Vipoglanstat

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Vipoglanstat

本产品不向个人销售，仅用作科学研究，不用于任何人体实验及非科研性质的动物实验。

CAS NO:	1360622-01-0
规格:	≥98%

理化性质和储存条件

Molecular Formula: C30H34Cl2F5N5O3;

Molecular Weight: 678.52

Synonym: Vipoglanstat; BI-1029539; GS-248; BI 1029539; GS248; BI1029539; GS 248

Chemical Name: 2-{2,6-dichloro-3-[(2,2- dimethylpropanamido)methyl]anilino}-6-(2,2- difluoroethoxy)-1-methyl-N-[trans-4- (trifluoromethyl)cyclohexyl]-1H-benzimidazole-5- carboxamide

InChi Key: PFORUFFGGNOLPJ-FITNRVMRSA-N

InChi Code: InChI=1S/C30H34Cl2F5N5O3/c1-29(2,3)27(44)38-13-15-5-10-19(31)25(24(15)32)41-28-40-20-11-18(22(45-14-23(33)34)12-21(20)42(28)4)26(43)39-17-8-6-16(7-9-17)30(35,36)37/h5,10-12,16-17,23H,6-9,13-14H2,1-4H3,(H,38,44)(H,39,43)(H,40,41)/t16?,17-

SMILES Code: O=C(C(C(OCC(F)F)=C1)=CC2=C1N(C)C(NC3=C(Cl)C(CNC(C(C)(C)C)=O)=CC=C3Cl)=N2)N[C@]4([H])CC[C@@]([H])(C(F)(F)F)CC4

In Vitro	Vipoglanstat (BI 1029539, GS-248) significantly inhibits mPGES-1 level (IC50: about 1 nM) in isolated brain capillaries from transgenic human-mPGES-1 mice. Vipoglanstat (BI 1029539, GS-248) blocks the up-regulation of P-gp and mPGES-1 levels on glutamate-mediatedin isolated brain capillaries. Vipoglanstat (BI 1029539, GS-248) reduces human peripheral blood inflammatory cell migration and inflammatory mediator release[3].
In Vivo	Vipoglanstat (BI 1029539, GS-248) (30 mg/kg; i.p.) can reduce LPS-induced lung injury, with reduction in neutrophil influx, protein content, TNF-ɑ, IL-1β and PGE2 levels in bronchoalveolar lavage (BAL), myeloperoxidase activity, expression of mPGES-1, cyclooxygenase (COX)-2 and intracellular adhesion molecule in lung tissue. Vipoglanstat (BI 1029539, GS-248) (30 mg/kg; p.o.; 2 hrs, 8 hrs and 22 hrs) significantly reduces sepsis-induced BAL inflammatory cell recruitment, lung injury score and lung expression of mPGES-1 and inducible nitric oxide synthase. Vipoglanstat (BI 1029539, GS-248) (30 mg/kg; p.o.; QD) also significantly prolongs survival of mice with severe sepsis[2]. Animal Model: LPS-induced acute lung injury models[2] 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[2] 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.

In Vitro

Vipoglanstat (BI 1029539, GS-248) significantly inhibits mPGES-1 level (IC50: about 1 nM) in isolated brain capillaries from transgenic human-mPGES-1 mice. Vipoglanstat (BI 1029539, GS-248) blocks the up-regulation of P-gp and mPGES-1 levels on glutamate-mediatedin isolated brain capillaries. Vipoglanstat (BI 1029539, GS-248) reduces human peripheral blood inflammatory cell migration and inflammatory mediator release[3].

In Vivo

Vipoglanstat (BI 1029539, GS-248) (30 mg/kg; i.p.) can reduce LPS-induced lung injury, with reduction in neutrophil influx, protein content, TNF-ɑ, IL-1β and PGE2 levels in bronchoalveolar lavage (BAL), myeloperoxidase activity, expression of mPGES-1, cyclooxygenase (COX)-2 and intracellular adhesion molecule in lung tissue. Vipoglanstat (BI 1029539, GS-248) (30 mg/kg; p.o.; 2 hrs, 8 hrs and 22 hrs) significantly reduces sepsis-induced BAL inflammatory cell recruitment, lung injury score and lung expression of mPGES-1 and inducible nitric oxide synthase. Vipoglanstat (BI 1029539, GS-248) (30 mg/kg; p.o.; QD) also significantly prolongs survival of mice with severe sepsis[2]. Animal Model: LPS-induced acute lung injury models[2] 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[2] 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.