Man , another HCV polymerase inhibitor!

Pharmasset announced today that a "Late Breaker" presentation describing the results of Study 303, a 48 week follow-on study to the Korean Phase 3 drug registration trial of Clevudine for the treatment of Hepatitis B, will be presented at the 57th Annual Meeting of the American Association for the Study of Liver Diseases (AASLD) being held in Boston, Massachusetts from October 27-31, 2006. The Clevudine abstract can be viewed on the AASLD website at http://www.aasld.org.

Clevudine is a nucleoside analogue that has shown potent anti-HBV activity in both in vitro and late-stage clinical studies in over 600 HBV-infected patients. The poster presentation at AASLD will describe the results of a study conducted by Bukwang Pharmaceuticals. In this study, Clevudine demonstrated potent antiviral activity in e-antigen positive (HBeAg+) and e-antigen negative (HBeAg-) patient populations, along with a marked 12-week post-treatment antiviral effect or sustained virological response (SVR) in both patient populations. Clevudine was generally well tolerated throughout the course of this study. Clevudine received conditional drug approval from the Korean Food & Drug Administration in July 2006, and the product launch in Korea is anticipated by the end of 2006.

"In this study, 31% of HBeAg+ patients and 92% of HBeAg -- patients have undetectable HBV 12 weeks after the end of treatment," stated Schaefer Price, Pharmasset's President & CEO. "The duration of Clevudine's post-treatment effect is unique. To our knowledge, Clevudine is the only HBV therapeutic agent, investigational or approved, that has demonstrated potentially clinically meaningful SVR levels at 12 weeks and 24 weeks post-treatment. We look forward to initiating our U.S. and European registration studies of Clevudine in 2007."

Clevudine acts directly on the HBV-polymerase to reduce its ability to incorporate nucleosides into new viral DNA chains. In preclinical animal models, Clevudine also demonstrated the ability to significantly reduce covalently closed circular DNA, or cccDNA, the form of HBV that is believed to be responsible for the persistence of an HBV infection.