Competitive Inhibition of Renal Tubular Secretion of Gemifloxacin by Probenecid
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| Published in | Antimicrobial Agents and Chemotherapy Vol. 53; no. 9; pp. 3902 - 3907 |
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American Society for Microbiology
01.09.2009
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| AbstractList | Probenecid interacts with transport processes of drugs at several sites in the body. For most quinolones, renal clearance is reduced by concomitant administration of probenecid. The interaction between gemifloxacin and probenecid has not yet been studied. We studied the extent, time course, site(s), and mechanism of this interaction. Seventeen healthy volunteers participated in a randomized, two-way crossover study. Subjects received 320 mg gemifloxacin as an oral tablet without and with 4.5 g probenecid divided in eight oral doses. Drug concentrations in plasma and urine were analyzed by liquid chromatography-tandem mass spectrometry. WinNonlin was used for noncompartmental analysis, compartmental modeling, and statistics, and NONMEM was used for visual predictive checks. Concomitant administration of probenecid increased plasma gemifloxacin concentrations and amounts excreted in urine compared to baseline amounts. Data are average estimates (percent coefficients of variation). Modeling showed a competitive inhibition of the renal tubular secretion of gemifloxacin by probenecid as the most likely mechanism of the interaction. The estimated K(m) and Vmax for the saturable part of renal elimination were 9.16 mg/liter (20%) and 113 mg/h (21%), respectively. Based on the molar ratio, the affinity for the renal transporter was 10-fold higher for gemifloxacin than for probenecid. Since probenecid reached an approximately 200-times-higher area under the molar concentration-time curve from 0 to 24 h than gemifloxacin, probenecid inhibited the active tubular secretion of gemifloxacin. Probenecid also reduced the nonrenal clearance of gemifloxacin from 25.2 (26%) to 21.0 (23%) liters/h. Probenecid inhibited the renal tubular secretion of gemifloxacin, most likely by a competitive mechanism, and slightly decreased nonrenal clearance of gemifloxacin.Probenecid interacts with transport processes of drugs at several sites in the body. For most quinolones, renal clearance is reduced by concomitant administration of probenecid. The interaction between gemifloxacin and probenecid has not yet been studied. We studied the extent, time course, site(s), and mechanism of this interaction. Seventeen healthy volunteers participated in a randomized, two-way crossover study. Subjects received 320 mg gemifloxacin as an oral tablet without and with 4.5 g probenecid divided in eight oral doses. Drug concentrations in plasma and urine were analyzed by liquid chromatography-tandem mass spectrometry. WinNonlin was used for noncompartmental analysis, compartmental modeling, and statistics, and NONMEM was used for visual predictive checks. Concomitant administration of probenecid increased plasma gemifloxacin concentrations and amounts excreted in urine compared to baseline amounts. Data are average estimates (percent coefficients of variation). Modeling showed a competitive inhibition of the renal tubular secretion of gemifloxacin by probenecid as the most likely mechanism of the interaction. The estimated K(m) and Vmax for the saturable part of renal elimination were 9.16 mg/liter (20%) and 113 mg/h (21%), respectively. Based on the molar ratio, the affinity for the renal transporter was 10-fold higher for gemifloxacin than for probenecid. Since probenecid reached an approximately 200-times-higher area under the molar concentration-time curve from 0 to 24 h than gemifloxacin, probenecid inhibited the active tubular secretion of gemifloxacin. Probenecid also reduced the nonrenal clearance of gemifloxacin from 25.2 (26%) to 21.0 (23%) liters/h. Probenecid inhibited the renal tubular secretion of gemifloxacin, most likely by a competitive mechanism, and slightly decreased nonrenal clearance of gemifloxacin. Probenecid interacts with transport processes of drugs at several sites in the body. For most quinolones, renal clearance is reduced by concomitant administration of probenecid. The interaction between gemifloxacin and probenecid has not yet been studied. We studied the extent, time course, site(s), and mechanism of this interaction. Seventeen healthy volunteers participated in a randomized, two-way crossover study. Subjects received 320 mg gemifloxacin as an oral tablet without and with 4.5 g probenecid divided in eight oral doses. Drug concentrations in plasma and urine were analyzed by liquid chromatography-tandem mass spectrometry. WinNonlin was used for noncompartmental analysis, compartmental modeling, and statistics, and NONMEM was used for visual predictive checks. Concomitant administration of probenecid increased plasma gemifloxacin concentrations and amounts excreted in urine compared to baseline amounts. Data are average estimates (percent coefficients of variation). Modeling showed a competitive inhibition of the renal tubular secretion of gemifloxacin by probenecid as the most likely mechanism of the interaction. The estimated K m and V max for the saturable part of renal elimination were 9.16 mg/liter (20%) and 113 mg/h (21%), respectively. Based on the molar ratio, the affinity for the renal transporter was 10-fold higher for gemifloxacin than for probenecid. Since probenecid reached an ∼200-times-higher area under the molar concentration-time curve from 0 to 24 h than gemifloxacin, probenecid inhibited the active tubular secretion of gemifloxacin. Probenecid also reduced the nonrenal clearance of gemifloxacin from 25.2 (26%) to 21.0 (23%) liters/h. Probenecid inhibited the renal tubular secretion of gemifloxacin, most likely by a competitive mechanism, and slightly decreased nonrenal clearance of gemifloxacin. Classifications Services AAC Citing Articles Google Scholar PubMed Related Content Social Bookmarking CiteULike Delicious Digg Facebook Google+ Mendeley Reddit StumbleUpon Twitter current issue AAC About AAC Subscribers Authors Reviewers Advertisers Inquiries from the Press Permissions & Commercial Reprints ASM Journals Public Access Policy AAC RSS Feeds 1752 N Street N.W. • Washington DC 20036 202.737.3600 • 202.942.9355 fax • journals@asmusa.org Print ISSN: 0066-4804 Online ISSN: 1098-6596 Copyright © 2014 by the American Society for Microbiology. For an alternate route to AAC .asm.org, visit: AAC Probenecid interacts with transport processes of drugs at several sites in the body. For most quinolones, renal clearance is reduced by concomitant administration of probenecid. The interaction between gemifloxacin and probenecid has not yet been studied. We studied the extent, time course, site(s), and mechanism of this interaction. Seventeen healthy volunteers participated in a randomized, two-way crossover study. Subjects received 320 mg gemifloxacin as an oral tablet without and with 4.5 g probenecid divided in eight oral doses. Drug concentrations in plasma and urine were analyzed by liquid chromatography-tandem mass spectrometry. WinNonlin was used for noncompartmental analysis, compartmental modeling, and statistics, and NONMEM was used for visual predictive checks. Concomitant administration of probenecid increased plasma gemifloxacin concentrations and amounts excreted in urine compared to baseline amounts. Data are average estimates (percent coefficients of variation). Modeling showed a competitive inhibition of the renal tubular secretion of gemifloxacin by probenecid as the most likely mechanism of the interaction. The estimated Km and Vmax for the saturable part of renal elimination were 9.16 mg/liter (20%) and 113 mg/h (21%), respectively. Based on the molar ratio, the affinity for the renal transporter was 10-fold higher for gemifloxacin than for probenecid. Since probenecid reached an ∼200-times-higher area under the molar concentration-time curve from 0 to 24 h than gemifloxacin, probenecid inhibited the active tubular secretion of gemifloxacin. Probenecid also reduced the nonrenal clearance of gemifloxacin from 25.2 (26%) to 21.0 (23%) liters/h. Probenecid inhibited the renal tubular secretion of gemifloxacin, most likely by a competitive mechanism, and slightly decreased nonrenal clearance of gemifloxacin. Probenecid interacts with transport processes of drugs at several sites in the body. For most quinolones, renal clearance is reduced by concomitant administration of probenecid. The interaction between gemifloxacin and probenecid has not yet been studied. We studied the extent, time course, site(s), and mechanism of this interaction. Seventeen healthy volunteers participated in a randomized, two-way crossover study. Subjects received 320 mg gemifloxacin as an oral tablet without and with 4.5 g probenecid divided in eight oral doses. Drug concentrations in plasma and urine were analyzed by liquid chromatography-tandem mass spectrometry. WinNonlin was used for noncompartmental analysis, compartmental modeling, and statistics, and NONMEM was used for visual predictive checks. Concomitant administration of probenecid increased plasma gemifloxacin concentrations and amounts excreted in urine compared to baseline amounts. Data are average estimates (percent coefficients of variation). Modeling showed a competitive inhibition of the renal tubular secretion of gemifloxacin by probenecid as the most likely mechanism of the interaction. The estimated Km and Vmax for the saturable part of renal elimination were 9.16 mg/liter (20%) and 113 mg/h (21%), respectively. Based on the molar ratio, the affinity for the renal transporter was 10-fold higher for gemifloxacin than for probenecid. Since probenecid reached an 200-times-higher area under the molar concentration-time curve from 0 to 24 h than gemifloxacin, probenecid inhibited the active tubular secretion of gemifloxacin. Probenecid also reduced the nonrenal clearance of gemifloxacin from 25.2 (26%) to 21.0 (23%) liters/h. Probenecid inhibited the renal tubular secretion of gemifloxacin, most likely by a competitive mechanism, and slightly decreased nonrenal clearance of gemifloxacin. Probenecid interacts with transport processes of drugs at several sites in the body. For most quinolones, renal clearance is reduced by concomitant administration of probenecid. The interaction between gemifloxacin and probenecid has not yet been studied. We studied the extent, time course, site(s), and mechanism of this interaction. Seventeen healthy volunteers participated in a randomized, two-way crossover study. Subjects received 320 mg gemifloxacin as an oral tablet without and with 4.5 g probenecid divided in eight oral doses. Drug concentrations in plasma and urine were analyzed by liquid chromatography-tandem mass spectrometry. WinNonlin was used for noncompartmental analysis, compartmental modeling, and statistics, and NONMEM was used for visual predictive checks. Concomitant administration of probenecid increased plasma gemifloxacin concentrations and amounts excreted in urine compared to baseline amounts. Data are average estimates (percent coefficients of variation). Modeling showed a competitive inhibition of the renal tubular secretion of gemifloxacin by probenecid as the most likely mechanism of the interaction. The estimated K(m) and Vmax for the saturable part of renal elimination were 9.16 mg/liter (20%) and 113 mg/h (21%), respectively. Based on the molar ratio, the affinity for the renal transporter was 10-fold higher for gemifloxacin than for probenecid. Since probenecid reached an approximately 200-times-higher area under the molar concentration-time curve from 0 to 24 h than gemifloxacin, probenecid inhibited the active tubular secretion of gemifloxacin. Probenecid also reduced the nonrenal clearance of gemifloxacin from 25.2 (26%) to 21.0 (23%) liters/h. Probenecid inhibited the renal tubular secretion of gemifloxacin, most likely by a competitive mechanism, and slightly decreased nonrenal clearance of gemifloxacin. |
| Author | Ulrike Holzgrabe George L. Drusano Jürgen B. Bulitta Fritz Sörgel Cornelia B. Landersdorfer Martina Kinzig Carl M. J. Kirkpatrick |
| AuthorAffiliation | IBMP—Institute for Biomedical and Pharmaceutical Research, Nürnberg-Heroldsberg, Germany, 1 The University of Queensland, School of Pharmacy, Brisbane, Australia, 2 Institute for Pharmacy and Food Chemistry, University of Würzburg, Würzburg, Germany, 3 Ordway Research Institute, Albany, New York, 4 Department of Pharmacology, University of Duisburg-Essen, Essen, Germany 5 |
| AuthorAffiliation_xml | – name: IBMP—Institute for Biomedical and Pharmaceutical Research, Nürnberg-Heroldsberg, Germany, 1 The University of Queensland, School of Pharmacy, Brisbane, Australia, 2 Institute for Pharmacy and Food Chemistry, University of Würzburg, Würzburg, Germany, 3 Ordway Research Institute, Albany, New York, 4 Department of Pharmacology, University of Duisburg-Essen, Essen, Germany 5 |
| Author_xml | – sequence: 1 givenname: Cornelia B. surname: Landersdorfer fullname: Landersdorfer, Cornelia B. organization: IBMP—Institute for Biomedical and Pharmaceutical Research, Nürnberg-Heroldsberg, Germany – sequence: 2 givenname: Carl M. J. surname: Kirkpatrick fullname: Kirkpatrick, Carl M. J. organization: The University of Queensland, School of Pharmacy, Brisbane, Australia – sequence: 3 givenname: Martina surname: Kinzig fullname: Kinzig, Martina organization: IBMP—Institute for Biomedical and Pharmaceutical Research, Nürnberg-Heroldsberg, Germany – sequence: 4 givenname: Jürgen B. surname: Bulitta fullname: Bulitta, Jürgen B. organization: IBMP—Institute for Biomedical and Pharmaceutical Research, Nürnberg-Heroldsberg, Germany – sequence: 5 givenname: Ulrike surname: Holzgrabe fullname: Holzgrabe, Ulrike organization: Institute for Pharmacy and Food Chemistry, University of Würzburg, Würzburg, Germany – sequence: 6 givenname: George L. surname: Drusano fullname: Drusano, George L. organization: Ordway Research Institute, Albany, New York – sequence: 7 givenname: Fritz surname: Sörgel fullname: Sörgel, Fritz organization: IBMP—Institute for Biomedical and Pharmaceutical Research, Nürnberg-Heroldsberg, Germany, Department of Pharmacology, University of Duisburg-Essen, Essen, Germany |
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| Cites_doi | 10.2165/00003088-200140001-00010 10.1007/BF00543976 10.1111/j.1365-2125.2008.03266.x 10.1128/AAC.01410-06 10.1067/mcp.2002.128388 10.2165/00044011-200121070-00008 10.1002/bdd.2510130603 10.1124/mol.107.042853 10.1128/AAC.23.1.1 10.1016/0009-9236(95)90173-6 10.2133/dmpk.21.432 10.1128/AAC.34.1.58 10.1152/ajprenal.00405.2002 10.1128/AAC.41.1.204 10.1128/AAC.39.12.2635 10.1007/s00228-005-0940-7 10.1074/jbc.272.48.30088 10.1128/AAC.01477-06 10.1146/annurev.pharmtox.44.101802.121444 10.1038/clpt.1989.53 10.1128/AAC.44.6.1604-1608.2000 10.1093/jac/40.6.903 10.1128/AAC.17.5.847 10.2165/00003088-199732020-00002 10.1124/jpet.105.085514 10.1002/1615-1003(200109)30:5<418::AID-PAUZ418>3.0.CO;2-# 10.1002/hep.510260641 10.1007/BF00315313 10.1007/BF00374180 10.2165/00003088-199325050-00002 |
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| Keywords | Gemifloxacin Fluoroquinolone derivatives Renal tubule Sulfonamides Secretion Antibacterial agent Competitive inhibition Uricosuric agent Quinolone derivatives Probenecid |
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Reddit... Probenecid interacts with transport processes of drugs at several sites in the body. For most quinolones, renal clearance is reduced by concomitant... |
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| SubjectTerms | Adjuvants, Pharmaceutic Adjuvants, Pharmaceutic - pharmacology Antibiotics. Antiinfectious agents. Antiparasitic agents Biological and medical sciences Female Fluoroquinolones Fluoroquinolones - blood Fluoroquinolones - pharmacokinetics Fluoroquinolones - urine Humans Kidney Function Tests Kidney Tubules Kidney Tubules - drug effects Kidney Tubules - metabolism Male Medical sciences Metabolic Clearance Rate - drug effects Naphthyridines Naphthyridines - blood Naphthyridines - pharmacokinetics Naphthyridines - urine Pharmacology Pharmacology. Drug treatments Probenecid Probenecid - blood Probenecid - pharmacology Probenecid - urine |
| Title | Competitive Inhibition of Renal Tubular Secretion of Gemifloxacin by Probenecid |
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