SB202190 (FHPI)

p38α；p38β

331.35

DMSO ：66 mg/mL (199.19 mM)
Ethanol ：12 mg/mL (36.21 mM)

Lyophilized powder

SB 202190 significantly inhibits both basal and anti-Fas antibody-induced MAPKAPK 2 activity in a dose-dependent manner. SB202190 by itself is sufficient to induce cell death in Jurkat and HeLa cells through activation of CPP32-like caspases, which can be blocked by expression of bcl-2. SB202190-induced apoptosis is attenuated by p38β but augmented by p38α. SB 202190 strongly inhibits UVB induced COX-2 protein expression in HaCaT cells, and markedly inhibits UVB induced cox-2 mRNA. SB 202190 treatment inhibits the expression of albumin-induced proinflammatory (monocyte chemoattractant protein-1) and transforming growth factor (TGF)-beta1-induced profibrotic (procollagen-Ialpha1) genes over 50% in renal tubular cells (normal rat kidney-52E). SB 202190 treatment induces phosphorylation of JNK in a dose- and time- dependent manner in A549 cells, induces phosphorylation of ATF-2 transcription factor, and increases AP-1 DNA binding. SB 202190 treatment enhances the growth of THP-1 and MV4-11 cells. SB 202190 increases the phosphorylation of c-Raf and ERK, suggesting that Ras-Raf-MEK-mitogen-activated protein kinase (MAPK) pathway activation is involved in the leukemia cell growth induced by SB 202190.

Inhibiting p38 by administration of SB 202190 inhibits PV IgG-induced blister formation in the passive transfer mouse model. In the endotoxin model of sepsis, SB 202190 treatment produces a statistically significant survival benefit compared with control.

SB202190；SB-202190

C₂₀H₁₄FN₃O

152121-30-7