Dimethandrolone undecanoate (DMAU) is an experimental oral steroid being developed as a male contraceptive pill. In the body it is broken down to dimethandrolone (DMA), a synthetic derivative of 19-nortestosterone (nandrolone) that acts on both the androgen receptor and the progesterone receptor. That dual action shuts down the brain signals (LH and FSH) that drive the testes, while the drug itself stands in for testosterone.
The single most important fact: DMAU is not an approved medicine anywhere. All human data come from a handful of small, short NIH-funded trials in healthy young men, the longest published one lasting 28 days. No trial has yet published data showing that it reliably stops sperm production or prevents pregnancy.
This page summarizes what the published trials, trial registries and regulators report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | Investigational 19-nor androgen with progestational activity; oral prodrug of dimethandrolone |
| Developer | Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), Contraceptive Development Program |
| Route studied | Oral capsule taken with food; injectable (IM and SC) forms in early testing |
| Doses studied in men | Single oral doses 25–800 mg; daily 100–400 mg for 28 days |
| Half-life (single oral dose, fed) | DMA ≈2.4–3.3 h; DMAU ≈1.7–2.3 h (group means, Ayoub 2017) |
| Converts to estrogen | No (in vitro aromatase study); estradiol falls during treatment |
| Development stage | Phase 1 and 2a trials completed; no approval |
| US status | Not FDA-approved; not named in the Schedule III anabolic steroid list |
| WADA status | Dimethandrolone named under S1.1 anabolic androgenic steroids; prohibited at all times |
What it is
DMAU is the 17β-undecanoate ester of dimethandrolone, whose full chemical name is 7α,11β-dimethyl-19-nortestosterone. PubChem lists DMAU as C₃₁H₅₀O₃ with a molecular weight of 470.7 g/mol, and the free steroid dimethandrolone as C₂₀H₃₀O₂, 302.5 g/mol (PubChem DMAU; PubChem dimethandrolone).
Compared with related steroids, the structure has two added methyl groups:
| Compound | Structure | Relationship |
|---|---|---|
| Nandrolone (19-nortestosterone) | Testosterone without the carbon-19 methyl | Parent 19-nor androgen |
| Trestolone (MENT) | Nandrolone + 7α-methyl | Earlier contraceptive candidate |
| Dimethandrolone (DMA) | Nandrolone + 7α-methyl + 11β-methyl | Active drug |
| DMAU | DMA with an undecanoate ester at 17β | Oral prodrug of DMA |
Chemists at the Research Triangle Institute described dimethandrolone in 2005 as a potent androgen in rat assays (Cook and Kepler, Bioorg Med Chem Lett 2005). The related pages on trestolone acetate (MENT) and nandrolone decanoate cover its closest chemical relatives.
How it works
In laboratory studies, dimethandrolone bound the androgen receptor with high affinity and also bound human progesterone receptors strongly, giving it both androgenic and progestational activity (Attardi et al., Endocrinology 2006). The 28-day human trial report summarizes its binding affinity at the androgen receptor as 400% of testosterone’s (Thirumalai et al., JCEM 2019).
Both actions suppress the hypothalamus and pituitary. With less LH and FSH, the testes make less testosterone and, over time, fewer sperm. The drug’s own androgen activity is meant to replace the testosterone that is lost.
Two other laboratory findings shape its profile:
- No conversion to estrogen. Incubated with recombinant human aromatase (the enzyme that turns testosterone into estradiol), dimethandrolone showed no detectable conversion over up to 180 minutes (Attardi et al., J Steroid Biochem Mol Biol 2008).
- No need for 5α-reduction. In castrated rats, blocking 5α-reductase with dutasteride did not reduce dimethandrolone’s effect on the prostate or seminal vesicles (Attardi et al., J Steroid Biochem Mol Biol 2010).
About “prostate-sparing.” The 2005 chemistry paper called dimethandrolone a “prostate-sparing” androgen based on rat assays. A later 16-week study in castrated rats found the opposite: prostate and seminal vesicle weights in DMAU-treated rats were 2.4–2.7 times those of intact rats (Attardi et al., J Androl 2011). In men, PSA did not change significantly over 28 days, but no study has looked at the prostate over the long term.
Pharmacokinetics
DMAU itself is inactive. Esterases (enzymes that cut ester bonds) remove the undecanoate chain and release dimethandrolone. The ester makes the drug fat-soluble, which is why it must be taken with food, much like oral testosterone undecanoate.
Food is essential
In the first-in-human study, men took single doses of 25–800 mg as powder in capsules, fasting and after a high-fat meal (Surampudi et al., Andrology 2014). Results:
- Fasting: DMA was detectable in only 4 of 10 men even after the 800 mg dose.
- With a high-fat meal: DMA was detectable in every man given 200 mg, rose with dose up to 800 mg and peaked 4–8 h after dosing.
- Hormones: LH, FSH and sex hormones were significantly suppressed 12 h after doses above 200 mg taken with food.
In the 28-day trial, a breakfast with 25–30 g of fat, about half the fat used in the single-dose study, still gave comparable DMA levels (Thirumalai et al., JCEM 2019).
Single-dose kinetics by formulation
A follow-up study compared three oral formulations in healthy men, 10 per formulation, given with a high-fat meal (Ayoub et al., Andrology 2017):
| Measure (mean, fed) | 200 mg | 400 mg |
|---|---|---|
| DMA half-life | 2.4–2.8 h | 3.1–3.3 h |
| DMAU half-life | 1.7–2.0 h | 1.8–2.3 h |
| DMA time to peak | 3.8–5.8 h | 3.8–6.4 h |
| DMA peak level | 12.5–19.2 ng/mL | 27.7–47.9 ng/mL |
| DMA exposure as a share of DMAU exposure (AUC ratio) | 0.03–0.06 | 0.03–0.11 |
Ranges span the powder, castor oil and self-emulsifying (SEDDS) capsules. Only a small fraction of the prodrug was converted to active DMA, and the powder formulation converted least. The SEDDS capsule was the only one that suppressed testosterone when taken fasting.
With daily dosing for 28 days, levels of both compounds were near the lower limit of detection by 24 h, and day-28 kinetics did not differ significantly from day 1. Average DMAU levels were about 20 times higher than DMA levels (Thirumalai et al., JCEM 2019).
Metabolism and variable absorption
In human liver cell experiments and in serum from men taking DMAU, the main metabolite was DMA-glucuronide, at levels over 100 times those of DMA (Sharma et al., Drug Metab Dispos 2022). The enzyme mainly responsible was UGT2B17, with a smaller role for UGT1A9. UGT2B17 is highly variable, with a reported gene deletion frequency of 20–80%, and the authors concluded that this variation in gut first-pass metabolism likely explains why oral DMA levels vary so much between men.
Lab measurement is also tricky. Blood esterases keep converting DMAU to DMA in the collection tube, which can overstate DMA levels. Using sodium fluoride tubes lowered measured DMA by 22% in men taking 200 mg DMAU (Ceponis et al., Andrology 2019).
Development and regulatory status
DMAU has never been approved by the FDA or any other regulator. Registered trials on ClinicalTrials.gov:
| Trial | Phase and design | What was tested | Registry status |
|---|---|---|---|
| NCT01382069 | Phase 1, single doses then 28 days daily | Oral DMAU 100, 200, 400 mg vs placebo | Completed 2017; published |
| NCT03455075 | Phase 2a, 12 weeks, 92 enrolled | Oral DMAU 200 or 400 mg alone, or 100 or 200 mg with levonorgestrel 30 mcg, vs placebo; endpoint sperm suppression | Completed March 2020; no results posted |
| NCT02927210 | Phase 1, single injection | IM 80–800 mg or SC 50–200 mg vs placebo | Completed April 2025; no results posted |
We could not find published results of the 12-week sperm-suppression trial or the injectable trial in PubMed as of October 2026. Without them, there is no human evidence yet on whether DMAU lowers sperm counts to contraceptive levels.
DMAU has also been described as a possible androgen therapy for men (Attardi et al., Endocrinology 2006), but no published trial has tested it as testosterone replacement in men with hypogonadism.
What the research shows
28-day oral trial in healthy men
The key human study was a double-blind, randomized, placebo-controlled phase 1b trial at two US academic centers (Thirumalai et al., JCEM 2019). It randomized 100 healthy men aged 18–50 to placebo or DMAU daily with food for 28 days, as castor oil capsules (C) or powder capsules (P); 82 men were in the efficacy analysis.
Average serum testosterone on day 28 (median):
| Group | n | Testosterone (ng/dL) | Men with testosterone under 50 ng/dL |
|---|---|---|---|
| Placebo | 23 | 474 | 0% |
| 100 mg (C) | 13 | 15.7 | 46% |
| 200 mg (C) | 14 | 24.3 | 64% |
| 200 mg (P) | 13 | 12.6 | 77% |
| 400 mg (P) | 6 | 7.0 | 100% |
| 400 mg (C) | 13 | 8.3 | 92% |
Testosterone was suppressed by day 7 and stayed down through day 28. Both LH and FSH fell below 1 IU/L in all men on 400 mg powder and 12 of 13 on 400 mg castor oil, compared with 64–69% on 200 mg and 54% on 100 mg. That threshold has been linked to sperm suppression in longer studies of other hormonal male contraceptives.
Even so, sperm concentration did not fall significantly in 28 days, which the authors expected because sperm production takes about 72 days. Four of 59 treated men had reached under 5 million/mL by day 28, compared with none on placebo.
Most men did not report symptoms of low testosterone such as hot flashes, which suggests DMA’s androgen activity largely replaced the lost testosterone at these doses.
Bone markers
Because DMA is not converted to estrogen, estradiol fell sharply, to under 5 pg/mL in the 400 mg groups. Low estradiol can speed bone loss in men, so the same trial measured bone turnover markers (Thirumalai et al., JCEM 2021):
| Marker (median % change, day 1 to 28) | Placebo | 200 mg | 400 mg |
|---|---|---|---|
| P1NP (bone formation) | −8% | +5% | +22% |
The rise in P1NP was statistically significant (p = 0.007 across groups). CTX, a marker of bone breakdown, did not differ between groups (p = 0.09). This is a 28-day blood marker study; it does not show what happens to bone density over months or years.
Acceptability
After the 28-day trial, 57 men completed a survey (Nguyen et al., Contraception 2020). 80% were satisfied with the method, 77% would recommend it and 54% said they would use it as their main contraceptive if it were available. Satisfaction was higher on DMAU than placebo (87% vs 67%, p = 0.05). 91% reported no difficulty taking up to four capsules after a high-fat meal.
Animal studies
These results come from animals and do not show the same effects in people:
- Rabbits: oral DMAU for 12–13 weeks caused severe oligospermia in most males at 2.5 and 5.0 mg/kg/day. In a mating trial, 0 of 4 and 2 of 5 males were fertile at those doses vs 4 of 4 on vehicle. Sperm counts returned to baseline by week 30 and all bred males were fertile at week 31. At 10 mg/kg/day sperm counts did not fall (Attardi et al., J Androl 2011).
- Monkeys: in cynomolgus and rhesus macaques, oral DMAU for 9 months or intramuscular injections suppressed testosterone, inhibin B, sperm counts and spermatogenesis. After five weekly injections, DMA stayed above 1 ng/mL for more than 500 days, consistent with a long-lasting depot at the injection site. Testosterone and sperm production recovered by the end of follow-up (Bunin et al., Andrology 2025).
Side effects and risks
No serious adverse events occurred in the published human trials, but they lasted 28 days or less. The largest enrolled 100 men, 73 of them on DMAU.
Adverse events in the 28-day trial
From Thirumalai et al., JCEM 2019:
| Event | Placebo (n = 27) | DMAU, all doses (n = 73) | DMAU 400 mg groups (n = 24) |
|---|---|---|---|
| Headache | 19% | 11% | — |
| Decreased libido | 4% | 11% | 25% |
| Erectile dysfunction | 0 of 27 | 3 of 73 (all in 400 mg groups) | 13% |
| Acne | 11% | 7% | 17% |
Nearly all events were mild. A questionnaire showed a dose-related drop in sexual desire, but no significant change in sexual activity, erectile function satisfaction or mood (PHQ-9 depression score). The authors suggested that lower estradiol or DMA’s progestational effect could explain the libido findings.
Lipids, weight, blood count and heart rhythm
Median change from day 1 to day 28 (Thirumalai et al., JCEM 2019):
| Group | HDL cholesterol (mg/dL) | Weight (kg) | Hematocrit (points) |
|---|---|---|---|
| Placebo | −0.5 | +0.3 | −1 |
| 100 mg (C) | −6 | +1.5 | +1.1 |
| 200 mg (C) | −13 | +1.7 | 0 |
| 200 mg (P) | −10 | +1.9 | +2 |
| 400 mg (P) | −15 | +3.8 | +0.4 |
| 400 mg (C) | −11 | +2.9 | +2 |
- HDL (“good”) cholesterol fell by about 6–15 mg/dL, a known effect of oral, non-aromatizable androgens. LDL did not change.
- Weight rose with dose; the trial did not measure whether this was muscle or fat.
- Hematocrit (the share of blood made up of red cells) rose slightly in treated groups, mostly within the normal range.
- QTc interval on the ECG was lower in all DMAU groups than placebo but stayed in the normal range.
- Liver enzymes and PSA did not change significantly.
A pooled analysis of the DMAU and 11β-MNTDC 28-day trials found no change in fasting glucose, fasting insulin or insulin resistance (HOMA-IR). DMAU slightly lowered adiponectin (a fat-tissue hormone linked to insulin sensitivity), and SHBG fell (Yuen et al., Andrology 2021).
Liver signal in animals
In a rabbit model, oral DMAU at 10 mg/kg/day for 14 days raised liver enzymes and slowed dye clearance, an effect ranked alongside 17α-methyltestosterone as the most liver-toxic of the androgens tested. Values returned to baseline 2 weeks after stopping, and 1 mg/kg/day had no effect (Hild et al., J Androl 2010). The 28-day human trial did not show significant liver enzyme changes, but long-term human liver data do not exist.
Unknowns
Key questions remain unanswered in humans:
- whether it suppresses sperm reliably enough to prevent pregnancy;
- how fast and how completely fertility returns after longer use;
- long-term effects on bone density, lipids, cardiovascular risk and the prostate;
- effects in women, which have not been studied.
Legal status and use outside medicine
DMAU is an investigational drug with no FDA approval. Dimethandrolone is not among the substances named in the DEA’s Schedule III anabolic steroid list (21 CFR 1308.13).
In sport, the WADA 2026 Prohibited List names dimethandrolone (7α,11β-dimethyl-19-nortestosterone) under S1.1 anabolic androgenic steroids. S1 substances are prohibited at all times, in and out of competition, and are non-Specified Substances. DMAU releases dimethandrolone in the body.
Key takeaways
- An experimental male pill, not a medicine. DMAU is an NIH-developed oral prodrug of dimethandrolone, a 19-nor androgen with progestational activity. It has no approval anywhere.
- Strong hormone suppression in 28 days. At 200–400 mg daily with food, median testosterone fell below 25 ng/dL, and most men on 400 mg suppressed LH and FSH below 1 IU/L.
- No proof of contraception yet. Sperm counts did not fall significantly within 28 days, and results from the completed 12-week sperm-suppression trial have not been published.
- Short half-life and erratic absorption. DMA’s half-life is about 2–3 h after a single dose; the drug barely works fasting, and gut UGT2B17 metabolism makes levels vary between men.
- Typical androgen side effects. HDL fell 6–15 mg/dL, weight rose up to about 4 kg, and decreased libido was reported by 25% of men on 400 mg.
- Banned in sport. Dimethandrolone is named on the WADA S1.1 list and is prohibited at all times.
Sources
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