Verified July 2026 · Cited to primary sources
The GH-axis peptides marketed for muscle and body recomposition, graded by human evidence and legal status. Most of the hype (CJC-1295/Ipamorelin) rests on a single pharmacokinetic study, which is not proof of muscle gain.
Evidence for this goal
An overall evidence grade reflects the indications studied; it does not establish a muscle-growth benefit. Compare each study's population, measured outcome and limitations before drawing conclusions. This catalog does not name a muscle-growth winner.
How to read this comparison
Compounds are listed alphabetically, not ranked for this goal. The overall grade reflects the evidence described in each record. Evidence for one condition, population or product form does not establish benefit for every use. Affiliate availability never changes a grade.
A historical FDA survey of compounded drugs found 31% failed standard potency testing. What is actually in the vial is a separate question from whether the compound works, and a rubric like this exists to keep the two apart. See the full A to F methodology →
Evidence scope: Grade C: one published human pharmacokinetic study (Teichman et al., JCEM 2006) shows CJC-1295 elevates GH and IGF-1 in healthy adults, which is real early human data (decision-tree rule 4 fired). But there is no efficacy RCT for muscle, fat loss or anti-aging, so the marketed body-composition benefits are unproven.
Sources: Teichman et al., J Clin Endocrinol Metab 2006: CJC-1295 human PK study (GH/IGF-1 elevation in healthy adults) · FDA 503A bulks list (CJC-1295 removed from Category 2; compounding nomination withdrawn) · Federal Register FDA-2025-N-6895 (April 2026 503A reclassification) · WADA Prohibited List (S2, GHRH analog / GH-releasing factors)
A modified GHRH analog that stimulates sustained pituitary GH and IGF-1 release; the "with DAC" (Drug Affinity Complex) version binds albumin to extend its half-life to days, versus the shorter-acting no-DAC form (Mod-GRF 1-29).
CJC-1295 (mono GHRH analog, usually "with DAC") is not FDA-approved and not legally compoundable; its nomination was withdrawn in April 2026. Human evidence is Grade C: one PK study proves it raises GH/IGF-1, but no trial shows muscle or fat-loss benefit. Most people search for the popular blend, so see our CJC-1295 / Ipamorelin page. We don't link gray-market sources.
See the evidence →Evidence scope: Graded to the stronger component. CJC-1295 has one published human PK study showing GH/IGF-1 elevation (Grade C: early human data, rule 4). Ipamorelin has only limited early-phase human development (Grade D). Neither has an efficacy RCT for muscle, fat, or anti-aging, so the marketed benefits are unproven.
Sources: FDA 503A bulks list (fda.gov/media/94155/download) · Federal Register FDA-2025-N-6895 (April 2026 503A reclassification) · WADA Prohibited List (S2, GHRH analog / GH secretagogue) · Teichman et al., J Clin Endocrinol Metab 2006: CJC-1295 human PK study
CJC-1295 (a GHRH analog) drives sustained pituitary GH/IGF-1 release while Ipamorelin (a selective ghrelin/GHS-R agonist) adds a clean GH pulse. The stack aims to raise GH/IGF-1.
CJC-1295/Ipamorelin is not FDA-approved and is not legally compoundable (CJC-1295 withdrawn April 2026). Human evidence is Grade C: one PK study proves it raises GH/IGF-1, but no trial shows muscle or fat-loss benefit. Researching CJC-1295 on its own (often "with DAC")? See our standalone CJC-1295 page.
See the evidence →Evidence scope: For the injectable follistatin peptide that people actually buy, human efficacy data is essentially absent; support is animal and mechanistic. The one legitimate human dataset, Mendell's Phase 1/2a trial, used AAV gene therapy delivering the FS344 gene by direct muscle injection in six patients, a fundamentally different modality from a peptide you inject. That is early human safety/signal data for gene therapy, not for the peptide. Since the peptide itself is preclinical and the human evidence belongs to a different technology, the honest grade for follistatin-as-a-peptide is D.
Sources: Mendell et al., A Phase 1/2a Follistatin Gene Therapy Trial for Becker Muscular Dystrophy, Molecular Therapy 2015 (n=6, AAV1.CMV.FS344, no serious adverse events, PMC full text) · Same trial, PubMed record (PMID 25322757)
Follistatin binds and neutralizes myostatin (GDF-8) and activins, removing a brake on skeletal-muscle growth. Blocking myostatin drives muscle-fiber hypertrophy, which is why it is attractive for muscle building. The catch is that follistatin is a large, short-lived glycoprotein, so a simple injected peptide does not durably produce the effect, which is why the credible human work used gene therapy to make muscle express it continuously.
A compelling target with a misleading reputation. The muscle-growth story rests almost entirely on animal work plus a tiny AAV gene-therapy trial that is not the same product as the injectable peptide being sold. For follistatin as a peptide, the human efficacy evidence is basically Grade D, safety is uncharacterized, systemic myostatin blockade carries real theoretical risks, and it is banned in sport. Interesting biology, not a justified purchase.
See the evidence →Evidence scope: GHRP-2 has the best-defined human pharmacology of the GHRPs (it is a licensed GH-stimulation diagnostic in Japan) and controlled human studies document both its GH-releasing potency and its appetite effect (Laferrere 2005; Gondo 2001). But 'approved as a one-time diagnostic test' is not the same as 'proven to build muscle over time.' There is no randomized controlled trial measuring muscle, body composition, recovery or any physique outcome from chronic use. Strong human pharmacology, no efficacy trial for the marketed use, so D.
Sources: Laferrere 2005, J Clin Endocrinol Metab, GHRP-2, like ghrelin, increases food intake ~36% in healthy men and raises GH · Gondo 2001, J Clin Endocrinol Metab, GHRP-2 stimulates GH secretion even in patients with a mutated GHRH receptor (GHRH-independent action) · WADA Prohibited List, GH-releasing peptides incl. GHRP-2 (pralmorelin) banned at all times (S2.2.4)
Ghrelin-receptor (GHS-R1a) agonist that drives some of the highest GH pulse amplitudes per unit dose in its class. It works partly independent of your own GHRH: in patients with a non-functional GHRH receptor it still produced a 4.5-fold GH rise, showing a direct action on pituitary somatotrophs. It also stimulates appetite and modestly raises ACTH, cortisol and prolactin.
The strongest GH-pulse trigger of the old GHRPs and a genuine diagnostic drug in Japan, which is more legitimacy than most peptides here can claim. But a single approved diagnostic test is not evidence it builds muscle, no such human trial exists, and in the US it is research-only. Grades D for the use case people search for.
See the evidence →Evidence scope: Human studies on GHRP-6 exist but they are pharmacodynamic, not efficacy: they measure GH, ACTH, cortisol and sleep EEG after a dose (Frieboes 1995), or map how much it depends on endogenous GHRH (Pandya 1998). There is no randomized controlled trial in humans measuring muscle, body composition, recovery or any clinical outcome that people take it for. Known to raise GH in people, but no proven benefit, and it comes with off-target cortisol/prolactin. That is a D.
Sources: Frieboes 1995, Neuroendocrinology, GHRP-6 stimulates sleep, GH, ACTH and cortisol in normal men (documents the non-selective cortisol rise) · Pandya 1998, J Clin Endocrinol Metab, GHRP-6 requires endogenous hypothalamic GHRH for maximal GH stimulation in humans · WADA Prohibited List, GH-releasing peptides incl. GHRP-6 banned at all times (S2.2.4)
Agonist at the ghrelin receptor (GHS-R1a) that triggers a pulse of pituitary growth hormone. Unlike ipamorelin it is non-selective: it also raises ACTH, cortisol and prolactin, stimulates appetite hard, and has gastric-motility effects. Human work shows it needs your own hypothalamic GHRH to hit maximal GH release, so its ceiling depends on an intact GHRH axis.
The granddaddy of GH peptides and a reliable appetite-and-GH trigger in the lab, but it is non-selective (cortisol and prolactin come along), the human data is decades-old pharmacology with no efficacy outcome, and it is not legal to compound. Newer selective secretagogues make it hard to justify even in theory.
See the evidence →Evidence scope: Hexarelin has legitimate human pharmacology data, including a distinctive controlled finding that it acutely improves cardiac ejection fraction independent of GH (Bisi 1999, both in healthy controls and in hypopituitary adults). But these are acute mechanism studies, not efficacy trials. There is no randomized controlled trial showing it builds muscle, improves body composition, or treats a cardiac condition over time, and its GH effect is undermined by tachyphylaxis. Real human data, no proven clinical benefit for any marketed use, so D.
Sources: Bisi 1999, J Endocrinol Invest, acute cardiovascular and hormonal effects of hexarelin in humans; short-lasting positive inotropic effect, GH-independent · Bisi 1999, Eur J Pharmacol, cardiac effects of hexarelin in hypopituitary adults (raised LVEF without BP/HR change, GH-independent) · WADA Prohibited List, GH-releasing peptides incl. examorelin (hexarelin) banned at all times (S2.2.4)
Agonist at the ghrelin receptor (GHS-R1a) that triggers pituitary GH release. Uniquely, it also acts on the cardiac scavenger receptor CD36, and human studies show an acute, short-lasting positive inotropic effect (better left-ventricular ejection fraction) that is independent of GH. The catch for GH use is desensitization: repeated dosing blunts the GH response (tachyphylaxis), so the hormonal effect fades.
The most scientifically interesting GHRP thanks to a real, human, GH-independent cardiac effect, but 'interesting mechanism' is not 'proven benefit.' No trial shows it builds muscle, its GH effect fades with repeat dosing, and it is research-only. Grades D for the use case people actually search.
See the evidence →Evidence scope: Grade D: there is no published human efficacy RCT of IGF-1 LR3 itself (rule 5 fired: animal/mechanistic evidence only, no human efficacy trial). The muscle-growth case rests on IGF-1's known biology and animal/tissue work, not on a controlled human trial of this specific analogue. Human efficacy for IGF-1 LR3 is effectively absent.
Sources: WADA Prohibited List (S2, IGF-1 and its analogues, banned at all times) · USADA, IGF-1 and the WADA Prohibited List (exogenous IGF-1 prohibited in and out of competition) · FDA 503A bulks list (no legal compounding pathway; research-chemical only)
A modified, long-acting form of IGF-1 that activates the IGF-1 receptor to drive the PI3K/Akt/mTOR protein-synthesis and satellite-cell pathways. That's the theoretical basis for its muscle-growth marketing.
IGF-1 LR3 is not FDA-approved and not legally compoundable; it's research-only. Human evidence is Grade D: there is no published human efficacy trial for the analogue itself, so the muscle-growth claims rest on mechanism, not proof. It is also WADA-prohibited (S2). We don't link gray-market sources.
See the evidence →Evidence scope: One genuine human Phase 2 randomized controlled trial exists (Beck 2014, 114 bowel-resection patients) but it missed every primary and secondary endpoint and the program was discontinued. That failure was in gut motility, not in muscle growth, so it does not brand ipamorelin a failure for the reason people actually buy it. But there is also zero human efficacy trial showing it builds lean mass, aids recovery or burns fat. So: real human exposure and a good safety/selectivity signal, no proof of the marketed benefit. That is a C, not higher.
Sources: Raun 1998, Eur J Endocrinol, 'Ipamorelin, the first selective growth hormone secretagogue' (defines its selectivity; no ACTH/cortisol rise vs GHRP-6/2) · Beck 2014, Int J Colorectal Dis, Phase 2 RCT for postoperative ileus; well tolerated but no significant benefit vs placebo on any endpoint · WADA Prohibited List, growth hormone secretagogues (incl. ipamorelin) banned at all times (S2.2.4)
Binds the ghrelin receptor (GHS-R1a) on pituitary somatotroph cells and triggers a pulse of stored growth hormone. Its selling point is selectivity: at GH-releasing doses it does not meaningfully raise ACTH, cortisol, prolactin, FSH, LH or TSH, which is what separates it from GHRP-6 and GHRP-2. It still needs your own GHRH axis to work, so it is not a substitute for GH itself.
The most selective GHRP on paper and the best-tolerated in a real human trial, but that trial failed and there is no human evidence it does the muscle or fat-loss job it is sold for. Interesting pharmacology, unproven benefit, not legal to compound.
See the evidence →Evidence scope: Evidence is preclinical only. The optimistic case rests on cell-culture and animal work suggesting the MGF-E peptide can activate satellite cells. But a well-controlled 2014 in-vitro study explicitly designed to test it found the peptide had no effect on myoblast or muscle-stem-cell proliferation at concentrations up to 500 ng/ml, and a 2012 review concluded its efficacy in humans is unproven. There are no human trials showing MGF injections build muscle. Grade D reflects animal/in-vitro-only evidence with a notable negative result.
Sources: Fornaro M, et al. MGF peptide has no apparent effect on myoblasts or primary muscle stem cells. Am J Physiol Endocrinol Metab, 2014 (PMID 24253050). · Zablocka B, et al. Mechano-Growth Factor: an important cog or a loose screw in the repair machinery? Front Endocrinol, 2012.
MGF is the C-terminal E-domain of the IGF-1Ec splice variant, produced locally in skeletal muscle in response to mechanical overload or damage. The proposed mechanism is autocrine/paracrine activation of muscle satellite cells (the resident stem cells that repair and enlarge fibers), acting through a receptor distinct from the classic IGF-1 receptor. In practice the receptor and downstream signaling remain poorly characterized, and whether the synthetic peptide reproduces the biology of the natural splice event is unresolved.
Skip it. The idea (a local muscle-repair growth factor you can inject) is attractive, but the honest read of the literature is preclinical at best and negative in the one rigorous cell study. There is no human evidence it builds muscle, it is banned in sport, and injecting an unverified growth factor is not a low-risk bet.
See the evidence →Evidence scope: MK-677 has real, multi-study human RCT data, well beyond anything the GHRPs have: a 2-year double-blind trial in older adults (Nass 2008) and randomized bone-turnover trials (Murphy 1999). It reliably raises GH and IGF-1 into a youthful range and modestly increases fat-free mass. But it is not FDA-approved, the 2-year trial showed no improvement in strength or function despite the lean-mass gain, and it measurably reduced insulin sensitivity and raised fasting glucose. Real human efficacy on a surrogate (FFM, IGF-1) but no approval and a meaningful metabolic downside puts it at C, the top of this group.
Sources: Nass 2008, Ann Intern Med, 2-year RCT of oral MK-677 in healthy older adults: increased fat-free mass and IGF-1 to youthful range, but raised fasting glucose and reduced insulin sensitivity · Murphy 1999, J Bone Miner Res, oral MK-677 increased markers of bone turnover in 187 elderly adults (randomized, placebo-controlled) · WADA Prohibited List, growth hormone secretagogues incl. ibutamoren (MK-677) banned at all times (S2.2.4)
Non-peptide agonist of the ghrelin receptor (GHS-R1a) that mimics ghrelin to drive sustained, roughly physiological increases in growth hormone and IGF-1. Because it is orally bioavailable and long-acting, one daily dose keeps GH/IGF-1 elevated, unlike the injectable peptide GHRPs. That same sustained GH/IGF-1 elevation is what drives its main downside: reduced insulin sensitivity and higher fasting glucose.
The most-studied and only orally-active option in this group, with genuine 2-year human RCT data behind it, which is why it grades C and not D. But the same trial that proves it works also shows the catch: modest lean-mass gain, no functional benefit, and worse insulin sensitivity. Not FDA-approved, research-only, and a poor idea for anyone with blood-sugar concerns.
See the evidence →Evidence scope: Evidence is animal and in-vitro only. Rodent muscle-injury models report increased satellite cell number and cross-sectional area with PEG-MGF, and the PEGylation rationale (extended half-life) is chemically sound. But there are no controlled human trials, and the parent peptide MGF failed to show activity in a rigorous cell study. Grade D reflects preclinical-only evidence with no human efficacy data.
Sources: Fornaro M, et al. MGF peptide has no apparent effect on myoblasts or primary muscle stem cells. Am J Physiol Endocrinol Metab, 2014 (PMID 24253050). · Zablocka B, et al. Mechano-Growth Factor: an important cog or a loose screw in the repair machinery? Front Endocrinol, 2012.
PEG-MGF is the MGF (IGF-1Ec E-domain) peptide conjugated to polyethylene glycol. Native MGF has a very short systemic half-life (minutes); PEGylation slows clearance and is meant to give the peptide time to reach tissue and act on satellite cells. The proposed downstream biology is identical to MGF: satellite cell activation, proliferation, and fusion to support fiber repair and hypertrophy. Whether extending the half-life of a peptide that may not be active in the first place produces a real anabolic effect is exactly the open question.
Skip it. PEG-MGF is a chemically reasonable attempt to fix MGF's short half-life, but fixing the delivery of a compound with no proven human effect does not create a proven human effect. Animal data only, banned in sport, unverified injectable. Not worth the risk.
See the evidence →Evidence scope: Grade B: previously FDA-approved (Geref) with human data for its approved indications, and still widely compounded (rule 3 fired: prior FDA approval backed by human trials). Withdrawn ~2008 for business reasons, not safety.
Sources: FDA 503A bulks list (fda.gov/media/94155/download) · Drugs@FDA: Geref (sermorelin) approval history · WADA Prohibited List (S2, GHRH analog)
Stimulates natural pituitary growth-hormone release as the shortest active GHRH(1-29) fragment. The "gentler," physiologic GH-axis peptide.
Sermorelin is legally compoundable (503A) thanks to its prior FDA approval as Geref. Human evidence is Grade B: real historical trial data. It is the best-evidenced GH-axis peptide with a legal supervised route today.
See the evidence →Evidence scope: Grade A: FDA-approved (2010) on multiple pivotal Phase 3 RCTs (rule 1 fired: FDA-approved for ≥1 indication). The only currently-marketed FDA-approved GHRH analog.
Sources: Drugs@FDA: Egrifta (tesamorelin) approval record · WADA Prohibited List (S2, GHRH analog) · Falutz et al., N Engl J Med 2007: tesamorelin pivotal Phase 3 (n=412)
A GHRH analog that stimulates the pituitary to release growth hormone, which reduces visceral (abdominal) fat.
Tesamorelin is an FDA-approved drug (Egrifta, 2010): Grade A, the strongest evidence tier here. But it is approved for HIV-associated visceral fat, not general weight loss; for that, approved GLP-1s are the evidence-backed route.
See the evidence →| Peptide | Overall grade | Legal & safety | Typical cost | Verdict | |
|---|---|---|---|---|---|
| CJC-1295 A GHRH analog, usually the long-acting "with DAC" version, that one human study shows raises GH/IGF-1. No trial shows it builds muscle or burns fat. | Grade C | See evidenceSee the evidence for CJC-1295 | |||
| CJC-1295 / Ipamorelin The classic GH-boosting stack. One human PK study shows it raises GH/IGF-1, but no trial shows it builds muscle or burns fat. | Grade C | See evidenceSee the evidence for CJC-1295 / Ipamorelin | |||
| Follistatin (FST-344 / FS344) A natural myostatin blocker that in theory should unlock muscle growth. The reality: the injectable peptide is essentially preclinical, and the only human evidence is from AAV gene therapy, a completely different technology, in a handful of muscular-dystrophy patients. | Grade D | See evidenceSee the evidence for Follistatin (FST-344 / FS344) | |||
| GHRP-2 The most potent GH-pulse trigger of the classic GHRPs per dose, and it is actually an approved diagnostic agent for GH deficiency in Japan. But like its cousins it also spikes appetite and modestly raises cortisol and prolactin, and there is no human trial showing it builds muscle. | Grade D | See evidenceSee the evidence for GHRP-2 | |||
| GHRP-6 The original GH-releasing peptide from the 1980s. It works as a GH pulse trigger and it makes you ravenously hungry, but it is non-selective, so it drags cortisol and prolactin up with it. Human data is all old pharmacology studies, none of it shows it builds muscle. | Grade D | See evidenceSee the evidence for GHRP-6 | |||
| Hexarelin The GHRP with the most interesting side story: beyond releasing GH it has a direct, GH-independent positive effect on heart contractility in humans via a cardiac receptor. That cardiac finding is real and human. What is missing is any trial showing it does the muscle-building it is sold for, plus it loses its GH punch fast with repeat dosing. | Grade D | See evidenceSee the evidence for Hexarelin | |||
| IGF-1 LR3 A long-acting IGF-1 analogue marketed for muscle growth on the strength of its mechanism alone. There is no published human efficacy trial for it, and it's banned in sport. | Grade D | See evidenceSee the evidence for IGF-1 LR3 | |||
| Ipamorelin The cleanest of the GH-releasing peptides on paper: it bumps GH without the cortisol and prolactin spike the older GHRPs cause. But the honest headline is that the one real human trial was for gut motility, not muscle, and it flat-out failed. Zero human data proving it builds muscle or burns fat. | Grade C | See evidenceSee the evidence for Ipamorelin | |||
| MGF (Mechano Growth Factor) A short splice variant of IGF-1 that muscle makes locally after mechanical stress. The theory is great, the human data barely exists, and the one well-run cell study said it did nothing. | Grade D | See evidenceSee the evidence for MGF (Mechano Growth Factor) | |||
| MK-677 (Ibutamoren) The odd one out: MK-677 is not a peptide, it is an orally-active small-molecule ghrelin mimetic, which is why people take it as a daily capsule instead of an injection. It has the best human evidence in this group by far, including a 2-year randomized trial, but that trial is also the cautionary tale: it raised lean mass a little while measurably worsening insulin sensitivity and blood sugar. | Grade C | See evidenceSee the evidence for MK-677 (Ibutamoren) | |||
| PEG-MGF (Pegylated Mechano Growth Factor) MGF with a polyethylene glycol tail bolted on to make it last longer in the blood. Longer half-life, same problem: the evidence is animal-only and no human trial has shown it does anything. | Grade D | See evidenceSee the evidence for PEG-MGF (Pegylated Mechano Growth Factor) | |||
| Sermorelin The "gentler," formerly-FDA-approved GH-axis peptide. It's the best-evidenced option you can still legally get through a compounding pharmacy. | Grade B | See evidenceSee the evidence for Sermorelin | |||
| Tesamorelin An FDA-approved peptide drug, not a research chemical. Proven to cut visceral fat, but approved for a narrow HIV indication. | Grade A | See evidenceSee the evidence for Tesamorelin |
Reading this table: Grades refer to each compound's stated evidence scope, not every use in this category. Legal status and Safety are separate badges; Verdict is the compound summary. Affiliate availability never changes a grade. Full methodology.
FAQ
This catalog does not establish a best peptide for muscle growth. Evidence for a different indication, or a change in a hormone measurement, should not be presented as proof of muscle gain. Read the studied population and outcomes on each compound profile.
There is no human trial showing CJC-1295/Ipamorelin builds muscle or burns fat. The only human data is a pharmacokinetic study confirming it raises GH and IGF-1, which is why we grade it C. It is also not legally compoundable.
Sermorelin is legally compoundable through a 503A pharmacy because of its prior FDA approval. CJC-1295/Ipamorelin is effectively research-only after CJC-1295's compounding nomination was withdrawn in April 2026. All of these are on the WADA Prohibited List for tested athletes.
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