Peptide transport
Experimental research shows that the PepT1 transporter can move KPV into intestinal epithelial and immune cells.
P—08 • Preclinical research profile
KPV
A concise educational overview of an alpha-MSH-derived tripeptide studied in preclinical models of inflammatory signaling, intestinal biology, and epithelial response.
Name
KPV
Sequence: Lys-Pro-Val
- Scientific classification
- Naturally occurring alpha-melanocyte-stimulating hormone-derived tripeptide corresponding to residues 11–13
- Library family
- Immune
- Research status
- Preclinical; published evidence is limited to cellular, tissue-model, and animal studies
- Regulatory status
- Not FDA approved; reviewed during the FDA's July 2026 compounding advisory process, with no identified human administration data
Compound overview
A short alpha-MSH fragment studied for inflammatory-pathway effects.
KPV is a three-amino-acid fragment derived from the C-terminal end of the naturally occurring hormone alpha-melanocyte-stimulating hormone.
Unlike the complete alpha-MSH molecule, KPV does not reproduce all melanocortin signaling functions. Researchers primarily study it in intestinal, immune, and skin-cell models.
Mechanism under study
Cellular uptake and inflammatory-pathway regulation
Preclinical research connects KPV with peptide-transporter uptake and reduced activation of several inflammatory signaling pathways. Its complete mechanism has not been established in humans.
NF-kappaB signaling
Cell studies report reduced NF-kappaB activation and lower expression of selected inflammatory mediators.
MAPK pathways
KPV has reduced MAP-kinase signaling and pro-inflammatory cytokine production in experimental models.
Some animal findings indicate that KPV's effects may occur at least partly independently of melanocortin-1 receptor signaling.
Current research areas
Questions under investigation
- Intestinal inflammation and experimental colitis
- Epithelial and immune-cell signaling
- NF-kappaB and MAPK pathway regulation
- Cytokine and oxidative-stress responses
- Inflammatory skin and wound-response models
Evidence summary
Reported preclinical findings
- Inflammatory signaling: Cell experiments report reduced NF-kappaB and MAPK activation and lower production of selected inflammatory cytokines.
- Intestinal inflammation: KPV reduced inflammatory measures in multiple mouse models of experimental colitis.
- Epithelial delivery: PepT1-mediated cellular uptake provides a possible explanation for activity observed in intestinal models.
- Skin-cell protection: A laboratory study reported reduced oxidative stress, inflammatory signaling, and cell death in keratinocytes and a three-dimensional skin model exposed to particulate matter.
- Clinical translation: The preclinical findings create a rationale for carefully designed human studies.
The consistent inflammatory-pathway signals across experimental models support continued investigation in intestinal, skin, wound, and systemic research contexts.
Educational notice
Education, not usage guidance.
This profile is provided for scientific education only. It is not medical advice, treatment guidance, dosing information, or instructions for KPV use. The FDA has identified no human administration data for KPV or KPV acetate and reports insufficient information to evaluate clinical safety, effectiveness, immunogenicity, or aggregation-related risks.
Key scientific referencesComing soon
A curated primary-source reference list will be added during the next educational expansion.