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提供 ≥98% 纯度,适用于对基线干扰要求严格的色谱和分析工作流程。
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在色谱分析、有机合成和交叉偶联反应领域已被 0 篇同行评审文献引用。
Trametiglue, a derivative of Trametinib , targets both KSR-MEK and RAF-MEK with unprecedented potency and selectivity via unique interfacial binding interactions
In Vitro
Trametiglue retains the strong binding potency and residence time of Trametinib on KSR-bound MEK. Trametiglue, unlike Trametinib but similar to Avutometinib , enhances interactions between endogenous BRAF and MEK1. Trametiglue (1 μM) demonstrates high selectivity towards MEK1 and MEK2 in direct binding assays. Trametiglue also displays high selectivity in a panel of active kinases measured for inhibition of MEK1 and MEK2 substrate phosphorylation or direct MEK1 phosphorylation by the upstream kinases. Trametiglue (5 days) inhibits HCT116, A375, A549 and SK-MEL-239 cells viability with IC 50 s of 0.07, 0.07, 0.12 and 0.47 nM, respectively. Trametiglue (10 nM; 10 days) inhibits colony formation in KRAS-mutant and BRAF-mutant cancer cell lines with higher potency than Trametinib. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Cell Viability AssayCell Line: SK-MEL-239, HCT116, A549 and A375 Concentration: Incubation Time: 5 days Result: Showed IC 50 s of 0.47, 0.07, 0.12 and 0.07 nM against SK-MEL-239, HCT116, A549 and A375 cells, respectively. Western Blot AnalysisCell Line: A549, HCT-116, A375 and SK-MEL-239 Concentration: 0.4, 0.8, 1.6, 3.1, 6.25, 12.5, 25 and 50 nM Incubation Time: 1 h Result: Inhibited the expression of pERK. And the effect was better than Trametinib.
Form:Solid
IC50& Target:MEK1 MEK2