GHRP-2 Research

GHRP-2, also called pralmorelin, is a synthetic six-amino-acid peptide with the sequence D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2. Chemistry databases list it under CAS 158861-67-7 and PubChem CID 6918245, formula C45H55N9O6 ^[1]. The codes KP-102 and GPA 748 name the same molecule ^[1][2]. Material sold as GHRP-2 is supplied for laboratory research use only, and is not for human consumption.

It is an agonist at the growth hormone secretagogue receptor GHS-R1a, cloned from pig and human pituitary tissue, whose natural ligand is ghrelin ^[3][4] (in vitro, animal).

What the human record covers

Human data on GHRP-2 exist, and they are narrow: they cover acute endocrine response to single administration, one validated diagnostic use, and one short study of repeated administration. Registry searches return no registered interventional trials for GHRP-2 or pralmorelin ^[5]. Most of this human work predates mandatory registration. Nothing in the record addresses body composition, lean mass, fat loss, strength or performance.

Cortisol and prolactin: the selectivity problem

In six healthy young adults, GHRP-2 and hexarelin released more growth hormone than GHRH did, and both also raised prolactin, ACTH and cortisol ^[6] (human). Prolactin release was lower than TRH produced, while ACTH and cortisol release matched that of human CRH, a maximal stimulus to the adrenal axis ^[6]. The authors concluded that these peptides are not fully specific ^[6]. Six subjects received every comparator in one crossover, which is very small, and administration was single and intravenous. GHRP-6 was never given in that study, despite frequent citation to the contrary.

A second human dataset supports the size of the cortisol effect. In 15 patients investigated for suspected hypopituitarism, peak cortisol during a GHRP-2 test tracked the insulin tolerance test closely, at r=0.817 and p<0.0001 ^[7] (human). That was a pilot study without a healthy control group ^[7].

Why cortisol rises is unresolved: two human hexarelin studies disagree over whether vasopressin mediates it ^[8][9] (human), and a rat study of GHRP-2 found it mainly CRF mediated ^[10] (animal). In conscious swine GHRP-2 raised ACTH and cortisol, but prolactin did not rise there ^[11] (animal).

Copy describing GHRP-2 as a selective growth hormone releaser is contradicted by the human data; that selectivity claim was made for ipamorelin, a different molecule ^[6][11].

Repeated administration

Nine healthy young men received GHRP-2 across five consecutive days ^[12] (human). The growth hormone response attenuated measurably, with mean peak values falling from 83 to 59 to 51 µg/L, ANOVA p<0.01. Serum IGF-1 did not rise at all, sitting between 22 and 25 nmol/L on every day measured ^[12]. Osteocalcin did rise, from 3.2 to 4.2 µg/L, p<0.01, so some tissue-level growth hormone effect did occur ^[12]. Five days is short, and the authors did not claim a later rise had been excluded. It is the only human measurement of IGF-1 across repeated GHRP-2 administration, and it was flat.

Circulating IGF-1 is associated with the risk of several common cancers in a meta-regression of case-control studies, including studies nested in cohorts ^[13] (human). Those associations come from lifelong endogenous IGF-1 across its normal range, not from an administered peptide. GHRP-2 has not been shown to raise IGF-1 in a person at all ^[12], so this article does not attach that literature to it. Where it does have a human anchor is tesamorelin, whose label quantifies the IGF-1 rise and carries a neoplasm warning ^[14]. Growth hormone is diabetogenic in humans ^[15] (review), and FDA's GHRP-2 entry cites reports of increased insulin requirement ^[16]. That is a regulator's stated concern, not a measured effect size.

The reported Japanese approval

GHRP-2 is often described as approved in Japan, and that claim needs care. A 2004 commercial development profile records that Kaken Pharmaceutical held worldwide rights, and that the compound was awaiting approval there as a diagnostic agent ^[2]. A validation study in 77 healthy subjects and 58 patients with growth hormone deficiency followed ^[17] (human), and the test appears in Japanese practice literature through 2023 ^[18]. Peak growth hormone came within 60 minutes in every subject, and averaged 1.36 µg/L in patients against 84.6 µg/L in controls ^[17]. The approval grant could not be confirmed against any primary regulatory database, so it is reported and unverified. The use is a diagnostic provocative test, a single challenge to see whether the pituitary responds, which is categorically different from a therapeutic approval. US development for growth hormone deficiency was discontinued ^[2].

Tesamorelin is not a credential for this compound

Tesamorelin holds FDA approval, granted 10 November 2010 and still in force, for reduction of excess abdominal fat in HIV-associated lipodystrophy ^[19]. It never obtained a European marketing authorization, and it was not refused: the applicant withdrew that application while it was under CHMP review ^[20]. 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 while GHRP-2 acts at GHS-R1a, so findings do not transfer between them. The honest contrast is not that tesamorelin works and the others might too. It is that tesamorelin is the only one of the nine compounds in this family that has been through the process that would let anyone know.

Regulatory status

FDA placed GHRP-2 on its Category 2 list of bulk drug substances that may present significant safety risks ^[16]. Its stated concerns include immunogenicity from impurities, and reports of increased insulin requirement, infection, pancreatitis and deaths among critically ill study subjects ^[16]. FDA states that causality has not been established, and those deaths concern critically ill populations rather than healthy people ^[16]. Pralmorelin is named in Section S2 of the 2026 WADA Prohibited List, prohibited at all times ^[21]. Chronic administration has been studied only in animal models ^[22] (animal). A 2026 review of this class lists prolactin and cortisol elevation, appetite change and dysglycemia among recognized adverse-effect domains ^[23] (review).

Conflicts of interest in the cited literature

Several sources above are not disinterested. The 2004 profile is a pipeline summary compiled from company disclosures ^[2], and the rat mechanism study was run by the company holding commercial rights ^[10]. The swine comparison was authored at Novo Nordisk, which was developing ipamorelin, the compound that emerged from it favorably ^[11]. The diagnostic validation study is academic work, run inside the Japanese regulatory program in which Kaken commercialized that test ^[17]. The 2026 review declares no commercial relationships ^[23].

Frequently Asked Questions

Is GHRP-2 approved anywhere? It is reported to be approved in Japan as a diagnostic agent, unconfirmed against any primary regulatory database ^[2]. A diagnostic provocative test is categorically different from a therapeutic approval, and the one documented approval in this family belongs to tesamorelin ^[19].

Does GHRP-2 raise IGF-1 in people? Not on the evidence available: the one human study measuring IGF-1 across five days of administration found it flat throughout, while the growth hormone response attenuated ^[12]. No longer human measurement of GHRP-2 exists.

What human evidence exists for muscle or fat loss? None specific to GHRP-2: the human record covers acute endocrine responses, a diagnostic application and one five-day study ^{[5][6][12][17]}. No body-composition, lean-mass or performance endpoint has been measured, and the chronic data are animal only ^[22].

References

1. 1

   PubChem Compound record CID 6918245, CAS 158861-67-7 (NIH/NLM).
2. 2

   Pralmorelin development profile. Drugs R&D 2004. PMID 15230633.
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   Howard AD et al. Science 1996. PMID 8688086.
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   Kojima M et al. Nature 1999. PMID 10604470.
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   ClinicalTrials.gov API v2 registry query for GHRP-2, pralmorelin and KP-102,
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   Arvat E et al. Peptides 1997. PMID 9285939.
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   Kano T et al. Peptides 2010. PMID 20045717.
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   Korbonits M et al. J Clin Endocrinol Metab 1999. PMID 10404825.
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    Hirotani C et al. Naunyn Schmiedebergs Arch Pharmacol 2005. PMID 15645295.
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    Nijland EA et al. Eur J Endocrinol 1998. PMID 9820615.
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    Renehan AG et al. Lancet 2004. PMID 15110491.
14. 14

    US FDA approved prescribing information for tesamorelin, sections 5.1 and 5.2.
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    Moller N, Jorgensen JOL. Endocr Rev 2009. PMID 19240267.
16. 16

    US FDA, Category 2 bulk drug substances that may present significant safety
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    Chihara K et al. Eur J Endocrinol 2007. PMID 17609397.
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    Teramoto S et al. Growth Horm IGF Res 2023. PMID 37295337.
19. 19

    US FDA regulatory record for tesamorelin, original approval 10 November 2010.
20. 20

    European Medicines Agency withdrawn-application record for tesamorelin, 2012.
21. 21

    World Anti-Doping Agency, 2026 Prohibited List, Section S2.
22. 22

    Xu XB et al. Am J Physiol Heart Circ Physiol 2005. PMID 15951341.
23. 23

    Dominikowski A et al. Front Endocrinol 2026. PMID 42395176.