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Hedi Raizer

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Kisspeptin-10: reported timelines in the literature

A research-supply summary of reported experimental timelines for Kisspeptin-10 across human, animal, and in vitro studies, with study durations and model details drawn from the cited literature.

peptides-pro Editorial

Kisspeptin-10 (also written Kp-10, KP-10, or KiSS-10) is the bioactive decapeptide core fragment of the kisspeptin neuropeptide family, corresponding to the C-terminal sequence of the KISS1 gene product. It is a peptide-class research reagent; the evidence block does not provide a sequence, formula, or molecular weight, so those identifiers are not stated here. In the literature summarised below, the work centres on the KISS1/KISS1R receptor axis and its downstream gonadotropin-releasing hormone (GnRH) and gonadotropin signalling.

Reported timelines vary by model and route. In healthy men, chronic subcutaneous administration has been reported to stimulate gonadotropin secretion for 12 days [1], while continuous intravenous infusion over 24 hours has been examined for its dynamic effect on luteinizing hormone (LH) [6]. In female mice, twice-daily intraperitoneal administration was studied over 21 days [5]. In pregnant rats, treatment began on gestational day 8 [8]. In human cardiac fibroblast cultures, effects on extracellular matrix components were assessed in vitro [3]. In ewe lambs, plasma concentrations were tracked in relation to puberty onset [4]. The sections below set out each study's model, intervention, and reported timeline.

Research Studies

Kisspeptin-10 and gonadotropin secretion in healthy men

A randomized, single-blinded, placebo-controlled study evaluated acute and chronic subcutaneous Kisspeptin-10 administration in healthy men. The protocol included an acute dose–response phase, a continuous 5-day infusion phase, and a daily intermittent phase (8 hours on, 16 hours off) for 12 days. Fifteen healthy men were recruited across the three study arms (study 1: n = 7; study 2: n = 4; study 3: n = 7), with 12 men serving as controls. The reported finding was that chronic subcutaneous Kisspeptin-10 stimulated gonadotropin secretion for 12 days in this population [1].

Kisspeptin-10 and dynamic LH secretion in healthy men

A separate study examined continuous intravenous infusion of Kisspeptin-10 at 12.5 mcg/kg/h for 24 hours in three healthy adult men, with frequent blood sampling to characterise the effect on LH secretion. The objective was to test whether continuous administration dampens kisspeptin-induced GnRH release, as had been reported in non-human primates, in a human model. The evidence block does not state the outcome direction, only the design and the 24-hour infusion timeline [6].

Kisspeptin-10 and obesity-diabetes in high-fat fed female mice

In high-fat diet (HFD) fed female mice, Kisspeptin-10 was administered twice daily by intraperitoneal injection at 25 nmol/kg for 21 days, with normal diet (ND) mice as an additional control. Reported effects included decreased body weight, blood glucose, and energy intake to ND levels. HFD increased circulating follicle-stimulating hormone (FSH), which was further modulated by treatment. The study also examined ileal enteroendocrine cells and pancreatic islet morphology. This is an animal model; the 21-day timeline applies to mice, not to humans [5].

Kisspeptin-10 and placental mTOR signalling in hypothyroid rats

In a rat model, maternal hypothyroidism was induced with propylthiouracil, and Kisspeptin-10 treatment began on gestational day 8. The study evaluated maternal energy homeostasis and placental expression of mTOR and glucose metabolism mediators. The reported finding was that Kisspeptin restored placental mTOR signalling and improved glucose homeostasis mediators disrupted by maternal hypothyroidism. This is an animal study; the gestational-day-8 start and subsequent timeline are specific to the rat model [8].

Kisspeptin-10 and extracellular matrix components in human cardiac fibroblast cultures

In human cardiac fibroblast cell cultures, the influence of Kisspeptin-10 on glycosaminoglycan and decorin content was assessed, with and without signalling inhibitors. Glycosaminoglycan levels were determined by the Farndale method and decorin secretion by ELISA. The reported finding was that Kisspeptin-10 regulates glycosaminoglycan and decorin content in this in vitro system. This is a cell-culture study; no in vivo timeline is reported [3].

Kisspeptin-10, neurokinin B, and dynorphin A in ewe lambs during puberty

Twenty-four ewe lambs from single and twin pregnancies were studied to determine changes in plasma concentrations of Kisspeptin-10, neurokinin B (NKB), and dynorphin A (Dyn A) during puberty in relation to first ovulation, and to examine relationships among these neuropeptides. The reported finding concerns the relationship between Kisspeptin-10, NKB, and Dyn A in the course of normal and delayed puberty in this animal model. The evidence block does not specify the sampling interval or total observation period [4].

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

A review of the KISS1/KISS1R axis in human placentation addressed molecular mechanisms and implications for foetal growth restriction and pre-eclampsia. The evidence block describes the diagnostic context (ultrasound, Doppler, PlGF, sFlt-1) and the potential for biomarkers directly associated with trophoblast signalling pathways. This is a review; it does not report a primary experimental timeline [7].

Kisspeptin-10 and comparative pharmacology with kisspeptin-54 and C6

An in vitro study characterised and directly compared the pharmacological profiles of hKp10, hKp54, and the synthetic agonist C6 in HEK293 cells. The reported finding was that the kisspeptin analog C6 elicits greater tachyphylaxis and transcriptional activation than Kisspeptin-10 and Kisspeptin-54. This is an in vitro comparison; no in vivo timeline is reported [2].

Kisspeptin-10 and ovarian cancer cell lines

A reference-only study explored the influence of exogenous Kisspeptin-10 on the SP1-ZEB1-hTERT pathway in SKOV-3 ovarian cancer cell lines using in vitro and computational methods. The reported finding was that exogenous Kisspeptin-10 inhibits ovarian cancer progression through targeting the SP1-hTERT-ZEB1 regulatory axis. This is an in vitro and computational study; no in vivo timeline is reported [11].

Kisspeptin-10 and ovarian follicle development in mice

A reference-only study in mice examined 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 reported finding was that Kisspeptin-10 promotes hormone secretion, ovarian follicle development, and fecundity via the PI3K/AKT/ERK signal pathway. This is an animal and cell-culture study [12].

Kisspeptin-10 and central precocious puberty versus premature thelarche

A reference-only study examined the Kisspeptin-10/basal LH ratio for improving differentiation of central precocious puberty and premature thelarche. The evidence block notes that distinguishing idiopathic central precocious puberty from premature thelarche remains a clinical challenge and often necessitates GnRH stimulation testing, and that Kisspeptin-10, NKB, and NPY are key regulators of GnRH secretion that may serve as surrogate biomarkers. This is a clinical study; the evidence block does not provide a timeline [10].

Kisspeptin-10 and KISS1R selectivity

A reference-only computational study reported structural insights into Kisspeptin-10 selectivity toward KISS1R. The evidence block notes that Kisspeptin-10 is the bioactive core fragment of kisspeptin neuropeptides and has emerged as a modulator of reward-related behaviours beyond its canonical role in reproductive neuroendocrinology, with behavioural studies indicating that KP-10 promotes impulsive and compulsive-like phenotypes in rodent models. This is a computational and behavioural study; no experimental timeline is provided [9].

Reported timelines at a glance

Model / populationInterventionReported timelineSource
Healthy menSubcutaneous Kisspeptin-10, daily intermittent (8 h on, 16 h off)12 days[1]
Healthy menContinuous intravenous Kisspeptin-10, 12.5 mcg/kg/h24 hours[6]
High-fat fed female miceIntraperitoneal Kisspeptin-10, 25 nmol/kg, twice daily21 days[5]
Pregnant rats (hypothyroid model)Kisspeptin-10 treatment beginning gestational day 8Gestational day 8 onward[8]
Human cardiac fibroblast culturesKisspeptin-10 with or without signalling inhibitorIn vitro; no in vivo timeline[3]
Ewe lambsPlasma Kisspeptin-10, NKB, Dyn A measurementDuring puberty to first ovulation[4]
HEK293 cellshKp10, hKp54, C6 comparisonIn vitro; no in vivo timeline[2]

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