AceclofenacAceclofenac
MedChemExpress (MCE)
HY-B0634
89796-99-6
99.91%
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Room temperature in continental US
may vary elsewhere.
Aceclofenac is an orally active nonsteroidal anti-inflammatory agent (NSAID), with analgesic and anti-inflammatory properties. Aceclofenac is used for the research of osteoarthritis, ankylosing spondylitis, rheumatoid arthritis.
Aceclofenac (1-30 μM
72 hours) significantly decreases interleukin-6 production and fully blocks prostaglandin E2 synthesis by IL-1β- or LPS-stimulated human chondrocytes[1]. Aceclofenac inhibits COX-1 with IC50 values superior to 100 μM, but decreases by 50% COX-2 activity at the concentration of 0.77 μM in the whole blood test[1]. Aceclofenac increases the synthesis of interleukin 1 receptor antagonist and decreases the production of nitric oxide in human articular chondrocytes[2].
Aceclofenac exhibits Cmax (4.59 μg/mL) following oral administration (rat 20 mg/kg)[3]. Aceclofenac exhibits terminal elimination half-life (rat 3.24 h) due to high plasma clearance (rat 1.10 L/h/kg) following intravenous injection (rat 10 mg/kg)[3].
COX-2 3 μM (IC50) COX-1 7.3 μM (IC50)
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[1]. Y Henrotin, et al. In vitro effects of aceclofenac and its metabolites on the production by chondrocytes of inflammatory mediators. Inflamm Res. 2001 Aug
50(8):391-9. [Content Brief]
[2]. E Maneiro, et al. Aceclofenac increases the synthesis of interleukin 1 receptor antagonist and decreases the production of nitric oxide in human articular chondrocytes. J Rheumatol. 2001 Dec
28(12):2692-9. [Content Brief]
[3]. E Maneiro, et al. Keumhan Noh, et al. Absolute bioavailability and metabolism of aceclofenac in rats. Arch Pharm Res. 2015 Jan
38(1):68-72. [Content Brief]