Post-treatment relapse was confirmed in patients with HCV-RNA level less than 25 IU/mL at the end of treatment and subsequent HCV-RNA level of 25 IU/mL or greater in 2 consecutive measurements. Efficacy analyses were performed using the intent-to-treat population, defined as all randomized 5-FU supplier HCV genotype 1b–infected patients who received

at least one dose of coformulated ABT-450/ritonavir/ombitasvir. The safety population included all patients who received at least one dose of study drug. A population of 90 patients per treatment arm was calculated to provide greater than 90% power to achieve noninferiority of the active regimen to the historical threshold (64%). SAS software (SAS Institute,

Inc, Cary, NC) for the UNIX operating system was used for all analyses. All statistical tests and all confidence intervals were 2-sided with a significance level of .05. Patient screening began on August 14, 2012, and the final SVR12 data were collected on January 16, 2014. Of 324 patients screened, 187 were randomized and 186 received study drug (91 in group 1, 95 in group 2) (Supplementary Consort Flow Chart). Null responders, partial responders, and relapsers to previous pegIFN/RBV treatment comprised 34.9%, 28.5%, and Protein Tyrosine Kinase inhibitor 36.6% of the study population, respectively,

evenly stratified between treatment arms (Table 1). Reasons for screen failures are provided in the Supplementary Appendix. Seven randomized patients, 3 in group 1 and 4 in group 2, were not included in the intent-to-treat efficacy population. Of these, 6 patients were enrolled before a protocol amendment and received noncoformulated ABT-450/ritonavir/ombitasvir, 3 of whom were genotype 1a; a seventh patient’s HCV subgenotype was not determined. After 12 weeks of treatment, 96.6% (85 of 88; 95% CI, 92.8–100) of group 1 and 100% (91 of 91; 95% CI, 95.9–100) PIK3C2G of group 2 patients achieved SVR12 using the intent-to-treat population for both groups (Figure 1; Table 2, Supplementary Figure 2). For the primary end point, SVR12 rates in both treatment groups were noninferior to the historical SVR rate for telaprevir plus pegIFN/RBV in comparable treatment-experienced patients. Both treatment groups also were superior to the historical rate. Noninferiority of group 2 to group 1 was shown because the treatment difference in SVR12 rates was 3.4% (95% CI, -0.4 to 7.2). No patients from either treatment group experienced on-treatment virologic failure or post-treatment relapse. Of the 3 patients in group 1 who did not achieve SVR12, there were 2 (2.