Kisspeptin-10 10 mg

Kisspeptin-10 is the C-terminal decapeptide of metastin, the 54-residue, carboxy-terminally amidated product of the KISS1 gene. KISS1 was characterised in the 1990s as a suppressor of melanoma and breast-carcinoma metastasis, but its peptide product was not matched to a receptor until 2001, when Ohtaki and colleagues at Takeda isolated metastin from human placenta and identified it as the endogenous ligand of the orphan G-protein-coupled receptor hOT7T175 — the receptor subsequently known as GPR54 and now designated KISS1R. The 45–54 fragment retains receptor-activating potency and is the form most commonly used in laboratory work. Like other members of the RFamide family, the decapeptide terminates in an amidated Arg-Phe motif; that C-terminal amide is a structural requirement rather than a formality, and the free-acid form YNWNSFGLRF-OH is a different compound, not KP-10.

Kisspeptin-10 is described in the literature as a high-affinity agonist at KISS1R (GPR54), a Gq/11-coupled receptor whose activation drives phospholipase C-β, inositol trisphosphate generation, intracellular calcium mobilisation and ERK1/2 phosphorylation. KISS1R is expressed on GnRH neurons of the hypothalamus, and the proposed mechanism situates kisspeptin one synaptic step upstream of the GnRH pulse generator: kisspeptinergic neurons in the arcuate nucleus and the anteroventral periventricular nucleus are held to relay gonadal steroid feedback and metabolic state onto GnRH neurons, which in turn govern pituitary gonadotropin release. The human loss-of-function genetics are the principal evidence for this placement — inactivating KISS1R mutations produce hypogonadotropic hypogonadism while the pituitary remains responsive to exogenous GnRH. Consistent with an action upstream of the pituitary rather than at it, the 2015 human comparison found GnRH associated with higher gonadotrophin output than either kisspeptin species at the levels tested. Receptor desensitisation on sustained exposure, and rapid enzymatic cleavage of the decapeptide, are recurring variables in the published pharmacology and remain areas of active investigation.

Kisspeptin-10 is classified as endogenous decapeptide, RFamide peptide family (Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH₂) — the C-terminal 45–54 fragment of the KISS1 gene product metastin / kisspeptin-54.

Short, and markedly shorter than that of the parent 54-mer. In the 2005 human infusion study by Dhillo and colleagues the plasma half-life of kisspeptin-54 was calculated at 27.6 ± 1.1 minutes. A comparably precise human plasma half-life for kisspeptin-10 could not be confirmed against the primary sources checked for this entry, so no figure is asserted for it here; the draft value of "approximately 4 minutes" was removed for that reason. What is documented is rapid loss of the decapeptide: Liu and colleagues (2013) reported decomposition half-lives of 6.8, 2.9 and 1.7 minutes in rat plasma at 4 °C, 25 °C and 37 °C respectively, with cleavage of the N-terminal tyrosine as the principal decomposition route, and rapid elimination in rats following intravenous bolus. Brief circulating persistence is therefore a defining experimental variable in the published record. Stated for interpretation of the research literature only; not a handling, preparation or administration instruction.

Lyophilized format gives ≥24 months sealed stability at -20°C — significantly longer than pre-reconstituted, which has a 30-day shelf life once in solution. You reconstitute at the moment of use, when potency is at its peak.

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