| Identification | Back Directory | [Name]
LXH254,LXH-254 | [CAS]
1800398-38-2 | [Synonyms]
LXH254
Naporafenib
LXH254,LXH-254
LXH254; LXH-254; LXH 254
4-Pyridinecarboxamide, N-[3-[2-(2-hydroxyethoxy)-6-(4-morpholinyl)-4-pyridinyl]-4-methylphenyl]-2-(trifluoromethyl)- | [Molecular Formula]
C25H25F3N4O4 | [MDL Number]
MFCD31657408 | [MOL File]
1800398-38-2.mol | [Molecular Weight]
502.49 |
| Chemical Properties | Back Directory | [Boiling point ]
601.9±55.0 °C(Predicted) | [density ]
1.353±0.06 g/cm3(Predicted) | [storage temp. ]
Store at -20°C | [solubility ]
DMSO:100.0(Max Conc. mg/mL);199.0(Max Conc. mM) | [form ]
A crystalline solid | [pka]
10.86±0.70(Predicted) | [color ]
Off-white to light yellow |
| Hazard Information | Back Directory | [Uses]
LXH254, is a kinase inhibitor used in the treatment of solid tumors. | [in vivo]
Treatment with Naporafenib (Compound A) generates tumor regression in several KRAS-mutant models including the NSCLC-derived Calu-6 (KRAS Q61K) and NCI-H358 (KRAS G12C). Naporafenib 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].
Naporafenib shows significant antitumor activity in models harboring BRAF mutations either alone or coincident with either activated NRAS or KRAS, and RAS mutants lacking ARAF are more sensitive to Naporafenib[2]. | Animal Model: | Outbred athymic (nu/nu) female mice and SCID Beige mice; BRAF-, NRAS-, and KRAS-mutant xenograft models, as well as a RAS/RAF wild-type model[2] | | Dosage: | 100 mg/kg | | Administration: | Orally, daily | | Result: | Significantly decreased tumor volume in models harboring BRAF mutations either alone or coincident with either activated NRAS or KRAS, slightly decreased tumor volume in KRAS model. |
| [IC 50]
CRAF: 0.072 nM (IC50); Braf: 0.21 nM (IC50); ARAF: 6.4 nM (IC50); p38α: 2.1 μM (IC50); Abl1: 4.9 μM (IC50) | [storage]
Store at -20°C |
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