GLPG-0634

本公司产品仅用于科研实验，不得用于人体或动物的临床与诊断

一种有效的 JAK1/JAK2 抑制剂，生化测定中 IC50 为 10 nM/28 nM；对 JAK3 和 TYK2 的作用较弱。

A potent JAK1/JAK2 inhibitor with IC50 of 10 nM/28 nM in biochemical assays; less potent for JAK3 and TYK2; reveals a selectivity of 30-fold for JAK1- over JAK2-dependent signaling in cellular and whole blood assays; inhibited Th1 and Th2 differentiation and to a lesser extent the differentiation of Th17 cells in vitro; shows efficacy in the collagen-induced arthritis models and orally active.Rheumatoid Arthritis Phase 3 Clinical(In Vitro):Filgotinib (GLPG0634) dose-dependently inhibits the differentiation of Th2 cells mediated by IL-4, a cytokine that signals through JAK1 and JAK3. Filgotinib also inhibits Th1 differentiation with similar potencies of 1 μM or lower. Filgotinib (GLPG0634) does not inhibit JAK2 homodimer-mediated signaling induced by EPO or PRL (IC50 > 10 μM). (In Vivo):Filgotinib (GLPG0634; 3, 10, 30 mg/kg, p.o.) dose-dependently prevents disease progression in the therapeutic rat CIA model. Filgotinib (50 mg/kg, o.p.) protects bone and cartilage from degradation, effectively reduces infiltration of T cells (CD3+?cells) and macrophages (F4/80+?cells) in the paw, and decreases the serum levels of all cytokines and chemokines measured, including IL-6, IP-10, XCL1, and MCP-1. Filgotinib (GLPG0634; 0.1 and 0.3 mg/kg) shows efficacy in the rat CIA model.

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Filgotinib | GLPG 0634 | GLPG0634

Angiogenesis

JAK

JAK1|JAK2|JAK3|Tyk2

Inflammation/Immunology

Rheumatoid Arthritis

1206161-97-8

425.504

C21H23N5O3S

>98% (HPLC)

DMSO: 6.8 mg/mL

O=C(C1CC1)NC2=NN3C(C4=CC=C(CN5CCS(CC5)(=O)=O)C=C4)=CC=CC3=N2.

Cyclopropanecarboxamide, N-[5-[4-[(1,1-dioxido-4-thiomorpholinyl)methyl]phenyl][1,2,4]triazolo[1,5-a]pyridin-2-yl]-

(-20℃)

With Ice Pack

≥ 2 years