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While the PARS1 inhibitor halofuginone exhibited toxicity, its optimized derivative DWN12088 demonstrated improved safety and efficacy in preclinical models and is currently under clinical investigation for IPF [143]

allopurinol, with its exquisite mechanistic precision, conducts a targeted biochemical silencing of xanthine oxidase enzymatic networks, fundamentally disrupting the pathophysiological cascade responsible for uric acid generation (Shuvo et al., 2025)