ArticleMarine drugs2016
Development of a Rapid Throughput Assay for Identification of hNav1.7 Antagonist Using Unique Efficacious Sodium Channel Agonist, Antillatoxin.
Article in Marine drugs, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- Molecular determinant of low-voltage dependence of human NaNature communications · 2026Article
- A High-Throughput Biosensing Approach for Rapid Screening of Compounds Targeting the hNav1.1 Channel: Marine Toxins as a Case Study.Marine drugs · 2025Article
- Screening an In-House Isoquinoline Alkaloids Library for New Blockers of Voltage-Gated NaMolecules (Basel, Switzerland) · 2022Article
- Painful and painless mutations of SCN9A and SCN11A voltage-gated sodium channels.Pflugers Archiv : European journal of physiology · 2020Review
- Article
- Functional and Mechanistic Neurotoxicity Profiling Using Human iPSC-Derived Neural 3D Cultures.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- Veratridine modifies the gating of human voltage-gated sodium channel Nav1.7.Acta pharmacologica Sinica · 2018Article
- Sodium channels and pain: from toxins to therapies.British journal of pharmacology · 2018Review
- Mechanism-specific assay design facilitates the discovery of Nav1.7-selective inhibitors.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Phenytoin: a step by step insight into its multiple mechanisms of action-80 years of mechanistic studies in neuropharmacology.Journal of neurology · 2017Article
- Bringing new dimensions to drug discovery screening: impact of cellular stimulation technologies.Drug discovery today · 2017Review
- Effects of Tetrodotoxin in Mouse Models of Visceral Pain.Marine drugs · 2017Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Voltage-gated sodium channels (VGSCs) are responsible for the generation of the action potential. Among nine classified VGSC subtypes (Nav1.1-Nav1.9), Nav1.7 is primarily expressed in the sensory neurons, contributing to the nociception transmission. Therefore Nav1.7 becomes a promising target for analgesic drug development. In this study, we compared the influence of an array of VGSC agonists including veratridine, BmK NT1, brevetoxin-2, deltamethrin and antillatoxin (ATX) on membrane depolarization which was detected by Fluorescence Imaging Plate Reader (FLIPR) membrane potential (FMP) blue dye. In HEK-293 cells heterologously expressing hNav1.7 α-subunit, ATX produced a robust membrane depolarization with an EC50 value of 7.8 ± 2.9 nM whereas veratridine, BmK NT1, and deltamethrin produced marginal response. Brevetoxin-2 was without effect on membrane potential change. The ATX response was completely inhibited by tetrodotoxin suggesting that the ATX response was solely derived from hNav1.7 activation, which was consistent with the results where ATX produced a negligible response in null HEK-293 cells. Six VGSC antagonists including lidocaine, lamotrigine, phenytoin, carbamazepine, riluzole, and 2-amino-6-trifluoromethylthiobenzothiazole all concentration-dependently inhibited ATX response with IC50 values comparable to that reported from patch-clamp experiments. Considered together, we demonstrate that ATX is a unique efficacious hNav1.7 activator which offers a useful probe to develop a rapid throughput screening assay to identify hNav1.7 antagonists.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.