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Mesterolone, sold under the brand name Proviron among others, is an androgen and anabolic steroid (AAS) medication which is used mainly in the treatment of low testosterone levels.



Mesterolone, sold under the brand name Proviron among others, is an androgen and anabolic steroid (AAS) medication which is used mainly in the treatment of low testosterone levels.[1][2] It has also been used to treat male infertility, although this use is controversial.[1][3][4] It is taken by mouth.[1]

Side effects of mesterolone include symptoms of masculinization like acneincreased hair growthvoice changes, and increased sexual desire.[1] It has no risk of liver damage.[1][2] The drug is a synthetic androgen and anabolic steroid and hence is an agonist of the androgen receptor (AR), the biological target of androgens like testosterone and dihydrotestosterone (DHT).[1][5] It has weak androgenic effects and weak anabolic effects, which make it useful for producing masculinization.[1] The drug has no estrogenic effects.[1][2]

Mesterolone was first described by 1966[6] and introduced for medical use by 1967.[7][8] In addition to its medical use, mesterolone has been used to improve physique and performance, although it is not commonly used for such purposes due to its weak anabolic effects.[1] The drug is a controlled substance in many countries and so non-medical use is generally illicit.[1][9]

Medical uses[edit]

Mesterolone is used in the treatment of androgen deficiency in male hypogonadismanemia, and to support male fertility among other indications.[1][10][11] It has also been used to treat delayed puberty in boys.[12] Because it lacks estrogenic effects, mesterolone may be indicated for treating cases of androgen deficiency in which breast tenderness or gynecomastia is also present.[13] The drug is described as a relatively weak androgen with partial activity and is rarely used for the purpose of androgen replacement therapy, but is still widely used in medicine.[1][11][14][2]

Mesterolone is used in androgen replacement therapy at a dosage of 50 to 100 mg 2 to 3 times per day.[15]

Androgen replacement therapy formulations and dosages used in men 

Non-medical uses[edit]

Mesterolone has been used for physique- and performance-enhancing purposes by competitive athletesbodybuilders, and powerlifters.[1]

Side effects[edit]

Side effects of mesterolone include virilization among others.[1]



Like other AAS, mesterolone is an agonist of the androgen receptor (AR).[1] It is not a substrate for 5α-reductase, as it is already 5α-reduced, and hence is not potentiated in so-called “androgenic” tissues such as the skinhair follicles, and prostate gland.[1] Mesterolone is described as a very poor anabolic agent due to inactivation by 3α-hydroxysteroid dehydrogenase (3α-HSD) in skeletal muscle tissue, similarly to DHT and mestanolone (17α-methyl-DHT).[1] In contrast, testosterone is a very poor substrate for 3α-HSD, and so is not similarly inactivated in skeletal muscle.[1] Because of its lack of potentiation by 5α-reductase in “androgenic” tissues and its inactivation by 3α-HSD in skeletal muscle, mesterolone is relatively low in both its androgenic potency and its anabolic potency.[1] However, it does still show a greater ratio of anabolic activity to androgenic activity relative to testosterone.[1]

Mesterolone is not a substrate for aromatase, and so cannot be converted into an estrogen.[1] As such, it has no propensity for producing estrogenic side effects such as gynecomastia and fluid retention.[1] It also has no progestogenic activity.[1]

Because mesterolone is not 17α-alkylated, it has little or no potential for hepatotoxicity.[1] However, its risk of deleterious effects on the cardiovascular system is comparable to that of several other oral AAS.[1]


The C1α methyl group of mesterolone inhibits its hepatic metabolism and thereby confers significant oral activity, although its oral bioavailability is still much lower than that of 17α-alkylated AAS.[1] In any case, mesterolone is one of the few non-17α-alkylated AAS that is active with oral ingestion.[1] Uniquely among AAS, mesterolone has very high affinity for human serum sex hormone-binding globulin (SHBG), about 440% that of DHT in one study and 82% of that of DHT in another study.[16][1][17] As a result, it may displace endogenous testosterone from SHBG and thereby increase free testosterone concentrations, which may in part be involved in its effects.[1]


Mesterolone, also known as 1α-methyl-4,5α-dihydrotestosterone (1α-methyl-DHT) or as 1α-methyl-5α-androstan-17β-ol-3-one, is a synthetic androstane steroid and derivative of DHT.[18][19][1] It is specifically DHT with a methyl group at the C1α position.[18][19][1] Closely related AAS include metenolone and its esters metenolone acetate and metenolone enanthate.[18][19][1] The antiandrogen rosterolone (17α-propylmesterolone) is also closely related to mesterolone.[20]


Mesterolone was developed in the 1960s[21] and was first described by 1966.[6][22][23][24] It was introduced for medical use by Schering under the brand name Proviron by 1967.[7][8] The well-established brand name Proviron had previously been used by Schering for testosterone propionate starting in 1936.[25] Following the introduction of mesterolone as Proviron, Schering continued to market testosterone propionate under the brand name Testoviron.[25] A number of sources incorrectly state that mesterolone was synthesized or introduced for medical use in 1934.[21][1][26][27]

Society and culture[edit]

Generic names[edit]

Mesterolone is the generic name of the drug and its INNUSANBAN, and DCIT, while mestérolone is its DCF.[18][19][28][29]

Brand names[edit]

Mesterolone is marketed mainly under the brand name Proviron.[18][19][29][1]


Mesterolone is available widely throughout the world, including in the United KingdomAustralia, and South Africa, as well as many non-English-speaking countries.[19][29] It is not available in the United StatesCanada, or New Zealand.[19][29] The drug has never been marketed in the United States.[26]

Legal status[edit]

Mesterolone, along with other AAS, is a schedule III controlled substance in the United States under the Controlled Substances Act and a schedule IV controlled substance in Canada under the Controlled Drugs and Substances Act.[9][30]


In one small scale clinical trial of depressed patients, an improvement of symptoms which included anxiety, lack of drive and desire was observed.[31] In patients with dysthymiaunipolar, and bipolar depression significant improvement was observed.[31] In this series of studies, mesterolone lead to a significant decrease in luteinizing hormone and testosterone levels.[31] In another study, 100 mg mesterolone cipionate was administered twice monthly.[32] With regards to plasma testosterone levels, there was no difference between the treated versus untreated group, and baseline luteinizing hormone levels were minimally affected.[32]


  1. Jump up to:a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af agah William Llewellyn (2011). Anabolics. Molecular Nutrition Llc. pp. 641–. ISBN 978-0-9828280-1-4.
  2. Jump up to:a b c d E. Nieschlag; H. M. Behre (1 April 2004). Testosterone: Action, Deficiency, Substitution. Cambridge University Press. pp. 411–. ISBN 978-1-139-45221-2.
  3. ^ T.B. Hargreave (6 December 2012). Male Infertility. Springer Science & Business Media. pp. 398–399. ISBN 978-1-4471-1029-3.
  4. ^ Larry I. Lipshultz; Stuart S. Howards; Craig S. Niederberger (24 September 2009). Infertility in the Male. Cambridge University Press. pp. 445–446. ISBN 978-0-521-87289-8.
  5. ^ Kicman AT (2008). “Pharmacology of anabolic steroids”Br. J. Pharmacol154 (3): 502–21. doi:10.1038/bjp.2008.165PMC 2439524PMID 18500378.
  6. Jump up to:a b Behre, H.M.; Wang, C.; Handelsman, D.J.; Nieschlag, E.; Nieschlag, E.; Behre, H. M.; Nieschlag, S. (2004). “Pharmacology of testosterone preparations”. Testosterone. pp. 405–444. doi:10.1017/CBO9780511545221.015ISBN 9780521833806.
  7. Jump up to:a b Rausch-Stroomann JG, Petry R, Hienz HA (1967). “The influence of mesterolone on testicular function”Research on Steroids. Pergamon. 3: 181–184.
  8. Jump up to:a b Tausk, M. (1968). “Practically Applicable Results of Twenty Years of Research in Endocrinology”. Prog Drug Res12: 137–164. doi:10.1007/978-3-0348-7065-8_3ISBN 978-3-0348-7067-2PMID 4307936.
  9. Jump up to:a b Karch SB (21 December 2006). Drug Abuse Handbook, Second Edition. CRC Press. pp. 30–. ISBN 978-1-4200-0346-8.
  10. ^ Gautam N. Allahbadia; Rita Basuray Das (12 November 2004). The Art and Science of Assisted Reproductive Techniques. CRC Press. pp. 824–. ISBN 978-0-203-64051-7.
  11. Jump up to:a b Kenneth L. Becker (2001). Principles and Practice of Endocrinology and Metabolism. Lippincott Williams & Wilkins. pp. 1186–. ISBN 978-0-7817-1750-2.
  12. ^ I. Hart; R.W. Newton (6 December 2012). Endocrinology. Springer Science & Business Media. pp. 119–. ISBN 978-94-010-9298-2.
  13. ^ Corona G, Rastrelli G, Vignozzi L, Maggi M (2012). “Emerging medication for the treatment of male hypogonadism”. Expert Opin Emerg Drugs17 (2): 239–59. doi:10.1517/14728214.2012.683411PMID 22612692S2CID 22068249.
  14. ^ Nieschlag E, Behre HM, Bouchard P, et al. (2004). “Testosterone replacement therapy: current trends and future directions”Hum. Reprod. Update10 (5): 409–19. doi:10.1093/humupd/dmh035PMID 15297434.
  15. ^ Rastrelli, G.; Reisman, Y.; Ferri, S.; Prontera, O.; Sforza, A.; Maggi, M.; Corona, G. (2019). “Testosterone Replacement Therapy”. Sexual Medicine. pp. 79–93. doi:10.1007/978-981-13-1226-7_8ISBN 978-981-13-1225-0.
  16. ^ Saartok T, Dahlberg E, Gustafsson JA (1984). “Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin”. Endocrinology114 (6): 2100–6. doi:10.1210/endo-114-6-2100PMID 6539197.
  17. ^ Pugeat MM, Dunn JF, Nisula BC (July 1981). “Transport of steroid hormones: interaction of 70 drugs with testosterone-binding globulin and corticosteroid-binding globulin in human plasma”. J. Clin. Endocrinol. Metab53 (1): 69–75. doi:10.1210/jcem-53-1-69PMID 7195405.
  18. Jump up to:a b c d e J. Elks (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. Springer. pp. 775–. ISBN 978-1-4757-2085-3.
  19. Jump up to:a b c d e f g Index Nominum 2000: International Drug Directory. Taylor & Francis. 2000. pp. 656–. ISBN 978-3-88763-075-1.
  20. ^ Brooks, J. R.; Primka, R. L.; Berman, C; Krupa, D. A.; Reynolds, G. F.; Rasmusson, G. H. (1991). “Topical anti-androgenicity of a new 4-azasteroid in the hamster”. Steroids56 (8): 428–33. doi:10.1016/0039-128x(91)90031-pPMID 1788861S2CID 21500107.
  21. Jump up to:a b Malcolm Carruthers (2006). Androgen Deficiency in the Adult Male: Causes, Diagnosis and Treatment. CRC Press. pp. 137–178. ISBN 978-0-367-80018-5.
  22. ^ Neumann F, Wiechert R, Kramer M, Raspé G (April 1966). “[Experimental animal studies with a new androgen–mesterolone (1-alpha-methyl-5-alpha-androstan-17-beta-ol-one)]”. Arzneimittelforschung (in German). 16 (4): 455–8. PMID 6014248.
  23. ^ Laschet, U.; Niermann, H.; Laschet, L.; Paarmann, H. F. (1967). “Mesterolone, a potent oral active androgen without gonadotropin inhibition”. Acta Endocrinologica56 (1_Suppl): S55. doi:10.1530/acta.0.056S055ISSN 0804-4643.
  24. ^ Tausk M (1968). “Practically applicable results of twenty years of research in endocrinology”. Prog Drug Res12: 137–64. doi:10.1007/978-3-0348-7065-8_3ISBN 978-3-0348-7067-2PMID 4307936.
  25. Jump up to:a b Nieschlag, Eberhard; Nieschlag, Susan (2017). “The History of Testosterone and The Testes: From Antiquity to Modern Times”. Testosterone. pp. 1–19. doi:10.1007/978-3-319-46086-4_1ISBN 978-3-319-46084-0.
  26. Jump up to:a b Alexandre Hohl (6 April 2017). Testosterone: From Basic to Clinical Aspects. Springer. pp. 204–. ISBN 978-3-319-46086-4.
  27. ^ Kalinchenko, Svetlana; Tyuzikov, Igor; Mskhalaya, George; Tishova, Yulia (2017). “Testosterone Therapy: Oral Androgens”. Testosterone. pp. 203–224. doi:10.1007/978-3-319-46086-4_10ISBN 978-3-319-46084-0.
  28. ^ I.K. Morton; Judith M. Hall (6 December 2012). Concise Dictionary of Pharmacological Agents: Properties and Synonyms. Springer Science & Business Media. pp. 176–177. ISBN 978-94-011-4439-1.
  29. Jump up to:a b c d
  30. ^ Linda Lane Lilley; Julie S. Snyder; Shelly Rainforth Collins (5 August 2016). Pharmacology for Canadian Health Care Practice. Elsevier Health Sciences. pp. 50–. ISBN 978-1-77172-066-3.
  31. Jump up to:a b c Itil TM, Michael ST, Shapiro DM, Itil KZ (June 1984). “The effects of mesterolone, a male sex hormone in depressed patients (a double blind controlled study)”. Methods Find Exp Clin Pharmacol6 (6): 331–7. PMID 6431212.
  32. Jump up to:a b Kövary PM, Lenau H, Niermann H, Zierden E, Wagner H (May 1977). “Testosterone levels and gonadotrophins in Klinefelter’s patients treated with injections of mesterolone cipionate”. Arch Dermatol Res258 (3): 289–94. doi:10.1007/bf00561132PMID 883846S2CID 1222130.

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