Side by side

1. 1.Binds the ghrelin/growth-hormone-secretagogue receptor in the pituitary gland.
2. 2.Triggers release of growth hormone in pulses rather than a continuous rise.
3. 3.Because growth hormone then drives IGF-1 production in the liver, effects on the whole body are indirect and slow.
4. 4.Animal work suggests it is more selective than earlier secretagogues, with less effect on ACTH, cortisol and prolactin.
5. 5.Its short half-life means growth-hormone release is brief, which is why research protocols used frequent dosing.

• Growth hormone deficiency assessment (as a diagnostic stimulus in research settings)
• Body composition and lean mass in small human studies
• Bone density and recovery markers (mostly animal)
• Sleep and growth-hormone pulse dynamics

• Dose-dependent growth-hormone release in healthy volunteers
• Modest rises in IGF-1 reported in small short-term studies
• Less appetite stimulation than ghrelin itself in early comparisons
• No convincing evidence of meaningful body-composition change from human trials

• Headache and flushing shortly after dosing, reported in early studies
• Increased hunger in some reports
• Water retention and joint discomfort reported anecdotally with growth-hormone-raising agents
• Long-term safety is unknown

Research context only — no approved human protocol exists. Published pharmacokinetic studies used single subcutaneous doses in the microgram-per-kilogram range and measured growth-hormone pulses over hours. Long multi-week 'cycle' schedules circulating online have no controlled human evidence behind them.

Research context only