Hexarelin was made to trigger growth hormone release. In animal hearts it kept doing things after that release was switched off, which is why it now has a second research identity.
Hexarelin · Growth hormone secretagogue
The pituitary releases growth hormone when it receives one of two signals: the hormone GHRH, or a trigger at the ghrelin receptor — the same receptor the “hunger hormone” ghrelin uses. Hexarelin is a synthetic trigger of the second kind. Researchers study it for that, and for a separate finding: it binds a receptor on heart and blood-vessel cells called CD36. Human data are 1990s hormone-release studies and one acute heart-function measurement during surgery; longer-term heart work is in animals.
Hexarelin is a synthetic six-amino-acid peptide from the growth hormone-releasing peptide (GHRP) family, first described in 1994 as a potent releaser of growth hormone in rats (Deghenghi et al., 1994). Like ipamorelin it acts at the growth hormone secretagogue receptor (the ghrelin receptor, GHS-R1a), a receptor on pituitary cells that, when activated, prompts growth hormone release.
CD36 is a different protein altogether: a scavenger receptor on the surface of many cells, including heart muscle and blood-vessel lining, that binds fatty acids and oxidised lipids. In 2002 hexarelin was shown to bind CD36 in rat heart membranes, and its effect on coronary blood flow in isolated hearts disappeared in animals lacking CD36 (Bodart et al., 2002). That is what gives hexarelin a second research target independent of growth hormone.
Human studies in the 1990s, largely from Turin, characterised the growth hormone response to hexarelin by intravenous, subcutaneous, intranasal and oral routes in healthy adults (Ghigo et al., 1994). Unlike ipamorelin, hexarelin also raised cortisol and prolactin in those studies. Repeated dosing was examined too: in a 16-week study of healthy adults, the growth hormone response to hexarelin declined over time and recovered after a washout, while IGF-1 rose only modestly (Rahim et al., 1998). These are pharmacology studies measuring hormone levels, not clinical-outcome trials.
Human cardiac data are acute and physiological. In 24 men with coronary artery disease undergoing bypass surgery under anaesthesia, a single intravenous dose of hexarelin raised left-ventricular ejection fraction, cardiac index and cardiac output within minutes and for up to 90 minutes, whereas GHRH, growth hormone and placebo did not (Broglio et al., 2002). That is a short-term measurement of heart performance, not a trial of a clinical outcome. Longer-term findings, such as protection of heart muscle cells after experimentally induced ischaemia–reperfusion injury, come from rats (Huang et al., 2017).
The desensitisation seen with repeated dosing means single-dose hormone responses cannot be assumed to persist. Cortisol and prolactin release limit how “selective” the compound can be called, and that selectivity was defined in specific study conditions. The CD36 findings come from animal tissue and the human cardiac data are acute haemodynamic measurements; neither establishes a cardiac benefit in people over time. Hexarelin has no regulatory approval and is prohibited in sport under WADA category S2 as a growth hormone secretagogue.
Hexarelin is not an approved medicine in Australia, and no approval elsewhere was identified. Growth hormone secretagogues are prohibited at all times in sport under WADA category S2.
Sources and status checked 2026-09-23
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