Yang S.-S.JIA-HORNG KAO2021-09-042021-09-0420151747-4124https://www.scopus.com/inward/record.uri?eid=2-s2.0-84918810280&doi=10.1586%2f17474124.2014.953930&partnerID=40&md5=30de1ef5b0593d7452062ca8b5a748cfhttps://scholars.lib.ntu.edu.tw/handle/123456789/581969Chronic hepatitis C virus (HCV) infection has been a tremendous health burden worldwide with an annual mortality of 300,000 people due to decompensated cirrhosis or hepatocellular carcinoma. A combination of interferon (IFN), ribavirin (RBV), and/or direct-acting antivirals (DAAs) can eradicate HCV in a various proportion of infected patients. Unfortunately, IFN-based therapy is associated with significant adverse effects, contraindications, and limited tolerability, leading to lower adherence or even treatment discontinuation. With the rapid evolution of newer DAAs or host-targeting agents, emerging HCV therapy is moving towards an IFN- and RBV-free strategy. To this end, a recently developed NS3 protease inhibitor, asunaprevir (ASV), in combination with other DAAs as IFN/RBV-containing or -free regimen, has shown promising results with fewer adverse effects. In this review, preclinical profiles and clinical proof-of-concept studies of ASV, including viral resistance, host polymorphism, and role of ASV in future HCV therapy are reviewed and discussed. ? 2015 Informa UK, Ltd.asunaprevir; direct-acting antivirals; hepatitis C virus; interferon; NS3 protease inhibitor; ribavirin[SDGs]SDG3alpha interferon; aminotransferase; asunaprevir; beclabuvir; bms 605339; ciluprevir; daclatasvir; nonstructural protein 3; nonstructural protein 4A; peginterferon alpha; peginterferon alpha2a; placebo; ribavirin; serine proteinase inhibitor; telaprevir; unclassified drug; antivirus agent; asunaprevir; isoquinoline derivative; NS3 protein, hepatitis C virus; proteinase inhibitor; sulfonamide; virus protein; antiviral activity; antiviral resistance; Article; asthenia; cardiovascular disease; diarrhea; drug disposition; drug dose reduction; drug exposure; drug fatality; drug liver level; drug potentiation; drug safety; drug structure; drug synthesis; drug tolerability; drug treatment failure; drug withdrawal; fatigue; fever; gastrointestinal symptom; genetic polymorphism; headache; hepatitis C; Hepatitis C virus; human; hyperbilirubinemia; liver cirrhosis; multiple drug dose; nausea; neutropenia; nonhuman; protein function; rhinopharyngitis; side effect; single drug dose; structure activity relation; unspecified side effect; virus inhibition; virus mutant; virus replication; animal; antagonists and inhibitors; drug combination; drug development; drug effects; enzymology; genetics; growth, development and aging; Hepacivirus; Hepatitis C, Chronic; metabolism; molecularly targeted therapy; treatment outcome; virology; Animals; Antiviral Agents; Drug Discovery; Drug Resistance, Viral; Drug Therapy, Combination; Hepacivirus; Hepatitis C, Chronic; Humans; Isoquinolines; Molecular Targeted Therapy; Protease Inhibitors; Sulfonamides; Treatment Outcome; Viral Nonstructural Proteins; Virus Replicationjournal article10.1586/17474124.2014.953930251742542-s2.0-84918810280