Hexarelin

updated

Hexarelin (examorelin) is a synthetic hexapeptide with no matching FDA application and no ClinicalTrials.gov record as of 9 October 2026. In small human studies it released about twice the GH of GHRH by intravenous injection, with prolactin and cortisol rising at the same doses, and its GH response fell on some repeated schedules. The only human study that measured body composition, 16 weeks in 12 healthy elderly people, found no change in fat, lean mass or bone density.

Synthetic hexapeptide growth hormone secretagogue

  • Hexarelin is a hexapeptide, His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2 (PubChem CID 6918297). Vendor material is normally the acetate salt (CID 88325556), so a milligram of powder is not a milligram of peptide.
  • Drugs@FDA queries for hexarelin and examorelin returned no matching application, and a ClinicalTrials.gov term search returned 0 records, on 9 October 2026.
  • In 12 healthy young volunteers, 1 mcg/kg intravenous hexarelin gave a GH AUC of 3175 micrograms/min/L versus 1544 for GHRH (P<0.001). Biological bioavailability was 77.0% subcutaneous, 4.8% intranasal and 0.3% oral.
  • Over 16 weeks of twice-daily subcutaneous dosing in 12 healthy elderly people, mean GH AUC fell from 19.1 to 10.5 micrograms/L.h and was back to 19.4 four weeks after stopping. Body fat, lean mass and bone density did not change.
  • In 7 male volunteers, intravenous hexarelin raised left ventricular ejection fraction from 64.0% to 70.7% (p<0.03), while recombinant GH did not.
  • A PubMed search on 9 October 2026 for hexarelin with recovery, exercise, athletes or healing returned 42 records; none tested training recovery, muscle gain or injury healing in healthy or trained adults.

What is hexarelin, and has anyone approved it?

Hexarelin (examorelin) is a synthetic hexapeptide with no matching Drugs@FDA application and no ClinicalTrials.gov record in searches on 9 October 2026. Vendor material is normally the acetate salt, so a milligram of powder is not a milligram of peptide.

Hexarelin, also called examorelin, is a synthetic hexapeptide with the sequence His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2 (PubChem CID 6918297, C47H58N12O6, molecular weight 887.0, CAS 140703-51-1). Listed synonyms include EP-23905 and MF-6003. The acetate salt is a separate identity (CID 88325556, C49H62N12O8, molecular weight 947.1, CAS 208251-52-9). Vendor material is normally the acetate, so a milligram of vendor powder is not a milligram of peptide.

openFDA Drugs@FDA substance-name queries for hexarelin and for examorelin each returned no matching application on 9 October 2026, and a ClinicalTrials.gov term search for hexarelin returned 0 records on the same date. There is no approved hexarelin product in the FDA record and no registered trial in that registry. This is a US-scoped and registry-scoped statement, not a worldwide legal claim, and approvals outside the United States are not covered.

PubChem: hexarelin peptide and acetate salt identity

Chemical identity record

National Library of Medicine. PubChem compound record CID 6918297 (hexarelin), with the acetate salt at CID 88325556.

Hexarelin, also called examorelin, is a synthetic hexapeptide, His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2: PubChem CID 6918297, C47H58N12O6, molecular weight 887.0, CAS 140703-51-1. Listed synonyms include EP-23905 and MF-6003. The acetate salt is a separate identity: CID 88325556, C49H62N12O8, molecular weight 947.1, CAS 208251-52-9.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined hexapeptide and acetate salt
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

Vendor material is normally the acetate, so a milligram of vendor powder is not a milligram of peptide.

Read the original source
Searches, 9 October 2026: no FDA application, 0 registered trials

Regulatory record

U.S. Food and Drug Administration. openFDA Drugs@FDA substance-name queries for hexarelin and for examorelin, run on 9 October 2026, with a ClinicalTrials.gov term search for hexarelin the same day.

openFDA Drugs@FDA substance-name queries for hexarelin and for examorelin each returned no matching application on 9 October 2026, and a ClinicalTrials.gov term search for hexarelin returned 0 records on the same date. There is no approved hexarelin product and no registered trial in that registry.

Participants / model
Regulator and registry databases, not a population
Treatment
Exact substance-name and term searches
Follow-up
Searches run on 9 October 2026
Study design
FDA API query and trial registry search
Funding
not stated in the source

This is a US-scoped and registry-scoped statement, not a worldwide legal claim.

Read the original source

How much growth hormone does hexarelin release, and by which routes?

In 12 healthy young volunteers, 1 mcg/kg intravenous hexarelin released about twice the GH of 1 mcg/kg GHRH (AUC 3175 versus 1544 micrograms/min/L, P<0.001). Biological bioavailability was 77.0% subcutaneous, 4.8% intranasal and 0.3% oral.

In 12 healthy young volunteers, hexarelin was given intravenously (1 and 2 mcg/kg), subcutaneously (1.5 and 3 mcg/kg), intranasally (20 mcg/kg) and orally (20 and 40 mg), and compared with intravenous saline and with GHRH 1 mcg/kg. GH release after 1 mcg/kg intravenous hexarelin (AUC 3175 micrograms/min/L) was about twice that after 1 mcg/kg GHRH (AUC 1544, P<0.001), and 2 mcg/kg gave a further increase (AUC 4422). Subcutaneous dosing was dose-dependent (AUC 3180 and 4459). Biological bioavailability was 77.0% subcutaneous, 4.8% intranasal and 0.3% oral. The claim that hexarelin out-releases GHRH is supported, and the oral route is almost completely unavailable.

In 6 normal young men, two or three daily subcutaneous injections of hexarelin 1.5 mcg/kg increased mean and integrated 24-hour serum GH to the same extent, amplifying GH secretory burst mass but not burst frequency. IGF-1, prolactin, ACTH and cortisol secretion did not change. Three daily injections gave the same 24-hour GH as two.

Routes and potency: 12 volunteers, GH AUC 3175 versus 1544 for GHRH, oral bioavailability 0.3%

Human study

Ghigo E et al. J Clin Endocrinol Metab. 1994;78(3):693-8. PMID 8126144.

GH release after 1 mcg/kg intravenous hexarelin (AUC 3175 micrograms/min/L) was about twice that after 1 mcg/kg GHRH (AUC 1544, P<0.001), and 2 mcg/kg gave a further increase (AUC 4422). Subcutaneous dosing was dose-dependent (AUC 3180 and 4459). Biological bioavailability was 77.0% subcutaneous, 4.8% intranasal and 0.3% oral.

Participants / model
12 healthy young volunteers
Treatment
Hexarelin intravenously (1 and 2 mcg/kg), subcutaneously (1.5 and 3 mcg/kg), intranasally (20 mcg/kg) and orally (20 and 40 mg), against intravenous saline and GHRH 1 mcg/kg
Follow-up
Single doses; total duration not stated in the source
Study design
Clinical study comparing routes against saline and GHRH
Funding
not stated in the source

The oral route is almost completely unavailable. Single doses in 12 people.

Read the original source
24-hour secretion: 6 young men, GH burst mass up, no change in IGF-1, prolactin, ACTH or cortisol

Human study

Maccario M et al. Eur J Endocrinol. 2002;146(3):310-8. PMID 11888836.

Two or three daily subcutaneous injections of hexarelin 1.5 mcg/kg increased mean and integrated 24-hour serum GH to the same extent, amplifying GH secretory burst mass but not burst frequency, with no change in IGF-1, prolactin, ACTH or cortisol secretion. An intravenous 1 mcg/kg dose at the end of each 24-hour profile still raised GH, prolactin, ACTH and cortisol, but prior hexarelin blunted the GH response and abolished the ACTH and cortisol responses. Three injections a day gave the same 24-hour GH as two.

Participants / model
6 normal young men
Treatment
Subcutaneous hexarelin 1.5 mcg/kg two or three times daily, with an intravenous 1 mcg/kg challenge
Follow-up
24-hour profiles
Study design
Clinical study with deconvolution analysis of 24-hour secretion
Funding
not stated in the source

Prior hexarelin blunted the GH response to a later intravenous dose.

Read the original source

Does hexarelin release only growth hormone?

No. In healthy adult males, intravenous hexarelin raised prolactin and cortisol at the same doses that raised GH. The GH curve plateaued at 140 mU/L with an ED50 of 0.48 mcg/kg, the prolactin curve at a 180% maximum rise with an ED50 of 0.39 mcg/kg, and cortisol showed a step increase of about 40% at 0.5 mcg/kg.

In healthy adult males given intravenous hexarelin at 0 to 1.0 mcg/kg, the GH dose-response curve plateaued at 140 mU/L with an ED50 of 0.48 mcg/kg. The prolactin curve plateaued at a 180% maximum rise from baseline with an ED50 of 0.39 mcg/kg, and cortisol showed a step increase of about 40% at 0.5 mcg/kg.

Co-administering GHRH 1.0 mcg/kg with low-dose hexarelin 0.125 mcg/kg produced large GH release (115 mU/L) with a moderate prolactin rise and no cortisol rise.

Prolactin and cortisol move at the same doses that move GH. The sellers' claim of maximal GH pulses is true, but it is not a GH-only effect.

Not GH-selective: prolactin and cortisol rise at the doses that raise GH

Human study

Massoud AF et al. J Clin Endocrinol Metab. 1996;81(12):4338-41. PMID 8954038.

The GH dose-response curve plateaued at 140 mU/L with an ED50 of 0.48 mcg/kg, the prolactin curve plateaued at a 180% maximum rise from baseline with an ED50 of 0.39 mcg/kg, and cortisol showed a step increase of about 40% at 0.5 mcg/kg. Co-administering GHRH 1.0 mcg/kg with low-dose hexarelin 0.125 mcg/kg produced large GH release (115 mU/L) with a moderate prolactin rise and no cortisol rise.

Participants / model
Healthy adult males; number not stated in the source
Treatment
Intravenous hexarelin 0 to 1.0 mcg/kg, with and without GHRH
Follow-up
Single doses; duration not stated in the source
Study design
Clinical dose-response study
Funding
not stated in the source

Prolactin and cortisol move at the same doses that move GH.

Read the original source

Does the growth hormone response fade with repeated dosing?

Partly and reversibly, depending on schedule and route. A second intravenous dose 120 minutes after the first lowered GH, and 16 weeks of twice-daily subcutaneous dosing cut mean GH AUC from 19.1 to 10.5 micrograms/L.h, which recovered 4 weeks after stopping. Intermittent intranasal or oral dosing for 8 to 15 days did not lower the response.

In 6 normal adults given two consecutive 1 mcg/kg intravenous boluses 120 minutes apart, the GH net incremental AUC fell from 1424 ng/mL/h after the first hexarelin bolus to 286.6 ng/mL/h after the second (p<0.02). The second response was still significantly larger than the response to a second GHRH bolus (74.5 ng/mL/h). In 6 healthy adult males aged 25.4 to 34.1 years given single or paired intravenous boluses of hexarelin 1 mcg/kg, GHRH 1 mcg/kg or both, a second bolus of hexarelin, or of hexarelin with GHRH, given 120 minutes after the first produced lower peak GH secretion rates (P=0.03), while reductions after 60-minute intervals were not statistically significant. Hexarelin and GHRH were synergistic on first dosing, and that synergy was lost on repeated administration.

Twelve healthy elderly individuals received hexarelin 1.5 mcg/kg subcutaneously twice daily for 16 weeks. Mean GH area under the curve was 19.1 micrograms/L.h at week 0, 13.1 at week 1, 12.3 at week 4 and 10.5 at week 16 (change over the study P=0.0003; week 4 P<0.05 and week 16 P<0.01 versus baseline). Four weeks after stopping, AUC rose to 19.4 micrograms/L.h, significantly above week 16 (P<0.05) and no different from week 0. Serum IGF-1 and IGFBP-3 did not change significantly over 20 weeks (P=0.24 and P=0.74). Total body fat, lean body mass and bone mineral density were unchanged at week 16 (P=0.6, 0.3 and 0.3). Attenuation was partial and reversible, and on this schedule nothing downstream moved.

In 7 elderly subjects given intranasal hexarelin 1.25 mg (about 18 mcg/kg) three times daily for 8 days, and 7 elderly women given oral hexarelin 20 mg (about 300 mcg/kg) three times daily for 15 days, the acute GH response to the peptide was maintained after treatment. With intranasal treatment IGF-1 did not change significantly but IGFBP-3 rose (2.4 versus 1.6 mg/L, p<0.02). With oral treatment IGF-1 and IGFBP-3 both rose slightly (156.0 versus 141.6 micrograms/L, p<0.03, and 3.4 versus 3.1 mg/L, p<0.03). Neither schedule changed prolactin or cortisol levels or caused side effects.

In 7 prepubertal constitutionally short children (mean age 7.6 years) given intranasal hexarelin 60 mcg/kg three times daily for 6 to 10 months, the mean peak GH rise to an intranasal bolus fell from 70.6 mU/L before treatment to 34.1 mU/L after 7 days (p<0.002) and stayed near that level at 6 months (37.5 mU/L, p<0.03). The response to an intravenous bolus fell from 84.8 to 19.8 mU/L (p<0.05) and recovered to 42.1 mU/L three months after stopping (p<0.005). Growth velocity rose from 5.3 to 7.4 cm/year (p<0.005). Partial suppression of the GH response did not abolish the clinical effect in this population, a group of short children rather than healthy adults.

In the 6 young men studied over 24 hours, an intravenous 1 mcg/kg dose at the end of each profile still raised GH, prolactin, ACTH and cortisol, but prior hexarelin blunted the GH response and abolished the ACTH and cortisol responses. Whether the GH response falls depends on schedule and route, not on the molecule alone.

Within-day fade: GH AUC 1424 to 286.6 ng/mL/h on a second bolus 120 minutes later

Human study

Sartorio A et al. J Endocrinol Invest. 1995;18(9):718-22. PMID 8719303.

The GH net incremental AUC fell from 1424 ng/mL/h after the first hexarelin bolus to 286.6 ng/mL/h after the second (p<0.02), although that second response was still significantly larger than the response to a second GHRH bolus (74.5 ng/mL/h). Repeated hexarelin reduces GH responsiveness within hours, and does so less than repeated GHRH does.

Participants / model
6 normal adults
Treatment
Two intravenous 1 mcg/kg hexarelin boluses 120 minutes apart
Follow-up
Single session
Study design
Clinical study of repeated boluses
Funding
not stated in the source

The first demonstration of acute within-day attenuation in the sources reviewed.

Read the original source
Interval matters: lower peak GH after a 120-minute repeat, not significant at 60 minutes

Human study

Massoud AF et al. Clin Endocrinol (Oxf). 1996;44(5):555-62. PMID 8762732.

A second bolus of hexarelin, or of hexarelin with GHRH, given 120 minutes after the first produced lower peak GH secretion rates (P=0.03), while reductions after 60-minute boluses were not statistically significant. Hexarelin and GHRH were synergistic on first dosing, and that synergy was lost on repeated administration.

Participants / model
6 healthy adult males aged 25.4 to 34.1 years
Treatment
Single or paired intravenous boluses of hexarelin 1 mcg/kg, GHRH 1 mcg/kg, or both, 60 or 120 minutes apart
Follow-up
Single sessions
Study design
Clinical study with deconvolution analysis of peak GH secretion rate
Funding
not stated in the source

The attenuation depends on the interval between doses.

Read the original source
16 weeks: 12 elderly people, GH AUC 19.1 to 10.5, recovered at 4 weeks off, body composition unchanged

Human study

Rahim A et al. J Clin Endocrinol Metab. 1998;83(5):1644-9. PMID 9589671.

Mean GH area under the curve was 19.1 micrograms/L.h at week 0, 13.1 at week 1, 12.3 at week 4 and 10.5 at week 16 (change over the study P=0.0003; week 4 P<0.05 and week 16 P<0.01 versus baseline). Four weeks after stopping, AUC rose to 19.4 micrograms/L.h, significantly above week 16 (P<0.05) and no different from week 0. Serum IGF-1 and IGFBP-3 did not change significantly over 20 weeks (P=0.24 and P=0.74). Total body fat, lean body mass and bone mineral density were unchanged at week 16 (P=0.6, 0.3 and 0.3).

Participants / model
12 healthy elderly individuals
Treatment
Subcutaneous hexarelin 1.5 mcg/kg twice daily
Follow-up
16 weeks of treatment, with a 4-week follow-up and measures over 20 weeks
Study design
Clinical study of chronic dosing
Funding
not stated in the source

Attenuation is partial and reversible, and on this schedule nothing downstream moved.

Read the original source
Intranasal 8 days and oral 15 days: GH response maintained, no side effects

Human study

Ghigo E et al. Eur J Endocrinol. 1996;135(4):407-12. PMID 8921821.

The acute GH response to the peptide was maintained after treatment. IGF-1 did not change significantly with intranasal treatment but IGFBP-3 rose (2.4 versus 1.6 mg/L, p<0.02); with oral treatment IGF-1 and IGFBP-3 both rose slightly (156.0 versus 141.6 micrograms/L, p<0.03, and 3.4 versus 3.1 mg/L, p<0.03). Neither schedule changed prolactin or cortisol levels or caused side effects.

Participants / model
7 elderly subjects (intranasal) and 7 elderly women (oral)
Treatment
Intranasal hexarelin 1.25 mg (about 18 mcg/kg) three times daily for 8 days; oral hexarelin 20 mg (about 300 mcg/kg) three times daily for 15 days
Follow-up
8 days (intranasal) and 15 days (oral)
Study design
Clinical study of short-term intermittent dosing
Funding
not stated in the source

Whether the GH response falls depends on schedule and route, not on the molecule alone.

Read the original source
Short children: 7 children, 6 to 10 months intranasal, GH response halved, growth velocity 5.3 to 7.4 cm/year

Human study

Klinger B et al. Eur J Endocrinol. 1996;134(6):716-9. PMID 8766941.

The mean peak GH rise to an intranasal bolus fell from 70.6 mU/L before treatment to 34.1 mU/L after 7 days (p<0.002) and stayed near that level at 6 months (37.5 mU/L, p<0.03). The response to an intravenous bolus fell from 84.8 to 19.8 mU/L (p<0.05) and recovered to 42.1 mU/L three months after stopping (p<0.005). Growth velocity rose from 5.3 to 7.4 cm/year (p<0.005).

Participants / model
7 prepubertal constitutionally short children (mean age 7.6 years)
Treatment
Intranasal hexarelin 60 mcg/kg three times daily
Follow-up
6 to 10 months
Study design
Clinical study of long-term intranasal dosing
Funding
not stated in the source

Partial suppression of the GH response did not abolish the clinical effect in this population. This was a group of short children, not healthy adults.

Read the original source
24-hour secretion: 6 young men, GH burst mass up, no change in IGF-1, prolactin, ACTH or cortisol

Human study

Maccario M et al. Eur J Endocrinol. 2002;146(3):310-8. PMID 11888836.

Two or three daily subcutaneous injections of hexarelin 1.5 mcg/kg increased mean and integrated 24-hour serum GH to the same extent, amplifying GH secretory burst mass but not burst frequency, with no change in IGF-1, prolactin, ACTH or cortisol secretion. An intravenous 1 mcg/kg dose at the end of each 24-hour profile still raised GH, prolactin, ACTH and cortisol, but prior hexarelin blunted the GH response and abolished the ACTH and cortisol responses. Three injections a day gave the same 24-hour GH as two.

Participants / model
6 normal young men
Treatment
Subcutaneous hexarelin 1.5 mcg/kg two or three times daily, with an intravenous 1 mcg/kg challenge
Follow-up
24-hour profiles
Study design
Clinical study with deconvolution analysis of 24-hour secretion
Funding
not stated in the source

Prior hexarelin blunted the GH response to a later intravenous dose.

Read the original source

What do the cardiac studies show?

In people, single intravenous hexarelin doses raised left ventricular ejection fraction within minutes in several small studies, while recombinant GH did not in the volunteer comparison. The infarct, fibrosis and remodeling work is in rats and mice, and the heart target CD36 also mediated dose-dependent coronary vasoconstriction in perfused hearts.

In 7 male volunteers studied by radionuclide angiocardiography, intravenous hexarelin raised left ventricular ejection fraction from 64.0% to 70.7% (p<0.03) without significant change in mean blood pressure or heart rate, rising at 15 minutes, peaking at 30 minutes and lasting up to 60 minutes. Recombinant human GH raised circulating GH to the same extent but did not change ejection fraction, which argues the inotropic effect is not GH-mediated. Hexarelin, but not rhGH, also raised cortisol.

In 7 adult men with GH deficiency and 9 male controls (PMID 10528131), intravenous hexarelin raised ejection fraction in both groups (peak 57 versus 70%, P<0.05 versus baseline) without changing catecholamines, mean blood pressure or cardiac output, even though the GH response in the GH-deficient men was negligible (peak 1.9 versus 45.7 micrograms/L). In 8 patients with dilated and 5 with ischemic cardiomyopathy (PMID 11959048), hexarelin raised ejection fraction in the ischemic group (22.6 to 26.2%, P<0.05) but not in the dilated group despite a similar GH rise. In 24 men with coronary artery disease during bypass surgery under general anesthesia (PMID 12144941), hexarelin 2.0 mcg/kg raised ejection fraction, cardiac index and cardiac output within 10 minutes and for up to 90 minutes and lowered wedge pressure, while GHRH, rhGH and placebo did nothing. All of these are single acute doses measured in minutes to hours. None is an outcome trial and none tested repeated dosing.

The cardiac protection literature is mostly animal. In hypophysectomized rats, hexarelin 80 mcg/kg subcutaneously for 7 days prevented the worsening of ischemia and reperfusion damage caused by hypophysectomy, prevented rises in left ventricular end diastolic pressure and coronary perfusion pressure, and improved recovery of contractility; GH 400 mcg/kg did the same, and a GH-releasing peptide that does not bind the heart did not (PMID 10465272). In rats 4 weeks after coronary ligation, hexarelin 100 mcg/kg/day subcutaneously for 2 weeks lowered total peripheral resistance and raised stroke volume and cardiac output, similar to rhGH (PMID 10614623). In C57BL/6J mice after coronary ligation, hexarelin 0.3 mg/kg/day for 21 days improved left ventricular function at 14 days, reduced left ventricular mass, interstitial collagen and TGF-beta 1, and lowered troponin-I, IL-1 beta and TNF-alpha (PMID 29756411).

The binding target in heart was identified as CD36 in rat cardiac membranes. In perfused hearts hexarelin raised coronary perfusion pressure dose-dependently, an effect absent in CD36-null mice, which the authors link to coronary vasospasm rather than to benefit (PMID 11988484). Sellers describe the cardiac data as protective only. CD36, the binding target identified in heart, also mediated this vasoconstrictor effect in the perfused hearts.

Cardiac, volunteers: 7 men, ejection fraction 64.0% to 70.7% with hexarelin, no change with rhGH

Human study

Bisi G et al. J Endocrinol Invest. 1999;22(4):266-72. PMID 10342360.

Intravenous hexarelin raised left ventricular ejection fraction from 64.0% to 70.7% (p<0.03) without significant change in mean blood pressure or heart rate, rising at 15 minutes, peaking at 30 minutes and lasting up to 60 minutes. Recombinant human GH raised circulating GH to the same extent but did not change ejection fraction, which argues the inotropic effect is not GH-mediated. Hexarelin, but not rhGH, also raised cortisol.

Participants / model
7 male volunteers
Treatment
Intravenous hexarelin and intravenous recombinant human GH
Follow-up
Single acute doses, measured over up to 60 minutes
Study design
Clinical study using radionuclide angiocardiography
Funding
not stated in the source

A single acute dose measured in minutes. Not an outcome trial and not a repeated-dose study.

Read the original source
Cardiac series: GH-deficient men, cardiomyopathy and bypass surgery, single intravenous doses

Human study

Broglio F et al. Eur J Pharmacol. 2002;448(2-3):193-200. PMID 12144941.

In 7 adult men with GH deficiency and 9 male controls (PMID 10528131), intravenous hexarelin raised left ventricular ejection fraction in both groups (peak 57 versus 70%, P<0.05 versus baseline) without changing catecholamines, mean blood pressure or cardiac output, even though the GH response in the GH-deficient men was negligible (peak 1.9 versus 45.7 micrograms/L). In 8 patients with dilated and 5 with ischemic cardiomyopathy (PMID 11959048), hexarelin raised ejection fraction in the ischemic group (22.6 to 26.2%, P<0.05) but not in the dilated group despite a similar GH rise. In 24 men with coronary artery disease during bypass surgery under general anesthesia (PMID 12144941), hexarelin 2.0 mcg/kg raised ejection fraction, cardiac index and cardiac output within 10 minutes and for up to 90 minutes and lowered wedge pressure, while GHRH, rhGH and placebo did nothing.

Participants / model
7 men with GH deficiency and 9 male controls; 8 patients with dilated and 5 with ischemic cardiomyopathy; 24 men with coronary artery disease during bypass surgery
Treatment
Single intravenous hexarelin
Follow-up
Single acute doses, measured over minutes to hours
Study design
Three clinical studies; the source link is the bypass surgery study
Funding
not stated in the source

All of these are single acute doses measured in minutes to hours. None is an outcome trial and none tested repeated dosing.

Read the original source
Cardiac, animals: rat and mouse protection studies; CD36 target and coronary vasoconstriction

Animal study

Bodart V et al. Circ Res. 2002;90(8):844-9. PMID 11988484.

In hypophysectomized rats, hexarelin 80 mcg/kg subcutaneously for 7 days prevented the worsening of ischemia and reperfusion damage caused by hypophysectomy, prevented rises in left ventricular end diastolic pressure and coronary perfusion pressure, and improved recovery of contractility; GH 400 mcg/kg did the same, and a GH-releasing peptide that does not bind the heart did not (PMID 10465272). In rats 4 weeks after coronary ligation, hexarelin 100 mcg/kg/day subcutaneously for 2 weeks lowered total peripheral resistance and raised stroke volume and cardiac output, similar to rhGH (PMID 10614623). In C57BL/6J mice after coronary ligation, hexarelin 0.3 mg/kg/day for 21 days improved left ventricular function at 14 days, reduced left ventricular mass, interstitial collagen and TGF-beta 1, and lowered troponin-I, IL-1 beta and TNF-alpha (PMID 29756411). The binding target in heart was identified as CD36 in rat cardiac membranes; in perfused hearts hexarelin raised coronary perfusion pressure dose-dependently, an effect absent in CD36-null mice, which the authors link to coronary vasospasm rather than to benefit (PMID 11988484).

Participants / model
Hypophysectomized rats, rats after myocardial infarction, mice after myocardial infarction, rat cardiac membranes and CD36-null mice
Treatment
Subcutaneous hexarelin in rodents; perfused hearts ex vivo
Follow-up
7 days, 2 weeks and 21 days in the rodent studies
Study design
Original animal and mechanistic studies; the source link is the CD36 study
Funding
not stated in the source

The cardiac protection literature is mostly animal. These are rodent results and do not transfer to people.

Read the original source

Do the sellers' claims about growth, recovery and cardiac protection hold up?

Partly. Maximal GH pulses and fading response are supported, with prolactin and cortisol rising alongside GH. Growth and recovery are not: 16 weeks of twice-daily dosing in 12 healthy elderly people changed no body composition measure, and a PubMed search on 9 October 2026 found no study of training recovery or injury healing.

Sellers say hexarelin produces maximal GH pulses for growth and recovery, has cardiac protection research behind it, and is limited to short bursts by rapid desensitization.

Maximal GH pulses are supported, with the caveat that prolactin and cortisol rise at the same doses. Rapid desensitization is supported and is more specific than the sellers state: the GH response falls within 120 minutes of a second intravenous dose, falls about 45% over 16 weeks of twice-daily subcutaneous dosing and returns to baseline 4 weeks after stopping, but did not fall with 8 to 15 days of intermittent intranasal or oral dosing.

Growth and recovery are not supported. A PubMed search on 9 October 2026 for hexarelin with recovery, exercise, athletes, muscle injury, tendon, healing, body composition or lean body mass returned 42 records. None tested hexarelin for training recovery, muscle gain or injury healing in healthy or trained adults; they covered rodent and dog models, analytical chemistry, cardiac work and the elderly-subject studies already cited. The one human study that measured body composition on hexarelin, 16 weeks of twice-daily subcutaneous dosing in 12 healthy elderly people, found no change in total body fat, lean body mass or bone mineral density.

A related study of 21 healthy elderly subjects found that the GH response to subcutaneous hexarelin falls as fat mass rises (peak GH versus fat mass r=-0.72, P=0.0001), so people with more body fat had smaller GH responses in that study.

Cardiac protection splits. The acute ejection fraction rise is in people, the infarct, fibrosis and remodeling work is in rats and mice, and CD36 also mediated dose-dependent coronary vasoconstriction in perfused hearts.

Fat mass and GH response: 21 elderly subjects, r=-0.72; recovery search returned 42 records, none on recovery

Human study

Rahim A et al. Clin Endocrinol (Oxf). 1998;49(5):659-64. PMID 10197083.

In 21 healthy elderly subjects given subcutaneous hexarelin 1.5 mcg/kg, the GH response fell as fat mass rose (peak GH versus fat mass r=-0.72, P=0.0001). A PubMed search run on 9 October 2026 for hexarelin with recovery, exercise, athletes, muscle injury, tendon, healing, body composition or lean body mass returned 42 records. None tested hexarelin for training recovery, muscle gain or injury healing in healthy or trained adults; they covered rodent and dog models, analytical chemistry, cardiac work and the elderly-subject studies cited elsewhere on this page. The one human study that measured body composition on hexarelin, 16 weeks of twice-daily subcutaneous dosing in 12 healthy elderly people, found no change in total body fat, lean body mass or bone mineral density.

Participants / model
21 healthy elderly subjects for the fat mass finding; records returned for the search, not a population
Treatment
Subcutaneous hexarelin 1.5 mcg/kg for the fat mass study; not applicable for the search
Follow-up
Search run on 9 October 2026
Study design
Human study plus a literature search; the source link is the fat mass study
Funding
not stated in the source

A search result shows what the database returned on that date. It is not proof that no unindexed study exists.

Read the original source
16 weeks: 12 elderly people, GH AUC 19.1 to 10.5, recovered at 4 weeks off, body composition unchanged

Human study

Rahim A et al. J Clin Endocrinol Metab. 1998;83(5):1644-9. PMID 9589671.

Mean GH area under the curve was 19.1 micrograms/L.h at week 0, 13.1 at week 1, 12.3 at week 4 and 10.5 at week 16 (change over the study P=0.0003; week 4 P<0.05 and week 16 P<0.01 versus baseline). Four weeks after stopping, AUC rose to 19.4 micrograms/L.h, significantly above week 16 (P<0.05) and no different from week 0. Serum IGF-1 and IGFBP-3 did not change significantly over 20 weeks (P=0.24 and P=0.74). Total body fat, lean body mass and bone mineral density were unchanged at week 16 (P=0.6, 0.3 and 0.3).

Participants / model
12 healthy elderly individuals
Treatment
Subcutaneous hexarelin 1.5 mcg/kg twice daily
Follow-up
16 weeks of treatment, with a 4-week follow-up and measures over 20 weeks
Study design
Clinical study of chronic dosing
Funding
not stated in the source

Attenuation is partial and reversible, and on this schedule nothing downstream moved.

Read the original source
Not GH-selective: prolactin and cortisol rise at the doses that raise GH

Human study

Massoud AF et al. J Clin Endocrinol Metab. 1996;81(12):4338-41. PMID 8954038.

The GH dose-response curve plateaued at 140 mU/L with an ED50 of 0.48 mcg/kg, the prolactin curve plateaued at a 180% maximum rise from baseline with an ED50 of 0.39 mcg/kg, and cortisol showed a step increase of about 40% at 0.5 mcg/kg. Co-administering GHRH 1.0 mcg/kg with low-dose hexarelin 0.125 mcg/kg produced large GH release (115 mU/L) with a moderate prolactin rise and no cortisol rise.

Participants / model
Healthy adult males; number not stated in the source
Treatment
Intravenous hexarelin 0 to 1.0 mcg/kg, with and without GHRH
Follow-up
Single doses; duration not stated in the source
Study design
Clinical dose-response study
Funding
not stated in the source

Prolactin and cortisol move at the same doses that move GH.

Read the original source
Cardiac, animals: rat and mouse protection studies; CD36 target and coronary vasoconstriction

Animal study

Bodart V et al. Circ Res. 2002;90(8):844-9. PMID 11988484.

In hypophysectomized rats, hexarelin 80 mcg/kg subcutaneously for 7 days prevented the worsening of ischemia and reperfusion damage caused by hypophysectomy, prevented rises in left ventricular end diastolic pressure and coronary perfusion pressure, and improved recovery of contractility; GH 400 mcg/kg did the same, and a GH-releasing peptide that does not bind the heart did not (PMID 10465272). In rats 4 weeks after coronary ligation, hexarelin 100 mcg/kg/day subcutaneously for 2 weeks lowered total peripheral resistance and raised stroke volume and cardiac output, similar to rhGH (PMID 10614623). In C57BL/6J mice after coronary ligation, hexarelin 0.3 mg/kg/day for 21 days improved left ventricular function at 14 days, reduced left ventricular mass, interstitial collagen and TGF-beta 1, and lowered troponin-I, IL-1 beta and TNF-alpha (PMID 29756411). The binding target in heart was identified as CD36 in rat cardiac membranes; in perfused hearts hexarelin raised coronary perfusion pressure dose-dependently, an effect absent in CD36-null mice, which the authors link to coronary vasospasm rather than to benefit (PMID 11988484).

Participants / model
Hypophysectomized rats, rats after myocardial infarction, mice after myocardial infarction, rat cardiac membranes and CD36-null mice
Treatment
Subcutaneous hexarelin in rodents; perfused hearts ex vivo
Follow-up
7 days, 2 weeks and 21 days in the rodent studies
Study design
Original animal and mechanistic studies; the source link is the CD36 study
Funding
not stated in the source

The cardiac protection literature is mostly animal. These are rodent results and do not transfer to people.

Read the original source

How does hexarelin work, and what happens to it in the body?

Hexarelin releases more GH than GHRH at an equal intravenous dose and also raises prolactin and cortisol. Its heart effect does not depend on GH, and CD36 was identified as the binding target in heart. The sources reviewed give no half-life; biological bioavailability was 77.0% subcutaneous, 4.8% intranasal and 0.3% oral.

In the 12-volunteer study, 1 mcg/kg intravenous hexarelin gave about twice the GH response of 1 mcg/kg GHRH. The two were synergistic on first dosing, and that synergy was lost on repeated administration. With low-dose hexarelin 0.125 mcg/kg and GHRH 1.0 mcg/kg together, GH release was large (115 mU/L) with a moderate prolactin rise and no cortisol rise.

The inotropic effect looks independent of GH. Recombinant human GH raised circulating GH to the same extent as hexarelin but did not change ejection fraction, and in GH-deficient men with a negligible GH response hexarelin still raised ejection fraction. In rat cardiac membranes the binding target in heart was identified as CD36.

The receptor through which hexarelin releases GH is not described in the sources reviewed, so none is named here.

No half-life, Tmax or clearance for hexarelin is given in the sources reviewed. In 12 healthy young volunteers, biological bioavailability was 77.0% subcutaneous, 4.8% intranasal and 0.3% oral.

Routes and potency: 12 volunteers, GH AUC 3175 versus 1544 for GHRH, oral bioavailability 0.3%

Human study

Ghigo E et al. J Clin Endocrinol Metab. 1994;78(3):693-8. PMID 8126144.

GH release after 1 mcg/kg intravenous hexarelin (AUC 3175 micrograms/min/L) was about twice that after 1 mcg/kg GHRH (AUC 1544, P<0.001), and 2 mcg/kg gave a further increase (AUC 4422). Subcutaneous dosing was dose-dependent (AUC 3180 and 4459). Biological bioavailability was 77.0% subcutaneous, 4.8% intranasal and 0.3% oral.

Participants / model
12 healthy young volunteers
Treatment
Hexarelin intravenously (1 and 2 mcg/kg), subcutaneously (1.5 and 3 mcg/kg), intranasally (20 mcg/kg) and orally (20 and 40 mg), against intravenous saline and GHRH 1 mcg/kg
Follow-up
Single doses; total duration not stated in the source
Study design
Clinical study comparing routes against saline and GHRH
Funding
not stated in the source

The oral route is almost completely unavailable. Single doses in 12 people.

Read the original source
Not GH-selective: prolactin and cortisol rise at the doses that raise GH

Human study

Massoud AF et al. J Clin Endocrinol Metab. 1996;81(12):4338-41. PMID 8954038.

The GH dose-response curve plateaued at 140 mU/L with an ED50 of 0.48 mcg/kg, the prolactin curve plateaued at a 180% maximum rise from baseline with an ED50 of 0.39 mcg/kg, and cortisol showed a step increase of about 40% at 0.5 mcg/kg. Co-administering GHRH 1.0 mcg/kg with low-dose hexarelin 0.125 mcg/kg produced large GH release (115 mU/L) with a moderate prolactin rise and no cortisol rise.

Participants / model
Healthy adult males; number not stated in the source
Treatment
Intravenous hexarelin 0 to 1.0 mcg/kg, with and without GHRH
Follow-up
Single doses; duration not stated in the source
Study design
Clinical dose-response study
Funding
not stated in the source

Prolactin and cortisol move at the same doses that move GH.

Read the original source
Interval matters: lower peak GH after a 120-minute repeat, not significant at 60 minutes

Human study

Massoud AF et al. Clin Endocrinol (Oxf). 1996;44(5):555-62. PMID 8762732.

A second bolus of hexarelin, or of hexarelin with GHRH, given 120 minutes after the first produced lower peak GH secretion rates (P=0.03), while reductions after 60-minute boluses were not statistically significant. Hexarelin and GHRH were synergistic on first dosing, and that synergy was lost on repeated administration.

Participants / model
6 healthy adult males aged 25.4 to 34.1 years
Treatment
Single or paired intravenous boluses of hexarelin 1 mcg/kg, GHRH 1 mcg/kg, or both, 60 or 120 minutes apart
Follow-up
Single sessions
Study design
Clinical study with deconvolution analysis of peak GH secretion rate
Funding
not stated in the source

The attenuation depends on the interval between doses.

Read the original source
Cardiac, volunteers: 7 men, ejection fraction 64.0% to 70.7% with hexarelin, no change with rhGH

Human study

Bisi G et al. J Endocrinol Invest. 1999;22(4):266-72. PMID 10342360.

Intravenous hexarelin raised left ventricular ejection fraction from 64.0% to 70.7% (p<0.03) without significant change in mean blood pressure or heart rate, rising at 15 minutes, peaking at 30 minutes and lasting up to 60 minutes. Recombinant human GH raised circulating GH to the same extent but did not change ejection fraction, which argues the inotropic effect is not GH-mediated. Hexarelin, but not rhGH, also raised cortisol.

Participants / model
7 male volunteers
Treatment
Intravenous hexarelin and intravenous recombinant human GH
Follow-up
Single acute doses, measured over up to 60 minutes
Study design
Clinical study using radionuclide angiocardiography
Funding
not stated in the source

A single acute dose measured in minutes. Not an outcome trial and not a repeated-dose study.

Read the original source
Cardiac series: GH-deficient men, cardiomyopathy and bypass surgery, single intravenous doses

Human study

Broglio F et al. Eur J Pharmacol. 2002;448(2-3):193-200. PMID 12144941.

In 7 adult men with GH deficiency and 9 male controls (PMID 10528131), intravenous hexarelin raised left ventricular ejection fraction in both groups (peak 57 versus 70%, P<0.05 versus baseline) without changing catecholamines, mean blood pressure or cardiac output, even though the GH response in the GH-deficient men was negligible (peak 1.9 versus 45.7 micrograms/L). In 8 patients with dilated and 5 with ischemic cardiomyopathy (PMID 11959048), hexarelin raised ejection fraction in the ischemic group (22.6 to 26.2%, P<0.05) but not in the dilated group despite a similar GH rise. In 24 men with coronary artery disease during bypass surgery under general anesthesia (PMID 12144941), hexarelin 2.0 mcg/kg raised ejection fraction, cardiac index and cardiac output within 10 minutes and for up to 90 minutes and lowered wedge pressure, while GHRH, rhGH and placebo did nothing.

Participants / model
7 men with GH deficiency and 9 male controls; 8 patients with dilated and 5 with ischemic cardiomyopathy; 24 men with coronary artery disease during bypass surgery
Treatment
Single intravenous hexarelin
Follow-up
Single acute doses, measured over minutes to hours
Study design
Three clinical studies; the source link is the bypass surgery study
Funding
not stated in the source

All of these are single acute doses measured in minutes to hours. None is an outcome trial and none tested repeated dosing.

Read the original source
Cardiac, animals: rat and mouse protection studies; CD36 target and coronary vasoconstriction

Animal study

Bodart V et al. Circ Res. 2002;90(8):844-9. PMID 11988484.

In hypophysectomized rats, hexarelin 80 mcg/kg subcutaneously for 7 days prevented the worsening of ischemia and reperfusion damage caused by hypophysectomy, prevented rises in left ventricular end diastolic pressure and coronary perfusion pressure, and improved recovery of contractility; GH 400 mcg/kg did the same, and a GH-releasing peptide that does not bind the heart did not (PMID 10465272). In rats 4 weeks after coronary ligation, hexarelin 100 mcg/kg/day subcutaneously for 2 weeks lowered total peripheral resistance and raised stroke volume and cardiac output, similar to rhGH (PMID 10614623). In C57BL/6J mice after coronary ligation, hexarelin 0.3 mg/kg/day for 21 days improved left ventricular function at 14 days, reduced left ventricular mass, interstitial collagen and TGF-beta 1, and lowered troponin-I, IL-1 beta and TNF-alpha (PMID 29756411). The binding target in heart was identified as CD36 in rat cardiac membranes; in perfused hearts hexarelin raised coronary perfusion pressure dose-dependently, an effect absent in CD36-null mice, which the authors link to coronary vasospasm rather than to benefit (PMID 11988484).

Participants / model
Hypophysectomized rats, rats after myocardial infarction, mice after myocardial infarction, rat cardiac membranes and CD36-null mice
Treatment
Subcutaneous hexarelin in rodents; perfused hearts ex vivo
Follow-up
7 days, 2 weeks and 21 days in the rodent studies
Study design
Original animal and mechanistic studies; the source link is the CD36 study
Funding
not stated in the source

The cardiac protection literature is mostly animal. These are rodent results and do not transfer to people.

Read the original source

What safety concerns do the studies raise?

There is no approved label, and every human study enrolled 6 to 24 people, so adverse-event and long-term data are thin. Prolactin and cortisol rise at the doses that raise GH, and in perfused hearts hexarelin raised coronary perfusion pressure through CD36, an effect the authors link to coronary vasospasm.

There is no approved hexarelin product, so there is no prescribing label with warnings. Every human study cited on this page enrolled between 6 and 24 participants, and none was an outcome study. The longest subcutaneous study used 1.5 mcg/kg twice daily for 16 weeks, and no higher repeated subcutaneous dose appears in the sources reviewed.

Hexarelin is not GH-selective. Prolactin and cortisol rose at the same doses that raised GH in healthy adult males, and cortisol showed a step increase of about 40% at 0.5 mcg/kg. In the 7-volunteer cardiac study, hexarelin but not rhGH also raised cortisol. In the 24-hour study, repeated dosing did not change IGF-1, prolactin, ACTH or cortisol secretion, and a later intravenous dose after prior hexarelin did not raise ACTH or cortisol. In 7 elderly subjects on intranasal dosing for 8 days and 7 elderly women on oral dosing for 15 days, prolactin and cortisol levels did not change and no side effects occurred.

In perfused hearts, hexarelin raised coronary perfusion pressure dose-dependently, an effect absent in CD36-null mice, which the authors link to coronary vasospasm rather than to benefit. In the human cardiac studies, single intravenous doses raised ejection fraction without changing mean blood pressure or heart rate in the volunteer study, but all of those were single acute doses measured in minutes to hours, and none tested repeated dosing.

Searches, 9 October 2026: no FDA application, 0 registered trials

Regulatory record

U.S. Food and Drug Administration. openFDA Drugs@FDA substance-name queries for hexarelin and for examorelin, run on 9 October 2026, with a ClinicalTrials.gov term search for hexarelin the same day.

openFDA Drugs@FDA substance-name queries for hexarelin and for examorelin each returned no matching application on 9 October 2026, and a ClinicalTrials.gov term search for hexarelin returned 0 records on the same date. There is no approved hexarelin product and no registered trial in that registry.

Participants / model
Regulator and registry databases, not a population
Treatment
Exact substance-name and term searches
Follow-up
Searches run on 9 October 2026
Study design
FDA API query and trial registry search
Funding
not stated in the source

This is a US-scoped and registry-scoped statement, not a worldwide legal claim.

Read the original source
Not GH-selective: prolactin and cortisol rise at the doses that raise GH

Human study

Massoud AF et al. J Clin Endocrinol Metab. 1996;81(12):4338-41. PMID 8954038.

The GH dose-response curve plateaued at 140 mU/L with an ED50 of 0.48 mcg/kg, the prolactin curve plateaued at a 180% maximum rise from baseline with an ED50 of 0.39 mcg/kg, and cortisol showed a step increase of about 40% at 0.5 mcg/kg. Co-administering GHRH 1.0 mcg/kg with low-dose hexarelin 0.125 mcg/kg produced large GH release (115 mU/L) with a moderate prolactin rise and no cortisol rise.

Participants / model
Healthy adult males; number not stated in the source
Treatment
Intravenous hexarelin 0 to 1.0 mcg/kg, with and without GHRH
Follow-up
Single doses; duration not stated in the source
Study design
Clinical dose-response study
Funding
not stated in the source

Prolactin and cortisol move at the same doses that move GH.

Read the original source
24-hour secretion: 6 young men, GH burst mass up, no change in IGF-1, prolactin, ACTH or cortisol

Human study

Maccario M et al. Eur J Endocrinol. 2002;146(3):310-8. PMID 11888836.

Two or three daily subcutaneous injections of hexarelin 1.5 mcg/kg increased mean and integrated 24-hour serum GH to the same extent, amplifying GH secretory burst mass but not burst frequency, with no change in IGF-1, prolactin, ACTH or cortisol secretion. An intravenous 1 mcg/kg dose at the end of each 24-hour profile still raised GH, prolactin, ACTH and cortisol, but prior hexarelin blunted the GH response and abolished the ACTH and cortisol responses. Three injections a day gave the same 24-hour GH as two.

Participants / model
6 normal young men
Treatment
Subcutaneous hexarelin 1.5 mcg/kg two or three times daily, with an intravenous 1 mcg/kg challenge
Follow-up
24-hour profiles
Study design
Clinical study with deconvolution analysis of 24-hour secretion
Funding
not stated in the source

Prior hexarelin blunted the GH response to a later intravenous dose.

Read the original source
Intranasal 8 days and oral 15 days: GH response maintained, no side effects

Human study

Ghigo E et al. Eur J Endocrinol. 1996;135(4):407-12. PMID 8921821.

The acute GH response to the peptide was maintained after treatment. IGF-1 did not change significantly with intranasal treatment but IGFBP-3 rose (2.4 versus 1.6 mg/L, p<0.02); with oral treatment IGF-1 and IGFBP-3 both rose slightly (156.0 versus 141.6 micrograms/L, p<0.03, and 3.4 versus 3.1 mg/L, p<0.03). Neither schedule changed prolactin or cortisol levels or caused side effects.

Participants / model
7 elderly subjects (intranasal) and 7 elderly women (oral)
Treatment
Intranasal hexarelin 1.25 mg (about 18 mcg/kg) three times daily for 8 days; oral hexarelin 20 mg (about 300 mcg/kg) three times daily for 15 days
Follow-up
8 days (intranasal) and 15 days (oral)
Study design
Clinical study of short-term intermittent dosing
Funding
not stated in the source

Whether the GH response falls depends on schedule and route, not on the molecule alone.

Read the original source
Cardiac, volunteers: 7 men, ejection fraction 64.0% to 70.7% with hexarelin, no change with rhGH

Human study

Bisi G et al. J Endocrinol Invest. 1999;22(4):266-72. PMID 10342360.

Intravenous hexarelin raised left ventricular ejection fraction from 64.0% to 70.7% (p<0.03) without significant change in mean blood pressure or heart rate, rising at 15 minutes, peaking at 30 minutes and lasting up to 60 minutes. Recombinant human GH raised circulating GH to the same extent but did not change ejection fraction, which argues the inotropic effect is not GH-mediated. Hexarelin, but not rhGH, also raised cortisol.

Participants / model
7 male volunteers
Treatment
Intravenous hexarelin and intravenous recombinant human GH
Follow-up
Single acute doses, measured over up to 60 minutes
Study design
Clinical study using radionuclide angiocardiography
Funding
not stated in the source

A single acute dose measured in minutes. Not an outcome trial and not a repeated-dose study.

Read the original source
Cardiac, animals: rat and mouse protection studies; CD36 target and coronary vasoconstriction

Animal study

Bodart V et al. Circ Res. 2002;90(8):844-9. PMID 11988484.

In hypophysectomized rats, hexarelin 80 mcg/kg subcutaneously for 7 days prevented the worsening of ischemia and reperfusion damage caused by hypophysectomy, prevented rises in left ventricular end diastolic pressure and coronary perfusion pressure, and improved recovery of contractility; GH 400 mcg/kg did the same, and a GH-releasing peptide that does not bind the heart did not (PMID 10465272). In rats 4 weeks after coronary ligation, hexarelin 100 mcg/kg/day subcutaneously for 2 weeks lowered total peripheral resistance and raised stroke volume and cardiac output, similar to rhGH (PMID 10614623). In C57BL/6J mice after coronary ligation, hexarelin 0.3 mg/kg/day for 21 days improved left ventricular function at 14 days, reduced left ventricular mass, interstitial collagen and TGF-beta 1, and lowered troponin-I, IL-1 beta and TNF-alpha (PMID 29756411). The binding target in heart was identified as CD36 in rat cardiac membranes; in perfused hearts hexarelin raised coronary perfusion pressure dose-dependently, an effect absent in CD36-null mice, which the authors link to coronary vasospasm rather than to benefit (PMID 11988484).

Participants / model
Hypophysectomized rats, rats after myocardial infarction, mice after myocardial infarction, rat cardiac membranes and CD36-null mice
Treatment
Subcutaneous hexarelin in rodents; perfused hearts ex vivo
Follow-up
7 days, 2 weeks and 21 days in the rodent studies
Study design
Original animal and mechanistic studies; the source link is the CD36 study
Funding
not stated in the source

The cardiac protection literature is mostly animal. These are rodent results and do not transfer to people.

Read the original source

Why does hexarelin sit in C tier?

Hexarelin has real, well-characterized human pharmacology, but no approval, no registered trial, no outcome study and no human study larger than 24 people. That is a plausible mechanism with thin outcome data.

Hexarelin has a real and well-characterized human pharmacology. It releases more GH than GHRH, it works by four routes with 77.0% subcutaneous and 0.3% oral biological bioavailability, and its acute effect on ejection fraction has been shown in several small human studies, including in patients under anesthesia where rhGH and GHRH did nothing.

What it lacks is any approval in the FDA record, any registered trial on ClinicalTrials.gov as of 9 October 2026, any outcome study, and any human study larger than 24 participants.

Of the supplier claims, maximal GH pulses are supported with prolactin and cortisol rising alongside. Rapid desensitization is supported and depends on schedule and route. Growth and recovery have no support, and the only body composition study found no change at 16 weeks. Cardiac protection splits between an acute human effect and animal remodeling work.

Searches, 9 October 2026: no FDA application, 0 registered trials

Regulatory record

U.S. Food and Drug Administration. openFDA Drugs@FDA substance-name queries for hexarelin and for examorelin, run on 9 October 2026, with a ClinicalTrials.gov term search for hexarelin the same day.

openFDA Drugs@FDA substance-name queries for hexarelin and for examorelin each returned no matching application on 9 October 2026, and a ClinicalTrials.gov term search for hexarelin returned 0 records on the same date. There is no approved hexarelin product and no registered trial in that registry.

Participants / model
Regulator and registry databases, not a population
Treatment
Exact substance-name and term searches
Follow-up
Searches run on 9 October 2026
Study design
FDA API query and trial registry search
Funding
not stated in the source

This is a US-scoped and registry-scoped statement, not a worldwide legal claim.

Read the original source
Routes and potency: 12 volunteers, GH AUC 3175 versus 1544 for GHRH, oral bioavailability 0.3%

Human study

Ghigo E et al. J Clin Endocrinol Metab. 1994;78(3):693-8. PMID 8126144.

GH release after 1 mcg/kg intravenous hexarelin (AUC 3175 micrograms/min/L) was about twice that after 1 mcg/kg GHRH (AUC 1544, P<0.001), and 2 mcg/kg gave a further increase (AUC 4422). Subcutaneous dosing was dose-dependent (AUC 3180 and 4459). Biological bioavailability was 77.0% subcutaneous, 4.8% intranasal and 0.3% oral.

Participants / model
12 healthy young volunteers
Treatment
Hexarelin intravenously (1 and 2 mcg/kg), subcutaneously (1.5 and 3 mcg/kg), intranasally (20 mcg/kg) and orally (20 and 40 mg), against intravenous saline and GHRH 1 mcg/kg
Follow-up
Single doses; total duration not stated in the source
Study design
Clinical study comparing routes against saline and GHRH
Funding
not stated in the source

The oral route is almost completely unavailable. Single doses in 12 people.

Read the original source
Cardiac series: GH-deficient men, cardiomyopathy and bypass surgery, single intravenous doses

Human study

Broglio F et al. Eur J Pharmacol. 2002;448(2-3):193-200. PMID 12144941.

In 7 adult men with GH deficiency and 9 male controls (PMID 10528131), intravenous hexarelin raised left ventricular ejection fraction in both groups (peak 57 versus 70%, P<0.05 versus baseline) without changing catecholamines, mean blood pressure or cardiac output, even though the GH response in the GH-deficient men was negligible (peak 1.9 versus 45.7 micrograms/L). In 8 patients with dilated and 5 with ischemic cardiomyopathy (PMID 11959048), hexarelin raised ejection fraction in the ischemic group (22.6 to 26.2%, P<0.05) but not in the dilated group despite a similar GH rise. In 24 men with coronary artery disease during bypass surgery under general anesthesia (PMID 12144941), hexarelin 2.0 mcg/kg raised ejection fraction, cardiac index and cardiac output within 10 minutes and for up to 90 minutes and lowered wedge pressure, while GHRH, rhGH and placebo did nothing.

Participants / model
7 men with GH deficiency and 9 male controls; 8 patients with dilated and 5 with ischemic cardiomyopathy; 24 men with coronary artery disease during bypass surgery
Treatment
Single intravenous hexarelin
Follow-up
Single acute doses, measured over minutes to hours
Study design
Three clinical studies; the source link is the bypass surgery study
Funding
not stated in the source

All of these are single acute doses measured in minutes to hours. None is an outcome trial and none tested repeated dosing.

Read the original source
16 weeks: 12 elderly people, GH AUC 19.1 to 10.5, recovered at 4 weeks off, body composition unchanged

Human study

Rahim A et al. J Clin Endocrinol Metab. 1998;83(5):1644-9. PMID 9589671.

Mean GH area under the curve was 19.1 micrograms/L.h at week 0, 13.1 at week 1, 12.3 at week 4 and 10.5 at week 16 (change over the study P=0.0003; week 4 P<0.05 and week 16 P<0.01 versus baseline). Four weeks after stopping, AUC rose to 19.4 micrograms/L.h, significantly above week 16 (P<0.05) and no different from week 0. Serum IGF-1 and IGFBP-3 did not change significantly over 20 weeks (P=0.24 and P=0.74). Total body fat, lean body mass and bone mineral density were unchanged at week 16 (P=0.6, 0.3 and 0.3).

Participants / model
12 healthy elderly individuals
Treatment
Subcutaneous hexarelin 1.5 mcg/kg twice daily
Follow-up
16 weeks of treatment, with a 4-week follow-up and measures over 20 weeks
Study design
Clinical study of chronic dosing
Funding
not stated in the source

Attenuation is partial and reversible, and on this schedule nothing downstream moved.

Read the original source
Fat mass and GH response: 21 elderly subjects, r=-0.72; recovery search returned 42 records, none on recovery

Human study

Rahim A et al. Clin Endocrinol (Oxf). 1998;49(5):659-64. PMID 10197083.

In 21 healthy elderly subjects given subcutaneous hexarelin 1.5 mcg/kg, the GH response fell as fat mass rose (peak GH versus fat mass r=-0.72, P=0.0001). A PubMed search run on 9 October 2026 for hexarelin with recovery, exercise, athletes, muscle injury, tendon, healing, body composition or lean body mass returned 42 records. None tested hexarelin for training recovery, muscle gain or injury healing in healthy or trained adults; they covered rodent and dog models, analytical chemistry, cardiac work and the elderly-subject studies cited elsewhere on this page. The one human study that measured body composition on hexarelin, 16 weeks of twice-daily subcutaneous dosing in 12 healthy elderly people, found no change in total body fat, lean body mass or bone mineral density.

Participants / model
21 healthy elderly subjects for the fat mass finding; records returned for the search, not a population
Treatment
Subcutaneous hexarelin 1.5 mcg/kg for the fat mass study; not applicable for the search
Follow-up
Search run on 9 October 2026
Study design
Human study plus a literature search; the source link is the fat mass study
Funding
not stated in the source

A search result shows what the database returned on that date. It is not proof that no unindexed study exists.

Read the original source

Studies and sources

PubChem: hexarelin peptide and acetate salt identity

Chemical identity record

National Library of Medicine. PubChem compound record CID 6918297 (hexarelin), with the acetate salt at CID 88325556.

Hexarelin, also called examorelin, is a synthetic hexapeptide, His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2: PubChem CID 6918297, C47H58N12O6, molecular weight 887.0, CAS 140703-51-1. Listed synonyms include EP-23905 and MF-6003. The acetate salt is a separate identity: CID 88325556, C49H62N12O8, molecular weight 947.1, CAS 208251-52-9.

Participants / model
Chemical identity, not a clinical population
Treatment
Defined hexapeptide and acetate salt
Follow-up
Not applicable
Study design
NLM chemical record
Funding
not stated in the source

Vendor material is normally the acetate, so a milligram of vendor powder is not a milligram of peptide.

Read the original source
Routes and potency: 12 volunteers, GH AUC 3175 versus 1544 for GHRH, oral bioavailability 0.3%

Human study

Ghigo E et al. J Clin Endocrinol Metab. 1994;78(3):693-8. PMID 8126144.

GH release after 1 mcg/kg intravenous hexarelin (AUC 3175 micrograms/min/L) was about twice that after 1 mcg/kg GHRH (AUC 1544, P<0.001), and 2 mcg/kg gave a further increase (AUC 4422). Subcutaneous dosing was dose-dependent (AUC 3180 and 4459). Biological bioavailability was 77.0% subcutaneous, 4.8% intranasal and 0.3% oral.

Participants / model
12 healthy young volunteers
Treatment
Hexarelin intravenously (1 and 2 mcg/kg), subcutaneously (1.5 and 3 mcg/kg), intranasally (20 mcg/kg) and orally (20 and 40 mg), against intravenous saline and GHRH 1 mcg/kg
Follow-up
Single doses; total duration not stated in the source
Study design
Clinical study comparing routes against saline and GHRH
Funding
not stated in the source

The oral route is almost completely unavailable. Single doses in 12 people.

Read the original source
Not GH-selective: prolactin and cortisol rise at the doses that raise GH

Human study

Massoud AF et al. J Clin Endocrinol Metab. 1996;81(12):4338-41. PMID 8954038.

The GH dose-response curve plateaued at 140 mU/L with an ED50 of 0.48 mcg/kg, the prolactin curve plateaued at a 180% maximum rise from baseline with an ED50 of 0.39 mcg/kg, and cortisol showed a step increase of about 40% at 0.5 mcg/kg. Co-administering GHRH 1.0 mcg/kg with low-dose hexarelin 0.125 mcg/kg produced large GH release (115 mU/L) with a moderate prolactin rise and no cortisol rise.

Participants / model
Healthy adult males; number not stated in the source
Treatment
Intravenous hexarelin 0 to 1.0 mcg/kg, with and without GHRH
Follow-up
Single doses; duration not stated in the source
Study design
Clinical dose-response study
Funding
not stated in the source

Prolactin and cortisol move at the same doses that move GH.

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Within-day fade: GH AUC 1424 to 286.6 ng/mL/h on a second bolus 120 minutes later

Human study

Sartorio A et al. J Endocrinol Invest. 1995;18(9):718-22. PMID 8719303.

The GH net incremental AUC fell from 1424 ng/mL/h after the first hexarelin bolus to 286.6 ng/mL/h after the second (p<0.02), although that second response was still significantly larger than the response to a second GHRH bolus (74.5 ng/mL/h). Repeated hexarelin reduces GH responsiveness within hours, and does so less than repeated GHRH does.

Participants / model
6 normal adults
Treatment
Two intravenous 1 mcg/kg hexarelin boluses 120 minutes apart
Follow-up
Single session
Study design
Clinical study of repeated boluses
Funding
not stated in the source

The first demonstration of acute within-day attenuation in the sources reviewed.

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Interval matters: lower peak GH after a 120-minute repeat, not significant at 60 minutes

Human study

Massoud AF et al. Clin Endocrinol (Oxf). 1996;44(5):555-62. PMID 8762732.

A second bolus of hexarelin, or of hexarelin with GHRH, given 120 minutes after the first produced lower peak GH secretion rates (P=0.03), while reductions after 60-minute boluses were not statistically significant. Hexarelin and GHRH were synergistic on first dosing, and that synergy was lost on repeated administration.

Participants / model
6 healthy adult males aged 25.4 to 34.1 years
Treatment
Single or paired intravenous boluses of hexarelin 1 mcg/kg, GHRH 1 mcg/kg, or both, 60 or 120 minutes apart
Follow-up
Single sessions
Study design
Clinical study with deconvolution analysis of peak GH secretion rate
Funding
not stated in the source

The attenuation depends on the interval between doses.

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16 weeks: 12 elderly people, GH AUC 19.1 to 10.5, recovered at 4 weeks off, body composition unchanged

Human study

Rahim A et al. J Clin Endocrinol Metab. 1998;83(5):1644-9. PMID 9589671.

Mean GH area under the curve was 19.1 micrograms/L.h at week 0, 13.1 at week 1, 12.3 at week 4 and 10.5 at week 16 (change over the study P=0.0003; week 4 P<0.05 and week 16 P<0.01 versus baseline). Four weeks after stopping, AUC rose to 19.4 micrograms/L.h, significantly above week 16 (P<0.05) and no different from week 0. Serum IGF-1 and IGFBP-3 did not change significantly over 20 weeks (P=0.24 and P=0.74). Total body fat, lean body mass and bone mineral density were unchanged at week 16 (P=0.6, 0.3 and 0.3).

Participants / model
12 healthy elderly individuals
Treatment
Subcutaneous hexarelin 1.5 mcg/kg twice daily
Follow-up
16 weeks of treatment, with a 4-week follow-up and measures over 20 weeks
Study design
Clinical study of chronic dosing
Funding
not stated in the source

Attenuation is partial and reversible, and on this schedule nothing downstream moved.

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Intranasal 8 days and oral 15 days: GH response maintained, no side effects

Human study

Ghigo E et al. Eur J Endocrinol. 1996;135(4):407-12. PMID 8921821.

The acute GH response to the peptide was maintained after treatment. IGF-1 did not change significantly with intranasal treatment but IGFBP-3 rose (2.4 versus 1.6 mg/L, p<0.02); with oral treatment IGF-1 and IGFBP-3 both rose slightly (156.0 versus 141.6 micrograms/L, p<0.03, and 3.4 versus 3.1 mg/L, p<0.03). Neither schedule changed prolactin or cortisol levels or caused side effects.

Participants / model
7 elderly subjects (intranasal) and 7 elderly women (oral)
Treatment
Intranasal hexarelin 1.25 mg (about 18 mcg/kg) three times daily for 8 days; oral hexarelin 20 mg (about 300 mcg/kg) three times daily for 15 days
Follow-up
8 days (intranasal) and 15 days (oral)
Study design
Clinical study of short-term intermittent dosing
Funding
not stated in the source

Whether the GH response falls depends on schedule and route, not on the molecule alone.

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Short children: 7 children, 6 to 10 months intranasal, GH response halved, growth velocity 5.3 to 7.4 cm/year

Human study

Klinger B et al. Eur J Endocrinol. 1996;134(6):716-9. PMID 8766941.

The mean peak GH rise to an intranasal bolus fell from 70.6 mU/L before treatment to 34.1 mU/L after 7 days (p<0.002) and stayed near that level at 6 months (37.5 mU/L, p<0.03). The response to an intravenous bolus fell from 84.8 to 19.8 mU/L (p<0.05) and recovered to 42.1 mU/L three months after stopping (p<0.005). Growth velocity rose from 5.3 to 7.4 cm/year (p<0.005).

Participants / model
7 prepubertal constitutionally short children (mean age 7.6 years)
Treatment
Intranasal hexarelin 60 mcg/kg three times daily
Follow-up
6 to 10 months
Study design
Clinical study of long-term intranasal dosing
Funding
not stated in the source

Partial suppression of the GH response did not abolish the clinical effect in this population. This was a group of short children, not healthy adults.

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24-hour secretion: 6 young men, GH burst mass up, no change in IGF-1, prolactin, ACTH or cortisol

Human study

Maccario M et al. Eur J Endocrinol. 2002;146(3):310-8. PMID 11888836.

Two or three daily subcutaneous injections of hexarelin 1.5 mcg/kg increased mean and integrated 24-hour serum GH to the same extent, amplifying GH secretory burst mass but not burst frequency, with no change in IGF-1, prolactin, ACTH or cortisol secretion. An intravenous 1 mcg/kg dose at the end of each 24-hour profile still raised GH, prolactin, ACTH and cortisol, but prior hexarelin blunted the GH response and abolished the ACTH and cortisol responses. Three injections a day gave the same 24-hour GH as two.

Participants / model
6 normal young men
Treatment
Subcutaneous hexarelin 1.5 mcg/kg two or three times daily, with an intravenous 1 mcg/kg challenge
Follow-up
24-hour profiles
Study design
Clinical study with deconvolution analysis of 24-hour secretion
Funding
not stated in the source

Prior hexarelin blunted the GH response to a later intravenous dose.

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Cardiac, volunteers: 7 men, ejection fraction 64.0% to 70.7% with hexarelin, no change with rhGH

Human study

Bisi G et al. J Endocrinol Invest. 1999;22(4):266-72. PMID 10342360.

Intravenous hexarelin raised left ventricular ejection fraction from 64.0% to 70.7% (p<0.03) without significant change in mean blood pressure or heart rate, rising at 15 minutes, peaking at 30 minutes and lasting up to 60 minutes. Recombinant human GH raised circulating GH to the same extent but did not change ejection fraction, which argues the inotropic effect is not GH-mediated. Hexarelin, but not rhGH, also raised cortisol.

Participants / model
7 male volunteers
Treatment
Intravenous hexarelin and intravenous recombinant human GH
Follow-up
Single acute doses, measured over up to 60 minutes
Study design
Clinical study using radionuclide angiocardiography
Funding
not stated in the source

A single acute dose measured in minutes. Not an outcome trial and not a repeated-dose study.

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Cardiac series: GH-deficient men, cardiomyopathy and bypass surgery, single intravenous doses

Human study

Broglio F et al. Eur J Pharmacol. 2002;448(2-3):193-200. PMID 12144941.

In 7 adult men with GH deficiency and 9 male controls (PMID 10528131), intravenous hexarelin raised left ventricular ejection fraction in both groups (peak 57 versus 70%, P<0.05 versus baseline) without changing catecholamines, mean blood pressure or cardiac output, even though the GH response in the GH-deficient men was negligible (peak 1.9 versus 45.7 micrograms/L). In 8 patients with dilated and 5 with ischemic cardiomyopathy (PMID 11959048), hexarelin raised ejection fraction in the ischemic group (22.6 to 26.2%, P<0.05) but not in the dilated group despite a similar GH rise. In 24 men with coronary artery disease during bypass surgery under general anesthesia (PMID 12144941), hexarelin 2.0 mcg/kg raised ejection fraction, cardiac index and cardiac output within 10 minutes and for up to 90 minutes and lowered wedge pressure, while GHRH, rhGH and placebo did nothing.

Participants / model
7 men with GH deficiency and 9 male controls; 8 patients with dilated and 5 with ischemic cardiomyopathy; 24 men with coronary artery disease during bypass surgery
Treatment
Single intravenous hexarelin
Follow-up
Single acute doses, measured over minutes to hours
Study design
Three clinical studies; the source link is the bypass surgery study
Funding
not stated in the source

All of these are single acute doses measured in minutes to hours. None is an outcome trial and none tested repeated dosing.

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Cardiac, animals: rat and mouse protection studies; CD36 target and coronary vasoconstriction

Animal study

Bodart V et al. Circ Res. 2002;90(8):844-9. PMID 11988484.

In hypophysectomized rats, hexarelin 80 mcg/kg subcutaneously for 7 days prevented the worsening of ischemia and reperfusion damage caused by hypophysectomy, prevented rises in left ventricular end diastolic pressure and coronary perfusion pressure, and improved recovery of contractility; GH 400 mcg/kg did the same, and a GH-releasing peptide that does not bind the heart did not (PMID 10465272). In rats 4 weeks after coronary ligation, hexarelin 100 mcg/kg/day subcutaneously for 2 weeks lowered total peripheral resistance and raised stroke volume and cardiac output, similar to rhGH (PMID 10614623). In C57BL/6J mice after coronary ligation, hexarelin 0.3 mg/kg/day for 21 days improved left ventricular function at 14 days, reduced left ventricular mass, interstitial collagen and TGF-beta 1, and lowered troponin-I, IL-1 beta and TNF-alpha (PMID 29756411). The binding target in heart was identified as CD36 in rat cardiac membranes; in perfused hearts hexarelin raised coronary perfusion pressure dose-dependently, an effect absent in CD36-null mice, which the authors link to coronary vasospasm rather than to benefit (PMID 11988484).

Participants / model
Hypophysectomized rats, rats after myocardial infarction, mice after myocardial infarction, rat cardiac membranes and CD36-null mice
Treatment
Subcutaneous hexarelin in rodents; perfused hearts ex vivo
Follow-up
7 days, 2 weeks and 21 days in the rodent studies
Study design
Original animal and mechanistic studies; the source link is the CD36 study
Funding
not stated in the source

The cardiac protection literature is mostly animal. These are rodent results and do not transfer to people.

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Fat mass and GH response: 21 elderly subjects, r=-0.72; recovery search returned 42 records, none on recovery

Human study

Rahim A et al. Clin Endocrinol (Oxf). 1998;49(5):659-64. PMID 10197083.

In 21 healthy elderly subjects given subcutaneous hexarelin 1.5 mcg/kg, the GH response fell as fat mass rose (peak GH versus fat mass r=-0.72, P=0.0001). A PubMed search run on 9 October 2026 for hexarelin with recovery, exercise, athletes, muscle injury, tendon, healing, body composition or lean body mass returned 42 records. None tested hexarelin for training recovery, muscle gain or injury healing in healthy or trained adults; they covered rodent and dog models, analytical chemistry, cardiac work and the elderly-subject studies cited elsewhere on this page. The one human study that measured body composition on hexarelin, 16 weeks of twice-daily subcutaneous dosing in 12 healthy elderly people, found no change in total body fat, lean body mass or bone mineral density.

Participants / model
21 healthy elderly subjects for the fat mass finding; records returned for the search, not a population
Treatment
Subcutaneous hexarelin 1.5 mcg/kg for the fat mass study; not applicable for the search
Follow-up
Search run on 9 October 2026
Study design
Human study plus a literature search; the source link is the fat mass study
Funding
not stated in the source

A search result shows what the database returned on that date. It is not proof that no unindexed study exists.

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Why is Hexarelin in C tier?

C fits a plausible mechanism with thin outcome data. Hexarelin releases more GH than GHRH in small human studies and acutely raises ejection fraction, but it has no approval, no registered trial on ClinicalTrials.gov as of 9 October 2026, no outcome study and no human study larger than 24 participants. The growth and recovery claim has no study behind it.