Randomized trial evaluates machine learning accuracy in predicting mitochondrial toxicity, highlighting model effectiveness.
Mitochondrial toxicity is a major concern in drug development and safety assessment. Machine learning models trained on mitochondrial membrane potential (MMP) assay data offer promising toxicity predictions, but cross-scaffold and cross-assay transferability remain uncharacterized. We evaluated classical machine learning and deep learning architectures across six molecular representations and both random and scaffold-based splitting strategies, assessing performance on an internal MMP test set and an independent external set comprising flux and glucose–galactose assay data. Across all model configurations, we observed a consistent cross-assay generalization gap, independent of model type, feature choice, or augmentation strategy. Mordred descriptors provided the most transferable predictive signal, outperforming fingerprint-based representations on the external set. SHAP analysis of the best CatBoost and Random Forest models identified autocorrelation-family descriptors as dominant predictors. C3SP3 contributed through feature interactions while ATS5i showed positive association with toxicity across assays. Motif-level and descriptor-level associations proved to be strongly assay-dependent, supporting a mechanism in which mitochondrial toxicity arises from multivariate physicochemical interactions rather than single structural alerts.
No takes yet. Share an insight, caveat, or question.
Lin et al. (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: