Loxoprofen (Koloxo) is an anti-inflammatory non-steroidal medicine.

Loxoprofen sodium(LOX) does not affect the proliferation and viability of LLC cells in vitro. HUVECs treated with LOX results in the inhibition of the tubular formation. Treatment with 50 mg/ml LOX reveals a 33% decline in in vitro angiogenesis, compared with vehicle-treated HUVECs. This inhibition is presumably due to inhibition of VEGF activity[1].

Loxoprofen sodium (LOX), inhibits in vivo growth of implanted Lewis lung carcinoma (LLC). Intratumoral vessel density in LOX-treated mice is significantly lower than that of mice without treatment. Intratumoral expressions of vascular endothelial growth factor (VEGF) mRNA are attenuated by the LOX treatment. LOX suppresses both intratumoral and systemic VEGF protein in LLC-implanted mice. LOX also inhibits tubular formation of primary cultured human umbilical vein endothelial cells, presumably due to the inhibition of VEGF. In patients with advanced non-small cell lung cancer, LOX medication (120 mg/day) for a week significantly decreases the plasma VEGF level[1].

To determine the proliferation of LLC cells with or without Loxoprofen, 2×104 cells are seeded into 100-mm dishes containing 10 ml culture medium supplemented with 50 μg/ml Loxoprofen or vehicle on day 0. On days 2, 3, 4 and 6, the cells are trypsinized and counted. (Only for Reference)