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Heegon Kim
ATHEROSCLEROSIS
Renatus goes beyond LDL lowering by targeting accumulated plaque cholesterol at the source of foam-cell dysfunction and inflammation.
Atherosclerosis: Biology and Unmet Need
Atherosclerosis is a chronic inflammatory disease of the arterial wall in which modified LDL is taken up by macrophages, driving intracellular cholesterol accumulation, foam-cell formation, and cholesterol crystal formation. Cholesterol crystals can activate the NLRP3 inflammasome and downstream IL-1β signaling, reinforcing vascular inflammation and promoting plaque growth and progression that can ultimately lead to major cardiovascular events.
Statins and other LDL-lowering therapies reduce circulating LDL and limit further cholesterol entry into the arterial wall, but they do not directly address cholesterol already accumulated within established plaques. As a result, plaque-associated cholesterol burden and inflammation can persist, leaving substantial residual cardiovascular risk.
Targeting Cholesterol at the Root of Plaque Disease
Renatus is developing a potential disease-modifying approach that targets pathological cholesterol accumulation within plaque macrophages, an upstream driver of foam-cell dysfunction, cholesterol crystal formation, and inflammatory signaling. By mobilizing intracellular cholesterol and restoring macrophage cholesterol homeostasis, our approach is designed to intervene earlier in the disease cascade and reshape plaque biology beyond conventional LDL lowering.
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