Discovery of Potent and Selective Blockers Targeting the Epilepsy-Associated KNa1.1 Channel

Gain-of-function (GOF) mutations of the sodium-activated potassium channel KNa1.1 (Slack, Slo2.2, or KCa4.1) induce severe, drug-resistant forms of epilepsy in infants and children. Although quinidine has shown promise in treating KCNT1-related epilepsie...

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Bibliographic Details
Main Author:	Ruqiu Zheng (10738206) (author)
Other Authors:	Zhongtang Li (6851987) (author), Qiufeng Wang (553607) (author), Shiqi Liu (1354662) (author), Ningfeng Liu (11009093) (author), Yiyan Li (10738203) (author), Guiwang Zhu (19939532) (author), Zhenming Liu (448850) (author), Zhuo Huang (167130) (author), Liangren Zhang (114208) (author)
Published:	2024
Subjects:	Biochemistry Medicine Molecular Biology Neuroscience Pharmacology Biotechnology Hematology Infectious Diseases Biological Sciences not elsewhere classified Chemical Sciences not elsewhere classified significant pharmacological profiles selective blockers targeting moderate oral bioavailability data also showed na </ sub ca </ sub z05 </ b vitro tool compound related epilepsies compared gof mutant y796h 1 channel gain selective potential k 1 channel inhibitors related epilepsies herg channel potential counteraction 1 inhibitor treating kcnt1 structural optimization shown promise resistant forms novel class new k mutation studies limited efficacy induce severe binding site associated k although quinidine
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Discovery of Potent and Selective Blockers Targeting the Epilepsy-Associated K<sub>Na</sub>1.1 Channel

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