ArticleFrontiers in drug discovery2025
Towards human cardiac new approach methodologies (NAMs) to evaluate the combination of repolarization prolonging and shortening drugs: a pilot study.
Article in Frontiers in drug discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Clinical trials in a dish: cardiometabolic drug development with biological and digital twins.The Journal of clinical investigation · 2026Review
- Comparative transcriptomics analysis of histone deacetylases, transcription factors, and ion channel genes in human iPSC-cardiomyocytes vs. the adult human heart.Journal of precision medicine (Amsterdam, Netherlands) · 2026Article
- Response of human iPSC-cardiomyocytes to adrenergic drugs assessed by high-throughput pericellular oxygen measurements and computational modeling.Journal of molecular and cellular cardiology plus · 2026Article
- Comparative transcriptomics analysis of histone deacetylases, transcription factors, and ion channel genes in human iPSC-cardiomyocytes vs. the adult human heart.bioRxiv : the preprint server for biology · 2026Article
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Authors and funding
5 authors.
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Abstract
Background and Purpose: Nonclinical human cardiac new approach methodologies (NAMs), including human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) combined with multielectrode array (MEA) represent a highly predictive Methods: To generate the Results: The combination of cobicistat and moxifloxacin resulted in a concentration-dependent shortening of the corrected field potential duration (FPDcF) relative to both vehicle control and moxifloxacin alone. This effect was observed at near clinical Cmax concentrations of cobicistat and moxifloxacin. Evaluation of local extracellular action potentials (LEAP) revealed early afterdepolarizations (EADs) with supratherapeutic concentrations of moxifloxacin which were subsequently eliminated by the addition of cobicistat at therapeutic concentrations. Finally, the Comprehensive Conclusion: We conclude that cobicistat can attenuate moxifloxacin induced FPDcF prolongation at clinically relevant concentrations
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