Ribozyme Pharmaceuticals, Inc. Demonstrates Potent Activity Of A Ribozyme Targeted Against The Hepatitis C Virus

Presented at Amer. Assoc. for the Study of Liver Diseases Conference

BOULDER, Colorado, November 9, 1998 -- Ribozyme Pharmaceuticals, Inc. (RPI) (Nasdaq: RZYM) today announced that HEPTAZYME®, a ribozyme designed to selectively destroy Hepatitis C Virus (HCV) RNA, was effective in decreasing Hepatitis C Viral RNA in cell culture assays. This work was presented at the American Association for the Study of Liver Diseases (AASLD) conference in Chicago by Dr. Lawrence Blatt, RPI's Senior Director of Biopharmacology and Preclinical Research. In these studies, HEPTAZYME® demonstrated significant inhibition of the HCV viral translation process in cells at very low doses, and in a manner that implies applicability across multiple forms of the virus.

Hepatitis C Virus (HCV) is the most common chronic bloodborne infection in the United States today. A recent Centers for Disease Control report stated that over 4 million Americans are chronically infected with HCV, and it is estimated that 500 million people are infected with HCV worldwide. The disease, which is more common than HIV, kills 8,000-10,000 Americans annually, and the death toll is expected to triple over the next 10-20 years. Furthermore, development of effective treatments has been hampered by the presence of multiple forms of HCV, with at least six genotypes and more than 90 subtypes known.

HEPTAZYME® contains many novel features believed to be important for HCV treatment. First, HEPTAZYME® is a ribozyme, a catalytic RNA molecule that has the unique potential to bind and cleave HCV RNA specifically and selectively, thus suggesting that viral replication can be inhibited without affecting other normal physiological processes. Next, HEPTAZYME® cleaves the HCV RNA at a location that is completely conserved in all known genotypes and subtypes of HCV, which gives HEPTAZYME® the potential to inhibit all forms of the virus. Finally, since HCV replicates in the cytoplas

Contact: Neil Cohen
415-677-4455 x. 205
Noonan/Russo Communications

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