NAD+
Price range: $69.99 through $119.99
1 published certificate
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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
We work directly with the manufacturers. 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 →Storage Instructions
All products from House of Compounds 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.
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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 research peptides
NAD dyshomeostasis in RYR1-related myopathies.
BACKGROUND: Pathogenic variants in RYR1 cause a spectrum of rare congenital myopathies associated with intracellular calcium dysregulation. NAD deficiency has been associated with skeletal muscle bioenergetic deficits in mitochondrial myopathy and sarcopenia.
View Full StudyREV-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 StudyNampt/SIRT2/LDHA pathway-mediated lactate production regulates follicular dysplasia in polycystic ovary syndrome.
Furthermore, target energy metabolomics and transcriptome results showed that NMN supplementation ameliorates the lactate production by activating glycolytic process in the ovary. Overall, these benefits of NMN were elucidated and the Nampt/SIRT2/LDHA pathway mediated lactate production in granulosa cells played an important role in the improvement of follicular development disorders in PCOS.
View Full StudyPhase 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 StudyNicotine rebalances NAD homeostasis and improves aging-related symptoms in male mice by enhancing NAMPT activity.
Nicotine, a metabolite of the NAD metabolic pathway, has been found to possess anti-inflammatory and neuroprotective properties, yet the underlying molecular mechanisms remained unknown. Here we find that, independent of nicotinic acetylcholine receptors, low-dose nicotine can restore the age-related decline of NAMPT activity through SIRT1 binding and subsequent deacetylation of NAMPT, thus increasing NAD synthesis.
View Full StudyGut microbiota-derived nicotinamide mononucleotide alleviates acute pancreatitis by activating pancreatic SIRT3 signalling.
BACKGROUND AND PURPOSE: Gut microbiota dysbiosis induced by acute pancreatitis (AP) exacerbates pancreatic injury and systemic inflammatory responses. Here, we aim to investigate the effect of gut microbiota and microbiota-derived metabolites on AP and further clarify the mechanisms associated with pancreatic damage and inflammation.
View Full Study