PEARL-IV – genotype 1a, treatment-naïve

PEARL-IV was a randomised, global multicentre, double-blind, controlled trial conducted in 305 treatment-naïve adults with genotype 1a chronic hepatitis C virus infection without cirrhosis. Subjects were randomised in a 1:2 ratio to receive Viekirax and dasabuvir with or without ribavirin for 12 weeks of treatment.

Treated subjects (N=305) had a median age of 54 years (range: 19 to 70); 65.2% were male; 11.8% were Black; 19.7% had a body mass index of at least 30 kg/m²; 20.7% had a history of depression or bipolar disorder; 69.2% had IL28B non-CC genotype; 86.6% had baseline HCV RNA levels of at least 800,000 IU/mL; 18.4% had portal fibrosis (F2) and 17.7% had bridging fibrosis (F3).

Table 9 shows the SVR12 rates for genotype 1a-infected, treatment-naïve subjects who received Viekirax and dasabuvir with or without ribavirin for 12 weeks in PEARL IV. Viekirax and dasabuvir without ribavirin was not non-inferior to Viekirax and dasabuvir with ribavirin.

Table 9. SVR12 for genotype 1a-infected treatment-naïve subjects in PEARL IV

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).

Clinical trials in peginterferon+ribavirin-experienced adults

SAPPHIRE-II – genotype 1, peginterferon+ribavirin-experienced

SAPPHIRE-II was a randomised, global multicentre, double-blind, placebo-controlled trial conducted in 394 subjects with genotype 1 chronic hepatitis C virus infection without cirrhosis who did not achieve SVR with prior treatment with pegIFN/RBV. Viekirax and dasabuvir in combination with ribavirin were given for 12 weeks of treatment. Subjects randomised to the placebo arm received placebo for 12 weeks, after which they received Viekirax and dasabuvir in combination with ribavirin for 12 weeks.

Treated subjects (N=394) had a median age of 54 years (range: 19 to 71); 49.0% were prior pegIFN/RBV null responders; 21.8/% were prior pegIFN/RBV partial responders, and 29.2% were prior pegIFN/RBV relapsers; 57.6% were male; 8.1% were Black; 19.8% had a body mass index of at least 30 kg/m²; 20.6% had a history of depression or bipolar disorder; 89.6% had IL28B non-CC genotype; 87.1% had baseline HCV RNA levels of at least 800,000 IU per mL; 17.8% had portal fibrosis (F2) and 14.5% had bridging fibrosis (F3); 58.4% had HCV genotype 1a infection; 41.4% had HCV genotype 1b infection.

Table 10 shows the SVR12 rates for treatment-experienced subjects with genotype 1-infection receiving Viekirax and dasabuvir in combination with ribavirin for 12 weeks in SAPPHIRE-II.

Table 10. SVR12 for genotype 1-infected peginterferon+ribavirin-experienced subjects in SAPPHIRE-II

CI = confidence interval, VF = virologic failure

a. On-treatment VF was defined as confirmed HCV ≥ 25 IU/mL after HCV R