ArticleCardio-oncology (London, England)2026
Entrectinib results in ventricular tachycardia and Brugada phenocopy through inhibition of sodium current.
Article in Cardio-oncology (London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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10 authors.
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Abstract
backgroundEntrectinib is a tropomyosin receptor kinase (TrK) inhibitor currently approved for the treatment of ROS1-positive non-small cell lung cancer (NSCLC) and neurotrophic tyrosine receptor kinase (NTRK) gene fusion-positive solid tumors. Two case reports of ventricular tachycardia and a Brugada ECG pattern following entrectinib treatment have been published, and we observed a third case in our clinical practice. Genetic testing on the patient showed no variants in SCN5A.
objectiveTo determine if entrectinib treatment of human cardiomyocytes results in alterations in sodium currents, which may lead to Brugada phenocopy and ventricular tachycardia.
methodsStudies were performed in human ventricular cardiomyocytes (hiPSC-vCMs) derived from population-control induced pluripotent stem cells. hiPSC-vCMs were treated with entrectinib (1 µM) for either a brief (15 min) or prolonged exposure (48 h) prior to experimental analysis.
resultsTreatment of hiPSC-vCMs with entrectinib (1 µM) for 48 h resulted in a significant decrease in sodium currents during channel activation and inactivation. Treatment with entrectinib for 15 min did not significantly change sodium currents. Western blot analysis revealed no changes in NaV1.5 protein expression after 48 h of entrectinib treatment.
conclusionProlonged treatment with entrectinib decreased sodium currents in hiPSC-vCMs, which may lead to Brugada phenocopy and ventricular arrhythmias. Brief treatment with entrectinib did not affect sodium currents, and no changes in NaV1.5 protein expression were observed following prolonged treatment, indicating that inhibition of sodium currents likely results through a phospho-signaling mechanism rather than by direct channel inhibition.
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