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Article

Chloroquine blocks a mutant Kir2.1 channel responsible for short QT syndrome and normalizes repolarization properties in silico.

Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology - 1 Jan 2009

Lopez-Izquierdo Angelica, Ponce-Balbuena Daniela, Ferrer Tania, Sachse Frank B, Tristani-Firouzi Martin, Sanchez-Chapula Jose A

Abstract excerpt

Short QT Syndrome (SQTS) is a novel clinical entity characterized by markedly rapid cardiac repolarization and lethal arrhythmias. A mutation in the Kir2.1 inward rectifier K+ channel (D172N) causes one form of SQTS (SQT3). Pharmacologic block of Kir2.1 channels may hold promise as potential therapy for SQT3. We recently reported that the anti-malarial drug chloroquine blocks Kir2.1 channels by plugging the...

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Identifiers

PMID: 19710529
DOI: 10.1159/000233241
PMCID: PMC3711575

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PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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