NAD+
Price range: $100.00 through $180.00
Description
A single-component research material supplied for controlled research environments. Suitable for studies involving nucleotide cofactor characterization and method development in model systems.g., NADH/NADP)
• Stability characterization under laboratory storage conditions (temperature, pH, light)
For qualified research professionals and institutional laboratories. Not for human use.
Documentation & Quality Assurance
Each lot is sourced through our verified global supply chain with emphasis on traceability and quality control.These documents are reviewed internally and displayed as they become available. Independent third-party testing is also performed on select lots to confirm identity, purity, and alignment with our internal specifications.
Important Notice
This product is intended for laboratory research use only. It is not intended for human or veterinary use, and must not be used for diagnostic, therapeutic, or clinical purposes.
This material is not a drug, medical device, or dietary supplement, and has not been evaluated by the U.S. Food and Drug Administration.
Quality & Manufacturing
All materials are sourced from carefully vetted domestic and international manufacturing partners who follow quality systems consistent with ISO and cGMP principles. Each supplier is reviewed for reliability, documentation integrity, and transparency in testing.
We require a verified purity of 99% or higher and perform independent third-party spot testing to confirm that select lots meet our internal standards for identity, purity, and composition. Where available, endotoxin testing results are included on Certificates of Analysis to verify laboratory purity; their inclusion is for research quality assessment only and does not imply suitability for human or veterinary use.
All research materials are sealed for integrity and packaged for stability during storage and transport from manufacturing through final delivery.
Additional information
| Weight | 0.0625 lbs |
|---|---|
| Dosage | 500mg, 1000mg |
Published Scientific Research
Explore the full library of peer-reviewed studies, clinical data, mechanism breakdowns, and molecular specifications for NAD+.
All research is sourced from PubMed-indexed journals for informational and educational purposes only. For Research Use Only (RUO). Not for human use.
View Full Research Library →Certificate of Analysis
Every batch undergoes independent third-party laboratory analysis to verify identity, potency, and safety. Testing includes quantitative assay verification, heavy metals screening, and comprehensive microbial analysis.
All Available COAs
Storage Instructions
All products from Apex Health Performance are manufactured using a lyophilization (freeze-drying) process. This method is designed to maintain product integrity and allows vials to remain stable during shipping for approximately 3–4 months.
Once a vial is reconstituted with bacteriostatic water, it should be stored in the refrigerator to help maintain stability. Under these conditions, reconstituted material is generally considered stable for up to 30 days.
Lyophilization is a dehydration technique in which compounds are frozen and then exposed to low pressure. This causes the water in the vial to sublimate directly from solid to gas, leaving behind a stable, crystalline white structure. This powder can be kept at room temperature until reconstitution.
Upon receipt, products should be stored away from heat and light. For short-term use, refrigeration at approximately 4°C (39°F) is suitable. For long-term storage (several months to years), vials may be placed in a freezer at approximately -80°C (-112°F). Freezing is the preferred method for preserving product stability over extended periods.
⚠️ Important Notice:
These products are intended for research use only. Not for human consumption.
Related products
Research Use Only
The following peer-reviewed publications reference compounds for laboratory and in vitro research purposes only. Not for human or animal use. Not intended to diagnose, treat, cure, or prevent any disease or condition.
Published Scientific Research
Peer-reviewed laboratory studies investigating nad+ precursors
REV-ERBα regulates brain NAD levels and tauopathy via an NFIL3-CD38 axis.
However, the molecular mechanisms of brain NAD regulation are incompletely understood. In cardiac tissue, the circadian nuclear receptor REV-ERBα has been shown to regulate NAD via control of the NAD-producing enzyme NAMPT.
View Full Study on PubMedVascular Endothelial NAMPT-Mediated NAD Biosynthesis Regulates Angiogenesis and Cardiometabolic Functions in Male Mice.
Aging is associated with metabolic dysfunction and cardiovascular abnormalities. However, the precise molecular mechanisms linking aging-associated NAD deficiency to cardiometabolic dysfunction remain unclear.
View Full Study on PubMedPhase separation of FSP1 promotes ferroptosis.
icFSP1-induced FSP1 condensates show droplet-like properties consistent with phase separation, an emerging and widespread mechanism to modulate biological activity. Hence, our results suggest that icFSP1 exhibits a unique mechanism of action and synergizes with ferroptosis-inducing agents to potentiate the ferroptotic cell death response, thus providing a rationale for targeting FSP1-dependent phase separation as an efficient anti-cancer therapy.
View Full Study on PubMedNAD metabolism modulates inflammation and mitochondria function in diabetic kidney disease.
Inflammation is closely associated with mitochondrial damage. These effects were associated with decreased inflammation, at least in part via inhibiting the activation of the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling pathway.
View Full Study on PubMedNAMPT-dependent NAD biosynthesis controls circadian metabolism in a tissue-specific manner.
NAMPT coordinates the rhythmicity of TCA cycle intermediates in BAT, but not in WAT, and loss of NAD abolishes these oscillations similarly to high-fat diet-induced circadian disruption.
View Full Study on PubMedInhibition of NAD+-Dependent Metabolic Processes Induces Cellular Necrosis and Tumor Regression in Rhabdomyosarcoma Models.
One such target is nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD+ salvage pathway. We used orthotopic xenograft models to examine tolerability, efficacy, and drug mechanism in vivo.
View Full Study on PubMedResearch Use Only
The following peer-reviewed publications reference compounds for laboratory and in vitro research purposes only. Not for human or animal use. Not intended to diagnose, treat, cure, or prevent any disease or condition.
Published Scientific Research
Peer-reviewed laboratory studies investigating nad+ precursors
REV-ERBα regulates brain NAD levels and tauopathy via an NFIL3-CD38 axis.
However, the molecular mechanisms of brain NAD regulation are incompletely understood. In cardiac tissue, the circadian nuclear receptor REV-ERBα has been shown to regulate NAD via control of the NAD-producing enzyme NAMPT.
View Full Study on PubMedVascular Endothelial NAMPT-Mediated NAD Biosynthesis Regulates Angiogenesis and Cardiometabolic Functions in Male Mice.
Aging is associated with metabolic dysfunction and cardiovascular abnormalities. However, the precise molecular mechanisms linking aging-associated NAD deficiency to cardiometabolic dysfunction remain unclear.
View Full Study on PubMedPhase separation of FSP1 promotes ferroptosis.
icFSP1-induced FSP1 condensates show droplet-like properties consistent with phase separation, an emerging and widespread mechanism to modulate biological activity. Hence, our results suggest that icFSP1 exhibits a unique mechanism of action and synergizes with ferroptosis-inducing agents to potentiate the ferroptotic cell death response, thus providing a rationale for targeting FSP1-dependent phase separation as an efficient anti-cancer therapy.
View Full Study on PubMedNAD metabolism modulates inflammation and mitochondria function in diabetic kidney disease.
Inflammation is closely associated with mitochondrial damage. These effects were associated with decreased inflammation, at least in part via inhibiting the activation of the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling pathway.
View Full Study on PubMedNAMPT-dependent NAD biosynthesis controls circadian metabolism in a tissue-specific manner.
NAMPT coordinates the rhythmicity of TCA cycle intermediates in BAT, but not in WAT, and loss of NAD abolishes these oscillations similarly to high-fat diet-induced circadian disruption.
View Full Study on PubMedInhibition of NAD+-Dependent Metabolic Processes Induces Cellular Necrosis and Tumor Regression in Rhabdomyosarcoma Models.
One such target is nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD+ salvage pathway. We used orthotopic xenograft models to examine tolerability, efficacy, and drug mechanism in vivo.
View Full Study on PubMedResearch Use Only
The following peer-reviewed publications reference compounds for laboratory and in vitro research purposes only. Not for human or animal use. Not intended to diagnose, treat, cure, or prevent any disease or condition.
Published Scientific Research
Peer-reviewed laboratory studies investigating nad+ precursors
REV-ERBα regulates brain NAD levels and tauopathy via an NFIL3-CD38 axis.
However, the molecular mechanisms of brain NAD regulation are incompletely understood. In cardiac tissue, the circadian nuclear receptor REV-ERBα has been shown to regulate NAD via control of the NAD-producing enzyme NAMPT.
View Full Study on PubMed →Vascular Endothelial NAMPT-Mediated NAD Biosynthesis Regulates Angiogenesis and Cardiometabolic Functions in Male Mice.
Aging is associated with metabolic dysfunction and cardiovascular abnormalities. However, the precise molecular mechanisms linking aging-associated NAD deficiency to cardiometabolic dysfunction remain unclear.
View Full Study on PubMed →Phase separation of FSP1 promotes ferroptosis.
icFSP1-induced FSP1 condensates show droplet-like properties consistent with phase separation, an emerging and widespread mechanism to modulate biological activity. Hence, our results suggest that icFSP1 exhibits a unique mechanism of action and synergizes with ferroptosis-inducing agents to potentiate the ferroptotic cell death response, thus providing a rationale for targeting FSP1-dependent phase separation as an efficient anti-cancer therapy.
View Full Study on PubMed →NAD metabolism modulates inflammation and mitochondria function in diabetic kidney disease.
Inflammation is closely associated with mitochondrial damage. These effects were associated with decreased inflammation, at least in part via inhibiting the activation of the cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING) signaling pathway.
View Full Study on PubMed →NAMPT-dependent NAD biosynthesis controls circadian metabolism in a tissue-specific manner.
NAMPT coordinates the rhythmicity of TCA cycle intermediates in BAT, but not in WAT, and loss of NAD abolishes these oscillations similarly to high-fat diet-induced circadian disruption.
View Full Study on PubMed →Inhibition of NAD+-Dependent Metabolic Processes Induces Cellular Necrosis and Tumor Regression in Rhabdomyosarcoma Models.
One such target is nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD+ salvage pathway. We used orthotopic xenograft models to examine tolerability, efficacy, and drug mechanism in vivo.
View Full Study on PubMed →Important Research Notice: These products are research chemicals intended exclusively for in vitro laboratory research by qualified professionals. Not for human or animal consumption. Not approved by the FDA for any therapeutic purpose. Sold strictly for scientific research applications only.