It exerts antiplatelet and vasodilator effects by inhibiting the activity of phosphodiesterase in platelets and vascular smooth muscle, increasing the cAMP concentration in platelets and smooth muscle; inhibiting the initial and secondary platelet aggregation and release reactions induced by ADP, adrenaline, collagen and arachidonic acid; not interfering with the synthesis of vascular protective prostacyclin by vascular endothelial cells; and increasing tissue blood flow in the foot and gastrocnemius muscles in patients with chronic arterial occlusion, thereby increasing the lower limb blood pressure index, skin blood flow and skin temperature of the limbs, and improving intermittent claudication.

Ca2 antagonists are highly selective for cerebral blood vessels. They inhibit the contraction of vascular smooth muscles and increase cerebral blood flow by blocking the influx of Ca2 in brain cells. They also have a neuroprotective effect, protecting the brain from damage caused by ischemia, reperfusion and hypoxia. They non-competitively inhibit the contraction of cerebral and peripheral arterial vessels induced by K, PGF2alpha and 5-hydroxytryptamine, and inhibit neuroinflammation such as plasma protein exudation caused by trigeminal nerve stimulation, thereby preventing the occurrence of migraines and having a preventive and therapeutic effect on migraines.

This product has a broad-spectrum antibacterial effect and strong antibacterial effect. It has strong antibacterial activity against most Enterobacteriaceae, such as Escherichia coli, Klebsiella, Proteus, Salmonella, Shigella, and Gram-negative bacteria such as Haemophilus influenzae, Legionella pneumophila, and Neisseria gonorrhoeae. It also has antibacterial effects on Gram-positive bacteria such as Staphylococcus aureus, Streptococcus pneumoniae, Streptococcus pyogenes, and Mycoplasma pneumoniae and Chlamydia pneumoniae, but has poor effects on anaerobic bacteria and enterococci. Its mechanism of action is to inhibit the activity of bacterial DNA gyrase, prevent the synthesis and replication of bacterial DNA, and cause bacterial death.

Calcium blockers (also known as slow channel blockers or calcium antagonists) block the entry of calcium ions across the membrane into myocardial and vascular smooth muscle cells.

Dihydropyridine calcium antagonists can selectively inhibit the transmembrane transport of calcium ions into myocardial cells and smooth muscle cells, and inhibit the release of calcium ions from intracellular pools without changing the plasma calcium ion concentration. It can simultaneously relax the coronary arteries in the normal blood supply area and the ischemic area, antagonize spontaneous or ergonovine-induced coronary artery spasm, increase the delivery of myocardial oxygen to patients with coronary artery spasm, and relieve and prevent coronary artery spasm. It can also inhibit myocardial contraction, reduce myocardial metabolism, and reduce myocardial oxygen consumption. On the other hand, it can relax peripheral resistance vessels, reduce peripheral resistance, reduce systolic and diastolic blood pressure, and reduce cardiac afterload. It can delay the sinoatrial node function and atrioventricular conduction of isolated hearts; electrophysiological studies on whole animals and humans have not found that this product has the effect of delaying atrioventricular conduction, prolonging the recovery time of the sinoatrial node, and slowing down the sinoatrial node rate.