[6] Hypotension, dizziness, increased cough, diarrhea, flu syndrome, fatigue, and flushing have been found to affect less than 6% of patients who were prescribed moexipril.

[7] The cardioprotective effects of ACE inhibitors are mediated through a combination of angiotensin II inhibition and bradykinin proliferation.

[8][9] Increased levels of bradykinin stimulate in the production of prostaglandin E2[10] and nitric oxide,[9] which cause vasodilation and continue to exert antiproliferative effects.

Indirectly, angiotensin II stimulates of the production of endothelin 1 and 3 (ET1, ET3)[11] and the transforming growth factor beta-1 (TGF-β1),[12] all of which have tissue proliferative effects that are blocked by the actions of moexipril.

A significant reduction in tissue ACE (lung, myocardium, aorta, and kidney) activity has been shown after moexipril use.

[16] The synthesis of the all-important dipeptide-like side chain involves alkylation of the tert-butyl ester of L-alanine (2) with ethyl 2-bromo-4-phenylbutanoate (1); the presominane of the desired isomer is attributable to asymmetric induction from the adjacent chiral center.