KPV Oral: Scientific Profile
Publicado el · Actualizado el
KPV (Lys-Pro-Val) is the C-terminal tripeptide of α-MSH and an inhibitor of the NF-κB pathway; its anti-inflammatory activity is independent of the melanocortin receptors. Reagent for in vitro and preclinical research (CAS 67727-97-3).
KPV (H-Lys-Pro-Val-OH) is the C-terminal tripeptide fragment of alpha-melanocyte-stimulating hormone (α-MSH), with molecular formula C16H30N4O4, molecular weight 342.43 g/mol and CAS 67727-97-3. Reagent for in vitro and preclinical research.
Mechanism: the tripeptide is internalized by the proton-coupled oligopeptide transporter PepT1 (SLC15A1) and acts intracellularly. It inhibits activation of the NF-κB pathway (blocking the nuclear translocation of p65/RelA) and reduces MAPK phosphorylation, with the consequent decrease in proinflammatory cytokines and adhesion molecules (TNF-α, IL-1β, IL-6, IL-8, and ICAM-1). Unlike the complete α-MSH peptide, KPV lacks the His-Phe-Arg-Trp motif for binding to melanocortin receptors, so its anti-inflammatory activity is independent of melanocortinergic signaling.
Research applications: in vitro and preclinical models of intestinal inflammation, epithelium, and immune cells. Reconstitution with bacteriostatic water and cold storage according to the standard handling of a lyophilized reagent.
Mechanism of action
The anti-inflammatory action of KPV is independent of the melanocortin receptors: as the C-terminal tripeptide of α-MSH, it lacks the HFRW pharmacophore needed to bind with relevant affinity to MC1R. Instead, KPV penetrates the cell (in the intestine, via the di/tripeptide transporter PepT1/SLC15A1) and intracellularly inhibits the nuclear translocation of NF-κB (p65) and the MAPK pathway, reducing the transcription of proinflammatory genes and the production of inducible nitric oxide synthase (iNOS).
Mechanism summary
Internalized by the oligopeptide transporter PepT1 (SLC15A1), it acts intracellularly by inhibiting the NF-κB pathway (it prevents the nuclear translocation of p65/RelA) and modulating MAPK, with a reduction of TNF-α, IL-1β, IL-6, IL-8 and ICAM-1. Its action is independent of the melanocortin receptors.
Clinical Studies (7)
- KPV and RAPA Self-Assembled into Carrier-Free Nanodrugs for Vascular Calcification Therapy (Zhang L et al. · Advanced healthcare materials · 2024) PMID 39252648.
- Transdermal Iontophoretic Delivery of Lysine-Proline-Valine (KPV) Peptide Across Microporated Human Skin (Pawar K et al. · Journal of pharmaceutical sciences · 2017) PMID 28343991.
- Inhibition of cellular and systemic inflammation cues in human bronchial epithelial cells by melanocortin-related peptides: mechanism of KPV action and a role for MC3R agonists (Land SC · International journal of physiology, pathophysiology and pharmacology · 2012) PMID 22837805.
- Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptides (Getting, et al. · The Journal of Pharmacology and Experimental Therapeutics · 2003) PMID 12750433.
- PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation (Dalmasso, et al. · Gastroenterology · 2008) PMID 18061177.
- Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease (Kannengiesser, et al. · Inflammatory Bowel Diseases · 2008) PMID 18092346.
- Lysine-Proline-Valine peptide mitigates fine dust-induced keratinocyte apoptosis and inflammation by regulating oxidative stress and modulating the MAPK/NF-κB pathway. (Sung J, et al. · Tissue Cell · 2025) PMID 40073467.
Warnings
KPV Oral is a compound exclusively for research use (RUO); the following warnings and handling considerations apply to its use in the laboratory:
- For laboratory research use only
- It must be handled under chemical biosafety protocols
- Study models with predisposition to melanocortin-dependent neoplasias
- Do not administer to experimental subjects with hypersensitivity to peptides
- Incompatibility with strong oxidizing agents in solution
Technical data
- CAS
- 67727-97-3
- Molecular formula
- C16H30N4O4
- Molecular weight
- 342.43 Da
- Compound type
- peptide
- Storage
- -20 °C liofilizado; 2-8 °C reconstituido
- Shelf life (lyophilized)
- 24 months
- Shelf life (reconstituted)
- 7-14 days refrigerated
- Light-sensitive
- No
Available for research
KPV Oral is available as a research reagent (RUO):
Frequently asked questions about KPV Oral
What is KPV Oral?
KPV (Lys-Pro-Val) is the C-terminal tripeptide of α-MSH and an inhibitor of the NF-κB pathway; its anti-inflammatory activity is independent of the melanocortin receptors. Reagent for in vitro and preclinical research (CAS 67727-97-3).
What is the mechanism of action of KPV Oral?
Internalized by the oligopeptide transporter PepT1 (SLC15A1), it acts intracellularly by inhibiting the NF-κB pathway (it prevents the nuclear translocation of p65/RelA) and modulating MAPK, with a reduction of TNF-α, IL-1β, IL-6, IL-8 and ICAM-1. Its action is independent of the melanocortin receptors.
What is Oral KPV investigated for?
In preclinical research, KPV Oral is studied mainly in: Research on the reduction of colonic inflammation; Modulation of the systemic immune response; Study of the integrity of the gastric mucosa. Material exclusively for scientific research.
What are the chemical properties of KPV Oral?
Molecular formula C16H30N4O4; molecular weight 342.43 Da; CAS number 67727-97-3.
How is KPV Oral stored?
Condiciones de conservación: -20 °C liofilizado; 2-8 °C reconstituido; estabilidad liofilizado: 24 meses; una vez reconstituido: 7-14 días refrigerado.
What routes of administration are studied for Oral KPV?
In research models the following are described: Oral (Gavage), Subcutaneous. Use is exclusively for scientific research.