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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

4C ) indicates a positive correlation

Approximately half of SSADH patients are affected by seizures because the illness is accompanied by disrupted GABA homeostasis

The FSP1-CoQ 10 -NAD(P)H pathway The FSP1 gene was initially identified as a pro-apoptotic gene, 230 but has also been identified as an anti-ferroptosis gene via FSP1s oxidoreductase activity, which reduces CoQ 10 to ubiquinol (CoQ 10 H 2 )

Partial responses occurred in 6%, stable disease in 50%, and progression in 44%

These data allow us to conclude that mitochondrial LPO is not sufficient for ferroptosis and that cytosolic ROS mediates additional oxidative events that stimulate ferroptosis in conjunction with mitochondrial LPO