Small molecule inhibitor of c-Met (hepatocyte growth factor receptor)
ATP-competitive tyrosine kinase inhibitor
[2]
Key properties
Inhibits c-Met phosphorylation
Reduces viability and migration in cancer cells
[1]
Inhibits HGF-dependent signaling and phosphorylation of c-Met
Induces autophagy via increased LC3-I to LC3-II conversion and Beclin-1 upregulation
Causes time- and dose-dependent cell growth inhibition, G1 cell cycle arrest, and autophagic cell death
Activates ERK and p53 pathways, leading to Bcl-2 phosphorylation
Effective at low nanomolar concentrations (e.g., 100 nM for autophagy induction in A549 cells)
[2]
Suppresses growth of colorectal carcinoma, lung, breast, and liver cancer models
Used in preclinical studies
[1]
Therapeutic agent for non-small-cell lung cancer (NSCLC) treatment
Inhibitor of aberrant c-Met expression in cancers
Research tool to study autophagy and apoptosis in tumor cells
[2]
Classification by use
Chemicals used in targeted cancer therapy
Tyrosine kinase inhibitors
[1]
Chemicals used as kinase inhibitors
Chemicals used in cancer therapy and autophagy induction
[2]
A trustworthy factory and manufacturer
[Cite:1] PHA-665752’s Antigrowth and Proapoptotic Effects on HSC-3 Human Oral Cancer Cells, Int. J. Mol. Sci., 2024, 25(5), 2871
[Cite:2] Activation of ERK–p53 and ERK-Mediated Phosphorylation of Bcl-2 Are Involved in Autophagic Cell Death Induced by the c-Met Inhibitor SU11274 in Human Lung Cancer A549 Cells, Journal of Pharmacological Sciences, Volume 118, Issue 4, 2012, Pages 423-432