Element of liver, can also promote with endothelial tissue factor through bay (TFPI) release, TFPI and factor X a combination and inactivated Xa, constitute the TFPI/factor Xa compounds, the compounds of TFPI and then inactivated and tissue factor Ⅶ a combination of factors.

　　It may be the main mechanism of preventing thrombus formation caused by endothelial injury and rupture of atheromatous plaque.

　　The anticoagulant activity and eradication rate of daheparin are affected by the chain length. High molecular weight fragments were removed from the cycle faster than low molecular weight fragments, resulting in increased accumulation of low molecular weight fragments and decreased resistance to IIa/Xa ratios.

　　In vitro, the combination of heparin and platelets can induce or suppress platelet aggregation according to different test conditions.

　　Daheparin activates daheparin cofactor II and directly inactivates coagulation factor IIa. This action is charge dependent and does not depend on pentose structure and requires a higher concentration of darheparin. The inactivation of IIa factor mediated by heparin cofactor II is also dependent on relative molecular weight, requiring at least 24 sugar units (relative molecular weight over 7200). In severe AT deficiency, this mechanism of darheparin can come into play.