Glucose oxidase compositions as a neonate anticonvulsant
AssigneeThe Penn State Research Foundation
InventorsGong Chen, Zheng Wu
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AssigneeThe Penn State Research Foundation
InventorsGong Chen, Zheng Wu
Estimating the term…
Neonatal seizure is different from adult seizure, and many anti epileptic drugs that are effective in adults often fail to treat neonatal seizure. Gluconic acid, a natural organic acid enriched in fruits and honey, and the glucose oxidase enzyme, is shown herein to potently inhibit neonatal epilepsy both in vitro and in vivo. Sodium gluconate is shown to inhibit epileptiform burst activity in cell cultures and protect neurons from kainic acid-induced cell death. Sodium gluconate also inhibited epileptiform burst activity in brain slices in a manner that was much more potent in neonatal animals than in older animals. Consistently, in vivo EEC recordings also revealed that sodium gluconate inhibited the epileptic seizure activity in a manner that was much more potent in neonates than in adult animals. Mechanistically, sodium gluconate inhibits voltage-dependent CLC-3 C1− channels both in neuronal cultures and in hippocampal slices. Together, these data suggest a novel antiepileptic drug gluconate that potently inhibits neonatal seizures through blocking CLC-3 C1− channels.
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An oral pharmaceutical composition comprising glucose oxidase and supplementary glucose, wherein said composition acts to reduce convulsion activity in a neonate having an upregulated CLC-3 Cl− channel compared to a non-neonate.
A pharmaceutical formulation for the use in treating convulsion activity in a neonate, wherein said formulation comprises a fixed dose of a CLC-3 Cl− channel inhibitor, supplemental glucose, and an inactive carrier.
Dependencies are inferred from the claim text.