Erastin

Cystine transporter inhibitor; Induces ferroptosis

Erastin

Cystine transporter inhibitor; Induces ferroptosis

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Cystine transporter inhibitor; Induces ferroptosis
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Overview

Erastin is a cystine transporter inhibitor that induces ferroptotic cell death in vitro (Li et al.). By blocking system Xc−, it induces iron-dependent programmed cell death that plays an important regulatory role in cancer, neurological disease, and acute kidney injury (Li et al.). It is shown to have increased activity in the presence of oncoproteins (Dolma et al.).

CANCER RESEARCH
· Induces cell death in cells expressing Ras and SV40 small T oncoprotein (IC50 = 1.25 - 5 μg/mL; Dolma et al.).
· Inhibits cystine uptake through the cystine-glutamate antiporter (system Xc−) as measured by glutamate release assay (IC50 = 0.20 μM; Larraufie et al.).
Cell Type
Cancer Cells and Cell Lines
Area of Interest
Cancer
CAS Number
571203-78-6
Chemical Formula
C30H31ClN4O4
Molecular Weight
547.1 g/mol
Purity
≥ 98%

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Product Name
Erastin
Catalog #
100-0545, 100-0544
Lot #
All
Language
English
Document Type
Safety Data Sheet
Product Name
Erastin
Catalog #
100-0545, 100-0544
Lot #
All
Language
English

Resources and Publications

Publications (3)

Ferroptosis: past, present and future. J. Li et al. Cell death {\&} disease 2020 feb

Abstract

Ferroptosis is a new type of cell death that was discovered in recent years and is usually accompanied by a large amount of iron accumulation and lipid peroxidation during the cell death process; the occurrence of ferroptosis is iron-dependent. Ferroptosis-inducing factors can directly or indirectly affect glutathione peroxidase through different pathways, resulting in a decrease in antioxidant capacity and accumulation of lipid reactive oxygen species (ROS) in cells, ultimately leading to oxidative cell death. Recent studies have shown that ferroptosis is closely related to the pathophysiological processes of many diseases, such as tumors, nervous system diseases, ischemia-reperfusion injury, kidney injury, and blood diseases. How to intervene in the occurrence and development of related diseases by regulating cell ferroptosis has become a hotspot and focus of etiological research and treatment, but the functional changes and specific molecular mechanisms of ferroptosis still need to be further explored. This paper systematically summarizes the latest progress in ferroptosis research, with a focus on providing references for further understanding of its pathogenesis and for proposing new targets for the treatment of related diseases.
Incorporation of metabolically stable ketones into a small molecule probe to increase potency and water solubility. M.-H. Larraufie et al. Bioorganic {\&} medicinal chemistry letters 2015 nov

Abstract

Introducing a reactive carbonyl to a scaffold that does not otherwise have an electrophilic functionality to create a reversible covalent inhibitor is a potentially useful strategy for enhancing compound potency. However, aldehydes are metabolically unstable, which precludes the use of this strategy for compounds to be tested in animal models or in human clinical studies. To overcome this limitation, we designed ketone-based functionalities capable of forming reversible covalent adducts, while displaying high metabolic stability, and imparting improved water solubility to their pendant scaffold. We tested this strategy on the ferroptosis inducer and experimental therapeutic erastin, and observed substantial increases in compound potency. In particular, a new carbonyl erastin analog, termed IKE, displayed improved potency, solubility and metabolic stability, thus representing an ideal candidate for future in vivo cancer therapeutic applications.
Identification of genotype-selective antitumor agents using synthetic lethal chemical screening in engineered human tumor cells. S. Dolma et al. Cancer cell 2003 mar

Abstract

We used synthetic lethal high-throughput screening to interrogate 23,550 compounds for their ability to kill engineered tumorigenic cells but not their isogenic normal cell counterparts. We identified known and novel compounds with genotype-selective activity, including doxorubicin, daunorubicin, mitoxantrone, camptothecin, sangivamycin, echinomycin, bouvardin, NSC146109, and a novel compound that we named erastin. These compounds have increased activity in the presence of hTERT, the SV40 large and small T oncoproteins, the human papillomavirus type 16 (HPV) E6 and E7 oncoproteins, and oncogenic HRAS. We found that overexpressing hTERT and either E7 or LT increased expression of topoisomerase 2alpha and that overexpressing RAS(V12) and ST both increased expression of topoisomerase 1 and sensitized cells to a nonapoptotic cell death process initiated by erastin.