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What it is
A synthetic hexapeptide growth-hormone secretagogue, structurally related to GHRP-6.
How it is proposed to work
GHS receptor agonism with high potency. It also binds CD36, which is the basis for the separate line of cardiovascular research and is unrelated to the growth-hormone effect people buy it for.
Approved medical uses
None. Hexarelin has no approved human medical indication in the jurisdictions we track. Any use is outside an approved label.
Human research
Each entry states what the study found and, separately, what it cannot show.
- Human open-label1998
Sixteen weeks of twice-daily hexarelin — growth-hormone response over time
Finding. Across 16 weeks of twice-daily subcutaneous hexarelin, the growth-hormone response to a single hexarelin injection fell rather than holding steady: the area under the GH curve changed significantly over the study period (P = 0.0003) and the decrease from baseline was significant at week 4 (P < 0.05) and at week 16 (P < 0.01). The decline reversed once treatment stopped — four weeks after the end of therapy the response had risen significantly above its week-16 value (P < 0.05) and was not significantly different from baseline. The authors describe this as a partial and reversible attenuation. Serum IGF-I and IGF binding protein-3 did not change significantly over the 20-week period (P = 0.24 and P = 0.74). Of the bone markers measured, only C-terminal propeptide of type I collagen changed significantly, being higher at week 16 than at baseline (P = 0.019); total body fat, lean body mass and bone mineral density had not changed significantly at week 16 (P = 0.6, P = 0.3 and P = 0.3).
Limitation. A single-arm before-and-after study with no control or comparison group described, so the fall in response cannot be separated from anything else changing across 20 weeks. The abstract states neither a participant total nor any characteristics of the group studied. What was measured is the response to a hexarelin injection itself, not spontaneous growth-hormone secretion. The attenuation the study found was partial and had recovered four weeks after stopping, so it is not evidence of a permanent loss of effect — and with no participant total stated, the week-20 return to baseline is a failure to detect a residual difference rather than demonstrated full recovery. It was measured on one schedule and one route only. The authors report that the biological impact of this schedule on the GH–IGF-I axis appears minimal and that the therapeutic potential of chronic hexarelin requires further investigation.
Preclinical research
Animal and laboratory work. Useful for generating hypotheses; it cannot establish that something works in people.
- Animal2003
Isolated ischaemic rat heart
Finding. In isolated working rat hearts subjected to 30 minutes of ischaemia followed by 120 minutes of reperfusion, hexarelin "significantly reduced infarct size, as estimated on the basis of triphenyltetrazolium chloride staining", while the non-peptidyl secretagogue MK-0677 "was ineffective"; ghrelin "was also protective" and desacylated ghrelin "did not modify ischemic injury". Under aerobic conditions "none of these substances produced any significant hemodynamic effects". The protection given by hexarelin "was partly abolished by the protein kinase C inhibitor chelerythrine", and the authors conclude the cardioprotective effect "is independent of growth hormone secretion, and might be related to protein kinase C activation".
Limitation. Isolated rat hearts rather than intact animals or people, with hexarelin applied directly in the perfusate at 1 micromolar rather than dosed systemically, a single short ischaemia-reperfusion protocol, and infarct size judged by tetrazolium staining. The mechanism advanced here is protein kinase C activation; the report tests no CD36 involvement. Preclinical evidence only — it says nothing about clinical outcomes.
Potential safety concerns
- CautionPreliminary
Documented desensitisation means continued use produces a diminishing effect — which tends to drive escalation.
- CautionInsufficient
Cortisol and prolactin elevation, and no long-term human safety dataset.
Known interactions and contraindication considerations
- Not characterised in humans.
This list is not exhaustive and is not a substitute for a clinician reviewing your full medication history.
Regulatory status
Status is shown per jurisdiction and is accurate only as of the date stated. Where a compound is approved, the approval is bound to a specific formulation, manufacturer and indication — shown in the detail column.
| Jurisdiction | Standing | Detail |
|---|---|---|
United States FDA | Unapproved / investigational as of 1 Jun 2026 | No marketing authorisation. Sold as research material, which is not an approval of any kind. |
European Union EMA | Unapproved / investigational as of 1 Jun 2026 | No marketing authorisation. |
India CDSCO | Unapproved / investigational as of 1 Jun 2026 | A first-time synthetically manufactured peptide falls under the new-drug pathway. Central Licensing Authority permission is required before import or manufacture for sale or distribution. |
How it is being used
What the grey community actually runs, the reasoning they give, and our read on whether it follows from known biology. This is observation, not evidence, and not a recommendation.
Short potent growth-hormone pulses
What is run
Deliberately short blocks, because the community has independently observed the response falling off with continued use.
Their mechanistic reasoning
That it is the most potent secretagogue available, and that keeping blocks short avoids the desensitisation that otherwise develops.
Reported in the community’s own terms. Not our position.
Stacked with
- A GHRH analogue—Separate receptor for a larger pulse.
Regimen shape
- Dose
- figure withheld
- Scale
- Microgram-scale
- Route
- Subcutaneous injection
- Frequency
- Daily during short blocks
- Timing
- Pre-sleep and fasted
- Duration
- Deliberately short blocks with longer breaks
Our read
The desensitisation the community works around is documented in human studies, so this is a case of practice correctly adapting to a real pharmacological property. The remaining problem is the same one facing the whole class — a bigger pulse has still not been shown to produce a functional outcome, and cycling to preserve a response does not establish that the response is worth having.
What the community reports
The comparison is between how sure the community is and how much is actually known — evidence strength, not direction. A compound can have solid research that came out negative.
Used by a minority who value potency, and avoided by others specifically because of desensitisation. The community's cycling practice is a reasonable adaptation to a documented property.
Commonly reported as helping
- A strong initial response, described as more pronounced than other secretagogues
Also reported, when it goes wrong
- Effects reported to diminish noticeably within weeks
- Increased prolactin and associated effects
- Water retention and lethargy
Why these reports can mislead
Diminishing reported effect is consistent with documented desensitisation, but it is equally consistent with novelty wearing off. Both explanations predict the same reports, so the reports cannot distinguish them.
Direct quotations are not published here yet. We will only carry verbatim reports once they are sourced, dated and checked — an unattributed quote is a testimonial, and testimonials are exactly what this section exists to replace.
Watch for, in this use specifically
- Diminishing response tends to drive escalation, which is the wrong response to desensitisation.
- Cortisol and prolactin elevation as with other non-selective GHRPs.
Active clinical trials
No registered trials currently tracked for Hexarelin.
What remains unknown
The questions that would change our assessment if they were answered.
- Is the desensitisation reversible, and over what timescale?
- Does the CD36 cardiac mechanism translate to humans at all?
References
- 1.Rahim A, O'Neill PA, Shalet SM. Growth hormone status during long-term hexarelin therapy. J Clin Endocrinol Metab. 1998;83(5):1644-9.PMID 9589671doi
- 2.Frascarelli S, Ghelardoni S, Ronca-Testoni S, Zucchi R. Effect of ghrelin and synthetic growth hormone secretagogues in normal and ischemic rat heart. Basic Res Cardiol. 2003 Nov;98(6):401-5.PMID 14556085doi
Editorial change history
When we change a grade or a regulatory note, we log it here rather than editing quietly.
Dossier created.
Spotted something wrong? Tell us — we publish corrections.