57821-29-1

Sulodexide is an orally active mixture of glycosaminoglycans composed of low molecular weight heparin (80%) and dermatan sulfate (20%). Sulodexide exhibits antithrombotic activity through interaction with antithrombin III (AT III) and heparin cofactor II (HC II), and inhibition of thrombin formation. Sulodexide exhibits profibrinolytic activity through release of tissue plasminogen activator (tPA). Sulodexide exhibits endothelial protective and anti-inflammatory effect, ameliorates chronic venous disease[1].

Sulodexide is a medium molecular weight glycosaminoglycan with effect on plasma viscosity by lowering plasma fibrinogen concentrations (Lunetta and Salanitri, 1992). Sulodexide disers from other glycosaminoglycans, like heparin, by having a longer half-life, reduced effect on systemic clotting and bleeding and increased lipolytic activity. Oral administration of sulodexide results in the release of tissue-type plasminogen activator (tPA) and an increase in fibrinolytic activities. Sulodexide has been used in chronic venous disease (Andreozzi, 2014), peripheral occlusive arterial disease with claudication (Shustov, 1997) and diabetic nephropathy (Vilayur and Harris, 2009). Parnetti et al. (1997) conducted a trial of sulodexide in patients fulfilling NINDSAIREN criteria for probable VaD; 46 patients were included in the active treatment group, compared with 40 in the pentoxifylline group. Larger reductions of plasma fibrinogen levels were seen with sulodexide, and both groups showed a slight reduction in activated factor VII levels. Dementia scores improved more in the sulodexide group.

[1] Andreozzi GM. Sulodexide in the treatment of chronic venous disease. Am J Cardiovasc Drugs. 2012 Apr 1;12(2):73-81. DOI:10.2165/11599360-000000000-00000
[2] Yung S, et al. Sulodexide decreases albuminuria and regulates matrix protein accumulation in C57BL/6 mice with streptozotocin-induced type I diabetic nephropathy[J]. PloS one, 2013, 8(1): e54501. DOI:10.1371/journal.pone.0054501
[3] Jo H, et al. Sulodexide inhibits retinal neovascularization in a mouse model of oxygen-induced retinopathy[J]. BMB reports, 2014, 47(11): 637. DOI:10.5483/bmbrep.2014.47.11.009
[4] Huang R, et al. Sulodexide attenuates liver fibrosis in mice by restoration of differentiated liver sinusoidal endothelial cell[J]. Biomedicine & Pharmacotherapy, 2023, 160: 114396. DOI:10.1016/j.biopha.2023.114396
[5] Ying J, et al. Sulodexide improves vascular permeability via glycocalyx remodelling in endothelial cells during sepsis[J]. Frontiers in immunology, 2023, 14: 1172892. DOI:10.3389/fimmu.2023.1172892