CV Therapeutics' Scientists Present New Data Suggesting a Novel Way To Increase "Good" Cholesterol

Search Blogs that Mention this News Release
Click this link to view linked Bookmarking Services
Click this link to view linked Blogging Services
CV Therapeutics' Scientists Present New Data Suggesting a Novel Way To Increase "Good" Cholesterol
 In-Vitro Study Highlights Potential to Use Drugs to Increase the Production
                    Of Cholesterol Transport Protein, ABC1

    NEW ORLEANS, Nov. 15 /PRNewswire/ -- Scientists at
CV Therapeutics, Inc. (Nasdaq: CVTX) today presented results of an in-vitro
study demonstrating that certain compounds can turn on production of the ABC1
protein which pumps excess cholesterol out of cells.   It is expected that
eliminating excess cholesterol from cells will also increase the levels of
High Density Lipoproteins ("HDL"), or the "good cholesterol," in the
bloodstream.  By discovering ways of controlling ABC1 with chemical
compounds, CV Therapeutics researchers hope to develop drugs that increase
levels of HDL in the bloodstream and lower cholesterol in the cells, thereby
decreasing the risk of heart disease.  These findings were presented today at
the 73rd Annual Scientific Sessions of the American Heart Association.
    "For heart disease, having too little HDL can be as dangerous as having
too much LDL.  We discovered last year that the cause of the extraordinarily
low levels of HDL seen in patients with the genetic disorder, Tangier disease,
is a defect in the gene coding for ABC1," said David Wade, Ph.D.,
Senior Scientist, Discovery Research at CV Therapeutics.  "In our current
study we have discovered a key regulatory mechanism that controls the
production of ABC1, a protein our work has already shown to be important in
determining HDL levels.  By identifying the intracellular signals that
increase ABC1 activity, we can begin to isolate compounds that can be tested
for their potential ability to raise HDL."
    The ABC1 protein pumps cholesterol out of cells where it is taken up by
HDL and disposed of in the liver.  HDL is believed to keep the heart healthy
by carrying cholesterol away from the coronary arteries and low HDL levels are
as much a risk factor for heart disease as high levels of low-density
lipoproteins (LDL) or bad cholesterol.  CV Therapeutics scientists first
identified the section of DNA, called the ABC1 promoter region, which controls
the rate of transcription of the ABC1 gene.  Transcription is the critical
step in producing a specific protein from the DNA blueprint.  By using cloning
techniques that allow the activity of the ABC1 promoter in cells to be
measured, researchers were able to identify a protein "key" that attaches to
and turns on the ABC1 gene.  This key is made up of two separate units, the
LXR and RXR proteins, that together bind DNA.  Many DNA-binding proteins can
be turned on and off by ligands, which are often drugs or chemicals produced
by the cell; for example, estrogen is a ligand for a DNA-binding protein that
stimulates the transcription of genes that lead to ovulation, breast
development and other female sexual characteristics.  This study confirmed
that the ligands for the LXR-RXR dimer, 9-cis retinoic acid and
20(S)-hydroxycholesterol, in fact, lead to increased production of the ABC1
protein and removal of cholesterol from cells.  These ligands can serve as
starting points for drug development programs.
    "We now know that ligands that activate LXR and RXR may increase
production of the ABC1 protein.  Future research will most likely focus on
finding new compounds that act via LXR and RXR, since these may have the
clinical benefits of both raising HDL levels and increasing the rate of
cholesterol removal from the fat-filled cells that cause atherosclerosis,"
said Richard M. Lawn, Ph.D., VP Discovery Research at CV Therapeutics.
    Last year, CVT's discovery of the ABC1 gene was selected by the
American Heart Association as one of the top ten 1999 research advances in
heart disease and stroke.
    Statements in this press release concerning the development, potential
application and commercialization of our products are forward-looking
statements that involve risks and uncertainties, including, but not limited
to, uncertainties related to CVT's early stage of development and clinical
trials.  Actual results could differ materially.  Factors that could cause or
contribute to such differences are more fully discussed in CVT's Annual Report
on Form 10-K for the year ended December 31, 1999.
    CV Therapeutics, Inc., headquartered in Palo Alto, CA, is a
biopharmaceutical company focused on applying molecular cardiology to the
discovery, development and commercialization of novel, small molecule drugs
for the treatment of cardiovascular diseases.  CVT currently has two compounds
in clinical trials.  Ranolazine, the first in a new class of compounds known
as partial fatty acid oxidation (pFOX) inhibitors, is in Phase III clinical
trials for the potential treatment of chronic angina.  CVT-510, an A1
adenosine receptor agonist, is in Phase II clinical trials for the potential
treatment of atrial arrhythmias.  For more information, please visit CV
Therapeutics' web site at http://www.cvt.com.
SOURCE CV Therapeutics, Inc.
http://www.cvt.com
CONTACT:
Dan Spiegelman, Chief Financial Officer,
650-812-9509, or Christopher Chai, Treasurer & Director of
Investor Relations, 650-812-9560, both of CV Therapeutics, Inc.;
or Carol Harrison of Fleishman-Hillard, 212-453-2442, for CV
Therapeutics, Inc.