The mechanism of action of Mafenide is not known, but is different from that of the sulfonamides. Mafenide is not antagonized by pABA, serum, pus or tissue exudates, and there is no correlation between bacterial sensitivities to mafenide and to the sulfonamides. Its activity is not altered by changes in the acidity of the environment. The osmolality of the 5% topical solution is approximately 340 mOsm/kg.

Applied topically, Mafenide Acetate diffuses through devascularized areas. Approximately 80% of a Mafenide Acetate dose is delivered to burned tissue over four hours following topical application of the 5% solution. Following application of Mafenide Acetate cream and solution, peak Mafenide concentrations in human burned skin tissue occur at two and four hours, respectively. Peak tissue concentrations are similar following administration of the solution or cream. Once absorbed, Mafenide is rapidly converted to an inactive metabolite (p-carboxybenzenesulfonamide) which is cleared through the kidneys. Clinical studies have shown that when applied topically to burns as an 11.2% Mafenide Acetate cream, blood levels of the parent drug peaked at 2 hours following application, ranging from 26 to 197 µg/mL for single doses of 14 to 77 g of Mafenide Acetate. Metabolite levels peaked at 3 hours, ranging from 10 to 340 µg/mL. Twenty-four hours after application, combined parent and metabolite blood levels had fallen to pretreatment levels.

Mafenide Acetate exerts broad bacteriostatic action against many gram-negative and gram-positive organisms, including Pseudomonas aeruginosa and certain strains of anaerobes.

Data from in vitro studies on cell culture suggests that Mafenide Acetate may have a deleterious effect on human keratinocytes. The clinical significance of this information is unknown. ^[1]

Adapted from the FDA Package Insert.