Peptide comparison
GHRP-2 vs GHRP-6
GHRP-2 and GHRP-6 are both research peptides. This side-by-side compares their mechanism, typical research dosing, half-life, routes and safety so you can see how they differ. For research use only.
| GHRP-2 | GHRP-6 | |
|---|---|---|
| Category | Hormonal | Hormonal |
| Overview | A synthetic growth-hormone secretagogue and ghrelin-receptor agonist that triggers pulsatile GH release; backed by real human pharmacology data and a Japanese diagnostic... | The prototypical growth-hormone-releasing peptide and ghrelin-receptor agonist, best known for strongly stimulating both GH release and appetite; characterized human... |
| How it works | GHRP-2 binds GHS-R1a, a Gq-coupled G-protein-coupled receptor expressed in the pituitary and hypothalamus. Receptor activation raises intracellular calcium through the phospholipase-C / protein-kinase-C pathway, driving release of stored growth hormone from somatotrophs in discrete pulses. Because GHRP-2 acts through a pathway distinct from GHRH (which signals via cAMP), submaximal doses of a GHRP combined with GHRH produce supra-additive (synergistic) GH release in humans - a property exploited in both diagnostic testing and community stacking. GHRP-2 also stimulates appetite in a ghrelin-like fashion and can transiently raise ACTH/cortisol and prolactin, generally in a dose-dependent way; its off-target hormonal profile sits between the more cortisol/prolactin-raising GHRP-6 and the highly selective ipamorelin. Additional CD36-mediated, GH-independent cytoprotective actions have been described, but these are largely preclinical. | GHRP-6 binds GHS-R1a, a Gq-coupled G-protein-coupled receptor in the pituitary and hypothalamus. Receptor activation drives the phospholipase-C / IP3 / diacylglycerol pathway, mobilizing intracellular calcium and triggering pulsatile GH release from somatotrophs. It also acts at the hypothalamus to promote GHRH release and to blunt somatostatin tone, so its GH effect synergizes with GHRH and GHRH analogs. The same GHS-R1a signaling that drives GH release also stimulates appetite and food intake, which is why hunger is GHRP-6's signature effect. In animal models GHRP-6 additionally shows cytoprotective and cardioprotective actions (reduced infarct size, lower oxidative stress, pro-survival signaling) that appear at least partly independent of GH release; these cardioprotective findings remain preclinical. |
| Half-life | Short. Human pharmacokinetic data show a biexponential disposition with an elimination half-life of roughly 30 minutes (about 0.55 hours) after intravenous dosing. The resulting GH pulse typically peaks around 15-60 minutes after administration. | Very short. A human pharmacokinetic study reported a rapid distribution half-life of about 7-8 minutes; the functionally relevant window is commonly summarized as roughly 15-30 minutes, with the GH pulse peaking around 15-30 minutes after injection. (The same study also detected a longer terminal elimination phase of a few hours, but the biologically active window is brief.) |
| Dosing reference | For its approved diagnostic use in Japan, pralmorelin is given as a single intravenous bolus of about 1 mcg/kg to provoke a measurable GH response. Published pediatric pharmacology studies used intravenous doses on the order of 100 mcg. There is no approved or established therapeutic (repeated-use) clinical dose for GH deficiency, anti-aging, or body-composition goals - the human data establish acute GH-releasing capacity and tolerability, not a validated treatment regimen. | No approved or established therapeutic dosing in humans. Published human pharmacology used weight-based dosing: a formal pharmacokinetic study administered single intravenous boluses of 100, 200, and 400 mcg/kg, and earlier dose-response work showed GH release in roughly the 1 mcg/kg range intravenously. These studies establish acute GH-releasing capacity and tolerability, not a validated treatment regimen. |
| Routes | subcutaneous, intramuscular, intravenous | subcutaneous, intramuscular, intravenous |
| Safety & side effects | In short-term studies GHRP-2 has generally been well tolerated, with no serious adverse events reported in pediatric GH-deficiency trials. The most consistent effects are increased hunger/food intake (a ghrelin-like action) and transient, dose-dependent rises in cortisol and prolactin; injection-site reactions and water retention are also reported anecdotally. Long-term human safety has not been established, and chronic stimulation of the GH/IGF-1 axis carries the same theoretical concerns as growth hormone itself (insulin resistance, fluid retention, and caution where there is active malignancy). Product quality is a real-world risk because research-grade material is unregulated and may be impure or mislabeled. GHRP-2 is not approved as a therapeutic drug in the US, EU, or most jurisdictions, and it is prohibited in sport by WADA. This information is for research reference only and is not a recommendation for human use. | GHRP-6's most distinctive effect is a marked increase in hunger and appetite, stronger than with other GHRPs. Other reported effects include transient, dose-dependent rises in cortisol and prolactin, injection-site reactions, water retention, transient changes in blood sugar, and occasional tingling/numbness. GH secretagogues as a class are described as generally well tolerated over the short term with few serious adverse events, but long-term human safety - including any effect on cancer risk - is unstudied, and chronic stimulation of the GH/IGF-1 axis carries the same theoretical concerns as growth hormone itself. Product quality is a real-world risk because research-grade material is unregulated and may be impure or mislabeled. GHRP-6 is not approved as a therapeutic drug, and it is prohibited in sport by WADA (category S2). This information is for research reference only and is not a recommendation for human use. |
For research use only. Not for human consumption. Always verify against current literature.