Lornoxicam

Lornoxicam (Chlortenoxicam) is an orally active oxycontin nonsteroidal anti-inflammatory drug (NSAID) with analgesic, anti-inflammatory, antipyretic and anticancer activities. Lornoxicam exhibits good inhibitory effects on both COX-1 and COX-2 (COX-1: IC₅₀=0.005 μM; COX-2:IC₅₀=0.008 μM) and inhibits the production of NO by iNOS (IC₅₀=65 μM) and the proinflammatory cytokine IL-6 (IC₅₀=54 μM). Lornoxicam also inhibits tumor cell proliferation and migration and induces tumor cell apoptosis. Lornoxicam can be used in the study of inflammatory pain, colorectal cancer and breast cancer^{[1][2][3][4][5][6][7]}. In Vitro:Lornoxicam (0.03-3 μM; 24 h) dose-dependently inhibites the formation of TXB2 in HEL cells, the formation of PGF1 in Mono Mac 6 cells stimulated by LPS (HY-D1056) and the accumulation of NO in the supernatant of RAW 264.7 cells stimulated by LPS (HY-D1056)^[6].
Lornoxicam (10-300 μM; 10 min) dose-dependently inhibites the formation of IL-6 in human monocytic THP-1 cells (IC₅₀=54 μM) and weakly stimulates the production of TNF-a, IL-1b and IL-8 at a dose of 300 μM^[6].
Lornoxicam (3.1-400 μg/mL; 0-48 h) concentration-dependently induces a decrease in the viability of cervical cancer, colorectal cancer, and breast cancer cell lines HeLa, MCF-7, and HT-29 and inhibites the proliferation of HT-29 cell line^[7].
Lornoxicam (400 μg/mL; 24 h) induces apoptosis in HT-29 and MCF-7 tumor cells^[7].
Lornoxicam (400 μg/mL; 0-72 h) inhibites the migration of HT-29 and MCF-7 tumor cells^[7].
In Vivo:Lornoxicam (1.3 mg/kg, i.p.; single dose) reduces the ability of central sensitization in rats to reduce hyperalgesia in the thermal hind paw hyperalgesia model^[3].