Mechanism overviews · 29 papers
Peptidoteca
Readypep ↗
↳ Referencia de Péptidos
Immune

NAD+

También conocido como: Nicotinamide adenine dinucleotide

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

Written by Peptidoteca Research Desk·Reviewed by Peptidoteca Research Desk·Last reviewed 2026-06-14·4 sources

§ In brief

NAD+ (also known as Nicotinamide adenine dinucleotide) is a coenzyme studied in cellular-energy, sirtuin-pathway and longevity research. It is supplied for laboratory research use only and is not approved for human or veterinary use. Its full amino-acid sequence is not characterised in this reference.

What is 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.

How is NAD+ studied?

NAD+ appears in the immune-modulation and cellular-energy literature, primarily in in-vitro and preclinical (animal) models. This page indexes 4 primary papers on NAD+, each tagged with its study type below. Peptidoteca summarizes the proposed mechanism class and the primary sources rather than human outcomes; for the wider library, see the research library.

Is NAD+ approved for human use?

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.

What are the research limitations?

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.

§ Primary literature

  1. 1.Wang X (2026). Mitochondrial NAD+ Transport Alleviates Cerebral Ischemia/Reperfusion Injury via Enhancement of Mitochondrial Function. Antioxidants & Redox Signaling.Rodent studyIn 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.
  2. 2.Heaselgrave SR (2026). Glucocorticoid excess disrupts NAD+ homeostasis in male and female mice. Journal of Endocrinology.Rodent studyIn 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.
  3. 3.Chen C (2026). Nicotinamide Ameliorates Deoxynivalenol-Induced Injury in Renal Cells via Inhibiting PARP1 Hyperactivation and Restoring NAD+ Homeostasis. Toxins (Basel).In-vitroIn 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.
  4. 4.Zhang SQ (2026). NAD+-circadian rhythm coupling in dementia. Alzheimer's & Dementia.ReviewThis 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.
Compound spec
Sequence not publicly characterised
ClassImmune
CAS53-84-9
Research vial500 / 1000 mg

Solo para investigación in-vitro. No es consejo médico, clínico ni de dosificación.