A 779 is a potent antagonist of the G-protein-coupled receptor Mas, the Ang1-7 receptor, which is distinct from conventional AngII.

A 779suppresses the proliferating cell nuclear antigen (PCNA) protein expression up-regulated by Ang II, but A 779alone has no effect to induce proliferation and migration of VSMCs.Pretreatment with Ang-(1-7) significantly retards Ang II-induced inflammatory responses of VSMCs associated with up-regulated MCP-1, VCAM-1 and IL-1β expressions, and this effect of Ang-(1-7) is blocked by A-779.But A 779alone has no effect to induce inflammatory response of VSMCs[1].

Inhibition of Ang1-7 cascade by A 779significantly eradicated captopril protective effects on bone metabolism, mineralization and micro-structure.A 779also restored OVX effects on RANKL expression and ACE-1/AngII/AT1R cascade and down-regulated OPG expression and ACE-2/Ang1-7/Mas pathway.In line with the clinical observations of the bone-preservative properties following ACE-1 inhibition, local activation of ACE-2/Ang1-7/Mas signaling and suppressed osteoclastogenesis seem responsible for the osteo-preservative effect of captopril, which could offers a potential therapeutic value in treatment of disabling bone and skeletal muscular diseases[2].