FGFR-IN-26

FGFR-IN-26 (Compound 13) (dose-response series) potently inhibits proliferation of Ba/F3 cells expressing FGFR1, FGFR2 (wild-type and clinically relevant resistance mutations), FGFR3, and FGFR4, with highest potency against FGFR2^K660E (IC₅₀ = 0.6 nM) and FGFR3 (IC₅₀ = 0.2 nM) and 23-fold selectivity for FGFR2 over FGFR4^[1].
FGFR-IN-26 binds potently to FGFR2 (K_d = 2.7 nM), FGFR2^(N550K) (K_d = 10 nM), FGFR1 (K_d = 21 nM), and FGFR3 (K_d = 3.5 nM), with 85-fold selectivity for FGFR2 over FGFR4, and shows weak reversible binding to FGFR2^(C491F) (K_d = 956 nM) consistent with a covalent mechanism^[1].
FGFR-IN-26 (72-120 h) potently inhibits viability of FGFR2-driven SNU-16 gastric cancer cells (IC₅₀ = 7.5 nM) and AN3CA endometrial cancer cells harboring FGFR2^N550K (IC₅₀ = 13 nM)^[1].
FGFR-IN-26 (1 μM) shows high selectivity against the human kinome, inhibiting only 13 wild-type kinases by >90%^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.