Ropinirole is a selective dopamine (DA) agonist with nonergoline structure. 1,2 It interacts with D2-like receptors in vitro and in vivo, showing greatest affinity for the D3 subtype, with little or no interaction with other neurotransmitter receptors. Ropinirole produces alterations in motor behavior indicative of antiparkinsonian activity, including contralateral rotation in 6hydroxydopamine-lesioned rats and reversal of disability on MPTP-treated primates. The administration of ropinirole over a 4week period in L-dopa-naive MPTP-treated marmosets induces significantly less dyskinesia than observed with L-dopa treatment over the same period of time with comparable efficacy. 3 As expected from any effective D2 agonist, clinical pharmacology studies have shown ropinirole to lower serum prolactin levels, and to induce symptomatic postural hypotension, nausea and vomiting. In vitro, ropinirole illustrates some potential neuroprotective properties. 4
PHARMACOKINETICS
After oral administration, ropinirole is rapidly absorbed, and has a median Tmax of about 1.4 hours after dosing. It has a bioavailability of 46 % and a mean elimination half-life of about 6 hours. Ropinirole is recommended as a t.i.d. dosing regimen. Plasma protein binding is low and concentration independent. Ropinirole is metabolized predominantly by the liver. The drug is oxidized, mainly through the cytochrome P450 1A2 pathway. Drug interactions (macrolides, theophilline) and hepatic insufficiency are, therefore, theoretically possible, although no such events have been reported in the clinical literature.
REVIEW OF CLINICAL STUDIES PREVENTION OF DISEASE PROGRESSION
No qualified studies were identified that assessed the efficacy of ropinirole in the prevention of disease progression. A large, 2year, L-dopa-controlled study in de novo patients with PD, is ongoing and is assessing the effect of ropinirole on disease progression relative to L-dopa, as measured using both 18F-dopa PET and clinical ratings as endpoints.