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Research profile · Peptide

Kisspeptin-10

Also known as KP-10, Metastin fragment 45-54

Early human — evidence level 3 of 4: Early human evidenceExperimental — UK regulatory status: Experimental — not authorised for human use in the UK

Overview

The shortest bioactive fragment of the kisspeptin family, studied as an upstream regulator of the reproductive hormone axis.

Category
Peptide
Highest evidence level identified
Early human evidence
Last scientifically reviewed
20 August 2026
Last regulatory review
20 August 2026

Mechanism under investigation

Kisspeptin-10 is the shortest bioactive fragment of the kisspeptin family, peptides encoded by the KISS1 gene that act as the endogenous ligands of the receptor KISS1R. That receptor is expressed on hypothalamic gonadotrophin-releasing hormone neurons, and kisspeptin binding depolarises them and stimulates endogenous GnRH release, placing kisspeptin upstream of the entire hypothalamic-pituitary-gonadal axis. Loss-of-function mutations in the receptor cause congenital hypogonadotrophic hypogonadism in humans, which establishes the pathway as essential for normal pubertal development.

Research areas

  • Reproductive endocrinology
  • Hypothalamic signalling

These are fields in which the compound has been investigated. Listing a field is not a statement that anything was demonstrated within it.

Current evidence

In-vitro evidence

Cells, tissues or biochemical systems outside a living organism.

Strong and foundational. The 2001 deorphanisation work identified kisspeptins as the natural ligands of the receptor, and subsequent electrophysiological and signalling work characterised the coupling, calcium mobilisation and sustained neuronal depolarisation that follow receptor activation.

Animal evidence

Studies in living non-human animals.

Strong. Receptor-null mice show hypogonadotrophic hypogonadism, and conditional and rescue models have dissected direct from indirect actions on GnRH neurons. Work in rats and sheep has characterised the role of hypothalamic kisspeptin in setting pulse frequency and in the pre-ovulatory hormone surge.

Human observational evidence

Studies observing people without assigning an intervention.

Moderate, and the human genetics is decisive: inactivating receptor variants cause congenital hypogonadotrophic hypogonadism across multiple independent families. Further observational work covers circulating kisspeptin in pregnancy and in polycystic ovary syndrome.

Clinical-trial evidence

Studies assigning an intervention to human participants.

Careful wording matters here. Human interventional evidence for this specific fragment is limited to small single-centre physiological studies, typically four to five participants per dosing group, showing it raises luteinising and follicle-stimulating hormone in men with a markedly attenuated response in women during the follicular phase. The larger and better-powered work — the assisted-reproduction trigger trials and the randomised crossover trials in hypoactive sexual desire disorder — used kisspeptin-54, a different and longer isoform. A direct head-to-head study found GnRH more potent than either kisspeptin isoform at the doses tested.

Study limitations

  • Human studies of this fragment are very small — commonly four to five participants per group — single-centre and physiological in design. There are no powered efficacy trials of the isoform itself.
  • The substantive clinical trial programme used kisspeptin-54, a different isoform with different pharmacokinetics. Evidence for one isoform should not be presented as evidence for the other, and frequently is.
  • Responses are strongly context-dependent: the effect in women varies markedly with menstrual cycle phase, and a direct comparison found GnRH more potent than either isoform.
  • Endpoints are almost entirely short-term hormonal or neuroimaging measures. There are no long-term outcome or safety data, and none on repeated or prolonged administration.

UK regulatory context

Experimental — not authorised for human use in the UK

A compound appearing in research literature that holds no UK authorisation for human use in any indication.

Source: The Human Medicines Regulations 2012, regulation 46 — prohibition on sale or supply of an unauthorised medicinal product (opens legislation.gov.uk in a new tab) (legislation.gov.uk)

Regulatory classification is jurisdiction-specific. A compound authorised elsewhere is not thereby authorised in the UK, and a supplier’s description of a substance does not determine how it is classified in law. See safety and regulation for the framework and the authoritative sources.

Safety and interpretation

Reported human studies describe the peptide as generally well tolerated in supervised research settings, with vital signs and laboratory parameters remaining stable during monitored intravenous administration and no serious adverse events attributed to it in the published academic programme. The total exposed population is small, follow-up is short, and administration has taken place under close clinical monitoring using pharmaceutical-grade material. No conclusion about safety outside those conditions follows from this evidence, and no regulator has assessed the compound.

References