Hexarelin

Examorelin, EP 23905, His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2

Growth hormone axis

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Summary

Class: Synthetic hexapeptide growth hormone secretagogue; GHRP-6 analogue with a methylated tryptophan for stability; GHS-R1a agonist that also binds CD36
Mechanism: Releases a large pulse of growth hormone via the ghrelin receptor; the most potent injectable GHRP, but also raises cortisol and prolactin and desensitises with repeated use
Routes studied: Intravenous, subcutaneous, intranasal and oral (human); subcutaneous (community)
Dose range reported: Human studies: 1–2 µg/kg IV; ~20 µg/kg intranasal; ~1.5–3 mg subcutaneous daily or twice daily in chronic studies. Community: 100–200 µg subcutaneous, 1–3 times daily. No approved human dose
Half-life: Roughly 55–70 minutes reported after IV dosing †; GH pulse lasts 2–3 hours
Storage: Lyophilised: refrigerate, protect from light. Reconstituted: refrigerate, use within ~4 weeks (community practice)
Regulatory status: Not approved for any indication; development for GH deficiency stopped in the late 1990s

Doses are as reported in studies or by the community — never recommendations.

1What it is

Hexarelin is a close chemical cousin of GHRP-6 developed in the early 1990s by Romano Deghenghi at Europeptides. The single change — a 2-methyl group on the D-tryptophan — makes the molecule more stable and roughly as potent or more potent at releasing GH. It is fully synthetic.

It was studied extensively in Italy and the UK through the 1990s, including in children with short stature, adults with GH deficiency and people with heart disease, and reached early clinical development. Two findings held it back: the GH response fades with continuous use, and the rise in IGF-1 is modest despite the large acute GH peaks. Development as a medicine stopped around 2000.

Hexarelin's second life in research came from its cardiac effects, which appear to be partly independent of GH and mediated through the CD36 receptor in heart muscle. In the community it is used as a "stronger" GHRP, typically in short cycles because of desensitisation.

2How it's thought to work

GH release. activation in the pituitary, with hypothalamic amplification, like GHRP-6. Synergistic with GHRH.

Cortisol and prolactin. hexarelin raises ACTH/cortisol and prolactin more than ipamorelin and similarly to or more than GHRP-6.

Appetite. ghrelin-receptor agonism increases hunger, though community reports describe it as less marked than GHRP-6.

Heart. binds CD36 on cardiomyocytes and coronary vessels; rodent work shows reduced ischaemia–reperfusion injury and improved contractility that persists in GH-deficient animals, pointing to a direct cardiac effect.

Desensitisation. repeated dosing down-regulates the GH response within weeks, while cortisol and prolactin responses decline too.

A ghrelin receptor agonist with the strongest growth hormone release of the GHRP series, and the fastest loss of effect with repeated use.Schematic — not to scale

3What the research shows

GH release

Dose–response studies in healthy adults show robust GH release after IV, , intranasal and oral routes, with oral bioavailability low but measurable (Ghigo 1994, J Clin Endocrinol Metab; Imbimbo 1994, Eur J Clin Pharmacol). Peak GH after 2 µg/kg IV is comparable to or larger than GHRH. [2][3]

Chronic dosing in adults

Sixteen weeks of twice-daily subcutaneous hexarelin in healthy adults produced an attenuated GH response by week 4 that partially recovered after stopping; IGF-1 rose only modestly (Rahim, O'Neill & Shalet 1998, J Clin Endocrinol Metab). A companion study found cortisol and prolactin responses also declined over time (Rahim 1998, Clin Endocrinol). These are the key human data on what happens with sustained use of a GHRP. [4][5]

Short stature in children

Intranasal hexarelin in short children maintained GH responsiveness over months in some reports despite partial desensitisation, with modest growth-velocity changes (Klinger 1996, Eur J Endocrinol). Development did not continue. [6]

Graded B (acute human) / C (chronic animal)

Cardiac effects

In healthy volunteers and GH-deficient adults, single IV hexarelin doses acutely increased left-ventricular ejection fraction, an effect not reproduced by GH itself (Bisi 1999, J Endocrinol Invest). In rats, hexarelin protected against ischaemia–reperfusion injury independently of GH (Locatelli 1999, Endocrinology), and the CD36 receptor was identified as mediating coronary effects (Bodart 2002, Circ Res). No chronic human cardiac trial. [7][8][9]

Body composition, recovery

No published human body-composition or strength trials. Community use for these purposes rests on GH physiology and anecdote.

4Reported side effects and interactions

Literature-reported

Flushing, transient sleepiness, mild increases in cortisol and prolactin after each dose, occasional nausea. Well tolerated in the short term. Reduced GH response (tachyphylaxis) with chronic dosing is the main documented limitation rather than a side effect.

Community-reported

flushing, warmth and lightheadedness after injection, hunger (less than GHRP-6), water retention, tingling in hands, lethargy, headache; some report raised prolactin-type symptoms with frequent dosing.

Theoretical. chronic cortisol stimulation; GH/IGF-1-related reduction in insulin sensitivity; concern in active malignancy; unknown long-term effects of CD36 agonism.

Interactions. synergistic with GHRH analogues; additive with other GHRPs; glucose-lowering medicines may need monitoring.

Markers researchers commonly monitor

Marker	Why it's watched
IGF-1	the integrated marker of GH effect; in the Rahim study it rose only modestly, so a flat IGF-1 is expected rather than alarming.
Fasting glucose and HbA1c	GH antagonises insulin.
Cortisol (morning) and prolactin	both are stimulated by hexarelin; relevant with frequent dosing.
Resting heart rate and blood pressure	given the direct cardiac actions; no established thresholds.
Fluid retention and weight	common early on.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Typically supplied in 2 mg or 5 mg vials. with , swirl gently. Community practice is short cycles (often 4–6 weeks) because of desensitisation.

Open in calculator, pre-loaded →

6Commonly studied alongside

GHRH analogues (CJC-1295 / mod GRF 1-29, sermorelin) for synergy. Compared with GHRP-6, GHRP-2 and ipamorelin in receptor-selectivity studies.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved. Compounding status under the 2023 bulk-substances review: †
European Union	Not authorised
United Kingdom	Not licensed
Australia	Prescription-only classification as a GH secretagogue; not an approved product †
South Africa	Not registered
Sport (WADA)	Prohibited (S2 — GHRPs including hexarelin are named)

8Open questions

Can intermittent dosing avoid desensitisation, as community practice assumes? Not tested.
Do the acute cardiac effects translate into any chronic benefit or harm?
Long-term effects of repeated cortisol and prolactin stimulation.

9References

1Deghenghi R et al. (1994). GH-releasing activity of hexarelin, a new growth hormone releasing peptide, in infant and adult rats. Life Sci. PubMed · DOI
2Ghigo E et al. (1994). Growth hormone-releasing activity of hexarelin, a new synthetic hexapeptide, after intravenous, subcutaneous, intranasal, and oral administration in man. J Clin Endocrinol Metab. PubMed · DOI
3Imbimbo BP et al. (1994). Growth hormone-releasing activity of hexarelin in humans: a dose-response study. Eur J Clin Pharmacol. PubMed · DOI
4Rahim A, O'Neill PA, Shalet SM (1998). Growth hormone status during long-term hexarelin therapy. J Clin Endocrinol Metab. PubMed · DOI
5Rahim A, O'Neill PA, Shalet SM (1998). The effect of chronic hexarelin administration on the pituitary-adrenal axis and prolactin. Clin Endocrinol (Oxf). PubMed · DOI
6Klinger B et al. (1996). Desensitization from long-term intranasal treatment with hexarelin does not interfere with the biological effects of this growth hormone-releasing peptide in short children. Eur J Endocrinol. PubMed · DOI
7Bisi G et al. (1999). Acute cardiovascular and hormonal effects of GH and hexarelin, a synthetic GH-releasing peptide, in humans. J Endocrinol Invest. PubMed · DOI
8Locatelli V et al. (1999). Growth hormone-independent cardioprotective effects of hexarelin in the rat. Endocrinology. PubMed · DOI
9Bodart V et al. (2002). CD36 mediates the cardiovascular action of growth hormone-releasing peptides in the heart. Circ Res. PubMed · DOI

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

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11Page history

25 Oct 2026Profile published — awaiting medical review

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