Sialyl-Lewis X  (Synonyms: sLeX)

Sialyl-Lewis X (sLeX) is a sialylated fucosylated tetrasaccharide, an endogenous antigen. Sialyl-Lewis X is a high-affinity ligand for selectins (E-, P-, and L-selectin)^[1]. Sialyl-Lewis X binds to ELAM-1 and CD62 and has the ability to inhibits CD62-mediated neutrophil recruitment to sites of inflammation^[2].

Sialyl-Lewis X is a high-affinity ligand of CD62, Antibodies [mAb CSLEX (IgM; anti-sLeX)] to sLeX inhibit CD62-mediated binding of HL-60 cells to activated platelets^[1].
Liposomes containing glycolipids with the sLeX structure prevents adhesion of HL-60 cells and human neutrophils. HL-60 cell adhesion is partially inhibited (50%) by liposomes containing Lex at 5 μg/ml. However, sLeX liposomes give maximal inhibition at only 1 ug/ml. sLeX liposomes inhibits adhesion with a 10-fold higher affinity than Lex liposomes^[1].
CD62 binding of neutrophils to activated platelets is inhibited a soluble human milk oligosaccharide that contains the LeX structure. the sLeX sugar is a 30-fold more potent inhibitor than the nonsialylated Lex sugar, which requires 2 μg/ml and 54 μg/ml to achieve 50% inhibition of neutrophil adhesion, respectively^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

820.74

C₃₁H₅₂N₂O₂₃

98603-84-0

Solid

White to off-white

OC([C@](O[C@@]([C@@H]1NC(C)=O)([H])[C@H](O)[C@H](O)CO)(C[C@@H]1O)O[C@@H]([C@H]([C@H]2CO)O)[C@H]([C@@H](O2)O[C@@]([C@H](O)CO)([H])[C@]([C@H](C=O)NC(C)=O)([H])O[C@H](O[C@H]3C)[C@H]([C@@H]([C@@H]3O)O)O)O)=O

Room temperature in continental US; may vary elsewhere.

-20°C, stored under nitrogen

*In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

• [1]. M J Polley, et al. CD62 and Endothelial Cell-Leukocyte Adhesion Molecule 1 (ELAM-1) Recognize the Same Carbohydrate Ligand, sialyl-Lewis X. Proc Natl Acad Sci U S A. 1991 Jul 15;88(14):6224-8.  [Content Brief]

  [2]. L A Lasky, et al. Selectins: Interpreters of Cell-Specific Carbohydrate Information During Inflammation. Science  [Content Brief]