The findings indicate that a new compound, 24-desmethylrifampicin, has much better antibacterial activity than rifampicin against multi-drug-resistant strains of the bacteria that cause tuberculosis.
Rifampicin and related drugs are important antibiotics, the key to an effective "drug cocktail" that already takes about six months of treatment to cure tuberculosis.
But two forms of tuberculosis, referred to as "multi-drug-resistant," or MDR, and "extensively drug-resistant," or XDR, have become resistant to rifampicin.
"Rifampicin is the most effective drug against tuberculosis, and it's very difficult to achieve a cure without it," Mahmud said.
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"The approach we're using should be able to create one or more analogs that could help take the place of rifampicin in TB therapy," said Mahmud, corresponding author the study that included collaborators from the University of Delhi and the Institute of Genomics and Integrative Biology in India.
A combination of genetic modification and synthetic drug development was used to create the new compound, which so far has only been developed in laboratory.
Drug resistance in rifampicin and related antibiotics has occurred when their bacterial RNA polymerase enzymes mutate, Mahmud said, leaving them largely unaffected by antibiotics that work by inhibiting RNA synthesis.
The new approach works by modifying the drug so it can effectively bind to this mutated enzyme and once again achieve its effectiveness.
In 1993, resurging levels of tuberculosis due to the antibiotic resistance led the World Health Organisation to declare it a global health emergency, researchers said.
Today more than 1 million people around the world are dying each year from tuberculosis, and after AIDS it remains the second most common cause of death by infectious disease.