This product is a fourth-generation quinolone antibacterial drug. Its mechanism of action is a DNA topoisomerase inhibitor, which prevents bacterial DNA from forming a supercoiled structure, causing bacterial cells to be unable to divide and proliferate and die.

It inhibits the action of plasmin, blocks the decomposition of fibrin, and has hemostatic, anti-allergic and anti-inflammatory effects; it can inhibit the production of agglutinins and other active substances that cause increased vascular permeability, allergic reactions and inflammatory lesions.

Fibrinolysis is related to the decomposition of fibrin in the physiological or pathological state, increased vascular permeability, etc., and is also related to the body's reaction caused by fibrinolysis, the occurrence, development and cure of various hemorrhagic symptoms and allergic reactions. This product can inhibit the action of this plasmin, and show hemostatic, anti-allergic and anti-inflammatory effects. The action of anti-plasmin Tranexamic acid can strongly adsorb to the lysine binding site (LBS) of the fibrin affinity site on plasminogen, inhibiting fibrinolytic acid, and the binding of fibrinolytic acidogen to fibrin, thereby strongly inhibiting the fibrinolysis caused by plasmin; in addition, in the presence of anti-plasmins such as macroglobulins in serum, the anti-fibrinolytic effect of tranexamic acid is more obvious, and the hemostatic effect is more significant. Abnormally hyperactive plasmin will cause platelet aggregation inhibition and decomposition of coagulation factors. Mild hyperactivity first leads to fibrin decomposition. Therefore, it is considered that in general bleeding, tranexamic acid can inhibit fibrin decomposition and play a hemostatic role. Anti-allergic and anti-inflammatory effects: Tranexamic acid can inhibit the production of agglutinins and other active substances that cause increased vascular permeability, allergic reactions and inflammatory lesions (pigs and rats).

Papaverine has a direct nonspecific relaxant effect on blood vessels, heart or other smooth muscles, which may be caused by the inhibition of cyclic nucleotide phosphodiesterase.

The drug can cause necrosis of the intrauterine decidual tissue and produce endogenous prostaglandins, which cause uterine contractions. Ethacridine (Rivanol) also has a direct excitatory effect on the uterine muscles.