Safinamide is a selective and reversible inhibitor of monoamine oxidase B (MAO-B, IC50=98 nM) with greater than 100-fold selectivity over MAO-A (1). It has demonstrated anticonvulsant activity (2) and protection against kainate-induced seizures and hippocampal neurodegeneration in rat models (3). Safinamide decreases overactive glutamatergic signaling via use-dependent sodium channel blockade (4). It has been considered a potential therapeutic for Parkinson’s disease (5). It’s already demonstrated to be effective as an add-on to dopamine agonist therapy in early Parkinson’s (6).
1) Strolin Benedetti et al. (1994), The anticonvulsant FCE 26743 is a selective and short-acting MAO-B inhibitor devoid of inducing properties towards cytochrome P450-dependent testosterone hydroxylation in mice and rats J. Pharm. Pharmacol., 46 814
2) Fariello et al. (1998), Preclinical evaluation of PNU-151774E as a novel anticonvulsant; J. Pharmacol. Exp. Ther. 285 397
3) Maj et al. (1998), PNU-151774E protects against kainite-induced status epilepticus and hippocampal lesions in the rat; Eur, J. Pharmacol., 59 27
4) Gardoni et al. (2018), Safinamide Modulates Striatal glutamatergic Signaling in a Rat Model of Levodopa-Induced Dyskinesia; J. Pharamcol. Exp. Ther., 367 442
5) Caccia et al. (2006), Safinamide: from molecular targets to a new anti-Parkinson drug; Neurology, 67(7 Suppl. 2) S18
6) Schapira et al. (2013), Long-term efficacy and safety of safinamide as add-on therapy in early Parkinson’s disease; Eur. J. Neurol., 20 271
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