Name: KPV
Brand: Amino Club
SKU: KPV - 10MG
Availability: InStock
Rating: 4.8 (61 reviews)

KPV | 99%+ Pure Peptide | Amino Club | Amino Club

How KPV Works

The Science, Simplified

NF-κB Inhibition via PepT1 Transport

KPV is the C-terminal tripeptide of alpha-melanocyte-stimulating hormone (α-MSH) that retains potent anti-inflammatory activity. Unlike full-length α-MSH which works through melanocortin receptors, KPV enters cells via the PepT1 di/tripeptide transporter. Once inside, it inhibits NF-κB and MAPK inflammatory signaling pathways at nanomolar concentrations, reducing pro-inflammatory cytokine production.

PepT1Primary

PepT1 Transport

Peptide Transporter 1 (SLC15A1)

High-affinity cellular uptake (Km ~160 μM)
Enhanced expression during IBD
Enables oral bioavailability

NF-κBPrimary

NF-κB Pathway

Nuclear Factor Kappa-B Inhibition

Shortens NF-κB activation duration
Interacts with IκB-α and p65RelA
Nuclear import inhibition

MAPKSecondary

MAPK Pathway

Mitogen-Activated Protein Kinase

Reduces ERK phosphorylation
Decreases inflammatory signaling
Synergizes with NF-κB inhibition

Gastroenterology — KPV Transport Study

Key Discovery

NOT Melanocortin Receptor-Mediated

A crucial finding is that KPV's anti-inflammatory effects are NOT mediated by melanocortin receptors (MC1R-MC5R). KPV does not bind to MC-1R and fails to increase cAMP levels. Instead, it is transported directly into cells by PepT1, where it accumulates in the nucleus to inhibit NF-κB activation. This explains why KPV remains effective even in MC1R knockout models.

Clinical significance: PepT1 expression is upregulated during inflammatory bowel disease, meaning inflamed tissue actually takes up MORE KPV — a self-targeting mechanism that enhances therapeutic potential.

α-MSH (13 AA)MCR-dependent signaling

KPV (3 AA)PepT1-mediated, MCR-independent

Km (intestinal)~160 μM

Km (immune cells)~700 μM

Oral Bioavailability

Effective via Oral Administration

Unlike most peptides that require injection, KPV can be administered orally. The PepT1 transporter is naturally expressed in the small intestine and is induced in the colon during IBD. Research shows oral KPV (100 μM in drinking water) significantly reduced inflammation in both DSS- and TNBS-induced colitis mouse models.

Practical advantage: Oral delivery combined with enhanced uptake at inflamed sites makes KPV uniquely suited for gastrointestinal inflammatory conditions.

Research Applications

Areas studied in preclinical models

IBD

Research

Primary focus: ulcerative colitis and Crohn's disease models with PepT1-mediated targeting to inflamed intestinal tissue

Dalmasso et al. 2008

Skin

Inflammation

Studied in contact dermatitis, cutaneous vasculitis, and wound healing models; topical application shows efficacy

Luger et al. 2007

Anti-

Microbial

KPV exhibits antimicrobial activity against Staphylococcus aureus and Candida albicans pathogens

Br J Pharmacol 2000

Arthritis

Models

α-MSH peptides showed efficacy comparable to prednisolone without causing weight loss in adjuvant-induced arthritis

Luger et al. 2007

Gastrointestinal

Inflammatory Bowel Disease Research

KPV's primary research focus is inflammatory bowel disease. The upregulation of PepT1 during IBD creates a self-targeting mechanism where inflamed tissue preferentially accumulates KPV. Oral administration is effective, making it uniquely practical for GI applications.

DSS colitis MPO↓ 50%

TNBS colitis MPO↓ 30%

IL-6/IL-12 mRNASignificantly reduced

Oral bioavailabilityYes (PepT1-mediated)

Gastroenterology 2008

Cellular

NF-κB Pathway Modulation

At the cellular level, KPV inhibits NF-κB at nanomolar concentrations. It shortens the duration of NF-κB activation by interacting with IκB-α, p65RelA, and Importin-α3 — critical mediators of the inflammatory cascade. The peptide accumulates in the nucleus where it exerts these effects.

NF-κB inhibition

+83%

IL-8 reduction

+35%

MAPK suppression

+60%

Dalmasso et al. 2008

Dermatological

Skin Inflammation Research

KPV and α-MSH peptides have been studied in various skin inflammation models including contact dermatitis, cutaneous vasculitis, and wound healing. Topical application of α-MSH showed effectiveness in nickel-induced contact eczema in preliminary human studies.

Contact dermatitisEffective in models

Cutaneous vasculitisAnti-inflammatory

Wound healingEnhanced epithelialization

RouteTopical application

Br J Pharmacol Review

Antimicrobial

Pathogen Inhibition

Beyond anti-inflammatory effects, KPV exhibits direct antimicrobial activity. Research demonstrates efficacy against common pathogens including Staphylococcus aureus and Candida albicans, suggesting dual therapeutic potential in infected inflammatory conditions.

Pathogen species inhibited

Dual action: Anti-inflammatory + antimicrobial properties may be particularly valuable in conditions where infection drives inflammation.

α-MSH Antimicrobial Activity

Frequently Asked Questions

Common questions about KPV research

KPV is a tripeptide (Lys-Pro-Val) that corresponds to the C-terminal amino acids 11-13 of alpha-melanocyte-stimulating hormone (α-MSH). Despite being only 3 amino acids compared to α-MSH's 13, KPV retains potent anti-inflammatory activity. It was discovered that this small fragment is responsible for much of α-MSH's anti-inflammatory effects, working through a mechanism independent of melanocortin receptors.

The key difference is mechanism: α-MSH works primarily through melanocortin receptors (MC1R-MC5R), while KPV does NOT bind to these receptors. Instead, KPV is transported into cells via PepT1 (peptide transporter 1), where it directly inhibits NF-κB signaling in the nucleus. This means KPV can work even in tissues lacking melanocortin receptors, and its uptake is actually enhanced in inflamed intestinal tissue where PepT1 is upregulated.

Yes, research demonstrates that KPV is effective via oral administration. The PepT1 transporter is naturally expressed in the small intestine, allowing KPV to be absorbed intact. In mouse colitis models, oral KPV (100 μM in drinking water) significantly reduced inflammation markers. This is unusual for peptides, which typically require injection due to degradation in the GI tract.

The primary research focus is inflammatory bowel disease (IBD), including ulcerative colitis and Crohn's disease models. KPV has also been studied in: contact dermatitis, cutaneous vasculitis, allergic airway inflammation, adjuvant-induced arthritis, ocular inflammation, and wound healing. Additionally, KPV shows antimicrobial activity against Staphylococcus aureus and Candida albicans.

PepT1 transport is clinically significant because this transporter is upregulated during inflammatory bowel disease. This means inflamed intestinal tissue preferentially accumulates KPV — essentially a self-targeting mechanism. The more inflamed the tissue, the more KPV it takes up. This could explain the enhanced efficacy seen in colitis models and suggests a built-in tissue selectivity.

No. KPV is a preclinical research compound that has not been approved by the FDA or any regulatory authority for therapeutic use in humans. While preclinical studies show promising anti-inflammatory effects and a favorable safety profile, human clinical trials are needed to establish safety and efficacy. It is currently available for research purposes only.

In cell culture studies, 10 nanomolar (nM) concentrations of KPV effectively inhibit NF-κB activation and reduce inflammatory cytokine production. In mouse colitis models, 100 micromolar (μM) KPV delivered in drinking water showed significant anti-inflammatory effects. Human therapeutic dosing has not been established as clinical trials have not been conducted.

Lyophilized (powder) KPV should be stored at -20°C for long-term stability. Once reconstituted, store at 2-8°C (refrigerated) and use within 7 days. Protect from light and avoid repeated freeze-thaw cycles. The small peptide size contributes to reasonable stability, but standard peptide handling precautions should be followed.

KPV

Certificate of Analysis

Frequently Researched Together

GHK-Cu

NF-κB Inhibition via PepT1 Transport

PepT1 Transport

NF-κB Pathway

MAPK Pathway

NOT Melanocortin Receptor-Mediated

Effective via Oral Administration

Anti-Inflammatory Effects in Colitis Models

Preclinical Efficacy Metrics

Inflammatory Bowel Disease Research

NF-κB Pathway Modulation

Skin Inflammation Research

Pathogen Inhibition

No observed toxicity

Minimal adverse effects

Preclinical Safety Summary

Important Considerations

💡Researcher Notes

What Is KPV?

Relationship to α-MSH

Stability Information

Where It Stands

What is KPV and where does it come from?

How does KPV differ from full-length α-MSH?

Can KPV be taken orally?

What conditions has KPV been studied for?

What is the significance of PepT1-mediated uptake?

Is KPV approved for human use?

What is the effective dose of KPV?

How should KPV be stored?

PepT1-Mediated Tripeptide KPV Uptake Reduces Intestinal Inflammation

α-MSH Related Peptides: A New Class of Anti-Inflammatory and Immunomodulating Drugs

Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis

Melanocortin-Derived Tripeptide KPV Has Anti-Inflammatory Potential in Murine Models of Inflammatory Bowel Disease

Alpha-Melanocyte-Stimulating Hormone and Related Tripeptides: Biochemistry, Antiinflammatory and Protective Effects

⚠️Important Research Notice

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Frequently Researched Together

GHK-Cu

Researcher Notes