|Other names||Fosinopril sodium|
|Drug class||ACE inhibitor|
|Main uses||High blood pressure, heart failure, diabetic kidney disease|
|Typical dose||10 to 40 mg OD|
|Protein binding||87% (fosinoprilat)|
|Metabolism||Liver, GIT mucosa (to fosinoprilat)|
|Elimination half-life||12 hours (fosinoprilat)|
|Chemical and physical data|
|Molar mass||563.672 g·mol−1|
|3D model (JSmol)|
Fosinopril, sold under the brand name Monopril among others, is a medication used to treat high blood pressure, heart failure, and diabetic kidney disease. It is one of a number of first line agents for high blood pressure. It is taken by mouth.
Common side effects include cough, nausea, and dizziness. Other side effects may include low blood pressure, liver problems, allergic reactions, high potassium, and kidney problems. Use during pregnancy may harm the baby. It is a angiotensin converting enzyme (ACE) inhibitor.
Fosinopril was patented in 1980 and approved for medical use in 1991. It is available as a generic medication. In the United Kingdom 4 weeks of 20 mg cost the NHS about £2 as of 2021. This amount in the United States costs about 10 USD.
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.
In heart failure patients, fosinopril increases exercise tolerance and lowers the frequency of events associated with worsening heart failure, such as dyspnea, the need for supplemental diuretics, fatigue, and hospitalizations.
It is started at 10 mg per day and may be increased to 40 mg per day.
In those with high blood pressure and kidney problems, a typical dose may be used.
Unlike other ACE inhibitors that are primarily excreted by the kidneys, fosinopril is eliminated from the body by both renal and liver pathways. This characteristic of fosinopril makes the drug a safer choice than other ACE inhibitors for heart failure patients with impaired kidney function resulting from poor perfusion as fosinopril can still be eliminated by the liver, preventing accumulation of the drug in the body.
Fosinopril is de-esterified by the liver or gastrointestinal mucosa and is converted to its active form, fosinoprilat. Fosinoprilat competitively binds to ACE, preventing ACE from binding to and converting angiotensin I to angiotensin II. Inhibiting the production of AII lowers peripheral vascular resistance, decreases afterload, and decreases blood pressure, thus helping to alleviate the negative effects of AII on cardiac performance.
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