Research Articles| May 27 2008 Zur Pharmakologie von Metaboliten des Imipramins Subject Area: Pharmacology W. Theobald; W. Theobald Aus den Forschungslaboratorien der J. R. Geigy A.G., Basel, Schweiz Search for other works by this author on: This Site PubMed Google Scholar O. Büch; O. Büch Aus den Forschungslaboratorien der J. R. Geigy A.G., Basel, Schweiz Search for other works by this author on: This Site PubMed Google Scholar H.A. Kunz; H.A. Kunz Aus den Forschungslaboratorien der J. R. Geigy A.G., Basel, Schweiz Search for other works by this author on: This Site PubMed Google Scholar C. Morpurgo C. Morpurgo Aus den Forschungslaboratorien der J. R. Geigy A.G., Basel, Schweiz Search for other works by this author on: This Site PubMed Google Scholar Medicina et Pharmacologia Experimentalis (1966) 15 (2): 187–197. https://doi.org/10.1159/000135868 Article history Received: December 03 1965 Published Online: July 01 1966 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation W. Theobald, O. Büch, H.A. Kunz, C. Morpurgo; Zur Pharmakologie von Metaboliten des Imipramins. Medicina et Pharmacologia Experimentalis 1 February 1966; 15 (2): 187–197. https://doi.org/10.1159/000135868 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsMedicina et Pharmacologia Experimentalis Search Advanced Search Article PDF first page preview Close Modal Journal Section: Paper This content is only available via PDF. Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. 1966 You do not currently have access to this content.
The disposition of the enantiomers of oxaprotiline has been investigated after single 100 mg oral doses of racemic 14C-labelled oxaprotiline X HCl in two healthy subjects. Absorption was complete. Peak blood concentrations of total 14C were 804 and 1010 ng equiv. g-1 after 4-6 h in the two subjects. After 9 days 85 and 80 per cent of the dose were excreted in urine, and a total of 93 and 87 per cent were found in the excreta. Mean peak blood concentrations of unchanged S(+)- and R(-)-oxaprotiline amounted to 25 and 10 ng g-1 before, and 474 and 422 ng g-1 after acid hydrolysis (free plus O-glucuronide). The mean blood half-lives of the S(+) and R(-) isomers were 22 and 23 h. Direct O-glucuronidation is the major metabolic pathway and N-demethylation a minor one. The former is more marked with the S(+) isomer and the latter with the R(-) isomer. For oxaprotiline, the AUC-ration of S(+) to R(-) was 2.2 before and 1.4 after hydrolysis. For desmethyl oxaprotiline the corresponding ration was 0.8 after hydrolysis. In urine, 0.8 and 0.5 per cent of total 14C were present as unchanged S(+)- and R(-)-oxaprotiline. After acid hydrolysis of the O-glucuronides, the enantiomers account for 44.7 and 37.1 per cent. The O-glucuronides of S(+)- and R(-)-desmethyl oxaprotiline account for 4.6 and 5.7 per cent.
