Quercetin seems to be. But following a quick Internet search (Google) it seems a bit inconclusive for EGCG.
Where the balance of evidence lies
- Most consistent: EGCG = HAT (p300/CBP) inhibitor that also modulates DNMTs. This readily explains increased histone acetylation at some loci (via network effects) and promoter-specific recruitment of HDACs. aacrjournals.org+1
- Less consistent / weaker: potent, direct HDAC inhibition across classes with reproducible biochemical IC₅₀ values. Reports exist, but they’re mixed and often cell-context or assay-format–dependent. PMC+1
https://claude.ai/share/90240dd1-051c-4fff-8ebc-431161b00975
Overall assessment: While EGCG does influence histone acetylation status and has been called an “HDAC inhibitor” in some literature, the mechanistic evidence suggests it functions primarily as a HAT inhibitor with possible weak, indirect effects on HDAC activity. The term “HDAC inhibitor” may be a misnomer for EGCG, though it does ultimately affect the acetylation balance in cells.
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Everything body talks about glitazone.
But what about saroglitazar??
Same effectiveness, no sides, and lower lipids!