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Alex Ankar, Kumar A

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

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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

Critical Reviews in Eukaryotic Gene Expression