Synthetic Routes to ATA and Related Derivatives

The complement system is an essential component of innate immunity, but also causes self-damage when the system is aberrantly activated or self-protective capacity is exceeded. There are many conditions where failure to protect against self-damage from the complement system has been implicated in the pathology, including Alzheimer’s disease, Parkinson’s disease, Lou Gehrig’s disease, paroxysmal nocturnal hemoglobinemia, atypical hemolytic uremia syndrome and age-related macular degeneration. Aurin tricarboxylic acid (ATA) and analogues have been shown to selectively block the harmful effects of unwanted complement activation. This project aims to develop synthetic routes to ATA and related analogues that generate the desired product in high yield and purity.

Intern: 
Matthew Wathier
Faculty Supervisor: 
Jennifer Love
Province: 
British Columbia
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