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Erastin

MCE China：Erastin

Brand：MedChemExpress (MCE)

Cat. No.HY-15763

CAS：571203-78-6

Purity：99.62%

Storage：Powder -20°C 3 years 4°C 2 years *The compound is unstable in solutions, freshly prepared is recommended.

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Erastin is a ferroptosis inducer. Erastin exhibits the mechanism of ferroptosis induction related to ROS and iron-dependent signaling. Erastin inhibits voltage-dependent anion channels (VDAC2/VDAC3) and accelerates oxidation, leading to the accumulation of endogenous reactive oxygen species. Erastin also disrupts mitochondrial permeability transition pore (mPTP) with anti-tumor activity. Furthermore, Erastin can block the uptake of cystine mediated by SLC7A11 and also spares UMRC6-EV and -C91A cells from disulfidptosis under glucose starvation.

In Vitro：Erastin (10 μM; 24 h) triggers ferroptosis in ectopic endometrial stromal cells (EESCs), and increases the total ROS level at 9 h[1]. Erastin shorts mitochondria and increases membrane density in EESCs[1]. Erastin (10 μM; 9 h) decreases the mRNA expression levels of iron-related proteins, such FPN (iron exporter) in EESCs. However, FPN overexpression significantly inhibits erastin-induced ferroptosis in EESCs[1]. Erastin (10 μM; 24 h) induces mitochondrial permeability transition pore (mPTP) opening in HT-29 colorectal cancer cells[2]. Erastin (30 μM; 72 h) significantly inhibits the growth of HT-29 colorectal cancer cells[2]. The molecular mechanism by which Erastin induces ferroptosis is related to genes regulating iron or mitochondrial fatty acid metabolism. Includes ribosomal protein L8, iron response element binding protein 2 (IREB2), ATP synthase F0 complex subunit C3, citrate synthase, tetrapeptide repeat domain 35, and acyl-CoA synthetase family member 2 (ACSF2)[3]. Note: 1. Different cell lines may have different sensitivity to a same compound. As reported, A549, HCT116, HepG2, H1299 cells may be insensitive to Erastin[3][4][5]. 2. Erastin is unstable in solution. Freshly prepared is recommended. Ferroptosis-sensitive Cell Lines Ferroptosis-sensitive Cells Test Conditions SKOV3[6] 5-20 μM; 1-7 days OVCA429[6] 5-20 μM; 1-7 days MCF10A-RAS[7] 0-30 μM; 48 h HT-22 neuron[8] 500 nM; 16 h NCI-H508[9] 0.1-10 μM; 48 h LoVo[9] 0.1-10 μM; 48 h LS513[9] 0.1-10 μM; 48 h SW480[9] 0.1-10 μM; 48 h SW620[9] 0.1-10 μM; 48 h SW1116[9] 0.1-10 μM; 48 h DLD-1[9] 0.1-10 μM; 48 h Caco-2[9] 0.1-10 μM; 48 h SW837[10] 0-40 μM; 24 h Pfa1[11] 0.1-5 μM; 48 h HT-1080[12] 0.1-5 μM; 48 h MAD-MB-231[13] 0-100 μM; 72 h; IC50: 9.55 μM HCC1937[13] 0-100 μM; 72 h; IC50: 11.58 μM Ferroptosis-insensitive Cell Lines Ferroptosis-insensitive Cells Test Conditions HCT116[11] 0-40 μM; 24 h SW48[11] 0-40 μM; 24 h HepG2[5] 0-20 μM; 24 h MDA-MB-436[13] 0.1-25 μM; 24 h HT-29[13] 0.1-25 μM; 24 h U-373[13] 0.1-25 μM; 24 h

In Vivo：Erastin can be used in animal modeling to construct ferroptosis induction model. Erastin (40 mg/kg; i.p.; once every 3 days for 2 weeks) suppresses endometriotic implants in the mouse endometriosis model, indicating Erastin regresses ectopic lesions by trigging ferroptosis[1]. Erastin (10 mg/kg, 30 mg/kg; i.p.; once daily for 4 weeks) suppresses HT-29 xenograft growth in SCID mice, with more potent efficacy under 30 mg/kg treatment[2].

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References：

[1]. Li Y, et al. Erastin induces ferroptosis via ferroportin-mediated iron accumulation in endometriosis. Hum Reprod. 2021 Mar 18;36(4):951-964.  [Content Brief]

[2]. Huo H, et al. Erastin Disrupts Mitochondrial Permeability Transition Pore (mPTP) and Induces Apoptotic Death of Colorectal Cancer Cells. PLoS One. 2016 May 12;11(5):e0154605.  [Content Brief]

[3]. Xie Y, et al. Ferroptosis: process and function. Cell Death Differ. 2016 Mar;23(3):369-79.  [Content Brief]

[4]. Gai C, et al. MT1DP loaded by folate-modified liposomes sensitizes erastin-induced ferroptosis via regulating miR-365a-3p/NRF2 axis in non-small cell lung cancer cells. Cell Death Dis. 2020 Sep 14;11(9):751.  [Content Brief]

[5]. Yang Y, et al. Piperlongumine Inhibits Thioredoxin Reductase 1 by Targeting Selenocysteine Residues and Sensitizes Cancer Cells to Erastin. Antioxidants (Basel). 2022 Apr 4;11(4):710.  [Content Brief]

[6]. Liu N, et al., Activation of the reverse transsulfuration pathway through NRF2/CBS confers erastin-induced ferroptosis resistance. Br J Cancer. 2020 Jan;122(2):279-292.  [Content Brief]

[7]. Romani P, et al., Mitochondrial fission links ECM mechanotransduction to metabolic redox homeostasis and metastatic chemotherapy resistance. Nat Cell Biol. 2022 Feb;24(2):168-180.  [Content Brief]

[8]. Chen T, et al., Mitochondrial transplantation rescues neuronal cells from ferroptosis. Free Radic Biol Med. 2023 Nov 1;208:62-72.   [Content Brief]

[9]. Zhu JF, et al., Ibrutinib facilitates the sensitivity of colorectal cancer cells to ferroptosis through BTK/NRF2 pathway. Cell Death Dis. 2023 Feb 23;14(2):151.   [Content Brief]

[10]. Xie Y, et al., The Tumor Suppressor p53 Limits Ferroptosis by Blocking DPP4 Activity. Cell Rep. 2017 Aug 15;20(7):1692-1704.  [Content Brief]

[11]. Doll S, et al., FSP1 is a glutathione-independent ferroptosis suppressor. Nature. 2019 Nov;575(7784):693-698.  [Content Brief]

[12]. Li P, et al., Inhibition of cannabinoid receptor type 1 sensitizes triple-negative breast cancer cells to ferroptosis via regulating fatty acid metabolism. Cell Death Dis. 2022 Sep 21;13(9):808.  [Content Brief]

[13]. Zheng J, et al., Sorafenib fails to trigger ferroptosis across a wide range of cancer cell lines. Cell Death Dis. 2021 Jul 13;12(7):698.   [Content Brief]

[14]. Wang J, et al. Tumor suppressor BAP1 suppresses disulfidptosis through the regulation of SLC7A11 and NADPH levels[J]. Oncogenesis, 2024, 13(1): 31.  [Content Brief]