Erastin

Catalog No.S7242

Erastin Chemical Structure

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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8 Customer Reviews

  • Indicated HCC cells were treated with sorafenib (5 μM) and erastin (10 μM) with or without cell death inhibitors (ferrostatin-1, 1 μM; liprostatin-1, 100 nM; ZVAD-FMK, 10 μM; necrosulfonamide, 0.5 μM) for 24 hours, and cell viability was assayed (n=3, *P < 0.05 versus sorafenib or erastin treatment group).

    Hepatology, 2016, 64(2):488-500.. Erastin purchased from Selleck.

    Western blot analysis indicated protein expression in PDAC cells following treatment with erastin (2.5-40 μmol/L) for 24 hours (n=3, * P < 0.05 vs. untreated group)

    Cancer Res, 2017, 77(8):2064-2077. Erastin purchased from Selleck.

  • 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.

    HeLa cells were treated with erastin (0.5 μM) for 24 h with or without Gö 6893 (0.5 μM) and calphostin C (0.1 μM), and HSPB1 phosphorylation at Ser 15 was assayed using western blot.

    Oncogene, 2015, 10.1038/onc.2015.32. Erastin purchased from Selleck.

  • F. Dramatically augmentation of the EF24 cytotoxicity to gastric cancer cells by GSH depletion. G. EF24 and erastin in combination dramatically activated ER-stress pathway.

    Oncotarget, 2016, 7(14):18050-64.. 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.

  • Baicalein suppresses erastin-induced GPX4 degradation. (A) PANC1 and BxPc3 cells were treated with erastin (20 μM) in the absence or presence of baicalein (10 μM) for 24 h. The indicated protein levels were assayed using western blot. (B) In parallel, the relative intensity of the western blot band of GPX4 was quantified using ImageJ densitometry software (n = 3, *, p < 0.05).

    Biochem Biophys Res Commun, 2016, 473(4):775-80.. Erastin purchased from Selleck.

    FANCD2 suppresses erastin-induced ferroptosis in BMSCs. (A) FANCD2+/+ and FANCD2 −/− BMSCs were treated with erastin (0.625–2.5 μM) for 24 h and cell viability was assayed (n = 3, *P < 0.05). (B) Interference contrast images of FANCD2+/+ and FANCD2 −/− BMSCs with or without erastin (1.25 μM) treatment for 24 h (C) FANCD2+/+ and FANCD2 −/− BMSCs were treated with erastin (1.25 μM) in the absence or presence of ferroptosis inhibitor (ferrostatin-1, 500 nM; liprostatin-1, 200 nM; β-mercaptoethanol, 50 μM; N-acetylcysteine, 100 mM) or autophagy inhibitor (chloroquine, 10 μM; 3-methyladenine, 5 mM) for 24 h. Cell viability was assayed (n = 3, *P < 0.05 versus erastin treatment group). (D) Western blot analysis of LC3-I and LC3-II expression in FANCD2+/+ and FANCD2 −/− BMSCs following erastin (1.25 μM) treatment for 24 h. (E) In parallel, the LC3-II/I ratio quantified by densitometry analysis of bands.

    Biochem Biophys Res Commun, 2016, 480(3):443-449.. Erastin purchased from Selleck.

Purity & Quality Control

Choose Selective Ferroptosis Inhibitors

Biological Activity

Description Erastin is a ferroptosis activator by acting on mitochondrial VDAC, exhibiting selectivity for tumor cells bearing oncogenic RAS.
Targets
Ferroptosis [1]
In vitro

Erastin is selectively lethal to oncogenic RAS-mutant cell lines, and triggers a unique iron-dependent form of non-apoptotic cell death called ferroptosis. [1] [2] 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. [3] In addition, erastin, via inducing ROS-mediated CID (Caspase-independent cell death), strongly enhances the effect of cisplatin in WT EGFR cells. [4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human CCF-STTG1 cells MoHnSpVv[3Srb36gZZN{[Xl? NVHWZlFJUW6qaXLpeIlwdiCxZjDYZ5QhcW5iaIXtZY4hS0OILWPUWGcyKGOnbHzzJIF{e2W|c3XkJIF{KGeudYThcYF1\SC{ZXzlZZNmKGGodHXyJFIhcHK|IHL5JIZtfW:{b33leJJ6NCCLQ{WwQVAvOiEQvF2u M{HobVI3OjNzMUW2
human HeLa cells NGCybHFHfW6ldHnvckBie3OjeR?= NEHNRVJKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDI[WxiKGOnbHzzMEBGSzVyPUCuOkDPxE1w NHW4fmoyPzV4OEe0PC=>
human BJ cells MoDwSpVv[3Srb36gZZN{[Xl? MXXJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCESjDj[YxteyCneIDy[ZN{cW6pIGTFVnQtKEyWLDDTWEBidmRiUlHTJGcyOlZibYX0ZY51KGenbnXzJINmdGy|IHnuJJBz\XOnbnPlJI9nKFCGLUm4NFU6KGK7IITyfZBidiCkbIXlJIV5[2y3c3nvckBu\XSqb3SsJGlEPTB;MD65JO69VS5? MlK1NVc2Pjh5NEi=
human HT1080 cells M4j6WWZ2dmO2aX;uJIF{e2G7 NWHQdXlNUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gTHQyODhyIHPlcIx{KGmwIIDy[ZNmdmOnIH;mJHBFNTl6MEW5JIJ6KHS{eYDhckBjdHWnIHX4Z4x2e2mxbjDt[ZRpd2RuIFnDOVA:OSEQvF2u M4DtNVE4PTZ6N{S4
human SVR cells NInEXYZHfW6ldHnvckBie3OjeR?= NWXSSmdVUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gV3ZTKGOnbHzzMEBGSzVyPUKuOUDPxE1w Mn3CNVc2Pjh5NEi=
human MES-SA cells MkDYSpVv[3Srb36gZZN{[Xl? NH65VWNKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDNSXMuW0FiY3XscJMtKEWFNUC9N{DPxE1w NGPCW4QyPzV4OEe0PC=>
human SKUT cells MYHGeY5kfGmxbjDhd5NigQ>? Mom1TY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iU1vVWEBk\WyuczygSWM2OD12IN88UU4> MWqxO|U3QDd2OB?=
human Calu1 cells NGHkVnhHfW6ldHnvckBie3OjeR?= NG\wNGNKdmirYnn0bY9vKG:oIHj1cYFvKEOjbIWxJINmdGy|IHX4dJJme3OrbnegT3JCWyC5aYToJIFkfGm4YYTpcochdXW2YYTpc45{KGK7IITyfZBidiCkbIXlJIV5[2y3c3nvckBie3OjeTygTWM2OD12IN88UU4> MoLJNVc2Pjh5NEi=
human LNCaP cells MXLGeY5kfGmxbjDhd5NigQ>? MlTiTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iTF7DZXAh[2WubIOsJGVEPTB;NjFOwG0v Mo\JNVc2Pjh5NEi=
human U2OS cells NX3GU4NKTnWwY4Tpc44h[XO|YYm= M1zRfmlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIGWyU3Mh[2WubIOsJGVEPTB;NjFOwG0v Ml[5NVc2Pjh5NEi=
human TC32 cells MWHGeY5kfGmxbjDhd5NigQ>? NGLBc29KdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDUR|MzKGOnbHzz M3;lR|E4PTZ6N{S4
human SK-N-MC cells MlPKSpVv[3Srb36gZZN{[Xl? NUnpSoltUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gV2suVi2PQzDj[YxteyxiRVO1NF0yOCEQvF2u NIn3TmoyPzV4OEe0PC=>
human U937 cells MoP4SpVv[3Srb36gZZN{[Xl? M{TRcmlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIGW5N|ch[2WubIOsJGVEPTB;MUCg{txONg>? MmHpNVc2Pjh5NEi=
human TC71 cells MWDGeY5kfGmxbjDhd5NigQ>? NGS0UnZKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDUR|cyKGOnbHzzMEBGSzVyPUGwJO69VS5? MkmyNVc2Pjh5NEi=
human BJ cells MnHBSpVv[3Srb36gZZN{[Xl? MVTJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDUSXJVKGW6cILld5NqdmdiaIXtZY4hSkpiY3XscJMtKEWFNUC9NVAh|ryPLh?= Mn24NVc2Pjh5NEi=
human EWS502 cells NUXQZY1uTnWwY4Tpc44h[XO|YYm= NYHZfpJxUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gSXdUPTB{IHPlcIx{NCCHQ{WwQVExKM7:TT6= M3zpWFE4PTZ6N{S4
human Hs51.T cells M4DZ[mZ2dmO2aX;uJIF{e2G7 NY\RV3BbUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gTJM2OS6WIHPlcIx{NCCHQ{WwQVEzKM7:TT6= MV6xO|U3QDd2OB?=
human Hs925.T cells NXLCbnVjTnWwY4Tpc44h[XO|YYm= M2D0W2lv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIFjzPVI2NlRiY3XscJMtKEWFNUC9NVch|ryPLh?= Mk\TNVc2Pjh5NEi=
human HOS cells NWC4VVJ{TnWwY4Tpc44h[XO|YYm= M3XEXGlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIFjPV{Bk\WyuczCsJGVEPTB;MUeg{txONg>? MnTaNVc2Pjh5NEi=
human MX2 cells NGHZe3VHfW6ldHnvckBie3OjeR?= MV7JcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCPWEKgZ4VtdHNuIFXDOVA:OThizszNMi=> MXuxO|U3QDd2OB?=
human A673 cells Mlr1SpVv[3Srb36gZZN{[Xl? NYfMPZpFUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gRVY4OyClZXzsd{whTUN3ME2zNEDPxE1w NEfRRlAyPzV4OEe0PC=>
human BJ cells Mn3pSpVv[3Srb36gZZN{[Xl? NVfIcJRrUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gRmoh[2WubIOg[ZhxemW|c3nu[{BVTVKWLDDMWEwhW1RiYX7kJHJCWyCJMULWJI12fGGwdDDn[Y5meyCrbjDwdoV{\W6lZTDv[kBWODF{NjDifUB1enmyYX6gZox2\SCneHPseZNqd25ibXX0bI9lNCCLQ{WwQVMyNjJizszNMi=> NXnUVpdIOTd3Nki3OFg>
human BJ cells MnfXSpVv[3Srb36gZZN{[Xl? NW\TfXk2QSEQvF2= MVLJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCESjDj[YxteyCneIDy[ZN{cW6pIGTFVnQtKEyWLDDTWEBidmRiUlHTJGcyOlZibYX0ZY51KGenbnXzJINmdGy|IHH0JFkhfU1w Mk\RNVc2Pjh5NEi=
human BJ cells NVq2Ro9HTnWwY4Tpc44h[XO|YYm= NIjvVIw1NjZizszN M37nfGlv[3KnYYPlJIlvKGmwdILhZ4VtdHWuYYKgc5hq\GG2aY\lJJNx\WOrZYOgbY4hcHWvYX6gRmoh[2WubIOg[ZhxemW|c3nu[{BVTVKWLDDMWEwhW1RiYX7kJHJCWyCJMULWJI12fGGwdDDn[Y5meyClZXzsd{BifCB2Lk[geW0> M17xfVE4PTZ6N{S4
human BJeLR cells MnW1R5l1d3SxeHnjxsBie3OjeR?= NUXOZWJMOTBizszN MUSxNkBp M{naOmN6fG:2b4jpZ4l1gSCjZ3HpcpN1KGi3bXHuJGJL\UyUIHPlcIx{KGW6cILld5NqdmdiUlHTJGcyOlZibYX0ZY51KGG2IEGwJJVOKGG2IEGyJIhzeyCkeTD0dplx[W5iYnz1[UB{fGGrbnnu[y=> M2LoU|IzQDN{M{Kx
human BJeH cells MYnGeY5kfGmxbjDhd5NigQ>? NV;kO25MPiCq NXnhN41XUW6mdXP0bY9vKG:oIILlZYN1cX[nIH;4fYdmdiC|cHXjbYV{KHC{b3T1Z5Rqd25iaX6gbJVu[W5iQlrlTEBk\WyuczDlfJBz\XO|aX7nJJdqdGRidInw[UBTSVNiYX\0[ZIhPiCqcoOgZpkhTEOILXLhd4VlKG[ub4egZ5l1d22ndILpZ{BidmGueYPpdy=> MlrONlI5OzJ|MkG=

... Click to View More Cell Line Experimental Data

Protocol

Cell Research:[1]
+ Expand
  • Cell lines: BJ-TERT/LT/ST/RASV12 cells
  • Concentrations: 5 or 10 μg/mL
  • Incubation Time: 6-11 hours
  • Method: BJ-TERT/LT/ST/RASV12 cells are seeded in 100 mm dishes and allowed to grow overnight. Cells are treated with erastin (5 or 10 μg/ml) for 6, 8, or 11 hr. A camptothecin-treated (0.4 μg/ml) control is maintained, treated at the time of seeding for 20 hours. After the treatment, cells are harvested with trypsin/EDTA and washed once with fresh medium containing serum and then twice with phosphate-buffered saline. Cells are resuspended in 1× binding buffer. 100 μL is incubated with 5 μL of Annexin V-FITC and propidium iodiode for 15 min in the dark at room temperature. Then 400 μl of the 1× binding buffer s added and the cells analyzed by flow cytometry. Data are acquired and analyzed using Cellquest software. Only viable cells that do not stain with propidium iodiode are analzyed for Annexin V-FITC staining using the FL1 channel.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 19 mg/mL (34.73 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order:
5% DMSO+corn oil
For best results, use promptly after mixing.
2.5mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 547.04
Formula

C30H31ClN4O4

CAS No. 571203-78-6
Storage powder
in solvent
Synonyms N/A

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Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID