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Kisspeptin-10 Reference

Educational, not medical advice reference for Kisspeptin-10: Hormonal, Reproductive; regulatory status, evidence posture, source review, and sch…

Reference summary

Kisspeptin-10 is the C-terminal decapeptide of the parent kisspeptin-54 (KP-54); both share the C-terminal RF-amide motif that activates KISS1R, but they differ pharmacokinetically. KP-10 plasma half-life in humans is about 4 minutes (Jayasena et al., 3.8 +/- 0.3 min in men, 4.1 +/- 0.4 min in women), while KP-54 plasma half-life is about 28 minutes (Dhillo 2005 reported 27.6 +/- 1.1 min IV). Most of the published human trial program (Imperial College London: Dhillo, Jayasena, Abbara) uses KP-54 for sustained signaling; the IVF-trigger paper is Jayasena 2014 J Clin Invest (PMID 25036713, 53 women, 12 clinical pregnancies with subsequent live births reported), and Abbara 2015 J Clin Endocrinol Metab (PMID 26192876, 60 women) extended the work in women at high risk of ovarian hyperstimulation syndrome. KP-10 work is dominated by single-pulse acute LH-response probes (peak ~20 to 40 minutes after IV bolus, with return toward baseline typically within ~1 hour at the doses studied). These findings do not validate self-directed fertility, testosterone, libido, or hormone-restart use.

Regulatory and posture

Categories
Hormonal, Reproductive
Aliases
Kp-10, KP10, Metastin fragment, KISS1-derived decapeptide
Evidence posture
human - KP-54 (not KP-10) is the peptide used in the IVF-trigger and amenorrhea-probe trials that the community often cites. The two fragments are pharmacokinetically distinct; equivalence by dose is not established. Research-vial KP-10 sold to the community is not the trial peptide. No FDA-approved product. No validated long-term outcome program.
Regulatory status
No FDA-approved kisspeptin-10 drug label. KISS1 was originally identified in 1996 as a melanoma metastasis suppressor gene at Penn State College of Medicine in Hershey, Pennsylvania (the name kisspeptin references Hershey's Kisses). The reproductive role was established in 2003 when de Roux (Proc Natl Acad Sci USA, PMID 12944565) and Seminara (N Engl J Med, PMID 14573733) independently reported that loss-of-function variants in KISS1R (formerly GPR54) cause normosmic hypogonadotropic hypogonadism, identifying kisspeptin signaling as the upstream activator of GnRH neurons. Kisspeptin-10 remains investigational worldwide; no human kisspeptin product is FDA-approved for any indication.
Content review status
research reference

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