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. 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 NWjiW2tPTnWwY4Tpc44h[XO|YYm= MWXJcohq[mm2aX;uJI9nKFildDDpckBpfW2jbjDDR2YuW1SWR{GgZ4VtdHNiYYPz[ZN{\WRiYYOg[4x2fGGvYYTlJJJmdGWjc3WgZYZ1\XJiMjDodpMh[nliZnz1c5JwdWW2comsJGlEPTB;MD6yJO69VS5? M1HOb|I3OjNzMUW2
human HeLa cells NYG4UYdjTnWwY4Tpc44h[XO|YYm= NHK1N3FKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDI[WxiKGOnbHzzMEBGSzVyPUCuOkDPxE1w Mn\yNVc2Pjh5NEi=
human BJ cells Ml;1SpVv[3Srb36gZZN{[Xl? NYrPNWt3UW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gRmoh[2WubIOg[ZhxemW|c3nu[{BVTVKWLDDMWEwhW1RiYX7kJHJCWyCJMULWJI12fGGwdDDn[Y5meyClZXzsd{BqdiCycnXz[Y5k\SCxZjDQSE06QDB3OTDifUB1enmyYX6gZox2\SCneHPseZNqd25ibXX0bI9lNCCLQ{WwQVAvQSEQvF2u M2PM[VE4PTZ6N{S4
human HT1080 cells NIHIb3NHfW6ldHnvckBie3OjeR?= MoTRTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iSGSxNFgxKGOnbHzzJIlvKHC{ZYPlcoNmKG:oIGDEMVk5ODV7IHL5JJRzgXCjbjDicJVmKGW6Y3z1d4lwdiCvZYToc4QtKEmFNUC9NUDPxE1w NWT2co9UOTd3Nki3OFg>
human SVR cells MkntSpVv[3Srb36gZZN{[Xl? M4LLU2lv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIGPWVkBk\WyuczygSWM2OD1{LkWg{txONg>? NF3TdYgyPzV4OEe0PC=>
human MES-SA cells NYLOTppTTnWwY4Tpc44h[XO|YYm= NGC3VmRKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDNSXMuW0FiY3XscJMtKEWFNUC9N{DPxE1w NYnhWFQ1OTd3Nki3OFg>
human SKUT cells MlqySpVv[3Srb36gZZN{[Xl? NWDmWpBZUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gV2tWXCClZXzsd{whTUN3ME20JO69VS5? NYixXnY3OTd3Nki3OFg>
human Calu1 cells MlzrSpVv[3Srb36gZZN{[Xl? MVfJcohq[mm2aX;uJI9nKGi3bXHuJGNidHVzIHPlcIx{KGW6cILld5NqdmdiS2LBV{B4cXSqIHHjeIl3[XSrbnegcZV1[XSrb37zJIJ6KHS{eYDhckBjdHWnIHX4Z4x2e2mxbjDhd5NigSxiSVO1NF01KM7:TT6= M13rVlE4PTZ6N{S4
human LNCaP cells M2eyXmZ2dmO2aX;uJIF{e2G7 NGXIR2VKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDMUmNiWCClZXzsd{whTUN3ME22JO69VS5? NWT1V4JiOTd3Nki3OFg>
human U2OS cells M2j2e2Z2dmO2aX;uJIF{e2G7 M3rWfWlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIGWyU3Mh[2WubIOsJGVEPTB;NjFOwG0v NGHIdXQyPzV4OEe0PC=>
human TC32 cells MoDhSpVv[3Srb36gZZN{[Xl? M4\EfGlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIGTDN|Ih[2WubIO= NELMSJcyPzV4OEe0PC=>
human SK-N-MC cells Ml3xSpVv[3Srb36gZZN{[Xl? MmXyTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iU1utUk1OSyClZXzsd{whTUN3ME2xNEDPxE1w MXWxO|U3QDd2OB?=
human U937 cells M{iyeGZ2dmO2aX;uJIF{e2G7 M{nzWGlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIGW5N|ch[2WubIOsJGVEPTB;MUCg{txONg>? MVexO|U3QDd2OB?=
human TC71 cells M3[wR2Z2dmO2aX;uJIF{e2G7 NIDFZYNKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDUR|cyKGOnbHzzMEBGSzVyPUGwJO69VS5? NVLSZm84OTd3Nki3OFg>
human BJ cells NUi1b|hXTnWwY4Tpc44h[XO|YYm= NXHnPYJTUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hXEWUVDDlfJBz\XO|aX7nJIh2dWGwIFLKJINmdGy|LDDFR|UxRTFyIN88UU4> MnLXNVc2Pjh5NEi=
human EWS502 cells M4Dr[mZ2dmO2aX;uJIF{e2G7 MWfJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCHV2O1NFIh[2WubIOsJGVEPTB;MUCg{txONg>? M{fBclE4PTZ6N{S4
human Hs51.T cells M2Ww[WZ2dmO2aX;uJIF{e2G7 M{myXGlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIFjzOVEvXCClZXzsd{whTUN3ME2xNkDPxE1w M3nVS|E4PTZ6N{S4
human Hs925.T cells Mn3MSpVv[3Srb36gZZN{[Xl? NHPkU3VKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDId|kzPS6WIHPlcIx{NCCHQ{WwQVE4KM7:TT6= MnXLNVc2Pjh5NEi=
human HOS cells NYfueIZTTnWwY4Tpc44h[XO|YYm= M1\GVGlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIFjPV{Bk\WyuczCsJGVEPTB;MUeg{txONg>? MnTUNVc2Pjh5NEi=
human MX2 cells MlT3SpVv[3Srb36gZZN{[Xl? M4DM[Wlv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJIh2dWGwIF3YNkBk\WyuczygSWM2OD1zODFOwG0v NXK3NWJrOTd3Nki3OFg>
human A673 cells NFHUTYlHfW6ldHnvckBie3OjeR?= MUXJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCDNkezJINmdGy|LDDFR|UxRTNyIN88UU4> MYmxO|U3QDd2OB?=
human BJ cells MWjGeY5kfGmxbjDhd5NigQ>? MoHGTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iQlqgZ4VtdHNiZYjwdoV{e2mwZzDUSXJVNCCOVDygV3Qh[W6mIGLBV{BIOTKYIH31eIFvfCCpZX7ld{BqdiCycnXz[Y5k\SCxZjDVNFEzPiCkeTD0dplx[W5iYnz1[UBmgGOudYPpc44hdWW2aH;kMEBKSzVyPUOxMlIh|ryPLh?= MmLENVc2Pjh5NEi=
human BJ cells NV3afmxxTnWwY4Tpc44h[XO|YYm= NHrLPW86KM7:TR?= NFrEXJdKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDCTkBk\WyuczDlfJBz\XO|aX7nJHRGWlRuIFzUMEBUXCCjbnSgVmFUKEdzMm[gcZV1[W62IHflcoV{KGOnbHzzJIF1KDlidV2u MUSxO|U3QDd2OB?=
human BJ cells MULGeY5kfGmxbjDhd5NigQ>? MoCzOE43KM7:TR?= NX;TWHFSUW6lcnXhd4UhcW5iaX70doFk\WyudXzhdkBwgGmmYYTpeoUhe3CnY3nld{BqdiCqdX3hckBDUiClZXzsd{BmgHC{ZYPzbY5oKFSHUmSsJGxVNCCVVDDhcoQhWkGVIFexNnYhdXW2YX70JIdmdmW|IHPlcIx{KGG2IESuOkB2VQ>? NEC4SIwyPzV4OEe0PC=>
human BJeLR cells NYfuU2M3S3m2b4TvfIlkyqCjc4PhfS=> MV6xNEDPxE1? M3PmO|EzKGh? MlvCR5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gRmpmVFJiY3XscJMh\XiycnXzd4lv\yCUQWOgS|EzXiCvdYThcpQh[XRiMUCgeW0h[XRiMUKgbJJ{KGK7IITyfZBidiCkbIXlJJN1[WmwaX7n Mme0NlI5OzJ|MkG=
human BJeH cells NV7RbIJ3TnWwY4Tpc44h[XO|YYm= MVW2JIg> NILn[HFKdmS3Y4Tpc44hd2ZicnXhZ5RqfmVib4j5[4VvKHOyZXPp[ZMheHKxZIXjeIlwdiCrbjDoeY1idiCESnXIJINmdGy|IHX4dJJme3Orbnege4lt\CC2eYDlJHJCWyCjZoTldkA3KGi{czDifUBFS0ZvYnHz[YQh\myxdzDjfZRwdWW2cnnjJIFv[Wy7c3nz NGi5UGgzOjh|MkOyNS=>

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 順序で溶剤を入れること:
5% DMSO+corn oil
2.5mg/mL

* 溶解度検測はSelleck技術部門によって行いますので、文献より提供された溶解度と差異がある可能性がありますが、生産工芸と不同ロット(lot)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
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、阻害剤の保管する方法、細胞実験や動物実験に注意すべきな点を全部含めており、製品を取扱う時よくあった質問に対して取扱説明書でお答えいたします。

Handling Instructions

他の質問がある場合は、お気軽くお問合せください。

  • * 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