322761-84-2

Upstream product

• 18162-48-6 tert-butyldimethylsilyl chloride 
• 322761-81-9 ethyl 3-O-[(1S)-1-(cyclohexylmethyl)-2-oxo-2-(phenylmethoxy)ethyl]-1-thio-β-D-galactopyranoside 2,4,6-tribenzoate 
• 322761-80-8 ethyl 3-O-[(1S)-1-(cyclohexylmethyl)-2-oxo-2-(phenylmethoxy)ethyl]-1-thio-β-D-galactopyranoside 
• 56245-60-4 ethyl 1-thio-β-D-galactopyranoside 
• 187404-16-6 benzyl (R)-3-cyclohexyl-2-trifluoromethanesulfonyloxy-propionate 
• 98-88-4 benzoyl chloride 
• 135214-83-4 1,5-Anhydro-2-deoxy-4,6-O-(phenylmethylene)-D-arabino-hexopyranoside 
• 322761-82-0 1,5-anhydro-2-deoxy-3-O-{2,4,6-tri-O-benzoyl-3-O-[(1S)-1-(cyclohexylmethyl)-2-oxo-2-(phenylmethoxy)ethyl]-β-D-galactopyranosyl}-D-arabino-hexitol 

Downstream Products

• 322761-78-4 O-3-O-[(1S)-1-cyclohexylmethyl)-2-oxo-2-(phenylmethoxy)ethyl]-2,4,6-tris-O-(phenylmethyl)-β-D-galactopyranosyl-(1->3)-O-[6-deoxy-2,3,4-tris-O-(phenylmethyl)-α-L-galactopyranosyl-(1->4)]-1,5-anhydro-2-deoxy-D-arabino-hexitol 

Relevant academic research and scientific papers

GLYCOMIMETIC ANTAGONISTS FOR BOTH E- AND P-SELECTINGS

Compounds and methods are provided for modulating in vivo and in vivo processes mediated by selectin biniding. More specifically, selectin modulators and their use are described, wherein the selectin modulators that modulate (e.g. inhibit or enhance) a selectin-mediated function comprise particular glycomimetics linked to a member of a class of compounds termed BASAs (Benzyl Amino Sulfonic Acids).

Potent E-selectin antagonists

In the search for drugs that could control excessive leukocyte extravasation, we now report on modifications of the already known potent E-selectin antagonist 3 containing a cyclohexyllactic acid residue and a glucal-derived building block. Thus, we describe the synthesis and biological evaluation of a series of derivatives 6 with modified glucal-derived moieties (CH2NR1R2 instead of CH2OH in 3) to explore a hypothetical potential complementary interaction with E-selectin. However, similar activity profiles of most derivatives 6 and compound 3 do not support such an interaction, but rather indicate topological-structure changes of 6 (and 3) in the orientation of the neighboring fucose and galactose due to intramolecular steric interactions. The most potent E-selectin antagonist 6v showed >50-fold improved E-selectin inhibition compared to the weak selectin ligand sialyl Lewis' (sLex, 1: IC50 = 1000-1500μM), but only a 2-fold improvement compared to 3. Compound 6x was tested in vivo in a murine model of acute inflammation and found to be as potent as 3 (ED50 = 15 mg/kg).