Ipamorelin and GHRP-2 act at the same receptor — the growth hormone secretagogue receptor GHS-R1a, the ghrelin receptor — but they differ in selectivity, and that is the whole basis for choosing between them. GHRP-2 descends from the enkephalin-derived GHRP-6 scaffold and has been reported to move cortisol, prolactin and appetite signalling alongside growth hormone; ipamorelin was characterised specifically as producing a comparatively clean growth hormone response in animal models. In an ipamorelin vs GHRP-2 comparison, the deciding question is whether your readouts include anything the broader neuroendocrine background would contaminate.
Both are supplied as lyophilized powder with lot-matched HPLC certificates — ipamorelin in 2, 5 and 10 mg vials and GHRP-2 in 5 and 10 mg vials — and both sit in GHRPs and secretagogues. Both are research chemicals for in-vitro and preclinical laboratory work only, not for human or veterinary use.
Ipamorelin vs GHRP-2 at a glance
| Attribute | Ipamorelin | GHRP-2 |
|---|---|---|
| Also called | NNC 26-0161 | Pralmorelin, KP-102 |
| Receptor | GHS-R1a (ghrelin receptor) | GHS-R1a (ghrelin receptor) |
| Length | 5 residues (pentapeptide) | 6 residues (hexapeptide) |
| Sequence | Aib-His-D-2-Nal-D-Phe-Lys-NH2 | D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2 |
| Lineage | Designed for selectivity; not derived from GHRP-6 | Descends from the enkephalin-derived GHRP-6 scaffold |
| CAS number | 170851-70-4 | 158861-67-7 |
| Molecular formula | C38H49N9O5 | C45H55N9O6 |
| Molecular weight | 711.85 g/mol | 817.97 g/mol |
| Reported selectivity | Comparatively clean GH response in animal models | Reported to also move cortisol, prolactin and appetite signalling |
| Unnatural residues | Aib, D-2-Nal, D-Phe, C-terminal amide | D-Ala, D-2-Nal, D-Phe, C-terminal amide |
| Photosensitive residue | None — no tryptophan | Tryptophan at position 4 |
| Typical research role | Isolating GHS-R1a signalling from neuroendocrine background | Reference agonist; potency calibration across the GHRP family |
| Research sizes stocked | 2 mg, 5 mg, 10 mg | 5 mg, 10 mg |
| Purity | ≥99% HPLC, MS identity, lot-matched COA | ≥99% HPLC, MS identity, lot-matched COA |
A shared pharmacophore with different flanks
Line the two sequences up and the family resemblance is obvious. Both carry D-2-naphthylalanine, both carry D-phenylalanine, and both terminate in Lys-NH2. That D-2-Nal residue is the potency-defining substitution across the GHRP family — it is what raised GHRP-2's potency above the parent GHRP-6 scaffold — and the C-terminal amide removes the negative charge a free carboxyl terminus would carry, which matters for receptor engagement and for resistance to carboxypeptidases.
Where they differ is at the N-terminal end and in length. GHRP-2 begins with D-alanine, a substitution that blunts aminopeptidase attack, and inserts alanine and tryptophan into the middle of the chain, giving six residues. Ipamorelin begins with alpha-aminoisobutyric acid, a non-proteinogenic residue that constrains the backbone conformation as well as resisting proteolysis, and reaches the same pharmacophore in five residues.
The consequence is that both are compact, protease-resistant molecules with well-defined synthesis, but ipamorelin is a smaller and more conformationally constrained ligand. Its 711.85 g/mol against GHRP-2's 817.97 g/mol also means a milligram of ipamorelin contains about 15 percent more material in molar terms — a difference large enough to distort a comparison prepared by mass.
Selectivity: the substantive difference
The GHS-R1a receptor sits within a neuroendocrine system that also touches the hypothalamic–pituitary–adrenal axis, prolactin release and appetite regulation. Earlier growth hormone secretagogues — GHRP-6, hexarelin and GHRP-2 among them — were reported to produce measurable movement in cortisol, ACTH and prolactin alongside the growth hormone response, and in the case of the GHRP-6 lineage, in food intake as well.
Ipamorelin was characterised against exactly that background. The published animal work describing it emphasised a growth hormone response without the accompanying cortisol and prolactin changes seen with the earlier compounds, and that reported selectivity is the reason it became a standard tool for isolating GHS-R1a signalling from the wider neuroendocrine picture.
Two qualifications belong here. First, selectivity claims of this kind derive from animal and cell work and are quantitative rather than absolute — "comparatively clean" is not "no off-target effects at any concentration". Second, GHRP-2's broader profile is not a defect. If the research question is about the interaction between secretagogue signalling and the HPA axis, or about appetite pathways, then the broader compound is the informative one and ipamorelin would show you nothing.
Historical role and what each is good for in the record
GHRP-2 has a specific historical importance: it was one of the compounds that established the growth hormone secretagogue receptor as a target distinct from the GHRH receptor, years before ghrelin was identified as the natural ligand. That lineage makes it a useful reference agonist — laboratories use it to characterise GHS-R1a binding, to calibrate calcium-flux and inositol-phosphate assays, and to anchor potency comparisons across the family alongside GHRP-6 and hexarelin. It also has a regulatory history in some jurisdictions as a diagnostic agent for growth hormone secretion testing, which is a use of the regulated pharmaceutical article and not of research-grade powder.
Ipamorelin's role is different. It is the compound of choice when a design needs GHS-R1a engagement without the confound, which makes it the more common partner in combination work with GHRH analogs — two different receptors, two different arms of the somatotropic axis. We stock co-formulated CJC-1295 with ipamorelin and ipamorelin with GHRP-2 vials for such designs, and CJC-1295 (No DAC) separately where single-component arms are needed. Our overview of the secretagogue landscape maps the whole family.
Which to choose for which research question
Choose ipamorelin when the readout must be clean
If the design measures growth hormone output, downstream IGF-1, or GHS-R1a signalling specifically, and cortisol, prolactin or feeding behaviour would be confounders, ipamorelin's reported selectivity is the reason it exists. It is also the appropriate secretagogue arm in a two-receptor combination study, where an off-target signal would be impossible to assign to one compound or the other.
Choose GHRP-2 when the broader profile is the subject
If the question concerns the relationship between secretagogue signalling and the HPA axis, prolactin release, or appetite pathways, GHRP-2 engages what you want to measure. It is also the better reference for potency calibration across the family and for replicating the older secretagogue literature, much of which used it.
Run both when selectivity itself is the variable
The pair is a well-defined two-point selectivity series: same receptor, shared pharmacophore, different reported off-target breadth. Running them together with the full panel of endocrine readouts — not only growth hormone — is the standard way to test a selectivity claim rather than inherit it. Adding GHRP-6 or hexarelin extends the series; see ipamorelin vs GHRP-6 and hexarelin vs ipamorelin for those pairings.
Handling, reconstitution and storage differences
Both are short, amidated peptides with unnatural residues and both are comparatively easy to work with: no lipid tails, no free thiols, no reactive linkers. The standard protocol covers both — sealed lyophilized vials held frozen, brought to room temperature before the stopper is pierced so moisture does not condense on cold powder, reconstituted by running diluent down the vial wall, dissolved without shaking, and aliquoted so stock is not repeatedly frozen and thawed. See our reconstitution guide and storage guide.
One difference is worth a specific note. GHRP-2 contains tryptophan at position 4, and tryptophan is the residue most susceptible to photo-oxidation in peptides — it degrades on exposure to light, particularly in aqueous solution and in the presence of dissolved oxygen or trace metals. GHRP-2 solutions should be protected from light and prepared reasonably fresh. Ipamorelin contains no tryptophan and is comparatively indifferent to light, though its naphthylalanine residue is still aromatic and prolonged strong illumination is best avoided with either.
Concentration is a laboratory calculation, not a recommendation for use: a 5 mg vial reconstituted with 2 mL of diluent gives 2.5 mg/mL, or 2,500 mcg/mL, so 0.1 mL contains 250 mcg. Because the two masses differ by about 15 percent, equal mass concentrations are not equal molarities, and any potency comparison should be prepared and reported in molar terms.
Purity, identity and COA checks
Request the lot-matched certificate for each vial and confirm HPLC purity with a visible chromatogram, a mass-spectrometric result matching the expected weight — 711.85 g/mol for ipamorelin and 817.97 g/mol for GHRP-2 — and a lot number matching the vial. Two checks apply specifically to this pair. Both peptides are C-terminally amidated, and a free-acid impurity differs by 1 Da, elutes close to the parent and is a different molecule for receptor purposes, so amidation should be confirmed rather than assumed. Both also contain D-amino acids, and epimerisation during synthesis produces diastereomers of identical mass that a mass spectrum cannot distinguish — which is why a visible chromatogram showing a single sharp peak matters more here than the numerical purity figure. For GHRP-2, a satellite peak 16 Da above the parent can indicate tryptophan oxidation in aged material. Our COA guide explains what a complete document should contain.
Regulatory framing
Ipamorelin and GHRP-2 are supplied as research chemicals for laboratory use only. Neither is an approved medicine in the United States. GHRP-2 has a regulatory history as a diagnostic agent in some jurisdictions, but that status attaches to a regulated pharmaceutical article rather than to research-grade powder. Nothing on this page is a protocol for human or veterinary use. For broader context see our growth and performance research overview.