KPV Peptide 10mg – Ac-KPV-NH₂

Chemical diagram for KPV by https://commons.wikimedia.org/w/index.php?curid=177340267

KEY SPECIFICATIONS

PRODUCT OVERVIEW

KPV (Ac-Lys-Pro-Val-NH₂) is a synthetic tripeptide representing the C-terminal fragment (residues 11-13) of alpha-melanocyte-stimulating hormone (α-MSH). This research peptide retains potent anti-inflammatory properties of the parent molecule while exhibiting minimal melanogenic activity—enabling investigation of inflammatory mechanisms independently of pigmentation pathways. Research demonstrates dual anti-inflammatory mechanisms: classical melanocortin receptor signaling (MC1R/MC3R/MC4R) and receptor-independent NF-κB pathway inhibition. PepT1 transporter-mediated uptake is critical for intestinal anti-inflammatory effects. With over 50 peer-reviewed publications spanning two decades, KPV is extensively characterized for inflammation research. BIONIX supplies KPV with ≥99% purity for immunological and cell signaling applications.

MECHANISM OF ACTION

KPV exhibits a unique dual mechanism engaging both receptor-mediated pathways and receptor-independent intracellular signaling—making it valuable for dissecting anti-inflammatory mechanisms.

Dual Signaling Pathways:

PepT1 Transporter Mechanism:

Structural Stability Features:

Proposed Signaling Pathway:

KPV Entry → PepT1 Transport (intestine) or Diffusion (other tissues) → 
Melanocortin Receptor Activation + NF-κB p65 Nuclear Translocation Blockade → 
Anti-inflammatory Cytokine Downregulation + Gene Transcription Modulation

Comparative Profile:

RESEARCH APPLICATIONS

• Intestinal Inflammation Models: DSS-induced colitis research documenting reduced MPO activity (neutrophil infiltration marker), preserved colon length, improved crypt architecture, and decreased pro-inflammatory cytokines (TNF-α, IL-6, IL-1β). Kannengiesser et al. (2008) demonstrated significant anti-inflammatory effects in murine colitis models.

• Skin Inflammation Studies: TPA-induced contact dermatitis models showing ear thickness reduction, decreased leukocyte infiltration, and reduced endothelial adhesion molecules. Research achieves anti-inflammatory effects without melanogenic stimulation—enabling mechanism isolation from pigmentation pathways.

• Wound Healing Research: Corneal epithelial wound healing studies demonstrating complete re-epithelialization within 60 hours versus no healing in controls. NO-dependent mechanism identified through synthesis inhibition studies. Fibroblast IL-8 pathway modulation and collagen type I/III ratio investigations.

• Antimicrobial Studies: Direct antimicrobial activity against Staphylococcus aureus and Candida albicans—dual anti-inflammatory/antimicrobial profile valuable for complex tissue repair investigations.

• Cytokine Modulation Research: TNF-α, IL-6, IL-1β downregulation studies; NF-κB pathway activation blockade; COX-2 expression reduction; evaluation of minimum effective concentrations across experimental models.

ANALYTICAL VERIFICATION

BIONIX KPV undergoes comprehensive analytical characterization:

• HPLC Analysis: ≥99% purity confirmation via optimized chromatographic separation; detects deletion sequences and byproducts • Mass Spectrometry: Molecular weight verification (441.5 g/mol) and sequence confirmation (Ac-Lys-Pro-Val-NH₂) • Amino Acid Analysis: Composition quantification • Terminal Modification Verification: N-acetylation and C-amidation confirmation • Endotoxin Testing: Laboratory quality assurance for cell culture applications

Physical Characteristics:

DEVELOPMENT STATUS

• Research History: Over 50 peer-reviewed publications spanning two decades • Mechanism Elucidation: Dual receptor-dependent and receptor-independent pathways characterized • Intestinal Research: PepT1 transporter mechanism established by Dalmasso et al. (2008) • Clinical Status: Not FDA or EMA approved for therapeutic use • Regulatory Classification: Research compound only • WADA Status: Research compound (verify current prohibited list)

BIONIX KPV is supplied exclusively for laboratory research purposes—not for therapeutic use, human administration, veterinary, or clinical applications.

FREQUENTLY ENCOUNTERED INQUIRIES

What is KPV and how does it differ from α-MSH?

KPV is a synthetic tripeptide (Ac-Lys-Pro-Val-NH₂) containing only the C-terminal three amino acids (positions 11-13) of full-length α-MSH. While α-MSH is a 13-amino acid peptide with strong melanocortin receptor activity including pigmentation control, KPV exhibits a focused anti-inflammatory profile with minimal melanogenic activity. KPV provides superior enzymatic stability, PepT1 transporter-mediated uptake, and receptor-independent NF-κB inhibition not present in the full-length parent peptide.

What is KPV’s dual mechanism of action?

KPV operates through two distinct pathways: (1) melanocortin receptor signaling (MC1R/MC3R/MC4R) with partial agonism and minimal cAMP elevation; (2) receptor-independent NF-κB pathway inhibition blocking p65 nuclear translocation and IKK activation. This dual mechanism persists even with complete melanocortin receptor blockade—confirming the receptor-independent pathway’s functional significance.

What is the significance of PepT1 transporter in KPV research?

The PepT1 (SLC15A1) proton-coupled oligopeptide transporter actively transports KPV into intestinal epithelial cells. PepT1 expression is upregulated in inflamed intestinal tissue and shows enhanced activity at acidic pH—precisely matching inflammatory microenvironments. This mechanism explains KPV’s particular efficacy in intestinal inflammation models and has stimulated targeted delivery research for inflammatory bowel disease applications.

What storage conditions are required?

Lyophilized powder requires -20°C storage for long-term stability (up to 24 months). Protect from moisture and light. Post-reconstitution, store at 2-8°C for 3-7 days or aliquot and freeze at -20°C (1-3 months) or -80°C (6-12 months). For short-term use, refrigerate at 2-8°C. Avoid repeated freeze-thaw cycles.

Does KPV have antimicrobial properties?

Affirmative. Research demonstrates direct antimicrobial activity against Staphylococcus aureus and Candida albicans at low concentrations. The dual anti-inflammatory and antimicrobial profile makes KPV valuable for wound healing research where infection control and inflammation reduction converge. Published studies (J Leukoc Biol, 2000) documented significant pathogen killing and viability reduction.

REFERENCES

• PMID: 18612139 — Comprehensive α-MSH/KPV pathway analysis (Endocr Rev, 2008)
• PMID: 18069684 — Murine colitis: MPO activity reduction (Inflamm Bowel Dis, 2008)
• PMID: 18061177 — PepT1-mediated uptake in intestinal epithelium (Gastroenterology, 2008)
• J Leukoc Biol, 2000 — Antimicrobial activity against S. aureus and C. albicans
• Catania A et al., 2010 — Melanocortin system and inflammation control (ScientificWorldJournal)