|Drug||EMA-approved indication in solid tumours||Main targets||Role in redox system|
|Afatinib||EGFR-mutated NSCLC||EGFR||Chronic oxidative stress associated with resistance.|
|Axitinib||RCC||VEGFR1–3, PDGFR, c-Kit||Oxidative stress-mediated genotoxic effects.|
|VEGF||Increases ROS levels.|
Combined with autophagy inhibitor enhances ROS levels and apoptosis.
|EGFR||Reduces the amount of GSH by internalizing EGFR and glutamine transport.|
Decreases Nox1 and Nox1-related effect of oxaliplatin.
|Crizotinib||ALK-positive NSCLC||ALK, c-MET||Increased O2•− production linked with cardiotoxicity. Prx II up-regulation associated with resistance.|
|Erlotinib||EGFR-mutated NSCLC Pancreatic cancer||EGFR||Increases ROS-mediated apoptosis in HNSCC and NSCLC.|
|Gefitinib||EGFR-mutated NSCLC||EGFR||Increases oxidative stress linked to EMT and cardiotoxicity. NFE2L2/Keap1-axis related to treatment resistance.|
|Imatinib||GISTs||PDGFRα, KIT, ABL, CSF-1 receptor||Induces ROS-dependent apoptosis in melanoma.|
|Lapatinib||HER2-positive breast cancer||HER1, HER2||Increases ROS; low ROS levels linked with resistance, which may be overcome with antioxidant mimics.|
|Pazopanib||RCC, sarcomas||Various kinases, for example, VEGFR1–3, (PDGFR-α and PDGFR-β), c-Kit, FGFR-1, and FGFR-3||May induce oxidative DNA damage-mediated erythrocyte apoptosis.|
|Rituximab||Non-Hodgkin’s lymphoma||CD-20||CD20 stimulation leads to the production of O2•−.|
|Sorafenib||HCC, RCC, radioiodine-refractory thyroid cancer||Various kinases, for example, VEGFR-2 and VEGFR-3, PDGFR-β, and RAF-kinases||Increases oxidative stress, which possibly is a predictive factor for sorafenib|
|Sunitinib||GISTs, pancreatic NET, RCC||Various kinases, for example, VEGFR1–3, (PDGFR-α and PDGFR-β), c-Kit||Enhances antioxidant defence, decreases NOS activity and expression.|
|Trastuzumab||HER2-positive breast cancer and HER2-positive gastric cancer||HER2 dimerization||Regulatory loop with NFE2L2|
NFE2L2 increases trastuzumab resistance.
|Vemurafenib||BRAF (V600E) mutated melanoma||BRAF V600E||Increases NO• and O2•− production increases depolarization of mitochondrial membranes. Induces PGC1α|