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The cardiovascular outcomes endpoint (REDEFINE 3) is event-driven and has not yet reported

NAFLD leads to a 2-3-fold increased risk of DM2 development, 1,2 since liver fat accumulation is a crucial pathogenetic component

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The aa 1419 and aa 42 in chain B were truncated because they had little interaction with chain A

Navitoclaxs precursor, ABT737, a BH3 mimetic, prevents the interaction between anti-apoptotic and pro-apoptotic proteins, also leading to senescent cell apoptosis [105]