At 4 hours, losartan blocked 43% of the << Ang II >>-induced systolic blood pressure increase; [[ valsartan ]], 51%; and irbesartan, 88% (P<0.01 between drugs).


At 4 hours, losartan blocked 43% of the << Ang II >>-induced systolic blood pressure increase; valsartan, 51%; and [[ irbesartan ]], 88% (P<0.01 between drugs).


This study thus demonstrates that the first administration of the recommended starting dose of << irbesartan >> induces a greater and longer lasting [[ Ang II receptor ]] blockade than that of valsartan and losartan in normotensive subjects.


This study thus demonstrates that the first administration of the recommended starting dose of irbesartan induces a greater and longer lasting << Ang II receptor >> blockade than that of [[ valsartan ]] and losartan in normotensive subjects.


This study thus demonstrates that the first administration of the recommended starting dose of irbesartan induces a greater and longer lasting << Ang II receptor >> blockade than that of valsartan and [[ losartan ]] in normotensive subjects.


In humans, prolonged administration of the << beta 2-adrenoceptor >> agonist [[ terbutaline ]] leads to a desensitization of beta 2-adrenoceptor-mediated cardiovascular responses, which can be blunted by concomitant administration of the antianaphylactic drug ketotifen.


In a double-blind, placebo-controlled, randomized design, nine healthy male volunteers received disodium cromoglycate (4 x 200 mg/day, p.o.) or placebo for 3 weeks with terbutaline (3 x 5 mg/day, p.o.) administered concomitantly during the last 2 weeks. beta 2-Adrenoceptor cardiovascular function was assessed by the increase in heart rate and reduction of diastolic blood pressure induced by an incremental intravenous infusion of the unselective << beta-adrenoceptor >> agonist [[ isoprenaline ]]; beta 1-adrenoceptor cardiovascular function was assessed by exercise-induced tachycardia.


OBJECTIVES: This study examined the effect of a small-molecule, direct << thrombin >> inhibitor, [[ argatroban ]], on reperfusion induced by tissue plasminogen activator (TPA) in patients with acute myocardial infarction (AMI).


In vitro and in vivo studies have shown that << argatroban >> has advantages over heparin for the inhibition of clot-bound [[ thrombin ]] and for the enhancement of thrombolysis with TPA.


The functional inhibitory characteristics of the << angiotensin II type 1 receptor >> blockers (ARB) candesartan; [[ irbesartan ]]; and losartan and its active metabolite EXP 3174 (EXP) were studied in rabbit aortic strips and rat portal vein preparations in vitro.


The functional inhibitory characteristics of the << angiotensin II type 1 receptor >> blockers (ARB) [[ candesartan ]]; irbesartan; and losartan and its active metabolite EXP 3174 (EXP) were studied in rabbit aortic strips and rat portal vein preparations in vitro.


The functional inhibitory characteristics of the << angiotensin II type 1 receptor >> blockers (ARB) candesartan; irbesartan; and [[ losartan ]] and its active metabolite EXP 3174 (EXP) were studied in rabbit aortic strips and rat portal vein preparations in vitro.


The functional inhibitory characteristics of the << angiotensin II type 1 receptor >> blockers (ARB) candesartan; irbesartan; and losartan and its active metabolite [[ EXP 3174 ]] (EXP) were studied in rabbit aortic strips and rat portal vein preparations in vitro.


The functional inhibitory characteristics of the << angiotensin II type 1 receptor >> blockers (ARB) candesartan; irbesartan; and losartan and its active metabolite EXP 3174 ([[ EXP ]]) were studied in rabbit aortic strips and rat portal vein preparations in vitro.


In both vascular preparations, << candesartan >> caused a marked decrease in the maximal contractile response of the [[ angiotensin II ]] (Ang II) concentration-response curve.


In both vascular preparations, << candesartan >> caused a marked decrease in the maximal contractile response of the angiotensin II ([[ Ang II ]]) concentration-response curve.


In addition, when << candesartan >> was given to conscious rats, the inhibitory effect on [[ Ang II ]]-induced blood pressure responses persisted during the 24-hour period despite nondetectable plasma concentrations of candesartan at 24 hours.


At clinically relevant concentrations, << candesartan >> is an insurmountable and long-lasting antagonist of the vascular contractile responses to [[ Ang II ]].


Dose-dependent inhibition of platelet << cyclooxygenase-1 >> and monocyte cyclooxygenase-2 by [[ meloxicam ]] in healthy subjects.


Dose-dependent inhibition of platelet cyclooxygenase-1 and monocyte << cyclooxygenase-2 >> by [[ meloxicam ]] in healthy subjects.


Concentration-response curves for the inhibition of monocyte << COX-2 >> and platelet COX-1 were obtained in vitro after the incubation of [[ meloxicam ]] with whole blood samples.


Concentration-response curves for the inhibition of monocyte COX-2 and platelet << COX-1 >> were obtained in vitro after the incubation of [[ meloxicam ]] with whole blood samples.


Before dosing and 24 h after the seventh dose of each regimen, heparinized whole blood samples were incubated with lipopolysaccharide (10 microgram/ml) for 24 h at 37 degrees C, and << prostaglandin E2 >> was measured in plasma as an index of monocyte [[ COX-2 ]] activity.


The production of << thromboxane B2 >> in whole blood allowed to clot at 37 degrees C for 60 min was assessed as an index of platelet [[ COX-1 ]] activity.


In contrast, the administration of 7.5 and 15 mg of << meloxicam >> caused dose-dependent reductions in monocyte [[ COX-2 ]] activity by 51% and 70%, respectively, and in platelet COX-1 activity by 25% and 35%, respectively.


In contrast, the administration of 7.5 and 15 mg of << meloxicam >> caused dose-dependent reductions in monocyte COX-2 activity by 51% and 70%, respectively, and in platelet [[ COX-1 ]] activity by 25% and 35%, respectively.


Although the IC50 value of << meloxicam >> for inhibition of [[ COX-1 ]] was 10-fold higher than the IC50 value of COX-2 in vitro, this biochemical selectivity was inadequate to clearly separate the effects of meloxicam on the two isozymes after oral dosing as a function of the daily dose and interindividual variation in steady-state plasma levels.


Although the IC50 value of << meloxicam >> for inhibition of COX-1 was 10-fold higher than the IC50 value of [[ COX-2 ]] in vitro, this biochemical selectivity was inadequate to clearly separate the effects of meloxicam on the two isozymes after oral dosing as a function of the daily dose and interindividual variation in steady-state plasma levels.


In distinction, the preferential << beta 1-AR >> antagonist, [[ betaxolol ]], and the preferential beta 2-AR antagonist, ICI118,551, did not increase basal levels of DA, NAD, or 5-HT.


In distinction, the preferential beta 1-AR antagonist, betaxolol, and the preferential << beta 2-AR >> antagonist, [[ ICI118,551 ]], did not increase basal levels of DA, NAD, or 5-HT.


The selective << 5-HT1A >> receptor antagonist, [[ WAY100,635 ]], slightly attenuated the (-)-pindolol-induced increase in DA and NAD levels, while the selective 5-HT1B antagonist, SB224,289, was ineffective.


The selective 5-HT1A receptor antagonist, WAY100,635, slightly attenuated the (-)-pindolol-induced increase in DA and NAD levels, while the selective << 5-HT1B >> antagonist, [[ SB224,289 ]], was ineffective.


UNLABELLED: << Entacapone >> is a potent and specific peripheral [[ catechol-O-methyltransferase ]] (COMT) inhibitor.


UNLABELLED: << Entacapone >> is a potent and specific peripheral catechol-O-methyltransferase ([[ COMT ]]) inhibitor.


<< 5-hydroxytryptamine >> evokes [[ endothelial nitric oxide synthase ]] activation in bovine aortic endothelial cell cultures.


Activation of << endothelial nitric oxide synthase >> (eNOS) results in the production of [[ nitric oxide ]] (NO) that mediates the vasorelaxing properties of endothelial cells.


Activation of endothelial nitric oxide synthase (<< eNOS >>) results in the production of [[ nitric oxide ]] (NO) that mediates the vasorelaxing properties of endothelial cells.


Activation of << endothelial nitric oxide synthase >> (eNOS) results in the production of nitric oxide ([[ NO ]]) that mediates the vasorelaxing properties of endothelial cells.


Activation of endothelial nitric oxide synthase (<< eNOS >>) results in the production of nitric oxide ([[ NO ]]) that mediates the vasorelaxing properties of endothelial cells.


Here, we tested the hypothesis that 5-HT receptors mediate << eNOS >> activation by measuring agonist-stimulated [[ [3H]L-citrulline ]] ([3H]L-Cit) formation in BAEC cultures.


Here, we tested the hypothesis that 5-HT receptors mediate << eNOS >> activation by measuring agonist-stimulated [3H]L-citrulline ([[ [3H]L-Cit ]]) formation in BAEC cultures.


We found that << 5-HT >> stimulated the conversion of [3H]L-arginine ([3H]L-Arg) to [3H]L-Cit, indicating [[ eNOS ]] activation.


We found that 5-HT stimulated the conversion of [3H]L-arginine ([3H]L-Arg) to << [3H]L-Cit >>, indicating [[ eNOS ]] activation.


We found that 5-HT stimulated the conversion of << [3H]L-arginine >> ([3H]L-Arg) to [3H]L-Cit, indicating [[ eNOS ]] activation.


We found that 5-HT stimulated the conversion of [3H]L-arginine (<< [3H]L-Arg >>) to [3H]L-Cit, indicating [[ eNOS ]] activation.


The high affinity << 5-HT1B >> receptor agonist, [[ 5-nonyloxytryptamine ]] (5-NOT)-stimulated [3H]L-Cit turnover responses were concentration-(0.01 nM to 100 microM) and time-dependent.


These responses were effectively blocked by the 5-HT1B receptor antagonist, isamoltane, the 5-HT1B/5-HT2 receptor antagonist, methiothepin, and the << eNOS >> selective antagonists (0.01-10 microM): [[ L-Nomega -monomethyl-L-arginine ]] (L-NMMA) and L-N omega-iminoethyl-L-ornithine (L-NIO).


These responses were effectively blocked by the 5-HT1B receptor antagonist, isamoltane, the << 5-HT1B >>/5-HT2 receptor antagonist, [[ methiothepin ]], and the eNOS selective antagonists (0.01-10 microM): L-Nomega -monomethyl-L-arginine (L-NMMA) and L-N omega-iminoethyl-L-ornithine (L-NIO).


These responses were effectively blocked by the 5-HT1B receptor antagonist, isamoltane, the 5-HT1B/<< 5-HT2 receptor >> antagonist, [[ methiothepin ]], and the eNOS selective antagonists (0.01-10 microM): L-Nomega -monomethyl-L-arginine (L-NMMA) and L-N omega-iminoethyl-L-ornithine (L-NIO).


These responses were effectively blocked by the 5-HT1B receptor antagonist, isamoltane, the 5-HT1B/5-HT2 receptor antagonist, methiothepin, and the << eNOS >> selective antagonists (0.01-10 microM): L-Nomega -monomethyl-L-arginine ([[ L-NMMA ]]) and L-N omega-iminoethyl-L-ornithine (L-NIO).


These responses were effectively blocked by the 5-HT1B receptor antagonist, isamoltane, the 5-HT1B/5-HT2 receptor antagonist, methiothepin, and the << eNOS >> selective antagonists (0.01-10 microM): L-Nomega -monomethyl-L-arginine (L-NMMA) and [[ L-N omega-iminoethyl-L-ornithine ]] (L-NIO).


These responses were effectively blocked by the 5-HT1B receptor antagonist, isamoltane, the 5-HT1B/5-HT2 receptor antagonist, methiothepin, and the << eNOS >> selective antagonists (0.01-10 microM): L-Nomega -monomethyl-L-arginine (L-NMMA) and L-N omega-iminoethyl-L-ornithine ([[ L-NIO ]]).


These findings lend evidence of a 5-HT1B receptor/eNOS pathway, accounting in part for the activation of << eNOS >> by [[ 5-HT ]].


<< Caffeine >> inhibits the checkpoint [[ kinase ]] ATM.


<< Caffeine >> inhibits the checkpoint kinase [[ ATM ]].


We report that the radiation-induced activation of the kinase Cds1 [4] (also known as Chk2 [5]) is inhibited by caffeine in vivo and that << ATM >> kinase activity is directly inhibited by [[ caffeine ]] in vitro.


We report that the radiation-induced activation of the kinase Cds1 [4] (also known as Chk2 [5]) is inhibited by caffeine in vivo and that ATM << kinase >> activity is directly inhibited by [[ caffeine ]] in vitro.


We report that the radiation-induced activation of the << kinase >> Cds1 [4] (also known as Chk2 [5]) is inhibited by [[ caffeine ]] in vivo and that ATM kinase activity is directly inhibited by caffeine in vitro.


We report that the radiation-induced activation of the kinase << Cds1 >> [4] (also known as Chk2 [5]) is inhibited by [[ caffeine ]] in vivo and that ATM kinase activity is directly inhibited by caffeine in vitro.


We report that the radiation-induced activation of the kinase Cds1 [4] (also known as << Chk2 >> [5]) is inhibited by [[ caffeine ]] in vivo and that ATM kinase activity is directly inhibited by caffeine in vitro.


Inhibition of << ATM >> provides a molecular explanation of the attenuation of DNA-damage checkpoint responses and for the increased radiosensitivity of [[ caffeine ]]-treated cells [6] [7] [8].


The turnover of << SERT >> was determined from the rate of recovery of binding after administration of [[ RTI-76 ]], an irreversible inhibitor of ligand binding.


In preliminary studies, in vitro incubation of rat cerebral cortex with << RTI-76 >> produced a wash and temperature resistant inhibition of [[ SERT ]] binding densities (Bmax).


Citalopram protected against the << RTI-76 >>-induced inhibition of [[ SERT ]] binding.


The decrease and recovery of << [3H]-5-HT >> uptake correlated highly (r = 0.93) with the recovery of [[ SERT ]] binding.


<< Losartan >> was the first, but by no means remained the only, [[ AT1 ]] receptor antagonist.


Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, telmisartan 10, E3174 (the active metabolite of [[ losartan ]]) 10, tasosartan 20, losartan 50, eprosartan 100 and the prodrug candesartan cilexetil 280.


Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, telmisartan 10, E3174 (the active metabolite of losartan) 10, [[ tasosartan ]] 20, losartan 50, eprosartan 100 and the prodrug candesartan cilexetil 280.


Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: [[ candesartan ]] 1, telmisartan 10, E3174 (the active metabolite of losartan) 10, tasosartan 20, losartan 50, eprosartan 100 and the prodrug candesartan cilexetil 280.


Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, [[ telmisartan ]] 10, E3174 (the active metabolite of losartan) 10, tasosartan 20, losartan 50, eprosartan 100 and the prodrug candesartan cilexetil 280.


Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, telmisartan 10, [[ E3174 ]] (the active metabolite of losartan) 10, tasosartan 20, losartan 50, eprosartan 100 and the prodrug candesartan cilexetil 280.


Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, telmisartan 10, E3174 (the active metabolite of losartan) 10, tasosartan 20, [[ losartan ]] 50, eprosartan 100 and the prodrug candesartan cilexetil 280.


Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, telmisartan 10, E3174 (the active metabolite of losartan) 10, tasosartan 20, losartan 50, [[ eprosartan ]] 100 and the prodrug candesartan cilexetil 280.


Among the current << AT1 >> receptor antagonists, the rank order of the relative binding affinities (highest affinity = 1) is: candesartan 1, telmisartan 10, E3174 (the active metabolite of losartan) 10, tasosartan 20, losartan 50, eprosartan 100 and the prodrug [[ candesartan cilexetil ]] 280.


The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, [[ saprisartan ]], zolasartan, irbesartan, valsartan, telmisartan, E3174).


The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, [[ zolasartan ]], irbesartan, valsartan, telmisartan, E3174).


The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, [[ irbesartan ]], valsartan, telmisartan, E3174).


The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, irbesartan, [[ valsartan ]], telmisartan, E3174).


The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, irbesartan, valsartan, [[ telmisartan ]], E3174).


The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, irbesartan, valsartan, telmisartan, [[ E3174 ]]).


The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive ([[ losartan ]], tasosartan, eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, irbesartan, valsartan, telmisartan, E3174).


The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, [[ tasosartan ]], eprosartan) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, irbesartan, valsartan, telmisartan, E3174).


The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, [[ eprosartan ]]) or insurmountable/noncompetitive (candesartan, saprisartan, zolasartan, irbesartan, valsartan, telmisartan, E3174).


The mode of (functional) << AT1 >> receptor antagonism has been characterized as surmountable/noncompetitive (losartan, tasosartan, eprosartan) or insurmountable/noncompetitive ([[ candesartan ]], saprisartan, zolasartan, irbesartan, valsartan, telmisartan, E3174).


<< Quinone oxidoreductases >> are flavoproteins that catalyze two-electron reduction and detoxification of [[ quinones ]].


A role of cytosolic << NQO1 >> in protection of cells from oxidative stress, cytotoxicity, and mutagenicity of [[ quinones ]] was established.


The << mNQO >> activity showed significantly higher affinity for NADH than NADPH as electron donors and catalyzed reduction of [[ 2,6-dichlorophenolindophenol ]] and menadione.


The << mNQO >> activity showed significantly higher affinity for NADH than NADPH as electron donors and catalyzed reduction of 2,6-dichlorophenolindophenol and [[ menadione ]].


The mNQO activity was insensitive to << dicoumarol >>, a potent inhibitor of cytosolic [[ NQO1 ]].


The << mu-opioid receptor >>-selective agonist [[ lofentanil ]] potently and competitively displaced [3H]nociceptin at rat brain receptors (IC(50) 62 nM).


<< Lofentanil >> exhibited full agonism for enhancement of [35S]GTPgammaS binding to human recombinant [[ ORL1 ]] receptors (EC(50) 50 nM).


The related piperidines ohmefentanyl and << sufentanil >> and the nonselective opioid receptor agonist etorphine were less potent [[ nociceptin receptor ]] agonists.


The related piperidines ohmefentanyl and sufentanil and the nonselective << opioid receptor >> agonist [[ etorphine ]] were less potent nociceptin receptor agonists.


The related piperidines ohmefentanyl and sufentanil and the nonselective opioid receptor agonist << etorphine >> were less potent [[ nociceptin receptor ]] agonists.


The related << piperidines >> ohmefentanyl and sufentanil and the nonselective opioid receptor agonist etorphine were less potent [[ nociceptin receptor ]] agonists.


The related piperidines << ohmefentanyl >> and sufentanil and the nonselective opioid receptor agonist etorphine were less potent [[ nociceptin receptor ]] agonists.


The kappa(1)+kappa(3)-opioid receptor agonist/mu-opioid receptor antagonist << naloxone benzoylhydrazone >> was a pure antagonist at both rat brain and human [[ ORL1 ]] receptors.


The kappa(1)+kappa(3)-opioid receptor agonist/<< mu-opioid receptor >> antagonist [[ naloxone benzoylhydrazone ]] was a pure antagonist at both rat brain and human ORL1 receptors.


The nonselective << opioid receptor >> partial agonist [[ buprenorphine ]] and the nonselective opioid receptor antagonist (-)-quadazocine exhibited pure antagonism at rat brain receptors, but displayed partial agonism at human ORL1 receptors.


The nonselective opioid receptor partial agonist buprenorphine and the nonselective opioid receptor antagonist << (-)-quadazocine >> exhibited pure antagonism at rat brain receptors, but displayed partial agonism at [[ human ORL1 ]] receptors.


The nonselective opioid receptor partial agonist buprenorphine and the nonselective << opioid receptor >> antagonist [[ (-)-quadazocine ]] exhibited pure antagonism at rat brain receptors, but displayed partial agonism at human ORL1 receptors.


<< Thymidylate synthase >> and thymidine kinase are key enzymes involved in the de novo and salvage pathways for [[ pyrimidine nucleotide ]] synthesis, respectively.


Thymidylate synthase and << thymidine kinase >> are key enzymes involved in the de novo and salvage pathways for [[ pyrimidine nucleotide ]] synthesis, respectively.


<< Thymidylate synthase >> is inhibited by [[ 5-fluorodeoxyuridine monophosphate ]], forming an inactive ternary complex with intracellular folate.


Thirty-week administration of << UFT >> with or without leucovorin markedly suppressed both colorectal carcinogenesis and tumor growth, resulted in the increase of [[ thymidylate synthase ]] inhibition and the decrease of thymidine kinase activity in the tumor cells.


Thirty-week administration of << UFT >> with or without leucovorin markedly suppressed both colorectal carcinogenesis and tumor growth, resulted in the increase of thymidylate synthase inhibition and the decrease of [[ thymidine kinase ]] activity in the tumor cells.


Thirty-week administration of UFT with or without << leucovorin >> markedly suppressed both colorectal carcinogenesis and tumor growth, resulted in the increase of [[ thymidylate synthase ]] inhibition and the decrease of thymidine kinase activity in the tumor cells.


Thirty-week administration of UFT with or without << leucovorin >> markedly suppressed both colorectal carcinogenesis and tumor growth, resulted in the increase of thymidylate synthase inhibition and the decrease of [[ thymidine kinase ]] activity in the tumor cells.


Ornithine decarboxylase (<< ODC >>) catalyses the first step in the synthesis of the polyamines putrescine, [[ spermidine ]] and spermine.


<< Ornithine decarboxylase >> (ODC) catalyses the first step in the synthesis of the polyamines putrescine, [[ spermidine ]] and spermine.


Ornithine decarboxylase (<< ODC >>) catalyses the first step in the synthesis of the polyamines putrescine, spermidine and [[ spermine ]].


<< Ornithine decarboxylase >> (ODC) catalyses the first step in the synthesis of the polyamines putrescine, spermidine and [[ spermine ]].


Ornithine decarboxylase (<< ODC >>) catalyses the first step in the synthesis of the polyamines [[ putrescine ]], spermidine and spermine.


<< Ornithine decarboxylase >> (ODC) catalyses the first step in the synthesis of the polyamines [[ putrescine ]], spermidine and spermine.


In << alpha(2A)-adrenoceptor >> transfected cells the rank order of agonist potency was [[ A-54741 ]] (mean pEC(50)=8.96)>dexmedetomidine (8.88)>UK-14304 (8.42)>B-HT 920 (7.05)>noradrenaline (6.92).


In << alpha(2A)-adrenoceptor >> transfected cells the rank order of agonist potency was A-54741 (mean pEC(50)=8.96)>[[ dexmedetomidine ]] (8.88)>UK-14304 (8.42)>B-HT 920 (7.05)>noradrenaline (6.92).


In << alpha(2A)-adrenoceptor >> transfected cells the rank order of agonist potency was A-54741 (mean pEC(50)=8.96)>dexmedetomidine (8.88)>[[ UK-14304 ]] (8.42)>B-HT 920 (7.05)>noradrenaline (6.92).


In << alpha(2A)-adrenoceptor >> transfected cells the rank order of agonist potency was A-54741 (mean pEC(50)=8.96)>dexmedetomidine (8.88)>UK-14304 (8.42)>[[ B-HT 920 ]] (7.05)>noradrenaline (6.92).


In << alpha(2A)-adrenoceptor >> transfected cells the rank order of agonist potency was A-54741 (mean pEC(50)=8.96)>dexmedetomidine (8.88)>UK-14304 (8.42)>B-HT 920 (7.05)>[[ noradrenaline ]] (6.92).


<< Glucocorticoid receptors >> were activated by [[ dexamethasone ]] as assessed using a glucocorticoid-responsive reporter plasmid, pTAT3-CAT.


The << glucocorticoid receptor >> antagonist [[ RU-486 ]] (mifepristone) significantly counteracted the effect of dexamethasone on glucocorticoid receptor activation, indicating that the dexamethasone effect is specific and is mediated through the glucocorticoid receptor.


The << glucocorticoid receptor >> antagonist RU-486 ([[ mifepristone ]]) significantly counteracted the effect of dexamethasone on glucocorticoid receptor activation, indicating that the dexamethasone effect is specific and is mediated through the glucocorticoid receptor.


RESULTS: << Quetiapine >> was an effective antipsychotic and improved the extrapyramidal symptoms and [[ prolactin ]] level elevation noted at baseline.


In a physiological K(+) gradient, << TWIK-2 >> is half inhibited by 0.1 mm [[ Ba(2+) ]], quinine, and quinidine.


In a physiological K(+) gradient, << TWIK-2 >> is half inhibited by 0.1 mm Ba(2+), [[ quinine ]], and quinidine.


In a physiological K(+) gradient, << TWIK-2 >> is half inhibited by 0.1 mm Ba(2+), quinine, and [[ quinidine ]].


Initial in vitro studies utilizing HEP-G2 liver cells revealed that addition of << eicosapentaenoic acid >> (EPA) blocked [[ Delta-5-desaturase ]] activity, the terminal enzymatic step in AA synthesis.


Initial in vitro studies utilizing HEP-G2 liver cells revealed that addition of eicosapentaenoic acid (<< EPA >>) blocked [[ Delta-5-desaturase ]] activity, the terminal enzymatic step in AA synthesis.


BACKGROUND: This study examines the effects of << nicorandil >>, a [[ K(+) channel ]] opener, on transmural dispersion of repolarization (TDR) and induction of torsade de pointes (TdP) under conditions mimicking the LQT1, LQT2, and LQT3 forms of the congenital long-QT syndrome (LQTS).


Isoproterenol (50 to 100 nmol/L) was used to mimic an increase in beta-adrenergic tone, << d-sotalol >> (100 micromol/L) to block [[ I(Kr) ]] (LQT2 model), and ATX-II (20 nmol/L) to augment late I(Na) (LQT3 model).


Isoproterenol (50 to 100 nmol/L) was used to mimic an increase in beta-adrenergic tone, << d-sotalol >> (100 micromol/L) to block I(Kr) (LQT2 model), and [[ ATX-II ]] (20 nmol/L) to augment late I(Na) (LQT3 model).


<< Isoproterenol >> (50 to 100 nmol/L) was used to mimic an increase in beta-adrenergic tone, d-sotalol (100 micromol/L) to block [[ I(Kr) ]] (LQT2 model), and ATX-II (20 nmol/L) to augment late I(Na) (LQT3 model).


<< Isoproterenol >> (50 to 100 nmol/L) was used to mimic an increase in beta-adrenergic tone, d-sotalol (100 micromol/L) to block I(Kr) (LQT2 model), and [[ ATX-II ]] (20 nmol/L) to augment late I(Na) (LQT3 model).


<< Peroxisome proliferator-activated receptor alpha >> (PPARalpha) activators, [[ bezafibrate ]] and Wy-14,643, increase uncoupling protein-3 mRNA levels without modifying the mitochondrial membrane potential in primary culture of rat preadipocytes.


Peroxisome proliferator-activated receptor alpha (<< PPARalpha >>) activators, [[ bezafibrate ]] and Wy-14,643, increase uncoupling protein-3 mRNA levels without modifying the mitochondrial membrane potential in primary culture of rat preadipocytes.


<< Peroxisome proliferator-activated receptor alpha >> (PPARalpha) activators, bezafibrate and [[ Wy-14,643 ]], increase uncoupling protein-3 mRNA levels without modifying the mitochondrial membrane potential in primary culture of rat preadipocytes.


Peroxisome proliferator-activated receptor alpha (<< PPARalpha >>) activators, bezafibrate and [[ Wy-14,643 ]], increase uncoupling protein-3 mRNA levels without modifying the mitochondrial membrane potential in primary culture of rat preadipocytes.


Peroxisome proliferator-activated receptor alpha (PPARalpha) activators, << bezafibrate >> and Wy-14,643, increase [[ uncoupling protein-3 ]] mRNA levels without modifying the mitochondrial membrane potential in primary culture of rat preadipocytes.


Peroxisome proliferator-activated receptor alpha (PPARalpha) activators, bezafibrate and << Wy-14,643 >>, increase [[ uncoupling protein-3 ]] mRNA levels without modifying the mitochondrial membrane potential in primary culture of rat preadipocytes.


<< Uncoupling proteins >> (UCPs) are inner mitochondrial membrane transporters which act as pores for [[ H(+) ]] ions, dissipating the electrochemical gradient that develops during mitochondrial respiration at the expense of ATP synthesis.


Uncoupling proteins (<< UCPs >>) are inner mitochondrial membrane transporters which act as pores for [[ H(+) ]] ions, dissipating the electrochemical gradient that develops during mitochondrial respiration at the expense of ATP synthesis.


Thus, << bezafibrate >> treatment resulted in an 8-fold induction in [[ UCP-3 ]] mRNA levels in preadipocytes compared with the 3.5-fold induction observed in adipocytes.


The induction in << UCP-3 >> expression was not accompanied by changes in the mitochondrial membrane potential of rat primary preadipocytes after [[ bezafibrate ]] or Wy-14,643 treatment.


The induction in << UCP-3 >> expression was not accompanied by changes in the mitochondrial membrane potential of rat primary preadipocytes after bezafibrate or [[ Wy-14,643 ]] treatment.


Since it has been proposed that UCP-3 could be involved in the regulation of the use of fatty acids as fuel substrates, the << UCP-3 >> induction achieved after [[ bezafibrate ]] and Wy-14, 643 treatment may indicate a higher oxidation of fatty acids, limiting their availability to be stored as triglycerides.


Since it has been proposed that UCP-3 could be involved in the regulation of the use of fatty acids as fuel substrates, the << UCP-3 >> induction achieved after bezafibrate and [[ Wy-14, 643 ]] treatment may indicate a higher oxidation of fatty acids, limiting their availability to be stored as triglycerides.


<< Schisandrin B >> protects against menadione-induced hepatotoxicity by enhancing [[ DT-diaphorase ]] activity.


Pretreating mice with schisandrin B (Sch B), a dibenzocyclooctadiene derivative isolated from the fruit of Schisandra chinensis, at a daily dose of 1 mmol/kg for 3 days protected against << menadione >>-induced hepatic oxidative damage in mice, as evidenced by decreases in plasma [[ alanine aminotransferase ]] activity (78%) and hepatic malondialdehyde level (70%), when compared with the menadione intoxicated control.


Hepatocytes isolated from << Sch B >> pretreated (a daily dose of 1 mmol/kg for 3 days) rats showed a significant increase (25%) in [[ DTD ]] activity.


The ensemble of results suggests that the ability of << Sch B >> pretreatment to enhance hepatocellular [[ DTD ]] activity may at least in part be attributed to the protection against menadione hepatotoxicity.


The group treated with << pyridostigmine >> alone showed decreased plasma [[ butyrylcholinesterase ]] (BChE) activity (87% of control), whereas pyridostigmine plus exercise significantly decreased the BChE activity (79% of control), indicating an interactive effect of the combination.


The group treated with << pyridostigmine >> alone showed decreased plasma butyrylcholinesterase ([[ BChE ]]) activity (87% of control), whereas pyridostigmine plus exercise significantly decreased the BChE activity (79% of control), indicating an interactive effect of the combination.


The group treated with pyridostigmine alone showed decreased plasma butyrylcholinesterase (BChE) activity (87% of control), whereas << pyridostigmine >> plus exercise significantly decreased the [[ BChE ]] activity (79% of control), indicating an interactive effect of the combination.


However, << AChE >> activity in triceps muscle decreased significantly (78% of control) in the group treated with [[ pyridostigmine ]] plus exercise.


<< Creatine phosphokinase >> activity in plasma increased slightly (compared to control, [[ pyridostigmine ]] or exercise group) in mice treated with pyridostigmine plus exercise, which may be indicative of perturbation in the integrity of the skeletal muscle due to combination.


<< Creatine phosphokinase >> activity in plasma increased slightly (compared to control, pyridostigmine or exercise group) in mice treated with [[ pyridostigmine ]] plus exercise, which may be indicative of perturbation in the integrity of the skeletal muscle due to combination.


RESULT(S): Buserelin acetate, a GnRH agonist (0.1-10 ng/mL), had no significant effect on MCP-1 expression, whereas << danazol >> (10(-7)-10(-5) M), a testosterone analog, and dexamethasone, an anti-inflammatory glucocorticoid hormone (10(-12)-10(-6)M), showed a direct and a dose-dependent inhibitory effect on [[ MCP-1 ]] expression.


RESULT(S): Buserelin acetate, a GnRH agonist (0.1-10 ng/mL), had no significant effect on MCP-1 expression, whereas danazol (10(-7)-10(-5) M), a << testosterone >> analog, and dexamethasone, an anti-inflammatory glucocorticoid hormone (10(-12)-10(-6)M), showed a direct and a dose-dependent inhibitory effect on [[ MCP-1 ]] expression.


RESULT(S): Buserelin acetate, a GnRH agonist (0.1-10 ng/mL), had no significant effect on MCP-1 expression, whereas danazol (10(-7)-10(-5) M), a testosterone analog, and << dexamethasone >>, an anti-inflammatory glucocorticoid hormone (10(-12)-10(-6)M), showed a direct and a dose-dependent inhibitory effect on [[ MCP-1 ]] expression.


RESULT(S): << Buserelin acetate >>, a [[ GnRH ]] agonist (0.1-10 ng/mL), had no significant effect on MCP-1 expression, whereas danazol (10(-7)-10(-5) M), a testosterone analog, and dexamethasone, an anti-inflammatory glucocorticoid hormone (10(-12)-10(-6)M), showed a direct and a dose-dependent inhibitory effect on MCP-1 expression.


The present studies were undertaken to compare two compounds, a vitamin D(3) analogue (<< CB1093 >>) with minimal calcaemic effects, and clenbuterol, a long-acting beta(2)-adrenoceptor agonist, both of which induce [[ NGF ]] synthesis in vivo.


The present studies were undertaken to compare two compounds, a vitamin D(3) analogue (CB1093) with minimal calcaemic effects, and << clenbuterol >>, a long-acting beta(2)-adrenoceptor agonist, both of which induce [[ NGF ]] synthesis in vivo.


The present studies were undertaken to compare two compounds, a << vitamin D(3) >> analogue (CB1093) with minimal calcaemic effects, and clenbuterol, a long-acting beta(2)-adrenoceptor agonist, both of which induce [[ NGF ]] synthesis in vivo.


The present studies were undertaken to compare two compounds, a vitamin D(3) analogue (CB1093) with minimal calcaemic effects, and << clenbuterol >>, a long-acting [[ beta(2)-adrenoceptor ]] agonist, both of which induce NGF synthesis in vivo.


<< Clenbuterol >> caused significant increases in both [[ NGF ]] mRNA and protein in 3T3 cells; with maxima at 10 nM and at 8-12 h exposure.


Mobility shift assays on whole cell extracts showed that << clenbuterol >> increased AP1 binding in 3T3 cells prior to increasing [[ NGF ]] synthesis.


Clenbuterol was without effect on NGF mRNA levels in L929 cells, whereas << CB1093 >> caused significant increases in both [[ NGF ]] mRNA and protein levels in both 3T3 and L929 cells.


This study demonstrates that << CB1093 >> and clenbuterol stimulate [[ NGF ]] levels in vitro and that AP-1 binding could be a commonality between the mechanism of NGF induction of these two compounds.


This study demonstrates that << CB1093 >> and clenbuterol stimulate NGF levels in vitro and that AP-1 binding could be a commonality between the mechanism of [[ NGF ]] induction of these two compounds.


This study demonstrates that CB1093 and << clenbuterol >> stimulate [[ NGF ]] levels in vitro and that AP-1 binding could be a commonality between the mechanism of NGF induction of these two compounds.


This study demonstrates that CB1093 and << clenbuterol >> stimulate NGF levels in vitro and that AP-1 binding could be a commonality between the mechanism of [[ NGF ]] induction of these two compounds.


Protective effect of << halothane >> anesthesia on retinal light damage: inhibition of metabolic [[ rhodopsin ]] regeneration.


RESULTS: << Halothane >> anesthesia reversibly inhibited metabolic [[ rhodopsin ]] regeneration and thus prevented rhodopsin from absorbing high numbers of photons during light exposure.


RESULTS: << Halothane >> anesthesia reversibly inhibited metabolic rhodopsin regeneration and thus prevented [[ rhodopsin ]] from absorbing high numbers of photons during light exposure.


CONCLUSIONS: After the initial bleach, << halothane >> impeded photon absorption by rhodopsin by inhibiting metabolic [[ rhodopsin ]] regeneration.


METHODS: Different classes of antidepressants [imipramine (tricyclic), maprotiline (noradrenline reuptake inhibitor), venlafaxine (mixed serotonin and noradrenaline reuptake inhibitors), fluvoxamine and sertraline (selective serotonin reuptake inhibitor)] were tested in the same randomised experimental session, alone and in combination with 5-HT1A and 5-HT1B receptor agonists [<< buspirone >> (partial [[ 5-HT1A ]] agonist), anpirtoline (5-HT1B agonist)] in the mouse forced swimming test.


METHODS: Different classes of antidepressants [imipramine (tricyclic), maprotiline (noradrenline reuptake inhibitor), venlafaxine (mixed serotonin and noradrenaline reuptake inhibitors), fluvoxamine and sertraline (selective serotonin reuptake inhibitor)] were tested in the same randomised experimental session, alone and in combination with 5-HT1A and 5-HT1B receptor agonists [buspirone (partial 5-HT1A agonist), << anpirtoline >> ([[ 5-HT1B ]] agonist)] in the mouse forced swimming test.


<< Pemetrexed disodium >> (Alimta, LY231514) is a novel, multitargeted antifolate that inhibits thymidylate synthase, [[ dihydrofolate reductase ]], and glycinamide ribonucleotide formyl transferase.


<< Pemetrexed disodium >> (Alimta, LY231514) is a novel, multitargeted antifolate that inhibits thymidylate synthase, dihydrofolate reductase, and [[ glycinamide ribonucleotide formyl transferase ]].


<< Pemetrexed disodium >> (Alimta, LY231514) is a novel, multitargeted antifolate that inhibits [[ thymidylate synthase ]], dihydrofolate reductase, and glycinamide ribonucleotide formyl transferase.


Pemetrexed disodium (<< Alimta >>, LY231514) is a novel, multitargeted antifolate that inhibits thymidylate synthase, [[ dihydrofolate reductase ]], and glycinamide ribonucleotide formyl transferase.


Pemetrexed disodium (<< Alimta >>, LY231514) is a novel, multitargeted antifolate that inhibits thymidylate synthase, dihydrofolate reductase, and [[ glycinamide ribonucleotide formyl transferase ]].


Pemetrexed disodium (<< Alimta >>, LY231514) is a novel, multitargeted antifolate that inhibits [[ thymidylate synthase ]], dihydrofolate reductase, and glycinamide ribonucleotide formyl transferase.


Pemetrexed disodium (Alimta, << LY231514 >>) is a novel, multitargeted antifolate that inhibits thymidylate synthase, [[ dihydrofolate reductase ]], and glycinamide ribonucleotide formyl transferase.


Pemetrexed disodium (Alimta, << LY231514 >>) is a novel, multitargeted antifolate that inhibits thymidylate synthase, dihydrofolate reductase, and [[ glycinamide ribonucleotide formyl transferase ]].


Pemetrexed disodium (Alimta, << LY231514 >>) is a novel, multitargeted antifolate that inhibits [[ thymidylate synthase ]], dihydrofolate reductase, and glycinamide ribonucleotide formyl transferase.


To mechanistically evaluate this regional selectivity, we assessed << cyclo-oxygenase-2 >> (COX-2) expression in the uninvolved mucosa and demonstrated a 3- to 4-fold excess in the distal relative to the proximal bowel in both MIN mice and [[ AOM ]]-treated rats.


To mechanistically evaluate this regional selectivity, we assessed cyclo-oxygenase-2 (<< COX-2 >>) expression in the uninvolved mucosa and demonstrated a 3- to 4-fold excess in the distal relative to the proximal bowel in both MIN mice and [[ AOM ]]-treated rats.


<< Diacylglycerol kinase >> (DGK) catalyzes the conversion of diacylglycerol to [[ phosphatidic acid ]], making it an attractive candidate for a signal transduction component.


Diacylglycerol kinase (<< DGK >>) catalyzes the conversion of diacylglycerol to [[ phosphatidic acid ]], making it an attractive candidate for a signal transduction component.


<< Diacylglycerol kinase >> (DGK) catalyzes the conversion of [[ diacylglycerol ]] to phosphatidic acid, making it an attractive candidate for a signal transduction component.


Diacylglycerol kinase (<< DGK >>) catalyzes the conversion of [[ diacylglycerol ]] to phosphatidic acid, making it an attractive candidate for a signal transduction component.


We took advantage of the previous observations that << phosphatidylserine >> inhibits [[ DGK-delta ]] (reviewed by Sakane, F., Imai, S., Kai, M., Wada, I., and Kanoh, H. (1996) J. Biol. Chem. 271, 8394-8401), and constitutively active RhoA inhibits DGK-theta (reviewed by Houssa, B., de Widt, J., Kranenburg, O., Moolenaar, W. H., and van Blitterswijk, W. J. (1999) J. Biol. Chem. 274, 6820-6822) to identify the activity induced by alpha-thrombin.


<< Nordihydroguaiaretic acid >> (NDGA) has been shown to inhibit both 5-lipoxygenase and [[ ornithine decarboxylase ]] and is active against several cancer cell lines and at least one mouse tumor model.


<< Nordihydroguaiaretic acid >> (NDGA) has been shown to inhibit both [[ 5-lipoxygenase ]] and ornithine decarboxylase and is active against several cancer cell lines and at least one mouse tumor model.


Nordihydroguaiaretic acid (<< NDGA >>) has been shown to inhibit both 5-lipoxygenase and [[ ornithine decarboxylase ]] and is active against several cancer cell lines and at least one mouse tumor model.


Nordihydroguaiaretic acid (<< NDGA >>) has been shown to inhibit both [[ 5-lipoxygenase ]] and ornithine decarboxylase and is active against several cancer cell lines and at least one mouse tumor model.


<< Carbonic anhydrase >> (CA) is a zinc enzyme that catalyses the reversible hydration reaction of [[ CO2 ]] and plays a major role in the acid-base balance.


Carbonic anhydrase (<< CA >>) is a zinc enzyme that catalyses the reversible hydration reaction of [[ CO2 ]] and plays a major role in the acid-base balance.


The temporal profile of butyrylcholinesterase (BuChE) and in vitro << pralidoxime >>-reactivated [[ BuChE ]] was studied in a cohort of 25 organophosphate-poisoned patients to examine their relationship to the development of intermediate syndrome and to understand reasons for lack of efficacy of oxime treatment.


Reactivation potentials of << BuChE >> (the difference between [[ oxime ]]-reactivated and -unreactivated enzyme activity) declined significantly with time after organophosphate ingestion.


Reactivation potentials of << BuChE >> (the difference between oxime-reactivated and -unreactivated enzyme activity) declined significantly with time after [[ organophosphate ]] ingestion.


Patients who received << oxime >> prior to hospitalization had a higher rate of intermediate syndrome and lower levels of [[ BuChE ]] at admission than those who had not.


The segments were contracted with the << alpha(2)-adrenoceptor >> agonists [[ brimonidine ]], apraclonidine, and oxymetazoline.


The segments were contracted with the << alpha(2)-adrenoceptor >> agonists brimonidine, [[ apraclonidine ]], and oxymetazoline.


The segments were contracted with the << alpha(2)-adrenoceptor >> agonists brimonidine, apraclonidine, and [[ oxymetazoline ]].


The following alpha(2)-adrenoceptor antagonists were applied: << BRL44408 >> ([[ alpha(2A) ]]-selective), ARC239 (alpha(2B)- and alpha(2C)-selective), and prazosin (alpha(2B)- and alpha(2C)-selective).


The following alpha(2)-adrenoceptor antagonists were applied: BRL44408 (alpha(2A)-selective), << ARC239 >> ([[ alpha(2B) ]]- and alpha(2C)-selective), and prazosin (alpha(2B)- and alpha(2C)-selective).


The following alpha(2)-adrenoceptor antagonists were applied: BRL44408 (alpha(2A)-selective), << ARC239 >> (alpha(2B)- and [[ alpha(2C) ]]-selective), and prazosin (alpha(2B)- and alpha(2C)-selective).


The following alpha(2)-adrenoceptor antagonists were applied: BRL44408 (alpha(2A)-selective), ARC239 (alpha(2B)- and alpha(2C)-selective), and << prazosin >> ([[ alpha(2B) ]]- and alpha(2C)-selective).


The following alpha(2)-adrenoceptor antagonists were applied: BRL44408 (alpha(2A)-selective), ARC239 (alpha(2B)- and alpha(2C)-selective), and << prazosin >> (alpha(2B)- and [[ alpha(2C) ]]-selective).


RESULTS: The << alpha(2)-adrenoceptor >> agonists induced vasoconstriction in the porcine ciliary artery with the following potency order (EC(50)) expressed in nanomolar: [[ brimonidine ]] 2.11, oxymetazoline 5.26, and apraclonidine 13.0.


RESULTS: The << alpha(2)-adrenoceptor >> agonists induced vasoconstriction in the porcine ciliary artery with the following potency order (EC(50)) expressed in nanomolar: brimonidine 2.11, [[ oxymetazoline ]] 5.26, and apraclonidine 13.0.


RESULTS: The << alpha(2)-adrenoceptor >> agonists induced vasoconstriction in the porcine ciliary artery with the following potency order (EC(50)) expressed in nanomolar: brimonidine 2.11, oxymetazoline 5.26, and [[ apraclonidine ]] 13.0.


Schild analyses for the antagonists against brimonidine yielded regression lines with slopes of unity and functional antagonist potencies (pK(B)) for << BRL44408 >> (7.8), ARC 239 (5.8) and for prazosin (6.0) suggesting the presence of functional [[ alpha(2A)-adrenoceptors ]].


Schild analyses for the antagonists against brimonidine yielded regression lines with slopes of unity and functional antagonist potencies (pK(B)) for BRL44408 (7.8), << ARC 239 >> (5.8) and for prazosin (6.0) suggesting the presence of functional [[ alpha(2A)-adrenoceptors ]].


Schild analyses for the antagonists against brimonidine yielded regression lines with slopes of unity and functional antagonist potencies (pK(B)) for BRL44408 (7.8), ARC 239 (5.8) and for << prazosin >> (6.0) suggesting the presence of functional [[ alpha(2A)-adrenoceptors ]].


CONCLUSIONS: The << alpha(2)-adrenoceptor >> agonists [[ brimonidine ]], apraclonidine, and oxymetazoline are potent vasoconstrictors in the porcine ciliary artery.


CONCLUSIONS: The << alpha(2)-adrenoceptor >> agonists brimonidine, [[ apraclonidine ]], and oxymetazoline are potent vasoconstrictors in the porcine ciliary artery.


CONCLUSIONS: The << alpha(2)-adrenoceptor >> agonists brimonidine, apraclonidine, and [[ oxymetazoline ]] are potent vasoconstrictors in the porcine ciliary artery.


<< Pemetrexed disodium >> (ALIMTA) is a novel antimetabolite that inhibits at least three folate-dependent enzymes, [[ thymidylate synthase ]], dihydrofolate reductase, and glycinamide ribonucleotide formyltransferase.


<< Pemetrexed disodium >> (ALIMTA) is a novel antimetabolite that inhibits at least three folate-dependent enzymes, thymidylate synthase, [[ dihydrofolate reductase ]], and glycinamide ribonucleotide formyltransferase.


<< Pemetrexed disodium >> (ALIMTA) is a novel antimetabolite that inhibits at least three folate-dependent enzymes, thymidylate synthase, dihydrofolate reductase, and [[ glycinamide ribonucleotide formyltransferase ]].


Pemetrexed disodium (<< ALIMTA >>) is a novel antimetabolite that inhibits at least three folate-dependent enzymes, [[ thymidylate synthase ]], dihydrofolate reductase, and glycinamide ribonucleotide formyltransferase.


Pemetrexed disodium (<< ALIMTA >>) is a novel antimetabolite that inhibits at least three folate-dependent enzymes, thymidylate synthase, [[ dihydrofolate reductase ]], and glycinamide ribonucleotide formyltransferase.


Pemetrexed disodium (<< ALIMTA >>) is a novel antimetabolite that inhibits at least three folate-dependent enzymes, thymidylate synthase, dihydrofolate reductase, and [[ glycinamide ribonucleotide formyltransferase ]].


<< DHFS >> is present exclusively in the mitochondria, making this compartment the sole site of synthesis of [[ dihydrofolate ]] in the plant cell.


UNLABELLED: << Rabeprazole >> is an inhibitor of the [[ gastric proton pump ]].


CONCLUSION: << Rabeprazole >> is a well tolerated [[ proton pump ]] inhibitor.


<< Angiotensin II >> suppression in humans by the orally active renin inhibitor [[ Aliskiren ]] (SPP100): comparison with enalapril.


<< Angiotensin II >> suppression in humans by the orally active renin inhibitor Aliskiren ([[ SPP100 ]]): comparison with enalapril.


Angiotensin II suppression in humans by the orally active << renin >> inhibitor [[ Aliskiren ]] (SPP100): comparison with enalapril.


Angiotensin II suppression in humans by the orally active << renin >> inhibitor Aliskiren ([[ SPP100 ]]): comparison with enalapril.


We tested the new orally active nonpeptidic << renin >> inhibitor [[ SPP100 ]] (Aliskiren, an octanamide with a 50% inhibitory concentration [IC50] in the low nanomolar range) in 18 healthy volunteers on a constant 100 mmol/d sodium diet using a double-blind, 3-way crossover protocol.


We tested the new orally active nonpeptidic << renin >> inhibitor SPP100 ([[ Aliskiren ]], an octanamide with a 50% inhibitory concentration [IC50] in the low nanomolar range) in 18 healthy volunteers on a constant 100 mmol/d sodium diet using a double-blind, 3-way crossover protocol.


We tested the new orally active nonpeptidic << renin >> inhibitor SPP100 (Aliskiren, an [[ octanamide ]] with a 50% inhibitory concentration [IC50] in the low nanomolar range) in 18 healthy volunteers on a constant 100 mmol/d sodium diet using a double-blind, 3-way crossover protocol.


There was a dose-dependent decrease in plasma renin activity, << Ang I >>, and Ang II following single doses of [[ Aliskiren ]] starting with 40 mg.


There was a dose-dependent decrease in plasma renin activity, Ang I, and << Ang II >> following single doses of [[ Aliskiren ]] starting with 40 mg.


There was a dose-dependent decrease in plasma << renin >> activity, Ang I, and Ang II following single doses of [[ Aliskiren ]] starting with 40 mg.


Inhibition was still marked and significant after repeated dosing with maximal decreases in << Ang II >> levels by 89% and 75% on Days 1 and 8, respectively, when the highest dose of [[ Aliskiren ]] was compared with placebo.


At the same time, mean plasma active << renin >> was increased 16- and 34-fold at the highest dose of [[ Aliskiren ]].


In conclusion, the renin inhibitor << Aliskiren >> dose-dependently decreases [[ Ang II ]] levels in humans following oral administration.


In conclusion, the << renin >> inhibitor [[ Aliskiren ]] dose-dependently decreases Ang II levels in humans following oral administration.


<< Aliskiren >> has the potential to become the first orally active [[ renin ]] inhibitor that provides a true alternative to ACE-inhibitors and Ang II receptor antagonists in therapy for hypertension and other cardiovascular and renal diseases.


<< Aliskiren >> has the potential to become the first orally active renin inhibitor that provides a true alternative to [[ ACE ]]-inhibitors and Ang II receptor antagonists in therapy for hypertension and other cardiovascular and renal diseases.


<< Aliskiren >> has the potential to become the first orally active renin inhibitor that provides a true alternative to ACE-inhibitors and [[ Ang II receptor ]] antagonists in therapy for hypertension and other cardiovascular and renal diseases.


The earliest known << AChE >> inhibitors, namely, [[ physostigmine ]] and tacrine, performed poorly in clinical trials (e.g., poor oral activity, brain penetration, and hepatotoxic liability).


The earliest known << AChE >> inhibitors, namely, physostigmine and [[ tacrine ]], performed poorly in clinical trials (e.g., poor oral activity, brain penetration, and hepatotoxic liability).


<< Donepezil hydrochloride >> inaugurates a new class of [[ AChE ]] inhibitors with longer and more selective action and with manageable adverse effects.


<< Thalidomide >>--removed from widespread clinical use by 1962 because of severe teratogenicity--has anti-angiogenic and immunomodulatory effects, including the inhibition of [[ TNF alpha ]].


As a prodrug << leflunomide >> is completely converted to its active metabolite A 77 1726 (M1) which blocks the [[ dihydroorotate dehydrogenase ]], a key enzyme of the pyrimidine de novo synthesis.


As a prodrug leflunomide is completely converted to its active metabolite << A 77 1726 >> (M1) which blocks the [[ dihydroorotate dehydrogenase ]], a key enzyme of the pyrimidine de novo synthesis.


A recent study showed that << anastrozole >>, an [[ aromatase ]] inhibitor, is as effective or even superior to tamoxifen when used as a first-line therapy.


<< Fulvestrant >>, the first agent in this new class, not only induces the degradation of the [[ estrogen receptor ]] but also is an estrogen antagonist; further, its lack of agonist activity provides a better safety profile.


<< Lovastatin >>, a specific inhibitor of [[ HMG-CoA reductase ]], induces a pronounced apoptotic response in a specific subset of tumor types, including HNSCC and CC.


Chronic treatment with the NET inhibitor, << desipramine >> (DMI), reduced [[ NET ]] levels in both control and Dbh -/- mice, demonstrating that NE is not required for the regulation of NET by antidepressant drugs.


Chronic treatment with the << NET >> inhibitor, [[ desipramine ]] (DMI), reduced NET levels in both control and Dbh -/- mice, demonstrating that NE is not required for the regulation of NET by antidepressant drugs.


Probes were perfused with artificial cerebrospinal fluid containing nicotine, the specific << alpha(4)beta(2*) nAChR >> agonist [[ metanicotine ]], or nicotine plus nAChR antagonists and norepinephrine measured in the microdialysates.


Probes were perfused with artificial cerebrospinal fluid containing nicotine, the specific << alpha(4)beta(2*) nAChR >> agonist metanicotine, or [[ nicotine ]] plus nAChR antagonists and norepinephrine measured in the microdialysates.


<< Cilostazol >> decreases levels of serum triglycerides and causes some increase in [[ HDL ]]-cholesterol levels.


<< Cilostazol >> undergoes intensive and finally complete hepatic metabolism via the [[ cytochrome P450 ]] systems.


We changed the residues to alanine using site-directed mutagenesis technique, expressed the mutants in a baculovirus/Sf9 cell system, and analyzed the kinetic characteristics of inhibition of the mutant enzymes by << milrinone >> and cilostazol, specific inhibitors of [[ PDE3 ]].


We changed the residues to alanine using site-directed mutagenesis technique, expressed the mutants in a baculovirus/Sf9 cell system, and analyzed the kinetic characteristics of inhibition of the mutant enzymes by milrinone and << cilostazol >>, specific inhibitors of [[ PDE3 ]].


Mutants << Y751A >>, D950A, and F1004A had reduced sensitivity to [[ milrinone ]] (K(i) changed from 0.66 microM for the recombinant PDE3A to 7.5 to 156 microM for the mutants), and diminished sensitivity to cilostazol (K(i) of the mutants were 18- to 371-fold higher than that of the recombinant PDE3A).


Mutants Y751A, << D950A >>, and F1004A had reduced sensitivity to [[ milrinone ]] (K(i) changed from 0.66 microM for the recombinant PDE3A to 7.5 to 156 microM for the mutants), and diminished sensitivity to cilostazol (K(i) of the mutants were 18- to 371-fold higher than that of the recombinant PDE3A).


Mutants Y751A, D950A, and << F1004A >> had reduced sensitivity to [[ milrinone ]] (K(i) changed from 0.66 microM for the recombinant PDE3A to 7.5 to 156 microM for the mutants), and diminished sensitivity to cilostazol (K(i) of the mutants were 18- to 371-fold higher than that of the recombinant PDE3A).


Mutants Y751A, D950A, and F1004A had reduced sensitivity to << milrinone >> (K(i) changed from 0.66 microM for the recombinant [[ PDE3A ]] to 7.5 to 156 microM for the mutants), and diminished sensitivity to cilostazol (K(i) of the mutants were 18- to 371-fold higher than that of the recombinant PDE3A).


Mutants Y751A, D950A, and F1004A had reduced sensitivity to milrinone (K(i) changed from 0.66 microM for the recombinant PDE3A to 7.5 to 156 microM for the mutants), and diminished sensitivity to << cilostazol >> (K(i) of the mutants were 18- to 371-fold higher than that of the recombinant [[ PDE3A ]]).


In contrast, the mutants T844A, F972A and Q975A showed increased K(i) for << cilostazol >> but no difference for milrinone from the recombinant [[ PDE3A ]].


In contrast, the mutants << T844A >>, F972A and Q975A showed increased K(i) for [[ cilostazol ]] but no difference for milrinone from the recombinant PDE3A.


In contrast, the mutants T844A, << F972A >> and Q975A showed increased K(i) for [[ cilostazol ]] but no difference for milrinone from the recombinant PDE3A.


In contrast, the mutants T844A, F972A and << Q975A >> showed increased K(i) for [[ cilostazol ]] but no difference for milrinone from the recombinant PDE3A.


In contrast, the mutants T844A, F972A and Q975A showed increased K(i) for cilostazol but no difference for << milrinone >> from the recombinant [[ PDE3A ]].


In contrast, the mutants << T844A >>, F972A and Q975A showed increased K(i) for cilostazol but no difference for [[ milrinone ]] from the recombinant PDE3A.


In contrast, the mutants T844A, << F972A >> and Q975A showed increased K(i) for cilostazol but no difference for [[ milrinone ]] from the recombinant PDE3A.


In contrast, the mutants T844A, F972A and << Q975A >> showed increased K(i) for cilostazol but no difference for [[ milrinone ]] from the recombinant PDE3A.


Molecular models show that the << PDE3 >> inhibitors [[ cilostazol ]] and milrinone share some of common residues but interact with distinct residues at the active site, suggesting that selective inhibitors can be designed with flexible size against PDE3 active site.


Molecular models show that the << PDE3 >> inhibitors cilostazol and [[ milrinone ]] share some of common residues but interact with distinct residues at the active site, suggesting that selective inhibitors can be designed with flexible size against PDE3 active site.


Our study implies that highly conserved residuals Y751, D950 and F1004 in the << PDE >> families are key residues for binding of both substrate and inhibitors, and nonconserved T844 may be responsible for the [[ cilostazol ]] selectivity of PDE3A.


Our study implies that highly conserved residuals Y751, D950 and F1004 in the PDE families are key residues for binding of both substrate and inhibitors, and nonconserved T844 may be responsible for the << cilostazol >> selectivity of [[ PDE3A ]].


The bacterial enzyme << maltodextrin phosphorylase >> (MalP) catalyses the phosphorolysis of an alpha-1,4-glycosidic bond in maltodextrins, removing the non-reducing glucosyl residues of linear oligosaccharides as [[ glucose-1-phosphate ]] (Glc1P).


The bacterial enzyme maltodextrin phosphorylase (<< MalP >>) catalyses the phosphorolysis of an alpha-1,4-glycosidic bond in maltodextrins, removing the non-reducing glucosyl residues of linear oligosaccharides as [[ glucose-1-phosphate ]] (Glc1P).


The bacterial enzyme << maltodextrin phosphorylase >> (MalP) catalyses the phosphorolysis of an alpha-1,4-glycosidic bond in maltodextrins, removing the non-reducing glucosyl residues of linear oligosaccharides as glucose-1-phosphate ([[ Glc1P ]]).


The bacterial enzyme maltodextrin phosphorylase (<< MalP >>) catalyses the phosphorolysis of an alpha-1,4-glycosidic bond in maltodextrins, removing the non-reducing glucosyl residues of linear oligosaccharides as glucose-1-phosphate ([[ Glc1P ]]).


OBJECTIVE: << Fondaparinux sodium >> is the first in a new class of synthetic [[ factor Xa ]] inhibitors that binds reversibly with high affinity to antithrombin III.


It is caused by a deficiency of << propionyl-CoA carboxylase >> (PCC, EC 6.4.1.3), a biotin-dependent enzyme that catalyzes the carboxylation of [[ propionyl-CoA ]] to D-methylmalonyl-CoA.


It is caused by a deficiency of propionyl-CoA carboxylase (<< PCC >>, EC 6.4.1.3), a biotin-dependent enzyme that catalyzes the carboxylation of [[ propionyl-CoA ]] to D-methylmalonyl-CoA.


It is caused by a deficiency of propionyl-CoA carboxylase (PCC, << EC 6.4.1.3 >>), a biotin-dependent enzyme that catalyzes the carboxylation of [[ propionyl-CoA ]] to D-methylmalonyl-CoA.


It is caused by a deficiency of << propionyl-CoA carboxylase >> (PCC, EC 6.4.1.3), a biotin-dependent enzyme that catalyzes the carboxylation of propionyl-CoA to [[ D-methylmalonyl-CoA ]].


It is caused by a deficiency of propionyl-CoA carboxylase (<< PCC >>, EC 6.4.1.3), a biotin-dependent enzyme that catalyzes the carboxylation of propionyl-CoA to [[ D-methylmalonyl-CoA ]].


It is caused by a deficiency of propionyl-CoA carboxylase (PCC, << EC 6.4.1.3 >>), a biotin-dependent enzyme that catalyzes the carboxylation of propionyl-CoA to [[ D-methylmalonyl-CoA ]].


Although only << clozapine >> and ziprasidone are directly acting 5-HT(1A) agonists, WAY100635, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined [[ 5-HT(2A) ]] and D(2) blockade.


Although only << clozapine >> and ziprasidone are directly acting 5-HT(1A) agonists, WAY100635, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined 5-HT(2A) and [[ D(2) ]] blockade.


Although only clozapine and << ziprasidone >> are directly acting 5-HT(1A) agonists, WAY100635, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined [[ 5-HT(2A) ]] and D(2) blockade.


Although only clozapine and << ziprasidone >> are directly acting 5-HT(1A) agonists, WAY100635, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined 5-HT(2A) and [[ D(2) ]] blockade.


Although only clozapine and ziprasidone are directly acting 5-HT(1A) agonists, << WAY100635 >>, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined [[ 5-HT(2A) ]] and D(2) blockade.


Although only clozapine and ziprasidone are directly acting 5-HT(1A) agonists, << WAY100635 >>, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined 5-HT(2A) and [[ D(2) ]] blockade.


Although only << clozapine >> and ziprasidone are directly acting [[ 5-HT(1A) ]] agonists, WAY100635, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined 5-HT(2A) and D(2) blockade.


Although only clozapine and << ziprasidone >> are directly acting [[ 5-HT(1A) ]] agonists, WAY100635, a selective 5-HT(1A) antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined 5-HT(2A) and D(2) blockade.


Although only clozapine and ziprasidone are directly acting 5-HT(1A) agonists, << WAY100635 >>, a selective [[ 5-HT(1A) ]] antagonist, partially attenuates these atypical APD-induced increases in cortical DA release that may be due to combined 5-HT(2A) and D(2) blockade.


However, << 5-HT(1A) >> agonism may be important only for [[ quetiapine ]]-induced ACh release.


BACKGROUND: The novel antiepileptic drug << retigabine >> is the first selective M-current potassium channel opener for [[ KCNQ2/3 ]] and KCNQ3/5 channels.


BACKGROUND: The novel antiepileptic drug << retigabine >> is the first selective M-current potassium channel opener for KCNQ2/3 and [[ KCNQ3/5 ]] channels.


BACKGROUND: The novel antiepileptic drug << retigabine >> is the first selective [[ M-current potassium channel ]] opener for KCNQ2/3 and KCNQ3/5 channels.


OBJECTIVE: Because of these physiological effects and the widespread use of the selective << COX-2 >> inhibitor, [[ celecoxib ]], we wanted to determine if inhibition of COX-2 would affect incisional skin wound healing.


METHODS: Using a cutaneous full-thickness, sutured, incisional wound model in hairless SKH-1 mice, we evaluated the role of COX-2 in the wound healing process by comparing the effects of a nonselective << COX >> inhibitor, [[ diclofenac ]], with a selective COX-2 inhibitor, SC-791.


<< Histamine H1-receptor >> antagonists, [[ promethazine ]] and homochlorcyclizine, increase the steady-state plasma concentrations of haloperidol and reduced haloperidol.


<< Histamine H1-receptor >> antagonists, promethazine and [[ homochlorcyclizine ]], increase the steady-state plasma concentrations of haloperidol and reduced haloperidol.


The effects of histamine H1-receptor antagonists, << promethazine >> and homochlorcyclizine, both of which are inhibitors of [[ CYP2D6 ]], on the steady-state plasma concentrations (Css) of haloperidol and reduced haloperidol were studied in 23 schizophrenic inpatients receiving haloperidol, 12 to 36 mg/d, for 2 to 29 weeks.


The effects of histamine H1-receptor antagonists, promethazine and << homochlorcyclizine >>, both of which are inhibitors of [[ CYP2D6 ]], on the steady-state plasma concentrations (Css) of haloperidol and reduced haloperidol were studied in 23 schizophrenic inpatients receiving haloperidol, 12 to 36 mg/d, for 2 to 29 weeks.


The effects of << histamine H1-receptor >> antagonists, [[ promethazine ]] and homochlorcyclizine, both of which are inhibitors of CYP2D6, on the steady-state plasma concentrations (Css) of haloperidol and reduced haloperidol were studied in 23 schizophrenic inpatients receiving haloperidol, 12 to 36 mg/d, for 2 to 29 weeks.


The effects of << histamine H1-receptor >> antagonists, promethazine and [[ homochlorcyclizine ]], both of which are inhibitors of CYP2D6, on the steady-state plasma concentrations (Css) of haloperidol and reduced haloperidol were studied in 23 schizophrenic inpatients receiving haloperidol, 12 to 36 mg/d, for 2 to 29 weeks.


Thus, the current study suggests that coadministration of clinical doses of << promethazine >> and homochlorcyclizine increases the Css of haloperidol and reduced haloperidol via the inhibitory effects on the [[ CYP2D6 ]]-catalyzed metabolism of haloperidol and reduced haloperidol.


Thus, the current study suggests that coadministration of clinical doses of promethazine and << homochlorcyclizine >> increases the Css of haloperidol and reduced haloperidol via the inhibitory effects on the [[ CYP2D6 ]]-catalyzed metabolism of haloperidol and reduced haloperidol.


Thus, the current study suggests that coadministration of clinical doses of promethazine and homochlorcyclizine increases the Css of haloperidol and reduced haloperidol via the inhibitory effects on the << CYP2D6 >>-catalyzed metabolism of haloperidol and reduced [[ haloperidol ]].


Thus, the current study suggests that coadministration of clinical doses of promethazine and homochlorcyclizine increases the Css of haloperidol and reduced haloperidol via the inhibitory effects on the << CYP2D6 >>-catalyzed metabolism of [[ haloperidol ]] and reduced haloperidol.


The four lysine residues located in the SMG loop, Lys-260, Lys-263, Lys-265, and Lys-268, also play an important role in mediating the sensitivity of << OTCase >> to [[ ornithine ]] and to arginase and appear to be involved in transducing and enhancing the signal given by ornithine for the closure of the catalytic domain.


Inhibition of binding of both << plasminogen >> and plasmin to gp330 by [[ benzamidine ]] was similar, although EACA inhibited the binding of plasmin to gp330 slightly more than the binding of plasminogen to gp330.


Inhibition of binding of both plasminogen and << plasmin >> to gp330 by [[ benzamidine ]] was similar, although EACA inhibited the binding of plasmin to gp330 slightly more than the binding of plasminogen to gp330.


Inhibition of binding of both plasminogen and plasmin to gp330 by benzamidine was similar, although << EACA >> inhibited the binding of [[ plasmin ]] to gp330 slightly more than the binding of plasminogen to gp330.


Inhibition of binding of both plasminogen and plasmin to gp330 by benzamidine was similar, although << EACA >> inhibited the binding of plasmin to gp330 slightly more than the binding of [[ plasminogen ]] to gp330.


Involvement of alpha(1)-adrenoceptors was established as mydriatic responses were inhibited by systemic administration of nonselective << alpha-adrenoceptor >> antagonists, [[ phentolamine ]] (0.3-3 mg/kg) and phenoxybenzamine (0.03-0.3 mg/kg), as well as by the selective alpha(1)-adrenoceptor antagonist, prazosin (0.3 mg/kg).


Involvement of alpha(1)-adrenoceptors was established as mydriatic responses were inhibited by systemic administration of nonselective << alpha-adrenoceptor >> antagonists, phentolamine (0.3-3 mg/kg) and [[ phenoxybenzamine ]] (0.03-0.3 mg/kg), as well as by the selective alpha(1)-adrenoceptor antagonist, prazosin (0.3 mg/kg).


Involvement of alpha(1)-adrenoceptors was established as mydriatic responses were inhibited by systemic administration of nonselective alpha-adrenoceptor antagonists, phentolamine (0.3-3 mg/kg) and phenoxybenzamine (0.03-0.3 mg/kg), as well as by the selective << alpha(1)-adrenoceptor >> antagonist, [[ prazosin ]] (0.3 mg/kg).


The << alpha(2)-adrenoceptor >> antagonist, [[ rauwolscine ]] (0.5 mg/kg), was without antagonistic effects.


<< alpha(1A)-Adrenoceptor >> selective antagonists, [[ 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane ]] (WB-4101; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), the alpha(1B)-adrenoceptor selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline (L-765314; 0.3-1 mg/kg), as well as the alpha(1D)-adrenoceptor selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.


<< alpha(1A)-Adrenoceptor >> selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane ([[ WB-4101 ]]; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), the alpha(1B)-adrenoceptor selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline (L-765314; 0.3-1 mg/kg), as well as the alpha(1D)-adrenoceptor selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.


<< alpha(1A)-Adrenoceptor >> selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane (WB-4101; 0.1-1 mg/kg) and [[ 5-methylurapidil ]] (0.1-1 mg/kg), the alpha(1B)-adrenoceptor selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline (L-765314; 0.3-1 mg/kg), as well as the alpha(1D)-adrenoceptor selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.


alpha(1A)-Adrenoceptor selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane (WB-4101; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), the << alpha(1B)-adrenoceptor >> selective antagonist, [[ 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline ]] (L-765314; 0.3-1 mg/kg), as well as the alpha(1D)-adrenoceptor selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.


alpha(1A)-Adrenoceptor selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane (WB-4101; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), the << alpha(1B)-adrenoceptor >> selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline ([[ L-765314 ]]; 0.3-1 mg/kg), as well as the alpha(1D)-adrenoceptor selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.


alpha(1A)-Adrenoceptor selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane (WB-4101; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), the alpha(1B)-adrenoceptor selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline (L-765314; 0.3-1 mg/kg), as well as the << alpha(1D)-adrenoceptor >> selective antagonist, [[ 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione ]] (BMY-7378; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.


alpha(1A)-Adrenoceptor selective antagonists, 2-([2,6-dimethoxyphenoxyethyl]aminomethyl)-1,4-benzodioxane (WB-4101; 0.1-1 mg/kg) and 5-methylurapidil (0.1-1 mg/kg), the alpha(1B)-adrenoceptor selective antagonist, 4-amino-2-[4-[1-(benzyloxycarbonyl)-2(S)- [[(1,1-dimethylethyl)amino]carbonyl]-piperazinyl]-6,7-dimethoxyquinazoline (L-765314; 0.3-1 mg/kg), as well as the << alpha(1D)-adrenoceptor >> selective antagonist, 8-[2-[4-(2-methoxyphenyl)-1-piperazinyl]ethyl]-8-azaspiro[4.5]decane-7,9-dione ([[ BMY-7378 ]]; 1 mg/kg), were used to delineate the adrenoceptor subtypes involved.


To further investigate this positive correlation and its possible therapeutic implications, a selective << COX-2 >> inhibitor, [[ etodolac ]], was tested on three variants of HT-29 colon cancer cell lines, HT-29/Inv1, HT-29/Inv2 and HT-29/Inv3, with graded increases of in vitro Matrigel invasive potential and COX-2 expression levels.


However, other << alpha(1)-adrenoceptor >> antagonists ([[ tamsulosin ]], WB4101 and corynanthine) did not inhibit the binding at a range of concentrations that generally exhibit alpha(1)-adrenoceptor antagonism, and noradrenaline, rauwolscine and propranolol were without effect on the [(3)H]prazosin binding.


However, other << alpha(1)-adrenoceptor >> antagonists (tamsulosin, [[ WB4101 ]] and corynanthine) did not inhibit the binding at a range of concentrations that generally exhibit alpha(1)-adrenoceptor antagonism, and noradrenaline, rauwolscine and propranolol were without effect on the [(3)H]prazosin binding.


However, other << alpha(1)-adrenoceptor >> antagonists (tamsulosin, WB4101 and [[ corynanthine ]]) did not inhibit the binding at a range of concentrations that generally exhibit alpha(1)-adrenoceptor antagonism, and noradrenaline, rauwolscine and propranolol were without effect on the [(3)H]prazosin binding.


The potency of MrIA was greater for inhibition of uptake by << hNET >> of [[ [3H]norepinephrine ]] (Ki 1.89 microM) than [3H]dopamine (Ki 4.33 microM), and the human dopamine transporter and serotonin transporter were not inhibited by MrIA (to 7 microM).


The potency of MrIA was greater for inhibition of uptake by << hNET >> of [3H]norepinephrine (Ki 1.89 microM) than [[ [3H]dopamine ]] (Ki 4.33 microM), and the human dopamine transporter and serotonin transporter were not inhibited by MrIA (to 7 microM).


A comparison of the results with previous data for desipramine and cocaine inhibition of << norepinephrine >> uptake by the mutant [[ hNETs ]] reveals that MrIA binding to hNET occurs at a site that is distinct from but overlaps with the binding sites for tricyclic antidepressants and cocaine.


A cDNA encoding the complete amino acid sequence of aminoacylase 1 (N-acylamino acid aminohydrolase, << ACY-1 >>) [EC 3.5.1.14], a dimeric metalloprotein having two Zn2+ in the molecule, which catalyzes the deacylation of [[ N-acylated L-amino acids ]] except L-aspartic acid, has been isolated from porcine kidney lambda gt10 cDNA library and sequenced.


A cDNA encoding the complete amino acid sequence of aminoacylase 1 (N-acylamino acid aminohydrolase, ACY-1) [<< EC 3.5.1.14 >>], a dimeric metalloprotein having two Zn2+ in the molecule, which catalyzes the deacylation of [[ N-acylated L-amino acids ]] except L-aspartic acid, has been isolated from porcine kidney lambda gt10 cDNA library and sequenced.


A cDNA encoding the complete amino acid sequence of aminoacylase 1 (N-acylamino acid aminohydrolase, ACY-1) [EC 3.5.1.14], a dimeric << metalloprotein >> having two Zn2+ in the molecule, which catalyzes the deacylation of [[ N-acylated L-amino acids ]] except L-aspartic acid, has been isolated from porcine kidney lambda gt10 cDNA library and sequenced.


A cDNA encoding the complete amino acid sequence of << aminoacylase 1 >> (N-acylamino acid aminohydrolase, ACY-1) [EC 3.5.1.14], a dimeric metalloprotein having two Zn2+ in the molecule, which catalyzes the deacylation of [[ N-acylated L-amino acids ]] except L-aspartic acid, has been isolated from porcine kidney lambda gt10 cDNA library and sequenced.


A cDNA encoding the complete amino acid sequence of aminoacylase 1 (<< N-acylamino acid aminohydrolase >>, ACY-1) [EC 3.5.1.14], a dimeric metalloprotein having two Zn2+ in the molecule, which catalyzes the deacylation of [[ N-acylated L-amino acids ]] except L-aspartic acid, has been isolated from porcine kidney lambda gt10 cDNA library and sequenced.


Patients stable on warfarin therapy and concurrently taking a << cyclooxygenase-2 >> (COX-2) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, [[ salsalate ]], or acetaminophen) randomly received celecoxib 200 mg/day or rofecoxib 25 mg/day for three weeks.


Patients stable on warfarin therapy and concurrently taking a cyclooxygenase-2 (<< COX-2 >>) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, [[ salsalate ]], or acetaminophen) randomly received celecoxib 200 mg/day or rofecoxib 25 mg/day for three weeks.


Patients stable on warfarin therapy and concurrently taking a << cyclooxygenase-2 >> (COX-2) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, salsalate, or [[ acetaminophen ]]) randomly received celecoxib 200 mg/day or rofecoxib 25 mg/day for three weeks.


Patients stable on warfarin therapy and concurrently taking a cyclooxygenase-2 (<< COX-2 >>) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, salsalate, or [[ acetaminophen ]]) randomly received celecoxib 200 mg/day or rofecoxib 25 mg/day for three weeks.


Patients stable on warfarin therapy and concurrently taking a << cyclooxygenase-2 >> (COX-2) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, salsalate, or acetaminophen) randomly received [[ celecoxib ]] 200 mg/day or rofecoxib 25 mg/day for three weeks.


Patients stable on warfarin therapy and concurrently taking a cyclooxygenase-2 (<< COX-2 >>) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, salsalate, or acetaminophen) randomly received [[ celecoxib ]] 200 mg/day or rofecoxib 25 mg/day for three weeks.


Patients stable on warfarin therapy and concurrently taking a << cyclooxygenase-2 >> (COX-2) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, salsalate, or acetaminophen) randomly received celecoxib 200 mg/day or [[ rofecoxib ]] 25 mg/day for three weeks.


Patients stable on warfarin therapy and concurrently taking a cyclooxygenase-2 (<< COX-2 >>) inhibitor comparator (traditional nonsteroidal antiinflammatory medications, salsalate, or acetaminophen) randomly received celecoxib 200 mg/day or [[ rofecoxib ]] 25 mg/day for three weeks.


<< AT1 >> antagonism by [[ eprosartan ]] lowers heart rate variability and baroreflex gain.


We sought to assess the effects of the << angiotensin type 1 (AT1) receptor >> blocker [[ eprosartan ]] on HRV and BRG.


RESULTS: << Eprosartan >> tended to lower mean AP, it slightly increased heart rate (HR) (p<0.05), and markedly increased circulating [[ Ang-II ]] levels (p<0.01).


CONCLUSIONS: << AT1 >> antagonism by [[ eprosartan ]] lowers heart rate variability and baroreflex gain.


The antinociceptive activity of the << alpha 2-adrenoceptor >> agonist [[ clonidine ]] was also increased in mice treated with alpha N-acetyl beta-endorphin-(1-31).


<< Loperamide >>, an opiate agonist of high specificity for mu-receptors, was recently reported to suppress [[ ACTH ]] and cortisol levels in normal subjects, but not in patients with proven ACTH-dependent Cushing's disease.


In seven normal subjects, basal << ACTH >> plasma levels were significantly suppressed 3 h after [[ loperamide ]] administration (16 mg, orally) from 5 +/- 1 to 2 +/- 0 pmol/L (P less than 0.0001).


After the combined pituitary stimulation test (100 micrograms << human CRH >>, 100 micrograms GnRH, 100 micrograms GH-releasing hormone, and 200 micrograms TRH), the ACTH peak (maximum increase at 30 min) was significantly blunted by [[ loperamide ]] from 9 +/- 1 to 4 +/- 1 pmol/L (P less than 0.001) and the area under the curve of ACTH from 0-120 min was reduced from 35 +/- 5 to 23 +/- 4 pmol/L.2 h (P less than 0.05).


After the combined pituitary stimulation test (100 micrograms human CRH, 100 micrograms << GnRH >>, 100 micrograms GH-releasing hormone, and 200 micrograms TRH), the ACTH peak (maximum increase at 30 min) was significantly blunted by [[ loperamide ]] from 9 +/- 1 to 4 +/- 1 pmol/L (P less than 0.001) and the area under the curve of ACTH from 0-120 min was reduced from 35 +/- 5 to 23 +/- 4 pmol/L.2 h (P less than 0.05).


After the combined pituitary stimulation test (100 micrograms human CRH, 100 micrograms GnRH, 100 micrograms << GH-releasing hormone >>, and 200 micrograms TRH), the ACTH peak (maximum increase at 30 min) was significantly blunted by [[ loperamide ]] from 9 +/- 1 to 4 +/- 1 pmol/L (P less than 0.001) and the area under the curve of ACTH from 0-120 min was reduced from 35 +/- 5 to 23 +/- 4 pmol/L.2 h (P less than 0.05).


After the combined pituitary stimulation test (100 micrograms human CRH, 100 micrograms GnRH, 100 micrograms GH-releasing hormone, and 200 micrograms << TRH >>), the ACTH peak (maximum increase at 30 min) was significantly blunted by [[ loperamide ]] from 9 +/- 1 to 4 +/- 1 pmol/L (P less than 0.001) and the area under the curve of ACTH from 0-120 min was reduced from 35 +/- 5 to 23 +/- 4 pmol/L.2 h (P less than 0.05).


After the combined pituitary stimulation test (100 micrograms human CRH, 100 micrograms GnRH, 100 micrograms GH-releasing hormone, and 200 micrograms TRH), the << ACTH >> peak (maximum increase at 30 min) was significantly blunted by [[ loperamide ]] from 9 +/- 1 to 4 +/- 1 pmol/L (P less than 0.001) and the area under the curve of ACTH from 0-120 min was reduced from 35 +/- 5 to 23 +/- 4 pmol/L.2 h (P less than 0.05).


After the combined pituitary stimulation test (100 micrograms human CRH, 100 micrograms GnRH, 100 micrograms GH-releasing hormone, and 200 micrograms TRH), the ACTH peak (maximum increase at 30 min) was significantly blunted by << loperamide >> from 9 +/- 1 to 4 +/- 1 pmol/L (P less than 0.001) and the area under the curve of [[ ACTH ]] from 0-120 min was reduced from 35 +/- 5 to 23 +/- 4 pmol/L.2 h (P less than 0.05).


In summary, << loperamide >> is able to reduce basal and [[ CRH ]]-induced ACTH and cortisol levels in normal subjects, but not in patients with Cushing's disease or secondary adrenal failure of hypothalamic origin.


In summary, << loperamide >> is able to reduce basal and CRH-induced [[ ACTH ]] and cortisol levels in normal subjects, but not in patients with Cushing's disease or secondary adrenal failure of hypothalamic origin.


We also examined the effects of << WEB 2086 >>, a [[ platelet-activating factor (PAF) receptor ]] antagonist, in parallel.


The unique role of the enzyme << 5-lipoxygenase >> (5-LO) in the production of [[ leukotrienes ]] (LTs) makes it a likely target for biochemical manipulation.


The unique role of the enzyme 5-lipoxygenase (<< 5-LO >>) in the production of [[ leukotrienes ]] (LTs) makes it a likely target for biochemical manipulation.


The unique role of the enzyme << 5-lipoxygenase >> (5-LO) in the production of leukotrienes ([[ LTs ]]) makes it a likely target for biochemical manipulation.


The unique role of the enzyme 5-lipoxygenase (<< 5-LO >>) in the production of leukotrienes ([[ LTs ]]) makes it a likely target for biochemical manipulation.


The compounds identified as 5-LO inhibitors can be divided into antioxidants, substrate-analogous, and a large miscellaneous group of inhibitors, where << hydroxamic acids >> are potent and more selective inhibitors of [[ 5-LO ]].


The << benzothiophene hydroxyurea >>, zileuton, is the first selective [[ 5-LO ]] inhibitor evaluated for the treatment of patients with IBD.


The benzothiophene hydroxyurea, << zileuton >>, is the first selective [[ 5-LO ]] inhibitor evaluated for the treatment of patients with IBD.


Ribonucleotide reductase (<< RR >>) is responsible for the de novo conversion of the ribonucleoside diphosphates to [[ deoxyribonucleoside diphosphates ]], which are essential for DNA synthesis and repair.


<< Ribonucleotide reductase >> (RR) is responsible for the de novo conversion of the ribonucleoside diphosphates to [[ deoxyribonucleoside diphosphates ]], which are essential for DNA synthesis and repair.


Ribonucleotide reductase (<< RR >>) is responsible for the de novo conversion of the [[ ribonucleoside diphosphates ]] to deoxyribonucleoside diphosphates, which are essential for DNA synthesis and repair.


<< Ribonucleotide reductase >> (RR) is responsible for the de novo conversion of the [[ ribonucleoside diphosphates ]] to deoxyribonucleoside diphosphates, which are essential for DNA synthesis and repair.


In PC3 cells, << hydroxyurea >> inhibited [[ hRRM2 ]] and resulted in increased sensitivity to UV irradiation.


In addition, << minocycline >> treatment significantly reduced the specific [[ caspase-3 ]] activity after SCI as compared to that of vehicle control.


Furthermore, RT-PCR analyses revealed that << minocycline >> treatment increased expression of [[ interleukin-10 ]] mRNA but decreased tumor necrosis factor-alpha expression.


Furthermore, RT-PCR analyses revealed that << minocycline >> treatment increased expression of interleukin-10 mRNA but decreased [[ tumor necrosis factor-alpha ]] expression.


RESULTS: The density of << AR >> in liver tissue in [[ NP ]] group was higher than that in control group (P < 0.05).


CONCLUSION: << Nandrolone phenylpropionate >> up-regulated the density of [[ AR ]] in liver tissue, whereas it had no significant effects on the density of AR in testis and ovary tissues.


Rats received a concomitant treatment with the selective beta(1)-adrenoceptor antagonist, bisoprolol (50 mg/kg/day p.o.) or were chronically pretreated with the selective << beta(2)-adrenoceptor >> agonist [[ salbutamol ]] (40 microg/kg/h) for 1 week to induce beta(2)-adrenoceptor desensitization.


Rats received a concomitant treatment with the selective << beta(1)-adrenoceptor >> antagonist, [[ bisoprolol ]] (50 mg/kg/day p.o.) or were chronically pretreated with the selective beta(2)-adrenoceptor agonist salbutamol (40 microg/kg/h) for 1 week to induce beta(2)-adrenoceptor desensitization.


The pretreatment with << salbutamol >> induced a 59% down-regulation of left ventricular [[ beta(2)-adrenoceptors ]] compared to control.


TRPM8 (<< CMR1 >>) is a Ca(2+)-permeable channel, which can be activated by low temperatures, menthol, [[ eucalyptol ]] and icilin.


TRPM8 (CMR1) is a << Ca(2+)-permeable channel >>, which can be activated by low temperatures, menthol, [[ eucalyptol ]] and icilin.


<< TRPM8 >> (CMR1) is a Ca(2+)-permeable channel, which can be activated by low temperatures, menthol, [[ eucalyptol ]] and icilin.


TRPM8 (<< CMR1 >>) is a Ca(2+)-permeable channel, which can be activated by low temperatures, [[ menthol ]], eucalyptol and icilin.


TRPM8 (CMR1) is a << Ca(2+)-permeable channel >>, which can be activated by low temperatures, [[ menthol ]], eucalyptol and icilin.


<< TRPM8 >> (CMR1) is a Ca(2+)-permeable channel, which can be activated by low temperatures, [[ menthol ]], eucalyptol and icilin.


TRPM8 (<< CMR1 >>) is a Ca(2+)-permeable channel, which can be activated by low temperatures, menthol, eucalyptol and [[ icilin ]].


TRPM8 (CMR1) is a << Ca(2+)-permeable channel >>, which can be activated by low temperatures, menthol, eucalyptol and [[ icilin ]].


<< TRPM8 >> (CMR1) is a Ca(2+)-permeable channel, which can be activated by low temperatures, menthol, eucalyptol and [[ icilin ]].


Known VR1 antagonists (BCTC, thio-BCTC and capsazepine) were also able to block the response of << TRPM8 >> to [[ menthol ]] (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).


Known VR1 antagonists (<< BCTC >>, thio-BCTC and capsazepine) were also able to block the response of [[ TRPM8 ]] to menthol (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).


Known VR1 antagonists (BCTC, << thio-BCTC >> and capsazepine) were also able to block the response of [[ TRPM8 ]] to menthol (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).


Known VR1 antagonists (BCTC, thio-BCTC and << capsazepine >>) were also able to block the response of [[ TRPM8 ]] to menthol (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).


Known << VR1 >> antagonists ([[ BCTC ]], thio-BCTC and capsazepine) were also able to block the response of TRPM8 to menthol (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).


Known << VR1 >> antagonists (BCTC, [[ thio-BCTC ]] and capsazepine) were also able to block the response of TRPM8 to menthol (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).


Known << VR1 >> antagonists (BCTC, thio-BCTC and [[ capsazepine ]]) were also able to block the response of TRPM8 to menthol (IC(50): 0.8+/-1.0, 3.5+/-1.1 and 18+/-1.1 microM, respectively).


The Ca(2+) response of << hVR1 >>-transfected HEK293 cells to the endogenous VR1 agonist [[ N-arachidonoyl-dopamine ]] was potentiated by low pH.


The Ca(2+) response of hVR1-transfected HEK293 cells to the endogenous << VR1 >> agonist [[ N-arachidonoyl-dopamine ]] was potentiated by low pH.


In contrast, << menthol >>- and icilin-activated [[ TRPM8 ]] currents were suppressed by low pH.


In contrast, menthol- and << icilin >>-activated [[ TRPM8 ]] currents were suppressed by low pH.


Inhibitory effects of the << monoamine oxidase >> inhibitor [[ tranylcypromine ]] on the cytochrome P450 enzymes CYP2C19, CYP2C9, and CYP2D6.


The inhibitory effects of << tranylcypromine >>, a nonselective irreversible inhibitor of [[ monoamine oxidase ]] (MAO), on three cytochrome P450 (CYP) enzymes, namely CYP2C9, CYP2C19, and CYP2D6, have been evaluated in vitro.


The inhibitory effects of << tranylcypromine >>, a nonselective irreversible inhibitor of monoamine oxidase ([[ MAO ]]), on three cytochrome P450 (CYP) enzymes, namely CYP2C9, CYP2C19, and CYP2D6, have been evaluated in vitro.


The results demonstrated that << tranylcypromine >> is a competitive inhibitor of [[ CYP2C19 ]] (Ki = 32 microM) and CYP2D6 (Ki = 367 microM) and a noncompetitive inhibitor of CYP2C9 (Ki = 56 microM).


The results demonstrated that << tranylcypromine >> is a competitive inhibitor of CYP2C19 (Ki = 32 microM) and [[ CYP2D6 ]] (Ki = 367 microM) and a noncompetitive inhibitor of CYP2C9 (Ki = 56 microM).


The results demonstrated that << tranylcypromine >> is a competitive inhibitor of CYP2C19 (Ki = 32 microM) and CYP2D6 (Ki = 367 microM) and a noncompetitive inhibitor of [[ CYP2C9 ]] (Ki = 56 microM).


Studies in rats, mice and monkeys show that GC-1 lowers cholesterol with 600- to 1400-fold more potency and approximately two- to threefold more efficacy than << atorvastatin >>, a compound that blocks [[ HMG-CoA reductase ]].


Although highly homologous to other class III RTKs, Flt3 is resistant to the << phenylaminopyrimidine >> STI571 (Gleevec, Imatinib), a potent inhibitor of other [[ RTKs ]] in the family, such as the PDGFbeta-receptor or c-Kit.


Although highly homologous to other class III RTKs, Flt3 is resistant to the << phenylaminopyrimidine >> STI571 (Gleevec, Imatinib), a potent inhibitor of other RTKs in the family, such as the [[ PDGFbeta-receptor ]] or c-Kit.


Although highly homologous to other class III RTKs, Flt3 is resistant to the << phenylaminopyrimidine >> STI571 (Gleevec, Imatinib), a potent inhibitor of other RTKs in the family, such as the PDGFbeta-receptor or [[ c-Kit ]].


Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine << STI571 >> (Gleevec, Imatinib), a potent inhibitor of other [[ RTKs ]] in the family, such as the PDGFbeta-receptor or c-Kit.


Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine << STI571 >> (Gleevec, Imatinib), a potent inhibitor of other RTKs in the family, such as the [[ PDGFbeta-receptor ]] or c-Kit.


Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine << STI571 >> (Gleevec, Imatinib), a potent inhibitor of other RTKs in the family, such as the PDGFbeta-receptor or [[ c-Kit ]].


Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (<< Gleevec >>, Imatinib), a potent inhibitor of other [[ RTKs ]] in the family, such as the PDGFbeta-receptor or c-Kit.


Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (<< Gleevec >>, Imatinib), a potent inhibitor of other RTKs in the family, such as the [[ PDGFbeta-receptor ]] or c-Kit.


Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (<< Gleevec >>, Imatinib), a potent inhibitor of other RTKs in the family, such as the PDGFbeta-receptor or [[ c-Kit ]].


Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (Gleevec, << Imatinib >>), a potent inhibitor of other [[ RTKs ]] in the family, such as the PDGFbeta-receptor or c-Kit.


Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (Gleevec, << Imatinib >>), a potent inhibitor of other RTKs in the family, such as the [[ PDGFbeta-receptor ]] or c-Kit.


Although highly homologous to other class III RTKs, Flt3 is resistant to the phenylaminopyrimidine STI571 (Gleevec, << Imatinib >>), a potent inhibitor of other RTKs in the family, such as the PDGFbeta-receptor or [[ c-Kit ]].


STI571 binding to Flt3 is prevented by the phenylalanine 691 side-chain in the ATP binding center and mutating this site to threonine renders the corresponding << Flt3 >> mutant sensitive to [[ STI571 ]].


Compounds of several other structural families, including the << quinoxaline >> AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.


Compounds of several other structural families, including the << quinoxaline >> AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].


Compounds of several other structural families, including the quinoxaline << AG1296 >>, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.


Compounds of several other structural families, including the quinoxaline << AG1296 >>, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].


Compounds of several other structural families, including the quinoxaline AG1296, the << bis(1H-2-indolyl)-1-methanone >> D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.


Compounds of several other structural families, including the quinoxaline AG1296, the << bis(1H-2-indolyl)-1-methanone >> D-65476, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].


Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone << D-65476 >>, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.


Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone << D-65476 >>, the indolinones SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].


Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the << indolinones >> SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.


Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the << indolinones >> SU5416 and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].


Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones << SU5416 >> and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of [[ Flt3 ]] kinase.


Compounds of several other structural families, including the quinoxaline AG1296, the bis(1H-2-indolyl)-1-methanone D-65476, the indolinones << SU5416 >> and SU11248, the indolocarbazoles PKC412 and CEP-701, and the piperazonyl quinazoline CT53518, are potent inhibitors of Flt3 [[ kinase ]].