DHT propionate (androstanolone propionate, dihydrotestosterone propionate) is dihydrotestosterone with a short propionate ester attached at the 17β position. Dihydrotestosterone (DHT) is the body’s most potent natural androgen. It is made from testosterone by the enzyme 5α-reductase and, unlike testosterone, cannot be converted to estrogen.

DHT propionate is not an approved medicine in the US, and we found no published study that measured its half-life in people. The human evidence on the propionate itself is a single small hormone study from 1983. Most of what is known about injected or applied DHT in people comes from other forms: the longer heptanoate ester and, above all, transdermal DHT gel.

This page summarizes what those studies and regulators report. It is for education only and is not medical advice.

Property	Detail
Drug class	Androgen; 17β-propionate ester of dihydrotestosterone (androstanolone)
Approval	No FDA-approved product containing DHT or a DHT ester
Route	Intramuscular injection (as studied)
Studied dose	100 mg IM daily for 4 days, in one study of 6 men with Klinefelter syndrome
DHT content	≈84% of the ester’s weight (100 mg ≈ 84 mg DHT)
Half-life	Not established in humans; no published pharmacokinetic study of the propionate
Converts to estrogen	No (DHT is not aromatizable)
US schedule	Schedule III (DHT is listed, including its esters)
WADA status	Prohibited at all times (S1.1 anabolic androgenic steroids)

What it is

DHT propionate has the formula C₂₂H₃₄O₃ and a molecular weight of 346.5 g/mol. DHT itself (androstanolone) is C₁₉H₃₀O₂, 290.4 g/mol (PubChem: DHT propionate; PubChem: DHT). The propionate ester therefore makes up about 16% of the weight, so each 100 mg of ester carries about 84 mg of DHT.

The ester has no hormonal action of its own. In a study of the heptanoate ester, its affinity for the human androgen receptor was 100 times lower than that of DHT, and the authors concluded that free DHT, released after the ester is cleaved, is the active hormone (Keenan et al., JCEM 1987). The ester only changes how fast DHT leaves the injection site.

The library has separate pages for the other DHT forms. They differ mainly in how DHT is delivered:

Form	Ester	Human data
DHT base	None	Crystalline DHT injected IM in hypogonadal men
DHT propionate (this page)	Propionate (3 carbons)	One 4-day hormone study in 6 men
DHT enanthate	Heptanoate, also called enanthate (7 carbons)	Pharmacokinetic studies in men and boys
DHT gel (10%, 20%)	None (applied to skin)	Randomized trials of up to 2 years

Not the same as Masteron. Several 1960s breast cancer studies tested “2α-methyl dihydrotestosterone propionate” (Thomas et al., Cancer 1962). That is drostanolone, the 2α-methyl derivative of DHT (21 CFR 1308.13), sold as Masteron. Those results do not apply to DHT propionate.

How it works in the body

DHT acts directly on the androgen receptor. A 2017 Endocrine Society review lists why it is the most potent natural androgen (Swerdloff et al., Endocr Rev 2017):

its binding affinity for the androgen receptor is about 4 times that of testosterone;
it dissociates from the receptor about 3 times more slowly;
it binds sex hormone-binding globulin (SHBG, the main carrier protein for sex hormones in blood) about 5 times more tightly than testosterone.

Two features set DHT apart from testosterone:

No conversion to estrogen. DHT is not aromatized, so it cannot form estradiol (Ly et al., JCEM 2001).
No further amplification. Testosterone gains potency in some tissues when 5α-reductase turns it into DHT. DHT is already the end product of that step.

Tissues break DHT down quickly. In men given DHT by infusion, its overall clearance was about 70% that of testosterone. Fat and skin convert much of it to an inactive metabolite, 3α-androstanediol, using the enzymes AKR1C1 and AKR1C2 (3α-hydroxysteroid dehydrogenase) (Swerdloff et al., Endocr Rev 2017). The review notes that muscle and fat cells tightly regulate their own androgen levels by metabolizing excess androgen.

Pharmacokinetics

No published study has measured the absorption, peak level or half-life of DHT propionate in people. Half-life figures quoted online for it could not be traced to a primary source.

Data on the other injectable DHT forms show how much the delivery method matters:

Study	Form and dose	Main finding
Keenan et al., JCEM 1987	DHT heptanoate, single IM injection, men and pubertal boys	DHT rose markedly within 24 h, peaked in the first week, and returned to baseline after 4–6 weeks. An estimated 43–55% was converted to DHT by 4–6 weeks.
Coutts et al., Clin Chem 1997	DHT heptanoate 250 mg IM, 6 healthy men	Urinary DHT markers exceeded published discrimination limits within 24 h and stayed above them for 10–14 days. All returned to baseline by day 28.
Díaz-Sánchez et al., Fertil Steril 1989	Crystalline DHT 40 mg IM, two groups of 6 hypogonadal men	Fine particles kept DHT above baseline for 17 days (absorption half-life 6 days); coarse particles for over 50 days (21 days).

The propionate is a shorter ester than the heptanoate, but how quickly it releases DHT in people has not been measured.

Regulatory status

Not an approved drug in the US. A search of Drugs@FDA for dihydrotestosterone or androstanolone returns no approved products. Any DHT propionate on sale comes from outside the regulated drug supply, with no control of dose, sterility or identity.
Controlled substance. The US Schedule III list names “4-dihydrotestosterone (17β-hydroxy-androstan-3-one)” and covers its salts, esters and ethers, which includes the propionate (21 CFR 1308.13).
Banned in sport. The WADA list names androstanolone (5α-dihydrotestosterone) under S1.1 anabolic androgenic steroids when administered exogenously, “including their esters.” It is prohibited in and out of competition and is a non-specified substance (WADA 2026 Prohibited List).

Because the body also makes DHT, the proposed detection methods rely on urinary ratios rather than on finding DHT itself. After DHT heptanoate, the urinary ratio of DHT to epitestosterone and related markers rose sharply (Southan et al., J Steroid Biochem Mol Biol 1992; Coutts et al., Clin Chem 1997).

What the research shows

No controlled trial has tested DHT propionate for muscle, strength or athletic performance. The available human data fall into three groups.

Hormone studies with DHT propionate

Six men with Klinefelter syndrome received testosterone propionate 100 mg IM daily for 4 days, and a month later DHT propionate 100 mg IM daily for 4 days (Forti et al., J Endocrinol Invest 1983). The findings were:

DHT propionate produced only a late, transient fall in LH and a very late fall in FSH, the pituitary hormones that drive the testes;
the authors concluded that DHT was less effective than testosterone at suppressing these hormones;
prolactin rose after testosterone propionate but not after DHT propionate, which the authors linked to testosterone’s conversion to estradiol.

A 1975 case report gave DHT propionate to a 16-year-old with partial androgen insensitivity; it did not lower LH or FSH (Perez-Palacios et al., JCEM 1975). This reflects the patient’s receptor defect, not the drug’s usual effect.

Randomized trials of DHT gel

The best human data on DHT come from daily 70 mg transdermal DHT gel. The hormone delivered is the same; the route and blood-level pattern differ from an injection.

Outcome	3 months, 37 men aged 60 or older (Ly et al., JCEM 2001)	24 months, 114 men over 50 (Idan et al., Ann Intern Med 2010)
Lean mass	Unchanged	+2.4% (95% CI 1.6–3.1)
Fat mass	Decreased	−5.2% (95% CI 2.6–7.7)
Muscle strength	Increased in 1 knee measure only; no change in mobility	Not a primary outcome
Prostate volume and PSA	Unchanged	No effect on prostate growth
Hemoglobin	Increased (with hematocrit)	+7% (95% CI 5–9)
Spinal bone density	Not reported	−1.4% (95% CI 0.6–2.3)
Testosterone, LH, FSH	Decreased	Suppressed
Estradiol	Unchanged	Suppressed

In the 3-month trial, total and LDL cholesterol fell and HDL did not change. A follow-up of the 2-year trial found no effect on 33 measures of sexual function and mood, except a mild decrease in sexual desire that reversed after stopping (Sartorius et al., J Sex Med 2014).

Gynecomastia

Because estradiol cannot be formed from DHT, DHT has been explored as a treatment for breast enlargement in males (Swerdloff et al., Endocr Rev 2017). Four boys with persistent pubertal gynecomastia received DHT heptanoate IM every 2–4 weeks for 16 weeks (Eberle et al., J Pediatr 1986):

breast size fell by 67–78%;
estradiol, LH, FSH and testosterone fell during treatment;
no regrowth was seen 6–15 months later.

In healthy men, DHT given with hCG cut the estradiol peak by 50% without changing the testosterone response (Cailleux-Bounacer et al., Int J Androl 2009). These were small, uncontrolled or mechanistic studies, and none used the propionate.

Side effects and risks

No safety study of DHT propionate exists. The risks below come from trials of other DHT forms and apply to DHT as a hormone.

“A dry, pure androgen without side effects.” DHT does avoid estrogen-driven water retention and gynecomastia, because it cannot form estradiol. But in controlled trials it shut down the body’s own testosterone, LH and FSH, suppressed estradiol, lowered spinal bone density and raised hemoglobin. None of that makes it free of side effects.

Suppression of natural hormones

Every DHT form studied lowered LH, FSH and testosterone. With DHT heptanoate in men, these fell by day 4, were lowest in week 2 and recovered after 4–6 weeks (Keenan et al., JCEM 1987). In the 2-year gel trial, suppression of testosterone, LH, FSH and estradiol was complete for the whole study (Sartorius et al., J Sex Med 2014). LH and FSH drive both testosterone and sperm production in the testes.

Low estrogen and bone

With estradiol suppressed by DHT for 2 years, spinal bone mineral density fell by 1.4%, while hip density did not change (Idan et al., Ann Intern Med 2010). The investigators attributed the bone loss to the selective estrogen deficiency that DHT creates (Sartorius et al., J Sex Med 2014).

Red blood cells

DHT raised hemoglobin by 7% over 2 years. Eight men stopped DHT because of an asymptomatic rise in hematocrit (the share of blood made up of red cells), which resolved after stopping (Idan et al., Ann Intern Med 2010).

Prostate

Two years of high blood DHT did not change prostate volume or PSA compared with placebo. Three men in the DHT group stopped because of a rise in PSA; none had prostate cancer. The authors note that the trial cannot exclude effects on the course of an existing prostate cancer (Idan et al., Ann Intern Med 2010).

Skin and hair

Drugs that lower DHT slow male pattern baldness, which points to a role for DHT in that process (Swerdloff et al., Endocr Rev 2017). The same review notes that the 2-year DHT gel study found no link with acne or male pattern baldness. In other DHT heptanoate studies summarized there, body and facial hair rose modestly and two cases of increased acne were reported.

Who has no data

There are no safety data for DHT propionate in women, adolescents, or people with heart, liver or kidney disease. The short-term gel and injection studies above involved small numbers of mostly older men.

Key takeaways

An ester of the body’s most potent androgen. About 84% of DHT propionate’s weight is DHT, which binds the androgen receptor about 4 times more strongly than testosterone and cannot form estrogen.
Almost no human data on this form. The only study of the propionate itself is a 4-day hormone study in 6 men. Its half-life in people has never been published.
DHT gel trials are the best evidence. Over 2 years, 70 mg/day of DHT gel raised lean mass by 2.4% and cut fat mass by 5.2% without growing the prostate.
Not side-effect free. DHT suppressed natural testosterone, LH, FSH and estradiol, lowered spinal bone density and raised hemoglobin.
Unapproved and controlled. There is no FDA-approved DHT product. DHT and its esters are Schedule III in the US and banned at all times by WADA.

Sources

National Center for Biotechnology Information. Dihydrotestosterone propionate, PubChem CID 13328. PubChem.
National Center for Biotechnology Information. Dihydrotestosterone, PubChem CID 10635. PubChem.
Keenan BS, Eberle AJ, Sparrow JT, Greger NG, Panko WB. Dihydrotestosterone heptanoate: synthesis, pharmacokinetics, and effects on hypothalamic-pituitary-testicular function. J Clin Endocrinol Metab. 1987;64(3):557–562. PubMed.
Swerdloff RS, Dudley RE, Page ST, Wang C, Salameh WA. Dihydrotestosterone: biochemistry, physiology, and clinical implications of elevated blood levels. Endocr Rev. 2017;38(3):220–254. PubMed; PMC.
Forti G, Vannucchi PL, Borghi A, Giusti G, Fusi S, Serio M. Effects of pharmacological doses of testosterone and dihydrotestosterone on the hypothalamic-pituitary axis function of Klinefelter patients. J Endocrinol Invest. 1983;6(4):297–300. PubMed.
Perez-Palacios G, Ortiz S, López-Amor E, et al. Familial incomplete virilization due to partial end organ insensitivity to androgens. J Clin Endocrinol Metab. 1975;41(5):946–952. PubMed.
Coutts SB, Kicman AT, Hurst DT, Cowan DA. Intramuscular administration of 5 alpha-dihydrotestosterone heptanoate: changes in urinary hormone profile. Clin Chem. 1997;43(11):2091–2098. PubMed.
Díaz-Sánchez V, Larrea F, Ulloa-Aguirre A, et al. Absorption of dihydrotestosterone (DHT) after its intramuscular administration. Fertil Steril. 1989;51(3):493–497. PubMed.
Southan GJ, Brooks RV, Cowan DA, et al. Possible indices for the detection of the administration of dihydrotestosterone to athletes. J Steroid Biochem Mol Biol. 1992;42(1):87–94. PubMed.
Ly LP, Jimenez M, Zhuang TN, et al. A double-blind, placebo-controlled, randomized clinical trial of transdermal dihydrotestosterone gel on muscular strength, mobility, and quality of life in older men with partial androgen deficiency. J Clin Endocrinol Metab. 2001;86(9):4078–4088. PubMed.
Idan A, Griffiths KA, Harwood DT, et al. Long-term effects of dihydrotestosterone treatment on prostate growth in healthy, middle-aged men without prostate disease: a randomized, placebo-controlled trial. Ann Intern Med. 2010;153(10):621–632. PubMed.
Sartorius GA, Ly LP, Handelsman DJ. Male sexual function can be maintained without aromatization: randomized placebo-controlled trial of dihydrotestosterone (DHT) in healthy, older men for 24 months. J Sex Med. 2014;11(10):2562–2570. PubMed.
Eberle AJ, Sparrow JT, Keenan BS. Treatment of persistent pubertal gynecomastia with dihydrotestosterone heptanoate. J Pediatr. 1986;109(1):144–149. PubMed.
Cailleux-Bounacer A, Rohmer V, Lahlou N, et al. Impact level of dihydrotestosterone on the hypothalamic-pituitary-leydig cell axis in men. Int J Androl. 2009;32(1):57–65. PubMed.
Thomas AN, Gordan GS, Goldman L, Lowe R. Antitumor efficacy of 2alpha-methyl dihydrotestosterone propionate in advanced breast cancer. Cancer. 1962;15:176–178. PubMed.
Food and Drug Administration. Drugs@FDA: FDA-approved drugs (searched for dihydrotestosterone and androstanolone, October 2026). FDA.
Drug Enforcement Administration. Schedules of controlled substances: Schedule III, 21 CFR 1308.13. eCFR.
World Anti-Doping Agency. World Anti-Doping Code International Standard: Prohibited List 2026. WADA 2026 Prohibited List.

DHT Propionate