NAD+

NAD+ Peptide Overview

Nicotinamide Adenine Dinucleotide (NAD+) is the essential oxidized form of the NAD+/NADH redox pair. It is a mandatory co-factor for the enzymes that drive the Citric Acid Cycle and the Electron Transport Chain. By facilitating the transfer of electrons, NAD+ is the primary driver of energy movement within every cell in the body. In addition to energy production, NAD+ is an active participant in extracellular signaling, influencing the health of the vascular and gastrointestinal systems.

Maintaining an optimal equilibrium between NAD+ synthesis and utilization is essential for sustaining biochemical networks. High metabolic demand or overactivation of certain pathways can reduce NAD+ availability, limiting cellular energy balance and the capacity for internal repair.

Research Observations by Physiological System

System

Primary Research Finding

Potential Biological Impact

Nervous

Enhanced DNA base-excision repair

Improved neuronal survival following oxidative stress.

Renal

Mitigated cellular hypertrophy

Protection against nephrotoxicity and age-related decline.

Skeletal

Increased ATP production

Enhanced mitochondrial efficiency and muscular endurance.

NAD+ Peptide Structure

The structure of NAD+ is characterized by the presence of a nicotinamide moiety and an adenine moiety, linked by a pair of bridging phosphate groups. This dinucleotide structure is what enables its role as a hydride acceptor in catabolic processes.

Structure Solution Formula: C21H27N7O14P2

NAD+ Peptide Research

Scientific Evidence on Interactions

Contemporary studies highlight the role of sirtuins and PARP enzymes as primary consumers of the NAD+ pool. Sirtuins are responsible for maintaining mitochondrial function and regulating energy balance, while PARPs safeguard genomic stability through DNA damage detection. Because these systems rely heavily on NAD+, maintaining its levels is vital for cellular energy balance and repair capacity.

Ischemic Stress and DNA Integrity

In neuronal culture models exposed to ischemic stress, the restoration of NAD+ levels enhanced DNA repair mechanisms and promoted cell survival. Mechanistically, PARP enzymes utilize NAD+ to catalyze the recruitment of repair proteins. Supplementation under stress conditions helps counteract depletion and restore cellular energy balance.

Organ Protection and Skeletal Resilience

Animal studies indicate that increasing circulating NAD+ concentrations provides organ-specific benefits. In liver and kidney models, NAD+ elevation was linked to improved glucose regulation and protection against oxidative stress. In skeletal tissue, administration of NAD+ precursors led to decreased inflammation and improved mitochondrial respiration.

Article Author

Dr. Shin-Ichiro Imai, M.D., Ph.D. is a Professor at Washington University School of Medicine and a world leader in longevity research. His work focus on how NAD+ biosynthesis and signaling pathways influence aging and metabolic balance.

Scientific Journal Author

Significant contributions to this field have been made by Dr. Imai and collaborators such as Dr. David Sinclair and Dr. Charles Brenner. Their work continues to define the relationship between NAD+ levels and systemic health.

Reference Citations

1. Schultz, Michael B, and David A Sinclair. "Why NAD(+) Declines during Aging: It's Destroyed." Cell metabolism vol. 23,6 (2016): 965-966.1617
2. Braidy N, Liu Y. NAD+ therapy in age-related degenerative disorders: A benefit/risk analysis. Exp Gerontol. 2020 Apr;132:110831.1819
3. Johnson, Sean, and Shin-Ichiro Imai20. "NAD+ biosynthesis, aging, and disease." F1000Research vol. 7 132. 1 Feb 2018.
4. Bieganowski P, Brenner C. Discoveries of nicotinamide riboside as a nutrient. Cell. 2004 May 14;117(4):495-502.
5. Fang, E. F., et al. (2017). NAD+ in Aging: Molecular Mechanisms and Translational Implications. Trends in molecular medicine, 23(10), 899-916.
6. Harden, A; Young, WJ (1906). "The alcoholic ferment of yeast-juice Part II." Proceedings of the Royal Society of London. 78 (526): 369-375.
7. Mills KF, et al. Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice. Cell Metab. 2016 Dec 13;24(6):795-806.
8. Long AN, et al. Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits. BMC Neurol. 2015 Mar 1;15:19.
9. Safety and Efficacy of Nicotinamide Riboside Supplementation. clinicaltrials.gov Identifier: NCT02921659.
10. Wang S, et al. Cellular NAD replenishment confers marked neuroprotection against ischemic cell death. Stroke. 2008 Sep;39(9):2587-95.
11. Rajman, Luis et al. "Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence." Cell metabolism vol. 27,3 (2018): 529-547.
12. Heer C, et al. Coronavirus infection and PARP expression dysregulate the NAD metabolome. Journal of Biological Chemistry. Dec 2020.
13. Mehmel, Mario et al. "Nicotinamide Riboside-The Current State of Research and Therapeutic Uses." Nutrients vol. 12,6 1616. 2020.
14. Leung A, et al. Poly(ADP-ribose) regulates post-transcriptional gene regulation in the cytoplasm. RNA Biol. 2012 May;9(5):542-8.

Storage

Peptides should be stored in a cold, dry, and dark environment. Lyophilized powder is stable at room temperature for transit but should be refrigerated (4 degrees Celsius) for short-term use or frozen (-80 degrees Celsius) for long-term storage. Once reconstituted, store the solution in the refrigerator and use within 30 days. Avoid repeated freeze-thaw cycles and direct light exposure.