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IKE (Imidazole ketone erastin )

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Chemical Structure| 1801530-11-9 同义名 : Imidazole Ketone Erastin;PUN30119;IKE
CAS号 : 1801530-11-9
货号 : A1155014
分子式 : C35H35ClN6O5
纯度 : 99%+
分子量 : 655.143
MDL号 : MFCD31813799
存储条件：

粉末 Sealed in dry,2-8°C

液体 -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 105 mg/mL(160.27 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO
动物实验配方：
生物活性
描述 Ferroptosis is a form of regulated cell death that can be induced by inhibition of the cystine-glutamate antiporter, system xc-. Among the existing system xc- inhibitors, imidazole ketone erastin (IKE) is a potent, metabolically stable inhibitor of system xc- and inducer of ferroptosis potentially suitable for in vivo applications[1]. The IC50 of GSH depletion by IKE was 34 nM in SUDHL6 cells. Analysis of lipid reactive oxygen species (ROS) by flow cytometry using the lipid peroxidation probe C11-BODIPY revealed a dose-dependent increase in lipid ROS upon IKE treatment in SUDHL6 cells. Immunofluorescence staining with an anti-dihydropyridine-MDA-lysine adduct antibody (mAb 1F83) revealed that dihydropyridine-MDA-lysine adduct abundance was increased upon IKE treatment[1]. The system xc- component SLC7A11, prostaglandin-endoperoxide synthase 2 (PTGS2, which encodes cyclooxygenase-2), and ChaC GSH-specific γ-glutamylcyclotransferase 1 (CHAC1) expression was significantly increased in SUDHL6 cells following IKE treatment[1]. IKE exhibits antitumor activity in DLBCL (diffuse large B cell lymphoma) xenograft model, which correlates with an increase of lipid peroxidation in tumors. These findings suggest that IKE can be effective as a potential therapeutic regimen for DLBCL[1].
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

1.53mL

0.31mL

0.15mL

7.63mL

1.53mL

0.76mL

15.26mL

3.05mL

1.53mL
参考文献

[1]Zhang Y, Tan H, Daniels JD, Zandkarimi F, Liu H, Brown LM, Uchida K, O'Connor OA, Stockwell BR. Imidazole Ketone Erastin Induces Ferroptosis and Slows Tumor Growth in a Mouse Lymphoma Model. Cell Chem Biol. 2019 May 16;26(5):623-633.e9. doi: 10.1016/j.chembiol.2019.01.008. Epub 2019 Feb 21. PMID: 30799221; PMCID: PMC6525071.