GHRP-6 (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) is the hexapeptide Bowers et al. used to show that a GH-releasing peptide can raise GH in normal men and act synergistically with GHRH. GHRP-2 is a later hexapeptide in the same chemical class. Both act at the ghrelin receptor (GHSR) pathway. They are not identical in every species or every second-messenger readout.
This page stays with verified papers. It does not invent a hunger ranking for GHRP-6 in humans. It does not publish a protocol.
Research notice: These peptides are discussed for laboratory research only. They are not approved for human consumption, medical treatment, or diagnosis.
| Parameter | GHRP-2 | GHRP-6 |
|---|---|---|
| Class | Synthetic GH-releasing peptide; GHSR agonist | Synthetic hexapeptide GHRP; GHSR agonist |
| Sequence (GHRP-6, published) | Hexapeptide analog in the GHRP series | His-D-Trp-Ala-Trp-D-Phe-Lys-NH2 |
| Rat pituitary (Cheng 1997) | Same receptor/mechanism as GHRP-6; no additive max effect | Same; synergistic with GRF |
| Sheep vs rat cAMP (Wu 1996) | Raises cAMP in sheep somatotrophs; not in rat pituitary cells | GH release without a cAMP increase in the sheep system described |
| Human GH release | Later GHRP in the same series; not the Bowers 1990 hexapeptide paper | Bowers 1990: GH in 18 normal men; synergy with GHRH |
| Human food intake | Increased in healthy men and in obese subjects (Laferrère) | Not cited as a human food-intake RCT here |
| ACTH/cortisol | Raised in swine (Raun 1998, with GHRP-6) | Raised in swine (Raun); ~2-fold PRL and cortisol at the highest IV dose in Bowers 1990 men |
| FDA-approved product | No | No |
Howard et al. cloned a pituitary and hypothalamus receptor that functions in GH release, the receptor this class uses. Kojima et al. identified ghrelin as the endogenous acylated GH-releasing peptide from stomach.
In rat primary pituitary cells, Cheng et al. compared GHRP-2 and GHRP-6 directly:
They concluded GHRP-2 stimulates GH from rat pituitary cells via the same receptor and mechanism as GHRP-6, despite structural difference.
Species matter. Wu, Chen, Zhang, Bowers, and Clarke compared GHRP-6 and GHRP-2 on cAMP and GH in ovine and rat somatotrophs. In partially purified sheep somatotrophs, GHRP-2 and GRF increased cAMP and GH; GHRP-6 did not increase cAMP. Combined GHRP-2 and GRF were additive on cAMP and GH; combined GHRP-2 and GHRP-6 were additive on GH only. A GRF-receptor antagonist reduced GHRP-2 and GRF effects on cAMP and GH, but not GHRP-6-induced GH. In rat pituitary cultures, GHRP-6 did not raise cAMP but potentiated GRF on cAMP; GHRP-2 caused cAMP accumulation in sheep somatotrophs but not in rat pituitary cells. The authors attributed this to species differences, probably different GHRP-receptor subtypes.
If a protocol assumes "GHRP-2 equals GHRP-6 in every system," Wu et al. already falsifies that for cAMP.
Neither peptide is an FDA-approved drug in the sources cited. Human papers below are healthy-volunteer GH-release, cortisol/PRL, or food-intake pharmacology.
Ipamorelin is a later GHSR ligand with more ACTH/cortisol selectivity in swine (Raun et al.). That comparison lives on Ipamorelin vs CJC-1295, not here.
Bowers et al. gave GHRP (the hexapeptide His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) by IV bolus to 18 normal men, alone and with GHRH-(1-44)-NH2. Mean peak serum GH after placebo and three GHRP dose levels was 1.2, 7.6, 16.5, and 68.7 micrograms/L. Submaximal GHRP plus GHRH stimulated GH synergistically. At the highest GHRP dose, serum PRL and cortisol rose about 2-fold; LH and TSH did not change over the first hour. No adverse clinical effects or laboratory abnormalities were observed for GHRP; GHRH caused brief mild facial flushing in 16 of 18 subjects.
Those IV amounts are trial methods, not a use protocol.
Laferrère, Abraham, Russell et al. (2005) reported that GHRP-2, like ghrelin, increased food intake in healthy men. Laferrère, Hart, and Bowers (2006) reported that obese subjects also responded to the stimulatory effect of GHRP-2 on food intake. That is GHRP-2, not a GHRP-6 human meal study.
In the ipamorelin discovery paper, administration of both GHRP-6 and GHRP-2 increased plasma ACTH and cortisol in swine. Ipamorelin did not. None of the secretagogues tested changed FSH, LH, PRL, or TSH in that model.
A statement that GHRP-6 causes "more hunger" than GHRP-2 in humans is not supported by a verified GHRP-6 food-intake RCT in the sources below. GHRP-2 has that human food-intake evidence. GHRP-6 has human GH-release and a cortisol/PRL rise at the highest IV dose in Bowers 1990.
| Question | GHRP-2 | GHRP-6 |
|---|---|---|
| Rat pituitary receptor vs GHRP-6 | Same (Cheng) | Reference hexapeptide in that assay |
| Additive at max with the other GHRP (rat cells) | No | No |
| cAMP in sheep somatotrophs | Increases | Does not, in Wu 1996 |
| cAMP in rat pituitary cells | Does not, in Wu 1996 | Does not; potentiates GRF on cAMP |
| Human GH + GHRH synergy | Same class; Cheng shows synergy with GRF in rat cells | Demonstrated in men (Bowers 1990) |
| Human food-intake RCT cited | Yes (Laferrère 2005, 2006) | Not cited |
| Swine ACTH/cortisol | Increased (Raun) | Increased (Raun) |
For GHSR-class work in rat pituitary, Cheng says they are functionally interchangeable at the receptor and competing at saturating concentrations. For second messengers, Wu says the species split is real. For human appetite data, GHRP-2 is the peptide with the Laferrère papers.
Related: Ipamorelin vs CJC-1295, GH secretagogues guide.
In rat primary pituitary cells, Cheng et al. concluded they act via the same receptor and mechanism. Co-administration at maximal concentrations added no further GH release. Each desensitized cells to the other, not to GRF. A GHRP antagonist blocked GHRP-2; a GRF antagonist did not.
Cheng et al. found no additive GH release in rat pituitary cells when both were used at maximal concentrations. That is a cell-system result, not a human protocol, and not a reason to stack them.
No. The cited papers are pituitary-cell, animal, or healthy-volunteer pharmacology. They are not approved-drug labels.
GHRP-2. Laferrère et al. reported that GHRP-2, like ghrelin, increased food intake in healthy men, and that obese subjects also increased food intake after GHRP-2. A comparable GHRP-6 human food-intake RCT is not among the sources cited here.
No. It compares published research. It is not medical advice and does not include human dosing protocols.
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