LC-MG-10

LC-MG-10 (0-10000 nM; 12 h) potently induces dose-dependent degradation of FGFR2 in KATO III gastric cancer cells, with a DC₅₀ of 230.2 nM^[1].
LC-MG-10 (0-1000 nM; 12 h) inhibits FGFR2-mediated PI3K/AKT and MAPK/ERK signaling pathways in KATO III gastric cancer cells following 12 h of treatment at concentrations of 300 nM and 1000 nM^[1].
LC-MG-10 (1 μM; 0-12 h) induces the internalization of FGFR2 from the plasma membrane into intracellular vesicles in KATO III gastric cancer cells^[1].
LC-MG-10 (1 μM; 0 h-8 h) induces time-dependent degradation of FGFR2 in KATO III gastric cancer cells^[1].
LC-MG-10 (96 h) potently inhibits the proliferation of KATO III gastric cancer cells, with an IC₅₀ value of 49.13 nM^[1].
Degradation of FGFR2 in KATO III gastric cancer cells induced by LC-MG-10 (200 nM) depends on the ubiquitin-proteasome system^[1].
LC-MG-10 (1 μM; 1 h) binds to the ATP-binding pocket of FGFR2 to mediate its degradation, whereas pre-treatment with the parent inhibitor Infigratinib (HY-13311) blocks this activity in KATO III gastric cancer cells^[1].

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