Diclofenac Sodium

Catalog No.S1903 Batch:S190302

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Technical Data

Formula

C14H10Cl2NNaO2
Molecular Weight 318.13 CAS No. 15307-79-6
Solubility (25°C)* In vitro DMSO 64 mg/mL (201.17 mM)
Ethanol 64 mg/mL (201.17 mM)
Water 14 mg/mL (44.0 mM)
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description Diclofenac Sodium (GP 45840) is a non-selective COX inhibitor with IC50 of 0.5 μg/ml and 0.5 μg/ml for COX-1 and -2 in intact cells, respectively, used as a nonsteroidal anti-inflammatory drug (NSAID) to relieve pain and reduce swelling in flammation.
Targets
COX-1 [1] COX-2 [1]
60 nM 200 nM
In vitro 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. [1] 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. [2] 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. [3]
In vivo Diclofenac (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). [4]

Protocol (from reference)

Selleck's Diclofenac Sodium has been cited by 4 publications

Propionibacterium acnes Induces Intervertebral Disc Degeneration by Promoting iNOS/NO and COX-2/PGE2 Activation via the ROS-Dependent NF-κB Pathway [ Oxid Med Cell Longev, 2018, 2018:3692752] PubMed: 30210652
The pharmacokinetics and metabolism of diclofenac in chimeric humanized and murinized FRG mice. [ Arch Toxicol, 2018, 92(6):1953-1967] PubMed: 29721588
Mutant KRAS Enhances Tumor Cell Fitness by Upregulating Stress Granules. [Grabocka E, et al. Cell, 2016, 167(7):1803-1813] PubMed: 27984728
Synergistic apoptosis in head and neck squamous cell carcinoma cells by co-inhibition of insulin-like growth factor-1 receptor signaling and compensatory signaling pathways [Axelrod MJ et al. Head Neck, 2014, 10.1002/hed.23822] PubMed: 24986420

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

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