NAD+

A coenzyme studied in cellular-energy, sirtuin-pathway and longevity research.

NAD+ is catalogued here as a reference compound for immune-modulation and cellular-energy research. The entry covers its chemical identity and the public databases that describe it; it is not a usage guide.

NAD+ appears in the immune-modulation and cellular-energy literature, primarily in in-vitro and preclinical (animal) models. This page indexes 4 verified primary papers on NAD+ (2 rodent, 1 in-vitro and 1 review), each resolvable by PMID or DOI. Peptidoteca summarizes the proposed mechanism class and the primary sources rather than human outcomes; for the wider library, see the research library.

Attributed, study-level findings from the verified literature indexed on this page — preclinical observations, not clinical outcomes:

• Wang X et al. (2026), Antioxidants & Redox Signaling [rodent] — In a rodent cerebral ischemia/reperfusion model, the report associates augmented SLC25A51-mediated mitochondrial NAD+ import with restored mitochondrial NAD+ pools, improved mitochondrial respiratory function, and reduced oxidative lipid damage in neuronal tissue.
• Heaselgrave SR et al. (2026), Journal of Endocrinology [rodent] — In male and female mice exposed to sustained corticosterone, this study reports tissue- and sex-specific changes in NAD+ and related metabolites in skeletal muscle and liver, and observes that nicotinamide riboside supplementation does not prevent the metabolic features associated with glucocorticoid excess in this rodent model.
• Chen C et al. (2026), Toxins (Basel) [in-vitro] — In an HEK293T renal cell-line model, the report links deoxynivalenol exposure to PARP1-driven NAD+ depletion and associates nicotinamide with suppressed PARP1 activity, replenished NAD+ pools, and attenuated cytotoxicity in vitro.
• Zhang SQ et al. (2026), Alzheimer's & Dementia [review] — This review synthesizes evidence on the bidirectional coupling between NAD+ metabolism and circadian regulation in dementia disorders, discussing NAMPT-mediated salvage synthesis and NAD+/sirtuin signaling in relation to reported sleep and cognitive phenotypes.

No. NAD+ is supplied for laboratory (in-vitro) research use only. It is not approved by the FDA or any comparable regulator for human or veterinary use, and nothing on this page constitutes medical advice, dosing guidance or a treatment recommendation.

Most available evidence for NAD+ is preclinical — in-vitro and animal models — and findings in those models do not establish efficacy or safety in humans. Human clinical data is limited or absent, and NAD+ is not an approved drug. Treat the literature as mechanistic research, not clinical guidance.