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U0126-EtOH

CAS No. : 1173097-76-1

MCE 國(guó)際站：U0126-EtOH

產(chǎn)品活性：U0126-EtOH 是一種有效，非 ATP 競(jìng)爭(zhēng)性的，選擇性的 MEK1 和 MEK2 抑制劑，IC₅₀ 分別為 72 nM 和 58 nM。U0126-EtOH 是一種自噬 (autophagy) 和線粒體自噬 (mitophagy) 抑制劑。

研究領(lǐng)域：MAPK/ERK Pathway  |  Autophagy  |  Anti-infection

作用靶點(diǎn)：MEK  |  Autophagy  |  Mitophagy  |  Influenza Virus

In Vitro: Treatment with U0126-EtOH (U0126) efficiently reduces progeny virus titers of all tested strains in A549 cells. While nM concentrations of U0126-EtOH are efficient to reduce H1N1v and H5N1 (MB1), μM concentrations of U0126-EtOH are required to reduce the virus titer of H5N1 (GSB) and H7N7. The EC₅₀ values for U0126-EtOH against H1N1v are 1.2±0.4 μM in A549 cells and 74.7±1.0 μM in MDCKII cells.
Rat hepatocarcinoma cells (FAO) stimulated by fetal calf serum (FCS) exhibits a significant proportion in S phase (32.62%) whereas U0126-EtOH (U0126) strongly decreases the proportion of cells in S phase (9.92%) and increases the proportion of cells in G₀-G₁ phase and to a lesser extent in G₂/M.

In Vivo: Mice are treated daily with U0126-EtOH (U0126; i.p., 10.5 mg/kg). In control experiment, tumor sizes are constant or slightly increase all over the kinetic. At the opposite, in all U0126-EtOH experiments, engraftment and early tumor growth are significantly decreased. Furthermore, a 60-70% reduction in the volume of tumors treated with U0126-EtOH is obtained 9 days after injection and thereafter.
Rats are subjected to 120 minutes transient middle cerebral artery occlusion (tMCAO) and thereafter treated with the U0126-EtOH (U0126; i.p., 30 mg/kg) at 0 and 24 hours of reperfusion. After treatment with U0126-EtOH, the vasoconstriction to S6c is markedly reduced.

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