Loxoprofen sodium dihydrate is a non-steroidal, orally active anti-inflammatory agent that has analgesic and anti-pyretic properties. Loxoprofen sodium dihydrate exhibits antitumor activity which also can reduce atherosclerosis. Loxoprofen sodium dihydrate is a nonselective inhibitor of COX with IC 50 s of 6.5 and 13.5 μM for COX-1 and COX-2, respectively [1] [2] [3] [4].

Loxoprofen sodium dihydrate, an anti-inflammatory prodrug (NSAID), is a nonselective COX inhibitor with IC 50 s of 6.5 and 13.5 μM for COX-1 and COX-2 in human whole blood assays, respectively [1]. Loxoprofen (LOX) sodium dihydrate is a non-selective cyclooxygenase inhibitor that is widely used for the reasearch of pain and inflammation caused by chronic and transitory conditions. Its alcoholic metabolites are formed by carbonyl reductase (CR) and they consist of trans-LOX, which is active, and cis-LOX, which is inactive. In addition, LOX sodium dihydrate can also be converted into an inactive hydroxylated metabolite (OH-LOXs) by cytochrome P450 (CYP) [2].

Loxoprofen sodium (4 mg/kg/day; p.o.; 1 or 8 weeks) dihydrate reduces atherosclerosis in mice by reducing inflammation [3]. Loxoprofen sodium (60 μg/mL; p.o.; 24 days) dihydrate suppresses mouse tumor growth by inhibiting VEGF [4]. Animal Model: ApoE -/- mice (C57BL/6J-Apoe tm1Unc ) with high-fat diet (0.2% cholesterol, 21% saturated fat) from 8 to 16 weeks of age [3] Dosage: 4 mg/kg/day in drinking water Administration: Oral dosing from 8 to 16 weeks of age or from 15 to 16 weeks of age Result: Inhibited platelet thromboxane production and platelet aggregation. Reduced extent of atherosclerosis. Suppressed the production of PGE 2, TxB 2 and PGI 2. Animal Model: 6-week-old male C57BL/6 and BDF1 mice, 100 μL suspensions (2 × 10 6 cells/mL) of LLC cells and KLN205 cells were injected subcutaneously into C57BL/6 and BDF1 mice, respectively [4]. Dosage: 60 μg/mL Administration: Oral dosing in drinking water, every day for 24 days Result: Suppressed tumor growth and angiogenesis, suppressed expression of VEGF in mice with LLC tumor, inhibited tubular formation of HUVECs.