[CAS NO. 571203-78-6]  Erastin

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 ^[1] . Cell death triggered by erastin is significantly inhibited by antioxidants (e.g., α-tocopherol, butylated hydroxytoluene, and β-carotene) and iron chelators, 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 ^[2] . Erastin potently inhibits HT-29 cell survival. Erastin shows a dose-dependent effect, and 30 μM of erastin displays the most dramatic effect ^[3] .

MCE has not independently confirmed the accuracy of these methods. They are for reference only.