GHRP-2: Research Overview

GHRP-2, also known by its INN pralmorelin, is a synthetic hexapeptide developed from Cyril Bowers' research program on growth hormone secretagogues in the 1980s. It is one of the most potent members of the GHRP family, acting as a full agonist at the ghrelin receptor (GHS-R1a) and producing robust GH release in both adults and children. While early clinical work explored diagnostic and therapeutic applications in growth hormone deficiency, GHRP-2 never advanced beyond phase 1–2 studies and is not approved for human use by the FDA or EMA. The compound remains available as a research chemical and serves as a pharmacological benchmark for the GHRP class.

What is GHRP-2?

GHRP-2 (D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2) is a six-residue amidated peptide with a molecular weight of approximately 817.94 Da. It belongs to the growth hormone releasing peptide class — synthetic, non-endogenous compounds that stimulate GH secretion through the GHSR pathway rather than the GHRH receptor. GHRP-2 is more potent on a molar basis than GHRP-6 but carries a less selective side-effect profile: at doses sufficient to release GH it also elevates cortisol and prolactin. It is sold by research-chemical suppliers as lyophilized powder and has no approved clinical indication anywhere in the world.

Mechanism of Action

GHRP-2 binds GHS-R1a on anterior pituitary somatotrophs, activating Gq/11-coupled phospholipase C, raising intracellular IP3 and diacylglycerol, and ultimately increasing cytosolic calcium to trigger GH exocytosis. This pathway is synergistic with — but mechanistically independent of — the GHRH/cAMP axis. GHRP-2 also acts at hypothalamic GHS-R1a to promote GHRH release, amplifying the pituitary response. At therapeutic-range doses it activates additional pathways that stimulate cortisol (via ACTH) and prolactin secretion, distinguishing it from the more selective ipamorelin.

What the Research Shows

The bulk of published GHRP-2 human data is diagnostic rather than therapeutic and was generated in the 1990s. Pihoker et al. (1997; PMID 9390009) studied intranasal GHRP-2 in short-stature children and found a modest but statistically significant increase in growth velocity, with the compound well tolerated. An earlier study by Pihoker et al. (1995; PMID 7559885) evaluated intravenous and intranasal administration in pediatric GH-deficiency workups, establishing that IV GHRP-2 produces peak GH responses useful for provocative testing. Mericq et al. (1998; PMID 9543135) published a phase 1 pharmacokinetic/pharmacodynamic study in children confirming dose-related GH release and acceptable tolerability.

A 2005 PMC-indexed review (Bowers, Growth Horm IGF Res, 2006; PMC article PMID 16950613) summarized the cytoprotective and metabolic research on the GHRP family. More recent work has characterized GHRP-2 as a ghrelin mimetic that increases food intake in healthy men (Laferrere et al., 2005; PMID 15699539). No modern phase 2 or phase 3 program for GHRP-2 exists in published literature; the compound has not progressed through the regulatory pathway required for therapeutic approval.

Reported Dose Ranges

Not medical advice. These are ranges reported in research literature, not personalized recommendations. Consult your physician.

Published dose-finding studies are limited; values reported here come from 1990s pediatric diagnostic studies and have not been validated in modern clinical trials. The Mericq et al. 1998 PK study in children used IV doses in the range of 1–3 mcg/kg. The Pihoker et al. studies used intranasal doses of approximately 2 mcg/kg. The Laferrere et al. 2005 food-intake study in healthy adult men used IV bolus doses. There are no published dose-finding studies for subcutaneous administration in adults establishing safety or efficacy.

References

Citations for this guide are listed below. All PubMed links resolve to the NCBI abstract page for the referenced article.