product name Diclofenac Sodium
Description: Diclofenac Sodium (also known as 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. 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.
318.13
Formula
C14H10Cl2NNaO2
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)
Solubility (In vivo)
Synonyms
GP 45840
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19407382
| 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. Kinase Assay: Cell Assay: |
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| 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). |
| Animal model | |
| Formulation & Dosage | |
| References | FEBS Lett. 2005 Aug 15;579(20):4213-8; Biochim Biophys Acta. 1997 Feb 15;1318(3):385-94. |
