Hexarelin has never been approved anywhere and its clinical development did not progress. The human studies below measured hormone release and cardiac performance over minutes to weeks — not clinical outcomes over months.
The short answer
Hexarelin does two distinct things, and the second is more interesting than the first. It is a potent growth hormone secretagogue — subcutaneous dosing raises 24-hour GH secretion by increasing the mass of each secretory burst (Maccario et al., Eur J Endocrinol 2002). Separately, and independently of GH, it acts directly on the heart: a single intravenous dose raised left ventricular ejection fraction, cardiac index and cardiac output in patients with coronary artery disease undergoing bypass surgery, while growth hormone itself did nothing (Broglio et al., Eur J Pharmacol 2002). Set against both: the GH response measurably declines over weeks of repeated dosing.
What it does to growth hormone
The most detailed human characterisation gave six healthy young men hexarelin 1.5 µg/kg subcutaneously, either two or three times in a day, with blood sampled every 20 minutes across 24 hours (Maccario 2002).
- Both schedules raised mean 24-hour GH concentrations to the same degree.
- The mechanism was larger secretory bursts, not more of them — burst mass increased, burst frequency did not.
- Over the same 24 hours, IGF-1, prolactin, ACTH and cortisol did not change.
That third bullet is the finding usually left out of hexarelin's reputation as a "dirty" secretagogue. Across a full day of subcutaneous dosing, basal lactotroph and corticotroph secretion were untouched. The hormonal spillover associated with this peptide family appears at large acute intravenous stimulation doses rather than at the doses and route studied here.
The cardiac finding, and why it is unusual
Growth hormone releasing peptides turned out to bind something in the heart that is not the ghrelin receptor. Labelling rat cardiac membranes with a photoactivatable hexarelin derivative and isolating the target identified an 84 kDa binding protein whose N-terminal sequence was identical to rat CD36 — a glycoprotein expressed in cardiomyocytes and microvascular endothelial cells. Hexarelin raised coronary perfusion pressure in perfused hearts dose-dependently, and that effect was absent in hearts from CD36-null mice and from spontaneously hypertensive rats genetically deficient in CD36 (Bodart et al., Circ Res 2002). Knocking out the receptor abolished the effect — about as clean a mechanistic demonstration as this literature offers.
The human counterpart is a small but well-designed study. Twenty-four men with coronary artery disease undergoing bypass surgery received hexarelin 2 µg/kg intravenously, GHRH, recombinant human GH, or placebo under general anaesthesia, with cardiac performance measured by transoesophageal echocardiography and arterial catheterisation. Recombinant GH, GHRH and placebo produced no haemodynamic effect at all. Hexarelin produced a prompt rise in ejection fraction, cardiac index and cardiac output within 10 minutes, lasting up to 90 minutes, with reduced wedge pressure and no change in heart rate or systemic vascular resistance index (Broglio 2002).
An earlier study found the same inotropic effect in seven healthy adults and seven people with severe GH deficiency — who release essentially no GH in response — but not in twelve patients with severe dilated cardiomyopathy (Broglio et al., Endocrine 2001). The GH-deficient result is the key one: the cardiac effect happened without a GH rise, so it is not GH acting downstream.
None of this makes hexarelin a cardiac therapy. These are acute studies of minutes to hours, in small groups, with no outcome endpoints and no follow-up programme. It is a mechanism with a clear demonstration behind it and no clinical development on top of it.
The catch — the response fades
Hexarelin is also the compound where attenuation of the GH response was measured most explicitly. Twelve healthy elderly volunteers received twice-daily subcutaneous hexarelin for 16 weeks, with the GH area under the curve measured at intervals. It fell from 19.1 µg/L/h at baseline to 13.1 at week 1, 12.3 at week 4 and 10.5 at week 16 — a significant decline overall (p = 0.0003). Four weeks after stopping, it had returned to 19.4, statistically indistinguishable from baseline (Rahim & Shalet, Growth Horm IGF Res 1998).
The authors' conclusion — that attenuation is "partial and reversible" — is the fairest summary. Roughly half the response is lost over four months, and it comes back after a month off. That is the empirical basis for cycling this class of compound, and hexarelin is the peptide where the numbers exist.
A single-day study captured a sharper version of the same phenomenon: after two or three subcutaneous doses, an intravenous hexarelin challenge produced a blunted GH response and an abolished ACTH and cortisol response, while prolactin was unaffected (Maccario 2002).
How it compares to related peptides
GHRP-6 — the parent hexapeptide. Hexarelin is a more potent analogue of it.
GHRP-2 — better documented in humans overall, with a diagnostic role and a 30-day dosing study, but no comparable cardiac literature.
Ipamorelin — chosen for selectivity rather than potency; no CD36 story, and no equivalent long-duration desensitisation data.
Hexarelin is prohibited in sport at all times under WADA section S2; it is metabolised extensively and both parent compound and metabolites are targeted in anti-doping urine assays (Semenistaya et al., Drug Test Anal 2015).
See also hexarelin side effects and dosing education.
Sport & Anti-Doping Warning
Hexarelin is another potent GHRP-family peptide that anti-doping laboratories monitor; it appears in WADA-target lists and in research focused on detecting GH secretagogue misuse.
Although less well-known than GHRP-2 or GHRP-6 in the media, hexarelin is handled the same way under anti-doping rules and remains prohibited.