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Hedi Raizer

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Kisspeptin-10: sourcing, documentation and price

Kisspeptin-10 is a decapeptide agonist of the KISS1R receptor. This page covers its identifiers, research-use documentation, and sourcing considerations for laboratory supply.

peptides-pro Editorial

Kisspeptin-10 (also known as Kp-10, KiSS-10, or hKp10) is a decapeptide fragment of the larger kisspeptin neuropeptide family, acting as an agonist at the KISS1R receptor (formerly GPR54). It is supplied as a research-use-only material, typically as a lyophilised powder for reconstitution. The evidence block for this page does not provide the full amino acid sequence, molecular formula, or molecular weight; those identifiers should be confirmed with the certificate of analysis provided by the supplier. The work described in the cited studies centres on the KISS1R receptor and its downstream signalling in reproductive neuroendocrinology, with additional investigation in metabolic, placental, and cardiac fibroblast models.

For laboratory sourcing, Kisspeptin-10 is offered as a 10 mg presentation. Documentation accompanying research peptides typically includes a certificate of analysis (CoA) stating purity (often by HPLC), identity (by mass spectrometry), and appearance. Researchers should verify that the CoA matches the lot number and that the material is intended for research purposes only. Price varies with quantity, purity grade, and supplier; no pricing information is provided in the evidence block, and this page does not quote a price.

Research Studies

Kisspeptin-10 and gonadotropin secretion in healthy men

A randomised, single-blinded, placebo-controlled study evaluated acute and chronic subcutaneous kisspeptin-10 administration in healthy men. The study included three protocols: acute dose–response, continuous infusion over 5 days, and daily intermittent administration (8 h on, 16 h off) for 12 days. In the 12-day intermittent protocol, kisspeptin-10 stimulated gonadotropin secretion persistently [1]. The same publication reported that 15 healthy men were recruited across the three studies, with 12 men serving as controls [1].

Kisspeptin-10 and LH secretion dynamics in healthy men

A separate study examined the effects of continuous intravenous kisspeptin-10 infusion on luteinizing hormone (LH) secretion in healthy men. Three healthy adult men received a continuous infusion at 12.5 mcg/kg/h for 24 h, with frequent blood sampling to characterise the LH response [6]. This study was designed to test whether continuous kisspeptin administration dampens kisspeptin-induced GnRH release, as had been observed in non-human primates but not consistently in limited human studies [6].

Kisspeptin-10 and in vitro pharmacological profiles

In vitro characterisation using HEK293 cells compared the pharmacological profiles of hKp10, hKp54, and the synthetic agonist C6. The kisspeptin analog C6 elicited greater tachyphylaxis and transcriptional activation than kisspeptin-10 and kisspeptin-54 [2]. This study provided direct comparative data on endogenous and synthetic agonists, which the authors noted had been limited both in vivo and in vitro [2].

Kisspeptin-10 and extracellular matrix components in human cardiac fibroblasts

In cultures of a human cardiac fibroblast cell line, kisspeptin-10 was found to regulate glycosaminoglycan and decorin content. The study assessed the effects of KiSS-10 on these extracellular matrix components with or without signalling inhibitors, measuring glycosaminoglycan levels by the Farndale method and decorin secretion by ELISA [3]. The authors stated that the effects of kisspeptin-10 on these components in the heart had previously been unknown [3].

Kisspeptin-10 and neuroendocrine markers in pubertal ewes

A study in ewe lambs investigated changes in plasma concentrations of kisspeptin-10, neurokinin B (NKB), and dynorphin A (Dyn A) during puberty, in relation to the time of first ovulation. Twenty-four ewe lambs from single or twin pregnancies were divided into two groups [4]. The aim was to examine the relationship between these neuropeptides and the onset of sexual maturity, as their roles in delayed puberty had not been fully elucidated [4].

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

In high-fat diet (HFD) fed female mice, twice-daily intraperitoneal administration of kisspeptin-10 at 25 nmol/kg for 21 days decreased body weight, blood glucose, and energy intake to levels comparable to normal diet (ND) mice. The study also examined morphology and function of ileal enteroendocrine cells and pancreatic islets. HFD increased circulating follicle-stimulating hormone (FSH) levels, which were further modulated by kisspeptin-10 treatment [5]. This work was conducted in an animal model and does not establish effects in humans.

Kisspeptin-10 and placental mTOR signalling in hypothyroid rats

In a rat model of maternal hypothyroidism induced by propylthiouracil, maternal treatment with kisspeptin-10 beginning on gestational day 8 was evaluated for effects on maternal energy homeostasis and placental expression of mTOR and glucose metabolism mediators. The study aimed to assess whether kisspeptin-10 could restore placental mTOR signalling and improve glucose homeostasis mediators disrupted by hypothyroidism [8]. This is an animal study; findings are not directly translatable to human pregnancy.

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

A review of the KISS1/KISS1R axis in human placentation discussed molecular mechanisms and implications for foetal growth restriction and pre-eclampsia. The authors noted that current diagnostic modalities for these pregnancy complications predominantly reflect established disease rather than early molecular disturbances, and that biomarkers directly associated with trophoblast signalling pathways could improve early risk stratification [7]. This is a review article; it does not present new primary data.

Kisspeptin-10 and comparative data on receptor selectivity

Computational studies have examined the structural basis for kisspeptin-10 selectivity toward KISS1R. One such report described kisspeptin-10 as the bioactive core fragment of kisspeptin neuropeptides and noted its modulation of reward-related behaviours beyond reproductive neuroendocrinology, with behavioural studies in rodent models indicating promotion of impulsive and compulsive-like phenotypes [9]. This is a reference-only item and is not the focus of this page.

Kisspeptin-10 and clinical differentiation in paediatric populations

A reference-only study reported that the ratio of kisspeptin-10 to basal LH may improve differentiation between idiopathic central precocious puberty and premature thelarche, conditions that are otherwise distinguished using GnRH stimulation testing [10]. The same report identified kisspeptin-10, neurokinin B, and neuropeptide Y as key regulators of GnRH secretion that may serve as surrogate biomarkers [10]. This finding is noted for completeness and is not a primary focus here.

Kisspeptin-10 and ovarian cancer cell lines

In vitro and computational work using SKOV-3 ovarian cancer cell lines explored the influence of exogenous kisspeptin-10 on the SP1-ZEB1-hTERT pathway. The study aimed to investigate the effect of kisspeptin-10 on this regulatory axis in the context of ovarian cancer progression [11]. This is a reference-only item; the findings are from cell-line experiments and do not establish clinical outcomes.

Kisspeptin-10 and ovarian follicle development in mice

A study in mice examined how kisspeptin-10 modulates hormone secretion, proliferation, and autophagy of ovarian follicles, using in vivo and in vitro approaches. Follicular granulosa cells were cultured and treated to assess associated genes and proteins, with the aim of elucidating the role of kisspeptin-10 via the PI3K/AKT/ERK signalling pathway [12]. This is a reference-only item and is not the main subject of this page.

If you are reading this for personal health reasons

This material is sold for laboratory research only. We do not provide dosing or medical guidance. Anyone considering a compound for themselves should speak to a licensed clinician.

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