Peptides & growth hormone

Hexarelin

Updated · 39 sources · Editorial policy

Hexarelin, also called examorelin, is a synthetic six-amino-acid peptide that makes the pituitary gland release growth hormone (GH). It is a chemically stabilized analog of GHRP-6, first described in 1994 by researchers in Milan, and it acts on the same ghrelin receptor as GHRP-2 and the stomach hormone ghrelin (Deghenghi et al., Life Sci 1994; Mao et al., J Geriatr Cardiol 2014).

Hexarelin was studied intensively in the 1990s, mostly as a research tool and a possible test for GH deficiency. Two features set it apart from the other GH-releasing peptides: it binds a second receptor in the heart (CD36), and a 16-week human study showed that its GH response fades with repeated dosing.

The single most important fact: hexarelin is not an approved medicine in the US (we found no approval elsewhere either), no controlled trial has tested it for muscle, fat loss or performance, and in the one 16-week adult study it did not change IGF-1, lean mass or body fat (Rahim et al., JCEM 1998). WADA bans it at all times.

This page summarizes what the published human studies, animal pharmacology and regulators report. It is for education only and is not medical advice.

Property Detail
Class Synthetic GH-releasing peptide (GHRP); ghrelin receptor (GHS-R1a) agonist that also binds CD36
Other names Examorelin (WADA lists it as “examorelin (hexarelin)”)
Structure Hexapeptide amide, C47H58N12O6, molecular weight 887.0 (PubChem)
Routes studied in humans Intravenous, subcutaneous, intranasal, oral
Doses in cited human studies 0.125–2 µg/kg IV single doses; 1.5 µg/kg subcutaneously twice daily for 16 weeks; 60 µg/kg intranasally three times daily in children
Half-life No published human plasma value found; 75.9 min in rats and 120 min in dogs after IV dosing
Bioavailability in humans ≈77% subcutaneous, ≈4.8% intranasal, ≈0.3% oral (estimated from GH response)
Hormones also raised Prolactin, ACTH and cortisol
US status Not an approved drug; not a scheduled controlled substance
WADA status Prohibited at all times, S2.2.4

What it is

Hexarelin was made by modifying GHRP-6. The researchers replaced one tryptophan-type amino acid with a 2-methyl-tryptophan, which is chemically more stable. In rats, the new peptide released GH as effectively as GHRP-6 after IV dosing, and slightly more effectively and for longer after subcutaneous injection (Deghenghi et al., 1994). Its molecular formula is C47H58N12O6 and its molecular weight is 887.0 (PubChem CID 6918297), one methyl group more than GHRP-6.

Early human studies included investigators from the Milan company Mediolanum Farmaceutici (Imbimbo et al., Eur J Clin Pharmacol 1994), and Pharmacia & Upjohn later investigated ways to improve its oral absorption (Westberg et al., J Pharm Pharmacol 2001). We found no approved hexarelin product. The history of the GHRP family and the discovery of ghrelin and its receptor are covered on the GHRP-6 page.

Two receptors

  • Ghrelin receptor (GHS-R1a). Like other GHRPs, hexarelin activates this receptor in the pituitary and hypothalamus to release GH (Mao et al., 2014). In people, its GH effect depends on an intact hypothalamus: in patients whose pituitary stalk was disconnected from the hypothalamus, hexarelin produced little or no GH response (Loche et al., JCEM 1995).
  • CD36. In rat heart tissue, hexarelin binds CD36, a scavenger receptor on heart muscle and blood vessel cells. Activating it raised coronary perfusion pressure in isolated rat hearts, an effect missing in hearts from mice lacking CD36 (Bodart et al., Circ Res 2002). This is the basis for interest in hexarelin’s heart effects (see below). It comes from animal tissue, not human trials.

How it compares with GHRP-2 and GHRP-6

Feature Hexarelin GHRP-2 GHRP-6
GH response at 1–2 µg/kg IV Similar to GHRP-2 in a head-to-head study Similar to hexarelin Less potent than GHRP-2 in the original GHRP series
Prolactin, ACTH, cortisol Raised Raised, to a similar degree as hexarelin Raised at higher doses
Approval None Japan, as a one-time diagnostic test (2004) None
FDA compounding Category 2 Not listed Listed (2023) Listed (2023)
Distinctive data CD36 binding; acute heart studies; 16-week desensitization study Large negative placebo-controlled trial in children Stroke trials with EGF

The head-to-head data come from a study in 6 young adults given 1 and 2 µg/kg IV of each peptide; GHRP-2 and hexarelin produced similar GH, prolactin, ACTH and cortisol responses (Arvat et al., Peptides 1997). The other comparison points come from the GHRP-2 and GHRP-6 pages and the FDA Category 2 list.

Pharmacokinetics

We found no published study that measured hexarelin itself in human blood. Human data describe the GH response instead.

Routes of administration in humans

In 12 healthy young volunteers, hexarelin released GH by every route tested (Ghigo et al., JCEM 1994):

Route and dose GH area under the curve (mean ± SEM, µg·min/L) Estimated bioavailability
IV, 1 µg/kg 3175 ± 506 Reference
IV, 2 µg/kg 4422 ± 626 Reference
Subcutaneous, 1.5 µg/kg 3180 ± 392 77.0 ± 10.5% (SC route)
Subcutaneous, 3 µg/kg 4459 ± 566
Intranasal, 20 µg/kg 2642 ± 452 4.8 ± 0.9% (intranasal route)
Oral, 20 mg 2278 ± 442 0.3 ± 0.1% (oral route)
Oral, 40 mg 4079 ± 514
GHRH, 1 µg/kg IV (comparison) 1544 ± 161 —

These “biological bioavailabilities” were estimated from GH levels, not from drug levels. Oral hexarelin needs doses thousands of times larger than injected doses: it is broken down by intestinal enzymes, including trypsin, and crosses the gut wall poorly (Westberg et al., 2001).

After an IV dose in 12 men, plasma GH peaked at about 30 minutes and returned to baseline within 240 minutes, with a GH half-life of about 55 minutes (Imbimbo et al., 1994). A 2026 review lists “t½ ≈55 min” for hexarelin citing this study (Dominikowski et al., Front Endocrinol 2026), but in the study abstract that figure describes the fall in GH, not the peptide’s own elimination.

Animal data

  • Rats. After an IV dose, hexarelin’s half-life was 75.9 ± 9.3 min. Subcutaneous bioavailability was 64%. It was cleared mainly through bile (60% of a radiolabeled dose in bile, 22% in urine), and most of what was excreted was unchanged peptide, showing resistance to breakdown (Roumi et al., Drug Metab Dispos 2000).
  • Dogs. After a 1 µg/kg IV dose, the terminal half-life was 120 min (Roumi et al., Peptides 1995).

In humans, an anti-doping study gave hexarelin nasally to one volunteer. It was heavily metabolized, and a three-amino-acid fragment was still detectable in urine after the parent peptide had disappeared (Semenistaya et al., Drug Test Anal 2015).

Regulatory status

  • Not an approved drug. FDA’s Drugs@FDA data contain no product listing hexarelin or examorelin as an active ingredient (Drugs@FDA via openFDA). A 2026 review notes that the pediatric findings for hexarelin do not establish a generalizable or approved therapeutic protocol (Dominikowski et al., 2026).
  • FDA compounding lists. Unlike GHRP-2, GHRP-6 and ipamorelin, hexarelin does not appear on FDA’s Category 2 list of bulk substances that may present significant safety risks (version current as of April 22, 2026) (FDA). Absence from that list is not an approval or a safety finding.
  • Not a controlled substance. Hexarelin is not named in the US anabolic steroid schedule (21 CFR 1308.13).
  • Banned in sport. WADA lists “examorelin (hexarelin)” among the GH-releasing peptides under S2.2.4, prohibited in and out of competition (WADA 2026 Prohibited List).

What the research shows

GH release in healthy adults

In a double-blind, placebo-controlled, rising-dose study in 12 healthy men, single IV doses raised GH in a dose-dependent way, with the response close to its maximum at 2 µg/kg (Imbimbo et al., 1994):

IV dose Mean peak GH (ng/mL) GH AUC 0–180 min (µg·min/mL)
Placebo 3.9 0.135
0.5 µg/kg 26.9 1.412
1 µg/kg 52.3 2.918
2 µg/kg 55.0 3.695

A London dose-response study in healthy men found a similar half-maximal dose (ED50 0.48 µg/kg) and showed that very low hexarelin (0.125 µg/kg) given with GHRH released a large amount of GH without raising cortisol (Massoud et al., JCEM 1996).

Other findings from single-dose studies:

  • Compared with GHRH and ghrelin. At maximal doses, hexarelin released more GH than GHRH in both young and elderly men (Arvat et al., JCEM 1994). Natural ghrelin at 1 µg/kg released more GH than hexarelin at the same dose (mean peak 92.1 vs 68.4 µg/L) in 7 young men (Arvat et al., JCEM 2001).
  • Age. The GH response was smaller in elderly men than in young men (AUC 2112 vs 4849 µg·min/L) (Arvat et al., 1994), and it was lower in prepubertal children and elderly adults than in pubertal children and young adults (Arvat et al., Eur J Endocrinol 1997).

Diagnostic testing for GH deficiency

Because it is a strong, reproducible stimulus, hexarelin was tested as a diagnostic tool. Unlike GHRP-2 in Japan, it never became an approved test.

  • Hexarelin plus GHRH. In 25 healthy adults, a low dose of hexarelin (0.25 µg/kg IV) with GHRH (1 µg/kg IV) produced a mean peak GH of 83.6 µg/L. In 19 adults with confirmed GH deficiency, the mean peak was 2.6 µg/L, and all 19 fell below the normal cut-off. The authors judged the test as sensitive as the insulin tolerance test when appropriate cut-offs are used (Gasperi et al., JCEM 1999).
  • Hexarelin alone. In 19 patients with possible pituitary disease, a 2 µg/kg dose identified GH deficiency well but was not a reliable test of cortisol reserve (Korbonits et al., Clin Endocrinol 1999).

Repeated dosing and loss of response

Several human studies looked at what happens to the GH response when hexarelin is given repeatedly:

Study Who and how long Dosing GH response IGF-1
Rahim et al., JCEM 1998; Rahim and Shalet, 1998 12 healthy elderly adults, 16 weeks 1.5 µg/kg SC twice daily GH AUC fell from 19.1 to 13.1 (week 1), 12.3 (week 4) and 10.5 µg/L·h (week 16); recovered to 19.4 four weeks after stopping No significant change
Klinger et al., Eur J Endocrinol 1996 7 short children, 6–10 months 60 µg/kg intranasal three times daily Peak GH to a nasal test dose halved within 7 days (70.6 to 34.1 mU/L); response to an IV test dose fell from 84.8 to 19.8 mU/L by the end; partial recovery 3 months after stopping Not reported in the abstract
Maccario et al., Eur J Endocrinol 2002 6 young men, 1 day 1.5 µg/kg SC two or three times daily 24-hour GH rose equally with either schedule; a final IV dose gave a blunted GH response No change

In the 16-week study, total body fat, lean body mass and bone mineral density did not change significantly. Of several bone markers, only one (C-terminal propeptide of type I collagen) rose. The authors concluded that this regimen had minimal biological impact on the GH-IGF-1 axis (Rahim et al., 1998).

Growth in short children

Small, uncontrolled Israeli studies reported faster growth with intranasal hexarelin:

  • In 8 prepubertal short children given 60 µg/kg three times daily for up to 8 months, IGF-1 rose from 10.4 to 14.1 nmol/L and growth velocity rose from 5.3 to 8.3 cm/year. Skinfold thickness fell while body weight rose (Laron et al., Clin Endocrinol 1995).
  • In 7 children followed for 6–10 months, growth velocity rose from 5.3 to 7.4 cm/year despite the fading GH response described above (Klinger et al., 1996).

Neither study had a placebo group, and growth velocity can change on its own. When GHRP-2 was tested in a 126-child placebo-controlled trial, it did not improve growth (see GHRP-2). No comparable controlled trial of hexarelin was found.

Heart function

Several small human studies looked for direct heart effects. All of them were single IV doses, measuring short-term changes in left ventricular ejection fraction (LVEF, the share of blood the main pumping chamber pushes out per beat):

Study Who Result after hexarelin
Bisi et al., J Endocrinol Invest 1999 7 healthy men LVEF rose from 64.0% to 70.7%, peaking at 30 min and lasting up to 60 min; GH injection raising GH to the same extent had no effect
Bisi et al., Eur J Pharmacol 1999 7 men with GH deficiency, 9 controls LVEF rose in both groups (peak 57% and 70%) although GH barely rose in the GH-deficient men
Imazio et al., Eur J Heart Fail 2002 8 patients with dilated and 5 with ischemic cardiomyopathy LVEF rose in ischemic cardiomyopathy (from 22.6% to a peak of 26.2%) but not in dilated cardiomyopathy
Broglio et al., Eur J Pharmacol 2002 24 men with coronary artery disease during bypass surgery, given hexarelin, GHRH, GH or placebo Only hexarelin (2 µg/kg) raised LVEF, cardiac index and cardiac output, from 10 to 90 min

Because GH injection and GHRH did not reproduce these effects, the investigators concluded that hexarelin acts directly on heart receptors rather than through GH. In rats, hexarelin protected isolated hearts from ischemia-reperfusion damage even after removal of the pituitary (Locatelli et al., Endocrinology 1999) and improved cardiac output after experimental heart attack (Tivesten et al., Endocrinology 2000).

No human trial has tested repeated hexarelin dosing for heart failure or any clinical cardiac outcome. The same CD36 activation that is studied for heart protection also caused coronary vasoconstriction in isolated rat hearts (Bodart et al., 2002).

Muscle, fat loss and performance

No controlled trial has tested hexarelin for muscle mass, strength, fat loss or athletic performance. A 2026 review concluded that claims for body-composition effects rest mainly on its ability to raise GH and IGF-1, not on trials designed to measure these outcomes (Dominikowski et al., 2026). The one long adult study found no change in lean mass, fat mass or IGF-1 after 16 weeks (Rahim et al., 1998).

About “the strongest GHRP, with no desensitization.” Hexarelin is often promoted as the most potent GH-releasing peptide. In the only head-to-head human study, its GH response matched GHRP-2’s, and natural ghrelin released more GH at the same dose. The fading response is not folklore either: in elderly adults, the GH response to twice-daily injections fell from 19.1 to 10.5 µg/L·h by week 16, and IGF-1, lean mass and fat mass did not change. The response recovered about four weeks after stopping.

Side effects and risks

The published human studies were small and short, and most reported no notable adverse effects. Long-term safety has not been studied.

Cortisol, ACTH and prolactin

Hexarelin is not selective for GH:

  • Dose-related rises. In healthy men, prolactin rose by up to ≈180% from baseline at 1 µg/kg, and cortisol rose by ≈40% from a dose of 0.5 µg/kg (Massoud et al., 1996).
  • Comparable to CRH. At 2 µg/kg, its ACTH and cortisol responses in healthy adults were similar to those from corticotropin-releasing hormone (hCRH). In Cushing’s disease (a pituitary tumor making ACTH) the ACTH rise was about 7-fold greater than with hCRH (Ghigo et al., JCEM 1997). The effect on the stress-hormone axis appears to involve vasopressin rather than CRH (Korbonits et al., JCEM 1999).
  • With repeated dosing. Over 16 weeks of twice-daily injections, the cortisol response to a morning dose actually fell (AUC 1506 to 1222 nmol/L·h) and recovered after stopping. Prolactin responses and 24-hour urinary cortisol did not change (Rahim et al., Clin Endocrinol 1999).

These rises can confound hormone blood tests in people using GHRPs (Dominikowski et al., 2026).

Sleep, appetite and thyroid

  • Sleep. In 7 young volunteers, four 50 µg doses given at night reduced deep (stage 4) sleep and raised GH, prolactin, ACTH and cortisol overnight (Frieboes et al., Psychoneuroendocrinology 2004).
  • Appetite. A single dose caused a small, acute rise in self-rated appetite in 15 healthy men (Korbonits et al., 1999).
  • Thyroid. In children, single doses caused a small fall in TSH (thyroid-stimulating hormone) that stayed within the normal range, with no change in thyroid hormones (Laron et al., Clin Endocrinol 1994).

Unknown long-term effects and product quality

There are no long-term human safety data for hexarelin, including on blood sugar, cancer risk or the heart. Because its purpose is to raise GH, the known effects of GH excess are plausible but unmeasured; see growth hormone and ibutamoren. With no approved product, material sold outside research has no regulator-verified identity, purity or dose.

Detection in sport

Hexarelin is prohibited at all times under WADA S2.2.4 (WADA 2026 Prohibited List). Anti-doping laboratories detect hexarelin and its metabolites in urine by liquid chromatography-mass spectrometry. Because hexarelin is extensively metabolized, a metabolite remained detectable after the parent peptide had cleared (Semenistaya et al., 2015).

Key takeaways

  • A stabilized GHRP-6 analog. Hexarelin is a synthetic hexapeptide that activates the ghrelin receptor to release GH, and in animal tissue it also binds the heart receptor CD36.
  • Potent but not unique. Single IV doses of 1–2 µg/kg raise GH strongly, about as much as GHRP-2 and less than natural ghrelin at the same dose. It also raises prolactin, ACTH and cortisol.
  • Responses fade with repeated use. Over 16 weeks of twice-daily injections in older adults, the GH response fell (AUC 19.1 to 10.5 µg/L·h) and IGF-1, lean mass and fat mass did not change.
  • Heart data are short-term only. Single doses raised ejection fraction in small human studies, but no trial has tested clinical heart outcomes.
  • No approved use and no performance evidence. It is not an approved drug in the US, no human plasma half-life has been published, no trial has tested muscle or performance outcomes, and WADA bans it at all times.

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