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It stimulates chondrocytes to produce proteoglycans with normal polymer structures, inhibits enzymes that damage cartilage such as collagenase and phospholipase A2, and prevents the production of superoxide free radicals that damage cells, thereby delaying the pathological process of bone and joint pain and the progression of the disease, improving joint movement and relieving pain.

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It has anti-thrombotic effect. Dipyridamole inhibits platelet aggregation, and high concentrations (50μg/ml) can inhibit platelet release. The mechanism of action may be: ⑴ Inhibit platelet uptake of adenosine, which is a platelet reaction inhibitor; ⑵ Inhibit phosphodiesterase, which increases cyclic adenosine monophosphate (cAMP) in platelets; ⑶ Inhibit the formation of thromboxane A2 (TXA2), which is a strong agonist of platelet activity; ⑷ Enhance endogenous PGI2. Dipyridamole has a vasodilatory effect. Dogs given 0.5-4.0 mg/kg of dipyridamole via the duodenum produce dose-related decreases in systemic and coronary vascular resistance, lower systemic blood pressure, and increased coronary blood flow. It takes effect 24 minutes after administration and lasts for about 3 hours. The same hemodynamic effects are observed in humans. However, acute intravenous administration can reduce local myocardial perfusion in the distal end of the stenotic coronary artery.