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Statements

Subject Item
n2:DB00691
rdf:type
n3:Drug
n3:description
Moexipril is a non-sulfhydryl containing precursor of the active angiotensin-converting enzyme (ACE) inhibitor moexiprilat. It is used to treat high blood pressure (hypertension). It works by relaxing blood vessels, causing them to widen. Lowering high blood pressure helps prevent strokes, heart attacks and kidney problems.
n3:dosage
n28:271B463F-363D-11E5-9242-09173F13E4C5 n28:271B4640-363D-11E5-9242-09173F13E4C5 n28:271B4641-363D-11E5-9242-09173F13E4C5 n28:271B4642-363D-11E5-9242-09173F13E4C5 n28:271B4643-363D-11E5-9242-09173F13E4C5 n28:271B4644-363D-11E5-9242-09173F13E4C5 n28:271B4645-363D-11E5-9242-09173F13E4C5 n28:271B4646-363D-11E5-9242-09173F13E4C5
n3:generalReferences
# Asmar R, Sayegh F, Tracz W, Hlawaty M, Olszowska M, Jourde M, Vincent M, Goujoun B, Maldonado J: Reversal of left ventricular hypertrophy with the ACE inhibitor moexipril in patients with essential hypertension. Acta Cardiol. 2002 Feb;57(1):31-2. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/11918132 # Blacher J, Raison J, Amah G, Schiemann AL, Stimpel M, Safar ME: Increased arterial distensibility in postmenopausal hypertensive women with and without hormone replacement therapy after acute administration of the ACE inhibitor moexipril. Cardiovasc Drugs Ther. 1998 Sep;12(4):409-14. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/9825188 # Brogden RN, Wiseman LR: Moexipril. A review of its use in the management of essential hypertension. Drugs. 1998 Jun;55(6):845-60. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/9617599 # Cawello W, Boekens H, Waitzinger J, Miller U: Moexipril shows a long duration of action related to an extended pharmacokinetic half-life and prolonged ACE inhibition. Int J Clin Pharmacol Ther. 2002 Jan;40(1):9-17. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/11837383 # Chrysant SG, Chrysant GS: Pharmacological and clinical profile of moexipril: a concise review. J Clin Pharmacol. 2004 Aug;44(8):827-36. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/15286086 # Chrysant SG, Chrysant GS: Pharmacological profile and clinical use of moexipril. Expert Rev Cardiovasc Ther. 2003 Sep;1(3):345-52. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/15030263 # Chrysant GS, Nguyen PK: Moexipril and left ventricular hypertrophy. Vasc Health Risk Manag. 2007;3(1):23-30. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/17583172 # Grass GM, Morehead WT: Evidence for site-specific absorption of a novel ACE inhibitor. Pharm Res. 1989 Sep;6(9):759-65. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/2554270 # Kalasz H, Petroianu G, Tekes K, Klebovich I, Ludanyi K, Gulyas Z: Metabolism of moexipril to moexiprilat: determination of in vitro metabolism using HPLC-ES-MS. Med Chem. 2007 Jan;3(1):101-6. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/17266629 # Persson B, Stimpel M: Evaluation of the antihypertensive efficacy and tolerability of moexipril, a new ACE inhibitor, compared to hydrochlorothiazide in elderly patients. Eur J Clin Pharmacol. 1996;50(4):259-64. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/8803515 # Spinar J, Vitovec J: MORE--MOexipril and REgression of left ventricle hypertrophy in combination therapy A multicentric open label clinical trial. Int J Cardiol. 2005 Apr 20;100(2):199-206. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/15823625 # Stimpel M, Koch B, Oparil S: Antihypertensive treatment in postmenopausal women: results from a prospective, randomized, double-blind, controlled study comparing an ACE inhibitor (moexipril) with a diuretic (hydrochlorothiazide). Cardiology. 1998 May;89(4):271-6. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/9643274 # White CM: Pharmacologic, pharmacokinetic, and therapeutic differences among ACE inhibitors. Pharmacotherapy. 1998 May-Jun;18(3):588-99. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/9620109 # White WB, Whelton A, Fox AA, Stimpel M, Kaihlanen PM: Tricenter assessment of the efficacy of the ACE inhibitor, moexipril, by ambulatory blood pressure monitoring. J Clin Pharmacol. 1995 Mar;35(3):233-8. "Pubmed":http://www.ncbi.nlm.nih.gov/pubmed/7608310
n3:group
approved
n3:halfLife
Moexipril elimination half-life is approximately 1 hour. Moexiprilat elimination half-life is 2 to 9 hours.
n3:indication
For the treatment of hypertension.
n3:manufacturer
n7:271B4639-363D-11E5-9242-09173F13E4C5 n7:271B463A-363D-11E5-9242-09173F13E4C5 n7:271B4637-363D-11E5-9242-09173F13E4C5 n7:271B4638-363D-11E5-9242-09173F13E4C5 n7:271B4636-363D-11E5-9242-09173F13E4C5
owl:sameAs
n16:DB00691 n24:DB00691
dcterms:title
Moexipril
adms:identifier
n9:82418 n10:DB00691 n11:50084673 n12:91270 n13:C07704 n14:0574-0110-01 n21:46508441 n25:PA164769059 n26:Moexipril
n3:mechanismOfAction
Moexipril is a prodrug for moexiprilat, which inhibits ACE in humans and animals. The mechanism through which moexiprilat lowers blood pressure is believed to be primarily inhibition of ACE activity. ACE is a peptidyl dipeptidase that catalyzes the conversion of the inactive decapeptide angiotensin I to the vasoconstrictor substance angiotensin II. Angiotensin II is a potent peripheral vasoconstrictor that also stimulates aldosterone secretion by the adrenal cortex and provides negative feedback on renin secretion. ACE is identical to kininase II, an enzyme that degrades bradykinin, an endothelium-dependent vasodilator. Moexiprilat is about 1000 times as potent as moexipril in inhibiting ACE and kininase II. Inhibition of ACE results in decreased angiotensin II formation, leading to decreased vasoconstriction, increased plasma renin activity, and decreased aldosterone secretion. The latter results in diuresis and natriuresis and a small increase in serum potassium concentration (mean increases of about 0.25 mEq/L were seen when moexipril was used alone). Whether increased levels of bradykinin, a potent vasodepressor peptide, play a role in the therapeutic effects of moexipril remains to be elucidated. Although the principal mechanism of moexipril in blood pressure reduction is believed to be through the renin-angiotensin-aldosterone system, ACE inhibitors have some effect on blood pressure even in apparent low-renin hypertension.
n3:packager
n7:271B4635-363D-11E5-9242-09173F13E4C5 n7:271B4633-363D-11E5-9242-09173F13E4C5 n7:271B4634-363D-11E5-9242-09173F13E4C5 n7:271B4631-363D-11E5-9242-09173F13E4C5 n7:271B4632-363D-11E5-9242-09173F13E4C5 n7:271B462F-363D-11E5-9242-09173F13E4C5 n7:271B4630-363D-11E5-9242-09173F13E4C5 n7:271B462D-363D-11E5-9242-09173F13E4C5 n7:271B462E-363D-11E5-9242-09173F13E4C5 n7:271B462B-363D-11E5-9242-09173F13E4C5 n7:271B462C-363D-11E5-9242-09173F13E4C5
n3:routeOfElimination
Moexiprilat undergoes renal elimination.
n3:synonym
Moexipril Univasc Uniretic Moexiprilum
n3:toxicity
Human overdoses of moexipril have not been reported. In case reports of overdoses with other ACE inhibitors, hypotension has been the principal adverse effect noted. Single oral doses of 2 g/kg moexipril were associated with significant lethality in mice. Rats, however, tolerated single oral doses of up to 3 g/kg. Common adverse effects include cough, dizziness, diarrhea, flu syndrome, fatigue, pharyngitis, flushing, rash, and myalgia
n3:volumeOfDistribution
* 183 L
n5:hasAHFSCode
n19:24-32-04
n3:foodInteraction
Herbs that may attenuate the antihypertensive effect of moexipril include: bayberry, blue cohash, cayenne, ephedra, ginger, ginseng (American), kola and licorice. High salt intake may attenuate the antihypertensive effect of moexipril. Moexipril may decrease the excretion of potassium. Salt substitutes containing potassium may increase the risk of hyperkalemia. Take moexipril one hour before or two hours after meals.
n3:mixture
n18:271B462A-363D-11E5-9242-09173F13E4C5
n3:proteinBinding
Moexiprilat is approxomately 50% protein bound.
n3:salt
n29:hasConcept
n30:M0162643
foaf:page
n23:moexip.htm n27:moexipril.html n31:uni1468.shtml
n3:IUPAC-Name
n4:271B464B-363D-11E5-9242-09173F13E4C5
n3:InChI
n4:271B4651-363D-11E5-9242-09173F13E4C5
n3:Molecular-Formula
n4:271B4650-363D-11E5-9242-09173F13E4C5
n3:Molecular-Weight
n4:271B464D-363D-11E5-9242-09173F13E4C5
n3:Monoisotopic-Weight
n4:271B464E-363D-11E5-9242-09173F13E4C5
n3:SMILES
n4:271B464F-363D-11E5-9242-09173F13E4C5
n3:Water-Solubility
n4:271B4661-363D-11E5-9242-09173F13E4C5 n4:271B4649-363D-11E5-9242-09173F13E4C5
n3:logP
n4:271B464A-363D-11E5-9242-09173F13E4C5 n4:271B4647-363D-11E5-9242-09173F13E4C5 n4:271B4662-363D-11E5-9242-09173F13E4C5
n3:logS
n4:271B4648-363D-11E5-9242-09173F13E4C5
n5:hasATCCode
n6:C09AA13
n3:H-Bond-Acceptor-Count
n4:271B4657-363D-11E5-9242-09173F13E4C5
n3:H-Bond-Donor-Count
n4:271B4658-363D-11E5-9242-09173F13E4C5
n3:InChIKey
n4:271B4652-363D-11E5-9242-09173F13E4C5
n3:Polar-Surface-Area--PSA-
n4:271B4653-363D-11E5-9242-09173F13E4C5
n3:Polarizability
n4:271B4655-363D-11E5-9242-09173F13E4C5
n3:Refractivity
n4:271B4654-363D-11E5-9242-09173F13E4C5
n3:Rotatable-Bond-Count
n4:271B4656-363D-11E5-9242-09173F13E4C5
n3:absorption
Moexipril is incompletely absorbed, with bioavailability as moexiprilat of about 13% compared to intravenous (I.V.) moexipril (both measuring the metabolite moexiprilat), and is markedly affected by food, which reduces C<sub>max</sub> and AUC by about 70% and 40%, respectively, after the ingestion of a low-fat breakfast or by 80% and 50%, respectively, after the ingestion of a high-fat breakfast.
n3:affectedOrganism
Humans and other mammals
n3:casRegistryNumber
103775-10-6
n3:category
n3:clearance
* 441 mL/min
n3:containedIn
n17:271B463E-363D-11E5-9242-09173F13E4C5 n17:271B463C-363D-11E5-9242-09173F13E4C5 n17:271B463D-363D-11E5-9242-09173F13E4C5 n17:271B463B-363D-11E5-9242-09173F13E4C5
n3:Bioavailability
n4:271B465D-363D-11E5-9242-09173F13E4C5
n3:Ghose-Filter
n4:271B465F-363D-11E5-9242-09173F13E4C5
n3:MDDR-Like-Rule
n4:271B4660-363D-11E5-9242-09173F13E4C5
n3:Number-of-Rings
n4:271B465C-363D-11E5-9242-09173F13E4C5
n3:Physiological-Charge
n4:271B465B-363D-11E5-9242-09173F13E4C5
n3:Rule-of-Five
n4:271B465E-363D-11E5-9242-09173F13E4C5
n3:Traditional-IUPAC-Name
n4:271B464C-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-acidic-
n4:271B4659-363D-11E5-9242-09173F13E4C5
n3:pKa--strongest-basic-
n4:271B465A-363D-11E5-9242-09173F13E4C5