| Name | CCT196969 |
| Description | CCT196969 is a novel orally available, pan-RAF inhibitor with anti-SRC activity. It also inhibits SRC, LCK, and the p38 MAPKs. |
| Cell Research | Cell lines: cell line derived from a vemurafenib-resistant melanoma. Method: The three cell lines derived from tumors displaying resistance to vemurafenib are incubated with DMSO (control),PLX4720,CCT196969,or CCT241161 (1 μM; 4 hr).Protein extracts are prepared in CLB1 lysis buffer,and samples are analyzed by Zeptosens RPPA(reverse phase protein arrays). |
| Animal Research | Animal Models: CD-1 mice. Formulation: 5% DMSO,95% water. Dosages: 20 mg/kg . Administration: oral gavage |
| In vitro | CCT196969 induces caspase 3 and PARP cleavage, thus induces apoptosis. CCT196969 does not drive paradoxical pathway activation and inhibit MEK/ERK in BRAF and NRAS mutant melanoma. CCT196969 is active against melanoma and colorectal cancer cell lines that are mutant for BRAF, but not cancer cells that are wild-type for BRAF and NRAS. |
| In vivo | Oral dosing at 10 mg/kg/day of CCT196969 results in plasma concentrations ～1 μM at 24 hr. It is orally bioavailable at ～55%. CCT196969 is extremely well tolerated at the doses assessed and does not produce any significant adverse effects in vivo. |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice. |
| Solubility Information | Ethanol : Insoluble
DMSO : 100 mg/mL (194.73 mM)
H2O : Insoluble
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| Keywords | Raf | CCT 196969 | CCT196969 | Inhibitor | inhibit | CCT-196969 | Raf kinases |
| Inhibitors Related | Nintedanib | Regorafenib monohydrate | Doramapimod | Vemurafenib | Sorafenib | Staurosporine | Ibrutinib | Dasatinib | Regorafenib | Dabrafenib | Sorafenib tosylate | PLX-4720 |
| Related Compound Libraries | Reprogramming Compound Library | Anti-Pancreatic Cancer Compound Library | Pain-Related Compound Library | Bioactive Compound Library | Kinase Inhibitor Library | Tyrosine Kinase Inhibitor Library | Anti-Obesity Compound Library | Anti-Ovarian Cancer Compound Library | Inhibitor Library | Bioactive Compounds Library Max |
United States
