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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Cited by 14 Publications

11 Customer Reviews

  • PANC1 and PANC2.03 cells were treated with staurosporine or erastin (D) in the absence or presence of indicated cell death inhibitors for 24 hours. Cell viability was assayed (n = 3, *P < 0.05).

    Gastroenterology, 2017, 153(5):1429-1443. Erastin purchased from Selleck.

    PANC1 cells were treated with JTC801 (10 μM), erastin (20 μM) in the absence or presence of ferrostatin-1 (500 nM) for 24 hours. Cell viability was assayed (n=3, **p < 0.01, ***p < 0.001, n.s.=not significant).

    Gastroenterology, 2018, 154(5):1480-1493. Erastin purchased from Selleck.

  • 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.

    Cancer Res Treat, 2018, 50(2):445-460. 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 NWjLZnRSTnWwY4Tpc44h[XO|YYm= MkTDTY5pcWKrdHnvckBw\iC[Y4SgbY4hcHWvYX6gR2NHNVOWVFexJINmdGy|IHHzd4V{e2WmIHHzJIdtfXSjbXH0[UBz\WynYYPlJIFnfGW{IEKgbJJ{KGK7IH\seY9zd22ndIL5MEBKSzVyPUCuNkDPxE1w NF\OWlAzPjJ|MUG1Oi=>
human HeLa cells M1PNdWZ2dmO2aX;uJIF{e2G7 NFG1ToFKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDI[WxiKGOnbHzzMEBGSzVyPUCuOkDPxE1w MVixO|U3QDd2OB?=
human BJ cells MYXGeY5kfGmxbjDhd5NigQ>? M1jhOGlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIFLKJINmdGy|IHX4dJJme3OrbnegWGVTXCxiTGSsJHNVKGGwZDDSRXMhTzF{VjDteZRidnRiZ3Xu[ZMh[2WubIOgbY4heHKnc3XuZ4Uhd2ZiUFStPVgxPTliYomgeJJ6eGGwIHLseYUh\XilbIXzbY9vKG2ndHjv[EwhUUN3ME2wMlkh|ryPLh?= M3\mTlE4PTZ6N{S4
human HT1080 cells M3nlbGZ2dmO2aX;uJIF{e2G7 M1u4W2lv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIFjUNVA5OCClZXzsd{BqdiCycnXz[Y5k\SCxZjDQSE06QDB3OTDifUB1enmyYX6gZox2\SCneHPseZNqd25ibXX0bI9lNCCLQ{WwQVEh|ryPLh?= MnS4NVc2Pjh5NEi=
human SVR cells MUHGeY5kfGmxbjDhd5NigQ>? MVfJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCVVmKgZ4VtdHNuIFXDOVA:Oi53IN88UU4> M3TUPFE4PTZ6N{S4
human MES-SA cells MlLGSpVv[3Srb36gZZN{[Xl? MYTJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCPRWOtV2Eh[2WubIOsJGVEPTB;MzFOwG0v M2DqSVE4PTZ6N{S4
human SKUT cells NEj5d5pHfW6ldHnvckBie3OjeR?= M3v1Nmlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIGPLWXQh[2WubIOsJGVEPTB;NDFOwG0v NIrJc5QyPzV4OEe0PC=>
human Calu1 cells Mor3SpVv[3Srb36gZZN{[Xl? M13EZmlvcGmkaYTpc44hd2ZiaIXtZY4hS2GudUGgZ4VtdHNiZYjwdoV{e2mwZzDLVmFUKHerdHigZYN1cX[jdHnu[{BufXSjdHnvcpMh[nlidIL5dIFvKGKudXWg[ZhkdHW|aX;uJIF{e2G7LDDJR|UxRTRizszNMi=> Mon1NVc2Pjh5NEi=
human LNCaP cells MXvGeY5kfGmxbjDhd5NigQ>? MnLMTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iTF7DZXAh[2WubIOsJGVEPTB;NjFOwG0v NI\id5EyPzV4OEe0PC=>
human U2OS cells NGi4[lRHfW6ldHnvckBie3OjeR?= MV\JcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCXMl;TJINmdGy|LDDFR|UxRTZizszNMi=> NHvTem8yPzV4OEe0PC=>
human TC32 cells MkDVSpVv[3Srb36gZZN{[Xl? M3HpdGlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIGTDN|Ih[2WubIO= MlXzNVc2Pjh5NEi=
human SK-N-MC cells MnS5SpVv[3Srb36gZZN{[Xl? NEfRc2dKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDTT{1PNU2FIHPlcIx{NCCHQ{WwQVExKM7:TT6= MV2xO|U3QDd2OB?=
human U937 cells NVv3PGh3TnWwY4Tpc44h[XO|YYm= MX\JcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCXOUO3JINmdGy|LDDFR|UxRTFyIN88UU4> NXXZWI5nOTd3Nki3OFg>
human TC71 cells NHy4UpRHfW6ldHnvckBie3OjeR?= NFGwO4pKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDUR|cyKGOnbHzzMEBGSzVyPUGwJO69VS5? M2\mUFE4PTZ6N{S4
human BJ cells MVnGeY5kfGmxbjDhd5NigQ>? NXnxbY1mUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hXEWUVDDlfJBz\XO|aX7nJIh2dWGwIFLKJINmdGy|LDDFR|UxRTFyIN88UU4> M1X3eVE4PTZ6N{S4
human EWS502 cells M2TNNWZ2dmO2aX;uJIF{e2G7 NYq5ZmVPUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gSXdUPTB{IHPlcIx{NCCHQ{WwQVExKM7:TT6= M1THSlE4PTZ6N{S4
human Hs51.T cells NHnzbJlHfW6ldHnvckBie3OjeR?= NWDWfGp6UW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gTJM2OS6WIHPlcIx{NCCHQ{WwQVEzKM7:TT6= MX[xO|U3QDd2OB?=
human Hs925.T cells MUnGeY5kfGmxbjDhd5NigQ>? NUW1VIJSUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gTJM6OjVwVDDj[YxteyxiRVO1NF0yPyEQvF2u NFj0W5UyPzV4OEe0PC=>
human HOS cells M{j3SmZ2dmO2aX;uJIF{e2G7 MUPJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCKT2OgZ4VtdHNiLDDFR|UxRTF5IN88UU4> NGLLTYEyPzV4OEe0PC=>
human MX2 cells Mo\lSpVv[3Srb36gZZN{[Xl? MXnJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCPWEKgZ4VtdHNuIFXDOVA:OThizszNMi=> NXTCc|RROTd3Nki3OFg>
human A673 cells NYHGeI95TnWwY4Tpc44h[XO|YYm= NXT1WIJ{UW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gRVY4OyClZXzsd{whTUN3ME2zNEDPxE1w MnP5NVc2Pjh5NEi=
human BJ cells MofySpVv[3Srb36gZZN{[Xl? NVPlSYgyUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gRmoh[2WubIOg[ZhxemW|c3nu[{BVTVKWLDDMWEwhW1RiYX7kJHJCWyCJMULWJI12fGGwdDDn[Y5meyCrbjDwdoV{\W6lZTDv[kBWODF{NjDifUB1enmyYX6gZox2\SCneHPseZNqd25ibXX0bI9lNCCLQ{WwQVMyNjJizszNMi=> NEC0XpEyPzV4OEe0PC=>
human BJ cells NEfOXpBHfW6ldHnvckBie3OjeR?= NWXzOmhzQSEQvF2= NFvne4hKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDCTkBk\WyuczDlfJBz\XO|aX7nJHRGWlRuIFzUMEBUXCCjbnSgVmFUKEdzMm[gcZV1[W62IHflcoV{KGOnbHzzJIF1KDlidV2u NIrq[mYyPzV4OEe0PC=>
human BJ cells M1ezPGZ2dmO2aX;uJIF{e2G7 MmTUOE43KM7:TR?= NHzyTnBKdmO{ZXHz[UBqdiCrboTyZYNmdGy3bHHyJI95cWSjdHn2[UB{eGWlaXXzJIlvKGi3bXHuJGJLKGOnbHzzJIV5eHKnc4PpcochXEWUVDygUHQtKFOWIHHu[EBTSVNiR{GyWkBufXSjboSg[4Vv\XNiY3XscJMh[XRiND62JJVO Ml\2NVc2Pjh5NEi=
human BJeLR cells NYPydHdRS3m2b4TvfIlkyqCjc4PhfS=> MXexNEDPxE1? NGPDO4kyOiCq MUHDfZRwfG:6aXPpeJkh[WejaX7zeEBpfW2jbjDCToVNWiClZXzsd{BmgHC{ZYPzbY5oKFKDUzDHNVJXKG23dHHueEBifCBzMDD1UUBifCBzMjDodpMh[nlidIL5dIFvKGKudXWgd5RicW6rbne= MWCyNlg{OjN{MR?=
human BJeH cells MUfGeY5kfGmxbjDhd5NigQ>? NXLi[VIyPiCq MWLJcoR2[3Srb36gc4YhemWjY4TpeoUhd3i7Z3XuJJNx\WOrZYOgdJJw\HWldHnvckBqdiCqdX3hckBDUmWKIHPlcIx{KGW6cILld5Nqdmdid3ns[EB1gXCnIGLBV{Bi\nSncjC2JIhzeyCkeTDER2Yu[mG|ZXSg[oxwfyCleYTvcYV1emmlIHHuZYx6e2m| MoixNlI5OzJ|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(Data is from Selleck tests instead of citations):
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