Cenobamate: Neuroprotective Potential of a New Antiepileptic Drug.


Journal

Neurochemical research
ISSN: 1573-6903
Titre abrégé: Neurochem Res
Pays: United States
ID NLM: 7613461

Informations de publication

Date de publication:
Mar 2021
Historique:
received: 19 07 2020
accepted: 20 11 2020
revised: 17 11 2020
pubmed: 1 12 2020
medline: 8 9 2021
entrez: 30 11 2020
Statut: ppublish

Résumé

Central nervous system (CNS) injuries annually afflict approximately 2.7 million people in United States only, inflicting costs of nearly 100 billion US dollars. The gravity of this problem is a consequence of severe and prolonged disability of patients due to a scarce regeneration of CNS, along with the lack of efficient neuroprotective and neuroregenrative therapies. Therefore, the first and most important task in managing the CNS injury is reduction of the damaged area, and apoptosis of neurons occurs not only during the trauma, but in great extent within the following minutes and hours. This process, called secondary injury phase, is a result of trauma-induced metabolic changes in nervous tissue and neuron apoptosis. Cenobamate is a new antiepileptic drug approved by FDA on November 21, 2019. Regardless of its primary purpose, cenobamate, as a blocker of voltage-gated sodium channels and positive modulator of GABAa receptors, it appears to be a promising neuroprotective agent. Moreover, through activation of PI3K/Akt-CREB-BDNF pathway, it leads to the increase of anti-apoptotic factor levels and the decrease of pro-apoptotic factor levels, which induce inhibition of apoptosis and increase neuron survival. Similarly to riluzole, cenobamate could be an important part of a perioperative procedure in neurosurgery, decreasing the occurrence of neurological deficits. Provided that cenobamate will be effective in aforementioned conditions, it could improve treatment outcomes of millions of patients every year, thereby an extensive investigation of its efficacy as a neuroprotective treatment after central nervous system trauma should follow.

Identifiants

pubmed: 33252771
doi: 10.1007/s11064-020-03188-8
pii: 10.1007/s11064-020-03188-8
doi:

Substances chimiques

Carbamates 0
Chlorophenols 0
GABA-A Receptor Agonists 0
Neuroprotective Agents 0
Tetrazoles 0
Voltage-Gated Sodium Channel Blockers 0
Glutamic Acid 3KX376GY7L
Cenobamate P85X70RZWS

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Pagination

439-446

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Auteurs

Michał Wiciński (M)

Department of Pharmacology and Therapeutics, Faculty of Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University, M. Curie 9, 85-090, Bydgoszcz, Poland.

Oskar Puk (O)

Department of Pharmacology and Therapeutics, Faculty of Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University, M. Curie 9, 85-090, Bydgoszcz, Poland. oskar.p.puk@gmail.com.

Bartosz Malinowski (B)

Department of Pharmacology and Therapeutics, Faculty of Medicine, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus University, M. Curie 9, 85-090, Bydgoszcz, Poland.

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