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These alternate metabolites of COX-1 may contribute to its activities. COX-1 promotes the production of the natural mucus lining that protects the inner stomach and contributes to reduced acid secretion and reduced pepsin content. [18] [19] COX-1 is normally present in a variety of areas of the body, including not only the stomach but any site ...
Ketorolac is a non-selective COX inhibitor. [26] It is considered a first-generation NSAID, [15]: 279 a group of drugs that non-selectively inhibit both COX-1 and COX-2 enzymes, which can lead to gastrointestinal side effects. [27]
Celecoxib, sold under the brand name Celebrex among others, is a COX-2 inhibitor and nonsteroidal anti-inflammatory drug (NSAID). [7] It is used to treat the pain and inflammation in osteoarthritis, acute pain in adults, rheumatoid arthritis, psoriatic arthritis, ankylosing spondylitis, painful menstruation, and juvenile rheumatoid arthritis. [7]
COX is a common target for anti-inflammatory drugs. The most significant difference between the isoenzymes, which allows for selective inhibition, is the substitution of isoleucine at position 523 in COX-1 with valine in COX-2. The smaller Val 523 residue in COX-2 allows access to a hydrophobic side-pocket in the enzyme (which Ile 523 ...
Newer NSAID drugs called COX-2 selective inhibitors have been developed that inhibit only COX-2, with the hope for reduction of gastrointestinal side-effects. [8] However, several COX-2 selective inhibitors have subsequently been withdrawn after evidence emerged that COX-2 inhibitors increase the risk of heart attack. [9]
Prostaglandin inhibitors are drugs that inhibit the synthesis of prostaglandin in human body. [1] There are various types of prostaglandins responsible for different physiological reactions such as maintaining the blood flow in stomach and kidney, regulating the contraction of involuntary muscles and blood vessels, and act as a mediator of inflammation and pain.
The VIGOR trial results were published in 2000 in the New England Journal of Medicine [47] Bombardier and her research team claimed that there was "an increase in myocardial infarction in the patients given rofecoxib (0.4%) compared with those given naproxen (0.1%)" and "patients given naproxen experienced 121 side effects compared with 56 in ...
The therapeutic recommended dosages were 12.5, 25, and 50 mg with an approximate bioavailability of 93%. [12] [13] [14] Rofecoxib crossed the placenta and blood–brain barrier, [12] [13] [15] and took 1–3 hours to reach peak plasma concentration with an effective half-life (based on steady-state levels) around 17 hours.