MK-677 side effects reported in human trials, study by study

MK-677 side effects reported in human trials include raised fasting glucose, lower insulin sensitivity, increased appetite, lower-limb oedema and muscle pain, and one hip-fracture trial was stopped early over a congestive heart failure signal. MK-677, also known as ibutamoren or MK-0677, is an investigational drug that was studied in a series of human trials published between 1996 and 2018. This guide walks through the published MK-677 clinical trials one at a time and sets out the MK-677 side effects reported in those that describe them: who took part, what was measured, what the numbers showed, what went wrong, and what the published results do and do not show.

Key takeaways

• Published human trials of ibutamoren span 4 days to 2 years and enrolled very different groups: healthy older adults, obese men, growth-hormone-deficient adults and children, hip-fracture patients, people with Alzheimer disease and dialysis patients.
• In nearly every trial that reported it, the drug raised blood levels of insulin-like growth factor 1 (IGF-1), a hormone made in response to growth hormone. That shows the drug engaged its target.
• Higher IGF-1 did not translate into clearer clinical benefit. The Alzheimer trial found no effect on disease progression, and the hip-fracture trials found no significant difference in most functional measures (one measure, gait speed, differed in the 2011 paper). The 2-year trial in healthy older adults found no change in strength or function, though the authors said it was underpowered to evaluate function.
• Trials repeatedly reported higher fasting glucose or reduced insulin sensitivity, and a hip-fracture trial published in 2011 was stopped early over a congestive heart failure signal.
• The randomised fat-free mass data in these papers come from older adults (Nass 2008) and obese men (Svensson 1998a). No randomised trial retrieved for this guide studied healthy, resistance-trained young adults; see the first item under "What the research does not tell us".
• Long-term safety, including cancer incidence and mortality, has not been established.
• For the main adverse findings from the human studies, case reports and reviews in one place, see the MK-677 side effects table; for how MK-677 differs from ipamorelin, IGF-1 LR3 and somatropin (HGH), see the comparison section.
• Ibutamoren is described in the literature as investigational. Nothing in this article is medical advice.

What is MK-677 (ibutamoren)?

Ibutamoren is a small, non-peptide molecule designed to be absorbed from the gut and to stimulate the release of growth hormone (GH). The names MK-677, MK-0677 and ibutamoren mesylate all refer to the same compound in the literature. A review by Smith describes this class, the growth hormone secretagogues, as the product of "reverse pharmacology": researchers built molecules that worked on a function before they knew which receptor or natural hormone was involved (Smith, 2005).

The human trials discussed here are described as oral in their titles or abstracts, apart from the Adunsky and Sevigny papers, whose abstracts do not state the route; a review describes ibutamoren as orally available (Sigalos and Pastuszak, 2018). The doses and schedules used in each paper are given in the paper itself, and this article deliberately does not repeat them. Participants were patients or volunteers in trial settings, and nothing in this guide should be read as describing what would happen in anyone else.

A plain-English note on terms. Growth hormone is released by the pituitary gland in pulses. IGF-1 is a hormone whose blood level rises when GH release increases, and it is the number most trials used as a marker of whether the GH system was being stimulated.

How researchers think it works

Ibutamoren acts on the ghrelin receptor (called GHS-R or GHSR in the cited papers). Ghrelin is often called the "hunger hormone" (Liu et al., 2021), and the same receptor also governs GH release from the pituitary. Smith reports that the receptor is found mainly in the brain, pituitary gland and pancreas, and that studies in mice lacking the receptor support the view that these drugs mimic ghrelin (Smith, 2005). The same review proposes four routes by which the drugs raise GH pulses: more GH-releasing hormone, stronger GH-releasing hormone signalling, less somatostatin release and blocking of somatostatin signalling.

In receptor binding and signalling assays, MK-677 behaved as a simple agonist, meaning it switched the receptor on, with a binding affinity of 6.5 nM and a potency of 0.2 to 1.4 nM (nanomolar) across several signalling read-outs. It did not boost or dampen ghrelin's own signal, which the authors described as neutral modulation (Holst et al., 2005). A 2021 cryo-electron microscopy paper then produced detailed three-dimensional structures of the receptor bound to ghrelin and to ibutamoren, which it calls an investigational new drug (Liu et al., 2021).

Because the receptor also drives appetite, the increased appetite reported in Nass et al., 2008 makes biological sense. That is an interpretation of the mechanism, not a finding of that trial.

Key studies at a glance

Smaller trials in children, dialysis patients, sleep research and bone and lipid markers are covered below.

The evidence, study by study

This section describes the 14 human studies covered in this guide. Every outcome below describes what happened to the named participants in that study. None of it can be assumed to apply to anyone else, and each study's adverse findings and limitations are reported alongside its results.

Chapman et al., 1996: healthy older adults and the GH axis

This randomised, double-blind, placebo-controlled trial enrolled 32 healthy volunteers (15 women, 17 men) aged 64 to 81. Participants received placebo or one of three oral dose levels across two study periods of 14 and 28 days. Blood was drawn every 20 minutes for 24 hours to track GH release (Chapman et al., 1996).

In the highest-dose group, mean 24-hour GH rose 97 plus or minus 23% after two weeks, through larger pulses rather than more of them. IGF-1 climbed from 141 to 219 micrograms/L at two weeks and 265 micrograms/L at four weeks, a level the authors described as typical of young adults. Cortisol was unchanged and prolactin rose 23% while staying within the normal range.

The adverse metabolic finding was clear: fasting glucose increased from 5.4 to 6.8 mmol/L at four weeks (P below 0.01 against baseline). The trial was short and small, so it says nothing about longer-term effects.

Chapman et al., 1997: severely GH-deficient men

Nine men aged 17 to 34 with severe GH deficiency, previously treated with GH in childhood, took part in a double-blind, rising-dose study lasting four days per period, with at least 28 days between periods (Chapman et al., 1997). IGF-1 rose 52% (65 to 99 micrograms/L) at the lower dose and 79% (84 to 150 micrograms/L) at the higher dose. Twenty-four-hour mean GH rose 79% and 82%.

The GH response was larger in men who were least GH-deficient at baseline; IGF-1 responses were not significantly related to any baseline measurement. Fasting and post-meal insulin and post-meal glucose all increased significantly, and the authors said longer studies would be needed to judge the clinical meaning. Cortisol, prolactin and thyroid hormones did not change significantly. With nine participants and four-day periods, the study is a pharmacology snapshot.

Murphy et al., 1998: calorie restriction and nitrogen balance

Eight healthy volunteers aged 24 to 39 took part in a double-blind, placebo-controlled crossover study in which each ate a calorie-restricted diet for two 14-day periods, receiving drug or placebo during the second week of each (Murphy et al., 1998). Nitrogen balance, the study's measure of diet-induced protein catabolism, was slightly positive on the drug (0.31, a daily average in grams of nitrogen) and clearly negative on placebo (-1.48; P below 0.01). Peak GH was 55.9 micrograms/L after the first dose and 22.6 after a week. IGF-1 averaged 264 ng/mL against 188 ng/mL on placebo.

The abstract reports no clinically significant adverse experiences in these eight volunteers; the limits are obvious: eight people, one week of treatment, and a dieting setting that does not resemble ordinary life.

Svensson et al., 1998a: obese men and body composition

Twenty-four obese men aged 18 to 50 were randomised, double-blind, to the drug (12) or placebo (12) for eight weeks (Svensson et al., 1998a). IGF-1 rose about 40%. Fat-free mass increased significantly by DXA scanning and by a four-compartment model, while total and visceral fat did not change significantly. Basal metabolic rate was higher at two weeks but not at eight.

The adverse finding was that fasting glucose and insulin were unchanged but an oral glucose tolerance test showed impaired glucose handling at both two and eight weeks. The authors noted that a higher dose or longer treatment might be needed to see any effect on body fat, so the study's fat-loss question remained open.

Svensson et al., 1998b and 1999: bone and lipid markers in obese men

Two further reports described bone markers and blood fats in obese men in a study of the same design (24 men, 12 on the drug and 12 on placebo, 8 weeks); the abstracts do not say whether these were the same participants as in the 1998a paper. For bone, markers of formation (a 23% rise in one procollagen marker and a 28% rise in another at two weeks, osteocalcin up 15% at eight weeks) and of resorption (a 26% rise in one marker at eight weeks, plus 23% and 46% rises in urinary ratios) all increased (Svensson et al., 1998b). These are blood and urine markers of bone turnover, not measurements of bone strength, and the authors called for longer studies to see whether bone mass changes.

For lipids, lipoprotein(a) did not change significantly, HDL cholesterol and triglycerides rose at two weeks but not at eight, and the LDL to HDL ratio fell at eight weeks (Svensson et al., 1999). The abstract describes the changes in apoA-I, apoE, triglycerides and LDL particle diameter as transient, and does not interpret them as harmful or beneficial; the sample was 24 men.

Murphy et al., 1999: three trials in elderly adults and bone turnover

This paper reported three randomised, double-blind, placebo-controlled studies lasting 2 to 9 weeks in 187 adults aged 65 or over, including 105 who met criteria for functional impairment (Murphy et al., 1999). In the first two studies IGF-1 rose 55 to 94%; the abstract gives no IGF-1 figure for the 9-week functional-impairment study. In that study, osteocalcin, bone-specific alkaline phosphatase and urinary N-telopeptide rose by 29.4%, 10.4% and 22.6% respectively (all differences against placebo statistically significant). Rises in both formation and resorption markers point to faster bone turnover, not to proven bone gain. The studies were short, and the abstract reports no clinical bone outcomes.

Copinschi et al., 1997: sleep recordings

Sleep laboratories tested the drug in eight young adults (three-period crossover, 7 days each) and six older adults aged 65 to 71 (two 14-day periods) (Copinschi et al., 1997). In young volunteers, stage IV sleep duration rose roughly 50% and REM sleep more than 20% against placebo. In the older group, REM sleep rose nearly 50%. The abstract describes no placebo period for the older group. These are laboratory sleep-stage measurements in very small groups. The abstract does not report adverse events or any daytime outcome, so it cannot show that anyone slept better in ordinary terms.

Codner et al., 2001: children with GH deficiency

Eighteen prepubertal children (15 boys, 3 girls) with idiopathic GH deficiency received ibutamoren mesylate for 7 to 8 days, with dose chosen per kilogram of body weight and shown in the paper (Codner et al., 2001). At the higher level, median GH peak rose 3.8 micrograms/L and IGF-1 rose 12 micrograms/L. Prolactin, glucose, insulin, thyroid hormones and cortisol measures did not change. The authors concluded the drug could now be tested for effects on growth velocity. The abstract says hormone levels rose in some children, with wide ranges between individuals (GH peak change 0 to 34.3 micrograms/L). The abstract states that safety and tolerability were evaluated but does not report adverse events; with 18 children and 7 to 8 days of treatment, it measured hormone levels only, not growth.

Nass et al., 2008: the 2-year trial in healthy older adults

This is the longest trial. Sixty-five healthy adults aged 60 to 81 were randomised, double-blind, to the drug or placebo in a modified crossover design over two years (Nass et al., 2008). At 12 months, fat-free mass changed by -0.5 kg on placebo and +1.1 kg on the drug (P below 0.001). Body weight rose 0.8 kg on placebo and 2.7 kg on the drug (P = 0.003). Visceral and total fat did not differ significantly, although limb fat rose more with the drug (1.1 kg against 0.24 kg).

The adverse and limiting findings matter as much. Fasting glucose rose by an average of 0.3 mmol/L and insulin sensitivity fell. The commonest side effects were increased appetite that eased within months, and transient, mild lower-limb swelling (oedema) and muscle pain. Cortisol rose, and bone density changes consistent with faster remodelling occurred. Critically, the added fat-free mass did not produce changes in strength or function, and the authors acknowledged that the study was underpowered for function in healthy older people.

Bach et al., 2004: hip fracture, 6 months

One hundred and sixty-one patients aged 65 or over, recruited between 3 and 14 days after surgery, or within 18 days of the fracture, at 13 centres in seven countries, were randomised to six months of drug or placebo and followed for six months afterwards (Bach et al., 2004). IGF-1 rose 84% (95% CI 63 to 107) on the drug and 17% on placebo. Functional performance measures and the overall Sickness Impact Profile score did not differ significantly. Some measures leaned in the drug's favour but not to a statistically significant degree. The authors said it was uncertain whether any clinically meaningful physical benefit had been achieved, and noted weaknesses in how function is measured after hip fracture.

Adunsky et al., 2011: the phase IIb hip-fracture trial that stopped early

A later phase IIb study randomised 123 elderly hip-fracture patients to the drug (62) or placebo (61) (Adunsky et al., 2011). At 24 weeks, IGF-1 was 51.4 ng/mL higher than on placebo (P below 0.001). Gait speed showed a difference (P = 0.011), and stair-climbing power did not differ significantly. Several other functional measures showed no improvement. Fewer falls were recorded in the drug group but the difference was not significant (P = 0.096).

The trial was terminated early because of a safety signal of congestive heart failure in a limited number of patients. The abstract does not give how many. The authors concluded the drug had an unfavourable safety profile in this patient population. This is the only study covered here that reports early termination.

Sevigny et al., 2008: Alzheimer disease, 12 months

The rationale was that IGF-1 helps clear beta-amyloid, a hallmark protein of Alzheimer disease, in animal studies. Five hundred and sixty-three patients with mild to moderate disease were randomised, double-blind, to the drug or placebo for 12 months, and 416 completed (Sevigny et al., 2008). IGF-1 rose 60.1% at six weeks and 72.9% at 12 months, yet there were no significant differences on the CIBIC-plus, ADAS-Cog, ADCS-ADL or CDR-sob scales. The authors concluded the drug was ineffective at slowing progression despite evidence of target engagement.

Campbell et al., 2018: haemodialysis patients

Twenty-six haemodialysis patients enrolled in a randomised, blinded crossover study, and 22 completed the three-month design (Campbell et al., 2018). IGF-1 was 1.76-fold higher after the drug (P below 0.001) and 1.07-fold after placebo. The adjusted difference was a 65% greater rise on the drug (95% CI 33 to 104%). No serious adverse effects were attributed to the drug. The primary outcome was IGF-1, and the authors said studies were needed to evaluate whether long-term therapy affects protein-energy wasting, lean body mass, physical strength, quality of life and survival.

Preclinical work: Jacks et al., 1996, beagles

In a balanced eight-dog crossover study, oral MK-0677 raised peak GH 5.3-fold, 9.0-fold and 15.8-fold across three dose levels, with IGF-1 up 30% at 480 minutes (Jacks et al., 1996). Cortisol rose about 2.4-fold after oral dosing. After intravenous dosing in the dogs, insulin and glucose were higher, LH and prolactin were unaltered and T4 was marginally lower, and the authors reported that each of these hormones stayed within the normal range for dogs. Animal data guide human trials but cannot be read across to people.

Safety signals, case reports and laboratory surveillance

Across the trials, the repeated adverse findings were glucose-related: higher fasting glucose (Chapman 1996; Nass 2008), impaired glucose tolerance (Svensson 1998a) and higher insulin and post-meal glucose (Chapman 1997). A review of growth hormone secretagogues noted some concern over blood glucose because of reduced insulin sensitivity, and concluded that long-term safety, including cancer incidence and mortality, still needs to be established (Sigalos and Pastuszak, 2018).

Outside controlled trials, the human safety literature retrieved for this guide consists of case reports, a surveillance study and a forensic case example. A man in his early thirties developed raised liver enzymes after consuming a MK-677 product, and tests normalised after he stopped (Cobani et al., 2025). Two other reports involved more than one compound and cannot be pinned on ibutamoren alone: a 25-year-old who took a selective androgen receptor modulator together with MK-677 showed changes in lipids, liver enzymes and hormones that mostly reversed afterwards (Cardaci et al., 2022), and a 40-year-old with breast tissue enlargement and low pituitary hormone signalling had consumed supplements found to contain several banned compounds plus undisclosed hormones (Chong et al., 2024). Case reports describe single individuals and cannot show how common a problem is. Anecdotal accounts from online forums are not evidence and are not used here.

Laboratory surveillance adds a quality concern. A European network of official medicines control laboratories examined 324 samples (the majority from illegal distribution) across 18 molecules from 13 countries. Ibutamoren was named first among the five most frequently reported molecules. The authors reported that 65% of the seized products were represented as medicines and 24% as dietary supplements; the abstract does not say how many of the 324 samples were seized products. From limited quantitative data, the authors assumed that most samples contained active doses and some were overdosed. The abstract does not give ibutamoren-specific figures (Barrios et al., 2025). Separately, forensic chemists have shown that ibutamoren can be detected in hair, a finding relevant to anti-doping interpretation: in one volunteer a single exposure gave 1.3 pg/mg in a 0 to 1 cm hair segment, while in one user described as using it for athletic enhancement a 0 to 4 cm segment tested at 224 pg/mg (Kintz and Gheddar, 2026). These are two individuals and different segment lengths, so the two figures are not directly comparable.

What the research does not tell us

• No trial in healthy, resistance-trained young adults. No randomised trial retrieved for this guide studied healthy, resistance-trained young adults. Younger adults appear in a small sleep-laboratory study (Copinschi et al., 1997), a calorie-restriction crossover study in eight healthy volunteers aged 24 to 39 (Murphy et al., 1998), a study in nine GH-deficient men aged 17 to 34 (Chapman et al., 1997), studies of obese men aged 18 to 50 (Svensson et al., 1998a), and in case reports, including one in which a 25-year-old took two compounds together (Cardaci et al., 2022). None of these abstracts describes its participants as resistance-trained, so applying the trial results to resistance-trained young adults is extrapolation.
• Clinical benefit is unproven. The hip-fracture trials, the 2-year trial in healthy older adults and the Alzheimer trial were all negative or inconclusive on function or clinical outcomes.
• Long-term safety is unknown. Long-term safety, including cancer incidence and mortality, has not been established (Sigalos and Pastuszak 2018). The trials above reported glucose changes and, in one trial, a heart failure signal in an unspecified number of patients (Adunsky 2011).
• Population differences. Participants were specific groups in trial settings. Results in dialysis patients or children do not describe anyone else.
• Formulation and purity. The formulation, purity and strength of any commercial product cannot be assumed to match the material used in the trials, and the abstracts used here do not describe how the trial material was made. For the surveillance findings on seized products, see the safety signals section above (Barrios 2025).
• Route. The human trials are described as oral in their titles or abstracts, apart from the Adunsky and Sevigny papers, which do not state the route. Their results cannot be assumed to apply to a commercial product of unknown formulation, or to anyone outside the study populations.
• Pharmacokinetics. No half-life or bioavailability figures for ibutamoren are given in the sources used here, so none are stated.
• Intermediate markers are not outcomes. IGF-1, osteocalcin and sleep-stage minutes are surrogate measures. Trials rarely showed they translated into how people function.

Most trials above were small or short, and the authors repeatedly called for longer studies.

MK-677 results: what the studies actually measured

This section groups the published findings by what was measured and reports the adverse findings and limits from the same papers alongside them. Every figure belongs to the named study group and to no one else.

Hormone markers. The most consistent finding was a rise in IGF-1. In a randomised, double-blind, placebo-controlled trial of 161 hip-fracture patients, serum IGF-1 rose 84% on the drug and 17% on placebo (Bach et al., 2004). In a double-blind trial that randomised 563 patients with mild to moderate Alzheimer disease, serum IGF-1 had risen 72.9% at 12 months on the drug (Sevigny et al., 2008), and in a randomised, blinded crossover study of 22 haemodialysis patients who completed it, the adjusted rise was 65% greater than on placebo (Campbell et al., 2018).

Body composition and metabolism. In the 2-year randomised trial of 65 healthy adults aged 60 to 81, fat-free mass at 12 months changed by 1.1 kg with the drug and -0.5 kg with placebo (Nass et al., 2008). In an eight-week randomised trial of 24 obese men, fat-free mass increased while total and visceral fat did not change significantly (Svensson et al., 1998a). In a crossover study of eight calorie-restricted volunteers, daily nitrogen balance was slightly positive on the drug (0.31) and negative on placebo (-1.48) (Murphy et al., 1998).

Function and clinical outcomes. Higher IGF-1 did not reliably translate into differences in function. The 2-year trial found no change in strength or function, the 2004 hip-fracture trial no significant functional difference, the Alzheimer trial none on four clinical scales, and the 2011 hip-fracture trial a gait-speed difference (P = 0.011) with most other measures unchanged (Adunsky et al., 2011).

Laboratory markers. Bone turnover markers rose in three randomised trials enrolling 187 older adults (Murphy et al., 1999) and sleep-stage durations changed in 8 young adults (Copinschi et al., 1997); these are surrogate laboratory measurements only.

Adverse findings and limits from the same papers. In the 2-year trial, fasting glucose rose by an average of 0.3 mmol/L and insulin sensitivity fell; the most frequent side effects were increased appetite and transient, mild lower-limb oedema and muscle pain. The obese-men study found impaired glucose tolerance, and the 2011 hip-fracture trial was stopped early over a congestive heart failure signal. Most trials were small or short, and the abstracts do not describe how the trial material was made, so none of these results can be assumed to apply to an oral capsule from any commercial source. The next section sets out the main adverse findings.

MK-677 side effects reported in the research

The table lists the adverse findings in the sources for this guide, from trials, case reports, reviews and a market-surveillance study; the last three rows (the two reviews and the market-surveillance study) are not specific to ibutamoren. Each row describes what happened to the named group in that paper.

Case reports need careful reading. A case report describes one person: it can flag a signal worth studying, such as liver enzymes that settled after a product was stopped, but it cannot show how common a problem is or prove its cause, and two of the three involved other compounds.

The data gaps are substantial. The abstracts give no event counts for oedema, appetite or muscle pain, do not say how many hip-fracture patients had heart failure, and report no adverse-event data for several trials (Bach 2004, Sevigny 2008, Murphy 1999, Copinschi 1997). The 2004 hip-fracture trial excluded patients with diabetes mellitus or congestive heart failure, so it cannot speak for them.

MK-677 vs ipamorelin vs IGF-1 LR3 vs HGH (somatropin): how they differ

This section sets out how four compounds that are sometimes discussed together differ. The table compares what each is, how far each has been studied in people, and the anti-doping and legal position as far as the sources establish it. It is not a ranking, and no source retrieved compares any pair head to head.

MK-677 and ipamorelin are both described as ghrelin-receptor agonists acting on the body's own GH release (for ipamorelin, see Beck et al., 2014; Raun et al., 1998), which a review says remains subject to negative feedback (Sigalos and Pastuszak, 2018). Somatropin is the hormone itself, and IGF-1 LR3 acts further downstream.

The evidence bases differ. Among the records retrieved for this guide, MK-677 has the largest set of published human trials; that reflects what was searched, not a ranking of the wider literature. Ipamorelin's human data in these sources are one pharmacokinetic study, one phase 2 trial in a different condition and a one-volunteer urinary metabolite study (Semenistaya et al., 2015), and for IGF-1 LR3 the retrieved evidence is animal and cell work only. Results from infusion, cell or animal studies cannot be assumed to apply to an oral capsule, and a 2026 review stresses uncertainty about the composition of unregulated products (Dominikowski et al., 2026).

Legal and anti-doping status in brief

This is general information, not legal advice. It reflects the legislation text and pages we checked on 2 October 2026.

• Medicines law. The Human Medicines Regulations 2012 define a medicinal product as a substance presented as treating or preventing disease, or one that may be administered to restore, correct or modify a physiological function through a pharmacological, immunological or metabolic action (regulation 2). Regulation 46 says a person may not sell or supply an unauthorised medicinal product (regulation 46). Neither page says whether ibutamoren falls within these definitions, which is a legal question. A 2021 structural paper (Liu et al., 2021) calls it an investigational new drug, and we did not find a marketing authorisation in anything we reviewed. We have not checked a regulator register.
• Controlled drugs. Ibutamoren is not named in the Schedule 2 text of the Misuse of Drugs Act 1971 that we checked on 2 October 2026 (Schedule 2). That says nothing about other legislation.
• Psychoactive Substances Act 2016. Section 2 defines a psychoactive substance by its capacity to affect the central nervous system and mental functioning (section 2). The page does not say whether ibutamoren is or is not covered, and we make no claim either way.
• Anti-doping. According to UK Anti-Doping, the Prohibited List is updated every 1 January, substances of similar structure or biological effect to listed ones are also prohibited, and athletes are strictly liable for anything found in their body. The page text we extracted does not name ibutamoren, so competitors should check the current list directly.
• MHRA context. A 2016 MHRA press release reported on unauthorised medicines sold as sports supplements and said some body-building products on sale in the UK are unacceptable even if considered legitimate elsewhere. It does not mention ibutamoren.

Full breakdown with sources: Is MK-677 legal in the UK?

About the Free Muscle MK-677 listings

Free Muscle sells research compounds and gym apparel online. Research compounds are sold for laboratory research use only, to customers aged 18 or over. They are not medicines or food supplements and not for human consumption. The Free Muscle MK-677 collection lists three products:

• MK-677 Ibutamoren 10mg
• MK-677 Ibutamoren 12.5mg
• MK-677 Ibutamoren 25mg

Strengths shown are product labels, not recommendations.

Every batch of research compounds is assayed for identity and purity by Janoshik Analytical, an independent laboratory. The Certificate of Analysis for a batch is sent on request: email the batch number printed on the label together with the product name, as described on the lab tests page. Our guide on how to read a certificate of analysis explains what the figures mean, and the companion explainer MK-677 (ibutamoren): what the research says is the broader overview of the topic, while this guide is the study-by-study version.

UK delivery is free and tracked, in plain packaging. Standard delivery takes 2 to 5 working days, and orders placed before 2pm UK time Monday to Friday are processed the same working day (shipping information). Unopened items in original packaging can be returned within 30 days (returns guarantee). Nothing on the site or in this article is medical advice.

Frequently asked questions

How many human studies of MK-677 does this guide cover?

This guide covers 14 human studies, from small pharmacology studies of four days to a two-year randomised trial, plus a beagle study and cell and structural work. Several papers describe very similar designs and may overlap in participants, so the number of separate participant groups may be smaller than 14.

What do the MK-677 clinical trials show about muscle?

They measured fat-free mass, not muscle alone. Randomised, placebo-controlled trials in older adults (Nass et al., 2008) and in obese men (Svensson et al., 1998a) reported increases in fat-free mass. The obese-men study also reported impaired glucose tolerance on an oral glucose tolerance test, and the 2-year trial in healthy older adults found no change in strength or function, though the authors said it was underpowered to evaluate function. No randomised trial retrieved for this guide studied healthy, resistance-trained young adults; see the unknowns section above. The same trial also reported higher fasting glucose, lower insulin sensitivity, more appetite, and transient mild lower-limb swelling and muscle pain.

Why was one hip-fracture trial stopped early, and what did the other trials find?

The phase IIb hip-fracture study published in 2011 was terminated early because of a safety signal of congestive heart failure in a limited number of patients (Adunsky et al., 2011). The abstracts of the other trials covered here do not report early termination. The Alzheimer trial found no effect on progression (Sevigny et al., 2008), and the earlier hip-fracture trial found no significant difference in functional performance measures (Bach et al., 2004). For the 2011 trial, the abstract does not say how many patients were affected.

What is the ghrelin receptor (GHSR)?

It is the ghrelin receptor (called GHS-R or GHSR in the cited papers), a protein found mainly in the brain, pituitary and pancreas according to a review (Smith, 2005). Ibutamoren switches it on, and the 2021 structural paper shows how the drug fits into it (Liu et al., 2021).

Was blood sugar affected in the trials?

Several trials reported higher fasting glucose, reduced insulin sensitivity or impaired glucose tolerance in the participants studied (Chapman 1996, Svensson 1998a, Nass 2008). A review noted some concern about increases in blood glucose linked to reduced insulin sensitivity (Sigalos and Pastuszak, 2018).

Is MK-677 legal in the UK?

That is a legal question we cannot settle. Ibutamoren was not named in the Misuse of Drugs Act Schedule 2 text we checked, but the Human Medicines Regulations definition of a medicinal product refers to how a substance is presented and to what it may be used by or administered to humans for (regulation 2, linked in the legal section), and whether ibutamoren falls within it is a legal question. No regulator register was checked. Our companion MK-677 UK legal status guide covers the UK position further. This is general information, not legal advice.

Has ibutamoren been detected in hair tests?

A 2026 forensic paper reported detection in the hair of one volunteer after a single exposure, with a limit of detection of 0.1 pg/mg, and in one user's hair after longer use (Kintz and Gheddar, 2026). Sports bodies publish their own rules, and UK Anti-Doping says athletes are strictly liable for what is found in their system.

Can trial results be assumed to apply to commercial products?

No. Results belong to the study populations, and the abstracts do not describe how the trial material was made. A surveillance study of seized products (Barrios et al., 2025) is summarised in the safety signals section above, including its lack of ibutamoren-specific figures.

What are the most commonly reported MK-677 side effects in studies?

In the 2-year randomised trial of 65 healthy older adults, the most frequent side effects were increased appetite that eased within a few months and transient, mild lower-limb oedema and muscle pain, alongside higher fasting glucose and lower insulin sensitivity (Nass et al., 2008). A 2011 hip-fracture trial was stopped early over a congestive heart failure signal (Adunsky et al., 2011). The side effects table sets out the main adverse findings reported in the human studies, case reports and reviews used for this guide.

Does MK-677 increase hunger, according to the research?

Increased appetite was among the most frequent side effects in the 2-year trial and subsided within a few months (Nass et al., 2008). The receptor involved is the ghrelin receptor, and ghrelin is often called the hunger hormone (Liu et al., 2021). A review of GH secretagogues also lists appetite stimulation among the changes described (Sigalos and Pastuszak, 2018). These findings describe the study participants only.

What did the MK-677 trials measure?

In a randomised, double-blind, placebo-controlled trial of 32 healthy adults aged 64 to 81, serum IGF-1 rose, and fasting glucose rose too (Chapman et al., 1996). IGF-1 also rose in the groups studied in a hip-fracture trial (Bach et al., 2004), an Alzheimer trial (Sevigny et al., 2008) and a haemodialysis crossover study (Campbell et al., 2018). The 2004 hip-fracture trial found no significant difference in functional performance measures, and the Alzheimer trial found no significant difference on its four clinical scales; the haemodialysis abstract reports IGF-1 only. The 2-year trial in 65 healthy older adults reported higher fasting glucose and lower insulin sensitivity (Nass et al., 2008), and a 2011 hip-fracture trial was stopped early over a congestive heart failure signal (Adunsky et al., 2011). These findings describe the study participants only. The results section gives the measured figures and the adverse findings together.

How does MK-677 differ from HGH and ipamorelin?

MK-677 and ipamorelin are both described as ghrelin-receptor agonists that act on the body's own GH release (for ipamorelin, see Beck et al., 2014; Raun et al., 1998), whereas somatropin is growth hormone itself. MK-677 has a larger set of published human trials than ipamorelin in the sources used here, and no head-to-head trial of any pair was found. The comparison table sets out the differences.

Does this article give instructions or doses for MK-677?

No. This article gives no doses or dosing instructions; it reports only study design facts such as who took part and how long each study ran, and the protocols used in the trials are in the linked papers. MK-677 is sold by Free Muscle for laboratory research use only, to customers aged 18 or over, and is not a medicine or food supplement or for human consumption. Nothing here is medical advice.

Is MK-677 named on the anti-doping Prohibited List?

The sources used for this guide do not state whether ibutamoren is on the Prohibited List, and the UK Anti-Doping page text we extracted does not name it, which is not the same as it being permitted. Whether a substance is prohibited is set by the current Prohibited List; the UK Anti-Doping page text we extracted does not name ibutamoren, and the legal and anti-doping section gives the detail. This guide could not confirm the listing status from the sources checked, so competitors should check the current WADA Prohibited List directly (wada-ama.org) and not rely on this article. The only data in the sources on detecting ibutamoren in a person's body are a 2026 hair-test case example in two individuals (see the hair-test question above).

What is the half-life of MK-677?

The abstracts used for this guide give no half-life or bioavailability figure for ibutamoren, so none is stated.

Related reading

• Short overview: MK-677 Ibutamoren UK 2026: What the Research Says

Sources

1. Chapman IM, Bach MA, Van Cauter E, et al. Stimulation of the growth hormone (GH)-insulin-like growth factor I axis by daily oral administration of a GH secretogogue (MK-677) in healthy elderly subjects. J Clin Endocrinol Metab. 1996;81(12):4249-57. doi:10.1210/jcem.81.12.8954023 PMID 8954023
2. Chapman IM, Pescovitz OH, Murphy G, et al. Oral administration of growth hormone (GH) releasing peptide-mimetic MK-677 stimulates the GH/insulin-like growth factor-I axis in selected GH-deficient adults. J Clin Endocrinol Metab. 1997;82(10):3455-63. doi:10.1210/jcem.82.10.4297 PMID 9329386
3. Murphy MG, Plunkett LM, Gertz BJ, et al. MK-677, an orally active growth hormone secretagogue, reverses diet-induced catabolism. J Clin Endocrinol Metab. 1998;83(2):320-5. doi:10.1210/jcem.83.2.4551 PMID 9467534
4. Svensson J, Lönn L, Jansson JO, et al. Two-month treatment of obese subjects with the oral growth hormone (GH) secretagogue MK-677 increases GH secretion, fat-free mass, and energy expenditure. J Clin Endocrinol Metab. 1998a;83(2):362-9. doi:10.1210/jcem.83.2.4539 PMID 9467542
5. Nass R, Pezzoli SS, Oliveri MC, et al. Effects of an oral ghrelin mimetic on body composition and clinical outcomes in healthy older adults: a randomized trial. Ann Intern Med. 2008;149(9):601-11. doi:10.7326/0003-4819-149-9-200811040-00003 PMID 18981485
6. Murphy MG, Bach MA, Plotkin D, et al. Oral administration of the growth hormone secretagogue MK-677 increases markers of bone turnover in healthy and functionally impaired elderly adults. J Bone Miner Res. 1999;14(7):1182-8. doi:10.1359/jbmr.1999.14.7.1182 PMID 10404019
7. Bach MA, Rockwood K, Zetterberg C, et al. The effects of MK-0677, an oral growth hormone secretagogue, in patients with hip fracture. J Am Geriatr Soc. 2004;52(4):516-23. doi:10.1111/j.1532-5415.2004.52156.x PMID 15066065
8. Adunsky A, Chandler J, Heyden N, et al. MK-0677 (ibutamoren mesylate) for the treatment of patients recovering from hip fracture: a multicenter, randomized, placebo-controlled phase IIb study. Arch Gerontol Geriatr. 2011;53(2):183-9. doi:10.1016/j.archger.2010.10.004 PMID 21067829
9. Sevigny JJ, Ryan JM, van Dyck CH, et al. Growth hormone secretagogue MK-677: no clinical effect on AD progression in a randomized trial. Neurology. 2008;71(21):1702-8. doi:10.1212/01.wnl.0000335163.88054.e7 PMID 19015485
10. Codner E, Cassorla F, Tiulpakov AN, et al. Effects of oral administration of ibutamoren mesylate, a nonpeptide growth hormone secretagogue, on the growth hormone-insulin-like growth factor I axis in growth hormone-deficient children. Clin Pharmacol Ther. 2001;70(1):91-8. doi:10.1067/mcp.2001.116514 PMID 11452249
11. Campbell GA, Patrie JT, Gaylinn BD, et al. Oral ghrelin receptor agonist MK-0677 increases serum insulin-like growth factor 1 in hemodialysis patients: a randomized blinded study. Nephrol Dial Transplant. 2018;33(3):523-530. doi:10.1093/ndt/gfw474 PMID 28340044
12. Copinschi G, Leproult R, Van Onderbergen A, et al. Prolonged oral treatment with MK-677, a novel growth hormone secretagogue, improves sleep quality in man. Neuroendocrinology. 1997;66(4):278-86. doi:10.1159/000127249 PMID 9349662
13. Svensson J, Ohlsson C, Jansson JO, et al. Treatment with the oral growth hormone secretagogue MK-677 increases markers of bone formation and bone resorption in obese young males. J Bone Miner Res. 1998b;13(7):1158-66. doi:10.1359/jbmr.1998.13.7.1158 PMID 9661080
14. Svensson J, Jansson JO, Ottosson M, et al. Treatment of obese subjects with the oral growth hormone secretagogue MK-677 affects serum concentrations of several lipoproteins, but not lipoprotein(a). J Clin Endocrinol Metab. 1999;84(6):2028-33. doi:10.1210/jcem.84.6.5799 PMID 10372705
15. Cobani E, Amin MS, Hasso M, Kumbar L. Hepatotoxicity induced by MK-677. BMJ Case Rep. 2025;18(7). doi:10.1136/bcr-2025-265728 PMID 40675653
16. Cardaci TD, Machek SB, Wilburn DT, et al. LGD-4033 and MK-677 use impacts body composition, circulating biomarkers, and skeletal muscle androgenic hormone and receptor content: A case report. Exp Physiol. 2022;107(12):1467-1476. doi:10.1113/EP090741 PMID 36303408
17. Chong S, Woolnough CA, Koyyalamudi SR, Perera NJ. Reversible gynecomastia and hypogonadism due to usage of commercial performance-enhancing supplement use. JCEM Case Rep. 2024;2(8):luae148. doi:10.1210/jcemcr/luae148 PMID 39145153
18. Sigalos JT, Pastuszak AW. The safety and efficacy of growth hormone secretagogues. Sex Med Rev. 2018;6(1):45-53. doi:10.1016/j.sxmr.2017.02.004 PMID 28400207
19. Smith RG. Development of growth hormone secretagogues. Endocr Rev. 2005;26(3):346-60. doi:10.1210/er.2004-0019 PMID 15814848
20. Liu H, Sun D, Myasnikov A, et al. Structural basis of human ghrelin receptor signaling by ghrelin and the synthetic agonist ibutamoren. Nat Commun. 2021;12(1):6410. doi:10.1038/s41467-021-26735-5 PMID 34737341
21. Holst B, Brandt E, Bach A, Heding A, Schwartz TW. Nonpeptide and peptide growth hormone secretagogues act both as ghrelin receptor agonist and as positive or negative allosteric modulators of ghrelin signaling. Mol Endocrinol. 2005;19(9):2400-11. doi:10.1210/me.2005-0059 PMID 15905359
22. Jacks T, Smith R, Judith F, et al. MK-0677, a potent, novel, orally active growth hormone (GH) secretagogue: GH, insulin-like growth factor I, and other hormonal responses in beagles. Endocrinology. 1996;137(12):5284-9. doi:10.1210/endo.137.12.8940347 PMID 8940347
23. Barrios MM, Deconinck E, Vanhee C, et al. SARMs, metabolic modulators and growth hormone secretagogues in suspected illegal medicines, bought as sport performance enhancers: a retro- and prospective study within the GEON. Drug Test Anal. 2025;17(10):2078-2085. doi:10.1002/dta.3918 PMID 40551438
24. Kintz P, Gheddar L. Knowing the minimal detectable dose can facilitate the interpretation of a hair test result: II. Case example with ibutamoren (MK-677), a growth hormone secretagogue. Clin Chim Acta. 2026;578:120578. doi:10.1016/j.cca.2025.120578 PMID 40882886
25. Raun K, Hansen BS, Johansen NL, et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552-61. doi:10.1530/eje.0.1390552 PMID 9849822
26. Gobburu JV, Agersø H, Jusko WJ, et al. Pharmacokinetic-pharmacodynamic modeling of ipamorelin, a growth hormone releasing peptide, in human volunteers. Pharm Res. 1999;16(9):1412-6. doi:10.1023/a:1018955126402 PMID 10496658
27. Beck DE, Sweeney WB, McCarter MD, et al. Prospective, randomized, controlled, proof-of-concept study of the Ghrelin mimetic ipamorelin for the management of postoperative ileus in bowel resection patients. Int J Colorectal Dis. 2014;29(12):1527-34. doi:10.1007/s00384-014-2030-8 PMID 25331030
28. Semenistaya E, Zvereva I, Thomas A, et al. Determination of growth hormone releasing peptides metabolites in human urine after nasal administration of GHRP-1, GHRP-2, GHRP-6, Hexarelin, and Ipamorelin. Drug Test Anal. 2015;7(10):919-25. doi:10.1002/dta.1787 PMID 25869809
29. Krug O, Thomas A, Malerød-Fjeld H, et al. Analysis of new growth promoting black market products. Growth Horm IGF Res. 2018;41:1-6. doi:10.1016/j.ghir.2018.05.001 PMID 29864719
30. Dominikowski A, Rękoś Z, Olejarz M, et al. The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration. Front Endocrinol (Lausanne). 2026;17:1822475. doi:10.3389/fendo.2026.1822475 PMID 42395176
31. Tomas FM, Knowles SE, Owens PC, et al. Insulin-like growth factor-I and more potent variants restore growth of diabetic rats without inducing all characteristic insulin effects. Biochem J. 1993;291 ( Pt 3):781-6. doi:10.1042/bj2910781 PMID 7683875
32. Prelle K, Stojkovic M, Boxhammer K, et al. Insulin-like growth factor I (IGF-I) and long R(3)IGF-I differently affect development and messenger ribonucleic acid abundance for IGF-binding proteins and type I IGF receptors in in vitro produced bovine embryos. Endocrinology. 2001;142(3):1309-16. doi:10.1210/endo.142.3.8038 PMID 11181549
33. Guha N, Cowan DA, Sönksen PH, et al. Insulin-like growth factor-I (IGF-I) misuse in athletes and potential methods for detection. Anal Bioanal Chem. 2013;405(30):9669-83. doi:10.1007/s00216-013-7229-y PMID 23934394
34. Rosenbloom AL. Mecasermin (recombinant human insulin-like growth factor I). Adv Ther. 2009;26(1):40-54. doi:10.1007/s12325-008-0136-5 PMID 19198769
35. Human Medicines Regulations 2012, regulations 2 and 46. legislation.gov.uk
36. Misuse of Drugs Act 1971, Schedule 2. legislation.gov.uk; Psychoactive Substances Act 2016, section 2. legislation.gov.uk
37. UK Anti-Doping. What's banned in sport: the Prohibited List. ukad.org.uk
38. MHRA. Review shows sports supplement industry improvement (3 August 2016). gov.uk