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Kisspeptin-10 10mg

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Kisspeptin-10 (KP-10) is the C-terminal 10-amino-acid biologically active fragment of kisspeptin (metastin), the endogenous ligand for GPR54 (KISS1R). GPR54 activation by kisspeptin-10 in hypothalamic KNDy neurons potently stimulates GnRH pulse release, positioning it as the master upstream regulator of the HPG axis. Research applications include GPR54 pharmacology, GnRH pulsatility investigation, KNDy neuron circuitry research, and HPG-axis neuroendocrinology.

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3D Molecular Structure

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Kisspeptin-10 10mg1 vial | KIT (10 vials)
Chemical Formula C258H401N79O78
Synonyms KISS-1 (68-121), Protein KISS-1, Gene KISS1 protein
Molar Mass 5857 g/mol
CAS Number 388138-21-4
PubChem CID 71306396
Total Compound Content 10 mg per vial
Shelf Life 36 months
Kisspeptin-10 (Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH₂) is the biologically active C-terminal decapeptide fragment of the kisspeptin peptide family and a selective agonist of the KISS1 receptor (KISS1R/GPR54), a Gq/11-coupled G protein-coupled receptor. KISS1R activation stimulates phospholipase C signaling, resulting in IP3/DAG generation, intracellular calcium mobilization, and downstream receptor-mediated signaling processes. Experimental investigations have examined kisspeptin signaling in relation to receptor activation mechanisms, ligand-receptor interactions, intracellular communication pathways, and GPCR-associated regulatory networks. The well-characterized interaction between Kisspeptin-10 and KISS1R makes it a valuable research tool for studies of peptide receptor pharmacology, signal transduction, receptor selectivity, and mechanistic evaluation of KISS1R-mediated signaling systems. Supplied as a lyophilized preparation (10 mg/vial). Independently third-party HPLC-tested; COA available per batch.

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What is the significance of kisspeptin in regulating the GnRH pulse generator?

Kisspeptin (via GPR54 activation on GnRH neurons) is the most potent known endogenous stimulator of GnRH pulsatility. Its identification in 2003 resolved a decades-long question about the upstream regulator of GnRH neurons — previously, the identity of the GnRH 'pulse generator' was unknown. KNDy neurons (co-expressing kisspeptin, NKB, and dynorphin) in the arcuate nucleus are now understood to generate the GnRH pulse signal, with kisspeptin as the primary GnRH secretagogue and NKB/dynorphin providing autocrine synchronisation. KP-10 is the research tool for directly activating this pathway.

How does kisspeptin-10 differ from full-length kisspeptin in research applications?

Full-length human kisspeptin-54 (hKP-54) and the shorter fragments KP-13 and KP-10 all bind GPR54 and stimulate GnRH release. KP-10 (the C-terminal decapeptide) retains the RF-amide motif essential for GPR54 binding and is equipotent with longer forms at the receptor. Its shorter length confers easier synthetic preparation, more consistent purity, and straightforward HPLC verification. KP-10 is the most widely used kisspeptin research tool in the published literature due to these practical advantages.

Why does kisspeptin-10's very short plasma half-life complicate research protocol design?

Kisspeptin-10 has a plasma half-life of approximately 3 minutes due to rapid C-terminal cleavage by endopeptidase 24.11 (neprilysin) and other peptidases. This necessitates continuous infusion or frequent bolus injections to maintain sustained GPR54 activation and GnRH stimulation in in vivo research. For studies requiring acute GnRH pulse stimulation, a single bolus is appropriate. For studies modelling tonic kisspeptin signalling (e.g. pubertal timing, continuous HPG axis activation), researchers must use infusion protocols or longer-acting kisspeptin analogues engineered for peptidase resistance.

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