Skip Navigation


JAC Advance Access originally published online on July 29, 2009
Journal of Antimicrobial Chemotherapy 2009 64(4):741-746; doi:10.1093/jac/dkp274
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
64/4/741    most recent
dkp274v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Smee, D. F.
Right arrow Articles by Furuta, Y.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Smee, D. F.
Right arrow Articles by Furuta, Y.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2009. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Original research

Intracellular metabolism of favipiravir (T-705) in uninfected and influenza A (H5N1) virus-infected cells

Donald F. Smee1,*, Brett L. Hurst1, Hiroyuki Egawa2, Kazumi Takahashi2, Takumi Kadota2 and Yousuke Furuta3

1 Department of Animal, Dairy and Veterinary Sciences, Institute for Antiviral Research, Utah State University, Logan, UT, USA 2 Research Laboratories, Toyama Chemical Co. Ltd, Toyama, Japan 3 Business Development Department, Toyama Chemical Co. Ltd, Tokyo, Japan

Received 13 May 2009; returned 9 June 2009; revised 1 July 2009; accepted 6 July 2009


* Corresponding author. Tel: +1-435-797-2897; Fax: +1-435-797-3959; E-mail: don.smee{at}usu.edu

Objectives: To determine the metabolism of favipiravir (T-705, 6-fluoro-3-hydroxy-2-pyrazinecarboxamide) to its ribosylated, triphosphorylated form (T-705 RTP) in uninfected and influenza A/Duck/MN/1525/81 (H5N1) virus-infected cells. Effects of treatment on intracellular guanosine triphosphate (GTP) pools and influenza virus-inhibitory activity were also assessed.

Methods: A strong anion exchange HPLC separation method with UV detection was used to quantify T-705 RTP and GTP levels in Madin–Darby canine kidney cells. Antiviral activity was determined by virus yield reduction assay.

Results: Accumulation of T-705 RTP in uninfected cells increased linearly from 3 to 320 pmol/106 cells in cells exposed to 1–1000 µM extracellular T-705 for 24 h, approaching maximum levels by 9 h. Virus infection did not result in greater T-705 RTP accumulation compared with uninfected cells. Catabolism of T-705 RTP occurred after removal of T-705 from the extracellular medium, with a half-life of decay of 5.6 ± 0.6 h. Based upon these results, short-term incubation of T-705 with H5N1 virus-infected cells was predicted to provide an antiviral benefit. Indeed, 4–8 h 10–100 µM T-705 treatment of cells resulted in virus yield reductions, but less than continuous exposure. A 100-fold higher extracellular concentration of T-705 was required to inhibit intracellular GTP levels compared with ribavirin, which helps explain ribavirin's greater toxicity.

Conclusions: The favourable intracellular metabolic properties of T-705 combined with its reduced cell-inhibitory properties make this compound an attractive candidate for treating human influenza virus infections.

Keywords: antiviral , phosphorylation , guanosine triphosphate , RNA polymerase , ribavirin


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.