The binding mechanism of IVR has been rationalized through docking simulations using the testicular ACE (tACE)−lisinopril complex at 2 Å resolution (PDB 108A). The best docking pose was located at the tACE catalytic site resembling the mode of inhibition exerted by lisinopril, an effective hypertensive synthetic drug. The degree of inhibition of this peptide correlated with the H-bond interaction between the C-terminal of IVR and Lys511 and Tyr520 residues of tACE, a significant inhibitor registration for lisinopril. |