What dose of hexarelin was used in human studies?

The longest human trial used 1.5 mcg/kg of body weight, injected subcutaneously twice daily, for 16 weeks. For a 80 kg person that is about 120 mcg per injection. Acute diagnostic and dose-response work in humans generally used 1 to 2 mcg/kg intravenously. Doses above roughly 2 mcg/kg do not produce proportionally larger growth hormone pulses, because the somatotroph response saturates. Nothing about this constitutes a protocol: hexarelin has never been approved by any regulator, and no dosing regimen has been validated for any outcome a person would actually want.

Does hexarelin stop working over time?

Partially, and the loss reverses. In the 16-week trial the area under the growth hormone curve fell from 19.1 to 13.1 mcg/L per hour after a single week, then drifted only slightly further to 12.3 at week 4 and 10.5 at week 16. Four weeks after stopping, it was back to 19.4, statistically indistinguishable from baseline. So the drop is real, front-loaded into the first week, roughly 45 percent at its worst, and fully reversible. That is a different picture from the 50 to 80 percent collapse within 2 to 4 weeks that vendor pages describe.

Did hexarelin change body composition in humans?

No. The same 16-week study measured total body fat, lean body mass and bone mineral density by scan, and none of them changed significantly (P values of 0.6, 0.3 and 0.3). Serum IGF-1 and IGFBP-3 also did not move over the full 20-week observation period. This is the single most important result on hexarelin and it is almost never cited, because it is the study that looked hardest for a physique effect and did not find one.

Does hexarelin raise cortisol and prolactin?

It depends on how it is given. Single boluses of GHRPs acutely raise ACTH, cortisol and prolactin, and repeated nighttime dosing at 4 x 50 mcg raised ACTH and cortisol in the first half of the night. But over 16 weeks of twice-daily dosing at 1.5 mcg/kg, prolactin AUC did not change at all, ACTH AUC did not change, 24-hour urinary free cortisol did not change, and cortisol AUC actually fell slightly before returning to baseline after stopping. The blanket claim that chronic hexarelin causes hypercortisolaemia was tested directly and did not hold.

Does hexarelin help you sleep?

The opposite, in the one study that measured it. Seven healthy volunteers given 4 x 50 mcg hexarelin across the evening showed a significant reduction in stage 4 sleep during the first half of the night and reduced EEG delta power across the whole night. Growth hormone and prolactin rose, and so did ACTH and cortisol early in the night. Since the standard pitch for GH peptides is to dose before bed and amplify the nocturnal growth hormone pulse, this is worth knowing: hexarelin raised the hormone and degraded the sleep.

How does hexarelin compare to ipamorelin?

Hexarelin is the more powerful growth hormone releaser and the more promiscuous one. Ipamorelin is selective for the GHS-R1a receptor and does not meaningfully move ACTH, cortisol or prolactin on acute dosing. Hexarelin binds GHS-R1a with high affinity and also binds CD36 in cardiac tissue, which is the basis of its separate cardiovascular literature. If the goal is a clean GH pulse, ipamorelin is the better-characterised choice. If the interest is the cardiac work, that literature only exists for hexarelin.

Hexarelin is not an FDA-approved drug and is not an approved medicine in any major market. It is sold only as a research chemical, which means it is not legal to sell for human consumption and carries no manufacturing, purity or sterility guarantee. Growth hormone secretagogues, hexarelin included, are prohibited at all times under section S2 of the WADA Prohibited List, so any tested athlete using it is doping regardless of intent.

Is hexarelin the same as GHRP-6?

No, but they are close relatives. Both are hexapeptides in the GHRP family and both act on the same receptor. Hexarelin differs from GHRP-6 by a methyl group on the second residue, which raises potency and metabolic stability. Practically, hexarelin releases more growth hormone per microgram and GHRP-6 produces a stronger hunger response. Neither has been approved for any indication.

Hexarelin: What 16 Weeks of Human Dosing Actually Showed

Hexarelin is unusual among research peptides in that somebody actually ran the long study. Twelve healthy older adults took it subcutaneously twice a day for sixteen weeks while researchers measured growth hormone response, IGF-1, bone turnover markers, body fat, lean mass and bone density. Almost every page selling hexarelin cites its potency as a growth hormone releaser. Almost none of them mention what the sixteen-week trial found when it weighed and scanned the participants at the end.

This guide is built on that trial and the handful of others like it, not on vendor copy. Where the published human data contradict what is commonly repeated about hexarelin, the data are quoted directly.

What hexarelin is

Hexarelin is a synthetic hexapeptide, His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2, developed in the 1990s as part of a family of growth hormone-releasing peptides that began with GHRP-6. It is structurally GHRP-6 with a methyl group added to the second residue, a change that increases potency and slows enzymatic breakdown.

These compounds were not designed from a known hormone. They were found by function first and explained later, in what Roy Smith later described as reverse pharmacology: build molecules that increase growth hormone pulse amplitude, then work backwards to find the receptor, then find the natural ligand. That process eventually produced the GHS receptor, the oral non-peptide secretagogue MK-677, and finally ghrelin, the endogenous hormone the whole class had been imitating without anyone knowing.

Hexarelin has never been approved as a medicine anywhere. It reached human trials, produced interesting endocrine data, and stopped. It is now sold exclusively as a research chemical. See growth hormone peptides for how it fits alongside sermorelin, ipamorelin and CJC-1295.

How hexarelin works: two receptors, not one

The growth hormone effect runs through GHS-R1a, the ghrelin receptor, in the pituitary and hypothalamus. GHRPs work through several mechanisms at once. They increase GHRH release, amplify GHRH signalling at the somatotroph, reduce somatostatin release, and antagonise somatostatin signalling. Behaving as a functional somatostatin antagonist is what allows hexarelin to work in states where GHRH alone fails.

The second receptor is CD36, and this is where hexarelin diverges from the rest of the class. Work published in Circulation Research in 2002 identified CD36 as the hexarelin binding protein in cardiac membranes, expressed in cardiomyocytes and microvascular endothelial cells. In perfused hearts, hexarelin raised coronary perfusion pressure in a dose-dependent way. In hearts from CD36-null mice and from spontaneously hypertensive rats genetically deficient in CD36, the effect was absent.

Binding studies using a radiolabelled hexarelin analogue found the highest density in human ventricles, then atria, aorta, coronaries, carotid, endocardium and vena cava. That binding was displaced by hexarelin, GHRP-6, GHRP-1 and GHRP-2, but not by MK-677. In other words the cardiac site recognises peptide GHRPs specifically and ignores the non-peptide secretagogue, which is strong evidence it is a distinct receptor from GHS-R1a rather than the same one in a different tissue. The practical consequence: hexarelin has cardiovascular actions that are independent of growth hormone release, and MK-677 does not share them.

What doses were actually used in humans

Three numbers cover most of the human literature.

1 to 2 mcg/kg intravenously for acute testing and dose-response work. Above roughly 2 mcg/kg the somatotroph response saturates, so larger doses buy little extra growth hormone.
1.5 mcg/kg subcutaneously, twice daily in the only long-term trial. That is roughly 120 mcg per injection for an 80 kg adult, or 240 mcg per day.
4 x 50 mcg fixed doses across the evening in the sleep study, which is closest to how the compound is discussed in fitness contexts.

Note how small these are. Milligram-per-vial quantities sold online represent many multiples of any dose that has ever been given to a person in a controlled setting, which makes accurate reconstitution and measurement the practical bottleneck rather than supply. The peptide calculator covers the arithmetic.

None of this is a recommendation. It is a description of published exposures, offered because the alternative on most sites is an invented protocol with no citation behind it at all.

The desensitization question, answered properly

Vendor pages generally say the growth hormone response to hexarelin drops 50 to 80 percent within two to four weeks, and prescribe 6 to 8 weeks on with 4 to 8 weeks off to manage it. The actual measurements look different.

In the 16-week study, the mean area under the growth hormone curve was 19.1 mcg/L per hour at baseline. After one week it was 13.1. At week 4, 12.3. At week 16, 10.5. Four weeks after the last injection, it was 19.4, no longer significantly different from where it started.

Three things follow. The decline is real and statistically robust. It is front-loaded: nearly all of it happens in the first week, and the following fifteen weeks add only a small further drift. And it reverses completely within a month of stopping. A 45 percent partial attenuation that plateaus early and washes out is a materially different phenomenon from a receptor that burns out and needs eight weeks to recover.

Shorter intermittent dosing did not produce measurable desensitization at all. An eight-day course of intranasal hexarelin at 1.25 mg three times daily, and a fifteen-day course of oral hexarelin at 20 mg three times daily, both left the acute growth hormone response intact in elderly subjects.

What 16 weeks did to body composition: nothing measurable

This is the finding that should anchor any honest hexarelin page, and it is the one that is systematically omitted.

The same trial that tracked the growth hormone response also tracked outcomes. Over 20 weeks, serum IGF-1 did not change significantly. IGFBP-3 did not change significantly. Of five markers of bone formation and resorption, only one, the C-terminal propeptide of type I collagen, moved at all. At week 16, total body fat had not changed significantly, lean body mass had not changed significantly, and bone mineral density had not changed significantly.

The authors concluded that the biological impact of this hexarelin schedule on the GH-IGF-1 axis appeared minimal. That is a careful way of saying the growth hormone pulses were real and the downstream consequences were not detectable.

There is an obvious caveat: this was 1.5 mcg/kg twice daily in healthy elderly people for sixteen weeks, not a higher dose in trained younger adults alongside heavy resistance training and a caloric surplus. Nobody has run that study. But the negative result is what exists, and a page that quotes the potency data while hiding the outcome data is selling rather than informing. The same asymmetry shows up across muscle-growth peptides and in the follistatin literature.

Cortisol and prolactin: the acute and chronic answers differ

GHRPs are not clean. As a class they raise prolactin, ACTH and cortisol alongside growth hormone, which is the standard argument for preferring ipamorelin. For hexarelin specifically, the acute and chronic pictures separate.

Acutely, boluses of GHRPs raise ACTH, cortisol and prolactin in humans, and repeated evening dosing at 50 mcg raised ACTH and cortisol through the first half of the night.

Chronically, a study designed specifically to test whether repeated hyperprolactinaemia and hypercortisolaemia occur found that they did not. Over 16 weeks at 1.5 mcg/kg twice daily, the prolactin AUC was 624 mU/L per hour at baseline and 641 at week 16, no significant change. ACTH AUC did not change. Cortisol-binding globulin did not change. Twenty-four hour urinary free cortisol did not change. Cortisol AUC fell from 1506 to 1222 nmol/L per hour by week 16, then rose to 1586 four weeks after stopping, back in line with baseline.

A decrease was not what anyone expected. The authors flagged it as contradicting the acute findings, noted it could not be explained by binding globulin changes, and judged it unlikely to be clinically meaningful given that urinary free cortisol was flat. The honest summary is that at that dose and schedule, adrenal and prolactin over-stimulation did not happen, and the mechanism behind the small drop is unresolved. See peptide side effects for how this compares across the class.

Hexarelin and sleep architecture

Growth hormone peptides are almost always pitched as pre-bed compounds, on the logic that the largest natural growth hormone pulse occurs during early deep sleep and the peptide amplifies it. One study put that logic on an EEG.

Seven healthy young volunteers received 50 mcg of hexarelin at 22:00, 23:00, midnight and 01:00, or placebo, with polysomnography and overnight hormone profiles. Growth hormone rose. Prolactin rose. ACTH and cortisol rose in the first half of the night. And stage 4 sleep in the first half of the night fell significantly, as did EEG delta power across the whole night. Leptin, TNF-alpha and soluble TNF receptors were unchanged, so there was no sign of an immune interaction.

The proposed explanation is that hexarelin shifts the balance between GHRH and CRH signalling toward CRH, and CRH degrades slow-wave sleep. It is worth contrasting this with the same group's observations that ghrelin itself promotes slow-wave sleep and GHRP-6 increases stage 2 non-REM sleep. Compounds that hit the same receptor do not have the same effect on sleep, and hexarelin sits at the unfavourable end.

One study, seven subjects, a dosing pattern chosen to probe the mechanism rather than to mimic real use. It is not the last word. It is also the only word, and it points the wrong way for a compound sold on the promise of better recovery.

Oral and intranasal routes: active, but inefficient

Hexarelin is orally and nasally active, which is genuinely unusual for a peptide. The relevant question is what it costs.

In elderly subjects, intranasal hexarelin at 1.25 mg per dose, roughly 18 mcg/kg, produced a growth hormone response that was not significantly greater than 1 mcg/kg of intravenous GHRH. Oral hexarelin at 20 mg per dose, roughly 300 mcg/kg, likewise did not significantly exceed intravenous GHRH.

Put the numbers side by side: about 1.5 mcg/kg subcutaneously produces a robust response, while 300 mcg/kg orally produces a response comparable to a modest GHRH injection. That is a two-order-of-magnitude penalty for swallowing it. Both routes did produce small significant increases in IGFBP-3, and in the oral arm a small rise in IGF-1, with no prolactin or cortisol change and no reported side effects. Oral hexarelin works. It is just an expensive way to do it.

Hexarelin versus the other secretagogues

Versus GHRP-6: same family, one methyl group apart. Hexarelin releases more growth hormone per microgram. GHRP-6 produces the stronger appetite response, which is either the point or the problem depending on the goal.

Versus ipamorelin: ipamorelin is the selective one. It activates GHS-R1a without meaningfully moving ACTH, cortisol or prolactin on acute dosing, which is why it displaced the older GHRPs in clinical practice. Hexarelin is more potent and less selective. Sermorelin versus ipamorelin covers the adjacent comparison.

Versus GHRH analogues: sermorelin, CJC-1295 and tesamorelin act on the GHRH receptor, a different target entirely. GHRPs and GHRH analogues are synergistic when combined, which is the entire rationale for the standard stacked protocols. Tesamorelin is the only one of the group with FDA approval, for HIV-associated lipodystrophy.

Versus MK-677: MK-677 is an orally active non-peptide secretagogue that hits GHS-R1a but does not bind the cardiac CD36 site. It raises IGF-1 durably in a way hexarelin did not in the 16-week trial, though it carries its own problems with appetite, water retention and insulin sensitivity.

Safety, legal status, and what is actually being sold

Hexarelin is not approved by the FDA or any comparable regulator, for any indication. There is no pharmaceutical-grade hexarelin product. Every vial available is a research chemical, sold with a not-for-human-consumption label, produced outside the manufacturing controls that apply to medicines. Purity, sterility and actual peptide content are unverified unless the buyer pays for independent testing, and mass-labelled contents are frequently wrong. Legal status of research peptides covers the regulatory position in more detail.

For competitive athletes: growth hormone secretagogues, including the GHRPs, are prohibited at all times under section S2 of the WADA Prohibited List. There is no in-competition-only carve-out and no therapeutic use exemption pathway for a compound with no approved therapeutic use. See peptides versus steroids for the broader anti-doping context.

Within the published human studies, tolerability was unremarkable. No side effects were reported in the intranasal and oral courses. The 16-week subcutaneous study found no adrenal or prolactin over-stimulation and no adverse change in bone density. The class-wide caution about GH secretagogues, that raising growth hormone and IGF-1 has implications for insulin sensitivity and for anyone with an active or suspected malignancy, still applies and is not addressed by any of these trials. Nobody has studied hexarelin for years of continuous use, in younger adults, or at the doses commonly discussed online.

The bottom line

Hexarelin is a genuinely potent growth hormone releaser with a real receptor story, a distinct cardiac binding site the rest of the class does not share, and more human data behind it than most research peptides will ever accumulate. It is also the compound where somebody ran the long study, measured the outcomes people care about, and found nothing.

Anyone weighing hexarelin should sit with that. The hormone response is not in question. The consequences of the hormone response, over sixteen weeks at the dose tested, were not measurable in fat, lean mass, bone density or IGF-1. Add a documented reduction in deep sleep at evening dosing, no approved product, and no supply chain accountability, and the case for it rests almost entirely on the potency figure rather than on any outcome.