Discovery of a selective antitubercular small-molecule inhibitor targeting CoaBC
Tuberculosis (TB) is one of the top ten causes of death worldwide, accounting for 1.8 million deaths per year.1 The emergence of multidrug resistant (MDR) and extensively drug resistant (XDR) strains of Mycobacterium tuberculosis (Mtb) has stimulated renewed efforts for the discovery of new anti-tubercular drugs.1
The biosynthesis pathway of coenzyme A (CoA) is essential in bacteria, and inhibiting the CoA pathway is considered a viable antibiotic strategy. In Mtb, the bifunctional enzyme CoaBC catalyses the formation of 4’-phosphopantothenoylcysteine from 4’-phosphopantothenate and L-cysteine through its CoaB domain, followed by decarboxylation of the cysteine moiety to 4’-phosphopantetheine via its CoaC domain.2 Due to its considerable different to the human orthologue, CoaBC is a highly promising target for the development of novel selective anti-tubercular drugs.3
We have developed novel inhibitors of Mtb CoaBC using a fragment-based approach in conjunction with structure-guided design by X-ray crystallography. Our campaign started from an original fragment hit, and using fragment-growing strategies, we obtained a lead series of compounds inhibiting the Mtb CoaBC enzyme at nanomolar concentrations. This is the first series of drug-like small-molecule inhibitor of Mtb CoaBC which is active on whole cell Mtb, confirming the druggability of Mtb CoaBC and opening avenues to develop a new class of antitubercular drugs.
[1] WHO, Global Tuberculosis Report, 2019.
[2] Ulrich Genschel, Molecular Biology and Evolution, 2004, 21, 1242–1251.
[3] Joanna C. Evans et al., ACS Infectious Diseases, 2016, 2, 958–968.