fak-in-7

FAK-IN-7 has potential antiproliferative activity and is a FAK inhibitor.

Chlorahololide D is a natural lindane-type sesquiterpene dimer and selective potassium channel blocker that stimulates reactive oxygen species ROS levels to cause cell cycle arrest in the G2 phase, modulates Bcl-2 and Bax and FAK, thereby inhibiting MCF-7 cell growth and triggering apoptosis. Chlorahololide D inhibits tumor proliferation, migration and angiogenesis in in vivo experiments and has anti-breast cancer potential.

FAK-IN-10 is an inhibitor of FAK (IC50: 76.3 μM) and demonstrates antitumor activity in MCF-7 and A431 cell lines with IC50 values of 4.23 μM and 0.78 μM, respectively.

Defactinib analogue-1 (Compound 7) serves as a ligand for the target protein FAK, and is utilized in the synthesis of PROTAC FAK degrader 1.

Azurin (50-77) is a peptide fragment derived from the copper-containing bacterial protein azurin, present in P. aeruginosa. It exhibits properties that regulate the cell cycle, inhibit cancer proliferation, and manage angiogenesis, proving its potential as an anticancer agent. Specifically, this compound acts as a VEGFR2 inhibitor with an IC20 of approximately 10.7 µM. At a concentration of 20 µM, it effectively induces cell cycle arrest at the G2 M phase in MCF-7 breast cancer cells, while a higher concentration of 50 µM significantly reduces the proliferation of both MCF-7 and ZR-75-1 breast cancer cell lines. Furthermore, Azurin (50-77) impedes VEGF-A-induced capillary tube formation with an IC50 of 12 µM, and alters the cellular and extracellular levels of critical signaling and structural proteins such as F-actin, focal adhesion kinase (FAK), paxillin, and platelet endothelial cell adhesion molecule-1 (PECAM-1) in human umbilical vein endothelial cells (HUVECs) at a concentration of 25 µM. Demonstrating its efficacy in vivo, Azurin (50-77) administered at 10 mg kg per day notably reduces tumor volume in an MCF-7 mouse xenograft model, highlighting its therapeutic potential.