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. 2022 Mar 17;13:858348. doi: 10.3389/fphar.2022.858348

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Copyright © 2022 Wisedchaisri and Gamal El-Din.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Toxins and drugs that physically block the pore. (A) Neurotoxin and drug receptor sites on Na_V channels. Receptor sites 1 to 4 are illustrated with their representative natural modulators. Anti-arrhythmic, anti-epileptic, and local anesthetic drugs enter the hydrophobic central cavity in the pore through the membrane fenestration and the activation gate. (B) Tetrodotoxin (TTX) binds to receptor site 1 at the selectivity filter and interacts with the DEKA motif of human Na_V1.7. (C) μ-Conotoxin KIIIA binds to receptor site 1 at the extracellular mouth of the channel above the selectivity filter of human Na_V1.2. (D,E) Anti-arrhythmic drug class IA quinidine, (D) and class IC propafenone, (E) bind to Na_V1.5 in the central cavity of the pore formed by DI and DIV. For clarity, the pore module of DII has been removed.