The short version
Ipamorelin, GHRP-2, GHRP-6 and hexarelin are synthetic peptides of five or six residues that bind GHS-R1a, the ghrelin receptor, and all four release growth hormone (GH) reliably. None has been approved as a treatment anywhere, and for none is there a controlled human trial showing a change in body composition, tissue repair or performance. The differences lie elsewhere.
- Selectivity. Ipamorelin released GH in pigs with ACTH and cortisol unchanged. The three older peptides nudge ACTH, cortisol and prolactin upward.
- Appetite. Pronounced with GHRP-6, measured once in humans for GHRP-2, poorly studied for the other two.
- Durability. Hexarelin loses part of its GH effect over weeks to months of dosing and regains it after a pause.
- Another family. CJC-1295 and tesamorelin are GHRH analogues. They use a second receptor, so they are set beside the four, not ranked among them.
Ipamorelin, GHRP-2, GHRP-6 and hexarelin side by side
| Peptide | Size | GH release | ACTH, cortisol, prolactin | Appetite | Repeated dosing | Furthest point reached |
|---|---|---|---|---|---|---|
| Ipamorelin | 5 residues, 711.9 Da | Same range as GHRP-6 in swine | ACTH and cortisol flat in swine, even beyond 200 times the half-maximal GH dose | Little reported; not ruled out | Not well characterised | Phase 2; no approval |
| GHRP-2 | 6 residues, 818.0 Da | Stronger than GHRP-6 per milligram | Modest, dose-related rises in human studies | About a third more food eaten by healthy lean men | Attenuation described for the class | Japanese diagnostic licence; not approved as a treatment |
| GHRP-6 | 6 residues, 873.0 Da | Reference compound for the others | Small rises reported | Pronounced | Class attenuation; human data too sparse for a figure | Research compound; never approved |
| Hexarelin | 6 residues, 887.0 Da | Among the most potent in human studies | Rises in prolactin, ACTH and cortisol | Less studied than GHRP-6 | Partial loss over weeks to months, reversible | Clinical research in the 1990s; never marketed |
Potency is given in words on purpose. The published comparisons use different species, routes and end points, and one number per peptide would claim a precision the literature does not have.
A receptor found after its ligands
GHRP-6 was designed in the early 1980s, from opioid peptide analogues that happened to release GH, and for more than a decade nobody knew what it bound to. The target was clearly not the receptor for growth hormone-releasing hormone (GHRH). That receptor signals through cyclic AMP, whereas GHRP-6 acts through phospholipase C and intracellular calcium. GHS-R1a itself was cloned in 1996. Its natural ligand was isolated from rat stomach in 1999 and named ghrelin.
GHS-R1a is present on the GH-producing cells of the pituitary and on hypothalamic neurons, and the peptides act at both sites. At the pituitary they push stored GH out of the cell. In the hypothalamus they increase the body’s own GHRH output and lower somatostatin, the hormone that holds GH secretion back. The second site is not optional: in patients whose pituitary has lost its connection to the hypothalamus, GHRP-6 releases very little GH. Because a secretagogue works through the gland, somatostatin and IGF-1 feedback stay in force and the pituitary sets the ceiling.
Selectivity: ACTH, cortisol and prolactin
GHS-R1a was never a receptor for GH release alone, and the three older peptides show it. With GHRP-6, ACTH, cortisol and prolactin all go up a little. GHRP-2 does the same in human studies, modestly and in proportion to dose. Hexarelin raises prolactin, ACTH and cortisol alongside its GH response.
Ipamorelin, developed at Novo Nordisk, was picked from a screening programme for the opposite behaviour. Raun and colleagues (1998, European Journal of Endocrinology) gave it to swine and saw dose-related GH release with efficacy in the range of GHRP-6. ACTH and cortisol stayed essentially flat, even at more than 200 times the dose that gave half the maximum GH response. Evidence level: one animal study. Nobody has published the equivalent cortisol dose-response in people, so the selectivity is established in pigs and presumed in humans. Human pharmacology does supply a terminal half-life of about two hours after intravenous infusion.
Appetite and the fading response
The ghrelin receptor is also present in the feeding circuits of the brain. Rats ate more after GHRP-6 was delivered directly into the brain, at doses too small to change blood GH. For GHRP-2 there is a direct human measurement: Laferrère and colleagues (2005) infused it in healthy lean men in a small acute study, and the men ate about a third more than on placebo. The ipamorelin literature reports little on appetite, which is not the same as ruling it out, and for hexarelin the question has had less attention than for GHRP-6. In a metabolic experiment extra food intake is a confounder; in a model of appetite regulation it is the point.
Desensitisation is documented most clearly for hexarelin. In human studies lasting weeks to months, repeated doses produced a partly smaller GH response, which recovered after a break. Continued stimulation of the ghrelin-receptor pathway is the likeliest cause, and the effect is treated as a property of the class. Long-term human dosing data for GHRP-6 are too sparse to quantify it, and for ipamorelin the question is not well characterised.
Hexarelin has one more feature the others lack: it binds CD36, a class B scavenger receptor found on heart muscle cells among other places. In rats without a pituitary, which cannot mount a GH response, pretreatment with hexarelin still protected the heart against ischaemia and reperfusion injury. Small Italian studies recorded a rise in left ventricular ejection fraction after a single intravenous dose. Evidence level: rodent models and acute human pilot work; no cardiac indication followed.
Where CJC-1295 and tesamorelin fit
The GHRH analogues copy the hypothalamic releasing hormone, modified so that enzymes do not destroy them within minutes. They occupy the GHRH receptor on the GH-producing cell, raise cyclic AMP and drive GH synthesis as well as release. What separates them from one another is how long they last.
| Compound | What it is | Duration | Human evidence | Status |
|---|---|---|---|---|
| CJC-1295 with DAC | 29-residue GHRH fragment, four substitutions, plus the DAC linker that bonds to albumin | Half-life about 6–8 days | Phase 1 (Teichman et al., 2006), one subcutaneous dose: GH up 2- to 10-fold and raised for at least six days; IGF-1 raised for 9 to 11 days | Development discontinued; never approved |
| CJC-1295 without DAC (Mod GRF 1-29) | Identical sequence, linker absent | Minutes | Nothing dose-ranging published under this name | Never approved |
| Tesamorelin | All 44 residues of human GHRH, with a trans-3-hexenoyl group on the N-terminal tyrosine | About 26–38 minutes | Randomised trials in HIV-associated abdominal fat: 2 mg once daily for 26 weeks, visceral fat down by roughly 15% | US approval as Egrifta; no EU authorisation |
The first two rows share a name and behave differently. The DAC form produces a sustained elevation that fills in the troughs between pulses; the form without the linker adds one pulse and is gone. No published trial has compared the two head to head. Tesamorelin is the only compound on this page that also exists as a licensed medicine. Its trials found that pulsatile secretion was preserved, that visceral fat returned once dosing stopped and that IGF-1 needed monitoring. The doses in the table are those of a phase 1 study and a licensed product; they are not guidance.
A GHRH analogue given with a ghrelin mimetic releases more GH than either alone, a finding reported in human studies since the 1990s. Whether the pair changes body composition, tendon repair or performance in people has not been tested in any controlled trial. The guide to peptide combinations takes that further.
Status in the Netherlands, Belgium and Luxembourg
None of the six compounds holds a marketing authorisation in the European Union, so none is an authorised medicine in the Netherlands, Belgium or Luxembourg. In Japan GHRP-2 has a licence for diagnostic testing of GH deficiency, which is permission to run a test, not to treat, and it does not extend to the EU. Ipamorelin stopped at phase 2, in postoperative ileus. CJC-1295 was discontinued after its early trials. Tesamorelin has been approved in the United States since 2010 for excess abdominal fat in HIV-associated lipodystrophy.
Material sold as a research peptide has no authorisation and is not sold for human use. What national law says about possession and personal import varies by member state, and institutions have rules of their own; the Benelux buying guide sets out the general frame. Growth hormone secretagogues, GHRH analogues, and IGF-1 with its analogues, the class to which IGF-1 LR3 belongs, all fall under section S2 of the WADA Prohibited List, which is in force in competition and outside it. Hexarelin is named there as examorelin.
What King Peptides lists, and what it does not
Three of the six compounds are listed, in two products. Ipamorelin and CJC-1295 are sold only together, as the CJC-1295 + Ipamorelin Blend 5/5 mg; the shop has no single-peptide vial of either. Tesamorelin is listed as Tesamorelin 10 mg.
GHRP-2, GHRP-6 and hexarelin are not listed. The closest product is the CJC-1295 + Ipamorelin Blend 5/5 mg, and in each case it is a different compound: it contains another ghrelin mimetic, chosen for its lack of cortisol and prolactin effects, together with a GHRH analogue. It is no substitute when GHRP-6 is the reference compound, when appetite is the subject, or in CD36 work, since neither of its components is known as a CD36 ligand.
On the certificate of analysis (CoA), a blend has to account for two peptides. Ipamorelin should appear at 711.9 Da. CJC-1295 appears at 3647.2 Da with the DAC linker or at 3367.9 Da without it; the product name does not say which form is in the vial, so check the product page first and the measured mass second. Tesamorelin should sit at 5135.9 Da. The shop’s lab reports page lists the blend at 99% or higher by HPLC and tesamorelin at 98% or higher, and every lot comes with a lot-specific CoA carrying HPLC and mass spectrometry. The lot number printed on the CoA and the one on your vial must be identical; the CoA guide goes through the document line by line.
Parcels are tracked and leave from the Netherlands. Delivery within the Netherlands usually takes 1–2 business days; Belgium, Luxembourg and other EU countries usually take 3–5 business days, and nothing has to clear customs inside the EU. Handling of the lyophilised powder is covered in the storage and reconstitution protocol.
Quick answers
Is ipamorelin as selective in humans as it was in pigs? Unknown. The flat ACTH and cortisol result comes from one swine study; the matching human dose-response has not been published.
Which of the four belongs in an appetite model? GHRP-6, whose appetite effect is pronounced. GHRP-2 has the only direct human figure.
Can the blend replace GHRP-2, GHRP-6 or hexarelin in a protocol? No. It holds ipamorelin and CJC-1295, different compounds with a different hormonal profile. A study that needs one of the older peptides needs that peptide.
Does one blood sample show whether a secretagogue worked? No. Between pulses GH is close to zero in a healthy person. Published work samples at intervals of 10 to 20 minutes across 12 or 24 hours, runs a provocation test, or reads IGF-1 as an integrated marker, and IGF-1 values from different assay platforms are not interchangeable.
Research use only. Everything on PeptidenBenelux.com describes peptides for laboratory research. Nothing here is medical advice. Always comply with the laws that apply in your jurisdiction.