Background:

Fosinopril sodium is an effective inhibitor of angiotensin-converting enzyme (ACE) with IC50 value of 9nM [1].

Fosinopril is a third type ACE inhibitor with a phosphinic acid. It binds to the active site of ACE via targeting the zinc ions with its phosphinic acid moiety. Fosinopril is an orally active prodrug which is hydrolysed and converted to its active diacid fosinoprilat after oral administration. The absorption of fosinopril ranges between 18 and 41 %. Antacids can affect the absorption of fosinopril and cause a decrease in its bioavailability by increasing the gastric pH. The pharmacokinetics assay shows fosinopril is hydrolysed completely into fosinoprilat after absorption. And fosinoprilat is slowly eliminated by renal and hepatic clearance. Fosinopril is proved to produce sustained blood pressure reduction through improving systemic and renal haemodynamics and reducing left ventricular mass [1].

参考文献:
[1] Shionoiri H,?Naruse M,?Minamisawa K,?Ueda S,?Himeno H,?Hiroto S,?Takasaki I. Fosinopril.?Clinical pharmacokinetics?and?clinical?potential. Clin Pharmacokinet.?1997 Jun;32(6):460-80.