Erastin

目录号:S7242

Erastin Chemical Structure

Molecular Weight(MW): 547.04

Erastin是一种ferroptosis激活剂,通过作用于线粒体VDAC而起作用,选择性作用于携带致癌基因RAS的肿瘤细胞。

规格 价格 库存 购买数量  
RMB 1199.29 现货
RMB 6303.21 现货
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客户使用Selleck该产品发表文献14篇:

客户使用该产品的11个实验数据:

  • 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.

产品安全说明书

Ferroptosis抑制剂选择性比较

生物活性

产品描述 Erastin是一种ferroptosis激活剂,通过作用于线粒体VDAC而起作用,选择性作用于携带致癌基因RAS的肿瘤细胞。
靶点
Ferroptosis [1]
体外研究

Erastin选择性致死致癌的Ras突变体细胞系,并触发独特的fe依赖性的称为ferroptosis的非凋亡细胞死亡。[1] [2] Erastin直接结合VDAC2并且使得通过NADH-依赖方式产生ROS导致线粒体损害,在一些表达激活突变的肿瘤细胞中,通过RAS-RAF-MEK途径诱导细胞死亡。[3] 此外,erastin通过诱导ROS介导的CID(胱天蛋白酶非依赖性细胞死亡),强烈增强了野生型EGFR细胞的作用。[4]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
human CCF-STTG1 cells Mn;6SpVv[3Srb36gZZN{[Xl? M3m2e2lvcGmkaYTpc44hd2ZiWHP0JIlvKGi3bXHuJGNETi2VVGTHNUBk\WyuczDhd5Nme3OnZDDhd{BodHW2YX3heIUhemWuZXHz[UBi\nSncjCyJIhzeyCkeTDmcJVwem:vZYTyfUwhUUN3ME2wMlIh|ryPLh?= MW[yOlI{OTF3Nh?=
human HeLa cells Ml\CSpVv[3Srb36gZZN{[Xl? MoTYTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iSHXMZUBk\WyuczygSWM2OD1yLk[g{txONg>? NHrpS4MyPzV4OEe0PC=>
human BJ cells NUPzeWtZTnWwY4Tpc44h[XO|YYm= Ml3UTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iQlqgZ4VtdHNiZYjwdoV{e2mwZzDUSXJVNCCOVDygV3Qh[W6mIGLBV{BIOTKYIH31eIFvfCCpZX7ld{Bk\WyuczDpckBxemW|ZX7j[UBw\iCSRD25PFA2QSCkeTD0dplx[W5iYnz1[UBmgGOudYPpc44hdWW2aH;kMEBKSzVyPUCuPUDPxE1w NH;zVpcyPzV4OEe0PC=>
human HT1080 cells M161VWZ2dmO2aX;uJIF{e2G7 Ml\xTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iSGSxNFgxKGOnbHzzJIlvKHC{ZYPlcoNmKG:oIGDEMVk5ODV7IHL5JJRzgXCjbjDicJVmKGW6Y3z1d4lwdiCvZYToc4QtKEmFNUC9NUDPxE1w MXKxO|U3QDd2OB?=
human SVR cells NFLKcVdHfW6ldHnvckBie3OjeR?= NWHMPHNEUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gV3ZTKGOnbHzzMEBGSzVyPUKuOUDPxE1w NF3RZ2cyPzV4OEe0PC=>
human MES-SA cells MYPGeY5kfGmxbjDhd5NigQ>? NV2wSoxJUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gUWVUNVODIHPlcIx{NCCHQ{WwQVMh|ryPLh?= MWWxO|U3QDd2OB?=
human SKUT cells M{nNOmZ2dmO2aX;uJIF{e2G7 NUHNeoZsUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gV2tWXCClZXzsd{whTUN3ME20JO69VS5? NGm2bZEyPzV4OEe0PC=>
human Calu1 cells MWjGeY5kfGmxbjDhd5NigQ>? NFjqR2NKdmirYnn0bY9vKG:oIHj1cYFvKEOjbIWxJINmdGy|IHX4dJJme3OrbnegT3JCWyC5aYToJIFkfGm4YYTpcochdXW2YYTpc45{KGK7IITyfZBidiCkbIXlJIV5[2y3c3nvckBie3OjeTygTWM2OD12IN88UU4> NWr6UYxKOTd3Nki3OFg>
human LNCaP cells NHvSbnFHfW6ldHnvckBie3OjeR?= MlPCTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iTF7DZXAh[2WubIOsJGVEPTB;NjFOwG0v NXPVPHU4OTd3Nki3OFg>
human U2OS cells M36yPGZ2dmO2aX;uJIF{e2G7 NHXHb4JKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDVNm9UKGOnbHzzMEBGSzVyPU[g{txONg>? Mn\YNVc2Pjh5NEi=
human TC32 cells NIPo[FNHfW6ldHnvckBie3OjeR?= Ml\VTY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iVFOzNkBk\Wyucx?= NFLFV3QyPzV4OEe0PC=>
human SK-N-MC cells MVjGeY5kfGmxbjDhd5NigQ>? MV7JcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCVSz3OMW1EKGOnbHzzMEBGSzVyPUGwJO69VS5? NHi4UmIyPzV4OEe0PC=>
human U937 cells M1PNN2Z2dmO2aX;uJIF{e2G7 NIP5T|dKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDVPVM4KGOnbHzzMEBGSzVyPUGwJO69VS5? MoLBNVc2Pjh5NEi=
human TC71 cells MX3GeY5kfGmxbjDhd5NigQ>? NVzRT21SUW6mdXP0bY9vKG:oIHPlcIwh\GWjdHigbY4hcHWvYX6gWGM4OSClZXzsd{whTUN3ME2xNEDPxE1w M2TvVlE4PTZ6N{S4
human BJ cells M4jBfGZ2dmO2aX;uJIF{e2G7 M33C[Glv\HWldHnvckBw\iClZXzsJIRm[XSqIHnuJHRGWlRiZYjwdoV{e2mwZzDoeY1idiCESjDj[YxteyxiRVO1NF0yOCEQvF2u MUexO|U3QDd2OB?=
human EWS502 cells Mli0SpVv[3Srb36gZZN{[Xl? NHf2T4dKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDFW3M2ODJiY3XscJMtKEWFNUC9NVAh|ryPLh?= NWDBTphpOTd3Nki3OFg>
human Hs51.T cells MUfGeY5kfGmxbjDhd5NigQ>? NGnnR2RKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDId|UyNlRiY3XscJMtKEWFNUC9NVIh|ryPLh?= NGPPOIMyPzV4OEe0PC=>
human Hs925.T cells MWHGeY5kfGmxbjDhd5NigQ>? MV;JcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCKc{myOU5VKGOnbHzzMEBGSzVyPUG3JO69VS5? MkHzNVc2Pjh5NEi=
human HOS cells M{PnZ2Z2dmO2aX;uJIF{e2G7 NFjUVVJKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDIU3Mh[2WubIOgMEBGSzVyPUG3JO69VS5? M4HyblE4PTZ6N{S4
human MX2 cells MWPGeY5kfGmxbjDhd5NigQ>? NED6ZpJKdmS3Y4Tpc44hd2ZiY3XscEBl\WG2aDDpckBpfW2jbjDNXFIh[2WubIOsJGVEPTB;MUig{txONg>? NEHrbWkyPzV4OEe0PC=>
human A673 cells M1TFbmZ2dmO2aX;uJIF{e2G7 MkPETY5lfWO2aX;uJI9nKGOnbHyg[IVifGhiaX6gbJVu[W5iQU[3N{Bk\WyuczygSWM2OD1|MDFOwG0v NIrKUJcyPzV4OEe0PC=>
human BJ cells MXLGeY5kfGmxbjDhd5NigQ>? MWXJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCESjDj[YxteyCneIDy[ZN{cW6pIGTFVnQtKEyWLDDTWEBidmRiUlHTJGcyOlZibYX0ZY51KGenbnXzJIlvKHC{ZYPlcoNmKG:oIGWwNVI3KGK7IITyfZBidiCkbIXlJIV5[2y3c3nvckBu\XSqb3SsJGlEPTB;M{GuNkDPxE1w MnjPNVc2Pjh5NEi=
human BJ cells NF[4bHBHfW6ldHnvckBie3OjeR?= M4Hod|kh|ryP MVvJcoR2[3Srb36gc4Yh[2WubDDk[YF1cCCrbjDoeY1idiCESjDj[YxteyCneIDy[ZN{cW6pIGTFVnQtKEyWLDDTWEBidmRiUlHTJGcyOlZibYX0ZY51KGenbnXzJINmdGy|IHH0JFkhfU1w M4e5SFE4PTZ6N{S4
human BJ cells M{DIT2Z2dmO2aX;uJIF{e2G7 M3W2fFQvPiEQvF2= MoLsTY5kemWjc3WgbY4hcW62cnHj[YxtfWyjcjDvfIll[XSrdnWgd5Bm[2mnczDpckBpfW2jbjDCTkBk\WyuczDlfJBz\XO|aX7nJHRGWlRuIFzUMEBUXCCjbnSgVmFUKEdzMm[gcZV1[W62IHflcoV{KGOnbHzzJIF1KDRwNjD1US=> MXWxO|U3QDd2OB?=
human BJeLR cells M2jodmN6fG:2b4jpZ:Kh[XO|YYm= NYWxRZplOTBizszN NU\KNVZ5OTJiaB?= Mlz0R5l1d3SxeHnjbZR6KGGpYXnud5QhcHWvYX6gRmpmVFJiY3XscJMh\XiycnXzd4lv\yCUQWOgS|EzXiCvdYThcpQh[XRiMUCgeW0h[XRiMUKgbJJ{KGK7IITyfZBidiCkbIXlJJN1[WmwaX7n NH\4[FMzOjh|MkOyNS=>
human BJeH cells NH7rc4xHfW6ldHnvckBie3OjeR?= NHu5enE3KGh? MmHsTY5lfWO2aX;uJI9nKHKnYXP0bZZmKG:6eXflckB{eGWlaXXzJJBzd2S3Y4Tpc44hcW5iaIXtZY4hSkqnSDDj[YxteyCneIDy[ZN{cW6pIIfpcIQhfHmyZTDSRXMh[W[2ZYKgOkBpenNiYomgSGNHNWKjc3XkJIZtd3diY4n0c41mfHKrYzDhcoFtgXOrcx?= NYPSO2pxOjJ6M{KzNlE>

... Click to View More Cell Line Experimental Data

推荐的实验操作(此推荐来自于公开的文献所以Selleck并不保证其有效性)

细胞实验:[1]
+ 展开
  • Cell lines: BJ-TERT/LT/ST/RASV12细胞
  • Concentrations: 5 or 10 μg/mL
  • Incubation Time: 6-11小时
  • Method: BJ-TERT/LT/ST/RASV12细胞接种在100 mm平皿中,并使其生长过夜。细胞用erastin(5或10微克/毫升)处理6,8,或11小时。camptothecin处理(0.4微克/毫升)的对照被维持,在接种的时候处理20小时。处理后,细胞用胰蛋白酶/EDTA孵育并用含血清的新鲜培养基洗1次,然后用磷酸盐缓冲盐水洗涤两次。细胞同1×结合缓冲液重悬。100 μL重悬细胞在5μL的膜联蛋白V-FITC和碘化丙啶iodiode在黑暗中孵育15分钟。然后加入400 μl的1×结合缓冲液S并用流式细胞仪分析。采集数据,并使用CellQuest软件进行分析。只有不被碘化丙啶染色的活细胞使用FL1通道的膜联蛋白V-FITC染色分析。
    (Only for Reference)

溶解度 (25°C)

体外 DMSO 19 mg/mL (34.73 mM)
Water Insoluble
Ethanol Insoluble
体内 从左到右依次将纯溶剂加入产品,现配现用(数据来自Selleck实验检测而非文献):
5% DMSO+corn oil
2.5mg/mL

* 溶解度检测是由Selleck技术部门检测的,可能会和文献中提供的溶解度有所差异,这是由于生产工艺和批次不同产生的正常现象。请按照顺序依次加入各个纯溶剂。

化学数据

分子量 547.04
化学式

C30H31ClN4O4

CAS号 571203-78-6
稳定性 powder
in solvent
别名 N/A

计算器

摩尔浓度计算器

摩尔浓度计算器

本计算器可帮助您计算出特定溶液中溶质的质量、溶液浓度和体积之间的关系,公式为:

质量 (g) = 浓度 (mol/L) x 体积 (L) x 分子量 (g/mol)

摩尔浓度计算公式

  • 质量
    浓度
    体积
    分子量

*在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。

稀释计算器

稀释计算器

用本工具协助配置特定浓度的溶液,使用的计算公式为:

开始浓度 x 开始体积 = 最终浓度 x 最终体积

稀释公式

稀释公式一般简略地表示为: C1V1 = C2V2 ( 输入 输出 )

  • C1
    V1
    C2
    V2

在配置溶液时,请务必参考Selleck产品标签上、MSDS / COA(可在Selleck的产品页面获得)批次特异的分子量使用本工具。.

连续稀释计算器方程

  • 连续稀释

  • 计算结果

  • 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):
分子量计算器

分子量计算器

通过输入化合物的化学式来计算其分子量:

总分子量:g/mol

注:化学分子式大小写敏感。C10H16N2O2 c10h16n2o2

摩尔浓度计算器

质量 浓度 体积 分子量
计算

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID