NJ500 - NAD+ - 500 MG - Research Use Only

Product definition

What is NAD+?

NAD+ is the central cellular redox coenzyme and substrate for sirtuins (SIRT1-7) and PARPs — declining ~50% with age, studied extensively in preclinical aging, metabolic, and neurodegenerative research.

NAD+ (nicotinamide adenine dinucleotide) is a dinucleotide coenzyme present in all living cells, functioning in two pharmacologically distinct roles: as an electron carrier (redox cycling between NAD+ and NADH) in glycolysis, the TCA cycle, and the mitochondrial electron transport chain; and as a consumed substrate for non-redox enzymes including sirtuins (SIRT1-7, histone deacylases), PARPs (DNA repair), CD38/CD157 (cAMP signaling), and SARM1 (axonal degeneration). The aging biology significance is the documented decline: NAD+ tissue concentrations fall approximately 50% between young adulthood and age 60 in humans, a decline attributed to increased CD38 NADase activity with age, decreased NAD+ biosynthesis pathway efficiency, and increased PARP consumption during accumulating DNA damage. This decline has been studied as a causal contributor to the hallmarks of aging: mitochondrial dysfunction, increased genomic instability, impaired cellular senescence regulation, and chronic inflammation (sirtuins regulate NF-κB activity). Preclinical NMN and NR studies in mice have demonstrated that restoring NAD+ levels reverses some of these aging-associated endpoints, driving substantial investment in clinical research.

Research context

What does the preclinical literature say about NAD+?

The NAD+ aging hypothesis was formalized by work from David Sinclair's group at Harvard, Johan Auwerx's group at EPFL, and Charles Brenner's group (discoverer of NR), among others. The foundational observation — that NAD+ levels decline with age and that restoring them in mice produces measurable improvements in aging endpoints — was published across multiple high-impact papers between 2013 and 2019, generating substantial academic and commercial interest. The sirtuin connection is central: SIRT1 deacetylates PGC-1α (mitochondrial biogenesis master regulator), p53 (DNA damage response), NF-κB (inflammation), and FOXO (stress resistance). As NAD+ declines with age, sirtuin activity decreases, potentially contributing to the mitochondrial dysfunction, increased inflammation, and impaired DNA damage response that characterize organismal aging. PARP competition for NAD+ is a parallel research thread: accumulated DNA damage with age activates PARP1, consuming NAD+ faster than it can be replenished — a potential positive feedback loop where aging causes DNA damage, DNA damage activates PARPs, PARP activation depletes NAD+, and NAD+ depletion further impairs the sirtuin-mediated repair pathways. CD38 inhibition and NAD+ repletion both represent pharmacological approaches to breaking this cycle. For injectable NAD+ research specifically: direct intravenous or subcutaneous NAD+ administration is used in clinical and translational research contexts to achieve rapid NAD+ repletion without dependence on NMN or NR conversion pathways, whose efficiency varies across tissues and individuals.