The involvement of EP1 and EP2 receptors is indicated by studies with the EP1 selective agonist 17-phenyl trinor PGE2, and the << EP2 >> selective agonist butaprost (which stimulate), as well as by studies with the antagonists SC-51089 (EP1 specific) and [[ AH 6809 ]] (EP1 and EP2 specific).


The involvement of EP1 and EP2 receptors is indicated by studies with the EP1 selective agonist 17-phenyl trinor PGE2, and the EP2 selective agonist butaprost (which stimulate), as well as by studies with the antagonists SC-51089 (EP1 specific) and << AH 6809 >> ([[ EP1 ]] and EP2 specific).


The involvement of EP1 and EP2 receptors is indicated by studies with the EP1 selective agonist 17-phenyl trinor PGE2, and the EP2 selective agonist butaprost (which stimulate), as well as by studies with the antagonists SC-51089 (EP1 specific) and << AH 6809 >> (EP1 and [[ EP2 ]] specific).


In addition to this evidence (for the involvement of EP2 receptors), evidence for the involvement of EP1 receptors in the << PGE1 >> mediated stimulation of [[ Na,K-ATPase beta ]] subunit gene transcription includes the stimulatory effect of 17-phenyl trinor PGE2, as well as the inhibitory effects of SC-51089.


In addition to this evidence (for the involvement of EP2 receptors), evidence for the involvement of EP1 receptors in the PGE1 mediated stimulation of << Na,K-ATPase beta >> subunit gene transcription includes the stimulatory effect of [[ 17-phenyl trinor PGE2 ]], as well as the inhibitory effects of SC-51089.


In addition to this evidence (for the involvement of EP2 receptors), evidence for the involvement of EP1 receptors in the PGE1 mediated stimulation of << Na,K-ATPase beta >> subunit gene transcription includes the stimulatory effect of 17-phenyl trinor PGE2, as well as the inhibitory effects of [[ SC-51089 ]].


Also consistent with the involvement of Gq coupled EP1 receptors, the PGE1 stimulation is inhibited by the PKCI vector (encoding the PKC inhibitory domain), the << PKC >> inhibitor Go 6976, [[ thapsigargin ]], as well as the calmodulin antagonists W7 and W13.


Also consistent with the involvement of Gq coupled EP1 receptors, the PGE1 stimulation is inhibited by the PKCI vector (encoding the PKC inhibitory domain), the << PKC >> inhibitor [[ Go 6976 ]], thapsigargin, as well as the calmodulin antagonists W7 and W13.


Also consistent with the involvement of Gq coupled EP1 receptors, the PGE1 stimulation is inhibited by the PKCI vector (encoding the PKC inhibitory domain), the PKC inhibitor Go 6976, thapsigargin, as well as the << calmodulin >> antagonists [[ W7 ]] and W13.


Also consistent with the involvement of Gq coupled EP1 receptors, the PGE1 stimulation is inhibited by the PKCI vector (encoding the PKC inhibitory domain), the PKC inhibitor Go 6976, thapsigargin, as well as the << calmodulin >> antagonists W7 and [[ W13 ]].


Spiro heterocycles as potential inhibitors of << SIRT1 >>: Pd/C-mediated synthesis of novel [[ N-indolylmethyl spiroindoline-3,2'-quinazolines ]].


Novel << N-indolylmethyl substituted spiroindoline-3,2'-quinazolines >> were designed as potential inhibitiors of [[ SIRT1 ]].


Cyclopentenone prostaglandins suppress activation of microglia: down-regulation of << inducible nitric-oxide synthase >> by [[ 15-deoxy-Delta12,14-prostaglandin J2 ]].


<< Cyclopentenone prostaglandins >> suppress activation of microglia: down-regulation of [[ inducible nitric-oxide synthase ]] by 15-deoxy-Delta12,14-prostaglandin J2.


<< Cyclopentenone prostaglandins >> were potent inhibitors of [[ iNOS ]] induction and were more effective than their precursors, prostaglandins E2 and D2.


Cyclopentenone prostaglandins were potent inhibitors of << iNOS >> induction and were more effective than their precursors, [[ prostaglandins E2 and D2 ]].


In activated microglia, << 15d-PGJ2 >> suppressed iNOS promoter activity, [[ iNOS ]] mRNA, and protein levels.


In activated microglia, << 15d-PGJ2 >> suppressed [[ iNOS promoter ]] activity, iNOS mRNA, and protein levels.


<< 15d-PGJ2 >> did not block nuclear translocation or DNA-binding activity of the transcription factor NFkappaB, but it did inhibit the activity of an [[ NFkappaB ]] reporter construct, suggesting that the mechanism of suppression of microglial iNOS by 15d-PGJ2 may involve interference with NFkappaB transcriptional activity in the nucleus.


15d-PGJ2 did not block nuclear translocation or DNA-binding activity of the transcription factor NFkappaB, but it did inhibit the activity of an NFkappaB reporter construct, suggesting that the mechanism of suppression of microglial << iNOS >> by [[ 15d-PGJ2 ]] may involve interference with NFkappaB transcriptional activity in the nucleus.


In vitro studies, however, revealed that << EO >> inhibits [[ fibrin ]] clot formation because of the Ca2+-chelating ability of its constituent ethanolamine, although oleate or benzyl alcohol exhibited procoagulant activity in FPA formation in vitro.


The activation may be accelerated by an acute inflammatory process provoked by << oleate >>, which is supported by such clinical manifestations as mild fever, retrosternal pain leukocytosis and an increase in plasma [[ fibrinogen ]] level which was observed in all during the period.


OBJECTIVE: Celecoxib and << rofecoxib >> are two relatively new nonsteroidal anti-inflammatory drugs (NSAIDs) that selectively inhibit the [[ cyclo-oxygenase-2 ]] (COX-2) isoenzyme at therapeutic concentrations.


OBJECTIVE: Celecoxib and << rofecoxib >> are two relatively new nonsteroidal anti-inflammatory drugs (NSAIDs) that selectively inhibit the cyclo-oxygenase-2 ([[ COX-2 ]]) isoenzyme at therapeutic concentrations.


OBJECTIVE: << Celecoxib >> and rofecoxib are two relatively new nonsteroidal anti-inflammatory drugs (NSAIDs) that selectively inhibit the [[ cyclo-oxygenase-2 ]] (COX-2) isoenzyme at therapeutic concentrations.


OBJECTIVE: << Celecoxib >> and rofecoxib are two relatively new nonsteroidal anti-inflammatory drugs (NSAIDs) that selectively inhibit the cyclo-oxygenase-2 ([[ COX-2 ]]) isoenzyme at therapeutic concentrations.


This study was conducted in order to understand the association between acute renal failure and the two << COX-2 >> inhibitors [[ celecoxib ]] and rofecoxib.


This study was conducted in order to understand the association between acute renal failure and the two << COX-2 >> inhibitors celecoxib and [[ rofecoxib ]].


<< (+)-Tamsulosin >>, (-)-tamsulosin, SL 89,0591, Rec 15/2739, SNAP 1069 and RS 17053 appeared to act as competitive antagonists of noradrenaline-mediated contractions of rat aorta yielding pA2 affinity estimates which were similar to binding affinities at cloned [[ human alpha 1D adrenoceptors ]].


(+)-Tamsulosin, << (-)-tamsulosin >>, SL 89,0591, Rec 15/2739, SNAP 1069 and RS 17053 appeared to act as competitive antagonists of noradrenaline-mediated contractions of rat aorta yielding pA2 affinity estimates which were similar to binding affinities at cloned [[ human alpha 1D adrenoceptors ]].


(+)-Tamsulosin, (-)-tamsulosin, << SL 89,0591 >>, Rec 15/2739, SNAP 1069 and RS 17053 appeared to act as competitive antagonists of noradrenaline-mediated contractions of rat aorta yielding pA2 affinity estimates which were similar to binding affinities at cloned [[ human alpha 1D adrenoceptors ]].


(+)-Tamsulosin, (-)-tamsulosin, SL 89,0591, << Rec 15/2739 >>, SNAP 1069 and RS 17053 appeared to act as competitive antagonists of noradrenaline-mediated contractions of rat aorta yielding pA2 affinity estimates which were similar to binding affinities at cloned [[ human alpha 1D adrenoceptors ]].


(+)-Tamsulosin, (-)-tamsulosin, SL 89,0591, Rec 15/2739, << SNAP 1069 >> and RS 17053 appeared to act as competitive antagonists of noradrenaline-mediated contractions of rat aorta yielding pA2 affinity estimates which were similar to binding affinities at cloned [[ human alpha 1D adrenoceptors ]].


(+)-Tamsulosin, (-)-tamsulosin, SL 89,0591, Rec 15/2739, SNAP 1069 and << RS 17053 >> appeared to act as competitive antagonists of noradrenaline-mediated contractions of rat aorta yielding pA2 affinity estimates which were similar to binding affinities at cloned [[ human alpha 1D adrenoceptors ]].


The potency of the antipsychotic drug, << risperidone >>, to antagonize alpha 1A-adrenoceptor-mediated contraction in rat vas deferens and vasoconstriction in rat perfused kidney, and [[ alpha 1B-adrenoceptor ]]-mediated contractions in spleen from guinea-pig and mouse was evaluated and compared to that of alpha 1-adrenoceptor subtype-discriminating antagonists.


The potency of the antipsychotic drug, << risperidone >>, to antagonize alpha 1A-adrenoceptor-mediated contraction in rat vas deferens and vasoconstriction in rat perfused kidney, and alpha 1B-adrenoceptor-mediated contractions in spleen from guinea-pig and mouse was evaluated and compared to that of [[ alpha 1-adrenoceptor ]] subtype-discriminating antagonists.


The potency of the antipsychotic drug, << risperidone >>, to antagonize [[ alpha 1A-adrenoceptor ]]-mediated contraction in rat vas deferens and vasoconstriction in rat perfused kidney, and alpha 1B-adrenoceptor-mediated contractions in spleen from guinea-pig and mouse was evaluated and compared to that of alpha 1-adrenoceptor subtype-discriminating antagonists.


In this article, the action of << dasatinib >> (BMS-354825) is contrasted with that of imatinib, a [[ kinase ]] inhibitor that is currently being used to treat chronic myelogenous leukemia and other disorders.


In this article, the action of dasatinib (<< BMS-354825 >>) is contrasted with that of imatinib, a [[ kinase ]] inhibitor that is currently being used to treat chronic myelogenous leukemia and other disorders.


In this article, the action of dasatinib (BMS-354825) is contrasted with that of << imatinib >>, a [[ kinase ]] inhibitor that is currently being used to treat chronic myelogenous leukemia and other disorders.


The work of Chen and colleagues shows that << dasatinib >> is a particularly potent inhibitor of [[ PDGFR ]] and that the compound also targets Src kinase.


The work of Chen and colleagues shows that << dasatinib >> is a particularly potent inhibitor of PDGFR and that the compound also targets [[ Src kinase ]].


From these data, it is inferred that both the << SERT >> and NET contribute to the active clearance of exogenously applied [[ 5-HT ]] in the dentate gyrus.


From these data, it is inferred that both the SERT and << NET >> contribute to the active clearance of exogenously applied [[ 5-HT ]] in the dentate gyrus.


In another experiment, << cyanopindolol >>, an antagonist of the [[ serotonin terminal autoreceptor ]], also prolonged the clearance of 5-HT from the CA3 region.


These and other data have generated a working hypothesis that activation of the terminal serotonin autoreceptor enhances the kinetics of << 5-HT >> uptake through an effect on the [[ serotonin transporter ]].


These and other data have generated a working hypothesis that activation of the terminal << serotonin autoreceptor >> enhances the kinetics of [[ 5-HT ]] uptake through an effect on the serotonin transporter.


The anti-amnesic effect of minaprine on the cycloheximide-induced memory impairment was also antagonized by a serotonin (5-HT) releaser, p-chloroamphetamine, and by a 5-HT precursor, 5-hydroxytryptophan, whereas a << 5-HT1A >>-selective agonist, [[ 8-hydroxy-2-(di-n-propylamino)tetralin ]], was inactive.


The memory-improving effect of minaprine on cycloheximide-induced amnesia was potentiated by a selective << 5-HT2 >> antagonist, [[ ritanserin ]].


Even though the activities of << MAT >> and GNMT were elevated, the concentration of liver S-adenosylmethionine was decreased (24%, p<0.001) and [[ S-adenosylhomocysteine ]] increased (113%, p<0.001) in the dwarf mice.


Even though the activities of MAT and << GNMT >> were elevated, the concentration of liver S-adenosylmethionine was decreased (24%, p<0.001) and [[ S-adenosylhomocysteine ]] increased (113%, p<0.001) in the dwarf mice.


Even though the activities of << MAT >> and GNMT were elevated, the concentration of liver [[ S-adenosylmethionine ]] was decreased (24%, p<0.001) and S-adenosylhomocysteine increased (113%, p<0.001) in the dwarf mice.


Even though the activities of MAT and << GNMT >> were elevated, the concentration of liver [[ S-adenosylmethionine ]] was decreased (24%, p<0.001) and S-adenosylhomocysteine increased (113%, p<0.001) in the dwarf mice.


Activation of << alpha 2B-adrenoceptors >> mediates the cardiovascular effects of [[ etomidate ]].


BACKGROUND: The intravenous anesthetic etomidate exhibits structural similarities to specific << alpha2-adrenoceptor >> agonists of the type such as [[ dexmedetomidine ]].


METHODS: Sedative and cardiovascular responses to etomidate and the alpha2-agonist, << dexmedetomidine >>, were determined in mice deficient in [[ alpha2-receptor ]] subtypes.


Inhibition of binding of the << alpha2-receptor >> antagonist [[ [3H]RX821002 ]] to recombinant alpha2-receptors by etomidate was tested in human embryonic kidney (HEK293) cells in vitro.


Inhibition of binding of the alpha2-receptor antagonist << [3H]RX821002 >> to recombinant [[ alpha2-receptors ]] by etomidate was tested in human embryonic kidney (HEK293) cells in vitro.


In membranes from HEK293 cells transfected with << alpha2-receptors >>, etomidate inhibited binding of the alpha2-antagonist, [[ [3H]RX821002 ]], with higher potency from alpha2B- and alpha2C-receptors than from alpha2A-receptors (Ki alpha2A 208 microm, alpha2B 26 microm, alpha2C 56 microm).


In membranes from HEK293 cells transfected with alpha2-receptors, etomidate inhibited binding of the alpha2-antagonist, << [3H]RX821002 >>, with higher potency from alpha2B- and alpha2C-receptors than from [[ alpha2A-receptors ]] (Ki alpha2A 208 microm, alpha2B 26 microm, alpha2C 56 microm).


In alpha2B-receptor-expressing HEK293 cells, << etomidate >> rapidly increased phosphorylation of the [[ extracellular signal-related kinases ]] ERK1/2.


In alpha2B-receptor-expressing HEK293 cells, << etomidate >> rapidly increased phosphorylation of the extracellular signal-related kinases [[ ERK1/2 ]].


CONCLUSIONS: These results indicate that << etomidate >> acts as an agonist at [[ alpha2-adrenoceptors ]], which appears in vivo primarily as an alpha2B-receptor-mediated increase in blood pressure.


Quantitative real-time polymerase chain reaction analysis showed that following the exposure of cells to << SiO(2) >> NPs, the messenger RNA level of apoptotic genes ([[ caspase-3 ]] and caspase-9) were upregulated in a dose-dependent manner.


Quantitative real-time polymerase chain reaction analysis showed that following the exposure of cells to << SiO(2) >> NPs, the messenger RNA level of apoptotic genes (caspase-3 and [[ caspase-9 ]]) were upregulated in a dose-dependent manner.


Moreover, activities of << caspase-3 >> and caspase-9 enzymes were also significantly higher in both kinds of cells exposed to [[ SiO(2) ]] NPs.


Moreover, activities of caspase-3 and << caspase-9 >> enzymes were also significantly higher in both kinds of cells exposed to [[ SiO(2) ]] NPs.


The << CYP2B6*6 >> Allele Significantly Alters the N-demethylation of [[ Ketamine ]] Enantiomers In Vitro.


<< Ketamine >> is primarily metabolized to norketamine by hepatic [[ cytochrome P450 (CYP) 2B6 ]] and CYP3A4-mediated N-demethylation.


<< Ketamine >> is primarily metabolized to norketamine by hepatic cytochrome P450 (CYP) 2B6 and [[ CYP3A4 ]]-mediated N-demethylation.


The << CYP2B6*6 >> allele is associated with reduced enzyme expression and activity that may lead to interindividual variability in [[ ketamine ]] metabolism.


We examined the N-demethylation of individual << ketamine >> enantiomers using human liver microsomes (HLMs) genotyped for the [[ CYP2B6*6 ]] allele, insect cell expressed recombinant CYP2B6 and CYP3A4 enzymes and COS-1 cell expressed recombinant CYP2B6.1 and CYP2B6.6 protein variant.


The intrinsic clearance for both << ketamine >> enantiomers by the high affinity enzyme in HLMs with [[ CYP2B6*1 ]]/*1 genotype were at least 2-fold and 6-fold higher, respectively, than those for CYP2B6*1/*6 genotype and CYP2B6*6/*6 genotype.


<< ThioTEPA >> ([[ CYP2B6 ]] inhibitor, 25 μM) and the monoclonal antibody against CYP2B6 but not troleandomycin (CYP3A4 inhibitor, 25 μM) or the monoclonal antibody against CYP3A4 inhibited ketamine N-demethylation at clinically relevant concentrations.


ThioTEPA (CYP2B6 inhibitor, 25 μM) and the monoclonal antibody against CYP2B6 but not << troleandomycin >> ([[ CYP3A4 ]] inhibitor, 25 μM) or the monoclonal antibody against CYP3A4 inhibited ketamine N-demethylation at clinically relevant concentrations.


These results indicate a major role of << CYP2B6 >> in [[ ketamine ]] N-demethylation in vitro and a significant impact of the CYP2B6*6 allele on enzyme-ketamine binding and catalytic activity.


These results indicate a major role of CYP2B6 in ketamine N-demethylation in vitro and a significant impact of the << CYP2B6*6 >> allele on enzyme-[[ ketamine ]] binding and catalytic activity.


PURPOSE: Testosterone-to-estradiol ratio levels in infertile men improve during treatment with the << aromatase >> inhibitor, [[ testolactone ]], and resulting changes in semen parameters.


We evaluated the effect of << anastrozole >>, a more selective [[ aromatase ]] inhibitor, on the hormonal and semen profiles of infertile men with abnormal baseline testosterone-to-estradiol ratios.


The results show that CYP2E1 inhibits << CYP2B4 >>-mediated metabolism of [[ benzphetamine ]] (BNZ) with a K(i) of 0.04 µM.


The results show that CYP2E1 inhibits << CYP2B4 >>-mediated metabolism of benzphetamine ([[ BNZ ]]) with a K(i) of 0.04 µM.


However, CYP2B4 is not an inhibitor of << CYP2E1 >>-mediated [[ p-nitrophenol ]] hydroxylation.


To explore for the existence of an auxiliary hydrophobic binding register remote from the active site of PSMA a series of << phenylalkylphosphonamidate >> derivatives of glutamic acid were synthesized and evaluated for their inhibitory potencies against [[ PSMA ]].


To explore for the existence of an auxiliary hydrophobic binding register remote from the active site of PSMA a series of phenylalkylphosphonamidate derivatives of << glutamic acid >> were synthesized and evaluated for their inhibitory potencies against [[ PSMA ]].


In PFC, << DEX >> caused activation of [[ AKT ]], augmentation of pro-survival Bcl-2 protein and enhanced Bcl-2/Bax protein ratio, as well Bcl-2 translocation to mitochondria.


In PFC, << DEX >> caused activation of AKT, augmentation of pro-survival [[ Bcl-2 ]] protein and enhanced Bcl-2/Bax protein ratio, as well Bcl-2 translocation to mitochondria.


In PFC, << DEX >> caused activation of AKT, augmentation of pro-survival Bcl-2 protein and enhanced [[ Bcl-2 ]]/Bax protein ratio, as well Bcl-2 translocation to mitochondria.


In PFC, << DEX >> caused activation of AKT, augmentation of pro-survival Bcl-2 protein and enhanced Bcl-2/[[ Bax ]] protein ratio, as well Bcl-2 translocation to mitochondria.


Results of RT-PCR analysis showed decrease of << p53 >> mRNA level and no significant difference in Bcl-2 and Bax mRNA expressions in [[ DEX ]]-treated rats.


Antitumor activity of << sorafenib >> in [[ FLT3 ]]-driven leukemic cells.


We show that << sorafenib >> (BAY 43-9006, Nexavar) potently inhibits [[ FLT3 ]] enzymatic and signaling activities.


We show that sorafenib (<< BAY 43-9006 >>, Nexavar) potently inhibits [[ FLT3 ]] enzymatic and signaling activities.


We show that sorafenib (BAY 43-9006, << Nexavar >>) potently inhibits [[ FLT3 ]] enzymatic and signaling activities.


In HEK293 cells stably transfected with FLT3-WT or FLT3-ITD, << sorafenib >> blocked basal and ligand dependent [[ FLT3 ]]-mediated tyrosine autophosphorylation as well as extracellular signal-regulated kinase1/2 and Stat5 phosphorylation.


In HEK293 cells stably transfected with FLT3-WT or FLT3-ITD, << sorafenib >> blocked basal and ligand dependent FLT3-mediated tyrosine autophosphorylation as well as [[ extracellular signal-regulated kinase1/2 ]] and Stat5 phosphorylation.


In HEK293 cells stably transfected with FLT3-WT or FLT3-ITD, << sorafenib >> blocked basal and ligand dependent FLT3-mediated tyrosine autophosphorylation as well as extracellular signal-regulated kinase1/2 and [[ Stat5 ]] phosphorylation.


In leukemia cell lines MV4-11 and EOL-1, << sorafenib >> treatment resulted in decreased cell proliferation and inhibition of [[ FLT3 ]] signaling.


The growth of the << FLT3 >>-independent RS4-11 cell line was only weakly inhibited by [[ sorafenib ]].


The demonstration that << sorafenib >> exhibits potent target inhibition and efficacy in [[ FLT3 ]]-driven models suggests that this compound may have a therapeutic benefit for patients with FLT3-driven leukemias.


The demonstration that << sorafenib >> exhibits potent target inhibition and efficacy in FLT3-driven models suggests that this compound may have a therapeutic benefit for patients with [[ FLT3 ]]-driven leukemias.


<< DBDCT >> up-regulated the expression of Bax, down-regulated the expression of Bcl-2, and significantly increased the ratio of [[ Bax ]]/Bcl-2.


<< DBDCT >> up-regulated the expression of Bax, down-regulated the expression of Bcl-2, and significantly increased the ratio of Bax/[[ Bcl-2 ]].


<< DBDCT >> up-regulated the expression of [[ Bax ]], down-regulated the expression of Bcl-2, and significantly increased the ratio of Bax/Bcl-2.


<< DBDCT >> up-regulated the expression of Bax, down-regulated the expression of [[ Bcl-2 ]], and significantly increased the ratio of Bax/Bcl-2.


<< DBDCT >> also caused the phosphorylation of [[ JNK ]] and p38(MAPK).


<< DBDCT >> also caused the phosphorylation of JNK and [[ p38 ]](MAPK).


<< DBDCT >> also caused the phosphorylation of JNK and p38([[ MAPK ]]).


Structure-based design of << aliskiren >>, a novel orally effective [[ renin ]] inhibitor.


This led to the discovery of << aliskiren >>, a highly potent and selective inhibitor of [[ human renin ]] in vitro, and in vivo; once-daily oral doses of aliskiren inhibit renin and lower blood pressure in sodium-depleted marmosets and hypertensive human patients.


This led to the discovery of aliskiren, a highly potent and selective inhibitor of human renin in vitro, and in vivo; once-daily oral doses of << aliskiren >> inhibit [[ renin ]] and lower blood pressure in sodium-depleted marmosets and hypertensive human patients.


<< Aliskiren >> represents the first in a novel class of [[ renin ]] inhibitors with the potential for treatment of hypertension and related cardiovascular diseases.


<< Everolimus >> (RAD001, Afinitor((R)) Novartis) is the first oral inhibitor of [[ mTOR ]] (mammalian target of rapamycin) to reach the oncology clinic.


<< Everolimus >> (RAD001, Afinitor((R)) Novartis) is the first oral inhibitor of mTOR ([[ mammalian target of rapamycin ]]) to reach the oncology clinic.


Everolimus (<< RAD001 >>, Afinitor((R)) Novartis) is the first oral inhibitor of [[ mTOR ]] (mammalian target of rapamycin) to reach the oncology clinic.


Everolimus (<< RAD001 >>, Afinitor((R)) Novartis) is the first oral inhibitor of mTOR ([[ mammalian target of rapamycin ]]) to reach the oncology clinic.


Everolimus (RAD001, << Afinitor((R)) Novartis >>) is the first oral inhibitor of [[ mTOR ]] (mammalian target of rapamycin) to reach the oncology clinic.


Everolimus (RAD001, << Afinitor((R)) Novartis >>) is the first oral inhibitor of mTOR ([[ mammalian target of rapamycin ]]) to reach the oncology clinic.


A phase III randomized placebo-controlled trial has examined the impact of everolimus in patients with clear cell renal cancers and progressive disease on or within 6 months of the << VEGFR >> tyrosine kinase inhibitors sunitinib and/or [[ sorafenib ]].


A phase III randomized placebo-controlled trial has examined the impact of everolimus in patients with clear cell renal cancers and progressive disease on or within 6 months of the VEGFR << tyrosine kinase >> inhibitors sunitinib and/or [[ sorafenib ]].


A phase III randomized placebo-controlled trial has examined the impact of everolimus in patients with clear cell renal cancers and progressive disease on or within 6 months of the << VEGFR >> tyrosine kinase inhibitors [[ sunitinib ]] and/or sorafenib.


A phase III randomized placebo-controlled trial has examined the impact of everolimus in patients with clear cell renal cancers and progressive disease on or within 6 months of the VEGFR << tyrosine kinase >> inhibitors [[ sunitinib ]] and/or sorafenib.


Synthesis and structure-activity relationship of << pyripyropene A >> derivatives as potent and selective [[ acyl-CoA:cholesterol acyltransferase 2 ]] (ACAT2) inhibitors: Part 2.


Synthesis and structure-activity relationship of << pyripyropene A >> derivatives as potent and selective acyl-CoA:cholesterol acyltransferase 2 ([[ ACAT2 ]]) inhibitors: Part 2.


<< Adrenaline >> inhibits [[ insulin ]] secretion via pertussis toxin-sensitive mechanisms.


<< Somatostatin >> which also inhibits [[ insulin ]] secretion was less efficient (inhibition by 20%).


In contrast to << adrenaline >> and somatostatin, galanin, another inhibitor of [[ insulin ]] secretion, reduced Ca2+ currents by about 40% in a pertussis toxin-insensitive manner.


In contrast to adrenaline and << somatostatin >>, galanin, another inhibitor of [[ insulin ]] secretion, reduced Ca2+ currents by about 40% in a pertussis toxin-insensitive manner.


These G-proteins are likely to be involved in the adrenaline-induced inhibition of dihydropyridine-sensitive Ca2+ currents and in other signal transduction pathways contributing to the << adrenaline >>-induced inhibition of [[ insulin ]] secretion.


Synthesis and in Vitro Characterisation of << Ifenprodil >>-Based Fluorescein Conjugates as [[ GluN1 ]]/GluN2B N-Methyl-D-aspartate Receptor Antagonists.


Synthesis and in Vitro Characterisation of << Ifenprodil >>-Based Fluorescein Conjugates as GluN1/[[ GluN2B ]] N-Methyl-D-aspartate Receptor Antagonists.


Synthesis and in Vitro Characterisation of << Ifenprodil >>-Based Fluorescein Conjugates as GluN1/GluN2B [[ N-Methyl-D-aspartate Receptor ]] Antagonists.


Synthesis and in Vitro Characterisation of Ifenprodil-Based << Fluorescein >> Conjugates as [[ GluN1 ]]/GluN2B N-Methyl-D-aspartate Receptor Antagonists.


Synthesis and in Vitro Characterisation of Ifenprodil-Based << Fluorescein >> Conjugates as GluN1/[[ GluN2B ]] N-Methyl-D-aspartate Receptor Antagonists.


Synthesis and in Vitro Characterisation of Ifenprodil-Based << Fluorescein >> Conjugates as GluN1/GluN2B [[ N-Methyl-D-aspartate Receptor ]] Antagonists.


<< Ifenprodil >>, known as the [[ GluNR2B ]] antagonist of reference, was chosen as the template for the elaboration of probes.


Molecular determinants for the selective inhibition of << cyclooxygenase-2 >> by [[ lumiracoxib ]].


Lumiracoxib is the first example of a marketed << COX-2 >> inhibitor of the [[ arylacetic acid ]] class, and it is reported to be the most selective COXIB in vivo.


<< Lumiracoxib >> is the first example of a marketed [[ COX-2 ]] inhibitor of the arylacetic acid class, and it is reported to be the most selective COXIB in vivo.


Using standard assays, << lumiracoxib >> was found to be a poor inhibitor of purified [[ ovine COX-1 ]] and a relatively weak inhibitor of purified human COX-2.


Using standard assays, << lumiracoxib >> was found to be a poor inhibitor of purified ovine COX-1 and a relatively weak inhibitor of purified [[ human COX-2 ]].


Kinetic studies with << lumiracoxib >> demonstrated that it was a time-dependent and slowly reversible inhibitor of [[ human COX-2 ]] that exhibited at least two binding steps during inhibition.


Inhibition studies demonstrated that the << methyl >> group on the phenylacetic acid ring is required for [[ COX-2 ]] selectivity.


Inhibition studies demonstrated that the methyl group on the << phenylacetic acid >> ring is required for [[ COX-2 ]] selectivity.


The chemical identity and position of the substituents on the lower << aniline >> ring were important in determining the potency and extent of [[ COX ]] inhibition as well as COX-2 selectivity.


Mutation of Ser-530 to Ala or Val-349 to Ala or Leu abolished the potent inhibition observed with wild-type << human COX-2 >> and key [[ lumiracoxib ]] analogs.


Interestingly, a << Val-349 to Ile >> mutant was inhibited with equal potency to human COX-2 with [[ 2,6-dichloro ]]-, 2,6-dimethyl-, or 2-chloro-6-methyl-substituted inhibitors and, in the case of lumiracoxib, actually showed an increase in potency.


Interestingly, a Val-349 to Ile mutant was inhibited with equal potency to << human COX-2 >> with [[ 2,6-dichloro ]]-, 2,6-dimethyl-, or 2-chloro-6-methyl-substituted inhibitors and, in the case of lumiracoxib, actually showed an increase in potency.


Interestingly, a << Val-349 to Ile >> mutant was inhibited with equal potency to human COX-2 with 2,6-dichloro-, [[ 2,6-dimethyl ]]-, or 2-chloro-6-methyl-substituted inhibitors and, in the case of lumiracoxib, actually showed an increase in potency.


Interestingly, a Val-349 to Ile mutant was inhibited with equal potency to << human COX-2 >> with 2,6-dichloro-, [[ 2,6-dimethyl ]]-, or 2-chloro-6-methyl-substituted inhibitors and, in the case of lumiracoxib, actually showed an increase in potency.


Interestingly, a << Val-349 to Ile >> mutant was inhibited with equal potency to human COX-2 with 2,6-dichloro-, 2,6-dimethyl-, or [[ 2-chloro-6-methyl ]]-substituted inhibitors and, in the case of lumiracoxib, actually showed an increase in potency.


Interestingly, a Val-349 to Ile mutant was inhibited with equal potency to << human COX-2 >> with 2,6-dichloro-, 2,6-dimethyl-, or [[ 2-chloro-6-methyl ]]-substituted inhibitors and, in the case of lumiracoxib, actually showed an increase in potency.


Interestingly, a << Val-349 to Ile >> mutant was inhibited with equal potency to human COX-2 with 2,6-dichloro-, 2,6-dimethyl-, or 2-chloro-6-methyl-substituted inhibitors and, in the case of [[ lumiracoxib ]], actually showed an increase in potency.


Interestingly, a Val-349 to Ile mutant was inhibited with equal potency to << human COX-2 >> with 2,6-dichloro-, 2,6-dimethyl-, or 2-chloro-6-methyl-substituted inhibitors and, in the case of [[ lumiracoxib ]], actually showed an increase in potency.


Taken together with a recent crystal structure of a lumiracoxib-COX-2 complex, the kinetic analyses presented herein of the inhibition of mutant << COX-2s >> by [[ lumiracoxib ]] allows the definition of the molecular basis of COX-2 inhibition.


The present study examined the effect of antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), on << VMAT2 >> activity by measuring adenosine triphosphate-dependent [[ [(3)H]dopamine ]] uptake into synaptic vesicles prepared from rat striatum.


Moreover, kinetic analysis revealed that inhibition by << reserpine >>, a typical [[ VMAT2 ]] inhibitor, was uncompetitive, decreasing maximum velocity and affinity for dopamine.


Moreover, kinetic analysis revealed that inhibition by reserpine, a typical << VMAT2 >> inhibitor, was uncompetitive, decreasing maximum velocity and affinity for [[ dopamine ]].


These results suggest that fluoxetine inhibited the activity of << VMAT2 >> by a mechanism different from that of [[ reserpine ]] and did not directly interact with the active site of VMAT2.


These results suggest that << fluoxetine >> inhibited the activity of VMAT2 by a mechanism different from that of reserpine and did not directly interact with the active site of [[ VMAT2 ]].


These results suggest that << fluoxetine >> inhibited the activity of [[ VMAT2 ]] by a mechanism different from that of reserpine and did not directly interact with the active site of VMAT2.


<< Betaxolol >>, a [[ beta(1)-adrenoceptor ]] antagonist, reduces Na(+) influx into cortical synaptosomes by direct interaction with Na(+) channels: comparison with other beta-adrenoceptor antagonists.


<< Betaxolol >>, a beta(1)-adrenoceptor antagonist, reduces Na(+) influx into cortical synaptosomes by direct interaction with Na(+) channels: comparison with other [[ beta-adrenoceptor ]] antagonists.


<< Betaxolol >>, a [[ beta(1)-adrenoceptor ]] antagonist used for the treatment of glaucoma, is known to be neuroprotective in paradigms of ischaemia/excitotoxicity.


In this study, we examined whether << betaxolol >> and other [[ beta-adrenoceptor ]] antagonists interact directly with neurotoxin binding to sites 1 and 2 of the voltage-sensitive sodium channel (Na(+) channel) in rat cerebrocortical synaptosomes.


Comparison of all the << beta-adrenoceptor >> antagonists tested revealed a potency order of [[ propranolol ]]>betaxolol approximately levobetaxolol>levobunolol approximately carteolol>/=timolol>atenolol.


Comparison of all the << beta-adrenoceptor >> antagonists tested revealed a potency order of propranolol>[[ betaxolol ]] approximately levobetaxolol>levobunolol approximately carteolol>/=timolol>atenolol.


Comparison of all the << beta-adrenoceptor >> antagonists tested revealed a potency order of propranolol>betaxolol approximately [[ levobetaxolol ]]>levobunolol approximately carteolol>/=timolol>atenolol.


Comparison of all the << beta-adrenoceptor >> antagonists tested revealed a potency order of propranolol>betaxolol approximately levobetaxolol>[[ levobunolol ]] approximately carteolol>/=timolol>atenolol.


Comparison of all the << beta-adrenoceptor >> antagonists tested revealed a potency order of propranolol>betaxolol approximately levobetaxolol>levobunolol approximately [[ carteolol ]]>/=timolol>atenolol.


Comparison of all the << beta-adrenoceptor >> antagonists tested revealed a potency order of propranolol>betaxolol approximately levobetaxolol>levobunolol approximately carteolol>/=[[ timolol ]]>atenolol.


Comparison of all the << beta-adrenoceptor >> antagonists tested revealed a potency order of propranolol>betaxolol approximately levobetaxolol>levobunolol approximately carteolol>/=timolol>[[ atenolol ]].


<< Leukotriene D4 >> induces cognitive impairment through enhancement of [[ CysLT₁ R ]]-mediated amyloid-β generation in mice.


<< Leukotriene D4 >> induces cognitive impairment through enhancement of CysLT₁ R-mediated [[ amyloid-β ]] generation in mice.


The results demonstrated that intracerebral infusions of << LTD4 >> (1 ng/mouse) produced memory impairment as determined by Morris water maze test and Y-maze test in mice, and caused the accumulation of [[ Aβ1-40 ]] and Aβ1-42 in the hippocampus and cortex through increased activity of β- and γ-secretases accompanied with increased expression of amyloid precursor protein (APP).


The results demonstrated that intracerebral infusions of << LTD4 >> (1 ng/mouse) produced memory impairment as determined by Morris water maze test and Y-maze test in mice, and caused the accumulation of Aβ1-40 and [[ Aβ1-42 ]] in the hippocampus and cortex through increased activity of β- and γ-secretases accompanied with increased expression of amyloid precursor protein (APP).


The results demonstrated that intracerebral infusions of << LTD4 >> (1 ng/mouse) produced memory impairment as determined by Morris water maze test and Y-maze test in mice, and caused the accumulation of Aβ1-40 and Aβ1-42 in the hippocampus and cortex through increased activity of β- and γ-secretases accompanied with increased expression of [[ amyloid precursor protein ]] (APP).


The results demonstrated that intracerebral infusions of << LTD4 >> (1 ng/mouse) produced memory impairment as determined by Morris water maze test and Y-maze test in mice, and caused the accumulation of Aβ1-40 and Aβ1-42 in the hippocampus and cortex through increased activity of β- and γ-secretases accompanied with increased expression of amyloid precursor protein ([[ APP ]]).


<< LTD4 >> also induced expression of [[ cysteinyl leukotriene receptor 1 ]] (CysLT(1)R) and NF-κB p65 in the hippocampus and cortex.


<< LTD4 >> also induced expression of cysteinyl leukotriene receptor 1 ([[ CysLT(1)R ]]) and NF-κB p65 in the hippocampus and cortex.


<< LTD4 >> also induced expression of cysteinyl leukotriene receptor 1 (CysLT(1)R) and [[ NF-κB ]] p65 in the hippocampus and cortex.


<< LTD4 >> also induced expression of cysteinyl leukotriene receptor 1 (CysLT(1)R) and NF-κB [[ p65 ]] in the hippocampus and cortex.


Pretreatment with << pranlukast >> (1.5 ng/mouse, intracerebroventricularly), a [[ CysLT(1)R ]] antagonist, blocked LTD4-induced amyloidogenesis, memory deficits.


Moreover, << LTD4 >>-induced increases in [[ CysLT(1)R ]] and NF-κB p65 in the brain were also attenuated by pranlukast.


Moreover, << LTD4 >>-induced increases in CysLT(1)R and [[ NF-κB ]] p65 in the brain were also attenuated by pranlukast.


Moreover, << LTD4 >>-induced increases in CysLT(1)R and NF-κB [[ p65 ]] in the brain were also attenuated by pranlukast.


Moreover, LTD4-induced increases in << CysLT(1)R >> and NF-κB p65 in the brain were also attenuated by [[ pranlukast ]].


Moreover, LTD4-induced increases in CysLT(1)R and << NF-κB >> p65 in the brain were also attenuated by [[ pranlukast ]].


Moreover, LTD4-induced increases in CysLT(1)R and NF-κB << p65 >> in the brain were also attenuated by [[ pranlukast ]].


These results suggest that << LTD4 >> increases Aβ peptide burden via activation of [[ CysLT(1)R ]], which further affects APP levels and activity of β- and γ-secretases via the NF-κB pathway.


These results suggest that << LTD4 >> increases [[ Aβ peptide ]] burden via activation of CysLT(1)R, which further affects APP levels and activity of β- and γ-secretases via the NF-κB pathway.


<< Statins >> increase [[ p21 ]] through inhibition of histone deacetylase activity and release of promoter-associated HDAC1/2.


<< Statins >> increase p21 through inhibition of histone deacetylase activity and release of promoter-associated [[ HDAC1/2 ]].


<< Statins >> increase p21 through inhibition of [[ histone deacetylase ]] activity and release of promoter-associated HDAC1/2.


<< Statins >> are [[ 3-hydroxy-3-methylglutaryl-CoA reductase ]] inhibitors broadly used for the control of hypercholesterolemia.


In the subsequent enzymatic assay, it was shown that << lovastatin >> inhibited [[ HDAC2 ]] activity competitively with a K(i) value of 31.6 micromol/L.


Recent studies have reported that << imatinib mesylate >>, a kinase inhibitor that targets the intracellular [[ tyrosine kinase ]] BCR-ABL and the platelet derived growth factor (PDGF) receptor, is an effective inhibitor of the macrophage colony stimulating factor (M-CSF) receptor, c-FMS.


Recent studies have reported that << imatinib mesylate >>, a kinase inhibitor that targets the intracellular tyrosine kinase [[ BCR ]]-ABL and the platelet derived growth factor (PDGF) receptor, is an effective inhibitor of the macrophage colony stimulating factor (M-CSF) receptor, c-FMS.


Recent studies have reported that << imatinib mesylate >>, a kinase inhibitor that targets the intracellular tyrosine kinase BCR-[[ ABL ]] and the platelet derived growth factor (PDGF) receptor, is an effective inhibitor of the macrophage colony stimulating factor (M-CSF) receptor, c-FMS.


Recent studies have reported that << imatinib mesylate >>, a kinase inhibitor that targets the intracellular tyrosine kinase BCR-ABL and the [[ platelet derived growth factor (PDGF) receptor ]], is an effective inhibitor of the macrophage colony stimulating factor (M-CSF) receptor, c-FMS.


Recent studies have reported that << imatinib mesylate >>, a kinase inhibitor that targets the intracellular tyrosine kinase BCR-ABL and the platelet derived growth factor (PDGF) receptor, is an effective inhibitor of the [[ macrophage colony stimulating factor (M-CSF) receptor ]], c-FMS.


Recent studies have reported that << imatinib mesylate >>, a kinase inhibitor that targets the intracellular tyrosine kinase BCR-ABL and the platelet derived growth factor (PDGF) receptor, is an effective inhibitor of the macrophage colony stimulating factor (M-CSF) receptor, [[ c-FMS ]].


Recent studies have reported that << imatinib mesylate >>, a [[ kinase ]] inhibitor that targets the intracellular tyrosine kinase BCR-ABL and the platelet derived growth factor (PDGF) receptor, is an effective inhibitor of the macrophage colony stimulating factor (M-CSF) receptor, c-FMS.


Given that << M-CSF >> signalling through c-FMS plays an important role in osteoclast biology, we speculated that blocking such a pathway with [[ imatinib ]] may modulate osteoclast activity.


Given that M-CSF signalling through << c-FMS >> plays an important role in osteoclast biology, we speculated that blocking such a pathway with [[ imatinib ]] may modulate osteoclast activity.


Imatinib was also found to inhibit M-CSF-induced osteoclast survival as well as M-CSF-induced osteoclast bone resorbing activity, but was without effect on interleukin 1alpha (IL-1alpha) and receptor activator of nuclear factor kappa B ligand (RANKL)-induced inhibition of osteoclasts apoptosis, further supporting the hypothesis that << imatinib >> may affect mature osteoclasts through the inhibition of [[ c-FMS ]].


<< Imatinib >> was also found to inhibit [[ M-CSF ]]-induced osteoclast survival as well as M-CSF-induced osteoclast bone resorbing activity, but was without effect on interleukin 1alpha (IL-1alpha) and receptor activator of nuclear factor kappa B ligand (RANKL)-induced inhibition of osteoclasts apoptosis, further supporting the hypothesis that imatinib may affect mature osteoclasts through the inhibition of c-FMS.


<< Imatinib >> was also found to inhibit M-CSF-induced osteoclast survival as well as [[ M-CSF ]]-induced osteoclast bone resorbing activity, but was without effect on interleukin 1alpha (IL-1alpha) and receptor activator of nuclear factor kappa B ligand (RANKL)-induced inhibition of osteoclasts apoptosis, further supporting the hypothesis that imatinib may affect mature osteoclasts through the inhibition of c-FMS.


Structural basis for << LFA-1 >> inhibition upon [[ lovastatin ]] binding to the CD11a I-domain.


We report here that << lovastatin >>, a drug clinically used for lowering cholesterol levels, inhibits the interaction of [[ human LFA-1 ]] with its counter-receptor intercellular adhesion molecule-1.


We report here that << lovastatin >>, a drug clinically used for lowering cholesterol levels, inhibits the interaction of human LFA-1 with its counter-receptor [[ intercellular adhesion molecule-1 ]].


Particularly, the effects of << doxycycline >> used as a non selective [[ MMP ]] inhibitor in experimental and clinical studies will be discussed.


Time-dependent changes in hepatic and intestinal induction of << cytochrome P450 3A >> after administration of [[ dexamethasone ]] to rats.


Abstract 1. We investigated the effects of the dose of and the number of times an inducer was administered and the duration of induction of hepatic and intestinal << cytochrome P450 3A >> (CYP3A) in rats using [[ dexamethasone 21-phosphate ]] (DEX-P) and midazolam (MDZ) as an inducer and a substrate to CYP3A, respectively.


Abstract 1. We investigated the effects of the dose of and the number of times an inducer was administered and the duration of induction of hepatic and intestinal cytochrome P450 3A (<< CYP3A >>) in rats using [[ dexamethasone 21-phosphate ]] (DEX-P) and midazolam (MDZ) as an inducer and a substrate to CYP3A, respectively.


Abstract 1. We investigated the effects of the dose of and the number of times an inducer was administered and the duration of induction of hepatic and intestinal cytochrome P450 3A (CYP3A) in rats using << dexamethasone 21-phosphate >> (DEX-P) and midazolam (MDZ) as an inducer and a substrate to [[ CYP3A ]], respectively.


Abstract 1. We investigated the effects of the dose of and the number of times an inducer was administered and the duration of induction of hepatic and intestinal << cytochrome P450 3A >> (CYP3A) in rats using dexamethasone 21-phosphate ([[ DEX-P ]]) and midazolam (MDZ) as an inducer and a substrate to CYP3A, respectively.


Abstract 1. We investigated the effects of the dose of and the number of times an inducer was administered and the duration of induction of hepatic and intestinal cytochrome P450 3A (<< CYP3A >>) in rats using dexamethasone 21-phosphate ([[ DEX-P ]]) and midazolam (MDZ) as an inducer and a substrate to CYP3A, respectively.


Abstract 1. We investigated the effects of the dose of and the number of times an inducer was administered and the duration of induction of hepatic and intestinal cytochrome P450 3A (CYP3A) in rats using dexamethasone 21-phosphate (<< DEX-P >>) and midazolam (MDZ) as an inducer and a substrate to [[ CYP3A ]], respectively.


Abstract 1. We investigated the effects of the dose of and the number of times an inducer was administered and the duration of induction of hepatic and intestinal cytochrome P450 3A (CYP3A) in rats using dexamethasone 21-phosphate (DEX-P) and << midazolam >> (MDZ) as an inducer and a substrate to [[ CYP3A ]], respectively.


Abstract 1. We investigated the effects of the dose of and the number of times an inducer was administered and the duration of induction of hepatic and intestinal cytochrome P450 3A (CYP3A) in rats using dexamethasone 21-phosphate (DEX-P) and midazolam (<< MDZ >>) as an inducer and a substrate to [[ CYP3A ]], respectively.


Abstract 1. We investigated the effects of the dose of and the number of times an inducer was administered and the duration of induction of hepatic and intestinal << cytochrome P450 3A >> (CYP3A) in rats using dexamethasone 21-phosphate (DEX-P) and [[ midazolam ]] (MDZ) as an inducer and a substrate to CYP3A, respectively.


Abstract 1. We investigated the effects of the dose of and the number of times an inducer was administered and the duration of induction of hepatic and intestinal cytochrome P450 3A (<< CYP3A >>) in rats using dexamethasone 21-phosphate (DEX-P) and [[ midazolam ]] (MDZ) as an inducer and a substrate to CYP3A, respectively.


Abstract 1. We investigated the effects of the dose of and the number of times an inducer was administered and the duration of induction of hepatic and intestinal cytochrome P450 3A (<< CYP3A >>) in rats using dexamethasone 21-phosphate (DEX-P) and midazolam ([[ MDZ ]]) as an inducer and a substrate to CYP3A, respectively.


3. << CYP3A >> induction in the liver increased depending on the dose of [[ DEX-P ]], whereas that in intestine showed a mild increase, but the induction level was almost constant regardless of the dose of DEX-P.


3. << CYP3A >> induction in the liver increased depending on the dose of DEX-P, whereas that in intestine showed a mild increase, but the induction level was almost constant regardless of the dose of [[ DEX-P ]].


4. Administration of a single dose of << DEX-P >> showed a temporal increase in [[ CYP3A ]] activity in both tissues and the induction ratios reached maximum values at 12 h after DEX-P administration.


4. Administration of a single dose of DEX-P showed a temporal increase in << CYP3A >> activity in both tissues and the induction ratios reached maximum values at 12 h after [[ DEX-P ]] administration.


<< LDH >> is responsible for pyruvate conversion to [[ lactate ]] through glycolysis.


<< LDH >> is responsible for [[ pyruvate ]] conversion to lactate through glycolysis.


Preclinical pharmacokinetics and in vitro metabolism of << dasatinib >> (BMS-354825): a potent oral multi-targeted [[ kinase ]] inhibitor against SRC and BCR-ABL.


Preclinical pharmacokinetics and in vitro metabolism of << dasatinib >> (BMS-354825): a potent oral multi-targeted kinase inhibitor against [[ SRC ]] and BCR-ABL.


Preclinical pharmacokinetics and in vitro metabolism of << dasatinib >> (BMS-354825): a potent oral multi-targeted kinase inhibitor against SRC and [[ BCR ]]-ABL.


Preclinical pharmacokinetics and in vitro metabolism of << dasatinib >> (BMS-354825): a potent oral multi-targeted kinase inhibitor against SRC and BCR-[[ ABL ]].


Preclinical pharmacokinetics and in vitro metabolism of dasatinib (<< BMS-354825 >>): a potent oral multi-targeted [[ kinase ]] inhibitor against SRC and BCR-ABL.


Preclinical pharmacokinetics and in vitro metabolism of dasatinib (<< BMS-354825 >>): a potent oral multi-targeted kinase inhibitor against [[ SRC ]] and BCR-ABL.


Preclinical pharmacokinetics and in vitro metabolism of dasatinib (<< BMS-354825 >>): a potent oral multi-targeted kinase inhibitor against SRC and [[ BCR ]]-ABL.


Preclinical pharmacokinetics and in vitro metabolism of dasatinib (<< BMS-354825 >>): a potent oral multi-targeted kinase inhibitor against SRC and BCR-[[ ABL ]].


PURPOSE: << Dasatinib >> (BMS-354825), a potent oral multi-targeted [[ kinase ]] inhibitor against SRC and BCR-ABL, has recently been approved for the treatment of chronic myelogenous leukaemia (CML) in imatinib-acquired resistance and intolerance.


PURPOSE: << Dasatinib >> (BMS-354825), a potent oral multi-targeted kinase inhibitor against [[ SRC ]] and BCR-ABL, has recently been approved for the treatment of chronic myelogenous leukaemia (CML) in imatinib-acquired resistance and intolerance.


PURPOSE: << Dasatinib >> (BMS-354825), a potent oral multi-targeted kinase inhibitor against SRC and [[ BCR ]]-ABL, has recently been approved for the treatment of chronic myelogenous leukaemia (CML) in imatinib-acquired resistance and intolerance.


PURPOSE: << Dasatinib >> (BMS-354825), a potent oral multi-targeted kinase inhibitor against SRC and BCR-[[ ABL ]], has recently been approved for the treatment of chronic myelogenous leukaemia (CML) in imatinib-acquired resistance and intolerance.


PURPOSE: Dasatinib (<< BMS-354825 >>), a potent oral multi-targeted [[ kinase ]] inhibitor against SRC and BCR-ABL, has recently been approved for the treatment of chronic myelogenous leukaemia (CML) in imatinib-acquired resistance and intolerance.


PURPOSE: Dasatinib (<< BMS-354825 >>), a potent oral multi-targeted kinase inhibitor against [[ SRC ]] and BCR-ABL, has recently been approved for the treatment of chronic myelogenous leukaemia (CML) in imatinib-acquired resistance and intolerance.


PURPOSE: Dasatinib (<< BMS-354825 >>), a potent oral multi-targeted kinase inhibitor against SRC and [[ BCR ]]-ABL, has recently been approved for the treatment of chronic myelogenous leukaemia (CML) in imatinib-acquired resistance and intolerance.


PURPOSE: Dasatinib (<< BMS-354825 >>), a potent oral multi-targeted kinase inhibitor against SRC and BCR-[[ ABL ]], has recently been approved for the treatment of chronic myelogenous leukaemia (CML) in imatinib-acquired resistance and intolerance.


The results of this study suggest that << noradrenaline >> predominantly, but not exclusively, mediates contraction of rat aorta through the activation of an [[ alphalD-adrenoceptor ]].


An increase in the << ADP >>/ATP ratio opens [[ K(ATP) channels ]], leading to membrane hyperpolarization.


An increase in the ADP/<< ATP >> ratio opens [[ K(ATP) channels ]], leading to membrane hyperpolarization.


Comparison of the effect of << rofecoxib >> (a [[ cyclooxygenase 2 ]] inhibitor), ibuprofen, and placebo on the gastroduodenal mucosa of patients with osteoarthritis: a randomized, double-blind, placebo-controlled trial.


OBJECTIVE: This randomized, double-blind study tested the hypothesis that << rofecoxib >>, a drug that specifically inhibits [[ cyclooxygenase 2 ]], would cause fewer gastroduodenal ulcers than ibuprofen (in a multicenter trial), and its side effects would be equivalent to those of placebo (in a prespecified analysis combining the results with another trial of identical design).


<< [-]-Huperzine A >> ([-]-Hup A), is a naturally occurring potent reversible [[ AChE ]] inhibitor that penetrates the blood-brain barrier.


[-]-Huperzine A (<< [-]-Hup A >>), is a naturally occurring potent reversible [[ AChE ]] inhibitor that penetrates the blood-brain barrier.


The synthetic stereoisomer, << [+]-Hup A >>, is less toxic due to poor [[ AChE ]] inhibition and is suitable for both pre-/post-exposure treatments of nerve agent toxicity.


Also, << vinblastine >> enhances the phosphorylation of [[ Ras homologous protein A ]], the accumulation of reactive oxygen species, the release of intracellular Ca(2+), as well as the activation of apoptosis signal-regulating kinase 1, c-jun-N-terminal kinase, p38, inhibitor of kappaBα (IκBα) kinase, and inositol requiring enzyme 1α.


Also, << vinblastine >> enhances the phosphorylation of Ras homologous protein A, the accumulation of reactive oxygen species, the release of intracellular Ca(2+), as well as the activation of [[ apoptosis signal-regulating kinase 1 ]], c-jun-N-terminal kinase, p38, inhibitor of kappaBα (IκBα) kinase, and inositol requiring enzyme 1α.


Also, << vinblastine >> enhances the phosphorylation of Ras homologous protein A, the accumulation of reactive oxygen species, the release of intracellular Ca(2+), as well as the activation of apoptosis signal-regulating kinase 1, [[ c-jun-N-terminal kinase ]], p38, inhibitor of kappaBα (IκBα) kinase, and inositol requiring enzyme 1α.


Also, << vinblastine >> enhances the phosphorylation of Ras homologous protein A, the accumulation of reactive oxygen species, the release of intracellular Ca(2+), as well as the activation of apoptosis signal-regulating kinase 1, c-jun-N-terminal kinase, [[ p38 ]], inhibitor of kappaBα (IκBα) kinase, and inositol requiring enzyme 1α.


Also, << vinblastine >> enhances the phosphorylation of Ras homologous protein A, the accumulation of reactive oxygen species, the release of intracellular Ca(2+), as well as the activation of apoptosis signal-regulating kinase 1, c-jun-N-terminal kinase, p38, [[ inhibitor of kappaBα ]] (IκBα) kinase, and inositol requiring enzyme 1α.


Also, << vinblastine >> enhances the phosphorylation of Ras homologous protein A, the accumulation of reactive oxygen species, the release of intracellular Ca(2+), as well as the activation of apoptosis signal-regulating kinase 1, c-jun-N-terminal kinase, p38, inhibitor of kappaBα ([[ IκBα ]]) kinase, and inositol requiring enzyme 1α.


Also, << vinblastine >> enhances the phosphorylation of Ras homologous protein A, the accumulation of reactive oxygen species, the release of intracellular Ca(2+), as well as the activation of apoptosis signal-regulating kinase 1, c-jun-N-terminal kinase, p38, inhibitor of kappaBα (IκBα) [[ kinase ]], and inositol requiring enzyme 1α.


Also, << vinblastine >> enhances the phosphorylation of Ras homologous protein A, the accumulation of reactive oxygen species, the release of intracellular Ca(2+), as well as the activation of apoptosis signal-regulating kinase 1, c-jun-N-terminal kinase, p38, inhibitor of kappaBα (IκBα) kinase, and [[ inositol requiring enzyme 1α ]].


In addition, << vinblastine >> induces the DNA-binding activities of the transcription factor [[ NF-κB ]], HSF1, AP-1, and ATF-2, together with the expression of HSP70 and Bax proteins.


In addition, << vinblastine >> induces the DNA-binding activities of the transcription factor NF-κB, [[ HSF1 ]], AP-1, and ATF-2, together with the expression of HSP70 and Bax proteins.


In addition, << vinblastine >> induces the DNA-binding activities of the transcription factor NF-κB, HSF1, [[ AP-1 ]], and ATF-2, together with the expression of HSP70 and Bax proteins.


In addition, << vinblastine >> induces the DNA-binding activities of the transcription factor NF-κB, HSF1, AP-1, and [[ ATF-2 ]], together with the expression of HSP70 and Bax proteins.


In addition, << vinblastine >> induces the DNA-binding activities of the transcription factor NF-κB, HSF1, AP-1, and ATF-2, together with the expression of [[ HSP70 ]] and Bax proteins.


In addition, << vinblastine >> induces the DNA-binding activities of the transcription factor NF-κB, HSF1, AP-1, and ATF-2, together with the expression of HSP70 and [[ Bax ]] proteins.


Cloning and characterization of a novel human phosphodiesterase that hydrolyzes both << cAMP >> and cGMP ([[ PDE10A ]]).


Cloning and characterization of a novel << human phosphodiesterase >> that hydrolyzes both [[ cAMP ]] and cGMP (PDE10A).


Cloning and characterization of a novel human phosphodiesterase that hydrolyzes both cAMP and << cGMP >> ([[ PDE10A ]]).


Cloning and characterization of a novel << human phosphodiesterase >> that hydrolyzes both cAMP and [[ cGMP ]] (PDE10A).


Recombinant << PDE10A >> transfected and expressed in COS-7 cells hydrolyzed [[ cAMP ]] and cGMP with Km values of 0.26 and 7.2 microM, respectively, and Vmax with cGMP was almost twice that with cAMP.


Recombinant << PDE10A >> transfected and expressed in COS-7 cells hydrolyzed cAMP and [[ cGMP ]] with Km values of 0.26 and 7.2 microM, respectively, and Vmax with cGMP was almost twice that with cAMP.


Recombinant << PDE10A >> transfected and expressed in COS-7 cells hydrolyzed cAMP and cGMP with Km values of 0.26 and 7.2 microM, respectively, and Vmax with [[ cGMP ]] was almost twice that with cAMP.


Recombinant << PDE10A >> transfected and expressed in COS-7 cells hydrolyzed cAMP and cGMP with Km values of 0.26 and 7.2 microM, respectively, and Vmax with cGMP was almost twice that with [[ cAMP ]].


Of the << PDE >> inhibitors tested, [[ dipyridamole ]] was most effective, with IC50 values of 1.2 and 0.45 microM for inhibition of cAMP and cGMP hydrolysis, respectively.


Of the << PDE >> inhibitors tested, dipyridamole was most effective, with IC50 values of 1.2 and 0.45 microM for inhibition of [[ cAMP ]] and cGMP hydrolysis, respectively.


Of the << PDE >> inhibitors tested, dipyridamole was most effective, with IC50 values of 1.2 and 0.45 microM for inhibition of cAMP and [[ cGMP ]] hydrolysis, respectively.


The << cytosine >> analog 5-aza-2'-deoxycytidine (decitabine) hypomethylates DNA by inhibiting [[ DNA methyltransferase ]].


The cytosine analog << 5-aza-2'-deoxycytidine >> (decitabine) hypomethylates DNA by inhibiting [[ DNA methyltransferase ]].


The cytosine analog 5-aza-2'-deoxycytidine (<< decitabine >>) hypomethylates DNA by inhibiting [[ DNA methyltransferase ]].


We examined if subcutaneous << decitabine >> could increase [[ HbF ]] levels and improve SSD pathophysiology without cytotoxicity.


Weekly subcutaneous << decitabine >> produces cumulative increases in [[ HbF ]] and total hemoglobin through a noncytotoxic mechanism of action.


Weekly subcutaneous << decitabine >> produces cumulative increases in HbF and total [[ hemoglobin ]] through a noncytotoxic mechanism of action.


<< Nox4 >> oxidase activity is thought to be constitutive and regulated at the transcriptional level; however, we challenge this point of view and suggest that specific [[ quinone ]] derivatives could modulate this activity.


Nox4 << oxidase >> activity is thought to be constitutive and regulated at the transcriptional level; however, we challenge this point of view and suggest that specific [[ quinone ]] derivatives could modulate this activity.


In fact, we demonstrated a significant stimulation of << Nox4 >> activity by 4 [[ quinone ]] derivatives (AA-861, tBuBHQ, tBuBQ, and duroquinone) observed in 3 different cellular models, HEK293E, T-REx™, and chondrocyte cell lines.


In fact, we demonstrated a significant stimulation of << Nox4 >> activity by 4 quinone derivatives ([[ AA-861 ]], tBuBHQ, tBuBQ, and duroquinone) observed in 3 different cellular models, HEK293E, T-REx™, and chondrocyte cell lines.


In fact, we demonstrated a significant stimulation of << Nox4 >> activity by 4 quinone derivatives (AA-861, [[ tBuBHQ ]], tBuBQ, and duroquinone) observed in 3 different cellular models, HEK293E, T-REx™, and chondrocyte cell lines.


In fact, we demonstrated a significant stimulation of << Nox4 >> activity by 4 quinone derivatives (AA-861, tBuBHQ, [[ tBuBQ ]], and duroquinone) observed in 3 different cellular models, HEK293E, T-REx™, and chondrocyte cell lines.


In fact, we demonstrated a significant stimulation of << Nox4 >> activity by 4 quinone derivatives (AA-861, tBuBHQ, tBuBQ, and [[ duroquinone ]]) observed in 3 different cellular models, HEK293E, T-REx™, and chondrocyte cell lines.


Such model of << Nox4 >> activity regulation could provide new insight into the understanding of the molecular mechanism of the electron transfer through the enzyme, i.e., its potential redox regulation, and could also define new therapeutic targets in diseases in which [[ quinones ]] and Nox4 are implicated.


Although the inhibition of << cyclooxygenases >> by [[ aspirin ]], which leads to its anti-inflammatory/analgesic properties, has been well studied, the mechanisms involved in its chemopreventive effects as well as some of its adverse effects are as yet ill-defined.


In a recent study using protein-specific anti-acetyl lysine antibodies and immunological methods, we demonstrated the ability of << aspirin >> to acetylate the [[ tumor suppressor protein p53 ]].


Second, << ICRF-187 >>, a [[ Top2 ]] catalytic inhibitor known to deplete Top2β, specifically sensitized MEFs to CPT.


Second, << ICRF-187 >>, a Top2 catalytic inhibitor known to deplete [[ Top2β ]], specifically sensitized MEFs to CPT.


To explore the molecular basis for CPT hypersensitivity in Top2β-deficient cells, we found that upon << CPT >> exposure, the [[ RNA polymerase II large subunit ]] (RNAP LS) became progressively depleted, followed by recovery to nearly the original level in wild-type MEFs, whereas RNAP LS remained depleted without recovery in Top2β-deficient cells.


To explore the molecular basis for CPT hypersensitivity in Top2β-deficient cells, we found that upon << CPT >> exposure, the RNA polymerase II large subunit ([[ RNAP LS ]]) became progressively depleted, followed by recovery to nearly the original level in wild-type MEFs, whereas RNAP LS remained depleted without recovery in Top2β-deficient cells.


To explore the molecular basis for CPT hypersensitivity in Top2β-deficient cells, we found that upon << CPT >> exposure, the RNA polymerase II large subunit (RNAP LS) became progressively depleted, followed by recovery to nearly the original level in wild-type MEFs, whereas [[ RNAP LS ]] remained depleted without recovery in Top2β-deficient cells.


Altogether, our findings support a model in which Top2β deficiency promotes << CPT >>-induced apoptosis in quiescent non-S-phase cells, possibly due to RNAP LS depletion and [[ p53 ]] accumulation.


Altogether, our findings support a model in which Top2β deficiency promotes << CPT >>-induced apoptosis in quiescent non-S-phase cells, possibly due to [[ RNAP LS ]] depletion and p53 accumulation.


Effects of << felodipine >> (a dihydropyridine [[ calcium channel ]] blocker) and analogues on calmodulin-dependent enzymes.


Effects of felodipine (a << dihydropyridine >> [[ calcium channel ]] blocker) and analogues on calmodulin-dependent enzymes.


We have examined the effects on the activities of three calmodulin-dependent enzymes (cAMP phosphodiesterase, caldesmon kinase and myosin light chain kinase) of the dihydropyridine << Ca2+ channel >> blocker [[ felodipine ]] and three analogues (p-chloro, oxidized and t-butyl) exhibiting different pharmacological potencies.


The << cAMP phosphodiesterase >> was inhibited completely by [[ felodipine ]] and the p-chloro analogue with IC50 values of 3.7 and 1.5 microM respectively.


The << cAMP phosphodiesterase >> was inhibited completely by felodipine and the [[ p-chloro ]] analogue with IC50 values of 3.7 and 1.5 microM respectively.


<< Felodipine >> and the p-chloro analogue inhibited the basal (Ca2+/calmodulin-independent) activity of [[ cAMP phosphodiesterase ]] as well as the calmodulin-stimulated activity.


<< Felodipine >> and the p-chloro analogue inhibited the basal (Ca2+/calmodulin-independent) activity of cAMP phosphodiesterase as well as the [[ calmodulin ]]-stimulated activity.


Felodipine and the << p-chloro >> analogue inhibited the basal (Ca2+/calmodulin-independent) activity of [[ cAMP phosphodiesterase ]] as well as the calmodulin-stimulated activity.


Felodipine and the << p-chloro >> analogue inhibited the basal (Ca2+/calmodulin-independent) activity of cAMP phosphodiesterase as well as the [[ calmodulin ]]-stimulated activity.


Calmodulin was relatively ineffective in preventing inhibition of << cAMP phosphodiesterase >> by [[ felodipine ]] and the p-chloro analogue.


Calmodulin was relatively ineffective in preventing inhibition of << cAMP phosphodiesterase >> by felodipine and the [[ p-chloro ]] analogue.


<< Felodipine >> and the p-chloro analogue inhibited Ca2+/calmodulin-dependent [[ caldesmon kinase ]] with similar potencies (IC50 = 17.4 microM), whereas the oxidized and t-butyl analogues caused no inhibition.


Felodipine and the << p-chloro >> analogue inhibited Ca2+/calmodulin-dependent [[ caldesmon kinase ]] with similar potencies (IC50 = 17.4 microM), whereas the oxidized and t-butyl analogues caused no inhibition.


Similarly, << felodipine >> and the p-chloro analogue inhibited [[ myosin light chain kinase ]] activity whether the isolated 20 kD light chain (IC50 = 12.6 microM) or intact myosin (IC50 = 11.0 microM) was used as substrate.


Similarly, felodipine and the << p-chloro >> analogue inhibited [[ myosin light chain kinase ]] activity whether the isolated 20 kD light chain (IC50 = 12.6 microM) or intact myosin (IC50 = 11.0 microM) was used as substrate.


Felodipine and the << p-chloro >> analogue inhibited the actin-activated [[ Mg2+-ATPase ]] activity of smooth muscle myosin (IC50 = 25.1 microM).


Felodipine and the << p-chloro >> analogue inhibited the actin-activated Mg2+-ATPase activity of smooth muscle [[ myosin ]] (IC50 = 25.1 microM).


<< Felodipine >> and the p-chloro analogue inhibited the actin-activated [[ Mg2+-ATPase ]] activity of smooth muscle myosin (IC50 = 25.1 microM).


<< Felodipine >> and the p-chloro analogue inhibited the actin-activated Mg2+-ATPase activity of smooth muscle [[ myosin ]] (IC50 = 25.1 microM).


Similarly, << felodipine >> and the p-chloro analogue blocked [[ myosin ]] filament assembly induced by low concentrations of calmodulin, whereas the oxidized and t-butyl analogues did not.


Similarly, felodipine and the << p-chloro >> analogue blocked [[ myosin ]] filament assembly induced by low concentrations of calmodulin, whereas the oxidized and t-butyl analogues did not.


Again, inhibition of the actin-activated << myosin >> Mg2+-ATPase and myosin filament assembly by [[ felodipine ]] and the p-chloro analogue could be reversed by raising the calmodulin concentration.


Again, inhibition of the actin-activated myosin << Mg2+-ATPase >> and myosin filament assembly by [[ felodipine ]] and the p-chloro analogue could be reversed by raising the calmodulin concentration.


Again, inhibition of the actin-activated myosin Mg2+-ATPase and << myosin >> filament assembly by [[ felodipine ]] and the p-chloro analogue could be reversed by raising the calmodulin concentration.


Again, inhibition of the actin-activated << myosin >> Mg2+-ATPase and myosin filament assembly by felodipine and the [[ p-chloro ]] analogue could be reversed by raising the calmodulin concentration.


Again, inhibition of the actin-activated myosin << Mg2+-ATPase >> and myosin filament assembly by felodipine and the [[ p-chloro ]] analogue could be reversed by raising the calmodulin concentration.


Again, inhibition of the actin-activated myosin Mg2+-ATPase and << myosin >> filament assembly by felodipine and the [[ p-chloro ]] analogue could be reversed by raising the calmodulin concentration.


These observations suggest that some of the pharmacological actions of << felodipine >> on smooth muscle may involve inhibition of [[ calmodulin-dependent enzymes ]] which are functionally involved in the regulation of smooth muscle contraction.


<< Aldosterone >>-induced [[ ENaC ]] and basal Na(+)/K(+)-ATPase trafficking via protein kinase D1-phosphatidylinositol 4-kinaseIIIβ trans Golgi signalling in M1 cortical collecting duct cells.


<< Aldosterone >>-induced ENaC and basal [[ Na(+)/K(+)-ATPase ]] trafficking via protein kinase D1-phosphatidylinositol 4-kinaseIIIβ trans Golgi signalling in M1 cortical collecting duct cells.


<< Aldosterone >> also induces the rapid phosphorylation of [[ Protein Kinase D1 ]] (PKD1).


<< Aldosterone >> also induces the rapid phosphorylation of Protein Kinase D1 ([[ PKD1 ]]).


This effect has been attributed to the antagonist effects of << pindolol >> at the [[ 5-HT(1A) ]] receptor.


In the present study, we compared the pharmacology of << (+/-)pindolol >>, WAY-100635 (a [[ 5-HT(1A) ]] antagonist), GR127935 (a 5-HT(1B/1D) antagonist), and isamoltane (a 5-HT(1B) antagonist), when given acutely in combination with fluoxetine, using in vivo microdialysis in the frontal cortex of the freely moving rat.


In the present study, we compared the pharmacology of (+/-)pindolol, << WAY-100635 >> (a [[ 5-HT(1A) ]] antagonist), GR127935 (a 5-HT(1B/1D) antagonist), and isamoltane (a 5-HT(1B) antagonist), when given acutely in combination with fluoxetine, using in vivo microdialysis in the frontal cortex of the freely moving rat.


In the present study, we compared the pharmacology of (+/-)pindolol, WAY-100635 (a 5-HT(1A) antagonist), GR127935 (a 5-HT(1B/1D) antagonist), and << isamoltane >> (a [[ 5-HT(1B) ]] antagonist), when given acutely in combination with fluoxetine, using in vivo microdialysis in the frontal cortex of the freely moving rat.


In addition, by comparing the combined administration of (+/-)pindolol with either WAY100635, GR127935 or isamoltane, we have determined that << (+/-)pindolol >> produces much of its acute potentiation of fluoxetine-induced increases in extracellular 5-HT via its action at the 5-HT(1B/D) receptor in addition to any activity it has at the presynaptic [[ 5-HT(1A) ]] receptor.


In the local presence into the LC of the << α2-adrenoceptor >> antagonist [[ RS79948 ]] (1 μM), systemic citalopram increased NA in the LC (Emax = 157 ± 25 %) and PFC (Emax = 175 ± 24 %).


Local LC citalopram effect was abolished by LC presence of the << 5-HT3 >> receptor antagonist [[ MDL72222 ]] (1 μM) but not the 5-HT1/2 receptor antagonist methiothepin (1 μM).


Local LC citalopram effect was abolished by LC presence of the 5-HT3 receptor antagonist MDL72222 (1 μM) but not the << 5-HT1/2 >> receptor antagonist [[ methiothepin ]] (1 μM).


alpha(1)-Adrenoceptor antagonists were tested against the << phenylephrine >> ([[ alpha(1)-adrenoceptor ]] agonist)-induced contraction in isolated hamster ureteral preparations using a functional experimental approach.


Noradrenaline and << phenylephrine >> ([[ alpha(1)-adrenoceptor ]] agonist) each produced a concentration-dependent tonic contraction, their pD(2) values being 6.87+/-0.08 and 6.10+/-0.05, respectively.


<< Noradrenaline >> and phenylephrine ([[ alpha(1)-adrenoceptor ]] agonist) each produced a concentration-dependent tonic contraction, their pD(2) values being 6.87+/-0.08 and 6.10+/-0.05, respectively.


Prazosin (nonselective << alpha(1)-adrenoceptor >> antagonist), silodosin (selective alpha(1A)-adrenoceptor antagonist) and BMY-7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione dihydrochloride) (selective alpha(1D)-adrenoceptor antagonist) competitively antagonized the [[ phenylephrine ]]-induced contraction (pA(2) values, 8.60+/-0.07, 9.44+/-0.06 and 5.75+/-0.07, respectively).


Prazosin (nonselective alpha(1)-adrenoceptor antagonist), silodosin (selective << alpha(1A)-adrenoceptor >> antagonist) and BMY-7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione dihydrochloride) (selective alpha(1D)-adrenoceptor antagonist) competitively antagonized the [[ phenylephrine ]]-induced contraction (pA(2) values, 8.60+/-0.07, 9.44+/-0.06 and 5.75+/-0.07, respectively).


Prazosin (nonselective alpha(1)-adrenoceptor antagonist), silodosin (selective alpha(1A)-adrenoceptor antagonist) and BMY-7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione dihydrochloride) (selective << alpha(1D)-adrenoceptor >> antagonist) competitively antagonized the [[ phenylephrine ]]-induced contraction (pA(2) values, 8.60+/-0.07, 9.44+/-0.06 and 5.75+/-0.07, respectively).


<< Prazosin >> (nonselective [[ alpha(1)-adrenoceptor ]] antagonist), silodosin (selective alpha(1A)-adrenoceptor antagonist) and BMY-7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione dihydrochloride) (selective alpha(1D)-adrenoceptor antagonist) competitively antagonized the phenylephrine-induced contraction (pA(2) values, 8.60+/-0.07, 9.44+/-0.06 and 5.75+/-0.07, respectively).


Prazosin (nonselective alpha(1)-adrenoceptor antagonist), << silodosin >> (selective [[ alpha(1A)-adrenoceptor ]] antagonist) and BMY-7378 (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione dihydrochloride) (selective alpha(1D)-adrenoceptor antagonist) competitively antagonized the phenylephrine-induced contraction (pA(2) values, 8.60+/-0.07, 9.44+/-0.06 and 5.75+/-0.07, respectively).


Prazosin (nonselective alpha(1)-adrenoceptor antagonist), silodosin (selective alpha(1A)-adrenoceptor antagonist) and << BMY-7378 >> (8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione dihydrochloride) (selective [[ alpha(1D)-adrenoceptor ]] antagonist) competitively antagonized the phenylephrine-induced contraction (pA(2) values, 8.60+/-0.07, 9.44+/-0.06 and 5.75+/-0.07, respectively).


Prazosin (nonselective alpha(1)-adrenoceptor antagonist), silodosin (selective alpha(1A)-adrenoceptor antagonist) and BMY-7378 (<< 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione dihydrochloride >>) (selective [[ alpha(1D)-adrenoceptor ]] antagonist) competitively antagonized the phenylephrine-induced contraction (pA(2) values, 8.60+/-0.07, 9.44+/-0.06 and 5.75+/-0.07, respectively).


BDZs and other positive GABA(A)R modulators, including << barbiturates >>, ethanol, and neurosteroids, can also inhibit [[ L-type voltage-gated calcium channels ]] (L-VGCCs), which could contribute to reduced neuronal excitability.


BDZs and other positive GABA(A)R modulators, including << barbiturates >>, ethanol, and neurosteroids, can also inhibit L-type voltage-gated calcium channels ([[ L-VGCCs ]]), which could contribute to reduced neuronal excitability.


BDZs and other positive GABA(A)R modulators, including barbiturates, << ethanol >>, and neurosteroids, can also inhibit [[ L-type voltage-gated calcium channels ]] (L-VGCCs), which could contribute to reduced neuronal excitability.


BDZs and other positive GABA(A)R modulators, including barbiturates, << ethanol >>, and neurosteroids, can also inhibit L-type voltage-gated calcium channels ([[ L-VGCCs ]]), which could contribute to reduced neuronal excitability.


BDZs and other positive GABA(A)R modulators, including barbiturates, ethanol, and << neurosteroids >>, can also inhibit [[ L-type voltage-gated calcium channels ]] (L-VGCCs), which could contribute to reduced neuronal excitability.


BDZs and other positive GABA(A)R modulators, including barbiturates, ethanol, and << neurosteroids >>, can also inhibit L-type voltage-gated calcium channels ([[ L-VGCCs ]]), which could contribute to reduced neuronal excitability.


<< BDZs >> and other positive GABA(A)R modulators, including barbiturates, ethanol, and neurosteroids, can also inhibit [[ L-type voltage-gated calcium channels ]] (L-VGCCs), which could contribute to reduced neuronal excitability.


<< BDZs >> and other positive GABA(A)R modulators, including barbiturates, ethanol, and neurosteroids, can also inhibit L-type voltage-gated calcium channels ([[ L-VGCCs ]]), which could contribute to reduced neuronal excitability.


<< Ca(v)1.3 >> channels were less sensitive to [[ pentobarbital ]] inhibition than Ca(v)1.2 channels, similar to dihydropyridine (DHP) L-VGCC antagonists.


Ca(v)1.3 channels were less sensitive to << pentobarbital >> inhibition than [[ Ca(v)1.2 ]] channels, similar to dihydropyridine (DHP) L-VGCC antagonists.


<< Ca(v)1.3 >> channels were less sensitive to pentobarbital inhibition than Ca(v)1.2 channels, similar to [[ dihydropyridine ]] (DHP) L-VGCC antagonists.


Ca(v)1.3 channels were less sensitive to pentobarbital inhibition than << Ca(v)1.2 >> channels, similar to [[ dihydropyridine ]] (DHP) L-VGCC antagonists.


<< Ca(v)1.3 >> channels were less sensitive to pentobarbital inhibition than Ca(v)1.2 channels, similar to dihydropyridine ([[ DHP ]]) L-VGCC antagonists.


Ca(v)1.3 channels were less sensitive to pentobarbital inhibition than << Ca(v)1.2 >> channels, similar to dihydropyridine ([[ DHP ]]) L-VGCC antagonists.


Ca(v)1.3 channels were less sensitive to pentobarbital inhibition than Ca(v)1.2 channels, similar to << dihydropyridine >> (DHP) [[ L-VGCC ]] antagonists.


Ca(v)1.3 channels were less sensitive to pentobarbital inhibition than Ca(v)1.2 channels, similar to dihydropyridine (<< DHP >>) [[ L-VGCC ]] antagonists.


All GABA(A)R modulators induced a negative shift in the steady-state inactivation curve of Ca(v)1.3 channels, but only << BDZs >> and pentobarbital induced a negative shift in [[ Ca(v)1.2 ]] channel inactivation.


All GABA(A)R modulators induced a negative shift in the steady-state inactivation curve of Ca(v)1.3 channels, but only BDZs and << pentobarbital >> induced a negative shift in [[ Ca(v)1.2 ]] channel inactivation.


Despite the structural similarity between benzothiazepines and BDZs, mutation of an amino acid important for diltiazem potency (<< I1150A >>) did not affect [[ diazepam ]] potency.


Although << L-VGCC >> inhibition by [[ BDZs ]] occurred at concentrations that are possibly too high to be clinically relevant and is not likely to play a role in the up-regulation of L-VGCCs during long-term treatment, pentobarbital and ethanol inhibited L-VGCCs at clinically relevant concentrations.


Although L-VGCC inhibition by BDZs occurred at concentrations that are possibly too high to be clinically relevant and is not likely to play a role in the up-regulation of L-VGCCs during long-term treatment, << pentobarbital >> and ethanol inhibited [[ L-VGCCs ]] at clinically relevant concentrations.


<< 5-Hydroxy-3,6,7,8,3'4'-hexamethoxyflavone >> inhibits nitric oxide production in lipopolysaccharide-stimulated BV2 microglia via NF-κB suppression and [[ Nrf-2 ]]-dependent heme oxygenase-1 induction.


<< 5-Hydroxy-3,6,7,8,3'4'-hexamethoxyflavone >> inhibits nitric oxide production in lipopolysaccharide-stimulated BV2 microglia via NF-κB suppression and Nrf-2-dependent [[ heme oxygenase-1 ]] induction.


<< 5-Hydroxy-3,6,7,8,3'4'-hexamethoxyflavone >> inhibits nitric oxide production in lipopolysaccharide-stimulated BV2 microglia via [[ NF-κB ]] suppression and Nrf-2-dependent heme oxygenase-1 induction.


In this study, we found that << 5-hydroxy-3,6,7,8,3'4'-hexamethoxyflavone >> (5HHMF) from Hizikia fusiforme considerably inhibits lipopolysaccharide (LPS)-stimulated NO production by suppressing the expression of [[ inducible NO synthase ]] (iNOS) in BV2 microglia.


In this study, we found that << 5-hydroxy-3,6,7,8,3'4'-hexamethoxyflavone >> (5HHMF) from Hizikia fusiforme considerably inhibits lipopolysaccharide (LPS)-stimulated NO production by suppressing the expression of inducible NO synthase ([[ iNOS ]]) in BV2 microglia.


In this study, we found that 5-hydroxy-3,6,7,8,3'4'-hexamethoxyflavone (<< 5HHMF >>) from Hizikia fusiforme considerably inhibits lipopolysaccharide (LPS)-stimulated NO production by suppressing the expression of [[ inducible NO synthase ]] (iNOS) in BV2 microglia.


In this study, we found that 5-hydroxy-3,6,7,8,3'4'-hexamethoxyflavone (<< 5HHMF >>) from Hizikia fusiforme considerably inhibits lipopolysaccharide (LPS)-stimulated NO production by suppressing the expression of inducible NO synthase ([[ iNOS ]]) in BV2 microglia.


In addition, << 5HHMF >> blocked LPS-induced phosphorylation of IκB, resulting in suppression of the nuclear translocation of [[ nuclear factor-κB ]] (NF-κB) subunits, namely p65 and p50, which are important molecules involved in the regulation of iNOS expression.


In addition, << 5HHMF >> blocked LPS-induced phosphorylation of IκB, resulting in suppression of the nuclear translocation of nuclear factor-κB ([[ NF-κB ]]) subunits, namely p65 and p50, which are important molecules involved in the regulation of iNOS expression.


In addition, << 5HHMF >> blocked LPS-induced phosphorylation of IκB, resulting in suppression of the nuclear translocation of nuclear factor-κB (NF-κB) subunits, namely [[ p65 ]] and p50, which are important molecules involved in the regulation of iNOS expression.


In addition, << 5HHMF >> blocked LPS-induced phosphorylation of IκB, resulting in suppression of the nuclear translocation of nuclear factor-κB (NF-κB) subunits, namely p65 and [[ p50 ]], which are important molecules involved in the regulation of iNOS expression.


In addition, << 5HHMF >> blocked LPS-induced phosphorylation of [[ IκB ]], resulting in suppression of the nuclear translocation of nuclear factor-κB (NF-κB) subunits, namely p65 and p50, which are important molecules involved in the regulation of iNOS expression.


<< Pyrrolidine dithiocarbamate >> (PDTC), a specific NF-κB inhibitor, along with 20S proteasome inhibitor (PSI) significantly inhibited LPS-induced [[ iNOS ]] expression, which indirectly suggested that 5HHMF downregulated iNOS expression by suppressing NF-κB activity.


Pyrrolidine dithiocarbamate (<< PDTC >>), a specific NF-κB inhibitor, along with 20S proteasome inhibitor (PSI) significantly inhibited LPS-induced [[ iNOS ]] expression, which indirectly suggested that 5HHMF downregulated iNOS expression by suppressing NF-κB activity.


Pyrrolidine dithiocarbamate (PDTC), a specific NF-κB inhibitor, along with 20S proteasome inhibitor (PSI) significantly inhibited LPS-induced iNOS expression, which indirectly suggested that << 5HHMF >> downregulated [[ iNOS ]] expression by suppressing NF-κB activity.


<< Pyrrolidine dithiocarbamate >> (PDTC), a specific [[ NF-κB ]] inhibitor, along with 20S proteasome inhibitor (PSI) significantly inhibited LPS-induced iNOS expression, which indirectly suggested that 5HHMF downregulated iNOS expression by suppressing NF-κB activity.


Pyrrolidine dithiocarbamate (<< PDTC >>), a specific [[ NF-κB ]] inhibitor, along with 20S proteasome inhibitor (PSI) significantly inhibited LPS-induced iNOS expression, which indirectly suggested that 5HHMF downregulated iNOS expression by suppressing NF-κB activity.


Pyrrolidine dithiocarbamate (PDTC), a specific NF-κB inhibitor, along with 20S proteasome inhibitor (PSI) significantly inhibited LPS-induced iNOS expression, which indirectly suggested that << 5HHMF >> downregulated iNOS expression by suppressing [[ NF-κB ]] activity.


Thus, we found that << 5HHMF >> enhances heme oxygenase-1 (HO-1) expression via [[ nuclear factor-erythroid 2-related factor 2 ]] (Nrf2) activation.


Thus, we found that << 5HHMF >> enhances heme oxygenase-1 (HO-1) expression via nuclear factor-erythroid 2-related factor 2 ([[ Nrf2 ]]) activation.


Thus, we found that << 5HHMF >> enhances [[ heme oxygenase-1 ]] (HO-1) expression via nuclear factor-erythroid 2-related factor 2 (Nrf2) activation.


Thus, we found that << 5HHMF >> enhances heme oxygenase-1 ([[ HO-1 ]]) expression via nuclear factor-erythroid 2-related factor 2 (Nrf2) activation.


In addition, << cobalt protoporphyrin >> (CoPP), a specific [[ HO-1 ]] inducer, predominantly suppressed LPS-induced NO production.


In addition, cobalt protoporphyrin (<< CoPP >>), a specific [[ HO-1 ]] inducer, predominantly suppressed LPS-induced NO production.


In contrast, << zinc protoporphyrin >> (ZnPP), a specific [[ HO-1 ]] inhibitor, showed a partial suppressive effect of 5HHMF on LPS-induced NO production.


In contrast, zinc protoporphyrin (<< ZnPP >>), a specific [[ HO-1 ]] inhibitor, showed a partial suppressive effect of 5HHMF on LPS-induced NO production.


Further, << 5HHMF >> increased specific DNA-binding activity of [[ Nrf2 ]], and transient knockdown with Nrf2 siRNA subsequently reversed 5HHMF-induced NO inhibition, which was followed by suppression of HO-1 activity.


Further, << 5HHMF >> increased specific DNA-binding activity of Nrf2, and transient knockdown with Nrf2 siRNA subsequently reversed 5HHMF-induced NO inhibition, which was followed by suppression of [[ HO-1 ]] activity.


Further, << 5HHMF >> increased specific DNA-binding activity of Nrf2, and transient knockdown with [[ Nrf2 ]] siRNA subsequently reversed 5HHMF-induced NO inhibition, which was followed by suppression of HO-1 activity.


Further, 5HHMF increased specific DNA-binding activity of << Nrf2 >>, and transient knockdown with Nrf2 siRNA subsequently reversed [[ 5HHMF ]]-induced NO inhibition, which was followed by suppression of HO-1 activity.


Further, 5HHMF increased specific DNA-binding activity of Nrf2, and transient knockdown with << Nrf2 >> siRNA subsequently reversed [[ 5HHMF ]]-induced NO inhibition, which was followed by suppression of HO-1 activity.


Further, 5HHMF increased specific DNA-binding activity of Nrf2, and transient knockdown with Nrf2 siRNA subsequently reversed 5HHMF-induced << NO >> inhibition, which was followed by suppression of [[ HO-1 ]] activity.


Further, 5HHMF increased specific DNA-binding activity of Nrf2, and transient knockdown with Nrf2 siRNA subsequently reversed << 5HHMF >>-induced NO inhibition, which was followed by suppression of [[ HO-1 ]] activity.


Taken together, our findings indicate that << 5HHMF >> suppresses NO production through modulation of iNOS, consequently suppressing NF-κB activity and induction of [[ Nrf2 ]]-dependent HO-1 activity.


Taken together, our findings indicate that << 5HHMF >> suppresses NO production through modulation of iNOS, consequently suppressing NF-κB activity and induction of Nrf2-dependent [[ HO-1 ]] activity.


Taken together, our findings indicate that 5HHMF suppresses << NO >> production through modulation of iNOS, consequently suppressing [[ NF-κB ]] activity and induction of Nrf2-dependent HO-1 activity.


Taken together, our findings indicate that 5HHMF suppresses << NO >> production through modulation of iNOS, consequently suppressing NF-κB activity and induction of [[ Nrf2 ]]-dependent HO-1 activity.


Taken together, our findings indicate that 5HHMF suppresses << NO >> production through modulation of iNOS, consequently suppressing NF-κB activity and induction of Nrf2-dependent [[ HO-1 ]] activity.


Taken together, our findings indicate that << 5HHMF >> suppresses NO production through modulation of iNOS, consequently suppressing [[ NF-κB ]] activity and induction of Nrf2-dependent HO-1 activity.


Synthesis and antitumor activity of << 1,3,4-oxadiazole >> possessing 1,4-benzodioxan moiety as a novel class of potent [[ methionine aminopeptidase type II ]] inhibitors.


Synthesis and antitumor activity of 1,3,4-oxadiazole possessing << 1,4-benzodioxan >> moiety as a novel class of potent [[ methionine aminopeptidase type II ]] inhibitors.


Discovery of novel cannabinoid receptor ligands by a virtual screening approach: further development of << 2,4,6-trisubstituted 1,3,5-triazines >> as [[ CB2 ]] agonists.


One of the << CB2 >> agonists, [[ N-cyclopentyl-4-ethoxy-6-(4-methylpiperidin-1-yl)-1,3,5-triazin-2-amine ]] (19, -logEC(50)=7.5, E(max)=255%) was selected for further development.


As far as we are aware, the compound's << 1,3,5-triazine >> scaffold represents a new core structure for [[ CB2 ]] agonists.


The discovery of an inducible << oxidase >> whose apparent substrate preference is [[ spermine ]] indicates that polyamine catabolism is more complex than that originally proposed.


Purified << PAOh1 >>/SMO oxidizes both [[ spermine ]] (K(m)=1.6 microM) and N(1)-acetylspermine (K(m)=51 microM), but does not oxidize spermidine.


Purified PAOh1/<< SMO >> oxidizes both [[ spermine ]] (K(m)=1.6 microM) and N(1)-acetylspermine (K(m)=51 microM), but does not oxidize spermidine.


Purified << PAOh1 >>/SMO oxidizes both spermine (K(m)=1.6 microM) and [[ N(1)-acetylspermine ]] (K(m)=51 microM), but does not oxidize spermidine.


Purified PAOh1/<< SMO >> oxidizes both spermine (K(m)=1.6 microM) and [[ N(1)-acetylspermine ]] (K(m)=51 microM), but does not oxidize spermidine.


The purified human enzyme also does not oxidize eight representative antitumor polyamine analogues; however, specific oligamine analogues were found to be potent inhibitors of the oxidation of << spermine >> by [[ PAOh1 ]]/SMO.


The purified human enzyme also does not oxidize eight representative antitumor polyamine analogues; however, specific oligamine analogues were found to be potent inhibitors of the oxidation of << spermine >> by PAOh1/[[ SMO ]].


The i.c.v. administration of very low doses of << okadaic acid >> (0.001-1 pg/mouse) and cantharidin (0.001-1 ng/mouse), which inhibit [[ PP2A ]], produced a dose-dependent antagonism of the antinociception induced by morphine (s.c.).


The i.c.v. administration of very low doses of okadaic acid (0.001-1 pg/mouse) and << cantharidin >> (0.001-1 ng/mouse), which inhibit [[ PP2A ]], produced a dose-dependent antagonism of the antinociception induced by morphine (s.c.).


On the other hand, high doses of << okadaic acid >> (10 ng/mouse, i.c.v.) and cantharidin (1 microg/mouse, i.c.v.), which also block [[ PP1 ]], and calyculin-A (0.1 fg/mouse-1 ng/mouse, i.c.v.), which inhibits equally both PP1 and PP2A, did not modify the morphine-induced antinociception.


On the other hand, high doses of okadaic acid (10 ng/mouse, i.c.v.) and << cantharidin >> (1 microg/mouse, i.c.v.), which also block [[ PP1 ]], and calyculin-A (0.1 fg/mouse-1 ng/mouse, i.c.v.), which inhibits equally both PP1 and PP2A, did not modify the morphine-induced antinociception.


On the other hand, high doses of okadaic acid (10 ng/mouse, i.c.v.) and cantharidin (1 microg/mouse, i.c.v.), which also block PP1, and << calyculin-A >> (0.1 fg/mouse-1 ng/mouse, i.c.v.), which inhibits equally both [[ PP1 ]] and PP2A, did not modify the morphine-induced antinociception.


On the other hand, high doses of okadaic acid (10 ng/mouse, i.c.v.) and cantharidin (1 microg/mouse, i.c.v.), which also block PP1, and << calyculin-A >> (0.1 fg/mouse-1 ng/mouse, i.c.v.), which inhibits equally both PP1 and [[ PP2A ]], did not modify the morphine-induced antinociception.


Inhibition of << mammalian isoforms I-XIV >> with a series of natural product [[ polyphenols ]] and phenolic acids.


Inhibition of << mammalian isoforms I-XIV >> with a series of natural product polyphenols and [[ phenolic acids ]].


A series of phenolic acids and phenol natural products, such as << p-hydroxybenzoic acid >>, p-coumaric acid, caffeic acid, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the [[ metalloenzyme ]] carbonic anhydrase (CA, EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as << p-hydroxybenzoic acid >>, p-coumaric acid, caffeic acid, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme [[ carbonic anhydrase ]] (CA, EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as << p-hydroxybenzoic acid >>, p-coumaric acid, caffeic acid, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme carbonic anhydrase ([[ CA ]], EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as << p-hydroxybenzoic acid >>, p-coumaric acid, caffeic acid, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme carbonic anhydrase (CA, [[ EC 4.2.1.1 ]]).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, << p-coumaric acid >>, caffeic acid, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the [[ metalloenzyme ]] carbonic anhydrase (CA, EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, << p-coumaric acid >>, caffeic acid, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme [[ carbonic anhydrase ]] (CA, EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, << p-coumaric acid >>, caffeic acid, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme carbonic anhydrase ([[ CA ]], EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, << p-coumaric acid >>, caffeic acid, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme carbonic anhydrase (CA, [[ EC 4.2.1.1 ]]).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, << caffeic acid >>, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the [[ metalloenzyme ]] carbonic anhydrase (CA, EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, << caffeic acid >>, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme [[ carbonic anhydrase ]] (CA, EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, << caffeic acid >>, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme carbonic anhydrase ([[ CA ]], EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, << caffeic acid >>, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme carbonic anhydrase (CA, [[ EC 4.2.1.1 ]]).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, << ferulic acid >>, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the [[ metalloenzyme ]] carbonic anhydrase (CA, EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, << ferulic acid >>, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme [[ carbonic anhydrase ]] (CA, EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, << ferulic acid >>, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme carbonic anhydrase ([[ CA ]], EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, << ferulic acid >>, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme carbonic anhydrase (CA, [[ EC 4.2.1.1 ]]).


A series of << phenolic acids >> and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the [[ metalloenzyme ]] carbonic anhydrase (CA, EC 4.2.1.1).


A series of << phenolic acids >> and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme [[ carbonic anhydrase ]] (CA, EC 4.2.1.1).


A series of << phenolic acids >> and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme carbonic anhydrase ([[ CA ]], EC 4.2.1.1).


A series of << phenolic acids >> and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, ferulic acid, gallic acid, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme carbonic anhydrase (CA, [[ EC 4.2.1.1 ]]).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, ferulic acid, << gallic acid >>, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the [[ metalloenzyme ]] carbonic anhydrase (CA, EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, ferulic acid, << gallic acid >>, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme [[ carbonic anhydrase ]] (CA, EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, ferulic acid, << gallic acid >>, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme carbonic anhydrase ([[ CA ]], EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, ferulic acid, << gallic acid >>, syringic acid, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme carbonic anhydrase (CA, [[ EC 4.2.1.1 ]]).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, ferulic acid, gallic acid, << syringic acid >>, quercetin, and ellagic acid, were investigated for their inhibitory effects against the [[ metalloenzyme ]] carbonic anhydrase (CA, EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, ferulic acid, gallic acid, << syringic acid >>, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme [[ carbonic anhydrase ]] (CA, EC 4.2.1.1).


A series of phenolic acids and phenol natural products, such as p-hydroxybenzoic acid, p-coumaric acid, caffeic acid, ferulic acid, gallic acid, << syringic acid >>, quercetin, and ellagic acid, were investigated for their inhibitory effects against the metalloenzyme carbonic anhydrase ([[ CA ]], EC 4.2.1.1).