产品
编 号：F744403
分子式：C30H34Cl2F5N5O3
分子量：678.52
分子式：C30H34Cl2F5N5O3
分子量：678.52
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
1mg
询价
询价
5mg
询价
询价
10mg
询价
询价
结构图
CAS No: 1360622-01-0
产品详情
生物活性：
Vipoglanstat (BI 1029539), a carboxamide, is a potent and selective, non-peptide and orally active small molecular inhibitor of human prostaglandin E synthase 1 (mPGES-1). Vipoglanstat also has anti-inflammatory activity.
体内研究：
Vipoglanstat (30 mg/kg; i.p.) can reduce LPS-induced lung injury, with reduction in neutrophil influx,protein content, TNF-ɑ, IL-1β and PGE2levels in bronchoalveolar lavage (BAL), myeloperoxidase activity, expression ofmPGES-1, cyclooxygenase (COX)-2 and intracellular adhesion molecule in lung tissue.Vipoglanstat (30 mg/kg; p.o.; 2 h, 8 h and 22 h) significantly reduces sepsis-induced BAL inflammatory cell recruitment, lung injury score and lung expression of mPGES-1 and inducible nitric oxide synthase.Vipoglanstat (30 mg/kg; p.o.; QD) also significantly prolongs survival of mice with severe sepsis.Animal Model:LPS-induced acute lung injury models
Dosage:30 mg/kg
Administration:30 mg/kg, i.p.
Result:Preserved lung architecture and reduced immune cell influx into the lungs of LPS?challenged mice.
Animal Model:CLP-induced sepsis models
Dosage:30 mg/kg
Administration:30 mg/kg, p.o., 2 hrs, 8 hrs and 22 hrs; 30 mg/kg, p.o., QD
Result:Attenuated CLP?induced lung injury and prolongs survival.
体外研究：
Vipoglanstat significantly inhibits mPGES-1 level (IC50: about 1 nM).Vipoglanstat blocks the up-regulation of P-gp and mPGES-1 levels on glutamate-mediatedinisolated brain capillaries. Vipoglanstat reduces human peripheral blood inflammatory cell migration and inflammatory mediator release.
Vipoglanstat (BI 1029539), a carboxamide, is a potent and selective, non-peptide and orally active small molecular inhibitor of human prostaglandin E synthase 1 (mPGES-1). Vipoglanstat also has anti-inflammatory activity.
体内研究：
Vipoglanstat (30 mg/kg; i.p.) can reduce LPS-induced lung injury, with reduction in neutrophil influx,protein content, TNF-ɑ, IL-1β and PGE2levels in bronchoalveolar lavage (BAL), myeloperoxidase activity, expression ofmPGES-1, cyclooxygenase (COX)-2 and intracellular adhesion molecule in lung tissue.Vipoglanstat (30 mg/kg; p.o.; 2 h, 8 h and 22 h) significantly reduces sepsis-induced BAL inflammatory cell recruitment, lung injury score and lung expression of mPGES-1 and inducible nitric oxide synthase.Vipoglanstat (30 mg/kg; p.o.; QD) also significantly prolongs survival of mice with severe sepsis.Animal Model:LPS-induced acute lung injury models
Dosage:30 mg/kg
Administration:30 mg/kg, i.p.
Result:Preserved lung architecture and reduced immune cell influx into the lungs of LPS?challenged mice.
Animal Model:CLP-induced sepsis models
Dosage:30 mg/kg
Administration:30 mg/kg, p.o., 2 hrs, 8 hrs and 22 hrs; 30 mg/kg, p.o., QD
Result:Attenuated CLP?induced lung injury and prolongs survival.
体外研究：
Vipoglanstat significantly inhibits mPGES-1 level (IC50: about 1 nM).Vipoglanstat blocks the up-regulation of P-gp and mPGES-1 levels on glutamate-mediatedinisolated brain capillaries. Vipoglanstat reduces human peripheral blood inflammatory cell migration and inflammatory mediator release.
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