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Description

Increases SIRT-1 activity as a result of enhanced NAD+ salvage, leading to beneficial epigenetic and metabolic reprogramming, including increased oxidative phosphorylation (OXPHOS) and muscle stem cell activation 1-3

3 Frontiers in Pharmacology (2024)NNMT as a candidate therapeutic target for metabolic syndrome (review)

The tirzepatide with B12 guide explains the rationale

By preserving SAM, NNMT inhibition may restore normal epigenetic control of metabolic gene expression in fat cells

When NNMT activity is elevated as documented in obese adipose tissue, several cancer types, and aged skeletal muscle intracellular NAD+ availability decreases, SAM availability decreases, and downstream sirtuin activity (particularly SIRT1 and SIRT3) is reduced