Finasteride
|
|
Clinical data |
Trade names |
Propecia, Proscar |
Synonyms |
MK-906; L-652,931; 17β-(N-tert-Butylcarbamoyl)-4-aza-5α-androst-1-en-3-one; |
AHFS/Drugs.com |
Monograph |
MedlinePlus |
a698016 |
Pregnancy
category |
- X (will cause birth defects)
|
Routes of
administration |
By mouth |
ATC code |
- G04CB01 (WHO) D11AX10 (WHO)
|
Legal status |
Legal status |
- UK: POM (Prescription only)
- US: ℞-only
|
Pharmacokinetic data |
Bioavailability |
63% |
Metabolism |
Liver |
Biological half-life |
Adults: 6 hours
Elderly: 8 hours |
Excretion |
Feces (57%) and urine (39%) as metabolites |
Identifiers |
IUPAC name
- N-(1,1-dimethylethyl)-3-oxo-
(5α,17β)-4-azaandrost-1-ene-17-carboxamide
|
CAS Number |
|
PubChem CID |
|
IUPHAR/BPS |
|
DrugBank |
|
ChemSpider |
|
UNII |
|
KEGG |
|
ChEBI |
|
ChEMBL |
|
Chemical and physical data |
Formula |
C23H36N2O2 |
Molar mass |
372.549 g/mol |
3D model (JSmol) |
|
SMILES
-
O=C(NC(C)(C)C)[C@@H]2[C@]1(CC[C@H]3[C@H]([C@@H]1CC2)CC[C@H]4NC(=O)\C=C/[C@]34C)C
|
InChI
-
InChI=1S/C23H36N2O2/c1-21(2,3)25-20(27)17-8-7-15-14-6-9-18-23(5,13-11-19(26)24-18)16(14)10-12-22(15,17)4/h11,13-18H,6-10,12H2,1-5H3,(H,24,26)(H,25,27)/t14-,15-,16-,17+,18+,22-,23+/m0/s1 Y
-
Key:DBEPLOCGEIEOCV-WSBQPABSSA-N Y
|
(verify) |
Finasteride, sold under the brand names Proscar and Propecia among others, is a medication used for the treatment of benign prostatic hyperplasia (enlarged prostate) and male pattern hair loss.[1][2] It is a type II and type III 5α-reductase inhibitor;[3] 5α-reductase, an enzyme, converts testosterone to dihydrotestosterone (DHT).[2]
Contents
- 1 Medical uses
- 1.1 Prostate enlargement
- 1.2 Pattern hair loss
- 1.3 Off-label uses
- 1.3.1 Excessive hair growth
- 1.3.2 Transgender women
- 2 Contraindications
- 3 Adverse effects
- 4 Mechanism of action
- 5 Chemistry
- 6 History
- 7 Society and culture
- 7.1 Athletics
- 7.2 Brand names
- 7.3 Controversy
- 8 References
- 9 External links
Medical uses
Prostate enlargement
Physicians sometimes use finasteride for the treatment of BPH, informally known as an enlarged prostate. Finasteride may improve the symptoms associated with BPH such as difficulty urinating, getting up during the night to urinate, hesitation at the start of urination, and decreased urinary flow. It provides less symptomatic relief than alpha-1 blockers such as tamsulosin and symptomatic relief is slower in onset (six months or more of treatment with finasteride may be required to determine the therapeutic results of treatment). Symptomatic benefits are mainly seen in those with prostate volume > 40 cm3. In long-term studies finasteride but not alpha-1 inhibitors reduce the risk of acute urinary retention (−57% at 4 years) and the need for surgery (−54% at 4 years). If the drug is discontinued, any therapeutic benefits reverse within about 6–8 months.[4][5][6]
Pattern hair loss
Finasteride is sometimes used to treat pattern hair loss (androgenetic alopecia) in men only.[7] Treatment slows further hair loss[8] and provides about 30% improvement in hair loss after six months of treatment, with effectiveness usually only persisting as long as the drug is taken,[9] although on occasion hair loss is slowed indefinitely following withdrawal. Finasteride has also been tested for pattern hair loss in women; the results were no better than placebo.[10]
Off-label uses
Excessive hair growth
Finasteride has been found to be effective in the treatment of hirsutism (excessive facial and/or body hair growth) in women.[11] In a study of 89 women with hyperandrogenism due to persistent adrenarche syndrome, finasteride produced a 93% reduction in facial hirsutism and a 73% reduction bodily hirsutism after 2 years of treatment.[11] Other studies using finasteride for hirsutism have also found it to be clearly effective.[11]
Transgender women
Finasteride is sometimes used in hormone replacement therapy for transgender women due to its antiandrogen properties, in combination with a form of estrogen . However, little clinical research of finasteride use for this purpose has been conducted and evidence of efficacy is limited.[12] Moreover, caution has been recommended when prescribing finasteride to transgender women, as finasteride may be associated with side effects such as depression, anxiety, and suicidal ideation, symptoms that are particularly prevalent in the transgender population and in others at high risk already.[13]
Contraindications
There are concerns that finasteride may cause birth defects if used during pregnancy.[14][15] It is classified in the FDA pregnancy category X.[7]
Adverse effects
A 2010 Cochrane review concluded that side effects from finasteride are rare when used for BPH.[4] Compared with placebo, men taking finasteride are, however, at increased risk for impotence, erectile dysfunction, decreased libido, and ejaculation disorder for the first year of treatment.[4] In this review the rates of these effects became indistinguishable from placebo after 2–4 years and these side effects usually got better over time.[4] Another 2010 review found that when used for hair loss finasteride increased rates of sexual problems.[16] A 2016 review of 5α-reductase inhibitors for prostatic hyperplasia found that sexual dysfunction was 2.5 times more likely in those who used them.[17]
In men with prostatic hyperplasia the use of both a 5α-reductase inhibitor and a α1-adrenergic receptor blocker resulted in a greater risk of erectile dysfunction compared to either agent alone.[18]
The FDA has added a warning to 5α-reductase inhibitors concerning an increased risk of high-grade prostate cancer, as the treatment of BPH lowers PSA (prostate-specific antigen), which could mask the development of prostate cancer.[19][20] Although overall incidence of male breast cancer in clinical trials for finasteride 5 mg was not increased, there are post-marketing reports of breast cancer in association with its use. Available evidence does not provide clarity as to whether there is a causative relationship between finasteride and these cancers.[7][21]
A 2015 meta analysis found that none of the clinical trials testing finasteride in hair loss had adequate safety reporting and did not provide sufficient information to establish the safety profile for finasteride as a treatment for hair loss. The study concluded the existing clinical trials of finasteride for hair loss provide very limited information on toxicity, are of poor quality, and seem to be systematically biased toward under-detection of adverse events. Moreover, the trials submitted to the FDA for approval for hair loss excluded most men who would normally be prescribed finasteride for androgenic alopecia.[22][23]
Although considered a cosmetic issue rather than necessarily an adverse effect, gynecomastia may also occur following finasteride usage and can be a source of psychological distress.[24][25][26][27]
Sexual dysfunction
Whether finasteride causes long-term sexual dysfunction in some men after stopping drug treatment is unclear.[22] There are case reports of persistent diminished libido or erectile dysfunction after stopping the drug and the FDA has updated the label to inform people of these reports.[9][28] A 2010 review found moderate quality evidence that finasteride increased the risk of sexual dysfunction, but not that people stopped using it because of sexual side effects.[16]
When finasteride was originally approved for hair loss in 1997, the FDA approval review reported that it appears well tolerated, with the most common side effects being related to sexual function.[29] In many people these side effects resolve if the medication is stopped and occasionally resolve even if the medication is continued.[29] They additionally state "the sexual functioning questionnaire seems to have given a sensitive reflection of the disturbance on sexual functioning".[29]
A meta-analysis and systematic review found that sexual dysfunction, including erectile dysfunction, loss of libido, and reduced ejaculate, may occur in 3.4 to 15.8% of men treated with finasteride or dutasteride.[30][31] This is linked to lower quality of life and can cause stress in relationships.[32] There is also an association with lowered sexual desire.[33] It has been reported that in a subset of men, these adverse sexual side effects may persist even after discontinuation of finasteride or dutasteride.[33]
Mechanism of action
Finasteride is a 5α-reductase inhibitor, specifically the type II and III isoenzymes.[3][34] By inhibiting 5α-reductase, finasteride prevents conversion of testosterone to dihydrotestosterone (DHT) by the type II and III isoenzymes, resulting in a decrease in serum DHT levels by about 65–70% and in prostate DHT levels by up to 85–90%,[3][35] where expression of the type II isoenzyme predominates. Unlike triple inhibitors of all three isoenzymes of 5α-reductase like dutasteride which can reduce DHT levels in the entire body by more than 99%,[3] finasteride does not completely suppress DHT production because it lacks significant inhibitory effects on the 5α-reductase type I isoenzyme, with 100-fold less affinity for I as compared to II.[7]
By blocking DHT production, finasteride reduces androgen activity in the scalp. In the prostate, inhibition of 5α-reductase reduces prostate volume, which improves BPH and reduces risk of prostate cancer. Inhibition of 5α-reductase also reduces epididymal weight, and decreases motility and normal morphology of spermatozoa in the epididymis.[36] Neurosteroids like 3α-androstanediol and allopregnanolone activate the GABAA receptor; because finasteride prevents the formation of neurosteroids, it may contribute to a reduction of GABAA activity (see also neurosteroidogenesis inhibitor). Reduction of GABAA receptor activation by these neurosteroids has been implicated in depression, anxiety, and sexual dysfunction.[37][38][39]
In addition to inhibiting 5α-reductase, finasteride has also been found to competitively inhibit 5β-reductase (AKR1D1),[40] although its affinity for the enzyme is substantially less than for 5α-reductase (an order of magnitude less than 5α-reductase type I) and hence is unlikely to be of clinical significance.[40]
Finasteride reduces prostate volume by 20 to 30% in men with benign prostatic hyperplasia.[41]
Chemistry
Finasteride, also known as 17β-(N-tert-butylcarbamoyl)-4-aza-5α-androst-1-en-3-one,[42] is a synthetic androstane steroid and 4-azasteroid. It is an analogue of androgen steroid hormones like testosterone and DHT.
Finasteride is a lipophilic compound.[43]
History
In 1942, James Hamilton observed that prepubertal castration prevents the later development of male pattern baldness in mature men.[44] In 1974, Julianne Imperato-McGinley of Cornell Medical College in New York attended a conference on birth defects. She reported on a group of intersex children in the Caribbean who appeared sexually ambiguous at birth, and were initially raised as girls, but then grew external male genitalia and other masculine characteristic after onset of puberty. Her research group found these children shared a genetic mutation, causing deficiency of the 5α-reductase enzyme and male hormone dihydrotestosterone (DHT), which was found to have been the etiology behind abnormalities in male sexual development. Upon maturation, these individuals were observed to have smaller prostates which were underdeveloped, and were also observed to lack incidence of male pattern baldness.[45][46]
In 1975, copies of Imperato-McGinley's presentation were seen by P. Roy Vagelos, who was then serving as Merck's basic-research chief. He was intrigued by the notion that decreased levels of DHT led to the development of smaller prostates. Dr. Vagelos then sought to create a drug which could mimic the condition found in these children to treat older men who were suffering from benign prostatic hyperplasia.[47]
Finasteride was developed under the code name MK-906.[citation needed] In 1992, finasteride (5 mg) was approved by the U.S. Food and Drug Administration (FDA) for treatment of BPH, which Merck marketed under the brand name Proscar.[citation needed] In 1997, Merck was successful in obtaining FDA approval for a second indication of finasteride (1 mg) for treatment of MPB, which was marketed under the brand name Propecia.[citation needed]
Society and culture
The Food and Drug Administration advises that donation of blood or plasma be deferred for at least one month after taking the last dose of finasteride.[48]
Harold Bornstein, Donald Trump's personal physician, stated Trump was taking finasteride to promote hair growth.[49]
Athletics
From 2005 to 2009, the World Anti-Doping Agency banned finasteride because it was discovered that the drug could be used to mask steroid abuse.[50] It was removed from the list effective January 1, 2009, after improvements in testing methods made the ban unnecessary.[51] Athletes who used finasteride and were banned from international competition include skeleton racer Zach Lund, bobsledder Sebastien Gattuso, footballer Romário and ice hockey goaltender José Théodore.[51][52]
Brand names
Drug trade names include Propecia, marketed for male pattern baldness (MPB), and Proscar, for benign prostatic hyperplasia (BPH); both are products of Merck & Co. There is 1 mg of finasteride in Propecia and 5 mg in Proscar. Merck's patent on finasteride for the treatment of BPH expired on June 19, 2006.[53] Merck was awarded a separate patent for the use of finasteride to treat MPB. This patent expired in November 2013.[54]
Controversy
Men in the US and Canada concerned about persistent sexual side effects "coined the phrase 'post finasteride syndrome', which they say is characterized by sexual, neurological, hormonal and psychological side effects that can persist in men who have taken finasteride for hair loss or an enlarged prostate".[55][56] In 2012, a health advocacy group called the Post-Finasteride Syndrome Foundation was formed with the primary goal of finding a cure for the reported syndrome and a secondary goal of raising awareness.[55] According to the company's 1Q2016 financial filing, Merck is a defendant in 1,385 product liability lawsuits which have been filed by customers alleging they have experienced persistent sexual side effects following cessation of treatment with finasteride.[57]
References
- ^ Buckingham J (1987). Dictionary of Organic Compounds. CRC Press. p. 3147. ISBN 978-0-412-54090-5.
- ^ a b Morton I, Hall JM (6 December 2012). Concise Dictionary of Pharmacological Agents: Properties and Synonyms. Springer Science & Business Media. pp. 121, 246. ISBN 978-94-011-4439-1.
- ^ a b c d Yamana K, Labrie F, Luu-The V (August 2010). "Human type 3 5α-reductase is expressed in peripheral tissues at higher levels than types 1 and 2 and its activity is potently inhibited by finasteride and dutasteride". Hormone Molecular Biology and Clinical Investigation. 2 (3): 293–9. PMID 25961201. doi:10.1515/hmbci.2010.035.
- ^ a b c d Tacklind J, Fink HA, Macdonald R, Rutks I, Wilt TJ (October 2010). "Finasteride for benign prostatic hyperplasia". The Cochrane Database of Systematic Reviews (10): CD006015. PMID 20927745. doi:10.1002/14651858.CD006015.pub3.
- ^ Proscar label
- ^ "Treatment of Non-neurogenic Male LUTS | Uroweb".
- ^ a b c d "Propecia label" (PDF).
- ^ Habif TP (23 April 2015). Clinical Dermatology. Elsevier Health Sciences. pp. 934–. ISBN 978-0-323-26607-9.
- ^ a b Varothai S, Bergfeld WF (July 2014). "Androgenetic alopecia: an evidence-based treatment update". American Journal of Clinical Dermatology. 15 (3): 217–30. PMID 24848508. doi:10.1007/s40257-014-0077-5.
- ^ Levy LL, Emer JJ (August 2013). "Female pattern alopecia: current perspectives". International Journal of Women's Health. 5: 541–56. PMC 3769411 . PMID 24039457. doi:10.2147/IJWH.S49337.
- ^ a b c Blume-Peytavi U, Whiting DA, Trüeb RM (26 June 2008). Hair Growth and Disorders. Springer Science & Business Media. p. 369. ISBN 978-3-540-46911-7.
- ^ Knezevich EL, Viereck LK, Drincic AT (January 2012). "Medical management of adult transsexual persons". Pharmacotherapy. 32 (1): 54–66. PMID 22392828. doi:10.1002/PHAR.1006.
- ^ Trüeb, Ralph M. (2017). "Discriminating in favour of or against men with increased risk of finasteride-related side effects?". Experimental Dermatology. ISSN 0906-6705. PMID 27489125. doi:10.1111/exd.13155.
[...] caution is recommended while prescribing oral finasteride to male-to-female transsexuals, as the drug has been associated with inducing depression, anxiety and suicidal ideation, symptoms that are particularly common in patients with gender dysphoria, who are already at a high risk.[9]
- ^ Wolverton SE (2007). Comprehensive Dermatologic Drug Therapy. Elsevier Health Sciences. ISBN 978-1-4377-2070-9.
- ^ Burchum, Jacqueline; Rosenthal, Laura. Lehne's Pharmacology for Nursing Care - E-Book. Elsevier Health Sciences. p. 802. ISBN 9780323340267.
- ^ a b Mella JM, Perret MC, Manzotti M, Catalano HN, Guyatt G (October 2010). "Efficacy and safety of finasteride therapy for androgenetic alopecia: a systematic review". Archives of Dermatology. 146 (10): 1141–50. PMID 20956649. doi:10.1001/archdermatol.2010.256.
- ^ Liu L, Zhao S, Li F, Li E, Kang R, Luo L, Luo J, Wan S, Zhao Z (September 2016). "Effect of 5α-Reductase Inhibitors on Sexual Function: A Meta-Analysis and Systematic Review of Randomized Controlled Trials". The Journal of Sexual Medicine. 13 (9): 1297–310. PMID 27475241. doi:10.1016/j.jsxm.2016.07.006.
- ^ Favilla V, Russo GI, Privitera S, Castelli T, Giardina R, Calogero AE, Condorelli RA, La Vignera S, Cimino S, Morgia G (September 2016). "Impact of combination therapy 5-alpha reductase inhibitors (5-ARI) plus alpha-blockers (AB) on erectile dysfunction and decrease of libido in patients with LUTS/BPH: a systematic review with meta-analysis". The Aging Male. 19 (3): 175–181. PMID 27310433. doi:10.1080/13685538.2016.1195361.
- ^ FDA. Posted 9 June 2011. 5-alpha reductase inhibitors (5-ARIs): Label Change – Increased Risk of Prostate Cancer
- ^ Walsh PC (April 2010). "Chemoprevention of prostate cancer". The New England Journal of Medicine. 362 (13): 1237–8. PMID 20357287. doi:10.1056/NEJMe1001045.
- ^ Medicines and Healthcare products Regulatory Agency Drug Safety Update. December 2009 Finasteride: potential risk of male breast cancer
- ^ a b Belknap SM, Aslam I, Kiguradze T, Temps WH, Yarnold PR, Cashy J, Brannigan RE, Micali G, Nardone B, West DP (June 2015). "Adverse Event Reporting in Clinical Trials of Finasteride for Androgenic Alopecia: A Meta-analysis". JAMA Dermatology. 151 (6): 600–6. PMID 25830296. doi:10.1001/jamadermatol.2015.36.
- ^ Moore TJ (June 2015). "Finasteride and the Uncertainties of Establishing Harms". JAMA Dermatology. 151 (6): 585–6. PMID 25831198. doi:10.1001/jamadermatol.2015.37.
- ^ Narula HS, Carlson HE (August 2014). "Gynaecomastia-pathophysiology, diagnosis and treatment". Nat Rev Endocrinol. 10 (11): 684–698. PMID 25112235. doi:10.1038/nrendo.2014.139.
- ^ Deepinder F, Braunstein GD (2012). "Drug-induced gynecomastia: an evidence-based review.". Expert opinion on drug safety. 11 (5): 779–795. PMID 22862307. doi:10.1517/14740338.2012.712109.
- ^ Bolignano D, Palmer SC, Navaneethan SD, Strippoli GF (April 2014). "Aldosterone antagonists for preventing the progression of chronic kidney disease". Cochrane Database of Systematic Reviews. 4: CD007004. PMID 24782282. doi:10.1002/14651858.CD007004.pub3.
- ^ Aiman, U; Haseen, MA; Rahman, SZ (December 2009). "Gynecomastia: An ADR due to drug interaction.". Indian journal of pharmacology. 41 (6): 286–287. PMC 2846505 . PMID 20407562. doi:10.4103/0253-7613.59929.
- ^ FDA (11 April 2012). "Questions and Answers: Finasteride Label Changes". US FDA. Retrieved 26 October 2014.
- ^ a b c FDA. "Summary of Key Safety Findings" (PDF). p. 98.
- ^ Hirshburg JM, Kelsey PA, Therrien CA, Gavino AC, Reichenberg JS (2016). "Adverse Effects and Safety of 5-alpha Reductase Inhibitors (Finasteride, Dutasteride): A Systematic Review". J Clin Aesthet Dermatol. 9 (7): 56–62. PMC 5023004 . PMID 27672412.
- ^ Liu, L; Zhao, S; Li, F; Li, E; Kang, R; Luo, L; Luo, J; Wan, S; Zhao, Z (September 2016). "Effect of 5α-Reductase Inhibitors on Sexual Function: A Meta-Analysis and Systematic Review of Randomized Controlled Trials.". The journal of sexual medicine. 13 (9): 1297–310. PMID 27475241. doi:10.1016/j.jsxm.2016.07.006.
- ^ Gur, S; Kadowitz, PJ; Hellstrom, WJ (January 2013). "Effects of 5-alpha reductase inhibitors on erectile function, sexual desire and ejaculation.". Expert opinion on drug safety. 12 (1): 81–90. PMID 23173718. doi:10.1517/14740338.2013.742885.
- ^ a b Traish, AM; Hassani, J; Guay, AT; Zitzmann, M; Hansen, ML (March 2011). "Adverse side effects of 5α-reductase inhibitors therapy: persistent diminished libido and erectile dysfunction and depression in a subset of patients.". The journal of sexual medicine. 8 (3): 872–84. PMID 21176115. doi:10.1111/j.1743-6109.2010.02157.x.
- ^ Aggarwal S, Thareja S, Verma A, Bhardwaj TR, Kumar M (February 2010). "An overview on 5alpha-reductase inhibitors". Steroids. 75 (2): 109–53. PMID 19879888. doi:10.1016/j.steroids.2009.10.005.
- ^ Bartsch G, Rittmaster RS, Klocker H (April 2000). "Dihydrotestosterone and the concept of 5alpha-reductase inhibition in human benign prostatic hyperplasia". European Urology. 37 (4): 367–80. PMID 10765065. doi:10.1159/000020181.
- ^ Robaire B, Henderson NA (May 2006). "Actions of 5alpha-reductase inhibitors on the epididymis". Molecular and Cellular Endocrinology. 250 (1-2): 190–5. PMID 16476520. doi:10.1016/j.mce.2005.12.044.
- ^ Finn DA, Beadles-Bohling AS, Beckley EH, Ford MM, Gililland KR, Gorin-Meyer RE, Wiren KM (2006). "A new look at the 5alpha-reductase inhibitor finasteride". CNS Drug Reviews. 12 (1): 53–76. PMID 16834758. doi:10.1111/j.1527-3458.2006.00053.x.
- ^ Römer B, Gass P (December 2010). "Finasteride-induced depression: new insights into possible pathomechanisms". Journal of Cosmetic Dermatology. 9 (4): 331–2. PMID 21122055. doi:10.1111/j.1473-2165.2010.00533.x.
- ^ Gunn BG, Brown AR, Lambert JJ, Belelli D (2011). "Neurosteroids and GABA(A) Receptor Interactions: A Focus on Stress". Frontiers in Neuroscience. 5: 131. PMC 3230140 . PMID 22164129. doi:10.3389/fnins.2011.00131.
- ^ a b Drury JE, Di Costanzo L, Penning TM, Christianson DW (July 2009). "Inhibition of human steroid 5beta-reductase (AKR1D1) by finasteride and structure of the enzyme-inhibitor complex". The Journal of Biological Chemistry. 284 (30): 19786–90. PMC 2740403 . PMID 19515843. doi:10.1074/jbc.C109.016931.
- ^ David G. Bostwick; Liang Cheng (24 January 2014). Urologic Surgical Pathology E-Book. Elsevier Health Sciences. pp. 402–. ISBN 978-0-323-08619-6.
- ^ Tian G, Stuart JD, Moss ML, Domanico PL, Bramson HN, Patel IR, Kadwell SH, Overton LK, Kost TA, Mook RA (1994). "17 beta-(N-tert-butylcarbamoyl)-4-aza-5 alpha-androstan-1-en-3-one is an active site-directed slow time-dependent inhibitor of human steroid 5 alpha-reductase 1". Biochemistry. 33 (8): 2291–6. PMID 8117686.
- ^ Azeem A, Khan ZI, Aqil M, Ahmad FJ, Khar RK, Talegaonkar S (May 2009). "Microemulsions as a surrogate carrier for dermal drug delivery". Drug Development and Industrial Pharmacy. 35 (5): 525–47. PMID 19016057. doi:10.1080/03639040802448646.
- ^ Hamilton J. 1942. Male hormone stimulation is prerequisite and an incitant in common baldness. American Journal of Anatomy 71(3):451–480 DOI 10.1002/aja.1000710306.
- ^ Imperato-McGinley J, Guerrero L, Gautier T, Peterson RE (December 1974). "Steroid 5alpha-reductase deficiency in man: an inherited form of male pseudohermaphroditism". Science. 186 (4170): 1213–5. PMID 4432067. doi:10.1126/science.186.4170.1213.
- ^ Isfort AH, Emerick JE, Paz RA (11 November 2016). "5-Alpha-Reductase Deficiency". WebMD. News & Perspective Drugs & Diseases CME & Education Academy Consult, Drugs & Diseases > Pediatrics: General Medicine.
- ^ Freudenheim M (February 16, 1992). "Keeping the Pipeline Filled at Merck". The New York Times.
- ^ "Deferral of Blood and Plasma donors – Medications" (PDF). FDA. 28 July 1993. Retrieved 4 February 2017.
- ^ Altman LK (1 February 2017). "Donald Trump’s Longtime Doctor Says President Takes Hair-Growth Drug". The New York Times. Retrieved 25 February 2017.
- ^ Sandomir R (2006-01-19). "Skin Deep; Fighting Baldness, and Now an Olympic Ban". The New York Times. Retrieved 2010-05-02.
- ^ a b Staff (28 October 2008). "WADA removes Finasteride from ban list". The Australian.
- ^ Staff (9 October 2008). "WADA takes Romario's drug off banned list". Sydney Morning Herald.
- ^ "Primary Patent Expirations for Selected High Revenue Drugs". RxNews. Prescription Solutions. Archived from the original on 21 March 2008.
- ^ FDA. "Patent Expiration for Propecia". Orange Book: Approved Drug Products with Therapeutic Equivalence Evaluations.
- ^ a b Margo J (26 September 2012). "Looking at care with a critical eye". Australian Financial Review.
- ^ "Post-Finasteride Syndrome Foundation official website".
- ^ "Form 10-Q 1st Quarter 2016" (PDF). Merck & Co., Inc. p. 19.
External links
- Proscar | Official website
- Propecia | Official website
Androgens and antiandrogens
|
Androgens
(incl. AAS) |
AR agonists |
- Testosterone derivatives: Androstenediol dipropionate
- Boldenone undecylenate
- Clostebol
- Clostebol acetate
- Clostebol caproate
- Clostebol propionate
- Cloxotestosterone acetate
- Dehydroepiandrosterone (DHEA) (androstenolone, prasterone)
- DHEA enanthate (prasterone enanthate)
- Quinbolone
- Testosterone#
- Testosterone ester mixtures (Deposterona, Omnadren, Sustanon)
- Testosterone esters
- Dihydrotestosterone derivatives: Bolazine capronate
- Dihydrotestosterone (DHT) (androstanolone, stanolone)
- Dihydrotestosterone esters
- Drostanolone propionate (dromostanolone propionate)
- Epitiostanol
- Mepitiostane
- Mesterolone
- Metenolone acetate (methenolone acetate)
- Metenolone enanthate (methenolone enanthate)
- Stenbolone acetate
- 19-Nortestosterone derivatives: Bolandiol dipropionate
- Norclostebol
- Norclostebol acetate
- Oxabolone cipionate (oxabolone cypionate)
- Trenbolone acetate
- Trenbolone hexahydrobenzylcarbonate (trenbolone cyclohexylmethylcarbonate)
- 17α-Alkylated testosterone derivatives: Bolasterone
- Calusterone
- Chlorodehydromethyltestosterone (CDMT)
- Fluoxymesterone
- Formebolone
- Metandienone (methandienone, methandrostenolone)
- Methandriol (methylandrostenediol)
- Methandriol bisenanthoyl acetate
- Methandriol dipropionate
- Methandriol propionate
- Methyltestosterone
- Methyltestosterone 3-hexyl ether
- Oxymesterone
- Penmesterol
- Tiomesterone (thiomesterone)
- 17α-Alkylated dihydrotestosterone derivatives: Androisoxazole
- Furazabol
- Mebolazine (dimethazine)
- Mestanolone
- Oxandrolone
- Oxymetholone
- Stanozolol
- 17α-Alkylated 19-nortestosterone derivatives: Ethylestrenol
- Mibolerone
- Norethandrolone
- Normethandrone (methylestrenolone, normethisterone)
- Propetandrol (propethandrol)
- 17α-Vinyltestosterone derivatives: Norvinisterone (vinylnortestosterone)
- 17α-Ethynyltestosterone derivatives: Danazol
- Gestrinone
- Progestins (e.g., ethisterone (ethynyltestosterone), levonorgestrel, norgestrel, norethisterone (norethindrone), lynestrenol, norgestrienone)
- Tibolone
- Progesterone derivatives: Medroxyprogesterone acetate
|
Progonadotropins |
- Antiestrogens (e.g., tamoxifen, clomifene)
- GnRH agonists (e.g., GnRH (gonadorelin), leuprorelin)
- Gonadotropins (e.g., LH, hCG)
|
|
Antiandrogens |
AR antagonists |
- Steroidal: Abiraterone acetate
- Canrenone
- Chlormadinone acetate
- Cyproterone acetate
- Delmadinone acetate
- Dienogest
- Drospirenone
- Medrogestone
- Megestrol acetate
- Nomegestrol acetate
- Osaterone acetate
- Oxendolone
- Potassium canrenoate
- Spironolactone
- Nonsteroidal: Apalutamide†
- Bicalutamide
- Cimetidine
- Darolutamide†
- Enzalutamide
- Flutamide
- Ketoconazole
- Nilutamide
- Seviteronel†
- Topilutamide (fluridil)
|
Steroidogenesis
inhibitors |
5α-Reductase |
- Alfatradiol
- Dutasteride
- Epristeride
- Finasteride
- Saw palmetto extract
|
Others |
- Abiraterone acetate
- Aminoglutethimide
- Bifluranol
- Cyproterone acetate
- Flutamide
- Ketoconazole
- Nilutamide
- Seviteronel†
- Spironolactone
|
|
Antigonadotropins |
- D2 receptor antagonists (prolactin releasers) (e.g., domperidone, metoclopramide, risperidone, haloperidol, chlorpromazine, sulpiride)
- Estrogens (e.g., bifluranol, diethylstilbestrol, estradiol, estradiol esters, ethinylestradiol, ethinylestradiol sulfonate, paroxypropione)
- GnRH agonists (e.g., leuprorelin)
- GnRH antagonists (e.g., cetrorelix)
- Progestogens (incl., chlormadinone acetate, cyproterone acetate, hydroxyprogesterone caproate, gestonorone caproate, medroxyprogesterone acetate, megestrol acetate)
|
Others |
- Androstenedione immunogens: Androvax (androstenedione albumin)
- Ovandrotone albumin (Fecundin)
|
|
- #WHO-EM
- ‡Withdrawn from market
- Clinical trials:
- †Phase III
- §Never to phase III
- See also
- Androgen receptor modulators
- Estrogens and antiestrogens
- Progestogens and antiprogestogens
- List of androgens/anabolic steroids
|
Drugs used in benign prostatic hyperplasia (G04C)
|
5α-Reductase inhibitors |
- Dutasteride
- Epristeride
- Finasteride
|
Alpha blockers (α1) |
- Alfuzosin
- Doxazosin
- Silodosin
- Tamsulosin
- Terazosin
|
Herbals |
- Pygeum africanum
- Saw palmetto extract
|
Other |
- Gestonorone caproate
- Mepartricin
- Osaterone acetate
- Oxendolone
|
Other dermatological preparations (D11)
|
Anti-seborrheics |
- Antiandrogens
- Bicalutamide
- Cyproterone acetate
- Flutamide
- Spironolactone
- Antifungals
- Bifonazole
- Cetrimonium bromide (cetrimide)
- Ciclopirox olamine (ciclopirox)
- Climbazole
- Clotrimazole
- Ketoconazole
- Miconazole
- Piroctone olamine
- Selenium disulfide (selenium sulfide)
- Xenysalate
- Zinc pyrithione (pyrithione zinc)
- Antihistamines
- Calcineurin inhibitors
- Cyclosporin
- Pimecrolimus
- Tacrolimus
- Isotretinoin
- Keratolytics
- Coal tar
- Resorcinol
- Salicylic acid
- Sulfur
- Urea (urea-containing cream)
- Lithium salts
- Lithium gluconate
- Lithium succinate
- Topical corticosteroids (e.g., hydrocortisone)
|
Skin lightening |
- Hydroquinone
- Mequinol
- Monobenzone
|
Skin darkening |
- Afamelanotide
- Melanotan II
|
Anti-inflammatories |
- Oxaceprol
- Gamolenic acid
- Pimecrolimus
- Tacrolimus
- Alitretinoin
|
Alopecia treatments |
- 5α-Reductase inhibitors
- Alfatradiol
- Finasteride
- Dutasteride
- Saw palmetto extract
- Antiandrogens
- Bicalutamide
- Cyproterone acetate
- Flutamide
- Spironolactone
- Topilutamide (fluridil)
- Potassium channel openers
- Others
|
Hair growth inhibitors |
- 5α-Reductase inhibitors
- Antiandrogens
- Bicalutamide
- Cyproterone acetate
- Flutamide
- Spironolactone
- Eflornithine
|
Others |
- Androgens (e.g., testosterone)
- Brimonidine
- Calcium gluconate
- Estrogens (e.g., estradiol)
- Hyaluronic acid
- Magnesium sulfate
- Pregnenolone acetate
- Progestogens (e.g., progesterone)
- Povidone-iodine
- Tiratricol
|
Merck & Co., Inc.
|
Corporate directors: |
- Richard Clark
- Johnnetta Cole
- William Harrison
- William Kelley
- Rochelle Lazarus
- Thomas Shenk
- Anne Tatlock
- Samuel Thier
- Wendell Weeks
- Peter Wendell
|
Products: |
- Alendronate
- Aprepitant
- Ertapenem
- Ezetimibe
- Ezetimibe/simvastatin
- Finasteride
- Fosaprepitant
- Indinavir
- Losartan
- Lovastatin
- Montelukast
- Omarigliptin
- Raltegravir
- Rizatriptan
- Rofecoxib
- Simvastatin
- Sitagliptin
- Vorinostat
|
Publications: |
- The Merck Manuals
- Index
- Manual
- Veterinary
- Geriatrics
|