≥99%HPLC Purity
COAIncluded
USAShipped
KPV Peptide
C-terminal tripeptide fragment of alpha-MSH. Studied for NF-kB pathway modulation and anti-inflammatory signaling research.
$55.00
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| Simple Peptide | GoAlpha Labs | AminoCore ✓ all‑in | |
|---|---|---|---|
| 10mg price | $45.00 | $39.74 | $55.00 |
| Shipping | +$13.00 | +$13.00 | FREE |
| Bac Water | +$30.00 | +$15.00 | FREE |
| Total paid | $88.00 | $67.74 | $55.00 save up to $33.00 |
Quick Facts
| SKU | ACR-KPV |
|---|---|
| CAS Number | 67727-97-3 |
| Molecular Formula | C16H31N5O4 |
| Molecular Weight | 357.45 g/mol |
| Sequence | Lys-Pro-Val |
| Purity | ≥99% |
| Physical Form | Lyophilized Powder |
| Storage | Store at -20°C |
What is KPV?
KPV (Lys-Pro-Val) is a tripeptide corresponding to the C-terminal amino acids 11-13 of alpha-melanocyte-stimulating hormone (alpha-MSH). Despite being only three amino acids in length, published research suggests KPV retains significant biological activity derived from the parent hormone.
Alpha-MSH is a 13-amino acid peptide produced from proopiomelanocortin (POMC) processing. Research identified that the C-terminal KPV sequence carries much of the anti-inflammatory signaling activity of the full-length peptide, independent of melanocortin receptor activation.
For laboratory research use only.
Mechanism of Action
NF-kB Pathway Modulation
Published research indicates KPV may directly inhibit NF-kB activation. Studies suggest the tripeptide can enter cells and interact with components of the NF-kB signaling cascade, potentially inhibiting IkB kinase (IKK) activity and preventing nuclear translocation of NF-kB. This mechanism is distinct from melanocortin receptor-mediated signaling.
Transepithelial Transport
Research has demonstrated that KPV can cross epithelial barriers via the peptide transporter PepT1 (SLC15A1). This oligopeptide transporter is expressed in intestinal epithelium and actively transports di- and tripeptides. The ability to cross epithelial barriers without degradation is notable for such a small peptide.
Inflammasome Modulation
Studies have investigated KPV interaction with inflammasome pathways, particularly NLRP3. Research suggests KPV may reduce inflammasome activation and downstream IL-1beta and IL-18 processing, providing an additional anti-inflammatory mechanism independent of NF-kB modulation.
Research & Clinical Studies
KPV and Inflammatory Bowel Disease Research
KPV has emerged as a key research compound in IBD studies. Oral and colonic administration of KPV in mouse models of colitis reduced disease activity scores by 60-70%, decreased pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), and preserved intestinal epithelial barrier integrity. The mechanism involves NF-κB inhibition in colonocytes and lamina propria macrophages, reducing the inflammatory cascade at its transcriptional root.
Remarkably, KPV retains anti-inflammatory activity when administered orally, as it is absorbed intact by intestinal epithelial cells via PepT1 transporter — a unique property for a peptide that enables direct delivery to inflamed gut tissue.
[1] Dalmasso G et al. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134(1):166-178. PubMed ↗
KPV and Skin Inflammation Research
In dermatological research, KPV reduces inflammatory responses in keratinocytes, melanocytes, and dermal fibroblasts. Studies show reduced IL-8, ICAM-1, and VCAM-1 expression in UV-irradiated skin models. KPV also inhibits contact hypersensitivity reactions (delayed-type allergy model) by reducing T-cell-mediated inflammatory infiltration. These findings position KPV as a research compound bridging immunology and dermatology.
KPV and NF-κB Signaling Pathway
KPV inhibits the NF-κB inflammatory pathway at multiple levels, making it one of the most potent peptide-based NF-κB modulators known:
- IκBα stabilization: KPV prevents phosphorylation and proteasomal degradation of IκBα, keeping NF-κB sequestered in the cytoplasm
- p65 nuclear translocation block: Even when IκBα is partially degraded, KPV reduces p65 (RelA) subunit nuclear import
- Transcriptional inhibition: KPV reduces NF-κB binding to DNA promoter elements, decreasing transcription of pro-inflammatory genes (TNF-α, IL-6, IL-1β, COX-2, iNOS)
The multi-level NF-κB inhibition is significant because NF-κB is the master transcription factor for inflammation. Unlike corticosteroids which broadly suppress immunity, KPV specifically targets the inflammatory cascade while preserving innate immune surveillance (phagocytosis, NK cell function remain intact).
[1] Brzoska T et al. Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory and protective effects in vitro and in vivo. Endocr Rev. 2008;29(5):581-602. PubMed ↗
KPV in Wound Healing and Dermal Research
KPV accelerates wound healing through a dual mechanism: reducing excessive inflammation (which delays healing) while promoting keratinocyte migration and proliferation. In full-thickness wound models, topical KPV reduced healing time by 30% compared to controls. The peptide also inhibited keloid fibroblast proliferation in vitro, suggesting potential in hypertrophic scar prevention research.
In atopic dermatitis models, KPV reduced scratching behavior (pruritus), decreased epidermal thickening, and normalized skin barrier function (transepidermal water loss). These effects were mediated through local NF-κB inhibition in skin-resident immune cells and keratinocytes.
Chemical Properties
| Sequence | Lys-Pro-Val (KPV) |
|---|---|
| Origin | C-terminal tripeptide of alpha-MSH (positions 11-13) |
| Formula | C₁₆H₃₁N₅O₄ (estimated free base) |
| MW | 357.45 g/mol |
| Amino Acids | 3 (tripeptide) |
| Mechanism | NF-κB pathway inhibition (p65 nuclear translocation block) |
| Oral Activity | Yes — absorbed via PepT1 transporter in intestinal epithelium |
| Purity | ≥98% HPLC |
Handling & Reconstitution
Reconstitution: Add bacteriostatic water slowly along the vial wall. KPV is a tiny tripeptide (357 Da) that dissolves almost instantly. Solution should be clear and colorless.
Concentration: For a 5 mg vial, 1 mL BAC water = 5 mg/mL. For research protocols requiring mcg-level doses, further dilution with sterile saline is recommended for accurate measurement.
Oral administration: KPV is one of the rare peptides with oral bioactivity. It can be dissolved in water for oral research protocols targeting intestinal inflammation. The PepT1 transporter actively absorbs KPV across the intestinal epithelium.
Storage & Stability
Lyophilized: -20°C for 24+ months. Reconstituted: 2-8°C, use within 21 days. KPV is a small, proline-containing tripeptide with excellent stability. No methionine or cysteine residues = no oxidation concerns.
Frequently Asked Questions
What is KPV?
KPV (Lys-Pro-Val) is a tripeptide fragment from the C-terminus of alpha-MSH. Despite its small size, research shows it retains anti-inflammatory signaling activity, primarily through NF-kB pathway modulation. It can cross epithelial barriers via the PepT1 transporter.
How does KPV differ from alpha-MSH?
Alpha-MSH is a 13-amino acid peptide that signals through melanocortin receptors. KPV is just the last 3 amino acids and appears to work through a different mechanism — direct NF-kB pathway modulation rather than melanocortin receptor activation. KPV lacks the melanogenic activity of full-length alpha-MSH.
Can KPV be taken orally?
Yes, uniquely for a peptide. KPV is absorbed intact by intestinal epithelial cells via the PepT1 (SLC15A1) oligopeptide transporter. This enables oral delivery directly to inflamed gut tissue, making it valuable for IBD and GI inflammation research.
What is the relationship between KPV and alpha-MSH?
KPV is the C-terminal tripeptide (positions 11-13) of alpha-melanocyte-stimulating hormone. While full-length alpha-MSH has broad melanocortin receptor activity (MC1-5R), KPV retains only the anti-inflammatory NF-κB inhibition without melanocortin receptor binding or skin-darkening effects.
KPV vs BPC-157 for inflammation research?
Different mechanisms: KPV inhibits NF-κB transcription factor (upstream inflammatory master switch). BPC-157 modulates NO/FAK-paxillin pathways (angiogenesis and tissue repair). KPV is more purely anti-inflammatory; BPC-157 is more pro-regenerative. They target complementary pathways.
What makes KPV unique among anti-inflammatory peptides?
Three unique properties: (1) Multi-level NF-κB inhibition (not just one step), (2) Oral bioavailability via PepT1 transporter (rare for peptides), (3) Anti-inflammatory without immunosuppression — preserves innate immunity while blocking inflammatory transcription.
Can KPV be used topically?
Yes, KPV is studied in topical formulations for dermal inflammation. Its small size (357 Da, 3 amino acids) allows skin penetration, and it reduces inflammatory mediators in keratinocytes and dermal immune cells directly at the application site.
For laboratory and research use only. Not intended for human or animal consumption. All product information is derived from published preclinical research and does not constitute medical advice or claims.