Erastin is a compound that interacts with VDAC, blocked and reversed mitochondrial depolarization after microtubule destabilizers in intact cells and antagonized tubulin-induced VDAC blockage in planar bilayers.

＞98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

本产品在溶液状态不稳定，建议您现用现配，即刻使用。

White solid

DMSO : 16 mg/mL (29.2 mM)

Ferroptosis

Erastin triggers oxidative, iron-dependent cell death. Treatment of NRAS-mutant HT-1080 fibrosarcoma cells with the RSL molecule erastin (10 µM) results in a time-dependent increase in cytosolic and lipid ROS beginning at 2 hours. Cell death triggered by erastin is significantly inhibited by antioxidants (e.g., α-tocopherol, butylated hydroxytoluene, and β-carotene) and iron chelators (e.g., deferoxamine), suggesting that ROS- and iron-dependent signaling is required for erastin-induced ferroptosis. Erastin can directly bind to VDAC2/3 in BJeLR cells. Knockdown of VDAC2 and VDAC3, but not VDAC1, leads to erastin resistance. Erastin has the ability to reduce glutathione level by directly inhibiting cystine/glutamate antiporter system Xc− activity, with activation of the ER stress response. Erastin potently inhibits HT-29 cell survival. Erastin shows a dose-dependent effect, and 30 μM of erastin displays the most dramatic effect.

Intraperitoneal injection of erastin at well-tolerated doses dramatically inhibits HT-29 xenograft growth in severe combined immunodeficient mice.