Catalog No.S1445 Synonyms: CI-912
Molecular Weight(MW): 212.23
Zonisamide is a voltage-dependent sodium channel and T-type calcium channel blocker, used as an antiepileptic drug.
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Choose Selective Sodium Channel Inhibitors
|Description||Zonisamide is a voltage-dependent sodium channel and T-type calcium channel blocker, used as an antiepileptic drug.|
Zonisamide inhibits monoamine oxidase B (MAO-B) activity in vitro with an IC(50) of 25 μM. 
|In vivo||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. |
-  Sonsalla PK, et al. Exp Neurol, 2010, 221(2), 329-334.
-  Tanabe M, et al. Naunyn Schmiedebergs Arch Pharmacol, 2005, 372(2), 107-114.
-  Hayakawa T, et al. Eur J Pharmacol, 1994, 257(1-2), 131-136.
|In vitro||DMSO||42 mg/mL (197.89 mM)|
|Ethanol||5 mg/mL (23.55 mM)|
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT02049073||Not yet recruiting||Noise-induced Hearing Loss||Washington University School of Medicine||June 2017||Phase 1|Phase 2|
|NCT02900352||Recruiting||Alcohol Use Disorder||Yale University||October 2016||Phase 1|
|NCT02901041||Not yet recruiting||Alcohol Dependence||Boston University|Mclean Hospital|University of Houston||September 2016||Phase 3|
|NCT02707965||Not yet recruiting||Epilepsy||Food and Drug Administration (FDA)|University of Maryland||March 2016||--|
|NCT02368431||Recruiting||Alcohol Use Disorder||VA Office of Research and Development||March 2015||Phase 3|
|NCT01847469||Recruiting||Alcohol Dependence|Post-Traumatic Stress Disorder (PTSD)||Yale University|United States Department of Defense||June 2013||Phase 2|
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