In vitro tests have destructive or inhibitory effects on the morphology or proliferation of cell lines such as liver cancer, esophageal cancer, laryngeal cancer, lung cancer, and cervical cancer; in vivo tests have a certain inhibitory effect on Ehrlich ascites carcinoma, sarcoma-180 and solid liver cancer in mice, and can increase the respiratory control rate and lysosomal enzyme activity of mitochondria in ascites liver cancer H22 mice, interfere with cancer cell division, block it in the M phase, and affect its cycle speed; it can destroy the skeleton of cancer cells (microfilaments, microtubules), affect the ultrastructure of cancer cells, and cause damage to mitochondria, microvilli and plasma membranes; it can inhibit the DNA synthesis of cancer cells, but has no inhibitory effect on normal bone marrow cells, and can increase white blood cells.

By inhibiting bacterial DNA gyrase and topoisomerase IV, it inhibits bacterial DNA replication, transcription and repair processes. It has antibacterial activity against the following microorganisms: 1. Gram-positive bacteria: Staphylococcus aureus (limited to strains sensitive to methicillin), Streptococcus pneumoniae (strains sensitive to penicillin). 2. Gram-negative bacteria: Escherichia coli, Haemophilus influenzae and parainfluenzae, Klebsiella pneumoniae, Moraxella catarrhalis, Neisseria gonorrhoeae, Proteus mirabilis. 3. Other microorganisms: Chlamydia pneumoniae, Legionella pneumophila, Mycoplasma pneumoniae.

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It inhibits the action of plasmin, blocks the decomposition of fibrin, and plays a hemostatic role; at the same time, it can inhibit the production of active substances that cause enhanced vascular permeability, allergic reactions and inflammatory lesions, and has anti-allergic and anti-inflammatory effects.

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).