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Ibuprofen is an inhibitor of cyclooxygenase 1 and cyclooxygenase 2 with IC50 values of 12 and 80 μM, respectively [1].

Cyclooxygenase (COX) is an enzyme that is responsible for the formation of prostaglandins, prostacyclin and thromboxane.

In HCT-116 p53wt or HCT-116 p53-/-colon carcinoma cell lines, S- and R-ibuprofen induced apoptosis and blocked cell cycle is in part dependent on p53. The anti-proliferative effects were significantly higher in the p53wt cell line than in the p53-deficient cells [2].

In nude mice model bearing HCT-116 p53wt and p53-/- xenografts, R-ibuprofen significantly inhibited the growth of p53wt expressing xenografts and only a small inhibition of p53-/- xenografts [2]. In hypercholesterolemic animals, ibuprofen reduced the levels of total cholesterol, VLDL, LDL, triglycerides and atherogenic index. Also, ibuprofen inhibited COX enzymes and inhibited the generation of free radicals during prostaglandins synthesis, which reduced the levels of lipid peroxidation, superoxide dismutase [3]. In rats, ibuprofen (60 mg/kg) improved mechanical hyperalgesia through reducing central hyperexcitability [4].

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