KPV (20mg – 100mg)

KPV

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Peptide Partners Manufacturer Id: VI32

Batch Id: KV202601

Research Studies

(for educational purposes only)

PepT1-Mediated Tripeptide KPV Uptake Reduces Intestinal Inflammation

Title: PepT1-Mediated Tripeptide KPV Uptake Reduces Intestinal Inflammation

Authors: Guillaume Dalmasso, Laetitia Charrier-Hisamuddin, Hang Thi Thu Nguyen, Yutao Yan, Shanthi Sitaraman, Didier Merlin

URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC2431115/

Published: Gastroenterology, 2007 Oct 17;134(1):166–178

Human intestinal epithelial cells (Caco2-BBE and HT29-Cl.19A) and human T cells (Jurkat) were stimulated with pro-inflammatory cytokines in the presence or absence of KPV to investigate its anti-inflammatory mechanisms. Nanomolar concentrations of KPV inhibited the activation of nuclear factor-kappa B (NF-κB) and mitogen-activated protein (MAP) kinase inflammatory signaling pathways and reduced pro-inflammatory cytokine secretion. Uptake experiments were performed using radiolabeled tritiated KPV ([3H]KPV) to determine kinetic characteristics of KPV cellular uptake. The study found that KPV acts via human peptide transporter 1 (hPepT1) expressed in both immune and intestinal epithelial cells. KPV anti-inflammatory effects were assessed using NF-κB luciferase gene reporter assays, western blot analysis for signaling proteins, real-time reverse transcription polymerase chain reaction (RT-PCR) for gene expression, and enzyme-linked immunosorbent assay (ELISA) for cytokine quantification. The study demonstrated that KPV is transported into cells by PepT1 and exerts anti-inflammatory effects through inhibition of pro-inflammatory signaling pathways at concentrations as low as nanomolar range.

In plain English

This research showed that KPV, a tiny three-amino-acid peptide, can reduce inflammation in intestinal and immune cells grown in the laboratory. The peptide enters cells through a specific transporter protein called PepT1, which normally helps absorb nutrients from food. Once inside the cells, even very small amounts of KPV block the activation of key inflammatory signaling pathways, particularly NF-κB, which is like a master switch for inflammation. This prevents the cells from producing inflammatory chemicals called cytokines. The researchers tracked KPV movement into cells using a radioactive version of the peptide and measured its anti-inflammatory effects using multiple laboratory techniques, demonstrating that KPV could potentially be developed as a treatment for inflammatory bowel diseases.

Lysine-Proline-Valine peptide mitigates fine dust-induced keratinocyte apoptosis and inflammation by regulating oxidative stress and modulating the MAPK/NF-κB pathway

Title: Lysine-Proline-Valine peptide mitigates fine dust-induced keratinocyte apoptosis and inflammation by regulating oxidative stress and modulating the MAPK/NF-κB pathway

Authors: Junghee Sung, Seo-Young Ju, SeungHyun Park, Won-Kyo Jung, Jae-Young Je, Sei-Jung Lee

URL: https://www.sciencedirect.com/science/article/abs/pii/S004081662500117X

Published: Tissue and Cell, Volume 95, August 2025, 102837

The study investigated the protective effects of KPV against oxidative damage and inflammation induced by fine particulate matter (PM10) in human HaCaT keratinocytes using in vitro cell culture methods. HaCaT cells were exposed to PM10 at different concentrations (0–200 μg/mL) for 24 hours, with significant cytotoxic effects observed at concentrations between 100 and 200 μg/mL. Treatment with 50 μg/mL of KPV restored cell viability and reduced interleukin-1 beta (IL-1β) secretion that had been disrupted by PM10 exposure. KPV inhibited reactive oxygen species (ROS) production, which is responsible for activating extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase (MAPK). KPV decreased the expression of apoptosis-related proteins including Bax, Bcl-2, and cleaved caspase-3, as well as IL-1β, through suppression of the redox-sensitive transcription factor nuclear factor-kappa B (NF-κB) in PM10-treated HaCaT cells. KPV effectively blocked ROS-mediated caspase-1 activation, thereby reducing IL-1β secretion. In a three-dimensional (3D) skin model, KPV treatment effectively attenuated the inflammatory cell death induced by PM10, demonstrating that KPV protects keratinocytes by mitigating PM10-induced pyroptosis.

In plain English

This study examined how KPV protects skin cells from damage caused by air pollution particles. When human skin cells were exposed to fine dust particles in laboratory dishes, the pollution triggered harmful reactions including production of damaging molecules called reactive oxygen species, activation of stress pathways, and ultimately cell death through inflammation. Adding KPV to the cell cultures prevented these harmful effects by blocking the production of reactive oxygen species and stopping the inflammatory signaling cascades that would normally kill the cells. The researchers tested this not only in simple cell cultures but also in a more realistic three-dimensional artificial skin model, showing that KPV could protect skin from environmental pollution damage. This suggests KPV might be useful in skin care products designed to protect against air pollution.

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

Title: 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

Authors: Stephen C Land

URL: https://pmc.ncbi.nlm.nih.gov/articles/PMC3403564/

Published: International Journal of Physiology, Pathophysiology and Pharmacology, 2012 Jun 23;4(2):59–73

Tumor necrosis factor-alpha (TNFα) and rhinosyncitial virus (RSV)-evoked nuclear factor-κB (NFκB) signaling was measured in immortalised human bronchial epithelial cells (16HBE14o-) in response to KPV using in vitro cell culture techniques. KPV evoked a dose-dependent inhibition of NFκB transcriptional activity, matrix metalloproteinase-9 (MMP-9) enzymatic activity, and secretion of the chemokines interleukin-8 (IL-8) and eotaxin. The anti-inflammatory effect of KPV was associated with its nuclear import into cells, stabilisation of the inhibitory protein IκBα, and suppressed nuclear translocation of yellow fluorescent protein (YFP)-tagged p65RelA, a key subunit of NFκB. Competition assays revealed a direct interaction between KPV and the importin-α3 (Imp-α3) binding site on p65RelA, which may involve blockade of the importin-α armadillo repeat domains 7 and 8. The study demonstrates that KPV translocates to the nucleus in human bronchial epithelial cells and competitively blocks the interaction between Imp-α3 and the p65RelA subunit of NFκB. Cellular and systemic inflammatory signaling was measured using NFκB luciferase reporter gene assays and chemokine secretion quantified by enzyme-linked immunosorbent assay (ELISA). The results show that KPV suppresses NFκB signalling in airway epithelium by directly inhibiting p65RelA nuclear import through competitive binding.

In plain English

This research uncovered exactly how KPV stops inflammation in lung cells at the molecular level. When lung cells are exposed to viruses or inflammatory signals, a protein complex called NFκB normally moves into the cell nucleus to turn on genes that cause inflammation. The researchers discovered that KPV actually travels into the cell and physically blocks this process by interfering with the transport system that carries NFκB into the nucleus. It’s like KPV acts as a decoy or competitor that prevents the inflammatory proteins from reaching their destination. Using cells that had fluorescent tags attached to key proteins, the scientists could watch this blocking action happen in real time under the microscope. This mechanism is different from many anti-inflammatory drugs and explains why KPV can reduce inflammation caused by various triggers including viruses and inflammatory chemicals in lung tissue.