产品
编 号：F195276
分子式：C25H27N5
分子量：397.52
分子式：C25H27N5
分子量：397.52
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规格
价格
是否有货
10mM*1mL in DMSO
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1mg
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5mg
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10mg
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25mg
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50mg
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100mg
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结构图
CAS No: 162640-98-4
产品详情
生物活性：
AT-56 is a potent, selective and orally active inhibitor of lipocalin-type prostaglandin D synthase (L-PGDS), with an IC50 of 95 μM and Ki of 75 μM. AT-56 could selectively suppress the drowsiness or pain reaction mediated by L-PGDS-catalyzed PGD2.
体内研究：
AT-56 (?1-30 mg/kg; p.o.) suppresses the PGD2 production in the stab-wounded brain.AT-56 (1-10 mg/kg; p.o.) suppresses the L-PGDS-mediated allergic airway inflammation in mice.AT-56 (10 mg/kg; p.o.) exhibits Cmax (2.15 μg/ml), half-life (1.71 h) and high oral bioavailability (82%).Animal Model:H-PGDS KO mice (14-16weeks, 25-30 g, C57BL/6 strain) with a stab wound brain injury
Dosage:0, 1, 3, 10, 30?mg/kg
Administration:P.o. 1 h before the stab wound injury
Result:Inhibited the L-PGDS reaction in the brain.Decreased the total amount of PGD2 in the brain to 40% with 30 mg/kg AT-56.
Animal Model:Human L-PGDS-overexpressing TG mice (males, 14-16 weeks, 25-30 g)
Dosage:?0, 1, 10 mg/kg
Administration:P.o. 1 h before and 24 h after the antigen exposure
Result:Prevented the eosinophil infiltration by inhibiting transgened human L-PGDS.
Animal Model:Male C57BL/6 mice (7 weeks, 22-26 g)
Dosage:10?mg/kg for p.o. and 2 mg/kg for i.v. (Pharmacokinetic Analysis)
Administration:P.o. and i.v. administration
Result:Oral bioavailability (82%); Cmax (2.15 μg/ml); T1/2 (1.71 h, p.o.); T1/2 (2.35 h, i.v.).
体外研究：
AT-56 (1-30 μM; 10 minutes) dose-dependently inhibits the production of PGD2 in L-PGDS-expressing human medulloblastoma TE-671 cells with an IC50 of about 3 μM.
AT-56 is a potent, selective and orally active inhibitor of lipocalin-type prostaglandin D synthase (L-PGDS), with an IC50 of 95 μM and Ki of 75 μM. AT-56 could selectively suppress the drowsiness or pain reaction mediated by L-PGDS-catalyzed PGD2.
体内研究：
AT-56 (?1-30 mg/kg; p.o.) suppresses the PGD2 production in the stab-wounded brain.AT-56 (1-10 mg/kg; p.o.) suppresses the L-PGDS-mediated allergic airway inflammation in mice.AT-56 (10 mg/kg; p.o.) exhibits Cmax (2.15 μg/ml), half-life (1.71 h) and high oral bioavailability (82%).Animal Model:H-PGDS KO mice (14-16weeks, 25-30 g, C57BL/6 strain) with a stab wound brain injury
Dosage:0, 1, 3, 10, 30?mg/kg
Administration:P.o. 1 h before the stab wound injury
Result:Inhibited the L-PGDS reaction in the brain.Decreased the total amount of PGD2 in the brain to 40% with 30 mg/kg AT-56.
Animal Model:Human L-PGDS-overexpressing TG mice (males, 14-16 weeks, 25-30 g)
Dosage:?0, 1, 10 mg/kg
Administration:P.o. 1 h before and 24 h after the antigen exposure
Result:Prevented the eosinophil infiltration by inhibiting transgened human L-PGDS.
Animal Model:Male C57BL/6 mice (7 weeks, 22-26 g)
Dosage:10?mg/kg for p.o. and 2 mg/kg for i.v. (Pharmacokinetic Analysis)
Administration:P.o. and i.v. administration
Result:Oral bioavailability (82%); Cmax (2.15 μg/ml); T1/2 (1.71 h, p.o.); T1/2 (2.35 h, i.v.).
体外研究：
AT-56 (1-30 μM; 10 minutes) dose-dependently inhibits the production of PGD2 in L-PGDS-expressing human medulloblastoma TE-671 cells with an IC50 of about 3 μM.
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