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Kisspeptin-10 — GPR54 (KISS1R) Agonist | Decapeptide GnRH Pulse-Generator Research Compound

Research-Grade Compound

Kisspeptin-10 (KP-10) is the 10-amino-acid C-terminal fragment of kisspeptin, the peptide product of the KISS1 gene, and acts as an agonist at GPR54 — the G protein-coupled receptor also designated KISS1R. Sequence: Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2 (YNWNSFGLRF-NH2). Molecular formula C63H83N17O14, molecular weight 1,302.5 Da, CAS 374675-21-5.

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Certificate Details

Purity≥99%

Methodology

HPLCLC-MS/MS

CAS Number374675-21-5

Molecular FormulaC63H83N17O14

Molecular Weight1302.5 g/mol

SequenceTyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2 (decapeptide, KP-10)

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This Certificate of Analysis was issued by an independent third-party laboratory. Peptide.Express does not conduct in-house testing. Results are provided as-is from the testing facility and confirm batch identity, purity, and analytical methodology. For questions about specific CoA results, contact [email protected].

≥99% by HPLCLC-MS/MS VerifiedCoA Every BatchIn-Vitro Research Use Only

What is Kisspeptin-10?

The compound has two research literatures that barely speak to each other. KISS1 was first characterised as a metastasis-suppressor gene in melanoma cells, and its product was named metastin on that basis. The reproductive function arrived later and from a different direction entirely — loss-of-function mutations in GPR54 were linked to hypogonadotropic hypogonadism, which established the receptor as the gate on the hypothalamic-pituitary-gonadal axis. One gene, one receptor, two fields that still cite each other sparingly.

Kisspeptin circulates as several processed forms — kisspeptin-54, -14, -13 and -10 — all sharing the same C-terminal decapeptide and the RF-amide terminus that the receptor recognises. KP-10 is the shortest form retaining full receptor activity, which is why it became the standard tool compound rather than the full-length peptide. The C-terminal amide is not optional: remove it and receptor binding falls off sharply.

How Does Kisspeptin-10 Work? Mechanism of Action

GPR54 couples to Gq/11 rather than Gs, which sets kisspeptin apart from most of the neuroendocrine compounds in this catalog. Receptor activation engages phospholipase C beta, which hydrolyses PIP2 into inositol trisphosphate and diacylglycerol. IP3 releases calcium from intracellular stores; DAG activates protein kinase C. The calcium transient, together with membrane depolarisation, drives vesicular GnRH release from the neuron.

That GnRH enters the hypophyseal portal circulation and acts on pituitary gonadotrophs, which secrete luteinising hormone and follicle-stimulating hormone. LH and FSH then drive gonadal steroidogenesis and gametogenesis. Kisspeptin sits one step upstream of the entire cascade — which is precisely why it is described as the gate on the HPG axis rather than one input among several.

The neuroanatomy carries most of the interesting detail. In the arcuate nucleus, kisspeptin neurons co-express neurokinin B and dynorphin — the KNDy population — and this group is the leading candidate for the GnRH pulse generator itself, with neurokinin B providing the excitatory drive and dynorphin the inhibitory brake that together set pulse frequency. A second population in the anteroventral periventricular nucleus is associated with the preovulatory surge in rodents. Human hypothalamic anatomy does not map cleanly onto the rodent nuclei, and translating between the two is an active methodological problem rather than a solved one.

One practical caution for study design: GPR54 desensitises under continuous agonist exposure. Bolus administration and constant infusion of the same compound can produce opposite readouts on LH output, because sustained receptor occupancy downregulates the very signalling the experiment is trying to measure. Protocols reporting a kisspeptin effect on gonadotropin secretion without specifying the exposure pattern are underspecified.

Research Applications of Kisspeptin-10

HPG Axis and Gonadotropin Regulation

LH pulse frequency studies: kisspeptin administration is the standard way to probe pulse generator output in reproductive neuroendocrinology models.
GnRH neuron electrophysiology: patch-clamp recording of depolarisation and firing rate after GPR54 activation links receptor signalling directly to neuronal output.
Gonadotroph responsiveness: separating hypothalamic from pituitary contributions requires a design that stimulates upstream with kisspeptin and downstream with GnRH in the same preparation.

GPR54 Receptor Pharmacology

Gq/11-PLC-IP3 calcium mobilisation assays: intracellular calcium flux in KISS1R-expressing cell lines is the direct in-vitro readout of receptor activation.
Desensitisation kinetics: continuous versus pulsatile exposure produces divergent receptor behaviour, and characterising that divergence is a research question in its own right.
Fragment structure-activity work: comparing KP-10 against longer processed forms and against C-terminally modified analogs isolates the contribution of the RF-amide terminus.

KISS1 Metastasis-Suppressor Research

Cell migration and invasion assays: the original KISS1 phenotype was suppression of metastatic behaviour in melanoma lines, and transwell migration remains the standard endpoint.
Matrix metalloproteinase regulation: MMP-9 downregulation is among the more consistently reported downstream effects in the oncology literature.
Cross-literature reconciliation: the reproductive and metastasis-suppression fields describe the same receptor with little overlap in method or model, which is itself worth noting when designing studies that draw on both.

Kisspeptin-10 vs Kisspeptin-54

Feature	Kisspeptin-10 (KP-10)	Kisspeptin-54 (metastin)
Identity	C-terminal decapeptide fragment	Full-length processed KISS1 gene product
Amino acid count	10	54
Sequence	YNWNSFGLRF-NH2	Contains the same C-terminal decapeptide
Receptor	GPR54 / KISS1R	GPR54 / KISS1R
Receptor-binding element	C-terminal RF-amide	Same C-terminal RF-amide
Reported plasma persistence	Shorter — cleared rapidly	Longer-lasting in circulation
Typical research use	Acute pulse and receptor-activation studies	Sustained-exposure and longer-duration designs
Molecular weight	1,302.5 Da (LC-MS/MS confirmed)	Substantially larger — verify against supplier CoA
Peptide.Express availability	Supplied as lyophilized powder	Not currently supplied

Both forms hit the same receptor through the same RF-amide terminus, so the choice between them is a pharmacokinetic decision rather than a pharmacological one. KP-10 is cleared faster, which makes it the better fit for acute pulse work and the worse fit for anything requiring sustained receptor occupancy — and since GPR54 desensitises under sustained occupancy, that trade-off is not simply a matter of dosing frequency.

Kisspeptin-10 Technical Specifications

Technical specifications for Kisspeptin-10, including molecular data, purity standard, testing methods and storage requirements.
Compound Name	Kisspeptin-10 (KP-10)
Common Synonyms	Kisspeptin 10, Kiss-10, KP-10, metastin fragment 45-54
Classification	RF-amide decapeptide, GPR54 (KISS1R) agonist
Gene of Origin	KISS1
Receptor Target	GPR54, also designated KISS1R
Receptor Coupling	Gq/11 — phospholipase C, IP3, intracellular calcium release
Amino Acid Sequence	Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2 (YNWNSFGLRF-NH2)
Amino Acid Count	10 (decapeptide)
C-Terminus	Amidated — required for receptor binding
CAS Number	374675-21-5
Molecular Formula	C63H83N17O14
Molecular Weight	1,302.5 Da
Purity	≥99% by HPLC
Purity Confirmation	LC-MS/MS molecular weight verification
Endotoxin Testing	LAL (Limulus Amebocyte Lysate) method
Physical Form	Lyophilized powder
Appearance	White to off-white powder
Reconstitution	Bacteriostatic water or sterile 0.9% sodium chloride
Storage (lyophilized)	-20°C, desiccated, protected from light
Storage (reconstituted)	2–8°C, use within 14–28 days
Shelf Life	24 months from manufacture (lyophilized)
Testing Methods	HPLC, LC-MS/MS, LAL Endotoxin
Documentation	Certificate of Analysis (CoA) per batch
FDA Status	Not approved for human use
Intended Use	In-vitro laboratory research only

How to Reconstitute Kisspeptin-10 for Research

Kisspeptin-10 contains tryptophan at position 3, and tryptophan-containing peptides are more light-sensitive than most. Keep the reconstituted vial protected from light rather than leaving it on an open bench between draws.

Bring the vial to room temperature before opening.
Draw the calculated volume of bacteriostatic water. For a 5 mg vial, 2.5 mL yields 2 mg/mL and 1 mL yields 5 mg/mL.
Swab the septum with alcohol and allow 30 seconds to dry.
Inject the diluent slowly down the inner vial wall rather than onto the lyophilized cake.
Swirl gently for 60–90 seconds until fully dissolved. Do not shake or vortex.
Confirm the solution is clear and colorless with no visible particulate matter.
Label with the reconstitution date and concentration, and return the vial to light-protected refrigerated storage promptly.
Store at 2–8°C and use within 14–28 days. Avoid repeated freeze-thaw cycles.

Diluent: bacteriostatic water for peptide reconstitution. Full protocol: step-by-step peptide reconstitution guide. Concentration maths: peptide reconstitution calculator.

Frequently Asked Questions — Kisspeptin-10

What is kisspeptin?

Kisspeptin is the peptide product of the KISS1 gene and the endogenous agonist at GPR54 (KISS1R), a G protein-coupled receptor expressed on hypothalamic GnRH neurons. Kisspeptin-10 is the 10-residue C-terminal fragment — sequence YNWNSFGLRF-NH2, 1,302.5 Da — and is the form most commonly used as a research tool compound.

What receptor does kisspeptin activate, and how?

GPR54, also written KISS1R. It is Gq/11-coupled, so activation runs through phospholipase C beta, PIP2 hydrolysis, IP3-mediated calcium release and PKC activation rather than through the cAMP pathway used by most peptide hormone receptors in this catalog.

What is the role of kisspeptin in GnRH regulation?

Kisspeptin sits directly upstream of GnRH. GPR54 activation on hypothalamic GnRH neurons produces a calcium transient and depolarisation, which triggers GnRH exocytosis into the hypophyseal portal circulation. GnRH then drives LH and FSH release from pituitary gonadotrophs. Without kisspeptin signalling the axis does not start — which is why GPR54 loss-of-function mutations produce hypogonadotropic hypogonadism.

What is the HPG axis?

The hypothalamic-pituitary-gonadal axis: hypothalamic GnRH drives pituitary LH and FSH, which drive gonadal steroid production and gametogenesis, and the gonadal steroids feed back on the hypothalamus and pituitary to close the loop. Kisspeptin neurons act as the entry point to that circuit and also relay the steroid feedback signal back into it.

What are KNDy neurons?

A population in the arcuate nucleus that co-expresses kisspeptin, neurokinin B and dynorphin — hence the acronym. Current models treat this group as the GnRH pulse generator, with neurokinin B supplying excitatory drive and dynorphin the inhibitory brake, the two together setting pulse frequency. The model is well supported in rodents and sheep; the mapping onto human hypothalamic anatomy is less settled.

What is the difference between kisspeptin-10 and kisspeptin-54?

Length and clearance, not receptor target. Both act on GPR54 through the same C-terminal RF-amide, and kisspeptin-10 is contained within kisspeptin-54. KP-10 is cleared from circulation faster, which suits acute pulse studies; KP-54 persists longer, which suits sustained-exposure designs. Because GPR54 desensitises under continuous occupancy, the two can give genuinely different readouts on gonadotropin output in the same model.

Is kisspeptin related to the KISS1 metastasis suppressor gene?

It is the product of that gene. KISS1 was identified as a metastasis suppressor in melanoma cells before the reproductive function was known, and the peptide was originally named metastin for that reason. Both literatures are active; they overlap less than one might expect.

Can kisspeptin-10 be used in LH pulse research?

It is one of the standard tools for it. The design point that matters most is exposure pattern — bolus and continuous-infusion protocols probe different receptor states, because GPR54 desensitises under sustained agonist occupancy. Any protocol reporting an LH effect should specify which pattern was used.

Why does kisspeptin-10 need an amidated C-terminus?

Because the RF-amide motif is what GPR54 recognises. The free-acid form binds far more weakly, so the amide is a structural requirement rather than a manufacturing convention. Verify the amidation on the Certificate of Analysis if a batch produces unexpectedly weak receptor activation.

What purity standard and testing does Peptide.Express apply to Kisspeptin-10?

≥99% by reverse-phase HPLC, LC-MS/MS confirming the 1,302.5 Da mass, LAL endotoxin testing, and visual QC — all through an independent third-party laboratory, with a batch-specific Certificate of Analysis issued per lot.

How should Kisspeptin-10 be stored before and after reconstitution?

Lyophilized: -20°C, desiccated and protected from light, stable for 24 months. Reconstituted: 2–8°C, used within 14–28 days, kept away from light because of the tryptophan residue. Do not freeze reconstituted solution.

Where is the Certificate of Analysis for Kisspeptin-10?

On this page and in the Peptide.Express lab results library, indexed by batch number, listing HPLC purity, mass confirmation, endotoxin result, testing laboratory and test date.

Research References

Han SK, Gottsch ML, Lee KJ, Popa SM, Smith JT, Jakawich SK, Clifton DK, Steiner RA, Herbison AE. Activation of gonadotropin-releasing hormone neurons by kisspeptin as a neuroendocrine switch for the onset of puberty. J Neurosci. 2005. Read Han et al. on kisspeptin-evoked depolarization of GnRH neurons
de Roux N, Genin E, Carel JC, Matsuda F, Chaussain JL, Milgrom E. Hypogonadotropic hypogonadism due to loss of function of the KiSS1-derived peptide receptor GPR54. Proc Natl Acad Sci U S A. 2003. Read de Roux et al.'s identification of GPR54 loss-of-function hypogonadotropic hypogonadism
Lee JH, Miele ME, Hicks DJ, Phillips KK, Trent JM, Weissman BE, Welch DR. KiSS-1, a novel human malignant melanoma metastasis-suppressor gene. J Natl Cancer Inst. 1996. Read Lee et al.'s identification of KiSS-1 as a melanoma metastasis suppressor

All products are sold for in-vitro laboratory research use only. Not intended for human consumption, clinical use, or veterinary use. Peptide.Express makes no medical claims. Consult the published literature for research application guidance.