Trestolone, also called MENT (7α-methyl-19-nortestosterone), is a synthetic anabolic-androgenic steroid. It is nandrolone with an extra methyl group at carbon 7. “Trestolone base” means the free steroid with no ester attached, which is the form that actually binds the androgen receptor. The acetate and enanthate esters are prodrugs that release this same molecule.
In the 1990s and 2000s the Population Council studied MENT as a possible long-acting androgen for male contraception and for testosterone replacement. Human studies stayed small and short, and it was never approved as a medicine anywhere (Piper et al., Drug Test Anal 2026). Free trestolone has a very short half-life in men: about 40 minutes after an intravenous dose.
This page summarizes what the published human studies, animal studies and regulators report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | Synthetic anabolic-androgenic steroid; 7α-methyl derivative of nandrolone (19-nortestosterone) |
| Other names | MENT, 7α-methylnandrolone, RU 27333 |
| Formula / molecular weight | C₁₉H₂₈O₂, 288.4 g/mol |
| Approval status | Never approved for medical use |
| Routes studied in men | Intravenous bolus (0.5 mg); intramuscular aqueous suspension (1–8 mg); the acetate ester in subdermal implants |
| Half-life | ≈40 min terminal half-life after a 0.5 mg intravenous dose in men |
| Key mechanism facts | Potent androgen receptor agonist; not 5α-reduced; aromatized to an estrogen in vitro; no detectable SHBG binding |
| US status | Not FDA approved; not among the anabolic steroids named in the DEA Schedule III list |
| WADA status | Named in class S1.1 (anabolic androgenic steroids); prohibited at all times |
What it is
Trestolone’s chemical name is 17β-hydroxy-7α-methylestr-4-en-3-one, CAS 3764-87-2 (PubChem). It has the same formula and molecular weight as testosterone (C₁₉H₂₈O₂, 288.4 g/mol), but a different structure (PubChem: testosterone):
- it lacks the carbon-19 methyl group, like nandrolone;
- it carries a methyl group at the 7α position.
Unlike oral steroids such as methyltestosterone, it has no 17α-alkyl group.
The 7α-methyl group blocks 5α-reductase, the enzyme that turns testosterone into the more potent dihydrotestosterone (DHT) in the prostate and skin (Kumar et al., Endocrinology 1992). MENT is still a substrate for aromatase. Human placental enzymes converted it to 7α-methylestradiol in vitro, and that product bound the estrogen receptor (LaMorte et al., J Steroid Biochem Mol Biol 1994).
In a cell-based reporter assay, MENT was the most potent androgen tested, ahead of DHT, nandrolone and testosterone. The authors attributed its high potency mainly to its higher affinity for the androgen receptor (Kumar et al., J Steroid Biochem Mol Biol 1999).
The library has separate pages for the esters:
| Form | Formula | Molecular weight | Trestolone share of weight |
|---|---|---|---|
| Trestolone (base, this page) | C₁₉H₂₈O₂ | 288.4 g/mol | 100% |
| Trestolone acetate | C₂₁H₃₀O₃ | 330.5 g/mol | ≈87% |
| Trestolone enanthate | C₂₆H₄₀O₃ | 400.6 g/mol | ≈72% |
Formulas and weights from PubChem (acetate, enanthate); share of weight calculated from them.
The esters have no activity of their own. In cynomolgus monkeys, continuous subcutaneous infusion of equimolar MENT or MENT acetate gave the same steady-state serum MENT (11.3 vs 13.1 nmol/L, not significantly different). The acetate was hydrolyzed to MENT in blood and plasma (Kumar et al., J Androl 1997). The Population Council used the acetate in its implants because its diffusion characteristics suited sustained release (Anderson et al., JCEM 1999).
Pharmacokinetics
Only two published human studies gave the unesterified steroid:
| Study | Dose and route | Findings |
|---|---|---|
| Kumar et al., J Androl 1997 | 500 µg single intravenous bolus, healthy men | Highest level at 3 min (first sample); undetectable by 180 min; terminal half-life 40 min; metabolic clearance rate 2,360 L/day |
| Suvisaari et al., Hum Reprod 1997 | 2, 4 or 8 mg single IM injection of micronized MENT in aqueous suspension, 18 healthy men | Peak at about 1–2 h; doubling the dose raised the peak by 60%; clearance 1,790 ± 140 L/day |
Kumar and colleagues reported clearance much faster than that of testosterone, and attributed it partly to the finding that MENT showed no binding to sex hormone-binding globulin (SHBG), the carrier protein that holds much of circulating testosterone in reserve (Kumar et al., J Androl 1997). The later research programs delivered it continuously from implants instead of injecting the free steroid.
In human liver preparations, MENT was metabolized by CYP3A4, 17β-hydroxysteroid dehydrogenase and 3-hydroxysteroid dehydrogenase. In rats, a labeled dose was excreted equally in urine and feces by 30 hours (Prasad et al., Steroids 2009).
Development history and regulatory status
MENT’s anabolic properties were first investigated in the 1960s, in cancer research (Piper et al., Drug Test Anal 2026). The Population Council later developed MENT systematically, both as testosterone substitution for hypogonadism and as part of male hormonal contraception (Nieschlag et al., Contraception 2013). The program did not lead to an approved product.
Current status:
- Approval. Trestolone “never received full approval for medical use” (Piper et al., Drug Test Anal 2026). There is no prescribing label, labeled dose or labeled list of contraindications.
- US controlled-substance status. Trestolone is not among the anabolic steroids named in Schedule III (21 CFR 1308.13). That does not make it an approved or legal drug or supplement.
- Sport. The WADA list names “Trestolone (7α-Methyl-19-nortestosterone, MENT)” under S1.1 anabolic androgenic steroids, prohibited in and out of competition; the class also covers esters (WADA 2026 Prohibited List).
What the research shows
No trial has tested trestolone for muscle mass or strength in people. The human evidence comes from a handful of small studies, most under 50 men, measuring hormones, sperm counts, sexual function and safety labs. All implant studies used the acetate ester; the circulating active hormone in them was MENT.
Suppression of LH, FSH and testosterone
Like other androgens, MENT signals the pituitary to cut LH and FSH, the hormones that drive the testes. In the IM study of the free steroid, 24 healthy men received six consecutive daily injections of 1, 2 or 4 mg (Suvisaari et al., Hum Reprod 1997). Falls were dose-dependent. At 4 mg/day:
| Hormone | Mean fall |
|---|---|
| Testosterone | 74% |
| LH | 70% |
| FSH | 57% |
With continuous release from implants, suppression was deeper. In 45 healthy men given one, two or four MENT acetate implants for 28 days (≈500 µg MENT released per implant per day), serum MENT reached 0.7, 1.2 and 2.0 nmol/L (Noé et al., Hum Reprod 1999). Two and four implants produced maximal suppression:
| Measure | Mean fall |
|---|---|
| Testosterone | 93% |
| DHT | 80% |
| LH | 97% |
| FSH | 95% |
Suppression reversed completely after the implants were removed.
Replacement therapy in hypogonadal men
In a crossover trial, 20 hypogonadal men in Edinburgh and Hong Kong received two 115 mg MENT acetate implants for 6 weeks, and testosterone enanthate 200 mg IM twice, 3 weeks apart (Anderson et al., JCEM 1999). MENT levels were stable at 1.3–1.4 nmol/L. Both treatments raised sexual interest and activity and spontaneous erections in the Edinburgh group, measured by diaries and nocturnal penile tumescence. In the Hong Kong group, both increased waking erections. The authors found only minor differences between MENT and testosterone.
A 24-week follow-up randomized 16 hypogonadal men to one or two implants (≈400 µg/day each) (Anderson et al., JCEM 2003):
| Outcome | 1 implant | 2 implants |
|---|---|---|
| Hemoglobin and hematocrit | Maintained | Maintained |
| Sexual behavior and erectile function | Declined | Maintained |
| Prostate volume | Fell | Small, nonsignificant fall |
| PSA | Fell significantly | Fell significantly |
| Lumbar spine bone mineral density | Decreased | Decreased |
The authors judged one implant to be under-replacement. Two implants maintained most androgen-dependent functions except bone. They read the bone loss as a sign that an androgen used for replacement needs enough estrogenic activity.
Male contraception
In a trial of 35 healthy men given one, two or four MENT acetate implants for 6–12 months, sperm suppression was dose-related (von Eckardstein et al., JCEM 2003):
| Group | Result |
|---|---|
| 1 implant (12 men) | None fell below 3 million sperm/mL |
| 2 implants (11 men) | 4 fell below 3 million/mL, 2 of them to zero (azoospermia) |
| 4 implants (12 men) | 8 azoospermic, 1 below 3 million/mL, 2 nonresponders |
A later trial randomized 29 men to two etonogestrel (progestin) implants plus either two MENT implants or 600 mg testosterone pellets every 12 weeks, for up to 48 weeks (Walton et al., J Androl 2007). At 12 weeks, sperm counts were under 1 million/mL in 8 of 10 MENT men and 13 of 16 testosterone men. Suppression was not maintained in the MENT group because release from the implants declined, and 6 men noted loss of libido. All 14 men who completed 48 weeks of testosterone became azoospermic.
The “prostate-sparing” idea
The rationale for MENT was that it would support muscle, libido and gonadotropin suppression while stimulating the prostate less, because it cannot be amplified to a DHT-like form there. The evidence:
- In castrated rats (given the acetate), MENT was about 10 times as potent as testosterone on the levator ani muscle, 12 times on gonadotropin suppression, and 4 times on prostate and seminal vesicle weight. Doses that maintained muscle did not maintain the prostate (Kumar et al., Endocrinology 1992).
- In castrated monkeys, MENT was 10 times as potent as testosterone for LH suppression and body weight, but only twice as potent for prostate growth (Cummings et al., JCEM 1998).
- In hypogonadal men, PSA fell on MENT implants and prostate volume did not rise, which the authors called the first human evidence of tissue selectivity (Anderson et al., JCEM 2003). PSA also fell in the 2007 contraceptive trial.
About “10 times stronger than testosterone.” The often-quoted 10× figure comes from rat and monkey dose comparisons, and the ratio differed by tissue. No study has established a human potency ratio for muscle, and no controlled trial has measured muscle mass or strength on trestolone in people.
Side effects and risks
No product label exists, so there are no labeled warnings, interaction lists or contraindications. The safety data below come from small trials of a few weeks to 12 months, at replacement-range or contraceptive doses, mostly using implants.
Shutdown of natural testosterone and sperm production
Suppression of LH, FSH and the body’s own testosterone is the intended effect in the contraceptive studies. At implant doses, testosterone fell by 93% (Noé et al., Hum Reprod 1999) and many men became azoospermic (von Eckardstein et al., JCEM 2003). Hormone suppression reversed after implant removal in the 28-day study. Recovery after long-term, high-dose non-medical use has not been studied.
Once the body’s own testosterone is shut down, MENT has to supply all androgen effect. In the trials, under-dosing showed up as reduced sexual function and libido (Anderson et al., JCEM 2003; Walton et al., J Androl 2007).
Blood count, lipids and bone
- Red cells. Red cell count, hematocrit (the share of blood made up of red cells) and hemoglobin rose and were reversible (von Eckardstein et al., JCEM 2003). Hemoglobin also rose in the 2007 trial.
- Cholesterol. HDL (“good”) cholesterol fell in both the MENT and testosterone arms of the 2007 trial. The 2003 contraceptive trial described lipid changes as moderate and transient.
- SHBG fell during treatment (von Eckardstein et al., JCEM 2003).
- Bone. Lumbar spine bone density decreased over 24 weeks in hypogonadal men on one or two implants (Anderson et al., JCEM 2003).
Liver
In the implant trials, liver enzymes showed only small changes (von Eckardstein et al., JCEM 2003), and the 28-day study found no consistent changes in clinical chemistry (Noé et al., Hum Reprod 1999).
Oral dosing has been tested only in animals. In rabbits given 10 mg/kg/day by mouth for 14 days, MENT raised ALT, AST, GGT and sorbitol dehydrogenase and slowed dye clearance by the liver, though less than methyltestosterone did. All values returned to baseline 2 weeks after stopping, and 1 mg/kg/day was a no-effect dose (Hild et al., J Androl 2010). How this translates to people is unknown.
Estrogenic and progestational activity
- Estrogen. MENT is aromatized to 7α-methylestradiol in vitro (LaMorte et al., 1994). How much estrogen forms in men at a given dose has not been well characterized.
- Progestin-like activity. In immature rabbits, MENT’s progestational activity was comparable to progesterone’s, and it bound the progesterone receptor with similar affinity (Beri et al., J Steroid Biochem Mol Biol 1998). This is animal and test-tube data. Its clinical significance in men is not known.
Anesthesia: a single case report
A 60-year-old man using testosterone 750–1,000 mg/week and trestolone acetate 300 mg/week showed unusually slow reversal of the muscle relaxant rocuronium with sugammadex. Neostigmine then restored full recovery (Farkas et al., Anaesth Rep 2023). The authors proposed that the steroids might bind sugammadex, but called this speculative; one case cannot establish an interaction.
Unregulated products
Trestolone is sold online, sometimes marketed as a “nutritional supplement.” Doping-control researchers bought two such products containing MENT acetate for their study (Piper et al., Drug Test Anal 2026). Products outside a regulated drug supply are not checked for identity, dose or sterility.
Detection in sport
Although it is easy to buy, MENT had not produced a single adverse analytical finding in WADA’s testing reports since 2003. A 2026 study suggests one reason is that its known urinary metabolites co-elute with natural steroids and are detectable only briefly (Piper et al., Drug Test Anal 2026). After a single oral dose of the acetate in volunteers:
| Target | Detection window |
|---|---|
| MENT itself (as glucuronide) | 23–43 h |
| Newly identified metabolites M5 and M10 | 3–4 days |
Key takeaways
- The active molecule. Trestolone base is MENT itself; the acetate and enanthate esters only change how it is released and convert to it in the body.
- Very short-lived when unesterified. After an intravenous dose in men, the terminal half-life was about 40 minutes, and MENT does not bind SHBG.
- Never approved. MENT reached small Population Council trials for contraception and hypogonadism, with up to 45 men per study, but no regulator approved it.
- Strongly suppressive. Implants cut testosterone by 93% and LH by 97% in healthy men, enough to stop sperm production in many.
- “Prostate-sparing,” not risk-free. It is not converted to a DHT-like form and lowered PSA, but trials still saw higher hemoglobin, lower HDL and bone loss, and it is aromatized to an estrogen.
- No human muscle data. The “10× testosterone” figure is from rats and monkeys; no controlled human trial has measured muscle or strength.
Sources
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