Description |
Erastin is a ferroptosis activator.
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In Vitro |
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 (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[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].
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In Vivo |
Intraperitoneal injection of erastin at well-tolerated doses dramatically inhibits HT-29 xenograft growth in severe combined immunodeficient mice[3].
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Cell Assay |
To test erastin’s activity on colorectal cancer cell survival, HT-29 cells are treated with increasing concentrations of erastin (0.1–30 μM). MTT assay was performed[3].
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Animal Admin |
Mice: Mice are treated daily with 10 or 30 mg/kg body weight of erastin (intraperitoneal injection, for 4 weeks) or vehicle control (Saline). Tumor volumes are calculated. Mice body weights are also recorded every week[3].
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Density | 1.3±0.1 g/cm3 |
Boiling Point | 721.9±70.0 °C at 760 mmHg |
Flash Point | 390.4±35.7 °C |
Exact Mass | 546.203369 |
PSA | 76.90000 |
LogP | 4.75 |
Vapour Pressure | 0.0±2.3 mmHg at 25°C |
Storage condition | −20°C |