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SULODEXIDE

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SULODEXIDE Basic information

Product Name:
SULODEXIDE
Synonyms:
  • SULODEXIDE
  • heparin-like substance: sulodexide*sodium from bo
  • HEPARIN-LIKE SUBSTANCE: SULODEXIDE*SODIU M FROM BOVI
  • heparin-like substance: sulodexide, sodium salt
  • Glucuronylglucosamineglicane sulfate
  • Vessel
  • 3Gs
  • Gluparin
CAS:
57821-29-1
MW:
0
EINECS:
615-070-3
Mol File:
Mol File
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SULODEXIDE Chemical Properties

form 
Solid-Liquid Mixture
color 
Colorless to light yellow
CAS DataBase Reference
57821-29-1
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SULODEXIDE Usage And Synthesis

Uses

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].

Pharmacology

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.

in vivo

Sulodexide (1 mg/kg, p.o., once daily for 12 weeks) significantly improves proteinuria and renal function in Streptozotocin (HY-13753)-induced type I diabetic nephropathy in mice[2]. Sulodexide (5 mg/kg and 15 mg/kg, i.p., once daily for 5 days) significantly inhibits retinal neovascularization and suppressed pro-angiogenic protein expression in the oxygen-induced retinopathy model in ICR mice[3]. Sulodexide (20 mg/kg, i.g., once daily for 4 weeks) significantly attenuats fibrosis in the Thioacetamide (HY-Y0698)-induced liver fibrosis model in mice[4]. Sulodexide (40 mg/kg, i.g., single dose) significantly improvs survival and reduced lung injury in the LPS (HY-D1056)-induced endotoxemia model in C57BL/6J mice[5].

Animal Model:Streptozotocin (HY-13753)-induced type I diabetic nephropathy in C57BL/6 mice model[2]
Dosage:1 mg/kg
Administration:Oral gavage (p.o.), once daily for 12 weeks
Result:Significantly reduced urinary albumin levels, improved renal function, increased GBM perlecan expression, reduced collagen I and IV deposition, and ERK activation.
Animal Model:Oxygen-induced retinopathy (OIR) model in ICR mice[3]
Dosage:5 mg/kg and 15 mg/kg
Administration:Intraperitoneal injection (i.p.), once daily for 5 days
Result:Significantly reduced avascular area, decreased neovascular tufts and lumens. Significantly inhibited expression of MMP-2, MMP-9, and VEGF
Animal Model:Thioacetamide (HY-Y0698)-induced liver fibrosis in C57BL/6 mice model[4]
Dosage:20 mg/kg
Administration:Intragastric administration (i.g.), once daily for 4 weeks
Result:Significantly reduced expression of fibrosis markers (Col1a1 and α-SMA), decreased hydroxyproline levels, and inhibited ECM deposition in liver tissue.
Animal Model:LPS (HY-D1056)-induced endotoxemia in C57BL/6J mice model[5]
Dosage:40 mg/kg
Administration:Intragastric administration (i.g.), single dose
Result:Significantly reduced plasma Syndecan-1 (SDC1) levels, increased survival rate, reduced lung injury, and restored endothelial glycocalyx damage.

References

[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

SULODEXIDESupplier

Beijing HuaMeiHuLiBiological Chemical
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010-56205725
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waley188@sohu.com
Hubei Jusheng Technology Co.,Ltd
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027-59599241 18871490274
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Dideu Industries Group Limited
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+86-29-89586680 +86-15129568250
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Amel Pharmatech Corporation
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027-888-4366503
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sales@amelpharmatech.com
Shaanxi Dideu Medichem Co. Ltd
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+86-29-81148696 +86-17392712697
Email
1022@dideu.com
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