Moexipril

Oral
Hypertension

CrCl (mL/min)	Dosage
≤40	Initially, 3.75 mg once daily. Max: 15 mg once daily.

Initially, 3.75 mg once daily.

Should be taken on an empty stomach. Take 1 hr before meals.

History of hypersensitivity or angioedema related to previous treatment w/ ACE inhibitors. Hereditary/idiopathic angioneurotic oedema. Concomitant use w/ aliskiren in patients w/ DM. Pregnancy.

Collagen vascular disease, hypovolaemia, renal artery stenosis (unilateral or bilateral), aortic or mitral valve stenosis, volume and/or salt depletion. Renal impairment. Lactation. Elderly.

Cough, flu syndrome, pharyngitis, headache, dizziness, fatigue, flushing and rash. GI disturbances, myalgia, hyperkalaemia, hyponatraemia and hypotension.
Potentially Fatal: Anaphylactic reactions and angioedema. Fulminant hepatic necrosis.

PO: D

May impair ability to drive or operate machinery.

Monitor BP, renal function, serum creatinine and K. Consider periodic monitoring of WBC in patients w/ collagen vascular disease and renal disease.

Symptoms: Severe hypotension, shock, stupor, bradycardia, electrolyte disturbances and renal failure. Management: Frequently monitor creatinine and serum electrolytes. Admin of absorbents if ingestion is w/in 1 hr. Consider angiotensin II infusion and/or IV catecholamines. Atropine should be used in the treatment of bradycardia or extensive vagal reactions. Pacemaker may also be considered.

Additive hyperkalaemic effects w/ K-sparing diuretics, K supplements, and other hyperkalaemic drugs. Concurrent treatment w/ NSAIDs reduces hypotensive action and increases the risk of nephrotoxicity. May increase nitritoid reactions of gold (Na aurothiomalate).
Potentially Fatal: Increased risk of hypotension, hyperkalaemia, and changes in renal function w/ aliskiren in patients w/ DM.

Food may reduce absorption. May worsen HTN w/ licorice.

Description: Moexipril, a prodrug of moexiprilat, is a competitive inhibitor of ACE. It prevents the conversion of angiotensin I to angiotensin II causing an increase in plasma renin activity and a reduction in aldosterone secretion. This promotes vasodilation and BP reduction.
Onset: Peak effect: 1-2 hr.
Duration: >24 hr.
Pharmacokinetics:
Absorption: Rapidly but incompletely absorbed from the GI tract. Reduced in the presence of food. Bioavailability: Approx 13% (moexiprilat). Time to peak plasma concentration: Approx 1.5 hr (moexiprilat).
Distribution: Volume of distribution: Approx 180 L (moexiprilat). Plasma protein binding: Moexipril (90%); moexiprilat (50-70%).
Metabolism: Metabolised to moexiprilat (active metabolite) in the GI mucosa and liver.
Excretion: Via urine (as moexiprilat, unchanged drug and other metabolites) and faeces (some moexiprilat). Elimination half-life: Approx 12 hr (moexiprilat).

Store between 20-25°C. Protect from excessive moisture.

ACE Inhibitors/Direct Renin Inhibitors

Anon. Moexipril. Lexicomp Online. Hudson, Ohio. Wolters Kluwer Clinical Drug Information, Inc. https://online.lexi.com. Accessed 25/11/2013.

Buckingham R (ed). Moexipril Hydrochloride. Martindale: The Complete Drug Reference [online]. London. Pharmaceutical Press. https://www.medicinescomplete.com. Accessed 25/11/2013.

McEvoy GK, Snow EK, Miller J et al (eds). Moexipril. AHFS Drug Information (AHFS DI) [online]. American Society of Health-System Pharmacists (ASHP). https://www.medicinescomplete.com. Accessed 25/11/2013.

Moexipril Hydrochloride. U.S. FDA. https://www.fda.gov/. Accessed 25/11/2013.

Wickersham RM. Moexipril Hydrochloride. Facts and Comparisons [online]. St. Louis, MO. Wolters Kluwer Clinical Drug Information, Inc. https://www.wolterskluwercdi.com/facts-comparisons-online/. Accessed 25/11/2013.