ARS-853 是选择性，共价的 KRAS G12C 抑制剂，IC₅₀ 为 2.5 μM。ARS-853 通过与 GDP 结合的癌蛋白结合并阻止激活来抑制突变 KRAS 驱动的信号传导。

ARS-853 is a cell-active, selective, covalent KRAS G12C inhibitor with an IC 50 of 2.5 μM. ARS-853 inhibits mutant KRAS-driven signaling by binding to the GDP-bound oncoprotein and preventing activation.

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KRAS(G12C) 2.5 μM (IC50)

ARS853 is designed to bind KRAS with high affinity. Treatment of KRAS-mutant lung cancer cells with ARS853 reduces the level of GTP-bound KRAS by more than 95% (10 μM). ARS853 inhibits proliferation with an inhibitory concentration 50% (IC50) of 2.5 μM, which is similar to its IC50 for target inhibition. ARS853 (10 μM) inhibits effector signaling and cell proliferation to varying degrees in six KRAS mutant lung cancer cell lines, but not in non-KRAS models. Similarly, it completely suppresses the effects of exogenous KRAS expression on KRAS-GTP levels, KRAS-BRAF interaction, and ERK signaling. ARS-853 treatment also induces apoptosis in four KRAS mutant cell lines. ARS853 selectively reduces KRAS-GTP levels and RAS-effector signaling in KRAS-mutant cells, while inhibiting their proliferation and inducing cell death. ARS-853 inhibits mutant KRAS-driven sig

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[1]. Lito P, et al. Allele-specific inhibitors inactivate mutant KRAS G12C by a trapping mechanism. Science. 2016 Feb 5;351(6273):604-8.
[2]. Patricelli MP, et al. Selective Inhibition of Oncogenic KRAS Output with Small Molecules Targeting the Inactive State. Cancer Discov. 2016 Mar;6(3):316-29.

In Vitro: DMSO : 25 mg/mL (57.74 mM; Need ultrasonic)配制储备液