Nitecapone (OR 462) was demonstrated to be well tolerated and modestly effective when administered to mice, rats, and monkeys (30-32). Its actions were confined to the periphery since it did not cross the blood-brain barrier (33), and its primary action appeared to be in the intestinal mucosa (34,35). In subsequent human studies, it was noted to "slightly but significantly" increase the relative bioavailability of lev-odopa and to reduce plasma 3-OMD (36), but it eventually ceded its place in clinical PD development to entacapone (OR 611), which was judged the more effective compound.

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