Ertapenem sodium

The main ingredient of this product is ertapenem sodium. Chemical name: (1R,5S,6S,8R,2S*,4S*)-2-[2-[3-carboxyl-phenylcarbamoyl]-pyrrolidinyl-4-thio]-6-(1-hydroxyethyl)-1-methylcarbapenem-3-carboxylic acid monosodium salt Chemical structure: Molecular formula: C22H24N3O7SNa Molecular weight: 497.50

When ertapenem is co-administered with probenecid, probenecid competes with ertapenem for active tubular secretion, thereby inhibiting the latter's renal excretion. This results in a small but statistically significant increase in elimination half-life (19%) and increased systemic drug exposure (25%). No dose adjustment of ertapenem is required when co-administered with probenecid. Due to the small effect on half-life, it is not recommended to prolong the half-life of ertapenem with co-administration of probenecid. In vitro studies have shown that ertapenem has no inhibitory effect on P-glycoprotein-mediated transport of digoxin or vinblastine, and ertapenem is not a substrate for P-glycoprotein-mediated transport. In vitro studies in human liver microsomes have shown that ertapenem has no inhibitory effect on metabolism mediated by the six major cytochrome P450 (CYP) isozymes (1A2, 2C9, 2C19, 2D6, 2E1, and 3A4). Ertapenem is unlikely to cause drug-drug interactions by inhibiting P-glycoprotein or CYP-mediated drug clearance (see Pharmacokinetics). Interactions with specific clinical drugs other than probenecid have not been studied. Concomitant use of carbapenems, including ertapenem, in patients receiving valproate or divalproex sodium has been documented to result in decreased valproate concentrations. Because of the drug interaction, valproate concentrations may fall below the therapeutic range, thus increasing the risk of seizures. Although the mechanism of the drug interaction is not clear, in vitro and animal data suggest that carbapenems may inhibit the hydrolysis of valproate glucuronide metabolite (VPA-g) to valproate, reducing serum valproate concentrations. (See PRECAUTIONS)

The main ingredient of this product is ertapenem sodium. Chemical name: (1R,5S,6S,8R,2S*,4S*)-2-[2-[3-carboxyl-phenylcarbamoyl]-pyrrolidinyl-4-thio]-6-(1-hydroxyethyl)-1-methylcarbapenem-3-carboxylic acid monosodium salt Chemical structure: Molecular formula: C22H24N3O7SNa Molecular weight: 497.50

When ertapenem is co-administered with probenecid, probenecid competes with ertapenem for active tubular secretion, thereby inhibiting the latter's renal excretion. This results in a small but statistically significant increase in elimination half-life (19%) and increased systemic drug exposure (25%). No dose adjustment of ertapenem is required when co-administered with probenecid. Due to the small effect on half-life, it is not recommended to prolong the half-life of ertapenem with co-administration of probenecid. In vitro studies have shown that ertapenem has no inhibitory effect on P-glycoprotein-mediated transport of digoxin or vinblastine, and ertapenem is not a substrate for P-glycoprotein-mediated transport. In vitro studies in human liver microsomes have shown that ertapenem has no inhibitory effect on metabolism mediated by the six major cytochrome P450 (CYP) isozymes (1A2, 2C9, 2C19, 2D6, 2E1, and 3A4). Ertapenem is unlikely to cause drug-drug interactions by inhibiting P-glycoprotein or CYP-mediated drug clearance (see Pharmacokinetics). Interactions with specific clinical drugs other than probenecid have not been studied. Concomitant use of carbapenems, including ertapenem, in patients receiving valproate or divalproex sodium has been documented to result in decreased valproate concentrations. Because of the drug interaction, valproate concentrations may fall below the therapeutic range, thus increasing the risk of seizures. Although the mechanism of the drug interaction is not clear, in vitro and animal data suggest that carbapenems may inhibit the hydrolysis of valproate glucuronide metabolite (VPA-g) to valproic acid, reducing serum valproate concentrations. (See PRECAUTIONS)