Etodolac (AY-24236) inhibits the activity of cyclooxygenase I and II, thereby preventing the formation of prostaglandin which is involved in the induction of pain, fever, and inflammation. Etodolac is a pyranocarboxylic acid and non-steroidal anti-inflammatory drug (NSAID) with antipyretic and analgesic activities. It also inhibits platelet aggregation by blocking platelet cyclooxygenase and the subsequent formation of thromboxane A2.

COX:53.5 nM

Etodolac markedly inhibits ICl, vol activation by TNFα as well as subsequent apoptotic events such as apoptotic cell volume decrease (AVD) and elevation of caspase-3/7 activity in isolated rabbit articular chondrocytes. [1]

Etodolac attenuates paclitaxel-induced peripheral neuropathy by a COX-independent pathway in a mouse model of mechanical allodynia. [2] Etodolac and other NSAIDs inhibits paw swelling and causes gastric mucosal lesions in adjuvant arthritic rats in a dose-dependent manner. Etodolac shows the highest UD(50) value and safety index among these NSAIDs in arthritic rats. Etodolac also shows the highest UD(50) value and safety index, except when its effects are assessed by acetic acid-induced writhing in normal rats. [3] Etodolac dose-dependently inhibits the development of gastric cancer, and no cancer is detected at a dose of 30 mg/kg/day. Etodolac does not affect the extent of inflammatory cell infiltration or oxidative DNA damage, but it significantly inhibits mucosal cell proliferation and dose-dependently represses the development of intestinal metaplasia in the stomachs of Helicobacter pylori (Hp)-infected Mongolian gerbils (MGs). [4] Etodolac alleviates heat-evoked hyperalgesia in the CCI rats and the increase in number of TRAP-positive multinucleated osteoclasts on the CCI-side is abrogated, however, it does not inhibit the decrease of bone mineral content (BMC) and bone mineral density (BMD) on the CCI-side. [5]