Redox cofactor (nicotinamide adenine dinucleotide)
NAD+
Essential hydride-transfer cofactor for dehydrogenases and substrate for sirtuins and PARPs; parenteral is a cofactor supply, not a drug.
Primary Mechanism of Action
Clinical / Scientific
/NADH is the central redox couple of , the TCA cycle, and oxidative phosphorylation. is also consumed by sirtuins (deacetylation) and PARPs (DNA-repair ADP-ribosylation). Raising extracellular does not automatically equal raising every tissue’s nuclear pool; pharmacokinetics of infusions and precursors differ.
Pathway Targets
Redox metabolism
Scientific explanation
Hydride transfer in dehydrogenase reactions.
Sirtuins
Scientific explanation
-dependent deacetylation.
PARP
Scientific explanation
consumption in ADP-ribosylation.
Pathway Convergence
Clinical / Scientific
Target → pathway → downstream effect → biological consequence. This is a mechanistic map, not a treatment claim.
Receptor to physiology
Target to downstream effect: Redox metabolism → Sirtuins → PARP
Mechanistically Relevant Repurposed & Adjunctive Applications
Research peptide context
PreclinicalMechanistic rationale
Catalogued as a research peptide. Mechanistic statements below describe known or pathway biology and do not establish a licensed therapeutic indication.
Mechanistic Application Matrix
| Biological Target | Mechanism | Potential Relevance | Evidence Level |
|---|---|---|---|
| Dehydrogenases | Cofactor | Cellular respiration | Established mechanism |
| Sirtuins / PARPs | Substrate | Stress signalling | Established mechanism |
In Plain Language
is a rechargeable chemical battery-helper that hundreds of enzymes use. Giving in a vial supplies that helper; it is not a hormone with one .
Mechanistic information is provided for scientific and educational purposes. Discussion of biological pathways or investigational applications does not establish clinical efficacy or constitute individualized medical advice.