Kisspeptin-10
Metastin (45-54) · HPG-axis research peptide
Overview
Kisspeptin-10 (also known as Metastin 45-54 or KP-10) is the 10-amino-acid C-terminal fragment of the larger kisspeptin family of peptides encoded by the KISS1 gene. The decapeptide retains essentially all of the KISS1 receptor (GPR54)-binding activity of the longer family members (Kisspeptin-54, -14, -13). Kisspeptin signaling at the hypothalamic level is the master regulator of GnRH neuron activation, which in turn drives downstream pituitary LH and FSH release, making kisspeptin-10 the canonical research tool for studying the apex of the hypothalamic-pituitary-gonadal (HPG) axis. Lyochem supplies Kisspeptin-10 as a lyophilized powder at ≥99.0% HPLC purity. The 10-residue sequence is straightforward in SPPS; the analytical packet covers peak-integration HPLC, mass spec, water content, and counter-ion. Sequence verification by LC-MS/MS is available on request. Buyers should note that Kisspeptin-10 has a relatively short plasma half-life (minutes) due to peptidase cleavage at the C-terminal RFamide motif, in vivo research protocols typically use continuous infusion or repeated bolus dosing to maintain HPG-axis stimulation, and intranasal preparations have been explored as a longer-duration alternative.
Who buys this, and why
Cognitive and neuropeptide buyers are predominantly research labs running in vivo rodent studies. The dominant administration route in the published literature is intranasal — Semax, Selank, DSIP, Pinealon — because these peptides are not meaningfully blood-brain-barrier permeable when delivered systemically. For in vivo workflows, endotoxin and microbial-limit testing is recommended at the CoA stage so the bioassay readout is not confounded by contamination unrelated to the test article.
Primary buyer fit: academic and contract research laboratories.
Specifications
- CAS
- 374675-21-5
- Purity (HPLC)
- ≥ 99.0%
- Common vial sizes
- 5 mg, 10 mg
- MOQ
- On request
- Lead time
- 10–18 days
- Storage
- -20°C, protect from light
Documentation available on request
- Lot-specific Certificate of Analysis (CoA)
- RP-HPLC chromatogram with peak integration
- ESI-MS identity confirmation (±0.5 Da)
- Sequence verification by LC-MS/MS
- Water content by Karl Fischer
- SDS / MSDS
- Bacterial endotoxin (LAL) on request — in vivo workflows
- Intranasal-formulation reconstitution guidance
- Sequence ladder (full b/y-ion) on request
Regulatory note
Sold for Research Use Only under the receiving laboratory's institutional and jurisdictional regulations. Not a finished dosage form and not labelled for human administration. In vivo research workflows should request endotoxin and microbial-limit testing on the specific lot so the bioassay readout is not confounded by contamination.
Frequently asked questions
What's the difference between Kisspeptin-10 and longer kisspeptin family members?▾
The KISS1 gene encodes a 145-amino-acid precursor that is processed into several biologically active C-terminal fragments: Kisspeptin-54 (the longest endogenous form, also called Metastin), Kisspeptin-14, Kisspeptin-13, and Kisspeptin-10. All four share the same C-terminal 10-amino-acid sequence ending in the RFamide motif that binds GPR54. Kisspeptin-10 retains essentially full binding activity at GPR54 and is the most commonly used research form because it's simpler to synthesize at high purity and avoids the variability that comes with longer-fragment processing. The longer forms (-54, -14) have slightly different pharmacokinetic profiles in vivo but similar receptor pharmacology.
Why is kisspeptin sometimes called the 'master regulator' of HPG-axis signaling?▾
Kisspeptin neurons in the hypothalamus (specifically in the arcuate nucleus and the rostral periventricular area) sit upstream of GnRH-releasing neurons. KISS1 signaling at GPR54 on GnRH neurons is the direct trigger for GnRH release into the hypophyseal portal system, which then drives pituitary LH and FSH release. In other words, kisspeptin is the proximate signal that determines whether the entire HPG cascade is active or quiescent, making it the master regulator of reproductive axis function. Disruption of kisspeptin signaling (loss-of-function mutations in KISS1 or GPR54) causes hypogonadotropic hypogonadism in humans, confirming the master-regulator role.
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