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Additionally, analogues containing the quinolinium scaffold lacked inhibitory activity against enzymes in the NAD + salvage pathway that bind nicotinamide-containing substrate, including NAMPT[27, 32] and the NAD + -dependent SIRT1 enzyme, which deacetylates NAD + to produce NA, a product inhibitor of SIRT1.[33] These results suggest that quinolinium-based NNMT inhibitors achieve selectivity by specifically interacting with the NA-binding pocket of NNMT,[17] unlike several known non-selective methyltransferase inhibitors that interact with the SAM-binding pocket, which is highly conserved among SAM-dependent methyltransferases.[34, 35] Membrane-permeable NNMT inhibitors reduced intracellular 1-MNA levels in a concentration-dependent manner and at pharmacologically relevant concentrations that did not impact cell viability, suggesting these small molecules interact directly with NNMT in cells

Common applications include: Obesity and Body-Weight Regulation Models : Studying how chronic exposure to AOD 9604 affects body weight, fat, and energy use in obese rodents, often using calorimetry (measuring energy expenditure) and body fat measurements

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In a cervical cancer cell line (HeLa), the compound reduced cell proliferation in a concentration- and time-dependent way and lowered expression of phospho-Akt and SIRT1, two proteins tied to tumor progression, while a non-cancer reference cell line was less affected