LC-MG-5

LC-MG-5 (1 μM; 12 h) significantly reduces the FGFR2 protein level in KATO III cells^[1].
LC-MG-5 (10 nM-10000 nM; 12 h) induces dose-dependent degradation of FGFR2 in KATO III cells, with a DC₅₀ of 231.7 nM^[1].
LC-MG-5 (0-1000 nM; 12 h) inhibits FGFR2-mediated PI3K/AKT and MAPK/ERK signaling pathways in KATO III cells^[1].
LC-MG-5 (1 μM; 6 h-12 h) induces the internalization of FGFR2 from the plasma membrane to intracellular vesicular compartments in KATO III cells^[1].
LC-MG-5 (1 μM; 0 h-8 h) induces time-dependent degradation of FGFR2 in KATO III cells, with the maximum clearance achieved at 8 h^[1].
LC-MG-5 (96 h) inhibits the proliferation of KATO III cells with an IC₅₀ value of 65.49 nM^[1].
LC-MG-5 (200 nM; co-incubated with 1 μM MG132 (HY-13259)) mediates the degradation of FGFR2 in KATO III cells, and this process is strictly dependent on the ubiquitin-proteasome system^[1].
LC-MG-5 (1 μM; co-incubated with 1 μM Infigratinib) mediates the degradation of FGFR2 in KATO III cells by binding to the ATP-binding pocket of FGFR2, whereas pretreatment with the parental inhibitor Infigratinib (HY-13311) blocks this degradation process^[1].

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