<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Titus SA</submitter><funding>Intramural NIH HHS</funding><funding>PHS HHS</funding><pagination>30-8</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2766802</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>394(1)</volume><pubmed_abstract>Long QT syndrome, either inherited or acquired from drug treatments, can result in ventricular arrhythmia (torsade de pointes) and sudden death. Human ether-a-go-go-related gene (hERG) channel inhibition by drugs is now recognized as a common reason for the acquired form of long QT syndrome. It has been reported that more than 100 known drugs inhibit the activity of the hERG channel. Since 1997, several drugs have been withdrawn from the market due to the long QT syndrome caused by hERG inhibition. Food and Drug Administration regulations now require safety data on hERG channels for investigative new drug (IND) applications. The assessment of compound activity on the hERG channel has now become an important part of the safety evaluation in the process of drug discovery. During the past dec</pubmed_abstract><journal>Analytical biochemistry</journal><pubmed_title>A new homogeneous high-throughput screening assay for profiling compound activity on the human ether-a-go-go-related gene channel.</pubmed_title><pmcid>PMC2766802</pmcid><funding_grant_id>NIH0012490817</funding_grant_id><pubmed_authors>Austin CP</pubmed_authors><pubmed_authors>Xia M</pubmed_authors><pubmed_authors>Shou L</pubmed_authors><pubmed_authors>Titus SA</pubmed_authors><pubmed_authors>Shahane SA</pubmed_authors><pubmed_authors>Southall N</pubmed_authors><pubmed_authors>Zheng W</pubmed_authors><pubmed_authors>Beacham D</pubmed_authors><pubmed_authors>Huang R</pubmed_authors><pubmed_authors>Hooten E</pubmed_authors><pubmed_authors>Zhao Y</pubmed_authors></additional><is_claimable>false</is_claimable><name>A new homogeneous high-throughput screening assay for profiling compound activity on the human ether-a-go-go-related gene channel.</name><description>Long QT syndrome, either inherited or acquired from drug treatments, can result in ventricular arrhythmia (torsade de pointes) and sudden death. Human ether-a-go-go-related gene (hERG) channel inhibition by drugs is now recognized as a common reason for the acquired form of long QT syndrome. It has been reported that more than 100 known drugs inhibit the activity of the hERG channel. Since 1997, several drugs have been withdrawn from the market due to the long QT syndrome caused by hERG inhibition. Food and Drug Administration regulations now require safety data on hERG channels for investigative new drug (IND) applications. The assessment of compound activity on the hERG channel has now become an important part of the safety evaluation in the process of drug discovery. During the past dec</description><dates><release>2009-01-01T00:00:00Z</release><publication>2009 Nov</publication><modification>2025-04-19T11:08:52.346Z</modification><creation>2019-03-27T00:26:09Z</creation></dates><accession>S-EPMC2766802</accession><cross_references><pubmed>19583963</pubmed><doi>10.1016/j.ab.2009.07.003</doi></cross_references></HashMap>