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Evidence: MediumPeptideResearch ChemicalGrowth Hormone SecretagogueGhrelin Receptor AgonistResearch Compound

GHRP-6

The original growth hormone-releasing hexapeptide: a strong, fast releaser in 1990s human tests that also raises ACTH and cortisol, and was never developed into a medicine.

GHRP-6 is a six-amino-acid peptide made in the early 1980s, before anyone knew the receptor it works through. In small human studies a single intravenous dose released as much growth hormone as GHRH, and far more when the two were given together. It also raised ACTH and cortisol, and it has never been tested as a treatment in people.

View Dosing Data Read Research →
Overview

What is it?

GHRP-6 came out of Cyril Bowers's laboratory, which in 1984 described a synthetic hexapeptide, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2, that released growth hormone in rat pituitary cells within minutes and did the same in rats, monkeys, lambs and calves. In those experiments it released growth hormone without releasing LH, FSH, TSH or prolactin, and it kept working when given into a vein, under the skin or into the abdomen. Nobody yet knew what it acted on: its receptor was cloned in the 1990s, and that receptor's natural hormone turned out to be ghrelin.

In people, GHRP-6 was used almost entirely as a probe. Endocrinologists gave one intravenous dose, usually 1 µg/kg, and measured growth hormone over the next hour or two, alone or together with GHRH. The two together released several times more than either alone, which made the pair the strongest growth hormone stimulus of its day and a candidate test for diagnosing deficiency. The same studies found the response depends on an intact connection between the hypothalamus and the pituitary, and changes with thyroid and adrenal disease.

Growth hormone was not the only thing it released. An overnight study in healthy men found higher ACTH and cortisol after GHRP-6, the opposite of GHRH, which blunts cortisol, and later studies found an exaggerated ACTH response in people with Addison's disease on replacement. That hormonal side effect, and the short action of an injected peptide, are part of why drug developers moved on: GHRP-6 became the template for orally active non-peptide secretagogues such as MK-0677 (ibutamoren).

Since the mid-2000s the research has shifted to animals and to a different question: whether GHRP-6 protects tissue. Rat and mouse studies report less organ damage after interrupted blood flow, antibiotic kidney injury and doxorubicin heart damage. None of this has been tested in people. GHRP-6 is not an approved medicine anywhere, and what is sold online as GHRP-6 is an unregulated research chemical.

7.6 min / 2.5 h
half-lives in blood
single IV doses, 9 healthy men (2013)
15.4 vs 5.5 ng/mL
night-time growth hormone
4 × 50 µg IV vs placebo
3,542 vs 1,221
GH response with GHRH vs alone
area under the curve, 7 controls
9 of 15
carded studies in people
all single-session endocrine tests
Science

Mechanism of Action

GHRP-6 activates the ghrelin receptor. At the pituitary that releases growth hormone directly, and at the hypothalamus it appears to amplify the brain's own signal, which is why the response collapses when the pituitary stalk is cut. The same receptor also drives ACTH and cortisol.

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Ghrelin receptor: growth hormone

In rat pituitary cells GHRP-6 released growth hormone at 1 to 10 ng/mL and, injected into rats, raised it within two minutes with a peak at 10 to 20 minutes. In people a single 1 µg/kg intravenous dose released about as much as GHRH, and the two together roughly three times more than either alone.

⇄

It needs an intact hypothalamus

Children whose pituitary stalk was cut around birth released almost no growth hormone after GHRP-6, less even than after GHRH, and none passed 5 µg/L with both together. A releaser that acted only on the pituitary would still work; GHRP-6 largely did not.

↑

ACTH and cortisol

Overnight doses raised ACTH and cortisol in healthy men, and the ACTH response was many times larger in Addison's disease on replacement. GHRH does the opposite and blunts cortisol, so this is a property of the ghrelin-receptor route, not of growth hormone release in general.

⚡

Inside the cell

In cultured rat somatotrophs GHRP-6 raised inositol phosphates, activated protein kinase C and triggered a calcium spike. Somatostatin given three minutes earlier blunted that spike, one reason GHRP-6 was described as a functional somatostatin antagonist.

Evidence

Published Research

Our evidence set holds 34 papers that name GHRP-6. Fifteen name it in their titles and have an abstract, and all fifteen are carded below: nine studies in people, four in animals, one in cultured cells and one review. The human studies are small single-session endocrine experiments from 1995 to 2013; none gave GHRP-6 for more than one night or tested it as a treatment. The animal studies since 2006 ask a different question, tissue protection, and have not been repeated in people. Two further sources, the 1984 discovery paper and a 1998 review of the whole peptide family, are listed under References without a card.

Human1995

Overnight doses in healthy men

Healthy men received four intravenous 50 µg boluses of GHRP-6 or placebo during the night. Between 22:00 and 03:00 growth hormone averaged 15.4 ng/mL against 5.5 on placebo, ACTH 21.0 against 16.6 pg/mL and cortisol 56.0 against 25.2 ng/mL. Stage 2 sleep lengthened from 245 to 270 minutes while slow-wave sleep did not change. GHRH, the authors note, blunts cortisol instead.

PMID: 7617137
Human1995

After pituitary stalk transection

Seven children with growth hormone deficiency from perinatal pituitary stalk transection and seven matched controls received 1 µg/kg intravenously of GHRH, GHRP-6, or both. In controls GHRP-6 released about as much growth hormone as GHRH (area 1,221 vs 1,029) and the pair released 3,542. In patients GHRP-6 released almost nothing (37, less than GHRH's 116), and no patient passed 5 µg/L even with both.

PMID: 7593423
Human1995

By mouth in short children

Thirteen prepubertal children of normal short stature took GHRP-6 by mouth at 300 µg/kg. In the first seven, growth hormone peaked at 60 minutes at 18.8 µg/L from a baseline of 1.1, close to the response to the maximally effective intravenous GHRH dose (20.8 µg/L). The oral dose was about 300 times the usual intravenous test dose.

PMID: 7581965
In Vitro1995

Signalling in rat pituitary cells

In cultured rat anterior pituitary cells GHRP-6 released growth hormone in a dose-dependent way, raised inositol phosphates, increased protein kinase C activity and set off a calcium spike in single somatotrophs. Somatostatin added three minutes beforehand diminished the calcium spike; added at the same time it had no effect.

PMID: 8903947
Review1996

As a test for growth hormone deficiency

Assessing GHRP-6 as a test of pituitary reserve, the authors found lower responses in growth hormone-deficient children than in normal children, but too much overlap to diagnose an individual. Responses to GHRP-6, alone or with GHRH, were almost completely blocked after pituitary stalk transection, and the combined GHRH-plus-GHRP-6 test looked promising for adult-onset deficiency.

PMID: 8887178
Human1997

Underactive thyroid

Eleven people with primary hypothyroidism and ten controls had three tests on separate days. GHRH released far less growth hormone in hypothyroidism (peak 4.1 vs 24.9 µg/L). GHRP-6 at 1 µg/kg did better (12.6 vs 22.1), and GHRP-6 plus GHRH gave 52.8 against 77.4. The authors read the difference as thyroid hormone acting on the two peptides by different routes.

PMID: 9156038
Human1997

With exercise

Eleven fit, non-obese young men did five randomised sessions, including 100 µg of GHRP-6 intravenously at rest and during 20 minutes of cycling near the lactate threshold. GHRP-6 produced long, high-amplitude growth hormone peaks, and GHRP-6 plus exercise added to each other. The authors concluded that exercise does not release growth hormone through a GHRP-6-like ligand and more likely acts through GHRH.

PMID: 9135702
Human1997

Cortisol excess

Six patients with endogenous cortisol excess, nine taking glucocorticoid drugs and ten controls received GHRH, GHRP-6 (1 µg/kg) or both. GHRH barely worked in either patient group (peaks 2.0 and 3.6 vs 24.9 µg/L). GHRP-6 still worked in patients on steroid drugs (27.4 vs 22.1 in controls) but was blunted in endogenous excess (7.7), as was the combination (18.8 vs 77.4).

PMID: 9274702
Human2003

Addison's disease

Six patients with Addison's disease on replacement and seven controls received 1 µg/kg intravenously. ACTH rose from 2.9 to 4.7 pmol/L in controls but from 38.1 to 174.9 in the patients, whose response area was about 30 times larger (5,490 vs 170). After 72 hours without replacement, basal ACTH was higher and the extra response was no longer clear (p = 0.053).

PMID: 12739742
Animal2006

Organ injury after interrupted blood flow, rats

In rats whose liver blood supply was cut off and restored, pretreatment with 120 µg/kg into the abdomen reduced liver and gut damage, neutrophil infiltration and lipid peroxidation by 50 to 85%, and lung and kidney injury were also lower; adding EGF helped further. In cell culture GHRP-6 tripled the migration rate of gut epithelial cells without increasing their proliferation.

PMID: 16417467
Human2009

Overactive thyroid

Twenty patients with hyperthyroidism and nine controls received ghrelin and GHRP-6 on separate occasions. Basal ACTH and cortisol were higher in hyperthyroidism. The cortisol response to GHRP-6 was similar in both groups, and its ACTH response was higher in patients but not significantly (927 vs 539), whereas ghrelin's ACTH response was significantly higher.

PMID: 19396632
Human2013

Pharmacokinetics in nine men

Nine healthy men received single intravenous doses of 100, 200 and 400 µg/kg, measured with a validated LC-MS assay. GHRP-6 left the blood in two phases, with half-lives of 7.6 minutes (distribution) and 2.5 hours (elimination), and exposure rose in proportion to dose. Four of the nine showed unexplained concentration spikes during the elimination phase.

PMID: 23099431
Animal2014

Antibiotic kidney injury, rats

Forty-four rats given an overdose of kanamycin for 20 days were treated with EGF, GHRP-6 or both. Damage to glomeruli, tubules and interstitium was lower with each treatment during acute injury, and recovery was faster; the combination repaired tissue most completely.

PMID: 25194405
Animal2024

Doxorubicin heart damage, rats

Given to otherwise healthy rats alongside doxorubicin, the chemotherapy drug that causes dilated cardiomyopathy, GHRP-6 prevented ventricular dilation and preserved left-ventricular pumping, limited damage and fibrosis in other organs and reduced deaths. It kept antioxidant defences up, raised the survival gene Bcl-2 and protected heart-cell mitochondria.

PMID: 38873418
Animal2025

Hydrogel in mouse kidney injury

A self-assembling GHRP-6 hydrogel improved recovery in a mouse model of acute kidney injury. Treated kidneys were enriched in spermidine, glutamine and acetyl-CoA, and the hydrogel improved the survival of tubular cells in low-oxygen conditions through the mTOR-P70 pathway.

PMID: 41327290
Dosing

Dosing Data

GHRP-6 has no approved dose. The human studies used it as a test: one intravenous dose, usually 1 µg/kg, with growth hormone or ACTH measured over the next hours. Other studies used fixed doses of 50 to 100 µg, a single oral dose of 300 µg/kg in children, and 100 to 400 µg/kg to measure how the body clears it.

Not a recommendation. No study gave GHRP-6 for longer than one night, measured a health outcome, or tested the repeated under-the-skin doses sold online; the community range of 100 to 300 µg two or three times a day does not come from these studies.
ProtocolDoseFrequencyDurationRoute
Endocrine test (1995–2003) Human studyPMID 91560381 µg/kgSingle doseSingle sessionIntravenous
Overnight study (1995) Human studyPMID 76171374 × 50 µgFour bolusesOne nightIntravenous
Exercise study (1997) Human studyPMID 9135702100 µgSingle doseSingle sessionIntravenous
Oral test in children (1995) Human studyPMID 7581965300 µg/kgSingle doseSingle sessionOral
Pharmacokinetics (2013) Human studyPMID 23099431100–400 µg/kgSingle doseSingle sessionIntravenous

Educational information, not medical advice. Each dose above is tagged with its source: an approved label, a published human study, animal data, or amounts reported by users. None is a recommendation for you. An unapproved compound has no established safe or effective human dose, and products sold for “research use only” are not made or tested for people. Talk to a doctor before acting on anything on this site, including before you start, stop or change any medicine or dose. Full medical disclaimer.

→ Full GHRP-6 dosage guide — the community figures, the per-kilogram test doses the studies used, and why a short-lived peptide is dosed several times a day

From µg/kg to a syringe
The standard test dose of 1 µg/kg is 70 µg for a 70 kg adult. The calculator turns a vial size and a water volume into the units to draw for any dose.
Open Calculator →
Safety

Side Effects & Contraindications

Reported Side Effects

These come from the single-dose studies above. None was designed to find side effects, so the list is short because the evidence is thin, not because GHRP-6 has been shown to be safe.

● Rises in ACTH and cortisol after single doses in healthy men, and a far larger ACTH response in Addison's disease on replacement
● Changes in sleep: more stage 2 sleep, no change in deep sleep, after four overnight doses
● Unexplained spikes in blood levels during elimination in four of nine volunteers, after large intravenous doses
● Appetite: often described by users and plausible for a ghrelin-receptor agonist, but not measured in any study on this page

Contraindications & Cautions

No trial defined who should avoid GHRP-6. These cautions follow from what the studies measured.

● Adrenal disease or cortisol excess: GHRP-6 raises ACTH and cortisol, and the response is altered in both Addison's disease and cortisol excess
● Pituitary or hypothalamic damage: expect little or no growth hormone response
● Thyroid disease: both underactive and overactive thyroid changed the hormonal response
● Pregnancy, breastfeeding and childhood: no safety data outside single diagnostic doses
● Research-chemical products: identity, dose and sterility are unverified
● Tested athletes: check the Sport (WADA) row in the table below
Questions

Frequently Asked Questions

?Does GHRP-6 make you hungry?

It is widely said to, and it acts on the ghrelin receptor, the receptor of the body's hunger hormone. But none of the studies on this page measured appetite or food intake, so the size of any effect in people is not established here.

?How long does GHRP-6 last in the body?

The one human measurement, in nine men given single intravenous doses in 2013, found two phases: a distribution half-life of 7.6 minutes and an elimination half-life of 2.5 hours. The growth hormone it releases rises within minutes. The 15 to 30 minute half-life often quoted online has no source we could find.

?Does GHRP-6 raise cortisol?

Yes. Four overnight doses raised ACTH and cortisol in healthy men, and the ACTH response was about 30 times larger in people with Addison's disease on replacement. GHRH, by contrast, blunts cortisol.

?Is GHRP-6 the same as GHRP-2 or hexarelin?

No. All three are hexapeptides that act on the ghrelin receptor, but they are different molecules. Hexarelin is GHRP-6 with one methyl group added to its first tryptophan; GHRP-2 (pralmorelin) has a different sequence.

?Can GHRP-6 be taken by mouth?

It was, once, in a 1995 study: 300 µg/kg by mouth in children of short stature gave a growth hormone peak close to the intravenous GHRH test. That is about 300 times the intravenous test dose, which is why oral secretagogues were later built on a non-peptide design.

?Can a pharmacy compound GHRP-6?

Not in the United States. FDA's 503A list places it in Category 3, nominated without adequate support, and FDA has listed it in 503B Category 2 for significant safety risks since September 29, 2023, so neither pharmacies nor outsourcing facilities can compound it.

Bibliography

References

  1. [Human] Frieboes RM, et al. "Growth hormone-releasing peptide-6 stimulates sleep, growth hormone, ACTH and cortisol release in normal man." Neuroendocrinology, 1995;61(5):584-9. PMID: 7617137.
  2. [Human] Pombo M, et al. "Absence of growth hormone (GH) secretion after the administration of either GH-releasing hormone (GHRH), GH-releasing peptide (GHRP-6), or GHRH plus GHRP-6 in children with neonatal pituitary stalk transection." J Clin Endocrinol Metab, 1995;80(11):3180-4. PMID: 7593423.
  3. [Human] Bellone J, et al. "Growth hormone-releasing effect of oral growth hormone-releasing peptide 6 (GHRP-6) administration in children with short stature." Eur J Endocrinol, 1995;133(4):425-9. PMID: 7581965.
  4. [In Vitro] Mau SE, et al. "Growth hormone releasing hexapeptide (GHRP-6) activates the inositol (1,4,5)-trisphosphate/diacylglycerol pathway in rat anterior pituitary cells." J Recept Signal Transduct Res, 1995;15(1-4):311-23. PMID: 8903947.
  5. [Review] Pombo M, et al. "Growth hormone releasing hexapeptide-6 (GHRP-6) test in the diagnosis of GH-deficiency." J Pediatr Endocrinol Metab, 1996;9 Suppl 3:333-8. PMID: 8887178.
  6. [Human] Pimentel-Filho FR, et al. "Growth hormone responses to GH-releasing peptide (GHRP-6) in hypothyroidism." Clin Endocrinol (Oxf), 1997;46(3):295-300. PMID: 9156038.
  7. [Human] Nooitgedagt A, et al. "Influence of endogenous cholinergic tone and growth hormone-releasing peptide-6 on exercise induced growth hormone release." Clin Endocrinol (Oxf), 1997;46(2):195-202. PMID: 9135702.
  8. [Human] Borges MH, et al. "Different effects of growth hormone releasing peptide (GHRP-6) and GH-releasing hormone on GH release in endogenous and exogenous hypercortisolism." Clin Endocrinol (Oxf), 1997;46(6):713-8. PMID: 9274702.
  9. [Human] Martins MR, et al. "GH-releasing peptide (GHRP-6)-induced ACTH release in patients with addison's disease: effect of glucocorticoid withdrawal." J Endocrinol Invest, 2003;26(2):143-7. PMID: 12739742.
  10. [Animal] Cibrián D, et al. "Use of growth-hormone-releasing peptide-6 (GHRP-6) for the prevention of multiple organ failure." Clin Sci (Lond), 2006;110(5):563-73. PMID: 16417467.
  11. [Human] Nascif SO, et al. "Ghrelin and GHRP-6-induced ACTH and cortisol release in thyrotoxicosis." Pituitary, 2009;12(4):315-21. PMID: 19396632.
  12. [Human] Cabrales A, et al. "Pharmacokinetic study of Growth Hormone-Releasing Peptide 6 (GHRP-6) in nine male healthy volunteers." Eur J Pharm Sci, 2013;48(1-2):40-6. PMID: 23099431.
  13. [Animal] Rodriguez Salgueiro S, et al. "Role of epidermal growth factor and growth hormone-releasing peptide-6 in acceleration of renal tissue repair after kanamycin overdosing in rats." Iran J Kidney Dis, 2014;8(5):382-8. PMID: 25194405.
  14. [Animal] Berlanga-Acosta J, et al. "Growth hormone releasing peptide-6 (GHRP-6) prevents doxorubicin-induced myocardial and extra-myocardial damages by activating prosurvival mechanisms." Front Pharmacol, 2024;15:1402138. PMID: 38873418.
  15. [Animal] Zhao X, et al. "Growth hormone-releasing peptide 6 (GHRP-6) hydrogel for acute kidney injury therapy via metabolic regulation." J Nanobiotechnology, 2025;24(1):15. PMID: 41327290.
  16. [pubmed] Bowers CY, et al. "On the in vitro and in vivo activity of a new synthetic hexapeptide that acts on the pituitary to specifically release growth hormone." Endocrinology, 1984;114(5):1537-45. PMID: 6714155.
  17. [pubmed] Camanni F, et al. "Growth hormone-releasing peptides and their analogs." Front Neuroendocrinol, 1998;19(1):47-72. PMID: 9465289.

Sources & Citations

Every citation on this page is PubMed-indexed and has been checked against its record. Two sources are listed without a card: the 1984 discovery paper, whose title predates the name GHRP-6, and a 1998 review titled for the whole peptide family. Grey Peptides sells nothing and links to no vendor.

Medical Disclaimer: This content is for educational and informational purposes only. It is not medical advice, and nothing here is an instruction to obtain or use any compound. Talk to a licensed clinician about your own situation.

Last reviewed: 2026-09-27