In the CORAL-I study, the safety and efficacy of Viekirax and dasabuvir with ribavirin for 24 weeks was studied in 34 HCV genotype 1-infected liver transplant recipients who were at least 12 months post transplantation at enrolment. The dose of ribavirin was left to the discretion of the investigator, with most patients receiving 600 to 800 mg per day as a starting dose, and most patients also receiving 600 to 800 mg per day at the end of treatment.

34 subjects (29 with HCV genotype 1a infection and 5 with HCV genotype 1b infection) were enrolled who had not received treatment for HCV infection after transplantation and had a METAVIR fibrosis score of F2 or less. 33 out of the 34 subjects (97.1%) achieved SVR12 (96.6% in subjects with genotype 1a infection and 100% in subjects with genotype 1b infection). One subject with HCV genotype 1a infection relapsed post-treatment.

Clinical trial in patients receiving opioid substitution therapy

In a phase 2, multicentre, open-label, single arm study, 38 treatment-naïve or pegIFN/RBV treatment experienced, non-cirrhotic subjects with genotype 1 infection who were on stable doses of methadone (N=19) or buprenorphine +/- naloxone (N=19) received 12 weeks of Viekirax and dasabuvir with ribavirin. Treated subjects had a median age of 51 years (range: 26 to 64); 65.8% were male and 5.3% were Black. A majority (86.8%) had baseline HCV RNA levels of at least 800,000 IU/mL and a majority (84.2%) had genotype 1a infection; 68.4% had IL28B non-CC genotype; 15.8% had portal fibrosis (F2) and 5.3% had bridging fibrosis (F3); and 94.7% were naïve to prior HCV treatment.

Overall, 37 (97.4%) of 38 subjects achieved SVR12. No subjects experienced on-treatment virologic failure or relapse.

Clinical trial in subjects with genotype 4 chronic hepatitis C

PEARL- I– genotype 4, treatment-naïve or peginterferon + ribavirin experienced

PEARL-I- was a randomised, global multicentre, open-label trial conducted in 135 adults with genotype 4 chronic hepatitis C virus infection without cirrhosis who were treatment-naïve or did not achieve SVR with prior treatment with pegIFN/RBV. Treatment naive subjects were randomised in a 1:1 ratio to receive ombitasvir, paritaprevir and ritonavir with or without ribavirin for 12 weeks of treatment. PegIFN/RBV-experienced subjects received ombitasvir, paritaprevir, and ritonavir in combination with ribavirin for 12 weeks

Treated subjects (N=135) had a median age of 51 years (range: 19 to 70); 63,7% were treatment-naïve, 17.0% were prior pegIFN/RBV null responders, 6.7% were prior pegIFN/RBV partial responders, 12.6% were prior pegIFN/RBV relapsers; 65.2%were male; 8.9% were Black, 14.1% had a body mass index of at least 30 kg/m²; 69.6% had baseline HCV RNA levels at least 800,000 IU/mL; 78.5% had IL28B non-CC genotype; 6.7% had bridging fibrosis (F3).

Table 16 shows the SVR12 rates for genotype 4 infected subjects, treatment-naïve or previously treated with pegIFN/RBV, who received ombitasvir, paritaprevir and ritonavir with or without ribavirin for 12 weeks in PEARL I.

Table 16. SVR12 for genotype 4-infected, subjects who were treatment-naïve or previously treated with pegIFN/RBV in PEARL I

VF = virologic failure

a. On-treatment VF was defined as confirmed HCV ≥ 25 IU/mL after HCV RNA < 25 IU/mL during treatme