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Its substrate site-targeting mechanism inhibiting NNMT at the nicotinamide binding site provides selectivity over related methyltransferases and other enzymes in the NAD salvage pathway, making it a precise tool compound for studying NNMT-specific enzymatic activity in controlled laboratory systems

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It is unknown whether suppressing the anti-cancer immune response generated by M2 macrophage polarization in the TME is more effective than boosting the anti-cancer immune response generated by M1 macrophage polarization because M2 macrophages consume more glutamine than M1 macrophages (Fig