It is the first dicarboxylate-containing ACE inhibitor and was developed partly to overcome these limitations of captopril.

As a prodrug, enalapril is hydrolyzed in vivo to the active form enalaprilat by various esterases.

Peak plasma enalaprilat concentrations occur 2 to 4 hours after oral enalapril administration.

Renal impairment [particularly creatinine clearance <20 mL/min (<1.2 L/h)] results in significant accumulation of enalaprilat and necessitates dosage reduction.

Accumulation is probably the cause of reduced elimination in healthy elderly individuals and in patients with concomitant diabetes, hypertension and heart failure.