Hexarelin: what it is, the research, dosage and side effects

Hexarelin is a synthetic hexapeptide from the same family as GHRP-6, to which it is structurally very close, and GHRP-2. It was developed in the early 1990s and studied extensively by endocrinologists at the University of Turin, whose 1994 paper showed that it released GH in healthy volunteers by intravenous, subcutaneous, nasal and oral routes ^[1].

Like other GHRPs, hexarelin mimics ghrelin at the growth hormone secretagogue receptor. It differs from ipamorelin, a later and more selective member of the family, in that it also stimulates ACTH, cortisol and prolactin.

Its sequence is His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2 ^[28]. The name hexarelin acetate describes the same hexarelin peptide as an acetate salt; the salt form does not make it a different compound, and the human studies described here refer to it simply as hexarelin. What hexarelin is used for today is research only. It was never approved as a medicine, but it was studied as a diagnostic test for GH deficiency ^[33], as a growth treatment in short children ^[11], and, most extensively in recent years, for its effects on the heart.

Hexarelin binds the GHS-R1a (ghrelin) receptor on the pituitary and hypothalamus and triggers GH release. In young men, the maximally effective dose of hexarelin released more GH than the maximally effective dose of GHRH, and giving the two together amplified the response further ^[2]. The GH response was clearly smaller in men aged 65 to 84 than in young men ^[2].

Hexarelin also appears to have effects on the heart that do not depend on GH. In patients undergoing heart bypass surgery, it improved cardiac performance, while GHRH and recombinant GH given for comparison did not, suggesting a direct action on receptors in heart or blood-vessel tissue ^[3].

That second receptor was later identified. Using a light-activated form of hexarelin to tag its binding partner in rat heart membranes, Canadian researchers found it was CD36, a scavenger receptor on heart muscle and small-vessel cells. In perfused hearts, hexarelin raised coronary perfusion pressure through CD36, and the effect was absent in hearts from mice lacking CD36 ^[22]. Hexarelin therefore acts on two receptors: the ghrelin receptor for GH release and CD36 in the heart.

Its GH effect still depends on the GHRH system. In four men with an inherited defect of the GHRH receptor, 2 µg/kg of hexarelin produced no rise in GH at all, while prolactin, ACTH and cortisol rose normally ^[30]. And although hexarelin is potent, ghrelin itself is stronger: at the same 1 µg/kg intravenous dose in young men, ghrelin released more GH than hexarelin, which in turn released more than GHRH ^[29].

In healthy young volunteers, hexarelin produced dose-dependent GH release. An intravenous dose of 1 µg/kg released about twice as much GH as the same dose of GHRH. Bioavailability relative to intravenous dosing was about 77% under the skin, 5% by nasal spray and 0.3% by mouth ^[1].

Repeated dosing blunts the response. In a Manchester study, 12 healthy older adults injected hexarelin twice daily for 16 weeks. The GH response fell significantly by week 4 and was about 45% lower than baseline by week 16; four weeks after stopping it had returned to baseline. The authors concluded the attenuation was partial and reversible ^[4]. In the same regimen, the cortisol response was modestly but significantly lower after 16 weeks, prolactin responses did not change, and there was no change in 24-hour urinary cortisol ^[5].

In healthy young men given two or three daily injections for one day, 24-hour GH secretion rose through larger pulses, not more frequent ones. A test dose given afterwards produced a smaller GH response, while its ACTH and cortisol responses were abolished ^[6]. Given at night, hexarelin reduced deep (stage 4) sleep and raised GH, prolactin, ACTH and cortisol in seven healthy volunteers ^[7].

The dose-response curve flattens early. In a placebo-controlled rising-dose study in 12 men, intravenous doses of 0.5, 1 and 2 µg/kg gave mean GH peaks of about 27, 52 and 55 ng/mL. GH peaked about 30 minutes after the injection and was back to baseline within four hours, and the 2 µg/kg dose was very close to the maximum possible response ^[28]. A later dose-response study found the GH response reached a plateau at 1 µg/kg, while prolactin and cortisol followed their own curves: cortisol stepped up by about 40% once the dose reached 0.5 µg/kg ^[14]. In the same study, a low dose of 0.125 µg/kg combined with GHRH released a very large amount of GH with a moderate prolactin rise and no cortisol rise.

Age changes the response. At 2 µg/kg intravenously, hexarelin was a strong stimulus in pubertal children and young adults, but the response in prepubertal children was no larger than to GHRH, and in people aged 53 to 79 it was well below that of young adults ^[31]. These differences are one reason the GH results from young volunteers cannot be applied to older people.

Hexarelin’s possible cardiac effects became a major focus of later research. In 13 patients with severe left ventricular dysfunction, a single intravenous dose increased ejection fraction in those with ischaemic cardiomyopathy but not in those with dilated cardiomyopathy ^[8]. During bypass surgery, a single 2 µg/kg dose raised ejection fraction, cardiac index and cardiac output within 10 minutes, lasting up to 90 minutes ^[3]. Both were small, acute studies.

Most of the rest of the cardiac evidence is from animals. In mice with an experimental heart attack, 0.3 mg/kg per day for 21 days preserved left ventricular function and reduced fibrosis compared with vehicle ^[9]. There are no long-term human trials of hexarelin for heart disease.

Two Turin studies in this line of hexarelin research separated the cardiac effect from GH. In seven adults with GH deficiency, whose pituitaries released almost no GH in response, an intravenous dose of hexarelin still raised left ventricular ejection fraction, from about 50% to 57%, and the rise in nine healthy controls was similar, from about 63% to 70%. Blood pressure, cardiac output and catecholamines did not change ^[16]. In seven healthy volunteers, injected recombinant GH and hexarelin raised GH to a similar degree, but only hexarelin raised ejection fraction, which rose within 15 minutes, peaked at 30 and lasted to 60 minutes ^[17].

The animal work points to direct protection of heart tissue. In rats whose pituitary glands had been removed, so that no GH could be released, seven days of hexarelin at 80 µg/kg under the skin protected the heart against damage from interrupted and restored blood flow; a related GHRP that does not bind heart tissue gave no protection ^[18]. In rats after a heart attack, 100 µg/kg a day for two weeks improved cardiac output and stroke volume and lowered peripheral resistance ^[19]. In spontaneously hypertensive rats, five weeks of treatment reduced heart fibrosis, left ventricular thickening and blood pressure, and a ghrelin-receptor blocker cancelled these effects ^[20]. In mice, a single oral dose given after an experimental heart attack preserved heart function in the longer term ^[21].

Not every cardiac effect is protective. The same CD36 binding that is thought to mediate these effects caused the coronary arteries of isolated rat hearts to constrict in a dose-dependent way ^[22]. The human cardiac data consist of single doses in small groups, measured over minutes to hours. None of the studies was designed to show a clinical benefit, and hexarelin has never been tested as a heart treatment in a controlled trial.

Most searches for hexarelin benefits are about muscle, fat loss, recovery or anti-ageing. The human evidence on those outcomes is thin and mostly negative. The longest adult study gave 1.5 µg/kg under the skin twice daily for 16 weeks to older adults. IGF-1 and IGFBP-3 did not change, and total body fat, lean body mass and bone mineral density were not significantly different from baseline after 16 weeks; of the bone markers measured, only one marker of bone formation rose ^[13]. The authors described the effect of this schedule on the GH–IGF-1 axis as minimal.

Shorter courses in older people gave similar results. Eight days of intranasal hexarelin did not change IGF-1, and 15 days by mouth raised IGF-1 and IGFBP-3 only slightly ^[32]. There are no human studies of hexarelin on muscle strength, fat loss, injury healing, sleep quality or skin.

The positive signals come from other settings. Short children treated with intranasal hexarelin grew faster (see below) ^[11][12]. In mice with a genetic form of insulin resistance, 12 days of hexarelin injections improved glucose and insulin tolerance, lowered triglycerides and reduced fat mass while raising lean mass, although food intake also rose ^[23]. In rats given the chemotherapy drug cisplatin, hexarelin protected muscle mitochondria and reduced muscle wasting ^[24]. These are animal results, and the heart findings above are covered separately. None shows a benefit in adults using the peptide for body composition.

The only human studies long enough to measure a physical outcome were in children. In Tel Aviv, eight short children received hexarelin by nasal spray at 60 µg/kg three times daily for up to eight months. IGF-1 rose, growth velocity increased from 5.3 to 8.3 cm a year, and skinfold thickness fell ^[11].

A follow-up paper in seven of these children measured tolerance. After one week of treatment the GH response to a nasal test dose had roughly halved, from 70.6 to 34.1 mU/L, and then stayed at that level for six months; the response to an intravenous test dose fell further by the end of treatment and partly recovered three months after stopping. Growth velocity still rose from 5.3 to 7.4 cm a year ^[12]. These were uncontrolled studies in a handful of children with a specific diagnosis, and they are not evidence about adults.

Searches for hexarelin before and after pictures or hexarelin results bodybuilding find forum photos, not research. The published studies do not report body-composition changes in adults (the 16-week study found none ^[13]), so there is no research basis for a before-and-after timeline.

What the studies do describe is the timing of the hormone response. After a single injection, GH peaks at about 30 minutes and returns to baseline within about four hours ^[28]. With repeated dosing the response shrinks. In adults injecting twice daily, it was lower by week 4 and about 45% lower by week 16, and it recovered within four weeks of stopping ^[4][13]. In children using a nasal spray, the drop appeared within the first week ^[12]. Intermittent use seemed to behave differently: eight days of intranasal or 15 days of oral hexarelin three times a day did not reduce the GH response in older people, and caused no side effects ^[32]. How much the dose, route and schedule each contribute to tolerance has not been worked out.

Hexarelin has been given intravenously, under the skin, by nasal spray and by mouth in human studies. Compared with intravenous dosing, bioavailability was about 77% under the skin, 5% nasally and 0.3% by mouth ^[1]. A study of oral hexarelin in humans and animals measured the same 0.3% and found the peptide was broken down in intestinal contents, which explains the low figure ^[27].

Hexarelin oral use therefore requires doses hundreds of times larger than an injection. The oral study in older women used 20 mg three times a day ^[32]. The nasal studies used 20 to 60 µg/kg per dose ^[1][11]. Research-grade products are sold as powder for injection, and oral or nasal products sold online have not been tested against these studies.

The peptide itself is cleared fairly quickly. Its terminal half-life was about 120 minutes after intravenous dosing in dogs ^[25] and about 76 minutes in rats, where most of it was excreted in bile ^[26]. In people, the GH it releases falls with a half-life of about 55 minutes ^[28]. A human study of nasal hexarelin found breakdown products in urine that anti-doping laboratories can use to detect it ^[34].

Both act on the ghrelin receptor, but they sit at opposite ends of the family. Hexarelin is one of the most potent GH releasers of its class and also raises prolactin, ACTH and cortisol ^[6][14]. Ipamorelin was designed to be selective: in pigs it released GH without raising ACTH or cortisol, even at doses far above those needed for GH release, unlike GHRP-6 and GHRP-2 ^[40].

Hexarelin has more human data, including the cardiac studies, the growth studies in children and the 16-week tolerance trial. Ipamorelin has fewer human studies. Neither has been approved for any use, and they have never been compared directly in people.

Sermorelin and tesamorelin are GHRH analogues. They act on a different receptor from hexarelin, so the comparison is between two ways of stimulating the pituitary. When hexarelin and GHRH were compared at the same intravenous dose in young men, hexarelin released more GH ^[29], and pairing a low dose of hexarelin with GHRH produced a much larger response than either alone ^[14]. Hexarelin also raises cortisol and prolactin, which GHRH analogues are not known for.

Their regulatory histories differ. Sermorelin was a licensed US medicine (Geref) until its manufacturer discontinued it, and the FDA later determined it was not withdrawn for safety or effectiveness reasons ^[39]. Tesamorelin is an approved medicine for reducing excess abdominal fat in adults with HIV and lipodystrophy ^[37]; in a 26-week trial of 412 patients, 2 mg daily reduced visceral fat by 15.2% compared with a 5.0% rise on placebo ^[38]. Hexarelin has no equivalent trial or approval. Anyone comparing hexarelin vs sermorelin vs tesamorelin is comparing an unapproved research peptide with two GHRH analogues that have been through formal drug development.

On evidence, hexarelin vs tesamorelin is an uneven comparison. Tesamorelin has phase 3 data for one outcome in one population, and its label states that it is not indicated for weight loss management ^[37]. Hexarelin has hormone and heart measurements taken over hours to weeks in small groups. Neither has been shown to build muscle or reduce fat in healthy adults.

Hexarelin is closest in structure to GHRP-6. In a direct comparison in six young adults, intravenous GHRP-2 and hexarelin at 1 and 2 µg/kg gave similar, strong GH responses, both higher than GHRH, with similar prolactin, ACTH and cortisol responses ^[15]. The main practical difference is the research that followed: the cardiac and CD36 work was done with hexarelin, not with GHRP-2 or GHRP-6.

A hexarelin CJC-1295 stack pairs a ghrelin-receptor agonist with a long-acting GHRH analogue, on the same reasoning as other GHRP and GHRH combinations. The reasoning comes from studies of hexarelin with GHRH itself: the two together released more GH than either alone in young and elderly adults ^[2][14], and hexarelin at a quarter of a microgram per kilogram plus GHRH was used as a diagnostic test because the combined response is so large ^[33]. The GHRH-receptor study shows why the pairing works at all: without GHRH signalling, hexarelin released no GH ^[30].

No study has combined hexarelin with CJC-1295, with or without DAC. There are no published doses, results or safety data for that stack. Any amounts quoted online are not drawn from research on the combination, and the hormonal side effects of hexarelin would still apply.

Human studies used single intravenous doses of 1 or 2 µg/kg, subcutaneous doses of 1.5 or 3 µg/kg, 20 µg/kg nasally and 20 or 40 mg by mouth ^[1][2][3]. Repeated-dosing studies used 1.5 µg/kg under the skin twice daily for 16 weeks ^[5] or two to three times in one day ^[6], and the sleep study gave four 50 µg intravenous doses an hour apart ^[7]. The mouse heart study used 0.3 mg/kg per day ^[9]. These are the doses researchers used, not recommendations; animal doses should not be converted to human ones.

Other human studies used intravenous doses of 0.5 to 2 µg/kg in dose-finding work ^[28], 0.25 µg/kg intravenously combined with GHRH as a diagnostic test ^[33], 1.25 mg by nasal spray or 20 mg by mouth three times daily in older adults ^[32], and 60 µg/kg by nasal spray three times daily in children ^[11]. The animal studies used 80 to 200 µg/kg in rats and mice ^[18][19][23]. None of these is a hexarelin dosage per day for anyone outside a study.

Products are sold as 2 mg or 5 mg vials, and the per-kilogram doses above do not translate into a vial count without a body weight and a volume of diluent. As arithmetic only: a 2 mg vial mixed with 2 mL of water contains 1 mg per mL, or 10 µg per unit on a U-100 insulin syringe. Our peptide calculator does this conversion for any vial size. It does not make any dose appropriate.

The published studies were short and small, and their abstracts focus on hormone responses rather than side effects. The effects that are documented are hormonal: acute rises in ACTH, cortisol and prolactin with single doses ^[6][7], loss of GH response with continued use ^[4], and reduced deep sleep when given at night ^[7]. Long-term safety has not been studied. Research-grade products are not made to medicine standards.

Hexarelin side effects in the studies were mainly the predictable hormonal ones. Cortisol rose once the intravenous dose reached 0.5 µg/kg, prolactin rose alongside GH, and hexarelin also raised cortisol in the volunteer cardiac study ^[14][17]. In the GHRH-receptor study, prolactin, ACTH and cortisol rose normally even when GH did not ^[30]. The intermittent intranasal and oral courses in older people reported no side effects and no change in prolactin or cortisol ^[32].

Injectable hexarelin side effects that the studies could not assess are those of the product itself: contamination, wrong content and poor sterility. These depend on the supplier. Our guides on third-party testing and spotting a fake supplier explain what to check. Nothing in the research shows hexarelin is safe for long-term use, and our disclaimer applies to all guide content.

Hexarelin is not an approved medicine in the UK, US, Canada, Australia or New Zealand. It is listed by WADA as examorelin (hexarelin) among the GH-releasing peptides in section S2 and is banned at all times ^[10]. For the rules on buying research peptides in each country, see our legal status overview.

The WADA listing is by name and applies at all times, in and out of competition. Section S2 also covers other substances with a similar chemical structure or biological effect, so products sold under other names are not exempt ^[10].

In Australia, hexarelin is a Schedule 4 prescription-only substance and is also listed in Appendix D of the Poisons Standard, which adds controls on possession; possessing it without authority is not permitted ^[35]. See Australia legal status. In New Zealand, Medsafe classifies hexarelin as a prescription medicine ^[36]; see New Zealand legal status. In the UK it is not listed under the Misuse of Drugs Act, but selling or supplying an unauthorised medicinal product is prohibited under the Human Medicines Regulations.

Research-grade hexarelin is supplied as freeze-dried powder with no published stability data. See our guides to storing peptides and bacteriostatic water for general practice.

Compare prices, check the COA with our guide on how to read a COA, and prefer third-party tested suppliers.

Searches to buy hexarelin online or find hexarelin for sale lead to research-chemical sellers, since there is no licensed product anywhere. Prices are listed by market, including hexarelin prices in the UK and in Australia, where possession needs authority. Our methodology explains how suppliers are scored. A low price does not show that a vial contains what its label says.