TL;DR
The strongest single-pulse GH release of any named GHRP. Two weeks later the response is gone.
What is it? A six-amino-acid ghrelin-receptor agonist designed by Deghenghi in 1991. Ghigo's 1994 paper showed 1 μg/kg IV produced roughly 2× the GH peak of equal-dose GHRH.
What does it do? Activates GHSR-1a on pituitary somatotrophs for GH pulses. Also binds CD36 on cardiomyocytes and triggers PI3K/Akt cardioprotective signaling without going through GH at all.
Does the evidence hold up? Deep 1990s pharmacology in humans (Ghigo 1994, Imbimbo 1994, Popovic 1999). Solid preclinical cardioprotection (Bodart 2002, Locatelli 1999). No Phase 3. Tachyphylaxis, ACTH, and prolactin elevation drove ipamorelin's displacement.
Who uses it? Labs probing GHSR/CD36 biology. A few niche clinics doing short pulse cycles.
Bottom line? Peak acute GH is unmatched. Chronic use doesn't work.
What It Is
Hexarelin (examorelin; originally EP 23905) is a synthetic hexapeptide growth hormone secretagogue (GHRP) developed in the early 1990s by Romano Deghenghi and colleagues at Europeptides. Its amino acid sequence is His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH₂ — a modification of the earlier reference compound GHRP-6 with an additional D-2-methyltryptophan substitution at position 2. That single substitution confers enhanced metabolic stability and higher GH-releasing potency compared to GHRP-6, giving hexarelin the strongest GH-release effect of any named small GHRP analog.
Hexarelin was extensively studied in the 1990s as a candidate provocative-test agent for growth hormone deficiency and as a therapeutic for adult GH replacement. Ghigo, Imbimbo, and colleagues in Italy generated most of the early clinical pharmacology, including the foundational observation that 1 μg/kg IV hexarelin produces approximately twice the peak GH response of 1 μg/kg IV GHRH in healthy young adults (Ghigo et al., J Clin Endocrinol Metab 1994). The compound was found to be active across intravenous, subcutaneous, intranasal, and oral routes — a breadth of bioavailability unusual for a peptide.
Despite the promising clinical pharmacology, hexarelin never achieved commercial approval anywhere. The single biggest reason was loss of GH response over chronic dosing (tachyphylaxis) and parallel increases in ACTH/cortisol and prolactin — problems that were ultimately solved by the later ipamorelin design, which achieves clean GH-selective pulses without the cortisol/prolactin burden. Hexarelin's development was superseded by ipamorelin for chronic use and by GHRH analogs (sermorelin, CJC-1295, tesamorelin) for GH restoration protocols.
What kept hexarelin clinically and scientifically interesting well past its GH-secretagogue era was the 2002 discovery by Bodart et al. (Circulation Research; PMID 11988484) that hexarelin binds the scavenger receptor CD36 in cardiac tissue with high affinity, triggering PI3K/Akt-mediated cardioprotective signaling independent of growth hormone release. That CD36 mechanism — unique to hexarelin and a small group of closely-related analogs — is the foundation for modern interest in hexarelin as a cardioprotective peptide rather than a chronic GH secretagogue.
Hexarelin sits within a broader class of small-molecule growth-hormone secretagogues developed in the 1990s, including GHRP-2, GHRP-6, ipamorelin, and the orally active non-peptide MK-677 (ibutamoren). Among the peptide GHRPs, hexarelin is the most potent single-dose GH releaser but also the least GH-selective — the cortisol / prolactin / ACTH elevation profile that defines its chronic-use liabilities is a feature of its receptor engagement pattern rather than a dose artifact. Ipamorelin, developed later and deliberately designed to minimize these off-target responses, achieves 60–70% of hexarelin's peak GH response with substantially cleaner hormone selectivity — which is why ipamorelin, not hexarelin, became the dominant GHRP in compounded men's-health and wellness peptide protocols over the past two decades. Hexarelin's modern research niche is almost entirely defined by the CD36 cardioprotective mechanism, not the GH-axis mechanism.
Mechanism of Action
Hexarelin operates through two mechanistically distinct pathways: GHSR-1a (ghrelin receptor) agonism producing GH release, and CD36-mediated cardioprotective signaling independent of the GH axis.
- GHSR-1a agonism (GH axis) — Binds the ghrelin receptor on anterior pituitary somatotrophs and hypothalamic neurons. Activates Gq/11 → phospholipase C → IP3/DAG → intracellular Ca²⁺ release → pulsed GH secretion. Potency is approximately 2× that of native GHRH at equivalent mass doses (Ghigo 1994).
- CD36 binding (cardioprotective) — Hexarelin binds CD36, a B-type scavenger receptor expressed on cardiomyocytes and coronary endothelium. CD36 activation by hexarelin signals via PI3K/Akt, producing anti-apoptotic, anti-oxidative, and pro-survival effects independent of GH (Bodart et al., Circ Res 2002). This pathway is not engaged by most other GHRPs; it is a hexarelin-signature mechanism.
- Direct cardiac effects — In rat post-MI models, hexarelin reduces infarct size, preserves left ventricular function, and reduces myocardial apoptosis even when GH receptor signaling is blocked. Improves mitochondrial function and reduces reactive oxygen species generation in hypoxic cardiomyocytes (Locatelli et al., Endocrinology 1999).
- ACTH/cortisol elevation (off-target) — Unlike ipamorelin, hexarelin raises ACTH and cortisol at therapeutic GH-release doses. The effect is mediated by GHSR-1a activation on anterior pituitary corticotrophs and by hypothalamic CRH release. This is dose-dependent and is the single most clinically significant off-target effect of hexarelin.
- Prolactin elevation — Parallel pattern to cortisol. Clinically meaningful in some users, particularly at higher doses.
- Nitric oxide modulation — CD36 signaling and downstream Akt pathway crosstalk with eNOS, contributing to vascular and coronary microcirculation benefits.
- Tachyphylaxis — GH response diminishes with chronic daily dosing over ~2–4 weeks. This desensitization is a hexarelin-specific liability and is why chronic-use protocols typically cycle or combine with a GHRH analog.
- Appetite stimulation — GHSR-1a activation drives orexigenic signaling. Hexarelin increases appetite but less dramatically than oral MK-677 given its shorter half-life and injection route.
- Sleep and slow-wave enhancement — Like other GHRPs, nighttime dosing aligns with the natural GH pulse and amplifies slow-wave sleep architecture.
- Somatostatin interaction — Hexarelin's GH release is partially somatostatin-sensitive; high somatostatin tone blunts response. Combining with a GHRH analog yields greater combined GH release than either alone.
What the Research Shows
Hexarelin has an unusually deep 1990s-era pharmacology database for a compound that never achieved approval. Modern interest has shifted substantially toward the cardioprotective signal.
- Discovery and early pharmacology (Deghenghi, 1991) — Original synthesis and characterization of hexarelin as a more potent GHRP-6 analog.
- GH dose-response in humans (Ghigo et al., J Clin Endocrinol Metab 1994; PMID 8126144) — Seminal paper demonstrating 1 μg/kg IV hexarelin produced approximately 2× the GH response of 1 μg/kg IV GHRH. Established SC, IN, and oral bioavailability as clinically meaningful for a peptide.
- Metabolic stability and PK (Imbimbo et al., Eur J Clin Pharmacol 1994) — Pharmacokinetic characterization of IV, SC, IN, and oral routes; plasma half-life ~70 minutes.
- Provocative diagnostic testing (Popovic et al., J Clin Endocrinol Metab 1999; PMID 10443652) — Low-dose GHRH + hexarelin proposed as alternative to insulin tolerance test for adult GHD diagnosis.
- Acromegaly / refractory GH (Arvat et al., 1997; PMID 9288722) — Hexarelin counteracted hydrocortisone-induced suppression of GH, suggesting upstream CNS activation independent of pituitary somatostatin tone.
- CD36 cardioprotection (Bodart et al., Circ Res 2002; PMID 11988484) — Landmark paper identifying CD36 as the cardiac receptor mediating hexarelin's GH-independent cardioprotective effects.
- CD36 binding-site characterization (Demers et al., Biochem J 2004; PMID 15285719) — Photoaffinity cross-linking study identifying the hexarelin binding site on CD36.
- Post-MI rat model (Locatelli et al., Endocrinology 1999; PMID 10465271) — Growth-hormone-independent cardioprotective effects of hexarelin in rat infarct models.
- Cushing's / Addison's axis interaction (Giordano et al., J Endocrinol Invest 1999; PMID 10516483) — Documented ACTH/cortisol response to hexarelin in pituitary-adrenal disorders, consistent with direct corticotroph activation.
- Hemodialysis patients (Imbimbo et al., Nephron 1999; PMID 10199757) — Dose, nutrition, and age effects on hexarelin-induced anterior pituitary hormone secretion in dialysis patients.
- Sleep architecture (Frieboes et al., Psychoneuroendocrinology 2004; PMID 15177700) — Hexarelin decreased slow-wave sleep and stimulated GH, ACTH, cortisol, and prolactin during sleep in healthy volunteers.
- Cardiovascular hexarelin review (Mao et al., J Geriatr Cardiol 2014; PMC4178518) — Summarized a decade of CD36 work and framed hexarelin's cardioprotective mechanism as clinically promising.
- Chronic administration and axis effects (Rahim et al., Clin Endocrinol 1999; PMID 10396327) — Effect of chronic hexarelin on the pituitary-adrenal axis and prolactin.
Honest Evidence Framing
Hexarelin has abundant acute-use human pharmacology data, solid preclinical cardioprotection data, but no approved indication and no Phase 3 cardioprotection trials in humans. Its chronic-use liabilities (GH tachyphylaxis, ACTH/cortisol, prolactin) are why ipamorelin displaced hexarelin for wellness/anti-aging indications. Modern community use is a narrow proposition: short courses or pulse-dosing for CD36-mediated cardiac benefit, or acute GH provocation, not chronic daily dosing.
Human Data
Hexarelin has been administered to humans in hundreds of published trial and provocative-test protocols. Key published human datasets:
- Phase 1 pharmacokinetics (Imbimbo 1994) — IV, SC, IN, and oral dose-response in healthy adults. ED50 ~0.48 μg/kg; plateau at ~1 μg/kg.
- GH dose-response (Ghigo 1994; PMID 8126144) — 12 healthy young volunteers; IV (1, 2 μg/kg), SC (1.5, 3 μg/kg), IN (20 μg/kg), oral (20, 40 mg). 1 μg/kg IV hexarelin produced ~2× GH response of equivalent-dose GHRH.
- Combined GHRH + hexarelin — Synergistic GH release in healthy adults and in patients with glucocorticoid excess.
- Acromegaly glucocorticoid counteraction (Arvat 1997) — Hexarelin reversed hydrocortisone-induced GH suppression.
- GHD diagnostic testing (Popovic 1999; PMID 10443652) — Low-dose hexarelin + GHRH as alternative to insulin tolerance test for adult GHD diagnosis.
- Addison's / Cushing's ACTH response (Giordano 1999; PMID 10516483) — Documented corticotropin-releasing activity of hexarelin, important for understanding the cortisol side-effect profile.
- Hemodialysis patients (Imbimbo 1999; PMID 10199757) — Dose, nutrition, and age effects on hexarelin-induced GH secretion in dialysis patients.
- Long-term dosing tachyphylaxis — Multiple groups documented that 2–4 weeks of chronic daily dosing leads to attenuated GH response.
- Elderly GH restoration short-term — Restoration of youthful GH pulse amplitude across small short-duration studies.
What is absent: a Phase 3 chronic-use trial for any indication. Hexarelin's 1990s development program delivered thorough pharmacology but no registrational commercial pathway. Modern human cardioprotection RCTs using hexarelin specifically have not been published.
Dosing from the Literature
The following synthesizes published trial doses and community practice. Because chronic-use tachyphylaxis is a documented liability, dosing patterns for hexarelin diverge from other peptides in this space.
| Protocol | Dose | Frequency | Notes |
|---|
| Acute GH provocation (Ghigo 1994) | 1 μg/kg IV | Single dose | Test dose for GH reserve. |
| SubQ short-course (community) | 100 μg | 1–2× daily, SubQ | Typical short-cycle body-comp dose. Often limited to 2–3 week courses to manage tachyphylaxis. |
| "Cardiac support" short-course | 200–300 μg/day | Split, 2–3 weeks on / 2–4 weeks off | Off-label pulse protocol for CD36-mediated cardiac support. |
| Pre-training dose | 100 μg | 30 min before training | Occasional use for GH pulse aligned to workout. |
| Pre-sleep dose | 100 μg | At bedtime | Aligned with natural nocturnal GH pulse. |
| Combined with GHRH analog | 100 μg hexarelin + sermorelin or CJC-1295 | Bedtime | Classical GHRH+GHRP pairing; larger combined GH pulse. |
| Cycle pattern | 2–3 weeks on / 2–4 weeks off | — | Designed to avoid tachyphylaxis. Continuous dosing beyond 3–4 weeks produces declining GH response. |
Dosing Disclaimer
Hexarelin doses >200 μg per dose raise ACTH, cortisol, and prolactin substantially without additional meaningful GH benefit. Chronic continuous dosing blunts the GH response you're seeking. Short pulse-dose cycles are the mechanistically coherent use pattern, not 3-month continuous protocols.
A practical framing for dose selection: 100 μg per injection sits in the "maximum GH release with manageable cortisol / prolactin burden" window for most users; 200 μg per injection delivers a modestly larger GH pulse with substantially larger cortisol / prolactin responses; 300+ μg per injection is pharmacologically possible but the marginal GH benefit is small while the cortisol / prolactin cost continues to rise. Higher is not better for hexarelin — the dose-response curve for GH plateaus at mid-range while off-target hormone responses continue to scale. This is a key practical distinction from ipamorelin, where dose-response tolerability is more forgiving.
Timing matters more for hexarelin than for GHRH analogs like sermorelin or CJC-1295. Hexarelin's brief pulsatile GH release is most productive when it reinforces an endogenous GH pulse — pre-sleep (aligned with nocturnal slow-wave-sleep GH burst) or immediately before resistance training (aligned with exercise-induced GH response) are the conventional windows. Post-meal dosing is generally avoided because post-prandial insulin and free fatty acid elevation blunt the GH response substantially.
Reconstitution & Storage
Hexarelin is typically supplied as a lyophilized powder in 2 mg or 5 mg vials.
| Vial Size | BAC Water | Concentration | 100 μg Dose | 200 μg Dose |
|---|
| 2 mg | 1 mL | 2 mg/mL | 5 units (0.05 mL) | 10 units (0.10 mL) |
| 2 mg | 2 mL | 1 mg/mL | 10 units (0.10 mL) | 20 units (0.20 mL) |
| 5 mg | 2 mL | 2.5 mg/mL | 4 units (0.04 mL) | 8 units (0.08 mL) |
| 5 mg | 2.5 mL | 2 mg/mL | 5 units (0.05 mL) | 10 units (0.10 mL) |
- Reconstitution — Inject BAC water slowly down the vial wall at 45°. Swirl gently; do not shake. Clear colorless solution.
- Storage — Unreconstituted: 2–8°C preferred. Reconstituted: 2–8°C, use within 21–28 days. Do not freeze reconstituted peptide.
- Injection sites — SubQ into abdomen, thigh, or upper arm. Rotate weekly.
- Timing — Empty stomach, ≥2 hours after last meal. Pre-sleep or pre-training are the most common timing strategies.
- Inspection — Discard if cloudy or discolored.
→ Use the Kalios Peptide Calculator for exact syringe units
Side Effects & Risks
Important
Hexarelin raises cortisol and prolactin and loses its GH punch within 2–4 weeks of continuous dosing. WADA-banned under S2. No Phase 3 human trials. Talk to someone licensed before deciding on continuous-dose hexarelin over a cleaner GHRP.
Hexarelin's side-effect profile is what separates it from ipamorelin as a chronic-use agent. The cortisol, prolactin, and tachyphylaxis signals are the dominant clinical considerations.
- Cortisol / ACTH elevation — Dose-dependent; measurable at therapeutic GH-release doses. Clinically meaningful with chronic use; can produce iatrogenic hypercortisolism markers over weeks to months. Not subtle at 200+ μg doses.
- Prolactin elevation — Parallel to cortisol. Can produce galactorrhea or libido changes with chronic use, particularly in women.
- Tachyphylaxis (GH desensitization) — Progressive loss of GH response over 2–4 weeks of daily dosing. Largely resolves with a 2–4 week break.
- Appetite stimulation — GHSR-1a activation; less pronounced than MK-677 but present.
- Mild water retention — Short duration, dose-dependent.
- Facial flushing / mild warmth — Transient, within minutes of injection.
- Injection site reactions — Mild; typical of SubQ peptides.
- Insulin sensitivity — Small dose-dependent impact via GH/IGF-1 axis.
- Sleep disturbance or vivid dreams — More pronounced with bedtime dosing.
- Cancer / IGF-1 concerns — Class-level caution for GH-axis stimulation.
- WADA status — Banned under S2. Not viable for competitive athletes.
- Cardiac risk paradox — Preclinical CD36 data support cardioprotection, but no Phase 3 human cardiac trials; any cardioprotective use remains extrapolation.
- Drug interactions — Chronic corticosteroids alter the GH response and may interact with the ACTH-axis activation. Somatostatin-active drugs (octreotide) blunt GH response.
- Purity concerns — Gray-market hexarelin quality varies. Oxidative degradation at tryptophan positions is common. Third-party HPLC/MS COAs are the floor.
- Hexarelin vs ipamorelin — chronic-use comparison — For anyone considering a chronic GH-secretagogue protocol, the practical question is almost always hexarelin vs ipamorelin. Hexarelin delivers a larger single-pulse GH release but carries the cortisol / prolactin / tachyphylaxis package that makes chronic use problematic; ipamorelin delivers a smaller but more GH-selective pulse without meaningful cortisol / prolactin elevation and without the tachyphylaxis signature. For chronic daily dosing, the evidence clearly favors ipamorelin. Hexarelin's sensible niche is short pulse-dose cycles, acute GH provocation in diagnostic contexts, or CD36-mediated cardiac work — not a 12-week continuous body-composition protocol.
- Hexarelin vs MK-677 — tachyphylaxis and receptor class — Both engage the GHSR-1a ghrelin receptor, but MK-677 is an orally active non-peptide with sustained receptor occupancy; hexarelin produces brief pulses. MK-677's sustained occupancy drives a more pronounced appetite, water retention, and insulin resistance profile; hexarelin's pulsatile action has a cleaner short-term tolerability profile. Neither should be combined with the other in practice — they act on the same receptor and would compound off-target effects.
Bloodwork & Monitoring
Because of the cortisol, prolactin, and tachyphylaxis liabilities, monitoring is more extensive for hexarelin than for ipamorelin or sermorelin.
- IGF-1 — Baseline and periodic during cycles to assess GH-axis response.
- Morning cortisol + ACTH — Baseline and after 2 weeks of dosing; rising values are a reason to reduce dose or switch to ipamorelin.
- Prolactin — Baseline and periodic, particularly in women.
- Fasting glucose + HbA1c — Baseline and periodic.
- CMP / CBC — Standard baseline; repeat periodically.
- Thyroid (TSH, free T4) — Baseline.
- Cardiac workup if cardioprotective use intent — EKG, echocardiography, cardiology consult if using for CD36-mediated cardiac support.
- Cancer screening — Age-appropriate baseline given GH-axis stimulation.
- Body composition (DEXA) — For objective tracking if that is an endpoint.
- 24-hour urinary free cortisol (in extended cycles) — Integrated assessment of adrenal axis load across extended dosing, more informative than a single morning draw; reasonable in users considering more than 2–3 weeks of continuous hexarelin.
- ECG (pre-initiation in cardiac-support intent) — Baseline 12-lead ECG if the rationale for hexarelin use is CD36-mediated cardiac support rather than body composition; provides a reference point for any future cardiac evaluation.
Monitoring should be tighter in the first 2–4 weeks of any hexarelin protocol because that is the window in which the GH response is largest (before tachyphylaxis), when cortisol / prolactin responses are also largest, and when most individual-specific tolerability is determined. After 4 weeks of continuous dosing, the GH response is typically blunted but the cortisol / prolactin pattern may persist — a mechanistic dissociation that argues for cycling rather than continuous use.
Commonly Stacked With
Classical GHRH + GHRP combination. Synergistic GH pulse; the short-duration hexarelin pulses plus sustained GHRH effect produce a larger combined GH release than either alone.
Same GHRH + GHRP mechanism as sermorelin pairing, with modified CJC-1295 providing slightly longer GHRH signaling. Common combination in short-course body-comp protocols.
Pairs for tissue repair + GH-axis support, particularly in injury recovery protocols. BPC-157's local VEGFR2/NO mechanism complements hexarelin's systemic GH pulse.
Both act at GHSR-1a; combining them amplifies GH-axis stimulation and compounds side-effect burden. Generally NOT recommended as a stack. Rotate rather than combine.
Full-axis protocols sometimes include hexarelin short-courses alongside TRT for body composition. Requires clinician oversight and monitoring of GH axis, androgen axis, and adrenal markers.
→ Check compound compatibility in the Stack Builder
Regulatory Status
Current Status — April 2026
Hexarelin is not approved by the FDA for any indication. Despite an extensive 1990s clinical development program, it never achieved commercial approval. It is classified by the FDA as a Category 2 Bulk Drug Substance, making it ineligible for compounding pharmacy use under 503A / 503B.
The February 27, 2026 HHS Secretary Robert F. Kennedy Jr. reclassification announcement has not publicly specified hexarelin's status among the candidates; as of April 2026 compounding remains prohibited.
Hexarelin is banned by WADA under S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics) as a named GH secretagogue. Athletes subject to anti-doping testing cannot use hexarelin.
Gray-market "research use only" hexarelin is the primary availability route. Pharmacy-compounded hexarelin is not legally available under current FDA enforcement.
Cost & Access
Hexarelin is not approved for human use in the United States. It is available through research suppliers for laboratory research purposes only.
U.S. compounding pharmacies cannot legally compound hexarelin under current FDA bulk-substance rules. Online research-chemical channels list hexarelin at varying price points, typically per 5 mg or 10 mg vial; a full month of community-typical 100 mcg × 1–2 daily dosing requires 1–2 vials per month depending on regimen. Vendor quality and purity vary substantially; independent HPLC/MS COAs are the practical floor.
Hexarelin is among the peptides under HHS Secretary Robert F. Kennedy Jr.'s February 27, 2026 Category 2 reclassification announcement (the GHRP family broadly is under review). If reclassified back to Category 1 (subject to Pharmacy Compounding Advisory Committee review and FDA implementation), 503A compounded hexarelin would become available through clinician-prescribed off-label channels. As of April 2026, this reclassification remains pending and hexarelin cannot be legally compounded by 503A or 503B pharmacies in the United States.
Estimated access context as of April 2026. Actual availability and costs vary by provider, location, and prescription status. Kalios does not sell compounds.
Related Compounds
Peptides hexarelin users end up weighing:
Second-generation growth hormone releasing peptide. Stronger GH pulse than ipamorelin with mild prolactin rise.
Ghrelin-receptor agonist with strong appetite-stimulating effect alongside GH release.
Selective ghrelin-receptor (GHS-R1a) agonist. The cleanest GHRP — minimal cortisol or prolactin spikes.
CJC-1295 + ipamorelin — the classic GHRH + GHRP combination for natural growth-hormone pulse amplification.
Key References
- Ghigo E, Arvat E, Gianotti L, Imbimbo BP, Lenaerts V, Deghenghi R, Camanni F. Growth hormone-releasing activity of hexarelin, a new synthetic hexapeptide, after intravenous, subcutaneous, intranasal, and oral administration in man. J Clin Endocrinol Metab. 1994;78(3):693-698. PMID: 8126144.
- Imbimbo BP, Mant T, Edwards M, Amin D, Dalton N, Boutignon F, Lenaerts V, Wüthrich P, Deghenghi R. Growth hormone-releasing activity of hexarelin in humans. A dose-response study. Eur J Clin Pharmacol. 1994;46(5):421-425. PMID: 7957536.
- Bodart V, Febbraio M, Demers A, McNicoll N, Pohankova P, Perreault A, Sejlitz T, Escher E, Silverstein RL, Lamontagne D, Ong H. CD36 mediates the cardiovascular action of growth hormone-releasing peptides in the heart. Circ Res. 2002;90(8):844-849. PMID: 11988484.
- Demers A, McNicoll N, Febbraio M, Servant M, Marleau S, Silverstein R, Ong H. Identification of the growth hormone-releasing peptide binding site in CD36: a photoaffinity cross-linking study. Biochem J. 2004;382(Pt 2):417-424. PMID: 15285719.
- Popovic V, Damjanovic S, Micic D, Djurovic M, Petakov M, Dieguez C, Casanueva FF. Low dose hexarelin and growth hormone (GH)-releasing hormone as a diagnostic tool for the diagnosis of GH deficiency in adults: comparison with insulin-induced hypoglycemia test. J Clin Endocrinol Metab. 1999;84(12):4374-4379. PMID: 10443652.
- Giordano R, Picu A, Broglio F, Bonelli L, Baldi M, Berardelli R, Ghigo E, Arvat E. Corticotropin-releasing effect of hexarelin, a peptidyl GH secretagogue, in normal subjects pretreated with metyrapone or RU-486. J Endocrinol Invest. 1999;22(9):617-622. PMID: 10516483.
- Imbimbo BP, Greco F, Marchiaro F, Mantovani V, Rocchi R, Ongini E. The effects of dose, nutrition, and age on hexarelin-induced anterior pituitary hormone secretion in adult patients on maintenance hemodialysis. Nephron. 1999;82(2):147-156. PMID: 10199757.
- Locatelli V, Rossoni G, Schweiger F, Torsello A, De Gennaro Colonna V, Bernareggi M, Deghenghi R, Müller EE, Berti F. Growth hormone-independent cardioprotective effects of hexarelin in the rat. Endocrinology. 1999;140(9):4024-4031. PMID: 10465271.
- Mao Y, Tokudome T, Kishimoto I. The cardiovascular action of hexarelin. J Geriatr Cardiol. 2014;11(3):253-258. PMCID: PMC4178518.
- Arvat E, Ramunni J, Bellone J, Di Vito L, Baffoni C, Broglio F, Deghenghi R, Bartolotta E, Ghigo E. The GH, prolactin, ACTH and cortisol responses to hexarelin, a peptidyl GH-releasing hormone, are not modified by pretreatment with dexamethasone or by cold exposure in man. Eur J Endocrinol. 1997;137(6):635-642. PMID: 9438997.
- Rahim A, O'Neill PA, Shalet SM. The effect of chronic hexarelin administration on the pituitary-adrenal axis and prolactin. Clin Endocrinol (Oxf). 1999;50(2):233-240. PMID: 10396327.
- Frieboes RM, Antonijevic IA, Held K, Murck H, Pollmächer T, Schuld A, Steiger A. Hexarelin decreases slow-wave sleep and stimulates the secretion of GH, ACTH, cortisol and prolactin during sleep in healthy volunteers. Psychoneuroendocrinology. 2004;29(6):728-739. PMID: 15177700.
- Broglio F, Gottero C, Benso A, Prodam F, Destefanis S, Gauna C, Maccario M, Deghenghi R, van der Lely AJ, Ghigo E. Effects of ghrelin on the insulin and glycemic responses to glucose, arginine, or free fatty acids load in humans. J Clin Endocrinol Metab. 2003;88(9):4268-4272. PMID: 12970297.
- Torsello A, Locatelli V, Melis MR, Succu S, Spano MS, Deghenghi R, Müller EE, Argiolas A. Differential orexigenic effects of hexarelin and its analogs in the rat hypothalamus: indication for multiple growth hormone secretagogue receptor subtypes. Neuroendocrinology. 2000;72(6):327-332. PMID: 11146416.
- Chen C. Growth hormone secretagogue actions on the pituitary gland: multiple receptors for multiple ligands? Clin Exp Pharmacol Physiol. 2000;27(5-6):323-329. PMID: 10779119.
- WADA. 2026 Prohibited List. Section S2 — Peptide hormones, growth factors, related substances and mimetics. World Anti-Doping Agency.
Last updated: April 2026 | Profile authored by Kalios Peptides research team