Bedaquiline, a newer anti-TB drug used in MDR-TB, acts by inhibiting:

• A Mycobacterial ATP synthase (F-type, subunit c), depleting cellular energy ✓
• B InhA (enoyl-ACP reductase), blocking mycolic acid elongation
• C DNA gyrase subunit B, preventing mycobacterial DNA supercoiling
• D Decaprenyl-phosphoryl-β-D-ribose 2'-epimerase (DprE1), blocking arabinogalactan synthesis

Explanation

Bedaquiline (diarylquinoline) selectively inhibits the mycobacterial F-type ATP synthase by binding to subunit c of the proton pump (c-ring), blocking the proton channel. This disrupts ATP synthesis and causes mycobacterial cell death due to energy depletion, with a prolonged post-antibiotic effect. It is active against both drug-susceptible and drug-resistant M. tuberculosis, including XDR-TB strains. InhA is the target of isoniazid and ethionamide; DprE1 is inhibited by BTZ043 (in development); fluoroquinolones target DNA gyrase.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.