Hexarelin is a synthetic hexapeptide growth hormone secretagogue first described by Deghenghi et al. in the 1990s. It belongs to the GHRP (growth hormone releasing peptide) class alongside GHRP-2, GHRP-6, and ipamorelin — but with a distinct selectivity profile that has produced unique cardiovascular research signals. This article maps the research.
Structure and sequence
Hexarelin: His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH₂. The D-amino acid substitutions and methylation confer protease resistance. The hexapeptide is one of the most potent GHRPs by molecular weight.
Receptor profile — GHS-R1a and beyond
Hexarelin is a potent agonist at the growth hormone secretagogue receptor 1a (GHS-R1a) — the same receptor activated by ghrelin and the other GHRPs. What distinguishes hexarelin is additional binding at the CD36 receptor in cardiac tissue, which appears responsible for its cardiovascular research signals.
Hexarelin vs other GHRPs
| Compound | GH potency | Cortisol | Prolactin | Cardiac CD36 binding |
|---|---|---|---|---|
| Hexarelin | Very high | Mild elevation | Mild elevation | Yes |
| GHRP-2 | High | Significant elevation | Mild elevation | Lower |
| GHRP-6 | Moderate | Elevation + appetite | Mild elevation | Lower |
| Ipamorelin | Selective | Negligible | Negligible | No |
Growth hormone pulse research
Hexarelin produces a strong, fast-rising GH pulse — peaking 15-30 minutes after subcutaneous administration in research models. Pulse amplitude is comparable to or greater than GHRP-2 at equivalent doses. The duration is moderate (2-3 hours to return to baseline).
Combined with a GHRH analogue (sermorelin, CJC-1295), hexarelin produces synergistic GH release. The two pathways — GHRH receptor and GHS-R1a — are independent, and their combined activation amplifies pulse magnitude.
Cardiovascular research signals
The most distinctive feature of hexarelin’s research record is cardiovascular activity independent of GH stimulation. Animal studies report:
- Cardioprotective effects in myocardial ischaemia models (Locatelli et al., 1999)
- Improved cardiac contractility post-ischaemic injury
- Reduced apoptotic cardiomyocyte death
- Possible angiogenic effects in cardiac tissue
These effects appear mediated by CD36 binding rather than GHS-R1a — and are observable in GHS-R1a knockout mice, demonstrating GH-independence.
Cortisol and prolactin off-target effects
Hexarelin produces mild elevation of cortisol and prolactin alongside GH release. The magnitude is lower than GHRP-2 or GHRP-6 but greater than ipamorelin. For research models requiring isolation of GH-specific effects, ipamorelin is preferred.
Where hexarelin fits in the GHRP landscape
- Maximum GH pulse research — hexarelin or GHRP-2
- Selective GH without cortisol — ipamorelin
- Cardiovascular protection studies — hexarelin (CD36 mechanism)
- Appetite-driven research — GHRP-6 (strongest appetite signal)
Receptor desensitisation
Like all GHRPs, hexarelin can produce receptor desensitisation under chronic or high-frequency dosing. The GHS-R1a receptor downregulates and pulse magnitude attenuates over time. Research protocols typically include rest periods to maintain pulse responsiveness.
Pharmacokinetic profile
- Subcutaneous bioavailability: ~70%
- Plasma half-life: ~70 minutes
- Peak GH response: 15-30 minutes after administration
- Primarily renal clearance
Stability and reconstitution
Hexarelin is supplied lyophilised. Reconstitution in bacteriostatic water at 1-2 mg/mL is standard. The methylated tryptophan provides resistance to oxidation. Refrigerated reconstituted hexarelin retains potency for approximately 4 weeks. Protect from light to preserve tryptophan integrity.
Research applications
- GHS-R1a pharmacology
- Cardiovascular protection studies (CD36 mechanism)
- GH/IGF-1 axis research
- Combined GHRH + GHRP synergy studies
- Receptor desensitisation kinetics
Chempeptides supplies HPLC-verified hexarelin with batch CoA — see the catalogue and our ipamorelin article for selective GHRP comparison.
Research use only.