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.
Because of established clinical benefits (e.g., reductions in overall mortality and in adverse cardiovascular, cerebrovascular, and renal outcomes), current evidence-based practice guidelines for the management of hypertension in adults generally recommend the use of drugs from 4 classes of antihypertensive agents (angiotensin-converting enzyme [ACE] inhibitors, angiotensin II receptor antagonists, calcium-channel blockers, and thiazide diuretics).501, 502, 503, 504, 1200 (See Uses: Hypertension in Adults, in the Thiazides General Statement 40:28.20.) Direct vasodilators, including minoxidil, may be used in combination with other antihypertensive therapies (e.g., a diuretic and a β-adrenergic blocking agent [β-blocker], an ACE inhibitor, a calcium-channel blocking agent, and/or an angiotensin II receptor antagonist) to achieve target blood pressure goals.504, 1200
Minoxidil often is effective in the management of hypertension resistant to other drugs. 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.110, 143 However, 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 some clinicians 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.1200 Such patients should be managed by intensification or reinstitution (e.g., following noncompliance) of the current antihypertensive regimen and treatment of anxiety if needed.1200
For additional information on overall principles and expert recommendations for treatment of hypertension, see Uses: Hypertension in Adults and also see Uses: Hypertension in Pediatric Patients, in the Thiazides General Statement 40:28.20.
Minoxidil is used topically to stimulate regrowth of hair in patients with androgenetic alopecia106, 107, 108, 109, 116, 117, 118, 119, 122, 123, 124, 128, 129, 130, 131, 132, 133, 134, 135, 137 (male pattern alopecia, hereditary alopecia, common male baldness) or alopecia areata†.102, 103, 104, 105, 106, 107, 116, 117, 118, 125, 126, 127 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.113 Instead, commercially available topical minoxidil preparations (e.g., Rogaine®) should be used. (See Minoxidil 84:92.) 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;110 in addition, skin intolerance to minoxidil110, 111, 116, 117, 118, 119, 124, 125, 133, 136 and/or an ingredient(s) in the formulation may occur.110
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-adrenergic blocking agent (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-blocker 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.)
For the management of hypertension in patients older than 12 years of age, the recommended initial dosage of minoxidil is 5 mg once daily.600 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.600 The manufacturer states that 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.600 Some experts state that the usual dosage range is 5-100 mg daily given as a single dose or in 2 or 3 divided doses.1200 If rapid control of hypertension is required, dosage may be adjusted every 6 hours while monitoring blood pressure closely.600
Clinical experience with minoxidil for the management of hypertension in children, particularly infants, is limited and dosage must be carefully titrated.600 In children younger than 12 years of age, the usual initial dosage of minoxidil is 0.2 mg/kg once daily.600 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.600 If rapid control of hypertension is required, dosage may be adjusted every 6 hours while monitoring blood pressure closely.600 The usual effective dosage of minoxidil in children is 0.25-1 mg/kg daily, and the maximum dosage recommended by the manufacturers is 50 mg daily.600
For rapid reduction of blood pressure in children and adolescents with severe hypertension and non-life-threatening symptoms†, some experts recommend an oral minoxidil dose of 0.1-0.2 mg/kg up to 10 mg per dose administered every 8-12 hours.1150
Blood Pressure Monitoring and Treatment Goals
Blood pressure should be monitored regularly during therapy and dosage of the antihypertensive drug adjusted until blood pressure is controlled.1200 In patients who develop unacceptable adverse effects with minoxidil, the drug should be discontinued and another antihypertensive agent from a different pharmacologic class should be initiated.1200, 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 A 2017 multidisciplinary hypertension guideline from the American College of Cardiology (ACC), American Heart Association (AHA), and a number of other professional organizations generally recommends a blood pressure goal of less than 130/80 mm Hg in all adults, regardless of comorbidities or level of atherosclerotic cardiovascular disease (ASCVD) risk.1200, 1207 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 target levels of blood pressure and on monitoring therapy, see Blood Pressure Monitoring and Treatment Goals under Dosage: Hypertension, in Dosage and Administration in the Thiazides General Statement 40:28.20.
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).
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 agent (β-blocker) 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-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;110, 139, 140, 141 however, the relationship of this effect to renal function is unclear.110
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 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-blocker 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.110 Patients receiving minoxidil also should be instructed to notify their clinician if resting pulse rate increases by 20 or more beats/minute 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.
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, see Uses: Hypertension in Pediatric Patients, in the Thiazides General Statement 40:28.20.
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.110 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.110 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.110
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.110 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.110
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.110 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.110 There was no evidence of carcinogenic potential in rats receiving the drug orally.110
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.114 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.115 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.115 However, it is not known whether these effects resulted from minoxidil, concurrently administered drugs, the maternal condition, or other factors.115 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.110 The effects of the drug on labor and delivery are not known.110
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.110 There has been no evidence of teratogenic effects in rats and rabbits.110 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.110, 153 Evidence of developmental toxicity was observed in rats receiving subcutaneous dosages exceeding 80 mg/kg daily.110, 153
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).110, 153
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.
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.
Limited information is available on the acute toxicity of minoxidil. Severe hypotension after ingestion of minoxidil is most likely to occur in patients with residual sympathetic nervous system blockade from previous therapy with guanethidine or α-adrenergic blockers. In these patients, IV administration of 0.9% sodium chloride injection helps maintain blood pressure and facilitates urine formation. Norepinephrine and epinephrine should be avoided, and vasopressors such as phenylephrine, vasopressin, and dopamine should be used only if a vital organ is underperfused.
Minoxidil reduces peripheral vascular resistance and blood pressure as a result of a direct vasodilating effect on vascular smooth muscle; like diazoxide and hydralazine, minoxidil's effect on arterioles is greater than on veins. Minoxidil delays the hydrolysis of cyclic 3',5'-adenosine monophosphate (cyclic AMP) and cyclic guanosine monophosphate (cyclic GMP) by inhibiting the enzyme phosphodiesterase, and relaxation of arterial smooth muscle by the drug may be, at least partly, mediated by cyclic AMP. Animal studies indicate that minoxidil does not have CNS or adrenergic neuronal blocking effects. The drug decreases blood pressure in both the supine and standing positions, and there is no orthostatic hypotension.
Minoxidil-induced decrease in blood pressure is accompanied by increased heart rate, cardiac output, and stroke volume due to a reflex response to the decreased peripheral resistance. Increased cardiac output may partially offset the hypotensive effect of arteriolar dilation and limit the antihypertensive effectiveness of the drug. Tachycardia and its sequelae may be minimized by administration of a β-adrenergic blocking agent (β-blocker). Pulmonary vascular resistance is decreased; when minoxidil is used in conjunction with a β-blocker, pulmonary artery pressure is usually unchanged. Renal blood flow and glomerular filtration rate are usually unchanged.
Minoxidil causes sodium and water retention which can result in expansion of fluid volume, edema, and congestive heart failure. The sodium- and water-retaining effects of minoxidil can be reversed by administration of a diuretic or, in patients on dialysis, by dialysis. (See Cautions: Other Adverse Effects.) Minoxidil usually increases plasma renin activity (PRA) appreciably, an effect which is most marked in patients with initially high PRA; PRA may return to pretreatment concentrations with continued therapy. Increased PRA is partially antagonized by β-blocker therapy.
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.101 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). 110 Minoxidil and its metabolites can be removed by hemodialysis or peritoneal dialysis.
Minoxidil is a piperidinopyrimidine-derivative hypotensive agent. The drug occurs as a white to off-white, crystalline powder and is slightly soluble in water and soluble in alcohol. Minoxidil has a pKa of 4.6.
Minoxidil tablets should be stored in well-closed containers at controlled room temperature of 20-25°C.
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 | 2.5 mg* | Minoxidil Tablets | |
10 mg* | Minoxidil Tablets |
* available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name
Only references cited for selected revisions after 1984 are available electronically.
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