1623784-80-4

Upstream product

• 1623784-81-5 p-methoxyphenyl 2,4-di-O-benzyl-α-L-rhamnopyranosyl-(1→3)-4-O-benzyl-2-O-benzoyl-α-L-rhamnopyranoside 
• 1352643-96-9 p-methoxyphenyl 2,3,4-tri-O-methyl-α-L-fucopyranosyl-(1→3)-2,4-di-O-benzyl-α-L-rhamnopyranosyl-(1→3)-4-O-benzyl-α-L-rhamnopyranoside 
• 943032-57-3 4-methoxyphenyl 2-O-benzoyl-4-O-benzyl-α-L-rhamnopyranoside 

Relevant academic research and scientific papers

Inhibition of cytokine release by mycobacterium tuberculosis phenolic glycolipid analogues

Infection by Mycobacterium tuberculosis causes tuberculosis, a disease characterized by alteration of host innate and adaptive immunity. These processes are mediated by a series of bacterial biomolecules, among which phenolic glycolipids (PGLs) and the related p-hydroxybenzoic acid derivatives have been suggested to play important roles. To probe the importance of structural features of these glycans on cytokine modulation, we synthesized three M. tuberculosis PGL analogues (1-3), which differ from the native glycoconjugates by possessing a simplified lipid algycone. The ability of 1-3 to modulate the release of proinflammatory cytokines (TNF-α, IL-1β, IL-6, MCP-1) and nitric oxide (NO) was evaluated. None of the compounds stimulated the secretion of these signalling molecules. However, all showed a Toll-like Receptor 2-mediated, concentration-dependent inhibition profile that was related to the methylation pattern on the glycan. Inflammatory contribution: Three simplified analogues of phenolic glycolipids from Mycobacterium tuberculosis were synthesized, and their ability to modulate the release of proinflammatory cytokines (TNF-α, IL-1β, IL-6, and MCP-1) and nitric oxide was evaluated. All demonstrated a Toll-like Receptor 2-mediated, concentration-dependent inhibition profile related to the methylation pattern on the glycan.