— peptide / anti-inflammatory —
Tripeptide C-terminal fragment of alpha-MSH investigated for anti-inflammatory activity in epithelial and mucosal research models.
α-MSH C-terminal tripeptide. Anti-inflammatory research (Catania 2000s). NF-κB modulation. Read more →
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Research-grade material. Documentation summarizes published literature in third-person scientific context. Not medical advice; not for human consumption.
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— The literature —
KPV is internalized into epithelial cells primarily through the proton-coupled oligopeptide transporter PepT1, which is highly expressed in small intestinal and colonic epithelium and upregulated under inflammatory conditions. Once internalized, the tripeptide has been reported to interact with nuclear factor-kappa B signaling components, inhibiting IkappaB kinase activity and reducing NF-kB nuclear translocation in response to inflammatory stimuli.
Downstream effects include reduced expression of tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, and interleukin-8 in stimulated epithelial preparations. KPV has also been reported to inhibit neutrophil chemotaxis and to attenuate mast cell degranulation in dermatological models. Unlike the parent alpha-MSH, the tripeptide shows limited activity at melanocortin receptors in standard binding assays, consistent with the observation that anti-inflammatory effects can be partly dissociated from melanocortin-1 receptor engagement.
All compounds discussed are intended for research use only. Not for human consumption. Research-context information is educational and does not constitute medical advice.
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