Abstract
Most patients with chronic hepatitis C virus (HCV) genotype 1 infection who have had a previous null response (<2-log10 reduction in HCV RNA by treatment week 12) to peginterferon/ribavirin (PegIFN/RBV) do not achieve a sustained virological response (SVR) when re-treated with a first-generation HCV protease inhibitor (PI) administered in combination with PegIFN/RBV. We studied the incremental benefits associated with adding mericitabine (nucleoside analog inhibitor of HCV polymerase) to PI plus PegIFN alfa-2a/RBV-based therapy in two double-blind randomized multicenter phase 2 trials (with boceprevir in DYNAMO 1, and with telaprevir in DYNAMO 2). The primary endpoint in both trials was SVR, defined as HCV RNA <25 IU/mL 12 weeks after the end of treatment (SVR12). Overall, the addition of mericitabine to PI plus PegIFN alfa-2a/RBV therapy resulted in SVR12 rates of 60-70% in DYNAMO 1 and of 71-96% in DYNAMO 2. SVR12 rates were similar in patients infected with HCV genotype 1a and 1b in both trials. The placebo control arms in both studies were stopped because of high rates of virological failure. Numerically lower relapse rates were associated with longer treatment with mericitabine (24 versus 12 weeks), telaprevir-containing regimens, and regimens that included 48 weeks of PegIFN alfa-2a/RBV therapy. No mericitabine resistance mutations were identified in any patient in either trial. The addition of mericitabine did not add to the safety burden associated with either telaprevir or boceprevir-based regimens. These studies demonstrate increased SVR rates and reduced relapse rates in difficult-to-treat patients when a nucleoside polymerase inhibitor with intermediate antiviral potency is added to regimens containing a first-generation PI.
Trial registration:
ClinicalTrials.gov NCT01482403 and ClinicalTrials.gov NCT01482390.
Publication types
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Multicenter Study
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Randomized Controlled Trial
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Research Support, Non-U.S. Gov't
MeSH terms
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Adult
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Antibodies, Viral / biosynthesis
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Antibodies, Viral / blood
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Antimetabolites / therapeutic use
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Antiviral Agents / therapeutic use*
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Deoxycytidine / analogs & derivatives*
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Deoxycytidine / therapeutic use
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Double-Blind Method
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Drug Administration Schedule
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Drug Therapy, Combination / methods
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Female
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Genotype
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Hepacivirus / drug effects
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Hepacivirus / enzymology
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Hepacivirus / growth & development
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Hepatitis C, Chronic / drug therapy*
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Hepatitis C, Chronic / immunology
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Hepatitis C, Chronic / pathology
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Hepatitis C, Chronic / virology
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Humans
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Interferon-alpha / therapeutic use*
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Male
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Middle Aged
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Oligopeptides / therapeutic use*
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Polyethylene Glycols / therapeutic use*
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Proline / analogs & derivatives*
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Proline / therapeutic use
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Protease Inhibitors / therapeutic use
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RNA, Viral / antagonists & inhibitors
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RNA, Viral / genetics
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Recombinant Proteins / therapeutic use
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Ribavirin / therapeutic use*
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Treatment Outcome
Substances
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2'-fluoro-2'-methyl-3',5'-diisobutyryldeoxycytidine
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Antibodies, Viral
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Antimetabolites
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Antiviral Agents
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Interferon-alpha
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Oligopeptides
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Protease Inhibitors
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RNA, Viral
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Recombinant Proteins
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Deoxycytidine
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Polyethylene Glycols
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Ribavirin
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telaprevir
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N-(3-amino-1-(cyclobutylmethyl)-2,3-dioxopropyl)-3-(2-((((1,1-dimethylethyl)amino)carbonyl)amino)-3,3-dimethyl-1-oxobutyl)-6,6-dimethyl-3-azabicyclo(3.1.0)hexan-2-carboxamide
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Proline
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peginterferon alfa-2a
Associated data
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ClinicalTrials.gov/NCT01482390
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ClinicalTrials.gov/NCT01482403
Grants and funding
These studies were funded by F. Hoffmann-La Roche Ltd. F. Hoffmann-La Roche Ltd and its subsidiaries Roche Products Ltd and Genentech Inc. provided support in the form of salaries for authors [AS, AV, SLP, IN, JAT]. The funders participated in the design and conduct of the study, in the analysis and interpretation of the data and in the preparation and review of the manuscript before submission. The specific roles of these authors are articulated in the ‘author contributions’ section. Third-party medical writing assistance, but not editorial content development sufficient to meet International Committee of Medical Journal Editors (ICMJE) authorship criteria, was funded by F. Hoffmann-La Roche Ltd.