Oxaprozin potassium is an orally active and potent inhibitor of COX, with IC50 values of 2.2 μM for human platelet COX-1 and 36 μM for IL-1-stimulated human synovial cell COX-2. It induces cell apoptosis and inhibits NF-κB activation. The inhibition of the Akt/IKK/NF-κB pathway by oxaprozin potassium contributes to its anti-inflammatory properties [1] [2].

Oxaprozin, across a concentration range of 0-100 μM, triggers apoptosis in a dose-dependent manner, with its most potent proapoptotic effect observed at 100 μM. This compound specifically elevates caspase-3 activity under activated conditions, while not affecting it in resting states. At a concentration of 50 μM, Oxaprozin effectively suppresses NF-κB activation and blocks the induction of the IKK system by IκBα. Furthermore, Oxaprozin significantly enhances apoptosis in CD40L-treated monocytes and abrogates CD40L-induced Akt and NF-κB (p65) phosphorylation, underscoring its potential in modulating inflammatory and apoptotic pathways.