“DHT base” is dihydrotestosterone (DHT, also called androstanolone or stanolone) with no ester attached. DHT is the body’s own most potent natural androgen. It is made from testosterone by the enzyme 5α-reductase, mainly inside target tissues such as the prostate, skin and liver (Swerdloff et al., Endocr Rev 2017). Unlike testosterone, it cannot be converted to estrogen.
The single most important fact: no injectable DHT product is approved anywhere we could verify, and no controlled trial has tested injectable DHT base for muscle, strength or physique. The only approved DHT product is a transdermal gel sold in a small number of countries outside the United States. Almost everything known about what high DHT levels do in people comes from trials of that gel. The human data on injected, unesterified DHT come from one small 1989 absorption study.
This page summarizes what those clinical studies and regulators report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Class | Endogenous androgen; 5α-reduced metabolite of testosterone |
| Other names | Androstanolone, stanolone, 5α-dihydrotestosterone, 17β-hydroxy-5α-androstan-3-one |
| Formula / weight | C₁₉H₃₀O₂, 290.4 g/mol; no ester, so 100% of the weight is DHT |
| Approved products | None in the US; a DHT gel is marketed in a few other countries; no approved injectable |
| Human injection data | One study: 40 mg crystalline DHT IM in 12 hypogonadal men |
| Release after IM injection | Absorption half-life ≈6 days (fine crystals) or ≈21 days (coarse crystals) in that study |
| Converts to estrogen | No |
| US status | Schedule III anabolic steroid (listed as “4-dihydrotestosterone”) |
| WADA status | Prohibited at all times (S1.1, androstanolone) |
What it is
DHT is testosterone with the double bond in its A-ring reduced. This small change has two consequences (Ly et al., JCEM 2001; Swerdloff et al., Endocr Rev 2017):
- It cannot be aromatized. Aromatase, the enzyme that turns testosterone into estradiol, cannot act on DHT. DHT therefore has no estrogen-mediated effects of its own.
- It cannot be “amplified” further. Testosterone gains potency in tissues that convert it to DHT. DHT is already the end product, so its activity does not depend on 5α-reductase.
PubChem lists the formula as C₁₉H₃₀O₂ and the molecular weight as 290.4 g/mol (PubChem CID 10635). Synonyms listed there include the brand names Andractim (the gel) and Anabolex. DHT has no 17α-methyl group, the chemical change that makes oral steroids such as oxandrolone survive the liver.
“Base” means the hormone is injected as-is, without an ester. Esters such as propionate or enanthate are prodrugs: the body cleaves them off to release DHT. A pharmacokinetic study of DHT heptanoate concluded that “unesterified DHT is the active principle” of such esters (Keenan et al., JCEM 1987). This page covers the unesterified form. The library has separate pages for the esters and the gels:
| Form | Library page |
|---|---|
| Unesterified DHT, injected | This page |
| DHT propionate | DHT Propionate |
| DHT enanthate | DHT Enanthate |
| Transdermal DHT gel | DHT Gel (10%), DHT Gel (20%) |
Several other anabolic steroids are chemical derivatives of DHT, including drostanolone, mesterolone and oxandrolone.
How it behaves in the body
Natural production and clearance
In men, most DHT in the blood comes from conversion of circulating testosterone rather than direct secretion. In a constant-infusion study of 15 people, about 4% of plasma testosterone was converted to plasma DHT (Mahoudeau et al., J Clin Invest 1971). The same study measured the following:
| Measure | Men (n = 3) | Women (n = 3) |
|---|---|---|
| DHT metabolic clearance rate (mean) | 336 L/24 h per m² | 153 L/24 h per m² |
| Range | 239–448 | 108–184 |
Two of DHT’s metabolites, 3α-androstanediol and 3β-androstanediol, were identified in plasma during the infusions. The authors noted that DHT and testosterone are cleared at broadly similar rates.
After intramuscular injection
The only human study of injected unesterified DHT gave 12 hypogonadal men a single 40 mg intramuscular dose of crystalline DHT, in two particle sizes (Díaz-Sánchez et al., Fertil Steril 1989):
| Crystal size | n | Serum DHT above baseline for | Absorption half-life | AUC |
|---|---|---|---|---|
| Under 50 microns | 6 | 17 days | 6 days | 14.5 ng/day/mL |
| 100–150 microns | 6 | Over 50 days | 21 days | 55.1 ng/day/mL |
Two points follow from this:
- With a crystalline depot, the release rate is set by how fast the crystals dissolve, not by an ester. Larger crystals released DHT more slowly.
- The duration of action depends heavily on the physical form of the product. Products sold outside medicine as “DHT base” do not report crystal size or vehicle, so their kinetics are unknown.
We found no primary human study reporting the elimination half-life of free DHT after an intravenous dose, so we do not give one.
Effects on other hormones
Raising DHT shuts down the body’s own testosterone production by lowering LH, the pituitary signal to the testes. In 25 men aged 60–80 using DHT gel at 16, 32 or 64 mg/day for 14 days, serum DHT reached steady state by day 2–3 (Wang et al., JCEM 1998):
| Daily gel dose | Mean serum DHT | Own testosterone (24 h AUC vs baseline) |
|---|---|---|
| 16 mg | 8–11 nmol/L | 75% |
| 32 mg | 12–17 nmol/L | 56% |
| 64 mg | 14–24 nmol/L | 36% |
Estradiol fell in a similar pattern, because less testosterone was available to convert.
Regulatory status
- United States. No DHT product of any form is approved. A 2017 Endocrine Reviews article noted that, of the DHT preparations used clinically, only DHT gel was commercially available, in a small number of countries that exclude the US (Swerdloff et al., Endocr Rev 2017).
- Controlled substance. DHT is named in the federal Schedule III list of anabolic steroids as “4-dihydrotestosterone (17β-hydroxy-androstan-3-one)” (21 CFR 1308.13).
- Sport. WADA lists androstanolone (5α-dihydrotestosterone) under S1.1 anabolic androgenic steroids, prohibited in and out of competition when administered exogenously (WADA 2026 Prohibited List).
Published medical uses of DHT gel include treatment of children with specific genital conditions. One randomized study gave 75 boys with hypospadias either 2.5% DHT gel on the penis for 3 months before surgery or no treatment. Reoperation was needed in 3% vs 24% (Kaya et al., J Urol 2008). This use is covered on the gel pages.
What the research shows
There are no trials of injectable DHT base for body composition, strength or athletic performance. The controlled human evidence on sustained high DHT levels comes from four placebo-controlled trials of DHT gel in middle-aged and older men:
| Trial | Design, n | Dose and duration | Main findings |
|---|---|---|---|
| Ly et al., JCEM 2001 | RCT, 37 men 60+ with testosterone ≤15 nmol/L | 70 mg/day gel, 3 months | Fat mass fell; lean mass unchanged; knee flexion strength rose; no change in gait, mobility, cognition or quality of life |
| Kunelius et al., JCEM 2002 | RCT, 120 men aged 50–70 | 125–250 mg/day gel, 6 months | Better ability to maintain erection; no change in well-being; hemoglobin and hematocrit rose |
| Idan et al., Ann Intern Med 2010 | RCT, 114 healthy men over 50 | 70 mg/day gel, 24 months | No effect on prostate growth; lean mass up, fat mass down; spinal bone density fell |
| Page et al., JCEM 2011 | RCT, 31 healthy men aged 35–55 | Daily gel, 4 weeks | Serum DHT up about 7-fold; DHT inside the prostate unchanged |
Body composition and strength
The longest trial gave 114 healthy men over 50 either 70 mg/day DHT gel or placebo for 2 years (Idan et al., Ann Intern Med 2010). Compared with placebo, DHT produced:
| Outcome | Change on DHT vs placebo (95% CI) |
|---|---|
| Lean mass | +2.4% (1.6–3.1) |
| Fat mass | −5.2% (−7.7 to −2.6) |
| Hemoglobin | +7% (5–9) |
| Serum creatinine | +9% (5–11) |
| Spinal bone mineral density | −1.4% (−2.3 to −0.6) |
In the shorter 3-month trial of 37 older men, DHT gel lowered fat mass but did not change lean mass (Ly et al., JCEM 2001). Of the strength measures, only knee flexion on the dominant side improved. Knee extension, shoulder strength, gait and balance did not change.
These are modest effects at doses that raised serum DHT roughly tenfold. They were measured in untrained middle-aged and older men, not in athletes.
About “hardening” claims. DHT base is often described online as a pre-contest “hardener” or strength drug. We found no human study of injected DHT that measured muscle, strength, water retention or appearance. The only controlled data are from DHT gel in older men, which showed small lean-mass gains and limited strength changes.
Prostate
Because DHT is the main androgen inside the prostate, it was long assumed that raising blood DHT would enlarge the prostate. The trials did not show this:
- Over 24 months, prostate volume and PSA rose with age in both groups, but DHT had no effect on either (P over 0.2) (Idan et al., Ann Intern Med 2010).
- After 4 weeks of DHT gel, DHT concentration inside prostate tissue was 3.1 vs 2.8 ng/g on placebo, a non-significant difference, despite serum DHT rising about 7-fold (Page et al., JCEM 2011).
The Idan authors cautioned that these negative results cannot exclude effects on the course of an existing prostate cancer.
Sexual function
In the 24-month trial, DHT fully suppressed testosterone and estradiol. It had no effect on any of 33 measures of sexual function and mood apart from a mild decrease in overall sexual desire, which reversed after stopping (Sartorius et al., J Sex Med 2014). In the 6-month Kunelius trial, the ability to maintain an erection improved compared with placebo (Kunelius et al., JCEM 2002).
Side effects and risks
Shutdown of natural testosterone and estradiol
The DHT gel trials consistently reported suppression of the body’s own testosterone, and those that measured them also reported lower LH and FSH. Over 24 months, mean serum testosterone fell by about 86% (Swerdloff et al., Endocr Rev 2017). Because DHT cannot become estradiol, estradiol falls too. This “selective estrogen deficiency” is the likely reason spinal bone density dropped 1.4% over 2 years (Idan et al., Ann Intern Med 2010; Sartorius et al., J Sex Med 2014). In the shorter 3-month trial, estradiol was unchanged (Ly et al., JCEM 2001).
Red blood cells
DHT raises hemoglobin and hematocrit (the share of blood made up of red cells):
- In the Kunelius trial, hematocrit rose from 43.5% to 45.8% and hemoglobin from 146.0 to 154.8 g/L over 6 months (Kunelius et al., JCEM 2002).
- In the 2-year Idan trial, 8 men on DHT stopped because hematocrit rose above the trial’s limit of 50%. None had symptoms, and the rise resolved after stopping. Mean hematocrit was 47.1% on DHT vs 43.4% on placebo (Swerdloff et al., Endocr Rev 2017).
Lipids and liver
In the trials of DHT gel, lipids did not worsen. The 3-month trial found lower total and LDL cholesterol with HDL unchanged (Ly et al., JCEM 2001). The 6-month trial found no effect on liver function or the lipid profile (Kunelius et al., JCEM 2002). These results come from transdermal doses in older men. They do not show what higher injected doses do.
PSA
In the 2-year trial, 3 men on DHT stopped because PSA rose; none was found to have prostate cancer (Idan et al., Ann Intern Med 2010).
Gaps in the evidence
- No safety data exist for injected DHT base beyond the single 12-man absorption study.
- No trial has studied DHT in women, in young trained men, or at the doses used outside medicine.
- Products sold as “DHT base” come from outside the regulated drug supply. Their content, sterility, crystal size and vehicle are not verified.
Key takeaways
- DHT without an ester. DHT base is the body’s most potent natural androgen, injected as-is. It cannot be converted to estrogen.
- No approved injectable and no performance trials. The only approved DHT product is a gel sold outside the US, and no study has tested injected DHT for muscle or strength.
- Kinetics depend on the physical form. In the one human injection study, 40 mg of crystalline DHT raised levels for 17 to over 50 days depending on crystal size.
- Modest body-composition effects in gel trials. Two years of DHT gel in men over 50 raised lean mass 2.4% and cut fat mass 5.2% compared with placebo, with no effect on prostate growth.
- Suppression is the main trade-off. DHT shuts down natural testosterone and, over time, estradiol, which was linked to a 1.4% loss of spinal bone density. Hematocrit also rises.
- Controlled and banned in sport. DHT is a Schedule III substance in the US and is prohibited at all times by WADA.
Sources
- 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.
- National Center for Biotechnology Information. Dihydrotestosterone (androstanolone), PubChem CID 10635. PubChem.
- 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.
- Mahoudeau JA, Bardin CW, Lipsett MB. The metabolic clearance rate and origin of plasma dihydrotestosterone in man and its conversion to the 5-alpha-androstanediols. J Clin Invest. 1971;50(6):1338–1344. PubMed.
- Keenan BS, Eberle AJ, Sparrow JT, et al. Dihydrotestosterone heptanoate: synthesis, pharmacokinetics, and effects on hypothalamic-pituitary-testicular function. J Clin Endocrinol Metab. 1987;64(3):557–562. PubMed.
- Wang C, Iranmanesh A, Berman N, et al. Comparative pharmacokinetics of three doses of percutaneous dihydrotestosterone gel in healthy elderly men–a clinical research center study. J Clin Endocrinol Metab. 1998;83(8):2749–2757. 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.
- Kunelius P, Lukkarinen O, Hannuksela ML, et al. The effects of transdermal dihydrotestosterone in the aging male: a prospective, randomized, double blind study. J Clin Endocrinol Metab. 2002;87(4):1467–1472. 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.
- Page ST, Lin DW, Mostaghel EA, et al. Dihydrotestosterone administration does not increase intraprostatic androgen concentrations or alter prostate androgen action in healthy men: a randomized-controlled trial. J Clin Endocrinol Metab. 2011;96(2):430–437. 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.
- Kaya C, Bektic J, Radmayr C, et al. The efficacy of dihydrotestosterone transdermal gel before primary hypospadias surgery: a prospective, controlled, randomized study. J Urol. 2008;179(2):684–688. PubMed.
- US Drug Enforcement Administration. Schedules of controlled substances: Schedule III, 21 CFR 1308.13(f). eCFR.
- World Anti-Doping Agency. The 2026 Prohibited List, International Standard. In effect January 1, 2026. WADA 2026 Prohibited List.