2. Metabolic Enzyme/Protease
  3. Endogenous Metabolite
  4. NAD sodium

NAD sodium  (Synonyms: β-DPN sodium; β-NAD sodium; β-Nicotinamide Adenine Dinucleotide sodium)

Cat. No.: HY-B0445A Purity: 99.44%
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NAD sodium is an orally effective cofactor and homeostatic regulator. NAD sodium can be reduced to β-nicotinamide adenine dinucleotide (NADH) during coupling with reactions that oxidize organic substrates. NAD sodium can be converted to β-nicotinamide adenine dinucleotide (NADH) and passes to the inside of mitochondria, which indirectly generates ATP. NAD sodium can be used for the research of non-alcoholic fatty liver disease, obesity, and glucose intolerance.

For research use only. We do not sell to patients.

CAS No. : 20111-18-6

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10 mM * 1 mL in Water
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Based on 45 publication(s) in Google Scholar

Other Forms of NAD sodium:

NAD sodium Related Antibodies

Top Publications Citing Use of Products

45 Publications Citing Use of MCE NAD sodium

Cell Proliferation/Viability Assay
IP
RT-PCR
WB
IF

    NAD sodium purchased from MedChemExpress. Usage Cited in: Redox Biol. 2024 Feb:69:103030.  [Abstract]

    LDH release assay showed the glioma cell death caused by SRT2183 (40 μmol/L) at 24 h was attenuated when the cells were pretreated 1 h with EX527 (200 μmol/L) or supplemented with exogenous NAD+ (2 mmol/L).

    NAD sodium purchased from MedChemExpress. Usage Cited in: Redox Biol. 2024 Feb:69:103030.  [Abstract]

    The declines of cysteine induced by SRT2183 (40 μmol/L) at 24 h were both suppressed by pretreating the cells 1 h with EX527 or supplementing exogenous NAD+ (2 mmol/L).

    NAD sodium purchased from MedChemExpress. Usage Cited in: Redox Biol. 2024 Feb:69:103030.  [Abstract]

    Western blotting revealed RSL3-induced downregulation of SLC7A11 and GPX4 was enhanced by FK866, but attenuated by exogenous NAD+ (2 mmol/L) supplement.

    NAD sodium purchased from MedChemExpress. Usage Cited in: Redox Biol. 2024 Feb:69:103030.  [Abstract]

    Pretreatment with FK866 (500 μmol/L) or supplement of exogenous NAD+ at 2 mmol/L for 1 h prevented RSL3-induced upregulation of ATF3 in both cytoplasmic and nuclear fractions.

    NAD sodium purchased from MedChemExpress. Usage Cited in: Redox Biol. 2024 Feb:69:103030.  [Abstract]

    Supplement of exogenous NAD+ at 1 mmol/L could inhibit ATF3 upregulation in the cells treated with FK866 (500 μmol/L) for 24 h, and this inhibition became more apparent by increasing NAD+ dosage to 2 mmol/L.

    NAD sodium purchased from MedChemExpress. Usage Cited in: Acta Pharmacol Sin. 2023 Oct;44(10):2125-2138.  [Abstract]

    Western blotting proved supplement of exterior NAD+ (0.5-2 mmol/L, 1 h) dosage-dependently alleviated DPT-induced downregulation of phospho-AKT and upregulation of NOX2, NAT10, phospho-CREB, PARP1, and PAR.

    NAD sodium purchased from MedChemExpress. Usage Cited in: Vascul Pharmacol. 2022 Dec:147:107126.  [Abstract]

    NAD+ significantly improves the expression of CD31 in the MI mice and DM + MI mice.

    NAD sodium purchased from MedChemExpress. Usage Cited in: Vascul Pharmacol. 2022 Dec:147:107126.  [Abstract]

    NAD+ significantly improves the expression of VEGF in the MI mice and DM + MI mice.

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    Description

    NAD sodium is an orally effective cofactor and homeostatic regulator. NAD sodium can be reduced to β-nicotinamide adenine dinucleotide (NADH) during coupling with reactions that oxidize organic substrates. NAD sodium can be converted to β-nicotinamide adenine dinucleotide (NADH) and passes to the inside of mitochondria, which indirectly generates ATP. NAD sodium can be used for the research of non-alcoholic fatty liver disease, obesity, and glucose intolerance[1][2][3][4][5].

    In Vitro

    NAD (sodium) (250 pM, 100 μM; 5-60 min, 10 min) is transported into NIH-3T3 cells with an apparent Km of ~190 μM, and co-treatment with unlabeled NAD competes for transport[4].
    NAD (sodium) (100 μM; 72 h) rescues FK866-induced cell death and replenishes intracellular NAD(P) levels in NIH-3T3 cells[4].
    NAD (sodium) (250 pM; 10 min) is transported into SH-SY5Y, HeLa, HaCaT, HMEC, and RAW 264.7 cells but not K562 cells, with sodium-dependent transport in SH-SY5Y cells[4].
    NAD (sodium) (100 μM; 72 h) rescues FK866-induced cell death and replenishes intracellular NAD(P) levels in SH-SY5Y cells[4].
    NAD (sodium) (100 μM; 36 h) reverts FK866-induced autophagy in SH-SY5Y cells[4].
    NAD (sodium) (0.5 mM) promotes M2 macrophage polarization and inhibits M1 macrophage polarization in both normal and high glucose-exposed RAW264.7 cells[5].
    NAD (sodium) (0.5 mM; 24 h) restores reduced VEGF secretion in high glucose-exposed mouse bone marrow-derived macrophages[5].
    NAD (sodium) (0.5 mM; 24 h) modulates BMDM to secrete factors that restore HUVEC tube formation, migration, and scratch wound closure impaired by high glucose exposure[5].
    NAD (sodium) (0.5 mM) promotes pro-angiogenic VEGF165 expression and inhibits anti-angiogenic VEGF165b expression in both normal and high glucose-exposed RAW264.7 cells[5].
    NAD (sodium) (0.5 mM) restores reduced SRSF1 expression and inhibits increased SRSF6 expression in high glucose-exposed RAW264.7 cells, and modulates these splicing factors in normal glucose cells[5].
    NAD (sodium) (0.5 mM; 24 h) reverses impaired HUVEC scratch wound closure caused by conditioned medium from NAD+-depleted RAW264.7 cells[5].
    NAD (sodium) (0.5 mM) restores reduced pro-angiogenic VEGF165 expression and inhibits increased anti-angiogenic VEGF165b expression in NAD+-depleted RAW264.7 cells[5].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    NAD sodium Related Antibodies

    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

    NAD+ (500 mg/kg/day; i.p.; daily; at least 28 days) attenuates cardiac injury and improves cardiac function after myocardial infarction in both diabetic and non-diabetic mice by restoring cardiac NAD+ levels, reducing infarct size, promoting M2 macrophage polarization, and enhancing angiogenesis, while also lowering blood glucose in diabetic mice[5].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    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
    Molecular Weight

    685.41

    Formula

    C21H26N7NaO14P2
    CAS No.
    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
    Shipping

    Room temperature in continental US; may vary elsewhere.
    Storage

    -20°C, sealed storage, away from moisture

    *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)

    Solvent & Solubility
    In Vitro: 

    H2O : ≥ 175 mg/mL (255.32 mM)

    *"≥" means soluble, but saturation unknown.

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 1.4590 mL 7.2949 mL 14.5898 mL
    5 mM 0.2918 mL 1.4590 mL 2.9180 mL
    View the Complete Stock Solution Preparation Table

    * Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
    Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

    * Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

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    Working solution concentration: mg/mL
    This product has good water solubility, please refer to the measured solubility data in water/PBS/Saline for details.
    The concentration of the stock solution you require exceeds the measured solubility. The following solution is for reference only.If necessary, please contact MedChemExpress (MCE).
    Purity & Documentation

    Purity: 99.44%

    SDS (557 KB)

    COA (261 KB)

    Handling Instructions (2659 KB)
    References

    Complete Stock Solution Preparation Table

    * Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
    Storage method and period of stock solution: -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture). When stored at -80°C, please use it within 6 months. When stored at -20°C, please use it within 1 month.

    Optional Solvent Concentration Solvent Mass 1 mg 5 mg 10 mg 25 mg
    H2O 1 mM 1.4590 mL 7.2949 mL 14.5898 mL 36.4745 mL
    5 mM 0.2918 mL 1.4590 mL 2.9180 mL 7.2949 mL
    10 mM 0.1459 mL 0.7295 mL 1.4590 mL 3.6475 mL
    15 mM 0.0973 mL 0.4863 mL 0.9727 mL 2.4316 mL
    20 mM 0.0729 mL 0.3647 mL 0.7295 mL 1.8237 mL
    25 mM 0.0584 mL 0.2918 mL 0.5836 mL 1.4590 mL
    30 mM 0.0486 mL 0.2432 mL 0.4863 mL 1.2158 mL
    40 mM 0.0365 mL 0.1824 mL 0.3647 mL 0.9119 mL
    50 mM 0.0292 mL 0.1459 mL 0.2918 mL 0.7295 mL
    60 mM 0.0243 mL 0.1216 mL 0.2432 mL 0.6079 mL
    80 mM 0.0182 mL 0.0912 mL 0.1824 mL 0.4559 mL
    100 mM 0.0146 mL 0.0729 mL 0.1459 mL 0.3647 mL

    * Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.

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    NAD sodium Related Classifications

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      Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

    Keywords:

    NAD20111-18-6β-DPNβ-NADβ-Nicotinamide Adenine DinucleotideEndogenous Metabolite辅酶因子巨噬细胞M2极化诱导剂Inhibitorinhibitorinhibit

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