GHRP-2 Research Peptide

GHRP-2 is a six-residue synthetic agonist of the ghrelin receptor, sequence D-Ala-D-2-Nal-Ala-Trp-D-Phe-Lys-NH2, formula C45H55N9O6, with a molecular weight close to 818 g/mol. It is the same molecule as pralmorelin. Crown Peptides offers it in a single 10mg fill size, and catalogues also list it as GHRP 2 or GHRP2.

Only in one specific form. Pralmorelin dihydrochloride is approved in Japan as a diagnostic reagent for testing growth-hormone reserve, marketed by Kaken Pharmaceutical as GHRP Kaken 100. That salt carries its own CAS number, 158827-34-0, distinct from the 158861-67-7 given for the peptide on this page. It holds no licence as a treatment, and the Japanese approval does not extend to research material.

Pralmorelin is the official non-proprietary name, and its -relin ending places it in the naming family for peptides that prompt pituitary hormone release, alongside sermorelin and tesamorelin. KP-102 was its code during the Japanese clinical programme, and some older pharmacology papers call it GPA-748. Searching all three names turns up far more of the literature than GHRP-2 on its own.

The pair share a receptor and four of their six residues. GHRP-2 trades the histidine at the front of GHRP-6 for D-alanine and its D-tryptophan for D-2-naphthylalanine. Merck researchers found the two worked through the same receptor and mechanism in rat pituitary cells, with no extra release when combined, while human studies from the Bowers group ranked GHRP-2 as the more effective growth-hormone releaser.

Prolonged critical illness silences growth-hormone pulses in a way that looks like a pituitary short of stimulation. Researchers in Leuven used GHRP-2 infusions to test that idea and found secretion could be restarted, with IGF-I and its binding proteins returning to normal. Giving TRH and GnRH alongside it revived the thyroid and reproductive axes too.

Both, according to the rat and dog work behind the KP-102 programme. GHRP-2 still released growth hormone from cultured rat pituitary cells, although it was weaker than GHRH there. Its effect vanished in rats without a pituitary and shrank in rats whose median eminence, the link between hypothalamus and pituitary, had been lesioned, so full activity relies on the hypothalamus supplying its own GHRH.

It does in human pharmacology studies. Prolactin rises, though less than after TRH, while ACTH and cortisol rise to roughly the degree seen after corticotrophin-releasing hormone. Rats respond a little differently, with ACTH and corticosterone going up but prolactin staying flat. Measuring these hormones alongside growth hormone is sound practice in any GHRP-2 design.

Somatostatin is the brake on growth-hormone release. In conscious rats it blunted GHRH far more than GHRP-2, so GHRP-2 appeared the stronger of the two; under pentobarbital anaesthesia, which lowers somatostatin output, they became roughly equal. Conscious dogs sharpened the contrast further, because GHRP-2 released growth hormone in them while GHRH failed to raise it at all.

The Japanese validation study looked for the growth-hormone level at which sensitivity and specificity crossed, which landed between 15 and 20 µg/L. A peak of 15 µg/L after GHRP-2 matched the 3 µg/L threshold long used with the insulin tolerance test. A lower GHRP-2 cut-off of 9 µg/L is now used in Japan to identify severe adult deficiency.

Only slightly. In the Japanese diagnostic study, peaks were a little lower in older volunteers and in those carrying more body fat, but not by enough to change who was classed as deficient. Men and women responded alike. That steadiness across groups is part of what suited GHRP-2 to a diagnostic role.

Its two swaps pull in opposite directions. Exchanging histidine for alanine removes about 66 Da, while exchanging D-tryptophan for the larger D-2-naphthylalanine adds about 11 Da, leaving GHRP-2 some 55 Da lighter despite its bulky ring system. Its monoisotopic mass of about 817.43 Da appears as [M+H]+ near m/z 818.4 and [M+2H]2+ near 409.7, readings that cannot be mistaken for GHRP-6.

Roughly 12.2 µmol, based on a molecular weight of about 818 g/mol; any counter-ion or water in the supplied material lowers the true figure slightly, so the net peptide content on the batch certificate is worth checking. Pituitary-cell assays run at nanomolar concentrations, so a single vial can supply a long series. The five- and ten-vial boxes help when every experiment in a project should draw on one production lot.

There is a clear precedent. In the Merck rat pituitary-cell study, GHRP-2 and GRF released more growth hormone together than either managed separately, and cells desensitised to GHRP-2 still answered GRF normally. Sermorelin is GRF(1-29), the shortest fully active stretch of GHRH, which makes it a natural partner on the GHRH side; Tesamorelin and CJC-1295 are modified GHRH analogues built to persist for longer.