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| Cas No.: | 1800398-38-2 |
| Chemical Name: | LXH254 free base |
| Synonyms: | LXH254;Naporafenib;LXH254 free base;15JL80DG6H;N-(3-(2-(2-hydroxyethoxy)-6-morpholinopyridin-4-yl)-4-methylphenyl)-2-(trifluoromethyl)isonicotinamide;N-[3-[2-(2-hydroxyethoxy)-6-morpholin-4-ylpyridin-4-yl]-4-methylphenyl]-2-(trifluoromethyl)pyridine-4-carboxamide;N-{3-[2-(2-hydroxyethoxy)-6-(morpholin-4-yl)pyridin-4-yl]-4-methylphenyl}-2-(trifluoromethyl)pyridine-4-carboxamide;K81;Naporafenib [INN] |
| SMILES: | FC(C1C([H])=C(C([H])=C([H])N=1)C(N([H])C1C([H])=C([H])C(C([H])([H])[H])=C(C=1[H])C1C([H])=C(N=C(C=1[H])N1C([H])([H])C([H])([H])OC([H])([H])C1([H])[H])OC([H])([H])C([H])([H])O[H])=O)(F)F |
| Formula: | C25H25F3N4O4 |
| M.Wt: | 502.49 |
| Sotrage: | 2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO |
| Description: | LXH254 is a potent CRAF inhibitor extracted from patent WO2018051306A1, Compound A. LXH254 also is a potent BRAF inhibitor. |
| In Vivo: | Treatment with LXH254 (Compound A) generates tumor regression in several KRAS-mutant models including the NSCLC-derived Calu-6 (KRAS Q61K) and NCI-H358 (KRAS G12C). LXH254 exhibits efficacy in numerous MAPK-driven human cancer cell lines and in xenograft tumors representing model tumors harboring human lesions in KRAS, NRAS and BRAF oncogenes[1]. |
| In Vitro: | LXH254 (Compound A) is an adenosine triphosphate (ATP)-competitive inhibitor of BRAF (also referred to herein as b-RAF or b-Raf) and CRAF (also referred to herein as c-RAF or c- Raf) protein kinases. Throughout the present disclosure, LXH254 is also referred to as a c-RAF (or CRAF) inhibitor or a C-RAF/c-Raf kinase inhibitor. In cell-based assays, LXH254 has demonstrated anti-proliferative activity in cell lines that contain a variety of mutations that activate MAPK signaling. Moreover, LXH254 is a Type 2 ATP -competitive inhibitor of both B-Raf and C-Raf that keeps the kinase pocket in an inactive conformation, thereby reducing the paradoxical activation seen with many B-Raf inhibitors, and blocking mutant RAS-driven signaling and cell proliferation[1]. |