Outside its diagnostic use in Japan, GHRP-2 has no approved therapeutic indication, so no regulator has reviewed a dose for ongoing use. The figures below describe what published studies administered and what research and community sources report. They are data points, not a protocol for the reader.
The short answer
Three sets of numbers exist and they were generated for three different purposes. Diagnostically, GHRP-2 is given as a single intravenous dose — 100 µg in adults, 2 µg/kg in children — to provoke one measurable GH pulse. In the only sustained-dosing study, it was delivered as a continuous subcutaneous infusion at 1 µg/kg/h for 30 days (Bowers et al., J Clin Endocrinol Metab 2004). Research and community sources describe something different again: roughly 100–300 µg subcutaneously, one to three times daily. That last pattern has never been studied.
Doses used in published studies
100 µg intravenously, single dose — the adult diagnostic stimulus, used to test both the GH and the adrenal axis; peak cortisol on this dose correlated with the insulin tolerance test at r = 0.817 (Kano et al., Peptides 2010). A peak GH below 9 µg/L defines severe adult GH deficiency in Japanese practice (Fukuda et al., Neurol Med Chir 2014).
2 µg/kg intravenously — the paediatric diagnostic dose, in 56 children with growth disorders; the test took an hour or less and correlated closely with the insulin tolerance test (Asakura et al., J Pediatr Endocrinol Metab 2010).
1 µg/kg/h subcutaneously, continuously for 30 days — 17 healthy older adults; GH secretion rose more than three-fold on day 1 and about 1.8-fold by days 14 and 30, with IGF-1 on a stable plateau and normal safety screening throughout (Bowers 2004).
1 µg/kg/h subcutaneously for 270 minutes — the appetite study, which produced a 35.9% increase in food intake (Laferrère et al., J Clin Endocrinol Metab 2005).
For scale: 1 µg/kg/h for a 70 kg adult is about 1,680 µg per day delivered continuously — an order of magnitude above the daily totals described in community protocols, but spread evenly rather than given as bolus injections. The two are not interchangeable, and neither predicts the other.
Commonly reported research protocols
Research and community sources most often describe 100–300 mcg per administration subcutaneously, one to three times daily, frequently paired with a GHRH analogue such as modified GRF 1-29, and taken on an empty stomach. Cycles of 8–12 weeks followed by a break are commonly described.
The 100 mcg figure is often called a "saturation dose," on the reasoning that the GH response plateaus above it. The dose-response work that exists is for related peptides given intravenously, not for repeated subcutaneous GHRP-2.
These numbers document what is reported, not what is validated.
Why timing and food come up
Two mechanistic points sit behind the timing conventions, and both are real pharmacology rather than folklore — though neither has been tested as a dosing instruction for this compound.
First, GHRP-2 and GHRH act at different receptors and their effects are synergistic rather than additive: submaximal GHRP doses given with GHRH stimulate GH release synergistically, implying independent systems (Bowers et al., J Clin Endocrinol Metab 1990), and 24-hour co-infusion of GHRP-2 with GHRH exceeded either agonist alone in older adults (Bowers 2004). That is the basis for stacking.
Second, the GH-releasing effect of this class is only partially blunted by influences — glucose, free fatty acids, glucocorticoids — that almost abolish the response to GHRH alone (Ghigo et al., Eur J Endocrinol 1997). The empty-stomach convention follows from that, though the effect it guards against is smaller for a GHRP than for a GHRH analogue.
Why schedules include breaks
The cycling convention has a measured basis. Across 30 days of continuous infusion, the acute GH response fell from more than three-fold on day 1 to about 1.8-fold at days 14 and 30, while IGF-1 stayed elevated (Bowers 2004). Class reviews describe this as partial desensitisation, more marked with continuous exposure and less with intermittent dosing (Ghigo 1997). The practical risk is not the tolerance itself but the response to it — escalating the dose into a range where no human data exists.
Why oversight matters
GHRP-2 does more than release GH. It raises cortisol enough to be used as an adrenal stimulation test, and it increases food intake by more than a third in a controlled setting. Both interact with the reasons people take it, and both are monitorable by a clinician and invisible to a protocol.
On the product side, material bought outside a pharmacy supply chain comes with no verified identity, purity, aggregate or endotoxin data. And on delivery, the dose is set by reconstitution — how much bacteriostatic water is added determines concentration, and the amount drawn is read in syringe units, which are frequently misread as micrograms.
GHRP-2 is prohibited in sport at all times under WADA section S2, with urinary detection of parent compound and metabolites for up to 47 hours after dosing (Semenistaya et al., Drug Test Anal 2015).
See also GHRP-2 side effects and the research and evidence overview.
Sport & Anti-Doping Warning
GHRP-2 is an older growth hormone–releasing peptide that appears explicitly on the WADA Prohibited List and has been a target compound in laboratory detection research.
Modern anti-doping testing panels routinely include GHRP-2 and related peptides, so its use is risky even at what might seem like 'research' doses.