Immune research
KPV
Lyophilized immune-signaling research peptide for pathway review
KPV is an alpha-MSH fragment research peptide studied around epithelial integrity, immune signaling, and inflammatory-pathway models.
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Get catalog updatesFor laboratory research use only. Not for human or veterinary use. Not intended to diagnose, treat, cure, mitigate, or prevent disease.
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研究背景
KPV 研究プロファイル
KPV is the tripeptide Lys-Pro-Val, a short fragment derived from the carboxyl end of alpha-melanocyte-stimulating hormone. Preclinical research examines epithelial integrity, cytokine signaling, inflammatory-pathway markers, microbial interactions, and gut or skin model systems. Unlike broader melanocortin analogs, KPV is generally studied for fragment-specific activity and may not reproduce the full receptor profile of alpha-MSH. It is a focused choice for projects comparing short melanocortin-derived peptides in epithelial or immune-signaling experiments. Evidence is primarily laboratory and animal based, and reported pathway effects depend on the model, concentration, formulation, and endpoints used in the original study.
Molecular class
Alpha-MSH-derived tripeptide
Sequence / composition
- K
- P
- V
Defined amino-acid chain, shown in standard one-letter notation.
Research design note
Its short sequence and proposed transporter-dependent cell entry make uptake and stability useful assay controls.
想定される機序
A Lys-Pro-Val tripeptide derived from the C-terminal region of alpha-MSH. Proposed actions include cell entry through peptide transport systems and suppression of NF-kappaB, MAPK, cytokine, and microbial-response pathways, sometimes independently of classical melanocortin receptors.
研究で報告された作用
- Cell studies reported reduced activation of inflammatory transcription pathways and lower production of selected cytokines.
- Animal and epithelial models reported reduced inflammation or tissue injury in selected gut, skin, and infection-related experiments.
- Mechanism, transport, and potency vary by model, and controlled human evidence is not established.
一般的な研究エンドポイント
NF-kappaB and MAPK activation, cytokines such as TNF-alpha and IL-6, epithelial permeability, histology, microbial growth, peptide transport, and tissue-injury scores.
エビデンスと限界
Evidence is primarily cell and animal based. Human pharmacokinetics, efficacy, and safety remain insufficiently characterized.
External reading
Literature for context—not product proof.
Third-party sources describe their own research materials and methods. They do not validate a specific Azure catalog batch.
Support and documentation
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