We Devoted Ourselves To The Development Of Biomedical Research Reagent.
Product Details
SB202190 (FHPI),152121-30-7,IC-012062
SB 202190 is a selective p38 MAP kinase inhibitor with IC50s of 50 nM and 100 nM for p38α and p38β2, respectively. SB 202190 binds to the ATP pocket of the active recombinant human p38 kinase with a Kd of 38 nM. SB 202190 has anti-cancer activity and rescued memory deficits[1,2]. SB202190 inhibits apoptosis of endothelial cells by inducing autophagy and heme oxidase 1 [3].
SB 202190(50 µM;24 hours) 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[4]. SB 202190 treatment(5/10 µM SB202190;4h) 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[5]. SB 202190(5µM;1h) strongly inhibits UVB induced COX-2 protein expression in HaCaT cells, and markedly inhibits UVB induced cox-2 mRNA[6].
SB 202190(12.5 µg; i.d.) attenuated blister formation induced by human poliomyelitis IgG(PV-IgG) in a passively transferred mouse model by inhibiting p38[7]. Inhibition of P38-MAPK by SB-202190(2.5µM/kg;24d; s.c.) resulted in increased primary tumor growth in tumor-bearing Balb-c mice (4T-1 cells) [8].
SB 202190 is a selective p38 MAP kinase inhibitor with IC50s of 50 nM and 100 nM for p38α and p38β2, respectively. SB 202190 binds to the ATP pocket of the active recombinant human p38 kinase with a Kd of 38 nM. SB 202190 has anti-cancer activity and rescued memory deficits[1,2]. SB202190 inhibits apoptosis of endothelial cells by inducing autophagy and heme oxidase 1 [3].
SB 202190(50 µM;24 hours) 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[4]. SB 202190 treatment(5/10 µM SB202190;4h) 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[5]. SB 202190(5µM;1h) strongly inhibits UVB induced COX-2 protein expression in HaCaT cells, and markedly inhibits UVB induced cox-2 mRNA[6].
SB 202190(12.5 µg; i.d.) attenuated blister formation induced by human poliomyelitis IgG(PV-IgG) in a passively transferred mouse model by inhibiting p38[7]. Inhibition of P38-MAPK by SB-202190(2.5µM/kg;24d; s.c.) resulted in increased primary tumor growth in tumor-bearing Balb-c mice (4T-1 cells) [8].