Novel peptide therapy for vascular inflammation
Challenge and innovation
Atherosclerosis is driven by chronic vascular inflammation, lipid deposition and chemokine‑mediated immune cell recruitment, leading to plaque growth and unstable lesions. In many patients, a high residual inflammatory risk persists despite optimal lipid‑lowering therapy. Existing anti‑ inflammatory and chemokine‑targeted drugs often lack selectivity and disrupt protective pathways, underscoring the need for pathway‑specific interventions.
The approach uses soluble CXCR4- mimicking peptides that bind selectively to the pro‑ inflammatory cytokine MIF while sparing the atheroprotective CXCL12/CXCR4 axis. These small, stable peptides localize to atherosclerotic plaques, inhibit MIF‑driven leukocyte recruitment, foam cell formation and vascular inflammation, and reduce plaque burden in relevant preclinical models. This chemokine‑selective, plaque‑targeted mode of action directly addresses residual inflammatory risk and provides a modular template for extending the concept to other chemokine receptors and indications.
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