Because this product has the physical and chemical characteristics of strong negative charge, it can interfere with many links of the blood coagulation process and has anticoagulant effect in vivo and in vitro. Its mechanism of action is relatively complex, mainly through binding with antithrombin III (AT-III), thereby enhancing the latter's inhibitory effect on activated coagulation factors II, IX, X, XI and XII. Its consequences involve preventing platelet aggregation and destruction, hindering the formation of coagulation activating enzymes; preventing prothrombin from turning into thrombin; inhibiting thrombin, thereby preventing fibrinogen from turning into fibrin.

After passing through the blood-cerebrospinal fluid barrier, it is decomposed into glutamate and gamma-aminobutyric acid (GABA). Glutamate is involved in the information transmission of the central nervous system. Gamma-aminobutyric acid can antagonize the excitotoxic effects of glutamate, improve nerve cell metabolism, maintain nerve stress resistance, reduce the effect of blood ammonia, and improve brain function.

This product is an anti-anemia drug. Vitamin B12 participates in methyl conversion and folic acid metabolism in the body, and promotes the conversion of 5-methyltetrahydrofolate into tetrahydrofolate. When it is deficient, it leads to DNA synthesis disorders and affects the maturation of red blood cells. This product also promotes the conversion of methylmalonic acid into succinic acid and participates in the tricarboxylic acid cycle. This effect is related to the synthesis of nerve myelin lipids and the maintenance of the integrity of myelinated nerve fiber function. The nerve damage caused by vitamin B12 deficiency may be related to this.

This product is an anti-anemia drug. Vitamin B12 participates in methyl conversion and folic acid metabolism in the body, and promotes the conversion of 5-methyltetrahydrofolate into tetrahydrofolate. When it is deficient, it leads to DNA synthesis disorders and affects the maturation of red blood cells. This product also promotes the conversion of methylmalonic acid into succinic acid and participates in the tricarboxylic acid cycle. This effect is related to the synthesis of nerve myelin lipids and the maintenance of the integrity of myelinated nerve fiber function. The nerve damage caused by vitamin B12 deficiency may be related to this.

It can inhibit the pathological excessive secretion of growth hormone, thyroid-stimulating hormone, gastrointestinal and pancreatic endocrine hormones; it can selectively reduce the blood flow and pressure of the portal vein and its collateral circulation, and reduce the pressure of varicose veins in the esophagus and gastric fundus; it can inhibit gallbladder emptying and have a therapeutic effect on pancreatic lesions; it can inhibit the secretion of gastric acid and gastrin, and improve the blood supply to the gastric mucosa; it can inhibit gastrointestinal motility.