Vanderbilt University scientists recently found that altering one small chemical in a current antibacterial drug may create a compound that effectively targets tuberculosis (TB) and its enzymes, improving TB treatments.
The new compound, further detailed in the Proceedings of the National Academy of Sciences, is derived from fluoroquinolone moxifloxacin. It shows heightened efficiency against the enzyme in wild-type TB. It also sustains its activity against the enzyme, even in the enzyme’s resistant forms.
"We're really excited about the translational potential of this work," Neil Osheroff, a professor of biochemistry at Vanderbilt, said.
TB is one of the deadliest illnesses in the world. Approximately one-third of the global population has TB infections, and World Health Organization (WHO) statistics show approximately 1.5 million people died because of TB in 2014 alone.
"By understanding how the drugs interact with the enzyme, we can learn how resistance occurs and then hopefully develop strategies for overcoming that resistance," Osheroff said.
Creating better treatments is just one way that researchers hope to eliminate TB from the world health scene.
"By making one small change in moxifloxacin, we've come up with a much better drug against the wild-type gyrase enzyme; it maintains activity against resistant enzymes; and in all cases, it forms more stable DNA strand breaks," Osheroff said.