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Fosinopril

Fosinopril
Fosinopril structure.svg
Clinical data
Trade names Monopril
AHFS/Drugs.com Monograph
MedlinePlus a692020
Pregnancy
category
  • AU: D
  • US: C (Risk not ruled out)
Routes of
administration
oral
ATC code
Legal status
Legal status
  • In general: ℞ (Prescription only)
Pharmacokinetic data
Bioavailability ~36%
Protein binding 87% (fosinoprilat)
Metabolism hepatic, GIT mucosa (to fosinoprilat)
Biological half-life 12 hours (fosinoprilat)
Excretion renal
Identifiers
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEMBL
Chemical and physical data
Formula C30H46NO7P
Molar mass 563.663 g/mol
3D model (Jmol)
 NYesY (what is this?)  

Fosinopril is an angiotensin converting enzyme (ACE) inhibitor used for the treatment of hypertension and some types of chronic heart failure. Fosinopril is the only phosphinate-containing ACE inhibitor marketed, by Bristol-Myers Squibb under the trade name Monopril.

Fosinoprilat proved to have the same problem as enalaprilat and the other carboxylate-containing ACE inhibitors (namely poor oral bioavailability). Addition of a hydrophobic side-chain modulated the ionisation characteristics of the molecule, making it more bioavailable. Fosinopril is administered as a prodrug and is converted in vivo to the active form fosinoprilat.

In congestive heart failure, the ability of the heart to pump enough blood to satisfy the physiological needs of the body is reduced. This condition has a variety of causes, including damaged heart valves, myocardial infarction, hypertension, vitamin B1 deficiency, and genetic mutations. When subsequent blood flow to the kidneys is reduced, the kidneys respond by increasing the secretion of renin from the juxtaglomerular apparatus. Renin converts the inactive angiotensinogen into angiotensin I, which is converted to angiotensin II (AII) by angiotensin converting enzyme (ACE). AII can have negative effects on the cardiovascular system after events such as heart failure and myocardial infarction. AII causes arterial vasoconstriction and hypertension, resulting in an increase in afterload, increasing the resistance against which the heart works. Additionally, chronic increase in production of AII is associated with structural changes to the myocardium which reduces the functionality of the heart.


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