GHRP-6 dosing — the studied doses and the reported pattern

The published human doses are intravenous, single, and measured in tenths of a microgram per kilogram: 0.1, 0.3 and 1.0 µg/kg by IV bolus in 18 healthy men (Bowers et al., J Clin Endocrinol Metab 1990). For a 70 kg adult that is 7 to 70 µg per administration. The figures circulating in research and community contexts are subcutaneous and larger — commonly 100–300 µg per injection, one to three times daily. No published study has administered repeated subcutaneous GHRP-6 to humans and reported what happened.

• 0.1, 0.3 and 1.0 µg/kg intravenous bolus, single administrations in 18 normal men, with GHRH(1-44) at 1.0 µg/kg as comparator and given in combination. Mean peak serum GH: 1.2 µg/L on placebo, then 7.6, 16.5 and 68.7 µg/L across the three ascending doses (Bowers 1990).

• Other routes, characterised only qualitatively. Class reviews report that GHRP-6's GH-releasing activity is "marked, dose related and reproducible after intravenous, subcutaneous, intranasal and even oral administration" (Ghigo et al., Eur J Endocrinol 1997) — but without a subcutaneous dose-response curve that could be compared with the intravenous one.

That absence is the central problem with any GHRP-6 dosing discussion. The route people use is the route with no published pharmacokinetics.

The 1990 numbers reward a second look, because they contain the strongest argument for restraint that exists for this compound. Going from 0.3 to 1.0 µg/kg — a roughly three-fold dose increase — raised peak GH from 16.5 to 68.7 µg/L, so the GH response was still climbing steeply at the top of the tested range. But the 1.0 µg/kg dose was also the only dose at which prolactin and cortisol rose, each about two-fold above baseline; at 0.1 and 0.3 µg/kg they did not move (Bowers 1990).

In other words, the hormonal spillover that distinguishes GHRP-6 from selective secretagogues appeared at exactly the point where the GH response was largest. That trade-off is measurable in the data; where a repeated subcutaneous dose sits on it is not.

The pairing convention has genuine experimental support. Submaximal GHRP-6 doses of 0.1 and 0.3 µg/kg given with 1 µg/kg GHRH stimulated GH release synergistically — evidence that the two peptides act through independent systems (Bowers 1990), later confirmed for the class in a 24-hour co-infusion study in older adults (Bowers et al., J Clin Endocrinol Metab 2004).

The empty-stomach convention is weaker than it is usually presented. The GH-releasing effect of this class is only partially blunted by glucose, free fatty acids and glucocorticoids — influences that nearly abolish the response to GHRH given alone (Ghigo 1997). Food matters more for the GHRH half of a stack than for the GHRP half.

Three things determine whether a GHRP-6 protocol is a bad idea for a particular person, and none of them are visible from a dosing chart: baseline glucose handling, since secretagogues reduce insulin sensitivity as a class (Sigalos & Pastuszak, Sex Med Rev 2018); any reason GH elevation would be unwise; and what is actually in the vial.

On the last point, the delivered dose is set by reconstitution rather than by the label — how much bacteriostatic water is added determines the concentration, and the volume drawn is read in syringe units, which are routinely misread as micrograms. Material sold outside a pharmacy supply chain also comes with no verified identity, impurity, aggregate or endotoxin data.

GHRP-6 is prohibited in sport at all times under WADA section S2; it is excreted mostly unchanged and has been detected in urine 23 hours after administration (Semenistaya et al., Drug Test Anal 2015).

See also GHRP-6 side effects and the research and evidence overview.