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TB-500 has been well-tolerated in various research applications, with its endogenous nature (as Thymosin Beta-4) suggesting compatibility with normal physiology

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In the context of HBV infection, PRMT1 is recruited to cccDNA and catalyzes H4R3me2a modification, which, in turn, alters the acetylation status of cccDNA, ultimately resulting in the suppression of HBV transcription (Figure 7F) [195]

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