U0126-EtOH,1173097-76-1,IC-0225284

U0126-EtOH-EtOH (U0126), as a non-ATP competitive and selective inhibitor, a has potent inhibition on MEK1 and MEK2 with IC50s of 72 nM and 58 nM, respectively.[1][6]

In vitro experiment it shown that treatment with 10 μM of U0126-EtOH-EtOH decreased the numbers of migration RA-FLSs induced by Sonic Hedgehog signaling. [2] In vitro, pretreatment with 50?μM SB203580 (the p38 inhibitor) and 50?μM U0126-EtOH-EtOH (ERK1/2 inhibitor) in the microglial cells obviously brogated the effects of isotalatizidine.[3] In addition, H9C2 cells pretreated with 10μM U0126-EtOH reduced ischemia/reperfusion-induced apoptosis and autophagy in myocardium and reduced cisplatin-induced renal injury by decreasing inflammation and apoptosis by inhibition of ERK1/2 phosphorylation.[4] Pretreatment with 10 μM of U0126-EtOH protected PC-12 Cells against hydrogen peroxide-induced cell death independent of MEK inhibition.[6] Moreover, at 1 μM to 20 μM of U0126-EtOH increased the half-width and decay time of action potential in a dose-dependent manner in primary hippocampal neurons. Bath application of 40?μM U0126-EtOH is more potent than 4-AP and TEA in suppressing maximal firing rate of pyramidal neurons in hippocampal slices.[5]

In vivo efficacy test it demonstrated that pretreatment with 1mg/kg U0126-EtOH in in STZ-induced diabetic mice improved cardiac function and ameliorated cardiac hypertrophy.[4] In the acute phase of experimental stroke, 30 mg/kg U0126-EtOH prevent activation of MMP-9, additionly, by adding U0126-EtOH in combination with rt-PA prevent activation of MMP-9 expression leading to BBB leakage and hemorrhagic transformation.[6]