Clinico-pharmacological studies and clinical evaluation of flurbiprofen. A new non-steroidal antirheumatic agent.

NO‐flurbiprofen reduces amyloid‐β, is neuroprotective in cell culture, and enhances cognition in response to cholinergic blockade

“…The etiology of the inflammatory reaction observed in AD is still debated, but Aβ has been implicated as a stimulus to induction of inflammation (Butterfield et al 2002). Flurbiprofen is an NSAID that inhibits COX and the activation of monocytes (Chalmers et al 1972, Hinz et al 2001). Flurbiprofen is also one of a subset of NSAIDs that have been reported to act as SALAs, reducing the levels of neurotoxic Aβ 1–42 and the ratio of Aβ 1–42 /Aβ 1–40 ; of common NSAIDs, flurbiprofen is the most efficacious in vitro (Morihara et al 2002, Eriksen et al 2003, Weggen et al 2001).…”

Intra-articular urokinase in rheumatoid arthritis.

“…The patients studied will be monitored for a considerable length of time and any changes which may emerge will be reported immediately. The numbers involved are small but, from previous experience of active compounds (Chalmers, Cathcart, Kumar, Dick and Buchanan, 1972), we should have expected to observe improvement in some of the patients whereas, even in the patients whose individual results showed slight though insignificant alteration, change was in the direction ofdeterioration rather than amelioration. It is also noteworthy that the dose employed was far in excess of tissue levels likely to be obtained in systemic urokinase treatment with standardly employed dose levels.…”

Studies on 2-(3-benzoylphenyl) propionic acid (Orudis). A double-blind cross-over trial in patients with rheumatoid arthritis and an assessment of its influence on hepatic drug-metabolizing enzymes.

“…The method has been previously described (Chalmers, Cathcart, Kumar, Dick, and Buchanan, 1972) and is a modification of that developed by Dick, Neufeld, Prentice, Woodburn, Whaley, Nuki, and Buchanan (1970) and Dick, Deodhar, Provan, Nuki, and Buchanan (1971).…”