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Published data shows this mechanism is particularly relevant in NSAID-induced gut damage models, where NO dysregulation contributes significantly to tissue destruction

48 It showed significantly higher proteolytic resistance (half-life of 165 h for a dose of 30 mg)

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Our previous study established transgenic fish expressing tropomyosin 3 ( TPM3 ) mutations and demonstrated that TPM3 (E151G) and TPM3 (E151A) exhibit different pathogenicity