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Best Peptides for Muscle Growth & Recovery

If you have been lifting heavy, eating right, and sleeping well but still feel like your body is not keeping pace with your effort, you are not alone. Thousands of people search for "peptides for muscle growth" every month looking for that missing piece. Some want faster recovery between sessions.

If you have been lifting heavy, eating right, and sleeping well but still feel like your body is not keeping pace with your effort, you are not alone. Thousands of people search for "peptides for muscle growth" every month looking for that missing piece. Some want faster recovery between sessions. Others want to push past a plateau that training alone has not broken.

Peptides have become one of the most talked-about topics in performance and recovery circles. But the gap between marketing hype and actual science is wide. Vendors oversell. Reddit threads contradict each other. And the published research, while promising in many areas, is not as clear-cut as the ads suggest.

This guide walks through every major peptide studied for muscle growth and recovery. For each one, you will get the mechanism of action, the strength of the evidence, known side effects, and regulatory status. No sales pitch. Just science, translated into plain language.

Table of Contents

How Peptides Influence Muscle Growth

Before diving into individual peptides, it helps to understand the three main biological pathways they target. Nearly every peptide on this list works through one or more of these routes.

The GH/IGF-1 Axis

Growth hormone (GH) is produced in the pituitary gland and released in pulses throughout the day, with the largest spikes during deep sleep. When GH enters the bloodstream, it triggers the liver to produce insulin-like growth factor 1 (IGF-1). IGF-1 is the real workhorse for muscle tissue. It drives protein synthesis through the PI3K/Akt/mTOR signaling pathway, the same pathway activated by resistance training and amino acid availability [1].

IGF-1 also blocks muscle breakdown. It suppresses ubiquitin ligases (the enzymes that tag muscle proteins for disposal) through the Akt/FoxO pathway [1]. So the GH/IGF-1 axis works both sides of the equation: building new protein while preventing existing protein from being broken down.

Most of the peptides in the "growth hormone releasing" category work by boosting GH output from the pituitary, which then raises circulating IGF-1. The goal is to amplify the body's own anabolic signaling.

One important caveat: raising GH levels does not automatically translate to bigger muscles. Studies in healthy adults have shown that even significant GH increases sometimes produce only modest changes in lean mass, with no measurable improvements in strength [2]. The relationship between the GH/IGF-1 axis and actual muscle performance is more complex than "more GH equals more muscle."

The Myostatin Pathway

Myostatin is a protein that acts as a brake on muscle growth. It belongs to the TGF-beta family and sends signals through activin type II receptors to limit how large muscles can get [3]. The famous "double muscled" cattle breeds (like Belgian Blues) have natural myostatin mutations that let their muscles grow far beyond normal.

Peptides that block myostatin, or its downstream signaling, remove this brake. Follistatin and ACE-031 both target this pathway, though through different mechanisms.

Repair and Regeneration

After intense training, muscle fibers sustain micro-damage. Recovery depends on satellite cells (muscle stem cells that sit dormant until activated), blood flow to the damaged area, and the inflammatory response that clears debris and triggers rebuilding.

Peptides like BPC-157 and TB-500 target these repair mechanisms directly. They promote blood vessel formation (angiogenesis), modulate inflammation, and appear to speed up satellite cell activation in animal models [4, 5].

Growth Hormone Releasing Peptides

This is the largest category, and it includes some of the most widely used peptides in clinical and off-label settings. They all share a common goal: stimulating the pituitary to release more growth hormone. But they differ in potency, selectivity, side effect profiles, and how long they stay active.

CJC-1295

CJC-1295 is a synthetic analog of growth hormone-releasing hormone (GHRH) with 30 amino acids. It comes in two forms: CJC-1295 without DAC (also called modified GRF 1-29) and CJC-1295 with DAC, which has a Drug Affinity Complex that extends its half-life significantly.

How it works: CJC-1295 binds to GHRH receptors on the pituitary gland, stimulating GH release. The version without DAC has a half-life of about 30 minutes, producing a GH pulse that mimics natural release patterns. CJC-1295 with DAC extends the half-life to 6-8 days, maintaining elevated GH levels over a much longer period.

Evidence: The strongest human data comes from a 2006 study in the Journal of Clinical Endocrinology & Metabolism. A single injection of CJC-1295 produced dose-dependent increases in mean plasma GH concentrations by 2- to 10-fold for 6 or more days, and IGF-1 levels by 1.5- to 3-fold for 9-11 days [6]. The peptide was safe and well tolerated at doses of 30 and 60 mcg/kg.

What's missing: These pharmacokinetic studies confirmed that CJC-1295 raises GH and IGF-1 levels effectively. But no published, peer-reviewed trial has measured actual muscle mass, strength, or body composition changes from CJC-1295 use in healthy adults. The leap from "raises GH" to "builds muscle" is assumed but not proven in clinical settings.

Side effects: Injection site reactions, headache, flushing, and diarrhea have been reported. CJC-1295 with DAC carries a theoretical risk of sustained GH elevation, which could affect blood sugar regulation over time.

Ipamorelin

Ipamorelin is a growth hormone secretagogue peptide (GHSP) that mimics ghrelin to stimulate GH release. It is often called the "cleanest" GH-releasing peptide because of its selectivity.

How it works: Ipamorelin binds to the ghrelin receptor (GHS-R1a) on the pituitary, triggering a GH pulse. Unlike GHRP-6 or GHRP-2, ipamorelin has minimal impact on cortisol, prolactin, or appetite hormones [7]. This selectivity is its main selling point.

Evidence: Pharmacokinetic studies in healthy adults show ipamorelin has a short half-life of about 2 hours and produces a single, time-limited GH pulse after dosing. A phase-2 trial (conducted for postoperative ileus, not muscle building) found it was well tolerated for up to 7 days [7]. No trials have measured muscle growth outcomes directly.

Common pairing: CJC-1295 and ipamorelin are frequently used together. The rationale is that CJC-1295 provides a sustained background GH elevation while ipamorelin produces acute GH pulses, mimicking a more natural secretion pattern. This combination is the most prescribed peptide stack in anti-aging clinics, though combination-specific clinical data on muscle outcomes is limited.

Side effects: Headache, nausea, and injection site reactions. The selective profile means less appetite stimulation and less cortisol release compared to other GH secretagogues.

GHRP-2

GHRP-2 (Growth Hormone Releasing Peptide-2) is a synthetic hexapeptide and one of the most potent GH secretagogues studied.

How it works: GHRP-2 binds to both the ghrelin receptor (GHS-R1a) and CD36 receptors. It stimulates GH release through cAMP production, mimicking the mechanism of endogenous GHRH, which sets it apart from GHRP-6 [8]. GHRP-2 releases more GH than GHRH itself in head-to-head comparisons.

Evidence: A retrospective review by Sigalos et al. assessed combined GHRP-2, GHRP-6, and sermorelin therapy in 14 hypogonadal men on testosterone therapy. After an average of 134 days of thrice-daily 100 mcg subcutaneous injections, participants showed significant increases in IGF-1 at all follow-up timepoints [9]. This is one of the few human studies examining GH secretagogues in a body composition context, though muscle mass was not directly measured.

Side effects: GHRP-2 raises cortisol and prolactin levels alongside GH, though less dramatically than GHRP-6 or hexarelin [8]. Some users report transient increases in appetite.

GHRP-6

GHRP-6 was the first growth hormone releasing peptide studied in humans and kicked off the entire GHRP field. It remains widely available but has largely been superseded by more selective alternatives.

How it works: GHRP-6 binds to the ghrelin receptor with strong affinity, triggering robust GH release. It works through intracellular calcium signaling and protein kinase C activation, a different pathway than GHRP-2 [8]. It also provokes a significant hunger response, likely through its ghrelin-mimicking activity.

Evidence: GHRP-6 has decades of research confirming its GH-releasing potency. Intravenous administration proved safe in a dose scale-up clinical trial in healthy volunteers, with no pharmacological interaction with common cardiovascular medications like metoprolol [10]. However, direct studies on muscle growth in healthy humans are absent.

Side effects: Strong appetite stimulation is the most notable effect, which some users view as a benefit (for bulking) and others as a drawback. GHRP-6 also raises cortisol and prolactin more than ipamorelin or GHRP-2.

Hexarelin

Hexarelin is the most potent growth hormone releasing peptide by raw GH output. It produces large, rapid GH spikes that exceed those of any other GHRP.

How it works: Like other GHRPs, hexarelin binds to the ghrelin receptor and stimulates GH release. It also has notable cardiovascular effects, interacting with CD36 receptors on cardiac tissue [10].

Evidence: In a pediatric study, Laron et al. gave 8 short prepubertal children intranasal hexarelin (60 mcg/kg three times daily) for up to 8 months. IGF-1 levels rose significantly (from 10.4 to 14.1 nmol/L, p < 0.004) and linear growth velocity increased from 5.3 to 8.3 cm/year [11]. In adults, hexarelin and GHRP-2 have similar GH-releasing activity, both exceeding GHRH [8].

One of hexarelin's most interesting research directions involves its cardiovascular protective effects. Chronic hexarelin treatment in spontaneously hypertensive rats reduced ventricular hypertrophy, diastolic dysfunction, and cardiac fibrosis [10].

Key limitation: Hexarelin desensitizes rapidly. The GH response diminishes significantly with continued use, typically within weeks. This makes it impractical for long-term muscle-building protocols.

Side effects: Cortisol and prolactin elevation. Rapid receptor desensitization. Water retention.

Sermorelin

Sermorelin is a 29-amino acid synthetic analog of GHRH, making it the shortest peptide with full GHRH biological activity. It was FDA-approved in 1990 for diagnosing and treating growth hormone deficiency in children, though it was discontinued in 2008 due to manufacturing difficulties, not safety issues [12].

How it works: Sermorelin binds to GHRH receptors on the pituitary gland and stimulates natural GH production. Because it works through the body's own feedback systems, overdosing is difficult. Somatostatin (the hormone that inhibits GH release) acts as a natural governor, preventing excessive GH output [12].

Evidence: Clinical results on muscle and body composition are mixed. One study failed to find significant changes in body weight, BMI, lean body mass, or total fat mass with sermorelin treatment. However, the same study noted improvements in 2 of 6 muscle strength tests and in muscle endurance [12]. Dosing frequency appears to matter: twice-daily administration produced more significant IGF-1 increases than nightly dosing alone.

Advantages: The built-in negative feedback mechanism makes sermorelin one of the safer GH-boosting peptides. It maintains natural GH pulsatility rather than creating constant elevation.

Side effects: Injection site reactions, headache, flushing, and dizziness. Generally mild.

Tesamorelin

Tesamorelin stands out among muscle-related peptides because it has the strongest clinical evidence and an actual FDA approval (granted in 2010 for HIV-associated lipodystrophy). It is a 44-amino acid GHRH analog that stimulates pulsatile, physiologic GH release.

How it works: Tesamorelin binds to GHRH receptors and prompts the pituitary to release GH in a natural pulsatile pattern. Phase III trials showed it raises IGF-1 levels by over 180% [13].

Evidence: Two Phase III trials (LIPO-010 and CTR-1011) involving 806 HIV-infected patients demonstrated significant visceral fat reduction (19.6% and 11.7%, respectively) [13]. A secondary analysis of these trials, published in the Journal of Frailty & Aging, found that tesamorelin responders showed significant increases in density across four trunk muscle groups (1.56-4.86 Hounsfield units, all p < 0.005) and significant increases in total area of the rectus and psoas muscles [14].

This is among the best clinical evidence any peptide has for actual measured changes in muscle tissue, though these findings came from secondary analyses of trials designed to study fat reduction, not muscle growth.

Limitations: All clinical data comes from HIV-positive populations with lipodystrophy. The effects in healthy adults without HIV remain to be established. Also, the trials did not measure muscle function or strength, so the clinical significance of the density and area increases is unknown. When treatment stops, visceral fat tends to return quickly [14].

Side effects: Injection site reactions, joint pain, peripheral edema, and hyperglycemia in some patients.

MK-677 (Ibutamoren)

MK-677 is not technically a peptide. It is a non-peptide, orally active ghrelin receptor agonist (a growth hormone secretagogue). It makes this list because it targets the same GH pathway and is frequently discussed alongside GH-releasing peptides.

How it works: MK-677 mimics ghrelin, binding to GHS-R1a receptors in the hypothalamus and pituitary to stimulate GH release. Its big advantage is oral bioavailability: no injections required. A single daily dose produces sustained GH and IGF-1 elevation [15].

Evidence: The landmark trial is the Nass et al. (2008) study published in Annals of Internal Medicine: a 2-year, double-blind, randomized, placebo-controlled trial in 65 healthy older adults (ages 60-81). Key findings [15]:

  • 24-hour mean GH levels increased 1.8-fold after one year
  • Serum IGF-1 increased 1.5-fold
  • Fat-free mass increased by 1.1 kg with MK-677 versus a 0.5 kg decrease with placebo
  • Changes were sustained through year two and reversed when treatment stopped

The catch? Increased fat-free mass did not translate to changes in strength or function. Researchers noted that some of the "lean mass" gains may represent intracellular water retention rather than new contractile muscle tissue [15].

Side effects: Increased appetite, ankle and leg edema (swelling), mild muscle aches, and a significant metabolic concern: fasting glucose increased by an average of 5 mg/dL, insulin sensitivity decreased, and cortisol rose by 47 nmol/L (p = 0.020) [15]. The insulin sensitivity issue is a serious consideration for long-term use.

Regulatory status: MK-677 is not FDA-approved for any indication and is prohibited by WADA.

IGF-1 Pathway Peptides

While the peptides above work upstream by boosting GH release (which then raises IGF-1), the following peptides act directly on the IGF-1 pathway. They skip the GH step entirely and deliver growth signals straight to muscle tissue.

IGF-1 LR3

IGF-1 LR3 (Long R3 Insulin-Like Growth Factor-1) is a modified version of IGF-1 with approximately 2-3 times the potency of the native hormone. The modification involves replacing glutamic acid at position 3 with arginine and adding 13 extra amino acids to the N-terminus.

How it works: These structural changes give IGF-1 LR3 very low binding affinity for IGF-binding proteins (IGFBPs), which normally sequester 95%+ of circulating IGF-1 and keep it inactive. With reduced IGFBP binding, more of the peptide remains free to activate IGF-1 receptors. It triggers the PI3K/Akt/mTOR pathway, the primary driver of muscle protein synthesis [1, 16].

IGF-1 LR3 acts systemically with a prolonged anabolic window compared to native IGF-1, working over hours to days rather than minutes.

Evidence: The science supporting IGF-1's role in muscle hypertrophy is extensive at the basic research level. IGF-1 activates satellite cell proliferation and differentiation, drives protein synthesis, and blocks protein degradation through multiple overlapping pathways [1]. However, the vast majority of this research involves native IGF-1, not the LR3 variant specifically. Human clinical trials of IGF-1 LR3 for muscle growth in healthy adults are essentially nonexistent.

Side effects: Hypoglycemia (because IGF-1 has insulin-like effects on glucose metabolism), joint pain, and potential for disproportionate tissue growth. The long duration of action raises concerns about sustained suppression of endogenous GH and IGF-1 production.

IGF-1 DES

IGF-1 DES (Des(1-3) IGF-1) is a truncated form of IGF-1 missing the first three amino acids of the N-terminus. This seemingly small change has big functional consequences.

How it works: The missing amino acids eliminate nearly all binding to IGFBPs, making IGF-1 DES roughly 10 times more potent than native IGF-1 at the receptor level [16]. However, it has a very short half-life (about 20-30 minutes), which means it acts rapidly but briefly. This makes it more of a localized peptide: when injected near a muscle, it delivers a concentrated growth signal to that specific area before being cleared.

Evidence: Like IGF-1 LR3, the mechanistic science is strong but specific clinical data on muscle building is almost entirely preclinical. The short half-life makes it impractical for systemic use but theoretically useful for targeted muscle growth.

Side effects: Similar to IGF-1 LR3 (hypoglycemia risk, joint pain), but the short duration limits systemic exposure. Localized injection site effects are possible.

MGF (Mechano Growth Factor)

MGF is a splice variant of IGF-1 that is naturally produced in muscle tissue after mechanical loading or damage. Its formal name is IGF-1Ec. When you lift heavy weights, the mechanical stress on muscle fibers triggers the production of MGF from the IGF-1 gene through alternative splicing [17].

How it works: MGF serves a different role than systemic IGF-1. It activates satellite cells, the dormant muscle stem cells that sit alongside muscle fibers. When satellite cells are activated, they proliferate and then fuse with damaged fibers or with each other to create new muscle tissue. MGF handles the first step: waking up and multiplying the satellite cells [17].

The body produces MGF quickly after exercise, with expression peaking in the hours following training. This is distinct from the liver-derived IGF-1 response, which takes longer to develop. Think of MGF as the "first responder" and systemic IGF-1 as the "construction crew."

Evidence: Research in both rodents and humans has confirmed that MGF expression increases in muscle after exercise and that it stimulates satellite cell proliferation [17]. A study in PLoS ONE showed that MGF is expressed in the growth plate during development and plays roles in tissue growth beyond just muscle [18]. However, clinical trials of synthetic MGF administration for muscle hypertrophy in humans have not been published.

Theoretical protocol: Some researchers have proposed that sequential use of MGF (to activate and multiply satellite cells) followed by IGF-1 LR3 (to drive differentiation and sustained protein synthesis) could optimize muscle hypertrophy. This mirrors the body's natural sequence, but the protocol remains theoretical and unvalidated in human trials.

Side effects: Limited data. The short half-life of unmodified MGF (minutes) has led to the development of PEGylated MGF (PEG-MGF), which lasts longer but introduces additional unknowns about safety.

Myostatin Inhibitors

Myostatin inhibitors take a completely different approach from everything listed above. Instead of adding more growth signals, they remove the body's built-in limit on muscle size. In theory, this is the most dramatic route to muscle growth. In practice, the science has been difficult to translate into safe therapies.

Follistatin

Follistatin is a naturally occurring glycoprotein that acts as a broad-spectrum inhibitor of the TGF-beta superfamily. It binds directly to myostatin, preventing myostatin from reaching its receptor and putting the brakes on muscle growth [3].

How it works: Follistatin does not just block myostatin. It also inhibits activin A and other TGF-beta ligands, which gives it a wider effect on muscle mass than myostatin-specific blockers. This broad mechanism is both its strength (more muscle growth potential) and its risk (more off-target effects).

Evidence: The most promising data comes from gene therapy approaches. AAV-delivered follistatin (FS344) has shown increased muscle size and strength in mice and monkeys [19]. In a small human gene therapy trial, patients with Becker muscular dystrophy and inclusion body myositis (sIBM) showed improved walking speed following FS344 gene transfer [19]. No organ system pathology or reproductive changes were observed in preclinical gene therapy studies.

For injectable follistatin peptide (as opposed to gene therapy), the evidence is far more limited. Most claims come from cell culture and animal studies.

Key concern: Follistatin's broad inhibition profile means it affects multiple systems beyond muscle. Activin signaling is involved in reproductive function, bone metabolism, and other processes. Long-term systemic follistatin administration could have unpredictable consequences.

Side effects: Limited safety data for injectable forms. Gene therapy trials reported no significant adverse events, but these involved localized delivery, not systemic administration.

ACE-031

ACE-031 (ramatercept) is a synthetic fusion protein that combines part of the activin type IIB receptor (ActRIIB) with the Fc region of human IgG1 antibody. It works as a decoy receptor, soaking up myostatin and related proteins before they can bind to actual muscle receptors [3].

How it works: ACE-031 latches onto myostatin, GDF11, and activins in the bloodstream. With these growth-limiting signals neutralized, muscle fibers can grow beyond their normal constraints. The approach is elegant in concept but difficult to control in practice.

Evidence: In healthy postmenopausal women, a single 3 mg/kg dose of ACE-031 led to significant increases in lean body mass and thigh muscle volume within 29 days [3]. That is a remarkable result for a single injection. A separate trial in boys with Duchenne muscular dystrophy showed promising trends in maintaining walking ability, increasing lean body mass, and improving bone mineral density [3].

Why it was discontinued: The DMD trial was halted early because of non-muscle-related adverse events: nosebleeds (epistaxis), gum bleeding, and telangiectasias (small dilated blood vessels near the skin surface). These vascular side effects were linked to cross-inhibition of BMP9 and BMP10, ligands involved in blood vessel maintenance [3]. A 43% decrease in follicle-stimulating hormone (FSH) was also observed in the healthy women study, indicating reproductive system disruption.

Current status: ACE-031 is no longer in active development. Its successor, ACE-083, is a follistatin-based fusion protein designed for local (intramuscular) injection to avoid systemic vascular side effects. ACE-083 showed localized muscle hypertrophy in mice without systemic effects [20], but its clinical development in neuromuscular diseases has had mixed results.

Recovery Peptides

Not all muscle-related peptides work by driving growth. Some of the most popular peptides in practice are valued for their role in speeding recovery from injury and intense training. Faster recovery means more frequent, higher-quality training sessions, which is often the real bottleneck for muscle growth.

BPC-157

BPC-157 (Body Protection Compound-157) is a 15-amino-acid synthetic peptide derived from a protein found in human gastric juice. It has become one of the most widely discussed peptides in the recovery and sports medicine world.

How it works: BPC-157 activates several overlapping repair pathways. It promotes angiogenesis (new blood vessel formation) through VEGFR2 and the Akt-eNOS axis. It engages ERK1/2 signaling, supports fibroblast activity, and reduces inflammation, particularly in poorly vascularized tissues like tendons and the myotendinous junctions where muscle meets tendon [4]. One intriguing finding: BPC-157 upregulates growth hormone receptor expression in tendon fibroblasts by up to sevenfold by day three of treatment [21].

Evidence: The animal data is extensive and consistently positive. In models of quadriceps transection, crush injury, and tendon rupture, BPC-157 treatment improved tissue regeneration, reduced fibrosis, and sped functional recovery [4, 21]. It has shown benefits in muscle, tendon, ligament, and bone healing models.

Human data is sparse. A 2021 retrospective study by Lee and Padgett compared BPC-157 knee injections (alone and combined with thymosin beta-4) in 16 patients with knee pain. At 6 months to 1 year follow-up, 14 of 16 patients reported significant pain relief [22]. However, most patients had ligamentous and tendinous sprains, which often heal on their own, and the study had no control group.

A 2025 systematic review in the Journal of Orthopaedic Sports Medicine concluded that while preclinical evidence for BPC-157 in musculoskeletal healing is promising, no rigorous human clinical trials have been completed [4].

Safety: In animal models, BPC-157 showed no acute toxicity across liver, spleen, lung, kidney, brain, thymus, prostate, and ovaries over a wide dose range (6 mcg/kg to 20 mg/kg) [4]. No lethal dose was established. However, no human clinical safety data exists.

Side effects: Reported anecdotally: nausea, dizziness, and headache, though these reports come from self-experimentation rather than controlled studies.

TB-500

TB-500 is a synthetic version of the active region of thymosin beta-4, a naturally occurring peptide found in high concentrations in platelets and wound fluid. Specifically, TB-500 is the N-acetylated 17-23 fragment (Ac-LKKTETQ) of thymosin beta-4 [5].

How it works: TB-500's core mechanism involves binding to G-actin monomers and regulating actin polymerization. This allows cells to rapidly reorganize their cytoskeleton and migrate into injured tissue [5]. It downregulates inflammatory cytokines and oxidative stress during acute injury, promotes endothelial cell differentiation and angiogenesis, and modulates myofibroblast activity to reduce scar tissue formation [5].

The anti-scarring property is particularly relevant for muscle injuries, where excessive scar tissue leads to stiffness, reduced function, and high re-injury risk.

Evidence: Like BPC-157, the evidence base is predominantly preclinical. Animal studies demonstrate faster healing, reduced inflammation, and improved tissue regeneration across multiple tissue types. Human clinical data is extremely limited, with most evidence coming from case reports and observational studies.

TB-500 and BPC-157 are frequently combined (the so-called "Wolverine Stack") based on the rationale that BPC-157 provides localized, targeted repair while TB-500 supports broader systemic healing and inflammation control [5].

Safety: Limited published safety data. The peptide is well-tolerated in animal models, but human safety profiles are not established.

Side effects: Anecdotal reports include headache, nausea, and lightheadedness. Some users report a temporary feeling of lethargy.

Comparing Muscle Growth Peptides

PeptidePrimary MechanismEvidence LevelAdministrationWADA StatusKey AdvantageKey Limitation
CJC-1295GHRH analog, raises GH/IGF-1Moderate (human PK data)Subcutaneous injectionProhibitedSustained GH elevationNo muscle outcome data
IpamorelinGhrelin mimetic, selective GH releaseModerate (human PK data)Subcutaneous injectionProhibitedMinimal cortisol/prolactin effectsNo muscle outcome data
GHRP-2Ghrelin receptor agonistModerate (human PK + limited body comp)Subcutaneous injectionProhibitedPotent GH releaseRaises cortisol/prolactin
GHRP-6Ghrelin receptor agonistModerate (human PK data)Subcutaneous injectionProhibitedStrong GH pulseIntense appetite stimulation
HexarelinGhrelin receptor agonistModerate (human PK data)Subcutaneous/intranasalProhibitedStrongest GH releaseRapid desensitization
SermorelinGHRH analogModerate (formerly FDA-approved)Subcutaneous injectionProhibitedNatural feedback regulationMixed body comp results
TesamorelinGHRH analogStrong (Phase III trials)Subcutaneous injectionProhibitedFDA-approved, real muscle dataOnly studied in HIV populations
MK-677Oral ghrelin mimeticStrong (2-year RCT)OralProhibitedNo injections neededLean mass gains may be water; insulin resistance
IGF-1 LR3Direct IGF-1 receptor activationStrong mechanistic, weak clinicalSubcutaneous injectionProhibitedBypasses GH step, potentHypoglycemia risk; no human muscle trials
IGF-1 DESDirect IGF-1 receptor activationPreclinical onlyIntramuscular injectionProhibited10x potency of native IGF-1Very short half-life; no human trials
MGFSatellite cell activationPreclinical onlyIntramuscular injectionProhibitedTargets muscle stem cellsExtremely short half-life; no human trials
FollistatinMyostatin/activin inhibitionModerate (gene therapy trials)Intramuscular injectionProhibited (S4 category)Removes muscle growth brakeBroad off-target effects possible
ACE-031ActRIIB decoy receptorModerate (human trials, discontinued)Subcutaneous injectionProhibited (S4 category)Rapid lean mass gains in trialsDiscontinued due to vascular side effects
BPC-157Angiogenesis, repair pathwaysStrong preclinical, weak clinicalSubcutaneous/oralProhibited (S0 category)Broad tissue healingNo rigorous human trials
TB-500Actin regulation, anti-inflammatoryPreclinicalSubcutaneous injectionProhibitedSystemic healing supportVery limited human data

Safety Considerations

Regulatory Status

No peptide on this list is FDA-approved for muscle building in healthy adults. Here is the regulatory picture:

  • FDA-approved for specific conditions: Tesamorelin (HIV-associated lipodystrophy). Sermorelin was previously approved for pediatric GH deficiency but was discontinued in 2008 due to manufacturing issues.
  • Research-only or off-label: CJC-1295, ipamorelin, GHRP-2, GHRP-6, hexarelin, MK-677, all IGF-1 variants, MGF, follistatin, ACE-031 (discontinued), BPC-157, TB-500.
  • Not FDA-approved for any indication: MK-677 cannot legally be sold as a dietary supplement in the United States.

The FDA has tightened regulations on peptide compounding in recent years, making several previously available peptides harder to access through compounding pharmacies.

WADA Status

Every peptide discussed here is prohibited by the World Anti-Doping Agency under the 2026 Prohibited List [23]:

  • S2.2.3: Growth hormone analogues and fragments (includes Fragment 176-191, AOD-9604)
  • S2.2.4: Growth hormone releasing factors (includes CJC-1295, sermorelin, tesamorelin) and growth hormone secretagogues and their mimetics (includes ipamorelin, GHRP-2, GHRP-6, hexarelin, MK-677)
  • S2 (growth factors): IGF-1 and all variants (LR3, DES, MGF)
  • S4 (hormone and metabolic modulators): Myostatin inhibitors including ACE-031, follistatin, and anti-activin receptor IIB antibodies
  • S0 (unapproved substances): BPC-157

If you compete in any sport governed by WADA or USADA rules, peptide use will result in a doping violation.

Common Side Effects Across Categories

GH-releasing peptides (CJC-1295, ipamorelin, GHRPs, sermorelin, tesamorelin, MK-677):

  • Water retention and joint swelling
  • Carpal tunnel-like symptoms (tingling, numbness in hands)
  • Increased blood sugar and reduced insulin sensitivity
  • Potential for abnormal tissue growth with sustained GH elevation
  • Injection site reactions

IGF-1 pathway peptides:

  • Hypoglycemia (IGF-1 has insulin-like effects)
  • Joint and muscle pain
  • Potential for disproportionate growth of non-target tissues

Myostatin inhibitors:

  • Off-target effects on vascular, reproductive, and bone systems
  • ACE-031 specifically caused nosebleeds and vascular abnormalities

Recovery peptides (BPC-157, TB-500):

  • Generally well-tolerated in animal studies
  • No established human safety profiles
  • Unknown long-term effects

The Medical Supervision Question

Every peptide on this list carries risks that are difficult to self-manage. Blood glucose monitoring, hormone panel testing, and awareness of contraindications all require medical oversight. Self-sourcing peptides from unregulated suppliers introduces additional risks: contamination, incorrect dosing, mislabeled products, and the absence of quality control that pharmaceutical manufacturing provides.

If you are considering any peptide discussed here, working with a physician who is knowledgeable about peptide therapies is not optional. It is essential.

Frequently Asked Questions

What is the best peptide for muscle growth?

There is no single "best" peptide because the answer depends on what you mean by "best." Tesamorelin has the strongest clinical evidence for measurable changes in muscle tissue, but it has only been studied in HIV populations. The CJC-1295/ipamorelin combination is the most widely prescribed in clinical practice. MK-677 has the most robust randomized controlled trial data in healthy adults, but the lean mass gains may partly reflect water retention rather than new muscle. For people focused on recovery from injuries, BPC-157 has the most extensive (though preclinical) evidence base.

Do peptides actually build muscle?

Peptides that raise GH and IGF-1 levels can increase lean body mass, as demonstrated in the MK-677 trial and tesamorelin studies. However, "lean body mass" is not the same as "contractile muscle tissue." The MK-677 study found lean mass increases but no strength improvements, suggesting some of the gains were water or connective tissue [15]. The honest answer: peptides can support muscle growth as part of a comprehensive program that includes resistance training, adequate protein, and recovery. They are not a substitute for those fundamentals.

How do peptides compare to anabolic steroids for muscle growth?

Steroids directly activate the androgen receptor in muscle tissue, producing rapid and significant muscle growth. Peptides work indirectly, primarily by boosting the body's GH and IGF-1 levels. The muscle-building effects of peptides are more subtle and slower than steroids. However, peptides generally have a milder side effect profile and do not suppress natural testosterone production the way anabolic steroids do. They occupy a different risk-benefit zone.

Can I stack multiple peptides together?

Stacking is common in practice. The most popular combination is CJC-1295 with ipamorelin, pairing sustained GH elevation with pulsatile release. Some protocols add BPC-157 and/or TB-500 for recovery support. Theoretically, sequential use of MGF followed by IGF-1 LR3 could optimize satellite cell activation and differentiation. However, stacking increases complexity, cost, potential interactions, and the difficulty of identifying which compound is causing any side effects.

In the United States, peptides exist in a regulatory gray area. They are not controlled substances in most cases, but they are also not approved for performance or physique use. Purchasing peptides labeled "for research use only" is legal, but using them on yourself puts you outside FDA oversight and medical regulation. In competitive sports, all peptides discussed here are prohibited. The legal picture continues to shift as the FDA tightens oversight of compounding pharmacies.

What are the side effects of growth hormone peptides?

The most common side effects across the GH-releasing peptide category include water retention, joint stiffness or swelling, tingling in the hands (carpal tunnel-like symptoms), increased appetite (especially with GHRP-6 and MK-677), elevated blood sugar, and reduced insulin sensitivity. Most of these effects are dose-dependent and reversible when treatment stops.

How long before I see results from peptides?

Most users report improved sleep quality and recovery within the first 2-4 weeks. Changes in body composition (reduced fat, modest lean mass increases) typically require 2-3 months of consistent use. The MK-677 trial showed measurable lean mass changes at 12 months [15]. Peptides work gradually by amplifying natural processes, not by creating overnight transformations.

Are peptides safe for long-term use?

Long-term safety data is limited for most peptides on this list. The longest controlled trial is the 2-year MK-677 study, which identified concerning trends in insulin sensitivity [15]. Tesamorelin has Phase III data spanning 26 weeks. For most other peptides, safety profiles are extrapolated from shorter studies or animal data. This is a real gap in the research, and one reason medical supervision is important.

The Bottom Line

The peptide space for muscle growth is a mix of solid mechanistic science, promising animal data, and surprisingly thin clinical evidence in healthy humans. Here is what we know with confidence:

The GH/IGF-1 axis is real and important. Peptides that raise GH and IGF-1 levels do so reliably. CJC-1295, ipamorelin, the GHRPs, sermorelin, tesamorelin, and MK-677 all have human data confirming their ability to increase these hormones.

Raising GH does not automatically equal muscle growth. The best clinical trial on this question (the 2-year MK-677 study) showed lean mass increases but no strength improvements. Tesamorelin shows muscle density and area changes, but only in secondary analyses of HIV populations.

Recovery peptides show real promise but lack human validation. BPC-157 and TB-500 have extensive and convincing animal data for tissue repair. Human evidence is limited to small, uncontrolled studies.

Myostatin inhibition is powerful but hard to control. ACE-031 produced rapid lean mass gains in a single dose but was discontinued due to vascular side effects. Follistatin gene therapy looks promising in disease populations.

Nothing replaces the basics. Progressive resistance training, adequate protein intake (1.6-2.2 g/kg/day), quality sleep, and creatine monohydrate remain the most evidence-backed strategies for building muscle. Peptides may offer incremental benefits on top of these foundations, not as replacements for them.

If you are interested in exploring peptides, start by having a conversation with a physician who understands both the science and the current regulatory environment. And read the research yourself: the references below are a good starting point.

Related guides:

This article is for educational purposes only and does not constitute medical advice. Peptides discussed here are not approved by the FDA for muscle building or athletic performance in healthy individuals. Always consult a qualified healthcare provider before considering any peptide therapy. PeptideJournal.org has no financial relationships with peptide vendors or clinics.

References

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