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Peroxides are a fundamental class of chemical compounds characterized by an oxygen-oxygen single bond, with hydrogen peroxide (H2O2) serving as the most significant biological representative. They play a dual role in cellular physiology: at low concentrations, they act as critical second messengers in redox signaling pathways that regulate cell proliferation, differentiation, and wound healing; conversely, at high concentrations, they function as potent oxidants capable of damaging DNA, proteins, and lipids. This metabolic balance is frequently disrupted in pathological states such as cancer, where elevated peroxide levels drive genomic instability, and in chronic wounds or inflammatory diseases where redox homeostasis is lost. Therapeutic strategies targeting peroxides range from the direct application of antiseptics like benzoyl peroxide for localized infection control to the development of sophisticated superoxide dismutase (SOD) mimetics like avasopasem manganese, which elevate peroxide levels to selectively induce apoptosis in tumor cells. Additionally, novel 'peroxide-activated' prodrugs are being designed to release active drugs only at sites of high oxidative stress, thereby improving therapeutic index and reducing systemic toxicity.
Drugs targeting peroxides primarily work by modulating their concentration to either induce selective oxidative damage in pathogens and cancer cells or to restore redox signaling in healing tissues. Mechanisms include the catalytic dismutation of superoxide into hydrogen peroxide (e.g., superoxide dismutase mimetics), the chemical reduction of peroxides to water (e.g., glutathione peroxidase mimetics), and the use of peroxide-activated prodrugs that leverage the reactive environment to release therapeutic agents specifically at sites of oxidative stress.
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