U0126-EtOH |
Catalog No.GC12807 |
U0126 (U0126-EtOH) est un inhibiteur MEK1 et MEK2 puissant, non compétitif et sélectif de l'ATP, avec des IC50 de 72 nM et 58 nM, respectivement. U0126 est un inhibiteur de l'autophagie et de la mitophagie.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 1173097-76-1
Sample solution is provided at 25 µL, 10mM.
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]
References:
[1]. Favata MF, et al. Identification of a novel inhibitor of mitogen-activated protein kinase kinase. J Biol Chem. 1998 Jul 17;273(29):18623-32.
[2]. Liu F, et al. Sonic Hedgehog Signaling Pathway Mediates Proliferation and Migration of Fibroblast-Like Synoviocytes in Rheumatoid Arthritis via MAPK/ERK Signaling Pathway. Front Immunol. 2018 Dec 5;9:2847.
[3]. Shao S, et al. Isotalatizidine, a C19-diterpenoid alkaloid, attenuates chronic neuropathic pain through stimulating ERK/CREB signaling pathway-mediated microglial dynorphin A expression. J Neuroinflammation. 2020 Jan 10;17(1):13.
[4]. Wang T, et al. The MEK inhibitor U0126-EtOH ameliorates diabetic cardiomyopathy by restricting XBP1's phosphorylation dependent SUMOylation. Int J Biol Sci. 2021 Jul 13;17(12):2984-2999.
[5]. Orset C, et al. Combination treatment with U0126-EtOH and rt-PA prevents adverse effects of the delayed rt-PA treatment after acute ischemic stroke. Sci Rep. 2021 Jun 7;11(1):11993.
[6]. Ong Q, et al. U0126-EtOH protects cells against oxidative stress independent of its function as a MEK inhibitor. ACS Chem Neurosci. 2015 Jan 21;6(1):130-7.
[7]. Wang JZ, et al. Potent block of potassium channels by MEK inhibitor U0126-EtOH in primary cultures and brain slices. Sci Rep. 2018 Jun 11;8(1):8808.
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