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Enobosarm

Also known as Ostarine, MK-2866, GTx-024, S-22, Ostabolic

Not a peptide but an oral non-steroidal SARM: heavily trialled, never approved, and a leading doping finding.

early-clinical Growth hormone research chemical

At a glance

Category
Growth hormone
Status
research chemical
Route
oral, once daily
Half-life
Approximately 24 hours in humans, which is why every trial dosed it once daily 12. Its long-lived metabolites are what make it detectable in urine at picogram concentrations weeks after use 6.
Onset
Changes in lean body mass were measurable at 12 weeks in the phase 2 trials 1
Molecular weight
389.3 g/mol (C19H14F3N3O3) 9

Enobosarm is not a peptide. It is a small non-steroidal molecule that acts as a selective androgen receptor modulator, included here because it is sold beside peptides and appears in the same searches and the same stacks. It is not approved as a medicine anywhere. It has, unusually for a compound in this reference, been through a full clinical development programme: phase 2 trials in healthy older adults and in cancer cachexia, two phase 3 trials in muscle wasting in non-small cell lung cancer, a phase 2 trial in advanced breast cancer, and most recently a phase 2 trial as a muscle-preserving add-on to GLP-1 receptor agonist therapy for weight management 12348. Seventeen studies are registered on ClinicalTrials.gov 10. None of that has produced a marketing authorisation. It is sold online as a 'research chemical' and is one of the SARMs most often detected in athlete urine samples 6.

Doping status: Prohibited at all times under S1.2, Other Anabolic Agents, where the 2026 Prohibited List names it explicitly as 'enobosarm (ostarine)' among the SARMs; all substances in class S1 are non-Specified Substances

Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.

Mechanism of action

Enobosarm binds the androgen receptor as a non-steroidal ligand. The selectivity claimed for the SARM class is tissue selectivity rather than receptor selectivity: the intention is to recruit the receptor's anabolic effects in muscle and bone while producing less of the effect in prostate, skin and hair follicle that limits the use of testosterone and its derivatives. Because it is not a steroid, it is not a substrate for aromatase or 5-alpha-reductase, so it does not convert to oestradiol or dihydrotestosterone.

The tissue selectivity is real but partial and dose-dependent, and it is worth being precise about what has been shown. In the trials, enobosarm increased lean body mass at doses that did not produce virilising effects in women or measurable prostate effects in men 1. It nevertheless suppresses the hypothalamic-pituitary-gonadal axis - an androgen receptor agonist does that by design, and total testosterone and SHBG fall on treatment. It is also hepatically metabolised, and elevated transaminases were among the most common grade 3-4 drug-related adverse events in the breast cancer trial 8.

The mechanism the compound is currently being repositioned around is different again. GLP-1 receptor agonists produce substantial weight loss of which a meaningful fraction is lean mass, and this has become a recognised clinical problem 11. The proposition is that an oral anabolic agent taken alongside a GLP-1 agonist preserves lean mass while fat loss continues. That is the question the phase 2 trial NCT06282458 was designed to answer 4.

What the research shows

There is more human evidence here than for almost anything else in this reference, and it has consistently produced the same shape of result: enobosarm reliably increases lean body mass, and reliably fails to convert that into an accepted functional or clinical benefit. The phase 3 POWER programme in cancer-related muscle wasting is the clearest illustration - it was a 321-patient double-blind placebo-controlled trial with co-primary endpoints of lean body mass and physical function, and the posted registry results show a lean mass responder rate of 41.9 per cent on drug against 30.4 per cent on placebo, but a stair-climb-power responder rate of only 29.4 per cent against 24.2 per cent 3. It has never been approved for any indication in any country.

Research in humans

Dalton and colleagues (2011) ran a 12-week double-blind placebo-controlled phase 2 trial in 120 healthy elderly men and postmenopausal women, reporting dose-dependent increases in total lean body mass by DXA, with significant improvements in physical function and insulin resistance at 3 mg against placebo 1. Dobs and colleagues (2013) randomised 159 patients with cancer and at least 2 per cent weight loss to 1 mg, 3 mg or placebo daily for up to 113 days: total lean body mass increased significantly in both enobosarm groups (median 1.5 kg at 1 mg, 1.0 kg at 3 mg) and not in the placebo group, and the serious adverse events reported were the expected events of advanced cancer rather than drug toxicity 2. The phase 3 POWER trial in non-small cell lung cancer patients on platinum-plus-taxane chemotherapy enrolled 321 patients with co-primary endpoints of stair climb power and lean body mass; the registry results are given above and did not support approval 3. In advanced breast cancer, an open-label randomised phase 2 trial of 9 mg against 18 mg daily in 136 postmenopausal women with AR-positive, ER-positive, HER2-negative disease reported clinical benefit at 24 weeks in 32 per cent and 29 per cent of the evaluable groups respectively, with grade 3-4 drug-related adverse events in 8 per cent and 16 per cent, most commonly raised hepatic transaminases 8. The current programme is NCT06282458, a completed 168-patient phase 2 dose-finding study of enobosarm 3 mg or 6 mg daily against placebo in patients taking semaglutide for chronic weight management, with percentage change in total lean body mass at day 112 as the primary endpoint 4.

Animal and lab research

Preclinical work established tissue-selective anabolic activity in muscle and bone with reduced activity in prostate. One line of rodent work is worth naming for balance: an androgen receptor knockout study in the satellite cell lineage found that enobosarm modulates adult skeletal muscle mass independently of the androgen receptor in that lineage, which complicates the simple account of how it works. Rodent exercise studies have been unimpressive - ostarine blunted the effect of endurance training on submaximal endurance in rats, and did not enhance the metabolic effect of exercise in obese rats.

Caveats. The pattern across the programme is that lean body mass on DXA responds and function does not follow, and lean body mass is a surrogate. Regulators did not accept it, and after fifteen years and a completed phase 3 programme there is still no approval anywhere. Almost all of the trials were funded by the sponsor, GTx and later Veru; the Lancet Oncology breast cancer paper states GTx funding directly 8. Hepatotoxicity is a genuine signal rather than a theoretical one: raised transaminases were the most frequent serious drug-related adverse event in the breast cancer trial 8, and a published case report describes drug-induced liver injury attributed to enobosarm taken outside medical supervision 7. Finally, none of the trial evidence describes the product people actually buy: material sold online as ostarine or MK-2866 has repeatedly been found to be mislabelled, underdosed, overdosed or to contain a different SARM entirely, so the clinical literature and the grey market are not describing the same substance.

What it is used for

  • Investigational treatment for cancer-related muscle wasting - the indication of the phase 3 POWER programme, which did not lead to approval 3
  • Investigational muscle-preserving add-on to GLP-1 receptor agonist therapy for weight management, currently the main line of development 411
  • Investigational endocrine therapy in androgen receptor-positive, ER-positive advanced breast cancer 8
  • Used without medical supervision for muscle gain and fat loss, in which context it is bought as a 'research chemical' of unverified identity 7
  • A frequent adverse analytical finding in anti-doping laboratories; in one high-throughput screening study of roughly 28,000 samples, ostarine was among the compounds most often identified alongside stanozolol, GW1516, LGD-4033 and clomiphene 6

Dosing

Dose
1-3 mg daily in the muscle-wasting trials; 9 mg and 18 mg daily in the breast cancer trial; 3 mg and 6 mg daily in the GLP-1 combination trial
Frequency
once daily
Route
oral
Duration
12 weeks to 113 days in most trials; 112 days plus an 84-day continuation in the GLP-1 trial
  • The dose ranges above come from published and registered trials: 1-3 mg daily in the muscle-wasting studies 12, 9 mg and 18 mg daily in the advanced breast cancer trial 8, and 3 mg or 6 mg daily for 112 days with an 84-day continuation in the GLP-1 combination study 4. They describe doses given under medical supervision in a trial. They are not a recommendation, and no dose of enobosarm has an approved indication anywhere in the world.
  • The doses used span an eighteen-fold range depending on indication 18, which is worth noticing: figures circulating online rarely say which trial they came from or what it was measuring.
  • The compound suppresses the hypothalamic-pituitary-gonadal axis. Trials monitored this; unsupervised use does not.
  • Any competitive athlete should treat this as a doping violation waiting to happen rather than as a dosing question. It is detectable at picogram concentrations long after the last dose 6, and it is named by name on the Prohibited List 5. Contamination of ordinary supplements with ostarine is a documented route to a positive test.
  • Material sold online is not the material used in these trials. Purity, identity and label accuracy are unverified for grey-market product.

These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.

Protocols

Bodybuilding self-dosing cycle (user-reported)

user protocol — not validated

Source: Bodybuilding and SARM forum posts and vendor labelling; no published basis

This is not a validated schedule. It is a pattern that circulates among users and sellers, reproduced because it is what people actually follow — not because it has been tested. No trial established these doses, this interval or this duration, and nobody is checking what is in the vial. Treat every number below as an assertion, not a finding.

Typical reported cycle10 to 25 mg once daily by mouth, most commonly around 15 to 20 mg
Cycle lengthroughly 6 to 12 weeks, often followed by a self-directed 'post-cycle therapy'
Reported upper end30 mg daily and above in some accounts, past any dose given in a trial

These figures come from forums and vendor labelling, not from research, and they sit above the trial doses: the muscle-wasting trials used 1 to 3 mg 12 and even the advanced breast cancer trial went only to 18 mg 8, while the circulating cycles cluster around 15 to 20 mg and run higher. The self-administered 'post-cycle therapy' is aimed at the axis suppression the compound genuinely causes but has no evidence base of its own. Two hard facts bound this practice: raised transaminases are the dominant serious adverse event and a published case of drug-induced liver injury followed unsupervised use 78, and grey-market 'ostarine' is frequently mislabelled, underdosed, overdosed or a different SARM entirely, so the milligrams on the label may not be what is in the product. For anyone in tested sport it is a doping violation detectable at picogram levels weeks after the last dose 6.

Enobosarm in cancer-related muscle wasting (phase 2)

published trial

Source: Lancet Oncology, 2013 - Dobs et al.; double-blind randomised placebo-controlled, 159 patients (NCT00467844)

Up to 113 days1 mg or 3 mg enobosarm once daily by mouth, against placebo

Total lean body mass increased significantly in both active groups and not in the placebo group. This trial measured body composition, not survival or symptoms, and the phase 3 programme that followed it did not meet its physical function endpoint - see the POWER protocol below.

Enobosarm with semaglutide for chronic weight management (phase 2 dose-finding)

published trial

Source: ClinicalTrials.gov NCT06282458 - Veru Inc.; completed, 168 participants, primary endpoint percentage change in total lean body mass at day 112

Weeks 1-4enobosarm 3 mg or 6 mg once daily by mouth (or placebo), with semaglutide 0.25 mg once weekly
Weeks 5-8enobosarm unchanged, semaglutide 0.5 mg once weekly
Weeks 9-12enobosarm unchanged, semaglutide 1 mg once weekly
Weeks 13-16enobosarm unchanged, semaglutide 1.7 mg once weekly
Day 112 to day 196enobosarm continued at the assigned dose; semaglutide discontinued

The semaglutide titration here is the standard chronic weight management escalation; the variable under study is the enobosarm dose. The trial is registered as completed but PeptideX has found no peer-reviewed publication of its results as of July 2026, so what is described here is the protocol, not an outcome.

POWER phase 3 in non-small cell lung cancer

published trial

Source: ClinicalTrials.gov NCT01355484 - GTx; 321 patients, co-primary endpoints stair climb power and lean body mass at day 84, results posted to the registry

Day 1 to day 84 (assessed), continuing for the duration of the trialGTx-024 (enobosarm) once daily by mouth, against placebo; the registry record does not state the milligram strength

Included because the result matters more than the schedule. At day 84 the proportion of patients with a stair climb power increase of 10 per cent or more was 29.4 per cent on drug against 24.2 per cent on placebo; the proportion with any increase in lean body mass was 41.9 per cent against 30.4 per cent. The body composition endpoint moved and the functional one did not, and no approval followed.

Schedules are reproduced as their source states them. Units, IU and milligrams explains why the figures are not interchangeable between products.

Reconstitution

An oral tablet or capsule in trials; sold online most often as a dissolved liquid to be taken by mouth. Nothing to reconstitute, and no injectable form exists.

Safety

Side effects

  • Raised hepatic transaminases - the most frequent grade 3 or 4 drug-related adverse event in the phase 2 breast cancer trial, at 4 per cent on 9 mg and 3 per cent on 18 mg 8
  • Drug-induced liver injury has been reported in a published case attributed to enobosarm used outside medical supervision 7
  • Suppression of the hypothalamic-pituitary-gonadal axis, with falls in total testosterone, SHBG and HDL cholesterol - the expected consequence of androgen receptor agonism
  • Hypercalcaemia, reported at 3 per cent in both dose groups of the breast cancer trial 8
  • Fatigue 8
  • In the muscle-wasting trials, adverse event rates were broadly similar to placebo at 1-3 mg daily 12 - the more serious events appear at the higher doses used in oncology
  • Long-term safety is unknown: no trial has exposed anyone for longer than a few months

Do not use if

  • Any athlete in a sport subject to anti-doping rules - enobosarm is named explicitly on the WADA Prohibited List under S1.2 and is prohibited at all times, in and out of competition 5
  • Pregnancy, and any possibility of pregnancy - an androgen receptor agonist during development is a foreseeable harm rather than an unknown one
  • Breastfeeding: no data
  • Children and adolescents: an androgen receptor agonist affects epiphyseal closure and pubertal development
  • Existing hepatic impairment or raised transaminases - hepatotoxicity is the established signal for this compound 78
  • Existing prostate cancer or a raised PSA in men: androgen receptor agonism in that setting is unstudied and the theoretical direction is unfavourable

Interactions

Enobosarm is metabolised in the liver, and a dedicated study examined its pharmacokinetic interactions with itraconazole, rifampin and probenecid. Combination with other hepatotoxic drugs or with alcohol is the interaction of practical concern, given that raised transaminases are the dominant adverse event 78. Effects on lipids and on endogenous testosterone mean it interacts, in a physiological rather than pharmacokinetic sense, with testosterone replacement and with any other androgenic agent. Interactions with GLP-1 receptor agonists were being studied in the current phase 2 programme 4.

Sources