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. 2019 Mar 18;6(4):723–738. doi: 10.1002/acn3.754

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© 2019 University of California. Annals of Clinical and Translational Neurology published by Wiley Periodicals, Inc on behalf of American Neurological Association.

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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The KCa3.1 inhibitor senicapoc is orally available and has excellent brain penetration. (A) Chemical structures of the three indicated KCa3.1 blockers and the synthetic scheme for senicapoc. (B) Total plasma and brain concentrations in mice (n = 3) and rats (n = 2) at 1 h after intraperitoneal administration of 50 mg/kg senicapoc in 1 mL miglyol per body weight. (C) Time course of total senicapoc brain and plasma concentrations in mice after intraperitoneal administration of 50 mg/kg senicapoc (n = 3 per time point). (D) Total senicapoc plasma concentrations after oral gavage of 50 mg/kg in rats (n = 3). Data are presented as mean ± SD.