Ampicillin 250 mg, Dicloxacillin 250 mg Tablets

Ampicillin is bactericidal at low concentrations and is clinically effective not only against the gram-positive organisms usually susceptible to penicillin G but also against a variety of gram-negative organisms. It is stable in the presence of gastric acid and is well absorbed from the gastrointestinal tract. It diffuses readily into most body tissues and fluids; however, penetration into the cerebrospinal fluid and brain occurs only with meningeal inflammation. Ampicillin is excreted largely unchanged in the urine; its excretion can be delayed by concurrent administration of probenecid which inhibits the renal tubular secretion of ampicillin. In blood serum, ampicillin is the least bound of all the penicillins; an average of about 20 percent of the drug is bound to plasma proteins as compared to 60 to 90 percent of the other penicillins. The administration of 500 mg dose of ampicillin capsules results in an average peak blood serum level of approximately 3.0 mcg/mL.

Mechanism of Action — Ampicillin is similar to penicillin in its bactericidal action against susceptible bacteria during the stage of active multiplication. It acts through the inhibition of cell wall biosynthesis that leads to the death of the bacteria.

Mechanism of Resistance — Resistance to ampicillin is mediated primarily through enzymes called beta-lactamases that cleave the beta-lactam ring of ampicillin, rendering it inactive.

Antimicrobial Activity — Ampicillin has been shown to be active against most isolates of the following bacteria, both in vitro and in clinical infections, as described in the INDICATIONS AND USAGE section.

The following in vitro data are available, but their clinical significance is unknown. At least 90 percent of the following bacteria exhibit an in vitro minimum inhibitory concentration (MIC) less than or equal to 0.12 mcg/mL for ampicillin. However the efficacy of ampicillin in treating clinical infections due to these bacteria has not been established in adequate and well-controlled trials.

Susceptibility Testing — For specific information regarding susceptibility test interpretive criteria and associated test methods and quality control standards recognized by FDA for this drug, please see: https://www.fda.gov/STIC.

Mechanism of Action — Penicillinase-resistant penicillins exert a bactericidal action against penicillin-susceptible microorganisms during the state of active multiplication. All penicillins inhibit the biosynthesis of the bacterial cell wall.

Antibacterial Activity — Dicloxacillin sodium has been shown to be active against most isolates of the following microorganisms, both in vitro and in clinical infections as described in the INDICATIONS AND USAGE section.

Dicloxacillin sodium is resistant to destruction by acid.

Absorption of dicloxacillin sodium after oral administration is rapid but incomplete; peak blood levels are achieved in 1 to 1.5 hours. In one study, after ingestion of a single 500 mg oral dose, peak serum concentrations range from 10 to 17 mcg/mL for dicloxacillin.

Oral absorption of dicloxacillin is delayed when the drugs are administered after meals.

Once absorbed, dicloxacillin sodium is 97.9 ± 0.6 percent bound to serum protein, mainly albumin. Dicloxacillin sodium vary in the extent to which they are distributed in the body fluids. With normal doses, insignificant concentrations are found in the cerebrospinal fluid and aqueous humor. Dicloxacillin sodium is found in therapeutic concentrations in the pleural, bile and amniotic fluids.

Dicloxacillin sodium is rapidly excreted, primarily as unchanged drug in the urine by glomerular filtration and active tubular secretion. The elimination half-life for dicloxacillin is about 0.7 hour. Nonrenal elimination includes hepatic inactivation and excretion in bile.

Dicloxacillin is not dialyzable. Only minimal amounts are removed by hemodialysis or peritoneal dialysis.