http://rdf.ncbi.nlm.nih.gov/pubchem/patent/WO-2016187228-A1

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http://rdf.ncbi.nlm.nih.gov/pubchem/patentcpc/A61K31-045
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http://rdf.ncbi.nlm.nih.gov/pubchem/patentipc/A61K31-045
filingDate 2016-05-17-04:00^^<http://www.w3.org/2001/XMLSchema#date>
inventor http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_2bd540038e3a3258815994e750902f4a
http://rdf.ncbi.nlm.nih.gov/pubchem/patentinventor/MD5_d05c053ee156e78f3dfd45c4cc6433dd
publicationDate 2016-11-24-04:00^^<http://www.w3.org/2001/XMLSchema#date>
publicationNumber WO-2016187228-A1
titleOfInvention Gluconate-based compositions as a neonate anticonvulsant
abstract Neonatal seizure is different from adult seizure, and many antiepileptic drugs that are effective in adults often fail to treat neonatal seizure. Gluconic acid, a natural organic acid enriched in fruits and honey, 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 EEG 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.
priorityDate 2015-05-19-04:00^^<http://www.w3.org/2001/XMLSchema#date>
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