This product is a gastric mucosal protective agent. It can prevent the occurrence of ulcers and promote ulcer healing. It can increase gastric mucosal blood flow, the synthesis of prostaglandin E2 and gastric mucus secretion. It can remove oxygen free radicals, promote the healing of peptic ulcers and improve inflammation.

Beta 2-receptor agonists have a high selectivity for beta 2-adrenergic receptors of bronchial smooth muscle, thereby relaxing bronchial smooth muscle. They also have a certain anti-allergic effect and promote the movement of respiratory cilia.

This product is an antiplatelet drug. It inhibits the activity of phosphodiesterase in platelets and vascular smooth muscle, thereby increasing the cAMP concentration in platelets and smooth muscle, exerting antiplatelet and vasodilatory effects. This product inhibits the initial and secondary aggregation and release reactions of platelets induced by ADP, adrenaline, collagen and arachidonic acid, and is dose-dependent. Oral administration of 100 mg of cilostazol is 7 to 78 times more effective than the corresponding amount of aspirin in inhibiting platelet aggregation in vitro (aspirin is ineffective against initial platelet aggregation). This product does not interfere with the synthesis of vascular protective prostacyclin by vascular endothelial cells. For patients with chronic arterial occlusion, the use of volume plethysmography shows that this product can increase tissue blood flow in the foot and gastrocnemius muscles, increase the blood pressure index of the lower limbs, increase skin blood flow and increase skin temperature of the limbs, and improve intermittent claudication.

It has high affinity for D2, D3, 5-HT1A, and 5-HT2A receptors, and moderate affinity for D4, 5-HT2c, 5-HT7, alpha 1, H1 receptors and 5-HT reabsorption sites; it is a partial agonist of D2 and 5-HT1A receptors, and an antagonist of 5-HT2A receptors; its mechanism of action may be mediated by partial agonism of D2 and 5-HT1A receptors and antagonism of 5-HT2A receptors, and its effects on other receptors may produce certain other clinical effects, such as the antagonism of alpha 1 receptors, which can explain the phenomenon of orthostatic hypotension.

It has high affinity for D2, D3, 5-HT1A, and 5-HT2A receptors, and moderate affinity for D4, 5-HT2C, 5-HT7, alpha;1, H1 receptors, and 5-HT reabsorption sites. It is a partial agonist of D2 and 5-HT1A receptors, and an antagonist of 5-HT2A receptors. Its mechanism of action may be mediated by partial agonism of D2 and 5-HT1A receptors and antagonism of 5-HT2A receptors. The action with other receptors may produce some other clinical effects, such as the antagonism of alpha;1 receptors, which can explain the phenomenon of postural hypotension.