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It accelerates the breakdown of existing fat stores and prevents new fat from forming, regardless of caloric intake

The primary theoretical concern is that sustained NAD+ elevation through chronic NNMT inhibition could activate pathways (PARP, SIRT1) that have context-dependent roles in cancer biology NAD+ supports DNA repair and cellular longevity, but also fuels rapidly dividing cells

Research published in Scientific Reports demonstrates that aged mice treated with NNMT inhibitors showed approximately 40% greater grip strength compared to untreated controls, remarkably surpassing even the benefits achieved through intensive exercise alone, which produced only 20% improvement

The compound appears to work by increasing intracellular NAD+ levels (through preventing nicotinamide consumption by NNMT), which activates sirtuins and enhances mitochondrial function and fatty acid oxidation, while also promoting a phenomenon called "browning" of white adipose tissue - the transformation of energy-storing white fat cells into metabolically active beige/brown adipocytes that burn fatty acids for thermogenesis rather than storing them