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GHRP-6

Growth hormone releasing hexapeptide, or GHRP-6, belongs to a group of synthetic peptides developed with the potential to stimulate the secretion and regulate growth hormone levels. Similar to most such peptides, GHRP-6 is an analog of the naturally occurring opioid peptide and neuromediator called met-enkephalin. Yet, researchers suggest it may lack the opioid activity generally associated with these enkephalins. Instead, GHRP-6 appears to interact with the so-called growth hormone secretagogue receptors (GHS-Rs) which eventually turn out to be ghrelin receptors. Initially, growth hormone releasing peptides (GHRP) were developed with the intention of mimicking the mechanism of action of growth hormone releasing hormones (GHRHs). When GHRH was first isolated in 1984, scientists hypothesized that these compounds might operate differently; with GHRPs exhibiting an apparent affinity to bind with ghrelin receptors. Ghrelin is also known as the hunger hormone, and it is naturally produced by the stomach when empty. Further research studies have suggested that GHRPs may act by binding with two receptors, GHS-R1a, and CD36. In addition to hGH release, GHRP-6 also appears to have the potential to reduce cellular death through binding with CD36 receptors, possibly stimulating prosurvival cellular pathways.

Size

$56.00 USD/ 10mg

Technical Specifications

Technical specifications for GHRP-6
Sequence	His-D-Trp-Ala-Trp-D-Phe-Lys-NH2
Molecular Formula	C46H56N12O6
Molecular Weight	873.03 g/mol
Purity	≥98% (HPLC)
Form	Lyophilized powder
Storage	-20°C, desiccated
CAS	87616-84-0
Also Known As	Growth Hormone Releasing Peptide-6

Application Areas

Tendon and ligament healing studies

Muscle injury recovery protocols

Gastrointestinal tissue repair research

Anti-inflammatory pathway research

Wound healing research

Veterinary wound healing applications

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For Research Use Only. Products are not for human or veterinary consumption. Not a drug, dietary supplement, or medical device. Sold exclusively to qualified research professionals.

Bio-Engineered Precision

Initially, growth hormone releasing peptides (GHRP) were developed with the intention of mimicking the mechanism of action of growth hormone releasing hormones (GHRHs). When GHRH was first isolated in 1984, scientists hypothesized that these compounds might operate differently; with GHRPs exhibiting an apparent affinity to bind with ghrelin receptors. Ghrelin is also known as the hunger hormone, and it is naturally produced by the stomach when empty.

Further research studies have suggested that GHRPs may act by binding with two receptors, GHS-R1a, and CD36. In addition to hGH release, GHRP-6 also appears to have the potential to reduce cellular death through binding with CD36 receptors, possibly stimulating prosurvival cellular pathways.

Purity Level≥98% (HPLC)

Molecular Weight873.03 g/mol

Molecular FormulaC46H56N12O6

SequenceHis-D-Trp-Ala-Trp-D-Phe-Lys-NH2

GHRP-6 Peptide and Hypothyroidism

Hypothyroidism is typically characterized by reduced levels of growth hormone secretion. The main aim of this study was to determine whether GHRP-6, a supposed hGH release-stimulating agent, might be used to mitigate hGH level reduction. Research models of hypothyroidism were evaluated following random exposure to three different concentrations of GHRH and GHRP-6. Models exposed to GHRP-6 alone and in combination with GHRH appeared to induce significantly higher levels of growth hormones than GHRH alone.

Proposed Mechanism

The possible reasoning behind GHRP-6's superior action in hypothyroidism is that it may differ from GHRH, with the potential as a functional antagonist of somatostatin at the pituitary level. This may be why GHRP-6 may exert possibly increased action on hypothyroidism compared to GHRH alone, suggesting a distinct pathway of action at the pituitary level that does not require full hypothalamic GHRH signaling.

GHRP-6 Peptide and Cortisol Hormone Release

In this study, the action of GHRP-6 peptide on hormone release and sleep electroencephalogram (EEG) during nighttime was studied. Research models were exposed with either the GHRP-6 peptide or a placebo. After the peptide, researchers observed that GHRP-6 appeared to induce higher secretion of both growth hormones and cortisol (ACTH) hormones. Throughout the night, particularly during the first half, cortisol hormone release and stage 2 sleep appeared to be enhanced, while other sleep EEG variables remained apparently unchanged.

GHRP-6 Peptide and Organ Function

The main goal of this study was to determine the action of GHRP-6, either alone or in combination with epidermal growth factor (EGF), on multiple organ failure. The first iteration was conducted on experimental models of injury and multiple organ failure, while the second was conducted on rat intestine and colonic cancer cells. The first study suggested that GHRP-6 may impact the gut epithelial cells and increase cell migration by three times a control rate, without apparent impact on cell proliferation.

Key Findings

In the second model, multiple organ failure caused severe hepatic and intestinal damage and lipid peroxidation. Presentation of GHRP-6 appeared to reduce these damages by a reported 50–85%, with additional activity when GHRP-6 was presented in combination with EGF. This suggests that GHRP-6 may serve a cytoprotective role in conditions of severe multi-organ stress.

GHRP-6 Peptide and Neuroprotection

Research explored the impact of GHRP-6 on the IGF-1 system within the brains of mouse models. Results indicated that exposure to GHRP-6 for a week appeared to elevate IGF-1 mRNA levels in the hypothalamus, cerebellum, and hippocampus, but not in the cerebral cortex, suggesting that GH and GHRP-6 might enhance IGF-1 production in specific areas of the brain.

Signaling Pathway

The phosphorylation of Akt and the Bcl-2-associated death promoter (BAD) was observed in areas with increased IGF-1 levels, indicating that GH and GHRP-6 may initiate cellular survival pathways in reaction to growth factors. There was also an increase in the antiapoptotic protein Bcl-2 in areas with raised IGF-1, while proapoptotic Bax levels remained consistent, hinting at a shift towards cell preservation over apoptosis. IGFBP-5, linked with neuronal survival, showed significant elevation primarily in the hypothalamus, pointing to a potential neuroendocrine role.

GHRP-6 Peptide and Tissue Recovery

GHRP-6 is believed to stimulate not only ghrelin (GHS-Rs) receptors linked to GH production, but also CD36 receptors, potentially mediating anti-inflammatory and other advantageous effects. A preclinical study involving murine models exposed to GHRP-6 for 30 days suggested a possibility for faster wound healing and diminished hypertrophic scar development by lessening inflammation and the expression of fibrotic cytokines.

Key Findings

In a separate preclinical investigation, stimulation of ghrelin receptors was posited to improve wound healing in rats subjected to combined radiation and burn injury, through a reduction in pro-inflammatory agents, particularly TNF-α, and the alteration of inflammation-related signaling pathways. Following 60 days of GHRP-6 exposure, a potential decrease in liver fibrosis and reduction in fibrogenic factors such as TGF-β and CTGF were noted, with fibrotic areas and nodularity decreasing by 75% and more than 60%, respectively.

[1]
Rico M, Lorenzo MT, Pazo JA, Vega FV, De la Cruz LF. GHRP-6 in heifer and cow adenohypophisial cells separated by elutriation. J Physiol Biochem. 1999 Mar;55(1):33-9. PMID: 10494658.
[2]
Berlanga-Acosta, Jorge et al. Synthetic Growth Hormone-Releasing Peptides (GHRPs): A Historical Appraisal of the Evidences Supporting Their Cytoprotective Effects. Clinical Medicine Insights. Cardiology vol. 11 1179546817694558. 2 Mar. 2017, doi:10.1177/1179546817694558https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5392015/
[3]
Bowers, C.Y., et al (2012). Ghrelin: A history of its discovery. In Ghrelin in Health and Disease (pp. 1-35), Human press Inchttps://mayoclinic.pure.elsevier.com/en/publications/ghrelin-a-history-of-its-discovery
[4]
Naushira Pandya et al. Growth Hormone (GH)-Releasing Peptide-6 Requires Endogenous Hypothalamic GH-Releasing Hormone for Maximal GH Stimulation. The Journal of Clinical Endocrinology & Metabolism, Volume 83, Issue 4, 1 April 1998, Pages 1186–1189https://academic.oup.com/jcem/article-abstract/83/4/1186/2865313
[5]
Popovic V, et al. Blocked growth hormone-releasing peptide (GHRP-6)-induced GH secretion and absence of the synergic action of GHRP-6 plus GH-releasing hormone in patients with hypothalamopituitary disconnection. J Clin Endocrinol Metab. 1995 Mar;80(3):942-7https://pubmed.ncbi.nlm.nih.gov/7883854/
[6]
Demers, A., et al. (2004). Identification of the growth hormone-releasing peptide binding site in CD36: a photoaffinity cross-linking study. The Biochemical journal, 382(Pt 2), 417–424https://doi.org/10.1042/BJ20040036
[7]
Pimentel-Filho FR, et al. Growth hormone responses to GH-releasing peptide (GHRP-6) in hypothyroidism. Clin Endocrinol (Oxf). 1997 Mar;46(3):295-300. doi: 10.1046/j.1365-2265.1997.1270942.xhttps://pubmed.ncbi.nlm.nih.gov/9156038/
[8]
Frieboes RM, et al. Growth hormone-releasing peptide-6 stimulates sleep, growth hormone, ACTH and cortisol release in normal man. Neuroendocrinology. 1995 May;61(5):584-9https://doi.org/10.1159/000126883
[9]
Cibrián D, et al. Use of growth-hormone-releasing peptide-6 (GHRP-6) for the prevention of multiple organ failure. Clin Sci (Lond). 2006 May;110(5):563-73https://pubmed.ncbi.nlm.nih.gov/16417467/
[10]
Zheng, Q., et al. (2008). Prokinetic effects of a ghrelin receptor agonist GHRP-6 in diabetic mice. World journal of gastroenterology, 14(30), 4795–4799https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2739343/
[11]
Frago LM, et al. Growth hormone (GH) and GH-releasing peptide-6 increase brain insulin-like growth factor-I expression and activate intracellular signaling pathways involved in neuroprotection. Endocrinology. 2002 Oct;143(10):4113-22. doi: 10.1210/en.2002-220261. PMID: 12239123.
[12]
Lim, C. J., et al. (2015). Growth hormone-releasing peptide-biotin conjugate stimulates myocytes differentiation through insulin-like growth factor-1 and collagen type I. BMB reports, 48(9), 501–506https://doi.org/10.5483/bmbrep.2015.48.9.258
[13]
Mendoza Marí, Y., et al. (2016). Growth Hormone-Releasing Peptide 6 Enhances the Healing Process and Improves the Esthetic Outcome of the Wounds. Plastic surgery international, 2016, 4361702https://doi.org/10.1155/2016/4361702
[14]
Liu, C., et al. (2016). Ghrelin accelerates wound healing through GHS-R1a-mediated MAPK-NF-κB/GR signaling pathways in combined radiation and burn injury in rats. Scientific reports, 6, 27499https://doi.org/10.1038/srep27499
[15]
Berlanga-Acosta, J., et al. (2012). Growth Hormone Releasing Peptide 6 (GHRP6) reduces liver fibrosis in CCl4 chronically intoxicated rats. Biotecnología Aplicada, 29(2), 60-72.

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Batch-level purity documentation

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≥99% purity guaranteed