NAD+ (and its precursors NMN / NR)

Identity NAD⁺ is a coenzyme — not a peptide — present in every cell and required for hundreds of enzymatic reactions: the electron-transport chain (ATP/energy), the sirtuins (SIRT1–SIRT7) ("longevity" deacylases), PARPs (DNA repair), and CD38 (immune signalling). Because oral NAD⁺ itself is poorly absorbed, the market sells precursors — mainly NMN and NR — that cells convert into NAD⁺, plus IV NAD⁺ infusions. It's included in this (mostly peptide) register because it is the biochemical hub that several register compounds act through. ## Mechanism (as proposed) NAD⁺ cycles between oxidized (NAD⁺) and reduced (NADH) forms to shuttle electrons in energy metabolism (ATP production). It's also the required substrate for three big consumer classes: sirtuins (SIRT1–7, which deacetylate histones/proteins to regulate metabolism, stress resistance, and gene expression — the "longevity" link), PARPs (DNA-damage repair), and CD38 (whose age-related rise consumes NAD⁺). With age, NAD⁺ falls (more consumption, less synthesis), so sirtuin and repair capacity drop — the rationale for precursor supplementation. NMN and NR feed the salvage pathway to regenerate NAD⁺. All of this biochemistry is solid and non-controversial; what's unresolved is whether pushing NAD⁺ back up in humans actually restores youthful function — the biomarker moves reliably, the clinical outcomes so far mostly don't.