Stereochemistry | ACHIRAL |
Molecular Formula | C16H13Cl2NO4 |
Molecular Weight | 354.185 |
Optical Activity | NONE |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
OC(=O)COC(=O)CC1=C(NC2=C(Cl)C=CC=C2Cl)C=CC=C1
InChI
InChIKey=MNIPYSSQXLZQLJ-UHFFFAOYSA-N
InChI=1S/C16H13Cl2NO4/c17-11-5-3-6-12(18)16(11)19-13-7-2-1-4-10(13)8-15(22)23-9-14(20)21/h1-7,19H,8-9H2,(H,20,21)
Molecular Formula | C16H13Cl2NO4 |
Molecular Weight | 354.185 |
Charge | 0 |
Count |
MOL RATIO
1 MOL RATIO (average) |
Stereochemistry | ACHIRAL |
Additional Stereochemistry | No |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Optical Activity | NONE |
Aceclofenac is a non-steroidal anti-inflammatory drug (NSAID) analog of Diclofenac. It is used for the relief of pain and inflammation in rheumatoid arthritis, osteoarthritis and ankylosing spondylitis. The dose is 100 mg twice daily, and should not be given to people with porphyria or breastfeeding mothers and is not recommended for children. Aceclofenac is a cytokine inhibitor. Aceclofenac works by blocking the action of a substance in the body called cyclo-oxygenase. Cyclo-oxygenase is involved in the production of prostaglandins (chemicals in the body which cause pain, swelling and inflammation). Aceclofenac is the glycolic acid ester of diclofenac. The incidence of gastric ulcerogenicity of aceclofenac has been reported to be significantly lower than that of other frequently prescribed NSAIDs: for instance, 2-fold less than naproxen, 4-fold less than diclofenac, and 7-fold less than indomethacin. Aceclofenac is metabolized in human hepatocytes and human microsomes to form [2-(2',6'-dichloro-4'-hydroxy- phenylamino)phenyl] acetoxyacetic acid as the major metabolite, which is then further conjugated.
Originator
Approval Year
PubMed
Patents
Sample Use Guides
In vitro adhesion assays were developed to examine the effects of aceclofenac on both neutrophil adhesion to tumor necrosis factor alpha stimulated human umbilical vein endothelial cells under nonstatic conditions, and homotypic neutrophil aggregation induced by anti-ICAM-3 and anti-CD18 monoclonal antibodies (Mab)