Diclofena-c Potassium CAS 15307-81-0 MDL NO MFCD00082254

Product Description:

Product Name: Diclofena-c potassium CAS NO: 15307-81-0

Synonyms:

potassium 2-(2-(2,6-dichlorophenylamino)phenyl)acetate;

2-[(2,6-Dichlorophenyl)amino]benzeneacetic acid potassium salt, Diclofena-c potassium salt;

Benzeneaceticacid, 2-[(2,6-dichlorophenyl)aMino]-, potassiuM salt (1:1);

Chemical & Physical Properties:

Appearance: White to yellowish crystalline powder

Assay :≥99.0%

Boiling Point: 412℃ at 760 mmHg

Melting Point: 156-158℃

Flash Point: 203℃

Vapor Pressure: 1.59E-07mmHg at 25℃

Solubility: Sparingly soluble in water, freely soluble in methanol, soluble in ethanol (96 per cent), slightly soluble in aceto-ne.

Safety Information:

HS Code: 2922499990

Hazard Codes: T,N

Symbols: GHS07, GHS09

Caution Statement: P273

Signal Word: Warning

Hazard Declaration: H302; H411

Diclofena-c Potassium Salt is a nonsteroidal anti-inflammatory compound an decycloxygenase (COX) inhibitor. Dichlofenac potassium is the potassium salt of dichlofenac. It is a nonsteroidal anti-inflammatory agent that can be used to reduce inflammation and as an analgesic to reduce pain in certain conditions. It can also used to treat dysmenorrhea. It can treat inflammatory disorders such as musculoskeletal complaints, dental pain, arthritis, actinic keratosis, joint pain, acute pain and chronic pain caused by certain kinds of cancers. Traditional opinion proposes that diclofena-c exerts its action via inhibition of prostaglandin synthesis by inhibiting cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) with relative equipotency. However, recent studies have shown that the pharmacologic activity of diclofena-c goes beyond COX inhibition, and includes multimodal and, in some instances, novel mechanisms of action (MOA). For example, research suggests diclofena-c can inhibit the thromboxane-prostanoid receptor, affect arachidonic acid release and uptake, inhibit lipoxygenase enzymes, and activate the nitric oxide–cGMP antinociceptive pathway. Other novel MOAs may include the inhibition of substrate P, inhibition of peroxisome proliferator activated receptor gamma (PPARγ), blockage of acid-sensing ion channels, alteration of interleukin-6 production, and inhibition of N-methyl-D-aspartate (NMDA) receptor hyperalgesia.

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