Kisspeptin-10

The C-terminal decapeptide of the KISS1 gene product that activates the KISS1R (GPR54) receptor on hypothalamic GnRH neurons, used in academic human physiology studies and early-phase reproductive-disorder trials; no approved product exists.

Also referenced as: KP-10, Kisspeptin 10, Kisspeptin 112-121, Kisspeptin-112-121, Metastin 45-54

Also appears in: Other

COA Public product evidence No certificate records are bound to a tracked Kisspeptin-10 product page A record counts here only when a vendor publishes a certificate against one of its own tracked Kisspeptin-10 product pages. Other certificates naming this compound may still exist — search the wider certificate database. →

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What is Kisspeptin-10?

Kisspeptin-10 is the ten-residue, C-terminally amidated fragment (Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2) at the end of the kisspeptin precursor encoded by the KISS1 gene — residues 112–121 of the human protein (UniProt Q15726), which is why most clinical-trial registrations call it “kisspeptin 112-121.” It is the shared active core of the longer kisspeptin-54, -14 and -13 forms, all of which terminate in the same RF-amide decapeptide.

The 2001 discovery of the kisspeptins and their receptor is covered on the kisspeptin-54 profile. Worth being precise about: the peptides actually isolated from human placenta in that work were the 54-, 14- and 13-residue forms. Kisspeptin-10 is the minimal C-terminal sequence that retains full intrinsic bioactivity, and it was not tested in humans until 2011 (George et al., Journal of Clinical Endocrinology & Metabolism, 2011).

It appears in the research-peptide market because it is a short, easily synthesized peptide with a genuine human literature behind it. Three academic groups account for nearly all of that literature: the Reproductive Endocrine Unit at Massachusetts General Hospital, the Dhillo group at Imperial College London, and the MRC reproductive-sciences group in Edinburgh (George and Anderson), which published the original human dose-finding work. It is now the molecule in early-phase trials for hypogonadotropic hypogonadism and hypothalamic amenorrhea. There is no approved kisspeptin product anywhere, and vials labeled simply “kisspeptin” are usually this decapeptide rather than the 54-mer used in much of the better-known clinical work.

How it works

• KISS1R (GPR54) agonism one step above the pituitary — kisspeptins bind KISS1R with low-nanomolar affinity and signal through Gq, driving PIP2 hydrolysis, calcium mobilization and ERK1/2 and p38 MAP kinase phosphorylation (Kotani et al., Journal of Biological Chemistry, 2001; Ohtaki et al., Nature, 2001). The receptor sits on hypothalamic GnRH neurons, so the peptide triggers endogenous GnRH release rather than acting on gonadotrophs directly.
• The pathway is required for human reproduction — the 2003 GPR54 loss-of-function genetics that validate the target are summarized on the kisspeptin-54 profile; for the decapeptide, the same genetics explain why exogenous kisspeptin-10 fails in patients whose GnRH network never developed (see below).
• A single bolus resets the GnRH pulse generator — in 13 healthy men, an intravenous bolus of kisspeptin 112-121 produced an immediate LH pulse regardless of when the previous endogenous pulse had occurred, and the induced pulses were larger than native ones (mean amplitude 5.0 ± 1.0 vs 2.1 ± 0.3 mIU/mL); it also delayed the next endogenous pulse by roughly one interpulse interval (Chan et al., Journal of Clinical Endocrinology & Metabolism, 2011, 96(6):E908–E915).
• Bolus dose response is bell-shaped — intravenous boluses from 0.01 to 3.0 µg/kg produced a rapid, dose-dependent LH rise with maximal stimulation at 1 µg/kg (4.1 ± 0.4 to 12.4 ± 1.7 IU/L at 30 minutes, n = 6) and a reduced response at 3 µg/kg. A 22.5-hour infusion at 4 µg/kg/h raised LH (5.4 to 20.8 IU/L) and testosterone (16.6 to 24.0 nmol/L); at the lower 1.5 µg/kg/h rate, where individual pulses remained resolvable, LH pulse frequency and secretory burst mass both rose (George et al., Journal of Clinical Endocrinology & Metabolism, 2011, 96(8):E1228–E1236).
• The response is gated by the sex-steroid milieu, and the two groups that looked do not fully agree — Imperial found that intravenous kisspeptin-10 raised LH and FSH in men at doses as low as 0.3 and 1.0 nmol/kg and in preovulatory-phase women, but produced no gonadotropin response in follicular-phase women even at 10 nmol/kg intravenously or 32 nmol/kg subcutaneously (Jayasena et al., Journal of Clinical Endocrinology & Metabolism, 2011, 96(12):E1963–E1972). MGH, giving 0.24 nmol/kg boluses to 27 women across the cycle (plus four more at 0.72 nmol/kg), saw immediate LH pulses in every luteal and preovulatory participant but in only about half of early-follicular women, and read that blunting as evidence of higher endogenous kisspeptin tone in the early follicular phase; in women, unlike men, the bolus did not appear to reset the pulse generator (Chan et al., Journal of Clinical Endocrinology & Metabolism, 2012, 97(8):E1458–E1467). Either way, because the peptide releases an endogenous GnRH pool, its effect depends on the state of the axis it acts on.

Research status

There is no approved kisspeptin-10 product in any jurisdiction, and no registrational (Phase 3) program for it exists. Every human exposure on record comes from investigator-led academic studies, with one small industry program for a synthetic analog that has since been discontinued. The human literature is real but small — typically 3 to 15 participants per study arm.

Healthy-volunteer physiology (kisspeptin-10). The foundational decapeptide studies are Chan et al. (2011), George et al. (2011) and Jayasena et al. (2011), described above. In the one direct human comparison, kisspeptin-10 and kisspeptin-54 produced similar gonadotropin responses at matched intravenous rates and GnRH outperformed both, roughly three-fold over the decapeptide (Jayasena et al., Human Reproduction, 2015, 30(8):1934–1941; the figures are on the kisspeptin-54 profile). In five men with type 2 diabetes and low testosterone, a 0.3 µg/kg bolus raised LH (4.7 to 10.7 IU/L) comparably to seven healthy age-matched controls (George et al., Clinical Endocrinology, 2013, 79(1):100–104). A 2026 MGH report of continuous intravenous infusion at 12.5 µg/kg/h for 24 hours in three men found LH rising five- to eight-fold within 12–20 hours, then declining 13–47% from peak while staying above baseline (Naveed et al., Hormones (Athens), 2026, online ahead of print; NCT01438073).

Chronic subcutaneous dosing — the newest and most relevant data. In a randomized, single-blind, placebo-controlled series of three sub-studies in 15 healthy men (n = 7, 4 and 7; 12 further men served as controls), acute 8-hour subcutaneous kisspeptin-10 infusions (1.25–10 nmol/kg/h) dose-dependently raised LH, FSH and testosterone; a continuous 5-day infusion at 180 nmol/h kept testosterone elevated but let gonadotropins fall back to vehicle levels; and daily 8-hour infusions at 150 nmol/h (8 hours on, 16 hours off) sustained the gonadotropin increase through day 12, with a 1 nmol/kg bolus afterward still eliciting a rise — indicating the receptor remained functional (Yeung et al., European Journal of Endocrinology, 2026, 195(2):206–216). This is the longest published human exposure to the decapeptide and the clearest demonstration that schedule, not dose, determines whether the axis keeps responding.

Diagnostic probe in reproductive disorders (kisspeptin-10). Eleven patients with congenital idiopathic hypogonadotropic hypogonadism failed to produce an LH response to a 0.24 nmol/kg kisspeptin 112-121 bolus that reliably works in healthy men and luteal-phase women, while a twelfth patient whose hypogonadism had reversed did respond (Chan et al., Journal of Clinical Endocrinology & Metabolism, 2014, 99(12):E2762–E2771). In 15 children with delayed or stalled puberty (11 boys, 4 girls), responses ranged from robust to absent, and the response pattern was later used to predict pubertal outcomes (Chan et al., JCI Insight, 2018, 3(8):e99109; Chan et al., Journal of Clinical Endocrinology & Metabolism, 2020, 105(8):e2717–e2725). In 11 women with hyperprolactinemia, hourly intravenous kisspeptin 112-121 boluses (0.24 nmol/kg for 10 hours) increased the total number of LH pulses, and in the 6 participants whose progesterone suggested an anovulatory state, mean LH and estradiol rose significantly (Hoskova et al., Journal of Clinical Endocrinology & Metabolism, 2022, 107(8):e3515–e3525; NCT02956447, Phase 2, completed with results posted). Exploratory MGH work using the same 0.24 nmol/kg bolus in 12 healthy adults found a transient oxytocin rise driven almost entirely by the men (31.9% vs 5.7%; Galbiati et al., European Journal of Endocrinology, 2025, 192(3):K24–K29) and no change in vasopressin in the same cohort (Galbiati et al., Journal of Neuroendocrinology, 2026, 38(1):e70114).

Registered trials, as of October 2026. Active clinical development is concentrated in one sponsor-investigator program at Massachusetts General Hospital, whose currently enrolling studies all register the intervention as “kisspeptin 112-121”: NCT04648969, a completed Phase 2 study of prolonged pulsatile dosing in hypogonadotropic hypogonadism (18 participants, results posted, primary completion August 2025); NCT05633966, a completed Phase 1 study of subcutaneous administration in reproductive disorders (13 participants); NCT05896293, a recruiting Phase 2 trial of subcutaneous kisspeptin in hypogonadotropic hypogonadism (started February 2023, 36 estimated participants, estimated primary completion May 2028); NCT07224438, a recruiting Phase 2 trial in hypothalamic amenorrhea that started in December 2025 (20 estimated participants); and NCT07224490, a recruiting Phase 1 study using kisspeptin to quantify GnRH neuronal function in health and disease, which opened in March 2026 (40 estimated participants). Two MGH studies of kisspeptin-10 and insulin secretion (NCT04532801, NCT05456854 — both registered under the name “Kisspeptin-10”) were withdrawn with zero enrollment, for insufficient power and futility respectively, and NCT05901467 was terminated in 2024 after 16 participants when the team lost access to its GnRH comparator. Three investigator studies at Pakistani universities (NCT03771326, NCT03286517, NCT03315325) are tagged Phase 3 in the registry but were 14- to 30-participant physiology studies completed in 2013–2014, not registrational trials; all three register their intervention as kisspeptin-10 (metastin 45-54), which is where that catalog alias comes from.

Failures and discontinuations. The only industry program built on this pharmacophore, Takeda’s TAK-448, an analog of the fully active 10-residue C terminus, drove testosterone below castration levels under continuous exposure in healthy men and prostate cancer patients, and all three of its registered trials were terminated (MacLean et al., Journal of Clinical Endocrinology & Metabolism, 2014, 99(8):E1445–E1453; the trial-by-trial record is on the kisspeptin-54 profile). No kisspeptin-10 program has produced an efficacy outcome in a patient population beyond the physiological endpoints above.

What the kisspeptin-54 trials do and do not say about kisspeptin-10. The best-known human kisspeptin results — the first human study, the IVF oocyte-maturation trigger program, and the fMRI work on sexual and emotional brain processing, all detailed on the kisspeptin-54 profile — used the 54-residue isoform, as did both randomized crossover trials in hypoactive sexual desire disorder, a 75-minute intravenous infusion of kisspeptin-54 in 32 women (Thurston et al., JAMA Network Open, 2022, 5(10):e2236131) and the same regimen in 32 men (Mills et al., JAMA Network Open, 2023, 6(2):e2254313). Those findings are often attached to retail kisspeptin-10 listings, but the decapeptide has never been tested as an IVF trigger or in sexual-desire disorders. The rodent pharmacokinetic difference between the two isoforms, and its failure to replicate in the human head-to-head infusion, is covered on the same page.

Common dosage forms

• Research-grade lyophilized powder — the dominant retail format is a single-use vial of synthetic peptide intended for reconstitution, offered in milligram quantities. Because the decapeptide is a short solid-phase synthesis, it is offered far more widely than kisspeptin-54, and a vial labeled only “kisspeptin” usually contains this fragment.
• Trial presentations — published human work used sterile solutions for intravenous bolus, intravenous infusion, subcutaneous bolus, and (since 2022) pulsatile or continuous subcutaneous infusion through a pump, with quantities expressed per kilogram or per hour rather than as fixed strengths. No fixed-dose, ready-to-use commercial presentation exists.
• Compounded preparations — kisspeptin-10 sits in Category 2 of the FDA’s interim 503A bulk-substance policy (see Key considerations), which places it outside the enforcement discretion the FDA extends to compounders under that policy.
• No validated alternative routes — there is no oral, intranasal, sublingual or topical kisspeptin-10 format with human data behind it.

Key considerations

• Regulatory status: unapproved and investigational, with an explicit FDA caution. No regulator has approved any kisspeptin product; the Investigational status reflects the registered investigator trials of kisspeptin-10 itself that are enrolling in 2026 (NCT05896293, NCT07224438, NCT07224490), with no pending marketing application. Separately, kisspeptin-10 is the isoform named in Category 2 of the FDA’s interim 503A bulks list (added September 29, 2023, still in place on the page marked current as of April 22, 2026), cited for possible immunogenicity by certain routes, impurity and characterization complexity, and limited route-specific safety information; the longer isoforms do not appear there (see the kisspeptin-54 profile).
• Isoform confusion is the main naming hazard. The kisspeptin isoforms share the same C-terminal decapeptide and receptor but are distinct molecules with distinct pharmacokinetics, as laid out on the kisspeptin-54 profile; for this page the practical points are that the IVF-trigger, fMRI and sexual-desire-disorder trials used kisspeptin-54, that the MGH diagnostic and pulsatile-dosing program, the Edinburgh dose-finding work and the 2026 chronic subcutaneous study used kisspeptin-10, and that the registry label “kisspeptin 112-121” and the catalog label “metastin 45-54” both denote this molecule.
• Dosing schedule inverts the effect. Sustained KISS1R stimulation suppresses the axis: a 5-day continuous subcutaneous infusion lost its gonadotropin effect in healthy men (Yeung et al., 2026), and 14-day continuous exposure to the decapeptide-derived analog TAK-448 produced below-castration testosterone (MacLean et al., 2014). Only intermittent or pulsatile schedules have sustained gonadotropin release, and only for 12 days in a handful of volunteers. Any framing of kisspeptin-10 as a durable “testosterone booster” is not supported by the human data.
• Evidence gaps are large. Total human exposure to kisspeptin-10 on record runs to the low hundreds of participants at most, almost all healthy volunteers or carefully phenotyped endocrine patients in supervised research units, with exposures measured in hours to two weeks. There are no efficacy outcomes (pregnancy, pubertal progression, symptom change) from a randomized trial in any patient population, no long-term safety data, no published data in people using exogenous androgens, and no pediatric data beyond single-bolus diagnostic use. Patients with congenital GnRH deficiency do not respond at all.
• Anti-doping status. Kisspeptin-54, its shorter isoforms including kisspeptin-10, and synthetic receptor agonists such as TAK-448 were added to the WADA Prohibited List in 2024 as testosterone-stimulating peptides, prohibited for male athletes. Doping-control laboratories have since published LC-HRMS methods for detecting them in serum and urine (Krombholz et al., Drug Testing and Analysis, 2026, 18(7):862–876).