Searches for "peptides for muscle growth" mostly return marketing. This page indexes the published laboratory research instead: which compounds have been studied against skeletal-muscle and growth-hormone-axis endpoints, what the studies actually reported, and where each record can be read on PubMed. Most of this literature is rodent and cell-culture work. None of it establishes an effect in people, and none of these compounds is approved for human use.
How to read this page. Compounds are ordered by how much published preclinical literature exists for the research area — not by how well anything is claimed to work. An "Extensive literature" label means many peer-reviewed studies exist to read, including negative and inconclusive ones. It is not a statement that the compound produces any effect, in a laboratory model or in a person. Every summary below describes what a specific study reported, with the PubMed record linked so you can read the source yourself.
01
BPC-157
Extensive literature
A synthetic pentadecapeptide derived from a sequence identified in gastric juice. It appears in the muscle literature mainly through studies of injured or impaired-healing rodent muscle, and in mechanistic work on growth-factor and nitric-oxide pathways.
Literature depth: One of the most-published research peptides, with a large rodent literature spanning muscle, tendon, and gastrointestinal tissue.
Skeletal muscle healing modelsTendon and ligament researchGrowth-factor pathway signalling
What the research reports
[1]Skeletal muscle healing. In a rat model of corticosteroid-impaired healing, BPC 157 was associated with improved recovery of injured skeletal muscle.
[2]Growth hormone receptor expression. In cell-culture research on rat tendon fibroblasts, pentadecapeptide BPC 157 was reported to upregulate growth hormone receptor expression, a pathway the study links to fibroblast proliferation.
A selective growth hormone secretagogue studied in rodent endocrinology for its effect on the growth-hormone axis. Muscle-relevant interest is indirect: the literature examines GH release and downstream tissue measures such as bone mineral content rather than muscle mass directly.
Literature depth: A focused but real body of rodent endocrinology work, mostly from growth-hormone-secretagogue research programmes.
Growth hormone secretagogue researchBone mineral content modelsGhrelin-receptor signalling
What the research reports
[1]Bone mineral content. In adult female rats, the growth hormone secretagogue ipamorelin was reported to increase bone mineral content in laboratory research.
[2]Secretagogue structure. In biochemical research, ipamorelin and related ghrelin derivatives were examined for their structural similarity to peptidyl growth hormone secretagogues.
A ghrelin-receptor agonist studied for its effect on growth hormone secretion. The literature also covers orexigenic (appetite) signalling and anti-inflammatory effects in rodent models, which is why it appears in metabolic research as well as endocrine research.
Literature depth: Studied across endocrinology and inflammation literature, including human GH-response studies in clinical research settings.
Growth hormone secretionGhrelin and feeding signallingAnti-inflammatory models
What the research reports
[1]Growth hormone secretion. In growth-hormone-deficient “little” mice, the growth hormone response to growth hormone-releasing peptide-2 was examined in preclinical research.
[2]Feeding and orexigenic signalling. In rodent research, regulation of ghrelin gene expression in the stomach was examined alongside feeding behaviour.
A synthetic hexapeptide growth hormone secretagogue. Beyond GH secretion, its research profile is distinctive for cardiovascular mechanism work — it acts at the CD36 receptor, which is why it appears in cardiac as well as endocrine literature.
Literature depth: A well-defined mechanistic literature, notably on the CD36 receptor and cardiac tissue, alongside GH-secretion work.
Growth hormone secretionCD36 receptor mechanismCardiac tissue research
What the research reports
[1]Cardiovascular mechanism (CD36). In laboratory research, CD36 was reported to mediate the cardiovascular action of growth hormone-releasing peptides.
A long-acting analogue of growth-hormone-releasing hormone. Its albumin-binding (DAC) design was built to extend half-life, and the published work measures what that does to the growth-hormone axis — hormone release patterns, not body composition.
Literature depth: A small but unusually well-controlled literature — the GHRH-analogue pharmacodynamics were characterised in randomised, placebo-controlled human studies.
[1]GRF receptor activation in rats. In rat research, hGRF(1-29)-albumin bioconjugates were reported to activate the GRF receptor on the anterior pituitary. The paper identifies CJC-1295 as a long-lasting GRF analogue in that preclinical model.
[2]GH/IGF-I axis pharmacodynamics. In a randomised, double-blind, placebo-controlled study in healthy adults, CJC-1295 was reported to produce prolonged increases in circulating growth hormone and IGF-I compared with placebo. The study characterised the pharmacodynamics of the GHRH analogue only — it did not measure muscle or body-composition outcomes.
[3]GH secretion pattern. In healthy adult volunteers, continuous GHRH-receptor stimulation by CJC-1295 was reported to raise mean GH concentrations while pulsatile GH secretion was retained. The endpoint studied was the pattern of endogenous GH release.
A modified IGF-I analogue with reduced affinity for IGF binding proteins. In the literature it functions largely as a research tool for probing IGF signalling in muscle precursor cells, rather than as a compound studied for its own sake.
Literature depth: Appears mainly as a laboratory reagent in muscle cell-culture work, where its low binding-protein affinity makes it a useful IGF-I analogue.
IGF signalling in myoblastsMuscle protein synthesis modelsIGF binding-protein research
What the research reports
[1]Rodent muscle protein synthesis. In streptozotocin-diabetic rats, infused IGF-I and two binding-protein-resistant variants — des(1-3)IGF-I and LR3-IGF-I — were reported to raise growth rate, nitrogen balance and muscle protein-synthesis rates, with the variants more potent than native IGF-I. The authors also reported that other insulin-dependent processes were not restored.
[2]In-vitro myogenic cell proliferation. In in-vitro research on L6 myogenic cells, long-R3-IGF-I was used alongside native IGF-I as a stimulus for proliferation and differentiation, to examine how recombinant porcine IGFBP-3 modulates those cellular responses.
The GHRH(1-29) fragment, the shortest sequence retaining growth-hormone-releasing activity. It appears in human endocrine physiology research as a tool for probing how GH pulses are generated, more than as a compound studied for an outcome.
Literature depth: Thin as a standalone modern literature — most recent PubMed hits are doping-control assays rather than research on the compound itself.
[1]GH pulse-generation physiology. This human physiology study used continuous GHRH(1-29)NH2 together with intermittent somatostatin(1-14) infusions to examine the relative contribution of each to growth hormone pulse generation, in healthy individuals and individuals studied after cranial irradiation.
[2]GH secretagogue comparison. In children with growth hormone insufficiency and idiopathic short stature, GH-releasing hormone(1-29)NH2 and GH-releasing peptide-2 were compared as acute GH-releasing stimuli. The study reports the GH response to each peptide in that specific clinical population.
For a study designed around the growth-hormone axis itself, the secretagogue literature (ipamorelin, GHRP-2, hexarelin) is where the mechanistic detail sits, and the compounds differ meaningfully in receptor selectivity — hexarelin's CD36 activity in particular gives it a different profile from the others. For work on damaged or impaired-healing muscle tissue rather than the endocrine axis, the BPC-157 literature is far deeper. Note that most of these records measure hormone release or tissue-level markers, not muscle mass, so match the compound to the endpoint you can actually measure.
Frequently asked questions
Do any of these build muscle?
That is not a question the published literature answers, and it is not a claim we make. The research indexed here measures things like growth hormone release, receptor expression, bone mineral content, and healing of injured tissue in animal models. None of it establishes that any of these compounds increases muscle mass in a person, and none of these compounds is approved for human use.
Why is MK-677 or a SARM not on this list?
We no longer supply oral compounds or SARMs, so they are excluded from this index. This page only covers compounds whose certificate of analysis we publish and can be independently verified.
What does the evidence level mean?
It describes how much published peer-reviewed literature exists for that compound in this research area — nothing more. A compound labelled "Extensive literature" simply has more studies available to read, including inconclusive and negative ones. It is not a ranking of effect.
This page summarises published laboratory research for reference. It is not medical guidance and makes no human safety, dosing, or efficacy claim. The compounds listed are unapproved research chemicals supplied by CertaPeptides (CERTALAB S.R.L.), a reseller, for laboratory research use only — not for human or animal consumption.
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