| Literature DB >> 33859800 |
Andrew M Griffin1, Kristopher M Kahlig1, Robert John Hatch1,2, Zoë A Hughes1, Mark L Chapman3, Brett Antonio3, Brian E Marron1, Marion Wittmann1, Gabriel Martinez-Botella1.
Abstract
The gene KCNT1 encodes the sodium-activated potassium channel KNa1.1 (Slack, Slo2.2). Variants in the KCNT1 gene induce a gain-of-function (GoF) phenotype in ionic currents and cause a spectrum of intractable neurological disorders in infants and children, including epilepsy of infancy with migrating focal seizures (EIMFS) and autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE). Effective treatment options for KCNT1-related disease are absent, and novel therapies are urgently required. We describe the development of a novel class of oxadiazole KNa1.1 inhibitors, leading to the discovery of compound 31 that reduced seizures and interictal spikes in a mouse model of KCNT1 GoF.Entities:
Year: 2021 PMID: 33859800 PMCID: PMC8040054 DOI: 10.1021/acsmedchemlett.0c00675
Source DB: PubMed Journal: ACS Med Chem Lett ISSN: 1948-5875 Impact factor: 4.345