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Free U.S. shipping on orders over $150Snapshot: Kisspeptin activates the KISS1R receptor, which regulates gonadotropin-releasing hormone (GnRH) secretion and various other targets. Exogenous kisspeptin-10 directly stimulates GnRH release and influences tumor cell behavior. Kisspeptin may also influence sexual and emotional brain processing, metabolic signaling, vascular and renal biology, and in tumor-cell migration and metastatic pathways.
Kisspeptins are biologically active peptides encoded by the KISS1 gene, which produces several biologically active peptides, including kisspeptin-54 and kisspeptin-10 [1]. All active fragments bind to the same G-protein-coupled receptor, KISS1R [2].
Kisspeptin-10 is the smallest active form of kisspeptin, with the amino acid sequence YNWNSFGLRFamide. Exogenously-administered kisspeptin-10 can directly stimulate GnRH, suggesting that it may have potential therapeutic effects in reproductive medicine and sexual health [3, 4].
KISS1 was originally identified as a metastasis suppressor gene, based on early findings that its expression could inhibit the spread of melanoma and breast cancer cells [5]. The gene is expressed in multiple tissues, including the hypothalamus, gonads, pancreas, adrenal gland, liver, and brain, reflecting both central and peripheral physiological roles [6].
Kisspeptin exerts primary endocrine effects through KISS1R-mediated stimulation of gonadotropin-releasing hormone (GnRH) neurons in the hypothalamus [2]. When it binds to KISS1R, the receptor activates G-protein-coupled intracellular signalling cascades, which increase the activity and firing of GnRH-secreting neurons [1]. GnRH is released into the hypothalamic-pituitary portal circulation and stimulates the anterior pituitary to release luteinizing hormone (LH) and follicle-stimulating hormone (FSH) [1].
Research suggests kisspeptin is a key upstream regulator of reproductive hormone activation, particularly around the onset of puberty, and the full extent of its regulatory control remains an active area of research [2, 7].
Beyond its central role in controlling reproductive hormones, kisspeptin is also studied for possible effects on sexual behavior and emotional processing, metabolic function, and in cancer biology.
Kisspeptin is best known for its central role in activating the reproductive hormone axis via stimulation of GnRH neurons, which in turn drives LH and FSH release and supports sexual maturation and fertility [6].
In a small clinical study enrolling 4–5 subjects per group per gender, subjects received subcutaneous bolus or IV infusion of kisspeptin-10. Healthy male participants had elevated LH and FSH in response to low-dose IV bolus at 0.3 and 1.0 nmol/kg. In contrast, female participants had no serum gonadotrophin responses during their follicular phase, even at doses as high as 720 pmol/kg/min. However, during their preovulatory phases, the serum LH and FSH were elevated after IV bolus of kisspeptin at 10 nmol/kg [3].
In a small comparative study enrolling 5 healthy men per group, vehicle, kisspeptin-10, kisspeptin-54, and GnRH were compared at doses of 0.1, 0.3, and 1.0 nmol/kg/h. Subjects received 3 hours of intravenous therapy. Subsequently, their LH and FSH were tested. The study found that GnRH produced about three-fold the LH and FSH elevation relative to kisspeptin-10, and twice that of kisspeptin-54 [8].
Emerging research also indicates that kisspeptin may influence aspects of emotional processing, bonding, and sexual behavior through its actions in the limbic and hypothalamic brain regions involved in motivation and affective regulation [6].
Both the hormonal and emotional effects appear to operate within reproductive and motivational circuits, rather than broad psychological pathways [6].
Kisspeptin signalling has been identified in several peripheral metabolic tissues, including the pancreas and adipose tissue, suggesting roles beyond reproduction. Experimental work in rodents and humans demonstrated that kisspeptin and its receptor are expressed in pancreatic islets and in vivo models, without affecting basal insulin release [6]. These findings support a context-dependent, glucose-linked action instead of a continuous insulin-stimulatory effect.
Consistent with this, animals created without kisspeptin signalling show increased adiposity, higher leptin levels, and impaired glucose tolerance [6]. This raises the possibility that loss of peripheral kisspeptin signalling may contribute to energy imbalances and metabolic dysregulation [6]. Current evidence supports a modulatory, rather than primary, metabolic role with kisspeptin influencing insulin signaling, adiposity, and glucose tolerance under specific physiological conditions, particularly those linked to reproductive or hormonal status [6].
Kisspeptin was first discovered in cancer research, where restoring KISS1 gene expression in highly metastatic melanoma cells strongly reduced the spread of tumors in animal models, without stopping the original tumor from growing [9]. This led to its classification as a metastasis-suppressor gene [9].
Cell-based studies suggest it does not mainly act by killing cancer cells, but by reducing their ability to move, invade, and migrate [9]. Kisspeptin peptides can slow chemotaxis and invasion, influence matrix-remodelling enzymes, and change cell shape and cytoskeleton dynamics in ways that make cells less mobile and more adhesive [9].
Clinical expression across several cancer types, including melanoma, breast, ovarian, bladder, esophageal, and endometrial cancers, consistently shows that lower KISS1 expression is associated with more advanced or metastatic disease, whereas higher expression is more common in earlier-stage tumors [9].
Current evidence primarily indicates that kisspeptin impacts metastatic potential rather than tumor growth itself, acting as a regulator of how readily cancer cells spread through the body [9].
1 Messager, S., Chatzidaki, E. E., Ma, D., Hendrick, A. G., Zahn, D., Dixon, J., et al. (2005) Kisspeptin directly stimulates gonadotropin-releasing hormone release via G protein-coupled receptor 54. Proc. Natl. Acad. Sci. U. S. A., Proceedings of the National Academy of Sciences 102, 1761–1766
2 Rønnekleiv, O. K. and Kelly, M. J. (2013) Kisspeptin excitation of GnRH neurons. Adv. Exp. Med. Biol., Springer New York 784, 113–131
3 Jayasena, C. N., Nijher, G. M. K., Comninos, A. N., Abbara, A., Januszewki, A., Vaal, M. L., et al. (2011) The effects of kisspeptin-10 on reproductive hormone release show sexual dimorphism in humans. J. Clin. Endocrinol. Metab., The Endocrine Society 96, E1963–72
4 Thurston, L., Hunjan, T., Ertl, N., Wall, M. B., Mills, E. G., Suladze, S., et al. (2022) Effects of kisspeptin administration in women with hypoactive sexual desire disorder: A randomized clinical trial: A randomized clinical trial. JAMA Netw. Open, American Medical Association (AMA) 5, e2236131
5 Lee, J. H., Miele, M. E., Hicks, D. J., Phillips, K. K., Trent, J. M., Weissman, B. E., et al. (1996) KiSS-1, a novel human malignant melanoma metastasis-suppressor gene. J. Natl. Cancer Inst., Oxford University Press (OUP) 88, 1731–1737
6 Bhattacharya, M. and Babwah, A. V. (2015) Kisspeptin: beyond the brain. Endocrinology, The Endocrine Society 156, 1218–1227
7 Skorupskaite, K., George, J. T. and Anderson, R. A. (2014) The kisspeptin-GnRH pathway in human reproductive health and disease. Hum. Reprod. Update 20, 485–500
8 Jayasena, C. N., Abbara, A., Narayanaswamy, S., Comninos, A. N., Ratnasabapathy, R., Bassett, P., et al. (2015) Direct comparison of the effects of intravenous kisspeptin-10, kisspeptin-54 and GnRH on gonadotrophin secretion in healthy men. Hum. Reprod., Oxford University Press (OUP) 30, 1934–1941
9 Mead, E. J., Maguire, J. J., Kuc, R. E. and Davenport, A. P. (2007) Kisspeptins: a multifunctional peptide system with a role in reproduction, cancer and the cardiovascular system: Kisspeptins are multifunctional peptides. Br. J. Pharmacol., Wiley 151, 1143–1153
Research Use Only. All findings described above are derived from preclinical studies (animal models and in vitro experiments). Kisspeptin is not approved by the FDA for any diagnostic or therapeutic use in humans. Genesis Peptides makes no claims regarding human clinical efficacy. This product is sold exclusively for laboratory research.
Every lot undergoes six independent assays before release. Results are published in the lot-specific Certificate of Analysis.
Kisspeptin-10 (KP-10), the minimal bioactive fragment of KISS1, exerts its effects through the G-protein-coupled receptor KISS1R. A review describes kisspeptin signalling via KISS1R as regulating trophoblast invasion, extracellular matrix remodelling, ERK1/2 activation, and angiogenic balance, which together modulate spiral artery transformation. A computational analysis indicates high selectivity for KISS1R compared with dopamine types 1 and 2 and serotonin types 1A and 2A receptors.
In a human clinical trial, LH concentrations under continuous kisspeptin-10 infusion peaked and then declined by 13-47% from the maximum to the end of the infusion. By the end of the infusion, LH had settled at 10.7-22.8 mIU/mL. In a human clinical trial of continuous kisspeptin-10 infusion, FSH and testosterone rose modestly in parallel with LH. A human clinical trial reported that chronic subcutaneous kisspeptin-10 administration sustained gonadotropin and testosterone secretion in healthy men for 12 days.
In a human clinical trial, gonadotropin rises were still detected after a kisspeptin-10 bolus of 1 nmol/kg following 12 days of daily infusions. The researchers reported this as indicating that the kisspeptin receptor remained functional after 12 days. Other human clinical trial evidence reports that chronic subcutaneous kisspeptin-10 administration sustained gonadotropin and testosterone secretion in healthy men for 12 days.
In a human review, maternal circulating kisspeptin concentrations were reported to rise exponentially during normal gestation. The same review reported that pregnancies later complicated by fetal growth restriction (FGR) or preeclampsia (PE), particularly in early gestation, are associated with reduced maternal circulating kisspeptin levels. In human studies summarised in the review, kisspeptin acting through its receptor KISS1R was described as regulating trophoblast invasion and spiral artery transformation.
In a study in epileptic rats with temporal lobe epilepsy, exogenous kisspeptin-10 (Kp-10) administration attenuated neuroinflammation and enhanced cognitive function and survival rate. The authors described this as highlighting a potential neuroprotective role of kisspeptin in temporal lobe epilepsy pathogenesis. In these rats, Kp-10 treatment upregulated the anti-inflammatory cytokine Il-10 in the hippocampus and anterior temporal lobe. In the hippocampus of epileptic rats, Kp-10 treatment downregulated the pro-inflammatory cytokine Il-1β, while no change was seen in the anterior temporal lobe.
In in vitro studies of microglial cells, KP-10 was found to suppress microglial pyroptosis and neuroinflammatory signaling. The authors describe this effect as arising from two mechanisms: inhibition of the NLRP3-caspase-1-GSDMD axis and activation of BAG3-dependent selective autophagy. In microglial cells in vitro, KP-10 markedly upregulated Bcl-2-associated athanogene 3 (BAG3), a co-chaperone involved in selective autophagy.
In mice, KP-10 administration suppressed food intake, with especially strong inhibition of feeding compared with KP-13.
In an in vitro study, kisspeptin-10 was extensively degraded after one week at 4 and 22 °C in serum and plasma. In in vitro work, all native kisspeptins investigated showed poor stability in urine and blood, although several degradation products could be identified. In in vitro testing, kisspeptin-10 was stable, with variation lower than 15%, for at least two months at -20 °C in all blood matrices considered. In in vitro dried matrices, kisspeptin-10 remained detectable throughout the entire duration of the stability study at non-refrigerated temperatures.
In an in vitro laboratory study, kisspeptin-10 was among the 54 prohibited peptidic and non-peptidic compounds detected in dried blood spots, serum, and plasma by the analytical workflow. The workflow was described as a fast, streamlined, and harmonized method for detecting these 54 compounds in dried blood spots, serum, and plasma. Separately, in an observational study of a human reference population, analysis of 20 serum samples and 100 urine samples revealed no detectable signals of endogenous kisspeptins and/or their degradation products.
Kisspeptin and its isoforms, including kisspeptin-10 (KP-10), were included in the World Anti-Doping Agency's Prohibited List in 2024. The source states that doping use of these substances is prohibited for male athletes. In a laboratory study, kisspeptin-10 was among the 54 prohibited peptidic and non-peptidic compounds that an analytical workflow detected in dried blood spots, serum, and plasma.
In ovarian cancer cells studied in vitro, KP-10 influenced the expression of the tumor-suppressive microRNAs miR-200, miR-345, and miR-577, which are known to inhibit epithelial-mesenchymal transition, invasion, and cancer development. In SKOV-3 ovarian cancer cells studied in vitro, KP-10 affected the regulation of the transcription factors SP1, CDX2, GATA2, FLI1, and ZEB1 and the expression of hTERT, which indicated modulation of telomerase-related oncogenic signaling.
FOR RESEARCH USE ONLY — Products are sold exclusively for in vitro and preclinical laboratory research. Not for human consumption or administration. Not intended for diagnostic or therapeutic use. These statements have not been evaluated by the FDA.