NMN
NAD+ Precursor | Cellular Energy & Longevity
Nicotinamide mononucleotide (NMN) is a naturally occurring nucleotide and a direct biosynthetic precursor to nicotinamide adenine dinucleotide (NAD+), a coenzyme essential for cellular energy metabolism, DNA repair, sirtuin activation, and hundreds of enzymatic reactions. NAD+ levels decline significantly with age, and this decline is implicated in mitochondrial dysfunction, genomic instability, and many hallmarks of aging. NMN supplementation aims to restore NAD+ levels by providing the immediate substrate for the enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT), which catalyzes the final step of NAD+ biosynthesis in the salvage pathway. Popularized by Harvard geneticist David Sinclair, NMN has become one of the most widely studied and used longevity supplements. While animal data is extensive and compelling, human clinical trial data is still accumulating, with several trials showing increases in blood NAD+ levels and improvements in various biomarkers of aging.
Moleküler Gösterim
M.W.: 334.22 Da
PubChem 2D yapı diyagramı
Referans Flakon
Referans illüstrasyonu — ürün listesi değildir
Etki Mekanizması
NMN is converted to NAD+ via the NAD+ salvage pathway. After oral ingestion, NMN is absorbed in the gut, where it may be partially converted to nicotinamide riboside (NR) by the enzyme CD73 for cellular uptake, then re-phosphorylated intracellularly back to NMN. The enzyme NMNAT then converts NMN to NAD+. The resulting increase in NAD+ levels activates multiple longevity-associated pathways: sirtuins (SIRT1-7), a family of NAD+-dependent deacetylases that regulate mitochondrial biogenesis, DNA repair, inflammation, and stress resistance; PARP enzymes involved in DNA damage repair; and CD38/CD157 involved in immune cell signaling. By restoring NAD+ pools, NMN supplementation supports mitochondrial electron transport chain function and ATP production, enhances oxidative metabolism in skeletal muscle, and may counteract age-related metabolic decline. In the Slc12a8 transporter discovery, a dedicated NMN transporter was identified in the small intestine, supporting direct NMN absorption without prior conversion to NR.
Nicotinamide mononucleotide (NMN) is a naturally occurring nucleotide and a direct biosynthetic precursor to nicotinamide adenine dinucleotide (NAD+), a coenzyme essential for cellular energy metabolism, DNA repair, sirtuin activation, and hundreds of enzymatic reactions. NAD+ levels decline significantly with age, and this decline is implicated in mitochondrial dysfunction, genomic instability, and many hallmarks of aging. NMN supplementation aims to restore NAD+ levels by providing the immediate substrate for the enzyme nicotinamide mononucleotide adenylyltransferase (NMNAT), which catalyzes the final step of NAD+ biosynthesis in the salvage pathway. Popularized by Harvard geneticist David Sinclair, NMN has become one of the most widely studied and used longevity supplements. While animal data is extensive and compelling, human clinical trial data is still accumulating, with several trials showing increases in blood NAD+ levels and improvements in various biomarkers of aging.
Moleküler Veri
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Doz Protokolleri
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| Hedef | Doz | Sıklık | Yol |
|---|---|---|---|
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Etkileşimler
NAD+
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Kaynaklar
- Nicotinamide mononucleotide increases muscle insulin sensitivity in prediabetic women — Yoshino, M., Yoshino, J., Kayser, B.D., et al.
- Chronic nicotinamide mononucleotide supplementation elevates blood nicotinamide adenine dinucleotide levels and alters muscle function in healthy older men — Igarashi, M., Nakagawa-Nagahama, Y., Miura, M., et al.
- Nicotinamide mononucleotide supplementation enhances aerobic capacity in amateur runners: a randomized, double-blind study — Liao, B., Zhao, Y., Wang, D., et al.
- Effect of 12-Week Intake of Nicotinamide Mononucleotide on Sleep Quality, Fatigue, and Physical Performance in Older Japanese Adults — Kim, M., Seol, J., Sato, T., et al.
- NAD+ metabolism and its roles in cellular processes during ageing — Covarrubias, A.J., Perrone, R., Grozio, A., Verdin, E.