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NSAIDs within a group tend to have similar characteristics and tolerability. There is little difference in clinical efficacy among the NSAIDs when used at equivalent doses. [153] Rather, differences among compounds usually relate to dosing regimens (related to the compound's elimination half-life), route of administration, and tolerability profile.
0.05 (3–6 min context-sensitive half-life; 7–18 min elimination half-life) Instantaneously (from 5 to 15 sec) 15 minutes; rapid offset of effects necessitates continuous infusion for maintenance of anesthesia Protonitazene: 200 50 μg Ocfentanil: 125–250 40–80 μg Ro4-1539: 240–480 20–40 μg Isotonitazene: 500 20 μg Sufentanil: 500 ...
Elimination half-life: 26.6-31.2 hours: Excretion: Feces (65%) Identifiers; ... Colchicine is an alternative for those unable to tolerate NSAIDs when treating gout.
Elimination half-life: Dose-dependent; 2–3 ... Other NSAIDs, such as ibuprofen and naproxen, may reduce the antiplatelet effect of aspirin. [228] [229] ...
Phenylbutazone has a plasma elimination half-life of 4–8 hours, however the inflammatory exudate half life is 24 hours, [10] so single daily dosing can be sufficient, although it is often used twice per day. [5] The drug is considered fairly non-toxic when given at appropriate doses (2.2-4.4 mg/kg/day), even when used repeatedly. [11]
As with other NSAIDs, ibuprofen has been reported to be a photosensitizing agent, [38] but it is considered a weak photosensitizing agent compared to other members of the 2-arylpropionic acid class. Like other NSAIDs, ibuprofen is an extremely rare cause of the autoimmune diseases Stevens–Johnson syndrome (SJS) and toxic epidermal necrolysis.
Acemetacin is a non-steroidal anti-inflammatory drug (NSAID) used for the treatment of osteoarthritis, ... Elimination half-life is 4.5±2.8 hours ...
Nabumetone is a non-acidic NSAID prodrug that is rapidly metabolized in the liver to the active metabolite, 6-methoxy-2-naphthyl acetic acid. Nabumetone's active metabolite inhibits the cyclooxygenase enzyme and preferentially blocks COX-2 activity (which is indirectly responsible for the production of inflammation and pain during arthritis).
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