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Hexapeptide · GHS-R1a agonist
Also known as Pralmorelin · KP-102 · GPA-748
Growth hormone-releasing peptide-2, a synthetic hexapeptide agonist at the ghrelin receptor (GHS-R1a). Supplied as a lyophilized powder for research purposes only.
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Tested lot by lot at ≥99% purity. The Janoshik certificate for your lot is emailed with the order.
Everything Valtrax Research ships is bench material for in-vitro work. None of it is a drug, a supplement, a cosmetic, or a medical device, and none of it is intended for human or animal use, ingestion, or administration. Placing an order is your confirmation that you are a qualified researcher buying for lawful research, under every Canadian law and regulation that applies to you.
Six residues, half of them unnatural: D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH₂, supplied as the acetate salt. GHRP-2 is a synthetic growth hormone secretagogue that works the ghrelin receptor (GHS-R1a) rather than the GHRH receptor — a distinction established directly in receptor work, and the reason it is studied as a separate axis into somatotroph signalling rather than as another GHRH analogue.
The D-amino acids and the C-terminal amide are the engineering. They are what keep a six-residue peptide intact long enough to produce a measurable response, and they are why this compound became the reference secretagogue in the GHRP series.
Two threads run through the literature. The first is endocrine: how cleanly a small synthetic peptide engages GHS-R1a and what the somatotroph does in response, measured as GH release and used diagnostically. The second is everything else the ghrelin receptor touches — appetite signalling and inflammatory readouts — plus a steady analytical-chemistry thread on detecting the compound in seized and adulterated material.
GHRP-2 binds GHS-R1a, the receptor ghrelin occupies, and the downstream readout is somatotroph activation and growth hormone release. Receptor work in GC cells showed the response survives when the GHRH receptor is taken out of the picture, which is what separates this pathway from GHRH analogues such as sermorelin or tesamorelin.
Beyond the endocrine readout, published work follows the ghrelin-receptor consequences that come with it: food-intake response in healthy volunteers, and inflammatory markers in arthritis models. The compound also shows up in analytical chemistry literature as a detection target in seized product and adulterated supplements.
The compound emerged from the growth-hormone-releasing-peptide line that began with the enkephalin-derived secretagogues of the 1980s, and was developed under the code KP-102 with its pharmacology characterized in that program. A 2004 profile catalogued it under the generic name pralmorelin alongside its several development codes.
Its most durable role has been diagnostic: GH-stimulation testing for hypothalamic-pituitary disorder, including work in pediatric and adolescent cohorts, where a reliable, short-acting secretagogue is more useful than a long one.
In vitro and animal studies
GHRP-2 is a synthetic hexapeptide agonist at the growth hormone secretagogue receptor, part of the growth hormone releasing peptide family developed from the pioneering work on enkephalin-derived secretagogues that preceded the discovery of ghrelin itself. Its history is notable: these peptides were designed to hit a receptor whose endogenous ligand had not yet been identified, and their existence is what prompted the search that eventually found ghrelin.
Preclinical work established a strong, reproducible GH response across species. Studies report GH release through a mechanism distinct from and complementary to GHRH receptor signalling, with the combination of both producing a greater response than either alone — a finding that has been replicated often enough to be considered settled.
The receptor is not confined to the pituitary. Ghrelin receptor expression in the hypothalamus underlies appetite effects, and expression in the gastrointestinal tract underlies prokinetic effects. Rodent work also covers cardiac tissue, where ghrelin receptor signalling has been studied in the context of ischemic injury and cardiac function.
Human data, where it exists
GHRP-2 has more human data than most secretagogues, largely because of its diagnostic use. It has been employed clinically as a provocative agent for testing growth hormone secretory capacity, particularly in Japan, where it was developed for that purpose. That application generated real human pharmacology — dose-response data for GH release, and observations of the accompanying hormonal changes.
Those accompanying changes are the important part of the human record. GHRP-2 administration produces measurable increases in cortisol and prolactin alongside GH, which is well documented and is the basis for describing it as less selective than ipamorelin.
There is no approval anywhere for therapeutic use in body composition, recovery, or the applications the compound is marketed around, and no long-term human safety data at sustained exposures. Its diagnostic use involves single administrations under supervision, which is a very different exposure pattern.
Common assertions, and what the record supports
The claim that GHRP-2 produces a strong GH response is well supported — arguably better supported than for any other secretagogue here, given the diagnostic literature.
The claim that it is a clean GH agent is not supported and is contradicted by the same literature. The cortisol and prolactin increases are consistent findings, not rare adverse events, and they are the reason more selective secretagogues were subsequently developed. Marketing that presents GHRP-2 as equivalent to ipamorelin while citing its stronger GH response omits the trade-off that distinguishes them.
A third claim treats appetite stimulation as an incidental bonus. It is a direct pharmacological consequence of ghrelin receptor agonism in the hypothalamus, it is dose-related, and in some research contexts it is a confound rather than a benefit.
Against the compounds it is most often confused with
Against ipamorelin, this is the classic selectivity trade-off within the ghrelin-receptor agonists. GHRP-2 delivers a stronger GH response; ipamorelin delivers a cleaner one, with substantially less effect on cortisol and prolactin. Neither is superior in the abstract — it depends on whether the experiment can tolerate confounding from other pituitary outputs.
Against GHRP-6, the other widely used peptide in the family, GHRP-2 is generally reported as more potent for GH release with comparatively less pronounced appetite stimulation, though both act on the same receptor.
Against CJC-1295 in either form, the difference is receptor system rather than potency: GHRH receptor versus growth hormone secretagogue receptor. Combined stimulation of both is reported to exceed either alone, which is why the pairing is conventional and why these two classes are usually discussed together rather than as alternatives.
Adverse findings, toxicology gaps, material hazards
The documented cortisol and prolactin elevation is the effect that distinguishes GHRP-2's risk profile from the more selective secretagogues. Sustained cortisol elevation carries recognised consequences for glucose handling, immune function, bone density and soft tissue. Prolactin elevation has its own endocrine consequences. These are not theoretical for this compound — they are consistently reported findings.
On top of that sit the effects common to GH axis stimulation: insulin resistance and impaired glucose tolerance, fluid retention, arthralgia and carpal tunnel symptoms. Sustained IGF-1 elevation raises the mitogenic concern that applies across this shelf, since IGF-1 promotes proliferation and inhibits apoptosis.
Ghrelin receptor agonism increases appetite and alters gastric motility as a direct consequence of the mechanism.
The compound is covered by the World Anti-Doping Agency Prohibited List. Long-term human safety at sustained exposure has not been characterised; the human data that exists comes overwhelmingly from single-administration diagnostic use.
Bench practice for this compound
GHRP-2 is a hexapeptide, short and relatively robust, and dissolves readily. Introduce bacteriostatic water against the vial wall rather than onto the powder cake, and swirl gently instead of shaking to avoid foaming losses at the air-water interface.
Store reconstituted material at 2–8 °C protected from light, and observe the working window given on this page. Unopened lyophilized powder held frozen is stable considerably longer. Aliquot before freezing if the vial will be drawn on more than once.
This summary describes published research. It is not a protocol, not a recommendation, and not a statement that this compound is safe or effective for any use. Not for human or animal use.
Doi, N. et al. (2004). Pharmacological characteristics of KP-102 (GHRP-2), a potent growth hormone-releasing peptide.
PubMedChen, C. et al. (1998). Growth hormone-releasing peptide-2 (GHRP-2) does not act via the human growth hormone-releasing factor receptor in GC cells.
PubMedLaferrère, B. et al. (2005). Growth hormone releasing peptide-2 (GHRP-2), like ghrelin, increases food intake in healthy men.
PubMedGranado, M. et al. (2005). Anti-inflammatory effect of the ghrelin agonist growth hormone-releasing peptide-2 (GHRP-2) in arthritic rats.
PubMedSuzuki, S. et al. (2022). Clinical Usefulness of the Growth Hormone-Releasing Peptide-2 Test for Hypothalamic-Pituitary Disorder.
PubMedIdentity, purity, and net content are established by independent Janoshik verification, and the certificate for your lot travels with the order.
Janoshik Analytical, a laboratory Valtrax does not own, runs the testing — identity by mass spectrometry, purity by RP-HPLC at ≥99%, on the lot you receive.
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