Research At a Glance
- Research Category
- Cellular Energy & Longevity Research
- Peptide Length
- Dinucleotide coenzyme (non-peptide)
- Purity
- ≥ 98% (HPLC)
- Published Studies
- 75,000+ indexed
- Storage
- Lyophilized: −20 °C long term, 2–8 °C short term. Reconstituted: 2–8 °C, use within 30 days.
Published-study figures are approximate PubMed result counts and indicate the volume of available literature only. Purity reflects third-party analytical testing on the corresponding lot; see the Quality Assurance Center for lot-matched certificates.
What Is NAD+?
Nicotinamide adenine dinucleotide (NAD+) is a coenzyme present in every living cell, playing a central role in cellular energy metabolism, redox reactions, and DNA repair processes. Unlike most compounds in this catalog, NAD+ is not itself a peptide, but it is frequently studied alongside mitochondrial peptides due to its foundational role in cellular bioenergetics.
Why Researchers Study It
NAD+ is one of the most heavily studied molecules in mitochondrial and aging research, relevant to:
- Mitochondrial bioenergetics — NAD+ serves as the primary electron donor in the mitochondrial respiratory chain, making it central to ATP production research
- Aging and cellular senescence models — declining NAD+ levels have been consistently observed in research models of aging, linked to reduced mitochondrial function and impaired DNA repair capacity
- Sirtuin pathway research — NAD+ availability is a required cofactor for sirtuin enzyme activity, a family of proteins studied for their role in mitochondrial biogenesis, metabolic regulation, and stress response
- Comparative mitochondrial peptide research — often studied in conjunction with mitochondrial-derived peptides such as MOTS-c to examine combined effects on cellular energy pathways
What the Published Literature Shows
A substantial and growing body of peer-reviewed literature has characterized NAD+'s role in mitochondrial and metabolic disease research. Research has established that declining cellular NAD+ levels are associated with impaired mitochondrial homeostasis, including disruption of mitophagy, the unfolded protein response, and antioxidant defense systems — processes implicated in research models of cognitive decline, sarcopenia, and metabolic disease.
Separate lines of research have investigated strategies for raising cellular NAD+ levels, including precursor-based approaches, as a means of restoring mitochondrial and organismal homeostasis in research models. Studies in cardiovascular and neurodegenerative disease research have similarly identified NAD+ metabolism as a relevant pathway, given its role in redox reactions and cellular stress adaptation across multiple organ systems.
This expanding literature base has positioned NAD+ as a foundational reference molecule in mitochondrial bioenergetics and aging-related research programs.
Source
Review literature available via PubMed — NAD+ metabolism and mitochondria .
Compound Specifications
| Classification | Cellular coenzyme (non-peptide) |
|---|---|
| Role | Electron carrier, sirtuin cofactor, DNA repair substrate |
| Format | Lyophilized powder |
| Purity | ≥99% (HPLC-verified per lot) |
| Storage | −20°C; refrigerate 2–8°C after laboratory handling |
Certificate of Analysis
Every lot is independently tested and lot-matched. View Certificates of Analysis