Samnir Mechanism of Action

Pharmacology: Pharmacodynamics: Cefdinir, a third-generation cephalosporin, is stable in the presence of some β-lactamases which is produced by the bacteria. Bactericidal activity results from Cefdinir inhibition of cell wall synthesis. It has bactericidal activity against gram-positive, gram-negative and including β-lactamases producing bacteria. Cefdinir is active in vitro against the following microorganisms which are Staphylococcus epidermidis (methicillin-susceptible strains), Staphylococcus aureus (methicillin-susceptible strains including β-lactamase-producing strains), Streptococcus pyogenes (Group A β-hemolytic streptococci), Streptococcus agalactiae (Group B), Streptococcus pneumoniae (penicillin-susceptible strains), Haemophilus influenzae (including β-lactamase-producing strains), Haemophilus parainfluenzae (including β-lactamase-producing strains), Klebsiella pneumoniae and Moraxella catarrhalis (including β-lactamase-producing strains). Cefdinir is inactive against most strains of Pseudomonas, Enterobacter, Enterococci, methicillin or oxacillin-resistant Staphylococci, penicillin-resistant Streptococci, Legionella pneumophila, Mycoplasma and Chlamydia pneumonia.
Pharmacokinetics: Cefdinir is rapidly absorbed after oral administration. The estimated absolute bioavailability of the suspension formulation is slightly greater than that of the capsule formulation. Cefdinir is 60-70% bound to plasma proteins; binding is independent of drug concentration. Cefdinir is distributed into blister fluid, middle ear fluid, tonsils, sinus tissue and bronchial mucosa. Cefdinir is less metabolized and eliminated unchanged in urine. Cefdinir is removed by hemodialysis. Clearance of Cefdinir is decreased in patients with impaired renal function.