Peptides for muscle growth: what the trials measured, and what they never did

Search "peptides for muscle growth" and the same pair comes back every time: CJC-1295 and ipamorelin, sold together, usually with a percentage attached. That percentage has no trial behind it. What exists is a handful of studies that measured two hormones in blood and stopped. One trial in this whole family put people on a scale for a year, and it found 1.1 kg. If peptides are new to you, start with the beginners guide first, because everything below assumes you know what an injectable peptide is.

What peptides are good for muscle growth, and what did their trials measure?

Sort the field by the endpoint each study collected and the ranking rearranges itself. The compounds people buy hardest for muscle sit at the top of the marketing and the bottom of the evidence, because the trials behind them stopped at a blood draw. The table below puts the strongest published human study next to each compound and names the measurement it ended on.

Growth-hormone secretagogues

Compounds that push your own pituitary to release more growth hormone. Every human trial behind them ended on a hormone concentration. None is FDA-approved for building muscle and none has a lawful US compounding pathway today.

CJC-1295The GH amplifier

IpamorelinThe selective GH releaser

TesamorelinThe visceral-fat GHRH

Tissue-repair compounds, covered elsewhere

Studied for tissue repair in animals, not for hypertrophy, and covered in full on our injury recovery page. Neither is FDA-approved for any use, and the July 2026 advisory recommendation on both still needs FDA rulemaking behind it.

BPC-157The one people take for injuries that will not heal

TB-500The systemic healer

Browse the full reference library →

Two other pages cover the parts of this question that are not hypertrophy. If your goal is recomposition, the fat side lives on our fat loss page. If your goal is getting a tendon or a muscle tear back to load, that is injury recovery, where BPC-157 and TB-500 have their own evidence review. If you are over 50 and the question is the ageing hormone axis instead of hypertrophy, peptides after 50 and our anti-aging page go there.

CJC-1295: six days of raised growth hormone, zero grams of muscle weighed

The trial everyone cites for CJC-1295 is Teichman and colleagues, published in the Journal of Clinical Endocrinology and Metabolism in 2006. It ran two randomised, placebo-controlled, double-blind ascending-dose studies lasting 28 and 49 days in healthy adults aged 21 to 61. After a single subcutaneous injection, mean plasma growth hormone rose 2 to 10 fold for 6 days or more and mean plasma IGF-1 rose 1.5 to 3 fold for 9 to 11 days, with an estimated half-life of 5.8 to 8.1 days; after repeat doses, IGF-1 stayed above baseline for up to 28 days ¹. The stated outcome measures were peak concentrations and area under the curve (total hormone exposure over time) for both hormones. The study ran no scan, no scale and no strength test.

A year of an oral secretagogue added 1.1 kg of fat-free mass

Nass and colleagues ran the closest thing to a controlled body-composition answer for this class: a 2-year, double-blind, randomised, placebo-controlled trial of MK-677 (an oral ghrelin mimic, the same mechanism ipamorelin uses) at 25 mg once daily in 65 healthy adults aged 60 to 81, published in Annals of Internal Medicine in 2008. Fat-free mass and abdominal visceral fat were the primary endpoints at one year. Fat-free mass fell 0.5 kg on placebo and rose 1.1 kg on MK-677 ². That is the number to hold every muscle-growth peptide claim against, because it is the only one that came from a long randomised trial with a scale, a scan and a strength test.

Two details from the same trial rarely travel with the 1.1 kg figure. Body weight rose 2.7 kg on MK-677 against 0.8 kg on placebo, and the average increase in limb fat was 1.1 kg on MK-677 against 0.24 kg on placebo ². So roughly as much fat arrived on the arms and legs as fat-free mass arrived overall. Fasting glucose rose about 5 mg/dL, insulin sensitivity fell and cortisol rose. The authors also flagged their own limitation plainly: study power was insufficient to evaluate functional endpoints in healthy older people, so "no strength change" here means "not detected in this trial", not "proven impossible".

What growth hormone itself did, which is the ceiling for anything that releases it

A secretagogue cannot beat the hormone it releases, so the pooled growth hormone literature sets the upper bound. Liu and colleagues at Stanford reviewed randomised controlled trials of growth hormone in healthy older adults for Annals of Internal Medicine in 2007: 18 unique study populations, 220 people in the treatment arms across 107 person-years, mean age 69, mean starting dose 14 micrograms per kilogram per day, mean treatment 27 weeks. Fat mass fell 2.1 kg (95% confidence interval -2.8 to -1.35) and lean body mass rose 2.1 kg (95% CI 1.3 to 2.9), while body weight did not change ³. Swelling, joint pain, carpal tunnel syndrome and breast tissue growth in men all became significantly more likely.

The literature published on randomized, controlled trials evaluating GH therapy in the healthy elderly is limited but suggests that it is associated with small changes in body composition and increased rates of adverse events. On the basis of this evidence, GH cannot be recommended as an antiaging therapy.Liu H, Bravata DM, Olkin I et al., Annals of Internal Medicine 2007, PMID 17227934

Note what those 2.1 kg are and are not. They are lean body mass measured on a scan, which includes water, and the reviewers listed several important outcomes as too infrequently or heterogeneously measured to pool. Strength never emerged as a pooled benefit anywhere in that review. Two kilograms of scan-measured lean mass in an older, overweight population after roughly six months is the honest ceiling for the entire growth-hormone axis, and everything sold as a secretagogue is trying to approach it indirectly.

Those two shares come from different trial sets inside the same meta-analysis, so this is a comparison across literatures and not a head-to-head ¹¹. It still matters here for one reason: the lever associated with a smaller muscle share of weight lost was resistance training, not the compound. That same lever is the only row in the table above with randomised evidence on muscle size and strength together.

Where the muscle-gain percentage on the sales pages comes from

A specific percentage of lean mass gain gets attached to CJC-1295 and ipamorelin across supplier sites and forum posts, and the reference underneath it is almost always Sigalos and Pastuszak, "The Safety and Efficacy of Growth Hormone Secretagogues", Sexual Medicine Reviews 2018. We read that review again in August 2026: it reports no percentage lean mass gain for CJC-1295, for ipamorelin, or for any secretagogue in healthy adults, and it reports no body-composition trial of either compound ⁵. It is a narrative summary of secretagogue studies in clinical populations. Here is its actual results sentence, which you can check against the abstract in one click.

To date, few long-term, rigorously controlled studies have examined the efficacy and safety of GHSs, although GHSs might improve growth velocity in children, stimulate appetite, improve lean mass in wasting states and in obese individuals, decrease bone turnover, increase fat-free mass, and improve sleep.Sigalos JT and Pastuszak AW, Sexual Medicine Reviews 2018, PMID 28400207

Read the populations in that sentence: children with slow growth, people who are wasting, people with obesity. None of them is a healthy adult who lifts four times a week, which is the exact person the compound is sold to. The review's own conclusion asks for more work on long-term impact, including cancer incidence and mortality ⁵. When a citation chain leads somewhere that does not contain the number being cited, the number has no source, and a claim with no source is not a small problem in a market where nothing is inspected.

What happened when a GHRH analog was injected nightly in older men

Sermorelin is the short GHRH(1-29) fragment that CJC-1295 was engineered from, and it has the one human study in this class where somebody measured muscle. Vittone and colleagues gave 11 healthy men aged 64 to 76 with low baseline IGF-1 nightly self-injections of 2 mg GHRH(1-29) for six weeks, published in Metabolism in 1997. They sampled growth hormone every 20 minutes overnight, ran DEXA scans, tested six strength measures and imaged muscle energy metabolism ⁴.

Nocturnal growth hormone release rose, and the peak amplitude rose. IGF-1 did not change, and neither did IGF binding protein-3 or growth hormone binding protein. Two of six strength measures improved (upright row and shoulder press) along with an abdominal endurance test, in 11 men against their own baselines with no placebo arm ⁴. The authors' own reading was that single nightly doses are less effective than multiple daily doses at producing growth-hormone-mediated effects. This is the most muscle-focused human data the GHRH class has, and the hormone one step downstream did not move.

Does the CJC-1295 and ipamorelin pairing have a trial behind it?

No controlled trial has tested CJC-1295 together with ipamorelin against either compound alone, or against placebo, on any endpoint. The pairing rests on a mechanism argument: CJC-1295 works through the growth-hormone-releasing-hormone receptor and ipamorelin works through the ghrelin receptor, so hitting both should produce a larger pulse than hitting either. That argument is reasonable pharmacology and it has never been checked in people. Ipamorelin's own human record is a phase 1 pharmacokinetic study in healthy men, which found a terminal half-life of about 2 hours and a single episode of growth hormone release per dose ⁸, and one phase 2 efficacy trial, in 114 bowel-resection patients with postoperative ileus, where the key endpoint was time to a tolerated meal and ipamorelin did not beat placebo (25.3 versus 32.6 hours, p = 0.15) ⁹. Its reputation for a clean profile comes from Raun's 1998 preclinical work in swine and rats, where it released growth hormone without much spillover into cortisol or prolactin: a selectivity result in animals, not a muscle result in humans ⁷. In evidence terms the stack is one compound with a hormone-kinetics trial bolted to one compound whose only controlled efficacy trial failed, sold as a system on the strength of a receptor diagram.

Muscle and body composition

CJC-1295 + Ipamorelin

10 mg vial

The growth-hormone pairing, and the one that has real logic behind it

5 mgCJC-1295

5 mgIpamorelin

Weight and metabolism

Tesamorelin + Ipamorelin

10 mg vial

An approved drug for belly fat, paired with a growth-hormone releaser

5 mgTesamorelin

5 mgIpamorelin

Compare every stack →

CJC-1295 with DAC and without DAC are two different drugs

The confusion is invisible on a vial label, and it changes what every number on this page applies to. Every number in the Teichman trial belongs to CJC-1295 with DAC, the albumin-binding group described above, which stretches the half-life to 5.8 to 8.1 days ¹. The form sold widely as plain "CJC-1295" (also labelled mod GRF 1-29) has no DAC, a half-life measured in minutes, and no published human trial at all. Vendors use one name for both.

A weekly-injection schedule copied from the with-DAC literature has no pharmacological basis for a compound that clears in minutes, and a purity or identity check is not something a home user can run. If you already have a vial: look for DAC or mod GRF 1-29 on the label. If it says neither, you cannot tell which of these two compounds you are holding, and no dosing schedule you find online applies to it. That vial, and the question of whether to use it at all, is a conversation to have with a clinician.

Is BPC-157 useful for muscle growth?

BPC-157 has no muscle-growth endpoint in any species. Neither BPC-157 nor TB-500 is FDA-approved for any use in any population, and the compounding status of both moved during 2026: removed from Category 2 in April, recommended for the 503A Bulks List by the FDA's advisory committee in July, with rulemaking still to come. An advisory vote is not an approval, and none of it makes a research-chemical vial legal to inject. The case for a training context is indirect: if recovery between hard sessions improves, you can hold more training volume, and the growth comes from the training. That is a plausible chain with an unmeasured first link in humans, and the compound's evidence sits on our injury recovery page, which reviews the animal repair studies properly.

The one published head-to-head is a rat study: 32 Sprague-Dawley rats with a transected and repaired Achilles tendon, randomised to control, BPC-157, TB-500 or both for four weeks. TB-500 alone was the only arm with a statistically significant gain in maximum load to failure, and combining the two compounds conferred no additional benefit over either alone ¹². That is animal biomechanics at four weeks, and it is the strongest comparative evidence either compound has anywhere.

For the training-side version of the same question, best peptides for muscle recovery covers what people run between sessions. Note that BPC-157 and TB-500 are also prohibited in tested sport, and that neither has a completed human clinical trial.

Are peptides safe for muscle growth?

Nobody can answer this for healthy trained adults, because no trial has run in that population. What exists is short-term tolerability from supervised trials in other populations, which is a narrow claim, and it came with measurable harms. Teichman reported no serious adverse reactions across 28 and 49 days ¹. Nass reported the oral secretagogue as generally well tolerated over 12 months, with increased appetite, transient mild lower-leg swelling and muscle pain as the most frequent complaints, alongside a 5 mg/dL rise in fasting glucose, reduced insulin sensitivity and a rise in cortisol ². The pooled growth hormone review found significantly higher rates of soft tissue swelling, joint pain, carpal tunnel syndrome and breast tissue growth in men ³.

• **Blood sugar.** Raising growth hormone reduces insulin sensitivity. The one 12-month controlled trial, MK-677 at 25 mg daily in 65 adults aged 60 to 81, recorded a fasting glucose rise of about 5 mg/dL directly ², which is why fasting glucose and HbA1c (a three-month average of blood sugar) are the labs clinicians watch. Existing diabetes or prediabetes is a specific reason not to start without a clinician: that fall in insulin sensitivity was measured, not theoretical.
• **IGF-1 and cancer history.** IGF-1 is a growth signal. Higher circulating IGF-1 is associated with modestly higher risk of prostate and premenopausal breast cancer in pooled epidemiology, with odds ratios around 1.5 comparing the 75th to the 25th percentile and associations that vary by cancer site ¹³. What has never been tested is whether raising IGF-1 with a drug changes that risk, and clinicians prescribing these compounds routinely exclude anyone with a personal or family cancer history instead of waiting for the argument to resolve.
• **Nerve compression.** Carpal tunnel syndrome and swelling were among the clearest signals in the pooled growth hormone data ³. Numbness or tingling in the hands is the symptom to stop for and take to a clinician.
• **Sterility, not just purity.** Research-grade vials are not manufactured to sterile pharmaceutical standards. Injecting material from one carries infection, abscess and endotoxin risk on top of the purity unknown, and no home test detects any of it.
• **Unknown purity.** These compounds arrive from unregulated suppliers as lyophilised (freeze-dried) powder. Nobody has measured what is in a typical vial, so every safety statement above describes the studied compound and not the one that arrives.
• **Nobody has studied these groups.** No trial of any compound on this page has enrolled anyone pregnant, breastfeeding or under 18. There is no safety data to reason from.
• **Long-term unknowns.** The longest controlled secretagogue exposure in the literature is 24 months in 65 older adults ². There is no long-term safety dataset in healthy trained adults at any dose.

Banned at all times in tested sport

CJC-1295, ipamorelin and sermorelin all fall under section S2 of the World Anti-Doping Agency Prohibited List, which covers peptide hormones, growth factors and related substances. S2 substances are prohibited at all times, in and out of competition, so an off-season cycle is a violation the same as an in-season one. Detection windows for these specific compounds are not publicly established, which means no washout period can be relied on. The list is revised annually, so check the current year instead of a forum post.

What CJC-1295 and ipamorelin cost, and how they are handled

PeptidesDNA does not sell, supply, ship or prescribe any compound on this page, and nothing here is an instruction to obtain one. Vendors list these vials for laboratory research use only; buying a research chemical to inject falls outside that stated purpose, is not lawful everywhere, and is a decision for a clinician instead of a checkout page. Both compounds ship as lyophilised powder in glass vials, most commonly 2 mg or 5 mg per vial. Vendor list prices for a single vial of either sit in the tens of dollars, not the hundreds, so the cost of any research protocol is dominated by frequency of use and not by the price of the powder. Current vendor pricing and which suppliers publish third-party purity testing are tracked on our comparison page. Those are affiliate links and we earn a commission on purchases made through them, which changes nothing about what the studies above measured.

• **These are handling facts, not a preparation guide.** This page gives no dose, schedule or route for any compound on it. What follows describes how suppliers document material sold for laboratory use.
• **Before reconstitution.** Sealed lyophilised powder is the stable state. Suppliers ship it at room temperature and document storage as cool, dark and dry until use.
• **After reconstitution.** Suppliers document reconstituted vials as requiring 2 to 8 degrees Celsius, protection from light, and a working life measured in weeks and not months. How to reconstitute peptides covers the arithmetic, and peptide injection hygiene covers the sterile side, which is where the real risk sits.
• **What degrades it.** Repeated freeze-thaw cycles, shaking the vial instead of swirling it, and warm shipping legs. None of this is measurable at home, which is a real limit on any personal experiment.
• **Timeline before anything is measurable.** The controlled trial that found 1.1 kg ran for 12 months with assessments every 6 months ². Judging a compound at 8 weeks against a mirror, during a training block that would move strength on its own, produces an answer about the training. For how people structure on and off periods, see our cycling protocol guide.

Which genes say anything about growth hormone response?

One variant in this area has real pharmacogenetic evidence, and it was collected in a population that has nothing to do with lifting. Dos Santos and colleagues, publishing in Nature Genetics in 2004, found in two cohorts of short children treated with growth hormone that an isoform of the growth hormone receptor gene lacking exon 3 (d3-GHR) was associated with 1.7 to 2 times more growth acceleration than the full-length isoform, with cell experiments showing the receptor passing on roughly 30% more signal. About half of Europeans carry at least one copy of the allele, and it is dominant over the full-length version ⁶. The replication history matters as much as the original result: a 2009 systematic review and meta-analysis of 15 studies in short children found the effect real but far smaller, roughly an extra 0.5 cm of growth velocity in the first year of treatment, and larger at lower doses ¹⁰.

• **GHR exon-3 (d3-GHR).** The only variant here with measured evidence of altered response to growth hormone, and a contested one: big in the original report, much smaller on meta-analysis ⁶¹⁰. It was tested against injected growth hormone in children, never against CJC-1295, ipamorelin, sermorelin or MK-677 in adults. It is a structural deletion, not a single-letter change, so consumer arrays infer it from a nearby tag marker instead of reading it directly.
• **ACTN3 rs1815739.** Sits on almost every consumer chip and tracks fast-twitch fibre proportion and power phenotype. That is useful training context. No study has ever tested it as a predictor of response to any peptide.
• **MSTN (myostatin) variants.** Loss-of-function variants produce dramatic muscle phenotypes and are individually rare, and they are largely absent from consumer genotyping chips, so a raw DNA file usually cannot speak to them.
• **"IGF-1 promoter variants".** A phrase that appears in peptide marketing and names no rsID, which makes it unauditable. We do not report a marker we cannot name.

No trial of any growth hormone secretagogue has stratified its results by genotype, so no report, ours included, can tell you that a protocol will work harder for you than for someone else. What a genotype legitimately contributes is context: fibre-type tendencies, metabolic and side-effect background, and a clear statement of which markers your file cannot read. Our DNA decision framework walks through where that line sits.