Kisspeptin

Dragon Pharma Kisspeptin-10 Peptide

Dragon Pharma Kisspeptin-10 is a research-grade synthetic decapeptide corresponding to the C-terminal 45–54 fragment of the KISS1 gene product. Carrying the sequence Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH₂ with a defining C-terminal amide characteristic of the kisspeptin RFamide family, Kisspeptin-10 is the shortest member of the kisspeptin peptide family that retains full binding activity at its cognate receptor KISS1R — also designated GPR54.

The compound has been characterized in laboratory research spanning neuroendocrine signaling, hypothalamic-pituitary-gonadal (HPG) axis regulation, cell motility inhibition, extracellular matrix biology, neuronal protection models, and cardiac fibroblast studies. Its established role as the primary endogenous ligand for KISS1R makes it a well-validated tool compound for GPR54 pharmacology and receptor signaling research across a broad range of in vitro applications.

Dragon Pharma Kisspeptin-10 is supplied as a lyophilized powder verified at ≥99% purity by HPLC, with LC-MS molecular identity confirmation and C-terminal amidation verification. Every batch ships with an independent third-party Certificate of Analysis. For research use only.

Compound Specifications

Molecular Biology and Receptor Background

Kisspeptin-10 is the C-terminal decapeptide fragment of the KISS1 gene product — the shortest naturally occurring kisspeptin family member that retains complete binding affinity at KISS1R (GPR54). The kisspeptin family includes four processed peptide products: kisspeptin-54, kisspeptin-14, kisspeptin-13, and kisspeptin-10. All four share the same C-terminal decapeptide sequence, with kisspeptin-10 representing the biologically active core unit that defines receptor interaction across the entire family.

KISS1R (GPR54) is a class A Gq/11-coupled G protein-coupled receptor located at chromosome 19p13.3. Upon binding kisspeptin-10, KISS1R activates phospholipase C (PLC) via Gq/11, generating inositol trisphosphate (IP3) and diacylglycerol (DAG). This initiates intracellular calcium mobilization, protein kinase C activation, and downstream ERK1/2 phosphorylation cascades. Binding assays using CHO-KISS1R membrane preparations have characterized Ki values of approximately 1.59 nM (rat) and 2.33 nM (human KISS1R), with EC50 approximately 1.0 nM in CHO-GPR54 IP accumulation assays.

The KISS1 gene was originally identified as a metastasis suppressor in melanoma research — the product name KiSS-1 reflects its discovery context as a "Kisspeptin Suppressor Sequence" — before the central role of KISS1R in reproductive endocrinology was established through loss-of-function genetic studies in the mid-2000s. This dual research heritage — metastasis biology and neuroendocrine regulation — defines the breadth of laboratory applications for which KP-10 serves as a tool compound.

The C-terminal amide (-NH₂) modification is an essential structural feature. It defines Kisspeptin-10 as a member of the RFamide neuropeptide superfamily and is required for KISS1R binding potency. Dragon Pharma's LC-MS verification specifically confirms C-terminal amidation alongside sequence identity and molecular mass — a critical quality checkpoint that distinguishes the correctly modified research-grade compound from synthesis artefacts lacking the amide terminus.

Mechanism of Action

KISS1R Activation and Gq/11 Signaling Cascade

Kisspeptin-10 binds KISS1R with sub-nanomolar to low-nanomolar affinity, triggering a well-characterized intracellular signaling cascade. Receptor activation mobilizes Gq/11, which stimulates phospholipase C to generate IP3 and DAG from membrane phosphoinositide substrates. IP3 triggers endoplasmic reticulum calcium release, producing a rapid intracellular Ca²⁺ surge. DAG activates protein kinase C, which phosphorylates downstream effectors including ERK1/2. The complete cascade — from receptor binding through ERK1/2 activation — provides multiple quantifiable research endpoints: IP1 accumulation (HTRF assay), Ca²⁺ flux (fluorometric), ERK1/2 phosphorylation (Western blot/ELISA), and β-arrestin recruitment assays.

Neuroendocrine Signaling and HPG Axis Regulation

In hypothalamic research models, KISS1R activation by KP-10 stimulates GnRH (gonadotropin-releasing hormone) release from KNDy neurons (co-expressing kisspeptin, neurokinin B, and dynorphin). This positions kisspeptin-10 at the apex of the hypothalamic-pituitary-gonadal (HPG) axis — the master regulatory cascade governing gonadotropin secretion. GnRH release drives pituitary LH (luteinizing hormone) and FSH (follicle-stimulating hormone) secretion, which in turn regulate gonadal steroid and gametogenesis biology downstream.

Cell Motility Inhibition

Independent of its neuroendocrine role, kisspeptin-10 has been characterized as an inhibitor of cell migration in placental and trophoblast cell models. In HTR8/SVneo cells, KP-10 reduced migration through an ERK1/2-p90rsk-GSK3β-FAK signaling feedback loop (Roseweir et al., 2012). In first-trimester trophoblast cultures, KP-10 raised intracellular calcium and inhibited cell motility without altering proliferation rates (Bilban et al., 2004) — consistent with a signaling-specific rather than cytotoxic mechanism of action.

KISS1R-Independent Neuroprotective Activity

A distinct and mechanistically significant finding is KP-10's documented neuroprotective activity in SH-SY5Y-derived cholinergic neurons via a pathway that operates independently of KISS1R. Simon et al. (2023) demonstrated that in neurons overexpressing wild-type or E46K mutant α-synuclein, kisspeptin-10 reduced apoptosis and mitochondrial depolarization through receptor-independent means. This finding opens a research avenue for investigating direct peptide-protein interactions that bypass GPR54 signaling entirely — mechanistically distinct from all other characterized KP-10 activities.

Cardiac Fibroblast and Extracellular Matrix Interactions

Radwańska et al. (2023) demonstrated that kisspeptin-10 increases intracellular collagen content in cardiac fibroblast cultures through focal adhesion kinase (FAK) phosphorylation, alongside shifts in matrix metalloproteinase and tissue inhibitor expression. This extends the documented biology of KP-10 beyond neuroendocrine and reproductive contexts into cardiovascular connective tissue research.

Research Applications

Kisspeptin Family: Understanding KP-10 in Context

Kisspeptin-10 is the shortest and most widely used member of a peptide family that all derive from the same KISS1 gene product but differ in chain length. All family members share the same C-terminal decapeptide sequence.

For most in vitro research applications, Kisspeptin-10 is the preferred tool compound. Its smaller size simplifies synthesis, reduces production cost, and enables precise structure-activity studies. Receptor binding potency is equivalent to longer family members since the C-terminal decapeptide is the receptor interaction domain for the entire family.

Quality Assurance

Kisspeptin-10's C-terminal amide is not a cosmetic modification — it is a structural requirement for KISS1R binding potency and defines membership in the RFamide neuropeptide family. Standard HPLC purity analysis cannot distinguish between correctly amidated and non-amidated peptide, since both may show equivalent chromatographic purity. Dragon Pharma addresses this through LC-MS verification that explicitly confirms C-terminal amidation alongside sequence identity and 1302.5 g/mol molecular mass — providing complete chemical characterization per batch.

• HPLC purity — ≥99% confirmed; reverse-phase chromatographic purity analysis
• LC-MS identity — sequence confirmation (YNWNSFGLRF-NH₂), molecular mass (1302.5 g/mol / monoisotopic 1301.63 Da), and C-terminal amidation verification
• Sterility and endotoxin screening — per batch specification
• Residual solvent screening — confirms clean synthesis
• Independent third-party COA per batch — traceable from vial label lot number to laboratory documentation; not reused across production runs

Storage and Handling

Lyophilized powder (unreconstituted): Store at -20°C, protected from light and moisture. Stable for 24 months or longer under these conditions. No cold chain required during standard domestic shipping as a lyophilized powder. Allow vial to equilibrate to room temperature before opening to prevent condensation.

Reconstituted solution: Store at 2–8°C (refrigerated). Use within 28–30 days. Avoid repeated freeze-thaw cycles, which compromise peptide integrity and assay reproducibility.

Reconstitution: Bacteriostatic water is the standard diluent. Introduce diluent slowly against the inner vial wall rather than directly into the lyophilized powder. Swirl gently until fully dissolved — do not shake or vortex. Maintain aseptic handling throughout. The decapeptide is water-soluble and dissolves readily at standard laboratory concentrations.

For research use only. Not for human consumption, veterinary use, or therapeutic application.

Key Features

• ✔ C-terminal amide verified by LC-MS — essential structural feature for KISS1R binding confirmed by mass spectrometry; not inferred from synthesis records alone
• ✔ ≥99% HPLC purity — highest research-grade threshold; suitable for receptor binding assays, cell signaling studies, and in vitro pharmacology
• ✔ Sub-nanomolar to low-nanomolar KISS1R affinity documented — Ki ~2.33 nM (human) characterizing it as a high-affinity GPR54 research ligand
• ✔ Multiple distinct research axes — neuroendocrine, cell motility, neuroprotection, cardiac fibroblast, and radiotheranostic applications documented in peer-reviewed literature
• ✔ Seven peer-reviewed references — more published research context than most decapeptides in the research market
• ✔ Lyophilized format — no fillers — maximum stability and assay compatibility; no excipients that could confound downstream experimental results
• ✔ Water-soluble — dissolves readily in bacteriostatic water; no organic co-solvent requirement for standard laboratory concentrations
• ✔ Batch-specific independent COA — per-lot documentation from third-party laboratory; not generic or reused

Frequently Asked Questions About Dragon Pharma Kisspeptin-10

Scientific References

The information presented on this page draws from published peer-reviewed scientific literature investigating Kisspeptin-10 and the KiSS-1/GPR54 system in laboratory and preclinical research settings. The following references document the specific research findings described above.

1. Zhu N, Zhao M, Song Y, Ding L, Ni Y. (2020). The KiSS-1/GPR54 system: Essential roles in physiological homeostasis and cancer biology. Genes & Diseases, 9(1), 28–40. https://doi.org/10.1016/j.gendis.2020.07.008
2. Kleynhans J, Reeve R, Driver CHS, Marjanovic-Painter B, Sathekge M, Zeevaart JR, Ebenhan T, Millar RP. (2025). Synthesis and characterisation of DOTA-kisspeptin-10 as a potential gallium-68/lutetium-177 pan-tumour radiopharmaceutical. Journal of Neuroendocrinology, 37(3), e13487. https://doi.org/10.1111/jne.13487
3. Roseweir AK, Katz AA, Millar RP. (2012). Kisspeptin-10 inhibits cell migration in vitro via a receptor-GSK3 beta-FAK feedback loop in HTR8SVneo cells. Placenta, 33(5), 408–415. https://doi.org/10.1016/j.placenta.2012.02.001
4. Bilban M, Ghaffari-Tabrizi N, Hintermann E, et al. (2004). Kisspeptin-10, a KiSS-1/metastin-derived decapeptide, is a physiological invasion inhibitor of primary human trophoblasts. Journal of Cell Science, 117(Pt 8), 1319–1328. https://doi.org/10.1242/jcs.00971
5. Francis VA, Abera AB, Matjila M, Millar RP, Katz AA. (2014). Kisspeptin regulation of genes involved in cell invasion and angiogenesis in first trimester human trophoblast cells. PLoS One, 9(6), e99680. https://doi.org/10.1371/journal.pone.0099680
6. Simon C, Soga T, Parhar I. (2023). Kisspeptin-10 Mitigates α-Synuclein-Mediated Mitochondrial Apoptosis in SH-SY5Y-Derived Neurons via a Kisspeptin Receptor-Independent Manner. International Journal of Molecular Sciences, 24(7), 6056. https://doi.org/10.3390/ijms24076056
7. Radwańska P, Gałdyszyńska M, Piera L, Drobnik J. (2023). Kisspeptin-10 increases collagen content in the myocardium by focal adhesion kinase activity. Scientific Reports, 13(1), 19977. https://doi.org/10.1038/s41598-023-47224-3

Dragon Pharma supplies Kisspeptin-10 exclusively for laboratory research purposes.