GHRP-6

The ten cited studies fall into two groups. Six are human endocrine studies published between 1995 and 2013: a phase 1 pharmacokinetic study in nine healthy men, and stimulation studies of hormone release in hyperthyroidism, primary hypothyroidism, endogenous and exogenous hypercortisolism, older adults and healthy men. The other four are preclinical papers from 2025 and 2026, covering acute lung injury, permanent coronary ligation, acute kidney injury and the maturation of human oocytes in culture.

The stimulation studies measured growth hormone, ACTH and cortisol responses, usually beside GHRH. In older adults, the growth hormone response to GHRP-6 was much larger than the response to GHRH, and the authors read the age-related fall in secretion as functional and potentially reversible. In primary hypothyroidism, responses to GHRP-6 were higher than the markedly blunted responses to GHRH, and in hyperthyroidism thyroid hormone excess affected the two pathways in similar ways. Hypercortisolism altered both pathways in its endogenous form, while GHRP-6 mechanisms appeared preserved in the exogenous form. In healthy men, GHRP-6 stimulated growth hormone, ACTH and cortisol release and increased stage 2 sleep without affecting slow-wave sleep. The pharmacokinetic study found a trend towards dose-proportional exposure and unexpected concentration spikes during elimination in four of the nine subjects. The preclinical papers reported less post-infarct remodelling and systolic dysfunction, less acute lung injury and less progression to interstitial fibrosis, greater survival of kidney tubular cells under ischaemic conditions via mTOR-P70 signalling, and nuclear maturation of oocytes within 24 hours without a significant change in cytoplasmic maturation.

The human evidence is limited in scale. The pharmacokinetic study enrolled nine men, and the other clinical studies, four of them from 1995 to 1997, measured hormone responses rather than clinical outcomes. The organ-injury and oocyte findings are recent and each rests on a single study; the lung-injury paper describes itself as the first assessment of its kind, and the cardiac paper's authors call their proteomic account of the mechanism theoretical. No cited study has tested the organ-injury findings in people.