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Drug News Perspect 2008, 21(2): 69
ISSN 0214-0934
Copyright 2008 Clarivate
CCC: 0214-0934


The mechanism of action of imiquimod and related imidazoquinolines in stimulating innate and acquired Th1 immunity allows these compounds to exhibit antiviral activity against a variety of viruses as well as against certain other intracellular pathogens.

The Antiviral Activity of Toll-Like Receptor 7 and 7/8 Agonists

by Richard L. Miller, Tze-Chiang Meng and Mark A. Tomai


Imiquimod 5% cream is approved for the topical treatment of external anogenital warts caused by human papillomavirus (HPV) and for the skin cancer conditions superficial basal cell carcinoma and actinic keratosis. This drug is the first approved topically active Toll-like receptor (TLR) 7 agonist. Imiquimod activates innate immune cells to produce interferon-a and other cytokines. The induced cytokine cascade, in combination with effects in enhancing antigen presentation, also promotes an antigen-specific T helper type 1 cell-mediated immune response. This immune-based mechanism provides activity against a number of viruses and other intracellular pathogens. Imiquimod was effective topically in clinical studies for HPV but caused mixed results for Molluscum contagiosum, and herpes simplex virus (HSV). Activity against several other viruses were reported in case reports or patient series involving "off-label" usage of imiquimod, while others were evaluated only in preclinical models. Resiquimod, a more potent investigational analogue of imiquimod with mixed TLR7/8 agonist activity, was evaluated in clinical studies topically for the treatment of HSV and systemically for hepatitis C virus also with mixed success. This review focuses on the mechanism of action and antiviral usage reported for the TLR7 agonist imiquimod, the TLR7/8 agonist resiquimod and related imidazoquinoline analogues. Copyright 2008 Prous Science, S.A.U. or its licensors. All rights reserved.

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