GHRP-6
GHRP-6 is a synthetic hexapeptide (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) and the compound that opened the entire growth hormone secretagogue field. It came out of Cyril Bowers' work in the early 1980s on opioid-derived peptides that released growth hormone without acting through GHRH. Every later secretagogue, including GHRP-2, hexarelin, ipamorelin, and the orally active MK-677, descends from this molecule and is usually benchmarked against it.
- class
- GHRP (hexapeptide secretagogue)
- half-life
- ~15–20 minutes
- route
- subcutaneous
- cadence
- 2–3x daily, fasted
- typical dose
- 100–300 mcg per injection
- cycle
- 12–16 weeks, then 4-week break
- storage
- refrigerated · 28-day max (reconstituted)
GHRP-6 Reconstitution & Dosage Protocol
weekly dose · reduces side effects| Phase | Window | Weekly dose | Draw (U-100, 2.5mL BAC) | Note |
|---|---|---|---|---|
| Introduction | Weeks 1–2 | 0.10 mg | 5 units· 0.05 mL | 100 mcg once daily, fasted, to gauge the hunger and facial flush response |
| Standard | Weeks 3–12 | 0.10 mg | 5 units· 0.05 mL | 100 mcg 2–3x daily (morning fasted, post-training, pre-sleep); stack with a GHRH analog |
| High output | Weeks 4–12 | 0.30 mg | 15 units· 0.15 mL | Optional 300 mcg ceiling during a bulk; hunger becomes the limiting factor before GH does |
| Maintenance | Weeks 13–16 | 0.10 mg | 5 units· 0.05 mL | Taper to 100 mcg once daily before a 4-week washout |
What is GHRP-6?
GHRP-6 is a synthetic hexapeptide (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) and the compound that opened the entire growth hormone secretagogue field. It came out of Cyril Bowers' work in the early 1980s on opioid-derived peptides that released growth hormone without acting through GHRH. Every later secretagogue, including GHRP-2, hexarelin, ipamorelin, and the orally active MK-677, descends from this molecule and is usually benchmarked against it.
GHRP-6 binds the growth hormone secretagogue receptor (GHS-R1a) in the pituitary and hypothalamus, the receptor whose natural ligand is ghrelin. Receptor activation does two things at once: it directly signals somatotroph cells to release stored growth hormone, and it suppresses somatostatin, the hypothalamic brake on GH output. That dual action is why a GHRP produces a much larger pulse than a GHRH analog used alone.
GHRP-6 does not work in isolation from the GHRH system. A 1998 JCEM study showed that blocking endogenous GHRH sharply reduced the GH response to GHRP-6, meaning the peptide needs intact hypothalamic GHRH signaling to reach its full effect. This is the pharmacological basis for stacking: pairing GHRP-6 with CJC-1295 without DAC or sermorelin produces a synergistic pulse rather than a simply additive one, and it is why the GHRH plus GHRP-6 combination became a standard clinical test for growth hormone deficiency.
The defining practical trait of GHRP-6 is hunger. Of all the GHRPs it produces the most pronounced appetite stimulation, often arriving 20–30 minutes after injection and strong enough to be disruptive for anyone in a caloric deficit. Rodent work showed that centrally administered GHRP-6 drives eating even when plasma GH does not change, confirming that the orexigenic effect is a separate central action and not a downstream consequence of the GH pulse. For a cutting phase, ipamorelin is the correct substitute.
GHRP-6 also raises cortisol and prolactin more than ipamorelin does, though less dramatically than hexarelin at equivalent doses. At 100 mcg per injection the spillover is usually minor. Above roughly 300 mcg the GH response flattens while the cortisol and prolactin curves keep climbing, so raising the dose past that point mostly buys side effects. Transient facial flushing and warmth in the first few minutes after injection are common and harmless.