D-23129: a potent anticonvulsant in the amygdala kindling model of complex partial seizures
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2014, Drug Discovery TodayCitation Excerpt :Electrophysiological experiments performed on Xenopus oocytes [114] and Chinese hamster ovary (CHO) cells [115,116] overexpressing the KCNQ2/3 heteromultimer showed that retigabine shifted the voltage dependence of channel activation to a more hyperpolarised membrane potential, increased the rate of channel activation and slowed channel deactivation. These results identified the mechanism by which retigabine reduced neuronal excitability in the animal seizure model studies [119–121]. The binding site of retigabine has since been identified as a hydrophobic pocket containing a tryptophan residue (Trp-236 in KV7.2; Trp-265 in KV7.3) in the cytoplasmic part of S5 and S6 to stabilise the channel in the open state [122,123].
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