No cirrhosis or compensated cirrhosis** No HBV or HIV co-infection HCV-trial.com COMMAND-3 Study: DCV vs TVR, in combination with PEG-IFN + RBV, for genotype 1a or 1b Design Randomisation* 2 : 1 Open-label ≥ 18 years Chronic HCV infection, Genotype 1a or 1b HCV RNA ≥ 10 000 IU/ml Treatment-naive No cirrhosis or compensated cirrhosis** No HBV or HIV co-infection N = 402 DCV + PEG-IFN + RBV (1) TVR + PEG-IFN + RBV (2) N = 200 * Randomisation was stratified on genotype (1a or 1b), IL28B (CC or non-CC), cirrhosis (yes or no) ** Liver biopsy or Fibroscan > 14.6 kPa (1): 24 weeks if undetectable HCV-RNA at W4 and W12 (eRVR) ; additional 24 weeks of PEG-IFN + RBV otherwise (2): 12 weeks + 12 weeks (if eRVR) or 36 weeks of PEG-IFN + RBV DCV: 60 mg qd ; TVR 750 mg tid ; PEG-IFNa-2a: 180 mg SC once weekly RBV: 1000 or 1200 mg/day (bid dosing) according to body weight (< or ≥ 75 kg) Objective Primary endpoint: SVR12 (HCV RNA < 25 IU/ml), with 2-sided 95% CI, noninferiority of DCV vs TVR in genotype 1b, lower margin of -12%, 91% power COMMAND-3 Jacobson I. World J Gastroenterol 2016;22:3418-31 1

Baseline characteristics and patient disposition COMMAND-3 Study: DCV vs TVR, in combination with PEG-IFN + RBV, for genotype 1a or 1b Baseline characteristics and patient disposition Genotype 1b Genotype 1a DCV N = 268 TVR N = 134 N = 66 Median age, years 46 48 49 51.5 Female 41% 46% 27% 29% Race : white / black 91% / 6% 96% / 2% 90% / 8% 96% / 3% IL28B CC genotype 20% 31% 30% HCV RNA log10 IU/ml, mean 6.23 6.30 6.31 Cirrhosis 9.7% 11.2% 11.9% 13.6% Discontinuation Virologic breakthrough Futility Lack of efficacy Adverse event Patient request Lost to follow-up Withdrew consent / other 39 11 3 1 14 6 20 17 2 44 4 8 COMMAND-3 Jacobson I. World J Gastroenterol 2016;22:3418-31 2

SVR12 (HCV RNA < 25 IU/ml) , mITT COMMAND-3 Study: DCV vs TVR, in combination with PEG-IFN + RBV, for genotype 1a or 1b SVR12 (HCV RNA < 25 IU/ml) , mITT 25 50 100 75 81.3 * % 85.1 * N = 134 66 268 69.7 64.9 DCV, genotype 1a TVR genotype 1a DCV, genotype 1b TVR, genotype 1b * Difference between treatment arms : 4.3% (95% CI: -3.3% to 11.9%) noninferiority Virologic breakthrough 11 NA Futility 3 4 HCV-RNA mssing/detectable at EOT 7 14 Relapse 12 20 9 Missing post treatment W12 data 2 COMMAND-3 Jacobson I. World J Gastroenterol 2016;22:3418-31 3

SVR12 in genotype 1b, by subgroups, mITT COMMAND-3 Study: DCV vs TVR, in combination with PEG-IFN + RBV, for genotype 1a or 1b SVR12 in genotype 1b, by subgroups, mITT IL28B 53 Cirrhosis 214 27 107 15 10 17 96.2 85.2 86.0 83.2 82.2 80.4 76.9 66.7 91.7 89.2 82.7 78.4 CC Non-CC No Yes Baseline HCV RNA < 800 000 IU/ml 25 50 100 75 % n DCV, genotype 1b TVR, genotype 1b COMMAND-3 Jacobson I. World J Gastroenterol 2016;22:3418-31 4

Resistance analysis in genotype 1b COMMAND-3 Study: DCV vs TVR, in combination with PEG-IFN + RBV, for genotype 1a or 1b Resistance analysis in genotype 1b NS5A population-based sequencing data At baseline, N = 249/268 43 (17.5%): ≥ 1 of NS5A polymorphisms L28M/V, R30H/Q, L31M or Y93H SVR12: 72.1% if NS5A polymorphisms vs 87% if no NS5A polymorphisms At virologic failure, N = 32/40 Same NS5A RAVs at baseline and failure, N = 2 Treatment-emergent NS5A RAVS, N = 30 L31F/I/M/V, N = 22 Y93H, N = 21 L31 and Y93 together, N = 18 COMMAND-3 Jacobson I. World J Gastroenterol 2016;22:3418-31 5

COMMAND-3 Study: DCV vs TVR, in combination with PEG-IFN + RBV, for genotype 1a or 1b Adverse events, N or % DCV + PEG-IFN + RBV N = 402 TVR + PEG-IFN + RBV N = 200 Serious adverse event, N (%) Drug-related SAE, N (%) 26 (6.5) 14 (3.5) * 20 (10) 16 (8) *, ** Death, N (%) (both unrelated) 1 (0.2) 1 (0.5) AE leading to discontinuation of any drug, N (%) 28 (7) 37 (18.5) AE leading to discontinuation of all 3 study drugs, N (%) 25 (6.2) 25 (12.5) Adverse event in ≥ 20% in either group, % Fatigue Headache Asthenia Pruritus Anemia Rash Nausea Neutropenia Alopecia Influenza-like illness Dry skin Pyrexia 34.8 34.1 27.2 26.6 23.9 23.1 21.9 21.6 21.4 21.1 20.9 19.9 40.5 28.5 26.5 37.5 49.5 34.5 37.0 13.5 16.0 19.0 17.0 21.0 * 1 case of DRESS in each group, ** 5 cases of anemia COMMAND-3 Jacobson I. World J Gastroenterol 2016;22:3418-31 6

Grade 3 or 4 emergent laboratory abnormalities, N (%) COMMAND-3 Study: DCV vs TVR, in combination with PEG-IFN + RBV, for genotype 1a or 1b Grade 3 or 4 emergent laboratory abnormalities, N (%) DCV + PEG-IFN + RBV N = 402 TVR + PEG-IFN + RBV N = 200 Hemoglobin 26 (6.5) 41 (20.5) Absolute neutrophil count 104 (25.9) Lymphocytes 67 (16.7) 44 (22) Platelet count 15 (3.7) 8 (4) ALT 3 (0.7) 4 (2) AST 7 (1.7) 1 (0.5) Total bilirubin 4 (1) 6 (3) Serum creatinine increased 1 (0.2) Safety secondary endpoints Hemoglobin < 10 g/dl in genotype 1b significantly lower in DCV vs TVR group (18.3% vs 47.4% ; 95% CI for difference: - 38.3% to – 19.4%) Grade 1-4 rash in genotype 1 not significantly different: 23.1% for DCV vs 34.5% for TVR (grade 3-4: 1.0% vs 3.5%) COMMAND-3 Jacobson I. World J Gastroenterol 2016;22:3418-31 7

COMMAND-3 Study: DCV vs TVR, in combination with PEG-IFN + RBV, for genotype 1a or 1b Summary This head-to-head comparison of two classes of DAAs in treatment naive genotype 1b infected patients demonstrates that DCV + PEG-IFN + RBV is noninferior to TVR + PEG-IFN + RBV for SVR12 High SVR12 was achieved in genotype 1b infected patients across all subgroups of baseline factors known to affect response rates to PEG-IFN + RBV (cirrhosis, IL28B genotype, age, sex, baseline viral load) In difficult-to-cure patients with cirrhosis, SVR12 was higher with DCV + PEG-IFN + RBV than with TVR+ PEG-IFN + RBV (76.9% vs 66.7%) Post treatment relapse was more frequent with TVR than with DCV (15% vs 5%), for genotype 1b SVR12 with DCV + PEG-IFN + RBV was lower and virologic failure was more frequent in patients infected with genotype 1a Lower resistance barrier of DCV in genotype 1a ? DCV + PEG-IFN + RBV was generally well tolerated, with a significantly lower rate of anemia, and an observed lower rate of rash-related events compared with TVR+ PEG-IFN + RBV COMMAND-3 Jacobson I. World J Gastroenterol 2016;22:3418-31 8