Zonisamide is a sulfonamide anticonvulsant approved for use as an adjunctive therapy in adults with partial-onset seizures. Zonisamide may be a carbonic anhydrase inhibitor although this is not one of the primary mechanisms of action. Zonisamide may act by blocking repetitive firing of voltage-gated sodium channels leading to a reduction of T-type calcium channel currents, or by binding allosterically to GABA receptors. This latter action may inhibit the uptake of the inhibitory neurotransmitter GABA while enhancing the uptake of the excitatory neurotransmitter glutamate.

98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

AD 810; CI 912

Soluble in DMSO

Sodium channel

Zonisamide inhibits monoamine oxidase B (MAO-B) activity in vitro with an IC(50) of 25 μM.

Zonisamide modifies dopamine (DA) activity, provides protection in ischemia mice models and influences antioxidant systems. Zonisamide attenuates the reduction in striatal contents of DA, its metabolite DOPAC and tyrosine hydroxylase (TH). Zonisamide (10 and 30 mg/kg) produces antihyperalgesic and antiallodynic effects in a dose-dependent manner, these effects are manifested by elevation of the withdrawal threshold in response to a thermal (plantar test) or mechanical (von Frey) stimulus, respectively.. Zonisamide produces antinociceptive effects against acute thermal and mechanical nociception in non-ligated mice. Zonisamide reduces the cortical infarction volume to 6% from 68% in vehicle-treated controls and the striatal volume to 8% from 78% in rats. Zonisamide also reduces neuronal necrosis in 5 hippocampal regions (the dentate gyrus, CA4, CA3, CA1, and the subiculum) in rats. Zonisamide causes increase in the quantity of EAAC-1 protein in hippocampus and cortex and down regulation of the GABA transporter GAT-1 in rats with hippocampal seizures. Zonisamide inhibits both the 50 mM KCl-evoked hippocampal glutamate release (AUC for 60 min) from 9.2 mM to 5.8 mM in urethane-anaesthetized rats, as well as the stimulatory effects of Ca2+ on KCl-evoked hippocampal glutamate release.

1. Tsujii S, et al. Eur J Pharmacol. 2015 Jan 5;746:301-7.

2. Sano H, et al. J Neurochem. 2015 Apr 10.

3. Eskandari D, et al. Eur Respir J. 2014 Jul;44(1):140-9.