HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Figures Only Full Text Correspondence: Submit a response Alert me when this article is cited Alert me when Correspondence are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Caccia, C. Articles by Fariello, R. G. Search for Related Content PubMed PubMed Citation Articles by Caccia, C. Articles by Fariello, R. G.

Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represent the opinions of the authors and are not endorsed by nor do they reflect the views of the American Academy of Neurology, Editor-in-Chief, or Associate Editors of Neurology.

Safinamide

From molecular targets to a new anti-Parkinson drug

From Newron Pharmaceuticals Spa, Bresso (MI), Italy (C.C., M.C., S.M., L.F., L.C., P.S., R.G.F.), and Mondo Biotech, Gentilino, Switzerland (R.M.).

Address correspondence and reprint requests to Dr. Carla Caccia, Newron Pharmaceuticals Spa, Via Ludovico Ariosto 21, 20091 Bresso (MI), Italy; e-mail: carla.caccia{at}newron.com

Ideal treatment in Parkinson’s disease (PD) aims at relieving symptoms and slowing disease progression. Of all remedies, levodopa remains the most effective for symptomatic relief, but the medical need for neuroprotectant drugs is still unfulfilled. Safinamide, currently in phase III clinical trials for the treatment of PD, is a unique molecule with multiple mechanisms of action and a very high therapeutic index. It combines potent, selective, and reversible inhibition of MAO-B with blockade of voltage-dependent Na⁺ and Ca²⁺ channels and inhibition of glutamate release. Safinamide has neuroprotective and neurorescuing effects in MPTP-treated mice, in the rat kainic acid, and in the gerbil ischemia model. Safinamide potentiates levodopa-mediated increase of DA levels in DA-depleted mice and reverses the waning motor response after prolonged levodopa treatment in 6-OHDA-lesioned rats. Safinamide has excellent bioavailability, linear kinetics, and is suitable for once-a-day administration. Therefore, safinamide may be used in PD to reduce l-dopa dosage and also represents a valuable therapeutic drug to test disease-modifying potential.

Publication of this supplement was supported by a grant from Newron Pharmaceuticals.

Disclosure: C.C., R.M., M.C., L.F., L.C., and P.S. are employees of the sponsor and have an equity interest or ownership interest in the sponsor. S.M. is an employee of the sponsor. R.G.F. was an employee of the sponsor until May 2005.

Neurology supplements are not peer-reviewed. Information contained in Neurology supplements represents the opinions of the authors and is not endorsed by nor does it reflect the views of the American Academy of Neurology, Editorial Board, Editor-in-Chief, or Associate Editors of Neurology.

This article has been cited by other articles:

				F. Stocchi, L. Vacca, P. Grassini, M. F. De Pandis, G. Battaglia, C. Cattaneo, and R. G. Fariello Symptom relief in Parkinson disease by safinamide: Biochemical and clinical evidence of efficacy beyond MAO-B inhibition. Neurology, October 10, 2006; 67(7 Suppl 2): S24 - S29. [Abstract] [Full Text]