Molecular Weight(MW): 547.04
Erastin is a ferroptosis activator by acting on mitochondrial VDAC, exhibiting selectivity for tumor cells bearing oncogenic RAS.
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Erastin induces HSF1-dependent HSPB1 expression in human cancer cells. Indicated human cancer cells were treated with erastin (HeLa, 0.5 μM; U2OS, 5 μM; LNCaP, 5 μM) for 24 h and the protein expressions of indicated HSPs were assayed by western blot.
Oncogene, 2015, 10.1038/onc.2015.32. Erastin purchased from Selleck.
Erastin exerts cytotoxic, but not cytostatic, effects to cultured colorectal cancer cells. Colorectal cancer cells (HT-29, DLD-1 and Caco-2 lines) or NCM460 colon epithelial cells were treated with vehicle control (0.1% DMSO, “Ctrl”) or indicated concentrations of erastin for applied time, cell survival was tested by MTT assay (A and E) and colony formation assay (C); The percentage of trypan blue positive (“dead” cells) was recorded (B); Cell proliferation was tested by BrdU incorporation assay (D and F). For each assay, n = 5. The data presented were mean ± SD. Experiments were repeated three times with similar results obtained. * p < 0.05 vs. group of “Ctrl”.
PLoS One, 2016, 11(5):e0154605.. Erastin purchased from Selleck.
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|Description||Erastin is a ferroptosis activator by acting on mitochondrial VDAC, exhibiting selectivity for tumor cells bearing oncogenic RAS.|
Erastin is selectively lethal to oncogenic RAS-mutant cell lines, and triggers a unique iron-dependent form of non-apoptotic cell death called ferroptosis.   Erastin binds directly to VDAC2 and causes mitochondrial damage via ROS production in an NADH-dependent manner, which induces cell death in some tumor cells harbouring activating mutations in the RAS-RAF-MEK pathway.  In addition, erastin, via inducing ROS-mediated CID (Caspase-independent cell death), strongly enhances the effect of cisplatin in WT EGFR cells. 
|In vitro||DMSO||19 mg/mL (34.73 mM)|
|In vivo||5% DMSO+corn oil||2.5mg/mL|
* 1 mg/ml means slightly soluble or insoluble.
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