Vancin-S Mechanism of Action

Pharmacology: Pharmacodynamics: Vancomycin, a tricyclic glycopeptide antibiotic, is bactericidal and appears to bind tightly to D-alanyl-D-alanine portion of cell wall precursor causing blockage of glycopeptide polymerization of cell wall biosynthesis. In addition, Vancomycin alters bacterial cell membrane permeability and RNA synthesis.
Pharmacokinetics: Vancin-S 125 mg: Absorption: Oral bioavailability usually is less than 5%. However, absorption may be enhanced in patients with inflammatory disorders of the intestinal mucosa or with Clostridium difficile-induced pseudomembranous colitis. Serum Vancomycin concentrations are higher in patients with renal dysfunction than in those with normal renal function, and toxic serum concentrations may result.
Distribution: Vancomycin is widely distributed in body tissues and diffuses readily into pericardial, pleural, ascitic, and synovial fluid. Small amounts of the drug are distributed into bile. Vancomycin does not readily distribute into CSF in absence of inflammation unless serum concentrations are exceedingly high. Vancomycin is 30-60% bound to serum proteins. Protein binding may be lower (19-29%) in patients with hypoalbuminemia (e.g. burn patients, those with end stage renal disease). Vancomycin readily crosses the placenta and is distributed into cord blood. Vancomycin is distributed into milk.
Metabolism: No apparent metabolism.
Elimination: The serum elimination half-life of Vancomycin in adults with normal renal function has been reported to average 4-7 hours and the serum elimination half-life of Vancomycin is increased in patients with renal dysfunction. Vancomycin does not appear to be metabolized. Following oral administration, the drug is excreted mainly in feces. Vancomycin is only minimally removed by hemodialysis or peritoneal dialysis, including continuous ambulatory peritoneal dialysis. The drug is substantially removed by hemofiltration.