How does tigecycline work in the body?
Tigecycline is a glycylcycline antibiotic. Its mechanism of action is to inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit. Specifically, it binds to the A-site of the ribosome and blocks the entry of aminoacyl-tRNA, which prevents formation of new peptide bonds and stops bacterial growth.
What does tigecycline target: Gram-positive, Gram-negative, or both?
Because tigecycline disrupts bacterial translation at the ribosome (rather than targeting a cell-wall or DNA-making pathway), it can inhibit a range of bacteria, including both Gram-positive and Gram-negative organisms.
How is tigecycline different from tetracycline?
Tigecycline is structurally related to tetracycline-class drugs but is modified (the glycyl group) to overcome some mechanisms that reduce tetracycline activity. Like other tetracyclines, it targets the ribosome; the difference is that tigecycline is designed to maintain binding in the bacterial ribosomal environment more effectively than older tetracyclines.
What happens to bacteria when tigecycline blocks translation?
When tigecycline prevents aminoacyl-tRNA entry into the ribosome A-site, protein synthesis halts. With translation blocked, bacteria cannot produce proteins needed for growth and replication, leading to suppression of bacterial proliferation (and, depending on the organism and conditions, bacterial killing or bacteriostatic effects).
Common clinical relevance: resistance and cross-resistance
Resistance to tetracycline-class antibiotics often involves mechanisms that reduce effective drug accumulation or ribosomal protection. Because tigecycline still acts on the ribosome, resistance that affects tetracycline-class binding or ribosomal function can also reduce tigecycline activity, though tigecycline was engineered to retain activity against some resistant strains.
Sources
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