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| |  Potential of Mutant Adenovirus for Killing p53-Deficient Tumors RICHMOND, Calif., Oct. 17, 1996 -- Researchers at ONYX Pharmaceuticals (NASDAQ:ONXX) have turned a common virus into one with the potential to become a highly specific new treatment for certain types of human cancers. ONYX scientists today published research in the journal "Science" describing an adenovirus that has been genetically engineered to selectively replicate in and kill p53-deficient human tumor cells, while leaving normal cells unaffected. "Mutations of the p53 tumor suppressor gene are found in over 50 percent of all human cancers," said Frank McCormick, Ph.D., F.R.S., ONYX chief scientific officer and senior author of the "Science" publication. "Tumors lacking p53 are especially resistant to chemotherapy and radiation, and are associated with decreased survival rates in breast, prostate, lung and bladder cancers. Thus, a therapeutic strategy that enables the selective killing of p53-deficient cells would potentially be of great value for the treatment of cancer." In April 1996, ONYX began Phase I human safety trials of its mutant adenovirus, called ONYX-015, in patients with head and neck cancer. Adenoviruses are relatively benign viruses that occur widely in the human population and cause only mild, self-limiting infections. When a normal adenovirus infects a cell, it takes control of the cell's genetic machinery and turns the cell into a factory for producing viral DNA and proteins. This viral replication kills the cell, releasing thousands of new virus particles to infect neighboring cells. To take control of the cell, the virus makes a protein called E1B 55K that binds to p53 and blocks its function. Once the virus inactivates p53, viral replication can proceed unchecked. In the "Science" publication, ONYX researchers first showed that a mutant adenovirus that does not express the E1B 55K protein can replicate in and kill a variety of p53-deficient human tumor cells, but not cells where p53 is functional. Dr. McCormick and his colleagues then studied the ability of the mutant virus to infect and destroy p53-deficient tumors in vivo, by injecting the virus directly into human tumors grown in nude mice. After six weeks, they measured the mean tumor volume in each group of mice. Injection of the mutant virus caused a significant reduction in tumor size in p53-deficient tumors, including complete regression in 60 percent of the tumors treated. The researchers observed those tumors responding completely for over three months without seeing evidence of tumor regrowth. In contrast, the researchers saw little change in tumor size when the mutant virus was injected into tumors with functional p53. To ensure that reduction of the p53-deficient tumors was due to virus replication, the researchers analyzed sections of the excised tumors for certain viral capsid proteins. The viral proteins were observed throughout the p53-deficient tumors. In contrast, the researchers detected no viral proteins in the tumors with functional p53. While these results are promising, the results in animal testing may not predict the results of clinical testing in humans. ONYX Pharmaceuticals was founded in 1992 for the purpose of discovering and developing novel therapeutics based upon the genetics of human disease, with an initial emphasis on cancer. The company focuses on defining the function of certain mutated genes which are known to cause cancer, and on developing innovative therapies to reverse the effects of the mutation or kill the cancer cell. ONYX pursues a strategy of establishing corporate partnerships that provide complementary skills in drug development, clinical trials, regulatory affairs, and marketing and sales. The statements made in this press release contain certain forward looking statements that involve a number of risks and uncertainties. Actual events or results may differ from the company's expectations. In addition to the matters described in this press release, timelines for clinical activity, results of pending or future clinical trials 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 SEC reports, including but not limited to its Registration Statement on Form SB-2, may affect the actual results achieved by the company.
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