Chondroitin sulfate A disodium
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Chondroitin sulfate A disodium is a mucopolysaccharide extracted from animal cartilages such as porcine nasal cartilage, and serves as a major structural component of cartilage. Chondroitin sulfate A disodium is one of the specific receptors for the adhesion of Plasmodium falciparum-infected red blood cells in the microcirculation. Chondroitin sulfate A disodium can be used together with selenium to prepare nanoparticles for protecting cartilage against T‑2 toxin-induced damage. Chondroitin sulfate A disodium is abnormally highly expressed in ameloblastoma, and is particularly enriched in stellate reticulum-like tumor cells. Chondroitin sulfate A disodium can be applied to studies on Plasmodium infection mechanisms, cartilage protection and oral tumors.
For research use only. We do not sell to patients.
- Purity : 99.95%
- CAS No.: 39455-18-0
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Storage:
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Biological Activity
Description
In Vitro
Chondroitin sulfate A disodium serves as a stable/targeting ligand. Na₂SeO₃ is used to reduce and prepare nano-selenium particles (CSA-SeNP). These nanoparticles activate autophagy through the SIRT1-AMPK-FOXO3 pathway, thereby protecting chondrocytes from the oxidative stress and mitochondrial dysfunction caused by T-2 toxin[1].
Chondroitin sulfate A disodium shows significantly higher expression in the epithelial component and stroma of solid/multicystic ameloblastoma than in odontogenic keratocyst or dentigerous cyst, with significantly stronger expression in stellate reticulum-like cells than in ameloblast-like cells within ameloblastoma[2].
Chondroitin sulfate A (1-10 μg/mL; 1 h) disodium potently inhibits and reverses cytoadherence of Plasmodium falciparum FAF-EA8CHO5-infected erythrocytes to wild-type (K1) CHO cells, with 99.2% inhibition at 10 μg/mL and 72.5% inhibition at 1 μg/mL[3].
Chondroitin sulfate A (1 h) disodium inhibits cytoadherence of Plasmodium falciparum FAF-EA8CHO5-, E10CHO6-, and D7CHO6-infected erythrocytes to C32 amelanotic melanoma cells, with 96.3% inhibition observed for FAF-EA8CHO5[3].
Chondroitin sulfate A (1-10 μg/mL; 1 h) disodium almost completely inhibits cytoadherence of Plasmodium falciparum laboratory strains, selected high-binding strains, and primary patient isolates to immobilized chondroitin sulfate A-phosphatidylethanolamine[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 39455-18-0
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Appearance Solid
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Color White to light yellow
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SMILES
O=C([C@@H]1C(O)[C@H](O)[C@@H](O)[C@H](O[C@@H]2[C@@H](NC(C)=O)[C@H](O[H])O[C@H](CO)[C@@H]2OS(=O)(O[Na])=O)O1)O[Na].[n]
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
4°C, sealed storage, away from moisture
* In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
Solvent & Solubility
In Vitro:
H2O : 8.33 mg/mL (ultrasonic and warming and heat to 60°C)
Protocols
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Research Protocol for Infectious Diseases
Infectious-disease experiments test how pathogens interact with host barriers, innate immune receptors, inflammatory signaling, pathogen replication, and tissue injury; pattern-recognition receptors such as TLRs, RIG-I-like receptors, NOD-like receptors, and inflammasomes detect microbial molecules and activate NF-κB, interferon, and cytokine responses. The central hypothesis is that infection severity reflects the balance between pathogen burden and host response: protective inflammation restricts pathogen growth, whereas excessive or mislocalized inflammation contributes to tissue damage and disease phenotype. Unresolved questions include which host pathways are protective versus pathogenic, why some infection models fail to translate to human disease, and which combined readouts best predict clinically relevant infection outcomes.
Purity & Documentation
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Data Sheet (278 KB)
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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)
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Handling Instructions (2659 KB)
References
[1]. Deng H, et al. Chondroitin sulfate A-selenium nanoparticles protect chondrocytes from T-2 toxin-induced oxidative stress and mitochondrial dysfunction through activating autophagy by the SIRT1-AMPK-FOXO3 pathway. Ecotoxicol Environ Saf. 2025;303:118797. [Content Brief]
[2]. Li X, et al. Potential involvement of chondroitin sulfate A in the pathogenesis of ameloblastoma. Acta Histochem. 2017;119(5):439-445. [Content Brief]
[3]. Rogerson SJ, et al. Chondroitin sulfate A is a cell surface receptor for Plasmodium falciparum-infected erythrocytes. J Exp Med. 1995;182(1):15-20. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- Chondroitin sulfate A disodium
- 39455-18-0
- Endogenous Metabolite
- Parasite
- ameloblastoma tumor cells
- infected erythrocyte surface proteins
- chondrocytes
- odontogenic keratocyst
- malaria pathogenesis
- SIRT1-AMPK-FOXO3 pathway
- odontogenic cysts
- dentigerous cyst
- infected erythrocyte cytoadherence
- Plasmodium falciparum
- Inhibitor
- inhibitor
- inhibit