cRIPGBM manufacturers
- cRIPGBM chloride
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- $0.00 / 1removed
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2025-11-10
- CAS:2361988-77-2
- Min. Order:
- Purity:
- Supply Ability: 10g
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| | cRIPGBM Basic information |
| Product Name: | cRIPGBM | | Synonyms: | 1-Benzyl-3-(4-fluorobenzyl)-2-methyl-4,9-dioxo-4,9- dihydro-1H-naphtho[2,3-d]imidazol-3-ium chloride;cRIPGBM(chloride);3-[(4-Fluorophenyl)methyl]-2-methyl-4,9-dioxo-1-(phenylmethyl)-1H-naphth[2,3-d]imidazolium chloride | | CAS: | 2361988-77-2 | | MF: | C26H20ClFN2O2 | | MW: | 446.91 | | EINECS: | | | Product Categories: | | | Mol File: | 2361988-77-2.mol |  |
| | cRIPGBM Chemical Properties |
| storage temp. | 2-8°C | | solubility | DMSO: 2mg/mL, clear | | form | Solid | | color | Light yellow to yellow |
| | cRIPGBM Usage And Synthesis |
| Uses | 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]. | | Biological Activity | cRIPGBM is an apoptosis inducer (GBM-1/-5/-39 EC50 = 63/95/290 nM; human neural progenitor cells (NPCs)/astrocytes/lung fibroblasts EC50 = 190/710/960 nM) th at binds receptor-interacting protein kinase 2 (RIPK2, RIP2) and promotes the formation of a proapoptotic RIPK2/caspase-1 complex. Cell type-selective metabolic redox conversion of RIPGBM to cRIPGBM in glioblastoma multiforme (GBM) cancer stem cells (CSCs) form the basis of selective GBM CSCs apoptosis induction by RIPGBM over non-GBM cultures. | | 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[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. |
| | IC 50 | Caspase-1; RIPK2 | | References | [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. DOI:10.1073/pnas.1816626116 |
| | cRIPGBM Preparation Products And Raw materials |
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