DHT enanthate, also called dihydrotestosterone heptanoate or androstanolone enanthate, is dihydrotestosterone (DHT) with a seven-carbon fatty acid ester attached. Like testosterone enanthate, it is dissolved in oil and injected into muscle, where the ester slows the release of the hormone. DHT itself is the potent androgen the body makes from testosterone, and unlike testosterone it cannot be converted to estrogen.
The single most important fact is that DHT enanthate is not an approved medicine in the US. Its human record consists of a handful of small studies from the 1980s and 1990s, mostly in adolescent boys, plus two anti-doping studies in a few healthy men. No controlled trial has measured its effects on muscle or strength in adults.
This page summarizes what those studies, related DHT research and regulators report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | Androgen; injectable ester of dihydrotestosterone (androstanolone) |
| Other names | Dihydrotestosterone heptanoate, DHT-hp, androstanolone enanthate |
| Approval | No FDA-approved product; investigational use in research studies only |
| Route | Intramuscular injection |
| Studied doses | 150 mg and 250 mg single injections in healthy men; repeated injections every 2–4 weeks in adolescent boys |
| Half-life | Not reported in humans; terminal half-life ≈7 days in monkeys |
| DHT content | ≈72% of the ester’s weight (100 mg ester ≈ 72 mg DHT) |
| Aromatizes to estrogen | No |
| US status | Schedule III controlled substance (DHT and its esters) |
| WADA status | Prohibited at all times (S1.1, androstanolone and its esters) |
What it is
DHT enanthate is the 17β-heptanoate ester of 5α-dihydrotestosterone: formula C₂₆H₄₂O₃, molecular weight 402.6 g/mol (PubChem CID 160230). DHT alone has the formula C₁₉H₃₀O₂ and weighs 290.4 g/mol (PubChem CID 10635). The ester therefore makes up about 28% of the weight, so 100 mg of the ester carries about 72 mg of DHT.
In the body, testosterone is converted to DHT by the enzyme 5α-reductase. DHT is described as a “nonaromatizable” androgen: the aromatase enzyme cannot turn it into estradiol (Idan et al., Ann Intern Med 2010). This is the main thing that separates it from testosterone and is the reason researchers used it to tell androgen effects apart from estrogen effects.
The ester itself is not the active hormone. In the original synthesis paper, DHT heptanoate bound the human androgen receptor with about 100 times lower affinity than DHT, and it showed no binding to the estrogen receptor. The authors concluded that free DHT, released once the ester is cleaved, is the active principle (Keenan et al., JCEM 1987).
The library has separate pages for other forms of the same hormone:
| Form | How it differs |
|---|---|
| DHT base | Unesterified DHT, no slow-release ester |
| DHT propionate | Shorter three-carbon ester |
| DHT enanthate (this page) | Seven-carbon ester; release over weeks |
| DHT gel 10% and DHT gel 20% | Applied to the skin daily; the form used in the largest DHT trial |
Related DHT-derived steroids include Masteron (drostanolone propionate) and Proviron (mesterolone).
Pharmacokinetics
In people
The only human kinetic description comes from Keenan and colleagues, who synthesized the ester and gave it by intramuscular injection to men and pubertal boys (Keenan et al., JCEM 1987):
| Measure | Finding |
|---|---|
| Plasma DHT | Rose markedly within 24 h |
| Peak | During the first week |
| Return to baseline | 4–6 weeks after injection |
| Share of ester converted to DHT | Estimated 43–55% by 4–6 weeks |
The paper’s abstract does not report a half-life. In adolescent boys given repeated injections, plasma DHT averaged 24.2 nmol/L (≈700 ng/dL) at 1 week and 29.2 nmol/L (≈850 ng/dL) at 2 weeks after a dose (Keenan et al., Metabolism 1996).
In monkeys
The only formal half-life estimates come from monkeys. Researchers in Münster compared single injections of testosterone enanthate and DHT enanthate carrying the same 23.6 mg of steroid in castrated cynomolgus monkeys (Weinbauer et al., Acta Endocrinol 1990):
| Measure | Testosterone enanthate | DHT enanthate |
|---|---|---|
| Peak rise of the hormone | ≈400% of baseline | ≈800% of baseline |
| Area under the curve | 2,920 ± 485 | 2,290 ± 340 (not significantly different) |
| Terminal half-life | ≈4 days | ≈7 days |
| Return to baseline | 4–5 weeks | 4–5 weeks |
In a second experiment in rhesus monkeys whose own hormones were suppressed with a GnRH agonist, the half-life estimates were about 5 days for testosterone enanthate and 7 days for DHT enanthate. These are animal figures and may not match human values.
Regulatory status
- FDA. A search of Drugs@FDA through the openFDA database returned no approved product containing androstanolone or dihydrotestosterone (openFDA Drugs@FDA). DHT enanthate has only been given in research studies.
- DEA. Dihydrotestosterone (17β-hydroxy-androstan-3-one) is named in Schedule III, and the listing covers “its salts, esters and ethers,” which includes the enanthate ester (21 CFR 1308.13).
- WADA. Androstanolone (5α-dihydrotestosterone) is listed under S1.1 anabolic androgenic steroids, prohibited at all times when given from outside the body, and the class explicitly includes their esters (WADA 2026 Prohibited List).
What the research shows
Pubertal gynecomastia
Gynecomastia is breast tissue growth in males. In an uncontrolled series, 4 boys with persistent pubertal gynecomastia received DHT heptanoate injections every 2–4 weeks for 16 weeks (Eberle et al., J Pediatr 1986):
- breast size fell by 67–78% in all four boys by the end of treatment;
- estradiol, LH, FSH and testosterone all fell during treatment;
- no breast regrowth was seen 6–15 months after treatment, and hormone levels were close to pretreatment values 2 months after the last injection.
With only four patients and no control group, this shows feasibility, not proof of efficacy.
Growth and puberty in boys
The same group used DHT heptanoate to ask whether the pubertal growth spurt depends on estrogen. In 9 boys with constitutional delay of growth and puberty, 3 received testosterone enanthate and 6 received DHT heptanoate (Keenan et al., JCEM 1993):
| Measure after 2.5 months | Testosterone enanthate (n = 3) | DHT heptanoate (n = 6) |
|---|---|---|
| Height velocity | 12.6 ± 2.8 cm/yr | 8.9 ± 1.7 cm/yr |
| Integrated growth hormone | Rose from 3.12 to 13.67 µg/L | Fell from 4.32 to 2.39 µg/L |
| IGF-I | Rose from 126.7 to 350.3 µg/L | 218.3 to 184.0 µg/L (not significant) |
| LH response to LHRH | 27.6 to 5.9 IU/L (not significant) | 45.7 to 10.7 IU/L (p under 0.05) |
Both groups grew within the range of a normal pubertal growth spurt. Because DHT did this without raising growth hormone, the authors concluded that the pubertal rise in growth hormone is estrogen-dependent.
A follow-up in 14 boys (7 per group) found similar results: growth hormone rose on testosterone but fell slightly on DHT (4.3 to 2.9 µg/L), height velocity was 9.3 cm/yr on DHT and not significantly different from testosterone, and growth hormone binding protein fell in both groups (Keenan et al., Metabolism 1996).
Anti-doping studies in men
DHT is also made naturally, so anti-doping labs studied how to detect an injection of it.
| Study | Dose | Men | Findings |
|---|---|---|---|
| Southan et al., 1992 | 150 mg IM, single | 2 | Plasma DHT rose; testosterone, LH and FSH fell; urinary DHT and its metabolites rose relative to testosterone and epitestosterone |
| Coutts et al., 1997 | 250 mg IM, single | 6 | All four urinary markers exceeded detection limits within 24 h and stayed above them for 10–14 days; all returned to baseline by day 28 |
Muscle and strength
No controlled trial has tested DHT enanthate for muscle mass or strength in adults. In castrated monkeys, it restored ejaculation, ejaculate size and sexual behavior as effectively as testosterone enanthate at equal steroid doses (Weinbauer et al., Acta Endocrinol 1990), but muscle was not studied.
The best human data on DHT and body composition come from a different form. In a 2-year randomized trial, 114 healthy men over 50 applied 70 mg of DHT gel or placebo daily (Idan et al., Ann Intern Med 2010). Compared with placebo, DHT increased lean mass by 2.4% (95% CI 1.6–3.1%) and decreased fat mass by 5.2% (95% CI 2.6–7.7%). Results from a daily gel kept near steady levels cannot be assumed to apply to large, intermittent injections.
About “hardening” and anabolic claims. DHT enanthate is often described online as a strong “hardener” or lean-mass compound. It is true that DHT does not convert to estrogen. But no human study has measured muscle, strength or appearance outcomes with the injectable ester, so claims about its size of effect are not backed by trial data.
Side effects and risks
There is no label and no safety database for DHT enanthate. The points below come from the small studies above and, where marked, from the DHT gel trial.
Suppression of natural hormones and fertility
DHT enanthate shuts down the body’s own hormone production. In men and boys, testosterone, estradiol, LH and FSH fell by 4 days after an injection, reached their lowest point in the second week, and returned to baseline after 4–6 weeks (Keenan et al., JCEM 1987). Repeated injections every 3 weeks for 15 weeks blunted the pituitary’s LH and FSH response to GnRH in pubertal boys.
LH and FSH drive sperm production, so suppression of this kind is expected to impair fertility. No study has measured sperm output with DHT enanthate in men.
Lower estrogen
Because DHT cannot become estradiol and it suppresses the testes, estradiol falls rather than rises. That is why it shrank breast tissue in the gynecomastia series. In the 2-year gel trial, DHT also suppressed estradiol and decreased spinal bone mineral density by 1.4% (95% CI 0.6–2.3%) at 24 months, with no change at the hip (Idan et al., Ann Intern Med 2010).
Blood counts and prostate (gel trial data)
In the same gel trial:
- hemoglobin rose by 7% (95% CI 5–9%);
- 8 men stopped DHT because of raised hematocrit (the share of blood made up of red cells), which resolved after stopping;
- 3 men stopped because of raised PSA, none of whom had prostate cancer;
- prostate volume did not change compared with placebo over 2 years.
The authors noted that these negative prostate findings cannot exclude effects on the course of an existing prostate cancer.
What is unknown
There are no published human data for DHT enanthate on blood lipids, blood pressure, liver function, cardiovascular events or long-term safety. Its effects on growth hormone are also different from testosterone: growth hormone fell in boys treated with DHT heptanoate (Keenan et al., JCEM 1993). Products sold outside a regulated supply are not tested for dose, purity or sterility.
Key takeaways
- An injectable ester of DHT, not an approved drug. DHT enanthate releases dihydrotestosterone over several weeks, and about 72% of its weight is DHT. No FDA-approved product exists.
- Slow release, measured mostly in animals. In people, DHT peaks in the first week and returns to baseline after 4–6 weeks. The only half-life estimate, about 7 days, comes from monkeys.
- Cannot become estrogen. DHT does not aromatize, and an injection lowers estradiol along with testosterone, LH and FSH.
- Very little human evidence. Studies cover a few dozen adolescent boys and eight healthy men in total. None tested muscle or strength in adults.
- Known risks come partly from other forms. Hormonal suppression is documented for the ester; higher hematocrit and lower spinal bone density come from a 2-year DHT gel trial.
- Controlled and banned in sport. It is Schedule III in the US and prohibited at all times by WADA, and after a 250 mg injection urinary markers stayed above detection limits for 10–14 days.
Sources
- 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.
- Eberle AJ, Sparrow JT, Keenan BS. Treatment of persistent pubertal gynecomastia with dihydrotestosterone heptanoate. J Pediatr. 1986;109(1):144–149. PubMed.
- Keenan BS, Richards GE, Ponder SW, Dallas JS, Nagamani M, Smith ER. Androgen-stimulated pubertal growth: the effects of testosterone and dihydrotestosterone on growth hormone and insulin-like growth factor-I in the treatment of short stature and delayed puberty. J Clin Endocrinol Metab. 1993;76(4):996–1001. PubMed.
- Keenan BS, Richards GE, Mercado M, Dallas JS, Eakman GD, Baumann G. Androgen regulation of growth hormone binding protein. Metabolism. 1996;45(12):1521–1526. PubMed.
- Weinbauer GF, Jackwerth B, Yoon YD, Behre HM, Yeung CH, Nieschlag E. Pharmacokinetics and pharmacodynamics of testosterone enanthate and dihydrotestosterone enanthate in non-human primates. Acta Endocrinol (Copenh). 1990;122(4):432–442. PubMed.
- Southan GJ, Brooks RV, Cowan DA, Kicman AT, Unnadkat N, Walker CJ. Possible indices for the detection of the administration of dihydrotestosterone to athletes. J Steroid Biochem Mol Biol. 1992;42(1):87–94. 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.
- 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.
- National Center for Biotechnology Information. Dihydrotestosterone heptanoate, PubChem CID 160230. PubChem.
- National Center for Biotechnology Information. Androstanolone, PubChem CID 10635. PubChem.
- U.S. Food and Drug Administration. Drugs@FDA data, queried via the openFDA drugsfda endpoint for androstanolone and dihydrotestosterone, October 2026. openFDA.
- Drug Enforcement Administration. Schedules of controlled substances: Schedule III. 21 CFR 1308.13. eCFR.
- World Anti-Doping Agency. The 2026 Prohibited List. In effect from January 1, 2026. WADA.