GHRP-2.
GHRP-2 (growth hormone-releasing peptide-2; international nonproprietary name pralmorelin; development codes KP-102/GPA-748) is a synthetic hexapeptide with the sequence D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2.
GHRP-2 (growth hormone-releasing peptide-2; international nonproprietary name pralmorelin; development codes KP-102/GPA-748) is a synthetic hexapeptide with the sequence D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2. GHRP-2 is research / preclinical, and PepCue grades its published evidence D tier (38/100). This is a research reference, not medical or dosing advice.
What it is
GHRP-2 (growth hormone-releasing peptide-2; international nonproprietary name pralmorelin; development codes KP-102/GPA-748) is a synthetic hexapeptide with the sequence D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2. It belongs to the "classical" growth hormone secretagogue (GHS) family pioneered by Cyril Bowers in the 1980s and is a synthetic agonist of the ghrelin receptor. Unlike GHRH, it is structurally unrelated to any hypothalamic releasing hormone and instead mimics the endogenous gut peptide ghrelin.
How it works
GHRP-2 binds and activates the growth hormone secretagogue receptor type 1a (GHS-R1a), the same Gq/11-coupled receptor targeted by ghrelin, expressed on anterior-pituitary somatotrophs and in the hypothalamus (including the arcuate nucleus). Receptor activation drives phospholipase C signaling, IP3/DAG generation, and intracellular calcium release, evoking pulsatile GH secretion. Because it acts through a pathway distinct from (and synergistic with) GHRH, GHRP-2 and GHRH together produce a markedly larger GH pulse than either alone. Its action on hypothalamic ghrelin-receptor circuits also explains its orexigenic (appetite-stimulating) effect and a degree of off-target activation of the corticotroph and lactotroph axes.
Mechanism pathways
Acting on the ghrelin / GH-secretagogue receptor, a pathway separate from GHRH.
The growth hormone secretagogue receptor, GHS-R1a, is a G-protein-coupled receptor expressed on pituitary somatotrophs and in hypothalamic nuclei. Its natural ligand is ghrelin, the stomach-derived hormone associated with hunger. Activation raises growth hormone through a route entirely separate from GHRH: it acts directly on somatotrophs, and it also suppresses hypothalamic somatostatin tone, effectively releasing the brake at the same time as pressing the accelerator. This dual action is why compounds at this receptor and GHRH analogs are often studied together, since combining them produces a larger growth hormone response than either produces alone. The history here is unusual. The synthetic peptides in this group were developed in the 1980s and 1990s by working backwards from observed growth hormone release, years before ghrelin itself was identified in 1999. They were the pharmacological tools that led researchers to the receptor. They are therefore best understood as synthetic ghrelin mimetics that happened to be discovered before the hormone they mimic. Members of this group differ chiefly in selectivity, which is the practical distinction that matters most. GHS-R1a activation is not confined to growth hormone. Because the receptor sits on cells that also govern prolactin and adrenocorticotropic hormone release, and because ghrelin signalling drives appetite and influences gastric motility, several of these compounds raise cortisol and prolactin and increase hunger alongside the intended growth hormone effect. Others were specifically designed to avoid that, producing a comparatively clean growth hormone response with minimal spillover onto the other axes. Some also show additional activity at the CD36 receptor, which has been studied in cardiac contexts. Honest assessment of clinical relevance: the acute receptor pharmacology is well characterised, including in short human studies where growth hormone reliably rises after administration. That is proof of mechanism. What does not exist for this class is proof of benefit. No compound in this group is an approved medicine, controlled trials of sustained use with body composition or clinical endpoints are essentially absent, and material sold under these names is unregulated research-grade product of uncertain content. Growth hormone secretagogues are also prohibited in sport by anti-doping authorities. A further consideration specific to this receptor is desensitisation: sustained agonism at a G-protein-coupled receptor commonly reduces its responsiveness over time, so the acute hormonal response observed in a short study is not a reliable guide to what happens with continued use.
The evidence
Human pharmacology is well characterized for acute, single-dose use: controlled studies show GHRP-2 reliably triggers a robust GH pulse, and in healthy men it increased subjective hunger and food intake, confirming it behaves as a ghrelin mimetic (Laferrère et al., JCEM 2005). On the strength of acute diagnostic data it is approved in Japan as a single-dose GH-deficiency provocation test, where the GH response separates GH-sufficient from GH-deficient subjects. Critically, the long-term therapeutic program failed: development for treating GH-deficient children/pituitary dwarfism reached Phase II but was not brought to market, in part because the GH response to GHRP-2 is blunted in people with GH deficiency relative to healthy individuals. There are essentially no rigorous long-term human trials demonstrating benefit for body composition, muscle, anti-aging, or performance. Claims in those areas rest on mechanism and short-term hormone changes, not proven clinical outcomes.
The evidence, in brief
A ghrelin-receptor agonist (pralmorelin) used mainly as a GH-deficiency diagnostic and a probe of ghrelin biology; small human studies show it raises GH and increases appetite. Evidence is short-term and mechanistic, with no long-term outcome trials; not FDA-approved for general use.
- Laferrère B et al.: GHRP-2, like ghrelin, increases food intake in healthy menJ Clin Endocrinol Metab, 2005 (PMID 15699539)
Evidence maturity
An evidence-only reading: approval status, human vs preclinical data, mechanism and safety. Popularity never raises it. Research file #023
Mostly preclinical or mechanistic; little human data.
Some early human evidence exists but isn't definitive.
Claim receipts
Popular claims about GHRP-2, checked against the state of the evidence. The verdict describes evidence maturity, never an invented study result.
Human pharmacology for acute use is well characterized, and it is approved in Japan as a single-dose GH-deficiency test.
That approval covers one-time diagnostic use only; repeated administration was never established.
Human studies show it also raises ACTH, cortisol and prolactin, which is why more selective secretagogues were developed.
Therapeutic development stopped at Phase 2, partly because the GH response is blunted in GH-deficient people.
Long-term body-composition and anti-aging outcomes have not been demonstrated in rigorous trials.
Safety profile
Documented acute effects in human studies include off-target stimulation of ACTH and cortisol and a transient rise in prolactin, a feature that distinguishes GHRP-2 from the more selective secretagogue ipamorelin (Arvat et al., Peptides 1997). As a ghrelin-receptor agonist it predictably stimulates appetite, and sustained GH/IGF-1 elevation carries the theoretical risks associated with the GH axis (insulin resistance, fluid retention, joint discomfort). The fundamental safety gap is that GHRP-2 has been studied chiefly as a one-time diagnostic agent; the consequences of repeated or chronic non-clinical use, including effects on the HPA axis, glucose metabolism, and any proliferative risk from prolonged IGF-1 elevation, have not been established in controlled long-term human trials. Material sold for "research" use is unregulated and may differ in identity, purity, or sterility from pharmaceutical-grade product.
Compound notes
- GHRP-2 (pralmorelin; development codes KP-102 and GPA-748) is a synthetic hexapeptide and an agonist at the growth hormone secretagogue receptor GHS-R1a, the same receptor targeted by ghrelin.
- It is structurally unrelated to GHRH, and because it acts through a separate pathway, GHRP-2 and GHRH together produce a markedly larger GH pulse than either alone.
- Its action on hypothalamic ghrelin-receptor circuits also makes it orexigenic: in healthy men it increased subjective hunger and food intake.
- It is approved in Japan (as GHRP Kaken 100) solely as a single-dose diagnostic test for growth hormone deficiency, making it the only GH secretagogue ever granted national regulatory approval, and only for diagnosis rather than therapy.
Both are ghrelin-receptor agonists, but GHRP-2 is less selective: human studies show it measurably raises ACTH, cortisol and prolactin, which ipamorelin was designed to avoid.
- Not FDA-approved for any indication; research-use-only in the US and prohibited in sport under the WADA list of growth hormone secretagogues.
- Documented acute effects include off-target ACTH and cortisol stimulation and a transient prolactin rise, plus predictable appetite stimulation.
- It has been studied chiefly as a one-time diagnostic agent. The long-term therapeutic program for GH-deficient children failed at Phase II, and the consequences of repeated use on the HPA axis, glucose metabolism, and prolonged IGF-1 elevation are not established.
Regulatory status
Approved in Japan (marketed by Kaken Pharmaceutical as GHRP Kaken 100) solely as a single-dose diagnostic agent for assessing growth hormone deficiency, making it the only GHS ever granted national regulatory approval, and only for diagnosis, not therapy. It is not FDA-approved for any indication; in the United States and most jurisdictions it is investigational/research-use-only, and it is prohibited in sport under the WADA Prohibited List (S2, growth hormone secretagogues).
Sold research-use-only; human evidence is limited or preclinical.
By the numbers
- 01Synthetic hexapeptide (D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2); a ghrelin-receptor (GHS-R1a) agonist, not a GHRH analog
- 02Approved in Japan only as a single-dose diagnostic test for GH deficiency (Kaken Pharmaceutical, GHRP Kaken 100)
- 03Acts synergistically with GHRH to amplify GH release; stimulates appetite consistent with ghrelin-mimetic action
- 04Unlike ipamorelin, it measurably raises ACTH, cortisol and prolactin in human studies
- 05Long-term therapeutic development for GH-deficient children failed at Phase II and was not marketed
- 06Banned in sport by WADA; not FDA-approved
GHRP-2: research formats
Choose the format you are researching to see route-specific notes.
Potent ghrelin mimetic; stimulates GH and appetite. Typically 3× daily at evenly spaced intervals.
GHRP-2 is sold as a 5 mg vial. Reconstituting 5 mg with 2.0 mL BAC water gives a concentrated 2,500 mcg/mL solution, with small injection volumes per dose. Research protocols commonly use GHRP-2 up to three times daily (morning, pre-workout, and pre-sleep).
At 2,500 mcg/mL, volumes are small and precise drawing is essential. A TB syringe (marked in mL) can be easier to read accurately than a U-100 at these tiny volumes.
GHRP-2 causes appetite stimulation; this is more pronounced than with ipamorelin and is a key differentiator between the two compounds.
Sources
Every factual claim above resolves to a real, published source.
- Pralmorelin (GHRP-2): drug profile, structure, ghrelin-receptor mechanism, and Japanese diagnostic approvalWikipedia (encyclopedic overview with cited primary references)
- Growth hormone releasing peptide-2 (GHRP-2), like ghrelin, increases food intake in healthy menJ Clin Endocrinol Metab, 2005; PMID 15699539
- Effects of GHRP-2 and hexarelin, two synthetic GH-releasing peptides, on GH, prolactin, ACTH and cortisol levels in manPeptides, 1997; PMID 9285939
- GHRP-2 / pralmorelin: PubMed literature search (mechanism, diagnostic and endocrine studies)PubMed query, NCBI
Cite this page
PepCue. “GHRP-2: the evidence.” PepCue, reviewed June 1, 2026. https://www.pepcue.app/p/ghrp-2.
Log your doses, run the vial math, and keep a provider-ready record in PepCue.