Heparin calcium (MW 15000-19000)

Heparin calcium (MW 15000-19000), an anticoagulant, forms a reversible complex with antithrombin III (ATIII), known as the heparin-antithrombin III complex. This complex binds to thrombin and the activated clotting factors IX, X, XI, and XII, leading to their irreversible inactivation and inhibiting the conversion of fibrinogen into fibrin [1] [2].

Heparin is a potent anticoagulant as it accelerates the inhibition of serine proteases in the coagulation cascade by antithrombin. Heparin and structurally related Heparan Sulfate are intricate linear polymers, consisting of a mixture of chains with variable lengths and sequences. These molecules interact most strongly with peptides containing complementarily high positive charge density binding sites. Both Heparin and Heparan Sulfate mainly exhibit a linear helical secondary structure, with sulfate and carboxyl groups displayed along the polysaccharide backbone at specific intervals and orientations. Similar to DNA, Heparin is a highly charged linear polymer and acts as a polyelectrolyte. Heparin's anticoagulant effect is primarily achieved by enhancing the AT-III mediated inhibition of coagulation factors, including thrombin and factor Xa, through its interaction with AT III. It forms a ternary complex with AT III and thrombin, increasing the bimolecular rate constant for thrombin inhibition by 2000-fold. Heparin is predominantly located in mast cell granules of tissues closely associated with immune responses. Additionally, it interacts extensively with FGF-2 and FGFR-1, stabilizing the FGF-FGFR binding and contacting FGFR-1 of adjacent FGF-FGFR complexes, which appears to promote FGFR dimerization [1].

Low-molecular-weight heparin calcium administered subcutaneously at a dosage of 4 mg/kg twice daily for two days (s.c. twice a day for 2 days) has been shown to mitigate skeletal muscle damage and systemic inflammatory response in ischemia-reperfusion injury (IRI) in adult male Sprague-Dawley rats weighing 200-300 g, demonstrating efficacy in an animal model with ischemic insult (IR) [2]. The regimen effectively alleviated the IRI caused by tourniquet application.