Bedaquiline, approved for MDR-TB, exerts its bactericidal activity by inhibiting:

• A DprE1 (decaprenylphosphoryl-β-D-ribose 2′-oxidase) in arabinogalactan synthesis
• B InhA (enoyl-ACP reductase) involved in mycobacterial fatty acid synthesis
• C RNA polymerase beta subunit (rpoB gene product)
• D Mycobacterial ATP synthase (subunit c of F0 component), depleting bacterial ATP ✓

Explanation

Bedaquiline specifically inhibits the c subunit of mycobacterial F0F1 ATP synthase, disrupting proton pumping across the bacterial membrane and collapsing the proton motive force needed for ATP generation. This is highly specific to mycobacteria (low off-target activity for human mitochondrial ATP synthase). DprE1 inhibition is the mechanism of delamanid/pretomanid; InhA is the target of isoniazid (via its active metabolite); rpoB is the rifampicin target.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.