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Free U.S. shipping on orders over $150GHRP-2 is a growth hormone–releasing peptide studied for its ability to stimulate endogenous GH and downstream IGF-1 signaling.
By engaging the GHS-R1a receptor and CD36-associated pathways such as PI3K-AKT, it influences tissue protection, inflammatory balance, pain modulation, and body composition through coordinated endocrine and cellular signaling.
Growth Hormone–Releasing Peptide-2 (GHRP-2) is a synthetic hexapeptide designed to stimulate the endogenous release of growth hormone (GH).
GHRP-2 activates GHS-R1a, a receptor expressed in both the pituitary gland and hypothalamus [1]. GHS-R1a increases GH secretion, which then stimulates hepatic and peripheral production of insulin-like growth factor-1 (IGF-1), a key mediator of GH’s effects on tissue growth, tissue repair, and metabolic regulation.
In addition to its role in GH release, GHRP-2 interacts with membrane glycoprotein CD36, which activates downstream pathways such as PI3K-AKT to help with cell survival, nutrient signaling, and anabolic processes [2].
While the functional relevance of these non-GHS-R pathways continues to be explored, they suggest that GHRP-2 may influence cellular metabolism beyond GH secretion alone.
GHRP-2 has been studied for its role in tissue-protective signaling, an effect that appears to arise from activating intracellular survival pathways.
A study investigated whether GHRP-2 could protect against glucocorticoid-induced muscle atrophy both in whole rats and muscle cell models [3].
Researchers found that dexamethasone significantly increased expression of the muscle-specific ubiquitin ligases Atrogin-1 and MuRF1, drivers of muscle protein breakdown.
Treatment with GHRP-2 resulted in:
These results support GHRP-2’s potential role in muscle preservation during catabolic states, such as steroid exposure, chronic illness, or disuse.
GHRP-2 may influence inflammatory signaling and immune modulation through both endocrine and intracellular pathways.
An animal study examined the effects of GHRP-2 on inflammation, metabolic disruption, and cachexia in a rat model of chronic inflammatory arthritis [4].
Arthritis and inflammation was induced in male Wistar rats using Freund’s adjuvant, followed by daily administration of GHRP-2 or saline for eight days.
Arthritis induction was associated with:
Despite not increasing food intake in arthritic animals, GRHP-2 administration resulted in:
These results suggest that GHRP-2’s benefits were not just driven by appetite stimulation.
GHRP-2 can influence pain modulation, an effect thought to arise from its interaction with growth hormone signaling as well as central opioid pathways.
An animal study investigated the role of GHRP-2 in central pain modulation using a mouse model of acute pain [5].
Researchers increased doses of GHRP-2 via intracerebroventricular (i.c.v.) administration (0.1, 0.3, 1, 3, and 10 nmol/L) and measured pain through the tail immersion test. Results showed:
Results indicate GHRP-2 modulates pain perception through central ghrelin receptor activation and opioid receptor crosstalk, supporting its value as a pain regulation adjunct.
GHRP-2 can influence body composition through IGF-1. A case study examined the effects of long-term GHRP-2 administration in a patient with a 20-year history of anorexia nervosa [6].
Although the patient’s fear of eating and desire to be thin had improved, persistent gastrointestinal dysfunction (vomiting, constipation, hypoglycemia, and sub-ileus) prevented meaningful increases in food intake or body weight.
GHRP-2 was administered intranasally before each meal for one year. Following treatment initiation, the patient experienced:
No significant adverse effects were recorded, presenting a new approach to managing treatment-resistant anorexia nervosa through GHRP-2 signaling.
Future studies will need to analyze greater sample sizes for reproducibility.
References
1 Laferrère, B., Abraham, C., Russell, C. D. and Bowers, C. Y. (2005) Growth hormone releasing peptide-2 (GHRP-2), like ghrelin, increases food intake in healthy men. J. Clin. Endocrinol. Metab., The Endocrine Society 90, 611–614
2 Demers, A., McNicoll, N., Febbraio, M., Servant, M., Marleau, S., Silverstein, R., et al. (2004) Identification of the growth hormone-releasing peptide binding site in CD36: a photoaffinity cross-linking study. Biochem. J., Portland Press Ltd. 382, 417–424
3 Yamamoto, D., Ikeshita, N., Matsubara, T., Tasaki, H., Herningtyas, E. H., Toda, K., et al. (2008) GHRP-2, a GHS-R agonist, directly acts on myocytes to attenuate the dexamethasone-induced expressions of muscle-specific ubiquitin ligases, Atrogin-1 and MuRF1. Life Sci., Elsevier BV 82, 460–466
4 Granado, M., Priego, T., Martín, A. I., Villanúa, M. A. and López-Calderón, A. (2005) Anti-inflammatory effect of the ghrelin agonist growth hormone-releasing peptide-2 (GHRP-2) in arthritic rats. Am. J. Physiol. Endocrinol. Metab., American Physiological Society 288, E486–92
5 Zeng, P., Li, S., Zheng, Y.-H., Liu, F.-Y., Wang, J.-L., Zhang, D.-L., et al. (2014) Ghrelin receptor agonist, GHRP-2, produces antinociceptive effects at the supraspinal level via the opioid receptor in mice. Peptides, Elsevier BV 55, 103–109
6 Haruta, I., Fuku, Y., Kinoshita, K., Yoneda, K., Morinaga, A., Amitani, M., et al. (2015) One-year intranasal application of growth hormone releasing peptide-2 improves body weight and hypoglycemia in a severely emaciated anorexia nervosa patient: GHRP-2 treatment for anorexia nervosa. J. Cachexia Sarcopenia Muscle, Wiley 6, 237–241
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). GHRP-2 is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
In clinical studies of patients, GHRP-2 (growth hormone-releasing peptide-2) was used as a stimulation test. In one study, a peak cortisol level below 12 μg/dL in the GHRP-2 stimulation test was specific to hypothalamic secondary adrenal insufficiency among patients with normal cortisol responses to CRH. GHRP2 was one of several tests, along with cosyntropin stimulation, CRH tests, and/or insulin tolerance tests, performed on 36 patients with hypothalamic-pituitary disorder. In patients with pituitary adenomas, GHRP-2 was used as a growth hormone-releasing stimulus in stimulation testing.
GHRP 2, also called GHRP2, acts through the GH secretagogue receptor (GHSR) in the hypothalamus, where ghrelin is a natural ligand. The source states that GHRP2 stimulates the hypothalamic-pituitary-adrenal axis through this receptor. Because it acts as a powerful stimulus for GH secretion, the cut-off peak GH level used in the GHRP2 loading test is higher than in other GH tests.
A liquid chromatography-tandem mass spectrometry procedure was developed to extract GHRP-2 and its main metabolite, AA-3, from dried blood spots and detect them. In authentic post-administration specimens analyzed with this dried blood spot method, GHRP-2 was successfully detected. GHRP-2 was chosen as a representative of the growth hormone-releasing peptides family to provide evidence that dried blood spots are suitable for detecting this group of substances in sport testing. In the in vitro analysis, the limit of detection for GHRP-2 in dried blood spot analysis was established at 50 pg/ml.
According to the reported analysis, seized powders were identified by LC-HRMS and comparison with reference standards as analogs of GHRP-2 (Pralmorelin). The same powders were also identified as analogs of GHRP-6, Ipamorelin, and modified growth hormone releasing factor (modified GRF 1-29). The study describes these compounds, including GHRP-2 (Pralmorelin), as growth hormone secretagogues that can be used as performance-enhancing substances in sports.
In a human observational study, the GHRP-2 test showed a sensitivity of 64% and a specificity of 79% for diagnosing adrenocortical insufficiency, relative to the insulin tolerance test. Across the whole cohort, the authors judged the GHRP-2 test not suitable for clinical use because of these values. A human observational analysis of male patients without functional adenoma (n = 104) reported a sensitivity of 95% and a specificity of 85% for the GHRP-2 test.
In a clinical trial in patients, the ACTH response in the GHRP2 test was useful for screening pituitary adrenal insufficiency, with a 1.55-fold cutoff giving 83% sensitivity and 88% specificity. Combining that ACTH response with a peak cortisol cutoff of 10 µg/dL gave 100% specificity and 0.94 accuracy for diagnosing pituitary adrenal insufficiency in patients. Separately, in a clinical trial in patients, a peak cortisol level below 12 μg/dL in the GHRP-2 stimulation test was specific to hypothalamic adrenal insufficiency only among patients with normal cortisol responses to CRH.
In a human observational study, overweight was associated with severe growth hormone deficiency diagnosed by GHRP-2 testing, with an odds ratio of 3.86 after adjustment for age, sex, creatinine, free thyroxine, tumor height and clinical diagnosis. This finding is an association observed in patients, not a measured effect of body weight on the growth hormone response to GHRP-2. In 48 human patients who underwent postoperative GHRP-2 tests, severe postoperative growth hormone deficiency was more common in overweight patients than in non-overweight individuals (100% vs. 48%).
In an observational study of 104 patients, 45 (43%) were found to have severe growth hormone deficiency when diagnosed using GHRP-2 tests. The 104 patients included 85 with non-functioning pituitary adenomas (NFPA) and 19 with Rathke's cysts. In a separate retrospective study of adolescents, median growth hormone peaks after GHRP2 were 3.4 ng/mL in the organic or genetic GHD group, 88.9 ng/mL in the idiopathic GHD group, and 90.1 ng/mL in the short stature group.
In a human observational study, two patients exceeded the cut-off for the GHRP-2 test but were below the cut-off on other growth hormone tests. From these results, the authors suggested that the current GHRP-2 test cut-off may miss some patients with growth hormone deficiency. Separately, a receiver operating characteristic analysis in humans identified a peak growth hormone cut-off of 8.08 ng/mL for the GHRP-2 test in relation to adrenocortical function, with specificity 0.868 and sensitivity 0.852.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.