NAD+ Peptide

NAD+ (nicotinamide adenine dinucleotide) is a coenzyme found in all living cells. Although it is listed with our peptides, NAD+ is a dinucleotide, not a peptide. It carries electrons in redox reactions and is consumed as a cosubstrate by sirtuins, poly(ADP-ribose) polymerases and CD38. Research has examined the decline of tissue NAD+ levels with age in rodents and humans, the NADase CD38 as a driver of that decline in mice, and NAD+ administration in a mouse model of brain ischemia. Research Market supplies NAD+ with identity and purity data for each lot reported on its certificate of analysis. It is sold strictly for laboratory research use.

Chemical structure and identification

• Molecular formula: C₂₁H₂₇N₇O₁₄P₂
• Molecular weight: 663.4 g/mol
• CAS number: 53-84-9
• PubChem CID: 5892
• Form: Lyophilized powder
• Analytical methods: HPLC for purity and mass spectrometry for identity, reported on the batch certificate of analysis

Research applications

• Coenzyme roles: Reviewed as a coenzyme for redox enzymes and a cosubstrate for sirtuins and poly(ADP-ribose) polymerases, with cellular NAD⁺ concentrations changing during aging [1]
• Cellular processes in aging: NAD⁺ influences metabolic pathways, DNA repair, chromatin remodeling, cellular senescence and immune cell function; tissue NAD⁺ declines gradually with age in model organisms including rodents and humans [2]
• Sirtuins and biosynthesis: Reviewed NAMPT-mediated NAD⁺ biosynthesis and SIRT1 function as joint regulators of metabolism and circadian rhythm [3]
• CD38 and NAD decline: In mice, expression and activity of the NADase CD38 increased with age and CD38 was required for age-related NAD decline and mitochondrial dysfunction, partly through SIRT3; CD38 was also the main enzyme degrading the precursor NMN in vivo [4]
• Brain ischemia model: In mice subjected to transient middle cerebral artery occlusion, intraperitoneal NAD⁺ given at reperfusion was associated with smaller infarcts and reduced ischemia-induced autophagy in cortex and hippocampus [5]

Reference citations

1. Verdin E. (2015). NAD⁺ in aging, metabolism, and neurodegeneration. Science, 350(6265):1208–1213. PMID 26785480 · DOI
2. Covarrubias A.J. et al. (2021). NAD⁺ metabolism and its roles in cellular processes during ageing. Nat Rev Mol Cell Biol, 22(2):119–141. PMID 33353981 · DOI
3. Imai S. et al. (2014). NAD⁺ and sirtuins in aging and disease. Trends Cell Biol, 24(8):464–471. PMID 24786309 · DOI
4. Camacho-Pereira J. et al. (2016). CD38 dictates age-related NAD decline and mitochondrial dysfunction through an SIRT3-dependent mechanism. Cell Metab, 23(6):1127–1139. PMID 27304511 · DOI
5. Zheng C. et al. (2012). NAD⁺ administration decreases ischemic brain damage partially by blocking autophagy in a mouse model of brain ischemia. Neurosci Lett, 512(2):67–71. PMID 22260797 · DOI

Compound data from PubChem CID 5892. Literature summaries describe published preclinical research and are not claims about this product’s effects in humans or animals.