Peptides & growth hormone

GHRP-6

Updated · 25 sources · Editorial policy

GHRP-6 (growth hormone-releasing peptide 6) is a synthetic six-amino-acid peptide that makes the pituitary gland release growth hormone (GH). It was designed in the early 1980s, years before anyone knew which receptor it acted on, and it later became the template for a whole family of drugs that mimic the stomach hormone ghrelin (Bowers et al., Endocrinology 1984; Bowers, Methods Enzymol 2012).

In people, GHRP-6 has been used almost entirely as a research and diagnostic tool: single injections to study GH regulation, and a combined test with GH-releasing hormone (GHRH) to diagnose adult GH deficiency. More recently, a Cuban group has tested it with epidermal growth factor in acute stroke.

The single most important fact: GHRP-6 has never been an approved medicine in the US, no controlled human trial has tested it for muscle growth, fat loss or performance, and FDA lists it among bulk drug substances that may present significant safety risks in compounding (FDA category 2 list).

This page summarizes what the published human studies, pharmacology papers and regulators report. It is for education only and is not medical advice.

Property Detail
Class Synthetic GH-releasing peptide (GHRP); ghrelin receptor (GHS-R1a) agonist
Structure Hexapeptide, C46H56N12O6, molecular weight 873.0 (PubChem)
Routes studied in humans Intravenous, oral, intranasal and sublingual
Doses in cited human studies 0.1–1 µg/kg IV for GH testing; 100–400 µg/kg IV in a pharmacokinetic study; 300 µg/kg orally
Half-life Distribution ≈7.6 min and elimination ≈2.5 h after an IV bolus in 9 healthy men
Key mechanism fact Needs the body’s own GHRH for most of its GH effect; acts synergistically with GHRH
Hormones also raised Cortisol, ACTH and prolactin, at least at higher test doses
US status Not an approved drug; FDA compounding category 2 (503B) since September 29, 2023; not a scheduled controlled substance
WADA status Prohibited at all times, S2.2.4 (named as GHRP-6)

What it is

GHRP-6 grew out of work by Cyril Bowers, Frank Momany and colleagues. They noticed that two modified forms of the opioid peptide met-enkephalin weakly released GH from rat pituitary cells in culture. Using conformational energy calculations, they designed a series of progressively more active analogs, reaching a pentapeptide about 1,000 times more active than the starting compounds (Momany et al., Endocrinology 1981).

The hexapeptide now called GHRP-6 was reported in 1984. In pituitary incubation assays it was active at 1–10 ng/mL, and it worked in rats, monkeys, lambs and calves. In those animal studies it released GH without releasing LH, FSH, TSH or prolactin (Bowers et al., 1984).

Structurally, GHRP-6 is a short chain of six amino acids. Two of them are D-amino acids (the mirror-image forms not normally used by the body), and the end of the chain is amidated. Its molecular formula is C46H56N12O6 and its molecular weight is 873.0 (PubChem CID 9919153).

A drug that predicted a hormone

For more than a decade, nobody knew what GHRP-6 bound to. Bowers argued early on that it was imitating an undiscovered natural hormone, because it acted differently from GHRH (Bowers, 2012). Two discoveries confirmed this:

  • 1996: Researchers cloned the receptor for these synthetic secretagogues, a G protein-coupled receptor found in the pituitary and hypothalamus of pigs and humans, now called GHS-R1a (Howard et al., Science 1996).
  • 1999: Kojima and Kangawa isolated the receptor’s natural ligand from the stomach, a 28-amino-acid acylated peptide they named ghrelin (Kojima et al., Nature 1999).

GHRP-6 is therefore best understood as an early synthetic ghrelin mimetic. Related compounds with their own pages include GHRP-2, hexarelin, ipamorelin and the oral non-peptide ibutamoren (MK-677). WADA lists all of them in the same class (WADA 2026 Prohibited List).

How it works in the body

Mechanism

GHRP-6 acts on the pituitary and on the hypothalamus. Three human findings shape how it works:

  • It depends on GHRH. In 9 healthy young men, blocking GHRH with a specific GHRH antagonist cut the GH rise after 1 µg/kg GHRP-6 from 33.8 to 6.2 µg/L, and the area under the GH curve from 1701 to 376 µg·min/L (Pandya et al., JCEM 1998). So most of its effect requires the body’s own GHRH.
  • It is synergistic with GHRH. Low doses of GHRP-6 given together with GHRH released more GH than either alone would predict (Bowers et al., JCEM 1990). This synergy is the basis of the diagnostic test described below.
  • It amplifies pulses rather than adding new ones. During a 34-hour infusion in 9 young men, GHRP-6 nearly doubled GH pulse amplitude but did not change pulse frequency (Jaffe et al., JCEM 1993).

In rats, somatostatin (the hypothalamic hormone that switches off GH release) blocked the GH response to GHRP-6 (Bowers et al., 1984).

Pharmacokinetics

Only one dedicated human pharmacokinetic study has been published. Nine healthy men received single IV bolus doses of 100, 200 and 400 µg/kg, and plasma GHRP-6 was measured by mass spectrometry (Cabrales et al., Eur J Pharm Sci 2013):

Parameter Result
Model Two-compartment (bi-exponential) disposition
Distribution half-life 7.6 ± 1.9 min
Elimination half-life 2.5 ± 1.1 h
Dose proportionality Exposure (AUC) rose roughly in proportion to dose
Unexpected finding Concentration spikes during the elimination phase in 4 of 9 subjects

These doses were far higher than the 1 µg/kg used in GH testing, and no human pharmacokinetic data exist for subcutaneous, oral or intranasal use. Oral GHRP-6 does release GH, but the oral human studies used 300 µg/kg (Ghigo et al., Eur J Endocrinol 1994; Bellone et al., Eur J Endocrinol 1995).

In an anti-doping excretion study, one volunteer took GHRP-6 by the nasal route. It was excreted mostly unchanged and was detectable in urine for 23 hours, while its metabolites were detectable for only 12 hours (Semenistaya et al., Drug Test Anal 2015).

Regulatory status

  • Not an approved drug. FDA’s Drugs@FDA data contain no product with GHRP-6 as an active ingredient (Drugs@FDA via openFDA), and a 2026 review of GH-axis peptides noted the absence of regulatory approval for physique or performance indications (Dominikowski et al., Front Endocrinol 2026).
  • FDA compounding category 2. FDA added GHRP-6 to category 2 for outsourcing facilities (503B) on September 29, 2023. FDA cited a risk of immunogenicity (an immune reaction against the peptide) for certain routes, due to aggregation and peptide-related impurities. It also said the limited safety data reveal concerns including a potential effect on cortisol and higher blood glucose from reduced insulin sensitivity (FDA).
  • Not a controlled substance. GHRP-6 is not named in the US anabolic steroid schedule (21 CFR 1308.13).
  • Banned in sport. WADA prohibits GHRP-6 at all times under S2.2.4, growth hormone releasing factors (WADA 2026 Prohibited List).

What the research shows

GH release in healthy adults

The first controlled human dose-response study gave single IV doses to 18 healthy men (Bowers et al., 1990):

IV dose Mean peak GH (µg/L)
Placebo 1.2
0.1 µg/kg 7.6
0.3 µg/kg 16.5
1.0 µg/kg 68.7

LH and TSH did not change in the first hour. Prolactin and cortisol about doubled, but only at the 1 µg/kg dose.

In the 34-hour infusion study, integrated GH concentration rose from 1374 to 2908 µg·min/L compared with saline, and IGF-1 (the growth factor made mainly in the liver in response to GH) rose from 252 to 312 µg/L. The pituitary stayed responsive, although the GH response to a further GHRP-6 bolus at the end of the infusion was smaller (Jaffe et al., 1993).

Diagnosing adult GH deficiency

Because GHRH plus GHRP-6 is a very strong combined stimulus, a European multicenter study tested it as a diagnostic tool (Popovic et al., Lancet 2000). It enrolled 125 adults with organic pituitary disease and 125 healthy controls, who received GHRH 1 µg/kg plus GHRP-6 1 µg/kg IV.

Test Mean peak GH, controls Mean peak GH, GH-deficient patients
GHRH + GHRP-6 59.2 µg/L 4.1 µg/L
Insulin tolerance test 14.3 µg/L 0.5 µg/L

A cut-off of 15 µg/L separated healthy from GH-deficient adults, and the authors reported no side effects.

Oral, intranasal and sublingual use

GHRP-6 is one of the few peptides shown to release GH after oral dosing in people, though at high doses:

  • Older women. In 7 women aged 65–82, oral GHRP-6 at 300 µg/kg raised peak GH to 10.7 µg/L, more than IV GHRH (5.1 µg/L). After 4 days of twice-daily oral dosing the response was maintained (16.8 µg/L), but IGF-1 did not rise significantly (77.1 vs 84.1 µg/L) (Ghigo et al., 1994).
  • Children with short stature. In 7 children, a single oral dose of 300 µg/kg raised GH from 1.1 to a peak of 18.8 µg/L, similar to IV GHRH (Bellone et al., 1995).
  • Sleep study in young men. An evening oral dose of 300 µg/kg in enteric-coated capsules did not change overnight GH, ACTH or cortisol. An intranasal dose of 30 µg/kg significantly raised overnight GH, while a sublingual dose only produced a trend (Frieboes et al., J Neuroendocrinol 1999).

Acute ischemic stroke (with epidermal growth factor)

The only recent clinical program comes from the Center for Genetic Engineering and Biotechnology in Havana, which tested IV GHRP-6 combined with recombinant epidermal growth factor (EGF), twice daily for 7 days:

Trial Design and n Doses Main result
Phase I/II (Hernández-Bernal et al., Front Neurol 2024) Open-label, randomized; 36 patients EGF 75 µg + GHRP-6 3.5 mg or 5 mg, vs standard care Serious adverse events in 30% and 20% of the two treated groups vs 56.2% of controls; only two events in one patient were attributed to treatment
Phase III, COURAGE-2 (Hernández-Bernal et al., J Clin Neurosci 2026) Open-label, randomized, multicenter; 188 patients (95 treated, 93 controls) EGF 75 µg + GHRP-6 5 mg, vs standard care Missed its primary endpoint. No difference in disability (modified Rankin scale), Barthel index or survival in the full population

In COURAGE-2, a subgroup of 27 patients with severe stroke did better on treatment, but subgroup results from an open-label trial that missed its main endpoint are hypothesis-generating only. Neither trial isolates the effect of GHRP-6 from that of EGF.

Muscle, fat loss and performance

No randomized trial has tested GHRP-6 for muscle mass, strength, fat loss or athletic performance. A 2026 review concluded that direct human evidence for meaningful body-composition changes is limited and that such claims extrapolate from its GH-releasing effect (Dominikowski et al., 2026).

The closest human data are uncontrolled. A retrospective chart review of men on testosterone therapy who were prescribed a combination of GHRP-6, GHRP-2 and sermorelin found that IGF-1 rose from 159.5 to 239.0 ng/mL over a mean of 134 days. Only 14 of 105 men met the compliance criteria, there was no control group, and the study measured hormone levels rather than body composition (Sigalos et al., Am J Mens Health 2017).

In immature rats, daily injections increased body-weight gain over 9 to 25 days (Bowers et al., 1984). This is animal data and does not show an effect on muscle in adults.

Appetite

GHRP-6 is often described as strongly appetite-stimulating. The direct evidence for GHRP-6 itself is from rats: injected into the brain ventricles of fed rats, it caused dose-related eating that was independent of GH release (Locke et al., Life Sci 1995). The controlled human food-intake studies cited in a 2026 review were done with GHRP-2, not GHRP-6 (Dominikowski et al., 2026), and we found no published human food-intake study of GHRP-6.

Side effects and risks

Short-term human studies reported GHRP-6 as well tolerated. In the 1990 dose-response study there were no adverse clinical effects or laboratory abnormalities (Bowers et al., 1990), and the large diagnostic study reported no side effects (Popovic et al., 2000). These were single doses under supervision. Most published human studies used single doses or a few days of dosing, so they say little about repeated use.

Cortisol, ACTH and prolactin

GHRP-6 is not purely selective for GH in humans:

  • At 1 µg/kg IV, prolactin and cortisol about doubled (Bowers et al., 1990).
  • Repeated IV boluses raised GH, ACTH and cortisol and increased stage 2 sleep, as summarized by the same research group (Frieboes et al., 1999).
  • The cortisol response is consistent enough that GHRP-6 (1 µg/kg) was evaluated as a test for adrenal insufficiency. It activated the stress-hormone (HPA) axis with no detectable side effects, but it was less accurate than the insulin tolerance test (sensitivity 71.0%, specificity 77.8%) (Alaioubi et al., Horm Metab Res 2010).

A 2026 clinical review notes that cortisol and prolactin rises from GHRP-6, GHRP-2 and hexarelin can confound hormone tests, whereas ipamorelin largely spares these axes (Dominikowski et al., 2026).

Blood glucose and insulin sensitivity

FDA named higher blood glucose from reduced insulin sensitivity as a safety concern for GHRP-6 (FDA). No published human trial has measured this for GHRP-6 over repeated dosing.

Immunogenicity and product quality

FDA’s compounding assessment flagged a risk of immune reactions for certain routes, linked to peptide aggregation and peptide-related impurities (FDA). Because GHRP-6 has no approved product, material sold outside clinical research has no regulator-verified identity, purity or dose.

Unknown long-term effects

There are no long-term human safety data for GHRP-6, and reported heart-protective effects come from animal and cell studies that have not been confirmed in human trials (Dominikowski et al., 2026). In COURAGE-2, serious adverse events occurred in 48 of 188 patients overall, 30 of them in the treated group of 95 (OR 1.92, 95% CI 0.98–3.77); the investigators judged none to be treatment-related (Hernández-Bernal et al., 2026).

Detection in sport

GHRP-6 is named on the WADA Prohibited List under S2.2.4 and is banned in and out of competition (WADA 2026 Prohibited List). Anti-doping laboratories detect it by liquid chromatography-mass spectrometry. In the nasal excretion study, the unchanged peptide was found in urine for 23 hours after one dose (Semenistaya et al., 2015).

Key takeaways

  • An early synthetic ghrelin mimetic. GHRP-6 was designed from enkephalin analogs in the early 1980s and helped lead to the discovery of the ghrelin receptor (1996) and ghrelin itself (1999).
  • A potent but GHRH-dependent GH releaser. Single IV doses of 1 µg/kg raised mean peak GH to 68.7 µg/L in healthy men, and blocking GHRH removed most of that effect.
  • Mainly a research and diagnostic tool. Its best-documented human use is the GHRH plus GHRP-6 test for adult GH deficiency.
  • No evidence for muscle or fat-loss benefits. No controlled human trial has tested body composition or performance, and the main recent trial (stroke, combined with EGF) missed its primary endpoint.
  • Not GH-selective. It also raises cortisol, ACTH and prolactin, and FDA has flagged effects on cortisol and blood glucose.
  • Unapproved and banned in sport. It has no FDA approval, sits on FDA’s compounding category 2 list, and is prohibited at all times by WADA.

Sources

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  16. Hernández-Bernal F, Estenoz-García D, Gutiérrez-Ronquillo JH, et al. Combination therapy of Epidermal Growth Factor and Growth Hormone-Releasing Hexapeptide in acute ischemic stroke: a phase I/II non-blinded, randomized clinical trial. Front Neurol. 2024;15:1303402. PubMed; PMC.
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  22. Food and Drug Administration. Certain bulk drug substances for use in compounding that may present significant safety risks (category 2 under the interim policies). Content current as of April 22, 2026. FDA.
  23. World Anti-Doping Agency. The 2026 Prohibited List, in effect January 1, 2026. WADA 2026 Prohibited List.
  24. Code of Federal Regulations. 21 CFR 1308.13, Schedule III. eCFR.
  25. Food and Drug Administration. Drugs@FDA data, openFDA drugsfda endpoint; no product listing GHRP-6 as an active ingredient (searched October 12, 2026). FDA.