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Dihydrotestosterone: Wikis


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Systematic (IUPAC) name
CAS number 521-18-6
ATC code A14AA01
PubChem 10635
ChemSpider 10189
Chemical data
Formula C 19H30O2  
Mol. mass 290.440 g/mol
Pharmacokinetic data
Bioavailability Oral 0-2%
Metabolism Hepatic
Half life  ?
Excretion Renal
Therapeutic considerations
Pregnancy cat. X


Legal status Schedule III (US), Schedule IV (CA)
Routes Intramuscular, transdermal
 Yes check.svgY(what is this?)  (verify)

Dihydrotestosterone (DHT) Full name: 5α-Dihydrotestosterone, abbreviating to 5α-DHT; INN: androstanolone is a biologically active metabolite of the hormone testosterone, formed primarily in the prostate gland, testes, hair follicles, and adrenal glands by the enzyme 5α-reductase by means of reducing the 4,5 double-bond. Dihydrotestosterone belongs to the class of compounds called androgens, also commonly called androgenic hormones or testoids. Androgens are part of the biology of gender by stimulating and controlling the development and maintenance of masculine characteristics.



Testosterone. Note the major difference -- the 4,5 double-bond on the A (leftmost) ring.

DHT is produced by males in vivo and is responsible for the formation of male sex-specific characteristics. DHT is an important contributor to other characteristics generally attributed to males, including facial and body hair growth, and deepening of the voice. Unlike other androgens such as testosterone, DHT cannot be converted by the enzyme aromatase to estradiol[1]. It therefore is frequently used in research settings to distinguish between 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.


DHT is the primary contributing factor in male-pattern baldness. Unlike men with male-pattern baldness, women with female-pattern baldness are characterized by increased production rates of T, but not of DHT. These results are compatible with the idea that 5α-reductase inhibition is of no therapeutical value in female-pattern baldness.[2] Women with increased levels of DHT may develop certain androgynous male secondary sex characteristics, including a deepened voice and facial hair. DHT may play a role in the development or exacerbation of benign prostatic hyperplasia, or BPH, and prostate cancer, by enlarging the prostate gland.[3] Prostate growth and differentiation are highly dependent on sex steroid hormones, particularly DHT[4]


The drugs belonging to the group known as 5α-reductase inhibitors, finasteride and dutasteride are used off-label for treatment of male-pattern alopecia. 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, which finasteride doesn't inhibit. It is noteworthy that in the patients treated with 2.5 mg dutasteride daily, 13% complained of decreased libido. Although dutasteride is not approved by the FDA for the treatment of androgenic alopecia, it is approved at a dose of 0.5 mg a day for the treatment of prostate enlargement. While both the type I and type II enzymes are found in the hair follicle, there is a recent study that shows that type I is present in the human brain. The function of this enzyme in the brain is still unclear.[5]

Currently, DHT supplementation is not used as a treatment for DHT androgen deficiency.


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