NAD+ Buffered

NAD+

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Product Format	900mg vials
Vial Size	900mg
Vial Capacity	10 mL
Box Combinations	1800mg, 4500mg, 9000mg
Cost per milligram	$0.08 – $0.11
Multi-vial Purity	99.55%
Endotoxin Screening	PASSED
Heavy Metals Screening	PASSED
Purity Screening	PASSED
Independently Tested	YES

Peptide Partners Manufacturer Id: WF03

Batch Id: NDB202606

 

Research Studies

(for educational purposes only)

 

Study 1: Dihydronicotinamide riboside is a potent NAD+ concentration enhancer in vitro and in vivo

Authors: Yue Yang, Farheen Sultana Mohammed, Ning Zhang, Anthony A. Sauve

Source: https://www.jbc.org/article/S0021-9258(20)35173-5/fulltext

Scientific Findings

The study reports the synthesis of dihydronicotinamide riboside (NRH) and its evaluation as a potent NAD+ precursor. In vitro experiments using various mammalian cell lines demonstrated that NRH administration led to a rapid and substantial increase in intracellular NAD+ concentrations, ranging from 2.5- to 10-fold over control values within one hour. Comparative analysis with established NAD+ precursors, nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN), revealed that NRH consistently exhibited superior efficacy in augmenting NAD+ levels at equivalent concentrations. Furthermore, NRH treatment significantly increased the NAD+/NADH ratio in cultured cells and conferred protection against cell death induced by genotoxic agents like hydrogen peroxide and methylmethane sulfonate. Mechanistic investigations indicated that NRH is not an inhibitor of NAD+ consumption but rather serves as a biochemical precursor. Cell lysates were found to possess an ATP-dependent kinase activity that efficiently converts NRH to nicotinamide mononucleotide (NMNH), independent of the known NR kinases Nrk1 or Nrk2, suggesting the existence of a novel metabolic pathway for NAD+ biosynthesis.

Plain English Interpretation

Researchers have developed a new compound called dihydronicotinamide riboside (NRH) that acts as a powerful booster for cellular energy. In laboratory experiments conducted on cells, NRH was found to be significantly more effective at increasing the levels of a crucial molecule called NAD+ compared to other similar substances. This increase in NAD+ helps to improve the cell's energy balance and protects it from damage caused by stress. The study suggests that NRH works through a previously unknown pathway in the cell, opening up new possibilities for developing therapies that target cellular metabolism and aging.

 

Study 2: NAD+/NADH redox alterations reconfigure metabolism and rejuvenate senescent human mesenchymal stem cells in vitro

Authors: Xuegang Yuan, Yijun Liu, Brent M. Bijonowski, Ang-Chen Tsai, Qin Fu, Timothy M. Logan, Teng Ma & Yan Li

Source: https://www.nature.com/articles/s42003-020-01514-y

Scientific Findings

This study investigates the role of NAD+/NADH redox balance in the replicative senescence of human mesenchymal stem cells (hMSCs) during in vitro expansion. The researchers found that prolonged cell culture leads to a decline in the intracellular NAD+/NADH ratio and reduced activity of Sirtuin-1 (Sirt-1), a NAD+-dependent deacetylase. This was accompanied by a metabolic shift towards glycolysis and diminished mitochondrial fitness, characteristic of cellular senescence. Treatment of late-passage hMSCs with the NAD+ precursor nicotinamide (NAM) successfully restored intracellular NAD+ levels, rebalanced the NAD+/NADH ratio, and enhanced Sirt-1 activity. Consequently, NAM-treated cells exhibited a partial reversal of the senescent phenotype, including improved mitochondrial function and a rejuvenated metabolic profile. In contrast, human dermal fibroblasts (hFBs) showed a more stable NAD+/NADH balance and limited senescence during in vitro expansion, highlighting a key metabolic distinction between stem cells and differentiated cells.

Plain English Interpretation

As we age, our bodies' stem cells, which are responsible for repairing tissues, can become old and less effective. Scientists have been studying why this happens by growing human stem cells in the lab. They discovered that as the stem cells multiply, their energy balance gets disrupted, leading to a decrease in a vital molecule called NAD+. This, in turn, causes the cells to age and lose their regenerative abilities. In this study, the researchers found that by giving the aging stem cells a vitamin B3 derivative, they could boost their NAD+ levels. This simple intervention helped to restore the cells' energy balance, improve their function, and essentially make them 'younger' again. This research provides important clues about how we might be able to combat the effects of aging and improve our bodies' natural repair mechanisms.

 

Study 3: Cellular NAD Replenishment Confers Marked Neuroprotection Against Ischemic Cell Death: Role of Enhanced DNA Repair

Authors: Suping Wang, Zili Xing, Peter S. Vosler, Hannah Yin, et al.

Source: https://www.ahajournals.org/doi/10.1161/strokeaha.107.509158

Scientific Findings

This in vitro study investigated the neuroprotective effects of direct NAD+ replenishment in primary rat neuronal cultures subjected to oxygen-glucose deprivation (OGD), a model for ischemic injury. The researchers demonstrated that exogenous NAD+ administration, either before or after the OGD insult, significantly reduced neuronal cell death in a dose- and time-dependent manner. Mechanistically, NAD+ replenishment was found to counteract the OGD-induced accumulation of oxidative DNA damage, including AP sites and single/double-strand breaks. This was achieved by restoring the activity of the base excision repair (BER) pathway. Specifically, NAD+ treatment inhibited the aberrant serine-specific phosphorylation of key BER enzymes, AP endonuclease (APE) and DNA polymerase-β (β-pol), which are typically inactivated during ischemic conditions. The critical role of the BER pathway in mediating the neuroprotective effects of NAD+ was confirmed by experiments where the knockdown of APE expression significantly diminished the pro-survival benefits of NAD+ replenishment. The study concludes that direct cellular NAD+ replenishment is a potent strategy to mitigate ischemic neuronal injury by enhancing DNA repair capacity.

Plain English Interpretation

When brain cells are deprived of oxygen and sugar, as happens during a stroke, they suffer from a kind of stress that damages their DNA and can lead to cell death. This study, conducted on rat brain cells in a dish, explored whether directly supplying NAD+, a vital molecule for cell survival and energy production, could protect them from this damage. The scientists found that adding NAD+ to the cells, even after the injury had occurred, acted as a powerful rescue mission. It significantly reduced cell death by helping the cells to repair their damaged DNA more effectively. Essentially, NAD+ helps to switch back on the cells' natural DNA repair machinery, which gets turned off during a stroke-like event. This research suggests that boosting NAD+ levels could be a promising new way to protect brain cells from the devastating effects of a stroke.