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 In Vitro cRIPGBM chloride (0.25 μM; 0-24 h) time-dependently activates caspase 1, caspase 9, and caspase 7, as well as PARP cleavage, in CBM-1 GBM CSCs. cRIPGBM chloride (0.125 μM, 0.25 μM; 24 h) induces cell apoptosis mediated by caspase 1 in CBM-1 GBM CSCs. MCE has not independently confirmed the accuracy of these methods. They are for reference only. Western Blot AnalysisCell 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; p.o.; twice daily for 5 weeks) inhibits tumor growth in patient-derived GBM CSC intracranial xenograft mouse models . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Animal Model: Orthotopic intracranial xenograft model in mouse 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. Form:Solid IC50& Target:Caspase-1 RIPK2