Disease relevance of mafenide

• However, the duration and area of mafenide application must be limited because of systemic toxicity associated with prolonged or extensive use [1].
• Using intact bacterial cells, it was found that Pseudomonas aeruginosa was more susceptible to mafenide than Escherichia coli, that p-aminobenzoic acid (pABA) did not reverse or prevent inhibition by mafenide and that pABA itself was inhibitory [2].
• Using burned guinea pigs infected with Pseudomonas aeruginosa, mafenide was applied every 12 hr as the dry foam or as the commercially available ointment [3].
• Inhibition of Pseudomonas burn wound infection by mafenide dry foam [3].
• Allergic contact dermatitis from topical mafenide [4].

High impact information on mafenide

• Mafenide did not qualitatively alter activation of plasminogen or affect generation of complexes with alpha 2 antiplasmin complexes [5].
• The presence of the inhibitor of CAs, p-aminomethylbenzensulfonamide (mafenide), at the start line in the course of electrophoresis of PSII membranes solubilized by n-dodecyl-beta-maltoside (DM) decreased the amount of PSII core complex in the gel [6].
• The effect of mafenide on dihydropteroate synthase [2].
• 'Peripheral' binding sites for benzodiazepines are under neural or homonal control in the pineal gland, olfactory bulb, and kidney [7].
• Evaluation of a prototype therapeutic system for prolonged, continuous topical delivery of homosulfanilamide in the management of Pseudomonas burn wound sepsis [8].

Chemical compound and disease context of mafenide

• Although not related statistically to survival time, the mafenide hydrochloride spray also controlled the Pseudomonas aeruginosa in these wounds [9].

Anatomical context of mafenide

• Therefore, mafenide could not be considered as an antidiabetic drug despite being oxidized and exhibiting insulin-mimicking effects in rat and mouse adipocytes [10].

Associations of mafenide with other chemical compounds

• A series of aromatic sulfonamides, most of which were Schiff's bases derived from sulfanilamide/homosulfanilamide/4-aminoethylbenzenesulfonamide and substituted-aromatic aldehydes, or ureido-substituted such sulfonamides, were investigated for in vitro inhibition of the malarial parasite enzyme (pfCA) and the growth of P. falciparum [11].
• Sulfamylon (mafenide) solution, a potent experimental topical antimicrobial, is used in our burn unit to treat burn wounds both before and after skin grafting [12].
• In human adipocytes, mafenide did not stimulate glucose transport since it was not a high-affinity substrate for SSAO and generated less hydrogen peroxide than benzylamine or methylamine [10].

Gene context of mafenide

• The first hCA IX-selective inhibitors were thus detected, as the chlorotriazinyl-sulfanilamide and the bis-ethoxytriazinyl derivatives of sulfanilamide/homosulfanilamide showed selectivity ratios for CA IX over CA II inhibition in the range of 166-706 [13].
• All of the quaternary ammonium salts prepared in the present study are potent inhibitors of both human carbonic anhydrase-II and recombinant human carbonic anhydrase-IV; they are significantly more potent as inhibitors of these carbonic anhydrase isozymes than the previously reported inhibitor quaternary ammonium homosulfanilamide [14].
• These were the control (group C); 20% body surface burn (group B); 20% burn, seeded with Pseudomonas aeruginosa (group BI); and burned-infected treated topically with mafenide (alpha-amino-p-toluenesulfonamide) acetate (group BIS), a treatment which controls P, aeruginosa burn-wound infection in humans [15].

Analytical, diagnostic and therapeutic context of mafenide

• The Maphenide group and S.S.D. group are compared statistically with the control group [16].

References