Minoxidil

Minoxidil, sold under the brand names Loniten and Rogaine among others, is a medication used for the treatment of high blood pressure and pattern hair loss.<ref name="Loniten SmPC" /><ref name="Regaine for Men SmPC" /><ref name="Regaine for Women SmPC" /> It is an antihypertensive and a vasodilator.<ref>Template:Cite web</ref> It is available as a generic medication by prescription in oral tablet form and over-the-counter as a topical liquid or foam.<ref name="Minoxidil tablet FDA label">Template:Cite web</ref><ref name="Minoxidil aerosol FDA label">Template:Cite web</ref><ref>Template:Cite web</ref><ref>Template:Cite web</ref>

Medical uses

High blood pressure

Minoxidil, when used for hypertension, is generally reserved for use in severe hypertension patients who do not respond to at least two agents and a diuretic.<ref name="pmid15133413" /> Minoxidil is also generally administered with a loop diuretic to prevent sodium retention and potassium retention.<ref name="pmid15133413" /> It may also cause a reflex tachycardia and thus is prescribed with a beta blocker.<ref name="pmid15133413" />

Hair loss

Minoxidil, when applied topically, is used for the treatment of hair loss.<ref name="Var2014" /> It is effective in helping promote hair growth in people with androgenic alopecia regardless of sex.<ref name="Var2014">Template:Cite journal</ref> Minoxidil must be used indefinitely for continued support of existing hair follicles and the maintenance of any experienced hair regrowth.<ref name="Regaine for Men SmPC" /><ref name="Regaine for Women SmPC" />

Low-dose oral minoxidil (LDOM) is used off-label against hair loss and to promote hair regrowth.<ref name=":0">Template:Cite news</ref> Oral minoxidil is an effective and well-tolerated treatment alternative for patients having difficulty with topical formulations.<ref name=":1">Template:Cite journal</ref><ref>Template:Cite journal</ref><ref>Template:Cite journal</ref>

Minoxidil requires at least 2 to 4Template:Nbspmonths before the first benefits on hair growth can be observed.<ref name="Anastassakis2022" /> Maximal effectiveness occurs after 12Template:Nbspmonths.<ref name="Anastassakis2022" />

Available forms

Minoxidil is available in the form of oral tablets, topical solution, topical foam, and topical spray.<ref name="GuptaTalukderVenkataraman2022" /> The tablets include 2.5 and 10Template:Nbspmg forms, the solutions include 2% and 5% forms, and the foam and spray are both 5% concentration.<ref name="Anastassakis2022" /><ref name="GuptaTalukderVenkataraman2022" /> The topical solutions are formulated with polyethylene glycol (PEG) to enhance absorption of minoxidil.<ref name="GuptaTalukderVenkataraman2022" /> The topical solution is often referred to as minoxidil topical solution (MTS) and the topical foam is known as minoxidil topical foam (MTF).<ref name="Anastassakis2022" />

Side effects

Top 10 most common side effects.<ref name=pmid27738338>Template:Cite journal</ref>

Side effects of oral minoxidil may include swelling of the face and extremities, rapid heartbeat, or lightheadedness. Cardiac lesions, such as focal necrosis of the papillary muscle and subendocardial areas of the left ventricle, have been observed in laboratory animals treated with minoxidil.<ref name="Minoxidil tablet FDA label" /> Pseudoacromegaly is an extremely rare side effect reported with large doses of oral minoxidil.<ref>Template:Cite journal</ref>

Topically applied minoxidil is generally well tolerated, but common side effects include itching of the eyes, general itching, irritation at the treated area, and unwanted hair growth elsewhere on the body.<ref name=effects>Template:Cite web</ref> Alcohol and propylene glycol present in some topical preparations may dry the scalp, resulting in dandruff and contact dermatitis.<ref>Template:Cite journal</ref>

Sublingual minoxidil may have reduced side effects with retained effectiveness compared to oral minoxidil.<ref name="ModhaPathania2022" /><ref name="Saceda-CorraloDomínguez-SantasVañó-Galván2023" /><ref name="BokhariJonesSinclair2022" /> This is due to less minoxidil sulfate being formed during first-pass metabolism and due to local activation of minoxidil into minoxidil sulfate within hair follicles.<ref name="ModhaPathania2022" /><ref name="Saceda-CorraloDomínguez-SantasVañó-Galván2023" /><ref name="BokhariJonesSinclair2022">Template:Cite journal</ref> In a preliminary clinical trial, no adverse effects or changes in blood pressure occurred with low-dose sublingual minoxidil.<ref name="Saceda-CorraloDomínguez-SantasVañó-Galván2023" /><ref name="BokhariJonesSinclair2022" />

Minoxidil has been implicated in causing pericardial effusions<ref>Template:Cite web</ref> including life-threatening cases of cardiac tamponade.<ref name = "Oye_2021">Template:Cite journal</ref> There have been case reports dating back to the 1980s describing this phenomenon, including topical<ref name = "Oye_2021" /> and oral formulations.<ref>Template:Cite journal</ref> The frequency of these occurrences has previously been reported at 3%, but the true frequency is difficult to determine as a large proportion of patients in this cohort also had renal insufficiency and may have had an effusion preceding the use of minoxidil.<ref>Template:Cite journal</ref>

Overdose

In 2013 or 2014, a seven-year-old girl was admitted to a children's hospital in Toulouse in France after accidentally ingesting a teaspoon of Alopexy (a brand name for minoxidil in France). The child vomited constantly after ingestion and showed hypotension and tachycardia for 40 hours.<ref>Template:Cite journal</ref> The authors of the report on the incident stressed that the product should be kept out of reach of children, and urged manufacturers to consider more secure child-resistant packaging.<ref>Template:Cite news</ref>

Interactions

Combination of oral minoxidil with guanethidine can result in profound orthostatic hypotension.<ref name="Loniten-Label" />

Low-dose daily aspirin can reduce the effectiveness of topical minoxidil for hair loss.<ref name="SuchonwanitThammaruchaLeerunyakul2019">Template:Cite journal</ref><ref name="OlsenSinclairHordinsky2025" /><ref name="GorenSharmaDhurat2018">Template:Cite journal</ref> This is thought to be because aspirin inhibits sulfotransferase activity and hence prevents conversion of aspirin into its active form minoxidil sulfate.<ref name="SuchonwanitThammaruchaLeerunyakul2019" /><ref name="OlsenSinclairHordinsky2025" /><ref name="GorenSharmaDhurat2018" /> Salicylic acid is also a sulfotransferase inhibitor and could likewise affect the effectiveness of topical minoxidil.<ref name="SuchonwanitThammaruchaLeerunyakul2019" /><ref name="GorenSharmaDhurat2018" /> In addition, paracetamol (acetaminophen) is a sulfate scavenger and may inhibit minoxidil activation into minoxidil sulfate and effectiveness.<ref name="OlsenSinclairHordinsky2025" /><ref name="BuhlWaldonBaker1990" />

Pharmacology

Pharmacodynamics

The mechanism by which minoxidil promotes hair growth is not fully understood. Minoxidil is an adenosine 5'-triphosphate-sensitive potassium channel opener,<ref>Template:Cite journal</ref> causing hyperpolarization of cell membranes. Theoretically, by widening blood vessels and opening potassium channels, it allows more oxygen, blood, and nutrients to the follicles. Moreover, minoxidil contains a nitric oxide moiety and may act as a nitric oxide agonist. This may cause follicles in the telogen phase to shed, which are then replaced by thicker hairs in a new anagen phase. Minoxidil is a prodrug that is converted by sulfation via the sulfotransferase enzyme SULT1A1 to its active form, minoxidil sulfate. The effect of minoxidil is mediated by adenosine, which triggers intracellular signal transduction via both adenosine A₁ receptors and two sub-types of adenosine A₂ receptors (A_2A and A_2B receptors).<ref name="maru 2001">Template:Cite journal</ref> Minoxidil acts as an activator of the Kir6/SUR2 channel upon selective binding to SUR2.<ref>Template:Cite journal</ref> The expression of SUR2B in dermal papilla cells might play a role in the production of adenosine.<ref name="maru 2001"/> Minoxidil induces cell growth factors such as VEGF, HGF, IGF-1 and potentiates HGF and IGF-1 actions by the activation of uncoupled sulfonylurea receptor on the plasma membrane of dermal papilla cells.<ref>Template:Cite journal</ref>

A number of in vitro effects of minoxidil have been described in monocultures of various skin and hair follicle cell types including stimulation of cell proliferation, inhibition of collagen synthesis, and stimulation of vascular endothelial growth factor, prostaglandin synthesis and leukotriene B4 expression.<ref>Template:Cite journal</ref>

Minoxidil causes a redistribution of cellular iron through its apparent capacity to bind this metal ion. By binding iron in a Fenton-reactive form, intracellular hydroxyl radical production would ensue, but hydroxyl would be immediately trapped and scavenged by the minoxidil to generate a nitroxyl radical. It is presumed that this nitroxyl radical will be capable of reduction by glutathione to reform minoxidil. Such a process would cycle until the minoxidil is otherwise metabolized and would result in rapid glutathione depletion with glutathione disulphide formation and therefore with concomitant consumption of NADPH/NADH and other reducing equivalents.<ref>Template:Cite book</ref> Minoxidil inhibited PHD by interfering with the normal function of ascorbate, a cofactor of the enzyme, leading to a stabilization of HIF-1α protein and a subsequent activation of HIF-1. In an in vivo angiogenesis assay, millimolar minoxidil increased blood vessel formation in a VEGF-dependent manner. Minoxidil inhibition of PHD occurs via interrupting ascorbate binding to iron.<ref>Template:Cite journal</ref> The structural feature of positioning amines adjacent to nitric oxide may confer the ability of millimolar minoxidil to chelate iron, thereby inhibiting PHD. Minoxidil is capable of tetrahydrobiopterin inhibition as a cofactor for nitric oxide synthase.<ref>Template:Cite patent</ref>

Minoxidil stimulates prostaglandin E₂ production by activating COX-1<ref>Template:Cite journal</ref> and prostaglandin endoperoxide synthase-1 but inhibits prostacyclin production. Additionally, expression of the prostaglandin E₂ receptor, the most upregulated target gene in the β-catenin pathway of DP cells, was enhanced by minoxidil, which may enable hair follicles to grow continuously and maintain the anagen phase.<ref name="pmid31496654">Template:Cite journal</ref>

Due to the anti-fibrotic activity of minoxidil inhibition of enzyme lysyl hydroxylase present in fibroblast may result in the synthesis of a hydroxylysine-deficient collagen. Minoxidil can also potentially stimulate elastogenesis in aortic smooth muscle cells, and in skin fibroblasts in a dose-dependent manner. In hypertensive rats, minoxidil increases elastin levels in the mesenteric, abdominal, and renal arteries by a decrease in elastase enzyme activity in these tissues. In rats, potassium channel openers decrease calcium influx which inhibits elastin gene transcription through extracellular signal-regulated kinase 1/2 (ERK 1/2)-activator protein 1 signaling pathway. ERK 1/2 increases, through elastin gene transcription, adequately cross-linked elastic fiber content synthesized by smooth muscle cells, and decreases the number of cells in the aorta.<ref>Template:Cite journal</ref>

Minoxidil possesses α₂-adrenergic receptor agonist activity,<ref>Template:Cite journal</ref> stimulates the peripheral sympathetic nervous system (SNS) by way of carotid and aortic baroreceptor reflexes. Minoxidil administration also brings an increase in plasma renin activity, largely due to the aforementioned activation of the SNS. This activation of the renin-angiotensin axis further prompts increased biosynthesis of aldosterone; whereas plasma and urinary aldosterone levels are increased early in the course of treatment with minoxidil, over time these values tend to normalize presumably because of accelerated metabolic clearance of aldosterone in association with hepatic vasodilation.<ref name="pmid15133413">Template:Cite journal</ref>

Minoxidil may be involved in the inhibition of serotonin 5-HT₂ receptors.<ref>Template:Cite journal</ref>

Minoxidil might increase blood-tumor barrier permeability in a time-dependent manner by down-regulating tight junction protein expression and this effect could be related to ROS/RhoA/PI3K/PKB signal pathway.<ref>Template:Cite journal</ref> Minoxidil significantly increases ROS concentration when compared to untreated cells.Template:Medcn

Minoxidil treatment resulted in a 0.22 fold change for 5α-R2 (p < 0.0001) in vitro. This antiandrogenic effect of minoxidil, shown by significant downregulation of 5α-R2 gene expression in HaCaT cells, may be one of its mechanisms of action in alopecia.<ref>Template:Cite journal</ref>

Minoxidil is less effective when the area of hair loss is large. In addition, its effectiveness has largely been demonstrated in younger men who have experienced hair loss for less than 5 years. Minoxidil use is indicated for central (vertex) hair loss only.<ref>Template:Cite journal</ref> Two clinical studies are being conducted in the US for a medical device that may allow patients to determine if they are likely to benefit from minoxidil therapy.<ref>Template:ClinicalTrialsGov</ref>

Conditions such as Cantú syndrome have been shown to mimic the pharmacological properties of minoxidil.<ref name="McClenaghanNichols2022">Template:Cite journal</ref><ref name="OhkoNakajimaNakajima2020">Template:Cite journal</ref>

Pharmacokinetics

Absorption

Minoxidil is readily absorbed from the gastrointestinal tract with oral administration.<ref name="GuptaTalukderVenkataraman2022" /> Its absorption from the gut is around 90% or more.<ref name="GuptaTalukderVenkataraman2022" /><ref name="Loniten-Label">https://www.accessdata.fda.gov/drugsatfda_docs/label/2015/018154s026lbl.pdf</ref><ref name="OngLiLipner2025" /> The drug reaches peak levels after about 30 to 60Template:NbspminutesTemplate:Nbsphour.<ref name="GuptaTalukderVenkataraman2022" /><ref name="Loniten-Label" /><ref name="OngLiLipner2025" /><ref name="FleishakerAndreadisWelshman1989" /> Following attainment of peak levels, concentrations of minoxidil rapidly decline.<ref name="Loniten-Label" /> Sublingual minoxidil is expected to have higher bioavailability than topical minoxidil.<ref name="ModhaPathania2022" /><ref name="SinclairTrindadedeCarvalhoFerialIsmail2020" /> Peak levels with sublingual administration occurred after 30Template:Nbspminutes.<ref name="BokhariJonesSinclair2022" /> The bioavailability of oral minoxidil is not affected by food and it can be taken in either a fasted or fed state.<ref name="GuptaTalukderShemer2023">Template:Cite journal</ref>

In the case of topical administration to the scalp, the absorption of minoxidil is only about 1.2 to 1.4%.<ref name="GuptaTalukderVenkataraman2022" /> With this route, serum levels of minoxidil are usually less than 5Template:Nbspng/mL and are frequently undetectable.<ref name="GuptaTalukderVenkataraman2022" /> It has been predicted that application of 5% topical minoxidil twice to the entire scalp might be equivalent to a single 5.4Template:Nbspmg oral dose of minoxidil in terms of systemic exposure.<ref name="GuptaTalukderVenkataraman2022" /><ref name="Franz1985">Template:Cite journal</ref> The stratum corneum of the scalp is saturated by minoxidil and acts as a reservoir for the drug.<ref name="Anastassakis2022" /> This results in a continuous flow of minoxidil in the scalp, with absorption being completed after about 10 to 12Template:Nbsphours.<ref name="Anastassakis2022" /> Based on these findings, topical minoxidil is generally applied twice daily.<ref name="Anastassakis2022" /> A wet scalp has been found to increase the absorption of topical minoxidil.<ref name="Anastassakis2022" />

Peak levels of minoxidil with oral minoxidil were 16.8Template:Nbspng/mL with 2.5Template:Nbspmg, 37.2Template:Nbspng/mL with 5Template:Nbspmg, and 74.7Template:Nbspng/mL with 10Template:Nbspmg doses.<ref name="GuptaTalukderShemer2023" /><ref name="FleishakerAndreadisWelshman1989">Template:Cite journal</ref> Mean peak minoxidil levels with a single 0.45Template:Nbspmg dose of sublingual minoxidil were 1.62Template:Nbspng/mL (range 0.3–5.3Template:Nbspng/mL).<ref name="BokhariJonesSinclair2022" /> Circulating levels of 0.6Template:Nbspng/mL with 2% solution and 1.6Template:Nbspng/mL with 5% solution occur with topical minoxidil.<ref name="Anastassakis2022" /> However, levels vary between individuals, with a range of undetectable to 7.5Template:Nbspng/mL with 3% solution in 12Template:Nbspindividuals in one study.<ref name="GuptaTalukderVenkataraman2022" /><ref name="Price1987">Template:Cite journal</ref> Significant cardiological and hemodynamic effects are said to occur with minoxidil when serum minoxidil levels exceed 20Template:Nbspng/mL.<ref name="Anastassakis2022" /><ref name="Ferry_1996">Template:Cite journal</ref>

Distribution

The volume of distribution of oral minoxidil is greater than 200Template:NbspL.<ref name="GuptaTalukderShemer2023" /> Minoxidil does not cross the blood–brain barrier and hence is peripherally selective.<ref name="GuptaTalukderVenkataraman2022" /><ref name="GuptaTalukderShemer2023" /><ref name="Loniten-Label" /> It shows minimal or negligible plasma protein binding.<ref name="GuptaTalukderVenkataraman2022" /><ref name="GuptaTalukderShemer2023" /><ref name="Loniten-Label" />

Metabolism

Minoxidil is a prodrug of minoxidil sulfate, which can be formed both systemically and locally within hair follicles.<ref name="GuptaTalukderVenkataraman2022" /><ref name="Anastassakis2022" /><ref name="BuhlWaldonBaker1990" /> This active metabolite is 14-fold more potent than minoxidil in stimulating cysteine incorporation in cultured rodent hair follicles ex vivo.<ref name="Anastassakis2022" /><ref name="BuhlWaldonBaker1990">Template:Cite journal</ref> Similarly to minoxidil, it also stimulates hair follicle growth.<ref name="Anastassakis2022" /><ref name="BuhlWaldonBaker1990" /> Minoxidil is sulfated into minoxidil sulfate by at least four cytosolic sulfotransferase enzymes found in skin, scalp, smooth muscle, liver, and fibroblasts.<ref name="Anastassakis2022" /> The primary sulfotransferase involved in sulfation of minoxidil in hair follicles is SULT1A1, whereas in the liver, it is SULT2A1.<ref name="GuptaTalukderVenkataraman2022" /><ref name="ModhaPathania2022" /> Expression of this enzyme has been found to predict the effectiveness of topical minoxidil.<ref name="GuptaTalukderVenkataraman2022" />

Oral minoxidil is subject to first-pass metabolism, including rapid and extensive metabolism in the liver.<ref name="Anastassakis2022" /> A majority of orally administered minoxidil, about 90%, is metabolized in the liver via glucuronidation, hydroxylation, and sulfation, with glucuronidation being the primary metabolic pathway and minoxidil glucuronide being the predominant metabolite of minoxidil.<ref name="GuptaTalukderVenkataraman2022" /><ref name="GuptaTalukderShemer2023" /><ref name="Loniten-Label" /><ref name="OngLiLipner2025" /> Conversely, topical minoxidil bypasses the first pass through the liver and is not subject to first-pass metabolism.<ref name="Anastassakis2022" /> Similarly, sublingual minoxidil also bypasses first-pass metabolism.<ref name="ModhaPathania2022">Template:Cite journal</ref><ref name="Saceda-CorraloDomínguez-SantasVañó-Galván2023">Template:Cite journal</ref><ref name="SinclairTrindadedeCarvalhoFerialIsmail2020">Template:Cite journal</ref>

Elimination

Minoxidil is excreted almost exclusively (>97%) in urine.<ref name="Anastassakis2022" /> About 10 to 15% is excreted in urine unchanged.<ref name="OlsenSinclairHordinsky2025">Template:Cite journal</ref> The elimination half-life of oral minoxidil is about 3 to 4Template:Nbsphours.<ref name="GuptaTalukderVenkataraman2022" /><ref name="Loniten-Label" /><ref name="OngLiLipner2025" /> Conversely, the half-life of topical minoxidil is 22Template:Nbsphours on average.<ref name="Anastassakis2022" /> Oral minoxidil is excreted within 12 to 20Template:Nbsphours in urine.<ref name="GuptaTalukderVenkataraman2022" /> Despite this however, the hypotensive effect of oral minoxidil lasts approximately 72Template:Nbsphours following a single dose.<ref name="GuptaTalukderShemer2023" /> With discontinuation of topical minoxidil, about 95% of systemically absorbed minoxidil is excreted within 4Template:Nbspdays.<ref name="GuptaTalukderVenkataraman2022" /> The renal clearance of oral minoxidil is 352Template:NbspmL/minute.<ref name="GuptaTalukderShemer2023" />

Chemistry

Properties

Minoxidil is an odorless, white to off-white, crystalline powder (crystals from methanol-acetonitrile). When heated to decomposition it emits toxic fumes of nitrogen oxides. It decomposes at 259-261 °C.<ref>Template:Cite web</ref> Its solubility (mg/ml) is propylene glycol 75, methanol 44, ethanol 29, 2-propanol 6.7, dimethylsulfoxide 6.5, water 2.2, chloroform 0.5, acetone <0.5, ethyl acetate <0.5, diethyl ether <0.5, benzene <0.5, acetonitrile <0.5. The pK_a of minoxidil is 4.61.

Synthesis

Another synthesis approach of Minoxidil<ref>Template:Cite journal</ref>

Minoxidil, 6-amino-1,2-dihydro-1-hydroxy-2-imino-4-piperidinopyrimidine, is synthesized from barbituric acid, the reaction of which with phosphorus oxychloride gives 2,4,6-trichloropyrimidine. Upon reaction with ammonium, this turns into 2,4-diamino-6-chloropyrimidine. Next, the resulting 2,4-diamino-6-chloropyrimidine undergoes a reaction with 2,4-dichlorophenol in the presence of potassium hydroxide, giving 2,4-diamino-6-(2,4-dichlorophenoxy)-pyrimidine. Oxidation of this product with 3-chloroperbenzoic acid gives 2,4-diamino-6-(2,4-dichlorophenoxy)pyrimidine-3-oxide, the 2,4-dichlorophenoxyl group of which is replaced with a piperidine group at high temperature, giving minoxidil.<ref>Template:Cite book</ref>

History

Initial development

Minoxidil was developed in the late 1950s by the Upjohn Company (later became part of Pfizer) to treat ulcers. In trials using dogs, the compound did not cure ulcers but proved to be a powerful vasodilator. Upjohn synthesized over 200 variations of the compound, including the one it developed in 1963 and named minoxidil.<ref name="kahn" /> These studies resulted in the U.S. Food and Drug Administration (FDA) approving minoxidil (with the brand name Loniten) in the form of oral tablets to treat high blood pressure in 1979.<ref>Template:Cite web</ref><ref name="medical">Template:Cite book</ref>

Repurposing for hair growth

When Upjohn received permission from the U.S. Food and Drug Administration (FDA) to test the new drug as medicine for hypertension they approached Charles A. Chidsey, at the University of Colorado School of Medicine.<ref name="kahn">Template:Cite news</ref> He conducted two studies,<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref> the second study showing unexpected hair growth. Puzzled by this side-effect, Chidsey consulted Guinter Kahn (who while a dermatology resident at the University of Miami had been the first to observe and report hair development on patients using the minoxidil patch) and discussed the possibility of using minoxidil for treating hair loss.Template:Cn

Kahn, along with his colleague Paul J. Grant, had obtained a certain amount of minoxidil and conducted their own research, since they were first to make the side effect observation. Neither Upjohn or Chidsey at the time were aware of the side effect of hair growth.<ref name="firstcl">Template:Cite journal</ref> The two doctors had been experimenting with a 1% solution of minoxidil mixed with several alcohol-based liquids.<ref name="gazette">Template:Cite web</ref> Both parties filed patents to use minoxidil for hair loss prevention, which resulted in a decade-long trial between Kahn and Upjohn, which ended with Kahn's name included in a consolidated patent (U.S. #4,596,812 Charles A Chidsey, III and Guinter Kahn) in 1986 and royalties from the company to both Kahn and Grant.<ref name="firstcl" />

Meanwhile, the effect of minoxidil on hair loss prevention was so clear that in the 1980s physicians were prescribing Loniten off-label to their balding patients.<ref name="medical" />

In August 1988, the FDA approved minoxidil for treating baldness in men<ref name="medical" /><ref name="gazette" /> under the brand name "Rogaine" (FDA rejected Upjohn's first choice, Regain, as misleading<ref name="hair">Template:Cite book (Google Books)</ref>). The agency concluded that although "the product will not work for everyone", 39% of the men studied had "moderate to dense hair growth on the crown of the head".<ref name="hair" /> "Men's Rogaine", marketed by Johnson & Johnson went off-patent on January 20, 2006.<ref name=":6">Template:Cite web</ref>

In 1991, Upjohn made the product available for women.<ref name="gazette" /> "Women's Rogaine", marketed by Johnson & Johnson, went off-patent in February 2014.<ref name=":6" />

Society and culture

Economics

In February 1996, the FDA approved both the over-the-counter sale and the production of generic formulations of minoxidil.<ref name="medical" /> Upjohn replied to that by lowering prices to half the price of the prescription drug<ref name="gazette" /> and by releasing a prescription 5% formula of Rogaine in 1997.<ref name="medical" /><ref>Template:Cite web</ref> In 1998, a 5% formulation of minoxidil was approved for nonprescription sale by the FDA.<ref>Template:Cite book (Google Books)</ref> The 5% aerosol foam formula was approved for medical use in the US in 2006.<ref>Template:Cite web</ref><ref>Template:Cite web</ref> The generic versions of the 5% aerosol foam formula were approved in 2017.<ref>Template:Cite web</ref><ref>Template:Cite web</ref>

In 2017, a study of pharmacy prices in four states for 41 over-the-counter minoxidil products which were "gender-specified" found that the mean price for minoxidil solutions was the same for women and men even though the women's formulations were 2% and the men's were 5%, while the mean price for minoxidil foams, which were all 5%, was 40% higher for women. The authors noted this was the first time gender-based pricing had been shown for a medication.<ref>Template:Cite journal</ref>

Brand names

Template:As of, Minoxidil is sold under many brand names worldwide, including but not limited to: Alomax, Alopek, Alopexy, Alorexyl, Alostil, Aloxid, Aloxidil, Anagen, Apo-Gain, Axelan, Belohair, Boots Hair Loss Treatment, Botafex, Capillus, Carexidil, Coverit, Da Fei Xin, Dilaine, Dinaxcinco, Dinaxil, Ebersedin, Eminox, Folcare, Follixil, Guayaten, Hair Grow, Hair-Treat, Hairgain, Hairgaine, Hairgrow, Hairway, Headway, Inoxi, Ivix, Keranique, Lacovin, Locemix, Loniten, Lonnoten, Lonolox, Lonoten, Loxon, M E Medic, Maev-Medic, Mandi, Manoxidil, Mantai, Men's Rogaine, Minodil, Minodril, Minostyl, Minovital, Minox, Minoxi, Minoxidil, Minoxidilum, Minoximen, Minoxiten, Minscalp, Mintop, Modil, Morr, Moxidil, Neo-Pruristam, Neocapil, Neoxidil, Nherea, Nioxin, Noxidil, Oxofenil, Pilfud, Pilogro, Pilomin, Piloxidil, Re-Stim, Re-Stim+, Recrea, Regain, Regaine, Regaxidil, Regro, Regroe, Regrou, Regrowth, Relive, Renobell Locion, Reten, Rexidil, Rogaine, Rogan, Scalpmed, Si Bi Shen, Splendora, Superminox, Trefostil, Tricolocion, Tricoplus, Tricovivax, Tricoxane, Trugain, Tugain, Unipexil, Vaxdil, Vius, Women's Regaine, Xenogrow, Xtreme Boost, Xtreme Boost+, Xue Rui, Ylox, and Zeldilon.<ref name=generic>Template:Cite web</ref> It is also sold as a combination medication with amifampridine under the brand names Gainehair and Hair 4 U; and as a combination with tretinoin and clobetasol under the brand name Sistema GB.<ref name=generic/>

Research

Hair loss

An extended-release formulation of low-dose oral minoxidil is under development for treatment of hair loss.<ref name="AdisInsight-VDPHL01">Template:Cite web</ref><ref name="Hebebrand2025">Template:Cite web</ref><ref name="Segal2025">Template:Cite magazine</ref><ref name="Robin2025" /> It is being developed by Veradermics under the developmental code name VDPHL01.<ref name="AdisInsight-VDPHL01" /><ref name="Hebebrand2025" /><ref name="Segal2025" /><ref name="Robin2025">Template:Cite web</ref> As of September 2025, it is in phase 3 clinical trials for this indication.<ref name="AdisInsight-VDPHL01" /><ref name="Segal2025" /><ref name="Robin2025" />

A low-dose sublingual formulation of minoxidil is under development for treatment of hair loss.<ref name="AdisInsight-SLM">Template:Cite web</ref><ref name="PRNewswire2025">Template:Cite web</ref><ref name="NCT06924632">Template:Cite journal</ref> It is being developed by Samson Clinical.<ref name="AdisInsight-SLM" /><ref name="PRNewswire2025" /><ref name="NCT06924632" /> As of September 2025, it is in phase 3 clinical trials for this indication.<ref name="AdisInsight-SLM" /><ref name="PRNewswire2025" /><ref name="NCT06924632" />

Finasteride/latanoprost/minoxidil (developmental code name TH-07 or TH07; Triple Hair) is a topical combination drug including minoxidil, finasteride, and latanoprost which is under development for the treatment of hair loss.<ref name="AdisInsight-TH-07">Template:Cite web</ref><ref name="SekhavatFordLepage2023">Template:Cite journal</ref> As of December 2023, it is in phase 2 clinical trials for this indication.<ref name="AdisInsight-TH-07" />

AB-103 is a minoxidil sulfotransferase stimulant which enhances minoxidil conversion into its active form minoxidil sulfate in hair follicles and is under development as a topical medication for the treatment of hair loss.<ref name="AdisInsight-AB-103">Template:Cite web</ref> Sulfotransferase activity in hair follicles has been associated with minoxidil's clinical effectiveness.<ref name="GorenNaccarato2018">Template:Cite journal</ref><ref name="Anastassakis2022">Template:Cite book</ref> As of February 2024, AB-103 is in phase 3 clinical trials for this indication, although there have been no new updates since 2019.<ref name="AdisInsight-AB-103" />

Beard growth

Minoxidil has been studied for enhancement of facial hair or beard growth in transgender men.<ref name="SmithPulminskasRogers2024">Template:Cite journal</ref><ref name="MarinelliBichiriCagnina2024">Template:Cite journal</ref><ref name="PangNguyenUpreti2021">Template:Cite journal</ref>

Nail problems

Minoxidil has been studied in the treatment of onychodystrophy (nail problems).<ref name="ThiagarajanWollHirpara2025">Template:Cite journal</ref> A 2025 systematic review found that it has been assessed in at least 6Template:Nbspclinical studies for this purpose and that the employed formulations included 2 to 5% topical minoxidil and 1.25 to 2.5Template:Nbspmg/day oral minoxidil.<ref name="ThiagarajanWollHirpara2025" /> The drug has been found to increase the rate of nail growth, improve nail appearance, increase nail strength, and resolve yellow nail discoloration.<ref name="ThiagarajanWollHirpara2025" />

Other uses

Minoxidil is being investigated as a potential treatment for ovarian cancer.<ref name=":2">Template:ClinicalTrialsGov</ref>

Toxicity to animals

Minoxidil is highly toxic to dogs and cats, even in doses as small as a drop or lick.<ref>Template:Cite journal</ref> There are reported cases of cats dying shortly after coming in contact with minimal amounts of the substance.<ref>Template:Cite journal</ref>

There is no specific antidote, but lipid rescue has been used successfully.<ref>Template:Cite journal</ref><ref>Template:Cite journal</ref>

External links

• Template:Cite web