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Original article

Rapid and sharp decline in HCV upon monotherapy with NS3 protease inhibitor, ACH-1625

Atul Agarwal, Bao Zhang, Elizabeth Olek, Heather Robison, Lisa Robarge, Milind Deshpande

Corresponding author name: Atul Agarwal
Corresponding author e-mail: aagarwal@achillion.com

Citation: Antiviral Therapy 2012; 17:1533-1539
doi: 10.3851/IMP2359

Date accepted: 03 April 2012
Date published online: 13 September 2012


Background: ACH-1625 is a linear peptidomimetic inhibitor that non-covalently binds to HCV NS3 protease with high potency and specificity. Short-term monotherapy of HCV genotype-1 infection with ACH-1625 was found to be safe and resulted in ≥3.3 log10 IU/ml mean viral load reduction. These viral load decay data were analysed to compare HCV dynamics with prior reports and estimate the antiviral efficiency of ACH-1625.

Methods: Drug efficiency was estimated by analysing the viral decay following initiation of up to 5 days of monotherapy with ACH-1625 in 36 chronically infected HCV genotype-1 patients. During this monotherapy study, ACH-1625 was administered either twice-a-day for 4.5 days or once daily for 5 days at 5 different dose levels in 36 patients.

Results: A sharp viral decay during the first 48 h following the initiation of ACH-1625 treatment afforded high drug efficiency estimates (≥0.9934). In addition, an increase in the estimated drug efficiency was observed with increasing ACH-1625 dose. The observed anti-HCV response was fairly uniform in this proof-of-concept study across the population of 36 patients.

Conclusions: Estimates of the treatment-independent viral kinetics parameters were consistent with prior reports and the estimated drug efficiency of ACH-1625 monotherapy was very high (≥0.9934) in fasted and fed states.


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