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NNMT normally catalyzes: Nicotinamide + SAM 1-Methylnicotinamide + SAH By inhibiting this pathway, 5-Amino-1MQ alters metabolic signaling relevant to: Energy expenditure Nicotinamide utilization Methyl donor conservation Adipocyte Metabolic Effects Experimental models suggest NNMT inhibition may influence: Fat-cell energy utilization Lipid storage signaling Cellular metabolic efficiency NAD+ Pathway Relevance Research suggests indirect effects on pathways related to: Nicotinamide salvage NAD+ precursor availability Mitochondrial metabolic signaling Preclinical Research Data Murine Adiposity Models Preclinical studies evaluating NNMT inhibition have reported effects involving: Reduced fat mass accumulation Altered adipocyte metabolism Increased energy expenditure markers Experimental outcomes vary by: Dose Duration Model system Route of administration Cellular Models In vitro studies have demonstrated: Target engagement at NNMT Metabolic pathway modulation Altered adipocyte signaling profiles Reconstitution & Handling Reconstitution 5-Amino-1MQ is supplied as lyophilized powder

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We use 5-fold cross-validation by splitting the dataset into five subsets to allow the models to be trained and evaluated on different pieces of data, ensuring consistency of results (see Fig

Byproducts of NNMT, SAH and 1-MNA inhibit NNMT activity via a feedback mechanism (107)

Jacob Temple and Dr