NAD+ 1000mg

Nicotinamide adenine dinucleotide (NAD⁺) is a ubiquitous pyridine dinucleotide cofactor central to cellular redox metabolism, sirtuin deacylase activity, poly(ADP-ribose) polymerase signaling, and CD38 ectoenzyme function. BioSim Peptides supplies NAD+ 1000mg as a lyophilized research-grade reference compound for in-vitro laboratory research use only.

This summary covers the chemistry, biochemistry, and published research surrounding NAD+ and NAD-boosting molecules to support investigators studying mitochondrial metabolism, aging biology, and redox signaling in cell, tissue, and preclinical model systems.

What is NAD+?

NAD⁺ (nicotinamide adenine dinucleotide, oxidized form) is a small dinucleotide composed of nicotinamide mononucleotide (NMN) and adenosine monophosphate (AMP) linked through a pyrophosphate bridge. Its molecular formula is C₂₁H₂₇N₇O₁₄P₂ with a molecular weight of approximately 663.4 g/mol. NAD⁺ cycles between oxidized (NAD⁺) and reduced (NADH) forms via hydride transfer at the nicotinamide ring, serving as the principal electron acceptor in glycolysis, the TCA cycle, and β-oxidation.

Although technically a nucleotide rather than a peptide, NAD⁺ is widely catalogued alongside research peptides for laboratories investigating mitochondrial bioenergetics, NAD-dependent enzyme activity, and aging-related metabolic decline. NAD⁺ was first identified by Harden and Young in 1906 as a yeast fermentation cofactor, and decades of biochemistry have refined our understanding of its biosynthetic routes from tryptophan (de novo), nicotinic acid (Preiss–Handler), nicotinamide (salvage), and the precursors nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN) (Yoshino et al., 2018).

Mechanism of Action in Research Models

Beyond its canonical role as a redox cofactor, NAD⁺ serves as a co-substrate for several enzyme families that consume rather than recycle the dinucleotide. The sirtuin family of NAD⁺-dependent deacylases (SIRT1–SIRT7) couples deacetylation of histone and non-histone targets to NAD⁺ hydrolysis, linking cellular energy status to transcription, mitochondrial function, and stress responses (Imai & Guarente, 2014). Poly(ADP-ribose) polymerases (PARPs) consume NAD⁺ during DNA-damage signaling, and the ectoenzyme CD38 hydrolyzes NAD⁺ in a tissue- and age-regulated manner (Camacho-Pereira et al., 2016).

Total cellular NAD⁺ declines with age in multiple tissues, a phenomenon driven in part by elevated CD38 activity and by accumulated DNA damage that activates PARPs (Camacho-Pereira et al., 2016; Rajman et al., 2018). NAD-boosting molecules — including NR and NMN — replenish the NAD⁺ pool through salvage-pathway enzymes (NRK1/2, NAMPT), enhancing sirtuin activity and mitochondrial oxidative metabolism in cultured cells and animal models (Cantó et al., 2012; Yoshino et al., 2018; Rajman et al., 2018).

Key Areas of Scientific Research

Mitochondrial Bioenergetics

NAD⁺/NADH ratios govern flux through the electron-transport chain and TCA cycle, making NAD⁺ a central variable in studies of mitochondrial oxidative capacity. Replenishment of NAD⁺ with precursors such as nicotinamide riboside enhances oxidative metabolism in murine skeletal muscle and protects against high-fat-diet-induced metabolic dysfunction (Cantó et al., 2012).

Sirtuin Biology and Aging Models

The NAD⁺–sirtuin axis is among the most-studied molecular nodes in aging research. NAD⁺ availability directly regulates SIRT1 and SIRT3 activity, which in turn deacetylate transcription factors (FOXO, PGC-1α, NF-κB) and mitochondrial substrates (SOD2, IDH2) implicated in lifespan and healthspan in model organisms (Imai & Guarente, 2014).

DNA-Damage Response and PARP Signaling

PARP1-driven NAD⁺ consumption during persistent DNA damage contributes to NAD⁺ depletion in stressed and aged tissues. Quantitative flux analyses have characterized NAD synthesis–breakdown dynamics in vivo, providing reference values for NAD-flux studies (Liu et al., 2018).

CD38 and NAD Decline

Camacho-Pereira and colleagues established that CD38 ectoenzyme activity rises with age and acts as a principal driver of NAD⁺ decline and mitochondrial dysfunction in a SIRT3-dependent manner (Camacho-Pereira et al., 2016). CD38 inhibitors and NAD precursors are studied together as complementary strategies in preclinical models.

Cardiovascular and Ischemia–Reperfusion Models

Recent preclinical work has examined NAD-boosting molecules in cardiac ischemia–reperfusion paradigms, where nicotinamide riboside attenuated injury via SIRT3/SOD2 signaling pathways (Zhao et al., 2024).

Published Research Highlights

• Imai and Guarente reviewed NAD⁺ and sirtuins in aging and disease, framing NAD⁺ as a metabolic linker between nutrient status and longevity pathways (Imai & Guarente, 2014, Trends in Cell Biology).
• Cantó and colleagues demonstrated that the NAD⁺ precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat-diet-induced obesity in mice (Cantó et al., 2012, Cell Metabolism).
• Yoshino, Baur, and Imai reviewed NMN and NR as NAD⁺ intermediates with therapeutic potential, consolidating preclinical evidence across tissues (Yoshino et al., 2018, Cell Metabolism).
• Camacho-Pereira and coauthors showed that CD38 dictates age-related NAD decline and mitochondrial dysfunction through SIRT3 (Camacho-Pereira et al., 2016, Cell Metabolism).
• Liu and colleagues quantified NAD synthesis–breakdown fluxes across tissues, providing kinetic reference data for NAD studies (Liu et al., 2018, Cell Metabolism).
• Rajman, Chwalek, and Sinclair reviewed in vivo evidence for NAD-boosting molecules across aging and disease models (Rajman et al., 2018, Cell Metabolism).

Neurological and Neurodegenerative Models

The brain is a metabolically demanding tissue, and disrupted NAD⁺ homeostasis has been implicated in models of neurodegeneration, axonal injury, and cognitive aging. NAD⁺ precursors have been investigated in cell-culture and rodent paradigms of Alzheimer-like pathology, Parkinsonian models, and traumatic neuronal injury, with mitochondrial function and sirtuin-dependent transcription serving as common mechanistic readouts (Rajman et al., 2018).

Inflammation and Immunometabolism

NAD⁺ is a substrate for CD38, which is highly expressed on activated immune cells, and CD38-driven NAD⁺ consumption couples inflammation to tissue NAD decline (Camacho-Pereira et al., 2016). Investigators studying immunometabolism use NAD⁺ and its precursors to interrogate macrophage polarization, inflammasome activation, and sirtuin-regulated cytokine programs in cultured cells.

Mitophagy and Mitochondrial Quality Control

NAD⁺-dependent sirtuin signaling has been linked to mitophagy regulation through deacetylation of FOXO transcription factors and components of the autophagy machinery. Reviews of mitophagy regulation by endogenous metabolites position NAD⁺ alongside acetyl-CoA and α-ketoglutarate as a master regulator of mitochondrial turnover (Zhang et al., 2022).

Methodological Notes for NAD Quantitation

Accurate measurement of intracellular NAD⁺ and NADH pools is essential for interpreting experiments with NAD⁺ or its precursors. Enzymatic cycling assays, HPLC with UV detection, and mass-spectrometry-based metabolomics each have characteristic dynamic ranges and interferences. Quantitative flux analyses such as those of Liu and colleagues provide complementary kinetic context, allowing investigators to interpret pool-size changes in the framework of synthesis and consumption rates (Liu et al., 2018).

Stability, Storage, and Handling in Laboratory Settings

Lyophilized NAD⁺ is supplied as a hygroscopic white-to-off-white powder and should be stored desiccated at -20°C protected from light. The dinucleotide is sensitive to moisture, elevated temperature, and alkaline pH, all of which can accelerate hydrolysis of the pyrophosphate bond and degradation of the nicotinamide moiety.

Reconstitution in the laboratory is typically performed with cold, neutral-pH buffered aqueous solutions and used promptly. Reconstituted NAD⁺ is commonly stored at 2–8°C for short-term assays and aliquoted at -20°C or -80°C for longer storage. Freeze–thaw cycles should be minimized, and concentration should be confirmed spectrophotometrically (ε₂₆₀ ≈ 18,000 M^-1cm^-1) when accuracy is critical.

Product Specifications

• CAS Number: 53-84-9 (NAD⁺, free acid)
• Molecular formula: C₂₁H₂₇N₇O₁₄P₂
• Molecular weight: ~663.43 g/mol
• Structure: nicotinamide mononucleotide linked to adenosine monophosphate via pyrophosphate bridge
• Purity: ≥98% by HPLC
• Presentation: 1000 mg per vial, lyophilized powder
• Identity confirmed by HPLC and mass spectrometry
• Certificate of Analysis: available on request
• Shipping: USA-based, tracked dispatch

Why Researchers Choose BioSim Peptides

BioSim Peptides supplies investigators across the United States with reference-grade research compounds suitable for demanding in-vitro and preclinical model work. Every batch produced under our supply program is independently tested by HPLC for chromatographic purity and confirmed by mass spectrometry for accurate molecular identity, with a Certificate of Analysis available on request for each lot.

Researchers working with our material benefit from a guaranteed minimum purity of 98%, lyophilized presentation in tamper-evident vials, domestic USA shipping with tracked carriers, and responsive technical support for handling, reconstitution, and storage questions. Our quality program is designed to deliver the lot-to-lot consistency that reproducible laboratory science requires.

Assay Considerations and In-Vitro Workflow Notes

NAD⁺ quantitation in cell-based assays is performed using enzymatic cycling kits, HPLC with UV detection at 260 nm, or LC–MS/MS-based targeted metabolomics. Each method has distinct strengths: enzymatic cycling offers throughput; HPLC provides direct NAD⁺/NADH discrimination; LC–MS/MS enables simultaneous measurement of NAD⁺, NADH, NMN, NR, NADP⁺, NADPH, and related intermediates with high specificity.

Investigators using exogenous NAD⁺ in cell culture should recognize that intact NAD⁺ is not efficiently taken up by mammalian cells due to its size and charge; the dinucleotide is instead degraded extracellularly to nicotinamide and other intermediates that enter cells through nucleoside transporters or other routes. For intracellular NAD⁺ elevation, NAD⁺ precursors such as nicotinamide riboside or nicotinamide mononucleotide are typically more effective tools, and NAD⁺ itself is most often used for in-vitro enzymatic assays of sirtuins, PARPs, and CD38.

For in-vitro sirtuin and PARP enzymatic assays, NAD⁺ is supplied as a defined cofactor, with reaction conditions optimized for pH (typically 7.5–8.0), ionic strength, and temperature. Stopped-reaction protocols and continuous fluorometric assays each require careful attention to NAD⁺ concentration relative to enzyme K_m, which differs substantially across the sirtuin family (SIRT1–SIRT7) and PARP isoforms.

Related Research Compounds

Investigators studying NAD⁺ biology frequently pair NAD⁺ with its precursors — nicotinamide riboside (NR), nicotinamide mononucleotide (NMN), nicotinic acid, and nicotinamide — to dissect biosynthetic flux through the salvage, Preiss–Handler, and de novo pathways. Inhibitors of NAMPT (e.g., FK866), PARP (e.g., olaparib), and CD38 (e.g., 78c) complete the toolkit for NAD⁺ pathway interrogation in cell-culture and tissue models.

References

1. Imai S, Guarente L. NAD+ and sirtuins in aging and disease. Trends Cell Biol. 2014;24(8):464-471. PMID: 24786309.
2. Cantó C, Houtkooper RH, Pirinen E, et al. The NAD(+) precursor nicotinamide riboside enhances oxidative metabolism and protects against high-fat diet-induced obesity. Cell Metab. 2012;15(6):838-847. PMID: 22682224.
3. Yoshino J, Baur JA, Imai SI. NAD+ intermediates: the biology and therapeutic potential of NMN and NR. Cell Metab. 2018;27(3):513-528. PMID: 29249689.
4. Camacho-Pereira J, Tarragó MG, Chini CCS, et al. CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism. Cell Metab. 2016;23(6):1127-1139. PMID: 27304511.
5. Liu L, Su X, Quinn WJ 3rd, et al. Quantitative analysis of NAD synthesis-breakdown fluxes. Cell Metab. 2018;27(5):1067-1080.e5. PMID: 29685734.
6. Rajman L, Chwalek K, Sinclair DA. Therapeutic potential of NAD-boosting molecules: the in vivo evidence. Cell Metab. 2018;27(3):529-547. PMID: 29514064.
7. Zhao K, et al. Nicotinamide riboside attenuates myocardial ischemia-reperfusion injury via regulating SIRT3/SOD2 signaling. Biomed Pharmacother. 2024;175:116689. PMID: 38703508.

This peptide is supplied by BioSim Peptides for in-vitro laboratory research use only. It is not a drug, supplement, cosmetic, or food product and is not intended for human or veterinary use, consumption, diagnosis, treatment, cure, or prevention of any disease. All research must comply with applicable institutional and regulatory guidelines.

Frequently Asked Questions about NAD+

What is NAD+?

NAD+ is a research peptide supplied by BioSim Peptides for in-vitro and laboratory use only. Each vial is lyophilized, lab-tested, and accompanied by a Certificate of Analysis (COA) verifying identity and purity above 98% by HPLC.

Is the NAD+ from BioSim Peptides third-party tested?

Yes. Every lot of NAD+ 1000mg is independently tested by HPLC and mass spectrometry. The COA for the current batch is available on request and packaged with every order.

How should NAD+ be stored?

Lyophilized NAD+ should be stored at -20°C for long-term stability. After reconstitution with bacteriostatic water it is typically stored at 2-8°C and used within the timeframe described in the published literature for the peptide.

How fast does BioSim Peptides ship?

Orders placed before 2 PM ET ship same business day from our USA facility via tracked carriers. Most domestic orders arrive in 2-4 business days.

Is NAD+ approved for human use?

No. NAD+ is supplied for in-vitro laboratory research only. It is not a drug, dietary supplement, cosmetic, or food, and is not intended for diagnosis, treatment, cure, or prevention of any disease in humans or animals.

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