Novel Anti-Tuberculosis Compounds

Ref.-No. 4941

Keywords: Tuberculosis, macrophage, antibiotic

The resurgence of tuberculosis, caused primarily by Mycobacterium tuberculosis (Mtb), and the appearance of multi‐drug and extensively drug resistant Mtb strains strengthen the need for new drugs with alternative modes of action. The interaction between the mycobacterial thioredoxin reductase (TrxR) and its substrate thioredoxin (Trx) is a promising new drug target for the treatment of tuberculosis, since Mtb lacks the common glutathione system and the mycobacterial TrxR shows a substantial difference in sequence, mechanism and structure to human TrxRs. It was shown that TrxR is essential for thiol redox homeostasis and genetic inactivation in vivo eradicates Mtb during acute and chronic mouse infections (Lin et al., PLoS Pathog. 2016). In order to further improve the bioactivity of promising compounds, researchers of the TU Dortmund University have focused on optimizing the physico-chemical properties that are important for permeability, since M. tuberculosis shows an unusual thick and impermeable cell wall.

Competitive Advantages

  • Novel class of compounds that inhibit a novel target with potential to overcome resistance problems of M. tuberculosis to other drugs
  • Viability of infected macrophages is not affected
  • Increased bioactivity by optimized permeability through the cell wall of M. tuberculosis

Commercial Opportunities

The technology is offered for licensing and further therapeutic development.

Current Status

The researcher are preparing the further development towards mice studies to confirm in vivo efficacy, as well as ADME‑Tox studies. In case of interest we are pleased to inform you about the patent status.

Relevant Puclications

Koch, O., et al. (2013) Identification of M. tuberculosis thioredoxin reductase inhibitors based on high-throughput docking using constraints J. Med. Chem. 56(12): 4849-59.

An invention of TU Dortmund.


Prof. Dr. Frank Entschladen

fe@provendis.info
+49 208 9410520