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minoxidil 10 mg tablet

Out of Stock Manufacturer MUTUAL PHARM CO 53489038701
Out of Stock



Minoxidil is used in the management of severe hypertension that is symptomatic or associated with end-organ damage. Because of the frequency and severity of adverse effects, minoxidil generally is reserved for hypertension that is not manageable with maximal therapeutic dosages of a diuretic and 2 other hypotensive drugs. Angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor antagonists, calcium-channel blockers, and thiazide diuretics are the preferred antihypertensive agents for the initial management of hypertension in adults.Direct vasodilators, including minoxidil, may be used in combination with other antihypertensive therapies (e.g., a diuretic and a β-adrenergic blocking agent, an ACE inhibitor, a calcium-channel blocking agent, and/or an angiotensin II receptor antagonist) to achieve target blood pressure goals.

Minoxidil often is effective in the management of hypertension resistant to other drugs. It should be considered that some clinicians and the manufacturers state that minoxidil should not be used in mild or moderate hypertension or severe hypertension that can be controlled with other drugs (i.e., reserved for refractory hypertension), because the benefit-to-risk ratio has not been clearly determined. However, some clinicians state that aggressive approaches to the management of severe hypertension may be necessary in some patients, reducing the intervals between changes in the antihypertensive regimen and maximum dosages employed, and they recommend that clinicians not hesitate to use the most potent agents, including minoxidil, when warranted, especially in patients with impaired renal function. Patients with markedly elevated blood pressure without acute target organ damage usually do not require hospitalization. Such patients should receive immediate oral combination antihypertensive therapy. Clinicians should carefully evaluate these patients and monitor them for development of hypertension-induced heart and kidney damage and identify causes of hypertension.

For additional information on overall principles and expert recommendations for treatment of hypertension,

Androgenetic Alopecia

Minoxidil is used topically to stimulate regrowth of hair in patients with androgenetic alopecia (male pattern alopecia, hereditary alopecia, common male baldness) or alopecia areata. Because the safety and efficacy of extemporaneously prepared formulations of topical minoxidil in promoting hair growth have not been fully evaluated and because such preparations may vary in strength and efficacy, the FDA requests that physicians and pharmacists refrain from preparing extemporaneous topical formulations using the commercially available tablets. Instead, commercially available topical minoxidil preparations (e.g., Rogaine) should be used. If minoxidil tablets are used to prepare extemporaneous topical formulations, such preparations should be considered to share the toxic potentials of the systemically administered drug; in addition, skin intolerance to minoxidil and/or an ingredient(s) in the formulation may occur.

Dosage and Administration


Minoxidil is administered orally. Minoxidil may be administered once or twice daily, depending on the patient's blood pressure response. The manufacturers recommend that the drug be administered once daily in patients whose supine diastolic pressure has been reduced by less than 30 mm Hg and twice daily in equally divided doses in those whose supine diastolic pressure has been reduced by more than 30 mm Hg during minoxidil therapy.

A β-blocker (e.g., equivalent to 80-160 mg of propranolol daily) must be given before minoxidil therapy is begun and should be continued during minoxidil therapy to minimize minoxidil-induced tachycardia and increased myocardial workload. If a β-adrenergic blocking drug is contraindicated, another sympathetic nervous system suppressant such as methyldopa (250-750 mg twice daily) should be used and must be started at least 24 hours before minoxidil because of the delayed onset of methyldopa's action. Limited clinical experience indicates that clonidine (0.1-0.2 mg twice daily) may be used as an alternative to methyldopa.

Minoxidil also must be used in conjunction with a thiazide (e.g., hydrochlorothiazide 50 mg twice daily, chlorthalidone 50-100 mg once daily) or loop diuretic (e.g., furosemide 40 mg twice daily) when initiating minoxidil therapy in patients dependent on renal function for maintenance of sodium and water balance. If excessive sodium and water retention results in weight gain exceeding 2.3 kg during minoxidil therapy, diuretic therapy should be changed to a loop diuretic or, in patients already receiving a loop diuretic, the dosage should be increased.


Dosage of minoxidil must be adjusted according to the patient's blood pressure response and tolerance.

The need for pretreatment with certain drugs (e.g., β-blockers) and possible concomitant use of a diuretic should be considered in patients receiving minoxidil. (See Dosage and Administration: Administration.)


Usual Dosage

For the management of hypertension in patients older than 12 years of age, the usual initial dosage of minoxidil is 2.5-5 mg once daily. Dosage may be gradually increased after at least 3-day intervals to 10 mg, 20 mg, and then to 40 mg daily in 1 or 2 doses until optimum blood pressure response is attained. The usual effective dosage of minoxidil in patients older than 12 years of age is 10-40 mg daily, and the maximum daily dosage is 100 mg. Some experts recommend a usual dosage of 2.5-80 mg daily given as a single dose or in 2 divided doses. If rapid control of hypertension is required, dosage may be adjusted every 6 hours while monitoring blood pressure closely.

Clinical experience with minoxidil for the management of hypertension in children, particularly infants, is limited and dosage must be carefully titrated. In children younger than 12 years of age, the usual initial dosage of minoxidil is 0.2 mg/kg (maximum 5 mg) once daily. If necessary, dosage is gradually increased at intervals of at least 3 days in increments of 50-100% until optimal blood pressure response is attained. If rapid control of hypertension is required, dosage may be adjusted every 6 hours while monitoring blood pressure closely. The usual effective dosage of minoxidil in children is 0.25-1 mg/kg daily in 1 or 2 doses, and the maximum dosage recommended by the manufacturers is 50 mg daily.

For rapid reduction of blood pressure in pediatric patients (1-17 year of age) with severe hypertension, some experts recommend an oral minoxidil dose of 0.1-0.2 mg/kg.

Blood Pressure Monitoring and Treatment Goals

Careful monitoring of blood pressure during initial titration or subsequent upward adjustment in dosage of minoxidil is recommended.

The goal of hypertension management and prevention is to achieve and maintain optimal control of blood pressure; specific target levels of blood pressure should be individualized based on consideration of multiple factors, including patient age and comorbidities, and the currently available evidence from clinical studies.

For additional information on initiating and adjusting dosage of minoxidil in the management of hypertension,

Dosage in Renal Impairment

Although minoxidil has been used safely in usual doses for the management of hypertension in patients with renal failure, patients with renal failure or those receiving dialysis may require smaller doses of minoxidil (about one-third less than in patients who are not receiving dialysis). Since minoxidil is removed by dialysis, some clinicians recommend that on the day of dialysis the drug be administered immediately after dialysis if dialysis is at 9 a.m.; if dialysis is after 3 p.m., the daily dose is given at 7 a.m. (i.e., 8 hours before dialysis).


Cardiovascular Effects

Sodium and water retention occur frequently in patients receiving minoxidil and may result in edema, weight gain, congestive heart failure (especially in uremic patients), pulmonary edema, and ''refractoriness'' to the antihypertensive effects of the drug. Congestive heart failure may worsen in some patients with preexisting heart failure, although many patients may improve due to the decrease in blood pressure and ventricular afterload. Concomitant administration of a diuretic (usually furosemide or ethacrynic acid) is required except in some patients who are undergoing hemodialysis. Diuretic therapy, alone or with salt restriction, usually minimizes fluid retention, although reversible edema did develop in approximately 10% of patients who were treated in this manner and were not undergoing dialysis. Ascites also has been reported. If fluid retention results in weight gain, diuretic therapy should be changed to furosemide or ethacrynic acid or, in patients already receiving one of these diuretics, the dosage should be increased. Diuretic effectiveness may be limited, especially in patients with impaired renal function, and a few patients have required 640 mg to 1.2 g of furosemide daily. Rarely, refractory fluid retention may occur, requiring discontinuance of minoxidil; in some patients who can be closely supervised, refractory fluid retention may be treated by discontinuing minoxidil for 1-2 days and then resuming minoxidil therapy in conjunction with vigorous diuretic therapy. In patients on hemodialysis, fluid retention can be controlled with more vigorous ultrafiltration.

Tachycardia occurs commonly during minoxidil therapy and can be minimized by concomitant administration of a β-adrenergic blocking drug such as propranolol or other sympathetic nervous system suppressant. Angina pectoris may worsen or occur in patients without previous angina, probably due to increased oxygen demand associated with increased heart rate and cardiac output and can usually be prevented by a β-adrenergic blocker or other sympathetic nervous system suppressant. Although rapid reduction in blood pressure may precipitate cerebrovascular accidents and myocardial infarction in patients with very severe hypertension, these adverse effects have not been unequivocally associated with minoxidil therapy.

Pericardial effusion, sometimes with tamponade, has been observed in about 3% of patients receiving minoxidil who were not on dialysis, especially in those with inadequate or compromised renal function. Although pericardial effusion has occurred most often in patients with a connective tissue disease, uremic syndrome, congestive heart failure, or marked fluid retention, there have been instances in which these potential causes of effusion were not present. Patients receiving minoxidil should be observed for signs and symptoms of pericarditis, pericardial effusion, and tamponade, and echocardiograms should be performed if necessary. More vigorous diuretic therapy, dialysis, pericardiocentesis, or surgery may be required and, if effusion persists, withdrawal of minoxidil should be considered. Pericardial effusion is thought to result from minoxidil-induced sodium and water retention. Pericarditis also has been reported in minoxidil-treated patients; however, the relationship of this effect to renal function is unclear.

Minoxidil has caused various cardiac lesions in animals, including necrosis of the papillary muscles and subendocardial areas of the left ventricle (incidence and severity were reduced by β-adrenergic blockade) and hemorrhagic lesions observed most prominently in the atria and occurring within the epicardium, endocardium, and walls of small coronary arteries and arterioles. In addition, long-term animal studies demonstrated cardiac hypertrophy and dilation (which were partly reversed by diuretic therapy) and epicarditis and serosanguineous fluid. Some of these cardiac lesions (e.g., hemorrhagic or necrotic lesions) are characteristic of agents that cause tachycardia and diastolic hypotension (e.g., β-adrenergic agonists such as isoproterenol, arterial vasodilators such as hydralazine) or of certain agents with arterial vasodilating properties (e.g., theobromine). The relevance of these findings to human use of minoxidil is not clear; the characteristic hemorrhagic lesions observed in animals have not been recognized in patients receiving oral minoxidil at systemically active dosages, despite formal review of more than 150 autopsies of treated patients. Although necrosis of papillary muscles has occurred in some patients with preexisting ischemic heart disease receiving minoxidil, such lesions also have occurred in patients who never received the drug.

ECG changes in the magnitude and direction of the T waves (i.e., positive T waves flatten or invert and negative T waves show increased negativity) occur commonly. Rarely, large negative amplitude of the T wave may encroach upon the ST segment, but the ST segment alone is not changed. ECG changes usually revert to the pretreatment state with continued therapy or when minoxidil is discontinued. No symptoms, evidence of myocardial damage, or deterioration of cardiac function have been associated with minoxidil-induced ECG changes.


Within 3-6 weeks after initiating minoxidil therapy, hypertrichosis (elongation, thickening, and increased pigmentation of fine body hair) commonly occurs but is not associated with an endocrine abnormality. At first, hypertrichosis occurs on the face (i.e., the temples, between the eyebrows, between the hairline and eyebrows, and in the sideburn area of the upper lateral cheek) and later extends to the back, arms, legs, scalp, and chest. Occasionally hypertrichosis may be associated with apparent coarsening of facial features, which may be due to mild generalized fluid retention; transient pruritus may also be associated with hair growth. Hypertrichosis can be controlled with shaving or depilatories. New hair growth stops when minoxidil is discontinued, but 1-6 months may be required before pretreatment appearance is restored.

Other Adverse Effects

Other adverse effects that have occurred rarely in patients receiving minoxidil include breast tenderness, gynecomastia, changes in skin pigmentation, polymenorrhea, headache, nausea, intermittent claudication, serosanguineous bullae on the legs, thrombocytopenia, and hypersensitivity (rash). Because of minoxidil-induced hemodilution, hematocrit, hemoglobin concentration, and erythrocyte count usually decrease about 7% and then return to pretreatment levels. Serum alkaline phosphatase may increase but no other evidence of liver or bone abnormality has occurred to date. Serum creatinine concentration and creatinine clearance are usually unchanged during minoxidil therapy, although serum creatinine and BUN concentrations may transiently increase slightly.

Precautions and Contraindications

Because about 80% of patients receiving minoxidil experience drug-induced hair growth (see Cautions: Hypertrichosis), which may be particularly disturbing to children and women, patients should be informed about this effect before therapy with the drug is begun.

Minoxidil should be used with caution in patients with recent myocardial infarction, since it is possible that a decrease in blood pressure and increase in heart rate may further limit blood flow to the myocardium; however, the decrease in blood pressure may be beneficial in decreasing oxygen demand. In patients with preexisting pulmonary hypertension, chronic congestive heart failure, or clinically important renal impairment, increased pulmonary artery pressure may occur and minoxidil should be used with caution in these patients.

Because rapid or excessive reductions in systolic or diastolic blood pressure in patients with very severe blood pressure elevation may precipitate syncope, cerebrovascular accidents, myocardial infarction, and ischemia of special sense organs with resulting decrease or loss of vision or hearing, patients with malignant hypertension and those already receiving guanethidine (see Drug Interactions: Diuretics and Hypotensive Agents) should be hospitalized during initial minoxidil therapy and monitored closely to assure that blood pressure is decreasing but not too rapidly.

Because serious adverse cardiovascular effects such as pericarditis, pericardial effusion with or without tamponade, exacerbation of angina pectoris, sodium and water retention, and tachycardia, as well as various cardiac lesions in animals, have been associated with minoxidil (see Cautions: Cardiovascular Effects), the drug must be used under close supervision, usually concomitantly with doses of a β-adrenergic blocking agent to prevent tachycardia and increased myocardial workload and with a diuretic, frequently one acting in the ascending limb of the loop of Henle, to prevent serious fluid accumulation. In addition, fluid and electrolyte balance and body weight should be monitored during minoxidil therapy, and patients with renal failure or those undergoing dialysis should be closely supervised to prevent exacerbation of renal failure or precipitation of cardiac failure.

Laboratory tests (e.g., urinalysis, renal function, ECG, chest radiograph, echocardiogram) that were abnormal at initiation of minoxidil therapy should be repeated initially at 1- to 3-month intervals and as stabilization occurs, at 6- to 12-month intervals. Patients receiving minoxidil also should be instructed to notify their clinician if resting pulse rate increases by 20 or more bpm above normal, if breathing becomes more difficult (especially when lying down), or if dizziness, lightheadedness, fainting, symptoms of edema (e.g., rapid weight gain, swelling or puffiness of face, hands, ankles, stomach area), or symptoms of angina occur.

Minoxidil is contraindicated in patients with pheochromocytoma, since the drug's hypotensive effect may stimulate secretion of catecholamines from the tumor. Minoxidil also is contraindicated in patients with known hypersensitivity to the drug or any ingredient in the formulation.

Pediatric Precautions

Clinical experience with minoxidil for the management of hypertension in children, particularly infants, is limited. In 3 pediatric patients who had received 40-50 mg of minoxidil daily for 47-158 weeks with other hypotensive agents, hypertensive encephalopathy occurred when minoxidil was discontinued (dosage was decreased gradually over a period of 4-8 weeks); however, a causal relationship has not been definitely established. For information on overall principles and expert recommendations for treatment of hypertension in pediatric patients,

Geriatric Precautions

Clinical studies of minoxidil did not include sufficient numbers of patients 65 years of age and older to determine whether geriatric patients respond differently than younger patients. Although other clinical experience has not revealed age-related differences in response, drug dosage generally should be titrated carefully in geriatric patients, usually initiating therapy at the low end of the dosage range. 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.

Mutagenicity and Carcinogenicity

In vitro studies using minoxidil in a microbial system (i.e., Ames test), the DNA damage/alkaline elution assay, unscheduled DNA synthesis assay, or mouse or rat micronucleus tests have not shown the drug to be mutagenic. An in vitro cytogenetic assay using Chinese hamster cells at long exposure times yielded equivocal results, but results of a similar assay in human lymphocytes were negative.

Oral administration of minoxidil for up to 2 years in mice was associated with an increased incidence of malignant lymphoma in females receiving minoxidil dosages of 10, 25, or 63 mg/kg daily and an increased incidence of hepatic nodules in males receiving minoxidil dosages of 63 mg/kg daily. Despite the increased incidence of hepatic nodules in these animals, there was no evidence of a drug-induced effect on the incidence of malignant hepatic tumors. There was no evidence of carcinogenic potential in rats receiving the drug orally.

Pregnancy, Fertility, and Lactation


Pronounced hypertrichosis and multiple congenital anomalies, including dysmorphic facial features (e.g., depressed nasal bridge, low-set ears, micrognathia), bilateral clinodactyly, omphalocele, undescended testes, midphallic constriction, unusual fat distribution, and ventriculoseptal defect, occurred in a neonate born to a woman who received minoxidil, captopril, furosemide, and propranolol throughout pregnancy. Hypertrichosis (which appeared as a general increase in bristly hair that was longest in the sacral area) occurred in another infant born to a woman who had received minoxidil as well as metoprolol and prazosin throughout pregnancy. Cyanotic heart disease resulting in death occurred in a neonate born to a woman receiving minoxidil, furosemide, hydralazine, methyldopa, and phenobarbital therapy during the pregnancy; an autopsy revealed transposition of the great vessels and pulmonic bicuspid valvular stenosis. However, it is not known whether these effects resulted from minoxidil, concurrently administered drugs, the maternal condition, or other factors. There are no adequate and controlled studies to date using minoxidil in pregnant women, and the drug should be used during pregnancy only when the potential benefits justify the possible risks to the fetus. The effects of the drug on labor and delivery are not known.

Oral administration of minoxidil has been associated with evidence of increased fetal resorption in rabbits, but not rats, when administered at 5 times the maximum recommended oral human dosage. There has been no evidence of teratogenic effects in rats and rabbits. There was no evidence of teratogenic effects in rats receiving subcutaneous minoxidil dosages of 80 mg/kg daily (about 2000 times the maximal systemic human exposure achieved with daily administration of topical minoxidil); however, maternal toxicity was observed with this dosage. Evidence of developmental toxicity was observed in rats receiving subcutaneous dosages exceeding 80 mg/kg daily.


Minoxidil produced a dose-dependent reduction in conception rate when administered orally to male and female rats in dosages 1 or 5 times the maximum recommended oral human dosage (based on a 50-kg patient).


Minoxidil is distributed into milk. Because of the potential for adverse reactions from minoxidil in nursing infants, the drug should not be administered in nursing women.

Drug Interactions

Diuretics and Hypotensive Agents

When minoxidil is administered with diuretics or other hypotensive drugs, the hypotensive effect of minoxidil is increased. The effect is usually used to therapeutic advantage, but careful adjustment of dosage is necessary when these drugs are used concomitantly. Minoxidil should be administered with caution to patients receiving guanethidine, since concurrent use may cause profound orthostatic hypotensive effects. If possible, guanethidine should be withdrawn several days (1-3 weeks) before minoxidil therapy is begun. If minoxidil must be started in patients receiving guanethidine, the patient should be hospitalized until severe orthostatic effects subside or the patient has learned to avoid activities that cause postural hypotension.



Minoxidil is rapidly and well absorbed from the GI tract. Following oral administration of a single 5- to 100-mg dose of minoxidil, plasma concentrations of unchanged drug peak within 1 hour and decline rapidly. Plasma concentrations of minoxidil do not correlate with extent or duration of action, probably because the drug exerts a persistent effect at receptor sites. After a single 2.5- to 25-mg oral dose of minoxidil, the hypotensive effect begins in 30 minutes, is maximal in 2-8 hours, and persists for about 2-5 days.


Minoxidil is widely distributed into body tissues. In animals, tissue concentrations (primarily the kidneys and to a lesser extent arterial tissue) of the drug are higher than plasma concentrations. The drug may be retained selectively by arterial tissue. Minoxidil is distributed into milk. The drug is not bound to plasma proteins.


In one study in patients with various degrees of renal function (i.e., normal to uremic), the mean plasma half-life of minoxidil and its metabolites was 4.2 hours. About 90% of an oral dose of minoxidil is metabolized, primarily by conjugation with glucuronic acid and also by conversion to more polar metabolites. Minoxidil's metabolites are considerably less active than the parent drug.

The drug and its metabolites are excreted principally in urine by glomerular filtration; with chronic therapy in patients with renal impairment, minoxidil's glucuronide metabolites accumulate in plasma but the unchanged drug does not. The clearance of minoxidil is directly affected by the glomerular filtration rate (GFR). Minoxidil and its metabolites can be removed by hemodialysis or peritoneal dialysis.

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