Kisspeptin 10mg

▎Kisspeptin Structure

▎Kisspeptin Research

Molecular Background

Kisspeptin-10 (KP-10) is a 10-amino-acid C-terminal fragment of the KISS1-derived kisspeptin precursor. Its amino acid sequence is Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2 (YNWNSFGLRF-NH2), and it binds the G protein-coupled receptor KISS1R. PubChem lists human Kisspeptin-10 under CID 25240297, with the molecular formula C63H83N17O14 and a molecular weight of approximately 1302.4 g/mol.[1,8]

Research Progress
Zhangsong Wu and colleagues determined cryo-EM structures of KISS1R-Gq and KISS1R-Gi complexes bound to the synthetic agonist TAK448, together with a KISS1R-Gq complex bound to endogenous KP54. Functional assays in the same study indicated that KISS1R can couple to the Gi/o pathway in addition to the established Gq/11 pathway. The authors reported structural differences in receptor extracellular and intracellular loops and in the Gα-subunit interface that may contribute to G-protein coupling selectivity. This structural study used KP54 and TAK448 rather than KP-10 as the bound ligands.[2]

Fig1. Cryo-EM structures of KISS1R-G protein complexes reported with TAK448 and KP54 in the cited study.[2]

(A) Schematic representation of KISS1R G-protein coupling examined in the source study. (B) NanoBiT G-protein dissociation assays for the indicated G-protein members following TAK448 exposure. (C-H) Cryo-EM models and maps of TAK448-KISS1R-Gq, TAK448-KISS1R-Gi, and KP54-KISS1R-Gq complexes. Experimental conditions and statistical details are reported in the original publication.[2]

Jenny Clarkson and Allan Herbison studied the postnatal development of kisspeptin neuron populations and their projections to GnRH neurons in mice. Using an antiserum raised against mouse kisspeptin-10, they identified kisspeptin-immunoreactive populations in the anteroventral periventricular/preoptic periventricular region, dorsomedial hypothalamus, and arcuate nucleus. The authors reported a marked female-dominant difference in AVPV/PeN kisspeptin neuron numbers and observed close appositions between kisspeptin fibers and GnRH neuron cell bodies emerging during postnatal development. This work characterized endogenous neuronal expression and development rather than the effects of an externally supplied KP-10 material.[3]

Alexander S. Kauffman and colleagues used adult wild-type (WT) and GPR54/KISS1R knockout (KO) mice to examine the role of kisspeptin-receptor signaling in sexually dimorphic behavior and neural development. Hormone-replaced GPR54 KO males and females retained sex-typical copulatory behavior, while differences were observed in olfactory partner preference and in several sexually dimorphic neural traits. The authors concluded that GPR54 signaling was not required for adult copulatory behavior under the hormone-replacement conditions used, but was involved in the development of selected sexually dimorphic traits.[4]

Fig2. GnRH-neuron Fos immunoreactivity and plasma LH measurements reported after intracerebroventricular kisspeptin exposure in WT and GPR54 KO male mice.[4]

*p < 0.05 versus the vehicle-treated WT group, as reported in the original study.[4]

Oscar González-Flores and colleagues examined intracerebroventricular kisspeptin exposure in ovariectomized rats primed with estradiol benzoate. The authors measured lordosis quotient and lordosis reflex intensity and then used the KISS1R antagonist Kiss-234, the progesterone receptor antagonist RU486, and the GnRH-1 receptor antagonist antide to examine receptor involvement. Kisspeptin exposure was associated with higher lordosis measurements in the rat model, while antagonist pretreatment reduced the response at selected time points. The findings supported involvement of KISS1R, progesterone-receptor, and GnRH-receptor signaling under the conditions of the study.[5]

Fig3. Lordosis measurements reported after kisspeptin exposure with or without the KISS1R antagonist Kiss-234 in ovariectomized rats.[5]

The source study compared kisspeptin and control groups and evaluated the effect of Kiss-234 pretreatment on lordosis quotient and lordosis reflex intensity. Group sizes, study doses, time points, and statistical comparisons are reported in the original publication.[5]

Suvi T. Ruohonen and colleagues generated mice with oocyte-selective deletion of Gpr54/Kiss1r by crossing a Gdf9-Cre line with a Gpr54 LoxP line. The resulting OoGpr54−/− mice underwent phenotypic, histological, hormonal, and molecular analyses across several postnatal ages. The authors reported normal puberty onset but progressive ovulatory failure with age, including histological changes and altered ovarian gene-expression profiles. Because this study used receptor deletion rather than administration of a kisspeptin peptide, its findings concern the biological role of ovarian KISS1R signaling and are not a direct KP-10 exposure study.[6]

Fig4. Progressive ovulatory changes reported in mice with oocyte-selective Gpr54/Kiss1r deletion.[6]

Panels (A-F) show representative ovarian histology from control and OoGpr54−/− mice at the indicated ages. Panel (G) summarizes the proportion of OoGpr54−/− females without corpora lutea, panel (H) presents selected RNA-sequencing findings, and panel (I) shows estrous-cycle measurements. Group sizes and statistical methods are reported in the original publication.[6]

Research Limitations

The studies summarized above do not all evaluate the same kisspeptin molecular form. The KISS1 precursor can be processed into several bioactive peptides, including KP54, KP14, KP13, and KP10, which share the same C-terminal decapeptide but differ in length and pharmacokinetic behavior. The Wu study used KP54 and TAK448, while other cited work examined endogenous kisspeptin signaling, receptor knockout models, or kisspeptin preparations that were not designed as direct comparisons of a commercial KP-10 research material.[2,3,4,6,7]

KISS1R is a class A G protein-coupled receptor and is best known for Gq/11 signaling, although recent structural and functional work also supports coupling to Gi/o under specific experimental conditions.[2] Differences in peptide isoform, receptor expression, species, tissue context, route of exposure, and experimental design may influence the observed response. Results from mouse and rat models therefore should remain tied to the exact peptide, receptor model, and experimental conditions described in each publication.[2,7]

COCER Peptides presents Kisspeptin-10 solely for laboratory research and analytical use. It is not intended for human or veterinary use. The research described above summarizes findings reported in third-party publications and is not a statement of clinical efficacy, safety, diagnosis, treatment, prevention, or an instruction for use.

▎Relevant Citations

References

[1] Xie Q, Kang Y, Zhang C, et al. The Role of Kisspeptin in the Control of the Hypothalamic-Pituitary-Gonadal Axis and Reproduction[J]. Frontiers in Endocrinology, 2022,13:925206.

DOI:10.3389/fendo.2022.925206.

[2] Wu Z, Chen G, Qiu C, et al. Structural basis for the ligand recognition and G protein subtype selectivity of kisspeptin receptor[J]. Science Advances, 2024,10(33):eadn7771.

DOI:10.1126/sciadv.adn7771.

[3] Clarkson J, Herbison A E. Postnatal development of kisspeptin neurons in mouse hypothalamus; sexual dimorphism and projections to gonadotropin-releasing hormone neurons[J]. Endocrinology, 2006,147(12):5817-5825.

DOI:https://doi.org/10.1210/en.2006-0787

[4] Kauffman A S, Park J H, McPhie-Lalmansingh A A, et al. The kisspeptin receptor GPR54 is required for sexual differentiation of the brain and behavior[J]. Journal of Neuroscience, 2007,27(33):8826-8835.

DOI:10.1523/JNEUROSCI.2099-07.2007.

[5] González-Flores O, Domínguez-Ordóñez R, Delgado-Macuil R J, et al. Participation of kisspeptin, progesterone, and GnRH receptors on lordosis behavior induced by kisspeptin[J]. Physiology & Behavior, 2024,283:114609.

DOI:10.1016/j.physbeh.2024.114609.

[6] Ruohonen S T, Gaytan F, Usseglio Gaudi A, et al. Selective loss of kisspeptin signaling in oocytes causes progressive premature ovulatory failure[J]. Human Reproduction, 2022,37(4):806-821.

DOI:10.1093/humrep/deab287.

[7] Chakraborty A P, Banerjee A A. Kisspeptin isoforms: versatile players in reproduction and beyond[J]. Journal of Molecular Endocrinology, 2025,75(1):e250001.

DOI:10.1530/jme-25-0001.

[8] NCBI PubChem. Kisspeptin-10, PubChem CID 25240297.

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