Repurposing Disease-Associated Inhibitors to Disrupt Thioredoxin Reductase in Cryptosporidium parvum

Session Number

CHEM 14

Advisor(s)

Dr. David Williams, Rush University Medical Center

Discipline

Chemistry

Start Date

17-4-2025 2:45 PM

End Date

17-4-2025 3:00 PM

Abstract

Cryptosporidiosis is a severe diarrheal disease caused by the protozoan parasite Cryptosporidium, posing a significant health risk to immunocompromised individuals and young children in low-resource settings. Current treatment options are limited, underscoring the urgent need for novel therapeutics. This project investigates thioredoxin reductase (CpTrxR), an essential enzyme in Cryptosporidium's redox homeostasis, as a potential drug target. We evaluated a panel of 20 inhibitors, previously shown to exhibit activity against diseases such as malaria, schistosomiasis, and cancer, for their efficacy against CpTrxR. Using a combination of biochemical assays, computational modeling, and structural analysis, we assessed each inhibitor’s potency and binding characteristics. While several compounds demonstrated measurable inhibition of CpTrxR, their IC₅₀ values were not sufficiently low to suggest strong potential as therapeutic candidates.

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Apr 17th, 2:45 PM Apr 17th, 3:00 PM

Repurposing Disease-Associated Inhibitors to Disrupt Thioredoxin Reductase in Cryptosporidium parvum

Cryptosporidiosis is a severe diarrheal disease caused by the protozoan parasite Cryptosporidium, posing a significant health risk to immunocompromised individuals and young children in low-resource settings. Current treatment options are limited, underscoring the urgent need for novel therapeutics. This project investigates thioredoxin reductase (CpTrxR), an essential enzyme in Cryptosporidium's redox homeostasis, as a potential drug target. We evaluated a panel of 20 inhibitors, previously shown to exhibit activity against diseases such as malaria, schistosomiasis, and cancer, for their efficacy against CpTrxR. Using a combination of biochemical assays, computational modeling, and structural analysis, we assessed each inhibitor’s potency and binding characteristics. While several compounds demonstrated measurable inhibition of CpTrxR, their IC₅₀ values were not sufficiently low to suggest strong potential as therapeutic candidates.