Rapid proliferation of human carcinoma results in increased levels of reactive oxygen species (ROS). This, in turn, results in elevated activity of ROS mediated pathways. Development of small molecules capable of disrupting these pathways through multiple mechanisms would provide insight as to how cancers tolerate increased ROS and indicate potential synergistic effects of small molecules capable of targeting multiple regulatory pathways. To this end, Au (I)-ferrocenylated <i>N</i>-heterocyclic carbenes capable of targeting specific ROS mediated pathways were designed, synthesized, and their drug mechanism of action elucidated in human cancer models.

Disrupting reactive oxygen species mediated pathways in human cancer models with ferrocenylated <i>N</i>-heterocyclic carbenes

249th National Meeting (2015)

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Disrupting reactive oxygen species mediated pathways in human cancer models with ferrocenylated N-heterocyclic carbenes