Mitochondrial coenzyme (pyridine nucleotide) Limited Human Data

NAD+

Also Known As: Nicotinamide Adenine Dinucleotide, NAD, β-NAD+

Nicotinamide adenine dinucleotide (NAD+) is a universal pyridine-nucleotide coenzyme that acts as an electron carrier in mitochondrial redox reactions and as a co-substrate for sirtuins (NAD+-dependent deacetylases), PARPs (poly-ADP-ribose polymerases) and CD38. It is NOT a peptide; it is listed alongside the research peptides for operational reasons. Limited human data — research use only.

NAD+ – peptide vial product image

Identity & Chemistry

Molecular Formula
C21H27N7O14P2
Molecular Weight
663.43 g/mol
CAS Number
53-84-9
PubChem CID
5893
IUPAC Name
[(2R,3S,4R,5R)-5-(6-aminopurin-9-yl)-3,4-dihydroxyoxolan-2-yl]methyl [hydroxy-[[(2R,3S,4R,5R)-3,4-dihydroxy-5-(3-carbamoylpyridin-1-ium-1-yl)oxolan-2-yl]methoxy]phosphoryl] phosphate

Mechanism of Action

Studies report that intracellular NAD+ stimulates SIRT1 / SIRT3 activity, mitochondrial biogenesis and PARP1-mediated DNA repair. Observed in research settings.

NAD+ transfers hydride ions through Complexes I and III of the respiratory chain. As a sirtuin co-substrate, it is consumed during each deacetylation and hydrolysed to nicotinamide + ADP-ribose. Tissue NAD+ levels decline with age, which Sinclair and Verdin have proposed as a mechanistic node for age-associated mitochondrial dysfunction. Direct intravenous NAD+ has been studied in small open-label trials; oral bioavailability is poor, so precursors (NR, NMN) dominate translational work.

Molecular Targets

  • Sirtuins (SIRT1, SIRT3)
  • PARP1
  • CD38
  • Mitochondrial complexes I/III (electron carrier)

Signaling Pathways

  • Oxidative phosphorylation
  • Sirtuin-mediated deacetylation
  • Poly-ADP-ribosylation / DNA repair

Research Applications

The published evidence base is dominated by animal studies and small human trials of NAD+ precursors (nicotinamide riboside, NMN); direct NAD+-infusion studies are small and uncontrolled.

Mitochondrial function in ageing — preclinical

in vivo

NAD+ restoration in aged mice partially reverses mitochondrial dysfunction and skeletal-muscle insulin resistance (Gomes 2013).

— Gomes AP et al. 2013, Cell 155(7):1624-1638

Clinical Status

Regulatory Status
NAD+ is NOT an approved drug by the FDA, EMA, MHRA or any other Western regulator. It is sold as a dietary-supplement ingredient (NAD precursors) and in some jurisdictions delivered as an off-label IV by non-traditional clinics — these uses are not regulatory approvals.
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Sponsor
None — public-domain coenzyme; academic research dominates

Safety Profile

Observed in research settings

Limited human data. Small open-label IV NAD+ studies report generally good tolerability; systematic pharmacovigilance data do not exist. Observed in research settings.

Adverse Events Reported in Studies

  • Flushing, nausea or chest pressure during IV infusion (reported with rapid infusion rates)
  • Injection-site reactions

References

  1. Rajman L, Chwalek K, Sinclair DA Therapeutic potential of NAD-boosting molecules: the in vivo evidence Cell Metabolism 2018;27(3):529-547. 2018 .

    DOI: 10.1016/j.cmet.2018.02.011 PMID: 29514064 View Source

  2. Verdin E NAD+ in aging, metabolism, and neurodegeneration Science 2015;350(6265):1208-1213. 2015 .

    DOI: 10.1126/science.aac4854 PMID: 26785480 View Source

  3. Cantó C, Menzies KJ, Auwerx J NAD+ metabolism and the control of energy homeostasis: a balancing act between mitochondria and the nucleus Cell Metabolism 2015;22(1):31-53. 2015 .

    DOI: 10.1016/j.cmet.2015.05.023 PMID: 26118927 View Source

Frequently Asked Questions

Is NAD+ a peptide?
No. NAD+ is a pyridine-nucleotide coenzyme, not a peptide. It is listed in this catalog alongside the research peptides for operational reasons.
Is NAD+ approved by the FDA or EMA?
No. NAD+ is NOT an approved drug. It is supplied for research use only.

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