Antiviral efficacy, as measured by the mean reduction in serum HBV DNA levels by PCR (log10 copies/mL) at Week 12, adjusted for baseline (Week 12 - baseline). A negative value = improvement.

As-randomized participants who completed 12 weeks of treatment

Antiviral efficacy, as measured by the mean reduction in serum HBV DNA levels by PCR (log10 copies/mL) at Week 48, adjusted for baseline (Week 48 - Baseline). A negative value = improvement.

Treated subjects who had both baseline and Week 12 HBV DNA measurements and who received the randomized treatment. 1 participant randomized to ADV actually received ETV and is not counted in secondary efficacy analyses.

Number of Subjects with HBV DNA <300 copies/mL by Roche COBAS® Amplicor (limit of quantitation 300 copies/mL)

Treated participants who had both baseline and Week 12 HBV DNA measurements and who received the randomized treatment. 1 participant randomized to ADV actually received ETV and is not counted in secondary efficacy analyses.

Number of participants with ALT ≤ 1 x upper limit of normal (ULN)

treated subjects who had both baseline and Week 12 HBV DNA measurements and who received the randomized treatment. 1 participant randomized to ADV actually received ETV and is not counted in secondary efficacy analyses.

The biphasic decline of HBV DNA is characterized via a 4-parameter exponential decay model previously published for HBV compounds. The model parameters of interest are the effectiveness of the drug in blocking virus production from infected cells (efficacy, ε) and effectiveness of the study treatment in blocking de novo infection of susceptible cells (η). The model parameters reflect the biphasic pattern that is typically observed after initiation of antiviral therapy. Parameters were estimated for each subject separately and then averaged within each treatment group.

Treated subjects who had both baseline and Week 12 HBV DNA measurements and who received the randomized treatment. 1 participant randomized to ADV actually received ETV and is not counted in secondary efficacy analyses.

The biphasic decline of HBV DNA is characterized via a 4-parameter exponential decay model previously published for HBV compounds. The model parameters of interest are the clearance rate of the free virus (c), the death rate of productively infected cells (δ), The model parameters reflect the biphasic pattern that is typically observed after initiation of antiviral therapy. Parameters were estimated for each subject separately and then averaged within each treatment group.

Treated subjects who had both baseline and Week 12 HBV DNA measurements and who received the randomized treatment. 1 participant randomized to ADV actually received ETV and is not counted in secondary efficacy analyses.

The biphasic decline of HBV DNA is characterized via a 4-parameter exponential decay model previously published for HBV compounds. An important derived parameter is the half-life of free virus (ie, the average amount of time for HBV particles in plasma to be reduced to half the initial level), calculated as 24*ln(2)/c. The model parameters reflect the biphasic pattern that is typically observed after initiation of antiviral therapy. Parameters were estimated for each subject separately and then averaged within each treatment group.

Treated subjects who had both baseline and Week 12 HBV DNA measurements and who received the randomized treatment. 1 participant randomized to ADV actually received ETV and is not counted in secondary efficacy analyses.

This analysis uses a 3-parameter piece-wise linear model and describes the biphasic decline in HBV DNA (measured by PCR assay) through Week 12. The 3 parameters are the values for the 2 slopes, describing the first and second phase declines, respectively, and the estimated HBV DNA at the knot (at day 10; the time point where the 2 phases join). The biphasic viral decay kinetics for each treatment were obtained using a spline fitting procedure to estimate the 3 parameters for each subject; these estimates were then averaged within each treatment group.

Treated subjects who had both baseline and Week 12 HBV DNA measurements and who received the randomized treatment. 1 participant randomized to ADV actually received ETV and is not counted in secondary efficacy analyses.

AE=new untoward medical occurrence or worsening of pre-existing medical condition regardless of causal relationship to treatment. SAE=untoward medical occurrence that is life-threatening, a congenital anomaly/birth defect, or an important medical event, or results in death, inpatient hospitalization/prolongation of hospitalization, or persistent/significant disability. AE grades: mild (1), moderate (2), severe (3), life-threatening (4), death (5). ALT flare= >2x baseline & >10x ULN up to end of therapy + 5 days. Hepatic SAE=SAEs consistent with worsening of hepatitis or hepatic decompensation.

As-treated population. 1 participant was randomized to ADV, but treated with ETV was counted in the ETV group.

Laboratory abnormalities reported as clinical AEs

As-treated population. 1 participant who was randomized to ADV, but treated with ETV was counted in the ETV group.