FGFR3-IN-12

FGFR3-IN-12 (Compound 10s) potently inhibits wild-type FGFR3 with an IC₅₀ of 6.8 nM, and exhibits 5 to 60-fold selectivity over wild-type FGFR1, FGFR2, and FGFR4^[1].
FGFR3-IN-12 (30 min) inhibits the FGFR3^V555M mutant with an IC₅₀ of 19.2 nM^[1].
FGFR3-IN-12 (5 days) potently inhibits proliferation of FGFR3-driven RT112/84 bladder carcinoma cells with an IC₅₀ of 9.2 nM, and exhibits 3.2- to 48.6-fold selectivity over FGFR1-amplified, FGFR2-mutant, and FGFR4-mutant cancer cell lines^[1].
FGFR3-IN-12 (0.5 μM) displays extraordinary kinome selectivity and potently inhibits TNK1 with an IC₅₀ of 16.9 nM^[1].
FGFR3-IN-12 (1 h) covalently binds to recombinant FGFR3, forming an adduct after 1 h incubation at a 1:2 (FGFR3:FGFR3-IN-12) molar ratio^[1].
FGFR3-IN-12 (2 h) covalently modifies the Cys482 residue in the FGFR3 kinase domain after 2 h incubation at a 1:5 (FGFR3:FGFR3-IN-12) molar ratio^[1].
FGFR3-IN-12 (6.25-100 nM; 6-48 h) concentration-dependently inhibits FGFR3 signaling and induces apoptosis in RT112/84 bladder carcinoma cells and inhibits FGFR3^V555M signaling in engineered Ba/F3 cells^[1].
FGFR3-IN-12 (20-80 nM; 96 h) concentration-dependently activates Caspase-3/7 in RT112/84 bladder carcinoma cells^[1].

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