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Research use only
· 7 min read
Two peptides, one receptor, and roughly a decade of chemistry between them. Ipamorelin and GHRP-6 both switch on the growth-hormone-secretagogue receptor, yet they were built to different specifications and carry very different research histories. GHRP-6 was synthesised before its own receptor even had a name; ipamorelin arrived years later as a deliberately trimmed-down, selective design. This page sets the two side by side by receptor pharmacology, selectivity, chemistry and evidence maturity, and nowhere by any effect on a living body.
Both are supplied by Kovalabs strictly as research reagents. Everything below describes verified molecular identity and what published studies set out to investigate, not any human use, benefit, dose or outcome. Neither compound is a licensed medicine.
| Property | Ipamorelin | GHRP-6 |
|---|---|---|
| Peptide class | Pentapeptide (5 residues) | Hexapeptide (6 residues) |
| Sequence | Aib-His-D-2-Nal-D-Phe-Lys-NH2 | His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 |
| Molecular formula | C38H49N9O5 | C46H56N12O6 |
| Molecular weight | 711.9 g/mol | 873.0 g/mol |
| CAS number | 170851-70-4 | 87616-84-0 |
| PubChem CID | 9831659 | 9919153 (CAS-anchored) |
| Synonym | NNC 26-0161 | SK&F-110679; Hexapeptide-2 |
| Receptor target | GHS-R1a (ghrelin receptor) | GHS-R1a (ghrelin receptor) |
| Receptor design note | Characterised as a selective GHS-R1a agonist | Prototypical, less selective GHS-R agonist |
Identifiers were cross-checked against the authoritative PubChem records. For GHRP-6 there is a well-known trap: a plain name search also surfaces PubChem CID 4345065, a connectivity-only record with the same formula and mass but no stereochemical descriptors and no CAS linkage. It is the same backbone, not a fully defined citation. The authoritative record for the defined compound is CID 9919153.
GHRP-6 (growth-hormone-releasing hexapeptide-6) is the older of the two and, in a neat inversion of the usual order, was characterised before the receptor it binds had been formally identified. Cyril Bowers built the growth-hormone-releasing peptide series, and Bowers (Cellular and Molecular Life Sciences, 1998; PMID 9893708) reviews GHRP-6 as a synthetic agonist at the growth-hormone-secretagogue receptor, with a binding site described as distinct from that of growth-hormone-releasing hormone. That receptor was later de-orphanised when ghrelin was discovered as its endogenous ligand.
Ipamorelin (NNC 26-0161) is the newer, leaner molecule. Raun et al. (European Journal of Endocrinology, 1998; PMID 9849822) is the primary report that introduced it and defined its pentapeptide structure, characterising ipamorelin as a selective growth-hormone secretagogue at the same GHS-R1a receptor. Two D-amino acids and an amide-capped C-terminus are structural signatures of its identity. In short, both sit in the family of GHS-R agonist peptides; one is the prototype, the other a later, more selective refinement. Each has its own reference monograph and product page: ipamorelin and GHRP-6.
The GHRP-6 vs ipamorelin distinction is not one of receptor identity. Both are agonists at GHS-R1a, the class-A G-protein-coupled receptor that ghrelin also binds. The difference is one of design and selectivity. GHRP-6 is the six-residue prototype: a broad, less selective ligand for the receptor system, and the peptide the whole GHS field was effectively built around. Ipamorelin is the five-residue successor, engineered as a selective GHS-R1a agonist.
That selectivity language is a receptor-pharmacology descriptor, not a statement about anything happening in a body. It matters at the level of study design: the foundational ipamorelin report named plasma ACTH and cortisol concentrations as comparator hormonal endpoints alongside the growth-hormone-secretagogue readout, which is how a molecule's selectivity profile is characterised in the first place. Naming those endpoints tells you what the experiment was built to measure. It says nothing about what the experiment found, and this page reproduces no result. The intracellular pathway on the GHRP-6 side has its own characterisation: Lei et al. (Journal of Molecular Endocrinology, 1995; PMID 7772238) ran an in-vitro assay in cultured human pituitary somatotroph cells with phosphatidylinositol turnover, a phospholipase-C second-messenger readout, as the pre-specified endpoint. Study design and endpoint name only; no effect is asserted.
For contrast, a mechanistically distinct sibling in the same growth-hormone axis is sermorelin, which is a growth-hormone-releasing-hormone analogue acting on the GHRH receptor rather than the ghrelin receptor. Same broad axis, a genuinely different door. Grouping ipamorelin and GHRP-6 together, and sermorelin separately, is a receptor-pharmacology call, not an indication one.
This is the question the search box really wants answered, and it is worth stating plainly why we will not answer it the way it is usually meant. "Better" only has meaning against a goal in a living organism, and neither compound has an established outcome in a person to be better or worse at. The one distinction that is properly sourced is selectivity. The foundational ipamorelin report characterised it as a selective growth-hormone secretagogue, naming plasma ACTH and cortisol as comparator hormonal endpoints against which that selectivity was defined; GHRP-6 is the earlier, less selective prototype of the class. That is a receptor-pharmacology descriptor about how each ligand was characterised in study design, and it is the correct level to keep it at. It is not a benefit, an indication, or a reason to pick one vial over another for any use.
So the ipamorelin GHRP-6 difference that actually holds up is chemical and historical, not clinical. One is a selective five-residue design; the other is the less selective six-residue prototype that came first. Choosing between them for research is a question about experimental aims and reference-standard quality, not about which one is stronger in a body, because that comparison has not been established for either.
Both compounds reward a sceptical, tiered read of their literature. The confidence drops sharply as you move from chemistry towards anything resembling a human outcome.
The honest close: neither ipamorelin nor GHRP-6 is a licensed medicine, and a mapped receptor plus a handful of design-stage studies is not the same as a demonstrated effect in people. Do not read the existence of a trial registration as evidence of an outcome, and do not import an expectation from any approved growth-hormone-axis product. The receptor is well described. The human ledger is thin, and this page keeps it that way.
A vial labelled ipamorelin is not automatically a vial that contains ipamorelin, and the same goes for GHRP-6. Peptide identifiers are easy to print and easy to get wrong, which is why every Kovalabs batch, and every variant and strength within a product, is tested at ILS Laboratories in San Diego, an ISO/IEC 17025 accredited lab. Net peptide content is measured per fill rather than assumed from one representative strength.
Each report carries peptide purity by RP-HPLC (area normalization at 214 nm) with the actual chromatogram shown, identity by HPLC retention-time matching against a reference standard, net peptide content against the label, and a fentanyl screen by immunoassay. The certificate is addressed "Tested for Kovalabs" as a chain-of-custody line, and a QR code verifies it at the lab's own portal. You can see a live example on the GHK-Cu certificate of analysis for lot CU50-242: 99.07% purity, net peptide content 50.84 mg against a 50 mg label, fentanyl not detected. That is what checking net peptide content and purity against the documented identifiers looks like in practice, rather than taking a label on trust. Browse current documents on the certificate of analysis page.
Both peptides ship lyophilised. As histidine-, tryptophan- and phenylalanine-bearing sequences, they are best held desiccated, cold and out of the light, with freeze-thaw cycles minimised; reconstituted solutions are typically kept at 2 to 8 C for a defined working window. The bench procedure and dilution maths live on the reconstitution guide. None of this is a preparation method for use in a human or an animal; it is handling information for a research reagent.
Publication titles are the original authors' own titles, not statements or claims by Kovalabs. Studies are cited by design and endpoint name only; no result, effect or magnitude is reproduced.
Both are synthetic agonists at the same growth-hormone-secretagogue receptor (GHS-R1a, the ghrelin receptor), so the difference is chemical and pharmacological, not a difference in receptor target. Ipamorelin is a five-residue pentapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2, C38H49N9O5) characterised as a selective GHS-R1a agonist. GHRP-6 is the older six-residue hexapeptide (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2, C46H56N12O6), the less selective prototype of the class. Both are research reference compounds, not medicines.
We cannot answer that, because "stronger" describes an effect in a living organism and neither compound has an established human outcome to compare. The literature on both is receptor-level and pre-clinical, reported here by study design and endpoint name only. Any comparison on this page is one of chemistry, selectivity and evidence maturity, never of potency in a body.
Yes. Both act at the growth-hormone-secretagogue receptor GHS-R1a, the receptor for which ghrelin is the endogenous ligand. Raun et al. (1998, PMID 9849822) characterised ipamorelin as a selective agonist at that receptor, and Bowers (1998, PMID 9893708) describes GHRP-6 as a synthetic agonist within the same series. That shared receptor is why they are grouped together by pharmacology.
Because the two were characterised to different specifications. The foundational ipamorelin report (Raun et al., 1998, PMID 9849822) characterised it as a selective growth-hormone secretagogue and named plasma ACTH and cortisol as comparator hormonal endpoints, which is how a selectivity profile is defined in study design. GHRP-6 (Bowers, 1998, PMID 9893708) is the earlier, less selective prototype of the class. That is a receptor-pharmacology descriptor about how each was characterised, not a benefit, an indication or a claim of any effect in a person or animal.
No. The published record for both consists of receptor-level, in-vitro and animal work, plus design-stage human study registrations reported here by design descriptor only. None of it establishes a benefit, effect, safety profile or outcome in humans. Neither is a licensed medicine, and both are supplied strictly as reference compounds for non-clinical laboratory research.
Check the batch certificate of analysis rather than trusting the label. Every Kovalabs batch is tested at the ISO/IEC 17025 accredited ILS Laboratories, with purity by RP-HPLC (the chromatogram shown), identity by HPLC retention-time matching against a reference standard, net peptide content measured per fill, and a fentanyl screen. A QR code verifies each report at the lab's own portal, so the net peptide content and purity can be checked against the documented identifiers.
Research use only
Research use only. Ipamorelin and GHRP-6 are supplied by Kovalabs strictly as reference compounds for in-vitro and laboratory research. Neither is a medicine, a supplement, or for human or veterinary use, and nothing on this page describes a dose, route, schedule or outcome. Every study above is reported by design and endpoint name only, with no result reproduced. Neither compound has been evaluated by the MHRA or any comparable regulator for safety or efficacy in humans or animals. Every batch ships with a third-party certificate of analysis. Read the full research disclaimer before ordering.