Chondroitin sulfate A disodium 

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^[1][2][3].

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.

39455-18-0

Solid

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]

Room temperature in continental US; may vary elsewhere.

• [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]