What it is
Kisspeptin is a natural hormone made in the brain that acts as a master switch for reproduction. It tells a small group of nerve cells to release GnRH, which in turn tells the pituitary gland to release the hormones that drive the ovaries and testes. People born without a working kisspeptin receptor do not go through puberty on their own.
The body makes kisspeptin in several lengths, from 54 amino acids down to 10. All of them end in the same 10-amino-acid tail, and that tail alone is enough to switch the receptor on. Kisspeptin-10 is a lab-made copy of that tail.
It is a research tool, not a medicine. No product containing it is approved anywhere, and the FDA lists it among substances that may pose significant safety risks in pharmacy compounding.
Kisspeptin-10 (Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2, C63H83N17O14, 1302.4 g/mol) corresponds to residues 112–121 of the KISS1 precursor and the C-terminal decapeptide common to kisspeptin-54, -14 and -13. Its C-terminal Arg-Phe-amide places it in the RF-amide peptide family. It is a full agonist at KISS1R (formerly GPR54), a Gq/11-coupled receptor on hypothalamic GnRH neurons; activation depolarises these neurons and releases GnRH into the portal circulation, which drives LH and FSH secretion.
Human pharmacology comes from small physiology studies. Intravenous boluses raise LH within 30 minutes in men, and continuous infusion increases LH pulse frequency and testosterone. In women the response depends on cycle phase. Kisspeptin-54 has been studied more often in women; its plasma half-life was 27.6 minutes in the first human study (Dhillo et al., JCEM 2005). A full human pharmacokinetic profile for kisspeptin-10 was not found in the sources reviewed for this article.
Who made it and when
The gene was found in 1996 at Penn State’s medical school in Hershey, Pennsylvania, by cancer researchers who noticed it stopped melanoma cells from spreading. They named it KiSS-1, a nod to the town’s famous chocolate. In 2001 drug-company and academic labs showed that the gene makes a hormone that fits an unclaimed receptor called GPR54.
The big surprise came in 2003, when two groups, in France and in Boston, found that people with broken copies of that receptor never enter puberty. That moved kisspeptin from cancer biology to reproductive medicine. Groups at Imperial College London, Edinburgh and Massachusetts General Hospital then began giving kisspeptins to volunteers. No company has taken kisspeptin-10 itself into development for approval.
Lee et al. (J Natl Cancer Inst 1996) cloned KiSS-1 as a melanoma metastasis-suppressor gene. In 2001 Ohtaki et al. (Takeda, Nature) isolated a 54-residue C-terminally amidated peptide from placenta, named metastin, as the endogenous ligand of GPR54, with parallel reports from other groups. de Roux et al. (PNAS 2003) and Seminara et al. (NEJM 2003) linked loss-of-function GPR54 mutations to hypogonadotropic hypogonadism.
Human studies followed: Dhillo et al. (Imperial, 2005) with kisspeptin-54 in men; George et al. (Edinburgh, 2011) and Chan et al. (MGH, 2011) with kisspeptin-10. Takeda designed TAK-448, a nonapeptide KISS1R agonist derived from kisspeptin-10; its prostate-cancer and hypogonadism trials were terminated (NCT01132404, NCT02369796), and the compound was later studied as MVT-602 with Myovant Sciences. MGH investigators led by Stephanie Seminara hold the current registered trials of kisspeptin-10, all listed as FDA-regulated drug studies; approval status is recorded as investigational on that basis. No patent held by a commercial developer of kisspeptin-10 itself could be verified.
What the data say
In small studies, kisspeptin-10 raised reproductive hormones in men. A single injection into a vein pushes up luteinising hormone within half an hour, and a steady drip over many hours raises testosterone. In women the picture is different: in one study it did nothing early in the menstrual cycle but worked just before ovulation.
A longer form, kisspeptin-54, has gone further. At Imperial College it was given instead of the usual hormone to trigger egg maturation in IVF, and it led to pregnancies, including in women at high risk of a dangerous over-stimulation reaction. That work is about kisspeptin-54, not kisspeptin-10. Trials in people with delayed or absent puberty and missing periods are ongoing in Boston. No long-term safety data exist for kisspeptin-10.
Men: George et al. reported a dose-dependent LH rise after IV bolus (maximal at 1 µg/kg, 4.1 to 12.4 IU/L at 30 minutes, n=6; reduced response at 3 µg/kg). Infusion at 4 µg/kg/h for 22.5 hours raised LH from 5.4 to 20.8 IU/L and testosterone from 16.6 to 24.0 nmol/L; at 1.5 µg/kg/h LH pulse frequency rose from 0.7 to 1.0 per hour. Chan et al. showed a single IV bolus resets the GnRH pulse generator. Jayasena et al. (Hum Reprod 2015) found kisspeptin-10 and -54 produced similar LH responses in men, both weaker than GnRH.
Women: Jayasena et al. (JCEM 2011) saw no gonadotropin response in the follicular phase at up to 10 nmol/kg IV, 32 nmol/kg SC or 720 pmol/kg/min infused, but a rise in the preovulatory phase.
Related molecules: kisspeptin-54 at 1.6–12.8 nmol/kg SC triggered oocyte maturation in 53 IVF patients, with 23% clinical pregnancy (Jayasena, Abbara et al. 2014); in 60 women at high OHSS risk, no moderate or severe OHSS occurred (Abbara 2015). MVT-602 produced a later LH peak than kisspeptin-54 (21.4 vs 4.7 hours) and larger LH exposure (Abbara 2020). Systematic safety data for kisspeptin-10 in humans are limited to these small studies.
Regulatory picture
Three separate facts. Approval: no medicine containing kisspeptin-10 is approved anywhere. Academic researchers in Boston are running small FDA-regulated trials with it, which is why this page records it as investigational rather than as having no programme at all. Compounding: since September 2023 the FDA has kept kisspeptin-10 in “Category 2”, meaning pharmacies that compound it risk FDA action, and in October 2024 an FDA advisory committee voted 11 to 0 against adding it to the list of allowed compounding ingredients. Unlike several other peptides, it was still in Category 2 when the FDA updated that list in April 2026. Enforcement: no FDA warning letters naming kisspeptin-10 were found.
Approval: investigational. No approved product; current US trials (NCT05896293, NCT07224438, NCT07224490) are investigator-sponsored at MGH and registered as FDA-regulated drug studies, which for an unapproved drug requires an IND; NCT05896293 lists FDA’s Office of Orphan Products Development as its funding source. No commercial development programme was identified.
Compounding: category-2. Kisspeptin-10 was placed in 503A Category 2 on 2023-09-29 and remains there on FDA’s page updated 2026-04-22; it was not among the substances withdrawn by nominators. At the 2024-10-29 Pharmacy Compounding Advisory Committee meeting FDA proposed not to include kisspeptin-10 on the 503A bulks list for secondary hypogonadism in men; the vote was 0 yes, 11 no. It is not a component of an approved drug and has no USP monograph.
Sport: WADA’s 2026 Prohibited List names “kisspeptin and its agonist analogues” under S2.2.1, testosterone-stimulating peptides in males.
