| Field | Specification |
|---|---|
| Alternative names | β-DPN sodium; β-NAD sodium; β-Nicotinamide Adenine Dinucleotide sodium |
| CAS no. | |
| Applications | |
| Molecular weight | |
| Molecular formula | C21H26N7NaO14P2 |
| Purity | |
| SMILES | |
| Form | Solid |
| Storage | |
| Shipping | |
| Catalog no. (Mfr.) | |
| Main SKU |
Compound Overview
NAD sodium, also known as β-DPN sodium, β-NAD sodium, or β-Nicotinamide Adenine Dinucleotide sodium, is an orally effective cofactor and homeostatic regulator. It can be reduced to β-nicotinamide adenine dinucleotide (NADH) while coupling with reactions that oxidize organic substrates, and the resulting NADH passes into mitochondria, where it indirectly generates ATP. It can be used to research non-alcoholic fatty liver disease, obesity, and glucose intolerance[1][2][3][4][5]. It is supplied as a white to off-white solid (C21H26N7NaO14P2, MW 685.41) at 99.44% purity.
Physical & Chemical Properties
| CAS Number | 20111-18-6 |
|---|---|
| Molecular Formula | C21H26N7NaO14P2 |
| Molecular Weight | 685.41 g/mol |
| Purity | 99.44% |
| Appearance | Solid |
| Color | White to off-white |
| SMILES | O[C@H]1[C@@H](O)[C@H]([N+]2=CC=CC(C(N)=O)=C2)O[C@@H]1COP([O-])(OP(OC[C@@H]3[C@@H](O)[C@@H](O)[C@H](N4C5=NC=NC(N)=C5N=C4)O3)(O[Na])=O)=O |
| Signaling Pathway | Metabolic Enzyme/Protease |
| Solubility | In Vitro: H2O: ≥ 175 mg/mL (255.32 mM) * "≥" means soluble, but saturation unknown. |
| Storage | -20°C, sealed storage, away from moisture. In solvent: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). |
| Shipping | Room temperature in continental US; may vary elsewhere. |
Literature Cited
Sources cited in this description and in the In Vitro & In Vivo Data tab. Peer-reviewed publications that used this product are listed under References.
[2]. 20260224132312.pdf
[4]. 15684.pdf
Safety
For Research Use Only. Not for use in diagnostic or therapeutic procedures, and not for human or veterinary use. Handle in accordance with the Safety Data Sheet and your institution's chemical hygiene plan.
In Vitro
| Solvent | Solubility | Notes |
|---|---|---|
| H2O | ≥ 175 mg/mL (255.32 mM) | — |
Aliquot the stock solution and store it at -80°C (up to 6 months) or -20°C (up to 1 month); sealed storage, away from moisture; avoid repeated freeze-thaw cycles.
If water is used as the stock solvent, dilute to the working solution and sterilize it through a 0.22 μm filter before use.
Data provided by the manufacturer.
In Vitro
NAD (sodium) (250 pM, 100 μM; 5-60 min, 10 min) enters NIH-3T3 cells with an apparent Km of ~190 μM, and unlabeled NAD co-treatment competes for uptake[4]. NAD (sodium) (100 μM; 72 h) prevents FK866-induced cell death and refills NAD(P) levels inside NIH-3T3 cells[4]. NAD (sodium) (250 pM; 10 min) enters HMEC, HaCaT, HeLa, SH-SY5Y, and RAW 264.7 cells, but not K562 cells, and transport in SH-SY5Y cells is sodium-dependent[4]. In SH-SY5Y cells, NAD (sodium) (100 μM; 72 h) prevents FK866-induced cell death and refills intracellular NAD(P) levels[4]. NAD (sodium) (100 μM; 36 h) reverses FK866-induced autophagy in SH-SY5Y cells[4]. NAD (sodium) (0.5 mM) favors M2 and suppresses M1 macrophage polarization, whether the RAW264.7 cells are under normal or high glucose exposure[5]. NAD (sodium) (0.5 mM; 24 h) restores the reduced VEGF secretion of mouse bone marrow-derived macrophages exposed to high glucose[5]. NAD (sodium) (0.5 mM; 24 h) makes BMDM secrete factors restoring HUVEC tube formation, migration, and scratch wound closure that high glucose exposure had impaired[5]. NAD (sodium) (0.5 mM) boosts pro-angiogenic VEGF165 expression and suppresses anti-angiogenic VEGF165b expression in RAW264.7 cells, under normal glucose as well as after high glucose exposure[5]. In high glucose-exposed RAW264.7 cells, NAD (sodium) (0.5 mM) restores the reduced SRSF1 expression and suppresses the increased SRSF6 expression, and it also modulates these splicing factors in cells under normal glucose[5]. NAD (sodium) (0.5 mM; 24 h) corrects the HUVEC scratch wound closure impairment caused by medium conditioned by NAD+-depleted RAW264.7 cells[5]. In NAD+-depleted RAW264.7 cells, NAD (sodium) (0.5 mM) restores the reduced pro-angiogenic VEGF165 expression and suppresses the increased anti-angiogenic VEGF165b expression[5].
Cell Viability Assay[4]
| Cell Line | NIH-3T3 murine epithelial cells |
|---|---|
| Concentration | 10-100 μM |
| Incubation Time | 24 h (NAD(P) replenishment); 72 h (cell viability rescue) |
| Result | Restored FK866-induced cell death to ~85% of control when used at 100 μM. Replenished intracellular NAD(P) levels concentration-dependently: reached ~30% of control at 10 μM, ~50% of control at 30 μM, and ~180% of control at 100 μM. Increased NAD(P) levels when treated alone. |
Cell Viability Assay[4]
| Cell Line | SH-SY5Y neuroblastoma cells |
|---|---|
| Concentration | 100 μM |
| Incubation Time | 72 h |
| Result | Restored FK866-induced cell death to ~78.6% of control when used at 100 μM. Replenished intracellular NAD(P) levels. |
Cell Autophagy Assay[4]
| Cell Line | SH-SY5Y neuroblastoma cells |
|---|---|
| Concentration | 100 μM |
| Incubation Time | 36 h |
| Result | Reverted FK866-induced increase in the percentage of cells with LC3-positive vacuoles (from 44.3% to near baseline). |
ELISA Assay[5]
| Cell Line | mouse bone marrow-derived macrophages (BMDM) |
|---|---|
| Concentration | 0.5 mM |
| Incubation Time | 24 h |
| Result | Rescued the significant reduction in secreted VEGF protein levels observed in high glucose-treated cells, restoring levels toward those of normal glucose control cells. |
In Vivo
In both diabetic and non-diabetic mice, NAD+ (500 mg/kg/day; i.p.; daily; at least 28 days) reduces cardiac injury and improves cardiac function after myocardial infarction by restoring cardiac NAD+ levels, shrinking infarct size, promoting M2 macrophage polarization, and enhancing angiogenesis, and it also lowers blood glucose in diabetic mice[5].
| Animal Model | Kunming (male, 25-30 g; induced diabetes via streptozocin, induced myocardial infarction via left anterior descending coronary artery ligation)[5] |
|---|---|
| Dosage | 500 mg/kg/day |
| Administration | i.p.; daily; at least 28 days |
| Result | Reinstated ejection fraction (EF) and fractional shortening (FS) values at 7 days and 28 days post-myocardial infarction in both diabetic and non-diabetic mice; Markedly reduced cardiac infarct size in both diabetic and non-diabetic mice after myocardial infarction; Significantly reduced fasting blood glucose levels in diabetic mice with or without myocardial infarction; Significantly restored cardiac tissue NAD+ levels (reduced in myocardial infarction mice, further reduced in diabetic myocardial infarction mice); Increased microvessel density and restored CD31 and VEGF expression to promote angiogenesis in the myocardial infarction area of both diabetic and non-diabetic mice; Reduced the number of F4/80-positive macrophages and increased the number of CD206-positive M2 macrophages in cardiac tissue of both diabetic and non-diabetic mice after myocardial infarction; Abolished the angiogenic effect in diabetic myocardial infarction mice when macrophages were depleted via clodronate liposomes |
Data provided by the manufacturer. Numbered citations refer to the Literature Cited list in the product description.
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TREM2 macrophage promotes cardiac repair in myocardial infarction by reprogramming metabolism via SLC25A53. Cell Death Differ 2024 Feb;31(2):239-253. PMID: 38182899
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