Safinamide mesylate

Research use only, not for human use.

Safinamide Mesylate, a mesylate salt of Safinamide, can reversibly and specifically inhibit MAO-B (IC50: 98 nM), has 5918-fold selectivity against MAO-A.

Safinamide Mesylate, a mesylate salt of Safinamide, can reversibly and specifically inhibit MAO-B (IC50: 98 nM), has 5918-fold selectivity against MAO-A.(In Vitro):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.(In Vivo):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.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.

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.

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.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.

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Microbiology/Virology

Antifungal

MAO

Neurological Disease

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202825-46-5

398.45

C18H23FN2O5S

>98% (HPLC)

In Vitro:?DMSO : 250 mg/mL (627.43 mM)

CS(=O)(=O)O.C[C@H](NCc1ccc(OCc2cc(F)ccc2)cc1)C(=O)N

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(-20℃)

With Ice Pack

≥ 2 years