ve Exviera and ombitasvir/paritaprevir/ritonavir with or without ribavirin for 12 weeks of treatment.
Treated subjects (N=179) had a median age of 57 years (range: 26 to 70); 35.2% were prior pegIFN/RBV null responders; 28.5% were prior pegIFN/RBV partial responders; and 36.3% were prior pegIFN/RBV relapsers; 54.2% were male; 3.9% were Black; 21.8% had a body mass index of at least 30 kg/m2; 12.8% had a history of depression or bipolar disorder; 90.5% had IL28B non-CC genotype; 87.7% had baseline HCV RNA levels of at least 800,000 IU/mL; 17.9% had portal fibrosis (F2) and 14.0% had bridging fibrosis (F3).
Table 11 shows the SVR12 rates for genotype 1b-infected, treatment-experienced subjects who received Exviera and ombitasvir/paritaprevir/ritonavir with or without ribavirin for 12 weeks in PEARL II. In this study, Exviera and ombitasvir/paritaprevir/ritonavir without ribavirin had a similar SVR12 rate (100%) compared to Exviera and ombitasvir/paritaprevir/ritonavir with ribavirin (97.7%).
Table 11. SVR12 for genotype 1b-infected peginterferon+ribavirin-experienced subjects in PEARL II
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 SVR4 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).
Clinical trial in subjects with compensated cirrhosis
TURQUOISE-II– genotype 1, treatment-naïve or peginterferon+ribavirin-experienced subjects with compensated cirrhosis
TURQUOISE-II was a randomised, global multicentre, open-label trial conducted exclusively in 380 genotype 1-infected subjects with compensated cirrhosis (Child-Pugh A) who were either treatment-naïve or did not achieve SVR with prior treatment with pegIFN/RBV. Exviera and ombitasvir/paritaprevir/ritonavir in combination with ribavirin were administered for either 12 or 24 weeks of treatment.
Treated subjects (N=380) had a median age of 58 years (range: 21 to 71); 42.1% were treatment-naïve, 36.1% were prior pegIFN/RBV null responders; 8.2% were prior pegIFN/RBV partial responders, 13.7% were prior pegIFN/RBV relapsers; 70.3% were male; 3.2% were Black; 28.4% had a body mass index of at least 30 kg/m2; 14.7% had platelet counts of less than 90 x 109/L; 49.7% had albumin less than 40 g/L; 86.1% had baseline HCV RNA levels of at least 800,000 IU/mL; 81.8% had IL28B non-CC genotype; 24.7% had a history of depression or bipolar disorder; 68.7% had HCV genotype 1a infection, 31.3% had HCV genotype 1b infection.
Table 12 shows the SVR12 rates for genotype 1-infected subjects with compensated cirrhosis who were treatment-naïve or previously treated with pegIFN/RBV.
Table 12. SVR12 for genotype 1-infected subjects with compensated cirrhosis who were treatment-naïve or previously treated with pegIFN/RBV
CI = confidence interval, VF = virologic failure
a. 97.5% confidence intervals are used for the primary efficacy endpoints (overall SVR12 rate); 95% confidence intervals are used for additional efficacy endpoints (SVR12 |
