2. Academic Validation
  3. An orally available, small-molecule interferon inhibits viral replication

An orally available, small-molecule interferon inhibits viral replication

  • Sci Rep. 2012;2:259. doi: 10.1038/srep00259.
Hideyuki Konishi 1,  Koichi Okamoto,  Yusuke Ohmori,  Hitoshi Yoshino,  Hiroshi Ohmori,  Motooki Ashihara,  Yuichi Hirata,  Atsunori Ohta,  Hiroshi Sakamoto,  Natsuko Hada,  Asao Katsume,  Michinori Kohara,  Kazumi Morikawa,  Takuo Tsukuda,  Nobuo Shimma,  Graham R Foster,  William Alazawi,  Yuko Aoki,  Mikio Arisawa,  Masayuki Sudoh
Affiliations

Affiliation

  • 1 Kamakura Research Laboratories, Chugai Pharmaceutical Co. Ltd., Kamakura, Kanagawa, Japan.
PMID: 22355771 DOI: 10.1038/srep00259
Abstract

Most acute hepatitis C virus (HCV) infections become chronic and some progress to liver cirrhosis or hepatocellular carcinoma. Standard therapy involves an interferon (IFN)-α-based regimen, and efficacy of therapy has been significantly improved by the development of Protease Inhibitors. However, several issues remain concerning the injectable form and the side effects of IFN. Here, we report an orally available, small-molecule type I IFN receptor agonist that directly transduces the IFN signal cascade and stimulates Antiviral gene expression. Like type I IFN, the small-molecule compound induces IFN-stimulated gene (ISG) expression for Antiviral activity in vitro and in vivo in mice, and the ISG induction mechanism is attributed to a direct interaction between the compound and IFN-α receptor 2, a key molecule of IFN-signaling on the cell surface. Our study highlights the importance of an orally active IFN-like agent, both as a therapy for Antiviral infections and as a potential IFN substitute.

Figures
Products