As the development of RVX-208 continues, many of you have asked, “What is the competition like?” The recent failures of two CETP inhibitors (torcetrapib and dalcetrapib), along with Niacin (extended release with or without antiflushing agent-Tredaptive) have weeded out some competitors. However, there are HDL therapeutic programs still in the race including peptides that look like parts of the ApoA-I protein, infusions of ApoA-I protein, delipidated HDL (i.e. HDL particles with cholesterol stripped off), and two CETP inhibitors anacetrapib and evacetrapib.
 
It is important to understand how these potential HDL targeted therapies differ from RVX-208. For the peptides, ApoA-I and delipidated HDL candidates in development, all three therapies are given by intravenous infusion. Moreover, they are really designed for use immediately following a heart attack, meaning these therapies are given within days after the event and require the use of hospital services for their administration.
 
In contrast, RVX-208 is an oral compound (“pill”) that can be taken at home and has been tested for up to 6 months in Phase 2b human clinical trials. Furthermore, the actions of RVX-208 are designed to be beneficial for chronic use and not limited to the period of time immediately following a heart attack or an episode of coronary ischemia. The net effect of RVX-208 is to raise functional HDL and facilitate cholesterol removal from atherosclerotic plaques.
 
The actions of CETP inhibitors have been reviewed previously. We believe that they do not raise the functional HDL required to lower cardiovascular disease risk. RVX-208 on the other hand has been shown to increase ApoA-I production and in turn create new particles of HDL that are highly active in pulling cholesterol out from atherosclerotic plaques.