During atherosclerosis, inflammatory cells (e.g., monocytes) invade the vessel wall and differentiate into foam cells which accumulate lipids and cholesterol. Existing therapies for the treatment of atherosclerosis intend to inhibit the uptake or the synthesis of cholesterol (e.g. by statins) which is, however, accompanied by negative secondary side effects.
CD68-Fc is a recombinant protein which specifically interferes with the generation of foam cells. This agent was originally conceived at the group of Meinrad Gawaz at the Medical Clinic III of the University of Tübingen. The drug inhibits the cellular uptake of cholesterol by binding to oxidized LDL (“oxLDL”), and thereby prevents oxLDL uptake to foam cells in atherosclerotic plaques, and reduced local inflammation of the vascular wall, with the potential to reverse plaque progression. CD68-Fc almost completely inhibited the progression of atherosclerosis in mouse models, and significantly reduced the risk of plaque rupture. CD68-Fc will be developed to treat high risk atherosclerotic patients.