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Br J Dermatol. 2007 Dec;157 Suppl 2:8-13.

Imiquimod: mode of action.

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Rudolf Virchow Center, DFG Research Center for Experimental Biomedicine and Department of Dermatology, Julius-Maximilians-University, Würzburg, Germany.



Since imiquimod, a nucleoside analogue of the imidazoquinoline family, has shown efficacy against many tumour entities, its mode of action has become a focus of scientific interest.


The major biologic effects of imiquimod are mediated through agonistic activity towards toll-like receptors (TLR) 7 and 8, and consecutively, activation of nuclear factor-kappa B (NF-kappaB). The result of this activity is the induction of pro-inflammatory cytokines, chemokines and other mediators leading to activation of antigen-presenting cells and other components of innate immunity and, eventually, the mounting of a profound T-helper (Th1)-weighted antitumoral cellular immune response. Several secondary effects on the molecular and cellular level may also be explained, at least in part, by the activation of NF-kappaB. Moreover, independent of TLR-7 and TLR-8, imiquimod appears to interfere with adenosine receptor signalling pathways, and the compound causes receptor-independent reduction of adenylyl cyclase activity. This novel mechanism may augment the pro-inflammatory activity of the compound through suppression of a negative regulatory feedback mechanism which normally limits inflammatory responses. Finally, imiquimod induces apoptosis of tumour cells at higher concentrations. The pro-apoptotic activity of imiquimod involves caspase activation and appears to depend on B cell lymphoma/leukemia protein (Bcl)-2 proteins.


Overall, imiquimod acts on several levels, which appear to synergistically underlie the profound antitumoral activity of the compound.

[Indexed for MEDLINE]

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