<unk>  mechanism<unk>  has a primarily bacteriostatic effect. At higher concentrations, it may be bactericidal. It is a bacterial protein synthesis inhibitor by inhibiting ribosomal translocation, in a similar way to macrolides. It does so by binding to the rRNA of the bacterial 50S ribosome subunit, overlapping with the binding sites of the oxazolidinone, pleuromutilin, and macrolide antibiotics, among others. The binding is reversible.<unk>  is more effective than lincomycin. The X-ray crystal structures of<unk>  bound to ribosomes (or ribosomal subunits) derived from Escherichia coli, Deinococcus radiodurans, and Haloarcura marismortui have been determined; the structure of the closely related antibiotic lincomycin bound to the 50S ribosomal subunit of Staphylococcus aureus has also been reported.
Clindamycin
Meropenem
Resistin
Rifamycin
Aztreonam
Cefepime
Levofloxacin
Spiramycin