymphoma. PPI-2458 has been shown to reduce the formation of germinal centers in lymphoid tissues in vivo, have direct anti-proliferative activity on NHL cells in vitro and inhibit the growth of NHL tumors in a preclinical model in vivo. The anti-tumor activity of PPI-2458 was dose-dependent in this preclinical in vivo model and directly correlated with the level of molecular target MetAP-2 enzyme inhibition in tumor tissue, as measured by a proprietary, pharmacodynamic assay developed by PRAECIS. Additionally, the activity of PPI-2458 in this preclinical model was synergistic with several chemotherapeutic agents that are routinely used in combination in NHL patients.",,,,PPI-2458 is investigational.,PPI-2458 is a solid.,True
18940,,,,,5-BROMO-2-{AMINO}BENZOIC ACID is experimental.,5-BROMO-2-{AMINO}BENZOIC ACID is a solid.,False
18941,,,,,5-METHYL-2-BENZOIC ACID is experimental.,5-METHYL-2-BENZOIC ACID is a solid.,False
18942,,,,,"2--5,6,7,8-TETRAHYDRONAPHTHALENE-1-CARBOXYLIC ACID is experimental.","2--5,6,7,8-TETRAHYDRONAPHTHALENE-1-CARBOXYLIC ACID is a solid.",False
18943,,,,,"2--4-FLUOROPHENYL}SULFONYL)AMINO]-5,6,7,8-TETRAHYDRONAPHTHALENE-1-CARBOXYLIC ACID is experimental.","2--4-FLUOROPHENYL}SULFONYL)AMINO]-5,6,7,8-TETRAHYDRONAPHTHALENE-1-CARBOXYLIC ACID is a solid.",False
18944,,,,,"N'-((2S,3R)-3-AMINO-2-HYDROXY-5-(ISOPROPYLSULFANYL)PENTANOYL)-N-3-CHLOROBENZOYL HYDRAZIDE is experimental.","N'-((2S,3R)-3-AMINO-2-HYDROXY-5-(ISOPROPYLSULFANYL)PENTANOYL)-N-3-CHLOROBENZOYL HYDRAZIDE is a solid.",False
18945,,,,,3-ETHYL-6-{AMINO}-2-METHYLBENZOIC ACID is experimental.,3-ETHYL-6-{AMINO}-2-METHYLBENZOIC ACID is a solid.,False
18946,"O-(chloroacetylcarbamoyl)fumagillol (TNP-470) has been used in trials studying the treatment of HIV Infections, Sarcoma, Kaposi, and Pancreatic Neoplasms.",,,,TNP-470 is investigational.,TNP-470 is a solid.,True
18947,,,,,2-Deoxy-2-Amino Glucitol-6-Phosphate is experimental.,2-Deoxy-2-Amino Glucitol-6-Phosphate is a solid.,False
18948,,,,,N-acetyl-D-glucosamine-6-phosphate is experimental.,N-acetyl-D-glucosamine-6-phosphate is a solid.,False
18949,,,,,"4-(1,3,2-Dioxaborolan-2-Yloxy)Butan-1-Aminium is experimental.","4-(1,3,2-Dioxaborolan-2-Yloxy)Butan-1-Aminium is a solid.",False
18950,,,,,4-Hydroxybutan-1-Aminium is experimental.,4-Hydroxybutan-1-Aminium is a solid.,False
18951,,,,,4-(Hydroxymethyl)Benzamidine is experimental.,4-(Hydroxymethyl)Benzamidine is a solid.,False
18952,,,,,Diamino-N-methaniminium is experimental.,Diamino-N-methaniminium is a solid.,False
18953,,,,,Guanidine-3-propanol is experimental.,Guanidine-3-propanol is a solid.,False
18954,,,,,Benzamidine is experimental.,Benzamidine is a solid.,False
18955,,,,,"1,3,2-Dioxaborolan-2-Ol is experimental.","1,3,2-Dioxaborolan-2-Ol is a solid.",False
18956,GW-3965 is a liver X receptor ligand.,,,,GW-3965 is experimental.,GW-3965 is a solid.,True
18957,,,,,Benzenesulfinic acid is experimental.,Benzenesulfinic acid is a solid.,False
18958,,,,,"1,1,1,3,3,3-HEXAFLUORO-2-{4-PHENYL}PROPAN-2-OL is experimental.","1,1,1,3,3,3-HEXAFLUORO-2-{4-PHENYL}PROPAN-2-OL is a solid.",False
18959,"Vorinostat (rINN) or suberoylanilide hydroxamic acid (SAHA), is a drug currently under investigation for the treatment of cutaneous T cell lymphoma (CTCL), a type of skin cancer, to be used when the disease persists, gets worse, or comes back during or after treatment with other medicines. It is the first in a new class of agents known as histone deacetylase inhibitors. A recent study suggested that vorinostat also possesses some activity against recurrent glioblastoma multiforme, resulting in a median overall survival of 5.7 months (compared to 4 - 4.4 months in earlier studies). Further brain tumor trials are planned using combinations of vorinostat with other drugs. For the treatment of cutaneous manifestations in patients with cutaneous T-cell lymphoma who have progressive, persistent or recurrent disease on or following two systemic therapies. Vorinostat inhibits the enzymatic activity of histone deacetylases HDAC1, HDAC2 and HDAC3 (Class I) and HDAC6 (Class II) at nanomolar concentrations (IC<sub>50</sub>&lt; 86 nM). These enzymes catalyze the removal of acetyl groups from the lysine residues of histones proteins. In some cancer cells, there is an overexpression of HDACs, or an aberrant recruitment of HDACs to oncogenic transcription factors causing hypoacetylation of core nucleosomal histones. By inhibiting histone deacetylase, vorinostat causes the accumulation of acetylated histones and induces cell cycle arrest and/or apoptosis of some transformed cells. The mechanism of the antineoplastic effect of vorinostat has not been fully characterized.",The molecular weight is 264.32.,Vorinostat has a topological polar surface area of 78.43.,The log p value of  is 0.99.,Vorinostat is approved and investigational.,Vorinostat is a solid.,True
18960,,,,,4-(dimethylamino)-N-benzamide is experimental.,4-(dimethylamino)-N-benzamide is a solid.,False
18961,,,,,N-Hydroxy-4-(Methyl{Sulfonyl}Amino)Benzamide is experimental.,N-Hydroxy-4-(Methyl{Sulfonyl}Amino)Benzamide is a solid.,False
18962,,,,,Trichostatin A is experimental.,Trichostatin A is a solid.,False
18963,,,,,(2E)-N-hydroxy-3-prop-2-enamide is experimental.,(2E)-N-hydroxy-3-prop-2-enamide is a solid.,False
18964,,,,,"5-(4-METHYL-BENZOYLAMINO)-BIPHENYL-3,4'-DICARBOXYLIC ACID 3-DIMETHYLAMIDE-4'-HYDROXYAMIDE is experimental.","5-(4-METHYL-BENZOYLAMINO)-BIPHENYL-3,4'-DICARBOXYLIC ACID 3-DIMETHYLAMIDE-4'-HYDROXYAMIDE is a solid.",False
18965,"Intracellular messenger formed by the action of phospholipase C on phosphatidylinositol 4,5-bisphosphate, which is one of the phospholipids that make up the cell membrane. Inositol 1,4,5-trisphosphate is released into the cytoplasm where it releases calcium ions from internal stores within the cell&#39;s endoplasmic reticulum. These calcium ions stimulate the activity of B kinase or calmodulin.",,,,"1D-myo-inositol 1,4,5-trisphosphate is experimental.","1D-myo-inositol 1,4,5-trisphosphate is a solid.",True
18966,,,,,Coproporphyrin I is experimental.,Coproporphyrin I is a solid.,False
18967,,,,,Coproporphyrinogen III is experimental.,Coproporphyrinogen III is a solid.,False
18968,,,,,N-Tridecanoic Acid is experimental.,N-Tridecanoic Acid is a solid.,False
18969,,,,,-Phosphonic Acid is experimental.,-Phosphonic Acid is a solid.,False
18970,,,,,4-(1-Benzyl-3-Carbamoylmethyl-2-Methyl-1h-Indol-5-Yloxy)-Butyric Acid is experimental.,4-(1-Benzyl-3-Carbamoylmethyl-2-Methyl-1h-Indol-5-Yloxy)-Butyric Acid is a solid.,False
18971,,,,,(1-Benzyl-5-methoxy-2-methyl-1H-indol-3-yl)acetic acid is experimental.,(1-Benzyl-5-methoxy-2-methyl-1H-indol-3-yl)acetic acid is a solid.,False
18972,,,,,6-phenyl-4(R)-(7-phenyl-heptanoylamino)-hexanoic acid is experimental.,6-phenyl-4(R)-(7-phenyl-heptanoylamino)-hexanoic acid is a solid.,False
18973,,,,,Elaidamide is experimental.,Elaidamide is a solid.,False
18974,,,,,(2R)-2-Acetamido-3-(octadecyloxy)propyl 2-(methylsulfanyl)ethyl hydrogen phosphate is experimental.,(2R)-2-Acetamido-3-(octadecyloxy)propyl 2-(methylsulfanyl)ethyl hydrogen phosphate is a solid.,False
18975,,,,,KH064 is experimental.,KH064 is a solid.,False
18976,,,,,Morpholine-4-Carboxylic Acid Amide is experimental.,Morpholine-4-Carboxylic Acid Amide is a solid.,False
18977,,,,,Morpholine-4-Carboxylic Acid (1-(3-Benzenesulfonyl-1-Phenethylallylcarbamoyl)-3-Methylbutyl)-Amide is experimental.,Morpholine-4-Carboxylic Acid (1-(3-Benzenesulfonyl-1-Phenethylallylcarbamoyl)-3-Methylbutyl)-Amide is a solid.,False
18978,,,,,Morpholine-4-Carboxylic Acid -Amide is experimental.,Morpholine-4-Carboxylic Acid -Amide is a solid.,False
18979,,,,,N--3-(MORPHOLIN-4-YLSULFONYL)-N~2~--L-ALANINAMIDE is experimental.,N--3-(MORPHOLIN-4-YLSULFONYL)-N~2~--L-ALANINAMIDE is a solid.,False
18980,,,,,N-(1-CYANOCYCLOPROPYL)-3-({METHYL}SULFONYL)-N~2~--L-ALANINAMIDE is experimental.,N-(1-CYANOCYCLOPROPYL)-3-({METHYL}SULFONYL)-N~2~--L-ALANINAMIDE is a solid.,False
18981,,,,,N--3-(BENZYLSULFONYL)-N~2~--L-ALANINAMIDE is experimental.,N--3-(BENZYLSULFONYL)-N~2~--L-ALANINAMIDE is a solid.,False
18982,,,,,"N~2~-1,3-BENZOXAZOL-2-YL-3-CYCLOHEXYL-N-{2-ETHYL}-L-ALANINAMIDE is experimental.","N~2~-1,3-BENZOXAZOL-2-YL-3-CYCLOHEXYL-N-{2-ETHYL}-L-ALANINAMIDE is a solid.",False
18983,,,,,"N--1H-1,2,3-TRIAZOL-4-YL}-1,2-DIMETHYLPROPYL]BENZAMIDE is experimental.","N--1H-1,2,3-TRIAZOL-4-YL}-1,2-DIMETHYLPROPYL]BENZAMIDE is a solid.",False
18984,,,,,(1R)-2--1-({SULFONYL}METHYL)-2-OXOETHYL MORPHOLINE-4-CARBOXYLATE is experimental.,(1R)-2--1-({SULFONYL}METHYL)-2-OXOETHYL MORPHOLINE-4-CARBOXYLATE is a solid.,False
18985,,,,,2-ETHANOL is experimental.,2-ETHANOL is a solid.,False
18986,,,,,N--1-(cyclohexylmethyl)-2-oxoethyl]morpholine-4-carboxamide is experimental.,N--1-(cyclohexylmethyl)-2-oxoethyl]morpholine-4-carboxamide is a solid.,False
18987,,,,,N-amino}-1-(cyclohexylmethyl)-2-oxoethyl]morpholine-4-carboxamide is experimental.,N-amino}-1-(cyclohexylmethyl)-2-oxoethyl]morpholine-4-carboxamide is a solid.,False
18988,"Camostat mesylate, or FOY-305, is a synthetic serine protease inhibitor. It was first described in the literature in 1981, as part of research on the inhibition of skin tumors in mice. Camostat mesylate inhibits cholecystokinin, pro-inflammatory cytokines, and serine proteases, leading to it being investigated for multiple indications including the treatment of COVID-19. Camostat mesylate is indicated in Japan to treat chronic pancreatitis and drug induced lung injury. It is also being investigated as a potential treatment for COVID-19. Camostat mesylate is a protease inhibitor used to treat chronic pancreatitis. The duration of action is not long, as it is typically given in 3 divided doses daily. Patients should be counselled regarding the risk of anaphylaxis, thrombocytopenia, hepatic dysfunction, and hyperkalemia. In rats, oral camostat mesylate may increase pancreatic secretions and hypertrophy by increasing cholecystokinin release. Administration in rats has also lead to lower levels of IL-1beta, IL-6, TNF-alpha, TGF-beta, and PSC. Similar activity is seem after administration in humans, leading to reduced pain and inflammation as well as improve the function of the pancrease in chronic pancreatitis.",The molecular weight is 398.42.,Camostat has a topological polar surface area of 134.81.,The log p value of  is 1.66.,Camostat is experimental.,Camostat is a solid.,True
18989,,,,,Tris(Hydroxyethyl)Aminomethane is experimental.,Tris(Hydroxyethyl)Aminomethane is a solid.,False
18990,"Ubenimex (also known as bestatin) is a competitive protease inhibitor. It is an inhibitor of aminopeptidase B, leukotriene A4 hydrolase, aminopeptidase N. It is being studied for use in the treatment of acute myelocytic leukemia. An adjuvant therapy used for acute and chronic myelonous leukemia, lung cancer and nasopharyngeal cancer. It is also used to treat hypercholesterolaemia.",The molecular weight is 308.38.,Ubenimex has a topological polar surface area of 112.65.,The log p value of  is -0.31.,Ubenimex is investigational.,Ubenimex is a solid.,True
18991,"DG051 is a novel small-molecule inhibitor of leukotriene A4 hydrolase (LTA4H), the protein made by one of the genes in the leukotriene pathway that has been shown to link to risk of heart attack. DG051 is designed to decrease risk of heart attack by decreasing the production of leukotriene B4 (LTB4), an end product of the leukotriene pathway and a potent promoter of inflammation.  Investigated for use/treatment in myocardial infarction. DG051 is an inhibitor of leukotriene A4 hydrolase (LTA4H)which has been shown to link to risk of heart attack, and is directly involved in the synthesis of LTB4. By inhibiting LTA4H, DG051 decreases risk of heart attack by decreasing the production of leukotriene B4 (LTB4), an end product of the leukotriene pathway and a potent promoter of inflammation.",,,,DG051 is investigational.,DG051 is a solid.,True
18992,,,,,5--1H-indole is experimental.,5--1H-indole is a solid.,False
18993,,,,,N-(pyridin-3-ylmethyl)aniline is experimental.,N-(pyridin-3-ylmethyl)aniline is a solid.,False
18994,,,,,(4-fluorophenyl)(pyridin-4-yl)methanone is experimental.,(4-fluorophenyl)(pyridin-4-yl)methanone is a solid.,False
18995,,,,,"1-(2,2'-bithiophen-5-yl)methanamine is experimental.","1-(2,2'-bithiophen-5-yl)methanamine is a solid.",False
18996,,,,,N-glycinamide is experimental.,N-glycinamide is a solid.,False
18997,,,,,(2S)-2-amino-5-oxo-5-pentanoic acid is experimental.,(2S)-2-amino-5-oxo-5-pentanoic acid is a solid.,False
18998,,,,,4-amino-N-butanamide is experimental.,4-amino-N-butanamide is a solid.,False
18999,,,,,N-methyl-1-(2-thiophen-2-ylphenyl)methanamine is experimental.,N-methyl-1-(2-thiophen-2-ylphenyl)methanamine is a solid.,False
19000,,,,,{4-phenyl}(4-thiophen-3-ylphenyl)methanone is experimental.,{4-phenyl}(4-thiophen-3-ylphenyl)methanone is a solid.,False
19001,,,,,(R)-pyridin-4-ylmethanol is experimental.,(R)-pyridin-4-ylmethanol is a solid.,False
19002,,,,,1-(4-thiophen-2-ylphenyl)methanamine is experimental.,1-(4-thiophen-2-ylphenyl)methanamine is a solid.,False
19003,,,,,N-benzyl-4-aniline is experimental.,N-benzyl-4-aniline is a solid.,False
19004,,,,,"4-(2-amino-1,3-thiazol-4-yl)phenol is experimental.","4-(2-amino-1,3-thiazol-4-yl)phenol is a solid.",False
19005,,,,,Kelatorphan is experimental.,Kelatorphan is a solid.,False
19006,,,,,"5-benzene-1,3-diol is experimental.","5-benzene-1,3-diol is a solid.",False
19007,"Tosedostat has been used in trials studying the treatment and supportive care of AML, Leukemia, Pancreas Cancer, Multiple Myeloma, and Pancreatic Cancer, among others. Tosedostat has pleiotropic effects against a range of human tumor cell lines originating from diverse tumor types in vitro and in vivo. Tosedostat is anti-proliferative agent which induces apoptosis in leukemic cell lines in vitro. The mechanism underlying these anti-cancer actions is unclear, particularly since normal cells are much less sensitive to the agents than transformed cells. It exerts potent anti-proliferative, pro-apoptotic and anti-angiogenic effects in vitro and shows selectivity for transformed over non-transformed cells. It inhibits a number of M1 aminopeptidase enzyme family members in vitro (eg puromycin-sensitive aminopeptidase (PSA), leukotriene A4 hydrolase (LTA4H)).",,,,Tosedostat is investigational.,,True
19008,,,,,"1,6-Fructose Diphosphate (Linear Form) is experimental.","1,6-Fructose Diphosphate (Linear Form) is a solid.",False
19009,"Dihydroxyacetone phosphate is an important intermediate in lipid biosynthesis and in glycolysis. Dihydroxyacetone phosphate has been investigated for the treatment of Lymphoma, Large-Cell, Diffuse.",,,,Dihydroxyacetone phosphate is investigational.,Dihydroxyacetone phosphate is a solid.,True
19010,,,,,"1,6-DI-O-PHOSPHONO-D-MANNITOL is experimental.","1,6-DI-O-PHOSPHONO-D-MANNITOL is a solid.",False
19011,,,,,N-(4-CHLOROPHENYL)-3-(PHOSPHONOOXY)NAPHTHALENE-2-CARBOXAMIDE is experimental.,N-(4-CHLOROPHENYL)-3-(PHOSPHONOOXY)NAPHTHALENE-2-CARBOXAMIDE is a solid.,False
19012,,,,,"(1'R,2'S)-9-(2-Hydroxy-3'-Keto-Cyclopenten-1-yl)Adenine is experimental.","(1'R,2'S)-9-(2-Hydroxy-3'-Keto-Cyclopenten-1-yl)Adenine is a solid.",False
19013,,,,,3'-Oxo-Adenosine is experimental.,3'-Oxo-Adenosine is a solid.,False
19014,,,,,D-Eritadenine is experimental.,D-Eritadenine is a solid.,False
19015,,,,,Adenosine monotungstate is experimental.,Adenosine monotungstate is a solid.,False
19016,,,,,Ado-P-Ch2-P-Ps-Ado is experimental.,Ado-P-Ch2-P-Ps-Ado is a solid.,False
19017,,,,,4-guanidinobenzoic acid is experimental.,4-guanidinobenzoic acid is a solid.,False
19018,"MLN2222 is a novel, proprietary recombinant protein that blocks both the C3 and C5 convertases, which are essential components of the complement activation pathway. Investigated for use/treatment in coronary artery disease. MLN2222 is a proprietary recombinant protein that blocks both the C3 and C5 convertases, which are essential components of the complement activation pathway. Complement activation is believed to contribute to harmful inflammatory responses to heart bypass surgery that can result in significant complications; MLN2222 is being developed to reduce the incidence of death and heart attacks in patients undergoing procedures involving the use of cardiopulmonary bypass (CPB), a heart-lung bypass machine.",,,,MLN2222 is investigational.,MLN2222 is a solid.,True
19019,,,,,Carba-nicotinamide-adenine-dinucleotide is experimental.,Carba-nicotinamide-adenine-dinucleotide is a solid.,False
19020,,,,,NU1025 is experimental.,NU1025 is a solid.,False
19021,,,,,2-{3-Propyl}-8-Methyl-4(3h)-Quinazolinone is experimental.,2-{3-Propyl}-8-Methyl-4(3h)-Quinazolinone is a solid.,False
19022,,,,,3-Methoxybenzamide is experimental.,3-Methoxybenzamide is a solid.,False
19023,,,,,2-(4-Chlorophenyl)-5-Quinoxalinecarboxamide is experimental.,2-(4-Chlorophenyl)-5-Quinoxalinecarboxamide is a solid.,False
19024,,,,,"3,4-Dihydro-5-Methyl-Isoquinolinone is experimental.","3,4-Dihydro-5-Methyl-Isoquinolinone is a solid.",False
19025,,,,,2-(3'-Methoxyphenyl) Benzimidazole-4-Carboxamide is experimental.,2-(3'-Methoxyphenyl) Benzimidazole-4-Carboxamide is a solid.,False
19026,,,,,"6-AMINO-BENZOISOQUINOLINE-1,3-DIONE is experimental.","6-AMINO-BENZOISOQUINOLINE-1,3-DIONE is a solid.",False
19027,,,,,Veliparib is investigational.,Veliparib is a solid.,False
19028,,,,,A-620223 is experimental.,A-620223 is a solid.,False
19029,,,,,"5-FLUORO-1-QUINAZOLINE-2,4(1H,3H)-DIONE is experimental.","5-FLUORO-1-QUINAZOLINE-2,4(1H,3H)-DIONE is a solid.",False
19030,"Talazoparib was approved by the FDA for use in germline BRCA mutated, HER2 negative, locally advanced or metastatic breast cancer on October 16, 2018 under the trade name Talzenna. Talzenna was granted approval based on the results of the EMBRACA trial in which talazoparib resulted in a mean 8.6 months progression-free survival time versus physician's choice chemotherapy which resulted in 5.6 months progression-free survival. Talazoparib is indicated for the treatment of deleterious or suspected deleterious germline BRCA mutated, HER2 negative locally advanced or metastatic breast cancer in adults. Talazoparib prevents PARP-mediated repair of DNA damage in cancer cells, allowing accumulation of damage and PARP-DNA complexes. Repair related errors by error prone secondary repair pathways may also contribute to the cytotoxicity of talazoparib. Talazoparib binds to and inhibits PARP1 and PARP2 at the NAD+ binding site with a Ki of 1.2 and 0.87 nM, respectively. The inhibitory effect on PAR synthesis has an EC50 of 2.51 nM.",,,,Talazoparib is approved and investigational.,Talazoparib is a solid.,True
19031,,,,,Iniparib is investigational.,Iniparib is a solid.,False
19032,,,,,2H-Benzimidazol-2-amine is experimental.,2H-Benzimidazol-2-amine is a solid.,False
19033,,,,,Bis(5-Amidino-Benzimidazolyl)Methane is experimental.,Bis(5-Amidino-Benzimidazolyl)Methane is a solid.,False
19034,,,,,"Nalpha-(2-Naphthylsulfonylglycyl)-3-Amidino-D,L-Phenylalanine-Isopropylester is experimental.","Nalpha-(2-Naphthylsulfonylglycyl)-3-Amidino-D,L-Phenylalanine-Isopropylester is a solid.",False
19035,,,,,CRA_17693 is experimental.,CRA_17693 is a solid.,False
19036,,,,,N-Alpha-(2-Naphthylsulfonyl)-N(3-Amidino-L-Phenylalaninyl)Isopipecolinic Acid Methyl Ester is experimental.,N-Alpha-(2-Naphthylsulfonyl)-N(3-Amidino-L-Phenylalaninyl)Isopipecolinic Acid Methyl Ester is a solid.,False
19037,,,,,CRA_10991 is experimental.,CRA_10991 is a solid.,False
19038,,,,,"-(3,4,5,6-Tetrahydro-2h-Bipyridinyl-4-Yl)-Methanone is experimental.","-(3,4,5,6-Tetrahydro-2h-Bipyridinyl-4-Yl)-Methanone is a solid.",False
19039,,,,,Bis(5-Amidino-2-Benzimidazolyl)Methanone is experimental.,Bis(5-Amidino-2-Benzimidazolyl)Methanone is a solid.,False
19040,,,,,5-Amidino-Benzimidazole is experimental.,5-Amidino-Benzimidazole is a solid.,False
19041,,,,,Amylamine is experimental.,Amylamine is a solid.,False
19042,,,,,CRA_16847 is experimental.,CRA_16847 is a solid.,False
19043,,,,,Bis-Benzamidine is experimental.,Bis-Benzamidine is a solid.,False
19044,,,,,CRA_17312 is experimental.,CRA_17312 is a solid.,False
19045,,,,,Zk-806450 is experimental.,Zk-806450 is a solid.,False
19046,,,,,-Amino}-Methyl)-Phenyl]-Trimethyl-Ammonium is experimental.,-Amino}-Methyl)-Phenyl]-Trimethyl-Ammonium is a solid.,False
19047,,,,,CRA-9334 is experimental.,CRA-9334 is a solid.,False
19048,,,,,4-{-Amino}-Benzamidine is experimental.,4-{-Amino}-Benzamidine is a solid.,False
19049,,,,,CRA_10762 is experimental.,CRA_10762 is a solid.,False
19050,,,,,Aminomethylcyclohexane is experimental.,Aminomethylcyclohexane is a solid.,False
19051,,,,,2-(2-Hydroxy-Phenyl)-1h-Indole-5-Carboxamidine is experimental.,2-(2-Hydroxy-Phenyl)-1h-Indole-5-Carboxamidine is a solid.,False
19052,,,,,Benzylamine is experimental.,Benzylamine is a solid.,False
19053,"A propylamine formed from the cyclization of the side chain of amphetamine. This monoamine oxidase inhibitor is effective in the treatment of major depression, dysthymic disorder, and atypical depression. It also is useful in panic and phobic disorders. (From AMA Drug Evaluations Annual, 1994, p311)",,,,"(1R,2S)-2-Phenylcyclopropanaminium is experimental.","(1R,2S)-2-Phenylcyclopropanaminium is a solid.",True
19054,,,,,RPR131247 is experimental.,RPR131247 is a solid.,False
19055,,,,,RWJ-56423 is experimental.,RWJ-56423 is a solid.,False
19056,,,,,CRA_1802 is experimental.,CRA_1802 is a solid.,False
19057,,,,,CRA_10972 is experimental.,CRA_10972 is a solid.,False
19058,,,,,CRA_1801 is experimental.,CRA_1801 is a solid.,False
19059,,,,,-D-(4-amidino-phenylalanyl)]-piperidine is experimental.,-D-(4-amidino-phenylalanyl)]-piperidine is a solid.,False
19060,,,,,CRA_10433 is experimental.,CRA_10433 is a solid.,False
19061,,,,,Bis(5-Amidino-2-Benzimidazolyl)Methane Ketone is experimental.,Bis(5-Amidino-2-Benzimidazolyl)Methane Ketone is a solid.,False
19062,,,,,4-Fluorobenzylamine is experimental.,4-Fluorobenzylamine is a solid.,False
19063,,,,,RWJ-51084 is experimental.,RWJ-51084 is a solid.,False
19064,,,,,1-(2-Amidinophenyl)-3-(Phenoxyphenyl)Urea is experimental.,1-(2-Amidinophenyl)-3-(Phenoxyphenyl)Urea is a solid.,False
19065,,,,,ZK-806711 is experimental.,ZK-806711 is a solid.,False
19066,"A product from the iodination of MONOIODOTYROSINE. In the biosynthesis of thyroid hormones, diiodotyrosine residues are coupled with other monoiodotyrosine or diiodotyrosine residues to form T4 or T3 thyroid hormones (THYROXINE and TRIIODOTHYRONINE). ",The molecular weight is 432.98.,"3,5-Diiodotyrosine has a topological polar surface area of 83.55.",The log p value of  is -0.28.,"3,5-Diiodotyrosine is experimental.","3,5-Diiodotyrosine is a solid.",True
19067,,,,,"(2S,3R)-2-amino]-6-(diaminomethylideneamino)-3-formylhexanoic acid is experimental.","(2S,3R)-2-amino]-6-(diaminomethylideneamino)-3-formylhexanoic acid is a solid.",False
19068,,,,,bis(5-amidino-benzimidazolyl)methanone zinc is experimental.,bis(5-amidino-benzimidazolyl)methanone zinc is a solid.,False
19069,,,,,CRA_11092 is experimental.,CRA_11092 is a solid.,False
19070,,,,,CRA_9785 is experimental.,CRA_9785 is a solid.,False
19071,,,,,CRA_1144 is experimental.,CRA_1144 is a solid.,False
19072,,,,,Zinc;benzimidazol-1-id-2-yl]methyl]benzimidazol-1-id-5-yl]methylidene]azanium is experimental.,Zinc;benzimidazol-1-id-2-yl]methyl]benzimidazol-1-id-5-yl]methylidene]azanium is a solid.,False
19073,,,,,-1-Methyl-1h-Benzoimidazol-5-Yl}-Cyclopropyl)-Pyridin-2-Yl-Methyleneaminooxy]-Acetic Acid Ethyl Ester is experimental.,-1-Methyl-1h-Benzoimidazol-5-Yl}-Cyclopropyl)-Pyridin-2-Yl-Methyleneaminooxy]-Acetic Acid Ethyl Ester is a solid.,False
19074,,,,,N-Alpha-(2-Naphthylsulfonyl)-N(3-Amidino-L-Phenylalaninyl)-4-Acetyl-Piperazine is experimental.,N-Alpha-(2-Naphthylsulfonyl)-N(3-Amidino-L-Phenylalaninyl)-4-Acetyl-Piperazine is a solid.,False
19075,,,,,CRA_9076 is experimental.,CRA_9076 is a solid.,False
19076,,,,,N-Alpha-(2-Naphthylsulfonyl)-N-(3-Amidino-L-Phenylalaninyl)-D-Pipecolinic Acid is experimental.,N-Alpha-(2-Naphthylsulfonyl)-N-(3-Amidino-L-Phenylalaninyl)-D-Pipecolinic Acid is a solid.,False
19077,,,,,CRA_23653 is experimental.,CRA_23653 is a solid.,False
19078,Cyclotheonamide A is a cyclic peptide isolated from the marine sponge Theonella.,,,,Cyclotheonamide A is experimental.,Cyclotheonamide A is a solid.,True
19079,,,,,Bis(5-Amidino-2-Benzimidazolyl)Methane Ketone Hydrate is experimental.,Bis(5-Amidino-2-Benzimidazolyl)Methane Ketone Hydrate is a solid.,False
19080,,,,,4-Phenylbutylamine is experimental.,4-Phenylbutylamine is a solid.,False
19081,,,,,Phenethylamine is experimental.,Phenethylamine is a solid.,False
19082,,,,,1-(4-Amidinophenyl)-3-(4-Chlorophenyl)Urea is experimental.,1-(4-Amidinophenyl)-3-(4-Chlorophenyl)Urea is a solid.,False
19083,,,,,Aeruginosin 98-B is experimental.,Aeruginosin 98-B is a solid.,False
19084,,,,,3-Phenylpropylamine is experimental.,3-Phenylpropylamine is a solid.,False
19085,,,,,RPR128515 is experimental.,RPR128515 is a solid.,False
19086,,,,,ZK-805623 is experimental.,ZK-805623 is a solid.,False
19087,,,,,Iminomethanaminium is experimental.,Iminomethanaminium is a solid.,False
19088,,,,,BenzoThiophene-2-Carboxamidine is experimental.,BenzoThiophene-2-Carboxamidine is a solid.,False
19089,,,,,CRA_10656 is experimental.,CRA_10656 is a solid.,False
19090,,,,,CRA_9678 is experimental.,CRA_9678 is a solid.,False
19091,,,,,"2,5-bis-O-{3-phenyl}-1,4:3,6-dianhydro-D-glucitol is experimental.","2,5-bis-O-{3-phenyl}-1,4:3,6-dianhydro-D-glucitol is a solid.",False
19092,,,,,"2-O-(4'-AMIDINOPHENYL)-5-O-(3''-AMIDINOPHENYL)-1,4:3,6-DIANHYDRO-D-SORBITOL is experimental.","2-O-(4'-AMIDINOPHENYL)-5-O-(3''-AMIDINOPHENYL)-1,4:3,6-DIANHYDRO-D-SORBITOL is a solid.",False
19093,,,,,"2,5-O,O-BIS-{4',4''-AMIDINOPHENYL}-1,4:3,6-DIANHYDRO-D-SORBITOL is experimental.","2,5-O,O-BIS-{4',4''-AMIDINOPHENYL}-1,4:3,6-DIANHYDRO-D-SORBITOL is a solid.",False
19094,,,,,"1,4:3,6-Dianhydro-2-O-(3-carbamimidoylphenyl)-5-O-(4-carbamimidoylphenyl)-D-glucitol is experimental.","1,4:3,6-Dianhydro-2-O-(3-carbamimidoylphenyl)-5-O-(4-carbamimidoylphenyl)-D-glucitol is a solid.",False
19095,,,,,diethyl boronate is experimental.,diethyl boronate is a solid.,False
19096,,,,,2-(2-METHYLPHENYL)-1H-INDOLE-6-CARBOXIMIDAMIDE is experimental.,2-(2-METHYLPHENYL)-1H-INDOLE-6-CARBOXIMIDAMIDE is a solid.,False
19097,,,,,2-(3-METHYLPHENYL)-1H-INDOLE-5-CARBOXIMIDAMIDE is experimental.,2-(3-METHYLPHENYL)-1H-INDOLE-5-CARBOXIMIDAMIDE is a solid.,False
19098,,,,,"3-{5--1H-INDOL-2-YL}-5-METHOXY-1,1'-BIPHENYL-2-OLATE is experimental.","3-{5--1H-INDOL-2-YL}-5-METHOXY-1,1'-BIPHENYL-2-OLATE is a solid.",False
19099,,,,,4-(METHYLSULFONYL)BENZENECARBOXIMIDAMIDE is experimental.,4-(METHYLSULFONYL)BENZENECARBOXIMIDAMIDE is a solid.,False
19100,,,,,"5-amino-2,4,6-tribromobenzene-1,3-dicarboxylic acid is experimental.","5-amino-2,4,6-tribromobenzene-1,3-dicarboxylic acid is a solid.",False
19101,,,,,+/-METHYL 4-(AMINOIMINOMETHYL)-BETA-BENZENE PENTANOATE is experimental.,+/-METHYL 4-(AMINOIMINOMETHYL)-BETA-BENZENE PENTANOATE is a solid.,False
19102,,,,,2-(2-METHYLPHENYL)-1H-INDOLE-5-CARBOXIMIDAMIDE is experimental.,2-(2-METHYLPHENYL)-1H-INDOLE-5-CARBOXIMIDAMIDE is a solid.,False
19103,,,,,1-{-AMINO}-2-(3-CYANO-PHENYL)-ETHANEBORONIC ACID is experimental.,1-{-AMINO}-2-(3-CYANO-PHENYL)-ETHANEBORONIC ACID is a solid.,False
19104,,,,,(4-AMIDINOPHENYL)METHANE-PHOSPHONATE is experimental.,(4-AMIDINOPHENYL)METHANE-PHOSPHONATE is a solid.,False
19105,,,,,Octanoyl-Coenzyme A is experimental.,Octanoyl-Coenzyme A is a solid.,False
19106,,,,,3-thiaoctanoyl-CoA is experimental.,3-thiaoctanoyl-CoA is a solid.,False
19107,,,,,Phosphomethylphosphonic acid guanosyl ester is experimental.,Phosphomethylphosphonic acid guanosyl ester is a solid.,False
19108,,,,,"5,6-Dihydro-BenzoCinnolin-3-Ylamine is experimental.","5,6-Dihydro-BenzoCinnolin-3-Ylamine is a solid.",False
19109,,,,,"6-(3-AMINOPROPYL)-4,9-DIMETHYLPYRROLOCARBAZOLE-1,3(2H,6H)-DIONE is experimental.","6-(3-AMINOPROPYL)-4,9-DIMETHYLPYRROLOCARBAZOLE-1,3(2H,6H)-DIONE is a solid.",False
19110,,,,,Fexaramine is experimental.,Fexaramine is a solid.,False
19111,The product of conjugation of cholic acid with taurine. Its sodium salt is the chief ingredient of the bile of carnivorous animals. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as a cholagogue and cholerectic.,,,,Taurocholic acid is approved and experimental.,Taurocholic acid is a solid.,True
19112,,,,,"(8alpha,10alpha,13alpha,17beta)-17-androsta-3,5-diene-3-carboxylic acid is experimental.","(8alpha,10alpha,13alpha,17beta)-17-androsta-3,5-diene-3-carboxylic acid is a solid.",False
19113,,,,,Deamido-Nad+ is experimental.,Deamido-Nad+ is a solid.,False
19114,,,,,"Inositol 1,3-Bisphosphate is experimental.","Inositol 1,3-Bisphosphate is a solid.",False
19115,"CHGN111 is an inhibitor of the mitochondrial enzyme CLK-1 which is a demethoxyubiquinone hydroxylase. Numerous parameters of mitochondrial function are altered when the activity of CLK-1 is reduced, which results in a decrease of ROS at critical cellular sites, as well as in a decrease of systemic oxidative stress. It was under investigation until approximately 2007. Investigated for use/treatment in skin infections/disorders. CHGN111 is an inhibitor of the mitochondrial enzyme CLK-1 which is a demethoxyubiquinone hydroxylase. Numerous parameters of mitochondrial function are altered when the activity of CLK-1 is reduced, which results in a decrease of ROS at critical cellular sites, as well as in a decrease of systemic oxidative stress. Compared to free radical scavengers or other detoxifying agents they directly modulate reactive oxygen species production and detoxification at an early stage to prevent damage and stop disease initiation as well as progression. Such drugs with a new mechanism of action allows Chronogen to target different pathological situations from acute and severe conditions like reperfusion-injury to more chronic situations in cardiovascular and central nervous system diseases.",,,,CHGN111 is investigational.,CHGN111 is a solid.,True
19116,,,,,"ethyl 3--6,7-dichloro-1-methyl-1H-indole-2-carboxylate is experimental.","ethyl 3--6,7-dichloro-1-methyl-1H-indole-2-carboxylate is a solid.",False
19117,,,,,S-(N-hydroxy-N-bromophenylcarbamoyl)glutathione is experimental.,S-(N-hydroxy-N-bromophenylcarbamoyl)glutathione is a solid.,False
19118,,,,,Fica is experimental.,Fica is a solid.,False
19119,,,,,"alpha,beta-Methyleneadenosine 5'-triphosphate is experimental.","alpha,beta-Methyleneadenosine 5'-triphosphate is a solid.",False
19120,,,,,2-Aminobenzyl alcohol is experimental.,2-Aminobenzyl alcohol is a solid.,False
19121,,,,,"3,4-Dichloroisocoumarin is experimental.","3,4-Dichloroisocoumarin is a solid.",False
19122,,,,,3-Phenol is experimental.,3-Phenol is a solid.,False
19123,,,,,Monastrol is experimental.,Monastrol is a solid.,False
19124,"Filanesib is a potent Kinesin Spindle Protein (KSP) inhibitor that caused marked tumor regression in preclinical models of human solid tumors and human leukemias, often leading to durable responses. Investigated for use/treatment in cancer/tumors (unspecified). This compound is a highly potent KSP inhibitor that demonstrates subnanomolar potency in both enzymatic and cellular assays and causes mitotic arrest, leading to cell death or apoptosis of the immensely proliferating cancer cells. KSP has been identified as an attractive drug target against cancer. Cancer results when normal cellular processes go awry and lead to a massive, uncontrolled cell division, proliferation, and growth. Inhibitors of KSP cause mitotic arrest by preventing the formation of bipolar spindle. The monopolar spindle thus prevents the separation of centrosomes, organizes the microtubules from a single locus in the cell, and aligns the chromosomes around this locus. This compound is a highly potent KSP inhibitor that demonstrates subnanomolar potency in both enzymatic and cellular assays and causes mitotic arrest, leading to cell death or apoptosis of the immensely proliferating cancer cells.",,,,Filanesib is investigational.,Filanesib is a solid.,True
19125,,,,,"(4R)-4-(3-HYDROXYPHENYL)-N,N,7,8-TETRAMETHYL-3,4-DIHYDROISOQUINOLINE-2(1H)-CARBOXAMIDE is experimental.","(4R)-4-(3-HYDROXYPHENYL)-N,N,7,8-TETRAMETHYL-3,4-DIHYDROISOQUINOLINE-2(1H)-CARBOXAMIDE is a solid.",False
19126,,,,,"N,N-DIETHYL-2--4,5,6,7-TETRAHYDRO-1-BENZOTHIOPHENE-3-CARBOXAMIDE is experimental.","N,N-DIETHYL-2--4,5,6,7-TETRAHYDRO-1-BENZOTHIOPHENE-3-CARBOXAMIDE is a solid.",False
19127,,,,,"(5R)-N,N-DIETHYL-5-METHYL-2--4,5,6,7-TETRAHYDRO-1-BENZOTHIOPHENE-3-CARBOXAMIDE is experimental.","(5R)-N,N-DIETHYL-5-METHYL-2--4,5,6,7-TETRAHYDRO-1-BENZOTHIOPHENE-3-CARBOXAMIDE is a solid.",False
19128,MK-0731 is a kinesin spindle protein inhibitor and antineoplastic agent.,,,,MK-0731 is experimental.,MK-0731 is a solid.,True
19129,,,,,(PHENYL)METHANONE is experimental.,(PHENYL)METHANONE is a solid.,False
19130,,,,,"(2S)-4-(2,5-DIFLUOROPHENYL)-N-METHYL-2-PHENYL-N-PIPERIDIN-4-YL-2,5-DIHYDRO-1H-PYRROLE-1-CARBOXAMIDE is experimental.","(2S)-4-(2,5-DIFLUOROPHENYL)-N-METHYL-2-PHENYL-N-PIPERIDIN-4-YL-2,5-DIHYDRO-1H-PYRROLE-1-CARBOXAMIDE is a solid.",False
19131,,,,,(1S)-1-CYCLOPROPYL-2--2-OXOETHANAMINE is experimental.,(1S)-1-CYCLOPROPYL-2--2-OXOETHANAMINE is a solid.,False
19132,,,,,"(2S)-4-(2,5-DIFLUOROPHENYL)-N,N-DIMETHYL-2-PHENYL-2,5-DIHYDRO-1H-PYRROLE-1-CARBOXAMIDE is experimental.","(2S)-4-(2,5-DIFLUOROPHENYL)-N,N-DIMETHYL-2-PHENYL-2,5-DIHYDRO-1H-PYRROLE-1-CARBOXAMIDE is a solid.",False
19133,,,,,"(5S)-5-(3-AMINOPROPYL)-3-(2,5-DIFLUOROPHENYL)-N-ETHYL-5-PHENYL-4,5-DIHYDRO-1H-PYRAZOLE-1-CARBOXAMIDE is experimental.","(5S)-5-(3-AMINOPROPYL)-3-(2,5-DIFLUOROPHENYL)-N-ETHYL-5-PHENYL-4,5-DIHYDRO-1H-PYRAZOLE-1-CARBOXAMIDE is a solid.",False
19134,"An amino alcohol with a long unsaturated hydrocarbon chain. Sphingosine and its derivative sphinganine are the major bases of the sphingolipids in mammals. (Dorland, 28th ed)",,,,Sphingosine is experimental.,Sphingosine is a solid.,True
19135,,,,,"3,4-Dihydroxycinnamic Acid is experimental and investigational.","3,4-Dihydroxycinnamic Acid is a solid.",False
19136,,,,,7-Hydroxy-2-Oxo-Chromene-3-Carboxylic Acid Ethyl Ester is experimental.,7-Hydroxy-2-Oxo-Chromene-3-Carboxylic Acid Ethyl Ester is a solid.,False
19137,,,,,"3-(4-HYDROXYPHENYL)-4,5-DIHYDRO-5-ISOXAZOLE-ACETIC ACID METHYL ESTER is experimental.","3-(4-HYDROXYPHENYL)-4,5-DIHYDRO-5-ISOXAZOLE-ACETIC ACID METHYL ESTER is a solid.",False
19138,,,,,4-HYDROXYBENZALDEHYDE O-(CYCLOHEXYLCARBONYL)OXIME is experimental.,4-HYDROXYBENZALDEHYDE O-(CYCLOHEXYLCARBONYL)OXIME is a solid.,False
19139,,,,,3-FLUORO-4-HYDROXYBENZALDEHYDE O-(CYCLOHEXYLCARBONYL)OXIME is experimental.,3-FLUORO-4-HYDROXYBENZALDEHYDE O-(CYCLOHEXYLCARBONYL)OXIME is a solid.,False
19140,,,,,"4-HYDROXYBENZALDEHYDE O-(3,3-DIMETHYLBUTANOYL)OXIME is experimental.","4-HYDROXYBENZALDEHYDE O-(3,3-DIMETHYLBUTANOYL)OXIME is a solid.",False
19141,A sulfhydryl reagent that is widely used in experimental biochemical studies. ,,,,N-Ethylmaleimide is experimental.,N-Ethylmaleimide is a solid.,True
19142,,,,,Dazoxiben is experimental.,Dazoxiben is a solid.,False
19143,"Nissan Chemical and Taisho have been jointly developing NM-702, a drug for the treatment of arteriosclerosis obliterans. Investigated for use/treatment in peripheral vascular disease. Intermittent claudication is a major symptom of arteriosclerosis obliterans. It is caused by insufficient oxygen supply to exercising muscles in the lower extremities due to decreased blood flow as a result of sclerosis of peripheral arteries. Patients with claudication experience significant disability, owing to their exercise limitation. Therapeutic options to improve exercise performance in these patients are limited. NM-702 is a novel drug that inhibits phosphodiesterase as well as thromboxane A2 synthase. NM-702 is a novel drug that inhibits phosphodiesterase as well as thromboxane A2 synthase.",,,,NM-702 is investigational.,NM-702 is a solid.,True
19144,,,,,"4-{4--1H-PYRAZOL-5-YL}-6-CHLOROBENZENE-1,3-DIOL is experimental.","4-{4--1H-PYRAZOL-5-YL}-6-CHLOROBENZENE-1,3-DIOL is a solid.",False
19145,,,,,"(5E)-14-CHLORO-15,17-DIHYDROXY-4,7,8,9,10,11-HEXAHYDRO-2-BENZOXACYCLOPENTADECINE-1,12(3H,13H)-DIONE is experimental.","(5E)-14-CHLORO-15,17-DIHYDROXY-4,7,8,9,10,11-HEXAHYDRO-2-BENZOXACYCLOPENTADECINE-1,12(3H,13H)-DIONE is a solid.",False
19146,,,,,"(5Z)-12-CHLORO-13,15-DIHYDROXY-4,7,8,9-TETRAHYDRO-2-BENZOXACYCLOTRIDECINE-1,10(3H,11H)-DIONE is experimental.","(5Z)-12-CHLORO-13,15-DIHYDROXY-4,7,8,9-TETRAHYDRO-2-BENZOXACYCLOTRIDECINE-1,10(3H,11H)-DIONE is a solid.",False
19147,,,,,"(5E)-12-CHLORO-13,15-DIHYDROXY-4,7,8,9-TETRAHYDRO-2-BENZOXACYCLOTRIDECINE-1,10(3H,11H)-DIONE is experimental.","(5E)-12-CHLORO-13,15-DIHYDROXY-4,7,8,9-TETRAHYDRO-2-BENZOXACYCLOTRIDECINE-1,10(3H,11H)-DIONE is a solid.",False
19148,,,,,"(5Z)-13-CHLORO-14,16-DIHYDROXY-3,4,7,8,9,10-HEXAHYDRO-1H-2-BENZOXACYCLOTETRADECINE-1,11(12H)-DIONE is experimental.","(5Z)-13-CHLORO-14,16-DIHYDROXY-3,4,7,8,9,10-HEXAHYDRO-1H-2-BENZOXACYCLOTETRADECINE-1,11(12H)-DIONE is a solid.",False
19149,"3-amino-5-phenylpentane is a solid. This compound belongs to the phenylpropylamines. These are compounds containing a phenylpropylamine moiety, which consists of a phenyl group substituted at the third carbon by a propan-1-amine. 3-amino-5-phenylpentane targets the proteins cathepsin K and cathepsin L2.",,,,3-amino-5-phenylpentane is experimental.,3-amino-5-phenylpentane is a solid.,True
19150,,,,,4-Methylpiperazin-1-Yl Carbonyl Group is experimental.,4-Methylpiperazin-1-Yl Carbonyl Group is a solid.,False
19151,,,,,S-4-Nitrobutyryl-CoA is experimental.,S-4-Nitrobutyryl-CoA is a solid.,False
19152,,,,,2'-Deoxyuridine 3'-Monophosphate is experimental.,2'-Deoxyuridine 3'-Monophosphate is a solid.,False
19153,,,,,3-(N-morpholino)propanesulfonic acid is experimental.,3-(N-morpholino)propanesulfonic acid is a solid.,False
19154,,,,,beta-D-Ribose-5-phosphate is experimental.,beta-D-Ribose-5-phosphate is a solid.,False
19155,The glycine conjugate of cholic acid. It acts as a detergent to solubilize fats for absorption and is itself absorbed.,,,,Glycocholic acid is experimental and investigational.,Glycocholic acid is a solid.,True
19156,,,,,N-Carbamoyl-Alanine is experimental.,N-Carbamoyl-Alanine is a solid.,False
19157,,The molecular weight is 315.69.,Fotemustine has a topological polar surface area of 97.3.,The log p value of  is 0.97.,Fotemustine is investigational.,Fotemustine is a solid.,False
19158,"Motexafin gadolinium is studied in the treatment of cancer by Pharmacyclics. It may make tumor cells more sensitive to radiation therapy, improve tumor images using magnetic resonance imaging (MRI), and kill cancer cells. It belongs to the family of drugs called metalloporphyrin complexes. Also called gadolinium texaphyrin. Investigated for use/treatment in brain cancer, cancer/tumors (unspecified), lung cancer, and lymphoma (non-hodgkin's). Motexafin gadolinium (Xcytrin) is Pharmacyclics' most advanced anti-cancer product candidate, a small-molecule drug with a novel mechanism of action. Xcytrin accumulates selectively in cancer cells due to their increased rates of metabolism. Once inside the cell, Xcytrin induces apoptosis (programmed cell death) by disrupting redox-dependent pathways. Xcytrin inhibits the enzyme thioredoxin reductase, which is a tumor growth promoter. This mechanism provides the opportunity to use Xcytrin in a wide range of cancers. Xcytrin is paramagnetic, and therefore is detectable by magnetic resonance imaging (MRI), allowing the visualization of the drug in tumors.",,,,Motexafin gadolinium is investigational.,Motexafin gadolinium is a solid.,True
19159,"PX-12 (1-methylpropyl 2-imidazolyl disulfide) is a small-molecule inhibitor of Trx-1 (thioredoxin-1), stimulates apoptosis, down-regulates HIF-1α and vascular endothelial growth factor (VEGF) and inhibits tumor growth in animal models. Since high levels of Trx-1 have been associated with colorectal, gastric and lung cancers, PX-12 is indicated as a potential cancer treatment in combination with chemotherapy for patients with advanced metastatic cancer. Initial trials correlated doses of Px-12 with increased patient survival. Investigated for use/treatment in cancer/tumors (unspecified), gastric cancer, and pancreatic cancer. PX-12 is a small molecule irreversible inhibitor of the redox protein thioredoxin. Thioredoxin is involved in the first unique step in DNA synthesis. Thioredoxin also provides control over a number of transcription factors affecting cell proliferation and death through the mechanism of redox regulation PX-12 irreversibly inhibits the redox protein thioredoxin, which has been associated with cancer and tumor growth.",,,,PX-12 is investigational.,PX-12 is a solid.,True
19160,"Metergoline is an ergot-derived psychoactive drug that acts as a ligand for serotonin and dopamine receptors. Metergoline is an antagonist at various 5-HT receptor subtypes at a relatively low concentration and agonist at dopamine receptors. Its use has been studied in various clinical settings such as a treatment for seasonal affective disorder, prolactin hormone regulation due to its inhibitory effect on prolactin release, premenstrual dysphoric disorder in women and antianxiety treatment.",The molecular weight is 403.53.,Metergoline has a topological polar surface area of 46.5.,The log p value of  is 4.69.,Metergoline is approved.,,True
19161,"Amylmetacresol is an antiseptic available in Canada over-the-counter in a number of lozenges for the treatment of sore throat and minor mouth infections ,. Amylmetacresol is often combined with dichlorobenzyl alcohol and menthol in the commonly used sore throat lozenges, known as Strepsils. Sore throat, minor mouth and throat infections , ,. The mixture of amylmetacresol throat lozenge medications markedly reduces the infectivity of certain infectious viruses in the throat and in cough droplets, thus reducing opportunities for person-to-person transmission.  In addition, it relieves symptoms of sore throat/irritation of the throat ,. The mechanism of virucidal action is not fully elucidated, however it is suggested that denaturation of external protein spikes, a pH-induced rearrangement of the tertiary structure of attachment proteins, or a selective effect on viral lipid membranes/protein–lipid interaction is responsible for this action.",,,,Amylmetacresol is approved.,Amylmetacresol is a solid.,True
19162,"P-chlorophenol is a white crystals with a strong phenol odor. Slightly soluble to soluble in water, depending on the isomer, and denser than water. Noncombustible. Used as an intermediate in organic synthesis of dyes and drugs. The major mode of action of chlorophenols appears to be the uncoupling of oxidative phosphorylation. The strength of the uncoupling effect is related to the degree of chlorination: PCP is the strongest inhibitor of oxidative phosphorylation, MCP the weakest. To a lesser extent, inhibition of oxidative phosphorylation is affected by the positions of the chlorine atoms on the molecule. ",,,,Parachlorophenol is approved.,Parachlorophenol is a solid.,True
19163,"Cyclic guanosine monophosphate (Cyclic GMP) is a guanine nucleotide containing one phosphate group which is esterified to the sugar moiety in both the 3&#39;- and 5&#39;-positions. It is a cellular regulatory agent and has been described as a second messenger. Its levels increase in response to a variety of hormones, including acetylcholine, insulin, and oxytocin and it has been found to activate specific protein kinases. (From Merck Index, 11th ed)",,,,Cyclic GMP is experimental.,Cyclic GMP is a solid.,True
19164,"ND7001, a selective PDE2 inhibitor is in clinical trials for the treatment of depression. ND7001 is a solid. Known drug targets of ND7001 including phosphodiesterase 2A, cGMP-stimulated and cGMP-dependent 3',5'-cyclic phosphodiesterase. It is a new type of antidepressant drug with anxiolytic activity. It is the first representative of a new generation of psycho-active compounds potentially devoid of several problems seen with existing treatments. Investigated for use/treatment in anxiety disorders and depression.",,,,ND7001 is investigational.,ND7001 is a solid.,True
19165,,,,,4-HYDROXY-N'-(4-ISOPROPYLBENZYL)BENZOHYDRAZIDE is experimental.,4-HYDROXY-N'-(4-ISOPROPYLBENZYL)BENZOHYDRAZIDE is a solid.,False
19166,,,,,p-Cumylphenol is experimental.,p-Cumylphenol is a solid.,False
19167,,,,,Bisphenol A is experimental.,Bisphenol A is a solid.,False
19168,,,,,Bisphenol Z is experimental.,Bisphenol Z is a solid.,False
19169,,,,,"3,5-Dinitrocatechol is experimental.","3,5-Dinitrocatechol is a solid.",False
19170,,,,,BIA is experimental.,BIA is a solid.,False
19171,,,,,"N-prop-2-enyl]-2,3-dihydroxy-5-nitrobenzamide is experimental.","N-prop-2-enyl]-2,3-dihydroxy-5-nitrobenzamide is a solid.",False
19172,"Withdrawn from the Canadian, US, and UK markets in 1963 due to interactions with food products containing tyrosine. Nialamide was one of the first MAOI (monoamine oxidase inhibitor) antidepressants. It is chemically related to iproniazide, another MAOI derived from isonicotinic acid. //",The molecular weight is 298.35.,Nialamide has a topological polar surface area of 83.12.,The log p value of  is 0.91.,Nialamide is approved and withdrawn.,Nialamide is a solid.,True
19173,,,,,"(3,4-DIHYDROXY-2-NITROPHENYL)(PHENYL)METHANONE is experimental.","(3,4-DIHYDROXY-2-NITROPHENYL)(PHENYL)METHANONE is a solid.",False
19174,,,,,"7,8-dihydroxy-4-phenyl-2H-chromen-2-one is experimental.","7,8-dihydroxy-4-phenyl-2H-chromen-2-one is a solid.",False
19175,"An antineoplastic agent that is a derivative of progesterone and used to treat advanced breast cancer. For palliative treatment of advanced breast cancer in postmenopausal women. Testolactone is a synthetic anti-neoplastic agent that is structurally distinct from the androgen steroid nucleus in possessing a six-membered lactone ring in place of the usual five-membered carbocyclic D-ring. Despite some similarity to testosterone, testolactone has no in vivo androgenic effect. No other hormonal effects have been reported in clinical studies in patients receiving testolactone. Although the precise mechanism by which testolactone produces its clinical antineoplastic effects has not been established, its principal action is reported to be inhibition of steroid aromatase activity and consequent reduction in estrone synthesis from adrenal androstenedione, the major source of estrogen in postmenopausal women. Based on in vitro studies, the aromatase inhibition may be noncompetitive and irreversible. This phenomenon may account for the persistence of testolactone's effect on estrogen synthesis after drug withdrawal.",The molecular weight is 300.4.,Testolactone has a topological polar surface area of 43.37.,The log p value of  is 2.63.,Testolactone is approved and investigational.,Testolactone is a solid.,True
19176,"MPI-674 is an aromatase inhibitor (AI) with a well-established, multi-year chronic safety and tolerability profile. AIs are a class of drugs that reduce the amount of estrogen circulating in the body by binding to and inhibiting the enzyme aromatase, which is responsible for converting certain hormones to estrogen. It is developed for the treatment of several serious women’s health conditions including endometrial thinning prior to endometrial ablations in premenopausal women with abnormal uterine bleeding (AUB). Investigated for use/treatment in menstrual disorders. MPI-674 is an aromatase inhibitor (AI). It reduces the amount of estrogen circulating in the body by binding to and inhibiting the enzyme aromatase, which is responsible for converting certain hormones to estrogen.",,,,MPI-674 is investigational.,MPI-674 is a solid.,True
19177,"Benralizumab is a humanized recombinant monoclonal antibody of the isotype IgG1k immunoglobulin that specifically binds to the alpha chain of the interleukin 5 receptor (IL-5R) expressed on eosinophils and basophils. It inhibits the binding of IL-5 as well as the hetero-oligomerization of the alpha and beta subunits of the IL-5R, thus blocking, signal transduction. Besides, it is an afucosylated IgG which gives it high affinity for the FcγRIIIα receptor in natural killer cells, macrophages and neutrophils. Benralizumab, FDA approved on November 14, 2017, was developed by MedImmune, the AstraZeneca's global biologic research and development arm. Benralizumab is indicated as a maintenance treatment of patients 12 years or older with severe asthma and an eosinophilic phenotype. The pathology of severe asthma with eosinophilic phenotype is also denotated as TH2-high phenotype. The patients with this phenotype are characterized by the expression of IL-5 and IL-13, airway hyperresponsiveness, responsiveness to inhaled corticosteroids, high serum IgE and eosinophilia in blood and airway. In the TH2-high phenotype, IL-5 presents a central role as it is responsible for eosinophil differentiation, survival, activation and migration to the lungs. Eosinophils are the key target of inflammatory respiratory diseases and they undergo apoptosis in absence of IL-5. Therefore, benralizumab action on the IL-5 receptor in basophils and eosinophils produces the apoptosis and its significant reduction in the blood. On the other hand, Benralizumab binding to natural killer cells FcγRIIIα receptor produces a direct antibody-dependent cell-mediated cytotoxicity. All these effects produce a reduction in eosinophil count in airway mucosa, submucosa, sputum, blood and bone marrow. Interleukin-5 (IL-5) induces an eosinophil-mediated inflammatory response by binding to the IL-5 receptor (IL-5R) expressed in eosinophils, basophils and some mast cells. Benralizumab, unlike IL-5 low-affinity binding, binds with high affinity to the domain I of the α-chain of IL-5R and blocks its signaling and the proliferation of IL-5-dependent cell lines. On the other hand, Benralizumab is an afucosylated antibody in the CH2 region which gives it a high affinity for the FcγRIIIa on natural killer cells, macrophages and neutrophils. This binding triggers a magnified apoptosis response in eosinophils via antibody-dependent cell-mediated cytotoxicity.",,,,Benralizumab is approved and investigational.,Benralizumab is a solid.,True
19178,"Latrunculin A is an actin binding macrolide purified from the red sea sponge Latrunculia magnifica. It is under investigation for the treatment of cancer. It disrupts actin polymerization, prevents mitotic spindle formation and thus cell replication.",,,,Latrunculin A is experimental.,Latrunculin A is a solid.,True
19179,,,,,Ulapualide A is experimental.,Ulapualide A is a solid.,False
19180,,,,,Kabiramide C is experimental.,Kabiramide C is a solid.,False
19181,,,,,Jaspisamide A is experimental.,Jaspisamide A is a solid.,False
19182,,,,,Tmr is experimental.,Tmr is a solid.,False
19183,,,,,1-Methylhistidine is experimental.,1-Methylhistidine is a solid.,False
19184,,,,,Aplyronine A is experimental.,Aplyronine A is a solid.,False
19185,,,,,Reidispongiolide A is experimental.,Reidispongiolide A is a solid.,False
19186,,,,,Reidispongiolide C is experimental.,Reidispongiolide C is a solid.,False
19187,,,,,Sphinxolide B is experimental.,Sphinxolide B is a solid.,False
19188,"Latrunculin B is a 14-membered macrolide attached to 2-thiazolidinone moiety, isolated from Red Sea sponge _Latrunculia magnifica_.",,,,Latrunculin B is experimental.,Latrunculin B is a solid.,True
19189,Resatorvid is an investigational compound designed for the treatment of severe sepsis. Investigated for use/treatment in sepsis and septicemia. TAK-242 suppresses production of inflammatory mediators such as cytokine by inhibiting the signal transduction through Toll-like receptor 4 (TLR4) which is one of the receptors recognizing the bacterial components.,,,,Resatorvid is investigational.,Resatorvid is a solid.,True
19190,"Tifuvirtide is the first members of a new class of anti-HIV drugs which is also called fusion inhibitors. It has received fast track designation from the FDA and is in Phase I/II clinical testing. Investigated for use/treatment in acquired immune deficiency syndrome (AIDS) and aids-related infections and HIV infection. Tifuvirtide binds to a slightly different region of the HIV virus than Fuzeon (enfuvirtide). As a result,it exhibits activity against Fuzeon-resistant viruses. Tifuvirtide is designed to block fusion of HIV with host cells before the virus enters the cell and begins its replication process.",,,,Tifuvirtide is investigational.,Tifuvirtide is a solid.,True
19191,"Chymopapain was first isolated in 1941 from the crude latex derived from the fruit of Carica papaya by squeezing the green papaya while on the plant prior to harvest.It is an extracellular plant cysteine proteinase similar to papain in specificity. Chymopapain was developed by Chart Medcl and FDA approved on November 10, 1982. It is currently discontinued. Chymopapain is indicated for the development of chemonucleolysis which is used for the digestion of the nucleus pulposus in patients with disc herniation confirmed by myelography. A disc herniation occurs when the outer portion of the spinal disc breaks down and the inner portion (nucleus pulposus) leaks out pressing surrounding nerves and leading to irradiating pain. The chemonucleolysis is a non-surgical treatment that involves the injection of an enzyme to dissolve the nucleus pulposus. The first studies showed that after intradiscal injection of chymopapain the effect involved the removal of the nucleus pulposus leaving the annulus intact. The clinical reports indicated a spontaneous remission of symptoms after the administration of chymopapain. It is also highly documented an increased urinary excretion of glycosaminoglycans. Chymopapain is thought to degrade proteoglycan content of the intervertebral disc causing loss of glycosaminoglycan and water. This effect will cause the shrinkage of the disc and a reduction of the pressure on the nerve root.",,,,Chymopapain is approved and withdrawn.,Chymopapain is a solid.,True
19192,"NPI 32101 possesses both anti-inflammatory and broad spectrum antimicrobial activities. This combination of pharmacological properties may have additional therapeutic uses beyond dermatology. Atopic dermatitis  NPI 32101 cream serves as a broad-spectrum antimicrobial barrier to organisms including Pseudomonas aeruginosa and Staphylococcus aureus, including strains resistant to Methicillin (MRSA). NPI 32101 has dual action against both the vegetative and spore forms of C. difficile could lead to a first-in-class drug that both treats and prevents disease recurrence.",,,,NPI 32101 is investigational.,NPI 32101 is a solid.,True
19193,"Bentiromide is a dipeptide that is used in the bentiromide test, which is a screening test for evaluating pancreatic exocrine function and monitoring the adequacy of supplemental pancreatic therapy. It is typically administered orally. Cases of headache and gastrointestinal disturbances have been reported with the use of bentiromide. Bentiromide is currently not available in the U.S. or Canada. Indicated as a screening test for exocrine pancreatic insufficiency and to monitor the adequacy of supplemental pancreatic therapy. Bentiromide is a peptide used as a screening test for exocrine pancreatic insufficiency and to monitor the adequacy of supplemental pancreatic therapy. The amount of <i>p</i>-aminobenzoic acid and its metabolites excreted in the urine is the quantitative measure of the chymotrypsin-secreting activity of the pancreas.  Bentiromide is a peptide that is broken down in the pancreas by chymotrypsin. By determining the output of unchanged bentiromide in the urine following oral administration, it is possible to determine the sufficiency of pancreatic activity.",The molecular weight is 404.42.,Bentiromide has a topological polar surface area of 115.73.,The log p value of  is 2.96.,Bentiromide is investigational and withdrawn.,Bentiromide is a solid.,True
19194,,,,,3-(3-methoxybenzyl)-1H-pyrrolopyridine is experimental.,3-(3-methoxybenzyl)-1H-pyrrolopyridine is a solid.,False
19195,,,,,(E)-pyridin-3-ylidene](3-methoxyphenyl)methanol is experimental.,(E)-pyridin-3-ylidene](3-methoxyphenyl)methanol is a solid.,False
19196,,,,,3--2-INDOLINONE is experimental.,3--2-INDOLINONE is a solid.,False
19197,"Teduglutide is a glucagon-like peptide-2 (GLP-2) analogue. It is made up of 33 amino acids and is manufactured using a strain of Escherichia coli modified by recombinant DNA technology. Teduglutide differs from GLP-2 by one amino acid (alanine is substituted by glycine). The significance of this substitution is that teduglutide is longer acting than endogenous GLP-2 as it is more resistant to proteolysis from dipeptidyl peptidase-4. FDA approved on December 21, 2012. Treatment of short bowel syndrome (SBS), malabsorption associated with the removal of the intestine, in adults patients who are dependent on parenteral support.  An enhancement of gastrointestinal fluid absorption (750-1000 mL/day) was observed following daily administrations of teduglutide. An increase in villus height and crypt depth of the intestinal mucosa was also noted. A decrease in fecal weight has also been observed. Teduglutide does not prolong the QTc interval.  Teduglutide is an analog of naturally occurring human glucagon-like peptide-2 (GLP-2), a peptide secreted by L-cells of the distal intestine in response to meals. GLP-2 increases intestinal and portal blood flow and inhibit gastric acid secretion. Teduglutide binds to the glucagon-like peptide-2 receptors located in enteroendocrine cells, subepithelial myofibroblasts and enteric neurons of the submucosal and myenteric plexus. This causes the release of insulin-like growth factor (IGF)-1, nitric oxide and keratinocyte growth factor (KGF). These growth factors may contribute to the increase in crypt cell growth and surface area of the gastric mucosa. Ultimately, absorption through the intestine is enhanced. ",The molecular weight is 3752.13.,Teduglutide has a topological polar surface area of 1624.22.,,Teduglutide is approved.,Teduglutide is a liquid.,True
19198,,The molecular weight is 212.25.,Felbinac has a topological polar surface area of 37.3.,The log p value of  is 3.3.,Felbinac is experimental.,Felbinac is a solid.,False
19199,"Neurotoxin produced by fermentation of clostridium botulinum type B. The protein exists in noncovalent association with hemagglutinin and nonhemagglutinin proteins as a neurotoxin complex. The neurotoxin complex is recovered from the fermentation process and purified through a series of precipitation and chromatography steps. For the treatment of patients with cervical dystonia to reduce the severity of abnormal head position and neck pain associated with cervical dystonia. Botulinum Toxin Type B inhibits acetylcholine release at the neuromuscular junction via a three stage process: 1) Heavy Chain mediated neurospecific binding of the toxin, 2) internalization of the toxin by receptor-mediated endocytosis, and 3) ATP and pH dependent translocation of the Light Chain to the neuronal cytosol where it acts as a zinc-dependent endoprotease cleaving polypeptides essential for neurotransmitter release. Botulinum Toxin Type B binds to and cleaves the synaptic Vesicle Associated Membrane Protein (VAMP, also known as synaptobrevin) which is a component of the protein complex responsible for docking and fusion of the synaptic vesicle to the presynaptic membrane, a necessary step to neurotransmitter release.",,,,Botulinum Toxin Type B is approved and investigational.,Botulinum Toxin Type B is a liquid.,True
19200,,,,,1-Hydroxy-1-Thio-Glycerol is experimental.,1-Hydroxy-1-Thio-Glycerol is a solid.,False
19201,,,,,S-oxy-L-cysteine is experimental.,S-oxy-L-cysteine is a solid.,False
19202,,,,,Z-Pro-Prolinal is experimental.,Z-Pro-Prolinal is a solid.,False
19203,,,,,Monothioglycerol is experimental.,Monothioglycerol is a solid.,False
19204,,,,,(6S)-1-chloro-3--6-(pyrrolidin-1-ylcarbonyl)pyrrolopyrazin-4(6H)-one is experimental.,(6S)-1-chloro-3--6-(pyrrolidin-1-ylcarbonyl)pyrrolopyrazin-4(6H)-one is a solid.,False
19205,,,,,1-{3-oxo-3-propyl}-3-phenylquinoxalin-2(1H)-one is experimental.,1-{3-oxo-3-propyl}-3-phenylquinoxalin-2(1H)-one is a solid.,False
19206,,,,,"2-{3--3-oxopropyl}-isoindole-1,3(2H)-dione is experimental.","2-{3--3-oxopropyl}-isoindole-1,3(2H)-dione is a solid.",False
19207,"Carbidopa presents a chemical denomination of N-amino-alpha-methyl-3-hydroxy-L-tyrosine monohydrate. It potently inhibits aromatic amino acid decarboxylase (DDC) and due to its chemical properties, it does not cross the blood-brain barrier. Due to its activity, carbidopa is always administered concomitantly with. An individual formulation containing solely carbidopa was generated to treat nausea in patients where the combination therapy /carbidopa is not efficient reducing nausea.  Carbidopa is indicated with for the treatment of symptoms of idiopathic Parkinson disease, postencephalitic parkinsonism and symptomatic parkinsonism followed by carbon monoxide or manganese intoxication. When mixed with , carbidopa inhibits the peripheral conversion of to dopamine and the decarboxylation of to serotonin by aromatic L-amino acid decarboxylase. This results in an increased amount of and available for transport to the central nervous system. Carbidopa also inhibits the metabolism of in the GI tract, thus, increasing the bioavailability of. Carbidopa is an inhibitor of the DDC which in order, inhibits the peripheral metabolism of levodopa. DDC is very important in the biosynthesis of L-tryptophan to serotonin and the modification of L-DOPA to dopamine. ",The molecular weight is 226.23.,Carbidopa has a topological polar surface area of 115.81.,The log p value of  is -0.44.,Carbidopa is approved.,Carbidopa is a solid.,True
19208,"When levodopa is used by itself as a therapy for treating Parkinson's disease, its ubiquitous metabolism into dopamine is responsible for a resultant increase in the levels of circulating dopamine in the blood and to various extracerebral tissues. This can result in a number of side effects like nausea, vomiting, or even cardiac arrhythmias that may diminish patient adherence. A decarboxylase inhibitor like benserazide is consequently an effective compound to combine with levadopa as it is incapable of crossing the blood-brain barrier itself but acts to prevent the formation of dopamine from levadopa in extracerebral tissues - thereby acting to minimize the occurrence of extracerebral side effects. The primary therapeutic use for which benserazide is currently indicated for is as a combination therapy with levadopa for the treatment of Parkinson's disease in adults > 25 years of age, with the exception of drug-induced parkinsonism. When used as a therapy for treating Parkinson's disease, levadopa's specific mechanism of action revolves around its metabolism into dopamine in the body. Unfortunately, the resultant increase in the levels of circulating dopamine in the blood and to various extracerebral tissues can result in a number of side effects like nausea, vomiting, or even cardiac arrhythmias that may diminish patient adherence. A decarboxylase inhibitor like benserazide is consequently an effective compound to combine with levadopa as it is incapable of crossing the blood-brain barrier itself and therefore allows levadopa to elicit its primary action in the central nervous system, but will prevent the formation of dopamine from levadopa in extracerebral tissues - thereby acting to minimize the occurrence of extracerebral side effects. The combination of levodopa and benserazide is an anti-Parkinsonian agent. Levodopa itself is the metabolic precursor of dopamine. In Parkinson's disease, dopamine is depleted to a large degree in the striatum, pallidum, and substantia nigra in the central nervous system (CNS). The administration of levodopa to treat the disease is subsequently proposed to facilitate raises in the levels of available dopamine in these areas. The metabolism of levodopa to dopamine occurs via the enzyme dopa decarboxylase, although unfortunately, this metabolism can also occur in extracerebral tissues. As a result, the full therapeutic effect of an administered dose of levodopa may not be obtained if portions of it are catabolized outside of the CNS and various patient adherence diminishing extracerebral side effects due to the extracerebral presence of dopamine like nausea, vomiting, or even cardiac arrhythmias can also happen.",The molecular weight is 257.25.,Benserazide has a topological polar surface area of 148.07.,The log p value of  is -2.9.,Benserazide is approved and investigational.,,True
19209,"Hexafluronium bromide is a neuromuscular blocking agent used in anesthesiology to prolong and potentiate the skeletal muscle relaxing action of suxamethonium during surgery. It is known to bind and block the activity of plasma cholinesterases. Used as an adjunct with succinylcholine (or suxamethonium chloride) to prolong muscle relaxation and to prevent succinylcholine-induced muscle fasciculations. Hexafluronium bromide is a cholinesterase antagonist that can be used to prolong the relaxation effects of succinylcholine or suxamethonium chloride. Suxamethonium acts as a depolarizing muscle relaxant. It imitates the action of acetylcholine at the neuromuscular junction and is degraded by pseudocholinesterase, a plasma cholinesterase. The prolonged stimulation of the acetylcholine receptor results first in disorganized muscle contractions, then in profound relaxation. Cholinesterases catalyze the hydrolysis of the neurotransmitter acetylcholine into choline and acetic acid, a reaction necessary to allow a cholinergic neuron to return to its resting state after activation. There are two types of cholinesterase acetylcholinesterase and pseuodocholinesterase. The first hydrolyses acetylcholine more quickly; the latter hydrolyses butyrylcholine and succinylcholine more quickly. An absence or mutation of the pseudocholinesterase enzyme leads to a medical condition known simply as pseudocholinesterase deficiency. This is a silent condition that only manifests itself when people who have the deficiency receive the muscle relaxants succinylcholine or mivacurium during a surgery. Hexafluronium bromide is a non-competitive reversible inhibitor of human plasma cholinesterase or pseudocholinesterase.",,,,Hexafluronium is approved.,Hexafluronium is a solid.,True
19210,,,,,Diethyl phosphonate is experimental.,Diethyl phosphonate is a solid.,False
19211,,,,,9-N-Phenylmethylamino-Tacrine is experimental.,9-N-Phenylmethylamino-Tacrine is a solid.,False
19212,,,,,DODECANESULFONATE ION is experimental.,DODECANESULFONATE ION is a solid.,False
19213,,,,,"9-(3-IODOBENZYLAMINO)-1,2,3,4-TETRAHYDROACRIDINE is experimental.","9-(3-IODOBENZYLAMINO)-1,2,3,4-TETRAHYDROACRIDINE is a solid.",False
19214,,,,,(1R)-menthyl hexyl phosphonate group is experimental.,(1R)-menthyl hexyl phosphonate group is a solid.,False
19215,,,,,(1S)-menthyl hexyl phosphonate group is experimental.,(1S)-menthyl hexyl phosphonate group is a solid.,False
19216,,,,,ETHYL HYDROGEN DIETHYLAMIDOPHOSPHATE is experimental.,ETHYL HYDROGEN DIETHYLAMIDOPHOSPHATE is a solid.,False
19217,"Tipiracil is a thymidine phosphorylase inhibitor. It is used in combination with trifluridine, in a ratio of 1:0.5, to form TAS-102. The main function of Tipiracil in TAS-102 is to increase trifluridine bioavailability by inhibiting its catabolism. TAS-102 is indicated for the treatment of metastatic colorectal cancer which has been previously treated with fluoropyrimidine-, oxaliplatin- and irinotecan-based chemotherapy, or with an anti-VEGF or anti-EGFR therapy. Tipiracil, in combination with trifluridine, is indicated for the treatment of refractory mestastatic colorectal cancer patients who keep progressing despite of treatment with standard chemotherapy and biologics. Tipiracil prevents trifluridine conversion into 5-trifluoromethyl-2,4(1H,3H)-pyrimidinedione, which is an inactive major metabolite, by inhibiting the enzyme thymidine phosphorylase. Thus, tipiracil is able to increase trifluridine bioavailability. On the other hand, thymidine phsophorylase is a known platelet-derived endothelial cell growth factor and its inhibition generates an indirect antiangiogenic benefit.  Tipiracil is a thymidine phosphorylase inhibitor. Its function prevents the breakdownof the active component of trifluridine, thus increasing the bioavailability of trifluridine and boosting its systemic presence. In addition, it is reported that thymidine phosphorylase is an angiogenic factor usually overexpressed in solid tumors. There is a direct association of thymidine phosphorylase with a poor prognosis; where the tumors with an elevated expression of this enzyme tend to present an increased angiogenesis and ergo, be more malignant. Therefore, it has been suggested that tipiracil presents an aditional function by downregulating tumoral angiogenesis.",The molecular weight is 242.66.,Tipiracil has a topological polar surface area of 85.29.,The log p value of  is -0.31.,Tipiracil is approved and investigational.,Tipiracil is a solid.,True
19218,"Methoxy arachidonyl fluorophosphonate, commonly referred as MAFP, is an irreversible active site-directed enzyme inhibitor that inhibits nearly all serine hydrolases and serine proteases. It inhibits phospholipase A2 and fatty acid amide hydrolase with special potency, displaying IC50 values in the low-nanomolar range.",,,,Methoxy arachidonyl fluorophosphonate is experimental.,Methoxy arachidonyl fluorophosphonate is a solid.,True
19219,"1-Dodecanol is a saturated 12-carbon fatty alcohol obtained from coconut oil fatty acids. It has a floral odor and is used in detergents, lubricating oils, and pharmaceuticals. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 5th ed)",,,,1-Dodecanol is experimental.,1-Dodecanol is a solid.,True
19220,,,,,4-(quinolin-3-ylmethyl)piperidine-1-carboxylic acid is experimental.,4-(quinolin-3-ylmethyl)piperidine-1-carboxylic acid is a solid.,False
19221,,,,,4-(3-{oxy}benzyl)piperidine-1-carboxylic acid is experimental.,4-(3-{oxy}benzyl)piperidine-1-carboxylic acid is a solid.,False
19222,"Isocarboxazid has the formula 1-benzyl-2-(5-methyl-3-isoxazolylcarbonyl)hydrazine-isocarboxazid. It is a monoamine oxidase inhibitor. It is used in the treatment of major depression, dysthymic disorder, atypical disorder, panic disorder and the phobic disorders. It was first introduced by Roche pharmaceuticals, further developed by Validus pharms Inc and first FDA approved as a prescription drug on July 1st, 1959. Isocarboxazid is indicated for the treatment of the enduring and debilitating symptoms of depression that have not responded to other antidepressant drugs. Depression is a common but serious mood disorder. The patient will present changes in its feelings, thoughts, and ability to handle everyday activities. For a mood disorder to be considered as depression, the symptoms should be present for at least two weeks. In vivo and in vitro studies demonstrated isocarboxazid-driven inhibition of MAO in the brain, heart, and liver. The reduced MAO activity, caused by isocarboxazid, results in an increased concentration of serotonin, epinephrine, norepinephrine, and dopamine in storage sites throughout the central nervous system (CNS) and sympathetic nervous system. The increase of one or more monoamines is the basis for the antidepressant activity of MAO inhibitors like isocarboxazid. Isocarboxazid works by irreversibly blocking the action of monoamine oxidases (MAO) in the nervous system. MAO subtypes A and B are involved in the metabolism of serotonin and catecholamine neurotransmitters such as epinephrine, norepinephrine, and dopamine. Isocarboxazid, as a nonselective MAO inhibitor, binds irreversibly to monoamine oxidase-A (MAO-A) and monoamine oxidase-B (MAO-B). Isocarboxacid, like other monoamine oxidase inhibitors, are unique psychopharmacological agents whose clinical effect is related to the direct action of the monoamine oxidases to transform them into reactive metabolites.",The molecular weight is 231.26.,Isocarboxazid has a topological polar surface area of 67.16.,The log p value of  is 0.99.,Isocarboxazid is approved.,Isocarboxazid is a solid.,True
19223,"Pargyline is a monoamine oxidase inhibitor with antihypertensive properties. For the treatment of moderate to severe hypertension. Pargyline is a monoamine oxidase B (MAO-B) inhibitor with antihypertensive properties. Patients taking pargyline must avoid concurrent consumption of tyramine-containing foods such as bleu cheese and beer, as this can lead to a hypertensive crisis. MAOIs act by inhibiting the activity of monoamine oxidase, thus preventing the breakdown of monoamine neurotransmitters and thereby increasing their availability. There are two isoforms of monoamine oxidase, MAO-A and MAO-B. MAO-A preferentially deaminates serotonin, melatonin, epinephrine and norepinephrine. MAO-B preferentially deaminates phenylethylamine and trace amines. Pargyline functions by inhibiting the metabolism of catecholamines and tyramine within presynaptic nerve terminals. Catecholamines cause general physiological changes that prepare the body for physical activity (fight-or-flight response). Some typical effects are increases in heart rate, blood pressure, blood glucose levels, and a general reaction of the sympathetic nervous system.",The molecular weight is 159.23.,Pargyline has a topological polar surface area of 3.24.,The log p value of  is 2.4.,Pargyline is approved.,Pargyline is a solid.,True
19224,,,,,"N-Dodecyl-N,N-Dimethyl-3-Ammonio-1-Propanesulfonate is experimental.","N-Dodecyl-N,N-Dimethyl-3-Ammonio-1-Propanesulfonate is a solid.",False
19225,,,,,N-METHYL-N-PROP-2-EN-1-AMINE is experimental.,N-METHYL-N-PROP-2-EN-1-AMINE is a solid.,False
19226,,,,,7--2-OXO-2H-CHROMENE-4-CARBALDEHYDE is experimental.,7--2-OXO-2H-CHROMENE-4-CARBALDEHYDE is a solid.,False
19227,,,,,7--4--2H-CHROMEN-2-ONE is experimental.,7--4--2H-CHROMEN-2-ONE is a solid.,False
19228,,,,,N-(2-AMINOETHYL)-P-CHLOROBENZAMIDE is experimental.,N-(2-AMINOETHYL)-P-CHLOROBENZAMIDE is a solid.,False
19229,,,,,(1Z)-4-(4-FLUOROPHENYL)-2-METHYLIDENEBUTAN-1-IMINE is experimental.,(1Z)-4-(4-FLUOROPHENYL)-2-METHYLIDENEBUTAN-1-IMINE is a solid.,False
19230,,,,,4-HYDROXY-N-PROPARGYL-1(R)-AMINOINDAN is experimental.,4-HYDROXY-N-PROPARGYL-1(R)-AMINOINDAN is a solid.,False
19231,,,,,(S)-(+)-2- is experimental.,(S)-(+)-2- is a solid.,False
19232,"Flortaucipir F-18, also known as <sup>18</sup>F-T807 and <sup>18</sup>F-AV-1451, is a small indole molecule synthesized with a radioactive fluorine isotope. It is used as a marker in positron emission tomography (PET) imaging of patients suspected of having Alzheimer's disease. After crossing the blood-brain barrier, flortaucipir F-18 binds to aggregated tau protein, a hallmark of Alzheimer's disease whose incidence correlates well with disease progression. Flortaucipir F-18 is a radioactive agent indicated for positron emission tomography (PET) imaging of aggregated tau neurofibrillary tangles (NFTs) in adult patients under evaluation for Alzheimer's disease. Flortaucipir F-18 is not indicated for use in patients under evaluation for chronic traumatic encephalopathy. Flortaucipir F-18 is a radioactive molecule that binds to and accumulates in tau NFT deposits allowing for imaging detection; however, non-specific binding and other factors allow for the possibility of misdiagnosis. As Flortaucipir F-18 is a radioactive substance, standard precautionary measures for protecting both patients and health care workers are advised. The safety and efficacy of flortaucipir F-18 in patients being evaluated for chronic traumatic encephalopathy are unknown and hence is not recommended. Alzheimer's disease is a progressive neurodegenerative disease characterized by the build-up of hyperphosphorylated tau protein aggregates. Hyperphosphorylated tau forms dimers termed paired helical filaments (PHFs), which aggregate further to form neurofibrillary tangles (NFTs) associated with neurodegeneration and severity of Alzheimer's symptoms.",,,,Flortaucipir F-18 is approved and investigational.,,True
19233,An antidepressive agent and monoamine oxidase inhibitor related to PARGYLINE.,,,,Clorgiline is experimental.,Clorgiline is a solid.,True
19234,"Posizolid (AZD2563) is an oxazolidinone antibiotic. In July 2002, after completion of phase I trials in December 2001, AstraZeneca announced that they were no longer pursuing the development of Posizolid, presumably due to negative trial results (though no results were reported). For the treatment of gram-positive infections, including multiresistant strains. AZD2563 is an oxazolidinone antibiotic. Oxazolidinones inhibit protein synthesis by binding at the P site at the ribosomal 50S subunit. Resistance to other protein synthesis inhibitors does not affect oxazolidinone activity, however rare development of oxazolidinone resistance cases, associated with 23S rRNA alterations during treatment have been reported. AZD2563 selectively inhibits bacterial protein synthesis through binding to sites on the bacterial ribosome and prevents the formation of a functional 70S-initiation complex. Specifically, AZD2563 binds to a site on the bacterial 23S ribosomal RNA of the 50S subunit and prevents the formation of a functional 70S initiation complex, which is an essential component of the bacterial translation process.",,,,Posizolid is investigational.,Posizolid is a solid.,True
19235,"CX157,3-fluoro-7-(2,2,2,-trifluoroethoxy)phenoxathiin-10,10-dioxide, is a reversible, selective inhibitor of MAO-A designed to have improved oral bioavailability and reduced clearance compared to previous MAO-A inhibitors of this class. Anxiety Disorders I, This drug increases the levels of three vital neurotransmitters that affect mood and anxiety: serotonin, norepinephrine and dopamine.",,,,CX157 is investigational.,CX157 is a solid.,True
19236,,,,,Decyl(dimethyl)phosphine oxide is experimental.,Decyl(dimethyl)phosphine oxide is a solid.,False
19237,,,,,Harmine is experimental.,Harmine is a solid.,False
19238,,,,,Brofaromine is experimental.,Brofaromine is a solid.,False
19239,,,,,"N-Alpha-Acetyl-3,5-Diiodotyrosylglycine is experimental.","N-Alpha-Acetyl-3,5-Diiodotyrosylglycine is a solid.",False
19240,,,,,"N-alpha-Acetyl-3,5-diiodotyrosyl-D-threonine is experimental.","N-alpha-Acetyl-3,5-diiodotyrosyl-D-threonine is a solid.",False
19241,,,,,2--Heptanoic Acid -Amide is experimental.,2--Heptanoic Acid -Amide is a solid.,False
19242,,,,,Bb-3497 is experimental.,Bb-3497 is a solid.,False
19243,,,,,Dioxo(sulfanyl)molybdenum is experimental.,Dioxo(sulfanyl)molybdenum is a solid.,False
19244,,,,,Niraxostat is experimental.,Niraxostat is a solid.,False
19245,"Febuxostat is a xanathine oxidase (XO) inhibitor indicated in patients with gout suffering from hyperuricemia and is used in its chronic management. Febuxostat is not recommended for the treatment of asymptomatic hyperuricemia. Febuxostat is marketed under the trade name Uloric by Takeda Pharmaceuticals America, Inc., and was approved by the FDA in February 2009. For the treatment of hyperuricemia in patients with gout. Febuxostat (ULORIC) is a novel, xanthine oxidase/dehydrogenase (XO/XDH) inhibitor being developed by Teijin, TAP Pharmaceuticals, and Ipsen for the treatment of gout. The currently available XO inhibitor, allopurinol, has been associated with serious instances of severe hypersensitivity, in some cases leading to fatalities. There is some suggestion that febuxostat is less prone to excacerbate systemic inflammatory events in animal studies. Febuxostat, a xanthine oxidase inhibitor, achieves its therapeutic effect by decreasing serum uric acid. Febuxostat is not expected to inhibit other enzymes involved in purine and pyrimidine synthesis and metabolism at therapeutic concentrations.",The molecular weight is 316.38.,Febuxostat has a topological polar surface area of 83.21.,The log p value of  is 4.1.,Febuxostat is approved.,Febuxostat is a solid.,True
19246,"Oxypurinol, an inhibitor of xanthine oxidase, is a metabolite of allopurinol. Intended for the treatment of congestive heart failure and hyperuricemia. Oxypurinol inhibits the enzyme xanthine oxidase, blocking the conversion of the oxypurines hypoxanthine and xanthine to uric acid. Elevated concentrations of oxypurine and oxypurine inhibition of xanthine oxidase through negative feedback results in a decrease in the concentrations of uric acid in the blood and urine. Oxypurinol also facilitates the incorporation of hypoxanthine and xanthine into DNA and RNA, resulting in further reductions of serum uric acid concentrations.",,,,Oxypurinol is investigational.,Oxypurinol is a solid.,True
19247,"FibroGen completed the phase I single-dose, dose escalation studies as of July 2007. Multiple dose, dose escalation and phase II US studies are listed as ongoing. In clinical development for the treatment of anemia of chronic inflammatory disease. FG-4592 represents one of several next generation PHI that has been optimized for multiple pharmacokinetic and pharmacodynamic parameters related to erythropoiesis, including selective inhibition of HIF prolyl and asparaginyl hydroxylases, potency, iron utilization, and ADME. FG-4592 represents one of several next generation HIF-PH inhibitors designed to selectively induce the expression of genes that mediate erythropoiesis for the treatment of anemia. FG-4592 is an orally active second generation HIF-PH inhibitor. Preclinical studies show that FG-4592 increases production of endogenous erythropoietin (EPO), increases iron mobilization and utilization, and overcomes the suppressive effects of inflammation on red blood cell production.",,,,Roxadustat is investigational.,Roxadustat is a solid.,True
19248,,,,,(2S)-2-({6--9-isopropyl-9H-purin-2-yl}amino)-3-methyl-1-butanol is experimental.,(2S)-2-({6--9-isopropyl-9H-purin-2-yl}amino)-3-methyl-1-butanol is a solid.,False
19249,,,,,Fisetin is experimental.,Fisetin is a solid.,False
19250,"A potent inhibitor of adenosine deaminase. The drug is effective in the treatment of many lymphoproliferative malignancies, particularly hairy-cell leukemia. It is also synergistic with some other antineoplastic agents and has immunosuppressive activity. For the treatment of hairy cell leukaemia refractory to alpha interferon. Pentostatin is an antineoplastic anti-metabolite used in the treatment of several forms of leukemia including acute nonlymphocytic leukemia and hairy cell leukemia. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA. They prevent these substances becoming incorporated in to DNA during the \S\"" phase (of the cell cycle), stopping normal development and division. It is a 6-thiopurine analogue of the naturally occurring purine bases hypoxanthine and guanine. Intracellular activation results in incorporation into DNA as a false purine base. An additional cytotoxic effect is related to its incorporation into RNA. Cytotoxicity is cell cycle phase-specific (S-phase)."" Pentostatin is a potent transition state inhibitor of adenosine deaminase (ADA), the greatest activity of which is found in cells of the lymphoid system. T-cells have higher ADA activity than B-cells, and T-cell malignancies have higher activity than B-cell malignancies. The cytotoxicity that results from prevention of catabolism of adenosine or deoxyadenosine is thought to be due to elevated intracellular levels of dATP, which can block DNA synthesis through inhibition of ribonucleotide reductase. Intracellular activation results in incorporation into DNA as a false purine base. An additional cytotoxic effect is related to its incorporation into RNA. Cytotoxicity is cell cycle phase-specific (S-phase).",The molecular weight is 268.27.,Pentostatin has a topological polar surface area of 112.13.,The log p value of  is -1.96.,Pentostatin is approved and investigational.,Pentostatin is a solid.,True
19251,,,,,FR221647 is experimental.,FR221647 is a solid.,False
19252,,,,,"7,8-dihydroinosine is experimental.","7,8-dihydroinosine is a solid.",False
19253,,,,,FR117016 is experimental.,FR117016 is a solid.,False
19254,,,,,FR236913 is experimental.,FR236913 is a solid.,False
19255,,,,,"6-hydroxy-1,6-dihydro purine nucleoside is experimental.","6-hydroxy-1,6-dihydro purine nucleoside is a solid.",False
19256,,,,,FR-234938 is experimental.,FR-234938 is a solid.,False
19257,,,,,FR239087 is experimental.,FR239087 is a solid.,False
19258,,,,,FR230513 is experimental.,FR230513 is a solid.,False
19259,,,,,1-Deaza-Adenosine is experimental.,1-Deaza-Adenosine is a solid.,False
19260,,,,,Nebularine is experimental.,Nebularine is a solid.,False
19261,,,,,"(2S,3R)-3-(6-amino-9H-purin-9-yl)nonan-2-ol is experimental.","(2S,3R)-3-(6-amino-9H-purin-9-yl)nonan-2-ol is a solid.",False
19262,,,,,1-((1R)-1-(HYDROXYMETHYL)-3-{6--1H-INDOL-1-YL}PROPYL)-1H-IMIDAZOLE-4-CARBOXAMIDE is experimental.,1-((1R)-1-(HYDROXYMETHYL)-3-{6--1H-INDOL-1-YL}PROPYL)-1H-IMIDAZOLE-4-CARBOXAMIDE is a solid.,False
19263,,,,,"1-{(1R,2S)-2-HYDROXY-1-PROPYL}-1H-IMIDAZONE-4-CARBOXAMIDE is experimental.","1-{(1R,2S)-2-HYDROXY-1-PROPYL}-1H-IMIDAZONE-4-CARBOXAMIDE is a solid.",False
19264,,,,,"1-((1R,2S)-1-{2-ETHYL}-2-HYDROXYPROPYL)-1H-IMIDAZOLE-4-CARBOXAMIDE is experimental.","1-((1R,2S)-1-{2-ETHYL}-2-HYDROXYPROPYL)-1H-IMIDAZOLE-4-CARBOXAMIDE is a solid.",False
19265,,,,,N-GLYCINE is experimental.,N-GLYCINE is a solid.,False
19266,A orally active prolyl-hydroxylase inhibitor which can stabilize hypoxia-inducible transcription factor independent of oxygen availability.  Investigated for use/treatment in anemia and kidney disease.,,,,FG-2216 is investigational.,FG-2216 is a solid.,True
19267,Saredutant (SR 48968) is a neurokinin-2 antagonist drug being developed as an antidepressant and anxiolytic by Sanofi-Aventis. Investigated for use/treatment in depression and anxiety disorders. Saredutant works by blocking the effects of Neurokinin A at the NK-2 receptor.,,,,Saredutant is investigational.,Saredutant is a solid.,True
19268,"Contulakin-G is a broad spectrum non-opioid analgesic. It is the synthetic form of a natural peptide extracted from the venom of the Conus Geographus sea snail. Investigated for use/treatment in pain (acute or chronic). CGX-1160 operates by activating the G-protein-coupled neurotensin NTR1 receptor (Prialt(R) inhibits the unrelated ion channel, n-type calcium channel), is a linear and smaller peptide, and has a significantly superior safety profile and therapeutic index than Prialt(R).",,,,Contulakin-G is investigational.,Contulakin-G is a solid.,True
19269,Sparfosic acid is a solid. This compound belongs to the n-acyl-alpha amino acids. These are compounds containing an alpha amino acid which bears an acyl group at the terminal nitrogen atom. This substance is known to target aspartate carbamoyltransferase catalytic chain and CAD protein.,,,,Sparfosic acid is experimental.,Sparfosic acid is a solid.,True
19270,"An amino acid analogue and antibiotic derived from the bacterium Streptomyces alanosinicus with antimetabolite and potential antineoplastic activities. Investigated for use/treatment in brain cancer and cancer/tumors (unspecified). L-alanosine inhibits adenylosuccinate synthetase, which converts inosine monophospate (IMP) into adenylosuccinate, an intermediate in purine metabolism. L-alanosine-induced disruption of de novo purine biosynthesis is potentiated by methylthioadenosine phosphorylase (MTAP) deficiency.",,,,Alanosine is investigational.,Alanosine is a solid.,True
19271,,,,,Hadacidin is experimental.,Hadacidin is a solid.,False
19272,,,,,6-O-Phosphoryl Inosine Monophosphate is experimental.,6-O-Phosphoryl Inosine Monophosphate is a solid.,False
19273,,,,,Adenylosuccinic acid is experimental.,Adenylosuccinic acid is a solid.,False
19274,Ethylmercurithiosalicylic acid is a topical antiseptic used on skin and mucous membranes. It is also used as a preservative in pharmaceuticals.,,,,Ethylmercurithiosalicylic acid is experimental.,Ethylmercurithiosalicylic acid is a solid.,True
19275,,,,,6-(Hydroxyethyldithio)-8-(Aminomethylthio)Octanoic Acid is experimental.,6-(Hydroxyethyldithio)-8-(Aminomethylthio)Octanoic Acid is a solid.,False
19276,,,,,"2,6,8-Trimethyl-3-Amino-9-Benzyl-9-Methoxynonanoic Acid is experimental.","2,6,8-Trimethyl-3-Amino-9-Benzyl-9-Methoxynonanoic Acid is a solid.",False
19277,,,,,"(2S,3S,4E,6E,8S,9S)-3-amino-9-methoxy-2,6,8-trimethyl-10-phenyldeca-4,6-dienoic acid is experimental.","(2S,3S,4E,6E,8S,9S)-3-amino-9-methoxy-2,6,8-trimethyl-10-phenyldeca-4,6-dienoic acid is a solid.",False
19278,"Encenicline has been investigated for the treatment of Cognition, Schizophrenia, Alzheimer's Disease, Cardiac Repolarization, and Central Nervous System Diseases. Encenicline, a selective, orally active, alpha 7 Nicotinic Acetylcholine Receptor agonist (alpha 7 NAchR agonist). Encenicline may have a similar mechanism of action to GTS-21. Auditory sensory gating, a biological measurement of the ability to suppress the evoked response to the second of two auditory stimuli, is diminished in people with schizophrenia. Deficits in sensory gating are associated with attentional impairment, and may contribute to cognitive symptoms and perceptual disturbances. This inhibitory process, which involves the alpha(7) nicotinic receptor mediated release of gamma-aminobutyric acid (GABA) by hippocampal interneurons, represents a potential new target for therapeutic intervention in schizophrenia. ",,,,Encenicline is investigational.,,True
19279,"Gamma hydroxybutyric acid, commonly abbreviated GHB, is a therapeutic drug which is illegal in multiple countries. It is currently regulated in the US and sold by Jazz Pharmaceuticals under the name Xyrem. However, it is important to note that GHB is a designated Orphan drug (in 1985). Today Xyrem is a Schedule III drug; however GHB remains a Schedule I drug and the illicit use of Xyrem falls under penalties of Schedule I. GHB is a naturally occurring substance found in the central nervous system, wine, beef, small citrus fruits and almost all other living creatures in small amounts. It is used illegally under the street names Juice, Liquid Ecstasy or simply G, either as an intoxicant, or as a date rape drug. Xyrem is a central nervous system depressant that reduces excessive daytime sleepiness and cataplexy in patients with narcolepsy. Used as a general anesthetic, to treat conditions such as insomnia, clinical depression, narcolepsy, and alcoholism, and to improve athletic performance.  GHB predominantly works at two distinct binding sites in the central nervous system: it works as an agonist at the newly-characterized excitatory GHB receptor, while acting as a weak agonist at the inhibitory GABAB receptor. Since it is a naturally occurring substance, its physiological action is similar to that of some endogenous neurotransmitters in mammalian brain. GHB is probably synthesized from GABA in GABAergic neurons, and released when the neurons fire. GHB is present at much higher concentrations in the brain, where it activates GABA-B receptors to exert its sedative effects. With high affinity, GHB binds to excitatory GHB receptors that are densely expressed throughout the brain, including the cotex and hippocampus. There is some evidence in research that upon activation of GHB receptors in some brain areas, the excitatory neurotransmitter glutamate is released. GHB stimulates dopamin release at low concentrations by acting on the GHB receptor, and the release of dopamine occurs in a biphasic manner. At higher concentrations, GHB inhibits dopamine release by acting on the GABA-B receptors, which is followed by GHB receptor signaling and increased release of dopamine. This explains the paradoxical mix of sedative and stimulatory properties of GHB, as well as the so-called \rebound\"" effect, experienced by individuals using GHB as a sleeping agent, wherein they awake suddenly after several hours of GHB-induced deep sleep. It is proposed that overtime, the level of GHB in the brain decreases below the threshold for significant GABA-B receptor activation, leading to preferential activation of GHB receptor over GABA-B receptors and enhanced wakefulness. """,,,,gamma-Hydroxybutyric acid is approved and illicit and investigational.,gamma-Hydroxybutyric acid is a solid.,True
19280,,,,,"(3AR,6R,6AS)-6-((S)-((S)-CYCLOHEX-2-ENYL)(HYDROXY)METHYL)-6A-METHYL-4-OXO-HEXAHYDRO-2H-FUROPYRROLE-6-CARBALDEHYDE is experimental.","(3AR,6R,6AS)-6-((S)-((S)-CYCLOHEX-2-ENYL)(HYDROXY)METHYL)-6A-METHYL-4-OXO-HEXAHYDRO-2H-FUROPYRROLE-6-CARBALDEHYDE is a solid.",False
19281,"Carfilzomib is an injectable antineoplastic agent (IV only). Chemically, it is a modified tetrapeptidyl epoxide and an analog of epoxomicin. It is also a selective proteasome inhibitor. FDA approved on July 20, 2012. Carfilzomib is indicated for the treatment of patients with multiple myeloma who have received at least two prior therapies including bortezomib and an immunomodulatory agent and have demonstrated disease progression on or within 60 days of completion of the last therapy. Approval is based on response rate.  Intravenous carfilzomib administration resulted in suppression of proteasome chymotrypsin-like activity when measured in blood 1 hour after the first dose. On Day 1 of Cycle 1, proteasome inhibition in peripheral blood mononuclear cells (PBMCs) ranged from 79% to 89% at 15 mg/m2, and from 82% to 83% at 20 mg/m2. In addition, carfilzomib administration resulted in inhibition of the LMP2 and MECL1 subunits of the immunoproteasome ranging from 26% to 32% and 41% to 49%, respectively, at 20 mg/m2. Proteasome inhibition was maintained for ≥ 48 hours following the first dose of carfilzomib for each week of dosing. Resistance against carfilzomib has been observed and although the mechanism has not been confirmed, it is thought that up-regulation of P-glycoprotein may be a contributing factor. Furthermore, studies suggest that carfilzomib is more potent than bortezomib.  Carfilzomib is made up of four modified peptides and acts as a proteasome inhibitor. Carfilzomib irreversibly and selectively binds to N-terminal threonine-containing active sites of the 20S proteasome, the proteolytic core particle within the 26S proteasome. This 20S core has 3 catalytic active sites: the chymotrypsin, trypsin, and caspase-like sites. Inhibition of the chymotrypsin-like site by carfilzomib (β5 and β5i subunits) is the most effective target in decreasing cellular proliferation, ultimately resulting in cell cycle arrest and apoptosis of cancerous cells. At higher doses, carfilzomib will inhibit the trypsin-and capase-like sites. ",The molecular weight is 719.92.,Carfilzomib has a topological polar surface area of 158.47.,The log p value of  is 6.4.,Carfilzomib is approved and investigational.,Carfilzomib is a solid.,True
19282,"Pracinostat is a novel HDAC inhibitor with improved in vivo properties compared to other HDAC inhibitors currently in clinical trials, allowing oral dosing. Data demonstrate that Pracinostat is a potent and effective anti-tumor drug with potential as an oral therapy for a variety of human hematological and solid tumors. For the treatment of various forms of cancer. SB939 is a novel compound with superior pharmaceutical, metabolic and pharmacokinetic properties. SB939 has demonstrated excellent in vivo anti-tumour activity in various animal models with dose proportional pharmacodynamic effects. The pharmacokinetics and pharmacodynamic attributes of SB939 explain and differentiate it as the best in class HDAC inhibitor. Inhibition of HDAC activity allows for the accumulation of acetyl groups on the histone lysine residues resulting in an open chromatin structure and transcriptional activation. In vitro, SB939 causes the accumulation of acetylated histones and induces cell cycle arrest and/or apoptosis of some transformed cells. The mechanism of the antineoplastic effect of SB939 has not been fully characterized.",,,,Pracinostat is investigational.,Pracinostat is a solid.,True
19283,"Mocetinostat has been used in trials studying the treatment of Lymphoma, Urothelial Carcinoma, Relapsed and Refractory, Myelodysplastic Syndrome, and Metastatic Leiomyosarcoma, among others. All HDAC inhibitors induce histone H3 hyperacetylation, correlating with inhibition of proliferation, induction of cell differentiation and apoptosis. Mocetinostat is a novel isotypic-selective inhibitor of the enzyme histone deacetylase (HDAC). HDAC inhibitors act by turning on tumour suppressor genes that have been inappropriately turned off. Tumour suppressor genes are a natural defense against cancer. It is therefore hypothesized that specifically inhibiting those HDACs involved in cancer with Mocetinostat may restore normal cell function and reduce or inhibit tumour growth.",,,,Mocetinostat is investigational.,,True
19284,"Abexinostat has been used in trials studying the treatment of Sarcoma, Lymphoma, Leukemia, Lymphocytic, and Hodgkin Disease, among others. It is a novel, broad-spectrum hydroxamic acid-based inhibitor of histone deacetylase (HDAC) with potential antineoplastic activity. Abexinostat is a novel histone deacetylase (HDAC) inhibitor. HDAC inhibitors target HDAC enzymes and inhibit the proliferation of cancer cells and induce cancer cell death, or apoptosis. Histone deacetylation is carried out by a family of related HDAC enzymes. Inhibition of these enzymes causes changes to chromatin structure and to gene expression patterns, which results in the inhibition of proliferation of cancer cells, and induction of apoptosis.",,,,Abexinostat is investigational.,,True
19285,"Telcagepant has been investigated for the treatment of Migraine. It is an antagonist of the receptor for calcitonin gene-related peptide (CGRP), a primary neuropeptide involved in the pathophysiology of migraine. CGRP and its receptors are found in areas of the central and peripheral nervous system that are important for the transmission of migraine pain. During migraine attacks, CGRP activates these receptors and facilitates the transmission of pain impulses. Telcagepant blocks the binding of CGRP to receptors within the areas of the central and peripheral nervous system that are important for the transmission of migraine pain and thereby is believed to inhibit the transmission of pain signals that lead to migraine headaches.",,,,Telcagepant is investigational.,,True
19286,"Eptinezumab is a fully-humanized IgG1 antibody manufactured using yeast (_Pichia pastoris_) and developed by Lundbeck Seattle Biopharmaceuticals. Eptinezumab has been specifically designed to bind to both alpha and beta forms of the human calcitonin gene-related peptide (CGRP). It was approved by the FDA in February 2020 for the preventive treatment of migraine headaches in adults. Eptinezumab is indicated for the preventive treatment of migraine in adults. Eptinezumab is experimentally administered as an intravenous infusion and/or subcutaneous injection. During Phase 3 clinical trials, it was noted that patients with episodic migraine who on average had 8.6 days of migraine per month demonstrated significant reductions in migraine frequency over weeks 1-12, associated with the 300mg dose arm. Additionally, 29.7% of patients achieved a 75% or greater reduction in migraine days from baseline, compared to 16.2% for placebo (p<0.0007). Moreover, a post hoc analysis revealed that those patients achieving a 75% or greater response rate had over an eight-fold increase in days between migraines. Eptinezumab is a fully-humanized IgG1 antibody manufactured and designed specifically to bind both alpha and beta forms of the human calcitonin gene-related peptide (CGRP).",,,,Eptinezumab is approved and investigational.,Eptinezumab is a solid.,True
19287,"Fremanezumab is a humanized monoclonal antibody targeted against human calcitonin gene-related peptide (CGRP) for the prevention of migraine headaches. It was developed by Teva Pharmaceuticals USA and approved by the FDA in September 2018. Along with other recently approved anti-CGRP therapies such as , , and the oral CGRP antagonist , fremanezumab represents an important step forward in the treatment and prevention of migraine headaches. Fremanezumab is indicated for the preventative treatment of migraine in adults. Fremanezumab is a subcutaneous injection that targets the calcitonin gene-related peptide (CGRP) ligand, preventing its binding to the CGRP receptor. It possesses a long duration of action requiring only monthly or quarterly administration and appears well-tolerated in clinical trials. Studies dating back to 1985 have demonstrated that CGRP levels increase during acute migraine attacks in migraine-suffering patients but normalize after administration of antimigraine therapy such as. Moreover, research has shown that intravenous administration of CGRP can induce migraine-like attacks in migraine-suffering patients. For these reasons, and despite the fact that their role in migraine headaches has not been entirely elucidated, CGRP and its receptors have become desirable targets for antimigraine therapies. Fremanezumab is a humanized monoclonal antibody directed against endogenous CGRP - it interferes with the activity of CGRP, preventing its downstream effects and ultimately mitigating the development of migraine headaches.",,,,Fremanezumab is approved and investigational.,Fremanezumab is a solid.,True
19288,"LY2951742/galcanezumab is a fully humanized monoclonal antibody against human calcitonin gene-related peptide (CGRP) that is developed by ELi Lilly and Company. This therapy is given as a single subcutaneous injection twice a month and ongoing clinical trials for the agent are for episodic and chronic migraine as well as cluster headaches. Galcanezumab is a humanized monoclonal antibody that is indicated for migraine prophylaxis and treatment of episodic cluster headaches in adults by binding endogenous human calcitonin gene-related peptide (CGRP). Galcanezumab is administered as a subcutaneous injection. During clinical trials, it was noted that galcanezumab therapy resulted in a significant reduction in the mean number of migraine headache days and a good tolerability profile. Additionally, post hoc efficacy analyses showed that 32% in the galcanezumab group versus 18% in the placebo group were complete responders. Finally, the most commonly reported adverse events associated with galcanezumab use are headache, nasopharyngitis, hematuria, dermatitis, diarrhea, toothache, and increased alanine aminotransferase (ALT). Galcanezumab is a fully humanized monoclonal antibody designed and manufactured specifically against calcitonin gene-related peptide (CGRP). It binds avidly to human CGRP, with a binding affinity (Kd) of 31 pM (4.5 ng/mL).",,,,Galcanezumab is approved and investigational.,Galcanezumab is a solid.,True
19289,"Developed by Sanofi-Aventis (formerly Sanofi-Synthelabo), osanetant (SR-142801) is an NK3 receptor antagonist which was under development for the treatment of schizophrenia and other Central Nervous System (CNS) disorders. In a review of its R&D portfolio, the company announced in August 2005 that it would cease any further development of osanetant. This follows an earlier decision to discontinue development of eplivanserin for schizophrenia. Potential therapy for schizophrenia, depression and visceral pain. Osanetant is a neurokinin-3 (NK3) receptor antagonist. Preliminary clinical trials have demonstrated that osanetant is superior to placebo on global assessment of efficacy and measures of positive symptoms in schizophrenia. The mechanism of action of osanetant is uncertain at this point. Various preclinical data indicate that activation of NK3 receptors enhances the release of biogenic amines, including dopamine and serotonin. NK3 receptor antagonists could block NK3-receptor-mediated activation of these systems.",,,,Osanetant is investigational.,Osanetant is a solid.,True
19290,"Talnetant (SB-223,412) is a neurokinin 3 receptor antagonist developed by GlaxoSmithKline, which is being researched for several different functions, primarily for irritable bowel syndrome and as a potential antipsychotic drug for the treatment of schizophrenia. Investigated for use/treatment in schizophrenia and schizoaffective disorders, irritable bowel syndrome (IBS), and chronic obstructive pulmonary disease (COPD).",,,,Talnetant is investigational.,Talnetant is a solid.,True
19291,Pavinetant has been used in trials studying the basic science and treatment of Safety and Schizophrenia.,,,,Pavinetant is investigational.,,True
19292,"AZD3409 is a farnesyl-transferase inhibitor (FAR) indicated for the treatment of solid tumors. Phase I trials were initiated January 2003, and were ongoing as of February 2004. As of February 2007 the development of AZD3409 had been discontinued. For the treatment of solid tumors. AZD3409 is a novel, oral, antitumor agent that acts as a prenyl transferase inhibitor. It has potentially broad antitumor activity both as monotherapy and in combination with other anticancer treatments. AZD3409 is a double pro-drug; its metabolism involves conversion to a thiol-ester intermediate, then, intracellularly, to a thiol-acid active species. Phase I trials were initiated January 2003, and were ongoing as of February 2004. Recent studies have shown that AZD3409 is a potent inhibitor of both prostate epithelial cell proliferation and cellular invasion, without an associated bone marrow cellular toxicity. In preclinical studies, AZD3409 achieves up to 90% inhibition of FTase in tumors at well tolerated doses. In enzyme studies AZD3409 is also known to inhibit GGTase-1.",,,,AZD3409 is investigational.,AZD3409 is a solid.,True
19293,"Tipifarnib (R-115777) is a substance that is being studied in the treatment of acute myeloid leukemia (AML) and other types of cancer. It belongs to the family of drugs called farnesyltransferase inhibitors. It is also called Zarnestra. In June 2005, the FDA issued a Not Approvable Letter for Zarnestra. Investigated for use/treatment in colorectal cancer, leukemia (myeloid), pancreatic cancer, and solid tumors. R115777, a nonpeptidomimetic farnesyl transferase inhibitor, suppresses the growth of human pancreatic adenocarcinoma cell lines. This growth inhibition is associated with modulation in the phosphorylation levels of signal transducers and activators of transcription 3 (STAT3) and extracellular signal-regulated kinases (ERK). The farnesyltransferase inhibitors (FTIs) are a class of experimental cancer drugs that target protein farnesyltransferase with the downstream effect of preventing the proper functioning of the Ras protein, which is commonly abnormally active in cancer. After translation, RAS goes through four steps of modification: isoprenylation, proteolysis, methylation and palmitoylation. Isoprenylation involves the enzyme farnesyltransferase (FTase) transferring a farnesyl group from farnesyl pyrophosphate (FPP) to the pre-RAS protein. Also, a related enzyme geranylgeranyltransferase I (GGTase I) has the ability to transfer a geranylgeranyl group to K and N-RAS. Farnesyl is necessary to attach RAS to the cell membrane. Without attachment to the cell membrane, RAS is not able to transfer signals from membrane receptors (Reuter et al., 2000).",,,,Tipifarnib is investigational.,Tipifarnib is a solid.,True
19294,,,,,2-CHLORO-5-(3-CHLORO-PHENYL)-6--NICOTINONITRILE is experimental.,2-CHLORO-5-(3-CHLORO-PHENYL)-6--NICOTINONITRILE is a solid.,False
19295,,,,,(11S)-8-CHLORO-11--6-PIPERAZIN-1-YL-11H-BENZOCYCLOHEPTAPYRIDINE is experimental.,(11S)-8-CHLORO-11--6-PIPERAZIN-1-YL-11H-BENZOCYCLOHEPTAPYRIDINE is a solid.,False
19296,,,,,-PHOSPHONIC ACID is experimental.,-PHOSPHONIC ACID is a solid.,False
19297,,,,,ALPHA-HYDROXYFARNESYLPHOSPHONIC ACID is experimental.,ALPHA-HYDROXYFARNESYLPHOSPHONIC ACID is a solid.,False
19298,,,,,"(20S)-19,20,21,22-TETRAHYDRO-19-OXO-5H-18,20-ETHANO-12,14-ETHENO-6,10-METHENO-18H-BENZIMIDAZOOXATRIAZA-CYCLOOCTADECOSINE-9-CARBONITRILE is experimental.","(20S)-19,20,21,22-TETRAHYDRO-19-OXO-5H-18,20-ETHANO-12,14-ETHENO-6,10-METHENO-18H-BENZIMIDAZOOXATRIAZA-CYCLOOCTADECOSINE-9-CARBONITRILE is a solid.",False
19299,,,,,"(20S)-19,20,22,23-TETRAHYDRO-19-OXO-5H,21H-18,20-ETHANO-12,14-ETHENO-6,10-METHENOBENZIMIDAZOOXATRIAZACYCLONOADECOSINE-9-CARBONITRILE is experimental.","(20S)-19,20,22,23-TETRAHYDRO-19-OXO-5H,21H-18,20-ETHANO-12,14-ETHENO-6,10-METHENOBENZIMIDAZOOXATRIAZACYCLONOADECOSINE-9-CARBONITRILE is a solid.",False
19300,"Investigated for use/treatment in cancer/tumors (unspecified) and solid tumors. ENMD-1198, a new chemical entity (NCE) based on a modified chemical structure of 2-methoxyestradiol (2ME2), is designed to decrease metabolism while retaining 2ME2's multiple mechanisms of action, including inducing apoptosis, disrupting microtubules, and inhibiting HIF-1 alpha. In preclinical studies, ENMD-1198 has been shown to be an orally active, antimitotic agent that leads to arrest of cell division and apoptosis in tumor cells. It also exerts antiangiogenic activity that further contributes to its overall antitumor effects.",,,,ENMD-1198 is investigational.,ENMD-1198 is a solid.,True
19301,"PX-478 is a small molecule inhibitor of hypoxia inducible factor (HIF)-1 alpha currently in a clinical trial in patients with advanced metastatic cancer and lymphoma. PX-478 was effective in models of both non-small cell lung cancer Investigated for use/treatment in cancer/tumors (unspecified). PX-478 is a novel small molecule compound that inhibits the activity of hypoxia inducible factor (HIF)-1 alpha, a transcription factor that controls the expression of a number of genes important for growth and survival of cancer cells. Genes regulated by HIF-1 alpha contribute to diverse functions including new blood vessel growth (angiogenesis), use of glucose for energy, and protection against apoptosis (programmed cell death). Preclinical data have demonstrated that PX-478 can induce apoptosis in experimental tumor models, as well as the down-regulation of factors which",,,,PX-478 is investigational.,PX-478 is a solid.,True
19302,"Castor oil is a vegetable oil obtained by pressing the seeds of the castor oil plant (_Ricinus communis_ L.) mainly cultivated in India, South America, Africa, and China. Castor oil is a rich source of , which represents up to 90% of the total castor oil content. It also consists up to 4% linoleic, 3% oleic, 1% stearic, and less than 1% linolenic fatty acids. has a hydroxyl group that provides a functional group location for various chemical reactions, making it a favourable substance in industrial applications. Castor oil does not contain ricin, which is a natural poison found in the castor oil plant; the toxic lectin remains in the bean pulp following oil isolation. Due to its renewability and high versatility in addition to being the only commercial source of a hydroxylated fatty acid , castor oil has been used as a vital raw material for the chemical industry. Castor oil was mainly used in the manufacturing of soaps, lubricants, and coatings. It is an FDA-approved food additive directly added to food products for human consumption. It can also be found in hard candies as a release agent and anti-sticking agent, or supplementary vitamins and mineral oral tablets as an ingredient for protective coatings. Castor oil is found in over-the-counter oral liquids as a stimulant laxative, and is also added in commercial cosmetic, hair, and skincare products. Indicated for over-the-counter use as a laxative for oral use and as a soothing agent for topical use on skin and hair.  Castor oil is a potent laxative that was shown to be effective for short-term constipation. In a prospective study, the group receiving oral castor oil was associated with a higher likelihood of initiation of labour compared to the placebo group. Castor oil is known to induce diarrhea, and has been used in studies to assess anti-diarrheal effect of some compounds.  Castor oil is a mix of triglycerides consisting of mainly ricinolein, linoleic acid, oleic acid, palmitic acid, stearic acid, dihydroxystearic acid, and traces of other fatty acids. The main pharmacodynamic effects of castor oil are mediated by ricinoleic acid, a hydroxylated fatty acid released from castor oil by intestinal lipases. It was believed that ricinoleic acid acts as an anionic surfactant that reduces net absorption of fluid and electrolytes, and stimulates intestinal peristalsis. However, a recent study suggests that ricinoleic acid interacts with EP3 prostanoid receptors expressed on intestinal and uterine smooth muscles. Via activating EP3 prostanoid receptors on intestinal and uterine smooth muscle cells, ricinoleic acid promotes laxation and uterus contraction, respectively. EP3 receptor act as the major prostanoid receptor in the intestine mediating propulsive effects on gut motility, and activation of EP3 receptors has been demonstrated to evoke contraction of uterine smooth muscle. ",,,,Castor oil is approved and investigational and nutraceutical and vet_approved.,Castor oil is a liquid.,True
19303,"Pilaralisib is an orally available small molecule that selectively inhibits the activity of phosphoinositide-3 kinase (PI3K). Pilaralisib has been used in trials studying the treatment of Cancer, Lymphoma, Solid Tumors, Glioblastoma, and Breast Cancer, among others. In preclinical studies, Pilaralisib slowed tumor growth or caused tumor shrinkage in multiple preclinical cancer models, including breast, lung, ovarian, and prostate cancers, and gliomas. Pilaralisib has also been shown to enhance the anti- tumor effects of several chemotherapeutic agents and an inhibitor of epidermal growth factor receptor (EGFR) in preclinical cancer models. Pilaralisib is an orally available small molecule that selectively inhibits the activity of phosphoinositide-3 kinase (PI3K). Activation of PI3K is a frequent event in human tumors, promoting tumor cell growth, survival, and resistance to chemotherapy and radiotherapy. Inactivation of PI3K has been shown to inhibit growth and induce apoptosis (programmed cell death) in tumor cells.",,,,Pilaralisib is investigational.,,True
19304,"DG031, deCODE genetics's lead compound, is being developed for the prevention of myocardial infarction, or heart attack. Investigated for use/treatment in heart disease and myocardial infarction. DG031 is an inhibitor of 5-lipoxygenase activating protein, or FLAP. deCODE has linked variants in the gene encoding FLAP, and the gene encoding leukotriene A4 hydrolase (LTA4H) to risk of heart attack. These variants appear to confer increased risk of heart attack by increasing the production of leukotriene B4 (LTB4), a potent driver of inflammation produced in atherosclerotic plaques. In Phase II trials completed last year, DG031 was shown to be well tolerated at all doses tested and to reduce the production of LTB4 in a dose-dependent manner. Late last year deCODE discovered that the HapK variant of the LTA4H gene, discovered in Iceland and which confers a moderate increase in risk of heart attack in people of predominantly European ancestry, confers a 250% increase in risk of the disease in African Americans. deCODE licensed DG031 from Bayer AG, which developed it originally for the treatment of asthma. In deCODE’s clinical trials and those conducted previously by Bayer, a total of approximately 2000 people have been dosed with DG031. DG031 inhibits the activity of the FLAP, or 5-lipoxygenase activating protein, that modulates the activity of the leukotriene pathway.",,,,DG031 is investigational.,DG031 is a solid.,True
19305,"AM103 is a novel inhibitor of 5-lipoxygenase-activiting protein (FLAP) that has demonstrated potential to treat asthma and cardiovascular disease by preventing the synthesis of LT, which triggers inflammation. It is being developed by Amira. For the treatment of asthma and cardiovascular disease. Results from the Phase I trial show that AM103 is safe and well-tolerated at doses up to 1,000 mg per day with no evidence of significant side effects. Pharmacodynamic data demonstrated a robust and statistically significant reduction of LTB4 and LTE4 in a dose-dependent manner. The exact mechanism of actions is not known, however, AM103 inhibits the 5-lipoxygenase-activiting protein (FLAP). This prevents the synthesis of LT, which normally triggers inflammation.",,,,AM103 is investigational.,AM103 is a solid.,True
19306,"Investigated for use/treatment in inflammatory disorders (unspecified). FLAP (5-Lipoxygenase Activating Protein) is a key component early in the leukotriene pathway, a complex signaling process that exerts control over biological processes, such as inflammation and immunity. Excessive production of leukotrienes exacerbates inflammatory diseases, such as asthma; the FLAP gene has also been linked to a significant increase in the risk of myocardial infarction and stroke. AM803 binds to FLAP, inhibiting the synthesis of leukotrienes that cause inflammation. ",,,,Fiboflapon is investigational.,Fiboflapon is a solid.,True
19307,"Rimiducid is a lipid-permeable tacrolimus analogue and a protein dimerizer. It was designed to overcome limitations of current cellular immunotherapies used for cancer and other blood disorders by enhancing the control of the immune cell activity and function. When administered via chemically-inducible dimerization (CID) technologies, rimiducid binds to switch proteins and dimerizes them, triggering downstream signaling cascade. The combination use of rimiducid with immunotherapies for enhanced therapeutic effectiveness is currently under investigation. Investigated for use/treatment in bone marrow transplant and graft versus host disease. Rimiducis is used to activate inducible caspase-9 produced by a modified gene included in some CAR T-cell therapies. This activation produces rapid induction of apoptosis in activated modified T-cells and resolution of the signs and symptoms of graft versus host disease within 24 hours. Rimiducid binds to a drug binding domain derived from human FK506-binding protein which is present on a modified form of inducible caspase-9. This binding results in dimerization and subsequent activation of caspase-9. This system was designed to function as a \safety switch\"" in CAR T-cell therapy used in hematological cancers. Retroviral vectors used in production of these modified cells preferentially integrate this gene nearby promoters associated with T-cell activation. This results in higher expression of the modified inducible caspase-9 product in activated T-cells. In practice, this allows for specific targeting of these active T-cells by rimiducid which results in a decrease in circulating cell numbers of over 90% in the setting of graft versus host disease. This specificity spares non-alloreactive T-cells and allows for successful reconstitution of the transplanted immune system from these cells. Additionally, these non-alloreactive cells retain their sensitivity to rimiducid.""",,,,Rimiducid is investigational.,Rimiducid is a solid.,True
19308,"Arimoclomol is an experimental drug compound developed by CytRx Corporation, a biopharmaceutical company based in Los Angeles, California. The orally administered drug is intended to treat amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, a neurodegenerative disease with no effective treatment. Investigated for use/treatment in amyotrophic lateral sclerosis (ALS), diabetes mellitus type 2, neurologic disorders, and neuropathy (diabetic). Arimoclomol is designed to stimulate a natural cellular repair pathway by activating compounds called “molecular chaperones.” Arimoclomol uses a unique 'molecular chaperone' co-induction mechanism. The small molecule drug candidate is believed to function by stimulating a normal cellular protein repair pathway through the activation of \molecular chaperones.\"" Since damaged proteins called aggregates are thought to play a role in many diseases, CytRx believes that activation of molecular chaperones could have therapeutic efficacy for a broad range of diseases.""",,,,Arimoclomol is investigational.,Arimoclomol is a solid.,True
19309,"AGRO100 is an oligonucleotide that functions as an aptamer and binds to nucleolin, a protein found intranuclear in all cells, but uniquely expressed on the surface of tumor cells. Such binding leads to internalization of the complex, and a strong anti-proliferative response in the tumor cell. Investigated for use/treatment in cancer/tumors (unspecified), kidney cancer, leukemia (myeloid), and pancreatic cancer. AGRO100, an experimental anticancer drug that recently entered human clinical trials, is a member of a novel class of antiproliferative agents known as G-rich oligonucleotides (GRO), which are non-antisense, guanosine-rich phosphodiester oligodeoxynucleotides that form stable G-quadruplex structures. The biological activity of GROs results from their binding to specific cellular proteins as aptamers. One important target protein of GROs has been previously identified as nucleolin, a multifunctional protein expressed at high levels by cancer cells. AGRO100 also associates with nuclear factor-{kappa}B (NF-{kappa}B) essential modulator (NEMO), which is a regulatory subunit of the inhibitor of {kappa}B (I{kappa}B) kinase (IKK) complex, and also called IKK{gamma}. In the classic NF-{kappa}B pathway, the IKK complex is required for phosphorylation of I{kappa}B{alpha} and subsequent activation of the transcription factor NF-{kappa}B. Research shows that treatment of cancer cells with AGRO100 inhibits IKK activity and reduces phosphorylation of I{kappa}B{alpha} in response to tumor necrosis factor-{alpha} stimulation. It also shows that AGRO100 blocks both tumor necrosis factor-{alpha}-induced and constitutive NF-{kappa}B activity in human cancer cell lines derived from cervical, prostate, breast, and lung carcinomas. In addition, in AGRO100-treated cancer cells, NEMO is coprecipitated by nucleolin, indicating that both proteins are present in the same complex. Studies suggest that abrogation of NF-{kappa}B activity may contribute to the anticancer effects of AGRO100 and that nucleolin may play a previously unknown role in regulating the NF-{kappa}B pathway. ",,,,AGRO100 is investigational.,AGRO100 is a solid.,True
19310,"Tarenflurbil is an investigational drug that was studied in patients with mild Alzheimer's disease. It is a selective amyloid lowering agent (SALA) that reduces levels of the toxic peptide amyloid beta 42 (Aβ42) in cultured human cells and in animal models. Aβ42 is the primary initiator of neurotoxicity and amyloid plaque development in the brains of Alzheimer's disease patients. In June 2008 development of the drug for Alzheimer's disease was discontinued. Tarenflurbil has also been used in trials studying the treatment of Prostate Cancer. Investigated for use/treatment in alzheimer's disease and prostate cancer. MPC-7869 is not an inhibitor of cyclooxygenase enzymes (COX-1 and COX-2). The compound modulates the signal transduction and transcription activation pathways associated with nuclear factor kappaB (NFkappaB), a principle transcription factor in the expression of many molecules involved in cell growth, cell death and inflammation. In addition, MPC-7869 has recently been shown to modulate gamma-secretase and selectively lower levels of Abeta42 peptide in vitro and in vivo, and to reduce amyloid pathology in the brain. MPC-7869 has an excellent safety profile and is very potent in animal models of cancer and Alzheimer's disease. In transgenic mouse studies, MPC-7869 reduced brain amyloid levels and prevented memory loss.",,,,Tarenflurbil is investigational.,Tarenflurbil is a solid.,True
19311,"Denufosol was an inhaled drug used for the treatment of cystic fibrosis (CF), showing various improvements in lung function during a phase III clinical trial. A new drug application (NDA) was filed with the FDA in 2011, however, the second phase III clinical trial showed a lack of improvement in lung function for cystic fibrosis patients taking denufosol. The drug was also evaluated in the treatment of retinal detachment and other diseases of the retina. Denufosol has not gained FDA approval, and clinical trials with this drug have ceased since 2011. For use as an inhaled treatment for cystic fibrosis. Denufosol is designed to enhance the lung's innate mucosal hydration and mucociliary clearance through stimulation of the P2Y2 receptor. The pharmacologic profile of denufosol parallels that of UTP, leading to increased chloride and water secretion, increased cilia beat frequency, and increased mucin release.  Denufosol tetrasodium is a selective P2Y2 agonist designed to enhance the lung's innate mucosal hydration and mucociliary clearance mechanisms by activating an alternative ion channel that acts in the same way as the defective ion channel in moving salt and water to the surface of the airways. Based on pre-clinical and clinical work, denufosol has several pharmacological actions contributing to its mechanism of action: hydration of the airways by stimulating chloride and liquid secretions on the epithelial cell surface; inhibition of epithelial sodium absorption; enhancement of ciliary beat frequency; and stimulation of mucin secretion. This unique mechanism of action represents a differentiated approach relative to other approved CF products and may be important in intervening in the early clinical course of CF lung disease.",,,,Denufosol is investigational.,Denufosol is a solid.,True
19312,"INS316 belongs to the family of drugs called nucleoside triphosphates.It is studied in the diagnosis of lung diseases, including lung cancer. It is selective P2y2 receptor antagonists claimed to be useful as anti-inflammatory agents. Investigated for use/treatment in lung cancer. INS316 helps to bring up a sample of mucus from deep in the lungs and improves the quality of the sample for testing.",,,,INS 316 is investigational.,INS 316 is a solid.,True
19313,"Tigapotide is a synthetic 15-mer peptide that is derived from the natural sequence of amino acids of the prostate secretory protein (PSP94), one of three predominant proteins found in human seminal fluid. For the treatment of late stage Hormone Refractory Prostate Cancer (HRPC) for which no effective therapy currently exists. PCK3145 is a synthetic 15-mer peptide that is derived from the natural sequence of amino acids of the prostate secretory protein (PSP94), one of three predominant proteins found in human seminal fluid. PSP94 expression in the prostate is down regulated in patients with advanced prostate cancer, and believed to be a survival mechanism for the cancer cells. Results from an earlier trial conducted in the U.K. showed PCK3145 to be safe and well tolerated at all doses tested and further suggest that it also plays a role in preventing the metastatic process as measured by its effect on MMP-9 levels, a Gelatinase B enzyme involved in angiogenesis, tumor invasion and metastasis. The mechanism of action and receptor for PCK3145 suggests PCK3145 to be a signal transduction inhibitor with multiple ways (apoptosis, anti-angiogenesis and anti-metastasis) to restrict disease development.",,,,Tigapotide is investigational.,Tigapotide is a liquid.,True
19314,"XL784 is a potent inhibitor of the ADAM-10 metalloprotease enzyme, a target of significant interest because of its important role in blood vessel formation and cell proliferation. XL784 was specifically optimized to be MMP-1 sparing, thus potentially enhancing its safety profile and enabling higher dosing compared with other previously studied metalloprotease inhibitors. Results of single dose Phase I clinical trials of XL784 administered orally to 96 healthy volunteers have demonstrated that XL784 has attractive safety and pharmacokinetic profiles. It is being developed by Exelixis, Inc. For treatment in patients with diabetes who have clinically significant proteinuria. XL784 is a potent inhibitor of the ADAM-10 metalloprotease (MP) enzyme, a target of significant interest because of its important role in blood vessel formation and cell proliferation. XL784 was specifically optimized to spare matrix metalloprotease 1 (MMP1), thus potentially significantly enhancing its safety profile and enabling higher dosing in comparison to other MMP inhibitors. Data from a Phase 1 clinical trial of orally administered XL784 in 70 healthy volunteers showed single doses of the compound to be free of side effects and to have an attractive pharmacokinetic profile. XL784 has been reformulated for chronic administration and has demonstrated dose-proportional absorption, was orally bioavailable and was well tolerated. XL784 is a potent small molecule inhibitor of the ADAM-10 metalloprotease enzyme, which plays a role in blood vessel formation and cell proliferation that can cause renal fibrosis and impairment.",,,,XL784 is investigational.,XL784 is a solid.,True
19315,,,,,"2-tert-butyl-9-fluoro-1,6-dihydrobenzoimidazoisoquinolin-7-one is experimental.","2-tert-butyl-9-fluoro-1,6-dihydrobenzoimidazoisoquinolin-7-one is a solid.",False
19316,"XL019 is a selective inhibitor of the cytoplasmic tyrosine kinase JAK2. An IND for XL019 was filed by Exelixis in May 2007. For the treatment of various forms of cancer. XL019 is a potent and selective JAK2 inhibitor with favorable pharmacodynamic properties and safety profile. XL019 is a selective inhibitor of the cytoplasmic tyrosine kinase JAK2. JAK2 is activated by cytokine and growth factor receptors and phosphorylates members of the STAT family of inducible transcription factors. Activation of the JAK/STAT pathway promotes cell growth and survival, and is a common feature of human tumors. JAK2 is activated by mutation in the majority of patients with polycythemia vera and essential thrombocytosis and appears to drive the inappropriate growth of blood cells in these conditions.",,,,XL019 is investigational.,XL019 is a solid.,True
19317,,,,,5-phenyl-1H-indazol-3-amine is experimental.,5-phenyl-1H-indazol-3-amine is a solid.,False
19318,,,,,4-(3-amino-1H-indazol-5-yl)-N-tert-butylbenzenesulfonamide is experimental.,4-(3-amino-1H-indazol-5-yl)-N-tert-butylbenzenesulfonamide is a solid.,False
19319,,,,,4--1H-PYRAZOL-3-YL}-1H-BENZIMIDAZOL-6-YL)METHYL]MORPHOLIN-4-IUM is experimental.,4--1H-PYRAZOL-3-YL}-1H-BENZIMIDAZOL-6-YL)METHYL]MORPHOLIN-4-IUM is a solid.,False
19320,"Rilapladib is the third genomics-derived small molecule drug arising from the Human Genome Sciences-GlaxoSmithKline collaboration to enter clinical development. It is a lipoprotein-associated phospholipase A2 (Lp-PLA2) inhibitor. Lp-PLA2 is an enzyme associated with the formation of atherosclerotic plaques. Investigated for use/treatment in atherosclerosis and cardiovascular disorders. Rilapladib is a Lp-PLA2 inhibitor. Lp-PLA2 has been found to be enriched in the highly atherogenic lipoprotein subfraction of small dense LDL, which is susceptible to oxidative modification. Moreover, enzyme levels are increased in patients with hyperlipidaemia, stroke, Type 1 and Type 2 diabetes mellitus, as well as in post-menopausal women. As such, plasma Lp-PLA2 levels tend to be elevated in those individuals who are considered to be at risk of developing accelerated atherosclerosis and clinical cardiovascular events. Thus, inhibition of the Lp-PLA2 enzyme would be expected to stop the build up of this fatty streak (by inhibition of the formation of lysophosphatidylcholine), and so be useful in the treatment of atherosclerosis. ",,,,Rilapladib is investigational.,Rilapladib is a solid.,True
19321,,,,,"(1R)-1,2,2-trimethylpropyl (R)-methylphosphinate is experimental.","(1R)-1,2,2-trimethylpropyl (R)-methylphosphinate is a solid.",False
19322,"GMX1777 is a water-soluble prodrug of the cyanoguanidine compound GMX1778 with potential antineoplastic activity. In vivo, apoptosis inducer GMX1777 is rapidly converted into GMX1778 through hydrolytic cleavage of a carbonate ester bond. Although the exact mechanism of action has yet to be fully elucidated, GMX1778 appears to antagonize nuclear factor-kappa B (NF-kB) transcription, resulting in the induction of tumor cell apoptosis. Intended for the treatment of solid tumors and lymphomas. GMX1777 exhibits unusually potent anti-tumor activity in preclinical animal models. The novel mechanism of action of GMX1778 supports the clinical use of GMX1777 as an anti-cancer agent. Moreover, the strong dependency of cancer cells on NAD+ to support DNA repair suggests a strong rationale for the use of GMX1777 in combination with DNA damaging agents for future trials. The cytotoxicity of GMX1777, a prodrug of GMX1778, occurs exclusively through its ability to selectively inhibit nicotinamide phosphoribosyl transferase (NAMPRT). Tumor cells have elevated NAMPRT, an enzyme involved in the biosynthesis of oxidized nicotinamide adenine dinucleotide (NAD+). These cells have a high rate of NAD+ turnover due to elevated glycolysis and high ADP-ribosylation activity required for DNA repair, genome stability and telomere maintenance. These latter characteristics make cancer cells more susceptible to NAMPRT inhibition than normal cells. Although the mechanism of action of GMX1778 was initially believed to include NF-κB inhibition, a transcriptional factor that plays a role in cancer cell survival, NF-κB inhibition occurs as a consequence of ATP loss following NAMPRT inhibition and NAD+ decline.",,,,GMX1777 is investigational.,GMX1777 is a solid.,True
19323,"Daporinad has been used in trials studying the treatment of Melanoma, Cutaneous T-cell Lymphoma, and B-cell Chronic Lymphocytic Leukemia.",,,,Daporinad is investigational.,,True
19324,"Glatiramer acetate consists of the acetate salts of synthetic polypeptides, containing four naturally occurring amino acids: L-glutamic acid, L-alanine, L-tyrosine, and L-lysine with an average molar fraction of 0.141, 0.427, 0.095, and 0.338, respectively. The average molecular weight of glatiramer acetate is 5,000-9,000 daltons. It is an immunomodulator, licensed in much of the world for reduced frequency of relapses in relapsing-remitting multiple sclerosis. For reduction of the frequency of relapses in patients with Relapsing-Remitting Multiple Sclerosis. Glatiramer acetate was originally designed to mimic a protein in myelin, called myelin basic protein, with the intention of inducing EAE (an animal model of MS). Quite to the contrary, it was found to suppress the disease and as a result came to be trialed in human MS. There is some evidence that Glatiramer acetate converts the body's immune response from a Th1 type to a Th2 one, promotes suppressor T cells or acts as an altered peptide ligand. Studies in animals and in vitro systems suggest that upon its administration, glatiramer acetate-specific suppressor T-cells are induced and activated in the periphery. Some fraction of the injected material, either intact or partially hydrolyzed, is presumed to enter the lymphatic circulation, enabling it to reach regional lymph nodes, and some may enter the systemic circulation intact. Glatiramer acetate (GA) exhibits strong and promiscuous binding to MHC molecules (HLA DRB1* variants) and consequent competition with various myelin antigens for their presentation to T cells. A further aspect of its action is potent induction of specific suppressor cells of the T helper 2 (Th2) type that migrate to the brain and lead to in situ bystander suppression. Furthermore, the GA-specific cells in the brain express the anti-inflammatory cytokines IL-10 and transforming growth factor beta, in addition to brain-derived neurotrophic factor, whereas they do not express the inflammatory cytokine IFN-gamma. Recent evidence also suggests that Glatiramer acetate directly inhibits dendritic cells and monocytes - both of which are circulating antigen presenting cells.",,,,Glatiramer is approved and investigational.,Glatiramer is a liquid.,True
19325,,,,,13-Acetylphorbol is experimental.,13-Acetylphorbol is a solid.,False
19326,"Peptide YY (3-36), a synthetic human PYY 3-36, is a compound being evaluated for the treatment of obesity. It reduces appetite and increases satiety in obese patients. Investigated for use/treatment in metabolic disease and obesity. PYY 3-36 acts via the presynaptic Y2 receptor in the ARC. It decreases neuropeptide Y (NPY) release from static hypothalamic explants and thus acts to decrease food intake.",,,,Peptide YY (3-36) is investigational.,Peptide YY (3-36) is a solid.,True
19327,"Obinepitide is a synthetic analogue of two natural human hormones, PYY and Pancreatic Polypeptide, which normally are released during a meal. These hormones are known to play a role in the regulation of food intake and appetite in man as satiety signal from the GI-tract to the CNS. In obinepitide, the properties of both of these hormones have been implanted into a single molecule. Investigated for use/treatment in obesity. TM30338 is a first-in-class compound, which in a single",,,,Obinepitide is investigational.,Obinepitide is a solid.,True
19328,"TM30339 is an analogue of the natural hormone Pancreatic Polypeptide (PP), which is released in connection with meals. TM30339 works through the same receptor as the natural satiety hormone, Pancreatic Polypeptide (PP), but TM30339 has improved properties compared with PP. TM30339 thus imitates a natural mechanism, a satiety signal from the gastrointestinal system involved in the regulation of food intake in humans. TM30339 is developed for the treatment of obesity. Investigated for use/treatment in schizophrenia and schizoaffective disorders. TM30339 works through the Y4 receptor like the natural satiety hormone, Pancreatic Polypeptide, PP, but TM30339 has improved properties over PP. Thus, TM30339 mimics a natural satiety signal from the gastrointestinal tract involved in the regulation of food intake in man. In pre-clinical studies in obese mice, the Y4 receptor selective TM30339 was highly efficacious with respect to long term body weight reduction.",,,,TM30339 is investigational.,TM30339 is a solid.,True
19329,"AER001, an IL4/13 receptor antagonist for severe asthma and eczema currently in Phase 2 studies. Investigated for use/treatment in asthma.",,,,AER001 is investigational.,AER001 is a solid.,True
19330,"Dupilumab is a fully human monoclonal antibody of the immunoglobulin G4 subclass that binds to the interleukin-4 (IL-4) receptor, inhibiting the receptor signaling pathways. As an interleukin-4 receptor alpha antagonist, dupilumab inhibits the signaling of pro-inflammatory cytokines, called interleukins (IL), that induce inflammatory and immunological reactions in several atopic or allergic conditions, such as eczema, allergic reaction, and rhinosinusitis. Dupilumab was generated by recombinant DNA technology in Chinese Hamster Ovary cell suspension culture. Dupilumab indicated, as monotherapy or in combination with topical corticosteroids, for the treatment of patients aged 12 years and older with moderate-to­-severe atopic dermatitis whose disease is not adequately controlled with topical prescription therapies or when those therapies are not advisable. Dupilumab is an recombinant human IgG4 antibody to the IL-4 receptor that works by inhibiting the activation of certain pro-inflammatory cytokines that are implicated in the pathophysiology of several allergic and atopic conditions, including asthma, chronic rhinosinusitis with nasal polyps, and food and environmental allergies. _In vivo_, dupilumab was shown to reduce the levels of type 2 inflammatory biomarkers associated with atopic dermatitis, such as thymus and activation-regulated chemokine (TARC/CCL17), total serum IgE, allergen-specific IgE, and lactate dehydrogenase (LDH). A decrease in the levels of biomarkers of asthma, such as FeNO, eotaxin-3, IgE, periostin, and eotaxin-3 (CCL26) was also observed. Since dupilumab works to suppress the immune response, it is proposed that it may influence the immune response against some infections, such as helminth infections, by inhibiting IL-4/IL-13 signaling. It is advised that infections are appropriately treated until resolved before initiating dupilumab therapy.  Type 2 inflammatory processes in various allergic and atopic conditions, such as asthma and atopic diseases, involve the type 2 helper T-cell (Th2) immunity. Upregulation of this Type 2/Th2 pathway is commonly observed in other inflammatory conditions and the activation of Th2 cells is linked to the production of Th2-associated cytokines, such as interleukin (IL) 4, IL-5, IL-9, and IL-13. IL-4 and IL-13 play a central role in inducing inflammatory conditions such as allergic rhinitis, asthma, and atopic dermatitis, by regulating Type 2 inflammation and immune function. These inflammatory cytokines work by modulating gene expression downstream of receptor signalling, regulating Th2 cell differentiation, and activating inflammatory cells such as mast cells and macrophages. ",,,,Dupilumab is approved and investigational.,,True
19331,"Ecabet is a prescription eye drop for the treatment of dry eye syndrome. Ecabet represents a new class of molecules that increases the quantity and quality of mucin produced by conjunctival goblet cells and corneal epithelia. Mucin is a glycoprotein component of tear film that lubricates while retarding moisture loss from tear evaporation. Ecabet is currently marketed in Japan as an oral agent for treatment of gastric ulcers and gastritis. For the treatment of reflux oesophagitis and peptic ulcer disease. Ecabet reduces the survival of H. pylori in the stomach and inhibits pepsin activity in the gastric juice of experimental animals. Here we have investigated the effects of ecabet on some of the factors involved in the dynamics of the mucosal barrier, i.e. pepsins and mucins. Pepsin, acid and Helicobacter pylori are major factors in the pathophysiology of peptic ulcer disease and reflux oesophagitis. Ecabet also acts as an inhibitor of H. pylori NADPH oxidase as well as urease. Inhibition of these enzymes prevents bacterial adhesion to gastric mucosa.",The molecular weight is 380.5.,Ecabet has a topological polar surface area of 91.67.,The log p value of  is 3.31.,Ecabet is investigational.,Ecabet is a solid.,True
19332,,,,,3'-THIO-THYMIDINE-5'-PHOSPHATE is experimental.,3'-THIO-THYMIDINE-5'-PHOSPHATE is a solid.,False
19333,,,,,"2,5-Anhydroglucitol-1,6-Biphosphate is experimental.","2,5-Anhydroglucitol-1,6-Biphosphate is a solid.",False
19334,,,,,{4--Thiazol-2-Yl}-Methanol is experimental.,{4--Thiazol-2-Yl}-Methanol is a solid.,False
19335,,,,,Mdl-29951 is experimental.,Mdl-29951 is a solid.,False
19336,"MB07803 is a second generation gluconeogenesis inhibitor for the treatment of type 2 diabetes. It is designed to block the metabolic pathway in the liver that is responsible for producing glucose. Investigated for use/treatment in diabetes mellitus type 2. MB07803 is a selective inhibitor of fructose-1, 6-bisphosphatase (FBPase), a regulatory enzyme in the pathway responsible for the production of glucose in the liver, known as the gluconeogenesis pathway. By specifically inhibiting this pathway, liver glucose production should be reduced and blood sugar levels decreased in patients with diabetes, independent of insulin levels and body weight. ",,,,MB-07803 is investigational.,MB-07803 is a solid.,True
19337,"CS-917 is a novel inhibitor of fructose 1,6-bisphphosphatase (FBPase) which is one of the rate-limiting enzymes of gluconeogenesis. Investigated for use/treatment in diabetes mellitus type 2. In type 2 diabetes, the liver produces excessive amounts of glucose through the gluconeogenesis (GNG) pathway and consequently is partly responsible for the elevated glucose levels characteristic of the disease. CS-917 targets the AMP binding site of fructose 1,6-bisphosphatase (FBPase), inhibiting the GNC pathway.",,,,Managlinat dialanetil is investigational.,Managlinat dialanetil is a solid.,True
19338,,,,,"N--2,5-DICHLOROBENZENESULFONAMIDE is experimental.","N--2,5-DICHLOROBENZENESULFONAMIDE is a solid.",False
19339,,,,,"2,5-DICHLORO-N-(5-CHLORO-1,3-BENZOXAZOL-2-YL)BENZENESULFONAMIDE is experimental.","2,5-DICHLORO-N-(5-CHLORO-1,3-BENZOXAZOL-2-YL)BENZENESULFONAMIDE is a solid.",False
19340,,,,,"2,5-DICHLORO-N-BENZENESULFONAMIDE is experimental.","2,5-DICHLORO-N-BENZENESULFONAMIDE is a solid.",False
19341,,,,,4-AMINO-N-BENZENESULFONAMIDE is experimental.,4-AMINO-N-BENZENESULFONAMIDE is a solid.,False
19342,,,,,alpha-Naphthoflavone is experimental.,alpha-Naphthoflavone is a solid.,False
19343,"Idronoxil is a substance that is being studied in the treatment of cancer. It belongs to the family of drugs called signal transduction inhibitors. Intended for the treatment of various forms of cancer. Phenoxodiol inhibits proliferation of many cancer cell lines and induces apoptosis by disrupting FLICE-inhibitory protein, FLIP, expression and by caspase-dependent and -independent degradation of the X-linked inhibitor of apoptosis, XIAP. In addition, phenoxodiol sensitizes drug-resistant tumour cells to anticancer drugs including paclitaxel, carboplatin and gemcitabine. The antiproliferative effects of phenoxodiol are associated with inhibition of plasma membrane electron transport in tumour cell lines and primary immune cells. Results from one study (PMID: 17904534) indicate that plasma membrane electron transport (PMET) may be a primary target for phenoxodiol in tumour cells and in activated T cells.",,,,Idronoxil is investigational.,Idronoxil is a solid.,True
19344,,,,,Metoprine is experimental.,Metoprine is a solid.,False
19345,,,,,SKF-91488 is experimental.,SKF-91488 is a solid.,False
19346,,,,,Harmaline is experimental.,Harmaline is a solid.,False
19347,"Cintredekin besudotox has been developed as a specific tumor-targeting agent, which is administered by positive-pressure convection-enhanced delivery (CED) directly to brain tissue at risk for residual infiltrating glioblastoma multiforme (GBM) after tumor resection. cintredekin besudotox is made from a human protein, Interleukin 13 (IL13), linked to a bacterial toxin, Pseudomonas exotoxin (PE). The IL13 portion binds to receptors on the tumor. Investigated for use/treatment in brain cancer. A recombinant chimeric protein with potent antitumor activity. Cintredekin besudotox is composed of interleukin-13 (IL13), a pleiotropic immunoregulatory cytokine, linked to a mutated form of pseudomonas exotoxin A; this agent targets and kills tumor cells that express the IL13 receptor (IL13R). The IL13 moiety attaches to the IL13R on the tumor cell membrane, facilitating the entry of the exotoxin. The exotoxin moiety induces caspase-mediated apoptosis of tumor cells via a mechanism involving mitochondrial damage; it also catalyzes the transfer of ADP ribose from nicotinamide adenine dinucleotide (NAD) to elongation factor-2 in eukaryotic cells, thereby inactivating elongation factor 2 and inhibiting protein synthesis.",,,,Cintredekin Besudotox is investigational.,Cintredekin Besudotox is a liquid.,True
19348,"Lebrikizumab has been used in trials studying the treatment of Asthma, Allergic Asthma, Atopic Dermatitis, Idiopathic Pulmonary Fibrosis, and COPD, Chronic Obstructive Pulmonary Disease. Anti-IL-13 humanized monoclonal antibody Lebrikizumab binds to and blocks the activity of IL-13, which may result in the inhibition of Hodkin lympoma cell proliferation. IL-13 cytokine, an important mediator in allergic inflammation, may be an autocrine growth factor for Hodgkin lymphoma cells.",,,,Lebrikizumab is investigational.,,True
19349,"Oregovomab is a murine monoclonal antibody that attaches to the tumor-associated antigen CA125. Investigated for use/treatment in ovarian cancer. Oregovomab is well tolerated and induces multiple antigen-specific immune responses, maintained during concomitant chemotherapy. A significant survival benefit has been observed in patients mounting a T-cell response to CA125 and/or autologous tumor. Vaccination with oregovomab may stimulate a host cytotoxic immune response against tumor cells that express CA125. Oregovomab targets the circulating tumour-associated antigen CA 125, which is shed from the surface of human ovarian cancer cells; the antibodies induce broad cellular and humoral immune responses against CA 125 via complex formation. Unlike free CA 125, CA 125-oregovomab complexes can prime dendritic cells, leading to downstream activation of T cells.",,,,Oregovomab is investigational.,Oregovomab is a liquid.,True
19350,"Ecallantide is a potent and selective human plasma kallikrein inhibitor that is indicated for the symptomatic treatment of hereditary angioedema. Ecallantide is a recombinant 60-amino-acid protein produced in _Pichia pastoris_ yeast cells that contains three intramolecular disulfide bonds. It was discovered by phage display technology. It shares sequence similarities with the naturally occurring human protein tissue-factor pathway inhibitor (TFPI), which is also known lipoprotein-associated coagulation inhibitor (LACI). The amino acid sequence of two compounds differ by seven amino acids.  Indicated for the symptomatic treatment of acute attacks of hereditary angioedema (HAE) in patients 12 years of age and older. Intravenous administration of ecallantide doses ≥20 mg/m^2 resulted in prolongation of activated partial thromboplastin time (aPTT) without an indication of bleeding. Ecallantide administration has been associated with instances of arrhythmia. In a clinical trial of patients experiencing acute attacks of hereditary angioedema (HAE), intravenous administration of ecallantide demonstrated a significant improvement in symptoms affecting the oropharynx, abdomen, gastrointestinal tract, and limbs within 4 hours post-administration compared to placebo. A substantial decrease in the severity and duration of attacks was also observed in patients with moderate-to-severe HAE attacks. In clinical trials, ecallantide had no significant effect on the QTc interval, heart rate, or any other components of the ECG. The kallikrein-kinin system is a complex proteolytic cascade that promotes inflammatory and coagulation pathways. Human plasma kallikrein acts as a protease to mediate the conversion of High Molecular Weight (HMW) kininogen to bradykinin, which is a vasoactive mediator that increases vascular permeability and induces localized swelling, inflammation, and pain. The actions of kallikrein is regulated by the major endogenous inhibitor, C1-esterase-inhibitor (C1-INH). C1-INH also functions to regulate the activation of the complement and intrinsic coagulation (contact system pathway) , which also initiates the production of bradykinin. Upon audoactivation via exposure to negatively charged surfaces, factor XII promotes the generation of factor XIIa and kallikrein. C1-INH inhibits both factor XIIa and kallikrein. Kallikrein may in turn reciprocally activate more FXII. Hereditary angioedema is associated with a deficiency of the C1 inhibitor is caused by a mutation in the C1 INH gene. Resulting effect is excessive production of the vasodilator, bradykinin. The actions of bradykinin produce typical edematous signs and symptoms of hereditary angioedema by enhancing vascular and endothelial permeability, leading to increased outflow of plasma into the interstitium to produce local edema. ",The molecular weight is 7053.9.,Ecallantide has a topological polar surface area of 2912.95.,,Ecallantide is approved and investigational.,Ecallantide is a solid.,True
19351,"Lanadelumab, also known as DX-2930, is a human IgG1 monoclonal antibody designed for subcutaneous self-injection. It is a fully human immunoglobulin, k-light-chain made in recombinant Chinese Hamster Ovary cells. The FDA and EU granted the designation of priority review, breakthrough therapy and orphan drug for rare diseases based on the results of the reported clinical trials. Lanadelumab was developed by Shire and FDA approved on August 28, 2018. Lanadelumab is indicated for the prophylaxis treatment to prevent attacks in patients 12 years and older with hereditary angioedema. In phase 1 studies, the level of kininogen, the substrate of kallikrein, was studied as a marker of kallikrein activity. In patients with C1 deficiency, the level of cleaved kininogen is 4-fold higher when compared with C1-normal individuals. When lanadelumab was administered, the levels of cleaved kininogen were significantly reduced with a dose of 300 and 400 mg of lanadelumab with a maximum reduction at day 22 corresponding with time for maximum concentration. This maximum reduction corresponded with the normal levels of cleaved kininogen. Similarly, the decreases of cleaved kininogen corresponded as well with reductions in the levels of the activated factor XII.  Lanadelumab is a plasma kallikrein inhibitor. This enzyme works by cleaving high molecular weight kininogen to generate the pro-inflammatory peptide bradykinin which is a potent vasodilator. The activity of plasma kallikrein is regulated by the activity of C1-inhibitor and thus, the patients that are deficient in C1 are known to be correlated to excessive production of bradykinin which will further lead to fatal angioedema. Hence, lanadelumab occludes the proteolytic active site of plasma kallikrein, preventing the cleavage of kininogen to bradykinin. It is a selective inhibitor as it has been reported that lanadelumab does not bind to prekallikrein or to inhibit any other serine proteases. The activity of lanadelumab works as an additional checkpoint for the patients suffering from C1 deficiency.",,,,Lanadelumab is approved and investigational.,Lanadelumab is a solid.,True
19352,,,,,(R)-3-hydroxytetradecanoic acid is experimental.,(R)-3-hydroxytetradecanoic acid is a solid.,False
19353,Eritoran is a structural analogue of the lipid A portion of lipopolysaccharide (LPS). It is being developed by Eisai Research Institute of Boston for the treatment of severe sepsis. Investigated for use/treatment in sepsis and septicemia. Eritoran has been shown to down-regulate the intracellular generation of pro-inflammatory cytokines IL-6 and TNF-alpha in human monocytes. Eritoran is a toll-like receptor 4 inhibitor.,The molecular weight is 1313.68.,Eritoran has a topological polar surface area of 293.63.,The log p value of  is 17.8.,Eritoran is investigational.,Eritoran is a solid.,True
19354,E5531 is an endotoxin antagonist. Investigated for use/treatment in sepsis and septicemia.,,,,E5531 is investigational.,E5531 is a solid.,True
19355,"Papain, also known as papaya proteinase I, is a cysteine protease (EC 3.4.22.2) enzyme that is found in species of papaya, _Carica papaya_ and _Vasconcellea cundinamarcensis_. The enzyme is found to be localized in the skin of papaya, and is collected from slashed unripe papayas as a crude latex. Papain is used in food, pharmaceutical, textile, and cosmetic industries. While it has been used for the treatment of inflammation and pain via topical administration, papain has also shown to have anthelmintic and tooth-whitening properties. Present in over-the-counter mixture products consisting of different digestive enzymes, its active site contains a catalytic diad that plays a role in breaking peptide bonds. Papain is also used as an ingredient in various enzymatic debriding preparations. No FDA-approved therapeutic indications.  Papain is a digestive enzyme and often acts as a skin allergen.  When topically applied, papain induces an allergen-like inflammatory response via recruiting neutrophils, mast cells, and CD3-positive cells and by induction of a TH2-biased antibody response. _In vitro_, treatment of papain resulted in the breakdown of tight junctions of primary human keratinocytes that maintain the epithelial barrier integrity. These tight junction proteins include zonula occludens-1, claudin-4, and occludin. It is proposed that papain induces allergic responses via activation of TLR4, leading to an increase in neutrophils, CD3+ cells, mast cells, and CCL8-positive cells.",,,,Papain is approved.,Papain is a solid.,True
19356,"Mifamurtide is an immunomodulator with antitumor activity via activation of macrophages and monocytes. Also called L-MTP-PE, mifamurtide may be a liposomal form of of the active ingredient MTP-PE, which is a synthetic, less pyrogenic, and longer-acting derivative of muramyl dipeptide (MDP). MDP is a motif present in all gram-positive and gram-negative bacterial walls that is recognized by different signalling molecules and activators such as nucleotide-binding and oligomerization domain (NOD)-like receptors (NLRs) and toll-like receptors present in macrophages and monocytes. The overall result of MDP recognition leads to the production of proinflammatory cytokines and promotion of bactericidal and tumoricidal effects. As a liposomal formulation, mifamurtide demonstrates an enhanced tumoricidal effect and improved safety profile. Indicated in children, adolescents and young adults for the treatment of high-grade, resectable, non-metastatic osteosarcoma after macroscopically complete surgical resection, typically in combination with post-operative multi-agent chemotherapy. Mifamurtide stimulates the innate immunity by activating monocytes and macrophages. Within hours following administration of mifamurtide in healthy adults or patients with osteosarcoma NOS, elevated plasma levels of proinflammatory molecules, such as TNF-α, IL-6, and IL-1β, and other indicators of immune stimulation like C-reactive protein and neopterine were observed. _In vivo_ administration of mifamurtide in rat and mouse model resulted in inhibition of tumour growth of lung metastasis, skin and liver cancer, and fibrosarcoma. In addition, increased disease-free survival rate was demonstrated when mifamurtide was given as an adjuvant in dog models of osteosarcoma and hemangiosarcoma. Administration of mifamurtide was associated with transient neutropenia, usually when used in conjunction with chemotherapy. Pronounced inflammatory responses are uncommon. It was discovered that tumor necrosis could be promoted by factors released by the host’s immune system (e.g. macrophages) in response to the endotoxins or bacterial products. Mifamurtide is referred to as MTP-PE or L-MTP-PE (in case of the liposomal formulation), which is a fully synthetic derivative of muramyl dipeptide (MDP), which is a motif within the peptidoglycan polymer in the cell wall of bacteria. ",,,,Mifamurtide is approved and experimental.,Mifamurtide is a solid.,True
19357,"VB4-845 is studied in the treatment of certain types of head and neck cancer. VB4-845 is made by linking a monoclonal antibody fragment to a toxic protein that may kill cancer cells. VB4-845 is a fusion protein containing humanized scFv specific for the epithelial cell adhesion molecule, Ep-CAM, a tumor cell-associated target highly expressed on carcinoma cells of epithelial origin and a truncated portion of Pseudomonas exotoxin A. Investigated for use/treatment in bladder cancer and head and neck cancer. VB4-845 binds to EpCAM (a protein on the surface of epithelial cells and some types of cancer cells). Also called anti-EpCAM-Pseudomonas-exotoxin fusion protein and Proxinium. It targets and kills Ep-CAM-positive tumors by apoptosis. ",,,,Oportuzumab monatox is investigational.,Oportuzumab monatox is a solid.,True
19358,"ING-1 is a high-affinity, human engineered trade mark monoclonal antibody that recognizes a 40 kilodalton epithelial cell adhesion molecule (EpCAM) glycoprotein that is expressed in high levels on most adenocarcinomas. It is an attractive target for immunotherapy. Investigated for use/treatment in cancer/tumors (unspecified). ING-1 is XOMA's proprietary anti-tumor Human Engineered(TM) monoclonal antibody with Triton's Targeted Nano-Therapeutics(TM) (TNT(TM)) System. The TNT(TM) System is an innovative product that ablates tumors by using tiny magnetic spheres delivered systemically with antibodies. The tiny spheres within the tumors are induced to heat by a localized externally applied magnetic field. ING-1, a Human Engineered(TM) monoclonal antibody with high affinity to the Ep-CAM antigen is expressed in high concentrations on many adenocarcinoma tumor cells. The combination of the ING-1 antibody with the TNT(TM) System is intended to create a novel, highly selective, safe, and effective treatment for adenocarcinomas, such as breast, colorectal, lung, ovary and prostate",,,,ING-1 is investigational.,ING-1 is a solid.,True
19359,"Hypromellose, or hydroxypropyl methylcellulose (HPMC) , is a semisynthetic, inert, and viscoelastic polymer that forms a colloid solution when dissolved in water. It acts as a thickening agent, coating polymer, bioadhesive, solubility enhancer in solid dispersions, and binder in the process of granulation and in modified release formulations. It is a commonly used as a delivery component in oral pharmaceutical products that provides the release of a drug in a controlled fashion, effectively increasing the duration of release of a drug to prolong its therapeutic effects. Hypromellose is also found in eye drops as a lubricant. Used as an ophthalmic protectant and lubricant, in artificial tears, and as a diagnostic aid (contact lens procedures; gonioscopy). Hypromellose is the most commonly used in hydrophilic matrix fabrication. It allows for controlled release of drug substances, increasing duration of therapeutic effects. The physical characteristics of this drug resemble natural tears, providing lubrication to the ocular surface and maintaining corneal hydration in dry eye syndromes. Promotes corneal wetting by the stabilization and thickening the precorneal tear film and prolonging the tear film breakdown time, which is usually shortened in dry eye conditions. Hypromellose also acts to lubricate and protect the eye.",,,,Hypromellose is approved.,,True
19360,"Afamelanotide is a first-in-class, synthetic, 13-amino acid peptide analogue of the endogenous alpha melanocyte-stimulating hormone (α-MSH). It differs structurally from its endogenous counterpart by only two amino acids - these structural differences improve biological efficacy by imparting a greater affinity for its target and a longer biological half-life. Afamelanotide is currently the only approved drug therapy used in the management of erythropoietic protoporphyria, having received approval in the EU in December 2014 and subsequent FDA approval in October 2019. Despite its relatively recent approval, afamelanotide has been available for use as an orphan drug in both the US and EU since 2008. Afamelanotide is indicated for the prevention of phototoxicity in adult patients with erythropoietic protoporphyria (EPP). Afamelanotide increases the production of eumelanin, an endogenous photoprotective agent, to attenuate UV-induced skin damage in patients with a condition that predisposes them to phototoxicity. It has a relatively long duration of therapeutic effect despite its short half-life due to its ability to increase melanosome density and therefore skin pigmentation. As afamelanotide may darken pre-existing skin pigmentary lesions, patients receiving afamelanotide should undergo a full body skin examination every 6 months to monitor for progression or worsening of any skin abnormalities. Standard sun safety measures should continue to be employed during afamelanotide therapy. Patients with erythropoietic porphyria (EPP) have a deficiency of ferrochelatase (FECH), an enzyme involved in the final step of heme biosynthesis. FECH is required to insert iron into protoporphyrin IX (PPIX) to generate heme, and a deficiency in FECH results in accumulation of PPIX (particularly in the liver and superficial skin vasculature). PPIX molecules are photodynamic - exposure to UV radiation causes these molecules to form reactive oxygen species that lead to subsequent tissue damage.",The molecular weight is 1646.87.,Afamelanotide has a topological polar surface area of 642.98.,The log p value of  is -6.07.,Afamelanotide is approved and investigational.,Afamelanotide is a solid.,True
19361,"CZEN-002 is a novel, non-azole anti-fungal synthetic octapeptide, derived from alpha-Melanocyte-Stimulating Hormone (a-MSH). CZEN-002 modulates inflammatory and immune responses. It has also been shown to kill Candida albicans (C. albicans), a single-celled fungal organism that causes a variety of infections, including vaginitis. This organism can invade tissues and produce fatal infections in individuals with compromised immune systems such as those suffering from HIV/AIDS or undergoing organ or bone transplants. The antimicrobial activity of CZEN-002 is unique in that it does not depend on direct damage to the microbial membrane. It appears that CZEN-002 works on a receptor in yeast that has yet to be identified.  Investigated for use/treatment in candidiasis and vaginitis. CZEN-002 is a novel, non-azole anti-fungal synthetic octapeptide, derived from alpha-Melanocyte-Stimulating Hormone (a-MSH). CZEN-002 modulates inflammatory and immune responses. It has also been shown to kill Candida albicans (C. albicans). The antimicrobial activity of CZEN-002 is unique in that it does not depend on direct damage to the microbial membrane. It appears that CZEN-002 works on a receptor in yeast that has yet to be identified.  The antimicrobial activity of CZEN-002 is unique in that it does not depend on direct damage to the microbial membrane. It appears that CZEN-002 works on a receptor in yeast that has yet to be identified. ",,,,CZEN 002 is investigational.,CZEN 002 is a solid.,True
19362,"GRN163L is a novel anti-cancer drug. It has been characterized preclinically and shown to inhibit telomerase in human tumor cells of many cancer types (including lung, breast, prostate, liver, and early stage of human breast cancer), in both cell culture systems and animal models. Study of this drug shows the its potential utility in the treatment of patients with hematologic and solid tumor malignancies. Investigated for use/treatment in leukemia (lymphoid) and solid tumors. GRN163L has been characterized preclinically and shown to inhibit telomerase in human tumor cells of many cancer types. It targets the template region, or active site, of telomerase. GRN163L does not exhibit antisense activity (binding to messenger RNA), but rather directly bind to the RNA component of telomerase at the active site of the enzyme, thereby acting like a conventional pharmaceutical drug. Inhibiting telomerase activity should result in telomere shortening and therefore cause aging and death of cancer cells. ",,,,Grn163l is investigational.,Grn163l is a solid.,True
19363,"Tertomotide is under investigation in clinical trial NCT01223209 (A Study, Combination, Immunologic Study of LTX-315 as adjunct to tertomotide in Patients Following Curative Surgery for Carcinoma). It is a peptide vaccine that activates the immune system so that it recognizes and kills cancer cells. It is being developed by Pharmexa A/S. Tertomotide is a peptide vaccine that activates the immune system so that it recognises and kills cancer cells. Tertomotide targets an enzyme called telomerase. Telomerase is seldom found in normal cell types but is overexpressed in most cancer cells.",,,,Tertomotide is investigational.,,True
19364,"GTI-2040 is a substance that is being studied as a treatment for cancer. It belongs to the family of drugs called antisense oligonucleotides. Investigated for use/treatment in breast cancer, colorectal cancer, leukemia (myeloid), leukemia (unspecified), myelodysplastic syndrome, prostate cancer, renal cell carcinoma, and solid tumors. GTI-2040 is an antisense drug that specifically targets the R2 component of ribonucleotide reductase, which is required for DNA synthesis and cell proliferation. R2 has also been described as a malignant determinant that is elevated in a wide range of tumors, and through deregulation can cooperate with a variety of cellular cancer causing genes known as oncogenes to enhance tumor growth and metastatic potential.",,,,GTI 2040 is investigational.,GTI 2040 is a solid.,True
19365,,,,,"N-(5-chloro-1,3-benzodioxol-4-yl)-6-methoxy-7-(3-piperidin-1-ylpropoxy)quinazolin-4-amine is experimental.","N-(5-chloro-1,3-benzodioxol-4-yl)-6-methoxy-7-(3-piperidin-1-ylpropoxy)quinazolin-4-amine is a solid.",False
19366,,,,,"N'-(5-CHLORO-1,3-BENZODIOXOL-4-YL)-N-(3,4,5- TRIMETHOXYPHENYL)PYRIMIDINE-2,4-DIAMINE is experimental.","N'-(5-CHLORO-1,3-BENZODIOXOL-4-YL)-N-(3,4,5- TRIMETHOXYPHENYL)PYRIMIDINE-2,4-DIAMINE is a solid.",False
19367,,,,,"N'-(3-CHLORO-4-METHOXY-PHENYL)-N-(3,4,5-TRIMETHOXYPHENYL)-1,3,5-TRIAZINE-2,4-DIAMINE is experimental.","N'-(3-CHLORO-4-METHOXY-PHENYL)-N-(3,4,5-TRIMETHOXYPHENYL)-1,3,5-TRIAZINE-2,4-DIAMINE is a solid.",False
19368,,,,,3-({4-pyrimidin-2-yl}amino)benzenesulfonamide is experimental.,3-({4-pyrimidin-2-yl}amino)benzenesulfonamide is a solid.,False
19369,,,,,"N'-(5-chloro-1,3-benzodioxol-4-yl)-N-(3-methylsulfonylphenyl)pyrimidine-2,4-diamine is experimental.","N'-(5-chloro-1,3-benzodioxol-4-yl)-N-(3-methylsulfonylphenyl)pyrimidine-2,4-diamine is a solid.",False
19370,,,,,N-PYRIMIDIN-2-YL]AMINO]PHENYL]METHANESULFONAMIDE is experimental.,N-PYRIMIDIN-2-YL]AMINO]PHENYL]METHANESULFONAMIDE is a solid.,False
19371,,,,,"N'-(5-CHLORO-1,3-BENZODIOXOL-4-YL)-N-(3-MORPHOLIN-4-YLPHENYL)PYRIMIDINE-2,4-DIAMINE is experimental.","N'-(5-CHLORO-1,3-BENZODIOXOL-4-YL)-N-(3-MORPHOLIN-4-YLPHENYL)PYRIMIDINE-2,4-DIAMINE is a solid.",False
19372,,,,,3-({4-PYRIMIDIN-2-YL}AMINO)BENZAMIDE is experimental.,3-({4-PYRIMIDIN-2-YL}AMINO)BENZAMIDE is a solid.,False
19373,SOT-107 is a drug that is a combination of a protein called transferrin and a poison called diphtheria toxin. This drug treat for a type of brain cancer called a high grade glioma brain tumour. About half of all brain tumours are gliomas.  Investigated for use/treatment in brain cancer. Its mechanism of action involves transferrin-mediated delivery of a modified diphtheria toxin that is capable of selectively killing cancer cells. The agent is administered directly into the glioma using convection enhanced delivery to circumvent the blood-brain barrier and achieve high local concentrations of the drug.,,,,SOT-107 is investigational.,SOT-107 is a solid.,True
19374,,,,,5-Benzylacyclouridine is experimental.,5-Benzylacyclouridine is a solid.,False
19375,"HspE7 is a recombinant chimeric protein composed of the heat shock protein 65 (Hsp65) from _Mycobacterium bovis_, and the human papilloma viral (HPV) protein E7. Hsp65, similar to other members of its family of proteins, elicits a strong immune response and may be used to design vaccines against a number of different cancers. E7 protein is involved in carcinogenesis of anal and cervical tumors, and represents a tumor antigen that may be specifically targeted by lymphocytes. It is being developed by StressGen Biotechnologies Corp. Investigated for use/treatment in anal dysplasia, cervical dysplasia/cancer, genital warts, HIV infection, infectious and parasitic disease (unspecified), pediatric indications, warts, and viral infection. HspE7 works by efficiently delivering the E7 antigen to dendritic cells, which have a natural affinity for Hsp. Dendritic cells are known to be the most potent cells in the body for triggering immune responses. Coupling E7 to Hsp takes advantage of the Hsp receptors that dendritic cells express on their surface to introduce E7, as part of a larger fusion protein, into the dendritic cells. ",,,,Verpasep caltespen is investigational.,Verpasep caltespen is a solid.,True
19376,"PCL-016 or Picolinic acid drug substance is a pyridine carboxylate metabolite of tryptophan. It acts as an anti-infective and immunomodulator and is produced in approximately 25-50 mg quantities by the body on a daily basis through the breakdown of tryptophan. PCL-016 plays a key role in zinc transport. As a therapeutic agent, the molecule works by binding to zinc finger proteins (ZFPs) in a way that changes their structures and disrupts zinc binding, inhibiting function. ZFPs are involved in viral replication and packaging as well as normal cell homeostatic functions. Picolinic acid has been shown to be an anti-viral in vitro and in vivo, and sometimes works in conjunction with other cytokines such as interferon gamma to affect immune responses. Acne vulgaris, herpes and other viral infections therefore pose potential therapeutic targets of PCL-016. Investigated for use/treatment in acne, herpes labialis infections (cold sores), and venereal disease. PCL-016 or Picolinic acid drug substance is a pyridine carboxylate metabolite of tryptophan. It acts as an anti-infective and immunomodulator through its role in zinc transport. ZFPs are involved in viral replication and packaging as well as normal cell homeostatic functions. Picolinic acid has been shown to be an anti-viral in vitro and in vivo. As a therapeutic agent, the molecule works by binding to zinc finger proteins (ZFPs) in a way that changes their structures and disrupts zinc binding, inhibiting function. ",,,,PCL-016 is investigational.,PCL-016 is a solid.,True
19377,"Selective inhibitor of SIRT1 that does not inhibit histone deacetylase (HDAC) or other sirtuin deacetylase family members (IC50 values are 98, 19600, 48700, > 100000 and > 100000 nM for SIRT1, SIRT2, SIRT3, HDAC and NADase respectively). Enhances p53 acetylation in response to DNA damaging agents.",,,,Selisistat is experimental.,Selisistat is a solid.,True
19378,"Cambinol is a beta-naphtol derivative that inhibits NAD-dependant deacetylases to reduce cell survival under stress. This activity is currently being investigated for its use as a cancer treatment. Cambinol inhibits the NAD-dependant deacetylases SIRT1 and SIRT2, members of a protein family known as sirtuins.",,,,Cambinol is experimental.,,True
19379,"Vercirnon is a novel, orally active anti-inflammatory agent that targets a chemokine receptor protein implicated in both Crohn's disease and ulcerative colitis, the two principal forms of IBD. It is under investigation in clinical trial NCT01611805 (Japanese Phase I of GSK1605786). Vercirnon, a small molecule, orally-available drug, is intended to control the inappropriate immune system response underlying IBD by blocking the activity of the CCR9 chemokine receptor. In adults, CCR9 is a highly specific receptor expressed by T cells that migrate selectively to the digestive tract. The trafficking of T cells to the small and large intestine causes persistent inflammation that may result in Crohn's disease or ulcerative colitis - the two principal forms of IBD.",,,,Vercirnon is investigational.,,True
19380,"Ribostamycin is an aminoglycoside antibiotic isolated from _Streptomyces ribosidificus_ listed as one of the World Health Organization's critically important antimicrobials. Aminoglycosides work by binding to the bacterial 30S ribosomal subunit (some work by binding to the 50S subunit), inhibiting the translocation of the peptidyl-tRNA from the A-site to the P-site and also causing misreading of mRNA, leaving the bacterium unable to synthesize proteins vital to its growth. However, their exact mechanism of action is not fully known.",The molecular weight is 454.48.,Ribostamycin has a topological polar surface area of 262.38.,The log p value of  is -5.02.,Ribostamycin is approved and experimental.,Ribostamycin is a solid.,True
19381,"PRLX 93936 is selectively toxic to cancer cells. Investigated for use/treatment in solid tumors. PRLX 93936 shows robust and selective toxicity in a wide variety of tumor cell-lines, and causes complete tumor regression in mouse xenograft models of fibrosarcoma, pancreatic cancer, ovarian cancer, colon cancer, and melanoma. PRLX 93936 appears to inhibit mitochondrial outer membrane protein VDACs (voltage-dependent anion channels) 2 and 3, resulting in an oxidative, non-apoptotic cell death.",,,,PRLX 93936 is investigational.,PRLX 93936 is a solid.,True
19382,"ROX-888 is ROXRO's lead compound which is currently in Phase 3 trials for the treatment of acute pain, including post-operative pain.  Investigated for use/treatment in pain (acute or chronic). ROX-888 is a intranasal formulation of the broadly used injectible analgesic, ketorolac. It has ability to provide effective analgesia in acute medical conditions resulting in moderate-severe pain, without the disabling side effects of opioid analgesics",,,,ROX-888 is investigational.,ROX-888 is a solid.,True
19383,The botanical drug product LLL-3348 is a once-daily oral formulation for treatment of chronic stable plaque type psoriasis. Investigated for use/treatment in psoriasis and psoriatic disorders. LLL-3348 acts by enhancing IL-10.,,,,LLL-3348 is investigational.,LLL-3348 is a solid.,True
19384,N-(carboxycarbonyl)-D-phenylalanine is a solid. This compound belongs to the n-acyl-alpha amino acids. These are compounds containing an alpha amino acid which bears an acyl group at its terminal nitrogen atom. It targets the protein hypoxia-inducible factor 1-alpha inhibitor.,,,,N-(carboxycarbonyl)-D-phenylalanine is experimental.,N-(carboxycarbonyl)-D-phenylalanine is a solid.,True
19385,,,,,(S)-wiskostatin is experimental.,(S)-wiskostatin is a solid.,False
19386,"Pradefovir mesilate (previously known as MB-06886, Hepavir B and remofovir mesylate) is an orally administered small molecule compound that belongs to a novel series of phosphate and phosphonate prodrugs of adefovir. (Hepsera) is an acyclic phosphonate analogue of adenine that is used to treat hepatitis B virus. As adefovir is poorly absorbed and associated with a high level of nephrotoxicity, pradefovir mesilate was designed to specifically target the liver and reduce risks to external tissue, especially the kidneys, while improving results of adefovir. Investigated for use as a prodrug for Hepsera in treating hepatitis (viral, B). Pradefovir is activated through oxidation that is mediated by cytochrome P-450 (CYP) 3A4, which is predominantly expressed in the liver. Accordingly, pradefovir allows Hepsera to be concentrated in the liver, while maintaining lower concentration levels in other tissue. The novel prodrug is an orally administered small molecule compound that belongs to a novel series of phosphate and phosphonate drugs. It is highly stable in both plasma and tissues. Pradefovir is activated through oxidation that is mediated by cytochrome P-450 (CYP) 3A4, which is predominantly expressed in the liver. In this way, it allows for increased Hepsera concentrations selectively in the liver. ",,,,Pradefovir mesylate is investigational.,Pradefovir mesylate is a solid.,True
19387,,,,,"Maltosyl-Alpha (1,4)-D-Gluconhydroximo-1,5-Lactam is experimental.","Maltosyl-Alpha (1,4)-D-Gluconhydroximo-1,5-Lactam is a solid.",False
19388,,,,,"N--4,6-dideoxy-4-aminoglucopyranoside is experimental.","N--4,6-dideoxy-4-aminoglucopyranoside is a solid.",False
19389,,,,,"4-O-(4,6-Dideoxy-4-{Amino}-Beta-D-Lyxo-Hexopyranosyl)-Alpha-D-Erythro-Hexopyranose is experimental.","4-O-(4,6-Dideoxy-4-{Amino}-Beta-D-Lyxo-Hexopyranosyl)-Alpha-D-Erythro-Hexopyranose is a solid.",False
19390,,,,,"4,6-Dideoxy-4-{Amino}-Alpha-D-Lyxo-Hexopyranosyl-(1->4)-Alpha-D-Threo-Hexopyranosyl-(1->6)-Alpha-L-Threo-Hexopyranose is experimental.","4,6-Dideoxy-4-{Amino}-Alpha-D-Lyxo-Hexopyranosyl-(1->4)-Alpha-D-Threo-Hexopyranosyl-(1->6)-Alpha-L-Threo-Hexopyranose is a solid.",False
19391,The pyranose form of D-quinovose with an α-configuration at the anomeric position.,,,,alpha-D-quinovopyranose is experimental.,alpha-D-quinovopyranose is a solid.,True
19392,,,,,"4,6-DIDEOXY-4-{-5,6-DIHYDROXY-3-(HYDROXYMETHYL)CYCLOHEX-2-EN-1-YL]AMINO}HEXOPYRANOSYL-(1->4)HEXOPYRANOSYL-(1->4)HEXOPYRANOSE is experimental.","4,6-DIDEOXY-4-{-5,6-DIHYDROXY-3-(HYDROXYMETHYL)CYCLOHEX-2-EN-1-YL]AMINO}HEXOPYRANOSYL-(1->4)HEXOPYRANOSYL-(1->4)HEXOPYRANOSE is a solid.",False
19393,,,,,(3E)-4-(1-METHYL-1H-INDOL-3-YL)BUT-3-EN-2-ONE is experimental.,(3E)-4-(1-METHYL-1H-INDOL-3-YL)BUT-3-EN-2-ONE is a solid.,False
19394,,,,,N-(3-AMINOPROPYL)-2-NITROBENZENAMINE is experimental.,N-(3-AMINOPROPYL)-2-NITROBENZENAMINE is a solid.,False
19395,,,,,Hydroxy-Phenyl-Acetic Acid 8-Methyl-8-Aza-BicycloOct-3-Yl Ester is experimental.,Hydroxy-Phenyl-Acetic Acid 8-Methyl-8-Aza-BicycloOct-3-Yl Ester is a solid.,False
19396,,,,,4-Piperidino-Piperidine is experimental.,4-Piperidino-Piperidine is a solid.,False
19397,,,,,"(1S,7S,8S,8AR)-1,2,3,7,8,8A-HEXAHYDRO-7-METHYL-8-ETHYL]-1-NAPHTHALENOL is experimental.","(1S,7S,8S,8AR)-1,2,3,7,8,8A-HEXAHYDRO-7-METHYL-8-ETHYL]-1-NAPHTHALENOL is a solid.",False
19398,"CEP-1347 is a semi-synthetic compound shown to protect multiple nerve cell types from a variety of insults leading to programmed cell death (apoptosis) which could improve the survival of dopamine neurons prior to and after transplantation. Investigated for use/treatment in asthma and parkinson's disease. CEP-1347, an orally active molecule, is a selective and potent inhibitor of the stress-activated protein kinase pathway, an intracellular signaling pathway that is an essential component of the stress response leading to neuronal death. In-vitro cell culture systems and in-vivo mouse and non-human primate models of Parkinson's disease have shown that CEP-1347 protects dopamine neurons in the substantia nigra, the area of the brain affected by Parkinson's disease.",,,,CEP-1347 is investigational.,CEP-1347 is a solid.,True
19399,"Elacytarabine is a fatty acid derivative of , an approved cytotoxic cancer drug. Cytarabine has limitations such as minimal uptake in solid tumours and is only used to treat leukaemia. Elacytarabine is designed to overcome this limitation and has shown considerable uptake in solid tumour cells. Elacytarabine is a patented new chemical entity of the nucleoside analog class, with improved biological properties and the potential to treat solid tumours such as non-small cell lung cancer, malignant melanoma and ovarian cancer. Investigated for use/treatment in leukemia (unspecified) and melanoma. CP-4055 is a fatty acid derivative of cytarabine, an approved cytotoxic cancer drug. Cytarabine has limitations such as minimal uptake in solid tumours and is only used to treat leukaemia. CP-4055 is designed to overcome this limitation and has shown considerable uptake in solid tumour cells. CP-4055 is a patented new chemical entity of the nucleoside analog class, with improved biological properties and the potential to treat solid tumours such as non-small cell lung cancer, malignant melanoma and ovarian cancer. CP-4055 is the lipophilic 5'-elaidic acid ester of the deoxycytidine analog cytosine arabinoside (cytarabine; Ara-C) with potential antineoplastic activity. As a prodrug, CP-4055 is converted intracellularly into cytarabine triphosphate by deoxycytidine kinase and subsequently competes with cytidine for incorporation into DNA, thereby inhibiting DNA synthesis. Compared to cytarabine, CP-4055 shows increased cellular uptake and retention, resulting in increased activation by deoxycytidine kinase to cytarabine triphosphate, decreased deamination and deactivation by deoxycytidine deaminase, and increased inhibition of DNA synthesis. This agent also inhibits RNA synthesis, an effect not seen with cytarabine.",,,,Elacytarabine is investigational.,Elacytarabine is a solid.,True
19400,,,,,alpha-L-fucose is experimental.,alpha-L-fucose is a solid.,False
19401,,,,,Biphenylalanine is experimental.,Biphenylalanine is a solid.,False
19402,,,,,3-(10-methyl-9-anthryl)propanoic acid is experimental.,3-(10-methyl-9-anthryl)propanoic acid is a solid.,False
19403,,,,,Etiocholanedione is experimental.,Etiocholanedione is a solid.,False
19404,,,,,3-{AMINO}PROPANOIC ACID is experimental.,3-{AMINO}PROPANOIC ACID is a solid.,False
19405,,,,,TRANS-2-(DIMETHYLPHENYLSILYL)-PIPERIDINE-N-OXIDE is experimental.,TRANS-2-(DIMETHYLPHENYLSILYL)-PIPERIDINE-N-OXIDE is a solid.,False
19406,,,,,Fluorescin is experimental.,Fluorescin is a solid.,False
19407,,,,,N-(P-CYANOPHENYL)-N'-DIPHENYLMETHYL-GUANIDINE-ACETIC ACID is experimental.,N-(P-CYANOPHENYL)-N'-DIPHENYLMETHYL-GUANIDINE-ACETIC ACID is a solid.,False
19408,,,,,N-{-2-PHENYLETHYL}-HYDROXYPHOSPHINYL)OXY]ACETYL}-2-PHENYLETHYLAMINE is experimental.,N-{-2-PHENYLETHYL}-HYDROXYPHOSPHINYL)OXY]ACETYL}-2-PHENYLETHYLAMINE is a solid.,False
19409,,,,,(2-AMINO-3-PHENYL-BICYCLOHEPT-2-YL)-PHENYL-METHANONE is experimental.,(2-AMINO-3-PHENYL-BICYCLOHEPT-2-YL)-PHENYL-METHANONE is a solid.,False
19410,,,,,"(1S,2S,5S)2-(4-GLUTARIDYLBENZYL)-5-PHENYL-1-CYCLOHEXANOL is experimental.","(1S,2S,5S)2-(4-GLUTARIDYLBENZYL)-5-PHENYL-1-CYCLOHEXANOL is a solid.",False
19411,,,,,2-(4-HYDROXY-3-NITROPHENYL)ACETIC ACID is experimental.,2-(4-HYDROXY-3-NITROPHENYL)ACETIC ACID is a solid.,False
19412,,,,,5-(PARA-NITROPHENYL PHOSPHONATE)-PENTANOIC ACID is experimental.,5-(PARA-NITROPHENYL PHOSPHONATE)-PENTANOIC ACID is a solid.,False
19413,,,,,9-(2-carboxyethyl)-10-methylanthracene endoperoxide is experimental.,9-(2-carboxyethyl)-10-methylanthracene endoperoxide is a solid.,False
19414,,,,,N--D-alanine is experimental.,N--D-alanine is a solid.,False
19415,,,,,PARA-NITROPHENYLPHOSPHONOBUTANOYL-GLYCINE is experimental.,PARA-NITROPHENYLPHOSPHONOBUTANOYL-GLYCINE is a solid.,False
19416,,,,,4-NITRO-BENZYLPHOSPHONOBUTANOYL-GLYCINE is experimental.,4-NITRO-BENZYLPHOSPHONOBUTANOYL-GLYCINE is a solid.,False
19417,,,,,PARA-NITROBENZYL GLUTARYL GLYCINIC ACID is experimental.,PARA-NITROBENZYL GLUTARYL GLYCINIC ACID is a solid.,False
19418,,,,,N--L-alanine is experimental.,N--L-alanine is a solid.,False
19419,,,,,6-{4--BUTYRYLAMINO}-HEXANOIC ACID is experimental.,6-{4--BUTYRYLAMINO}-HEXANOIC ACID is a solid.,False
19420,,,,,4-(4-STYRYL-PHENYLCARBAMOYL)-BUTYRIC ACID is experimental.,4-(4-STYRYL-PHENYLCARBAMOYL)-BUTYRIC ACID is a solid.,False
19421,,,,,3-Cyclohexyl-L-alanine is experimental.,3-Cyclohexyl-L-alanine is a solid.,False
19422,"LJP 1082 is a Toleragen that is designed to shut down the B cells that produce antibodies to ß2 GP1. LJP 1082 is undergoing trial for for the treatment of stroke, deep-vein thrombosis and other conditions associated with antibody-mediated thrombosis. Antibody-mediated thrombosis, also called antiphospholipid syndrome (APS), is a blood clotting disorder. Patients with high levels of anticardiolipin antibodies (ACA) have an increased risk of stroke, heart attack, deep vein thrombosis, and recurrent fetal loss. The target of the LJP 1082's clot-promoting antibodies is a small region on a key blood protein called beta 2-glycoprotein I. To date, our scientists have shown that approximately 90% of patients studied with antibody-mediated thrombosis have antibodies that bind to this region. Investigated for use/treatment in autoimmune diseases, strokes, and thrombosis. LJP 1082, a Toleragen that is designed to shut down the B cells that produce antibodies to ß2 GP1. The target of the LJP 1082's clot-promoting antibodies is a small region on a key blood protein called beta 2-glycoprotein I.",,,,LJP 1082 is investigational.,LJP 1082 is a solid.,True
19423,,,,,{pteridin-8-yl]methyl dihydrogenato(2-) phosphate}(dioxo)sulfanylmolybdenum is experimental.,{pteridin-8-yl]methyl dihydrogenato(2-) phosphate}(dioxo)sulfanylmolybdenum is a solid.,False
19424,,,,,Pantothenoylaminoethenethiol is experimental.,Pantothenoylaminoethenethiol is a solid.,False
19425,,,,,Heptaethylene glycol is experimental.,Heptaethylene glycol is a solid.,False
19426,,,,,"2-(2-{2--Ethoxy}-Ethoxy)-Ethoxy]-Ethoxy}-Ethoxy)-Ethanol, Polyethyleneglycol Peg400 is experimental.","2-(2-{2--Ethoxy}-Ethoxy)-Ethoxy]-Ethoxy}-Ethoxy)-Ethanol, Polyethyleneglycol Peg400 is a solid.",False
19427,,,,,"2-ACETAMIDO-2-DEOXY-BETA-D-GLUCOPYRANOSE(BETA1-4)-2-ACETAMIDO-1,6-ANHYDRO-3-O--2-DEOXY-BETA-D-GLUCOPYRANOSE-L-ALANYL-GAMMA-D-GLUTAMYL-MESO-DIAMINOPIMELYL-D-ALANINE is experimental.","2-ACETAMIDO-2-DEOXY-BETA-D-GLUCOPYRANOSE(BETA1-4)-2-ACETAMIDO-1,6-ANHYDRO-3-O--2-DEOXY-BETA-D-GLUCOPYRANOSE-L-ALANYL-GAMMA-D-GLUTAMYL-MESO-DIAMINOPIMELYL-D-ALANINE is a solid.",False
19428,,,,,"7-PYRIDIN-2-YL-N-(3,4,5-TRIMETHOXYPHENYL)-7H-PYRROLOPYRIMIDIN-2-AMINE is experimental.","7-PYRIDIN-2-YL-N-(3,4,5-TRIMETHOXYPHENYL)-7H-PYRROLOPYRIMIDIN-2-AMINE is a solid.",False
19429,,,,,2-({5-CHLORO-2-PYRIMIDIN-4-YL}AMINO)-N-METHYLBENZAMIDE is experimental.,2-({5-CHLORO-2-PYRIMIDIN-4-YL}AMINO)-N-METHYLBENZAMIDE is a solid.,False
19430,,,,,"Adenosine-5'-diphosphate-2',3'-vanadate is experimental.","Adenosine-5'-diphosphate-2',3'-vanadate is a solid.",False
19431,"5'-Adenylic acid, monoanhydride with sulfuric acid. The initial compound formed by the action of ATP sulfurylase on sulfate ions after sulfate uptake. Synonyms: adenosine sulfatophosphate; APS.",,,,Adenosine 5'-phosphosulfate is experimental and investigational.,Adenosine 5'-phosphosulfate is a solid.,True
19432,,,,,2'-Deoxyguanosine-5'-Triphosphate is experimental.,2'-Deoxyguanosine-5'-Triphosphate is a solid.,False
19433,"A naturally occurring amino acid in both eukaryotic and prokaryotic organisms. It is found in tRNAs and in the catalytic site of some enzymes. The genes for glutathione peroxidase and formate dehydrogenase contain the TGA codon, which codes for this amino acid. ",,,,Selenocysteine is experimental.,Selenocysteine is a solid.,True
19434,,,,,"2',3'-Dehydro-2',3'-Deoxy-Thymidine 5'-Diphosphate is experimental.","2',3'-Dehydro-2',3'-Deoxy-Thymidine 5'-Diphosphate is a solid.",False
19435,,,,,Adenosine Phosphonoacetic Acid is experimental.,Adenosine Phosphonoacetic Acid is a solid.,False
19436,,,,,Stavudine triphosphate is experimental.,Stavudine triphosphate is a solid.,False
19437,,,,,Thymidine-5'- Diphosphate is experimental.,Thymidine-5'- Diphosphate is a solid.,False
19438,,,,,2'-Deoxyguanosine-5'-Diphosphate is experimental.,2'-Deoxyguanosine-5'-Diphosphate is a solid.,False
19439,,,,,"2',3'-dideoxy-3'-fluoro-urididine-5'-diphosphate is experimental.","2',3'-dideoxy-3'-fluoro-urididine-5'-diphosphate is a solid.",False
19440,,,,,3'-Deoxy 3'-Amino Adenosine-5'-Diphosphate is experimental.,3'-Deoxy 3'-Amino Adenosine-5'-Diphosphate is a solid.,False
19441,,,,,Zidovudine diphosphate is experimental.,Zidovudine diphosphate is a solid.,False
19442,,,,,6-METHYL-2(PROPANE-1-SULFONYL)-2H-THIENODIAZABORININ-1-OL is experimental.,6-METHYL-2(PROPANE-1-SULFONYL)-2H-THIENODIAZABORININ-1-OL is a solid.,False
19443,,,,,S-palmitoyl-L-cysteine is experimental.,S-palmitoyl-L-cysteine is a solid.,False
19444,,,,,4-Nitrocatechol sulfate is experimental.,4-Nitrocatechol sulfate is a solid.,False
19445,,,,,2-Amino-3-Hydroxy-3-Phosphonooxy-Propionic Acid is experimental.,2-Amino-3-Hydroxy-3-Phosphonooxy-Propionic Acid is a solid.,False
19446,,,,,"2,6-Diamino-Hexanoic Acid Amide is experimental.","2,6-Diamino-Hexanoic Acid Amide is a solid.",False
19447,"A guanido-neuraminic acid that is used to inhibit neuraminidase. For the prevention and treatment of influenza A and B. Zanamivir, an antiviral agent, is a neuraminidase inhibitor indicated for treatment of uncomplicated acute illness due to influenza A and B virus in adults and pediatric patients 7 years and older who have been symptomatic for no more than 2 days. Zanamivir has also been shown to significantly inhibit the human sialidases NEU3 and NEU2 in the micromolar range (Ki 3.7 +/-0.48 and 12.9+/-0.07 microM, respectively), which could account for some of the rare side effects of zanamivir. The proposed mechanism of action of zanamivir is via inhibition of influenza virus neuraminidase with the possibility of alteration of virus particle aggregation and release. By binding and inhibiting the neuraminidase protein, the drug renders the influenza virus unable to escape its host cell and infect others.",The molecular weight is 332.31.,Zanamivir has a topological polar surface area of 198.22.,The log p value of  is -5.56.,Zanamivir is approved and investigational.,Zanamivir is a solid.,True
19448,,,,,"2-deoxy-2,3-dehydro-N-acetylneuraminic acid is experimental.","2-deoxy-2,3-dehydro-N-acetylneuraminic acid is a solid.",False
19449,,,,,"5-ACETAMIDO-5,6-DIHYDRO-4-HYDROXY-6-ISOBUTOXY-4H-PYRAN-2-CARBOXYLIC ACID is experimental.","5-ACETAMIDO-5,6-DIHYDRO-4-HYDROXY-6-ISOBUTOXY-4H-PYRAN-2-CARBOXYLIC ACID is a solid.",False
19450,"A viscous, hygroscopic amino alcohol with an ammoniacal odor. It is widely distributed in biological tissue and is a component of lecithin. It is used as a surfactant, fluorimetric reagent, and to remove CO2 and H2S from natural gas and other gases.",,,,Ethanolamine is experimental.,Ethanolamine is a solid.,True
19451,"MDX-1303 is a fully human antibody against the inhalation anthrax, the most lethal form of illness in humans caused by the Bacillus anthracis bacterium, and targets a protein component of these lethal toxins known as the anthrax protective antigen. Investigated for use/treatment in anthrax exposure and bacterial infection. MDX-1303 targets a protein component of lethal toxins produced by the bacterium known as the anthrax protective antigen. The anthrax protective antigen initiates the onset of the illness by attaching to cells in the infected person, and then facilitates the entry of additional destructive toxins into the cells. MDX-1303 is designed to target anthrax protective antigen and protect the cells from damage by the anthrax toxins.",,,,MDX-1303 is investigational.,MDX-1303 is a solid.,True
19452,,,,,2-(3-GUANIDINOPHENYL)-3-MERCAPTOPROPANOIC ACID is experimental.,2-(3-GUANIDINOPHENYL)-3-MERCAPTOPROPANOIC ACID is a solid.,False
19453,,,,,(2S)-2--3-{(S)-HYDROXYAMINO}PROPYL]PHOSPHORYL}PROPANOIC ACID is experimental.,(2S)-2--3-{(S)-HYDROXYAMINO}PROPYL]PHOSPHORYL}PROPANOIC ACID is a solid.,False
19454,,,,,(2S)-2--3-PROPYL}PHOSPHORYL]PROPANOIC ACID is experimental.,(2S)-2--3-PROPYL}PHOSPHORYL]PROPANOIC ACID is a solid.,False
19455,,,,,BX-528 is experimental.,BX-528 is a solid.,False
19456,,,,,"(5R,6S,8S)-8--6-HYDROXY-5-ISOPROPYL-3-OXO-1-PHENYL-2,7-DIOXA-4-AZA-6-PHOSPHANONAN-9-OIC ACID 6-OXIDE is experimental.","(5R,6S,8S)-8--6-HYDROXY-5-ISOPROPYL-3-OXO-1-PHENYL-2,7-DIOXA-4-AZA-6-PHOSPHANONAN-9-OIC ACID 6-OXIDE is a solid.",False
19457,,,,,(2S)-2-(3-Carbamimidamidophenyl)-3-propanoic acid is experimental.,(2S)-2-(3-Carbamimidamidophenyl)-3-propanoic acid is a solid.,False
19458,,,,,(2S)-2--3-AMINO}-2-METHYLPROPYL](HYDROXY)PHOSPHORYL]PROPANOIC ACID is experimental.,(2S)-2--3-AMINO}-2-METHYLPROPYL](HYDROXY)PHOSPHORYL]PROPANOIC ACID is a solid.,False
19459,,,,,Guanosine-5'-Diphosphate-Rhamnose is experimental.,Guanosine-5'-Diphosphate-Rhamnose is a solid.,False
19460,"ABX-PTH is a fully human monoclonal antibody generated by Abgenix's technology platform. This drug targets and neutralizes the action of parathyroid hormone (PTH) for the treatment of a secondary hyperparathyroidism. Investigated for use/treatment in chronic renal failure and parathyroid disorders. ABX-PTH is being developed for the treatment of secondary hyperparathyroidism (SHPT). SHPT is a chronic disorder that is frequently observed in patients with chronic kidney disease. Preclinical studies demonstrate ABX-PTH to be highly potent in vivo models of SHPT. ABX-PTH takes a novel approach to addressing secondary hyperparathyroidism (SHPT), because it directly lowers serum levels of free parathyroid hormone.",,,,ABX-PTH is investigational.,ABX-PTH is a solid.,True
19461,,,,,3'-Phosphate-Adenosine-5'-Diphosphate is experimental.,3'-Phosphate-Adenosine-5'-Diphosphate is a solid.,False
19462,,,,,Cytidine 3'-monophosphate is experimental.,Cytidine 3'-monophosphate is a solid.,False
19463,,,,,2'-Monophosphoadenosine-5'-Diphosphate is experimental.,2'-Monophosphoadenosine-5'-Diphosphate is a solid.,False
19464,,,,,"2'-deoxycytidine-2'-deoxyadenosine-3',5'-monophosphate is experimental.","2'-deoxycytidine-2'-deoxyadenosine-3',5'-monophosphate is a solid.",False
19465,,,,,3'-Uridinemonophosphate is experimental.,3'-Uridinemonophosphate is a solid.,False
19466,,,,,Arabinouridine 3'-phosphate is experimental.,Arabinouridine 3'-phosphate is a solid.,False
19467,,,,,Cysteine-S-acetamide is experimental.,Cysteine-S-acetamide is a solid.,False
19468,,,,,2'-fluoro-2'-deoxyuridine 3'-monophosphate is experimental.,2'-fluoro-2'-deoxyuridine 3'-monophosphate is a solid.,False
19469,,,,,Adenylate-3'-phosphate--3'-phosphate] is experimental.,Adenylate-3'-phosphate--3'-phosphate] is a solid.,False
19470,,,,,"Deoxycytidylyl-3',5'-guanosine is experimental.","Deoxycytidylyl-3',5'-guanosine is a solid.",False
19471,,,,,Uridylyl-2'-5'-phospho-adenosine is experimental.,Uridylyl-2'-5'-phospho-adenosine is a solid.,False
19472,,,,,"Uridine-2',3'-vanadate is experimental.","Uridine-2',3'-vanadate is a solid.",False
19473,,,,,Purine Riboside-5'-Monophosphate is experimental.,Purine Riboside-5'-Monophosphate is a solid.,False
19474,,,,,2'-cytidylic acid is experimental.,2'-cytidylic acid is a solid.,False
19475,,,,,5-Aminouracil is experimental.,5-Aminouracil is a solid.,False
19476,,,,,Uridylyl-2'-5'-phospho-guanosine is experimental.,Uridylyl-2'-5'-phospho-guanosine is a solid.,False
19477,,,,,5'-deoxy-5'-piperidin-1-ylthymidine is experimental.,5'-deoxy-5'-piperidin-1-ylthymidine is a solid.,False
19478,,,,,"1-(2,5-dideoxy-5-pyrrolidin-1-yl-beta-L-erythro-pentofuranosyl)-5-methylpyrimidine-2,4(1H,3H)-dione is experimental.","1-(2,5-dideoxy-5-pyrrolidin-1-yl-beta-L-erythro-pentofuranosyl)-5-methylpyrimidine-2,4(1H,3H)-dione is a solid.",False
19479,"1-benzylimidazole, an N-imidazole derivative, has been shown to have strong cardiotonic activity.",,,,1-benzylimidazole is experimental.,1-benzylimidazole is a solid.,True
19480,,,,,N-acetylhistamine is experimental.,N-acetylhistamine is a solid.,False
19481,,,,,Glutamine t-butyl ester is experimental.,Glutamine t-butyl ester is a solid.,False
19482,,,,,3-hydroxyglutaric acid is experimental.,3-hydroxyglutaric acid is a solid.,False
19483,,,,,IC261 is experimental.,IC261 is a solid.,False
19484,,,,,N-(2-Aminoethyl)-5-Chloroisoquinoline-8-Sulfonamide is experimental.,N-(2-Aminoethyl)-5-Chloroisoquinoline-8-Sulfonamide is a solid.,False
19485,,,,,"9-HYDROXY-4-PHENYL-6H-PYRROLOCARBAZOLE-1,3-DIONE is experimental.","9-HYDROXY-4-PHENYL-6H-PYRROLOCARBAZOLE-1,3-DIONE is a solid.",False
19486,,,,,"9-HYDROXY-6-(3-HYDROXYPROPYL)-4-(2-METHOXYPHENYL)PYRROLOCARBAZOLE-1,3(2H,6H)-DIONE is experimental.","9-HYDROXY-6-(3-HYDROXYPROPYL)-4-(2-METHOXYPHENYL)PYRROLOCARBAZOLE-1,3(2H,6H)-DIONE is a solid.",False
19487,,,,,N-CARBAZOL-9-YL]FORMAMIDE is experimental.,N-CARBAZOL-9-YL]FORMAMIDE is a solid.,False
19488,,,,,"4-(2-chlorophenyl)-8-(2-hydroxyethyl)-6-methylpyrroloindole-1,3(2H,6H)-dione is experimental.","4-(2-chlorophenyl)-8-(2-hydroxyethyl)-6-methylpyrroloindole-1,3(2H,6H)-dione is a solid.",False
19489,,,,,"3-(9-HYDROXY-1,3-DIOXO-4-PHENYL-2,3-DIHYDROPYRROLOCARBAZOL-6(1H)-YL)PROPANOIC ACID is experimental.","3-(9-HYDROXY-1,3-DIOXO-4-PHENYL-2,3-DIHYDROPYRROLOCARBAZOL-6(1H)-YL)PROPANOIC ACID is a solid.",False
19490,,,,,"8-bromo-4-(2-chlorophenyl)-N-(2-hydroxyethyl)-6-methyl-1,3-dioxo-1,2,3,6-tetrahydropyrroloindole-7-carboxamide is experimental.","8-bromo-4-(2-chlorophenyl)-N-(2-hydroxyethyl)-6-methyl-1,3-dioxo-1,2,3,6-tetrahydropyrroloindole-7-carboxamide is a solid.",False
19491,"MK-1775 has been used in trials studying the treatment of LYMPHOMA, Neoplasms, Ovarian Cancer, Tongue Carcinoma, and Adult Glioblastoma, among others.",,,,MK-1775 is investigational.,,True
19492,,,,,"N,N-DIMETHYL(5-(PYRIDIN-3-YL)FURAN-2-YL)METHANAMINE is experimental.","N,N-DIMETHYL(5-(PYRIDIN-3-YL)FURAN-2-YL)METHANAMINE is a solid.",False
19493,,,,,N-METHYL(5-(PYRIDIN-3-YL)FURAN-2-YL)METHANAMINE is experimental.,N-METHYL(5-(PYRIDIN-3-YL)FURAN-2-YL)METHANAMINE is a solid.,False
19494,,,,,(5-(PYRIDIN-3-YL)FURAN-2-YL)METHANAMINE is experimental.,(5-(PYRIDIN-3-YL)FURAN-2-YL)METHANAMINE is a solid.,False
19495,,,,,"4,4'-DIPYRIDYL DISULFIDE is experimental.","4,4'-DIPYRIDYL DISULFIDE is a solid.",False
19496,,,,,4-amino]-4-methylpentanoyl]amino]butyl-(diaminomethylidene)azanium is experimental.,4-amino]-4-methylpentanoyl]amino]butyl-(diaminomethylidene)azanium is a solid.,False
19497,,,,,N--L-leucyl-N--L-leucinamide is experimental.,N--L-leucyl-N--L-leucinamide is a solid.,False
19498,,,,,(2S)-4-METHYL-2-(3-PHENYLTHIOUREIDO)-N-((3S)-TETRAHYDRO-2-HYDROXY-3-FURANYL)PENTANAMIDE is experimental.,(2S)-4-METHYL-2-(3-PHENYLTHIOUREIDO)-N-((3S)-TETRAHYDRO-2-HYDROXY-3-FURANYL)PENTANAMIDE is a solid.,False
19499,,,,,(2R)-3-{OXY}(HYDROXY)PHOSPHORYL]OXY}-2-PROPYL (9E)-OCTADEC-9-ENOATE is experimental.,(2R)-3-{OXY}(HYDROXY)PHOSPHORYL]OXY}-2-PROPYL (9E)-OCTADEC-9-ENOATE is a solid.,False
19500,,,,,Phosphatidyl ethanol is experimental.,Phosphatidyl ethanol is a solid.,False
19501,,,,,2'-O-Acetyl Adenosine-5-Diphosphoribose is experimental.,2'-O-Acetyl Adenosine-5-Diphosphoribose is a solid.,False
19502,"WF10 is a chlorite-based, immunomodulating drug is developed by Nuvo Research Inc. Certain preclinical evidence and clinical pilot data suggest that WF10 may be effective in treating certain cancers. The Corporation believes the research to-date demonstrates that WF10 acts on macrophages (a type of white blood cell) by modulating the balance between inflammation and phagocytosis, a state in which the body digests foreign, potentially harmful substances. The Corporation has commenced a Phase II clinical trial in an effort to demonstrate the efficacy of WF10 in combination with Xeloda (capecitabine) in the treatment of pancreatic cancer. The trial is being conducted in Germany at the University of Heidelberg and the National Centre for Tumor Diseases. Investigated for use/treatment in acquired immune deficiency syndrome (AIDS) and aids-related infections, cancer/tumors (unspecified), HIV infection, and inflammatory disorders (unspecified). WF 10 is a 1: 10 dilution of tetrachlorodecaoxide (TCDO) formulated for intravenous injection. It was developed by Oxo Chemie in Switzerland as an adjunctive therapy to combination antiretroviral and opportunistic infection prophylaxis regimens in AIDS patients. WF 10 specifically targets macrophages. WF10 potentially modulates disease-related up-regulation of immune responses both in vitro and in vivo. Thus immune response is influenced in a way that inappropriate inflammatory reactions are downregulated.",,,,Tetrachlorodecaoxide is approved and investigational.,Tetrachlorodecaoxide is a solid.,True
19503,"Although leptin is a circulating signal that reduces appetite, in general, obese people have an unusually high circulating concentration of leptin. These people are said to be resistant to the effects of leptin, in much the same way that people with type 2 diabetes are resistant to the effects of insulin. Thus, obesity develops when people take in more energy than they use over a prolonged period of time, and this excess food intake is not driven by hunger signals, occurring in spite of the anti-appetite signals from circulating leptin. The high sustained concentrations of leptin from the enlarged fat stores result in the cells that respond to leptin becoming desensitized. Investigated for use/treatment in lipodystrophy and obesity. It is unknown whether leptin can cross the blood-brain barrier to access receptor neurons, because the blood-brain barrier is somewhat absent in the area of the median eminence, close to where the NPY neurons of the arcuate nucleus are. If it does cross the blood-brain barrier, it is unknown whether this occurs via an active or passive process. It is generally thought that leptin might enter the brain at the choroid plexus, where there is intense expression of a form of leptin receptor molecule that might act as a transport mechanism.",,,,Leptin is investigational.,Leptin is a solid.,True
19504,"Metreleptin, a recombinant analog of the human hormone leptin, is an orphan drug used to treat complications of leptin deficiency in people with congenital or acquired lipodystrophy. Affecting less than 500 people worldwide, lipodystrophy is characterized by a lack of adipose tissue, fat deposition in the muscles and liver, and metabolic complications such as hypertriglyceridemia, insulin resistance, diabetes mellitus, and fatty liver disease. These metabolic abnormalities are often aggravated by excessive food intake, which is further aggravated by leptin deficiency, a protein secreted by adipose tissue. Administration of Metreleptin results in improvement of metabolic symptoms including improvements in insulin resistance, reduced HbA1c and fasting glucose, reduced triglycerides, and reductions in food intake. Metreleptin is produced in E. coli and differs from native human leptin by the addition of a methionine residue at its amino terminus. It is administered as a once daily subcutaneous injection. On Feb. 24, 2014, Metreleptin was approved by the FDA for the treatment of complications of leptin deficiency, in addition to diet, in patients with congenital generalized or acquired generalized lipodystrophy. Metreleptin is marketed under the brand Myalept® by Aegerion Pharmaceuticals, Inc. Metreleptin is indicated as an adjunct to diet as replacement therapy to treat the complications of leptin deficiency in patients with congenital or acquired generalized lipodystrophy. In patients with leptin deficiency, clinical trials demonstrated that exogenous leptin administration results in weight loss, reduction in mean HbA1c and fasting glucose levels, reduced blood insulin, and reduced triglyceride levels leading to improved insulin sensitivity and reductions in food intake.  Metreleptin functions by binding to and activating the human leptin receptor (ObR), which belongs to the Class I cytokine family of receptors that signals through the JAK/STAT transduction pathway.",The molecular weight is 16155.67.,Metreleptin has a topological polar surface area of 6610.67.,,Metreleptin is approved.,Metreleptin is a solid.,True
19505,"C31G is a potent broad spectrum antimicrobial agent, effective against gram positive and gram negative bacteria, yeast and fungi.C31G, vaginal gel is developed by Biosyn Inc. and has commenced enrollment in a phase III pivotal clinical trial for the reduction of sexual transmission of human immunodeficiency virus (HIV). Investigated for use/treatment in contraception, HIV infection, and prevention of stdis. The range of organisms killed by C31G has been extended to include enveloped viruses. Coupled with data indicating a low toxicity for mammalian cells, and a much wider range of anti-microbial activity than Nonoxynol-9, it appears that C31G is an ideal agent for use in decreasing the risk of transmission of organisms associated with STD. C31G is developed as a topical vaginal microbicide with broad-spectrum antibacterial and antiviral properties. C31G which has a high affinity for bacteria, fungi, yeast, and viruses while exhibiting low mammalian cell toxicity. ",,,,C31G is investigational.,C31G is a solid.,True
19506,"APD668 is a novel, highly potent and orally active glucose-dependent insulinotropic receptor (GDIR) agonist intended to more efficiently stimulate insulin release by beta cells in response to elevated blood glucose levels, and to also avoid hypoglycemia.  Investigated for use/treatment in diabetes mellitus type 2. The GDIR mechanism is glucose dependent: in preclinical studies, GDIR agonists only lowered blood glucose when it rose above normal levels, such as after a meal. Therefore, unlike the glucose-insensitive sulfonylureas, Arena's GDIR agonists are not expected to lower normal fasting blood glucose levels or cause hypoglycemia. In addition, GDIR stimulation has been found to increase the levels and activity of intracellular factors thought to be involved in the preservation of beta cells. ",,,,APD668 is investigational.,APD668 is a solid.,True
19507,,,,,N-{4-METHYL-3-PHENYL}-3-(TRIFLUOROMETHYL)BENZAMIDE is experimental.,N-{4-METHYL-3-PHENYL}-3-(TRIFLUOROMETHYL)BENZAMIDE is a solid.,False
19508,,,,,Triethyl phosphate is experimental.,Triethyl phosphate is a solid.,False
19509,AZD 3355 is a reflux inhibitor used for the treatment of Gastroesophageal Reflux Disease. It is developed by AstraZeneca and is currently in phase I/II trials. Investigated for use/treatment in gastroesophageal reflux disease (GERD). AZD3355 is reflux inhibitors which offer a new approach to the treatment of Gastroesophageal reflux disease (GERD) by improving the function of the lower oesophageal sphincter (LOS) through receptors responsible for opening and closing the sphincter.,,,,AZD 3355 is investigational.,AZD 3355 is a solid.,True
19510,,,,,1-(9-ethyl-9H-carbazol-3-yl)-N-methylmethanamine is experimental.,1-(9-ethyl-9H-carbazol-3-yl)-N-methylmethanamine is a solid.,False
19511,"XL844 is investigated for the use and treatment solid tumors. XL844 is a solid. XL844 is a potent inhibitor of the checkpoint kinases CHK1 and CHK2, which induce cell cycle arrest in response to a variety of DNA damaging agents. Known drug targets of XL844 including serine/threonine-protein kinase Chk1 and serine/threonine-protein kinase Chk2. Investigated for use/treatment in cancer/tumors (unspecified) and solid tumors. XL844 is a potent inhibitor of the checkpoint kinases CHK1 and CHK2, which induce cell cycle arrest in response to a variety of DNA damaging agents. Activation of these checkpoints following DNA damage allows for DNA repair and protects tumor cells from the cytotoxic effects of chemo- and radio-therapy. XL844 abrogates these cell cycle blocks and enhances tumor cell killing by a wide variety of chemotherapeutic agents and radiation in in vitro assays. XL844 has good pharmacokinetic properties and oral bioavailability, and in in vivo tumor models increases the efficacy of chemotherapeutic agents without increasing systemic toxicity.",,,,XL844 is investigational.,XL844 is a solid.,True
19512,CHIR-124 is a potent inhibitor of Chk1 that potentiates the cytotoxicity of topoisomerase I poisons in vitro and in vivo.,,,,CHIR-124 is experimental.,CHIR-124 is a solid.,True
19513,,,,,N-{5--1H-PYRROLOPYRIDIN-3-YL}NICOTINAMIDE is experimental.,N-{5--1H-PYRROLOPYRIDIN-3-YL}NICOTINAMIDE is a solid.,False
19514,,,,,3-(5-{METHYL}-1H-INDOL-2-YL)QUINOLIN-2(1H)-ONE is experimental.,3-(5-{METHYL}-1H-INDOL-2-YL)QUINOLIN-2(1H)-ONE is a solid.,False
19515,,,,,"2,2'-{BIS(OXY)}DIACETIC ACID is experimental.","2,2'-{BIS(OXY)}DIACETIC ACID is a solid.",False
19516,,,,,(2S)-1-AMINO-3-PROPAN-2-OL is experimental.,(2S)-1-AMINO-3-PROPAN-2-OL is a solid.,False
19517,,,,,2-(cyclohexylamino)benzoic acid is experimental.,2-(cyclohexylamino)benzoic acid is a solid.,False
19518,,,,,3-(5-{METHYL}-1H-INDOL-2-YL)-1H-INDAZOLE-6-CARBONITRILE is experimental.,3-(5-{METHYL}-1H-INDOL-2-YL)-1H-INDAZOLE-6-CARBONITRILE is a solid.,False
19519,,,,,"(3Z)-6-(4-HYDROXY-3-METHOXYPHENYL)-3-(1H-PYRROL-2-YLMETHYLENE)-1,3-DIHYDRO-2H-INDOL-2-ONE is experimental.","(3Z)-6-(4-HYDROXY-3-METHOXYPHENYL)-3-(1H-PYRROL-2-YLMETHYLENE)-1,3-DIHYDRO-2H-INDOL-2-ONE is a solid.",False
19520,,,,,"5-ETHYL-3-METHYL-1,5-DIHYDRO-4H-PYRAZOLOQUINOLIN-4-ONE is experimental.","5-ETHYL-3-METHYL-1,5-DIHYDRO-4H-PYRAZOLOQUINOLIN-4-ONE is a solid.",False
19521,,,,,"(5-{3--1H-INDAZOL-6-YL}-2H-1,2,3-TRIAZOL-4-YL)METHANOL is experimental.","(5-{3--1H-INDAZOL-6-YL}-2H-1,2,3-TRIAZOL-4-YL)METHANOL is a solid.",False
19522,,,,,1-(5-CHLORO-2-METHOXYPHENYL)-3-{6-PYRAZIN-2-YL}UREA is experimental.,1-(5-CHLORO-2-METHOXYPHENYL)-3-{6-PYRAZIN-2-YL}UREA is a solid.,False
19523,,,,,(3-ENDO)-8-METHYL-8-AZABICYCLOOCT-3-YL 1H-PYRROLOPYRIDINE-3-CARBOXYLATE is experimental.,(3-ENDO)-8-METHYL-8-AZABICYCLOOCT-3-YL 1H-PYRROLOPYRIDINE-3-CARBOXYLATE is a solid.,False
19524,,,,,"18-CHLORO-11,12,13,14-TETRAHYDRO-1H,10H-8,4-(AZENO)-9,15,1,3,6-BENZODIOXATRIAZACYCLOHEPTADECIN-2-ONE is experimental.","18-CHLORO-11,12,13,14-TETRAHYDRO-1H,10H-8,4-(AZENO)-9,15,1,3,6-BENZODIOXATRIAZACYCLOHEPTADECIN-2-ONE is a solid.",False
19525,,,,,"1-(5-CHLORO-2,4-DIMETHOXYPHENYL)-3-(5-CYANOPYRAZIN-2-YL)UREA is experimental.","1-(5-CHLORO-2,4-DIMETHOXYPHENYL)-3-(5-CYANOPYRAZIN-2-YL)UREA is a solid.",False
19526,,,,,"4-(6-{METHYL}-1,4-DIHYDROINDENOPYRAZOL-3-YL)BENZOIC ACID is experimental.","4-(6-{METHYL}-1,4-DIHYDROINDENOPYRAZOL-3-YL)BENZOIC ACID is a solid.",False
19527,,,,,4--2-METHOXYPHENOL is experimental.,4--2-METHOXYPHENOL is a solid.,False
19528,,,,,(2R)-1-PYRIMIDIN-4-YL)AMINO]PROPAN-2-OL is experimental.,(2R)-1-PYRIMIDIN-4-YL)AMINO]PROPAN-2-OL is a solid.,False
19529,,,,,"(2R)-3-{PYRIMIDIN-4-YLIDENE]AMINO}PROPANE-1,2-DIOL is experimental.","(2R)-3-{PYRIMIDIN-4-YLIDENE]AMINO}PROPANE-1,2-DIOL is a solid.",False
19530,,,,,"N-(5,6-DIPHENYLFUROPYRIMIDIN-4-YL)GLYCINE is experimental.","N-(5,6-DIPHENYLFUROPYRIMIDIN-4-YL)GLYCINE is a solid.",False
19531,,,,,"(5,6-DIPHENYL-FUROPYRIMIDIN-4-YLAMINO)-ACETIC is experimental.","(5,6-DIPHENYL-FUROPYRIMIDIN-4-YLAMINO)-ACETIC is a solid.",False
19532,,,,,"3-AMINO-3-BENZYL-BICYCLO-1,6-DIAZANONAN-2-ONE is experimental.","3-AMINO-3-BENZYL-BICYCLO-1,6-DIAZANONAN-2-ONE is a solid.",False
19533,,,,,3-(1H-BENZIMIDAZOL-2-YL)-1H-INDAZOLE is experimental.,3-(1H-BENZIMIDAZOL-2-YL)-1H-INDAZOLE is a solid.,False
19534,,,,,2-PYRIMIDIN-4-YLAMINO]-ETHANOL is experimental.,2-PYRIMIDIN-4-YLAMINO]-ETHANOL is a solid.,False
19535,,,,,2-PYRIMIDIN-4-YL)AMINO]ETHANOL is experimental.,2-PYRIMIDIN-4-YL)AMINO]ETHANOL is a solid.,False
19536,,,,,"REL-(9R,12S)-9,10,11,12-TETRAHYDRO-9,12-EPOXY-1H-DIINDOLOPYRROLOBENZODIAZOCINE-1,3(2H)-DIONE is experimental.","REL-(9R,12S)-9,10,11,12-TETRAHYDRO-9,12-EPOXY-1H-DIINDOLOPYRROLOBENZODIAZOCINE-1,3(2H)-DIONE is a solid.",False
19537,,,,,1-pyridin-4-yl)morpholin-2-yl]methanamine is experimental.,1-pyridin-4-yl)morpholin-2-yl]methanamine is a solid.,False
19538,,,,,"N-(4-OXO-5,6,7,8-TETRAHYDRO-4H-THIAZOLOAZEPIN-2-YL)ACETAMIDE is experimental.","N-(4-OXO-5,6,7,8-TETRAHYDRO-4H-THIAZOLOAZEPIN-2-YL)ACETAMIDE is a solid.",False
19539,,,,,"5,6,7,8-TETRAHYDROBENZOTHIENOPYRIMIDIN-4(3H)-ONE is experimental.","5,6,7,8-TETRAHYDROBENZOTHIENOPYRIMIDIN-4(3H)-ONE is a solid.",False
19540,,,,,(phenyl)methanone is experimental.,(phenyl)methanone is a solid.,False
19541,,,,,2-(methylsulfanyl)-5-(thiophen-2-ylmethyl)-1H-imidazol-4-ol is experimental.,2-(methylsulfanyl)-5-(thiophen-2-ylmethyl)-1H-imidazol-4-ol is a solid.,False
19542,,,,,6-MORPHOLIN-4-YL-9H-PURINE is experimental.,6-MORPHOLIN-4-YL-9H-PURINE is a solid.,False
19543,,,,,1-PYRIDIN-4-YL)MORPHOLIN-2-YL]METHANAMINE is experimental.,1-PYRIDIN-4-YL)MORPHOLIN-2-YL]METHANAMINE is a solid.,False
19544,"Ulimorelin is a novel small molecule ghrelin agonist being developed by Tranzyme Pharma as a first-in-class treatment for both POI and diabetic gastroparesis, serious medical conditions in which motility of the GI tract is severely impaired. Data gathered thus far demonstrate that Ulimorelin induces a dose-dependent increase of gastric emptying that effectively reverses the delay caused by surgically induced postoperative ileus (POI). Treatment levels as low as 30µg/kg have been shown to be effective in stimulating GI transit in this model. Furthermore, Ulimorelin significantly stimulates gastric emptying in naïve rats with 100-fold greater potency than metoclopramide, a compound currently marketed as a prokinetic treatment for gastroparesis. Postoperative ileus (POI) is a major cause of postoperative complications and prolonged hospitalization. Ghrelin, which is the endogenous ligand for the growth hormone secretagogue receptor, has been found to stimulate gastric motility and accelerate gastric emptying. Ulimorelin is a synthetic ghrelin-receptor agonist, and has been shown to improve gastrointestinal transit in rats with POI.",,,,Ulimorelin is investigational.,,True
19545,"TBC3711 is a next-generation endothelin antagonist that is being studied through oral and intravenous formulations by Encysive Pharmaceuticals. Investigated for use/treatment in congestive heart failure, hypertension, and pulmonary hypertension. TBC3711 is a small molecule that blocks the action of endothelin, a potent mediator of blood vessel constriction and growth of smooth muscle in vascular walls. It is a next-generation endothelin A antagonist which possesses high oral bioavailability and is more selective and potent than THELIN(tm) (sitaxsentan sodium) Encysive's oral treatment for pulmonary arterial hypertension. TBC3711 is greater than 100,000-fold selective in the targeting of the endothelin A receptor versus the endothelin B receptor.",,,,TBC-3711 is investigational.,TBC-3711 is a solid.,True
19546,INCB3284 is a CCR2 antagonist for Inflammation-driven Diseases. Investigated for use/treatment in inflammatory disorders (unspecified).,,,,INCB3284 is investigational.,INCB3284 is a solid.,True
19547,"CCX915 is developed by ChemoCentryx which targets the chemokine receptor CCR2 and is in phase 1 of clinical trial for the treatment of Multiple Sclerosis and Neurologic Disorders. The CCR2 receptor is thought to be of central importance to inflammatory diseases, such as multiple sclerosis (MS), Type II diabetes and atherosclerosis. Investigated for use/treatment in multiple sclerosis and neurologic disorders. Mechanism of action indicates that CCX915 selectively inhibits CCR2-mediated migration of inflammatory white blood cells, but do not inhibit migration mediated by other chemokine receptors, even when administered at high concentrations. Based on the high degree of target specificity observed, CCX915 has the potential to avoid the undesirable side effects of traditional immunosuppressive therapies used in MS and other autoimmune disease indications.",,,,CCX915 is investigational.,CCX915 is a solid.,True
19548,"Plozalizumab has been investigated for the treatment of Atherosclerosis. Plozalizumab, a novel humanized monoclonal antibody, specifically targets CCR2 chemokine receptors found on the surface of certain white blood cells including macrophages and monocytes. Preclinical studies suggest that CCR2 plays an important role in the trafficking of monocytes and macrophages to sites of inflammation. The recruitment of macrophages to the arterial wall is believed to be a critical step in the development of atherosclerosis. Preclinical studies suggest that CCR2 plays an important role in the trafficking of monocytes and macrophages to sites of inflammation. The recruitment of macrophages to the arterial wall is believed to be a critical step in the development of atherosclerosis. Plozalizumab targets CCR2 chemokine receptors found on the surface of certain white blood cells including macrophages and monocytes.",,,,Plozalizumab is investigational.,,True
19549,"CAT-213 is a fully human anti-eotaxin monoclonal antibody with potential in the treatment of allergic disorders, has moved into pre-clinical development. It is developed by MedImmune for the treatment of Allergic Rhinitis. Investigated for use/treatment in allergic rhinitis. CAT-213 targets eotaxin, a member of the chemokine family of proteins that acts as messenger molecules between the cells of the immune system. During an allergic response the levels of eotaxin1 are elevated. This attracts eosinophils, a type of white blood cell, into tissues where they can degranulate causing tissue damage that occurs in a variety of allergic disorders.",,,,CAT-213 is investigational.,CAT-213 is a solid.,True
19550,,,,,L-methionine (R)-S-oxide is experimental.,L-methionine (R)-S-oxide is a solid.,False
19551,"An organic amine proton acceptor. It is used in the synthesis of surface-active agents and pharmaceuticals; as an emulsifying agent for cosmetic creams and lotions, mineral oil and paraffin wax emulsions, as a biological buffer, and used as an alkalizer. (From Merck, 11th ed; Martindale, The Extra Pharmacopoeia, 30th ed, p1424) For the prevention and correction of metabolic acidosis.",The molecular weight is 121.14.,Tromethamine has a topological polar surface area of 86.71.,The log p value of  is -0.94.,Tromethamine is approved.,Tromethamine is a solid.,True
19552,"Tetrathiomolybdate is an oral, small-molecule, anticopper agent that is highly specific for lowering the levels of free copper in serum. COPREXA has completed pivotal clinical trials for the treatment of neurologic Wilson's disease. It is also developed for fibrotic disorders based upon the rationale that the fibrotic disease process is dependent upon the availability of free copper in the body. Investigated for use/treatment in liver disease and pulmonary fibrosis. Tetrathiomolybdate demonstrated the ability to reduce toxic free copper levels and substantially improve clinical neurologic outcomes in Wilson’s patients. Studies also showed it is capable of specifically inhibiting chronic fibrotic disease processes in the lung. Tetrathiomolybdate has demonstrated the ability to inhibit fibrosis in a number of well established animal models through the sequestration of available copper and inhibition of key fibrotric cytokines, including secreted protein acid rich in cysteine (SPARC), NFkappaB, TGF-beta, FGF-2, IL-1, IL-6, IL-8, and connective tissue growth factor (CTGF).",,,,Tetrathiomolybdate is investigational.,Tetrathiomolybdate is a solid.,True
19553,"CAD106 is an immunotherapeutic product in development for the treatment of Alzheimer's disease. It is designed to induce antibodies against the beta-amyloid-protein that inhibit the formation of plaques in the brain of Alzheimer's disease patients.  Investigated for use/treatment in alzheimer's disease. CAD106 can block the formation of beta-amyloid plaques in the brain. Since the formation of such plaques is considered a hallmark of the disease, CAD106 may offer the potential to advance the treatment of Alzheimer's disease. CAD106 is designed to induce antibodies against the beta-amyloid-protein that inhibit the formation of",,,,CAD106 is investigational.,CAD106 is a solid.,True
19554,"Mito-4509 is a non-feminizing estrogen analog that could affect mitochondrial metabolic pathways. It is used to treat Parkinson's Disease, Alzheimer's Disease, Retinal Disorders and other neurologic Disorders.  Investigated for use/treatment in alzheimer's disease, neurologic disorders, parkinson's disease, and retinal disorders (unspecified). MITO-4509 is an orally-administered drug candidate that shows neuro-protective activity and reductions in beta-amyloid in animal models of Alzheimer's disease, and is well tolerated in a completed human Phase I trial. In addition to Alzheimer's disease, MITO-4509 shows potential for use in Parkinson's disease, Friedreich's ataxia, retinitis pigmentosa, and mild cognitive impairment (\MCI\"" is often considered a precursor to Alzheimer's disease).""",,,,Mito-4509 is investigational.,Mito-4509 is a solid.,True
19555,"Edonerpic is a neurotrophic agent intended for the treatment of Alzheimer's disease which is under phase I clinical trial. Investigated for use/treatment in alzheimer's disease. T-817MA has neuroprotective properties. Toyama Chemical has demonstrated that T-817MA prevents neurodegeneration induced by Amyloid-b protein. Accumulation of Amyloid-b protein is considered to be central to the pathogenesis of Alzheimer's disease. The neuroprotective properties of T-817MA were also observed in a mutant tau induced Alzheimer's disease model. Besides these neuroprotective properties, T-817MA also promotes neurite outgrowth.",,,,Edonerpic is investigational.,Edonerpic is a solid.,True
19556,"Dimercaprol is a traditional chelating agent developed by British biochemists at Oxford University during World War II. It was developed as an experimental antidote against the arsenic-based poison gas Lewisite. It has been used clinically since 1949 in arsenic, cadmium and mercury poisoning. In addition, it has in the past been used for the treatment of Wilson's disease, a genetic disorder in which the body tends to retain copper. Dimercaprol has toxic potential, and its use may be followed by a variety of adverse effects. For the treatment of arsenic, gold and mercury poisoning. Indicated in acute lead poisoning when used concomitantly with edetate calcium disodium (DB00974). Due to its oily nature, dimercaprol is not absorbed orally and its administration requires a deep intra-muscular injection that is extremely painful and allergenic. It was found to mobilize and relocate lead to the brain, increasing its neurotoxic effects. Despite that fact that dimercaprol increases cadmium excretion, there is an associated increase in kidney cadmium concentration. Because of this, dimercaprol must be avoided in patients with cadmium toxicity. The sulfhydryl groups of dimercaprol form complexes with certain heavy metals thus preventing or reversing the metallic binding of sulfhydryl-containing enzymes. The complex is excreted in the urine.",The molecular weight is 124.22.,Dimercaprol has a topological polar surface area of 20.23.,The log p value of  is 0.18.,Dimercaprol is approved.,Dimercaprol is a solid.,True
19557,"Florbetapir (18F) is a radiopharmaceutical compound containing the radionuclide fluorine-18 bound to the compound florbetapir, a molecule that binds with high affinity to beta amyloid plaque, a peptide that plays a key role in Alzheimer's Disease pathogenesis. Marketed as the product Amyvid, florbetapir 18F is indicated for positron emission tomography (PET) imaging of the brain to estimate β-amyloid neuritic plaque density in adult patients with cognitive impairment who are being evaluated for Alzheimer's Disease (AD) and other causes of cognitive decline.  Florbetapir 18F is indicated for Positron Emission Tomography (PET) imaging of the brain to estimate β-amyloid neuritic plaque density in adult patients with cognitive impairment who are being evaluated for Alzheimer's Disease (AD) and other causes of cognitive decline. Following intravenous injection, florbetapir F 18 diffuses across the human blood-brain barrier and produces a radioactivity signal detectable throughout the brain. Subsequently, cerebral perfusion decreases the brain florbetapir F 18 content, with differential retention of the drug in areas that contain β-amyloid aggregates compared to areas that lack the aggregates. Florbetapir (18F) is a radiopharmaceutical compound containing the radionuclide fluorine-18 bound to the compound florbetapir, a molecule that binds with high affinity to beta amyloid plaque, a peptide that plays a key role in Alzheimer's Disease pathogenesis. The radionucleide fluorine-18 was chosen as it has a half life of 110 minutes allowing it to accumulate sufficiently in the brain before undergoing positon emission decay.",The molecular weight is 359.43.,Florbetapir (18F) has a topological polar surface area of 52.61.,The log p value of  is 3.48.,Florbetapir (18F) is approved and investigational.,Florbetapir (18F) is a solid.,True
19558,"Flutemetamol (18F) is a PET scanning radiopharmaceutical containing the radionuclide fluorine-18. It is indicated for Positron Emission Tomography (PET) imaging of the brain to estimate β amyloid neuritic plaque density in adult patients with cognitive impairment who are being evaluated for Alzheimer's disease (AD) or other causes of cognitive decline. Flutemetamol F18 is indicated for Positron Emission Tomography (PET) imaging of the brain to estimate β amyloid neuritic plaque density in adult patients with cognitive impairment who are being evaluated for Alzheimer's disease (AD) or other causes of cognitive decline.  Following intravenous injection, flutemetamol F 18 diffuses across the human blood-brain barrier and produces a radioactivity signal detectable throughout the brain. Subsequently, cerebral perfusion decreases the brain flutemetamol F 18 content, with differential retention of the drug in cortical areas that contain β-amyloid aggregates compared to areas that lack the aggregates. Fluorine-18 (F 18) is a cyclotron-produced radionuclide that decays by positron emission (β+ decay, 96.7%) and orbital electron capture (3.3%) to stable oxygen-18 with a physical half-life of 109.8 minutes. The positron can undergo annihilation with an electron to produce two gamma rays; the energy of each gamma ray is 511 keV. After flumetamol F18 is given intravenously, it accumulates in beta amyloid plaques in the brain, and thus becomes visible via positron emission tomography (PET).",The molecular weight is 273.32.,Flutemetamol (18F) has a topological polar surface area of 45.15.,The log p value of  is 4.3.,Flutemetamol (18F) is approved and investigational.,Flutemetamol (18F) is a solid.,True
19559,BMS-488043 has been investigated as an anti-HIV agent. Investigated for use/treatment in HIV infection.,,,,BMS-488043 is investigational.,BMS-488043 is a solid.,True
19560,"PRO 542 belongs to a new class of drugs, viral-entry inhibitor, which is intended to prevent HIV from entering and infecting cells. PRO 542 (CD4-immunoglobulin G2) is a tetravalent CD4-immunoglobulin fusion protein that broadly neutralizes primary HIV-1 isolates.  Investigated for use/treatment in acquired immune deficiency syndrome (AIDS) and aids-related infections, HIV infection, and pediatric indications. PRO 542 binds to the viral surface glycoprotein gp120 and blocks attachment and entry of virus into CD4(+) cells.Unlike currently approved therapies that block viral replication in cells already infected with HIV, PRO 542 is an antibody-like molecule that is designed to target and neutralize the virus in the bloodstream.",,,,PRO-542 is investigational.,PRO-542 is a solid.,True
19561,"FX06 is a naturally occurring peptide derived from the neo-N-terminus of fibrin (Bbeta(15-42)). It prevents leukocyte migration through the gap junctions of endothelial cells. FX06 has proven safe in acute and subchronic toxicological studies and recently entered clinical development. It is being developed by Fibrex Medical Inc. Investigated for use/treatment in cardiac reperfusion injury and myocardial infarction. FX06 has a novel mechanism of action: it is a competitive inhibitor of the binding of fibrin E1 fragments to vascular endothelial (VE)-cadherin. Through this inhibition, it potently blocks the transmigration of inflammatory leukocytes through the endothelial barrier and prevents the downstream release of tissue-damaging mediators.",,,,FX06 is investigational.,FX06 is a liquid.,True
19562,Hesperidin is a flavan-on glycoside found in citrus fruits.,,,,Hesperidin is approved and investigational.,Hesperidin is a solid.,True
19563,,,,,Reversine is experimental.,Reversine is a solid.,False
19564,"Farletuzumab (MORAb-003) is a fully humanized monoclonal antibody against the folate receptor alpha, for the potential treatment of epithelial ovarian cancer. Investigated for use/treatment in ovarian cancer.",,,,Farletuzumab is investigational.,Farletuzumab is a liquid.,True
19565,AZD-9684 is the first member of a new anti-thrombotic class (CPU inhibitors). It is being developed by AstraZeneca. Investigated for use/treatment in thrombosis. AZD-9684 enhances endogenous fibrinolysis. AZD-9684 is a Carboxypeptidase U inhibitor (CPUi).,,,,AZD-9684 is investigational.,AZD-9684 is a solid.,True
19566,"An alkaloid from Hydrastis canadensis L., Berberidaceae. It is also found in many other plants. It is relatively toxic parenterally, but has been used orally for various parasitic and fungal infections and as antidiarrheal.",,,,Berberine is approved and investigational.,Berberine is a solid.,True
19567,"LY2181308 is investigated in clinical trials for treating solid tumors. LY2181308 is a solid. LY2181308 is directed against a molecular target called survivin. LY2181308 is known to target baculoviral IAP repeat-containing protein 5. LY2181308 is an anti-sense oligonucleotide that potently downregulated survivin expression in human cancer cells derived from lung, colon, breast, prostate, ovary, cervix, skin and brain. Investigated for use/treatment in cancer/tumors (unspecified) and solid tumors. LY2181308 is directed against a molecular target called survivin. Survivin belongs to a family of proteins, called Inhibitor of Apoptosis Proteins, which play a key role in the regulation of apoptosis and cell division. The protein is expressed in a majority of human cancers but not in normal adult tissues, making it a potential target for cancer therapies. LY2181308 potently downregulates survivin expression in human cancer cells derived from lung, colon, breast, prostate, ovary, cervix, skin and brain.",,,,LY2181308 is investigational.,LY2181308 is a solid.,True
19568,"E-2012 is a gamma secretase modulator that is being evaluated as a potential new treatment for Alzheimer's disease. Investigated for use/treatment in alzheimer's disease. Gamma secretase plays a role in the production of beta-amyloid, a major component of plaque in the brain, which is thought to be a cause of Alzheimer's disease. E2012 is a new chemical entity discovered by Eisai and, in preclinical (laboratory) research, has shown some potential to reduce the production of beta-amyloid by modulating the function of gamma secretase.",,,,E-2012 is investigational.,E-2012 is a solid.,True
19569,"CR002 is a novel investigational fully human monoclonal antibody that blocks the activity of excess platelet-derived growth factor-D (PDGF-D), a target shown to play a role in kidney inflammation. This is a novel therapeutic approach to treat kidney inflammation. Investigated for use/treatment in nephropathy. CR002 blocks the activity of excess platelet-derived growth factor-D (PDGF-D), a target shown to play a role in kidney inflammation. Diabetic nephropathy, IgA nephropathy, and lupus nephritis are histologically characterized by glomerular mesangial cell proliferation and extracellular matrix accumulation. PDGF-D and its receptors play an important role in the pathogenesis of nephritis, based on their potent induction of mesangial cell proliferation and extracellular matrix accumulation shown both in vitro and in vivo. A fully human monoclonal antibody that neutralizes PDGF-D represents a novel therapeutic approach to block nephritides.",,,,CR002 is investigational.,CR002 is a solid.,True
19570,"INCB7839 is a novel, orally available ADAM metalloprotease inhibitor that is designed to block activation of the epidermal growth factor (EGFR) pathways. It represents a potentially important new class of targeted breast cancer therapy. It has shown promising clinical activity in heavily pretreated, refractory breast cancer patients. Investigated for use/treatment in breast cancer. INCB7839 is a novel, orally available ADAM metalloprotease inhibitor that is designed to block activation of the epidermal growth factor (EGFR) pathways. Currently approved therapies that target the EGFR pathways have shown promising efficacy in metastatic disease, validating these pathways as targets; however, efficacy may be limited due to the fact that these drugs inhibit only one or two of the four HER receptor pathways. In contrast, the sheddase inhibitor, INCB7839, has the potential to inhibit activation through all four of the HER receptors, resulting in more complete inhibition of these pathways.",,,,INCB7839 is investigational.,INCB7839 is a solid.,True
19571,"Guselkumab is a human immunoglobulin G1 lambda (IgG1λ) monoclonal antibody that selectively blocks interleukin-23. IL-23 is an inflammatory cytokine that activates the CD4+ T-helper (Th17) cell pathway to mediate the inflammatory cascade that induces psoriatic plaque formation. In clinical trials, guselkumab demonstrated improved skin clearance and symptomatic improvements in dermatological manifestations of psoriasis.  Indicated for the treatment of adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy. Guselkumab is shown to reduce serum levels of IL-17A, IL-17F and IL-22.  Guselkumab targets the p19 alpha subunit of IL-23. While IL-23 promotes the normal inflammatory and immune responses, the p19 and p40 subunits of IL-23 are found to be over-expressed in the condition of psoriasis and other autoimmune inflammatory skin diseases. Guselkumab selectively binds to the p19 subunit of IL-23 in dendritic cells and keratinocytes and blocks its interaction with IL-23 receptor, which further prevents the release of other pro-inflammatory cytokines and chemokines via stimulation of immune cells such as Th17 cells. Thus, guselkumab blocks the abnormally-heightened signalling of inflammatory cascades that promote epidermal abnormalities including keratinocyte hyperproliferation and psoriatic plaque formation. ",,,,Guselkumab is approved and investigational.,Guselkumab is a liquid.,True
19572,,,,,Methyl (1s)-1-Pentylcarbamate is experimental.,Methyl (1s)-1-Pentylcarbamate is a solid.,False
19573,,,,,N2--N--L-leucyl}-4-oxo-3-pyrrolidinyl]-L-leucinamide is experimental.,N2--N--L-leucyl}-4-oxo-3-pyrrolidinyl]-L-leucinamide is a solid.,False
19574,N2--n1--l-leucinamide is a solid. This compound belongs to the n-acyl-alpha amino acids and derivatives. These are compounds containing an alpha amino acid (or a derivative thereof) which bears an acyl group at its terminal nitrogen atom. It is known to target cathepsin K.,,,,N2--n1--l-leucinamide is experimental.,N2--n1--l-leucinamide is a solid.,True
19575,,,,,N-amino}-2-pentanyl]-1-benzofuran-2-carboxamide is experimental.,N-amino}-2-pentanyl]-1-benzofuran-2-carboxamide is a solid.,False
19576,,,,,"Dibenzyl (carbonylbis{2,1-hydrazinediyl})biscarbamate is experimental.","Dibenzyl (carbonylbis{2,1-hydrazinediyl})biscarbamate is a solid.",False
19577,,,,,N2-({Oxy}Carbonyl)-N1--L-Leucinamide is experimental.,N2-({Oxy}Carbonyl)-N1--L-Leucinamide is a solid.,False
19578,,,,,(2R)-2-(3-Biphenylyl)-N-{(2R)-2-hydroxy-3-propyl}-4-methylpentanamide is experimental.,(2R)-2-(3-Biphenylyl)-N-{(2R)-2-hydroxy-3-propyl}-4-methylpentanamide is a solid.,False
19579,,,,,Tert-Butyl(1s)-1-Cyclohexyl-2-Oxoethylcarbamate is experimental.,Tert-Butyl(1s)-1-Cyclohexyl-2-Oxoethylcarbamate is a solid.,False
19580,"MIV-701 is a selective, potent inhibitor of the protease Cathepsin K. It is developed for the treatment of osteoporosis. Investigated for use/treatment in osteoporosis. MIV-701 inhibits an enzyme, cathepsin K, which degrades bone, but most probably also contributes to cartilage damage in joint diseases. It greatly reduces degradation of bone.",,,,MIV-701 is investigational.,MIV-701 is a solid.,True
19581,"Investigated for use/treatment in osteoporosis and bone metastases. Relacatib is a small-molecule drug that inhibits the activity of cathepsin K, an enzyme that appears to be implicated in osteoporosis, osteoarthritis and certain other disorders causing bone degradation. ",,,,Relacatib is investigational.,Relacatib is a solid.,True
19582,,,,,1-{7-cyclohexyl-6--7H-pyrrolopyrimidin-2-yl}methanamine is experimental.,1-{7-cyclohexyl-6--7H-pyrrolopyrimidin-2-yl}methanamine is a solid.,False
19583,,,,,(2R)-3-Methyl-1-phenyl-2-butanyl carbamate is experimental.,(2R)-3-Methyl-1-phenyl-2-butanyl carbamate is a solid.,False
19584,,,,,1-(PHENYLMETHYL)CYCLOPENTYLCARBAMATE is experimental.,1-(PHENYLMETHYL)CYCLOPENTYLCARBAMATE is a solid.,False
19585,,,,,6-(cyclohexylamino)-9--9H-purine-2-carbonitrile is experimental.,6-(cyclohexylamino)-9--9H-purine-2-carbonitrile is a solid.,False
19586,,,,,9-CYCLOPENTYL-6--9H-PURINE-2-CARBONITRILE is experimental.,9-CYCLOPENTYL-6--9H-PURINE-2-CARBONITRILE is a solid.,False
19587,,,,,"N-(2-AMINOETHYL)-N~2~-{(1S)-1--2,2,2-TRIFLUOROETHYL}-L-LEUCINAMIDE is experimental.","N-(2-AMINOETHYL)-N~2~-{(1S)-1--2,2,2-TRIFLUOROETHYL}-L-LEUCINAMIDE is a solid.",False
19588,,,,,"(1R,2R)-N-(2-Aminoethyl)-2-{methyl}cyclohexanecarboxamide is experimental.","(1R,2R)-N-(2-Aminoethyl)-2-{methyl}cyclohexanecarboxamide is a solid.",False
19589,,,,,TERT-BUTYL 2-CYANO-2-METHYLHYDRAZINECARBOXYLATE is experimental.,TERT-BUTYL 2-CYANO-2-METHYLHYDRAZINECARBOXYLATE is a solid.,False
19590,,,,,MIV-711 is investigational.,,False
19591,"A novel anti-cancer compound synthesized by scientists at the University of California, San Diego more than a decade ago from toxins of the poisonous jack-o-lantern mushroom, has been granted “fast track” status by the U.S. Food and Drug Administration (FDA) after demonstrating promise against one of the most deadly cancers.  Investigated for use/treatment in brain cancer, breast cancer, endometrial cancer, liver cancer, lung cancer, ovarian cancer, pancreatic cancer, pediatric indications, prostate cancer, and sarcoma. MGI-114(Irofulven) has unique mechanism of action as an anti-tumor agent is due to its ability to be rapidly absorbed by tumor cells. Once inside the cells, the compound binds to DNA and protein targets. This binding interferes with DNA replication and cell division of tumor cells, leading to tumor-specific apoptotic cell death, or “cell suicide.” During this process, tumor cells tend to automatically shut themselves down when they sense their function is compromised.",The molecular weight is 246.31.,Irofulven has a topological polar surface area of 57.53.,The log p value of  is 0.59.,Irofulven is investigational.,Irofulven is a solid.,True
19592,GEM231 is a second-generation antisense oligonucleotide targeting the mRNA of the R1alpha regulatory subunit of cAMP dependent protein kinase. A monoclonal antibody combined with a toxic substance that is used treat certain types of acute myeloid leukemia in older patients and is being studied in the treatment of other types of cancer. Monoclonal antibodies are made in the laboratory and can locate and bind to cancer cells. Investigated for use/treatment in solid tumors. GEM-231 has also demonstrated potentiation of the effects of certain conventional cytotoxic chemotherapy drugs. Hybridon is conducting studies of the DNA methyltransferase gene and has identified specific sequences on mRNA as targets for chemically-modified antisense oligonucleotides.,,,,GEM-231 is investigational.,GEM-231 is a solid.,True
19593,,,,,(Rp)-cAMPS is experimental.,(Rp)-cAMPS is a solid.,False
19594,"Cyclic adenosine monophosphate (cAMP, cyclic AMP or 3'-5'-cyclic adenosine monophosphate) is a molecule that is important in many biological processes; it is derived from adenosine triphosphate (ATP).",,,,Cyclic adenosine monophosphate is experimental.,Cyclic adenosine monophosphate is a solid.,True
19595,"AZD-8330 is a potent, selective, orally active MEK inhibitor that blocks signal transduction pathways implicated in cancer cell proliferation and survival. AZD-8330 has shown tumor suppressive activity in multiple preclinical models of human cancer including melanoma, pancreatic, colon, lung, and breast cancers. Investigated for use/treatment in cancer/tumors (unspecified). AZD8330 specifically inhibits mitogen-activated protein kinase kinase 1 (MEK or MAP/ERK kinase1), resulting in inhibition of growth factor-mediated cell signaling and tumor cell proliferation. MEK is a key component of the RAS/RAF/MEK/ERK signaling pathway that regulates cell growth; constitutive activation of this pathway has been implicated in many cancers.",,,,AZD-8330 is investigational.,AZD-8330 is a solid.,True
19596,"KAI-1455 is a selective epsilon protein kinase C (εPKC) activator designed to reduce ischemic organ injury during procedures where blood supply may be compromised, such as coronary artery bypass grafting (CABG), congenital cardiac defect repair, and hip replacement and may protect against renal injury associated with contrast media. Several studies have demonstrated that epsilon PKC plays a key role in cytoprotection during periods of ischemia. In preclinical studies, KAI-1455 showed a dramatic reduction in infarct size when delivered prior to the ischemic insult. Investigated for use/treatment in ischemic reperfusion injury. KAI-1455 is a selective epsilon protein kinase C (εPKC) activator. It reduces damage during surgical procedures, such as coronary artery bypass grafting, vascular surgery and pediatric cardiac surgery N.B. begun dosing protein tyrosine phosphatase 1B (PTP1B).",,,,KAI-1455 is investigational.,KAI-1455 is a solid.,True
19597,"Apatorsen is a second generation antisense drug which in preclinical experiments, inhibits production of Heat Shock Protein 27 (Hsp27) a cell survival protein found at elevated levels in many human cancers including prostate, lung, breast, ovarian, bladder, renal, pancreatic, multiple myeloma and liver cancer. Investigated for use/treatment in cancer/tumors (unspecified). OGX-427 significantly decreases levels of Hsp27, induces apoptosis in several human cancer cell lines, has single agent anti-tumor activity, and acts as a chemosensitizer in combination with several cytotoxic drugs including docetaxel.",,,,Apatorsen is investigational.,Apatorsen is a solid.,True
19598,"HGS-TR2J is a novel agonistic human monoclonal antibody to TRAIL Receptor 2, in patients with advanced solid malignancies. It is developed by Human Genome Sciences, Inc and is under Phase I of clinical trial. Investigated for use/treatment in solid tumors. HGS-TR2J binds TRAIL Receptor 2 with high affinity, induces apoptosis and has anti-tumor activity, both as a single agent and in combination with chemotherapy. HGS-TR2J mimics the activity of native TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) and, thus, is considered an agonistic antibody. Numerous nonclinical studies have shown that cell lines derived from a broad array of solid and hematological human tumors, including lung, colon, breast, multiple myeloma, prostate and pancreas, are sensitive to killing by apoptosis (programmed cell death) induced by native TRAIL or by agonistic antibodies to TRAIL Receptors 1 and 2.2-24.",,,,HGS-TR2J is investigational.,HGS-TR2J is a solid.,True
19599,"Lexatumumab is a fully humanized, high-affinity immunoglobulin G(1 lambda) monoclonal antibody (mAb). Investigated for use/treatment in cancer/tumors (unspecified). Lexatumumab agonizes the tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) receptor 2 (TRAIL-R2), triggering the extrinsic apoptotic pathway.",,,,Lexatumumab is investigational.,Lexatumumab is a solid.,True
19600,"GSK-923295 is a small-molecule inhibitor of the mitotic kinesin centromere-associated protein E (CENP-E), and the third novel drug candidate to arise from Cytokinetics' broad strategic alliance with GlaxoSmithKline (GSK). GSK-923295 demonstrated a broad spectrum of activity against a range of human tumor xenografts grown in nude mice, including models of colon, breast, ovarian, lung and other tumors. GSK-923295 is the first drug candidate to enter human clinical trials that specifically targets CENP-E and is currently in Phase I human clinical trials being conducted by GSK. Investigated for use/treatment in cancer/tumors (unspecified) and solid tumors. GSK-923295 is an inhibitor of the mitotic kinesin centromere-associated protein E (CENP-E). CENP-E plays an essential role in chromosome movement during early cell division or mitosis and integrates mitotic spindle mechanics with regulators of the mitotic checkpoint regulating cell-cycle transition from metaphase to anaphase. Inhibition of CENP-E induces cell cycle arrest during cell duplication leading to subsequent apoptosis or cell death.",,,,GSK-923295 is investigational.,GSK-923295 is a solid.,True
19601,"MYO-029 is a human anti-GDF-8 monoclonal antibody, which is being developed to treat muscle-wasting diseases including muscular dystrophy and age-related sarcopenia.  Investigated for use/treatment in muscular dystrophy. MYO-029 is used to treat muscular dystrophy. It binds to and inhibit the activity of myostatin (growth and differentiation factor 8 or GDF-8), a protein that prevents skeletal muscle formation. Muscular dystrophy is characterized by a progressive wasting and weakening of muscle fibers. The disorder can be classified into six major types, all of which are inherited. The common feature of these disorders is absence of one of several proteins involved in linking F-actin (a muscle fiber component) to the sheath of tissue surrounding the fiber.",,,,MYO-029 is investigational.,MYO-029 is a solid.,True
19602,"CT-011 is a humanized monoclonal antibody directed against a B7 family-associated protein, in patients with advanced haematological malignancies. It is directed against human PD-1 (programmed cell death 1; PDCD1), with immunomodulating and antitumor activities. Investigated for use/treatment in cancer/tumors (unspecified). CT-011 blocks interaction between the receptor PD-1 with its ligands, PD-1 ligand 1 (PD-1L1) and PD-1 ligand 2 (PD-1L2), resulting in the attenuation of apoptotic processes in lymphocytes, primarily effector/memory T cells, and the augmentation of the anti-tumor activities of NK cells. PD-1 is an inhibitory receptor belonging to the B7-receptor family that is expressed on lymphocytes and myeloid cells; its ligands, PD-1L1 and PD-1L2, are expressed not only by hematopoietic cells but also by cells in non-lymphoid tissues.",,,,CT-011 is investigational.,CT-011 is a solid.,True
19603,"Nivolumab is a fully human IgG4 antibody targeting the immune checkpoint programmed death receptor-1 (PD-1). This antibody was produced entirely in mice and grafted onto human kappa and IgG4 Fc region with the mutation _S228P_ for additional stability and reduced variability. It was developed by Bristol Myers Squibb. Nivolumab is indicated to treat unresectable or metastatic melanoma, adjuvant treatment of melanoma, metastatic non-small cell lung cancer, small cell lung cancer, advanced renal cell carcinoma, classical Hodgkin lymphoma, squamous cell carcinoma of the head and neck, urothelial carcinoma, microsatellite instability-high or mismatch repair deficient metastatic colorectal cancer, and hepatocellular carcinoma. Nivolumab blocks PD-1 inhibitory signalling to T-cells. It has a long duration of action as it is administered every 2-4 weeks. Patients should be counselled regarding the risk of immune-mediated adverse effects, infusion-related adverse effects, complications of allogenic hematopoietic stem cell transplants, embryo-fetal toxicity. The ligands PD-L1 and PD-L2 bind to the PD-1 receptor on T-cells, inhibiting the action of these cells. Tumor cells express PD-L1 and PD-L2. Nivolumab binds to PD-1, preventing PD-L1 and PD-L2 from inhibiting the action of T-cells, restoring a patient's tumor-specific T-cell response.",,,,Nivolumab is approved.,Nivolumab is a liquid.,True
19604,"Pembrolizumab is a highly selective IgG4-kappa humanized monoclonal antibody against PD-1 receptor. It was generated by grafting the variable sequences of a very high-affinity mouse antihuman PD-1 antibody onto a human IgG4-kappa isotype with the containing a stabilizing S228P Fc mutation. It contains 32 cysteine residues and the complete folded molecule includes 4 disulfide linkages as interchain bonds and 23 interchain bonds. It was developed by Merck & Co and firstly approved for the treatment of metastatic malignant melanoma. This is the first approved therapy against PD-1. It was approved firstly by the FDA on September 4, 2014. Its approval in melanoma was extended to several countries such as Australia, Israel, Korea, Macau, the European Union and the United Arab Emirates. On June 12, 2018, Pembrolizumab was approved for the treatment of cervical cancer under the status of accelerated approval. Pembrolizumab is indicated for the treatment of: Pembrolizumab pharmacodynamic reports indicate that there are not effector functions by binding to C1q and CD64 not by cytokine release. On clinical trials, the objective response rate, defined as the proportion of patients with tumor size reduction of a predefined amount for a minimum time period, was assessed based on independent central review and a response duration. These studies performed for different classes of cancer showed a response either partial or complete in a range of 14.3-26% of the individuals. The response duration was estimated to be of 11 months and 45-91% of the patients had a response equal or greater than 6 months.  Pembrolizumab, as an IgG4 subclass antibody, is preferred over other subclasses as it only induces weakly the complement and cell activation due to low affinity to C1q and Fc receptors. It binds with high affinity to the cell surface receptor programmed cell death protein 1 (PD-1) and it antagonizes its interaction with its known ligands PD-L1 and PD-L2. In normal circumstances, the binding of the ligands of PD-1 to the receptor inhibits the TCR-mediated T cell proliferation and cytokine production. This inhibitory signal seems to be essential for self-tolerance, collateral damage minimizing after immune response against a pathogen and maternal tolerance to fetal tissue. Therefore, the binding of pembrolizumab to PD-1 prevents the inhibitory pathway causing a physiological shift to immune reactivity and enhancing tumor immunosurveillance and anti-tumor immune response.",,,,Pembrolizumab is approved.,Pembrolizumab is a solid.,True
19605,"The U.S. Food and Drug Administration (FDA) approved Cemiplimab (_Libtayo_), manufactured by Regeneron Pharmaceuticals, on September 28, 2018. This drug is a programmed death receptor-1 (PD-1) blocking antibody indicated for the treatment of patients with metastatic cutaneous squamous cell carcinoma (CSCC) or locally advanced CSCC who are not candidates for curative surgery or curative radiation. Cemiplimab inhibits tumor growth by an immune-mediated mechanism, specifically by the inhibition of the programmed death receptor 1 (PD-1), treating cutaneous squamous cell carcinoma , ,. Binding of the programmed death receptor (PD) ligands PD-L1 and PD-L2, to the PD-1 receptor, which is found on T cells, inhibits T-cell proliferation and cytokine production. The upregulation of PD-1 ligands occurs in some tumors and signaling through this pathway may contribute to the inhibition of active T-cell immune surveillance of tumors. Cemiplimab is a recombinant human immunoglobulin G4 (IgG4) monoclonal antibody that binds to the PD-1 receptor and blocks its interaction with PD-L1 and PD-L2 ligands, causing PD-1 pathway-mediated inhibition of the immune response, including the anti-tumor immune response. In mouse tumor models, blocking PD-1 activity resulted in decreased rates of tumor growth.",,,,Cemiplimab is approved and investigational.,,True
19606,Camrelizumab is under investigation in clinical trial NCT03417895 (SHR-1210 Combined With Apatinib in Treatment of ED-SCLC After Failure of First Line Standard Therapy).,,,,Camrelizumab is investigational.,,True
19607,Spartalizumab is under investigation in clinical trial NCT02605967 (Safety and Efficacy Study of PDR001 in Patients With Recurrent or Metastatic Nasopharyngeal Carcinoma).,,,,Spartalizumab is investigational.,,True
19608,"Tislelizumab is under investigation in clinical trial NCT02660034 (The Safety, Pharmacokinetics and Antitumor Activity of BGB-A317 in Combination With BGB-290 in Subjects With Advanced Solid Tumors).",,,,Tislelizumab is investigational.,,True
19609,Toripalimab is under investigation in clinical trial NCT03919383 (Phase II of Lenvatinib Plus Toripalimab for Advanced HCC).,,,,Toripalimab is investigational.,,True
19610,Dostarlimab is under investigation in clinical trial NCT03981796 (A Study of Dostarlimab (TSR-042) Plus Carboplatin-paclitaxel Versus Placebo Plus Carboplatin-paclitaxel in Patients With Recurrent or Primary Advanced Endometrial Cancer).,,,,Dostarlimab is investigational.,,True
19611,"Romiplostim is a thrombopoiesis stimulating dimer Fc-peptide fusion protein (peptibody) to increase platelet production through activation of the thrombopoietin receptor. The peptibody molecule has two identical single-chain subunits, each one is made up of 269 amino acid residues. Each subunit consists of an IgG1 Fc carrier domain that is covalently attached to a polypeptide sequence that contains two binding domains to interact with thrombopoietin receptor c-Mpl. Each domain consists of 14 amino acids. Interestingly, romiplostim's amino acid sequence is not similar to that of endogenous thrombopoietin. Romiplostim is produced by recombinant DNA technology in Escherichia coli. FDA approved on August 22, 2008. Treatment of chronic immune thrombocytopenic purpura.  Responses to platelet increase varies between patients thus indicating a need for individualization of dose. However, a dose dependent-increase in platelet counts have been observed in clinical trials. Does not affect platelet destruction.  Romiplostim is a thrombopoietin receptor agonist that activates intracellular transcriptional pathways via c-Mpl to increase production of platelets. It also works similarly to thrombopoietin (TPO), an endogenous glycoprotein hormone that regulates the production of platelets in the bone marrow. ",,,,Romiplostim is approved.,Romiplostim is a solid.,True
19612,"SB-559448 is a small-molecule drug that mimics the activity of thrombopoietin (TPO), a protein factor that promotes growth and production of blood platelets. This drug is developed by GlaxoSmithKline and used to treat Thrombocytopenia.Thrombocytopenia (decreased platelet count) is a common side effect of many chemotherapies and can lead to uncontrolled bleeding, thus representing a significant problem in the treatment of cancer patients. Investigated for use/treatment in thrombocytopenia.",,,,SB-559448 is investigational.,SB-559448 is a solid.,True
19613,Investigated for use/treatment in thrombocytopenia.,,,,Thrombopoietin is investigational.,Thrombopoietin is a solid.,True
19614,"Atezolizumab is a humanized monoclonal antibody used to prevent the interaction of PD-L1 and PD-1, removing inhibition of immune responses seen in some cancers. This medication is reserved for patients whose tumors express PD-L1, cannot receive platinum based chemotherapy, or whose tumors do not respond to platinum based chemotherapy. Atezolizumab was granted FDA approval on 18 October 2016. Atezolizumab is indicated to treat locally or advanced metastatic urothelial carcinoma in patients ineligible for cicplatin-containing chemotherapy with tumors expressing PD-L1, in patients ineligible for cisplatin-containing chemotherapy irrespective of PD-L1, have disease progression following platinum containing chemotherapy, or have disease progression within 12 months of neoadjuvant or adjuvant chemotherapy. Atezolizumab is a humanized monoclonal antibody used to prevent the interaction of PD-L1 and PD-1, removing inhibition of immune responses seen in some cancers. This drug has a long duration of action as it is usually given every 3-4 weeks. Atezolizumab should not be used in patients with immune mediated penumonitis, hepatitis, colitis, and some endocrinopathies. Atezolizumab is a humanized IgG antibody that binds PD-L1, preventing its interaction with PD-1 and B7-1. Preventing the interaction of PD-L1 and PD-1 removes inhibition of immune responses such as the anti-tumor immune response but not antibody dependent cellular cytotoxicity.",,,,Atezolizumab is approved and investigational.,Atezolizumab is a solid.,True
19615,"Durvalumab is a human immunoglobulin G1 kappa (IgG1κ) monoclonal antibody and a novel immune-checkpoint inhibitor for cancer treatment. Produced by recombinant DNA technology in Chinese Hamster Ovary (CHO) cell suspension culture, durvalumab is a programmed death-ligand 1 (PD-L1) blocking antibody that works to promote normal immune responses that attack tumour cells. Durvalumab is indicated for the treatment of patients with locally advanced or metastatic urothelial carcinoma who have disease progression during or following platinum-containing chemotherapy, or within 12 months of neoadjuvant or adjuvant treatment with platinum-containing chemotherapy. Durvalumab is an anticancer antibody that works to promote the antitumour responses mediated by immune cells. By blocking the action of PD-L1, durvalumab exerts its anticancer effects by increasing T-cell activation, enhancing detection and ablation of tumour cells. In _in vitro_ assays, durvalumab inhibited the activity of PD-L1 in a concentration-dependent manner. In co-engrafted human tumor and immune cell xenograft mouse models, durvalumab was effective in decreasing tumour size. Durvalumab does not mediate antibody-dependent cell-mediated cytotoxicity (ADCC). Because cancer cells express antigens that are recognized and taken up by antigen-presenting cells (APCs), the immune responses prime and activate cytotoxic T cells, and allow them to travel to the site of tumour to destroy cancer cells. However, tumours often evade T cell-mediated immune responses to enhance their survival. Inflammatory mediators, such as IFN-gamma, induce the expression of programmed cell death ligand-1 (PD-L1), which is a type 1 transmembrane protein expressed on tumour cells and tumour-associated immune cells in the tumour microenvironment. PD-L1 acts as an immune checkpoint to regulate immune responses. PD-L1 is a ligand to PD-1, which is a cell surface receptor expressed on activated T cells in peripheral tissues following antigen exposure. Both PD-L1 and PD-1 are co-inhibitory molecules involved in blocking T cell-mediated immune responses. PD-L1 also interacts with CD-80, which is a receptor constitutively expressed by T cells and is upregulated early after T cell activation.",,,,Durvalumab is approved and investigational.,Durvalumab is a liquid.,True
19616,"Avelumab is a programmed death ligand-1 (PD-L1) blocking antibody indicated for the treatment of adults and pediatric patients 12 years and older with metastatic Merkel cell carcinoma (MCC). It is a fully human anti-PD immunoglobulin G1 (IgG1) lambda monoclonal antibody with antineoplastic actions. It was granted accelerated approval in March 2017 under the name Bavencio. Indicated for the treatment of adults and pediatric patients 12 years and older with metastatic Merkel cell carcinoma (MCC).  Avelumab is a whole antibody that binds the immunosuppressive programmed death-ligand 1 and inhibits the interaction between PD-1 and PD-L1. It prevents the formation of a PD-1/PD-L1 receptor/ligand complex that normally leads to inhibition of CD8+ T cells, and therefore inhibition of an immune reaction. Alevumab is an immunotherapeutic and antineoplastic agent that belongs to the group of immune checkpoint blockade cancer therapies. By retaining a native Fc-region, avelumab is thought to engage the innate immune system and may induce antibody-dependent cell-mediated cytotoxicity (ADCC). PD-L1 may be expressed on tumor cells and tumor-infiltrating immune cells and can contribute to the inhibition of the anti-tumor immune response in the tumor microenvironment. Binding of PD-L1 to the PD-1 and B7.1 receptors found on T cells and antigen presenting cells suppresses cytotoxic T-cell activity, T-cell proliferation and cytokine production. Avelumab binds PD-L1 through the FG loops and blocks the interaction between PD-L1 and its receptors PD-1 and B7.1. This interaction releases the inhibitory effects of PD-L1 on the immune response resulting in the restoration of immune responses, including anti-tumor immune responses. Avelumab has also been shown to induce antibody-dependent cell-mediated cytotoxicity (ADCC) in vitro. In syngeneic mouse tumor models, blocking PD-L1 activity resulted in decreased tumor growth.",,,,Avelumab is approved and investigational.,Avelumab is a liquid.,True
19617,"MK-0354, is an orally administered drug candidate under development by Merck for the treatment of atherosclerosis and related disorders. It targets G protein-coupled receptor, or GPCR, that have the potential to regulate plasma lipid profiles, including HDL, or the good cholesterol, similar to the therapeutic action of niacin. Investigated for use/treatment in atherosclerosis.",,,,MK-0354 is investigational.,MK-0354 is a solid.,True
19618,"Sifalimumab is a fully human monoclonal antibody targeting interferon-alpha. The levels of interferon-alpha are elevated in many patients with active systemic lupus erythematosus (SLE, or lupus) and other autoimmune disorders, and may be associated with disease activity. Sifalimumab may suppress the abnormal immune activity associated with lupus by binding to multiple interferon-alpha subtypes seen in the serum of lupus patients.",,,,Sifalimumab is investigational.,,True
19619,"Mirococept (APT070) is a complement inhibitor currently under development for treatment of rheumatoid arthritis and I/RI. It is a truncated form of the human Complement Receptor 1 (CR1) linked to a unique Prodaptin™ construct that regulates the over-production of complement at the cell surface, which occurs in inflammation. It consists of the first three short consensus domains of human complement receptor 1 (CR1), manufactured in recombinant bacteria and modified with a membrane-targeting amphiphilic peptide based on the naturally occurring membrane-bound myristoyl-electrostatic switch peptide. Investigated for use/treatment in transplant (rejection), kidney disease, and rheumatoid arthritis. Mirococept comprises the C3/C5 convertase-inhibiting region of CR1. This complement inhibitory domains of CR1 (in APT070) contain C3b-binding sites that lead to dissociation and inactivation of C3b from the classical and alternative pathway convertases. Mirococept effectively blocks and reduces the generation of the activated form of C3, and thwarts the release of both C3a and C5a.",,,,Mirococept is investigational.,Mirococept is a solid.,True
19620,"Blinatumomab is a BiTE-class (bi-specific T-cell engagers) constructed monoclonal antibody indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). Blinatumomab is manufactured by Amgen Inc. and marketed under the brand Blincyto™. A full treatment regimen consisting of two cycles of four weeks each, is priced at $178 000 USD. Blinatumomab was approved in December 2014 under the FDA’s accelerated approval program, which allows approval of a drug to treat a serious or life-threatening disease based on clinical data showing the drug has an effect on a surrogate endpoint reasonably likely to predict clinical benefit to patients. Indicated for the treatment of Philadelphia chromosome-negative relapsed or refractory B-cell precursor acute lymphoblastic leukemia (ALL). Blinatumomab is a bispecific CD19-directed CD3 T-cell engager that binds to CD19 expressed on the surface of cells of B-lineage origin and CD3 expressed on the surface of T cells. It activates endogenous T cells by connecting CD3 in the T-cell receptor (TCR) complex with CD19 on benign and malignant B cells. Blinatumomab mediates the formation of a synapse between the T cell and the tumor cell, upregulation of cell adhesion molecules, production of cytolytic proteins, release of inflammatory cytokines, and proliferation of T cells, which result in redirected lysis of CD19+ cells.",,,,Blinatumomab is approved and investigational.,Blinatumomab is a solid.,True
19621,"Amatuximab has been used in trials studying the treatment and basic science of Mesothelioma, Ovarian Cancer, Ovarian Neoplasms, Pancreatic Cancer, and Mesothelioma, Malignant, among others.",,,,Amatuximab is investigational.,,True
19622,"Bardoxolone has been used in trials studying the treatment of LYMPHOMA and Solid Tumors. It is a synthetic triterpenoid and a highly potent activator of redox-sensitive signaling pathways that induce programmed cell death (apoptosis) in cancer cells that are under high levels of intrinsic oxidative stress. In contrast, Bardoxolone in normal cells induces protective antioxidant/anti-inflammatory responses. Bardoxolone, a synthetic triterpenoid, is a highly potent activator of redox-sensitive signaling pathways that induce programmed cell death (apoptosis) in cancer cells that are under high levels of intrinsic oxidative stress. In contrast, Bardoxolone in normal cells induces protective antioxidant/anti-inflammatory responses. Intensive research in animal models of human cancer has demonstrated that Bardoxolone is a potent anticancer agent with a well-characterized ability to inhibit growth and cause regression of tumors as a single agent and in combination with radiation and chemotherapy. Bardoxolone also suppresses radiation- and chemotherapy-induced damage (e.g., oral mucositis) in normal tissues at dose levels that also produce an anti-cancer effect. Bardoxolone induces apoptosis through both caspase-independent and -dependent mechanisms, the latter involving caspase-8 activation, Bid cleavage, cytochrome c release, and caspase-3 activation. Furthermore, JNK, p38, and ERK pathways are involved in Bardoxolone-induced apoptosis of tumor cell lines mediated by disrupted intracellular redox balance and involving decreased glutathione and increased reactive oxygen species. Study shows that Bardoxolone enhances p42 CEBPA protein at the level of translation. ",,,,Bardoxolone is investigational.,,True
19623,"Urelumab has been used in trials studying the treatment of Leukemia, Multiple Myeloma, Malignant Tumors, and Cancer - Solid Tumors and B-Cell Non-Hodgkin's Lymphoma. Urelumab is a fully human antibody that targets CD137. The antibody product was developed using Medarex's UltiMAb(R) technology and was the first UltiMAb- derived antibody in clinical development by Bristol-Myers Squibb under the December 2003 agreement with Medarex.",,,,Urelumab is investigational.,,True
19624,"Lumiliximab is a chimeric monoclonal antibody which is used as an immunosuppressive drug. It is a primatized anti-CD23 macaque/human chimeric antibody that inhibits the production of the IgE antibody, for the potential treatment of allergic conditions. Lumiliximab was developed by IDEC Pharmaceuticals, which was acquired by Biogen. Clinical trials for CLL were terminated in 2010, and for allergic asthma in 2007. Results published from the CLL clinical trial failed to meet primary endpoints. Investigated for use/treatment in asthma and leukemia (lymphoid). Lumiliximab is a chimeric macaque-human monoclonal antibody to CD23, a protein expressed on virtually all chronic lymphocytic leukemia (CLL) cells. CD23, also known as Fc epsilon RII, or Fc&epsilon;RII, is the \low affinity\"" receptor for IgE, an antibody isotype involved in allergy and resistance to parasites and is important in regulation of IgE levels. Unlike many of the antibody receptors, CD23 is a C-type lectin. It is found on mature B cells, activated macrophages, eosinophils, follicular dendritic cells and platelets.""",,,,Lumiliximab is investigational.,Lumiliximab is a liquid.,True
19625,"Radezolid has been used in trials studying the treatment of Abscess, Bacterial Skin Diseases, Streptococcal Infections, Infectious Skin Diseases, and Staphylococcal Skin Infections, among others.",,,,Radezolid is investigational.,,True
19626,"Investigated for use/treatment in cancer/tumors (unspecified) and liver cancer. CRS-100 is a bacteria-based immune therapy that targets liver metastases. Liver metastases arise from a number of cancers, including colon and pancreas cancers. Despite recent advances, metastasized colorectal and pancreatic cancers remain significant unmet medical needs.",,,,ANZ-100 is investigational.,ANZ-100 is a solid.,True
19627,"Investigated for use/treatment in lymphoma (unspecified), multiple myeloma, and solid tumors. RTA 402 inhibits the activity of nuclear factor kappa-B (NF-kB) activated by tumor necrosis factor (TNF) and other inflammatory agents in a variety of cancer cells. It is a novel targeted cancer therapy with a unique mechanism of action. It exploits fundamental physiological differences between cancerous and noncancerous cells by modulating oxidative stress response pathways. As a result, the drug is toxic to cancer cells but induces protective antioxidant and anti-inflammatory responses in normal cells.",,,,Bardoxolone methyl is investigational.,Bardoxolone methyl is a solid.,True
19628,"Astaxanthin is a keto-carotenoid in the terpenes class of chemical compounds. It is classified as a xanthophyll but it is a carotenoid with no vitamin A activity. It is found in the majority of aquatic organisms with red pigment. Astaxanthin has shown to mediate anti-oxidant and anti-inflammatory actions. It may be found in fish feed or some animal food as a color additive. Investigated for use/treatment in eye disorders/infections, cancer/tumors (unspecified), and asthma.",,,,Astaxanthin is investigational.,Astaxanthin is a solid.,True
19629,"C-101, also called Myodur, is developed for the treatment of Duchenne’s muscular dystrophy (DMD) which is a morbid genetic disease that can lead to death in late adolescence due to accelerated skeletal muscle breakdown. C-101 includes a carnitine carrier molecule and a leupeptin analogue, a known calpain inhibitor. Calpain is the primary protease that degrades skeletal muscle. Investigated for use/treatment in muscular dystrophy. C-101 targets muscle cells by using a carnitine carrier molecule and inhibits calpain by attaching a leupeptin analogue onto the carrier. Leupeptin has been studied extensively in a variety of animal models and was shown to be an effective means of slowing or delaying muscle wasting. Carnitine is a compound present in skeletal muscle involved in the transfer of fatty acids across mitochondrial membranes. In C-101, the carnitine carrier molecule directs the leupeptin analogue into targeted cells where it inhibits the up-regulation of calpain. Therefore, by targeting a calpain inhibitor to muscle cells, it is believed that C-101 will prevent the degradation and promote the preservation of functional muscle.",,,,L-aminocarnityl-succinyl-leucyl-argininal-diethylacetal is investigational.,L-aminocarnityl-succinyl-leucyl-argininal-diethylacetal is a solid.,True
19630,"Sotatercept has been used in trials studying the supportive care and treatment of Anemia, Leukemia, Solid Tumors, Bladder Cancer, and multiple myeloma, among others.",,,,Sotatercept is investigational.,,True
19631,"A conjugate of an anti-glycoprotein non-metastatic melanoma protein B mAb and monomethyl auristatin E for the treatment of melanoma and breast cancer. Investigated for use/treatment in melanoma. CR011 is a fully-human monoclonal antibody which utilizes antibody-drug conjugation (ADC) technology licensed from Seattle Genetics. The ADC technology links vcMMAE, a potent chemotherapeutic, to the CR011 antibody resulting in the antibody-drug conjugate CR011-vcMMAE. CR011-vcMMAE targets GPNMB, a protein located specifically on the surface of melanoma cells. After CR011-vcMMAE binds to GPNMB, it is transported inside the cancer cell where the chemotherapy payload, Auristatin E, is cleaved from the antibody and activated.",,,,Glembatumumab vedotin is investigational.,Glembatumumab vedotin is a solid.,True
19632,,,,,L-tyrosinamide is experimental.,L-tyrosinamide is a solid.,False
19633,"XmAb 2513 is a humanized monoclonal antibody that targets the antigen CD30, a molecule expressed on the surface of a number of tumor cell types. It has been investigated for the treatment of hodgkin’s lymphoma. Investigated for use/treatment in lymphoma (unspecified) and lymphoma (non-hodgkin's). XmAb™2513 is a humanized monoclonal antibody that targets the antigen CD30, a molecule expressed on the surface of a number of tumor cell types. XmAb™2513 has an XmAb™ Fc domain which increases its cytotoxic potency. XmAb™2513 recruits primary human immune cells to kill tumor cells in vitro models and is active in blocking tumor growth in rodent models. ",,,,XmAb 2513 is investigational.,XmAb 2513 is a solid.,True
19634,"Talarozole has been investigated for the treatment of Psoriasis and Cutaneous Inflammation. Rambazole is a new generation all-trans retinoic acid metabolism blocking agent, highly specific against the retinoic acid 4-hydroxylase. The drug alleviates hyperproliferation and normalizes differentiation of the epidermis in animal models of psoriasis. All-trans-retinoic acid (RA) regulates epithelial differentiation and growth through activation of specific nuclear RA receptors (RARs). Rambazole acts by inhibiting the metabolic breakdown of the retinoid, increasing the biological efficacy of RA.",,,,Talarozole is investigational.,,True
19635,,,,,3-Indolebutyric Acid is experimental.,3-Indolebutyric Acid is a solid.,False
19636,"Investigated for use/treatment in prostate cancer and breast cancer. NeuVax is a HER2/neu peptide-based T-cell immunotherapy aimed at preventing disease recurrence and prolonging survival in cancer patients that have tumors which express the HER2/neu oncoprotein. To date, clinical study results have demonstrated that NeuVax significantly reduces the rate of cancer recurrence while showing minimal side effects. ",,,,Nelipepimut-S is investigational.,Nelipepimut-S is a solid.,True
19637,Coccidioides immitis spherule is a skin test antigen indicated to detect delayed-type hypersensitivity to Coccidioides immitis in individuals with a history of pulmonary coccidioidomycosis. Indicated to detect delayed-type hypersensitivity to Coccidioides immitis in individuals with a history of pulmonary coccidioidomycosis. Use in 18-64 year old patients. A positive result occurs if 48h after administration if the diameter of the induration is >5mm.  Illicit cellular immune response if patient has been exposed to Coccidiodes immitis.  Delayed type hypersensitivity reaction begin with the C.immitis antigen is presented to CD4 and CD8 lymphocytes by antigen presenting cells. This causes the secretion of interleukins and other lymphokines from macrophage cells. The release of effector molecules causes blood vessels to become permeable and allows fibrinogen to escape into the surrounding tissue where it is converted to fibrin. The deposition of fibrin and the movement of T-cells and monocytes in the extracellular spaces cause the tissue to become indurated. The induration is usually detectable in 18 hours and peaks at 48 hours. ,,,,Coccidioides immitis spherule is approved.,,True
19638,Clenoliximab is a chimeric monoclonal antibody from _Macaca irus_ against CD4 which acts as an immunomodulator. It has investigated for the treatment of rheumatoid arthritis. Investigated for use/treatment in rheumatoid arthritis. Clenoliximab is a macaque-human chimeric monoclonal antibody (immunoglobulin G4)that binds specifically to the CD4 receptor present on T-lympocytes (Helper T lymphocytes). CD-4 lymphocytes are implicated in the pathogenesis of rheumatoid arthritis (RA). Clenoliximab coats the CD4 T-lymphocytes and thus down-modulates the CD4 T-lympocytes in a dose and concentration-dependent manner without decreasing the amount of CD4 T-lympocytes in circulation.,,,,Clenoliximab is investigational.,Clenoliximab is a solid.,True
19639,"Investigated for use/treatment in asthma, chronic obstructive pulmonary disease (COPD), cystic fibrosis, and rheumatoid arthritis. Amelubant is a long-acting oral Leukotriene B4 (LTB4) receptor antagonist. Amelubant is a prodrug which is metabolized by ubiquitous esterases to BIIL 260 and its glucuronidated metabolite BIIL 315.14. BIIL 260 and BIIL 315.14 interact directly with the LTB4 receptors. LTB4 is a chemotactic factor for immune cells and potentiates the immune response. The G-protein coupled receptors BLT1, (high affinity for LTB4, expressed in most leukocytes) and BLT2 (low affinity for LTB4) are responsible for mediating LTB4's effects.",,,,Amelubant is investigational.,Amelubant is a solid.,True
19640,,,,,M-Cresol is experimental.,M-Cresol is a solid.,False
19641,"Elotuzumab is a humanized IgG1 (Immunoglobulin G) monoclonal antibody indicated in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received one to three prior therapies. Elotuzumab targets SLAMF7, also known as Signaling Lymphocytic Activation Molecule Family member 7, a cell surface glycoprotein. Elotuzumab consists of the complementary determining regions (CDR) of the mouse antibody, MuLuc63, grafted onto human IgG1 heavy and kappa light chain frameworks. Elotuzumab is produced in NS0 cells by recombinant DNA technology. Elotuzumab has a theoretical mass of 148.1 kDa for the intact antibody. Elotuzumab was approved on November 30, 2015 by the U.S. Food and Drug Administration. Elotuzumab is marketed under the brand Empliciti™ by Bristol-Myers Squibb. Indicated in combination with lenalidomide and dexamethasone for the treatment of patients with multiple myeloma who have received one to three prior therapies. Elotuzumab is a humanized IgG1 monoclonal antibody that specifically targets the SLAMF7 (Signaling Lymphocytic Activation Molecule Family member 7) protein. SLAMF7 is expressed on myeloma cells independent of cytogenetic abnormalities. SLAMF7 is also expressed on Natural Killer cells, plasma cells, and at lower levels on specific immune cell subsets of differentiated cells within the hematopoietic lineage. Elotuzumab directly activates Natural Killer cells through both the SLAMF7 pathway and Fc receptors. Elotuzumab also targets SLAMF7 on myeloma cells and facilitates the interaction with Natural Killer cells to mediate the killing of myeloma cells through antibody-dependent cellular cytotoxicity (ADCC). In preclinical models, the combination of elotuzumab and lenalidomide resulted in enhanced activation of Natural Killer cells that was greater than the effects of either agent alone and increased anti-tumor activity in vitro and in vivo.",,,,Elotuzumab is approved.,Elotuzumab is a solid.,True
19642,"Investigated for use/treatment in autoimmune diseases. R438 is a selective Janus tyrosine kinase 3 (JAK3) inhibitor prodrug which is converted to its active metabolite R333. JAKs are cytoplasmic tyrosine kinases that are involved in immune system activation and cytokine signaling. They achieve their effects when coupled with signal tranducers and activators of transcription (STATs). JAK3 is critical to immune system activation, and high levels of JAK3 are expressed in cells and thyocytes, and are inducible in T and B cells. JAK3 is also found in nonhematopoietic cells, but its function in these cells is currently undetermined. JAK3 inhibitors impede the development of CD8 memory cells by attenuating the interleukin 7 (IL7) and interleukin 15 (IL-15) pathways, making it a promising drug for treatment of autoimmune disorders.",,,,R-348 is investigational.,R-348 is a solid.,True
19643,"Investigated for use/treatment in solid tumors. TRC105 is a first-in-class human chimeric monoclonal antibody that inhibits tumor growth by binding to CD105 (endoglin), a receptor over-expressed on proliferating endothelium that is required for angiogenesis (growth of new blood vessels). TRC105 has shown activity, as monotherapy or when combined with chemotherapy, in pre-clinical studies of breast and colorectal cancer. Pre-clinical data also indicate CD105 expression is increased following treatment of human cancer with anti-VEGF therapy. The target of TRC105 shares many features with the VEGF receptor. Most importantly, both the VEGF and CD105 receptors are essential for angiogenesis, in that deletion of either receptor prevents blood vessel formation in utero.",,,,Carotuximab is investigational.,Carotuximab is a solid.,True
19644,"Investigated for use/treatment in macular degeneration and eye disorders/infections. E10030 is an aptamer based, anti-platelet-derived growth factor (PDGF) which inhibits PDGF-B with high specificity and affinity. E10030 may be efficacious in treating neovascular age-related macular degeneration when combined with a vascular endothelial growth factor A (VEGF-A) inhibitor. PDGF-B is implicated in vascular stability and function through its role in activating the recruitment of mural cells (pericytes) by endothelial cells to envelop the developing vasculature. Pericyte recruitment is part of the maturation process in blood vessel development and pericytes act as support cells for mature blood vessels. ",,,,Pegpleranib is investigational.,Pegpleranib is a solid.,True
19645,"Inappropriate growth of or self-directed antibody production by B-cells is the etiological underpinning of a variety of conditions, including the multiple sclerosis-like neurological condition neuromyelitis optica spectrum disorder (NMOSD). Inebilizumab is a humanized afucosylated monoclonal IgG1 antibody directed against the broadly expressed B-cell surface antigen CD19. Inebilizumab is cytolytic, resulting in B-cell depletion and offering therapeutic benefit to patients suffering from NMOSD. Compared to the anti-CD20 antibody , which is also used to treat NMOSD, inebilizumab has broader specificity. Inebilizumab is indicated for the treatment of aquaporin-4 (AQP4) immunoglobulin-positive (AQP4-IgG) neuromyelitis optica spectrum disorder (NMOSD) in adult patients. Inebilizumab is a CD19-directed monoclonal antibody that results in immunosuppression through B-cell depletion with sufficient efficacy to allow a six-month dosing schedule. Due to this mechanism of action, patients undergoing inebilizumab treatment may be at higher risk of infections and should be monitored for active infections and immunoglobulin levels while undergoing treatment; vaccination is not recommended during inebilizumab treatment. Also, there is a risk of severe infusion reactions. Animal data suggests the possibility of fetal harm with inebilizumab and therefore, effective contraception during and for six months following inebilizumab treatment is recommended. Neuromyelitis optica spectrum disorder (NMOSD), formerly referred to as Devic's disease, is an antibody-mediated autoimmune condition resulting in astroglial cell death, demyelination, and central nervous system (CNS) inflammation. The presence of anti-aquaporin 4 immunoglobulin (AQP4-IgG) is the most frequent biomarker, although AQP4-IgG negative, anti-myelin oligodendrocyte glycoprotein (anti-MOG) positive, variants with similar presentation also exist. The theoretical origin of symptoms is through AQP4-IgG-mediated astrocyte cytotoxicity and subsequent infiltration of neutrophils, eosinophils, and macrophages, leading to inflammatory-mediated oligodendrocyte damage and myelin sheath loss. In general, this manifests as optic neuritis and transverse myelitis with occasional involvement of the diencephalic, brainstem, and cerebral hemisphere.",,,,Inebilizumab is approved and investigational.,Inebilizumab is a solid.,True
19646,"Tisagenlecleucel is a CD19-directed genetically modified autologous T cell immunotherapy, or a CAR-T cell therapy for B-cell acute lymphoblastic leukemia. It was granted approval by FDA in August 2017 under the market name Kymriah. Tisagenlecleucel is an immunocellular therapy that involves autologous T cells that are collected from each individual patient and genetically engineered to express a specific protein called a chimeric antigen receptor (CAR) that specifically target CD19 antigens. Modified T cells are infused back into the patient's body. These CD19-directed chimeric antigen receptors (CD19 CAR-T cells) direct the T cells to targt and kill leukiemia cells that express a specific antigen (CD19) on the cell surface. Indicated for the treatment of patients up to 25 years of age with B-cell precursor acute lymphoblastic leukemia (ALL) that is refractory or in second or later relapse.  Tisagenlecleucel demonstrates efficacy in re-inducing remission in patients with refractory B-cell precursor acute lymphoblastic leukemia. The sole purpose of the therapy is to eliminate Tisagenlecleucel is a CD19-directed genetically modified autologous T cell immunotherapy that involves genetically modified autologous T cells isolated from each individual patient. The reprogramming of the patient's T cells uses a lentiviral vector to encode an anti-CD19 chimeric antigen receptor (CAR). The CAR is comprised of a murine single-chain antibody fragment (scFv) specific for CD19, followed by a CD8 hinge and transmembrane region that is fused to the intracellular signaling domains from 4-1BB (CD137) and CD3 zeta. These intracellular costimulatory signaling domains increase the expansion, longer-term persistence and potency of CAR T cells : the CD3 zeta component is critical for initiating T-cell activation and antitumor activity, while 4-1BB enhances the expansion and persistence of tisagenlecleucel {FDA Label, A20379]. Upon binding to CD19-expressing cells, the CAR transmits a signal to promote T-cell expansion, activation, target cell elimination, and persistence of the tisagenlecleucel cells.",,,,Tisagenlecleucel is approved and investigational.,,True
19647,"Axicabtagene ciloleucel is a chimeric antigen receptor (CAR) T cell therapy for the treatment of Diffuse large B-cell lymphoma (DLBCL), which is a type of a non-Hodgkin lymphoma (NHL). It is the second cell-based gene therapy that is FDA-approved but the first in the treatment of large B-cell lymphoma in adult patients. Uniquely, axicabtagene ciloleucel utilizes each patient’s own immune system where each dose of the drug consists of the patient's genetically modified T-cells that were previously collected. The modified version of the T-cell expresses a new gene that targets and kills the lymphoma cells and is infused back into the patient.  Indicated for the treatment of adult patients with relapsed or refractory large B-cell lymphoma after two or more lines of systemic therapy, including diffuse large B-cell lymphoma (DLBCL) not otherwise specified, primary mediastinal large B-cell lymphoma, high grade B-cell lymphoma, and DLBCL arising from follicular lymphoma.  The levels of cytokines, chemokines and other blood molecules were measured over a 4-week interval after the drug infusion. There were transient elevations of chemokines such as IL-6, IL-8, IL-10, IL-15, TNF-α, IFN-γ, and sIL2Rα where the peak elevation was reached within the first 14 days after infusion, and the levels gradually returned to baseline within 28 days. It is likely that axicabtagene ciloleucel may lead to B cell aplasia, or low numbers of B cells or absent B cells, as expected by other chimeric anntigen receptor T-cell therapies.  The CD 19 antigen is a 95 kDa integral membrane glycoprotein expressed on lymphocytes of the B-cell lineage but noton pluripotent stem cell. While this antigen is ubiquitously expressed on B lymphocyte lineage, the expression of this Ig protein is downregulated during terminal differentiation of premature and mature B cells into plasma cells. In blood disorders, however, the expression CD19 is maintained in in B-lineage cells that has undergone neoplastic transformation. Thus CD19 plays a critical role in clinical oncolgy as it aids in the diagnosis of blood cancers such as leukemias and lymphomas and serves as a therapeutic target for immunotherapies.",,,,Axicabtagene ciloleucel is approved.,Axicabtagene ciloleucel is a solid.,True
19648,"Tafasitamab is a humanized, CD19-directed cytolytic monoclonal antibody intended for the treatment of B-cell malignancies. It is produced using recombinant DNA technology in Chinese hamster ovary cells, and contains an IgG1/2 hybrid Fc-domain which has been modified with 2 amino acid substitutions to enhance its cytotoxicity relative to non-engineered anti-CD19 antibodies. Tafasitamab is indicated, in combination with , for the treatment of adult patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) not otherwise specified whom are ineligible for autologous stem cell transplant (ASCT). Tafasitamab induces a reduction in circulating B-cell counts by binding to a surface antigen, CD19, which is important for their survival. Patients with relapsed or refractory diffuse large B-cell lymphoma (DLBCL) experienced a 97% reduction in peripheral blood B-cell counts following 8 days of treatment, with a 100% reduction reached within 16 weeks of treatment. The CD19 surface antigen is a protein expressed on the surface of pre-B and mature B-lymphocytes that appears to play a role in enhancing B-cell receptor signaling and is considered integral to their survival. These surface proteins are also highly expressed on several B-cell malignancies, such as chronic lymphocytic leukemia (CLL), small lymphocytic lymphoma (SLL), and diffuse large B-cell lymphoma (DLBCL).",,,,Tafasitamab is approved and investigational.,Tafasitamab is a solid.,True
19649,"TRC093 is a recombinant humanized IgG1k monoclonal antibody. Investigated for use/treatment in solid tumors and cancer/tumors (unspecified). TRC093 (MT293) is a recombinant humanized IgG1 monoclonal antibody that inhibits angiogenesis, tumor cell growth and metastasis by binding cleaved collagen, which is predominantly produced in the extracellular matrix of tumors. TRC093 targets collagen found in the basement membrane of tumor blood vessels. Collagen is a essential triple helix of polypeptide chains found in the extracellular matrix which is involved with many cellular processs including cell proliferation, adhesion, migration, and angiogenesis (neovascularization - growth of new blood vessels). Matrix metalloproteinase enzymes (MMPs) remodel and denature collagen during angiogenesis, causing changes in bioactive sites which results in altered proliferation, adhesion and migration of cells. TRC093 specifically binds to mice breast cancer blood vessel tumors, inhibiting tumor growth. It is proposed that TRC093 binds to hydroxyproline residues of GPO sequences (the major platelet-activating motif within collagen and essential for collagen folding) when they are exposed by thermal denaturation or partially proteolytically degraded by MMPs. TRC093 may target many different types of cancer as a critical component of the TRC093 epitope is a GPOG sequence which are present in high numbers in many different types of collagen. ",,,,TRC093 is investigational.,TRC093 is a solid.,True
19650,"Linaclotide is an orally administered, peptide agonist of guanylate cyclase 2C for the treatment of irritable bowel syndrome. Chemically, it is a heterodetic cyclic peptide and consists of fourteen amino acids. The protein sequence is as follows: Cys Cys Glu Tyr Cys Cys Asn Pro Ala Cys Thr Gly Cys Tyr. There are three disulfide bonds which are located between Cys1 and Cys6; between Cys2 and Cys10; and between Cys5 and Cys13. FDA approved on August 30, 2012. Treatment of irritable bowel syndrome (IBS) with constipation and chronic idiopathic constipation.  Changes in the appearance and consistency of stools as measured by the Bristol Stool Form Scale (BSFS) have been noted after taking linaclotide.  Linaclotide is an agonist of guanylate cyclase-C (GC-C). Once linaclotide and its active metabolite binds to GC-C, it has local effect on the luminal surface of the intestinal epithelium. Activation of GC-C by linaclotide results in the intra- and extracellular increase of cyclic guanosine monophosphate concentrations (cGMP). This elevation of cGMP levels stimulates the secretion of chloride and bicarbonate into the intestinal lumen via activation of cystic fibrosis transmembrane conductance regulator (CFTR) ion channel. Ultimately, linaclotide helps patients with IBS (especially with constipation) as GI transit is accelerated and the release of intestinal fluid is increased. In animal models, a decrease in visceral pain after administration of linaclotide may be observed. A decrease in the activity of pain-sensing nerves occurs as a result of an increase in extracellular cGMP. ",The molecular weight is 1526.73.,Linaclotide has a topological polar surface area of 573.91.,The log p value of  is -3.12.,Linaclotide is approved.,Linaclotide is a solid.,True
19651,ORE1001 has been used in trials studying the treatment of Mild to Moderate Ulcerative Colitis. It is an ACE2 inhibitor.,,,,ORE-1001 is investigational.,,True
19652,"An indolizidine alkaloid from the plant Swainsona canescens that is a potent alpha-mannosidase inhibitor. Swainsonine also exhibits antimetastatic, antiproliferative, and immunomodulatory activity. Tridolgosir competitively inhibits the alpha manosidase II (alphaMII), which processes N linked carbohydrates of newly synthesized glycoproteins passing through the Golgi apparatus to the cell surface. Highly branched carbohydrate structures are created which bind to Lectin-phytohemagglutinin (L-PHA) and are subsequently expressed in different tumor types which results in metastatic phenotype, which is correlated with an increased aggressiveness in animals and causes other human malignancies. Inhibition of alphaMII reduces carbohydrates that bind to L-PHA, reducing aggressiveness, metastatic phenotype cells, slows tumor growth, and increases“hybrid type” carbohydrates on the cell surface. Hybrid type carbohydrates may increase cytokine activation of lymphocytes, increasing tumor susceptibility to lymphokine activated and natural killer cells.",,,,Tridolgosir is experimental.,Tridolgosir is a solid.,True
19653,,,,,2-deoxy-2-fluoro-alpha-D-mannosyl fluoride is experimental.,2-deoxy-2-fluoro-alpha-D-mannosyl fluoride is a solid.,False
19654,,,,,Ghavamiol is experimental.,Ghavamiol is a solid.,False
19655,,,,,5-fluoro-beta-L-gulosyl fluoride is experimental.,5-fluoro-beta-L-gulosyl fluoride is a solid.,False
19656,,,,,5-Thio-a/B-D-Mannopyranosylamine is experimental.,5-Thio-a/B-D-Mannopyranosylamine is a solid.,False
19657,An alpha-glucosidase inhibitor with antiviral action. Derivatives of deoxynojirimycin may have anti-HIV activity. ,,,,1-deoxymannojirimycin is experimental.,1-deoxymannojirimycin is a solid.,True
19658,,,,,"(1R,2R,3R,4S,5R)-4-(BENZYLAMINO)-5-(METHYLTHIO)CYCLOPENTANE-1,2,3-TRIOL is experimental.","(1R,2R,3R,4S,5R)-4-(BENZYLAMINO)-5-(METHYLTHIO)CYCLOPENTANE-1,2,3-TRIOL is a solid.",False
19659,,,,,"(1S,2S,3R,6R)-4-(hydroxymethyl)-6-(octylamino)cyclohex-4-ene-1,2,3-triol is experimental.","(1S,2S,3R,6R)-4-(hydroxymethyl)-6-(octylamino)cyclohex-4-ene-1,2,3-triol is a solid.",False
19660,"Sibrotuzumab is a humanized monoclonal antibody directed against fibroblast activation protein (FAP). It is used to treat cancer. Investigated for use/treatment in cancer/tumors (unspecified), colorectal cancer, and lung cancer. Human FAP is unique in its selective expression by tumor stromal fibroblasts in epithelial carcinomas, but not by epithelial carcinoma cells, normal fibroblasts, or other normal tissues. Therefore, FAP is an attractive target for the study of tumor stromal cell biology and provides valuable insights into the roles of the tumor microenvironment. Sibrotuzumab is a humanized monoclonal antibody designed to attack the cell-surface antigen FAP.",,,,Sibrotuzumab is investigational.,Sibrotuzumab is a solid.,True
19661,"Abaloparatide is an analog of PTHrP (parathyroid hormone-related protein). It was approved in April 28, 2017 by the FDA (as Tymlos) for the treatment of postmenopausal women with osteoporosis at high risk for fracture. Abaloparatide is a synthetic peptide that is related to hPTHrP and has demonstrated in preclinical testing the potential to widen the anabolic window for bone therapeutics, stimulating bone formation with a limited effect on bone resorption and mineral mobilization. This could enable improved convenience over currently available anabolic therapies, resulting in greater compliance and, ultimately, greater benefit to patients. Investigated for use/treatment in postmenopausal osteoporosis to reduce vertebral and/or non-vertebral fractures. Abaloparatide (BA058), a proprietary analog of human parathyroid hormone-related protein (hPTHrP), is currently undergoing clinical trials by the company for the treatment of osteoporosis in postmenopausal women. PTHrP is a critical peptide for promoting new bone formation, with a distinct role from parathyroid hormone, or PTH, which primarily regulates calcium homeostasis and bone resorption. Clinical studies show increased bone mineral density (BMD) and levels of bone formation markers in a dose-response relationship. In target cells, abaloparatide acts as an agonist on PTH type 1 receptor (PTH1R) and activates both G protein–mediated cAMP signaling and β-arrestin-mediated ERK-1/2 signaling pathways with similar potency. Abaloparatide binds to RG conformation of PTH1R with greater selectivity that results in more transient cell signalling responses. ",The molecular weight is 3960.66.,Abaloparatide has a topological polar surface area of 1738.6.,,Abaloparatide is approved and investigational.,Abaloparatide is a liquid.,True
19662,"Parathyroid hormone (PTH) is a single-chain polypeptide composed of 84 amino acids. Available as Preotact, it is an identical form of human recombinant hormome which produced as a fusion protein undergoeing post-translational processing involving the cleavage of the OmpA leader sequence, leaving the mature protein as a single-chain 84 amino-acids polypeptide (9.4 kDa). For use/treatment in osteoporosis. Parathyroid hormone is responsible for the fine regulation of serum calcium concentration on a minute-to-minute basis. This is achieved by the acute effects of the hormone on calcium resorption in bone and calcium reabsorption in the kidney. The phosphate mobilized from bone is excreted into the urine by means of the hormone's influence on renal phosphate handling. Parathyroid hormone also stimulates calcium absorption in the intestine, this being mediated indirectly by 1,25-dihydroxyvitamin D. Thus, a hypocalcemic stimulus of parathyroid hormone secretion results in an increased influx of calcium from three sources (bone, kidney, and intestine), resulting in a normalization of the serum calcium concentration without change in the serum phosphate concentration. The biological actions of rhPTH are mediated through binding to at least two distinct high- affinity cell-surface receptors specific for the N-terminal and C-terminal regions of the molecule, both of which are required for normal bone metabolism. The N-terminal portion of the molecule is primarily responsible for the bone building effects of parathyroid hormone. The C-terminal portion of the molecule has antiresorptive activity and is necessary for normal regulation of N-terminal fragment activity.",,,,Parathyroid hormone is approved and investigational.,Parathyroid hormone is a solid.,True
19663,"Teriparatide (recombinant human parathyroid hormone) is a potent anabolic agent used in the treatment of osteoporosis. It is manufactured and marketed by Eli Lilly and Company. For the treatment of osteoporosis in men and postmenopausal women who are at high risk for having a fracture. Also used to increase bone mass in men with primary or hypogonadal osteoporosis who are at high risk for fracture. Clinical trials indicate that teriparatide increases predominantly trabecular bone in the lumbar spine and femoral neck; it has less significant effects at cortical sites. The combination of teriparatide with antiresorptive agents is not more effective than teriparatide monotherapy. The most common adverse effects associated with teriparatide include injection-site pain, nausea, headaches, leg cramps, and dizziness. After a maximum of two years of teriparatide therapy, the drug should be discontinued and antiresorptive therapy begun to maintain bone mineral density. Teriparatide is the portion of human parathyroid hormone (PTH), amino acid sequence 1 through 34 of the complete molecule which contains amino acid sequence 1 to 84. Endogenous PTH is the primary regulator of calcium and phosphate metabolism in bone and kidney. Daily injections of teriparatide stimulates new bone formation leading to increased bone mineral density.",The molecular weight is 4117.77.,Teriparatide has a topological polar surface area of 1752.65.,,Teriparatide is approved and investigational.,Teriparatide is a liquid.,True
19664,,,,,"4'-FLUORO-1,1'-BIPHENYL-4-CARBOXYLIC ACID is experimental.","4'-FLUORO-1,1'-BIPHENYL-4-CARBOXYLIC ACID is a solid.",False
19665,Gossypol has been used in trials studying the treatment of Non-small Cell Lung Cancer.,The molecular weight is 518.56.,Gossypol has a topological polar surface area of 155.52.,The log p value of  is 5.76.,Gossypol is investigational.,,True
19666,"Anatibant is a selective, very potent, small-molecule Bradykinin B2 receptor antagonist. It is developed for the for the treatment of traumatic brain injury (TBI). Investigated for use/treatment in traumatic brain injuries. Anatibant is a new potent and selective non-peptide antagonist of the bradyknin B2 receptor. Anatibant crosses the blood brain barrier, reduces brain edema formation and brain damage, and improves neurological function following experimental traumatic brain injury. The underlying mechanisms are still not well understood. So far bradykinin B2 receptor-mediated neuroprotection was mainly explained by the reduction of vascular permeability and subsequent reduction of post-ischemic or post-traumatic brain edema. ",,,,Anatibant is investigational.,Anatibant is a solid.,True
19667,Investigated for use/treatment in brain cancer and pediatric indications.,,,,Labradimil is investigational.,Labradimil is a solid.,True
19668,"Bimoclomol is an investigational drug that induces stress proteins and has cytoprotective effects. Investigated for use/treatment in neuropathy (diabetic) and wounds. Bimoclomol binds to HSF-1 and induces a prolonged binding of HSF-1 to the respective DNA elements. Since HSF-1 does not bind to DNA in the absence of stress, the bimoclomol-induced extension of HSF-1/DNA interaction may contribute to the chaperone co-induction of bimoclomol observed previously. These findings indicate that bimoclomol may be of value in targeting HSF-1 so as to induce up-regulation of protective Hsp-s in a non-stressful manner and for therapeutic benefit.",,,,Bimoclomol is investigational.,Bimoclomol is a solid.,True
19669,Vinylglycine is an irreversible inhibitor of aspartate aminotransferase.,,,,Vinylglycine is experimental.,Vinylglycine is a solid.,True
19670,Recombinant osteoprotegerin (AMGN-0007) is a recombinant OPG construct developed as a potential therapeutic agent in the treatment of bone disease. Investigated for use/treatment in osteoporosis and bone metastases.,,,,AMGN-0007 is investigational.,AMGN-0007 is a solid.,True
19671,"Denosumab is a novel, fully human IgG2 monoclonal antibody specific to receptor activator of nuclear factor kappa-B ligand (RANKL), suppresses bone resorption markers in patients with a variety of metastatic tumors and is being investigated in multiple clinical trials for the prevention and treatment of bone metastases. Chemically, it consists of 2 heavy and 2 light chains. Each light chain consists of 215 amino acids. Each heavy chain consists of 448 amino acids with 4 intramolecular disulfides. FDA approved on June 1, 2010. Prolia is indicated for the treatment of postmenopausal women with osteoporosis at high risk for fracture. It reduces the incidence of vertebral, nonvertebral, and hip fractures. Prolia is also indicated as a treatment to increase bone mass in women at high risk for fracture receiving adjuvant aromatase inhibitor therapy for breast cancer. It can also be used in men with osteoporosis at high risk for fracture or in men receiving androgen deprivation therapy for nonmetastatic prostate cancer to increase bone mass. Xgeva is indicated for the prevention of skeletal-related events in patients with bone metastases from solid tumors. In clinical studies, treatment with 60 mg of Prolia resulted in reduction in the bone resorption marker serum type 1 C-telopeptide (CTX) by approximately 85% by 3 days. Consistent with the physiological coupling of bone formation and resorption in skeletal remodeling, subsequent reductions in bone formation markers (i.e. osteocalcin and procollagen type 1 N-terminal peptide ) were observed starting 1 month after the first dose of Prolia. Denosumab is designed to target RANKL (RANK ligand), a protein that acts as the primary signal to promote bone removal/resorption. In many bone loss conditions, RANKL overwhelms the body's natural defense against bone destruction. Denosumab prevents RANKL from activating its receptor, RANK, on the surface of osteoclasts and their precursors. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function, and survival, thereby decreasing bone resorption and increasing bone mass and strength in both cortical and trabecular bone.",,,,Denosumab is approved.,Denosumab is a solid.,True
19672,"Pascolizumab (SB 240683) is a humanized anti-interleukin-4 antibody with therapeutic potential in asthma. Investigated for use/treatment in asthma. Pascolizumab is a humanized anti-IL-4 monoclonal antibody that can inhibit upstream and downstream events associated with asthma, including (T(H)2) cell activation and immunoglobulin E production.",,,,Pascolizumab is investigational.,Pascolizumab is a solid.,True
19673,,,,,N-hydroxy-5-pyrazin-7(8H)-yl)carbonyl]thiophene-2-carboxamide is experimental.,N-hydroxy-5-pyrazin-7(8H)-yl)carbonyl]thiophene-2-carboxamide is a solid.,False
19674,,,,,"2,2,2-TRIFLUORO-1-{5-PYRAZIN-7(8H)-YL)CARBONYL]THIOPHEN-2-YL}ETHANE-1,1-DIOL is experimental.","2,2,2-TRIFLUORO-1-{5-PYRAZIN-7(8H)-YL)CARBONYL]THIOPHEN-2-YL}ETHANE-1,1-DIOL is a solid.",False
19675,"Dotatate gallium (Ga-68) is a somatostatin-2 receptor analog which is radiolabeled with gallium 68 as a positron-emitting radioisotope. Ga-68 dotatate has a high affinity for somatostatin-2 receptor and it is rapidly excreted from the nontarget sites which gives it an ideal candidate for imaging neuroendocrine tumors. Dotatate gallium (Ga-68) explotes its ability to detect somatostatin receptor scintigraphy and this characteristic tends to change with tumor grade which gives Ga-68 dotate a high diagnostic value. Dotatate gallium 68 was developed by Advanced Accelerator Applications USA, Inc. and FDA approved in June 1, 2016. Dotatate gallium 68 is one of the most prominent radiopharmaceuticals used in imaging with positron emission tomography. It binds to the somatostatin-2 receptor which is usually overexpressed in many neuroendocrine tumors in both adult and pediatric patients. The neuroendocrine tumors are bening or malignant tumors produced in the hormone producing cells of the neuroendocrine system.  The overexpression of somatostatin receptor in tumor tissue has been widely studied and the usage of scintigraphy for the diagnostic of neuroendocrine tumors has been happening since the beggining of the 90s. The development of positron-emission tomography there has been an emerging and growing field for the discovery of tracer labeled somatostatin analogues like dotatate gallium 68. Even after all the reportes, the pharmacodynamic profile of dotatate gallium 68 has not been studied. The somatostatin receptor-based imaging is the preferred choice in the diagnostic and management of neuroendocrine tumors. The basis for the mechanism of dotatate gallium 68 is the binding of a ligand analog that is radiolabeled, in this case thye preferred binding site is the receptors of the subtype 2. The malignant cells are reported to overexpress the somatostatin subtype 2 receptor. Dotatate gallium 68 is a β+ emiting radionuclide with an emission yield that can be detected by the positron emission tomography and thus the seletive binding to the overexpressed somatostatin receptor will be detected.",,,,Dotatate gallium Ga-68 is approved and investigational.,Dotatate gallium Ga-68 is a solid.,True
19676,,,,,Trans-O-Hydroxy-Alpha-Methyl Cinnamate is experimental.,Trans-O-Hydroxy-Alpha-Methyl Cinnamate is a solid.,False
19677,,,,,"2,4-Dihydroxy-Trans Cinnamic Acid is experimental.","2,4-Dihydroxy-Trans Cinnamic Acid is a solid.",False
19678,,,,,Phenylethane Boronic Acid is experimental.,Phenylethane Boronic Acid is a solid.,False
19679,,,,,"1,1,1-TRIFLUORO-3-ACETAMIDO-4-PHENYL BUTAN-2-ONE(N-ACETYL-L-PHENYLALANYL TRIFLUOROMETHYL KETONE) is experimental.","1,1,1-TRIFLUORO-3-ACETAMIDO-4-PHENYL BUTAN-2-ONE(N-ACETYL-L-PHENYLALANYL TRIFLUOROMETHYL KETONE) is a solid.",False
19680,,,,,"N-(1-BENZYL-3,3,3-TRIFLUORO-2,2-DIHYDROXY-PROPYL)-ACETAMIDE is experimental.","N-(1-BENZYL-3,3,3-TRIFLUORO-2,2-DIHYDROXY-PROPYL)-ACETAMIDE is a solid.",False
19681,,,,,3-(4-DIETHYLAMINO-2-HYDROXY-PHENYL)-2-METHYL-PROPIONIC ACID is experimental.,3-(4-DIETHYLAMINO-2-HYDROXY-PHENYL)-2-METHYL-PROPIONIC ACID is a solid.,False
19682,,,,,2-ACETYLAMINO-4-METHYL-PENTANOIC ACID (1-FORMYL-2-PHENYL-ETHYL)-AMIDE is experimental.,2-ACETYLAMINO-4-METHYL-PENTANOIC ACID (1-FORMYL-2-PHENYL-ETHYL)-AMIDE is a solid.,False
19683,,,,,(2S) N-acetyl-L-alanyl-αL-phenylalanyl-chloroethylketone is experimental.,(2S) N-acetyl-L-alanyl-αL-phenylalanyl-chloroethylketone is a solid.,False
19684,,,,,"1,1,1-TRIFLUORO-3-((N-ACETYL)-L-LEUCYLAMIDO)-4-PHENYL-BUTAN-2-ONE(N-ACETYL-L-LEUCYL-L-PHENYLALANYL TRIFLUOROMETHYL KETONE) is experimental.","1,1,1-TRIFLUORO-3-((N-ACETYL)-L-LEUCYLAMIDO)-4-PHENYL-BUTAN-2-ONE(N-ACETYL-L-LEUCYL-L-PHENYLALANYL TRIFLUOROMETHYL KETONE) is a solid.",False
19685,,,,,Phenylalanylmethylchloride is experimental.,Phenylalanylmethylchloride is a solid.,False
19686,,,,,L-1-naphthyl-2-acetamido-ethane boronic acid is experimental.,L-1-naphthyl-2-acetamido-ethane boronic acid is a solid.,False
19687,,,,,D-1-naphthyl-2-acetamido-ethane boronic acid is experimental.,D-1-naphthyl-2-acetamido-ethane boronic acid is a solid.,False
19688,,,,,D-1-(4-chlorophenyl)-2-(acetamido)ethane boronic acid is experimental.,D-1-(4-chlorophenyl)-2-(acetamido)ethane boronic acid is a solid.,False
19689,,,,,L-1-(4-chlorophenyl)-2-(acetamido)ethane boronic acid is experimental.,L-1-(4-chlorophenyl)-2-(acetamido)ethane boronic acid is a solid.,False
19690,,,,,7-(5-DEOXY-BETA-D-RIBOFURANOSYL)-5-IODO-7H-PYRROLOPYRIMIDIN-4-AMINE is experimental.,7-(5-DEOXY-BETA-D-RIBOFURANOSYL)-5-IODO-7H-PYRROLOPYRIMIDIN-4-AMINE is a solid.,False
19691,,,,,5--6-PYRIMIDIN-4-AMINE is experimental.,5--6-PYRIMIDIN-4-AMINE is a solid.,False
19692,Indirubin is under investigation in clinical trial NCT01735864 (Dosage Determination Trial for Indigo Naturalis Extract in Oil Ointment).,,,,Indirubin is investigational.,,True
19693,,,,,4-(4-Chlorophenyl)Imidazole is experimental.,4-(4-Chlorophenyl)Imidazole is a solid.,False
19694,,,,,Cyclohexyl-pentyl-maltoside is experimental.,Cyclohexyl-pentyl-maltoside is a solid.,False
19695,,,,,1-(biphenyl-4-ylmethyl)-1H-imidazole is experimental.,1-(biphenyl-4-ylmethyl)-1H-imidazole is a solid.,False
19696,"A complex of gadolinium with a chelating agent, diethylenetriamine penta-acetic acid (DTPA see pentetic acid), that is given to enhance the image in cranial and spinal MRIs. (From Martindale, The Extra Pharmacopoeia, 30th ed, p706) For use with magnetic resonance imaging (MRI) in adults, and pediatric patients (2 years of age and older) to visualize lesions with abnormal vascularity in the brain (intracranial lesions), spine and associated tissues as well as lesions with abnormal vascularity in the head and neck. Also used to facilitate the visualization of lesions with abnormal vascularity in the body (excluding the heart). Based on the behavior of protons when placed in a strong magnetic field, which is interpreted and transformed into images by magnetic resonance (MR) instruments. MR images are based primarily on proton density and proton relaxation dynamics. MR instruments are sensitive to two different relaxation processes, the T1 (spin-lattice or longitudinal relaxation time) and T2 (spin-spin or transverse relaxation time). Paramagnetic agents contain one or more unpaired electrons that enhance the T1 and T2 relaxation rates of protons in their molecular environment. The proton relaxation effect (PRE) of an unpaired electron is 700 times stronger than that of a proton itself. In MRI, visualization of normal and pathological brain tissue depends in part on variations in the radio frequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in T2. When placed in a magnetic field, gadopentetate dimeglumine shortens the T1 and T2 relaxation times in tissues where it accumulates. In the central nervous system (CNS), gadopentetate dimeglumine enhances visualization of normal tissues that lack a blood-brain barrier, such as the pituitary gland and the meninges. Gadopentetate dimeglumine does not cross the intact blood-brain barrier; therefore, it does not accumulate in normal brain tissue or in CNS lesions that have not caused an abnormal blood-brain barrier (e.g., cysts, mature post-operative scars). Abnormal vascularity or disruption of the blood-brain barrier allows accumulation of gadopentetate dimeglumine in lesions such as neoplasms, abscesses, and subacute infarcts. Outside the CNS, gadopentetate dimeglumine rapidly reaches equilibrium in the interstitial compartment and enhances signal in all tissues as a function of delivery and size of the interstitial compartment.",The molecular weight is 545.56.,,,Gadopentetic acid is approved.,Gadopentetic acid is a solid.,True
19697,,,,,Nicotinamide 8-bromo-adenine dinucleotide phosphate is experimental.,Nicotinamide 8-bromo-adenine dinucleotide phosphate is a solid.,False
19698,,,,,"(5E,13E)-11-HYDROXY-9,15-DIOXOPROSTA-5,13-DIEN-1-OIC ACID is experimental.","(5E,13E)-11-HYDROXY-9,15-DIOXOPROSTA-5,13-DIEN-1-OIC ACID is a solid.",False
19699,Dinoprost has been investigated in Headache.,The molecular weight is 354.49.,Dinoprost has a topological polar surface area of 97.99.,The log p value of  is 2.27.,Dinoprost is approved and investigational.,,True
19700,Ramatroban has been used in trials studying the treatment of Asthma.,The molecular weight is 416.47.,Ramatroban has a topological polar surface area of 88.4.,The log p value of  is 3.97.,Ramatroban is investigational.,,True
19701,,,,,Octylphenoxy polyethoxyethanol is experimental.,Octylphenoxy polyethoxyethanol is a solid.,False
19702,The bafilomycins refer to a category of toxic macrolide antibiotics that are derivatives of Streptomyces griseus. These compounds all appear in the same fermentation and have similar biological activity. Bafilomycins are specific inhibitors of vacuolar-type H+-ATPase. (V-ATPase). The most commonly utilized bafilomycin is bafilomycin A1. This is a useful tool as it can prevent the re-acidification of synaptic vesicles once they have undergone exocytosis. The bafilomycins are a family of toxic macrolide antibiotic derived from Streptomyces griseus. These compounds all appear in the same fermentation and have quite similar biological activity. Bafilomycins are specific inhibitors of vacuolar-type H+-ATPase. (V-ATPase).,,,,Bafilomycin A1 is experimental.,Bafilomycin A1 is a solid.,True
19703,,,,,Bafilomycin B1 is experimental.,Bafilomycin B1 is a solid.,False
19704,,,,,Farnesyl thiopyrophosphate is experimental.,Farnesyl thiopyrophosphate is a solid.,False
19705,,,,,"(1-HYDROXYHEPTANE-1,1-DIYL)BIS(PHOSPHONIC ACID) is experimental.","(1-HYDROXYHEPTANE-1,1-DIYL)BIS(PHOSPHONIC ACID) is a solid.",False
19706,,,,,"(1-HYDROXYNONANE-1,1-DIYL)BIS(PHOSPHONIC ACID) is experimental.","(1-HYDROXYNONANE-1,1-DIYL)BIS(PHOSPHONIC ACID) is a solid.",False
19707,,,,,"(2,2-DIPHOSPHONOETHYL)(DODECYL)DIMETHYLPHOSPHONIUM is experimental.","(2,2-DIPHOSPHONOETHYL)(DODECYL)DIMETHYLPHOSPHONIUM is a solid.",False
19708,,,,,-PHOSPHONIC ACID is experimental.,-PHOSPHONIC ACID is a solid.,False
19709,,,,,Lauryl alcohol diphosphonic acid is experimental.,Lauryl alcohol diphosphonic acid is a solid.,False
19710,,,,,"(6E,11E)-HEPTADECA-6,11-DIENE-9,9-DIYLBIS(PHOSPHONIC ACID) is experimental.","(6E,11E)-HEPTADECA-6,11-DIENE-9,9-DIYLBIS(PHOSPHONIC ACID) is a solid.",False
19711,"Plecanatide is a drug approved in January 2017 by the FDA for the treatment of chronic idiopathic constipation (CIC). It should not be used in children less than six years of age, and should be avoided in patients six years to 18 years of age Plecanatide stimulates intestinal fluid secretions in the gastrointestinal tract to support regular bowel function. Plecanatide, taken orally once daily, works locally in the upper GI tract to stimulate secretion of intestinal fluid and support regular bowel function. Food Effect Subjects who received either a low-fat, low calorie (LF-LC) meal or a high fat, high calorie (HF-HC) meal reported looser stools than fasted subjects up to 24 hours after a single dose of 9 mg (3 times the recommended dose). In clinical studies, Plecanatide was administered with or without food. Guanylate cyclase C (GC-C) agonist",The molecular weight is 1681.89.,Plecanatide has a topological polar surface area of 718.13.,,Plecanatide is approved and investigational.,Plecanatide is a solid.,True
19712,"A central respiratory stimulant with a brief duration of action. (From Martindale, The Extra Pharmocopoeia, 30th ed, p1225) For use as a temporary measure in hospitalized patients with acute respiratory insufficiency superimposed on chronic obstructive pulmonary disease. Doxapram is an analeptic agent (a stimulant of the central nervous system). The respiratory stimulant action is manifested by an increase in tidal volume associated with a slight increase in respiratory rate. A pressor response may result following doxapram administration. Provided there is no impairment of cardiac function, the pressor effect is more marked in hypovolemic than in normovolemic states. The pressor response is due to the improved cardiac output rather than peripheral vasoconstriction. Following doxapram administration, an increased release of catecholamines has been noted. Doxapram produces respiratory stimulation mediated through the peripheral carotid chemoreceptors. It is thought to stimulate the carotid body by inhibiting certain potassium channels.",The molecular weight is 378.52.,Doxapram has a topological polar surface area of 32.78.,The log p value of  is 3.24.,Doxapram is approved and vet_approved.,Doxapram is a solid.,True
19713,"Gantacurium chloride is a new, investigational, non-depolarizing ultra-short acting neuromuscular blocker. It is being developed by Avera Pharmaceuticals. Investigated for use/treatment in anesthesia (unspecified). Gantacurium chloride administered to anesthetized and ventilated healthy volunteers, caused dose dependent transient decrease in arterial blood pressure, mild histamine release at higher doses and no consistent changes in pulmonary compliance.",,,,Gantacurium is investigational.,Gantacurium is a solid.,True
19714,,,,,5beta-dihydrotestosterone is experimental.,5beta-dihydrotestosterone is a solid.,False
19715,,,,,"N,4-Dimethyl-N-(1-phenyl-1H-pyrazol-5-yl)benzenesulfonamide is experimental.","N,4-Dimethyl-N-(1-phenyl-1H-pyrazol-5-yl)benzenesulfonamide is a solid.",False
19716,,,,,Undecyl-Phosphinic Acid Butyl Ester is experimental.,Undecyl-Phosphinic Acid Butyl Ester is a solid.,False
19717,,,,,alpha-D-mannose 6-phosphate is experimental.,alpha-D-mannose 6-phosphate is a solid.,False
19718,"Cerliponase alfa is an enzyme replacement treatment for a specific form of Batten disease. It was the first FDA-approved treatment to slow loss of walking ability (ambulation) in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase-1 (TPP1) deficiency. Intraventricular administration of the drug allows significant uptake into the brain. Cerliponase alfa was approved in April, 2017 (as Brineura). Cerliponase alfa is a treatment for late infantile neuronal ceroid lipofuscinosis type 2 (CLN2) disease to decelerate the progressive motor function decline in patients 3 years of age and older. CLN2 disease is a form of Batten disease, a rare inherited neurodegenerative disorder and is associated with seizures, ataxia, rapid loss of language and motor functions, blindness, and early death. It is caused by the lack the lysosomal enzyme tripeptidyl peptidase-1 (TPP1) and subsequent accumulation of lysosomal storage materials normally metabolized by this enzyme in the central nervous system. Cerliponase alfa contains the active substance tripeptidyl peptidase-1 (rhTPP1), a recombinant human lysosomal exopeptidase which cleaves the N-terminal of tripeptides with a broad substrate specificity. Cerliponase alfa slows the progressive decline in motor function caused by abnormal motor signalling in the brain by restoring the normal levels and activity of TPP1.  The mature form of enzyme contains 5 consensus N-glycosylation sites with high mannose, phosphorylated high mannose and complex glycosylation structures. It is taken up by LINCL fibroblasts and translocated to the lysosomes through the Cation Independent Mannose-6-Phosphate Receptor (CI-MPR, also known as",,,,Cerliponase alfa is approved and investigational.,Cerliponase alfa is a liquid.,True
19719,Saccharin has been investigated for the treatment of Hypertension and Hyperglycemia.,,,,Saccharin is investigational.,,True
19720,"Mafenide is a sulfonamide-type antimicrobial agent used to treat severe burns. It acts by reducing the bacterial population present in the burn tissue and promotes healing of deep burns. Indicated for use as an adjunctive topical antimicrobial agent to control bacterial infection when used under moist dressings over meshed autografts on excised burn wounds. The precise mechanism of mafenide is unknown. However, mafenide reduces the bacterial population in the avascular burn tissue and promotes spontaneous heeling of deep burns. ",The molecular weight is 186.23.,Mafenide has a topological polar surface area of 86.18.,The log p value of  is -0.74.,Mafenide is approved and vet_approved.,Mafenide is a solid.,True
19721,,,,,"N-(4-chlorobenzyl)-N-methylbenzene-1,4-disulfonamide is experimental.","N-(4-chlorobenzyl)-N-methylbenzene-1,4-disulfonamide is a solid.",False
19722,"Volixibat, also known as SHP626 or LUM002, is an investigational drug that will potentially be used for the treatment of Non-Alcoholic Steatohepatitis (NASH). If approved for use, it will be the first available agent for the treatment of NASH. Volixibat is an investigational drug that has not been approved for use in any conditions. Volixibat is a selective inhibitor of the apical sodium-dependent bile acid transporter (ASBT), a transmembrane protein primarily expressed by enterocytes of the ileum. ASBT is primarily responsible for the recirculation of bile acids and therefore for hepatic lipid and glucose metabolism. Inhibiting this enzyme results in a decrease of bile acids returning to the liver, which is helpful for the treatment of NASH as abnormal cholesterol metabolism and accumulation of free cholesterol in the liver have been implicated in its pathogenesis. ",,,,Volixibat is experimental and investigational.,Volixibat is a solid.,True
19723,"Ginsenosides are a class of steroid glycosides, and triterpene saponins, found exclusively in the plant genus Panax (ginseng). Ginsenosides have been the target of research, as they are viewed as the active compounds behind the claims of ginseng's efficacy. Because ginsenosides appear to affect multiple pathways, their effects are complex and difficult to isolate. Rb1 appears to be most abundant in Panax quinquefolius (American Ginseng). Rb1 seems to affect the reproductive system in animal testicles. Recent research shows that Rb1 affects rat embryo development and has teratogenic effects, causing birth defects. Another study shows that Rb1 may increase testosterone production in male rats indirectly through the stimulation of the luteinizing hormone.",,,,Ginsenoside Rb1 is nutraceutical.,Ginsenoside Rb1 is a solid.,True
19724,"Ginsenosides are a class of steroid glycosides, and triterpene saponins, found exclusively in the plant genus Panax (ginseng). Ginsenosides have been the target of research, as they are viewed as the active compounds behind the claims of ginseng's efficacy. Because ginsenosides appear to affect multiple pathways, their effects are complex and difficult to isolate. Rg1 Appears to be most abundant in Panax ginseng (Chinese/Korean Ginseng). It improves spatial learning and increase hippocampal synaptophysin level in mice, plus demonstrates estrogen-like activity.",,,,Ginsenoside Rg1 is nutraceutical.,Ginsenoside Rg1 is a solid.,True
19725,,,,,"(1R)-N,6-DIHYDROXY-7-METHOXY-2--1,2,3,4-TETRAHYDROISOQUINOLINE-1-CARBOXAMIDE is experimental.","(1R)-N,6-DIHYDROXY-7-METHOXY-2--1,2,3,4-TETRAHYDROISOQUINOLINE-1-CARBOXAMIDE is a solid.",False
19726,,,,,"N4-HYDROXY-2-ISOBUTYL-N1-(9-OXO-1,8-DIAZA-TRICYCLONONADECA-12(19),13,15,17-TETRAEN-10-YL)-SUCCINAMIDE is experimental.","N4-HYDROXY-2-ISOBUTYL-N1-(9-OXO-1,8-DIAZA-TRICYCLONONADECA-12(19),13,15,17-TETRAEN-10-YL)-SUCCINAMIDE is a solid.",False
19727,,,,,"5-METHYL-3-(9-OXO-1,8-DIAZA-TRICYCLONONADECA-12(19),13,15,17-TETRAEN-10-YLCARBAMOYL)-HEXANOIC ACID is experimental.","5-METHYL-3-(9-OXO-1,8-DIAZA-TRICYCLONONADECA-12(19),13,15,17-TETRAEN-10-YLCARBAMOYL)-HEXANOIC ACID is a solid.",False
19728,,,,,Nα-amino}-2-phenylethyl](hydroxy)phosphoryl]methyl}-5-phenylpentanoyl]-L-tryptophanamide is experimental.,Nα-amino}-2-phenylethyl](hydroxy)phosphoryl]methyl}-5-phenylpentanoyl]-L-tryptophanamide is a solid.,False
19729,"Diosmin is a semisynthetic drug indicated for the treatment of venous disease. Diosmin is a flavone that can be found in the plant Teucrium gnaphalodes. Diosmin is available as a prescription medicine in several European countries, and is available as a nutritional supplement in the United States and the rest of Europe. It should be noted that clinical studies have been inconclusive and no articles have been published pertaining to its use in the treatment of vascular disease. When used in rats, diosmin has been effective at mitigating hyperglycaemia, and may also have antineurodegenerative properties.",The molecular weight is 608.55.,Diosmin has a topological polar surface area of 234.29.,The log p value of  is 0.23.,Diosmin is approved and investigational.,Diosmin is a solid.,True
19730,"Indolesulfonic acid is a blue-colored dye used a marker in urological procedures, also known as _indigo carmine_. This drug was initially used as a kidney function test. The main application of indigo carmine at this time is localizing and visualizing ureteral orifices during cystoscopy and ureteral catheterization procedures.  This drug dyes tissues blue, enabling easier visualization for accuracy during medical procedures. Indigo carmine works as a dye that accumulates in crevices, cysts, and foveolae and stains the tissue blue.",,,,Indigotindisulfonic acid is approved.,Indigotindisulfonic acid is a liquid.,True
19731,Kynurenic Acid is under investigation in clinical trial NCT02340325 (FS2 Safety and Tolerability Study in Healthy Volunteers).,,,,Kynurenic Acid is investigational.,,True
19732,"Cantharidin is a naturally occurring odorless, colorless fatty substance of the terpenoid class that is produced as an oral fluid in the alimentary canal of the male blister beetle. For its natural purpose, the male blister beetle secretes and presents the cantharidin to a female beetle as a copulatory gift during mating. Post-copulation, the female beetle places the cantharidin over her eggs as protection against any potential predators. The only therapeutic use for which cantharidin is currently primarily indicated for is as an active ingredient in topical agents for treating common warts (verruca vulgaris), periungual warts, plantar warts, and molluscum contagiosum.  Cantharidin is a natural toxin produced by the blistering beetle that possesses both vesicant (blistering) and keratolytic effects. The substance elicits these effects by inducing acantholysis (loss of intercellular connections) through the targeting of the desmosomal dense plaque, resulting in the detachment of the desmosomes from the tonofilaments. Cantharidin's effectiveness against warts is proposed to be a result of the exfoliation of the wart body as a consequence of the compound's acantholytic action. This acantholytic action generally does not go beyond the epidermal cells so that the basal layer remains intact and minimal effect occurs on the corium. There is consequently no scarring from the topical application of cantharidin.  Cantharidin is specifically absorbed by lipids in the membrane of epidermal keratinocytes, where it activates the release of neutral serine proteases. These enzymes subsequently break the peptide bonds in surrounding proteins, leading to the progressive degeneration of desmosomal dense plaques, which are important cellular structures that participate in cell-to-cell adhesion. Such degeneration results in the detachment of the tonofilaments that hold cells together. This process as a whole leads to the selective acantholysis (loss of cellular connections) and blistering of the skin when the cantharidin topical application is applied upon specific topical developments like warts. A blister(s) at the application site develop within 24 to 48 hours of application and typically resolve within 4 to 7 days. Factors that can modify this proposed time frame include the volume or concentration of cantharidin used, physical contact time of the applied compound (usually between 4 to 24 hours), the presence of any occlusive dressings, or even patient sensitivity to cantharidin. The blistered lesions ultimately heal without scarring.",,,,Cantharidin is approved and investigational.,,True
19733,,,,,1-CYCLOHEXYL-N-{METHYL}METHANAMINE is experimental.,1-CYCLOHEXYL-N-{METHYL}METHANAMINE is a solid.,False
19734,,,,,(2R)-N~4~-hydroxy-2-(3-hydroxybenzyl)-N~1~-butanediamide is experimental.,(2R)-N~4~-hydroxy-2-(3-hydroxybenzyl)-N~1~-butanediamide is a solid.,False
19735,"N-hydroxy-4-({4-phenyl}sulfonyl)tetrahydro-2H-pyran-4-carboxamide is a solid. This compound belongs to the diarylethers. These are organic compounds containing the dialkyl ether functional group, with the formula ROR', where R and R' are aryl groups. This substance is known to target a disintegrin and metalloproteinase with thrombospondin motifs 5.",,,,N-hydroxy-4-({4-phenyl}sulfonyl)tetrahydro-2H-pyran-4-carboxamide is experimental.,N-hydroxy-4-({4-phenyl}sulfonyl)tetrahydro-2H-pyran-4-carboxamide is a solid.,True
19736,,,,,"2',5'-DIDEOXY-ADENOSINE 3'-MONOPHOSPHATE is experimental.","2',5'-DIDEOXY-ADENOSINE 3'-MONOPHOSPHATE is a solid.",False
19737,,,,,1-(1'-{carbonyl}spiro-5-yl)methanamine is experimental.,1-(1'-{carbonyl}spiro-5-yl)methanamine is a solid.,False
19738,,,,,1--5-yl]methanamine is experimental.,1--5-yl]methanamine is a solid.,False
19739,,,,,"3,6,9,12,15,18-HEXAOXAICOSANE is experimental.","3,6,9,12,15,18-HEXAOXAICOSANE is a solid.",False
19740,,,,,3-amino}isoxazolopyridin-3-yl)phenyl]propan-1-ol is experimental.,3-amino}isoxazolopyridin-3-yl)phenyl]propan-1-ol is a solid.,False
19741,,,,,3-amino}-1H-pyrazolopyridin-1-yl)phenyl]propanamide is experimental.,3-amino}-1H-pyrazolopyridin-1-yl)phenyl]propanamide is a solid.,False
19742,,,,,"1--3-amino]ethyl]-1,3-thiazol-2-yl]urea is experimental.","1--3-amino]ethyl]-1,3-thiazol-2-yl]urea is a solid.",False
19743,,,,,1-guanidine is experimental.,1-guanidine is a solid.,False
19744,,,,,2-(2-HYDROXY-CYCLOPENTYL)-PENT-4-ENAL is experimental.,2-(2-HYDROXY-CYCLOPENTYL)-PENT-4-ENAL is a solid.,False
19745,"A clear, colorless, viscous organic solvent and diluent used in pharmaceutical preparations.",,,,(R)-Propylene glycol is experimental.,(R)-Propylene glycol is a solid.,True
19746,,,,,4-methyl-umbelliferyl-N-acetyl-chitobiose is experimental.,4-methyl-umbelliferyl-N-acetyl-chitobiose is a solid.,False
19747,An arsenical which has been used as a feed additive for enteric conditions in pigs and poultry. It causes blindness and is ototoxic and nephrotoxic in animals. ,The molecular weight is 217.06.,Arsanilic acid has a topological polar surface area of 83.55.,The log p value of  is -1.17.,Arsanilic acid is experimental and vet_approved.,Arsanilic acid is a solid.,True
19748,,,,,p-Toluenesulfonic acid is experimental.,p-Toluenesulfonic acid is a solid.,False
19749,A colorless liquid made by oxidation of aliphatic hydrocarbons that is used as a solvent and chemical intermediate.,The molecular weight is 60.1.,Propyl alcohol has a topological polar surface area of 20.23.,The log p value of  is 0.29.,Propyl alcohol is approved.,Propyl alcohol is a solid.,True
19750,,,,,Cu-Cyclam is experimental.,Cu-Cyclam is a solid.,False
19751,,,,,(S)-Aspartimide is experimental.,(S)-Aspartimide is a solid.,False
19752,,,,,Dodecyl sulfate is experimental.,Dodecyl sulfate is a solid.,False
19753,,,,,Triacetylchitotriose is experimental.,Triacetylchitotriose is a solid.,False
19754,,,,,Methylumbelliferyl chitotriose is experimental.,Methylumbelliferyl chitotriose is a solid.,False
19755,,,,,"UNDECA-3,7-DIENE-1,3,7,11-TETRACARBALDEHYDE is experimental.","UNDECA-3,7-DIENE-1,3,7,11-TETRACARBALDEHYDE is a solid.",False
19756,,,,,(S)-3-phenyllactic acid is experimental.,(S)-3-phenyllactic acid is a solid.,False
19757,,,,,L-Phenylalanine is experimental.,L-Phenylalanine is a solid.,False
19758,,,,,Phenylalanine-N-Sulfonamide is experimental.,Phenylalanine-N-Sulfonamide is a solid.,False
19759,A thiol-containing non-essential amino acid that is oxidized to form CYSTINE.,,,,D-Cysteine is experimental.,D-Cysteine is a solid.,True
19760,,,,,2-Benzyl-3-Iodopropanoic Acid is experimental.,2-Benzyl-3-Iodopropanoic Acid is a solid.,False
19761,,,,,N-Carbamoylphenylalanine is experimental.,N-Carbamoylphenylalanine is a solid.,False
19762,,,,,D-Phenylalanine is experimental.,D-Phenylalanine is a solid.,False
19763,,,,,(2R)-2-benzyl-3-nitropropanoic acid is experimental.,(2R)-2-benzyl-3-nitropropanoic acid is a solid.,False
19764,,,,,O-(((1R)-((N-(PHENYL-METHOXY-CARBONYL)-ALANYL)-AMINO)METHYL)HYDROXYPHOSPHINYL)3-L-PHENYLLACTATE is experimental.,O-(((1R)-((N-(PHENYL-METHOXY-CARBONYL)-ALANYL)-AMINO)METHYL)HYDROXYPHOSPHINYL)3-L-PHENYLLACTATE is a solid.,False
19765,,,,,"(2R)-4,4-dihydroxy-5-nitro-2-(phenylmethyl)pentanoic acid is experimental.","(2R)-4,4-dihydroxy-5-nitro-2-(phenylmethyl)pentanoic acid is a solid.",False
19766,,,,,L-BENZYLSUCCINIC ACID is experimental.,L-BENZYLSUCCINIC ACID is a solid.,False
19767,,,,,"OCTANE-1,3,5,7-TETRACARBOXYLIC ACID is experimental.","OCTANE-1,3,5,7-TETRACARBOXYLIC ACID is a solid.",False
19768,,,,,O-(((1R)-((N-PHENYLMETHOXYCARBONYL-L-ALANYL)AMINO)ETHYL)HYDROXYPHOSPHONO)-L-BENZYLACETIC ACID is experimental.,O-(((1R)-((N-PHENYLMETHOXYCARBONYL-L-ALANYL)AMINO)ETHYL)HYDROXYPHOSPHONO)-L-BENZYLACETIC ACID is a solid.,False
19769,(3S)-1-{sulfonyl}pyrrolidine-3-thiol is a solid. This compound belongs to the benzenesulfonamides. These are organic compounds containing a sulfonamide group that is S-linked to a benzene ring. This substance is known to target disintegrin and metalloproteinase domain-containing protein 17.,,,,(3S)-1-{sulfonyl}pyrrolidine-3-thiol is experimental.,(3S)-1-{sulfonyl}pyrrolidine-3-thiol is a solid.,True
19770,,,,,3-{sulfonyl}propane-1-thiol is experimental.,3-{sulfonyl}propane-1-thiol is a solid.,False
19771,,,,,"4-({4-PHENYL}SULFONYL)-N-HYDROXY-2,2-DIMETHYLTHIOMORPHOLINE-3-CARBOXAMIDE is experimental.","4-({4-PHENYL}SULFONYL)-N-HYDROXY-2,2-DIMETHYLTHIOMORPHOLINE-3-CARBOXAMIDE is a solid.",False
19772,,,,,(2R)-N-HYDROXY-2-PHENYL}-2-OXOPYRROLIDIN-1-YL]PROPANAMIDE is experimental.,(2R)-N-HYDROXY-2-PHENYL}-2-OXOPYRROLIDIN-1-YL]PROPANAMIDE is a solid.,False
19773,,,,,"methyl (1R,2S)-2-(hydroxycarbamoyl)-1-{4-benzyl}cyclopropanecarboxylate is experimental.","methyl (1R,2S)-2-(hydroxycarbamoyl)-1-{4-benzyl}cyclopropanecarboxylate is a solid.",False
19774,,,,,"(1S,3R,6S)-4-oxo-6-{4-phenyl}-5-azaspiroheptane-1-carboxylic acid is experimental.","(1S,3R,6S)-4-oxo-6-{4-phenyl}-5-azaspiroheptane-1-carboxylic acid is a solid.",False
19775,,,,,N-{sulfonyl}-5-methyl-D-tryptophan is experimental.,N-{sulfonyl}-5-methyl-D-tryptophan is a solid.,False
19776,,,,,"(3S)-4-{SULFONYL}-N-HYDROXY-2,2-DIMETHYLTHIOMORPHOLINE-3-CARBOXAMIDE is experimental.","(3S)-4-{SULFONYL}-N-HYDROXY-2,2-DIMETHYLTHIOMORPHOLINE-3-CARBOXAMIDE is a solid.",False
19777,,,,,Cumidine is experimental.,Cumidine is a solid.,False
19778,,,,,"2--N-(3,3,3-Trifluoro-1-Isopropyl-2-Oxopropyl)Acetamide is experimental.","2--N-(3,3,3-Trifluoro-1-Isopropyl-2-Oxopropyl)Acetamide is a solid.",False
19779,,,,,N-{4-benzoyl}-L-valyl-N--L-prolinamide is experimental.,N-{4-benzoyl}-L-valyl-N--L-prolinamide is a solid.,False
19780,,,,,N-{carbonyl}-L-alanyl-L-alaninamide is experimental.,N-{carbonyl}-L-alanyl-L-alaninamide is a solid.,False
19781,,,,,N--Methanesulfonamide is experimental.,N--Methanesulfonamide is a solid.,False
19782,,,,,(3R)-3-ethyl-N--L-aspartic acid is experimental.,(3R)-3-ethyl-N--L-aspartic acid is a solid.,False
19783,,,,,(TERT-BUTYLOXYCARBONYL)-ALANYL-AMINO ETHYL-FORMAMIDE is experimental.,(TERT-BUTYLOXYCARBONYL)-ALANYL-AMINO ETHYL-FORMAMIDE is a solid.,False
19784,,,,,(2-BROMOETHYL)(2-'FORMYL-4'-AMINOPHENYL) ACETATE is experimental.,(2-BROMOETHYL)(2-'FORMYL-4'-AMINOPHENYL) ACETATE is a solid.,False
19785,,,,,-CARBAMIC ACID TERT-BUTYL ESTER is experimental.,-CARBAMIC ACID TERT-BUTYL ESTER is a solid.,False
19786,,,,,METHYL(2-ACETOXY-2-(2-CARBOXY-4-AMINO-PHENYL))ACETATE is experimental.,METHYL(2-ACETOXY-2-(2-CARBOXY-4-AMINO-PHENYL))ACETATE is a solid.,False
19787,,,,,(2R)-3-{AMINO}-2-HYDROXYPROPANOIC ACID is experimental.,(2R)-3-{AMINO}-2-HYDROXYPROPANOIC ACID is a solid.,False
19788,,,,,3-AMINO]-2-OXO-6-PHENYL-N--1(2H)-PYRIDINE ACETAMIDE is experimental.,3-AMINO]-2-OXO-6-PHENYL-N--1(2H)-PYRIDINE ACETAMIDE is a solid.,False
19789,,,,,"(2S,3S)-3-FORMYL-2-({AMINO}METHYL)PENTANOIC ACID is experimental.","(2S,3S)-3-FORMYL-2-({AMINO}METHYL)PENTANOIC ACID is a solid.",False
19790,,,,,"(2S,3S)-3-FORMYL-2-({AMINO}METHYL)PENTANOIC ACID is experimental.","(2S,3S)-3-FORMYL-2-({AMINO}METHYL)PENTANOIC ACID is a solid.",False
19791,Pentanal is a solid. This compound belongs to the polyamines. These are compounds containing more than one amine group. This drug targets the protein cAMP-dependent protein kinase catalytic subunit alpha.,,,,Pentanal is experimental.,Pentanal is a solid.,True
19792,,,,,Balanol Analog 2 is experimental.,Balanol Analog 2 is a solid.,False
19793,,,,,3-azepan-4-yl 4-(2-hydroxy-5-methoxybenzoyl)benzoate is experimental.,3-azepan-4-yl 4-(2-hydroxy-5-methoxybenzoyl)benzoate is a solid.,False
19794,,,,,Balanol Analog 1 is experimental.,Balanol Analog 1 is a solid.,False
19795,,,,,Balanol is experimental.,Balanol is a solid.,False
19796,,,,,(2S)-1-(3H-Indol-3-yl)-3-{oxy}-2-propanamine is experimental.,(2S)-1-(3H-Indol-3-yl)-3-{oxy}-2-propanamine is a solid.,False
19797,,,,,(2S)-1-{oxy}-3-(7aH-indol-3-yl)-2-propanamine is experimental.,(2S)-1-{oxy}-3-(7aH-indol-3-yl)-2-propanamine is a solid.,False
19798,,,,,(1S)-2-(1H-INDOL-3-YL)-1-PYRIDIN-3-YL}OXY)METHYL]ETHYLAMINE is experimental.,(1S)-2-(1H-INDOL-3-YL)-1-PYRIDIN-3-YL}OXY)METHYL]ETHYLAMINE is a solid.,False
19799,,,,,(2S)-1-(6H-INDOL-3-YL)-3-{PYRIDIN-5-YL)PYRIDIN-3-YL]OXY}PROPAN-2-AMINE is experimental.,(2S)-1-(6H-INDOL-3-YL)-3-{PYRIDIN-5-YL)PYRIDIN-3-YL]OXY}PROPAN-2-AMINE is a solid.,False
19800,,,,,(1S)-1-(1H-INDOL-3-YLMETHYL)-2-(2-PYRIDIN-4-YL-NAPHTYRIDIN-5-YLOXY)-EHYLAMINE is experimental.,(1S)-1-(1H-INDOL-3-YLMETHYL)-2-(2-PYRIDIN-4-YL-NAPHTYRIDIN-5-YLOXY)-EHYLAMINE is a solid.,False
19801,,,,,N--5-THIOPHENE-2-CARBOXAMIDE is experimental.,N--5-THIOPHENE-2-CARBOXAMIDE is a solid.,False
19802,,,,,"3-(1H-indol-3-yl)-4-{1--1H-indol-3-yl}-1H-pyrrole-2,5-dione is experimental.","3-(1H-indol-3-yl)-4-{1--1H-indol-3-yl}-1H-pyrrole-2,5-dione is a solid.",False
19803,,,,,"(4R,2S)-5'-(4-(4-CHLOROBENZYLOXY)PYRROLIDIN-2-YLMETHANESULFONYL)ISOQUINOLINE is experimental.","(4R,2S)-5'-(4-(4-CHLOROBENZYLOXY)PYRROLIDIN-2-YLMETHANESULFONYL)ISOQUINOLINE is a solid.",False
19804,,,,,N-METHYL-1-METHANAMINE is experimental.,N-METHYL-1-METHANAMINE is a solid.,False
19805,,,,,(S)-1-PHENYL-1-METHANAMINE is experimental.,(S)-1-PHENYL-1-METHANAMINE is a solid.,False
19806,,,,,6-{4-PHENYL}-9H-PURINE is experimental.,6-{4-PHENYL}-9H-PURINE is a solid.,False
19807,,,,,(2R)-2-(4-chlorophenyl)-2-ethanamine is experimental.,(2R)-2-(4-chlorophenyl)-2-ethanamine is a solid.,False
19808,,,,,(2S)-2-(4-chlorophenyl)-2-ethanamine is experimental.,(2S)-2-(4-chlorophenyl)-2-ethanamine is a solid.,False
19809,,,,,(2R)-2-(4-CHLOROPHENYL)-2-PHENYLETHANAMINE is experimental.,(2R)-2-(4-CHLOROPHENYL)-2-PHENYLETHANAMINE is a solid.,False
19810,,,,,H-89 is experimental.,H-89 is a solid.,False
19811,,,,,5-(2-methylpiperazine-1-sulfonyl)isoquinoline is experimental.,5-(2-methylpiperazine-1-sulfonyl)isoquinoline is a solid.,False
19812,,,,,N--5-ISOQUINOLINESULFONAMIDE is experimental.,N--5-ISOQUINOLINESULFONAMIDE is a solid.,False
19813,,,,,2-ETHANAMINE is experimental.,2-ETHANAMINE is a solid.,False
19814,,,,,3-pyridin-4-yl-1H-indazole is experimental.,3-pyridin-4-yl-1H-indazole is a solid.,False
19815,,,,,"5-benzyl-1,3-thiazol-2-amine is experimental.","5-benzyl-1,3-thiazol-2-amine is a solid.",False
19816,,,,,1-pyrimidin-4-yl)piperidin-4-yl]methanamine is experimental.,1-pyrimidin-4-yl)piperidin-4-yl]methanamine is a solid.,False
19817,,,,,1-pyrimidin-4-yl)piperidin-4-yl]methanamine is experimental.,1-pyrimidin-4-yl)piperidin-4-yl]methanamine is a solid.,False
19818,,,,,4-(4-chlorobenzyl)-1-(7H-pyrrolopyrimidin-4-yl)piperidin-4-aminium is experimental.,4-(4-chlorobenzyl)-1-(7H-pyrrolopyrimidin-4-yl)piperidin-4-aminium is a solid.,False
19819,,,,,A-674563 is experimental.,A-674563 is a solid.,False
19820,,,,,"3-PYRIDIN-4-YL-2,4-DIHYDRO-INDENO PYRAZOLE is experimental.","3-PYRIDIN-4-YL-2,4-DIHYDRO-INDENO PYRAZOLE is a solid.",False
19821,,,,,N-sulfo-flavin mononucleotide is experimental.,N-sulfo-flavin mononucleotide is a solid.,False
19822,,,,,Benzoylformic Acid is experimental.,Benzoylformic Acid is a solid.,False
19823,,,,,"3-Decyl-2,5-Dioxo-4-Hydroxy-3-Pyrroline is experimental.","3-Decyl-2,5-Dioxo-4-Hydroxy-3-Pyrroline is a solid.",False
19824,,,,,Phenylpyruvic acid is experimental.,Phenylpyruvic acid is a solid.,False
19825,,,,,"4-Carboxy-5-(1-Pentyl)Hexylsulfanyl-1,2,3-Triazole is experimental.","4-Carboxy-5-(1-Pentyl)Hexylsulfanyl-1,2,3-Triazole is a solid.",False
19826,,,,,"5-(dodecylthio)-1H-1,2,3-triazole-4-carboxylic acid is experimental.","5-(dodecylthio)-1H-1,2,3-triazole-4-carboxylic acid is a solid.",False
19827,,,,,3-(INDOL-3-YL) LACTATE is experimental.,3-(INDOL-3-YL) LACTATE is a solid.,False
19828,,,,,(2S)-2-HYDROXYOCTANOIC ACID is experimental.,(2S)-2-HYDROXYOCTANOIC ACID is a solid.,False
19829,,,,,1-naphthaleneacetic acid is experimental.,1-naphthaleneacetic acid is a solid.,False
19830,,,,,(2S)-2-(1H-indol-3-yl)hexanoic acid is experimental.,(2S)-2-(1H-indol-3-yl)hexanoic acid is a solid.,False
19831,,,,,(2S)-2-(1H-indol-3-yl)pentanoic acid is experimental.,(2S)-2-(1H-indol-3-yl)pentanoic acid is a solid.,False
19832,,,,,(2S)-8--2-(1H-indol-3-yl)octanoic acid is experimental.,(2S)-8--2-(1H-indol-3-yl)octanoic acid is a solid.,False
19833,,,,,9-Hydroxy-8-Methoxy-6-Nitro-PhenanthrolDioxole-5-Carboxylic Acid is experimental.,9-Hydroxy-8-Methoxy-6-Nitro-PhenanthrolDioxole-5-Carboxylic Acid is a solid.,False
19834,,,,,Indolepropionic acid is experimental.,Indolepropionic acid is a solid.,False
19835,,,,,P-Anisic Acid is experimental.,P-Anisic Acid is a solid.,False
19836,,,,,(2E)-1--3-(4-hydroxyphenyl)prop-2-en-1-one is experimental.,(2E)-1--3-(4-hydroxyphenyl)prop-2-en-1-one is a solid.,False
19837,,,,,(2-CARBAMOYLMETHYL-5-PROPYL-OCTAHYDRO-INDOL-7-YL)ACETIC ACID is experimental.,(2-CARBAMOYLMETHYL-5-PROPYL-OCTAHYDRO-INDOL-7-YL)ACETIC ACID is a solid.,False
19838,,,,,3-{3--1H-INDOL-7-YL}PROPAN-1-OL is experimental.,3-{3--1H-INDOL-7-YL}PROPAN-1-OL is a solid.,False
19839,,,,,{4-PHENYL}SULFAMIC ACID is experimental.,{4-PHENYL}SULFAMIC ACID is a solid.,False
19840,,,,,"(4-{4--2,2-BIS(ETHOXYCARBONYL)BUTYL}PHENYL)SULFAMIC ACID is experimental.","(4-{4--2,2-BIS(ETHOXYCARBONYL)BUTYL}PHENYL)SULFAMIC ACID is a solid.",False
19841,,,,,{4-PHENYL}SULFAMIC ACID is experimental.,{4-PHENYL}SULFAMIC ACID is a solid.,False
19842,,,,,(4-ETHYLPHENYL)SULFAMIC ACID is experimental.,(4-ETHYLPHENYL)SULFAMIC ACID is a solid.,False
19843,,,,,4-BENZOIC ACID is experimental.,4-BENZOIC ACID is a solid.,False
19844,,,,,1-(2-DEOXY-5-O-PHOSPHONO-BETA-D-ERYTHRO-PENTOFURANOSYL)-4-METHYL-1H-INDOLE is experimental.,1-(2-DEOXY-5-O-PHOSPHONO-BETA-D-ERYTHRO-PENTOFURANOSYL)-4-METHYL-1H-INDOLE is a solid.,False
19845,,,,,3-benzoic acid is experimental.,3-benzoic acid is a solid.,False
19846,,,,,N-{3-phenyl}furan-2-carboxamide is experimental.,N-{3-phenyl}furan-2-carboxamide is a solid.,False
19847,,,,,"(2R,3R,4S,5R)-2-purin-9-yl]-5-(hydroxymethyl)oxolane-3,4-diol is experimental.","(2R,3R,4S,5R)-2-purin-9-yl]-5-(hydroxymethyl)oxolane-3,4-diol is a solid.",False
19848,,,,,Myristoyl-Coa is experimental.,Myristoyl-Coa is a solid.,False
19849,,,,,S-(2-oxo)pentadecylcoa is experimental.,S-(2-oxo)pentadecylcoa is a solid.,False
19850,,,,,"1-(CYCLOHEXYLAMINO)-3-(6-METHYL-3,4-DIHYDRO-1H-CARBAZOL-9(2H)-YL)PROPAN-2-OL is experimental.","1-(CYCLOHEXYLAMINO)-3-(6-METHYL-3,4-DIHYDRO-1H-CARBAZOL-9(2H)-YL)PROPAN-2-OL is a solid.",False
19851,,,,,(Z)-3-BENZYL-5-(2-HYDROXY-3-NITROBENZYLIDENE)-2-THIOXOTHIAZOLIDIN-4-ONE is experimental.,(Z)-3-BENZYL-5-(2-HYDROXY-3-NITROBENZYLIDENE)-2-THIOXOTHIAZOLIDIN-4-ONE is a solid.,False
19852,,,,,4-(3-Pyridin-2-Yl-1h-Pyrazol-4-Yl)Quinoline is experimental.,4-(3-Pyridin-2-Yl-1h-Pyrazol-4-Yl)Quinoline is a solid.,False
19853,,,,,Naphthyridine Inhibitor is experimental.,Naphthyridine Inhibitor is a solid.,False
19854,,,,,"3-(4-Fluorophenyl)-2-(6-Methylpyridin-2-Yl)-5,6-Dihydro-4h-PyrroloPyrazole is experimental.","3-(4-Fluorophenyl)-2-(6-Methylpyridin-2-Yl)-5,6-Dihydro-4h-PyrroloPyrazole is a solid.",False
19855,,,,,N-acetamide is experimental.,N-acetamide is a solid.,False
19856,,,,,2-(6-methylpyridin-2-yl)-N-pyridin-4-ylquinazolin-4-amine is experimental.,2-(6-methylpyridin-2-yl)-N-pyridin-4-ylquinazolin-4-amine is a solid.,False
19857,,,,,N-1H-indazol-5-yl-2-(6-methylpyridin-2-yl)quinazolin-4-amine is experimental.,N-1H-indazol-5-yl-2-(6-methylpyridin-2-yl)quinazolin-4-amine is a solid.,False
19858,,,,,4-Nitrophenyl Phosphate is experimental.,4-Nitrophenyl Phosphate is a solid.,False
19859,,,,,4-(6-{amino}imidazopyridazin-3-yl)benzoic acid is experimental.,4-(6-{amino}imidazopyridazin-3-yl)benzoic acid is a solid.,False
19860,,,,,"6-CHLORO-9-HYDROXY-1,3-DIMETHYL-1,9-DIHYDRO-4H-PYRAZOLOQUINOLIN-4-ONE is experimental.","6-CHLORO-9-HYDROXY-1,3-DIMETHYL-1,9-DIHYDRO-4H-PYRAZOLOQUINOLIN-4-ONE is a solid.",False
19861,,,,,"N-(4-AMINO-5-CYANO-6-ETHOXYPYRIDIN-2-YL)-2-(4-BROMO-2,5-DIMETHOXYPHENYL)ACETAMIDE is experimental.","N-(4-AMINO-5-CYANO-6-ETHOXYPYRIDIN-2-YL)-2-(4-BROMO-2,5-DIMETHOXYPHENYL)ACETAMIDE is a solid.",False
19862,,,,,"5-CYANO-N-(2,5-DIMETHOXYBENZYL)-6-ETHOXYPYRIDINE-2-CARBOXAMIDE is experimental.","5-CYANO-N-(2,5-DIMETHOXYBENZYL)-6-ETHOXYPYRIDINE-2-CARBOXAMIDE is a solid.",False
19863,"Anthralin (1,8‐dihydroxy‐9anthrone, dithranol) is an older anti-psoriatic agent that was first synthesized as a derivative of chrysarobin, obtained from the araroba tree in Brazil over 100 years ago. Adverse effects of anthralin include irritation and discoloration of the skin. Stable plaque psoriasis of the skin and scalp.",The molecular weight is 226.23.,Anthralin has a topological polar surface area of 57.53.,The log p value of  is 4.06.,Anthralin is approved.,Anthralin is a solid.,True
19864,,,,,2-({2-PYRIMIDIN-4-YL}AMINO)BENZAMIDE is experimental.,2-({2-PYRIMIDIN-4-YL}AMINO)BENZAMIDE is a solid.,False
19865,,,,,2-fluoro-6-{phenyl}amino)-7H-pyrrolopyrimidin-4-yl]amino}benzamide is experimental.,2-fluoro-6-{phenyl}amino)-7H-pyrrolopyrimidin-4-yl]amino}benzamide is a solid.,False
19866,"BOS172722 is a novel and selective Monopolar spindle 1 (Mps1) kinase inhibitor identified as a potential anticancer agent. Normally, Mps1 supports the proper division of cancer cells, ensuring survival and replication. The key role of Mps1 in the growth of cancer cells renders it an appealing target for cancer treatment, as its inhibition could lead to favorable effects. An in vivo study combined BOS172722 with for the treatment of triple hormone receptor negative breast cancer, and demonstrated promising synergistic effects. Mps1 is a protein kinase that is expressed in normal proliferating tissues and in certain actively dividing tumors. It acts during mitosis (cell division) and plays a crucial role in the alignment of chromosomes in cancer cells. Checkpoint activities by Mps1 normally inhibit the advancement of cancer cells from metaphase to anaphase until structural integrity and alignment occur. BOS172722 binds to Mps1, inhibiting its regulatory checkpoint activities. This inhibition causes accelerated cell division with increased missegregation errors that ultimately reduce the viability of malignant cells.",,,,BOS172722 is experimental.,BOS172722 is a solid.,True
19867,,,,,-6-(methylamino)pyrimidin-2-yl}amino)phenyl]acetonitrile is experimental.,-6-(methylamino)pyrimidin-2-yl}amino)phenyl]acetonitrile is a solid.,False
19868,,,,,"5-(2-hydroxyethyl)nonane-1,9-diol is experimental.","5-(2-hydroxyethyl)nonane-1,9-diol is a solid.",False
19869,,,,,3-(3-aminophenyl)-N-(3-chlorophenyl)pyrazolopyrimidin-5-amine is experimental.,3-(3-aminophenyl)-N-(3-chlorophenyl)pyrazolopyrimidin-5-amine is a solid.,False
19870,,,,,(2S)-2-{pyridazin-6-yl]amino}-3-methylbutan-1-ol is experimental.,(2S)-2-{pyridazin-6-yl]amino}-3-methylbutan-1-ol is a solid.,False
19871,,,,,p-Coumaric acid is experimental.,p-Coumaric acid is a solid.,False
19872,,,,,"5--N,2,4-trimethyl-1H-pyrrole-3-carboxamide is experimental.","5--N,2,4-trimethyl-1H-pyrrole-3-carboxamide is a solid.",False
19873,,,,,Methylecgonine is experimental.,Methylecgonine is a solid.,False
19874,,,,,1-METHYLPHOSPHONIC ACID is experimental.,1-METHYLPHOSPHONIC ACID is a solid.,False
19875,,,,,3-OXO-N-DODECANAMIDE is experimental.,3-OXO-N-DODECANAMIDE is a solid.,False
19876,,,,,5-ALPHA-PREGNANE-3-BETA-OL-HEMISUCCINATE is experimental.,5-ALPHA-PREGNANE-3-BETA-OL-HEMISUCCINATE is a solid.,False
19877,,,,,PROGESTERONE-11-ALPHA-OL-HEMISUCCINATE is experimental.,PROGESTERONE-11-ALPHA-OL-HEMISUCCINATE is a solid.,False
19878,,,,,3-(HYDROXY-PHENYL-PHOSPHINOYLOXY)-8-METHYL-8-AZA-BICYCLOOCTANE-2-CARBOXYLIC ACID METHYL ESTER is experimental.,3-(HYDROXY-PHENYL-PHOSPHINOYLOXY)-8-METHYL-8-AZA-BICYCLOOCTANE-2-CARBOXYLIC ACID METHYL ESTER is a solid.,False
19879,,,,,"3,6,9,12,15-PENTAOXAHEPTADECAN-1-OL is experimental.","3,6,9,12,15-PENTAOXAHEPTADECAN-1-OL is a solid.",False
19880,,,,,"1,3-Propanediol is experimental.","1,3-Propanediol is a solid.",False
19881,,,,,Guanosine-3'-monophosphate-5'-diphosphate is experimental.,Guanosine-3'-monophosphate-5'-diphosphate is a solid.,False
19882,"Anisomycin (sometimes known as flagecidin), is an antibiotic retrieved from the bacteria _Streptomyces griseolus_. This drug acts to inhibit bacterial protein and DNA synthesis.",,,,Anisomycin is experimental.,Anisomycin is a solid.,True
19883,"Puromycin is an antibiotic that prevents bacterial protein translation. It is utilized as a selective agent in laboratory cell cultures. Puromycin is toxic to both prokaryotic and eukaryotic cells, resulting in significant cell death at appropriate doses.",,,,Puromycin is experimental.,Puromycin is a solid.,True
19884,,,,,PUROMYCIN AMINONUCLEOSIDE-5'-MONOPHOSPHATE is experimental.,PUROMYCIN AMINONUCLEOSIDE-5'-MONOPHOSPHATE is a solid.,False
19885,"One of the components of virginiamycin, a cyclic polypeptide antibiotic complex from streptomyces virginiae, s. Loidensis, s. Mitakaensis, s. Pristina-spiralis, s. Ostreogriseus, and others. It is used to treat infections with gram-positive organisms and as a growth promoter in cattle, swine, and poultry.",,,,Virginiamycin S1 is experimental.,Virginiamycin S1 is a solid.,True
19886,"Omacetaxine mepesuccinate (formerly known as HHT or Homoharringtonine), is a cephalotaxine ester and protein synthesis inhibitor with established clinical activity as a single agent in hematological malignancies. Omacetaxine mepesuccinate is synthesized from cephalotaxine, which is an extract from the leaves of the plant, Cephalotaxus species. In October 2005, omacetaxine mepesuccinate received Orphan Drug designation from the EMEA for the treatment of chronic myeloid leukemia (CML). Then in March 2006, it received Orphan Drug status from the FDA for the treatment of CML. In November 2006, omacetaxine mepesuccinate, for the treatment of CML, was granted Fast Track designation by the FDA. Most recently, in October 2012, omacetaxine mepesuccinate was marketed under the brand name Synribo and FDA approved for patients who are intolerant and/or resistant to two or more tyrosine kinase inhibitors used to treat accelerated or chronic phase CML. Used in patients who are intolerant and/or resistant to two or more tyrosine kinase inhibitors used to treat accelerated or chronic phase CML.  The pharmacodynamics of homoharringtonine is not fully understood. It is known that homoharringtonine is involved Homoharringtonine inhibits protein synthesis by not directly binding to Bcr-Abl. It binds to the A-site cleft in the large ribosomal subunit, which affects chain elongation and prevents protein synthesis.",The molecular weight is 545.63.,Omacetaxine mepesuccinate has a topological polar surface area of 123.99.,The log p value of  is 2.33.,Omacetaxine mepesuccinate is approved and investigational.,Omacetaxine mepesuccinate is a solid.,True
19887,,,,,Tetrabutylammonium Ion is experimental.,Tetrabutylammonium Ion is a solid.,False
19888,,,,,(2S)-2-(BUTYRYLOXY)-3-HYDROXYPROPYL NONANOATE is experimental.,(2S)-2-(BUTYRYLOXY)-3-HYDROXYPROPYL NONANOATE is a solid.,False
19889,,,,,"(4Z)-2,8:7,12:11,15:14,18:17,22-PENTAANHYDRO-4,5,6,9,10,13,19,20,21-NONADEOXY-D-ARABINO-D-ALLO-D-ALLO-DOCOSA-4,9,20-TRIENITOL is experimental.","(4Z)-2,8:7,12:11,15:14,18:17,22-PENTAANHYDRO-4,5,6,9,10,13,19,20,21-NONADEOXY-D-ARABINO-D-ALLO-D-ALLO-DOCOSA-4,9,20-TRIENITOL is a solid.",False
19890,,,,,UNDEC-1-YLCARBAMOYLOXY]-ACETIC ACID is experimental.,UNDEC-1-YLCARBAMOYLOXY]-ACETIC ACID is a solid.,False
19891,,,,,4-{4-NAPHTHALEN-4-YL) -ACETYLAMINO]-PHENYLCARBAMOYL}-BUTYRIC ACID is experimental.,4-{4-NAPHTHALEN-4-YL) -ACETYLAMINO]-PHENYLCARBAMOYL}-BUTYRIC ACID is a solid.,False
19892,,,,,PHENYLPHOSPHONATE is experimental.,PHENYLPHOSPHONATE is a solid.,False
19893,,,,,N-(PARA-GLUTARAMIDOPHENYL-ETHYL)-PIPERIDINIUM-N-OXIDE is experimental.,N-(PARA-GLUTARAMIDOPHENYL-ETHYL)-PIPERIDINIUM-N-OXIDE is a solid.,False
19894,,,,,METHYL-PHOSPHONIC ACID MONO-(4-NITRO-PHENYL) ESTER is experimental.,METHYL-PHOSPHONIC ACID MONO-(4-NITRO-PHENYL) ESTER is a solid.,False
19895,,,,,TRAZEOLIDE is experimental.,TRAZEOLIDE is a solid.,False
19896,"A phthalic indicator dye that appears yellow-green in normal tear film and bright green in a more alkaline medium, such as the aqueous humor, and is used therapeutically as a diagnostic aid in corneal injuries and corneal trauma. It has been approved by FDA for use in externally applied drugs and cosmetics. (From Merck Index, 12th ed; American Medical Association Drug Evaluations; 1995, p2275) For diagnostic imaging. Primarily indicated in diagnostic fluorescein angiography or angioscopy of the fundus and of the iris vasculature. Fluorescein sodium is used extensively as a diagnostic tool in the field of ophthalmology. Fluorescein is a fluorescent compound or fluorophore having a maximum absorbance of 494 m and an emission maximum of 521 nm. The yellowish-green fluorescence of the compound can be used to demarcate the vascular area under observation, distinguishing it from adjacent areas. It is applied topically in the form of a drop or it can be injected intravenously to produce a fluorescein angiogram. Topical fluorescein is a useful tool in the diagnosis of corneal abrasions, corneal ulcers, herpetic corneal infections, and dry eye. Fluorescein angiography is used to diagnose and categorize macular degeneration, diabetic retinopathy, inflammatory intraocular conditions, and intraocular tumors.",,,,Fluorescein is approved.,Fluorescein is a solid.,True
19897,,,,,"N~2~-1H-benzimidazol-5-yl-N~4~-(3-cyclopropyl-1H-pyrazol-5-yl)pyrimidine-2,4-diamine is experimental.","N~2~-1H-benzimidazol-5-yl-N~4~-(3-cyclopropyl-1H-pyrazol-5-yl)pyrimidine-2,4-diamine is a solid.",False
19898,,,,,1-ACETYL-2-CARBOXYPIPERIDINE is experimental.,1-ACETYL-2-CARBOXYPIPERIDINE is a solid.,False
19899,,,,,AUROVERTIN B is experimental.,AUROVERTIN B is a solid.,False
19900,,,,,Piceatannol is experimental.,Piceatannol is a solid.,False
19901,,,,,N1-(2-AMINO-4-METHYLPENTYL)OCTAHYDRO-PYRROLO PYRIMIDINE is experimental.,N1-(2-AMINO-4-METHYLPENTYL)OCTAHYDRO-PYRROLO PYRIMIDINE is a solid.,False
19902,,,,,N-Hydroxy-4-Phosphono-Butanamide is experimental.,N-Hydroxy-4-Phosphono-Butanamide is a solid.,False
19903,,,,,Phosphoglycolohydroxamic Acid is experimental.,Phosphoglycolohydroxamic Acid is a solid.,False
19904,,,,,3-(2-Benzothiazolylthio)-1-Propanesulfonic Acid is experimental.,3-(2-Benzothiazolylthio)-1-Propanesulfonic Acid is a solid.,False
19905,,,,,-Phosphonic Acid is experimental.,-Phosphonic Acid is a solid.,False
19906,,,,,2-Carboxyethylphosphonic Acid is experimental.,2-Carboxyethylphosphonic Acid is a solid.,False
19907,,,,,3-phospho-D-glyceric acid is experimental.,3-phospho-D-glyceric acid is a solid.,False
19908,,,,,3-(BUTYLSULPHONYL)-PROPANOIC ACID is experimental.,3-(BUTYLSULPHONYL)-PROPANOIC ACID is a solid.,False
19909,,,,,"16,17-Androstene-3-Ol is experimental.","16,17-Androstene-3-Ol is a solid.",False
19910,,,,,"4-AMINO}PHENYL)SULFONYL]-N,N-DIMETHYLBENZAMIDE is experimental.","4-AMINO}PHENYL)SULFONYL]-N,N-DIMETHYLBENZAMIDE is a solid.",False
19911,,,,,"1,2,3-TRIHYDROXY-1,2,3,4-TETRAHYDROBENZOPYRENE is experimental.","1,2,3-TRIHYDROXY-1,2,3,4-TETRAHYDROBENZOPYRENE is a solid.",False
19912,,,,,"1--2,4-DIFLUORO-5-METHYL-BENZENE-5'MONOPHOSPHATE is experimental.","1--2,4-DIFLUORO-5-METHYL-BENZENE-5'MONOPHOSPHATE is a solid.",False
19913,,,,,2'-deoxy-N-(naphthalen-1-ylmethyl)guanosine 5'-(dihydrogen phosphate) is experimental.,2'-deoxy-N-(naphthalen-1-ylmethyl)guanosine 5'-(dihydrogen phosphate) is a solid.,False
19914,,,,,N--(S)-Leucyl-(R)--Phosphonic Acid is experimental.,N--(S)-Leucyl-(R)--Phosphonic Acid is a solid.,False
19915,,,,,Furoyl-Leucine is experimental.,Furoyl-Leucine is a solid.,False
19916,,,,,Ilomastat is experimental.,Ilomastat is a solid.,False
19917,,,,,2-(Thiomethylene)-4-Methylpentanoic Acid is experimental.,2-(Thiomethylene)-4-Methylpentanoic Acid is a solid.,False
19918,,,,,"(2R,3R)-N^1^--N^4^-HYDROXY-2-(2-METHYLPROPYL)-3-{METHYL}BUTANEDIAMIDE is experimental.","(2R,3R)-N^1^--N^4^-HYDROXY-2-(2-METHYLPROPYL)-3-{METHYL}BUTANEDIAMIDE is a solid.",False
19919,,,,,Leucine Phosphonic Acid is experimental.,Leucine Phosphonic Acid is a solid.,False
19920,,,,,(2S)-3-(hydroxy)phosphoryl]-2-benzylpropanoic acid is experimental.,(2S)-3-(hydroxy)phosphoryl]-2-benzylpropanoic acid is a solid.,False
19921,,,,,Zofenoprilat is experimental.,Zofenoprilat is a solid.,False
19922,,,,,"2,5-di-tert-butylhydroquinone is experimental.","2,5-di-tert-butylhydroquinone is a solid.",False
19923,,,,,"(6AR,11AS,11BR)-10-ACETYL-9-HYDROXY-7,7-DIMETHYL-2,6,6A,7,11A,11B-HEXAHYDRO-11H-PYRROLOISOINDOLOINDOL-11-ONE is experimental.","(6AR,11AS,11BR)-10-ACETYL-9-HYDROXY-7,7-DIMETHYL-2,6,6A,7,11A,11B-HEXAHYDRO-11H-PYRROLOISOINDOLOINDOL-11-ONE is a solid.",False
19924,,,,,(S)-blebbistatin is experimental.,(S)-blebbistatin is a solid.,False
19925,,,,,Mant-Adp is experimental.,Mant-Adp is a solid.,False
19926,,,,,"(3aS)-3a-hydroxy-5-methyl-1-phenyl-1,2,3,3a-tetrahydro-4H-pyrroloquinolin-4-one is experimental.","(3aS)-3a-hydroxy-5-methyl-1-phenyl-1,2,3,3a-tetrahydro-4H-pyrroloquinolin-4-one is a solid.",False
19927,,,,,"(3aS)-3a-hydroxy-7-methyl-1-phenyl-1,2,3,3a-tetrahydro-4H-pyrroloquinolin-4-one is experimental.","(3aS)-3a-hydroxy-7-methyl-1-phenyl-1,2,3,3a-tetrahydro-4H-pyrroloquinolin-4-one is a solid.",False
19928,,,,,"(3aS)-3a-hydroxy-1-phenyl-1,2,3,3a-tetrahydro-4H-pyrroloquinolin-4-one is experimental.","(3aS)-3a-hydroxy-1-phenyl-1,2,3,3a-tetrahydro-4H-pyrroloquinolin-4-one is a solid.",False
19929,,,,,trifluoro-phosphoryl]oxy-phosphoryl]oxy-beryllium(1-) is experimental.,trifluoro-phosphoryl]oxy-phosphoryl]oxy-beryllium(1-) is a solid.,False
19930,,,,,acetylleucyl-leucyl-norleucinal is experimental.,acetylleucyl-leucyl-norleucinal is a solid.,False
19931,,,,,12-Bromododecanoic Acid is experimental.,12-Bromododecanoic Acid is a solid.,False
19932,,,,,"{4-Amino-2--1,3-thiazol-5-yl}(4-methoxyphenyl)methanone is experimental.","{4-Amino-2--1,3-thiazol-5-yl}(4-methoxyphenyl)methanone is a solid.",False
19933,,,,,"4-Amino-2--5-(4-fluorobenzoyl)-1,3-thiazol-3-ium is experimental.","4-Amino-2--5-(4-fluorobenzoyl)-1,3-thiazol-3-ium is a solid.",False
19934,,,,,"(3-EXO)-3-(10,11-DIHYDRO-5H-DIBENZOANNULEN-5-YLOXY)-8,8-DIMETHYL-8-AZONIABICYCLOOCTANE is experimental.","(3-EXO)-3-(10,11-DIHYDRO-5H-DIBENZOANNULEN-5-YLOXY)-8,8-DIMETHYL-8-AZONIABICYCLOOCTANE is a solid.",False
19935,,,,,Thiacloprid is experimental.,Thiacloprid is a solid.,False
19936,"Imidacloprid is a neonicotinoid, which is a class of neuro-active insecticides modeled after nicotine. Imidacloprid is a patented chemical, Imidacloprid is manufactured by Bayer Cropscience (part of Bayer AG) and sold under trade names Kohinor, Admire, Advantage, Gaucho, Merit, Confidor, Hachikusan, Premise, Prothor, and Winner. It is marketed as pest control, seed treatment, an insecticide spray, termite control, flea control, and a systemic insecticide.",,,,Imidacloprid is vet_approved.,,True
19937,,,,,N1-(1-Dimethylcarbamoyl-2-Phenyl-Ethyl)-2-Oxo-N4-(2-Pyridin-2-Yl-Ethyl)-Succinamide is experimental.,N1-(1-Dimethylcarbamoyl-2-Phenyl-Ethyl)-2-Oxo-N4-(2-Pyridin-2-Yl-Ethyl)-Succinamide is a solid.,False
19938,,,,,CARBOBENZYLOXY-(L)-LEUCINYL-(L)LEUCINYL METHOXYMETHYLKETONE is experimental.,CARBOBENZYLOXY-(L)-LEUCINYL-(L)LEUCINYL METHOXYMETHYLKETONE is a solid.,False
19939,,,,,"2,4,6-Triaminoquinazoline is experimental.","2,4,6-Triaminoquinazoline is a solid.",False
19940,,,,,METHYL 1-(4-{AMINO}BENZOYL)PIPERIDINE-4-CARBOXYLATE is experimental.,METHYL 1-(4-{AMINO}BENZOYL)PIPERIDINE-4-CARBOXYLATE is a solid.,False
19941,,,,,METHYL 1-(4-{(METHYL)AMINO}BENZOYL)PIPERIDINE-4-CARBOXYLATE is experimental.,METHYL 1-(4-{(METHYL)AMINO}BENZOYL)PIPERIDINE-4-CARBOXYLATE is a solid.,False
19942,,,,,-1H-indazol-1-yl}pyrazin-2-yl)-1H-pyrrol-3-yl]acetic acid is experimental.,-1H-indazol-1-yl}pyrazin-2-yl)-1H-pyrrol-3-yl]acetic acid is a solid.,False
19943,,,,,Heptanoic acid is experimental and investigational.,Heptanoic acid is a solid.,False
19944,,,,,1-O-Octyl-2-Heptylphosphonyl-Sn-Glycero-3-Phosphoethanolamine is experimental.,1-O-Octyl-2-Heptylphosphonyl-Sn-Glycero-3-Phosphoethanolamine is a solid.,False
19945,"An organic compound used often as a reagent in organic synthesis, as a flavoring agent, and in tanning. It has been demonstrated as an intermediate in the metabolism of acetone and its derivatives in isolated cell preparations, in various culture media, and in vivo in certain animals. ",,,,Pyruvaldehyde is experimental.,Pyruvaldehyde is a solid.,True
19946,,,,,PHOSPHONIC ACID 2-DODECANOYLAMINO-HEXYL ESTER PROPYL ESTER is experimental.,PHOSPHONIC ACID 2-DODECANOYLAMINO-HEXYL ESTER PROPYL ESTER is a solid.,False
19947,,,,,1-DECYL-3-TRIFLUORO ETHYL-SN-GLYCERO-2-PHOSPHOMETHANOL is experimental.,1-DECYL-3-TRIFLUORO ETHYL-SN-GLYCERO-2-PHOSPHOMETHANOL is a solid.,False
19948,,,,,"5-Chloryl-2,4,6-Quinazolinetriamine is experimental.","5-Chloryl-2,4,6-Quinazolinetriamine is a solid.",False
19949,,,,,"5--2,4-Quinazolinediamine is experimental.","5--2,4-Quinazolinediamine is a solid.",False
19950,,,,,"5-(4-Morpholin-4-Yl-Phenylsulfanyl)-2,4-Quinazolinediamine is experimental.","5-(4-Morpholin-4-Yl-Phenylsulfanyl)-2,4-Quinazolinediamine is a solid.",False
19951,,,,,"5-(4-Methoxyphenoxy)-2,4-Quinazolinediamine is experimental.","5-(4-Methoxyphenoxy)-2,4-Quinazolinediamine is a solid.",False
19952,,,,,"5-Phenylsulfanyl-2,4-Quinazolinediamine is experimental.","5-Phenylsulfanyl-2,4-Quinazolinediamine is a solid.",False
19953,,,,,"5--2,4-Quinazolinediamine is experimental.","5--2,4-Quinazolinediamine is a solid.",False
19954,,,,,"7-(1-ETHYL-PROPYL)-7H-PYRROLO-QUINAZOLINE-1,3-DIAMINE is experimental.","7-(1-ETHYL-PROPYL)-7H-PYRROLO-QUINAZOLINE-1,3-DIAMINE is a solid.",False
19955,,,,,"7--7H-PYRROLO QUINAZOLINE-1,3-DIAMINE is experimental.","7--7H-PYRROLO QUINAZOLINE-1,3-DIAMINE is a solid.",False
19956,,,,,N-(5-{amino}-1H-indazol-3-yl)benzamide is experimental.,N-(5-{amino}-1H-indazol-3-yl)benzamide is a solid.,False
19957,"AVI-4557 is an oral antisense compound that selectively inhibits the metabolic enzyme cytochrome P450 3A4 (CYP), a liver enzyme responsible for the metabolism or breakdown of approximately half of currently marketed drugs. Studies indicate that AVI-4557 can successfully reduce the rate of metabolism for certain drugs, therefore allowing greater and longer availability of the drug in the patient's system through a decrease in clearance and an increase in maximal blood concentration (Cmax). AVI-4557 is therefore indicated to limit toxicity for patients receiving highly-toxic therapeutic drugs for treatment of anxiety, cancer, and a number of other serious conditions. Investigated for use/treatment in adverse effects (chemotherapy) and adverse effects (drug). selectively inhibits the metabolic enzyme cytochrome P450 3A4 (CYP), a liver enzyme responsible for the metabolism or breakdown of approximately half of currently marketed drugs. Studies indicate that AVI-4557 can successfully reduce the rate of metabolism when co-administered with certain therapeutic drugs, allowing greater and longer availability of the drug in the patient's system without an increase in toxicity. selectively inhibits the metabolic enzyme cytochrome P450 3A4 (CYP), a liver enzyme responsible for the metabolism or breakdown of approximately half of currently marketed drugs. S",,,,AVI-4557 is investigational.,AVI-4557 is a solid.,True
19958,,,,,"2-quinazolin-2-yl]iminocyclohexa-2,5-dien-1-yl]acetonitrile is experimental.","2-quinazolin-2-yl]iminocyclohexa-2,5-dien-1-yl]acetonitrile is a solid.",False
19959,,,,,"2-methyl-3,5,7,8-tetrahydro-4H-thiopyranopyrimidin-4-one is experimental.","2-methyl-3,5,7,8-tetrahydro-4H-thiopyranopyrimidin-4-one is a solid.",False
19960,,,,,4-phthalazin-1(2H)-one is experimental.,4-phthalazin-1(2H)-one is a solid.,False
19961,,,,,"N~2~,N~2~-DIMETHYL-N~1~-(6-OXO-5,6-DIHYDROPHENANTHRIDIN-2-YL)GLYCINAMIDE is experimental.","N~2~,N~2~-DIMETHYL-N~1~-(6-OXO-5,6-DIHYDROPHENANTHRIDIN-2-YL)GLYCINAMIDE is a solid.",False
19962,,,,,S-(Methylmercury)-L-Cysteine is experimental.,S-(Methylmercury)-L-Cysteine is a solid.,False
19963,,,,,"(7R,12R,13R)-13-formyl-12,14-dihydroxy-3,5,7-trimethyltetradeca-2,4-dienoic acid is experimental.","(7R,12R,13R)-13-formyl-12,14-dihydroxy-3,5,7-trimethyltetradeca-2,4-dienoic acid is a solid.",False
19964,"MRTX849 is a KRAS inhibitor developed by Mirati and is currently undergoing trials for KRAS G12C mutant cancers. This mutation makes up >50% of all KRAS mutations. MRTX849 is an experimental KRAS inhibitor being investigated for the treatment of KRAS G12C mutant lung and colon adenocarcinomas. Normally GTP binds to KRAS, activating the protein and promoting effectors to the MAP kinase pathway. GTP is hydrolyzed to GDP, and KRAS is inactivated. KRAS G12C mutations impair hydrolysis of GTP, leaving it in the active form.",,,,MRTX849 is investigational.,,True
19965,"AMG-510 is an acrylamide derived KRAS inhibitor developed by Amgen and is currently undergoing clinical trials for solid tumors with KRAS G12C mutations. This mutation makes up >50% of all KRAS mutations. It is the first experimental KRAS inhibitor. AMG-510 is being investigated for the treatment of KRAS G12C mutant non small cell lung cancer, colorectal cancer, and appendix cancer. Normally GTP binds to KRAS, activating the protein and promoting effectors to the MAP kinase pathway. GTP is hydrolyzed to GDP, and KRAS is inactivated. KRAS G12C mutations impair hydrolysis of GTP, leaving it in the active form.",,,,AMG-510 is investigational.,AMG-510 is a solid.,True
19966,,,,,Hexatantalum Dodecabromide is experimental.,Hexatantalum Dodecabromide is a solid.,False
19967,,,,,"(2Z,3E)-2,3'-biindole-2',3(1H,1'H)-dione 3-{O-oxime} is experimental.","(2Z,3E)-2,3'-biindole-2',3(1H,1'H)-dione 3-{O-oxime} is a solid.",False
19968,,,,,Gibberellic acid is experimental.,Gibberellic acid is a solid.,False
19969,,,,,Gibberellin A4 is experimental.,Gibberellin A4 is a solid.,False
19970,,,,,pyridin-3-yl)phenyl]acetic acid is experimental.,pyridin-3-yl)phenyl]acetic acid is a solid.,False
19971,,,,,4-(5-phenyl-1H-pyrrolopyridin-3-yl)benzoic acid is experimental.,4-(5-phenyl-1H-pyrrolopyridin-3-yl)benzoic acid is a solid.,False
19972,,,,,"2,4-Dihydroxy-7-(Methyloxy)-2h-1,4-Benzoxazin-3(4h)-One is experimental.","2,4-Dihydroxy-7-(Methyloxy)-2h-1,4-Benzoxazin-3(4h)-One is a solid.",False
19973,,,,,(S)-4-hydroxymandelonitrile is experimental.,(S)-4-hydroxymandelonitrile is a solid.,False
19974,,,,,PARA-NITROPHENYL 1-THIO-BETA-D-GLUCOPYRANOSIDE is experimental.,PARA-NITROPHENYL 1-THIO-BETA-D-GLUCOPYRANOSIDE is a solid.,False
19975,,,,,5-CHLORO-6-METHYL-N-(2-PHENYLETHYL)-2-PYRIDIN-2-YLPYRIMIDIN-4-AMINE is experimental.,5-CHLORO-6-METHYL-N-(2-PHENYLETHYL)-2-PYRIDIN-2-YLPYRIMIDIN-4-AMINE is a solid.,False
19976,,,,,TERT-BUTYL {2-PYRIDIN-3-YL}CARBAMATE is experimental.,TERT-BUTYL {2-PYRIDIN-3-YL}CARBAMATE is a solid.,False
19977,,,,,"3--N-1,3-THIAZOL-2-YLPYRIDINE-2-CARBOXAMIDE is experimental.","3--N-1,3-THIAZOL-2-YLPYRIDINE-2-CARBOXAMIDE is a solid.",False
19978,,,,,7-HYDROXY-4-METHYL-3-(2-HYDROXY-ETHYL)COUMARIN is experimental.,7-HYDROXY-4-METHYL-3-(2-HYDROXY-ETHYL)COUMARIN is a solid.,False
19979,,,,,2-OXOHEPTYLPHOSPHONIC ACID is experimental.,2-OXOHEPTYLPHOSPHONIC ACID is a solid.,False
19980,,,,,(3R)-3-HYDROXYDODECANOIC ACID is experimental.,(3R)-3-HYDROXYDODECANOIC ACID is a solid.,False
19981,,,,,5-carbamoyl}phenyl)amino]pyridine-3-carboxamide is experimental.,5-carbamoyl}phenyl)amino]pyridine-3-carboxamide is a solid.,False
19982,,,,,"3,4-Dihydro-2h-Pyrrolium-5-Carboxylate is experimental.","3,4-Dihydro-2h-Pyrrolium-5-Carboxylate is a solid.",False
19983,,,,,Imino-Tryptophan is experimental.,Imino-Tryptophan is a solid.,False
19984,"Tryptophan is one of the 20 standard amino acids, as well as an essential amino acid in the human diet. It is encoded in the standard genetic code as the codon UGG. The D-stereoisomer is occasionally found in naturally produced peptides (for example, the marine venom peptide contryphan). The distinguishing structural characteristic of tryptophan is that it contains an indole functional group. It is an essential amino acid as defined by its growth effects on rats.",,,,D-Tryptophan is experimental.,D-Tryptophan is a solid.,True
19985,,,,,Flavin-adenine dinucleotide-N5-isobutyl ketone is experimental.,Flavin-adenine dinucleotide-N5-isobutyl ketone is a solid.,False
19986,,,,,Anthranilic acid is experimental.,Anthranilic acid is a solid.,False
19987,,,,,"(2E)-3-(3,4-DIHYDROXYPHENYL)-2-IMINOPROPANOIC ACID is experimental.","(2E)-3-(3,4-DIHYDROXYPHENYL)-2-IMINOPROPANOIC ACID is a solid.",False
19988,,,,,PD150606 is experimental.,PD150606 is a solid.,False
19989,SU-11652 is a tyrosine kinase inhibitor.,,,,SU-11652 is experimental.,SU-11652 is a solid.,True
19990,,,,,L-Alpha-Glycerophosphorylserine is experimental.,L-Alpha-Glycerophosphorylserine is a solid.,False
19991,,,,,L-thioproline is experimental.,L-thioproline is a solid.,False
19992,,,,,K201 free base is experimental and investigational.,K201 free base is a solid.,False
19993,,,,,sn-glycero-3-phosphoethanolamine is experimental.,sn-glycero-3-phosphoethanolamine is a solid.,False
19994,,,,,L-alanyl-N--L-alaninamide is experimental.,L-alanyl-N--L-alaninamide is a solid.,False
19995,,,,,Kaempherol is experimental.,Kaempherol is a solid.,False
19996,,,,,Matairesinol is experimental.,Matairesinol is a solid.,False
19997,"Labetuzumab is a humanized monoclonal antibody to carcinoembryonic antigen that inhibits tumor growth. It is used in radioimmunotherapy. Labetuzumab is a humanized monoclonal antibody used to treat cancer. Retrieved from \http://en.wikipedia.org/wiki/Labetuzumab\"""" labetuzumab could significantly increase the",,,,Labetuzumab is investigational.,Labetuzumab is a solid.,True
19998,,,,,N-thiophene-2-carboxamide is experimental.,N-thiophene-2-carboxamide is a solid.,False
19999,,,,,"(2S)-2-(3-bromophenyl)-3-(5-chloro-2-hydroxyphenyl)-1,3-thiazolidin-4-one is experimental.","(2S)-2-(3-bromophenyl)-3-(5-chloro-2-hydroxyphenyl)-1,3-thiazolidin-4-one is a solid.",False
20000,,,,,4-HYDROXY-5-IODO-3-NITROPHENYLACETYL-EPSILON-AMINOCAPROIC ACID ANION is experimental.,4-HYDROXY-5-IODO-3-NITROPHENYLACETYL-EPSILON-AMINOCAPROIC ACID ANION is a solid.,False
20001,,,,,4-HYDROXY-3-NITROPHENYLACETYL-EPSILON-AMINOCAPROIC ACID ANION is experimental.,4-HYDROXY-3-NITROPHENYLACETYL-EPSILON-AMINOCAPROIC ACID ANION is a solid.,False
20002,,,,,2-({6--9-isopropyl-9H-purin-2-yl}amino)ethanol is experimental.,2-({6--9-isopropyl-9H-purin-2-yl}amino)ethanol is a solid.,False
20003,,,,,"2-(6-HYDROXY-1,3-BENZOTHIAZOL-2-YL)-1,3-THIAZOL-4(5H)-ONE is experimental.","2-(6-HYDROXY-1,3-BENZOTHIAZOL-2-YL)-1,3-THIAZOL-4(5H)-ONE is a solid.",False
20004,,,,,Diphthamide is experimental.,Diphthamide is a solid.,False
20005,,,,,"4-benzene-1,3-diol is experimental.","4-benzene-1,3-diol is a solid.",False
20006,,,,,"4,4'-BIS(METHYLSULFONYL)-2,2',5,5'-TETRACHLOROBIPHENYL is experimental.","4,4'-BIS(METHYLSULFONYL)-2,2',5,5'-TETRACHLOROBIPHENYL is a solid.",False
20007,,,,,4--4-HYDROXY-BUTYRIC ACID is experimental.,4--4-HYDROXY-BUTYRIC ACID is a solid.,False
20008,,,,,Pentaglyme is experimental.,Pentaglyme is a solid.,False
20009,,,,,4-{amino}butanoic acid is experimental.,4-{amino}butanoic acid is a solid.,False
20010,,,,,N-(TRANS-4'-NITRO-4-STILBENYL)-N-METHYL-5-AMINO-PENTANOIC ACID is experimental.,N-(TRANS-4'-NITRO-4-STILBENYL)-N-METHYL-5-AMINO-PENTANOIC ACID is a solid.,False
20011,,,,,2-Methoxy-3-Isopropylpyrazine is experimental.,2-Methoxy-3-Isopropylpyrazine is a solid.,False
20012,,,,,"(4R)-limonene 1α,2α-epoxide is experimental.","(4R)-limonene 1α,2α-epoxide is a solid.",False
20013,,,,,2-(Sec-Butyl)Thiazole is experimental.,2-(Sec-Butyl)Thiazole is a solid.,False
20014,,,,,6-Hydroxy-6-Methyl-Heptan-3-One is experimental.,6-Hydroxy-6-Methyl-Heptan-3-One is a solid.,False
20015,,,,,2-Isobutyl-3-methoxypyrazine is experimental.,2-Isobutyl-3-methoxypyrazine is a solid.,False
20016,,,,,N-(5-METHYL-1H-PYRAZOL-3-YL)-2-PHENYLQUINAZOLIN-4-AMINE is experimental.,N-(5-METHYL-1H-PYRAZOL-3-YL)-2-PHENYLQUINAZOLIN-4-AMINE is a solid.,False
20017,,,,,(1-Methyl-1h-Imidazol-2-Yl)-(3-Methyl-4-{3--Propoxy}-Benzofuran-2-Yl)-Methanone is experimental.,(1-Methyl-1h-Imidazol-2-Yl)-(3-Methyl-4-{3--Propoxy}-Benzofuran-2-Yl)-Methanone is a solid.,False
20018,,,,,(R)-1-Para-Nitro-Phenyl-2-Azido-Ethanol is experimental.,(R)-1-Para-Nitro-Phenyl-2-Azido-Ethanol is a solid.,False
20019,,,,,"D-gluconhydroximo-1,5-lactam is experimental.","D-gluconhydroximo-1,5-lactam is a solid.",False
20020,,,,,alpha-D-Xylopyranose is experimental.,alpha-D-Xylopyranose is a solid.,False
20021,,,,,2-deoxy-2-fluoro-α-D-glucose is experimental.,2-deoxy-2-fluoro-α-D-glucose is a solid.,False
20022,"Gluconolactone is a naturally-occurring food additive used as a sequestrant, an acidifier, or a curing, pickling, or leavening agent. It is a cyclic ester of D-gluconic acid. Pure gluconolactone is a white odorless crystalline powder.",The molecular weight is 178.14.,Gluconolactone has a topological polar surface area of 107.22.,The log p value of  is -2.23.,Gluconolactone is approved and experimental.,Gluconolactone is a solid.,True
20023,,,,,"(1S,2S,3R,4S,5S)-2,3,4-TRIHYDROXY-5-(HYDROXYMETHYL)CYCLOHEXYL (1E)-2-PHENYL-N-(SULFOOXY)ETHANIMIDOTHIOATE is experimental.","(1S,2S,3R,4S,5S)-2,3,4-TRIHYDROXY-5-(HYDROXYMETHYL)CYCLOHEXYL (1E)-2-PHENYL-N-(SULFOOXY)ETHANIMIDOTHIOATE is a solid.",False
20024,,,,,ETHYL (1E)-2-PHENYL-N-(SULFOOXY)ETHANIMIDOTHIOATE is experimental.,ETHYL (1E)-2-PHENYL-N-(SULFOOXY)ETHANIMIDOTHIOATE is a solid.,False
20025,,,,,"(5R)-2-sulfanyl-5--1,3-thiazol-4(5H)-one is experimental.","(5R)-2-sulfanyl-5--1,3-thiazol-4(5H)-one is a solid.",False
20026,,,,,1-(3-HYDROXYPROPYL)-2--1H-BENZIMIDAZOL-5-YL PIVALATE is experimental.,1-(3-HYDROXYPROPYL)-2--1H-BENZIMIDAZOL-5-YL PIVALATE is a solid.,False
20027,,,,,"4-({(2R,5S)-2,5-DIMETHYL-4-PIPERAZIN-1-YL}CARBONYL)BENZONITRILE is experimental.","4-({(2R,5S)-2,5-DIMETHYL-4-PIPERAZIN-1-YL}CARBONYL)BENZONITRILE is a solid.",False
20028,,,,,"(2R)-N-{4--2-methylphenyl}-3,3,3-trifluoro-2-hydroxy-2-methylpropanamide is experimental.","(2R)-N-{4--2-methylphenyl}-3,3,3-trifluoro-2-hydroxy-2-methylpropanamide is a solid.",False
20029,,,,,N-(2-AMINOETHYL)-2-{3-CHLORO-4-PHENYL} ACETAMIDE is experimental.,N-(2-AMINOETHYL)-2-{3-CHLORO-4-PHENYL} ACETAMIDE is a solid.,False
20030,,,,,"1,1,1-TRIFLUORO-3-(OCTYLTHIO)ACETONE is experimental.","1,1,1-TRIFLUORO-3-(OCTYLTHIO)ACETONE is a solid.",False
20031,,,,,"9-ACETYL-2,3,4,9-TETRAHYDRO-1H-CARBAZOL-1-ONE is experimental.","9-ACETYL-2,3,4,9-TETRAHYDRO-1H-CARBAZOL-1-ONE is a solid.",False
20032,,,,,2-Undecanone is experimental.,2-Undecanone is a solid.,False
20033,,,,,1-tert-butyl-3-(3-methylbenzyl)-1H-pyrazolopyrimidin-4-amine is experimental.,1-tert-butyl-3-(3-methylbenzyl)-1H-pyrazolopyrimidin-4-amine is a solid.,False
20034,,,,,"12-(2-hydroxyethyl)-2-(1-methylethoxy)-13,14-dihydronaphthopyrrolocarbazol-5(12H)-one is experimental.","12-(2-hydroxyethyl)-2-(1-methylethoxy)-13,14-dihydronaphthopyrrolocarbazol-5(12H)-one is a solid.",False
20035,,,,,2-(4-CHLORO-PHENYLAMINO)-NICOTINIC ACID is experimental.,2-(4-CHLORO-PHENYLAMINO)-NICOTINIC ACID is a solid.,False
20036,,,,,"Inositol-(1,3,4,5,6)-Pentakisphosphate is experimental.","Inositol-(1,3,4,5,6)-Pentakisphosphate is a solid.",False
20037,,,,,Uridine is experimental and investigational.,Uridine is a solid.,False
20038,,,,,"D-Myo-Inositol-1,4-Bisphosphate is experimental.","D-Myo-Inositol-1,4-Bisphosphate is a solid.",False
20039,,,,,4-phospho-L-threonic acid is experimental.,4-phospho-L-threonic acid is a solid.,False
20040,,,,,Malonate Ion is experimental.,Malonate Ion is a solid.,False
20041,"3-Fluoro-L-tyrosine is a solid. This compound belongs to the phenylpropanoic acids. These are compounds whose structure contain a benzene ring conjugated to a propanoic acid. 3-Fluoro-L-tyrosine targets the protein superoxide dismutase , mitochondrial.",,,,3-Fluoro-L-tyrosine is experimental.,3-Fluoro-L-tyrosine is a solid.,True
20042,,,,,S-Mercaptocysteine is experimental.,S-Mercaptocysteine is a solid.,False
20043,,,,,"1,4-dithio-alpha-D-glucopyranose is experimental.","1,4-dithio-alpha-D-glucopyranose is a solid.",False
20044,,,,,4-Methylthio-Alpha-D-Mannose is experimental.,4-Methylthio-Alpha-D-Mannose is a solid.,False
20045,,,,,alpha-maltotriose is experimental.,alpha-maltotriose is a solid.,False
20046,"A dextrodisaccharide from malt and starch. It is used as a sweetening agent and fermentable intermediate in brewing. (Grant & Hackh&#39;s Chemical Dictionary, 5th ed)",The molecular weight is 342.3.,Maltose has a topological polar surface area of 189.53.,The log p value of  is -4.4.,Maltose is experimental and investigational.,Maltose is a solid.,True
20047,,,,,Trifluoroacetonyl coenzyme A is experimental.,Trifluoroacetonyl coenzyme A is a solid.,False
20048,,,,,alpha-Fluoro-carboxymethyldethia coenzyme A complex is experimental.,alpha-Fluoro-carboxymethyldethia coenzyme A complex is a solid.,False
20049,,,,,Nitromethyldethia coenzyme A is experimental.,Nitromethyldethia coenzyme A is a solid.,False
20050,A 2-phosphoglyceric acid in which the glyceric acid moiety has D (R) configuration.,,,,2-phospho-D-glyceric acid is experimental.,2-phospho-D-glyceric acid is a solid.,True
20051,,,,,Phosphonoacetohydroxamic Acid is experimental.,Phosphonoacetohydroxamic Acid is a solid.,False
20052,,,,,"Alpha-D-Glucose 1,6-Bisphosphate is experimental.","Alpha-D-Glucose 1,6-Bisphosphate is a solid.",False
20053,,,,,Alpha-D-Glucose-1-Phosphate-6-Vanadate is experimental.,Alpha-D-Glucose-1-Phosphate-6-Vanadate is a solid.,False
20054,,,,,Benzene Hexacarboxylic Acid is experimental.,Benzene Hexacarboxylic Acid is a solid.,False
20055,,,,,Porphyrin Fe(III) is experimental.,Porphyrin Fe(III) is a solid.,False
20056,,,,,N-Butyl Isocyanide is experimental.,N-Butyl Isocyanide is a solid.,False
20057,,,,,Methylethylamine is experimental.,Methylethylamine is a solid.,False
20058,,,,,Tetrazolyl Histidine is experimental.,Tetrazolyl Histidine is a solid.,False
20059,,,,,Nitrosoethane is experimental.,Nitrosoethane is a solid.,False
20060,,,,,1-Methylimidazole is experimental.,1-Methylimidazole is a solid.,False
20061,,,,,Ethyl Isocyanide is experimental.,Ethyl Isocyanide is a solid.,False
20062,,,,,N-Propyl Isocyanide is experimental.,N-Propyl Isocyanide is a solid.,False
20063,,,,,Isocyanomethane is experimental.,Isocyanomethane is a solid.,False
20064,"Carbon monoxide (CO) is a colorless, odorless, and tasteless gas that has a slightly lower density than air. It is toxic to hemoglobin utilizing animals (including humans), when encountered in concentrations above about 35 ppm, although it is also formed in normal animal metabolism in low quantities, and is thought to have some normal biological/homeostatic functions. Carbon monoxide (CO), is a ubiquitous environmental product of organic combustion, which is also formed endogenously in the human body, as the byproduct of heme metabolism. Exhaled CO (eCO), similar to exhaled nitric oxide (eNO), has been evaluated as a candidate breath biomarker of pathophysiological states, including smoking status, and inflammatory diseases of the lung and other organs. Exhalation of corbon monoxide values have been studied as potential indicators of inflammation in asthma, stable COPD and exacerbations, cystic fibrosis, lung cancer, and during surgery or critical care. Used as a marker of respiratory status in spirometry tests ,. Carbon monoxide is used to measure the diffusing capacity for carbon monoxide (DLCO), also known as the transfer factor for carbon monoxide. It is a measure of the gas transfer from inspired gas to the circulatory system (red blood cells in particular). It is used in a particular pulmonary function test called \the single-breath test\"".""",,,,Carbon monoxide is approved and investigational.,Carbon monoxide is a gas.,True
20065,,,,,6-hydroxyuridine-5'-phosphate is experimental.,6-hydroxyuridine-5'-phosphate is a solid.,False
20066,"A non-hydrolyzable analog of GTP, in which the oxygen atom bridging the beta to the gamma phosphate is replaced by a nitrogen atom. It binds tightly to G-protein in the presence of Mg2+. The nucleotide is a potent stimulator of adenylate cyclase.",,,,Phosphoaminophosphonic acid guanylate ester is experimental.,Phosphoaminophosphonic acid guanylate ester is a solid.,True
20067,,,,,Methyl N-{-L-prolyl-6-ammonio-L-norleucyl}amino)-2-phenylethyl](hydroxy)phosphoryl}-L-alanyl-L-prolinate is experimental.,Methyl N-{-L-prolyl-6-ammonio-L-norleucyl}amino)-2-phenylethyl](hydroxy)phosphoryl}-L-alanyl-L-prolinate is a solid.,False
20068,,,,,O3-Sulfonylgalactose is experimental.,O3-Sulfonylgalactose is a solid.,False
20069,,,,,Methyl alpha-D-mannoside is experimental.,Methyl alpha-D-mannoside is a solid.,False
20070,,,,,4-(Hydrogen sulfate)-beta-D-galactopyranose is experimental.,4-(Hydrogen sulfate)-beta-D-galactopyranose is a solid.,False
20071,,,,,Methyl beta-L-fucopyranoside is experimental.,Methyl beta-L-fucopyranoside is a solid.,False
20072,,,,,alpha-L-methyl-fucose is experimental.,alpha-L-methyl-fucose is a solid.,False
20073,,,,,Alpha-Methyl-N-Acetyl-D-Glucosamine is experimental.,Alpha-Methyl-N-Acetyl-D-Glucosamine is a solid.,False
20074,,,,,"2',3'-Dideoxyadenosine triphosphate is experimental.","2',3'-Dideoxyadenosine triphosphate is a solid.",False
20075,,,,,"Inositol 2,4,5-trisphosphate is experimental.","Inositol 2,4,5-trisphosphate is a solid.",False
20076,"Thiodigalactoside is a solid. This compound belongs to the dihexoses. These are disaccharides containing two hexose carbohydrates. This medication is known to target galectin-1, heat-labile enterotoxin b chain, neurocan core protein, and lactose permease.",,,,Thiodigalactoside is experimental.,Thiodigalactoside is a solid.,True
20077,"Aglucosidase alfa consists of the human enzyme acid alpha-glucosidase (GAA) which is essential for the degradation of glygogen to glucose in lysosomes. It is encoded by the most predominant of nine observed haplotypes of this gene. Aglucosidase alfa is produced by recombinant DNA technology in a Chinese hamster ovary cell line. Alglucosidase alfa degrades glycogen by catalyzing the hydrolysis of a-1,4- and a-1,6- glycosidic linkages of lysosomal glycogen. Structurally, Alglucosidase alfa is a glycoprotein with a calculated mass of 98,008 daltons for the 883 residue mature polypeptide chain, and a total mass of approximately 109,000 daltons, including carbohydrates. It is used for the treatment of Pompe disease (GAA deficiency) in infants and pediatric patients. For the treatment of Pompe disease (GAA deficiency) in infants and pediatric patients. Pompe disease (glycogen storage disease type II, GSD II, glycogenosis type II, acid maltase deficiency) is an inherited disorder of glycogen metabolism caused by the absence or marked deficiency of the lysosomal enzyme GAA. In the infantile-onset form, Pompe disease results in intralysosomal accumulation of glycogen in various tissues, particularly cardiac and skeletal muscles, and hepatic tissues, leading to the development of cardiomyopathy, progressive muscle weakness, and impairment of respiratory function. In the juvenile- and adult-onset forms, intralysosomal accumulation of glycogen is limited primarily to skeletal muscle, resulting in progressive muscle weakness. Death in all forms is usually related to respiratory failure. Alglucosidase alfa provides an exogenous source of GAA. Binding to mannose-6-phosphate receptors on the cell surface has been shown to occur via carbohydrate groups on the GAA molecule, after which it is internalized and transported into lysosomes, where it undergoes proteolytic cleavage that results in increased enzymatic activity. It then exerts enzymatic activity in cleaving glycogen. Alglucosidase alfa is designed to act as an exogenous source of GAA, acting to correct GAA deficiency that is the hallmark of Pompe disease. Alglucosidase alfa binds to mannose-6-phosphate receptors on the cell surface via carbohydrate groups on the GAA molecule, after which it is internalized and transported into lysosomes, where it undergoes proteolytic cleavage that results in increased enzymatic activity. It then exerts enzymatic activity in cleaving glycogen. Specifically, it hydrolyses alpha-1,4-glucose bonds.",,,,Alglucosidase alfa is approved.,Alglucosidase alfa is a liquid.,True
20078,,,,,1-3 Sugar Ring of Pentamannosyl 6-Phosphate is experimental.,1-3 Sugar Ring of Pentamannosyl 6-Phosphate is a solid.,False
20079,,,,,cis-tetracosenoyl sulfatide is experimental.,cis-tetracosenoyl sulfatide is a solid.,False
20080,,,,,2-Deoxy-D-Glucitol 6-(E)-Vinylhomophosphonate is experimental.,2-Deoxy-D-Glucitol 6-(E)-Vinylhomophosphonate is a solid.,False
20081,,,,,2-Deoxy-Glucitol-6-Phosphate is experimental.,2-Deoxy-Glucitol-6-Phosphate is a solid.,False
20082,,,,,Hexanoyl-CoA is experimental.,Hexanoyl-CoA is a solid.,False
20083,,,,,"4-(N,N-Dimethylamino)cinnamoyl-CoA is experimental.","4-(N,N-Dimethylamino)cinnamoyl-CoA is a solid.",False
20084,,,,,Arginineamide is experimental.,Arginineamide is a solid.,False
20085,,,,,4-Hydroxy-Aconitate Ion is experimental.,4-Hydroxy-Aconitate Ion is a solid.,False
20086,,,,,Alpha-Methylisocitric Acid is experimental.,Alpha-Methylisocitric Acid is a solid.,False
20087,,,,,Aconitate Ion is experimental.,Aconitate Ion is a solid.,False
20088,,,,,Tricarballylic acid is experimental.,Tricarballylic acid is a solid.,False
20089,,,,,"1-Ethyl-Pyrrolidine-2,5-Dione is experimental.","1-Ethyl-Pyrrolidine-2,5-Dione is a solid.",False
20090,,,,,Cordycepin Triphosphate is experimental.,Cordycepin Triphosphate is a solid.,False
20091,"Used as water softener, peptizing agent, emulsifier & dispersing agent; ingredient of cleansers; meat preservative.",,,,Triphosphoric acid is experimental.,Triphosphoric acid is a solid.,True
20092,"Trimetazidine is a drug for angina pectoris sold under the brand name Vastarel MR. Trimetazidine is described as the first cytoprotective anti-ischemic agent developed and marketed by Laboratoires Servier (France). Trimetazidine is an anti-ischemic (anti-anginal) metabolic agent, which improves myocardial glucose utilization through inhibition of long-chain 3-ketoacyl CoA thiolase activity, which results in a reduction in fatty acid oxidation and a stimulation of glucose oxidation. High fatty acid oxidation rates are detrimental during ischemia due to an inhibition of glucose oxidation leading to uncoupling of glycolysis and an increase in proton production, which has the potential to accelerate sodium and calcium overload in the heart, which leads to an exacerbation of ischemic injury and decreased cardiac efficiency during reperfusion. Trimetazidine is indicated for use in angina pectoris. Trimetazidine is an anti-ischemic (anti-anginal) metabolic agent, which improves myocardial glucose utilization through inhibition of long-chain 3-ketoacyl CoA thiolase activity, which results in a reduction in fatty acid oxidation and a stimulation of glucose oxidation. High fatty acid oxidation rates are detrimental during ischemia due to an inhibition of glucose oxidation leading to uncoupling of glycolysis and an increase in proton production, which has the potential to accelerate sodium and calcium overload in the heart. This leads to an exacerbation of ischemic injury and decreased cardiac efficiency during reperfusion.",The molecular weight is 266.34.,Trimetazidine has a topological polar surface area of 42.96.,The log p value of  is 1.18.,Trimetazidine is approved and investigational.,Trimetazidine is a solid.,True
20093,"Thonzonium is a monocationic surface-active agent with surfactant and detergent properties. It is widely used as an additive to in ear and nasal drops to enhance dispersion and penetration of cellular debris and exudate, thereby promoting tissue contact of the administered medication. A common pharmaceutical formulation of thonzonium bromide is cortisporin-TC ear drops. It is also reported that thonzonium also confers an antifungal property and antiresorptive effect on bone. Used as a monocationic surfactant and detergent to help penetration of active ingredients through cellular debris for its antibacterial action. Thonzonium bromide causes dispersion and penetration of cellular debris and exudate, thereby promoting tissue contact of the active ingredients contained in the administered medication. It is an inhibitor of vacuolar ATPase that uncouples and blocks the function of the pump without inhibiting ATP hydrolysis.  Thonzonium bromide is a suface-active agent added in nasal and ear drops that potentiates and lenghten the time of skin contact with the active compounds and penetration through the cellular debris. ",,,,Thonzonium is approved.,Thonzonium is a solid.,True
20094,,,,,D-Myo-Inositol-Hexasulphate is experimental.,D-Myo-Inositol-Hexasulphate is a solid.,False
20095,,,,,O-Benzylsulfonyl-Serine is experimental.,O-Benzylsulfonyl-Serine is a solid.,False
20096,,,,,"(R,R)-2,3-Butanediol is experimental.","(R,R)-2,3-Butanediol is a solid.",False
20097,,,,,Acetoacetic acid is experimental.,Acetoacetic acid is a solid.,False
20098,,,,,4-]-3-Oxo-Butanoic Acid is experimental.,4-]-3-Oxo-Butanoic Acid is a solid.,False
20099,,,,,L-methionine (S)-S-oxide is experimental.,L-methionine (S)-S-oxide is a solid.,False
20100,,,,,Hexadecanesulfonyl fluoride is experimental.,Hexadecanesulfonyl fluoride is a solid.,False
20101,,,,,"(1R,2R,3S,4R,6S)-3,4,6-Trihydroxy-5-{oxy}-1,2-cyclohexanediyl bis is experimental.","(1R,2R,3S,4R,6S)-3,4,6-Trihydroxy-5-{oxy}-1,2-cyclohexanediyl bis is a solid.",False
20102,Component of human seminal plasma & spermatozoa.,,,,Cholesterol sulfate is experimental.,Cholesterol sulfate is a solid.,True
20103,,,,,Aspartate Beryllium Trifluoride is experimental.,Aspartate Beryllium Trifluoride is a solid.,False
20104,,,,,"2,8-bis-1,1,1,3,5,5,7,7,9,9,9-undecaoxopentavanadoxane-2,8-diium is experimental.","2,8-bis-1,1,1,3,5,5,7,7,9,9,9-undecaoxopentavanadoxane-2,8-diium is a solid.",False
20105,,,,,(4s)-5-Fluoro-L-Leucine is experimental.,(4s)-5-Fluoro-L-Leucine is a solid.,False
20106,,,,,Leucine - Reduced Carbonyl is experimental.,Leucine - Reduced Carbonyl is a solid.,False
20107,A nucleoside monophosphate sugar which donates N-acetylneuraminic acid to the terminal sugar of a ganglioside or glycoprotein. ,,,,Cytidine-5'-Monophosphate-5-N-Acetylneuraminic Acid is experimental.,Cytidine-5'-Monophosphate-5-N-Acetylneuraminic Acid is a solid.,True
20108,,,,,Guanidinoethylmercaptosuccinic acid is experimental.,Guanidinoethylmercaptosuccinic acid is a solid.,False
20109,,,,,Fusicoccin is experimental.,Fusicoccin is a solid.,False
20110,,,,,S-Acetyl-Cysteine is experimental.,S-Acetyl-Cysteine is a solid.,False
20111,,,,,4-Deoxy-Alpha-D-Glucose is experimental.,4-Deoxy-Alpha-D-Glucose is a solid.,False
20112,,,,,CoA-S-trimethylene-acetyl-tryptamine is experimental.,CoA-S-trimethylene-acetyl-tryptamine is a solid.,False
20113,,,,,CoA-s-acetyl tryptamine is experimental.,CoA-s-acetyl tryptamine is a solid.,False
20114,,,,,CoA-S-acetyl 5-bromotryptamine is experimental.,CoA-S-acetyl 5-bromotryptamine is a solid.,False
20115,,,,,Sinapoyl coenzyme A is experimental.,Sinapoyl coenzyme A is a solid.,False
20116,,,,,Feruloyl Coenzyme A is experimental.,Feruloyl Coenzyme A is a solid.,False
20117,,,,,3-Phosphono-D-alanine is experimental.,3-Phosphono-D-alanine is a solid.,False
20118,"99mTc 14F7 Mab has strong anti tumor activity against myeloma cells in vivo. Growth inhibition and prolonged survival of the myeloma tumor were obtained as evidences of anti tumor effect after treatment with 99mTc 14F7 Mab.  Investigated for use/treatment in breast cancer. The 99mTc 14F7 Mab has shown to bind specifically to GM3 (NeuGc) and that it also reacts with human breast and melanoma tumors in contrast with its low reactivity in normal tissues. N-Glycolyl GM3 is considered a heterophilic antigen since is not present in all species, humans are normally lacking them. The discovery of the presence of this molecule in significant amounts in breast tumors allowed considering it as an advantageous target for cancer immunotherapy.",,,,99mTc-14 F7 Mab is investigational.,99mTc-14 F7 Mab is a solid.,True
20119,,,,,Dansyllysine is experimental.,Dansyllysine is a solid.,False
20120,,,,,Aminophosphonic acid-guanylate ester is experimental.,Aminophosphonic acid-guanylate ester is a solid.,False
20121,,,,,beta-Hydroxyasparagine is experimental.,beta-Hydroxyasparagine is a solid.,False
20122,"Brivudine is used in the treatment of herpes zoster. Although not approved in the U.S. or Canada, it is approved in several European countries.",The molecular weight is 333.14.,Brivudine has a topological polar surface area of 99.1.,The log p value of  is -0.82.,Brivudine is approved and investigational.,Brivudine is a solid.,True
20123,"Thymidine is a pyrimidine deoxynucleoside. Thymidine is the DNA nucleoside T, which pairs with deoxyadenosine (A) in double-stranded DNA. In cell biology it is used to synchronize the cells in S phase.",,,,Thymidine is experimental and investigational.,Thymidine is a solid.,True
20124,"Carglumic acid is a drug used for the treatment of hyperammonemia in patients with a deficiency in N-acetyl glutamate synthase. This rare genetic disorder results in elevated blood levels of ammonia, which can eventually cross the blood–brain barrier and cause neurologic problems, cerebral edema, coma, and death. Carglumic acid was approved by the U.S. Food and Drug Administration (FDA) on 18 March 2010. For the treatment of acute and chronic hyperammonaemia in patients with N-acetylglutamate synthase (NAGS) deficiency. This enzyme is an important component of the urea cycle to prevent build up of neurotoxic ammonium in the blood.  The median Tmax of Carbaglu was 3 hours (range: 2-4). The daily dose of carglumic acid ranges from 100 to 250 mg/kg and this does are normally adjusted to maintain normal plasma levels of ammonia. Carglumic acid is a synthetic structural analogue of N-acetylglutamate (NAG), which is an essential allosteric activator of the liver enzyme carbamoyl phosphate synthetase 1 (CPS1). CPS1 is found in the mitochondria and is the first enzyme of the urea cycle, which converts ammonia into urea. Carglumic acid acts as a replacement for NAG in NAGS deficiency patients by activating CPS1 but it does not help to regulate the urea cycle.",The molecular weight is 190.16.,Carglumic acid has a topological polar surface area of 129.72.,The log p value of  is -1.94.,Carglumic acid is approved.,Carglumic acid is a solid.,True
20125,"Ethanolamine oleate is a mild sclerosing agent. It is composed of ethanolamine, a basic substance, which when combined with oleic acid forms a clear, straw to pale yellow colored, deliquescent oleate. For the treatment of patients with esophageal varices that have recently bled, to prevent rebleeding. When injected intravenously, ethanolamine oleate acts primarily by irritation of the intimal endothelium of the vein and produces a sterile dose-related inflammatory response. This results in fibrosis and possible occlusion of the vein. Ethanolamine oleate also rapidly diffuses through the venous wall and produces a dose-related extravascular inflammatory reaction. The oleic acid component of ethanolamine oleate is responsible for the inflammatory response, and may also activate coagulation in vivo by release of tissue factor and activation of Hageman factor. The ethanolamine component, however, may inhibit fibrin clot formation by chelating calcium, so that a procoagulant action of ethanolamine oleate has not been demonstrated.",The molecular weight is 343.55.,Ethanolamine oleate has a topological polar surface area of 37.3.,,Ethanolamine oleate is approved.,Ethanolamine oleate is a solid.,True
20126,"Dimethyl fumarate is an anti-inflammatory. It is indicated for multiple sclerosis patients with relapsing forms and is also being investigated for the treatment of psoriasis. The mechanism of action of dimethyl fumarate in multiple sclerosis is not well understood. It is thought to involve dimethyl fumarate degradation to its active metabolite monomethyl fumarate (MMF) then MMF up-regulates the Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathway that is activated in response to oxidative stress. Dimethyl fumarate is marketed under the brand name Tecfidera. Used in multiple sclerosis patients with relapsing forms. The physiological effects dimethyl fumarate has on the body is not well understood. It is known that dimethyl fumarate has anti-inflammatory and cytoprotective effects, which both are likely involved in its actions in multiple sclerosis patients. The mechanism of action of dimethyl fumarate in multiple sclerosis is not well understood. It is thought to involve dimethyl fumarate degradation to its active metabolite monomethyl fumarate (MMF). MMF up-regulates the Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) pathway that is activated in response to oxidative stress. As well MMF is an agonist at the nicotinic acid receptor, but the relevance of this is not known.",The molecular weight is 144.13.,Dimethyl fumarate has a topological polar surface area of 52.6.,The log p value of  is 0.78.,Dimethyl fumarate is approved and investigational.,Dimethyl fumarate is a solid.,True
20127,"1D09C3, a monoclonal antibody against lymphoid cancers, is an anti-MHC (major histocompatibility complex) class II monoclonal antibody. The antibody was isolated in collaboration with MorphoSys from its HuCAL(R) library of human antibodies. 1D09C3 binds to certain cell surface receptors, selectively killing activated, proliferating MHC class II-positive tumor cells, which include those in B-cell and T-cell lymphomas. 1D09C3 has been shown to induce programmed cell death and does not require a functioning immune system for its cell-killing effect. Intended for the treatment of various forms of cancer. 1D09C3 binds specifically to the MHC (major histocompatibility complex) class II molecule, which is found mainly on the surface of blood cells and certain tumor cells. It selectively kills activated, proliferating MHC class II-positive tumor cells, which include those in B-cell and T-cell lymphomas. 1D09C3 has been shown to kill these tumor cells by inducing programmed cell death.",,,,1D09C3 is investigational.,1D09C3 is a liquid.,True
20128,"Ethchlorvynol is a sedative and hypnotic drug. It has been used to treat insomnia, but has been largely superseded and is only offered where an intolerance or allergy to other drugs exists. Used for short-term hypnotic therapy in the management of insomnia for periods of up to one week in duration; however, this medication generally has been replaced by other sedative-hypnotic agents. Ethchlorvynol is a sedative drug and schedule IV (USA) controlled substance. It produces cerebral depression, however the exact mechanism of action is not known. Although the exact mechanism of action is unknown, ethchlorvynol appears to depress the central nervous system in a manner similar to that of barbiturates. Barbiturates bind at a distinct binding sites associated with a Cl<sup>-</sup> ionopore at the GABA<sub>A</sub> receptor, increasing the duration of time for which the Cl<sup>-</sup> ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged.",The molecular weight is 144.6.,Ethchlorvynol has a topological polar surface area of 20.23.,The log p value of  is 1.39.,Ethchlorvynol is approved and illicit and withdrawn.,Ethchlorvynol is a liquid.,True
20129,"An anxiolytic benzodiazepine derivative with anticonvulsant, sedative, and amnesic properties. It has also been used in the symptomatic treatment of alcohol withdrawal. For the management of anxiety disorders or for the short-term relief of symptoms of anxiety, withdrawal symptoms of acute alcoholism, and preoperative apprehension and anxiety. Chlordiazepoxide has antianxiety, sedative, appetite-stimulating and weak analgesic actions. The drug seems to block EEG arousal from stimulation in the brain stem reticular formation. The drug has been studied extensively in many species of animals and these studies are suggestive of action on the limbic system of the brain, which recent evidence indicates is involved in emotional responses. Hostile monkeys were made tame by oral drug doses which did not cause sedation. Chlordiazepoxide revealed a \taming\"" action with the elimination of fear and aggression. The taming effect of chlordiazepoxide was further demonstrated in rats made vicious by lesions in the septal area of the brain. The drug dosage which effectively blocked the vicious reaction was well below the dose which caused sedation in these animals."" Chlordiazepoxide binds to stereospecific benzodiazepine (BZD) binding sites on GABA (A) receptor complexes at several sites within the central nervous system, including the limbic system and reticular formation. This results in an increased binding of the inhibitory neurotransmitter GABA to the GABA(A) receptor. BZDs, therefore, enhance GABA-mediated chloride influx through GABA receptor channels, causing membrane hyperpolarization. The net neuro-inhibitory effects result in the observed sedative, hypnotic, anxiolytic, and muscle relaxant properties.",The molecular weight is 299.76.,Chlordiazepoxide has a topological polar surface area of 53.14.,The log p value of  is 3.79.,Chlordiazepoxide is approved and illicit and investigational.,Chlordiazepoxide is a solid.,True
20130,"Halazepam is a _benzodiazepine_ derivative drug exerting anxiolytic, anticonvulsant, sedative, a muscle relaxing effects. It has been shown to be less toxic than chlordiazepoxide or diazepam. This drug is no longer marketed in the United States, and was withdrawn by _Schering_, its manufacturer, in 2009. Used to relieve anxiety, nervousness, and tension associated with anxiety disorders. Benzodiazepines bind nonspecifically to benzodiazepine receptors BNZ1, which mediates sleep, and BNZ2, which affects affects muscle relaxation, anticonvulsant activity, motor coordination, and memory. As benzodiazepine receptors are thought to be coupled to gamma-aminobutyric acid-A (GABAA) receptors, this enhances the effects of GABA by increasing GABA affinity for the GABA receptor. Binding of GABA to the site opens the chloride channel, resulting in a hyperpolarized cell membrane that prevents further excitation of the cell.",The molecular weight is 352.74.,Halazepam has a topological polar surface area of 32.67.,The log p value of  is 3.75.,Halazepam is approved and illicit and withdrawn.,Halazepam is a solid.,True
20131,"Camazepam is a benzodiazepine which is a dimethyl carbamate ester of tamzepam, a metabolite of diazepam. Similarly to other drugs in its class, it has antxiolytic, anticonvulsant, hypnotic, and skeletal muscle relaxant properties. However, unlike other benzodiapeines camazepam is predominantly anxiolytic and is relatively weak as an anticonvulsant, hypnotic and skeletal muscle relaxant. Camazepam has been used in placebo controlled studies for the treatment of patients suffering from anxiety and depression.  Camazepam has been shown to bind competitively to benzodiazepine receptors in the brain with a relatively low affinity in animal models. This binding of benzodiazepine receptors by camazepam and its active metabolites is responsible for its anticonvulsant effects. Notably, only three metabolites were shown to exert anticonvulsant activity, temazepam, oxazepam, and hydroxy camazepam. ",The molecular weight is 371.82.,Camazepam has a topological polar surface area of 62.21.,The log p value of  is 3.44.,Camazepam is experimental and illicit.,Camazepam is a solid.,True
20132,"Delorazepam is a benzodiazepine which, like other drugs in its class, possesses anxiolytic, skeletal muscle relaxant, hypnotic and anticonvulsant properties. It may have adverse effects such as drowsiness, and cognitive impairments such as short term memory impairment.   Mainly used as an anti-anxiety agent. Studies have found delorazepam to be more effective in the first 4 weeks of use than antidepressants; however, after 4 weeks, antidepressants showed superior anti-anxiety effects. Anti-anxiety effects also appear to be weaker in elderly patients. ",The molecular weight is 305.16.,Delorazepam has a topological polar surface area of 41.46.,The log p value of  is 3.08.,Delorazepam is experimental and illicit.,Delorazepam is a solid.,True
20133,,The molecular weight is 360.77.,Ethyl loflazepate has a topological polar surface area of 67.76.,The log p value of  is 3.19.,Ethyl loflazepate is experimental and illicit.,Ethyl loflazepate is a solid.,False
20134,"Cloxazolam is a benzodiazepine with anxiolytic, sedative/hypnotic, muscle relaxant, and antiepileptic effects. It is marketed in the Argentina, Australia, Portugal, Belgium, Switzerland, Luxembourg, Germany, Taiwan and Japan -- mainly for anti-anxiety. The usual dose of cloxazolam in adults is 3-12mg/day for anti-anxiety. Although less commonly noted, it has also been reported as clinically effective in the treatment of depression, schizophrenia, and neurosis. As well, it has also been studied in Japan in doses of 15-30mg/day as an adjunct in the treatment of intractable epilepsy, for which it has demonstrated effectiveness. Used primarily as an anti-anxiety agent. Typically used short term, and may be given as a single dose of up to 100mcg/kg to reduce anxiety and tension experienced prior to surgery.  Studies have shown a superiority of 4mg/day of cloxazepam to 12mg/day of bromazepam in terms of anxiety, depressed mood, and sleep; an insignificant difference in terms of sedative effect; and less muscle relaxant effects.   Cloxazolam is a long acting benzodiazepine. It acts as a prodrug, with pharmacologically active metabolites, which bind to to the GABAa receptor, which other benzodiazepines bind to, to illicit a physiological response.  ",The molecular weight is 349.21.,Cloxazolam has a topological polar surface area of 41.57.,The log p value of  is 4.3.,Cloxazolam is experimental.,Cloxazolam is a solid.,True
20135,"Cinolazepam is a benzodiazepine derivative with anxiolytic, anticonvulsant, sedative and skeletal muscle relaxant activity. It is not approved in Canada or America. For the management of anxiety disorders or for the short-term relief of the symptoms of anxiety or anxiety associated with depressive symptoms. Cinolazepam is a benzodiazepine derivative with anxiolytic, anticonvulsant, sedative and skeletal muscle relaxant activity. It is not approved in Canada or America. Cinolazepam binds to central benzodiazepine receptors which interact allosterically with GABA receptors. This potentiates the effects of the inhibitory neurotransmitter GABA, increasing the inhibition of the ascending reticular activating system and blocking the cortical and limbic arousal that occurs following stimulation of the reticular pathways.",The molecular weight is 357.77.,Cinolazepam has a topological polar surface area of 76.69.,The log p value of  is 1.91.,Cinolazepam is experimental.,Cinolazepam is a solid.,True
20136,,The molecular weight is 308.77.,Pinazepam has a topological polar surface area of 32.67.,The log p value of  is 3.38.,Pinazepam is experimental.,,False
20137,,The molecular weight is 270.76.,Medazepam has a topological polar surface area of 15.6.,The log p value of  is 4.12.,Medazepam is experimental.,,False
20138,"Loprazolam is an imidazobenzodiazepine with anxiolytic, anticonvulsant, hypnotic, sedative and skeletal muscle relaxant properties. It is indicated for the short-term treatment of insomnia including difficulty in falling asleep and/or frequent nocturnal awakenings. Loprazolam is recommended as a short-term therapy only, due to adverse events associated with the drug including dependence and withdrawal symptoms. It is a positive modulator of GABA-A receptor that enhances the inhibitory neurotransmission. It is not an FDA-approved drug.",The molecular weight is 464.91.,Loprazolam has a topological polar surface area of 97.33.,The log p value of  is 0.43.,Loprazolam is experimental.,,True
20139,,The molecular weight is 348.76.,Doxefazepam has a topological polar surface area of 73.13.,The log p value of  is 1.59.,Doxefazepam is experimental.,,False
20140,"Lormatazepam is an orally available benzodiazepine used in the UK for the treatment of short-term insomnia. It is marketed by Auden Mckenzie (Pharma Division) in 0.5 and 1 mg tablet formulations. For the treatment of short-term insomnia  Lormetazepam is a benzodiazepine which reduces central nervous system (CNS) activity. It produces anxiolytic, muscle relaxant, sedative and hypnotic effects. Because it is a short-acting benzodiapine, it does not produce significant sedation after waking. Lormetazepam, as a benzodiazepine, binds to the regulatory site between the α and γ subunits of γ-aminobutryic acid (GABA) A receptors with γ2 and α1, α2, α3, or α5 subunits. This facilitates the opening of the chloride channel allowing chloride ions to flow into the neuron resulting in hyperpolarization. Hyperpolarized neurons require greater simulation to reach their action potential threshold. The general inhibitory effect on neuronal depolarization produces the effects of lormetazepam.",The molecular weight is 335.18.,Lormetazepam has a topological polar surface area of 52.9.,The log p value of  is 2.4.,Lormetazepam is approved.,Lormetazepam is a solid.,True
20141,An intermediate in the metabolism of DIAZEPAM to OXAZEPAM. It may have actions similar to those of diazepam.,The molecular weight is 270.72.,Nordazepam has a topological polar surface area of 41.46.,The log p value of  is 3.02.,Nordazepam is experimental.,Nordazepam is a solid.,True
20142,,,,,Oxazepam acetate is experimental.,,False
20143,,,,,Cinazepam is experimental.,,False
20144,,The molecular weight is 296.39.,Bentazepam has a topological polar surface area of 41.46.,The log p value of  is 3.51.,Bentazepam is experimental.,,False
20145,"Magnesium acetate tetrahydrate is a hydrated form of anhydrous magnesium acetate salt with the chemical formula of Mg(CH3COO)2 • 4H2O. As a salt form of magnesium, magnesium acetate is one of the bioavailable forms of magnesium and forms a very water soluble compound. Magnesium is an essential element and second most abundant cation in the body that plays a key role in maintaining normal cellular function such as production of ATP and efficient enzyme activity. Magnesium acetate tetrahydrate can be used as an electrolyte supplementation or a reagent in molecular biology experiments. Used as magnesium salf-containing laxatives to prevent constipation. It can bring synergistic effect to restore normal bowel function when using in combination with aluminum salts that induce bowel retention. Magnesium acetate tetrahydrate is used as a source of water and electrolytes when combined with dextrose and other salts to form intravenous infusions. This injection can be used for patients with carbohydrate or magnesium deficiency, insulin hypoglycemia, constipation or hypertension during pregnancy. Magnesium is an essential cofactor for many enzymatic reactions such as protein synthesis and ATP production. It also participates in adenylyl cyclase pathway and tyrosine kinase signalling pathways. Magnesium may also play a role in regulating glucose metabolism. It serves as an essential cation for a number of biochemical processes involved in nerve signaling, bone mineralization and muscle contractions.  Magnesium ions electrostatically stabilize the adenylyl cyclase complex and enhance its catalytic actions and production of cAMP. They also regulate the level of phosphorylation in various pathways by formation of transition state of phosphoryl transfer reaction by protein kinases and stabilize ATP binding to protein kinases via electrostatic interactions. Many metabolic enzymes involved in glycolysis and Krebs cycle are magnesium-dependent. Magnesium-containing laxatives cause diarrhea through water retention and increased fecal mass that stimulates peristalsis. When used as an electrolyte supplementation, magnesium acetate tetrahydrate induces diuresis and metabolic alkalinizing effect. Magnesium ions enhance reactivity of arteries to vasoconstrictors, promotes vasoconstriction, and increases peripheral resistance, leading to increased blood pressure through potential competition with calcium ions in the vascular system. Magnesium ions also regulate other ions entering and exiting the cell membrane by acting as a ligand in N-methyl-D-aspartate receptor.",,,,Magnesium acetate tetrahydrate is approved.,Magnesium acetate tetrahydrate is a solid.,True
20146,"Magnesium carbonate, also known as magnesite, is a common over the counter remedy for heartburn and upset stomach caused by overproduction of acid in the stomach. Used as an over the counter antacid. Neutralizes acid in the stomach. Magnesium carbonate reacts with hydrochloric acid in the stomach to form carbon dioxide and magnesium chloride thus neutralizing excess acid in the stomach.",The molecular weight is 84.31.,,,Magnesium carbonate is approved and investigational.,Magnesium carbonate is a solid.,True
20147,"Setiptiline is a tetracyclic antidepressant (TeCA) which acts as a noradrenergic and specific serotonergic antidepressant (NaSSA). In Japan, the company Mochida started its commercialization for the treatment of depression started in 1989. For the treatment of depression. Setiptiline is a tertacyclic antidepressant. It acts to reduce the symptoms of major depressive disorder. Setiptiline is an antagonist at the α2 adrenergic receptor and at serotonin receptors. The antagonism of the α2 receptors likely relieves presynaptic inhibition of adrenergic neurotransmission, allowing for greater and longer sustained release of noradrenaline into the synapse. The antagonism of serotonin receptors may produce an upregulation of the receptors leading to an eventual increase in serotonergic signalling. The actual physiological mechanisms behind the antidepressant effect of setiptiline is unknown but the listed possibilities exist as likely explanations.",The molecular weight is 261.37.,Setiptiline has a topological polar surface area of 3.24.,The log p value of  is 4.44.,Setiptiline is experimental.,Setiptiline is a solid.,True
20148,"Synephrine, also referred to as, p-synephrine, is naturally occurring alkaloid. It is present in approved drug products as neo-synephrine, its m-substituted analog. p-synephrine and m-synephrine are known for their longer acting adrenergic effects compared to norepinephrine.",The molecular weight is 167.21.,Synephrine has a topological polar surface area of 52.49.,The log p value of  is -0.09.,Synephrine is experimental.,Synephrine is a solid.,True
20149,"Levonordefrin acts as a topical nasal decongestant and vasoconstrictor, most often used in dentistry. Used as a topical nasal decongestant and vasoconstrictor in dentistry. Levonordefrin is a sympathomimetic amine used as a vasoconstrictor in local anesthetic solutions. It has pharmacologic activity similar to that of Epinephrine but it is more stable than Epinephrine. In equal concentrations, Levonordefrin is less potent than Epinephrine in raising blood pressure, and as a vasoconstrictor. It is designed to mimic the molecular shape of adrenaline. It binds to alpha-adrenergic receptors in the nasal mucosa. Here it can, therefore, cause vasoconstriction.",The molecular weight is 183.21.,Levonordefrin has a topological polar surface area of 86.71.,The log p value of  is -0.68.,Levonordefrin is approved.,Levonordefrin is a solid.,True
20150,"Xylazine is a clonidine analog which acts as an agonist at α2 adrenoceptors. Veterinarians also use xylazine as an emetic, especially in cats.",,,,Xylazine is vet_approved.,,True
20151,"A sympathomimetic agent with mainly indirect effects on adrenergic receptors. It is used to maintain blood pressure in hypotensive states, for example, following spinal anesthesia. Although the central stimulant effects of mephentermine are much less than those of amphetamine, its use may lead to amphetamine-type dependence. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1248) Used to maintain blood pressure in hypotensive states. Mephentermine is a sympathomimetic agent with mainly indirect effects on adrenergic receptors. It is used to maintain blood pressure in hypotensive states, for example, following spinal anesthesia. Although the central stimulant effects of mephentermine are much less than those of amphetamine, its use may lead to amphetamine-type dependence. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1248) Mephentermine is an alpha adrenergic receptor agonist, but also acts indirectly by releasing endogenous norepinephrine. Cardiac output and systolic and diastolic pressures are usually increased. A change in heart rate is variable, depending on the degree of vagal tone. Sometimes the net vascular effect may be vasodilation. Large doses may depress the myocardium or produce central nervous system (CNS) effects.",The molecular weight is 163.26.,Mephentermine has a topological polar surface area of 12.03.,The log p value of  is 2.29.,Mephentermine is approved.,Mephentermine is a liquid.,True
20152,"Pipradrol (Meratran) was initially developed in the 1950s as an antidepressant, however, the adverse effects associated with its use and its abuse potential led to its withdrawal and international regulation. Pipradrol was made illegal in many countries in 1970s because of its potential for abuse. It is currently classified under the Misuse of Drugs Act as a Class C substance. Used to manage fatigue and depression , , ,. Used as an adjunct therapy in the management of obesity. Pipradrol (Meratran) is a psychoactive agent and a central nervous system stimulant that has proven useful in the field of psychiatry. Pipradrol and pipradrol derivatives are norepinephrine and dopamine reuptake inhibitors. ",The molecular weight is 267.37.,Pipradrol has a topological polar surface area of 32.26.,The log p value of  is 3.27.,Pipradrol is approved.,Pipradrol is a solid.,True
20153,"Metixene (or methixene) is a anticholinergic used as an antiparkinsonian agent. Used for the symptomatic treatment of parkinsonism. Metixene is a tertiary antimuscarinic with actions similar to those of atropine; it also has antihistaminic and direct antispasmodic properties. It is used for the symptomatic treatment of parkinsonism, including the alleviation of the extrapyramidal syndrome induced by other drugs such as phenothiazines, but, like other antimuscarinics, it is of no value against tardive dyskinesias. Metixene has been discontinued. Parkinsonism is thought to result from an imbalance between the excitatory (cholinergic) and inhibitory (dopaminergic) systems in the corpus striatum. The mechanism of action of centrally active anticholinergic drugs such as metixene is considered to relate to competitive antagonism of acetylcholine at muscarinic receptors in the corpus striatum, which then restores the balance.",The molecular weight is 309.47.,Metixene has a topological polar surface area of 3.24.,The log p value of  is 5.84.,Metixene is approved.,Metixene is a liquid.,True
20154,"Dichlorobenzyl alcohol is a mild antiseptic with a broad spectrum for bacterial and virus associated with mouth and throat infections. Dichlorobenzyl alcohol is considered as an active ingredient found in several marketed OTC products by Health Canada which has categorized this agent as an anatomical therapeutic chemical. On the other hand, dichlorobenzyl alcohol is categorized by the FDA in the inactive ingredient for approved drug products. Dichlorobenzyl alcohol in combination with is available in over-the-counter products used for symptomatic relief of acute sore throat and postoperative sore throat. In vitro studies with the combination of dichlorobenzyl alcohol and amylmetacresol have shown a virucidal against a number of viruses associated with the common cold which is observed by a reduction in the viral load. In clinical trials, administration of dichlorobenzyl alcohol lozenges has been shown to generate a reduced throat soreness and to provide pain relief and relief from difficulty in swallowing 5 minutes after administration. This effect can last for even 2 hours. The relief effect was shown to reach a steady-state after 45 minutes. The use of dichlorobenzyl alcohol has been related to its antibacterial, antiviral and local anesthetic properties. The local anesthetic action of dichlorobenzyl alcohol is thought to be due to a reduced sodium channel blockade. The antiseptic mechanism of action of dichlorobenzyl alcohol is not fully understood but it is thought to be related to a denaturation of external proteins and rearrangement of the tertiary structure proteins.",The molecular weight is 177.02.,Dichlorobenzyl alcohol has a topological polar surface area of 20.23.,The log p value of  is 2.53.,Dichlorobenzyl alcohol is approved.,Dichlorobenzyl alcohol is a solid.,True
20155,"Investigated for use/treatment in atopic dermatitis, inflammatory disorders (unspecified), and skin infections/disorders.",,,,NF-kappaB Decoy is investigational.,NF-kappaB Decoy is a solid.,True
20156,"A compound composed of a two cyclic peptides attached to a phenoxazine that is derived from streptomyces parvullus. It binds to DNA and inhibits RNA synthesis (transcription), with chain elongation more sensitive than initiation, termination, or release. As a result of impaired mRNA production, protein synthesis also declines after dactinomycin therapy. (From AMA Drug Evaluations Annual, 1993, p2015) For the treatment of Wilms' tumor, childhood rhabdomyosarcoma, Ewing's sarcoma and metastatic, nonseminomatous testicular cancer as part of a combination chemotherapy and/or multi-modality treatment regimen Generally, the actinomycins exert an inhibitory effect on gram-positive and gram-negative bacteria and on some fungi. However, the toxic properties of the actinomycins (including dactinomycin) in relation to antibacterial activity are such as to preclude their use as antibiotics in the treatment of infectious diseases. Because the actinomycins are cytotoxic, they have an antineoplastic effect which has been demonstrated in experimental animals with various types of tumor implant. This cytotoxic action is the basis for their use in the treatment of certain types of cancer. Dactinomycin is believed to produce its cytotoxic effects by binding DNA and inhibiting RNA synthesis. Good evidence exists that this drug bind strongly, but reversibly, to DNA, interfering with synthesis of RNA (prevention of RNA polymerase elongation) and, consequently, with protein synthesis.",The molecular weight is 1255.44.,Dactinomycin has a topological polar surface area of 355.54.,The log p value of  is 8.05.,Dactinomycin is approved and investigational.,Dactinomycin is a solid.,True
20157,"Guaifenesin possesses a storied history, having been originally formally approved by the US FDA in 1952 and continues to be one of very few - if not perhaps the only drug that is readily available and used as an expectorant. Since that time the agent has been a combination component of various prescription and non-prescription over-the-counter cough and cold products and is currently a widely available over-the-counter generic medication. Although it is principally believed that guaifenesin elicits an action to facilitate productive cough to manage chest congestion , it is not known whether the agent can reliably mitigate coughing. Guaifenesin is an expectorant that is indicated for providing temporary symptomatic relief from congested chests and coughs which may be due to a cold, bronchitis, and/or other breathing illnesses. Guaifenesin is categorized as an expectorant that acts by enhancing the output of phlegm (sputum) and bronchial secretions via decreasing the adhesiveness and surface tension of such material. Furthermore, guaifenesin elicits an increased flow of less viscous gastric secretions that subsequently promote ciliary action - all actions that ultimately change dry, unproductive coughing to coughs that are more productive and less frequent. Essentially, by decreasing the viscosity and adhesiveness of such secretions, guaifenesin enhances the efficacy of mucociliary activity in removing accumulated secretions from the upper and lower airway. Although the exact mechanism of action of guaifenesin may not yet be formally or totally elucidated, it is believed that expectorants like guaifenesin function by increasing mucus secretion. Moreover, it is also further proposed that such expectorants may also act as an irritant to gastric vagal receptors, and recruit efferent parasympathetic reflexes that can elicit glandular exocytosis that is comprised of a less viscous mucus mixture. Subsequently, these actions may provoke coughing that can ultimately flush difficult to access, congealed mucopurulent material from obstructed small airways to facilitate a temporary improvement for the individual.",The molecular weight is 198.22.,Guaifenesin has a topological polar surface area of 58.92.,The log p value of  is 0.1.,Guaifenesin is approved and investigational and vet_approved.,Guaifenesin is a solid.,True
20158,"Daratumumab is an immunoglobulin G1 kappa monoclonal antibody developed by Janssen and Genmab. It was first described in the literature in 2010 as a monoclonal antibody that targets CD38+ multiple myeloma cells; the first of its kind. Daratumumab is indicated as an intravenous injection alone or in combination with other medications for the treatment of multiple myeloma. Subcutaneous daratumumab with is also indicated alone or in combination for the treatment of multiple myeloma. Daratumumab is a monoclonal antibody that targets and induces apoptosis in cells that highly express CD38, including multiple myeloma cells. It has a long duration of action as it is given every 1-4 weeks. Patients should be counselled regarding the risk of hypersensitivity, neutropenia, thrombocytopenia, embryo-fetal toxicity, and interferences with cross-matching and red blood cell antibody screening. CD38 is a glycoprotein present on the surface of hematopoietic cells and is responsible for a number of cell signalling functions. Daratumumab is an immunoglobulin G1 kappa (IgG1κ) monoclonal antibody that targets CD38. Cancers like multiple myeloma overexpress CD38, allowing daratumumab to have higher affinity for these cells. This binding allows daratumumab to induce apoptosis, antibody dependent cellular phagocytosis, and antibody and complement-dependent cytotoxicity. Antibody dependent cellular phagocytosis is mediated by the FC region of the antibody inducing phagocytes such as macrophages, antibody dependent cellular cytotoxicity is mediated by the FC region of the antibody inducing effector cells such as natural killer cells, and complement dependent cytotoxicity is mediated by the FC region of the antibody binding to and inducing complement protein activity.",,,,Daratumumab is approved.,Daratumumab is a liquid.,True
20159,"Isatuximab (formerly SAR650984) is a humanized, IgG1-derived monoclonal antibody (mAb) produced from a Chinese hamster ovary (CHO) cell line. Structurally, isatuximab is comprised of two identical immunoglobulin kappa light chains and two identical immunoglobulin gamma heavy chains. It is a cytolytic antibody targeted against CD38, a glycoprotein found on the surface of some immune cells that is highly expressed by malignant plasma cells in multiple myeloma. Along with , another anti-CD38 mAb, isatuximab constitutes a novel treatment modality for patients with difficult-to-treat multiple myeloma. Isatuximab is indicated in combination with and for the treatment of multiple myeloma in adults who have received at least two prior therapies including and a proteasome inhibitor. Isatuximab results in the apoptosis of malignant plasma cells via inhibition of a surface protein key to their survival and proliferation. It has a relatively long residence time in the body, taking approximately 2 months to clear following the final dose, and may therefore be infused on a weekly or bimonthly schedule. Isatuximab is given in combination with due to a synergy that exists between the two - isatuximab can induce a depletion in host NK lymphocytes, yet the ADCC effect of anti-CD38 mAbs has been shown to be superior in patient samples with a high ratio of NK to myleoma cells. Pomalidomide, another antineoplastic agent, has the ability to induce and enhance NK lymphocyte activity and thus works synergistically to enhance isatuximab-mediated killing of myeloma cells. Multiple myeloma is a blood cancer characterized by an overproduction of malignant plasma cells in the bone marrow. A unique characteristic of myeloma cells is their dense and uniform expression of CD38 surface glycoproteins - these proteins, also expressed in relatively minor quantities on other lymphoid and myeloid cells, have been identified as performing several critical cellular functions, and this, along with their relative abundance on myeloma cells, has made them an attractive target for multiple myeloma treatment. CD38 was first identified as an activation marker, but has subsequently demonstrated roles in adhesion to endothelial CD31 proteins, as an accessory component of the synapse complex, and as an ectoenzyme involved in the metabolism of extracellular NAD+ and cytoplasmic NADP. The products of CD38’s ectoenzymatic activity include the calcium-mobilizing compound adenosine diphosphate ribose (ADPR), which can be further metabolized by CD203a/PC-1 and CD73 to adenosine, an immunosuppressive molecule that may play a role in tumour cell evasion of the immune system.",,,,Isatuximab is approved and investigational.,Isatuximab is a solid.,True
20160,"Secukinumab (Cosentyx) is a human monoclonal antibody designed for the treatment of uveitis, rheumatoid arthritis, ankylosing spondylitis, and psoriasis. Secukinumab is an interleukin-17A (IL-17A) inhibitor marketed by Novartis. IL-17 is a group of proinflammatory cytokines released by cells of the immune system and and exist in higher levels in many immune conditions associated with chronic inflammation. By targeting IL-17A, secukinumab has shown excellent efficacy in psoriasis by normalizing skin histology and was approved by the United States Food and Drug Administration on January 21, 2015 to treat adults with moderate-to-severe plaque psoriasis. For the treatment of moderate to severe plaque psoriasis in patients that are candidates for systemic therapy or phototherapy.  Secukinumab is a human monoclonal antibody that targets IL-17A cytokine to downregulate inflammation in psoriasis, an autoimmune dermatological disease. The pathophysiology of psoriasis has not been fully established, however it is known that dysregulation of innate and adaptive immune responses plays part in the chronic inflammation associated with the disease. IL-17 represents is a six-membered family (IL-17A to F) of pleiotropic pro-inflammatory cytokines, expression of which is found to be elevated in psoriatic skin. These cytokines act on many different cell types and provide defense against different extracellular pathogens causing fungal or bacterial infections. IL-17 cytokines are produced by many cells involved in immune system defense, such as Th17, mast cells, neutrophils, and dendritic cells - all implicated in promoting inflammation. There is evidence linking IL-17 to pathogenesis of multiple autoimmune diseases including rheumatoid arthritis, spondyloarthritis, psoriasis, Crohn's disease, multiple sclerosis, and even atherosclerosis. ",,,,Secukinumab is approved.,Secukinumab is a solid.,True
20161,"Ixekizumab is a humanized immunoglobulin G subclass 4 (IgG4) monoclonal antibody (mAb) against interleukin-17A (IL-17A) and prevents it from interacting with the IL-17A receptor. As IL-17A is a pro-inflammatory cytokine involved in inflammation and immune responses, blocking its effect is beneficial for use in inflammatory conditions. In particular, IL-17A has been found to be implicated in a variety of autoimmune diseases including Rheumatoid Arthritis and plaque psoriasis.   Ixekizumab is indicated for the treatment of adults with moderate-to-severe plaque psoriasis who are candidates for systemic therapy or phototherapy.  Ixekizumab is a humanized immunoglobulin G subclass 4 (IgG4) monoclonal antibody (mAb) against interleukin-17A (IL-17A) and prevents it from interacting with the IL-17A receptor. As IL-17A is a pro-inflammatory cytokine involved in inflammation and immune responses, blocking its effect is beneficial for use in inflammatory conditions. In particular, IL-17A has been found to be implicated in a variety of autoimmune diseases including Rheumatoid Arthritis and plaque psoriasis. ",,,,Ixekizumab is approved and investigational.,Ixekizumab is a solid.,True
20162,"Alirocumab is a biopharmaceutical that obtained FDA approval in July 2015 as a second line treatment for high cholesterol in adults whose LDL-cholesterol (LDL-C) is not controlled by the combination of diet and statin treatment. It is a human monoclonal antibody part of the family of the PCSK9 inhibitors which are a novel class of anticholesterol therapeutics. From this family, it was the first agent to receive FDA approval. The FDA approval was contingent on the completion of further clinical trials to better determine efficacy and safety. PCSK9 inhibition facilitates more LDL-C clearance from the blood. Alirocumab is an antibody eliciting proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitor activity that is indicated for: Alirocumab reduces levels of PCSK9 in a concentration-dependent manner.  Alirocumab is a fully human IgG1 monoclonal antibody that binds and inhibits proprotein convertase subtilisin/kexin type 9 (PCSK9), an enzyme found to have \gain of function\"" mutations in autosomal dominant hypercholesterolemia. PCSK9 is secreted by the liver and typically binds to the LDL receptors in serum and marks them for lysosomal degradation. In result, the LDL receptors are not able to recycle to the plasma membrane, reducing their binding to LDL-C and therefore reducing the clearance of LDL-C from plasma. Therefore by inhibiting PCSK9's actions, alirocumab allows for more LDL-C reuptake by the liver and facilitates a higher rate of clearance. Lower LDL cholesterol concentrations are associated with a reduced risk of coronary heart disease.""",,,,Alirocumab is approved.,Alirocumab is a liquid.,True
20163,"Inclisiran is a long-acting, synthetic small interfering RNA (siRNA) directed against proprotein convertase subtilisin-kexin type 9 (PCSK9), which is a serine protease that regulates plasma low-density lipoprotein cholesterol (LDL-C) levels. By binding to PCSK9 messenger RNA, inclisiran prevents protein translation of PCSK9, leading to decreased concentrations of PCSK9 and plasma concentrations of LDL cholesterol. Lowering circulating plasma LDL-C levels contributes to an additional benefit of lowering the risk of cardiovascular disease (CVD) and improving cardiovascular outcomes, as hypercholesterolemia is a major known risk factor for CVD.  Inclisiran is a long-acting small interfering RNA (siRNA) that works to lower plasma LDL-cholesterol (LDL-C). In clinical trials comprising healthy adult volunteers, inclisiran caused a reduction of PCSK9 levels by 70-80% and LDL-C levels by 27-60% following subcutaneous injection. In a clinical trial consisting of subjects with atherosclerotic cardiovascular disease with or without diabetes, inclisiran reduced LDL-C levels by 28-52%. Low-density lipoprotein (LDL) receptors expressed on hepatocytes are responsible for the removal of circulating LDL-C from plasma via receptor-mediated endocytosis. Proprotein convertase subtilisin-kexin type 9 (PCSK9) is a serine protease that is mainly produced by hepatocytes. It binds to LDL receptors and targets them for lysosomal degradation, thereby reducing the levels of LDL receptors, attenuating the recycling of LDL receptors, and elevating the levels of circulating plasma LDL-C.",,,,Inclisiran is approved and investigational.,,True
20164,"Asfotase alfa is a first-in-class bone-targeted enzyme replacement therapy designed to address the underlying cause of hypophosphatasia (HPP)—deficient alkaline phosphatase (ALP). Hypophosphatasia is almost always fatal when severe skeletal disease is obvious at birth. By replacing deficient ALP, treatment with Asfotase Alfa aims to improve the elevated enzyme substrate levels and improve the body's ability to mineralize bone, thereby preventing serious skeletal and systemic patient morbidity and premature death. Asfotase alfa was first approved by Pharmaceuticals and Medicals Devices Agency of Japan (PMDA) on July 3, 2015, then approved by the European Medicine Agency (EMA) on August 28, 2015, and was approved by the U.S. Food and Drug Administration (FDA) on October 23, 2015. Asfotase Alfa is marketed under the brand name Strensiq® by Alexion Pharmaceuticals, Inc. The annual average price of Asfotase Alfa treatment is $285,000. Indicated for the treatment of patients with perinatal/infantile and juvenile onset hypophosphatasia (HPP).  Perinatal/infantile- and juvenile-onset HPP patients treated with Asfotase alfa had reductions in plasma TNSALP (tissue non-specific alkaline phosphatase) substrates, PPi and pyridoxal 5'-phosphate (PLP) within 6 to 12 weeks of treatment. Reductions in plasma PPi and PLP levels did not correlate with clinical outcomes. Bone biopsy data from perinatal/infantile-onset and juvenile-onset HPP patients treated with Asfotase alfa demonstrated decreases in osteoid volume and thickness indicating improved bone mineralization.  HPP is caused by a deficiency in TNSALP (tissue non-specific alkaline phosphatase) enzyme activity, which leads to elevations in several TNSALP substrates, including inorganic pyrophosphate (PPi). Elevated extracellular levels of PPi block hydroxyapatite crystal growth which inhibits bone mineralization and causes an accumulation of unmineralized bone matrix which manifests as rickets and bone deformation in infants and children and as osteomalacia (softening of bones) once growth plates close, along with muscle weakness. Replacement of the TNSALP enzyme upon Asfotase alfa treatment reduces the enzyme substrate levels. ",,,,Asfotase alfa is approved and investigational.,Asfotase alfa is a liquid.,True
20165,"Protirelin is the pharmaceutically available synthetic analogue of the endogenous peptide thyrotropin-releasing hormone (TRH). It is a tri-peptide tropic hormone, released by the hypothalamus, that stimulates the release of Thyroid Stimulating Hormone (TSH) and prolactin from the anterior pituitary. ",The molecular weight is 362.39.,Protirelin has a topological polar surface area of 150.28.,The log p value of  is -2.79.,Protirelin is approved and investigational.,,True
20166,"Risankizumab is a fully humanized IgG1 monoclonal antibody (mAb) that is selective for interleukin 23 (IL-23). On April 23, 2019 it was approved by the FDA (as _SKYRIZI_) for the treatment of moderate-to-severe plaque psoriasis in adults who are clinically considered eligible for systemic therapy or phototherapy for psoriasis. This drug has been commercialized through collaboration between the German pharmaceutical company, Boehringer Ingelheim, and Abbvie. This drug is for the treatment of moderate-to-severe plaque psoriasis in adults who are eligible to receive systemic therapy or phototherapy based on their disease process. No formal studies examining pharmacodynamic properties have been completed with risankizumab , however, this drug is expected to relieve symptoms of psoriasis by targeting interleukin 23 (IL-23) and preventing the initiation of the inflammatory cascade that is implicated in psoriasis. Risankizumab acts to prevent the release of pro-inflammatory cytokines and chemokines that often lead to inflammatory skin symptoms, such as redness, pain, and plaques. Risankizumab binds with a high affinity to the p19 subunit of human interleukin 23 (IL-23) cytokine , thereby preventing its action on the IL-23 receptor. IL-23 is a cytokine released in the human body that is involved in inflammatory and immune processes, especially in peripheral tissues.",,,,Risankizumab is approved and investigational.,,True
20167,Adipiplon is an nonbenzodiazepine anxiolytic developed by Neurogen Corporation. It is known by the standardized identifier NG2-73. Investigated for use/treatment in insomnia and sleep disorders.,,,,Adipiplon is investigational.,Adipiplon is a solid.,True
20168,"5,7,2′-trihydroxy-6,8-dimethoxyflavone (K36) is a high-affinity, naturally occurring flavonoid derivative isolated from the medicinal herb _Scutellaria baicalensis_ Georgi.",,,,"5,7,2′-trihydroxy-6,8-dimethoxyflavone is experimental.","5,7,2′-trihydroxy-6,8-dimethoxyflavone is a solid.",True
20169,"A small colorless crystal used as an anticonvulsant, a cathartic, and an electrolyte replenisher in the treatment of pre-eclampsia and eclampsia. It causes direct inhibition of action potentials in myometrial muscle cells. Excitation and contraction are uncoupled, which decreases the frequency and force of contractions. (From AMA Drug Evaluations Annual, 1992, p1083) Used for immediate control of life-threatening convulsions in the treatment of severe toxemias (pre-eclampsia and eclampsia) of pregnancy and in the treatment of acute nephritis in children. Also indicated for replacement therapy in magnesium deficiency, especially in acute hypomagnesemia accompanied by signs of tetany similar to those of hypocalcemia. Also used in uterine tetany as a myometriat relaxant. Magnesium sulfate is a small colorless crystal used as an anticonvulsant, a cathartic, and an electrolyte replenisher in the treatment of pre-eclampsia and eclampsia. It causes direct inhibition of action potentials in myometrial muscle cells. Excitation and contraction are uncoupled, which decreases the frequency and force of contractions. Magnesium sulfate is gaining popularity as an initial treatment in the management of various dysrhythmias, particularly torsades de pointes, and dyrhythmias secondary to TCA overdose or digitalis toxicity. Magnesium is the second most plentiful cation of the intracellular fluids. It is essential for the activity of many enzyme systems and plays an important role with regard to neurochemical transmission and muscular excitability. Magnesium sulfate reduces striated muscle contractions and blocks peripheral neuromuscular transmission by reducing acetylcholine release at the myoneural junction. Additionally, Magnesium inhibits Ca<sup>2+</sup> influx through dihydropyridine-sensitive, voltage-dependent channels. This accounts for much of its relaxant action on vascular smooth muscle.",The molecular weight is 120.36.,,,Magnesium sulfate is approved and investigational and vet_approved.,Magnesium sulfate is a solid.,True
20170,"Volanesorsen is an antisense oligonucleotide that binds to apoC-III mRNA to prevent its translation. It is indicated to treat familial chylomicronemia, a genetic condition that prevents breakdown of triglycerides and chylomicrons. This drug is not commonly prescribed as it is used as an adjunct to diet in patients at high risk for pancreatitis, who have had inadequate response to triglyceride lowering therapy. Volanesorsen is conditionally approved by the EMA as an adjunct to diet in adults with familial chylomicronemia, at high risk for pancreatitis, and who have had an inadequate response to diet and triglyceride lowering therapy. Volanesorsen is an antisense oligonucleotide that prevents the translation of apoC-III. It has a long duration of action as it has a half life of >2 weeks. Patients should be counselled regarding the risk of thrombocytopenia, raised LDL-C levels, renal toxicity, hepatotoxicity, and immunogenicity. Volanesorsen is an antisense oligonucleotide that binds to apoC-III mRNA, leading to its degradation, and preventing translation of apoC-III protein. Normally, apoC-III would inhibit triglyceride metabolism and hepatic clearance of chylomicrons. Preventing translation of apoC-III allows for metabolism and breakdown of these triglycerides and chylomicrons.",,,,Volanesorsen is approved and investigational.,Volanesorsen is a liquid.,True
20171,"Titanium dioxide, also known as titanium(IV) oxide or titania, is the naturally occurring oxide of titanium. It is used as a pigment under the names titanium white, Pigment White 6 (PW6), or CI 77891. It is typically extracted from ilmenite, rutile and anatase. Titanium dioxide is used in most sunscreens to block UVA and UVB rays, similar to. Diminish the penetration of ultraviolet (UV) light through the epidermis by absorbing UV radiation within a specific wavelength range. The amount and wavelength of UV radiation absorbed are affected by the molecular structure of the sunscreen agent. ",The molecular weight is 79.86.,Titanium dioxide has a topological polar surface area of 34.14.,,Titanium dioxide is approved.,Titanium dioxide is a solid.,True
20172,"Silicon dioxide, or silica, is an oxide of silicon with the chemical formula SiO2. It is found in nature as agate, amethyst, chalcedony, cristobalite, flint, sand, QUARTZ, and tridymite as transparent and tasteless crystals. Inhalation of fine crystals is toxic to humans leading to respiratory toxicity. In powdered food products and pharmaceutical tablets, silicon dioxide is added as a flow agent to absorb water. Colloidal silica is also used as a wine, beer, and juice fining agent or stabilizer.",The molecular weight is 60.08.,Silicon dioxide has a topological polar surface area of 34.14.,,Silicon dioxide is approved.,Silicon dioxide is a solid.,True
20173,"Rocaglamide, also referred to as rocaglamide-A, is the eponymous member of a class of anti-cancer phytochemicals known as rocaglamides. Rocaglamides are secondary metabolites of the plant genus _Aglaia_, and extracts of the plant have traditionally been used as a form of insect repellant due to its natural insecticidal properties. Reports of _Aglaia_ anti-tumor activity date back as far as 1973, and rocaglamide-A was first isolated in 1982 from the species _A. elliptifolia_. Rocaglamide and a number of its derivatives (e.g. ) are currently being studied for use as chemotherapeutic agents in the treatment of various leukemias, lymphomas, and carcinomas, as well as adjuvant therapy in the treatment of certain chemotherapy-resistant cancers. Rocaglamide’s anti-tumor activity is driven primarily via inhibition of protein synthesis in tumor cells. Inhibition of protein synthesis is accomplished via inhibition of prohibitin 1 (PHB1) and prohibitin 2 (PHB2) - these proteins are necessary in the proliferation of cancer cells and are implicated in the Ras-mediated CRaf-MEK-ERK signaling pathway responsible for phosphorylating eIF4E, a key factor in the initiation of protein synthesis. The rocaglamide derivative silvestrol has also been observed to act directly on eIF4A, another translation initiation factor of the eIF4F complex ultimately responsible for initiation of protein synthesis.",,,,Rocaglamide is experimental.,,True
20174,"Didesmethylrocaglamide is a naturally-occurring derivative of and belongs to a class of anti-cancer phytochemicals referred to as \rocaglamides\"" derived from plants of the genus _Aglaia_. While traditionally used for their insecticidal benefits, this class of compounds is now being studied for use as chemotherapeutic agents in the treatment of various leukemias, lymphomas, and carcinomas. Of the known derivatives of rocaglamide, didesmethylrocaglamide appears to carry the most potent anti-tumour activity."" Little research has been conducted specifically regarding didesmethylrocaglamide, but its mechanism of action is likely to be congruent with the rest of the rocaglamide class.",,,,Didesmethylrocaglamide is experimental.,,True
20175,"Boehringer Ingelheim Pharmaceuticals’ olcegepant (BIBN 4096) is a selective Calcitonin Gene-Related Peptide (CGRP) antagonist, a new class of drugs in development for the treatment of acute migraine attacks. Olcegepant is undergoing phase II trials in Europe and the US, with preliminary results suggesting that CGRP antagonists may represent a potential new approach to the treatment of migraine. For the treatment of migraine headaches. Olcegepant is a calcitonin gene-related peptide (CGRP) antagonist. In preclinical studies, olcegepant attenuated arterial dilation induced by CGRP or electrical stimulation. In a phase II clinical trial, olcegepant reduced the severity of headache in 60% of migraine sufferers and met secondary endpoints including headache-free rate and rate of sustained response. Only mild-to-moderate transient adverse events were observed, with no adverse cardiovascular symptoms reported. The compound appears to be an effective anti-migraine medication that is well tolerated and does not display the vasoconstrictive effect that precludes the use of triptans and dihydroergotamine in certain patients. Migraine involves dysfunction of brainstem pathways that normally modulate sensory input. The involvement of calcitonin gene-related peptide (CGRP) in migraine pathology is supported by both clinical and experimental evidence. The release of CGRP and other neuropeptides from trigeminal nerves is thought to mediate neurogeate inflammation within the meninges which contributes to the generation of severe cerebral pain experienced during migraine attack. CGRP antagonists such as olcegepant bind at CGRP receptors, blocking the effect CGRP and thus reducing inflammation.",,,,Olcegepant is investigational.,Olcegepant is a solid.,True
20176,"Erenumab (AMG-334) (INN; trade name Aimovig) is a human monoclonal antibody designed specifically to bind and antagonize the calcitonin gene-related peptide receptor (CGRPR) as a means to prevent migraines. Aimovig, as released and marketed by Novartis and Amgen, is in fact a novel therapeutic approach as the first and only FDA approved treatment specifically developed to prevent migraine by blocking the CGRP receptor, which is believed to play a critical role in migraine. Erenumab is indicated for the preventative treatment of migraine in adults. As a human monoclonal antibody designed to specifically bind with and antagonize the calcitonin gene-related peptide (CGRP) receptor, there is the possibility that erenumab could interfere with natural activities of CGRP that may not be immediately or directly associated with migraines. For example, at peripheral synapses, CGRP released from trigeminal terminals results in vasodilation by way of CGRP receptor on smooth muscle cells of meningeal and cerebral blood vessels, making CGRP a potent general arterial vasodilator. Antagonism of CGRP receptors responsible for such vasodilation could theoretically result in vasoconstriction and raises in blood pressure. Erenumab is a human monoclonal antibody that has been designed to bind specifically to the calcitonin gene-related peptide (CGRP) receptor and antagonize the CGRP receptor function.",,,,Erenumab is approved and investigational.,Erenumab is a liquid.,True
20177,"Vazegepant is an antagonist of the calcitonin gene-related peptide (CGRP) receptor currently in phase 3 trials in an intranasal formulation for the treatment of migraine. If FDA approved, it will join other previously-approved \-gepant\"" drugs and as an additional treatment alternative for patients with migraine, particularly those for whom traditional triptan therapy has proven ineffective.""",,,,Vazegepant is investigational.,,True
20178,"Coagulation Factor XIII A-Subunit (Recombinant), also known as catridecacog, is a recombinant form of the Factor XIII-A2 homodimer composed of two factor XIII (FXIII) A-subunits. For people with congenital deficiency or mutation of Factor XIII, a rare bleeding disorder, exogenous replacement of this key coagulation factor is essential for management and prevention of bleeding episodes.  For routine prophylaxis of bleeding in patients with congenital factor XIII A-Subunit deficiency.",,,,Catridecacog is approved.,Catridecacog is a solid.,True
20179,"Voretigene Neparvovec-rzyl (VN-rzyl) is an adeno-associated virus vector-based gene therapy. An adeno-associated virus is a small virus that infects humans and other primates. It is not pathogenic and it causes a very mild immune response. This type of virus is vastly used as vectors for gene therapy because they can infect dividing and quiescent cell integrating just the carried genes into the host genome without fully integrating into the genome. An advantage of this adeno-associated virus is the high predictability, unlike retrovirus, as they associate with a specific region of the human cellular genome localized in the chromosome 19. When used in genetic therapy, this virus is modified for the elimination of its negligible integrative capacity by the removal of *rep* and *cap* and the insertion of the desired gene with its promoter between the inverted terminal repeats. VN-rzyl was developed by Spark Therapeutics Inc. and FDA approved on December 19, 2017. VN-rzyl is indicated for the treatment of children and adult patients with confirmed biallelic RPE65 mutation-associated retinal dystrophy. The administration of VN-rzyl is conditioned to the physician determination of the presence of viable retinal cells. The RPE65 represents the LCA2 form of the Leber's congenital amaurosis (LCA). LCA is a group of inherited conditionts that involves retinal degeneration and severe vision loss in early childhood leading to total blindness by 30-40 years old. The LCA2 form is associated with a mutation that interferes with the isomerohydrolase activity of the retinal pigment epithelium. The isomerohydrolase activity transforms the trans-retinyl esters to 11-cis-retinal which is the natural ligand and chromophore of the opsins of rod and cones photoreceptors. In the presence of RPE65 mutations, the opsins cannot capture light or transduce it into electrical responses to initiate vision. Subretinal injection generates the transduction of retinal pigment epithelial cells, restoring the visual cycle. In clinical trials, there was a significant increase in the mean bilateral multi-luminance mobility testing scores with a shown maximum possible improvement. The eyes receiving the treatment presented also a more effective drive in pupillary response even 3 times greater than the baseline. There was also a significant reduction of nystagmus. The improved vision was determined by the ability of the treated patients to cross an obstacle course at various light levels which showed a significant amelioration. VN-rzyl is designed for the delivery, in the cells of the retina, of a normal copy of the gene encoding for the human retinal pigment epithelial protein whose molecular weight is 65 kDa. The delivery of this gene will allow the production of the RPE65 protein re-establishing the visual cycle and restoring the visual function. ",,,,Voretigene neparvovec is approved.,Voretigene neparvovec is a liquid.,True
20180,"Dibotermin alfa is a recombinant human bone morphogenetic protein-2 (rhBMP-2) derived from a recombinant Chinese Hamster Ovary (CHO) cell line. It is implanted in patients undergoing bone surgeries or those with fractures. BMPs are subfamily of the transforming growth factor-β (TGF-β) superfamily that have different actions on the bone matrix. BMP-2 is a potent osteoinductive protein that plays a critical role in the differentiation of osteoprogenitor cells into osteoblasts, thus promoting bone and cartilage formation. Through enhancing osteogenesis at the site of implantation, dibotermin alfa accelerates the healing of open tibial shaft fractures and reduces the need for secondary intervention. In a prospective clinical study of patients with an open tibial fracture, administration of dibotermin alfa resulted in faster fracture- or wound-healing, significantly fewer secondary invasive interventions, and reduced infection rate post-operation. Dibotermin alfa was approved by the EMA in 2002 as Inductos for implantation matrix. In 2004, it was approved by the FDA and is marketed as Infuse. In Infuse, rhBMP is a disulfide-linked dimeric protein molecule with two major subunit species of 114 and 131 amino acids. Each subunit is glycosylated with high-mannose-type glycans. - indicated for the treatment of acute tibia fractures in adults, as an adjunct to standard care using open fracture reduction and intramedullary unreamed nail fixation. Dibotermin alfa promotes bone and cartilage formation through anabolic effects in human osteoblastic cells. Radiographic, biomechanical and histologic evaluation of the induced bone at the site of implantation supports that induced bone from dibotermin alfa therapy is capable of biological and biochemical function as native bone and repair abilities. In the same pathway shared by endogenous BMPs, recombinant human BMP-2 (rhBMP-2) binds and initiates intracellular signal cascade through an oligomeric transmembrane receptor complex formed by type I and II serine/threonine kinase receptor proteins. These BMP receptors are expressed on the surface of mesenchymal cells and upon binding of BMP-2 to the BMP receptor type II, type II receptor phosphorylates and activates type I receptor. Type I receptor may also undergo autophosphorylation. Activated BMP type I receptor then phosphorylates intracellular effector proteins, the receptor-regulated Smads (R-Smads). Smad1, Smad 5 and Smad 8 associate with the Co-Smad, Smad4 and once activated via complex formation, they translocate to the nucleus where they associate with other transcription factors and bind promoters of target genes to control their expression. This ultimately results in bone formation at the site of implantation. Dibotermin alfa causes mesenchymal cells to differentiate into cartilage- and bone-forming cells. Implantation of dibotermin alfa in trabecular bone results in transient resorption of the bone surrounding the implant, followed by replacement of degraded matrix by newly differentiated cells.",The molecular weight is 25795.62.,Dibotermin alfa has a topological polar surface area of 10367.0.,,Dibotermin alfa is approved and investigational.,,True
20181,"Technetium Tc-99m tilmanocept is a radiopharmaceutical diagnostic imaging agent approved by the U.S. Food and Drug Administration (FDA) for the imaging of lymph nodes with or without scintigraphic imaging. It is a macromolecule consisting of multiple units of diethylenetriaminepentaacetic acid (DTPA) and mannose, each covalently attached to a 10 kDa dextran backbone. DTPA serves as a chelating agent for technetium Tc 99m to bind. Technetium Tc-99m tilmanocept is used in lymphatic mapping and lymph node localization in breast cancer, melanoma, clinically node-negative squamous cell carcinoma of the oral cavity, and other solid tumors. Detecting sentinel lymph node (SLN) is clinically useful in the prognosis and management of the disease, as it is considered as the first lymph node that receives afferent lymphatic drainage from a primary tumor, and may be used to predict tumour staging and metastasis. However, as nodal micrometastasis in breast cancer may not be associated with significant changes in survival, it is also important to identify clinically node-negative patients.  Indicated with or without scintigraphic imaging for lymphatic mapping using a handheld gamma counter to locate lymph nodes draining a primary tumor site in patients with solid tumors for which this procedure is a component of intraoperative management. Technetium Tc 99m tilmanocept binds to the CD206 receptors on the surface of reticuloendothelial cells, such as macrophages and dendritic cells, which are highly expressed in lymph nodes. In clinical studies, technetium Tc 99m tilmanocept has been shown to be detectable in lymph nodes within 10 minutes and up to 30 hours after injection. Moreover, Phase 1 clinical studies showed approximately 0.5 to 1.8% of a dose accumulating in draining lymph nodes via specific binding after about 30 minutes. Technetium Tc99m tilmanocept bindng appears to be independent of tumor type or severity. It displays rapid injection site clearance, rapid accumulation, long retention in the sentinel node, and low distal node accumulation. The mannose of the molecule acts as a ligand and guides the molecule to selectively bind to human mannose binding receptors (CD206) located on the surface of reticuloendothelial cells residing within lymph nodes, such as macrophages and dendritic cells. According to _in vitro_ studies, technetium Tc 99m tilmanocept demonstrates selective binding to CD206 with a primary binding site affinity of Kd = 2.76 x 10^-11 M. ",,,,Technetium Tc-99m tilmanocept is approved and investigational.,Technetium Tc-99m tilmanocept is a solid.,True
20182,"SR-9009 is a REV-ERB agonist. SR-9011 has been demonstrated that it is specifically lethal to cancer cells and oncogene-induced senescent cells, including melanocytic naevi, and has no effect on the viability of normal cells or tissues.",,,,SR-9009 is experimental.,SR-9009 is a solid.,True
20183,"SR-9011 is a REV-ERB agonist. SR-9011 has been demonstrated that it is specifically lethal to cancer cells and oncogene-induced senescent cells, including melanocytic naevi, and has no effect on the viability of normal cells or tissues.",,,,SR-9011 is experimental.,SR-9011 is a solid.,True
20184,"H3B-8800 is a novel spliceosome inhibitor developed by H3 Biomedicine. It offers the benefit of preferentially killing spliceosome-mutant cancer cells whereas other splicesome inhibitors, such as the pladienolide analogue E7107, show no such preferential targeting. H3B-8800 was granted orphan drug status by the FDA in August 2017 and is in clinical trials for the treatment of acute myelogenous leukemia and chronic myelomonocytic leukemia. H3B-8800 preferentially targets cells with spliceosome complexes containing mutant splicing factor 3B1 (SF3B1) protein, modulating intron splicing leading to increased death in cancer cells while having little effect on the viability cells with wild-type SF3B1. Both normal and aberrant mature mRNA are suppressed in mutant and wild-type cells, the selectivity of the lethal effect is thought to be due to the presence of mutant SF3B1 and its implications rather than a change in mechanism or potency of effect on the mutant protein over the wild-type. H3B-8800 is thought to bind to a site similar to pladienolides on the SF3B complex within the spliceosome. Once bound it induces increased retention of short (<300 nucleotide) GC-rich introns through modulation of pre-mRNA processing. These intron-retained mRNA sequences are then thought to be destroyed through the nonsense-mediated decay pathway. It has been suggested that modulation by H3B-8800 is mediated by disruption of branchpoint sequence recognition by the SF3B complex as there is overall less preference for adenosine as the branchpoint nucleotide and a greater amount of sequences with weaker association to the SFB3 in introns retained with H3B-8800.",,,,H3B-8800 is investigational.,H3B-8800 is a solid.,True
20185,"Epicriptine is also known as beta-dihydroergocryptine presents a molecular formula of 9,10 alpha-dihydro-13'-epi-b-ergocryptine. Together with the alpha-dihydroergocryptine, it represents one-third of the ergoloid mesylate mixture. Epicriptine differs from the alpha form on the position of one methyl group. To know more about the mixture please visit  Please refer to and to know more about the isomer please refer to. Please refer to and to know more about the isomer please refer to. Epicriptine effect is mainly due to the agonistic activity on dopamine receptor. This activity is categorized as part of the ergoline class which is defined as a producer of a vasoconstrictive effect. Please refer to and to know more about the isomer please refer to.",The molecular weight is 577.73.,Epicriptine has a topological polar surface area of 118.21.,The log p value of  is 5.6.,Epicriptine is approved.,Epicriptine is a solid.,True
20186,"SC-236 is a potent, selective, orally active inhibitor of cyclooxygenase-2 (COX-2) that has been studied in cancer therapy , lower back pain , and inflammation , ,,. This drug is a selective inhibitor of the COX-2 enzyme ,. COX-2 is expressed in the brain, in the kidney, in bone, and likely in the female reproductive system. Its expression at other sites is increased during inflammation, experimentally, in response to mitogenic stimuli. Growth factors, phorbol esters, and interleukin (IL)-1 stimulate the expression of COX-2 in fibroblasts, while endotoxin serves the same function in monocytes/macrophages.",,,,SC-236 is experimental and investigational.,SC-236 is a solid.,True
20187,Potent and selective histone methyltransferase EZH2 inhibitor.,,,,CPI-1205 is investigational.,,True
20188,"Sennosides (also known as senna glycoside or senna) is a medication used to treat constipation and empty the large intestine before surgery. The medication is taken by mouth or via the rectum. It typically begins working in minutes when given by rectum and within twelve hours when given by mouth. It is a weaker laxative than bisacodyl or castor oil. Sennoside A, one of the sennosides present in the laxative medication, has recently proven effective in inhibiting the ribonuclease H (RNase H) activity of human immunodeficiency virus (HIV) reverse transcriptase. For the over the counter treatment of constipation. Senna stimulates peristalsis and increases fecal water content to increase motility of feces through the large intestine. Sennoside A and B, the components of senna, are metabolized by gut bacteria into the active metabolite rheinanthrone. Rheinanthrone appears to increase cyclooxegenase 2 (COX2) expression in macrophage cells leading to an increase in prostaglandin E2 (PGE2). This increase in PGE2 is associated with a decrease in aquaporin 3 expression in mucosal epithelial cells of the large intestine. A decrease in aquaporin 3 expression likely produces the laxative effect by restricting water reabsorption by the large intestine thereby increasing fecal water content. The exact mechanism by which rheinanthrone increases COX2 expression is unknown. Rheinanthrone also stimulates peristalsis in the large intestine although the mechanism behind this effect is unknown. Rhein , another active metabolite is thought to excite submucosal acetylcholinergic neurons resulting in increased chloride and prostaglandin secretion. The movement of chloride ions into the large intestine would also help to draw water into the lumen.",,,,Sennosides is experimental.,Sennosides is a solid.,True
20189,"Romosozumab is a humanized monoclonal antibody indicated for the treatment of osteoperosis in postmenopausal women at high risk of fracture and patients who have failed in other treatments or are intolerant to other osteoperosis therapies. Romosozumab prevents bone resorption and induces the formation of bone though it is associated with an increased risk of cardiac death, heart attack, and stroke in one study. In a comparison study of post menopausal women with osteoporosis and a past fracture, romosozumab for 12 months followed by alendronic acid for 12 months was superior to alendronic acid alone for 24 months. Romosozumab also demonstrates a faster and larger increase in bone density than teriparatide. Romosozumab is marketed in the United States by Amgen under the brand name Evinity. Romosozumab was granted FDA approval on April 9,2019. Romosozumab is indicated for the treatment of osteoporosis in post menopausal women at high risk of fractures and also in patients with osteoperosis who are intolerant to other treatments or who have failed in other treatments. Romosozumab is a subcutaneously injected humanized monoclonal antibody that inhibits the secreted protein sclerostin. Inhibition of this protein allows Wnt signalling in osteoblasts to promote bone formation and allows for the inhibition of receptor activator of nuclear factor kappa-beta-ligand (RANKL) mediated bone resorption by osteoclasts. Osteocytes secrete sclerostin which inhibits bone formation by binding to low-density lipoprotein (LDL) receptor-related proteins 5 and 6 of osteoblasts, inhibiting the Wnt signal pathway.",,,,Romosozumab is approved and investigational.,Romosozumab is a solid.,True
20190,"PT2977 is an HIF-2α inhibitor. A kidney cancer treatment, it is the lead candidate drug for Peloton. Peloton was acquired by Merck & Co Inc on May 21, 2019.",,,,PT2977 is investigational.,,True
20191,"Setmelanotide is the first available treatment for patients with pro-opiomelanocortin, proprotein subilisin/kexin type 1, or leptin deficiencies. It is an agonist of the melanocortin 4 receptor. Earlier attempts at agonizing MC4R (such as LY2112688) lead to successful weight loss, but also an increase in blood pressure and heart rate. Other earlier treatments for these patients included gastric bypass surgery. Patients taking setmelanotide experienced an average weight loss of 0.6 kg/week. Setmelanotide is indicated for chronic weight management in patients 6 years and older with obesity due to pro-opiomelanocortin deficiency, proprotein subtilisin/kexin type 1 deficiency, or leptin receptor deficiency. These conditions affect the MC4R signalling pathway. Setmelanotide agonizes MC4R, downstream of multiple potential genetic deficiencies, to induce a feeling of satiety for chronic weight management. It has a moderate duration of action as it is given daily. Patients should be counselled regarding the risk of disturbances in sexual arousal, depression and suicidal ideation, and darkening of skin pigmentation. Exercise caution in neonates and low birth weight infants, as they may experience serious adverse effects due to benzyl alcohol. Grehlin and other hunger signals from the gastrointestinal tract stimulate orexigenic neurons, stimulating the release of agouti-related protein. Agouti-related protein inhibits melanocortin 4 receptor (MC4R) activation until satiety signals such as insulin or leptin stimulate anorexigenic neurons. Insulin and leptin stimulate production of the POMC-derived melanocortin peptide α-melanocyte simulating hormone, which is a ligand of MC4R.",,,,Setmelanotide is approved and investigational.,Setmelanotide is a liquid.,True
20192,"Despite the introduction of using cocaine injections for regional anesthesia in 1884, non-addictive substitutes were sought after immediately. Finally, in 1903 the world's first synthetic and non-addictive local anesthetic, amylocaine, was synthesized and patented under the name Forneaucaine by Ernest Fourneau at the Pasteur Institute. Elsewhere in English speaking countries it was referred to as Stovaine, given the meaning of the French word 'fourneau' as 'stove' in English. The most common indication for the usage of amylocaine was spinal anesthesia. Like all other local anesthetics, amylocaine acts as a membrane stabilizing drug that reversibly decreases the rate of depolarization and depolarization of excitable membranes. In this way, the conduction of neuronal signals for certain bodily movements can be blocked. In particular, when administered for spinal anesthesia, the resultant anesthesia can typically extend from the chest to the legs. In particular, amylocaine, much like other local anesthetics, bind and blockade voltage gated sodium channels located in the excitable membranes of various sensory receptors. Once blocked, the influx of sodium across the channels and membrane is inhibited. Because the influx of sodium is necessary to facilitate neuronal action potentials and signal conduction across sensory receptor membranes, the influx inhibition subsequently prevents the body reactions that would normally result from the neuronal signals.",The molecular weight is 235.33.,Amylocaine has a topological polar surface area of 29.54.,The log p value of  is 3.43.,Amylocaine is approved and withdrawn.,Amylocaine is a solid.,True
20193,"Pramocaine (also known as pramoxine or pramoxine HCI) is a topical anesthetic and antipruritic. It is used for many dermatological and anorectal/anogenital conditions including minor cuts/burns, insect bites, hives/rashes due to poison ivy exposure, hemorrhoids and other anorectal/anogenital disorders. Pramocaine is available by itself and in combination with other medications in various topical preparations. It works by preventing ionic fluctuations needed for neuron membrane depolarization and action potential propagation. It is indicated for temporary relief of pain and pruritus from minor lip and skin irritations as well as for temporary relief from pain, burning, itching and discomfort associated with hemorrhoids and other anorectal/anogenital disorders.  Pramocaine temporarily relieves pain, pruritis, burning and discomfort associated with minor lip and skin irritations and hemorrhoid's by inhibiting voltage gated sodium channels on neurons.  Pramocaine reversibly binds and inhibits voltage gated sodium channels on neurons decreasing sodium permeability into the cell. This stabilizes the membrane and prevents ionic fluctuations needed for depolarization stopping any action potential propagation. ",The molecular weight is 293.41.,Pramocaine has a topological polar surface area of 30.93.,The log p value of  is 4.16.,Pramocaine is approved.,Pramocaine is a solid.,True
20194,"Mogamulizumab is a humanized monoclonal antibody (mAb) directed against CC chemokine receptor 4 (CCR4) for the treatment of Mycosis Fungoides (MF) and Sézary Syndrome (SS), the most common subtypes of cutaneous T-cell lymphoma. Cutaneous T-cell lymphomas occur when certain white blood cells, called T cells, become cancerous; these cancers typically affect the skin, causing various types of skin lesions.   For the intravenous use for the treatment of adult patients with relapsed or refractory mycosis fungoides (MF) or Sézary syndrome (SS) after at least one prior systemic therapy. This approval provides a new treatment option for patients with MF and is the first FDA approval of a drug specifically for Sézary Syndrome. This drug is a CC chemokine receptor 4 (CCR4) antagonist. It is a monoclonal antibody which blocks T cell proliferation, which leads to malignancy ,. Mogamulizumab selectively binds to and inhibits the activity of CCR4, which may block CCR4-mediated signal transduction pathways and, so, chemokine-mediated cellular migration and proliferation of T cells, as well as chemokine-mediated angiogenesis. Additionally, this agent may induce antibody-dependent cell-mediated cytotoxicity (ADCC) against CCR4-positive T cells. CCR4, a G-coupled-protein receptor for C-C chemokines such MIP-1, RANTES, TARC and MCP-1, is expressed on the surfaces of some types of T cells, endothelial cells, and certain types of neurons. CCR4, also known as CD194, may be overexpressed on adult T-cell lymphoma (ATL) and peripheral T-cell lymphoma (PTCL) cells. In addition to directly targeting malignant T cells expressing CCR4, mogamulizumab depletes Treg cells, an important therapeutic target in many human cancers because of their role in suppressing host antitumor immunity.",,,,Mogamulizumab is approved and investigational.,,True
20195,FLX475 is a small molecule CCR4 antagonist being investigated for the treatment of cancer.,,,,FLX475 is investigational.,FLX475 is a solid.,True
20196,"Golodirsen is a morpholino antisense oligomer designed to treat about 8% of patients with Duchenne Muscular Dystrophy (DMD). This is an X-linked condition leading to progressive muscle degeneration that begins in early childhood, rendering many patients wheelchair-bound by age 12. Often, patients succumb to this condition by age 30 or younger due to cardiac and respiratory complications. A similar drug used in the treatment of other types of DMD is , which targets a different genetic mutation. Golodirsen is indicated to treat Duchenne muscular dystrophy (DMD) in patients with a confirmed mutation of the DMD gene that would benefit from exon 53 skipping. Continued FDA approval of this drug is contingent upon the results of clinical trials to confirm its benefit. Golodirsen masks genetic mutations that result in a cascade of events which treat Duchenne Muscular Dystrophy in about 8% of patients. Golodirsen indirectly induces the production of dystrophin, an important protein for muscle function. It is not yet confirmed whether motor function is improved by golodirsen, however, clinical trials are underway to examine its clinical benefits.  The hallmark of Duchenne Muscular Dystrophy is the absence of the important muscle stabilizing protein, dystrophin, that is caused by a deletion mutation on the DMD (dystrophin) gene. This results in the production of a non-functional protein. Lack of dystrophin protein leads to progressive muscle weakness and degeneration. ",,,,Golodirsen is approved.,Golodirsen is a solid.,True
20197,,,,,Halicin is experimental.,,False
20198,"Opaganib, also known as ABC294640, is a selective (https://go.drugbank.com/polypeptides/Q9NRA0) inhibitor that is orally administered. This drug has potential anticancer, anti-inflammatory, and antiviral activities, with potential applications in oncology, inflammation, the gastrointestinal system, and COVID-19. Opaganib selectively inhibits (https://go.drugbank.com/polypeptides/Q9NRA0). This inhibition blocks the synthesis of sphingosine 1-phosphate (S1P) and its activities (which includes regulation of fundamental biological processes such as cell proliferation, migration, immune cell trafficking, angiogenesis, immune-modulation, and suppression of innate immune responses from T-cells). This drug has dual anti-inflammatory and antiviral activity targeting a host cell component and is unaffected by viral mutation, contributing to minimization of the likelihood of resistance. It is currently being investigated against COVID-19 as it has demonstrated anti-SARS-CoV-2 activity in studies. ",,,,ABC-294640 is investigational.,,True
20199,"Tauroursodeoxycholic acid is the more hydrophilic form of ursodeoxycholic acid, which is the more abundant naturally produced bile acid in humans. Tauroursodeoxycholic acid, on the other hand, is produced abundantly in bears and has been used for centuries as a natural remedy in some Asian countries. It is approved in Italy and Turkey for the treatment of cholesterol gallstones and is an investigational drug in China, Unites States, and Italy. Tauroursodeoxycholic acid is being investigated for use in several conditions such as Primary Biliary Cirrhosis (PBC), insulin resistance, amyloidosis, Cystic Fibrosis, Cholestasis, and Amyotrophic Lateral Sclerosis. The only completed clinical trial thus far is a phase III clinical trial comparing tauroursodeoxycholic acid and ursofalk in PBC adult patients, but as of June 2013 no results of this trial have been published. Used in the treatment of cholesterol gallstones. Tauroursodeoxycholic acid is also being investigated for use in several conditions such as Primary Biliary Cirrhosis (PBC), insulin resistance, amyloidosis, Cystic Fibrosis, Cholestasis, and Amyotrophic Lateral Sclerosis. Tauroursodeoxycholic acid is the more hydrophilic form of ursodeoxycholic acid, which is naturally produced in the body. In patients with properly functioning gallbladders, both of these bile acids inhibit liver cholesterol secretion and synthesis as well as intestinal cholesterol absorption allowing for the promotion of cholesterol gallstone dissolution. The mechanism of action of tauroursodeoxycholic acid in the other conditions is still being investigated.",,,,Tauroursodeoxycholic acid is experimental and investigational.,Tauroursodeoxycholic acid is a solid.,True
20200,"Ferumoxytol is an intravenously administered iron preparation indicated in the EU and the US for the treatment of iron deficiency anemia in adult patients with chronic kidney disease (CKD). This drug is indicated for the treatment of iron deficiency anemia in adult patients who have experienced intolerance to oral iron or have experienced an unsatisfactory response to oral iron or Feraheme (ferumoxytol) is comprised of a superparamagnetic iron oxide that is coated with a carbohydrate shell, aiding in the isolation the bioactive iron from plasma components until the iron-carbohydrate complex enters the reticuloendothelial system macrophages of the liver, spleen and the bone marrow. ",,,,Ferumoxytol is approved and investigational.,Ferumoxytol is a solid.,True
20201,"Gallium citrate Ga 67 is the citrate salt of the radioisotope gallium Ga 67. Although the mechanism is unknown, gallium Ga 67 concentrates in lysosomes and is bound to a soluble intracellular protein in certain viable primary and metastatic tumors and focal sites of inflammation, allowing scintigraphic localization. Ga-67 scintigraphy (GS) cannot differentiate between tumor and acute inflammation.  Gallium Citrate Ga 67 Injection may be useful to demonstrate the presence and extent of Hodgkin's disease, lymphoma, and bronchogenic carcinoma. Positive gallium Ga-67 uptake in the absence of prior symptoms warrants follow-up as an indication of a potential disease state. Gallium Citrate Ga 67 Injection may be useful as an aid in detecting some acute inflammatory lesions. It has been reported in the scientific literature that following intravenous injection, the highest tissue concentration of gallium Ga-67 - other than tumors and sites of infection - is the renal cortex. After the first day, the maximum concentration shifts to bone and lymph nodes and after the first week, to liver and spleen. Gallium Ga-67 is excreted relatively slowly from the body. The average whole body retention is 65 percent after seven days, with 26 percent having been excreted in the urine and 9 percent in the stools. Gallium Citrate Ga 67, with no carrier added, has been found to concentrate in certain viable primary and metastatic tumors as well as focal sites of infection. The body generally handles Ga3+ as though it were ferric iron (Fe-III), and thus the free isotope ion is bound (and concentrates) in areas of inflammation, such as an infection site, and also areas of rapid cell division. Ga-67 binds to transferrin, leukocyte lactoferrin, bacterial siderophores, inflammatory proteins, and cell-membranes in neutrophils, both living and dead. Lactoferrin is contained within leukocytes. Ga-67 may bind to lactoferrin and be transported to sites of inflammation, or binds to lactoferrin released during bacterial phagocytosis at infection sites (and remains due to binding with macrophage receptors). Ga-67 also attaches to the siderophore molecules of bacteria themselves, and for this reason can be used in leukopenic patients with bacterial infection (here it attaches directly to bacterial proteins, and leukocytes are not needed). Uptake is thought to be associated with a range of tumour properties including transferring receptors, anaerobic tumor metabolism and tumor perfusion and vascular permeability.",The molecular weight is 256.03.,Gallium citrate Ga-67 has a topological polar surface area of 140.62.,,Gallium citrate Ga-67 is approved.,Gallium citrate Ga-67 is a solid.,True
20202,"The glycine amide of 4-aminobenzoic acid. Its sodium salt is used as a diagnostic aid to measure effective renal plasma flow (ERPF) and excretory capacity.  Used to measure effective renal plasma flow (ERPF) and to determine the functional capacity of the tubular excretory mechanism. Aminohippurate (p-aminohippuric acid, PAH, PAHA) is the glycine amide of p-aminobenzoic acid. It is filtered by the glomeruli and is actively secreted by the proximal tubules. At low plasma concentrations (1.0 to 2.0 mg/100 mL), an average of 90 percent of aminohippurate is cleared by the kidneys from the renal blood stream in a single circulation. It is ideally suited for measurement of ERPF since it has a high clearance, is essentially nontoxic at the plasma concentrations reached with recommended doses, and its analytical determination is relatively simple and accurate. Aminohippurate is also used to measure the functional capacity of the renal tubular secretory mechanism or transport maximum (Tm<sub>PAH</sub>). This is accomplished by elevating the plasma concentration to levels (40-60 mg/100 mL) sufficient to saturate the maximal capacity of the tubular cells to secrete aminohippurate. Inulin clearance is generally measured during Tm<sub>PAH</sub> determinations since glomerular filtration rate (GFR) must be known before calculations of secretory Tm measurements can be done. Aminohippurate is filtered by the renal glomeruli and secreted into the urine by the proximal tubules. By measuring the amount of drug in the urine it is possible to determine functional capacity and effective renal plasma flow.",The molecular weight is 194.19.,Aminohippuric acid has a topological polar surface area of 92.42.,The log p value of  is -0.25.,Aminohippuric acid is approved and investigational.,Aminohippuric acid is a solid.,True
20203,"Semisynthetic, broad-spectrum antibacterial derived from cephaloridine and used especially for Pseudomonas and other gram-negative infections in debilitated patients. For the treatment of patients with infections caused by susceptible strains of organisms in the following diseases: lower respiratory tract infections,skin and skin structure infections, urinary tract infections, bacterial septicemia, bone and joint infections, gynecologic infections, intra abdominal infections (including peritonitis), and central nervous system infections (including meningitis). Ceftazidime is a semisynthetic, broad-spectrum, beta-lactam antibiotic for parenteral administration. Ceftazidime is bactericidal in action exerting its effect by inhibition of enzymes responsible for cell-wall synthesis, primarily penicillin binding protein 3 (PBP3). A wide range of gram-negative organisms is susceptible to ceftazidime in vitro, including strains resistant to gentamicin and other aminoglycosides. In addition, ceftazidime has been shown to be active against gram-positive organisms. It is highly stable to most clinically important beta-lactamases, plasmid or chromosomal, which are produced by both gram-negative and gram-positive organisms and, consequently, is active against many strains resistant to ampicillin and other cephalosporins. Ceftazidime has activity against the gram-negative organisms <i>Pseudomonas</i> and <i>Enterobacteriaceae</i>. Its activity against <i>Pseudomonas</i> is a distinguishing feature of ceftazidime among the cephalosporins. The bactericidal activity of ceftazidime results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs).",The molecular weight is 547.58.,Ceftazidime has a topological polar surface area of 188.39.,The log p value of  is -3.75.,Ceftazidime is approved.,Ceftazidime is a solid.,True
20204,"Cefixime, an antibiotic, is a third-generation cephalosporin like ceftriaxone and cefotaxime. Cefixime is highly stable in the presence of beta-lactamase enzymes. As a result, many organisms resistant to penicillins and some cephalosporins due to the presence of beta-lactamases, may be susceptible to cefixime. The antibacterial effect of cefixime results from inhibition of mucopeptide synthesis in the bacterial cell wall. For use in the treatment of the following infections when caused by susceptible strains of the designated microorganisms: (1) uncomplicated urinary tract infections caused by <i>Escherichia coli</i> and <i>Proteus mirabilis</i>, (2) otitis media caused by <i>Haemophilus influenzae</i> (beta-lactamase positive and negative strains), <i>Moraxella catarrhalis</i> (most of which are beta-lactamase positive), and <i>S. pyogenes</i>, (3) pharyngitis and tonsillitis caused by <i>S. pyogenes</i>, (4) acute bronchitis and acute exacerbations of chronic bronchitis caused by <i>Streptococcus pneumoniae</i> and <i>Haemophilus influenzae</i> (beta-lactamase positive and negative strains), and (5) uncomplicated gonorrhea (cervical/urethral) caused by <i>Neisseria gonorrhoeae</i> (penicillinase- and non-penicillinase-producing strains). Cefixime, an antibiotic, is a third-generation cephalosporin like ceftriaxone and cefotaxime. Cefixime is highly stable in the presence of beta-lactamase enzymes. As a result, many organisms resistant to penicillins and some cephalosporins due to the presence of beta-lactamases, may be susceptible to cefixime. The antibacterial effect of cefixime results from inhibition of mucopeptide synthesis in the bacterial cell wall. Like all beta-lactam antibiotics, cefixime binds to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, causing the inhibition of the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that cefixime interferes with an autolysin inhibitor.",The molecular weight is 453.44.,Cefixime has a topological polar surface area of 184.51.,The log p value of  is 0.25.,Cefixime is approved and investigational.,Cefixime is a solid.,True
20205,A cephalorsporin antibiotic that is no longer commonly used. For treatment of severe infections caused by susceptible bacteria. Cephaloglycin is an antibiotic related to cephalosporin but no longer in common use. It is an orally absorbed derivative of cephalosporin C. The bactericidal activity of cephaloglycin results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs).,The molecular weight is 405.43.,Cephaloglycin has a topological polar surface area of 139.03.,The log p value of  is -2.56.,Cephaloglycin is approved.,Cephaloglycin is a solid.,True
20206,"A cyclohexylamido analog of penicillanic acid. For the treatment of bacterial infections caused by susceptible organisms. Cyclacillin, a penicillin, is a cyclohexylamido analog of penicillanic acid. Cyclacillin is more resistant to beta-lactamase hydrolysis than ampicillin, is much better absorbed when given by mouth and, as a result, the levels reached in the blood and in the urine are considerably higher than those obtained with the same dose of ampicillin. Cyclacillin has been replaced by newer penicillin treatments. The bactericidal activity of cyclacillin results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs). Cyclacillin is stable in the presence of a variety of b-lactamases, including penicillinases and some cephalosporinases.",The molecular weight is 341.43.,Cyclacillin has a topological polar surface area of 112.73.,The log p value of  is -0.82.,Cyclacillin is approved.,Cyclacillin is a solid.,True
20207,"Long-acting, broad-spectrum, water-soluble, cephalexin derivative. For the treatment of the following infections (skin, UTI, ENT) caused by; <i>S. pneumoniae, H. influenzae, staphylococci, S. pyogenes</i> (group A beta-hemolytic streptococci), <i>E. coli, P. mirabilis, Klebsiella</i> sp, coagulase-negative staphylococci and <i>Streptococcus pyogenes</i> Cefadroxil, a first-generation cephalosporin antibiotic, is used to treat urinary tract infections, skin and skin structure infections, pharyngitis, and tonsillitis. Like all beta-lactam antibiotics, cefadroxil binds to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, causing the inhibition of the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that cefadroxil interferes with an autolysin inhibitor.",The molecular weight is 363.39.,Cefadroxil has a topological polar surface area of 132.96.,The log p value of  is -2.51.,Cefadroxil is approved and vet_approved and withdrawn.,Cefadroxil is a solid.,True
20208,"Cefepime is a fourth-generation cephalosporin antibiotic developed in 1994. Cefepime is active against Gram-positive and Gram-negative bacteria, with greater activity against both than third-generation antibiotics. Cefepime is usually reserved to treat severe nosocomial pneumonia, infections caused by multi-resistant microorganisms (e.g. Pseudomonas aeruginosa) and empirical treatment of febrile neutropenia. For the treatment of pneumonia (moderate to severe) caused by <i>Streptococcus pneumoniae</i>, including cases associated with concurrent bacteremia, <i>Pseudomonas aeruginosa</i>, <i>Klebsiella pneumoniae</i>, or <i>Enterobacter</i> species. Also for empiric treatment of febrile neutropenic patients and uncomplicated and complicated urinary tract infections (including pyelonephritis) caused by <i>Escherichia coli</i> or <i>Klebsiella pneumoniae</i>, when the infection is severe, or caused by <i>Escherichia coli</i>, <i>Klebsiella pneumoniae</i>, or <i>Proteus mirabilis</i>, when the infection is mild to moderate, including cases associated with concurrent bacteremia with these microorganisms. Also for the treatment of uncomplicated skin and skin structure infections caused by <i>Staphylococcus aureus</i> (methicillin-susceptible strains only) or <i>Streptococcus pyogenes</i> and complicated intra-abdominal infections (used in combination with metronidazole) caused by <i>Escherichia coli</i>, viridans group streptococci, <i>Pseudomonas aeruginosa</i>, <i>Klebsiella pneumoniae</i>, <i>Enterobacter</i> species, or <i>Bacteroides fragilis</i>. Cefepime is a fourth-generation cephalosporin antibiotic developed in 1994. Cefepime is active against Gram-positive and Gram-negative bacteria, with greater activity against both than third-generation antibiotics. Cefepime has good activity against important pathogens including Pseudomonas aeruginosa, Staphylococcus aureus, Enterobacteriaceae, and multiple drug resistant Streptococcus pneumoniae. Whereas other cephalosporins are degraded by many plasmid- and chromosome-mediated beta-lactamases, cefepime is stable and is a front line agent when infection with Enterobacteriaceae is known or suspected Cephalosporins are bactericidal and have the same mode of action as other beta-lactam antibiotics (such as penicillins). Cephalosporins disrupt the synthesis of the peptidoglycan layer of bacterial cell walls. The peptidoglycan layer is important for cell wall structural integrity, especially in Gram-positive organisms. The final transpeptidation step in the synthesis of the peptidoglycan is facilitated by transpeptidases known as penicillin binding proteins (PBPs).",The molecular weight is 480.56.,Cefepime has a topological polar surface area of 150.04.,The log p value of  is -5.97.,Cefepime is approved and investigational.,Cefepime is a solid.,True
20209,,,,,Degraded Cephaloridine is experimental.,Degraded Cephaloridine is a solid.,False
20210,"Azidocillin is a penicillin antibiotic similir to ampicillin. For treatment of infection (Respiratory, GI, UTI and meningitis) due to E. coli, P. mirabilis, enterococci, Shigella, S. typhosa and other Salmonella, nonpenicillinase-producing N. gononhoeae, H. influenzae, staphylococci, streptococci including streptoc By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, Azidocillin inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that Azidocillin interferes with an autolysin inhibitor.",The molecular weight is 375.4.,Azidocillin has a topological polar surface area of 116.14.,The log p value of  is 2.6.,Azidocillin is experimental.,Azidocillin is a solid.,True
20211,"Acetylcarnitine is an investigational drug in the United states, Italy, United Kingdom, China, Israel, and Norway, and it is approved in Italy, Portugal, Argentina, Chile, Philippines, Australia, and India. Acetylcarnitine can be synthesized, but it is also naturally found in adequate amounts in healthy humans. In human plasma and tissues, acetylcarnitine is the most predominant acylated ester of carnitine, which is an amino acid derivative that is made in the kidney, liver, and brain from lysine and methionine. The main role of acetylcarnitine is to help transport fatty acids into the mitochondrial matrix where fatty acid metabolism occurs. Acetylcarnitine is not approved for any indication in the United states and Canada, but it is approved and indicated in Italy for cerebrovascular disorders, mental function disorders, peripheral nerve disorders, diabetic neuropathy, and nutritional supplementation; Portugal for mental function disorders; Argentina for cerebral vasculopathy, nutritional supplementation, and peripheral neuropathy; Chile for dementia; Philippines for cerebrovascular disorders and mental function disorders; Australia for nutritional supplementation; and India for nutritional supplementation to increase sperm count. Acetylcarnitine also has several potential therapeutic indications for which it is still being investigated: in Norway, acetylcarnitine is in a phase IV trial for prophylactic treatment of migraines; in Italy acetylcarnitine is in a phase II trial for use in patients with type 2 Diabetes Mellitus, a phase III trial for alleviating fatigue in patients with chronic hepatitis C, and for use in patients with Minimal Hepatic Encephalopathy; in the United States acetylcarnitine is in a phase II trial for the neurodegenerative disorder Progressive Supranuclear Palsy, a phase II and III trial for reducing peripheral neuropathy in cancer patients as an adjunct to chemotherapy, a phase I and II trial for treating patients in septic shock, a phase II trial for bipolar depression, a phase II trial to reduce oxidative stress in patients with Sickle Cell disease, a phase I and II trial for chronic fatigue syndrome, and a study for preventing nerve damage in HIV patients; in China acetylcarnitine is in a phase III trial for reducing peripheral neuropathy in cancer patients as an adjunct to chemotherapy; in the United Kingdom acetylcarnitine is being investigated for preventing nerve damage in HIV patients; and in Israel acetylcarnitine is being studied for the treatment of male infertility. The complete physiological effects of acetycarnitine are still being studied. What has been discovered so far is that acetylcarinitine has positive effects on mental fatigue, neurodegenerative disorders, cognitive functions, peripheral neuropathy, and sperm motility. Specifically, in one study involving patients with HIV, patients on acetylcarnitine supplementation had increased CD4 cells, decreased lymphocyte apoptosis, improved polyneuropathy and cardiovascular damage, and decreased triglyceride and TNF alpha levels in the blood. Another study showed that acetylcarnitine increased glucose disposal in type 2 diabetic patients through possibly increasing the activity of glycogen synthase. The mechanisms of action of acetylcarnitine have not been fully elucidated, but it seems that the main role of acetylcarnitine is to donate an acetyl group during fatty acid metabolism to help transport fatty acids, such as acetyl CoA, into the mitochondrial matrix where fatty acid metabolism occurs. Additionally several studies have found that separate from its metabolic role, acetylcarnitine has neuromodulatory, neurotrophic, and neuroprotective effects that most likely are involved in its positive effects in neurological diseases. In its role in treating male infertility, acetylcarnitine increases the active movement of sperm cells. One study has also mentioned a role for acetylcarnitine as an antioxidant. The study found that through the receptor, tyrosine kinase A, acetylcarnitine was able to decrease the production of free radicals, peroxidation of lipids, and oxidation of proteins as well as decrease glutathione levels and increase thioredoxin.",The molecular weight is 203.24.,Acetylcarnitine has a topological polar surface area of 66.43.,The log p value of  is -6.88.,Acetylcarnitine is approved and investigational.,Acetylcarnitine is a solid.,True
20212,"An alkylating nitrogen mustard that is used as an antineoplastic in the form of the levo isomer - melphalan, the racemic mixture - merphalan, and the dextro isomer - medphalan; toxic to bone marrow, but little vesicant action; potential carcinogen. For the palliative treatment of multiple myeloma and for the palliation of non-resectable epithelial carcinoma of the ovary. Has also been used alone or as part of various chemotherapeutic regimens as an adjunct to surgery in the treatment of breast cancer, alone or in combination regimens for palliative treatment of locally recurrent or unresectable in-transit metastatic melanoma of the extremities, as well as for the treatment of amyloidosis with prednisone. Melphalan is an antineoplastic in the class of alkylating agents and is used to treat various forms of cancer. Alkylating agents are so named because of their ability to add alkyl groups to many electronegative groups under conditions present in cells. They stop tumor growth by cross-linking guanine bases in DNA double-helix strands - directly attacking DNA. This makes the strands unable to uncoil and separate. As this is necessary in DNA replication, the cells can no longer divide. In addition, these drugs add methyl or other alkyl groups onto molecules where they do not belong which in turn inhibits their correct utilization by base pairing and causes a miscoding of DNA. Alkylating agents are cell cycle-nonspecific. Alkylating agents work by three different mechanisms all of which achieve the same end result - disruption of DNA function and cell death. Alkylating agents work by three different mechanisms: 1) attachment of alkyl groups to DNA bases (primarily at the N-7 position of guanine and to a lesser extent, at the N-3 position of adenine), forming monoadducts and resulting in the DNA being fragmented by repair enzymes in their attempts to replace the alkylated bases, preventing DNA synthesis and RNA transcription from the affected DNA, 2) DNA damage via the formation of cross-links (bonds between atoms in the DNA) which prevents DNA from being separated for synthesis or transcription, and 3) the induction of mispairing of the nucleotides leading to mutations.",The molecular weight is 305.2.,Melphalan has a topological polar surface area of 66.56.,The log p value of  is -0.21.,Melphalan is approved.,Melphalan is a solid.,True
20213,An essential branched-chain amino acid important for hemoglobin formation. ,,,,D-Leucine is experimental.,D-Leucine is a solid.,True
20214,"Potassium bicarbonate is a white, crystalline, slightly alkaline and salty substance. It is produced by the passage of carbon dioxide through an aqueous potassium carbonate solution. It is used in medicine as an antacid. It is registered in the FDA under the section of suitable, safe and effective ingredients for OTC antacids. This FDA denomination classifies potassium bicarbonate as a GRAS ingredient. Potassium bicarbonate is used as an antacid, electrolyte replenisher and potassium supplement. It can also be used as an excipient in drug formulations. An antacid is a medication used to neutralize gastric acid in a short timeframe after ingestion and the effect is soon overcome by meal-stimulated acid secretion. Potassium is the principal intracellular cation in most body tissues. The concentration of potassium ions is essential to conduct nerve impulses in specialized tissues like brain, heart and skeletal muscle, as well as to maintain normal renal function, acid-base balance, and cellular metabolic functions. The use of compounds containing bicarbonate is showed to produce the release of CO2. This effect has been one of the problems of the use of potassium bicarbonate as it can cause eructation.  The antacid potential of potassium bicarbonate is attained by increasing the gastrointestinal pH by neutralizing hydrochloric acid. The increase in pH results in suppression of the action of pepsin which is the enzyme that exacerbates ulceration due to the presence of acid.",The molecular weight is 100.11.,Potassium bicarbonate has a topological polar surface area of 60.36.,,Potassium bicarbonate is approved.,Potassium bicarbonate is a solid.,True
20215,"Valganciclovir hydrochloride (Valcyte, manufactured by Roche) is an antiviral medication used to treat cytomegalovirus infections. As the L-valyl ester of ganciclovir, it is actually a prodrug for ganciclovir. After oral administration, it is rapidly converted to ganciclovir by intestinal and hepatic esterases. Valganciclovir is an antiviral medication used for the treatment of cytomegalovirus infections. Valganciclovir is an antiviral medication used to treat cytomegalovirus infections. As the L-valyl ester of ganciclovir, it is actually a prodrug for ganciclovir. After oral administration, it is rapidly converted to ganciclovir by intestinal and hepatic esterases. After this, it (being an analogue of guanosine) gets incorporated into DNA and thus cannot be properly read by DNA polymerase. This results in the termination of the elongation of viral DNA. Valganciclovir is a prodrug of ganciclovir that exists as a mixture of two diastereomers. After administration, these diastereomers are rapidly converted to ganciclovir by hepatic and intestinal esterases. In cytomegalovirus (CMV)-infected cells, ganciclovir is initially phosphorylated to the monophosphate form by viral protein kinase, then it is further phosphorylated via cellular kinases to produce the triphosphate form. This triphosphate form is slowly metabolized intracellularly. The phosphorylation is dependent upon the viral kinase and occurs preferentially in virus-infected cells. The virustatic activity of ganciclovir is due to the inhibition of viral DNA synthesis by ganciclovir triphosphate. Ganciclovir triphosphate is incorporated into the DNA strand replacing many of the adenosine bases. This results in the prevention of DNA synthesis, as phosphodiester bridges can longer to be built, destabilizing the strand. Ganciclovir inhibits viral DNA polymerases more effectively than it does cellular polymerase, and chain elongation resumes when ganciclovir is removed.",,,,Valganciclovir is approved and investigational.,Valganciclovir is a solid.,True
20216,"A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed)",,,,D-Lactic acid is experimental.,D-Lactic acid is a solid.,True
20217,"A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed) Sodium lactate is the sodium salt of lactic acid, and has a mild saline taste. It is produced by fermentation of a sugar source, such as corn or beets, and then, by neutralizing the resulting lactic acid to create a compound having the formula NaC3H5O3. For use as an alkalinizing agent. Lactic acid produces a metabolic alkalinizing effect. Lactate ions are metabolized ultimately to carbon dioxide and water, which requires the consumption of hydrogen cations.",The molecular weight is 90.08.,Lactic acid has a topological polar surface area of 57.53.,The log p value of  is -0.73.,Lactic acid is approved and vet_approved.,Lactic acid is a solid.,True
20218,"Sodium citrate is the sodium salt of citric acid. It is white, crystalline powder or white, granular crystals, slightly deliquescent in moist air, freely soluble in water, Used as an anticoagulant during plasmophoresis as well as a neutralizing agent in the treatment of upset stomach and acidic urine . Citrate prevents activation of the clotting cascade by chelating calcium ions. Citrate neutralizes acid in the stomach and urine, raising the pH. Citrate chelates free calcium ions preventing them from forming a complex with tissue factor and coagulation factor VIIa to promote the activation of coagulation factor X. This inhibits the extrinsic initiation of the coagulation cascade. Citrate may also exert an anticoagulant effect via a so far unknown mechanism as restoration of calcium concentration does not fully reverse the effect of citrate. Citrate is a weak base and so reacts with hydrochloric acid in the stomach to raise the pH. It it further metabolized to bicarbonate which then acts as a systemic alkalizing agent, raising the pH of the blood and urine. It also acts as a diuretic and increases the urinary excretion of calcium.",The molecular weight is 258.07.,Sodium citrate has a topological polar surface area of 140.62.,,Sodium citrate is approved and investigational.,Sodium citrate is a solid.,True
20219,,,,,Glyoxylic acid is experimental.,Glyoxylic acid is a solid.,False
20220,"Synthetic guanethidine derivative that locates phaeochromocytomas and neuroblastomas. The radioisotope used can either be iodine-123 for imaging or iodine-131 for destruction of tissues that metabolize noradrenaline. Iodine 123 is a cyclotron-produced radionuclide that decays to Te 123 by electron capture. Images are produced by a I123 MIBG scintigraphy. FDA approved on September 19, 2008. Detection of primary and metastatic pheochromocytoma or neuroblastoma  AdreView is a diagnostic radiopharmaceutical which contains a small quantity of iobenguane that is not expected to produce a pharmacodynamic effect. Patients with renal insufficiency may experience increased radiation exposure and impaired imaging results.  Structure of iobenguane is similar to noradrenaline so it can be taken up by adrenergic tissue in the adrenal medulla, liver, heart, and spleen. Once taken up by noradrenaline transporters in the adrenergic nerve terminals, it is stored in the presynaptic storage vesicles. The radioactive iodine component is responsible for its imaging properties. ",,,,Iobenguane is approved and investigational.,Iobenguane is a liquid.,True
20221,Iobenguane sulfate I-123 is a radiopharmaceutical used in gamma-scintigraphy of adrenergically inervated tissues. For use in the diagnostic imaging of adrenergically inervated tissues for the purposes of detecting metastatic pheochromocytoma or neuroblastoma. Also used to assess the sympathetic inervation of the myocardium via determination of the heart to mediastinum ratio of radioactivity in patients with New York Heart Association class II or III heart failure. Iobenguane I-123 is taken up by and stored in adrenergic nerve terminals allowing for the radiographic imaging of adrenergically inervated organs and tissues. Iobenguane I-123 is transported into adrenergic nerve terminals via the noradrenaline uptake transporter. It is rapidly cleared from systemic circulation and collected in adrenergically invervated tissues. This allows for gamma-scintigraphic imaging of these tissues and their associated organs for diagnostic purposes.,,,,Iobenguane sulfate I-123 is approved and investigational.,Iobenguane sulfate I-123 is a liquid.,True
20222,"D-proline is an isomer of the naturally occurring amino acid, L-Proline. D-amino acids have been found in relatively high abundance in human plasma and saliva. These amino acids may be of bacterial origin, but there is also evidence that they are endogenously produced through amino acid racemase activity.",,,,D-Proline is experimental.,D-Proline is a solid.,True
20223,"Gaboxadol also known as 4,5,6,7-tetrahydroisoxazolo(5,4-c)pyridin-3-ol (THIP) is an experimental sleep aid drug developed by Lundbeck and Merck, who reported increased deep sleep without the reinforcing effects of benzodiazepines. Development of Gaboxadol was stopped in March 2007 after concerns regarding safety and efficacy. It acts on the GABA system, but in a seemingly different way from benzodiazepines and other sedatives. Investigated for use/treatment in sleep disorders and insomnia.",,,,Gaboxadol is investigational.,Gaboxadol is a solid.,True
20224,"Hydroxyproline is a neutral heterocyclic protein amino acid. It is found in collagen and as such it is common in many gelatin products. Hydroxyproline is mostly used as a diagnostic marker of bone turnover and liver fibrosis. Therapeutically, hydroxyproline is being studied as an an experimental medicine but is approved in France as a combination topical gel product called Cicactive for small, superficial wounds. Used in France as a combination product for the treatment of small, superficial wounds. Hydroxyproline as well as proline and glycine are the major components of collagen. Collagen is on one of the main building blocks of connective tissue such as skin, bone, and cartilage. Thus when these tissues are damaged, hydroxyproline is necessary for repair of the damaged area.",The molecular weight is 131.13.,Hydroxyproline has a topological polar surface area of 69.56.,The log p value of  is -1.91.,Hydroxyproline is experimental.,Hydroxyproline is a solid.,True
20225,,,,,Nipecotic acid is experimental.,Nipecotic acid is a solid.,False
20226,"Ioflupane (I-123) is a radiopharmaceutical used to image dopamine neurons and diagnose Parkinsonian syndromes. Ioflupane I-123 is a SPECT (single photon emission computerized tomography) agent used to distinguish between Parkinson’s syndrome tremors and essential tremor.  iodine-123 labeled ioflupanebinds selectively to striatal presynaptic dopamine neurons by binding reversibly to presynaptic dopamine transporters. Iodine-123 labeled ioflupane binds to presynaptic dopamine transporters. When Iodine-123 decays, a gammay ray is emmitted and detected through SPECT.",The molecular weight is 427.29.,Ioflupane I-123 has a topological polar surface area of 29.54.,The log p value of  is 4.42.,Ioflupane I-123 is approved.,Ioflupane I-123 is a liquid.,True
20227,"An antiviral agent used in the treatment of cytomegalovirus retinitis. Foscarnet also shows activity against human herpes viruses and HIV. For the treatment of CMV retinitis in patients with acquired immunodeficiency syndrome (AIDS) and for treatment of acyclovir-resistant mucocutaneous HSV infections in immunocompromised patients. Foscarnet is an organic analogue of inorganic pyrophosphate that inhibits replication of herpes viruses <i>in vitro</i> including cytomegalovirus (CMV) and herpes simplex virus types 1 and 2 (HSV-1 and HSV-2). Foscarnet does not require activation (phosphorylation) by thymidine kinase or other kinases and therefore is active in vitro against HSV TK deficient mutants and CMV UL97 mutants. Thus, HSV strains resistant to acyclovir or CMV strains resistant to ganciclovir may be sensitive to foscarnet. However, acyclovir or ganciclovir resistant mutants with alterations in the viral DNA polymerase may be resistant to foscarnet and may not respond to therapy with foscarnet. The combination of foscarnet and ganciclovir has been shown to have enhanced activity in vitro. Foscarnet exerts its antiviral activity by a selective inhibition at the pyrophosphate binding site on virus-specific DNA polymerases at concentrations that do not affect cellular DNA polymerases.",The molecular weight is 126.0.,Foscarnet has a topological polar surface area of 94.83.,The log p value of  is -2.17.,Foscarnet is approved.,Foscarnet is a solid.,True
20228,"Acetic acid is a product of the oxidation of ethanol and of the destructive distillation of wood. It is used locally, occasionally internally, as a counterirritant and also as a reagent. (Stedman, 26th ed) Acetic acid otic (for the ear) is an antibiotic that treats infections caused by bacteria or fungus. Used to treat infections in the ear canal.",The molecular weight is 60.05.,Acetic acid has a topological polar surface area of 37.3.,The log p value of  is -0.19.,Acetic acid is approved.,Acetic acid is a solid.,True
20229,"A bile salt formed in the liver from chenodeoxycholate and glycine, usually as the sodium salt. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is a cholagogue and choleretic. ",,,,Glycochenodeoxycholic Acid is experimental.,Glycochenodeoxycholic Acid is a solid.,True
20230,Pilsicainide has been investigated for the treatment of Paroxysmal Atrial Fibrillation.,The molecular weight is 272.39.,Pilsicainide has a topological polar surface area of 32.34.,The log p value of  is 2.05.,Pilsicainide is investigational.,,True
20231,"A cyclododecadepsipeptide ionophore antibiotic produced by Streptomyces fulvissimus and related to the enniatins. It is composed of 3 moles each of L-valine, D-alpha-hydroxyisovaleric acid, D-valine, and L-lactic acid linked alternately to form a 36-membered ring. (From Merck Index, 11th ed) Valinomycin is a potassium selective ionophore and is commonly used as a tool in biochemical studies.",,,,Valinomycin is experimental.,Valinomycin is a solid.,True
20232,,,,,Rhodamine 6G is experimental.,Rhodamine 6G is a solid.,False
20233,"Technetium Tc-99m sestamibi (commonly sestamibi) is a pharmaceutical agent used in nuclear medicine imaging. The drug is a coordination complex consisting of the radioisotope technetium-99m bound to six methoxyisobutylisonitrile (MIBI) ligands, hence the name sesta (6) MIBI.. Following intravenous injection of the drug, Technetium Tc-99m sestamibi is taken up by the myocardium, parathyroid, and/or breast tissue. The mechanism by which sestamibi localizes to these tissues has not been established. Single photon emission computed tomography (SPECT) is then performed to detect the gamma ray emmitted by the decay of Technetium-99m to Technetium-99. Technetium Tc 99m Sestamibi is indicated for: 1) detecting coronary artery disease by localizing myocardial ischemia (reversible defects) and infarction (non-reversible defects); and 2) evaluating myocardial function and developing information for use in patient management decisions.",The molecular weight is 777.87.,Technetium Tc-99m sestamibi has a topological polar surface area of 81.54.,,Technetium Tc-99m sestamibi is approved and investigational.,Technetium Tc-99m sestamibi is a solid.,True
20234,"Novobiocin is an antibiotic compound derived from _Streptomyces niveus_. It has a chemical structure similar to coumarin. Novobiocin binds to DNA gyrase, and blocks adenosine triphosphatase (ATPase) activity. (From Reynolds, Martindale The Extra Pharmacopoeia, 30th ed, p189) For the treatment of infections due to staphylococci and other susceptible organisms Novobiocin is an aminocoumarin antibiotic that was produced by the actinomycete <i>Streptomyces niveus</i>. Novobiocin binds to DNA gyrase, and blocks adenosine triphosphatase (ATPase) activity. Other antibiotics in the aminocoumarin class include coumermycin A1 and clorobiocin. Novobiocin is an aminocoumarinthat works by inhibiting the GyrB subunit of the bacterial DNA gyrase enzyme involved in energy tranduction. Similar to other aminocoumarin antibiotics, it acts as a competitive inhibitor of the ATPase reaction catalysed by GyrB.",The molecular weight is 612.63.,Novobiocin has a topological polar surface area of 196.1.,The log p value of  is 3.98.,Novobiocin is approved and investigational and vet_approved.,Novobiocin is a solid.,True
20235,"Cefamandole is also known as cephamandole. It is a parenterally administered broad-spectrum cephalosporin antibiotic. It is generally formulated as a formate ester. It is no longer marketed in the United States. For the treatment of serious infections caused by susceptible strains of microorganisms. The parenteral prodrug formate ester cefamandole nafate is a broad-spectrum cephalosporin antibiotic. The bactericidal action of cefamandole results from inhibition of cell-wall synthesis. Cephalosporins have in vitro activity against a wide range of gram-positive and gram-negative organisms. Like all beta-lactam antibiotics, cefamandole binds to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, causing the inhibition of the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that cefamandole interferes with an autolysin inhibitor.",The molecular weight is 462.5.,Cefamandole has a topological polar surface area of 150.54.,The log p value of  is 0.21.,Cefamandole is approved and experimental.,Cefamandole is a solid.,True
20236,,,,,Glutaric Acid is experimental.,Glutaric Acid is a solid.,False
20237,"Relebactam is a diazabicyclooctane beta-lactamase inhibitor, similar in structure to. It includes a piperidine ring which reduces export from bacterial cells by producing a positive charge. It is currently available in a combination product which includes and to treat complicated urinary tract infections (UTIs), pyelonephritis, and complicated intra-abdominal infections in adults. It is considered to be a last-line treatment option and gained FDA approval as part of the combination product RecarbrioⓇ in July 2019. Relebactam is indicated in combination with and for the treatment of complicated urinary tract infections (including pyelonephritis), and complicated intra-abdominal infections caused by susceptible organisms in adults. Relebactam prevents the hydrolysis of , allowing it to exert its bactericidal effect. Relebactam is a beta-lactamase inhibitor known to inhibit many types of beta-lactamases including Ambler class A and Ambler class C enzymes, helping to prevent from degrading in the body. Similar to the structurally-related , first, relebactam binds non-covalently to a beta-lactamase binding site, then, it covalently acylates the serine residue in the active site of the enzyme. In contrast to some other beta-lactamase inhibitors, once relebactam de-acylates from the active site, it can reform it's 5 membered ring and is capable of rebinding to target enzymes.",,,,Relebactam is approved and investigational.,Relebactam is a solid.,True
20238,"Nystatin is a polyene antifungal drug that has broad-spectrum fungicidal and fungistatic activity against a number of yeasts and fungi, most notably _Candida_ species. It is one of the most effective antifungal agents synthesized by bacteria, in this case a strain of _Streptomyces noursei_, and is closely related to , differing only slightly in structure. Nystatin has a greater antifungal activity than amphotericin B - parenterally administered nystatin, however, is associated with significant toxicity and is not available in a formulation appropriate for systemic use. As it undergoes very little absorption following oral or topical administration, nystatin's efficacy is limited to the treatment/prevention of cutaneous, mucocutaneous, and gastrointestinal fungal infections. Nystatin is available in oral formulations for the treatment and/or prevention of oral candidiasis (a.k.a. thrush), intestinal candidiasis, and anal candidiasis. It is indicated topically for the treatment of vulvovaginal candidiasis and other cutaneous candida infections. A combination product containing nystatin alongside , , and (Viaderm K.C.®) is indicated in the treatment of corticosteroid-responsive dermatoses caused by bacterial or candidal infections and for pruritus ani/vulvae. It is also available in combination with for the treatment of mixed infections due to _Trichomonas vaginalis_ and _Candida albicans_. Nystatin is an antifungal that is both fungistatic and fungicidal in vitro against a wide variety of yeasts and yeast-like fungi. It exerts its antifungal effects via disruption of the fungal cell membrane. Resistance to nystatin is minimal in _Candida albicans_, but tends to develop in other species of _Candida_. Nystatin carries no significant activity against bacteria, protozoa, or viruses. It carries significant systemic toxicity and is currently unavailable in a formula appropriate for systemic use - its efficacy is currently restricted, therefore, to topical, oral, and gastrointestinal infections. Nystatin is a channel-forming ionophore, meaning it exerts its therapeutic effect via formation of a membrane-spanning pore in the fungal plasma membrane. The formation of this pore results in a change in membrane permeability that allows for leakage of intracellular contents and the subsequent disruption of electrochemical gradients necessary for proper cell function. Selectivity for fungal cells over mammalian cells is due to nystatin’s greater binding affinity for ergosterol, a key sterol found in fungal cell walls, as opposed to its mammalian counterpart, cholesterol.",The molecular weight is 926.11.,Nystatin has a topological polar surface area of 319.61.,The log p value of  is -3.2.,Nystatin is approved and vet_approved.,Nystatin is a solid.,True
20239,"Penicillamine is a pharmaceutical of the chelator class. The pharmaceutical form is D-penicillamine, as L-penicillamine is toxic (it inhibits the action of pyridoxine). It is an α-amino acid metabolite of penicillin, although it has no antibiotic properties. For treatment of Wilson's disease, cystinuria and active rheumatoid arthritis. Penicillamine is a chelating agent used in the treatment of Wilson's disease. It is also used to reduce cystine excretion in cystinuria and to treat patients with severe, active rheumatoid arthritis unresponsive to conventional therapy. Penicillamine is used as a form of immunosuppression to treat rheumatoid arthritis. Penicillamine inhibits macrophages, decreases IL-1 and the number of T-lymphocytes, and prevents collagen cross linkage. In Wilson's disease it binds copper, allowing it to be eliminated in the urine. Penicillamine is a chelating agent recommended for the removal of excess copper in patients with Wilson's disease. From in vitro studies which indicate that one atom of copper combines with two molecules of penicillamine. Penicillamine also reduces excess cystine excretion in cystinuria. This is done, at least in part, by disulfide interchange between penicillamine and cystine, resulting in formation of penicillamine-cysteine disulfide, a substance that is much more soluble than cystine and is excreted readily. Penicillamine interferes with the formation of cross-links between tropocollagen molecules and cleaves them when newly formed. The mechanism of action of penicillamine in rheumatoid arthritis is unknown although it appears to suppress disease activity. Unlike cytotoxic immunosuppressants, penicillamine markedly lowers IgM rheumatoid factor but produces no significant depression in absolute levels of serum immunoglobulins. Also unlike cytotoxic immunosuppressants which act on both, penicillamine in vitro depresses T-cell activity but not B-cell activity.",The molecular weight is 149.21.,Penicillamine has a topological polar surface area of 63.32.,The log p value of  is -1.73.,Penicillamine is approved.,Penicillamine is a solid.,True
20240,Gimatecan is an orally available 7-t-butoxyiminomethyl-substituted lipophilic camptothecin derivative.,,,,Gimatecan is investigational.,Gimatecan is a solid.,True
20241,"A delta-selective opioid (ANALGESICS, OPIOID). It can cause transient depression of mean arterial blood pressure and heart rate.",,,,DADLE is experimental.,DADLE is a solid.,True
20242,Bamet-UD2 is a novel bile acid-platinum derivative.,,,,Bamet-UD2 is experimental.,Bamet-UD2 is a solid.,True
20243,,,,,cis-Diamminechlorocholylglycinateplatinum(II) is experimental.,cis-Diamminechlorocholylglycinateplatinum(II) is a solid.,False
20244,"Gadoxetic acid (gadoxetate) is a paramagnetic gadolinium-containing contrast agent in which its salt form, gadoxetate disodium, is used for intravenous injection. Ethoxybenzyl diethylenetriaminepentaacetic acid is the moiety that chelates with a gadolinium ion and forms a stable complex with it to make up the drug. It is marketed by Bayer HealthCare Pharmaceuticals and FDA approved on July 3, 2008. Gadoxetate is used as a contrast medium for magnetic resonance imaging (MRI) to detect and characterize lesions in the liver.  Gadoxetate disodium is an amphipathic compound in which gadoxetate is hydrophillic and its moiety, the ethoxybenyzl group, is lipophillic. Consequently, gadoxetate disodium has a biphasic mode of action in which it first distributes into the extracellular space after bolus injection and then hepatocytes selectively takes up the drug.  When gadoxetate disodium is placed in an external magnetic field, a large magnetic moment is produced. As a result, a magnetic field is induced around the tissue. The water protons in the vicinity are disrupted such that the change the proton density and spin characteristics are detected and visualized by a device. ",The molecular weight is 679.74.,,,Gadoxetic acid is approved.,Gadoxetic acid is a solid.,True
20245,"Technetium Tc 99m Mebrofenin is a diagnostic radiopharmaceutical composed of diisopropyl-iminodiacetic acid (DISIDA) attached to a technetium-99m ion. Following intravenous injection, single photon emission computer tomography (SPECT) imaging of the liver or gallbladder is performed using a gamma camera to detect the gamma rays emitted by the technetium-99m as it decays. This is possible as Technetium-99m decays by isomeric transition to technetium-99 through the release of a gamma ray. Liver and gallbladder imaging is enabled through attachment to mebrofenin as this molecule has high hepatic uptake and fast biliary excretion, resulting in improved hepatic imaging. More specifically, mebrofenin is taken up into hepatocytes through the action of OATP1B1 and OATP1B3 transporters. Technetium Tc 99m Mebrofenin is indicated as a hepatobiliary imaging agent. Technetium Tc 99m Mebrofenin has no known pharmacologic activity at the recommended doses. It is used as a diagnostic agent as Technetium-99m decays by isomeric transition to technetium-99 through the release of a detectable gamma ray.",,,,Technetium Tc-99m mebrofenin is approved.,Technetium Tc-99m mebrofenin is a solid.,True
20246,"Valspodar has been used in trials studying the treatment of Cancer, Sarcoma, Leukemia, Lymphoma, and Breast Cancer, among others.",,,,Valspodar is investigational.,,True
20247,"Bisabolol, or more formally α-(−)-bisabolol or also known as levomenol, (-)-alpha-Bisabolol is found in fats and oils. (-)-alpha-Bisabolol is isolated from essential oil of Matricaria chamomilla (German chamomile) (-)-alpha-Bisabolol belongs to the family of Sesquiterpenes. These are terpenes with three consecutive isoprene units. Levomenol has been known to elicit a number of potentially beneficial pharmacological effects, including anti-irritant, anti-inflammatory, and anti-microbial actions. Bisabolol is also demonstrated to enhance the percutaneous absorption of certain molecules Levomenol is an anti-inflammatory and natural moisturizing agent that has been found to diminish the signs of photodamage, reduce pruritus, and ameliorate skin texture and elasticity.",The molecular weight is 222.37.,Levomenol has a topological polar surface area of 20.23.,The log p value of  is 4.66.,Levomenol is approved and experimental.,Levomenol is a solid.,True
20248,"Loracarbef is a carbacephem antibiotic sometimes grouped together with the second-generation cephalosporin antibiotics. It is marketed under the trade name Lorabid. Used to treat upper respiratory tract bacterial infections, chronic bronchitis, pneumonia, sinusitis, pharyntitis and tonsillitis, skin absceses, urinary tract infections and pyelonephritis caused by <i>E. coli</i>, <i>S. pyogenes</i>, <i>S. aureus</i>, <i>S. saprphyticus</i>, <i>S. penumoniae</i>, <i>H. influenzae</i> and <i>M. catarrhalis</i>. Loracarbef is considered a second generation cephalosporin antibiotic. The advantages of cephalosporin antibiotics include a broad range of activity, a safe record in children with almost no dose-related toxicity, and the lack of need to monitor levels. Adverse reactions are rare and consist primarily of hypersensitivity reactions with urticaria, nonspecific rash, and pruritus. Loracarbef can be used to treat a large number of bacterial infections caused by gram-negative and gram-positive bacteria, including upper respiratory tract bacterial infections, chronic bronchitis, pneumonia, sinusitis, pharyntitis and tonsillitis, skin absceses, urinary tract infections and pyelonephritis caused by <i>E. coli</i>, <i>S. pyogenes</i>, <i>S. aureus</i>, <i>S. saprphyticus</i>, <i>S. penumoniae</i>, <i>H. influenzae</i> and <i>M. catarrhalis</i>. Loracarbef is an oral, synthetic beta-lactam antibiotic of the carbacephem class. Chemically, carbacephems differ from cephalosporin-class antibiotics in the dihydrothiazine ring where a methylene group has been substituted for a sulfur atom. Loracarbef has a spectrum of activity similar to that of the second generation cephalosporins. It is structurally identical to cefaclor except for a sulfur atom that has been replaced by a methylene group. This change gives greater chemical stability in solution and allows storage at room temperature. Loracarbef, like all b-lactams and cephalosporins, inhibits penicillin binding proteins, enzymes that create the cross-linkage of the peptidoglycan polymer. This binding leads to interference with the formation and remodeling of the cell wall structure.",The molecular weight is 349.77.,Loracarbef has a topological polar surface area of 112.73.,The log p value of  is -0.47.,Loracarbef is approved and investigational and withdrawn.,Loracarbef is a solid.,True
20249,"Broad-spectrum cephalosporin antibiotic resistant to beta-lactamase. It has been proposed for infections with gram-negative and gram-positive organisms, gonorrhea, and haemophilus. For the treatment of many different types of bacterial infections such as bronchitis, sinusitis, tonsillitis, ear infections, skin infections, gonorrhea, and urinary tract infections. Cefuroxime is a &beta;-lactam type antibiotic. More specifically, it is a second-generation cephalosporin. Cephalosporins work the same way as penicillins: they interfere with the peptidoglycan synthesis of the bacterial wall by inhibiting the final transpeptidation needed for the cross-links. This effect is bactericidal. Cefuroxime is effective against the following organisms: Aerobic Gram-positive Microorganisms: <i>Staphylococcus aureus</i>, <i>Streptococcus pneumoniae</i>, <i>Streptococcus pyogenes</i>. Aerobic Gram-negative Microorganisms: <i>Escherichia coli</i>, <i>Haemophilus influenzae</i> (including beta-lactamase-producing strains), <i>Haemophilus parainfluenzae</i>, <i>Klebsiella pneumoniae</i>, <i>Moraxella catarrhalis</i> (including beta-lactamase-producing strains), <i>Neisseria gonorrhoeae</i> (including beta-lactamase-producing strains). Spirochetes: <i>Borrelia burgdorferi</i>. Cefuroxime axetil is the prodrug  Cefuroxime, like the penicillins, is a beta-lactam antibiotic. By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, it inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that cefuroxime interferes with an autolysin inhibitor.",The molecular weight is 424.38.,Cefuroxime has a topological polar surface area of 173.76.,The log p value of  is 0.23.,Cefuroxime is approved.,Cefuroxime is a solid.,True
20250,"A semisynthetic cephalosporin antibiotic which can be administered intravenously or by suppository. The drug is highly resistant to a broad spectrum of beta-lactamases and is active against a wide range of both aerobic and anaerobic gram-positive and gram-negative organisms. It has few side effects and is reported to be safe and effective in aged patients and in patients with hematologic disorders. Cetizoxime was previously indicated for the treatment of infections due to susceptible strains of bacteria. Ceftizoxime is highly resistant to a broad spectrum of beta-lactamases and is active against a wide range of both aerobic and anaerobic gram-positive and gram-negative organisms. It has few side effects and is reported to be safe and effective in aged patients and in patients with hematologic disorders. Ceftizoxime is an aminothiazolyl cephalosporin with an extended spectrum of activity against many gram-negative, nosocomially acquired pathogens. It has excellent beta-lactamase stability, with good in vitro activity against Haemophilus influenzae, Neisseria gonorrhoeae and Klebsiella pneumoniae. Ceftizoxime, like the penicillins, is a beta-lactam antibiotic. By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, it inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that ceftizoxime interferes with an autolysin inhibitor.",The molecular weight is 383.4.,Ceftizoxime has a topological polar surface area of 147.21.,The log p value of  is 0.34.,Ceftizoxime is approved and withdrawn.,Ceftizoxime is a solid.,True
20251,"Ceftibuten is a third-generation cephalosporin antibiotic that is orally-administered. It is typically used to treat acute bacterial exacerbations of chronic bronchitis (ABECB), acute bacterial otitis media, pharyngitis, and tonsilitis. Indicated for the treatment of acute bacterial exacerbations of chronic bronchitis (ABECB), acute bacterial otitis media, pharyngitis, and tonsilitis. Ceftibuten is an antibiotic with bactericidal actions.  Ceftibuten exerts its bactericidal action by binding to essential target proteins of the bacterial cell wall. This binding leads to inhibition of cell-wall synthesis.",The molecular weight is 410.42.,Ceftibuten has a topological polar surface area of 162.92.,The log p value of  is -1.21.,Ceftibuten is approved and investigational.,Ceftibuten is a solid.,True
20252,"Gramcidin D is a heterogeneous mixture of three antibiotic compounds, gramicidins A, B and C, making up 80%, 6%, and 14% respectively all of which are obtained from the soil bacterial species Bacillus brevis and called collectively gramicidin D. Gramcidins are 15 residue peptides with alternating D and L amino acids, which assemble inside of the hydrophobic interior of the cellular lipid bilayer to form a β-helix. Active against most Gram-positive bacteria and some Gram-negative organisms, Gramicidin D is used primarily as a topical antibiotic and is also found in Polysporin ophthalmic solution. For treatment of skin lesions, surface wounds and eye infections. Gramicidin is particularly effective against gram-positive bacteria. Because the drug is highly hemolytic, it cannot be administered internally and so is used only on the skin as a lotion or ointment. It is used primarily in the treatment of infected surface wounds, and in eye, nose, and throat infections. It is normally given with two other antibiotics (neomycin and polymixin B) as an ophthalmic solution. Gramicidin D binds to and inserts itself into bacterial membranes (with a strong preference to gram-positive cell membranes). This results in membrane disruption and permeabilization (it acts as a channel). This leads to (i) loss of intracellular solutes (e.g., K+ and amino acids); (ii) dissipation of the transmembrane potential; (iii) inhibition of respiration; (iv) a reduction in ATP pools; and (v) inhibition of DNA, RNA, and protein synthesis, which leads to cell death.",The molecular weight is 9354.6.,Gramicidin D has a topological polar surface area of 548.99.,,Gramicidin D is approved.,Gramicidin D is a liquid.,True
20253,"Ledipasvir is a direct acting antiviral (DAA) medication used as part of combination therapy to treat chronic Hepatitis C, an infectious liver disease caused by infection with Hepatitis C Virus (HCV). HCV is a single-stranded RNA virus that is categorized into nine distinct genotypes, with genotype 1 being the most common in the United States, and affecting 72% of all chronic HCV patients. Treatment options for chronic Hepatitis C have advanced significantly since 2011, with the development of Direct Acting Antivirals (DAAs) such as ledipasvir. More specifically, ledipasvir is an inhibitor of the Hepatitis C Virus (HCV) Non-Structural Protein 5A (NS5A), which is required for viral RNA replication and assembly of HCV virions. Although its exact mechanism of action is unknown, it is postulated to prevent hyperphosphorylation of NS5A which is required for viral protein production. It is effective against genotypes 1a, 1b, 4a, and 5a and with a lesser activity against genotypes 2a and 3a of HCV. Ledipasvir and other direct acting antivirals are very potent options for the treatment of Hepatitis C, as they exhibit a high barrier to the development of resistance. This is an important advantage relative to HCV drugs that target other viral enzymes such as the protease, for which rapid development of resistance has proven to be an important cause of therapeutic failure.  When used in combination with the antiviral medication as the commercially available product Harvoni, ledipasvir is indicated for the treatment of HCV genotypes 1, 4, 5, and 6 with or without depending on the level of liver damage or cirrhosis. Its use has also proven successful in the treatment of HCV in patients co-infected with HIV. Ledipasvir acts against HCV and is categorized as a direct-acting antiviral agent (DAA). Ledipasvir is an inhibitor of the Hepatitis C Virus (HCV) NS5A protein required for viral RNA replication and assembly of HCV virions. Although its exact mechanism of action is unknown, it is postulated to prevent hyperphosphorylation of NS5A which is required for viral production. ",The molecular weight is 889.02.,Ledipasvir has a topological polar surface area of 174.64.,The log p value of  is 6.71.,Ledipasvir is approved.,Ledipasvir is a solid.,True
20254,"Polyethylene glycol (PEG) is a synthetic polymer produced via polymerization of ethylene oxide molecules to make joining units of ethylene glycol by an ether linkage. PEGs are water-soluble polymers that can form hydrogen bonds in a ratio of 100 water molecules per one PEG molecule. Molecular weights of PEGs vary by time of the polymerization process and the molecular weight represents the weighted average of the individual PEG molecules. PEGs differ in their physical and chemical properties depending on their molecular weight: PEGs are liquids when molecular weights are <1000 and the molecule turns to waxy solids with increasing molecular weights. The most common preparations of PEGs include PEG 3350 and PEG 400. PEGs have various applications in many fields, ranging from medical to industrial areas. PEGs have a long history of gastroenterology: PEG 3350 is a common over-the-counter osmotic laxative used to relieve occasional constipation. PEG 3350 is also used for cleansing of the colon in preparation for colonoscopy in adults. Polyethylene glycol is indicated for use as an over-the-counter osmotic laxative to relieve occasional constipation. When used in combination with sodium ascorbate, sodium sulfate, ascorbic acid, sodium chloride and potassium chloride, it is used for cleansing of the colon in preparation for colonoscopy in adults. The osmotic effect of PEG produces a copious watery diarrhea. The onset of action of PEG 3350 is about 1 to 2 hours after oral ingestion. The colonic transit of polyethylene glycol occurs in a dose-dependent manner. When used for bowel preparation before colonscopy, electrolytes are typically added in the oral solution to prevent dehydration and electrolyte disturbances. As an over-the-counter laxative, the OTC product does not contain any salts that can be absorbed. In a study involving healthy subjects, PEG 3350 had negligible effects on colonic fluid absorption or with the ability of the colonic mucosa to generate and sustain steep electrochemical gradients. Osmotic laxatives contain substances that are poorly absorbable and draw water into the lumen of the bowel. Polyethylene glycol functions is an osmotic laxative that causes increased water retention in the lumen of the colon by binding to water molecules, thereby producing loose stools.",,,,Polyethylene glycol is approved and vet_approved.,Polyethylene glycol is a solid.,True
20255,Monensin is a polyether isolated from _Streptomyces cinnamonensis_ that presents antibiotic properties. It is widely used in ruminant animal feeds.,,,,Monensin is experimental and vet_approved.,,True
20256,,,,,Salinomycin is vet_approved.,,False
20257,"Sarecycline is a semi-synthetic derivative of tetracycline that was initially discovered by Paratek Pharmaceuticals from Boston, MA but then licensed to Warner Chilcott of Rockaway, NJ in July of 2007. After completing various phase-II and phase-III trials demonstrating its effectiveness in treating moderate to severe facial acne vulgaris the US Food and Drug Administration approved Barcelona based Almirall, S.A.'s Seysara (sarecylcine) as a new first in class narrow spectrum tetracycline derived oral antibiotic for the treatment of inflammatory lesions of non-nodular moderate to severe acne vulgaris in patients nine years of age and older. Seysara (sarecycline) was originally part of Allergan's US Medical Dermatology portfolio, before Almirall acquired the portfolio in the second half of 2018 as a means of consolidating and reinforcing the dermatology-focused pharmaceutical company's presence in the United States. Sarecycline is a tetracycline-class drug indicated for the treatment of inflammatory lesions of non-nodular moderate to severe acne vulgaris in patients 9 years of age and older. Compared to various examples of first-line tetracycline therapies for moderate to severe acne like doxycycline and minocycline, studies have shown that sarecycline can be sixteen to thirty-two fold less active against aerobic Gram-negative bacilli present within the normal human intestinal microbiome. Furthermore, it has also been demonstrated that sarecycline may be four to eight fold less active against various anaerobic bacteria that also comprise the normal human intestinal microbiome. Subsequently, while doxycycline and minocycline typically elicit broad-spectrum antimicrobial activity that can often cause adverse effects like diarrhea, fungal overgrowth, vaginal candidiasis, etc. due to undesirable off-target antibacterial effects on endogenous intestinal flora, sarecycline demonstrates a noticeably more target specific narrow spectrum activity with lower incidence of such side effects. It has been demonstrated that tetracyclines like sarecycline elicit their antimicrobial action by targeting and inhibiting protein synthesis in microbial agents like Cutibacterium acnes present in acne lesions. In particular, it is believed that sarecycline's mechanism of action revolves around the inhibition of various macromolecular biosynthesis activities like the macromolecular biosynthesis of microbial DNA, RNA, proteins, lipids, and cell wall. Specifically, it has been observed that while sarecycline demonstrates appreciable inhibition of microbial macromolecular DNA and protein synthesis, the compound has little to no effect on lipid biosynthesis, cell wall synthesis, and RNA synthesis. In addition, because Cutibacterium acnes also generates proteins and enzymes that are capable of causing inflammation, it is also believed that tetracyclines like sarecyclines can also affect an anti-inflammatory effect via the inhibition of such microbial protein synthesis.",,,,Sarecycline is approved and investigational.,Sarecycline is a solid.,True
20258,Laniquidar has been used in trials studying the treatment of Breast Cancer.,,,,Laniquidar is investigational.,,True
20259,"Dehydroascorbic acid is made from the oxidation of ascorbic acid. This reaction is reversible, but dehydroascorbic acid can instead undergo irreversible hydrolysis to 2,3-diketogulonic acid. Dehydroascorbic acid as well as ascorbic acid are both termed Vitamin C, but the latter is the main form found in humans. In the body, both dehydroascorbic acid and ascorbic acid have similar biological activity as antivirals but dehydroascorbic acid also has neuroprotective effects. Currently dehydroascorbic acid is an experimental drug with no known approved indications. There is no approved indication for dehydroascorbic acid, but it has potential therapeutic use in patients with certain viruses and ischemic stroke. Dehydroascorbic acid has similar biological activity as ascorbic acid. Both compounds have been shown to have antiviral effects against herpes simplex virus type 1, influenza virus type A and poliovirus type 1 with dehydroascorbic acid having the stronger effect. In addition, unlike ascorbic acid, dehydroascorbic acid can cross the blood brain barrier and is then converted to ascorbic acid to enable retention in the brain. This is important because one study has found that after an ischemic stroke, dehydroascorbic acid has neuroprotective effects by reducing infarct volume, neurological deficits, and mortality. Even though dehydroascorbic acid and ascorbic acid have similar effects, their mechanism of action seems to be different. The exact mechanism of action is still being investigated, but some have been elucidated. Concerning dehydroascorbic acid's antiviral effect against herpes simplex virus type 1, it is suggested that dehydroascorbic acid acts after replication of viral DNA and prevents the assembly of progeny virus particles.",,,,Dehydroascorbic acid is experimental.,Dehydroascorbic acid is a solid.,True
20260,"2-deoxyglucose is predominantly used as a diagnostic agent in its radiolabelled form (fluorine-18 is used as the radiolabel). By using positron emission tomography (PET), radiolabelled 2-deoxyglucose can determine glucose metabolism, which is altered in diseases such as cardiovascular disease, tumors, and Alzheimer's disease. Therapeutically, 2-deoxyglucose is an investigational drug that is being studied as an anticancer and antiviral agent. Concerning the former, 2- deoxyglucose was used as an adjunct to chemotherapy and radiotherapy in the treatment of solid tumors (lung, breast, pancreas, head, neck, and gastric tumors). The exact mechanisms of action of 2-deoxyglucose is still being investigated, but it is known that in hypoxic cancer cells, 2-deoxyglucose is a glycolysis inhibitor that prevents ATP production and, ultimately, cell survival. With respect to antiviral therapy, 2-deoxyglucose was shown to be effective against herpes simplex virus by affecting the virus' ability to penetrate cells. As an experimental drug, 2-deoxyglucose was demonstrated to work as an anticonvulsant in temporal lobe epilepsy. In this condition, 2-deoxyglucose represses the expression of certain proteins that are at high levels after a seizure. Although there are several possible therapeutic indications for 2-deoxyglucose, presently there is no approved indication for 2-deoxyglucose as a therapeutic agent. As of July 2013, there is no approved therapeutic indication for 2-deoxyglucose. 2-deoxyglucose may have several potential indications as an adjunct to chemotherapy and radiotherapy in the treatment of solid tumors, as an antiviral treatment in herpes simplex patients, and as an antiepileptic in temporal lobe epilepsy patients. Physiologically 2-deoxyglucose is an inhibitor of glycolysis, certain viruses, and seizures.  Solid tumors have hypoxic areas with slow growing cells that are resistant to chemotherapy, which attacks rapidly dividing cells. In the hypoxic area of the tumor, the cells rely on anaerobic glycolysis to produce energy in the form of ATP while non-tumor cells can rely on additional pathways such as fatty acid and amino acid metabolism to produce ATP. 2-deoxyglucose is an inhibitor of glycolysis because as a modified glucose molecule (it has a hydrogen at the carbon 2 position instead of a hydroxyl group), it is unable to complete the glycolysis process, and as such will hinder the survival of slow growing cancer cells. Regarding 2-deoxyglucose's antiviral activity, it prevents the glycosylation of specific proteins and lipids as well as prevents proper penetration of the virus into the target cells. In temporal lobe epilepsy, 2-deoxyglucose represses the overactive brain-derived neurotrophic factor (BDNF) promoter and prevents the increased expression of BDNF protein and TrkB receptor (BDNF's receptor) that is observed in epileptic patients.",,,,2-deoxyglucose is experimental and investigational.,2-deoxyglucose is a solid.,True
20261,One of the cephalosporins that has a broad spectrum of activity against both gram-positive and gram-negative microorganisms. For treatment of severe infections caused by susceptible bacteria. Cefotiam is a third generation beta-lactam cephalosporin antibiotic that works by inhibiting bacterial cell wall biosynthesis. It is a broad spectrum antibiotic that is effective against Gram positive and Gram negative bacteria. The bactericidal activity of cefotiam results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs).,The molecular weight is 525.62.,Cefotiam has a topological polar surface area of 172.46.,The log p value of  is -3.48.,Cefotiam is approved and investigational.,Cefotiam is a solid.,True
20262,"Semisynthetic, broad-spectrum, ampicillin derived ureidopenicillin antibiotic proposed for pseudomonas infections. It is also used in combination with other antibiotics. For the treatment of polymicrobial infections. Piperacillin is a penicillin beta-lactam antibiotic used in the treatment of bacterial infections caused by susceptible, usually gram-positive, organisms. The name \penicillin\"" can either refer to several variants of penicillin available, or to the group of antibiotics derived from the penicillins. Piperacillin has <i>in vitro</i> activity against gram-positive and gram-negative aerobic and anaerobic bacteria. The bactericidal activity of Piperacillin results from the inhibition of cell wall synthesis and is mediated through Piperacillin binding to penicillin binding proteins (PBPs). Piperacillin is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, and cephalosporinases and extended spectrum beta-lactamases."" By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, Piperacillin inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that Piperacillin interferes with an autolysin inhibitor.",,,,Piperacillin is approved.,Piperacillin is a solid.,True
20263,"An acyclovir analog that is a potent inhibitor of the Herpesvirus family including cytomegalovirus. Ganciclovir is used to treat complications from AIDS-associated cytomegalovirus infections. For induction and maintenance in the treatment of cytomegalovirus (CMV) retinitis in immunocompromised patients, including patients with acquired immunodeficiency syndrome (AIDS). Also used in the treatment of severe cytomegalovirus (CMV) disease, including CMV pneumonia, CMV gastrointestinal disease, and disseminated CMV infections, in immunocompromised patients. Ganciclovir is a synthetic nucleoside analogue of 2'-deoxyguanosine that inhibits replication of herpes viruses both <i>in vitro</i> and <i>in vivo</i>. Sensitive human viruses include cytomegalovirus (CMV), herpes simplex virus -1 and -2 (HSV-1, HSV-2), Epstein-Barr virus (EBV) and varicella zoster virus (VZV), however clinical studies have been limited to assessment of efficacy in patients with CMV infection. Ganciclovir is a prodrug that is structurally similar to acyclovir. It inhibits virus replication by its encorporation into viral DNA. This encorporation inhibits dATP and leads to defective DNA, ceasing or retarding the viral machinery required to spread the virus to other cells. Ganciclovir's antiviral activity inhibits virus replication. This inhibitory action is highly selective as the drug must be converted to the active form by a virus-encoded cellular enzyme, thymidine kinase (TK). TK catalyzes phosphorylation of ganciclovir to the monophosphate, which is then subsequently converted into the diphosphate by cellular guanylate kinase and into the triphosphate by a number of cellular enzymes. <i>In vitro</i>, ganciclovir triphosphate stops replication of herpes viral DNA. When used as a substrate for viral DNA polymerase, ganciclovir triphosphate competitively inhibits dATP leading to the formation of 'faulty' DNA. This is where ganciclovir triphosphate is incorporated into the DNA strand replacing many of the adenosine bases. This results in the prevention of DNA synthesis, as phosphodiester bridges can longer to be built, destabilizing the strand. Ganciclovir inhibits viral DNA polymerases more effectively than it does cellular polymerase, and chain elongation resumes when ganciclovir is removed.",The molecular weight is 255.23.,Ganciclovir has a topological polar surface area of 134.99.,The log p value of  is -2.54.,Ganciclovir is approved and investigational.,Ganciclovir is a solid.,True
20264,"A derivative of 7-aminocephalosporanic acid. Cefacetrile is a broad-spectrum first generation cephalosporin antibiotic effective in Gram-positive and Gram-negative bacterial infections. Cefacetrile is effective against many Gram-positive bacterial strains and somewhat less effective against Gram-negative species. It works by inhibition of bacterial cell wall synthesis. It attains high serum levels and is excreted quickly via the urine. In vitro tests demonstrate that the bactericidal action of cephalosporins results from inhibition of cell wall synthesis. By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, it inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins.",The molecular weight is 339.32.,Cefacetrile has a topological polar surface area of 136.8.,The log p value of  is -1.62.,Cefacetrile is experimental and vet_approved.,Cefacetrile is a solid.,True
20265,"Tazobactam is an antibiotic of the beta-lactamase inhibitor class that prevents the breakdown of other antibiotics by beta-lactamase enzyme producing organisms. It is combined with and for the treatment of a variety of bacterial infections. Tazobactam is used in combination with piperacillin or ceftolozane to broaden the spectrum of piperacillin antibacterial action, treating susceptible infections. As with any other antibiotic, tazobactam should only be used for infections that are either proven or strongly suspected to be susceptible to the tazobactam containing drug. Tazobactam inhibits the action of bacterial beta-lactamase producing organisms, which are normally resistant to beta-lactam antibiotics. This augments the effects of antibiotics which would otherwise not be effective in treating certain infections. These antibiotics contain a beta-lactam ring in their chemical structure, which is destroyed by beta-lactam resistant organisms. When combined with other antibiotics, a variety of infections, including serious and life-threatening infections may be treated. Tazobactam broadens the spectrum of piperacillin and ceftolozane by making them effective against organisms that express beta-lactamase and would normally degrade them. This occurs through the irreversible inhibition of beta-lactamase enzymes. In addition, tazobactam may bind covalently to plasmid-mediated and chromosome-mediated beta-lactamase enzymes. Tazobactam is predominantly effective against the OHIO-1, SHV-1, and TEM groups of beta-lactamases, but may also inhibit other beta-lactamases.",The molecular weight is 300.29.,Tazobactam has a topological polar surface area of 122.46.,The log p value of  is -0.65.,Tazobactam is approved.,Tazobactam is a solid.,True
20266,,,,,GS 0573 is investigational.,GS 0573 is a solid.,False
20267,"Uric acid is the last product of purine metabolism in humans. The formation of uric acid is through the enzyme xanthine oxidase, which oxidizes oxypurines. Normally a small amount of uric acid is present in the body, but when there is an excess amount in the blood, called hyperuricemia, this can lead to gout and formation of kidney stones. As a therapeutic agent, it is known that uric acid is increased in response to oxidative stress, and as such, uric acid acts as an antioxidant. At present (August 2013), there is no approved formulation or indication for uric acid. In one country, Spain, uric acid is an investigational drug in a phase 3 trial studying its effects as an adjunct to alteplase in acute ischemic stroke. At present (August 2013), there is no approved indication for uric acid. The potential therapeutic use for uric acid is as an adjunct in acute ischemic stroke. Uric acid is a strong reducing agent (donates electrons) and an antioxidant. Normally in humans, one of the main antioxidants in plasma is uric acid. Several animal studies have found that animals given exogenous uric acid within 3 hours after a stroke had decreased infarct volume, improved neurologic function, and diminished inflammatory responses providing evidence for the neuroprotective effects of uric acid. In some early human studies, uric acid has so far shown similar neuroprotective effects, in both the cortex and subcortex areas, due to its antioxidant effects such as decreased lipid peroxidation, and there appears to be no significant toxicities. The exact mechanism of action for uric acid's antioxidant effects have not yet been elucidated.",,,,Uric acid is investigational.,Uric acid is a solid.,True
20268,Cephaloridine or cefaloridine is a first generation semisynthetic cephalosporin. It is derived from cephalosporin C and is a zwitterion at physiological pH.,The molecular weight is 415.48.,Cefaloridine has a topological polar surface area of 93.42.,The log p value of  is -6.68.,Cefaloridine is experimental and withdrawn.,Cefaloridine is a solid.,True
20269,Cabotegravir has been investigated for the treatment of Acquired Immunodeficiency Syndrome.,,,,Cabotegravir is approved and investigational.,,True
20270,"Edaravone is a free radical scavenger approved in May, 2017 for the treatment of amyotrophic lateral scleorosis (ALS). Clinical studies showed that the treatment attenuated deterioration of the disease when compared to placebo. It has been previously investigated for the treatment of ischemic stroke, reperfusion Injury, and myocardial Infarction as it possesses antioxidant and anti-apoptotic properties. Being a low molecular weight molecule with good water and lipid-soluble properies, it is therapeutically advantageous in crossing the blood-brain barrier to mediate nootropic and neuroprotective effects. Oral formulation of edaravone is currently under development. Indicated for improving neurological symptoms and damage from acute ischemic stroke and delaying disease progression of ALS. Edaravone scavenges free hydroxyl radicals and peroxynitrite radicals which are highly associated with neuronal damage/death from many cerebral vascular disorders such as ischemic strokes and degenerative neurological disorders such as ALS. It exerts a neuroprotective and antioxidant effect and delays disease progression by limiting the extent of lipid peroxidation via free radical generation and cell membrane damage from oxidative stress. It reversed the reduction in regional blood flow and cerebral edema in a case of ischemic stroke.  Nootropic and neuroprotective effects are mediated through inhibiting lipid peroxidation and scavenging free radicals. Edaravone acts to increase prostacyclin production, decrease lipoxygenase metabolism of arachidonic acid by trapping hydroxyl radicals, and inhibit alloxan-induced lipid peroxidation and quench active oxygen species. It targets various kinds of cells, including neurons, endothelial cells and myocardial cells. There is also evidence of reduction of neuronal nitric oxide synthase (nNOS) levels and potentiation of SOD1 levels after transient ischemia in rabbits thus preventing spinal cord injury. ",The molecular weight is 174.2.,Edaravone has a topological polar surface area of 32.67.,The log p value of  is 1.33.,Edaravone is approved and investigational.,Edaravone is a solid.,True
20271,,,,,"(1,10 Phenanthroline)-(Tri-Carbon Monoxide) Rhenium (I) is experimental.","(1,10 Phenanthroline)-(Tri-Carbon Monoxide) Rhenium (I) is a solid.",False
20272,"Avibactam is a non-β-lactam β-lactamase inhibitor that is available in combination with ceftazidime (Avycaz). This combination was approved by the FDA on February 25, 2015 for the treatment of complicated intra-abdominal infections in combination with metronidazole, and the treatment of complicated urinary tract infections, including pyelonephritis caused by antibiotic resistant-pathogens, including those caused by multi-drug resistant gram-negative bacterial pathogens. As there is limited clinical safety and efficacy data, Avycaz should be reserved for patients over 18 years old who have limited or not alternative treatment options. AVYCAZ (ceftazidime-avibactam), in combination with metronidazole, is indicated for the treatment of complicated intra-abdominal infections caused by the following susceptible microorganisms: Escherichia coli, Klebsiella pneumoniae, Proteus mirabilis, Providencia stuartii, Enterobacter cloacae, Klebsiella oxytoca, and Pseudomonas aeruginosa in patients 18 years or older. Avibactam is a non-β lactam β-lactamase inhibitor that inactivates some β-lactamases (Ambler class A β-lactamases, including Klebsiella pneumoniae carbapenemases, Ambler class C and some Ambler class D β-lactamases) by a unique covalent and reversible mechanism, and protects ceftazidime from degradation by certain β-lactamases. Avibactam rapidly reaches the periplasm of bacteria at high enough concentrations to restore activity of ceftazidime against ceftazidime-resistant, β-lactamase-producing strains. Avibactam does not decrease the activity of ceftazidime against ceftazidime­ susceptible organisms. ",The molecular weight is 265.24.,Avibactam has a topological polar surface area of 130.24.,The log p value of  is -1.63.,Avibactam is approved.,Avibactam is a solid.,True
20273,"Polymyxin B was discovered in the 1940s. They are basic polypeptides of about eight amino acids and have cationic detergent action on cell membranes. Polymyxin B is used for infections with gram-negative organisms, but may be neurotoxic and nephrotoxic. All gram-positive bacteria, fungi, and the gram-negative cocci, are resistant. It is appropriate for treatment of infections of the urinary tract, meninges, and blood stream, caused by susceptible strains of _Pseudomonas aeruginosa_. Polymyxin B has a narrow therapeutic index and so its use is limited and unlikely to be used first line. Polymyxin B is indicated for the treatment of infections of the urinary tract, meninges, and blood stream, caused by susceptible strains of <i>Pseudomonas aeruginosa</i>. Polymyxin B is an antibiotic that disrupts the outer cell membrane of Gram negative bacteria, binds and neutralizes lipopolysaccharide, and inhibits respiration of Gram-negative bacterial cells. Polymyxin B can be given by a number of routes to treat susceptible Gram negative bacterial infections. Absorption of the drug is poor (though not necessary for most of its activity) and the excreted drug is unchanged by metabolic processes. Polymyxin B is generally indicated for susceptible Gram negative infections of the urinary tract, meninges, and blood stream. The alpha and gamma diaminobutyric acid of a positively charged polymyxin B forms an electrostatic interaction with the phosphate groups of a negatively charged lipid A on the outer membrane of a Gram negative bacterium. Calcium and Magnesium ions are displaced from phosphates of the membrane lipids, destabalising the lipopolysaccharide (LPS), increasing membrane permeability, causing cytoplasmic leaking, and killing the cell.",,,,Polymyxin B is approved and vet_approved.,Polymyxin B is a solid.,True
20274,"Folinic Acid (also known as 5-formyl tetrahydrofolic acid or leucovorin) is the 5-formyl derivative of tetrahydrofolic acid, a necessary co-factor in the body. Commercially available leucovorin is composed of a 1:1 racemic mixture of the dextrorotary and levorotary isomers, while levoleucovorin contains only the pharmacologically active levo-isomer. In vitro, the levo-isomer has been shown to be rapidly converted to the biologically available methyl-tetrahydrofolate form while the dextro form is slowly excreted by the kidneys. Despite this difference in activity, the two commercially available forms have been shown to be pharmacokinetically identical and may be used interchangeably with limited differences in efficacy or side effects (Kovoor et al, 2009).  For the treatment of osteosarcoma (after high dose methotrexate therapy). Used to diminish the toxicity and counteract the effects of impaired methotrexate elimination and of inadvertent overdosages of folic acid antagonists, and to treat megaloblastic anemias due to folic acid deficiency. Also used in combination with 5-fluorouracil to prolong survival in the palliative treatment of patients with advanced colorectal cancer. Leucovorin is one of several active, chemically reduced derivatives of folic acid. It is useful as an antidote to drugs which act as folic acid antagonists. Leucovorin is a mixture of the diastereoisomers of the 5-formyl derivative of tetrahydrofolic acid (THF). The biologically active compound of the mixture is the (-)-l-isomer, known as Citrovorum factor or (-)-folinic acid. Leucovorin does not require reduction by the enzyme dihydrofolate reductase in order to participate in reactions utilizing folates as a source of &ldquo;one-carbon&rdquo; moieties. Administration of leucovorin can counteract the therapeutic and toxic effects of folic acid antagonists such as methotrexate, which act by inhibiting dihydrofolate reductase. Leucovorin has also been used to enhance the activity of fluorouracil. As leucovorin is a derivative of folic acid, it can be used to increase levels of folic acid under conditions favoring folic acid inhibition (following treatment of folic acid antagonists such as methotrexate). Leucovorin enhances the activity of fluorouracil by stabilizing the bond of the active metabolite (5-FdUMP) to the enzyme thymidylate synthetase.",The molecular weight is 473.45.,Leucovorin has a topological polar surface area of 215.55.,The log p value of  is -3.49.,Leucovorin is approved.,Leucovorin is a solid.,True
20275,,,,,trans-2-hydroxycinnamic acid is experimental.,trans-2-hydroxycinnamic acid is a solid.,False
20276,Pradigastat has been used in trials studying the treatment of Non-alcoholic Fatty Liver Disease (NAFLD).,,,,Pradigastat is investigational.,,True
20277,"A dye that is a mixture of violet rosanilinis with antibacterial, antifungal, and anthelmintic properties. For the treatment of bacterial and fungal infections inside the mouth (thrush) and skin, also for the prevention of transmission of Chagas' disease (as a blood additive). Gentian violet is a mutagen, a mitotic poison, and a clastogen. Gentian violet has been used in medicine for almost 100 years: as an antiseptic for external use, as a topical antibiotic, as a topical antifungal agent, as an antihelminthic agent by oral administration, and more recently, as a blood additive to prevent transmission of Chagas' disease. It is thought to work by binding to the DNA of target organisms and causing disruption, mutation or inhibition of DNA replication. In aqueous solutions Gentian violet (GV) dissociates into positive (GV+)and negative ions (Cl-) that penetrate through the wall and membrane of both gram-positive and gram-negative bacterial cells. The GV+ interacts with negatively charged components of bacterial cells including the lipopolysaccharide (on the cell wall), the peptidoglycan and DNA. A similar cell penetration and DNA binding process is thought to take place for fungal cells as well. Because Gentian violet is a mutagen and mitotic poison, cell growth is consequently inhibited. A photodynamic action of gentian violet, apparently mediated by a free-radical mechanism, has recently been described in bacteria and in the protozoan T. cruzi. Evidence also suggests that gentian violet dissipates the bacterial (and mitochondrial) membrane potential by inducing permeability. This is followed by respiratory inhibition. This anti-mitochondrial activity might explain gentian violet's efficacy towards both bacteria and yeast with relatively mild effects on mammalian cells.",,,,Gentian violet cation is approved.,Gentian violet cation is a solid.,True
20278,"Buformin is an anti-diabetic drug of the biguanide class, chemically related to metformin and phenformin. It was withdrawn from the market in most countries due to a high risk of causing lactic acidosis.",The molecular weight is 157.22.,Buformin has a topological polar surface area of 97.78.,The log p value of  is -1.54.,Buformin is investigational and withdrawn.,Buformin is a solid.,True
20279,"Tyramine (4-hydroxyphenethylamine; para-tyramine, mydrial or uteramin) is a naturally occurring monoamine compound and trace amine derived from the amino acid tyrosine. Tyramine acts by inducing the release of catecholamine. An important characteristic of this product is its impediment to cross the blood-brain barrier which restrains its side effects to only nonpsychoactive peripheral sympathomimetic effects. There have been reports of hypertensive crisis in patients ingesting tyramine-rich diet in conjunction with monoamine oxidase inhibitors (MAOIs).",The molecular weight is 137.18.,Tyramine has a topological polar surface area of 46.25.,The log p value of  is 0.77.,Tyramine is investigational and nutraceutical.,Tyramine is a solid.,True
20280,The D-enantiomer of alanine.,,,,D-Alanine is experimental.,D-Alanine is a solid.,True
20281,"beta-Alanine is an amino acid formed in vivo by the degradation of and. Since neuronal uptake and neuronal receptor sensitivity to beta-alanine have been demonstrated, the compound may be a false transmitter replacing GAMMA-AMINOBUTYRIC ACID. A rare genetic disorder, hyper-beta-alaninemia, has been reported.",,,,beta-Alanine is experimental.,beta-Alanine is a solid.,True
20282,A non-essential amino acid. In animals it is synthesized from PHENYLALANINE. It is also the precursor of EPINEPHRINE; THYROID HORMONES; and melanin.,,,,D-Tyrosine is experimental.,D-Tyrosine is a solid.,True
20283,An aldotriose which is an important intermediate in glycolysis and in tryptophan biosynthesis. ,,,,Glyceraldehyde-3-Phosphate is experimental.,Glyceraldehyde-3-Phosphate is a solid.,True
20284,"Developed by Achaogen biopharmaceuticals, plazomicin is a next-generation aminoglycoside synthetically derived from. The structure of plazomicin was established via appending hydroxylaminobutyric acid to at position 1 and 2-hydroxyethyl group at position 6'. It was designed to evade all clinically relevant aminoglycoside-modifying enzymes, which contribute to the main resistance mechanism for aminoglycoside therapy. However, acquired resistance of aminoglycosides may arise through over expression of efflux pumps and ribosomal modification by bacteria, which results from amino acid or rRNA sequence mutations. Like other aminoglycosides, plazomicin is ineffective against bacterial isolates that produce 16S rRNA methyltransferases. Plazomicin mediates the antibacterial activity against pathogens including carbapenem-resistant (CRE) and extended-spectrum beta-lactamase (ESBL) producing _Enterobacteriaceae_. It mediates the antibacterial activity by binding to bacterial 30S ribosomal subunit and inhibiting protein synthesis. On June 28th, 2018, plazomicin sulfate was approved by the FDA for use in adult patients for the treatment of complicated urinary tract infections (cUTI) including Pyelonephritis. It is marketed as Zemdri and is administered via once-daily intravenous infusion. Plazomicin is indicated for the treatment of patients 18 years of age or older with Complicated Urinary Tract Infections (cUTI) including Pyelonephritis, who have limited or no alternative treatment options. It should only be used to treat infections that are proven or strongly suspected to be caused by susceptible microorganisms.  Plazomicin exerts its antibacterial activity in a dose-dependent manner with a post-antibiotic effect ranging from 0.2 to 2.6 hours at 2X MIC against _Enterobacteriaceae_, as demonstrated by _in vitro_ studies. In clinical trials comprising of hospitalized adult patients with cUTI (including pyelonephritis), resolution or improvement of clinical cUTI symptoms and a microbiological outcome of eradication were observed at day 5 following the first dose administration of plazomicin. Plazomicin has shown to elicit nephrotoxic, ototoxic, and neuromuscular blocking effects. In clinical trials, it did not induce any clinically relevant QTc-prolonging effects.  Plazomicin exerts a bactericidal action against susceptible bacteria by binding to bacterial 30S ribosomal subunit. Aminoglycosides typically bind to the ribosomal aminoacyl-tRNA site (A-site) and induce a conformational change to further facilitate the binding between the rRNA and the antibiotic. This leads to codon misreading and mistranslation of mRNA during bacterial protein synthesis. ",,,,Plazomicin is approved and investigational.,,True
20285,"A heterodetic cyclic peptide that is a cyclic enkephalin analogue, having D-penicillaminyl residues located at positions 2 and 5, which form the heterocycle via a disulfide bond.",,,,DPDPE is experimental.,DPDPE is a solid.,True
20286,"Sincalide is a medication given by injection to assist in the diagnosis of gallbladder and pancreas disorders. It is identified as the 8-amino acid C-terminal segment of cholecystokinin and is also known as _CCK-8_. Naturally occurring cholecystokinin is a gastrointestinal peptide hormone normally essential for stimulating protein and fat digestion in the body. When injected intravenously, sincalide produces a substantial reduction in gallbladder size by causing this organ to contract. The evacuation of bile that results is similar to that which occurs physiologically in response to endogenous cholecystokinin. Furthermore, sincalide stimulates pancreatic secretion of bicarbonate and enzymes. As the product Kinevac (FDA), sincalide is used for the following indications: 1) to stimulate gallbladder contraction, as may be assessed by various methods of diagnostic imaging, or to obtain by duodenal aspiration a sample of concentrated bile for analysis of cholesterol, bile salts, phospholipids, and crystals; (2) to stimulate pancreatic secretion (especially in conjunction with secretin) prior to obtaining a duodenal aspirate for analysis of enzyme activity, composition, and cytology; (3) to accelerate the transit of a barium meal through the small bowel, thereby decreasing the time and extent of radiation associated with fluoroscopy and x-ray examination of the intestinal tract. When injected intravenously, sincalide produces a substantial reduction in gallbladder size by causing this organ to contract. The evacuation of bile that results is similar to that which occurs physiologically in response to endogenous cholecystokinin. Like cholecystokinin, sincalide stimulates pancreatic secretion; concurrent administration with secretin increases both the volume of pancreatic secretion and the output of bicarbonate and protein (enzymes) by the gland. This combined effect of secretin and sincalide permits the assessment of specific pancreatic function through measurement and analysis of the duodenal aspirate. ",The molecular weight is 1143.27.,Sincalide has a topological polar surface area of 426.8.,The log p value of  is -4.65.,Sincalide is approved.,Sincalide is a solid.,True
20287,"Agalsidase beta is a recombinant human α-galactosidase A similar to. While patients generally do not experience a clinically significant difference in outcomes between the two drugs, some patients may experience greater benefit with agalsidase beta. Use of agalsidase beta has decreased in Europe, in favor of agalsidase alfa, after a contamination event in 2009. Agalsidase beta is indicated in the treatment of Fabry disease. Agalsidase beta is a recombinant human α-galactosidase A used as enzyme replacement therapy in the treatment of Fabry disease. It has a long duration of action and a wide therapeutic index. Patients should be counselled regarding the risk of infusion related reactions and hypersensitivity. α-galactosidase A is uptaken by cells via the mannose 6 phosphate receptor. Agalsidase beta hydrolyzes globotriaosylceramide and other glycosphingolipids that would normally be hydrolyzed by endogenous α-galactosidase A. Preventing the accumulation of glycosphingolipids prevents or reduces the severity of manifestations of Fabry disease such as renal failure, cardiomyopathy, or cerebrovascular events.",,,,Agalsidase beta is approved and investigational.,Agalsidase beta is a liquid.,True
20288,"Sodium bicarbonate is a white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions. Sodium bicarbonate is used for the treatment of metabolic acidosis which may occur in severe renal disease, uncontrolled diabetes, circulatory insufficiency due to shock or severe dehydration, extracorporeal circulation of blood, cardiac arrest and severe primary lactic acidosis. Also is indicated in severe diarrhea which is often accompanied by a significant loss of bicarbonate. Further indicated in the treatment of certain drug intoxications, including barbiturates (where dissociation of the barbiturateprotein complex is desired), in poisoning by salicylates or methyl alcohol and in hemolytic reactions requiring alkalinization of the urine to diminish nephrotoxicity of blood pigments. Intravenous sodium bicarbonate therapy increases plasma bicarbonate, buffers excess hydrogen ion concentration, raises blood pH and reverses the clinical manifestations of acidosis. Sodium bicarbonate is a systemic alkalizer, which increases plasma bicarbonate, buffers excess hydrogen ion concentration, and raises blood pH, thereby reversing the clinical manifestations of acidosis. It is also a urinary alkalizer, increasing the excretion of free bicarbonate ions in the urine, thus effectively raising the urinary pH. By maintaining an alkaline urine, the actual dissolution of uric acid stones may be accomplished. Sodium bicarbonate acts as an antacid and reacts chemically to neutralize or buffer existing quantities of stomach acid but has no direct effect on its output. This action results in increased pH value of stomach contents, thus providing relief of hyperacidity symptoms. ",The molecular weight is 84.01.,,,Sodium bicarbonate is approved.,Sodium bicarbonate is a solid.,True
20289,"Clavulanic acid is a beta-lactamase inhibitor that is frequently combined with or to fight antibiotic resistance by preventing their degradation by beta-lactamase enzymes, broadening their spectrum of susceptible bacterial infections. Clavulanic acid is derived from the organism Streptomyces clavuligerus.When it is combined with amoxicillin, clavulanic acid is frequently known as Augmentin, Co-Amoxiclav, or Clavulin. Clavulanic acid combined with other antibiotics is indicated to prevent the development of drug-resistant strains of bacteria and promotes their therapeutic antibacterial effects. Clavulanic acid inactivates some beta-lactamase enzymes that are produced by bacteria, therefore preventing enzymatic destruction of amoxicillin. This helps to treat a variety of bacterial infections which would otherwise be resistant to antibiotics without the addition of clavulanic acid. Clavulanic acid contains a beta-lactam ring in its structure that binds in an irreversible fashion to beta-lactamases, preventing them from inactivating certain beta-lactam antibiotics, with efficacy in treating susceptible gram-positive and gram-negative infections.",The molecular weight is 199.16.,Clavulanic acid has a topological polar surface area of 87.07.,The log p value of  is -1.07.,Clavulanic acid is approved and vet_approved.,Clavulanic acid is a solid.,True
20290,Sodium phosphate is a saline laxative that is thought to work by increasing fluid in the small intestine. It usually results in a bowel movement after 30 minutes to 6 hours. Used to treat constipation or to clean the bowel before a colonoscopy. Sodium phosphate inceases fecal water content to increase mobility through the large intestine. Sodium phosphate is thought to work by increasing the amount of solute present in the intestinal lumen thereby creating an osmotic gradient which draws water into the lumen.,The molecular weight is 119.98.,,,"Sodium phosphate, monobasic is approved.","Sodium phosphate, monobasic is a solid.",True
20291,Used to treat constipation or to clean the bowel before a colonoscopy. Sodium phosphate inceases fecal water content to increase mobility through the large intestine. Sodium phosphate is thought to work by increasing the amount of solute present in the intestinal lumen thereby creating an osmotic gradient which draws water into the lumen.,The molecular weight is 141.96.,"Sodium phosphate, dibasic has a topological polar surface area of 83.42.",,"Sodium phosphate, dibasic is approved.",,True
20292,Used to treat constipation or to clean the bowel before a colonoscopy. Sodium phosphate inceases fecal water content to increase mobility through the large intestine. Sodium phosphate is thought to work by increasing the amount of solute present in the intestinal lumen thereby creating an osmotic gradient which draws water into the lumen.,,,,"Sodium phosphate, monobasic, unspecified form is approved.",,True
20293,"Inositol is a collection of nine different stereoisomers but the name is usually used to describe only the most common type of inositol, myo-inositol. Myo-inositol is the cis-1,2,3,5-trans-4,6-cyclohexanehexol and it is prepared from an aqueous extract of corn kernels by precipitation and hydrolysis of crude phytate. These molecules have structural similarities to glucose and are involved in cellular signaling. It is considered a pseudovitamin as it is a molecule that does not qualify to be an essential vitamin because even though its presence is vital in the body, a deficiency in this molecule does not translate into disease conditions. Inositol can be found as an ingredient of OTC products by Health Canada but all current product whose main ingredient is inositol are discontinued. By the FDA, inositol is considered in the list of specific substances affirmed as generally recognized as safe (GRAS). Inositol may be used in food without any limitation. As a drug, inositol is used as a nutrient supplement in special dietary foods and infant formula. As it presents a relevant role in ensuring oocyte fertility, inositol has been studied for its use in the management of polycystic ovaries. Inositol is also being researched for the treatment of diabetes, prevention of metabolic syndrome, aid agent for weight loss, treatment of depression, psychiatric disorder and anxiety disorder and for prevention of cancer. Inositol can stimulate glucose uptake in skeletal muscle cells which allows the decrease in blood sugar levels. This effect is later seen as a reduction in urine glucose concentration and indicates a decrease in high blood sugar levels. The mechanism of action of inositol in brain disorders is not fully understood but it is thought that it may be involved in neurotransmitter synthesis and it is a precursor to the phosphatidylinositol cycle. The change that occurs in the cycle simulates when the postsynaptic receptor is activated but without activating the receptor. This activity provokes a fake activation which regulated the activity of monoamines and other neurotransmitters.",The molecular weight is 180.16.,Inositol has a topological polar surface area of 121.38.,The log p value of  is -0.12.,Inositol is approved and investigational and withdrawn.,Inositol is a solid.,True
20294,"Phenyltoloxamine is an antihistamine drug with sedative and analgesic effects. It is a H1 receptor blocker and a member of the ethanolamine class of antihistaminergic drugs. It is available in combination products that also contain other analgesics and antitussives such as acetaminophen. Phenyltoloxamine citrate is the more common salt form that acts as an active ingredient in pharmaceutical products and promotes hay fever relief via reversing the effects of histamine. Phenyltoloxamine acts as an adjuvant analgesic, which augments the analgesic effect of acetaminophen. It also potentiates the effects of other drugs, such as codeine and codeine derivatives. The primary therapeutic use for which phenyltoloxamine is currently indicated is as an adjuvant therapy in various combination products containing an analgesic(s) (either narcotic or non-narcotic), where it is expected to potentiate the pain relieving, anti-tussive, etc. effect(s) of the analgesic component of the product. As a member of the first generation H1 antihistamines, it is known that phenyltoloxamine - like virtually all first generation H1 antihistamines - has a propensity for crossing the blood-brain barrier and acting on H1 histamine receptors there to interfere with neurotransmission. The most common results of this kind of first generation H1 antihistamine CNS neurotransmission interference are adverse effects like drowsiness, sedation, somnolence, and fatigue. Given these effects, under specific circumstances like a patient experiencing a pain or a cough that may be preoccupying all of their waking energy and attention, it is perhaps possible that the sedative and tranquilizing characteristics of phenyltoloxamine may be the factors that contribute to its apparent adjunctive analgesic and antitussive actions.  As a first-generation H1 antihistamine, phenyltoloxamine interferes with the agonist activity of histamine at the H1 receptor and are ostensibly used to attenuate inflammatory processes as a means to treat conditions like allergic rhinitis, allergic conjunctivitis, and urticaria. Reduction of the activity of the NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) immune response transcription factor via the phospholipase C and phosphatidylinositol (PIP2) signaling pathways also serves to decrease antigen presentation and the expression of pro-inflammatory cytokines, cell adhesion molecules, and chemotactic factors. Moreover, lowering calcium ion concentration leads to increased mast cell stability which reduces further histamine release.",The molecular weight is 255.36.,Phenyltoloxamine has a topological polar surface area of 12.47.,The log p value of  is 4.23.,Phenyltoloxamine is approved.,,True
20295,"Methapyrilene, formerly marketed in many drug products, was shown to be a potent carcinogen. Manufacturers voluntarily withdrew methapyriline drug products from the market in May and June 1979.",The molecular weight is 261.39.,Methapyrilene has a topological polar surface area of 19.37.,The log p value of  is 2.95.,Methapyrilene is withdrawn.,Methapyrilene is a solid.,True
20296,"Polyvinyl alcohol is a water-soluble synthetic polymer obtained by polymerization of vinyl alcohol. It has varying roles in commercial and industrial applications such as papermaking, textiles, and printing. Polyvinyl alcohol is found in ophthalmic solutions as a lubricant to prevent irritation or to relieve dryness of the eyes. For use as a lubricant to prevent further irritation or to relieve dryness of the eye(s). As a synthetic resin with hydrophilic properties, it increases the persistence of tear film and therefore lubricates and soothes dry/irritated eyes.",,,,Polyvinyl alcohol is approved.,Polyvinyl alcohol is a solid.,True
20297,"Imidapril has been investigated for the treatment of Kidney, Polycystic, Autosomal Dominant.",The molecular weight is 405.45.,Imidapril has a topological polar surface area of 116.25.,The log p value of  is 1.53.,Imidapril is investigational.,,True
20298,"Potassium citrate (also known as tripotassium citrate) is a potassium salt of citric acid. It is a white, hygroscopic crystalline powder. It is odorless with a saline taste. It contains 38.3% potassium by mass. In the monohydrate form it is highly hygroscopic and deliquescent. For the management of renal tubular acidosis, hypocitraturic calcium oxalate nephrolithiasis, and uric acid lithiasis with or without calcium stones. Potassium citrate induces changes in the urine which renders urine less susceptible to the formation of crystals and stones from salts e.g. calcium oxalate, calcium phosphate and uric acid. Increased citrate levels in the urine will make complexation with calcium which decrease the calcium ion activity and decrease the chance for the formation of calcium phosphate crystals.  After oral administration of potassium citrate, its metabolism yields alkaline load. Potassium Citrate therapy appears to increase urinary citrate mainly by modifying the renal handling of citrate, rather than by increasing the filtered load of citrate. In addition to raising urinary pH and citrate, Potassium Citrate increases urinary potassium by approximately the amount contained in the medication. In some patients, Potassium Citrate causes a transient reduction in urinary calcium.",The molecular weight is 306.39.,Potassium citrate has a topological polar surface area of 140.62.,,Potassium citrate is approved and investigational and vet_approved.,Potassium citrate is a solid.,True
20299,"Medetomidine is a synthetic compound used as a surgical anesthetic and analgesic. It is normally found as its hydrochloride salt, medetomidine hydrochloride. Medetomidine is an intravenously available alpha-2 adrenergic agonist. The drug has been developed by Orion Pharma. In the United States, it is currently approved for its veterinary use in dogs and distributed by Pfizer Animal Health. In Canada, medetomidine is distributed by Novartis Animal Health. The marketed product is a racemic mixture of two stereoisomers from which dexmedetomidine is the main active isomer.",The molecular weight is 200.28.,Medetomidine has a topological polar surface area of 28.68.,The log p value of  is 3.11.,Medetomidine is experimental and vet_approved.,,True
20300,"Perazine has been used in trials studying the treatment of Dementia, Depression, Schizophrenia, Anxiety Disorders, and Psychosomatic Disorders, among others.",The molecular weight is 339.5.,Perazine has a topological polar surface area of 9.72.,The log p value of  is 3.68.,Perazine is approved and investigational.,,True
20301,,The molecular weight is 452.55.,Delapril has a topological polar surface area of 95.94.,The log p value of  is 2.45.,Delapril is investigational.,,False
20302,"Saturated solution of Potassium Iodide (SSKI) is used pharmaceutically for emergency use in patients experiencing acute symptoms of severe hyperthyroidism (also known as thyroid storm or thyrotoxic crisis). SSKI can also be used for radioiodine-contamination emergencies or in preparation of thyrotoxic patients for thyroidectomy. Potassium Iodide is oral antithyroid agent used in the prevention of radioactive iodine uptake into the thyroid gland during a nuclear radiation emergency. Potassium Iodide may be used as an adjunct to other antithyroid agents in the treatment of hyperthyroidism and thyrotoxicosis and preoperatively to induce thyroid involution. It works in the thyroid gland. By inhibiting thyroid hormone synthesis and release, thyroid gland vascularity is reduced, thyroid gland tissue becomes firmer, thyroid cell size is reduced, follicular colloid reaccumulates, and bound iodine levels increase. As a protectant following radiation exposure, KI blocks the uptake of radioactive iodine isotopes by the thyroid gland thereby minimizing the risk of radiation-induced thyroid neoplasms.",The molecular weight is 166.0.,,,Potassium Iodide is approved.,Potassium Iodide is a solid.,True
20303,,The molecular weight is 284.18.,Trolnitrate has a topological polar surface area of 168.39.,The log p value of  is -5.27.,Trolnitrate is experimental.,,False
20304,"Salicylamide is the common name for the substance o-hydroxybenzamide, or amide of salicyl. Salicylamide is a non-prescription drug with analgesic and antipyretic properties. It has similar medicinal uses to aspirin. Salicylamide is used in combination with both aspirin and caffeine in the over-the-counter pain remedies",The molecular weight is 137.14.,Salicylamide has a topological polar surface area of 63.32.,The log p value of  is 1.28.,Salicylamide is approved.,Salicylamide is a solid.,True
20305,"A sympathomimetic agent that was formerly used as an anorectic. It has properties similar to those of dextroamphetamine. It has been implicated in lipid storage disorders and pulmonary hypertension. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1223) Used as an appetite suppressant. Chlorphentermine is a relatively weak stimulant with little abuse potential. It presents a prominent serotonergic profile leading to pulmonary hypertension and cardiac fibrosis after prolonged use. Thus, this drug is no longer used. ",The molecular weight is 183.68.,Chlorphentermine has a topological polar surface area of 26.02.,The log p value of  is 2.85.,Chlorphentermine is illicit and withdrawn.,Chlorphentermine is a solid.,True
20306,"Zinc gluconate is a zinc salt of gluconic acid comprised of two gluconic acid molecules for each zinc cation (2+). Zinc gluconate is a generally recognized as safe (GRAS) substance by FDA. It is available as a trace mineral supplement and over the counter as a lozenge form for a reduced duration of common colds and with decreased symptom severity. Zinc gluconate is mainly indicated in conditions like zinc deficiency, and can also be administered in adjunctive therapy as an alternative drug of choice in diarrhea. Zinc is an important mineral found in almost every cell in the human body. It promotes the activity of about 100 enzymes. Zinc deficiency is often associated with an increased risk of infection. When they are used to treat the common cold, zinc supplements may interfere with rhinovirus cleavage or adhesion and may play a role in protecting plasma membranes from microbial toxins and complement. Although the mechanism of action is not completely known, zinc supplementation may be used to increase immunity against viruses or may interfere with the replication of certain viruses, such as the human papillomavirus (HPV).",The molecular weight is 455.67.,Zinc gluconate has a topological polar surface area of 141.28.,,Zinc gluconate is approved and vet_approved.,Zinc gluconate is a solid.,True
20307,,The molecular weight is 269.31.,Endralazine has a topological polar surface area of 84.14.,The log p value of  is 0.94.,Endralazine is experimental.,,False
20308,"Telavancin is a semi-synthetic derivative of vanocymycin that has bactericidal activity against Methicillin-resistant Staphylococcus aureus (MRSA) and other gram-positive bacteria. MRSA is an important pathogen capable of causing hospital-acquired pneumonia (HAP), ventilator-associated pneumonia (VAP), and skin and subcutaneous tissue infections among others. For the treatment of complicated skin and skin structure infections (cSSSI) caused by gram-positive bacteria like methicillin-susceptible or -resistant Staphylococcus aureus, vancomycin-susceptible Enterococcus faecalis, and Streptococcus pyogenes, Streptococcus agalactiae, or Streptococcus anginosus group. Also for the treatment of adult patients with hospital-acquired bacterial pneumonia (HAP) and ventilator-associated bacterial pneumonia (VAP), known or suspected to be caused by susceptible isolates of Staphylococcus aureus (including methicillin-susceptible and methicillin-resistant S. aureus). Telavancin is a semi-synthetic derivative of vancomycin, therefore the mode of bactericidal action is similar to vancomycin in which both antibiotics inhibit cell wall synthesis. Not only that, it displays concentration-dependent bactericidal action. Furthermore, telavancin is a more potent inhibitor (10-fold) of peptidoglycan synthesis and, unlike vancomycin, disrupts cell membrane integrity via its interaction with lipid II. AUC/MIC ratio best predicts the extent of in-vivo response in which the higher the ratio, the greater the bactericidal activity. The smallest ratio in which one would be able to observe no bacterial growth at 24 hours is 50. Maximal bactericidal activity is observed at a AUC/MIC ratio of 404.  Telavancin is a bactericidal lipoglycopeptide that is active against a broad range of gram-positive bacteria. Telavancin prevents polymerization of N-acetylmuramic acid (NAM) and N-acetylglucosamine (NAG) and cross-linking of peptidoglycan by binding to D-Ala-D-Ala. As a result, inhibition of bacterial cell wall synthesis occurs. Furthermore, telavancin disrupts membrane potential and cell permeability as a result of the lipophillic side chain moiety. This additional bactericidal mechanism is what sets telavancin apart from vancomycin. ",The molecular weight is 1755.65.,Telavancin has a topological polar surface area of 598.09.,The log p value of  is 1.87.,Telavancin is approved.,Telavancin is a solid.,True
20309,"Etidocaine is marketed under the name Duranest. It is an injectable local anesthetic during surgery, labor, and delivery. Etidocaine has a long duration of activity, but has the main disadvantage of increased bleeding during oral surgery.",The molecular weight is 276.42.,Etidocaine has a topological polar surface area of 32.34.,The log p value of  is 3.32.,Etidocaine is approved.,Etidocaine is a solid.,True
20310,Trimazosin is a sympatholytic alpha blocker.,The molecular weight is 435.48.,Trimazosin has a topological polar surface area of 132.5.,The log p value of  is 2.63.,Trimazosin is experimental.,Trimazosin is a solid.,True
20311,"Calcium gluconate is used as mineral supplement and medication when there is insufficient calcium in the diet. Supplementation may be done to treat or prevent osteoporosis or rickets, consequences of hypocalcemia. It can also be taken by mouth but is not recommended by injection into a muscle. Oral calcium salts are used as dietary supplemental therapy for person who may not get enough calcium in their regular diet. Calcium gluconate is used as a cardioprotective agent in high blood potassium. Calcium gluconate is the antidote for magnesium sulfate toxicity. Calcium Gluconate is the gluconate salt of calcium. An element or mineral necessary for normal nerve, muscle, and cardiac function, calcium as the gluconate salt helps to maintain calcium balance and prevent bone loss when taken orally. This agent may also be chemopreventive for colon and other cancers. Calcium is essential for the functional integrity of the nervous, muscular, and skeletal systems. It plays a role in normal cardiac function, renal function, respiration, blood coagulation, and cell membrane and capillary permeability. Also, calcium helps to regulate the release and storage of neurotransmitters and hormones, the uptake and binding of amino acids, absorption of vitamin B 12, and gastrin secretion. The major fraction (99%) of calcium is in the skeletal structure primarily as hydroxyapatite, Ca 10(PO 4) 6(OH) 2; small amounts of calcium carbonate and amorphous calcium phosphates are also present. The calcium of bone is in a constant exchange with the calcium of plasma. Since the metabolic functions of calcium are essential for life, when there is a disturbance in the calcium balance because of dietary deficiency or other causes, the stores of calcium in bone may be depleted to fill the body's more acute needs. Therefore, on a chronic basis, normal mineralization of bone depends on adequate amounts of total body calcium. ",The molecular weight is 430.37.,Calcium gluconate has a topological polar surface area of 141.28.,,Calcium gluconate is approved and vet_approved.,,True
20312,"Difenoxin is a 4-phenylpiperidine which is closely related to the opioid analgesic meperidine. Difenoxin alone is a USA Schedule I controlled drug, as it may be habit forming. However, it is listed as a Schedule IV controlled drug if combined with atropine, which is added to decrease deliberate misuse. Motofen(R) is a brand mixture which combines atropine sulfate and difenoxin hydrochloride. It is approved by the FDA to treat acute and chronic diarrhea.  Motofen(R) is a combination of atropine, an anticholinergic drug, and difenoxin, an antidiarrheal drug. It has been used in many countries for many years as a second line opioid-agonist antidiarrheal, which exists an intermediate between loperamide and paragoric.  Difenoxin acts as a potent antidiarrheal by slowing the movement of the intestines. It also crosses the blood brain barrier to a slight degree to exert weak sedative and analgesic effects.  Difenoxin acts as an antidiarrheal by activating peripheral opioid receptors in the small intestine and thereby inhibiting peristalsis. However, research has suggested that non-opioid receptor pathways exist. This would explain the potent antidiarrheal effects of difenoxin despite only limited opioid action. ",The molecular weight is 424.54.,Difenoxin has a topological polar surface area of 64.33.,The log p value of  is 2.13.,Difenoxin is approved and illicit.,Difenoxin is a solid.,True
20313,"Polyethylene glycol 300 (PEG 300) is a water-miscible polyether with an average molecular weight of 300 g/mol. It is a clear viscous liquid at room temperature with non-volatile, stable properties. Polyethylene glycols are widely used in biochemistry, structural biology, and medicine in addition to pharmaceutical and chemical industries. They serve as solubilizers, excipients, lubricants, and chemical reagents. Low molecular weight glycols are observed to exhibit antibacterial properties as well. PEG 300 is found in eye drops as a lubricant to temporarily relieve redness, burning and irritation of the eyes. Indicated as a lubricant in over-the-counter ophthalmic solutions to temporarily relieve redness, burning and irritation of the eyes. PEGs act as nonionic surfactant to decrease surface tension and condition the stratum corneum, thus enhance the diffusion of other molecules or drugs through the skin.  Due to their physical properties, PEG acts as a surfactant by coating the eye. It provides lubrication and surface protection in dry eyes. ",,,,Polyethylene glycol 300 is approved.,Polyethylene glycol 300 is a liquid.,True
20314,,,,,Polyethylene glycol 3500 is experimental.,,False
20315,Articaine is a dental local anesthetic. Articaine is widely used around the world and is the most popular local anesthetic in many European countries.,The molecular weight is 284.37.,Articaine has a topological polar surface area of 67.43.,The log p value of  is 1.98.,Articaine is approved.,Articaine is a solid.,True
20316,"Epitizide is an agent, commonly found in combination , used to produce diuresis.",The molecular weight is 425.84.,Epitizide has a topological polar surface area of 118.36.,The log p value of  is 1.07.,Epitizide is experimental.,Epitizide is a solid.,True
20317,,The molecular weight is 306.45.,Butacaine has a topological polar surface area of 55.56.,The log p value of  is 5.01.,Butacaine is vet_approved.,,False
20318,"An anti-infective agent that is used topically to treat skin infections and orally for urinary tract infections. For the treatment of bacterial vaginitis, keratitis, acute conjunctivitis, and blepharitis. Sulfacetamide is a sulfonamide antibiotic with bacteriostatic actions and broad-spectrum activity against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of <i>p</i>-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus. Sulfacetamide is a competitive inhibitor of bacterial para-aminobenzoic acid (PABA), an essential component for bacterial growth (according to the Woods-Fildes theory). The inhibited reaction is necessary in these organisms for the synthesis of folic acid.",The molecular weight is 214.24.,Sulfacetamide has a topological polar surface area of 89.26.,The log p value of  is -0.98.,Sulfacetamide is approved.,Sulfacetamide is a solid.,True
20319,,The molecular weight is 354.81.,Xipamide has a topological polar surface area of 109.49.,The log p value of  is 1.93.,Xipamide is experimental.,,False
20320,,The molecular weight is 1329.37.,Cobalamin has a topological polar surface area of 488.71.,,Cobalamin is experimental.,Cobalamin is a solid.,False
20321,"Methscopolamine is a quaternary ammonium derivative of scopolamine and antagonist at muscarininc (mACh) receptors. Methscopolamine bromide is the most common form of the active ingredient in oral pharmaceutical products. The oral tablets are used as an adjunct therapy for the treatment of peptic ulcer and is shown to be effective in decreasing the rate of recurrence of peptic ulcers as well as preventing complications. Methscopolamine bromide is an anticholinergic agent which possesses most of the pharmacologic actions of that drug class. These include reduction in volume and total acid content of gastric secretion, inhibition of gastrointestinal motility, inhibition of salivary excretion, dilation of the pupil and inhibition of accommodation with resulting blurring of vision. Large doses may result in tachycardia.",The molecular weight is 318.39.,Methscopolamine has a topological polar surface area of 59.06.,The log p value of  is -2.47.,Methscopolamine is approved.,,True
20322,"Zinc oxide is an inorganic compound used in a number of manufacturing processes. It can be found in rubbers, plastics, ceramics, glass, cement, lubricants, paints, ointments, adhesives, sealants, pigments, foods, batteries, ferrites, fire retardants, and first-aid tapes. It occurs naturally as the mineral zincite, but most zinc oxide is produced synthetically. It is also widely used to treat a variety of other skin conditions, in products such as baby powder and barrier creams to treat diaper rashes, calamine cream, anti-dandruff shampoos, and antiseptic ointments. For adjunctive treatment of diaper dermatitis. Also, it can be used to treat minor skin irritations (eg, cuts, burns, and scrapes, poison ivy). Zinc oxide has astringent, soothing and protective properties and is used in topical preparations for eczema, slight excoriations, wounds and haemorrhoids. It also reflects ultraviolet radiation and can be used as a physical sunscreen. It acts by providing a physical barrier to prevent skin irritation and help heal damaged skin.",The molecular weight is 81.38.,Zinc oxide has a topological polar surface area of 17.07.,,Zinc oxide is approved.,Zinc oxide is a solid.,True
20323,Ammonium chloride is an inorganic compound with the formula NH4Cl. It is highly soluble in water producing mildly acidic solutions. 1. Expectorant in cough syrups. Systemic acidifier. In liver ammonium chloride is converted into urea with the liberation of hydrogen ions ( which lowers the pH) and chloride.  Ammonium chloride increases acidity by increasing the amount of hydrogen ion concentrations.,The molecular weight is 53.49.,,,Ammonium chloride is approved and investigational and vet_approved.,Ammonium chloride is a solid.,True
20324,"Triethylenetatramine (TETA) is a highly selective divalent Cu(II) chelator and orphan drug that revereses copper overload in tissues. Its salt form, trientine (triethylenetetramine dihydrochloride or 2,2,2-tetramine) was introduced in 1969 as an alternative to D-penicillamine. It consists of a polyamine-like structure different from D-penicillamine, as it lack sulfhydryl groups. It was previously approved by FDA in 1985 as second-line pharmacotherapy for Wilson's disease. Although penicillamine treatment is believed to be more extensive, TETA therapy has been shown to be an effective initial therapy, even with patients with decompensated liver disease at the outset, and prolonged TETA treatment is not associated with adverse effects as expected in penicillamine treatment. Its clinical applications on cancer, diabetes mellitus, Alzheimer's disease and vascular demetia are being studied. Trientine is a copper chelator used in the treatment of Wilson's disease as an alternative to D-penicillamine. It tends to be used in patients who are experiencing serious adverse effects from penicillamine therapy or intolerance of penicillamine.  TETA is a selective copper (II) chelator. tightly binds and facilitates systemic elimination of Cu(II) into the urine whilst neutralizing its catalytic activity, but does not cause systemic copper deficiency even after prolonged use. It may also act as an antioxidant as it suppresses the copper-mediated oxidative stress. TETA not only increases urinary Cu excretion, but also decreases intestinal copper absorption by 80%.  Copper is chelated by forming a stable complex with the four constituent nitrogens in a planar ring as copper displays enhanced ligand binding properties for nitrogen compared to oxygen. It binds Cu(II) very tightly, having a dissociation constant from Cu(II) of 10^−15 mol/L at pH 7.0. TETA reacts in a stoichiometric ratio 1:1 with copper and is also able to complex with iron and zinc in vivo. TETA is considered a potential chemotherapeutic agent as it could be a telomerase inhibitor because it is a ligand for G-quadruplex, and stabilizes both intra- and intermolecular G-quadruplexes. It may mediate a selective inhibitory effect or cytotoxicity on tumor growth. Chelating excess copper may affect copper-induced angiogenesis. Other mechanisms of action of TETA for alternative therapeutic implications include improved antioxidant defense against oxidative stress, pro-apoptosis, and reduced inflammation. ",The molecular weight is 146.24.,Triethylenetetramine has a topological polar surface area of 76.1.,The log p value of  is -2.37.,Triethylenetetramine is approved and investigational.,Triethylenetetramine is a liquid.,True
20325,Meticrane is a diuretic medication. It has been marketed in Japan under the trade name Arresten and is used to lower blood pressure.,The molecular weight is 275.34.,Meticrane has a topological polar surface area of 94.3.,The log p value of  is 0.48.,Meticrane is approved.,,True
20326,Tramazoline is under investigation in clinical trial NCT01601509 (Nasal Tramazoline and Dexamethazone in Obstructive Sleep Apnea (OSA) Patients Tramazoline and).,The molecular weight is 215.3.,Tramazoline has a topological polar surface area of 36.42.,The log p value of  is 2.59.,Tramazoline is investigational.,,True
20327,"Hydroxyamphetamine is a derivative of amphetamines. Hydroxyamphetamine is intended mainly as local eye drops for diagnostic purposes. It is indirect sympathomimetic agent which cause dilation of the eye pupil before diagnostic test. Among the minor side effects from its use are: change in color vision, difficulty seeing at night, dry mouth, headache, increased sensitivity of eyes to sunlight, muscle stiffness or tightness and temporary stinging in the eyes. Mydriatic agent (eye pupil dilatation) for diagnosis of ophthalmic nerve lesions. Hydroxyamphetamine hydrobromide is an indirect acting sympathomimetic agent which causes the release of norepinephrine from adrenergic nerve terminals, resulting in mydriasis. ",The molecular weight is 151.21.,Hydroxyamphetamine has a topological polar surface area of 46.25.,The log p value of  is 1.07.,Hydroxyamphetamine is approved.,,True
20328,"Methenamine is a heterocyclic organic compound with a cage-like structure similar to adamantane. In salt form it is used for the treatment of urinary tract infection (Example: methenamine hippurate which is the hippuric acid salt of methenamine). For prophylactic or suppressive treatment of frequently recurring urinary tract infections when long-term therapy is considered necessary. This drug is not used to treat infection and should only be used after appropriate eradication of infection with antimicrobial agents. Ingestion of a 1-gram dose of methenamine hippurate produces antibacterial activity in the urine within 1/2 hour. Administration of 1 g twice daily produces continuous antibacterial activity in the urine. Methenamine does not have antibacterial properties in an alkaline environment (pH≥6); however, in a more acidic environment (pH<6), methenamine is hydrolyzed to formaldehyde. (1) Formaldehyde is considered to be highly bactericidal. (1) Formaldehyde has nonspecific antibacterial activity and works by denaturing proteins and nucleic acid of bacteria. (1) Certain bacteria such as Proteus sp. can alkalize urine, inhibiting the beneficial activity of formaldehyde. (1) The key role of the salt component of the drug, for example hippuric acid, is to maintain the acidic state of the urine. (1)",The molecular weight is 140.19.,Methenamine has a topological polar surface area of 12.96.,The log p value of  is 2.43.,Methenamine is approved and vet_approved.,Methenamine is a solid.,True
20329,"Clobutinol is a cough suppressant that is withdrawn from the US and EU markets. Clobutinol may prolong the QT interval. In 2007, Clobutinol was determined to cause cardiac arrhythmia in some patients.",The molecular weight is 255.79.,Clobutinol has a topological polar surface area of 23.47.,The log p value of  is 3.28.,Clobutinol is withdrawn.,Clobutinol is a solid.,True
20330,"Dichlorophen is an antimicrobial agent shown to exert activity against cestodes, protozoa, fungi, and bacteria. It is often combined with toluene to remove parasites including ascarids, tapeworm, and hookworm from dogs and cats.",The molecular weight is 269.12.,Dichlorophen has a topological polar surface area of 40.46.,The log p value of  is 4.79.,Dichlorophen is experimental and vet_approved.,,True
20331,Iopanoic acid contains iodine and is useful as a contrast medium in cholecystography.,The molecular weight is 570.93.,Iopanoic acid has a topological polar surface area of 63.32.,The log p value of  is 4.7.,Iopanoic acid is approved and withdrawn.,Iopanoic acid is a solid.,True
20332,"Investigated for use/treatment in cardiovascular disorders and coronary artery disease. M118 is a novel drug candidate that has been, through Momenta's proprietary technology, rationally engineered with attributes of monitorability, reversibility, flexible administration (intravenous and subcutaneous), and both potent and predictable anti-Xa (aXa) and anti-IIa (aIIa) activity to provide anticoagulant therapy to patients with ACS. M118 is designed to interact at multiple points in the coagulation cascade by selectively binding to anti-thrombin III and thrombin, two critical factors in the formation of clots. ",,,,Adomiparin is investigational.,Adomiparin is a solid.,True
20333,Parnaparin is an heparin of low molecular weight with antithrombotic effects. Used in the prevention and treatment of venous thromboembolism (deep vein thrombosis and pulmonary embolism) and in the treatment of myocardial infarction.,,,,Parnaparin is approved and investigational.,Parnaparin is a solid.,True
20334,"Heparin, bovine is under investigation in clinical trial NCT01072747 (Efficacy And Safety Of Unfractionated Heparin In Patients With Cardiovascular Surgery Using Cardiopulmonary Bypass).",,,,"Heparin, bovine is investigational.",,True
20335,,The molecular weight is 156.27.,Racementhol has a topological polar surface area of 20.23.,The log p value of  is 3.23.,Racementhol is approved and experimental.,,False
20336,"Temozolomide (Temodar and Temodal) is an oral alkylating agent used for the treatment of refractory anaplastic astrocytoma -- a type of cancerous brain tumor. Temozolomide is not active until it is converted at physiologic pH to the active form, 5-(3-methyltriazen-1-yl)imidazole-4-carboxamide (MTIC). For the treatment of adult patients diagnosed with anaplastic astrocytoma whose disease has progressed after therapy with nitrosourea and procarbazine, as well as concomitantly with radiation therapy for treatment of newly diagnosed glioblastoma multiforme. Also used as maintenance therapy for glioblastoma multiforme. Temozolomide is an imidazotetrazine deritave and an antineoplastic agent. It is a prodrug that has little to no pharmacological activity until it is hydrolyzed in vivo to 5-(3-methyltriazen-1-yl)imidazole-4-carboxamide (MTIC). After administration, temozolomide undergoes rapid, nonenzymatic hydrolysis at physiological pH to MTIC, which is the active form of the drug. MTIC is generated through the effect of water at the highly electropositive C4 position of temozolomide, causing the ring of temozolomide to open, release carbon dioxide, and generate MTIC. Temozolomide is not active until it is converted at physiologic pH to MTIC. It is suggested that MTIC then alkylates DNA at the N7 position of guanine, O3 position of adenosine, and O6 position of guanosine, with the most common site being the N7 position. This methylation of guanine residues lead to single and double-strand DNA breaks and subsequent apoptotic cell death. It is suggested that the N7-methylguanine plays a critical role in the antitumor activity of the drug, as there is a correlation between the sensitivity of tumor cell lines to temozolomide and the activity of O6-alkylguanine alkyltransferase, which is the DNA repair protein that specifically removes alkyl groups at the O6 position of guanine. Cells lines that have lower levels of AGT are more sensitive to the cytotoxicity of temozolomide. It is also suggested that cytotoxic mechanism of temozolomide is related to the failure of the DNA MMR system to find a complementary base for methylated guanine. The DNA MMR system is involved in the formation of a number of proteins that remove methylated guanine. Evidence shows that when this repair process is targeted to the DNA strand opposite the O6-methylguanine, its inability to find the correct target leads to long-lived nicks in the DNA. The accumulation of these nicks lead to the inhibition of replication in the daughter cells, thereby blocking the cell cycle at the G<sub>2</sub>-M boundary.",The molecular weight is 194.15.,Temozolomide has a topological polar surface area of 105.94.,The log p value of  is -0.81.,Temozolomide is approved and investigational.,Temozolomide is a solid.,True
20337,"Monopotassium phosphate, MKP, (also potassium dihydrogenphosphate, KDP, or monobasic potassium phosphate), KH2PO4, is a soluble salt of potassium and the dihydrogen phosphate ion. It is a source of phosphorus and potassium as well as a buffering agent. It can be used in fertilizer mixtures to reduce escape of ammonia by keeping pH low. Used in buffers (determination of pH, pharmaceutical production, urinary acidifier, paper processing, baking powder, and food), nutrient solutions, yeast foods, special liquid fertilizers, sonar systems and other electronic applications;  Potassium is the major cation of intracellular fluid and is essential for maintenance of acid-base balance, isotonicity, and electrodynamic characteristics of the cell. Potassium is an important activator in many enzymatic reactions and is essential to a number of physiologic processes including transmission of nerve impulses; contraction of cardiac, smooth, and skeletal muscles; gastric secretion; renal function; tissue synthesis; and carbohydrate metabolism. hosphorus has a number of important functions in the biochemistry of the body. The bulk of the body's phosphorus is located in the bones, where it plays a key role in osteoblastic and osteoclastic activities. Enzymatically catalyzed phosphate-transfer reactions are numerous and vital in the metabolism of carbohydrate, lipid and protein, and a proper concentration of the anion is of primary importance in assuring an orderly biochemical sequence. ln addition, phosphorus plays an important role in modifying steady-state tissue concentrations of calcium. Phosphate ions are important buffers of the intracellular fluid, and also play a primary role in the renal excretion of the hydrogen ion. Oral administration of inorganic phosphates increases serum phosphate levels. Phosphates lower urinary calcium levels in idiopathic hypercalciuria.",The molecular weight is 136.08.,Monopotassium phosphate has a topological polar surface area of 80.59.,,Monopotassium phosphate is approved and investigational and vet_approved.,,True
20338,,The molecular weight is 152.24.,Synthetic camphor has a topological polar surface area of 17.07.,The log p value of  is 2.18.,Synthetic camphor is approved and experimental.,,False
20339,"Mannitol is an osmotic diuretic that is metabolically inert in humans and occurs naturally, as a sugar or sugar alcohol, in fruits and vegetables. Mannitol elevates blood plasma osmolality, resulting in enhanced flow of water from tissues, including the brain and cerebrospinal fluid, into interstitial fluid and plasma. As a result, cerebral edema, elevated intracranial pressure, and cerebrospinal fluid volume and pressure may be reduced. Mannitol may also be used for the promotion of diuresis before irreversible renal failure becomes established; the promotion of urinary excretion of toxic substances; as an Antiglaucoma agent; and as a renal function diagnostic aid. Used for the promotion of diuresis before irreversible renal failure becomes established, the reduction of intracranial pressure, the treatment of cerebral edema, and the promotion of urinary excretion of toxic substances. Chemically, mannitol is an alcohol and a sugar, or a polyol; it is similar to xylitol or sorbitol. However, mannitol has a tendency to lose a hydrogen ion in aqueous solutions, which causes the solution to become acidic. For this reason, it is not uncommon to add a substance to adjust its pH, such as sodium bicarbonate. Mannitol is commonly used to increase urine production (diuretic). It is also used to treat or prevent medical conditions that are caused by an increase in body fluids/water (e.g., cerebral edema, glaucoma, kidney failure). Mannitol is frequently given along with other diuretics (e.g., furosemide, chlorothiazide) and/or IV fluid replacement. Mannitol is an osmotic diuretic that is metabolically inert in humans and occurs naturally, as a sugar or sugar alcohol, in fruits and vegetables. Mannitol elevates blood plasma osmolality, resulting in enhanced flow of water from tissues, including the brain and cerebrospinal fluid, into interstitial fluid and plasma. As a result, cerebral edema, elevated intracranial pressure, and cerebrospinal fluid volume and pressure may be reduced. As a diurectic mannitol induces diuresis because it is not reabsorbed in the renal tubule, thereby increasing the osmolality of the glomerular filtrate, facilitating excretion of water, and inhibiting the renal tubular reabsorption of sodium, chloride, and other solutes. Mannitol promotes the urinary excretion of toxic materials and protects against nephrotoxicity by preventing the concentration of toxic substances in the tubular fluid. As an Antiglaucoma agent mannitol levates blood plasma osmolarity, resulting in enhanced flow of water from the eye into plasma and a consequent reduction in intraocular pressure. As a renal function diagnostic aid mannitol is freely filtered by the glomeruli with less than 10% tubular reabsorption. Therefore, its urinary excretion rate may serve as a measurement of glomerular filtration rate (GFR).",The molecular weight is 182.17.,Mannitol has a topological polar surface area of 121.38.,The log p value of  is -2.05.,Mannitol is approved and investigational.,Mannitol is a solid.,True
20340,"A second-line antitubercular agent that inhibits mycolic acid synthesis. It also may be used for treatment of leprosy. (From Smith and Reynard, Textbook of Pharmacology, 1992, p868) For use in the treatment of pulmonary and extrapulmonary tuberculosis when other antitubercular drugs have failed. Ethinamate is bacteriostatic against <i>M. tuberculosis</i>. In a study examining ethionamide resistance, ethionamide administered orally initially decreased the number of culturable <i>Mycobacterium tuberculosis</i> organisms from the lungs of H37Rv infected mice. Drug resistance developed with continued ethionamide monotherapy, but did not occur when mice received ethionamide in combination with streptomycin or isoniazid. Ethionamide may be bacteriostatic or bactericidal in action, depending on the concentration of the drug attained at the site of infection and the susceptibility of the infecting organism. Ethionamide, like prothionamide and pyrazinamide, is a nicotinic acid derivative related to isoniazid. It is thought that ethionamide undergoes intracellular modification and acts in a similar fashion to isoniazid. Isoniazid inhibits the synthesis of mycoloic acids, an essential component of the bacterial cell wall. Specifically isoniazid inhibits InhA, the enoyl reductase from <i>Mycobacterium tuberculosis</i>, by forming a covalent adduct with the NAD cofactor. It is the INH-NAD adduct that acts as a slow, tight-binding competitive inhibitor of InhA.",The molecular weight is 166.24.,Ethionamide has a topological polar surface area of 38.91.,The log p value of  is 1.73.,Ethionamide is approved.,Ethionamide is a solid.,True
20341,,The molecular weight is 157.17.,Ethadione has a topological polar surface area of 46.61.,The log p value of  is 0.41.,Ethadione is experimental.,,False
20342,Iodamide is a contrast medium molecule that is no longer marketed in the United States.,The molecular weight is 627.94.,Iodamide has a topological polar surface area of 95.5.,The log p value of  is 0.72.,Iodamide is withdrawn.,Iodamide is a solid.,True
20343,"A hypnotic and sedative used in the treatment of insomnia. The safety margin is too narrow for chloral hydrate to be used as a general anesthetic in humans, but it is commonly used for that purpose in animal experiments. It is no longer considered useful as an anti-anxiety medication. Mainly used as a hypnotic in the treatment of insomnia; however, it is only effective as a hypnotic for short-term use. May be used as a routine sedative preoperatively to decrease anxiety and cause sedation and/or sleep with respiration depression or cough reflex. ",The molecular weight is 165.39.,Chloral hydrate has a topological polar surface area of 40.46.,The log p value of  is 0.71.,Chloral hydrate is approved and illicit and investigational and vet_approved.,Chloral hydrate is a solid.,True
20344,"Tigecycline is a glycylcycline antibiotic developed and marketed by Wyeth under the brand name Tygacil. It was developed in response to the growing prevalence of antibiotic resistance in bacteria such as Staphylococcus aureus. It was granted fast-track approval by the U.S. Food and Drug Administration (FDA) on June 17, 2005. For the treatment of infections caused by susceptible strains of the designated microorganisms in the following conditions: Complicated skin and skin structure infections caused by <i>Escherichia coli</i>, <i>Enterococcus faecalis</i> (vancomycin-susceptible isolates only), <i>Staphylococcus aureus</i> (methicillin-susceptible and -resistant isolates), <i>Streptococcus agalactiae</i>, <i>Streptococcus anginosus</i> grp. (includes <i>S. anginosus</i>, <i>S. intermedius</i>, and <i>S. constellatus</i>), <i>Streptococcus pyogenes</i> and <i>Bacteroides fragilis</i>. Complicated intra-abdominal infections caused by <i>Citrobacter freundii</i>, <i>Enterobacter cloacae</i>, <i>Escherichia coli</i>, <i>Klebsiella oxytoca</i>, <i>Klebsiella pneumoniae</i>, <i>Enterococcus faecalis</i> (vancomycin-susceptible isolates only), <i>Staphylococcus aureus</i> (methicillin-susceptible isolates only), <i>Streptococcus anginosus</i> grp. (includes <i>S. anginosus</i>, <i>S. intermedius</i>, and <i>S. constellatus</i>), <i>Bacteroides fragilis</i>, <i>Bacteroides thetaiotaomicron</i>, <i>Bacteroides uniformis</i>, <i>Bacteroides vulgatus</i>, <i>Clostridium perfringens</i>, and <i>Peptostreptococcus micros</i>. Tigecycline is the first clinically-available drug in a new class of antibiotics called the glycylcyclines. Glycylcyclines are a new class of antibiotics derived from tetracycline. These tetracycline analogues are specifically designed to overcome two common mechanisms of tetracycline resistance, namely resistance mediated by acquired efflux pumps and/or ribosomal protection. Glycylcycline antibiotics have a similar mechanism of action as tetracycline antibiotics. Both classes of antibiotics bind to the 30S ribosomal subunit to prevent the amino-acyl tRNA from binding to the A site of the ribosome. However, the glycylcyclines appear to bind more effectively than the tetracyclines. Tigecycline, a glycylcycline, inhibits protein translation in bacteria by binding to the 30S ribosomal subunit and blocking entry of amino-acyl tRNA molecules into the A site of the ribosome. This prevents incorporation of amino acid residues into elongating peptide chains. Tigecycline carries a glycylamido moiety attached to the 9-position of minocycline. The substitution pattern is not present in any naturally occurring or semisynthetic tetracycline and imparts certain microbiologic properties to tigecycline. Tigecycline is not affected by the two major tetracycline resistance mechanisms, ribosomal protection and efflux. Accordingly, tigecycline has demonstrated in vitro and in vivo activity against a broad spectrum of bacterial pathogens. There has been no cross resistance observed between tigecycline and other antibiotics. Tigecycline is not affected by resistance mechanisms such as beta-lactamases (including extended spectrum beta-lactamases), target site modifications, macrolide efflux pumps or enzyme target changes (e.g. gyrase/topoisomerase). In vitro studies have not demonstrated antagonism between tigecycline and other commonly used antibacterial drugs. In general, tigecycline is considered bacteriostatic.",The molecular weight is 585.66.,Tigecycline has a topological polar surface area of 205.76.,The log p value of  is -0.03.,Tigecycline is approved.,Tigecycline is a solid.,True
20345,"Metaxalone is a moderate to strong muscle relaxant used in the symptomatic treatment of musculoskeletal pain caused by strains, sprains, and other musculoskeletal conditions. It is marketed by King Pharmaceuticals under the brand name Skelaxin®. Its main mechanism of action is thought to involve general central nervous system depression. Metaxalone is associated with few side effects and is available as a 800 mg scored tablet. For the treatment of painful peripheral musculoskeletal conditions and spasticity from upper motor neuron syndromes. Metaxalone is a skeletal muscle relaxant indicated as an adjunct to rest, physical therapy, and other measures for the relief of discomforts associated with acute, painful musculoskeletal conditions. The mode of action of this drug has not been clearly identified, but may be related to its sedative properties. Metaxalone does not directly relax tense skeletal muscles in man. The mechanism of action of metaxalone in humans has not been established, but may be due to general central nervous system depression.",The molecular weight is 221.26.,Metaxalone has a topological polar surface area of 47.56.,The log p value of  is 2.14.,Metaxalone is approved.,Metaxalone is a solid.,True
20346,Iocetamic acid is a diagnostic aid (radiopaque medium),The molecular weight is 613.96.,Iocetamic acid has a topological polar surface area of 83.63.,The log p value of  is 2.82.,Iocetamic acid is approved.,,True
20347,"An antibiotic produced by Streptomyces lincolnensis var. lincolnensis. It has been used in the treatment of staphylococcal, streptococcal, and Bacteroides fragilis infections. Lincomycin is an antibiotic used in the treatment of staphylococcal, streptococcal, and <i>Bacteroides fragilis</i> infections. Lincomycin is a lincosamide antibiotic that produced by <i>Streptomyces lincolnensis</i>. Lincomycin has been shown to be active in vitro against the following microorganisms: Aerobic gram-positive cocci: <i>Streptococcus pyogenes</i> and <i>Viridans group streptococci</i>; Aerobic gram-positive bacilli: <i>Corynebacterium diphtheriae</i>; Anaerobic gram-positive non-sporeforming bacilli: <i>Propionibacterium acnes</i>; Anaerobic gram-positive sporeforming bacilli: <i>Clostridium tetani</i> and <i>Clostridium perfringens</i>. Lincomycin inhibits protein synthesis in susceptible bacteria by binding to the 50 S subunits of bacterial ribosomes and preventing peptide bond formation upon transcription. It is usually considered bacteriostatic, but may be bactericidal in high concentrations or when used against highly susceptible organisms.",The molecular weight is 406.54.,Lincomycin has a topological polar surface area of 122.49.,The log p value of  is 1.28.,Lincomycin is approved and vet_approved.,Lincomycin is a solid.,True
20348,,The molecular weight is 365.98.,Meglumine antimoniate has a topological polar surface area of 117.76.,,Meglumine antimoniate is experimental and investigational.,,False
20349,"Methyl salicylate (oil of wintergreen or wintergreen oil) is an organic ester naturally produced by many species of plants, particularly wintergreens. The compound was first extracted and isolated from plant species Gaultheria procumbens in 1843. It can be manufactured synthetically and it used as a fragrance, in foods, beverages, and liniments. It forms a colorless to yellow or reddish liquid and exhibits a characteristic odor and taste of wintergreen. For acute joint and muscular pain, methyl salicylate is used as a rubefacient and analgesic in deep heating liniments. It is used as a flavoring agent in chewing gums and mints in small concentrations and added as antiseptic in mouthwash solutions. Ointments or liniments containing methyl salicylate are applied topically as counter irritant for relief of acute pain associated with lumbago,sciatica and rheumatic conditions. Local analgesics for human and veterinary medicine. Methyl salicylate relieve musculoskeletal pain in the muscles, joints, and tendons by causing irritation and reddening of the skin due to dilated capillaries and increased blood flow. It is pharmacologically similar to aspirin and other NSAIDs but as a topical agent it primarily acts as a rubefacient and skin irritant. Counter-irritation is believed to cause a soothing sensation of warmth. Counter-irritation is thought to be effective at alleviating musculoskeletal pain as the irritation of the sensory nerve endings is thought to alter or offset pain in the underlying muscle or joints that are served by the same nerves. This is thought to mask the underlying musculoskeletal pain and discomfort. When applied topically, methyl salicylate is thought to penetrate the skin and underlying tissues where it reversibly inhibits cyclooxygenase enzyme and locally and peripherally prevents the production of inflammatory mediators such as prostaglandin and thromboxane A2. ",The molecular weight is 152.15.,Methyl salicylate has a topological polar surface area of 46.53.,The log p value of  is 2.33.,Methyl salicylate is approved and vet_approved.,Methyl salicylate is a liquid.,True
20350,,The molecular weight is 136.15.,Pentaerithrityl has a topological polar surface area of 80.92.,The log p value of  is -0.93.,Pentaerithrityl is experimental.,,False
20351,"Meropenem is a broad-spectrum carbapenem antibiotic. It is active against Gram-positive and Gram-negative bacteria. Meropenem exerts its action by penetrating bacterial cells readily and interfering with the synthesis of vital cell wall components, which leads to cell death. For use as single agent therapy for the treatment of the following infections when caused by susceptible isolates of the designated microorganisms: <b>complicated skin and skin structure infections</b> due to <i>Staphylococcus aureus</i> (b-lactamase and non-b-lactamase producing, methicillin-susceptible isolates only), <i>Streptococcus pyogenes</i>, <i>Streptococcus agalactiae</i>, viridans group streptococci, <i>Enterococcus faecalis</i> (excluding vancomycin-resistant isolates), <i>Pseudomonas aeruginosa</i>, <i>Escherichia coli</i>, <i>Proteus mirabilis</i>, <i>Bacteroides fragilis</i> and <i>Peptostreptococcus</i> species; <b>complicated appendicitis and peritonitis</b> caused by viridans group streptococci, <i>Escherichia coli</i>, <i>Klebsiella pneumoniae</i>, <i>Pseudomonas aeruginosa</i>, <i>Bacteroides fragilis</i>, <i>B. thetaiotaomicron</i>, and <i>Peptostreptococcus</i> species. Also for use in the treatment of bacterial meningitis caused by <i>Streptococcus pneumoniae</i>, <i>Haemophilus influenzae</i> (b-lactamase and non-b-lactamase-producing isolates), and <i>Neisseria meningitidis</i>. Meropenem is a broad-spectrum carbapenem antibiotic. It is active against Gram-positive and Gram-negative bacteria. Meropenem exerts its action by penetrating bacterial cells readily and interfering with the synthesis of vital cell wall components, which leads to cell death. The bactericidal activity of meropenem results from the inhibition of cell wall synthesis. Meropenem readily penetrates the cell wall of most Gram-positive and Gram-negative bacteria to reach penicillin-binding- protein (PBP) targets. Its strongest affinities are toward PBPs 2, 3 and 4 of <i>Escherichia coli</i> and <i>Pseudomonas aeruginosa</i>; and PBPs 1, 2 and 4 of <i>Staphylococcus aureus</i>.",The molecular weight is 383.46.,Meropenem has a topological polar surface area of 110.18.,The log p value of  is -3.28.,Meropenem is approved and investigational.,Meropenem is a solid.,True
20352,"Providone, also known as polyvinylpyrrolidone (PVP) or polyvidone, is a synthetic water-soluble polymer made from the monomer N-vinylpyrrolidone that is used as a binder in many pharmaceutical tablets and lubricant in eye drops. It is also used in many technical applications with various roles as an adhesive, additive, and emulsifier. When in complex with iodine, displays antiseptic properties where the iodine, a bactericidal component, mainly contributes to this effect and povidone acts as a carrier. can be found in over-the-counter topical solutions, ointment, pessaries, liquid soaps and surgical scrubs. The clinical effectiveness of on wound healing remains somewhat controversial, as it was demonstrated in few clinical studies that application of the compound in wounds was associated with impaired wound healing, reduced wound strength, or infection in open wounds. When in complex with iodine, indicated for inducing antisepsis for prevention of infection in minor cuts, scrapes, and burns.  Povidone itself has no microbicidal activity. exhibits rapid, potent, broad-spectrum antimicrobial properties. The clinical effectiveness of povidon-iodine on wound healing remains somewhat controversial; in few clinical studies investigating the effects of povidone-iodine on wound healing, topical administration of the complex was associated with no significant infections, but slower healing and mild to moderate discomfort on application.  Povidone-iodine is a water-soluble complex that mediates a bactericidal or virucidal action following the gradual liberation of free iodine from the complex at the application site to react with the pathogen. Please refer to the drug entry for for the full mechanism of action of the complex. ",,,,Povidone is approved.,Povidone is a solid.,True
20353,"A polyvinyl polymer of variable molecular weight; used as suspending and dispersing agent and vehicle for pharmaceuticals; also used as blood volume expander. See for full details. When in complex with iodine, indicated for inducing antisepsis for prevention of infection in minor cuts, scrapes, and burns.  Povidone itself has no microbicidal activity. exhibits rapid, potent, broad-spectrum antimicrobial properties. The clinical effectiveness of povidon-iodine on wound healing remains somewhat controversial; in few clinical studies investigating the effects of povidone-iodine on wound healing, topical administration of the complex was associated with no significant infections, but slower healing and mild to moderate discomfort on application.  Povidone-iodine is a water-soluble complex that mediates a bactericidal or virucidal action following the gradual liberation of free iodine from the complex at the application site to react with the pathogen. Please refer to the drug entry for for the full mechanism of action of the complex. ",,,,Povidone K30 is approved and experimental.,,True
20354,"Phensuximide is a member of the succinimide class with anticonvulsant properties. It suppresses the paroxysmal three cycle per second spike and wave EEG pattern associated with lapses of consciousness in petit mal seizures. The frequency of attacks is reduced by depression of nerve transmission in the motor cortex. For the treatment of epilepsy. Phensuximide suppresses the paroxysmal three cycle per second spike and wave EEG pattern associated with lapses of consciousness in absence (petit mal) seizures. The frequency of attacks is reduced by depression of nerve transmission in the motor cortex. Phensuximide's mechanism of action not understood, but may act in inhibitory neuronal systems that are important in the generation of the three per second rhythm. It's effects may be related to its ability to inhibit depolarization-induced accumulation of cyclic AMP and cyclic GMP in brain tissue.",The molecular weight is 189.21.,Phensuximide has a topological polar surface area of 37.38.,The log p value of  is 0.94.,Phensuximide is approved.,Phensuximide is a solid.,True
20355,,The molecular weight is 261.36.,Alphaprodine has a topological polar surface area of 29.54.,The log p value of  is 2.89.,Alphaprodine is illicit.,Alphaprodine is a solid.,False
20356,Ethoheptazine is marketed under the name Zactane. It is a phenazepine based opioid analgesic. It was invented in the 1950s and is related to other drugs such as proheptazine. Ethoheptazine is no longer marketed in the United States.,The molecular weight is 261.36.,Ethoheptazine has a topological polar surface area of 29.54.,The log p value of  is 2.79.,Ethoheptazine is approved and withdrawn.,Ethoheptazine is a solid.,True
20357,"Bisacodyl is an organic stimulant laxative that acts directly on the colon to promote bowel movement. Bisacodyl is prescribed for constipation, neurogenic bowel dysfunction, and bowel preparation before medical examinations.  Indicated for cleansing of the colon as a preparation for colonoscopy in adults.  Bisacodyl is hydrolyzed by intestinal brush border enzymes and colonic bacteria to form an active metabolite that acts directly on the colonic mucosa to produce colonic peristalsis. Induces diarrhea which cleanses the colon. ",The molecular weight is 361.4.,Bisacodyl has a topological polar surface area of 65.49.,The log p value of  is 2.85.,Bisacodyl is approved.,Bisacodyl is a solid.,True
20358,"Povidone-iodine is a stable chemical complex of polyvinylpyrrolidone (povidone, PVP) and elemental iodine. It contains from 9.0% to 12.0% available iodine, calculated on a dry basis. This unique complex was discovered in 1955 at the Industrial Toxicology Laboratories in Philadelphia by H. A. Shelanski and M. V. Shelanski. During in vitro testing to demonstrate anti-bacterial activity it was found that the complex was less toxic in mice than tincture of iodine. Human clinical trials showed the product to be superior to other iodine formulations. Povidone-iodine was immediately marketed, and has since become the universally preferred iodine antiseptic. For topical application in the treatment and prevention of infection in wounds. Povidone iodine is a kind of iodine disinfectant which directly cause in vivo protein denaturation, precipitation of bacteria, and further resulting in the death of pathogenic microorganisms. Therefore, it is effective in disinfection and sterilization. It can kill viruses, bacteria, spores, fungi, and protozoa with low toxicity to human. Povidone-iodine aqueous solution has strong pharmacological activity against Staphylococcus aureus, Neisseria gonorrhoeae, Pseudomonas aeruginosa, syphilis, hepatitis B virus, HIV, and Trichomonas vaginalis. Povidone-iodine is called iodophore which means povidone acts as a carrier of iodine. Iodine is considered as the active moiety that mediates microbicidal actions. When released from the complex, free iodine (I2) penetrates the cell wall of microorganisms quickly, and the lethal effects are believed to result from disruption of protein and nucleic acid structure and synthesis. While the full mechanism of action is not fully elucidated, iodine is thought to inhibit vital bacterial cellular mechanisms and structures, and oxidizes nucleotides fatty or amino acids in bacterial cell membranes. Additionally, free iodine disrupts the function of the cytosolic enzymes involved in the respiratory chain, causing them to become denatured and deactivated. _In vitro_ evidence suggests that iodine also counteracts inflammation elicited by both pathogens and the host response via multifactorial effects. In hosts, povidone-iodine was demonstrated to modulate the redox potential, inhibit the release of inflammatory mediators such as TNF-α and β-galactosidase, inhibit metalloproteinase production, and potentiate the healing signals from pro-inflammatory cytokines by activation of monocytes, T-lymphocytes, and macrophages, _in vitro_.",,,,Povidone-iodine is approved.,Povidone-iodine is a solid.,True
20359,"A long acting sulfonamide that is used, usually in combination with other drugs, for respiratory, urinary tract, and malarial infections. Sulfadoxine is used in combination with pyrimethamine for the treatment or prevention of malaria. It can also be used to treat various infections in livestock as well. Sulfadoxine helps inhibit the enzyme dihydropteroate synthetase which is an enzyme necessary in the conversion of PABA to folic acid. As folic acid is vital to the synthesis, repair, and methylation of DNA which is vital to cell growth in Plasmodium falciparum. With this vital nutrient lacking, the parasite has difficulty in reproducing. Sulfadoxine is a sulfa drug, often used in combination with pyrimethamine to treat malaria. This medicine may also be used to prevent malaria in people who are living in, or will be traveling to, an area where there is a chance of getting malaria. Sulfadoxine targets Plasmodium dihydropteroate synthase and dihydrofolate reductase. Sulfa drugs or Sulfonamides are antimetabolites. They compete with para-aminobenzoic acid (PABA) for incorporation into folic acid. The action of sulfonamides exploits the difference between mammal cells and other kinds of cells in their folic acid metabolism. All cells require folic acid for growth. Folic acid (as a vitamin) diffuses or is transported into human cells. However, folic acid cannot cross bacterial (and certain protozoan) cell walls by diffusion or active transport. For this reason bacteria must synthesize folic acid from p-aminobenzoic acid.",The molecular weight is 310.33.,Sulfadoxine has a topological polar surface area of 116.43.,The log p value of  is 1.23.,Sulfadoxine is approved and investigational.,Sulfadoxine is a solid.,True
20360,"Ertapenem is a carbapenem antibiotic drug that is marketed under the trade name Invanz by Merck & Co. pharmaceutical company. It is structurally similar to and possesses a 1-beta-methyl group. For the treatment the following moderate to severe infections caused by susceptible isolates of the designated microorganisms: (1) complicated intra-abdominal infections due to <i>Escherichia coli</i>, <i>Clostridium clostridioforme</i>, <i>Eubacterium lentum</i>, <i>Peptostreptococcus</i> species, <i>Bacteroides fragilis</i>, <i>Bacteroides distasonis</i>, <i>Bacteroides ovatus</i>, <i>Bacteroides thetaiotaomicron</i>, or <i>Bacteroides uniformis</i>, (2) complicated skin and skin structure infections, including diabetic foot infections without osteomyelitis due to <i>Staphylococcus aureus</i> (methicillin susceptible isolates only), <i>Streptococcus agalactiae</i>, <i>Streptococcus pyogenes</i>, <i>Escherichia coli</i>, <i>Klebsiella pneumoniae</i>, <i>Proteus mirabilis</i>, <i>Bacteroides fragilis</i>, <i>Peptostreptococcus</i> species, <i>Porphyromonas asaccharolytica</i>, or <i>Prevotella bivia</i>, (3) community acquired pneumonia due to <i>Streptococcus pneumoniae</i> (penicillin susceptible isolates only) including cases with concurrent bacteremia, <i>Haemophilus influenzae</i> (beta-lactamase negative isolates only), or <i>Moraxella catarrhalis</i>, (4) complicated urinary tract infections including pyelonephritis due to <i>Escherichia coli</i>, including cases with concurrent bacteremia, or <i>Klebsiella pneumoniae</i>, (5) acute pelvic infections including postpartum endomyometritis, septic abortion and post surgical gynecologic infections due to <i>Streptococcus agalactiae</i>, <i>Escherichia coli</i>, <i>Bacteroides fragilis</i>, <i>Porphyromonas asaccharolytica</i>, <i>Peptostreptococcus</i> species, or <i>Prevotella bivia</i>. Ertapenem has in vitro activity against gram-positive and gram-negative aerobic and anaerobic bacteria. The bactericidal activity of ertapenem results from the inhibition of cell wall synthesis and is mediated through ertapenem binding to penicillin binding proteins (PBPs). In <i>Escherichia coli</i>, it has strong affinity toward PBPs 1a, 1b, 2, 3, 4 and 5 with preference for PBPs 2 and 3. Ertapenem is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, and cephalosporinases and extended spectrum beta-lactamases. Ertapenem is hydrolyzed by metallo-beta-lactamases.",The molecular weight is 475.52.,Ertapenem has a topological polar surface area of 156.27.,The log p value of  is -1.82.,Ertapenem is approved and investigational.,Ertapenem is a solid.,True
20361,"An RNA synthesis inhibitor that is used as an antiviral agent in the prophylaxis and treatment of influenza. For the prophylaxis and treatment of illness caused by various strains of influenza A virus in adults. Rimantadine, a cyclic amine, is a synthetic antiviral drug and a derivate of adamantane, like a similar drug amantadine. Rimantadine is inhibitory to the in vitro replication of influenza A virus isolates from each of the three antigenic subtypes (H1N1, H2H2 and H3N2) that have been isolated from man. Rimantadine has little or no activity against influenza B virus. Rimantadine does not appear to interfere with the immunogenicity of inactivated influenza A vaccine. The mechanism of action of rimantadine is not fully understood. Rimantadine appears to exert its inhibitory effect early in the viral replicative cycle, possibly inhibiting the uncoating of the virus. The protein coded by the M2 gene of influenza A may play an important role in rimantadine susceptibility.",The molecular weight is 179.31.,Rimantadine has a topological polar surface area of 26.02.,The log p value of  is 3.96.,Rimantadine is approved and investigational.,Rimantadine is a solid.,True
20362,"Magnesium oxide is an inorganic compound that occurs in nature as the mineral periclase. In aqueous media combines quickly with water to form magnesium hydroxide. It is used as an antacid and mild laxative and has many nonmedicinal uses. Indicated for over-the-counter use as a supplement for cardiovascular and neuromuscular health, and as an antacid for relief of acid indigestion and upset stomach. The term \Milk of Magnesia\"" was first used to describe a white aqueous, mildly alkaline suspension of magnesium hydroxide formulated at about 8%w/v. Milk of magnesia is primarily used to alleviate constipation, but can also be used to relieve indigestion and heartburn. When taken internally by mouth as a laxative, the osmotic force of the magnesia suspension acts to draw fluids from the body and to retain those already within the lumen of the intestine, serving to distend the bowel, thus stimulating nerves within the colon wall, inducing peristalsis and resulting in evacuation of colonic contents. Magnesium supplements have also been shown to reduce platelet aggregation by inhibiting in the influx of calcium, a crucial component of platelet aggregation.""",The molecular weight is 40.3.,Magnesium oxide has a topological polar surface area of 17.07.,,Magnesium oxide is approved.,Magnesium oxide is a solid.,True
20363,,The molecular weight is 98.14.,Methylpentynol has a topological polar surface area of 20.23.,The log p value of  is 0.89.,Methylpentynol is experimental.,,False
20364,,The molecular weight is 237.1.,Carbromal has a topological polar surface area of 72.19.,The log p value of  is 1.62.,Carbromal is experimental.,,False
20365,"Sertaconazole nitrate is an antifungal medication of the imidazole class. It is available in topical formulations for the treatment of skin infections such as athlete's foot. For the topical treatment of interdigital tinea pedis in immunocompetent patients 12 years of age and older, caused by <i>Trichophyton rubrum</i>, <i>Trichophyton mentagrophytes</i>, and <i>Epidermophyton floccosum</i>. Sertaconazole is an imidazole/triazole type antifungal agent. Sertaconazole is a highly selective inhibitor of fungal cytochrome P-450 sterol C-14 &alpha;-demethylation via the inhibition of the enzyme cytochrome P450 14&alpha;-demethylase. This enzyme converts lanosterol to ergosterol, and is required in fungal cell wall synthesis. The subsequent loss of normal sterols correlates with the accumulation of 14 &alpha;-methyl sterols in fungi and may be partly responsible for the fungistatic activity of fluconazole. Mammalian cell demethylation is much less sensitive to fluconazole inhibition. Sertaconazole exhibits <i>in vitro</i> activity against <i>Cryptococcus neoformans</i> and <i>Candida spp.</i> Fungistatic activity has also been demonstrated in normal and immunocompromised animal models for systemic and intracranial fungal infections due to <i>Cryptococcus neoformans</i> and for systemic infections due to Candida albicans. Sertaconazole interacts with 14-&alpha; demethylase, a cytochrome P-450 enzyme necessary to convert lanosterol to ergosterol. As ergosterol is an essential component of the fungal cell membrane, inhibition of its synthesis results in increased cellular permeability causing leakage of cellular contents. Sertaconazole may also inhibit endogenous respiration, interact with membrane phospholipids, inhibit the transformation of yeasts to mycelial forms, inhibit purine uptake, and impair triglyceride and/or phospholipid biosynthesis.",The molecular weight is 437.76.,Sertaconazole has a topological polar surface area of 27.05.,The log p value of  is 6.16.,Sertaconazole is approved and investigational.,Sertaconazole is a solid.,True
20366,"Haloprogin is used as a topical ointment or cream in the treatment of Tinea infections. Tinea infections are superficial fungal infections caused by three species of fungi collectively known as dermatophytes (Trichophyton, Microsporum and Epidermophyton). Commonly these infections are named for the body part affected, including tinea corporis (general skin), tinea cruris (groin), and tinea pedis (feet). Haloprogin is a halogenated phenolic ether administered topically for dermotaphytic infections. The mechanism of action is unknown, but it is thought to be via inhibition of oxygen uptake and disruption of yeast membrane structure and function. Haloprogin is no longer available in the United States and has been discontinued.  Used to treat fungal (Tinea) skin infections such as athlete's foot, jock itch, ringworm, and tinea versicolor. Used as a topical ointment or cream in the treatment of Tinea infections. Tinea infections are superficial fungal infections caused by three species of fungi collectively known as dermatophytes (Trichophyton, Microsporum and Epidermophyton). Commonly these infections are named for the body part affected, including tinea corporis (general skin), tinea cruris (groin), and tinea pedis (feet). Haloprogin is a halogenated phenolic ether administered topically for dermotaphytic infections. The mechanism of action is unknown, but is thought to be via inhibition of oxygen uptake and disruption of yeast membrane structure and function. There is a higher incidence of cutaneous side effects with haloprogin, including irritation, burning, vesiculation (blisters), scaling, and itching. It is generally used when the infection is unresponsive to other antifungals.",The molecular weight is 361.38.,Haloprogin has a topological polar surface area of 9.23.,The log p value of  is 5.1.,Haloprogin is approved and withdrawn.,Haloprogin is a solid.,True
20367,"Tolnaftate is a synthetic over-the-counter anti-fungal agent. It may come as a cream, powder, spray, or liquid aerosol, and is used to treat jock itch, athlete's foot and ringworm. It is sold under several brand names, most notably Tinactin and Odor Eaters. Tolnaftate topical is used to treat skin infections such as athlete's foot, jock itch, and ringworm infections. Tolnaftate is also used, along with other antifungals, to treat infections of the nails, scalp, palms, and soles of the feet. The powder and powder aerosol may be used to prevent athlete's foot. Tolnaftate is a synthetic over-the-counter anti-fungal agent. Tolnaftate is a topical fungicide. Though its exact mechanism unknown, it is believed to prevent ergosterol biosynthesis by inhibiting squalene epoxidase. It has also been reported to distort the hyphae and to stunt mycelial growth in susceptible organisms.",The molecular weight is 307.41.,Tolnaftate has a topological polar surface area of 12.47.,The log p value of  is 5.34.,Tolnaftate is approved and investigational and vet_approved.,Tolnaftate is a solid.,True
20368,"Clioquinol was withdrawn in 1983 due to neurotoxicity. Used as a topical antifungal treatment. Clioquinol is a broad-spectrum antibacterial with antifungal properties. Application of clioquinol to extensive or eroded areas of the skin may lead to increased protein-bound iodine (PBI) levels within 1 week. In addition, elevated PBI levels may occur when relatively small areas of the skin are treated with clioquinol for more than 1 week. Clioquinol is bacteriostatic, however, the precise mechanism of its action is unknown.",The molecular weight is 305.5.,Clioquinol has a topological polar surface area of 33.12.,The log p value of  is 3.73.,Clioquinol is approved and vet_approved and withdrawn.,Clioquinol is a solid.,True
20369,"Undecylenate, or undecylenic acid, is an unsaturated fatty acid with a terminal double bond that is derived from castor oil. Undecylenic acid is also found naturally in the human sweat. It is used as a precursor in the manufacture of aromatic chemicals, polymers or modified silicones. Undecylenic acid was first isolated from the products of distillation of castor oil in 1877 via pyrolysis of ricinoleic acid, and has been polymerized for vinyl production. It it suggested that many organic fatty acids exert fungicidal or fungistatic actions. Undecylenic acid also possesses antifungal properties, but is never used on its own for antifungal purposes. Salts of undecylenate are found in topical over-the-counter or mixture products as antifungal agents. Zinc undecylenate is an example of a topical antifungal agent that treats skin infections such as athlete’s foot and relieves itching, burning, and irritation associated with the skin condition. Due to its bifunctional properties, undecylenate is also used as a linking molecule to conjugate other biomolecules such as proteins. It serves as an acid moiety for anabolic steroid boldenone. Indicated for the treatment of fungal infections as a salt form. No therapeutic indications on its own. Zinc undecylendate acts as a fungistatic agent but fungicidal activity may be observed with chronic exposure in high concentrations. It is effective against _Candida albicans_. It is proposed that undecylenic acid exerts antimicrobial actions via interacting with nonspecific components in the cell membrane.  Undecylenic acid demonstrated effectiveness against _Candida albicans_, which is an opportunistic pathogenic yeast with two cellular morphologies: the round yeast form and the filamentous form with elongated hyphae. Hyphae formation is associated with active infections and virulence. A study proposed that undecylenic acid inhibits biofilm formation of _Candida albicans_ with optimal concentration above 3 mM and disrupts hyphal growth, which is the morphological transition from yeast to filamentous phase, at concentration above 4 mM. Under the drug treatment, hyphal formation related genes, like HWP1, were significantly reduced in transcriptional level leading to poor biofilm formation. Both biofilm and hyphae formation are critical virulence factors for the initiation of skin infection and late development of disseminated infection. Undecylenic acid may also inhibit enzyme involved in lipid metabolism and abolish germ tube formation by carrying protons across the plasma membrane, thus altering cytoplasmic pH.",The molecular weight is 184.28.,Undecylenic acid has a topological polar surface area of 37.3.,The log p value of  is 4.08.,Undecylenic acid is approved and investigational.,Undecylenic acid is a solid.,True
20370,"Oxitropium has been investigated for the treatment of Pulmonary Disease, Chronic Obstructive.",The molecular weight is 332.42.,Oxitropium has a topological polar surface area of 59.06.,The log p value of  is -1.94.,Oxitropium is investigational.,,True
20371,Neltenexine is an elastase inhibitor. It may be useful for preventing pulmonary emphysema.,The molecular weight is 488.24.,Neltenexine has a topological polar surface area of 61.36.,The log p value of  is 2.22.,Neltenexine is experimental.,,True
20372,Vonoprazan has been used in trials studying the treatment of Erosive Esophagitis.,The molecular weight is 345.39.,Vonoprazan has a topological polar surface area of 63.99.,The log p value of  is 2.54.,Vonoprazan is investigational.,,True
20373,,The molecular weight is 435.01.,Chlorbenzoxamine has a topological polar surface area of 15.71.,The log p value of  is 6.81.,Chlorbenzoxamine is experimental.,,False
20374,,The molecular weight is 294.35.,Troxipide has a topological polar surface area of 68.82.,The log p value of  is 0.78.,Troxipide is experimental.,,False
20375,"Aluminum hydroxide is an inorganic salt used as an antacid. It is a basic compound that acts by neutralizing hydrochloric acid in gastric secretions. Subsequent increases in pH may inhibit the action of pepsin. An increase in bicarbonate ions and prostaglandins may also confer cytoprotective effects. For relief of heartburn and acid indigestion.  Gastric-peptic disease occurs as a result of an imbalance between protective factors, such as mucus, bicarbonate, and prostaglandin secretion, and aggressive factors, such as hydrochloric acid, pepsin, and Helicobacter pylori (H. pylori). Antacids work by restoring acid-base balance, attenuating the pepsin activity and increasing bicarbonate and prostaglandin secretion.  Aluminum hydroxide is a basic inorganic salt that acts by neutralizing hydrochloric acid in gastric secretions. Aluminum hydroxide is slowly solubilized in the stomach and reacts with hydrochloric acid to form aluminum chloride and water. It also inhibits the action of pepsin by increasing the pH and via adsorption. Cytoprotective effects may occur through increases in bicarbonate ion (HCO<sub>3</sub><sup>-</sup>) and prostaglandins.",The molecular weight is 78.0.,Aluminum hydroxide has a topological polar surface area of 60.69.,,Aluminum hydroxide is approved and investigational.,Aluminum hydroxide is a solid.,True
20376,"Magnesium hydroxide is an inorganic compound. It is naturally found as the mineral brucite. Magnesium hydroxide can be used as an antacid or a laxative in either an oral liquid suspension or chewable tablet form.  Magnesium hydroxide can be used as an antacid or a laxative depending on the administered dose. As an antacid, magnesium hydroxide suspension neutralizes gastric acid by reacting with hydrochloric acid in the stomach to form magnesium chloride and water. It is practically insoluble in water and does not have any effect until it reacts with the hydrochloric acid in the stomach. There, it decreases the direct acid irritant effect and increases the pH in the stomach leading to inactivation of pepsin. Magnesium hydroxide enhances the integrity of the mucosal barrier of the stomach as well as improving the tone of both the gastric and esophageal sphincters.  The suspension of magnesium hydroxide is ingested and enters the stomach. According to the amount ingested, the magnesium hydroxide will either act as an antacid or a laxative. ",The molecular weight is 58.32.,Magnesium hydroxide has a topological polar surface area of 40.46.,,Magnesium hydroxide is approved and investigational.,Magnesium hydroxide is a solid.,True
20377,"Benzoyl peroxide (BPO) is an organic compound in the peroxide family. It is formed by two benzoyl groups which are connected by a peroxide link. It is one of the most important organic peroxides in terms of applications. In medicine, benzoyl peroxide is used as a topical treatment for acne, either in combination with antibiotics or as a single agent. These products are available over-the-counter or by prescription in gels, creams or liquids at concentrations of 2.5%, 5% or 10%. Benzoyl peroxide is also used for bleaching flour or hair, teeth whitening, for cross-linking polyester resins, and many other chemical uses. It is on the World Health Organization's List of Essential Medicines, the most important medications needed in a basic health system. Benzoyl peroxide is indicated for the treatment of mild to moderate acne vulgaris and rosacea. Combined with other agents, it may be used in the treatment of more severe acne. Benzoyl peroxide acts as an antibacterial, irritant, keratolytic, comedolytic, and anti-inflammatory agent when applied topically to the human epithelium.  Benzoyl peroxide decomposes to release oxygen after topical application. This oxygen acts as a bactericidal agent towards Proprionibacterium acnes, the bacteria present in acne vulgaris. Benzoyl peroxide also increases the turnover rate of epithelial cells, thereby peeling the skin and promoting the resolution of comedones. ",The molecular weight is 242.23.,Benzoyl peroxide has a topological polar surface area of 52.6.,The log p value of  is 2.78.,Benzoyl peroxide is approved.,Benzoyl peroxide is a solid.,True
20378,"Trioxsalen (trimethylpsoralen, trioxysalen or trisoralen) is a furanocoumarin and a psoralen derivative obtained from several plants, mainly Psoralea corylifolia. Like other psoralens it causes photosensitization of the skin. It is administered either topically or orally in conjunction with UV-A (the least damaging form of ultraviolet light) for phototherapy treatment of vitiligo and hand eczema. The photoactivated form produces interstrand linkages in DNA resulting in cell apoptosis. In research it can be conjugated to dyes for confocal microscopy and used to visualize sites of DNA damage. The compound is has been explored for development of antisense oligonucleotides that can be cross-linked specifically to a mutant mRNA sequence without affecting normal transcripts differing at even a single base pair. Trioxsalen is a pigmenting photosensitizing agent used in conjunction with ultraviolet light in the treatment of vitiligo. Trioxsalen ispharmacologically inactive but when exposed to ultraviolet radiation or sunlight it is converted to its active metabolite to produce a beneficial reaction affecting the diseased tissue. After photoactivation it creates interstrand cross-links in DNA, which can cause programmed cell death.",The molecular weight is 228.25.,Trioxsalen has a topological polar surface area of 39.44.,The log p value of  is 3.47.,Trioxsalen is approved.,Trioxsalen is a solid.,True
20379,"Methyl aminolevulinate is a prodrug that is metabolised to Protoporphyrin IX (a photosensitizer) used in photodynamic therapy. For topical use, in combination with 570 to 670 nm wavelength red light illumination, in the treatment of non-hyperkeratotic actinic keratoses of the face and scalp in immunocompetent patients when used in conjunction with lesion preparation (debridement using a sharp dermal curette). After topical application of methyl aminolevulinate, porphyrins will accumulate intracellularly in the treated skin lesions. The intracellular porphyrins (including PpIX) are photoactive, fluorescing compounds and, upon light activation in the presence of oxygen, singlet oxygen is formed which causes damage to cellular compartments, in particular the mitochondria. Light activation of accumulated porphyrins leads to a photochemical reaction and thereby phototoxicity to the light-exposed target cells. Photosensitization following application of methyl aminolevulinate cream occurs through the metabolic conversion of methyl aminolevulinate (prodrug) to photoactive porphyrins (PAP), which accumulates in the skin lesions to which the cream has been applied. When exposed to light of appropriate wavelength and energy, the accumulated photoactive porphyrins produce a photodynamic reaction, resulting in a cytotoxic process dependent upon the simultaneous presence of oxygen. The absorption of light results in an excited state of porphyrin molecules, and subsequent spin transfer from photoactive porphyrins to molecular oxygen generates singlet oxygen, which can further react to form superoxide and hydroxyl radicals.",The molecular weight is 145.16.,Methyl aminolevulinate has a topological polar surface area of 69.39.,The log p value of  is -0.67.,Methyl aminolevulinate is approved and investigational.,Methyl aminolevulinate is a solid.,True
20380,"Trichloroacetate, or trichloroacetic acid, is a strong acid prepared by the reaction of chlorine with acetic acid in the presence of a suitable catalyst. In clinical chemistry and biochemistry, it is used as a precipitant of macromolecules including proteins, DNA and RNA. Trichloroacetate is also found in cosmetic treatments and topical formulations as a cauterant, which removes condyloma or warts on the skin.",The molecular weight is 163.38.,Trichloroacetate has a topological polar surface area of 37.3.,The log p value of  is 1.68.,Trichloroacetate is approved.,,True
20381,"An antioxidant flavonoid, occurring especially in woody plants as both (+)-catechin and (-)-epicatechin (cis) forms.",The molecular weight is 290.27.,Cianidanol has a topological polar surface area of 110.38.,The log p value of  is 0.53.,Cianidanol is approved and withdrawn.,Cianidanol is a solid.,True
20382,"Benzoin is a white crystalline compound prepared by condensation of benzaldehyde in potassium cyanide, and is used in organic syntheses. This should not be confused with benzoin gum from STYRAX (see ). Benzoin is an FDA-approved colour additive used for marking fruits and vegetables. No approved therapeutic indications. ",The molecular weight is 212.25.,Benzoin has a topological polar surface area of 37.3.,The log p value of  is 2.38.,Benzoin is approved and experimental.,Benzoin is a solid.,True
20383,"Mequinol is a phenol used in various applications. It is used as an inhibitor for acrylic monomers and acrylonitirles, as a stabilizer for chlorinated hydrocarbons and ethyl cellulose, as an ultraviolet inhibitor, as a chemical intermediate in the manufacture of antioxidants, pharmaceuticals, plasticizers, and dyestuffs. It is found as an active ingredient in topical drugs used for skin depigmentation indicated for the treatment of solar lentigines. Mequinol is currently primarily available only as an active ingredient in combination products combined with tretinoin that are indicated for the treatment of solar lentigines and related hyperpigmented lesions resulting from chronic sun exposure. Mequinol is in fact considered a melanocytotoxic chemical which when oxidized in melanocytes results in the formation of toxic entities like quinones. Such cytotoxic compounds subsequently have the potential to damage and destroy pigment cells, therefore causing skin depigmentation. In response, skin cells are naturally capable of protecting themselves against such cytotoxic agents with the help of endogenous intracellular glutathione and the detoxification action of glutathione S-transferase on the cytotoxic compounds. Regardless, it is consequently by way of this seemingly negative and damaging pharmacodynamic profile by which the mechanism of action of mequinol is sometimes described. Solar lentigines and related hyperpigmented lesions are localized, pigmented, macular lesions of the skin, usually on the areas of the body which have been chronically exposed to sunlight. These lesions are characterized by increased numbers of active melanocytes and increased melanin production.",The molecular weight is 124.14.,Mequinol has a topological polar surface area of 29.46.,The log p value of  is 1.57.,Mequinol is approved.,,True
20384,"Mebanazine, also known as _Actomol_, is a monoamine oxidase inhibitor (MAOI) belonging to the _hydrazine_ class of chemicals. It was used in the past as an antidepressant in the 1960s, but has since been discontinued because of its hepatotoxic potential. For the treatment of depression.",The molecular weight is 136.2.,Mebanazine has a topological polar surface area of 38.05.,The log p value of  is 1.01.,Mebanazine is withdrawn.,Mebanazine is a solid.,True
20385,"Iproclozide is an irreversible and selective hydrazine class based monoamine oxidase inhibitor (MAOI). Although it was employed as an antidepressant for a time, the fact that the agent is capable of causing fulminant hepatitis and that its use has been documented as the cause for at least three reported fatalities has resulted ultimately in the agent being discontinued. For the treatment of depression.",The molecular weight is 242.7.,Iproclozide has a topological polar surface area of 50.36.,The log p value of  is 2.06.,Iproclozide is withdrawn.,Iproclozide is a solid.,True
20386,"Opipramol has been used in trials studying the treatment of Dementia, Depression, Schizophrenia, Anxiety Disorders, and Psychosomatic Disorders.",The molecular weight is 363.5.,Opipramol has a topological polar surface area of 29.95.,The log p value of  is 3.79.,Opipramol is investigational.,,True
20387,Demexiptiline is marketed under the names Deparon or Tinoran. It is a tricyclic antidepressant which acts primarily as a norepinephrine reuptake inhibitor.,The molecular weight is 278.36.,Demexiptiline has a topological polar surface area of 33.62.,The log p value of  is 3.05.,Demexiptiline is experimental.,Demexiptiline is a solid.,True
20388,,The molecular weight is 418.97.,Lofepramine has a topological polar surface area of 23.55.,The log p value of  is 7.29.,Lofepramine is experimental.,,False
20389,"Caroxazone is an antidepressant that has been withdrawn from the market. It is a reversible monoamine oxidase inhibitor (MAOI) of both A and B monoamine oxidase subtypes. However, it presents a five-fold preference for the MAO-B subtype. For the treatment of depression.",The molecular weight is 206.2.,Caroxazone has a topological polar surface area of 72.63.,The log p value of  is 0.2.,Caroxazone is withdrawn.,Caroxazone is a solid.,True
20390,"A highly fluorescent anti-infective dye used clinically as a topical antiseptic and experimentally as a mutagen, due to its interaction with DNA. It is also used as an intracellular pH indicator.",The molecular weight is 194.24.,Aminacrine has a topological polar surface area of 38.91.,The log p value of  is 3.09.,Aminacrine is experimental.,Aminacrine is a solid.,True
20391,"Silver sulfadiazine is a sulfa derivative topical antibacterial used primarily on second- and third-degree burns. Indicated as an adjunct for the prevention and treatment of wound sepsis in patients with second- and third-degree burns. Silver sulfadiazine has broad antimicrobial activity. It is bactericidal for many gram- negative and gram-positive bacteria as well as being effective against yeast. Silver sulfadiazine is not a carbonic anhydrase inhibitor and may be useful in situations where such agents are contraindicated. Studies utilizing radioactive micronized silver sulfadiazine, electron microscopy, and biochemical techniques have revealed that the mechanism of action of silver sulfadiazine on bacteria differs from silver nitrate and sodium sulfadiazine. Silver sulfadiazine acts only on the cell membrane and cell wall to produce its bactericidal effect. A specific mechanism of action has not been determined, but silver sulfadiazine's effectiveness may possibly be from a synergistic interaction, or the action of each component. Silver is a biocide, which binds to a broad range of targets. Silver ions bind to nucleophilic amino acids, as well as sulfhydryl, amino, imidazole, phosphate, and carboxyl groups in proteins, causing protein denaturation and enzyme inhibition. ",The molecular weight is 357.14.,,,Silver sulfadiazine is approved and vet_approved.,Silver sulfadiazine is a solid.,True
20392,"Sulfacytine is a short-acting sulfonamide. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of p-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Used orally in the treatment of acute urinary tract infections. Sulfacytine is a short-acting sulfonamide. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of p-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus. Sulfacytine is a competitive inhibitor of the enzyme dihydropteroate synthetase. It inhibits bacterial synthesis of of dihydrofolic acid by preventing the condensation of the pteridine with para-aminobenzoic acid (PABA), a substrate of the enzyme dihydropteroate synthetase. The inhibited reaction is necessary in these organisms for the synthesis of folic acid.",The molecular weight is 294.33.,Sulfacytine has a topological polar surface area of 104.86.,The log p value of  is -0.33.,Sulfacytine is approved.,Sulfacytine is a solid.,True
20393,"Verteporfin, marketed as Visudyne, is a benzoporphyrin derivative. It is used as a photosensitizer in photodynamic therapy to eliminate abnormal blood vessels in wet form macular degeneration. Verteporfin accumulates in these abnormal blood vessels and, when stimulated by nonthermal red light with a wavelength of 693 nm in the presence of oxygen, produces highly reactive short-lived singlet oxygen and other reactive oxygen radicals, resulting in local damage to the endothelium and blockage of the vessels. For the treatment of patients with predominantly classic subfoveal choroidal neovascularization due to age-related macular degeneration, pathologic myopia or presumed ocular histoplasmosis syndrome. Verteporfin can also be used to destroy tumors. Verteporfin, otherwise known as benzoporphyrin derivative, is a medication used in conjunction with laser treatment to eliminate the abnormal blood vessels in the eye associated with conditions such as the wet form of macular degeneration. Verteporfin accumulates in these abnormal blood vessels and, when stimulated by nonthermal red light with a wavelength of 693 nm in the presence of oxygen, produces highly reactive short-lived singlet oxygen and other reactive oxygen radicals, resulting in local damage to the endothelium and blockage of the vessels. Verteporfin is transported in the plasma primarily by lipoproteins. Once verteporfin is activated by light in the presence of oxygen, highly reactive, short-lived singlet oxygen and reactive oxygen radicals are generated. Light activation of verteporfin results in local damage to neovascular endothelium, resulting in vessel occlusion. Damaged endothelium is known to release procoagulant and vasoactive factors through the lipo-oxygenase (leukotriene) and cyclo-oxygenase (eicosanoids such as thromboxane) pathways, resulting in platelet aggregation, fibrin clot formation and vasoconstriction. Verteporfin appears to somewhat preferentially accumulate in neovasculature, including choroidal neovasculature. However, animal models indicate that the drug is also present in the retina. As singlet oxygen and reactive oxygen radicals are cytotoxic, Verteporfin can also be used to destroy tumor cells.",The molecular weight is 1437.61.,Verteporfin has a topological polar surface area of 173.56.,,Verteporfin is approved and investigational.,Verteporfin is a solid.,True
20394,Sulfabenzamide is an antimicrobial agent often used in conjunction with sulfathiazole and sulfacetamide as a topical intravaginal antibacterial preparation.,The molecular weight is 276.31.,Sulfabenzamide has a topological polar surface area of 89.26.,The log p value of  is 1.76.,Sulfabenzamide is approved.,,True
20395,"A starch found in the tubers and roots of many plants. Since it is hydrolyzable to fructose, it is classified as a fructosan. It has been used in physiologic investigation for determination of the rate of glomerular function. Historically used in an important medical test of renal function, specifically a measure of glomerular filtration rate. Sometimes used to help relieve symptoms of diabetes mellitus - a condition characterised by hyperglycemia and/or hyperinsulinemia. The inulin test is a procedure by which the filtering capacity of the glomeruli (the main filtering structures of the kidney) is determined by measuring the rate at which inulin, the test substance, is cleared from blood plasma. Inulin is one of the more suitable and accurate substance to measure because it is a small, inert polysaccharide molecule that readily passes through the glomeruli. The inulin clearance test is performed by injecting inulin, waiting for it to be distributed, and then measuring plasma and urine inulin concentrations by various assays. As nutraceutical agents inulins may have antitumor, antimicrobial, hypolipidemic and hypoglycemic actions. They may also help to improve mineral absorption and balance and may have antiosteoporotic activity. As a diagnostic agent, inulin is readily soluble and essentially indigestible. It readily passes through the blood and into the urine. It is neither secreted nor resorbed by the kidney making it an excellent indicator for renal clearance rates. The inulin clearance test has largely been succeeded by the creatinine clearance test as a measure of glomerular filtration rate. ",,,,Inulin is approved and investigational and nutraceutical.,Inulin is a solid.,True
20396,"Calcium lactate is a salt that consists of two lactate anions for each calcium cation (Ca2+). It is prepared commercially by the neutralization of lactic acid with calcium carbonate or calcium hydroxide. Approved by the FDA as a direct food substance affirmed as generally recognized as safe, calcium lactate is used as a firming agent, flavoring agent, leavening agent, stabilizer, and thickener. Calcium lactate is also found in daily dietary supplements as a source of calcium. It is also available in various hydrate forms, where calcium lactate pentahydrate is the most common. Indicated for use as the nutritional supplement.  Both components of calcium lactate, calcium ion and lactic acid, play essential roles in the human body as a skeletal element an energy source, respectively.  In aqueous environments such as the gastrointestinal (GI) tract, calcium lactate will dissociate into calcium cation and lactic acid anions, the conjugate base of lactic acid. Lactic acid is a naturally-occurring compound that serves as fuel or energy in mammals by acting as an ubiquitous intermediate in the metabolic pathways. Lactic acid diffuses through the muscles and is transported to the liver by the bloodstream to participate in gluconeogenesis. ",The molecular weight is 218.22.,Calcium lactate has a topological polar surface area of 60.36.,,Calcium lactate is approved and investigational and vet_approved.,Calcium lactate is a solid.,True
20397,"Pantothenic acid, also called pantothenate or vitamin B5 (a B vitamin), is a water-soluble vitamin discovered by Roger J. Williams in 1919. For many animals, pantothenic acid is an essential nutrient as it is required to synthesize coenzyme-A (CoA), as well as to synthesize and metabolize proteins, carbohydrates, and fats. Pantothenic acid is the amide between pantoic acid and β-alanine and commonly found as its alcohol analog, the provitamin panthenol, and as calcium pantothenate. Small quantities of pantothenic acid are found in nearly every food, with high amounts in whole-grain cereals, legumes, eggs, meat, royal jelly, avocado, and yogurt. Pantothenic acid is an ingredient in some hair and skin care products. Only the dextrorotatory (D) isomer of pantothenic acid possesses biological activity. while the levorotatory (L) form may antagonize the effects of the dextrorotatory isomer. Studied for the treatment of many uses such as treatment of testicular torsion, diabetic ulceration, wound healing, acne, obesity, diabetic peripheral polyneuropathy. It has also been investigated for its hypolipidemic effects and as cholesterol lowering agent. Pantothenic acid is used in the synthesis of coenzyme A (CoA). CoA is thought to act as a carrier molecule, allowing the entry of acyl groups into cells. This is of critical importance as these acyl groups are used as substrates in the tricarboxylic acid cycle to generate energy and in the synthesis of fatty acids, cholesterol, and acetylcholine. Additionally, CoA is part of acyl carrier protein (ACP), which is required in the synthesis of fatty acids in addition to CoAs use as a substrate.  Pantothenic acid is incorporated into COENZYME A and protects cells against peroxidative damage by increasing the level of GLUTATHIONE.",The molecular weight is 219.24.,Pantothenic acid has a topological polar surface area of 106.86.,The log p value of  is -1.49.,Pantothenic acid is approved and nutraceutical and vet_approved.,Pantothenic acid is a solid.,True
20398,"A monocyclic beta-lactam antibiotic originally isolated from Chromobacterium violaceum. It is resistant to beta-lactamases and is used in gram-negative infections, especially of the meninges, bladder, and kidneys. It may cause a superinfection with gram-positive organisms. For the treatment of the following infections caused by susceptible gram-negative microorganisms: urinary tract infections, lower respiratory tract infections, septicemia, skin and skin-structure infections, intra-abdominal infections, and gynecologic infections. Aztreonam is a monocyclic beta-lactam antibiotic (a monobactam) originally isolated from <i>Chromobacterium violaceum</i>. Aztreonam exhibits potent and specific activity in vitro against a wide spectrum of gram-negative aerobic pathogens including <i>Pseudomonas aeruginosa</i>. It has no useful activity against gram-positive bacteria or anaerobes, but has very broad spectrum against gram-negative aerobes, including <i>Pseudomonas aeruginosa</i>. This has given it the nickname \the magic bullet for aerobic gram-negative bacteria\"". Aztreonam, unlike the majority of beta-lactam antibiotics, does not induce beta-lactamase activity and its molecular structure confers a high degree of resistance to hydrolysis by beta-lactamases (such as penicillinases and cephalosporinases) produced by most gram-negative and gram-positive pathogens; it is, therefore, usually active against gram-negative aerobic microorganisms that are resistant to antibiotics hydrolyzed by beta-lactamases. It is active against many strains that are multiply-resistant to other antibiotics, such as certain cephalosporins, penicillin, and aminoglycosides. Aztreonam maintains its antimicrobial activity over a pH range of 6 to 8 in vitro, as well as in the presence of human serum and under anaerobic conditions."" The bactericidal action of aztreonam results from the inhibition of bacterial cell wall synthesis due to a high affinity of aztreonam for penicillin binding protein 3 (PBP3). By binding to PBP3, aztreonam inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins. It is possible that aztreonam interferes with an autolysin inhibitor.",The molecular weight is 435.43.,Aztreonam has a topological polar surface area of 201.58.,The log p value of  is 0.34.,Aztreonam is approved.,Aztreonam is a solid.,True
20399,"Magnesium chloride salts are highly soluble in water and the hydrated form of magnesium chloride can be extracted from brine or sea water. Magnesium chloride is used in several medical and topical (skin related) applications. Magnesium chloride usp, anhydrous uses as electrolyte replenisher, pharmaceutic necessity for hemodialysis and peritoneal dialysis fluids. Magnesium is important as a cofactor in many enzymatic reactions in the body involving protein synthesis and carbohydrate metabolism (at least 300 enzymatic reactions require magnesium). Actions on lipoprotein lipase have been found to be important in reducing serum cholesterol and on sodium/potassium ATPase in promoting polarization (eg, neuromuscular functioning). Mechanism of action of magnesium chloride studied in 10 adult volunteers. Results suggested magnesium ion in duodenum is relatively weak stimulus to pancreas and gall bladder. It is weak stimulant to cholecystokinin release and inhibits net jejunal water absorption.",The molecular weight is 95.21.,,,Magnesium chloride is approved.,,True
20400,"Dipotassium phosphate (K2HPO4) is a highly water-soluble salt often used as a fertilizer and food additive as a source of phosphorus and potassium as well as a buffering agent. Dipotassium phosphate is used in imitation dairy creamers, dry powder beverages, mineral supplements, and starter cultures as an additive. It is used in non-dairy creamers to prevent coagulation. Dipotassium phosphate is also used to make buffer solutions and it is used in the production of trypticase soy agar which is used to make agar plates for culturing bacteria. Phosphate is a major intracellular anion which participates in providing energy for metabolism of substances and contributes to important metabolic and enzymatic reactions in almost all organs and tissues. Phosphate exerts a modifying influence on calcium concentrations, a buffering effect on acid-base equilibrium, and has a major role in the renal excretion of hydrogen ions. Once phosphate gains access to the body fluids and tissues, it exerts little pharmacological effect. If the ion is introduced into the intestine, the absorbed phosphate is rapidly excreted. If large amounts are given by this route, much of it may escape absorption. Because this property leads to a cathartic action, phosphate salts are employed as mild laxatives.",The molecular weight is 174.17.,Dipotassium phosphate has a topological polar surface area of 83.42.,,Dipotassium phosphate is approved.,,True
20401,"An oligosaccharide antibiotic produced by various streptomyces.  For the treatment of acute and chronic intestinal amebiasis (it is not effective in extraintestinal amebiasis). Also for the management of hepatic coma as adjunctive therapy. Paromomycin is a broad spectrum aminoglycoside antibiotic produced by <i>Streptomyces rimosus</i> var. paromomycinus. The in vitro and in vivo antibacterial action of paromomycin closely parallels that of neomycin. Paromomycin inhibits protein synthesis by binding to 16S ribosomal RNA. Bacterial proteins are synthesized by ribosomal RNA complexes which are composed of 2 subunits, a large subunit (50s) and small (30s) subunit, which forms a 70s ribosomal subunit. tRNA binds to the top of this ribosomal structure. Paramomycin binds to the A site, which causes defective polypeptide chains to be produced. Continuous production of defective proteins eventually leads to bacterial death.",The molecular weight is 615.63.,Paromomycin has a topological polar surface area of 347.32.,The log p value of  is -6.52.,Paromomycin is approved and investigational.,Paromomycin is a solid.,True
20402,"An antitubercular agent that inhibits the transfer of mycolic acids into the cell wall of the tubercle bacillus. It may also inhibit the synthesis of spermidine in mycobacteria. The action is usually bactericidal, and the drug can penetrate human cell membranes to exert its lethal effect. (From Smith and Reynard, Textbook of Pharmacology, 1992, p863) For use, as an adjunct, in the treatment of pulmonary tuberculosis. Ethambutol is an oral chemotherapeutic agent which is specifically effective against actively growing microorganisms of the genus Mycobacterium, including <i>M. tuberculosis</i>. Ethambutol inhibits RNA synthesis and decreases tubercle bacilli replication. Nearly all strains of <i>M. tuberculosis</i> and <i>M. kansasii</i> as well as a number of strains of MAC are sensitive to ethambutol. Ethambutol inhibits arabinosyl transferases which is involved in cell wall biosynthesis. By inhibiting this enzyme, the bacterial cell wall complex production is inhibited. This leads to an increase in cell wall permeability.",The molecular weight is 204.31.,Ethambutol has a topological polar surface area of 64.52.,The log p value of  is 0.12.,Ethambutol is approved.,Ethambutol is a solid.,True
20403,"Almasilate is a buffering antacid that has been used in peptic ulcers and dyspepsia. It is a crystalline polyhydrate of aluminium/magnesium silicate and mediates its buffering activity by binding hydrogen ions within the polymer. However its therapeutic efficacy is not comparable to other approved antacids, as it is no more effective in neutralizing acid and binding bile salts than other conventional antacids. Almasilate is indicated for use as an antacid for the neutralization of excess stomach acid. It is subsequently also used for the symptomatic treatment of diseases where it is necessary to neutralize acid in the stomach, for example, for treating stomach and duodenal ulcers or heartburn and stomach conditions caused by excess stomach acid. Various non-prescription antacid products are available to the general public to purchase and use as a treatment for relieving the occasional, limited, and non-severe sensation of heartburn (or acid indigestion) that may frequently be associated with stomach indigestion (or dyspepsia) or gastroesophageal reflux disease (when stomach contents may rise back up into the esophagus and cause a taste of acid in the back of the mouth, among other symptoms). Almasilate is a crystalline polyhydrate of aluminum/magnesium silicate and mediates its buffering activity by binding hydrogen ions within the polymer. Specifically, the aluminosilicate minerals dissolve, and in doing so consume acidic hydrogen ions and release moieties like H4SiO4, Al3+, and other cations, including the magnesium associated with the compound. Almasilate consequently contributes to the overall acid-neutralization by consuming acid hydrogen ion in this way. Additionally, aluminum and other metals released from the original compound may also accumulate into secondary aluminum and magnesium based antacid like products that can act as secondary pH buffers.",The molecular weight is 262.43.,Almasilate has a topological polar surface area of 27.69.,,Almasilate is approved and experimental.,,True
20404,"Sulbactam is a β-lactamase inhibitor given in combination with β-lactam antibiotics to inhibit β-lactamase, an enzyme produced by bacteria that destroys antibiotic activity. Sulbactam is currently available in combination products with ampicillin. Within this formulation it is indicated for the treatment of infections due to susceptible strains of the designated microorganisms in the conditions listed below. Sulbactam is an irreversible inhibitor of β-lactamase; by binding and inhibiting β-lactamase produced by bacterial cells, sulbactam is thereby able to prevent it from reducing antibiotic activity. Although sulbactam alone possesses little useful antibacterial activity, except against the Neisseriaceae, whole organism studies have shown that sulbactam restores ampicillin activity against beta-lactamase producing strains. In particular, sulbactam has good inhibitory activity against the clinically important plasmid mediated beta-lactamases most frequently responsible for transferred drug resistance. The presence of sulbactam in formulations with ampicillin effectively extends the antibacterial spectrum of ampicillin to include many bacteria normally resistant to it and to other beta-lactam antibacterials. Thus, products with ampicillin + sulbactam possess the properties of a broad-spectrum antibacterial and a beta-lactamase inhibitor.",The molecular weight is 233.24.,Sulbactam has a topological polar surface area of 91.75.,The log p value of  is 0.31.,Sulbactam is approved.,Sulbactam is a solid.,True
20405,"The chemical compound calcium acetate is the calcium salt of acetic acid. It has been commonly referred to as the acetate of lime. The anhydrous form is very hygroscopic, therefore the monohydrate is the common form. Calcium acetate is one of a number of calcium salts used to treat hyperphosphatemia (too much phosphate in the blood) in patients with kidney disease. Patients with advanced renal insufficiency (creatinine clearance less than 30 ml/min) exhibit phosphate retention and some degree of hyperphosphatemia. The retention of phosphate plays a pivotal role in causing secondary hyperparathyroidism associated with osteodystrophy, and soft-tissue calcification. The mechanism by which phosphate retention leads to hyperparathyroidism is not clearly delineated. Therapeutic efforts directed toward the control of hyperphosphatemia include reduction in the dietary intake of phosphate, inhibition of absorption of phosphate in the intestine with phosphate binders, and removal of phosphate from the body by more efficient methods of dialysis. The rate of removal of phosphate by dietary manipulation or by dialysis is insufficient. Dialysis patients absorb 40% to 80% of dietary phosphorus. Therefore, the fraction of dietary phosphate absorbed from the diet needs to be reduced by using phosphate binders in most renal failure patients on maintenance dialysis. Calcium acetate when taken with meals combines with dietary phosphate to form insoluble calcium phosphate which is excreted in the feces. Maintenance of serum phosphorus below 6.0 mg/dl is generally considered as a clinically acceptable outcome of treatment with phosphate binders. Calcium acetate is highly soluble at neutral pH, making the calcium readily available for binding to phosphate in the proximal small intestine. Calcium acetate and other calcium salts are phosphate binders. They work by binding with the phosphate in the food you eat, so that it is eliminated from the body without being absorbed.",The molecular weight is 158.17.,Calcium acetate has a topological polar surface area of 40.13.,,Calcium acetate is approved and investigational.,Calcium acetate is a solid.,True
20406,"One of the penicillins which is resistant to penicillinase but susceptible to a penicillin-binding protein. It is inactivated by gastric acid so administered by injection. Used to treat infections caused by susceptible Gram-positive bacteria, particularly beta-lactamase-producing organisms such as <i>Staphylococcus aureus</i> that would otherwise be resistant to most penicillins. Meticillin (INN, BAN) or methicillin (USAN) is a narrow spectrum beta-lactam antibiotic of the penicillin class. It is no longer clinically used. Its role in therapy has been largely replaced by flucloxacillin and dicloxacillin, however the term methicillin-resistant <i>Staphylococcus aureus</i> (MRSA) continues to be used to describe <i>Staphylococcus aureus</i> strains resistant to all penicillins. Similar to other beta-lactam antimicrobials, meticillin blocks synthesis of the bacterial cell wall. Meticillin stops cross-linkage between the peptidoglycan polymer chains, which make up a large portion of gram-positive bacterial cell walls. It does this by binding to and competitively inhibiting the transpeptidase enzyme used by bacteria to cross-link the peptide (D-alanyl-alanine) used in peptidogylcan synthesis.",The molecular weight is 380.42.,Meticillin has a topological polar surface area of 105.17.,The log p value of  is 1.78.,Meticillin is approved and investigational.,Meticillin is a solid.,True
20407,"Kanamycin (also known as kanamycin A) is an aminoglycoside bacteriocidal antibiotic, available in oral, intravenous, and intramuscular forms, and used to treat a wide variety of infections. Kanamycin is isolated from the bacterium Streptomyces kanamyceticus and its most commonly used form is kanamycin sulfate. For treatment of infections where one or more of the following are the known or suspected pathogens: <i>E. coli</i>, <i>Proteus</i> species (both indole-positive and indole-negative), <i>E. aerogenes, K. pneumoniae, S. marcescens,</i> and <i>Acinetobacter</i> species. Kanamycin is an aminoglycoside antibiotic. Aminoglycosides work by binding to the bacterial 30S ribosomal subunit, causing misreading of t-RNA, leaving the bacterium unable to synthesize proteins vital to its growth. Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. In addition, some mycobacteria, including the bacteria that cause tuberculosis, are susceptible to aminoglycosides. Infections caused by Gram-positive bacteria can also be treated with aminoglycosides, but other types of antibiotics are more potent and less damaging to the host. In the past the aminoglycosides have been used in conjunction with penicillin-related antibiotics in streptococcal infections for their synergistic effects, particularly in endocarditis. Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses. Aminoglycosides like kanamycin \irreversibly\"" bind to specific 30S-subunit proteins and 16S rRNA. Specifically Kanamycin binds to four nucleotides of 16S rRNA and a single amino acid of protein S12. This interferes with decoding site in the vicinity of nucleotide 1400 in 16S rRNA of 30S subunit. This region interacts with the wobble base in the anticodon of tRNA. This leads to interference with the initiation complex, misreading of mRNA so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes.""",The molecular weight is 484.5.,Kanamycin has a topological polar surface area of 282.61.,The log p value of  is -3.88.,Kanamycin is approved and investigational and vet_approved.,Kanamycin is a solid.,True
20408,"Netilmicin is a semisynthetic 1-N-ethyl derivative of sisomycin, an aminoglycoside antibiotic with action similar to gentamicin, but less ear and kidney toxicity. Netilmicin inhibits protein synthesis in susceptible organisms by binding to the bacterial 30S ribosomal subunit and interfering with mRNA binding and the acceptor tRNA site. The bactericidal effect of netilmiicin is not fully understood. For the treatment of bacteremia, septicaemia, respiratory tract infections, skin and soft-tissue infection, burns, wounds, and peri-operative infections caused by susceptible strains. Netilmicin is a semisynthetic, water soluble antibiotic of the aminoglycoside group, produced by the fermentation of Micromonospora inyoensis, a species of actinomycete. Aminoglycosides are useful primarily in infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. It is active at low concentrations against a wide variety of pathogenic bacteria including <i>Escherichia coli</i>, bacteria of the <i>Klebsiella-Enterobacter-Serratia </i>group, <i>Citrobacter </i>sp., <i>Proteus </i>sp. (indole-positive and indole-negative), including <i>Proteus mirabilis</i>, <i>P. morganii, P. rettgrei, P. vulgaris, Pseudomonas aeruginosa </i>and <i>Neisseria gonorrhoea</i>. Netilmicin is also active <i>in vitro </i>against isolates of <i>Hemophilus influenzae, Salmonella </i>sp., <i>Shigella </i>sp. and against penicillinase and non-penicillinase-producing <i>Staphylococcus </i>including methicillin-resistant strains. Some strains of <i>Providencia </i>sp., <i>Acinetobacter </i>sp. and <i>Aeromonas </i>sp. are also sensitive to netilmicin. Many strains of the above organisms which are found to be resistant to other aminoglycosides, such as kanamycin, gentamicin, tobramycin and sisomicin, are susceptible to netilmicin <i>in vitro</i>. Occasionally, strains have been identified which are resistant to amikacin but susceptible to netilmicin. The combination of netilmicin and penicillin G has a synergistic bactericidal effect against most strains of <i>Streptococcus faecalis</i> (enterococcus). The combined effect of netilmicin and carbenicillin or ticarcillin is synergistic for many strains of <i>Pseudomonas aeruginosa</i>. In addition, many isolates of <i>Serratia</i>, which are resistant to multiple antibiotics, are inhibited by synergistic combinations of netilmicin with carbenicillin, azlocillin, mezlocillin, cefamandole, cefotaxime or moxalactam. Aminoglycosides are mostly ineffective against anaerobic bacteria, fungi and viruses. Aminoglycosides like netilmicin \irreversibly\"" bind to specific 30S-subunit proteins and 16S rRNA. Specifically netilmicin binds to four nucleotides of 16S rRNA and a single amino acid of protein S12. This interferes with decoding site in the vicinity of nucleotide 1400 in 16S rRNA of 30S subunit. This region interacts with the wobble base in the anticodon of tRNA. This leads to interference with the initiation complex, misreading of mRNA so incorrect amino acids are inserted into the polypeptide leading to nonfunctional or toxic peptides and the breakup of polysomes into nonfunctional monosomes, leaving the bacterium unable to synthesize proteins vital to its growth.""",The molecular weight is 475.59.,Netilmicin has a topological polar surface area of 199.73.,The log p value of  is -2.39.,Netilmicin is approved and investigational.,Netilmicin is a solid.,True
20409,"Procaine benzylpenicillin (INN), also known as procaine G penicillin, is an injectable antiobiotic. It is a poorly soluble salt form of penicillin which is a combination of naturally occuring benzylpenicillin (penicillin G) and the local anaesthetic agent procaine in equimolar amounts. Procaine benzylpenicillin is administered by deep intramuscular injection. It is slowly absorbed and hydrolyzed to benzylpenicillin. This drug is used where prolonged exposure to benzylpenicillin at a low concentration is required. This combination is aimed at reducing the pain and discomfort associated with a large intramuscular injection of penicillin. It is widely used in veterinary settings. Benzylpenicillin is active against a wide range of organisms and is the drug of first choice for many infections. For the treatment of a number of bacterial infections such as syphilis, anthrax, mouth infections, pneumonia and diphtheria.  It is an antibiotic against penicillin-susceptible microorganisms with bactericidal effect. Like all penicillins, procaine benzylpenicillin interferes with the synthesis of the bacterial cell wall peptidoglycan. It acts through the inhibition of biosynthesis of cell-wall peptidoglycan, rendering the cell wall osmotically unstable. It is part of the penicillin and beta lactam family of antibacterial drugs.  Procaine benzylpenicillin is hydrolyzed into penicillin G once it is released from the injection site. Penicillin G attaches to the penicillin-binding proteins on bacterial cell wall and inhibit the transpeptidation enzyme that crosslinks the peptide chains attached to the backbone of the peptidoglycan. The final bactericidal event involves the inactivation of an inhibitor of autolytic enzymes in the cell wall, leading to lysis of the bacterium. ",The molecular weight is 570.71.,Procaine benzylpenicillin has a topological polar surface area of 86.71.,,Procaine benzylpenicillin is approved and vet_approved.,Procaine benzylpenicillin is a solid.,True
20410,"Semisynthetic ampicillin-derived acylureido penicillin. It has been proposed for infections with certain anaerobes and may be useful in inner ear, bile, and CNS infections. Used to treat serious gram&ndash;negative infections of the lungs, urinary tract, and skin. Mezlocillin is a penicillin beta-lactam antibiotic used in the treatment of bacterial infections caused by susceptible, usually gram-positive, organisms. The name \penicillin\"" can either refer to several variants of penicillin available, or to the group of antibiotics derived from the penicillins. Mezlocillin has <i>in vitro</i> activity against gram-positive and gram-negative aerobic and anaerobic bacteria. The bactericidal activity of mezlocillin results from the inhibition of cell wall synthesis and is mediated through mezlocillin binding to penicillin binding proteins (PBPs). Mezlocillin is stable against hydrolysis by a variety of beta-lactamases, including penicillinases, and cephalosporinases and extended spectrum beta-lactamases. Mezlocillin can be used to treat susceptible strains of <i>H. influenzae</i>, <i>Klebsiella</i> species, <i>Pseudomonas</i> species, <i>Proteus mirabilis</i>, <i>E. coli</i>, <i>Enterobacter</i> species, <i>Streptococcus faecelis</i>, <i>Peptococcus</i> species, <i>Peptostreptococcus</i> species, <i>Bacteriodes</i> species (including <i>B. fragilis</i>), <i>Morganella morganii</i>, <i>Serratia</i> species, <i>N. gonorrhoeae</i>, <i>P. vulgaris</i>, and <i>Providencia rettgeri</i>. This drug is discontinued in the U.S."" By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, mezlocillin inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that mezlocillin interferes with an autolysin inhibitor.",The molecular weight is 539.58.,Mezlocillin has a topological polar surface area of 173.5.,The log p value of  is 1.5.,Mezlocillin is approved and investigational.,Mezlocillin is a solid.,True
20411,"Bacampicillin is a prodrug of ampicillin and is microbiologically inactive. It is absorbed following oral administration. During absorption from the gastrointestinal tract, bacampicillin is hydrolyzed by esterases present in the intestinal wall. It is microbiologically active as ampicillin, and exerts a bactericidal action through the inhibition of the biosynthesis of cell wall mucopeptides. It is used to cure infection of upper and lower respiratory tract; skin and soft tissue; urinary tract and acute uncomplicated gonococcal urethritis etc. For infections at the following sites: upper and lower respiratory tract; skin and soft tissue; urinary tract and acute uncomplicated gonococcal urethritis, when due to sensitive strains of the following organisms: Gram-positive: streptococci (including <i>S. faecalis</i> and <i>S. pneumoniae</i>) and nonpenicillinase-producing staphylococci; Gram-negative: <i>H. influenzae</i>, <i>N. gonorrhoeae</i>, <i>E. coli</i>, <i>P. mirabilis</i>, <i>Salmonellae</i> and <i>Shigellae</i>. Bacampicillin is a prodrug of ampicillin and is microbiologically inactive. During absorption from the gastrointestinal tract, bacampicillin is hydrolyzed by esterases present in the intestinal wall. It is microbiologically active as ampicillin, and exerts a bactericidal action through the inhibition of the biosynthesis of cell wall mucopeptides.",The molecular weight is 465.52.,Bacampicillin has a topological polar surface area of 137.26.,The log p value of  is 2.06.,Bacampicillin is approved and investigational.,Bacampicillin is a solid.,True
20412,"Amikacin is a semi-synthetic aminoglycoside antibiotic that is derived from kanamycin A. Amikacin is synthesized by acylation with the l-(-)-γ-amino-α-hydroxybutyryl side chain at the C-1 amino group of the deoxystreptamine moiety of kanamycin A. The amikacin sulfate injection is indicated in the short-term treatment of serious bacterial infections due to susceptible strains of gram-negative bacteria, including Pseudomonas species, Escherichia coli, species of indole-positive and indole-negative Proteus, Providencia species, Klebsiella-Enterobacter-Serratia species, as well as Acinetobacter (Mima-Herellea) species. Amikacin is an aminoglycoside antibiotic. Aminoglycosides bind to the bacteria, causing misreading of t-RNA, leaving bacteria unable to synthesize proteins vital to their growth. Aminoglycosides are useful mainly in the treatment infections involving aerobic, Gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. In addition, some mycobacteria, including the bacteria that cause tuberculosis, are susceptible to aminoglycosides. Infections caused by Gram-positive bacteria can also be treated with aminoglycosides, however, other antibiotics may be more potent and less toxic to humans. The primary mechanism of action of amikacin is the same as that for all aminoglycosides. It binds to bacterial 30S ribosomal subunits and interferes with mRNA binding and tRNA acceptor sites, interfering with bacterial growth. This leads to disruption of normal protein synthesis and production of non-functional or toxic peptides. Other actions have been postulated for drugs of this class. Amikacin, as well as the rest of the aminoglycosides, are generally bacteriocidal against gram-positive and gram-negative bacteria.",The molecular weight is 585.61.,Amikacin has a topological polar surface area of 331.94.,The log p value of  is -4.12.,Amikacin is approved and investigational and vet_approved.,Amikacin is a solid.,True
20413,"Azlocillin is a semisynthetic ampicillin-derived acylureido penicillin. For the treatment of infections caused by <i>Pseudomonas aeruginosa</i>, <i>Escherichia coli</i>, and <i>Haemophilus influenzae</i>. Similar to and , azlocillin is an acylampicillin that exhibits an extended-spectrum of activity and _in vitro_ potency that is greater than that of the carboxy penicillins. Azlocillin is shown to be effective against a broad spectrum of bacteria, including <i>Pseudomonas aeruginosa</i> and enterococci.  By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, azlocillin inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that azlocillin interferes with an autolysin inhibitor.",The molecular weight is 461.49.,Azlocillin has a topological polar surface area of 148.15.,The log p value of  is 1.56.,Azlocillin is approved.,Azlocillin is a solid.,True
20414,"Cefoxitin is a semi-synthetic, broad-spectrum cepha antibiotic for intravenous administration. It is derived from cephamycin C, which is produced by <i>Streptomyces lactamdurans</i>. For the treatment of serious infections caused by susceptible strains microorganisms. Cefoxitin is a cephamycin antibiotic often grouped with the second-generation cephalosporins. It is active against a broad range of gram-negative bacteria including anaerobes. The methoxy group in the 7a position provides cefoxitin with a high degree of stability in the presence of beta-lactamases, both penicillinases and cephalosporinases, of gram-negative bacteria. The bactericidal action of cefoxitin results from inhibition of cell wall synthesis.",The molecular weight is 427.45.,Cefoxitin has a topological polar surface area of 148.26.,The log p value of  is -0.81.,Cefoxitin is approved.,Cefoxitin is a solid.,True
20415,"An antibiotic derived from penicillin similar to carbenicillin in action. For the treatment of bacterial infections. Ticarcillin is a semisynthetic antibiotic with a broad spectrum of bactericidal activity against many gram-positive and gram-negative aerobic and anaerobic bacteria. Ticarcillin is, however, susceptible to degradation by ß-lactamases, and therefore, the spectrum of activity does not normally include organisms which produce these enzymes. Ticarcillin's principal mechanism of action revolves around its capacity to prevent the cross-linking of peptidoglycan during bacterial cell wall synthesis. Consequently, when the offending bacteria attempt to undergo cell division, cell death occurs.",The molecular weight is 384.42.,Ticarcillin has a topological polar surface area of 124.01.,The log p value of  is 1.28.,Ticarcillin is approved and investigational and vet_approved.,Ticarcillin is a solid.,True
20416,"Telbivudine is a synthetic thymidine nucleoside analog with specific activity against the hepatitis B virus. Telbivudine is orally administered, with good tolerance, lack of toxicity and no dose-limiting side effects. For the treatment of chronic hepatitis B in adult and adolescent patients ≥16 years of age with evidence of viral replication and either evidence of persistent elevations in serum aminotransferases (ALT or AST) or histologically active disease. Telbivudine is a synthetic thymidine nucleoside analogue with activity against hepatitis B virus (HBV). Telbivudine is the unmodified β–L enantiomer of the naturally occurring nucleoside, thymidine. It undergoes phosphorylation via interaction with cellular kinases to form the active metabolite, telbivudine 5'-triphosphate. Telbivudine 5'–triphosphate inhibits HBV DNA polymerase (reverse transcriptase) by competing with the natural substrate, thymidine 5'–triphosphate. This leads to the chain termination of DNA synthesis, thereby inhibiting viral replication. Incorporation of telbivudine 5'–triphosphate into viral DNA also causes DNA chain termination, resulting in inhibition of HBV replication. Telbivudine inhibits anticompliment or second-strand DNA.",The molecular weight is 242.23.,Telbivudine has a topological polar surface area of 99.1.,The log p value of  is -1.38.,Telbivudine is approved and investigational.,Telbivudine is a solid.,True
20417,Magnesium citrate is a low volume and osmotic cathartic agent. The cathartic action works primarily through the high osmolarity of the solution which draws large amounts of fluid into space where is used. Magnesium citrate is considered by the FDA as an approved inactive ingredient for approved drug products under the specifications of oral administration of a maximum concentration of 237 mg. It is also considered as an active ingredient in over-the-counter products. Magnesium citrate has been used in bowel preparations prior to a colonoscopy as a cathartic agent.  The onset of action can be as early as 30 minutes after administration with a mean onset time of approximately 2 hours and a maximum action of 4 hours. The effect of magnesium citrate is highly dependent on the individual's hydration status. It mainly works through its property of high osmolality which will draw large amounts of fluid into the colonic lumen. There is also a possible stimulation of fluid excretion by cholecystokinin release and activation of muscle peristalsis.,The molecular weight is 451.11.,Magnesium citrate has a topological polar surface area of 140.62.,,Magnesium citrate is approved.,Magnesium citrate is a solid.,True
20418,"An aminoglycoside, broad-spectrum antibiotic produced by Streptomyces tenebrarius. It is effective against gram-negative bacteria, especially the pseudomonas species. It is a 10% component of the antibiotic complex, nebramycin, produced by the same species. For the treatment of pseudomonas aeruginosa lung infections. Also being investigated for use in the treatment of sinus infections. Tobramycin, an aminoglycoside antibiotic obtained from cultures of <i>Streptomyces tenebrarius</i>, is used in combination with other antibiotics to treat urinary tract infections, gynecologic infections, peritonitis, endocarditis, pneumonia, bacteremia and sepsis, respiratory infections including those associated with cystic fibrosis, osteomyelitis, and diabetic foot and other soft-tissue infections. It acts primarily by disrupting protein synthesis, leading to altered cell membrane permeability, progressive disruption of the cell envelope, and eventual cell death. Tobramycin has in vitro activity against a wide range of gram-negative organisms including <em>Pseudomonas aeruginosa</em>. Tobramycin binds irreversibly to one of two aminoglycoside binding sites on the 30 S ribosomal subunit, inhibiting bacterial protein synthesis. Tobramycin may also destabilize bacterial memebrane by binding to 16 S 16 S r-RNA. An active transport mechanism for aminoglycoside uptake is necessary in the bacteria in order to attain a significant intracellular concentration of tobramycin.",The molecular weight is 467.52.,Tobramycin has a topological polar surface area of 268.17.,The log p value of  is -3.44.,Tobramycin is approved and investigational.,Tobramycin is a solid.,True
20419,"Calcium supplements such as calcium gluceptate are taken by individuals who are unable to get enough calcium in their regular diet or who have a need for more calcium. They are used to prevent or treat several conditions that may cause hypocalcemia (not enough calcium in the blood). The body needs calcium to make strong bones. Calcium is also needed for the heart, muscles, and nervous system to work properly. For treatment of mild hypocalcemia due to neonatal tetany, tetany due to parathyroid deficiency or vitamin D deficiency, and alkalosis, as prophylaxis of hypocalcemia during exchange transfusions, in the treatment of intestinal malabsorption, and to replenish electrolytes. Calcium supplements such as calcium gluceptate are taken by individuals who are unable to get enough calcium in their regular diet or who have a need for more calcium. They are used to prevent or treat several conditions that may cause hypocalcemia (not enough calcium in the blood). The body needs calcium to make strong bones. Calcium is also needed for the heart, muscles, and nervous system to work properly. The bones serve as a storage site for the body's calcium. They are continuously giving up calcium to the bloodstream and then replacing it as the body's need for calcium changes from day to day. When there is not enough calcium in the blood to be used by the heart and other organs, your body will take the needed calcium from the bones. When you eat foods rich in calcium, the calcium will be restored to the bones and the balance between your blood and bones will be maintained. Calcium gluceptate replenishes the deminished levels of calcium in the body, returning them to normal levels.",The molecular weight is 490.42.,Calcium glucoheptonate has a topological polar surface area of 161.51.,,Calcium glucoheptonate is approved.,Calcium glucoheptonate is a solid.,True
20420,"Calcium glycerophosphate is a salt of glycerophosphoric acid that forms a white, fine, slightly hygroscopic powder. The commercial product is a mixture of calcium beta-, and D-, and L -alpha-glycerophosphate. By FDA, calcium glycerophosphate is considered a generally recognized as safe (GRAS) food ingredient as a nutrient supplement (source of calcium or phosphorus), or in food products such as gelatins, puddings, and fillings. It is also present in dental or oral hygiene products due to its cariostatic effects. It is suggested that calcium glycerophosphate promotes plaque-pH buffering, elevation of plaque and phosphate levels and direct interaction with dental mineral. Calcium glycerophosphate is found in OTC dental products such as toothpastes for the prevention of dental caries. As OTC products these do not have an official indication. It is thought that calcium glycerophosphate may act through a variety of mechanisms to produce an anti-caries effect. These include increasing acid-resistance of the enamel, increasing enamel mineralization, modifying plaque, acting as a pH-buffer in plaque, and elevating and phosphate levels.  Calcium glycerophosphate in combination with sodium monofluorophosphate was found to reduce the acid solubility of enamel. This is thought to be due to increased uptake of fluoride in a non-alkali soluble form at the expense of a fraction remaining in the alkali-soluble form of calcium fluoride. It is also thought that calcium glycerophosphate enhances the remineralization effect of sodium monofluorophosphate leading to greater remineralization of enamel but the mechanism behind this is unknown.",The molecular weight is 210.14.,Calcium glycerophosphate has a topological polar surface area of 112.88.,,Calcium glycerophosphate is approved.,Calcium glycerophosphate is a solid.,True
20421,"An antibiotic produced by Streptomyces fradiae. For the treatment of uncomplicated urinary tract infections (acute cystitis) in women due to susceptible strains of <i>Escherichia coli</i> and <i>Enterococcus faecalis</i>. Fosfomycin is a broad spectrum antibiotic that concentrates in kidney and bladder and is used to treat uncomplicated urinary tract infections. Fosfomycin also reduces nephrotoxicity and ototoxicity of platinum-containing anti-tumor agents. Fosfomycin is a phosphoenolpyruvate analogue produced by Streptomyces that irreversibly inhibits enolpyruvate transferase (MurA), which prevents the formation of N-acetylmuramic acid, an essential element of the peptidoglycan cell wall.",The molecular weight is 138.06.,Fosfomycin has a topological polar surface area of 70.06.,The log p value of  is -0.23.,Fosfomycin is approved.,Fosfomycin is a solid.,True
20422,"Meclocycline is under investigation in clinical trial NCT00385515 (Efficacy of SNX-1012 in the Treatment of Oral Mucositis). Currently under investigation for the topical treatment of ulcerative oral mucositis  Tetracyclines such as meclocycline are broad spectrum bacteriostatic agents. Meclocyclin likely inhibits the growth of bacterial species present in the damaged oral mucosa, allowing the immune system to more easily eliminate infections. As a tetracycline, meclocycline likely works by reversably associating with the 30s subint of the bacterial ribosome. A likely binding site for tetracyclines has been identified on protein S7 of this subunit. This association blocks the association of aminoacyl-tRNA with the ribosome, inhibiting protein synthesis. Ultimately this inhibits bacterial growth due to a lack of proteins necessary for reproduction.",The molecular weight is 476.87.,Meclocycline has a topological polar surface area of 181.62.,The log p value of  is 0.04.,Meclocycline is investigational.,Meclocycline is a solid.,True
20423,A member of the vitamin B complex. It used to be common in sunscreening agents until found to also be a sensitizer. The potassium salt is used therapeutically in fibrotic skin disorders.,The molecular weight is 137.14.,Aminobenzoic acid has a topological polar surface area of 63.32.,The log p value of  is 0.98.,Aminobenzoic acid is approved and experimental.,Aminobenzoic acid is a solid.,True
20424,"Magnesium trisilicate is an inorganic compound that is used as an antacid in the treatment of peptic ulcers. For the treatment of peptic ulcers. Magnesium trisilicate works by increasing the pH of gastric juice via a neutralisation reaction. It also precipitates colloidal silica, which can coat gastrointestinal mucosa conferring further protection. The gelatinous silicon dioxide, formed by the reaction of magnesium trisilicate with gastric contents is said to protect ulcerated mucosal surfaces and favor healing. ",The molecular weight is 260.86.,Magnesium trisilicate has a topological polar surface area of 144.84.,,Magnesium trisilicate is approved.,Magnesium trisilicate is a solid.,True
20425,Chromium picolinate has a chemical formula CrPic3 and reddish-pink color. It is a coordination complex consisting of chromium(III) and picolinic acid. Chromium picolinate is used as a nutritional supplement for optimal insulin function in patients with Type 2 diabetes or promotion of weight loss. Chromium ions are shown to regulate insulin by promoting glucose utilization and increasing the sensitivity of the insulin receptor.,The molecular weight is 418.3.,,,Chromium picolinate is approved.,,True
20426,"Trimethobenzamide is a novel antiemetic which prevents nausea and vomiting in humans. Its actions are unclear but most likely involves the chemoreceptor trigger zone (CTZ). In dogs pretreated with trimethobenzamide HCl, the emetic response to apomorphine is inhibited, while little or no protection is afforded against emesis induced by intragastric copper sulfate. For the treatment of postoperative nausea and vomiting and for nausea associated with gastroenteritis. Trimethobenzamide is a novel antiemetic which prevents nausea and vomiting in humans. Its actions are unclear but most likely involves the chemoreceptor trigger zone (CTZ). In dogs pretreated with trimethobenzamide HCl, the emetic response to apomorphine is inhibited, while little or no protection is afforded against emesis induced by intragastric copper sulfate. The mechanism of action of trimethobenzamide as determined in animals is obscure, but may involve the chemoreceptor trigger zone (CTZ), an area in the medulla oblongata through which emetic impulses are conveyed to the vomiting center; direct impulses to the vomiting center apparently are not similarly inhibited.",The molecular weight is 388.46.,Trimethobenzamide has a topological polar surface area of 69.26.,The log p value of  is 2.33.,Trimethobenzamide is approved and investigational.,Trimethobenzamide is a solid.,True
20427,"Cholestyramine or colestyramine is a bile acid sequestrant. Bile acid sequestrants are polymeric compounds which serve as ion exchange resins. Cholestyramine resin is quite hydrophilic, but insoluble in water. Indicated as adjunctive therapy to diet for the reduction of elevated serum cholesterol in patients with primary hypercholesterolemia (elevated low density lipoprotein cholesterol) who do not respond adequately to diet. Also for the relief of pruritus associated with partial biliary obstruction. Cholesterol is probably the sole precursor of bile acids. During normal digestion, bile acids are secreted into the intestines. A major portion of the bile acids is absorbed from the intestinal tract and returned to the liver via the enterohepatic circulation. Only very small amounts of bile acids are found in normal serum. Cholestyramine resin adsorbs and combines with the bile acids in the intestine to form an insoluble complex which is excreted in the feces. This results in a partial removal of bile acids from the enterohepatic circulation by preventing their absorption. Cholestyramine forms a resin that acts as a bile acid sequestrant to limit the reabsorption of bile acids in the gastrointestinal tract. Cholestyramine resin is a strong anion exchange resin, allowing it to exchange its chloride anions with anionic bile acids present in the gastrointestinal tract and form a strong resin matrix. Cholestyramine consists of a functional group, which is a quaternary ammonium group attached to an inert styrene-divinylbenzene copolymer, in the anion exchange resin.",The molecular weight is 1161.81.,,,Cholestyramine is approved and investigational.,Cholestyramine is a solid.,True
20428,"Cyclic peptide antibiotic similar to viomycin. It is produced by Streptomyces capreolus. Used in the treatment of tuberculosis in combination with other drugs. Capreomycin is a member of the aminoglycoside family of antibiotics. These antibiotics have the ability to kill a wide variety of bacteria, including bacteria responsible for causing tuberculosis (TB). Little is known about capreomycin's exact mechanism of action, but it is thought to inhibit protein synthesis by binding to the 70S ribosomal unit. Capreomycin also binds to components in the bacterial cell which result in the production of abnormal proteins. These proteins are necessary for the bacteria's survival. Therefore the production of these abnormal proteins is ultimately fatal to the bacteria.",The molecular weight is 1321.44.,Capreomycin has a topological polar surface area of 378.42.,,Capreomycin is approved.,Capreomycin is a solid.,True
20429,"Cyclic polypeptide antibiotic from Bacillus colistinus. It is composed of Polymyxins E1 and E2 (or Colistins A, B, and C) which act as detergents on cell membranes. Colistin is less toxic than Polymyxin B, but otherwise similar; the methanesulfonate is used orally. For the treatment of acute or chronic infections due to sensitive strains of certain gram-negative bacilli, particularly <i>Pseudomonas aeruginosa</i>. Colistin is a polymyxin antibiotic agent. Polymyxins are cationic polypeptides that disrupt the bacterial cell membrane through a detergentlike mechanism. With the development of less toxic agents, such as extended-spectrum penicillins and cephalosporins, parenteral polymyxin use was largely abandoned, except for the treatment of multidrug-resistant pulmonary infections in patients with cystic fibrosis. More recently, however, the emergence of multidrug-resistant gram-negative bacteria, such as <i>Pseudomonas aeruginosa</i> and <i>Acinetobacter baumannii</i>, and the lack of new antimicrobial agents have led to the revived use of the polymyxins. Colistin is a surface active agent which penetrates into and disrupts the bacterial cell membrane. Colistin is polycationic and has both hydrophobic and lipophilic moieties. It interacts with the bacterial cytoplasmic membrane, changing its permeability. This effect is bactericidal. There is also evidence that polymyxins enter the cell and precipitate cytoplasmic components, primarily ribosomes.",The molecular weight is 2324.94.,Colistin has a topological polar surface area of 490.66.,,Colistin is approved.,Colistin is a solid.,True
20430,Sodium monofluorophosphate is used in OTC dental preparations to help protect against cavities. Sodium monofluorophosphate is indicated for the treatment of cavities,The molecular weight is 143.95.,Sodium fluorophosphate has a topological polar surface area of 63.19.,,Sodium fluorophosphate is approved.,,True
20431,"Diiodohydroxyquinoline, also known as uidoquinol and iodoquinol, is a quinoline derivative that can be used in the treatment of amoebiasis. The exact mechanism of action is unknown. Iodoquinol is not currently available in any FDA-approved products. Used in the treatment of amoebiasis. Unknown.",The molecular weight is 396.95.,Diiodohydroxyquinoline has a topological polar surface area of 33.12.,The log p value of  is 4.14.,Diiodohydroxyquinoline is approved.,Diiodohydroxyquinoline is a solid.,True
20432,"Nandrolone, also known as 19-nortestosterone or 19-norandrostenolone, is a synthetic anabolic-androgenic steroid (AAS) derived from testosterone.",The molecular weight is 274.4.,Nandrolone has a topological polar surface area of 37.3.,The log p value of  is 2.89.,Nandrolone is experimental and investigational.,Nandrolone is a solid.,True
20433,"Anidulafungin or Eraxis is an anti-fungal drug manufactured by Pfizer that gained approval by the Food and Drug Administration (FDA) in February 21, 2006; it was previously known as LY303366. There is preliminary evidence that it has a similar safety profile to caspofungin. For use in the treatment of the following fungal infections: Candidemia and other forms of <i>Candida</i> infections (intra-abdominal abscess, and peritonitis), Aspergillus infections, and esophageal candidiasis. Also considered an alternative treatment for oropharyngeal canaidiasis. Anidulafungin is a semi-synthetic lipopeptide synthesized from a fermentation product of <i>Aspergillus nidulans</i>. Anidulafungin is an echinocandin, a class of antifungal drugs that inhibits the synthesis of 1,3-&beta;-D-glucan, an essential component of fungal cell walls. Anidulafungin is active in vitro against many <i>Candida</i>, as well as some <i>Aspergillus</i>. Like other echinocandins, anidulafungin is not active against <i>Cryptococcus neoformans</i>, <i>Trichosporon</i>, <i>Fusarium</i>, or zygomycetes. Anidulafungin is a semi-synthetic echinocandin with antifungal activity. Anidulafungin inhibits glucan synthase, an enzyme present in fungal, but not mammalian cells. This results in inhibition of the formation of 1,3-&beta;-D-glucan, an essential component of the fungal cell wall, ultimately leading to osmotic instability and cell death.",The molecular weight is 1140.25.,Anidulafungin has a topological polar surface area of 377.42.,The log p value of  is 2.2.,Anidulafungin is approved and investigational.,Anidulafungin is a solid.,True
20434,"An alkylating agent proposed as an antineoplastic. It also acts as a chemosterilant for male houseflies and other insects. For use as a single agent in the palliative treatment of patients with persistent or recurrent ovarian cancer following first-line therapy with a cisplatin and/or alkylating agent-based combination. Altretamine is a novel antineoplastic agent. The precise mechanism by which altretamine exerts its cytotoxic effect is unknown, although a number of theoretical possibilities have been studied. Structurally, altretamine resembles the alkylating agent triethylenemelamine, yet <i>in vitro</i> tests for alkylating activity of altretamine and its metabolitics have been negative. Altretamine has been demonstrated to be efficacious for certain ovarian tumors resistant to classical alkylating agents. Metabolism of altretamine is a requirement of cytotoxicity. Synthetic monohydroxymethylmelamines, and products of altretamine metabolism, <i>in vitro</i> and <i>in vivo</i>, can form covalent adducts with tissue macromolecules including DNA, but the relevance of these reactions to antitumor activity is unknown. The precise mechanism by which altretamine exerts its cytotoxic effect is unknown although it is classified as an alkylating anti-neoplastic agent. Through this mechanism, the drug is metabolized into alkylating agents by N-demethylation. These alkylating species consequently damage tumor cells.",The molecular weight is 210.28.,Altretamine has a topological polar surface area of 48.39.,The log p value of  is 1.66.,Altretamine is approved.,Altretamine is a solid.,True
20435,"Inotersen is a transthyretin-directed antisense oligonucleotide for the treatment of the polyneuropathy caused by hereditary transthyretin-mediated amyloidosis in adults. It was FDA approved in October 2018. Inotersen has been shown to improve the course of neurologic disease and quality of life in patients with hereditary transthyretin amyloidosis. Inotersen is a transthyretin-directed antisense oligonucleotide indicated for treatment of the polyneuropathy of hereditary transthyretin-mediated amyloidosis in adults.  The pharmacodynamic effects of inotersen were studied in hereditary transthyretin-mediated amyloidosis (hATTR) amyloidosis patients treated with 284 mg of inotersen via subcutaneous injection once weekly. With repeated dosing, the mean percentage decreases from baseline in serum TTR (transthyretin) from week 13 to Week 65 of treatment were measured from 68%-74% (median range: 75% to 79%). Similar TTR reductions were seen regardless of TTR mutation, sex, age, or race. Inotersen is an antisense oligonucleotide that causes degradation of mutant and wild-type TTR mRNA through binding to the TTR mRNA, which results in a reduction of serum TTR protein and TTR protein deposits in tissues.",,,,Inotersen is approved and investigational.,Inotersen is a solid.,True
20436,"Dexpanthenol is an alcohol derivative of pantothenic acid, a component of the B complex vitamins and an essential component of a normally functioning epithelium. Dexpanthenol is enzymatically cleaved to form pantothenic acid, which is an essential component of Coenzyme A, which acts as a cofactor in many enzymatic reactions that are important for protein metabolism in the epithelium.  Injection: Prophylactic use immediately after major abdominal surgery to minimize the possibility of paralytic ileus. Intestinal atony causing abdominal distention; postoperative or postpartum retention of flatus, or postoperative delay in resumption of intestinal motility; paralytic ileus. Pantothenic acid is a precursor of coenzyme A, which serves as a cofactor for a variety of enzyme-catalyzed reactions involving transfer of acetyl groups. The final step in the synthesis of acetylcholine consists of the choline acetylase transfer of acetyl group from acetylcoenzyme A to choline. Acetylcholine is the neurohumoral transmitter in the parasympathetic system and as such maintains the normal functions of the intestine. Decrease in acetylcholine content would result in decreased peristalsis and in extreme cases adynamic ileus.  Dexpanthenol is an alcohol derivative of pantothenic acid, a component of the B complex vitamins and an essential component of a normally functioning epithelium. Dexpanthenol is enzymatically cleaved to form pantothenic acid, which is an essential component of Coenzyme A, which acts as a cofactor in many enzymatic reactions that are important for protein metabolism in the epithelium. ",The molecular weight is 205.25.,Dexpanthenol has a topological polar surface area of 89.79.,The log p value of  is -1.65.,Dexpanthenol is approved.,,True
20437,"Ammonium lactate is the ammonium salt of lactic acid. For the treatment of dry, scaly skin (xerosis) and ichthyosis vulgaris and for temporary relief of itching associated with these conditions. Lactic acid is an alpha-hydroxy acid. It is a normal constituent of tissues and blood. The alpha-hydroxy acids (and their salts) may act as humectants when applied to the skin. This property may influence hydration of the stratum corneum. In addition, lactic acid, when applied to the skin, may act to decrease corneocyte cohesion. Unknown.",The molecular weight is 107.11.,Ammonium lactate has a topological polar surface area of 60.36.,,Ammonium lactate is approved.,Ammonium lactate is a solid.,True
20438,"Iron(III) oxide or ferric oxide is the inorganic compound with the formula Fe2O3. It is one of the three main oxides of iron, the other two being iron(II) oxide (FeO) the rarer form, and iron(II,III) oxide (Fe3O4) which naturally as magnetite.",The molecular weight is 159.69.,Ferric oxide has a topological polar surface area of 43.37.,,Ferric oxide is experimental.,Ferric oxide is a solid.,True
20439,"An analog of deoxyuridine that inhibits viral DNA synthesis. The drug is used as an antiviral agent. For use in keratoconjunctivitis and keratitis caused by herpes simplex virus. In chemical structure idoxuridine closely approximates the configuration of thymidine, one of the four building blocks of DNA (the genetic material of the Herpes virus). As a result, idoxuridine is able to replace thymidine in the enzymatic step of viral replication or \growth\"". The consequent production of faulty DNA results in a pseudostructure which cannot infect or destroy tissue. In short, by pre-empting a vital building block in the genetic material of the Herpes simplex virus, Herplex-D topical solution destroys the infective and destructive capacity of the viral material. The virus infected cell may only be attacked during the period of active synthesis of DNA. This occurs early in the development of the Herpes simplex lesion, but at different times in different cells. Therefore, ideally, the affected area should remain saturated with the antiviral agent."" Idoxuridine acts as an antiviral agent by inhibiting viral replication by substituting itself for thymidine in viral DNA. This in turn inhibits thymidylate phosphorylase and viral DNA polymerases from properly functioning. The effect of Idoxuridine results in the inability of the virus to reproduce or to infect/destroy tissue.",The molecular weight is 354.1.,Idoxuridine has a topological polar surface area of 99.1.,The log p value of  is -0.42.,Idoxuridine is approved and investigational.,Idoxuridine is a solid.,True
20440,,The molecular weight is 277.15.,Neridronic Acid has a topological polar surface area of 161.31.,The log p value of  is -4.58.,Neridronic Acid is experimental and investigational.,Neridronic Acid is a solid.,False
20441,"Brodalumab has been used in trials studying the treatment of Asthma, Psoriasis, Crohn's Disease, Psoriatic Arthritis, and Rheumatoid Arthritis. Brodalumab was FDA approved in February, 2017 as Siliq for the treatment of moderate-to-severe plaque psoriasis. Brodalumab has been approved for the treatment of psoriasis vulgaris, psoriatic arthritis, pustular psoriasis and psoriatic erythroderma.  Increase in the level of IL-17 due to blocking of its receptors.  Brodalumab binds with high affinity to interleukin (IL)-17 receptor A, thereby inhibiting several pro-inflammatory cytokines from the IL-17 family.",,,,Brodalumab is approved and investigational.,,True
20442,"Rebamipide has been investigated for the treatment of Stomach Ulcer, Keratoconjunctivitis Sicca, and Gastric Adenoma and Early Gastric Cancer.",The molecular weight is 370.79.,Rebamipide has a topological polar surface area of 95.5.,The log p value of  is 1.97.,Rebamipide is approved and investigational.,,True
20443,,The molecular weight is 340.44.,Poldine has a topological polar surface area of 46.53.,The log p value of  is 0.22.,Poldine is experimental.,,False
20444,,The molecular weight is 340.5.,Penthienate has a topological polar surface area of 46.53.,The log p value of  is -0.04.,Penthienate is experimental.,,False
20445,Ilaprazole has been investigated in Helicobacter Infections.,The molecular weight is 366.44.,Ilaprazole has a topological polar surface area of 72.8.,The log p value of  is 3.13.,Ilaprazole is investigational.,,True
20446,,The molecular weight is 634.51.,,,Hematin is experimental.,,False
20447,"Docusate, or dioctyl sulfosuccinate, is a stool softener indicated for the treatment of constipation. Docusate acts by increasing the amount of water the stool absorbs in the gut, making the stool softer and easier to pass. Docusate can be orally or rectally administered. Docusate is on the World Health Organization's List of Essential Medicines. However the effectiveness of docusate in treating constipation remains unclear, as several studies report docusate to be no more effective than placebo for increasing the frequency of stool or stool softening. Recently there has been pressure to stop prescribing docusate as it has been identified as an ineffective medicine. Additionally, it does not appear to lessen symptoms associated with constipation such as abdominal cramps. Still docusate is available in over-the-counter products as a common laxative. Indicated for the treatment of constipation associated with dry, hard stools or opioid induced constipation. Though recently, pressure has been building to end the use of docusate over concerns of efficacy. Docusate sodium is a laxative and an anionic detergent that supposedly promotes incorporation of water and fats into stool through a reduction in surface tension, resulting in softer fecal mass. Docusate's onset of action is 6-72 hours orally and 2-15 minutes rectally. The effects of docusate are thought to be exerted locally in the jejunum.  Recent studies suggest that docusate's mechanism of action is due largely to it's surfactant effect in the intestines, which allow fat and water into the feces to soften the stool.",The molecular weight is 422.58.,Docusate has a topological polar surface area of 106.97.,The log p value of  is 5.46.,Docusate is approved.,Docusate is a solid.,True
20448,Aceclidine has been marketed in Europe but has not been used clinically in the United States. It is used in the treatment of open-angle glaucoma and is a parasympathomimetic agent.,The molecular weight is 169.22.,Aceclidine has a topological polar surface area of 29.54.,The log p value of  is 0.74.,Aceclidine is approved.,,True
20449,,The molecular weight is 285.27.,Flunoxaprofen has a topological polar surface area of 63.33.,The log p value of  is 3.25.,Flunoxaprofen is experimental.,,False
20450,,The molecular weight is 844.45.,Proglumetacin has a topological polar surface area of 139.72.,The log p value of  is 6.72.,Proglumetacin is experimental.,,False
20451,"The use of benoxaprofen, formerly marketed as Oraflex tablets, was associated with fatal cholestatic jaundice among other serious adverse reactions. The holder of the approved application voluntarily withdrew Oraflex tablets from the market on August 5, 1982.",The molecular weight is 301.73.,Benoxaprofen has a topological polar surface area of 63.33.,The log p value of  is 3.82.,Benoxaprofen is approved and withdrawn.,Benoxaprofen is a solid.,True
20452,Iguratimod is under investigation in Rheumatoid Arthritis.,The molecular weight is 374.37.,Iguratimod has a topological polar surface area of 110.8.,The log p value of  is 1.93.,Iguratimod is investigational.,,True
20453,,The molecular weight is 320.75.,Tenidap has a topological polar surface area of 83.63.,The log p value of  is 2.3.,Tenidap is experimental.,,False
20454,"Mupirocin, formerly termed pseudomonic acid A, is a novel antibacterial agent with a unique chemical structure and mode of action apart from other antibiotic agents. Produced by fermentation using the organism _Pseudomonas fluorescens_, mupirocin is a naturally-occurring antibiotic that displays a broad-specturm activity against many gram-positive bacteria and certain gram-negative bacteria _in vitro_. It primarily works by inhibiting bacterial protein synthesis. Due to its unique mode of action of inhibiting the activity of bacterial isoleucyl-tRNA synthetase, mupirocin does not demonstrate cross-resistance with other classes of antimicrobial agents, giving it a therapeutic advantage. It is available in topical formulations only due to extensive systemic metabolism and is used in the treatment of impetigo caused by _Staphylococcus aureus_ and _Streptococcus pyogenes_ and traumatic skin lesions due to secondary skin infections caused by _S. aureus_ and _S. pyogenes_. There is also some clinical evidence that suggests the potential role of mupirocin in eradicating nasal carriage of Staphylococci when administered intranasally. Mupirocin is commonly marketed under the brand name Bactroban. Indicated for the treatment of impetigo and secondary skin infections, leading to traumatic skin lesions, due to _Staphylococcus aureus_ and _Streptococcus pyogenes_.  Mupirocin is reported to be active against susceptible aerobic gram-positive cocci, such as _Staphylococcus aureus_, _Staphylococcus epidermidis_, and other beta-hemolytic streptococci_Streptococcus pyogenes_. It mediates its antibacterial activity by inhibiting the bacterial protein synthesis and formation of bacterial proteins essential for survival. The minimum bactericidal concentration (MBC) against relevant pathogens is generally eight-fold to thirty-fold higher than the minimum inhibitory concentration (MIC). In one clinical study investigating the therapeutic effectiveness of topical mupirocin in impetigo, the therapeutic response rate was about 94 to 98% after one week following the end of therapy. In clinical studies of patients with primary and secondary skin infections, both elimination of the bacterial pathogen and clinical cure or improvement hav been demonstrated in over 90% of patients receiving topical mupirocin. Mupirocin resistance as high as 81% has been reported previously. Resistance to mupirocin, which occurs more frequently in methicillin-resistant than methicillin-susceptible staphylococci, may occur with the production of a modified isoleucyl-tRNA synthetase, or the acquisition of, by genetic transfer, a plasmid mediating a new isoleucyl-tRNA synthetase. Mupirocin specifically and reversibly binds to bacterial isoleucyl transfer-RNA (tRNA) synthetase, which is an enzyme that promotes the conversion of isoleucine and tRNA to isoleucyl-tRNA. Inhibition of this enzyme subsequently leads to the inhibition of the bacterial protein and RNA synthesis. Mupirocin is bacteriostatic at lower concentrations but it exerts bactericidal effects with prolonged exposure, killing 90-99% of susceptible bacteria over a 24 hour period.",The molecular weight is 500.63.,Mupirocin has a topological polar surface area of 146.05.,The log p value of  is 1.54.,Mupirocin is approved and investigational and vet_approved.,Mupirocin is a solid.,True
20455,Clopenthixol is a thioxanthene with therapeutic actions similar to the phenothiazine antipsychotics. It is an antagonist at D1 and D2 dopamine receptors.,The molecular weight is 400.97.,Clopenthixol has a topological polar surface area of 26.71.,The log p value of  is 4.13.,Clopenthixol is experimental.,,True
20456,"Daptomycin is a naturally-occurring lipopeptide antibiotic that kills susceptible gram positive bacteria by disrupting their membrane potential. It is found in the soil bacterium called <i>Streptomyces roseosporus</i>. Antibiotics are used in the treatment of infections caused by bacteria. They work by killing bacteria or preventing their growth. Daptomycin will not work for colds, flu, or other virus infections. It was approved in September 2003 for the treatment of complicated skin and soft tissue infections. It has a safety profile similar to other agents commonly administered to treat gram-positive infections. For the treatment of complicated skin and skin structure infections caused by susceptible strains of Gram-positive microorganisms. Daptomycin is a 13 member amino acid cyclic lipopeptide antibiotic active against Gram-positive bacteria only. It has proven in vitro activity against enterococci (including glycopeptide-resistant Enterococci (GRE)), staphylococci (including methicillin-resistant <i>Staphylococcus aureus</i>), streptococci and corynebacteria. Daptomycin is derived from the fermentation product of Streptomyces roseosporus.  Daptomycin appears to bind or insert into the outer membrane of gram positive bacteria. The binding and integration of daptomycin into the cell membrane is calcium dependent. Calcium ions cause a conformational change in daptomycin, augmenting its amphipathicity (hydrophilic head group and hydrophobic tail group), leading to incorporation into the cell membrane.",The molecular weight is 1620.69.,Daptomycin has a topological polar surface area of 702.02.,The log p value of  is -2.43.,Daptomycin is approved and investigational.,Daptomycin is a solid.,True
20457,Ozagrel has been used in trials studying the treatment of Dry Eye Syndromes.,The molecular weight is 228.25.,Ozagrel has a topological polar surface area of 55.12.,The log p value of  is 1.6.,Ozagrel is investigational.,,True
20458,"Pemirolast potassium is a slightly yellow powder that is soluble in water. It is a mast cell stabilizer that acts as an antiallergic agent. As an ophthalmic aqueous sterile solution, pemirolast is used for the prevention of itching of the eyes caused by allergies such as hay fever, and allergic conjunctivitis. Pemirolast is potentially useful for prophylaxis of pulmonary hypersensitivity reactions to drugs such as paclitaxel. For the prevention of itching of the eyes caused by allergies such as hay fever, and allergic conjunctivitis Pemirolast is used for the prophylactic treatment of itching of the eye associated with allergic conjunctivitis. Pemirolast potassium is a mast cell stabilizer that inhibits the <i>in vivo</i> Type I immediate hypersensitivity reaction. Pemirolast inhibits the antigen-induced release of inflammatory mediators (e.g., histamine, leukotriene C4, D4, E4) from human mast cells. Allergic reactions lead to cell-degranulation and the release of histamine (and other chemical mediators) from the mast cell or basophil. Once released, histamine can react with local or widespread tissues through histamine receptors. Histamine, acting on H<sub>1</sub>-receptors, produces pruritis and vasodilatation (allowing blood fluids to enter the area to cause swelling). Pemirolast is a histamine H1 antagonist. It competes with histamine for the normal H<sub>1</sub>-receptor sites on effector cells of blood vessels to provide effective, temporary relief of watery and itchy eyes. Pemirolast binds to the histamine H<sub>1</sub> receptor. This blocks the action of endogenous histamine, which subsequently leads to temporary relief of the negative symptoms brought on by histamine. Pemirolast has also been observed to inhibit antigen-stimulated calcium ion influx into mast cells through the blockage of calcium channels. Pemirolast inhibits the chemotaxis of eosinophils into ocular tissue, and prevents inflammatory mediator release from human eosinophils.",The molecular weight is 228.22.,Pemirolast has a topological polar surface area of 87.13.,The log p value of  is 0.57.,Pemirolast is approved and investigational.,Pemirolast is a solid.,True
20459,"Reproterol has been used in trials studying the treatment of Asthma, Exercise-Induced.",The molecular weight is 389.41.,Reproterol has a topological polar surface area of 131.16.,The log p value of  is -0.47.,Reproterol is investigational.,,True
20460,,The molecular weight is 929.16.,Atracurium has a topological polar surface area of 126.44.,The log p value of  is 3.5.,Atracurium is approved and experimental and investigational.,,False
20461,Cobamamide is one of the active forms of vitamin B12 that is also known as _adenosylcobalamin_ or _dibencozide_. This drug is available as a nutritional supplement to prevent vitamin B12 deficiency.,The molecular weight is 1579.61.,Cobamamide has a topological polar surface area of 608.02.,,Cobamamide is approved.,Cobamamide is a solid.,True
20462,,The molecular weight is 512.73.,Acetoxolone has a topological polar surface area of 80.67.,The log p value of  is 7.42.,Acetoxolone is experimental.,,False
20463,,The molecular weight is 276.38.,Mebhydrolin has a topological polar surface area of 8.17.,The log p value of  is 4.01.,Mebhydrolin is experimental.,,False
20464,,The molecular weight is 420.48.,Isoflupredone acetate has a topological polar surface area of 100.9.,The log p value of  is 1.8.,Isoflupredone acetate is vet_approved.,,False
20465,,The molecular weight is 293.41.,Quifenadine has a topological polar surface area of 23.47.,The log p value of  is 2.62.,Quifenadine is experimental.,,False
20466,"Lucinactant is a new synthetic peptide-containing surfactant for intratracheal use. It contains sinapultide, a novel, hydrophobic, 21-amino acid peptide (leucine and lysine repeating units, KL4 peptide) designed to mimic human surfactant protein-B (SB-P). More specifically, it mimics the C-terminal amphipathic helical domain of this protein. It also consists of phospholipids (dipalmitoylphosphatidylcholine, DPPC and palmitoyloleoyl phosphatidylglycerol, POPG) and a fatty acid (palmitic acid). It is completely devoid of animal-derived components. FDA approved on March 6, 2012. Intended for the prevention of respiratory distress syndrome (RDS) in premature infants at high risk for RDS.  Lucinactant is a new synthetic surfactant containing a protein that mimics human surfactant protein-B, is effective at preventing respiratory distress syndrome (RDS) and related complications in preterm infants. Lucinactant has been shown to have antiinflammatory properties, is resistant to proteolytic degradation and oxidation, and has no potential for transmitting animal-derived diseases. Lucinactant has proven safe and effective in the prevention of RDS in preterm infants and as a treatment for MAS in full-term infants and for adult ARDS. Pulmonary surfactant is a lipoprotein complex that is produced naturally in the lungs, where it lines the alveolar epithelium and serves to reduce surface tension, which facilitates alveoli expansion and allows gas exchange. Human surfactants contain phospholipids, predominantly dipalmitoylphosphatidylcholine (DPPC), in addition to surfactant proteins A, B, C and D. Surfactant is also a physical barrier to inhaled particle and noxious agents, enhances particle clearance, is involved in host defense against infection and possesses antiinflammatory properties. Several serious respiratory disorders have been associated with a loss or lack of endogenous surfactant. Lucinactant was designed to mimic the essential endogenous human surfactant protein B (SP-B). ",The molecular weight is 4209.96.,,,Lucinactant is approved and investigational.,Lucinactant is a liquid.,True
20467,"Colfosceril palmitate is a synthetic pulmonary surfactant administered in infants with respiratory distress syndrome. It was part of the first generation of commercially available artificial surfactants. It was developed by Burroughs Wellcome and it was FDA approved on August 6, 1990. Nowadays colfosceril palmitate is under the state of canceled post-marketing. Colfosceril palmitate is indicated for the treatment of respiratory distress syndrome (RDS) in premature infants. The official label is referred as a intratracheal suspension for prophylactic treatment of infants of less than 1350 grams of birth weight under risk of developing RDS, or in infants with birth weight greater than 1350 grams with pulmonary immaturity, or as rescue treatment of infants that already developed RDS. The central feature of RDS is a surfactant deficiency due to lung immaturity. This lung condition is more frequently presented due to risk factors like prematurity, delayed lung maturation caused by maternal diabetes or male gender, or surfactant dysfuntion due to perinatal asphyxia, pulmonary infection or delivery without labor. Colfosceril palmitate has shown to significantly reduce the risk of pneumothoraces, pulmonary interstitial emphysema and mortality. Unlike naturals surfactants, colfosceril palmitate reduces the risk of bronchopulmonary dysplasia, intraventricular hemorrhage and patent ductus arteriosus. In clinical placebo-controlled trials, there was a significant reduction in the number of deaths attributed to hyaline membrane disease, the incidence of pulmonary air leaks, oxygen requirements and mean airway pressure. Some reports have indicated a lack of therapeutic effect due to the absence of surfactant protein. Treatment with colfosceril palmitate aims to reinflate a collapsed area of the lung, improve compliance and reduce intrapulmonary shunting. The actions of colfosceril palmitate are perfomed by replacing the defficient or innefective endogenous lung surfactant and thus, reducing the tension and stabilizing the alveoli from collapsing. Colfosceril palmitate will form a very thin film that will cover the surface of the alveolar cells and therefore it will reduce surface tension.",The molecular weight is 734.05.,Colfosceril palmitate has a topological polar surface area of 111.19.,The log p value of  is 4.0.,Colfosceril palmitate is approved and investigational and withdrawn.,Colfosceril palmitate is a solid.,True
20468,"Cetyl alcohol, also known as 1-hexadecanol or n-hexadecyl alcohol, is a 16-C fatty alcohol with the chemical formula CH3(CH2)15OH. It can be produced from the reduction of palmitic acid. Cetyl alcohol is present in a waxy white powder or flake form at room temperature, and is insoluble in water and soluble in alcohols and oils. Discovered by Chevrenl in 1913, cetyl alcohol is one of the oldest known long-chain alcohol. It may be contained in cosmetic and personal care products such as shampoos, creams and lotions. Mainly it is used as an opacifier, emulsifier, and thickening agent that alter the thickness of the liquid, and increase and stabilize the foaming capacity. Due to its water-binding property, cetyl alcohol is commonly used as an emollient that prevents drying and chapping of the skin. According to the FDA Code of Federal Regulations, cetyl alcohol is a safe synthetic fatty acid in food and in the synthesis of food components under the condition that it contain not less than 98 percent of total alcohols and not less than 94 percent of straight chain alcohols. Cetyl alcohol is also listed in the OTC ingredient list as a skin protectant for skin irritations caused by poison ivy, oak, sumac, and insect bites or stings. Cetyl alcohol is reported to be a mild skin or eye irritant. No therapeutic indications in medicinal products. Indicated to be used as an indirect additive in food contact substances, or an ingredient in commercial or cosmetic products.  Cetyl alcohol exhibits skin protect properties against skin irritations caused by bites, rashes and stings. The inhibitory action of cetyl alcohol against the growth of _Mycoplasma gallisepticum_ and _Mycopiasma pneumoniae_ has been reported. Cetyl alcohol has hydrating properties that makes it a suitable emulsifier and stabilizer in pharmaceutical formulations. It is also present in washable ointment base due to its dispersant abilities and stabilizing properties. Potential antimicrobial activity of cetyl alcohol may be due to a change in cell membrane permeability that either blocks absorption of essential nutrients and induction of outward diffusion vital cellular components. This proposed mechanism of action is thought to be similar for other long-chain aliphatic alcohols with same antimicrobial activity, such as myristyl alcohol and behenyl alcohol. ",The molecular weight is 242.45.,Cetyl alcohol has a topological polar surface area of 20.23.,The log p value of  is 7.17.,Cetyl alcohol is approved.,Cetyl alcohol is a solid.,True
20469,"Calfactant is a sterile, non-pyrogenic lung surfactant intended for intratracheal instillation. It is an off-white suspension of an extract of natural surfactant from calf lungs suspended in 0.9% saline. Each milliliter of calfactant contains 35mg of phospholipids (including 26 mg phosphatidylcholine of which 16 mg is disaturated phosphatidylcholine) and 0.65mg of proteins including surfactant-associated proteins B and C. Calfactant is indicated for prophylaxis therapy to prevent respiratory distress syndrome (RDS) in premature infants <29 weeks of gestational age with low lung surfactant and at high risk for RDS. Calfactant therapy is also indicated for the treatment of respiratory distress syndrome in infants 72 hours or less of age with RDS confirmed by clinical and radiologic findings and requiring endotracheal intubation. Pulmonary surfactant is an endogenous substance produced in the lungs that functions to decrease surface tension at the air:fluid interface on the alveolar surface. In premature infants with pulmonary surfactant deficiency, surface tension can increase to the point where sections of lung collapse and respiratory distress syndrome (RDS) develops. Calfactant adsorbs rapidly to the surface of the alveolar air:fluid interface and modifies surface tension to a minimum of less than 3 mN/m. It acts in a manner similar to natural lung surfactant, thus preventing or treating respiratory distress syndrome.",,,,Calfactant is approved.,Calfactant is a liquid.,True
20470,"Poractant alfa is a pulmonary surfactant marketed as Curosurf in the United States and Canada. It is used to treat Respiratory Distress Syndrome (RDS) in premature infants with an endogenous pulmonary surfactant deficiency. Poractant alfa is an extract of natural porcine lung surfactant consisting of 99% polar lipids (mainly phospholipids) and 1% hydrophobic low molecular weight proteins (surfactant associated proteins SP-B and SP-C). The phospholipid content of the extract consists primarily of phosphatidylcholine and dipaImitoylphosphatidylcholine. Poractant alfa is a creamy white suspension of this extract in 0.9% sodium chloride solution. It contains no preservatives. Poractant alfa is indicated for the treatment of Respiratory Distress Syndrome (RDS) in premature infants. Poractant alfa improved lung compliance, pulmonary gas exchange and survival in preterm rabbits. Endogenous pulmonary surfactant reduces surface tension at the air-liquid interface of the alveoli in the lungs, thus stabilizing them against collapse under transpulmonary pressures. A deficiency of pulmonary surfactant in premature infants allows surface tension to increase to the point where sections of lung collapse and respiratory distress syndrome (RDS) develops. Poractant alfa lowers minimum surface tension to less than or equal to 4 mN/m. This compensates for the lack of endogenous surfactant and restores adequate surface activity to the lungs.",,,,Poractant alfa is approved.,Poractant alfa is a liquid.,True
20471,"Beractant is a pulmonary surfactant used for the treatment of Respiratory Distress Syndrome (RDS) in premature infants. Considered a natural source of surfactant as it is made from bovine lung extract, beractant contains a mixture of phospholipids, neutral lipids, fatty acids, and surfactant-associated proteins such as SP-B and SP-C. The final composition provides 25 mg/mL phospholipids (including 11.0-15.5 mg/mL disaturated phosphatidylcholine), 0.5-1.75 mg/mL triglycerides, 1.4-3.5 mg/mL free fatty acids, and less than 1.0 mg/mL protein. It is suspended in 0.9% sodium chloride solution, and heat-sterilized.  Beractant is indicated for prevention and treatment of Respiratory Distress Syndrome (RDS) in premature infants. In vitro, Beractant reproducibly lowers minimum surface tension to less than 8 dynes/cm as measured by the pulsating bubble surfactometer and Wilhelmy Surface Balance. In situ, it restores pulmonary compliance to excised rat lungs artificially made surfactant-deficient. In vivo, single doses improve lung pressure-volume measurements, lung compliance, and oxygenation in premature rabbits and sheep. Beractant replenishes lung surfactant and restores surface activity to the lungs by lowering surface tension on alveolar surfaces during respiration and stabilizing the alveoli against collapse at resting transpulmonary pressures. ",,,,Beractant is approved.,Beractant is a solid.,True
20472,"Lactulose is a synthetic disaccharide derivative of lactose that is most commonly used as a laxative agent despite also being formally indicated to serve as an adjunct therapy in treating portal-systemic encephalopathy (PSE). Despite being first synthesized in 1929, investigations regarding its possible use as a laxative for the treatment of chronic constipation did not occur until the 1960s and its first clinical use for treating PSE was not until 1966.  Lactulose is indicated for use as a laxative in the treatment of chronic constipation in adults and geriatric patients. Lactulose formulations are most commonly administered via the oral route or the rectal route. Consequently, because the substance experiences minimal absorption by the gut it typically remains localized in the gastrointestinal tract environment and ultimately demonstrates almost all of its pharmacologic effects within the gut. In particular, as lactulose elicits its laxative effects in enhancing stool amounts and softening stool, such biochemical and physiologic activities can cause increased bowel sounds (borborygmi), a feeling of bloatedness, belching, frequent flatus, and diarrhea.   Lactulose is a synthetic disaccharide derivative of lactose that consists of one molecule of galactose and one molecule of fructose. Saccharolytic bacteria present in the large intestine subsequently break the substance down into organic acids like lactic acid and small amounts of formic and acetic acids. Such resultant volatile fatty acid metabolites, in combination with hydrogen and methane that is also generated consequently enhance intraluminal gas formation, peristaltic gut motility, and elicit an osmotic effect that facilitates an increase in the water content of stool as well as associated stool softening. All of these actions ultimately assist in facilitating and increasing the frequency of bowel movements in patients experiencing constipation, although it may take 24 to 48 hours after using the medication for this laxative effect to become evident.",The molecular weight is 342.3.,Lactulose has a topological polar surface area of 189.53.,The log p value of  is -3.59.,Lactulose is approved.,Lactulose is a solid.,True
20473,"Nitrogen mustard derivative of uracil. It is a alkylating antineoplastic agent that is used in lymphatic malignancies, and causes mainly gastrointestinal and bone marrow damage. Used for its antineoplastic properties. Uracil Mustard selectively inhibits the synthesis of deoxyribonucleic acid (DNA). The guanine and cytosine content correlates with the degree of Uracil Mustard-induced cross-linking. At high concentrations of the drug, cellular RNA and protein synthesis are also suppressed. After activation, it binds preferentially to the guanine and cytosine moieties of DNA, leading to cross-linking of DNA, thus inhibiting DNA synthesis and function.",The molecular weight is 252.1.,Uracil mustard has a topological polar surface area of 61.44.,The log p value of  is 0.6.,Uracil mustard is approved.,Uracil mustard is a solid.,True
20474,"Talimogene laherparepvec is an oncolytic treatment used in local treatment of unresectable cutaneous, subcutaneous, and nodal lesions in patients with recurrent melanoma. It is a genetically administered herpes simplex virus 1 (HSV-1) that expresses human cytokine granulocyte-macrophage colony stimulating factor (GM-CSF) with antitumor and immune-stimulating activities. It specifically replicates within tumor cells and causes lysis. It was approved by the FDA in 2015 under the market name Imlygic. This medication is a genetically modified oncolytic viral therapy indicated for the local treatment of unresectable, cutaneous, subcutaneous, and nodal lesions in patients with melanoma recurrent after initial surgery. Elsewhere, the EMA notes that the agent is indicated for the treatment of adults with unresectable melanoma that is regionally or distantly metastatic (Stage IIIB, IIIC, and IVM1a) with no bone, brain, lung, or other visceral diseases. Talimogene laherparepvec has been genetically modified to replicate within tumors and to produce the immune stimulatory protein GM-CSF (granulocyte macrophage colony stimulating factor). The medication causes lysis of tumors, followed by the release of tumor-derived antigens, which together with virally derived GM-CSF may promote an anti-tumor immune response in the body. Talimogene laherparepvec is an oncolytic immunotherapy that is derived from Herpes Simplex Virus type-1 (HSV-1). It has been modified to replicate within tumor cells and to produce the immune response stimulatory protein, human GM-CSF (granulocyte macrophage colony stimulating factor). The medication causes the death of tumor cells and the release of tumor-derived antigens. It is believed that together with GM-CSF, talimogene laherparepvec can promote a systemic anti-tumor immune response and an effector T-cell response. Mice subjects involved in talimogene laherparepvec treatment studies that had complete regression of their primary tumors following therapy were resistant to subsequent tumor rechallenge.",,,,Talimogene laherparepvec is approved and experimental and investigational.,,True
20475,"Beclabuvir has been used in trials studying the treatment of Hepatitis C, Chronic.",The molecular weight is 659.85.,Beclabuvir has a topological polar surface area of 104.19.,The log p value of  is 6.2.,Beclabuvir is investigational.,,True
20476,"Vaniprevir has been used in trials studying the treatment and diagnostic of Hepatitis C, Chronic Hepatitis C, Hepatitis C, Chronic, Chronic Hepatitis C Infection, and Chronic Genotype 1 Hepatitis C Virus Infection.",The molecular weight is 757.94.,Vaniprevir has a topological polar surface area of 180.52.,The log p value of  is 7.78.,Vaniprevir is investigational.,,True
20477,"Investigated for use/treatment in hepatitis (viral, B).",The molecular weight is 260.22.,Clevudine has a topological polar surface area of 99.1.,The log p value of  is -0.94.,Clevudine is investigational.,Clevudine is a solid.,True
20478,"Entecavir is an oral antiviral drug used in the treatment of hepatitis B infection. It is marketed under the trade name Baraclude (BMS). For the treatment of chronic hepatitis B virus infection in adults with evidence of active viral replication and either evidence of persistent elevations in serum aminotransferases (ALT or AST) or histologically active disease. Entecavir is a guanosine nucleoside analogue with selective activity against hepatitis B virus (HBV). It is designed to selectively inhibit the Hepatitis B virus, blocking all three steps in the replication process. Entecavir is more efficient than an older Hepatitis B drug, lamivudine. By competing with the natural substrate deoxyguanosine triphosphate, entecavir functionally inhibits all three activities of the HBV polymerase (reverse transcriptase, rt): (1) base priming, (2) reverse transcription of the negative strand from the pregenomic messenger RNA, and (3) synthesis of the positive strand of HBV DNA. Upon activation by kinases, the drug can be incorporated into the DNA which has the ultimate effect of inhibiting the HBV polymerase activity.",The molecular weight is 277.28.,Entecavir has a topological polar surface area of 125.76.,The log p value of  is -2.58.,Entecavir is approved and investigational.,Entecavir is a solid.,True
20479,"Mandelic acid is an approved aromatic, alpha hydroxy acid. Mandelic acid is used as an ingredient in cosmetics and drug products applied topically.",The molecular weight is 152.15.,Mandelic acid has a topological polar surface area of 57.53.,The log p value of  is 0.5.,Mandelic acid is approved.,,True
20480,"Ceftolozane is a semi-synthetic broad-spectrum fifth generation cephalosporin. It was approved by the FDA in 2014 for use in combination with for the treatment of serious infections, such as intra-abdominal infections and complicated urinary tract infections. The manufacturer of this drug is Cubist Pharmaceuticals. Most recently, in June 2019, ceftolozane-tazobactam was approved for the treatment of hospital-acquired bacterial pneumonia and ventilator-associated bacterial pneumonia. This drug is administered in combination with tazobactam for the treatment of complicated intra-abdominal infections (in combination with metronidazole) and complicated urinary tract infections, which may include pyelonephritis. Ceftolozane-tazobactam is also indicated in the treatment of bacterial ventilator-associated pneumonia and bacterial hospital-acquired pneumonia. Ceftolozane exerts bactericidal activities against susceptible gram-negative and gram-positive infections by interfering with bacterial cell wall synthesis. When it is combined with tazobactam, it exerts further activity against beta-lactamase enzyme producing bacteria, which are normally resistant to beta-lactam antibiotics and interfere with infection treatment. The addition of tazobactam strengthens the therapeutic response to ceftolozane, giving it the ability to treat a broader range of bacterial infections and resistant organisms. Ceftolozane belongs to the cephalosporin class of antibacterial drugs. Ceftolozane exerts antibacterial effects, preventing the formation of cell walls that protect bacteria from injury and confer resistance to some antibiotics. Its antibacterial activity is also mediated through ceftolozane binding to penicillin-binding proteins (PBPs), which are required for peptidoglycan cross-linking for bacterial cell wall synthesis. As a result of cell wall synthesis inhibition, bacterial cells are killed, treating various infections. Ceftolozane has a particularly high affinity to the penicillin-binding proteins for Pseudomonas aeruginosa and Escherichia coli as well as Klebsiella pneumoniae and other enteric bacteria. In particular, a high affinity has been seen in vitro for penicillin-binding proteins 1b, 1c, 2, and 3 when compared to other antibiotics, ceftazidime and imipenem. ",The molecular weight is 667.7.,Ceftolozane has a topological polar surface area of 299.38.,The log p value of  is -9.85.,Ceftolozane is approved and investigational.,Ceftolozane is a solid.,True
20481,"Cefapirin (INN, also spelled cephapirin), commonly marketed under the trade name Cefadyl, is a first-generation cephalosporin antibiotic that is available in injectable formulations. Production for use in humans has been discontinued in the United States. Cefapirin is partly plasma-bound and is effective against gram-negative and gram-positive organisms. For treatment of infections caused by susceptible bacteria. Cephapirin is a first-generation cephalosporin that has a wide spectrum of activity against gram-positive and gram-negative organisms. Cephapirin is more resistant to beta-lactamases than are the penicillins and so is effective against staphylococci, with the exception of methicillin-resistant staphylococci. The bactericidal activity of cephapirin results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs).",The molecular weight is 423.46.,Cefapirin has a topological polar surface area of 125.9.,The log p value of  is -0.29.,Cefapirin is approved and vet_approved.,Cefapirin is a solid.,True
20482,,The molecular weight is 264.2.,Furazidin has a topological polar surface area of 118.05.,The log p value of  is 0.02.,Furazidin is experimental.,,False
20483,"Alatrofloxacin is a fluoroquinolone antibiotic developed by Pfizer, delivered as a mesylate salt. It was withdrawn from the U.S. market in 2001.",The molecular weight is 558.52.,Alatrofloxacin has a topological polar surface area of 157.96.,The log p value of  is -1.58.,Alatrofloxacin is approved and withdrawn.,Alatrofloxacin is a solid.,True
20484,,The molecular weight is 268.18.,Nifurtoinol has a topological polar surface area of 132.17.,The log p value of  is -0.78.,Nifurtoinol is experimental.,,False
20485,"Cefprozil is a cephalosporin antibiotic that is commonly employed to treat a variety of bacterial infections, including those of the ear and skin, bronchitis, and others. For the treatment of the following infections (respiratory, skin, soft tissue, UTI, ENT) caused by; S. pneumoniae, H. influenzae, staphylococci, S. pyogenes (group A beta-hemolytic streptococci), E. coli, P. mirabilis, Klebsiella sp, coagulase-negative staph Cefprozil, a semisynthetic, second-generation cephalosporin, is used to treat otitis media, soft-tissue infections, and respiratory tract infections. Cefprozil, like the penicillins, is a beta-lactam antibiotic. By binding to specific penicillin-binding proteins (PBPs) located inside the bacterial cell wall, it inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that cefprozil interferes with an autolysin inhibitor.",The molecular weight is 389.43.,Cefprozil has a topological polar surface area of 132.96.,The log p value of  is -1.87.,Cefprozil is approved.,Cefprozil is a solid.,True
20486,"Rasburicase is a recombinant urate-oxidase enzyme produced by a genetically modified <i>Saccharomyces cerevisiae</i> strain. The cDNA coding for rasburicase was cloned from a strain of _Aspergillus flavus_. For treatment of hyperuricemia, reduces elevated plasma uric acid levels (from chemotherapy) Drugs used to treat lympohoid leukemia, non-Hodgkin's lymphoma and acute myelogenous leukemia often lead to the accumulation of toxic plasma levels of purine metabolites (i.e. uric acid). The injection of rasburicase reduces levels of uric acid and mitigates the toxic effects of chemotherapy induced tumor lysis. Rasburicase catalyzes enzymatic oxidation of uric acid into an inactive and soluble metabolite (allantoin).",,,,Rasburicase is approved and investigational.,Rasburicase is a liquid.,True
20487,A beta-adrenergic agonist that causes direct relaxation of uterine and vascular smooth muscle. Its vasodilating actions are greater on the arteries supplying skeletal muscle than on those supplying skin. It is used in the treatment of peripheral vascular disease and in premature labor.,The molecular weight is 301.39.,Isoxsuprine has a topological polar surface area of 61.72.,The log p value of  is 2.61.,Isoxsuprine is approved and withdrawn.,Isoxsuprine is a solid.,True
20488,"Pegloticase is a recombinant porcine-like uricase drug indicated for the treatment of severe, treatment-refractory, chronic gout. Similarly to rasburicase, pegloticase metabolises the conversion of uric acid to allantoin. This reduces the risk of precipitate formation and development of gout, since allantoin is five to ten times more soluble than uric acid. Pegloticase is a pegylated form of uricase which offers an extended half-life of ten-12 days compared to rasburicase's 8 hours. It also offers reduced immunogenicity due to the bulky PEG group. The longer haf-life allows for less frequent dosing at once every 2-4 weeks making pegloticase more convenient for chronic use. For the treatment of chronic gout in adult patients refractory to conventional therapy. Pegloticase is a recombinant uricase that catalyzes the metabolism of uric acid to allantoin.",,,,Pegloticase is approved and investigational.,Pegloticase is a solid.,True
20489,,The molecular weight is 249.27.,Cinchophen has a topological polar surface area of 50.19.,The log p value of  is 4.28.,Cinchophen is experimental.,,False
20490,,The molecular weight is 400.58.,Tiocarlide has a topological polar surface area of 42.52.,The log p value of  is 6.23.,Tiocarlide is experimental.,,False
20491,Cyclic basic peptide related to viomycin. It is isolated from an induced mutant of Streptomyces griseoverticillatus var. tuberacticus and acts as an antitubercular agent with less ototoxicity than tuberactinomycin.,The molecular weight is 685.7.,Enviomycin has a topological polar surface area of 392.86.,The log p value of  is -6.42.,Enviomycin is experimental.,Enviomycin is a solid.,True
20492,Amithiozone has been used in trials studying the treatment of Mycobacterium Avium-intracellulare Infection.,The molecular weight is 236.29.,Amithiozone has a topological polar surface area of 79.51.,The log p value of  is 0.88.,Amithiozone is investigational.,,True
20493,Vincamine is a monoterpenoid indole alkaloid obtained from the leaves of *Vinca minor* with a vasodilatory property. Studies indicate that vincamine increases the regional cerebral blood flow.,The molecular weight is 354.45.,Vincamine has a topological polar surface area of 54.7.,The log p value of  is 3.16.,Vincamine is experimental.,,True
20494,,The molecular weight is 353.51.,Motretinide has a topological polar surface area of 38.33.,The log p value of  is 6.16.,Motretinide is experimental.,,False
20495,"To date, ozenoxacin has been used in trials studying the treatment of impetigo. Ozenoxacin cream is indicated for the topical treatment of impetigo caused by *Staphylococcus aureus* or *Streptococcus pyogenes* in patients aged 2 months of age and older. Although the exposure response relationship for ozenoxacin after it has been applied topically has not yet been studied, a formal relationship is unlikely because systemic exposure of ozenoxacin following its topical application has been measured to be negligible. Ozenoxacin is a quinolone antibiotic drug. And, like most quinolones, ozenoxacin predominately executes its mechanism of action by entering into bacterial cells and acting to inhibit the bacterial DNA replication enzymes DNA gyrase A and topoisomerase IV. ",The molecular weight is 363.42.,Ozenoxacin has a topological polar surface area of 82.53.,The log p value of  is 3.39.,Ozenoxacin is approved and investigational.,Ozenoxacin is a solid.,True
20496,Nadifloxacin has been used in trials studying the treatment of Acne Vulgaris.,The molecular weight is 360.38.,Nadifloxacin has a topological polar surface area of 81.08.,The log p value of  is 1.3.,Nadifloxacin is investigational.,,True
20497,A direct-acting peripheral vasodilator that causes flushing and may decrease blood pressure. It is used in vasospasm and threatened gangrene. ,The molecular weight is 109.13.,Nicotinyl alcohol has a topological polar surface area of 33.12.,The log p value of  is 0.06.,Nicotinyl alcohol is experimental.,Nicotinyl alcohol is a solid.,True
20498,"Cetylpyridinium is a quaternary ammonium with broad-spectrum antiseptic properties. Its salt form, cetylpyridinium chloride, is typically found as an active ingredient in mouthwashes, toothpastes, lozenges, throat sprays, breath sprays, and nasal sprays. In these products, it generally mediates an antiseptic activity and protective action against dental plaque and reducing gingivitis. Typically employed as the cetylpyridinium chloride salt, this compound is commonly used as an active ingredient in various over-the-counter mouthwashes, toothpastes, lozenges, and mouth sprays where it is generally indicated for antiseptic actions, gingivitis and plaque prevention, as well as action or prevention against some other oropharyngeal bacterial infections. Cetylpyridinium chloride is considered a cationic disinfectant with properties and uses similar to other such cationic surfactants. In particular, cetylpyridinium chloride has demonstrated a rapid bactericidal and fungicide effect on gram-positive pathogens and yeasts, respectively. Cetylpyridinium chloride is subsequently utilized in a variety of preparations for the local treatment of minor infections. Despite the variety of formulations in which cetylpyridinium chloride may appear as an active ingredient, it is generally accepted that it only elicits a local effect owing to the compound's relatively poor absorption by route of exposure. When incorporated into mouthwashes, toothpastes, lozenges, or mouth sprays, cetylpyridinium chloride is expected to elicit a mechanism of action that decreases new dental plaque growth, decreases or removes existing dental plaque, diminishes the growth of pathogenic bacteria, and inhibits the production of virulence factors. Cetylpyridinium chloride is a quaternary ammonium compound that demonstrates a broad spectrum anti-bacterial activity. It possesses a cationic surface active agent surfactant which can absorb readily to oral surfaces. The molecules of this agent have both hydrophilic and hydrophobic groups. In action, the positively charged hydrophilic region of cetylpyridinium chloride molecules enables the compound to interact with microbial cell surfaces and even integrate into the bacterial cytoplasmic membrane. Consequently, there is a resultant disruption of bacterial membrane integrity causing a leakage of bacterial cytoplasmic components, interference with cellular metabolism, inhibition of cell growth, and ultimately - cell death. Moreover, cetylpyridinium chloride can also inhibit the synthesis of insoluble glucan by streptococcal glucosyltransferase, adsorb to pellicle-covered enamel, and inhibit co-adhesion of bacteria, and bind streptococcus mutans biofilms. This ability of cetylpyridinium chloride to be able to adsorb to pellicle covered enamel imparts substantivity to the compound molecules - that is retention in the mouth and continued antimicrobial activity for a period of time after rinsing. Taking these mechanisms into consideration, cetylpyridinium chloride may be considered an active ingredient that is effective in the treatment and prevention of bacterial or fungal disorders of the oropharyngeal cavity.",The molecular weight is 304.54.,Cetylpyridinium has a topological polar surface area of 3.88.,The log p value of  is 3.74.,Cetylpyridinium is approved.,,True
20499,"Nitrogen is a chemical element with symbol N and atomic number 7. At room temperature, it is a transparent, odorless diatomic gas.  Liquid nitrogen is used mainly as a cryogenic agent for the treatment of various benign and malignant skin lesions.  In cryotherapy, mechanism of action could be classified into three stages: 1. heat transfer, 2. cell injury and 3. inflammation.",The molecular weight is 28.01.,Nitrogen has a topological polar surface area of 47.58.,,Nitrogen is approved and vet_approved.,Nitrogen is a solid.,True
20500,,The molecular weight is 99.09.,Succinimide has a topological polar surface area of 46.17.,The log p value of  is -1.17.,Succinimide is experimental.,,False
20501,"Icosapent ethyl or ethyl eicosapentaenoic acid is a synthetic derivative of the omega-3 fatty acid eicosapentaenoic acid (EPA). It is used as adjunct therapy for severe hypertriglyceridemia (TG levels > 500 mg/dL). FDA approved on July 26, 2012. Icosapent ethyl is used as adjunct therapy to reduce triglyceride (TG) levels in adults with severe (>500 mg/dL) hypertriglyceridemia.  Studies suggest that EPA reduces hepatic very low-density lipoprotein triglycerides (VLDL-TG) synthesis and/or secretion and enhances TG clearance from circulating VLDL particles. Potential mechanisms of action include increased β-oxidation; inhibition of acyl-CoA:1,2-diacylglycerol acyltransferase (DGAT); decreased lipogenesis in the liver; and increased plasma lipoprotein lipase activity.",The molecular weight is 330.51.,Icosapent ethyl has a topological polar surface area of 26.3.,The log p value of  is 7.81.,Icosapent ethyl is approved and investigational and nutraceutical.,Icosapent ethyl is a solid.,True
20502,"Colesevelam is a bile acid sequestrant. Colesevelam is used with exercise and diet changes (restriction of cholesterol and fat intake) to reduce the amount of cholesterol and certain fatty substances in the blood. It works by binding bile acids in the intestine. Bile acids are made when cholesterol is broken down in the body. Removing these bile acids helps to lower blood cholesterol. For use, alone or in combination with an HMG-CoA reductase inhibitor, as adjunctive therapy to diet and exercise for the reduction of elevated LDL cholesterol in patients with primary hypercholesterolemia (Fredrickson Type IIa). Colesevelam is a high capacity bile-acid binding molecule. Colesevelam binds to bile acids in the intestine which reduces the amount of bile acids that are returned to the liver via enterohepatic circulation. Clinical studies have demonstrated that elevated levels of total cholesterol (total-C), LDL-C, and apolipoprotein B (Apo B, a protein associated with LDL-C) are associated with an increased risk of atherosclerosis in humans. Similarly, decreased levels of high-density lipoprotein cholesterol (HDL-C) are associated with the development of atherosclerosis. Epidemiological investigations have established that cardiovascular morbidity and mortality vary directly with the levels of total-C and LDL-C, and inversely with the level of HDL-C. The combination of colesevelam and an HMG-CoA reductase inhibitor is effective in further lowering serum total-C and LDL-C levels beyond that achieved by either agent alone. Colesevelam binds bile acids in the intestine and prevents their reabsorption. Colesevelam is not absorbed itself. The depletion of bile acid causes the upregulation of cholesterol 7-alpha-hydroxylase and conversion of cholesterol to bile acid. this increases the production and activity of hydroxymethyl-glutaryl-coenzyme A (HMG-CoA) reductase in the liver as well as an increase in the number of low density lipoprotein (LDL) receptors. This process clears LDL cholesterol from the blood.",,,,Colesevelam is approved.,Colesevelam is a solid.,True
20503,"Calcium carbonate is an inorganic salt used as an antacid. It is a basic compound that acts by neutralizing hydrochloric acid in gastric secretions. Subsequent increases in pH may inhibit the action of pepsin. An increase in bicarbonate ions and prostaglandins may also confer cytoprotective effects. Calcium carbonate may also be used as a nutritional supplement or to treat hypocalcemia. For relief of heartburn and acid indigestion. May also be used as a nutritional supplement or to treat hypocalcemia.  Gastric-peptic disease occurs as a result of an imbalance between protective factors, such as mucus, bicarbonate, and prostaglandin secretion, and aggressive factors, such as hydrochloric acid, pepsin, and <i>Helicobacter pylori</i> (<i>H. pylori</i>). Antacids work by restoring acid-base balance, attenuating the pepsin activity and increasing bicarbonate and prostaglandin secretion. The acid-neutralizing capacity of calcium carbonate is 58 mEq/15 ml.  Calcium carbonate is a basic inorganic salt that acts by neutralizing hydrochloric acid in gastric secretions. It also inhibits the action of pepsin by increasing the pH and via adsorption. Cytoprotective effects may occur through increases in bicarbonate ion (HCO<sub>3</sub><sup>-</sup>) and prostaglandins. Neutralization of hydrochloric acid results in the formation of calcium chloride, carbon dioxide and water. Approximately 90% of calcium chloride is converted to insoluble calcium salts (e.g. calcium carbonate and calcium phosphate).",The molecular weight is 100.09.,,,Calcium carbonate is approved and investigational.,Calcium carbonate is a solid.,True
20504,,The molecular weight is 324.3.,Calcium lactate gluconate has a topological polar surface area of 141.28.,,Calcium lactate gluconate is experimental.,,False
20505,,The molecular weight is 319.4.,Oxetorone has a topological polar surface area of 25.61.,The log p value of  is 4.65.,Oxetorone is experimental.,,False
20506,Colestilan is an ingredient in the EMA-withdrawn product BindRen.,,,,Colestilan chloride is approved and investigational and withdrawn.,,True
20507,,The molecular weight is 211.73.,Mefenorex has a topological polar surface area of 12.03.,The log p value of  is 2.81.,Mefenorex is experimental.,,False
20508,"Fenproporex is an orally active stimulant drug, which was developed in the 1960s. It is used as an appetite suppressant and a treatment for obesity. It is listed as an illicit substance in many countries due to addiction issues and listed as a prohibited substance by the World Anti-Doping Agency. Structurally, fenproporex (N-2-cyanoethylamphetamine) falls within the phenylethamine and amphetamine chemical class of drugs. The N-2-cyanoethyl substituent was once believed to be resistant to cleavage, because fenproporex -- once recommended as an obesity treatment for patients with cardiovascular disease -- was originally claimed to lack stimulant properties. Contrary to the claim, research has demonstrated easy in vivo cleavage of the N-2-cyanothyl substituent to yield amphetamine as a metabolite. However, in clinical practice, central nervous system stimulative effects are less notorious than with some other agents such as diethylpropion and mazindol.  Fenproporex is used as an appetite suppressant, and anti-obesity agent ; however, due to substance abuse potential, it is an illicit substance in many countries. In some countries, such as Brazil, it is still prescribed -- often in the form of diet pills (ie. Brazilian Diet Pills) which combine amphetamines, benzodiazepines, antidepressants, diuretics and laxatives.  Fenproporex was first claimed to not exert a stimulant effect on the body, however research into its metabolism has shown that it is converted into a considerable amount of amphetamine in the body, which leads to stimulant effects.  Fenproporex is an amphetamine based anorectic which is rapidly metabolized into amphetamine in the body. Both acute and chronic fenproporex administration has been shown to increase brain energy metabolism in young rats, by increasing the activity of citrate synthase, malate dehydrogenase, succinate dehydrogenase, creatine kinase and complexes I,II, III, and IV. ",The molecular weight is 188.27.,Fenproporex has a topological polar surface area of 35.82.,The log p value of  is 1.73.,Fenproporex is experimental and illicit and withdrawn.,Fenproporex is a solid.,True
20509,Belotecan has been investigated for the treatment of Epithelial Ovarian Cancer.,The molecular weight is 433.51.,Belotecan has a topological polar surface area of 91.76.,The log p value of  is 0.87.,Belotecan is investigational.,,True
20510,"Acipimox is a niacin derivative used as a hypolipidemic agent. It is used in low doses and may have less marked adverse effects, although it is unclear whether the recommended dose is as effective as are standard doses of nicotinic acid. Acipimox inhibits the production of triglycerides by the liver and the secretion of VLDL, which leads indirectly to a modest reduction in LDL and increase in HDL. Long-term administration is associated with reduced mortality, but unwanted effects limit its clinical use. Adverse effects include flushing (associated with Prostaglandin D2), palpitations, and GI disturbances. Flushing can be reduced by taking aspirin 20-30 min before taking Acipimox. High doses can cause disorders of liver function, impair glucose tolerance and precipitate gout. Used in the treatment of hyperlipidemias (abnormally elevated levels of any or all lipids and/or lipoproteins in the blood). Acipimox inhibits the production of triglycerides by the liver and the secretion of VLDL, which leads indirectly to a modest reduction in LDL and increase in HDL.",The molecular weight is 154.12.,Acipimox has a topological polar surface area of 75.65.,The log p value of  is -0.16.,Acipimox is approved and investigational.,Acipimox is a solid.,True
20511,"Givosiran is a small interfering RNA (siRNA) directed towards 5-aminolevulinic acid synthase, a critical enzyme in the heme biosynthesis pathway. It is manufactured by Alnylam Pharmaceuticals and was first approved for use in the United States in November 2019 for the treatment of adults with acute hepatic porphyria, a genetic disorder in which the overproduction of toxic heme intermediates leads to neuro-, nephro-, and gastrotoxicity. Givosiran represents an important step forward in the treatment of acute hepatic porphyria as it is the first approved pharmacotherapy for the prevention of acute attacks - previous strategies involved non-therapeutic measures (e.g. trigger avoidance), intravenous for the treatment of attacks, and liver transplantation in refractory cases. Givosiran is the second-ever FDA-approved member of the siRNA drug class (the first being ), a new class of drugs promising an important and exciting step forward in the treatment of genetic disorders. Givosiran is indicated for the treatment of adults with acute hepatic porphyria. Givosiran decreases the rate at which toxic byproducts of heme synthesis are produced in the livers of patients with acute hepatic porphyria, thus preventing their accumulation and associated neuro-, nephro-, and gastrotoxicity. As givosiran works at the transcriptional level, it has a long duration of action and can be administered subcutaneously on a monthly basis. Although givosiran appears to be relatively well-tolerated, hepatic and renal toxicity were noted during clinical trials. Patients receiving therapy with givosiran should undergo routine laboratory monitoring of liver and kidney function. Acute hepatic porphyrias are a class of genetic disorders involving deficiencies in the pathway responsible for heme synthesis in liver hepatocytes. The rate-limiting step in heme synthesis is the first enzyme in the pathway, 5-aminolevulinic acid synthase (ALAS1), which is controlled via a negative feedback loop by the presence of heme end-product in the liver. Deficiencies in later enzymes in the pathway result in low circulating levels of heme, which in turn stimulates the up-regulation of ALAS1. The overexpression of ALAS1, in combination with downstream enzyme deficiencies, leads to the overproduction and accumulation of toxic heme intermediates which are ultimately responsible for the neurovisceral symptoms characteristic of acute hepatic porphyrias.",,,,Givosiran is approved and investigational.,Givosiran is a solid.,True
20512,"Lanthanum carbonate is a phosphate binder commonly used in clinical practice. It is marketed under the trade name _Fosrenol_ by Shire Pharmaceuticals. It is the largest of all pills filled in community pharmacies. Sometimes patients forget that Fosrenol is not swallowed whole, but instead should be chewed. This has led to severe choking. It is prescribed for treating high phosphate levels, mainly found in patients with chronic kidney disease. Lanthanum should be taken with meals and binds to phosphate in the diet, preventing phosphate absorption in the intestine. Used to reduce serum phosphate in patients with end stage renal disease (ESRD). In vitro studies have shown that lanthanum binds phosphate in the physiologically relevant pH range of 3 to 7. In simulated gastric fluid, lanthanum binds approximately 97% of the available phosphate at pH 3-5 and 67% at pH 7, when lanthanum is present in a two-fold molar excess to phosphate. Bile acids have not been shown to affect the phosphate binding affinity of lanthanum. In order to bind dietary phosphate, lanthanum carbonate must be administered with or immediately after meals. Lanthanum carbonate is a phosphate binder that reduces absorption of phosphate by forming insoluble lanthanum phosphate complexes that pass through the gastrointestinal (GI) tract unabsorbed. Both serum phosphate and calcium phosphate product are reduced as a consequence of the reduced dietary phosphate absorption.",The molecular weight is 457.84.,Lanthanum carbonate has a topological polar surface area of 63.19.,,Lanthanum carbonate is approved.,Lanthanum carbonate is a solid.,True
20513,Gemigliptin is under investigation in Type 2 Diabetes Mellitus. Gemigliptin has been investigated for the treatment of Cancer and Cisplatin Adverse Reaction.,The molecular weight is 489.37.,Gemigliptin has a topological polar surface area of 92.42.,The log p value of  is 0.57.,Gemigliptin is investigational.,,True
20514,Tofogliflozin has been used in trials studying the treatment and prevention of Diabetes Mellitus Type 2.,The molecular weight is 386.44.,Tofogliflozin has a topological polar surface area of 99.38.,The log p value of  is 3.06.,Tofogliflozin is investigational.,,True
20515,"Luseogliflozin has been used in trials studying the treatment of Diabetes Melltius, Type 2.",The molecular weight is 434.55.,Luseogliflozin has a topological polar surface area of 99.38.,The log p value of  is 3.96.,Luseogliflozin is investigational.,,True
20516,"Trelagliptin is under investigation in clinical trial NCT03555591 (Specified Drug-Use Survey of Trelagliptin Tablets \Survey on Long-term Use in Patients With Type 2 Diabetes Mellitus\"").""",The molecular weight is 357.39.,Trelagliptin has a topological polar surface area of 93.67.,The log p value of  is 1.13.,Trelagliptin is investigational.,,True
20517,"Ipragliflozin is under investigation in Type 2 Diabetes and Diabetes Mellitus, Type 2.",The molecular weight is 404.45.,Ipragliflozin has a topological polar surface area of 90.15.,The log p value of  is 3.38.,Ipragliflozin is investigational.,,True
20518,Teneligliptin has been investigated for the treatment of Type 2 Diabetes Mellitus.,The molecular weight is 426.58.,Teneligliptin has a topological polar surface area of 56.64.,The log p value of  is 2.24.,Teneligliptin is investigational.,,True
20519,"Anagliptin is under investigation for the treatment of LDL Cholesterol, Coronary Disease, Diabetes Mellitus, Glycosylated Hemoglobin, and Dipeptidyl-Peptidase 4 Inhibitors.",The molecular weight is 383.46.,Anagliptin has a topological polar surface area of 115.42.,The log p value of  is 0.57.,Anagliptin is investigational.,,True
20520,Omarigliptin has been used in trials studying the treatment of Type 2 Diabetes Mellitus and Chronic Renal Insufficiency.,The molecular weight is 398.43.,Omarigliptin has a topological polar surface area of 90.45.,The log p value of  is -0.91.,Omarigliptin is investigational.,,True
20521,"Evogliptin has been used in trials studying the treatment and screening of Osteoporosis, Renal Impairment, Type 2 Diabetes Mellitus, Diabetes Mellitis Type 2, and Diabetes Mellitus, Type 2.",The molecular weight is 401.43.,Evogliptin has a topological polar surface area of 84.66.,The log p value of  is 2.8.,Evogliptin is investigational.,,True
20522,Omidenepag isopropyl is under investigation in clinical trial NCT02179008 (Multi-center Phase II Study Assessing the Safety and Efficacy of DE-117 Ophthalmic Solution in Subjects With Primary Open-angle Glaucoma or Ocular Hypertension).,,,,Omidenepag isopropyl is investigational.,,True
20523,"Pramiracetam has been previously approved in some eastern European countries under the brand names Pramistar, Neupramir, and Remen. It was also previously approved in the United States with orphan drug designation. Pramiracetam has been studied for the use in Alzheimer's disease and as an adjunct treatment to restore cognitive functioning post-electroconvulsive therapy in severe depression.",The molecular weight is 269.39.,Pramiracetam has a topological polar surface area of 52.65.,The log p value of  is 1.41.,Pramiracetam is approved.,,True
20524,"Chloroxine is a synthetic antibacterial compound. Chloroxine is a compound used in some shampoos for the treatment of dandruff and seborrheic dermatitis of the scalp. Used in the treatment of dandruff and mild to moderately severe seborrheic dermatitis of the scalp. Chloroxine has an antibacterial action, inhibiting the growth of gram-positive as well as some gram-negative organisms. Also, chloroxine has shown some antifungal activity against certain dermatophytes and yeasts. Although the mechanism of action is not understood, chloroxine may slow down mitotic activity in the epidermis, thereby reducing excessive scaling associated with dandruff or seborrheic dermatitis of the scalp. Chloroxine induces SOS-DNA repair in E. coli, so chloroxine may be genotoxic to bacteria.",The molecular weight is 214.05.,Chloroxine has a topological polar surface area of 33.12.,The log p value of  is 3.34.,Chloroxine is approved.,Chloroxine is a solid.,True
20525,"Selenium Sulfide is an antifungal agent as well as a cytostatic agent, slowing the growth of hyperproliferative cells in seborrhea. Selenium Sulfide is the active ingredient often used in shampoos for the treatment of dandruff, seborrheic dermatitis and tinea capitis, a fungal infection that is primarily a disease of preadolescent children. For treatment of tinea versicolor, tinea capitis, dandruff and seborrheic dermatitis of the scalp. Selenium sulfide is an antifungal agent often used in shampoos for the treatment of dandruff and seborrheic dermatitis. Selenium sulfide is highly active in inhibiting the growth of <i>P. ovale</i>. It is also a proven cytostatic agent, slowing the growth of both hyperproliferative and normal cells in dandruff and seborrheic dermatitis. A 0.6% micronized form of selenium sulfide is also safe and effective for dandruff. Topical selenium sulfide may act by an antimitotic action, resulting in a reduction in the turnover of epidermal cells. It also has local irritant, antibacterial, and mild antifungal activity, which may contribute to its effectiveness. An antimitotic mechanism of action is suggested by data showing that selenium sulfide decreases the rate of incorporation of radioactively labeled thymidine into the DNA of dermal epithelial cells. The following organisms are generally considered susceptible to selenium sulfide in vitro: <i>Malassezia furfur</i>, <i>Microsporum sp.</i> including <i>Microsporum audouinii</i> and <i>Microsporum canis</i>, <i>Pityrosporon sp.</i>, <i>Trichophyton sp.</i> including <i>Trichophyton schoenleinii</i> and <i>Trichophyton tonsurans</i>. Selenium sulfide has been shown to be sporicidal to <i>T. tonsurans</i>, the most common etiologic agent of tinea capitis. One in-vitro study demonstrated that 2.5% selenium sulfide was equivalent in sporicidal activity to both 1% and 2% zinc pyrithione.",The molecular weight is 143.09.,,,Selenium Sulfide is approved.,Selenium Sulfide is a solid.,True
20526,,The molecular weight is 292.76.,Climbazole has a topological polar surface area of 44.12.,The log p value of  is 3.43.,Climbazole is experimental.,,False
20527,"Piperonyl butoxide (PBO) is an organic compound used as a component of pesticide formulations. It is used for the treatment of head, pubic (crab), and body lice. Piperonyl butoxide is a synergist. It has no pesticidal activity of its own, but acts to increase the activity of pesticides such as carbamates, pyrethrins, pyrethroids, and rotenone. Piperonyl butoxide is a semisynthetic derivative of safrole. For the treatment of head, pubic (crab), and body lice. Piperonyl butoxide does not affect the mixed-function oxidase system in humans. In small trials in human volunteers, usual doses of piperonyl butoxide had no effect on humans. Piperonyl butoxide is not a pesticide, but acts as a synergist to increase the activity of pesticides such as carbamates, pyrethrins, pyrethroids, and rotenone. Piperonyl butoxide inhibits the mixed-function oxidase (MFO) system of an insect. The MFO system is the insects natural defense system and causes the oxidative breakdown of insecticides. Thus, by inhibiting this system piperonyl butoxide promotes higher levels of insecticide and allows for lower doses to be used for a lethal effect.",The molecular weight is 338.44.,Piperonyl butoxide has a topological polar surface area of 46.15.,The log p value of  is 4.4.,Piperonyl butoxide is approved and vet_approved.,Piperonyl butoxide is a solid.,True
20528,"Crotamiton is a scabicidal and antipruritic agent available as a cream or lotion for topical use only. It is a colorless to slightly yellowish oil, having a faint amine-like odor. It is miscible with alcohol and with methanol. For eradication of scabies (<i>Sarcoptes scabiei</i>) and for symptomatic treatment of pruritic skin. Crotamiton is usually used to treat pruritis (itching of the skin) caused by scabies or sunburn. Crotamiton relieves itching by producing what is called a counter-irritation. As crotamiton evaporates from the skin, it produces a cooling effect. This cooling effect helps to divert your body's attention away from the itching. Due to this cooling effect it is also effective for the relief of sunburn. The drug is also believed to kill scabies through an unknown mechanism. Crotamiton is an antiparasitic that is toxic to the scabies mite. Crotamiton also relieves itching by producing what is called a counter-irritation. As crotamiton evaporates from the skin, it produces a cooling effect. This cooling effect helps to divert your body's attention away from the itching.",The molecular weight is 203.28.,Crotamiton has a topological polar surface area of 20.31.,The log p value of  is 3.43.,Crotamiton is approved.,Crotamiton is a liquid.,True
20529,"Acetarsol, with the molecular formula N-acetyl-4-hydroxy-m-arsanilic acid, is a pentavalent arsenical compound with antiprotozoal and antihelmintic properties. It was first discovered in 1921 by Ernest Fourneau at the Pasteur Institute. It was developed by Neolab Inc, and approved by Health Canada as an antifungal on December 31, 1964. It has been canceled and withdrawn from the market since August 12, 1997. Acetarsol has been used for the treatment of different diseases such as syphilis, amoebiasis, yaws, trypanosomiasis, and malaria. Acetarsol was used commonly for the treatment of vaginitis due to _Trichomonas vaginalis_ and _Candida albicans_. When orally administered, acetarsol can be used for the treatment of intestinal amoebiasis and in the form of suppositories it has been researched for the treatment of proctitis. Some reports indicate a certain infection remission with the use of acetarsol but this reports also demonstrate the absorption of systemic arsenic which can be physiologically dangerous. The mechanism of action of acetarsol is not well known but it is thought to bind to protein-containing sulfhydryl groups located in the infective microorganism and to form a lethal As-S bond. The formation of this bond impairs the protein to function and it eventually kills the microorganism.",The molecular weight is 275.09.,Acetarsol has a topological polar surface area of 106.86.,The log p value of  is -1.36.,Acetarsol is approved and withdrawn.,Acetarsol is a solid.,True
20530,Quinfamide has been used in trials studying the treatment of Amoebiasis and Helminthiasis.,The molecular weight is 354.18.,Quinfamide has a topological polar surface area of 59.75.,The log p value of  is 3.75.,Quinfamide is investigational.,,True
20531,"Diloxanide is used alone as a primary agent in the treatment of asymptomatic (cyst passers) intestinal amebiasis caused by Entamoeba histolytica. Diloxanide may also be used concurrently, or sequentially, with other agents such as the nitroimidazoles (eg. metronidazole) in the treatment of invasive or extraintestinal forms of amebiasis. Diloxanide is a luminal amebicide, however the mechanism of action of diloxanide is unknown. Diloxanide destroys the trophozoites of E. histolytica that eventually form into cysts. The cysts are then excreted by persons infected with asymptomatic amebiasis. Diloxanide furoate is a prodrug, and is hydrolyzed in the gastrointestinal tract to produce diloxanide, the active ingredient.  Unknown. Diloxanide may inhibit protein synthesis. ",The molecular weight is 328.15.,Diloxanide furoate has a topological polar surface area of 59.75.,The log p value of  is 3.09.,Diloxanide furoate is approved.,,True
20532,"Sotagliflozin has been used in trials studying the treatment of Renal impairment, Hepatic Impairment, Type 1 Diabetes Mellitus, and High Level of Sugar (Glucose) in the Blood.",,,,Sotagliflozin is approved and investigational.,,True
20533,Distigmine is a parasympathomimetic agent with a longer duration of action and enhanced drug accumulation compared to and. It is an anticholinergic drug and long-acting reversible carbamate cholinesterase inhibitor that binds directly and competitively to the agonist binding sites of muscurinic receptors. Distigmine is available in several countries as a treatment of underactive detrusor and voiding dysfunction in the urinary tract where the active ingredient is distigmine bromide. It improves detrusor function thereby restoring normal voiding patterns in patients suffering from detrusor underactivity.,The molecular weight is 416.52.,Distigmine has a topological polar surface area of 66.84.,The log p value of  is -7.11.,Distigmine is experimental.,,True
20534,Gepirone has been used in trials studying the treatment of Cocaine-Related Disorders.,The molecular weight is 359.47.,Gepirone has a topological polar surface area of 69.64.,The log p value of  is 1.79.,Gepirone is investigational.,,True
20535,,The molecular weight is 183.68.,Clortermine has a topological polar surface area of 26.02.,The log p value of  is 2.85.,Clortermine is experimental.,Clortermine is a solid.,False
20536,"Raxibacumab is a human IgG1λ monoclonal antibody that binds the protective antigen (PA) component of B. anthracis toxin. Raxibacumab has a molecular weight of approximately 146 kilodaltons. Raxibacumab is produced by recombinant DNA technology in a murine cell expression system. FDA approved on December 14, 2012. Raxibacumab is indicated for the treatment of adult and pediatric patients with inhalational anthrax due to Bacillus anthracis in combination with appropriate antibacterial drugs, and for prophylaxis of inhalational anthrax when alternative therapies are not available or are not appropriate.  Raxibacumab is a monoclonal antibody that binds free PA with an affinity equilibrium dissociation constant (Kd) of 2.78 ± 0.9 nM. Raxibacumab inhibits the binding of PA to its cellular receptors, preventing the intracellular entry of the anthrax lethal factor and edema factor, the enzymatic toxin components responsible for the pathogenic effects of anthrax toxin. It does not have direct antibacterial activity. ",,,,Raxibacumab is approved.,Raxibacumab is a liquid.,True
20537,"Obiltoxaximab, an affinity-enhanced monoclonal antibody (Mab), is used for prevention and treatment of infection and death caused by anthrax toxin. Obiltoxaximab is a chimeric IgG1 kappa monoclonal antibody (mAb) that binds the PA component of B. anthracis toxin. It has an approximate molecular weight of 148 kDa. Investigated for use/treatment in anthrax exposure, bacterial infection, crohn's disease, and graft versus host disease. ETI-204 is an affinity-enhanced, de-immunized antibody, which means that its ability to bind to its target pathogen has been strengthened and that elements that might cause an immune response have been removed. ETI-204 targets and binds to Protective Antigen, which prevents the anthrax toxins from binding to and entering the cells in the body, thereby preventing death.",,,,Obiltoxaximab is approved.,Obiltoxaximab is a liquid.,True
20538,"Radium Ra 223 Dichloride is a radiopharmaceutical containing the radioisotope radium-223 that emits short range but high linear energy alpha particles. As a cation, radium mimics calicum and binds to hydroxyapatite, which is a bone mineral found in areas of high bone turnover as seen in bone metastases. It was first approved by the FDA in May 2013 and is currently marketed under the brand name Xofigo, which was formerly called Alpharadin. Xofigo is indicated in patients who have metastatic bone cancer that is symptomatic with no visceral metastases and patients who have prostate cancer that is castration resistant. The FDA label includes a warning that Radium Ra 223 Dichloride should not be used in women who are pregnant or may become pregnant due to the high risk of fetal harm. Used in patients who have metastatic bone cancer that is symptomatic with no visceral metastases and patients who have prostate cancer that is castration resistant. Physiologically, Radium Ra 223 Dichloride, prevents the spread of bone cancer by killing the associated bone cancer cells. Radium Ra 223 Dichloride is the radioisotope radium-223 that emits short range but high linear energy alpha particles. As a cation, radium mimics calicum and binds to hydroxyapatite, which is a bone mineral found in areas of high bone turnover as seen in bone metastases. The high energy damages bone cells by introducing double-stranded DNA breaks. This leads to cell death and prevention of the spread of the bone cancer cells. As well because of the alpha particle's short range of less than 10 cell diameters, its damaging effects would less likely affect the non-cancerous cells nearby. ",The molecular weight is 293.92.,,,Radium Ra 223 dichloride is approved and investigational.,Radium Ra 223 dichloride is a liquid.,True
20539,"Iron sucrose (sucroferric oxyhydroxide or iron saccharate) is used as a source of iron in patients with iron deficiency anemia with chronic kidney disease (CKD), including those who are undergoing dialysis (hemodialysis or peritoneal) and those who do not require dialysis. Due to less side effects than iron dextran, iron sucrose is more preferred in chronic kidney disease patients. Iron sucrose is elemental iron as an injection. It replenishes body iron stores in patients with iron deficiency. Significant increases in serum iron and serum ferritin and significant decreases in total iron binding capacity occurred four weeks from the initiation of iron sucrose treatment. Following intravenous administration, iron sucrose is dissociated into iron and sucrose and the iron is transported as a complex with transferrin to target cells including erythroid precursor cells. The iron is then incorporated into hemoglobin as the cells mature into red blood cells.",,,,Iron sucrose is approved.,Iron sucrose is a solid.,True
20540,Pyronaridine has been investigated for the treatment of Malaria.,The molecular weight is 518.06.,Pyronaridine has a topological polar surface area of 73.75.,The log p value of  is 6.9.,Pyronaridine is investigational.,,True
20541,"Plicamycin is an antineoplastic antibiotic produced by Streptomyces plicatus. It has been used in the treatment of testicular cancer, Paget's disease of bone, and, rarely, the management of hypercalcemia. The manufacturer discontinued plicamycin in 2000. For the treatment of testicular cancer, as well as hypercalcemia and hypercalciuria associated with a variety of advanced forms of cancer. Plicamycin is lethal to Hela cells in 48 hours at concentrations as low as 0.5 micrograms per milliliter of tissue culture medium. Plicamycin has shown significant anti-tumor activity against experimental leukemia in mice when administered intraperitoneally. Plicamycin is presumed to inhibit cellular and enzymic RNA synthesis by forming a complex with DNA. Plicamycin may also lower calcium serum levels by inhibiting the effect of parathyroid hormone upon osteoclasts or by blocking the hypercalcemic action of pharmacologic doses of vitamin D.",The molecular weight is 1085.16.,Plicamycin has a topological polar surface area of 358.2.,The log p value of  is -3.07.,Plicamycin is approved and investigational and withdrawn.,Plicamycin is a solid.,True
20542,,The molecular weight is 142.96.,Sodium phosphate P 32 has a topological polar surface area of 83.42.,,Sodium phosphate P 32 is approved.,,False
20543,,The molecular weight is 235.33.,Azapetine has a topological polar surface area of 3.24.,The log p value of  is 4.14.,Azapetine is experimental.,,False
20544,"Dehydrocholic acid is a synthetic bile acid that was prepared from the oxidation of cholic acid with chromic acid. It has been used for stimulation of biliary lipid secretion. The use of dehydrocholic acid in over-the-counter products has been discontinued by Health Canada. No approved therapeutic indications.  Following infusion of dehydrocholic acid (DHCA) in rats, the secretions of all the endogenous biliary bile acids were decreased within 30-60 minutes of infusion. Phospholipid secretion as well as cholesterol levels were also declined. The bile flow was increased after administration of dehydrocholic acid.  It is proposed that dehydrocholic acid induces choleresis, which is associated with biliary lipid secretion and reduced secretion of endogenous and/or exogenous biliary components. Dehydrocholic acid may decrease bile phospholipid secretion due to a lack of micelle formation by dehydrocholic acid-produced bile. A study suggests that due to enhanced permeability of tight junctions in the canalicular membranes, dehydrocholic acid facilitates direct exchange between bile and plasma. ",The molecular weight is 402.53.,Dehydrocholic acid has a topological polar surface area of 88.51.,The log p value of  is 2.23.,Dehydrocholic acid is approved and investigational.,Dehydrocholic acid is a solid.,True
20545,"A polyhydric alcohol with about half the sweetness of sucrose. Sorbitol occurs naturally and is also produced synthetically from glucose. It was formerly used as a diuretic and may still be used as a laxative and in irrigating solutions for some surgical procedures. Used as a non-stimulant laxative via an oral suspension or enema. Sorbitol exerts its laxative effect by drawing water into the large intestine, thereby stimulating bowel movements.",The molecular weight is 182.17.,Sorbitol has a topological polar surface area of 121.38.,The log p value of  is -2.05.,Sorbitol is approved.,Sorbitol is a solid.,True
20546,A laxative that undergoes enterohepatic circulation. It may cause jaundice.,The molecular weight is 317.34.,Oxyphenisatin has a topological polar surface area of 69.56.,The log p value of  is 2.49.,Oxyphenisatin is investigational and withdrawn.,Oxyphenisatin is a solid.,True
20547,,The molecular weight is 401.42.,Oxyphenisatin acetate has a topological polar surface area of 81.7.,The log p value of  is 2.52.,Oxyphenisatin acetate is approved and investigational and withdrawn.,,False
20548,,The molecular weight is 280.32.,Ipriflavone has a topological polar surface area of 35.53.,The log p value of  is 3.92.,Ipriflavone is experimental.,,False
20549,"Strontium ranelate, a strontium (II) salt of ranelic acid, is a medication for osteoporosis. Some reports have shown that strontium ranelate can slow down the progression of osteoarthritis of the knee. This agent presents an atypical mechanism of action in which it increases deposition of new bone by osteoblasts and, simultaneously, reduces the resorption of bone by osteoclasts. It is therefore promoted as a \dual action bone agent\"" (DABA) indicated for use in treatment of severe osteoporosis."" Strontium ranelate is therapeutically indicated for the treatment of severe osteoperosis in: a) postmenopasual women, and b) adult men, who are at high risk of fractures, for whom treatment with other medical products approved for the treatment of osteoperosis is not possible due to, for example, contraindications or intolerance.  In general, it is believed that strontium ranelate is capable of affecting a rebalance in bone turnover in favour of bone formation by: (1) increasing osteoblast differentiation from progenitors, osteoblast activity and survival, as well as regulating osteoblast-induced osteoclastogenesis, and (2) decreasing osteoclast differentiation and activity, as well as increasing osteoclast apoptosis.  The underlying pathogenesis of osteperosis involves an imbalance between bone resorption and bone formation. Osteoclasts are a kind of differentiated or specialized bone cell that breaks down bone tissue while osteoblasts are another set of differentiated bone cells that synthesize and rebuild bone tissue. When osteoclasts degrade bone tissue faster than the osteoblasts are capable of rebuilding the bone tissue, low or inadequate bone mass density and osteoperosis can resula One of the mechanisms with which strontium ranelate is thought to act is its functionality as an agonist of the extracellular calcium sensing receptors (CaSRs) of osteoblasts and osteoclasts. Ordinary interaction between calcium 2+ divalent cations with mature osteoclast CaSRs is known to induce osteoclast apoptosis. Subsequently, strontium 2+ divalent cations from strontium ranelate use can also bind CaSRs on osteoclasts to induce their apoptosis because of the strontium 2+ cation's close resemeblance to calcium 2+. Contact between extracelluar calcium 2+ and osteoclast CaSRs stimulates the phospholipase C (PLC) dependant breakdown of phosphatidylinositol 4,5-biphosphate (PIP2) into the two secondary messengers inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). Whereas the calcium-CaSRs interaction then performs IP3 Adependent translocation of nuclear factor NF-kB from the cytoplasm to the nucleus in mature osteoclasts, strontium-CaSRs interactions involves a DAG-PKC beta II (protein kinase C beta II) signalling pathway for translocating NF-kB from the cytoplasm to the nucleus in an IP3-independent manner. Although the calcium 2+ and strontium 2+ mediated signalling pathways are different, both CaSR interactions induce osteoclast apoptosis and are in fact capable of potentiating each other, leading to enhanced osteoclast apoptosis and decreased bone tissue degradation.",The molecular weight is 513.49.,Strontium ranelate has a topological polar surface area of 187.55.,,Strontium ranelate is approved and withdrawn.,Strontium ranelate is a solid.,True
20550,,The molecular weight is 201.27.,Indanazoline has a topological polar surface area of 36.42.,The log p value of  is 2.03.,Indanazoline is experimental.,,False
20551,,The molecular weight is 230.33.,Metizoline has a topological polar surface area of 24.39.,The log p value of  is 4.13.,Metizoline is experimental.,,False
20552,"Oteracil is an adjunct to antineoplastic therapy, used to reduce the toxic side effects associated with chemotherapy. Approved by the European Medicines Agency (EMA) in March 2011, Oteracil is available in combination with and within the commercially available product \Teysuno\"". The main active ingredient in Teysuno is , a pro-drug of (5-FU), which is a cytotoxic anti-metabolite drug that acts on rapidly dividing cancer cells. By mimicking a class of compounds called \""pyrimidines\"" that are essential components of RNA and DNA, 5-FU is able to insert itself into strands of DNA and RNA, thereby halting the replication process necessary for continued cancer growth."" Oteracil is used as an adjunct to antineoplastic therapy. When used within the product Teysuno, oteracil is indicated for the treatment of adults with advanced gastric (stomach) cancer when given in combination with cisplatin. Oteracil's main role within Teysuno is to reduce the activity of 5-FU within normal gastrointestinal mucosa, and therefore reduce's gastrointestinal toxicity. It functions by blocking the enzyme orotate phosphoribosyltransferase (OPRT), which is involved in the production of 5-FU.",The molecular weight is 157.08.,Oteracil has a topological polar surface area of 107.86.,The log p value of  is -2.13.,Oteracil is approved.,Oteracil is a solid.,True
20553,,The molecular weight is 269.39.,Bifemelane has a topological polar surface area of 21.26.,The log p value of  is 3.97.,Bifemelane is experimental.,,False
20554,,The molecular weight is 383.53.,Naftidrofuryl has a topological polar surface area of 38.77.,The log p value of  is 5.44.,Naftidrofuryl is experimental.,,False
20555,"Lodoxamide is a mast-cell stabilizer for topical administration into the eye. Mast-cell stabilizers, first one approved being cromolyn sodium, are used in treatment of ocular hypersensitivity reactions such as vernal conjunctivitis. These conditions often require treatment with anti-inflammatory medications such as ophthalmic NSAIDs or topical steroids which may cause systemic or toxic effects long-term. Although less effective than topical steroids at decreasing inflammation, mast-cell stabilizers offer another treatment option and exhibit minimal adverse effects. Lodoxamide is marketed under the brand name Alomide by Alcon. Indicated in the treatment of the ocular disorders referred to by the terms vernal keratoconjunctivitis, vernal conjunctivitis, and vernal keratitis. Lodoxamide is a mast cell stabilizer that inhibits the in vivo Type 1 immediate hypersensitivity reaction. Lodoxamide therapy inhibits the increases in cutaneous vascular permeability that are associated with reagin or IgE and antigen-mediated reactions. Although lodoxamide's precise mechanism of action is unknown, it is postulated that it prevents calcium influx into mast cells upon antigen stimulation and therefore stabilizes the membrane. By stabilizing the mast cell membrane from degranulation, lodoxamide consequently inhibits the release of intracellular histamine and other chemoattractant factors that primarily cause ocular symptoms. Lodoxamide's mechanism of action may be similar to cromolyn sodium, as both exhibit cross-tachyphylaxis. ",The molecular weight is 311.63.,Lodoxamide has a topological polar surface area of 156.59.,The log p value of  is -2.24.,Lodoxamide is approved.,Lodoxamide is a solid.,True
20556,"Dornase alfa is a biosynthetic form of human deoxyribunuclease I (DNase I) enzyme. It is produced in genetically modified Chinese hamster ovary (CHO) cells using recombinant DNA technology. The 260-amino acid sequence of dornase alfa is identical to the endogenous human enzyme. Dornase alfa cleaves extracellular DNA to 5´-phosphodinucleotide and 5´-phosphooligonucleotide end products without affecting intracellular DNA. In individuals with cystic fibrosis, extracellular DNA, which is an extremely viscous anion, is released by degenerating leukocytes that accumulate during inflammatory responses to infections. Enzymatic breakdown of this extracellular DNA appears to reduce sputum viscosity and viscoelasticity. Used as adjunct therapy in the treatment of cystic fibrosis.  Cystic fibrosis (CF) is a disease characterized by the retention of viscous purulent secretions in the airways. These thick secretions contribute both to reduced pulmonary function and to frequent pulmonary infection. Purulent pulmonary secretions of individuals with cystic fibrosis contain very high concentrations of extracellular DNA released by degenerating leukocytes that accumulate in response to these infections. Dornase alfa hydrolyzes the DNA in sputum of CF patients and reduces sputum viscosity and viscoelasticity. The enzyme does not appear to affect sputum in the absence of an inflammatory response to infection, nor does it affect the sputum of healthy individuals.  Dornase alfa is a biosynthetic form of human DNase I. The enzyme is involved in endonucleolytic cleavage of extracellular DNA to 5´-phosphodinucleotide and 5´-phosphooligonucleotide end products. It has no effect on intracellular DNA. Optimal activity is dependent on the presence of divalent cations such as calcium and magnesium. Extracellular DNA is a viscous anionic polymer and its breakdown appears to improve the viscosity and viscoelasticity of purulent sputum of individuals with CF, thus reducing airflow obstruction. Dornase alfa does not seem to have any effect on non-purulent sputum.",,,,Dornase alfa is approved.,Dornase alfa is a liquid.,True
20557,,,,,Alipogene tiparvovec is approved and investigational.,,False
20558,,The molecular weight is 423.72.,Omoconazole has a topological polar surface area of 36.28.,The log p value of  is 6.06.,Omoconazole is experimental.,,False
20559,,The molecular weight is 280.42.,Bamipine has a topological polar surface area of 6.48.,The log p value of  is 4.13.,Bamipine is experimental.,,False
20560,,The molecular weight is 479.07.,Mosapramine has a topological polar surface area of 38.82.,The log p value of  is 5.93.,Mosapramine is experimental.,,False
20561,,The molecular weight is 379.5.,Oxypertine has a topological polar surface area of 40.73.,The log p value of  is 4.37.,Oxypertine is experimental.,,False
20562,"Tavaborale is a novel, boron-based topical antifungal medication for the treatment of onychomycosis, a fungal infection of the nail and nail bed due to *Trichophyton rubrum* or *Trichophyton mentagrophytes* infection. Tavaborole functions by inhibiting Leucyl-tRNA synthetase, or LeuRS, an essential fungal enzyme required for protein synthesis and for the catalysis of ATP-dependent ligation of L-leucine to tRNA(Leu). Indicated for the treatment of onychomycosis (a fungal infection) of the toenails due to <i>Trichophyton rubrum</i> or <i>Trichophyton mentagrophytes</i>.  After a single dose, the mean (± standard deviation) peak concentration (Cmax) of tavaborole was 3.54 ± 2.26 ng/mL (n=21 with measurable concentrations, range 0.618-10.2 ng/mL, LLOQ=0.5 ng/mL), and the mean AUClast was 44.4 ± 25.5 ng*hr/mL (n=21). After 2 weeks of daily dosing, the mean Cmax was 5.17 ± 3.47 ng/mL (n=24, range 1.51­-12.8 ng/mL), and the mean AUCτ was 75.8 ± 44.5 ng*hr/mL.  Tavaborole exerts its antifungal activity by blocking cellular protein synthesis through the formation of an adduct with cytoplasmic leucyl-aminoacyl transfer RNA (tRNA) synthetase.",The molecular weight is 151.93.,Tavaborole has a topological polar surface area of 29.46.,The log p value of  is 1.24.,Tavaborole is approved and investigational.,Tavaborole is a solid.,True
20563,"Efinaconazole is a 14 alpha-demethylase inhibitor indicated in the treatment of fungal infection of the nail, known as onychomycosis. It was approved for use in Canada and the USA in 2014 and is marketed by Valeant Pharmaceuticals North America LLC under the name Jublia. Indicated in the treatment of fungal infection of the nail, known as onychomycosis. mean ± SD plasma Cmax on Day 28 of treatment: 0.67 ± 0.37 ng/mL. Efinaconazole is an azole antifungal. Efinaconazole inhibits fungal lanosterol 14α-demethylase involved in the biosynthesis of ergosterol, a constituent of fungal cell membranes. ",The molecular weight is 348.4.,Efinaconazole has a topological polar surface area of 54.18.,The log p value of  is 2.15.,Efinaconazole is approved.,Efinaconazole is a solid.,True
20564,"Reviparin is a low molecular weight heparin which seems to have a better safety profile than unfractionated heparin. It is prepared from porcine intestinal mucosa by nitrous acid depolymerization. Reviparin has a molecular weight of 3.9 kDa. It was developed by Abbott laboratories and in 2009, reviparin presented an orphan drug designation by the FDA. By the FDA, reviparin is indicated for the treatment of deep vein which may lead to pulmonary embolism in pediatric patients. It is also indicated for the long-term treatment of acute deep vein thrombosis with or without pulmonary embolism in pregnant patients. Reviparin is been shown to present significant inhibition of smooth muscle cell migration and proliferation in human cell cultures without affecting endothelial cell growth.",,,,Reviparin is approved and investigational.,Reviparin is a solid.,True
20565,"Elosulfase alfa is a synthetic version of the enzyme N-acetylgalactosamine-6-sulfatase. It was approved by the FDA in 2014 for the treatment of Morquio syndrome. Elosulfase alfa was developed by BioMarin Pharmaceutical Inc. and is marketed under the brand Vimizim™. The recommended dose is 2 mg per kg given intravenously over a minimum range of 3.5 to 4.5 hours, based on infusion volume, once every week. Vimizim is a hydrolytic lysosomal glycosaminoglycan (GAG)-specific enzyme indicated for patients with Mucopolysaccharidosis type IVA (MPS IVA; Morquio A syndrome).  AUC: 238 min x μg/mL, standard deviation 100.  Mucopolysaccharidoses comprise a group of lysosomal storage disorders caused by the deficiency of specific lysosomal enzymes required for the catabolism of glycosaminoglycans (GAG). Mucopolysaccharidosis IVA (MPS IVA, Morquio A Syndrome) is characterized by the absence or marked reduction in N-acetylgalactosamine-6-sulfatase activity. The sulfatase activity deficiency results in the accumulation of the GAG substrates, KS and C6S, in the lysosomal compartment of cells throughout the body. The accumulation leads to widespread cellular, tissue, and organ dysfunction. Vimizim is intended to provide the exogenous enzyme N-acetylgalactosamine-6-sulfatase that will be taken up into the lysosomes and increase the catabolism of the GAGs KS and C6S. Elosulfase alfa uptake by cells into lysosomes is mediated by the binding of mannose-6-phosphate-terminated oligosaccharide chains of elosulfase alfa to mannose-6-phosphate receptors.",,,,Elosulfase alfa is approved and investigational.,Elosulfase alfa is a solid.,True
20566,"Polysorbate, a substance formulated by the reaction of sorbitan fatty acid ester (a nonionic surfactant) with ethylene oxide, is used in many foreign countries, including the U.S. and the EU, where it acts as an emulsifier, a solubilizer in many foods, including bread, cake mix, salad dressing, shortening oil and chocolate. It is used as a solubilizer, antimicrobial preservative and disinfectant. Polysorbates are widely used to protect biological drug products from protein unfolding, aggregation, and precipitation during both shipping and handling. The polysorbates are amphipathic, nonionic surfactants made of fatty acid esters of polyoxyethylene sorbitan. Polysorbate 80 is one of the most common surfactants currently used in the formulation of protein-based biopharmaceuticals. Polysorbate 80 is one of the primary components of protein formulations. This drug inhibits interfacial damage of the protein molecule that undergoes mechanical stress during shipping and handling. Polysorbate 80 also affects the formulation photostability. Exposure to light of polysorbate 80 aqueous solution results in peroxide generation, which in turn may lead to oxidation of the susceptible amino acid residues in the protein molecule.",,,,Polysorbate 80 is approved.,Polysorbate 80 is a liquid.,True
20567,"A clear, colorless, viscous organic solvent and diluent used in pharmaceutical preparations.",The molecular weight is 76.1.,Propylene glycol has a topological polar surface area of 40.46.,The log p value of  is -1.06.,Propylene glycol is approved and investigational.,Propylene glycol is a solid.,True
20568,"Polidocanol is a sclerosing agent indicated to treat uncomplicated spider veins (varicose veins ≤1 mm in diameter) and uncomplicated reticular veins (varicose veins 1 to 3 mm in diameter) in the lower extremity. It is marketed under the brand names Asclera and Varithena. The formula for Polidocanol has the structural formula C12H25(OCH2CH2)nOH, a mean extent of polymerization (n) of approximately 9 and a mean molecular weight of approximately 600. Polidocanol is a sclerosing agent indicated to treat uncomplicated spider veins and uncomplicated reticular veins in the lower extremity.  Polidocanol has a concentration and volume dependent damaging effect on the blood vessel endothelium.  When administered, polidocanol locally damages blood vessel endothelium. Following the endothelial damage, platelets aggregate at the site and attach to the venous wall eventually resulting in a dense network of platelets, cellular debris, and fibrin that occludes the vessel. Eventually the vessel is replaced by connective fibrous tissue.",,,,Polidocanol is approved.,Polidocanol is a liquid.,True
20569,"Moxidectin is a potent, broad-spectrum endectocide (antiparasitic that is active against endo- and ecto-parasites) with activity against nematodes, insects, and acari. It was first used in cattle followed by an approved use in general animals. It is a semi-synthetic methoxine derivative of nemadectin which is a 16-member pentacyclic lactone of the milbemycin class. Moxidectin differs by the absence of a disaccharide moiety on carbon 13, a substituted olefinic side chain at carbon 25 and a unique methoxime moiety at carbon 23. Due to these modifications, moxidectin is classified as a second generation macrocyclic lactone. Moxidectin was developed by Medicines Development for Global Health and FDA approved in June 13, 2018. Moxidectin is indicated for the treatment of river blindness, also called onchocerciasis, in patients aged 12 years and older. River blindness is caused by a parasitic worm _Onchocerca volvulus_ and it is manifested as severe itching, disfiguring skin conditions and visual impairment caused by the worm's larvae.  Moxidectin has been reported to be highly effective against _Onchocerca volvulus_ when compared to ivermectin. When moxidectin was administered in infected individuals, the microfilarial load in the skin was lower even when compared to the current therapy, ivermectin. The levels of microfilarial got reduced to an undetectable level while being safe to be used in mass drug administration. Moxidectin selectively binds to the parasite's GABA-A and glutamate-gated chloride ion channels which are vital for the function of invertebrate nerve and muscle cells. It presents activity against the parasite but it does not kill him. Once moxidectin is bound, there is an increased permeability leading to an influx of chloride ions and flaccid paralysis of the parasite.",,,,Moxidectin is approved and investigational and vet_approved.,Moxidectin is a solid.,True
20570,"Sevelamer is a phosphate binding drug used to prevent hyperphosphataemia in patients with chronic renal failure. It is marketed by Genzyme under the trade name Renagel. For the control of serum phosphorus in patients with Chronic Kidney Disease (CKD) on hemodialysis. Patients with end-stage renal disease (ESRD) retain phosphorus and can develop hyperphosphatemia. High serum phosphorus can precipitate serum calcium resulting in ectopic calcification. When the product of serum calcium and phosphorus concentrations (Ca x P) exceeds 55 mg<sup>2</sup>/dL<sup>2</sup>, there is an increased risk that ectopic calcification will occur. Hyperphosphatemia plays a role in the development of secondary hyperparathyroidism in renal insufficiency. An increase in parathyroid hormone (PTH) levels is characteristic of patients with chronic renal failure. Increased levels of PTH can lead to osteitis fibrosa, a bone disease. A decrease in serum phosphorus may decrease serum PTH levels. Treatment of hyperphosphatemia includes reduction in dietary intake of phosphate, inhibition of intestinal phosphate absorption with phosphate binders, and removal of phosphate with dialysis. Sevelamer taken with meals has been shown to decrease serum phosphorus concentrations in patients with ESRD who are on hemodialysis. <i>In vitro</i> studies have shown that the capsule and tablet formulations bind phosphate to a similar extent. Sevelamer treatment also results in a lowering of low-density lipoprotein (LDL) and total serum cholesterol levels. Sevelamer prevents hyperphosphatemia by binding to dietary phosphate in the gut, preventing its absorption and thus decreasing serum parathyroid hormone levels.",,,,Sevelamer is approved.,Sevelamer is a solid.,True
20571,Imrecoxib has been used in trials studying the treatment of Knee Osteoarthritis.,The molecular weight is 369.48.,Imrecoxib has a topological polar surface area of 54.45.,The log p value of  is 2.71.,Imrecoxib is investigational.,,True
20572,,The molecular weight is 173.17.,Oxaceprol has a topological polar surface area of 77.84.,The log p value of  is -1.25.,Oxaceprol is experimental.,,False
20573,"Polmacoxib has been used in trials studying the treatment of Osteoarthritis, Osteoarthritis, Hip, Osteoarthritis, Knee, Localized Primary Osteoarthritis of Hip, and Localized Primary Osteoarthritis of Knee.",The molecular weight is 361.39.,Polmacoxib has a topological polar surface area of 86.46.,The log p value of  is 2.28.,Polmacoxib is investigational.,,True
20574,Butylphthalide has been used in trials studying the prevention of Restenosis.,The molecular weight is 190.24.,Butylphthalide has a topological polar surface area of 26.3.,The log p value of  is 2.9.,Butylphthalide is investigational.,,True
20575,,The molecular weight is 188.27.,Ipidacrine has a topological polar surface area of 38.91.,The log p value of  is 2.9.,Ipidacrine is experimental.,,False
20576,"Taliglucerase alfa is the recombinant active form of the human lysosomal enzyme, β-glucocerebrosidase. It was approved in 2012 and is marketed under the name Elelyso for use in patients with type 1 Gaucher's disease. For the treatment of adult Type 1 Gaucher disease.  Patient's with Type 1 Gaucher disease have a long-term deficiency in the enzyme, glucocerebrosidase. Taliglucerase alfa is a modified form of glucocerebrosidase and is provided to counter this enzyme deficiency, resulting in smaller liver and spleen size, and improved thrombocytopenia and anemia. Taliglucerase alfa is different from human glucocerebrosidase by two amino acids at the N terminal and up to 7 amino acids at the C terminal. This recombinant enzyme allows the hydrolysis reaction of glucocerebroside to glucose and ceramide that naturally occurs in healthy individuals.",,,,Taliglucerase alfa is approved and investigational.,Taliglucerase alfa is a solid.,True
20577,"Human Beta-glucocerebrosidase or Beta-D-glucosyl-N-acylsphingosine glucohydrolase E.C. 3.2.1.45. 497 residue protein with N-linked carbohydrates, MW=59.3 kD. Alglucerase is prepared by modification of the oligosaccharide chains of human Beta-glucocerebrosidase. The modification alters the sugar residues at the non-reducing ends of the oligosaccharide chains of the glycoprotein so that they are predominantly terminated with mannose residues. For the treatment of Gaucher's disease (deficiency in glucocerebrosidase) Gaucher disease is characterized by a functional deficiency in Beta-glucocerebrosidase enzymatic activity and the resultant accumulation of lipid glucocerebroside in tissue macrophages which become engorged and are termed Gaucher cells. Gaucher cells are typically found in liver, spleen and bone marrow. This can lead to an enlarged spleen and liver (hepatosplenomegaly). Secondary hematologic sequelae include severe anemia and thrombocytopenia. Injections of alglucerase into Gaucher disease patients leads to elevated serum levels of the enzyme and reduction in the accumulation of glucocerebroside Alglucerase catalyzes the hydrolysis of the glycolipid, glucocerebroside, to glucose and ceramide as part of the normal degradation pathway for membrane lipids.",,,,Alglucerase is approved and investigational.,Alglucerase is a liquid.,True
20578,Tandospirone has been used in trials studying the treatment of Schizophrenia.,The molecular weight is 383.5.,Tandospirone has a topological polar surface area of 69.64.,The log p value of  is 1.9.,Tandospirone is investigational.,,True
20579,"Eteplirsen is a phosphoramidite morpholino sequence complementary to a portion of exon 51.  It exerts it's mechanism of action by forcing the exclusion of exon 51 from the mature DMD mRNA.  Eteplirsen is indicated for treatment of certain individuals with Duchenne muscular dystrophy (DMD). Its use is limited to those with a confirmed mutation of the DMD gene which would benefit from exon 51 skipping. Based on clinical studies showing increased dystrophin production in skeletal muscle in some patients given this drug, the above indication was approved under accelerated approval.  Further confirmatory trials are required to demonstrate clinical benefit of eteplirsen. The defining characteristic of DMD is lack of dystrophin, which is a protein that plays a vital role in maintaining muscle cell membrane integrity. (2) This is caused by a mutation in the DMD gene which leads to disruption of the translational reading frame, and ultimately in a non-functional protein. (2) Eteplirsen, is a targeted oligonucleotide that causes exon skipping of exon 51 and restores the translational reading frame. (2) The expected result is production of an internally deleted but functional dystrophin protein. (2)  Eteplirsen, is a targeted oligonucleotide that causes exon skipping of exon 51 and restores the translational reading frame. (2) The expected result is production of an internally deleted but functional dystrophin protein. (2) ",The molecular weight is 10305.89.,Eteplirsen has a topological polar surface area of 3305.26.,,Eteplirsen is approved and investigational.,Eteplirsen is a solid.,True
20580,"Bezlotoxumab is a human monoclonal antibody that binds to Clostridium difficile toxin B and neutralizes its effects. Used to reduce the recurrence of Clostridium difficle infection in adults receiving antibiotic therapy to treat C. difficile infection and high risk of recurrence. Prevents recurrence of Clostridium difficile infection in people 18 years or older who are either currently receiving treatment for C. difficile infection or have a high risk of recurrence.  Bezlotoxumab binds to C.difficile toxin B, a virulence factor common to practically all C.difficile, which prevents the bacteria from infecting host cells. Bezlotoxumab binds two epitopes of toxin B, via two Fab regions, which partially blocks the carbohydrate binding pockets of the toxin resulting in the prevention of toxin B from binding to host cells. A single molecule of bezlotoxumab neutralizes Toxin B by binding its two Fab regions to two epitopes within the N-terminal half of the Toxin B CROP domain, partially blocking the carbohydrate binding pockets of the toxin and preventing toxin binding to host cells.",,,,Bezlotoxumab is approved and investigational.,Bezlotoxumab is a solid.,True
20581,An antibiotic produced by Streptomyces spectabilis. It is active against gram-negative bacteria and used for the treatment of gonorrhea. For use in the treatment of acute gonorrheal urethritis and proctitis in the male and acute gonorrheal cervicitis and proctitis in the female when due to susceptible strains of <i>Neisseria gonorrhoeae</i>. Spectinomycin is an aminocyclitol antibiotic produced by a species of soil microorganism designated as S<i>treptomyces spectabilis</i>. In vitro studies have shown spectinomycin to be active against most strains of <i>Neisseria gonorrhoeae</i> (minimum inhibitory concentration <7.5 to 20 mcg/mL). Footprint studies indicate that spectinomycin exerts regional effects on ribosomal structure. Spectinomycin is an inhibitor of protein synthesis in the bacterial cell; the site of action is the 30S ribosomal subunit. It is bactericidal in its action.,The molecular weight is 332.35.,Spectinomycin has a topological polar surface area of 129.51.,The log p value of  is -2.88.,Spectinomycin is approved and investigational and vet_approved.,Spectinomycin is a solid.,True
20582,Evocalcet has been used in trials studying the treatment of Hyperparathyroidism and Secondary Hyperparathyroidism.,,,,Evocalcet is investigational.,,True
20583,"Xylitol is a naturally occurring five-carbon sugar alcohol found in most plant material, including many fruits and vegetables. Xylitol-rich plant materials include birch and beechwood. It is widely used as a sugar substitute and in \sugar-free\"" food products. The effects of xylitol on dental caries have been widely studied, and xylitol is added to some chewing gums and other oral care products to prevent tooth decay and dry mouth. Xylitol is a non-fermentable sugar alcohol by most plaque bacteria, indicating that it cannot be fermented into cariogenic acid end-products. It works by inhibiting the growth of the microorganisms present in plaque and saliva after it accummulates intracellularly into the microorganism. The recommended dose of xylitol for dental caries prevention is 6–10 g/day, and most adults can tolerate 40 g/day without adverse events."" Indicated for use as a sugar substitute, and oral hygiene active ingredient.  There has been evidence of xylitol in dental hygiene in reducing dental caries disease and also reversing the process of early caries. Xylitol increases salivary flow and pH, reduces the levels of _Streptococcus mutans_ in plaque and saliva and reduces the adhesion on the microorganism to the teeth surface. _Streptococcus mutans_ is the main target plaque microorganism , but xylitol may potentially have inhibitory actions against several other bacterial species. Xylitol is initially taken up by the microorganism and accumulates intracellularly. Accumulated xylitol is transported into an energy-consuming cycle, or the inducible fructose transport system. It is converted to non-metabolizable, toxic xylitol-5-phosphate via phosphoenolpyruvate: a constitutive fructose phosphotransferase system by _S. mutans_. This metabolic process of xylitol, without the gain of any energy molecules, results in the development of intracellular vacuoles and cell membrane degradation. _S. mutans_ dephosphorylates xylitol-5-phosphate and expels it from the cell, in which requires energy consumption. This ultimately leading to starving of microorganism and growth inhibition. Long-term exposure to xylitol can cause microorganisms to develop resistance to xylitol. This clinically beneficial selection process creates xylitol-resistant mutans strains that are less virulent and less cariogenic than their parent strains. Xylitol also increases the concentrations of ammonia and amino acids in plaque, thereby neutralizing plaque acids. A study suggests that xylitol may also promote remineralization of deeper layers of demineralized enamel by facilitating Ca2+ and phosphate movement and accessibility.",The molecular weight is 152.15.,Xylitol has a topological polar surface area of 101.15.,The log p value of  is -1.88.,Xylitol is experimental and investigational.,Xylitol is a solid.,True
20584,"Stannous Fluoride, or Tn(II) Fluoride, is a compound commonly used in toothpastes for the prevention of gingivitis, dental infections, cavities, and to relieve dental hypersensitivity. Although similar in function and activity to Sodium Fluoride (NaF), the conventionally added ingredient in toothpastes, stannous fluoride has been shown to be more effective at stopping and reversing dental lesions. It manages and prevents dental caries and gingivitis by promoting enamel mineralization , reducing gingival inflammation and bleeding through its potential broad-spectrum antibiotic effect and modulation of the microbial composition of the dental biofilm. It is an FDA-approved over-the-counter product. Indicated for use to relieve dental hypersensitivity, increase enamel production, prevent gingivitis and cavities, and control periodontal infections.  Stannous fluoride mediates both bactericidal and bacteriostatic properties and provides an anti-erosive action on tooth enamel.  Stannous fluoride has been shown to manage and prevent dental caries and gingivitis by promoting enamel mineralization, reducing gingival inflammation and bleeding, its potential broad-spectrum antibiotic effect, and through modulation of the microbial composition of the dental biofilm. It works by depositing a stable acid-resistant layer on the tooth surfaces which is composed of calcium fluoride produced when stannous fluoride converts the calcium mineral apatite into fluorapatite. Tin and fluoride mediate anti-erosive actions by interacting with and modifying the absorbent layer composed of salivary proteins such as mucins, perhaps by enhancing the cross-linking between the proteins to result in a more resistant and protective layer against erosion. The efficacy of stannous fluoride solutions seems to depend mainly on the incorporation of tin in the mineralized dentine when the organic portion is preserved but on surface precipitation when the organic portion is continuously digested. Moreover, the relative erosion-inhibiting effects of stannous fluoride strongly depend on the presence or absence of the demineralized organic dentine matrix.",The molecular weight is 158.72.,,,Stannous fluoride is approved.,Stannous fluoride is a solid.,True
20585,Mebeverine has been investigated for the treatment of Irritable Bowel Syndrome and Post-cholecystectomy Gastrointestinal Spasms.,The molecular weight is 429.56.,Mebeverine has a topological polar surface area of 57.23.,The log p value of  is 5.23.,Mebeverine is approved and investigational.,,True
20586,"Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour. It is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse. Dinutuximab is indicated, in combination with granulocyte-macrophage colony-stimulating factor (GM-CSF), interleukin-2 (IL-2), and 13-cis-retinoic acid (RA), for the treatment of pediatric patients with high-risk neuroblastoma who achieve at least a partial response to prior first-line multiagent, multimodality therapy. Despite a high clinical response seen after first-line treatment, the complete eradication of neuroblastoma is rarely achieved and the majority of patients with advanced disease suffer a relapse. Current strategies for treatment include immunotherapy with drugs such as dinutuximab to target surviving neuroblastoma cells and to prevent relapse. In vitro dinutuximab binds to neuroblastoma tumour cells and mediates the lysis of tumour cells via cell-mediated and complement-mediated cytotoxicity.  Dinutuximab is an IgG1 monoclonal human/mouse chimeric antibody against GD2, a disialoganglioside expressed on tumors of neuroectodermal origin, including human neuroblastoma and melanoma, with highly restricted expression on normal tissues. It is composed of the variable heavy- and light-chain regions of the murine anti-GD2 mAb 14.18 and the constant regions of human IgG1 heavy-chain and kappa light-chain. By binding to GD2, dinutiximab induces antibody-dependent cell-mediated cytotoxicity and complement-dependent cytotoxicity of tumor cells thereby leading to apoptosis and inhibiting proliferation of the tumour.",,,,Dinutuximab is approved and investigational.,Dinutuximab is a solid.,True
20587,,The molecular weight is 455.4.,Fenticonazole has a topological polar surface area of 27.05.,The log p value of  is 6.72.,Fenticonazole is experimental.,,False
20588,"Terconazole is an anti-fungal drug that is mainly used to treat vaginal yeast infections (or vaginal candidiasis). It is classified as a _triazole ketal derivative_. Terconazole was initially approved by the FDA in 1987. This drug is available in cream and suppository forms and both have demonstrated high levels of safety, efficacy, and tolerability in clinical trials.  For the treatment of candidiasis (a yeast-like fungal infection) of the vulva and vagina. Terconazole is a triazole antifungal agent available for intravaginal use. It is structurally related to imidazole-derivative antifungal agents, although terconazole and other triazoles have 3 nitrogens in the azole ring. By inhibiting the 14-alpha-demethylase (lanosterol 14-alpha-demethylase), Terconazole inhibits ergosterol synthesis. Depletion of ergosterol in fungal membrane disrupts the structure and many functions of fungal membrane leading to inhibition of fungal growth. Terconazole may exert its antifungal activity by disrupting normal fungal cell membrane permeability. Terconazole and other triazole antifungal agents inhibit cytochrome P450 14-alpha-demethylase in susceptible fungi, which leads to the accumulation of lanosterol and other methylated sterols and a decrease in ergosterol concentration. Depletion of ergosterol in the membrane disrupts the structure and function of the fungal cell leading to a decrease or inhibition of fungal growth.",The molecular weight is 532.47.,Terconazole has a topological polar surface area of 64.88.,The log p value of  is 4.81.,Terconazole is approved.,Terconazole is a solid.,True
20589,"Menatetrenone has been used in trials studying the treatment of Diabetes, Osteoporosis, Prediabetic State, and Hepatocellular Carcinoma.",The molecular weight is 444.66.,Menatetrenone has a topological polar surface area of 34.14.,The log p value of  is 10.56.,Menatetrenone is investigational.,,True
20590,"Anecortave acetate (Retaane) is an analog of cortisol acetate; among the modifications to the steroid are the removal of the 11ß hydroxyl OH group and an addition of a 21-acetate group. As a result of these modifications, anecortave acetate lacks the typical antiinflammatory and immunosuppressive properties of glucocorticoids.Alcon Inc. is developing and marketing Retaane. Investigated for use/treatment in glaucoma and macular degeneration. Anecortave acetate functions as an antiangiogenic agent, inhibiting blood vessel growth by decreasing extracellular protease expression and inhibiting endothelial cell migration. Its angiostatic activity does not seem to be mediated through any of the commonly known pharmacological receptors. (Ophthalmology 2004;111:2316-7) RETAANE blocks signals from multiple growth factors because it acts downstream and independent of the initiating angiogenic stimuli and inhibits angiogenesis subsequent to the angiogenic stimulation. ",The molecular weight is 386.49.,Anecortave acetate has a topological polar surface area of 80.67.,The log p value of  is 2.87.,Anecortave acetate is investigational.,Anecortave acetate is a solid.,True
20591,,The molecular weight is 211.22.,Melevodopa has a topological polar surface area of 92.78.,The log p value of  is -0.29.,Melevodopa is experimental.,,False
20592,"Sacrosidase is a liquid enzyme preparation from S.cerevisiae used for the treatment of congenital sucrose-isomaltase deficiency (CSID). People with CSID have variable amounts of sucrose-isomaltase enzyme activity and therefore have issues metabolizing dietary disaccharide sucrose causing chronic or intermittent watery diarrhea in infants and children. Treatment options for these patients are limited and usually consists of a lifelong sucrose-free diet; therefore, sacrosidase offers a potential alternative for symptom relief. For the treatment of congenital sucrose-isomaltase deficiency (CSID). Sacrosidase is a -fructofuranoside fructohydrolase that hydrolyzes sucrose. Unlike human intestinal sucrase-isomaltase, it has no activity with oligosaccharides containing 1,6 glucosyl bonds.",,,,Sacrosidase is approved.,Sacrosidase is a solid.,True
20593,"Dalbavancin is a second-generation lipoglycopeptide antibiotic that was designed to improve on the natural glycopeptides currently available, such as vancomycin and teicoplanin. Modifications from these older glycoprotein classes facilitated a similar mechanism of action for dalbavancin but with increased activity and once-weekly dosing. Its use is indicated for the treatment of acute bacterial skin and skin structure infections (ABSSSI) caused by the following gram-positive microorganisms: Staphylococcus aureus (including methicillin-susceptible and methicillin-resistant strains), S. pyogenes, S. agalactiae, S. dysgalactiae, the S. anginosus group (including S. anginosus, S. intermedius, and S. constellatus), and Enterococcus faecalis (vancomycin susceptible strains). Dalbavancin acts by interfering with bacterial cell wall synthesis by binding to the D-alanyl-D-alanine terminus of nascent cell wall peptidoglycan and preventing cross-linking. Dalbavancin for injection is indicated for the treatment of adult patients with acute bacterial skin and skin structure infections (ABSSSI), caused by susceptible isolates of the following gram-positive microorganisms: Staphylococcus aureus (including methicillin-susceptible and methicillin-resistant strains), Streptococcus pyogenes, Streptococcus agalactiae, Streptococcus dysgalactiae, Streptococcus anginosus group (including Streptococcus anginosus, Streptococcus intermedius, Streptococcus constellatus) and Enterococcus faecalis (vancomycin susceptible strains). The antibacterial activity of dalbavancin appears to best correlate with the ratio of area under the concentration-time curve to minimal inhibitory concentration (AUC/MIC) for Staphylococcus aureus based on animal models of infection. An exposure-response analysis of a single study in patients with complicated skin and skin structure infections supports the two-dose regimen for which dalbavancin injection is administered. Dalbavancin has a spectrum and mechanism of action similar to vancomycin, a naturally formed glycopeptide antimicrobial. The bactericidal action of dalbavancin results primarily from inhibition of cell-wall biosynthesis. Specifically, dalbavancin prevents incorporation of N-acetylmuramic acid (NAM)- and N-acetylglucosamine (NAG)-peptide subunits from being incorporated into the peptidoglycan matrix; which forms the major structural component of Gram-positive cell walls. The large hydrophilic molecule is able to form hydrogen bond interactions with the terminal D-alanyl-D-alanine moieties of the NAM/NAG-peptides, which is normally a five-point interaction. Binding of dalbavancin to the D-Ala-D-Ala prevents the incorporation of the NAM/NAG-peptide subunits into the peptidoglycan matrix. In addition, dalbavancin alters bacterial-cell-membrane permeability and RNA synthesis. ",The molecular weight is 1816.71.,Dalbavancin has a topological polar surface area of 572.51.,The log p value of  is 5.64.,Dalbavancin is approved and investigational.,Dalbavancin is a solid.,True
20594,"Faropenem medoxomil is an ester prodrug derivative of the beta-lactam antibiotic. The prodrug form of faropenem offers dramatically improved oral bioavailability and leads to higher systemic concentrations of the drug. Faropenem medoxomil is a broad-spectrum antibiotic that is highly resistant to beta-lactamase degradation. It is being developed jointly by Replidyne, Inc. and Forest Laboratories, Inc. Investigated for use/treatment in bacterial infection, bronchitis, otitis media, and pediatric indications. Faropenem has demonstrated excellent in vitro activity against common respiratory pathogens, many aerobic gram-positive organisms, and anaerobes. Activity against gram-negative organisms is more reserved. In vivo data suggest that faropenem is efficacious in treating community-acquired infections including uncomplicated skin and skin structure infections; however, more data may help to characterize faropenem's place in antimicrobial therapy. Like other beta-lactam antibiotics, faropenem acts by inhibiting the synthesis of bacterial cell walls. It inhibits cross-linkage between the linear peptidoglycan polymer chains that make up a major component of the cell wall of Gram-positive bacteria. It does this by binding to and competitively inhibiting the transpeptidase enzyme used by bacteria to cross-link the peptide (D-alanyl-alanine) used in peptidogylcan synthesis.",The molecular weight is 397.4.,Faropenem medoxomil has a topological polar surface area of 111.6.,The log p value of  is -0.25.,Faropenem medoxomil is investigational.,Faropenem medoxomil is a solid.,True
20595,"Faropenem has been used in trials studying the treatment of Tuberculosis, Pulmonary Tuberculosis, and Community Acquired Pneumonia.",The molecular weight is 285.31.,Faropenem has a topological polar surface area of 87.07.,The log p value of  is 0.16.,Faropenem is investigational.,,True
20596,Bunazosin has been used in trials studying the treatment of High Blood Pressure.,The molecular weight is 373.46.,Bunazosin has a topological polar surface area of 93.81.,The log p value of  is 2.1.,Bunazosin is investigational.,,True
20597,"Tivozanib has been used in trials studying the treatment and basic science of Solid Tumors, Glioblastoma, Ovarian Cancer, Prostate Cancer, and Stage IV Disease, among others.",The molecular weight is 454.87.,Tivozanib has a topological polar surface area of 107.74.,The log p value of  is 4.62.,Tivozanib is approved and investigational.,,True
20598,,The molecular weight is 307.39.,Ibopamine has a topological polar surface area of 64.63.,The log p value of  is 1.77.,Ibopamine is experimental.,,False
20599,"A non-benzodiazepine that is used in the management of anxiety. It has been suggested for use in the treatment of muscle spasm. Used in the management of anxiety and in the treatment of muscle spasm. Chlormezanone is a non-benzodiazepine muscle relaxant. It was discontinued worldwide in 1996 by its manufacturer due to confirmed serious and rare cutaneous reactions (toxic epidermal necrolysis). Chlormezanone binds to central benzodiazepine receptors which interact allosterically with GABA receptors. This potentiates the effects of the inhibitory neurotransmitter GABA, increasing the inhibition of the ascending reticular activating system and blocking the cortical and limbic arousal that occurs following stimulation of the reticular pathways.",The molecular weight is 273.73.,Chlormezanone has a topological polar surface area of 54.45.,The log p value of  is 1.58.,Chlormezanone is approved and investigational and withdrawn.,Chlormezanone is a solid.,True
20600,,The molecular weight is 273.3.,Oxaflozane has a topological polar surface area of 12.47.,The log p value of  is 3.45.,Oxaflozane is experimental.,,False
20601,,The molecular weight is 198.23.,Mebicar has a topological polar surface area of 47.1.,The log p value of  is 0.51.,Mebicar is experimental.,,False
20602,"Hemin (trade name Panhematin) is an iron-containing porphyrin. More specifically, it is protoporphyrin IX containing a ferric iron ion (heme B) with a chloride ligand. Used in the management of porphyria attacks, particularly in acute intermittent porphyria.",The molecular weight is 651.95.,Hemin has a topological polar surface area of 92.22.,,Hemin is approved and investigational.,Hemin is a solid.,True
20603,"Amenamevir has been used in trials studying the treatment of Herpes Zoster, Herpes Simplex, Herpes Genitalis, and Safety of Amenamevir.",The molecular weight is 482.56.,Amenamevir has a topological polar surface area of 122.47.,The log p value of  is 1.82.,Amenamevir is investigational.,,True
20604,"Human Beta-glucocerebrosidase or Beta-D-glucosyl-N-acylsphingosine glucohydrolase E.C. 3.2.1.45. 497 residue protein with N-linked carbohydrates, MW=59.3 kD. Alglucerase is prepared by modification of the oligosaccharide chains of human Beta-glucocerebrosidase. The modification alters the sugar residues at the non-reducing ends of the oligosaccharide chains of the glycoprotein so that they are predominantly terminated with mannose residues. For the treatment of Gaucher's disease (deficiency in glucocerebrosidase) Gaucher disease is characterized by a functional deficiency in Beta-glucocerebrosidase enzymatic activity and the resultant accumulation of lipid glucocerebroside in tissue macrophages which become engorged and are termed Gaucher cells. Gaucher cells are typically found in liver, spleen and bone marrow. This can lead to an enlarged spleen and liver (hepatosplenomegaly). Secondary hematologic sequelae include severe anemia and thrombocytopenia. Injections of imiglucerase into Gaucher disease patients leads to elevated serum levels of the enzyme and reduction in the accumulation of glucocerebroside leading to reduced anemia and thrombocytopenia, reduced spleen and liver size, and decreased cachexia Imiglucerase catalyzes the hydrolysis of the glycolipid, glucocerebroside, to glucose and ceramide as part of the normal degradation pathway for membrane lipids.",,,,Imiglucerase is approved.,Imiglucerase is a liquid.,True
20605,"In 2005, the Food and Drug Administration (FDA) withdrew approval for pemoline. In March 2005, Abbott Laboratories (Cylert marketer) had discontinued the production of Cylert arguing economic reasons. For treatment of Attention Deficit Hyperactivity Disorder (ADHD) Pemoline belongs to the group of medicines called central nervous system (CNS) stimulants. It is used to treat attention deficit hyperactivity disorder (ADHD). Pemoline stimulates the brain, probably by affecting neurotransmitters, the chemicals in the brain that nerves use to communicate with each other.",The molecular weight is 176.18.,Pemoline has a topological polar surface area of 64.68.,The log p value of  is 0.46.,Pemoline is approved and illicit and investigational and withdrawn.,Pemoline is a solid.,True
20606,"Secnidazole is a second-generation 5-nitroimidazole antimicrobial that is structurally related to other 5-nitroimidazoles including and , but displays improved oral absorption and longer terminal elimination half-life than antimicrobial agents in this class. Secnidazole is selective against many anaerobic Gram-positive and Gram-negative bacteria and protozoa. In September 2017, FDA granted approval to secnidazole under the market name Solosec as a single-dose oral treatment for bacterial vaginosis, which is a common vaginal infection in women aged 15 to 44 years. The antimicrobial therapy is only intended to treat or prevent infections that are proven or strongly suspected to be caused by susceptible bacteria. Indicated for the treatment of bacterial vaginosis in adult women.  Secnidazole is a nitroimidazole antimicrobial drug that displays selectivity against many anaerobic Gram-positive and Gram-negative bacteria and protozoa. In vitro studies demonstrates the effectiveness of the drug against *Bacteroides fragilis*, *Trichomonas vaginalis*, *Entamoeba histolytica* and *Giardia lamblia*. There is no significant bacterial or protozoal resistance reported from secnidazole treatment.  Secnidazole enters the bacterial cell as a prodrug without an antimicrobial activity. The drug is converted to an active form via reduction of nitro groups to radical anions by bacterial enzymes. The radical anions are thought to interfere with bacterial DNA synthesis of susceptible isolates. ",The molecular weight is 185.18.,Secnidazole has a topological polar surface area of 81.19.,The log p value of  is -0.15.,Secnidazole is approved.,,True
20607,"Idebenone is a synthetic analogue of ubiquinone (also known as Coenzyme Q10), a vital cell antioxidant and essential component of the Electron Transport Chain (ETC). It has been proposed that by interacting with the ETC, idebenone increases ATP production required for mitochondrial function, reduces free radicals, inhibits lipid peroxidation, and consequently protects the lipid membrane and mitochondria from oxidative damage. More specifically, idebenone is thought to transfer electrons directly to complex III of the mitochondrial ETC, thereby circumventing complex I and restoring cellular energy (ATP) generation.  Idebenone is indicated for use by the European Medicines Agency (EMA) for the treatment of visual impairment in adolescent and adult patients with Idebenone is a synthetic analogue of ubiquinone (also known as Coenzyme Q10), a vital cell antioxidant and essential component of the Electron Transport Chain (ETC). It has been proposed that by interacting with the ETC, idebenone increases ATP production required for mitochondrial function, reduces free radicals, inhibits lipid peroxidation, and consequently protects the lipid membrane and mitochondria from oxidative damage. More specifically, idebenone is thought to transfer electrons directly to complex III of the mitochondrial ETC, thereby circumventing complex I and restoring cellular energy (ATP) generation. ",The molecular weight is 338.44.,Idebenone has a topological polar surface area of 72.83.,The log p value of  is 3.42.,Idebenone is approved and investigational.,Idebenone is a solid.,True
20608,Epalrestat is under investigation in clinical trial NCT03244358 (Evaluation of Epalrestat in Metastatic Triple-negative Breast Cancer).,The molecular weight is 319.39.,Epalrestat has a topological polar surface area of 57.61.,The log p value of  is 2.43.,Epalrestat is investigational.,,True
20609,"Racecadotril has been investigated for the basic science and treatment of Diarrhea, Acute Diarrhea, and Acute Gastroenteritis.",The molecular weight is 385.48.,Racecadotril has a topological polar surface area of 72.47.,The log p value of  is 3.85.,Racecadotril is investigational.,,True
20610,,The molecular weight is 331.41.,Tetramethrin has a topological polar surface area of 63.68.,The log p value of  is 4.56.,Tetramethrin is experimental.,,False
20611,"Spinosad is a pediculicide mixture of spinosyn A and spinosyn D (in an approximately 5:1 ratio, respectively) used in the topical treatment of head lice in children (four years old and older) and in adults. Spinosad is an insecticide based on a compound found in S. spinosa, a bacterial species. Spinosad has also been experimented for use in cats for treatment of flea infestations, and has also been experimented for use against the KS1 Ctenocephalides felis flea strain infesting dogs, in addition to many investigations for use in other animals and agricultural plants. Spinosad is indicated for the topical treatment of head lice in children four years old and over and in adults. Spinosyn A does not appear to directly interact with any known relevant insecticidal targets, but instead boasts a novel mechanism that resembles a GABA antagonist. Spinosyn A is also slightly more biologically active than spinosyn D.   Spinosad is a mixture of spinosyn A and spinosyn D in a 5:1 ratio. This combination causes neuronal hyperexcitation through mostly alteration of nicotinic acetylcholine receptors, which ultimately leads to lice paralysis and death.",The molecular weight is 1477.96.,Spinosad has a topological polar surface area of 111.22.,,Spinosad is approved and investigational and vet_approved.,Spinosad is a liquid.,True
20612,,The molecular weight is 339.7.,Phenylmercuric nitrate has a topological polar surface area of 55.05.,,Phenylmercuric nitrate is experimental.,,False
20613,"Azosemide is a loop diuretic used to treat hypertension, edema, and ascites. Diuretic affects upon oral administration match those of furosemide. However, upon intravenous administration azosemide displays 5.5 to 8 times greater effect.  Exact mechanism of action is unclear. However, it acts primarily on the loop of Henle, in both the medullary and cortical segments of the thick ascending limb.",The molecular weight is 370.83.,Azosemide has a topological polar surface area of 126.65.,The log p value of  is 1.36.,Azosemide is investigational.,Azosemide is a solid.,True
20614,,The molecular weight is 768.19.,Padeliporfin has a topological polar surface area of 157.56.,,Padeliporfin is approved and experimental.,,False
20615,"Ethyl chloride, or chloroethane, has a chemical formula C2H5Cl. It was commonly used in the production of tetraethyllead (TEL), which is an additive for gasoline. It was also used in other commerical applications as a chemical reagent. It is still used in the treatment of cellulose to make ethylcellulose for commercial products. Ethyl chloride is used as a diagnostic tool to detect a dead tooth with nonviable pulp.",The molecular weight is 64.51.,,The log p value of  is 1.47.,Ethyl chloride is approved and experimental and investigational.,,True
20616,Melarsoprol is under investigation in clinical trial NCT00330148 (Randomized Clinical Trial of Three Drug Combinations for Late-Stage Gambiense Human African Trypanosomiasis).,The molecular weight is 398.33.,Melarsoprol has a topological polar surface area of 122.97.,The log p value of  is 2.48.,Melarsoprol is investigational.,,True
20617,"Carmofur is a derivative of fluorouracil, and is an antineoplastic agent that has been used in the treatment of breast and colorectal cancer. Carmofur has been known to induce leukoencephalopathy.",The molecular weight is 257.26.,Carmofur has a topological polar surface area of 78.51.,The log p value of  is 2.55.,Carmofur is withdrawn.,Carmofur is a solid.,True
20618,"Teicoplanin is a glycopeptide antibiotic consisting of a mixture of several compounds, five major (named teicoplanin A2-1 through A2-5) and four minor (named teicoplanin RS-1 through RS-4). All teicoplanins share a same glycopeptide core, teicoplanin A3-1, but differ in the length and conformation of side chains attached to their β-D-glucosamine moiety. For the treatment of bacterial infections caused by susceptible microorganisms. It is a glycopeptide antiobiotic extracted from <i>Actinoplanes teichomyceticus</i>, with a similar spectrum of activity to vancomycin. Its mechanism of action is to inhibit bacterial cell wall synthesis. Oral teicoplanin has been demonstrated to be effective in the treatment of pseudomembranous colitis and Clostridium difficile-associated diarrhoea, with comparable efficacy to vancomycin. Teicoplanin inhibits peptidoglycan polymerization, resulting in inhibition of bacterial cell wall synthesis and cell death.",,,,Teicoplanin is approved and investigational.,Teicoplanin is a solid.,True
20619,,The molecular weight is 310.35.,Trepibutone has a topological polar surface area of 82.06.,The log p value of  is 2.69.,Trepibutone is experimental.,,False
20620,"Docosanol is a drug used for topical treatment for recurrent herpes simplex labialis episodes (episodes of cold sores or fever blisters). A saturated 22-carbon aliphatic alcohol, docosanol exhibits antiviral activity against many lipid enveloped viruses including herpes simplex virus (HSV). Docosanol inhibits fusion between the plasma membrane and the herpes simplex virus (HSV) envelope, thereby preventing viral entry into cells and subsequent viral replication. For the topical treatment of recurrent oral-facial herpes simplex episodes (cold sores or fever blisters). Docosanol is a saturated 22-carbon aliphatic alcohol which exhibits antiviral activity against many lipid enveloped viruses including herpes simplex virus (HSV). Docosanol speeds the healing of cold sores and fever blisters on the face or lips. It also relieves the accompanying symptoms, including tingling, pain, burning, and itching. Docosanol cannot, however, prevent cold sores or fever blisters from appearing. Docosanol works by inhibiting fusion between the human cell plasma membrane and the herpes simplex virus (HSV) envelope, thereby preventing viral entry into cells and subsequent viral replication. Unlike other cold-sore antivirals, docosanol does not act directly on the virus, and as such it is unlikely it will produce drug resistant mutants of HSV.",The molecular weight is 326.61.,Docosanol has a topological polar surface area of 20.23.,The log p value of  is 10.34.,Docosanol is approved and investigational.,Docosanol is a solid.,True
20621,"Penciclovir is a synthetic acyclic guanine derivative with antiviral activity used for the treatment of various herpes simplex virus (HSV) infections. Displaying low toxicity and good selectivity, penciclovir is a nucleoside analogue. Used to treat recurrent cold sores on the lips and face from various herpesvirus invections. Penciclovir is the active metabolite of the oral product famciclovir. The more favorable results observed with topical penciclovir versus topical acyclovir for the treatment of herpes labialis may be due to the longer intracellular half-life of penciclovir in HSV-infected cells. The activated drug inhibits the viral DNA polymerase. This impairs the ability of the virus to replicate within the cell. Penciclovir has <i>in vitro</i> activity against herpes simplex virus types 1 (HSV-1) and 2 (HSV-2). In cells infected with HSV-1 or HSV-2, viral thymidine kinase phosphorylates penciclovir to a monophosphate form. The monophosphate form of the drug is then converted to penciclovir triphosphate by cellular kinases. The intracellular triphosphate of penciclovir is retained <i>in vitro</i> inside HSV-infected cells for 10-20 hours, compared with 0.7-1 hour for acyclovir. <i>in vitro</i> studies show that penciclovir triphosphate selectively inhibits viral DNA polymerase by competing with deoxyguanosine triphosphate. Inhibition of DNA synthesis of virus-infected cells inhibits viral replication. In cells not infected with HSV, DNA synthesis is unaltered. Resistant mutants of HSV can occur from qualitative changes in viral thymidine kinase or DNA polymerase. The most commonly encountered acyclovir-resistant mutants that are deficient in viral thymidine kinase are also resistant to penciclovir.",The molecular weight is 253.26.,Penciclovir has a topological polar surface area of 125.76.,The log p value of  is -2.9.,Penciclovir is approved.,Penciclovir is a solid.,True
20622,Talaporfin has been investigated for the treatment of Port-Wine Stain and Benign Prostatic Hyperplasia.,The molecular weight is 711.77.,Talaporfin has a topological polar surface area of 235.66.,The log p value of  is 7.3.,Talaporfin is investigational.,,True
20623,"Lactitol, also known as 4-β-D-galactopyranosyl-D-glucitol, is a sugar alcohol synthesized from. It is used in food manufacturing as a nutritive sweetener and is approximately 35% as sweet as table sugar (i.e. ). Clinically, lactitol has been investigated for use as an osmotic laxative and, along with other non-absorbable disaccharides such as , in the treatment of hepatic encephalopathy in patients with cirrhosis. Lactitol is indicated for the treatment of chronic idiopathic constipation in adults. Lactitol helps to facilitate bowel movements by drawing water into the gastrointestinal tract. The oral administration of lactitol may reduce the absorption of concomitant medications - other oral medications should be administered at least 2 hours before or 2 hours after lactitol. Lactitol is an osmotic laxative - it exerts its pharmacologic effect by creating a hyperosmotic environment within the small intestine. The osmotic effect generated by lactitol draws water into the small intestine, which loosens stools and ultimately facilitates bowel movements.",The molecular weight is 344.31.,Lactitol has a topological polar surface area of 200.53.,The log p value of  is -4.23.,Lactitol is approved and investigational.,Lactitol is a solid.,True
20624,"Carbamide peroxide, also known as urea-hydrogen peroxide, is a water-soluble, white crystalline solid compound consisting of hydrogen peroxide and urea. As it is a source of hydrogen peroxide, it can be found in disinfecting and dental bleaching products. Some adverse effects of carbamide peroxide as a dental bleaching agent include dentin sensitivity and/or gingival irritation led by unstable and reactive H+ free radicals and low pH from prolonged use. It may also alter enamel surface morphology via enamel mineral loss and surface roughening. The FDA considers carbamide peroxide to be safe in oral mucosal injury drug products as an oral wound healing agent, although there is insufficient data to establish general recognition of the effectiveness of this ingredient as an oral wound healing agent. It is available in OTC otic drugs as non-water, non-oil-based solutions used to soften, loosen and remove excessive ear wax, or cerumen. Indicated as a dental bleaching agent.  Carbamide peroxide releases hydrogen peroxide and free radicals upon contact with water or outer surfaces of ear and tooth. Hydrogen peroxide exerts cerumenolytic, enamel-bleaching and antiseptic actions. _In vitro_, the chemical stability of ceramics against bleaching agents was observed after treatment with 15% carbamide peroxide for 56 h, 16% carbamide peroxide for 126 h, 10% or 15% carbamide peroxide and 38% hydrogen peroxide for 30 minutes or 45 minutes, respectively. According to _in vitro_ studies, high (37%) or low (10 or 16%) concentrated carbamide peroxide agents were similarly effective as oral bleaching agents. Treatment with carbamide peroxide may lead to demineralization which involves decreased mineral content of enamel calcium, phosphate, and fluoride, and alteration of the chemical, structural, and mechanical properties. Carbamide peroxide may affect the organic components of the enamel and lead to increased susceptibility to erosion, fracture stability or decreased abrasion resistance of the treated area. Carbamide peroxide release hydrogen peroxide upon contact with teeth, which is a strong oxidizing and bleaching agent. It also release free radicals such as H+ or H3O+. Hydrogen peroxide also acts as an antiseptic, especially in sites with relative anaerobiosis. Following otic administration, carbamide peroxide complex releases hydrogen peroxide that breaks up the hardened wax. The hydrogen peroxide component, which further breaks down into water, is also a cerumenolytic that hydrates the desquamated sheets of corneocytes, which are the major constituent of cerumen plugs. The glycerol and urea facilitates softening of the cerumen, either with or without syringing. Both hydrogen peroxide and urea mildly induce keratolysis with disintegration of the ear wax to help reduce the keratin-load in the ear debris and allow other active components to reach the skin under the debris. ",The molecular weight is 94.07.,Carbamide peroxide has a topological polar surface area of 69.11.,,Carbamide peroxide is approved.,Carbamide peroxide is a solid.,True
20625,,The molecular weight is 350.46.,Phenothrin has a topological polar surface area of 35.53.,The log p value of  is 7.43.,Phenothrin is experimental.,,False
20626,,The molecular weight is 418.62.,Maxacalcitol has a topological polar surface area of 69.92.,The log p value of  is 4.17.,Maxacalcitol is investigational.,Maxacalcitol is a solid.,False
20627,"Stibophen is used in the treatment of schistosomiasis, a disease of parasitic flatworms.",The molecular weight is 895.2.,Stibophen has a topological polar surface area of 160.52.,,Stibophen is experimental.,,True
20628,"Pancrelipase, in general, is composed of a mixture of pancreatic enzymes which include amylases, lipases, and proteases. These enzymes are extracted from porcine pancreatic glands. The pancrelipase mixture was developed by Ortho-McNeil-Janssen Pharmaceuticals, Inc and FDA approved on April 12, 2010. For further information on the components of this mixture please visit , and. The use of pancrelipase amylase is part of the pancreatic enzyme replacement therapy. This therapy is indicated for the treatment of pancreatic insufficiency attributed to cystic fibrosis, chronic pancreatitis or any other medically defined pancreatic disease that might require it. Pancreatic diseases are associated with the deterioration of pancreatic parenchyma and of the dual physiological functions of the pancreas. Once established, pancreatic insufficiency results in malnutrition, weight loss, and steatorrhea. The major maldigestion/malabsorption problems arise from incomplete fat digestion. In clinical trials, the administration of pancrelipase as a mixture of amylase, lipase, and protease demonstrated a significant improvement in the coefficient of fat absorption and nitrogen absorption. These effects are accompanied by increased in body weight and body mass index. Pancrelipase is used to replace the deficiency of pancreatic enzymes. As abovementioned, pancrelipase is formed by a mixture of lipase, protease, and amylase which are able to break down fat, protein, and starches, respectively, in the small intestine. For a more specific description of each mechanism of action, please visit , and. ",,,,Pancrelipase is approved and investigational.,Pancrelipase is a solid.,True
20629,,The molecular weight is 309.45.,Levomethadone has a topological polar surface area of 20.31.,The log p value of  is 4.17.,Levomethadone is experimental.,,False
20630,"For use in females, for palliation of androgenresponsive recurrent mammary cancer in women who are more than one year but less than five years postmenopausal. Dromostanolone is a synthetic androgen, or male hormone, similar to testosterone. Dromostanolone works by attaching itself to androgen receptors; this causes it to interact with the parts of the cell involved in the making of proteins. It may cause an increase in the synthesis of some proteins or a decrease in the synthesis of others. These proteins have a variety of effects, including blocking the growth of some types of breast cancer cells, stimulating cells that cause male sexual characteristics, and stimulating the production of red blood cells. Dromostanolone is a synthetic androgenic anabolic steroid and is approximately 5 times as potent as natural methyltestosterone. Like testosterone and other androgenic hormones, dromostanolone binds to the androgen receptor. This causes downstream genetic transcriptional changes. This ultimately causes retention of nitrogen, potassium, and phosphorus; increases protein anabolism; and decreases amino acid catabolism. The antitumour activity of dromostanolone appears related to reduction or competitive inhibition of prolactin receptors or estrogen receptors or production.",The molecular weight is 360.54.,Drostanolone propionate has a topological polar surface area of 43.37.,The log p value of  is 5.55.,Drostanolone propionate is approved and illicit.,,True
20631,"Burosumab (KRN23) is an entirely human monoclonal IgG1 antibody that binds excess fibroblast growth factor 23 (FGF23) and has been successfully tested in clinical trials in children with X-linked hypophosphatemic rickets.  This drug is indicated for the treatment of X-linked hypophosphatemia with radiological evidence of bone disease in children of 1 year of age and older and adolescents with growing skeletons. This drug has the ability to reduce the loss of phosphate, to improve pathologically low serum phosphate concentrations and other metabolic changes, as well as to reduce the severity of rickets as seen radiographically. In summary, this drug works to support of bone mineralization. Burosumab is a recombinant human monoclonal antibody (IgG1) that both binds to and inhibits the actions of fibroblast growth factor 23 (FGF23). By inhibiting this growth factor, burosumab increases the tubular reabsorption of phosphate from the kidney and thus increases serum concentration of 1, 25 dihydroxy-Vitamin D. This form of vitamin D enhances intestinal absorption of phosphate and calcium, supporting bone mineralization.",,,,Burosumab is approved and investigational.,Burosumab is a solid.,True
20632,"A highly reactive aldehyde gas formed by oxidation or incomplete combustion of hydrocarbons. In solution, it has a wide range of uses: in the manufacture of resins and textiles, as a disinfectant, and as a laboratory fixative or preservative. Formaldehyde solution (formalin) is considered a hazardous compound, and its vapor toxic. (From Reynolds, Martindale The Extra Pharmacopoeia, 30th ed, p717) Use for drying skin before or after surgical removal of warts or where dryness is required. ",The molecular weight is 30.03.,Formaldehyde has a topological polar surface area of 17.07.,The log p value of  is 0.35.,Formaldehyde is approved and vet_approved.,Formaldehyde is a gas.,True
20633,,The molecular weight is 171.2.,Moroxydine has a topological polar surface area of 98.22.,The log p value of  is -3.29.,Moroxydine is experimental.,,False
20634,"Peramivir is an antiviral agent developed by Biocryst Pharmaceuticals to treat influenza A/B. The development of peramivir has been supported by the US Department of Health and Human Services as part of the government's effort to prepare for a flu pandemic. Being an influenza virus neuraminidase inhibitor, peramivir works by preventing new viruses from emerging from infected cells. Due to the poor oral bioavailability, the oral formulation of the drug was previously abandoned by Johnson and Johnson Company. The injectable intravenous formulation of peramivir was approved by the FDA in September 2017 for the treatment of acute uncomplicated influenza to pediatric patients 2 years and older who have been symptomatic for no more than two days. Indicated for the treatment of acute uncomplicated influenza in patients 18 years and older who have been symptomatic for no more than two days. Peramivir is an inhibitor of influenza neuraminidase, preventing new virus particles from leaving infected cells.",The molecular weight is 328.41.,Peramivir has a topological polar surface area of 148.53.,The log p value of  is -1.31.,Peramivir is approved and investigational.,Peramivir is a solid.,True
20635,Laninamivir octanoate has been used in trials studying the treatment of Asthma.,The molecular weight is 472.54.,Laninamivir octanoate has a topological polar surface area of 193.29.,The log p value of  is -2.21.,Laninamivir octanoate is investigational.,,True
20636,,The molecular weight is 255.27.,Tenonitrozole has a topological polar surface area of 85.13.,The log p value of  is 1.5.,Tenonitrozole is experimental.,,False
20637,,,,,Hachimycin is experimental.,,False
20638,"Uridine triacetate, formerly known as vistonuridine, is an orally active prodrug of the naturally occurring nucleoside uridine. It is used for the treatment of hereditary orotic aciduria (Xuriden), or for the emergency treatment of fluorouracil or capecitabine overdose or toxicity (Vistogard). It is provided in the prodrug form as uridine triacetate as this form delivers 4- to 6-fold more uridine into the systemic circulation compared to equimolar doses of uridine itself.  Marketed as the product Xuriden (FDA), uridine triacetate is indicated for the treatment of hereditary orotic aciduria. Uridine triacetate is a synthetic uridine pro-drug that is converted to uridine in vivo. When used for the treatment or prevention of toxicity associated with fluorouracil and other antimetabolites, uridine triacetate is utilized for its ability to compete with 5-fluorouracil (5-FU) metabolites for incorporation into the genetic material of non-cancerous cells. It reduces toxicity and cell-death associated with two cytotoxic intermediates: 5-fluoro-2'-deoxyuridine-5'-monophosphate (FdUMP) and 5-fluorouridine triphosphate (FUTP). By pre-administering with uridine (as the prodrug uridine triacetate), higher doses of 5-FU can be given allowing for improved efficacy and a reduction in toxic side effects such as neutropenia, mucositis, diarrhea, and hand–foot syndrome. ",The molecular weight is 356.29.,Uridine triacetate has a topological polar surface area of 137.54.,The log p value of  is -0.59.,Uridine triacetate is approved and investigational.,Uridine triacetate is a solid.,True
20639,,The molecular weight is 354.45.,Hexamidine has a topological polar surface area of 118.2.,The log p value of  is 2.84.,Hexamidine is approved and experimental.,Hexamidine is a solid.,False
20640,,The molecular weight is 314.47.,Sulbentine has a topological polar surface area of 6.48.,The log p value of  is 4.26.,Sulbentine is experimental.,,False
20641,Urapidil has been investigated for the treatment of Hypertension During Pre-Eclampsia.,The molecular weight is 387.48.,Urapidil has a topological polar surface area of 68.36.,The log p value of  is 2.44.,Urapidil is investigational.,,True
20642,"Luspatercept is a recombinant fusion protein comprised of a modified extracellular domain of activin receptor type IIB fused to the FC domain of human IgG1. It was first approved for use in the United States in November 2019 under the brand name Reblozyl® for the treatment of anemia in patients with beta thalassemia who require regular blood transfusions. Luspatercept is novel in that it ameliorates anemia via action on late-stage erythropoiesis, in contrast to typical erythropoiesis-stimulating agents (ESAs), such as and , which act only on early-stage erythropoiesis. Luspatercept's novel mechanism of action, then, is uniquely suited for the treatment of conditions in which late-stage erythropoiesis is defective, such as beta thalassemia and other myelodysplastic diseases. Luspatercept is indicated for the treatment of anemia in adults with beta thalassemia who require regular red blood cell transfusions. Luspatercept binds to, and inhibits, several ligands that act as negative regulators of late-stage erythropoiesis, thereby alleviating the ineffective erythropoiesis observed in patients with beta thalassemia. Thromboembolic events (e.g. deep vein thrombosis, pulmonary embolism, ischemic stroke) have been reported in patients with beta thalassemia receiving luspatercept - patients with a greater baseline risk of thromboembolism may benefit from concomitant thromboprophylaxis while undergoing therapy with luspatercept. Luspatercept may carry some degree of embryo-fetal toxicity and should therefore be avoided in pregnancy. Women of child-bearing age should use an effective form of contraception during therapy and for 3 months after completion of therapy. Beta thalassemia is a genetic red blood cell disorder caused by mutations in the β-globin gene - these mutations cause oxidative stress and premature apoptosis of erythroblasts, thereby leading to ineffective erythropoesis. The transforming growth factor beta (TGF-β) superfamily of endogenous ligands (including activins, growth differentiation factors, and bone morphogenetic proteins) are involved in the inhibition of erythroid differentiation via activation of the Smad2/3 subfamily of intracellular effectors.",,,,Luspatercept is approved and investigational.,Luspatercept is a solid.,True
20643,"Temoporfin is a photosensitizing agent used in the treatment of squamous cell carcinoma of the head and neck. It was first authorized for market by the European Medicines Agency in October 2001. It is currently available under the brand name Foscan. For use in the treatment of patients with advanced squamous cell carcinoma of the head and neck failing standard therapies and who are unsuitable for radiotherapy, surgery, or systemic chemotherapy. Temoporfin is a photosensitizing agent. It enters cancer cells and is activated via light to produce reactive species which destroy the cell. Temoporfin is excited from ground state to the first excited singlet state by the application of 652 nm light. It is then thought to undergo intersystem crossing to an excited triplet state which is longer lived and able to interact with surrounding molecules. It is then thought to produce cytotoxic species by either a Type I or Type II reaction typical of agents used in photodynamic therapy. Type I involves either hydrogen abstraction of electron transfer from the excited photosensitizer to a substrate molecule to produce free radicals or radical ions. Type II reactions involve a similar reaction with oxygen as the substrate to produce reactive oxygen species. These reactive products cause oxidative damage to the cancer cell resulting in cell death.",The molecular weight is 680.76.,Temoporfin has a topological polar surface area of 138.28.,The log p value of  is 12.13.,Temoporfin is approved and investigational.,Temoporfin is a solid.,True
20644,"Monoxerutin is a flavonol, a type of flavonoid.",The molecular weight is 654.57.,Monoxerutin has a topological polar surface area of 274.75.,The log p value of  is -1.67.,Monoxerutin is experimental.,,True
20645,"Benznidazole was granted accelerated approval for the treatment of Chagas disease in children 2-12 years of age by the FDA on August 29, 2017. It is the first treatment made available in the United States for Chagas disease. For use in the treatment of Chagas disease in children 2-12 years of age. Benznidazole is a trypanocidal agent which kills the causative organism in Chagas disease, *Trypanosoma cruzi*. Benznidazole is thought to be reduced to various electrophilic metabolites by nitroreductases present in *Trypanosoma cruzi*. These metabolites likely bind to proteins, lipids, DNA, and RNA resulting in damage to these macromolecules. Benznidazole has been found to increase trypanosomal death through interferon-γ which is likely present in increased amounts due to inflammation caused by macromolecule damage. DNA in parasites affected by benznidazole has been found to undergo extensive unpacking with overexpression of DNA repair proteins supporting the idea of DNA damage contributing to the mechanism of the drug.",The molecular weight is 260.25.,Benznidazole has a topological polar surface area of 90.06.,The log p value of  is 0.9.,Benznidazole is approved and investigational.,,True
20646,"Eftrenonacog alfa is a long-acting recombinant fusion protein used in the treatment of hemophilia B. It is comprised of a single molecule of human factor IX (FIX) covalently linked to the constant region (Fc) domain of human IgG1 via recombinant DNA technology in a human embryonic kidney cell line (HEK293H). The presence of the Fc domain extends the terminal half-life which confers clinical benefits of prolonged therapeutic efficacy, less frequent intravenous injections for patient convenience and improved adherence to prophylaxis.  Indicated for the treatment and prophylaxis of bleeding in patients of all age with haemophilia B (congenital factor IX deficiency). In two multinational, phase III studies in previously treated children, adolescents and adults with severe haemophilia B, eftrenonacog alfa prophylaxis resulted in low median annualized bleeding rates (ABRs), and was associated with reductions in median weekly factor consumption and dosing frequency compared with pre-study FIX regimens. The extension of those studies demonstrated effectiveness in the treatment of bleeding episodes and when used in the perioperative setting in all age groups. In animal models, a single intravenous dose of eftrenonacog alfa displayed half values approximately three- to four-fold longer than those seen with recombinant FIX. The coagulation protein factor IX (FIX) is a vitamin K-dependent coagulation factor and one of the critical serine proteases involved in the coagulation cascade. Upon activation by factor XIa in the intrinsic coagulation pathway and by the factor VII/tissue factor complex in the extrinsic pathway, factor IX, in combination with factor VIII, activates factor X. Activated factor X mediates the conversion of prothrombin to thrombin which sequentially leads to thrombin converting fibrinogen into fibrin. A blood clot is then formed. With a mutation in the gene encoding the coagulation protein factor IX (FIX), patients with hemophilia B have factor IX deficiency and are at high risk for recurrent bleeding episodes. ",,,,Eftrenonacog alfa is approved and investigational.,Eftrenonacog alfa is a solid.,True
20647,"Human recombinant alpha-L-iduronidase, 628 residues (mature form), produced by recombinant DNAtechnology in a Chinese hamster ovary cell line. Laronidase is a glycoprotein with a molecular weight of approximately 83 kD. The predicted amino acid sequence of the recombinant form, as well as the nucleotide sequence that encodes it, are identical to a polymorphic form of human a-L-iduronidase. It contains 6 N-linked oligosaccharide modification sites. For the treatment of mucopolysaccharidosis Laronidase is used to treat mucopolysaccharide storage disorders (specifically mucopolysaccharidosis 1 or Hurlers syndrome) caused by deficiencies of alpha-L-iduronidase. Reduced or absent a-L-iduronidase activity results in the accumulation of the GAG substrates, dermatan sulfate and heparan sulfate, throughout the body and leads to widespread cellular, tissue, and organ dysfunction. Laronidase catalyses the hydrolysis of terminal alpha-L-iduronic acid residues of dermatan sulfate and heparin sulfate.",,,,Laronidase is approved.,Laronidase is a liquid.,True
20648,"Benperidol has been used in trials studying the treatment of Dementia, Depression, Schizophrenia, Anxiety Disorders, and Psychosomatic Disorders, among others.",The molecular weight is 381.45.,Benperidol has a topological polar surface area of 52.65.,The log p value of  is 3.8.,Benperidol is approved and investigational.,,True
20649,"Vestronidase alfa, or vestronidase alfa-vjbk, is a recombinant human lysosomal beta glucuronidase that is a purified enzyme produced by recombinant DNA technology in a Chinese hamster ovary cell line. The enzyme is a homotetramer consisted of 4 monomers with 629 amino acids, and holds the same amino acid sequence as human beta-glucuronidase (GUS). Vestronidase alfa is an enzyme replacement therapy for the treatment of mucopolysaccharidosis type VII (MPS VII), also known as Sly syndrome, which is an inherited, rare genetic metabolic condition that targets a small subset of population. MPS VII is a progressive condition that affects most tissues and organs due to the lack of a lysosomal enzyme called beta-glucuronidase, leading to buildup of toxic metabolites. The disorder is initiated with skeletal abnormalities, including short stature, along with other pathological conditions including enlarged liver and spleen, heart valve abnormalities, and narrowed airways which can lead to lung infections and trouble breathing. Last two conditions are leading causes of fatalities in patients with MPS VII.  Indicated in pediatric and adult patients for the treatment of Mucopolysaccharidosis VII (MPS VII, Sly syndrome). In all patients evaluated, MEPSEVII treatment resulted in reduction of urinary excretion of GAGs including chondroitin sulfate and dermatan sulfate, which was sustained with continued treatment. Beta-glucuronidase (GUS) is a lysosomal enzyme responsible for degradation of glucuronate-containing glycosaminoglycan (GAG). Resulting lysosomal storage and GAG accumulation in cells from incomplete metabolic degradation of macromolecules leads to damage to multiple tissues and organs. Vestronidase alfa serves as an exogenous source of GUS enzyme for uptake into cellular lysosomes, which is facilitated by the presence of mannose-6-phosphate (M6P) residues on the oligosaccharide chains of the recombinant enzyme. The chains allow binding of the enzyme to cell surface receptors to promote cellular uptake, and targets the lysosomes to achieve catabolism of accumulated GAGs in affected tissues.",,,,Vestronidase alfa is approved and investigational.,Vestronidase alfa is a liquid.,True
20650,"Prussian blue is described as a deep blue pigment that is produced when the oxidation of ferrous ferrocyanide salts occurs. It contains ferric hexacyanoferrate(II) in a cubic lattice crystal structure. It is insoluble in water but also tends to form a colloid thus can exist in either colloidal or water-soluble form, and an insoluble form. It is orally administered for clinical purposes to be used as an antidote for certain kinds of heavy metal poisoning, such as thallium and radioactive isotopes of caesium. Prussian blue is included in the World Health Organization Model List of Essential Medicines as a specific antidote used in poisonings to provide symptomatic and supportive treatment. It was also administered in individuals exposed to 137-Cs+ during Goiânia accident, one of the worst radioactive contamination incidents that occured in Brazil, 1983. Indicated for treatment of patients with known or suspected internal contamination with radioactive cesium and/or radioactive or non-radioactive thallium to increase their rates of elimination.  Prussian blue is an insoluble radioactive metals chelating agent and absorbent. It acts by ion-exchange, adsorption, and mechanical trapping within the crystal structure and has a very high affinity for radioactive and non-radioactive cesium and thallium. The antidote therapy greatly minimizes the extent of contamination and reduces the half life of radioactive isotopes which have relatively long physicall half life and uniform tissue distribution. Data suggest that in humans, Prussian blue can reduce cesium’s half-life by approximately 43% and reduce total body burdens by significantly increasing the feces-to-urine excretion ratio.  Prussian blue binds cesium and thallium isotopes in the gastrointestinal tract after ingestion or excreted in the bile by the liver, therby reduces gastrointestinal reabsorption into the enterohepatic circulation. It serves as an ion exchanger for univalent cations and it preferentially binds to cesium or thallium as its affinity for cations increases as the ionic radius of the cation increases. Prussian blue exchanges potassium for cesium or thallium at the surface of the crystal in the intestinal lumen. The insoluble complex is excreted without being absorbed from the intestinal walls. Insoluble prussian blue decreases the half life of cesium by 33% and from 3.8 to 2.2 days for thallium. The rate of cesium and thallium elimination is proportional to the dose and duration of prussian blue. ",The molecular weight is 859.24.,Prussian blue has a topological polar surface area of 142.74.,,Prussian blue is approved.,Prussian blue is a solid.,True
20651,"Sebelipase alfa is a recombinant form of the enzyme lysosomal acid lipase (LAL) approved for the treatment of lysosomal acid lipase deficiency (LAL-D). The amino acid sequence for sebelipase alfa is the same as the amino acid sequence for human LAL. Sebelipase alfa is an orphan drug which is expected to cost about $310,000 for annual treatment in the United States. Sebelipase alfa is marketed under the brand name Kanuma™ by Alexion Pharmaceuticals, Inc. Sebelipase alfa is a hydrolytic lysosomal cholesteryl ester and triacylglycerol-specific enzyme indicated for the treatment of patients with a diagnosis of Lysosomal Acid Lipase (LAL) deficiency.  LAL deficiency is an autosomal recessive lysosomal storage disorder characterized by a genetic defect resulting in a marked decrease or loss in activity of the lysosomal acid lipase (LAL) enzyme. The primary site of action of the LAL enzyme is the lysosome, where the enzyme normally causes the breakdown of lipid particles including LDL-c. Deficient LAL enzyme activity results in progressive complications due to the lysosomal accumulation of cholesteryl esters and triglycerides in multiple organs, including the liver, spleen, intestine, and the walls of blood vessels. The resulting lipid accumulation in the liver may lead to increased liver fat content and progression of liver disease, including fibrosis and cirrhosis. Lipid accumulation in the intestinal wall leads to malabsorption and growth failure. In parallel, dyslipidemia due to impaired degradation of lysosomal lipid is common with elevated LDL-c and triglycerides and low HDL-cholesterol (HDL-c). Sebelipase alfa binds to cell surface receptors via glycans expressed on the protein and is subsequently internalized into lysosomes. Sebelipase alfa catalyzes the lysosomal hydrolysis of cholesteryl esters and triglycerides to free cholesterol, glycerol and free fatty acids. ",,,,Sebelipase alfa is approved and investigational.,Sebelipase alfa is a liquid.,True
20652,"Sivelestat has been used in trials studying the treatment of Acute Lung Injury and Respiratory Distress Syndrome, Adult.",The molecular weight is 434.46.,Sivelestat has a topological polar surface area of 138.87.,The log p value of  is 2.77.,Sivelestat is investigational.,,True
20653,"An antisense oligonucleotide that induces survival motor neuron (SMN) protein expression, it was approved by the U.S. FDA in December, 2016 as Spinraza for the treatment of children and adults with spinal muscular atrophy (SMA). It is adminstrated as direct intrathecal injection. Indicated for the treatment of spinal muscular atrophy (SMA) in pediatric and adult patients.  Autopsy samples from patients (n=3) had higher levels of SMN2 messenger ribonucleic acid (mRNA) containing exon 7 in the thoracic spinal cord compared to untreated SMA infants. Nusinersen is a survival motor neuron-2 (SMN2)-directed antisense oligonucleotide (ASO) designed to treat SMA caused by mutations in chromosome 5q that lead to SMN protein deficiency. Using in vitro assays and studies in transgenic animal models of SMA, nusinersen was shown to increase exon 7 inclusion in SMN2 messenger ribonucleic acid (mRNA) transcripts and production of full-length SMN protein. ",The molecular weight is 7500.86.,Nusinersen has a topological polar surface area of 2257.9.,,Nusinersen is approved and investigational.,Nusinersen is a solid.,True
20654,"Cefmenoxime is a novel broad-spectrum and third-generation cephalosporin antibiotic that is typically used in the treatment of female gynecologic and obstetric infections. It is reported to exhibit high activity against a wide variety of gram-positive and gram-negative bacteria. Used to treat female gynecologic and obstetric infections caused by susceptible aerobic (including the gonococcus) and anaerobic bacteria. Cefmenoxime is a semisynthetic beta-lactam cephalosporin antibiotic with activity similar to that of cefotaxime. It has broad spectrum activity against Gram positive and Gram negative bacteria. The bactericidal activity of cefmenoxime results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs). Cefmenoxime is stable in the presence of a variety of b-lactamases, including penicillinases and some cephalosporinases.",The molecular weight is 511.55.,Cefmenoxime has a topological polar surface area of 190.81.,The log p value of  is 0.25.,Cefmenoxime is approved.,Cefmenoxime is a solid.,True
20655,"Ceforanide is administered parenterally. It has a longer elimination half-life than any currently available cephalosporin. Its activity is very similar to that of cefamandole, another second-generation cephalosporin antibiotic, except that ceforanide is less active against most gram-positive organisms. Many coliforms, including Escherichia coli, Klebsiella, Enterobacter, and Proteus, are susceptible to ceforanide, as are most strains of Salmonella, Shigella, Hemophilus, Citrobacter and Arizona species. For the treatment of infections caused by susceptible organisms. Ceforanide is a semisynthetic second-generation cephalosporin. The cephalosporins are bactericidal drugs with both gram-positive and gram-negative activity. They inhibit bacterial cell wall synthesis in a way similar to the penicillins. The bactericidal activity of ceforanide results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs).",The molecular weight is 519.55.,Ceforanide has a topological polar surface area of 193.63.,The log p value of  is -3.35.,Ceforanide is approved.,Ceforanide is a solid.,True
20656,"Cefditoren is an oral third-generation cephalosporin. It is commonly marketed under the trade name Spectracef by Cornerstone BioPharma. For the treatment of mild to moderate infections in adults and adolescents (12 years of age or older) which are caused by susceptible strains of microorganisms in acute bacterial exacerbation of chronic bronchitis, community-acquired pneumonia, pharyngitis/tonsillitis, and uncomplicated skin and skin-structure infections. Cefditoren pivoxil is a prodrug which is hydrolyzed by esterases during absorption, and the drug is distributed in the circulating blood as active cefditoren. Cefditoren is a cephalosporin with antibacterial activity against gram-positive and gram-negative pathogens. Cefditoren is effective against <i>Staphylococcus aureus</i> (methicillin-susceptible strains, including b-lactamase-producing strains), penicillin-susceptible strains of <i>Staphylococcus aureus</i> and <i>Streptococcus pneumoniae</i>, <i>Streptococcus pyogenes</i>, <i>Haemophilus influenzae</i> (including b-lactamase-producing strains), <i>Haemophilus parainfluenzae</i> (including b-lactamase-producing strains), <i>Moraxella catarrhalis</i> (including b-lactamase-producing strains), <i>Streptococcus agalactiae</i>, <i>Streptococcus</i> Groups C and G, and <i>Streptococcus</i>, viridans group (penicillin-susceptible and -intermediate strains). The bactericidal activity of cefditoren results from the inhibition of cell wall synthesis via affinity for penicillin-binding proteins (PBPs). Cefditoren is stable in the presence of a variety of b-lactamases, including penicillinases and some cephalosporinases.",,,,Cefditoren is approved and investigational.,Cefditoren is a solid.,True
20657,"Cefpodoxime is an oral third generation cephalosporin antibiotic with effectiveness against most Gram positive and Gram negative bacteria. Commonly used to treat acute otitis media, pharyngitis, and sinusitis, cefpodoxime proxetil is a prodrug which is absorbed and de-esterified by the intestinal mucosa to Cefpodoxime. Indicated for the treatment of patients with mild to moderate infections caused by susceptible strains of the designated microorganisms. Cefpodoxime is shown to be effective against most Gram positive and Gram negative bacteria, except <i>Pseudomonas aeruginosa</i>, <i>Enterococcus</i>, and <i>Bacteroides fragilis</i>. Cefpodoxime is active against a wide spectrum of Gram-positive and Gram-negative bacteria. Cefpodoxime is stable in the presence of beta-lactamase enzymes. As a result, many organisms resistant to penicillins and cephalosporins, due to their production of beta-lactamase, may be susceptible to cefpodoxime. Cefpodoxime is inactivated by certain extended spectrum beta-lactamases. The bactericidal activity of cefpodoxime results from its inhibition of cell wall synthesis. The active metabolite of cefpodoxime binds preferentially to penicillin binding protein 3, which inhibits production of peptidoglycan, the primary constituent of bacterial cell walls.",,,,Cefpodoxime is approved and vet_approved.,Cefpodoxime is a solid.,True
20658,"4-Hydroxytestosterone is testosterone substituted with a hydroxy group on the fourth carbon atom. It is an anabolic steroid with no therapeutic indications, which is prohibited from use in sports by the World Anti-Doping Agency. Aanabolic steroids have a similar effect to testosterone in the body. Effects include an increase in protein production within cells, (ie. skeletal muscle cells) and well as the development and maintenance of masculine characteristics.  4-hydroxytestosterone is a fat soluble compound which can cross the lipid bilayers of cell membranes to enter the cytoplasm of cells. In the cytoplasm, 4-hydroxytestosterone can bind to an androgen receptor, which then gets transported to the nucleus of the cell to alter protein transcription and translation.  ",,,,4-Hydroxytestosterone is experimental and illicit.,4-Hydroxytestosterone is a solid.,True
20659,,,,,Dehydrochloromethyltestosterone is experimental and illicit.,Dehydrochloromethyltestosterone is a solid.,False
20660,,,,,18-methyl-19-nortestosterone is experimental and illicit.,18-methyl-19-nortestosterone is a solid.,False
20661,Methyl-1-testosterone is a synthetic and orally active anabolic–androgenic steroid (AAS) which was never marketed for medical use. It is a derivative of 1-testosterone with a methyl group in the carbon 17. Methyl-1-testosterone is considered a prohibited doping substance.,,,,Methyl-1-testosterone is experimental and illicit.,Methyl-1-testosterone is a solid.,True
20662,,,,,Taxifolin is experimental.,Taxifolin is a solid.,False
20663,,,,,4-hydroxycoumarin is experimental.,4-hydroxycoumarin is a solid.,False
20664,"Latamoxef is a broad- spectrum beta-lactam antibiotic similar in structure to the cephalosporins except for the substitution of an oxaazabicyclo moiety for the thiaazabicyclo moiety of certain cephalosporins. It has been proposed especially for the meningitides because it passes the blood-brain barrier and for anaerobic infections. Latamoxef is an oxacephem antibiotic usually grouped with the cephalosporins. It is used to treat bacterial infections. Latamoxef is primarily indicated in conditions like Bone and joint infection, GI infections, Gynecological infections, Meningitis, Respiratory tract infections, Septicaemia, Skin infections, Soft tissue infections, UTI.  Latamoxef works by inhibiting bacterial cell wall biosynthesis. Penicillins acylate the penicillin-sensitive transpeptidase C-terminal domain (the penicillin-binding protein) by opening the lactam ring. This inactivation of the enzyme prevents the formation of a cross-link of two linear peptidoglycan strands, inhibiting the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins; it is possible that amoxicllin interferes with an autolysin inhibitor.",The molecular weight is 520.47.,Latamoxef has a topological polar surface area of 206.3.,The log p value of  is -0.82.,Latamoxef is approved and investigational.,Latamoxef is a solid.,True
20665,"Ceftobiprole is a cephalosporin antibiotic with activity against methicillin-resistant <i>Staphylococcus aureus</i>. It was discovered by Basilea Pharmaceutica and is being developed by Johnson & Johnson Pharmaceutical Research and Development. Ceftobiprole is the first cephalosporin to demonstrate clinical efficacy in patients with infections due to methicillin-resistant staphylococci and, if approved by regulatory authorities, is expected to be a useful addition to the armamentarium of agents for the treatment of complicated skin infections and pneumonia. For the treatment of serious bacterial infections in hospitalised patients. Ceftobiprole, a cephalosporin antibiotic, is active against methicillin-resistant <i>Staphylococcus aureus</i>. Cephalosporins, such as ceftobiprole, are bactericidal and have the same mode of action as other beta-lactam antibiotics (such as penicillins). Cephalosporins disrupt the synthesis of the peptidoglycan layer of bacterial cell walls. The peptidoglycan layer is important for cell wall structural integrity, especially in Gram-positive organisms. The final transpeptidation step in the synthesis of the peptidoglycan is facilitated by transpeptidases known as penicillin binding proteins (PBPs). PBPs bind to the D-Ala-D-Ala at the end of muropeptides (peptidoglycan precursors) to crosslink the peptidoglycan. Beta-lactam antibiotics mimic this site and competitively inhibit PBP crosslinking of peptidoglycan.",,,,Ceftobiprole is approved and investigational.,Ceftobiprole is a solid.,True
20666,"Trestolone (7α-methyl-19-nortestosterone) is a synthetic androgen developed by the Population Council as a potential candidate drug for use in hormonal male contraceptive methods. In males, regular administration of sufficient quantities of trestolone induces a state of temporary infertility. Investigated for use/treatment in contraception and male hormonal deficiencies/abnormalities. Trestolone is a potent inhibitor of the release of the luteinizing hormone (LH) and follicle stimulating hormone (FSH). As spermatogenesis requires both testosterone and FSH, it is impaired by the reduction in FSH caused by trestolone as well as the reduction in LH, and subsequent reduction in testosterone.",,,,Trestolone is investigational.,Trestolone is a solid.,True
20667,"Sugammadex is a selective relaxant binding agent indicated for reversal of neuromuscular blockade induced by rocuronium bromide and vecuronium bromide during surgery in adults. Rocuronium bromide and vecuronium bromide are neuromuscular blocking medications that cause temporary paralysis and are especially useful for general anesthesia, ventilation, or tracheal intubation that patients may require for surgery. Sugammadex provides a new treatment option to reverse the effects of those medications and possibly help patients recover sooner post-surgery. Sugammadex (brand name Bridion) is marketed by Merck Sharp and Dohme, and was approved by the United States FDA on December 15, 2015. Sugammadex is indicated for the reversal of neuromuscular blockade induced by rocuronium bromide and vecuronium bromide in adults undergoing surgery. Sugammadex is a modified gamma-cyclodextrin which forms very tight water soluble complexes at a 1:1 ratio with steroidal neuromuscular blocking drugs (rocuronium > vecuronium >> pancuronium). Sugammadex creates a concentration gradient which favors movement of rocurionium from the neuromuscular junction into the plasma, which quickly reverses rocuronium-induced neuromuscular blockade. The free rocuronium in the plasma are then bound tightly to sugammadex, assisting the diffusion of the remaining rocuronium molecules out of the neuromuscular junction and increasing bound and free rocuronium in the plasma.",The molecular weight is 2002.12.,Sugammadex has a topological polar surface area of 769.76.,The log p value of  is -11.9.,Sugammadex is approved.,Sugammadex is a solid.,True
20668,Investigated for use/treatment in inflammatory bowel disease.,,,,Dersalazine is investigational.,Dersalazine is a solid.,True
20669,Investigated for use/treatment in thrombosis.,,,,Semuloparin is investigational.,Semuloparin is a solid.,True
20670,Ceftaroline fosamil is a cephalosporin antibacterial indicated for the treatment of the following infections caused by designated susceptible bacteria: Ceftaroline fosamil is indicated for the treatment of patients with the following infections caused by susceptible isolates of the designated microorganisms. The time that unbound plasma concentration of ceftaroline exceeds the minimum inhibitory concentration (MIC) of the infecting organism has been shown to best correlate with efficacy in a neutropenic murine thigh infection model with S. aureus and S. pneumoniae. Ceftaroline fosamil is an antibacterial drug. ,,,,Ceftaroline fosamil is approved and investigational.,Ceftaroline fosamil is a solid.,True
20671,"Amediplase is a recombinant chimeric plasminogen activator, consisting of the kringle 2 domain from the A-chain of tissue plasminogen activator (t-PA) and the carboxy terminal region of pro-urokinase.  Investigated for use/treatment in myocardial infarction and thrombosis.",,,,Amediplase is investigational.,Amediplase is a solid.,True
20672,,The molecular weight is 229.24.,Phenyl aminosalicylate has a topological polar surface area of 72.55.,The log p value of  is 2.77.,Phenyl aminosalicylate is approved.,Phenyl aminosalicylate is a solid.,False
20673,,,,,Ferulic acid is experimental.,Ferulic acid is a solid.,False
20674,,,,,Testosterone succinate is experimental.,Testosterone succinate is a solid.,False
20675,Kebuzone (also known as ketophenylbutazone ) is a non-steroidal anti-inflammatory drug.,The molecular weight is 322.36.,Kebuzone has a topological polar surface area of 57.69.,The log p value of  is 0.9.,Kebuzone is experimental.,Kebuzone is a solid.,True
20676,Isoxicam is a non-steroidal anti-inflammatory drug that is not marketed in the United States.,The molecular weight is 335.33.,Isoxicam has a topological polar surface area of 112.74.,The log p value of  is 1.61.,Isoxicam is approved and withdrawn.,Isoxicam is a solid.,True
20677,A drug that has analgesic and anti-inflammatory properties. Following reports of adverse reactions including reports of carcinogenicity in animal studies it was withdrawn from the market worldwide.,The molecular weight is 281.31.,Indoprofen has a topological polar surface area of 57.61.,The log p value of  is 2.74.,Indoprofen is withdrawn.,Indoprofen is a solid.,True
20678,Ibuproxam is a non steroidal anti-inflammatory drug (NSAID).,The molecular weight is 221.3.,Ibuproxam has a topological polar surface area of 49.33.,The log p value of  is 2.61.,Ibuproxam is withdrawn.,Ibuproxam is a solid.,True
20679,Floctafenine is an anti-inflammatory analgesic similar in action to aspirin. Floctafenine inhibits prostaglandin synthesis.,The molecular weight is 406.36.,Floctafenine has a topological polar surface area of 91.68.,The log p value of  is 4.24.,Floctafenine is approved and withdrawn.,Floctafenine is a solid.,True
20680,"Fenbufen is a non-steroidal anti-inflammatory drug used primarily to treat inflammation in osteoarthritis, ankylosing spondylitis, and tendinitis. It can also be used to relieve backaches, sprains, and fractures. Fenbufen is available as a capsule or tablet sold with the brand names Cepal, Cinopal, Cybufen, Lederfen, and Reugast. Fenbufen acts by preventing cyclooxygenase from producing prostaglandins which can cause inflammation.",The molecular weight is 254.28.,Fenbufen has a topological polar surface area of 54.37.,The log p value of  is 3.14.,Fenbufen is approved.,Fenbufen is a solid.,True
20681,Epirizole is an oral nonsteroidal anti-inflammatory drug (NSAID) used for muscle and joint pain.,The molecular weight is 234.26.,Epirizole has a topological polar surface area of 62.06.,The log p value of  is 1.98.,Epirizole is experimental.,Epirizole is a solid.,True
20682,"Ditazole is a non-steroidal anti-inflammatory drug (NSAID). Ditazole's analgesic and antipyretic effects are similar to phenylbutazone. Additionally, ditazole is a platelet aggregation inhibitor marketed in Spain and Portugal with trade name Ageroplas.",The molecular weight is 324.38.,Ditazole has a topological polar surface area of 69.73.,The log p value of  is 2.65.,Ditazole is experimental and withdrawn.,Ditazole is a solid.,True
20683,Cefminox (INN) is a second generation cephalosporin antibiotic. It is approved for use in Japan.,The molecular weight is 519.57.,Cefminox has a topological polar surface area of 202.86.,The log p value of  is -3.2.,Cefminox is experimental.,Cefminox is a solid.,True
20684,"Benzydamine (also known as Tantum Verde or Difflam), available as the hydrochloride salt, is a locally-acting nonsteroidal anti-inflammatory drug (NSAID) with local anaesthetic and analgesic properties. It is used topically for pain relief and anti-inflammatory treatment of the mouth, throat, or muscoskeletal system. Available predominantly as a liquid mouthwash, oromucosal spray, or topical cream, benzydamine is most frequently employed as a locally acting analgesic and anti-inflammatory treatment for the relief of painful inflammatory conditions.  Benzydamine is a non-steroidal anti-inflammatory drug (NSAID) designed to elicit local anesthetic and analgesic effects mainly for the mouth and throat. It specifically acts on the local mechanisms of inflammation such as pain, oedema, or granuloma. Typically applied topically, the drug demonstrates anti-inflammatory activity reducing oedema as well as exudate and granuloma formation. Moreover, benzydamine exhibits analgesic properties and local anaesthetic activity if pain is caused by an inflammatory condition. Benzydamine can be absorbed into the oral mucosa and intact skin. Once absorbed in the local area of pain or inflammation, benzydamine binds selectively to local inflamed tissues, usually allowing it to act with few adverse systemic effects. On average a period of 2 to 4 hours is necessary for the substance to reach peak plasma concentration.  Despite being categorized as a non-steroidal anti-inflammatory drug (NSAID), benzydamine demonstrates various mechanisms of action that differ from those of traditional aspirin-like NSAIDs. In particular, benzydamine predominantly acts by inhibiting the synthesis of pro inflammatory cytokines like tumour necrosis factor-alpha (TNF-α) and interleukin-1β (IL-1β) without largely affecting other pro inflammatory cytokines (ie. such as IL-6 and IL-8) or anti-inflammatory cytokines (ie. like IL-10 or IL-1 receptor antagonist). ",The molecular weight is 309.41.,Benzydamine has a topological polar surface area of 30.29.,The log p value of  is 4.24.,Benzydamine is approved.,Benzydamine is a solid.,True
20685,Clonixin is a non-steroidal anti-inflammatory drug. Indicated for use in the management of chronic arthritic conditions and certain soft tissue disorders associated with pain and inflammation. Clonixin is a non-steroidal anti-inflammatory drug (NSAID) similar in structure to. It produces vasodilation and analgesia. The mechanism of clonixin does not appear to have been investigated on a molecular level. It is presumed to function similarly to other NSAIDs by inhibiting cycloxygenase enzymes 1 and 2 resulting in a reduction in prostaglandin production.,The molecular weight is 262.69.,Clonixin has a topological polar surface area of 62.22.,The log p value of  is 5.03.,Clonixin is experimental.,Clonixin is a solid.,True
20686,"Fibrinogen concentrate (human) is a hematological agent. It works by replacing a certain protein in the blood that helps with blood clotting. Fibrinogen (factor I) is a soluble plasma glycoprotein with a molecular weight of about 340 kDa. It is a physiological substrate for three enzymes: plasmin, factor XIIIa and thrombin. It is indicated for the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenemia and hypofibrinogenemia. For the treatment of acute bleeding episodes in patients with congenital fibrinogen deficiency, including afibrinogenemia and hypofibrinogenemia. Fibrinogen replaces the missing, or low coagulation factor. Fibrinogen (factor I) is a soluble plasma glycoprotein with a molecular weight of about 340 kDa. The native molecule is a dimer and consists of three pairs of polypeptide chains (Aα, Bβ and γ). Fibrinogen is a physiological substrate of three enzymes: thrombin, factor XIIIa, and plasmin. During the coagulation process, thrombin cleaves the Aα and Bβ chains releasing fibrinopeptides A and B (FPA and FPB, respectively). FPA is separated rapidly and the remaining molecule is a soluble fibrin monomer (fibrin I). The slower removal of FPB results in formation of fibrin II that is capable of polymerization that occurs by aggregation of fibrin monomers. The resulting fibrin is stabilized in the presence of calcium ions and by activated factor XIII, which acts as a transglutaminase. Factor XIIIa-induced cross-linking of fibrin polymers renders the fibrin clot more elastic and more resistant to fibrinolysis. Cross-linked fibrin is the end result of the coagulation cascade, and provides tensile strength to a primary hemostatic platelet plug and structure to the vessel wall.",,,,Fibrinogen human is approved.,Fibrinogen human is a solid.,True
20687,"Hydracarbazine is a pyridazine that has found use as an antihypertensive agent It was once marketed in France under the tradename Normatensyl. Was used for the treatment of hypertension. Relaxes vascular smooth muscle. Likely acts similarly to hydralazine, a related compound, which interferes with calcium release from the sarcoplasmic reticulum in response to inositol.",The molecular weight is 153.15.,Hydracarbazine has a topological polar surface area of 105.86.,The log p value of  is -1.6.,Hydracarbazine is experimental.,Hydracarbazine is a solid.,True
20688,"Benmoxin is an irreversible and nonselective monoamine oxidase inhibitor (MAOI) of the hydrazine class. It was first synthesized in 1967 and rapidly used in Europe as an antidepressant. However, this agent is no longer marketed. For the treatment of depression.",The molecular weight is 240.31.,Benmoxin has a topological polar surface area of 41.13.,The log p value of  is 2.25.,Benmoxin is withdrawn.,Benmoxin is a solid.,True
20689,"Octamoxin, also known as _2-octylhydrazine_, is both an irreversible and nonselective monoamine oxidase enzyme inhibitor (MAOI) of the _hydrazine_ chemical class. This drug was used in the past as an antidepressant agent in the 1960s, however, has since been discontinued. For the treatment of depression.",The molecular weight is 144.26.,Octamoxin has a topological polar surface area of 38.05.,The log p value of  is 2.42.,Octamoxin is withdrawn.,Octamoxin is a solid.,True
20690,"Pheniprazine is an irreversible and nonselective monoamine oxidase inhibitor (MAOI) of the hydrazine chemical class that was used as an antidepressant in the 1960s. In addition, it was used for the treatment of other conditions, such as angina pectoris and schizophrenia. Pheniprazine was withdrawn by its manufacturer due to its ability to cause toxicity in the liver and its ability to cause optic neuritis. For the treatment of depression, schizophrenia, and angina pectoris.",The molecular weight is 150.22.,Pheniprazine has a topological polar surface area of 38.05.,The log p value of  is 1.34.,Pheniprazine is withdrawn.,Pheniprazine is a solid.,True
20691,"Phenoxypropazine is a non-selective and irreversible monoamine oxidase enzyme inhibitor (MAOI), belonging to the _hydrazine_ chemical class. It was marketed as an antidepressant in 1961 but was later withdrawn in 1966 because of its hepatotoxic potential. For the treatment of depression.",The molecular weight is 166.22.,Phenoxypropazine has a topological polar surface area of 47.28.,The log p value of  is 1.27.,Phenoxypropazine is withdrawn.,Phenoxypropazine is a solid.,True
20692,"Pivhydrazine, also known as pivazide, is a member of the hydrazine family with irreversible and non-selective inhibitory activity against monoamine oxidases. In 1960, it was widely used as an antidepressant agent but it is now discontinued. For the treatment of depression.",The molecular weight is 206.29.,Pivhydrazine has a topological polar surface area of 41.13.,The log p value of  is 1.4.,Pivhydrazine is withdrawn.,Pivhydrazine is a solid.,True
20693,"Safrazine is a member of the hydrazine family with non-selective and irreversible inhibitor effects against monoamine oxidases. In 1960, it was used as an antidepressant but it is now discontinued. For the treatment of depression.",,,,Safrazine is withdrawn.,Safrazine is a solid.,True
20694,"Dextran is a polysaccharide that differs from others in that its glucose units are joined together 1:6 glucoside links. The main chain of glucose has short branches at frequent intervals which are probably joined by 1:3 and 1:4 glucoside links. The chains can be composed of about 200,000 glucose units. Many bacteria, like _Leuconostoc_, can synthesize dextran from sucrose, and this activity is used commercially to obtain dextran. Dextran is used as the restoration of blood mass during surgical interventions if there is hypovolemia due to trauma or dehydration. It is as well used after the presence of hemorrhage in cases of blood loss to a level inferior to 15% of the blood mass, if compatibility test cannot be completed or when blood lots need to be tested for pathogen detection. Dextran is also used for the prevention of profound postoperative venous thrombosis. It is reported that dextran presents an effect on the hemostatic system in particular by prolonging bleeding time. In the same trials, dextran is reported to reduce emboli, reduce platelet adhesiveness and produce hemodilution. These effects have been showed to be greater proportionally with the increase in the molecular weight of the dextran. In preclinical studies, the mechanism of action is thought to be related to the blockage of the uptake of tissue plasminogen activator by mannose-binding receptors. This process has a direct effect by enhancing endogenous fibrinolysis.",,,,Dextran is approved and investigational and vet_approved.,Dextran is a solid.,True
20695,"Azficel-T is an autologous cellular product composed of fibroblasts indicated for improvement of the appearance of moderate to severe nasolabial fold wrinkles in adults. Dermal fibroblasts are collected from the post-auricular biopsy tissue and aseptically expanded using standard tissue-culture procedures until sufficient cells for three doses are obtained. Expanded cells are then suspended in a cell medium. As a replacement for lost dermal constituents in the aging or skin deformation process, treatment with autologous fibroblasts has shown to improve wrinkle and acne scar appearance than with placebo treatment. Intradermal administration of autologous dermal fibroblasts into irradiated skin following surgical procedures was associated with an improved healing process of subsequent surgical wounds. Azficel-T is marketed in the US as Laviv for intradermal injection. Indicated for improvement of the appearance of moderate to severe nasolabial fold wrinkles in adults. In clinical studies involving patients with moderate to severe bilateral nasolabial fold wrinkles, there was a substantial improvement in the wrinkle appearance. In a randomized multicenter, double-blind, placebo-controlled trial in subjects with bilateral moderate to severe acne scarring, treatment of autologous fibroblast treatment was associated with a significant improvement in the appearance of acne scars without permanent adverse reactions. The mechanism of action of azficel-T, or autologous human fibroblasts, is not fully elucidated. Autologous fibroblasts correct dermal defects such as acne or other dermal conditions associated with aging, such as reduced elasticity. The importance of collagen matrix production by fibroblasts in maintaining skin integrity and reducing the appearance of scars has been highlighted. The appearance of acne scars is also associated with the loss of collagen at the site of inflammation following resolution of localized intense inflammation and wound healing associated with inflammatory acne. Fragmentation of the dermal collagen matrix occurs in the natural aging process; due to UV-induced photodamage and the actions of collagen-degrading enzymes (matrix metalloproteinases, MMPs) overtime, the structural integrity of the dermis and function of fibroblasts may be impaired. While fibroblasts are responsible in the synthesis, organization, regulation and the maintenance of collagen network, the function of fibroblasts are strongly dependent on the physical properties of collagen fibres, and vice versa. The aging process is associated with a reduced rate of collagen turnover and formation of modified crosslinks that normally give structural support for collagen fibres. These crosslinks prevent the removal of degraded collagen, leading to accumulation of collagen fragments within the extracellular matrix, and compromised structural and mechanical integrity of the dermis. Integrins that are expressed by the fibroblasts allow the cell to bind to collagen matrix and allow mechanical tension within fibroblasts and the collagenous matrix. In the presence of fragmented collagen, the fibroblasts lose attachment to the collagen matrix and collapse within the dermis and subsequently leads to reduced collagen production and increased production of MMPs. Autologous human fibroblasts have the ability to increase the formation of human collagen _in vivo_ and promote remodelling of pre-existing extracellular matrix in the scarred tissue. They may also decrease the degradation of collagen.",,,,Azficel-T is approved and investigational.,,True
20696,"Zinc citrate is a zinc salt of citric acid. It is available as dietary supplements as a treatment of zinc deficiency and source of zinc, which is an essential trace element. Zinc citrate demonstrates effective absorption following oral administration.",,,,Zinc citrate is investigational.,,True
20697,"Calcium threonate is a calcium salt of threnoic acid and a novel drug developed for the treatment of osteoporosis and as a calcium supplement. It is found in dietary supplements as a source of L-threonate used in the treatment of calcium deficiency and prevention of osteoporosis. The most common form is calcium L-threonate, or (2R,3S)-2,3,4-trihydroxy butyric acid calcium. L-threonate is an active metabolite of vitamin C that mediates a stimulatory action on vitamin C uptake. Therapeutic efficacy of calcium threonate in reducing was studied and investigated due to the hypothesis that it may play a role in the mineralization process through its positive action on vitamin C. No approved therapeutic indications.  In a preclinical study, calcium L-theronate inhibited the bone resorption of osteoclasts _in vitro_.  Once dissociated to calcium and L-theronic acid, L-threonic acid exhibits significant stimulatory action on vitamin C uptake and prolongs the retention of vitamin C in human T-lymphoma cells. Vitamin C is a marker for osteoblast formation and has been shown to stimulate procollagen and enhance collagen synthesis. Via stimulation of vitamin C uptake, L-threonic acid acts as a metabolite that influences the mineralization process. ",The molecular weight is 310.27.,Calcium threonate has a topological polar surface area of 100.82.,,Calcium threonate is approved.,Calcium threonate is a solid.,True
20698,"Also known as protocatechuic aldehyde, protocatechualdehyde is a naturally-occuring phenolic aldehyde that is found in barley, green cavendish bananas, grapevine leaves and root of the herb S. miltiorrhiza. Protocatechualdehyde possesses antiproliferative and pro-apoptotic properties against human breast cancer cells and colorectal cancer cells by reducing the expression of pro-oncogenes β-catenin and cyclin D1.",The molecular weight is 138.12.,Protocatechualdehyde has a topological polar surface area of 57.53.,The log p value of  is 1.03.,Protocatechualdehyde is experimental.,,True
20699,"Factor IX Complex is a sterile, lyophilized concentrate composed of a number of Vitamin K-dependent clotting factors found in functioning human plasma. Also known as prothrombin complex concentrate, products containing this complex often include Factor IX (antihemophilic factor B), Factor II (prothrombin), Factor X (Stuart-Prower Factor), and low levels of Factor VII (proconvertin) derived from human plasma. Many commercially available products also contain low levels of other antithrombotic proteins. For example, Kcentra (FDA) also contains the antithrombotic proteins C and S, while Bebulin VH (FDA) contains heparin. Coagulation factors are purified from pooled human plasma and subsequently sterilized and treated.  Factor IX Complex is indicated for the prevention and control of hemorrhagic episodes in hemophilia B patients. It is also indicated for the urgent reversal of acquired coagulation factor deficiency induced by Vitamin K antagonist (VKA, e.g., warfarin) therapy in adult patients with acute major bleeding or who require rapid reversal of therapy.  Factor IX Complex is a sterile, lyophilized concentrate composed of a number of Vitamin K-dependent clotting factors found in functioning human plasma. Also known as prothrombin complex concentrate, products containing this complex often include Factor IX (antihemophilic factor B), Factor II (prothrombin), Factor X (Stuart-Prower Factor), and low levels of Factor VII (proconvertin) derived from human plasma. Many commercially available products also contain low levels of other antithrombotic proteins. For example, Kcentra(FDA) also contains the antithrombotic proteins C and S, while Bebulin VH (FDA) contains heparin.",,,,Factor IX Complex (Human) is approved and investigational.,,True
20700,"Cefroxadine is an orally available cephalosporin antibiotic. As part of its drug class, it shares structural properties to as well as its activity spectrum. It was used in Italy but has since been withdrawn. Was used for the treatment of bacterial infections. Cefroxadine is a cephalosporin antibiotic which produces a bactericidal effect on susceptible bacteria. Cefrixadine is a cephalosporin antibiotic, a class of β-lactam antibiotics similar to penicillins, which binds to and inhibits penicillin binding proteins (PBPs). PBPs are responsible for catalyzing the transpeptidase reaction which cross-links the peptide side chains on the sugar residues of a peptidoglycan unit, adding the unit to the peptidoglycan layer. This disrupts the balance between the hydrolysis of peptidoglycan, in order to insert new peptidoglycan units, by murein hydrolase and the attachment of the new units which leads to overall destruction of the peptidoglycan layer. With the loss of its peptidoglycan layer the cell also loses its resistance to the high osmotic pressure inside its membrane and lyses.",The molecular weight is 365.4.,Cefroxadine has a topological polar surface area of 121.96.,The log p value of  is -1.95.,Cefroxadine is withdrawn.,Cefroxadine is a solid.,True
20701,"Altrenogest, also known as allyltrenbolone, is a steroidal progestin that is widely used in veterinary medicine to suppress estrus in animals.",,,,Altrenogest is vet_approved.,,True
20702,Robenacoxib is a non-steroidal anti-inflammatory drug used in veterinary medicine for the relief of pain and inflammation in cats and dogs.,,,,Robenacoxib is experimental and vet_approved.,,True
20703,Tepoxalin is a nonsteroidal anti-inflammatory drug approved for veterinary use in the United States and many other countries. It is primarily used to reduce inflammation and relief of pain caused by musculoskeletal disorders such as hip dysplasia and arthritis.,,,,Tepoxalin is vet_approved.,,True
20704,,,,,Cloprostenol is vet_approved.,,False
20705,"Flunixin is a non-steroidal anti-inflammatory drug for use in pigs, cattle and horses.  It exerts analgesic and antipyretic effects. This drug is often prepared for use in meglumine salt form. Flunixin is regulated in the United States by the Food and Drug Administration (FDA) and must be prescribed by a licensed veterinarian. Flunixin may be also referred to as _Banamine_, and other trade names.",,,,Flunixin is vet_approved.,,True
20706,Chrysalin has been used in trials studying the treatment of Radius Fracture.,,,,Rusalatide acetate is investigational.,,True
20707,Hyodeoxycholic Acid has been used in trials studying the treatment of Hypercholesterolemia.,,,,Hyodeoxycholic Acid is investigational.,,True
20708,Flomoxef has been used in trials studying the treatment of Urinary Tract Infection.,The molecular weight is 496.46.,Flomoxef has a topological polar surface area of 169.0.,The log p value of  is -1.24.,Flomoxef is investigational.,,True
20709,Letaxaban has been used in trials studying the treatment and prevention of Venous Thromboembolism and Acute Coronary Syndrome.,,,,Letaxaban is investigational.,,True
20710,"Triptolide has been used in trials studying the treatment of HIV, Crohn's Disease, Intestinal Diseases, Gastrointestinal Diseases, and Digestive System Diseases, among others.",,,,Triptolide is investigational.,,True
20711,"Darexaban has been used in trials studying the prevention and basic science of Japanese, Caucasian, Thromboembolism, Pharmacodynamics, and Pharmacokinetics, among others.",,,,Darexaban is investigational.,,True
20712,"Ifetroban has been used in trials studying the treatment of Skin Diseases, Autoimmune Diseases, Pathologic Processes, Scleroderma, Limited, and Scleroderma, Diffuse, among others.",,,,Ifetroban is investigational.,,True
20713,"Vatreptacog Alfa (Activated) has been used in trials studying the treatment of Haemophilia B, Haemophilia A, Congenital Bleeding Disorder, Haemophilia A With Inhibitors, and Haemophilia B With Inhibitors.",,,,Vatreptacog alfa is investigational.,,True
20714,Indobufen has been used in trials studying the supportive care and prevention of Atrial Fibrillation.,The molecular weight is 295.34.,Indobufen has a topological polar surface area of 57.61.,The log p value of  is 3.27.,Indobufen is investigational.,,True
20715,Monteplase has been used in trials studying the treatment of Pulmonary Embolism.,,,,Monteplase is investigational.,,True
20716,Hydroxytyrosol has been used in trials studying the prevention of Breast Cancer.,,,,Hydroxytyrosol is investigational.,,True
20717,"Factor XIII (human) is a heat-treated, lyophilized concentrate of coagulation factor XIII, an endogenous enzyme responsible for the crosslinking of fibrin and an essential component of the coagulation cascade. For people with congenital deficiency or mutation of Factor XIII, a rare bleeding disorder, exogenous replacement of this key coagulation factor is essential for management and prevention of bleeding episodes.  Factor XIII (Human), available as the commercially available product Corifact, is approved by the Food and Drug Administration for routine prophylactic treatment and peri-operative management of surgical bleeding in adult and pediatric patients with congenital FXIII deficiency. Also known as Fibrin Stabilizing Factor (FSF), Factor XIII is an endogenously produced coagulation factor and the final enzyme within the blood coagulation cascade. Within the body, FXIII circulates as a heterotetramer composed of 2 A-subunits and 2 B-subunits (A2B2). When activated by thrombin at the site of injury, the FXIII pro-enzyme is cleaved resulting in activation of the catalytic A-subunit and dissociation from its carrier B-subunit. As a result, the active transglutaminase from subunit A cross-links fibrin and other proteins resulting in increased mechanical strength and resistance to fibrinolysis of the fibrin clot. This contributes to enhanced platelet and clot adhesion to injured tissue, thereby improving blood coagulation and maintenance of hemostasis. Exogenous replacement of Factor XIII is a cornerstone of treatment for bleeding associated with congenital Factor XIII deficiency. ",,,,Factor XIII (human) is approved and investigational.,,True
20718,Tinoridine is under investigation in clinical trial NCT01224756 (Efficacy of Tinoridine in Treating Pain and Inflammation in Adults).,The molecular weight is 316.42.,Tinoridine has a topological polar surface area of 55.56.,The log p value of  is 4.28.,Tinoridine is investigational.,,True
20719,Troxerutin has been used in trials studying the treatment of Chronic Venous Insufficiency.,The molecular weight is 742.68.,Troxerutin has a topological polar surface area of 293.21.,The log p value of  is -2.49.,Troxerutin is investigational.,,True
20720,,The molecular weight is 286.37.,Methallenestril has a topological polar surface area of 46.53.,The log p value of  is 4.63.,Methallenestril is experimental.,Methallenestril is a solid.,False
20721,"Coagulation Factor X (Human), is a plasma-derived human blood coagulation factor is used by adults and children (aged 12 years and above) with hereditary Factor X deficiency. However its use is limited in the perioperative setting for the management of bleeding in major surgery in patients with moderate and severe hereditary Factor X deficiency.  Indicated in adults and children (aged 12 years and above) with hereditary Factor X deficiency for on-demand treatment and control of bleeding episodes, or for perioperative management of bleeding in patients with mild hereditary Factor X deficiency.  Clinical human coagulation Factor X solution increases plasma levels of Factor X and can temporarily correct the coagulation defect in these patients, as reflected by decrease in the activated Partial Thromboplastin Time (aPTT) and prothrombin time (PT). Factor X is an inactive zymogen that is synthesized in the liver, which can be activated by Factor IXa (via the intrinsic pathway) or by Factor VIIa (via the extrinsic pathway). It is composed of a light chain which contains the Gla (glutamic acid) domain and two epidermal growth factor domains, and a heavy chain that contains the catalytic serine protease domain. The conversion of inactive Factor X into the active form Factor Xa requires the cleavage of a 52-residue peptide from the heavy chain and the release of 52-residue activation peptide that contains the His236, Asp228 and Ser379 catalytic site. This activation step can occur through the extrinsic or intrinsic pathway and is considered to be the first step in the common pathway to fibrin formation. ",,,,Coagulation factor X human is approved and investigational.,Coagulation factor X human is a solid.,True
20722,,,,,Kallidinogenase is experimental.,,False
20723,,,,,Brinase is experimental.,,False
20724,"Human coagulation factor IX (EC 3.4.21.22, Christmas factor, plasma thromboplastin component), produced in CHO cells.",,,,Trenonacog alfa is investigational.,,True
20725,,The molecular weight is 329.8.,Fentiazac has a topological polar surface area of 50.19.,The log p value of  is 4.37.,Fentiazac is experimental.,,False
20726,Gestonorone is often mistaken for gestonorone capproate which has a different chemical structure.,The molecular weight is 316.44.,Gestonorone has a topological polar surface area of 54.37.,The log p value of  is 2.82.,Gestonorone is experimental.,,True
20727,,The molecular weight is 438.48.,Suxibuzone has a topological polar surface area of 104.22.,The log p value of  is 3.66.,Suxibuzone is experimental.,,False
20728,Alaproclate was developed as one of the first selective serotonin reuptake inhibitor (SSRI) antidepressants by Astra AB (now AstraZeneca) in the 1970s. Development was discontinued due to concerns over hepatotoxicity observed in animal studies. Alaproclate has also been found to act as a non-competitive NMDA receptor antagonist although without discriminative stimulus properties similar to phencyclidine.,,,,Alaproclate is experimental.,,True
20729,,The molecular weight is 462.5.,Cefatrizine has a topological polar surface area of 174.53.,The log p value of  is -3.09.,Cefatrizine is experimental.,,False
20730,"Clorindione is a vitamin K antagonist, which may be useful to decrease prothrombin levels in humans.",The molecular weight is 256.69.,Clorindione has a topological polar surface area of 34.14.,The log p value of  is 3.52.,Clorindione is experimental.,,True
20731,"Bumadizone has been approved for use in Germany and Austria, it is a drug with anti-inflammatory, antipyretic, and analgesic properties, and was marketed for the treatment of both rheumatoid arthritis and gout. Its use is restricted to these conditions, due to risks this drug poses.",The molecular weight is 326.4.,Bumadizone has a topological polar surface area of 69.64.,The log p value of  is 4.67.,Bumadizone is approved.,,True
20732,,The molecular weight is 457.61.,Ormeloxifene has a topological polar surface area of 30.93.,The log p value of  is 7.54.,Ormeloxifene is experimental.,,False
20733,Alminoprofen is a non-steroidal anti-inflammatory drug (NSAID) whose physiochemical characteristics make it a member of the phenylpropionic acid class of chemical substances.,The molecular weight is 219.28.,Alminoprofen has a topological polar surface area of 49.33.,The log p value of  is 2.39.,Alminoprofen is experimental.,,True
20734,,The molecular weight is 376.42.,Picotamide has a topological polar surface area of 93.21.,The log p value of  is 0.95.,Picotamide is experimental.,,False
20735,,The molecular weight is 395.88.,Cloricromen has a topological polar surface area of 65.07.,The log p value of  is 3.87.,Cloricromen is experimental.,,False
20736,,The molecular weight is 288.35.,Difenpiramide has a topological polar surface area of 41.99.,The log p value of  is 3.92.,Difenpiramide is experimental.,,False
20737,,The molecular weight is 302.41.,Epimestrol has a topological polar surface area of 49.69.,The log p value of  is 3.79.,Epimestrol is experimental.,,False
20738,,The molecular weight is 170.17.,Linsidomine has a topological polar surface area of 57.79.,The log p value of  is -0.14.,Linsidomine is experimental.,,False
20739,,The molecular weight is 308.34.,Nifenazone has a topological polar surface area of 65.54.,The log p value of  is 0.13.,Nifenazone is experimental.,,False
20740,,The molecular weight is 326.44.,Moxestrol has a topological polar surface area of 49.69.,The log p value of  is 2.46.,Moxestrol is experimental.,,False
20741,,The molecular weight is 381.89.,Mebutizide has a topological polar surface area of 118.36.,The log p value of  is 2.54.,Mebutizide is experimental.,,False
20742,,The molecular weight is 312.75.,Lonazolac has a topological polar surface area of 55.12.,The log p value of  is 4.0.,Lonazolac is experimental.,,False
20743,,The molecular weight is 447.33.,Tioclomarol has a topological polar surface area of 66.76.,The log p value of  is 5.49.,Tioclomarol is experimental.,,False
20744,,The molecular weight is 453.49.,Cefcapene has a topological polar surface area of 177.94.,The log p value of  is -0.87.,Cefcapene is experimental.,,False
20745,,The molecular weight is 584.66.,Cefodizime has a topological polar surface area of 197.4.,The log p value of  is 1.1.,Cefodizime is experimental.,,False
20746,,The molecular weight is 532.54.,Cefsulodin has a topological polar surface area of 190.88.,The log p value of  is -9.81.,Cefsulodin is experimental.,,False
20747,,The molecular weight is 397.42.,Cefetamet has a topological polar surface area of 147.21.,The log p value of  is 0.86.,Cefetamet is experimental.,,False
20748,,,,,Aloxiprin is experimental.,,False
20749,,The molecular weight is 307.39.,Buflomedil has a topological polar surface area of 48.0.,The log p value of  is 2.93.,Buflomedil is experimental.,,False
20750,,The molecular weight is 230.31.,Propyphenazone has a topological polar surface area of 23.55.,The log p value of  is 1.35.,Propyphenazone is experimental.,,False
20751,"Cyclopenthiazide is a thiazide diuretic with antihypertensive properties. In a double blind, randomized crossover study, cyclopenthiazide was effective in reducing diastolic blood pressure in mildly hypertensive non-insulin dependent diabetic patients. It is a positive allosteric modulator at AMPA-A receptors.",The molecular weight is 379.87.,Cyclopenthiazide has a topological polar surface area of 118.36.,The log p value of  is 2.25.,Cyclopenthiazide is approved.,,True
20752,,The molecular weight is 288.43.,Methylestrenolone has a topological polar surface area of 37.3.,The log p value of  is 3.41.,Methylestrenolone is experimental.,,False
20753,,The molecular weight is 286.28.,Guacetisal has a topological polar surface area of 61.83.,The log p value of  is 2.66.,Guacetisal is experimental.,,False
20754,,The molecular weight is 165.19.,Ethenzamide has a topological polar surface area of 52.32.,The log p value of  is 1.29.,Ethenzamide is experimental.,,False
20755,,The molecular weight is 294.39.,Norgestrienone has a topological polar surface area of 37.3.,The log p value of  is 1.91.,Norgestrienone is experimental.,,False
20756,,The molecular weight is 458.44.,Carbaspirin calcium has a topological polar surface area of 66.43.,,Carbaspirin calcium is experimental and investigational.,,False
20757,,,,,Melagatran is experimental.,,False
20758,,The molecular weight is 232.28.,Mofebutazone has a topological polar surface area of 49.41.,The log p value of  is 1.98.,Mofebutazone is experimental.,,False
20759,,The molecular weight is 627.65.,Cefbuperazone has a topological polar surface area of 229.49.,The log p value of  is -0.8.,Cefbuperazone is experimental.,,False
20760,,The molecular weight is 142.18.,Methylthiouracil has a topological polar surface area of 41.13.,The log p value of  is -0.09.,Methylthiouracil is experimental.,,False
20761,,,,,Saruplase is experimental.,,False
20762,,The molecular weight is 278.36.,Proquazone has a topological polar surface area of 32.67.,The log p value of  is 3.65.,Proquazone is experimental.,,False
20763,,The molecular weight is 313.31.,Benorilate has a topological polar surface area of 81.7.,The log p value of  is 2.05.,Benorilate is approved.,,False
20764,,The molecular weight is 515.52.,Cefozopran has a topological polar surface area of 184.11.,The log p value of  is -6.65.,Cefozopran is experimental.,,False
20765,,The molecular weight is 514.58.,Cefpirome has a topological polar surface area of 153.92.,The log p value of  is -5.56.,Cefpirome is approved.,,False
20766,,The molecular weight is 251.71.,Pirprofen has a topological polar surface area of 40.54.,The log p value of  is 2.6.,Pirprofen is experimental.,,False
20767,,The molecular weight is 548.43.,Cefazedone has a topological polar surface area of 132.8.,The log p value of  is -0.8.,Cefazedone is experimental.,,False
20768,,The molecular weight is 218.27.,Benzylthiouracil has a topological polar surface area of 41.13.,The log p value of  is 1.48.,Benzylthiouracil is experimental.,,False
20769,,The molecular weight is 440.47.,Ceftezole has a topological polar surface area of 156.09.,The log p value of  is -1.59.,Ceftezole is experimental.,,False
20770,,,,,Imidazole salicylate is experimental.,Imidazole salicylate is a solid.,False
20771,,,,,Testosterone enantate benzilic acid hydrazone is approved and experimental.,,False
20772,"Trestolone acetate is a synthetic and injected anabolic–androgenic steroid (AAS) and a derivative of nandrolone (19-nortestosterone) which was never marketed. It is an androgen ester – specifically, the C17 acetate ester of.",,,,Trestolone acetate is experimental.,Trestolone acetate is a solid.,True
20773,,,,,Thiosalicylic acid is experimental.,Thiosalicylic acid is a solid.,False
20774,NS-398 is a COX-2 inhibitor. It was developed as part of the mechanistic study of the cyclooxygenases.,,,,NS-398 is experimental.,NS-398 is a solid.,True
20775,,,,,"(1,2,6,7-3H)Testosterone is experimental.","(1,2,6,7-3H)Testosterone is a solid.",False
20776,,,,,Tocopherylquinone is experimental and investigational.,Tocopherylquinone is a solid.,False
20777,Beroctocog alfa is indicated for the prevention and control of bleeding in patients with hemophilia A or acquired Factor VIII (FVIII) deficiency. It is also indicated for surgical/invasive procedures in adult and pediatric patients with von Willebrand Disease in who desmopression is either ineffective or contraindicated. It is not indicated for patients with severe (i.e. type 3) von Willebrand Disease whom are undergoing major surgery.,,,,Beroctocog alfa is approved and investigational.,,True
20778,,,,,Calcium cation is experimental.,,False
20779,,The molecular weight is 408.58.,Quingestanol acetate has a topological polar surface area of 35.53.,The log p value of  is 6.23.,Quingestanol acetate is experimental.,,False
20780,,,,,Cefamandole nafate is approved.,,False
20781,,,,,Dabigatran is investigational.,,False
20782,Flurbiprofen axetil is under investigation in clinical trial NCT02043366 (Effect of Butorphanol Combined With Flurbiprofen Axetil on Preventing Hyperalgesia Induced by Remifentanil in Patients).,The molecular weight is 330.36.,Flurbiprofen axetil has a topological polar surface area of 52.6.,The log p value of  is 4.33.,Flurbiprofen axetil is investigational.,,True
20783,Biochanin A is under investigation in clinical trial NCT02174666 (Isoflavone Treatment for Postmenopausal Osteopenia.).,,,,Biochanin A is investigational.,,True
20784,Formononetin is under investigation in clinical trial NCT02174666 (Isoflavone Treatment for Postmenopausal Osteopenia.).,,,,Formononetin is investigational.,,True
20785,"Gadodiamide is a paramagnetic gadolinium-based contrast agent (GBCA) that is used in MR imaging procedures to assist in the visualization of blood vessels. It is intravenously injected and is commonly marketed under the trade name Omniscan. For intravenous use in MRI to visualize lesions with abnormal vascularity (or those thought to cause abnormalities in the blood-brain barrier) in the brain (intracranial lesions), spine, and associated tissues. Based on the behavior of protons when placed in a strong magnetic field, which is interpreted and transformed into images by magnetic resonance (MR) instruments. Paramagnetic agents have unpaired electrons that generate a magnetic field about 700 times larger than the proton's field, thus disturbing the proton's local magnetic field. When the local magnetic field around a proton is disturbed, its relaxation process is altered. MR images are based on proton density and proton relaxation dynamics. MR instruments can record 2 different relaxation processes, the T1 (spin-lattice or longitudinal relaxation time) and the T2 (spin-spin or transverse relaxation time). In magnetic resonance imaging (MRI), visualization of normal and pathological brain tissue depends in part on variations in the radiofrequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in the T2. When placed in a magnetic field, gadodiamide shortens both the T1 and the T2 relaxation times in tissues where it accumulates. At clinical doses, gadodiamide primarily affects the T1 relaxation time, thus producing an increase in signal intensity. Gadodiamide does not cross the intact blood-brain barrier; therefore, it does not accumulate in normal brain tissue or in central nervous system (CNS) lesions that have not caused an abnormal blood-brain barrier (e.g., cysts, mature post-operative scars). Abnormal vascularity or disruption of the blood-brain barrier allows accumulation of gadodiamide in lesions such as neoplasms, abscesses, and subacute infarcts.",The molecular weight is 573.66.,,,Gadodiamide is approved and investigational.,Gadodiamide is a solid.,True
20786,"A commonly used x-ray contrast medium. As diatrizoate meglumine and as Diatrizoate sodium, it is used for gastrointestinal studies, angiography, and urography. Used, alone or in combination, for a wide variety of diagnostic imaging methods, including angiography, urography, cholangiography, computed tomography, hysterosalpingography, and retrograde pyelography. It can be used for imaging the gastrointestinal tract in patients allergic to barium. Diatrizoate is the most commonly used water-soluble, iodinated, radiopaque x-ray contrast medium. Radiopaque agents are drugs used to help diagnose certain medical problems. They contain iodine, which blocks x-rays. Depending on how the radiopaque agent is given, it localizes or builds up in certain areas of the body. The resulting high level of iodine allows the x-rays to make a \picture\"" of the area. The areas of the body in which the radiopaque agent localizes will appear white on the x-ray film. This creates the needed distinction, or contrast, between one organ and other tissues. The contrast will help the doctor see any special conditions that may exist in that organ or part of the body."" Diatrizoate is an iodine-containing X-ray contrast agent. Iodated contrast agents were among the first contrast agents developed. Iodine is known to be particular electron-dense and to effectively scatter or stop X-rays. A good contrast agent requires a high density of electron-dense atoms. Therefore, the more iodine, the more \dense\"" the x-ray effect. Iodine based contrast media are water soluble and harmless to the body. These contrast agents are sold as clear colorless water solutions, the concentration is usually expressed as mg I/ml. Modern iodinated contrast agents can be used almost anywhere in the body. Most often they are used intravenously, but for various purposes they can also be used intraarterially, intrathecally (the spine) and intraabdominally - just about any body cavity or potential space.""",The molecular weight is 613.92.,Diatrizoate has a topological polar surface area of 95.5.,The log p value of  is 0.76.,Diatrizoate is approved and vet_approved.,Diatrizoate is a solid.,True
20787,"Gadoteridol provides contrast enhancement of the brain, spine and surrounding tissues resulting in improved visualization (compared with unenhanced MRI) of lesions with abnormal vascularity or those thought to cause a disruption of the normal blood brain barrier. Gadoteridol can also be used for whole body contrast enhanced MRI including the head, neck, liver, breast, musculoskeletal system and soft tissue pathologies. n MRI, visualization of normal and pathological brain tissue depends in part on variations in the radiofrequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in T2. When placed in a magnetic field, gadoteridol shortens the T1 relaxation time in tissues where it accumulates. Abnormal vascularity or disruption of the blood-brain barrier allows accumulation of gadoteridol in lesions such as neoplasms, abscesses, and subacute infarcts. Gadoteridol is an MRI contrast agent used for contrast enhancement of the brain, spine and surrounding tissues resulting in improved visualization (compared with unenhanced MRI) of lesions with abnormal vascularity or those thought to cause a disruption of the normal blood brain barrier. Gadoteridol can also be used for whole body contrast enhanced MRI including the head, neck, liver, breast, musculoskeletal system and soft tissue pathologies. Based on the behavior of protons when placed in a strong magnetic field, which is interpreted and transformed into images by magnetic resonance (MR) instruments. Paramagnetic agents have unpaired electrons that generate a magnetic field about 700 times larger than the proton's field, thus disturbing the proton's local magnetic field. When the local magnetic field around a proton is disturbed its relaxation process is altered. MR images are based on proton density and proton relaxation dynamics. MR instruments can record two different relaxation processes, the T1 (spin-lattice or longitudinal relaxation time) and T2 (spin-spin or transverse relaxation time). In MRI, visualization of normal and pathological brain tissue depends in part on variations in the radiofrequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in T2. When placed in a magnetic field, gadoteridol shortens the T1 relaxation time in tissues where it accumulates. Gadoteridol does not cross the intact blood-brain barrier; therefore, it does not accumulate in normal brain tissue or in central nervous system (CNS) lesions that have not caused an abnormal blood-brain barrier (e.g., cysts, mature post-operative scars). Abnormal vascularity or disruption of the blood-brain barrier allows accumulation of gadoteridol in lesions such as neoplasms, abscesses, and subacute infarcts.",The molecular weight is 557.68.,,,Gadoteridol is approved and investigational.,Gadoteridol is a solid.,True
20788,"Colistimethate is an antibiotic that has been shown to have bactericidal activity against aerobic gram-negative microorganisms. Colistimethate is particularly indicated when the infection is caused by sensitive strains of Pseudomonas aeruginosa. For the treatment of acute or chronic infections due to sensitive strains of certain gram-negative bacilli, particularly _Pseudomonas aeruginosa_. Colistimethate is a polymyxin antibiotic agent. Originally, colistimethate sodium was thought to be less toxic than polymyxin B; however, if the drugs are administered at comparable doses, their toxicities may be similar. Polymyxins are cationic polypeptides that disrupt the bacterial cell membrane through a detergentlike mechanism. With the development of less toxic agents, such as extended-spectrum penicillins and cephalosporins, parenteral polymyxin use was largely abandoned, except for the treatment of multidrug-resistant pulmonary infections in patients with cystic fibrosis. More recently, however, the emergence of multidrug-resistant gram-negative bacteria, such as _Pseudomonas aeruginosa_ and _Acinetobacter baumannii_, and the lack of new antimicrobial agents have led to the revived use of the polymyxins. Colistimethate is a surface active agent which penetrates into and disrupts the bacterial cell membrane. Colistimethate is polycationic and has both hydrophobic and lipophilic moieties. It interacts with the bacterial cytoplasmic membrane, changing its permeability. This effect is bactericidal. There is also evidence that polymyxins enter the cell and precipitate cytoplasmic components, primarily ribosomes.",,,,Colistimethate is approved and vet_approved.,Colistimethate is a solid.,True
20789,"Iodixanol is a nonionic hydrophilic compound commonly used as a contrast agent during coronary angiography, particularly in individuals with renal dysfunction, as it is believed to be less toxic to the kidneys than most other intravascular contrast agents. Iodixanol is a contrast agent during coronary angiography. Iodixanol is a contrast agent commonly used during coronary angiography, particularly in individuals with renal dysfunction, as it is believed to be less toxic to the kidneys than most other intravascular contrast agents. It is an imaging contrast agent with the same osmolality as blood (290mOsm/kg H20). Organic iodine compounds attenuate x-rays as they pass through the body, thereby allowing the body structures containing iodine to be delineated in contrast to those structures that do not contain iodine. The degree of opacity produced by these compounds is directly proportional to the total amount (concentration and volume) of the iodinated contrast agent in the path of the x-rays. After intravascular administration, iodixanol makes opaque those internal structures in its path of flow, allowing their visualization until significant hemodilution and elimination occur.",The molecular weight is 1550.19.,Iodixanol has a topological polar surface area of 339.09.,The log p value of  is -4.28.,Iodixanol is approved.,Iodixanol is a solid.,True
20790,,,,,Hydrolyzed Cephalothin is experimental.,Hydrolyzed Cephalothin is a solid.,False
20791,"Cephalothin group is a solid. This compound belongs to the 1,3-thiazines. These are organic compounds containing 1,3-thiazine, a six-member ring with a nitrogen and a sulfur atom in ring positions 1 and 3 respectively, as well as two double bonds. This substance is known to target beta-lactamase Toho-1 and D-alanyl-D-alanine carboxypeptidase.",,,,Cephalothin Group is experimental.,Cephalothin Group is a solid.,True
20792,"Apramycin is an aminoglycoside antibiotic and has a bactericidal action against many gram-negative bacteria. Apramycin is a structurally unique antibiotic that contains a bicyclic sugar moiety and a monosubstituted deoxystreptamine. It is not approved for use in humans. For the treatment of bacterial infections in animals. Apramycin stands out among aminoglycosides for its mechanism of action which is based on blocking translocation and its ability to bind also to the eukaryotic decoding site despite differences in key residues required for apramycin recognition by the bacterial target. The drug binds in the deep groove of the RNA which forms a continuously stacked helix comprising non-canonical C.A and G.A base pairs and a bulged-out adenine. The binding mode of apramycin at the human decoding-site RNA is distinct from aminoglycoside recognition of the bacterial target, suggesting a molecular basis for the actions of apramycin in eukaryotes and bacteria.",,,,Apramycin is experimental and vet_approved.,Apramycin is a solid.,True
20793,,,,,Gentamicin C1a is experimental.,Gentamicin C1a is a solid.,False
20794,,,,,Neamine is experimental.,Neamine is a solid.,False
20795,"An semisynthetic aminoglycoside antibiotic. Often used for treatment of multi-resistant bacterial infection such as methicillin-resistant _Staphylococcus aureus_ (MRSA). Arbekacin is used for the short term treatment of multi-resistant bacterial infections, such as methicillin-resistant <i>Staphylococcus aureus</i> (MRSA). Arbekacin is an aminoglycoside. Aminoglycosides function by binding to bacterial 30S ribosomal subunits, causing t-RNA misreads, and preventing the production of proteins. Anaerobes are less susceptible to aminoglycosides because they do not spend as much energy as aerobes on taking up chemicals like aminoglycosides. Aminoglycosides are useful primarily in infections involving aerobic, gram-negative bacteria, such as Pseudomonas, Acinetobacter, and Enterobacter. Arbekacin irreversibly binds bacterial 30S and 16S ribosomal subunits inhibiting protein synthesis. Arbekacin binds to 4 nucleotides of the 16S subunit and 1 amino acid of protein S12 to interfere with the decoding site around nucleotide 1400 in the 16S subunit. Interference with the decoding site interferes with its interaction with the wobble base of tRNA. This hindered interaction causes mRNA to be misread and the incorrect amino acids are inserted into protein. These error filled proteins are not able to function or may even be toxic.",The molecular weight is 552.63.,Arbekacin has a topological polar surface area of 297.27.,The log p value of  is -3.64.,Arbekacin is experimental and investigational.,Arbekacin is a solid.,True
20796,"Pyrithione zinc, or zinc pyrithione or zinc pyridinethione, is a coordination complex consisted of pyrithione ligands chelated to zinc (2+) ions via oxygen and sulfur centers. In the crystalline state, it exists as a centrosymmetric dimer. Due to its dynamic fungistatic and bacteriostatic properties, pyrithione zinc is used to treat dandruff and seborrheic dermatitis. Dandruff is a common scalp disease affecting >40% of the world's adult population, and may be caused by fungi such as _Malassezia globosa_ and _M. restricta_. Indicated for the treatment of dandruff and seborrheic dermatitis.  Pyrithione zinc has a broad antimicrobial spectrum of activity, including fungi, gram-positive and gram-negative bacteria. Pyrithione zinc is effective against Malassezia and all other fungi, especially the Malassezia species found on scalp. In patients with dandruff, treatment with pyrithione zinc reduced the amount of fungus on the scalp, which reduces the amount of free fatty acids, thereby reducing scalp flaking and itch. Inhibition of fungal growth by pyrithione zinc is linked to increased copper uptake and cellular levels of copper, which is demonstrated by decreased CTR1-lacZ expression and slightly increased CUP1-lacZ expression in affected microorganisms. The coordination complex of pyrithione zinc dissociates, and pyrithione ligand forms a CuPT complex from available extracellular copper in the target organism. Pyrithione acts as an ionophore, interacting nonspecifically with the plasma membrane to shuttle copper into the cell, and facilitates copper transport across intracellular membranes. Copper may be shuttled into the mitochondria. Copper inactivates iron-sulfur (Fe-S) cluster-containing proteins via a mechanism similar to that described for copper-induced growth inhibition in bacteria. Decreased activity of Fe-S proteins leads to inhibition of fungal metabolism and fungal growth. Pyrithione zinc has been shown to slightly increase the levels of zinc.",,,,Pyrithione is approved.,Pyrithione is a solid.,True
20797,"Magaldrate is an antacid drug used for the treatment of esophagitis, duodenal and gastric ulcers, and gastroesophageal reflux. Magaldrate has been discontinued in the US market.",,,,Magaldrate is approved and withdrawn.,Magaldrate is a solid.,True
20798,"Canrenoic acid (as the salt potassium canrenoate) is an aldosterone antagonist. Like spironolactone, it is a prodrug, which is metabolized to canrenone in the body.",,,,Canrenoic acid is approved and withdrawn.,Canrenoic acid is a solid.,True
20799,"Hydroxyethyl starch (HES/HAES) is a nonionic starch derivative. Hydroxyethyl starches (HES) are synthetic colloids commonly used for fluid resuscitation to replace intravascular volume. An intravenous solution of hydroxyethyl starch is used to prevent shock following severe blood loss caused by trauma, surgery, or other issues. After isovolemic exchange of blood with 500 mL of HES in healthy volunteers, blood volume is maintained for at least 6 hours Hydroxyethyl starch (HES) is one of the most frequently used plasma substitutes. Recent studies have indicated that HES may reduce capillary leakage.",,,,Hydroxyethyl Starch is approved.,Hydroxyethyl Starch is a solid.,True
20800,"Pentastarch is an artificial colloid (hydroxyethyl starch derivative). Pentastarch is characterized by presenting five hydroxyethyl groups, which signifies an approximate 50% hydroxyethylation. It is sold under the name Pentaspan by Bristol-Myers Squibb and is used for fluid resuscitation. When administered, pentastarch remains mainly in the circulatory system and hence, it is considered a plasma expander. The primary intended use of pentastarch is as a substitute for older colloids such as albumin or hetastarch for use in plasma volume expansion. ",,,,Pentastarch is approved and investigational.,Pentastarch is a solid.,True
20801,"Gadoteric acid is a macrocycle-structured gadolinium-based MRI contrast agent. It is composed of the organic acid DOTA (1,4,7,10-tetraazacyclododecane-1,4,7,10-tetraacetic acid) used for its chelating properties, and gadolinium (Gd3+). As a paramagnetic molecule, gadoterate develops a magnetic moment when placed in a magnetic field. This magnetic moment enhances the relaxation rates of water protons in its vicinity, leading to an increase in signal intensity (brightness) of tissues. More specifically, it reduces the T1 relaxation time (and to some extent the T2 and T2* relaxation times) in NMR, which is the source of its clinical utility. Increased signal brightness allows it to be used in imaging of blood vessels and of inflamed or diseased tissue where the blood vessels become 'leaky'.  Gadoteric acid is indicated for intravenous use with magnetic resonance imaging (MRI) in brain (intracranial), spine and associated tissues in adult and pediatric patients (2 years of age and older) to detect and visualize areas with disruption of the blood brain barrier (BBB) and/or abnormal vascularity. Gadoterate affects proton relaxation times and consequently the MR signal, and the contrast obtained is characterized by the relaxivity of the gadoterate molecule. The relaxivity values for gadoterate are similar across the spectrum of magnetic field strengths used in clinical MRI (0.2 - 1.5 T). Gadoterate is a paramagnetic molecule that develops a magnetic moment when placed in a magnetic field. The magnetic moment enhances the relaxation rates of water protons in its vicinity, leading to an increase in signal intensity (brightness) of tissues. When placed in a magnetic field, gadoterate shortens the T1 and T2 relaxation times in target tissues. ",The molecular weight is 558.65.,,,Gadoteric acid is approved.,Gadoteric acid is a solid.,True
20802,"Iothalamic acid is an iodine containing organic anion used as a diagnostic contrast agent. Conray is indicated for use in excretory urography, cerebral angiography, peripheral arteriography, venography, arthrography, direct cholangiography, endoscopic retrograde cholangiopancreatography, contrast enhancement of computed tomographic brain images, cranial computerized angiotomography, intravenous digital subtraction angiography and arterial digital subtraction angiography.",The molecular weight is 613.92.,Iothalamic acid has a topological polar surface area of 95.5.,The log p value of  is 0.47.,Iothalamic acid is approved.,Iothalamic acid is a solid.,True
20803,"Ioversol is classified as an _organoiodine_ compound and is used as a contrast dye in diagnostic procedures. It contains high levels of iodine in addition to various hydrophilic groups. Optiray 350 is indicated in adults for peripheral and coronary arteriography and left ventriculography. Optiray 350 is also indicated for contrast enhanced computed tomographic imaging of the head and body, intravenous excretory urography, intravenous digital subtraction angiography and venography. Optiray 350 is indicated in children for angiocardiography. Intravascular injection of ioversol opacifies those vessels in the path of the flow of the contrast medium, permitting radiographic visualization of the internal structures until significant hemodilution occurs. Optiray enhances computed tomographic imaging through augmentation of radiographic efficiency with the degree of density enhancement directly related to the iodine content in an administered dose.",The molecular weight is 807.12.,Ioversol has a topological polar surface area of 199.89.,The log p value of  is -2.73.,Ioversol is approved.,Ioversol is a solid.,True
20804,"Ioxilan is a tri-iodinated diagnostic contrast agent. Intravascular injection results in opacification of vessels in the path of flow of the contrast medium, permitting radiographic visualization of the internal structures of the human body until significant hemodilution occurs. When administered intra-arterially, Ioxilan is indicated for the following diagnostic tests: cerebral arteriography (300 mgI/mL), coronary arteriography and left ventriculography (350 mgI/mL), visceral angiography(350 mgI/mL), aortography(350 mgI/mL), and peripheral arteriography(350 mgI/mL). As with other iodinated contrast agents the degree of contrast enhancement is directly related to the iodine content in the administered dose. Intravascular injection results in opacification of vessels in the path of flow of the contrast medium, permitting radiographic visualization of the internal structures of the human body until significant hemodilution occurs.",The molecular weight is 791.12.,Ioxilan has a topological polar surface area of 179.66.,The log p value of  is -2.31.,Ioxilan is approved.,Ioxilan is a solid.,True
20805,"Isosulfan Blue is a synthetic visual lymphatic imaging agent. Isosulfan blue upon subcutaneous administration, delineates the lymphatic vessels draining the region of injection. It is an adjunct to lymphography in: primary and secondary lymphedema of the extremities; chyluria, chylous ascites or chylothorax; lymph node involvement by primary or secondary neoplasm; lymph node response to therapeutic modalities.  Following subcutaneous administration, Lymphazurin 1% binds to serum proteins and is picked up by the lymphatic vessels. Thus, the lymphatic vessels are delineated by the blue dye.  Isosulfan Blue is injected into the periphery of the tumor site, it localizes to the lymphatic system and aids in the surgical identification of tumor sentinel nodes which stain blue.",,,,Isosulfan blue is approved.,Isosulfan blue is a solid.,True
20806,"Iopromide is a low osmolar, non-ionic X-ray contrast agent for intravascular administration. It functions as a contrast agent by opacifying blood vessels in the path of flow of the contrast agent, permitting radiographic visualization of the internal structures until significant hemodilution occurs. Iopromide, as the product Iovist, is indicated for use as an X-ray contrast agent in the following procedures: Iopromide is a low osmolar, non-ionic X-ray contrast agent for intravascular administration. It functions as a contrast agent by opacifying blood vessels in the path of flow of the contrast agent, permitting radiographic visualization of the internal structures until significant hemodilution occurs.",The molecular weight is 791.12.,Iopromide has a topological polar surface area of 168.66.,The log p value of  is -1.73.,Iopromide is approved.,Iopromide is a solid.,True
20807,"Technetium Tc-99m exametazime is a radiopharmaceutical sold under the trade name Ceretec used in the detection of altered regional cerebral perfusion in stroke and other cerebrovascular diseases. It can also be used for the labelling of leukocytes to localise intra-abdominal infections and inflammatory bowel disease. Exametazime, also known as hexamethylpropyleneamine oxime or HMPAO, acts as a chelating agent for the Tc-99m radioisotope. Technetium Tc99m exametazime scintigraphy (with or without methylene blue stabilization) may be useful as an adjunct in the detection of altered regional cerebral perfusion in stroke. Tc99m exametazime without methylene blue stabilization is indicated for leukocyte labeled scintigraphy as an adjunct in the localization of intra-abdominal infection and inflammatory bowel disease. During the first hour following injection of Tc99m labeled leukocytes, activity is seen in the lungs, liver, spleen, blood pool, bone marrow and the bladder. The kidneys (parenchyma and/or renal pelvis) and gall bladder may also be visualized. Over the first 1-6 hours, the Tc99m is visualized in the bowel. At 24 hours post-injection substantial colonic activity is seen. ",The molecular weight is 384.27.,Technetium Tc-99m exametazime has a topological polar surface area of 149.38.,,Technetium Tc-99m exametazime is approved.,Technetium Tc-99m exametazime is a solid.,True
20808,"A radionuclide imaging agent used primarily in scintigraphy or tomography of the heart to evaluate the extent of the necrotic myocardial process. It has also been used in noninvasive tests for the distribution of organ involvement in different types of amyloidosis and for the evaluation of muscle necrosis in the extremities. For use as a skeletal imaging agent used to demonstrate areas of altered osteogenesis, and a cardiac imaging agent used as an adjunct in the diagnosis of acute myocardial infarction. May also be used to image gated blood pools and detect gastrointetinal bleeding. Technetium Tc-99m pyrophosphate collects in areas of altered osteogenesis and injured myocardium. It also has an affinity for red blood cells, enabling imaging of blood pools. It is thought that technetium Tc-99m pyrophosphate is adsorbed onto the surface of amorphous calcium phosphate deposits , insoluble hydroxyapatite crystals, and possibly other organic macromolecules. This would result in selective localization to necrotic muscle tissue such as that of a myocardial infarction where calcium deposition has begun as a result of cell damage. In areas of altered osteogenesis where hydroxyapatite formation is actively occuring, the surface area to volume ratio is high and favors a greater amount of technetium Tc-99m pyrophosphate to the surface of the crystals than in other areas of bone where crystal formation is less active. The localization of technetium Tc-99m pyrophosphate to these areas allows for their specific radioimaging.",,,,Technetium Tc-99m pyrophosphate is approved.,Technetium Tc-99m pyrophosphate is a solid.,True
20809,"Piracetam is a nootropic drug in the racetams group, with chemical name 2-oxo-1-pyrrolidine acetamide. It shares the same 2-oxo-pyrrolidone base structure with pyroglutamic acid and is a cyclic derivative of the neurotransmitter γ-aminobutyric acid (GABA). However its mechanism of action differ from that of endogenous GABA.Piracetam has neuroprotective and anticonvulsant properties and is reported to improve neural plasticity. Its efficacy is documented in cognitive disorders and dementia, vertigo, cortical myoclonus, dyslexia, and sickle cell anemia although the clinical application in these conditions is not yet established. Piracetam has effects on the vascular system by reduce erythrocyte adhesion to vascular endothelium, hinder vasospasm and facilitate microcirculation. Indicated in adult patients suffering from myoclonus of cortical origin, irrespective of aetiology, and should be used in combination with other anti-myoclonic therapies. Piracetam is known to mediate various pharmacodynamic actions: Piracetam interacts with the polar heads in the phospholipids membrane and the resulting mobile drug-lipid complexes are thought to reorganize the lipids and influence membrane function and fluidity. Such interaction has been reported in a study that investigated the effects of neuronal outgrowth induced by beta amyloid peptides; while amyloid peptides cause lipid disorganization within the cell membranes leading to neuronal death, piracetam demonstrated to decrease the destabilizing effects of amyloid peptide. The authors suggest that piracetam induces a positive curvature of the membrane by occupying the polar groups in the phospholipids to counteract the negative curvature induced by amyloid peptides , which in turn would decrease the likelihood of membrane fusion. This mechanism of action is thought to improve membrane stability, allowing the membrane and transmembrane proteins to maintain and recover the three-dimensional structure or folding for normal function such as membrane transport, chemical secretion, and receptor binding and stimulation. ",The molecular weight is 142.16.,Piracetam has a topological polar surface area of 63.4.,The log p value of  is -1.18.,Piracetam is approved and investigational.,Piracetam is a solid.,True
20810,Bisoxatin is a stimulant laxative which increases peristalsis and inhibits absorbtion of water and ions in the intestine. It is marketed in Belgium under the tradename Wylaxine and used for the treatment of constipation and for preparation of the colon for surgical procedures. For use in the treatment of constipation in the absence of bowel obstruction and for surgical preparation of the colon. Bisoxatin is a stimulant laxative which increases peristalsis and inhibits the absorbtion of water and ions in the intestine. This increases the water content of the feces and increases its movement through the intestine. The precise mechanism of the bisoxatin's stimulant effect and inhibition of water and ion movement is unknown.,The molecular weight is 333.34.,Bisoxatin has a topological polar surface area of 78.79.,The log p value of  is 2.77.,Bisoxatin is approved.,Bisoxatin is a solid.,True
20811,"Idarucizumab is a humanized monoclonal antibody fragment (Fab) derived from an immunoglobulin G1 isotype molecule that binds to and inactivates the oral anticoagulant dabigatran, thereby reversing its anticoagulant effect. As a direct acting oral anticoagulant (DOAC), one of the risks associated with the use of dabigatran includes bleeding, espeically when given to patients at increased risk (elderly, chronic kidney disease, concomitant NSAID or warfarin use, etc).  For use in patients treated with Dabigatran when reversal of the anticoagulant effects of dabigatran is needed for emergency surgery/urgent procedures and in life-threatening or uncontrolled bleeding. Idarucizumab is a specific reversal agent for dabigatran. It is a humanized monoclonal antibody fragment (Fab) that binds to dabigatran and its acylglucuronide metabolites with higher affinity than the binding affinity of dabigatran to thrombin, neutralizing their anticoagulant effect.",,,,Idarucizumab is approved.,Idarucizumab is a solid.,True
20812,"Picosulfuric acid is found in laxative products. Sodium picosulfate is a used to treat constipation or induce colon cleansing to prepare the large bowels before colonoscopy or surgery. The combination product containing sodium picosulfate and magnesium citrate was introduced to the Canadian market in 2005 and has been used in European countries for many years. Indicated for cleansing of the colon as a preparation for colonoscopy in adults. Sodium picosulfate is a stimulant laxative that in conjunction with magnesium citrate, produces a purgative effect on stools. In a multicentre, observational study comprising of patients undergoing colonoscopy, more than 93.0% of the patients receiving sodium picosulfate-containing preparations reported the colon cleansing effect to be effective.  Picosulfuric acid, as sodium picosulfate, is a contact laxative. Sodium picosulfate inhibits the absorption of water and",,,,Picosulfuric acid is approved.,Picosulfuric acid is a solid.,True
20813,"Choline C 11 is a marker for cellular proliferation as its main molecule is a precursor for the biosynthesis of phospholipids which are essential components of all cell membranes. It was developed by MCPRF and FDA first approved in September 2012. Choline C11 is indicated for its use in positron emission tomography (PET) imaging in patients with suspected prostate cancer recurrence and non-informative bone scintigraphy, computerized tomography or magnetic resonance imaging. Choline is phosphorylated by choline kinase into phosphorylcholine. This phosphorylated form gets trapped inside the cell. Cancer cells exhibit an increased cell wall membrane synthesis as well as an increased activity of choline kinase. Choline C11 presents a small tracer activity in the urinary collecting system and this property makes it a very noble compound in the evaluation of ureters and bladder. Choline is incorporated into phosphatidylcholine which is a major membrane phospholipid in mammalian cells. The use of choline C11 is based on the knowledge that malignant tumors with increased cellular proliferation take up more choline when compared with normal cells for the formation of cellular membranes. The increased uptake of choline is explained by its use as a substrate in phospholipid synthesis in cell membranes, transmembrane signaling, and lipid and cholesterol transport and metabolism.",,,,Choline C 11 is approved and investigational.,Choline C 11 is a solid.,True
20814,"Phosphoric Acid is a colorless, odorless phosphorus-containing inorganic acid. Phosphoric acid is a sequestering agent which binds many divalent cations, including Fe++, Cu++, Ca++, and Mg++. Phosphoric acid is used in dentistry and orthodontics as an etching solution, to clean and roughen the surfaces of teeth where dental appliances or fillings will be placed. Transport of phosphate from the gut lumen is an active, energy-dependent process that is modified by several factors.... Vitamin D stimulates phosphate absorption, an effect reported to precede its action on calcium ion transport. Phosphate supplementation of the diet of rodents has been shown to lead to reduction in the incidence of dental caries and different phosphates have different powers in reducing the cariogenic potential of the carbohydrates in a diet. Phosphate supplements seem to exert their cariostatic effect on the tooth surface either directly during eating or by excretion in the saliva.",The molecular weight is 97.99.,Phosphoric acid has a topological polar surface area of 77.76.,,Phosphoric acid is approved.,,True
20815,"Octinoxate is a cinnamate ester and common ingredient in sunscreen and other skin care products to minimize DNA photodamage. It was originally developed in 1950's as an organic UV-B filter that absorbs UV-B rays from sun. It is often combined with nanoparticles or other water-resistant liposomes in formulations to increase the localization at the epidermis and decrease the risk of percutaneous absorption. Its use in pharmaceutical and cosmetic formulations is approved by FDA. As an active ingredient in sunscreens and lip balms. Used for protection against damaging effects of sun rays.  Acts as a photoprotective agent that protects the skin by preventing and minimizing the damaging effects of ultraviolet (UV) rays of natural light. The cellular effects of UV irradiation include DNA damage, cell cycle arrest, immunological depression, apoptosis, and transcriptional changes. Absorbs UV-B (predominantly) and UV-A rays while accumulating in the outermost layer of the epidermis. Like any other photoprotective agents, octinoxate prevents the damage to cells and deoxyribonucleic acid (DNA) by reducing the p53 protein expression following UV exposure and also increases the skin's tolerability to UV rays. ",The molecular weight is 290.4.,Octinoxate has a topological polar surface area of 35.53.,The log p value of  is 5.96.,Octinoxate is approved and investigational.,Octinoxate is a liquid.,True
20816,"N-acetyltyrosine, also referred to as N-acetyl-L-tyrosine, is used in place of as a tyrosine precursor. is a non-essential amino acid with a polar side group. N-acetyltyrosine is administered as parenteral nutrition or intravenous infusion due to its enhanced solubility compared to tyrosine. It is typically administered as a source of nutritional support where oral nutrition is inadequate or cannot be tolerated. N-acetyltyrosine is indicated, in combination with several other amino acids and dextrose, as a peripherally administered source of nitrogen for nutritional support in patients with adequate stores of body fat in whom, for short periods, oral administration cannot be tolerated, is undesirable, or inadequate. N-acetyltyrosine is used as a high solubility precursor to used due to 's poor solubility. It is deacetylated to form. Used as a source of. See for more information on its role and pharmacology.",The molecular weight is 223.23.,N-acetyltyrosine has a topological polar surface area of 86.63.,The log p value of  is 0.15.,N-acetyltyrosine is approved.,N-acetyltyrosine is a solid.,True
20817,"Eucalyptus oil is a distilled oil derived from the leaves of the tree Eucalyptus. It is shown to be effective in reducing pain, swelling, and inflammation via its modulatory effect on the immune response. It is also shown to exhibit antibacterial activity against some bacterial species and cough suppressant actions. Eucalyptus oil can be applied directly to the skin for pain and swelling of respiratory tract mucous membranes, joint pain, genital herpes, and nasal stuffiness. As an active agent, eucalyptus oil has been indicated for relief of the symptoms of catarrhal colds, and/or the relief of the symptoms of minor muscular sprains and cramps. Lipophilic monoterpene formulations of eucalyptus oil appear to be readily absorbed orally, with a primarily oxidative metabolism that might necessitate induction of the cytochrome P450 enzyme system and subsequent urinary excretion. Gastrointestinal absorption of eucalyptus appears to be rapid and may be enhanced by the intake of lipids and milk. 1,8-cineole (which makes up to as much as 90% of most commonly used cineole-based eucalyptus oils) has also been found in vitro and in animals to possess cytochrome P450 inducing activity. The general consensus is that the exact mechanism of action of eucalyptus oil is largely unknown at this time but comprises various hypotheses from various studies.",,,,Eucalyptus oil is approved.,,True
20818,"Chloroxylenol, or para-chloro-meta-xylenol (PCMX), is an antiseptic and disinfectant agent used for skin disinfection and surgical instruments. It is found in antibacterial soaps, wound-cleansing applications, and household antiseptics. The halophenol is shown to be most effective against Gram positive bacteria where it disrupts the cell wall due to its phenolic nature. Chloroxylenol is on the World Health Organization's List of Essential Medicines. The predominant medical applications for which chloroxylenol is formally indicated for therapeutic use is as an application to the skin for use in cuts, bites, stings, abrasions, and for use as antiseptic hand cleaner. Chloroxylenol is a substituted phenol which has been widely used for many years as an ingredient of antiseptic and disinfectant products intended for external use. It is known to be bactericidal in low concentration to a wide range of Gram positive and Gram negative bacteria. As a phenol antiseptic, it is believed that the hydroxyl -OH groups of the chloroxylenol molecule binds to certain proteins on the cell membrane of bacteria, and disrupts the membrane so as to allow the contents of the bacterial cell to leak out. This allows chloroxylenol to enter the bacterial cell to bind further with more proteins and enzymes to disable the cell's functioning. At particularly high concentrations of chloroxylenol, the protein and nucleic acid content of targeted bacterial cells become coagulated and cease to function, leading to rapid cell death.",The molecular weight is 156.61.,Chloroxylenol has a topological polar surface area of 20.23.,The log p value of  is 3.48.,Chloroxylenol is approved.,Chloroxylenol is a liquid.,True
20819,"Oxyquinoline is a heterocyclic phenol and derivative of quinoline with antiseptic, disinfectant, and pesticide properties. It is used as a stabilizer for hydrogen peroxide, where it is sometimes added in cosmetic products. Oxyquinoline is used as a biocidal component of several over the counter products. These products are marketed for the purposes of inhibiting abnormal biological growth in the vagina and restoring natural pH.  Oxyquinoline acts as a biocide to eliminate bacteria and fungi. The mechanism by which oxyquinoline exerts its biocidal effect is unknown.",The molecular weight is 145.16.,Oxyquinoline has a topological polar surface area of 33.12.,The log p value of  is 2.08.,Oxyquinoline is approved and vet_approved.,Oxyquinoline is a solid.,True
20820,"Bicisate, also known as ethyl cysteinate dimer (ECD), is a N,N'-1,2-ethylene-di-yl-bis-L-cysteinate diethyl ester. It is used in conjunction with technetium Tc99m as a tracer to measure cerebral blood flow with single-photon emission computed tomography (SPECT). The complex of bicisate and technetium Tc99m as a kit was developed by Lantheus Medcl and FDA-approved on November 23, 1994. Bicisate as a complex with technetium Tc-99m is used in single photon emission computerized tomography (SPECT) as an adjunct to conventional CT or MRI in the localization of stroke in patients whom the presence of a stroke has already been diagnosed. It is not indicated to assess the functional viability of brain tissue or to distinguish between a stroke and other brain lesions. The neutral and lipophilic nature of bicisate provides it with high stability. This property is given by its N2S2 core. This characteristic has been proven to allow bicisate to be used even several hours after preparation and to present an easy passage through the blood-brain barrier. Bicisate is rapidly uptaken by the brain. The retention of bicisate in the brain is associated with stereospecific de-esterification to hydrophilic acid derivatives. Even though both DD and LL isomers demonstrate brain uptake, only the LL presents brain retention. Bicisate brain localization is performed by passive diffusion and the presence of slow hydrolysis in the blood and rapid hydrolysis in the brain. The hydrolysis of bicisate forms the monoacid and diacid bicisate derivatives. The formation of these derivatives results in high brain uptake and retention. The uptake of bicisate depends on the blood flow directed to the brain and thus the presence of a stroke will be translated into specific zones in the brain that would not include the complex of bicisate and technetium Tc-99m.",,,,Bicisate is approved and investigational.,Bicisate is a solid.,True
20821,"Pidotimod is a synthetic dipeptide with immunomodulatory properties. For use as immunostimulant therapy for treatment of cell-mediated immunosuppression with respiratory or urinary infections. Pidotimod modulates the immune system to induce an immune response against bacterial or viral pathogens  Pidotimod inhibits tumor necrosis factor α (TNF-α) induced increases in extracellular signal-related kinase (ERK) phosphorylation. It also increases nuclear factor κB (NFκB) expression and translocation to the nucleus. It is these to modulatory effects on ERK and NFκB signalling which are thought to produce the increase in toll-like receptor expression seen with pidotimod. Pidotimod increase maturation of dendritic cells responsible for presenting antigens to naive Th-cells. It also appears to result in a greater population these cells diiferentiating to Th1 cells which are believed to mediate the immune response to pathogens like bacteria and viruses. Lastly, pidotimod appears to increase antigen-specific antibody titer and cytotoxic response with antigen exposure. The precise mechanism and timeline of events leading to these effects is unknown.",The molecular weight is 244.27.,Pidotimod has a topological polar surface area of 86.71.,The log p value of  is -0.14.,Pidotimod is experimental.,Pidotimod is a solid.,True
20822,Dihydrostreptomycin is an antibiotic.,The molecular weight is 583.6.,Dihydrostreptomycin has a topological polar surface area of 334.59.,The log p value of  is -3.55.,Dihydrostreptomycin is approved and investigational and vet_approved and withdrawn.,,True
20823,"Hygromycin B is an aminoglycoside antibiotic produced by the bacterium Streptomyces hygroscopicus which kills bacteria, fungi and higher eukaryotic cells by inhibiting protein synthesis.",,,,Hygromycin B is vet_approved.,,True
20824,"Vaborbactam is a β-lactamase inhibitor based on a cyclic boronic acid pharmacophore. It has been used in trials investigating the treatment of bacterial infections in subjects with varying degrees of renal insufficiency. In August 2017, a combination antibacterial therapy under the market name Vabomere was approved by the FDA for the treatment of adult patients with complicated urinary tract infections (cUTI). Vabomere consists of vaborbactam and for intravenous administration. Vaborbactam is added to the therapy to reduce the extent meropenem degradation by inhibiting the serine beta-lactamases expressed by the microorganism of target. The treatment aims to resolve infection-related symptoms of cUTI and achieve negative urine culture, when the infections are proven or strongly suspected to be caused by susceptible bacteria. Indicated in combination with meropenem for the treatment of patients 18 years of age and older with complicated urinary tract infections (cUTI) including pyelonephritis caused by the following susceptible microorganisms: _Escherichia coli_, _Klebsiella pneumoniae_, and _Enterobacter cloacae_ species complex. Vaborbactam shows no antibacterial activity alone; it serves to restore the antibacterial activity of other antibacterial agents such as meropenem by attenuating their degradation by inhibiting certain serine beta-lactamases of microorganisms. Vaborbactam does not decrease the activity of meropenem against meropenem-susceptible organisms. Vaborbactam in combination with meropenem, which is a penem antibacterial drug, potentiates the bactericidal actions of meropenem against carbapenem-resistant KPC-containing _Escherichia coli_, _Klebsiella pneumoniae_, and _Enterobacter cloacae_ in a concentration-dependent manner. It restored the antimicrobial activity of meropenem in animal models of infection caused by some meropenem non-susceptible KPC-producing Enterobacteriaceae. Vaborbactam is a cyclic boronic acid pharmacophore β-lactamase inhibitor that elicits potent inhibition of _Klebsiella pneumoniae_ carbapenemase (KPC) enzymes and other Ambler class A and C enzymes such as serine β-lactamases that confer resistance to commonly-used antibiotics such as Carbapenems. Vaborbactam is a potent inhibitor of class A carbapenemases, such as KPC, as well as an inhibitor of other class A (CTX-M, SHV, TEM) and class C (P99, MIR, FOX) beta-lactamases. Vaborbactam interacts with β-lactamases of Ambler classes A and C via precovalent and covalent binding. It exerts no inhibitory actions on class D or class B carbapenemases. The production of contemporary β-lactamase by bacterial isolates potentiate the degradation of β-lactam antibiotic agents, rendering them clinically ineffective and posing challenges for patients receiving the standard antibiotic therapy. In combination with meropenem, varborbactam acts as a non-suicidal beta-lactamase inhibitor that protects meropenem from degradation mediated by serine beta-lactamases such as _Klebsiella pneumoniae_ carbapenemase (KPC).",The molecular weight is 297.13.,Vaborbactam has a topological polar surface area of 95.86.,The log p value of  is 0.52.,Vaborbactam is approved and investigational.,Vaborbactam is a solid.,True
20825,"Brincidofovir is under investigation for the prevention of Outcomes, Survival Rates, and Cytomegalovirus Disease. Brincidofovir has been investigated for the prevention and treatment of CMV, Adenovirus, BK Virus (BKV), Adenoviruses (AdV), and Epstein-Barr (EBV), among others.",,,,Brincidofovir is investigational.,,True
20826,Canrenone has been used in trials studying the diagnostic of Heart Failure.,The molecular weight is 340.46.,Canrenone has a topological polar surface area of 43.37.,The log p value of  is 2.91.,Canrenone is investigational.,,True
20827,Sisomicin has been used in trials studying the treatment of Pyoderma.,The molecular weight is 447.53.,Sisomicin has a topological polar surface area of 213.72.,The log p value of  is -2.69.,Sisomicin is investigational.,,True
20828,Spiradoline has been investigated for the basic science of Bipolar Depression.,,,,Spiradoline is investigational.,,True
20829,"Cicletanine is under investigation for the treatment of Diabetes, Hypokalemia, Hyponatremia, and Arterial Hypertension.",The molecular weight is 261.71.,Cicletanine has a topological polar surface area of 42.35.,The log p value of  is 3.14.,Cicletanine is investigational.,,True
20830,"Lafutidine has been investigated in Peptic Ulcer, Community-acquired Pneumonia, and Gastroesophageal Reflux Disease (GERD).",,,,Lafutidine is investigational.,,True
20831,"Lavoltidine has been used in trials studying the diagnostic of Reflux, Gastroesophageal and Gastroesophageal Reflux Disease.",,,,Lavoltidine is investigational.,,True
20832,"Nedaplatin is a second generation platinum analog. It is less nephrotoxic than but has proven equally effective. It was approved for use in Japan in 1995. Used in the treatment of non-small cell lung cancer, small cell lung cancer, oesophygeal cancer, and head and neck cancers. Nedaplatin damages DNA and induces cell death in cancer cells. It also functions as a radiosensitizer, increasing the susceptibility of the affected cells to radiation therapy. As a platinum analog, nedaplatin likely works similarly to on which the following mechanistic description is based. Once it has entered the cell it is hydrolyzed to its active form which complexes with water molecules. This form binds to to nucleophiles in the cytoplasm such as glutathione and other cyteine rich proteins resulting in an overall increase in oxidative stress as the cell loses antioxidant proteins. It also binds to purine nucleotides in the DNA. The active form allows for two binding interactions to form cross-links between these nucleotides. High mobility group proteins-1 and -2 induce apoptosis in response to guanine cross-links and their binding serves to shield the cross-linked DNA from repair mechanisms. The mismatch repair (MMR) protein complex also recognizes the distortion caused by platinum complexes and attempts to repair the DNA. This results in single strand breaks when the MMR complex attempts to remove the platinum cross-link. The MMR complex induces apoptosis after the repair attempt has failed. The single strand break in DNA makes it easier to form lethal double strand breaks with radiation treatment thus creating the radiosensitizing effect of nedaplatin.",,,,Nedaplatin is approved and investigational.,Nedaplatin is a solid.,True
20833,"Inosine pranobex (Isoprinosine or Methisoprinol) is a combination of inosine, acetamidobenzoic acid, and dimethylaminoisopropanol used as an antiviral drug. Inosine pranobex is also indicated for mucocutaneous infections due to herpes simplex virus (type 1 and type II) and for treatment of genital warts as adjunctive therapy to podophyllin or carbon dioxide laser.  Works by slowing the growth and spread of the virus in the body. It may also stimulate the immune system in the body, which helps to increase the body's ability to fight these infections. Inosine pranobex stimulates cell-mediated immune processes to viral infections.",The molecular weight is 550.57.,Inosine pranobex has a topological polar surface area of 129.2.,,Inosine pranobex is approved.,Inosine pranobex is a solid.,True
20834,"Oxabolone cipionate is the C17β cypionate ester and a prodrug of. A synthetic anabolic-androgenic (AAS) steroid, it is a derivative of 19-nortestosterone (nandrolone). It is considered as a performance enhancing drug thus is prohibited from use in sports. Used as a performance enhancing drug illicitly in athletes.  Androgenic effects include enhanced secondary sexual characteristics. ",The molecular weight is 414.59.,Oxabolone cipionate has a topological polar surface area of 63.6.,The log p value of  is 6.31.,Oxabolone cipionate is experimental.,Oxabolone cipionate is a solid.,True
20835,"Bismuth subnitrate, also referred to as bismuth oxynitrate or bismuthyl nitrate, is a highly water-soluble crystalline compound that has been used as a treatment for duodenal ulcers and anti-diarrheic agent. The use of bismuth substrate as an active ingredient in over-the-counter antacids is approved by the FDA. Indicated for over-the-counter use as an antacid.  Bismuth subnitrate acts as an antacid that exert protective effects on the gastric mucosa. In a double-blind endoscopically controlled study, bismuth substrate was demonstrated to be effective for symptomatic relief in duodenal ulcers. In the alcohol model of mucosal injury in the rat, bismuth substrate was shown to be cytoprotective. In a randomized clinical study consisting of patients with _H. pylori_-associated duodenal ulcer, adjunctive use of colloidal bismuth subnitrate in a short treatment regimen with omeprazole and clarithromycin resulted in improved eradication rate of _H. pylori_.  Based on the findings of a clinical investigation in patients with duodenal ulcer disease and healthy volunteers receiving oral bismuth subnitrate tablets, the protective effects of bismuth subnitrate may be secondary to endogenous mucosal prostaglandin (PGE2) production, which is one of the deficient factors observed in peptic ulcer disease. Antacid neutralizing activity of bismuth subnitrate was demonstrated to have a significant postprandial effect on gastric pH. ",The molecular weight is 1461.98.,Bismuth subnitrate has a topological polar surface area of 92.83.,,Bismuth subnitrate is approved.,Bismuth subnitrate is a solid.,True
20836,"Magnesium silicate is a compound of magnesium oxide and silicon. It is the magnesium salt of silicic acid containing an unspecified amount of water. The molecular formula can be expressed more clearly as MgSiO3.xH2O. It is known as talc and it presents many uses in the cosmetic industry, food industry and pharmaceutical industry. Under the FDA, magnesium silicate is determined as a member of the substances generally recognized as safe (GRAS) to be used as an anticaking agent. Magnesium silicate is used to absorb moisture, prevent caking, and to improve the feel of a product. In the pharmaceutical companies, it is used as a dietary supplement, as part of the formulation ingredients in drug production, in antacid and antiulcer preparations, as a component of antiepileptic drugs, in antifungal topical agents and in the treatment of acne and as a facial moisturizer.  As a supplement, magnesium silicate acts by replacing the factor that is missing. In the case of antacids, it is a non-absorbable antacid whose main activity is related to the absorption of hydrochloric acid. More specifically, magnesium silicate acts as a neutralizing and astringent agent.",,,,Magnesium silicate is approved.,Magnesium silicate is a solid.,True
20837,Aluminium acetoacetate is an aluminum containing antacid.,The molecular weight is 330.22.,,,Aluminium acetoacetate is experimental.,,True
20838,,,,,Hydrotalcite is approved and experimental and investigational.,,False
20839,,The molecular weight is 382.87.,Mefruside has a topological polar surface area of 106.77.,The log p value of  is 1.66.,Mefruside is experimental.,,False
20840,,The molecular weight is 56.3.,Magnesium peroxide has a topological polar surface area of 21.76.,,Magnesium peroxide is experimental.,,False
20841,,The molecular weight is 569.61.,Isepamicin has a topological polar surface area of 297.72.,The log p value of  is -2.66.,Isepamicin is experimental.,,False
20842,,The molecular weight is 328.81.,Clorexolone has a topological polar surface area of 80.47.,The log p value of  is 2.08.,Clorexolone is experimental.,,False
20843,,,,,Aluminium glycinate is experimental.,,False
20844,"Aloglutamol is an antacid salt of aluminium, gluconic acid, and tris. Proprietary names include Altris, Pyreses, Tasto and Sabro.",The molecular weight is 413.31.,,,Aloglutamol is experimental.,,True
20845,,The molecular weight is 270.7.,Clofenamide has a topological polar surface area of 120.32.,The log p value of  is -0.39.,Clofenamide is experimental.,,False
20846,,The molecular weight is 337.78.,Fenquizone has a topological polar surface area of 101.29.,The log p value of  is 1.28.,Fenquizone is experimental.,,False
20847,,The molecular weight is 434.51.,Niperotidine has a topological polar surface area of 102.04.,The log p value of  is 2.39.,Niperotidine is experimental and investigational.,,False
20848,"Clopamide is an oral diuretic agent with antihypertensive activity. Like thiazide diuretics, it has an aromatic sulfonamide base but with no double-ring structure.",The molecular weight is 345.84.,Clopamide has a topological polar surface area of 92.5.,The log p value of  is 2.37.,Clopamide is experimental.,,True
20849,,The molecular weight is 272.13.,Muzolimine has a topological polar surface area of 58.69.,The log p value of  is 1.33.,Muzolimine is approved and withdrawn.,,False
20850,,The molecular weight is 116.16.,Calcium silicate has a topological polar surface area of 63.19.,,Calcium silicate is experimental.,,False
20851,,,,,Adefovir is investigational.,Adefovir is a solid.,False
20852,"Strontium chloride (SrCl2) is a salt of strontium and chloride. SrCl2 is useful in reducing tooth sensitivity by forming a barrier over microscopic tubules in the dentin containing nerve endings that have become exposed by gum recession. This kind of barrier protection for tooth hypersensitivity has, however, been superseded by other toothpaste formulations and ingredients designed to be nerve calming agents instead. Such strontium chloride toothpaste formulations may subsequently not be available for sale anymore in certain parts of the world. When employed as an ingredient in toothpaste formulations, strontium chloride is predominantly indicated for treating teeth hypersensitivity. As an active ingredient in a toothpaste formulation, strontium chloride and the rest of the toothpaste product that it is incorporated into is designed to come into contact with and topically coat the teeth that are being brushed and is not supposed to be swallowed. The regular use of the toothpaste maintains protection that strontium chloride provides against tooth sensitivity despite the normal everyday wear, tear, and cleaning of teeth. For dental hypersensitivity, strontium ions in strontium chloride toothpaste formulations appear to relieve pain and sensitivity by blocking fluid flow in dentinal tubules, which are essentially microscopic canals in the dentin. Regular use of such toothpastes maintains the strontium chloride barricading of the tubules despite normal everyday wear, tear, and washing of teeth.",,,,Strontium chloride is approved.,Strontium chloride is a solid.,True
20853,"Sodium zirconium cyclosilicate is approved as the trade product Lokelma developed by AstraZeneca - an insoluble, non-absorbed sodium zirconium silicate, formulated as a powder for oral suspension that acts as a highly selective potassium removing agent. It is administered orally and is odorless, tasteless, and stable at room temperature. Approval of the medication is supported by data from three double-blind, placebo-controlled trials and two open-label trials which showed that the onset of action was approximately 1.0 hour and the median time to achieving normal potassium levels in the blood was 2.2 hours, with 92% of patients achieving normal potassium levels within 48 hours following administration. The treatment effect was maintained for up to 12 months. Sodium zirconium cyclosilicate is a potassium binder indicated for the treatment of hyperkalemia in adult patients. Sodium zirconium cyclosilicate is capable of reducing serum potassium concentrations as quickly as one hour after ingestion and normokalaemia can be achieved typically within 24 to 48 hours. Sodium zirconium cyclosilicate does not affect serum calcium or magnesium concentrations, or urinary sodium excretion. A close correlation is observed between starting serum potassium levels and effect size; patients with higher starting serum potassium levels have greater reductions in serum potassium. As a consequence of the resultant reduction in serum potassium concentration, there is a reduction in urinary potassium excretion as well. In a study of healthy subjects given sodium zirconium cyclosilicate 5 or 10 grams daily for four days, a dose-dependent reduction in serum potassium concentration and total urinary potassium excretion were accompanied by mean increases in fecal potassium excretion. No statistically significant changes in urinary sodium excretion were observed. Hyperkalemia is a condition defined by elevated potassium levels in the blood, often caused by cardiovascular, renal, and metabolic diseases. Hyperkalemia occurs in 23 to 47% of patients with chronic kidney disease and/or chronic heart failure, and may lead to cardiac arrest and death.",,,,Sodium zirconium cyclosilicate is approved and investigational.,Sodium zirconium cyclosilicate is a solid.,True
20854,Used for tryptophan determinations in proteins & foods.,,,,Lithium hydroxide is approved and withdrawn.,,True
20855,Salvianolic acid A is under investigation in clinical trial NCT03908242 (Phase I Study of Continuous Administration of Salvianolic Acid A Tablet).,,,,Salvianolic acid A is investigational.,,True
20856,"Perflutren, a diagnostic drug that is intended to be used for contrast enhancement during the indicated echocardiographic procedures, is comprised of lipid-coated microspheres filled with octafluoropropane(OFP) gas. When exposed to ultrasound waves, the microspheres resonate and \echo\"" strong signals back to the ultrasound machine. The difference in density between the gas-filled bubbles and the blood around them creates an increased level of contrast visible in the resulting ultrasound image. During echocardiography, activated Perflutren enhances images of the inner edges or borders of the heart, producing an improved image that may enable physicians to better diagnose patients."" Used as an ultrasound contrast imaging in cardiology and radiology. Perflutren, a diagnostic drug that is intended to be used for contrast enhancement during the indicated echocardiographic procedures, comprised of lipid-coated microspheres filled with octafluoropropane(OFP) gas. It provide contrast enhancement of the endocardial borders during echocardiography. The perflutren lipid microspheres exhibit lower acoustic impedance than blood and enhance the intrinsic backscatter of blood. Perflutren is comprised of gas-filled microspheres that are injected or infused into the body. When exposed to ultrasound waves, the microspheres resonate and \echo\"" strong signals back to the ultrasound machine. The difference in density between the gas-filled bubbles and the blood around them creates an increased level of contrast visible in the resulting ultrasound image. During echocardiography, activated Perflutren enhances images of the inner edges or borders of the heart, producing an improved image that may enable physicians to better diagnose patients.""",The molecular weight is 188.02.,,The log p value of  is 2.36.,Perflutren is approved.,Perflutren is a liquid.,True
20857,"Strepronin is a mucolytic drug. A mucolytic agent is any agent which dissolves thick mucus usually used to help relieve respiratory difficulties. The viscosity of mucous secretions in the lungs is dependent upon the concentrations of mucoprotein as well as the presence of disulfide bonds between these macromolecules and DNA. Strepronin is a mucolytic (expectorant) drug. The drug promotes drainage of mucus from the lungs by thinning the mucus and lubricating the irritated respiratory tract An expectorant increases bronchial secretions and mucolytics help loosen thick bronchial secretions. Expectorants reduce the thickness or viscosity of bronchial secretions thus increasing mucus flow that can be removed more easily through coughing, Mucolytics break down the chemical structure of mucus molecules. The mucus becomes thinner and can be removed more easily through coughing.",The molecular weight is 273.32.,Stepronin has a topological polar surface area of 83.47.,The log p value of  is 1.18.,Stepronin is experimental.,Stepronin is a solid.,True
20858,,,,,Castanospermine is experimental.,Castanospermine is a solid.,False
20859,,,,,2-Methoxyethanol is experimental.,2-Methoxyethanol is a solid.,False
20860,"G17DT is a vaccine that neutralises gastrin-17, a hormone required for the growth of a number of cancers of the gastrointestinal tract. It is in phase III trials for advanced pancreatic cancer as a monotherapy and in combination with gemcitabine. It is also in a phase II/III trial for advanced stomach cancer in combination with 5-fluorouracil and cisplatin and in a late phase II trial for advanced colorectal cancer in combination with irinotecan. Intended for the treatment of various forms of cancer. G17DT is a vaccine which neutralizes the gastrin 17 (G17) hormone and glycine-extended gastrin 17. G17 is a growth factor for pancreatic, stomach and colorectal cancers, and a potent stimulator of gastric acid secretion. G17DT consists of a protein carrier (Diptheria Toxoid) and a synthetic peptide which is similar to a portion of the gastrin 17 hormone. These are contained in a 'slow-release' liquid suspension vehicle for intramuscular administration. G17DT is administered by injection, the initial schedule for injection is unclear at present but booster  When administered, G17DT induces an immune response producing antibodies which bind with the peptide and also cross-react and neutralise gastrin 17 thus inhibiting the growth of gastrointestinal cancers and metastasis. In addition the product neutralizes glycine-extended gastrin 17 which is also a stomach and pancreatic cancer growth factor.",,,,G17DT is investigational.,G17DT is a liquid.,True
20861,PEV3A is a prophylactic malaria vaccine that acts against various stages of the disease. It is a two-component vaccine that contains the virosome formulated peptide mimetics PEV301 and PEV302. The two synthetic peptide vaccine components mimic the native structure of important antigens of the malaria parasite. The elicited antibodies are highly specific and able to inhibit the parasite’s ability to invade liver tissue _in vitro_. Investigated for use/treatment in malaria.,,,,PEV3A is investigational.,PEV3A is a solid.,True
20862,"INGN 225 is a therapeutic consisting of a cancer patient's own immune cells treated with an adenovector carrying the human p53 gene, Ad-p53. INGN 225 is currently in Phase 1/2 trials in patients with small cell lung cancer and breast cancer. Investigated for use/treatment in breast cancer, head and neck cancer, and lung cancer. INGN 225 uses the p53 tumor suppressor in a different manner than ADVEXIN to create a molecular immunotherapy for cancer that stimulates a particular type of immune system cell known as a dendritic cell. Testing has shown that the human immune system can recognize and kill tumors after treatment with dendritic cells stimulated by the p53 tumor suppressor, which suggests this therapy could have broad utility as a treatment for solid tumors. INGN 225 may also sensitize tumors to the effects of platinum and taxane chemotherapies.",,,,INGN 225 is investigational.,INGN 225 is a solid.,True
20863,"SRP 299 is a preparation of killed Mycobacterium vaccae that has been tested in uses related to inhibiting periodontal disease, in treating asthma and in treating eczema, itching and inflammation. Mycobacterium vaccae is a non-pathogenic, saprophytic bacteria whose antigens can be used to induce peripheral immune activation through the activity of regulatory T-cells that surpress inappropriate Th2 activity. A specific subset of serotonergic neurons in the interfascicular part of the dorsal raphe nucleus (DRI) is believed to be involved, based on studies with mice.  Investigated for use/treatment in asthma, atopic dermatitis, and pediatric atopic dermatitis indications. Induces peripheral immune activation through the activity of regulatory T-cells Induces activity of regulatory t-cells that surpress Th2 activity. CD11c+ cells act as the primary target for M. vaccae.",,,,SRP 299 is investigational.,SRP 299 is a solid.,True
20864,"GI-5005 is GlobeImmune's lead infectious disease product from its proprietary Tarmogen active immunotherapy platform for the treatment of chronic hepatitis C infection. GI-5005 is whole, heat-killed recombinant yeast genetically modified to express HCV-specific protein targets. Tarmogens are believed to activate both an innate immune response via Toll-like receptors (TLRs), as well as an adaptive, antigen specific cellular immune response. Investigated for use/treatment in hepatitis (viral, C). The mechanism of action for GI-5005 (i.e. immune elimination of infected hepatic cells) may work synergistically in combination with the current or emerging standard of care, which directly inhibits viral replication, to more effectively eradicate hepatitis C virus from the liver. Additionally, this mechanism of action may offer an option for interferon-intolerant or interferon-contraindicated patients as a long term monotherapy.",,,,GI-5005 is investigational.,GI-5005 is a solid.,True
20865,"Tedisamil (planned trade name Pulzium) is an investigational drug for atrial fibrillation and atrial flutter. It is currently being developed by Solvay and is currently under regulatory review by the United States Food and Drug Administration. Investigated for use/treatment in arrhythmia, atrial fibrillation, and angina. It is hypothesized tedisamil prevents Ca2+ overload by the cAMP dependent SR Ca2+ uptake.",The molecular weight is 288.48.,Tedisamil has a topological polar surface area of 6.48.,The log p value of  is 3.32.,Tedisamil is investigational.,Tedisamil is a solid.,True
20866,Investigated for use/treatment in cancer/tumors (unspecified). Chidamide is an orally bioavailable histone deacetylase (HDAC) inhibitor derived from the benzamide class. Histone deacetylase inhibitors are a class of cancer drugs that induce selective regulation of gene expression in cancer cells. ,,,,Tucidinostat is investigational.,Tucidinostat is a solid.,True
20867,"Investigated for use/treatment in kidney cancer, melanoma, renal cell carcinoma, lymphoma (unspecified), colorectal cancer, and brain cancer. HSPPC-96 is a protein peptide complex consisting of a 96 kDa heat shock protein (Hsp), gp96, and an array of gp96-associated cellular peptides. Immunisation with HSPPC-96 induces T-cell specific immunity against these peptides; gp96 is not immunogenic per se. The non-covalent binding of gp96 to peptides is neither selective nor restricted to cell types. Thus, the collection of gp96-associated peptides represents the antigenic peptide pool of a cell; this is the basis of the peptide-specific immunogenicity elicited by HSPPC-96.",,,,Vitespen is investigational.,Vitespen is a solid.,True
20868,Abetimus was developed by La Jolla Pharmaceuticals as an immunosuppressant but was never marketed in American or Europe despite application for marketing authorization in the mid-2000s. Investigated for use/treatment in kidney disease and systemic lupus erythematosus.,,,,Abetimus is investigational.,Abetimus is a solid.,True
20869,"Barbexaclone, a salt compound of propylhexedrine and phenobarbital, is a potent antiepileptic. By weight, barbexaclone is 40% propylhexedrine and 60% phenobarbital. While barbexaclone has sedative properties, propylhexedrine has psychostimulant properties intended to offset these sedative effects. Pharmacokinetic studies have demonstrated that the pharmacokinetics of phenobarbital given as barbexaclone are not affected by propylhexedrine. Several reports from Spanish and Italian literature suggest that barbexaclone is at least as effective as phenobarbital in adults and children, while being better tolerated and having less sedative properties. These reports were conducted in a small series of patients in the 1970s and 1980s, and have yet to be confirmed by larger controlled trials. Despite the lack of controlled trials, barbexaclone was used widely in Turkey until it was discontinued in 2009.  Created for the treatment for epilepsy, with the intent of creating an antiepileptic with less sedative properties than phenobarbital.  Phenobarbitol targets GABA receptors in the CNS. ",The molecular weight is 387.52.,Barbexaclone has a topological polar surface area of 75.27.,,Barbexaclone is experimental.,Barbexaclone is a solid.,True
20870,"Anthrax immune globulin is a human antibody given with antibiotics for the treatment of anthrax. It is derived from the plasma of humans immunized with BioThrax (adsorbed anthrax vaccine), which is then further purified. Available as the product Anthrasil (FDA), the result is a solution for slow IV infusion containing polyclonal antibodies that bind the protective antigen (PA) component of Bacillus anthracis lethal and edema toxins. This binding of antibody to PA prevents PA-mediated cellular entry of toxic factors. It is administered in combination with appropriate antibiotic therapy as the immunoglobulin itself is not known to have direct antibacterial activity against anthrax bacteria, which otherwise may continue to grow and produce anthrax toxins. Anthrax immune globulin is indicated for the treatment of inhalational anthrax in adult and pediatric patients in combination with appropriate antibacterial drugs. Polyclonal anthrax immune globulin is a passive immunizing agent that neutralizes anthrax toxin by binding to Protective Antigen (PA) to prevent PA-mediated cellular entry of anthrax edema factor and lethal factor. It is administered in combination with appropriate antibiotic therapy as the immunoglobulin itself is not known to have direct antibacterial activity against anthrax bacteria, which otherwise may continue to grow and produce anthrax toxins.",,,,Anthrax immune globulin human is approved.,Anthrax immune globulin human is a solid.,True
20871,"Equine anti-thymocyte globulin is composed of purified gamma globulin containing primarily IgG against human thymus lymphocytes. It is formed by inoculating a horse with an antigen (human thymoyctes) which then induces the horse immune system's B-lymphocytes to produce IgG immunoglobulins specific for that antigen. The result is polyclonal IgG that is then purified from the horse's serum to produce a usable drug product that can be used for immunosuppression. Although the exact mechanism of action is unknown, equine anti-thymocyte globulin targets a variety of immune system proteins including lymphocyte surface proteins, granulocytes, platelets, bone marrow cells, and other cell types. Equine ATG is currently indicated for the suppression of the immune system to prevent renal transplant rejection and in the treatment of aplastic anemia. Induction of T cell apoptosis and resulting T-cell lymphopenia found in vivo is credited for its therapeutic effect in these conditions.  For prevention of renal transplant rejection and for the treatment of aplastic anemia.",,,,Antilymphocyte immunoglobulin (horse) is approved and investigational.,Antilymphocyte immunoglobulin (horse) is a solid.,True
20872,Inactivated rabies virus antigen B is a component of rabies vaccines used for pre- and post-exposure prophylaxis against rabies. Inactivated rabies virus antigen B is indicated for pre- and post-exposure prophylaxis against rabies.,,,,"Rabies virus inactivated antigen, B is approved.",,True
20873,"Haemophilus influenzae type b strain 1482 capsular polysaccharide tetanus toxoid conjugate antigen is a vaccine for intramuscular injection used in the prevention of invasive disease caused by *Haemophilus influenzae* type b. *H. influenzae* is a Gram-negative coccobacillus that can cause infections including sepsis and meningitis. The vaccine contains the *Haemophilus influenzae* type b capsular polysaccharide (polyribosyl-ribitol-phosphate, PRP), a high-molecular-weight polymer prepared from the *H. influenzae* type b strain 1482 grown in a semi-synthetic medium, covalently bound to tetanus toxoid. The toxoid antigen is purified and toxin-inactivated.",,,,Haemophilus influenzae type B strain 1482 capsular polysaccharide tetanus toxoid conjugate antigen is approved and investigational.,,True
20874,"Rotavirus commonly infects children and infants causing severe diarrhea and vomiting leading to potentially fatal dehydration. Two rotavirus vaccines are available for the prevention of rotavirus gastroenteritis, Rotateq and Rotarix. Rotateq is a live vaccine consisting of 5 reassorted human-bovine viral strains. Rotarix is a live attenuated vaccine containing the 89-12 human strain. Rotavirus vaccines are 90% effective in protecting against severe rotavirus infection. Rotarix is indicated for prevention of rotavirus gastroenteritis caused by G1, G3, G4, and G9 types in infants aged 6-24 weeks. Rotarix and Rotateq contain live attenuated and live virus respectively. The virus replicates in the intesine and interacts with the patient's immune system to produce immunity. Seroconversion has been defined as the appearance of anti-rotavirus IgA antibodies at concentrations greater than 20 U/mL post-vaccination in the serum of infants previously negative for rotavirus. The exact mechanism specific to the rotavirus vaccines' interaction with the immune system is uncharacterized.",,,,Rotavirus vaccine is approved.,,True
20875,"Rabies virus inactivated antigen, A is an inactivated virus vacine for the intramuscular injection. It is an active immunization against rabies that can be administered pre- or post-exposure to the rabies virus.",,,,"Rabies virus inactivated antigen, A is approved and investigational.",,True
20876,"Rubella virus vaccine is a live attenuated virus vaccine for active immunization against rubella (German measles) that is subcutaneously administered. It is prepared from RA 27/3 strain of live attenuated rubella virus. Rubella is a common childhood disease, caused by rubella virus (togavirus).",,,,Rubella virus vaccine is approved and investigational.,,True
20877,"Live attenuated zoster vaccine is available as two products: Zostavax for the prevention of shingles in immunocompetent people over the age of 50, and Varivax for the prevention of chickenpox in individuals 12 months of age and older. While the two vaccines contain the same immunological components and provide protection against the same virus, Zostavax contains a higher dose and is used in older adults to prevent the development of shingles and post-herpetic neuralgia.  Zostavax vaccine is indicated for the prevention of herpes zoster (shingles) in immunocompetent adults aged 50 years and older. Zostavax provides protection against Herpes Zoster reactivation by eliciting an immune response to Varicella Zoster Virus (VZV). ",,,,Varicella Zoster Vaccine (Live/attenuated) is approved.,,True
20878,Haemophilus influenzae type b capsular polysaccharide meningococcal outer membrane protein conjugate antigen is a vaccine containing outer membrane antigen extracted from *Haemophilus influenzae*.,,,,Haemophilus influenzae type B capsular polysaccharide meningococcal outer membrane protein conjugate antigen is approved and investigational.,,True
20879,Bacillus calmette-guerin substrain tice live antigen is a vaccine containing attenuated live culture preparation of the Bacillus of Calmette and Guerin (BCG) strain of *Mycobacterium bovis* for percutaneous use. It is administered to prevent the development of tuberculosis.,,,,Bacillus calmette-guerin substrain tice live antigen is approved.,,True
20880,"Clostridium tetani toxoid antigen (formaldehyde inactivated) is a vaccine for intramuscular injection. It is used for active immunization of children 7 years of age or older, and adults, for prevention of tetanus. The toxoid in the Clostridium tetani culture is grown and detoxified followed by purification via ammonium sulfate filtration and precipation.",,,,Clostridium tetani toxoid antigen (formaldehyde inactivated) is approved.,,True
20881,,,,,Corynebacterium diphtheriae toxoid antigen (formaldehyde inactivated) is approved and investigational.,,False
20882,"A seasonally-specific component of the influenza vaccine. The influenza vaccine, also known as the \flu shot\"", is a vaccine that protects against infection from the influenza viruses. Vaccines provide protection from influenza by exposing the immune system to the virus (or parts of the virus) which stimulates an immunological defence against future exposure to the virus, or \""antigen\"". This defence includes the production of humoral immunity through the development of antibodies (through memory B cells) and of cell-mediated immunity through the production of T-lymphocytes. Upon re-exposure to infectious influenza virus, the immune system is prepared to identify and destroy the virus as there are circulating antibodies that recognize that particular component of the virus that it was previously exposed to.""",,,,Influenza A virus A/California/7/2009 X-181 (H1N1) antigen (propiolactone inactivated) is approved.,,True
20883,,,,,Japanese encephalitis virus strain sa 14-14-2 antigen (formaldehyde inactivated) is approved.,,False
20884,"A seasonally-specific component of the influenza vaccine. The influenza vaccine, also known as the \flu shot\"", is a vaccine that protects against infection from the influenza viruses. Vaccines provide protection from influenza by exposing the immune system to the virus (or parts of the virus) which stimulates an immunological defence against future exposure to the virus, or \""antigen\"". This defence includes the production of humoral immunity through the development of antibodies (through memory B cells) and of cell-mediated immunity through the production of T-lymphocytes. Upon re-exposure to infectious influenza virus, the immune system is prepared to identify and destroy the virus as there are circulating antibodies that recognize that particular component of the virus that it was previously exposed to.""",,,,Influenza B virus B/Brisbane/60/2008 antigen (formaldehyde inactivated) is approved.,,True
20885,"Typhoid Vi polysaccharide vaccine is a vaccine that is administered intramuscularly. It is an active immunization for the prevention of typhoid fever caused by S typhi and is approved for use in persons two years of age or older. The vaccine contains the purified cell surface Vi polysaccharide extracted from *Salmonella enterica* serovar *Typhi, S typhi Ty2* strain. The bacterial culture is inactivated in the medium with the capsular polysaccharides precipated from the solution.",,,,Typhoid Vi polysaccharide vaccine is approved.,,True
20886,"Bacillus calmette-guerin substrain connaught live antigen is intravesically administered for the treatment and prophylaxis of carcinoma in situ (CIS) of the urinary bladder and for the prophylaxis of primary or recurrent stage Ta and/or T1 papillary tumors following transurethral resection (TUR). The solution contains live, attenuated strain of Mycobacterium bovis. It is prepared from the Connaught strain of Bacillus Calmette and Guérin. Indicated for intravesical use in the treatment and prophylaxis of carcinoma in situ (CIS) of the urinary bladder and for the prophylaxis of primary or recurrent stage Ta and/or T1 papillary tumors following transurethral resection (TUR). ",,,,Bacillus calmette-guerin substrain connaught live antigen is approved and investigational.,,True
20887,"Yellow Fever vaccine prevents against Yellow Fever, a viral hemorrhagic disease caused by the transmission of a _flavivirus_ through the bite of an infected mosquito. Symptoms of Yellow Fever can range from asymptomatic, to mild flu-like illness, to more severe symptoms such as shock, jaundice, internal bleeding, and organ failure. Interestingly, Yellow Fever got its name from the characteristic yellowing of the skin and eyes that occurs from the development of jaundice when the virus attacks the liver. Although there is supportive treatment available for managing Yellow Fever, there are currently no antivirals developed to specifically treat Yellow Fever. Vaccination with Yellow Fever vaccine is therefore considered to be the most important and effective measure to protect against Yellow Fever, with protective immunity developing within 10 days after vaccination; in two separate clinical trials of Yellow Fever Vaccine, 90% of subjects seroconverted within 10 days after vaccination, and 100% of subjects seroconverted within 14 days. The World Health Organization no longer recommends the use of a 10-year booster dose following primary immunization, as a single dose is \sufficient to confer life-long immunity against yellow fever disease\"". "" Yellow Fever Vaccine is indicated for active immunization for the prevention of yellow fever in persons 9 months of age and older in the following categories: Yellow Fever Vaccine is composed of two live, attenuated strains of yellow fever virus, 17D-204 and 17DD, which have been shown to elicit an immune response identical to that induced by wild-type infection. Vaccination with Yellow Fever vaccine is considered to be the most important and effective measure to protect against Yellow Fever, with protective immunity developing within 10 days after vaccination; in two separate clinical trials of Yellow Fever Vaccine, 90% of subjects seroconverted within 10 days after vaccination, and 100% of subjects seroconverted within 14 days. ",,,,Yellow Fever Vaccine is approved and investigational.,,True
20888,"Hepatitis A viral infection can lead to significant morbidity and mortality, with signs and symptoms that include anorexia, nausea, vomiting, and liver failure. Known by several trade names, such as Havrix and Twinrix, the Hepatitis A vaccine has been formulated for immunization against hepatitis A virus (HAV) infection and safely confers strong protection against the disease caused by infection with this virus. In the US, the approved vaccine is inactivated while live Hepatitis A vaccines are currently available in other countries. Hepatitis A vaccine is indicated for immunization against hepatitis A virus (HAV) infection in patients aged 12 months and older, and the first dose should be administered at least 2 weeks before expected exposure to the Hepatitis A virus. Hepatitis A vaccine stimulates the immune-mediated production of anti-Hepatitis A antibodies, allowing for protection against Hepatitis A infection via the production of specific antibodies against the virus and other immune cells that prevent infection with Hepatitis A virus. The administration of the hepatitis A vaccine leads to immune activation of lymphocytes, which proceed to engulf the hepatitis A antigen, leading to the release of inflammatory mediators that stimulate B and T cells to attack the viral antigen. Following this stimulation, the B cells and T cells then differentiate into memory cells, antibody-producing B cells, cytotoxic T cells, and helper T cells to provide immunity against infection with Hepatitis A.",,,,Hepatitis A Vaccine is approved.,Hepatitis A Vaccine is a liquid.,True
20889,"Haemophilus influenzae type b strain 20752 capsular polysaccharide tetanus toxoid conjugate antigen is an active immunization as a booster dose given intramuscularly to pediatric patients who have received a primary series with a Haemophilus b Conjugate Vaccine that is licensed for primarly immunization. The vaccine contains Haemophilus b capsular polysaccharide (polyribosyl-ribitol-phosphate ), which is a high molecular weight polymer prepared from the *Haemophilus influenzae* type b strain 20,752. These are heat inactivated and purified. Indicated for active immunization in pediatric patients 15 months through 4 years of age as a booster dose for the prevention of invasive disease caused by Haemophilus influenzae type b. ",,,,Haemophilus influenzae type B strain 20752 capsular polysaccharide tetanus toxoid conjugate antigen is approved and investigational.,,True
20890,"Anthrax vaccine is a vaccine used for the pre- or post-exposure prophylaxis of disease in at high risk of, suspected or confirmed exposure to *Bacillus anthracis*. It is subcutaneously or intramuscularly administered. It is derived from cell-free filtrates of microaerophilic cultures of an avirulent, nonencapsulated strain of Bacillus anthracis which are grown in a chemically defined protein-free medium.",,,,Anthrax vaccine is approved.,,True
20891,"A seasonally-specific component of the influenza vaccine. The influenza vaccine, also known as the \flu shot\"", is a vaccine that protects against infection from the influenza viruses. Vaccines provide protection from influenza by exposing the immune system to the virus (or parts of the virus) which stimulates an immunological defence against future exposure to the virus, or \""antigen\"". This defence includes the production of humoral immunity through the development of antibodies (through memory B cells) and of cell-mediated immunity through the production of T-lymphocytes. Upon re-exposure to infectious influenza virus, the immune system is prepared to identify and destroy the virus as there are circulating antibodies that recognize that particular component of the virus that it was previously exposed to.""",,,,Influenza A virus A/Brisbane/59/2007(H1N1) hemagglutinin antigen (propiolactone inactivated) is approved.,,True
20892,"A seasonally-specific component of the influenza vaccine. The influenza vaccine, also known as the \flu shot\"", is a vaccine that protects against infection from the influenza viruses. Vaccines provide protection from influenza by exposing the immune system to the virus (or parts of the virus) which stimulates an immunological defence against future exposure to the virus, or \""antigen\"". This defence includes the production of humoral immunity through the development of antibodies (through memory B cells) and of cell-mediated immunity through the production of T-lymphocytes. Upon re-exposure to infectious influenza virus, the immune system is prepared to identify and destroy the virus as there are circulating antibodies that recognize that particular component of the virus that it was previously exposed to.""",,,,Influenza B virus B/Brisbane/60/2008 hemagglutinin antigen (propiolactone inactivated) is approved.,,True
20893,"A seasonally-specific component of the influenza vaccine. The influenza vaccine, also known as the \flu shot\"", is a vaccine that protects against infection from the influenza viruses. Vaccines provide protection from influenza by exposing the immune system to the virus (or parts of the virus) which stimulates an immunological defence against future exposure to the virus, or \""antigen\"". This defence includes the production of humoral immunity through the development of antibodies (through memory B cells) and of cell-mediated immunity through the production of T-lymphocytes. Upon re-exposure to infectious influenza virus, the immune system is prepared to identify and destroy the virus as there are circulating antibodies that recognize that particular component of the virus that it was previously exposed to.""",,,,Influenza A virus A/California/7/2009 X-181 (H1N1) hemagglutinin antigen (propiolactone inactivated) is approved.,,True
20894,"A seasonally-specific component of the influenza vaccine. The influenza vaccine, also known as the \flu shot\"", is a vaccine that protects against infection from the influenza viruses. Vaccines provide protection from influenza by exposing the immune system to the virus (or parts of the virus) which stimulates an immunological defence against future exposure to the virus, or \""antigen\"". This defence includes the production of humoral immunity through the development of antibodies (through memory B cells) and of cell-mediated immunity through the production of T-lymphocytes. Upon re-exposure to infectious influenza virus, the immune system is prepared to identify and destroy the virus as there are circulating antibodies that recognize that particular component of the virus that it was previously exposed to.""",,,,Influenza B virus B/Brisbane/60/2008 antigen (propiolactone inactivated) is approved.,,True
20895,"Salmonella typhi Ty21a live antigen is a live attenuated vaccine for oral administration only. It contains the attenuated strain *Salmonella typhi* Ty21a. The vaccine prevents the development of typhoid fever, an acute, febrile enteric disease caused by *Salmonella typhi* by inducing a local immune response in the intestinal tract.",,,,Typhoid Vaccine Live is approved.,,True
20896,"This drug is a fat-soluble phosphorothioate agent that kills both insects and mites. It is non-volatile in nature and is well known by a variety of names as such a _dip_ or _wash_. Coumaphos is widely used for both farm and domestic animals to control ticks, mites, flies and fleas.",,,,Coumaphos is vet_approved.,,True
20897,,,,,Famphur is vet_approved.,,False
20898,"Fenthion is an _organothiophosphate_ drug used as an insecticide, avicide, and acaricide. Its mode of action is explained by cholinesterase enzyme inhibition, which is similar to other organophosphates. Fenthion is listed as a restricted use compound by the United States Environmental Protection Agency due to its potential to cause cholinesterase inhibition in humans and animals.",,,,Fenthion is vet_approved.,,True
20899,"Phosmet is a phthalimide-derived organophosphate. It is a non-specific insecticide. It is mainly used on apple trees to control codling moths. It is also used on other fruit crops, ornamentals, and vines to control aphids, suckers, mites, and fruit flies.",,,,Phosmet is vet_approved.,,True
20900,"IMOGAM Rabies Pasteurized is indicated for post-exposure prophylaxis in persons suspected of exposure to rabies, who have not previously received a complete immunization regimen with a cell culture produced rabies vaccine. For use in prophylaxis against rabies virus in patients who have been exposed to the virus and are immunocompromised or have not previously recieved the rabies vaccine. Rabies immune globulin prevents viral invasion of the central nervous system. Rabies immune globulin binds the rabies virus, preventing it from invading the central nervous system. This affords time for the rabies vaccine, which is also administered in cases of rabies exposure, to induce an immune response to destroy the virus. Rabies immunoglobulin should only be administered up to eight days after exposure as the host begins to produce sufficient antibodies to the virus one week after exposure. Repeat dosing should also be avoided as it may interfere with induction of immune response by the rabies vaccine.",,,,Human rabies virus immune globulin is approved.,Human rabies virus immune globulin is a solid.,True
20901,,The molecular weight is 627.64.,Pirarubicin has a topological polar surface area of 204.3.,The log p value of  is 1.76.,Pirarubicin is investigational.,Pirarubicin is a solid.,False
20902,"Hepatitis B Vaccine is an ingredient in the EMA-withdrawn product Quintanrix. It is marketed in Canada as Engerix B. It is also a part of Twinrix (Hep A/Hep B vaccine) available also in Canada. Active immunization against hepatitis B virus infection. ENGERIX-B induces specific humoral antibodies against the surface antigen of hepatitis B virus (anti-HBs antibodies). An anti-HBs antibody titre above 10 IU/l correlates with protection to HBV infection. ENGERIX®-B induces specific humoral antibodies against HBsAg (anti-HBs antibodies). It is generally accepted that an anti-HBs titre greater than 10 IU/L correlates with protection against hepatitis B virus infection. More than 90% of healthy adults, children and neonates developed protective anti-HBs titres one month after completing a",,,,Hepatitis B Vaccine (Recombinant) is approved and withdrawn.,,True
20903,"Peficitinib has been used in trials studying the treatment and basic science of Psoriasis, Pharmacodynamics, Drug Interactions, Colitis, Ulcerative, and RHEUMATOID ARTHRITIS, among others.",,,,Peficitinib is investigational.,,True
20904,"Sirukumab has been used in trials studying the treatment and basic science of Giant Cell Arteritis and Arthritis, Rheumatoid.",,,,Sirukumab is investigational.,,True
20905,"Entinostat is under investigation for the treatment and other of Volunteers, Breast Cancer, Human Volunteers, and Normal Volunteers. Entinostat has been investigated for the treatment of Non-Small Lung Cancer, Epigenetic Therapy.",,,,Entinostat is investigational.,,True
20906,"CUDC-907 has been used in trials studying the treatment of Lymphoma, Solid Tumors, BREAST CANCER, Multiple Myeloma, and NUT Midline Carcinoma, among others.",,,,CUDC-907 is investigational.,,True
20907,"CUDC-101 has been used in trials studying the treatment of Cancer, Tumors, Liver Cancer, Breast Cancer, and Gastric Cancer, among others.",,,,CUDC-101 is investigational.,,True
20908,Diphos has been used in trials studying the treatment of Plasmodium Falciparum Malaria.,,,,Temefos is investigational.,,True
20909,Simendan is under investigation in clinical trial NCT00527059 (Renal Effects of Levosimendan in Patients Admitted With Acute Decompensated Heart Failure).,,,,Simendan is investigational.,,True
20910,Ricolinostat is under investigation for the treatment of Breast Carcinoma and Metastatic Breast Cancer.,,,,Ricolinostat is investigational.,,True
20911,BCG SSI has been used in trials studying Tuberculosis.,,,,Bacillus calmette-guerin substrain danish 1331 live antigen is investigational.,,True
20912,Lobucavir has been used in trials studying the treatment of HIV Infections and Cytomegalovirus Infections.,,,,Lobucavir is investigational.,,True
20913,"Tecemotide has been used in trials studying the treatment of Prostate Cancer and Carcinoma, Non-Small-Cell Lung.",,,,Tecemotide is investigational.,,True
20914,Mizoribine has been investigated for the treatment of Rheumatoid Arthritis.,The molecular weight is 259.22.,Mizoribine has a topological polar surface area of 151.06.,The log p value of  is -1.36.,Mizoribine is investigational.,,True
20915,"Givinostat has been used in trials studying the treatment of Polycythemia Vera, Juvenile Idiopathic Arthritis, Duchenne Muscular Dystrophy (DMD), Chronic Myeloproliferative Neoplasms, and Polyarticular Course Juvenile Idiopathic Arthritis.",,,,Givinostat is investigational.,,True
20916,"Gusperimus has been used in trials studying the treatment of Lupus Nephritis, Wegeners Granulomatosis, and Wegener's Granulomatosis.",The molecular weight is 387.53.,Gusperimus has a topological polar surface area of 178.38.,The log p value of  is -2.72.,Gusperimus is investigational.,,True
20917,"BCG vaccine has been investigated for the treatment of Neoplasms, Bladder Cancer, Neoplasms by Site, Urologic Diseases, and Urologic Neoplasms, among others.",,,,BCG vaccine is investigational.,,True
20918,"Oxatomide has been used in trials studying the treatment of Muscular Dystrophy, Duchenne.",The molecular weight is 426.56.,Oxatomide has a topological polar surface area of 38.82.,The log p value of  is 5.62.,Oxatomide is approved and investigational.,,True
20919,"Trofosfamide has been used in trials studying the treatment of Ependymomas, Medulloblastomas, Sarcoma, Soft Tissue, Supratentorial PNETs, and Recurrent Brain Tumors.",The molecular weight is 323.58.,Trofosfamide has a topological polar surface area of 32.78.,The log p value of  is 1.18.,Trofosfamide is investigational.,,True
20920,Cafedrine is under investigation in clinical trial NCT01311414 (Effect of Cafedrine/Theodrenaline and Urapidil on Cerebral Oxygenation).,The molecular weight is 357.41.,Cafedrine has a topological polar surface area of 90.7.,The log p value of  is 0.9.,Cafedrine is investigational.,,True
20921,Theodrenaline is under investigation in clinical trial NCT01311414 (Effect of Cafedrine/Theodrenaline and Urapidil on Cerebral Oxygenation).,The molecular weight is 375.38.,Theodrenaline has a topological polar surface area of 131.16.,The log p value of  is -0.67.,Theodrenaline is investigational.,,True
20922,Doxifluridine has been investigated for the treatment of Stomach Cancer.,The molecular weight is 246.19.,Doxifluridine has a topological polar surface area of 99.1.,The log p value of  is -1.19.,Doxifluridine is investigational.,,True
20923,"Deoxyspergualin has been used in trials studying the treatment of Lupus Nephritis, Chronic Rejection, and Diabetes Mellitus, Type 1.",,,,Deoxyspergualin is investigational.,,True
20924,Acteoside is under investigation in clinical trial NCT02662283 (Validity and Security of Reh-acteoside Therapy for Patients of IgA Nephropathy).,,,,Acteoside is investigational.,,True
20925,9-(N-methyl-L-isoleucine)-cyclosporin A (NIM811) has been used in trials studying the treatment of Chronic Hepatitis C Genotype-1 Relapse.,,,,9-(N-methyl-L-isoleucine)-cyclosporin A is investigational.,,True
20926,Fluocortin has been studied as a corticosteroid for treatment of dermatitis and eczema Spain.,,,,Fluocortin is experimental.,,True
20927,,,,,Begelomab is experimental and investigational.,,False
20928,"Sultopride is used in Japan, Hong Kong, and Europe to treat schizophrenia. It is of the drug class atypical antipsychotics.",The molecular weight is 354.47.,Sultopride has a topological polar surface area of 75.71.,The log p value of  is 1.93.,Sultopride is approved.,,True
20929,,The molecular weight is 262.36.,Cibenzoline has a topological polar surface area of 24.39.,The log p value of  is 4.13.,Cibenzoline is experimental.,,False
20930,,,,,Fluperolone is experimental.,,False
20931,,The molecular weight is 412.87.,Nizofenone has a topological polar surface area of 83.95.,The log p value of  is 4.4.,Nizofenone is experimental.,,False
20932,,The molecular weight is 369.53.,Prajmaline has a topological polar surface area of 43.7.,The log p value of  is 1.4.,Prajmaline is experimental.,,False
20933,,The molecular weight is 402.92.,Lorajmine has a topological polar surface area of 53.01.,The log p value of  is 3.17.,Lorajmine is experimental.,,False
20934,,The molecular weight is 326.48.,Bunaftine has a topological polar surface area of 23.55.,The log p value of  is 5.1.,Bunaftine is experimental.,,False
20935,,The molecular weight is 370.92.,Lorcainide has a topological polar surface area of 23.55.,The log p value of  is 4.48.,Lorcainide is experimental.,,False
20936,,,,,Acetyldigoxin is experimental.,,False
20937,,The molecular weight is 3363.83.,Elcatonin has a topological polar surface area of 1435.94.,The log p value of  is 0.0.,Elcatonin is experimental.,,False
20938,,The molecular weight is 288.31.,Piromidic acid has a topological polar surface area of 86.63.,The log p value of  is 0.63.,Piromidic acid is experimental.,,False
20939,,The molecular weight is 447.32.,Fluclorolone has a topological polar surface area of 94.83.,The log p value of  is 2.42.,Fluclorolone is experimental.,,False
20940,"Recombinant zoster vaccine, manufactured as the product Shingrix by GlaxoSmithKline, is an adjuvanted non-live recombinant vaccine indicated for prevention of shingles. First approved in October 2017 by the Food and Drug Administration, Shingrix is the preferred vaccine for preventing varicella zoster infection in people aged 50 years and older, replacing Zostavax as first line therapy.  Shingrix vaccine is indicated for the prevention of herpes zoster (shingles) in adults aged 50 years and older. Shingrix provides protection against Herpes Zoster reactivation by eliciting an immune response to Varicella Zoster Virus (VZV). The main immunological component of Shingrix vaccine is glycoprotein E (gE), a protein found on the surface of varicella zoster virus (VZV). Immune exposure to gE protein stimulates the development of anti-gE antibodies, and therefore adaptive immunity to VZV. The adjuvant system, AS01B, is also included in Shingrix to enhance the immunological response to the vaccine leading to longer lasting and greater immunogenicity to the herpes zoster virus.",,,,Varicella Zoster Vaccine (Recombinant) is approved and investigational.,Varicella Zoster Vaccine (Recombinant) is a solid.,True
20941,,,,,Typhoid vaccine is approved.,Typhoid vaccine is a solid.,False
20942,,,,,Monomethyl fumarate is approved and experimental and investigational.,,False
20943,"A seasonally-specific component of the influenza vaccine. The influenza vaccine, also known as the \flu shot\"", is a vaccine that protects against infection from the influenza viruses. Vaccines provide protection from influenza by exposing the immune system to the virus (or parts of the virus) which stimulates an immunological defence against future exposure to the virus, or \""antigen\"". This defence includes the production of humoral immunity through the development of antibodies (through memory B cells) and of cell-mediated immunity through the production of T-lymphocytes. Upon re-exposure to infectious influenza virus, the immune system is prepared to identify and destroy the virus as there are circulating antibodies that recognize that particular component of the virus that it was previously exposed to.""",,,,Influenza A virus A/Victoria/210/2009 X-187 (H3N2) hemagglutinin antigen (formaldehyde inactivated) is approved.,,True
20944,"A seasonally-specific component of the influenza vaccine. The influenza vaccine, also known as the \flu shot\"", is a vaccine that protects against infection from the influenza viruses. Vaccines provide protection from influenza by exposing the immune system to the virus (or parts of the virus) which stimulates an immunological defence against future exposure to the virus, or \""antigen\"". This defence includes the production of humoral immunity through the development of antibodies (through memory B cells) and of cell-mediated immunity through the production of T-lymphocytes. Upon re-exposure to infectious influenza virus, the immune system is prepared to identify and destroy the virus as there are circulating antibodies that recognize that particular component of the virus that it was previously exposed to.""",,,,Influenza B virus B/Brisbane/60/2008 hemagglutinin antigen (formaldehyde inactivated) is approved and investigational.,,True
20945,"A seasonally-specific component of the influenza vaccine. The influenza vaccine, also known as the \flu shot\"", is a vaccine that protects against infection from the influenza viruses. Vaccines provide protection from influenza by exposing the immune system to the virus (or parts of the virus) which stimulates an immunological defence against future exposure to the virus, or \""antigen\"". This defence includes the production of humoral immunity through the development of antibodies (through memory B cells) and of cell-mediated immunity through the production of T-lymphocytes. Upon re-exposure to infectious influenza virus, the immune system is prepared to identify and destroy the virus as there are circulating antibodies that recognize that particular component of the virus that it was previously exposed to.""",,,,Influenza A virus A/California/7/2009 (H1N1) live (attenuated) antigen is approved.,,True
20946,Human adenovirus e serotype 4 strain cl-68578 antigen is a vaccine.,,,,Human adenovirus e serotype 4 strain cl-68578 antigen is approved.,,True
20947,"_Vibrio cholerae_ CVD 103-HgR strain live antigen is a component of Vaxchora, an oral vaccine for immunization against _Vibrio cholerae_ serogroup O1. _Vibrio cholerae_ CVD 103-HgR strain live antigen is indicated for active oral immunization against infection caused by _Vibrio cholerae_ serogroup O1 in patients between 18 and 64 years of age.",,,,Vibrio cholerae CVD 103-HgR strain live antigen is approved and investigational.,,True
20948,"A seasonally-specific component of the influenza vaccine. The influenza vaccine, also known as the \flu shot\"", is a vaccine that protects against infection from the influenza viruses. Vaccines provide protection from influenza by exposing the immune system to the virus (or parts of the virus) which stimulates an immunological defence against future exposure to the virus, or \""antigen\"". This defence includes the production of humoral immunity through the development of antibodies (through memory B cells) and of cell-mediated immunity through the production of T-lymphocytes. Upon re-exposure to infectious influenza virus, the immune system is prepared to identify and destroy the virus as there are circulating antibodies that recognize that particular component of the virus that it was previously exposed to.""",,,,Influenza A virus A/Victoria/210/2009 X-187 (H3N2) antigen (formaldehyde inactivated) is approved.,,True
20949,"A seasonally-specific component of the influenza vaccine. The influenza vaccine, also known as the \flu shot\"", is a vaccine that protects against infection from the influenza viruses. Vaccines provide protection from influenza by exposing the immune system to the virus (or parts of the virus) which stimulates an immunological defence against future exposure to the virus, or \""antigen\"". This defence includes the production of humoral immunity through the development of antibodies (through memory B cells) and of cell-mediated immunity through the production of T-lymphocytes. Upon re-exposure to infectious influenza virus, the immune system is prepared to identify and destroy the virus as there are circulating antibodies that recognize that particular component of the virus that it was previously exposed to.""",,,,Influenza A virus A/Perth/16/2009 (H3N2) live (attenuated) antigen is approved.,,True
20950,"A seasonally-specific component of the influenza vaccine. The influenza vaccine, also known as the \flu shot\"", is a vaccine that protects against infection from the influenza viruses. Vaccines provide protection from influenza by exposing the immune system to the virus (or parts of the virus) which stimulates an immunological defence against future exposure to the virus, or \""antigen\"". This defence includes the production of humoral immunity through the development of antibodies (through memory B cells) and of cell-mediated immunity through the production of T-lymphocytes. Upon re-exposure to infectious influenza virus, the immune system is prepared to identify and destroy the virus as there are circulating antibodies that recognize that particular component of the virus that it was previously exposed to.""",,,,Influenza A virus A/Uruguay/716/2007(H3N2) antigen (propiolactone inactivated) is approved.,,True
20951,"A seasonally-specific component of the influenza vaccine. The influenza vaccine, also known as the \flu shot\"", is a vaccine that protects against infection from the influenza viruses. Vaccines provide protection from influenza by exposing the immune system to the virus (or parts of the virus) which stimulates an immunological defence against future exposure to the virus, or \""antigen\"". This defence includes the production of humoral immunity through the development of antibodies (through memory B cells) and of cell-mediated immunity through the production of T-lymphocytes. Upon re-exposure to infectious influenza virus, the immune system is prepared to identify and destroy the virus as there are circulating antibodies that recognize that particular component of the virus that it was previously exposed to.""",,,,Influenza A virus A/Brisbane/59/2007(H1N1) antigen (propiolactone inactivated) is approved.,,True
20952,,,,,Adenovirus type 7 vaccine live is approved.,,False
20953,"The New York City Board of Health strain of _Vaccinia_ is a viral strain used as a component of some smallpox vaccinations. ACAM2000, a percutaneously administered smallpox vaccine that was approved by the FDA in 2007, contains live antigens of this strain. The live antigen of the New York City Board of Health strain of _Vaccinia_ is indicated (within the ACAM2000 formulation) for active immunization against smallpox disease in patients determined to be at high risk of contracting smallpox infection.",,,,Vaccinia virus strain new york city board of health live antigen is approved.,Vaccinia virus strain new york city board of health live antigen is a solid.,True
20954,"Rozanolixizumab is under investigation in clinical trial NCT03861481 (A Study to Assess the Efficacy, Safety and Tolerability of Rozanolixizumab in Subjects With Chronic Inflammatory Demyelinating Polyradiculoneuropathy).",,,,Rozanolixizumab is investigational.,,True
20955,Bleselumab is under investigation in clinical trial NCT02921789 (Study to Assess the Efficacy and Safety of Bleselumab in Preventing the Recurrence of Focal Segmental Glomerulosclerosis in de Novo Kidney Transplant Recipients).,,,,Bleselumab is investigational.,,True
20956,Thyrotropin is under investigation in clinical trial NCT01348191 (Detection of Thyrotrophin Receptor in Human Myometrium).,,,,Thyrotropin is investigational.,,True
20957,Pertussis vaccine is under investigation in clinical trial NCT01698346 (Pertussis (Tdap) Vaccination in Pregnancy).,,,,Pertussis vaccine is approved and investigational.,,True
20958,Yersinia pestis 195/p antigen (formaldehyde inactivated) is under investigation in clinical trial NCT02596308 (Immunogenicity and Safety of Subunit Plague Vaccine).,,,,Yersinia pestis 195/p antigen (formaldehyde inactivated) is investigational.,,True
20959,,,,,Modified vaccinia ankara is approved.,,False
20960,"Ebola virus vaccine is a vaccine used to prevent Ebola virus disease caused by _Zaire ebolavirus_ in adults, prevent outbreaks, and reduce the extent of the virus spreading in case of outbreaks. Ebola virus disease, formerly known as Ebola hemorrhagic fever, is a rare but severe and often deadly disease. It is highly contagious: human to human transmission occurs from contact with body fluids from infected patients. It is characterized by fever, headache, myalgia, and gastrointestinal symptoms. These may be accompanied by hypotension and respiratory, kidney and liver failure, as well as internal and external bleeding. In the _Filoviridae_ family, there are five unique Ebolavirus species that are each named after the geographical region where it was first identified. The mortality rate of the Zaire species is about 80%. Ebola Zaire vaccine is indicated for active immunization of individuals 18 years of age or older to protect against Ebola Virus Disease (EVD) caused by _Zaire Ebolavirus_. Ebola Zaire vaccine protects against the Ebola virus infection and disease by introducing a protein produced by the _Zaire ebolavirus_ and initiating the body's normal immune responses against the virus. In clinical trials consisting of subjects receiving the Ebola virus vaccine, the vaccine virus RNA was detected in the plasma samples of most subjects within the first week after intramuscular injection. Ebola virus disease occurs when the virus comes into contact with the host tissue and invades the tissue by breaking in the mucosa or skin. Exposure can occur through animal-to-human or human-to-human transmission from blood and other bodily fluids of the virus-infected animal or human. The viral genome then replicates inside the cell, causing gene modulation in host cells - including monocytes, macrophages, and dendritic cells - and promote cell apoptosis, releasing the viral particles to extracellular tissue. The virus can further disseminate the infection by migrating to the regional lymph nodes, liver, and spleen to cause lymphadenopathy, hepatocellular necrosis, and lymphopenia. Ebola virus can cause dysregulation of the host immune system by inducing the host expression and release of pro-inflammatory mediators, including interferons, interleukins (IL-2, IL- 6, IL-8, and IL-10), and tumour necrosis factor α (TNF-α). These inflammatory processes promote endothelial activation and reduced vascular integrity. Furthermore, the release of tissue factors and increased nitric oxide levels lead to disseminated intravascular coagulation (DIC) and hypotension seen in the Ebola virus disease, respectively. The incubation period after the Ebola virus infection is 1-21 days.",,,,"Ebola Zaire vaccine (live, attenuated) is approved.",,True
20961,"The Moderna COVID-19 Vaccine (mRNA-1273) is a novel mRNA-based vaccine encapsulated in a lipid nanoparticle that encodes for a full-length pre-fusion stabilized spike (S) protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Coronavirus disease 2019 (COVID-19) is a highly contagious infectious disease caused by the novel coronavirus, SARS-CoV-2, leading to a respiratory illness alongside other complications. COVID-19 has high interpatient variability in symptoms, ranging from mild symptoms to severe illness. A phase I, open-label, dose-ranging clinical trial (NCT04283461) was initiated in March 2020 in which 45 subjects received two intramuscular doses (on days 1 and 29). This trial was later followed by phase II and III trials, where the Moderna COVID-19 Vaccine demonstrated vaccine efficacy of 94.1%. The Moderna COVID-19 Vaccine is authorized for use under an Emergency Use Authorization (EUA) for active immunization to prevent coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in individuals 18 years of age and older. It is administered in two doses, one month (28 days) apart. The Moderna COVID-19 Vaccine contains nucleoside-modified messenger RNA (mRNA) encoding the pre-fusion stabilized Spike glycoprotein (S) of SARS-CoV-2 virus. It has the potential to elicit a highly S-protein specific antiviral response. In clinical trials, the Moderna COVID-19 Vaccine demonstrated vaccine efficacy of 94.1%; however, the manufacturing company emphasizes that the vaccine may not protect all vaccine recipients against COVID-19, as some vaccinated patients still contracted the virus. The Moderna COVID-19 Vaccine is a vaccine that contains synthetic nucleoside-modified messenger RNA (mRNA) encapsulated in Lipid nanoparticle (LNP) which codes for the full-length, pre-fusion stabilized spike protein (S) of SARS-CoV-2. The S glycoprotein is a large transmembrane protein that plays a critical role in viral attachment, fusion, and entry into the host cell. Upon vaccination, human cells express the SARS-CoV-2 S antigen and immune response to the S antigen is elicited, leading to the protection against SARS-CoV-2.",,,,mRNA-1273 is investigational.,,True
20962,"Bile acid sequestrants like colestipol have been in use since the 1970s. And even though such an agent may very well be useful in reducing elevated cholesterol levels and decreasing the risk for atherosclerotic vascular disease due to hypercholesterolemia, colestipol is still generally only employed as an adjunct therapy and the relatively physical nature of its pharmacological activity sometimes limits its usefulness. Colestipol is indicated as adjunctive therapy to diet for the reduction of elevated serum total and low-density lipoprotein cholesterol (LDL-C) in patients with primary hypercholesterolemia (a condition that features elevated LDL-C) who do not respond adequately to dietary changes. Cholesterol is the major, and probably the sole precursor of bile acids. During normal digestion, bile acids are secreted via the bile from the liver and gall bladder into the intestines. Bile acids emulsify the fat and lipid materials present in food, thus facilitating absorption. A major portion of the bile acids secreted is reabsorbed from the intestines and returned via the portal circulation to the liver, thus completing the enterohepatic cycle. Only very small amounts of bile acids are found in normal serum. Colestipol is a lipid-lowering polymer that binds with bile acids in the intestine forming a complex that is excreted in the feces. This non-systemic action results in a continuous, partial removal of bile acids from the enterohepatic circulation preventing their reabsorption. This increased fecal loss of bile acids due to colestipol hydrochloride administration leads to increased oxidation of cholesterol to bile acids. This results in an increase in the number of hepatic low-density lipoprotein (LDL) receptors, and consequently an increased uptake of LDL and a decrease in serum/plasma beta lipoprotein or total and LDL cholesterol levels. Although hydrochloride produces an increase in the hepatic synthesis of cholesterol in man, serum cholesterol levels fall. ",,,,Colestipol is approved.,Colestipol is a solid.,True
20963,"Bentoquatam is a topical medication intended to act as a shield against exposure to the irritating substance urushiol, found in plants such as poison ivy or poison oak. Bentoquatam contains bentonite, a clay, and is only effective as long as the film is visible on the skin. Used to prevent or reduce the severity of allergic contact dermatitis due to urushiol, the allergenic resin of poison ivy, poison oak, and poison sumac. Bentoquatam protects the skin like a shield against poison ivy, poison oak, and poison sumac by physically blocking skin contact with their resin. The best protection against getting these conditions is to avoid contact with these plants. This medicine does not dry oozing and weeping caused by the rash of poison ivy, poison oak, or poison sumac. The mechanism of action is unknown. It is thought topically applied bentoquatam acts as a physical barrier that interferes with the adsorption of antigens onto the skin and reduces absorption of antigens into the skin. It probably does not work by modifying the systemic allergic response.",,,,Bentoquatam is approved.,Bentoquatam is a solid.,True
20964,"Kaolin is a layered silicate mineral. Kaolin is used in ceramics, medicine, coated paper, as a food additive, in toothpaste, as a light diffusing material in white incandescent light bulbs, and in cosmetics. Until the early 1990s it was the active substance of anti-diarrhoea medicine Kaopectate. Used for upset stomach and diarrhea, a traditional medicine used in China, South America and Africa. Kaolin is also used to treat AIDs-related diarrhea. Kaolin based bandages are also under investigation.  Kaolin is an adsorptive agent. Kaolin adsorbs water, toxins and bacteria, contributing to firmer stools, reducing fluid loss from diarrhea. ",,,,Kaolin is approved.,Kaolin is a solid.,True
20965,Zinc picolinate is a zinc salt of picolinic acid. It is available as OTC dietary supplements as a source of zinc to treat and prevent zinc deficiency. The absorption of zinc after oral administration of zinc picolinate is shown to be effective.,,,,Zinc picolinate is investigational.,,True
20966,"Aluminum (Al), also spelled aluminum, chemical element, a lightweight, silvery-white metal of main Group 13 (IIIa, or boron group) of the periodic table. Solutions containing 5 to 10% aluminum sulfate have been used as local applications to ulcers and to arrest foul discharges from mucous surfaces. Aluminum sulfate is also used in the preparation of aluminum acetate ear drops. It is often purchased over the counter and is available in solid stick or powder form for minor cuts and abrasions after shaving ,. Aluminum sulfate is also used as an adjuvant in vaccines. Aluminum sulfate may be used as a deodorant, as well as an astringent. Aluminum sulfate is also known as an astringent. Astringents are substances that cause contraction or shrinkage of tissues and that dry up secretion. When used as a deodorant, the volume of sweat produced is reduced by narrowing sweat ducts. The inhibition of body odor causing bacteria is another important strategy for deodorization. ",,,,Aluminum sulfate is approved.,Aluminum sulfate is a solid.,True
20967,,,,,Bentonite is approved.,,False
20968,"Magnesium aspartate is a magnesium salt of aspartic acid that is commonly used as a mineral supplement. It displays high oral bioavailability and water solubiltiy compared to other magnesium salts such as magnesium citrate, magnesium carbonate and magnesium oxide.",,,,Magnesium aspartate is experimental.,,True
20969,,,,,Montmorillonite is experimental and investigational.,,False
20970,"Magnesium orotate is a magnesium salt of orotic acid and is poorly soluble in water. It is a source of magnesium and is used as a mineral supplement to treat Mg deficiency. Orotic acid acts as a transporter that carries magnesium into the cells. It also exhibits antioxidant properties, since it is a key intermediate in the biosynthetic pathway of pyrimidines that promotes the synthesis of enzymes which act as free radical scavengers. Experiments investigating the potential cardioprotective actions of orotic acid in pathological heart conditions are still ongoing.",The molecular weight is 334.48.,,,Magnesium orotate is experimental.,,True
20971,,,,,Acetylcysteine zinc is experimental.,,False
20972,,,,,Zinc ascorbate is approved and nutraceutical.,,False
20973,Glycoprotein marker of gastrointestinal cancer.,,,,Zinc glycinate is experimental.,,True
20974,,,,,Zinc cation is experimental.,,False
20975,Etofibrate is a fibrate produced by the combination of clofibrate ester linked to niacin. These components separate in the body slowly allowing for pharmacokinetics similar to controlled-release formulations.,The molecular weight is 363.79.,Etofibrate has a topological polar surface area of 74.72.,The log p value of  is 3.75.,Etofibrate is experimental.,Etofibrate is a solid.,True
20976,,The molecular weight is 469.36.,Simfibrate has a topological polar surface area of 71.06.,The log p value of  is 6.72.,Simfibrate is experimental.,,False
20977,,The molecular weight is 377.82.,Ronifibrate has a topological polar surface area of 74.72.,The log p value of  is 4.15.,Ronifibrate is experimental.,,False
20978,,The molecular weight is 471.26.,,,Aluminium clofibrate is experimental.,,False
20979,,The molecular weight is 327.81.,Clofibride has a topological polar surface area of 55.84.,The log p value of  is 3.11.,Clofibride is experimental.,,False
20980,,,,,Dihydroetorphine is experimental and illicit.,Dihydroetorphine is a solid.,False
20981,"Bezitramide is a narcotic analgesic which was discovered in 1961, clinically tested around the 1970's , and marketed under the name Burgodin. After cases of fatal overdose in the Netherlands in 2004 the drug was withdrawn from the market.  A narcotic analgesic once used for the treatment of severe chronic pain.  Bezitramide acts in the body to relieve pain with a potency 20 times that of methadone. Its duration of action is relatively long, lasting up to 12 hours post oral administration, after the achievement of steady state. Its onset of action is slow, with a peak in analgesic effect noted between 2.5-3.5 hours after dosing. ",The molecular weight is 492.62.,Bezitramide has a topological polar surface area of 67.65.,The log p value of  is 5.28.,Bezitramide is experimental and illicit and withdrawn.,Bezitramide is a solid.,True
20982,"An opioid analgesic structurally related to methadone and used in the treatment of severe pain. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1070)",The molecular weight is 392.54.,Dextromoramide has a topological polar surface area of 32.78.,The log p value of  is 4.07.,Dextromoramide is experimental and illicit.,Dextromoramide is a solid.,True
20983,,The molecular weight is 271.36.,Desomorphine has a topological polar surface area of 32.7.,The log p value of  is 2.43.,Desomorphine is experimental and illicit.,Desomorphine is a solid.,False
20984,A narcotic analgesic with a long onset and duration of action. It is used mainly in the treatment of narcotic dependence. ,,,,Alphacetylmethadol is experimental and illicit.,Alphacetylmethadol is a solid.,True
20985,A muscarinic antagonist that has been used to treat neuroleptic-induced parkinsonism. Benzetimide is the (-)-enantimorph of dexetimide.,The molecular weight is 362.47.,Dexetimide has a topological polar surface area of 49.41.,The log p value of  is 3.31.,Dexetimide is withdrawn.,Dexetimide is a solid.,True
20986,Chlorphenoxamine is marketed under the name Phenoxene. It is an antihistamine and anticholinergic used to treat itching as well as for its antiparkinsonian effect.,The molecular weight is 303.83.,Chlorphenoxamine has a topological polar surface area of 12.47.,The log p value of  is 4.56.,Chlorphenoxamine is withdrawn.,Chlorphenoxamine is a solid.,True
20987,Benactyzine is an anticholinergic drug used as an antidepressant in the treatment of depression and associated anxiety.,The molecular weight is 327.42.,Benactyzine has a topological polar surface area of 49.77.,The log p value of  is 3.76.,Benactyzine is withdrawn.,Benactyzine is a solid.,True
20988,Lofentanil is an analog of fentanyl and is one of the most potent opioids available today. It displays most similarity to carfentanil (4-carbomethoxyfentanyl) and is considered to be slightly more potent than this drug.,,,,Lofentanil is illicit.,Lofentanil is a solid.,True
20989,"Polycarbophil calcium is a synthetic polymer manufactured from the cross-linking of polyacrylic acid with divinyl glycol and a calcium counter-ion. Polycarbophil is used to treat constipation and to help maintain regular bowel movements. Relieves constipation or diarrhea associated with bowel disorders and acute nonspecific diarrhea. It is known as a bulk-forming laxative. It increases the bulk in the stool, an effect that helps to cause movement of the intestines. It also works by increasing the amount of water in the stool, making the stool softer and easier to pass.",,,,Polycarbophil is experimental.,Polycarbophil is a solid.,True
20990,"Mineral oil, or paraffin oil, is a mixture of higher alkanes from a mineral source, such as petroleum. Petroleum mineral oil is manufactured from crude oils by vacuum distillation to produce several distillates and a residual oil that are then further refined. During the modern refining process, aromatics are reduced by solvent extraction, catalytic hydrotreating, or hydrocracking. Unrefined or mildly treated mineral oils are classified as Group 3 carcinogens by the World Health Organizations, as chronic exposure to these aromatics including alkylated polycyclic aromatic compounds (PAC) can lead to skin cancer.  Mineral oil is not considered an active pharmacological ingredient in pharmaceutical preparations and so has no official indication. It is typically present in topical formulations as an emollient and occlusive agent. Mineral oil blocks the loss of water from the skin allowing greater hydration of the epidermis. Mineral oil sits on the surface of the skin and in spaces between cells and provides a hydrophobic barrier. This barrier prevents trans-epidermal water loss to trap water in the skin. Overall this leads to greater hydration, flexibility, and softness of the stratum corneum.",,,,Mineral oil is approved and vet_approved.,Mineral oil is a liquid.,True
20991,"Platango seeds refer to the seeds collected from various species of plantago trees. It is found in some laxatives for treating occasional constipation and restoring regularity in bowel movements. Its potential benefit in maintaining remission in ulcerative colitis has been studied. Indications include the treatment of patients needing a high fibre regime, perhaps for: (a) the relief of constipation, including constipation in pregnancy and the maintenance of regularity; (b) the management of bowel function in patients with colostomy, ileostomy, hemorrhoids, anal fissure, chronic diarrhea with diverticular disease, irritable bowel syndrome, and ulcerative colitis. The active ingredient psyllium husk is comprised of the episperm and collapsed adjacent layers removed from the seeds of Plantago afar L. or Plantago indica L.. Psyllium husk is abundant in alimentary fibres and mucilages, with its mucilage content in particular being higher than that of other plantago species. Specifically, psyllium husk is capable of absorbing up to 40 times its own weight in water. Psyllium husk consists of 85% water-soluble fibre - it is subsequently partly fermentable (in vitro 72% unfermentable residue) and acts by hydration in the bowel. Psyllium seeds are comprised of dietary fibre which, when mixed with water forms a gel-like mass that works as a mild laxative. This gel-like mass subsequently moves down a patient's digestive system and makes stools softer by increasing their water contents. At the same time psyllium seed lubricates the intestine, which improves the transit of stools. Moreover, as the presence of the gel-like mass increases the stool bulk it also increases the tension and/or the stretch stimulus in the bowel wall which serves to trigger bowel movements.",,,,Plantago seed is approved and investigational.,,True
20992,Magnesium glycinate is a magnesium salt of glycine that is available as dietary supplements as a source of magnesium. It is used in the treatment of magnesium deficiency.,,,,Magnesium glycinate is approved.,,True
20993,"Methyl cellulose polymer consisting of numerous linked glucose molecules used as a stabiliser, thickener and emulsifier for foodstuffs and cosmetics. The Degree of Substitution (DS) of a given form of methyl cellulose is defined as the average number of substituted hydroxyl groups per glucose with a theoretical maximum of 3, however more typical values are 1.3 2.6. Methyl cellulose is a hydrophilic white powder in pure form and dissolves in cold (but not in hot) water, forming a clear viscous solution or gel. It is available under a variety of trade names as a treatment for constipation. Like cellulose, it is not digestible, not toxic, and not allergenic Solutions containing methyl cellulose are used as substitute for tears or saliva if the natural production of these fluids is disturbed. It is also used or constipation, diverticulosis, hemorrhoids and irritable bowel syndrome. Used in the manufacture of capsules in nutritional supplements. Its edible and nontoxic properties provide a vegetarian alternative to the use of gelatin. It increases the bulk in your stool, an effect that helps to cause movement of the intestines. It also works by increasing the amount of water in the stool, making the stool softer and easier to pass. Methylcellulose absorbs water in the gastrointestinal lumen thereby increasing the bulk of the stool. This leads to distension and stimulation of peristalsis. The ability of methylcellulose to absorb water may contribute to its efficacy in the management of diarrhea by once again increasing the bulk and consistency of the stool.",,,,Methylcellulose is approved.,,True
20994,Normethadone is used as an opioid antitussive in combination with. It is marketed in Canada by Valeant under the tradename Cophylac. For use in the treatment of cough when other less potent treatments have failed. Normethadone is an opioid which suppresses coughing by central and peripheral mechanisms. Normethadone activates central opioid receptors in the medulla to supress the cough reflex. It also likely activates peripheral opioid receptors to inhibit signalling by irritant receptors of the airway.,The molecular weight is 295.43.,Normethadone has a topological polar surface area of 20.31.,The log p value of  is 3.86.,Normethadone is approved and illicit.,Normethadone is a solid.,True
20995,"Piritramide is under investigation for the treatment of Colon Cancer and Minimal Residual Disease. Piritramide has been investigated for the supportive care of Pain, Postoperative and Postoperative Nausea and Vomiting.",The molecular weight is 430.6.,Piritramide has a topological polar surface area of 73.36.,The log p value of  is 3.19.,Piritramide is approved and investigational.,,True
20996,"Batefenterol has been used in trials studying the treatment of Pulmonary Disease, Chronic Obstructive.",,,,Batefenterol is investigational.,,True
20997,Tropatepine has been used in France for its antiparkinsons activities.,The molecular weight is 333.49.,Tropatepine has a topological polar surface area of 3.24.,The log p value of  is 5.05.,Tropatepine is experimental.,,True
20998,Prifinium is an antimuscarinic agent with antispasmodic and antiemetic properties. It may be useful for the treatment of irritable bowel syndrome.,,,,Prifinium is experimental.,,True
20999,,The molecular weight is 323.44.,Piperidolate has a topological polar surface area of 29.54.,The log p value of  is 4.58.,Piperidolate is experimental.,,False
21000,,The molecular weight is 354.47.,Benzilone has a topological polar surface area of 46.53.,The log p value of  is 0.66.,Benzilone is experimental.,,False
21001,,The molecular weight is 327.42.,Difemerine has a topological polar surface area of 49.77.,The log p value of  is 3.41.,Difemerine is experimental.,,False
21002,,The molecular weight is 288.39.,Phenglutarimide has a topological polar surface area of 49.41.,The log p value of  is 2.53.,Phenglutarimide is experimental.,,False
21003,,The molecular weight is 405.57.,Mazaticol has a topological polar surface area of 49.77.,The log p value of  is 3.66.,Mazaticol is experimental.,,False
21004,,The molecular weight is 495.54.,Nicomorphine has a topological polar surface area of 90.85.,The log p value of  is 2.72.,Nicomorphine is experimental.,,False
21005,,The molecular weight is 321.46.,Etybenzatropine has a topological polar surface area of 12.47.,The log p value of  is 4.05.,Etybenzatropine is experimental.,,False
21006,,The molecular weight is 233.36.,Meptazinol has a topological polar surface area of 23.47.,The log p value of  is 3.71.,Meptazinol is experimental.,,False
21007,,The molecular weight is 282.45.,,The log p value of  is -0.5.,Emepronium is experimental.,,False
21008,,The molecular weight is 354.47.,Bevonium has a topological polar surface area of 46.53.,The log p value of  is 0.78.,Bevonium is experimental.,,False
21009,,The molecular weight is 510.83.,Gallamine has a topological polar surface area of 27.69.,The log p value of  is -5.4.,Gallamine is experimental.,,False
21010,,The molecular weight is 367.49.,Phenoperidine has a topological polar surface area of 49.77.,The log p value of  is 3.5.,Phenoperidine is experimental.,,False
21011,,,,,Phenazocine is experimental.,,False
21012,,The molecular weight is 329.48.,Bornaprine has a topological polar surface area of 29.54.,The log p value of  is 5.26.,Bornaprine is experimental.,,False
21013,,,,,Etanautine is experimental.,,False
21014,A non-depolarizing skeletal muscle relaxant similar to. It is used as an anesthesia adjuvant.,The molecular weight is 666.91.,Alcuronium has a topological polar surface area of 46.94.,The log p value of  is -3.49.,Alcuronium is experimental.,,True
21015,,,,,Tiemonium iodide is experimental.,,False
21016,,The molecular weight is 321.5.,Dihexyverine has a topological polar surface area of 29.54.,The log p value of  is 6.29.,Dihexyverine is experimental.,,False
21017,"Sodium tartrate is a disodium salt of l-( + )-tartaric acid that is identified by transparent, colorless, and odorless crystals. It is obtained as a byproduct of wine manufacturing. Sodium tartrate is generally recognized as safe (GRAS) as a direct human food ingredient. It acts as an emulsifier and pH control agent in food products.  It acts as an emulsifier and pH control agent in food products ,. Sodium tartrate is a white, crystalline powder, used as an emulsifier and a binding agent. It can be used in jellies, cheeses, sausage casings and any foods which contain fats or oils. ",The molecular weight is 194.05.,Sodium tartrate has a topological polar surface area of 120.72.,,Sodium tartrate is approved.,Sodium tartrate is a solid.,True
21018,,The molecular weight is 320.48.,Camylofin has a topological polar surface area of 41.57.,The log p value of  is 4.72.,Camylofin is experimental.,,False
21019,,The molecular weight is 337.49.,Fenpiverinium has a topological polar surface area of 43.09.,The log p value of  is -0.03.,Fenpiverinium is experimental.,,False
21020,,The molecular weight is 298.45.,Emetonium iodide has a topological polar surface area of 9.23.,The log p value of  is 0.54.,Emetonium iodide is experimental.,,False
21021,,The molecular weight is 273.38.,Tilidine has a topological polar surface area of 29.54.,The log p value of  is 3.76.,Tilidine is experimental.,,False
21022,,The molecular weight is 354.47.,Pipenzolate has a topological polar surface area of 46.53.,The log p value of  is 0.69.,Pipenzolate is experimental.,,False
21023,,,,,Timepidium is experimental.,,False
21024,,,,,Deacetylbisacodyl is experimental.,,False
21025,,,,,Sodium ascorbate is approved and nutraceutical.,,False
21026,,,,,"Sodium phosphate, dibasic, unspecified form is approved and experimental.",,False
21027,,,,,Sodium cation is experimental.,,False
21028,,,,,Sulfate ion is experimental and investigational.,,False
21029,,,,,Plantago ovata seed is approved and experimental and investigational.,,False
21030,"Calcium polycarbophil is a stool stabilizer. Based on its chemical structure, it is a synthetic polymer of polyacrylic acid cross-linked with divinyl glycol presenting a calcium atom as a counter-ion. Polycarbophil is used to treat constipation. This drug may also be used to help relieve the symptoms of irritable bowel syndrome or diarrhea. Polycarbophil is used to treat constipation and to help maintain regular bowel movements. Relieves constipation or diarrhea associated with bowel disorders and acute nonspecific diarrhea. It is known as a bulk-forming laxative. It increases the bulk in the stool, an effect that helps to cause movement of the intestines. It also works by increasing the amount of water in the stool, making the stool softer and easier to pass.",,,,Calcium polycarbophil is approved.,,True
21031,Konjac mannan is under investigation in clinical trial NCT01709955 (The Effects of Glucomannan on Weight Loss).,,,,Konjac mannan is investigational.,,True
21032,"Carfentanil, C-11 is under investigation in clinical trial NCT01899170 (Towards Individualized Deep Brain Stimulation Treatment of Chronic Neuropathic Pain).",,,,"Carfentanil, C-11 is investigational.",,True
21033,"Benzhydrocodone is a benzylic prodrug of hydrocodone. It was developed in an effort to reduce parenteral bioavailability of the active metabolite as a deterrent to abuse. Benzhydrocodone is indicated for use in the short-term management of pain. It was first approved by the FDA in February 2018 in combination with under the trade name Apadaz, marketed by KVK Tech and developed by KemPharm. Benzyhydrocodone is indicated, in combination with , for the short-term management of acute pain requiring opioid therapy. Benzhydrocodone is rapidly metabolized to which acts on the central nervous system to produce analgesia. The action of hydrocodone in the brain can also produce euphoria, leading to addiction. Benzyhydrocodone is not reported to have pharmacological activity of its own and it not present in the plasma at detectable concentrations. Its active metabolite, is a mu-opioid receptor agonist.",,,,Benzhydrocodone is approved.,Benzhydrocodone is a solid.,True
21034,,,,,Alloin is approved and experimental.,,False
21035,,,,,Frangula purshiana bark is approved and experimental.,,False
21036,Resolvin E1 (RX 10001) is under investigation in clinical trial NCT00941018 (Single and Multiple Ascending Oral Dose Study of Resolvin E1 in Healthy Volunteers).,,,,Resolvin E1 is investigational.,,True
21037,"Tumor associated glycoprotein (TAG) 72 (B72.3) monoclonal antibody conjugated with Indium 111 for radioimaging colon tumors. Satumomab Pendetide (trade name: OncoScint®) is no longer commercially available. For diagnosis of extrahepatic malignant cancers Binds to the tumor associated glycoprotein 72 antigen, which is a cell surface protein generally over-expressed in colorectal cancers. The radioactive Indium 111, which is covalently attached to the antibody, allows radiodiagnostic detection of TAG-72 expressing cells and tumors. Satumomab Pendetide is a monoclonal antibody which is attached to the chelator pentetic acid (DTPA) linked to the tripeptide glycine (G) – L-tyrosine (Y) – L-lysine (K), which chelates Indium 111. Satumomab pendetide binds selectively to cell-surface TAG-72 expressed on colorectal tumors. ",,,,Indium In-111 satumomab pendetide is experimental and withdrawn.,Indium In-111 satumomab pendetide is a liquid.,True
21038,"Digoxin Immune Fab is a sheep antibody (26-10) FAB fragment from sheep immunized with the digoxin derivative Digoxindicarboxymethylamine. It is used as an antidote for overdose of digoxin. For treatment of digitoxin overdose or digitalis glycoside toxicity. DigiFab binds molecules of digoxin, making them unavailable for binding at their site of action on cells in the body. The Fab fragment-digoxin complex accumulates in the blood, from which it is excreted by the kidney. The net effect is to shift the equilibrium away from binding of digoxin to its receptors in the body, thereby reversing its effects. Binds excess digoxin or digitoxin molecules circulating in the blood.",,,,Digoxin Immune Fab (Ovine) is approved.,Digoxin Immune Fab (Ovine) is a liquid.,True
21039,,,,,Dexpropranolol is experimental.,Dexpropranolol is a solid.,False
21040,"Pexelizumab is a humanized monoclonal antibody used as an immunosuppressive drug. It is being investigated by Alexion Pharmaceuticals. For the treatment of inflammation during cardiac surgery. Myocardial injury and dysfunction in acute infarction and during cardiac surgery with cardiopulmonary bypass (CPB) are associated with an undesirable systemic inflammatory response, in which the complement cascade plays a major role. In animal models C5 inhibition has been found to significantly reduce myocardial infarct size and decrease cellular necrosis and apoptosis. Pexelizumab is a humanized, monoclonal, single-chain antibody fragment that inhibits C5, thereby blocking its cleavage into active forms.  Although inflammation is a normal response, continued exposure to foreign surfaces, toxic antigens, and tissue injury results in pathologic local and systemic inflammation (SIRS). This response involves multiple humoral and cellular components, including the coagulation (Factor XII, thrombin, Proteins C and S, platelets) and complement systems, cytokines (TNF-alpha, interleukins), leukocytes, monocytes, adhesion molecules (ICAM-1), and endothelial cells, among others. The complement system is a group of glycoproteins, which, when activated, results in the formation of C3-convertase, which converts C3 to C3a and C3b. C3a cleaves C5 to C5a and C5b. C5b, in conjunction with C6, C7, C8, and C9, forms the membrane attack or terminal complement complex (TCC) C5b-9. Both C5a and C5b-9 activate, promote, and amplify inflammatory components, and likely play central roles in the development of SIRS, tissue injury, reperfusion injury, and apoptosis. Pexelizumab, a recombinant humanized single chain monoclonal antibody to C5, blocks the conversion of C5 to C5a and C5b-9.",,,,Pexelizumab is investigational.,Pexelizumab is a liquid.,True
21041,"Bectumomab (marketed under the trade name LymphoScan®) is a mouse monoclonal antibody and which it's used to treat non-Hodgkin's lymphoma. It has a radioisotope, technetium (99m TC) which it's added. Investigated for use/treatment in lymphoma (non-hodgkin's). Using bectumomab, a mouse-derived monoclonal antibody labeled with technetium-99m (Tc-99m), a widely available, inexpensive radioisotope, medical professionals can determine through nuclear imaging the extent of CD22-expressing lymphomas.",,,,Bectumomab is investigational.,Bectumomab is a liquid.,True
21042,"Adecatumumab is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Investigated for use/treatment in breast cancer and prostate cancer. Adecatumumab (MT201) is a recombinant human monoclonal antibody of the IgG1 subclass with a binding specificity to epithelial cell adhesion molecule (EpCAM). EpCAM (CD326) is a cell surface protein that is frequently expressed at high level on most solid tumor types, including prostate, breast, colon, gastric, ovarian, pancreatic and lung cancer. Overexpression of EpCAM has been shown to promote the proliferation, migration and invasiveness of breast cancer cells. Moreover, expression of EpCAM is associated with decreased survival in a number of cancer indications, including breast, gall bladder, bile duct, ovarian and ampullary pancreatic cancer. EpCAM has recently been shown to be expressed on cancer stem cells from breast, prostate, colon and pancreatic cancer. Clinical studies have shown a favorable safety profile and that clinical activity depends on the EpCAM target expression.",,,,Adecatumumab is investigational.,Adecatumumab is a solid.,True
21043,"Bavituximab is a chimeric Anti-PS monoclonal antibody analog which is used to potentially treat cancers and viral infections. It binds to phosphatidylserine and other exposed host cell lipids when induced by cellular stress. Additional analogs in the class include 3G4, 2aG4, 9d2 and Hu3g4. Investigated for use/treatment in breast cancer, cancer/tumors (unspecified), HIV infection, hepatitis (viral, C), and solid tumors. Bavituximab Anti-Cancer is a monoclonal antibody that binds to a basic component of the cell structure called a phospholipid that is exposed only on the surface of tumor blood vessel cells or on cells infected with certain viruses. Bavituximab binding to the tumor blood vessel cells alerts the body’s immune system to attack the tumor and its blood supply. This has been shown to inhibit tumor growth and development. Because in healthy cells the phospholipids are concealed inside the cell, the bavituximab does not bind to them. This targets the bavituximab to the malignant cells and potentially minimizes unwanted side effects. ",,,,Bavituximab is investigational.,Bavituximab is a solid.,True
21044,Rozrolimupab is a recombinant polyclonal antibody consisting of 25 different anti-Rhesus D (RhD) antibodies to replace existing anti-RhD hyperimmune immunoglobulins for the treatment of Idiopathic Thrombocytopenic Purpura (ITP) and the prevention of Hemolytic Disease of Newborns (HDN). Investigated for use/treatment in thrombocytopenia.,,,,Rozrolimupab is investigational.,Rozrolimupab is a solid.,True
21045,"XTL001 is an investigational monoclonal antibody (MAb) product developed by XTL Biopharmaceuticals to evaluate the safety profile and antiviral activity of the compound in patients chronically infected with hepatitis B virus (HBV). Investigated for use/treatment in hepatitis (viral, B). XTL001 is a combination of two high-affinity, fully human monoclonal antibodies that bind to distinct sites on the surface antigen of HBV to neutralize the virus and limit viral escape. ",,,,XTL-001 is investigational.,XTL-001 is a solid.,True
21046,"RIGScan CR49, a 125I-labelled CR monoclonal antibody directed against the tumour-associated antigen TAG-72, is undergoing development with Neoprobe for the intraoperative detection of metastatic colorectal cancer. Investigated for use/treatment in colorectal cancer and solid tumors. RIGScan CR49 is used to locate cancerous tissue during surgery for patients with metastatic cancer of the colon or rectum (colorectal). In multicenter Phase II and pivotal Phase III clinical trials, RIGScan CR49 located tumor confirmed by pathology tests in 90 percent of evaluable patients who participated in the studies. The product found pathology-confirmed tumor that was missed by the surgeon and by preoperative diagnostic scans in one of five of the evaluable patients.",,,,NAV 1800 is investigational.,NAV 1800 is a solid.,True
21047,"Otelixizumab is a monoclonal antibody that binds to a receptor found on all T cells called CD3, which is involved in normal T cell signaling. Otelixizumab is believed to inhibit the function of autoreactive T cells, which are important in propagating autoimmune diseases, while inducing regulatory T cell pathways that promote immunological tolerance and inhibit autoreactive disease activity. Tolerx is developing otelixizumab to treat patients with type 1 diabetes, psoriasis and other autoimmune diseases such as rheumatoid arthritis. Investigated for use/treatment in diabetes mellitus type 1, pediatric indications, and psoriasis and psoriatic disorders. Otelixizumab is a monoclonal antibody that binds to a receptor found on all T cells called CD3, which is involved in normal T cell signaling. Tolerx is developing otelixizumab to treat patients with type 1 diabetes, psoriasis and other autoimmune diseases such as rheumatoid arthritis. Otelixizumab is a monoclonal antibody that binds to a receptor found on all T cells called CD3, which is involved in normal T cell signaling. Otelixizumab is believed to inhibit the function of autoreactive T cells, which are important in propagating autoimmune diseases, while inducing regulatory T cell pathways that promote immunological tolerance and inhibit autoreactive disease activity.",,,,Otelixizumab is investigational.,Otelixizumab is a solid.,True
21048,AMG 108 was investigated for use as an antirheumatic agent. Investigated for use/treatment in osteoarthritis and rheumatoid arthritis.,,,,AMG 108 is investigational.,AMG 108 is a solid.,True
21049,"Immunoglobulin G1, anti-(human CD30 (antigen)) (human monoclonal MDX-060 heavy chain), disulfide with human monoclonal MDX-060 light chain, dimer. Molecular weight is approximately 170,000 daltons. In phase I/II clinical trials for treatment of CD30+ lymphomas. Investigated for use/treatment in lymphoma (unspecified).",,,,Iratumumab is investigational.,Iratumumab is a solid.,True
21050,A humanized immunoglobulin G1k anti-interleukin-9 mAb. Investigated for use/treatment in asthma.,,,,Enokizumab is investigational.,Enokizumab is a solid.,True
21051,"Veltuzumab is a monoclonal antibody which, as of October 2009, is undergoing Phase I/II clinical trials for the treatment of non-Hodgkin's lymphoma. Investigated for use/treatment in lymphoma (non-hodgkin's).",,,,Veltuzumab is investigational.,Veltuzumab is a solid.,True
21052,"IPH-2101 (NN-1975), a fully human monoclonal antibody developed for patients with acute myeloid leukemia. Investigated for use/treatment in leukemia (myeloid) and multiple myeloma. The therapeutic principle of IPH 2101 (NN 1975) is based on the activation of Natural Killer (NK) cells by a monoclonal antibody which blocks the NK’s KIR inhibitory receptors, thereby potentiating NK cells anti-cancer action.",,,,IPH 2101 is investigational.,IPH 2101 is a solid.,True
21053,"Investigated for use/treatment in head and neck cancer, brain cancer, pediatric indications, pancreatic cancer, lung cancer, and colorectal cancer.",,,,Nimotuzumab is investigational.,Nimotuzumab is a solid.,True
21054,"BIIB015 is a humanized, IgG1 , DM4-Conjugated, anti-cripto, monoclonal antibody. It has been investigated for the treatment of subjects with relapsed or refractory solid tumours. Investigated for use/treatment in solid tumors.",,,,BIIB015 is investigational.,BIIB015 is a solid.,True
21055,"A humanized monoclonal antibody directed against sphingosine 1-phosphate (S1P) with potential antiangiogenic and antineoplastic activities. Upon administration, sonepcizumab binds S1P, which may result in the inhibition of tumor angiogenesis. S1P is the extracellular ligand for the G protein-coupled lysophospholipid receptor EDG-1 (endothelial differentiation gene-1). Investigated for use/treatment in solid tumors.",,,,Sonepcizumab is investigational.,Sonepcizumab is a solid.,True
21056,"Investigated for use/treatment in viral infection and pediatric indications. Motavizumab is a second generation, ultra-potent, affinity-matured, humanized mAb derived from palivizumab that reduces replication of Respiratory Syncytial Virus (RSV), a pathogen which causes lower respiratory tract disease. ",,,,Motavizumab is investigational.,Motavizumab is a solid.,True
21057,"Investigated for use/treatment in renal cell carcinoma, pancreatic cancer, melanoma, and lung cancer.",,,,Diethylnorspermine is investigational.,Diethylnorspermine is a solid.,True
21058,"Apolizumab is a humanized monoclonal antibody that is being studied as a treatment for hematologic cancers. Investigated for use/treatment in lymphoma (non-hodgkin's), leukemia (lymphoid), and solid tumors. Apolizumab is a humanized monoclonal antibody directed against 1D10, a polymorphic determinant on the HLA-DR beta chain that is expressed on normal and neoplastic B cells. Apolizumab induces complement-mediated cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and apoptosis of 1D10 antigen-positive B cells in vitro.",,,,Apolizumab is investigational.,Apolizumab is a solid.,True
21059,Investigated for use/treatment in glaucoma and cataracts.,,,,Lerdelimumab is investigational.,Lerdelimumab is a solid.,True
21060,Investigated for use/treatment in diabetes mellitus type 1.,,,,Teplizumab is investigational.,Teplizumab is a solid.,True
21061,"Investigated for use/treatment in solid tumors, renal cell carcinoma, melanoma, pancreatic cancer, lung cancer, and ovarian cancer.",,,,Volociximab is investigational.,Volociximab is a solid.,True
21062,"Tetanus Immune Globulin is manufactured from human plasma. It contains antibodies against tetanus toxoid and is primarily used as prophylaxis against tetanus in wounded patients. For use as prophylaxis against tetanus in patients who are injured and have incomplete of uncertain immunization statu. May also be used in the treatment of active tetanus. Human clostridium tetani toxoid immune globulin prevents tetanus toxoid from damaging tissue and producing the symptoms associated with tetanus. The immune globulin binds to tetanus toxiod, interfering with the normal interaction of the toxoid with human tissue. This prevents the toxoid from invading the nervous system and producing painful muscle spasms as well as autonomic dysfunction. The Clostridium tetani bacterium is killed either via antibiotic treatment of the host's immune system and immune globulin-bound toxoid is likely broken down by phagocytic immune cells.",,,,Tetanus Immune Globulin is approved.,Tetanus Immune Globulin is a solid.,True
21063,"Human Varicella-Zoster Immune Globulin is a solvent/detergent-treated sterile liquid preparation of purified human immune globulin G (IgG) containing antibodies to varicella zoster virus (anti-VZV). It is prepared from pools of healthy human donors' plasma via anion-exchange column chromatography and was approved in 2012 under the name VariZIG to reduce the disease severity in high-risk patients who lack evidence of immunity to varicella and for whom varicella vaccine is contraindicated. The therapeutic efficacy is proven if administered within 4 days of exposure to varicella zoster virus. Indicated for preventing and reducing the severity of chicken pox (varicella zoster virus) infections in high risk individuals within 4 days of exposure to varicella zoster virus. Varicella zoster immune globuline provides passive immunization for non-immune individuals exposed to VZV, reducing the severity of varicella infections.  Immunoglobulins are derived from human plasma and synthesized from plasma cells that recognize a broad spectrum of specific antigenic determinants.",,,,Human Varicella-Zoster Immune Globulin is approved.,Human Varicella-Zoster Immune Globulin is a liquid.,True
21064,"Conatumumab has been used in trials studying the treatment of Sarcoma, Lymphoma, Oncology, Colon Cancer, and Rectal Cancer, among others.",,,,Conatumumab is investigational.,,True
21065,"Tabalumab has been used in trials studying the treatment of Autoimmune Disease, Rheumatoid Arthritis, Kidney Failure, Chronic, Connective Tissue Disease, and Systemic Lupus Erythematosus, among others.",,,,Tabalumab is investigational.,,True
21066,"Ficlatuzumab has been used in trials studying the treatment of Acute Myeloid Leukemia, Non-small Cell Lung Cancer, Mullerian Mixed Tumor of Ovary, Relapsed Acute Myeloid Leukemia, and Refractory Acute Myeloid Leukemia, among others.",,,,Ficlatuzumab is investigational.,,True
21067,"Figitumumab has been used in trials studying the treatment of Sarcoma, Solid Tumor, Breast Cancer, Lung Neoplasms, and Advanced Cancer, among others.",,,,Figitumumab is investigational.,,True
21068,Bapineuzumab has been investigated for the treatment of Alzheimer's Disease.,,,,Bapineuzumab is investigational.,,True
21069,TXA127 has been investigated for the treatment of Miscellaneous Peripheral Blood Cell Abnormalities.,,,,Angiotensin 1-7 is investigational.,,True
21070,"Onartuzumab has been used in trials studying the treatment of Neoplasms, Lung Cancer, Glioblastoma, Gastric Cancer, and Colorectal Cancer, among others.",,,,Onartuzumab is investigational.,,True
21071,"Solanezumab is under investigation for the treatment of Dementia, Alzheimers Disease, and Alzheimers Disease, Familial.",,,,Solanezumab is investigational.,,True
21072,Lampalizumab has been used in trials studying the treatment of Geographic Atrophy.,,,,Lampalizumab is investigational.,,True
21073,"Dalotuzumab has been investigated for the treatment of Breast Cancer, Non Small Cell Lung Cancer, and Metastatic Colorectal Cancer.",,,,Dalotuzumab is investigational.,,True
21074,"Emibetuzumab has been used in trials studying the treatment of Advanced Cancer, Renal Cell Carcinoma, Hepatocellular Cancer, Gastric Adenocarcinoma, and Non-Small Cell Lung Cancer, among others.",,,,Emibetuzumab is investigational.,,True
21075,"Ublituximab has been used in trials studying the treatment of B-cell Lymphoma, Neuromyelitis Optica, Mantle Cell Lymphoma, Non-Hodgkins Lymphoma, and Marginal Zone Lymphoma, among others.",,,,Ublituximab is investigational.,,True
21076,"Ligelizumab has been used in trials studying the basic science and treatment of Asthma, Allergy, Peanut Allergy, Allergic Asthma, and Atopic Dermatitis, among others.",,,,Ligelizumab is investigational.,,True
21077,"Seribantumab has been used in trials studying the treatment of NSCLC, Heregulin, Adenocarcinoma, Colorectal Cancer, and Solid Tumor Cancers, among others.",,,,Seribantumab is investigational.,,True
21078,"Landogrozumab has been used in trials studying the treatment of Advanced Cancer, Muscular Atrophy, and Pancreatic Cancer.",,,,Landogrozumab is investigational.,,True
21079,"Vadastuximab Talirine has been used in trials studying the treatment of Acute myeloid leukemia, Myelodysplastic Syndrome, Acute Myelogenous Leukemia, and Acute Promyelocytic Leukemia.",,,,Vadastuximab Talirine is investigational.,,True
21080,"Varlilumab has been used in trials studying the treatment of MELANOMA, Skin Ulcer, Burkett's Lymphoma, Mantle cell lymphoma, and Any T-cell Malignancy, among others.",,,,Varlilumab is investigational.,,True
21081,Crenezumab has been used in trials studying the treatment of Alzheimer's Disease.,,,,Crenezumab is investigational.,,True
21082,"Rilotumumab has been investigated for the treatment of Cancer, Lung Cancer, Solid Tumors, Gastric Cancer, and Prostate Cancer, among others.",,,,Rilotumumab is investigational.,,True
21083,Anifrolumab has been investigated for the treatment of Scleroderma.,,,,Anifrolumab is investigational.,,True
21084,"Gantenerumab is under investigation for the treatment of Dementia, Alzheimers Disease, and Alzheimers Disease, Familial.",,,,Gantenerumab is investigational.,,True
21085,Visilizumab has been investigated for the treatment of Ulcerative Colitis.,,,,Visilizumab is investigational.,,True
21086,"BQ-123 has been investigated for the basic science and treatment of Coronary Artery Disease, Aorto-coronary Bypass Grafting, and ST-Elevation Myocardial Infarction.",,,,BQ-123 is investigational.,,True
21087,"Patritumab has been used in trials studying the treatment of LUNG CANCER, Solid Tumors, Neoplasms by Site, Head and Neck Neoplasms, and Non-small Cell Lung Cancer, among others.",,,,Patritumab is investigational.,,True
21088,"Fulranumab has been used in trials studying the treatment of Pain, Cystitis, Neuralgia, Joint Pain, and Arthralgia, among others.",,,,Fulranumab is investigational.,,True
21089,"Tarextumab has been used in trials studying the treatment of Solid Tumors, Stage IV Pancreatic Cancer, and Stage IV Small Cell Lung Cancer.",,,,Tarextumab is investigational.,,True
21090,"Duligotuzumab has been used in trials studying the treatment of Neoplasms, Colorectal Cancer, Head and Neck Cancer, and Epithelial Tumors, Malignant.",,,,Duligotuzumab is investigational.,,True
21091,"Simtuzumab has been used in trials studying the treatment and basic science of Myelofibrosis, Pancreatic Cancer, Colorectal Cancer, and Idiopathic Pulmonary Fibrosis.",,,,Simtuzumab is investigational.,,True
21092,"Fasinumab has been used in trials studying the basic science and treatment of Sciatica, Back Pain, Low Back Pain, Osteoarthritis, Hip, and Abdominal Pain Upper, among others.",,,,Fasinumab is investigational.,,True
21093,Tralokinumab is under investigation for the treatment of Alopecia Areata. Tralokinumab has been investigated for the treatment of Asthma.,,,,Tralokinumab is investigational.,,True
21094,Etrolizumab has been used in trials studying the treatment of Crohn Disease and Ulcerative Colitis.,,,,Etrolizumab is investigational.,,True
21095,"Ganitumab has been used in trials studying the treatment of Colon Cancer, Rectal Cancer, Breast Cancer, Breast Tumors, and Breast Neoplasms, among others.",,,,Ganitumab is investigational.,,True
21096,"Etaracizumab has been investigated for the treatment of Psoriasis, Renal Cell Carcinoma, Stage IV Renal Cell Cancer, Recurrent Renal Cell Cancer, and Stage III Renal Cell Cancer.",,,,Etaracizumab is investigational.,,True
21097,"Inclacumab has been used in trials studying the treatment and prevention of Myocardial Infarction, Peripheral Arterial Disease (PAD), and Coronary Heart Disease, Graft Occlusion, Vascular.",,,,Inclacumab is investigational.,,True
21098,"Ascrinvacumab has been used in trials studying the treatment and basic science of Neoplasms, Advanced Solid Tumors, Carcinoma, Hepatocellular, and Malignant Pleural Mesothelioma.",,,,Ascrinvacumab is investigational.,,True
21099,Aducanumab has been used in trials studying the treatment of Alzheimer's Disease.,,,,Aducanumab is investigational.,,True
21100,"GS-5745 has been used in trials studying the treatment of Tumors, Breast Cancer, Crohn's Disease, Colorectal Cancer, and Pancreatic Cancer, among others.",,,,GS-5745 is investigational.,,True
21101,Vanucizumab has been used in trials studying the treatment of ColoRectal Cancer and Advanced/Metastatic Solid Tumors.,,,,Vanucizumab is investigational.,,True
21102,"Labetuzumab govitecan has been used in trials studying the treatment of Colon Cancer, Rectal Cancer, and Metastatic Colorectal Cancer.",,,,Labetuzumab govitecan is investigational.,,True
21103,"Tanezumab has been investigated for the treatment of Osteoarthritis, Knee and Neuralgia, Postherpetic.",,,,Tanezumab is investigational.,,True
21104,"Ensituximab has been used in trials studying the treatment of Pancreatic Cancer, Adult, Metastatic Colorectal Cancer, and Metastatic Pancreatic Cancer.",,,,Ensituximab is investigational.,,True
21105,Fezakinumab has been used in trials studying the treatment of Atopic Dermatitis and Rheumatoid Arthritis.,,,,Fezakinumab is investigational.,,True
21106,"Dusigitumab has been used in trials studying the treatment of Cancer, Advanced Solid Malignancies, Unresectable or Metastatic Hepatocellular Carcinoma (HCC), and Hormone-sensitive, HER-2 Negative Metastatic Breast Cancer.",,,,Dusigitumab is investigational.,,True
21107,"Fresolimumab has been used in trials studying the treatment of Primary Brain Tumors, Metastatic Breast Cancer, Diffuse Systemic Sclerosis, Pleural Malignant Mesothelioma, and Primary Focal Segmental Glomerulosclerosis.",,,,Fresolimumab is investigational.,,True
21108,"Indusatumab vedotin has been used in trials studying the treatment of Pancreatic Adenocarcinoma, Adenocarcinoma of the Stomach, Recurrent Gastric Adenocarcinoma, Metastatic Gastric Adenocarcinoma, and Advanced Gastrointestinal Carcinoma, among others.",,,,Indusatumab vedotin is investigational.,,True
21109,"Bococizumab has been used in trials studying the treatment and prevention of Dyslipidemia, Hyperlipidemia, Hypercholesterolemia, Cardiovascular Disease, and Heterozygous Familial Hypercholesterolemia.",,,,Bococizumab is investigational.,,True
21110,Promestriene has been used in trials studying the prevention of Hypospadias.,The molecular weight is 328.5.,Promestriene has a topological polar surface area of 18.46.,The log p value of  is 6.14.,Promestriene is investigational.,,True
21111,Mavrilimumab has been investigated for the treatment of Rheumatoid Arthritis.,,,,Mavrilimumab is investigational.,,True
21112,"Blosozumab has been used in trials studying the basic science and treatment of Osteoporosis and Osteoporosis, Postmenopausal.",,,,Blosozumab is investigational.,,True
21113,"Bimagrumab has been used in trials studying the treatment and supportive care of Sarcopenia, Skeletal Muscle, Mechanical Ventilation, Sporadic Inclusion Body Myositis, and Sporadic Inclusion Body Myositis (sIBM), among others.",,,,Bimagrumab is investigational.,,True
21114,"Tovetumab has been used in trials studying the treatment of Cancer, Glioblastoma Multiforme, and Advanced Solid Malignancies.",,,,Tovetumab is investigational.,,True
21115,"Lumretuzumab has been used in trials studying the treatment of Neoplasms, Breast Cancer, Squamous Non-Small Cell Lung Cancer, and Non-Squamous Non-Small Cell Lung Cancer.",,,,Lumretuzumab is investigational.,,True
21116,Intetumumab has been used in trials studying the treatment of Melanoma.,,,,Intetumumab is investigational.,,True
21117,Carlumab has been used in trials studying the treatment of Cancer and Prostate Cancer.,,,,Carlumab is investigational.,,True
21118,Demcizumab is under investigation for the treatment of Nonsquamous Nonsmall Cell Neoplasm of Lung.,,,,Demcizumab is investigational.,,True
21119,Abituzumab has been used in trials studying the treatment of Prostate Cancer Metastatic.,,,,Abituzumab is investigational.,,True
21120,Ecromeximab has been used in trials studying the treatment of Cutaneous Melanoma and Metastatic Melanoma.,,,,Ecromeximab is investigational.,,True
21121,"Naptumomab Estafenatox has been used in trials studying the treatment of Pancreatic Cancer, Renal Cell Carcinoma, and Non-Small-Cell Lung Carcinoma.",,,,Naptumomab Estafenatox is investigational.,,True
21122,"Crotedumab has been used in trials studying the treatment of Diabetes Mellitus, Type 2.",,,,Crotedumab is investigational.,,True
21123,Concizumab has been used in trials studying the treatment of Haemophilia A and Congenital Bleeding Disorder.,,,,Concizumab is investigational.,,True
21124,Depatuxizumab has been used in trials studying the treatment and diagnostic of Adenocarcinoma and Advanced Solid Tumors.,,,,Depatuxizumab is investigational.,,True
21125,Rontalizumab has been used in trials studying the treatment of Systemic Lupus Erythematosus.,,,,Rontalizumab is investigational.,,True
21126,Clazakizumab has been used in trials studying the treatment of Rheumatoid Arthritis.,,,,Clazakizumab is investigational.,,True
21127,"Ozanezumab has been used in trials studying the treatment of Multiple Sclerosis, Amyotrophic Lateral Sclerosis, and Multiple Sclerosis, Relapsing-Remitting.",,,,Ozanezumab is investigational.,,True
21128,"Bimekizumab has been used in trials studying the treatment of Psoriatic arthritis, Ankylosing Spondylitis, Chronic Plaque Psoriasis, and Mild to Moderate Psoriasis.",,,,Bimekizumab is investigational.,,True
21129,"Milatuzumab has been used in trials studying the treatment of Lupus Nephritis, Multiple Myeloma (MM), GVHD (Acute or Chronic), Myelodysplastic Syndrome, and Chronic Lymphocytic Leukemia, among others.",,,,Milatuzumab is investigational.,,True
21130,"Robatumumab has been used in trials studying the treatment of Osteosarcoma, Sarcoma, Ewing's, and Peripheral Neuroectodermal Tumor.",,,,Robatumumab is investigational.,,True
21131,"Rovalpituzumab Tesirine has been used in trials studying the treatment of GLIOBLASTOMA, Malignant Melanoma, Other Solid Tumors, Small Cell Lung Cancer, and Medullary Thyroid Cancer, among others.",,,,Rovalpituzumab Tesirine is investigational.,,True
21132,"Namilumab has been used in trials studying the treatment of Plaque Psoriasis and Rheumatoid Arthritis. Namilumab is a human antibody which neutralizes the activity of granulocyte/macrophage colony stimulating factor (GM-CSF), which has potential applications in the treatment of various inflammatory and autoimmune diseases, such as rheumatoid arthritis, psoriasis, or multiple sclerosis.",,,,Namilumab is investigational.,,True
21133,"Racotumomab has been used in trials studying the treatment of Glioma, Wilm's Tumor, Neuroblastoma, Retinoblastoma, and Ewing's Sarcoma.",,,,Racotumomab is investigational.,,True
21134,Tregalizumab has been used in trials studying the treatment of Rheumatoid Arthritis.,,,,Tregalizumab is investigational.,,True
21135,Olokizumab has been used in trials studying the treatment of Crohn's Disease.,,,,Olokizumab is investigational.,,True
21136,Guanoxan is an antihypertensive agent similar in its mechanism of action to guanethidine; may cause liver damage.,The molecular weight is 207.23.,Guanoxan has a topological polar surface area of 80.36.,The log p value of  is 0.55.,Guanoxan is approved.,,True
21137,,,,,Edrecolomab is experimental and investigational.,,False
21138,,The molecular weight is 247.08.,Guanoxabenz has a topological polar surface area of 80.5.,The log p value of  is 1.53.,Guanoxabenz is experimental.,,False
21139,,The molecular weight is 209.68.,Tolonidine has a topological polar surface area of 36.42.,The log p value of  is 1.97.,Tolonidine is experimental.,,False
21140,,The molecular weight is 283.33.,Cadralazine has a topological polar surface area of 99.61.,The log p value of  is 0.93.,Cadralazine is experimental.,,False
21141,,,,,Nebacumab is experimental.,,False
21142,,The molecular weight is 707.86.,Bietaserpine has a topological polar surface area of 110.16.,The log p value of  is 5.54.,Bietaserpine is experimental.,,False
21143,,The molecular weight is 184.29.,Guanazodine has a topological polar surface area of 73.93.,The log p value of  is 0.8.,Guanazodine is experimental.,,False
21144,,The molecular weight is 608.69.,Methoserpidine has a topological polar surface area of 117.78.,The log p value of  is 3.86.,Methoserpidine is experimental.,,False
21145,,The molecular weight is 263.12.,Guanoclor has a topological polar surface area of 83.16.,The log p value of  is 1.52.,Guanoclor is experimental.,,False
21146,"Cytomegalovirus immunoglobulin is obtained from pooled adult human plasma selected for high titers of antibody for cytomegalovirus (CMV). It contains purified immunoglobulin G (IgG) antibodies targeting cytomegalovirus (CMV). It is used to prevent cytomegalovirus (CMV) disease after organ transplant. CytoGam (cytomegalovirus immune globulin) contains IgG antibodies representing those of the large number of normal individuals who have contributed to the plasma pools from which the product was derived. The globulin contains a relatively high concentration of antibodies which are directed against cytomegalovirus (CMV). In the case of persons who may possibly be exposed to CMV, CytoGam can increase the relevant antibodies to levels sufficient to prevent or reduce the incidence of serious CMV disease.  CMV—IGIV mainly consists of immunoglobulin G (IgG), specifically subclasses _IgG1_ and _IgG3_. IgG1 and IgG3 play important roles in viral neutralization in addition to tissue protection and complement activation. ",,,,Human cytomegalovirus immune globulin is approved.,Human cytomegalovirus immune globulin is a liquid.,True
21147,Market product is Tc99m-labeled murine antibody fragment for nuclear imaging of activated granulocytes.,,,,Sulesomab is approved.,Sulesomab is a solid.,True
21148,"Besilesomab is a mouse monoclonal antibody labelled with the radioactive isotope technetium-99m for determining the location of inflammation/infection in peripheral bone in adults with suspected osteomyelitis. Utilised only as a diagnostic agent, besilesomab is currently approved by the EMEA for marketing and use in various European countries like Italy, France, Germany, Spain, Portugal, Norway, Sweden, the Netherlands, and the United Kingdom. Besilesomab is radiolabelled with sodium pertechnetate (Tc99m) solution to develop technetium (Tc99m) besilesomab solution. This solution is indicated in adults for scintigraphic imaging - in conjunction with other appropriate imaging modalities, when possible - in determining the location of inflammation/infection in peripheral bone in adults with suspected osteomyelitis. When utilized as such, this medicinal product is for diagnostic use only. In a study employing cryo-preserved human tissues using an indirect alkaline phosphatase anti-alkaline phosphatase technique, besilesomab antibody from hybridoma supernatants demonstrated staining to cytoplasmic, membranous, and interstitial areas of primary colon carcinoma tissue, to single granulocytic cells in normal human liver and lung and to a large proportion of granulocytic cells in normal human bone marrow but not to blood vessels or connective tissue. Additionally, the antibody also shows binding to the granulocytic cells of breast, kidney, parotid gland, pituitary, lymph nodes, and spleen tissues, as well as colonic, pancreatic, and some lung and breast carcinomas. Nonspecific cross-reacting antigens (NCA) is the name of a collection of highly glycosylated bacterial binding receptors expressed on human granulocytes and other tissues. In particular, these glycoprotein receptors are members of the immunoglobulin supergene family and are related structurally to carcinoembryonic antigen (CEA). CEA is found naturally in the human body and its expression may be increased in both cancer and non-cancerous (benign) circumstances.",,,,Besilesomab is approved.,Besilesomab is a solid.,True
21149,,,,,Benazeprilat is experimental.,,False
21150,"Fosinoprilat is the active phosphinic acid metabolite of prodrug , which is activated by esterases in vivo. It binds zinc with phosphinic acid group.",,,,Fosinoprilat is experimental.,,True
21151,The active metabolite of the prodrug.,,,,Ramiprilat is experimental.,,True
21152,,,,,Fanolesomab is approved and experimental.,,False
21153,The active metabolite of the prodrug.,,,,Perindoprilat is experimental.,,True
21154,The active metabolite of the prodrug.,,,,Quinaprilat is experimental.,,True
21155,Lecanemab is an experimental drug that is currently in clinical trials for the treament of Alzheimer's disease.,,,,Lecanemab is investigational.,,True
21156,Setrusumab is under investigation in clinical trial NCT01406548 (Safety and Efficacy of Multiple Dosing Regimens of BPS804 in Post Menopausal Women With Low Bone Mineral Density).,,,,Setrusumab is investigational.,,True
21157,Gancotamab is under investigation in clinical trial NCT02213744 (MM-302 Plus Trastuzumab vs. Chemotherapy of Physician's Choice Plus Trastuzumab in HER2-Positive Locally Advanced/Metastatic Breast Cancer Patients).,,,,Gancotamab is investigational.,,True
21158,Anetumab ravtansine is under investigation in clinical trial NCT03455556 (Anetumab Ravtansine and Atezolizumab in Treating Participants With Advanced Non-small Cell Lung Cancer).,,,,Anetumab ravtansine is investigational.,,True
21159,Icrucumab is under investigation in clinical trial NCT01111604 (A Study of IMC-1121B or IMC-18F1 in Colorectal Cancer).,,,,Icrucumab is investigational.,,True
21160,Codrituzumab is under investigation in clinical trial NCT01507168 (A Study of RO5137382 (GC33) in Patients With Advanced or Metastatic Hepatocellular Carcinoma).,,,,Codrituzumab is investigational.,,True
21161,Xentuzumab is under investigation in clinical trial NCT02191891 (Xentuzumab (BI 836845) Plus Afatinib in Patients With Epidermal Growth Factor Receptor (EGFR) Mutant Non-small Cell Lung Cancer (NSCLC)).,,,,Xentuzumab is investigational.,,True
21162,Lintuzumab is under investigation in clinical trial NCT00016159 (Chemotherapy Plus Monoclonal Antibody in Treating Patients With Acute Promyelocytic Leukemia).,,,,Lintuzumab is investigational.,,True
21163,Vobarilizumab is under investigation in clinical trial NCT02101073 (ALX-0061 Phase I Bioavailability Study in Healthy Volunteers).,,,,Vobarilizumab is investigational.,,True
21164,"Parsatuzumab is under investigation in clinical trial NCT01366131 (Study Evaluating the Safety and Efficacy of MEGF0444A in Combination With Carboplatin, Paclitaxel and Bevacizumab in Patients With Advanced or Recurrent Non-Squamous Non-Small Cell Lung Cancer Who Have Not Received Prior Chemotherapy for Advanced Disease (NILE)).",,,,Parsatuzumab is investigational.,,True
21165,Emactuzumab is under investigation in clinical trial NCT01494688 (A Study of RO5509554 as Monotherapy and in Combination With Paclitaxel in Participants With Advanced Solid Tumors).,,,,Emactuzumab is investigational.,,True
21166,Bevacizumab zirconium Zr-89 is under investigation in clinical trial NCT01338090 (89Zr-bevacizumab PET Imaging in Patients With Neuroendocrine Tumors).,,,,Bevacizumab zirconium Zr-89 is investigational.,,True
21167,"Refanezumab is under investigation in clinical trial NCT00833989 (Safety Escalating Repeat IV, in Stroke Patients).",,,,Refanezumab is investigational.,,True
21168,"Bermekimab is under investigation in clinical trial NCT01384630 (Safety, Pharmacokinetics, and Efficacy of RA-18C3 in Subjects With Moderate to Severe Psoriasis).",,,,Bermekimab is investigational.,,True
21169,Pamrevlumab is under investigation in clinical trial NCT00913393 (Study of FibroGen (FG)-3019 in Subjects With Type 2 Diabetes Mellitus and Kidney Disease on ACEi and/or ARB Therapy).,,,,Pamrevlumab is investigational.,,True
21170,"Opicinumab is under investigation in clinical trial NCT02641041 (Safety, Tolerability, and Pharmacokinetics of Single and Multiple Doses of BIIB033 in Healthy Japanese Participants).",,,,Opicinumab is investigational.,,True
21171,Dalantercept is under investigation in clinical trial NCT00996957 (Study of ACE-041 in Patients With Advanced Solid Tumors or Relapsed/Refractory Multiple Myeloma).,,,,Dalantercept is investigational.,,True
21172,Pateclizumab is under investigation in clinical trial NCT01225393 (A Study to Evaluate the Efficacy and Safety of MLTA3698A in Combination With a Disease-Modifying Anti-Rheumatic Drug (DMARD) Compared With Adalimumab in Combination With a DMARD in Patients With Active Rheumatoid Arthritis).,,,,Pateclizumab is investigational.,,True
21173,Gremubamab is under investigation in clinical trial NCT02255760 (Phase 1 Randomized Double-blind Placebo Controlled Study to Evaluate Safety and PK of MEDI3902 in Healthy Adults).,,,,Gremubamab is investigational.,,True
21174,"Apomab is under investigation in clinical trial NCT00851136 (A Study of PRO95780 Administered in Combination With the FOLFOX Regimen and Bevacizumab in Patients With Previously Untreated, Locally Advanced, Recurrent, and Metastatic Colorectal Cancer (APM4566g)).",,,,Apomab is investigational.,,True
21175,Ipafricept is under investigation in clinical trial NCT01608867 (A Dose Escalation Study of OMP-54F28 in Subjects With Solid Tumors).,,,,Ipafricept is investigational.,,True
21176,"Abrilumab is under investigation in clinical trial NCT01290042 (Study to Evaluate Safety, Tolerability, Pharmacokinetics and Pharmacodynamics of AMG 181.).",,,,Abrilumab is investigational.,,True
21177,Frovocimab is under investigation in clinical trial NCT01671085 (A Study of LY3015014 in Healthy Participants With High Cholesterol).,,,,Frovocimab is investigational.,,True
21178,Tezepelumab is under investigation in clinical trial NCT03406078 (Study to Evaluate the Efficacy and Safety of Tezepelumab in Reducing Oral Corticosteroid Use in Adults With Oral Corticosteroid Dependent Asthma).,,,,Tezepelumab is investigational.,,True
21179,Tigatuzumab is under investigation in clinical trial NCT00991796 (CS-1008 With Carboplatin/Paclitaxel in Chemotherapy naïve Subjects With Metastatic or Unresectable Non-small Cell Lung Cancer (NSCLC)).,,,,Tigatuzumab is investigational.,,True
21180,"Telisotuzumab vedotin is under investigation in clinical trial NCT02099058 (A Study Evaluating the Safety, Pharmacokinetics (PK), and Preliminary Efficacy of ABBV-399 in Subjects With Advanced Solid Tumors.).",,,,Telisotuzumab vedotin is investigational.,,True
21181,Utomilumab is under investigation in clinical trial NCT03318900 (T Cell Immunotherapy for Advanced Ovarian Cancer).,,,,Utomilumab is investigational.,,True
21182,Zolbetuximab is under investigation in clinical trial NCT01630083 (Efficacy and Safety of IMAB362 in Combination With the EOX Regimen for CLDN18.2-positive Gastric Cancer).,,,,Zolbetuximab is investigational.,,True
21183,"Ponezumab is under investigation in clinical trial NCT00607308 (A Phase I, Single Dose Study Of PF-04360365 In Japanese Patients With Mild To Moderate Alzheimer's Disease).",,,,Ponezumab is investigational.,,True
21184,Asunercept is under investigation in clinical trial NCT02853565 (A Study of CAN008 for Newly Diagnosed Glioblastoma Multiforme).,,,,Asunercept is investigational.,,True
21185,Suvratoxumab is under investigation in clinical trial NCT02296320 (Study of the Efficacy and Safety of MEDI4893).,,,,Suvratoxumab is investigational.,,True
21186,Mitazalimab is under investigation in clinical trial NCT02379741 (ADC-1013 First-in-Human Study).,,,,Mitazalimab is investigational.,,True
21187,Nemolizumab is under investigation in clinical trial NCT03921411 (A Pharmacokinetics and Safety Study of Nemolizumab in Adolescent Subjects With Atopic Dermatitis (AD)).,,,,Nemolizumab is investigational.,,True
21188,"Chronic kidney disease (CKD) is a progressive and irreversible disease that represents a significant burden for both the individual and healthcare system at large. Currently available treatments for end-stage renal disease are limited to dialysis and renal transplantation, with the former associated with significant costs and lower quality of life.  Imlifidase is indicated for desensitization of highly sensitized adult kidney transplant patients with a positive crossmatch against an available deceased donor. The treatment is reserved for patients unlikely to receive a transplant under the available kidney allocation system including prioritization programs for highly sensitized patients. Imlifidase is highly specific to all four human IgG subclasses and does not cleave any other immunoglobulins (IgM, IgA, IgE, IgD). The inactivation of human IgG antibodies occurs rapidly and efficiently after administration of imlifidase, with the effect lasting for several weeks. Imlifidase is a cysteine protease derived from _Streptococcus pyogenes_ which degrades immunoglobulin G (IgG) in a multistep process. In the first step, imlifidase cleaves one of the two IgG heavy chains at the lower hinge leaving the other intact, resulting in a single cleaved IgG molecule. In the second step, the second heavy chain is cleaved yielding one homodimeric Fc fragment and one F(ab’)<sub>2</sub> fragment. ",,,,Imlifidase is approved and investigational.,Imlifidase is a liquid.,True
21189,Gedivumab is under investigation in clinical trial NCT01877785 (A Study of MHAA4549A to Assess Safety And Pharmacokinetics in Healthy Volunteers).,,,,Gedivumab is investigational.,,True
21190,Valanafusp alfa is under investigation in clinical trial NCT03071341 (Extension Study Evaluating Long Term Safety and Activity of AGT-181 in Children With MPS I).,,,,Valanafusp alfa is investigational.,,True
21191,Sofituzumab vedotin is under investigation in clinical trial NCT01335958 (Safety and Pharmacokinetics of DMUC5754A Administered Intravenously to Patients With Platinum-Resistant Ovarian Cancer or Unresectable Pancreatic Cancer).,,,,Sofituzumab vedotin is investigational.,,True
21192,Evinacumab is under investigation in clinical trial NCT03146416 (Study of Evinacumab (REGN1500) in Caucasian and in Japanese Healthy Volunteers).,,,,Evinacumab is investigational.,,True
21193,Istiratumab is under investigation in clinical trial NCT02399137 (A Phase 2 Study of MM-141 Plus Nab-paclitaxel and Gemcitabine in Front-line Metastatic Pancreatic Cancer).,,,,Istiratumab is investigational.,,True
21194,Pidilizumab is under investigation in clinical trial NCT01952769 (Anti PD1 Antibody in Diffuse Intrinsic Pontine Glioma).,,,,Pidilizumab is investigational.,,True
21195,GMA-161 is under investigation in clinical trial NCT00244257 (Safety Study of GMA161 in Patients With Idiopathic Thrombocytopenic Purpura (ITP)).,,,,GMA-161 is investigational.,,True
21196,Ladiratuzumab vedotin is under investigation in clinical trial NCT01969643 (A Safety Study of SGN-LIV1A in Breast Cancer Patients).,,,,Ladiratuzumab vedotin is investigational.,,True
21197,Tomaralimab is under investigation in clinical trial NCT01794663 (Placebo-Controlled Study to Evaluate the Safety and Efficacy of OPN-305 in Preventing Delayed Renal Graft Function).,,,,Tomaralimab is investigational.,,True
21198,Vesencumab is under investigation in clinical trial NCT00747734 (A Study of MNRP1685A in Patients With Locally Advanced or Metastatic Solid Tumors).,,,,Vesencumab is investigational.,,True
21199,Pinatuzumab vedotin is under investigation in clinical trial NCT01691898 (A Study of Pinatuzumab Vedotin (DCDT2980S) Combined With Rituximab or Polatuzumab Vedotin (DCDS4501A) Combined With Rituximab or Obinutuzumab in Participants With Relapsed or Refractory B-Cell Non-Hodgkin's Lymphoma (NHL)).,,,,Pinatuzumab vedotin is investigational.,,True
21200,Lulizumab pegol is under investigation in clinical trial NCT02843659 (Proof of Concept Study to Evaluate the Efficacy and Safety of BMS-931699 (Lulizumab) or BMS-986142 in Primary Sjögren's Syndrome).,,,,Lulizumab pegol is investigational.,,True
21201,"Lorukafusp alfa is under investigation in clinical trial NCT01334515 (Biological Therapy, Sargramostim, and Isotretinoin in Treating Patients With Relapsed or Refractory Neuroblastoma).",,,,Lorukafusp alfa is investigational.,,True
21202,Naratuximab emtansine is under investigation in clinical trial NCT01534715 (IMGN529 in Treating Patients With Relapsed or Refractory Non-Hodgkin's Lymphoma and Chronic Lymphocytic Leukemia).,,,,Naratuximab emtansine is investigational.,,True
21203,Zenocutuzumab is under investigation in clinical trial NCT03321981 (MCLA-128 With Trastuzumab/chemotherapy in HER2+ and With Endocrine Therapy in ER+ and Low HER2 Breast Cancer).,,,,Zenocutuzumab is investigational.,,True
21204,"Oxaprotiline is a norepinephrine reuptake inhibitor of the tetracyclic antidepressant family that is related to maprotiline. This drug was never marketed. Oxaprotiline is a racemic mixture of the isomers levoprotiline and dextroprotiline. Levoprotiline is the R or levo isomer of oxaprotiline (CGP-12,103-A). Dextroprotiline is the S or dextro isomer of oxaprotiline (CGP-12,104-A). Both enantiomers have antidepressant effects but levoprotiline also is an antihistamine and dextroprotiline has many other pharmacological actions. Investigated for the treatment of depression.",,,,Oxaprotiline is experimental.,Oxaprotiline is a solid.,True
21205,Amitriptylinoxide has been used in trials studying Major Depression.,The molecular weight is 293.41.,Amitriptylinoxide has a topological polar surface area of 23.06.,The log p value of  is 4.32.,Amitriptylinoxide is approved and investigational.,,True
21206,Dibenzepin is approved for use in Europe.,The molecular weight is 295.39.,Dibenzepin has a topological polar surface area of 26.79.,The log p value of  is 3.31.,Dibenzepin is approved.,,True
21207,"Quinupramine has been approved in France under the brand name Kinupril, as an antidepressant.",The molecular weight is 304.44.,Quinupramine has a topological polar surface area of 6.48.,The log p value of  is 4.78.,Quinupramine is approved.,,True
21208,,The molecular weight is 291.44.,Melitracen has a topological polar surface area of 3.24.,The log p value of  is 5.48.,Melitracen is experimental and investigational.,,False
21209,,The molecular weight is 284.45.,Iprindole has a topological polar surface area of 8.17.,The log p value of  is 5.66.,Iprindole is experimental.,,False
21210,,The molecular weight is 296.41.,Imipramine oxide has a topological polar surface area of 30.12.,The log p value of  is 4.58.,Imipramine oxide is experimental.,,False
21211,,,,,Calcium ascorbate is approved and nutraceutical.,,False
21212,,,,,Niacinamide ascorbate is approved and nutraceutical.,,False
21213,"NBI-6024 is an altered peptide ligand that is designed to cause an immune response which result in preservation of beta-cell function and endogenous insulin production.  Investigated for use/treatment in diabetes mellitus type 1 and pediatric indications. NBI-6024 is designed specifically to generate an immune response that could result in preservation of beta-islet cell function in patients with Type I diabetes or juvenile-onset diabetes. Because there is progressive beta-islet destruction in Type I diabetes, an early intervention strategy with a product like NBI-6024 could delay or prevent insulin dependence.",,,,NBI-6024 is investigational.,NBI-6024 is a solid.,True
21214,Benfluorex is an anorectic and hypolipidemic agent that is structurally related to fenfluramine. It was patented and manufactured by a French pharmaceutical company Servier. The European Medicines Agency (EMA) recommended withdrawing all benfluorex containing medicines on 18 December 2009. This recommendation was based on the risks (especially fenfluramine-like cardiovascular side-effects) outweighing the benefits.,The molecular weight is 351.37.,Benfluorex has a topological polar surface area of 38.33.,The log p value of  is 4.89.,Benfluorex is investigational and withdrawn.,Benfluorex is a solid.,True
21215,Garlic allergenic extract is used in allergenic testing.,,,,Garlic is approved and nutraceutical.,,True
21216,Allicin has been used in trials studying the treatment of Follicular Lymphoma.,,,,Allicin is investigational.,,True
21217,"Thiazolidinedione has been investigated for the treatment of Type 2 Diabetes, Diabetes Mellitus, and DIABETES MELLITUS, TYPE 2.",,,,"2,4-thiazolidinedione is investigational.",,True
21218,Carmegliptin has been used in trials studying the treatment of Diabetes Mellitus Type 2.,,,,Carmegliptin is investigational.,,True
21219,"Remogliflozin etabonate has been used in trials studying the treatment and basic science of Type 2 Diabetes Mellitus and Diabetes Mellitus, Type 2.",,,,Remogliflozin etabonate is investigational.,,True
21220,,The molecular weight is 794.98.,Metildigoxin has a topological polar surface area of 192.06.,The log p value of  is 1.73.,Metildigoxin is experimental.,,False
21221,,,,,Guar gum is experimental.,,False
21222,"Taspoglutide is a pharmaceutical drug, a glucagon-like peptide-1 agonist (GLP-1 agonist), under investigation for treatment of type 2 diabetes being codeveloped by Ipsen and Roche. In September 2010 Roche halted Phase III clinical trials due to incidences of serious hypersensitivity reactions and gastrointestinal side effects. As of May 2013 no new trials had been registered.",,,,Taspoglutide is investigational.,Taspoglutide is a solid.,True
21223,Englitazone is a hypoglycemic agent.,,,,Englitazone is experimental.,Englitazone is a solid.,True
21224,Tirzepatide is under investigation in clinical trial NCT03311724 (A Study of Tirzepatide (LY3298176) in Participants With Type 2 Diabetes).,,,,Tirzepatide is investigational.,,True
21225,Gastric inhibitory polypeptide is under investigation in clinical trial NCT03081676 (The Effect of GIP and GLP-1 on Insulin and Glucagon Secretion in Patients With HNF1A-diabetes Treated With or Without Sulphonylurea).,,,,Gastric inhibitory polypeptide is investigational.,,True
21226,The active metabolite of the prodrug.,,,,Trandolaprilat is experimental.,,True
21227,The active metabolite of the prodrug.,,,,Moexiprilat is experimental.,,True
21228,,,,,Quinoline Yellow WS is experimental.,,False
21229,Xanomeline is under investigation in clinical trial NCT02831231 (Pilot Study Comparing Effects of Xanomeline Alone to Xanomeline Plus Trospium).,The molecular weight is 281.42.,Xanomeline has a topological polar surface area of 38.25.,The log p value of  is 4.42.,Xanomeline is investigational.,,True
21230,"Three paclitaxel molecules linked by a cleavable succinyl ester linkage to a brain peptide vector, Angiopep-2, conjugate named ANG1005. Investigated for use/treatment in brain cancer.",,,,Paclitaxel trevatide is investigational.,Paclitaxel trevatide is a solid.,True
21231,"Nitrous oxide, commonly known as \laughing gas\"", is a chemical compound with the chemical formula N2O. At room temperature, it is a colorless non-flammable gas, with a pleasant, slightly sweet odor and taste. It is used in surgery and dentistry for its anesthetic and analgesic effects. It is known as \""laughing gas\"" due to the euphoric effects of inhaling it, a property that has led to its recreational use as an inhalant drug."" Findings to date indicate that nitrous oxide induces opioid peptide release in the brain stem leading to the activation of descending noradrenergic neurones, which results in modulation of the nociceptive process in the spinal cord. Several receptor–effector mechanisms including dopamine receptors, α2 adrenoceptors, benzodiazepine receptors and -methyl- -aspartate (NMDA) receptors have been implicated although the relationship of one with the other is not known.",The molecular weight is 44.01.,Nitrous oxide has a topological polar surface area of 54.46.,,Nitrous oxide is approved and vet_approved.,Nitrous oxide is a solid.,True
21232,Oleandrin has been used in trials studying the treatment of Lung Cancer and Chemotherapeutic Agent Toxicity.,The molecular weight is 576.73.,Oleandrin has a topological polar surface area of 120.75.,The log p value of  is 2.85.,Oleandrin is experimental and investigational.,,True
21233,,The molecular weight is 548.67.,Cymarin has a topological polar surface area of 131.75.,The log p value of  is 0.22.,Cymarin is experimental.,,False
21234,"Proscillaridin is a cardiac glycoside that is derived from plants of the genus Scilla and in Drimia maritima (Scilla maritima). Studies suggest the potential cytotoxic and anticancer property of proscillaridin, based on evidence of the drug potently disrupting topoisomerase I and II activity at nanomolar drug concentrations and triggering cell death and blocking cell proliferation of glioblastoma cell lines.",The molecular weight is 530.66.,Proscillaridin has a topological polar surface area of 125.68.,The log p value of  is 2.55.,Proscillaridin is experimental.,,True
21235,,The molecular weight is 985.13.,Lanatoside C has a topological polar surface area of 288.28.,The log p value of  is 0.93.,Lanatoside C is experimental.,,False
21236,,The molecular weight is 921.0.,Gitoformate has a topological polar surface area of 233.41.,The log p value of  is 3.19.,Gitoformate is experimental.,,False
21237,,The molecular weight is 548.67.,Peruvoside has a topological polar surface area of 131.75.,The log p value of  is 0.32.,Peruvoside is experimental.,,False
21238,,,,,Paclitaxel poliglumex is experimental and investigational.,,False
21239,"Lymecycline is a broad-spectrum second-generation tetracycline antibiotic used for the treatment of acne and other susceptible bacterial infections. It has been proven a cost-effective alternative to treatment with with comparable safety and efficacy. Lymecycline was initially discovered in 1961. It is marketed by Galderma and used in the UK as well as New Zealand in addition to other countries. Lymecycline is not marketed in the USA, however, equivalent drugs are available, such as minocycline and. Lymecycline is used for the treatment of acne in addition to other susceptible infections; propionibacterium is often the cause of acne. Some of the infections that can be treated with lymecycline include upper respiratory tract infections, urinary tract infections, bronchitis, chlamydial infections, and rickettsial infections. Lymecycline, like other tetracyclines, exerts bacteriostatic actions on intracellular and extracellular bacteria, treating susceptible bacterial infections. It has been shown to be safe and effective in the treatment of moderate to severe acne. Normally, the ribosome synthesizes proteins through the binding of aminoacyl-tRNA to the mRNA-ribosome complex. Lymecycline binds to the 30S ribosomal subunit, preventing amino-acyl tRNA from binding to the A site of the ribosome, which prevents the elongation of polypeptide chains. This results in bacteriostatic actions, treating various infections.",The molecular weight is 602.64.,Lymecycline has a topological polar surface area of 242.98.,The log p value of  is -3.63.,Lymecycline is approved and investigational.,Lymecycline is a solid.,True
21240,"Clomocycline is a tetracycline used to treat bacterial infections. For the treatment and management of Brucellosis, mycoplasma infection, acne vulgaris, chlamydial infection;Chronic bronchitis Clomocycline is a tetracycline antibiotic that is commonly prescribed by medical doctors for infections and to treat acne. It may also be used to treat urinary tract infections, gum disease, and other bacterial infections such as gonorrhea and chlamydia. Clomocycline is also used commonly as a prophylactic treatment for infection by Bacillus anthracis (anthrax). It is also effective against Yersinia pestis and malaria and is also prescribed for the treatment of Lyme disease. Clomocycline inhibits cell growth by inhibiting translation. It binds to the 30S ribosomal subunit and prevents the amino-acyl tRNA from binding to the A site of the ribosome. The binding is reversible in nature. Cells become resistant to Clomocycline by at least two mechanisms: efflux and ribosomal protection. In efflux, a resistance gene encodes a membrane protein that actively pumps Clomocycline out of the cell. This is the mechanism of action of the tetracycline resistance gene on the artificial plasmid pBR322. In ribosomal protection, a resistance gene encodes a protein which binds to the ribosome and prevents Clomocycline from acting on the ribosome. Clomocycline inhibits cell growth by inhibiting translation. It binds to the 30S ribosomal subunit and prevents the amino-acyl tRNA from binding to the A site of the ribosome. The binding is reversible in nature. Clomocycline is lipophilic and can easily pass through the cell membrane or passively diffuses through porin channels in the bacterial membrane.",The molecular weight is 508.91.,Clomocycline has a topological polar surface area of 187.86.,The log p value of  is -0.05.,Clomocycline is experimental.,Clomocycline is a solid.,True
21241,"Long-acting plasma-bound sulfonamide used for respiratory and urinary tract infections and also for malaria. For the treatment of urinary tract infection and chronic bronchitis. Sulfametopyrazine is a sulfonamide antibiotic. The sulfonamides are synthetic bacteriostatic antibiotics with a wide spectrum against most gram-positive and many gram-negative organisms. However, many strains of an individual species may be resistant. Sulfonamides inhibit multiplication of bacteria by acting as competitive inhibitors of <i>p</i>-aminobenzoic acid in the folic acid metabolism cycle. Bacterial sensitivity is the same for the various sulfonamides, and resistance to one sulfonamide indicates resistance to all. Most sulfonamides are readily absorbed orally. However, parenteral administration is difficult, since the soluble sulfonamide salts are highly alkaline and irritating to the tissues. The sulfonamides are widely distributed throughout all tissues. High levels are achieved in pleural, peritoneal, synovial, and ocular fluids. Although these drugs are no longer used to treat meningitis, CSF levels are high in meningeal infections. Their antibacterial action is inhibited by pus. Sulfametopyrazine is a competitive inhibitor of the bacterial enzyme dihydropteroate synthetase. Para-aminobenzoic acid (PABA), a substrate of the enzyme is prevented from binding. The inhibited reaction is necessary in these organisms for the synthesis of folic acid.",The molecular weight is 280.3.,Sulfametopyrazine has a topological polar surface area of 107.2.,The log p value of  is 1.05.,Sulfametopyrazine is approved and withdrawn.,Sulfametopyrazine is a solid.,True
21242,"A pyrrolidinylmethyl tetracycline. Rolitetracycline is a broad-spectrum antibiotic used in cases needing high concentrations or when oral administration is impractical. Rolitetracycline is a semisynthetic broad-spectrum tetracycline antibiotic used especially for parenteral administration in cases requiring high concentrations or when oral administration is impractical. Rolitetracycline passively diffuses through porin channels in the bacterial membrane and reversibly binds to the 30S ribosomal subunit, preventing binding of tRNA to the mRNA-ribosome complex, and thus interfering with protein synthesis.",The molecular weight is 527.57.,Rolitetracycline has a topological polar surface area of 170.87.,The log p value of  is 0.48.,Rolitetracycline is approved.,Rolitetracycline is a solid.,True
21243,"A macrolide antibiotic from Streptomyces narbonensis. The drug has antimicrobial activity against a wide spectrum of pathogens. For the treatment of bacterial infections. Josamycin is a macrolide antibiotic from <i>Streptomyces narbonensis</i>. The drug has antimicrobial activity against a wide spectrum of pathogens.  The mechanism of action of macrolides such as Josamycin is via inhibition of bacterial protein biosynthesis by binding reversibly to the subunit 50S of the bacterial ribosome, thereby inhibiting translocation of peptidyl tRNA. This action is mainly bacteriostatic, but can also be bactericidal in high concentrations. Macrolides tend to accumulate within leukocytes, and are therefore actually transported into the site of infection.",The molecular weight is 828.01.,Josamycin has a topological polar surface area of 206.05.,The log p value of  is 3.67.,Josamycin is investigational.,Josamycin is a solid.,True
21244,,,,,"4-Bromo-2,5-dimethoxyamphetamine is experimental and illicit.","4-Bromo-2,5-dimethoxyamphetamine is a solid.",False
21245,Dichloralphenazone is a sedative composed of chloral hydrate and phenazone. It is typically found in combination products Nodolor and Midrin containing and used for the relief of tension and vascular headaches. It is a US Schedule IV drug and its clinical use is limited.,,,,Dichloralphenazone is approved and illicit.,Dichloralphenazone is a solid.,True
21246,An amphetamine derivative that inhibits uptake of catecholamine neurotransmitters. It is a hallucinogen. It is less toxic than its methylated derivative but in sufficient doses may still destroy serotonergic neurons and has been used for that purpose experimentally. ,,,,Tenamfetamine is experimental and illicit.,Tenamfetamine is a solid.,True
21247,Chlorhexadol is a sedative and hypnotic which is regulated in the United States as a Schedule III controlled substance. It is a derivative of chloral hydrate. Chloral hydrate has sedative/hypnotic activity which has been shown to extend the sleep of normal made adults via a dose-response relationship. ,The molecular weight is 265.56.,Chlorhexadol has a topological polar surface area of 49.69.,The log p value of  is 2.15.,Chlorhexadol is experimental and illicit.,Chlorhexadol is a solid.,True
21248,,The molecular weight is 333.43.,Drotebanol has a topological polar surface area of 62.16.,The log p value of  is 0.43.,Drotebanol is experimental and illicit.,Drotebanol is a solid.,False
21249,"Cathinone is a monoamine alkaloid found in the shrub Catha edulis (Khat). Closely related to ephedrine, cathine and other amphetamines, it is probably the main contributor to the stimulant effect of Catha edulis. Cathinone differs from many other amphetamines in that its structure is a ketone. Other amphetamines to share this structure include the antidepressant bupropion and the stimulant methcathinone, among others. Internationally, cathinone is categorized as a Schedule I drug. Cathinone was added to the Controlled Substances Act's Schedule I in 1993 in compliance with international laws.",,,,Cathinone is illicit.,Cathinone is a solid.,True
21250,,,,,"7,9-Dimethylguanine is experimental.","7,9-Dimethylguanine is a solid.",False
21251,,,,,7-Deazaguanine is experimental.,7-Deazaguanine is a solid.,False
21252,"5-Hydroxytryptophan (5-HTP), also known as oxitriptan (INN), is a naturally occurring amino acid and metabolic intermediate in the synthesis of serotonin and melatonin. 5-HTP is sold over-the-counter in the United Kingdom, United States and Canada as a dietary supplement for use as an antidepressant, appetite suppressant, and sleep aid, and is also marketed in many European countries for the indication of major depression under trade names like Cincofarm, Levothym, Levotonine, Oxyfan, Telesol, Tript-OH, and Triptum. Several double-blind placebo-controlled clinical trials have demonstrated the effectiveness of 5-HTP in the treatment of depression, though a lack of high quality studies has been noted. More study is needed to determine efficacy in treating depression. For use as an antidepressant, appetite suppressant, and sleep aid. The psychoactive action of 5-HTP is thought to be due to increased serotonin production in central nervous system tissue. ",The molecular weight is 220.23.,Oxitriptan has a topological polar surface area of 99.34.,The log p value of  is -2.23.,Oxitriptan is approved and investigational and nutraceutical.,Oxitriptan is a solid.,True
21253,,,,,Valpromide is experimental.,Valpromide is a solid.,False
21254,Investigated for use/treatment in strokes and alzheimer's disease.,,,,Tramiprosate is investigational.,Tramiprosate is a solid.,True
21255,Investigated for use/treatment in anxiety disorders.,,,,Ocinaplon is investigational.,Ocinaplon is a solid.,True
21256,Investigated for use/treatment in herpes zoster infections and viral infection.,,,,Valomaciclovir is investigational.,Valomaciclovir is a solid.,True
21257,Investigated for use/treatment in irritable bowel syndrome (IBS).,,,,Dextofisopam is investigational.,Dextofisopam is a solid.,True
21258,Investigated for use/treatment in obesity.,,,,Taranabant is investigational.,Taranabant is a solid.,True
21259,,The molecular weight is 229.37.,Triclofos has a topological polar surface area of 66.76.,The log p value of  is -0.11.,Triclofos is approved and withdrawn.,Triclofos is a solid.,False
21260,Mebutamate is a sedative and anxiolytic drug with anti-hypertensive (blood pressure lowering) effects comparable to those of other barbiturates but is only around 1/3rd the potency of secobarbital as a sedative. Side effects include dizziness and headaches.,The molecular weight is 232.28.,Mebutamate has a topological polar surface area of 104.64.,The log p value of  is 1.31.,Mebutamate is approved.,Mebutamate is a solid.,True
21261,"Long acting sulfonamide used in leprosy, urinary, and respiratory tract infections.",The molecular weight is 280.3.,Sulfameter has a topological polar surface area of 107.2.,The log p value of  is 0.65.,Sulfameter is approved.,Sulfameter is a solid.,True
21262,"Unoprostone isopropyl is a prostaglandin analogue. Ophthalmic Solution 0.15% is a synthetic docosanoid. Unoprostone isopropyl has the chemical name isopropyl (+)-(Z)-7--5-heptenoate. For the lowering of intraocular pressure in patients with open-angle glaucoma or ocular hypertension who are intolerant of other intraocular pressure lowering medications or insufficiently responsive (failed to achieve target IOP determined after multiple measurements over time) to another intraocular pressure lowering medication. Unoprostone will begin to reduce IOP 30 minutes after ocular instillation. Unoprostone is believed to reduce elevated intraocular pressure (IOP), by increasing the outflow of aqueous humor. The mechanism of action for the IOP-lowering effect of unoprostone is controversial. Early studies showed that unoprostone increases aqueous humor outflow through the uveoscleral pathway similar to the 20-carbon prostaglandin analogs, such as latanoprost.8 More recent evidence, however, shows that it may work, at least in part, through stimulation of Ca2+-activated BK and CIC-2 type channels, leading to increased trabecular meshwork outflow.",,,,Unoprostone is approved and investigational.,Unoprostone is a liquid.,True
21263,Viomycin is a tuberactinomycin antibiotic that was used to treat Mycobacterium tuberculosis until it was replaced by the less toxic capreomycin. These drugs bind RNA in bacterial ribosomes and inhibit protein synthesis. Viomycin was derived from the actinomycete _Streptomyces puniceus_. Viomycin is an essential component in the drug cocktail currently used to fight infections of Mycobacterium tuberculosis. Viomycin binds to a site on the ribosome which lies at the interface between helix 44 of the small ribosomal subunit and helix 69 of the large ribosomal subunit. The structures of this complexes suggest that the viomycin inhibits translocation by stabilizing the tRNA in the A site in the pretranslocation state. This inhibits protein synthesis.,The molecular weight is 685.7.,Viomycin has a topological polar surface area of 392.86.,The log p value of  is -7.14.,Viomycin is approved.,Viomycin is a solid.,True
21264,"Etifoxine is an anxiolytic and anticonvulsant drug developed by Hoechst in the 1960s. It is used in anxiety disorders and to promote peripheral nerve healing. It does not bind to the benzodiazepine receptor though the effects are similar to that of benzodiazepines. It is more effective than lorazepam as an anxiolytic, and has fewer side effects. Etifoxine has been associated with acute liver injury.",The molecular weight is 300.79.,Etifoxine has a topological polar surface area of 33.62.,The log p value of  is 5.29.,Etifoxine is investigational and withdrawn.,Etifoxine is a solid.,True
21265,"Cyclopentamine is a sympathomimetic alkylamine, classified as a vasoconstrictor. Cyclopentamine was an over the counter treatment for nasal congestion in Europe and Australia. It has been widely discontinued due to the safety, effectiveness, and availability of a similar drug, propylhexedrine.",The molecular weight is 141.26.,Cyclopentamine has a topological polar surface area of 12.03.,The log p value of  is 2.41.,Cyclopentamine is withdrawn.,Cyclopentamine is a solid.,True
21266,"Cyamemazine (Tercian), also known as cyamepromazine, is a typical antipsychotic drug of the phenothiazine class used primarily in the treatment of schizophrenia and psychosis-associated anxiety. Cyamemazine actually behaves like an atypical antipsychotic, due to its potent anxiolytic effects (5-HT2C) and lack of extrapyramidal side effects (5-HT2A).",The molecular weight is 323.46.,Cyamemazine has a topological polar surface area of 30.27.,The log p value of  is 4.87.,Cyamemazine is experimental.,Cyamemazine is a solid.,True
21267,"Beclamide (N-benzyl-B-chloropropionamide) is a no longer used drug that possesses anticonvulsant and sedative activity. It was studied in the 1950s for generalised tonic-clonic seizures but was not effective for absence seizures. Has been used in the management of epilepsy and epilepsy related behavioural disorders. It was used for generalised tonic-clonic seizures, and was not effective for absence seizures. Beclamide has been used for over three decades with little knowledge of how it acts in the CNS. In one study using rats, beclamide was seen to reduce striatal dopamine and serotonin levels and increase the levels of dopamine's major metabolites (and thus dopamine turnover), while reducing the levels of serotonin's major metabolite below detectable levels. A similar effect on neurotransmitter levels was seen in the rat frontal cortices. It is theorized that animal aggression is linked to levels of biogenic monoamines such as dopamine and serotonin, however the exact role is unclear. ",The molecular weight is 197.66.,Beclamide has a topological polar surface area of 29.1.,The log p value of  is 1.54.,Beclamide is experimental.,Beclamide is a solid.,True
21268,"Benzoctamine is a drug with two main uses. It can be used as a sedative which does not depress the respiratory system, but rather stimulates it. It can also be used as an anxiolytic with the same efficacy as chlordiazepoxide for treating anxiety neurosis. Benzoctamine acts as a sedative and axiolytic agent. The exact mechanism by which bezoctamine reduces anxiety and produces sedation is unknown. It has been found to increase serotonin levels in the forebrain which may mediate anxiolytic effects similar to those of serotonin selective reuptake inhibitors.",The molecular weight is 249.36.,Benzoctamine has a topological polar surface area of 12.03.,The log p value of  is 3.62.,Benzoctamine is experimental.,Benzoctamine is a solid.,True
21269,Edivoxetine is a drug which acts as a selective norepinephrine reuptake inhibitor and is currently under development by Eli Lilly for attention-deficit hyperactivity disorder (ADHD) and as an antidepressant treatment. Edivoxetine failed to be approved for major depressive disorder after phase III clinical trials in 2012.,,,,Edivoxetine is investigational.,Edivoxetine is a solid.,True
21270,"Lortalamine (LM-1404) is a selective norepinephrine reuptake inhibitor developed in the 1980s. This drug never made it past clinical trials, likely due to ocular toxicity in animals, but has been used in positron emission tomography studies to label norepinephrine transporters.",,,,Lortalamine is experimental.,Lortalamine is a solid.,True
21271,Talopram is a selective norepinephrine reuptake inhibitor (SNRI) that is structurally similar to citalopram and melitracen. It was researched in the 1960s and 1970s but never marketed.,,,,Talopram is experimental.,Talopram is a solid.,True
21272,"Brilaroxazine (RP5063) is an investigational atypical antipsychotic which is under development by Reviva Pharmaceuticals for the treatment of schizophrenia and schizoaffective disorder. Reviva Pharmaceuticals also intends to investigate RP5063 for the treatment of bipolar disorder, major depressive disorder, psychosis/agitation associated with Alzheimer's disease, Parkinson's disease psychosis, attention deficit hyperactivity disorder (ADD/ADHD), and autism. As of May 2015, it is in phase III clinical trials for schizophrenia. Investigated for the treatment of schizophrenia and schizoaffective disorder.",,,,Brilaroxazine is investigational.,Brilaroxazine is a solid.,True
21273,"Magnesium aluminum silicate is a naturally occurring mineral obtained from silicate ores of the montmorillonite group. It is refined to a powder for use in cosmetic and pharmaceutical applications as an absorbent, anticaking agent, opacifying agent, viscosity-increasing agent, suspending agent, tablet and capsule disintegrant, and Magnesium aluminum silicate is used as an over the counter antacid for the self-treatment of heartburn, sour stomach, or acid indigestion. Magnesium aluminum silicate neutralizes excess acid in the stomach to reduce or eliminate symptoms of heartburn, sour stomach, or acid indigestion  Magnesium aluminum silicate reacts with acid in the stomach to increase the pH.",,,,Magnesium Aluminum Silicate is approved.,Magnesium Aluminum Silicate is a solid.,True
21274,"Alfaxalone, also known as alphaxalone or alphaxolone, is a neuroactive steroid and general anaesthetic. It is used in veterinary practice under the trade name Alfaxan, and is licensed for use in both dogs and cats. Along with alfadolone, it is also one of the constituents of anesthetic drug mixture althesin.",The molecular weight is 332.48.,Alfaxalone has a topological polar surface area of 54.37.,The log p value of  is 3.73.,Alfaxalone is vet_approved.,,True
21275,"Azaperone is a pyridinylpiperazine and butyrophenone agent that is capable of eliciting neuroleptic sedative and antiemetic effects. It is subsequently employed predominantly as a veterinary tranquilizer and mainly for pigs and elephants. At the same time, the agent generally does not see equine use as particular adverse reactions may happen. More rarely it may be used in humans as an antipsychotic drug, but this is uncommon.",,,,Azaperone is investigational and vet_approved.,,True
21276,,,,,Clorsulon is vet_approved.,,False
21277,A sulfonamide antimicrobial used for urinary tract infections and in veterinary medicine.,The molecular weight is 284.72.,Sulfachlorpyridazine has a topological polar surface area of 97.97.,The log p value of  is 0.71.,Sulfachlorpyridazine is vet_approved.,,True
21278,,,,,Sulfaethoxypyridazine is vet_approved.,,False
21279,,,,,Sulfanitran is vet_approved.,,False
21280,Sulfaquinoxaline is a veterinary medicine which can be given to cattle and sheep to treat coccidiosis.It is available in Pakistan with Sanna Laboratories in combination with Amprolium and Vitamin K as potential treatment of coccidiosis.,,,,Sulfaquinoxaline is vet_approved.,,True
21281,,,,,Propiopromazine is experimental and vet_approved.,,False
21282,"Romifidine is a veterinary drug utilized as a sedative primarily in large animals, most frequently horses. It is also used less commonly in a wide variety of other animal species. This drug's chemical structure closely resembles that of clonidine, however, romifidine is not approved for use in humans.",,,,Romifidine is vet_approved.,,True
21283,"This drug is a dissociative anesthetic agent that falls under the drug category of _NMDA receptor antagonists_. Tiletamine is chemically similar to another dissociative anesthetic, ketamine. Tiletamine hydrochloride, the salt form, exists as odorless white crystals.",,,,Tiletamine is vet_approved.,,True
21284,"Tricaine (as tricaine methanesulfonate) is white powder used for anesthesia, sedation, or euthanasia of fish. It is also the only anesthetic licensed in the United States for use in fin fish that are intended for human consumption.",,,,Tricaine is vet_approved.,,True
21285,Zolazepam is a pyrazolodiazepinone derivative used as an anaesthetic in veterinary medicine. Zolazepam is typically used in combination with the NMDA antagonist tiletamine or the α2 adrenoceptor agonist xylazine. It is around four times the potency of diazepam but it is both water-soluble and un-ionized at physiological pH meaning that its onset is very fast.,,,,Zolazepam is vet_approved.,,True
21286,"Detomidine is an α2-adrenergic agonist that is used as a horse sedative. Normally, it is administered in the salt form, detomidine hydrochloride. This drug is prescribed by veterinarians and is marketed as _Dormosedan_. Currently, it is only approved by the FDA for use in horses but has been studied for use in other large animals. Used as a large animal sedative, primarily in horses.",,,,Detomidine is vet_approved.,Detomidine is a solid.,True
21287,"Psilocybin has been investigated for the treatment of Anxiety and Stage IV Melanoma. In November, 2019, it was granted Breakthrough Therapy status by the FDA.",,,,Psilocybin is investigational.,,True
21288,"Mosapride is under investigation for the treatment and prevention of Postoperative Ileus and Gastric Peroral Endoscopic Pyloromyotomy (G-POEM). Mosapride has been investigated for the treatment and diagnostic of Constipation, Type 2 Diabetes, Functional Dyspepsia, Functional Constipation, and Epigastric Pain Syndrome, among others.",The molecular weight is 421.9.,Mosapride has a topological polar surface area of 76.82.,The log p value of  is 3.44.,Mosapride is investigational.,,True
21289,Iferanserin has been investigated for the treatment of Hemorrhoids.,,,,Iferanserin is investigational.,,True
21290,Etiracetam is under investigation in clinical trial NCT01137110 (Comparison of Short Duration Levetiracetam to Extended Course for Seizure Prophylaxis After Subarachnoid Hemorrhage (SAH)).,,,,Etiracetam is investigational.,,True
21291,"Lanicemine has been used in trials studying the treatment and basic science of Depression, Major Depressive Disorder, and Treatment Resistant Major Depressive Disorder.",,,,Lanicemine is investigational.,,True
21292,"GW842166X has been used in trials studying the treatment of Pain, Analgesia, Inflammation, Osteoarthritis, and Pain, Inflammatory, among others.",,,,GW842166 is investigational.,,True
21293,"Idalopirdine has been used in trials studying the treatment of Cognition, Schizophrenia, and Alzheimer's Disease.",,,,Idalopirdine is investigational.,,True
21294,"Setrobuvir has been used in trials studying the treatment of Hepatitis C, Chronic.",,,,Setrobuvir is investigational.,,True
21295,Vabicaserin has been used in trials studying the health services research and treatment of Schizophrenia.,,,,Vabicaserin is investigational.,,True
21296,Imagabalin has been investigated in Generalized Anxiety Disorder.,,,,Imagabalin is investigational.,,True
21297,MK-212 has been used in trials studying the treatment of Alcoholism.,,,,MK-212 is investigational.,,True
21298,"Ajulemic acid has been used in trials studying the treatment of Cystic Fibrosis, Dermatomyositis, and Diffuse Cutaneous Systemic Sclerosis.",,,,Ajulemic acid is investigational.,,True
21299,Cerlapirdine has been investigated for the treatment of Alzheimer Disease.,,,,Cerlapirdine is investigational.,,True
21300,"Ecopipam has been used in trials studying the treatment of Tourette's Syndrome, Lesch-Nyhan Disease, Pathological Gambling, and Self-injurious Behavior.",,,,Ecopipam is investigational.,,True
21301,Eltanolone is under investigation in clinical trial NCT02603926 (Treatment of Fragile-X Associated Tremor/Ataxia Syndrome (FXTAS) With Allopregnanolone).,The molecular weight is 318.5.,Eltanolone has a topological polar surface area of 37.3.,The log p value of  is 4.51.,Eltanolone is investigational.,,True
21302,Salvinorin A has been investigated for the basic science of Pharmaceutical Preparations.,,,,Salvinorin A is investigational.,,True
21303,"Carisbamate has been investigated in Alcohol Abuse, Substance Abuse, and Alcohol Dependence.",The molecular weight is 215.63.,Carisbamate has a topological polar surface area of 72.55.,The log p value of  is 0.96.,Carisbamate is investigational.,,True
21304,Piclozotan has been investigated for the treatment of Parkinson's Disease.,,,,Piclozotan is investigational.,,True
21305,Esreboxetine has been used in trials studying the treatment and basic science of Fibromyalgia.,,,,Esreboxetine is investigational.,,True
21306,"Bromperidol has been used in trials studying the treatment of Dementia, Depression, Schizophrenia, Anxiety Disorders, and Psychosomatic Disorders, among others.",The molecular weight is 420.32.,Bromperidol has a topological polar surface area of 40.54.,The log p value of  is 4.0.,Bromperidol is approved and investigational.,,True
21307,"Orvepitant has been used in trials studying the treatment of Depressive Disorder, Depressive Disorder, Major, Post-Traumatic Stress Disorder, and Posttraumatic Stress Disorder (PTSD).",,,,Orvepitant is investigational.,,True
21308,Glpg0492 is under investigation in clinical trial NCT01130818 (First-in-Human Single Ascending Dose of GLPG0492).,,,,GLPG-0492 is investigational.,,True
21309,"AZD3043 has been used in trials studying the treatment and basic science of Safety, Sedation, Tolerability, and Pharmacokinetics.",,,,AZD-3043 is investigational.,,True
21310,Indiplon has been used in trials studying the treatment of Insomnia and Depression.,,,,Indiplon is investigational.,,True
21311,Ibipinabant has been used in trials studying the treatment of Obesity and Obesity and Type 2 Diabetes.,,,,Ibipinabant is investigational.,,True
21312,TD-8954 has been used in trials studying the treatment of Enteral Feeding Intolerance and Gastrointestinal Motility Disorder.,,,,TD-8954 is investigational.,,True
21313,Eltoprazine has been used in trials studying the treatment of Schizophrenia and Cognitive Impairment.,,,,Eltoprazine is investigational.,,True
21314,Chlorsulfaquinoxaline has been used in trials studying the treatment of Lung Cancer and Colorectal Cancer.,,,,Chlorsulfaquinoxaline is investigational.,,True
21315,Pivagabine has been used in trials studying the treatment of Stress and Anxiety.,The molecular weight is 187.24.,Pivagabine has a topological polar surface area of 66.4.,The log p value of  is 0.56.,Pivagabine is investigational.,,True
21316,"Prothipendyl has been used in trials studying the treatment of Dementia, Depression, Schizophrenia, Anxiety Disorders, and Psychosomatic Disorders.",The molecular weight is 285.41.,Prothipendyl has a topological polar surface area of 19.37.,The log p value of  is 3.83.,Prothipendyl is investigational.,,True
21317,Neosaxitoxin is under investigation in clinical trial NCT01786655 (Safety Study of Long-Acting Local Anesthetic).,,,,Neosaxitoxin is investigational.,,True
21318,Surinabant has been investigated for the treatment of Smoking Cessation.,,,,Surinabant is investigational.,,True
21319,Nefiracetam has been used in trials studying the treatment of Alzheimer's Disease.,The molecular weight is 246.31.,Nefiracetam has a topological polar surface area of 49.41.,The log p value of  is 0.64.,Nefiracetam is investigational.,,True
21320,"Valnoctamide has been used in trials studying the treatment of Mania and Schizoaffective Disorder, Manic Type.",The molecular weight is 143.23.,Valnoctamide has a topological polar surface area of 43.09.,The log p value of  is 1.71.,Valnoctamide is investigational.,,True
21321,"Butaperazine was approved in 1967 , and possibly discontinued in the 1980s.",The molecular weight is 409.59.,Butaperazine has a topological polar surface area of 26.79.,The log p value of  is 4.5.,Butaperazine is approved.,,True
21322,,The molecular weight is 254.3.,Sulfadicramide has a topological polar surface area of 89.26.,The log p value of  is 0.4.,Sulfadicramide is experimental.,,False
21323,"Medifoxamine was marketed as an atypical antidepressant, with anxiolyitc properties in France, Spain, and Morrocco in the 1990s but was later withdrawn from the market due to it causing cases of hepatotoxicity.",The molecular weight is 257.33.,Medifoxamine has a topological polar surface area of 21.7.,The log p value of  is 3.38.,Medifoxamine is approved.,,True
21324,Apronalide is approved in Japan. Apronalide has been withdrawn from the market in many other countries due to patient development of thrombocytopenic purpura.,The molecular weight is 184.24.,Apronalide has a topological polar surface area of 72.19.,The log p value of  is 1.31.,Apronalide is approved.,,True
21325,"An intravenous anesthetic that has been used for rapid induction of anesthesia and for maintenance of anesthesia of short duration. (From Martindale, The Extra Pharmacopoeia, 30th ed, p918)",The molecular weight is 337.42.,Propanidid has a topological polar surface area of 65.07.,The log p value of  is 2.78.,Propanidid is experimental.,,True
21326,"Phthalylsulfathiazole is a broad spectrum antibiotic which is part of the drug class, sulfonamides. It was used as an antibiotic for bowel surgery, and for infections of the colon.",The molecular weight is 403.43.,Phthalylsulfathiazole has a topological polar surface area of 125.46.,The log p value of  is 1.25.,Phthalylsulfathiazole is approved.,,True
21327,"Proxibarbal is a derivative of barbiturates, which has been used to treat migraines. Proxibarbal was approved in France but was withdrawn from the market due to the risk of inducing immunoallergic thrombocytopenia.",The molecular weight is 226.23.,Proxibarbal has a topological polar surface area of 95.5.,The log p value of  is -0.98.,Proxibarbal is approved.,,True
21328,"Clothiapine has been approved in European countries and is an atypical antipsychotic, shown to be useful in some treatment-resistant patients.",The molecular weight is 343.87.,Clothiapine has a topological polar surface area of 18.84.,The log p value of  is 4.28.,Clothiapine is approved.,,True
21329,"Penimepicycline is a tetracycline-class antibiotic. It is mentioned on List A produced by the Government of Canada, which is a list of antimicrobial active pharmaceutical ingredients. In the classification of the active ingredients included on this list, the classification document states that tetracycline class antibiotics are of medium importance, and are used in humans.",The molecular weight is 937.03.,,,Penimepicycline is experimental.,,True
21330,"Sulfaisodimidine also called sulfisomidine is an antibacterial product that has been studied for the treatment of urinary tract infections in the 1950s, however, it is unclear whether this drug has been officially approved for use anywhere.",The molecular weight is 278.33.,Sulfaisodimidine has a topological polar surface area of 97.97.,The log p value of  is 1.1.,Sulfaisodimidine is experimental.,,True
21331,,The molecular weight is 405.45.,Febarbamate has a topological polar surface area of 128.03.,The log p value of  is 1.82.,Febarbamate is experimental.,,False
21332,,The molecular weight is 264.3.,Sulfaperin has a topological polar surface area of 97.97.,The log p value of  is 0.6.,Sulfaperin is experimental.,,False
21333,"Trichloroethylene is a halocarbon commonly used as an industrial solvent, not to be confused with the similar 1,1,1-trichloroethane, also known as chlorothene. It has been sold under a variety of trade names including Trimar and Trilene and used as a volatile anesthetic and as an inhaled obstetrical analgesic. Environmental exposure, particularly groundwater and drinking water contamination from industrial discharge, is a major concern for human health and has been the subject of numerous incidents and lawsuits.",The molecular weight is 131.38.,,The log p value of  is 2.63.,Trichloroethylene is approved.,,True
21334,,The molecular weight is 288.78.,Tetrazepam has a topological polar surface area of 32.67.,The log p value of  is 3.69.,Tetrazepam is experimental.,,False
21335,,The molecular weight is 167.21.,Pyrithyldione has a topological polar surface area of 46.17.,The log p value of  is 1.3.,Pyrithyldione is experimental.,,False
21336,"Deanol is commonly referred to as 2-(dimethylamino)ethanol, dimethylaminoethanol (DMAE) or dimethylethanolamine (DMEA). It holds tertiary amine and primary alcohol groups as functional groups. Deanol has been used in the treatment of attention deficit-hyperactivity disorder (ADHD), Alzheimer's disease, autism, and tardive dyskinesia. It has been also used as an ingredient in skin care, and in cognitive function- and mood-enhancing products.",The molecular weight is 89.14.,Deanol has a topological polar surface area of 23.47.,The log p value of  is -0.4.,Deanol is experimental.,,True
21337,,The molecular weight is 179.22.,Phenprobamate has a topological polar surface area of 52.32.,The log p value of  is 1.77.,Phenprobamate is experimental.,,False
21338,,The molecular weight is 181.19.,Styramate has a topological polar surface area of 72.55.,The log p value of  is 0.25.,Styramate is experimental.,,False
21339,,The molecular weight is 206.24.,Pheneturide has a topological polar surface area of 72.19.,The log p value of  is 1.71.,Pheneturide is experimental.,,False
21340,,The molecular weight is 223.07.,Bromisoval has a topological polar surface area of 72.19.,The log p value of  is 1.18.,Bromisoval is experimental.,,False
21341,,The molecular weight is 224.26.,Vinbarbital has a topological polar surface area of 75.27.,The log p value of  is 2.03.,Vinbarbital is experimental.,,False
21342,,The molecular weight is 346.92.,Chlorproethazine has a topological polar surface area of 6.48.,The log p value of  is 6.56.,Chlorproethazine is experimental.,,False
21343,,The molecular weight is 281.51.,,,Acetylglycinamide chloral hydrate is experimental.,,False
21344,,The molecular weight is 214.27.,Fenyramidol has a topological polar surface area of 45.15.,The log p value of  is 1.92.,Fenyramidol is experimental.,,False
21345,,The molecular weight is 299.46.,Thiazinam has a topological polar surface area of 3.24.,The log p value of  is 0.48.,Thiazinam is experimental.,,False
21346,,The molecular weight is 179.22.,Phenibut has a topological polar surface area of 63.32.,The log p value of  is -1.33.,Phenibut is experimental.,,False
21347,,The molecular weight is 294.33.,Sulfametomidine has a topological polar surface area of 107.2.,The log p value of  is 1.55.,Sulfametomidine is experimental.,,False
21348,,The molecular weight is 383.46.,Veralipride has a topological polar surface area of 110.96.,The log p value of  is 0.84.,Veralipride is experimental.,,False
21349,,,,,Gedocarnil is experimental.,,False
21350,,The molecular weight is 264.29.,Iprazochrome has a topological polar surface area of 108.02.,The log p value of  is 1.36.,Iprazochrome is experimental.,,False
21351,,The molecular weight is 417.52.,Sulfatolamide has a topological polar surface area of 98.21.,,Sulfatolamide is experimental.,,False
21352,,The molecular weight is 409.42.,Trifluperidol has a topological polar surface area of 40.54.,The log p value of  is 4.02.,Trifluperidol is experimental.,,False
21353,,The molecular weight is 355.45.,Moperone has a topological polar surface area of 40.54.,The log p value of  is 3.63.,Moperone is experimental.,,False
21354,,The molecular weight is 560.6.,Sulfamazone has a topological polar surface area of 171.13.,The log p value of  is -1.53.,Sulfamazone is experimental.,,False
21355,,The molecular weight is 446.01.,Thiopropazate has a topological polar surface area of 36.02.,The log p value of  is 4.91.,Thiopropazate is experimental.,,False
21356,,The molecular weight is 145.2.,Emylcamate has a topological polar surface area of 52.32.,The log p value of  is 1.59.,Emylcamate is experimental.,,False
21357,,The molecular weight is 208.22.,Allobarbital has a topological polar surface area of 75.27.,The log p value of  is 0.75.,Allobarbital is experimental.,,False
21358,,The molecular weight is 355.38.,Succinylsulfathiazole has a topological polar surface area of 125.46.,The log p value of  is 0.73.,Succinylsulfathiazole is experimental.,,False
21359,Mesterolone is a synthetic anabolic-androgenic steroid (AAS) and derivative of dihydrotestosterone (DHT). It is inactivated by 3α-hydroxysteroid dehydrogenase in skeleta muscules so it is considered a weak androgen. It is not a substrate for aromatase so it is not converted into estrogen. Mesterolone demonstrated to have minimal effect on sperm counts and levels of FSH or LH. Experiments of mesterolone serving as a potential treatment of depression are still undergoing.,The molecular weight is 304.47.,Mesterolone has a topological polar surface area of 37.3.,The log p value of  is 4.07.,Mesterolone is experimental.,,True
21360,,The molecular weight is 74.12.,Diethyl ether has a topological polar surface area of 9.23.,The log p value of  is 0.87.,Diethyl ether is experimental.,,False
21361,,The molecular weight is 158.16.,Oxiracetam has a topological polar surface area of 83.63.,The log p value of  is -1.2.,Oxiracetam is experimental.,,False
21362,,The molecular weight is 307.41.,Fabomotizole has a topological polar surface area of 50.38.,The log p value of  is 3.51.,Fabomotizole is experimental.,,False
21363,,The molecular weight is 295.43.,Pridinol has a topological polar surface area of 23.47.,The log p value of  is 4.07.,Pridinol is experimental.,,False
21364,,The molecular weight is 181.24.,Hexapropymate has a topological polar surface area of 52.32.,The log p value of  is 1.9.,Hexapropymate is experimental.,,False
21365,,The molecular weight is 569.06.,Formocortal has a topological polar surface area of 108.36.,The log p value of  is 3.56.,Formocortal is experimental.,,False
21366,,,,,Fluanisone is experimental.,,False
21367,Niaprazine is a selective brain catecholamine depletor.,The molecular weight is 356.44.,Niaprazine has a topological polar surface area of 48.47.,The log p value of  is 3.33.,Niaprazine is experimental.,,True
21368,,The molecular weight is 70.09.,Vinyl ether has a topological polar surface area of 9.23.,The log p value of  is 1.12.,Vinyl ether is experimental.,,False
21369,,The molecular weight is 231.29.,Sulfathiourea has a topological polar surface area of 98.21.,The log p value of  is 0.49.,Sulfathiourea is experimental.,,False
21370,,The molecular weight is 214.24.,Sulfaguanidine has a topological polar surface area of 122.06.,The log p value of  is -1.24.,Sulfaguanidine is experimental.,,False
21371,,The molecular weight is 236.27.,Cyclobarbital has a topological polar surface area of 75.27.,The log p value of  is 1.87.,Cyclobarbital is experimental.,,False
21372,,,,,Fazadinium bromide is experimental.,,False
21373,,The molecular weight is 223.23.,Mephenoxalone has a topological polar surface area of 56.79.,The log p value of  is 0.89.,Mephenoxalone is experimental.,,False
21374,,The molecular weight is 224.26.,Vinylbital has a topological polar surface area of 75.27.,The log p value of  is 2.03.,Vinylbital is experimental.,,False
21375,,The molecular weight is 280.3.,Sulfamethoxypyridazine has a topological polar surface area of 107.2.,The log p value of  is 0.56.,Sulfamethoxypyridazine is experimental.,,False
21376,,The molecular weight is 427.61.,Dixyrazine has a topological polar surface area of 39.18.,The log p value of  is 3.59.,Dixyrazine is experimental.,,False
21377,"Reposal is a barbiturate derivative invented in the 1960s in Denmark that has sedative, hypnotic and anticonvulsant properties. It was used primarily in the treatment of insomnia.",The molecular weight is 262.31.,Reposal has a topological polar surface area of 75.27.,The log p value of  is 2.71.,Reposal is experimental.,,True
21378,,,,,Magnesium phosphate is experimental.,Magnesium phosphate is a solid.,False
21379,"Cyclopropane was initially investigated because it was thought to be the toxic element in ethylene. Instead, it turned out to be an excellent anesthetic with very rapid onset and recovery while maintaining stable hemodynamics. Its use was ultimately limited because it was highly explosive.",,,,Cyclopropane is experimental.,Cyclopropane is a solid.,True
21380,MRK-409 is a GABA-A receptor agonist.,,,,MRK-409 is experimental.,MRK-409 is a solid.,True
21381,A cannabinoid receptor-inactive eCB-related molecule used as prophylactic in helping to prevent respiratory viral infection. Palmidrol is available for human use as a supplement (400 mg capsules) and as food for medical purposes In Italy and Spain (300 mg and 600 mg tablets).,The molecular weight is 299.5.,Palmidrol has a topological polar surface area of 49.33.,The log p value of  is 6.0.,Palmidrol is experimental and nutraceutical.,Palmidrol is a solid.,True
21382,,,,,Magnesium stearate is investigational.,Magnesium stearate is a solid.,False
21383,Salvia miltiorrhiza root is a plant/plant extract used in some OTC (over-the-counter) products. It is not an approved drug.,,,,Salvia miltiorrhiza root is experimental.,,True
21384,,,,,Loteprednol is approved and experimental.,,False
21385,,The molecular weight is 472.58.,Methylprednisolone aceponate has a topological polar surface area of 106.97.,The log p value of  is 3.35.,Methylprednisolone aceponate is approved and vet_approved.,,False
21386,,,,,Perphenazine enanthate is experimental.,,False
21387,,,,,Pyrazolam is experimental.,,False
21388,Cannabinol (CBN) is a physiologically inactive constituent of Cannabis sativa.,,,,Cannabinol is experimental and investigational.,,True
21389,PCS-499 is under investigation in clinical trial NCT01487109 (A Phase 2 Study to Evaluate the Safety and Efficacy of CTP-499 in Type 2 Diabetic Nephropathy Patients).,,,,PCS-499 is investigational.,,True
21390,JNJ-26489112 is under investigation in clinical trial NCT00579384 (A Study of the Effects of JNJ-26489112 on the Photic Induced Paroxysmal Electroencephalogram (EEG) Response in Patients With Photosensitive Epilepsy).,,,,JNJ-26489112 is investigational.,,True
21391,,,,,"2,5-Dimethoxy-4-ethylamphetamine is experimental and illicit.","2,5-Dimethoxy-4-ethylamphetamine is a solid.",False
21392,,,,,Methylenedioxyethamphetamine is experimental and illicit.,Methylenedioxyethamphetamine is a solid.,False
21393,,,,,"1,10-Phenanthroline is experimental.","1,10-Phenanthroline is a solid.",False
21394,,The molecular weight is 912.06.,Saralasin has a topological polar surface area of 355.05.,The log p value of  is -3.98.,Saralasin is investigational.,Saralasin is a solid.,False
21395,"Adrafinil is a mild central nervous system stimulating drug typically employed to relieve excessive sleepiness and inattention in geriatric patients. It is also been used off-label to prevent fatigue or falling asleep for extended periods of time. Adrafinil does not currently have FDA approval and is thus unregulated in the United States. It was marketed in France and elsewhere in Europe under the trade name Olmifon until September 2011 when France's FDA equivalent reassessed the drug and withdrew marketing permission. Used to relieve excessive sleepiness and inattention in elderly patients. Adrafinil is a prodrug; it is primarily metabolized in vivo to modafinil, resulting in nearly identical pharmacological effects. Unlike modafinil, the active metabolite must accumulate before the drug is able to act. Oral adrafinil without food usually begins to act within 45 minutes to 1 hour.",The molecular weight is 289.35.,Adrafinil has a topological polar surface area of 66.4.,The log p value of  is 0.61.,Adrafinil is withdrawn.,Adrafinil is a solid.,True
21396,"Hexoprenaline is a stimulant of beta 2 adrenergic receptors. It is used as a bronchodilator, antiasthmatic, and tocolytic agent.",The molecular weight is 420.51.,Hexoprenaline has a topological polar surface area of 145.44.,The log p value of  is 0.05.,Hexoprenaline is experimental and withdrawn.,Hexoprenaline is a solid.,True
21397,Etilefrine is an adrenergic agonist that appears to interact with beta-2 and some alpha adrenergic receptors. It has been used as a vasoconstrictor agent.,The molecular weight is 181.24.,Etilefrine has a topological polar surface area of 52.49.,The log p value of  is 0.44.,Etilefrine is approved and withdrawn.,Etilefrine is a solid.,True
21398,Cimetropium is a semi-synthetic belladonna alkaloid and derivative of scopolamine. It is a potent antimuscarinic and an effective antispasmodic drug. It is also endowed of a direct myolitic action which partially accounts for its antispasmodic activity. It has never been approved for use in the U.S. or Canada.,,,,Cimetropium is experimental and investigational.,Cimetropium is a solid.,True
21399,,,,,Iofetamine I-123 is approved.,,False
21400,Secretin porcine stimulates pancreatic and gastric secretions to aid in the diagnosis of pancreatic exocrine dysfunction and the diagnosis of gastrinoma.,The molecular weight is 3055.46.,Secretin porcine has a topological polar surface area of 1421.45.,,Secretin porcine is approved.,,True
21401,"Amitraz is a non-systemic acaricide and insecticide. It was generated in 1969 by the Boots Co. in England. Amitraz presents insect repellent effects and hence, it can be used as an insecticide and pesticide. Its insecticide effect is due to its agonistic activity in the alpha-adrenergic system, its interaction with the octopamine receptors in the central nervous system and its driven inhibition of the synthesis of monoamine oxidases and prostaglandins. All the abovementioned effects are translated into the overexcitation, paralysis, and death in insects. ",,,,Amitraz is experimental and vet_approved.,,True
21402,"Metrifonate or trichlorfon is an irreversible organophosphate acetylcholinesterase inhibitor. It is a prodrug which is activated non-enzymatically into 2,2-dichlorovinyl dimethyl phosphate.",The molecular weight is 257.43.,Metrifonate has a topological polar surface area of 55.76.,The log p value of  is 0.68.,Metrifonate is vet_approved.,,True
21403,Atipamezole is a synthetic α2 adrenoceptor antagonistused to reverse the sedative and analgesic effects of dexmedetomidine and medetomidine in dogs. It has also been undergone research as a potential anti-Parkinsonian drug for humans. For the reversal of the sedative and analgesic effects of dexmedetomidine and medetomidine in dogs.,,,,Atipamezole is investigational and vet_approved.,Atipamezole is a solid.,True
21404,"PF-00610355 has been used in trials studying the treatment of Lung Disease, Moxifloxacin, Pulmonary Disease, Asthma, Bronchial, and Bronchial Diseases, among others.",,,,PF-00610355 is investigational.,,True
21405,Ritobegron is under investigation in clinical trial NCT02256735 (Study to Investigate the Effect of KUC 7483 CL on the QT/QTc Interval of the ECG in Comparison to Placebo and Moxifloxacin in Healthy Male and Female Volunteers).,,,,Ritobegron is investigational.,,True
21406,"Abediterol has been used in trials studying the treatment of Asthma, Chronic Obstructive Pulmonary Disease (COPD), and Chronic Obstructive Pulmonary Disease (COPD) and Asthma.",,,,Abediterol is investigational.,,True
21407,"Dopexamine has been used in trials studying the diagnostic and treatment of Free Flap, Oral Cancer, Hypotension, Septic Shock, and Head and Neck Cancer.",The molecular weight is 356.51.,Dopexamine has a topological polar surface area of 64.52.,The log p value of  is 3.32.,Dopexamine is approved and investigational.,,True
21408,Acotiamide has been used in trials studying the treatment of Dyspepsia and Functional Dyspepsia.,The molecular weight is 450.55.,Acotiamide has a topological polar surface area of 113.02.,The log p value of  is 4.06.,Acotiamide is investigational.,,True
21409,"Idazoxan has been used in trials studying the basic science of Molecular Imaging, Alzheimer Disease, and Major Depressive Disorder.",,,,Idazoxan is investigational.,,True
21410,Higenamine is under investigation in clinical trial NCT01451229 (Pharmacokinetics and Pharmacodynamics of Higenamine in Chinese Healthy Subjects).,,,,Higenamine is investigational.,,True
21411,Methanesulfonyl Fluoride has been used in trials studying the treatment of Safety.,,,,Methanesulfonyl Fluoride is investigational.,,True
21412,Mephedrone has been investigated in Alcohol-Related Disorders and Amphetamine-Related Disorders.,,,,Mephedrone is investigational.,,True
21413,"Octopamine is structurally similar to norepinephrine. It has been used as a nootropic, and therefore it and all of its enantiomer are prohibited by the World Anti-doping Agency (WADA) as of 2014.",The molecular weight is 153.18.,Octopamine has a topological polar surface area of 66.48.,The log p value of  is -0.39.,Octopamine is experimental.,,True
21414,,The molecular weight is 204.23.,Fenozolone has a topological polar surface area of 50.69.,The log p value of  is 1.46.,Fenozolone is experimental.,,False
21415,,The molecular weight is 153.18.,Norfenefrine has a topological polar surface area of 66.48.,The log p value of  is -0.39.,Norfenefrine is experimental.,,False
21416,,The molecular weight is 313.4.,Oxyfedrine has a topological polar surface area of 58.56.,The log p value of  is 2.84.,Oxyfedrine is experimental.,,False
21417,,The molecular weight is 131.29.,,,Xenon is experimental.,,False
21418,,The molecular weight is 275.2.,Paraoxon has a topological polar surface area of 90.58.,The log p value of  is 1.88.,Paraoxon is experimental.,,False
21419,,The molecular weight is 223.27.,Rimiterol has a topological polar surface area of 72.72.,The log p value of  is 0.57.,Rimiterol is experimental.,,False
21420,,The molecular weight is 179.26.,Methoxyphenamine has a topological polar surface area of 21.26.,The log p value of  is 1.81.,Methoxyphenamine is approved.,,False
21421,,The molecular weight is 367.45.,Tiracizine has a topological polar surface area of 61.88.,The log p value of  is 3.07.,Tiracizine is experimental.,,False
21422,,The molecular weight is 413.54.,Ethacizine has a topological polar surface area of 61.88.,The log p value of  is 3.93.,Ethacizine is experimental.,,False
21423,,The molecular weight is 345.4.,Tretoquinol has a topological polar surface area of 80.18.,The log p value of  is 1.57.,Tretoquinol is experimental.,,False
21424,,The molecular weight is 151.21.,Gepefrine has a topological polar surface area of 46.25.,The log p value of  is 1.07.,Gepefrine is experimental.,,False
21425,,The molecular weight is 326.44.,Hydroquinine has a topological polar surface area of 45.59.,The log p value of  is 3.27.,Hydroquinine is experimental.,,False
21426,,The molecular weight is 225.29.,Prenalterol has a topological polar surface area of 61.72.,The log p value of  is 1.09.,Prenalterol is experimental.,,False
21427,,,,,Fosfructose is experimental.,Fosfructose is a solid.,False
21428,"Sympathomimetic, vasoconstrictor agent.",,,,Deoxyepinephrine is experimental.,Deoxyepinephrine is a solid.,True
21429,,,,,Chloride ion is experimental.,,False
21430,,,,,Racephedrine is approved and experimental.,,False
21431,Hydroquinidine is under investigation in clinical trial NCT00927732 (Hydroquinidine Versus Placebo in Patients With Brugada Syndrome).,The molecular weight is 326.44.,Hydroquinidine has a topological polar surface area of 45.59.,The log p value of  is 3.27.,Hydroquinidine is investigational.,,True
21432,"Posiphen is under investigation in clinical trial NCT02925650 (Safety, Tolerability, PK and PD of Posiphen® in Subjects With Early Alzheimer's Disease).",,,,Posiphen is investigational.,,True
21433,SOR-C13 is under investigation in clinical trial NCT01578564 (Safety and Tolerability Study of SOR-C13 in Subjects With Advanced Cancers Commonly Known to Express the TRPV6 Channel).,,,,SOR-C13 is investigational.,,True
21434,"Mipomersen sodium, which was known as the investigational drug, isis-301012, is the salt form of a synthetic phosphorothioate oligonucleotide. Mipomersen sodium prevents the formation of apo B-100, resulting in a decrease in the levels of apolipoprotein B (apo B), low density lipoprotein (LDL), and total cholesterol. Mipomersen is indicated in patients with homozygous familial hypercholesterolemia as an adjunct to diet and other lipid-lowering medications. It is marketed under the brand name Kynamro in the United States, and the FDA label includes a black box warning of hepatoxicity. Specifically, elevations in the liver enzymes, i.e. transaminases, and in liver fat (hepatic steatosis) have been reported. Due to this serious risk of liver toxicity, mipomersen sodium is only available to patients under the restricted program called Kynamro Risk Evaluation and Mitigation Strategy program. Used in patients with homozygous familial hypercholesterolemia as an adjunct to diet and other lipid-lowering medications. Mipomersen sodium decreases the levels of apolipoprotein B (apo B), low density lipoprotein (LDL) non-high density lipoprotein-cholesterol, and total cholesterol. Mipomersen binds to the mRNA that codes for apoB-100. This binding leads to double-stranded RNA, which is degraded by RNase H and prevents translation of the mRNA to form the apo B-100 protein.",,,,Mipomersen is approved and investigational.,Mipomersen is a liquid.,True
21435,,The molecular weight is 269.17.,Propatyl nitrate has a topological polar surface area of 165.15.,The log p value of  is -3.66.,Propatyl nitrate is experimental and investigational.,,False
21436,,,,,Methylpropylpropanediol dinitrate is experimental.,,False
21437,,The molecular weight is 416.3.,Tenitramine has a topological polar surface area of 226.68.,The log p value of  is -6.48.,Tenitramine is experimental.,,False
21438,,,,,Nitrate is experimental and investigational.,Nitrate is a solid.,False
21439,"Hetacillin is a penicillin beta-lactam antibiotic used in the treatment of bacterial infections caused by susceptible, usually gram-positive, organisms. The name \penicillin\"" can either refer to several variants of penicillin available, or to the group of antibiotics derived from the penicillins. Hetacillin has in vitro activity against gram-positive and gram-negative aerobic and anaerobic bacteria. The bactericidal activity of Hetacillin results from the inhibition of cell wall synthesis and is mediated through Hetacillin binding to penicillin binding proteins (PBPs). Hetacillin has been withdrawn from the market since it has been discovered that it has no therapeutic advantage compared to non-ester derivatives like ampicillin."" Hetacillin is a beta-lactam antibiotic prodrug used to treat bacterial infections. In the body it gets converted to ampicillin. Hetacillin is a penicillin beta-lactam antibiotic used in the treatment of bacterial infections caused by susceptible, usually gram-positive, organisms. The name \penicillin\"" can either refer to several variants of penicillin available, or to the group of antibiotics derived from the penicillins. Hetacillin has in vitro activity against gram-positive and gram-negative aerobic and anaerobic bacteria. The bactericidal activity of Hetacillin results from the inhibition of cell wall synthesis and is mediated through Hetacillin binding to penicillin binding proteins (PBPs)."" Hetacillin is a semisynthetic penicillin prodrug which itself has no antibacterial activity, but is converted in the body to ampicillin and has actions and uses similar to those of ampicillin. Hetacillin is prepared by reacting ampicillin with acetone. Ampicillin rapidly decomposes because of the intramolecular attack of the side chain amino group on the lactam ring. _In vitro_ studies have shown that hetacillin is resistant to beta lactamase activity. However, this effect is transient, as the hydrolysis product, ampicillin, is readily inactivated by beta lactamase. Hetacillin locks up the offending amino group and prevents the decomposition of Hetacillin. Once hydrolyzed to ampicillin (and acetone), ampicillin binds to the penicillin binding proteins found in susceptible bacteria. This inhibits the third and last stage of bacterial cell wall synthesis. Cell lysis is then mediated by bacterial cell wall autolytic enzymes such as autolysins.",The molecular weight is 389.47.,Hetacillin has a topological polar surface area of 89.95.,The log p value of  is 0.81.,Hetacillin is approved and vet_approved and withdrawn.,Hetacillin is a solid.,True
21440,"Amidinopenicillanic acid derivative with broad spectrum antibacterial action. It is poorly absorbed if given orally and is used in urinary infections and typhus. Amdinocillin is not available in the United States. Used in the treatment of urinary tract infections caused by some strains of E. coli and klebsiella and enterobacter species. Used mainly against Gram negative organisms. Amdinocillin is a novel, semisynthetic penicillin effective against many gram-negative bacteria. The antibacterial activity of amdinocillin is derived from its ability to bind specifically and avidly to Penicillin Binding Protein-2 (PBP 2). Amdinocillin is active alone against many gram-negative organisms. Pseudomonas and non-fermenting gram-negative bacteria, however, are usually resistant. Amdinocillin, in combination with many beta-lactams, exhibits marked synergy against many enterobacteriaceae. No such synergy can be demonstrated for gram-positive organisms or pseudomonas species. Amdinocillin is not beta-lactamase stable. Organisms which produce high levels of plasma-mediated beta-lactamase are resistant to the drug. Co-administration of probenecid results in markedly elevated plasma levels of amdinocillin and delays its excretion. Amdinocillin is a stong and specific antagonist of Penicillin Binding Protein-2 (PBP 2). It is active against gram negative bacteria, preventing cell wall synthesis by inhibiting the activity of PBP2. PBP2 is a peptidoglycan elongation initiating enzyme. Peptidoglycan is a polymer of sugars and amino acids that is the main component of bacterial cell walls. ",The molecular weight is 325.43.,Amdinocillin has a topological polar surface area of 73.21.,The log p value of  is 2.5.,Amdinocillin is investigational and withdrawn.,Amdinocillin is a solid.,True
21441,"Pivalate ester analog of ampicillin. or the treatment of respiratory tract infections (including acute bronchitis, acute exacerbations of chronic bronchitis and pneumonia); ear, nose and throat infections; gynecological infections; urinary tract infections (including acute uncomplicated gonococcal urethritis) when caused by non penicillinase-producing susceptible strains of the following organisms: gram-positive organisms, e.g., streptococci, pneumococci and staphylococci; gram-negative organisms, e.g., H. influenzae, N. gonorrhoeae, E. coli, P. mirabilis.  Pivampicillin is the pivaloyloxymethyl ester of (the semi-synthetic penicillin) ampicillin. It is an inactive pro-drug, which is converted during its absorption from the gastrointestinal tract to the microbiologically active ampicillin, together with formaldehyde and pivalic acid, by non-specific esterases present in most body tissues. Amounts in excess of 99% of the pivampicillin absorbed are converted to ampicillin within 15 minutes of absorption. Ampicillin (the active metabolite of pivampicillin) has a bactericidal action resulting from inhibition of cell wall mucopeptide biosynthesis.",The molecular weight is 463.55.,Pivampicillin has a topological polar surface area of 128.03.,The log p value of  is 2.52.,Pivampicillin is approved.,Pivampicillin is a solid.,True
21442,"Pivmecillinam is a mecillinam prodrug, a pivaloyloxymethyl ester of amdinocillin that is well absorbed orally, but broken down to amdinocillin in the intestinal mucosa. It is active against gram-negative organisms and used as for amdinocillin.  Used to treat infections due to mecillinam-sensitive organisms such as urinary tract infections, salmonellosis and typhoid fever. Pivmecillinam is a pivaloyloxymethyl ester of amdinocillin that is well absorbed orally, but broken down to amdinocillin in the intestinal mucosa. It is active against gram-negative organisms and used as for amdinocillin. Pivmecillinam interferes with the biosynthesis of the bacterial cell wall however its activity is slightly different from that of other penicillins and cephalosporins",The molecular weight is 439.57.,Pivmecillinam has a topological polar surface area of 88.51.,The log p value of  is 3.96.,Pivmecillinam is approved.,Pivmecillinam is a solid.,True
21443,,,,,4-Oxoretinol is experimental.,4-Oxoretinol is a solid.,False
21444,"Carindacillin or Carbenicillin isdanyl was an oral penicillin prodrug of marketed by Pfizer as Geocillin. It is no longer marketed in the United States. For the treatment of acute and chronic infections of the upper and lower urinary tract and in asymptomatic bacteriuria (due to susceptible strains Escherichia coli, Proteus mirabilis, Morganella morganii, Providencia rettgeri, Proteus vulgaris, Pseudomonas, Enterobacter, and Enterococci.). Also indicated in the treatment of prostatitis (due to susceptible strains Escherichia coli Enterococcus (S. faecalis), Proteus mirabilis Enterobacter sp.).",The molecular weight is 494.56.,Carindacillin has a topological polar surface area of 113.01.,The log p value of  is 4.18.,Carindacillin is approved and investigational.,Carindacillin is a solid.,True
21445,"Zuretinol acetate has been used in trials studying the treatment of Impaired Dark Adaptation, RP (Retinitis Pigmentosa), Retinitis Pigmentosa (RP), and LCA (Leber Congenital Amaurosis).",,,,Zuretinol acetate is investigational.,,True
21446,Sultamicillin has been used in trials studying the prevention and treatment of Ventilator Associated Pneumonia and Chronic Obstructive Pulmonary Disease (COPD).,The molecular weight is 594.65.,Sultamicillin has a topological polar surface area of 182.48.,The log p value of  is 1.74.,Sultamicillin is approved and investigational.,,True
21447,"Temocillin has been investigated in Infection, Liver Dysfunction, and Urinary Tract Infection.",The molecular weight is 414.45.,Temocillin has a topological polar surface area of 133.24.,The log p value of  is 1.52.,Temocillin is approved and investigational.,,True
21448,,The molecular weight is 351.42.,Epicillin has a topological polar surface area of 112.73.,The log p value of  is -1.09.,Epicillin is experimental.,,False
21449,Pheneticillin (or phenethicillin) is a penicillin antibiotic which is approved for use internationally.,The molecular weight is 364.42.,Pheneticillin has a topological polar surface area of 95.94.,The log p value of  is 2.25.,Pheneticillin is approved.,,True
21450,,The molecular weight is 454.5.,Carfecillin has a topological polar surface area of 113.01.,The log p value of  is 3.17.,Carfecillin is experimental.,,False
21451,,The molecular weight is 378.44.,Propicillin has a topological polar surface area of 95.94.,The log p value of  is 2.78.,Propicillin is experimental.,,False
21452,,The molecular weight is 433.3.,Clometocillin has a topological polar surface area of 95.94.,The log p value of  is 3.23.,Clometocillin is experimental.,,False
21453,,The molecular weight is 414.45.,Sulbenicillin has a topological polar surface area of 141.08.,The log p value of  is -0.12.,Sulbenicillin is experimental.,,False
21454,,The molecular weight is 406.45.,Penamecillin has a topological polar surface area of 102.01.,The log p value of  is 1.96.,Penamecillin is experimental.,,False
21455,,The molecular weight is 481.52.,Talampicillin has a topological polar surface area of 128.03.,The log p value of  is 1.59.,Talampicillin is experimental.,,False
21456,,The molecular weight is 493.54.,Aspoxicillin has a topological polar surface area of 191.16.,The log p value of  is -3.2.,Aspoxicillin is experimental.,Aspoxicillin is a solid.,False
21457,Metampicillin is a penicillin antibiotic prepared by the reaction of ampicillin with formaldehyde. It is hydrolysed in aqueous solution to form ampicillin. Hydrolysis is rapid under acid conditions like the stomach.,The molecular weight is 361.42.,Metampicillin has a topological polar surface area of 99.07.,The log p value of  is 1.22.,Metampicillin is experimental.,,True
21458,"Aramchol has been used in trials studying the treatment of HIV, Gallstones, Fatty Liver, Metabolic Syndrome, and Nonalcoholic Steatohepatitis, among others.",,,,Aramchol is investigational.,,True
21459,,,,,Ox bile extract is approved and experimental and investigational.,Ox bile extract is a solid.,False
21460,"Asparaginase is an important agent used to treat acute lymphoblastic leukemia (ALL). Asparagine is incorporated into most proteins, and the synthesis of proteins is stopped when asparagine is absent, which inhibits RNA and DNA synthesis, resulting in a halt in cellular proliferation. This forms the basis of asparaginase treatment in ALL , ,. This drug is is an asparagine specific enzyme indicated as a component of a multi-agent chemotherapeutic regimen for the treatment of acute lymphoblastic leukemia in pediatric and young adult patients age 1 month to 21 years. The effect of this drug is believed to occur by selective killing of leukemic cells due to depletion of plasma L-asparagine. Leukemic cells with low expression of asparagine synthetase are less capable of producing L-asparagine, and therefore rely on exogenous L-asparagine for survival. When asparagine is depleted, tumor cells cannot proliferate. L-asparaginase (the main component of this drug) is an enzyme that catalyzes the conversion of the amino acid L-asparagine into both aspartic acid and ammonia ,. This process depletes malignant cells of their required asparagine. The depletion of asparagine then blocks protein synthesis and tumor cell proliferation, especially in the G1 phase of the cell cycle. As a result, tumor cell death occurs. Asparagine is important in protein synthesis in acute lymphoblastic leukemia (ALL) cells which, unlike normal cells, cannot produce this amino acid due to lack of the enzyme _asparagine synthase_ ,. ",,,,Calaspargase pegol is approved.,Calaspargase pegol is a liquid.,True
21461,,,,,Prostaglandin B2 is experimental.,Prostaglandin B2 is a solid.,False
21462,,,,,Penicillin G Acyl-Serine is experimental.,Penicillin G Acyl-Serine is a solid.,False
21463,Certoparin is part of the heparins of low molecular weight that presents high activity against the coagulation factor Xa. It is normally used to prevent deep venous thrombosis. Used in the prevention and treatment of venous thromboembolism (deep vein thrombosis and pulmonary embolism) and in the treatment of myocardial infarction.,,,,Certoparin is approved and investigational.,Certoparin is a solid.,True
21464,,The molecular weight is 128.17.,Potassium lactate has a topological polar surface area of 60.36.,,Potassium lactate is approved.,,False
21465,"Potassium bitartate, also referred to as potassium acid tartrate or cream of tartar, is the potassium acid salt of l-( + )-tartaric acid. It is obtained as a byproduct of wine manufacture during the fermentation process. Approved by the FDA as a direct food substance, potassium bitartrate is used as an additive, stabilizer, pH control agent, antimicrobial agent, processing aid, or thickener in various food products. Potassium bitartrate has a long history of medical use as a laxative administered as a rectal suppository and is an approved third-class OTC drug in Japan. Indicated for the treatment of constipation.  Potassium bitartrate potentiates bowel movements. In medical studies, it was shown to be an effective treatment for chronic constipationwhen combined with sodium bicarbonate in a polyethylene glycol-based suppository.  Potassium bitartrate is a carbon dioxide-releasing laxative that works by forming carbon dioxide gas, which creates a mechanical distension against the intestinal wall and induces bowel contractions. Rectal suppositories of carbon dioxide-releasing type of laxative were demonstrated to be useful and safe in the treatment of patients at risk for electrolyte disorders such as the elderly or patients with renal or cardiovascular disorders. ",The molecular weight is 188.18.,Potassium bitartrate has a topological polar surface area of 117.89.,,Potassium bitartrate is experimental.,Potassium bitartrate is a solid.,True
21466,"Potassium hydroxide, also known as _lye_ is an inorganic compound with the chemical formula _KOH_. Also commonly referred to as _caustic potash_, it is a potent base that is marketed in several forms including pellets, flakes, and powders. It is used in various chemical, industrial and manufacturing applications. Potassium hydroxide is also a precursor to other potassium compounds. Potassium hydroxide is used in food to adjust pH, as a stabilizer, and as a thickening agent. This ingredient has been considered as generally safe as a direct human food ingredient by the FDA, based upon the observance of several good manufacturing practice conditions of use. The corrosiveness of potassium hydroxide renders it a very useful agent in the decomposition/removal soft tissue and hair removal. It is incorporated into some nail products, shaving creams, and soaps. The exact mechanism of action of KOH is not known but the speculated one is that topical application of KOH digests keratin, and induces inflammation.",,,,Potassium hydroxide is approved.,Potassium hydroxide is a solid.,True
21467,,,,,Fenprostalene is vet_approved.,,False
21468,,,,,Luprostiol is experimental and vet_approved.,,False
21469,Analog of prostaglandin F2 alpha.,,,,Prostalene is vet_approved.,,True
21470,,,,,Fluprostenol is vet_approved.,,False
21471,"Mm has been used in trials studying the treatment of Cocaine Dependence and Diabetes Mellitus, Type 2.",,,,Mannitol busulfan is approved and investigational.,,True
21472,Betulinic Acid has been used in trials studying the treatment of Dysplastic Nevus Syndrome.,,,,Betulinic Acid is investigational.,,True
21473,,The molecular weight is 320.39.,Feprazone has a topological polar surface area of 40.62.,The log p value of  is 3.3.,Feprazone is experimental.,,False
21474,,The molecular weight is 255.27.,Pranoprofen has a topological polar surface area of 59.42.,The log p value of  is 2.49.,Pranoprofen is experimental and investigational.,,False
21475,Guaiacolsulfonate is an aromatic sulfonic acid. Potassium guaiacolsulfonate salt is an expectorant that thins the mucus in the lungs and reduces chest congestion.,,,,Potassium Guaiacolsulfonate is experimental.,,True
21476,,The molecular weight is 400.47.,Enprostil has a topological polar surface area of 93.06.,The log p value of  is 1.27.,Enprostil is experimental.,,False
21477,,The molecular weight is 158.03.,Potassium permanganate has a topological polar surface area of 74.27.,,Potassium permanganate is experimental and investigational.,,False
21478,"Potassium carbonate (K2CO3) is a white salt, soluble in water (insoluble in ethanol) which forms a strongly alkaline solution. It can be made as the product of potassium hydroxide's absorbent reaction with carbon dioxide. It presents a large capacity to absorb moisture.",,,,Potassium carbonate is approved.,Potassium carbonate is a solid.,True
21479,,,,,Potassium triiodide is experimental.,,False
21480,,,,,"(6S)-5,6,7,8-tetrahydrofolic acid is experimental.","(6S)-5,6,7,8-tetrahydrofolic acid is a solid.",False
21481,"Levoleucovorin is the enantiomerically active form of Folinic Acid (also known as 5-formyl tetrahydrofolic acid or leucovorin). Commercially available leucovorin is composed of a 1:1 racemic mixture of the dextrorotary and levorotary isomers, while levoleucovorin contains only the pharmacologically active levo-isomer. In vitro, the levo-isomer has been shown to be rapidly converted to the biologically available methyl-tetrahydrofolate form while the dextro form is slowly excreted by the kidneys. Despite this difference in activity, the two commercially available forms have been shown to be pharmacokinetically identical and may be used interchangeably with limited differences in efficacy or side effects (Kovoor et al, 2009).  Levoleucovorin is indicated for use as rescue therapy following high-dose methotrexate in the treatment of osteosarcoma or for diminishing the toxicity associated with inadvertent overdosage of folic acid antagonists. Levoleucovorin, as the product Fusilev (FDA, dosed at one-half the usual dose of racemic d,l-leucovorin), has an additional indication for use in combination chemotherapy with 5-fluorouracil in the palliative treatment of patients with advanced metastatic colorectal cancer (although they should not be mixed in the same infusion as a precipitate may form). Levoleucovorin is actively and passively transported across cell membranes. In vivo, levoleucovorin is converted to 5-methyltetrahydrofolic acid (5-methyl-THF), the primary circulating form of active reduced folate. Levoleucovorin and 5-methyl-THF are polyglutamated intracellularly by the enzyme folylpolyglutamate synthetase. Folylpolyglutamates are active and participate in biochemical pathways that require reduced folate. Folic acid is an essential B vitamin required by the body for the synthesis of purines, pyrimidines, and methionine before incorporation into DNA or protein. However, in order to function in this role, it must first be reduced by the enzyme dihydrofolate reductase (DHFR) into the cofactors dihydrofolate (DHF) and tetrahydrofolate (THF). This important pathway, which is required for de novo synthesis of nucleic acids and amino acids, is disrupted when high-dose methotrexate is used for cancer therapy. As methotrexate functions as a DHFR inhibitor to prevent DNA synthesis in rapidly dividing cells, it also prevents the formation of DHF and THF. This results in a deficiency of coenzymes and a resultant buildup of toxic substances that are responsible for numerous adverse side effects of methotrexate therapy. As levoleucovorin and leucovorin are analogs of tetrahydrofolate (THF), they are able to bypass DHFR reduction and act as a cellular replacement for the co-factor THF, thereby preventing these toxic side effects.",,,,Levoleucovorin is approved and investigational.,Levoleucovorin is a solid.,True
21482,"Sodium polystyrene sulfonate is a medication used to treat abnormally high potassium levels. It may be taken orally or by rectum, as an enema, and functions as a potassium-binding resin in the intestines. It is also an effective topical microbicide and spermicide, inhibiting the genital transfection of, among others, HIV. Used to treat abnormally high potassium levels. Polystyrene sulfonate affects the exchange of sodium and potassium in the body. Polystyrene sulfonate is used to treat high levels of potassium in the blood, also called hyperkalemia. It is a potassium-binding ion-exchange resin that can be administered orally (25 grams in 20% sorbitol) or rectally (50 grams in 20% sorbitol). Polystyrene sulfonate, which is not absorbed, binds excess potassium, carrying it out of the body. The indigestible potassium polystryene sulfonate complex is excreted with the faeces, preventing the absorption of potassium into the blood stream. Hence, the serum potassium level decreases.",,,,Tolevamer is approved and investigational.,Tolevamer is a solid.,True
21483,,,,,"3-Aza-2,3-Dihydrogeranyl Diphosphate is experimental.","3-Aza-2,3-Dihydrogeranyl Diphosphate is a solid.",False
21484,,,,,Thiopyrophosphate is experimental.,Thiopyrophosphate is a solid.,False
21485,,,,,Pyrophosphoric acid is approved and experimental.,Pyrophosphoric acid is a solid.,False
21486,"OXI-4503 is investigated in clinical trials for treating cancer/tumors. OXI-4503 is a solid. OXI-4503 blocks and destroys tumor vasculature, resulting in extensive tumor cell death and necrosis. OXI-4503 (combretastatin A1 di-phosphate / CA1P) is a unique and highly potent, dual-mechanism vascular disrupting agent (VDA). In addition, however, preclinical data demonstrates that OXI-4503 is metabolized by oxidative enzymes (e.g., tyrosinase and peroxidases), which are elevated in many solid tumors and tumor infiltrates, to an orthoquinone chemical species that has direct cytotoxic effects on tumor cells. Preclinical studies have demonstrated that OXI-4503 has (i) single-agent activity against a range of xenograft tumor models; and (ii) synergistic or additive effects when incorporated in various combination regimens with chemotherapy, molecularly-targeted therapies (including tumor-angiogenesis inhibitors), and radiation therapy. Investigated for use/treatment in cancer/tumors (unspecified). OXi4503 blocks and destroys tumor vasculature, resulting in extensive tumor cell death and necrosis. In addition, however, preclinical data demonstrates that OXi4503 is metabolized by oxidative enzymes (e.g., tyrosinase and peroxidases), which are elevated in many solid tumors and tumor infiltrates, to an orthoquinone chemical species that has direct cytotoxic effects on tumor cells. OXi4503 blocks and destroys tumor vasculature, resulting in extensive tumor cell death and necrosis. It induced the shutdown of tumor blood vessels and affected peripheral tumor regions less than central regions.",,,,OXI-4503 is investigational.,OXI-4503 is a solid.,True
21487,"LR-103 is a naturally occurring D-hormone that is produced by the kidneys from vitamin D. LR-103 is one of the D-hormones produced from Hectorol. It is developed for the treatment of secondary hyperparathyroidism in patients with chronic kidney disease (CKD). Studies have shown LR-103 has the same potency as calcitriol, but much lower toxicity. Investigated for use/treatment in parathyroid disorders. LR-103 is effective in normalizing serum calcium and PTH levels without causing hypercalcemia. Importantly, LR-103 also normalized bone abnormalities consequent to SHPT and active vitamin D deficiency.",,,,"1alpha,24S-Dihydroxyvitamin D2 is investigational.","1alpha,24S-Dihydroxyvitamin D2 is a solid.",True
21488,"Sodium tripolyphosphate is an inorganic compound with formula Na5P3O10 and the sodium salt of the polyphosphate penta-anion. It is used as a component of a wide range domestic and industrial products, particularly detergents.",,,,Sodium tripolyphosphate is vet_approved.,Sodium tripolyphosphate is a solid.,True
21489,"1alpha-Hydroxyvitamin D5 (CARD-024) has been used in trials studying the treatment of Drug Safety and Heart; Disease, Activity.",,,,1alpha-Hydroxyvitamin D5 is investigational.,,True
21490,,,,,Phosphate ion is experimental.,,False
21491,"Investigated for use/treatment in fungal infections, bacterial infection, skin infections/disorders, and onychomycosis. Abafungin has been shown to have fungicidal and fungistatic effects on a wide variety of pathogens, including dermatophytes, yeasts (Candida) and moulds. The drug acts on the infecting organisms in two ways: by interfering with the formation of a vital sterol in the fungal cell membrane, thereby preventing cell growth, and also by direct interaction with another membrane component resulting in membrane disruption, leakage of cellular contents and death of the cell and independent of whether it is in a non-metabolising (`resting') phase of development or actively growing. These features of abafungin, combined with the attainment of microbicidal concentrations in the skin from a 1% preparation, its long residence at the site of dermal application and the lack of significant systemic absorption, mean that Abasol(tm) is particularly attractive for the topical treatment of dermatomycoses, which is the first indication under review for marketing approval.",,,,Abafungin is investigational.,Abafungin is a solid.,True
21492,"Investigated for use/treatment in fungal infections, aspergillosis, candidiasis, and onychomycosis.",,,,Ravuconazole is investigational.,Ravuconazole is a solid.,True
21493,Albaconazole has been used in trials studying the basic science of Onychomycosis.,,,,Albaconazole is investigational.,,True
21494,"Calcium glubionate (or glubionate calcium) is a mineral supplement to prevent or treat low blood calcium levels in people who do not get enough calcium from their diets. Calcium glubionate is indicated to treat conditions caused by low calcium levels such as bone loss (osteoporosis), weak bones (osteomalacia/rickets), decreased activity of the parathyroid gland (hypoparathyroidism), and a certain muscle disease (latent tetany). It may also be used in certain patients to make sure they are getting enough calcium (e.g., women who are pregnant, nursing, or postmenopausal, people taking certain medications such as phenytoin, phenobarbital, or prednisone). Essential for nervous, muscular, and skeletal systems. Maintain cell membrane and capillary permeability. Act as an activator in the transmission of nerve impulses and contraction of cardiac, skeletal, and smooth muscle. Essential for bone formation and blood coagulation.",,,,Calcium glubionate anhydrous is approved.,Calcium glubionate anhydrous is a solid.,True
21495,Commonly found in salts with sodium and calcium. Gluconic acid or gluconate is used to maintain the cation-anion balance on electrolyte solutions. For use as part of electrolyte supplementation in total parenteral nutrition. Used as part of electrolyte salts to maintain cation-anion balance in solutions.,The molecular weight is 196.16.,Gluconic Acid has a topological polar surface area of 138.45.,The log p value of  is -3.11.,Gluconic Acid is approved and investigational.,Gluconic Acid is a liquid.,True
21496,,The molecular weight is 600.58.,Calcium pangamate has a topological polar surface area of 150.59.,,Calcium pangamate is experimental.,,False
21497,,,,,PD173955 is experimental.,PD173955 is a solid.,False
21498,Investigated for use/treatment in solid tumors.,,,,Motesanib is investigational.,Motesanib is a solid.,True
21499,Investigated for use/treatment in cancer/tumors (unspecified).,,,,Glesatinib is investigational.,Glesatinib is a solid.,True
21500,Pacritinib is under investigation for the prevention of Acute Myeloid Leukemia (AML).,,,,Pacritinib is investigational.,,True
21501,Crenolanib is under investigation for the treatment of Diffuse Intrinsic Pontine Glioma and Progressive or Refractory High-Grade Glioma.,,,,Crenolanib is investigational.,,True
21502,"Flumatinib has been used in trials studying the treatment of Myelogenous Leukemia, Chronic.",,,,Flumatinib is investigational.,,True
21503,"Savolitinib has been used in trials studying the treatment and health services research of Tumor, Food Effect, Gastric Cancer, Health Subjects, and Colorectal Cancer, among others.",,,,Savolitinib is investigational.,,True
21504,"Iodide I-131 (as Sodium iodide I-131) is a radioisotopic drug used for the treatment and palliation of thyroid malignancy. Iodine-131 is notable for causing mutation and death in cells that it penetrates, which is due to its mode of beta decay. As a result of beta decay, approximately 10% of its energy and radiation dose is via gamma radiation, while the other 90% (beta radiation) causes tissue damage without contributing to any ability to see or image the isotope. Low levels of beta radiation are also known for causing cancer as this dose is highly mutagenic. For this reason, less toxic iodine isotopes such as I-123 are more frequently used in nuclear imaging, while I-131 is reserved for its tissue destroying effects. Because the thyroid gland naturally takes up iodine from the body, therapeutic methods using radioisotopes can take advantage of this mechanism for localization of drug to the site of malignancy.  Therapeutic solutions of Sodium Iodide-131 are indicated for the treatment of hyperthyroidism and thyroid carcinomas that take up iodine. Palliative effects may be observed in patients with advanced thyroid malignancy if the metastatic lesions take up iodine. It is also indicated for use in performance of the radioactive iodide (RAI) uptake test to evaluate thyroid function. The therapeutic effects of sodium iodide I-131 are a result of the ionizing radiation absorbed by the thyroidal tissue. Tissue damage is the result of direct insult to molecules by ionization and excitation and the consequent dissociation of those molecules. About 90% of local irradiation from sodium iodide I-131 is the result of beta radiation and 10% is the result of gamma radiation.  Taken orally, sodium iodide I-131 is rapidly absorbed and distributed within the extracellular fluid of the body. The iodide is concentrated in the thyroid via the sodium/iodide symporter, and subsequently oxidized to iodine. The destruction of thyroidal tissue is achieved by the beta emission of sodium iodide I-131. ",,,,Iodide I-131 is approved and investigational.,Iodide I-131 is a solid.,True
21505,,The molecular weight is 480.65.,Emetine has a topological polar surface area of 52.19.,The log p value of  is 4.95.,Emetine is experimental.,,False
21506,"A bismuth compound used for peptic ulcer and gastro-oesophageal reflux disease (GORD). For the treatment of peptic ulcer and gastro-oesophageal reflux disease (GORD). Bismuth subcitrate is very effective in the treatment of gastroduodenal disorders and appears to act via several mechanisms. It has little acid-neutralizing effect and does not affect acid secretion. Colloidal bismuth subcitrate is very effective in the treatment of gastroduodenal disorders and appears to act via several mechanisms. It has little acid-neutralizing effect and does not affect acid secretion. It is uncertain whether it affects pepsin secretion, but it does inhibit peptic activity. It causes an increase in mucus glycoprotein secretion and may also bind to the gastric mucus layer to act as a diffusion barrier to HCl. It accelerates ulcer healing and causes an accumulation of epidermal growth factor around the ulcer. In addition, it has a cytoprotective effect and increases mucosal secretion of prostaglandins and bicarbonate. It has bactericidal effects against Helicobacter pylori (which is associated with gastritis and peptic ulcers). It also prevents adhesion of H. pylori to epithelial cells and can inhibit enzymes secreted by H. pylori, such as proteases, lipases, glycosidases, and phospholipases.",,,,Bismuth subcitrate potassium is approved and investigational.,Bismuth subcitrate potassium is a solid.,True
21507,,,,,Bismuth subcarbonate is experimental and vet_approved.,,False
21508,"Pirlimycin hydrochloride is an antibiotic belonging to the _lincosamide_ class. Often marketed as _Pirsue_, this drug is used to treat mastitis in cattle.",,,,Pirlimycin is vet_approved.,,True
21509,Valproate bismuth is available in Canada in the over-the-counter medication Neo-Laryngobis.,,,,Valproate bismuth is approved.,Valproate bismuth is a solid.,True
21510,"A synthetic fluoroquinolone (FLUOROQUINOLONES) antibacterial agent that inhibits the supercoiling activity of bacterial DNA GYRASE, halting DNA REPLICATION.",,,,D-Levofloxacin is experimental.,D-Levofloxacin is a solid.,True
21511,25-desacetylrifapentine is under investigation in clinical trial NCT00023387 (TBTC Study 25PK: Intensive Pharmacokinetic Study of Three Doses of Rifapentine and 25-Desacetyl Rifapentine).,,,,25-desacetylrifapentine is investigational.,,True
21512,"Chloroform is an organic small molecule, member of the family of the chloromethanes that presents a formula of CHCl3. It is a colorless, sweet-smelling, dense liquid that is produced on a large scale as a precursor to PTFE and refrigerants, but the latter application is declining.",The molecular weight is 119.37.,,The log p value of  is 1.95.,Chloroform is approved and vet_approved.,,True
21513,,The molecular weight is 303.16.,Enibomal has a topological polar surface area of 66.48.,The log p value of  is 1.93.,Enibomal is experimental.,,False
21514,"2-Hydroxyestradiol is classified as an endogenous steroid, catechol estrogen, and metabolite of estradiol. It is also a positional isomer of estriol. ",,,,2-Hydroxyestradiol is experimental.,2-Hydroxyestradiol is a solid.,True
21515,,,,,Insulin argine is experimental.,Insulin argine is a solid.,False
21516,Aminomethylbenzoic acid may be useful as an antifibrinolytic agent.,The molecular weight is 151.16.,Aminomethylbenzoic acid has a topological polar surface area of 63.32.,The log p value of  is -1.43.,Aminomethylbenzoic acid is experimental.,,True
21517,,The molecular weight is 416.65.,Tacalcitol has a topological polar surface area of 60.69.,The log p value of  is 6.04.,Tacalcitol is experimental and investigational.,,False
21518,,,,,Ferric ammonium citrate is approved and experimental.,,False
21519,,,,,Ferumoxsil is approved and experimental.,,False
21520,,,,,Ferumoxides is approved.,,False
21521,"Ferric sulfate has the molecular formula of Fe2SO4, and it is a dark brown or yellow chemical agent with acidic properties. It is produced by the reaction of sulfuric acid and an oxidizing agent. It is used in different fields such as dermatology, dentistry and it is thought to present hemostatic properties by interacting chemically with blood proteins. By the FDA, ferric sulfate is a direct food substance affirmed in the GRAS category (Generally Recognized As Safe). Ferric sulfate was first used in dermatology as part of the Monsel's solution. This solution is an antihemorrhagic agent used in skin and mucosal biopsies. The use of ferric sulfate in dermatology is under review as ferric sulfate is corrosive and injurious and it can cause degenerative changes that are not observed with other alternatives like collagen. The administration of ferric sulfate as a dermatologic agent has showed delayed reepithelialization and dyspigmentation. Some studies have reported the generation of inflammation in the sites of administration of ferric sulfate. The main function of ferric sulfate is as a hemostatic agent in different medical practices. This hemostatic function is achieved when ferric sulfate is applied directly in the damaged tissue. Once applied, ferric sulfate forms ferric ion-protein complex which helps the sealing of the damaged vessels mechanically. The formation of agglutinated protein complexes produces the generation of occlusion in the capillary orifices. The formation of the ferric protein complex is thought to be due to a chemical reaction between the acidic form of ferric sulfate and the blood proteins.",The molecular weight is 399.86.,Ferric sulfate has a topological polar surface area of 80.26.,,Ferric sulfate is approved.,Ferric sulfate is a solid.,True
21522,"Colloid solution of ferric hydroxide, dextran & glucoheptonic acid.",,,,Gleptoferron is vet_approved.,,True
21523,"Perflubutane has been used in trials studying the diagnostic of Liver Mass, Liver Diseases, Liver Metastasis, Portal Hypertension, and Peripheral Artery Disease. It is a cardiovascular drug designed to enable ultrasound to compete more effectively with nuclear stress testing; currently the leading procedure for detecting coronary heart disease. Perflubutane perfusion echocardiography has the potential to be a cost-effective and convenient alternative to nuclear perfusion imaging. Perflubutane is easy to use and echocardiographers in the clinical trials can be trained to use it after imaging only a few patients. Based on data from previous clinical trials, ultrasound enhanced with Perflubutane was able to image myocardial perfusion and obtain information that appears comparable to nuclear imaging. Acusphere's Phase 3 program is designed with the appropriate comparative standards to determine the value of Perflubutane perfusion echocardiography relative to nuclear perfusion imaging. These standards are coronary angiography, nuclear perfusion imaging, and patient outcome.",The molecular weight is 238.03.,,The log p value of  is 3.21.,Perflubutane is approved and investigational.,,True
21524,,The molecular weight is 367.05.,,,Sodium feredetate is approved.,,False
21525,,The molecular weight is 106.87.,Ferric hydroxide has a topological polar surface area of 60.69.,,Ferric hydroxide is experimental.,,False
21526,An antiferromagnetic material; constitutes the core of natural ferritin.,,,,Ferric oxyhydroxide is experimental.,,True
21527,"TMC-310911 (also known as ASC-09) is a novel investigational protease inhibitor (PI) that is structurally similar to the currently available. It is being investigated for use in HIV-1 infections. TMC-310911 has shown marked activity against a variety of HIV-1 strains, including multi-PI-resistant strains, and may be less likely to generate resistance, making it a potentially desirable therapy for both treatment-naive and PI-experienced patients.",,,,TMC-310911 is investigational.,TMC-310911 is a solid.,True
21528,"PEG-uricase, a polyethylene glycol (\PEG\"") conjugate of recombinant porcine uricase (urate oxidase), which breaks down the uric acid deposits is being studied in Phase III clinical trials for the treatment of severe, treatment-refractory gout in the United States in 2006."" Investigated for use/treatment in hyperuricemia. PEG-uricase is a recombinant, PEGylated formulation of a modified porcine urate oxidase intended to dramatically lower the blood level of uric acid safely and continuously in patients who have not benefited from conventional therapeutic approaches. Urate oxidase is a hepatic enzyme present in almost all mammals – but not in humans – that lowers uric acid levels in the blood by converting uric acid into allantoin, a benign substance which is then easily excreted in the urine.",,,,PEG-uricase is investigational.,PEG-uricase is a liquid.,True
21529,"PEGylation is a technology for the chemical attachment of polyethylene glycol (PEG) polymer chains to a broad range of drug substances such as peptides and proteins including antibody fragments; small molecules, and other drugs. is a bio-engineered type I interferon alpha that is FDA-approved for the treatment of patients with chronic hepatitis C infections. Investigated for use/treatment in hepatitis (viral, C). The effect of PEGylation is to increase drug circulation time in the bloodstream, improve drug solubility and stability, and reduce immunogenicity. The potential advantages of PEGylation are to decrease dosing frequency, improve drug efficacy and safety, improve stability, and simplify drug formulation.",,,,Peginterferon alfacon-1 is investigational.,Peginterferon alfacon-1 is a solid.,True
21530,"GlycoPEG-GCSF is a long-acting GlycoPEGylated granulocyte colony stimulating factor for the treatment of chemotherapy-induced neutropenia. Investigated for use/treatment in adverse effects (chemotherapy) and neutropenics. GlycoPEG-GCSF is a long-acting, GlycoPEGylated granulocyte colony stimulating factor for the treatment of neutropenia. G-CSF is prescribed to stimulate the production of neutrophils, and is approved for sale in major markets around the world for the treatment of neutropenia associated with myelosuppressive chemotherapy. Neutropenia is a severe reduction in the number of neutrophils (mature white blood cells) in the circulating blood, commonly associated with cancer chemotherapy. Patients with neutropenia are at increased risk of developing serious infection. If not treated promptly, neutropenia can be life-threatening. ",,,,GlycoPEG-GCSF is investigational.,GlycoPEG-GCSF is a solid.,True
21531,"Investigated for use/treatment in thrombosis, coronary artery disease, and vascular diseases.",,,,Pegnivacogin is investigational.,Pegnivacogin is a solid.,True
21532,Pegsunercept is used for treating rheumatoid arthritis. Phase II clinical trials were completed in January 2010. Investigated for use/treatment in rheumatoid arthritis.,,,,Pegsunercept is investigational.,Pegsunercept is a solid.,True
21533,"Eptacog alfa pegol (activated) has been used in trials studying the prevention and treatment of Haemophilia A, Haemophilia B, Congenital Bleeding Disorder, Haemophilia B With Inhibitors, and Haemophilia A With Inhibitors.",,,,Eptacog alfa pegol (activated) is investigational.,,True
21534,Olaptesed Pegol has been investigated for the treatment of Hematopoietic Stem Cell Transplantation.,,,,Olaptesed Pegol is investigational.,,True
21535,Abicipar Pegol has been used in trials studying the treatment of Macular Edema and Macular Degeneration.,,,,Abicipar Pegol is investigational.,,True
21536,"Lexaptepid Pegol has been used in trials studying the treatment of Anemia, Inflammation, Chronic Diseases, End Stage Renal Disease, and Anemia of Chronic Disease.",,,,Lexaptepid Pegol is investigational.,Lexaptepid Pegol is a solid.,True
21537,"Pegvaliase is a recombinant phenylalanine ammonia lyase (PAL) enzyme derived from _Anabaena variabilis_ that converts phenylalanine to ammonia and _trans_-cinnamic acid. Both the U.S. Food and Drug Administration and European Medicines Agency approved pegvaliase-pqpz in May 2018 for the treatment of adult patients with phenylketonuria (PKU). Phenylketonuria is a rare autosomal recessive disorder that is characterized by deficiency of the enzyme phenylalanine hydroxylase (PAH) and affects about 1 in 10,000 to 15,000 people in the United States. PAH deficiency and inability to break down an amino acid phenylalanine (Phe) leads to elevated blood phenylalanine concentrations and accumulation of neurotoxic Phe in the brain, causing chronic intellectual, neurodevelopmental and psychiatric disabilities if untreated. Individuals with PKU also need to be under a strictly restricted diet as Phe is present in foods and products with high-intensity sweeteners. The primary goal of lifelong treatment of PKU, as recommended by the American College of Medical Genetics and Genomics (ACMG) guidelines, is to maintain blood Phe concentration in the range of 120 µmol/L to 3690 µmol/L. Pegvaliase-pqpz, or PEGylated pegvaliase, is used as a novel enzyme substitution therapy and is marketed as Palynziq for subcutanoues injection. It is advantageous over currently available management therapies for PKU, such as , that are ineffective to many patients due to long-term adherence issues or inadequate Phe-lowering effects. The presence of a PEG moiety in pegvaliase-pqpz allows a reduced immune response and improved pharmacodynamic stability. Pegvaliase is indicated for the management of phenylketonuria (PKU) in adult patients who have uncontrolled blood phenylalanine concentrations greater than 600 micromol/L on existing management.  In a phase 3 clinical trial of adult patients with phenylketonuria and blood phenylalanine concentrations greater than 600 µmol/L on existing management therapies, subcutaneous administration of pegvaliase resulted in significantly reduced blood phenylalanine concentrations in most patients compared to their pre-treatment baseline levels within 24 months in addition to improved neuropsychiatric symptoms.  Pegvaliase is a phenylalanine ammonia lyase (PAL) enzyme that temporarily restores the levels of deficient enzyme and reduces blood phenylalanine concentrations by converting phenylalanine to ammonia and _trans_-cinnamic acid. Formed conversion products are metabolized in the liver and later excreted in the urine. ",,,,Pegvaliase is approved and investigational.,Pegvaliase is a solid.,True
21538,"Pegamotecan has been used in trials studying the treatment of Cancer of Stomach, Sarcoma, Soft Tissue, and Gastroesophageal Cancer.",,,,Pegamotecan is investigational.,,True
21539,"Elapegademase is a PEGylated recombinant adenosine deaminase. It can be defined molecularly as a genetically modified bovine adenosine deaminase with a modification in cysteine 74 for serine and with about 13 methoxy polyethylene glycol chains bound via carbonyl group in alanine and lysine residues. Elapegademase is generated in _E. coli_, developed by Leadiant Biosciences and FDA approved on October 5, 2018. Elapegademase is approved for the treatment of adenosine deaminase severe combined immune deficiency (ADA-SCID) in pediatric and adult patients. This condition was previously treated by the use of bovine pegamedase as part of an enzyme replacement therapy. In clinical trials, elapegademase was shown to increase adenosine deaminase activity while reducing the concentrations of toxic metabolites which are the hallmark of ADA-SCID. As well, it was shown to improve the total lymphocyte count. The ADA-SCID is caused by the presence of mutations in the ADA gene which is responsible for the synthesis of adenosine deaminase. This enzyme is found throughout the body but it is mainly active in lymphocytes. The normal function of adenosine deaminase is to eliminate deoxyadenosine, created when DNA is degraded, by converting it into deoxyinosine. This degradation process is very important as deoxyadenosine is cytotoxic, especially for lymphocytes. Immature lymphocytes are particularly vulnerable as deoxyadenosine kills them before maturation making them unable to produce their immune function.",,,,Elapegademase is approved.,Elapegademase is a solid.,True
21540,"Ferric Carboxymaltose is an iron replacement product and chemically, an iron carbohydrate complex. FDA approved on July 25, 2013. Ferric carboxymaltose is a iron replacement product indicated for the treatment of iron deficiency anemia in adult patients who have intolerance to oral iron or have had unsatisfactory response to oral iron or those who have non-dialysis dependent chronic kidney disease.  When measured using positron emission tomography (PET), the red cell uptake of 59-Fe and 52-Fe from INJECTAFER ranged from 61% to 99%. In patients with iron deficiency, the red cell uptake ranged from 91% to 99%. In patients with renal anemia, the red cell uptake ranged from 61% to 84%.  Ferric carboxymaltose is a colloidal iron (III) hydroxide in complex with carboxymaltose, a carbohydrate polymer that release iron. ",,,,Ferric carboxymaltose is approved.,Ferric carboxymaltose is a solid.,True
21541,"Ferrous bisglycinate is a chelate that is used as a source of dietary iron. Forming a ring structure when reacting with glycine, ferrous bisglycinate acts as both a chelate and a nutritionally functional. It is found in foods for food enrichment or in supplements for the treatment of iron deficiency or iron deficiency anemia.",The molecular weight is 203.96.,Ferrous bisglycinate has a topological polar surface area of 85.82.,,Ferrous bisglycinate is approved.,,True
21542,"Iron isomaltoside 1000 is under investigation in Iron Deficiency Anaemia. Iron isomaltoside 1000 has been investigated for the treatment and basic science of Anemia, Gastric Cancer, Esophageal Cancer, Chronic Kidney Disease, and Anemia, Iron-Deficiency, among others.",,,,Iron isomaltoside 1000 is approved and investigational.,,True
21543,,The molecular weight is 126.75.,,,Ferrous chloride is experimental.,,False
21544,Mephenesin is a synthetic cresol glyceryl ether which produces transient muscle relaxation and paralysis via central nervous system depression. It first entered use in the 1950s. Mephenesin was used for the treatment of muscle spasticity in diseases like Parkinson's or Multiple Sclerosis. Mephenesin reduced neuronal excitability leading to decreases action potentials to muscle fibers which ultimately produces a reduction in spasticity. The exact mechanism of action of mephenesin is not known. It has been observed to block both inward sodium and inward calcium currents in neurons. It has a physiological effect which opposes that of strychnine.,The molecular weight is 182.22.,Mephenesin has a topological polar surface area of 49.69.,The log p value of  is 0.86.,Mephenesin is approved.,Mephenesin is a solid.,True
21545,,,,,Ecgonine is experimental and illicit.,Ecgonine is a solid.,False
21546,Dimetotiazine has considerable antiemetic & serotonin antagonistic action used mainly in allergic skin conditions.,The molecular weight is 391.55.,Dimetotiazine has a topological polar surface area of 43.86.,The log p value of  is 4.13.,Dimetotiazine is approved.,Dimetotiazine is a solid.,True
21547,"Aptazapine (CGS-7525A) was a tetracyclic antidepressant developed in the 1980s. Aptazapine had noradrenergic and specific serotonergic activity. It antagonised α2 adrenergic receptors approximately 10 times more effectively than mianserin, antagonised 5-HT2 receptors, agonised H1 receptors, and did not affect reuptake of serotonin or norepinephrine. Although Aptazapine reached clinical trials, it was never marketed. Investigated for the treatment of depression.",,,,Aptazapine is experimental.,Aptazapine is a solid.,True
21548,ORM-12741 has been used in trials studying the basic science and treatment of Alzheimer's Disease.,,,,ORM-12741 is investigational.,,True
21549,"Gsk1004723 has been investigated for the treatment of Allergic Rhinitis and Rhinitis, Allergic, Seasonal.",,,,GSK-1004723 is investigational.,,True
21550,,The molecular weight is 333.48.,Deptropine has a topological polar surface area of 12.47.,The log p value of  is 4.21.,Deptropine is experimental.,,False
21551,,The molecular weight is 500.55.,Tritoqualine has a topological polar surface area of 110.94.,The log p value of  is 2.72.,Tritoqualine is approved.,,False
21552,,,,,Magnesium ascorbate is approved and nutraceutical.,,False
21553,GSK-239512 is under investigation in clinical trial NCT00474513 (An Imaging Study to Investigate the Distribution of GSK239512 in the Brain.).,,,,GSK-239512 is investigational.,,True
21554,ABT-288 is under investigation in clinical trial NCT01018875 (Efficacy and Safety Study of ABT-288 in Subjects With Mild-to-Moderate Alzheimer's Disease).,,,,ABT-288 is investigational.,,True
21555,Artefenomel has been investigated for the treatment of Malaria.,,,,Artefenomel is investigational.,,True
21556,Chlorproguanil has been used in trials studying the treatment of MALARIA. It is a dichloro-derivative of chloroguanide.,The molecular weight is 288.18.,Chlorproguanil has a topological polar surface area of 83.79.,The log p value of  is 3.22.,Chlorproguanil is investigational.,,True
21557,"Artemotil, also known as β-arteether, is a semi-synthetic derivative of artemisinin and a fast acting blood schizonticide specifically indicated for the treatment of chloroquine-resistant _Plasmodium falciparum_ malaria and cerebral malaria cases.",The molecular weight is 312.41.,Artemotil has a topological polar surface area of 46.15.,The log p value of  is 3.44.,Artemotil is approved.,,True
21558,Cycloguanil is the active metabolite of.,The molecular weight is 251.72.,Cycloguanil has a topological polar surface area of 80.0.,The log p value of  is 1.07.,Cycloguanil is approved.,,True
21559,"Pristinamycin IIA is a macrolide antibiotic, a member of the streptogramin A group of antibiotics, and one component of pristinamycin. It is produced by Streptomyces graminofaciens and other bacteria. For the treatment of bacterial infections. Virginiamycin M1 is a macrocyclic lactone antibiotic that acts syngeristically with the structurally unrelated cyclic depsipeptides more commonly known as the virginiamycins B (ostreogrycin B or streptogramin B) and S to inhibit peptide elongation. This is achieved by blocking formation of a peptide bond between the growing peptide chain (peptidyl-tRNA) linked to the 50S ribosome and aminoacyl-tRNA. Virginiamycin M1 has proven to be highly active against Gram positive bacteria, particularly methicillin-resistant S. aureus.",,,,Virginiamycin M1 is experimental.,Virginiamycin M1 is a solid.,True
21560,"Sinefungin is a solid. This compound belongs to the purine nucleosides and analogues. These are compounds comprising a purine base attached to a sugar. The proteins that adenosyl-ornithine target include RdmB, modification methylase TaqI, rRNA (adenine-N6-)-methyltransferase, and modification methylase RsrI.",,,,Sinefungin is experimental.,Sinefungin is a solid.,True
21561,,,,,Maltotetraose is experimental.,Maltotetraose is a solid.,False
21562,"A phenol obtained from thyme oil or other volatile oils. It is used as a stabilizer in pharmaceutic preparations. It has been used for its antiseptic, antibacterial, and antifungal actions, and was formerly used as a vermifuge. (Dorland, 28th ed)",The molecular weight is 150.22.,Thymol has a topological polar surface area of 20.23.,The log p value of  is 3.2.,Thymol is approved.,Thymol is a solid.,True
21563,Pyroquilon is a commercial blasticide which binds in the naphthol pocket of fungal trihydroxynaphthalene reductase active site.,,,,Pyroquilon is experimental.,Pyroquilon is a solid.,True
21564,,,,,Fosmidomycin is experimental and investigational.,Fosmidomycin is a solid.,False
21565,,,,,GE-2270A is experimental.,GE-2270A is a solid.,False
21566,,,,,Salicylhydroxamic Acid is experimental.,Salicylhydroxamic Acid is a solid.,False
21567,Aurodox is an antibiotic obtained from a streptomyces variant considered as possibly effective against streptococcus pyogenes infections. It may promote growth in poultry.,,,,Aurodox is experimental.,Aurodox is a solid.,True
21568,,,,,Lawsone is experimental.,Lawsone is a solid.,False
21569,"Streptolydigin is an antibiotic isolated from culture filtrates of Streptomyces lydicus. It is active against gram-postive bacteria except micrococci. Streptolydigin is an antibiotic which works by blocking nucleic acid chain elongation by binding to the polymerase, thus stopping RNA polymerase activity inside a cell. Specifically, it inhibits the assembly of the RNA polymerase II transcription complex and DNA polymerase III transcription. It is active against a number of gram positive bacteria.",,,,Streptolydigin is experimental.,Streptolydigin is a solid.,True
21570,"Ramoplanin is a novel glycolipodepsipeptide antibiotic under development for the treatment of CDAD. For the treatment of bacterial infections. Ramoplanin represents a new class of antibiotics with a novel mechanism of action that is highly effective against <i>Staphylococci</i>. Ramoplanin is the first in a new class of antimicrobials to reach clinical trials. It is a glycolipodepsipeptide produced by the fermentation of <i>Actinoplanes spp.</i>. Ramoplanin blocks bacterial cell wall biosynthesis by interfering with peptidoglycan production. Ramoplanin inhibits the N-acetylglucosaminyltransferase-catalysed conversion of lipid intermediate I to lipid intermediate II, a step that occurs before the transglycosylation and transpeptidation reactions. Ramoplanin’s mechanism of action is distinct from that of glycopeptides. Unlike glycopeptides, ramoplanin does not complex with the D-Ala–D-Ala sequence of cell wall precursors.",,,,Ramoplanin is investigational.,Ramoplanin is a solid.,True
21571,"Spiramycin is a primarily bacteriostatic macrolide antimicrobial agent with activity against Gram-positive cocci and rods, Gram-negative cocci and also Legionellae, mycoplasmas, chlamydiae, some types of spirochetes, Toxoplasma gondii and Cryptosporidium. Macrolide antibiotic for treatment of various infections. The absolute bioavailability of oral spiramycin is generally within the range of 30 to 40%. After a 1 g oral dose, the maximum serum drug concentration was found to be within the range 0.4 to 1.4 mg/L. The mechanism of action of macrolides has been a matter of controversy for some time. Spiramycin, a 16-membered macrolide, inhibits translocation by binding to bacterial 50S ribosomal subunits with an apparent 1 : 1 stoichiometry. This antibiotic is a potent inhibitor of the binding to the ribosome of both donor and acceptor substrates. The primary mechanism of action is done by stimulation of dissociation of peptidyl-tRNA from ribosomes during translocation.I ",The molecular weight is 843.06.,Spiramycin has a topological polar surface area of 195.38.,The log p value of  is 2.01.,Spiramycin is approved.,Spiramycin is a solid.,True
21572,"Investigated for use/treatment in ovarian cancer, lung cancer, and macular degeneration.",,,,Squalamine is investigational.,Squalamine is a solid.,True
21573,,The molecular weight is 356.21.,Thiamphenicol has a topological polar surface area of 103.7.,The log p value of  is -0.1.,Thiamphenicol is experimental and investigational.,Thiamphenicol is a solid.,False
21574,A bactericidal and fungicidal antiseptic. It is used as a 0.1% mouthwash for local infections and oral hygiene.,The molecular weight is 339.61.,Hexetidine has a topological polar surface area of 32.5.,The log p value of  is 8.14.,Hexetidine is approved and investigational.,Hexetidine is a solid.,True
21575,"Fusafungine is an antibiotic from Fusarium lateririum, and is used for the treatment of respiratory infections.",,,,Fusafungine is approved and withdrawn.,Fusafungine is a solid.,True
21576,,,,,Avilamycin is vet_approved.,,False
21577,"Bambermycins are antibiotic complexes which are retrieved from the organism, _Streptomyces bambergiensis_. They are used as an additive in food ingested by chickens and swine. The bambermycin complex of antibiotics consists primarily of moenomycins A and C.",,,,Bambermycins is vet_approved.,,True
21578,,,,,Efrotomycin is vet_approved.,,False
21579,Florfenicol is a fluorinated synthetic analog of thiamphenicol.,,,,Florfenicol is experimental and vet_approved.,,True
21580,Gamithromycin is an antibiotic used in cattle.,,,,Gamithromycin is vet_approved.,,True
21581,Lasalocid is an agent that presents antibacterial and coccidiostat activities. It is produced by strains of _Streptomyces lasaliensis_.,,,,Lasalocid is vet_approved.,,True
21582,"Marbofloxacin is a carboxylic acid, part of the third generation of antibiotic fluoroquinolones. It is used in veterinary. A formulation of marbofloxacin combined with clotrimazole and dexamethasone is available under the name Aurizon.",,,,Marbofloxacin is vet_approved.,,True
21583,Narasin is an agent with coccidiostatic and antibacterial properties.,,,,Narasin is experimental and vet_approved.,,True
21584,Roxarsone is an organoarsenic molecule added to poultry feed. The addition of this compound to poultry feed improves weight gain and feed efficiency as well as prevent the growth of coccidian parasites. The drug is also approved in the United States for use in pigs.,,,,Roxarsone is vet_approved.,,True
21585,"Thiostrepton is a natural cyclic oligopeptide antibiotic, derived from several strains of streptomycetes including Streptomyces azureus and Streptomyces laurentii. Thiostrepton is a natural product of the ribosomally synthesized and post-translationally modified peptide class.",,,,Thiostrepton is vet_approved.,,True
21586,Tiamulin is a pleuromutilin antibiotic drug that is used in veterinary medicine particularly for pigs and poultry.,,,,Tiamulin is vet_approved.,,True
21587,Tulathromycin is a macrolide antibiotic used to treat bovine respiratory disease in cattle and swine respiratory disease in pigs. It is marketed by Pfizer Inc. under the tradename Draxxin.,,,,Tulathromycin A is vet_approved.,,True
21588,"Ceftiofur is a third generation cephalosporin antibiotic, first described in 1987, and now used in veterinary medicine. It is marketed by pharmaceutical company Zoetis as Excenel, and is the active ingredient in that company's Specramast LC (lactating cow formula) product. It is resistant to hydrolysis by beta-lactamase, and has activity against both Gram-positive and Gram-negative bacteria. E. coli strains resistant to ceftiofur have been reported. The metabolite desfurolyceftiofur also has antibiotic activity, consequently the two compounds are measured together to monitor for antibiotic activity in the milk.",,,,Ceftiofur is vet_approved.,Ceftiofur is a solid.,True
21589,"Maduramicin is an antiprotozoal agent used in veterinary medicine as prophylaxis against coccidiosis. It is a naturally occurring compound which was first isolated from the actinomycete, Actinomadura rubra.",,,,Maduramicin is vet_approved.,,True
21590,,,,,Isatoic anhydride is experimental.,Isatoic anhydride is a solid.,False
21591,"Epetraborole has been used in trials studying the treatment of Infections, Bacterial, Infections, Intestinal, Infections, Urinary Tract, and Community-acquired Infection.",,,,Epetraborole is investigational.,,True
21592,"Lanopepden has been used in trials studying the treatment of Pneumonia, Infections, Bacterial, Skin Diseases, Infectious, and Skin Infections, Bacterial.",,,,Lanopepden is investigational.,,True
21593,Cordycepin has been used in trials studying the treatment of Leukemia.,,,,Cordycepin is investigational.,,True
21594,Prothionamide has been used in trials studying the treatment of MDR-TB and HIV Infections.,The molecular weight is 180.27.,Protionamide has a topological polar surface area of 38.91.,The log p value of  is 2.26.,Protionamide is approved and investigational.,,True
21595,Nikkomycin Z has been used in trials studying the treatment and basic science of Coccidioidomycosis.,,,,Nikkomycin Z is investigational.,,True
21596,Biapenem has been used in trials studying the treatment of Bacterial Infections.,The molecular weight is 350.39.,Biapenem has a topological polar surface area of 102.37.,The log p value of  is -8.73.,Biapenem is investigational.,,True
21597,"Lcb01 0371 is under investigation in clinical trial NCT01554995 (A Clinical Study, Randomized, Double-blind, Placebo-controlled, Single Dose Study).",,,,LCB01-0371 is investigational.,,True
21598,"Tunicamycin is a mixture of homologous nucleoside antibiotics that inhibits the UDP-HexNAc: polyprenol-P HexNAc-1-P family of enzymes. One member of this family is the enzyme GlcNAc phosphotransferase (GPT), which catalyzes the transfer of N-acetylglucosamine-1-phosphate from UDP-N-acetylglucosamine to dolichol phosphate in the first step of glycoprotein synthesis in eukaryotes. Tunicamycin blocks N-linked glycosylation (N-glycans) resulting in cell cycle arrest at the G1 phase in human cells. It is used as an experimental tool to induce unfolded protein response. Tunicamycin is produced by Streptomyces clavuligerus and Streptomyces lysosuperficus bacteria along with several other species.",,,,Tunicamycin is experimental.,Tunicamycin is a solid.,True
21599,,The molecular weight is 295.26.,Azidamfenicol has a topological polar surface area of 144.81.,The log p value of  is 0.9.,Azidamfenicol is experimental.,,False
21600,,The molecular weight is 291.39.,Pecilocin has a topological polar surface area of 57.61.,The log p value of  is 1.58.,Pecilocin is experimental.,,False
21601,,The molecular weight is 670.84.,Pentamycin has a topological polar surface area of 228.6.,The log p value of  is 2.47.,Pentamycin is experimental.,,False
21602,,The molecular weight is 257.07.,Pyrrolnitrin has a topological polar surface area of 61.61.,The log p value of  is 3.67.,Pyrrolnitrin is experimental.,,False
21603,,The molecular weight is 1349.51.,Pristinamycin has a topological polar surface area of 224.72.,,Pristinamycin is experimental and investigational.,,False
21604,,The molecular weight is 623.02.,Decamethoxine has a topological polar surface area of 52.6.,The log p value of  is 3.54.,Decamethoxine is experimental.,,False
21605,,The molecular weight is 285.27.,Nifuratel has a topological polar surface area of 100.86.,The log p value of  is 0.79.,Nifuratel is experimental.,,False
21606,"Malacidin A, along with , is a member of a class of chemicals made by bacteria found in soil that can kill Gram-positive bacteria. Malacidins are 10-member macrocycle lipopeptides discovered via gene sequencing and bioinformatic analysis. While structurally similar to other macrocycle drugs like and , Malacidin A appears to act via its own distinct mechanism. Malacidin A is being investigated for its antibiotic action and has potential for use as an antibacterial agent in the future. Malacidin A disrupts bacterial cell wall synthesis likely leading to cell death in Gram-positive bacteria. This bactericidal effect reduces the number of live bacteria present during infection. Malacidin A has exhibited broad spectrum activity against Gram-positive bacteria including several multi-drug resistant pathogens. Malacidin A appears to bind Lipid II via a calcium dependent mechanism despite the absence of the typical Asp-X-Asp-Gly motif associate with calcium binding. The structure of Malacidin A includes a 3-hydroxy-aspartate residue while the \X\"" variable spacer residue is absent. It is unknown how these unique structural features may impact the drug's mechanism of action. The binding of Malacidin A to Lipid II prevents the incorporation of the subunit into the cell wall, disrupting synthesis and likely resulting in death of the bacterial cell. Malacidin A does not appear to form pores nor does it seem to integrate into the cell wall. While this mechanism is similar to that of , Malacidin A retains its activity against -resistant pathogens. Unlike other antibiotic agents, Malacidin A also retains its activity in the presence of pulmonary surfactants.""",,,,Malacidin A is experimental.,Malacidin A is a solid.,True
21607,"Malacidin B, along with , is a member of a class of chemicals made by bacteria found in soil that can kill Gram-positive bacteria. Malacidins are 10-member macrocycle lipopeptides discovered via gene sequencing and bioinformatic analysis. While structurally similar to other macrocycle drugs like and , Malacidin B appears to act via its own distinct mechanism. Malacidin B is being investigated for its antibiotic action and has potential for use as an antibacterial agent in the future. Malacidin B disrupts bacterial cell wall synthesis likely leading to cell death in Gram-positive bacteria. This bactericidal effect reduces the number of live bacteria present during infection. Malacidin B has exhibited broad spectrum activity against Gram-positive bacteria including several multi-drug resistant pathogens. Malacidin B appears to bind Lipid II via a calcium dependent mechanism despite the absence of the typical Asp-X-Asp-Gly motif associate with calcium binding. The structure of Malacidin B includes a 3-hydroxy-aspartate residue while the \X\"" variable spacer residue is absent. It is unknown how these unique structural features may impact the drug's mechanism of action. The binding of Malacidin B to Lipid II prevents the incorporation of the subunit into the cell wall, disrupting synthesis and likely resulting in death of the bacterial cell. Malacidin B does not appear to form pores nor does it seem to integrate into the cell wall. While this mechanism is similar to that of , Malacidin B retains its activity against -resistant pathogens. Unlike other antibiotic agents, Malacidin B also retains its activity in the presence of pulmonary surfactants.""",,,,Malacidin B is experimental.,Malacidin B is a solid.,True
21608,"A polyether antibiotic which affects ion transport and ATPase activity in mitochondria. It is produced by Streptomyces hygroscopicus. (From Merck Index, 11th ed)",,,,Nigericin is experimental.,Nigericin is a solid.,True
21609,"Basifungin, also known as _aureuobacidin A_, is a phosphorylceramide synthase inhibitor ,.",,,,Basifungin is experimental.,Basifungin is a solid.,True
21610,Ceftobiprole medocaril is a prodrug.,The molecular weight is 690.66.,Ceftobiprole medocaril has a topological polar surface area of 256.48.,The log p value of  is -2.18.,Ceftobiprole medocaril is experimental and investigational.,,True
21611,Murepavadin is under investigation in clinical trial NCT02110459 (Pharmacokinetics and Safety of POL7080 in Patients With Renal Impairment).,,,,Murepavadin is investigational.,,True
21612,Olorofim is under investigation in clinical trial NCT03340597 (Assessment of Varying Oral Dosing Regimens for F901318 in Healthy Subjects).,,,,Olorofim is investigational.,,True
21613,"Ala-geninthiocin is a novel thiopeptide antibacterial compound derived from marine _Streptomyces_ species. It has exhibited potent _in vitro_ activity against gram-positive bacteria including _Staphylococcus aureus_, _Bacillus subtilis_, _Mycobacterium smegmatis_, and _Micrococcus luteus_.",,,,Ala-geninthiocin is experimental.,,True
21614,"Corticorelin, available commercially as corticorelin ovine triflutate (tradename Acthrel), is a synthetic form of the peptide human corticotropin-releasing hormone (hCRH), a potent stimulator of adrenocorticotropic hormone (ACTH) release from the anterior pituitary. Endogenous forms hCRH are involved in the stress response and its main function is stimulation of the pituitary to release ACTH.  Corticorelin is indicated for use in differentiating pituitary and ectopic production of ACTH in patients with ACTH-dependent Cushing's syndrome. In normal subjects, intravenous administration of corticorelin results in a rapid and sustained increase of plasma ACTH levels and a near parallel increase of plasma cortisol. In addition, intravenous administration of corticorelin to normal subjects causes a concomitant and prolonged release of the related proopiomelanocortin peptides β- and γ-lipotropins (β -and γ-LPH) and β-endorphin (β -END). Corticorelin is a potent stimulator of adrenocorticotropic hormone (ACTH) release from the anterior pituitary. It is used as a diagnostic agent to evaluate the status of the pituitary-adrenal axis in the differentiation of a pituitary source from an ectopic source of excessive ACTH secretion.",,,,Corticorelin ovine triflutate is approved.,Corticorelin ovine triflutate is a solid.,True
21615,"Amorolfine or amorolfin, is a morpholine antifungal drug that inhibits the fungal enzymes D14 reductase and D7-D8 isomerase. This inhibition affects fungal sterol synthesis pathways, depleting ergosterol and causing ignosterol to accumulate in the fungal cytoplasmic cell membranes. Amorolfine is marketed as Curanail, Loceryl, Locetar, and Odenil. It is available in the form of a 5% amorolfine nail lacquer used to treat onychomycosis (fungal infection of the toe- and fingernails). Amorolfine 5% nail lacquer in once or twice weekly applications is 60-71% effective in treating toenail onychomycosis; complete cure rates three months after stopping treatment (after six months of treatment) were 38-46%. However, full experimental details of these trials were not available and since they were first reported in 1992 there have been no subsequent trials.",The molecular weight is 317.52.,Amorolfine has a topological polar surface area of 12.47.,The log p value of  is 6.43.,Amorolfine is approved and investigational.,Amorolfine is a solid.,True
21616,"Ethiodized oil is used by injection as a radio-opaque contrast agent. The composition of the oil is comprised of iodine combined with ethyl esters of fatty acids of poppyseed oil. And although these esters are primarily as ethyl monoiodostearate and ethyl diiodostearate, the actual, specific structure is unknown. For use as a radio-opaque medium for hysterosalpingography and lymphography, and as an antineoplastic agent when part of the iodine is 131-I. It is also used in follow-up imaging for chemoembolization. There has been little detailed investigation of the metabolic fate of ethiodized oil in either man or animals. However, the fate of ethiodized oil following Iymphangiography in dogs has been reported. Koehler <i>et al</i>. employed I<sup>131</sup>-tagged ethiodol for lymphangiography in dogs and analyses of individual organs at various time intervals were done. The investigators reported an average of only 25% of the injected medium was retained in the lymphatics at the end of three days. An average of 50% was recovered from the lungs. They found the remainder of injected activity was fairly uniformly distributed throughout the body. Urinary excretion in the form of inorganic iodine was revealed as the chief mode of iodine loss from the system. Ethiodized oil is selectively retained in tumor vessels for long periods, and is used for imaging organs such as liver, lung, stomach, and thyroid. Labeled with I-131 or other beta emitters (Y-90 or P-32), ethiodized oil can deliver a high internal radiation dose to certain tumors with minimal effect on healthy tissues.",,,,Ethiodized oil is approved and investigational.,Ethiodized oil is a liquid.,True
21617,"Iohexol is an effective non-ionic, water-soluble contrast agent which is used in myelography, arthrography, nephroangiography, arteriography, and other radiographic procedures. Its low systemic toxicity is the combined result of low chemotoxicity and low osmolality. Iohexol ia used in myelography, arthrography, nephroangiography, arteriography, and other radiographic procedures. Iohexol is an effective non-ionic, water-soluble contrast agent which is used in myelography, arthrography, nephroangiography, arteriography, and other radiographic procedures. Its low systemic toxicity is the combined result of low chemotoxicity and low osmolality. Organic iodine compounds block x-rays as they pass through the body, thereby allowing body structures containing iodine to be delineated in contrast to those structures that do not contain iodine. The degree of opacity produced by these compounds is directly proportional to the total amount (concentration and volume) of the iodinated contrast agent in the path of the x-rays. After intrathecal administration into the subarachnoid space, diffusion of iohexol in the CSF allows the visualization of the subarachnoid spaces of the head and spinal canal. After intravascular administration, iohexol makes opaque those vessels in its path of flow, allowing visualization of the internal structures until significant hemodilution occurs.",The molecular weight is 821.14.,Iohexol has a topological polar surface area of 199.89.,The log p value of  is -2.44.,Iohexol is approved.,Iohexol is a solid.,True
21618,"Iopamidol is a contrast agent developed by Bracco with nonionic, low-osmolar properties.",The molecular weight is 777.09.,Iopamidol has a topological polar surface area of 188.45.,The log p value of  is -2.24.,Iopamidol is approved.,Iopamidol is a solid.,True
21619,"Glucarpidase is the recombinant form of the Pseudomonas sp. (strain RS-16) enzyme carboxypeptidase G2 that is produced in Escherichia coli. In patients, glucarpidase inactivates methotrexate, and other antifolates, by hydrolyzing glutamate on the carboxyl terminal of these compounds. Therefore since methotrexate is eliminated enzymatically and not by the kidneys, glucarpidase is indicated in patients on methotrexate treatment who have kidney dysfunction, and are experiencing an abnormally high plasma concentration of methotrexate (>1 micromole per liter). Glucarpidase is marketed under the brand name Voraxaze®. Used in patients on methotrexate treatment who have kidney dysfunction, and are experiencing an abnormally high plasma concentration of methotrexate (> 1 micromole per liter). Glucarpidase acts as an antidote to toxic methotrexate levels by elminating methotrexate by a non-kidney route. Glucarpidase inactivates methotrexate, and other antifolates, by hydrolyzing glutamate on the carboxyl terminal of these compounds. For methotrexate specifically, it is hydrolyzed to the inactive metabolites glutamate and 4-deoxy-4-amino-N10-methylpteroic acid (DAMPA).",,,,Glucarpidase is approved and investigational.,Glucarpidase is a solid.,True
21620,"MAXY-G34 is a pegylated variant of human granulocyte-colony stimulating factor (G-CSF). This variant contains multiple non-naturally occurring lysines that have been introduced into alpha helixes of wild type human G-CSF as PEGylation sites, and from which multiple undesired, naturally occurring lysines have been removed as compared to wild type human G-CSF to avoid PEGylation of such sites. Specifically, the amino acid sequence of MAXY-G34 differs from that of human wild type G-CSF at residues 16, 34, 40, 105 and 159. This was accomplished by removing the three lysine residues at positions 16, 34 and 40, and replacing them with arginine, and substituting two new lysine residues at positions 105 and 159. MAXY-G34 is pegylated with 5 kd mPEG SPA (succinimidyl propionate) groups at 3 amino acid residues, including PEG groups attached at the amino terminal end of the protein and at two internal lysine residues, while Neulasta has a single 20 Kd PEG group attached at the N terminal end of the wild type G-CSF protein. It is being developed by Maxygen, Inc. for the treatment of chemotherapy-induced neutropenia. Investigated for use/treatment in adverse effects (chemotherapy) and neutropenics. Maxy-G34 is a PEGylated proprietary G-CSF variant designed to be administered as a single subcutaneous injection once per chemotherapy cycle. Maxygen has made changes in the G-CSF gene sequence that code for novel PEGylation sites in the resulting protein. In contrast to the currently marketed PEGylated G-CSF, Maxy-G34 has multiple PEG groups attached at specifically selected sites on the molecule. In several in vivo models, Maxy- G34 has demonstratedimproved pharmacokinetics and pharmacodynamics compared to the currently marketed PEGylated G-CSF. Neutropenia is a severe decrease in neutrophil cell counts in the blood. Neutropenia is a common side effect of chemotherapeutic treatments for many forms of cancer, including breast cancer, lung cancer, lymphomas and leukemias. Neutropenic patients contract bacterial infections more easily and often, some of which can be life threatening. Further, and most importantly, neutropenic patients may receive reduced or delayed chemotherapy treatment, which can result in cancer progression. Maxy-G34, like natural G-CSF is a protein that stimulates the body's bone marrow to produce neutrophils, a specific type of white blood cell that plays an important role in the defense against bacterial infections.",,,,Maxy-G34 is investigational.,Maxy-G34 is a liquid.,True
21621,Epoetin Delta is an ingredient in the EMA-withdrawn product Dynepo.,,,,Epoetin delta is approved and investigational and withdrawn.,,True
21622,"Muplestim is under investigation in clinical trial NCT00002258 (A Phase I, Open Label Trial to Evaluate the Safety, Tolerance and Biological Effects of SDZ ILE-964 (Recombinant Human Interleukin-3, RhIL-3) in HIV Infected Patients With Cytopenia).",,,,Muplestim is investigational.,,True
21623,"Molgramostim has been used in trials studying the treatment of Bronchiectasis, Cystic Fibrosis, Pulmonary Alveolar Proteinosis, Acute Respiratory Distress Syndrome, and Autoimmune Pulmonary Alveolar Proteinosis.",,,,Molgramostim is investigational.,,True
21624,Balugrastim has been used in trials studying the treatment of Solid Tumors.,,,,Balugrastim is investigational.,,True
21625,Leridistim is under investigation in clinical trial NCT00004215 (Leridistim Compared With Filgrastim in Treating Older Patients With Acute Myeloid Leukemia).,,,,Leridistim is investigational.,,True
21626,Pegteograstim is under investigation in clinical trial NCT02787876 (Pegteograstim in Children With Solid Tumors).,,,,Pegteograstim is investigational.,,True
21627,Sodium bisulfite has been used externally for parasitic skin diseases and as gastrointestinal antiseptic.,,,,Sodium bisulfite is approved.,Sodium bisulfite is a solid.,True
21628,Flubendazole is an anthelmintic that is used to treat worm infection in humans. It is available OTC in Europe.,The molecular weight is 313.29.,Flubendazole has a topological polar surface area of 84.08.,The log p value of  is 3.25.,Flubendazole is experimental and withdrawn.,Flubendazole is a solid.,True
21629,,,,,Cambendazole is experimental and vet_approved.,,False
21630,"Fenbendazole is a benzimidazole that presents a wide spectrum anthelmintic effect. It is used against a number of gastrointestinal parasites including giardia, roundworms, hookworms, whipworms, the Taenia genus of tapeworms, pinworms, aelurostrongylus, paragonimiasis, strongyles, and Strongyloides. Fenbendazole is approved to be administered under veterinary to sheep, cattle, horses, fish, dogs, cats, rabbits and seals.",The molecular weight is 299.35.,Fenbendazole has a topological polar surface area of 67.01.,The log p value of  is 4.18.,Fenbendazole is vet_approved.,,True
21631,"Oxfendazole is a sulfoxide metabolite of fenbendazole. This benzimidazole antihelminthic protects livestock from roundworm. strongyles, and pinworn.",,,,Oxfendazole is investigational and vet_approved.,,True
21632,Agn 201904 has been used in trials studying the prevention of Peptic Ulcer.,,,,AGN-201904 is investigational.,,True
21633,,The molecular weight is 281.33.,Albendazole oxide has a topological polar surface area of 84.08.,The log p value of  is 1.7.,Albendazole oxide is experimental.,Albendazole oxide is a solid.,False
21634,,,,,Cephalosporin analog is experimental.,Cephalosporin analog is a solid.,False
21635,,,,,Cephalosporin C is experimental.,Cephalosporin C is a solid.,False
21636,,,,,Deacetoxycephalosporin C is experimental.,Deacetoxycephalosporin C is a solid.,False
21637,"Levopropoxyphene is a stereoisomer of propoxyphene in the form of 2S, 3R enantiomer. It was sold as an antitussive, but it was removed from the market in the 70s. Levopropoxyphene was developed by Lilly and FDA approved on March 21st, 1962. This drug presented different dosages and it was administered as a capsule or suspension. Levopropoxyphene was used as an antitussive. An antitussive is a medication often recommended for the treatment of cough and associated respiratory tract disorders. Its enantiomer, dextropropoxyphene, presents an analgesic effect.",The molecular weight is 339.48.,Levopropoxyphene has a topological polar surface area of 29.54.,The log p value of  is 5.21.,Levopropoxyphene is withdrawn.,Levopropoxyphene is a solid.,True
21638,"Sage oil is extracted from sage or *Salvia officinalis*, the herb commonly used for culinary purposes. *Salvia officinalis* is a common sage and a member of the genus *Salvia*, that includes aromatic and perennial plants with flowers. Essential oil has been traditionally used in medicine for the relief of pain and the treatment of inflammation and infections, as it is reported to exhibit carminative, antispasmodic, antiseptic, and astringent properties. The main constituents of sage oil include camphor, 1,8-cineole, α-thujone, β-thujone, borneol, and viridiflorol, which are thought to mainly produce the biological effects of sage oil. Sage oil also contains flavonoids and polyphenolic compounds that mediate strong antioxidant, radical-scavenging, and antibacterial activities. It is found in cosmetics, personal care products and dietary supplements.",,,,Sage oil is nutraceutical.,,True
21639,"Borage oil, or borage seed oil, is a rich source of gamma-linolenic acid (GLA) that is obtained from the seeds of the Borago officinalis (borage). Borage oil is used as an herbal treatment of skin disorders including eczema, seborrheic dermatitis, and neurodermatitis as well as other inflammatory, cardiovascular and endocrine disorders, although its clinical efficacy and long-term effects are not fully elucidated yet. GLA, which accounts for approximately 24% of the oil, is converted to dihomo-γ-linolenic acid (DGLA) which acts as a precursor to anti-inflammatory mediators such as 1-series prostaglandins and the 3-series leukotrienes. Borage oil may be found in foods or in skin care products.",,,,Borage oil is approved and investigational.,,True
21640,Misonidazole is under investigation in clinical trial NCT00038038 (Assessment of Head and Neck Tumor Hypoxia Using 18F-Fluoromisonidazole).,,,,Misonidazole is investigational.,,True
21641,"Gamolenic acid, or gamma-linolenic acid (γ-Linolenic acid) or GLA, is an essential fatty acid (EFA) comprised of 18 carbon atoms with three double bonds that is most commonly found in human milk and other botanical sources. It is an omega-6 polyunsaturated fatty acid (PUFA) also referred to as 18:3n-6; 6,9,12-octadecatrienoic acid; and cis-6, cis-9, cis-12- octadecatrienoic acid. Gamolenic acid is produced minimally in the body as the delta 6-desaturase metabolite of. It is converted to , a biosynthetic precursor of monoenoic prostaglandins such as PGE1. While Gamolenic acid is found naturally in the fatty acid fractions of some plant seed oils , and are rich sources of gamolenic acid. Evening primrose oil has been investigated for clinical use in menopausal syndrome, diabetic neuropathy, and breast pain, where gamolenic acid is present at concentrations of 7-14%. Gamolenic acid may be found in over-the-counter dietary supplements. Gamolenic acid is also found in some fungal sources and also present naturally in the form of triglycerides. Various clinical indications of gamolenic acid have been studied, including rheumatoid arthritis, atopic eczema, acute respiratory distress syndrome, asthma, premenstrual syndrome, cardiovascular disease, ulcerative colitis, ADHD, cancer, osteoporosis, diabetic neuropathy, and insomnia. Indicated as a dietary supplement for over-the-counter uses.  Gamolenic acid is converted to PGE1, which exhibits anti-inflammatory, antithrombotic, antiproliferative, and lipid-lowering effects. PGE1 also induces smooth muscle relaxation and vasodilation. Gamolenic acid is an essential component of membrane phospholipids, including the mitochondrial membrane, where it enhances the the integrity and the fluidity of the membrane.  Once gamolenic acid (GLA) is absorbed and converted to dihomo-gamolenic acid (DGLA), circulating DGLA fatty acids are converted to several lipid mediators with predominantly anti-inflammatory properties, such as prostaglandin-E1 (PGE1) and 15-HETrE. The anti-inflammatory effects of DGLA are attributed to both the anti-inflammatory properties of DGLA-derived metabolites and the ability of DGLA and its products to compete with arachidonic acid (AA) in the synthesis of pro-inflammatory potent eicosanoid products, such as prostaglandins, thromboxane and leukotrienes. Both PGE1 and 15-HETrE are known to suppress inflammation, promote vasodilation, lower blood pressure, inhibit smooth muscle cell proliferation, inhibit platelet aggregation, and exert anti-neoplastic activities. PGE1 is a potent vasodilator that binds to surface receptors on smooth muscle cells, increasing intracellular cAMP. PGE1 is binds to G protein coupled surface PGE (EP) receptors and prostacyclin (IP) receptors as a natural ligand. ",The molecular weight is 278.44.,Gamolenic acid has a topological polar surface area of 37.3.,The log p value of  is 6.82.,Gamolenic acid is approved and investigational.,Gamolenic acid is a liquid.,True
21642,Centella asiatica is a plant/plant extract used in some OTC (over-the-counter) products. It is not an approved drug.,,,,Centella asiatica is approved and experimental and investigational.,,True
21643,"Satraplatin is a platinum compound that is currently under investigation as one treatment of patients with advanced prostate cancer who have failed previous chemotherapy. As an investigation drug, it has not yet received U.S. Food and Drug Administration (FDA) approval and is not available in retail pharmacies. Investigated for use/treatment in lung cancer, prostate cancer, and solid tumors. This drug binds to the DNA of cancer cells, inhibiting cell division.",The molecular weight is 500.28.,,,Satraplatin is investigational.,Satraplatin is a solid.,True
21644,"Platinum is under investigation for the treatment of Metastatic Breast Cancer, Non-small Cell Lung Cancer, Gastric Large Cell Neuroendocrine Carcinoma, Colorectal Large Cell Neuroendocrine Carcinoma, and Pancreatic Large Cell Neuroendocrine Carcinoma, among others. Platinum has been investigated for the treatment and supportive care of Ovarian Cancer, Fallopian Tube Cancer, Peritoneal Primary Cancer, Non Small Cell Lung Cancer, and Primary Peritoneal Carcinoma, among others.",,,,Platinum is investigational.,,True
21645,Cg200745 has been used in trials studying the treatment of Solid Tumour.,,,,CG-200745 is investigational.,,True
21646,OBP-801 has been used in trials studying the treatment of Solid Tumor.,,,,OBP-801 is investigational.,,True
21647,R306465 has been used in trials studying the treatment of Neoplasms.,,,,R-306465 is investigational.,,True
21648,Tefinostat is under investigation in clinical trial NCT02759601 (Dose Escalation Trial of Tefinostat for Cancer Associated Inflamation in Hepatocellular Carcinoma (HCC)).,,,,Tefinostat is investigational.,,True
21649,"Nanatinostat is under investigation in clinical trial NCT00697879 (Safety Study of the Histone Deacetylase Inhibitor, CHR-3996, in Patients With Advanced Solid Tumours).",,,,Nanatinostat is investigational.,,True
21650,"Talc is a mineral composed primarily of magnesium, silicon and oxygen. It is a substance often found in cosmetic and personal hygiene products including baby powder, adult body powders and facial powders. Talc helps absorb moisture, freshen materials, and reduce friction to prevent rashes. Indicated to prevent recurrence of malignant pleural effusions in symptomatic patients during thoracoscopy or open thoracotomy. It has very good absorptive properties. ",,,,Talc is approved.,,True
21651,"Ascorbyl phosphate is a synthetic form of Vitamin C and is found in different salt forms such as magnesium ascorbyl phosphate and sodium ascorbyl phosphate. These salts are present in cosmetic products at concentrations ranging from 0.001 % to 3%. As vitamin C is susceptible to breakdown of compound and discoloration in cosmetic formulations, ascorbyl phosphate, along with other Vitamin C derivatives, acts as an active and stable precursor of vitamin C that is readily absorbed into the skin with a hydrating effect on the skin. While ascorbyl phosphate salts provide a constant delivery of vitamin C into the skin, they also mediate an antioxidant action to act as a free radical scavenger and increases collagen production *in vitro*.",,,,Ascorbyl phosphate is approved.,,True
21652,Benziodarone is a uricostatic and a uricosuric agent which is sold also under the name Amplivex-Labaz. It is used in the treatment of gout. It was withdrawn from France markets and British markets due to its effects causing Jaundice in patients.,The molecular weight is 518.09.,Benziodarone has a topological polar surface area of 50.44.,The log p value of  is 6.36.,Benziodarone is approved and withdrawn.,,True
21653,"19-Norandrostenedione refers to two steroid isomers that were once marketed as dietary supplements and mainly used by body builders. After 2005, 19-Norandrostenedione was regulated in the United States as a schedule III controlled substance, as well as banned from use in competitive sports by the World Anti-Doping Agency.  The claim that supplemental 19-norandrostenedione has anabolic effects is unsubstantiated. 19-Norandrostenedione may be metabolized to 19-nortestosterone in both men and women. 19-Norandrostenedione, also known as nandrolone, is the basic substance of some very popular injectable anabolic steroids, however 19-norandrostenedione is not metabolized to testosterone. Whether or not increases in 19-nortestosterone levels would be sustained long enough by taking 19-norandrostenedione to show an increase in nitrogen retention and muscle strength and mass is unknown.",,,,19-norandrostenedione is experimental and illicit.,19-norandrostenedione is a solid.,True
21654,,,,,Bolasterone is experimental and illicit.,Bolasterone is a solid.,False
21655,,The molecular weight is 322.87.,Clostebol has a topological polar surface area of 37.3.,The log p value of  is 4.18.,Clostebol is experimental and illicit.,Clostebol is a solid.,False
21656,"Androstenediol is an intermediate in biosynthesis, found in the testis or the adrenal glands. Androstenediol, derived from dehydroepiandrosterone by the reduction of the 17-keto group (17-hydroxysteroid dehydrogenases), is converted to testosterone by the oxidation of the 3-beta hydroxyl group to a 3-keto group (3-hydroxysteroid dehydrogenases).",The molecular weight is 290.45.,Androstenediol has a topological polar surface area of 40.46.,The log p value of  is 3.47.,Androstenediol is experimental and illicit.,Androstenediol is a solid.,True
21657,,The molecular weight is 388.55.,Bolandiol has a topological polar surface area of 52.6.,The log p value of  is 6.1.,Bolandiol is experimental and illicit.,Bolandiol is a solid.,False
21658,"Has antiproliferative effects on HIV-1 and reduces HIV-1 replication. Investigated for use/treatment in psoriasis and psoriatic disorders, hyperlipidemia, metabolic disease, cancer/tumors (unspecified), and obesity. Fluasterone is a synthetically stable adrenocortical steroid fluorinated analogue of dehydroepiandrosterone (DHEA), a powerful anti-inflammatory molecule with androgenic or estrogenic side effects. It is proposed that fluasterone inhibits NF-kB activation and reduces oxidative stress, but other mechanisms may play a role. Fluasterone suppresses",,,,Fluasterone is investigational.,Fluasterone is a solid.,True
21659,"Atamestane has been used in trials studying the treatment of Breast Cancer, Breast Neoplasms, and Neoplasms, Hormone-Dependent.",,,,Atamestane is investigational.,,True
21660,,The molecular weight is 302.46.,Metenolone has a topological polar surface area of 37.3.,The log p value of  is 3.93.,Metenolone is experimental.,,False
21661,"Verinurad has been used in trials studying the basic science and treatment of Gout, Gout and Hyperuricemia, and Gout and Asymptomatic Hyperuricemia.",,,,Verinurad is investigational.,,True
21662,,The molecular weight is 301.14.,Isobromindione has a topological polar surface area of 34.14.,The log p value of  is 3.71.,Isobromindione is experimental.,,False
21663,,The molecular weight is 152.18.,Tisopurine has a topological polar surface area of 53.07.,The log p value of  is -1.09.,Tisopurine is experimental.,,False
21664,An antineoplastic agent that acts by alkylation. For the treatment of polycythaemia vera and refractory chronic myeloid leukaemia. Pipobroman is an antineoplastic agent. Specifically it is a piperazine derivative with a chemical structure close to that of many DNA alkylating agents. Pipobroman has well documented clinical activity against polycythemia vera and essential thrombocythemia. The mechanism of action is uncertain but pipobroman is thought to alkylate DNA leading to disruption of DNA synthesis and eventual cell death.,The molecular weight is 356.06.,Pipobroman has a topological polar surface area of 40.62.,The log p value of  is 0.23.,Pipobroman is approved.,Pipobroman is a solid.,True
21665,"An antibiotic purine ribonucleoside that readily substitutes for adenosine in the biological system, but its incorporation into DNA and RNA has an inhibitory effect on the metabolism of these nucleic acids.",,,,Tubercidin is experimental.,Tubercidin is a solid.,True
21666,,,,,"3,4-Dihydroxybenzoic Acid is experimental.","3,4-Dihydroxybenzoic Acid is a solid.",False
21667,An antitumor antibiotic produced by Streptomyces sparsogenes. It inhibits protein synthesis in 70S and 80S ribosomal systems. ,,,,Sparsomycin is experimental.,Sparsomycin is a solid.,True
21668,"Thymalfasin is a chemically synthesized version of thymosin alpha 1 that is identical to human thymosin alpha 1. Thymosin alpha 1 is an acetylated polypeptide. Thymosin alpha 1 is now approved in 35 developing countries for the treatment of Hepatitis B and C. It is also used to boost the immune response in the treatment of other diseases. Indicated as an adjuvant for influenza vaccine in elderly patients and as an adjuvant for both influenza and hepatitis B vaccines in chronic hemodialysis patients who failed to achieve adequate antibody titers from previous immunization. Thymalfasin is a 28-amino acid polypeptide produced synthetically but originally isolated from thymosin fraction 5, a bovine thymus extract containing a number of immunologically active peptides. In vitro studies have shown that Thymalfasin can influence T-cell production and maturation, stimulate production of Th1 cytokines such as interferon-gamma and interleukin-2, and activate natural killer cell-mediated cytotoxicity. The mechanism of action of thymalfasin is not completely understood but is thought to be related to its immunomodulating activities, centered primarily around augmentation of T-cell function. In various in vitro assays, thymosin alpha 1 has been shown to promote T-cell differentiation and maturation; for example, CD4+, CD8+, and CD3+ cells have all been shown to be increased. Thymosin alpha 1 has also been shown to increase production of IFN-g, IL-2, IL-3, and expression of IL-2 receptor following activation by mitogens or antigens, increase NK cell activity, increase production of migratory inhibitory factor (MIF), and increase antibody response to T-cell dependent antigens. Thymosin alpha 1 has also been shown to antagonize dexamethasone-induced apoptosis of thymocytes in vitro. In vivo administration of thymosin alpha 1 to animals immunosuppressed by chemotherapy, tumor burden, or irradiation showed that thymosin alpha 1 protects against cytotoxic damage to bone marrow, tumor progression and opportunistic infections, thereby increasing survival time and number of survivors. Many of the in vitro and in vivo effects of thymosin alpha 1 have been interpreted as influences on either differentiation of pluripotent stem cells to thymocytes or activation of thymocytes into activated T-cells. Thymalfasin also has been shown in vitro to upregulate expression of toll like receptors (TLR) including TLR2 and TLR9 in mouse and human dendritic cells, as well as activate NF-kB and JNK/P38/AP1 pathways. Thymalfasin's activation of dendritic cells provides another possible pathway explaining thymalfasin's immunomodulatory and antiviral effects. ",The molecular weight is 3108.32.,Thymalfasin has a topological polar surface area of 1456.35.,The log p value of  is 0.0.,Thymalfasin is investigational.,Thymalfasin is a solid.,True
21669,"Sitimagene ceradenovec is a novel gene-based product for the treatment of patients with operable high grade glioma, a type of malignant brain tumour, given in addition to standard surgery and radiotherapy/chemotherapy. It is being developed by Ark Therapeutics. Intended for the treatment of brain cancer. EG009 is comprised of a gene encased in a virus vector. Vectors transfer their gene payload into target cells, a process known as transfection, which use this new genetic material as a blueprint for the production of new beneficial proteins. EG009 uses a well-established adenoviral vector (Ad5) to introduce the gene that causes cells to express a protein called thymidine kinase (TK). Following the standard surgery to remove the solid tumour mass, EG009 is injected through the wall of the cavity left behind by the surgical removal of the solid tumour, into the surrounding healthy brain tissue. In the following days, the healthy cells in the wall of the cavity express TK. Five days after surgery, the drug ganciclovir (GCV) is given to the patient as part of the overall EG009 treatment regimen. Neither TK nor GCV is individually active but they react together to produce a substance which destroys cells when they try to divide. Since cell division is a key characteristic of cancer and the normal brain cells are not dividing, cells that try to divide to form a new tumour around the site of the removal of the original tumour are targeted for destruction by the EG009 treatment. EG009 thus works by harnessing healthy cells to produce the substances necessary to destroy newly growing cancer cells. EG009 works by delivering a gene into the healthy brain cells remaining after the tumour has been removed. These then produce an enzyme that kills the cells trying to divide, preventing a recurrence of a tumour.",,,,Sitimagene ceradenovec is investigational.,Sitimagene ceradenovec is a liquid.,True
21670,"Ranpirnase is a ribonuclease enzyme found in <i>Rana pipiens</i> oocytes. It is being studied in the treatment of cancer. It is manufactured by Alfacell Corporation. It is the first ribonuclease to enter cancer clinical trials. For the treatment of various forms of cancer. Ranpirnase controls tumour growth by degrading RNA within cancer cells, resulting in inhibition of protein synthesis and arresting mitosis in G(1)phase.",,,,Ranpirnase is investigational.,Ranpirnase is a solid.,True
21671,"Oglufanide is a synthetic dipeptide immunomodulator in development for the treatment of chronic hepatitis C viral infection. Oglufanide was originally developed to treat severe infectious disease in Russia (where it is a registered pharmaceutical), and was extensively studied in cancer clinical trials in the United States before being acquired by Implicit Bioscience in 2005. Oglufanide works as a regulator of the body's immune response, is being given by intranasal administration to patients with chronic hepatitis C viral infection. Investigated for use/treatment in hepatitis (viral, C). Oglufanide regulates the body's innate immune response to defeat invading germs and cancer cells. It may control or reverse the suppression of the immune system which the hepatitis virus uses to defeat our normally healthy defenses.",,,,Oglufanide is investigational.,Oglufanide is a solid.,True
21672,"Vitamin A-analog that increases diffusivity of oxygen in aqueous solutions, including plasma. Investigated for use/treatment in cancer/tumors (unspecified), hemorrhage, hypoxia, respiratory failure, and strokes. Trans sodium crocetinate is a novel drug, which has been shown to increase whole-body oxygen consumption during hemorrhagic shock. It works by increasing the diffusion rate of oxygen through plasma rather than on a specific symptom of hemorrhagic shock and has been suggested as a general treatment for hypoxemia. Thus it could also be beneficial for treating respiratory insufficiencies.",,,,Transcrocetinate is investigational.,Transcrocetinate is a solid.,True
21673,"Investigated for use/treatment in pancreatic cancer, solid tumors, gastric cancer, lung cancer, and colorectal cancer.",,,,Plevitrexed is investigational.,Plevitrexed is a solid.,True
21674,"Investigated for use/treatment in renal cell carcinoma, solid tumors, and lung cancer.",,,,IMO-2055 is investigational.,IMO-2055 is a solid.,True
21675,"Pixantrone is an aza-anthracenedione and DNA intercalator which inhibits topoisomerase II. It is similar in structure to anthracyclines such as mitoxantrone, but exerts fewer toxic effects on cardiac tissue. The lower cardio-toxic effects of pixantrone may be explained, in part, by its redox inactivity. Pixantrone does not bind iron and promotes the formation of reactive oxygen species to a lesser degree than other anthracyclines. It also inhibits doxorubicinol formation in human myocardium. As a result, it is believed to be less cardiotoxic while still exerting efficacy.  Currently in Phase III investigation for treatment of relapsed or refractory aggressive non-Hodgkin's lymphoma in patients who have failed two prior lines of therapy. Presently, no standard therapy exists for patients with relapsed or refractory NHL. After first line therapy has been initiated, most patients have received their lifetime limit of doxorubicin and further use of anthracyclines may potentially lead to anthracycline-induced congestive heart failure (CHF). Pixantrone is an attractive alternative as a second line agent, due to its lack of cardiac toxicity.  Pixantrone has a wide range of antitumor activity, especially in terms of treating leukemias and lymphomas.  Pixantrone is an aza-anthracenedione which acts as a DNA intercalator. By intercalating between DNA, with modest affinity, it stimulates DNA cleavage by topoisomerase II. (Pixantrone acts as a poison to topoisomerase II by stabilizing protein-DNA complexes which are usually transient, giving rise to double stranded DNA breaks.)",,,,Pixantrone is approved and investigational.,Pixantrone is a solid.,True
21676,"Investigated for use/treatment in solid tumors, cutaneous t-cell lymphoma, myelodysplastic syndrome, and leukemia (lymphoid). Sapacitabine appears to act through a dual mechanism. It interferes with DNA synthesis by causing single-strand DNA breaks and also induces arrest of cell cycle progression mainly at G2/M-Phase. Both sapacitabine and CNDAC, its major metabolite or a substance into which the drugs converts after ingestion by patients, have demonstrated potent anti-tumor activity in preclinical studies.",,,,Sapacitabine is investigational.,Sapacitabine is a solid.,True
21677,,,,,Ginsenoside C is nutraceutical.,Ginsenoside C is a solid.,False
21678,"Roquinimex is a derivative of quinoline that presents immunostimulant properties. Its effects are suggested to increase the activity of NK cells and macrophage cytotoxicity. Additionally, roquinimex is known to inhibit angiogenesis and to decrease the synthesis of TNF alpha. Roquinimex is investigated to be used as a treatment of a number of cancers and autoimmune conditions. ",The molecular weight is 308.34.,Roquinimex has a topological polar surface area of 60.85.,The log p value of  is 1.7.,Roquinimex is investigational.,Roquinimex is a solid.,True
21679,"Masitinib is a tyrosine-kinase inhibitor used in the treatment of mast cell tumors in dogs. It has been available in Europe since 2009, under the brand name Masivet. In the USA it is distributed under the name Kinavet and has been available for veterinaries since 2011.",,,,Masitinib is investigational and vet_approved.,,True
21680,,The molecular weight is 811.88.,Aclarubicin has a topological polar surface area of 217.05.,The log p value of  is 3.43.,Aclarubicin is investigational.,Aclarubicin is a solid.,False
21681,Zorubicin is a drug of the anthracycline class - a class of medications that have historically demonstrated effective chemotherapy for a variety of cancer types.,The molecular weight is 645.66.,Zorubicin has a topological polar surface area of 210.23.,The log p value of  is 2.23.,Zorubicin is experimental.,Zorubicin is a solid.,True
21682,"Dactolisib has been used in trials studying the treatment of Cancer, Solid Tumor, Renal Cancer, Breast Cancer, and Cowden Syndrome, among others.",,,,Dactolisib is investigational.,,True
21683,"Rabusertib has been used in trials studying the treatment of Cancer, Solid Tumors, Advanced Cancer, Pancreatic Neoplasms, and Non Small Cell Lung Cancer.",,,,Rabusertib is investigational.,,True
21684,"Ortataxel has been used in trials studying the treatment of Lymphoma, Lung Cancer, Glioblastoma, and Kidney Cancer.",,,,Ortataxel is investigational.,,True
21685,"Treosulfan is under investigation in Allogeneic Haematopoietic Stem Cell Transplantation. Treosulfan has been investigated for the treatment of Lymphoblastic Leukemia, Acute, Childhood.",The molecular weight is 278.29.,Treosulfan has a topological polar surface area of 127.2.,The log p value of  is -2.2.,Treosulfan is approved and investigational.,,True
21686,"2-chloroethyl-3-sarcosinamide-1-nitrosourea has been used in trials studying the treatment of Colorectal Cancer, Brain and Central Nervous System Tumors, and Unspecified Adult Solid Tumor, Protocol Specific.",,,,2-chloroethyl-3-sarcosinamide-1-nitrosourea is investigational.,,True
21687,"Ilorasertib has been used in trials studying the treatment of Myelodysplasia, Solid Neoplasm, Advanced Cancers, Advanced Solid Tumors, and Acute Myelogenous Leukemia, among others.",,,,Ilorasertib is investigational.,,True
21688,"Epacadostat has been used in trials studying the treatment of HL, Melanoma, Glioblastoma, Mucosal Melanoma, and Ovarian Carcinoma, among others.",,,,Epacadostat is investigational.,,True
21689,Endostar is under investigation for the treatment of Nasopharyngeal Carcinoma. Endostar has been investigated for the treatment of Non-small Cell Lung Cancer.,,,,Endostar is investigational.,,True
21690,"GSK2636771 has been used in trials studying the treatment of CANCER, LYMPHOMA, Solid Neoplasm, Recurrent Solid Neoplasm, and Advanced Malignant Neoplasm, among others.",,,,GSK-2636771 is investigational.,,True
21691,Acridine Carboxamide has been used in trials studying the treatment of Lung Cancer and Brain and Central Nervous System Tumors.,,,,Acridine Carboxamide is investigational.,,True
21692,Infigratinib is under investigation for the treatment of Head and Neck Squamous Cell Carcinoma.,,,,Infigratinib is investigational.,,True
21693,"Efatutazone has been used in trials studying the treatment of Lymphoma, Liposarcoma, Solid Tumors, Multiple Myeloma, and Recurrent Thyroid Cancer, among others.",,,,Efatutazone is investigational.,,True
21694,"Rociletinib has been used in trials studying the treatment and prevention of Nonsmall Cell Lung Cancer, Non-small Cell Lung Cancer, and Locally Advanced or Metastatic Non-small Cell Lung Cancer.",,,,Rociletinib is investigational.,,True
21695,Guadecitabine is under investigation for the treatment of Previously Treated Metastatic Colorectal Cancer.,,,,Guadecitabine is investigational.,,True
21696,"Vosaroxin is under investigation for the treatment of Leukemia, Myeloid, Acute.",,,,Vosaroxin is investigational.,,True
21697,"Broxuridine has been used in trials studying the treatment of Leukemia, Stage I Prostate Cancer, Stage IIB Prostate Cancer, and Stage IIA Prostate Cancer.",The molecular weight is 307.1.,Broxuridine has a topological polar surface area of 99.1.,The log p value of  is -0.68.,Broxuridine is investigational.,,True
21698,"Naquotinib has been used in trials studying the treatment of Solid Tumors, Non-small Cell Lung Cancer, Non-Small-Cell Lung Cancer (NSCLC), Epidermal Growth Factor Receptor Mutations, and Epidermal Growth Factor Receptor (EGFR) Mutations, among others.",,,,Naquotinib is investigational.,,True
21699,"Trebananib is under investigation for the treatment of Ovarian Cancer, Peritoneal Cancer, and Fallopian Tube Cancer. Trebananib has been investigated for the treatment of Cancer, Oncology, Carcinoma, Metastases, and Colon Cancer, among others.",,,,Trebananib is investigational.,,True
21700,"Volasertib has been used in trials studying the treatment of Leukemia, Neoplasms, Leukemia, Myeloid, Acute, Myelodysplastic Syndromes, and Leukemia, Monocytic, Acute, among others.",,,,Volasertib is investigational.,,True
21701,Anecortave is under investigation in clinical trial NCT00691717 (Anecortave Acetate Safety in Patients With Open-Angle Glaucoma or Ocular Hypertension).,,,,Anecortave is investigational.,,True
21702,"Vesnarinone has been used in trials studying the treatment of HIV Infections and Sarcoma, Kaposi.",The molecular weight is 395.46.,Vesnarinone has a topological polar surface area of 71.11.,The log p value of  is 1.82.,Vesnarinone is investigational.,,True
21703,"Mafosfamide has been used in trials studying the treatment of Lymphoma, Leukemia, Meningeal Neoplasm, and Brain and Central Nervous System Tumors.",,,,Mafosfamide is investigational.,,True
21704,"LCL161 has been used in trials studying the treatment of Leukemia, Neoplasms, Solid Tumors, Breast Cancer, and Ovarian Cancer, among others.",,,,LCL-161 is investigational.,,True
21705,"Taselisib has been used in trials studying the treatment and basic science of LYMPHOMA, Breast Cancer, Ovarian Cancer, Solid Neoplasm, and HER2/Neu Negative, among others.",,,,Taselisib is investigational.,,True
21706,Namitecan has been used in trials studying the treatment of Solid Tumors.,,,,Namitecan is investigational.,,True
21707,"Rigosertib has been used in trials studying the treatment and basic science of MDS, RAEB, Cancer, Hepatoma, and Neoplasms, among others.",,,,Rigosertib is investigational.,,True
21708,"Binetrakin has been used in trials studying the treatment of HIV Infections, Sarcoma, Kaposi, Non-Hodgkin's Lymphoma (NHL), Myelodysplastic Syndrome (MDS), and Leukemia, Acute Myelogenous (AML), among others.",,,,Binetrakin is investigational.,,True
21709,"Exatecan has been used in trials studying the treatment of Sarcoma, Leukemia, Lymphoma, Lung Cancer, and Liver Cancer, among others.",The molecular weight is 435.46.,Exatecan has a topological polar surface area of 105.75.,The log p value of  is 0.65.,Exatecan is investigational.,,True
21710,Lurtotecan is under investigation in clinical trial NCT00022594 (Liposomal Lurtotecan in Treating Patients With Metastatic or Locally Recurrent Head and Neck Cancer).,,,,Lurtotecan is investigational.,,True
21711,"KRN7000 has been used in trials studying the treatment of Lung Cancer, Chronic Hepatitis C, Hepatitis B, Chronic, Unspecified Adult Solid Tumor, Protocol Specific, and Prevention of GvHD in Patients With Hematological Malignancies Undergoing AHSCT.",,,,KRN-7000 is investigational.,,True
21712,"Bizelesin has been used in trials studying the treatment of Unspecified Adult Solid Tumor, Protocol Specific.",,,,Bizelesin is investigational.,,True
21713,"Merestinib has been used in trials studying the treatment of Cancer, Solid Tumor, Advanced cancer, ColoRectal Cancer, and Metastatic Cancer, among others.",,,,Merestinib is investigational.,,True
21714,10-hydroxycamptothecin is under investigation in clinical trial NCT00956787 (Study of AR-67 (DB-67) in Myelodysplastic Syndrome (MDS)).,,,,10-hydroxycamptothecin is investigational.,,True
21715,Sulforaphane is under investigation for the treatment of Autism Spectrum Disorder. It is a naturally occurring isothiocyanate found in high concentration in a variety of broccoli.,,,,Sulforaphane is investigational.,,True
21716,"Taurolidine has been investigated for the prevention of Central Venous Catheter, Home Parenteral Nutrition, and Catheter-Related Infections.",The molecular weight is 284.35.,Taurolidine has a topological polar surface area of 98.82.,The log p value of  is -0.09.,Taurolidine is approved and investigational.,,True
21717,"Oltipraz has been used in trials studying the treatment and prevention of Lung Cancer, Liver Fibrosis, Liver Cirrhosis, and Non-alcoholic Fatty Liver Disease.",,,,Oltipraz is investigational.,,True
21718,"Pyrazoloacridine has been used in trials studying the treatment of Lung Cancer, Liver Cancer, Breast Cancer, Melanoma (Skin), and Metastatic Cancer, among others.",,,,Pyrazoloacridine is investigational.,,True
21719,Fosbretabulin has been investigated for the treatment of Anaplastic Thyroid Cancer.,,,,Fosbretabulin is investigational.,,True
21720,Apaziquone has been investigated for the treatment of Bladder Cancer and Bladder Neoplasms.,,,,Apaziquone is investigational.,,True
21721,Combretastatin has been investigated for the treatment of Anaplastic Thyroid Cancer.,,,,Combretastatin is investigational.,,True
21722,"PU-H71 has been used in trials studying the treatment of LYMPHOMA, Solid Tumors, Metastatic Solid Tumor, and Myeloproliferative Neoplasms (MPN).",,,,PU-H71 is investigational.,,True
21723,"Beloranib has been used in trials studying the treatment of Obesity, Over-weight, Type 2 Diabetes, Craniopharyngioma, and Hypothalamic Injury, among others.",,,,Beloranib is investigational.,,True
21724,"Soblidotin has been used in trials studying the treatment of Sarcoma, Lung Cancer, and Unspecified Adult Solid Tumor, Protocol Specific.",,,,Soblidotin is investigational.,,True
21725,"Salirasib has been used in trials studying the diagnostic of Carcinoma, Non-Small-Cell Lung.",,,,Salirasib is investigational.,,True
21726,Methylselenocysteine has been used in trials studying the prevention of Prostate Carcinoma and No Evidence of Disease.,,,,Methylselenocysteine is investigational.,,True
21727,"Dolastatin 10 has been used in trials studying the treatment of Sarcoma, Leukemia, Lymphoma, Liver Cancer, and Kidney Cancer, among others.",,,,Dolastatin 10 is investigational.,,True
21728,"Etanidazole has been used in trials studying the diagnostic of Adult Ependymoma, Malignant Ascites, Adult Gliosarcoma, Adult Mixed Glioma, and Adult Glioblastoma, among others.",,,,Etanidazole is investigational.,,True
21729,"Lometrexol has been used in trials studying the treatment of Lung Cancer, Drug/Agent Toxicity by Tissue/Organ, and Unspecified Adult Solid Tumor, Protocol Specific.",,,,Lometrexol is investigational.,,True
21730,Prednimustine has been used in trials studying the treatment of Lymphoma.,The molecular weight is 646.65.,Prednimustine has a topological polar surface area of 104.14.,The log p value of  is 5.79.,Prednimustine is investigational.,,True
21731,Buthionine Sulfoximine has been used in trials studying the treatment of Neuroblastoma and Melanoma (Skin).,,,,Buthionine Sulfoximine is investigational.,,True
21732,"Dianhydrogalactitol has been used in trials studying the treatment of GBM, Glioma, Glioblastoma, Brain Cancer, and Glioblastoma Multiforme.",,,,Dianhydrogalactitol is investigational.,,True
21733,Indole 3 Carbinol is under investigation in clinical trial NCT00033345 (Indole-3-Carbinol in Preventing Breast Cancer in Nonsmoking Women Who Are at High Risk For Breast Cancer).,,,,Indole-3-carbinol is investigational.,,True
21734,Fiacitabine has been used in trials studying the treatment of HIV Infections and Cytomegalovirus Infections.,,,,Fiacitabine is investigational.,,True
21735,Nolatrexed is under investigation in clinical trial NCT00012324 (Nolatrexed Dihydrochloride Compared With Doxorubicin in Treating Patients With Recurrent or Unresectable Liver Cancer).,,,,Nolatrexed is investigational.,,True
21736,Mitolactol has been used in trials studying the treatment of Brain and Central Nervous System Tumors.,The molecular weight is 307.97.,Mitolactol has a topological polar surface area of 80.92.,The log p value of  is -0.38.,Mitolactol is investigational.,,True
21737,"Pinometostat has been used in trials studying the treatment of Leukemia, Acute Leukemias, Acute Myeloid Leukemia, Myelodysplastic Syndrome, and Acute Lymphocytic Leukemia, among others.",,,,Pinometostat is investigational.,,True
21738,Didox has been used in trials studying the supportive care of Gastric Cancer.,,,,Didox is investigational.,,True
21739,"Mitoguazone has been used in trials studying the treatment of Lymphoma, HIV Infections, and Lymphoma, Non-Hodgkin.",The molecular weight is 184.21.,Mitoguazone has a topological polar surface area of 148.52.,The log p value of  is -2.58.,Mitoguazone is investigational.,,True
21740,"Penclomedine has been used in trials studying the treatment of Lymphoma and Unspecified Adult Solid Tumor, Protocol Specific.",,,,Penclomedine is investigational.,,True
21741,Rebastinib has been used in trials studying the treatment of Chronic Myeloid Leukemia. It is an inhibitor of Tie2 tyrosine kinase receptor and an antineoplastic agent.,,,,Rebastinib is investigational.,,True
21742,Tocladesine has been used in trials studying the treatment of Colorectal Cancer and Multiple Myeloma and Plasma Cell Neoplasm.,,,,Tocladesine is investigational.,,True
21743,"Liarozole has been used in trials studying the treatment of Ichthyosis, Lamellar.",,,,Liarozole is investigational.,,True
21744,Nimustine has been used in trials studying the treatment of Glioblastoma.,The molecular weight is 272.69.,Nimustine has a topological polar surface area of 113.57.,The log p value of  is 0.47.,Nimustine is investigational.,,True
21745,X-396 has been used in trials studying the treatment of Advanced Solid Tumors and Non-small Cell Lung Cancer.,,,,X-396 is investigational.,,True
21746,"A beta-D-glucan obtained from the Aphyllophoral fungus Schizophyllum commune. It is used as an immunoadjuvant in the treatment of neoplasms, especially tumors found in the stomach. Sizofiran has been used in trials studying the treatment of Cervical Cancer.",,,,Sizofiran is investigational.,,True
21747,,,,,Daidzein is experimental.,Daidzein is a solid.,False
21748,Tiazofurine has potential clinical use in cancer treatment as it is a potential inhibitor of Inosine- 5’-monophosphate (IMP) dehydrogenase.,The molecular weight is 260.26.,Tiazofurine has a topological polar surface area of 125.9.,The log p value of  is -1.86.,Tiazofurine is experimental.,,True
21749,,The molecular weight is 231.26.,Triaziquone has a topological polar surface area of 43.17.,The log p value of  is -1.79.,Triaziquone is experimental.,,False
21750,,The molecular weight is 371.43.,Demecolcine has a topological polar surface area of 66.02.,The log p value of  is 1.76.,Demecolcine is experimental.,,False
21751,,The molecular weight is 494.51.,Mannosulfan has a topological polar surface area of 213.94.,The log p value of  is -2.79.,Mannosulfan is experimental.,,False
21752,,The molecular weight is 262.3.,Etoglucid has a topological polar surface area of 61.98.,The log p value of  is -1.02.,Etoglucid is experimental.,,False
21753,,,,,Lentinan is experimental and investigational.,,False
21754,,The molecular weight is 307.97.,Mitobronitol has a topological polar surface area of 80.92.,The log p value of  is -0.38.,Mitobronitol is experimental.,,False
21755,,The molecular weight is 247.72.,Semustine has a topological polar surface area of 61.77.,The log p value of  is 3.27.,Semustine is experimental and investigational.,,False
21756,,The molecular weight is 321.33.,Carboquone has a topological polar surface area of 101.71.,The log p value of  is -1.21.,Carboquone is experimental.,,False
21757,,The molecular weight is 324.77.,Vorozole has a topological polar surface area of 61.42.,The log p value of  is 2.2.,Vorozole is experimental.,,False
21758,,,,,Oblimersen is experimental and investigational.,,False
21759,,The molecular weight is 327.72.,Ranimustine has a topological polar surface area of 140.92.,The log p value of  is -0.16.,Ranimustine is experimental.,,False
21760,,,,,Coumermycin A1 is experimental.,Coumermycin A1 is a solid.,False
21761,"4-Amino-5-cyano-7-(D-ribofuranosyl)-7H- pyrrolo(2,3-d)pyrimidine. Antibiotic antimetabolite isolated from Streptomyces toyocaensis cultures. It is an analog of adenosine, blocks RNA synthesis and ribosome function, and is used mainly as a tool in biochemistry.",,,,Toyocamycin is experimental.,Toyocamycin is a solid.,True
21762,,,,,Combretastatin A4 is experimental.,,False
21763,Rivoceranib is under investigation in clinical trial NCT02726854 (Apatinib as Second-line Treatment of Advanced Pancreatic Cancer).,The molecular weight is 397.48.,Rivoceranib has a topological polar surface area of 90.7.,The log p value of  is 3.66.,Rivoceranib is investigational.,,True
21764,AZD-5991 is under investigation in clinical trial NCT03218683 (Study of AZD5991 in Relapsed or Refractory Haematologic Malignancies.).,,,,AZD-5991 is investigational.,,True
21765,ONC-201 is under investigation in clinical trial NCT03394027 (ONC201 in Recurrent/Refractory Metastatic Breast Cancer and Advanced Endometrial Carcinoma).,,,,ONC-201 is investigational.,,True
21766,Ensartinib is under investigation in clinical trial NCT03420508 (Treating Patients With Melanoma and ALK Alterations With Ensartinib).,,,,Ensartinib is investigational.,,True
21767,Human interleukin-2 is under investigation in clinical trial NCT03475134 (TIL-ACT After NMA Chemo With IL-2 and Nivo Rescue in mMEL).,,,,Human interleukin-2 is investigational.,,True
21768,Etirinotecan pegol is under investigation in clinical trial NCT01663012 (Phase II NKTR-102 In Bevacizumab-Resistant High Grade Glioma).,,,,Etirinotecan pegol is investigational.,,True
21769,NUC-1031 is under investigation in clinical trial NCT03610100 (Acelarin First Line Randomised Pancreatic Study).,,,,NUC-1031 is investigational.,,True
21770,Voruciclib is under investigation in clinical trial NCT03547115 (A Phase 1 Study of Voruciclib in Subjects With B-Cell Malignancies or AML).,,,,Voruciclib is investigational.,,True
21771,KRN-5500 is under investigation in clinical trial NCT00002923 (KRN5500 in Treating Patients With Metastatic Solid Tumors).,,,,KRN-5500 is investigational.,,True
21772,Perillyl alcohol is under investigation in clinical trial NCT02704858 (Safety and Efficacy Study in Recurrent Grade IV Glioma).,,,,Perillyl alcohol is investigational.,,True
21773,"Tallimustine, a benzoyl mustard derivative of distamycin A, is an alkylating agent that binds to the minor groove of DNA. It's association with severe myelotoxicity lead to the end of its development in favour of α-halogenoacrylamide derivatives such as , which have a favourable cytotoxicity/myelotoxicity ratio. Newer generations of DNA minor groove binding agents can more specifically recognize base pair sequences. Tallimustine was being investigated for its use in treating tumors. Derivatives of tallimustine with similar DNA binding ability and reduced myelotoxicity are being investigated for their antitumor activity. Tallimustine binds to the minor groove of DNA while avoiding targets like glutathione. Currently, the mechanism of DNA minor groove binding agents is poorly understood. Though, they may act by directly inhibiting the interaction of protein and DNA.",,,,Tallimustine is experimental.,,True
21774,"DTS-201 is a prodrug of doxorubicin, a widely used anti-cancer drug that Diatos intends to develop for the treatment of various solid tumors. It is activated in the tumor environment. Investigated for use/treatment in cancer/tumors (unspecified). DTS-201 is a prodrug: it remains inactive while circulating in the blood stream and healthy tissues and does not enter cells. In the vicinity of tumors, extracellular enzymes overexpressed and oversecreted specifically in the tumor environment cleave DTS-201 to yield an intermediate, L-dox (leucyl doxorubicin), which is capable of penetrating cells. Once in the cell, intracellular peptidases release free doxorubicin which is then able to interact with its targets.",,,,DTS-201 is investigational.,DTS-201 is a solid.,True
21775,"Sabarubicin has been used in trials studying the treatment of Prostate Cancer, Testicular Germ Cell Tumor, and Unspecified Adult Solid Tumor, Protocol Specific.",,,,Sabarubicin is investigational.,,True
21776,"Zoptarelin doxorubicin has been used in trials studying the treatment of Breast Cancer, Ovarian Cancer, Prostate Cancer, Endometrial Cancer, and Urothelial Carcinoma, among others.",,,,Zoptarelin doxorubicin is investigational.,,True
21777,GPX-150 has been used in trials studying the treatment of Soft Tissue Sarcoma and Advanced Solid Tumors - Phase 1 Population.,,,,GPX-150 is investigational.,,True
21778,Deslorelin acetate is an injectable gonadotropin releasing hormone super-agonist also known as an LHRH agonist. It stops the production of sex hormones.,,,,Deslorelin is investigational and vet_approved.,,True
21779,"Activated charcoal, or activated carbon, is an amorphous form of carbon prepared from incomplete combustion of carbonaceous organic matter. It is activated by an oxidizing gas flow at high temperature passed over its surface to make a fine network of pores, producing a material with large surface area and high affinity for various substances. It is used as a gastric decontaminant and emergency medication to treat poisonings following excessive oral ingestion of certain medications or poisons by absorbing most drugs and toxins. However its effects is rendered poor on some compounds including strong acids or bases, methanol and substances with limited absorptive capacity (including iron, lithium, arsenic). It works by binding to the poison in the gastric contents in a reversible fashion thus may be adminstered together with a cathartic to reduce the small intestine transit time. The clinical applications of activated charcoal occured in the early 1800's. While this management for acute poisoning is considered fairly invasive, it is on the World Health Organization's List of Essential Medicines that includes the most important medications needed in a basic health system. Used as a antidote to treat poisonings following excessive oral ingestion of certain medications or poisons.  Activated charcoal is used as a gastric decontamination agent in emergency clinical settings in case of poison or medication overdose. Studies show that early administration of one dose of activated charcoal can adsorb poison in the stomach and reduce absorption while it also works long after ingestion, by interruption of enterohepatic and enterovascular cycling of poison.  Active charcoal acts by binding to the pharmaceutical drugs or poisons such as organophosphates and decreasing the systemic absorption of toxic agents. Molecules with large volume of distribution, thus likely having higher lipid solubility, tends to bind have better absorptive binding to activated charcoal. Following the administration of activated charcoal, cathartics are indicated to evacuate the charcoal-poison bonded complex from the gastrointestinal tract. ",,,,Activated charcoal is approved.,Activated charcoal is a solid.,True
21780,Albusomatropin has been used in trials studying the treatment of Growth Hormone-Deficiency and Growth Hormone Deficiency.,,,,Albusomatropin is investigational.,,True
21781,"Somatropin pegol is under investigation in clinical trial NCT00715689 (Dose Study in Growth Hormone Deficient Adults Investigating Safety, Pharmacokinetics and Pharmacodynamics of NNC126-0083).",,,,Somatropin pegol is investigational.,,True
21782,,,,,Oseltamivir acid is experimental.,Oseltamivir acid is a solid.,False
21783,"Rupintrivir is a rhinovirus 3C protease inhibitor in development for use against human rhinoviral (HRV) infections. Rupintrivir was active against all 48 HRV serotypes tested in a cell protection assay in H1-HeLa cells. It is designed to combat colds caused by rhinovirus. Investigated for use/treatment in viral infection. The 3C protease (3CP) enzyme is central to rhinovirus replication. By binding to and inhibiting this enzyme, AG7088 prevents rhinovirus replication in cells of the respiratory tract and stops cold symptoms developing.",,,,Rupintrivir is investigational.,Rupintrivir is a solid.,True
21784,"Pleconaril is an antiviral drug from _viral capsid inhibitor_ class, manufactured by _Schering-Plough_ and intended for the prevention of acute asthma exacerbations and common cold symptoms in asthmatic patients who have had exposure to _picornavirus_. It acts by inhibiting viral replication. The use of pleconaril has not gained approval by the U.S. Food and Drug Administration (FDA) due to the fact that it has been found to induce CYP3A enzyme activity, therefore increasing the risk for serious drug interactions. Investigated for use/treatment in upper respiratory infection. Pleconaril binds to a hydrophobic pocket in viral protein 1, the major protein which makes up the capsid (shell) of picornaviruses. This renders the viral capsid rigid and compressed and prevents the uncoating of its RNA. As a result, the virus is stopped from attaching to the host cell and causing infection.",The molecular weight is 381.36.,Pleconaril has a topological polar surface area of 74.18.,The log p value of  is 4.04.,Pleconaril is investigational.,Pleconaril is a solid.,True
21785,"UC-781 is a thiocarboxanilide non-nucleoside reverse transcriptase inhibitor (NNRTI). It is a topical microbicide targeted against the AIDS virus. Investigated for use/treatment in HIV infection. UC-781 is an HIV non-nucleoside reverse transcriptase inhibitor (NNRTI) that has shown in vitro to be very active specifically against HIV-1. UC-781 exhibits synergy with the NRTI zidovudine in vitro. The combination of UC-781 and another candidate microbicide, cellulose acetate 1,2-benzenedicarboxylate, resulted in effective synergy for inhibition of HIV-1 in vitro and in peripheral blood mononuclear cells",,,,UC-781 is investigational.,UC-781 is a solid.,True
21786,Investigated for use/treatment in HIV infection.,,,,Alovudine is investigational.,Alovudine is a solid.,True
21787,"Investigated for use/treatment in viral infection, transplantation (organ or tissue), cytomegalovirus (CMV) retinitis, and retinal disorders (unspecified). Maribavir is part of a new class of anti-cytomegalovirus (CMV) , benzimidazole ribosides, that inhibit viral DNA assembly and inhibits egress of viral capsids from the nucleus of infected cells. Maribavir is active in vitro against strains of CMV that are resistant to commonly used anti-CMV drugs. Maribavir inhibits the human CMV UL97 viral protein kinase which prevents the virus from encapsulating and leaving infected cells.",,,,Maribavir is investigational.,Maribavir is a solid.,True
21788,"Investigated for use/treatment in hepatitis (viral, B) and HIV infection. Elvucitabine is a L-cytosine Nucleoside analog Reverse Transcriptase Inhibitor (NRTIs) anti-HIV drug. NRTI's inhibit the activity of viral RNA-directed DNA polymerase (i.e., reverse transcriptase). It is believed that inhibition of reverse transcriptase interferes with the generation of DNA copies of viral RNA, which, in turn, are necessary for synthesis of new virions. Intracellular enzymes subsequently eliminate the HIV particle that previously had been uncoated, and left unprotected, during entry into the host cell. Thus, reverse transcriptase inhibitors are virustatic and do not eliminate HIV from the body. ",,,,Elvucitabine is investigational.,Elvucitabine is a solid.,True
21789,Emivirine has been used in trials studying the treatment of HIV Infections.,,,,Emivirine is investigational.,Emivirine is a solid.,True
21790,Dapivirine has been investigated for the prevention of HIV-1 Infections and Topical Penile Exposures.,,,,Dapivirine is investigational.,Dapivirine is a solid.,True
21791,"Ruzasvir has been used in trials studying the treatment of Hepatitis C, Hepatitis C, Chronic, and Hepatitis C Infection.",,,,Ruzasvir is investigational.,,True
21792,"Cenicriviroc has been used in trials studying the treatment of HIV-infection/AIDS, AIDS Dementia Complex, Nonalcoholic Steatohepatitis, Human Immunodeficiency Virus, and HIV-1-Associated Cognitive Motor Complex.",,,,Cenicriviroc is investigational.,,True
21793,Faldaprevir has been investigated for the treatment of Chronic Hepatitis C.,,,,Faldaprevir is investigational.,,True
21794,Pritelivir has been used in trials studying the prevention of HSV-2 and Genital Herpes.,,,,Pritelivir is investigational.,,True
21795,Ingavirin has been used in trials studying the treatment of Influenza and Common Cold.,,,,Ingavirin is investigational.,,True
21796,Sorivudine has been used in trials studying the treatment of Chickenpox and HIV Infections.,The molecular weight is 349.14.,Sorivudine has a topological polar surface area of 119.33.,The log p value of  is -1.15.,Sorivudine is investigational.,,True
21797,"Vedroprevir has been investigated for the treatment of Hepatitis C, Chronic.",,,,Vedroprevir is investigational.,,True
21798,Atevirdine has been used in trials studying the treatment of HIV Infections.,,,,Atevirdine is investigational.,,True
21799,Dexelvucitabine has been used in trials studying the treatment of HIV Infections and Human Immunodeficiency Virus.,,,,Dexelvucitabine is investigational.,,True
21800,Vesatolimod has been used in trials studying the treatment of Hepatitis B and Chronic Hepatitis B.,,,,Vesatolimod is investigational.,,True
21801,"Racivir, also known as RCV, is an oxothiolane nucleoside reverse transcriptase inhibitor similar to emtricitabine and lamivudine. Racivir is a 50:50 mixture of emtricitabine and its positive enantiomer. Racivir has been used in trials studying the prevention of HIV Infections.",,,,Racivir is investigational.,,True
21802,Laninamivir has been used in trials studying the treatment of Influenza.,,,,Laninamivir is investigational.,,True
21803,"Odalasvir has been used in trials studying the treatment of Hepatitis C, Chronic and Chronic Hepatitis C Infection.",,,,Odalasvir is investigational.,,True
21804,,The molecular weight is 234.28.,Metisazone has a topological polar surface area of 70.72.,The log p value of  is 1.16.,Metisazone is experimental.,,False
21805,,The molecular weight is 353.12.,Ibacitabine has a topological polar surface area of 108.38.,The log p value of  is -0.67.,Ibacitabine is experimental.,,False
21806,PF-232798 is under investigation in clinical trial NCT01140425 (Study To Evaluate The Effect Of A Multiple Oral Dose Of PF-00232798 On QT Intervals In Healthy Subjects).,,,,PF-232798 is investigational.,,True
21807,Adafosbuvir is under investigation in clinical trial NCT02894905 (A Study to Evaluate the Effect of Renal Impairment on the Pharmacokinetics of AL-335).,,,,Adafosbuvir is investigational.,,True
21808,Alovudine F-18 is under investigation in clinical trial NCT02819024 (Dexamethasone Effects in Patients With Refractory Non-Small Cell Lung Cancer Using FLT Positron Emission Tomography).,,,,Alovudine F-18 is investigational.,,True
21809,BMS-955176 is under investigation in clinical trial NCT02415595 (Dose-finding Study of BMS-955176 to Treat HIV-1 Infected Treatment-naive Adults).,,,,BMS-955176 is investigational.,,True
21810,Uprifosbuvir is under investigation in clinical trial NCT02332707 (Efficacy and Safety of Grazoprevir (MK-5172) and Uprifosbuvir (MK-3682) With Elbasvir (MK-8742) or Ruzasvir (MK-8408) for Chronic Hepatitis C Genotype (GT)1 and GT2 Infection (MK-3682-011)).,,,,Uprifosbuvir is investigational.,,True
21811,Radavirsen is under investigation in clinical trial NCT01375985 (Safety Study of Single Administration Intravenous Treatment for Influenza).,,,,Radavirsen is investigational.,,True
21812,Fialuridine is under investigation in clinical trial NCT01337466 (Biodistribution and Dosimetry Evaluation of FIAU).,,,,Fialuridine is investigational.,,True
21813,"Onasemnogene abeparvovec is an adeno-associated virus vector-based gene therapy that has been approved by the FDA in May 2019 for the treatment of infant patients (less than 2 years of age) with spinal muscular atrophy (SMA) and a specific mutation in the survival motor neuron 1 (SMN1) gene. SMA is a rare genetic disease that affects the survival and function of motor neurons, leading to debilitating and often fatal muscle weakness. As there is no cure for SMA, onasemnogene abeparvovec is a disease-modifying agent that decelerates the disease progression, improves motor function, and manages the symptoms. The use and effectiveness of onasemnogene abeparvovec in patients with advanced SMA, such as those with complete paralysis of the limbs and permanent dependence on ventilators, has not been evaluated. Onasemnogene abeparvovec is the first gene therapy that was approved for this indication in the USA. is another gene therapy that is currently approved by the FDA for the treatment of SMA in pediatric and adult patients. Onasemnogene abeparvovec is indicated for the treatment of pediatric patients less than 2 years of age (neonatal and infant patients) with spinal muscular atrophy (SMA) with bi-allelic mutations in the survival motor neuron 1 (SMN1) gene. Onasemnogene abeparvovec is a gene therapy that restores the levels of SMN protein in the spinal cord to promote the survival and function of motor neurons. Acute serious liver injury and elevated aminotransferases were observed with the treatment of onasemnogene abeparvovec in clinical trials. Spinal muscular atrophy is a genetic disorder caused by mutations in the SMN gene, which encodes the SMN protein. SMN protein is found ubiquitously but it is highly expressed in the spinal cord where it is responsible for the survival and maintenance of specialized nerve cells called motor neurons. SMN1 and SMN2 genes encode the SMN protein but many mutations in the SMN1 gene have been found to cause spinal muscular atrophy, as SMN1 is the primary gene responsible for functional production of SMN protein. A common mutation that causes spinal muscular atrophy involves a bi-allelic deletion of exon 7 in the SMN1 gene. The number of copies of the SMN2 gene varies among individuals: while higher number of SMN2 gene copies may protect against SMN protein deficiency caused by SMN1 gene mutations, it is generally proposed that the bi-allelic mutation in the SMN1 gene cannot be compensated by the SMN2 gene. The mutation results in insufficient SMN protein expression and inefficient assembly of the machinery needed to process pre-mRNA for motor neuron development and survival. Spinal muscular atrophy involves a progressive degeneration and loss of lower motor neurons, leading to muscle weakness and atrophy.",,,,Onasemnogene abeparvovec is approved.,,True
21814,"GS-441524 is an adenosine nucleotide analog antiviral, similar to. This molecule was patented in 2009. _In vitro_ studies of GS-441524 have determined it has a higher EC<sub>50</sub> than remdesivir against a number of viruses, meaning GS-441524 is less potent. GS-441524 continues to be studied in the treatment of Feline Infectious Peritonitis Virus, a coronavirus that only infects cats. GS-441524 is phosphorylated 3 times to form the active nucleoside triphosphate, which is incorporated into the genome of virions, terminating its replication.",,,,GS-441524 is experimental.,GS-441524 is a solid.,True
21815,"Hexaminolevulinate is an optical imaging drug. In solution form it is instilled intravesically for use with photodynamic blue light cystoscopy as an adjunct to white light cystoscopy. On May 28, 2010, the U.S. Food and Drug Administration (FDA) granted approval for hexaminolevulinate hydrochloride (Cysview for Intravesical Solution, Photocure ASA), as an optical imaging agent for use in combination with the Karl Storz Photodynamic Diagnostic D-Light C (PDD) System for cystoscopic detection of non-muscle invasive papillary cancer of the bladder for patients suspected or known to have lesion(s) on the basis of a prior cystoscopy. Hexaminolevulinate is manufactured under the brand Cysview® by Photocure ASA. In Europe, Hexaminolevulinate is marketed under the brand Hexvix®. Hexaminolevulinate is indicated for use in the cystoscopic detection of non-muscle invasive papillary cancer of the bladder among patients suspected or known to have lesion(s) on the basis of a prior cystoscopy.  In vitro studies have shown increased porphyrin fluorescence in normal urothelium after exposure to hexaminolevulinate hydrochloride intravesical solution. In the human bladder, a greater accumulation of porphyrins is proposed in neoplastic or inflamed cells, compared to normal urothelium. After bladder instillation of hexaminolevulinate hydrochloride intravesical solution for approximately 1 hour and subsequent illumination with blue light at wavelengths 360 – 450nm, the porphyrins will fluoresce red. Hexaminolevulinate is an ester of the heme precursor, aminolevulinic acid. After bladder instillation, hexaminolevulinate enters the bladder mucosa and is proposed to enter the intracellular space of mucosal cells where it is used as a precursor in the formation of the photoactive intermediate protoporphyrin IX (PpIX) and other photoactive porphyrins (PAPs). PpIX and PAPs are reported to accumulate preferentially in neoplastic cells as compared to normal urothelium, partly due to altered enzymatic activity in the neoplastic cells. After excitation with light at wavelengths between 360 and 450 nm, PpIX and other PAPs return to a lower energy level by fluorescing, which can be detected and used for cystoscopic detection of lesions. The fluorescence from tumor tissue appears bright red and demarcated, whereas the background normal tissue appears dark blue. Similar processes may occur in inflamed cells.",The molecular weight is 215.29.,Hexaminolevulinate has a topological polar surface area of 69.39.,The log p value of  is 1.97.,Hexaminolevulinate is approved.,Hexaminolevulinate is a solid.,True
21816,Dibekacin is an aminoglycoside antibiotic marketed in Japan.,The molecular weight is 451.52.,Dibekacin has a topological polar surface area of 247.94.,The log p value of  is -3.41.,Dibekacin is approved.,,True
21817,"Micronomicin is an aminoglycoside antibiotic which is marketed in Japan, and sold under the brand names Sagamicin and Luxomicina.",The molecular weight is 463.58.,Micronomicin has a topological polar surface area of 199.73.,The log p value of  is -2.11.,Micronomicin is approved.,,True
21818,,The molecular weight is 483.52.,Bekanamycin has a topological polar surface area of 288.4.,The log p value of  is -3.85.,Bekanamycin is experimental.,,False
21819,,,,,Silver cation is experimental.,,False
21820,Paspalum notatum pollen is the pollen of the Paspalum notatum plant. Paspalum notatum pollen is mainly used in allergenic testing.,,,,Paspalum notatum pollen is approved.,,True
21821,"Cynodon dactylon pollen, also known as bermuda grass pollen, is a standardized grass pollen extracts used for the diagnosis and treatment of allergic disease to grass pollen. It can be cutaneously, intradermally and subcutaneously administered to initiate an immune response in case of an allergic reaction. Diagnostic allergenic extracts are primarily indicated for establishing clinical relevance of specific allergens to which the patient has been exposed and the degree of sensitivity the patient has toward that allergen.",,,,Cynodon dactylon pollen is approved.,,True
21822,Poa annua pollen is the pollen of the Poa annua plant. Poa annua pollen is mainly used in allergenic testing.,,,,Poa annua pollen is approved.,,True
21823,Sorghum halepense pollen is the pollen of the Sorghum halepense plant. Sorghum halepense pollen is mainly used in allergenic testing.,,,,Sorghum halepense pollen is approved.,,True
21824,Poa pratensis pollen is the pollen of the Poa pratensis plant. Poa pratensis pollen is mainly used in allergenic testing.,,,,Poa pratensis pollen is approved.,,True
21825,Festuca pratensis pollen is the pollen of the Festuca pratensis plant. Festuca pratensis pollen is mainly used in allergenic testing.,,,,Festuca pratensis pollen is approved.,,True
21826,Dactylis glomerata pollen is the pollen of the Dactylis glomerata plant. Dactylis glomerata pollen is mainly used in allergenic testing.,,,,Dactylis glomerata pollen is approved.,,True
21827,Lolium perenne pollen is the pollen of the Lolium perenne plant. Lolium perenne pollen is mainly used in allergenic testing.,,,,Lolium perenne pollen is approved.,,True
21828,Phleum pratense pollen allergenic extract is used in allergenic testing.,,,,Phleum pratense pollen is approved and investigational.,,True
21829,Holcus lanatus pollen is the pollen of the Holcus lanatus plant. Holcus lanatus pollen is mainly used in allergenic testing.,,,,Holcus lanatus pollen is approved.,,True
21830,Agrostis gigantea pollen is the pollen of the Agrostis gigantea plant. Agrostis gigantea pollen is mainly used in allergenic testing.,,,,Agrostis gigantea pollen is approved.,,True
21831,Anthoxanthum odoratum pollen is the pollen of the Anthoxanthum odoratum plant. Anthoxanthum odoratum pollen is mainly used in allergenic testing.,,,,Anthoxanthum odoratum pollen is approved.,,True
21832,Elymus repens pollen is the pollen of the Elymus repens plant. Elymus repens pollen is mainly used in allergenic testing.,,,,Elymus repens pollen is approved.,,True
21833,Distichlis spicata pollen is the pollen of the Distichlis spicata plant. Distichlis spicata pollen is mainly used in allergenic testing.,,,,Distichlis spicata pollen is approved.,,True
21834,Poa compressa pollen is the pollen of the Poa compressa plant. Poa compressa pollen is mainly used in allergenic testing.,,,,Poa compressa pollen is approved.,,True
21835,Phalaris arundinacea pollen is the pollen of the Phalaris arundinacea plant. Phalaris arundinacea pollen is mainly used in allergenic testing.,,,,Phalaris arundinacea pollen is approved.,,True
21836,Bouteloua gracilis pollen is the pollen of the Bouteloua gracilis plant. Bouteloua gracilis pollen is mainly used in allergenic testing.,,,,Bouteloua gracilis pollen is approved.,,True
21837,Urochloa mutica pollen is the pollen of the Urochloa mutica plant. Urochloa mutica pollen is mainly used in allergenic testing.,,,,Urochloa mutica pollen is approved.,,True
21838,Secale cereale pollen is the pollen of the Secale cereale plant. Secale cereale pollen is mainly used in allergenic testing.,,,,Secale cereale pollen is approved.,,True
21839,Pascopyrum smithii pollen is the pollen of the Pascopyrum smithii plant. Pascopyrum smithii pollen is mainly used in allergenic testing.,,,,Pascopyrum smithii pollen is approved.,,True
21840,Bromus secalinus pollen is the pollen of the Bromus secalinus plant. Bromus secalinus pollen is mainly used in allergenic testing.,,,,Bromus secalinus pollen is approved.,,True
21841,Arrhenatherum elatius pollen is the pollen of the Arrhenatherum elatius plant. Arrhenatherum elatius pollen is mainly used in allergenic testing.,,,,Arrhenatherum elatius pollen is approved.,,True
21842,Koeleria macrantha pollen is the pollen of the Koeleria macrantha plant. Koeleria macrantha pollen is mainly used in allergenic testing.,,,,Koeleria macrantha pollen is approved.,,True
21843,Agrostis stolonifera pollen is the pollen of the Agrostis stolonifera plant. Agrostis stolonifera pollen is mainly used in allergenic testing.,,,,Agrostis stolonifera pollen is approved.,,True
21844,Phalaris minor pollen is the pollen of the Phalaris minor plant. Phalaris minor pollen is mainly used in allergenic testing.,,,,Phalaris minor pollen is approved.,,True
21845,Lolium perenne subsp. multiflorum pollen is the pollen of the Lolium perenne subsp. multiflorum plant. Lolium perenne subsp. multiflorum pollen is mainly used in allergenic testing.,,,,Lolium perenne subsp. multiflorum pollen is approved.,,True
21846,Sorghum bicolor subsp. drummondii pollen is the pollen of the Sorghum bicolor subsp. drummondii plant. Sorghum bicolor subsp. drummondii pollen is mainly used in allergenic testing.,,,,Sorghum bicolor subsp. drummondii pollen is approved.,,True
21847,,The molecular weight is 373.88.,Clebopride has a topological polar surface area of 67.59.,The log p value of  is 2.61.,Clebopride is experimental.,,False
21848,Fallypride is under investigation in clinical trial NCT02310360 (Striatal and Extra-striatal Dopamine Release in Response to Food in Healthy Humans).,,,,Fallypride is investigational.,,True
21849,,,,,Eticlopride is experimental.,,False
21850,Investigated for use/treatment in parkinson's disease.,The molecular weight is 225.24.,Etilevodopa has a topological polar surface area of 92.78.,The log p value of  is 0.24.,Etilevodopa is investigational.,Etilevodopa is a solid.,True
21851,,The molecular weight is 293.45.,Budipine has a topological polar surface area of 3.24.,The log p value of  is 5.58.,Budipine is experimental.,,False
21852,Dexpramipexole is under investigation in clinical trial NCT01511029 (Study to Evaluate the QTC Interval in Healthy Volunteers Dosed With Dexpramipexole (QTC = Electrocardiogram (ECG) Interval Measured From the Onset of the QRS Complex to the End of the T Wave Corrected for Heart Rate)).,,,,Dexpramipexole is investigational.,,True
21853,,,,,Lanthanum III cation is experimental.,,False
21854,,,,,"4-butyl-5-propyl-1,3-selenazol-2-amine is experimental.","4-butyl-5-propyl-1,3-selenazol-2-amine is a solid.",False
21855,,,,,Dioxyselenocysteine is experimental.,Dioxyselenocysteine is a solid.,False
21856,,,,,Selenoinosine is experimental.,Selenoinosine is a solid.,False
21857,,,,,Selenomethionine Selenoxide is experimental.,Selenomethionine Selenoxide is a solid.,False
21858,,,,,(S)-2-Amino-3-(6h-Selenolo-Pyrrol-4-Yl)-Propionic Acid is experimental.,(S)-2-Amino-3-(6h-Selenolo-Pyrrol-4-Yl)-Propionic Acid is a solid.,False
21859,,,,,S-Selanyl Cysteine is experimental.,S-Selanyl Cysteine is a solid.,False
21860,,,,,Acetate is experimental.,Acetate is a solid.,False
21861,,,,,S-Adenosyl-L-Homoselenocysteine is experimental.,S-Adenosyl-L-Homoselenocysteine is a solid.,False
21862,,,,,(S)-2-Amino-3-(4h-Selenolo-Pyrrol-6-Yl)-Propionic Acid is experimental.,(S)-2-Amino-3-(4h-Selenolo-Pyrrol-6-Yl)-Propionic Acid is a solid.,False
21863,"An organoselenium drug previously studied by Oxis International in Phase-II clinical trials for ulcerative colitis patients. Some indications of efficacy were demonstrated. BXT-51072 has enthusiastic endorsement for treatment in cardiovascular indications, primarily because of its ability to mimic the function of glutathione peroxidase. Investigated for use/treatment in cardiovascular disorders and diabetes mellitus type 1 and 2.",,,,ALT-2074 is investigational.,ALT-2074 is a solid.,True
21864,,,,,Selenomethionine Se-75 is approved.,,False
21865,"Selenic acid is an organic compound with the chemical formula H2SeO4. It may be found in over-the-counter daily dietary supplements as a source of , an essential trace mineral for human health. Indicated for use as a nutritional supplement.   is an essential trace mineral that plays a critical role in antioxidant actions, anti-inflammatory effects, immune function, and the production of active thyroid hormone.   is a constituent of selenoproteins thus has structural and enzymatic roles. It acts as an antioxidant via the actions of selenoproteins for protection against oxidative stress, and acts as a catayst for the production of active thyroid hormone. It may also play a role in sperm motility. ",,,,Selenic acid is approved.,Selenic acid is a solid.,True
21866,"Selenomethionine is a naturally occuring amino acid in some plant materials such as cereal grains, soybeans and enriched yeast but it cannot be synthesized from animals or humans. It can be produced from post-structural modifications. *In vivo*, selenomethionine plays an essential role in acting as an antioxidant, where it depletes reactive oxygen species (ROS) and aids in the formation and recycling of glutathione, another important antioxidant. In comparison to selenite, which is the inorganic form of selenium, the organic form of selenomethionine is more readily absorbed in the human body. Selenomethionin is used in biochemical laboratories where its incorporation into proteins that need to be visualized enhances the performance of X-ray crystallography.",The molecular weight is 196.12.,Selenomethionine has a topological polar surface area of 63.32.,The log p value of  is -1.89.,Selenomethionine is approved and investigational.,,True
21867,"Aluminum oxide has a chemical formula Al2O3. It is amphoteric in nature, and is used in various chemical, industrial and commercial applications. It is considered an indirect additive used in food contact substances by the FDA.",The molecular weight is 101.96.,Aluminum oxide has a topological polar surface area of 27.69.,,Aluminum oxide is approved.,,True
21868,,,,,Selenium (75Se) norcholesterol is experimental.,,False
21869,Ethaselen is under investigation in clinical trial NCT02166242 (Ethaselen for the Treatment of Thioredoxin Reductase High Expression Advanced Non-small Cell Lung Cancers).,,,,Ethaselen is investigational.,,True
21870,"Withdrawn from the Canadian, US, and UK markets in 1963 due to concerns involving neutropenia.",The molecular weight is 286.44.,Thenalidine has a topological polar surface area of 6.48.,The log p value of  is 3.78.,Thenalidine is approved and withdrawn.,Thenalidine is a solid.,True
21871,Pimethixene is approved for use in Brazil and is marketed under the trade name Muricalm. It is an anticholinergic used in the treatment of bronchitis.,The molecular weight is 293.43.,Pimethixene has a topological polar surface area of 3.24.,The log p value of  is 4.92.,Pimethixene is approved.,,True
21872,,The molecular weight is 307.4.,Talastine has a topological polar surface area of 35.91.,The log p value of  is 2.15.,Talastine is experimental.,,False
21873,,The molecular weight is 280.42.,Histapyrrodine has a topological polar surface area of 6.48.,The log p value of  is 4.79.,Histapyrrodine is experimental.,,False
21874,,The molecular weight is 321.46.,Sequifenadine has a topological polar surface area of 23.47.,The log p value of  is 3.52.,Sequifenadine is experimental.,,False
21875,,The molecular weight is 330.45.,Oxomemazine has a topological polar surface area of 40.62.,The log p value of  is 2.52.,Oxomemazine is experimental.,,False
21876,,The molecular weight is 329.48.,Hydroxyethylpromethazine has a topological polar surface area of 23.47.,The log p value of  is 1.38.,Hydroxyethylpromethazine is experimental.,,False
21877,,The molecular weight is 311.85.,Pyrrobutamine has a topological polar surface area of 3.24.,The log p value of  is 5.72.,Pyrrobutamine is experimental.,,False
21878,"Nalorphine is a mixed opioid agonist–antagonist. It acts at two opioid receptors—at the mu receptor it has antagonistic effects, and at the kappa receptors it exerts high-efficacy agonistic characteristics. It is used to reverse opioid overdose and (starting in the 1950s) in a challenge test to determine opioid dependence. Used to reverse opioid overdose.",The molecular weight is 311.38.,Nalorphine has a topological polar surface area of 52.93.,The log p value of  is 1.18.,Nalorphine is experimental and vet_approved.,Nalorphine is a solid.,True
21879,Axelopran has been used in trials studying the treatment of OIC and Opioid-induced Constipation.,,,,Axelopran is investigational.,,True
21880,Ly2456302 has been used in trials studying the health services research and basic science of Anxiety Disorders and Alcohol Dependence.,,,,LY-2456302 is investigational.,,True
21881,"Samidorphan has been used in trials studying the treatment of Schizophrenia, Alcohol Dependence, and Binge Eating Disorder.",,,,Samidorphan is investigational.,,True
21882,Ondelopran has been used in trials studying the treatment of Alcohol Dependence.,,,,Ondelopran is investigational.,,True
21883,,The molecular weight is 364.44.,Cyclofenil has a topological polar surface area of 52.6.,The log p value of  is 5.12.,Cyclofenil is experimental.,,False
21884,Nefopam is under investigation for the prevention of Cholecystitis and Post Anaesthetic Shivering. Nefopam has been investigated for the prevention of Kidney Transplantation.,The molecular weight is 253.34.,Nefopam has a topological polar surface area of 12.47.,The log p value of  is 2.91.,Nefopam is approved and investigational.,,True
21885,"Gsk256066 has been used in trials studying the treatment and diagnostic of SAR, Asthma, Mild Asthma, Allergic Rhinitis, and Seasonal Allergic Rhinitis, among others.",,,,GSK-256066 is investigational.,,True
21886,E6005 has been used in trials studying the treatment of Atopic Dermatitis.,,,,E-6005 is investigational.,,True
21887,MK-0873 has been used in trials studying the treatment of Rheumatoid Arthritis.,,,,MK-0873 is investigational.,,True
21888,VTP-27999 has been used in trials studying the basic science of Renal Function.,,,,VTP-27999 is investigational.,,True
21889,"Clorobiocin is an aminocoumarin antibiotic, similar to and coumermycin A1.",,,,Clorobiocin is experimental.,Clorobiocin is a solid.,True
21890,,The molecular weight is 176.17.,Hymecromone has a topological polar surface area of 46.53.,The log p value of  is 2.12.,Hymecromone is experimental and investigational.,Hymecromone is a solid.,False
21891,,,,,Haloxon is vet_approved.,,False
21892,Bergapten is under investigation in clinical trial NCT00533195 (Comparison of UVA1 Phototherapy Versus Photochemotherapy for Patients With Severe Generalized Atopic Dermatitis).,The molecular weight is 216.19.,Bergapten has a topological polar surface area of 48.67.,The log p value of  is 2.31.,Bergapten is investigational.,,True
21893,Tecarfarin has been used in trials studying the prevention of Thrombosis and Thromboembolism.,,,,Tecarfarin is investigational.,,True
21894,,,,,4-methylumbelliferyl beta-D-glucoside is experimental.,4-methylumbelliferyl beta-D-glucoside is a solid.,False
21895,"Carbocromen was marketed for use in Germany as a vasodilator, however, it has been discontinued due to the risk of arrhythmia development.",The molecular weight is 361.44.,Carbocromen has a topological polar surface area of 65.07.,The log p value of  is 3.37.,Carbocromen is approved and withdrawn.,,True
21896,,,,,Acetophenone is experimental.,Acetophenone is a solid.,False
21897,"Motexafin lutetium (MLu) is a second-generation photosensitizer for photodynamic therapy (PDT) of cancer. It belongs to the family of drugs called metallotexaphyrins. Also called lutetium texaphyrin. Motexafin lutetium is a pentadentate aromatic metallotexaphyrin with photosensitizing properties. Investigated for use/treatment in brain cancer, breast cancer, cervical dysplasia/cancer, prostate cancer, cancer/tumors (unspecified), coronary artery disease, macular degeneration, and peripheral vascular disease. Motexafin lutetium has the potential to combine the features of selective localization, ability to be activated by deeply penetrating far-red light, low incidence of skin photosensitization and water solubility. The product is in clinical development as a treatment for several types of solid tumors (as Lutrin), age-related macular degeneration (as Optrin), atherosclerosis and prevention of restenosis (as Antrin). Motexafin lutetium preferentially accumulates in tumor cells due to their increased rates of metabolism and absorbs light, forming an extended high energy conformational state that produces high quantum yields of singlet oxygen, resulting in local cytotoxic effects.",,,,Motexafin lutetium is investigational.,Motexafin lutetium is a solid.,True
21898,Investigated for use/treatment in macular degeneration.,,,,Rostaporfin is investigational.,Rostaporfin is a solid.,True
21899,,The molecular weight is 181.19.,Adrenalone has a topological polar surface area of 69.56.,The log p value of  is 0.32.,Adrenalone is experimental.,,False
21900,,The molecular weight is 1042.2.,Ornipressin has a topological polar surface area of 425.55.,The log p value of  is -2.98.,Ornipressin is experimental.,,False
21901,,,,,Angiotensinamide is experimental.,,False
21902,"Sodium chloride, also known as salt, common salt, table salt or halite, is an ionic compound with the chemical formula NaCl, representing a 1:1 ratio of sodium and chloride ions. Sodium chloride is the primary salt in seawater and in the extracellular fluid of many multicellular organisms. It is listed on the World Health Organization Model List of Essential Medicines. This intravenous solution is indicated for use in adults and pediatric patients as a source of electrolytes and water for hydration. Also, designed for use as a diluent and delivery system for intermittent intravenous administration of compatible drug additives.  Sodium, the major cation of the extracellular fluid, functions primarily in the control of water distribution, fluid balance, and osmotic pressure of body fluids. Sodium is also associated with chloride and bicarbonate in the regulation of the acid-base equilibrium of body fluid. Sodium and chloride — major electrolytes of the fluid compartment outside of cells (i.e., extracellular) — work together to control extracellular volume and blood pressure. Disturbances in sodium concentrations in the extracellular fluid are associated with disorders of water balance.",The molecular weight is 58.44.,,,Sodium chloride is approved and vet_approved.,Sodium chloride is a solid.,True
21903,,,,,Phenylacetaldehyde is experimental.,Phenylacetaldehyde is a solid.,False
21904,Malonaldehyde is the dialdehyde of.,,,,Malonaldehyde is experimental.,Malonaldehyde is a solid.,True
21905,,,,,Phosphonoacetaldehyde is experimental.,Phosphonoacetaldehyde is a solid.,False
21906,"One of the protein CROSS-LINKING REAGENTS that is used as a disinfectant for sterilization of heat-sensitive equipment and as a laboratory reagent, especially as a fixative.",The molecular weight is 100.12.,Glutaral has a topological polar surface area of 34.14.,The log p value of  is -0.17.,Glutaral is experimental.,Glutaral is a solid.,True
21907,,,,,P-Hydroxybenzaldehyde is experimental.,P-Hydroxybenzaldehyde is a solid.,False
21908,Tucaresol has been used in trials studying the treatment of HIV Infections.,,,,Tucaresol is investigational.,,True
21909,Cinnamaldehyde is a naturally occurring flavonoid that gives the spice cinnamon its flavour and odour. It occurs naturally in the bark of cinnamon trees and other species of the genus Cinnamomum such as camphor and cassia.  Cinnamaldehyde is approved by the FDA for use within allergenic epicutaneous patch tests which are indicated for use as an aid in the diagnosis of allergic contact dermatitis (ACD) in persons 6 years of age and older.,,,,Cinnamaldehyde is approved and experimental.,,True
21910,"Tosylchloramide, also known as chloramine-T, is a chlorinated and deprotonated sulfonamide used as a mild disinfectant. It is not stable in the water dissolved form.",,,,Tosylchloramide is experimental.,,True
21911,Dinitolmide is a fodder additive for prophylaxis against coccidiosis infections in poultry.,,,,Zoalene is experimental and vet_approved.,,True
21912,Iodohippuric acid is under investigation in clinical trial NCT02599844 (Impact of Pediatric Acute Renal Injury in Severe Sepsis in Young Adults).,,,,Iodohippuric acid is investigational.,,True
21913,"Patiromer is a powder for suspension in water for oral administration, approved in the U.S. as Veltassa in October, 2015. Patiromer is supplied as patiromer sorbitex calcium which consists of the active moiety, patiromer, a non-absorbed potassium-binding polymer, and a calcium-sorbitol counterion. Each gram of patiromer is equivalent to a nominal amount of 2 grams of patiromer sorbitex calcium. The chemical name for patiromer sorbitex calcium is cross-linked polymer of calcium 2-fluoroprop-2-enoate with diethenylbenzene and octa-1,7-diene, combination with D-glucitol. Patiromer sorbitex calcium is an amorphous, free-flowing powder that is composed of individual spherical beads. For the treatment of hyperkalemia. In clinical studies, patiromer decreased systemic exposure of some coadministered oral medications. Binding of patiromer to other oral medications could cause decreased gastrointestinal absorption and loss of efficacy when taken close to the time patiromer is administered. Administer oral medications at least 3 hours before or 3 hours after patiromer. Patiromer is a non-absorbed, cation exchange polymer that contains a calcium-sorbitol counterion. It increases fecal potassium excretion through binding of potassium in the lumen of the gastrointestinal tract. Binding of potassium reduces the concentration of free potassium in the gastrointestinal lumen, resulting in a reduction of serum potassium levels.",,,,Patiromer is approved and investigational.,Patiromer is a solid.,True
21914,Calcitonin is a polypeptide hormone secreted by the parafollicular cells of the thyroid gland in mammals. It inhibits bone resorption and lowers both serum and urinary calcium concentrations. Human calcitonin is available only in very small quantities but has been used in some studies. The first commercially available preparation in Britain was porcine calcitonin (brand name Calcitare).,,,,Calcitonin porcine is experimental.,Calcitonin porcine is a solid.,True
21915,,The molecular weight is 398.47.,Flumedroxone has a topological polar surface area of 54.37.,The log p value of  is 3.08.,Flumedroxone is experimental.,,False
21916,,The molecular weight is 339.19.,Brodimoprim has a topological polar surface area of 96.28.,The log p value of  is 2.16.,Brodimoprim is experimental.,,False
21917,"Alferminogene tadenovec, Cardium’s lead product candidate, is being developed for the potential treatment of myocardial ischemia that gives rise to angina symptoms associated with coronary heart disease. Alferminogene tadenovec represents a new therapeutic class of biologics designed to promote angiogenesis and thereby improve blood flow following a one-time intracoronary administration from a standard cardiac infusion catheter. Investigated for use/treatment in angina, coronary artery disease, and heart disease. Alferminogene tadenovec holds the potential to promote a disease-modifying improvement by leveraging the body’s natural healing processes in response to myocardia ischemia (insufficient blood flow and myocardial oxygen supply). Angiogenesis, the growth of new collateral blood vessels, is a natural biologic response to repeated myocardial ischemia. These newly formed vessels provide alternate routes of blood flow and oxygen delivery to parts of the patient’s heart downstream from a blockage in a coronary artery. In many patients however, including those with recurrent angina, coronary collateral vessel formation is insufficient to meet the heart’s needs during stress. Currently available anti-anginal drugs, which may provide symptomatic relief, are generally designed to alter the oxygen demand of the heart muscle or dilate vessels to temporarily relieve angina. Alferminogene tadenovec is designed to promote the heart’s natural response of collateral growth and to increase blood flow in the microcirculation.",,,,Alferminogene tadenovec is investigational.,Alferminogene tadenovec is a liquid.,True
21918,"A 37-amino acid peptide derived from the calcitonin gene. It occurs as a result of alternative processing of mRNA from the calcitonin gene. The neuropeptide is widely distributed in the brain, gut, perivascular nerves, and other tissue. The peptide produces multiple biological effects and has both circulatory and neurotransmitter modes of action. In particular, it is a potent endogenous vasodilator. Investigated for use/treatment in myocardial infarction, heart disease, and asthma. While current drugs for treating HF and MI have a single mechanism of action, CGRP appears to work on several levels: for example, it (1) increases local blood flow enhancing hemodynamic proficiency; (2) protects heart muscle cells from the damage due to lack of oxygen (ischemia); and, (3) modulates the immune system by boosting anti-inflammatory cytokine expression while suppressing pro-inflammatory cytokines, which reduces the inflammatory response to provide a cardioprotective effect. All these actions are meant to minimize heart muscle damage and subsequent scar tissue formation, while promoting the healing process.",,,,Calcitonin gene-related peptide is investigational.,Calcitonin gene-related peptide is a solid.,True
21919,Imolamine is a compound with a molecular weight of 260.33 g/mol with the formula diethylamine. It is developed under the brand name Coremax by Novartis consumer health SA. Imolamine is indicated for the treatment of angina pectoris. The hydrochloride form is used as a local anesthetic.,The molecular weight is 260.34.,Imolamine has a topological polar surface area of 51.92.,The log p value of  is 2.67.,Imolamine is investigational.,Imolamine is a solid.,True
21920,Cinepazide has been used in trials studying the treatment of Ischemic Stroke.,The molecular weight is 417.51.,Cinepazide has a topological polar surface area of 71.55.,The log p value of  is 1.62.,Cinepazide is investigational.,,True
21921,Bradykinin has been investigated for the basic science and treatment of Hypertension and Diabetes Type 2.,,,,Bradykinin is investigational.,,True
21922,Puerarin has been investigated for the treatment of Alcohol Abuse.,,,,Puerarin is investigational.,,True
21923,,The molecular weight is 209.29.,Bamethan has a topological polar surface area of 52.49.,The log p value of  is 1.5.,Bamethan is experimental.,,False
21924,"Flosequinan was approved in the USA and the UK for a year prior to being withdrawn from the market due to increased mortality in chronic heart failure patients, found in drug trials.",The molecular weight is 239.26.,Flosequinan has a topological polar surface area of 37.38.,The log p value of  is -0.75.,Flosequinan is approved.,,True
21925,"Hexobendine is a medication used to cause vasodilation, to treat several conditions including angina pectoris. It has not been approved in the United States or the United Kingdom, but has been used widely in Austria and Germany.",The molecular weight is 592.69.,Hexobendine has a topological polar surface area of 114.46.,The log p value of  is 4.63.,Hexobendine is approved.,,True
21926,,The molecular weight is 337.57.,Suloctidil has a topological polar surface area of 32.26.,The log p value of  is 5.99.,Suloctidil is experimental.,,False
21927,,The molecular weight is 600.54.,Nicofuranose has a topological polar surface area of 186.22.,The log p value of  is 1.27.,Nicofuranose is experimental.,,False
21928,,The molecular weight is 316.45.,Butalamine has a topological polar surface area of 54.19.,The log p value of  is 5.78.,Butalamine is experimental.,,False
21929,,The molecular weight is 604.7.,Dilazep has a topological polar surface area of 114.46.,The log p value of  is 3.54.,Dilazep is experimental.,,False
21930,,The molecular weight is 349.53.,Cetiedil has a topological polar surface area of 29.54.,The log p value of  is 5.97.,Cetiedil is experimental.,,False
21931,,The molecular weight is 294.4.,Vinburnine has a topological polar surface area of 25.24.,The log p value of  is 4.03.,Vinburnine is experimental.,,False
21932,Etafenone is a vasodilator.,The molecular weight is 325.45.,Etafenone has a topological polar surface area of 29.54.,The log p value of  is 5.05.,Etafenone is experimental.,,True
21933,Ornidazole has been used in trials studying the prevention of Elective Colorectal Surgery.,The molecular weight is 219.63.,Ornidazole has a topological polar surface area of 81.19.,The log p value of  is 0.06.,Ornidazole is investigational.,,True
21934,,The molecular weight is 267.24.,Propenidazole has a topological polar surface area of 107.01.,The log p value of  is 0.43.,Propenidazole is experimental.,,False
21935,"Diethyltoluamide (DEET) is the common active ingredient in many insect repellent products. It is widely used to repel biting pests such as mosquitoes and ticks. Every year, DEET formulations are used to protect populations from mosquito-borne illnesses like West Nile Virus, the Zika virus, malaria, and/or tick-borne illnesses like Lyme disease and Rocky Mountain spotted fever. And, despite concerns over excessive exposure to the chemical, appropriate usage of the chemical at the recommended dosages and routes of administration have generally proven to be safe - even when most DEET products are largely designed to be applied directly to human skin, where the exact mechanisms of actions in which DEET is capable of repelling insects and causing toxicity to humans is still not fully elucidated. Diethyltoluamide, or DEET, is an active ingredient that is predominantly indicated for as an insect repellant used to repel biting pests like mosquitoes and ticks. Products containing DEET currently are available to the public in a variety of liquids, lotions, sprays, and impregnated materials like towelettes or roll-ons. When used appropriately, diethyltoluamide (DEET) containing products are designed to be applied directly to people's skin as a means to elicit a repelling action to keep insects from targeting human skin. At the amounts and doses recommended for use on human children and adults, noticeable absorption or systemic exposure is not expected. Owing to the proportional difference in size between humans and insects, however, the exposure of insects to the applied DEET (whether topically or via inhalation of DEET) is expected to be enough to interfere with the insects' sensory attraction to human skin. The exact mechanism(s) of action by which both (a) insects are repelled by diethyltoluamide (DEET), and (b) humans can be affected deleteriously by exposure to toxic amounts of DEET have not yet been formally elucidated.",The molecular weight is 191.27.,Diethyltoluamide has a topological polar surface area of 20.31.,The log p value of  is 2.16.,Diethyltoluamide is approved.,,True
21936,"Icaridin, also known as Picaridin or hydroxy-ethyl isobutyl piperidine carboxylate, is a cyclic amine and a member of the piperidine chemical family. Piperidines are structural components of , which is a plant extract from the genus _Piper _, or pepper. Icaridin has been commonly used as a topically-applied insect repellent in various countries but was officially licensed for use in the United States in 2001 and Canada in 2012. Icaridin was synthesized by Bayer in the 1980s based on molecular modeling. It is considered to be the first choice of repellent by the Public Health Agency of Canada’s Canadian Advisory Committee on Tropical Medicine and Travel for travelers six months to 12 years of age. Icaridin is reported to be less irritating than , another common insect repellant, and products containing up to 20% of icaridin are considered safe for long-term use in adults. Icaridin is indicated for use to repel insects, such as mosquitoes, biting flies, ticks, chiggers, and fleas, via topical use or over clothing.  Icaridin is a cyclic amine and piperidine compound that is expected to stimulate the sensory hairs on the antennae of insects. The exact mechanism and target molecules of icaridin repelling insects are not fully understood; it is presumed that piperine interacts with the olfactory system consisting of odorant receptors (ORs) that need a common co-receptor (ORCO), and of ionotropic receptors (IR) , leading to the insect's inability to recognize its host's cues. It is also suggested that icaridin may bind to odorant binding protein 1 (AgamOBP1) at different binding sites. A study demonstrated that icaridin inhibited the odorant-induced responses of AaOR2 and AaOR8 expressed in Xenopus oocytes, leading to altered olfactory inputs by olfactory sensory neurons (OSN).",,,,Icaridin is experimental.,Icaridin is a liquid.,True
21937,"A mercaptodicarboxylic acid used as an antidote to heavy metal poisoning because it forms strong chelates with them. For the treatment of lead poisoning in pediatric patients with blood lead levels above 45 &micro;g/dL. May also be used to treat mercury or arsenic poisoning. Succimer is an orally active, heavy metal chelating agent. It forms water soluble chelates and, consequently, increases the urinary excretion of lead. Succimer is not to be used for prophylaxis of lead poisoning in a lead-containing environment. In addition, the use of succimer should always be accompanied by identification and removal of the source of the lead exposure. Succimer is a heavy metal chelator. It binds with high specificity to ions of lead in the blood to form a water-soluble complex that is subsequently excreted by the kidneys. Succimer can also chelate mercury, cadmium, and arsenic in this manner.",The molecular weight is 182.21.,Succimer has a topological polar surface area of 74.6.,The log p value of  is -1.48.,Succimer is approved.,Succimer is a solid.,True
21938,,,,,Dipicolinic acid is experimental.,Dipicolinic acid is a solid.,False
21939,"Tagatose is a functional sweetener. It is a naturally occurring monosaccharide, specifically a hexose. It is commonly found in dairy with a similar texture and sweetened capacity to sucrose but with only a third of the calories. It is approved as a food additive as a low calorie sweetener. Additionally, it is under investigation by Spherix for the treatment of obesity and type II diabetes. Intended for use as a therapeutic adjunct in the treatment of type II diabetes. Oral tagatose significantly blunts the rise in plasma glucose seen after oral glucose in patients with diabetes mellitus in a dose-dependent manner without significantly affecting insulin levels. The minimal elevation of plasma tagatose levels in normal patients and the adverse gastrointestinal effects seen following larger doses of tagatose support poor absorption of this hexose and suggest that tagatose may act by attenuating glucose absorption in the intestine. he steps in the metabolism of tagatose are identical to those for fructose or fruit sugar but tagatose is incompletely absorbed. Only 15-20 percent of tagatose is absorbed in the small intestine. The major part of ingested tagatose is fermented in the colon by indigenous microflora, resulting in the production of short-chain fatty acids. The short chain fatty acids are absorbed almost completely and metabolized.",,,,Tagatose is investigational.,Tagatose is a solid.,True
21940,"Poliglusam, or chitosan, is a linear polysaccharide consisting of D-glucosamine and N-acetyl-D-glucosamine. Naturally-occuring poliglusam is found in the cell walls of fungi, soil and sediments where it is produced from degradation of chitin induced by certain groups of bacteria that produce the enzymes deacetylase or chitosanase enzymes. In comparison, commercial poliglusam is derived from deacetylation of chitin contained in the shells of various sea crustaceans such as shrimps. As a rich source of dietary fiber, chitosan is used as a food ingredient or additive. It is also reported to have an effect on protein aggregation, emulsification capacity, film-forming ability, clarifying ability, and fatty acid absorption capability. In addition, chitosan also exhibits antimicrobial and antioxidant activities.",,,,Poliglusam is experimental.,,True
21941,Emeramide has been used in trials studying the treatment of Mercury Poisoning.,,,,Emeramide is investigational.,,True
21942,Dichloroisoproterenol has been used in trials studying the treatment and basic science of Insulin Resistance and Polycystic Ovary Syndrome.,,,,Dichloroisoproterenol is investigational.,,True
21943,"Dimethicone is a silicone oil that is also known as polydimethylsiloxane (PDMS). It has viscoelastic properties. Dimethicone is used as a surfactant, antifoaming agent, carminative in various products such as medical devices, food products, and lubricants. It is used in a number of health and beauty products including hair care products such as shampoo, conditioner, leave-in conditioner, and de-tangling products. On skin, it is also observed to have moisturizing actions. Dimethicone is a colorless liquid with both cosmetic and therapeutic uses. It is used in topical creams and ointments to help distribute the active ingredients. Dimethicone is used as an anti-foaming agent, a hair and skin conditioner, and in the treatment of head lice and, as an anti-bloating/anti-flatulence agent ,. This drug acts as a skin protectant by helping to treat and prevent minor skin irritation due to diaper rash and seals out moisture from the diaper area. This drug temporarily protects and helps prevent chafed, chapped, cracked or windburned skin.. When applied topically, dimethicone forms a layer to delay the evaporation of water.",,,,Dimethicone is approved.,,True
21944,Tocotrienol has been investigated for the treatment of Cholesterol Lowering.,,,,Tocotrienol is investigational.,,True
21945,Menaquinone 7 is under investigation in clinical trial NCT00402974 (The Effect of Vitamin K Supplementation on Osteocalcin Carboxylation in Healthy Children).,,,,Menaquinone 7 is investigational.,,True
21946,,,,,DL-alpha-Tocopherol is approved and experimental and investigational.,,False
21947,Menaquinone 6 is under investigation in clinical trial NCT01194778 (Comparison of Efficacy of Different Dosages Vitamin K2).,,,,Menaquinone 6 is investigational.,,True
21948,Menaquinone is under investigation in clinical trial NCT01533441 (Vitamin K2 Intervention in Patients With Vitamin K Antagonists).,,,,Menaquinone is investigational.,,True
21949,gamma-Tocopherol is under investigation in clinical trial NCT00836368 (In Vitro Basophil Responsiveness to Allergen Challenge After Gamma-tocopherol Supplementation in Allergic Asthmatics).,,,,gamma-Tocopherol is investigational.,,True
21950,,,,,Aluminum cation is experimental.,,False
21951,,,,,Sodium aurotiosulfate is approved and experimental.,,False
21952,"Sulprostone has been used in trials studying Abortion, Induced.",The molecular weight is 465.56.,Sulprostone has a topological polar surface area of 130.0.,The log p value of  is 0.18.,Sulprostone is investigational.,,True
21953,,The molecular weight is 992.18.,Demoxytocin has a topological polar surface area of 373.51.,The log p value of  is 0.02.,Demoxytocin is experimental.,,False
21954,,The molecular weight is 254.76.,Butanilicaine has a topological polar surface area of 41.13.,The log p value of  is 2.15.,Butanilicaine is experimental.,,False
21955,,The molecular weight is 236.32.,Metabutethamine has a topological polar surface area of 64.35.,The log p value of  is 2.34.,Metabutethamine is experimental.,,False
21956,,The molecular weight is 272.39.,Quinisocaine has a topological polar surface area of 25.36.,The log p value of  is 4.82.,Quinisocaine is experimental.,,False
21957,,The molecular weight is 253.35.,Meladrazine has a topological polar surface area of 83.2.,The log p value of  is 3.36.,Meladrazine is experimental.,,False
39887,"Galactose has been used in trials studying the treatment and diagnosis of Hepatitis C, Hepatic Cancer, Wilsons Disease, Diabetic Macular Oedema, and Focal Segmental Glomerulosclerosis, among others. There are even proposals for its use in accelerating senescence in mice, rats, and Drosophila, for its association with ovarian cancer, or even for the potential treatment of focal segmental glomerulosclerosis. Nevertheless, none of these ongoing studies have yet provided formal elucidation for their proposals. There are limited therapeutic uses for which galactose is formally indicated. Some predominant indications include (a) the use of galactose to facilitate the construction of structurally and immunologically effective attenuated vaccines , and (b) the role galactose plays as an essential element in the formation of lactulose - a synthetic disaccharide indicated for the treatment of constipation and/or hepatic encephalopathy (HE); hepatic coma. Galactose is a naturally occurring monosaccharide that forms the disaccharide lactose when combined with glucose (another monosaccharide). Subsequently, when lactose or small amounts of free galactose found in various common dairy products (and other foods) are consumed, the hydrolysis of lactose to glucose and galactose occurs and galactose is itself further metabolized to generate glucose. Such glucose is, of course, ultimately relied upon and used as the primary metabolic fuel for humans in a variety of biological reactions. In the development of typhoid Ty21a live oral vaccine, the use of exogenous galactose is critical. When dealing with Salmonella typhimurium, it has been shown that rough strains with incomplete lipopolysaccharide (LPS) lacking O-specific side chains are much less virulent than smooth strains with complete LPS with O-specific side chains. Salmonella typhimurium gal E mutants used to produce the vaccine are effectively avirulent and highly protective but lack the specific UDP-galactose 4-epimerase enzyme which allows for the normal synthesis of UDP-galactose from UDP-glucose. The consequence of this mutant defect is that the gal E mutants can only generate incomplete LPS without O-specific antigen side chains, which are not capable enough as the complete LPS with O-specific side chains at generating an immunologic response. When exogenous galactose is added to the vaccine medium, however, it allows the mutants to generate UDP-galactose via galactose 1-phosphate. This ultimately allows the mutants to form smooth-type LPS with O-specific side chains. Regardless, the mutant's epimerase defect ultimately results in the accumulation of such intermediary products like galactose 1-phosphate and UDP-galactose, which consequently causes lysis of the mutant cells. The resultant vaccine is subsequently effective enough to elicit an immunologic response while the bacteriolysis prevents the mutant cells from regaining virulence under conditions where smooth type LPS similar to the active parental strain is synthesized.",The molecular weight is 180.16.,Galactose has a topological polar surface area of 110.38.,The log p value of  is -2.21.,Galactose is approved and investigational.,,True
39888,"Benzyl benzoate is one of the older preparations used to treat scabies. Scabies is a skin infection caused by the mite sarcoptes scabiei. It is characterised by severe itching (particularly at night), red spots, and may lead to a secondary infection. Benzyl benzoate is lethal to this mite and so is useful in the treatment of scabies. It is also used to treat lice infestation of the head and body. Benzyl benzoate is not the treatment of choice for scabies due to its irritant properties. Used to kill lice and the mites responsible for the skin condition scabies. Benzyl benzoate is one of the older preparations used to treat scabies. Scabies is a skin infection caused by the mite sarcoptes scabiei. It is characterised by severe itching (particularly at night), red spots, and may lead to a secondary infection. Benzyl benzoate is lethal to this mite and so is useful in the treatment of scabies. It is also used to treat lice infestation of the head and body. Benzyl benzoate is not the treatment of choice for scabies due to its irritant properties. Benzyl benzoate exerts toxic effects on the nervous system of the parasite, resulting in its death. It is also toxic to mite ova, though its exact mechanism of action is unknown. In vitro, benzyl benzoate has been found to kill the Sarcoptes mite within 5 minutes.",The molecular weight is 212.25.,Benzyl benzoate has a topological polar surface area of 26.3.,The log p value of  is 3.94.,Benzyl benzoate is approved.,Benzyl benzoate is a liquid.,True
39889,"Bromhexine is an expectorant/mucolytic agent. Bromhexine is not available in the United States. It is marketed under the trade name Bisolvon(R) in Germany, England, Belgium, France, Italy, Netherlands, Norway, Sweden, Australia, and South Africa.",The molecular weight is 376.14.,Bromhexine has a topological polar surface area of 29.26.,The log p value of  is 4.88.,Bromhexine is approved.,Bromhexine is a solid.,True
39890,,,,,Protamine is experimental and investigational.,,False
39891,"Nonionic, isotonic contrast medium designed for intrathecal use.",The molecular weight is 1626.24.,Iotrolan has a topological polar surface area of 399.78.,The log p value of  is -4.2.,Iotrolan is approved.,,True
39892,"Ioxaglic acid is marketed as Hexabrix. This drug is an ionic tri-iodinated benzoate used as a low-osmolality contrast agent during diagnostic imaging procedures. Like other organic iodine compounds, ioxaglic acid blocks x-rays and is opaque in its appearance on x-ray film, improving the visualization of important structures and organs during angiography, arteriography, arthrography, cholangiography, urography, and computed tomography. This medicinal product is for diagnostic use only in adults and children as a low-osmolality medium ,.  This drug allows for the visualization of important organs and structures in the body. It binds to tissues, allowing the blockage of X-rays and diagnostic visualization in various soft tissues and body cavities.  Ioxaglic acid is an iodine-containing, low osmolality contrast agent. Ioxaglate is a molecule that consists of six iodine atoms and achieves water solubility by ionization; thus, it is a 3.0 ratio ionic agent. ",The molecular weight is 1268.89.,Ioxaglic acid has a topological polar surface area of 194.24.,The log p value of  is -0.84.,Ioxaglic acid is approved and investigational.,Ioxaglic acid is a solid.,True
39893,"Cathine, also known as d-norpseudoephedrine and (+)-norpseudoephedrine, is a psychoactive drug with stimulant properties. It belongs to the phenethylamine and amphetamine chemical classes. In the United States, it is classified as a Schedule IV controlled substance. Used to decrease appetite. Closely related to ephedrine, cathinone and other amphetamines, it may contribute to the stimulant effect of <i>Catha edulis</i>, although another constituent, cathinone appears to show stronger activity.",The molecular weight is 151.21.,Cathine has a topological polar surface area of 46.25.,The log p value of  is 0.58.,Cathine is experimental and illicit.,Cathine is a solid.,True
39894,"Sulfur hexafluoride is an ultrasound contrast agent indicated for use  Echocardiography: Sulfur hexafluoride is indicated for use in adult patients with suboptimal echocardiograms to opacify the left ventricular chamber and to improve the delineation of the left ventricularendocardial border.  Sulfur hexafluoride provides useful echocardiographic signal intensity for two minutes after the injection. Sulfur hexafluoride microspheres are destroyed and contrast enhancement decreases as the mechanical index increases (values of 0.8 or less are recommended).  Within the blood, the acoustic impedance of Lumason microspheres is lower than that of the surrounding non-aqueous tissue. Therefore, an ultrasound beam is reflected from the interface between the microspheres and the surrounding tissue. The reflected ultrasound signal provides a visual image that shows a contrast between the blood and the surrounding tissues. ",The molecular weight is 146.05.,,,Sulfur hexafluoride is approved.,,True
39895,"Butoconazole is an imidazole antifungal used in gynecology. For the local treatment of vulvovaginal candidiasis (infections caused by Candida) Butoconazole is an imidazole derivative that has fungicidal activity <i>in vitro</i> against <i>Candida</i> spp. and has been demonstrated to be clinically effective against vaginal infections due to <i>Candida albicans</i>. <i>Candida albicans</i> has been identified as the predominant species responsible for vulvovaginal candidasis. The exact mechanism of the antifungal action of butoconazole is unknown, however, it is presumed to function as other imidazole derivatives via inhibition of steroid synthesis. Imidazoles generally inhibit the conversion of lanosterol to ergosterol via the inhibition of the enzyme cytochrome P450 14&alpha;-demethylase, resulting in a change in fungal cell membrane lipid composition. This structural change alters cell permeability and, ultimately, results in the osmotic disruption or growth inhibition of the fungal cell.",,,,Butoconazole is approved.,Butoconazole is a solid.,True
39896,"Gadoversetamide, marketed under the trade name OptiMARK, is a gadolinium compound used as a contrast agent in magnetic resonance imaging (MRI), particularly imaging of the brain, spine and liver. Gadoversetamide is an MRI contrast agent used for MRI diagnostic procedures to provide increased enhancement and visualization of lesions of the brain, spine and liver, including tumors. Based on the behavior of protons when placed in a strong magnetic field, which is interpreted and transformed into images by magnetic resonance (MR) instruments. MR images are based primarily on proton density and proton relaxation dynamics. MR instruments are sensitive to two different relaxation processes, the T1 (spin-lattice or longitudinal relaxation time) and T2 (spin-spin or transverse relaxation time). Paramagnetic agents contain one or more unpaired electrons that enhance the T1 and T2 relaxation rates of protons in their molecular environment. In MRI, visualization of normal and pathological brain, spinal and hepatic tissue depends in part on variations in the radio frequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in T2. When placed in a magnetic field, gadoversetamide shortens the T1 and T2 relaxation times in tissues where it accumulates. At the recommended dose, the effect is primarily on T1 relaxation time, and produces an increase in signal intensity (brightness). Gadoversetamide does not cross the intact blood-brain barrier; therefore, it does not accumulate in normal brain tissue or in CNS lesions that may have a normal blood-brain barrier (e.g., cysts, mature post-operative scars). Abnormal vascularity or disruption of the blood-brain barrier allows accumulation of gadoversetamide in lesions such as neoplasms, abscesses, and subacute infarcts.",The molecular weight is 661.77.,,,Gadoversetamide is approved and investigational.,Gadoversetamide is a solid.,True
39897,"Intravenous gadobutrol is a second-generation extracellular non-ionic macrocyclic GBCA (gadolinium-based contrast agent) used in magnetic resonance imaging (MRI) in adults and children older than 2 years of age. It may help visualize and detect vascular abnormalities in the blood brain barrier (BBB) and central nervous system (CNS).  For diagnostic use only. Indicated for adults and children age 2 and over for contrast enhancement during cranial and spinal MRI, and for contrast-enhanced magnetic resonance angiography (CE-MRA). Gadobutrol is particularly suited for the detection of very small lesions and for the visualization of tumors that do not readily take up contrast media. It may be a desired agent when the exclusion or demonstration of an additional pathology may influence the choice of therapy or patient management. It may also be suitable for perfusion studies in the diagnosis of stroke, detection of focal cerebral ischemia, and in studies of tumor perfusion.  Even at low concentrations Gadobutrol can lead to distinct shortening of relaxation times of protons in plasma. At physiological conditions (pH=7, temperature=37°C), and 1.5T, the relaxivity (r1) is 5.2L/(mmol·sec) based on the relaxation times (T1), while the relativity (r2) is 6.1L/(mmol·sec) based on relaxation times (T2).  MRI tissue visualization is dependent, in part, on variations in intensity of radiofrequency signals which occur due to differences in proton density, differences of the spin-lattice or longitudinal relaxation times (T1), and differences in the spin-spin or transverse relaxation times (T2).",The molecular weight is 604.72.,Gadobutrol has a topological polar surface area of 181.08.,,Gadobutrol is approved.,Gadobutrol is a liquid.,True