571203-78-6
Chemical Structure
Erastin
- CAS No.: 571203-78-6
- Formula:C30H31ClN4O4
- Molecular Weight:547.04
IUPAC Name: 2-(1-(4-(2-(4-chlorophenoxy)acetyl)piperazin-1-yl)ethyl)-3-(2-ethoxyphenyl)quinazolin-4(3H)-one
InChIKey: BKQFRNYHFIQEKN-UHFFFAOYSA-N
SMILES: O=C1N(C2=CC=CC=C2OCC)C(C(N3CCN(C(COC4=CC=C(Cl)C=C4)=O)CC3)C)=NC5=C1C=CC=C5
Biological Activity: 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[1][2][3][4][5][6][7][8][9][10][11][12][13][14].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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Erastin | 99.91% | 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. | ||||||||||||||||||||
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- [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]
Keywords
