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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9 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.

    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 MXrGeY5kfGmxbjDhd5NigQ>? M1npeGlvcGmkaYTpc44hd2ZiWHP0JIlvKGi3bXHuJGNETi2VVGTHNUBk\WyuczDhd5Nme3OnZDDhd{BodHW2YX3heIUhemWuZXHz[UBi\nSncjCyJIhzeyCkeTDmcJVwem:vZYTyfUwhUUN3ME2wMlIh|ryPLh?= NULnc2NvOjZ{M{GxOVY>
human HeLa cells M3HhWWZ2dmO2aX;uJIF{e2G7 MkTmTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iSHXMZUBk\WyuczygSWM2OD1yLk[g{txONg>? MXWxO|U3QDd2OB?=
human BJ cells M4HsZmZ2dmO2aX;uJIF{e2G7 NIXJWJlKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDCTkBk\WyuczDlfJBz\XO|aX7nJHRGWlRuIFzUMEBUXCCjbnSgVmFUKEdzMm[gcZV1[W62IHflcoV{KGOnbHzzJIlvKHC{ZYPlcoNmKG:oIGDEMVk5ODV7IHL5JJRzgXCjbjDicJVmKGW6Y3z1d4lwdiCvZYToc4QtKEmFNUC9NE46KM7:TT6= NEHIZ3IyPzV4OEe0PC=>
human HT1080 cells Mn\iSpVv[3Srb36gZZN{[Xl? NVvEbY1RUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gTHQyODhyIHPlcIx{KGmwIIDy[ZNmdmOnIH;mJHBFNTl6MEW5JIJ6KHS{eYDhckBjdHWnIHX4Z4x2e2mxbjDt[ZRpd2RuIFnDOVA:OSEQvF2u MXWxO|U3QDd2OB?=
human SVR cells M2DhbGZ2dmO2aX;uJIF{e2G7 MnfwTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iU2\SJINmdGy|LDDFR|UxRTJwNTFOwG0v M2LPOlE4PTZ6N{S4
human MES-SA cells MWrGeY5kfGmxbjDhd5NigQ>? NX3nbYE5UW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gUWVUNVODIHPlcIx{NCCHQ{WwQVMh|ryPLh?= NY\2b3hWOTd3Nki3OFg>
human SKUT cells MmC3SpVv[3Srb36gZZN{[Xl? NWjyN4M1UW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gV2tWXCClZXzsd{whTUN3ME20JO69VS5? Mn\uNVc2Pjh5NEi=
human Calu1 cells NXrOepV3TnWwY4Tpc44h[XO|YYm= M3fXdWlvcGmkaYTpc44hd2ZiaIXtZY4hS2GudUGgZ4VtdHNiZYjwdoV{e2mwZzDLVmFUKHerdHigZYN1cX[jdHnu[{BufXSjdHnvcpMh[nlidIL5dIFvKGKudXWg[ZhkdHW|aX;uJIF{e2G7LDDJR|UxRTRizszNMi=> M4ixZlE4PTZ6N{S4
human LNCaP cells NYfudZBxTnWwY4Tpc44h[XO|YYm= NImw[5JKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDMUmNiWCClZXzsd{whTUN3ME22JO69VS5? MX6xO|U3QDd2OB?=
human U2OS cells Mlv0SpVv[3Srb36gZZN{[Xl? MUXJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCXMl;TJINmdGy|LDDFR|UxRTZizszNMi=> NHr2[IIyPzV4OEe0PC=>
human TC32 cells NY\KR3BsTnWwY4Tpc44h[XO|YYm= MWTJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCWQ{OyJINmdGy| NWjTT49oOTd3Nki3OFg>
human SK-N-MC cells MX\GeY5kfGmxbjDhd5NigQ>? NU\KVlY1UW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gV2suVi2PQzDj[YxteyxiRVO1NF0yOCEQvF2u M17qOVE4PTZ6N{S4
human U937 cells NYTvd3RTTnWwY4Tpc44h[XO|YYm= MUnJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCXOUO3JINmdGy|LDDFR|UxRTFyIN88UU4> NYjUNm1xOTd3Nki3OFg>
human TC71 cells MYXGeY5kfGmxbjDhd5NigQ>? NVTn[pd3UW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gWGM4OSClZXzsd{whTUN3ME2xNEDPxE1w M1XsOVE4PTZ6N{S4
human BJ cells M37qTmZ2dmO2aX;uJIF{e2G7 NYeyS3JwUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hXEWUVDDlfJBz\XO|aX7nJIh2dWGwIFLKJINmdGy|LDDFR|UxRTFyIN88UU4> NVrOZZpGOTd3Nki3OFg>
human EWS502 cells M1LiZWZ2dmO2aX;uJIF{e2G7 MUXJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCHV2O1NFIh[2WubIOsJGVEPTB;MUCg{txONg>? MUmxO|U3QDd2OB?=
human Hs51.T cells M3rReWZ2dmO2aX;uJIF{e2G7 MljmTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iSIO1NU5VKGOnbHzzMEBGSzVyPUGyJO69VS5? NETRPVgyPzV4OEe0PC=>
human Hs925.T cells M2fJdGZ2dmO2aX;uJIF{e2G7 MXfJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCKc{myOU5VKGOnbHzzMEBGSzVyPUG3JO69VS5? Mk\HNVc2Pjh5NEi=
human HOS cells NFmxSVNHfW6ldHnvckBie3OjeR?= NHfEbmdKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDIU3Mh[2WubIOgMEBGSzVyPUG3JO69VS5? M3;KNlE4PTZ6N{S4
human MX2 cells M4X4RmZ2dmO2aX;uJIF{e2G7 NVX0[2Z{UW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gUXgzKGOnbHzzMEBGSzVyPUG4JO69VS5? Mlz1NVc2Pjh5NEi=
human A673 cells MYPGeY5kfGmxbjDhd5NigQ>? NXywZlRsUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gRVY4OyClZXzsd{whTUN3ME2zNEDPxE1w MVyxO|U3QDd2OB?=
human BJ cells M2SyNWZ2dmO2aX;uJIF{e2G7 NEniclhKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDCTkBk\WyuczDlfJBz\XO|aX7nJHRGWlRuIFzUMEBUXCCjbnSgVmFUKEdzMm[gcZV1[W62IHflcoV{KGmwIIDy[ZNmdmOnIH;mJHUxOTJ4IHL5JJRzgXCjbjDicJVmKGW6Y3z1d4lwdiCvZYToc4QtKEmFNUC9N|EvOiEQvF2u M1rCSlE4PTZ6N{S4
human BJ cells M2rVNGZ2dmO2aX;uJIF{e2G7 NYDxcGZTQSEQvF2= MVnJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCESjDj[YxteyCneIDy[ZN{cW6pIGTFVnQtKEyWLDDTWEBidmRiUlHTJGcyOlZibYX0ZY51KGenbnXzJINmdGy|IHH0JFkhfU1w MmP2NVc2Pjh5NEi=
human BJ cells MnqxSpVv[3Srb36gZZN{[Xl? M2nQeFQvPiEQvF2= MmHVTY5kemWjc3WgbY4hcW62cnHj[YxtfWyjcjDvfIll[XSrdnWgd5Bm[2mnczDpckBpfW2jbjDCTkBk\WyuczDlfJBz\XO|aX7nJHRGWlRuIFzUMEBUXCCjbnSgVmFUKEdzMm[gcZV1[W62IHflcoV{KGOnbHzzJIF1KDRwNjD1US=> NIHVNoQyPzV4OEe0PC=>
human BJeLR cells NXvNR4szS3m2b4TvfIlkyqCjc4PhfS=> NI\i[nEyOCEQvF2= NVfZR|Q6OTJiaB?= NWjHfVNlS3m2b4TvfIlkcXS7IHHnZYlve3RiaIXtZY4hSkqnTGKgZ4VtdHNiZYjwdoV{e2mwZzDSRXMhTzF{VjDteZRidnRiYYSgNVAhfU1iYYSgNVIhcHK|IHL5JJRzgXCjbjDicJVmKHO2YXnubY5o NXPSU4ZZOjJ6M{KzNlE>
human BJeH cells NHHWVFBHfW6ldHnvckBie3OjeR?= NG\ESHM3KGh? NHXqSHFKdmS3Y4Tpc44hd2ZicnXhZ5RqfmVib4j5[4VvKHOyZXPp[ZMheHKxZIXjeIlwdiCrbjDoeY1idiCESnXIJINmdGy|IHX4dJJme3Orbnege4lt\CC2eYDlJHJCWyCjZoTldkA3KGi{czDifUBFS0ZvYnHz[YQh\myxdzDjfZRwdWW2cnnjJIFv[Wy7c3nz M1[2fFIzQDN{M{Kx

... 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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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.

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID