product name Lumiracoxib
Description: Lumiracoxib (also known as COX-189) is a novel, selective COX-2 inhibitor with IC50 and Ki of 0.14 μM and 0.06 μM, exhibits 515-fold selectivity over COX-1. Lumiracoxib has anti-inflammatory, analgesic and antipyretic activities comparable with diclofenac, the reference NSAID, but with much improved gastrointestinal safety. Lumiracoxib has an IC50 of 0.14 μm in COX-2-expressing dermal fibroblasts, but caused no inhibition of COX-1 at concentrations up to 30 μm.
References: Br J Pharmacol. 2005 Feb;144(4):538-50.
293.72
Formula
C15H13ClFNO2
CAS No.
220991-20-8
Storage
-20℃ for 3 years in powder form
-80℃ for 2 years in solvent
Solubility (In vitro)
DMSO: 59 mg/mL (200.9 mM)
Water: <1 mg/mL
Ethanol: <1 mg/mL
Solubility (In vivo)
Synonyms
COX-189
other peoduct :References PubMed ID：:http://www.ncbi.nlm.nih.gov/pubmed/19408653
| In Vitro |
In vitro activity: Lumiracoxib has an IC50 of 0.14 μm in COX-2-expressing dermal fibroblasts, but caused no inhibition of COX-1 at concentrations up to 30 μm (HEK 293 cells transfected with human COX-1). In a human whole blood assay, IC50 values for Lumiracoxib are 0.13 μM for COX-2 and 67 μM for COX-1 (COX-1/COX-2 selectivity ratio 515). Kinase Assay: Cell Assay: |
|---|---|
| In Vivo | Lumiracoxib is a highly selective COX-2 inhibitor with anti-inflammatory, analgesic and antipyretic activities comparable with diclofenac, the reference NSAID, but with much improved gastrointestinal safety. Lumiracoxib is rapidly absorbed following oral administration in rats with peak plasma levels being reached between 0.5 and 1 h. Efficacy of Lumiracoxib in rat models of hyperalgesia, oedema, pyresis and arthritis is dose-dependent and similar to diclofenac. However, consistent with its low COX-1 inhibitory activity, Lumiracoxib at a dose of 100 mg/kg orally causes no ulcers and is significantly less ulcerogenic than diclofenac. |
| Animal model | Female Lewis rats |
| Formulation & Dosage | Dissolved in phosphate-buffered saline; 0.2–2 mg/kg; Oral gavage |
| References | Br J Pharmacol. 2005 Feb;144(4):538-50. |
