New Research in Emerging Role of Safinamide in Parkinson’s Disease Therapy

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European Neurological Review, a peer-reviewed, open access, bi-annual neurology journal publish cutting-edge article by Jaime Kulisevsky.

Chemical Structure of Safinamide

Chemical Structure of Safinamide

Safinamide improves motor symptoms, motor complications, quality of life and ‘on’ and ‘off’ time even in combination with other Parkinson’s disease (PD) medications

Parkinson’s disease (PD) is a neurodegenerative disorder characterised by the loss of dopaminergic neurons in the substantia nigra pars compacta – non-dopaminergic neurotransmission is also involved. In the basal ganglia circuitry there are many non-dopaminergic neurotransmitters and neuromodulators involved in the control of motor symptoms and implicated in the development of motor complications following long-term levodopa (LD) therapy. Indeed, PD is no longer seen purely as a disease of the dopaminergic system. In particular, overactive glutamate transmission plays a role in the progression of PD. Targeting non-dopaminergic systems is thus a complementary approach to improve and control such motor complications, removing the need for further increases in LD, which may otherwise worsen motor fluctuations.

Safinamide (see Figure 1) is an oral, once-a-day adjunctive therapy developed for any stage of PD. Safinamide is a unique molecule with novel mechanisms of action (dopaminergic and non-dopaminergic) that include monoamine oxidase-B (MAO-B) inhibition, sodium channel blockade and calcium channel modulation, thus inhibiting the excessive glutamate release. The sodium channel inhibition is concentration- and state-dependent, and does not influence physiological activity, avoiding depressant effects on the central nervous system (CNS). Safinamide does not affect L-type calcium channels (no effects in blood pressure and heart rate).

Safinamide is more selective for MAO-B versus MAO-A than selegiline and rasagiline: 1,000-fold in humans, compared with 127-fold for selegiline and 103-fold for rasagiline. This higher selectivity is related to the absence of diet restrictions pertaining to the clinical use of the drug. Moreover, the MAO-B inhibition is totally reversible, allowing better clinical manageability and limiting possible drug–drug interactions.

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