All information below describes the compound's chemical identity, laboratory handling, and the published research literature. It describes molecular targets and results in laboratory and animal models only — not effects in humans — and is not evidence of any human benefit.
What Is GHRP-2?
GHRP-2 (Growth Hormone Releasing Peptide-2), also known by the international nonproprietary name pralmorelin and the development code KP-102, is a synthetic hexapeptide (molecular formula C45H55N9O6; CAS 158861-67-7). It belongs to the growth hormone secretagogue (GHS) class of peptides. It does not occur freely in nature; it is a synthetic ligand designed to interact with the growth hormone secretagogue receptor, and it has been used as a reference agonist in neuroendocrine laboratory investigation.
It is supplied as a reference compound for in vitro and animal research use only. The sections below summarize its chemical identity, laboratory handling, the molecular targets and model systems examined in the published literature, and the primary references — without describing outcomes, efficacy, or effects in humans.
Research Targets & Pathways
Published preclinical literature has examined GHRP-2 in relation to several molecular systems. These are pathway associations reported in laboratory and animal models; refer to the cited studies for methods and findings.
- Growth hormone secretagogue receptor (GHS-R1a / ghrelin receptor) — examined in relation to receptor binding and activation in transfected cell lines and pituitary systems.
- Somatotropic axis / pituitary GH secretion — studied in relation to pituitary GH-secretion signaling, characterized as a pathway distinct from the growth-hormone-releasing-hormone (GHRH) receptor.
- IP3 / Ca2+ second-messenger signaling — examined as a downstream GHS-R signal-transduction pathway in cell-based assays.
- NF-κB signaling — investigated in relation to inflammatory-pathway markers in rodent tissue-injury models.
- Cardiac / vascular GHS-R expression — examined in relation to receptor distribution in cardiac tissue and vasculature.
Model Systems Studied
GHRP-2 has been used as a test compound across a range of published preclinical model systems, including in vitro cell assays, rodents, and other animal models. Refer to the cited literature for study designs, endpoints, and findings.
- In vitro — pituitary-cell stimulation assays and receptor-binding assays targeting the GHS-R1a receptor.
- Somatotropic axis — rat pituitary GH-secretion models and stimulation-test protocols.
- Cardiovascular — isolated blood-perfused rabbit-heart ischemia models and permanent-coronary-ligation rodent models (some using GHRP-6).
- Musculoskeletal — rat rotator-cuff / tendon-to-bone interface models.
- Inflammation / tissue — rodent sepsis, liver-injury, and organ-fibrosis models.
Note: several cited references reflect broader GHRP-class findings (e.g., GHRP-6 and other ghrelin mimetics) relevant to shared receptor mechanisms; species and model differences should be considered when interpreting translatability, and independent replication varies across endpoints.
Molecular & Technical Profile
C45H55N9O6 | MW 817.94 g/mol | CAS 158861-67-7 | Synthetic hexapeptide
Storage, Reconstitution & Working Concentrations
Storage, reconstitution, and working-concentration values are general laboratory guidance for in vitro and animal research; always confirm against the lot-specific Certificate of Analysis.
Current Research Status
As of the time of this writing, GHRP-2 (pralmorelin) has not been approved by the U.S. Food and Drug Administration (FDA) for any human therapeutic use. The material supplied by Explicit Research is a reference compound for laboratory research use only and is not an approved drug product. The available literature is drawn from in vitro assays and animal models, together with a body of human physiology and stimulation-test studies; translation of these model findings to clinical contexts has not been established through the compound as supplied here. Ongoing research continues to characterize its receptor pharmacology and the model systems in which it has been examined.
Research FAQ
Is GHRP-2 approved for human use?
GHRP-2 (pralmorelin) has not been approved by the FDA for any human therapeutic use. The material supplied by Explicit Research is a reference compound for laboratory research use only and is not an approved drug product — not for human consumption.
What is GHRP-2's molecular formula?
A synthetic hexapeptide — molecular formula C45H55N9O6, MW 817.94 g/mol, CAS 158861-67-7.
How is GHRP-2 stored and reconstituted?
Store lyophilized at −20°C, protected from light and moisture. Reconstitute in sterile or bacteriostatic water (or 0.1% acetic acid); store the reconstituted solution at 2–8°C for up to ~28 days and avoid repeated freeze–thaw.
What targets and model systems has GHRP-2 been studied in?
Preclinical work has examined GHRP-2 at the growth hormone secretagogue receptor (GHS-R1a / ghrelin receptor) — a pathway reported as distinct from the GHRH receptor — across pituitary-cell and receptor-binding assays and rodent and other animal models. Note that several cited references reflect broader GHRP-class findings; species and model differences should be considered.
Selected References
- Bowers et al. (1991). Characterized dose-dependent GH secretion and receptor-binding actions of GHRP in pituitary and in vivo models. Endocrinology.
- Mori et al. (2004). Profiled the general pharmacology of GHRP-2 (KP-102), including GH-release potency, cortisol, and prolactin responses across dose ranges. Eur J Pharmacol.
- Bowers et al. (1993). Defined the GHRP-family structural requirements for GHS-receptor activation and peptide activity in pituitary cell assays. J Pediatr Endocrinol.
- Howard et al. (1996). Identified and cloned the growth hormone secretagogue receptor (GHS-R), characterizing ligand binding and signal transduction via IP3/Ca2+ second messengers distinct from the GHRH receptor. Science.
- Kojima et al. (1999). Identified ghrelin as the endogenous GHS-R ligand and characterized its GH-releasing and orexigenic signaling in rat stomach and pituitary. Nature.
- Cornejo et al. (2025). Measured brain GHS-R engagement and downstream ghrelin signaling following intranasal ghrelin-mimetic delivery in mouse models. Endocrinology.
- Tannenbaum et al. (2003). Measured GH secretion when GHRP-2 and GHRH were co-administered, characterizing non-competing receptor pathways in rat pituitary models. Endocrinology.
- Arvat et al. (1995). Quantified GH, cortisol, and prolactin secretory responses to GHRP-2 and GHRH co-administration in human subjects. J Endocrinol Invest.
- Akamizu et al. (2023). Measured pituitary GH reserve and secretory response to GHRP-2 stimulation testing in elderly subjects, evaluating assay reliability and adverse-event monitoring. Growth Horm IGF Res.
- Ghigo et al. (2000). Compared GHRP-2, arginine, and GHRH stimulation tests for GH-reserve assessment in adults with suspected GH deficiency. Eur J Endocrinol.
- Chapman et al. (1996). Measured IGF-1, GH pulse frequency, and body-composition changes during GHS administration in elderly men and women in a double-blind RCT. J Clin Endocrinol Metab.
- Bisi et al. (2000). Measured diastolic-function and myocardial-stunning parameters in an isolated blood-perfused rabbit-heart model following GHRP-2 pretreatment before ischemic challenge. Endocrinology.
- Locatelli et al. (2000). Reviewed GHS-R expression in cardiac tissue and vasculature and noted species differences as a limitation in translating preclinical cardiovascular findings. Ann Endocrinol (Paris).
- Rosenblatt et al. (2026). Measured ventricular-remodeling indices, ejection fraction, and systolic-function parameters in a permanent coronary-ligation rat model following GHRP-6 administration. Pharmaceuticals (Basel).
- Broglio et al. (2003). Quantified acute hemodynamic and cardiac-output responses to GHRP-2 infusion in healthy human subjects using echocardiography and invasive monitoring. J Clin Endocrinol Metab.
- Berthold et al. (2025). Measured macrophage-polarization markers, histologic scores, and tendon-bone interface biomechanical properties in a rat rotator-cuff-tear model following GHRP-2 treatment. Arthroscopy.
- Granado et al. (2012). Quantified NF-κB pathway activation and cytokine profiles (TNF-α, IL-6) in a rodent sepsis model following GHRP-2 treatment. Am J Physiol Endocrinol Metab.
- Dios-Barbeito et al. (2009). Measured hepatic inflammatory signaling, oxidative-stress indices, and NF-κB activation in a rat liver-injury model following GHRP-2 administration. J Hepatol.
- Garcia-Ojalvo et al. (2014). Assessed pro-fibrotic cytokine levels, collagen deposition, and tissue-remodeling markers in a rat model of organ fibrosis following GHRP-class peptide treatment. Peptides.
