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Infectious disease


Mycobacterium tuberculosis decaprenylphosphoryl-b-d-ribose 2ʹ-oxidase (dprE1); M. tuberculosis molybdopterin biosynthesis protein (moeW)

Mouse and cell culture studies suggest an inhibitor of dprE1 and moeW could help treat drug-resistant tuberculosis infection. In multidrug-resistant and extensively drug-resistant strains of tuberculosis, the small molecule TCA1 showed potent bactericidal activity. In mouse models for acute and chronic M. tuberculosis infection, oral TCA1 decreased infection in the lung and spleen compared with no treatment and without causing weight loss or other adverse effects. In a series of genetic studies, dprE1 and moeW were implicated as the targets of TCA1. Next steps include optimizing the potency and pharmacokinetics of the compound.

SciBX 6(28); doi:10.1038/scibx.2013.727
Published online July 25, 2013

Patent application filed; available for licensing

Wang, F. et al. Proc. Natl. Acad. Sci. USA; published online June 17, 2013;
Contact: Peter G. Schultz, The Scripps Research Institute, La Jolla, Calif.
Contact: William R. Jacobs Jr., Albert Einstein College of Medicine of Yeshiva University, Bronx, N.Y.