DOCUMENTED BY BATCHIdentity (HPLC)
High-performance liquid chromatography records the compound’s retention profile against a reference.
Research peptide
NAD+
Lyophilized powder, catalogued by compound identity and backed by a certificate of analysis for its production batch.
For laboratory research only. Not for human or veterinary use.
Indicative · checkout opens at launch
Research use only
≥99% purity*
Batch tested
$100.00In stock
Size
1,000 mg
Buying option
Buy now · $100.00100 in stock
Sealed, labelled vials · US delivery
| Quantity | 5–9 | 10+ |
|---|---|---|
| Discount | 10% | 15% |
| Price | $90.00 | $85.00 |
Indicative volume pricing, confirmed at launch.
View specifications Batch documentation Certificate of analysis
- Third-party tested
- Secure packaging
- Supplied for laboratory research
- Identity by HPLC & LC-MS Compound identity documented per batch.
- Batch-specific COA A certificate of analysis per batch.
- Secure packaging Sealed, labelled research vials.
- Third-party tested Independent testing per batch.
Documented by batch
Every batch is catalogued, tested and recorded.
Overview
NAD+ (Nicotinamide Adenine Dinucleotide)
Research grade NAD+ for scientific and laboratory research. Nicotinamide adenine dinucleotide (NAD+) is an essential coenzyme and metabolite present throughout living systems. It is not a peptide. Chemically, NAD+ is a dinucleotide composed of nicotinamide and adenine nucleotides linked through their phosphate groups. NAD+ participates in cellular energy metabolism, oxidation-reduction chemistry, DNA-damage responses and intracellular signalling, making it a major subject of investigation across biochemistry, molecular biology, mitochondrial research, metabolism, neuroscience and ageing biology.
Understanding NAD+
NAD+ was identified during early twentieth-century investigations of fermentation and cellular respiration. Subsequent research established that it functions as an electron carrier by alternating between its oxidised form, NAD+, and its reduced form, NADH. In redox reactions, NAD+ accepts electrons and a proton to form NADH. NADH can then transfer reducing equivalents into pathways including mitochondrial electron transport, supporting the processes that generate adenosine triphosphate (ATP).
This NAD+/NADH redox pair is required for central metabolic pathways including central carbon metabolism, the tricarboxylic acid pathway and oxidative phosphorylation. NAD+ availability and the NAD+/NADH ratio influence metabolic flux, cellular redox state and the capacity of cells to respond to changing energy demand. NAD+ is compartmentalised among the cytosol, nucleus and mitochondria, and these pools are regulated through interconnected but distinct biosynthetic and consumption pathways.
NAD+ as a consumable signalling substrate
The biological importance of NAD+ extends beyond redox metabolism. NAD+ is consumed as a substrate by several enzyme families, including sirtuins, poly(ADP-ribose) polymerases (PARPs), CD38 and related NADases. Unlike reversible redox interconversion between NAD+ and NADH, these reactions cleave NAD+ and therefore require continual resynthesis through de novo, Preiss-Handler and salvage pathways.
Why NAD+ is a focus of research
Sirtuins are NAD+-dependent protein deacylases that regulate diverse cellular processes. The seven mammalian sirtuins, SIRT1 through SIRT7, are distributed across the nucleus, cytosol and mitochondria. Experimental research examines their roles in gene regulation, mitochondrial function, metabolic adaptation, circadian biology and cellular stress responses. NAD+ availability can influence sirtuin activity, but changes in NAD+ do not necessarily produce uniform biological effects across tissues or experimental conditions.
PARP enzymes use NAD+ to transfer ADP-ribose units to target proteins during processes that include DNA-damage signalling and processing. PARP1 is activated in response to several forms of DNA damage. Sustained or excessive PARP activity can consume substantial amounts of NAD+, linking genomic stress to cellular energy metabolism. Researchers continue investigating how NAD+ availability, PARP activity and DNA-damage-response capacity interact under normal and pathological conditions.
CD38 is a multifunctional NAD+-consuming enzyme involved in the production of signalling molecules including cyclic ADP-ribose and ADP-ribose. These metabolites participate in calcium signalling and immune-cell biology. Animal and cellular studies implicate CD38 activity in age-associated changes in NAD+ metabolism, but the magnitude, timing and tissue distribution of age-related NAD+ changes in humans remain incompletely characterised.
Mitochondrial biology is one of the largest areas of NAD+ research. Mitochondria rely on NADH-derived reducing equivalents to support electron transport and ATP production. Experimental studies investigate how NAD+ metabolism relates to mitochondrial respiration, substrate oxidation, redox balance, mitochondrial biogenesis and cellular adaptation to energetic stress. Because NAD+ pools are compartmentalised, measurements from blood or one tissue cannot automatically be assumed to represent mitochondrial NAD+ availability in another tissue.
Ageing research has generated substantial interest in NAD+ metabolism. Many animal studies report declines in NAD+ availability with age in particular tissues and experimental conditions. Human data are more limited and tissue-specific, and current reviews caution against assuming that findings from rodents apply uniformly to people. Research continues to examine whether changes in NAD+ synthesis, consumption, compartmentalisation or precursor availability contribute to age-associated biological changes.
Endogenous NAD+, direct materials and precursors
A major distinction is required between endogenous NAD+ biology, direct use of NAD+, and use of NAD+ precursors. Much of the human intervention literature evaluates precursors such as nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), nicotinamide or nicotinic acid. These compounds enter NAD+ biosynthetic pathways but are not identical to NAD+ itself. Findings from precursor studies should not be represented as direct evidence for an NAD+ research product.
Systematic reviews of human research report that NAD+-raising interventions can alter NAD+-related biomarkers, particularly when precursor compounds are used. However, evidence for broad claims about ageing biology or general physiological outcomes remains inconclusive. Published evidence for direct exogenous NAD+ is substantially more limited than the literature on oral precursors, and available studies are generally small or exploratory.
Current NAD+ research spans cellular bioenergetics, mitochondrial function, metabolic regulation, DNA-damage responses, sirtuin biology, PARP signalling, CD38 activity, neurobiology, immune-cell metabolism, skeletal-tissue physiology and exercise adaptation. The breadth of these research areas reflects the central biochemical role of NAD+, but it does not mean that direct use of an NAD+ research product has been validated for each field.
Documentation and quality considerations
At livvmore, NAD+ should be classified as a research coenzyme or laboratory research compound rather than a research peptide. Each production batch should be supported by product-specific analytical documentation. Appropriate documentation may include identity testing, purity analysis, assay or content measurement, water content where relevant, residual-solvent information and batch traceability. Product claims should match the results reported on the batch-specific Certificate of Analysis.
Researchers should consider the chemical form, salt form, purity, water content, storage conditions and analytical method when comparing NAD+ materials. A chromatographic purity percentage alone does not necessarily establish total assay, identity, stability or suitability for a particular experiment.
livvmore NAD+ is supplied exclusively for laboratory research and analytical investigation. Mechanistic findings involving endogenous NAD+, animal models or NAD+ precursors should not be interpreted as evidence of activity for this product.
For laboratory research use only. Not for human or veterinary use.
Documented by batchCatalogued by compound identity
Compound identityCAS · Molecular weight · Sequence
Batch recordsBatch · Lot · Production date
Independent testingHPLC · LC-MS
Specifications
Product specifications
Format
Lyophilized powder
Appearance
Powder
Molecular weight
663.43 g/mol
CAS number
53-84-9
Sequence
Not a peptide – a dinucleotide coenzyme (C21H27N7O14P2)
Storage
Store refrigerated at 2–8°C, protected from light and moisture. For extended storage, follow your laboratory's standard storage procedures.
Batch documentation
The certificate for the current batch
Every batch is third-party tested. The batch-specific certificate of analysis is available on request; the layout below shows the fields it records.
Certificate of analysis
Specimen layout
- Compound
- product identity
- Batch
- batch number
- Produced
- production date
- Appearance
- recorded appearance
- Identity (HPLC)
- recorded
- Mass (LC-MS)
- recorded
Specimen layout. A batch-specific certificate of analysis is issued for each production run and is available on request.
- Compound and batch identify the exact material supplied.
- Batch and production date tie the certificate to its production run.
- Identity records (HPLC, LC-MS) document what was tested on the batch.
Testing records
What each batch record documents
Every batch is accompanied by laboratory records. The entries below describe what each record documents.
Mass (LC-MS)
Mass spectrometry records the compound’s measured mass to document molecular identity.
Appearance
The physical appearance of the material is recorded, for example a white lyophilized powder.
Batch record
Each batch is logged with a lot number and production date for traceability.
These are records of laboratory testing carried out on the batch. They document compound identity for research use and are not a statement of safety, suitability, or fitness for any use.
Research information
NAD+ research context
Nicotinamide adenine dinucleotide is both a redox coenzyme and a consumable substrate for signalling enzymes. This dual role places NAD+ at the intersection of cellular energy metabolism, mitochondrial function, genome maintenance and intracellular communication.
Interpretation of NAD+ research requires careful separation of four related but different subjects: endogenous NAD+ metabolism; experimental manipulation of NAD+ biosynthesis or consumption; use of NAD+ precursors; and direct use of NAD+ itself. Evidence from one category should not automatically be applied to another. This information is provided solely for scientific, analytical and educational purposes.
Current areas of scientific investigation
- Cellular bioenergetics. NAD+ and NADH transfer reducing equivalents through central carbon metabolism, the tricarboxylic acid pathway, beta-oxidation and mitochondrial oxidative phosphorylation. Researchers examine how the NAD+/NADH ratio affects metabolic flux, ATP-generating capacity, lactate production and cellular responses to energetic demand.
- Mitochondrial function. Mitochondrial NADH supplies electrons to respiratory complex I. Research investigates mitochondrial NAD+ pools, electron transport, respiratory efficiency, redox balance, substrate oxidation and mitochondrial stress responses. NAD+ is compartmentalised, so whole-blood or plasma measurements may not reflect mitochondrial concentrations in specific tissues.
- NAD+ biosynthesis and salvage pathways. Mammalian cells maintain NAD+ through de novo synthesis from tryptophan, the Preiss-Handler pathway from nicotinic acid and salvage pathways using nicotinamide and related precursors. The nicotinamide salvage pathway is a major source of NAD+ in many tissues. Researchers investigate enzymes including NAMPT, NMNATs and NAPRT as regulators of NAD+ availability.
- Sirtuin biology. SIRT1 through SIRT7 require NAD+ for deacylation and related enzymatic reactions. Studies examine their roles in transcriptional regulation, mitochondrial metabolism, chromatin biology, circadian signalling and stress adaptation. Sirtuin biology is tissue- and context-dependent, and increased NAD+ availability does not guarantee a uniform functional response.
- PARP signalling and DNA-damage response. PARPs consume NAD+ during ADP-ribosylation reactions involved in DNA-damage signalling and genome maintenance. Excessive PARP activation can deplete cellular NAD+ and impair energy metabolism. Current research examines the balance between DNA-damage response, NAD+ consumption and cellular survival.
- CD38 and calcium signalling. CD38 metabolises NAD+ and produces ADP-ribose-related second messengers involved in calcium mobilisation. Experimental studies investigate CD38 in immune-cell function and age-related NAD+ metabolism. Much of the causal evidence for age-associated NAD+ loss through CD38 comes from animal and cellular models.
- Metabolic research. NAD+ metabolism is investigated in relation to energy-substrate handling, lipid oxidation and metabolic flexibility. Human intervention findings vary by compound, amount, tissue and outcome. Evidence involving NR, NMN, nicotinamide or nicotinic acid should be identified as precursor evidence rather than direct NAD+ evidence.
- Neurobiology. Neurons depend heavily on mitochondrial energy metabolism and NAD+ homeostasis. Research examines axonal degeneration, SARM1-mediated NAD+ cleavage, neuroinflammation, mitochondrial dysfunction and neurodegenerative disease models. Most proposed translational applications remain investigational.
- Exercise and skeletal-tissue physiology. Studies investigate changes in NAD+ metabolism during exercise, skeletal-tissue adaptation, mitochondrial biogenesis and ageing. Human evidence on NAD+-raising interventions is mixed and frequently based on precursors rather than direct NAD+.
- Ageing biology. Preclinical research links altered NAD+ metabolism with several hallmarks of ageing. Human evidence that NAD+ declines uniformly across tissues is sparse, and tissue-specific measurements remain limited. Current research therefore focuses on defining where, when and why NAD+ changes occur rather than assuming age-associated decline is a universal established fact.
Current evidence landscape
The mechanistic evidence establishing NAD+ as a central coenzyme and signalling substrate is extensive. Its roles in redox chemistry, mitochondrial metabolism, sirtuin activity, PARP reactions and CD38 biology are supported by a large body of biochemical, cellular and animal research.
Human intervention evidence is narrower. Most studies intended to raise NAD+ have used precursor compounds, particularly NR and NMN. These studies generally show that some precursors can increase NAD+-related metabolites, but physiological and experimental outcomes are inconsistent and often limited by small samples, short follow-up and varied study designs.
Evidence for direct exogenous NAD+ is substantially less developed. Recent systematic reviews identify very limited eligible human-study evidence for exogenous NAD+ itself and conclude that activity for broad ageing-biology or general physiological outcomes remains inconclusive.
The page should therefore avoid presenting established endogenous functions of NAD+ as proof that a research NAD+ product produces the same effects. It should also avoid transferring results from NR, NMN, nicotinamide or nicotinic acid studies directly to NAD+.
Scientific limitations
- Human tissue data on age-related NAD+ changes remain limited and tissue-specific.
- Many influential findings derive from cell culture and animal models.
- Most human intervention studies use NAD+ precursors rather than direct NAD+.
- Biomarker increases do not automatically establish functional relevance.
- Results from one NAD+ precursor cannot be assumed to apply to another precursor or to NAD+ itself.
- Published studies of direct exogenous NAD+ are limited and generally exploratory.
- NAD+ pools are compartmentalised, complicating interpretation of blood measurements.
- Optimal analytical methods, handling parameters and long-term safety data for direct use are not established for broad application.
- Product purity alone does not establish identity, assay, stability or experimental suitability.
Recommended product and batch documentation
- Product name: NAD+ (Nicotinamide Adenine Dinucleotide)
- Product classification: Research Coenzyme / Laboratory Research Compound
- Chemical form and salt form, where applicable
- Identity confirmation by an appropriate analytical method
- Chromatographic purity
- Assay or content measurement
- Water content, where relevant
- Residual solvents, where relevant
- Batch or lot number
- Manufacture or test date
- Storage and stability information supported by available data
- Batch-specific Certificate of Analysis
Selected scientific references
- Covarrubias AJ, Perrone R, Grozio A, Verdin E. NAD+ metabolism and its roles in cellular processes during ageing. Nature Reviews Molecular Cell Biology. 2021;22:119-141.
- Xie N, Zhang L, Gao W, et al. Signal Transduct Target Ther. 2020;5:227.
- Verdin E. NAD+ in aging, metabolism, and neurodegeneration. Science. 2015;350:1208-1213.
- Camacho-Pereira J, Tarragó MG, Chini CCS, et al. CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism. Cell Metabolism. 2016;23:1127-1139.
- Cantó C, Menzies KJ, Auwerx J. NAD+ metabolism and the control of energy homeostasis: a balancing act between mitochondria and the nucleus. Cell Metabolism. 2015;22:31-53.
- Gallagher C, et al. 2026.
- Vinten KT, et al. 2025.
- Yaku K, Okabe K, Nakagawa T. NAD+ precursors in human health and disease. 2023.
For laboratory research use only. Not for human or veterinary use.
Frequently asked questions
Questions and documentation
What is NAD+?
NAD+ is catalogued in the Other research compounds collection and supplied as a lyophilized powder for in-vitro laboratory research. It is listed by CAS number 53-84-9 and a molecular weight of 663.43 g/mol. It is not for human or veterinary use.
What is the CAS number for NAD+?
The CAS number recorded for NAD+ is 53-84-9.
What is the molecular weight of NAD+?
The molecular weight recorded for NAD+ is 663.43 g/mol.
How is NAD+ supplied and stored?
NAD+ is supplied as a lyophilized powder. Store refrigerated at 2–8°C, protected from light and moisture. For extended storage, follow your laboratory's standard storage procedures.
What does research use only mean?
All products are supplied strictly for in-vitro laboratory research and are not for human or veterinary use, diagnosis, treatment, or personal consumption.
How are the products documented?
Every batch is third-party tested and documented. The certificate of analysis is available on request.
Is a certificate of analysis available?
Every batch is third-party tested, and the batch-specific certificate of analysis is available on request.
Who can purchase?
By placing an order, purchasers acknowledge that the product is intended solely for laboratory research use and agree to the Research Use Terms.
Fulfilment
How orders are handled
-
Secure packaging
Sealed, labelled research vials, packed to protect integrity in transit.
-
Third-party tested
Every batch is third-party tested; the certificate of analysis is available on request.
-
Research customers only
Supplied to qualified researchers for laboratory research use.
Shipping options and timelines are shown at checkout.
- Third-party tested Independent testing per batch
- Documented by batch Batch and lot records
- Certificate of analysis Available on request
- Identity by HPLC & LC-MS Compound identity documented
- Secure packaging Sealed, labelled research vials
- Supplied for laboratory research Research use only
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NAD+
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