What the literature reports on GHRP-6 dosage: the 1 µg/kg intravenous bolus, subcutaneous, intranasal and oral routes, animal cadences, the 15–60 minute half-life and 5 mg vial reconstitution math.
GHRP-6 is the original growth hormone-releasing peptide: the synthetic hexapeptide from Cyril Bowers's laboratory that in 1984 became the first such compound to release growth hormone in a living animal, fifteen years before the receptor's natural ligand, ghrelin, was identified. Its dosing literature is almost entirely human physiology — single doses given to volunteers to map the GH axis — plus animal protocols with a different purpose. This page collects what those studies administered, the half-life behind their design, and the reconstitution arithmetic for the 5 mg vial sold here. It is a research reference beside the GHRP-6 profile, not a protocol and not medical advice.
Plasma half-life after intravenous dosing is reported on the order of 15 to 60 minutes. The two D-amino acids — D-tryptophan at position 2 and D-phenylalanine at position 5 — let the 1984 sequence survive peptidases long enough to act in vivo, but the peptide is still cleared quickly. The GH pulse it triggers peaks around 15 to 30 minutes and returns to baseline within roughly two hours; the half-life calculator plots the decay of a single exposure. Human pharmacokinetic data for repeated subcutaneous dosing is sparse, so the two-hour window is an intravenous single-dose figure carried across by inference.
GHRP-6 was used as a probe: investigators wanted one measurable pulse, sampled over an hour or two, and the dosing record reflects that.
The recurring figure is 1 µg/kg body weight as a single intravenous bolus. Bowers and colleagues (Journal of Clinical Endocrinology and Metabolism, 1990) gave it to normal men and reported a reliable GH peak within 15 to 30 minutes; the same paper co-administered 1 µg/kg GHRH and found the combined response larger than the sum of the two alone, the synergy behind every GHRH-plus-GHRP design since. Ghigo and colleagues (European Journal of Endocrinology, 1997) reviewed a decade of studies in adults, children and patients with pituitary disease built on the same probe dose.
For scale, 1 µg/kg in a 70 kg adult is 70 µg — a fraction of a milligram, chosen to produce a measurable pulse in a laboratory, not to reach any outcome. The comparative studies that placed GHRP-6 between GHRP-2 and ipamorelin on potency and off-target hormone release used the same design; the GHRP-2 vs GHRP-6 comparison sets out the differences.
Subcutaneous studies used single doses in a range similar to the intravenous work, with a slower and lower peak. Intranasal and oral studies used far larger amounts — up to milligrams — to compensate for bioavailability that was measured as low but sufficient to raise GH; that finding is why GHRP-6 was once considered as an oral secretagogue before non-peptide molecules took that role. A microgram figure carries its route with it: the intravenous bolus, the subcutaneous injection and the oral dose are three different exposures, not one dose given three ways.
Animal and mechanistic protocols dosed once to three times daily, subcutaneously or intraperitoneally, over days to weeks. The cytoprotection work from a Cuban institute — rodent and porcine models of myocardial infarction, ischaemia–reperfusion and fibrosis — used substantially higher weight-based doses delivered intraperitoneally or intravenously around an injury. None of it has been tested in humans, and the doses were chosen for an injury model.
Two pharmacological facts shape repeated dosing. Repeated GHRP administration desensitises the ghrelin receptor to some degree — less with GHRP-6 than with hexarelin, but measurably — which is one reason continuous protocols are not how the compound was studied. And anything that raises somatostatin tone — glucose, free fatty acids, glucocorticoids, obesity — blunts the GH response, a property physiology studies used deliberately by giving GHRP-6 after a glucose load.
GHRP-6 5MG ships as a lyophilised powder, and the concentration after reconstitution is set by the volume of bacteriostatic water added: mass ÷ diluent = concentration. On a U-100 insulin syringe, 100 units = 1 mL.
The trade-off is shelf life: a larger diluent volume means the reconstituted vial stays open longer, and GHRP-6 is light-sensitive in solution because of its two tryptophan residues, so it belongs refrigerated and in the dark. The vial planner works out how many measured draws a vial yields at each concentration and the dosage calculator converts between micrograms and syringe units; the reconstitution walkthrough shows the procedure and the dosing-math guide works through the arithmetic.
There is no validated human dose of GHRP-6 for any purpose. The physiology studies established that a single 1 µg/kg bolus produces a GH pulse; they tested no outcome, and no trial has dosed GHRP-6 for months and followed participants. Repeated-dose regimens circulated online are not derived from controlled studies. The secretagogues primer sets the class's dosing record in context and the research overview covers the history and mechanism.
GHRP-6 has no Health Canada market authorisation or DIN and is sold in Canada for research use only. In 2023 the U.S. FDA placed it in category 2 of its 503A compounding evaluation, and the World Anti-Doping Agency lists it by name under S2, prohibited at all times.
What is the half-life of GHRP-6? On the order of 15 to 60 minutes after intravenous dosing. The GH pulse it triggers peaks within 15 to 30 minutes and returns to baseline in roughly two hours. Pharmacokinetic data for repeated subcutaneous dosing in humans is sparse.
What dose did the human studies use? Most often a single 1 µg/kg intravenous bolus, sometimes combined with 1 µg/kg GHRH (Bowers et al., 1990). Subcutaneous studies used single doses in a similar range; intranasal and oral studies used up to milligrams because of low bioavailability.
How often was GHRP-6 given? Once, in most human studies — they were physiology probes. Animal protocols dosed once to three times daily, and those cadences do not translate to a human figure.
How is a 5 mg vial reconstituted? With bacteriostatic water; the volume sets the concentration. 2 mL gives 2.5 mg/mL (25 µg per U-100 unit); 5 mL gives 1 mg/mL (10 µg per unit), which resolves small quantities better at the cost of a longer-open vial.
Why is GHRP-6 studied with GHRH analogues? Because the two act on different receptors and co-administration produced a larger GH pulse than either alone in the 1990 study. That is a mechanism described in the literature, not an endorsed design.
Is this medical advice? No. GHRP-6 is a research-grade compound for laboratory use only, not for human or veterinary use. Every number here reports what a study administered; none is a recommendation, a protocol or a validated dose.
