Flurbiprofen (dl-Flurbiprofen) is an anti-inflammatory analgesic and antipyretic of the phenylalkynoic acid series. It has been shown to reduce bone resorption in periodontal disease by inhibiting CARBONIC ANHYDRASE.

Flurbiprofen effectively inhibits the growth of various tumor cells in a dose-dependent manner and causes a noticeable change in the progression of cells through cell cycle stages in tumor cell lines derived from medulloblastoma and glioblastoma multiforme. Flurbiprofen reduces the number of cells in G1 and G2, and significantly increases their numbers in S phase, suggesting that, Flurbiprofen accelerates G1/S entry, and/or delays cell exit from S to G2/M stages. Flurbiprofen causes a minor change in the RNA level of different cyclins, there is a significant decrease in the level of cyclin B protein upon flurbiprofen treatment. [1]

Flurbiprofen affords significant neuroprotection from ischemic injury as evidenced by reduction in cerebral infarct volume and neurobehavioral deficit. Flurbiprofen significantly reduces an early calcium dependent rise in levels of nitrite and MDA in ischemic brain regions of rats. Flurbiprofen also reduces the proteolytic products (SBDPs) caused by ischemic activation of calcium dependent protease calpain. [2] Flurbiprofen (5 mg/kg and 10 mg/kg) significantly attenuates brain ischemia/reperfusion injury in rats, as shown by a reduction in the infarct volume, neurological deficit scores and cell apoptosis. Flurbiprofen not only inhibits the expression of Bax protein and p-GSK-3β, but also increases the expression of Bcl-2 protein, the ratio of Bcl-2/Bax as well as the P-Akt level in rats. [3]