MK-0773 is an experimental oral selective androgen receptor modulator (SARM) developed by Merck. Unlike most SARMs sold online, such as ostarine or ligandrol, it is a steroid: its core is a 4-azasteroid, the same ring system used in the hair-loss and prostate drugs finasteride and dutasteride.
Merck tested MK-0773 as a treatment for sarcopenia (age-related loss of muscle mass and strength). Its one published randomized trial, in 170 frail older women, is often cited in discussions of whether SARMs do more than add lean mass. The drug raised lean body mass by about 1 kg more than placebo over 6 months, but did not improve strength or physical function more than placebo, and it raised liver enzymes and hematocrit. MK-0773 was never approved, and no trials of it have appeared on ClinicalTrials.gov since 2009.
This page summarizes what the published trial, trial registries and regulators report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | Steroidal (4-aza-steroid) selective androgen receptor modulator |
| Other names | MK0773; also listed in PubChem as PF-05314882 |
| Developer | Merck Research Laboratories |
| Route | Oral tablet, twice daily in trials |
| Doses studied in trials | 25 mg and 100 mg twice daily (phase 1, women); three 25 mg tablets twice daily (phase 1, older men); 50 mg twice daily (phase 2a) |
| Half-life | No published human value located |
| Highest stage reached | Phase 2a in women with sarcopenia (completed 2009) |
| US status | Not FDA-approved for any use; not named in the DEA Schedule III list |
| WADA status | Prohibited at all times as a SARM (class S1.2, other anabolic agents) |
What it is
MK-0773’s chemical name is N-(3H-imidazo[4,5-b]pyridin-2-ylmethyl)-2-fluoro-4-methyl-3-oxo-4-aza-5α-androst-1-ene-17β-carboxamide: formula C₂₇H₃₄FN₅O₂, molecular weight 479.6 g/mol (PubChem). “4-aza” means a nitrogen atom replaces carbon 4 in the steroid’s A-ring. Doping-control chemists describe it, alongside YK-11, as a steroidal SARM in a class that is otherwise mostly nonsteroidal (Thevis and Schänzer, Mol Cell Endocrinol 2018; Lagojda et al., Eur J Mass Spectrom 2016).
Merck’s 2010 discovery paper explains the design logic (Schmidt et al., J Biol Chem 2010):
- The team screened more than 1,000 synthetic androgen receptor ligands in cell assays, which ranged from no activity to full agonist activity.
- In ovariectomized rats, ligands that activated the receptor only partially (40–80% of a full agonist) and recruited coactivator proteins weakly still built bone, with smaller effects on the uterus and sebaceous (oil) glands.
- The authors concluded that moderate receptor activation can produce a full anabolic response, while reproductive tissues need more complete activation. MK-0773 was selected using these criteria.
The tissue-selectivity evidence behind this design is from cell assays and rats. Whether the same separation holds in people is a question for the human trials below.
5α-reductase inhibition
Because MK-0773 shares the 4-azasteroid scaffold with finasteride, a 2026 laboratory study tested it against 5α-reductase type 2, the enzyme that converts testosterone to DHT in reproductive tissues. In an enzyme assay, MK-0773 was a moderate inhibitor with an IC50 (the concentration that blocks half of the enzyme’s activity) of 1.70 µM. Computer modeling suggested it does not bind the enzyme covalently the way finasteride does (Kędzierski et al., Toxicol Lett 2026). This is an in-vitro finding; it has not been studied in people.
Pharmacokinetics
Human pharmacokinetic data for MK-0773 have not been published in a peer-reviewed paper we could locate. Merck’s phase 1 studies were registered as pharmacokinetic studies, but no results were posted (NCT01011725; NCT01017458). We therefore do not give a half-life.
What is documented:
| Finding | Detail | Source |
|---|---|---|
| Dosing in trials | Twice daily; in the phase 2a trial, tablets were taken about 12 h apart | Papanicolaou et al., 2013 |
| Drug interactions | The phase 2a trial excluded people taking strong inhibitors or inducers of CYP3A4, a liver enzyme that breaks down many drugs | Papanicolaou et al., 2013 |
| Metabolism (human liver microsomes, in vitro) | At least 10 monooxygenated metabolites; hydroxylation of the methyl group on the A-ring nitrogen was especially prominent; at least two N-oxygenated metabolites | Lagojda et al., 2016 |
The metabolism study was done in lab preparations because, in the authors’ words, there were no controlled elimination studies in people. Its purpose was to give doping laboratories metabolites to test for.
Clinical development
ClinicalTrials.gov lists three Merck studies of MK-0773, all completed between 2008 and 2009:
| Study | Population | Design | Status |
|---|---|---|---|
| NCT01011725 (phase 1) | 67 healthy postmenopausal women | MK-0773 25 mg or 100 mg twice daily vs placebo, 12 weeks | Completed 2009; no results posted |
| NCT01017458 (phase 1) | 68 healthy men aged 50–75 | Three 25 mg MK-0773 tablets twice daily vs testosterone enanthate 200 mg injection every 14 days vs placebo, 12 weeks | Completed 2008; no results posted |
| NCT00529659 (phase 2a) | 170 women aged 65 and older with sarcopenia | MK-0773 50 mg twice daily vs placebo, 6 months | Completed 2009; results posted and published |
Two facts about the phase 1 work come from the phase 2a paper (Papanicolaou et al., J Nutr Health Aging 2013):
- In a 12-week phase 1 study in postmenopausal women, MK-0773 increased appendicular lean body mass (lean mass in the arms and legs) without signs of skin androgenization.
- The 100 mg twice-daily dose caused liver test (transaminase) abnormalities at a rate Merck considered unacceptable for further clinical development. That is why the phase 2a trial used 50 mg twice daily.
No later MK-0773 trials appear on ClinicalTrials.gov, and the drug was never approved.
What the research shows
Sarcopenia in older women (phase 2a)
The only published efficacy trial was randomized, double-blind and placebo-controlled, run at sites in 15 countries (Papanicolaou et al., 2013). It enrolled 170 women aged 65 and older (mean age 75.9) who had low muscle mass and mobility problems. Of these, 81 received MK-0773 50 mg twice daily and 89 received placebo for 6 months; 136 (80%) completed treatment. All participants also received a protein drink (25–35 g protein/day) and vitamin D (2,800–5,600 IU/week).
Changes from baseline at 6 months:
| Outcome | MK-0773 | Placebo | Difference (95% CI) | p |
|---|---|---|---|---|
| Total lean body mass | +1.26 kg | +0.29 kg | 1.00 kg (0.59–1.41) | under 0.001 |
| Appendicular lean body mass | +0.72 kg | +0.15 kg | 0.56 kg (0.35–0.78) | under 0.001 |
| Leg press, one-repetition maximum | +17.4 lb | +16.0 lb | 5.19 lb (−4.04 to 14.43) | 0.269 |
| Stair-climbing power | +19.7 W | +15.0 W | 5.03 W (−3.10 to 13.16) | 0.224 |
| SPPB score (0–12 physical performance scale) | +0.92 | +0.88 | 0.15 (−0.38 to 0.68) | 0.576 |
| Gait speed | +6.2 cm/s | +8.9 cm/s | −1.49 cm/s (−6.79 to 3.82) | 0.581 |
| Total fat mass | +0.84 kg | +1.12 kg | −0.48 kg (−1.19 to 0.23) | 0.186 |
| Bone mineral content | +0.02 kg | 0.00 kg | 0.02 kg (−0.01 to 0.04) | 0.137 |
Key points from the trial:
- Lean mass rose, function did not separate from placebo. Most of the lean-mass effect appeared by month 3. Leg-press strength was significantly better than placebo at month 1 only, not at months 3 or 6.
- Both groups improved. Strength and physical performance rose from baseline in both arms. The authors suggested the protein and vitamin D supplements may explain much of the placebo group’s improvement.
- DXA limits. The scan used to measure lean mass (dual-energy X-ray absorptiometry) cannot separate muscle from fluid. The authors noted that part of the gain could be fluid, although they considered this unlikely.
- Dose ceiling. The tested dose was capped by liver toxicity at a higher dose, and the trial had no exercise component. The authors wrote that a higher dose, longer treatment or added strength training might be needed to show a functional benefit, but this was never tested.
MK-0773 in the wider SARM evidence
A 2025 systematic review pooled 9 randomized trials with 970 participants testing six SARMs, including MK-0773, LGD-4033 and enobosarm (ostarine). It concluded that SARMs have a positive effect on body composition and physical performance, with moderate rates of mild-to-moderate side effects (Wen et al., Clin Endocrinol 2025). The MK-0773 trial itself is a reminder that a gain in lean mass measured by DXA does not automatically mean better strength or function.
No trial has tested MK-0773 in young adults or alongside exercise training, and the 12-week phase 1 study in men has not been published.
Side effects and risks
All quantified human safety data come from the phase 2a trial in older women (Papanicolaou et al., 2013; NCT00529659 results).
| Event | MK-0773 (n = 81) | Placebo (n = 89) |
|---|---|---|
| Any drug-related adverse event | 18.5% | 9.0% |
| ALT (liver enzyme) increased | 6.2% | 1.1% |
| AST (liver enzyme) increased | 4.9% | 1.1% |
| Hematocrit increased | 4.9% | 0% |
| Hemoglobin increased | 2.5% | 0% |
| Serious adverse events (registry) | 12 participants | 9 participants |
Liver enzymes
Transaminase elevations were the main safety signal and the most common reason for stopping the drug. Five women, all on MK-0773, were withdrawn because of transaminase elevations that were classed as serious. Their levels returned to normal after stopping. All five cases occurred 6–8 weeks after starting treatment, the same window seen in the earlier phase 1 study. At 100 mg twice daily, liver abnormalities were frequent enough to rule that dose out (Papanicolaou et al., 2013).
NIH’s LiverTox notes that SARMs sold in supplements have been linked to multiple cases of severe cholestatic jaundice resembling anabolic steroid jaundice (LiverTox: SARMs). That statement covers the class; no such cases specific to MK-0773 were found.
Blood counts and blood pressure
- Hemoglobin and hematocrit (the share of blood made up of red cells) rose on MK-0773, by about 0.6 g/dL and about 2% more than placebo at 6 months. Neither curve had leveled off by the end of the trial. The authors called the rise clinically meaningful and an expected androgen effect.
- Systolic blood pressure rose 2.84 mmHg on MK-0773 and fell 2.39 mmHg on placebo, a gap of about 5 mmHg that persisted through the study.
- No difference in cardiovascular events was seen, but people with heart disease were excluded from the trial.
Androgenic effects in women
Acne and hirsutism (male-pattern hair growth) scores did not rise significantly more on MK-0773 than on placebo over 6 months, and the authors reported no evidence of androgenization (Papanicolaou et al., 2013). This was the main tissue-selectivity finding in humans. Effects on hormones, fertility, the prostate or lipids in men have not been published.
Unknowns
- No long-term safety data exist; the longest exposure studied was 6 months.
- Effects on testosterone, LH and FSH, and sperm production have not been reported in a published human study, and the phase 2a paper did not report cholesterol results.
- The in-vitro 5α-reductase inhibition has not been studied in people.
Legal status and use outside medicine
- FDA. MK-0773 was never approved. FDA states that SARMs are not FDA approved and “cannot be legally marketed in the U.S. as a dietary supplement or drug at this time.” It lists reported risks of SARMs as a class, including liver injury, heart attack and stroke, and infertility (FDA consumer update).
- DEA. MK-0773 is not among the anabolic steroids named in Schedule III (21 CFR 1308.13).
- Sport. The 2026 WADA Prohibited List bans SARMs at all times under S1.2, other anabolic agents. MK-0773 is not one of the named examples, but the class is listed as “including but not limited to” (WADA 2026 Prohibited List). Anti-doping and forensic laboratories have characterized MK-0773 metabolites and added the drug to urine and hair screening methods (Lagojda et al., 2016; Stacchini et al., J Pharm Biomed Anal 2021; Gheddar et al., J Chromatogr B 2021).
Products sold online as MK-0773 come from outside any regulated drug supply, and their content has not been verified.
Key takeaways
- A steroidal SARM. MK-0773 is a 4-azasteroid, structurally related to finasteride, designed by Merck to activate the androgen receptor only partially.
- More lean mass, not more function. In 170 frail older women, 50 mg twice daily for 6 months added about 1 kg of lean mass over placebo, but strength, stair climbing, gait speed and SPPB scores were no better than placebo.
- Liver enzymes limited the dose. 100 mg twice daily caused unacceptable transaminase abnormalities in phase 1, and at 50 mg twice daily five women stopped because of transaminase rises.
- Androgen-type effects still appeared. Hemoglobin, hematocrit and systolic blood pressure rose, although acne and hirsutism did not.
- Development ended without approval. No trials have appeared on ClinicalTrials.gov since 2009, no human half-life has been published, and MK-0773 is prohibited in sport as a SARM.
Sources
- Papanicolaou DA, Ather SN, Zhu H, et al. A phase IIA randomized, placebo-controlled clinical trial to study the efficacy and safety of the selective androgen receptor modulator (SARM), MK-0773 in female participants with sarcopenia. J Nutr Health Aging. 2013;17(6):533–543. PubMed.
- Merck Sharp & Dohme LLC. A Phase IIa Randomized, Placebo-Controlled Clinical Trial to Study the Efficacy and Safety of MK-0773 in Patients With Sarcopenia (NCT00529659). ClinicalTrials.gov.
- Merck Sharp & Dohme LLC. A Randomized, Double-Blind, Placebo-Controlled, Multiple-Dose Study to Assess the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamic Efficacy of MK0773 in Healthy Postmenopausal Women (NCT01011725). ClinicalTrials.gov.
- Merck Sharp & Dohme LLC. A Randomized, Double-Blind, Placebo-Controlled, Double-Dummy, Multiple-Dose Study to Assess the Safety, Tolerability, Pharmacokinetics, and Pharmacodynamic Endpoints of MK0773 in Healthy Older Men (NCT01017458). ClinicalTrials.gov.
- Schmidt A, Kimmel DB, Bai C, et al. Discovery of the selective androgen receptor modulator MK-0773 using a rational development strategy based on differential transcriptional requirements for androgenic anabolism versus reproductive physiology. J Biol Chem. 2010;285(22):17054–17064. PubMed.
- Lagojda A, Kuehne D, Krug O, et al. Identification of selected in vitro generated phase-I metabolites of the steroidal selective androgen receptor modulator MK-0773 for doping control purposes. Eur J Mass Spectrom (Chichester). 2016;22(2):49–59. PubMed.
- Kędzierski J, van Diest RE, Allard JA, et al. Identification of xenobiotics interfering with 5α-reductase (SRD5A2) activity. Toxicol Lett. 2026;418:111859. PubMed.
- Thevis M, Schänzer W. Detection of SARMs in doping control analysis. Mol Cell Endocrinol. 2018;464:34–45. PubMed.
- Stacchini C, Botrè F, Comunità F, et al. Simultaneous detection of different chemical classes of selective androgen receptor modulators in urine by liquid chromatography-mass spectrometry-based techniques. J Pharm Biomed Anal. 2021;195:113849. PubMed.
- Gheddar L, Raul JS, Kintz P. Development and validation of SARMs and metabolic modulators screening in hair using UHPLC-MS/MS: Application to a doping case and first identification of S23 in authentic human hair. J Chromatogr B Analyt Technol Biomed Life Sci. 2021;1187:123048. PubMed.
- Wen J, Syed B, Leapart J, et al. Selective Androgen Receptor Modulators (SARMs) Effects on Physical Performance: A Systematic Review of Randomized Control Trials. Clin Endocrinol (Oxf). 2025;102(1):3–27. PubMed.
- Hoofnagle JH. Selective Androgen Receptor Modulators. In: LiverTox: Clinical and Research Information on Drug-Induced Liver Injury. National Institute of Diabetes and Digestive and Kidney Diseases; 2012–. PubMed.
- National Center for Biotechnology Information. PubChem Compound Summary for CID 11950726, MK-0773. PubChem.
- US Food and Drug Administration. FDA Warns of Use of Selective Androgen Receptor Modulators (SARMs) Among Teens, Young Adults. Consumer Update; 2023. FDA.
- Drug Enforcement Administration. Schedules of controlled substances: Schedule III. 21 CFR 1308.13. eCFR.
- World Anti-Doping Agency. World Anti-Doping Code International Standard: Prohibited List 2026. WADA.