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Peptide Research Library

GHRP-6

the original growth-hormone-releasing hexapeptide
Growth Hormone Releasing Peptide-6, Hexapeptide-2, SKF-110679, U-75799E, HWAWFK-NH2
For research use only Evidence grade B — limited human pharmacology, strong animal data GH Secretagogues / GH Axis

GHRP-6 (Growth Hormone Releasing Peptide-6) is a synthetic hexapeptide and one of the first growth hormone secretagogues ever characterized. It was reported in 1984 by Cyril Bowers and colleagues as a peptide that releases growth hormone (GH) from the pituitary through a pathway distinct from growth hormone-releasing hormone (GHRH)12. Researchers later identified its molecular target as the growth hormone secretagogue receptor (GHS-R1a), cloned in 1996 and subsequently recognized as the endogenous receptor for ghrelin4. GHRP-6 is supplied strictly for laboratory research use only; it is not an approved drug and has no authorized therapeutic indication. The human data below come from small early pharmacology and endocrine studies, not from large clinical efficacy trials. This monograph does not provide usage directions.

Structure

Sequence & identity

His-D-Trp-Ala-Trp-D-Phe-Lys-NH₂ · C₄₆H₅₆N₁₂O₆ · 873.0 g/mol

Chemical identity per PubChem CID 4345065: molecular formula C₄₆H₅₆N₁₂O₆, average mass approximately 873.0 g/mol6. The sequence incorporates two D-amino acids (D-Trp at position 2, D-Phe at position 5) and a C-terminal amide, so it is not a simple linear L-peptide; the stereochemically defined InChIKey is WZHKXNSOCOQYQX-FUAFALNISA-N.

What the research shows

Mechanisms studied

Researchers reported that GHRP-6 acts as an agonist at the growth hormone secretagogue receptor (GHS-R1a), a class A G-protein-coupled receptor expressed in the anterior pituitary and hypothalamus that was cloned by Howard and colleagues in 19964. This receptor was later identified as the receptor for the endogenous hormone ghrelin. Investigators described the downstream signaling as Gq/11-coupled: receptor activation stimulates phospholipase C, generating IP3 and triggering release of intracellular calcium, which in turn promotes GH secretion from somatotrophs5. In rat pituitary cell culture, GH release evoked by the hexapeptide was suppressed by calcium-channel blockade and showed an ED50 near 9 nM, and the response was additive with GHRH — observations the authors interpreted as action through a receptor separate from the GHRH receptor2. In human studies, the GH response to GHRP-6 persisted when pituitary GHRH responsiveness had been desensitized, consistent with a GHRH-independent mechanism3.

Reported in studies

Dosing in the research literature

The figures below summarise regimens as reported in published research — they are not recommendations or directions for use.

Source / modelRegimen reportedNotes
Robinson et al., J Clin Endocrinol Metab 1992 (PMID 1400881)31 µg/kg as a single intravenous bolus in healthy male volunteersUsed in a mechanistic study showing GH release independent of endogenous GHRH; not a usage recommendation.
Cabrales et al., Eur J Pharm Sci 2013 (PMID 23099431)7Single IV bolus of 100, 200, and 400 µg/kg in nine healthy men (pharmacokinetic study)Dedicated PK study; plasma disposition best fit a bi-exponential model (distribution t½ ≈ 7.6 min, elimination t½ ≈ 2.5 h).
Bowers et al., Endocrinology 19841; Sartor et al., Endocrinology 1985 (PMID 3918849)2Nanomolar concentrations in vitro (reported ED₅₀ ≈ 9 nM) for GH release from rat pituitary cellsIn-vitro potency from the original characterization work; not a human dose.
Research use only. Peptigo products are sold to qualified researchers for laboratory use. This information summarises published research for reference and is not medical advice, a dosing recommendation, or directions for human or animal use.
Reported in studies

Effects observed in research

In the original characterization, studies reported that GHRP-6 released growth hormone both in vitro and in vivo across several species through a mechanism distinct from GHRH12. In small human pharmacology studies, an intravenous bolus produced a marked, transient rise in plasma GH, and the response persisted under conditions of GHRH desensitization3. Because the GHS-R1a target is the same receptor activated by ghrelin, researchers have observed appetite-related and orexigenic signaling associated with this receptor class5. Investigators have also reported that, in conscious swine, GHRP-6 administration increased ACTH and cortisol, whereas the later secretagogue ipamorelin did not — an observation interpreted as GHRP-6 having more limited receptor selectivity8. Reported effects are observations from research models and small studies; they are not established clinical outcomes, and no therapeutic benefit is claimed.

Honest assessment

Strength of evidence

Grade B

Evidence is graded B. There is a coherent, reproduced body of work: the discovery and in-vitro/in-vivo characterization12, identification and cloning of the GHS-R1a target4, mechanistic human studies confirming GH release and GHRH-independence3, and a dedicated human pharmacokinetic study7. However, the human studies are small (single-digit to low-dozens of subjects) and largely physiologic or pharmacokinetic in design; there are no large randomized clinical efficacy or safety trials, and GHRP-6 is not an approved therapeutic. The frequently cited “2-3 hour half-life” is supported by the Cabrales PK study (elimination t½ ≈ 2.5 h)7; other figures circulating on vendor pages are generally uncited. Effects on cortisol, ACTH, and appetite are reported but should be regarded as research observations rather than defined clinical findings.

Handling

Reconstitution & storage

Reconstitute with bacteriostatic water for laboratory handling. Store lyophilised material frozen and reconstituted material refrigerated. Use Peptigo’s reconstitution calculator and storage cheat sheet for working figures.

References

References

  1. Bowers CY, Momany FA, Reynolds GA, Hong A. 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):1537-1545.
  2. Sartor O, Bowers CY, Chang D. Parallel studies of His-DTrp-Ala-Trp-DPhe-Lys-NH2 and human pancreatic growth hormone-releasing factor-44-NH2 in rat primary pituitary cell monolayer culture. Endocrinology. 1985;116(3):952-957. PMID 3918849.
  3. Robinson BM, Friberg RD, Bowers CY, Barkan AL. Acute growth hormone (GH) response to GH-releasing hexapeptide in humans is independent of endogenous GH-releasing hormone. J Clin Endocrinol Metab. 1992;75(4):1121-1124. PMID 1400881.
  4. Howard AD, Feighner SD, Cully DF, et al. A receptor in pituitary and hypothalamus that functions in growth hormone release. Science. 1996;273(5277):974-977. PMID 8688086.
  5. Yin Y, Li Y, Zhang W. The growth hormone secretagogue receptor: its intracellular signaling and regulation. Int J Mol Sci. 2014;15(3):4837-4855. PMC3975427.
  6. National Center for Biotechnology Information. PubChem Compound Summary for CID 4345065, Ghrp-6. https://pubchem.ncbi.nlm.nih.gov/compound/4345065
  7. Cabrales A, Gil J, Fernández E, 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):40-46. PMID 23099431.
  8. Raun K, Hansen BS, Johansen NL, et al. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998;139(5):552-561. PMID 9849822.
Written by the Peptigo Research Team · scientifically reviewed by Peter, Peptigo Research Team · Last reviewed June 2026. We cite primary literature and flag where evidence is limited. Our sourcing & RUO policy →