K4 Elite
K4 Elite
NAD+ (nicotinamide adenine dinucleotide) is a fundamental coenzyme central to cellular energy metabolism and redox reactions, and a major focus of aging research due to its decline with age and role in sirtuin and PARP signaling.
Nicotinamide adenine dinucleotide (NAD+) is one of the most fundamental coenzymes in biology, present in every living cell. It exists in oxidized (NAD+) and reduced (NADH) forms and functions as a central electron carrier in metabolic pathways including glycolysis, the citric acid cycle, and oxidative phosphorylation.
Beyond its classical redox role, NAD+ serves as a substrate for enzymes such as sirtuins and PARPs, linking it to DNA repair, gene regulation, and cellular stress responses. Because cellular NAD+ levels decline with age, it has become a central molecule in aging and metabolic research.
This entry describes NAD+ as a research reference compound. While NAD+ and its precursors are widely studied, the material here is intended for laboratory investigation, not therapeutic use.
NAD+ operates as a hydride-accepting coenzyme, cycling between NAD+ and NADH to shuttle reducing equivalents through central metabolism and drive ATP production via the electron transport chain.
As a consumed substrate, NAD+ is used by sirtuin deacylases (which regulate metabolism and stress responses) and by PARP enzymes (involved in DNA-damage repair), as well as CD38 and other NAD+-consuming enzymes. Research on NAD+ precursors such as nicotinamide riboside and nicotinamide mononucleotide focuses on restoring the age-associated decline in these pathways.
Trammell and colleagues (2016) administered the NAD+ precursor nicotinamide riboside to mice and healthy human volunteers, measuring blood NAD+ metabolome by mass spectrometry; the study reported dose-dependent increases in circulating NAD+ and related metabolites [1].
Yoshino and colleagues investigated nicotinamide mononucleotide in rodent models of diet- and age-induced metabolic dysfunction, using glucose tolerance and mitochondrial function endpoints, and reported improvements in these metabolic measures in the treated animals at the doses studied [2].
Review work by Verdin (2015) synthesized evidence across species describing the decline of NAD+ with age and the effects of restoring NAD+ on sirtuin activity and mitochondrial function [3].
Combinations examined in the research literature. Descriptive only — not a recommendation to combine compounds.