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BACKGROUND AND AIMS: ITX 5061 is a clinical stage small molecule compound that promotes high-density lipoprotein (HDL) levels in animals and patients by targeting the scavenger receptor BI protein pathway. Since SR-BI is a known co-receptor for HCV infection, we evaluated these compounds for their effects on HCV entry. METHODS: We obtained ITX 5061 and related compounds to characterize their interaction with SR-BI and effects on HCV entry and infection. RESULTS: We confirmed that a tritium-labeled compound analog (ITX 7650) binds cells expressing SR-BI, and both ITX 5061 and ITX 7650 compete for HDL-mediated lipid transfer in an SR-BI dependent manner. Both molecules inhibit HCVcc and HCVpp infection of primary human hepatocytes and/or human hepatoma cell lines and have minimal effects on HCV RNA replication. Kinetic studies suggest that the compounds act at an early post-binding step. CONCLUSIONS: These results suggest that the ITX compounds inhibit HCV infection with a mechanism of action distinct from other HCV therapies under development. Since ITX 5061 has already been evaluated in over 280 patients with good pharmacokinetic and safety profiles, it warrants proof-of-concept clinical studies in HCV infected patients.

Original publication

DOI

10.1016/j.jhep.2010.06.024

Type

Journal article

Journal

J Hepatol

Publication Date

01/2011

Volume

54

Pages

48 - 55

Keywords

Amides, Animals, Antiviral Agents, CHO Cells, Cell Line, Cricetinae, Cricetulus, Hepacivirus, Hepatitis C, Chronic, Hepatocytes, Humans, Kinetics, Lipoproteins, HDL, Receptors, Virus, Scavenger Receptors, Class B, Virus Internalization