icon-folder.gif   Conference Reports for NATAP  
61th Annual Meeting of the American Association for the Study of Liver Diseases
Boston, MA, Hynes Convention Center
October 30-November 3, 2010
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High rates of early viral response, promising safety profile and lack of resistance-related breakthrough in HCV GT 1/4 patients treated with RG7128 plus PegIFN alfa-2a (40KD)/RBV: Planned Week 12 interim analysis from the PROPEL study
  Reported by Jules Levin
AASLD Nov 1 2010 Boston
Donald M. Jensen, Heiner Wedemeyer, Robert Herring Jr., Peter Ferenci, Mang-Ming Ma, Stefan Zeuzem, Maribel Rodriguez-Torres, Natalie Bzowej, Paul Pockros, John Vierling, David Ipe, George Hill
from Jules: this is another important study because it looks at a nucleoside R7128 from Roche and Pharmasset and the potency of this regimen was very good with 88% the 82 patients in the arm of the study receiving 1000,g bid of R7128 plus pegasys/rbv achieving undetectable viral load after 12 weeks of therapy and the other dosing arms doing also well. Of note genotype 1As in this study responded equally well as genotype 1Bs because this is a nucleoside which has a high genetic barrier to drug resistance so the authors reported that of the patients who completed therapy 11 had viral load >1000 at the end of triple therapy but they did not detect the S282T mutation. So a nucleoside or nucleotide is an important element in therapy, other classes of drugs can develop resistance pretty quick which is why we need combinationtherapy with several drugs like in HIV but the nucleoside has this special characteristic where it does not appear to develop resistance easily thus helping to suppress virus for genotypes 1A and incombination with a protease or other drug will also provide protection in supppressing virus in 1A genotypes and in overall potency. In earlier Roche combination studies of their protease RG7227 now called danoprevir and which is now boosted with low dose ritonavir I recall the combination of these 2 drugs suppressed 1A genotypes as well. Ritonavir boosting of HCV protease inhibitors appear to increase potency and help suppress the early development of resistance in genotype 1a.