NF-κB Pathway Modulation
KPV has been shown to inhibit NF-κB activation in cell culture models, reducing transcription of pro-inflammatory cytokines including IL-1β, IL-6, and TNF-α.
Overview
What is KPV?
KPV is a tripeptide representing the C-terminal fragment (11-13) of alpha-melanocyte-stimulating hormone (α-MSH). Research has characterized KPV as the biologically active anti-inflammatory portion of α-MSH, with studies examining its effects on NF-κB signaling, cytokine production, and mucosal inflammation in cell culture and animal models.
KPV (Lys-Pro-Val Tripeptide) is supplied strictly as a reference material for in vitro and preclinical investigation. All characterization data described here is drawn from peer-reviewed literature and laboratory analysis; nothing herein constitutes a claim of clinical effect in humans.
Investigational Scope
Documented Research Areas
The following domains summarize directions explored across published studies and laboratory models. Each reflects observations reported in rodent models, in vitro systems, or the peer-reviewed record.
Mucosal Inflammation Models
Studies using DSS-induced colitis models in mice have examined KPV's effects on mucosal inflammation, with observed reductions in inflammatory markers and mucosal damage scores.
MC1R & MC3R Receptor Biology
KPV exerts its anti-inflammatory effects primarily through melanocortin receptors MC1R and MC3R, both of which are expressed on immune cells and intestinal epithelium.
Dermal Inflammation Research
Research has examined KPV's effects in cutaneous inflammation models, with studies documenting reduced keratinocyte cytokine production and immune cell infiltration in skin tissue.
Proposed Mechanism
Mechanistic Pathway
Mechanistic steps below are hypothesized from in vitro assays and animal-model data reported in the literature. They describe biochemical interactions observed under controlled experimental conditions.
-
1
Melanocortin Receptor Agonism
KPV binds MC1R and MC3R on macrophages, dendritic cells, and epithelial cells. Receptor activation triggers intracellular cAMP elevation and downstream suppression of inflammatory signaling cascades.
-
2
NF-κB Inhibition
Research has documented KPV's ability to prevent nuclear translocation of NF-κB p65 subunit in LPS-stimulated macrophages, reducing transcription of TNF-α, IL-1β, and IL-6.
-
3
Cytokine Profile Modulation
Cell culture studies have shown KPV shifts macrophage cytokine production from pro-inflammatory (M1) toward anti-inflammatory (M2) profiles, with increased IL-10 and decreased TNF-α output.
-
4
Intestinal Barrier Research
In vitro studies using Caco-2 intestinal epithelial cells have examined KPV's effects on tight junction protein expression and epithelial barrier integrity under inflammatory conditions.
Technical Data
Molecular Specifications
| Amino Acid Sequence | Lys-Pro-Val |
|---|---|
| Molecular Weight | 340.4 g/mol |
| Molecular Formula | C₁₆H₃₂N₄O₄ |
| CAS Number | 131866-22-3 |
| Storage | −20°C long-term, 4°C short-term up to 4 weeks |
References
Selected Literature
The following peer-reviewed references informed the research summaries on this page. Citations are provided for scientific context only.
- Luger TA, et al. (2003). The role of alpha-MSH as a modulating peptide in inflammation and autoimmunity. Annals of the New York Academy of Sciences, 999, 315–320.
- Bhatt DL, et al. (2000). Anti-inflammatory effects of alpha-MSH. Journal of Leukocyte Biology, 67(4), 493–501.
- Kannengiesser K, et al. (2008). Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine experimental colitis. Inflammatory Bowel Diseases, 14(3), 324–331.
- Catania A & Lipton JM. (1993). Alpha-melanocyte stimulating hormone in the modulation of host reactions. Endocrine Reviews, 14(5), 564–576.
- Brzoska T, et al. (2008). Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory and protective effects in vitro and in vivo. Endocrine Reviews, 29(5), 581–602.
Research Disclaimer
This product is intended strictly for laboratory research purposes only. It is not a drug, food, cosmetic, or dietary supplement and is not intended to diagnose, treat, cure, or prevent any disease. It is not for human or animal consumption. All information presented is derived from published scientific literature and is provided for educational reference only. By purchasing, the buyer affirms they are a qualified researcher or institution and assume full responsibility for the safe and lawful handling of this material.