Moexipril is available as a prodrug moexipril hydrochloride, and is metabolized in the liver to form the pharmacologically active compound moexiprilat. Formation of moexiprilat is caused by hydrolysis of an ethyl ester group. Moexipril is incompletely absorbed after oral administration, and its bioavailability is low. The long pharmacokinetic half-life and persistent ACE inhibition of moexipril allows once-daily administration.
Moexipril is highly lipophilic, and is in the same hydrophobic range as quinapril, benazepril, and ramipril. Lipophilic ACE inhibitors are able to penetrate membranes more readily, thus tissue ACE may be a target in addition to plasma ACE. A significant reduction in tissue ACE (lung, myocardium, aorta, and kidney) activity has been shown after moexipril use.
It has additional PDE4-inhibiting effects.