AMINO+LABS
Research purposes only. This information does not constitute medical advice. BPC-157, TB-500, CJC-1295, and related peptides are not approved for human use. Semaglutide and tirzepatide are FDA-approved drugs — consult a licensed healthcare provider for any clinical use.
← All peptides

NAD+

Also known as: Nicotinamide Adenine Dinucleotide

An essential cellular coenzyme and substrate for sirtuins and PARP enzymes, studied for its role in energy metabolism, DNA repair, and its decline with age.

Molecular Data

Class
Nucleotide coenzyme (oxidized dinucleotide) — cellular metabolism research compound
Molecular Weight
663.43 Da
Molecular Formula
C₂₁H₂₇N₇O₁₄P₂
Half-Life
Short in circulation (minutes to roughly an hour, estimated); intracellular pools are continuously regenerated via salvage and de novo synthesis pathways
Sequence / Structure
Dinucleotide (adenine nucleotide + nicotinamide nucleotide joined by a pyrophosphate bond) — not a peptide

Mechanism of Action

NAD+ (nicotinamide adenine dinucleotide) is a nucleotide coenzyme present in every living cell, functioning both as an electron carrier in metabolic redox reactions and as a consumed substrate for several enzyme families. Unlike the peptides in this library, NAD+ is not an amino acid chain — it is included here as a widely studied research compound in cellular metabolism and aging biology.

  • Cellular respiration: NAD+ (and its reduced form, NADH) shuttles electrons through the mitochondrial electron transport chain, a step required for oxidative phosphorylation and ATP production.
  • Sirtuin activation: NAD+ is a required substrate for the SIRT1–7 family of deacetylase enzymes, which regulate mitochondrial biogenesis, epigenetic modification, and stress-response pathways implicated in aging research.
  • DNA repair: NAD+ is consumed by poly-ADP-ribose polymerase (PARP) enzymes during DNA damage repair, linking cellular NAD+ availability to genomic stability.
  • Metabolic cofactor function: As a cofactor for dehydrogenase enzymes, NAD+ supports glycolysis, the TCA cycle, and fatty acid beta-oxidation.

Because NAD+ is consumed by sirtuins and PARPs faster than it can always be regenerated, and because total NAD+ pools decline with age, restoring or maintaining NAD+ availability is a central research question in metabolic and aging biology — studied both through direct NAD+ administration and through precursor compounds.

Research History

NAD+'s role as a metabolic redox cofactor has been established biochemistry since the early 20th century, but research interest accelerated substantially after the discovery that sirtuins — enzymes linked to caloric-restriction-associated longevity in model organisms — require NAD+ as an obligate substrate. This connected cellular NAD+ status directly to aging biology research.

Imai, Guarente, and others established that NAD+ levels decline with age across multiple tissues in animal models, and that this decline correlates with reduced sirtuin activity and impaired mitochondrial function. Cantó, Auwerx, and colleagues (2015, Cell Metabolism) reviewed the broader network of NAD+-dependent metabolic processes and the rationale for NAD+ or NAD+-precursor research.

Because directly administered NAD+ has practical limitations (poor cell permeability, rapid extracellular metabolism), much current research has shifted toward NAD+ precursor compounds — nicotinamide mononucleotide (NMN), nicotinamide riboside (NR), and others — that are more readily taken up by cells and converted to NAD+ intracellularly. Clinical research on both direct NAD+ administration (commonly via intravenous infusion in research and wellness settings) and precursor compounds is ongoing; as of current published literature, effects in healthy humans remain an active area of investigation rather than an established clinical intervention.

Notable Studies

NAD+ and Sirtuins in Aging and Disease

2014

Imai S, Guarente L. · Trends in Cell Biology

Review establishing the mechanistic link between declining NAD+ availability, reduced sirtuin activity, and age-related cellular dysfunction.

NAD+ Metabolism and Its Roles in Cellular Processes

2015

Cantó C, Menzies KJ, Auwerx J. · Cell Metabolism

Comprehensive review of NAD+ biosynthesis, consumption, and its roles across metabolic regulation, positioning NAD+ decline as a research target in metabolic disease and aging.

NAD+ in Aging, Metabolism, and Neurodegeneration

2015

Verdin E. · Science

Review synthesizing evidence connecting NAD+ metabolism to aging and neurodegenerative disease research, and potential intervention strategies via precursor compounds.

Research Protocols

The following protocols describe doses used in published research studies. They are not prescriptions or recommendations for human use.

Clinical/research intravenous administration

Dose
250–750 mg per session
Route
Intravenous infusion
Frequency
Once or twice weekly
Duration
Varies by study protocol

Common dose range reported across published research and clinical wellness protocols. Direct NAD+ administration research is distinct from NAD+ precursor (NMN/NR) research, which uses different dosing.

Related Peptides

This information is for research purposes only and does not constitute medical advice. The information presented is drawn from published preclinical and clinical research. Peptides listed here may not be approved for human use in your jurisdiction. Always consult a qualified healthcare professional before considering any substance for personal use.