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Its effect in people with [[alopecia areata]] is unclear.<ref>{{cite journal | vauthors = Hordinsky M, Donati A | title = Alopecia areata: an evidence-based treatment update | journal = American Journal of Clinical Dermatology | volume = 15 | issue = 3 | pages = 231–46 | date = July 2014 | pmid = 25000998 | doi = 10.1007/s40257-014-0086-4 | s2cid = 32253 }}</ref>
Its effect in people with [[alopecia areata]] is unclear.<ref>{{cite journal | vauthors = Hordinsky M, Donati A | title = Alopecia areata: an evidence-based treatment update | journal = American Journal of Clinical Dermatology | volume = 15 | issue = 3 | pages = 231–46 | date = July 2014 | pmid = 25000998 | doi = 10.1007/s40257-014-0086-4 | s2cid = 32253 }}</ref>

It takes time for finasteride to work and deliver noticeable effects. Men can go as long as 3-4 months before noticing hair regrowth with minoxidil.<ref>{{Cite web|title=What Happens If I Stop Using Minoxidil Or Finasteride?|url=https://upguys.com/blog/what-happens-if-i-stop-using-minoxidil-or-finasteride|url-status=live|website=UPGUYS}}</ref>


==Side effects==
==Side effects==

Revision as of 15:19, 3 August 2021

Minoxidil
A space filling model of the molecule.
Clinical data
Trade namesRogaine
AHFS/Drugs.comMonograph
MedlinePlusa682608
License data
Pregnancy
category
  • AU: C
Routes of
administration
By mouth / topical
ATC code
Legal status
Legal status
Pharmacokinetic data
MetabolismPrimarily liver
Elimination half-life4.2 h
ExcretionKidney
Identifiers
  • 3-hydroxy-2-imino-6-piperidin-1-ylpyrimidin-4-amine
CAS Number
PubChem CID
IUPHAR/BPS
DrugBank
ChemSpider
UNII
KEGG
ChEBI
ChEMBL
PDB ligand
CompTox Dashboard (EPA)
ECHA InfoCard100.048.959 Edit this at Wikidata
Chemical and physical data
FormulaC9H15N5O
Molar mass209.253 g·mol−1
3D model (JSmol)
Melting point248 °C (478 °F)
Solubility in water<1 mg/mL (20 °C)
  • Nc1cc(nc(N)[n+]1[O-])N2CCCCC2
  • InChI=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
  • Key:ZFMITUMMTDLWHR-UHFFFAOYSA-N ☒N
 ☒NcheckY (what is this?)  (verify)

Minoxidil (2,4-diamino-6-piperidinopyrimidine 3-oxide) is a medication used for the treatment of high blood pressure and pattern hair loss in males and females.[2] It is an antihypertensive vasodilator.[3] It is available as a generic medication by prescription in oral tablet form and over the counter as a topical liquid or foam.

Medical uses

Minoxidil, applied topically, is widely used for the treatment of hair loss. It is effective in helping promote hair growth in people with androgenic alopecia regardless of sex.[4] Minoxidil must be used indefinitely for continued support of existing hair follicles and the maintenance of any experienced hair regrowth.[2]

Its effect in people with alopecia areata is unclear.[5]

It takes time for finasteride to work and deliver noticeable effects. Men can go as long as 3-4 months before noticing hair regrowth with minoxidil.[6]

Side effects

Topically applied minoxidil is generally well tolerated, but common side effects include itching of the eye, itching, redness or irritation at the treated area, and unwanted hair growth elsewhere on the body. Exacerbation of hair loss/alopecia has been reported.[7] Other side effects may include rash, itching, difficulty breathing, swelling of the mouth, face, lips, or tongue, chest pain, dizziness, fainting, tachycardia, headache, sudden and unexplained weight gain, or swelling of the hands and feet.[7] Temporary hair loss is a common side effect of minoxidil treatment.[8] Manufacturers note that minoxidil-induced hair loss is a common side effect and describe the process as "shedding".

Alcohol and propylene glycol present in some topical preparations may dry the scalp, resulting in dandruff and contact dermatitis.[9]

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 observered in laboratory animals treated with minoxidil.[10] Cases of allergic reactions to minoxidil or the non-active ingredient propylene glycol, which is found in some topical minoxidil formulations, have been reported. Pseudoacromegaly is an extremely rare side effect reported with large doses of oral minoxidil.[11]

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.[12] 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.[13]

Minoxidil may cause hirsutism, although it is exceedingly rare and reversible by discontinuation of the drug.[14]

Minoxidil is suspected to be highly toxic to cats, even in small doses, as there are reported cases of cats dying shortly after coming in contact with minimal amounts of the substance.[15][16]

Mechanism of action

The mechanism by which minoxidil promotes hair growth is not fully understood. Minoxidil is an adenosine 5'-triphosphate-sensitive potassium channel opener,[17] 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 and A2 receptors[disambiguation needed], and that the expression of SUR2B in dermal papilla cells might play a role in the production of adenosine.[18] Minoxidil acts as an activator of the Kir6/SUR2 channel upon selective binding to SUR2.[19] 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.[20]

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.[21]

Minoxidil stimulates prostaglandin E2 production by activating COX-1[22] and prostaglandin endoperoxide synthase-1 but inhibites 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.[23]

Due to anti-fibrotic activity of minoxidil inhibition of enzyme lysyl hydroxylase present in fibroblast may result in 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 level 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 ½ (ERK 1/2)-activator protein 1 signaling pathway. ERK 1/2 increases, through elastin gene transcription, adequately cross-linked elastic fiber content synthetized by smooth muscle cells, and decreases the number of cells in the aorta.[24]

Minoxidil possesses alpha 2-adrenoceptor agonist activity,[25] 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.[26]

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.[27] Minoxidil significantly increases ROS concentration when compared to untreated cells.

In vitro Minoxidil treatment resulted in a 0.22 fold change for 5α-R2 (p < 0.0001). 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.[28]

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.[29] 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.[30]

History

Initial application

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.[31] These studies resulted in FDA approving minoxidil (with the trade name 'Loniten') in the form of oral tablets to treat high blood pressure in 1979.[32]

Hair growth

When Upjohn received permission from the FDA to test the new drug as medicine for hypertension they approached Charles A. Chidsey MD, Associate Professor of Medicine at the University of Colorado School of Medicine.[31] He conducted two studies,[33][34] 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.

Kahn along with his colleague Paul J. Grant MD had obtained a certain amount of the drug 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.[35] The two doctors had been experimenting with a 1% solution of minoxidil mixed with several alcohol-based liquids.[36] Both parties filed patents to use the drug 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.[35]

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.[32]

In August 1988, the FDA finally approved the drug for treating baldness in men[32][36] under the trade name "Rogaine" (FDA rejected Upjohn's first choice, Regain, as misleading[37]). 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".[37]

In 1991, Upjohn made the product available for women.[36]

On February 12, 1996, the FDA approved both the over-the-counter sale of the drug and the production of generic formulations of minoxidil.[32] Upjohn replied to that by lowering prices to half the price of the prescription drug[36] and by releasing a prescription 5% formula of Rogaine in 1997.[32]

In 1998, a 5% formulation of minoxidil was approved for nonprescription sale by the FDA.[38]

In 2017, JAMA published a study of pharmacy prices in four states for 41 over-the-counter minoxidil products which were "gender-specified." The authors 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.[39]

Trade names

As of June 2017, Minoxidil was marketed under many trade 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, 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, Noxidil, Oxofenil, Pilfud, Pilogro, Pilomin, Piloxidil, Recrea, Regain, Regaine, Regaxidil, Regro, Regroe, Regrou, Regrowth, Relive, Renobell Locion, Reten, Rexidil, Rogaine, Rogan, Si Bi Shen, Splendora, Superminox, Trefostil, Tricolocion, Tricoplus, Tricovivax, Tricoxane, Trugain, Tugain, Unipexil, Vaxdil, Vius, Womens Regaine, Xenogrow, Xue Rui, Ylox, and Zeldilon.[40] It was also marketed as combination drug 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.[40]

Side effects

Topical Minoxidil for hair growth have been reported by a small percentage of users to cause serious side effects, some of which were not reverted upon stopping the application.[41] Male users applying 5% topical application, once or twice a day, aged between 17 and 50, users reported a Post Minoxidil Syndrome of any or a combination of:

More than 60,000 reported cases in FDA database[42]

See also

References

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  2. ^ a b "Minoxidil Regular Strength". UK Electronic Medicines Compendium. 18 August 2015. Archived from the original on 8 January 2017. Retrieved 8 January 2017.
  3. ^ "Vasodilators". mayoclinic.com. Archived from the original on 2011-03-09.
  4. ^ Varothai S, Bergfeld WF (July 2014). "Androgenetic alopecia: an evidence-based treatment update". American Journal of Clinical Dermatology. 15 (3): 217–30. doi:10.1007/s40257-014-0077-5. PMID 24848508. S2CID 31245042.
  5. ^ Hordinsky M, Donati A (July 2014). "Alopecia areata: an evidence-based treatment update". American Journal of Clinical Dermatology. 15 (3): 231–46. doi:10.1007/s40257-014-0086-4. PMID 25000998. S2CID 32253.
  6. ^ "What Happens If I Stop Using Minoxidil Or Finasteride?". UPGUYS.{{cite web}}: CS1 maint: url-status (link)
  7. ^ a b "Rogaine Side Effects in Detail". Drugs.com. Retrieved 8 December 2020.
  8. ^ "FAQs for Men - Hair Growth Education". ROGAINE. Archived from the original on 2009-11-10. Retrieved 2009-11-20.
  9. ^ "Dandruff and Seborrheic Dermatitis". Medscape.com. Archived from the original on 2010-10-28. Retrieved 2009-10-09.
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  11. ^ Nguyen KH, Marks JG (June 2003). "Pseudoacromegaly induced by the long-term use of minoxidil". Journal of the American Academy of Dermatology. 48 (6): 962–5. doi:10.1067/mjd.2003.325. PMID 12789195.
  12. ^ "Minoxidil Topical Solution: An Unsafe Product for Children". Pediatric Emergency Care. 31 (1): 44–46. January 2015. doi:10.1097/PEC.0000000000000301. PMID 12789195. S2CID 205932483. {{cite journal}}: Cite uses deprecated parameter |authors= (help)
  13. ^ Neumann J (10 December 2014). "Hair loss treatment may be dangerous to kids". Reuters.
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  42. ^ "Qlik Sense". fis.fda.gov. Retrieved 2021-04-07.

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