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KPV

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.

Plage de prix : 48.99 $ à 208.99 $
98.8%-99.4% Poudre lyophilisée 10 mg
Available documentation

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Pour la recherche en laboratoire uniquement. Pas pour un usage humain ou vétérinaire. Non destiné à diagnostiquer, traiter, guérir, atténuer ou prévenir une maladie.

Stockage

Conserver scellé, froid, sec et protégé des variations de chaleur. Confirmez le stockage spécifique au produit à l'arrivée.

Notes d'expédition

Emballé pour la stabilité du transit avec une assistance aux commandes disponible pour les itinéraires par temps chaud.

Batch reference

Batch-linked certificate support is available through the documentation desk.

Contexte de recherche

Profil de recherche KPV

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

  1. K
  2. P
  3. 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.

Mécanisme proposé

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.

Effets rapportés dans les études

  • 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.

Critères de recherche courants

NF-kappaB and MAPK activation, cytokines such as TNF-alpha and IL-6, epithelial permeability, histology, microbial growth, peptide transport, and tissue-injury scores.

Preuves et limites

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.

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