Abstract
Helicobacter pylori is a gram‐negative pathogenic bacteria responsible for ulcer progression and contributing to stomach cancer in humans. We targeted 5′‐methylthioadenosine nucleosidase (MTAN) in the futalosine pathway, a critical enzyme in menaquinone metabolism. A potent inhibitor, BTDIA, was previously designed from the MTAN transition state. It is a powerful inhibitor of bacterial growth. This study evaluates a small library of compounds stemming from this initial design. Through in vitro and culture inhibition assays, we compare this new series of potential inhibitors against the lead compound BTDIA. Future studies aim to test other analogs as potential therapeutic agents for H. pylori as well as to continue pre‐clinical trials with the current library of compounds for treatment of H. pylori infections.Support or Funding InformationAlbert Einstein SURP Program
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