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cRIPGBM Sale

目录号 : GC34543

cRIPGBM是RIPGBM的促凋亡衍生物,是通过与受体相互作用蛋白激酶2(RIPK2)结合,诱导GBM肿瘤干细胞凋亡的选择性诱导剂,对GBM-1细胞的EC50值为68nM。

cRIPGBM Chemical Structure

Cas No.:2361988-76-1

规格 价格 库存 购买数量
5mg
¥4,950.00
现货
10mg
¥7,650.00
现货

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Sample solution is provided at 25 µL, 10mM.

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产品描述

cRIPGBM, a proapoptotic derivative of RIPGBM, a cell type-selective inducer of apoptosis in GBM cancer stem cells (CSCs) by binding to receptor-interacting protein kinase 2 (RIPK2), with an EC50 of 68 nM in GBM-1 cells[1]. RIPK2[1].

[1]. Lucki NC, et al. A cell type-selective apoptosis-inducing small molecule for the treatment of brain cancer. Proc Natl Acad Sci U S A. 2019 Mar 26;116(13):6435-6440.

Chemical Properties

Cas No. 2361988-76-1 SDF
Canonical SMILES O=C1C2=C([N+](CC3=CC=CC=C3)=C(C)N2CC4=CC=CC=C4)C(C5=C1C=CC=C5)=O
分子式 C26H21N2O2 分子量 393.46
溶解度 Soluble in DMSO 储存条件 Store at -20°C
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1 mg 5 mg 10 mg
1 mM 2.5416 mL 12.7078 mL 25.4155 mL
5 mM 0.5083 mL 2.5416 mL 5.0831 mL
10 mM 0.2542 mL 1.2708 mL 2.5416 mL
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Research Update

A cell type-selective apoptosis-inducing small molecule for the treatment of brain cancer

Proc Natl Acad Sci U S A 2019 Mar 26;116(13):6435-6440.PMID:30846550DOI:PMC6442583

Glioblastoma multiforme (GBM; grade IV astrocytoma) is the most prevalent and aggressive form of primary brain cancer. A subpopulation of multipotent cells termed GBM cancer stem cells (CSCs) play a critical role in tumor initiation, tumor maintenance, metastasis, drug resistance, and recurrence following surgery. Here we report the identification of a small molecule, termed RIPGBM, from a cell-based chemical screen that selectively induces apoptosis in multiple primary patient-derived GBM CSC cultures. The cell type-dependent selectivity of this compound appears to arise at least in part from redox-dependent formation of a proapoptotic derivative, termed cRIPGBM, in GBM CSCs. cRIPGBM induces caspase 1-dependent apoptosis by binding to receptor-interacting protein kinase 2 (RIPK2) and acting as a molecular switch, which reduces the formation of a prosurvival RIPK2/TAK1 complex and increases the formation of a proapoptotic RIPK2/caspase 1 complex. In an orthotopic intracranial GBM CSC tumor xenograft mouse model, RIPGBM was found to significantly suppress tumor formation in vivo. Our chemical genetics-based approach has identified a drug candidate and a potential drug target that provide an approach to the development of treatments for this devastating disease.