PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
27449698-3	2016	Here, we describe GS-6615, a selective inhibitor of late INa , already in clinical development for the treatment of long QT syndrome 3 (LQT3).	eleclazine	18-25	LOW QUALITY PROTEIN: alpha-internexin	Oryctolagus cuniculus	57-60
27449698-3	2016	Here, we describe GS-6615, a selective inhibitor of late INa , already in clinical development for the treatment of long QT syndrome 3 (LQT3).	eleclazine	18-25	sodium voltage-gated channel alpha subunit 5	Homo sapiens	136-140
27449698-4	2016	EXPERIMENTAL APPROACH: The effects of GS-6615 to inhibit late INa , versus other ion currents to shorten the ventricular action potential duration (APD), monophasic APD (MAPD) and QT interval, and decrease to the incidence of ventricular arrhythmias was determined in rabbit cardiac preparations.	eleclazine	38-45	LOW QUALITY PROTEIN: alpha-internexin	Oryctolagus cuniculus	62-65
27449698-6	2016	KEY RESULTS: GS-6615 inhibited ATX-II enhanced late INa in ventricular myocytes (IC50  = 0.7 muM), shortened the ATX-II induced prolongation of APD, MAPD, QT interval, and decreased spatiotemporal dispersion of repolarization and ventricular arrhythmias.	eleclazine	13-20	LOW QUALITY PROTEIN: alpha-internexin	Oryctolagus cuniculus	52-55
27449698-8	2016	In contrast to flecainide, GS-6615 had the minimal effects on peak INa .	eleclazine	27-34	LOW QUALITY PROTEIN: alpha-internexin	Oryctolagus cuniculus	67-70
27449698-10	2016	CONCLUSIONS AND IMPLICATIONS: GS-6615 was a selective inhibitor of late INa , stabilizes the ventricular repolarization and suppresses arrhythmias in a model of LQT3.	eleclazine	30-37	LOW QUALITY PROTEIN: alpha-internexin	Oryctolagus cuniculus	72-75
27449698-10	2016	CONCLUSIONS AND IMPLICATIONS: GS-6615 was a selective inhibitor of late INa , stabilizes the ventricular repolarization and suppresses arrhythmias in a model of LQT3.	eleclazine	30-37	sodium voltage-gated channel alpha subunit 5	Homo sapiens	161-165
29017927-2	2018	OBJECTIVES: The goals of this study were to investigate the inhibition of late INa by eleclazine using a sample of long QT syndrome type 3 (LQT3) and overlap LQT3/Brugada syndrome mutant channels; to compare the apparent binding rates for eleclazine with those for other class 1 antiarrhythmic agents; and to investigate the binding site.	eleclazine	86-96	sodium voltage-gated channel alpha subunit 5	Homo sapiens	140-144
29017927-4	2018	RESULTS: Eleclazine inhibited anemone toxin II-enhanced late INa from wild-type hNaV1.5 with a drug concentration that causes 50% block of 0.62 +- 0.12 muM (84-fold selectivity over peak INa).	eleclazine	9-19	neuron navigator 1	Homo sapiens	80-85
29017927-5	2018	The drug concentration that causes 50% block of eleclazine to inhibit the enhanced late INa from LQT3 mutant channels ranged from 0.33 to 1.7 muM.	eleclazine	48-58	sodium voltage-gated channel alpha subunit 5	Homo sapiens	97-101
29017927-7	2018	Eleclazine was found to interact with hNaV1.5 significantly faster than ranolazine and 6 other class 1 antiarrhythmic agents.	eleclazine	0-10	neuron navigator 1	Homo sapiens	38-43
29017927-9	2018	CONCLUSION: At predicted therapeutic concentrations, eleclazine elicits potent inhibition of late INa across a cohort of NaV1.5 mutant channels.	eleclazine	53-63	sodium voltage-gated channel alpha subunit 5	Homo sapiens	121-127