NexVas™ Plaque Regression (NexVas PR) is our lead program focused on developing novel small molecules to target ApoA-I to stabilize and regress atherosclerotic plaque. High levels of ApoA-I have been clinically proven to reduce the risk of cardiovascular disease (CVD). The process by which this happens is called reverse cholesterol transport, where cholesterol is removed from the arteries and delivered to the liver for elimination from the body.
The lead drug in the NexVas PR program, RVX-208 is a novel small molecule that stimulates endogenous ApoA-I production to trigger the synthesis of HDL. The use of this approach will enhance the functionality of HDL. ApoA-I is the major protein component of HDL. The main role of these particles is to act as the body's natural defense system against atherosclerosis by mediating a normal physiologic process called RCT. This pathway enables cholesterol, including that within atherosclerotic plaques of vessel walls, to be transported to the liver for further processing and elimination from the body. Enhanced RCT clearance of cholesterol from vessel walls should reduce or prevent atherosclerosis. The ability of RVX-208 to increase ApoA-I production and thereby augment RCT makes it highly differentiated from all other HDL therapies. Thus RVX-208 is positioned to be one of the most promising drugs in development for the treatment of atherosclerosis.
Our NexVas PR program has the capacity to become a leading force in the largest life science market in the world for the following reasons:
- It is fundamentally different from other therapies focused on increasing HDL. Resverlogix’s small molecules have been shown to enhance the functionality of ApoA-I particles resulting in cholesterol excretion.
- Resverlogix has taken the unique and physiological approach to pharmaceutical discovery by activating the body’s own health promoting genes (such as ApoA-I) to fight diseases.
- This therapeutic approach of increasing the body’s endogenous ApoA-I production may avoid any immunologic complications associated with peptide or recombinant ApoA-I therapies currently in development, and more importantly facilitates continual enhancement of ApoA-I levels.
