From:  Reactive oxygen species (ROS) in cancer: from redox signaling and metabolic plasticity to therapeutic vulnerabilities

 Summary of redox-targeted therapeutic strategies in cancer.

StrategyKey agentsMechanism of actionCancer typesClinical statusAdvantagesReferences
Pro-oxidant therapyDoxorubicin, arsenic trioxide (ATO), β-lapachone, elesclomolRedox cycling; superoxide via mitochondrial ETC disruption; exceeds cytotoxic ROS threshold.Leukaemia, APL, solid tumoursApproved/Phase I–IIISelective cancer cell killing due to elevated basal ROS[120]
GSH synthesis inhibitionButhionine sulfoximine (BSO), erastin, imuthiolInhibits γ-GCS; depletes GSH; erastin blocks system Xc causing GPX4-mediated ferroptosis.Melanoma, ovarian, neuroblastoma, glioblastomaPhase I–IISensitises drug-resistant tumours; induces ferroptosis[132, 133]
Thioredoxin system inhibitionAuranofin (TrxR inhibitor), PX-12, PMX464Covalent TrxR selenocysteine modification; impairs peroxiredoxin recycling; elevates ROS.Lung, ovarian, colorectal cancerPhase I–IIWell-tolerated; repurposed gold-based drug[133, 134]
Nrf2 pathway suppressionML385, brusatol, trigonelline, halofuginoneBlocks Nrf2-Keap1 axis; reduces NQO1, HO-1, GPx; sensitizes to oxidative damage.Lung, pancreatic, liver, breast cancerPreclinical/Phase IOvercomes chemo-resistance; broad spectrum[131, 132]
Radiotherapy and ROS modulationIonising radiation ± nimorazole, ATOHydroxyl radicals via water radiolysis; ROS amplifiers enhance DNA DSB formation.Head & neck, brain, breast, prostateStandard of care and trialsWell-established; synergistic with antioxidant inhibition[99, 143]
Photodynamic therapy (PDT)Photofrin, talaporfin, 5-ALA, temoporfinPhotosensitizer + light → singlet oxygen (1O2); oxidizes lipids, proteins, nucleic acids.Skin, oesophageal, lung, bladder, H&NApproved/Phase II–IIITumour-localised; minimal systemic toxicity[144, 145]
ROS + immunotherapy combinationAnti-PD-1/PD-L1 + pro-oxidant agentsInduces ICD; releases DAMPs (CRT, HMGB1, ATP); activates DCs; enhances checkpoint blockade.Melanoma, NSCLC, colorectal, bladderPhase I–IIIConverts ‘cold’ to ‘hot’ tumours; broadens IO response[134, 144]
Nanoparticle-based CDTIron oxide NPs, Cu-MOFs, GOx nanoplatforms, TiO2-NPsFenton/Fenton-like reactions; tumor microenvironment H2O2 amplification; chemodynamic therapy.Liver, breast, glioma, lung cancerPreclinical/Phase ISpatially controlled ROS; reduced systemic toxicity[134, 149]
Ferroptosis inductionErastin, RSL3, sulfasalazine, FIN56Inhibits system Xc or GPX4; promotes iron-dependent lipid peroxidation and lethal lipid ROS accumulation.Pancreatic, lung, liver, glioblastoma, therapy-resistant tumorsPreclinical/early phaseTargets redox-adapted and drug-resistant cancer cells; synergistic with chemotherapy and immunotherapy[156, 157]
ROS-responsive drug delivery and prodrugsThioketal nanoparticles, boronic ester prodrugs, ROS-responsive polymersROS-triggered drug release selectively within oxidative tumor microenvironments.Solid tumors, hypoxic tumorsPreclinical/early phaseReduced systemic toxicity; enhanced tumor specificity[34, 134, 149]