NMN (Nicotinamide Mononucleotide)
A direct precursor to NAD+ (nicotinamide adenine dinucleotide), a coenzyme essential for cellular energy production, DNA repair, and sirtuin activation. NAD+ levels decline 50% between ages 40 and 60, contributing to age-related cognitive decline and neurodegeneration. NMN supplementation restores NAD+ levels and improves mitochondrial function, memory, and neuroplasticity in animal models.
Dosage
Standard: 250-1000 mg daily. Sublingual may improve bioavailability by bypassing first-pass metabolism. Take in the morning — NAD+ follows circadian rhythm and morning supplementation aligns with natural peaks. Effects build over weeks.
Dosages shown are for research reference only. Always consult a qualified healthcare provider.
Half-Life
2-3 minutes in blood (rapidly converted to NAD+). NAD+ half-life: 1-2 hours in tissue
Administration
Oral (capsules, powder, sublingual). Sublingual may improve bioavailability. Store in cool, dry place.
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Mechanism of Action
NMN is transported into cells via the Slc12a8 transporter (highly expressed in the small intestine and brain) and converted to NAD+ by nicotinamide mononucleotide adenylyltransferases (NMNAT1 in the nucleus, NMNAT2 in axons/Golgi, NMNAT3 in mitochondria). Elevated NAD+ activates the sirtuin family of NAD+-dependent protein deacetylases: SIRT1 deacetylates PGC-1alpha to promote mitochondrial biogenesis, SIRT3 activates superoxide dismutase 2 (SOD2) and isocitrate dehydrogenase 2 (IDH2) for mitochondrial antioxidant defense, and SIRT6 promotes base excision repair of oxidative DNA damage. NAD+ is also consumed by poly(ADP-ribose) polymerases (PARP1/2) during DNA repair — age-related NAD+ depletion impairs PARP function, allowing DNA damage accumulation. In neurons, NAD+ is required for glycolysis (GAPDH cofactor), the TCA cycle, and Complex I of the electron transport chain, directly fueling the enormous ATP demands of synaptic transmission. NAD+ decline with aging (approximately 50% reduction between ages 40-60) reduces all of these processes simultaneously, creating a cascade of mitochondrial dysfunction, impaired DNA repair, and neuroinflammation that NMN supplementation aims to reverse.
Regulatory Status
Dietary supplement. FDA issued warning that NMN may not qualify as a supplement (ongoing regulatory debate). Available OTC in most countries.
Risks & Safety
Common
Mild flushing, nausea, headache initially.
Serious
Long-term human safety data still limited (first human trials completed 2020-2023). Theoretical concern about promoting cancer growth in existing tumors (NAD+ fuels fast-growing cells).
Rare
Insomnia if taken late.
Compare NMN (Nicotinamide Mononucleotide) With
Research Papers
10Published: September 4, 2023
AI Summary
In stress conditions, NAD+ biosynthesis and levels decrease as well as the activity of consuming enzymes rises. In this review, we will show the biochemistry and metabolism of NAD+ precursors NR (nicotinamide riboside) and NMN (nicotinamide mononucleotide), the latest findings on their beneficial physiological effects, their i...
Published: June 28, 2022
AI Summary
The mitophagy is highly responsive to the dynamics of endogenous metabolites, including iron-, calcium-, glycolysis-TCA-, NAD+-, amino acids-, fatty acids-, and cAMP-associated metabolites. Herein, we summarize the recent advances toward the molecular details of mitophagy regulation in mammalian cells.
Published: April 24, 2022
AI Summary
By using Echs1 heterogeneous knockout (Echs1 +/-) mice, we found that ECHS1 deficiency caused cardiac dysfunction, as evidenced by diffuse myocardial fibrosis and upregulated fibrosis-related genes. ECHS1 deficiency promotes p300 nuclear translocation, leading to increased H3K9 acetylation, a known risk factor for cardiomyopathy.
Published: December 28, 2025
AI Summary
While mitophagy has emerged as a promising target for neuroprotection and geroprotection, its potential to restore age-associated defects in organellar crosstalk remains unclear. Calcium chelation abolishes UA-induced mitophagy, blocking its beneficial impact on muscle function and lifespan, underscoring the critical role of calcium signaling in...
Published: June 26, 2017
AI Summary
In various animal models, NMN has been shown to mitigate age-associated physiological changes in liver, adipose tissue, muscle, pancreas, kidney, retina, and central nerve system. In this review, recent findings in the NMN research will be summarized, and the potential of NMN on the regulation of age-associated diseases in humans will be discussed.
Published: November 17, 2015
AI Summary
Using bioinformatics tools, we found two NMNAT sequences in Giardia lamblia (glnmnat-a and glnmnat-b). Double-reciprocal plots showed no cooperativity for this enzyme.
Published: September 4, 2022
AI Summary
Also, significant alterations in the composition and abundance of intestinal flora in IBD mice were found. The abundance of Firmicutes, Verrucomicrobia, Akkermansia and Lactobacillus, considered as beneficial bacteria, increased, while Bacteroidetes and Muribaculaceae unclassifiably decreased.
Published: July 21, 2022
AI Summary
Declines in NAD+ levels are associated with metabolic and inflammatory diseases, aging, and neurodegenerative disorders. Due to its silenced IgG4 Fc, TNB-738 did not deplete CD38-expressing cells, in contrast to the clinically available anti-CD38 antibodies, daratumumab, and isatuximab.
Published: August 11, 2020
AI Summary
A selective reactivation of autophagy/mitophagy by Tat-Beclin 1 also reduced stroke occurrence, restored autophagy/mitophagy and improved mitochondrial function. Endothelial progenitor cells (EPCs) from subjects homozygous for the thymine allele variant at NDUFC2/rs11237379, which is associated with NDUFC2 deficiency and increased stroke risk, d...
Published: September 25, 2022
AI Summary
The level of lncRNA-ZFAS1 was elevated in MIRI hearts, and artificial knockdown of lncRNA-ZFAS1 in mice improved cardiac function. Nicotinamide mononucleotide could promote the expression of Notch1 by competitively inhibiting the expression of DNMT3b and improving the apoptosis of cardiomyocytes and cardiac function.
Frequently Asked Questions
What is NMN (Nicotinamide Mononucleotide) used for?
A direct precursor to NAD+ (nicotinamide adenine dinucleotide), a coenzyme essential for cellular energy production, DNA repair, and sirtuin activation. NAD+ levels decline 50% between ages 40 and 60, contributing to age-related cognitive decline and neurodegeneration. NMN supplementation restores NAD+ levels and improves mitochondrial function, memory, and neuroplasticity in animal models.
What are the side effects of NMN (Nicotinamide Mononucleotide)?
Common: Mild flushing, nausea, headache initially. Serious: Long-term human safety data still limited (first human trials completed 2020-2023). Theoretical concern about promoting cancer growth in existing tumors (NAD+ fuels fast-growing cells). Rare: Insomnia if taken late.
How is NMN (Nicotinamide Mononucleotide) administered?
NMN (Nicotinamide Mononucleotide) is administered via oral (capsules, powder, sublingual). sublingual may improve bioavailability. store in cool, dry place..
What is the half-life of NMN (Nicotinamide Mononucleotide)?
The half-life of NMN (Nicotinamide Mononucleotide) is 2-3 minutes in blood (rapidly converted to NAD+). NAD+ half-life: 1-2 hours in tissue.
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