ABSTRACT
O-methylation, catalyzed by the enzyme catechol-O-methyl transferase (COMT), converts levodopa to a clinically inactive metabolite. One class of antiparkinsonian medications has been developed to inhibit this enzymatic pathway in an attempt to augment the effect of levodopa on Parkinson’s disease (PD) symptoms. Subsequent clinical investigation of COMT inhibition in PD patients has led to further refinement of how to utilize these medications. This chapter will focus on entacapone, the most widely used inhibitor of COMT. The biochemistry, pharmacology, toxicology, and clinical controversies surrounding entacapone will be reviewed.
