GHRP-2
clinical trialsAlso known as: Pralmorelin, KP-102
**Mechanism of Action** GHRP-2 (Pralmorelin) is a synthetic hexapeptide that acts as a potent agonist of the ghrelin receptor (growth hormone secretagogue receptor, GHS-R1a). By binding to this receptor in the pituitary gland and hypothalamus, it stimulates the release of growth hormone (GH) in a dose-dependent manner, surpassing the efficacy of natural ghrelin. Additionally, GHRP-2 activates downstream pathways that increase appetite, cortisol secretion, and prolactin release, reflecting its broader neuroendocrine effects beyond GH regulation. **Key Research Findings** Clinical trials have demonstrated GHRP-2’s ability to significantly elevate GH levels in healthy adults and GH-deficient patients, with a rapid onset and short half-life. Studies show its potential for diagnosing GH deficiency (e.g., via stimulation tests) and for enhancing muscle mass or recovery in catabolic states. However, its non-specific effects—including elevated cortisol and prolactin—raise concerns about long-term safety, and research has not established consistent benefits for aging or athletic performance. Most trials remain small-scale, with limited data on chronic use. **Clinical Relevance** GHRP-2 is approved in some regions (e.g., Japan) for diagnostic use in GH deficiency but not for therapeutic indications. Its off-label use for anti-aging or bodybuilding is unsupported by robust evidence and carries risks of hormonal imbalance, including hypercortisolism and prolactin-related side effects. Ongoing research explores its utility in cachexia and metabolic disorders, but regulatory approval for such uses remains pending. For research purposes only — not medical advice.
Key data
C45H55N9O6Research & studies
AGHD is characterized by abnormal body composition, dyslipidemia, insulin resistance, and impaired quality of life.; The GHRP-2 test with a peak GH cutoff of 9 μg/L is recommended for diagnosing severe AGHD in Japan.; GH therapy for adults should start at 3 μg/kg/day and be individually titrated based on clinical status and IGF-I levels.; Favorable effects of GH replacement have been shown, but a direct reduction in mortality is not yet confirmed.
Limits of detection for all seven peptides were less than 50 pg/mL.; Method validated for specificity, precision, and recovery.; Detected N-acetylated LKKTETQ and its metabolite in plasma after TB-500 administration.; First identification of in vitro metabolites for all studied peptides except TB-500 in horses.
Peak GH responses were significantly lower with the arginine test (median 4.43 μg/L) and higher with the GHRP-2 test (median 28.88 μg/L) compared to ITT (median 9.38 μg/L).; Among AGHD patients, no significant difference in peak GH responses was found between the arginine test and ITT.; Sensitivity and specificity for severe AGHD were 93.8% and 85.5% for arginine test, and 81.3% and 94.5% for GHRP-2 test, respectively.; Both arginine and GHRP-2 tests are acceptable alternatives to ITT for diagnosing AGHD in Japanese patients.
GHRP-2, a peptide with verified growth-hormone-releasing properties, was identified and quantified in tablets offered as an over-the-counter nutritional supplement.; Qualitative identification used high-resolution/high-accuracy mass spectrometry after liquid chromatographic separation, considering accurate masses and fragment ion ratios from collisionally induced dissociation.; Quantification used LC coupled to a triple quadrupole mass spectrometer with an external calibration curve adjusted via internal standard (Hexarelin).; GHRP-2 content was determined at approximately 50 g per tablet; the authors note no routinely performed assay currently exists for such peptides in athletes' biological fluids.
GHRP-2 attenuated dexamethasone-induced Atrogin-1 mRNA in rat soleus muscle.; GHRP-2 decreased MuRF1 mRNA levels regardless of dexamethasone presence.; GHRP-2 did not alter plasma or muscle IGF-I levels.; The suppressive effect of GHRP-2 on Atrogin-1 and MuRF1 was blocked by a GHS-R1a antagonist.
Arthritis increased skeletal muscle MuRF1, MAFbx, and TNF-alpha mRNA expression.; Arthritis decreased serum IGF-I and hepatic IGF-I gene expression but increased muscular IGF-I and IGFBP-5 expression.; GHRP-2 for 8 days prevented the arthritis-induced increases in muscular MuRF1, MAFbx, and TNF-alpha.; GHRP-2 increased serum IGF-I and hepatic and cardiac IGF-I mRNA and decreased muscular IGFBP-5 mRNA in both control and arthritic rats.
GHRP-2 decreased arthritis score and paw volume in arthritic rats.; GHRP-2 reduced circulating IL-6 levels in arthritic rats.; GHRP-2 and ghrelin prevented endotoxin-induced IL-6 release from peritoneal macrophages in vitro.; GHRP-2 increased food intake in control rats but not in arthritic rats.
GHRP-2 infusion increased food intake by 35.9% vs. saline in all subjects.; Energy intake per kg body weight was higher with GHRP-2 (136.0 kJ/kg) than saline (101.3 kJ/kg).; Macronutrient composition of consumed food did not differ between conditions.; Serum GH levels rose significantly during GHRP-2 infusion.
Frequently asked questions
What is GHRP-2?
**Mechanism of Action** GHRP-2 (Pralmorelin) is a synthetic hexapeptide that acts as a potent agonist of the ghrelin receptor (growth hormone secretagogue receptor, GHS-R1a). By binding to this receptor in the pituitary gland and hypothalamus, it stimulates the release of growth hormone (GH) in a dose-dependent manner,
How does GHRP-2 work?
Synthetic hexapeptide ghrelin receptor agonist that potently stimulates GH secretion; also raises appetite, cortisol, and prolactin.
What is the research status of GHRP-2?
GHRP-2 is currently classified as clinical trials, with 206 research references on record. This is for research purposes only and is not medical advice.
What is the molecular weight of GHRP-2?
GHRP-2 has a molecular weight of approximately 818 g/mol (formula C45H55N9O6).
Related peptides
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First-generation ghrelin receptor agonist hexapeptide that stimulates GH release and strongly increases appetite.
Potent GHRP-family ghrelin receptor agonist with studied cardioprotective effects independent of GH release.
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Selective ghrelin receptor (GHS-R1a) agonist that stimulates GH release with minimal effect on cortisol or prolactin.
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