Bedaquiline, approved for drug-resistant tuberculosis, is unique because it targets:

• A Mycobacterial RNA polymerase (rpoB), different from rifampicin binding site
• B Mycobacterial ATP synthase (atpE subunit), depleting bacterial ATP production ✓
• C Mycobacterial folate synthesis (dihydropteroate synthase)
• D Mycobacterial ribosomal translocation (EF-G equivalent)

Explanation

Bedaquiline selectively inhibits mycobacterial F-ATP synthase by binding the c-ring of the Fo subunit (encoded by atpE), blocking proton translocation and ATP synthesis; this is a first-in-class mechanism with no cross-resistance to existing anti-TB drugs. Bedaquiline is bactericidal against both replicating and non-replicating (dormant) mycobacteria. Key adverse effects include QT prolongation and hepatotoxicity.

Reference: KD Tripathi, Essentials of Medical Pharmacology, 8th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.