Tesamorelin vs MK-677 vs CJC-1295, compared by what each one was measured on

Tesamorelin, MK-677 and CJC-1295 answer three different questions, and no trial has ever put them side by side or even measured them against the same endpoint. So the ranking here is a ranking of what was measured, and two of the three borrow their body composition credentials from the third. Tesamorelin was tested on deep belly fat, the fat packed around the organs, as the main result in 412 people over 26 weeks ². MK-677 was tested on lean mass in 65 adults aged 60 to 81 over two years, and in that trial fat mass did not move and neither did grip strength or walking speed ³. CJC-1295 was tested on hormone levels in blood, in both of the two human studies that exist, and on nothing else ever ⁴⁵. And the CJC-1295 number everyone quotes is attached to the wrong paper. The 2 to 10-fold growth hormone rise belongs to a study that never weighed anybody, while the study it is usually credited to reported 46 percent.

What each compound was measured on

The table below is the whole argument in one screen. Read the second column first, because it decides what every other number on this page is worth.

TesamorelinThe visceral-fat GHRH

CJC-1295The GH amplifier

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There are two cards above because MK-677 has no entry in our catalogue. Ibutamoren is an orally active non-peptide small molecule that imitates ghrelin at the growth hormone secretagogue receptor, and the trial authors call it "an oral ghrelin mimetic" throughout their paper ³. A compound people take to lose fat also raises appetite, by design, and that is not a side effect bolted on at the edges.

Tesamorelin was measured on deep belly fat, in people with HIV

Tesamorelin is a modified copy of growth hormone releasing hormone, the instruction the pituitary gland receives to release growth hormone in its natural pulses. In the registration trial, 412 people with HIV and fat accumulation around the middle received 2 mg by daily injection under the skin or a placebo for 26 weeks. Deep belly fat fell 15.2 percent on tesamorelin and rose 5.0 percent on placebo, IGF-1 rose 81.0 percent against a 5.0 percent fall, and triglycerides fell 50 mg/dL against a 9 mg/dL rise, all at P<0.001 ².

The label is stricter than any trial summary suggests. Egrifta is contraindicated in active malignancy, in pregnancy, and where the hypothalamic-pituitary axis has been disrupted, and it carries warnings for glucose intolerance, fluid retention and an increased risk of new malignancy, because growth hormone signalling can accelerate the growth of a tumour that is already present. The same label states that it is not indicated for weight loss, on the grounds that its effect on body weight is neutral, and that its long-term cardiovascular safety has not been established ⁹. Those are label restrictions, not inferences from the trials. Two formulations are marketed, Egrifta SV and Egrifta WR, they are not substitutable, and both are mixed from a freeze-dried powder with the supplied diluent and injected under the skin once daily ⁹.

That pooled analysis, published in Obesity Research & Clinical Practice in 2026, is the largest pooled dataset on this page, and its conclusion includes the sentence that tesamorelin improved body composition, liver fat, lean mass and IGF-1 "without serious side effects or perturbation of glucose" ¹. That is the authors' conclusion about their pooled population rather than a general safety statement. The trials ran 26 weeks to 12 months, in adults with HIV-associated fat redistribution, under monitoring, and the approved label still carries a glucose warning ⁹. The side effects the analysis did record were joint pain, muscle pain, pins and needles, and redness where the injection went in ¹.

Across 26 weeks in the registration trial and across the five pooled trials, glucose measures did not differ significantly from placebo ²¹. That is the trial evidence, and it is what the meta-analysis authors mean by no perturbation of glucose. It is not the same as no glucose signal at all. Growth hormone works against insulin by mechanism, and the US label for Egrifta carries a warning for glucose intolerance and diabetes mellitus and directs that glucose be evaluated before and during therapy ⁹. The fair reading is that tesamorelin's glucose effect is smaller and less consistent than MK-677's, not that it is absent, and monitoring is on the label for a reason. Anyone with prediabetes or diabetes should treat that monitoring as part of the treatment rather than as optional, and the decision sits with the prescriber.

The newest data in people taking modern HIV therapy is smaller than it is usually described. Russo and colleagues, writing in AIDS in 2024, analysed the 38 participants on integrase-inhibitor regimens (the HIV drug class most people take now) inside a randomised double-blind trial of 61 people, of whom 15 on tesamorelin and 16 on placebo completed 12 months. Deep belly fat fell a median 25 cm2 against a 14 cm2 rise on placebo (P=0.001), liver fat fell 4.2 percent against 0.5 percent (P=0.01), with "no exacerbation of glycemic control" ⁶. That is a subgroup analysis of a small trial, not a new standalone trial, and it should be read as support rather than as fresh proof.

Does tesamorelin work for fat loss if you do not have HIV?

Nobody has measured it. All five randomised trials in the 2026 pooled analysis were run in people with HIV-associated fat redistribution ¹, and the approved indication is that same population: Russo and colleagues open their 2024 paper by describing tesamorelin as "the only FDA-approved therapy to treat abdominal fat accumulation in people with HIV" ⁶. Anyone outside that group who expects the same 15.2 percent is extrapolating from a different body, on a different backdrop of medication, with a different reason for the fat being there. That extrapolation has not been tested. The compound detail, including how it is handled and what the monograph says about its genetics, sits on the tesamorelin page, and the named combination is covered at tesamorelin and ipamorelin.

MK-677 moved lean mass over two years, and nothing else moved

The MK-677 evidence is stronger than tesamorelin's in one way and much weaker in another. It is a two-year, double-blind, randomised, placebo-controlled trial, a longer run of human data than tesamorelin or CJC-1295 has. In it, 65 healthy adults aged 60 to 81 took 25 mg by mouth once daily. Lean mass rose 1.1 kg, a small but statistically solid gain, against a 0.5 kg fall on placebo (P<0.001), and growth hormone and IGF-1 rose into the range normally seen in healthy young adults ³. Everyone in that trial was over 60, which is also the group with the most reason to be interested, so if that is you, peptides after 50 and the anti-aging goal page cover the age-specific picture.

What the trial did not find matters as much. Deep belly fat and total fat mass showed no significant difference. Limb fat rose more on MK-677 than on placebo, 1.1 kg against 0.24 kg (P=0.001), and body weight rose 2.7 kg against 0.8 kg ³. Someone reading only the lean-mass headline would picture a recomposition that the scan did not show.

Increased fat-free mass did not result in changes in strength or function.Nass and colleagues, Annals of Internal Medicine, 2008 [[3]]

Two years of an oral drug produced a real and statistically significant gain in lean tissue, and grip strength, walking speed and stair climbing did not improve. Lean mass on a scan is a measurement, not an outcome, and this trial shows the two can separate. What happens across 12 to 24 months in more detail is covered on our MK-677 long-term results page, which owns that ground.

Why does MK-677 raise blood sugar?

Because raising growth hormone raises blood sugar. Growth hormone pushes the liver to release glucose and makes muscle and fat tissue respond less readily to insulin, and MK-677 raises growth hormone every day for as long as it is taken. In the two-year trial, fasting blood glucose rose an average 0.3 mmol/L, about 5 mg/dL (P=0.015), and insulin sensitivity fell. Cortisol, the stress hormone, rose 47 nmol/L (P=0.020) and LDL cholesterol fell 5.4 mg/dL. The commonest side effects were increased appetite, short-lived mild swelling in the lower legs, and muscle pain ³. You will see a specific "15 to 34 percent reduction in insulin sensitivity" quoted around this topic, including on an earlier version of this page. It does not appear in the source it is attributed to, and it should not be used. The verified number is the 5 mg/dL fasting glucose rise ³. For anyone already taking it, the practical follow-through is a fasting glucose and an HbA1c with whoever prescribes or supervises their care, alongside the IGF-1 pair described below, and how to read peptide bloodwork covers what those numbers look like.

How long does it take for MK-677 to show body composition changes?

In the trial that measured it properly, the answer is 12 months for the lean-mass difference to be established and 24 months for it to be confirmed, with IGF-1 running roughly 60 percent above baseline throughout ³. Nobody has published a credible shorter timeline on body composition, so the four-week and eight-week transformations circulating online are describing weight and water, not a scan. Body weight rose 2.7 kg in that trial while fat mass did not significantly fall ³, which is what a compound that raises appetite and holds fluid would be expected to do early.

CJC-1295 has never been measured on body composition

Two human studies of CJC-1295 have been published, both of them using the DAC form, and both of them measured hormone concentrations in blood. Neither weighed, scanned or measured anybody's body. Every claim you have read about what CJC-1295 does to fat or muscle is inferred from an IGF-1 number, not observed ⁴⁵. The line nobody has ever plotted is body fat, because no human trial of this compound measured it.

Teichman and colleagues, Journal of Clinical Endocrinology & Metabolism, 2006, ran two ascending-dose placebo-controlled trials of 28 and 49 days in healthy subjects aged 21 to 61, using CJC-1295 with DAC. That study owns the 2 to 10-fold rise in growth hormone, the 1.5 to 3-fold rise in IGF-1 lasting 9 to 11 days after a single injection, the estimated half-life of 5.8 to 8.1 days, and the finding that after repeat doses IGF-1 stayed above baseline for up to 28 days. Its stated outcome measures were peak concentrations and area under the curve for growth hormone and IGF-1, and nothing else ⁴.

Ionescu and Frohman, in the same journal later that year, did something different. They sampled blood every 20 minutes overnight in healthy men aged 20 to 40, before and one week after a single 60 or 90 mcg/kg injection of the DAC form, and reported mean growth hormone up 46 percent (P<0.01), IGF-1 up 45 percent (P<0.001), and trough growth hormone up 7.5-fold (P<0.0001), with natural pulsing preserved rather than flattened ⁵. The "21 healthy adults" figure attached to this study appears to be a garble of Teichman's "ages 21-61 yr". Preserved pulsing is a genuinely interesting finding, because a hormone that arrives in pulses behaves differently from one held at a constant level.

A verdict on CJC-1295 has to be split in two. One injection of the DAC form raises growth hormone and IGF-1 substantially and keeps them raised for over a week, without flattening the body's own pulsing ⁴⁵. Whether any of that changes fat, muscle, strength or anything else you can see is unmeasured, and the numbers above say nothing at all about the no-DAC version that most blends contain. The compound detail, including which form is which, sits on the CJC-1295 page, the named combination is covered at CJC-1295 and ipamorelin, and ipamorelin has its own entry.

Is CJC-1295 safe for long-term use?

There is no long-term human safety data on CJC-1295, in either direction. The longest published human exposure, again to the DAC form, is 49 days ⁴. Everything past that is unmeasured, including what continuous elevation of IGF-1 does over months, which is exactly the kind of question that needs years of follow-up to answer. The sensible reading is that CJC-1295 is untested rather than proven safe, and the absence of a signal in a 49-day study is not evidence of absence over a year. Separately, the growth hormone axis does not respond to constant stimulation indefinitely, and the way receptors dial down is covered on our GH receptor reset timeline.

How does MK-677 compare with tesamorelin for losing belly fat?

On the evidence that exists, tesamorelin is the one with a fat result and MK-677 is the one with a lean-mass result, and swapping them around is not supported by anything published. The columns are not scores. They are not comparable measurements, and the difference in who was studied (adults with HIV-associated fat redistribution against healthy adults over 60) is large enough on its own to explain any difference you might want to attribute to the compounds.

What "measured" means here, and why borrowed numbers travel badly

A trial's primary endpoint is the one thing it was designed, sized and statistically powered to detect, chosen and registered before anybody was dosed. Every other number in the paper is something that happened to be recorded along the way. Both kinds of number are real. Only the first kind carries the trial's full weight, because only the first kind was protected from the ordinary ways a result can turn up by chance in a dataset with dozens of measurements in it.

This is why the CJC-1295 numbers travel so badly. A 2 to 10-fold growth hormone rise sounds decisive next to tesamorelin's 15.2 percent fat reduction, and the two are not the same kind of claim at all. One is a blood concentration, the other is a scanned change in a person's body. Our MK-677 page puts the marker itself in context: "IGFBP-3 is the carrier protein that holds most IGF-1 out of circulation until tissues call for it" (PeptidesDNA, MK-677 long-term results), so two people with the same IGF-1 reading are not necessarily delivering the same amount to their tissues. Reading those numbers properly is a subject of its own, covered at IGF-1 against its binding protein, with when to draw the test and what an IGF-1 that is too high looks like as further reading.

The protocols the studies used, as reported research

The honest unknowns

Nobody knows what tesamorelin does to belly fat in people without HIV, nobody knows what MK-677 does past two years or in people under 60, and nobody knows what CJC-1295 does to any tissue in any population, because it has never been measured. Long-term cardiovascular and cancer-related outcomes on sustained IGF-1 elevation are unstudied for all three, and Egrifta's own label states that its long-term cardiovascular safety has not been established ⁹. All three raise IGF-1, which is a growth signal, so an active or recent cancer is a reason to rule this class out rather than to monitor it, and poorly controlled diabetes is a reason to raise the glucose question before anything else. Both are clinician calls, and both sit on the label of the one compound here that has a label ⁹. There is also no pharmacy price for MK-677 or CJC-1295 in the US, because there is no legal pharmacy route to price ¹⁰.

Why two people get different results on the same compound

Before reaching for genetics, rank the ordinary explanations, because they are bigger and they are nearly always the answer. What follows explains why published results differ and why self-reported results differ from them. None of it is a suggestion to start, extend or adjust anything, and two of these three compounds are not approved for human use.

1. Dose and how long it was taken. The MK-677 lean-mass result needed two years to establish ³, and the tesamorelin fat result needed 26 weeks of daily injections ². Most self-reported accounts describe shorter exposure than either trial, so they are not measuring the same thing the trials measured.
2. What the person was eating. MK-677 raises appetite by mechanism, and the two-year trial did not isolate how much of its flat fat result that explains ³.
3. What training they were doing. A lean-mass number on a scan and a stronger person are different things, as the trial that measured both demonstrated ³.
4. Whether the product contained what the label said. Two of these three have no legal pharmacy route in the US ¹⁰¹¹, so purity and identity are open questions rather than assumptions.
5. Where they were starting from. Trial participants were selected: people with HIV-associated fat gain in one case, adults over 60 with declining growth hormone in the other.
6. How long they had been on it without a break, since receptors respond less to continuous stimulation over time. The GH receptor reset timeline covers what is known about that, and peptide cycling protocols covers the practice.

No randomised trial of tesamorelin, MK-677 or CJC-1295 has ever sorted responders from non-responders by genotype, and anybody telling you your genotype picks between these three is telling you something no study has tested.

The best evidence for the growth hormone receptor exon-3 deletion, a missing chunk of the gene for the docking point on cells where growth hormone lands, is a Bayesian meta-analysis of 18 datasets from 12 studies covering 1,527 children treated with recombinant growth hormone. The median difference in one-year height response was small, about 0.09 standard deviations for one copy of the variant and 0.14 for two, which is less than the ordinary variation between the studies themselves (0.18). In other words the variant moved the needle less than the choice of study did. The authors call the effect "modest" and conclude that "considerable unexplained variability in responsiveness remains" ⁷. Our own MK-677 page states it more strongly, that carriers "grew 1.7 to 2 times faster, with roughly 30% more signal getting through the receptor" (PeptidesDNA, MK-677 long-term results). The pooled figure is the one to trust, and that page is queued for correction against it.

Count the jumps between that and the question you came here with. A small effect, in children rather than adults, on injected growth hormone rather than on a compound that prompts your own, measured as height rather than as belly fat. Three jumps, each of which could reverse the direction. This page will not make them.

Where this leaves genetics is that it describes the machinery rather than predicting the outcome. In research and in clinical practice, response to growth hormone axis treatment is followed by measuring IGF-1 before and during treatment under consistent conditions, which says more about one person's response than any current genetic claim about these three compounds does. Whether any measurement or any treatment is appropriate for you, and what it would mean, is a conversation with a clinician. Genotype belongs in how results are interpreted, not in which compound gets picked.

Where these three stand legally, and in sport

Tesamorelin is approved and prescription only, sold as Egrifta by Theratechnologies under biologics licence 022505, with a labelling revision dated March 2025 ⁹. Because it is an approved biologic, a compounding pharmacy cannot legally make a copy of it ¹⁰.

An earlier version of this page had the other two wrong. The FDA removed 12 substances from its restricted Category 2 compounding list in April 2026, by nomination withdrawal rather than by any safety finding, and neither ibutamoren nor CJC-1295 was among them ¹⁰. CJC-1295 went the other way. The Pharmacy Compounding Advisory Committee voted against recommending it on 4 December 2024, and ipamorelin on 29 October 2024 ¹¹. The same committee then met on 23 to 24 July 2026 to evaluate seven of those 12 removed substances for the approved list ¹¹; none of the three compounds on this page was part of that review, any positive recommendation would still require rulemaking before it authorised anything, and neither ibutamoren nor CJC-1295 is any closer to a legal compounding route because of it. Our legal page, which owns this ground, quotes the Frier Levitt client alert directly on what removal from that list does and does not mean.

If you compete, there is a second layer that a prescription does nothing about. Our legal page states it directly: "WADA's 2026 Prohibited List, Section S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics) bans the peptides that prompt your body to release growth hormone, including ipamorelin, CJC-1295, GHRP-2, GHRP-6, and MK-677, both in competition and out of it", and "a valid prescription is irrelevant to a WADA tribunal" (PeptidesDNA, are peptides legal in the US in 2026). Tesamorelin is not named in that sentence, so anyone under a testing programme should check the current list directly ¹² rather than infer where a given compound sits. Full detail, including the hearing schedule, lives at are peptides legal in the US in 2026. Of the growth hormone axis peptides, sermorelin is the one with a clean US prescription route, and its dosing guide covers how it is used.

Ask what each number measured

Ask what each number measured before you compare it to another number. Tesamorelin has a fat result in a population unlike most readers. MK-677 has a lean-mass result with the fat and the function sitting still, plus a blood sugar cost and a heart signal that made a regulator write letters. CJC-1295 has a blood result and nothing else, and two of the three are not obtainable through a US pharmacy. That is the whole field as it currently stands, and anyone who hands you a clean ranking of all three is ranking things that were never measured together.

If that leaves you with nothing you can obtain, that is a fair conclusion to reach here. The fat-loss and recovery options with a cleaner availability picture are covered at AOD-9604 for fat loss, MOTS-c and how to build a peptide stack.