Resverlogix highlights features of RVX-208 drug at ATVB conference

Apr 12 2010

Resverlogix Corp. ("Resverlogix" or the "Company") (TSX:RVX) announced today that key scientific data was communicated in an oral presentation highlighting the novel features of RVX-208, the Company's lead drug, during the Atherosclerosis, Thrombosis, Vascular Biology (ATVB) conference being held in San Francisco, California. The presentation titled "RVX-208, an Orally Active Small Molecule, Raises ApoA-I Production and HDL Levels in Human Trials and Also Reduces Plaque Numbers in a Mouse Model of Atherosclerosis" was presented by Dr. Norman Wong, MD, Chief Scientific Officer of Resverlogix.

Resverlogix's oral small molecule therapy for the treatment of atherosclerosis is currently being studied in two parallel Phase 2 clinical trials. The first trial focuses on stable coronary artery disease patients, while the second trial examines patients with unstable acute coronary syndrome and includes the use of intravascular ultrasound (IVUS). Both of these studies are chaired by Dr. Steven Nissen, MD, Chairman of the Cleveland Clinic Department of Cardiovascular Medicine and the principal investigator is Dr. Stephen Nicholls, Medical Director of Intravascular Ultrasound at the Cleveland Clinic.

Cardiovascular disease is the leading cause of death in the US and other developed nations costing the American health care system an estimated $448.5 billion in 2008. According to the American Heart Association's Heart Disease & Stroke Statistics 2010 publication, approximately every 25 seconds an American will have a coronary event and approximately every minute, someone will die from such an event. A key underlying cause of cardiovascular disease is atherosclerosis, a build-up of plaque in the arteries often referred to as 'hardening of the arteries'.

Apolipoprotein A-I (ApoA-I), the main component of high-density lipoprotein (HDL), represents the body's natural defense system against atherosclerosis by mediating reverse cholesterol transport, i.e. transport of peripheral cholesterol including that within the atherosclerotic plaques of the vessel wall to the liver for processing. In multiple human and animal studies over-expression or repeated infusion of ApoA-I inhibits progression and induces regression of atherosclerosis in animals and humans. Developing small molecules that increase ApoA-I would satisfy a vast unmet medical need.