Journal September 16, 2026 6 min read

Kisspeptin-10: what the published research shows

Kisspeptin-10 is the bioactive decapeptide fragment of the KISS1 gene product, acting at the KISS1R receptor. This page summarises published research on its pharmacology, from gonadotropin regulation to metabolic and pla

peptides-pro Editorial

Kisspeptin-10 (KP-10) is a decapeptide with the sequence YNWNSFGLRF-NH2, corresponding to the C-terminal bioactive fragment of the KISS1 gene product. It is also known as metastin 45–54, and its molecular formula is C63H83N17O14, with a molecular weight of approximately 1302.5 Da. Kisspeptin-10 is classified as a neuropeptide and functions as an agonist at the KISS1R receptor (also known as GPR54), a G protein-coupled receptor.

The work described on this page centres on the KISS1/KISS1R signalling axis and its downstream effects on gonadotropin-releasing hormone (GnRH) neurons and other tissues.

Research Studies

Kisspeptin-10 and gonadotropin secretion in healthy men

A randomized, single-blinded, placebo-controlled study investigated the effects of acute and chronic subcutaneous kisspeptin-10 administration on reproductive hormones in healthy men. The study included three protocols: an acute dose–response infusion, a continuous 5-day infusion, and daily intermittent administration (8 hours on, 16 hours off) for 12 days. A total of 15 healthy men were recruited across the three studies (n=7, n=4, and n=7, respectively), with 12 men serving as controls. The authors reported that chronic subcutaneous kisspeptin-10 stimulated gonadotropin secretion for 12 days [1].

Kisspeptin-10 and LH secretion dynamics in healthy men

A separate study examined the effects of continuous kisspeptin administration on luteinizing hormone (LH) secretion in healthy men. Three healthy adult men received a continuous intravenous infusion of kisspeptin-10 at a dose of 12.5 mcg/kg/h for 24 hours and underwent frequent blood sampling. The objective was to assess whether continuous kisspeptin administration dampens kisspeptin-induced GnRH release, as had been observed in non-human primates. The authors noted that this phenomenon had not been replicated in the limited human studies reported to date [6].

Kisspeptin-10 and in vitro pharmacology: comparison with other agonists

An in vitro study characterised and directly compared the pharmacological profiles of hKp10, hKp54, and the synthetic agonist C6 using HEK293 cells. The authors noted that direct comparative data on these molecules remain limited. The study reported that the kisspeptin analog C6 elicits greater tachyphylaxis and transcriptional activation than kisspeptin-10 and -54 [2].

Kisspeptin-10 and extracellular matrix components in human cardiac fibroblasts

An in vitro study using a human cardiac fibroblast cell line investigated the effects of kisspeptin-10 on glycosaminoglycan and decorin content. Cardiac fibroblasts play a key role in extracellular matrix remodelling through the synthesis of glycosaminoglycans and proteoglycans such as decorin. The study aimed to determine the influence of KiSS-10 on these components and to identify its mechanism, assessing glycosaminoglycan levels by the Farndale method and decorin secretion by ELISA, with or without signalling inhibitors [3].

Kisspeptin-10 and neuroendocrine regulation in ewes

A study in ewe lambs examined changes in kisspeptin-10, neurokinin B (NKB), and dynorphin A (Dyn A) concentrations in blood plasma during puberty in relation to the first ovulation time. Twenty-four ewe lambs were divided into two groups: from single and twin pregnancies. The authors noted that the roles of these neuropeptides in the onset of sexual maturity and the pathomechanism of delayed puberty have not been fully elucidated [4].

Kisspeptin-10 and metabolic effects in high-fat fed female mice

An animal study examined the effects of twice-daily intraperitoneal administration of saline vehicle or kisspeptin-10 (25 nmol/kg) for 21 days on glucose homeostasis, energy balance, circulating hormones, and the morphology–function of enteroendocrine and islet cells in high-fat diet (HFD) fed female mice, with normal diet (ND) mice as an additional control group. The authors reported that kisspeptin-10 decreased body weight, blood glucose, and energy intake to ND levels. HFD increased circulating follicle-stimulating hormone (FSH) levels, which were further modulated by kisspeptin-10 [5].

Kisspeptin-10 and placental mTOR signalling in hypothyroid rats

A study in rats evaluated the effects of maternal hypothyroidism, with and without kisspeptin-10 treatment, on maternal energy homeostasis and placental expression of mTOR and glucose metabolism mediators. Maternal hypothyroidism was induced by administration of propylthiouracil, and kisspeptin-10 treatment began on gestational day 8. The authors noted that reduced placental mTOR signalling is associated with intrauterine growth restriction and impaired maternal and placental metabolism, and that maternal treatment with kisspeptin-10 has been shown to improve feto-placental development in hypothyroid rats [8].

Kisspeptin-10 and the KISS1/KISS1R axis in human placentation

A review discussed the KISS1/KISS1R axis in human placentation, molecular mechanisms, and implications for foetal growth restriction and pre-eclampsia. The authors noted that pre-eclampsia and foetal growth restriction are major pregnancy complications primarily driven by placental dysfunction, and that current diagnostic modalities predominantly reflect established disease rather than early molecular disturbances. The identification of biomarkers directly associated with trophoblast signalling pathways has the potential to improve early risk stratification [7].

Kisspeptin-10 and structural selectivity at KISS1R

A computational study provided structural insights into the selectivity of kisspeptin-10 toward KISS1R. The authors noted that kisspeptin-10, the bioactive core fragment of kisspeptin neuropeptides, has emerged as a modulator of reward-related behaviours beyond its canonical role in reproductive neuroendocrinology, and that behavioural studies indicate it promotes impulsive and compulsive-like phenotypes in rodent models [9].

Kisspeptin-10 and clinical differentiation of central precocious puberty

A clinical study reported that the kisspeptin-10/basal LH ratio improves the differentiation of central precocious puberty and premature thelarche. The authors noted that distinguishing idiopathic central precocious puberty from premature thelarche remains a clinical challenge and often necessitates GnRH stimulation testing, and that kisspeptin-10, neurokinin B, and neuropeptide Y are key regulators of GnRH secretion that may serve as surrogate biomarkers [10].

Kisspeptin-10 and ovarian cancer progression

An in vitro and computational study explored the influence of exogenous kisspeptin-10 on the SP1–ZEB1–hTERT pathway in SKOV-3 ovarian cancer cell lines. The authors noted that ovarian cancer is one of the deadliest female gynaecological cancers, known to have high metastatic ability and telomerase reactivation [11].

Kisspeptin-10 and ovarian follicle development in mice

A study in mice aimed to elucidate how kisspeptin-10 modulates hormone secretion, proliferation, and autophagy of ovarian follicles by regulating in vivo and in vitro levels of associated genes and proteins. Follicular granulosa cells were cultured in EMDM/F12 medium. The authors reported that kisspeptin-10 promotes hormone secretion, ovarian follicle development, and fecundity via the PI3K/AKT/ERK signalling pathway [12].

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