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Systematic (IUPAC) name
Clinical data
  • X
Routes of
Intramuscular, transdermal
Pharmacokinetic data
Bioavailability Oral 0-2%
Metabolism Hepatic
Excretion Renal
CAS Number 521-18-6 YesY
ATC code A14AA01 (WHO)
PubChem CID 10635
DrugBank DB02901 YesY
ChemSpider 10189 YesY
UNII 08J2K08A3Y YesY
ChEBI CHEBI:16330 YesY
Chemical data
Formula C19H30O2
Molar mass 290.442 g/mol
 NYesY (what is this?)  (verify)

Dihydrotestosterone (commonly abbreviated to DHT), or 5α-dihydrotestosterone (5α-DHT), also known as 5α-androstan-17β-ol-3-one, is a sex steroid and androgen hormone. The enzyme 5α-reductase synthesizes DHT from testosterone in the prostate, testes, hair follicles, and adrenal glands. This enzyme reduces the 4,5 double-bond of the testosterone. Relative to testosterone, DHT is much more potent as an agonist of the androgen receptor.

DHT is also known as androstanolone (INN) and stanolone (BAN), and is used clinically under brand names including Anabolex, Anaprotin, Andractim, Androlone, Gelovit, Neoprol, Pesomax, and Stanaprol as an androgen and anabolic steroid.[1][2] Unlike testosterone and some anabolic steroids, DHT cannot be aromatized, and hence, has no risk of estrogenic side effects such as gynecomastia.[3]

Biological activity[edit]

DHT has an affinity (Kd) of 0.25 to 0.5 nM for the human androgen receptor (AR), which is about 2- to 3-fold higher than that of testosterone (Kd = 0.4 to 1.0 nM).[4] The EC50 of DHT for activation of the AR is 0.13 nM, which is about 5-fold higher than that of testosterone (EC50 = 0.66 nM).[5] In bioassays, DHT has been found to be 2.5- to 10-fold more potent than testosterone.[4] The half-life of DHT in the body (53 minutes) is longer than that of testostrone (34 minutes), and this may account for some of the potency difference.[6] A study of transdermal DHT and testosterone treatment reported half-lives of 2.83 hours and 1.29 hours, respectively.[7]

Sexual development[edit]

Chemical structure of testosterone. Compared with DHT, there is a double bond in the A ring (left).

In men, approximately 5% of testosterone undergoes 5α-reduction to form the more potent androgen, dihydrotestosterone (DHT). DHT has two to three times greater androgen receptor affinity than testosterone and has 15–30 times greater affinity than adrenal androgens.[8] The dissociation rate of testosterone from the receptor is five-fold faster than DHT.[9] During embryogenesis DHT has an essential role in the formation of the male external genitalia, while in the adult DHT acts as the primary androgen in the prostate and in hair follicles.[10]

An example illustrating the significance of DHT for the development of secondary sex characteristics is congenital 5α-reductase deficiency. This gene lesion can result in pseudohermaphroditism.[11] This condition typically presents with underdeveloped male genitalia and prostate. These individuals are often raised as girls due to their lack of conspicuous male genitalia.[11] In the onset of puberty, although their DHT levels remain very low, their testosterone levels elevate normally. Their musculature develops like that of other male adults. After puberty, men with this condition have a large deficiency of pubic and body hair, and no incidence of male pattern baldness.[12] They also have no incidence of prostate cancer.[13]

Unlike other androgens such as testosterone, DHT cannot be converted by the enzyme aromatase to estradiol. Therefore, it is frequently used in research settings to distinguish between the effects of testosterone caused by binding to the androgen receptor and those caused by testosterone's conversion to estradiol and subsequent binding to estrogen receptors.[14]


DHT created locally at the site of hair follicles by 5α-reductase, and not systemic levels of DHT, is the primary causal factor in male pattern baldness that results from hair follicle miniaturisation, although the pathology regarding this phenomenon is poorly understood.[15][16] However, female hair loss is more complex, and DHT is only one of several possible causes.[17] Women with increased levels of DHT may develop certain androgynous male secondary sex characteristics, including a deepened voice and facial hair. It was once believed that DHT played a role in the development and exacerbation of benign prostatic hyperplasia, as well as prostate cancer, but this has largely been disproven.[18] Prostate growth and differentiation are highly dependent on sex steroid hormones, particularly DHT.[19]

Treatment for DHT-related conditions[edit]

5α-Reductase inhibitors are commonly used for the treatment of two DHT-related conditions, male pattern baldness (MPB), and benign prostatic hyperplasia (BPH). Dutasteride is approved for the treatment of benign prostatic hyperplasia, and is prescribed off-label for the treatment of male pattern baldness, whereas finasteride is approved for both conditions. Dutasteride is three times more potent than finasteride in inhibiting the type II enzyme and 100 times more potent than finasteride in inhibiting the type I form of the DHT-producing enzyme. Both finasteride and dutasteride are potent inhibitors of the third isotype of the enzyme.[20]


DHT is synthesized from testosterone by the enzyme 5α-reductase.[21] It is inactivated to 3α-androstanediol and 3β-androstanediol by the enzymes 3α-hydroxysteroid dehydrogenase and 3β-hydroxysteroid dehydrogenase, respectively.[22] Unlike testosterone, DHT cannot be aromatized, and therefore has no propensity for estrogenic effects.[23]


Serum DHT levels are about 10% of those of testosterone, but levels in the prostate gland are several-fold higher than those of testosterone due to extensive conversion of testosterone into DHT by locally expressed 5α-reductase.[24] Moreover, DHT is considerably more potent than testosterone as an androgen.[4] As such, DHT is considered to be the major androgen of the prostate, although testosterone can mediate similar effects.[24]


Synthetic derivatives of DHT employed as anabolic steroids include mesterolone (1α-methyl-DHT) and drostanolone (2α-methyl-DHT).

See also[edit]


  1. ^ J. Elks (14 November 2014). The Dictionary of Drugs: Chemical Data: Chemical Data, Structures and Bibliographies. Springer. pp. 640–. ISBN 978-1-4757-2085-3. 
  2. ^ Index Nominum 2000: International Drug Directory. Taylor & Francis. January 2000. pp. 63–. ISBN 978-3-88763-075-1. 
  3. ^ Paul V. Malven (12 January 1993). Mammalian Neuroendocrinology. CRC Press. pp. 228–. ISBN 978-0-8493-8757-9. 
  4. ^ a b c Ashraf Mozayani; Lionel Raymon (18 September 2011). Handbook of Drug Interactions: A Clinical and Forensic Guide. Springer Science & Business Media. pp. 656–. ISBN 978-1-61779-222-9. 
  5. ^ Treatise on Water Science, Four-Volume Set. Newnes. 1 September 2010. pp. 1805–. ISBN 978-0-444-53199-5. 
  6. ^ Bentham Science Publishers (September 1999). Current Pharmaceutical Design. Bentham Science Publishers. pp. 708–. 
  7. ^ Ashraf Mozayani; Lionel Raymon (15 October 2003). Handbook of Drug Interactions: A Clinical and Forensic Guide. Springer Science & Business Media. pp. 510–. ISBN 978-1-59259-654-6. 
  8. ^ Hemat RAS (2004). Principles Of Orthomolecularism. Urotext. p. 426. ISBN 1-903737-05-2. 
  9. ^ Grino, P. B.; Griffin, J. E.; Wilson, J. D. (1990). "Testosterone at high concentrations interacts with the human androgen receptor similarly to dihydrotestosterone". Endocrinology. 126 (2): 1165–1172. doi:10.1210/endo-126-2-1165. PMID 2298157. 
  10. ^ Amory JK, Anawalt BD, Matsumoto AM, Page ST, Bremner WJ, Wang C, Swerdloff RS, Clark RV (June 2008). "The effect of 5alpha-reductase inhibition with dutasteride and finasteride on bone mineral density, serum lipoproteins, hemoglobin, prostate specific antigen and sexual function in healthy young men". J. Urol. 179 (6): 2333–8. doi:10.1016/j.juro.2008.01.145. PMC 2684818free to read. PMID 18423697. 
  11. ^ a b Imperato-McGinley J, Peterson RE, Gautier T, Sturla E (May 1979). "Androgens and the Evolution of Male-Gender Identity among Male Pseudohermaphrodites with 5α-Reductase Deficiency". New England Journal of Medicine. 300: 1233–1237. doi:10.1056/NEJM197905313002201. PMID 431680. 
  12. ^ Marks LS (2004). "5α-reductase: history and clinical importance". Rev Urol. 6 Suppl 9: S11–21. PMC 1472916free to read. PMID 16985920. 
  13. ^ N. K. Jain; Maqsood Siddiqi; J. H. Weisburger (2006). Protective Effects of Tea on Human Health. CABI. pp. 95–. ISBN 978-1-84593-113-1. 
  14. ^ Swerdloff RS, Wang C (October 1998). "Dihydrotestosterone: a rationale for its use as a non-aromatizable androgen replacement therapeutic agent". Baillieres Clin. Endocrinol. Metab. 12 (3): 501–6. doi:10.1016/s0950-351x(98)80267-x. PMID 10332569. 
  15. ^ Nordqvist C (2012-02-23). "What Is DHT (Dihydrotestosterone)? What Is DHT's Role In Baldness?". Medical News Today. 
  16. ^ "Male Pattern Baldness Causes". Hair Loss Health Center. WebMD, LLC. 
  17. ^ McAndrews PJ. "Women's Hair Loss / Causes of Hair Loss". American Hair Loss Association. 
  18. ^ "Long-Term Effects of Dihydrotestosterone Treatment on Prostate Growth in Healthy, Middle-Aged Men Without Prostate Disease: A Randomized, Placebo-Controlled Trial". Annals of Internal Medicine. 
  19. ^ Freedland SJ, Isaacs WB, Platz EA, Terris MK, Aronson WJ, Amling CL, Presti JC, Kane CJ (October 2005). "Prostate size and risk of high-grade, advanced prostate cancer and biochemical progression after radical prostatectomy: a search database study". J. Clin. Oncol. 23 (30): 7546–54. doi:10.1200/JCO.2005.05.025. PMID 16234520. 
  20. ^ Olsen EA, Hordinsky M, Whiting D, Stough D, Hobbs S, Ellis ML, Wilson T, Rittmaster RS (December 2006). "The importance of dual 5alpha-reductase inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride". J. Am. Acad. Dermatol. 55 (6): 1014–23. doi:10.1016/j.jaad.2006.05.007. PMID 17110217. Lay summaryIAHRS Hair Transplant & Hair Loss Info Center. 
  21. ^ Ulrike Blume-Peytavi; David A. Whiting; Ralph M. Trüeb (26 June 2008). Hair Growth and Disorders. Springer Science & Business Media. pp. 161–. ISBN 978-3-540-46911-7. 
  22. ^ Rizner TL, Lin HK, Peehl DM, Steckelbroeck S, Bauman DR, Penning TM (July 2003). "Human type 3 3alpha-hydroxysteroid dehydrogenase (aldo-keto reductase 1C2) and androgen metabolism in prostate cells". Endocrinology. 144 (7): 2922–32. doi:10.1210/en.2002-0032. PMID 12810547. 
  23. ^ Irving B. Weiner; Michela Gallagher (2003). Handbook of Psychology, Biological Psychology. John Wiley & Sons. pp. 333–. ISBN 978-0-471-38403-8. 
  24. ^ a b Ian D. Hay; John A. H. Wass (26 January 2009). Clinical Endocrine Oncology. John Wiley & Sons. pp. 37–. ISBN 978-1-4443-0023-9.