What are hexarelin and ipamorelin?
Hexarelin and ipamorelin are both synthetic growth hormone releasing peptides (GHRPs) that act on the growth hormone secretagogue receptor (GHS-R1a), the same receptor ghrelin activates naturally. Researchers who pair a GHRP with CJC-1295 have to pick one of the two, and the choice changes what else gets measured alongside growth hormone in a research protocol.
Hexarelin is a synthetic hexapeptide (His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2) developed by Romano Deghenghi's group in the early 1990s. Ghigo et al. tested it by intravenous, subcutaneous, intranasal, and oral routes in a 1994 study in the Journal of Clinical Endocrinology and Metabolism (PMID 8126144). At 1 microgram/kg intravenously, hexarelin produced a GH response roughly twice that of an equal dose of GHRH.
Subcutaneous bioavailability reached 77 percent; intranasal dropped to 4.8 percent; oral doses of 20 to 40 mg reached only 0.3 percent bioavailability but still raised GH in a dose-related pattern.
Ipamorelin is a pentapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2) developed by Novo Nordisk. Raun et al. described it in a 1998 paper in the European Journal of Endocrinology (PMID 9849822) as the first GHRP-receptor agonist with a selectivity for GH release similar to that displayed by GHRH. The CJC-1295 and ipamorelin research overview covers ipamorelin's pairing with CJC-1295 in more depth, and the hexarelin research overview covers hexarelin on its own.
Mechanism: one receptor, two different outcomes
Both peptides bind GHS-R1a on pituitary somatotrophs and trigger the same downstream signal, a rise in intracellular calcium that drives growth hormone secretion. The difference shows up off-target. Hexarelin also binds CD36, a scavenger receptor expressed in cardiac tissue that has nothing to do with growth hormone release.
Bodart et al. identified CD36 as hexarelin's cardiac binding site in a 2002 study in Circulation Research (PMID 11988484), using a radioactive hexarelin derivative to label rat cardiac membranes. Hexarelin activation of CD36 raised coronary perfusion pressure in a dose-dependent manner in perfused hearts, an effect that disappeared entirely in CD36-knockout mice while staying intact in GHS-R1a-knockout mice. The cardiac activity runs through a separate receptor from the one that releases GH.
Ipamorelin does not show this dual-receptor behavior. Raun et al. reported that ipamorelin failed to raise ACTH or cortisol above GHRH-stimulation levels even at doses more than 200 times its ED50 for GH release, a selectivity margin the paper described as unmatched among the GHRP-receptor agonists tested at that point. The pentapeptide structure appears to restrict binding to the pituitary GHS-R1a population without engaging CD36 or the corticotroph pathways that hexarelin and other GHRPs activate.
What the dose-response studies show
Massoud, Hindmarsh, and Brook ran a dose-response study of intravenous hexarelin (0 to 1.0 microgram/kg) in healthy adult men, published in 1996 in the Journal of Clinical Endocrinology and Metabolism (PMID 8954038). GH response plateaued at 140 mU/L with an ED50 of 0.48 microgram/kg. Prolactin rose in step with dose, peaking at 180 percent above baseline. Cortisol showed a stepped increase at higher doses rather than a smooth curve.
When the researchers combined a low dose of hexarelin with GHRH, GH release increased sharply while prolactin rose only moderately and cortisol barely moved, which suggests the co-release effects depend partly on dose rather than being fixed to the compound.
Ipamorelin's clinical program went further than a dose-response study. Novo Nordisk and later Helsinn Therapeutics advanced it into a Phase 2 trial (ClinicalTrials.gov NCT01280344) testing whether intravenous ipamorelin, dosed at 0.03 to 0.06 mg/kg two or three times daily, could speed recovery of gastrointestinal function in 320 patients following bowel resection.
The trial reached completion, but no synthetic GHRP, ipamorelin included, has received regulatory approval for human use. Hexarelin has not been taken past early-phase human dose-response and physiology studies either. Neither peptide has become an approved drug.
Hexarelin vs ipamorelin: key differences at a glance
| Feature | Hexarelin | Ipamorelin |
|---|---|---|
| Structure | Hexapeptide, 6 amino acids | Pentapeptide, 5 amino acids |
| Receptor targets | GHS-R1a plus CD36 (cardiac tissue) | GHS-R1a selectively |
| Acute GH response (IV) | Roughly 2x GHRH at matched dose (Ghigo et al., 1994) | Lower acute response than hexarelin at matched dose |
| Cortisol/ACTH effect | Stepped, dose-dependent rise (Massoud et al., 1996) | No significant rise even above 200x ED50 (Raun et al., 1998) |
| Prolactin effect | Dose-dependent rise, up to 180% above baseline | Not significantly elevated in the selectivity studies |
| Cardiac receptor activity | CD36-mediated, independent of GHS-R1a (Bodart et al., 2002) | No documented CD36 activity |
| Furthest human trial phase | Dose-response and physiology studies only | Phase 2, GI motility recovery (NCT01280344) |
Choosing between them in a research protocol
The practical question for a researcher pairing a GHRP with CJC-1295 is what happens to cortisol and prolactin readings alongside the GH data. If the protocol needs to isolate the GH axis without confounding stress-hormone activation, ipamorelin's selectivity profile is the more defensible pick. The Raun et al. data give researchers a documented basis for treating cortisol and prolactin as largely unaffected across the concentration ranges studied.
If a protocol specifically targets the CD36-mediated cardiac pathway or calls for maximum acute GH output regardless of secondary hormone shifts, hexarelin's dual-receptor mechanism is the reason a study would choose it, not a limitation to design around.
Neither peptide should be reconstituted with anything other than bacteriostatic water at research-grade purity. See the peptide reconstitution guide for the general procedure and the dosing calculator for volume math specific to each vial's labeled concentration. Both peptides degrade with repeated freeze-thaw cycling, so aliquoting reconstituted solution into single-use volumes cuts down on how often a stock vial leaves the freezer.
Storage and sourcing in Indonesia
Lyophilized hexarelin and ipamorelin both tolerate short transit at ambient temperature, but Indonesia's climate does not offer much margin. Bali, Jakarta, and most of the archipelago sit above 28 degrees C for most of the year, and a package left on a doorstep in direct sun for several hours degrades faster than the same vial held indoors at room temperature. Move lyophilized stock into a refrigerator within a few hours of delivery, and into a -20 degrees C freezer if it will sit for more than a week before use.
Once reconstituted, both peptides should stay refrigerated and get used within roughly two to four weeks, consistent with the general handling guidance in the lyophilized peptide storage guide. Hexarelin, ipamorelin, and CJC-1295 are available through Zurich Biotech, each shipped with a third-party HPLC certificate of analysis to Bali, Jakarta, Surabaya, and other tier-1 Indonesian cities.