What Is GHRP-2 (Pralmorelin)? The Growth Hormone-Releasing Peptide, Examined

GHRP-2 is one of the most thoroughly characterized members of the growth-hormone-releasing peptide family, and unlike most compounds in that family it has an actual regulatory paper trail: a Japanese approval, a defined diagnostic protocol, and a developer who published the full chemistry. It is a synthetic hexapeptide that behaves like ghrelin at a specific pituitary receptor, and its story is really the story of how a laboratory tool for probing growth hormone reserve was built. Everything below describes laboratory and literature findings, not use in people.

What is GHRP-2, structurally?

GHRP-2 is a synthetic hexapeptide — six amino acids — and it goes by an unusually long list of names: pralmorelin (its international nonproprietary name), KP-102, GPA-748, and the developmental codes attached to it over the years. The base compound carries CAS number 158861-67-7; the diagnostic drug form is the dihydrochloride salt.¹

The sequence, taken from the developer’s own primary paper and corroborated by the Japanese regulatory dossier, is D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2 — formally D-alanyl-3-(2-naphthyl)-D-alanyl-L-alanyl-L-tryptophyl-D-phenylalanyl-L-lysinamide.^1,3 Two structural details matter and are frequently mangled in secondary sources. Position 2 is D-2-naphthylalanine, a bulky non-natural residue, not plain phenylalanine. And the C-terminus is amidated (the -NH2), not a free carboxylic acid. Both features are what you would expect from a peptide engineered for receptor affinity and resistance to peptidase degradation rather than one lifted from a natural protein. The IUPHAR/BPS Guide to Pharmacology classifies pralmorelin as a met-enkephalin analogue, which places it in the same design lineage as the earlier growth-hormone-releasing peptides that grew out of enkephalin chemistry.⁴

6 amino acids — GHRP-2 is a hexapeptide, but two of its residues are non-natural D-amino acids that no ribosome would ever assemble.

How does it work?

GHRP-2 is a ghrelin mimetic. It is an agonist at the growth hormone secretagogue receptor, GHS-R1a, expressed in the pituitary and hypothalamus. That receptor was cloned by Howard and colleagues in 1996 as “a receptor in pituitary and hypothalamus that functions in growth hormone release.”⁵ At the time its natural ligand was unknown; it was defined by the synthetic secretagogues, GHRP-2 among them, that activated it. Three years later Kojima and colleagues identified ghrelin, an acylated peptide from the stomach, as the endogenous ligand.⁶ GHRP-2 therefore does artificially what ghrelin does naturally: it binds GHS-R1a and drives growth hormone release.

The Japanese regulatory review makes the mechanistic attribution explicit, treating KP-102 as a ghrelin/GHS-R agonist and citing both the Howard and Kojima papers directly.³ A 2018 clinical study describing the GHRP-2 test states the same thing in operational terms — that GHRP-2 stimulates its targets through GHS-R in the hypothalamus, ghrelin’s natural ligand.¹²

In the developer’s own pharmacology, GHRP-2 in conscious rats was more potent than exogenous GHRH at releasing growth hormone, was relatively resistant to suppression by somatostatin, and produced no response in hypophysectomized rats — confirming the pituitary as its site of action.^1,2 The relative somatostatin resistance is pharmacologically interesting: somatostatin is the brake on GH release, and a secretagogue that partly bypasses that brake produces a robust, reproducible GH pulse. That reproducibility is exactly what a diagnostic test needs.

GHRP-2 was defined by the receptor it activated years before anyone knew what that receptor was naturally for.

The regulatory reality: a Japan-only diagnostic

This is where GHRP-2 diverges sharply from the gray-market framing it usually receives. Pralmorelin hydrochloride is an approved drug — but in Japan only, and for one narrow purpose. Kaken Pharmaceutical markets it as “GHRP Kaken 100,” approved in 2004, with the indication “diagnosis of growth hormone secretion deficiency.”^3,4 It is a single-dose diagnostic agent, administered once to provoke a measurable growth hormone response. It is not approved as a treatment for anything, and it is not approved in the European Union or the United States.

The diagnostic protocol in the PMDA label is specific: 100 µg given intravenously in the fasting state (2 µg/kg for ages 4 to under 18, capped at 100 µg), with growth hormone sampled at 0, 15, 30, 45 and 60 minutes. Severe GH deficiency is defined by a peak GH at or below 15 ng/mL, or at or below 9 ng/mL when measured against a recombinant GH standard.³

Summary of the documented record for GHRP-2 / pralmorelin. The “approved use” line refers to a single-dose diagnostic test in Japan and must not be read as endorsement of any therapeutic or non-clinical use.

In human diagnostic studies GHRP-2 raises plasma growth hormone reliably and markedly, and does so largely independent of sex, age or obesity — the property that makes it a dependable provocative test where other stimuli can be blunted.⁷ An early study in 24 children of short stature found that intravenous and intranasal GHRP-2 evoked GH responses as reliable as GHRH for predicting pituitary reserve, with GHRH and GHRP-2 acting synergistically when combined.⁷ A modern validation in 36 patients with hypothalamic-pituitary disorder confirmed the test’s usefulness for diagnosing GH deficiency.¹¹

Where GHRP-2 sits among the secretagogues

The GHRP series traces back to work begun by C.Y. Bowers at Tulane University in the late 1970s, and Bowers’s name recurs as a co-author across the core GHRP-2 clinical papers, reflecting his role in co-developing KP-102.^7,8,9 Against its siblings, GHRP-2 is distinguished by potency and by its off-target profile. In a direct in-vitro comparison in rat primary pituitary cells, GHRP-2 was more potent than GHRP-6 at releasing growth hormone.¹³

The contrast with ipamorelin is instructive. Ipamorelin is a more selective secretagogue with minimal effect on ACTH and cortisol.¹⁴ GHRP-2 is not so clean: in humans it is a potent GH releaser that also modestly stimulates ACTH and cortisol, though not prolactin.¹⁰ That off-target activity on the hypothalamic-pituitary-adrenal axis was once a confounder; more recently it has been turned into a feature, with the ACTH response during the GHRP-2 test used to screen for secondary adrenal insufficiency at the same time.^11,12 If you want to read GHRP-6, ipamorelin, and CJC-1295 against this same axis, see the GHRP-6 guide, the ipamorelin guide, and the CJC-1295 DAC guide, or the broader overview of growth hormone secretagogues.

An honest read of the evidence

The strong parts of the GHRP-2 record are the mechanism and the diagnostic use. The GHS-R1a target is well established, the ghrelin-mimetic identity is settled, and the Japanese approval as a single-dose diagnostic rests on a real regulatory dossier and reproducible GH-provocation data. That much is solid.

The weak parts are everything beyond acute diagnosis. There is no approved therapeutic indication for GHRP-2 anywhere, and there is no robust long-term human safety or efficacy data outside the acute diagnostic setting. Framing GHRP-2 as a “growth hormone therapy” or a performance agent is unsupported by any regulator; the primary evidence supports only acute GH provocation. Several of the foundational clinical papers date from the 1990s and are small — 24 children in one, similar numbers in others — and frequently list the compound’s own discoverer, Bowers, as a co-author.^7,8,9 Large independent modern efficacy trials outside the diagnostic indication are lacking, and development for short stature was discontinued.

There is also a sourcing concentration worth naming. Much of the detailed potency and general-pharmacology data comes from the developer, Kaken, published in a single 2004 journal, and from animal models — rats and dogs.^1,2 Single-sponsor sourcing plus species differences are real limitations on how far those numbers generalize. And GHRP-2 is not receptor-selective for growth hormone: it also raises ACTH, cortisol and in some settings prolactin, so any GH signal has to be interpreted against that off-target activity rather than treated as a clean GH-only readout.¹⁰ Finally, gray-market “GHRP-2” is not the diagnostic drug product. Identity, purity and endotoxin status of research-grade material are unverified in the absence of a compound-specific certificate of analysis, and no such claim is made here.

All materials supplied by Condor Research are Research Use Only (RUO). Everything above describes in-vitro findings, animal studies, and the published regulatory and clinical literature — it is not a dosing protocol, clinical guidance, or a safety assessment for any organism. Nothing here concerns human or veterinary use.

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