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JKE-1674 Sale

目录号 : GC47477

A GPX4 inhibitor and active metabolite of ML-210

JKE-1674 Chemical Structure

Cas No.:2421119-60-8

规格 价格 库存 购买数量
1 mg
¥480.00
现货
5 mg
¥2,039.00
现货

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Sample solution is provided at 25 µL, 10mM.

产品文档

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产品描述

JKE-1674 is an inhibitor of glutathione peroxidase 4 (GPX4) and an active metabolite of the GPX4 inhibitor ML-210 .1 JKE-1674 reduces viability of LOX-IMVI cancer cells (EC50 = 0.03 µM) and in a panel of additional cancer cell lines, an effect that can be blocked by the ferroptosis inhibitor ferrostatin-1 .

1.Eaton, J.K., Furst, L., Ruberto, R.A., et al.Selective covalent targeting of GPX4 using masked nitrile-oxide electrophilesNat. Chem. Biol.16(5)497-506(2020)

Chemical Properties

Cas No. 2421119-60-8 SDF
Canonical SMILES O=C(C(C[N+]([O-])=O)=NO)N1CCN(C(C2=CC=C(Cl)C=C2)C3=CC=C(Cl)C=C3)CC1
分子式 C20H20Cl2N4O4 分子量 451.3
溶解度 DMSO: soluble 储存条件 4°C, protect from light
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.2158 mL 11.0791 mL 22.1582 mL
5 mM 0.4432 mL 2.2158 mL 4.4316 mL
10 mM 0.2216 mL 1.1079 mL 2.2158 mL
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Research Update

RB1-deficient prostate tumor growth and metastasis are vulnerable to ferroptosis induction via the E2F/ACSL4 axis

J Clin Invest 2023 Mar 16;e166647.PMID:36928314DOI:10.1172/JCI166647

Inactivation of the RB1 tumor suppressor gene is common in several types of therapy-resistant cancers, including metastatic castration-resistant prostate cancer, and predicts poor clinical outcomes. Effective therapeutic strategies against RB1-deficient cancers, however, remain elusive. Here we showed that RB1-loss/E2F activation sensitized cancer cells to ferroptosis, a form of regulated cell death driven by iron-dependent lipid peroxidation, by upregulating expression of ACSL4 and enriching ACSL4-dependent arachidonic acid-containing phospholipids, which are key components of ferroptosis execution. ACSL4 appeared to be a direct E2F target gene and was critical to RB1 loss-induced sensitization to ferroptosis. Importantly, using cell line-derived xenografts and genetically engineered tumor models, we demonstrated that induction of ferroptosis in vivo by JKE-1674, a highly selective and stable GPX4 inhibitor, blocked RB1-deficient prostate tumor growth and metastasis and led to improved survival of the mice. Thus, our findings uncover an RB/E2F/ACSL4 molecular axis that governs ferroptosis, and also suggest a promising approach for the treatment of RB1-deficient malignancies.