Quinapril

438.52

438.52

1312995-182-4

RJ84Y44811

DTXSID4023547

C62074

C09AA06|C - Cardiovascular system

95.9

1.2

Solid

1.217±0.06 g/cm3(Predicted)

120-130°C

662ºC

354.1ºC

8.50e-03 g/L

2.8None

2.8

204.4 Ų [M+H]+ [CCS Type: DT, Method: single field calibrated]

22-24/25

The oral LD50 in rats is 3541mg/kg and in mice is 1739mg/kg. Patients experiencing an overdose may present with symptoms of severe hypotension. Due to the extensive protein binding of quinapril and the active metabolite quinaprilat, hemodialysis is not expected to remove the drug from circulation. Treat patients with symptomatic and supportive measures, including normal saline infusions to restore normal blood pressure.

Quinapril, like other ACE inhibitors, has been associated with a low rate of serum aminotransferase elevations (

Quinapril and the active metabolite quinaprilat are 97% protein bound in plasma.

Quinapril is indicated for the treatment of hypertension and as an adjunct therapy in the treatment of heart failure. Quinapril in combination with hydrochlorothiazide is indicated for the treatment of hypertension.

Quinapril is an angiotensin-converting enzyme (ACE) inhibitor used in the therapy of hypertension and congestive heart failure. Quinapril is associated with a low rate of transient serum aminotransferase elevations, but has yet to be linked to instances of acute liver injury.

Angiotensin-Converting Enzyme Inhibitors

Quinapril is a prodrug of an angiotensin converting enzyme (ACE) inhibitor used in the treatment of hypertension or adjunct in the treatment of heart failure. Quinapril has a wide therapeutic window and a long duration of action as it is given in doses of 10-80mg once daily.

A class of drugs whose main indications are the treatment of hypertension and heart failure. They exert their hemodynamic effect mainly by inhibiting the renin-angiotensin system. They also modulate sympathetic nervous system activity and increase prostaglandin synthesis. They cause mainly vasodilation and mild natriuresis without affecting heart rate and contractility. (See all compounds classified as Angiotensin-Converting Enzyme Inhibitors.)|Drugs used in the treatment of acute or chronic vascular HYPERTENSION regardless of pharmacological mechanism. Among the antihypertensive agents are DIURETICS; (especially DIURETICS, THIAZIDE); ADRENERGIC BETA-ANTAGONISTS; ADRENERGIC ALPHA-ANTAGONISTS; ANGIOTENSIN-CONVERTING ENZYME INHIBITORS; CALCIUM CHANNEL BLOCKERS; GANGLIONIC BLOCKERS; and VASODILATOR AGENTS. (See all compounds classified as Antihypertensive Agents.)|Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume. (See all compounds classified as Cardiovascular Agents.)

Quinapril if 50-80% bioavailable. Quinapril has a T_max of <1 hour, while quinaprilat has a T_max of 2.5h. The C_max of quinaprilat is highly variable but reaches 1526ng/mL with an AUC of 2443ng\*h/mL in healthy males given a 10mg dose. A high fat meal reduces the absorption of quinapril by 25-30%.|Quinaprilat is up to 96% eliminated in the urine. The eliminated metabolites PD109488 and PD113413 account for approximately 6% of a dose of quinapril each. A small fraction of the dose recovered in the urine is accounted for by unmetabolized quinapril.|The mean volume of distribution of quinaprilat is 13.9L.|The clearance of quinaprilat is 68mL/min.

Quinapril is de-esterified to the active quinaprilat or dehydrated to form the inactive PD109488. PD109488 can undergo O-deethylation to form another inactive metabolite, PD113413.

The active metabolite quinaprilat has an elimination half life of 2.3 hours.

Angiotensin II constricts coronary blood vessels and is positively inotropic, which under normal circumstances, would increase vascular resistance and oxygen consumption. This action can eventually lead to myocyte hypertrophy and vascular smooth muscle cell proliferation. Angiotensin II also stimulates production of plasminogen activator inhibitor-1 (PAI-1), increasing the risk of thrombosis. Quinaprilat prevents the conversion of angiotensin I to angiotensin II by inhibition of angiotensin converting enzyme, and also reduces the breakdown of bradykinin. Reduced levels of angiotensin II lead to lower levels of PAI-1, reducing the risk of thrombosis, especially after a myocardial infarction.

2-(2-((1-(ethoxycarbonyl)-3-phenylpropyl)amino)-1-oxopropyl)-1,2,3,4-tetrahydro-3-isoquinolinecarboxylic acid

Human Drugs -> FDA Approved Drug Products with Therapeutic Equivalence Evaluations (Orange Book) -> Active Ingredients