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The logic is that base epithalon has a short half-life and gets degraded quickly, so flooding the system at a higher concentration each day pushes more surviving peptide into target tissues per research dose

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However, in the reperfusion period, its mutual inhibitory interaction with Bcl-2 reduces the function of Bcl-2, which promotes the formation of apoptosome and thereby makes autophagy change from a protective role to a pro-apoptotic one [116]