cebo for 12 weeks, after which they received open-label Viekirax and dasabuvir in combination with ribavirin for 12 weeks.
Treated subjects (N=631) had a median age of 52 years (range: 18 to 70); 54.5% were male; 5.4% were Black; 16.2% had a body mass index of at least 30 kg/m2; 15.2% had a history of depression or bipolar disorder; 69.3% had IL28B non-CC genotype; 79.1% had baseline HCV RNA levels of at least 800,000 IU/mL; 15.4% had portal fibrosis (F2) and 8.7% had bridging fibrosis (F3); 67.7% had HCV genotype 1a infection; 32.3% had HCV genotype 1b infection.
Table 7 shows the SVR12 rates for genotype 1-infected treatment-naïve subjects receiving Viekirax and dasabuvir in combination with ribavirin for 12 weeks in SAPPHIRE-I.
Table 7. SVR12 for genotype 1-infected treatment-naïve subjects in SAPPHIRE-I
CI = confidence interval, VF = virologic failure
a. On-treatment VF was defined as confirmed HCV ≥ 25 IU/mL after HCV RNA < 25 IU/mL during treatment, confirmed 1 log10 IU/mL increase in HCV RNA from nadir, or HCV RNA persistently ≥ 25 IU/mL with at least 6 weeks of treatment.
b. Relapse was defined as confirmed HCV RNA ≥ 25 IU/mL post-treatment before or during SVR12 window among subjects with HCV RNA less than 25 IU/mL at last observation during at least 11 weeks of treatment.
c. Other includes subjects not achieving SVR12 but not experiencing on-treatment VF or relapse (e.g. missing HCV RNA values in the SVR12 window).
No subjects with HCV genotype 1b infection experienced on-treatment virologic failure and one subject with HCV genotype 1b infection experienced relapse.
PEARL-III – genotype 1b, treatment-naïve
PEARL-III was a randomised, global multicentre, double-blind, controlled trial conducted in 419 treatment-naïve adults with genotype 1b chronic hepatitis C virus infection without cirrhosis. Subjects were randomised in a 1:1 ratio to receive Viekirax and dasabuvir with or without ribavirin for 12 weeks of treatment.
Treated subjects (N=419) had a median age of 50 years (range: 19 to 70), 45.8% were male; 4.8% were Black; 16.5% had a body mass index of at least 30 kg/m2; 9.3% had a history of depression or bipolar disorder; 79.0% had IL28B non-CC genotype; 73.3% had baseline HCV RNA of at least 800,000 IU/mL; 20.3% had portal fibrosis (F2) and 10.0% had bridging fibrosis (F3).
Table 8 shows the SVR12 rates for genotype 1b-infected treatment-naïve subjects who received either Viekirax and dasabuvir with ribavirin or Viekirax and dasabuvir without ribavirin for 12 weeks in PEARL III. In this study Viekirax and dasabuvir without ribavirin had similar SVR12 rates (100%) compared to Viekirax and dasabuvir with ribavirin (99.5%).
Table 8. SVR12 for genotype 1b-infected treatment-naïve subjects in PEARL III
CI = confidence interval, VF = virologic failure
a. On-treatment VF was defined as confirmed HCV ≥ 25 IU/mL after HCV RNA < 25 IU/mL during treatment, confirmed 1 log10 IU/mL increase in HCV RNA from nadir, or HCV RNA persistently ≥ 25 IU/mL with at least 6 weeks of treatment.
b. Relapse was defined as confirmed HCV RNA ≥ 25 IU/mL post-treatment before or during SVR12 window among subjects with HCV RNA less than 25 IU/mL at last observation during at least 11 weeks of treatment.
c. Other includes subjects not achieving SVR12 but not experiencing on-treatment VF or relapse (e.g. missing HCV RNA values
