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Research-grade compound with certificate of analysis. Full analytical testing on every lot.
Snapshot: Hexarelin is a synthetic hexapeptide and potent growth hormone secretagogue that selectively activates GHS-R (ghrelin) receptors to simulate endogenous, pulsatile GH release. Preclinical studies suggest potential roles in cardiomyocyte protection under ischemic stress, metabolic and lipid-regulating pathways, skeletal muscle mass preservation, and organ-protective stress-response signalling.
Hexarelin (examorelin) is a synthetic hexapeptide (His-D-2-Methyl-Trp-Ala-Trp-D-Phe-Lys-NH2) belonging to the group of growth hormone secretagogues (GHS) [1]. It was developed as a selective GHS-R ghrelin receptor agonist to enhance the body’s natural growth-hormone output, rather than replace it with exogenous hormone [1]. Through high-affinity receptor binding in the hypothalamus and pituitary, hexarelin activates G-protein coupled signalling, intracellular calcium mobilization, and cAMP-linked pathways that support pulsatile GH release patterns [2].
The peptide incorporates non-natural amino acids including D-2-methyltryptophan, D-phenylalanine, and lysine amide, increasing resistance to enzymatic degradation and improving its pharmacokinetic stability [3]. It is metabolized in the liver with renal elimination and remains analytically detectable for up to 8 hours post-administration [3].
In addition to GH signalling, hexarelin is widely used in experimental and preclinical research to study cardiometabolic stress responses, intracellular calcium regulation, oxidative stress and inflammatory markers, and survival-associated pathways in cardiac and skeletal muscle models.
Hexarelin activates two key receptors found directly in cardiac muscle and blood vessels, GHSR-1a receptor and CD36 [4]. Because these receptors are present in heart muscle cells themselves, many of hexarelin’s effects appear to come from local, tissue-level signalling inside the heart, rather than through increasing circulating growth hormone [4].
In many experimental models, hexarelin enhanced myocardial contractility. Hexarelin has been shown to improve intracellular calcium handling and activates downstream kinase pathway (including protein kinase C signalling), resulting in a positive inotropic effect without increasing heart rate or imposing excess hemodynamic load [4].
Hexarelin has also demonstrated cytoprotective effects under stress conditions, including heart failure, ischemia, and toxin exposure [4]. It attenuates cardiomyocyte and endothelial apoptosis, reduces DNA fragmentation, and promotes survival-associated signalling, thereby supporting the preservation of myocardial tissue over time [4].
In ischemic-reperfusion models, hexarelin reduced infarct size and improved recovery of post-ischemic ventricular performance, and heart conduction stabilization [4]. Chronic cardiovascular stress is a driver of fibrotic remodelling, and hexarelin seems to mitigate this process by downregulating collagen I and III expression, reducing profibrotic signaling, and enhancing metalloprotease activity – changes consistent with reduced myocardial stiffness and improved diastolic function [4].
Combined, these findings suggest hexarelin may help the heart contract more efficiently, withstand stress, and recover more efficiently following injury, with actions driven largely by its direct interaction with cardiac receptors [4].
Hexarelin and related growth-hormone secretagogues have been investigated for their effects on lipid metabolism, insulin-resistance markers, skeletal muscle mass preservation, and cachexia-induced signalling pathways.
In a study of healthy older adults, those with higher total fat mass, body fat percentage, BMI or bodyweight showed a smaller growth hormone response after a single dose of hexarelin [5]. Fat mass was the strongest predictor of response, while gender’s predictive effect was not significant once body composition was adjusted [5]. This trend occurred across a continuum, with even moderate increases in body fat linked to reduced GH response. This suggests higher adiposity can blunt GH-sectretagogue signalling [5].
Beyond hormone responsiveness, preclinical research indicates hexarelin may support metabolic resilience and cellular protection [6]. In models of chemically induced pancreatic beta-cell damage, hexarelin reduced mitochondrial injury, oxidative stress, and activation of cell-death pathways, while preserving beta-cell structure and insulin levels [6]. These findings suggest a potential role in protecting beta-cell mass under oxidative and metabolic stress conditions [6].
Additional animal models have shown improvements in glucose and insulin tolerance, lowered liver and plasma triglycerides, and enhanced fat-cell differentiation and lipid handling [7]. These improvements occurred without increases in total body weight and were accompanied by a shift toward lower fat mass and higher lean mass, despite increased food intake [7]. These effects may relate, in part, to CD36-linked lipid metabolism pathways [7].
Research across cardiac, metabolic, and skeletal muscle systems indicates that hexarelin may exert organ-protective effects. It is thought these effects occur through activation of survival- and stress-response pathways, modulation of fibrosis and remodelling signals, stabilization of intracellular calcium dynamics, and protection of mitochondrial function under metabolic or toxic stress [8, 9, 10, 6].
These effects are currently described within experimental frameworks and mechanistic investigations, rather than clinical outcome studies.
1 Carpino, P. A. (2002) Recent developments in ghrelin receptor (GHS-R1a) agonists and antagonists. Expert Opin. Ther. Pat., Informa Healthcare 12, 1599–1618
2 Imbimbo, B. P., Mant, T., Edwards, M., Amin, D., Dalton, N., Boutignon, F., et al. (1994) Growth hormone-releasing activity of hexarelin in humans. A dose-response study. Eur. J. Clin. Pharmacol., Springer 46, 421–425
3 Ghigo, E., Arvat, E., Gianotti, L., Imbimbo, B. P., Lenaerts, V., Deghenghi, R., et al. (1994) Growth hormone-releasing activity of hexarelin, a new synthetic hexapeptide, after intravenous, subcutaneous, intranasal, and oral administration in man. J. Clin. Endocrinol. Metab., The Endocrine Society 78, 693–698
4 Mao, Y., Tokudome, T. and Kishimoto, I. (2014) The cardiovascular action of hexarelin. J. Geriatr. Cardiol. 11, 253–258
5 Rahim, A., O’Neill, P. and Shalet, S. M. (1998) The effect of body composition on hexarelin-induced growth hormone release in normal elderly subjects. Clin. Endocrinol. (Oxf.), Wiley 49, 659–664
6 Zhao, Y., Zhang, X., Chen, J., Lin, C., Shao, R., Yan, C., et al. (2016) Hexarelin protects rodent pancreatic Β-cells function from cytotoxic effects of streptozotocin involving mitochondrial signalling pathways in vivo and in vitro. PLoS One, Public Library of Science (PLoS) 11, e0149730
7 Mosa, R., Huang, L., Wu, Y., Fung, C., Mallawakankanamalage, O., LeRoith, D., et al. (2017) Hexarelin, a growth hormone secretagogue, improves lipid metabolic aberrations in nonobese insulin-resistant male MKR mice. Endocrinology, Endocrinology 158, 3174–3187
8 Guan, C., Li, C., Shen, X., Yang, C., Liu, Z., Zhang, N., et al. (2023) Hexarelin alleviates apoptosis on ischemic acute kidney injury via MDM2/p53 pathway. Eur. J. Med. Res., Springer Science and Business Media LLC 28, 344
9 Rossoni, G., De Gennaro Colonna, V., Bernareggi, M., Polvani, G. L., Müller, E. E. and Berti, F. (1998) Protectant activity of hexarelin or growth hormone against postischemic ventricular dysfunction in hearts from aged rats. J. Cardiovasc. Pharmacol., Ovid Technologies (Wolters Kluwer Health) 32, 260–265
10 Zambelli, V., Rizzi, L., Delvecchio, P., Bresciani, E., Rezoagli, E., Molteni, L., et al. (2021) Hexarelin modulates lung mechanics, inflammation, and fibrosis in acute lung injury. Drug Target Insights, Aboutscience Srl 15, 26–33
Every lot undergoes five independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Every lot undergoes our 4-panel testing protocol: HPLC purity analysis, ESI-MS identity confirmation, LAL endotoxin screening, and amino acid analysis (for peptides >15 residues). Full analytical data is published in the Certificate of Analysis for each lot.
Lyophilized peptides should be stored at -20°C or below for long-term stability. Once reconstituted, peptides should be stored at 2–8°C and used within a reasonable timeframe depending on the specific compound. Avoid repeated freeze-thaw cycles. Always store in a dry environment away from direct light.
Orders placed before noon PST, Monday–Saturday, ship the same day. We offer free standard shipping on orders over $150. All orders are shipped in insulated packaging with ice packs when necessary. Standard delivery typically takes 2–4 business days within the continental US.
No. All compounds sold by Genesis Peptides are strictly for in vitro and preclinical laboratory research purposes only. They are not approved for human consumption, therapeutic use, or diagnostic purposes. By purchasing, you confirm the products will be used solely for legitimate research applications.
A Certificate of Analysis (COA) is a document issued by our analytical laboratory that reports the results of all quality control tests performed on a specific lot of product. Each COA includes HPLC chromatograms, mass spectra, endotoxin results, and amino acid analysis where applicable. COAs are available in our COA Library for every lot we have shipped.
Yes. We offer volume pricing for universities, research institutions, and laboratories with recurring needs. Discounts begin at 10+ units and scale with volume. Contact our team for a custom quote tailored to your research requirements.
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Hexarelin 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.
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.
