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Imiquimod, an immune response modifier, is dependent on the OGF-OGFr signaling pathway
Date:7/24/2008

ation of OGF or knockdown of OGFr by siRNA technology eliminated the inhibitory effects of imidazoquinolines on cell replication. "Thus our data," Dr. Zagon said, "brings a paradigm shift to our thinking about a drug widely used in the clinics. Rather than imiquimod activity being mediated by induction of various cytokines, including interferon (IFN)-α, IFN-γ, tumor necrosis factor-α (TNFα) interleukin (IL)-1α, and IL-12 as currently thought, an entirely new pathway - native to body chemistry - has been discovered to regulate cell proliferation by imidazoquinolines." Co-author, Moshe Rogosnitzky adds: "The elucidation of imiquimod's immune-independent mechanism of action in cancer also creates exciting new therapeutic possibilities for a number of non-cancer conditions, and these are now being further explored. Such studies could lead to new off-label applications for imiquimod as well as development of imiquimod analogues and unique combination therapies." Dr. Steven R. Goodman, Editor-in-Chief of Experimental Biology and Medicine stated "Through decades of elegant and ground-breaking work, Zagon and colleagues have identified the role of met-enkephalin (the opioid growth factor OGF) and the OGF receptor in regulating cell proliferation. The current study demonstrates that the mechanism of imidazoquinoline activity is via OGF and OGFr which will have a profound impact on its use as a therapeutic for cancer and many other non-cancerous disorders."


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Contact: Dr. Ian S. Zagon
isz1@psu.edu
717-531-8650
Society for Experimental Biology and Medicine
Source:Eurekalert

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