VA Class:CV800
Moexipril hydrochloride is a nonsulfhydryl angiotensin-converting enzyme (ACE) inhibitor.1
Moexipril hydrochloride is used alone or in combination with other classes of antihypertensive agents (e.g., thiazide diuretics) in the management of hypertension.1, 2, 5, 25, 83, 1200
Because captopril, another angiotensin-converting enzyme (ACE) inhibitor, may cause serious adverse effects (e.g., neutropenia, agranulocytosis), particularly in patients with renal impairment (especially those with collagen vascular disease)1, 8 or in patients receiving immunosuppressive therapy,8, 61 the possibility that similar adverse effects may occur with moexipril should be considered since current experience is insufficient to rule out such risk.1 (See Cautions: Hematologic Effects, in Captopril 24:32.04.)
Moexipril is used alone or in combination with other classes of antihypertensive agents in the management of hypertension.1, 2, 5, 25, 83, 1200 ACE inhibitors are considered one of several preferred antihypertensive drugs for the initial management of hypertension according to current evidence-based hypertension guidelines; other preferred options include angiotensin II receptor antagonists, calcium-channel blockers, and thiazide diuretics.501, 502, 503, 504, 1200 While there may be individual differences with respect to recommendations for initial drug selection and use in specific patient populations, current evidence indicates that these antihypertensive drug classes all generally produce comparable effects on overall mortality and cardiovascular, cerebrovascular, and renal outcomes.501, 502, 504, 1200, 1213 ACE inhibitors may be particularly useful in the management of hypertension in patients with certain coexisting conditions such as heart failure, ischemic heart disease, diabetes mellitus, chronic kidney disease (CKD), or cerebrovascular disease or following myocardial infarction.501, 502, 504, 523, 524, 525, 526, 527, 534, 535, 536, 543, 1200, 1214, 1215 (See Uses: Hypertension, in Captopril 24:32.04 and in Enalapril/Enalaprilat 24:32.04.)
In patients with hypertension and compelling indications (e.g., CKD with albuminuria [urine albumin 300 mg/day or greater, or urine albumin:creatinine ratio of 300 mg/g or equivalent in the first morning void]), angiotensin II receptor antagonists are usually considered an alternative for ACE inhibitor-intolerant patients.1218 However, data indicate no difference in efficacy between ACE inhibitors and angiotensin II receptor antagonists with regard to blood pressure lowering and clinical outcomes (i.e., all-cause mortality, cardiovascular mortality, MI, heart failure, stroke, and end-stage renal disease).1200, 1218 Adverse events (e.g., cough, angioedema) leading to drug discontinuance occur more frequently with ACE inhibitor therapy than with angiotensin II receptor antagonist therapy.1218 Because of similar efficacy and a lower frequency of adverse effects, some experts believe that angiotensin II receptor antagonists should be used instead of an ACE inhibitor for the treatment of hypertension or hypertension with certain compelling indications.1218
Most patients with hypertension, especially black patients, will require at least 2 antihypertensive drugs to achieve adequate blood pressure control.1200 In general, black hypertensive patients tend to respond better to monotherapy with thiazide diuretics or calcium-channel blockers than to monotherapy with ACE inhibitors.25, 83, 92, 93, 108, 109, 501, 504, 1200 Although ACE inhibitors have lowered blood pressure in all races studied, monotherapy with these agents has produced a smaller reduction in blood pressure in black hypertensive patients, a population associated with low renin hypertension.92, 93 However, the combination of an ACE inhibitor or an angiotensin II receptor antagonist with a calcium-channel blocker or thiazide diuretic produces similar blood pressure lowering in black patients as in other racial groups.1200 In addition, ACE inhibitors appear to produce a higher incidence of angioedema in black patients than in other races.1, 93, 1200 (See Race under Hypertension: Other Special Considerations for Antihypertensive Drug Therapy, in Uses in Captopril 24:32.04 and in Enalaprilat/Enalapril 24:32.04.)
For additional information on the role of ACE inhibitors in the management of hypertension, see Uses in Captopril 24:32.04 and in Enalaprilat/Enalapril Maleate 24:32.04. For information on overall principles and expert recommendations for treatment of hypertension, see Uses: Hypertension in Adults, in the Thiazides General Statement 40:28.20.
ACE inhibitors have been used in the management of heart failure†, usually in conjunction with other agents such as cardiac glycosides, diuretics, and β-adrenergic blocking agents (β-blockers).10, 11, 12, 14, 96, 524, 800
Current guidelines for the management of heart failure in adults generally recommend a combination of drug therapies to reduce morbidity and mortality, including neurohormonal antagonists (e.g., ACE inhibitors, angiotensin II receptor antagonists, angiotensin receptor-neprilysin inhibitors [ARNIs], β-blockers, aldosterone receptor antagonists) that inhibit the detrimental compensatory mechanisms in heart failure.524, 701, 703, 800 Additional agents (e.g., cardiac glycosides, diuretics, sinoatrial modulators [i.e., ivabradine]) added to a heart failure treatment regimen in selected patients have been associated with symptomatic improvement and/or reduction in heart failure-related hospitalizations.524, 800 Experts recommend that all asymptomatic patients with reduced left ventricular ejection fraction (LVEF) (American College of Cardiology Foundation [ACCF]/American Heart Association [AHA] stage B heart failure) receive therapy with an ACE inhibitor and β-blocker to prevent symptomatic heart failure and to reduce morbidity and mortality.524, 800 In patients with prior or current symptoms of chronic heart failure and reduced LVEF (ACCF/AHA stage C heart failure), ACCF, AHA, and the Heart Failure Society of America (HFSA) recommend inhibition of the renin-angiotensin-aldosterone (RAA) system with an ACE inhibitor, angiotensin II receptor antagonist, or ARNI in conjunction with a β-blocker, and an aldosterone antagonist in selected patients, to reduce morbidity and mortality.800 While ACE inhibitors have been the preferred drugs for inhibition of the renin-angiotensin-aldosterone (RAA) system because of their established benefits in patients with heart failure and reduced ejection fraction,524 some evidence indicates that therapy with sacubitril/valsartan, an ARNI, may be more effective than ACE inhibitor therapy (enalapril) in reducing cardiovascular death and heart failure-related hospitalization.702, 800 ACCF, AHA, and HFSA recommend that patients with chronic symptomatic heart failure and reduced LVEF (New York Heart Association [NYHA] class II or III) who are able to tolerate an ACE inhibitor or angiotensin II receptor antagonist be switched to therapy containing an ARNI to further reduce morbidity and mortality.800 However, in patients in whom an ARNI is not appropriate, continued use of an ACE inhibitor for all classes of heart failure with reduced ejection fraction remains strongly advised.800 In patients in whom an ARNI or ACE inhibitor is not appropriate, an angiotensin II receptor antagonist may be used.800 For additional information on the use of ACE inhibitors in the management of heart failure, see Uses: Heart Failure in Captopril 24:32.04 and in Enalaprilat/Enalapril 24:32.04.For further information on the use of ARNIs in patients with heart failure, see Uses: Heart Failure, in Sacubitril and Valsartan 24:32.92.
Both ACE inhibitors and angiotensin II receptor antagonists have been shown to slow the rate of progression of renal disease in patients with diabetes mellitus and persistent albuminuria†, 103, 104, 105, 106, 107, 1232 and use of a drug from either class is recommended in such patients with modestly elevated (30-300 mg/24 hours) or higher (exceeding 300 mg/24 hours) levels of urinary albumin excretion.535, 536, 1232 The usual precautions of ACE inhibitor or angiotensin II receptor antagonist therapy in patients with substantial renal impairment should be observed.99 For additional information on the use of ACE inhibitors in the treatment of diabetic nephropathy, see Diabetic Nephropathy under Uses: Nephropathy, in Captopril 24:32.04.
Moexipril hydrochloride is administered orally.1 Because food decreases oral bioavailability (e.g., by 40-50%) and peak plasma concentrations (e.g., 70-80%), the manufacturer recommends that moexipril hydrochloride be taken in a fasting state (e.g., 1 hour before meals).1, 3, 83
Dosage of moexipril hydrochloride must be adjusted according to the patient's tolerance and response.1, 83 Because of the risk of inducing hypotension, initiation of angiotensin-converting enzyme (ACE) inhibitor therapy, including moexipril hydrochloride, requires consideration of recent and current antihypertensive therapy, the extent of blood pressure elevation, sodium intake, fluid status, and other clinical circumstances.1, 37, 46, 58 If therapy is initiated in patients already receiving a diuretic, symptomatic hypotension may occur following the initial dose of the ACE inhibitor.1, 2, 30, 46 To minimize the possibility of hypotension, it is recommended that volume and salt depletion be corrected, if present, and that diuretic therapy be discontinued, if possible, 2-3 days before initiating moexipril hydrochloride; such precautions may be particularly important in patients in whom diuretic therapy was recently initiated.1, 8, 9, 10, 11, 12, 13, 14, 37, 46 If blood pressure is not controlled adequately with the ACE inhibitor alone, diuretic therapy may be resumed.1, 28, 29, 30, 39 If diuretic therapy cannot be discontinued, moexipril hydrochloride therapy should be initiated at a reduced dosage.1, 8, 10, 11, 12, 13, 14, 83, 84 Dosage should be adjusted carefully under close medical supervision in patients with heart failure, with or without associated renal impairment, because of the risk of hypotension; such patients should be followed closely prior to and for at least 2 weeks after initiation of moexipril hydrochloride or diuretic therapy or dosage adjustment of either drug.1, 12, 91 For more information on the use of ACE inhibitors in patients with heart failure and renal impairment, see Cautions: Precautions and Contraindications in Captopril 24:32.04.
For the management of hypertension in patients not receiving a diuretic, the usual initial adult dosage of moexipril hydrochloride is 7.5 mg once daily.1, 5 In patients currently receiving diuretic therapy, an initial moexipril hydrochloride dose of 3.75 mg is recommended and should be administered under close medical supervision until blood pressure has stabilized.1 However, discontinuance of the diuretic is preferred in such patients.1 (See the introductory discussion under Dosage and Administration: Dosage.) Subsequent dosage of moexipril hydrochloride should be adjusted based on blood pressure response.1 If blood pressure response diminishes toward the end of the dosing interval during once daily administration, increasing the dosage or giving the drug in 2 divided doses daily should be considered.1
The recommended maintenance dosage of moexipril hydrochloride is 7.5-30 mg daily, given as a single dose or in 2 divided doses.1, 1200 Limited data from dose ranging studies do not consistently indicate a dose response relationship with doses ranging from 7.5-60 mg once daily.4 Dosages exceeding 60 mg daily have not been extensively evaluated in hypertensive patients.1, 5 During chronic therapy, the antihypertensive effect of moexipril generally is evident within 2 weeks, with a maximum effect after 4 weeks.1
Moexipril/Hydrochlorothiazide Fixed-combination Therapy
When combination therapy is required, the manufacturer recommends that the commercially available preparation containing moexipril hydrochloride in fixed combination with hydrochlorothiazide should not be used for initial therapy.83 The fixed combination containing moexipril hydrochloride with hydrochlorothiazide may be used in patients who have been receiving the drugs separately and in whom dosage of the individual drugs has been adjusted.83 Therapy with the commercially available preparations containing moexipril hydrochloride in fixed combination with hydrochlorothiazide should be initiated only after an adequate response is not achieved with moexipril hydrochloride or hydrochlorothiazide monotherapy.83 Such fixed combinations also may be used to prevent hydrochlorothiazide-induced potassium loss.83 Patients whose blood pressure is not adequately controlled with moexipril or hydrochlorothiazide monotherapy may receive the fixed combination containing 7.5 mg of moexipril hydrochloride and 12.5 mg of hydrochlorothiazide, the preparation containing 15 mg of moexipril hydrochloride and 12.5 mg of hydrochlorothiazide or, alternatively, the preparation containing 15 mg of moexipril hydrochloride and 25 mg of hydrochlorothiazide.83 Further increases of either or both drugs depend on clinical response; however, generally, dosage of hydrochlorothiazide should not be increased for about 2-3 weeks after initiation of therapy.83 Combined dosage of moexipril hydrochloride and hydrochlorothiazide exceeding 30 and 50 mg daily, respectively, has not been studied.83 In addition, patients whose blood pressure has been adequately controlled with a hydrochlorothiazide dosage of 25 mg daily, but who experienced potassium loss, may achieve similar blood pressure control without electrolyte disturbance if they are switched to therapy with the fixed-combination preparation containing 3.75 mg of moexipril hydrochloride and 6.25 mg of hydrochlorothiazide (one-half tablet of the preparation containing 7.5 mg of moexipril hydrochloride and 12.5 mg of hydrochlorothiazide).83 Patients who experience excessive decreases in blood pressure while receiving the fixed combination containing 7.5 mg of moexipril hydrochloride and 12.5 mg of hydrochlorothiazide alternatively may receive therapy with the fixed-combination preparation containing 3.75 mg of moexipril hydrochloride and 6.25 mg of hydrochlorothiazide (one-half tablet of the preparation containing 7.5 mg of moexipril hydrochloride and 12.5 mg of hydrochlorothiazide).83
Blood Pressure Monitoring and Treatment Goals
Blood pressure should be monitored regularly (i.e., monthly) during therapy and dosage of the antihypertensive drug adjusted until blood pressure is controlled.1200 If an adequate blood pressure response is not achieved with ACE inhibitor monotherapy, the dosage may be increased or another antihypertensive agent with demonstrated benefit and preferably with a complementary mechanism of action (e.g., calcium-channel blocker, thiazide diuretic) may be added; if target blood pressure is still not achieved with the use of 2 antihypertensive agents, a third drug may be added.1200, 1216 (See Uses: Hypertension.) In patients who develop unacceptable adverse effects with moexipril, the drug should be discontinued and another antihypertensive agent from a different pharmacologic class should be initiated.1216
The goal of hypertension management and prevention is to achieve and maintain optimal control of blood pressure.1200 However, the optimum blood pressure threshold for initiating antihypertensive drug therapy and specific treatment goals remain controversial.505, 506, 507, 508, 515, 523, 530, 1201, 1207, 1209, 1222 While other hypertension guidelines have based target blood pressure goals on age and comorbidities,501, 504, 536 a 2017 multidisciplinary hypertension guideline from the American College of Cardiology (ACC), American Heart Association (AHA), and a number of other professional organizations incorporates underlying cardiovascular risk into decision making regarding treatment and generally recommends the same target blood pressure (i.e., less than 130/80 mm Hg) in all adults.1200 Many patients will require at least 2 drugs from different pharmacologic classes to achieve this blood pressure goal; the potential benefits of hypertension management and drug cost, adverse effects, and risks associated with the use of multiple antihypertensive drugs also should be considered when deciding a patient's blood pressure treatment goal.1200, 1220
For additional information on initiating and adjusting moexipril hydrochloride dosage in the management of hypertension, see Blood Pressure Monitoring and Treatment Goals under Dosage: Hypertension, in Dosage and Administration in the Thiazides General Statement 40:28.20.
If moexipril hydrochloride is used in patients with impaired renal function, dosage must be modified in response to the degree of renal impairment, and the theoretical risk of neutropenia must be considered.1, 12, 54, 72, 81 In hypertensive adults with creatinine clearances of 40 mL/minute or less per 1.73 m2, dosage of moexipril hydrochloride should be initiated cautiously at 3.75 mg daily.1 If an adequate response is not achieved, dosage may be increased gradually until blood pressure is controlled or a maximum dosage of 15 mg daily is reached.1 The effect of hemodialysis or peritoneal dialysis on elimination of the drug has not been determined.1
If concomitant diuretic therapy is required in patients with severe renal impairment (creatinine clearance of 40 mL/minute or less per 1.73 m2), a loop diuretic is preferred to a thiazide diuretic.83 Therefore, use of commercially available preparations containing moexipril in fixed combination with hydrochlorothiazide is not recommended for patients with severe renal impairment.83
Peak plasma concentrations and bioavailability of moexipril hydrochloride are increased and those of the active metabolite moexiprilat are decreased following oral administration in patients with mild to moderate cirrhosis.1 However, the manufacturer currently makes no specific recommendations for dosage adjustment in patients with impaired hepatic function. 1
Dosage of moexipril generally should be titrated carefully in geriatric patients, usually initiating therapy at the low end of the dosage range.1 Because geriatric patients may have decreased renal function, the manufacturer states that monitoring renal function may be useful and dosage of the fixed combination should be selected with care in these patients.83
Known hypersensitivity to moexipril, other angiotensin-converting enzyme (ACE) inhibitors, or any ingredient in the formulation.1, 83
History of angioedema related to previous ACE inhibitor treatment.1, 83
Concomitant therapy with aliskiren in patients with diabetes mellitus.1, 83
Fetal/Neonatal Morbidity and Mortality
Drugs that act on the renin-angiotensin system (e.g., ACE inhibitors, angiotensin II receptor antagonists) reduce fetal renal function and increase fetal and neonatal morbidity and mortality when used in pregnancy, especially during the second and third trimesters.1, 12, 53, 54, 74, 75, 76, 83, 84 ACE inhibitors also have been reported to increase the risk of major congenital malformations when administered during the first trimester of pregnancy.110, 111 Resulting oligohydramnios can be associated with fetal lung hypoplasia and skeletal deformations.1, 83 Potential neonatal effects include skull hypoplasia, anuria, hypotension, renal failure, and death.1, 83 ACE inhibitors (e.g., moexipril) should be discontinued as soon as possible when pregnancy is detected, unless continued use is considered lifesaving.1, 12, 53, 54, 74, 111 Nearly all women can be transferred successfully to alternative therapy for the remainder of their pregnancy.75 For additional information on the risk of ACE inhibitors during pregnancy, see Cautions: Pregnancy, Fertility, and Lactation, in Captopril 24:32.04 and in Enalaprilat/Enalapril Maleate 24:32.04.
Like other ACE inhibitors, moexipril rarely is associated with hypotension in patients with uncomplicated hypertension.1 Symptomatic hypotension may occur; patients at particular risk include those with severe volume and/or salt depletion secondary to prolonged diuretic therapy, dietary salt restriction, dialysis, diarrhea, or vomiting.1 Volume and/or salt depletion should be corrected before starting moexipril therapy.1
Marked hypotension may occur in patients with heart failure (with or without associated renal impairment) and may be associated with oliguria and/or progressive azotemia and rarely with acute renal failure and/or death.1 In patients with heart failure, moexipril therapy should be started under close medical supervision and patients should be followed closely for at least 2 weeks after initiation of moexipril or diuretic therapy or dosage adjustment of either drug.1 Other patients at risk for hypotension include those with ischemic heart disease, aortic stenosis, or cerebrovascular disease, in whom an excessive decrease in blood pressure could result in myocardial infarction or cerebrovascular accident (stroke).1, 12, 34, 35, 36
If hypotension occurs, the patient should be placed in the supine position, and if necessary, an IV infusion of 0.9% sodium chloride injection to expand fluid volume may be administered.1 Moexipril therapy usually may be continued following restoration of blood pressure and volume.1
Neutropenia/agranulocytosis, particularly in patients with renal impairment (especially those with a concomitant collagen vascular disease such as systemic lupus erythematosus or scleroderma), has been reported with ACE inhibitor therapy.1 (See Cautions: Hematologic Effects, in Captopril 24:32.04.) Data are insufficient to rule out similar incidence of agranulocytosis with moexipril in patients without prior reactions to other ACE inhibitors.1 Monitoring of leukocytes in patients with collagen vascular disease, especially if renal impairment exists, should be considered.1, 83
Rare ACE inhibitor-associated clinical syndrome manifested initially by cholestatic jaundice; may progress to fulminant hepatic necrosis and is potentially fatal.1, 83 Patients receiving an ACE inhibitor, including moexipril, who develop jaundice or marked elevations of hepatic enzymes should discontinue the drug and receive appropriate monitoring.1, 83
Sensitivity reactions, including anaphylactoid reactions and angioedema (including laryngeal angioedema and tongue edema), are potentially fatal.1, 83 Head and neck angioedema have occurred in patients receiving an ACE inhibitor; angioedema has been reported at a higher rate in black patients compared with patients of other races.1, 83 Head and neck angioedema involving the tongue, glottis, or larynx may cause airway obstruction.1, 83 If laryngeal stridor or angioedema of the face, lips, tongue, or glottis occurs, ACE inhibitors (e.g., moexipril) should be discontinued and appropriate therapy (e.g., epinephrine) should be initiated immediately.1, 83
Intestinal angioedema (occasionally without a prior history of facial angioedema or elevated serum levels of complement 1 [C1] esterase inhibitor) also has been reported in patients receiving ACE inhibitors.1, 83 Intestinal angioedema, which frequently presents as abdominal pain (with or without nausea or vomiting), usually is diagnosed by abdominal CT scan, ultrasound, or surgery;1, 83 symptoms usually have resolved after discontinuance of the ACE inhibitor.1, 83 Intestinal angioedema should be considered in the differential diagnosis of patients who develop abdominal pain during therapy with an ACE inhibitor.1, 83
Life-threatening anaphylactoid reactions have been reported in at least 2 patients receiving ACE inhibitors while undergoing desensitization treatment with hymenoptera venom.1, 83 When ACE inhibitors were temporarily discontinued before desensitization with the venom, anaphylactoid reactions did not recur; however, such reactions recurred after inadvertent rechallenge.1, 83 Anaphylactoid reactions have been reported following initiation of hemodialysis that used a high-flux membrane in patients receiving an ACE inhibitor.1, 83 In addition, anaphylactoid reactions also have been reported in patients undergoing low-density lipoprotein (LDL) apheresis with dextran sulfate absorption.1, 83
Inhibition of the renin-angiotensin-aldosterone (RAA) system may cause renal impairment and rarely renal failure and/or death in susceptible patients (e.g., those whose renal function depends on the activity of the RAA system such as hypertensive patients with severe heart failure).1, 83
Deterioration of renal function, manifested as transient increases in BUN and serum creatinine concentrations, may occur following administration of ACE inhibitor therapy in hypertensive patients with unilateral or bilateral renal artery stenosis.1, 83 This effect usually was reversible following discontinuance of ACE inhibitor and/or diuretic therapy.1, 83 Renal function should be monitored closely during the first few weeks of therapy and periodically thereafter in such patients.1, 83 Dosage reduction of moexipril and/or discontinuance of diuretic therapy may be required.1, 83
Hyperkalemia can develop, especially in those with renal impairment or diabetes mellitus and those receiving drugs that can increase serum potassium concentration (e.g., potassium-sparing diuretics, potassium supplements, potassium-containing salt substitutes).1
Persistent and nonproductive; resolves after drug discontinuance.1
Moexipril may block the effects of compensatory renin release; hypotension may occur in patients undergoing surgery or during anesthesia with agents that produce hypotension.1 Hypotension in such patients may be corrected by volume expansion.1
When hydrochlorothiazide is used in fixed combination with moexipril hydrochloride, the usual cautions, precautions, and contraindications associated with hydrochlorothiazide must be considered in addition to those associated with moexipril.83 (See Cautions, in the Thiazides General Statement 40:28.20.)
Category D.1, 83 (See Users Guide.)
Moexipril can cause fetal and neonatal morbidity and mortality when administered to a pregnant woman.1, 83 (See Fetal/Neonatal Morbidity and Mortality under Warnings/Precautions: Warnings, in Cautions.)
Not known whether moexipril is distributed into milk.1 Caution is advised if the drug is administered in nursing women.1
If oliguria or hypotension occurs in neonates with a history of in utero exposure to moexipril, blood pressure and renal function should be supported; exchange transfusions or dialysis may be required.1, 83 (See Fetal/Neonatal Morbidity and Mortality under Warnings/Precautions: Warnings, in Cautions.)
Safety and efficacy not established in pediatric patients 16 years of age or younger.1, 112 For information on overall principles and expert recommendations for treatment of hypertension in pediatric patients, see Uses: Hypertension in Pediatric Patients, in the Thiazides General Statement 40:28.20.
Experience in those 65 years of age or older insufficient to determine whether they respond differently than younger adults.1 No substantial differences in safety and efficacy relative to younger adults.1
Drug dosage generally should be titrated carefully in geriatric patients, usually initiating therapy at the low end of the dosage range.1, 2, 3 The greater frequency of decreased hepatic, renal, and/or cardiac function and of concomitant disease and drug therapy observed in the elderly also should be considered.1
Renal function may decrease with ACE inhibitor therapy in susceptible patients.1 Use with caution in those with renal impairment.1 (See Dosage and Administration: Special Populations and also Renal Effects under Warnings/Precautions: General Precautions, in Cautions.)
ACE inhibitors generally are not as effective for blood pressure reduction in black patients compared with other races.1, 801, 802, 803, 804, 805, 806 (See Uses: Hypertension.)
Adverse effects considered at least possibly related to treatment and reported in greater than 1% of patients receiving moexipril include increased cough,1 dizziness,1 diarrhea,1 flu syndrome,1 fatigue,1 pharyngitis,1 flushing,1 rash,1 and myalgia.1 Adverse effects considered at least possibly related to treatment and reported in greater than 1% of patients receiving moexipril in fixed combination with hydrochlorothiazide include cough,83 dizziness,83 and fatigue.83
Agents that Increase Serum Potassium Concentration
Potential pharmacologic interaction (additive hyperkalemic effect) with potassium-sparing diuretics, potassium supplements, and other drugs that can cause hyperkalemia.1, 83 Caution is advised; serum potassium concentrations should be monitored in patients receiving such concomitant therapy.1
Interaction studies with warfarin have not identified any clinically important effect of moexipril therapy on the serum concentrations or effects of warfarin.1, 83
Concomitant therapy with cimetidine and moexipril did not reveal any clinically important pharmacokinetic interactions.1, 83
Concomitant therapy with digoxin and moexipril did not reveal any clinically important pharmacokinetic interactions.1, 83
Potential pharmacokinetic and pharmacologic interaction (hypotensive effect).1 No clinically important pharmacokinetic interaction observed with concomitant hydrochlorothiazide.1, 83
Drugs that Block the Renin-Angiotensin System
Dual blockade of the renin-angiotensin system with angiotensin receptor blocking agents, angiotensin-converting enzyme (ACE) inhibitors, or aliskiren is associated with increased risks of hypotension, hyperkalemia, and changes in renal function (including acute renal failure) compared with monotherapy.1, 83 Blood pressure, renal function, and electrolytes should be closely monitored in patients receiving moexipril and other agents that affect the renin-angiotensin system.1, 83
Nitroid reactions (manifestations include facial flushing, nausea, vomiting, and hypotension) have been reported rarely in patients receiving concomitant therapy with injectable gold (sodium aurothiomalate) and an ACE inhibitor.1, 83
Potential pharmacokinetic interaction (increased lithium concentrations and clinical toxicity).1, 83
Nonsteroidal Anti-inflammatory Agents
In geriatric patients, patients who are volume depleted (including those who are receiving diuretic therapy), or patients with compromised renal function, concomitant use of nonsteroidal anti-inflammatory agents (NSAIAs), including cyclooxygenase-2 (COX-2) inhibitors, and ACE inhibitors may result in the deterioration of renal function, including possible renal failure.1, 83 These effects are usually reversible.1, 83 Renal function should be monitored periodically in patients receiving concomitant moexipril and NSAIA therapy.1, 83
Moexipril hydrochloride is an angiotensin-converting enzyme (ACE, bradykininase, kininase II) inhibitor.1 Unlike captopril or lisinopril but similar to benazepril, enalapril, fosinopril, perindopril, quinapril, ramipril, and trandolapril, moexipril is a prodrug and has little pharmacologic activity until hydrolyzed in the liver to moexiprilat.1, 2, 3, 5, 8, 9, 10, 11, 12, 13, 14 Like benazepril, enalapril, fosinopril, lisinopril, perindopril, quinapril, ramipril, and trandolapril, but unlike captopril, moexipril does not contain a sulfhydryl group.1, 8, 9, 10, 11, 12, 13, 14
Risk of angioedema, anaphylactoid, and other sensitivity reactions and importance of reporting suggestive manifestations (e.g., edema of face, extremities, lips, or tongue; hoarseness; swallowing or breathing with difficulty).1
Risk of hypotension (e.g., lightheadedness, syncope), especially during initial therapy or with volume depletion secondary to excessive perspiration, vomiting, or diarrhea.1 Importance of adequate fluid intake.1 Importance of discontinuing drug and contacting clinician if symptoms of syncope occur.1
Importance of contacting a clinician promptly if manifestations of infection (e.g., sore throat, fever) develop.1
Risk of hyperkalemia.1 Importance of avoiding the use of potassium supplements or salt substitutes containing potassium without consultation with a clinician.1
Importance of advising patients to take moexipril hydrochloride in a fasting state (e.g., 1 hour before meals).1, 3, 83
Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs.1
Importance of women informing clinicians immediately if they are or plan to become pregnant or plan to breast-feed.1, 111 Risk of use during first, second, and third trimesters of pregnancy; importance of discussing other options for hypertension treatment if pregnancy occurs.1, 110, 111
Importance of informing patients of other important precautionary information. (See Cautions.)
Additional Information
Overview® (see Users Guide). For additional information on this drug until a more detailed monograph is developed and published, the manufacturers' labelings should be consulted. It is essential that the manufacturers' labelings be consulted for more detailed information on usual cautions, precautions, contraindications, potential drug interactions, laboratory test interferences, and acute toxicity.
Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.
Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets, film-coated | 7.5 mg* | Moexipril Hydrochloride Tablets | |
15 mg* | Moexipril Hydrochloride Tablets |
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Routes | Dosage Forms | Strengths | Brand Names | Manufacturer |
|---|---|---|---|---|
Oral | Tablets, film-coated | 7.5 mg with Hydrochlorothiazide 12.5 mg* | Moexipril Hydrochloride and Hydrochlorothiazide Tablets | |
15 mg with Hydrochlorothiazide 12.5 mg* | Moexipril Hydrochloride and Hydrochlorothiazide Tablets | |||
15 mg with Hydrochlorothiazide 25 mg* | Moexipril Hydrochloride and Hydrochlorothiazide Tablets |
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
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