Sulodexide solution
Based on 1 Customer Validation
Sulodexide solution is a mixture of glycosaminoglycans that can be administered by injection. It is 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.
For research use only. We do not sell to patients.
- CAS No.: 57821-29-1
-
Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
In Vitro
Sulodexide (0–200 μg/mL, 24 hours) promotes fibronectin and collagen type III synthesis in mouse mesangial cells[2]. Sulodexide (50 µg/mL, 48 hours) significantly inhibits capillarization marker expression in LSECs[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
Clinical Trial
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
-
CAS No. 57821-29-1
-
Appearance Liquid
-
Color Colorless to light yellow
-
SMILES
[Sulodexide solution]
-
Shipping
Room temperature in continental US; may vary elsewhere.
-
Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
-
How to Select the Route of Administration for Mammals
Route-of-administration selection in mammals is a pharmacokinetic, pharmacodynamic, formulation, animal-welfare, and translational decision, not a default technical choice. The selected route should match the study goal: intravenous dosing is most useful when complete systemic exposure and rapid onset are required, oral dosing is most translational for orally intended medicines but is affected by absorption and first-pass metabolism, subcutaneous or intramuscular dosing can provide slower systemic exposure, and intraperitoneal dosing can be useful in rodent proof-of-concept studies but may have limited clinical translation. Published route-comparison studies show that the same compound can produce different exposure, onset, bioavailability, tissue distribution, and tolerability depending on route; therefore, route choice should be supported by pilot pharmacokinetic or pharmacodynamic evidence when the literature is insufficient. Unresolved questions include how to standardize route sel
-
Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
Purity & Documentation
-
Data Sheet (273 KB)
-
SDS (252 KB)
- English - EN (252 KB)
- Français - FR (252 KB)
- Deutsch - DE (252 KB)
- Norwegian - NO (252 KB)
- Español - ES (252 KB)
- Swedish - SV (252 KB)
- Italian - IT (252 KB)
- Korean - KR (252 KB)
- Portuguese - PT (252 KB)
-
Handling Instructions (2659 KB)
References
[1]. Andreozzi GM. Sulodexide in the treatment of chronic venous disease. Am J Cardiovasc Drugs. 2012 Apr 1;12(2):73-81. [Content Brief]
[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. [Content Brief]
[3]. Jo H, et al. Sulodexide inhibits retinal neovascularization in a mouse model of oxygen-induced retinopathy[J]. BMB reports, 2014, 47(11): 637. [Content Brief]
[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. [Content Brief]
[5]. Ying J, et al. Sulodexide improves vascular permeability via glycocalyx remodelling in endothelial cells during sepsis[J]. Frontiers in immunology, 2023, 14: 1172892. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)