Erastin |
Catalog No.GC16630 |
Erastin is a cell-permeable ferroptosis activatior and antitumor agent.
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Cas No.: 571203-78-6
Sample solution is provided at 25 µL, 10mM.
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Erastin is a cell-permeable ferroptosis activatior and an antitumor agent that is selective for cell expressing oncogene RAS.
Erastin induces ferroptosis through directly binding to VDAC2/3 to alter the permeability of the outer mitochondrial membrane, which decreases the rate of NADH oxidation. Besides exerting targeted effects, erastin also enhances chemotherapy, targeted therapy, and immunotherapy in certain cancer cells, suggesting a potential role of erastin in cancer cell treatment.[3]
Erastin and its analogs specifically inhibited cystine uptake via system xc−, and triggered ferroptosis in a variety of cellular contexts and act much more potently than SAS. Moreover, Erastin was ∼2500 times more potent than SAS as an inhibitor of system xc− function in both HT-1080 and Calu-1 cells (HT-1080: erastin IC50 = 0.20 µM, SAS IC50 = 450 µM; Calu-1: erastin IC50 = 0.14 µM, SAS IC50 = 460 µM).[1]
Erastin, an inhibitor of SLC7A11, was found to hold a remarkably stronger cytotoxic effect on colorectal CSCs via in vitro and in vivo experiments. Besides, Erastin attenuated the chemoresistance of colorectal CSCs (colorectal cancer stem cells). For in vivo experiment, Erastin (10 mg/kg) was intravenously injected into mice with colorectal cancer every two days. It was found that Erastin inhibited ALDH1 activity, and reduced sphere size and number in colorectal cancer cells. [2]
References:
[1]. Dixon SJ, et al. Pharmacological inhibition of cystine-glutamate exchange induces endoplasmic reticulum stress and ferroptosis. Elife. 2014 May 20;3:e02523.
[2]. Xu X, et al. Targeting SLC7A11 specifically suppresses the progression of colorectal cancer stem cells via inducing ferroptosis. Eur J Pharm Sci. 2020 Sep 1;152:105450.
[3]. Yang Y, et al. Nedd4 ubiquitylates VDAC2/3 to suppress erastin-induced ferroptosis in melanoma. Nat Commun. 2020 Jan 23;11(1):433.
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