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    Sodium salicylate
    Sodium salicylate

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0767
    CAS #: 54-21-7Purity ≥98%

    Description: Sodium salicylate (Magsalyl; Kerasalicyl; Kerosal), the sodium salt of salicylic acid and a metabolite of acetylsalicylic acid, is an inhibitor of NF-kB with potential anti-inflammatory activity. It has been used as a nonsteroidal anti-inflammatory drug (NSAID), and acts by irreversibly acetylating COX I/II (cyclooxygenases I and II), thereby inhibiting prostaglandin synthesis and associated inflammation and pain.

    References: Science. 1994 Aug 12;265(5174):956-9; Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):2869-73.

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    Molecular Weight (MW)161.11
    CAS No.54-21-7
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 32 mg/mL (198.6 mM)
    Water: 32 mg/mL (198.6 mM)
    Ethanol: <1 mg/mL
    Other info

    Chemical Name: Benzoic acid, 2-hydroxy-, monosodium salt


    InChi Code: InChI=1S/C7H6O3.Na/c8-6-4-2-1-3-5(6)7(9)10;/h1-4,8H,(H,9,10);/q;+1/p-1

    SMILES Code: O=C([O-])C1=CC=CC=C1O.[Na+]           


    Sodium salicylate; Magsalyl; Kerasalicyl; Kerosal; 

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    In Vitro

    In vitro activity: Sodium salicylate acts as non-steroidal anti-inflammatory drug (NSAID), and induces apoptosis in cancer cells and also necrosis. Sodium salicylate inhibits the activation of NF-kappa B, and also inhibits NF-kappa B-dependent transcription from the Ig kappa enhancer and the human immunodeficiency virus (HIV) long terminal repeat (LTR) in transfected T cells. Sodium salicylate also induces apoptosis via p38 MAPK and inhibits TNF-induced JNK/stress-activated protein kinase activation.

    Kinase Assay: Human purified COX-2 are and the cofactors Glutathione (5 mM), Adrenaline (5 mM), and Hematin (1 μM) are dissolved in 50 mM Tris buffer (pH 7.5). Hematin is first dissolved in a concentrated stock of 100 mM in 1 M NaOH before being further diluted in Tris buffer. Enzyme reactions are carried out in individual wells of 96-well plates with a final reaction volume of 200 μL. Different concentrations of Sodium Salicylate are added to the plate, followed by the addition of 10 units of enzyme (180 μL). The plates are incubated at 37° for 30 min before Arachidonic acid (10 nM to 30 μM) is added for a further 15 min. The reaction is stopped by heating the plate to 100°C for 5 min. The 96-well plate is then centrifuged at 10,000 × g for 10 min, and appropriated samples are removed and added into the radioimmunoassay

    Cell Assay: To assess the direct effect of Sodium Salicylate on COX-2 activity after induction has occurred, A549 cells are first treated with IL-1β for 24 hr, and the culture medium is replaced with DMEM containing different concentrations of Sodium Salicylate(10, 100 and 1000 μg/mL). Cells are incubated at 37°C for 30 min. Arachidonic acid (1-30 μM) is then added for 15 min, and the medium is removed for the measurement of PGE2

    In VivoIn C57Bl/6 DIO mice, Salicylate decreases both fasting and postprandial plasma glucose levels. Furthermore, there is a trend to reduce plasma triglyceride levels after Salicylate treatment in C57Bl/6 DIO mice (P=0.059). Salicylate significantly reduces 11β-HSD1 mRNA in omental adipose tissue in C57Bl/6 DIO mice, with a similar trend in mesenteric adipose (P=0.057). In mesenteric adipose of C57Bl/6 DIO mice, Salicylate also reduces 11β-HSD1 enzyme activity
    Animal modelMice: Adult male C57Bl/6 mice are at age 12 weeks. Diet-induced obese C57Bl/6 mice (C57Bl/6 DIO) are given 10 weeks of high-fat diet (58% fat, 12% sucrose) before treatment. Sodium Salicylate (120 mg/kg/day) or distilled water (vehicle) is administered from 1 week after arriving (C57Bl/6 Lean), after 10 weeks of high-fat feeding (C57Bl/6 DIO), or after achieving target weight (HSD1KO-DIO) for 4 weeks to groups of n=8 via osmotic minipumps implant subcutaneously between the scapulae.
    Formulation & Dosage120 mg/kg

    Science. 1994 Aug 12;265(5174):956-9; Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):2869-73.

    These protocols are for reference only. InvivoChem does not independently validate these methods.


    Sodium salicylate

    Inhibition of TNF-induced JNK activation by NaSal. Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):2869-73.

    Sodium salicylate

    Inhibition of TNF-induced c-fos mRNA induction by NaSal. Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):2869-73.

    Sodium salicylate

    Activation of p38 MAPK by NaSal. Proc Natl Acad Sci U S A. 1997 Apr 1;94(7):2869-73.


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