Tigecycline

Tigecycline is a broad spectrum glycylcycline antibiotic useful for multi-drug resistant organisms and approved by the FDA in June 2005. Tigecycline is a semisynthetic derivative of tetracycline, that is structurally similar to minocycline; however, it contains a large glycylamido group at the D-9 position. This substitution is thought to be the reason behind its broad-spectrum activity.
Tigecycline is a protein synthesis inhibitor, that show bacteriostatic activity against both Gram-positive and Gram-negative bacteria. It was designed be less affected by the two major tetracycline-resistance mechanisms, ribosomal protection and efflux. Additionally, Tigecycline is not affected by resistance mechanisms such as beta-lactamases (including extended spectrum beta-lactamases), target-site modifications, macrolide efflux pumps or enzyme target changes (e.g. gyrase/topoisomerases). However, some ESBL-producing isolates may confer resistance to Tigecycline via other resistance mechanisms. Tigecycline resistance in some bacteria (e.g. Acinetobacter calcoaceticus-Acinetobacter baumannii complex) is associated with multi-drug resistant (MDR) efflux pumps.
Tigecycline has recently shown anti-tumor properties and is being evaluated for Tigecycline’s inhibitory effects on several activating signaling pathways and abnormal mitochondrial function in cancer cells.
Tigecycline is soluble in water (0.45 mg/mL) and DMSO (>3 mg/mL).

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Background

Tigecycline inhibits protein translation in bacteria by binding to the 30S ribosomal subunit and blocking entry of amino-acyl tRNA molecules into the A site of the ribosome. This prevents incorporation of amino acid residues into elongating peptide chains. In general, Tigecycline is considered bacteriostatic; however, Tigecycline has demonstrated bactericidal activity against isolates of S. pneumoniae and L. pneumophila.