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NAD+Important information. The data compiled from scientific literature is provided for educational purposes. Dosage ranges reflect what is reported in studies and do not constitute a recommendation, prescription, or usage guidance. Health decisions should always be made with a qualified professional.
Scientific literature related to NAD+ and its potential applications.
Macromolecular crowding by dextran alters YADH kinetics in a substrate-dependent manner: crowding reduces Vmax for ethanol (likely due to slower NADH release) but increases Vmax for larger alcohols (where hydride transfer is rate-limiting).
In murine osteoclast progenitors, Sirt1 activation (by SRT2104/SRT3025) suppresses osteoclastogenesis via deacetylation and activation of FoxO transcription factors, which induce genes (e.g., HO-1, catalase) that impair mitochondrial ATP production; FoxOs are required for the antiosteoclastogenic effects.
In this preclinical report, nicotinamide (an NAD+ precursor) was associated with preserved mitochondrial integrity, improved autophagy-lysosome function, activation of pro-survival signaling, reduced Aβ and tau pathologies, and improved cognition in 3xTgAD mice, but the abstract lacks critical methodological and quantitative details.
Low-intensity ultrasound can trigger single-electron reduction of aromatic azide prodrugs in the presence of NADH and a riboflavin-based electron-transfer catalyst (TBR); co-loading prodrug and catalyst into nanoparticles enables tumor-selective activation, robust antitumor immunity, and near-complete tumor suppression in a murine CT26 model.
miR-10b-5p is upregulated in primary liver cancer and promotes tumor growth and metabolic reprogramming in vitro and in vivo by directly targeting and downregulating the amino acid transporter SLC38A2; miR-10b-5p overexpression is associated with increased tumor NAD+ levels among other metabolite changes.
In Jingyuan chicken breast muscle, beta-nicotinamide adenine dinucleotide (annotated as NAD+) showed a marked age-dependent pattern—substantially increased from 42 to 126 days and then decreased from 126 to 180 days—and was enriched in longevity-regulating and oxidative phosphorylation pathways; in older birds (126 vs 180 days) NAD+ abundance correlated positively with muscle lipid content and several meat quality traits, but these are associative findings from untargeted metabolomics and require targeted validation and functional studies.
The study reports a bacterial antiphage immune pathway that uses deaminated nucleotides (dITPs) as signaling molecules; dITP activates an effector that depletes cellular NAD+ to kill infected cells, while phages counter by depleting the dITP precursor (dAMP).
Bioinformatics analysis identified an 11-gene set related to disulfidptosis and a four-gene signature (BRK1, NDUFA11, RAC1, NDUFS1) that discriminates cervical cancer from normal tissue with high AUCs; NDUFA11 and BRK1 associate with improved survival, but results require experimental and clinical validation. The peptide NAD+ is not mentioned or studied in the supplied content.
In this mouse study, oral ferulic acid increased serum NAD+ levels and decreased oxidative and inflammatory markers after 6.0 Gy whole-body irradiation, coinciding with improved hematopoietic progenitor recovery and reduced JAK/STAT pathway protein levels in bone marrow.
The abstract reports a stretchable printed electrode lactate sensor using LDH with NAD+ cofactor and a Toluidine Blue O/MWCNT electron-transfer layer that produces concurrent electrochemical and fluorescence signals, with a reported ultrahigh active surface area (648%) and apparent robustness under simulated deformation and shifted excitation conditions; however, quantitative analytical metrics and in vivo/human testing are not provided in the abstract.