Kisspeptin-10
KP-10 / Metastin fragment
Hypothalamic peptide that drives GnRH pulsatility — the most upstream signal in the entire reproductive hormone cascade. Studied for libido fertility and hypogonadism research.
Mechanism of action
Binds Kiss1R GPR54 receptors on GnRH neurons in hypothalamus — the most upstream point in the reproductive hormone cascade. Drives GnRH which drives LH and FSH which drives testosterone and estrogen. Also has direct effects on sexual motivation independent of hormonal pathway.
Effects in the body
Kisspeptin is the on-switch for the entire reproductive hormone axis sitting upstream of GnRH which is upstream of LH and FSH which drives sex hormones. Research spans fertility enhancement libido and hypothalamic hormone regulation.
Pros & cons (from the literature)
- Upstream control of entire reproductive hormone axis
- Studied for fertility enhancement in clinical trials
- Direct sexual motivation effects independent of hormones
- Potential for hypogonadotropic hypogonadism treatment
- RUO status not compoundable
- Very short half-life requiring complex dosing
- Limited human therapeutic trial data
- May have adverse effects in hormone-sensitive conditions
Protocol summary (from published research)
Dosing ranges reproduced from published research literature. Not a prescription, not medical advice.
FDA & regulatory status
Evidence base
Multiple Phase I and II human trials published. Dhillo et al. published key human GnRH stimulation data. Mechanistically well characterized. Not yet at clinical approval stage.
Primary research sources
Peer-reviewed literature referenced throughout this profile is drawn from PubMed, Cell Metabolism, and clinical trial registries cited in the evidence base above.