GHRP-6

Typical use cases

Dosing guidelines

Titration

Sources describe starting low and increasing gradually; doses are typically reported as taken on an empty stomach (food, especially carbohydrate/fat, is reported to blunt the GH pulse), with at least ~3 hours between doses to allow receptor recovery. This is educational information, not a dosing recommendation.

Reconstitution

Lyophilized powder reconstituted with bacteriostatic water (e.g., adding 2-3 mL to a 5 mg vial); add water slowly down the vial wall and swirl gently rather than shaking

Injection sites

Subcutaneous injection (commonly abdomen/lower stomach fat); intravenous administration has also been used in research settings

Storage & handling

Lyophilized powder stored frozen or refrigerated and protected from light; after reconstitution, refrigerated at 2-8 C and used within several weeks per common guidance

Side effects

• Strong hunger / increased appetite Mild · Common
• Water retention and tingling/numbness in extremities Mild · Uncommon
• Injection-site redness or irritation Mild · Common
• Transient rise in cortisol and prolactin (more at higher doses) Moderate · Uncommon
• Lightheadedness or flushing shortly after dosing Mild · Uncommon
• Reduced insulin sensitivity / altered glucose with chronic GH elevation Moderate · Rare

Research summary

GHRP-6 (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2) was characterized by Cyril Bowers in the 1980s as one of the first synthetic peptides to dose-dependently release growth hormone through a mechanism distinct from GHRH; it acts mainly as an agonist at the growth hormone secretagogue receptor 1a (GHS-R1a, later identified as the ghrelin receptor) and has also been reported to engage the scavenger receptor CD36. In preclinical models it produces robust, pulsatile GH secretion and strong orexigenic (appetite-stimulating) effects, and a substantial animal literature reports GH-independent cytoprotective actions in cardiac, neuronal, hepatic and gastrointestinal tissue via PI-3K/AKT and prosurvival signaling. Rodent work indicates that GHRP-6's effects on weight gain and visceral fat accrual depend on insulin/glucose status, acting additively with insulin rather than alone. Human data are limited and largely preliminary: small studies in GH-deficient patients and surgical cohorts suggested acute, GH-independent positive inotropic effects, and intravenous safety has been described in healthy volunteers, but no large controlled efficacy trials exist. Compared with newer secretagogues such as GHRP-2 and ipamorelin, GHRP-6 is reported to cause the most pronounced hunger and can raise cortisol and prolactin at higher doses. GHRP-6 is not approved by the FDA for any indication, is prohibited in sport by WADA, and is sold only as a research chemical. Overall the evidence base is comparatively strong preclinically but thin and inconclusive in humans, limiting any clinical conclusions.

Key references

• https://pmc.ncbi.nlm.nih.gov/articles/PMC5392015/
• https://pubmed.ncbi.nlm.nih.gov/20219977/
• https://pubchem.ncbi.nlm.nih.gov/compound/9919153
• https://www.guidetopharmacology.org/GRAC/LigandDisplayForward?ligandId=1093
• https://www.frontiersin.org/journals/pharmacology/articles/10.3389/fphar.2024.1402138/full
• https://en.wikipedia.org/wiki/GHRP-6

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