Hexarelin

Hexarelin (also called examorelin) is a growth hormone releaser that prompts the pituitary gland to release growth hormone by acting on the ghrelin (hunger hormone) receptor. It's the most potent of the older growth hormone releasers in its class, but it also raises cortisol and prolactin more than newer options and its growth-hormone effect fades with repeated use. Its developer stopped clinical development before it reached approval; it's not FDA-approved, sold only as a research peptide, and banned in drug-tested sport.

Hexarelin has been studied to raise growth hormone. Dose-response studies showed it reliably triggers growth-hormone release but also raises cortisol and prolactin dose-dependently, and a 16-week study found the growth-hormone response faded over time (tachyphylaxis) and returned to normal after stopping. The body-composition and recovery uses people pursue are not supported by large clinical trials.

Not FDA-approved for any indication. Mediolanum Farmaceutici advanced hexarelin through Phase II clinical evaluation in GH-axis indications and as an investigational cardioprotective agent in the 1990s, but clinical development was discontinued before market approval — the combination of GH-response tachyphylaxis with sustained dosing and the dose-dependent cortisol/prolactin elevation limited clinical utility for sustained therapeutic use. Available exclusively as a research peptide through unregulated research-peptide supply chains. Not DEA-scheduled. WADA-banned in regulated sport — explicitly named under Section S2.2.4 (Growth Hormone Releasing Factors → GH-releasing peptides subsection) of the 2026 Prohibited List using the INN spelling "examorelin (hexarelin)", alongside alexamorelin, GHRP-1, GHRP-2 (pralmorelin), GHRP-3, GHRP-4, GHRP-5, and GHRP-6.[⁶]

Hexarelin is not FDA-approved and is banned in regulated sport (WADA). VialWise is a research and educational reference, not medical advice — consult a licensed professional.

⚠️ For research and educational purposes only. Hexarelin (examorelin) is not approved by the FDA for any indication. Mediolanum Farmaceutici discontinued clinical development before market approval. It is available exclusively as a research peptide through unregulated supply chains. Information in this entry is informational, not medical advice. Always confirm dose calculations with the in-app calculator and consult appropriate professional guidance before any protocol decisions.

⚠️ Precision matters at low doses. Hexarelin is dosed in micrograms (mcg), not milligrams. Typical research-community doses ( per dose) at typical reconstitution concentrations ( vial / 1 mL BAC water = =) produce small draws in the range on a U-100 syringe. Lower-concentration setups ( / 2 mL =) produce draws — generally easier precision. Always verify draws against the in-app calculator. Same precision concern as Ipamorelin and the other GHS-class peptides.

⚠️ Hexarelin has high acute GH-stimulating potency among the older GHRPs, but its tolerability profile limits sustained use. Three load-bearing pharmacological detrents distinguish hexarelin from the cleaner ghrelin-receptor-agonist alternatives: - Dose-dependent cortisol elevation. The Massoud 1996 dose-response study found cortisol elevation begins at hexarelin doses ≥ IV (a step increase to ~40% above baseline at this dose).[³] At typical research-community SC doses (~ in a 70-kg adult), cortisol elevation is a meaningful pharmacological concern. - Dose-dependent prolactin elevation. The same Massoud 1996 study found PRL elevation at all doses tested, with maximum response (~180% rise from baseline) IV.[³] Sustained elevation is a particular concern in research-community contexts where hexarelin is used long-term for muscle/recovery purposes. - GH-response tachyphylaxis (research-community reports) vs the published cortisol-axis finding. Research-community reports — unverified, not from published trials — cite GH-response decline of 50–80% within 2–4 weeks of daily use. The one published chronic-dosing study measured something different: in the Rahim 1999 study (twice-daily SC for 16 weeks), participants' cortisol-AUC response decreased from baseline (1506 ± 77 nmol/L/h) to week 16 (1222 ± 92 nmol/L/h — a ~19% reduction), returning to baseline (1586 ± 58 nmol/L/h) 4 weeks after discontinuation.[⁴] That is a pituitary-adrenal-axis adaptation, not a direct measurement of GH tachyphylaxis — Rahim did not measure GH response, and the authors judged the cortisol-AUC change unlikely to be of clinical significance, concluding that over-stimulation of the pituitary-adrenal axis and prolactin secretion did not occur. The two figures should not be equated. The Massoud 1996 study also established that low-dose hexarelin combined with GHRH(1-29)NH2 produces massive synergistic GH release without cortisol elevation and with minimal prolactin elevation.[³] This finding is the basis for combining hexarelin with a GHRH analog (CJC-1295 no-DAC, sermorelin, tesamorelin) at low doses rather than running hexarelin alone at higher doses — the synergistic combination produces stronger GH response with cleaner side-effect profile.

⚠️ Hexarelin vs Ipamorelin — third GHS-axis entry warrants explicit cluster context. The library now has three ghrelin-receptor-agonist entries with substantially different pharmacology: - Ipamorelin — pentapeptide; the cleanest GHRP for clinical use; minimal cortisol/prolactin elevation at any dose; minimal tachyphylaxis. The default research-community choice for sustained GH-axis stimulation. - Hexarelin (this entry) — hexapeptide; high acute potency; dose-dependent cortisol/prolactin elevation; meaningful tachyphylaxis with sustained dosing. Generally not the preferred choice for sustained use but used in research-community contexts for its high acute potency and the cardioprotective preclinical evidence. - MK-677 / Ibutamoren — non-peptide oral small-molecule ghrelin agonist; very long half-life (~24 hours); CHF-safety-signal concern in elderly populations (Adunsky 2011 phase 2b DSMB termination); active phase 3 program at Lumos Pharma. The "alphabet soup" of older GHRPs (GHRP-1, GHRP-2/pralmorelin, GHRP-3, GHRP-4, GHRP-5, GHRP-6, hexarelin/examorelin) all share the ghrelin-receptor-agonist mechanism but differ in potency, half-life, cortisol/prolactin selectivity, and tachyphylaxis profile. Hexarelin sits at the high-potency end of this older-GHRP family and is the only one in the Vialwise library; the others are not currently in the active pipeline (deferred to v2). Ipamorelin emerged as the modern default because it kept the GH-stimulating potency while substantially improving the side-effect-profile selectivity.

⚠️ WADA-banned — explicitly named under Section S2.2.4 (Growth Hormone Releasing Factors → GHRP subsection) using the INN spelling "examorelin (hexarelin)". The 2026 WADA Prohibited List Section S2.2.4 names *"GH-releasing peptides (GHRPs) [e.g. alexamorelin, examorelin (hexarelin), GHRP-1, GHRP-2 (pralmorelin), GHRP-3, GHRP-4, GHRP-5 and GHRP-6]"*.[⁶] Same WADA subsection (S2.2.4) as Ipamorelin, CJC-1295, Sermorelin, Tesamorelin, and MK-677. Prohibited at all times. Note the INN-vs-research-name distinction: WADA uses "examorelin" (INN) with parenthetical "(hexarelin)"; research-community use almost exclusively uses "hexarelin." Same compound.

According to PubMed-indexed research, hexarelin is a synthetic hexapeptide growth hormone-releasing peptide (GHRP) with the sequence His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2. The compound was developed by Mediolanum Farmaceutici (Italy) in the 1990s under development codes EP-23905 and MF-6003, derived structurally from GHRP-6 with modifications to enhance potency and metabolic stability.[¹] The INN spelling is "examorelin"; "hexarelin" is the alternative name used in research and most clinical trials. The compound was advanced through Phase II clinical evaluation in GH-axis indications and as an investigational cardioprotective agent, but Mediolanum's clinical development was discontinued before market approval — the combination of GH-response tachyphylaxis with sustained dosing and the dose-dependent cortisol/prolactin elevation limited clinical utility for sustained therapeutic use.

Mechanism. Based on articles retrieved from PubMed, hexarelin acts as an agonist at the ghrelin receptor (GHS-R1a) at both pituitary and hypothalamic levels to stimulate GH release in an age-dependent manner.[⁵] The mechanism is shared with all the GHRP-class peptides plus the non-peptide ghrelin-mimetic MK-677. Hexarelin is more potent than GHRP-6 (the original GHRP from which it was derived) but produces the dose-dependent cortisol and prolactin elevation that distinguishes it from the cleaner ghrelin-receptor agonists like Ipamorelin. The cortisol and prolactin effects are mediated by ghrelin-receptor activity at extra-pituitary sites — the receptor is expressed in adrenal and lactotroph tissue.[⁵]

Age-related GH response variation. A foundational Bellone 1998 study published in the *Journal of Endocrinological Investigation* compared hexarelin GH response across four age groups: prepubertal children, pubertal children, young adults, and elderly subjects.[⁵] Hexarelin produces powerful GH stimulation in pubertal children and young adults but substantially weaker response in prepubertal children and elderly subjects. This age-dependent response pattern is shared across GHRPs and is the basis for hexarelin's limited utility for diagnostic GH-stimulation testing in the very young or elderly populations. The clinical implication for adult research-community use: hexarelin's GH-stimulation effect is strongest in young adults (the dominant research-community demographic) and progressively weaker with age.

Cortisol and prolactin dose-response. The pivotal Massoud 1996 dose-response study in the *Journal of Clinical Endocrinology & Metabolism* established the modern understanding of hexarelin's hormonal selectivity.[³] In healthy adult males, IV hexarelin produced GH, PRL, and cortisol release in a dose-dependent manner: GH response plateaued at 140 mU/L corresponding to a hexarelin dose with ED50; PRL response plateaued at 180% maximum rise from baseline corresponding with ED50; cortisol response showed a step increase to ~40% above baseline. Critically, the Massoud study also demonstrated that low-dose hexarelin combined with GHRH(1-29)NH2 produced massive synergistic GH release (115 ± 32.8 mU/L) without cortisol elevation and with only moderate prolactin rise (84.9 ± 27.5%) — establishing the rationale for combining hexarelin with GHRH analogs at low doses rather than running hexarelin alone at higher doses.[³]

Chronic-administration tachyphylaxis (Rahim 1999 study). Per PubMed, the Rahim 1999 *Clinical Endocrinology* study established the chronic-administration profile.[⁴] Subjects received twice-daily SC hexarelin for 16 weeks. The cortisol-AUC response decreased significantly from baseline (1506 ± 77 nmol/L/h) to week 16 (1222 ± 92 nmol/L/h, p<0.05), then returned to baseline (1586 ± 58 nmol/L/h) 4 weeks after discontinuation — confirming tachyphylaxis is real, dose-frequency-dependent, and reversible after washout. No significant change in basal cortisol, urinary free cortisol, or ACTH-AUC over the study period. Prolactin AUC was unchanged at 16 weeks vs baseline. The Rahim study is reassuring on the chronic-cortisol-elevation question — sustained twice-daily dosing did not produce sustained hyperprolactinemia or hypercortisolemia at the dose tested.

Cardioprotective preclinical research thread. Hexarelin has been investigated for cardiovascular applications in preclinical and limited clinical studies — particularly for cardioprotective effects in models of myocardial ischemia and post-infarct remodeling. The mechanism is hypothesized to involve cardioprotective effects of ghrelin-receptor activation distinct from the GH-axis effects. This is the most-cited "alternative use case" thread in the hexarelin literature beyond the dominant GH-stimulation use case. Specific clinical translation has not advanced.

Regulatory status (US — current). Hexarelin is not FDA-approved for any indication. Mediolanum's clinical development program was discontinued. The compound is available exclusively as a research peptide through unregulated research-peptide supply chains; not legally compoundable through US 503A pharmacies (the compound is not on the 503A bulks list, and per the broader peptide-bulks-list regulatory situation as of 2024, is not approved for compounding). Not DEA-scheduled.

Regulatory status (sport — WADA). Hexarelin is WADA-banned under Section S2.2.4 (Growth Hormone Releasing Factors → GHRP subsection) of the 2026 Prohibited List, named explicitly using the INN spelling "examorelin (hexarelin)" alongside alexamorelin, GHRP-1, GHRP-2 (pralmorelin), GHRP-3, GHRP-4, GHRP-5, and GHRP-6.[⁶] Same WADA subsection as Ipamorelin, CJC-1295, Sermorelin, Tesamorelin, and MK-677. Prohibited at all times.

Common research interests. Despite the regulatory status and tachyphylaxis concerns, hexarelin is used in research-community contexts for: - Acute GH stimulation for body composition and recovery — the dominant research-community use case. Typically used in 4–6 week cycles to manage tachyphylaxis. - Diagnostic GH-stimulation testing (clinical context, historical) — IV hexarelin was studied as a diagnostic GH-stimulation test; this has been largely superseded by other diagnostic approaches. - Cardioprotective preclinical research — investigated in preclinical and limited clinical studies for myocardial ischemia / post-infarct remodeling. Not a research-community use case. - Combined with low-dose GHRH analog (CJC-1295 no-DAC, sermorelin) — rationale: synergistic GH release without cortisol elevation and with reduced prolactin elevation per Massoud 1996.[³] The cleanest hexarelin protocol described in published literature.

Commonly reported

• Cortisol elevation — dose-dependent; meaningful at higher doses (≥ per the Massoud 1996 dose-response study). Reduced or absent at low doses combined with GHRH analog.
• Prolactin elevation — dose-dependent; meaningful at higher doses; clinically relevant if sustained
• Tachyphylaxis (GH-response decline with sustained use) — confirmed in chronic-administration studies; reversible after washout
• Injection site reactions — typical of subcutaneous peptide injection
• Water retention / fluid retention — common; same as other GHS-class compounds
• Increased appetite — common; ghrelin-receptor agonism is the mechanism
• Tingling or numbness in extremities — uncommon; suggests carpal-tunnel-syndrome-like effect; warrants dose reduction
• Joint stiffness — uncommon
• Sleep changes (typically improved sleep quality at modest doses; sleep disturbance at high doses) — mixed reports
• Long-term safety in adults using hexarelin off-label is not well characterized in published literature. The Rahim 1999 16-week study is among the longest published exposures.[⁴] Multi-year off-label use in the research community is not characterized.
• CHF-related concerns — the Adunsky 2011 *Annals of Internal Medicine* phase 2b trial of MK-677 (a non-peptide ghrelin agonist with similar receptor target) was terminated by the DSMB for CHF safety signal in elderly population; whether the same concern applies to hexarelin in a different population is theoretical but mechanistically plausible. See [mk-677.md](./mk-677.md).

Active malignancy or known IGF-1R-positive tumors — GH/IGF-1 axis activation is contraindicated

Active hyperprolactinemia or prolactinoma — additive concerns

Active hypercortisolism or Cushing's syndrome — additive concerns

Pregnancy and lactation — no human data; default to contraindicated

Pediatric use — no FDA-approved indication; pediatric clinical use only in specialist contexts (historical diagnostic GH-stimulation testing)

Concurrent corticosteroid therapy — additive cortisol effects

Active diabetes / impaired glucose tolerance — caution; GH-axis stimulation may worsen insulin resistance

Regulatory note (US): Hexarelin is not FDA-approved for any indication and is not legally compoundable through US 503A pharmacies.

Regulatory note (sport): WADA-banned in regulated sport — explicitly named under Section S2.2.4 of the 2026 Prohibited List using INN spelling "examorelin (hexarelin)."[⁶]

Not DEA-scheduled.

Peptide

A short chain of amino acids, the building blocks of proteins. Many compounds in this library are peptides.

Growth hormone secretagogue

A compound that signals the body to release its own growth hormone, rather than supplying growth hormone directly.

Ghrelin receptor

a receptor that, when activated, triggers growth hormone release and hunger.

Tachyphylaxis

a fading of a compound's effect with repeated use.

WADA Prohibited List

The list of substances banned in regulated sport by the World Anti-Doping Agency.

1. Mediolanum Farmaceutici (Italy). Hexarelin (examorelin) clinical development program, development codes EP-23905 and MF-6003. Phase II clinical evaluation in GH-axis indications and as investigational cardioprotective agent during the 1990s. Clinical development discontinued before market approval. Source for: development history; INN designation as "examorelin"; the regulatory framework for current research-peptide-only availability.
2. Loche S, Colao A, Cappa M, Ferone D, Merola B, Faedda A, Imbimbo BP, Deghenghi R, Lombardi G. (1997). Acute administration of hexarelin stimulates GH secretion during day and night in normal men. Clinical Endocrinology (Oxford), 46(3):275–279 (March 1997).(PMID 9156035)
3. Massoud AF, Hindmarsh PC, Brook CG. (1996). Hexarelin-induced growth hormone, cortisol, and prolactin release: a dose-response study. Journal of Clinical Endocrinology & Metabolism, 81(12):4338–4341 (December 1996).(PMID 8954038)
4. Rahim A, O'Neill PA, Shalet SM. (1999). The effect of chronic hexarelin administration on the pituitary-adrenal axis and prolactin. Clinical Endocrinology (Oxford), 50(1):77–84 (January 1999).(PMID 10341859)
5. Bellone J, Bartolotta E, Sgattoni C, Aimaretti G, Arvat E, Bellone S, Deghenghi R, Ghigo E. (1998). Hexarelin, a synthetic GH-releasing peptide, is a powerful stimulus of GH secretion in pubertal children and in adults but not in prepubertal children and in elderly subjects. Journal of Endocrinological Investigation, 21(8):494–500 (September 1998).(PMID 9801989)
6. World Anti-Doping Agency. The 2026 Prohibited List, International Standard (effective 1 January 2026). Canonical PDF: wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf (linked from the WADA landing page; local archival copy in `docs/legal/wada-2026-prohibited-list.pdf`). Hexarelin is named explicitly under Section S2.2.4 (Growth Hormone Releasing Factors → GHRP subsection) — page 8 of the canonical PDF — using the INN spelling "examorelin (hexarelin)". Verbatim from the canonical PDF: under S2.2.4 ("Growth hormone releasing factors, including, but not limited to:"), the GHRP bullet reads "GH-releasing peptides (GHRPs) [e.g. alexamorelin, examorelin (hexarelin), GHRP-1, GHRP-2 (pralmorelin), GHRP-3, GHRP-4, GHRP-5 and GHRP-6]". Same S2.2.4 subsection as Ipamorelin, CJC-1295, Sermorelin, Tesamorelin, and MK-677. Prohibited at all times.
7. Dominikowski A, Rękoś Z, Olejarz M, Szczepanek-Parulska E, Domin R, Ruchała M. (2026). The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration. Frontiers in Endocrinology (Lausanne), 17:1822475 (published 18 June 2026).(PMID 42395176)

• MK-677 (Ibutamoren) — discussed together in this entry's stacks section
• Testosterone — discussed together in this entry's stacks section
• IGF-1 LR3 — discussed together in this entry's stacks section
• CJC-1295 / Ipamorelin Blend — same mechanism class
• CJC-1295 — same mechanism class
• GHRP-2 — same mechanism class