Name | cRIPGBM chloride |
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Description | cRIPGBM(chloride), an orally active, proapoptotic derivative. cRIPGBM can be generated from glioblastoma multiforme (GBM) cancer stem cells (CSCs). cRIPGBM(chloride) targets to receptor-interacting protein kinase 2 (RIPK2) to induce caspase 1-dependent apoptosis. cRIPGBM(chloride) suppresses the formation of RIPK2/TAK1 (prosurvival complex), and increases the formation of RIPK2/caspase 1 (proapoptotic complex). cRIPGBM(chloride) exerts potent anti-tumor activity in vivo in animal models[1]. |
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Related Catalog | |
Target |
Caspase-1 RIPK2 |
In Vitro | cRIPGBM(chloride) (0.25 μM;0-24 小时) 时间依赖性地激活半胱天冬酶 1、半胱天冬酶 9 和半胱天冬酶 7,以及 PARP 裂解[1]。 cRIPGBM(chloride) (0.125 μM, 0.25 μM;24 小时) 在 CBM-1 GBM CSCs[1] 中诱导 caspase 1 介导的细胞凋亡[1]。 Western Blot Analysis[1] Cell Line: GBM-1 GBM CSCs Concentration: 50 nM, 100 nM, 125 nM, 250 nM, and 500 nM Incubation Time: 3 h, 6 h, 12 h, and 24 h Result: Had the ability to regulate RIPK2 to act as a prosurvival or proapoptotic molecule. Significantly reduced RIPK2 binding to cIAP2 in a dose-dependent manner. |
In Vivo | cRIPGBM(chloride) (50 mg/kg;口服;每天两次,持续 5 周) 在携带患者来源的 GBM CSC 颅内异种移植的小鼠模型再,抑制肿瘤生长[1]。 Animal Model: Orthotopic intracranial xenograft model in mouse[1] Dosage: 50 mg/kg Administration: PO; twice daily, 8 h apart, starting at day 7 postinjection; last for 5 weeks Result: Monitored by Fluorescence Tomography System. Decreased the tumor signal, as well as tumor size. |
References |
Molecular Formula | C26H20ClFN2O2 |
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Molecular Weight | 446.90 |