{"history":[],"article":{"id":"3d8be292-b185-4d25-adbb-06fbd36a00f5","title":"Minoxidil","slug":"minoxidil","content":":::summary\n![Minoxidil](https://upload.wikimedia.org/wikipedia/commons/9/94/Minoxidil///structure.svg)\n**Verifiedfields:** changed \n**Watchedfields:** changed \n**Verifiedrevid:** 394534793 \n**Width:** 150 \n**Image 2:** Minoxidil-from-xtal-3D-balls.png \n**Width 2:** 135 \n**Tradename:** Loniten, Rogaine, others \n**Medlineplus:** a682608 \n**Dailymedid:** Minoxidil \n**Pregnancy Au:** C \n**Routes Of Administration:** [By mouth](https://bliptext.com/articles/oral-administration), [topical](https://bliptext.com/articles/topical-administration) \n**Atc Prefix:** C02 \n**Atc Suffix:** DC01 \n**Legal Au:** S4 \n**Legal Au Comment:** / S2 \n**Legal Uk:** GSL \n**Legal Uk Comment:** / POM \n**Legal Us:** OTC \n**Legal Us Comment:** / Rx-only \n**Metabolism:** Primarily liver \n**Elimination Half -life:** 4.2 h \n**Excretion:** Kidney \n**Cas Number:** 38304-91-5 \n**Pubchem:** 4201 \n**Iuphar Ligand:** 4254 \n**Drugbank:** DB00350 \n**Chemspiderid:** 10438564 \n**Unii:** 5965120SH1 \n**Kegg:** D00418 \n**Chebi:** 6942 \n**Chembl:** 802 \n**Pdb Ligand:** MXD \n**Synonyms:** 2,4-Diamino-6-piperidinopyrimidine 3-oxide \n**Iupac Name:** 2,6-diamino-4-(piperidin-1-yl)pyrimidine 1-oxide \n**C:** 9 \n**H:** 15 \n**N:** 5 \n**O:** 1 \n**Smiles:** Nc1cc(nc(N)[n+]1[O-])N2CCCCC2 \n**Stdinchi:** 1S/C9H15N5O/c10-7-6-8(12-9(11)14(7)15)13-4-2-1-3-5-13/h6H,1-5,10H2,(H2,11,12) \n**Stdinchikey:** ZFMITUMMTDLWHR-UHFFFAOYSA-N \n**Melting Point:** 248 \n**Solubility:** <1 \n:::\n\n# \n**Minoxidil** is a [medication](https://bliptext.com/articles/medication) used for the treatment of [high blood pressure](https://bliptext.com/articles/high-blood-pressure) and [pattern hair loss](https://bliptext.com/articles/pattern-hair-loss).\nIt is an [antihypertensive](https://bliptext.com/articles/antihypertensive) and a [vasodilator](https://bliptext.com/articles/vasodilator).\nIt is available as a [generic medication](https://bliptext.com/articles/generic-medication) by prescription in [oral](https://bliptext.com/articles/oral-administration) [tablet](https://bliptext.com/articles/tablet-pharmacy) form and [over the counter](https://bliptext.com/articles/over-the-counter-drug) as a [topical](https://bliptext.com/articles/topical-medication) liquid or foam.\n\n# Medical uses\nMinoxidil, 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](https://bliptext.com/articles/diuretic).\nMinoxidil is also generally administered with a [loop diuretic](https://bliptext.com/articles/loop-diuretic) to prevent [sodium](https://bliptext.com/articles/sodium-retention) and [potassium retention](https://bliptext.com/articles/potassium-retention).\nIt may also cause a [reflex tachycardia](https://bliptext.com/articles/reflex-tachycardia) and thus is prescribed with a [beta blocker](https://bliptext.com/articles/beta-blocker).\n\n## Hair loss\nMinoxidil, when applied topically, is used for the treatment of hair loss.\nIt is effective in helping promote hair growth in people with [androgenic alopecia](https://bliptext.com/articles/androgenic-alopecia) regardless of sex.\nMinoxidil must be used indefinitely for continued support of existing hair follicles and the maintenance of any experienced hair regrowth.\nLow-dose oral minoxidil (LDOM) is used [off-label](https://bliptext.com/articles/off-label-use) against hair loss and to promote hair regrowth.\nOral minoxidil is an effective and well-tolerated treatment alternative for patients having difficulty with topical formulations.\n\n# Side effects\nTopically 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.\n[Alcohol](https://bliptext.com/articles/alcohol-chemistry) and [propylene glycol](https://bliptext.com/articles/propylene-glycol) present in some topical preparations may dry the scalp, resulting in [dandruff](https://bliptext.com/articles/dandruff) and [contact dermatitis](https://bliptext.com/articles/contact-dermatitis).\nSide effects of oral minoxidil may include swelling of the face and extremities, rapid heartbeat, or lightheadedness.\nCardiac lesions, such as focal [necrosis](https://bliptext.com/articles/necrosis) of the [papillary muscle](https://bliptext.com/articles/papillary-muscle) and subendocardial areas of the left ventricle, have been observed in laboratory animals treated with minoxidil.\n[Pseudoacromegaly](https://bliptext.com/articles/pseudoacromegaly) is an extremely rare side effect reported with large doses of oral minoxidil.\nIn 2013 or 2014, a seven-year-old girl was admitted to a children's hospital in [Toulouse](https://bliptext.com/articles/toulouse) in France after accidentally ingesting a teaspoon of Alopexy (a brand name for minoxidil in France).\nThe child vomited constantly after ingestion and showed [hypotension](https://bliptext.com/articles/hypotension) and [tachycardia](https://bliptext.com/articles/tachycardia) for 40 hours.\nThe 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.\n# [296x296px | upload.wikimedia.org/wikipedia/commons/d/d0/Minoxidil///and///Finasteride///side///effects.jpg]\n\n# Pharmacology\n\n## Mechanism of action\nThe [mechanism](https://bliptext.com/articles/mechanism-of-action) by which minoxidil promotes hair growth is not fully understood.\nMinoxidil is an [adenosine 5'-triphosphate](https://bliptext.com/articles/adenosine-triphosphate)-sensitive [potassium channel opener](https://bliptext.com/articles/potassium-channel-opener), causing [hyperpolarization](https://bliptext.com/articles/hyperpolarization-biology) of cell membranes.\nTheoretically, by widening blood vessels and opening potassium channels, it allows more oxygen, blood, and nutrients to the [follicles](https://bliptext.com/articles/hair-follicle).\nMoreover, minoxidil contains a [nitric oxide](https://bliptext.com/articles/nitric-oxide) moiety and may act as a [nitric oxide](https://bliptext.com/articles/nitric-oxide) agonist.\nThis may cause follicles in the [telogen phase](https://bliptext.com/articles/telogen-phase) to shed, which are then replaced by thicker hairs in a new [anagen phase](https://bliptext.com/articles/anagen-phase).\nMinoxidil is a [prodrug](https://bliptext.com/articles/prodrug) that is converted by [sulfation](https://bliptext.com/articles/sulfation) via the [sulfotransferase](https://bliptext.com/articles/sulfotransferase) [enzyme](https://bliptext.com/articles/enzyme) [SULT1A1](https://bliptext.com/articles/sult1a1) to its active form, [minoxidil sulfate](https://bliptext.com/articles/minoxidil-sulfate).\nThe effect of minoxidil is mediated by [adenosine](https://bliptext.com/articles/adenosine), which triggers intracellular signal transduction via both [adenosine](https://bliptext.com/articles/adenosine) A1 receptors and two sub-types of [adenosine](https://bliptext.com/articles/adenosine) A2 receptors ([A2A](https://bliptext.com/articles/adenosine-a2a-receptor) and [A2B](https://bliptext.com/articles/adenosine-a2b-receptor) receptors).\nMinoxidil acts as an activator of the [Kir6](https://bliptext.com/articles/inward-rectifier-potassium-channel)/[SUR2](https://bliptext.com/articles/sur2) channel upon selective binding to [SUR2](https://bliptext.com/articles/sur2).\nThe expression of [SUR2B](https://bliptext.com/articles/sulfonylurea-receptor) in dermal papilla cells might play a role in the production of adenosine.\nMinoxidil induces cell growth factors such as VEGF, HGF, IGF-1 and potentiates HGF and IGF-1 actions by the activation of uncoupled [sulfonylurea receptor](https://bliptext.com/articles/sulfonylurea-receptor) on the plasma membrane of dermal papilla cells.\nA number of [in vitro](https://bliptext.com/articles/in-vitro) effects of minoxidil have been described in monocultures of various skin and hair follicle cell types including stimulation of cell [proliferation](https://bliptext.com/articles/cell-proliferation), inhibition of collagen synthesis, and stimulation of [vascular endothelial growth factor](https://bliptext.com/articles/vascular-endothelial-growth-factor), [prostaglandin](https://bliptext.com/articles/prostaglandin) synthesis and [leukotriene B4](https://bliptext.com/articles/leukotriene-b4) expression.\nMinoxidil causes a redistribution of cellular iron through its apparent capacity to bind this metal ion.\nBy binding iron in a Fenton-reactive form, intracellular [hydroxyl radical](https://bliptext.com/articles/hydroxyl-radical) production would ensue, but hydroxyl would be immediately trapped and scavenged by the minoxidil to generate a nitroxyl radical.\nIt is presumed that this nitroxyl radical will be capable of reduction by [glutathione](https://bliptext.com/articles/glutathione) to reform minoxidil.\nSuch a process would cycle until the minoxidil is otherwise metabolized and would result in rapid [glutathione](https://bliptext.com/articles/[glutathione](https://bliptext.com/articles/glutathione)) depletion with [glutathione](https://bliptext.com/articles/[glutathione](https://bliptext.com/articles/glutathione)) disulphide formation and therefore with concomitant consumption of [NADPH](https://bliptext.com/articles/nadph)/ [NADH](https://bliptext.com/articles/nadh) and other reducing equivalents.\nMinoxidil inhibited [PHD](https://bliptext.com/articles/hif-prolyl-hydroxylase) by interfering with the normal function of [ascorbate](https://bliptext.com/articles/ascorbate), a [cofactor](https://bliptext.com/articles/cofactor-biochemistry) of the enzyme, leading to a stabilization of [HIF-1α protein](https://bliptext.com/articles/hif1a) and a subsequent activation of [HIF-1](https://bliptext.com/articles/hif-1).\nIn an in vivo angiogenesis assay, millimolar minoxidil increased blood vessel formation in a VEGF-dependent manner.\nMinoxidil inhibition of PHD occurs via interrupting [ascorbate](https://bliptext.com/articles/ascorbate) binding to iron.\nThe 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](https://bliptext.com/articles/tetrahydrobiopterin) inhibition as a cofactor for nitric oxide synthase.\nMinoxidil stimulates [prostaglandin E2](https://bliptext.com/articles/prostaglandin-e2) production by activating [COX-1](https://bliptext.com/articles/ptgs1) and [prostaglandin endoperoxide synthase-1](https://bliptext.com/articles/prostaglandin-endoperoxide-synthase-1) but inhibits [prostacyclin](https://bliptext.com/articles/prostacyclin) production.\nAdditionally, expression of the [prostaglandin](https://bliptext.com/articles/prostaglandin) E2 receptor, the most upregulated target gene in the [β-catenin](https://bliptext.com/articles/beta-catenin) pathway of DP cells, was enhanced by minoxidil, which may enable hair follicles to grow continuously and maintain the anagen phase.\nDue to the anti-fibrotic activity of minoxidil inhibition of enzyme [lysyl hydroxylase](https://bliptext.com/articles/lysyl-hydroxylase) present in [fibroblast](https://bliptext.com/articles/fibroblast) may result in the synthesis of a [hydroxylysine](https://bliptext.com/articles/hydroxylysine)-deficient collagen.\nMinoxidil can also potentially stimulate [elastogenesis](https://bliptext.com/articles/elastogenesis) in aortic smooth muscle cells, and in skin fibroblasts in a dose-dependent manner.\nIn hypertensive rats, minoxidil increases elastin levels in the mesenteric, abdominal, and renal arteries by a decrease in \"[elastase](https://bliptext.com/articles/elastase)\" enzyme activity in these tissues.\nIn rats, potassium channel openers decrease calcium influx which inhibits elastin gene transcription through [extracellular signal-regulated kinase 1/2](https://bliptext.com/articles/extracellular-signal-regulated-kinases) ([ERK 1/2](https://bliptext.com/articles/erk1))-activator protein 1 signaling pathway.\nERK 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.\nMinoxidil possesses [alpha 2-adrenoceptor](https://bliptext.com/articles/alpha-2-adrenergic-receptor) [agonist](https://bliptext.com/articles/agonist) activity, stimulates the peripheral [sympathetic nervous system](https://bliptext.com/articles/sympathetic-nervous-system) (SNS) by way of carotid and aortic [baroreceptor reflexes](https://bliptext.com/articles/baroreceptor).\nMinoxidil administration also brings an increase in plasma [renin](https://bliptext.com/articles/renin) activity, largely due to the aforementioned activation of the [SNS](https://bliptext.com/articles/sympathetic-nervous-system).\nThis activation of the [renin-angiotensin](https://bliptext.com/articles/renin-angiotensin-system) axis further prompts increased biosynthesis of [aldosterone](https://bliptext.com/articles/aldosterone); whereas plasma and urinary [aldosterone](https://bliptext.com/articles/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](https://bliptext.com/articles/aldosterone) in association with hepatic vasodilation.\nMinoxidil may be involved in the inhibition of [serotonergic](https://bliptext.com/articles/5-ht-receptor) ([5-HT2](https://bliptext.com/articles/5-ht2-receptor)) receptors.\nMinoxidil might increase blood-tumor barrier permeability in a time-dependent manner by down-regulating [tight junction protein](https://bliptext.com/articles/tight-junction-proteins) expression and this effect could be related to [ROS](https://bliptext.com/articles/reactive-oxygen-species)/[RhoA](https://bliptext.com/articles/rhoa)/[PI3K](https://bliptext.com/articles/pi3k)/[PKB](https://bliptext.com/articles/protein-kinase-b) signal pathway.\nMinoxidil significantly increases [ROS](https://bliptext.com/articles/reactive-oxygen-species) concentration when compared to untreated cells.\nIn vitro Minoxidil treatment resulted in a 0.22 fold change for [5α-R2](https://bliptext.com/articles/5-reductase) (p < 0.0001).\nThis 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.\nMinoxidil is less effective when the area of hair loss is large.\nIn addition, its effectiveness has largely been demonstrated in younger men who have experienced hair loss for less than 5 years.\nMinoxidil use is indicated for central ([vertex](https://bliptext.com/articles/vertex-anatomy)) hair loss only.\nTwo 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.\nConditions such as [Cantú syndrome](https://bliptext.com/articles/cant-syndrome) have been shown to mimic the pharmacological properties of minoxidil.\n\n# Chemistry\nMinoxidil is an odorless, white to off-white, crystalline powder (crystals from methanol-acetonitrile).\nWhen heated to decomposition it emits toxic fumes of nitrogen oxides.\nIt decomposes at 259-261 °C.\n[Solubility](https://bliptext.com/articles/solubility) (mg/ml): [propylene glycol](https://bliptext.com/articles/propylene-glycol) 75, [methanol](https://bliptext.com/articles/m[ethanol](https://bliptext.com/articles/ethanol)) 44, [ethanol](https://bliptext.com/articles/ethanol) 29, [2-propanol](https://bliptext.com/articles/2-propanol) 6.7, [dimethylsulfoxide](https://bliptext.com/articles/dimethylsulfoxide) 6.5, water 2.2, [chloroform](https://bliptext.com/articles/chloroform) 0.5, [acetone](https://bliptext.com/articles/acetone) <0.5, [ethyl acetate](https://bliptext.com/articles/ethyl-acetate) <0.5, [diethyl ether](https://bliptext.com/articles/diethyl-ether) <0.5, [benzene](https://bliptext.com/articles/benzene) <0.5, [acetonitrile](https://bliptext.com/articles/acetonitrile) <0.5.\n[Acid strength](https://bliptext.com/articles/acid-strength) 4.61\nMinoxidil, 6-amino-1,2-dihydro-1-hydroxy-2-imino-4-piperidinopyrimidine, is synthesized from [barbituric acid](https://bliptext.com/articles/barbituric-acid), the reaction of which with [phosphorus oxychloride](https://bliptext.com/articles/phosphoryl-chloride) gives 2,4,6-trichloropyrimidine.\nUpon reaction with ammonium, this turns into 2,4-diamino-6-chloropyrimidine.\nNext, 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.\nOxidation 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.\nAnother synthesis approach is depicted here:\n# [Minoxidil synthesis | upload.wikimedia.org/wikipedia/commons/c/c3/Minoxidil///synthesis///1.svg]\n\n# History\n\n## Initial application\nMinoxidil was developed in the late 1950s by the [Upjohn Company](https://bliptext.com/articles/upjohn) (later became part of [Pfizer](https://bliptext.com/articles/pfizer)) to treat [ulcers](https://bliptext.com/articles/peptic-ulcer).\nIn trials using dogs, the compound did not cure ulcers but proved to be a powerful vasodilator.\nUpjohn synthesized over 200 variations of the compound, including the one it developed in 1963 and named minoxidil.\nThese studies resulted in the U.S. [Food and Drug Administration](https://bliptext.com/articles/food-and-drug-administration) (FDA) approving minoxidil (with the brand name 'Loniten') in the form of oral [tablets](https://bliptext.com/articles/tablet-pharmacy) to treat [high blood pressure](https://bliptext.com/articles/arterial-hypertension) in 1979.\n\n## Hair growth\nWhen Upjohn received permission from the U.S. [Food and Drug Administration](https://bliptext.com/articles/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](https://bliptext.com/articles/university-of-colorado-school-of-medicine).\nHe conducted two studies, the second study showing unexpected hair growth.\nPuzzled 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](https://bliptext.com/articles/hair-loss).\nKahn, 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.\nNeither Upjohn or Chidsey at the time were aware of the side effect of hair growth.\nThe two doctors had been experimenting with a 1% solution of minoxidil mixed with several alcohol-based liquids.\nBoth 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.\nMeanwhile, the effect of minoxidil on hair loss prevention was so clear that in the 1980s physicians were prescribing Loniten [off-label](https://bliptext.com/articles/off-label-use) to their balding patients.\nIn August 1988, the FDA approved minoxidil for treating baldness in men under the brand name \"Rogaine\" (FDA rejected Upjohn's first choice, Regain, as misleading ).\nThe 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\".\n\"Men's Rogaine\", marketed by Johnson & Johnson went off-patent on January 20, 2006.\nIn 1991, Upjohn made the product available for women.\n\"Women's Rogaine\", marketed by Johnson & Johnson, went off-patent in February 2014.\n\n## Pericardial effusion\nMinoxidil has been implicated in causing pericardial effusions including life-threatening cases of cardiac tamponade.\nThere have been case reports dating back to the 1980s describing this phenomenon, including topical.\nand oral formulations.\nThe 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.\n\n# Society and culture\n\n## Economics\nIn February 1996, the FDA approved both the [over-the-counter](https://bliptext.com/articles/over-the-counter-drug) sale and the production of [generic formulations](https://bliptext.com/articles/generic-drug) of minoxidil.\nUpjohn replied to that by lowering prices to half the price of the prescription drug and by releasing a prescription 5% formula of Rogaine in 1997.\nIn 1998, a 5% formulation of minoxidil was approved for nonprescription sale by the FDA.\nThe 5% aerosol foam formula was approved for medical use in the US in 2006.\nThe generic versions of the 5% aerosol foam formula were approved in 2017.\nIn 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.\nThe authors noted this was the first time [gender-based pricing](https://bliptext.com/articles/gender-based-price-discrimination-in-the-united-states) had been shown for a medication.\n\n## Brand names\n, Minoxidil is sold under many brand names worldwide: 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, Regain, 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.\nIt is also sold as a [combination medication](https://bliptext.com/articles/combination-medication) with [amifampridine](https://bliptext.com/articles/amifampridine) under the brand names Gainehair and Hair 4 U; and as a combination with [tretinoin](https://bliptext.com/articles/tretinoin) and [clobetasol](https://bliptext.com/articles/clobetasol) under the brand name Sistema GB.\n\n# Research\nMinoxidil is being investigated as a potential treatment for treating ovarian cancer.\n\n# Toxicity to animals\nMinoxidil is highly [toxic](https://bliptext.com/articles/toxicity) to [dogs](https://bliptext.com/articles/dog) and [cats](https://bliptext.com/articles/cat), even in doses as small as a drop or lick.\nThere are reported cases of cats dying shortly after coming in contact with minimal amounts of the substance.\nThere is no specific [antidote](https://bliptext.com/articles/antidote), but [lipid rescue](https://bliptext.com/articles/lipid-rescue) has been used successfully.","current_revision":null,"created_by":"kACnuQmH5k9Nr5VNVEpVeg7XpvUmMctD","created_at":"2025-01-25T19:35:32.303Z","updated_at":"2025-01-25T19:35:32.303Z","search_vector":"'minoxidil':1","search_content":" \n \n**Verifiedfields:** changed \n**Watchedfields:** changed \n**Verifiedrevid:** 394534793 \n**Width:** 150 \n**Image 2:** Minoxidil-from-xtal-3D-balls.png \n**Width 2:** 135 \n**Tradename:** Loniten, Rogaine, others \n**Medlineplus:** a682608 \n**Dailymedid:** Minoxidil \n**Pregnancy Au:** C \n**Routes Of Administration:** [By mouth](https://bliptext.com/articles/oral-administration), [topical](https://bliptext.com/articles/topical-administration) \n**Atc Prefix:** C02 \n**Atc Suffix:** DC01 \n**Legal Au:** S4 \n**Legal Au Comment:** / S2 \n**Legal Uk:** GSL \n**Legal Uk Comment:** / POM \n**Legal Us:** OTC \n**Legal Us Comment:** / Rx-only \n**Metabolism:** Primarily liver \n**Elimination Half -life:** 4.2 h \n**Excretion:** Kidney \n**Cas Number:** 38304-91-5 \n**Pubchem:** 4201 \n**Iuphar Ligand:** 4254 \n**Drugbank:** DB00350 \n**Chemspiderid:** 10438564 \n**Unii:** 5965120SH1 \n**Kegg:** D00418 \n**Chebi:** 6942 \n**Chembl:** 802 \n**Pdb Ligand:** MXD \n**Synonyms:** 2,4-Diamino-6-piperidinopyrimidine 3-oxide \n**Iupac Name:** 2,6-diamino-4-(piperidin-1-yl)pyrimidine 1-oxide \n**C:** 9 \n**H:** 15 \n**N:** 5 \n**O:** 1 \n**Smiles:** Nc1cc(nc(N)[n+]1[O-])N2CCCCC2 \n**Stdinchi:** 1S/C9H15N5O/c10-7-6-8(12-9(11)14(7)15)13-4-2-1-3-5-13/h6H,1-5,10H2,(H2,11,12) \n**Stdinchikey:** ZFMITUMMTDLWHR-UHFFFAOYSA-N \n**Melting Point:** 248 \n**Solubility:** <1 \n \n\n# \n**Minoxidil** is a [medication](https://bliptext.com/articles/medication) used for the treatment of [high blood pressure](https://bliptext.com/articles/high-blood-pressure) and [pattern hair loss](https://bliptext.com/articles/pattern-hair-loss).\nIt is an [antihypertensive](https://bliptext.com/articles/antihypertensive) and a [vasodilator](https://bliptext.com/articles/vasodilator).\nIt is available as a [generic medication](https://bliptext.com/articles/generic-medication) by prescription in [oral](https://bliptext.com/articles/oral-administration) [tablet](https://bliptext.com/articles/tablet-pharmacy) form and [over the counter](https://bliptext.com/articles/over-the-counter-drug) as a [topical](https://bliptext.com/articles/topical-medication) liquid or foam.\n\n# Medical uses\nMinoxidil, 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](https://bliptext.com/articles/diuretic).\nMinoxidil is also generally administered with a [loop diuretic](https://bliptext.com/articles/loop-diuretic) to prevent [sodium](https://bliptext.com/articles/sodium-retention) and [potassium retention](https://bliptext.com/articles/potassium-retention).\nIt may also cause a [reflex tachycardia](https://bliptext.com/articles/reflex-tachycardia) and thus is prescribed with a [beta blocker](https://bliptext.com/articles/beta-blocker).\n\n## Hair loss\nMinoxidil, when applied topically, is used for the treatment of hair loss.\nIt is effective in helping promote hair growth in people with [androgenic alopecia](https://bliptext.com/articles/androgenic-alopecia) regardless of sex.\nMinoxidil must be used indefinitely for continued support of existing hair follicles and the maintenance of any experienced hair regrowth.\nLow-dose oral minoxidil (LDOM) is used [off-label](https://bliptext.com/articles/off-label-use) against hair loss and to promote hair regrowth.\nOral minoxidil is an effective and well-tolerated treatment alternative for patients having difficulty with topical formulations.\n\n# Side effects\nTopically 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.\n[Alcohol](https://bliptext.com/articles/alcohol-chemistry) and [propylene glycol](https://bliptext.com/articles/propylene-glycol) present in some topical preparations may dry the scalp, resulting in [dandruff](https://bliptext.com/articles/dandruff) and [contact dermatitis](https://bliptext.com/articles/contact-dermatitis).\nSide effects of oral minoxidil may include swelling of the face and extremities, rapid heartbeat, or lightheadedness.\nCardiac lesions, such as focal [necrosis](https://bliptext.com/articles/necrosis) of the [papillary muscle](https://bliptext.com/articles/papillary-muscle) and subendocardial areas of the left ventricle, have been observed in laboratory animals treated with minoxidil.\n[Pseudoacromegaly](https://bliptext.com/articles/pseudoacromegaly) is an extremely rare side effect reported with large doses of oral minoxidil.\nIn 2013 or 2014, a seven-year-old girl was admitted to a children's hospital in [Toulouse](https://bliptext.com/articles/toulouse) in France after accidentally ingesting a teaspoon of Alopexy (a brand name for minoxidil in France).\nThe child vomited constantly after ingestion and showed [hypotension](https://bliptext.com/articles/hypotension) and [tachycardia](https://bliptext.com/articles/tachycardia) for 40 hours.\nThe 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.\n# [296x296px | upload.wikimedia.org/wikipedia/commons/d/d0/Minoxidil///and///Finasteride///side///effects.jpg]\n\n# Pharmacology\n\n## Mechanism of action\nThe [mechanism](https://bliptext.com/articles/mechanism-of-action) by which minoxidil promotes hair growth is not fully understood.\nMinoxidil is an [adenosine 5'-triphosphate](https://bliptext.com/articles/adenosine-triphosphate)-sensitive [potassium channel opener](https://bliptext.com/articles/potassium-channel-opener), causing [hyperpolarization](https://bliptext.com/articles/hyperpolarization-biology) of cell membranes.\nTheoretically, by widening blood vessels and opening potassium channels, it allows more oxygen, blood, and nutrients to the [follicles](https://bliptext.com/articles/hair-follicle).\nMoreover, minoxidil contains a [nitric oxide](https://bliptext.com/articles/nitric-oxide) moiety and may act as a [nitric oxide](https://bliptext.com/articles/nitric-oxide) agonist.\nThis may cause follicles in the [telogen phase](https://bliptext.com/articles/telogen-phase) to shed, which are then replaced by thicker hairs in a new [anagen phase](https://bliptext.com/articles/anagen-phase).\nMinoxidil is a [prodrug](https://bliptext.com/articles/prodrug) that is converted by [sulfation](https://bliptext.com/articles/sulfation) via the [sulfotransferase](https://bliptext.com/articles/sulfotransferase) [enzyme](https://bliptext.com/articles/enzyme) [SULT1A1](https://bliptext.com/articles/sult1a1) to its active form, [minoxidil sulfate](https://bliptext.com/articles/minoxidil-sulfate).\nThe effect of minoxidil is mediated by [adenosine](https://bliptext.com/articles/adenosine), which triggers intracellular signal transduction via both [adenosine](https://bliptext.com/articles/adenosine) A1 receptors and two sub-types of [adenosine](https://bliptext.com/articles/adenosine) A2 receptors ([A2A](https://bliptext.com/articles/adenosine-a2a-receptor) and [A2B](https://bliptext.com/articles/adenosine-a2b-receptor) receptors).\nMinoxidil acts as an activator of the [Kir6](https://bliptext.com/articles/inward-rectifier-potassium-channel)/[SUR2](https://bliptext.com/articles/sur2) channel upon selective binding to [SUR2](https://bliptext.com/articles/sur2).\nThe expression of [SUR2B](https://bliptext.com/articles/sulfonylurea-receptor) in dermal papilla cells might play a role in the production of adenosine.\nMinoxidil induces cell growth factors such as VEGF, HGF, IGF-1 and potentiates HGF and IGF-1 actions by the activation of uncoupled [sulfonylurea receptor](https://bliptext.com/articles/sulfonylurea-receptor) on the plasma membrane of dermal papilla cells.\nA number of [in vitro](https://bliptext.com/articles/in-vitro) effects of minoxidil have been described in monocultures of various skin and hair follicle cell types including stimulation of cell [proliferation](https://bliptext.com/articles/cell-proliferation), inhibition of collagen synthesis, and stimulation of [vascular endothelial growth factor](https://bliptext.com/articles/vascular-endothelial-growth-factor), [prostaglandin](https://bliptext.com/articles/prostaglandin) synthesis and [leukotriene B4](https://bliptext.com/articles/leukotriene-b4) expression.\nMinoxidil causes a redistribution of cellular iron through its apparent capacity to bind this metal ion.\nBy binding iron in a Fenton-reactive form, intracellular [hydroxyl radical](https://bliptext.com/articles/hydroxyl-radical) production would ensue, but hydroxyl would be immediately trapped and scavenged by the minoxidil to generate a nitroxyl radical.\nIt is presumed that this nitroxyl radical will be capable of reduction by [glutathione](https://bliptext.com/articles/glutathione) to reform minoxidil.\nSuch a process would cycle until the minoxidil is otherwise metabolized and would result in rapid [[glutathione](https://bliptext.com/articles/glutathione)](https://bliptext.com/articles/[glutathione](https://bliptext.com/articles/glutathione)) depletion with [[glutathione](https://bliptext.com/articles/glutathione)](https://bliptext.com/articles/[glutathione](https://bliptext.com/articles/glutathione)) disulphide formation and therefore with concomitant consumption of [NADPH](https://bliptext.com/articles/nadph)/ [NADH](https://bliptext.com/articles/nadh) and other reducing equivalents.\nMinoxidil inhibited [PHD](https://bliptext.com/articles/hif-prolyl-hydroxylase) by interfering with the normal function of [ascorbate](https://bliptext.com/articles/ascorbate), a [cofactor](https://bliptext.com/articles/cofactor-biochemistry) of the enzyme, leading to a stabilization of [[HIF-1](https://bliptext.com/articles/hif-1)α protein](https://bliptext.com/articles/hif1a) and a subsequent activation of [HIF-1](https://bliptext.com/articles/hif-1).\nIn an in vivo angiogenesis assay, millimolar minoxidil increased blood vessel formation in a VEGF-dependent manner.\nMinoxidil inhibition of PHD occurs via interrupting [ascorbate](https://bliptext.com/articles/ascorbate) binding to iron.\nThe 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](https://bliptext.com/articles/tetrahydrobiopterin) inhibition as a cofactor for nitric oxide synthase.\nMinoxidil stimulates [prostaglandin E2](https://bliptext.com/articles/prostaglandin-e2) production by activating [COX-1](https://bliptext.com/articles/ptgs1) and [prostaglandin endoperoxide synthase-1](https://bliptext.com/articles/prostaglandin-endoperoxide-synthase-1) but inhibits [prostacyclin](https://bliptext.com/articles/prostacyclin) production.\nAdditionally, expression of the [prostaglandin](https://bliptext.com/articles/prostaglandin) E2 receptor, the most upregulated target gene in the [β-catenin](https://bliptext.com/articles/beta-catenin) pathway of DP cells, was enhanced by minoxidil, which may enable hair follicles to grow continuously and maintain the anagen phase.\nDue to the anti-fibrotic activity of minoxidil inhibition of enzyme [lysyl hydroxylase](https://bliptext.com/articles/lysyl-hydroxylase) present in [fibroblast](https://bliptext.com/articles/fibroblast) may result in the synthesis of a [hydroxylysine](https://bliptext.com/articles/hydroxylysine)-deficient collagen.\nMinoxidil can also potentially stimulate [elastogenesis](https://bliptext.com/articles/elastogenesis) in aortic smooth muscle cells, and in skin fibroblasts in a dose-dependent manner.\nIn hypertensive rats, minoxidil increases elastin levels in the mesenteric, abdominal, and renal arteries by a decrease in \"[elastase](https://bliptext.com/articles/elastase)\" enzyme activity in these tissues.\nIn rats, potassium channel openers decrease calcium influx which inhibits elastin gene transcription through [extracellular signal-regulated kinase 1/2](https://bliptext.com/articles/extracellular-signal-regulated-kinases) ([ERK 1/2](https://bliptext.com/articles/erk1))-activator protein 1 signaling pathway.\nERK 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.\nMinoxidil possesses [alpha 2-adrenoceptor](https://bliptext.com/articles/alpha-2-adrenergic-receptor) [agonist](https://bliptext.com/articles/agonist) activity, stimulates the peripheral [sympathetic nervous system](https://bliptext.com/articles/sympathetic-nervous-system) (SNS) by way of carotid and aortic [baroreceptor reflexes](https://bliptext.com/articles/baroreceptor).\nMinoxidil administration also brings an increase in plasma [renin](https://bliptext.com/articles/renin) activity, largely due to the aforementioned activation of the [SNS](https://bliptext.com/articles/sympathetic-nervous-system).\nThis activation of the [renin-angiotensin](https://bliptext.com/articles/renin-angiotensin-system) axis further prompts increased biosynthesis of [aldosterone](https://bliptext.com/articles/aldosterone); whereas plasma and urinary [aldosterone](https://bliptext.com/articles/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](https://bliptext.com/articles/aldosterone) in association with hepatic vasodilation.\nMinoxidil may be involved in the inhibition of [serotonergic](https://bliptext.com/articles/5-ht-receptor) ([5-HT2](https://bliptext.com/articles/5-ht2-receptor)) receptors.\nMinoxidil might increase blood-tumor barrier permeability in a time-dependent manner by down-regulating [tight junction protein](https://bliptext.com/articles/tight-junction-proteins) expression and this effect could be related to [ROS](https://bliptext.com/articles/reactive-oxygen-species)/[RhoA](https://bliptext.com/articles/rhoa)/[PI3K](https://bliptext.com/articles/pi3k)/[PKB](https://bliptext.com/articles/protein-kinase-b) signal pathway.\nMinoxidil significantly increases [ROS](https://bliptext.com/articles/reactive-oxygen-species) concentration when compared to untreated cells.\nIn vitro Minoxidil treatment resulted in a 0.22 fold change for [5α-R2](https://bliptext.com/articles/5-reductase) (p < 0.0001).\nThis 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.\nMinoxidil is less effective when the area of hair loss is large.\nIn addition, its effectiveness has largely been demonstrated in younger men who have experienced hair loss for less than 5 years.\nMinoxidil use is indicated for central ([vertex](https://bliptext.com/articles/vertex-anatomy)) hair loss only.\nTwo 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.\nConditions such as [Cantú syndrome](https://bliptext.com/articles/cant-syndrome) have been shown to mimic the pharmacological properties of minoxidil.\n\n# Chemistry\nMinoxidil is an odorless, white to off-white, crystalline powder (crystals from methanol-acetonitrile).\nWhen heated to decomposition it emits toxic fumes of nitrogen oxides.\nIt decomposes at 259-261 °C.\n[Solubility](https://bliptext.com/articles/solubility) (mg/ml): [propylene glycol](https://bliptext.com/articles/propylene-glycol) 75, [m[ethanol](https://bliptext.com/articles/ethanol)](https://bliptext.com/articles/m[ethanol](https://bliptext.com/articles/ethanol)) 44, [ethanol](https://bliptext.com/articles/ethanol) 29, [2-propanol](https://bliptext.com/articles/2-propanol) 6.7, [dimethylsulfoxide](https://bliptext.com/articles/dimethylsulfoxide) 6.5, water 2.2, [chloroform](https://bliptext.com/articles/chloroform) 0.5, [acetone](https://bliptext.com/articles/acetone) <0.5, [ethyl acetate](https://bliptext.com/articles/ethyl-acetate) <0.5, [diethyl ether](https://bliptext.com/articles/diethyl-ether) <0.5, [benzene](https://bliptext.com/articles/benzene) <0.5, [acetonitrile](https://bliptext.com/articles/acetonitrile) <0.5.\n[Acid strength](https://bliptext.com/articles/acid-strength) 4.61\nMinoxidil, 6-amino-1,2-dihydro-1-hydroxy-2-imino-4-piperidinopyrimidine, is synthesized from [barbituric acid](https://bliptext.com/articles/barbituric-acid), the reaction of which with [phosphorus oxychloride](https://bliptext.com/articles/phosphoryl-chloride) gives 2,4,6-trichloropyrimidine.\nUpon reaction with ammonium, this turns into 2,4-diamino-6-chloropyrimidine.\nNext, 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.\nOxidation 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.\nAnother synthesis approach is depicted here:\n# [Minoxidil synthesis | upload.wikimedia.org/wikipedia/commons/c/c3/Minoxidil///synthesis///1.svg]\n\n# History\n\n## Initial application\nMinoxidil was developed in the late 1950s by the [Upjohn Company](https://bliptext.com/articles/upjohn) (later became part of [Pfizer](https://bliptext.com/articles/pfizer)) to treat [ulcers](https://bliptext.com/articles/peptic-ulcer).\nIn trials using dogs, the compound did not cure ulcers but proved to be a powerful vasodilator.\nUpjohn synthesized over 200 variations of the compound, including the one it developed in 1963 and named minoxidil.\nThese studies resulted in the U.S. [Food and Drug Administration](https://bliptext.com/articles/food-and-drug-administration) (FDA) approving minoxidil (with the brand name 'Loniten') in the form of oral [tablets](https://bliptext.com/articles/tablet-pharmacy) to treat [high blood pressure](https://bliptext.com/articles/arterial-hypertension) in 1979.\n\n## Hair growth\nWhen Upjohn received permission from the U.S. [Food and Drug Administration](https://bliptext.com/articles/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](https://bliptext.com/articles/university-of-colorado-school-of-medicine).\nHe conducted two studies, the second study showing unexpected hair growth.\nPuzzled 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](https://bliptext.com/articles/hair-loss).\nKahn, 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.\nNeither Upjohn or Chidsey at the time were aware of the side effect of hair growth.\nThe two doctors had been experimenting with a 1% solution of minoxidil mixed with several alcohol-based liquids.\nBoth 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.\nMeanwhile, the effect of minoxidil on hair loss prevention was so clear that in the 1980s physicians were prescribing Loniten [off-label](https://bliptext.com/articles/off-label-use) to their balding patients.\nIn August 1988, the FDA approved minoxidil for treating baldness in men under the brand name \"Rogaine\" (FDA rejected Upjohn's first choice, Regain, as misleading ).\nThe 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\".\n\"Men's Rogaine\", marketed by Johnson & Johnson went off-patent on January 20, 2006.\nIn 1991, Upjohn made the product available for women.\n\"Women's Rogaine\", marketed by Johnson & Johnson, went off-patent in February 2014.\n\n## Pericardial effusion\nMinoxidil has been implicated in causing pericardial effusions including life-threatening cases of cardiac tamponade.\nThere have been case reports dating back to the 1980s describing this phenomenon, including topical.\nand oral formulations.\nThe 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.\n\n# Society and culture\n\n## Economics\nIn February 1996, the FDA approved both the [over-the-counter](https://bliptext.com/articles/over-the-counter-drug) sale and the production of [generic formulations](https://bliptext.com/articles/generic-drug) of minoxidil.\nUpjohn replied to that by lowering prices to half the price of the prescription drug and by releasing a prescription 5% formula of Rogaine in 1997.\nIn 1998, a 5% formulation of minoxidil was approved for nonprescription sale by the FDA.\nThe 5% aerosol foam formula was approved for medical use in the US in 2006.\nThe generic versions of the 5% aerosol foam formula were approved in 2017.\nIn 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.\nThe authors noted this was the first time [gender-based pricing](https://bliptext.com/articles/gender-based-price-discrimination-in-the-united-states) had been shown for a medication.\n\n## Brand names\n, Minoxidil is sold under many brand names worldwide: 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, Regain, 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.\nIt is also sold as a [combination medication](https://bliptext.com/articles/combination-medication) with [amifampridine](https://bliptext.com/articles/amifampridine) under the brand names Gainehair and Hair 4 U; and as a combination with [tretinoin](https://bliptext.com/articles/tretinoin) and [clobetasol](https://bliptext.com/articles/clobetasol) under the brand name Sistema GB.\n\n# Research\nMinoxidil is being investigated as a potential treatment for treating ovarian cancer.\n\n# Toxicity to animals\nMinoxidil is highly [toxic](https://bliptext.com/articles/toxicity) to [dogs](https://bliptext.com/articles/dog) and [cats](https://bliptext.com/articles/cat), even in doses as small as a drop or lick.\nThere are reported cases of cats dying shortly after coming in contact with minimal amounts of the substance.\nThere is no specific [antidote](https://bliptext.com/articles/antidote), but [lipid rescue](https://bliptext.com/articles/lipid-rescue) has been used successfully.","revisionCount":0},"hasMore":false,"nextCursor":null}