EmergingResearch compound

MK‑2866 (Ostarine, Enobosarm)

Non-steroidal SARM (Enobosarm), GTx Inc 2007. The SARM with the MOST clinical trial data: Phase II cachexia (Dalton 2011 PMID 21833506, 159 patients), Phase III POWER cancer-cachexia trials (Crawford 2016 PMID 26944362). The most popular SARM on the bodybuilding market, UGL marketing under 'soft first-SARM' label. WADA-banned S1.2.

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MK-2866 (Ostarine, Enobosarm) vial

WHAT IS MK-2866 (OSTARINE, ENOBOSARM)?

Detailed overview

Ostarine (MK-2866, Enobosarm, GTx-024, S-22) is a non-steroidal selective androgen receptor modulator (SARM) developed by GTx Inc. (Memphis, USA) in 2007. Structurally an aryl-propionamide derivative (NOT a steroid), AR-binding affinity ~30-40% of testosterone-level in vitro (Bhasin 2012 PMID 22573713). Clinical development: the MOST clinically tested molecule of the SARM class – Phase I 2007-2010, Phase II 2010-2012 cancer-cachexia (Dalton 2011 PMID 21833506 – 159 patients, 16 weeks, 1-3 mg/day, result: 1.3 kg lean body mass gain @ 3 mg vs placebo), Phase III POWER 1+2 trials 2013-2016 non-small-cell lung cancer cachexia (Crawford 2016 PMID 26944362 – NCT01355484/NCT01355497, ~600 patients, 3 mg/day, result: lean body mass + physical function co-primary endpoints STATISTICALLY did NOT reach clinical-meaningfulness threshold → Phase III FAILED). GTx halted clinical development for cachexia indication after 2016, later focused on urinary incontinence (Asahi, Phase II, 2018) + breast cancer (ER+ adjunct, Phase II, 2017) trials, but FDA approval still pending. On the bodybuilding market the MOST POPULAR SARM, UGL marketing as 'soft first-SARM' (lower HPTA suppression than RAD/LGD, more moderate hepatotoxicity). Hepatotoxicity cases documented (4+ known cases, Vilaca 2018 PMID 30171122 review), but rarer than RAD/LGD. WADA-banned year-round (S1.2 – other anabolic agents) since 2008 – common target since 2013.

Mechanism

Non-steroidal selective AR modulator (aryl-propionamide). Strong AR agonist in muscle, moderate prostate.

Anabolic activity (Dalton 2011)

1.3 kg lean body mass gain @ 3 mg/day, 16 weeks, cancer cachexia patients.

Half-life

~24 h (oral)

Onset

2-4 weeks

Legal status

Never FDA-approved (Phase III POWER failed 2016). UGL 'research chemical'. WADA-banned S1.2.

Data console

Lab data

/lab/molecular-data.jsonLIVE
> Androgenic:Anabolic~50:20 (muscle:prostate selectivity – high, better than LGD).
> AR bindingNon-steroidal SARM, AR-binding affinity ~30-40% of testoste…
> Active half-life~24 h
> Detection windowUrinary: 2-4 weeks Ostarine metabolites by LC-MS/MS (WADA-accredited). The most common cause of NFL/MLB suspension cases between 2015-2020.
> AromatizationNO – non-steroidal, NOT a CYP19 substrate. E2 does not rise (Dalton 2011 Phase II).
> Hepatotoxicity**Moderate-high – 4+ documented hepatocellular injury case reports (Vilaca 2018 PMID 30171122). In clinical trials (Dalton 2011, Crawford 2016) ALT/AST elevation moderate (~1.5-2x normal at 3 mg).** At UGL doses (20-30 mg/day) more severe. TUDCA + milk-thistle + monthly ALT/AST recommended (not strictly mandatory, but strongly suggested).

Safety

Side effects, stop signs, contraindications

Side effects · 7

  • HPTA suppression: lowered testosterone, LH and FSH. At the clinical 3 mg/day dose Total T fell ~23% (Dalton 2011); at UGL doses (20-30 mg/day) suppression can be complete, with reduced libido and lethargy.
  • Adverse lipid profile: HDL ("good" cholesterol) drops ~20-30%, a class effect of SARMs. Longer or high-dose use shifts the cardiovascular risk profile unfavourably.
  • Hepatotoxicity (drug-induced liver injury, DILI): at least 4+ documented hepatocellular injury case reports (Vilaca 2018). In trials ALT/AST rose moderately (~1.5-2x); worse at UGL doses. Mechanism: a CYP3A4-mediated reactive metabolite (Solomon 2019).
  • Androgenic effects: hair loss (androgenic alopecia) in genetically predisposed users, plus acne. Milder than with more androgenic SARMs (e.g. RAD-140), but present.
  • Virilisation in women: at higher doses masculinisation (voice deepening, increased body hair, clitoral enlargement), which can be partly irreversible. Voice deepening is permanent.
  • Insomnia and lethargy: sleep disturbance and fatigue are commonly reported, partly secondary to HPTA suppression.
  • Slow clearance due to the long half-life (~24 h): if a side effect appears, the compound cannot be stopped quickly and effects persist for days.

Contraindications · 7

  • Pregnancy and breastfeeding: absolutely contraindicated due to the risk of fetal androgenisation and virilisation of a female fetus.
  • Pre-existing liver dysfunction or elevated liver enzymes: avoid given the documented DILI cases.
  • Concurrent alcohol use or other hepatotoxic agents (e.g. other oral SARMs, 17-alpha-alkylated steroids): cumulative liver burden.
  • Planned fatherhood / fertility window: due to HPTA suppression and reduced sperm parameters; full recovery takes 2-4 months.
  • Competitive athletes: banned by WADA year-round (S1.2 "other anabolic agents"), urine detection window 2-4 weeks. The most frequent cause of doping suspensions in 2015-2020.
  • Undiagnosed or androgen-sensitive conditions (e.g. prostate disease, hormone-sensitive tumours): avoid without medical evaluation.
  • Pre-existing dyslipidaemia or cardiovascular risk: the HDL drop further worsens the lipid profile.

Related Performance Compounds

Same therapeutic category

Studies

Related research and clinical findings

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MolekulaX Editorial Team·Source-verified · PubMed · FDA · EMA
Updated: June 19, 2026

The information here is for educational and scientific purposes only. Performance-enhancing compounds (AAS, prohormones, stimulants, doping agents) are illegal without prescription in Hungary and most of the EU, and carry serious health and legal risks. WADA bans them in competitive sport. This is NOT a usage guide, and we do not encourage any illegal use. If you do use them, medical supervision and regular bloodwork are ESSENTIAL. Severe endocrine, cardiovascular, hepatic and psychiatric side effects are possible.