# Kisspeptin-10

> Kisspeptin-10 is a ten-amino-acid amidated peptide that forms the C-terminal end of kisspeptin, the hypothalamic hormone encoded by the KISS1 gene. Also called KP-10 or metastin 45-54, it activates the KISS1R (GPR54) receptor on gonadotropin-releasing hormone neurons and is studied as a research tool for the reproductive axis, puberty and anti-doping analysis.

Canonical: https://peptideproperties.com/compounds/kisspeptin-10/

## Identity

- **Class:** Reproductive & HPG-Axis Compounds
- **Also known as:** Metastin 45-54, KP-10
- **Molecular formula:** C63H83N17O14
- **Molecular weight:** 1302.4 g/mol
- **Monoisotopic mass:** 1301.6305 Da
- **CAS number:** 374675-21-5
- **PubChem CID:** 25240297
- **InChIKey:** RITKWYDZSSQNJI-INXYWQKQSA-N
- **Sequence:** YNWNSFGLRF
- **Sequence notes:** C-terminal amide (Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe-NH2); the PubChem formula C63H83N17O14 matches this sequence with an amidated C-terminus.

## Key facts

- Class: kisspeptin peptide, an agonist of the KISS1R (GPR54) receptor
- Length: 10 residues (YNWNSFGLRF) with a C-terminal amide
- Origin: residues 45-54 of human kisspeptin-54 (metastin), encoded by the KISS1 gene
- Formula C63H83N17O14; molecular weight 1302.4 g/mol (PubChem CID 25240297)
- CAS number 374675-21-5; also known as KP-10 and metastin 45-54
- Not approved by the FDA for any medical use
- Listed on the 2024 World Anti-Doping Agency Prohibited List

## What Is Kisspeptin-10?

Kisspeptin-10 is the ten-residue C-terminal fragment of kisspeptin, a peptide hormone encoded by the KISS1 gene that is now recognized as a key orchestrator of the reproductive axis.[1] It corresponds to residues 45-54 of the longer kisspeptin-54, also called metastin, and is often abbreviated KP-10.Kisspeptins bind their cognate receptor, KISS1R (also called GPR54), on gonadotropin-releasing hormone (GnRH) neurons and stimulate their activity. This provides an obligatory signal for GnRH secretion and so gates the downstream hormonal events that support reproduction.[2]Kisspeptin-10 itself has been described as capable of increasing circulating follicle-stimulating hormone (FSH), luteinizing hormone (LH) and testosterone in humans. That profile has drawn interest in infertility research and also led to its inclusion on the 2024 World Anti-Doping Agency (WADA) Prohibited List.[3]The sections below cover its chemical identity, the mechanisms studied for kisspeptin signaling, and the published findings that address kisspeptin-10 by name.

## Chemical Structure and Molecular Identity

Kisspeptin-10 is a linear decapeptide with the sequence Tyr-Asn-Trp-Asn-Ser-Phe-Gly-Leu-Arg-Phe and an amidated C-terminus (YNWNSFGLRF-NH2). PubChem lists the human form under CID 25240297 with the molecular formula C63H83N17O14 and a molecular weight of 1302.4 g/mol, which corresponds exactly to these ten residues with a C-terminal amide.All ten residues are standard L-amino acids, and the only modification is the terminal phenylalaninamide. The C-terminal Arg-Phe-amide ending places kisspeptin-10 among the RFamide peptides, the neuropeptide family defined by that motif.
### Key identifiers

- CAS number: 374675-21-5
- InChIKey: RITKWYDZSSQNJI-INXYWQKQSA-N
- Synonyms: KP-10, metastin 45-54, human kisspeptin-10Stability is a practical analytical concern. While developing a urine test, one research group observed a degradation product that was probably caused by oxidation of the tryptophan residue into kynurenine, and noted that the kinetics of this reaction still need to be characterized.[3]
### Comparison with GnRH decapeptides
Kisspeptin-10 is often discussed alongside the GnRH decapeptides because all three are ten residues long and act on the same axis, but their structures and targets differ.PeptideFormulaMW (g/mol)ReceptorTerminal groupsKisspeptin-10C63H83N17O141302.4KISS1R (GPR54)Free N-terminus; C-terminal amideGonadorelinC55H75N17O131182.3GnRH receptorPyroglutamate; C-terminal glycinamideTriptorelinC64H82N18O131311.4GnRH receptorPyroglutamate; D-Trp at position 6; glycinamide

## Research History and Development

Interest in kisspeptin peptides grew out of human reproductive genetics, where the kisspeptin-GPR54 signaling system was identified as a regulator of puberty. A 2007 review of puberty genetics described the then recently discovered kisspeptin-GPR54 system as one of several single-gene pathways that affect puberty by modulating GnRH neurons and pituitary gonadotrophs.[4]Later work tied the same system to early puberty. A 2018 review of central precocious puberty stated that the kisspeptin system plays a key role in pubertal initiation and that mutations in it have been identified in sporadic and familial cases.[5]Over the following years, kisspeptin research broadened from puberty to energy balance, prolactin regulation and behavior.[6][7][1] In parallel, researchers began designing kisspeptin antagonists to probe the system; by 2013, four peptide antagonists and one small-molecule antagonist had been reported.[2]Authors of a 2019 review of kisspeptin and behavior argued that these broader roles could inform the pharmacological development of kisspeptin for reproductive, emotional and cognitive disorders, a direction that remains investigational.[1]

## Mechanisms Studied in Research

The central mechanism studied for kisspeptin peptides is activation of KISS1R on GnRH neurons, which drives GnRH release and, downstream, pituitary gonadotropin secretion.[2] Kisspeptin neurons are themselves targets of steroid hormone feedback and of nutritional and metabolic signals, positioning them as an integration point above GnRH.[2]Most of this mechanistic literature concerns endogenous kisspeptin signaling as a whole rather than kisspeptin-10 specifically.
### Metabolic regulation
A 2020 review described hypothalamic kisspeptin neurons as the nodal regulatory center of reproductive function and summarized how metabolic factors control KISS1 expression and kisspeptin release at stages ranging from early development to adulthood, reflecting the need for sufficient energy reserves before reproduction can succeed. It also discussed evidence that these neurons take part in circuits governing energy balance, a bidirectional link between metabolism and reproduction.[6]
### Prolactin
Extensive evidence indicates that elevated prolactin inhibits kisspeptin secretion, a pathway proposed to explain hyperprolactinemia-associated hypogonadotropic hypogonadism and infertility. More recent data suggest kisspeptin neurons may also help control prolactin secretion.[7]
### Limbic and behavioral signaling
Kisspeptin neuronal populations have been identified in limbic and paralimbic brain regions across several species. Studies from zebrafish through humans have linked kisspeptin signaling to olfactory and auditory cues in sexual partner preference, copulatory behavior, mood and emotion, with emerging work on memory and learning.[1]

## Key Findings From Published Studies

Published findings on kisspeptin-10 cover its hormonal effects in humans and, most specifically, its detection and breakdown in analytical studies. Only a small share of the indexed literature names kisspeptin-10 directly; most addresses kisspeptin signaling broadly.
### Hormonal effects
Kisspeptin-10 has been reported to increase circulating FSH, LH and testosterone in humans.[3] These effects are consistent with the receptor pathway described in reviews, in which kisspeptin acts upstream of GnRH.[2]
### Detection and metabolism
A 2024 study in Biomedical Chromatography validated an initial screening procedure and a confirmation procedure for kisspeptin-10 in urine using liquid chromatography-mass spectrometry. Because earlier rat research had shown elimination within about 30 minutes, the team incubated kisspeptin-10 in human serum to mimic endogenous metabolism and identified four metabolites, the y9, y8, y7 and y5 fragments, which they added to the screening method.[3]Using the confirmation procedure, the same group analyzed a black-market vial of kisspeptin-10. It contained no unexpected impurities but appeared more degraded than the purchased reference standard.[3]
### Genetic evidence
Human genetic studies link kisspeptin signaling to disorders of pubertal timing. The 2007 review counted at least 17 single-gene mutations associated with delayed or absent puberty, including the kisspeptin-GPR54 system, and estimated that such mutations account for about 30% of individuals with disorders of puberty.[4]
### Clinical context
In central precocious puberty, GnRH analogs remain the mainstay of treatment, and targeted therapies are listed among areas still to be explored.[5] Kisspeptin antagonists have been proposed as possible agents for hormone-dependent reproductive disorders such as precocious puberty, endometriosis and metastatic prostate cancer.[2]Because kisspeptin-10's tryptophan can oxidize and degraded material has turned up in unregulated vials, researchers typically confirm identity with HPLC-MS certificates of analysis.

## Regulatory and Research Status

Kisspeptin-10 is not approved by the US Food and Drug Administration for any medical use and remains an investigational research compound. No kisspeptin-based drug is currently marketed in the United States.In sport, kisspeptin-10 appears on the 2024 WADA Prohibited List because of its testosterone-increasing effect, and validated liquid chromatography-mass spectrometry methods now exist for detecting it and its metabolites in urine.[3]Research use centers on reproductive neuroendocrinology, where kisspeptin peptides serve as tools for studying the hypothalamic-pituitary-gonadal axis, puberty and the interface between metabolism and fertility.[6][5] Kisspeptin antagonists, the opposite pharmacological approach, were likewise still at the design stage in a 2013 review of the field, which described peripherally active antagonists as a possible future direction.[2]

## FAQ

**What is kisspeptin-10?**
Kisspeptin-10 is a ten-amino-acid peptide, YNWNSFGLRF with a C-terminal amide, that makes up the C-terminal end of kisspeptin-54 (metastin), the product of the KISS1 gene. It binds the KISS1R (GPR54) receptor on gonadotropin-releasing hormone neurons, the signal that gates GnRH secretion. It is used in research on the reproductive axis and puberty.

**Is kisspeptin-10 the same as kisspeptin?**
Not exactly. Kisspeptin is a family of peptides derived from the KISS1 gene product, including the longer kisspeptin-54, also called metastin. Kisspeptin-10 is the shortest common form, corresponding to residues 45-54. All kisspeptins share this C-terminal decapeptide, which carries the Arg-Phe-amide ending, and they act through the same receptor, KISS1R.

**What is the molecular weight of kisspeptin-10?**
Kisspeptin-10 has a molecular weight of 1302.4 g/mol and the molecular formula C63H83N17O14, according to PubChem (CID 25240297). That value refers to the free peptide with its C-terminal amide. Salt forms such as the trifluoroacetate salt, which appears among PubChem synonyms, have a higher formula weight because of the counterion.

**Is kisspeptin-10 FDA approved?**
No. Kisspeptin-10 is not approved by the US Food and Drug Administration for any medical use and remains an investigational research compound. It is also on the 2024 World Anti-Doping Agency Prohibited List, because it has been reported to raise circulating LH, FSH and testosterone in humans.

**How is kisspeptin-10 different from gonadorelin?**
Kisspeptin-10 acts one step higher in the reproductive axis. It stimulates GnRH neurons through the KISS1R receptor, prompting them to release GnRH. Gonadorelin is synthetic GnRH itself, a decapeptide with a pyroglutamate start that acts directly on pituitary GnRH receptors. The two peptides have unrelated sequences and target different receptors.

**Can kisspeptin-10 be detected in drug tests?**
Yes. A 2024 study validated screening and confirmation procedures for kisspeptin-10 in urine using liquid chromatography-mass spectrometry. Because the peptide is cleared rapidly, the researchers also identified four serum metabolites, the y9, y8, y7 and y5 fragments, and added them to the screening method to improve sensitivity.

## References

1. Mills EGA, O'Byrne KT, Comninos AN. Kisspeptin as a Behavioral Hormone. Seminars in reproductive medicine 2019. PMID: 31847025
2. Roseweir AK, Millar RP. Kisspeptin antagonists. Advances in experimental medicine and biology 2013. PMID: 23550006
3. Colpaert T, Risseeuw M, Deventer K, et al. [Not Available]. Biomedical chromatography : BMC 2024. PMID: 38978171
4. Herbison AE. Genetics of puberty. Hormone research 2007. PMID: 18174715
5. Aguirre RS, Eugster EA. Central precocious puberty: From genetics to treatment. Best practice & research. Clinical endocrinology & metabolism 2018. PMID: 30086862
6. Navarro VM. Metabolic regulation of kisspeptin - the link between energy balance and reproduction. Nature reviews. Endocrinology 2020. PMID: 32427949
7. Grattan DR, Szawka RE. Kisspeptin and Prolactin. Seminars in reproductive medicine 2019. PMID: 31847029