« Previous
Next »
Gastroenterology
Volume 141, Issue 6
, Pages 2047-2055
, December 2011
Efficacy of the Protease Inhibitor BI 201335, Polymerase Inhibitor BI 207127, and Ribavirin in Patients With Chronic HCV Infection
References
- Boceprevir for untreated chronic HCV genotype 1 infection. N Engl J Med. 2011;364:1195–1206
- Telaprevir in combination with peginterferon and ribavirin in genotype 1 HCV treatment-naïve patients: final results of phase 3 ADVANCE study (abstr 211). Hepatology. 2010;52(Suppl 1):427A
- Telaprevir in combination with peginterferon alfa2a and ribavirin for 24 or 48 weeks in treatment-naïve genotype 1 HCV patients who achieved an extended rapid viral response: final results of phase 3 ILLUMINATE study (abstr LB-2). Hepatology. 2010;52(Suppl 1):401A–402A
- SILEN-C1: sustained virologic response (SVR) and safety of BI201335 combined with peginterferon alfa-2a and ribavirin (P/R) in treatment-naïve patients with chronic genotype 1 HCV infection (abstr 60). J Hepatol. 2011;54(Suppl 1):S27
- Combination of the NS3/4A protease inhibitor ITMN-191 (R7227) with the active moiety of the NS5B inhibitors R1626 or R7128 enhances replicon clearance and reduces the emergence of drug resistant variants (abstr 1885). Hepatology. 2008;48(Suppl 1):1153A
- A triple combination of direct-acting antiviral agents demonstrates robust anti-HCV activity in vitro (abstr 769). J Hepatol. 2010;52(Suppl 1):S299
- Oral combination therapy with a nucleoside polymerase inhibitor (RG7128) and danoprevir for chronic hepatitis C genotype 1 infection (INFORM-1): a randomised, double-blind, placebo-controlled, dose-escalation trial. Lancet. 2010;376:1467–1475
- Potency, safety and pharmacokinetics of the NS3/4A protease inhibitor BI201335 in patients with chronic HCV genotype-1 infection. J Hepatol. 2011;54:1114–1122
- SILEN-C2: sustained virologic response (SVR) and safety of BI201335 combined with peginterferon alfa-2a and ribavirin (P/R) in chronic HCV genotype-1 patients with non-response to P/R (abstr 66). J Hepatol. 2011;54(Suppl 1):S30
- 4 week therapy with the non-nucleoside polymerase inhibitor BI 207127 in combination with peginterferon-alfa2a and ribavirin in treatment naïve and treatment experienced chronic HCV GT1 patients (abstr 2007). J Hepatol. 2010;52(Suppl 1):S466
- Binding site characterization and resistance to a class of non-nucleoside inhibitors of the hepatitis C virus NS5B polymerase. J Biol Chem. 2005;280:39260–39267
- Effects of ribavirin monotherapy on ALT, HCV viral levels, serum cytokines, and hepatic interferon-stimulated gene expression in chronic hepatitis C (abstr 908). Hepatology. 2010;52(Suppl 1):756A
- Tolerance and efficacy of oral ribavirin treatment of chronic hepatitis C: a multicenter trial. Hepatology. 1997;26:473–477
- . Side effects of therapy of hepatitis C and their management. Hepatology. 2002;36(Suppl 1):S237–S244
- Peginterferon alfa-2b or alfa-2a with ribavirin for treatment of hepatitis C infection. N Engl J Med. 2009;361:580–593
- Surprisingly small effect of antiviral treatment in patients with hepatitis C. Ann Intern Med. 2002;136:288–292
- Predictors of treatment in patients with chronic hepatitis C infection—role of patient versus nonpatient factors. Hepatology. 2007;46:1741–1749
- Dual, triple, and quadruple combination treatment with a protease inhibitor (GS-9256) and a polymerase inhibitor (GS-9190) alone and in combination with ribavirin (RBV) or PegIFN/RBV for up to 28 days in treatment naïve, genotype 1 HCV subjects (abstr LB-1). Hepatology. 2010;52(Suppl 1):400A–401A
- VX-222 with TVR alone or in combination with peginterferon alfa-2a and ribavirin in treatment-naive patients with chronic hepatitis C: ZENITH study interim results (abstr 1363). J Hepatol. 2011;54(Suppl 1):S540
- Quadruple therapy with BMS-790052, BMS-650032 and Peg-IFN/RBV for 24 weeks results in 100% SVR12 in HCV genotype 1 null responders (abstr 1356). J Hepatol. 2011;54(Suppl 1):S536
- Once daily dual-nucleotide combination of PSI-938 and PSI-7977 provides 94% HCV RNA <LOD at Day 14: first purine/pyrimidine clinical combination data (the NUCLEAR study) (abstr 1370). J Hepatol. 2011;54(Suppl 1):S543
- The hepatitis C virus replicon presents a higher barrier to resistance to nucleoside analogs than to nonnucleoside polymerase or protease inhibitors. Antimicrob Agents Chemother. 2008;52:1604–1612
- . Resistance to direct antiviral agents in patients with hepatitis C virus infection. Gastroenterology. 2010;138:447–462
- Rapid emergence of protease inhibitor resistance in hepatitis C virus. Sci Transl Med. 2010;2:30–32
- Mechanisms of isolated unconjugated hyperbilirubinemia induced by the HCV NS3/4A protease inhibitor BI201335 (abstr 1236). J Hepatol. 2011;54(Suppl 1):S488
- . Bilirubin metabolism and its disorders. In: Zakim D, Boyer TD editor. Hepatology: a textbook of liver disease. 4th ed.. Philadelphia, PA: WB Saunders; 2003;p. 233–270
- In vitro studies investigating the mechanism of interaction between TMC435 and hepatic transporters (abstr 278). Hepatology. 2010;52(Suppl 1):461A
- Gilbert's disease and atazanavir: from phenotype to UDP-glucuronosyltransferase haplotype. Hepatology. 2006;44:1324–1332
- . Drug-induced liver injury associated with antiretroviral therapy that includes HIV-1 protease inhibitors. Clin Infect Dis. 2004;38(Suppl 2):S90–S97
- The antiviral efficacy of ribavirin priming (A follow up of 93 patients treated with ribavirin monotherapy followed by standard combination treatment (abstr 980)). Hepatology. 2010;52(Suppl 1):793A
Watch this article's video abstract and others at http://tiny.cc/j026c.
This article has an accompanying continuing education activity on page e14. Learning Objective: Upon completion of this CME activity, successful learners will be able to explain details on the design and results of the SOUND-C1 clinical trial (BI 201335, BI 207127 and RBV in treatment-naïve patients with chronic HCV GT-1 infection) and assess the potential for this regimen as a future treatment for this patient population.
Conflicts of interest The authors disclose the following: S.Z. is a consultant for Abbott Laboratories, Achillion Pharmaceuticals, Anadys Pharmaceuticals, Boehringer Ingelheim, Bristol-Myers Squibb, Gilead Sciences, iTherX, Janssen/Tibotec, Merck, Novartis, Pfizer, Pharmasset, Roche/Genentech, Santaris Pharma, and Vertex Pharmaceuticals. T.A. is a consultant for Boehringer Ingelheim, Bristol-Myers Squibb, Gilead Sciences, Janssen, Merck, Novartis, and Roche. J.-P.Z. is a consultant for Boehringer Ingelheim, Bristol-Myers Squibb, Gilead Sciences, Roche, Janssen, and Merck/Schering-Plough. D.L. is a consultant for Boerhinger Ingelheim, Bristol-Myers Squibb, Roche, Janssen, Merck, and Cytheris. B.M. is a consultant for MSD, Roche, Janssen, and Gilead Sciences. M.S. is a consultant for Bristol-Myers Squibb and Roche and a speaker for Bristol-Myers Squibb, Falk, Gilead Sciences, Merck, and Roche. A.L. has participated in trials for Boehringer Ingelheim, Roche, MSD, Janssen, and Falk and has received lecture fees from MSD, Roche, and Falk. S.P. is a consultant for Bristol-Myers Squibb, Boehringer Ingelheim, Tibotec/Janssen-Cilag, Gilead Sciences, Roche, Merck/Schering-Plough, and Abbott Laboratories; is a speaker for GlaxoSmithKline, Bristol-Myers Squibb, Boehringer Ingelheim, Tibotec/Janssen-Cilag, Gilead Sciences, Roche, and Schering-Plough; and has received grants from Bristol-Myers Squibb, Gilead Sciences, Roche, and Merck/Schering-Plough. J.-P.B. is a consultant for Boehringer Ingelheim, Bristol-Myers Squibb, Gilead Sciences, GlaxoSmithKline, Janssen, Merck, Novartis, and Roche. F.Z. is a consultant for Janssen, Schering-Plough, and Vertex Pharmaceuticals. M.H. is a consultant for Novartis, MSD, Roche, Jansen, and Gilead Sciences. J.O.S., G.K., G.N., C.H., and W.O.B. are employees of Boehringer Ingelheim. The remaining authors disclose no conflicts.
PII: S0016-5085(11)01248-0
doi: 10.1053/j.gastro.2011.08.051
© 2011 AGA Institute. Published by Elsevier Inc. All rights reserved.
« Previous
Next »
Gastroenterology
Volume 141, Issue 6
, Pages 2047-2055
, December 2011

