P Palthera
Signalling Peptides

KPV

Lys-Pro-Val / α-MSH(11-13)

KPV is the C-terminal of α-melanocyte-stimulating hormone (α-MSH). Research has demonstrated anti-inflammatory activity in models of intestinal inflammation (colitis) and keratinocyte biology, with the PepT1 transporter implicated in cellular uptake.

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Abstract reference visual for Signalling Peptides.
Signalling Peptides
Classification
C-terminal tripeptide of α-melanocyte-stimulating hormone (α-MSH 11-13)
Research stage
Active in vitro and rodent inflammation literature; in vivo colitis models and dermatology research
Sequence
Lys-Pro-Val
Molecular weight
342.4 Da

Snapshot

Key takeaways

A three-bullet snapshot before reading the full dossier.

  1. 01

    Three- of α-MSH (Lys-Pro-Val).

  2. 02

    Active and rodent literature on intestinal inflammation and dermatology.

  3. 03

    Anti-inflammatory activity appears largely independent of melanocortin .

Dossier overview

4

research areas

3

references

3

handling notes

01

Mechanism of action

KPV is taken up by intestinal cells via the PepT1 di/ transporter and reduces inflammatory signalling (NF-κB, IL-1β) in epithelial and immune cells. Research suggests KPV's anti-inflammatory effects are largely melanocortin--independent.

02

Research applications

  • Inflammatory bowel disease research (colitis models)
  • Dermatology and keratinocyte research
  • Melanocortin pharmacology
  • PepT1 transporter pharmacology

Evidence at a glance

What's behind this profile

3 citations · 2003–2008

Animal
1

Studies in rodents or other animal models.

In vitro
2

Cell, tissue, or biochemical assays outside a living organism.

Publication years

  1. 03
  2. 04
  3. 05
  4. 06
  5. 07
  6. 08
20032008

Counts are derived from the cited studies below. A study covering both in vivo and in vitro work is counted by its primary model. Sample size is reported in 0 of 3 citations. Findings remain model-specific and are not extrapolated to therapeutic use.

03

Study references

Each profile cites a minimum of two peer-reviewed sources, with model type and reported sample size where the source provides it. Findings are model-specific and must not be extrapolated to therapeutic use.

Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) α-melanocyte-stimulating hormone peptides

2003

Getting SJ et al. · Journal of Pharmacology and Experimental Therapeutics

Model
In vivo — C57BL/6 and recessive yellow e/e mouse peritonitis model
Sample
Not reported in abstract

KPV exhibited anti-inflammatory effects in the murine peritonitis model that appeared largely independent of melanocortin , likely involving IL-1β inhibition.

PMID 12750433 DOI 10.1124/jpet.103.051623

α-Melanocyte-stimulating hormone, MSH 11-13 KPV and adrenocorticotropic hormone signalling in human keratinocyte cells

2004

Elliott RJ et al. · Journal of Investigative Dermatology

Model
In vitro — HaCaT cells and normal human keratinocytes
Sample
N/A (cell culture)

KPV was associated with elevated intracellular calcium in human keratinocytes via a pathway independent of the classical cAMP melanocortin- signalling.

PMID 15102092 DOI 10.1111/j.0022-202X.2004.22404.x

PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation

2008

Dalmasso G et al. · Gastroenterology

Model
In vitro intestinal cell models + in vivo murine DSS- and TNBS-induced colitis
Sample
Not reported in abstract

KPV taken up via the PepT1 transporter reduced inflammatory signalling in intestinal cells and was associated with reduced colitis severity in the murine models used.

PMID 18061177 DOI 10.1053/j.gastro.2007.10.026

Evidence caveats

  • Primary clinical evidence in humans is limited. Most published primary work is in vitro or rodent.
  • KPV is not approved as a medicine for any indication.

04

Storage and handling

Store under controlled laboratory conditions with batch and preparation details recorded.

  • Maintain batch and supplier documentation.
  • Research-only inventory; not for human use.
  • Limited modern clinical protocol documentation.