Product Name: Clofenac
Generic Name: Diclofenac Sodium
Mechanism of Action:
The anti-inflammatory effects of Diclofenac are believed to be due to inhibition of enzyme cyclooxygenase (COX-1 and COX-2), leading to the peripheral inhibition of prostaglandin synthesis. As prostaglandins sensitize pain receptors, inhibition of their synthesis is responsible for the analgesic effects of Diclofenac.
Product Name: Miclofenac
Generic Name: Diclofenac + Misoprostol
Mechanism of Action:
Prostaglandins are produced by the enzyme cyclooxygenase (Cox).
There actually are two Cox enzymes, Cox-1 and Cox-2.
Both enzymes produce prostaglandins that promote inflammation, pain, and fever.
However, only Cox-1 produces prostaglandins that support platelets and protect the stomach. Diclofenac blocks both Cox enzymes and reduces prostaglandins throughout the body.
As a consequence, ongoing inflammation, pain, and fever are reduced.
Since prostaglandins that protect the stomach and support platelets and blood clotting also are reduced, NSAIDs can cause ulcers in the stomach and promote bleeding.
Misoprostol is a synthetic (man-made) prostaglandin that stimulates secretion of mucus in the gastrointestinal tract.
Mucus protects the lining of the stomach from acid.
Misoprostol has been shown to reduce the frequency of ulcers of the stomach caused by NSAIDs.
Product Name: Panodin SR-Tab
Generic Name: Etodolac
Mechanism of Action:
Similar to other NSAIDs, the anti-inflammatory effects of Etodolac result from inhibition of the enzyme cyclooxygenase (COX).
This decreases the synthesis of peripheral prostaglandins involved in mediating inflammation.
Etodolac binds to the upper portion of the COX enzyme active site and prevents its substrate, arachidonic acid, from entering the active site. Etodolac was previously thought to be a non-selective COX inhibitor, but it is now known to be 5 – 50 times more selective for COX-2 than COX-1.
