NAD⁺ Precursor / Nicotinamide Nucleotide / Longevity Research Compound
NMN Research Compound — Nicotinamide Mononucleotide (NAD⁺ Precursor)
NMN (Nicotinamide Mononucleotide, β-NMN) is a naturally occurring nucleotide derivative and the immediate biosynthetic precursor to NAD⁺ (nicotinamide adenine dinucleotide). It sits at the center of NAD⁺ metabolism research — the study of how NAD⁺ levels decline with aging, what cellular consequences that decline produces, and whether restoring NAD⁺ through its precursors can modulate aging-associated biology in model systems.
Compound identity
- Name
- NMN (Nicotinamide Mononucleotide)
- Class
- NAD⁺ Precursor / Nicotinamide Nucleotide / Longevity Research Compound
- CAS number
- 1094-61-7
- Molecular formula
- C₁₁H₁₅N₂O₈P
- Also known as
- Nicotinamide Mononucleotide, β-NMN, NMN supplement research, NAD+ precursor NMN
- Sequence
- Not applicable (nucleotide derivative; MW 334.22 Da; β-D-ribofuranose-5-phosphate conjugated to nicotinamide via N-glycosidic bond; immediate NAD⁺ biosynthesis precursor)
Research context
NMN (CAS 1094-61-7, MW 334.22 Da, C₁₁H₁₅N₂O₈P) is the mononucleotide form of nicotinamide — consisting of the nicotinamide base, a ribose sugar (β-D-ribofuranose), and a 5'-phosphate group. It is the direct precursor to NAD⁺ in the Preiss-Handler salvage pathway: NMN + ATP → NAD⁺ + PPi, catalyzed by NMNAT (nicotinamide mononucleotide adenylyltransferase) enzymes (NMNAT1/2/3 with different subcellular localizations). NMN is also a product of NRK1/2 (nicotinamide riboside kinases) acting on NR (nicotinamide riboside), placing it downstream of NR in the NAD⁺ salvage cascade. NAD⁺ is an essential coenzyme in over 500 enzyme-catalyzed reactions — serving as a hydride acceptor in oxidative metabolism (glycolysis, TCA cycle, β-oxidation, oxidative phosphorylation) and as a substrate for NAD⁺-consuming enzymes including sirtuins (SIRT1-7, NAD⁺-dependent deacylases), PARPs (poly-ADP-ribose polymerases, DNA damage response), and CD38/CD157 (cyclic ADP-ribose synthesis).
Research interest in NMN derives primarily from the discovery that NAD⁺ levels decline progressively with aging in multiple tissues (liver, muscle, brain, adipose) in rodents and humans, and that supplementation with NAD⁺ precursors (including NMN) can restore NAD⁺ levels and produce metabolic, mitochondrial, and longevity-associated phenotypes in preclinical models. Key findings from David Sinclair's group (Harvard) and others include: (1) NMN administration in aged mice restores muscle NAD⁺ to youthful levels and improves mitochondrial function, exercise capacity, and insulin sensitivity; (2) NMN activates SIRT1 signaling, which regulates PGC-1α-mediated mitochondrial biogenesis; (3) NMN has been studied in models of metabolic syndrome, type 2 diabetes, NAFLD, cardiovascular aging, neurodegeneration (Alzheimer's disease models), and reproductive biology (oocyte quality in aged female mice). The 2023 Nature Aging human clinical trial (Igarashi et al.) demonstrated NMN's ability to increase blood NAD⁺ levels in healthy volunteers, opening research questions about tissue-specific NAD⁺ bioavailability. Relationship to Sinclair's broader longevity research: NMN was one of the compounds studied in the 'epigenetic reprogramming' aging model and the 'information theory of aging' hypothesis.
As a research reagent, NMN is used in studies of NAD⁺ metabolism, sirtuin signaling, mitochondrial function, aging biology, metabolic disease models, DNA damage/repair (PARP pathway), circadian regulation (NAD⁺ oscillates with the circadian clock via NAMPT-SIRT1 feedback), and NAD⁺ precursor pharmacokinetics/bioavailability. DMV Research supplies NMN as a lyophilized compound with per-batch Certificate of Analysis confirming identity by mass spectrometry and purity ≥99% by HPLC.
Frequently asked questions
What is NMN?+
NMN (Nicotinamide Mononucleotide, CAS 1094-61-7, MW 334.22 Da) is a naturally occurring nucleotide and the direct precursor to NAD⁺ (nicotinamide adenine dinucleotide) in the salvage biosynthesis pathway. NAD⁺ is an essential coenzyme in metabolism (glycolysis, TCA cycle, oxidative phosphorylation) and a substrate for sirtuins (SIRT1-7), PARPs, and CD38 — enzymes central to longevity research, DNA damage response, and metabolic regulation. NMN is studied because NAD⁺ levels decline with aging, and restoring them via precursors like NMN produces metabolic and aging-associated phenotypes in preclinical models. Supplied by DMV Research for research use only.
What is the difference between NMN and NR (Nicotinamide Riboside)?+
NMN (Nicotinamide Mononucleotide) and NR (Nicotinamide Riboside) are both NAD⁺ precursors in the salvage pathway but at different metabolic steps. NR is upstream of NMN: NR + ATP → NMN (catalyzed by NRK1/2 nicotinamide riboside kinases). NMN is then directly converted to NAD⁺ by NMNAT enzymes. The key research question is cellular uptake: NMN (MW 334 Da, charged phosphate group) was initially thought to require extracellular dephosphorylation to NR before cellular entry, but the Slc12a8 (SLC12A8) transporter in intestinal and some other cells can transport NMN directly. NR enters cells via nucleoside transporters without dephosphorylation. Both increase intracellular NAD⁺ in research models; the relative bioavailability and tissue distribution differ and are active research questions.
What are sirtuins and why do they matter in NMN research?+
Sirtuins (SIRT1-7) are NAD⁺-dependent protein deacylases — they use NAD⁺ as a co-substrate (not a cofactor) to remove acyl modifications from target proteins, consuming one NAD⁺ molecule per reaction cycle. SIRT1 (nuclear/cytoplasmic) deacetylates PGC-1α (mitochondrial biogenesis), FOXO3a (stress resistance), p53, and NF-κB — making it a key regulator of metabolism, stress response, and longevity pathways. SIRT3/4/5 are mitochondrial sirtuins regulating fatty acid oxidation and TCA cycle enzymes. Because sirtuins deplete NAD⁺ and compete with PARPs (DNA repair) and CD38 (immune signaling), NAD⁺ availability is a metabolic bottleneck; NMN research tests whether restoring NAD⁺ can reactivate sirtuin signaling in aged tissues where NAD⁺ has declined.
Is NMN approved for human use?+
NMN is generally recognized as safe (GRAS) in some jurisdictions and is sold as a dietary supplement in several countries. In 2022, the FDA issued guidance reclassifying NMN as not eligible for dietary supplement status in the United States following IND submission by Metro International Biotech (as the FDA requires that a substance cannot be marketed as both a drug-IND and a dietary supplement under 21 CFR 101). As supplied by DMV Research, NMN is a research compound for in-vitro and pre-clinical laboratory research use only — not for human consumption.
Research use only
All products are intended for laboratory and research use only (RUO) and are not for human consumption, ingestion, or any in-vivo use.
The statements on this page have not been evaluated by the FDA. NMN (Nicotinamide Mononucleotide) is not intended to diagnose, treat, cure, or prevent any disease. Content is provided for laboratory research reference only.