Diclofenac sodium

SKU: orb1308210

Description

Diclofenac sodium is a widely used non-steroidal anti-inflammatory drug (NSAID) with analgesic and antipyretic properties. It is commonly applied in research to study inflammation, pain mechanisms, and cyclooxygenase (COX) inhibition in both in vitro assays and in vivo animal models.

Research Area

Cell Biology, Immunology & Inflammation, Neuroscience

Key Properties

• CAS Number: 15307-79-6
• MW: 318.13
• Purity: 99.92% (May vary between batches)
• Formula: C₁₄H₁₀Cl₂NNaO₂
• SMILES: [Na+].C(=O)(Cc1c(cccc1)Nc1c(cccc1Cl)Cl)[O-]
• Target: COX,Apoptosis
• Solubility: H2O:15.9 mg/mL (49.98 mM);DMSO:45 mg/mL (141.45 mM)

Bioactivity

• Target IC50:
  COX-1 (ovine):0.84 μM|COX-1 (ovine):5.1 μM|COX-2:200 nM|COX-1 (human, CHO cells):4 nM|COX-2 (human, CHO cells):1.3 nM|COX-1:60 nM
• 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).
• 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. 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.

Storage & Handling

• Storage: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

stem, Diclofenac, Diclofenac sodium, Cyclooxygenase, CHO, COX, COX-1, COX-2, cells, caspase, cascade, Apoptosis, anti-inflammatory, neural, ovine, NSCs, inhibit, GP 45840, GP-45840, GP45840, Inhibitor

Compound Identifiers

PubChem CID

5018304