Peptide Medix product catalog

ET
Editorial Team
August 16, 2026 6 min read

GHRP-2, also catalogued as pralmorelin, is a synthetic hexapeptide agonist of the growth hormone secretagogue receptor GHS-R1a with the sequence D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2 — a second-generation refinement of the GHRP-6 scaffold in which a D-2-naphthylalanine at position 2 sharply increased potency. It occupies a specific historical position: GHRP-2 was one of the compounds that proved a receptor distinct from the GHRH receptor must exist, years before ghrelin was identified as its natural ligand. It is also the only member of the class with a regulatory approval anywhere, having been authorised in Japan as a diagnostic agent for assessing growth hormone secretion.

This page covers the structure and what each modification contributes, the receptor mechanism, the published research, and how the material is specified and handled. GHRP-2 is supplied for laboratory research use only.

GHRP-2 at a glance

PropertyValue
Also known asPralmorelin; KP-102
SequenceD-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2
Length6 residues, C-terminally amidated
CAS number158861-67-7
Molecular formulaC45H55N9O6
Molecular weight817.97 g/mol
ReceptorGHS-R1a (ghrelin receptor), class A GPCR
SignallingGq → phospholipase C → IP3 / DAG → intracellular calcium
Reported off-target movementProlactin, ACTH and cortisol reported to rise more than with ipamorelin
Regulatory noteApproved in Japan as a diagnostic agent for growth hormone secretion testing
Sizes supplied5 mg, 10 mg lyophilized vials
Purity specification≥99% by RP-HPLC with lot-matched COA

Origin and structure: a second-generation hexapeptide

The growth hormone-releasing peptide series began with work on met-enkephalin analogues in the 1980s, which produced GHRP-6, His-D-Trp-Ala-Trp-D-Phe-Lys-NH2. The discovery that these opioid-derived fragments released growth hormone through a mechanism GHRH antagonists could not block implied an unknown receptor, and the medicinal chemistry that followed aimed at greater potency on the same scaffold.

GHRP-2 is the product of that effort. Two changes distinguish it from GHRP-6. The first is the substitution of D-2-naphthylalanine for the D-tryptophan at position 2 — a bicyclic aromatic side chain in place of an indole, larger and more hydrophobic, and the change most responsible for the increase in potency. The second is D-alanine at the N-terminus in place of histidine, which removes the imidazole side chain and, more importantly, places a D-residue at the position aminopeptidases attack first. The rest of the scaffold is conserved: the tryptophan at position 4, the D-phenylalanine at position 5 and the amidated lysine at position 6 are common to both compounds and to hexarelin.

At 817.97 g/mol GHRP-2 sits between ipamorelin at 711.85 and GHRP-6 at 873.01. All three are small enough that molar quantities per milligram are high compared with any GHRH analogue, which is the practical reason 5 mg and 10 mg vials cover a great deal of work.

How GHRP-2 is thought to work

GHRP-2 is an agonist at GHS-R1a, a class A G protein-coupled receptor expressed on pituitary somatotrophs and in the hypothalamus. Receptor occupancy activates Gq, which stimulates phospholipase C, generates inositol trisphosphate and diacylglycerol, and raises intracellular calcium to trigger secretory granule release. A second reported contribution is suppression of somatostatin tone, which lifts an inhibitory brake at the same time as the stimulatory signal is applied. The receptor also displays high constitutive activity in the absence of ligand, which is why it features so heavily in inverse-agonist pharmacology.

The clinically relevant characteristic of GHRP-2 in the comparative literature is that its effects are not confined to growth hormone. Published studies report increases in prolactin, ACTH and cortisol alongside growth hormone release, more so than with ipamorelin at equivalent growth-hormone-releasing potency. Whether that is a drawback depends entirely on the experiment: it is a confound in a study isolating somatotroph signalling, and it is the phenomenon itself in work on secretagogue receptor involvement in the hypothalamic-pituitary-adrenal axis. GHRP-2 has also been reported to have a weaker effect on appetite signalling than GHRP-6, which is the axis on which the two older hexapeptides most differ from each other.

What research has examined

Receptor discovery and characterisation

GHRP-2 is one of the tool compounds that established GHS-R1a as a target distinct from the GHRH receptor before the endogenous ligand was known. It remains a standard reference agonist in binding assays, calcium flux and inositol phosphate accumulation experiments, and in potency ranking across the growth hormone secretagogue class.

Diagnostic endocrinology

Pralmorelin is approved in Japan as a diagnostic agent for evaluating growth hormone secretory capacity, where a defined stimulus with a predictable response is exactly what is required. This is a diagnostic authorisation for a pharmaceutical product administered under medical supervision, and it does not transfer to research-grade material.

Comparative secretagogue pharmacology

Almost every study ranking this class includes GHRP-2, usually alongside GHRP-6, hexarelin and ipamorelin. The selectivity contrast with ipamorelin is examined in ipamorelin vs GHRP-2.

Combination designs

Because GHS-R1a and the GHRH receptor act on the same cell through different second messengers, pairing a secretagogue with a GHRH analogue is a standard experimental design; pre-blended research material exists as CJC-1295 with GHRP-2. Any such study should state both molar concentrations, since the two peptides differ in molecular weight by roughly fourfold.

Forms and sizes we supply

GHRP-2 is stocked as a lyophilized powder in 5 mg (USD 50) and 10 mg (USD 80) sealed vials. At 817.97 g/mol a 5 mg vial contains approximately 6.11 micromoles, roughly four times the molar content of a 5 mg vial of a GHRH analogue — the reason mass-based comparisons across the two receptor systems are misleading. The class sits under GHRPs and secretagogues.

Reconstitution and storage in a laboratory context

The calculation: a 5 mg vial reconstituted with 2 mL of bacteriostatic water gives 2.5 mg/mL, equivalently 2,500 mcg/mL; 0.1 mL (10 units on a U-100 syringe) contains 250 mcg. In molar terms the stock is approximately 3.06 mM, so an assay running at 10 nanomolar requires roughly a 300,000-fold dilution, performed in stages rather than in one step.

GHRP-2 has no cysteine, no methionine and no asparagine, which removes the disulfide, oxidation and deamidation problems that dominate stability discussions elsewhere. Its one sensitivity is the tryptophan at position 4: indole side chains are photosensitive and can degrade under prolonged light exposure, which is a practical reason to keep both powder and solution protected from light rather than a purely precautionary one. Two large aromatic side chains also make the peptide less hydrophilic than its size suggests, so allow the cake to dissolve fully and inspect for clarity. Lyophilized vials are stored at −20 °C protected from light and moisture; reconstituted solution is refrigerated and aliquoted. Detail is in the peptide storage guide.

Purity, COA and how to read one

Each lot is purified by reversed-phase HPLC to at least 99% with mass confirmation and a lot-matched certificate. Three checks apply. First, confirm the mass against 817.97 g/mol for the amidated hexapeptide; a value about 1 Da higher indicates the free acid. Second, distinguish it from its siblings, which is easy by mass and worth doing: GHRP-6 is 873.01 g/mol and ipamorelin is 711.85, so a mis-labelled vial is immediately apparent from the certificate. Third, understand the limit of the method: the D configurations at positions 1, 2 and 5 are isobaric with their L counterparts and cannot be confirmed by mass spectrometry, so stereochemical confidence rests on synthesis documentation, clean chromatographic resolution or dedicated chiral analysis. Our COA reading guide sets out what each analytical section establishes.

Regulatory status

Pralmorelin holds a diagnostic approval in Japan as a pharmaceutical product used under medical supervision. It has no marketing authorisation in the United States, is not a dietary supplement ingredient, and is not a generally available compounded medication. Material supplied here is research use only, for in-vitro and preclinical laboratory investigation by qualified researchers, and is not intended for human or veterinary administration. A foreign diagnostic approval is not a licence for any other use of research-grade peptide.

Related peptides and further reading

GHRP-6 is the founding compound of the class and the appropriate comparator for appetite-related work; ipamorelin is the selective modern standard; hexarelin is the most potent and least selective of the group. On the other arm of the axis, sermorelin, Modified GRF 1-29 and tesamorelin act at the GHRH receptor through cyclic AMP rather than calcium. The whole picture is mapped in the GH secretagogue landscape explained.

Frequently Asked Questions

What is GHRP-2?
GHRP-2, also called pralmorelin or KP-102, is a synthetic hexapeptide with the sequence D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2. It weighs 817.97 g/mol and carries CAS number 158861-67-7. It is an agonist at the growth hormone secretagogue receptor GHS-R1a, the receptor whose endogenous ligand is ghrelin.
How does GHRP-2 differ from GHRP-6?
Two substitutions. GHRP-2 carries D-2-naphthylalanine at position 2 in place of GHRP-6's D-tryptophan, a larger and more hydrophobic bicyclic side chain that is chiefly responsible for its higher potency. It also has D-alanine at the N-terminus in place of histidine, which places a D-residue where aminopeptidases attack first. The remainder of the scaffold is conserved.
Does GHRP-2 affect anything besides growth hormone?
Published studies report increases in prolactin, ACTH and cortisol alongside growth hormone release, more so than with ipamorelin at equivalent growth-hormone-releasing potency. Whether that matters depends on the experiment: it is a confound when isolating somatotroph signalling, and it is the phenomenon of interest in work on secretagogue receptor involvement in the adrenal axis.
Is GHRP-2 approved anywhere?
Pralmorelin holds an approval in Japan as a diagnostic agent for evaluating growth hormone secretory capacity, used as a pharmaceutical product under medical supervision. It has no marketing authorisation in the United States, is not a dietary supplement and is not a generally available compounded medication. A foreign diagnostic approval does not licence any other use of research-grade peptide.
How does GHS-R1a signalling work?
GHS-R1a is a class A receptor coupling predominantly to Gq. Agonist binding activates phospholipase C, generating inositol trisphosphate and diacylglycerol and raising intracellular calcium, which triggers secretory granule release. Suppression of somatostatin tone is a second reported contribution, and the receptor also displays high constitutive activity in the absence of ligand.
How can GHRP-2 be told apart from GHRP-6 and ipamorelin on a certificate?
By mass, easily. GHRP-2 is 817.97 g/mol, GHRP-6 is 873.01 g/mol and ipamorelin is 711.85 g/mol, so a mislabelled vial is immediately apparent from the mass spectrometry section. A value about 1 Da above the expected mass indicates the free acid rather than the required C-terminal amide.
What are the storage sensitivities of GHRP-2?
It contains no cysteine, methionine or asparagine, so disulfide scrambling, oxidation and deamidation do not apply. Its one real sensitivity is the tryptophan at position 4, whose indole side chain is photosensitive and can degrade under prolonged light exposure. Powder and solution should therefore be protected from light, with vials at minus 20 degrees Celsius and solution refrigerated and aliquoted.
Why is GHRP-2 historically important?
It was one of the tool compounds showing that growth hormone could be released through a mechanism GHRH antagonists could not block, implying a receptor distinct from the GHRH receptor. That receptor was cloned as GHS-R1a in 1996 and its endogenous ligand ghrelin identified in 1999. GHRP-2 remains a widely cited reference agonist in that literature.

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