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Research Guide · KPV

What is KPV?

The C-terminal alpha-MSH tripeptide with potent anti-inflammatory and immunomodulating properties for research into inflammatory disease, wound healing, and immune response.

Updated September 2026 Research Use Only 10 min read

What is KPV

A three-amino-acid peptide derived from the C-terminal fragment of alpha-MSH with distinct receptor-independent anti-inflammatory activity.

01

Structure & Chemistry

KPV (Lys-Pro-Val) is a tripeptide representing amino acids 11–13 of alpha-MSH. Unlike the parent molecule, KPV lacks the N-terminal residues responsible for melanocortin receptor binding, exerting anti-inflammatory effects through a receptor-independent intracellular mechanism. Molecular weight 342.43 Da; sequence H-Lys-Pro-Val-OH.

02

Cellular Mechanism

KPV crosses cell membranes via the peptide transporter PepT1 (SLC15A1), expressed in small intestinal epithelium and strongly upregulated in inflamed colon. Once intracellular, KPV blocks NF-κB activation at nanomolar concentrations, suppressing pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8).

03

Regulatory Status

KPV is not approved as a therapeutic agent and is used exclusively for research in cell culture, tissue engineering, and animal studies.

Mechanism of Action

KPV’s intracellular anti-inflammatory signalling through PepT1-mediated uptake and NF-κB pathway inhibition.

01
PepT1-Mediated Cellular Entry
KPV enters target cells through the SLC15A1 peptide transporter (PepT1), constitutively expressed in small intestinal epithelium and markedly upregulated in colonic epithelium during inflammatory bowel disease. This self-targeting principle makes KPV particularly suitable for oral delivery research in colitis models, where the peptide concentrates precisely in inflamed sites.
02
NF-κB Inhibition
KPV inhibits the canonical NF-κB inflammatory cascade by preventing IκBα phosphorylation, sequestering NF-κB in the cytoplasm and blocking pro-inflammatory gene expression. At nanomolar concentrations (1–10 nM in vitro), KPV reduces TNF-α, IL-1β, IL-6, and IL-8 production in activated immune cells and intestinal epithelium (Brzoska et al., 2008).
03
MAPK Pathway Modulation
Beyond NF-κB inhibition, KPV suppresses MAPK signalling, a parallel inflammatory cascade. By simultaneously blocking both pathways, KPV produces a potent additive anti-inflammatory effect, offering a multi-target model for studying combined pathway inhibition (Luger et al., 2003).
04
Mast Cell Stabilisation
KPV stabilises mast cell degranulation and reduces local production of inflammatory mediators. By suppressing NF-κB activation in mast cells, it decreases preformed mediator release (histamine, tryptase) and limits synthesis of newly formed mediators (prostaglandins, leukotrienes).

KPV vs Related Peptides

Comparing KPV to parent alpha-MSH and tissue-repair peptides.

Property
KPV (Tripeptide)
Alpha-MSH (Full Hormone)
Amino Acid Count
3 (residues 11–13 of α-MSH)
13 (Full sequence)
Molecular Weight
342.43 Da
~1,817 Da
Receptor Mechanism
Receptor-independent (intracellular)
Melanocortin R agonist + intracellular
Pigmentation Effects
None
Yes (melanin induction)
Cellular Entry
PepT1 transporter
Endocytosis + receptor-mediated
Intestinal Targeting
High (PepT1 upregulation in IBD)
Systemic circulation

Comparative Perspective: BPC-157 is studied for gut barrier repair via growth factor induction; TB-500 promotes tissue remodelling via actin signalling. KPV operates through rapid NF-κB blockade — complementary rather than directly comparable. MT-2 is a synthetic melanocortin agonist with full receptor activation; KPV offers an alternative when researchers want anti-inflammatory benefit without melanocortin signalling.

Research Applications

Primary domains in which KPV demonstrates experimental utility.

01
Inflammatory Bowel Disease
KPV’s primary research focus. Murine colitis models (DSS, TNBS) demonstrate that KPV reduces colonic inflammation, diminishes pro-inflammatory cytokine expression, and improves disease histology. PepT1 upregulation in inflamed intestinal epithelium creates preferential KPV accumulation at disease sites (Brzoska et al., 2008; Garczorz et al., 2016).
02
Atopic Dermatitis & Skin Barrier
KPV reduces inflammatory mediators driving atopic dermatitis flares — TNF-α, IL-6, IL-8 — and stabilises mast cell degranulation. Topical and transdermal delivery studies have explored KPV’s efficacy in restoring skin barrier function impaired by chronic inflammation. Provides a research model distinct from corticosteroids and calcineurin inhibitors.
03
Mast Cell & Immune Tolerance
KPV is studied in mast cell-associated pathologies including mastocytosis, MCAS, and histamine intolerance models. By stabilising mast cell degranulation and reducing local histamine and tryptase release, KPV provides a tool for understanding intracellular signalling control of immune cell activation.
04
Wound Healing & Tissue Repair
KPV accelerates wound closure in acute and chronic injury models by modulating the inflammatory phase of healing. Excessive NF-κB inflammation delays healing and promotes hypertrophic scarring; KPV suppression permits earlier transition to the proliferative phase. Studies show reduced scar formation and enhanced dermal remodelling.
05
Antimicrobial Activity
KPV exhibits direct antimicrobial activity against Gram-positive bacteria (Staphylococcus aureus, Bacillus) and fungi (Candida albicans), independent of host inflammation effects. This dual activity makes KPV useful for antimicrobial peptide research with multi-target therapeutic implications for chronic infected wounds and dysbiotic intestinal diseases.

Quick Reference Specifications

Essential biochemical parameters.

P · 01
Peptide Designation
KPV (Lys-Pro-Val); Alpha-MSH 11–13 fragment
P · 02
CAS Number
67727-97-3
P · 03
Molecular Weight
342.43 Da
P · 04
Sequence
H-Lys-Pro-Val-OH
P · 05
Molecular Formula
C16H30N4O4
P · 06
Form & Purity
Lyophilised powder; 98–99%+ HPLC
P · 07
Half-Life
<4 hours (rapid proteolysis)
P · 08
Primary Mechanism
NF-κB inhibitor; MAPK suppression
P · 09
Cellular Entry
PepT1 (SLC15A1) transporter
P · 10
Active Range
1–100 nM (varies by cell type)

Reconstitution & Storage

Best practices for KPV stability and bioactivity.

01
Reconstitution & Aseptic Technique
Reconstitute with sterile WFI or bacteriostatic saline (0.9% NaCl with 0.9% benzyl alcohol). Bacteriostatic formulations are preferred when multiple aliquots are required. Use sterile syringes and 23–27 gauge needles; the powder dissolves readily without heat or vigorous agitation.
02
Storage Timeline
Lyophilised KPV vials remain stable for 12–24 months at 2–8°C. Reconstituted solutions are stable for 2–4 weeks refrigerated. Protect from light. Avoid freeze-thaw cycles — even one cycle induces aggregation. For extended storage, aliquot into sterile microfuge tubes and store at −20°C.
03
Quality Control
Visually inspect for clarity. A clear, colourless to pale yellow solution is expected. Any turbidity or visible particles indicates degradation. Confirm peptide identity by HPLC or LC-MS for critical applications. Ensure supplier documentation includes batch purity >99%.
04
Handling Best Practices
Maintain 2–8°C; minimise light exposure; use dedicated sterile supplies for each withdrawal; equilibrate refrigerated solutions to room temperature slowly before use. Document reconstitution date; discard solutions older than 4 weeks.

Key Published Research

Peer-reviewed studies behind KPV’s research profile.

2008
PepT1 uptake and colitis
KPV entered intestinal epithelial and immune cells via the PepT1 transporter, reduced NF-κB and MAP kinase inflammatory signalling, and lessened colitis in DSS and TNBS mouse models.1
2008
Murine IBD models
A separate study confirmed KPV’s anti-inflammatory activity in mouse models of inflammatory bowel disease.2
2008
α-MSH tripeptide review
A review in Endocrine Reviews summarised the biochemistry and anti-inflammatory effects of α-MSH and its C-terminal tripeptides, including KPV.3
2010
Colon-targeted delivery
KPV-loaded nanoparticles in a polysaccharide hydrogel, delivered orally, reduced colitis in mice at far lower doses than free peptide.4
2017
Oral nanoparticle KPV
Hyaluronic-acid-functionalised nanoparticles delivered KPV to inflamed colonic tissue and alleviated ulcerative colitis in mice.5

Regulatory & Research Status

Where KPV stands in 2026.

APR 26
FDA Category 2 removal
KPV was one of twelve peptides removed from the US FDA’s Category 2 compounding list. This is not an approval.
JUL 26
Advisory committee vote
The FDA’s Pharmacy Compounding Advisory Committee voted 8–6 (one abstention) to recommend KPV for the 503A bulks list for proposed wound-healing and inflammatory uses. FDA reviewers had noted the absence of human exposure data. The vote is non-binding.

Evidence Quality & Limitations

There are no published human studies of KPV. Its anti-inflammatory profile rests on cell and mouse models, and several of the strongest colitis results used specialised nanoparticle formulations that differ from a simple reconstituted peptide. Half-life and active-concentration figures vary between models and should be treated as approximate.

References

  1. Dalmasso G, et al. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134:166–78. PubMed
  2. Kannengiesser K, et al. Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflamm Bowel Dis. 2008;14:324–31. PubMed
  3. Brzoska T, et al. Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory and protective effects in vitro and in vivo. Endocr Rev. 2008;29:581–602. PubMed
  4. Laroui H, et al. Drug-loaded nanoparticles targeted to the colon with polysaccharide hydrogel reduce colitis in a mouse model. Gastroenterology. 2010;138:843–53. PubMed
  5. Xiao B, et al. Orally targeted delivery of tripeptide KPV via hyaluronic acid-functionalized nanoparticles efficiently alleviates ulcerative colitis. Mol Ther. 2017;25:1628–40. PubMed
⚠ Research Use Only. The compounds discussed in this guide are intended strictly for in-vitro laboratory research. They are not intended for human consumption, therapeutic use, or veterinary application. Researchers must comply with all applicable local regulations.
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