Mark J. Murray, Ph.D., President and CEO; formerly of Protiva, Zymogentics, and Xcyte Therapeutics
Patrick T. Higgins, Chief Business Officer; co-founder of OnCore BioPharma; formerly of Pharmasset and Roche
Bruce Cousins, Chief Financial Officer; formerly of Aspreva and Johnson & Johnson
Michael J. Sofia, Ph.D., Chief Scientific Officer; co-founder of OnCore BioPharma; formerly of Pharmasset (inventor of sofosbuvir for hepatitis C), Bristol-Myers Squibb, and Eli Lilly
William T. Symonds, Pharm.D., Chief Development Officer; formerly of Gilead Sciences, Pharmasset (clinical development of sofosbuvir for hepatitis C), and GlaxoSmithKline
Mark Kowalski, MD, Chief Medical Officer; formerly of Gilead Sciences, YM BioSciences, and Viventia Biotechnologies
Peter Lutwyche Ph.D., Chief Technology Officer, formerly of Protiva, QLT, and Inex Pharmaceuticals 作者: newchinabok 时间: 2015-10-27 12:33
The therapeutic goals of chronic hepatitis B treatment are to restore normal liver function and prevent the development of cirrhosis, HCC, and liver failure. It has been convincingly demonstrated thus far that inhibition of HBV replication by the currently available antiviral drugs results in significant histological, biochemical, and serological improvement and reduction of HCC mortality and morbidity (60). However, the current antiviral therapeutics fail to resolve HBV infection in the vast majority of treated patients, and the achievement of therapeutic goals in these patients requires long-term, possibly life-long, treatment, which may ultimately fail due to the emergence of drug resistance and/or intolerability from the long-term use of these drugs (10). Hence, there is a pressing need for therapeutics that are able to either cure HBV infection or induce a durable off-drug suppression of the virus, which requires elimination and/or transcriptional silencing of cccDNA, the most stable HBV replication intermediate. We believe that therapeutic regimes with such pharmacological properties are most likely to come in the form of combination therapies with multiple drugs that target different steps of HBV replication. Thus, cccDNA formation can be prevented through more efficient inhibition of nucleocapsid assembly or rcDNA production and conversion to cccDNA, as well as by suppressing the emergence of drug-resistant mutants and accelerating the loss of preformed cccDNA.
To fulfill this goal, we have been developing cell-based assays suitable for the discovery of antiviral drugs that inhibit HBV replication in a high-throughput manner (33, 61, 62). 作者: newchinabok 时间: 2015-10-27 13:29