SULODEXIDE manufacturers
- SULODEXIDE
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- $3880.00
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2026-09-10
- CAS:57821-29-1
- Min. Order: 500g
- Purity: 99%
- Supply Ability: 10 kg
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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;3Gs;Gluparin;Krx-101 | | CAS: | 57821-29-1 | | MF: | | | MW: | 0 | | EINECS: | 615-070-3 | | Product Categories: | | | Mol File: | Mol File | ![SULODEXIDE Structure]() |
| | SULODEXIDE Chemical Properties |
| form | Solid-Liquid Mixture | | color | Colorless to light yellow | | CAS DataBase Reference | 57821-29-1 |
| | 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. | | Synthesis | A method for the production of sulodexide, using heparin by-product as raw material, oxidizing to obtain intermediate crude heparin solution; adding acetate to intermediate crude heparin solution, ultrafiltration separation, obtaining fast-moving heparin crude and dermatoxylin sulfate crude; and then refining fast-moving heparin crude and dermatoxylin sulfate crude, respectively; and finally, mixing and dissolving precipitate obtained from the refining, filtration, collection of filtrate, and lyophilization treatment, obtaining raw material of sulodexide. lyophilization treatment to obtain the raw material of sulodexide, specifically including the following steps:
(1) oxidation: dissolve the heparin by-products, then adjust the pH and temperature of the solution, then add hydrogen peroxide to the solution to oxidize it, after oxidation is completed, adjust the pH of the solution to 6.0-8.0, centrifugation to remove the precipitate, filtration of the supernatant, collection of the filtrate, and obtain the crude heparin solution of the intermediate;
(2) ultrafiltration: add sodium acetate to the intermediate crude heparin solution, recycle ultrafiltration, collect the retention solution to get the crude dermatoxylin sulfate, collect the permeate to get the crude fast-moving heparin, and store the crude fast-moving heparin at 38;
3) Refining: the fast-moving heparin crude and the dermatoxylin sulfate crude were refined separately;
4Mixing: the precipitates obtained from refining are mixed and dissolved, filtered, and the filtrate is collected and lyophilized to obtain the raw material of sulodexide.
| | 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 |
| | SULODEXIDE Preparation Products And Raw materials |
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