What it is
Kisspeptin is a natural hormone made in the brain. It works like a master switch for making babies. It tells a small group of nerve cells to release a signal called GnRH. GnRH then tells the pituitary gland (a small gland under the brain) to release more hormones. Those hormones drive the ovaries and testes. People born without a working kisspeptin receptor (the “lock” the hormone fits into) do not go through puberty on their own.
The body makes kisspeptin in several lengths. The longest has 54 amino acids and the shortest has 10. All of them end in the same tail of 10 amino acids. That tail alone is enough to switch the receptor on. Kisspeptin-10 is a lab-made copy of that tail. It is a short chain of amino acids (a peptide).
It is a research tool, not a medicine. No product with it is approved anywhere. The FDA lists it among substances that may carry serious safety risks when pharmacies mix it themselves.
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. Cancer researchers noticed it stopped skin cancer (melanoma) cells from spreading. They named it KiSS-1, a nod to the town’s famous chocolate. In 2001, drug-company and university labs found that the gene makes a hormone. That hormone fits a receptor called GPR54, which had no known partner before.
The big surprise came in 2003. Two groups, one in France and one in Boston, found something new. People with broken copies of that receptor never start puberty. This moved kisspeptin from cancer research to the study of fertility and sex hormones. Teams at Imperial College London, Edinburgh and Massachusetts General Hospital then began giving kisspeptins to volunteers. No company has tried to get kisspeptin-10 itself approved as a medicine.
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 sex hormones in men. One shot into a vein raises luteinising hormone (LH) within half an hour. LH is a hormone that tells the testes and ovaries to work. A slow, steady drip into a vein over many hours raises testosterone. Women responded differently. In one study it did nothing early in the monthly cycle. But it worked just before the egg was released.
A longer form, kisspeptin-54, has been studied further. At Imperial College it was used in IVF instead of the usual hormone to help eggs mature. It led to pregnancies. This included women at high risk of a dangerous reaction from too much fertility treatment. That work was on kisspeptin-54, not kisspeptin-10. Trials in Boston are still running. They include people with late or missing puberty and people with missing periods. There is no long-term safety data 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
There are three separate points here.
Approval: No medicine with kisspeptin-10 is approved anywhere. University researchers in Boston are running small trials with it. The FDA oversees these trials. That is why this page calls it still being tested, rather than saying no one is working on it.
Pharmacy mixing: Since September 2023, the FDA has kept kisspeptin-10 in “Category 2”. This means pharmacies that mix it risk FDA action. In October 2024, an FDA expert panel voted 11 to 0 against adding it to the list of ingredients pharmacies may mix. The FDA updated its Category 2 list in April 2026. Several other peptides were taken off it. Kisspeptin-10 was not. It was still in Category 2.
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.
