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Research profile · Peptide

KPV

Also known as Lysine-proline-valine, Lys-Pro-Val

Animal — evidence level 2 of 4: Animal evidenceExperimental — UK regulatory status: Experimental — not authorised for human use in the UK

Overview

The C-terminal tripeptide of alpha-melanocyte-stimulating hormone, studied in cell culture and in mouse models of intestinal inflammation.

Category
Peptide
Highest evidence level identified
Animal evidence
Last scientifically reviewed
19 August 2026
Last regulatory review
19 August 2026

Mechanism under investigation

KPV is the C-terminal tripeptide of alpha-melanocyte-stimulating hormone. It is proposed to act intracellularly rather than through melanocortin receptor binding, with reported inhibition of nuclear factor kappa B translocation and of MAP kinase inflammatory signalling, and consequent reduction in pro-inflammatory cytokine output. In intestinal tissue it is reported to be taken up by the di- and tripeptide transporter PepT1.

Research areas

  • Inflammatory signalling
  • Intestinal models

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.

The mechanistic work is reasonably clear at this level. Nanomolar concentrations inhibited activation of nuclear factor kappa B and MAP kinase signalling and reduced pro-inflammatory cytokine secretion in intestinal epithelial and immune cell lines, with uptake shown to depend on the PepT1 transporter.

Animal evidence

Studies in living non-human animals.

Confined almost entirely to murine colitis. Orally administered peptide reduced disease severity and pro-inflammatory cytokine expression in two chemically induced mouse colitis models, and an independent group reported anti-inflammatory effects in two further murine models. Later work has focused on delivery systems rather than the free peptide.

Human observational evidence

Studies observing people without assigning an intervention.

There is no substantial published human observational work. What circulates is anecdotal user report, not data.

Clinical-trial evidence

Studies assigning an intervention to human participants.

There are no registered or published human clinical trials for any indication. Searches of ClinicalTrials.gov return no records. This is the most important fact on this page: the entire evidence base is cell culture and mice, and every claim made for this compound in humans crosses both a species gap and an evidence-level gap.

Study limitations

  • The entire evidence base is in vitro and murine. There is no human efficacy or safety data whatsoever.
  • Animal work is concentrated in acute, chemically induced mouse colitis, which models a narrow slice of human inflammatory bowel disease over short durations.
  • A substantial portion of the in vivo literature originates from a single research group, so independent replication is limited.
  • Much of the later work tests engineered nanoparticle delivery systems rather than free peptide, and those findings do not transfer to unformulated material.

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 2 — definition of a 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

Human safety data are essentially absent: there are no human trials, no pharmacokinetic data and no systematic adverse-event reporting. The animal literature reports the peptide as well tolerated in short-term rodent colitis studies, but that provides no basis for estimating adverse-event frequency, immunogenicity or long-term effects in people.

References