{"id":2864,"date":"2026-08-25T10:39:25","date_gmt":"2026-08-25T10:39:25","guid":{"rendered":"https:\/\/officialcorepeptides.brandloom.net\/fr\/?post_type=product&p=2864"},"modified":"2026-08-25T10:39:25","modified_gmt":"2026-08-25T10:39:25","slug":"buy-kisspeptin-10-in-switzerland","status":"publish","type":"product","link":"https:\/\/officialcorepeptides.ch\/fr\/product\/buy-kisspeptin-10-in-switzerland\/","title":{"rendered":"Kisspeptin-10 (10MG)"},"content":{"rendered":"

What Is Kisspeptin-10 and Why Buy It for Research?<\/strong><\/h2>\n

Buy Kisspeptin-10 in Switzerland for research into reproductive endocrinology, GPR54 signaling, and neuroendocrine regulation. Specifically, Kisspeptin-10 (also known as Kp-10, Metastin 45-54, or Kisspeptin-10 human) is a synthetic decapeptide composed of ten amino acids with the sequence H-Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH\u2082 (one-letter code: YNWNSFGLRF-NH\u2082). It is the shortest bioactive fragment of the larger kisspeptin-54 protein, which is encoded by the KISS1 gene first identified in 1996 at Pennsylvania State University.<\/p>\n

Kisspeptin-10 has a molecular weight of 1302.4 g\/mol and the molecular formula C\u2086\u2083H\u2088\u2083N\u2081\u2087O\u2081\u2084. The C-terminal amide group (-NH\u2082) on the final phenylalanine residue is a defining structural feature of the peptide, distinguishing it from truncated variants lacking this modification. In scientific research, Kisspeptin-10 serves as a molecular tool for studying GPR54 (KISS1R) signaling, HPG axis regulation, and reproductive endocrinology. Furthermore, Core Peptides supplies Kisspeptin-10 as a lyophilized powder exclusively for laboratory use. Therefore, researchers seeking to source this compound for their work will find it readily available when they buy Kisspeptin-10 in Switzerland.<\/p>\n

Kisspeptin-10 Research Overview: Buy Kisspeptin-10 in Switzerland for GPR54 Studies<\/strong><\/h2>\n

Centrally, research into Kisspeptin-10 has focused on its function as a potent endogenous agonist of the G protein-coupled receptor GPR54 (also known as KISS1R or AXOR12). Among the kisspeptin isoforms, Kp-10 is the smallest and is reported to activate KISS1R to its full functional potential. Kisspeptin-10 exhibits the same binding and agonist activity as the parent molecule, kisspeptin-54, and contains the basic residues required to retain full functional activity with higher receptor affinity and biopotency than longer forms of the peptide.<\/p>\n

Kisspeptin-10 binds to the G protein-coupled receptor KISS1R\/GPR54 with high affinity: Ki values of 1.59 nM for rat KISS1 receptors and 2.33 nM for human KISS1 receptors. This binding triggers G protein-coupled receptor signaling via activation of G(q) and phosphatidylinositol 4,5-bisphosphate hydrolysis. The activation of KISS1R by kisspeptin-10 recruits phosphatase DUSP18 and SRC to the KISS1R C-terminus. Measurement of calcium kinetics has revealed that kisspeptin-10 elicits a remarkable increase in intracellular calcium concentration in target cells.<\/p>\n

Kisspeptins are reported to be the most potent activators of the hypothalamus-pituitary-gonadal (HPG) axis known to date. Kisspeptin potently elicits gonadotropin-releasing hormone (GnRH) release and luteinizing hormone (LH) secretion, even in the pre-pubertal period. Accordingly, researchers who buy Kisspeptin-10 in Switzerland from Core Peptides can support their investigations into GPR54 signaling, reproductive endocrinology, and neuroendocrine regulation.<\/p>\n

How Does Kisspeptin-10 Work in Research?<\/strong><\/h2>\n

Mechanistically, Kisspeptin-10’s proposed action involves functioning as a GPR54 agonist that activates Gq\/11-coupled signaling to stimulate GnRH release and downstream gonadotropin secretion. The peptide operates through several interconnected mechanisms.<\/p>\n

GPR54 Receptor Activation<\/strong><\/h3>\n

Kisspeptin-10 binds to and activates the G protein-coupled receptor GPR54 (KISS1R), which is expressed on hypothalamic GnRH neurons and in other tissues. This binding event initiates a conformational change in the receptor, leading to the activation of downstream signaling pathways. Kisspeptin-10 exhibits higher receptor affinity and biopotency than longer forms of the peptide. The binding affinity (Ki) of Kisspeptin-10 for human KISS1R is approximately 2.33 nM.<\/p>\n

Intracellular Signaling Cascade<\/strong><\/h3>\n

The primary signaling pathway involves the coupling of activated KISS1R to the G\u03b1q\/11 subunit of the heterotrimeric G protein. This activation stimulates phospholipase C (PLC), which hydrolyzes phosphatidylinositol 4,5-bisphosphate (PIP2) into two key second messengers: inositol trisphosphate (IP3) and diacylglycerol (DAG). IP3 triggers the release of stored calcium (Ca\u00b2\u207a) from the endoplasmic reticulum, and this sharp increase in intracellular calcium is critical for GnRH neuron depolarization and subsequent gonadotropin secretion.<\/p>\n

GnRH and Gonadotropin Secretion<\/strong><\/h3>\n

Kisspeptin-10 stimulates the release of gonadotropin-releasing hormone (GnRH) from hypothalamic neurons, which in turn drives the secretion of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) from the anterior pituitary. George et al. reported that kisspeptin-10 increased LH pulse frequency and LH secretion in healthy men, supporting its role in physiological GnRH pulse generation. Kisspeptin-10 significantly increased LH and testosterone concentrations, highlighting its potential therapeutic relevance in hypogonadal states. Studies have also demonstrated a central mechanism of action of kisspeptin-10 that is independent of sex steroids.<\/p>\n

Osteoblast Differentiation<\/strong><\/h3>\n

Beyond its neuroendocrine functions, Kisspeptin-10 has been shown to regulate osteoblast differentiation through GPR54-mediated activation of NFATc4 transcription factor. In mesenchymal stem cells, KP-10 enhances osteogenic gene expression, such as BMP2, Runx2, and Dlx5. This signaling pathway promotes Smad1\/5\/9 phosphorylation, a key step in BMP2-induced osteoblast differentiation. The mechanism involves NFATc4 binding to the BMP2 promoter, establishing Kisspeptin-10 as a regulator of bone formation through GPR54\/NFATc4\/BMP2 signaling.<\/p>\n

Vasoconstriction and Angiogenesis Inhibition<\/strong><\/h3>\n

Kisspeptin-10 is also a potent vasoconstrictor and inhibitor of angiogenesis. It acts as a tumor metastasis suppressor via its receptor GPR54. The ability of Kp-10 to inhibit signaling and chemotaxis induced by SDF-1 indicates that activation of GPR54 signaling may negatively regulate the role of CXCR4 in programming tumor metastasis.<\/p>\n

Why Is Kisspeptin-10 Studied in Switzerland?<\/strong><\/h2>\n

Primarily, researchers study Kisspeptin-10 because it represents the shortest bioactive kisspeptin isoform with full GPR54 agonist activity, enabling investigation of reproductive endocrinology, neuroendocrine regulation, and GPR54-mediated signaling pathways. In fact, this compound offers a focused tool for studying the molecular mechanisms underlying HPG axis function, fertility regulation, and gonadotropin secretion.<\/p>\n

Research has demonstrated Kisspeptin-10’s relevance across multiple domains. Recent studies have revealed that the KISS1\/KISS1R system plays an essential role in the neuroendocrine control of the reproductive axis. Development and functional analysis of Kp-10 analogs may help in the search for new agonists and antagonists as valuable tools to manipulate the KISS1\/KISS1R system and hence fertility.<\/p>\n

Furthermore, Kisspeptin-10 has been studied for its potential in treating stress-induced reproductive dysfunction. Kisspeptin-10 has also been studied for its antidepressant-like effects. Ultimately, researchers who buy Kisspeptin-10 in Switzerland gain access to a comprehensive research tool for investigating GPR54 signaling, reproductive endocrinology, and neuroendocrine regulation.<\/p>\n

Kisspeptin-10 Research Areas in Laboratory Studies<\/strong><\/h2>\n\n\n\n\n\n\n\n\n\n\n\n\n
Research Area<\/th>\nFocus<\/th>\nEvidence Level<\/th>\n<\/tr>\n<\/thead>\n
GPR54 Receptor Pharmacology<\/td>\nReceptor binding, Gq\/11 signaling, calcium mobilization<\/td>\nMechanistic \/ In Vitro<\/td>\n<\/tr>\n
HPG Axis Regulation<\/td>\nGnRH release, LH secretion, FSH regulation, puberty onset<\/td>\nMechanistic \/ In Vivo \/ Clinical<\/td>\n<\/tr>\n
Fertility Research<\/td>\nOvulation induction, gametogenesis, reproductive function<\/td>\nPreclinical \/ Clinical<\/td>\n<\/tr>\n
Neuroendocrine Research<\/td>\nHypothalamic-pituitary signaling, stress-induced dysfunction<\/td>\nPreclinical<\/td>\n<\/tr>\n
Osteoblast Differentiation<\/td>\nBMP2 expression, NFATc4 activation, bone formation<\/td>\nMechanistic \/ In Vitro<\/td>\n<\/tr>\n
Vasoconstriction and Angiogenesis<\/td>\nVascular tone regulation, angiogenesis inhibition<\/td>\nMechanistic \/ Preclinical<\/td>\n<\/tr>\n
Metastasis Research<\/td>\nTumor suppression, CXCR4 regulation, migration inhibition<\/td>\nMechanistic \/ Preclinical<\/td>\n<\/tr>\n
Metabolic Regulation<\/td>\nObesity-diabetes, insulin secretion, energy metabolism<\/td>\nPreclinical<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Kisspeptin-10 Compared With Related Research Compounds<\/strong><\/h2>\n\n\n\n\n\n\n\n\n
Compound<\/th>\nResearch Focus<\/th>\nMechanism \/ Target<\/th>\nKey Difference<\/th>\n<\/tr>\n<\/thead>\n
Kisspeptin-10 (Kp-10)<\/td>\nGPR54 signaling, HPG axis, fertility, osteogenesis<\/td>\nKISS1R\/GPR54 agonist (Gq\/11 signaling)<\/td>\nShortest bioactive kisspeptin; full GPR54 agonist activity<\/td>\n<\/tr>\n
Kisspeptin-54 (Metastin)<\/td>\nGPR54 signaling, metastasis suppression<\/td>\nKISS1R\/GPR54 agonist<\/td>\nLonger isoform; proteolytically cleaved to generate Kp-10<\/td>\n<\/tr>\n
Kisspeptin-234 (Antagonist)<\/td>\nGPR54 antagonism, receptor blockade<\/td>\nKISS1R antagonist<\/td>\nReceptor antagonist; opposite mechanism<\/td>\n<\/tr>\n
Gonadorelin (GnRH)<\/td>\nGnRH receptor activation, gonadotropin secretion<\/td>\nGnRH receptor agonist<\/td>\nActs downstream of kisspeptin; different receptor target<\/td>\n<\/tr>\n<\/tbody>\n<\/table>\n

Comparatively, Kisspeptin-10 differs from other kisspeptin isoforms in its length and research applications. On the one hand, Kisspeptin-10 is the shortest isoform (10 amino acids) that retains full GPR54 agonist activity and exhibits higher receptor affinity than longer forms. On the other hand, Kisspeptin-54 is the full-length protein that is proteolytically cleaved to generate Kp-10 and other isoforms.<\/p>\n

Research Applications for Kisspeptin-10 in Switzerland<\/strong><\/h2>\n

Scientists have investigated Kisspeptin-10 across several research domains:<\/p>\n