M64HCl is a specific small molecule, water-soluble focal adhesion kinase (FAK) activator, interacts directly with the FAK kinase domain to activate FAK, induces epithelial sheet migration in vitro, and stimulates gut mucosal wound healing in vivo.
M64HCl activates FAK-Tyr397 phosphorylation at 100 pM and 1 ​nM by 8.7 ​± ​3.0%, 9.1 ​± ​3.9% respectively in Caco-2 ​cells.
M64HCl increases FAK-Tyr-397 phosphorylation in comparison to H2O controls by 20.2 ​± ​7.4% at 100 ​nM.
M64HCl does not activate the FAK paralog, proline-rich tyrosine kinase 2 (Pyk2), and non-receptor protein tyrosine kinase Src.
M64HCl not only activates FAK but also stimulates epithelial sheet migration.
M64HCl dose-responsively activates the FAK kinase domain vs. the non-salt M64, increasing the Vmax of ATP-binding.
M64HCl (25 ​mg/kg/day) promotes mucosal healing in two murine small intestinal injury models.