Novel peptide therapy for vascular inflammation

Atherosclerosis is driven by chronic vascular inflammation, lipid accumulation and immune cell recruitment, leading to plaque formation and vessel narrowing. Even in optimally treated patients, substantial residual inflammatory risk remains. CXCR4 is widely expressed but has a key role on leukocytes and aortic endothelial cells: activation by the pro‑inflammatory cytokine MIF drives vascular inflammation, foam cell formation and plaque progression, whereas CXCR4 engagement by CXCL12 can exert both cell‑dependent atheroprotective and disease‑promoting effects.
Life Sciences
Therapeutics
Reference
b80034
IP right year
2021
IP status
PCT filed in AU, CA, EP, US
Applicant
Technical University of Munich
Contact
Linda Keil

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.

Talk to an expert

Interested in learning more about this technology offer, exploring potential applications or discussing a possible collaboration? Get in touch to learn more.

Linda Keil