Safinamide mesylateSafinamide mesylate
MedChemExpress (MCE)
HY-70057A
202825-46-5
FCE 26743 mesylate
EMD 1195686 mesylate
99.87%
4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months
-20°C, 1 month (sealed storage, away from moisture)
Room temperature in continental US
may vary elsewhere.
Safinamide (FCE 26743
EMD 1195686) mesylate is a potent, selective, and reversible monoamine oxidase B (MAO-B) inhibitor (IC50=0.098 μM) over MAO-A (IC50=580 nM). Safinamide mesylate also blocks sodium channels and modulates glutamate (Glu) release, showing a greater affinity at depolarized (IC50=8?μM) than at resting (IC50=262?μM) potentials. Safinamide mesylate has neuroprotective and neurorescuing effects and can be used for the study of parkinson disease, ischemia stroke et.al.
Safinamide mesylate (1-300?μM) reduces the amplitude of the peak sodium currents in a concentration-dependent manner.?When currents are stimulated to a?Vtest?of +10 mV from a?Vh?of -110 mV, the IC50?value was 262?μM. When the holding potential is depolarized to -53 mV, the inhibitory effect of Safinamide mesylate with a lower IC50?value (8?μM) in rat cortical neurons[1].
Safinamide mesylate (intraperitoneal?injection
90 mg/kg
once daily
14 days) treatment prior to MCAO significantly ameliorates MCAO-caused cerebral infarction volume, neurological deficit, disruption of the brain-blood barrier (BBB), and impairs expression of tight junction protein occludin and ZO-1 in mice[3].Safinamide mesylate (intraperitoneal?injection
5 mg/kg, 15 mg/kg and 30 mg/kg) dose dependently inhibits the veratridine-induced GABA release and Glu release in vivo. At the dose 30 mg/kg, ?Safinamide mesylate prevents the effect of veratridine both on Glu (treatment?F1,8=1.31
time×treatment interaction?F8,64=2.4) and GABA (treatment?F1,8=4.04
time?F8,64=3.76, time×treatment interaction?F8,64=2.83) release.Safinamide mesylate causes a slight, albeit not significant, reduction of veratridine-stimulated Glu release at 0.5 mg/kg and full inhibition at 5 and 15 mg/kg in rat[3].
MAO-B 98 nM (IC50) MAO-A 580 nM (IC50)
| | | |
| | | | | |
[1]. Leonetti F, et al. Solid-phase synthesis and insights into structure-activity relationships of safinamide analogues as potent and selective inhibitors of type B monoamine oxidase. J Med Chem, 2007, 50(20), 4909-4916. [Content Brief]
[2]. C Caccia, et al.Safinamide: from molecular targets to a new anti-Parkinson drug. Neurology. 2006 Oct 10
67(7 Suppl 2):S18-23. [Content Brief]
[3]. Michele Morari, et al. Safinamide Differentially Modulates In Vivo Glutamate and GABA Release in the Rat Hippocampus and Basal Ganglia.J Pharmacol Exp Ther. 2018 Feb
364(2):198-206. [Content Brief]