Indobufen is a drug that hinders the aggregation of platelets by reversibly repressing the cyclo-oxygenase enzyme, further bringing about diminished thromboxane production. It may also be effective in many prothrombotic conditions, in restenosis thromboembolism with heart disease and in intermittent claudication. This drug suppresses thromboxane synthesis, but its effect is due to the impairment of neutrophil access through Cox inhibition. It has the same efficacy as warfarin in the prevention of thromboembolic events in patients with non-rheumatic atrial fibrillation who are at high risk. Additionally, the ability of indobufen is recently highlighted, as it suppresses enhanced TxA2 synthesis in platelet activation during the acute phase of unstable angina. The effect is not shared with aspirin and is been attributed to the inhibition of Cox-2, which is given by the monocytes to a local inflammatory milieu as a response. It also contributes to certain changes in the tissues.
In recent studies, the drug said drug was proven to prevent the occurrence of thrombotic activity in both isolated and whole blood monocytes. This also leads to a reduction of TxA2 synthesis, with a less effect on PGE2 levels and the prevention of ERK1/2 phosphorylation. These are the mechanisms by which indobufen negatively affects thrombosis.
Some data also show the down-regulation of thrombosis in monocytes due to the antiplatelet effects of the drug, thus preventing atherothrombosis.
