Hexarelin Research

Hexarelin is a synthetic hexapeptide from the growth hormone releasing peptide series, sequence His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2 ^[1]. It differs from GHRP-6 by one methyl group on the D-tryptophan residue ^[1]. PubChem lists CID 6918297, CAS 140703-51-1, C47H58N12O6 and molecular weight 887.0 ^[1]. Hexarelin

Hexarelin has no registered interventional trials, and ranking it by that number is a mistake ^[2]. Roughly fourteen human studies exist, including 16 weeks in older adults, six months in children, sleep architecture work and two cardiac studies ^{[3][4][5][13][15]}. Almost all of it predates mandatory registration, so the accurate phrasing is no registered interventional trials ^[2].

Two receptors, not one

Hexarelin acts at the growth hormone secretagogue receptor GHS-R1a, cloned from pituitary and hypothalamus as the target of this class (in vitro) ^[6]. Its endogenous ligand ghrelin was identified later (animal) ^[7].

Hexarelin also binds CD36, a scavenger receptor genuinely separate from GHS-R1a. Radiolabeled hexarelin bound an 84 kDa protein in rat cardiac membranes matching CD36, and in perfused hearts the result was coronary vasoconstriction (animal) ^[8]. The effect was absent in CD36-null mice, and the authors tied it to atherosclerotic vasospasm ^[8]. Promotional material cites CD36 for cardioprotection while omitting that result. Cholesterol efflux and adipocyte mitochondrial findings downstream of CD36 are cell culture and rodent work (in vitro and animal) ^[9]. No CD36-mediated metabolic effect of hexarelin has been measured in a human ^[9].

What has been measured in humans

A double-blind placebo-controlled rising-dose study in 12 adult men found dose-dependent GH release peaking near 30 minutes (human) ^[10]. The roughly 55 minute figure quoted from that paper is the decay of the GH response, not a plasma half-life ^[10]. No human plasma half-life for hexarelin was located.

Hexarelin is not selective for growth hormone: in six healthy young adults it raised prolactin, ACTH and cortisol alongside GH (human) ^[11]. Its corticotropic activity was similar to human CRH, and the investigators concluded it is not fully specific ^[11]. A separate study found the GH response roughly halves from young adulthood to old age, while prolactin and cortisol responses do not vary with age (human) ^[12]. The off-target effects hold constant as the on-target effect fades.

Across 16 weeks in healthy elderly subjects, cortisol AUC fell rather than rose (human) ^[4]. Whether the replicated acute rise accumulates over months is unresolved, and the one long study that looked found it did not ^[4]. In seven volunteers dosed at night, stage 4 sleep fell during the first half and EEG delta power fell across the whole night (human) ^[13]. GH and prolactin rose across the whole night, while ACTH and cortisol rose during the first half ^[13]. That is the reverse of the common marketing claim.

Desensitization on repeated dosing

This is real and under-reported. Across 16 weeks in 12 healthy elderly subjects, GH AUC fell from 19.1 to 10.5 µg/L per hour, most of it in the first week (human) ^[3]. The response returned to baseline four weeks after stopping ^[3]. In seven prepubertal short children, the GH response to an intravenous bolus fell roughly 77% by the end of treatment (human) ^[5]. Growth velocity rose over the same uncontrolled period, so a lost provoked GH response is not a lost biological effect ^[5].

The picture is schedule dependent rather than settled. Two intermittent-exposure arms of one small uncontrolled study in elderly subjects found the response maintained over 8 and 15 days (human) ^[14]. Those arms were tiny and far shorter than the studies finding attenuation ^[14].

Cardiac effects, human and rat

Acute inotropy has human data: in 24 men with coronary artery disease under anesthesia, intravenous hexarelin raised ejection fraction, cardiac index and cardiac output within 10 minutes (human) ^[15]. Recombinant GH, GHRH and placebo produced no hemodynamic effect, so circulating GH does not explain it, and mean arterial pressure also rose ^[15].

The null belongs beside it: hexarelin raised ejection fraction in five patients with ischemic cardiomyopathy but not in eight with dilated cardiomyopathy (human) ^[16]. Cardioprotection, anti-remodeling and plaque suppression are rat findings only, and no human study has tested repeated dosing for a cardiac endpoint (animal) ^[17]. The CD36 vasoconstriction above is ex vivo rat ^[8]. An acute ejection fraction change under anesthesia is not evidence of therapeutic benefit.

Regulatory and evidentiary standing

Tesamorelin holds an FDA approval granted in November 2010, for reduction of excess abdominal fat in HIV-associated lipodystrophy ^[18]. It never obtained a European marketing authorization, because the applicant, Ferrer Internacional, withdrew that application under CHMP review ^[19]. No refusal decision was ever issued ^[19].

The approval belongs to the molecule tesamorelin and to one indication. It is not a family credential and must never be written as one. Tesamorelin acts at the GHRH receptor ^[18] and hexarelin does not ^[6]. The honest contrast is not that tesamorelin works and the others might too. It is that tesamorelin has been through the process that would let anyone know, and hexarelin has not.

One further read-across should be blocked, although it does not involve hexarelin's receptor. Tesamorelin's mean elimination half-life is formulation-specific, 8 minutes and 11 minutes, and it is given daily ^[18]. CJC-1295 with DAC, at the same receptor, has an estimated half-life of 5.8 to 8.1 days ^[20], with trough GH raised 7.5-fold ^[21]. GHRH analogue names a receptor target, not a duration of action.

GHRP-2 is sometimes described as approved in Japan. That report concerns a diagnostic agent for pituitary function testing, is unverified against any primary regulatory database, and is not a therapeutic approval ^[22]. It is not comparable to tesamorelin's. Hexarelin holds no approval anywhere identified here, and is prohibited at all times as examorelin under Section S2 of the WADA Prohibited List ^[23].

The IGF-1 and cancer literature is often attached to this whole family, and it should not be. Those odds ratios come from lifelong endogenous IGF-1 levels in cohort studies, not administered peptides ^[24]. They apply only where a compound has been shown to raise IGF-1 in people. Hexarelin's record is thin: IGF-1 was unchanged by one route and marginally raised by another in one small uncontrolled study with two short arms ^[14].

Limitations

Almost every human hexarelin study is small, uncontrolled and acute, and none reports a body composition, lean mass, fat loss or performance endpoint ^[3][5]. At GH exposures higher than any secretagogue produces, lean mass rose about 2.1 kg with no gain in strength or exercise capacity (human) ^[25]. Much of the favorable literature comes from a few groups, including the CD36 laboratory that holds related intellectual property ^[8]. Clinical development was abandoned rather than completed ^[2]. Hexarelin is supplied for laboratory research use only and is not for human consumption.

Frequently Asked Questions

Does hexarelin have human data, given that it has no registered trials? Yes, although hexarelin has no registered interventional trials: roughly fourteen published human studies exist, almost all predating mandatory registration ^[2]. These include 16 weeks in older adults, six months in children, sleep architecture work and two cardiac studies ^{[3][5][13][15][16]}.

Is hexarelin the same molecule as GHRP-6? No, hexarelin carries one extra methyl group on the D-tryptophan residue, giving C47H58N12O6 and molecular weight 887.0 ^[1]. Findings on one should not be transferred to the other, and the CD36 work described here was done with hexarelin (animal) ^[8].

Is the CD36 activity supported by human evidence? No, CD36 binding was identified in rat cardiac membranes, and the functional result there was coronary vasoconstriction (animal) ^[8]. The cholesterol efflux and adipocyte findings downstream of it are cell culture and rodent work (in vitro and animal) ^[9]. No CD36-mediated metabolic effect of hexarelin has been measured in a human ^[9].

References

1. 1

   PubChem Compound CID 6918297 (examorelin), CAS 140703-51-1, C47H58N12O6, MW 887.0. NIH/NLM, queried 27 August 2026. GHRP-6 comparison: CID 9919153, CAS 87616-84-0, C46H56N12O6, MW 873.0.
2. 2

   ClinicalTrials.gov v2 API, queries for hexarelin under query.intr and query.term, re-run 27 August 2026. Registry observation, not a publication.
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