ArticleThe Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology2009
Block of HERG k channel by classic histamine h(1) receptor antagonist chlorpheniramine.
Article in The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Serotonergic Toxicity and Hyponatremia Associated with Antidepressant Therapy: The Pivotal Role of SIADH.Clinical drug investigation · 2026Review
- A hERG Blocker Facilitates KbioRxiv : the preprint server for biology · 2026Article
- Cardiac Safety of Intranasal Chlorpheniramine: An Exposure-Based Risk Assessment.Pharmaceuticals (Basel, Switzerland) · 2026Review
- The interplay between serotonin syndrome and syndrome of inappropriate antidiuresis: a fatal case of acute hyponatremia during treatment with duloxetine, chlorphenamine, amitriptyline, and L-tryptophan.Therapeutic advances in psychopharmacology · 2026Article
- Long QT syndrome in chromosome 7q35q36.3 deletion involving KCNH2 gene: Warning for chlorpheniramine prescription.Molecular genetics & genomic medicine · 2019Article
- Effects of the histamine H(1) receptor antagonist hydroxyzine on hERG K(+) channels and cardiac action potential duration.Acta pharmacologica Sinica · 2011Article
- Torsades de pointes tachycardia induced by common cold compound medication containing chlorpheniramine.European journal of clinical pharmacology · 2010Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chlorpheniramine is a potent first-generation histamine H(1) receptor antagonist that can increase action potential duration and induce QT prolongation in several animal models. Since block of cardiac human ether-a-go-go-related gene (hERG) channels is one of leading causes of acquired long QT syndrome, we investigated the acute effects of chlorpheniramine on hERG channels to determine the electrophysiological basis for its proarrhythmic potential. We examined the effects of chlorpheniramine on the hERG channels expressed in Xenopus oocytes using two-microelectrode voltage-clamp techniques. Chlorpheniramine induced a concentration-dependent decrease of the current amplitude at the end of the voltage steps and hERG tail currents. The IC(50) of chlorpheniramine-dependent hERG block in Xenopus oocytes decreased progressively relative to the degree of depolarization. Chlorpheniramine affected the channels in the activated and inactivated states but not in the closed states. The S6 domain mutations Y652A and F656A partially attenuated (Y652A) or abolished (F656A) the hERG current block. These results suggest that the H(1) antihistamine, chlorpheniramine is a blocker of the hERG channels, providing a molecular mechanism for the drug-induced arrhythmogenic side effects.
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