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Radioprotective compounds may suppress free radical formation, remove free radicals, induce natural radioprotector production (such as superoxide dismutase, glutathione peroxidase, and catalase), enhance DNA repair, reduce the post-radiation inflammatory response, or even delay cellular division allowing more time for cells to repair or undergo apoptosis [10] (Table 1)

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Conventional DMARDs (e.g., methotrexate, leflunomide, sulfasalazine): Methotrexate slows joint damage and suppresses inflammation but causes hepatic toxicity and bone marrow suppression, leading to 30% treatment discontinuation within one year (8)

The high reactivity of vinyl-ether bonds makes them preferentially oxidized, thereby protecting membrane polyunsaturated fatty acids from oxidative damage by free radicals