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    Diclofenac Sodium (GP 45840)
    Diclofenac Sodium (GP 45840)

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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 #: V1051
    CAS #: 15307-79-6Purity ≥98%

    Description: Diclofenac Sodium (Abitren, Blesin, Delimon, Allvoran, Berifen, Delphimix, Voltaren, Voltarol; Assaren, Batafil, GP-45840) is a nonsteroidal anti-inflammatory drug (NSAID), acting as a non-selective COX inhibitor with potential anti-inflammatory activity. It inhibits COX-1/2 with IC50 of 0.5 μg/ml and 0.5 μg/ml in intact cells, respectively, and is used to relieve pain and reduce swelling in flammation. Diclofenac inhibits Wnt/beta-catenin signaling without altering the level of beta-catenin protein and reduces the expression of beta-catenin/TCF-dependent genes. Diclofenac induces the degradation of IkappaBalpha, which increases free nuclear factor kappaB (NF-kappaB) in colon cancer cells.

    References: FEBS Lett. 2005 Aug 15;579(20):4213-8; Biochim Biophys Acta. 1997 Feb 15;1318(3):385-94.

    Related CAS #: 15307-86-5 (free base) 

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    Molecular Weight (MW)318.13 
    FormulaC14H10Cl2NNaO2 
    CAS No.15307-79-6 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 64 mg/mL (201.2 mM) 
    Water: 14 mg/mL (44.0 mM)
    Ethanol: 64 mg/mL (201.2 mM) 
    Other info

    Chemical Name: Benzeneacetic acid, 2-((2,6-dichlorophenyl)amino)-, monosodium salt

    InChi Key: KPHWPUGNDIVLNH-UHFFFAOYSA-M

    InChi Code: 1S/C14H11Cl2NO2.Na/c15-10-5-3-6-11(16)14(10)17-12-7-2-1-4-9(12)8-13(18)19;/h1-7,17H,8H2,(H,18,19);/q;+1/p-1

    SMILES: c1ccc(c(c1)CC(=O)[O-])Nc2c(cccc2Cl)Cl.[Na+]

    SynonymsGP-45840; Abitren, Voltaren, Voltaren-XR, Allvoran, Delimon, Neriodin, Orthophen, Sodium diclofenac, Voltarene, Voltarol; GP45840; GP 45840; Assaren, Batafil, Berifen, Delphimix, Diclofenac sodium, Blesin


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    In Vitro

    In vitro activity: Diclofenac inhibits Wnt/beta-catenin signaling without altering the level of beta-catenin protein and reduces the expression of beta-catenin/TCF-dependent genes. Diclofenac induces the degradation of IkappaBalpha, which increases free nuclear factor kappaB (NF-kappaB) in colon cancer cells. Diclofenac suppresses both fast tetrodotoxin-sensitive (TTX-S) and the slow tetrodotoxin-resistant (TTX-R) sodium currents in a dose-dependent manner. Diclofenac produces shifts of the steady-state inactivation curves in the hyperpolarizing direction in both types of sodium currents in a dose-dependent manner. Diclofenac may bind to sodium channels with a greater affinity when they are in the inactivated state than when they are in the resting state. Diclofenac results in a severe accumulation of protein in the tubular cells (so called hyaline droplet degeneration), macrophage infiltration and structural alterations (dilation, vesiculation) of the endoplasmic reticulum (ER) in the proximal and distal renal tubules of kidney. Diclofenac also results in shortening of podocytes and their retraction from the basal lamina, a thickening of the basal lamina, the formation of desmosomes, and necrosis of endothelial cells in the renal corpuscles of kidney.

    In VivoDiclofenac (0.01 to 0.2 mM) stimulates state-4 respiration and slightly inhibits state 3 in rats, decreasing the respiratory control ratio, while the membrane potential is decreased or collapsed (depending on the drug concentration).  
    Animal modelRats
    Formulation & Dosage0.01 to 0.2 mM
    References

    FEBS Lett. 2005 Aug 15;579(20):4213-8; Biochim Biophys Acta. 1997 Feb 15;1318(3):385-94. 


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

    Purity ≥99%

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