Tigecycline differs from classical tetracyclines primarily because it:

• A Inhibits the 50S ribosomal subunit rather than the 30S
• B Overcomes both efflux pump-mediated and ribosomal protection mechanisms of tetracycline resistance ✓
• C Is renally excreted and dose-adjusted in renal failure
• D Has superior activity against Pseudomonas aeruginosa

Explanation

Tigecycline, a glycylcycline, has a bulky 9-glycylamide substituent that sterically prevents efflux pumps (such as TetB) from removing it and also overcomes ribosomal protection proteins (TetM, TetO), the two main mechanisms of tetracycline resistance. Like classical tetracyclines, it binds the 30S subunit. It is predominantly hepatically excreted (biliary) without need for renal dose adjustment. Notably, tigecycline has little to no activity against Pseudomonas aeruginosa.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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