Lincosamides (eg. lincomycin, clindamycin) are a class of antibiotics.
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Lincosamides kill bacteria by interfering with the synthesis of proteins. They bind to the 23s portion of the 50S subunit of bacterial ribosomes and cause premature dissociation of the peptidyl-tRNA from the ribosome.[1] Lincosamides do not interfere with protein synthesis in human cells (or those of other eukaryotes) because our ribosomes are structurally different from those of bacteria.
The first lincosamide to be discovered is lincomycin, isolated from Streptomyces lincolnensis in a soil sample from Lincoln, Nebraska (hence the bacterial name).
Lincomycin has been superseded by clindamycin, which exhibits improved antibacterial activity. Clindamycin also exhibits some activity against parasitic protozoa, and has been used in toxoplasmosis and malaria.
They are normally used to treat staphylococci and streptococci, and have proved useful in treating Bacteroides fragilis and some other anaerobes. They are used in the treatment of Toxic Shock Syndrome and thought to directly block the M protein production that leads to the severe inflammatory response.
Target bacteria may alter the drug's binding site (similar to resistance found in macrolides and streptogramins). The resistance mechanism is methylation of the 23s binding site. If this occurs then the bacteria are resistant to both the macrolides and the lincosamides. Also, enzymatic inactivation of clindamycin has been described (rare).
The lincosamides, as the hydrochloride salt, are bitter to taste, so for oral formulation they are given as the palmitate esters, or formulated in capsules. Clindamycin is given intravenously as clindamycin phosphate, which is then converted into active clindamycin within the body.
These are bacteriostatic drugs and antagonists of macrolides and streptogramins.
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