Preclinical cardiac screens routinely clear drug candidates based on basic cell viability. But because cardiomyocytes demand ATP production to function, a compound that impairs mitochondrial health will cause damage before overt death. Since standard endpoint assays only capture late-stage cytotoxicity, metabolic liabilities can slip through in vitro testing unnoticed.
This application note shows how live-cell oxygen monitoring identifies deficits directly in standard 96-well plates. In iPSC-derived cardiomyocytes, the technique reveals respiration falling to 0.24-fold of baseline levels while the cells still look morphologically intact.
Download this application note to see
- How continuous oxygen consumption tracking resolves dose-dependent suppression over a multi-day exposure window
- Bioenergetic profiles that pinpoint which respiratory step a compound targets
- How metabolic readouts complement standard electrophysiology screens
