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Free U.S. shipping on orders over $150GHRP-6 is a ghrelin receptor agonist studied for its ability to stimulate endogenous growth hormone release and modulate appetite, energy balance, and neuroendocrine signaling.
Through activation of GHS-R1a and downstream pathways such as GH/IGF-1 and prolactin, GHRP-6 has been explored for effects on body composition, organ protection, immune regulation, and sleep physiology.
Growth Hormone–Releasing Peptide-6 (GHRP-6) is a synthetic hexapeptide that promotes growth hormone (GH) release by activating hypothalamic and pituitary signaling pathways.
What distinguishes GHRP-6 from other GHRPs is its orexigenic and neuroendocrine signaling [1]. GHRP-6 is a potent appetite-stimulating agent, reflecting strong activation of central ghrelin pathways involved in hunger perception and meal initiation.
This characteristic has made it a valuable research tool for studying the neural integration of appetite, growth hormone dynamics, and metabolic signaling.
At the receptor level, GHRP-6 activates GHS-R1a, triggering downstream GH/IGF-1 axis activity. Through this pathway, GHRP-6 indirectly influences:
In experimental settings, GHRP-6 increases secretion of other pituitary hormones, including prolactin and cortisol, highlighting its broader impact on neuroendocrine regulation [2, 3].
GHRP-6 can cause release of GH and downstream IGF-1 effects independent of GHRH or somatostatin. This occurs through activation of GHS-R1a [4].
GHRP-6 has unique effects on appetite regulation and body composition.
An animal study investigated the effects of GHRP-6 on food intake, body weight, and fat accumulation. Researchers compared adrenal-intact with adrenalectomised (ADX) rats (no glucocorticoid secretion) [5].
Rats received twice-daily subcutaneous injections of GHRP-6 (250 μg/kg) for two weeks. Results showed:
GHRP-6–induced body weight gain is not dependent on glucocorticoids, but activation of the HPA axis contributes to fat mass accumulation.
A study evaluated the effects of GHRP-6 on epithelial repair and organ protection in cell models of intestinal injury and rat models of multiple organ failure (MOF) induced by hepatic ischaemia–reperfusion [6].
In cells, GHRP-6 administration tripled cell migration compared with controls (p < 0.01). No increase in cell proliferation measured by [³H]-thymidine incorporation, indicating enhanced cellular motility rather than uncontrolled growth.
In the in vivo MOF model, ischaemia–reperfusion caused substantial tissue injury, including:
In the rat MOF model, results showed that:
GHRP-6 directly enhances epithelial repair through increased cell migration and provides broad organ-protective effects, supporting further investigation as a research strategy for mitigating inflammatory and ischemic organ injury.
GHRP-6 has been studied for its influence on sleep architecture.
A clinical study investigated how different routes of administration of GHRP-6 influence sleep architecture and endocrine hormone secretion in healthy young men [7].
Participants received either 300 μg/kg orally, 30 μg/kg intranasally, or 30 μg/kg sublingually at night.
Results showed that:
Results indicate that GHRP-6 can modulate both endocrine secretion and sleep, but that intranasal delivery was the most effective in influencing nocturnal GH secretion and sleep-related parameters.
References
1 Yahashi, S., Kang, K. S., Kaiya, H. and Matsuda, K. (2012) GHRP-6 mimics ghrelin-induced stimulation of food intake and suppression of locomotor activity in goldfish. Peptides, Elsevier BV 34, 324–328
2 Carmignac, D. F., Bennett, P. A. and Robinson, I. C. (1998) Effects of growth hormone secretagogues on prolactin release in anesthetized dwarf (dw/dw) rats. Endocrinology, The Endocrine Society 139, 3590–3596
3 Oliveira, J. H. A., Vieira, J. G. H., Abucham, J. and Lengyel, A. M. J. (2003) GHRP-6 is able to stimulate cortisol and ACTH release in patients with Cushing’s disease: comparison with DDAVP. J. Endocrinol. Invest., Springer Science and Business Media LLC 26, 230–235
4 Micic, D., Mallo, F., Peino, R., Cordido, F., Leal-Cerro, A., Garcia-Mayor, R. V., et al. (1993) Regulation of growth hormone secretion by the growth hormone releasing hexapeptide (GHRP-6). The Journal of pediatric endocrinology, J Pediatr Endocrinol 6 https://doi.org/10.1515/JPEM.1993.6.3-4.283
5 Tung, Y. L., Hewson, A. K. and Dickson, S. L. (2004) Glucocorticoid-dependent stimulation of adiposity and appetite by a ghrelin mimetic in the rat. Eur. J. Endocrinol., Oxford University Press (OUP) 150, 905–911
6 Cibrián, D., Ajamieh, H., Berlanga, J., León, O. S., Alba, J. S., Kim, M. J.-T., et al. (2006) Use of growth-hormone-releasing peptide-6 (GHRP-6) for the prevention of multiple organ failure. Clin. Sci. (Lond.), Portland Press Ltd. 110, 563–573
7 Frieboes, R. M., Murck, H., Antonijevic, I. A. and Steiger, A. (1999) Effects of growth hormone-releasing peptide-6 on the nocturnal secretion of GH, ACTH and cortisol and on the sleep EEG in man: role of routes of administration: Sleep endocrinology after GHRP-6. J. Neuroendocrinol., Wiley 11, 473–478
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). GHRP-6 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.
GHRP-6, also written GHRP6 or growth hormone-releasing peptide-6, is described as a growth hormone secretagogue hexapeptide. A review lists GHRP-6 among growth hormone secretagogues (GHS), which it names among the agents most commonly encountered in clinical practice and online self-administration protocols. In one study, GHRP6 was co-administered with epidermal growth factor (EGF), and the authors describe this combination as a promising neuroprotective candidate.
No, the facts do not describe GHRP-6 as a steroid. One source describes GHRP-6 as a growth hormone secretagogue hexapeptide. A review names GHRP-6 as a growth hormone secretagogue (GHS) among the agents most commonly encountered in clinical practice and online self-administration protocols. Neither fact mentions steroid structure, so this answer rests only on how the compound is named and classified.
In animal studies, D-Lys-3-GHRP-6 is a ghrelin receptor antagonist, and the authors used it to test the role of ghrelin. [D-Lys3]-GHRP-6 is described as a growth hormone secretagogue receptor (GHSR) antagonist. In animal work, molecular docking and a pharmacological experiment with [D-Lys3]-GHRP-6 (D-Lys3) were used to verify the Ghrelin/GHSR pathway. In one rat study of traumatic brain injury, [D-Lys3]-GHRP-6 was injected intraperitoneally after the rats woke up.
In the randomized open-label human acute stroke trial, GHRP6 was tested as part of a combined EGF+GHRP6 therapy given twice daily for 7 days to 95 patients, while 93 patients received standard care. In that trial, severe adverse events occurred in 48 of 188 patients, and none were considered treatment-related. These findings are about the combined EGF+GHRP6 therapy in that trial, not about GHRP6 given alone.
In a clinical trial in humans, GHRP6 combined with EGF showed no differences from standard care in the intention-to-treat population for modified Rankin Scale, Barthel index, or survival. In a human clinical trial, patients in the middle cerebral artery territory treated with EGF+GHRP6 had greater infarct volume reduction at 30 days. The COURAGE-2 study missed its primary endpoint but suggested potential benefit of EGF+GHRP6 in moderate-to-severe stroke in humans, and its authors said this warranted further studies targeting that subpopulation.
In a rat model of acute ischemic stroke, EGF combined with GHRP6 modulated 40 proteins at 3 hours and 223 proteins at 24 hours after treatment in the ischemic penumbra. In these rats, anti-apoptotic and mitochondrial proteins were modulated in the ischemic penumbra after EGF plus GHRP6 treatment. At 24 hours after treatment in rats, proteins linked to reactive oxygen species detoxification, heat shock factor 1 activation, and negative regulation of cellular hypoxia response were significantly modulated by GHRP6 combined with EGF.
In human oocytes cultured in vitro, GHRP-6 showed potential in promoting nuclear maturation by significantly inducing the appearance of the first polar body (PB1) within 24 hours. In the same in vitro study, GHRP-6 did not show statistically significant improvements in cytoplasmic maturation in metaphase 2 (MII) oocytes during that timeframe. Real-time PCR in human oocytes cultured in vitro found that, despite the early PB1 appearance at 24 hours, GHRP-6 did not elevate the expression of the CENP-E or LINGO2 genes. In the in vitro maturation procedure, the optimal GHRP-6 concentration was determined to be 75 ng/ml, resulting in a maturation rate of 70% on the first day and 80% on the second day.
In animal studies, GHRP-6 hydrogel treatment was found to have beneficial therapeutic effects on acute kidney injury (AKI) by targeting metabolic reprogramming. In the same animal studies, GHRP-6 hydrogel treatment enhanced the survival of tubular epithelial cells in the ischemic microenvironment by activating the mTOR-P70 pathway.
In a mouse study, GHRP-6 was examined for its ability to attenuate pulmonary damage caused by intratracheal LPS or zymosan combined with platelet activating factor. In the acute lung injury scenario in mice, GHRP-6 reduced neutrophilic alveolitis, attenuated lung compliance failure, and contributed to improved alveolar-capillary permeability. In the chronic scenario in mice, GHRP-6 preserved lung parenchymal integrity and accounted for meager collagen accumulation.
In broiler chickens, co-injection of the (D-Lys-3)-GHRP-6 form of GHRP6 with LEAP2 was reported to significantly decrease LEAP2-induced hypophagia (P<0.05). The same paper also reports that this co-injection significantly increased the hypophagic effect of LEAP2 in broiler chickens (P<0.05), a result that conflicts with the decrease reported in the same results section. The authors concluded that LEAP2-induced hypophagia is mediated via ghrelin and CB1 and CB2 receptors in neonatal chickens, a conclusion drawn in part from the (D-Lys-3)-GHRP-6 co-injection experiment.
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.