Target intelligence / Profile preview

Mycobacterium tuberculosis leucyl-tRNA synthetase (LeuRS)

Target
LeuRS
Molecular classification
Enzyme, Aminoacyl-tRNA synthetase, Class I aminoacyl-tRNA synthetase
01

Overview

Mycobacterium tuberculosis leucyl-tRNA synthetase is a class I aminoacyl-tRNA synthetase enzyme responsible for linking the amino acid leucine to its cognate tRNA^Leu during translation, a process essential for bacterial protein synthesis[2][5][7]. This enzyme is required for viability and plays a key role in the growth, survival, and biofilm formation of M. tuberculosis[2][5]. Its unique structural features, particularly in the editing and tRNA-binding domains, make it an attractive therapeutic target for anti-tubercular drug development[1][4][5]. Small molecule inhibitors of LeuRS, especially those utilizing the oxaborole tRNA-trapping (OBORT) mechanism, block protein synthesis and show efficacy against drug-sensitive and drug-resistant M. tuberculosis, validating LeuRS as a promising target for next-generation antituberculosis agents[1][4][6][8].

Other names
LeuRSMtb LeuRSMtLeuRSMycobacterium tuberculosis LeuRS
02

Mechanism of action

Inhibition of LeuRS blocks leucylation of tRNA^Leu, halting protein synthesis in Mycobacterium tuberculosis[1][2][4] OBORT (oxaborole tRNA-trapping): covalent trapping of tRNA in the enzyme editing site, preventing protein translation[1][4][6] Direct enzymatic inhibition via small molecule binding (competitive or allosteric), including by dual-acting compounds targeting both LeuRS and other synthetases[8]

03

Biological functions

Protein synthesis (translation)Aminoacylation of tRNA^LeuProofreading/editing of charged tRNARegulation of mycobacterial growth and developmentBiofilm formation in Mycobacterium tuberculosis
04

Disease associations

Infection (specifically tuberculosis caused by Mycobacterium tuberculosis)Antimicrobial resistance (target for anti-tubercular drug development)Other (NTM infection in related pathogens, e.g., M. abscessus)
05

Safety considerations

Potential for off-target inhibition of human mitochondrial or cytoplasmic leucyl-tRNA synthetase, leading to toxicity[4]Emergence of resistance through mutations in leuS affecting inhibitor binding[4]Null (no major clinical safety liabilities reported yet for first-in-class TB agents)
06

Interacting drugs

Benzoxaboroles (e.g., EC/11770, AN3016, AN3017, compound 1)

2 more in the full profile.

07

Biomarkers

Expression of the leuS gene (encodes LeuRS) for molecular drug resistance studies and target validation[4]Mutations in leuS associated with drug resistance to LeuRS inhibitors[4]Null (no widely accepted clinical LeuRS biomarker yet)

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