The site of binding appears to be in the 50S sub-unit of the ribosome. Binding occurs to the soluble RNA fraction of certain ribosomes, thereby inhibiting the binding of amino acids to those ribosomes. Clindamycin differs from cell wall inhibitors in that it causes irreversible modification of the protein-synthesizing subcellular elements at the ribosomal level. The following clindamycin in vitro data are available but their clinical significance is unknown. Most C. perfringens are susceptible, but other species may be resistant to clindamycin.
Most mycoplasma species are susceptible to clindamycin.
Clindamycin and erythromycin show parallel resistance. Partial cross resistance has been demonstrated between clindamycin, erythromycin and macrolide antibiotics. Clindamycin hydrochloride is rapidly absorbed from the canine gastrointestinal tract. Dogs orally dosed with therapeutic amounts of clindamycin hydrochloride demonstrated antibacterial serum levels of the drug within 15 minutes post-dosing. This same study revealed that average peak serum concentrations occurred 1 hour and 15 minutes after dosing.