Why the study?
QTc prolongation crossing the regulatory threshold was observed with supratherapeutic transdermal buprenorphine, prompting electrophysiological investigation into whether it directly blocks cardiac ion channels.
Does buprenorphine cause QT prolongation via direct hERG channel block in cardiac cells?
Population
Cells expressing hERG, CaV1.2, and NaV1.5, and human iPSC-CMs
Comparison
Buprenorphine and norbuprenorphine vs methadone, naltrexone, and naloxone
Design
In vitro electrophysiological study
Authors
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Buprenorphine QTc effects appear hERG-independent; leaves open whether non-hERG mechanisms confer clinical TdP risk.
Does buprenorphine cause QT prolongation via direct hERG channel block in cardiac cells?
Buprenorphine-induced QTc prolongation is not mediated by direct hERG channel block, unlike methadone, suggesting a different mechanism that may not carry the same Torsades de Pointes risk.
Tran et al. (2020) studied this question.
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