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• W2000718634 endingPage "3069" @default.
• W2000718634 startingPage "3013" @default.
• W2000718634 abstract "Redox dysregulation originating from metabolic alterations and dependence on mitogenic and survival signaling through reactive oxygen species represents a specific vulnerability of malignant cells that can be selectively targeted by redox chemotherapeutics. This review will present an update on drug discovery, target identification, and mechanisms of action of experimental redox chemotherapeutics with a focus on pro- and antioxidant redox modulators now in advanced phases of preclinal and clinical development. Recent research indicates that numerous oncogenes and tumor suppressor genes exert their functions in part through redox mechanisms amenable to pharmacological intervention by redox chemotherapeutics. The pleiotropic action of many redox chemotherapeutics that involves simultaneous modulation of multiple redox sensitive targets can overcome cancer cell drug resistance originating from redundancy of oncogenic signaling and rapid mutation. Moreover, some redox chemotherapeutics may function according to the concept of synthetic lethality (i.e., drug cytotoxicity is confined to cancer cells that display loss of function mutations in tumor suppressor genes or upregulation of oncogene expression). The impressive number of ongoing clinical trials that examine therapeutic performance of novel redox drugs in cancer patients demonstrates that redox chemotherapy has made the crucial transition from bench to bedside. Antioxid. Redox Signal. 11, 3013–3069. Introduction The (redox) war on cancer Developing anticancer redox chemotherapeutics Redox chemotherapeutics: More than neocytotoxics? Redox chemotherapeutics: Pleiotropic ‘dirty’ drugs? Redox chemotherapeutics: Combinatorial or stand-alone drugs? Redox chemotherapeutics and personalized medicine Redox dysregulation as anticancer drug target ROS in cancer chemotherapy: From toxicological liability to therapeutic asset Reactive Pharmacophores for Anticancer Redox Chemotherapy Organic endoperoxides: Artemisinins Arsenicals: As2O3 and darinaparsin As2O3 Darinaparsin Redox cyclers: Motexafin gadolinium Motexafin gadolinium Menadione Acetaminophen and O-acetylsalicylic acid Geldanamycin 3,7-Diaminophenothiazinium redox dyes 2-(Phenyltelluryl)-3-methyl-[1,4]naphthoquinone Metal chelators: Disulfiram and triapine Disulfiram Triapine and others Di- and polysulfides: Varacin and diallyltrisulfide Calicheamicin γ1I Varacin and other polysulfides Leinamycin Diallyldisulfide and diallyltrisulfide Isothiocyanate organosulfur agents: β-Phenylethylisothiocyanate Sulforaphane β-Phenylethylisothiocyanate Electrophilic Michael acceptors: Parthenolide and neratinib Parthenolide Curcumin Cinnamaldehyde Neratinib Sacrificial antioxidants: L-Ascorbate 3014Molecular Targets for Anticancer Redox Chemotherapy Targeting the SOD system SOD inhibitors: ATN-224 TETA ATN-224 2-Methoxyestradiol SOD mimetics: Mangafodipir M40403 Mangafodipir cis-FeMPy2P2P MnTBAP and others TEMPO and others Targeting the glutathione redox system: Imexon and NOV002 NOV-002 Imexon L-Buthionine-S,R-sulfoximine PABA/NO Targeting the thioredoxin system: PX-12 and PMX464 PX-12 PMX464 PX-916 Chaetocin and gliotoxin Targeting the Nrf2/Keap1-ARE pathway Targeting HO-1: Zinc protoporphyrin IX Targeting NQO1: Dicoumarol and ES936 Dicoumarol ES936 Targeting APE/Ref1: E3330 and PNRI-299 E3330 PNRI-299 and resveratrol Lucanthone and CRT0044876 Targeting Cdc25 phosphatases: NSC 67121 and F-NSC 67121 NSC 67121 and F-NSC 67121 Indolyldihydroxyquinones Targeting zinc finger transcription factors: DIBA DIBA In search of a molecular target: elesclomol Functional Targets for Anticancer Redox Chemotherapy Prooxidant intervention targeting glucose metabolism: 2-DG and DCA 2-Deoxyglucose 3-Bromopyruvate Dichloroacetate Oxythiamine Prooxidant intervention targeting mitochondria Targeting mitochondrial respiration: α-TOS, DIM, and Bz-423 α-TOS 3,3′-Diindolylmethane Bz-423 Targeting VDACs: Erastin Erastin RSL5 Targeting tumor hypoxia Hypoxia-activated redox chemotherapeutics: TPZ, AQ4N, and PR-104 Tirapazamine AQ4N and PR-104 Targeting HIF-1α: PX-478 PX-478 Conclusions3015" @default.
• W2000718634 created "2016-06-24" @default.
• W2000718634 creator A5081187066 @default.
• W2000718634 date "2009-12-01" @default.
• W2000718634 modified "2023-10-17" @default.
• W2000718634 title "Redox-Directed Cancer Therapeutics: Molecular Mechanisms and Opportunities" @default.
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