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Hexarelin: What the Research Shows on Potency, Desensitisation and the Heart

Hexarelin is a synthetic six-residue growth hormone secretagogue that acts on the ghrelin receptor. In human endocrine studies it released growth hormone (GH) in a dose-dependent way, with cortisol and prolactin rising at higher doses. In a 16-week study the GH response fell by roughly 45% and recovered four weeks after stopping. It also binds CD36 in heart tissue, where the animal data are mixed. It was never marketed and is research material only.

These are endocrine and animal results, not outcome claims. The 16-week study found no significant change in IGF-I, body composition or bone density, and the heart work is in rats, isolated hearts and one short human study. Research context only; nothing here is medical or dosing guidance.

At a glance

Hexarelin Class Growth hormone secretagogue, a GHRP-family hexapeptide; also called examorelin Sequence His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH 2 (about 887 Da) Targets Ghrelin receptor (GHS-R1a); CD36 in heart tissue (animal data) Development Reached Phase II for growth hormone deficiency and congestive heart failure; never marketed Status in sport On the WADA Prohibited List

What it is

Hexarelin belongs to the growth hormone-releasing peptide (GHRP) family, whose members release GH through the ghrelin receptor, a G protein-coupled receptor originally cloned from pituitary tissue (Bodart et al., 2002). Two D-amino acids in the sequence, D-2-methyltryptophan and D-phenylalanine, are what separate it from the natural residues. For where it sits among related compounds see the hexarelin research guide and the growth hormone secretagogue hub.

The human endocrine studies

Most of what is known in people comes from short endocrine challenge studies in healthy adults, not from treatment trials.

Dose-response (Massoud et al., 1996, JCEM ). Hexarelin released GH, prolactin and cortisol in a dose-dependent way. Cortisol rose by about 40% at the higher doses tested. At a low dose combined with GHRH it produced what the authors called massive GH release with no rise in cortisol, which is the synergy the secretagogue literature is built on.

Repeated administration (Massoud et al., 1996, Clin Endocrinol ). In six healthy men, a second hexarelin bolus given 120 minutes after the first produced a lower GH peak. The synergy with GHRH was lost on repeated administration.

Two points limit what this shows. The studies measure a hormone pulse over hours, and the subjects were healthy adults rather than people with a condition. A large pulse is a pharmacology result, not evidence of any downstream effect.

Desensitisation over 16 weeks

The longest human study is Rahim and colleagues’ 16-week trial in 12 healthy older adults ( JCEM , 1998; Growth Hormone & IGF Research , 1998). The GH response to a hexarelin challenge fell steadily over the course of repeated administration:

Study week Week 0 Week 1 Week 4 Week 16 Week 20 GH area under the curve (µg/L·h) 19.1 13.1 12.3 10.5 19.4

Four weeks after the last administration the response had returned to baseline, so the authors described the attenuation as partial and reversible . Over the same 16 weeks, serum IGF-I, IGF-binding protein-3, total body fat, lean body mass and bone mineral density did not change significantly, and the authors concluded that, in this study, the biological impact on the GH–IGF-I axis seemed minimal.

The CD36 heart research

Hexarelin has also been studied at a second, cardiac target. The evidence is a mixture of findings that do not all point the same way:

Protection in rats (Locatelli et al., 1999). In hypophysectomised rats, which cannot make GH, seven days of hexarelin prevented the added damage that ischaemia and reperfusion caused in explanted hearts. A second GHRP that does not bind the heart was ineffective, so the authors proposed specific cardiac receptors rather than GH.

The receptor is CD36 (Bodart et al., 2002). A cardiac binding protein for hexarelin was identified as CD36. In perfused hearts, hexarelin raised coronary perfusion pressure in a dose-dependent way, an effect absent in CD36-null mice; the authors suggest CD36 may mediate coronary vasospasm.

A short human study (Bisi et al., 1999). In 7 adults with GH deficiency and 9 controls, acute hexarelin produced a short-lasting increase in left ventricular ejection fraction, probably independent of GH.

A 2014 review of the cardiovascular action of hexarelin (Mao et al., J Geriatr Cardiol ) gathers the animal work. The honest summary is that the direction of the cardiac effect depends on the model, and that no treatment trial supports a heart claim.

Where claims outrun the evidence

Potency is not outcome. The strongest figure in the literature is an acute GH pulse, and the 16-week study found no significant change in IGF-I, body composition or bone density.

“Cardioprotective” is an animal-model label. The same receptor raised coronary perfusion pressure in isolated hearts.

Endocrine side signals are documented. Cortisol and prolactin rise with dose. A 2026 endocrinology review of GH–IGF-1 axis compounds sold as research chemicals, hexarelin among them, lists prolactin and cortisol elevations among the reported adverse effects and notes that the class has no regulatory approval for physique or performance uses (Dominikowski et al., 2026).

No regulatory approval. Hexarelin never completed development as a medicine.

Identity is harder than it looks. A mass spectrum confirms composition but not stereochemistry, and hexarelin contains two D-amino acids. Documentation that shows only a matching mass (about 887 Da) does not by itself distinguish the intended molecule from its stereoisomers. See how to read a certificate of analysis.

Research takeaway

Hexarelin is a ghrelin-receptor agonist that releases GH potently and dose-dependently, with cortisol and prolactin rising at higher doses.

The GH response attenuated by roughly 45% over 16 weeks and recovered after four weeks off, without measurable change in IGF-I, body composition or bone density.

The heart data are animal-model findings plus one short human study, and they are not uniformly favourable.

It was never marketed, and it is sold as laboratory research material only.

Primary sources

Journal of Clinical Endocrinology & Metabolism — Hexarelin-induced growth hormone, cortisol, and prolactin release: a dose-response study (Massoud et al., 1996)

Clinical Endocrinology — The effect of repeated administration of hexarelin and growth hormone releasing hormone on growth hormone responsivity (Massoud et al., 1996)

Journal of Clinical Endocrinology & Metabolism — Growth hormone status during long-term hexarelin therapy (Rahim et al., 1998)

Growth Hormone & IGF Research — Does desensitization to hexarelin occur? (Rahim & Shalet, 1998)

Endocrinology — Growth hormone-independent cardioprotective effects of hexarelin in the rat (Locatelli et al., 1999)

Circulation Research — CD36 mediates the cardiovascular action of growth hormone-releasing peptides in the heart (Bodart et al., 2002)

European Journal of Pharmacology — Cardiac effects of hexarelin in hypopituitary adults (Bisi et al., 1999)

Journal of Geriatric Cardiology — The cardiovascular action of hexarelin (Mao et al., 2014)

Frontiers in Endocrinology — The emerging landscape of performance-enhancing peptides modulating the GH-IGF1 axis (Dominikowski et al., 2026)

Background

Wikipedia — Examorelin (hexarelin): development history, including Phase II and no marketing

World Anti-Doping Agency — Prohibited List (class S2: peptide hormones, growth factors, related substances and mimetics)

Hexarelin as laboratory research material

New-U lists hexarelin as laboratory research material. The studies above describe published endocrine and animal work, not this material. Research use only – all claims made on this site are for testing and research use only.

Frequently asked questions

What is hexarelin?

Hexarelin, also called examorelin, is a synthetic hexapeptide growth hormone secretagogue. It acts on the ghrelin receptor to release growth hormone, and it also binds CD36 in heart tissue. It is research material, not an approved medicine.

Is hexarelin approved?

No. It reached Phase II trials for growth hormone deficiency and congestive heart failure but was never marketed. It has no marketing authorisation as a medicine and is on the WADA Prohibited List.

Does hexarelin lose effect over time?

In a 16-week study in 12 healthy older adults, the growth hormone response to hexarelin fell from 19.1 to 10.5 µg/L·h and returned to 19.4 four weeks after stopping. The authors called the attenuation partial and reversible.

Does hexarelin raise cortisol and prolactin?

In healthy men it raised both in a dose-dependent way, with cortisol up by about 40% at the higher doses tested. At a low dose combined with GHRH, growth hormone release was large and cortisol did not rise.

What is the CD36 heart research?

Hexarelin binds CD36 in rat heart tissue. It protected explanted hearts from ischaemia and reperfusion damage in rats, yet also raised coronary perfusion pressure in isolated hearts. The findings are animal-model results and are not uniformly favourable.

External links are provided for research reference only; New-U is not affiliated with the cited organisations or authors. All figures are published study results shown for research context, not dosing guidance. New-U Research Compounds supplies research compounds strictly for laboratory research use only — not for human consumption .

Part of the Growth hormone secretagogue research research area — explore related compounds, guides and sources.

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Research peptides at >99% HPLC-verified purity, third-party tested by Janoshik Analytical & Freedom Diagnostics, with Certificates of Analysis published per released batch. Supplied strictly for laboratory research use.

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