KRA-533 是一种有效的 KRAS 激动剂。KRA-533 与 KRAS 蛋白中的 GTP/GDP binding pocket 结合，防止 GTP 切割，导致 GTP 结合 KRAS 的组成性活性积累，触发癌细胞中凋亡和自噬细胞死亡途径。

KRA-533 is a potent KRAS agonist. KRA-533 binds to the GTP/GDP binding pocket in the KRAS protein to prevent GTP cleavage, resulting in the accumulation of constitutively active GTP-bound KRAS that triggers both apoptotic and autophagic cell death pathways in cancer cells.

Solid

KRAS

KRA-533 (10 μM; 48 hours; HCC827 cells) enhances KRAS activity to a greater extent.
KRA-533 (0~15 μM; 48 hours; H157 cells) enhances KRAS activity in a dose-dependent manner, which is associated increased levels of pERK, ratio of active caspase 3/procaspase 3 and PARP cleavage, leading to apoptotic cell death.
KRA-533 (10 μM; 10 days; H292 cells) mediates cell growth suppression than those without KRAS mutation. KRA-533 (5~15 μM) can directly bind to WT, G12C, G12D and G13D mutant KRAS proteins. KRA-533 activates WT KRAS to increase its activity in a dose-dependent manner. KRA-533 further enhances the activities of active KRAS mutants. has not independently confirmed the accuracy of these methods. They are for reference only.

KRA-533 (0~30 mg/kg; i.p.; 28 days) suppresses tumor growth in a dose-dependent manner in lung cancer mutant KRAS xenografts and induces apoptosis and autophagy in tumor tissues in a dose-dependent manner.
KRA-533 shows optimal therapeutic index between 7.5 mg/kg and 30 mg/kg doses. has not independently confirmed the accuracy of these methods. They are for reference only.

Room temperature in continental US; may vary elsewhere.

Powder -20°C 3 years；In solvent -80°C 6 months

[1]. Xu K, et al. Small Molecule KRAS Agonist for Mutant KRAS Cancer Therapy [published correction appears in Mol Cancer. 2020 May 20;19(1):93]. Mol Cancer. 2019;18(1):85. Published 2019 Apr 10.

In Vitro: DMSO : 250 mg/mL (795.72 mM; Need ultrasonic)配制储备液