Ningetinib

1394820-69-9

C31H29FN4O5

H2O : < 0.1 mg/mL (insoluble); DMSO : 16.67 mg/mL (29.95 mM; Need ultrasonic)

Protein Tyrosine Kinase/RTK; Protein Tyrosine Kinase/RTK; Protein Tyrosine Kinase/RTK

Ningetinib is a potent, orally bioavailable small molecule tyrosine kinase inhibitor (TKI) with IC₅₀s of 6.7, 1.9 and <1.0 nM for c-Met, VEGFR2 and Axl, respectively. IC50 & Target: VEGFR, c-Met, and Axl^[1] In Vitro: Ningetinib is a potent, orally bioavailable small molecule tyrosine kinase inhibitor (TKI) with IC₅₀s of 6.7, 1.9 and <1.0 nM for c-Met, VEGFR2 and Axl, respectively. In cell-based functional assays, Ningetinib (CT053PTSA) inhibits HGF and VEGF-stimulated HUVEC proliferation and microvascular angiogenesis in rat aortic rings with IC₅₀ values of 8.6 and 6.3 nM, respectively^[1]. In Vivo: When single dosed orally (3 mg/kg) to U87MG tumor-bearing nude mice, Ningetinib (CT053PTSA) potently inhibits the phosphorylation of c-Met and its downstream signaling kinases AKT and ERK1/2 for up to 6 hours in tumor tissues. In orthotopic U87MG human glioblastoma xenograft model, Ningetinib prolongs the median survival time (MST) and yields significant increase in life-span value (ILS=32%, p=0.003) at an oral dose of 20 mg/kg/day (dosed 21 days) versus the vehicle-treated group^[1].