155666-58-3

Upstream product

• 98510-20-4 myo-Inositol orthoformate 
• 824-94-2 p-methoxybenzyl chloride 

Downstream Products

• 796883-94-8 1-O-diphenylphosphate-2,4,6-O-tri-para-methoxybenzyl-D-myo-inositol 
• 900159-84-4 2,4,6-tri-O-p-methoxybenzyl-D-myo-inositol-3-diphenyl phosphate 
• 796883-97-1 1-O-dibenzylphosphate-2,4,6-O-tri-para-methoxybenzyl-D-myo-inositol 
• 796883-95-9 3,5-O-bis(tert-butyldimethylsilyl)-1-O-diphenylphosphate-2,4,6-O-tri-para-methoxybenzyl-D-myo-inositol 
• 796883-96-0 3,5-O-bis(tert-butyldimethylsilyl)-1-O-dibenzylphosphate-2,4,6-O-tri-para-methoxybenzyl-D-myo-inositol 
• 1428567-02-5 2,4,6-tri-O-(4-methoxybenzyl)-1,3,5-tri-O-(o-xylylenephospho)-myo-inositol 

Relevant academic research and scientific papers

Small-Molecule Allosteric Triggers of Clostridium difficile Toxin B Auto-proteolysis as a Therapeutic Strategy

Clostridium difficile causes increasing numbers of life-threatening intestinal infections. Symptoms associated with C. difficile infection (CDI) are mediated by secreted protein toxins, whose virulence is modulated by intracellular auto-proteolysis following allosteric activation of their protease domains by inositol hexakisphosphate (IP6). Here, we explore the possibility of inactivating the C. difficile toxin B (TcdB) by triggering its auto-proteolysis in the gut lumen prior to cell uptake using gain-of-function small molecules. We anticipated that high calcium concentrations typically found in the gut would strongly chelate IP6, precluding it from pre-emptively inducing toxin auto-proteolysis if administered exogenously. We therefore designed IP6 analogs with reduced susceptibility to complexation by calcium, which maintained allosteric activity at physiological calcium concentrations. We found that oral administration of IP6 analogs attenuated inflammation and promoted survival in mouse models of CDI. Our data provide impetus to further develop small-molecule allosteric triggers of toxin auto-proteolysis as a therapeutic strategy. Ivarsson et al. describe a therapeutic strategy that targets the C. difficile toxin B (TcdB). They designed analogs of the natural co-factor IP6 that can induce pre-emptive toxin auto-proteolysis at physiological calcium concentrations. Oral administration of analogs attenuated inflammation and promoted survival in mouse models of CDI.

CALCIUM OXALATE CRYSTALLIZATION INHIBITORS FOR RENAL DISORDERS

The present invention relates to inositol derivatives comprising two or more cyclohexanolpentakisester moieties linked by a common central linker and their use in therapy or prevention of a condition related to pathological crystallization. The invention

Unified total syntheses of the inositol polyphosphates: D-I-3,5,6P 3, D-I-3,4,5P3, D-I-3,4,6P3, and D-I-3,4,5,6P4 via catalytic enantioselective and site-selective phosphorylation

Synthetic routes to various inositol polyphosphates have been discovered utilizing catalytic enantioselective and site-selective phosphorylation reactions. The syntheses described herein exploit a common intermediate to gain efficient access to eight unique inositol polyphosphates.