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Sustained GHRHR activation by CJC-1295 with DAC could theoretically cause receptor downregulation or feedback suppression of endogenous GHRH release
Updated Sept 2022
More recent evidence demonstrates that although reduced ACC1 activity may decrease fatty acid synthesis, there is a paradoxical promotion of a pro-tumorigenic phenotype due to increased availability of acetyl-CoA for use by the enzyme histone acetyltransferase P300
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DAC is therefore the main reason why CJC-1295 with DAC behaves differently from the version without DAC
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