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COX-1 is inhibited by nonsteroidal anti-inflammatory drugs (NSAIDs) such as aspirin. Thromboxane A2, the major product of COX-1 in platelets, induces platelet aggregation. [20] [21] The inhibition of COX-1 is sufficient to explain why low dose aspirin is effective at reducing cardiac events.
COX-2 is an enzyme facultatively expressed in inflammation, and it is inhibition of COX-2 that produces the desirable effects of NSAIDs. [125] When nonselective COX-1/COX-2 inhibitors (such as aspirin, ibuprofen, and naproxen) lower stomach prostaglandin levels, ulcers of the stomach or duodenum and internal bleeding can result. [126]
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 ...
The existing nonsteroidal anti-inflammatory drugs differ in their relative specificities for COX-2 and COX-1; while aspirin and ibuprofen inhibit COX-2 and COX-1 enzymes, other NSAIDs appear to have partial COX-2 specificity, particularly meloxicam . [39] Aspirin is ≈170-fold more potent in inhibiting COX-1 than COX-2. [40]
Like aspirin and indomethacin, ibuprofen is a nonselective COX inhibitor, in that it inhibits two isoforms of cyclooxygenase, COX-1 and COX-2. The analgesic , antipyretic , and anti-inflammatory activity of NSAIDs appears to operate mainly through inhibition of COX-2, which decreases the synthesis of prostaglandins involved in mediating ...
NSAIDs inhibits the synthesis of prostaglandin by inhibiting cyclooxygenase (COX-1 and COX-2). NSAIDs with higher selectivity on COX-2 such as indomethacin, zomepirac and diclofenac have potent anti- inflammatory activity and fewer side effects on stomach and kidney. [28] [29]
Aspirin acts as an acetylating agent where an acetyl group is covalently attached to a serine residue in the active site of the COX enzyme. [1] This makes aspirin different from other NSAIDs (such as diclofenac and ibuprofen), which are reversible inhibitors; aspirin creates an allosteric change in the structure of the COX enzyme. [2]
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]