Kisspeptin

Synthetic Decapeptide Research Compound

Kisspeptin-10 occupies a unique position in peptide research. Discovered first as a tumor metastasis suppressor in melanoma biology — the KISS1 gene name itself traces to that origin — it was later identified as the master upstream regulator of the hypothalamic-pituitary-gonadal (HPG) axis, controlling reproductive endocrinology at the level of GnRH pulse release from hypothalamic KNDy neurons. Few research peptides carry dual biological heritage across two fields as distinct as oncology and reproductive neuroendocrinology.

Dragon Pharma Kisspeptin-10 delivers the biologically active C-terminal decapeptide sequence Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH₂ in lyophilized research-grade form — the shortest naturally occurring fragment of the kisspeptin family that retains complete binding activity at its cognate receptor KISS1R (GPR54). The critical C-terminal amide (-NH₂), which defines the kisspeptin RFamide family and is structurally required for KISS1R engagement, is explicitly confirmed by LC-MS in every Dragon Pharma batch — a quality checkpoint that HPLC purity analysis alone cannot provide.

Product Specifications

KISS1R Pharmacology and Downstream Signaling

At its most fundamental level, Dragon Pharma Kisspeptin-10 is a tool compound for GPR54 pharmacology. KISS1R is a class A G protein-coupled receptor belonging to the Gq/11 subfamily, located at chromosome 19p13.3. It is the sole endogenous receptor for the kisspeptin family and serves as one of the most well-validated entry points for studying the neuroendocrine regulation of reproductive biology in laboratory settings.

When KP-10 engages KISS1R, the following signaling cascade is initiated:

• Gq/11 activation — G-protein coupling triggers phospholipase C (PLC) activation
• IP3 and DAG generation — PLC cleaves phosphatidylinositol 4,5-bisphosphate into inositol trisphosphate (IP3) and diacylglycerol (DAG)
• Intracellular Ca²⁺ mobilization — IP3 triggers endoplasmic reticulum calcium release producing rapid [Ca²⁺]i elevation
• PKC activation — DAG activates protein kinase C, which phosphorylates downstream substrates
• ERK1/2 phosphorylation — downstream MAPK signaling; a commonly measured endpoint in KISS1R activation studies
• β-arrestin recruitment — receptor desensitization pathway, measurable in KISS1R-expressing cell lines

Quantified receptor pharmacology: Ki ~2.33 nM (human KISS1R), ~1.59 nM (rat KISS1R); EC50 ~1.0 nM in CHO-GPR54 IP accumulation assays. These values establish Kisspeptin-10 as a high-affinity reference ligand suitable for binding competition assays, dose-response characterization, and comparative GPR54 pharmacology studies.

Five Active Research Domains

1. Neuroendocrine and HPG Axis Research

KP-10 is the primary tool compound for investigating hypothalamic-pituitary-gonadal axis regulation at the GnRH level. In hypothalamic models, KISS1R activation on KNDy neurons (co-expressing kisspeptin, neurokinin B, and dynorphin) drives pulsatile GnRH secretion, which governs downstream pituitary LH and FSH release and gonadal sex steroid biology. Research areas include GnRH pulsatility modeling, KNDy neuron circuitry characterization, puberty onset mechanisms, hypogonadotropic hypogonadism pathway investigation, and HPG axis regulation in both male and female reproductive biology contexts.

2. Cell Motility and Trophoblast Biology

The KISS1 gene was originally identified as a metastasis suppressor in melanoma — its product inhibits cell migration and invasion. In placental trophoblast research, KP-10 has been studied as a physiological inhibitor of cell motility. Research in HTR8/SVneo placental cells demonstrated reduced migration via an ERK1/2-p90rsk-GSK3β-FAK signaling feedback loop. In first-trimester trophoblast cultures, KP-10 raised intracellular calcium and inhibited motility without altering proliferation — consistent with a signaling-specific rather than cytotoxic mechanism. Downstream investigations have examined associated changes in MMP and TIMP expression, alongside VEGF-A modulation through KISS1R/ERK1/2 pathways.

3. Neuronal Protection Models

Published research has characterized a neuroprotective activity of Kisspeptin-10 in cholinergic neuronal models that operates independently of KISS1R binding — a mechanistically significant finding that opens a research thread entirely separate from GPR54 pharmacology. In SH-SY5Y-derived neurons engineered to overexpress wild-type or E46K mutant α-synuclein, KP-10 was shown to reduce α-synuclein-linked apoptosis and mitochondrial depolarization through receptor-independent direct peptide-protein interactions. This positions Kisspeptin-10 as a research tool for neurodegeneration biology relevant to conditions characterized by α-synuclein pathology, alongside its established role in GPR54 signaling.

4. Cardiac Fibroblast and ECM Biology

Research in cardiac fibroblast cultures has documented that Kisspeptin-10 increases intracellular collagen content through focal adhesion kinase (FAK) phosphorylation, alongside shifts in the balance between matrix metalloproteinases and their tissue inhibitors. This extends KP-10's documented biology into cardiovascular connective tissue research, creating a research application profile that spans neuroendocrine, reproductive, neuronal, and cardiac tissue systems — an unusually broad multi-system footprint for a ten-residue peptide.

5. Radiotheranostic and Imaging Research

Published work from 2025 demonstrated that a DOTA-conjugated Kisspeptin-10 analogue retained comparable KISS1R activation capacity to unconjugated KP-10, measured by inositol phosphate accumulation in KISS1R-expressing HEK293 cells. The conjugate was characterized for serum stability and evaluated as a potential gallium-68/lutetium-177 pan-tumour radiopharmaceutical targeting KISS1R-expressing tumours. This work positions the KISS1R system as a target for receptor-targeted radiotheranostic research — an emerging application domain for which unconjugated Kisspeptin-10 serves as the essential reference comparator.

In Vitro Research Applications

Key Features

• ✔ C-terminal amide (-NH₂) confirmed by LC-MS per batch — the structural feature required for KISS1R binding potency; verified independently of HPLC purity which cannot detect this modification
• ✔ ≥99% purity by reverse-phase HPLC — research-grade threshold for receptor pharmacology, cell signaling, and in vitro biology applications
• ✔ Quantified KISS1R affinity (Ki ~2.33 nM human) — characterized as a high-affinity GPR54 ligand in published receptor binding assays; not inferred from biological activity observations alone
• ✔ Five distinct research domains in published literature — neuroendocrine, trophoblast motility, neuroprotection, cardiac fibroblast, and radiotheranostic applications, each supported by peer-reviewed studies
• ✔ Water-soluble — no organic co-solvent needed — dissolves directly in bacteriostatic water for standard laboratory concentrations; simplifies reconstitution protocol
• ✔ Lyophilized white powder without fillers — no excipients that could confound downstream assay results
• ✔ Independent third-party COA per batch — lot-specific documentation traceable from vial label to laboratory results; not reused across production runs
• ✔ Dual heritage: oncology + neuroendocrinology — KISS1 originally identified as metastasis suppressor in melanoma; later established as HPG axis master regulator; both research threads remain active

Research Benefits

The only endogenous high-affinity KISS1R ligand available in research-grade form. Kisspeptin-10 is the natural ligand for GPR54 — not a synthetic agonist analogue. This makes it the appropriate reference compound for any study establishing baseline receptor pharmacology, characterizing KISS1R-selective drug candidates, or building structure-activity relationships around the GPR54 binding domain. Synthetic analogues require KP-10 as the comparator; KP-10 requires no comparator.

Seven peer-reviewed publications directly supporting its research applications. Unlike many research peptides backed primarily by manufacturer descriptions or forum reports, Kisspeptin-10's research profile spans publications in Placenta, Journal of Cell Science, PLoS One, International Journal of Molecular Sciences, Scientific Reports, Genes & Diseases, and Journal of Neuroendocrinology — covering receptor pharmacology, trophoblast biology, neuronal protection, cardiac fibroblast, and radiotheranostic research respectively.

Receptor-independent mechanism opens a second research axis. The KISS1R-independent neuroprotective activity documented in SH-SY5Y models creates a research angle that does not require GPR54-expressing cell systems — expanding the compound's utility beyond receptor pharmacology into direct peptide-protein interaction research relevant to neurodegeneration biology.

A precision quality checkpoint other suppliers omit. Standard peptide quality assurance verifies purity by HPLC. Dragon Pharma additionally confirms C-terminal amidation by LC-MS — a structural feature that is invisible to chromatographic methods but is the defining characteristic of KISS1R-active kisspeptin. A non-amidated KP-10 at 99% purity is a different and inferior research compound.

Why Dragon Pharma Quality Matters for KP-10

Kisspeptin-10 presents a specific quality challenge that most research peptides do not: the C-terminal amide. This modification is not detectable by HPLC purity analysis. A batch of non-amidated YNWNSFGLRF-OH can show 99% HPLC purity while being pharmacologically inactive at KISS1R — it would fail every receptor binding assay while appearing flawless on a chromatogram.

Dragon Pharma's batch testing for Kisspeptin-10 explicitly includes:

• Reverse-phase HPLC — ≥99% purity, main peak area confirmation
• LC-MS — molecular ion confirmation at 1302.5 g/mol (average) / 1301.63 Da (monoisotopic); sequence verification; explicit C-terminal amide confirmation distinguishing YNWNSFGLRF-NH₂ from YNWNSFGLRF-OH
• Sterility and endotoxin testing — per batch
• Residual solvent screening
• Batch-specific independent COA — lot-traceable documentation from third-party laboratory

Product Summary

Dragon Pharma Kisspeptin-10 is a synthetic decapeptide (Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH₂ / KP-10 / CAS 374675-21-5) corresponding to the C-terminal 45–54 fragment of the KISS1 gene product. It is the primary endogenous ligand for KISS1R (GPR54), a Gq/11-coupled class A GPCR, with characterized binding affinity of Ki ~2.33 nM (human). Research applications span five documented domains: GPR54 pharmacology and neuroendocrine HPG axis signaling, trophoblast cell motility inhibition, KISS1R-independent neuroprotection in α-synuclein neuronal models, cardiac fibroblast collagen and FAK biology, and DOTA-conjugate radiotheranostic research. Supplied as lyophilized white powder at ≥99% HPLC purity, with LC-MS confirmation of sequence, molecular mass, and C-terminal amidation. Independent third-party COA per batch. For research use only.

Research domains: GPR54 pharmacology • Neuroendocrine signaling • Cell motility • Neuroprotection • Cardiac fibroblast • ECM biology • Radiotheranostic research