GHRP-6 Research

GHRP-6 is a synthetic hexapeptide, sequence His-D-Trp-Ala-Trp-D-Phe-Lys-NH2. PubChem records it as CID 9919153, CAS 87616-84-0, formula C46H56N12O6, molecular weight 873.0 ^[1]. It is a single defined molecule, not a marketing name. It differs from hexarelin only by the absence of a 2-methyl group on the D-Trp residue ^[1].

Material supplied as GHRP-6 is a research chemical. It is not for human consumption.

Receptor and pathway

GHRP-6 acts at the growth hormone secretagogue receptor, later designated GHS-R1a. That receptor was cloned from pig and human pituitary and hypothalamus and identified as the target of this peptide class (in vitro) ^[2]. Ghrelin, an acylated stomach peptide, was later shown to be its endogenous ligand (animal) ^[3]. GHRP-6 is therefore a synthetic ghrelin-receptor agonist, and this is not the growth hormone releasing hormone receptor, so GHRH analogue findings do not carry across to it.

What has been measured in humans

The human record is two acute intravenous studies, roughly 27 subjects in total.

The first gave intravenous GHRP-6 to 18 normal men (human) ^[4]. Mean peak serum growth hormone rose from 1.2 micrograms per liter after placebo to 68.7 at the highest of three ascending levels tested. Prolactin and cortisol each rose about two-fold above basal, but only at that top level. Luteinizing hormone and thyroid-stimulating hormone were unchanged over the first hour. GHRP-6 and GHRH together released growth hormone synergistically, indicating separate mechanisms. The study was single-dose, and measured no IGF-1 and no clinical outcome. Its senior author originated the GHRP series and held an inventor interest through a university patent ^[4].

The second is a phase I pharmacokinetic study in nine healthy men (human) ^[5]. Disposition was bi-exponential, with a distribution half-life of 7.6 minutes and an elimination half-life of 2.5 hours. The authors reported unexplained concentration spikes during the elimination phase in four of the nine subjects. It measured concentrations only, with no growth hormone, cortisol or prolactin endpoint. It was run by the state institute developing the compound ^[5].

That is the whole of it: there is no repeat-dose study, no IGF-1 measurement, no body composition or performance endpoint, and no controlled trial of any clinical outcome. There are also no registered interventional trials of GHRP-6 (registry query) ^[6]. The compound has been given to people, but no trial of it was ever registered.

The cortisol and prolactin question

The human cortisol and prolactin finding most often attached to GHRP-6 is not its own. That study gave GHRP-2 and hexarelin to six young adults, finding ACTH and cortisol release similar to human CRH ^[7]. GHRP-6 appears in it only in the introduction, and was never administered ^[7]. Its actual human cortisol datum is the roughly two-fold rise at the top level in the 1990 study, and nothing else ^[4].

In conscious swine, GHRP-6 raised ACTH and cortisol, while ipamorelin at the same receptor did not (animal) ^[8]. Prolactin did not rise in those swine, the reverse of the human GHRP finding, so the species model is incomplete ^[8]. That paper also came from the company developing ipamorelin, its favorable comparator ^[8]. Whether repeated administration produces meaningful hypercortisolism has never been studied in people.

What has not been shown in people

No human study of GHRP-6 has measured IGF-1. The nearest evidence in this series is five days of GHRP-2, a different molecule, in which the growth hormone response attenuated while IGF-1 did not move (human) ^[9]. No one has shown that GHRP-6 raises IGF-1 in a person. The cohort literature linking lifelong endogenous IGF-1 to cancer risk therefore does not apply here, and is not cited on this page.

Body composition, lean mass, fat loss and performance endpoints do not exist for GHRP-6 in humans at all. GHRP-6 analogues bind CD36, a scavenger receptor, in structure-activity work (in vitro) ^[10]. Downstream CD36 effects claimed for this family, including cholesterol efflux and mitochondrial biogenesis in fat cells, are cell culture and rodent findings (in vitro and animal) ^[10]. Chronic GHRP-6 improved ejection fraction in rats with pressure-overload heart failure (animal) ^[11]. No human study has tested chronic administration for any cardiac or metabolic endpoint. The human appetite datum for this receptor belongs to hexarelin, a different molecule (human) ^[12]. A 2026 review lists appetite changes, prolactin and cortisol elevations, dysglycemia and fluid retention among this class's reported adverse effects ^[13].

Regulatory position

GHRP-6 holds no marketing authorization in any jurisdiction located in this evidence base. FDA placed it on its Category 2 list of bulk drug substances that may present significant safety risks, dated 29 September 2023 ^[14]. The entry cites a potential effect on cortisol and increased blood glucose from decreased insulin sensitivity ^[14]. That is a regulator's stated concern in a listing entry, with no underlying study cited. No controlled human trial of GHRP-6 has measured insulin sensitivity. GHRP-6 is named in Section S2 of the 2026 WADA Prohibited List, prohibited at all times ^[15].

Two approval claims circulate near this compound. Tesamorelin holds FDA approval, granted 10 November 2010, for reduction of excess abdominal fat in adults with HIV-associated lipodystrophy ^[16]. It remains in force, with supplements running to 25 March 2025 and labeling current to 2026 ^[16]. It never obtained a European authorization: the application was withdrawn by the applicant while under CHMP review, and the committee's position at withdrawal was provisional ^[17]. The approval belongs to the molecule tesamorelin and to one indication. It is not a family credential and must never be written as one.

Tesamorelin acts at the GHRH receptor and GHRP-6 does not, so they share no target. Duration does not transfer either: tesamorelin's mean elimination half-life is formulation-specific, reported as 8 minutes and as 11 minutes, and it is given daily ^[18]. CJC-1295 with DAC, at that same GHRH receptor, has a reported half-life of 5.8 to 8.1 days ^[19], and it raised trough growth hormone 7.5-fold in healthy men ^[20]. A receptor name states a target, not a duration of action and not a credential.

The honest contrast is not that tesamorelin works and the others might too. It is that tesamorelin is the only one of these compounds that has been through the process that would let anyone know.

The second claim concerns GHRP-2, again a different molecule. Its reported Japanese approval as a diagnostic agent traces to a 2004 trade profile that recorded approval as still pending, with a 2007 validation study ^[21]. It is unverified against any primary regulatory database. A provocative test approval is diagnostic, not therapeutic, and says nothing about GHRP-6. Material sold under peptide names in this family has also, in documented cases, not been the labeled molecule. One vial sold as IGF-1 LR3 held a His-tagged research construct instead ^[22].

Frequently Asked Questions

How much human evidence exists for GHRP-6?

Two acute intravenous studies, roughly 27 subjects in total, both single-dose ^{[4] [5]}. Neither measured IGF-1, body composition or any clinical outcome, and no interventional trial of the compound is registered ^[6].

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

No. GHRP-6 is His-D-Trp-Ala-Trp-D-Phe-Lys-NH2, hexarelin differs from it by a single 2-methyl group on the D-Trp residue, and GHRP-2 is a separate peptide again ^[1]. This matters for the cortisol and prolactin study most often attributed to GHRP-6, which tested GHRP-2 and hexarelin and never administered GHRP-6 ^[7].

Has GHRP-6 been shown to raise IGF-1 in humans?

No human study of GHRP-6 has measured IGF-1 ^{[4] [5]}. The nearest evidence is five days of GHRP-2, a different molecule, in which IGF-1 did not move ^[9]. Nothing about a sustained IGF-1 effect has been demonstrated for GHRP-6 in people.

Is anything in this group of compounds approved?

Tesamorelin is, for one HIV-related indication, and that approval belongs to that molecule alone ^[16]. GHRP-2 has a reported Japanese diagnostic approval that is unverified against any primary regulatory database and is not therapeutic ^[21]. GHRP-6 holds no authorization located here, and instead appears on an FDA list of bulk substances that may present significant safety risks ^[14].

References

1. 1

   PubChem Compound record CID 9919153, CAS 87616-84-0. PubChem (NIH/NLM), queried 27 August 2026.
2. 2

   Howard AD, et al. Science 1996. PMID 8688086.; DOI: 10.1126/science.273.5277.974.
3. 3

   Kojima M, et al. Nature 1999. PMID 10604470.; DOI: 10.1038/45230.
4. 4

   Bowers CY, et al. J Clin Endocrinol Metab 1990. PMID 2108187.; DOI: 10.1210/jcem-70-4-975.
5. 5

   Cabrales A, et al. Eur J Pharm Sci 2013. PMID 23099431.; DOI: 10.1016/j.ejps.2012.10.006.
6. 6

   ClinicalTrials.gov v2 API, per-compound queries by intervention and general term, 27 August 2026. GHRP-6 returns zero registered studies.
7. 7

   Arvat E, et al. Peptides 1997. PMID 9285939.; DOI: 10.1016/s0196-9781(97)00016-8. GHRP-2 and hexarelin only, n=6; GHRP-6 was not administered.
8. 8

   Raun K, et al. Eur J Endocrinol 1998. PMID 9849822.; DOI: 10.1530/eje.0.1390552.
9. 9

   Nijland EA, et al. Eur J Endocrinol 1998. PMID 9820615.; DOI: 10.1530/eje.0.1390395. GHRP-2.
10. 10

    Avallone R, et al. Mol Endocrinol 2006. PMID 16959872.; DOI: 10.1210/me.2006-0146. Rodrigue-Way A, et al. Endocrinology 2007. PMID 17138655.; DOI: 10.1210/en.2006-0975. Sabatino D, et al. J Am Chem Soc 2011. PMID 21692501.; DOI: 10.1021/ja203007u.
11. 11

    Xu XB, et al. Am J Physiol Heart Circ Physiol 2005. PMID 15951341.; DOI: 10.1152/ajpheart.01042.2004.
12. 12

    Korbonits M, et al. J Clin Endocrinol Metab 1999. PMID 10404825.; DOI: 10.1210/jcem.84.7.5811. Hexarelin.
13. 13

    Dominikowski A, et al. Front Endocrinol (Lausanne) 2026. PMID 42395176.; DOI: 10.3389/fendo.2026.1822475.
14. 14

    FDA, Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks, Category 2 entry for GHRP-6, dated 29 September 2023; page current 22 April 2026.
15. 15

    World Anti-Doping Agency, 2026 Prohibited List, Section S2, in force 1 January 2026.
16. 16

    FDA regulatory record for tesamorelin: original approval 10 November 2010; latest supplement approved 25 March 2025; current Structured Product Label effective 29 July 2026.
17. 17

    European Medicines Agency, withdrawn-application record for tesamorelin, EMEA/H/C/002427. Withdrawal notified to the CHMP by the applicant on 21 June 2012.
18. 18

    FDA Structured Product Label for tesamorelin, section 12.3, effective 29 July 2026. Mean elimination half-life is formulation-specific: 8 minutes and 11 minutes.
19. 19

    Teichman SL, et al. J Clin Endocrinol Metab 2006. PMID 16352683.; DOI: 10.1210/jc.2005-1536. CJC-1295 with DAC.
20. 20

    Ionescu M, et al. J Clin Endocrinol Metab 2006. PMID 17018654.; DOI: 10.1210/jc.2006-1702. CJC-1295 with DAC.
21. 21

    Drugs R&D development profile, pralmorelin, 2004. PMID 15230633.; DOI: 10.2165/00126839-200405040-00011. Chihara K, et al. Eur J Endocrinol 2007. PMID 17609397.; DOI: 10.1530/EJE-07-0066.
22. 22

    Kohler M, et al. Growth Horm IGF Res 2010. PMID 20675162.; DOI: 10.1016/j.ghir.2010.07.001.