Cancer Cell Publishes Onyx Pharmaceuticals' Paper on New

                         Oncolytic Virus, 

  RICHMOND, Calif., May 20 /PRNewswire-FirstCall/ -- 
Onyx Pharmaceuticals, Inc. (Nasdaq: ONXX) today announced that a paper 
describing its new virus, ONYX-411, had been published on-line in Cancer Cell 
(May 2002, Volume1 (4)), a leading scientific journal in the field of cancer 
research (  In the paper entitled, "Selectively 
Replicating Adenoviruses Targeting Deregulated E2F Activity Are Potent, 
Systemic Anti-Tumor Agents," lead author, Leisa Johnson, Ph.D., and colleagues 
describe the construction and properties of ONYX-411.  This novel virus 
replicates selectively in cancer cells and not in normal cells.  This 
selectivity is based on defects that nearly all cancer cells have in a pathway 
that controls normal cell replication, known as the Rb pathway.  
In the same issue of Cancer Cell, in a preview article written by 
Thomas W. Dubensky, Jr., of Cerus Corporation, Dr. Dubensky opines, " ... the 
potency and selectivity of ONYX-411 could be an important step to making a 
selectively replicating adenovirus that can be used for systemic treatment."  
Onyx Pharmaceuticals has pioneered the development of cancer-selective 
viruses as cancer therapeutics by utilizing the genetic differences between 
normal and cancer cells.  Its compound, ONYX-015, is currently being evaluated 
in a Phase III clinical trial in recurrent head and neck cancer as well as in 
other cancers in earlier-stage human clinical trials.  ONYX-015 has been 
engineered to lose the ability to inactivate a key regulatory protein known as 
p53 in healthy cells.  Because p53 functions have already been eliminated in 
cancer cells, when ONYX-015 infects normal cells, the virus growth proceeds 
and cancer cells are killed.  
ONYX-411 has been similarly engineered to target cancer cells that have 
lost control of the regulatory pathway known as Rb, but not healthy cells that 
maintain a properly controlled Rb pathway.  Onyx recently reported at the 
annual meeting of the American Association for Cancer Research that ONYX-411 
can be used as a vector for tumor-selective expression of genes, to further 
enhance the killing power of this virus.  
Leonard E. Post, Ph.D., Senior Vice President, Research and Development, 
commented, "The data in this paper shows that while ONYX-015 is the first 
generation of an entirely new kind of cancer therapy, there are opportunities 
for construction of viruses with improved potency and selectivity.  We believe 
that ONYX-411, or a derivative that is armed with a gene to further improve 
anticancer activity, will be the next virus product in development for Onyx."  
Onyx Pharmaceuticals is engaged in the discovery and development of novel 
cancer therapies.  Based on its proprietary technologies that target the 
molecular basis of cancer, the company is developing two lead products, 
BAY 43-9006 and ONYX-015.  For more information about Onyx's pipeline and 
activities, visit the company's web site at  
This press release may contain certain forward-looking statements 
regarding the development of potential human therapeutic products that involve 
a number of risks and uncertainties.  Actual events may differ from the 
company's expectations.  In addition to the matters described in this press 
release, the timeline for clinical activity, results of pending or future 
clinical trials, dependency on third parties to manufacture our products, and 
changes in the status of the company's collaborative relationships, as well as 
the risk factors listed from time to time in the company's periodic reports 
filed with the Securities and Exchange Commission, including but not limited 
to its Annual Report on Form 10-K, may affect the actual results achieved by 
the company.  
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SOURCE  Onyx Pharmaceuticals, Inc.  

    -0-                             05/20/2002 
    /CONTACT:  Shari Annes of Onyx Pharmaceuticals, Inc., +1-510-262-8775/ 
    /Web site: 
    /Web site: 

CO:  Onyx Pharmaceuticals, Inc. 
ST:  California 
-0- May/20/2002 16:31 GMT
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