Molecular Formula | C20H14FN3O |
Molar Mass | 331.34 |
Density | 1.31 |
Melting Point | 240-243℃ |
Boling Point | 565.7±50.0 °C(Predicted) |
Solubility | Soluble in DMSO, not in water |
Appearance | Pale yellow solid |
Color | pale yellow |
pKa | 9.14±0.15(Predicted) |
Storage Condition | 2-8°C |
Stability | Stable for 2 years from date of purchase as supplied. Solutions in DMSO may be stored at -20° for up to 2 months. |
Use | SB 202190 is a selective p38 MAPK inhibitor, and the IC50 for inhibiting p38α and p38β2 is 50 nM and 100 nM, respectively. SB 202190 binds to the ATP pocket of recombinant human active p38 kinase with a Kd value of 38 nM. SB 202190 has anti-cancer activity and can save memory impairment. |
In vitro study | SB 202190 significantly inhibited both endogenous background and anti-Fas antibody-induced MAPKAPK 2 activity in a dose-dependent manner. SB 202190 alone is sufficient to induce the death of Jurkat and Hela cells: by activating the CPP 32-like cysteine protease, the expression of Bcl-2 can be blocked. p38β may be attenuated and p38α may exacerbate apoptosis induced by SB 202190. SB 202190 strongly inhibited cox - 2 protein expression and mRNA levels induced by UV light in HaCaT cells. Treatment of renal tubular epithelial cells (normal rat k livers-52E) with SB 202190 can induce inflammation induced by albumin (monocyte chemoattractant protein -1, MCP-1). Or tumor growth factor beta -1(TGFβ-1)-induced profibrosis (procollagen I a1,procollagen-i Alpha 1)-related genes were reduced by 50%. Treatment of A549 cells with SB 202190 induced JNK phosphorylation (a time-and dose-dependent effect), transcription factor ATF-2 phosphorylation, and increased DNA binding by AP-1. SB 202190 treatment promoted the growth of THP-1 and MV4-11 cells. SB 202190 can increase the phosphorylation of c-Raf and ERK (extracellular signal-regulated kinase), suggesting that Ras-Raf-MEK-mitogen activated MAPK pathway is involved in the proliferation of leukemia cells induced by SB 202190. |
In vivo study | SB 202190 attenuated blister formation induced by human polio IgG(PV-IgG) in a passive transfer mouse model by inhibiting p38. In the sepsis endotoxin model, treatment with SB 202190 significantly improved survival compared to the control group. |
Hazard Symbols | Xi - Irritant![]() |
Risk Codes | 36/37/38 - Irritating to eyes, respiratory system and skin. |
Safety Description | S26 - In case of contact with eyes, rinse immediately with plenty of water and seek medical advice. S36/37 - Wear suitable protective clothing and gloves. |
WGK Germany | 3 |
RTECS | SL4584000 |
HS Code | 29333990 |
1mg | 5mg | 10mg | |
---|---|---|---|
1 mM | 3.018 ml | 15.09 ml | 30.18 ml |
5 mM | 0.604 ml | 3.018 ml | 6.036 ml |
10 mM | 0.302 ml | 1.509 ml | 3.018 ml |
5 mM | 0.06 ml | 0.302 ml | 0.604 ml |
application | 4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)-1H-imidazole can be used as an organic synthesis intermediate and a pharmaceutical intermediate, mainly used in laboratory research and development processes and chemical production processes. |
biological activity | SB202190 (FHPI) is an effective p38 MAPK inhibitor, targeting p38α/β, IC50 is 50 nM/100 nM in cell-free test, and is sometimes used to study its potential effect on SAPK2a/p38 in vivo instead of SB 203580. SB202190 can inhibit apoptosis of endothelial cells by inducing autophagy and heme oxygenase-1. SB202190 can significantly inhibit Erastin-dependent iron death ferroptosis. |
target | TargetValue Ferroptosis () p38α (cell-free assay) 50 nM p38β (cell-free assay) 100 nM |
Target | Value |
Ferroptosis () | |
p38α (Cell-free assay) | 50 nM |
p38β (Cell-free assay) | 100 nM |
in vitro study | SB 202190 significantly inhibited endogenous background and MAPKAPK 2 activity induced by anti-Fas antibody, and the inhibitory effect was dose-dependent. SB 202190 itself is sufficient to induce the death of Jurkat cells and Hela cells: by activating CPP 32-like cysteine protease, the expression of Bcl-2 can be blocked. P38β can reduce and p38α can aggravate apoptosis induced by SB 202190. SB 202190 strongly inhibited UV-induced cox - 2 protein expression and mRNA levels in HaCaT cells. Treatment of renal tubular epithelial cells (normal rat krypton-52E) with SB 202190 reduced the genes associated with albumin-induced inflammation (monocyte chemoattractant protein -1, MCP-1) or tumor growth factor β-1(TGFβ-1)-induced primary fibrosis (primary collagen I a1,procollagen-i alpha1) by 50%. SB 202190 treatment of A549 cells can induce JNK phosphorylation (the phosphorylation effect is time-and dose-dependent), transcription factor ATF-2 phosphorylation, and increase the binding of AP-1 to DNA. SB 202190 treatment promotes the growth of THP-1 and MV4-11 cells. SB 202190 can increase phosphorylation of c-Raf and ERK (extracellular signal-regulated kinase), suggesting that Ras-Raf-MEK-mitogen activated MAPK pathway is involved in the proliferation process of leukemia cells induced by SB 202190. |
in vivo study | SB 202190 attenuates the formation of blisters induced by human polio IgG(PV-IgG) in a passive transfer mouse model by inhibiting p38. In septic endotoxin model, SB 202190 treatment can significantly improve survival rate compared with control group. |