Incyte Gene gets some Press. From Quicken:
CV Therapeutics Scientists Demonstrate a Novel Approach to Remove
Cholesterol From Cells
Thursday, October 14, 1999 04:25 PM
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Study Finding May Lead to New Treatments for Cholesterol Management to Reduce Heart Disease
Risk
PALO ALTO, Calif., Oct. 14 /PRNewswire/ -- A study published in The Journal of Clinical Investigation
(October 15, 1999) reports that scientists at CV Therapeutics, Inc. (Nasdaq: CVTX) have demonstrated
that increasing levels of a gene known as ABC1 enhances the removal of cholesterol from cultured
cells. This research provides the first biological evidence suggesting that therapies which increase the
level of ABC1 might aid in removing cholesterol from the body, which could reduce the risk of heart
disease, the leading killer in the United States.
Using gene expression microarray analysis along with other techniques, CV Therapeutics, working with
Incyte Pharmaceuticals, Inc. (Nasdaq: INCY) and University of Washington, determined that ABC1 is a
key gene involved in the formation of high density lipoprotein (HDL or the "good" cholesterol). Scientists
have known for some time that HDL removes excess cholesterol from the body. CVT researchers have
now established that ABC1 shuttles cholesterol outside the cell, where it can be converted to HDL.
Moreover, CVT scientists have utilized recombinant gene expression techniques to successfully
modulate the level of ABC1 within cultured cells. "Low HDL cholesterol is as much a risk factor as high
LDL, or "bad," cholesterol for heart disease," explained study lead investigator, Richard Lawn, Ph.D.,
Vice President, Discovery Research at CV Therapeutics. "By increasing ABC1 in cultured cells, we
were able to boost the efficiency of cholesterol removal from the cell. This could lead to increased
production of HDL cholesterol in the body, and hence, the eventual removal of cholesterol from the
body."
"We believe this new finding holds the promise of discovering new treatment solutions for cholesterol
management that could substantially impact treatment for heart disease, similar to how statins, such
as Lipitor(R) and Zocor(R), changed the way we manage high LDL," added Dr. Lawn.
Study Findings
The authors reported their findings that mutations in the gene encoding the transporter protein known
as ABC1 cause Tangier disease, a rare genetic disorder that results in very low levels of HDL and is
associated with increased risk of heart disease. This work, followed by additional studies, enabled the
authors to demonstrate that by controlling the amount of the ABC1 gene in cells, the level of
cholesterol removal from the cells can be modulated.
CV Therapeutics' scientists believe that these discoveries may lead to the development of compounds
that could increase the amount of ABC1 protein in humans and remove excess cholesterol from artery
walls. Efforts may also be directed to developing gene therapy approaches to raise HDL levels in
patients with pathologically low HDL, thus reducing the incidence of heart disease.
"Studying a disease that affects a small population, such as Tangier disease," noted Dr. Lawn, "has
led us to the discovery of a possible pathway that may eventually lead to therapies for those suffering
from or at risk for heart disease."
Background
LDL and HDL Cholesterol. There are two forms of cholesterol carrying particles that act in opposing
pathways to control cholesterol levels in tissues: LDL (bad) and HDL (good). As LDL delivers
cholesterol to tissues and vessels, HDL removes excess cholesterol from the body. Excessive
amounts of LDL can lead to cholesterol accumulation and vessel blockage and ultimately heart
disease. Low amounts of HDL can also lead to heart disease; slower removal of cholesterol means
greater buildup of arterial plaques, which can cause heart attacks and angina.
Gene Expression Microarray Technology. This study also represented the first time gene expression
microarray analysis has been used to identify the defect associated with a human genetic condition.
This technique uses a micro-chip with thousands of genes covering its surface. When researchers
place patient RNA samples on the chip, they can determine, through comparison with normal RNA
samples, which of the affected person's genes are defective. This technology dramatically reduces the
time needed to find one mutated gene within the entire human genome.
In addition to historical information, this press release contains forward-looking statements that involve
risks and uncertainties, including, but not limited to, uncertainties related to the Company'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 the Company's Annual Report on Form 10-K
for the year ended December 31, 1998.
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. The Company currently has three drug
candidates in clinical trials. Ranolazine, the first in a new class of drugs known as partial fatty acid
oxidation (pFOX) inhibitors for the potential treatment of angina, is in Phase III clinical trials. CVT-124,
for the potential treatment of congestive heart failure (CHF), is in Phase II clinical trials. A third product,
CVT-510, for the potential treatment of atrial arrhythmias, is in Phase I clinical trials. For more
information, please visit CV Therapeutics' web site at www.cvt.com.
SOURCE CV Therapeutics, Inc.
CONTACT: Dan Spiegelman, Chief Financial Officer, 650-812-9560, or Christopher Chai, Director,
Strategic Planning & Investor Relations, 650-812-9509, both of CV Therapeutics; or Carol Harrison,
212-453-2442, or Caroline Yu, 415-356-1075, both of Fleishman-Hillard for CV Therapeutics
Quote for referenced ticker symbols: INCY, CVTX
© 1999, PR Newswire |
