Anti-tumor drug lenvatinib induced cardiotoxicity via mitochondrial oxidative stress and apoptosis

Lenvatinib was approved by FDA for the treatment of radioiodine-refractory thyroid cancer in 2015，receiving a significant progression-free survival improvement in cancer survivors. Clinical side-effects decreases by targeted vascular endothelial growth factor receptors VEGFR 1–3, fibroblast growth factor receptors FGFR 1–4, platelet derived growth factor alpha PDGFRa, RET, and c-KIT. Nevertheless, several cases reported severe cardiac dysfunction had occurred. The aim of our study is to investigate the mechanism of cardiotoxicity induced by lenvatinib.