This may be a particular advantage in enabling expression of cartilage protective effects of the drug. Radiolabelled oxaprozin accumulated in cartilage to a much greater extent than observed with other NSAIDs.

Oxaprozin did not exacerbate the IL-1β and/or TNFα-induced proteoglycan destruction in pig or bovine cartilage in organ culture as observed with indomethacin and aspirin. Oxaprozin (1.0-100 μM) did not affect NO production from porcine synovial tissue, whereas indomethacin and nimesulide reduced production of NO. Among the major effects of oxaprozin (10-100 μM) observed on components of joint destruction was (a) the inhibition of the production of interleukin-1β (IL-1β) from pig synovial tissues in organ culture and IL-1β, IL-6 and IL-8, as well as tumour necrosis factor-α (TNFα) from THP-1 mononuclear cells at 50-100 μM. The latter in vitro pharmacokinetic study can be considered as a basis for understanding both safety and therapeutic activity of the drug. We have investigated the pharmacology of oxaprozin on (a) the biochemical components of joint destruction in vitro, and (b) the pharmacokinetic interactions of this drug with albumin in vitro in which drug interactions are modelled by competitive binding of the drug with endogenous ligands or drugs that are commonly prescribed with NSAIDs. Being an unselective COX-1 and COX-2 inhibitor the drug may have advantages in more effective pain relief related to both COX-1 as well as COX-2 effects. It has a low incidence of gastrointestinal side effects making it a particularly attractive therapy.

Oxaprozin has proven a safe and effective treatment for arthritic conditions.

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