RE: Press ReleaseAmerican College of Cardiology Meeting Highlights the Need for ApoA-I
Enhancement Small Molecules
CETP failure demonstrate ApoA-l focused therapeutics clearly differentiated as the key target for
cardiovascular disease risk reduction
Calgary, AB April 2, 2007 – Resverlogix Corp. (“Resverlogix”) (TSX:RVX) released today that
subsequent to important findings announced last week from numerous presentations at the
American College of Cardiology (ACC) meeting in New Orleans, attendees learned that merely
increasing HDL is not good enough. The goal for future HDL therapies is ApoA-I/HDL
enhancement, a process to increase functional HDL which occurs by increasing endogenous
Apolipoprotein (ApoA-l) production.
Functional HDL, often referred to as nascent HDL, is an early form of HDL known to be the most
efficient particle for uptake of cholesterol from macrophage foam cells. These foam cells are
responsible for the unstable atherosclerosis plaque which causes heart attacks. Presentations at
the recent ACC conference demonstrated that previous failings in HDL therapies were a result of
targeting other HDL, not nascent HDL. Simply put, ApoA-I enhancement creates hungry young
HDL particles whereas CETP creates mature congested HDL particles. The CETP drug debacle
actually supports the clinical importance of the pathway Resverlogix is working along, ApoA-I
enhancement. Resverlogix lead drug, RVX-208, is the first small molecule drug that has illustrated
proof in multiple animal models to enhance endogenous ApoA-l synthesis thereby increasing the
amount of functional HDL in plasma.
Donald McCaffrey, CEO and President of Resverlogix stated, “We are very pleased to see that
large human studies support the type of small molecules that we are developing. Our lead ApoA-I
enhancement drug, RVX-208, has the potential to fill an unmet medical need namely the removal
of atherosclerosis plaque.”
McCaffrey continued, “I was particularly pleased with several supportive statements made during
the ACC conference. In an interview in Medscape with Dr. Brian Brewer, he stated that ‘Another
approach to increasing HDL is to increase the level of expression of the ApoA-l’. Adding further
evidence to the importance of ApoA-l was Dr. Daniel Rader’s statements in the ACC News
whereby he said, ‘We have an abundance of clinical data. The most compelling is that the hepatic
expression of apoA-1 reduces - and even regresses - atherosclerosis in mice. This data suggest a
link to atherosclerosis.’ We absolutely agree with both of these statements which is why the timing
of our white paper, which examines the future of HDL therapies, could not be any better.”
To view Resverlogix’s white paper on the future of HDL therapies please go to the company’s
website at www.resverlogix.com/media/fact_sheets.html.
There exists a huge unmet medical need for new cardiovascular disease therapies. Currently
cardiovascular disease is the leading cause of death in industrialized countries and future
estimates indicate that mortality will increase by 90% by the year 2020 versus rates in 1990. The
American Heart Association estimates the direct and indirect costs of CVD in the United States
alone for 2006 are US $403.1 billion. ApoA-I is the key protein in high-density lipoprotein (HDL or
the “good cholesterol”).