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MedChemExpressModel Lornoxicam - 70374-39-9

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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].
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Lornoxicam

MCE China:Lornoxicam

Brand:MedChemExpress (MCE)

Cat. No.HY-B0367

CAS:70374-39-9

Synonyms:Chlortenoxicam; Ro 13-9297

Purity:99.36%

Storage:Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year

Shipping:Room temperature in continental US; may vary elsewhere.

Description: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.

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].

IC50 & Target:COX-1 5 nM (IC50, in cells) COX-2 45 nM (IC50, in cells)

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References:

[1]. Spyra S, et al. COX-2-selective inhibitors celecoxib and deracoxib modulate transient receptor potential vanilloid 3 channels. Br J Pharmacol. 2017 Aug;174(16):2696-2705.  [Content Brief]

[2]. Rose, P. and C. Steinhauser, Comparison of Lornoxicam and Rofecoxib in Patients with Activated Osteoarthritis (COLOR Study). Clin Drug Investig, 2004. 24(4): p. 227-36.  [Content Brief]

[3]. Bianchi, M. and A.E. Panerai, Effects of lornoxicam, piroxicam, and meloxicam in a model of thermal hindpaw hyperalgesia induced by formalin injection in rat tail. Pharmacol Res, 2002. 45(2): p. 101-5.  [Content Brief]

[4]. Balfour J A, et al. Lornoxicam: a review of its pharmacology and therapeutic potential in the management of painful and inflammatory conditions[J]. Drugs, 1996, 51: 639-657.  [Content Brief]

[5]. Pohlmeyer-Esch G, et al. Evaluation of chronic oral toxicity and carcinogenic potential of lornoxicam in rats[J]. Food and chemical toxicology, 1997, 35(9): 909-922.  [Content Brief]

[6]. Berg J, et al. The analgesic NSAID lornoxicam inhibits cyclooxygenase (COX)-1/-2, inducible nitric oxide synthase (iNOS), and the formation of interleukin (IL)-6 in vitro[J]. Inflammation Research, 1999, 48: 369-379.  [Content Brief]

[7]. Marinov L, et al. The effects of meloxicam, lornoxicam, ketoprofen, and dexketoprofen on human cervical, colorectal, and mammary carcinoma cell lines[J]. Pharmacia, 2024, 71: 1-12.

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