SB 202190

152121-30-7

C20H14FN3O

DMSO : >= 40 mg/mL (120.72 mM)

MAPK/ERK Pathway; Autophagy

SB 202190 is a cell-permeable p38 MAP kinase inhibitor with IC₅₀s of 50 nM and 100 nM for p38 and p38beta2, respectively. IC50 & Target: IC50: 50 nM (p38), 100 nM (p38beta2)^[1] In Vitro: Treatment of cells with SB 202190 (SB202190) significantly inhibits both basal and anti-Fas antibody-induced MAPKAPK 2 activity in a dose-dependent manner as measured in immune complex kinase assays with GST-hsp27 as a substrate. Jurkat cells are treated with SB202190 or left untreated. After 24 h, cells are harvested, and the activity of CPP32-like caspases in cell extracts is measured by cleavage of the fluorescent peptide DEVD-AMC, which is a specific substrate of CPP32-like caspases. The cleavage of DEVD-AMC is significantly increased in cells treated with SB202190 but not in the control^[2]. In Vivo: In HCT-116-derived colorectal tumors, administration of SB 202190 (SB202190), Bay 43-9006 or a combination of both give similar results in terms of measurement of external tumor size (around 58% growth reduction compare with control tumors). SB202190 induces a 28% reduction of tumor growth, compare with a 31% reduction promoted by Bay 43-9006, while combination of both drugs reduce tumor growth by 55%^[3]. Compare to the model group, the SB202190 group exhibits significantly shorter escape latencies in the Morris water maze hidden platform trials (P<0.01) and longer times in the original platform quadrant during probe trials (P<0.01). The SB202190 group also shows significantly reduced neuronal apoptosis in the hippocampus compared to VaD model rats (P<0.01) as well as higher (antiapoptotic) Bcl-2 expression and lower (proapoptotic) caspase-3 expression (P<0.01 for both). In conclusion, blockade of the p38 MAPK signaling pathway by SB202190 following permanent 2-OV reduced apoptosis of hippocampal neurons and rescued spatial learning and memory deficits^[4].