ALK-IN-37

ALK-IN-37 (Compound C04) (48 h) selectively inhibits the proliferation of ALK-overexpressing H2228 cells (IC₅₀ = 0.10 μM) and ALK-positive Karpas299 cells (IC₅₀ = 0.53 μM), shows weak activity against ALK-negative A549 cells, and exhibits no activity against WML2 cells^[1].
ALK-IN-37 (50-200 nM; 14 days) dose-dependently inhibits colony formation of H2228 cells, with 200 nM reducing the colony formation efficiency to 36.3%^[1].
ALK-IN-37 (50-200 nM; 24-48 h) inhibits the migration of H2228 cells in a dose-dependent manner, and a concentration of 200 nM reduces the 48-hour scratch wound healing rate to 28.5%^[1].
ALK-IN-37 (100-200 nM; 24 h) inhibits the invasion of H2228 cells in a dose-dependent manner, with 200 nM reducing the relative invasion area to 36.6%^[1].
ALK-IN-37 (50-200 nM; 24 h) induces G0/G1 cell cycle arrest in H2228 cells in a dose-dependent manner, and treatment with 200 nM increases the proportion of G0/G1 phase cells to 85.0%^[1].
ALK-IN-37 (50-200 nM; 24 h) induces apoptosis in H2228 cells in a dose-dependent manner, and treatment with 200 nM increases the proportion of apoptotic cell population to 55.9%^[1].
ALK-IN-37 (50-200 nM) dose-dependently inhibits the phosphorylation of ALK and the downstream STAT3/AKT signaling pathway in H2228 cells, with the strongest inhibitory effect observed at 200 nM^[1].

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