Everything below reports findings from cell cultures, isolated tissue and animals. This material is for research use only, not for human or veterinary use.
Kisspeptin-10 is a C-terminally amidated decapeptide. It is the shortest ligand that still engages KISS1R, the receptor formerly called GPR54.
Indexed papers in people exist. Those human endpoints sit outside this profile. The useful laboratory questions are identity, receptor chemistry, and what animal and cell systems actually measured.
Chemical identity
A decapeptide, amidated at the C-terminus, corresponding to residues 45 to 54 of the larger parent peptide.
| Property | Value |
|---|---|
| Sequence | Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2 |
| Common names | Kisspeptin-10, KP-10, metastin 45-54, kisspeptin 112-121 |
| Molecular formula | C63H83N17O14 |
| Molecular weight | 1302.4 |
| CAS | 374675-21-5 |
| PubChem CID | 25240297 |
| InChIKey | RITKWYDZSSQNJI-INXYWQKQSA-N |
| C-terminus | Primary amide |
| Family motif | RF-amide |
Kimera supplies the material as Kisspeptin-10.
The two numbering systems
The same molecule carries two positional names, and both appear in the literature. Metastin 45-54 numbers from the processed 54-residue peptide. Kisspeptin 112-121 numbers from the full KISS1 gene product.
Papers use them interchangeably without explanation. A search on one misses the other. That is the ordinary reason a literature review on this compound comes back thinner than it should.
The C-terminal amide is not optional
The RF-amide motif at the C-terminus defines the family and the receptor interaction. An unamidated peptide is a different compound with the same residue sequence.
That matters for verification, because the amide costs one dalton against the free acid. A synthesis that failed to amidate produces material 1 Da heavier that a low-resolution instrument will not flag.
Four of the ten residues carry liabilities. Tryptophan and tyrosine photodegrade. Two asparagines deamidate. That is a high proportion for a short peptide.
How it sits next to related ligands
| Ligand | Length | Receptor | Distinguishing fact |
|---|---|---|---|
| Kisspeptin-10 | 10 residues, amidated | KISS1R | Also numbered metastin 45-54 and kisspeptin 112-121 |
| Metastin | 54 residues | KISS1R | Parent peptide; this decapeptide is its C-terminus |
| RF9 | Small molecule | KISS1R | Second agonist, not a peptide [8] |
| Gonadorelin | Decapeptide | GnRH receptor | One step downstream of kisspeptin |
Shared receptor is not shared mass. Shared length is not shared receptor. A certificate that says “decapeptide” has not named Kisspeptin-10.
The RF-amide family is larger than this table. Cross-reactivity inside that family is why RF9 exists as a complication [8]. A method that detects an RF-amide motif has not identified this sequence.
The name records a hypothesis that turned out wrong
Kisspeptin-10 is a fossil of its own discovery, and the fossil is still in the synonym list.
Found as a metastasis suppressor
KISS1 entered the literature as a metastasis suppressor gene. Early work showed the peptide product, named metastin, suppressing motility and growth in cells transfected with its receptor [3].
That is why the compound’s PubChem synonyms still include “Human metastin 45-54” and why the CAS registry entry sits under that lineage.
Then found to run reproduction
The receptor, KISS1R and formerly GPR54, turned out to sit upstream of gonadotropin-releasing hormone. Loss-of-function mutations map to that receptor [4]. The system is now understood as central to reproductive function.
The cancer thread did not disappear. Work on KISS1 and KISS1R in metastasis continues [5]. The compound’s importance moved to a different organ system than the one it was named for.
Why this is worth knowing
Anyone reading across this literature will meet the same molecule under four names, in two fields, numbered two ways. The oncology papers and the reproductive endocrinology papers rarely cite each other.
That split has a practical cost. A search on “kisspeptin” returns the reproductive literature. A search on “metastin” returns the cancer literature. Neither returns both. A review that used only one term will look complete while missing half the field.
The two roles are not obviously connected
It would be tidy if the reproductive and metastatic functions shared a mechanism. Published work does not make that case cleanly.
Reproduction runs through hypothalamic neurons and GnRH release [6]. The cancer literature concerns cell motility and invasion in peripheral tissue [3][5]. Same receptor, very different context. The connection between them is an open question rather than a settled story.
Treat a paper that explains one role by reference to the other as making an argument, not reporting a finding.
The receptor and where it sits
KISS1R is a G-protein coupled receptor, and the neurons expressing it sit upstream of GnRH release [6].
KNDy neurons
The relevant population co-expresses kisspeptin, neurokinin B and dynorphin, and is known by the acronym KNDy. Reviews of reproductive physiology treat this population as the pulse generator for GnRH [7].
Kisspeptin-10 acts at the top of that cascade. It does not release LH directly. It drives GnRH release, which drives LH. An intact downstream network is a precondition for any response at all.
The receptor is not exclusive
At least one small molecule, RF9, acts as a KISS1R agonist both in vivo and in vitro [8]. The RF-amide family is broad, and cross-reactivity within it is a known complication rather than a curiosity.
A lot labelled Kisspeptin-10 is not the only ligand that can move that receptor. Name the ligand. Name the assay. A cAMP number on an unnamed RF-amide is not a Kisspeptin-10 result.
Neurokinin B and dynorphin sit on the same neurons [7]. Those peptides are not this decapeptide. A KNDy experiment that names only “kisspeptin” has not named the fragment length. Kisspeptin-10 is residues 45 to 54. Longer products of KISS1 are different reagents.
Pulse generation is a network property. Oride and Kanasaki treat the KNDy population as the generator [7]. A receptor agonist can report whether that network can fire. It cannot replace the other two peptides in the acronym. Keep those names on separate labels.
What a cell assay can report
A KISS1R-expressing cell line can report calcium or a Gq readout. Hori and colleagues used CHO cells transfected with the receptor [3]. That is a potency pair against the decapeptide, not a use claim.
Name the species of the receptor. Confirm the C-terminal amide on the map. A free-acid lot is a different reagent.
Gonadorelin sits one step downstream. It is GnRH itself and acts at the pituitary receptor. That write-up sits at Gonadorelin. The two peptides are not substitutes.
Indexed papers and what they do not decide
Indexed papers that mention people exist. Human endpoints from those papers sit outside the scope of this profile.
What the citations are for
Jayasena and colleagues published a dimorphism paper [1]. Chan and colleagues published a cycle-phase paper [2]. Lippincott and colleagues published an estradiol-background paper [9]. A later Chan paper asked about network integrity [10]. Shahab and colleagues published a receptor-genetics case [11]. Use them to find the record. Do not use this page as a use document.
A development programme does not turn a KISS1R decapeptide into a laboratory dosing recipe. Identity, receptor chemistry and animal systems remain the useful questions.
What a laboratory can take from the paper trail
The papers confirm that Kisspeptin-10 entered formal study under more than one name. They do not prove that a research-grade lot matches any historical programme lot. They do not replace a receptor assay.
Dhillo and colleagues mapped the neuroendocrine physiology of the ligand [4]. Joy and Chaube reviewed hypothalamic-pituitary-ovarian control [6]. Those reviews are maps. They are not dosing documents.
Animal and cell readouts
The fragment is not inert in animals. Species transfer is the part that fails.
Ovulation in the mare
Equine Kisspeptin-10 was given to Welsh pony mares by bolus and by short and long perfusion, in anestrus and at several cycle stages [12]. Gonadotropins rose reliably every time.
The rise was rapid and essentially transient, even under continuous perfusion, and ovulation was not triggered. In sheep the same approach had controlled ovulation. Species did not transfer.
The transience is the mechanism
That the response fades under continued exposure is the most practically important property in this article. A single bolus and a continuous infusion do not produce proportionally different results.
Anyone designing an experiment on the assumption that more exposure means more effect is designing against the published behaviour.
The underlying reason is structural rather than pharmacological. GnRH release is pulsatile, and the KNDy population generates that rhythm [7]. A system built to produce pulses does not respond to a flat signal the way a simple dose-response would predict.
This is well established for the downstream receptor. Continuous GnRH agonism suppresses the axis rather than stimulating it. Kisspeptin-10 sits one step above that. The mare file is consistent with a system that reads rhythm rather than level [12].
Cell motility is a different context
Hori and colleagues showed the peptide suppressing motility and growth in CHO cells that expressed the receptor [3]. That is a transfected-cell result. It is not a hypothalamic result.
Li and colleagues reviewed KISS1 and KISS1R in metastasis [5]. Same receptor, peripheral tissue. Keep the two files in separate piles.
A later reader should not have to guess which file a methods section used. Write Kisspeptin-10, write 1302.4 Da, and write the host. A paper that says “kisspeptin” without a residue range has not specified the reagent. That habit is how the 54-residue parent and this decapeptide contaminate each other in a notebook.
What this means for experimental design
Three consequences follow from the receptor chemistry, and they are unusual enough to state directly.
A ligand is not a specification
For most compounds, reporting the structure and the route describes the exposure. Here it describes only half of it. The other half is the state of the GnRH network receiving it [6][7].
An experiment that does not record sex, cycle stage and estradiol background in an intact animal has an uncontrolled variable larger than the one under study.
Non-response can be network data
In most contexts a null result invites a dose increase. Indexed papers asked that question in people [2]. Those human figures stay out. The mare file already shows that more exposure is not more effect [12].
Non-response instead says something about the preparation or the axis. That is the property a probe exploits.
Matched controls matter more than usual
Comparing two groups that differ in hormonal background will produce a difference whether or not the intervention did anything. RF9 is a second agonist at the same receptor [8]. A study that does not name the ligand has not named the experiment.
How to read a Kisspeptin-10 study
Five questions, and the first three are unusual to need at all.
Which structure was measured?
Formula C63H83N17O14, mass 1302.4, InChIKey RITKWYDZSSQNJI-INXYWQKQSA-N, C-terminal amide present. A free acid is one dalton heavier and is a different reagent.
Which numbering?
Metastin 45-54 and kisspeptin 112-121 are the same molecule. Confirm rather than assume.
Bolus or infusion?
Transience under continuous exposure is documented in the mare [12]. A flat signal is not a stronger signal.
Which species?
Sheep and horses diverged on ovulation induction under comparable protocols [12].
Was the downstream network intact?
Without functioning GnRH neurons there is no response to measure [6][7]. In a disease model this is the variable under study rather than a nuisance. Indexed papers asked that question in people [10]. Those human figures stay out.
Verifying research material
Kisspeptin-10 is a defined chemical entity with published identifiers, so verification is arithmetic rather than judgement. Batch documentation sits on the certificates of analysis page.
Identity
Formula C63H83N17O14, molecular weight 1302.4, InChIKey RITKWYDZSSQNJI-INXYWQKQSA-N. At ten residues, tandem mass spectrometry sequences the peptide readily.
The amidation check
Confirm the C-terminal amide. The free acid weighs one dalton more and is a plausible synthesis failure. The RF-amide motif is what the receptor recognises.
High-resolution mass spectrometry resolves one dalton at 1302 without difficulty. A nominal-mass instrument does not. That makes the instrument specification on a certificate worth reading.
Asparagine deamidation is the other one-dalton trap, and it runs in the opposite direction on the sequence. Two asparagines sit at positions two and four. Deamidation converts each to aspartate, adding one dalton per event.
So a sample reading 1303 has two plausible explanations: a failed amidation, or a deamidated asparagine. They are different defects with different causes. Mass alone cannot separate them. Peptide mapping locates which residue changed.
Why the sequence is worth reading before ordering
Four of the ten residues carry liabilities. Tryptophan and tyrosine photodegrade. The two asparagines deamidate. That is a high proportion for a short peptide.
None of it makes the compound difficult to work with. It does mean a vial that has sat reconstituted for a month is not the same material as a fresh one. A purity figure from the date of manufacture says little about the state on the bench.
Handling
Tryptophan at position three and tyrosine at position one both absorb ultraviolet light and photodegrade, the same liability that affects the melanocortin peptides. Arginine and asparagine add deamidation routes.
Store the lyophilised powder cold, dry and dark, and reconstitute close to the point of use.
Storage guidance is a house recommendation. Analytical documentation is per-lot release testing.
Compare with the shorter Gonadorelin, which acts one step downstream at the GnRH receptor and carries its own stability profile.
A second handling question is the counterion. Trifluoroacetate from cleavage cocktails is common on research peptides. That salt changes both the mass of the weighed vial and the peptide content. Name it on the certificate.
At ten residues a tryptic map is almost empty. Full tandem mass spectrometry of the intact ion is the sequence check. Cover every residue. A deletion of asparagine or phenylalanine is easy to miss inside a broad chromatographic peak.
Reversed-phase chromatography with mass detection finds those deletions. Ultraviolet detection alone often does not. Tryptophan and tyrosine give a strong UV signal. That signal does not prove the amide is present.
Peptide content differs from chromatographic purity. Lyophilised material carries counterions and water. A vial labelled by weight holds less peptide than that. Acetate or trifluoroacetate content belongs on the certificate.
Freeze-thaw cycling drives aggregation in short peptides as well as long ones. Aliquot on reconstitution. Do not sample one vial repeatedly.
A later reader should be able to match the Kisspeptin-10 lot to the notebook without asking what was in the vial. Intact mass, amide state, and a mapped spectrum are the three lines that make that possible.
Common questions about Kisspeptin-10
Identity and naming
Is Kisspeptin-10 the same as metastin? It is the C-terminal decapeptide of it. Metastin is the 54-residue peptide. This is residues 45 to 54, also numbered 112 to 121 from the full gene product.
Why is it named after metastasis? KISS1 was characterised first as a metastasis suppressor gene, and early work showed the peptide suppressing cell motility and growth [3]. Its reproductive role was established later.
What is GPR54? The former name for KISS1R, its receptor. Older papers use it.
Effects and evidence
Does this page report human outcomes? No. Indexed papers are listed so they can be found. This profile stops at chemistry, receptor logic and animal systems.
Does it induce ovulation? Not in mares, despite reliably raising gonadotropins [12]. It did in sheep, so the result is species-dependent.
Does more exposure give more effect? Not in the mare file. Gonadotropin rises were transient even under continuous perfusion [12].
Why would a pulse generator ignore a constant signal? Because GnRH release is rhythmic and the KNDy population produces that rhythm [7]. Systems built on pulses respond to pattern, not level.
Is RF9 the same ligand? No. RF9 is a small-molecule KISS1R agonist [8]. Shared receptor is not shared structure.
Handling and verification
What is the main identity risk? A missing C-terminal amide. The free acid is one dalton heavier and needs high-resolution mass spectrometry to catch.
Why does it photodegrade? Tryptophan at position three and tyrosine at position one both absorb ultraviolet light. Asparagine and arginine add deamidation routes.
Is it related to Gonadorelin? They act one step apart. Kisspeptin-10 drives GnRH release. Gonadorelin is GnRH and acts at the pituitary receptor below it.
Summary of the evidence
Write the name, the mass and the amide on the first line of a notebook page. Kisspeptin-10 is C63H83N17O14, 1302.4 Da, amidated RF-amide, agonist at KISS1R.
Identity: ten residues, two numbering systems, one amide. A certificate that omits intact mass is not finished.
Receptor: KNDy neurons sit upstream of GnRH [6][7]. RF9 is a second agonist at the same receptor [8]. Transfected CHO cells report motility suppression [3].
Animal file: mares raise gonadotropins without ovulation under bolus or perfusion [12]. Sheep diverged on that endpoint.
Indexed papers that mention people remain in the list so a reader can find them. Human endpoints stay out.
The rest of this class sits in the endocrine category.
Status: supplied for laboratory research use only.
References
- Jayasena CN, Nijher GM, Comninos AN, Abbara A, Januszewki A, Vaal ML, Sriskandarajah L, Murphy KG, et al.. The effects of kisspeptin-10 on reproductive hormone release show sexual dimorphism in humans. J Clin Endocrinol Metab. 2011;96(12):E1963-72. PMID 21976724. DOI
- Chan YM, Butler JP, Sidhoum VF, Pinnell NE, Seminara SB. Kisspeptin administration to women: a window into endogenous kisspeptin secretion and GnRH responsiveness across the menstrual cycle. J Clin Endocrinol Metab. 2012;97(8):E1458-67. PMID 22577171. DOI
- Hori A, Honda S, Asada M, Ohtaki T, Oda K, Watanabe T, Shintani Y, Yamada T, et al.. Metastin suppresses the motility and growth of CHO cells transfected with its receptor. Biochem Biophys Res Commun. 2001;286(5):958-63. PMID 11527393. DOI
- Dhillo WS, Murphy KG, Bloom SR. The neuroendocrine physiology of kisspeptin in the human. Rev Endocr Metab Disord. 2007;8(1):41-6. PMID 17323132. DOI
- Li Z, Liu J, Inuzuka H, Wei W. Functional analysis of the emerging roles for the KISS1/KISS1R signaling pathway in cancer metastasis. J Genet Genomics. 2022;49(3):181-184. PMID 34767970. DOI
- Joy KP, Chaube R. Kisspeptin control of hypothalamus-pituitary-ovarian functions. Vitam Horm. 2025;127:153-206. PMID 39864941. DOI
- Oride A, Kanasaki H. The role of KNDy neurons in human reproductive health. Endocr J. 2024;71(8):733-743. PMID 38866494. DOI
- Min L, Leon S, Li H, Pinilla L, Carroll RS, Tena-Sempere M, Kaiser UB. RF9 Acts as a KISS1R Agonist In Vivo and In Vitro. Endocrinology. 2015;156(12):4639-48. PMID 26418326. DOI
- Lippincott MF, Chan YM, Rivera Morales D, Seminara SB. Continuous Kisspeptin Administration in Postmenopausal Women: Impact of Estradiol on Luteinizing Hormone Secretion. J Clin Endocrinol Metab. 2017;102(6):2091-2099. PMID 28368443. DOI
- Chan YM, Lippincott MF, Butler JP, Sidhoum VF, Li CX, Plummer L, Seminara SB. Exogenous kisspeptin administration as a probe of GnRH neuronal function in patients with idiopathic hypogonadotropic hypogonadism. J Clin Endocrinol Metab. 2014;99(12):E2762-71. PMID 25226293. DOI
- Shahab M, Lippincott M, Chan YM, Davies A, Merino PM, Plummer L, Mericq V, Seminara S. Discordance in the Dependence on Kisspeptin Signaling in Mini Puberty vs Adolescent Puberty: Human Genetic Evidence. J Clin Endocrinol Metab. 2018;103(4):1273-1276. PMID 29452377. DOI
- Decourt C, Caraty A, Briant C, Guillaume D, Lomet D, Chesneau D, Lardic L, Duchamp G, et al.. Acute injection and chronic perfusion of kisspeptin elicit gonadotropins release but fail to trigger ovulation in the mare. Biol Reprod. 2014;90(2):36. PMID 24429215. DOI
Kisspeptin-10 is sold for laboratory research use only. Not for human consumption, nor medical, veterinary, or household uses.
