Erastin

製品コードS7242

Erastin化学構造

分子量(MW):547.04

Erastin is a ferroptosis activator by acting on mitochondrial VDAC, exhibiting selectivity for tumor cells bearing oncogenic RAS.

サイズ 価格(税別)  
JPY 24402.00
JPY 127820.00

カスタマーフィードバック(8)

  • 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.

製品安全説明書

Ferroptosis阻害剤の選択性比較

生物活性

製品説明 Erastin is a ferroptosis activator by acting on mitochondrial VDAC, exhibiting selectivity for tumor cells bearing oncogenic RAS.
ターゲット
Ferroptosis [1]
体外試験

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]

細胞データ
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human CCF-STTG1 cells MYPGeY5kfGmxbjDhd5NigQ>? M4XkUGlvcGmkaYTpc44hd2ZiWHP0JIlvKGi3bXHuJGNETi2VVGTHNUBk\WyuczDhd5Nme3OnZDDhd{BodHW2YX3heIUhemWuZXHz[UBi\nSncjCyJIhzeyCkeTDmcJVwem:vZYTyfUwhUUN3ME2wMlIh|ryPLh?= MVKyOlI{OTF3Nh?=
human HeLa cells NXP4[Y1ETnWwY4Tpc44h[XO|YYm= MkniTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iSHXMZUBk\WyuczygSWM2OD1yLk[g{txONg>? MoD3NVc2Pjh5NEi=
human BJ cells M3;zPGZ2dmO2aX;uJIF{e2G7 NIfU[XJKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDCTkBk\WyuczDlfJBz\XO|aX7nJHRGWlRuIFzUMEBUXCCjbnSgVmFUKEdzMm[gcZV1[W62IHflcoV{KGOnbHzzJIlvKHC{ZYPlcoNmKG:oIGDEMVk5ODV7IHL5JJRzgXCjbjDicJVmKGW6Y3z1d4lwdiCvZYToc4QtKEmFNUC9NE46KM7:TT6= MUexO|U3QDd2OB?=
human HT1080 cells NEHrO2RHfW6ldHnvckBie3OjeR?= MoHLTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iSGSxNFgxKGOnbHzzJIlvKHC{ZYPlcoNmKG:oIGDEMVk5ODV7IHL5JJRzgXCjbjDicJVmKGW6Y3z1d4lwdiCvZYToc4QtKEmFNUC9NUDPxE1w M3yyWlE4PTZ6N{S4
human SVR cells Mm\TSpVv[3Srb36gZZN{[Xl? Mn7HTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iU2\SJINmdGy|LDDFR|UxRTJwNTFOwG0v M1TjdFE4PTZ6N{S4
human MES-SA cells MVfGeY5kfGmxbjDhd5NigQ>? NV7QcYMxUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gUWVUNVODIHPlcIx{NCCHQ{WwQVMh|ryPLh?= MWOxO|U3QDd2OB?=
human SKUT cells NEWwcXJHfW6ldHnvckBie3OjeR?= MnjFTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iU1vVWEBk\WyuczygSWM2OD12IN88UU4> MlzaNVc2Pjh5NEi=
human Calu1 cells NF7SeHVHfW6ldHnvckBie3OjeR?= M2r4XGlvcGmkaYTpc44hd2ZiaIXtZY4hS2GudUGgZ4VtdHNiZYjwdoV{e2mwZzDLVmFUKHerdHigZYN1cX[jdHnu[{BufXSjdHnvcpMh[nlidIL5dIFvKGKudXWg[ZhkdHW|aX;uJIF{e2G7LDDJR|UxRTRizszNMi=> NUPxb2NXOTd3Nki3OFg>
human LNCaP cells NXewdmc3TnWwY4Tpc44h[XO|YYm= M2HKPGlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIFzOR4FRKGOnbHzzMEBGSzVyPU[g{txONg>? NFXlTGsyPzV4OEe0PC=>
human U2OS cells NFHZ[JJHfW6ldHnvckBie3OjeR?= MkO0TY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iVULPV{Bk\WyuczygSWM2OD14IN88UU4> MlnONVc2Pjh5NEi=
human TC32 cells MniySpVv[3Srb36gZZN{[Xl? M2jzOmlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIGTDN|Ih[2WubIO= M1rEclE4PTZ6N{S4
human SK-N-MC cells NFzNcG5HfW6ldHnvckBie3OjeR?= MXnJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCVSz3OMW1EKGOnbHzzMEBGSzVyPUGwJO69VS5? NVr2WmwxOTd3Nki3OFg>
human U937 cells MmmxSpVv[3Srb36gZZN{[Xl? NXzzc4VlUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gWVk{PyClZXzsd{whTUN3ME2xNEDPxE1w MV2xO|U3QDd2OB?=
human TC71 cells MkDrSpVv[3Srb36gZZN{[Xl? MXvJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCWQ{exJINmdGy|LDDFR|UxRTFyIN88UU4> NWDuNVRYOTd3Nki3OFg>
human BJ cells MUjGeY5kfGmxbjDhd5NigQ>? M{nhO2lv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJHRGWlRiZYjwdoV{e2mwZzDoeY1idiCESjDj[YxteyxiRVO1NF0yOCEQvF2u MXuxO|U3QDd2OB?=
human EWS502 cells NFLpOWpHfW6ldHnvckBie3OjeR?= MUnJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCHV2O1NFIh[2WubIOsJGVEPTB;MUCg{txONg>? MYexO|U3QDd2OB?=
human Hs51.T cells NY\1NoZLTnWwY4Tpc44h[XO|YYm= MVnJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCKc{WxMnQh[2WubIOsJGVEPTB;MUKg{txONg>? NEfZU2gyPzV4OEe0PC=>
human Hs925.T cells NEXyVGdHfW6ldHnvckBie3OjeR?= M2L2NGlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIFjzPVI2NlRiY3XscJMtKEWFNUC9NVch|ryPLh?= MUCxO|U3QDd2OB?=
human HOS cells NX\BOFNrTnWwY4Tpc44h[XO|YYm= MYPJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCKT2OgZ4VtdHNiLDDFR|UxRTF5IN88UU4> MonBNVc2Pjh5NEi=
human MX2 cells NIXWdHpHfW6ldHnvckBie3OjeR?= MUnJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCPWEKgZ4VtdHNuIFXDOVA:OThizszNMi=> M4W4e|E4PTZ6N{S4
human A673 cells M3HL[WZ2dmO2aX;uJIF{e2G7 NYntdJh{UW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gRVY4OyClZXzsd{whTUN3ME2zNEDPxE1w NUfaeIQzOTd3Nki3OFg>
human BJ cells M1\aSWZ2dmO2aX;uJIF{e2G7 MoHQTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iQlqgZ4VtdHNiZYjwdoV{e2mwZzDUSXJVNCCOVDygV3Qh[W6mIGLBV{BIOTKYIH31eIFvfCCpZX7ld{BqdiCycnXz[Y5k\SCxZjDVNFEzPiCkeTD0dplx[W5iYnz1[UBmgGOudYPpc44hdWW2aH;kMEBKSzVyPUOxMlIh|ryPLh?= MnzUNVc2Pjh5NEi=
human BJ cells NUDQT2VVTnWwY4Tpc44h[XO|YYm= Mm\ZPUDPxE1? NVnafZB1UW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gRmoh[2WubIOg[ZhxemW|c3nu[{BVTVKWLDDMWEwhW1RiYX7kJHJCWyCJMULWJI12fGGwdDDn[Y5meyClZXzsd{BifCB7IIXNMi=> NH3KT5IyPzV4OEe0PC=>
human BJ cells NIjmT2JHfW6ldHnvckBie3OjeR?= M1nWcFQvPiEQvF2= NXvKVpBkUW6lcnXhd4UhcW5iaX70doFk\WyudXzhdkBwgGmmYYTpeoUhe3CnY3nld{BqdiCqdX3hckBDUiClZXzsd{BmgHC{ZYPzbY5oKFSHUmSsJGxVNCCVVDDhcoQhWkGVIFexNnYhdXW2YX70JIdmdmW|IHPlcIx{KGG2IESuOkB2VQ>? M4m3eFE4PTZ6N{S4
human BJeLR cells MUTDfZRwfG:6aXRCpIF{e2G7 MYexNEDPxE1? NWDmRYp[OTJiaB?= NHPVe2lEgXSxdH;4bYNqfHliYXfhbY5{fCCqdX3hckBDUmWOUjDj[YxteyCneIDy[ZN{cW6pIGLBV{BIOTKYIH31eIFvfCCjdDCxNEB2VSCjdDCxNkBpenNiYomgeJJ6eGGwIHLseYUhe3SjaX7pcoc> MlzUNlI5OzJ|MkG=
human BJeH cells MWPGeY5kfGmxbjDhd5NigQ>? MUi2JIg> M2LiUmlv\HWldHnvckBw\iC{ZXHjeIl3\SCxeInn[Y4he3CnY3nld{Bxem:mdXP0bY9vKGmwIHj1cYFvKEKMZVigZ4VtdHNiZYjwdoV{e2mwZzD3bYxlKHS7cHWgVmFUKGGodHXyJFYhcHK|IHL5JGRETi2kYYPl[EBndG:5IHP5eI9u\XS{aXOgZY5idHm|aYO= MWCyNlg{OjN{MR?=

多くの細胞株試験データを見る場合、クリックしてください

お薦めの試験操作(参考用のみ)

細胞試験: [1]
+ 展開
  • 細胞株: BJ-TERT/LT/ST/RASV12 cells
  • 濃度: 5 or 10 μg/mL
  • 反応時間: 6-11 hours
  • 実験の流れ: 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.
    (参考用のみ)

溶解度 (25°C)

体外 DMSO 19 mg/mL (34.73 mM)
Water Insoluble
Ethanol Insoluble
体内 左から(NMPから)右の順に溶剤を製品に加えます:
5% DMSO+corn oil
混合させたのち直ちに使用することを推奨します。
2.5mg/mL

* 溶解度測定はSelleck技術部門によって行われており、その他文献に示されている溶解度と差異がある可能性がありますが、同一ロットの生産工程で起きる正常な現象ですからご安心ください。

化学情報

分子量 547.04
化学式

C30H31ClN4O4

CAS No. 571203-78-6
保管
in solvent
別名 N/A

便利ツール

モル濃度計算器

モル濃度計算器

解決のために必要とされるマス、ボリュームまたは濃度を計算してください。

マス (g) = 濃度 (mol/L) x ボリューム (L) x 分子量 (g/mol)

モル濃度計算器方程式

  • マス
    濃度
    ボリューム
    分子量

*貯蔵液を準備するとき、常に、オンであるとわかる製品のバッチに特有の分子量を使って、を通してラベルとMSDS/COA(製品ページで利用可能な)。

希釈計算器

希釈計算器

貯蔵液を準備することを要求される希釈剤を計算してください. セレック希釈計算器は、以下の方程式に基づきます:

開始濃度 x 開始体積 = 最終濃度 x 最終体積

希釈の計算式

この方程式は、一般に略語を使われます:C1V1 = C2V2 ( 輸入 輸出 )

  • C1
    V1
    C2
    V2

常に貯蔵液を準備するとき、小びんラベルとMSDS/COA(オンラインで利用できる)で見つかる製品のバッチに特有の分子量を使ってください。

連続希釈計算器方程式

  • 連続希釈剤

  • 計算結果

  • C1=C0/X C1: LOG(C1):
    C2=C1/X C2: LOG(C2):
    C3=C2/X C3: LOG(C3):
    C4=C3/X C4: LOG(C4):
    C5=C4/X C5: LOG(C5):
    C6=C5/X C6: LOG(C6):
    C7=C6/X C7: LOG(C7):
    C8=C7/X C8: LOG(C8):
分子量計算器

分子量计算器

そのモル質量と元素組成を計算するために、合成物の化学式を入力してください:

総分子量:g/mol

チップス: 化学式は大文字と小文字の区別ができます。C10H16N2O2 c10h16n2o2

モル濃度計算器

マス 濃度 ボリューム 分子量

技術サポート

ストックの作り方、阻害剤の保管方法、細胞実験や動物実験の際に注意すべき点など、製品を取扱う時に問い合わせが多かった質問に対しては取扱説明書でお答えしています。

Handling Instructions

他に質問がある場合は、お気軽にお問い合わせください。

  • * 必須
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細胞株 試験類型 濃度 培養時間 溶剤類型 活性叙述 PMID