Description

Niagen Nicotinamide Riboside Vitamin B3 Nootropic Powder

CAS Number	1341-23-7
Other Names	Nicotinamide Riboside, Nicotinamide Ribose, N-Ribosylnicotinamide, Nicotinamide-Beta-Riboside
IUPAC Name	1-[(2R,3R,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]pyridin-1-ium-3-carboxamide
Molecular Formula	C₁₁H₁₅ClN₂O₅
Molecular Weight	290.7
Purity	≥99% Pure (LC-MS)
Liquid Availability	N/A
Powder Availability	10 grams
Gel Availability	N/A
Storage	Store in cool dry environment, away from direct sunlight.
Terms	All products are for laboratory developmental research USE ONLY. Products are not for human consumption.

 

Mechanisms of NRC Niagen

Nicotinamide riboside, more commonly referred to as niagen, is a vitamin B3 alternative known for its ability to convert to NAD+ As NAD+ levels naturally decrease with age, many supplements that promote substrate conversion to NAD+ are labeled as “anti-aging”. That being said, NAD+ is an important part of many biological processes and helps to combat age-related decline. Additionally, the presence of NAD+ helps to activate various enzymes that are involved in the process of healthy aging. One of the main groups of enzymes are referred to as sirtuins. Evidence has found that sirtuins improve overall health and increase lifespan. Animal-based studies have indicated that sirtuins can potentially repair DNA, improve resistance to stress, and reduce inflammation.

Furthermore, NAD+ is crucial to healthy aging of brain cells due to its ability to regulate the production of proliferator-activated receptor-γ coactivators (PGC-1𝜶). PGC-1𝜶 is a protein that is crucial to protecting brain cells against oxidative stress and impaired mitochondrial functioning. This is important to note considering that dysfunction throughout the mitochondria can facilitate the development of diseases such as Parkinson’s and Alzheimer’s.

Amyloid-𝜷 plaques are one of the core components of Alzheimer’s Disease as it has the tendency to trigger neurodegeneration by decreasing expression of the vitamin D receptor (VDR) protein. Researchers Wang et. Al examined how PGC-1𝜶 has the potential to act as a coactivator for VDR in an attempt to protect against oxidative stress. In order to determine the involvement of PGC-1𝜶 in the development of Alzheimer’s Disease, 6 month old mice with deficient levels of PGC-1𝜶 and VDR were studied. Results reported that low expression of PGC-1𝜶 led to decreased VDR expression and increased oxidative stress in the neurons. These mice were then compared to subjects with induced overexpression of PGC-1𝜶. The overexpression led to improvement of VDR expression and a reduction of the amyloid-𝜷 plaques. The results of this study indicate that niagen is capable of reducing instances of Alzheimer’s Disease as the compound is efficiently converted into NAD+, and in turn promotes the expression of PGC-1𝜶 (https://pubmed.ncbi.nlm.nih.gov/33373677/).

This claim was supported by the work of Gong et. Al in which they state that niagen is an NAD+ precursor that increases PGC-1𝜶 levels in the brain. The researchers tested the hypothesis that niagen can potentially treat Alzheimer’s Disease because PGC-1𝜶 is considered a crucial step of Amyloid-𝜷 regulation due to its effects on 𝜷-secretase (BACE-1) degradation. The study was conducted on the Tg2576 AD mouse model and results were measured through use of behavioral analyses, gene silencing, and electrophysiological recordings. Results reported that after daily administration of 250 mg/kg of niagen over the course of 3 months, NAD+ levels in the cerebral cortex had increased while there was a drastic decrease in any measured cognitive deterioration. Additional findings explained that applying niagen to hippocampal slices had the tendency to abolish deficits in long term potentiation as well. Furthermore, the study was able to confirm that niagen promotes the expression of PGC-1𝜶, resulting in enhanced degradation of BACE-1 and decreased production of Amyloid-𝜷. Overall, the researchers were able to conclude that niagen could be an effective treatment for Alzheimer’s Disease due to its mechanism of action (https://pubmed.ncbi.nlm.nih.gov/23312803/).

In addition to niagen’s potential to combat Alzheimer’s Disease, evidence has shown the compound could potentially reverse the degeneration of skeletal muscle due to its role as an NAD+ precursor. Availability of NAD+ is known to decrease during periods of genotoxic stress. While low NAD+ levels in the brain lead to decreased expression of PGC-1𝜶 and can result in the production of Amyloid-𝜷 plaques, the effect of low NAD+ levels in skeletal muscle tissues is unclear. Researchers Frederick et. Al conducted a study to try to understand this pathway. It initially began by depleting Nampt, an enzyme involved in NAD+ salvaging, from the skeletal muscles of mice.

The knockout mice experienced an 85% decrease in NAD+ levels as well as fiber degeneration and a loss of muscle strength and endurance. After observing this change the subjects were administered niagen, which immediately helped improve functional deficits and muscle mass. It’s important to note that these benefits were seen in the animals without a drastic increase in intramuscular NAD+. Further research found that overexpression of Nampt preserved the NAD+ pool as well as the exercise capacity and endurance of the mice. Overall, Frederick et. Al were able to conclude that NAD+ is crucial for maintaining healthy muscle mass and that the compound is regulated through the administration of niagen (https://pubmed.ncbi.nlm.nih.gov/27508874/).

The nootropics sold by Umbrella Labs are sold for laboratory research only. The description above is not medical advice and is for informative purposes only.

NRC Niagen Nicotinamide Riboside is sold for laboratory research use only. Terms of sale apply. Not for human consumption, nor medical, veterinary, or household uses. Please familiarize yourself with our Terms & Conditions prior to ordering.

File Name	View/Download
01-19-2023-Umbrella-Labs-NRC-Niagen-Certificate-Of-Analysis-COA.pdf

VIEW CERTIFICATES OF ANALYSIS (COA)

Additional information