<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zheng Y</submitter><funding>NCRR NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>2516-26</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4891189</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>32(8)</volume><pubmed_abstract>&lt;h4>Purpose&lt;/h4>Recent controversial publications, citing studies purporting to show that P-gp mediates the transport of propranolol, proposed that passive biological membrane transport is negligible. Based on the BDDCS, the extensively metabolized-highly permeable-highly soluble BDDCS class 1 drug, propranolol, shows a high passive permeability at concentrations unrestricted by solubility that can overwhelm any potential transporter effects. Here we reinvestigate the effects of passive diffusion and carrier-mediated transport on S-propranolol.&lt;h4>Methods&lt;/h4>Bidirectional permeability and inhibition of efflux transport studies were carried out in MDCK, MDCK-MDR1 and Caco-2 cell lines at different concentrations. Transcellular permeability studies were conducted at different apical pHs in </pubmed_abstract><journal>Pharmaceutical research</journal><pubmed_title>pH Dependent but not P-gp Dependent Bidirectional Transport Study of S-propranolol: The Importance of Passive Diffusion.</pubmed_title><pmcid>PMC4891189</pmcid><funding_grant_id>U01 GM061390</funding_grant_id><funding_grant_id>R43 RR031474</funding_grant_id><funding_grant_id>U19 GM061390</funding_grant_id><funding_grant_id>RR031474</funding_grant_id><funding_grant_id>GM061390</funding_grant_id><pubmed_authors>Zheng Y</pubmed_authors><pubmed_authors>Benet LZ</pubmed_authors><pubmed_authors>Chen X</pubmed_authors><pubmed_authors>Okochi H</pubmed_authors></additional><is_claimable>false</is_claimable><name>pH Dependent but not P-gp Dependent Bidirectional Transport Study of S-propranolol: The Importance of Passive Diffusion.</name><description>&lt;h4>Purpose&lt;/h4>Recent controversial publications, citing studies purporting to show that P-gp mediates the transport of propranolol, proposed that passive biological membrane transport is negligible. Based on the BDDCS, the extensively metabolized-highly permeable-highly soluble BDDCS class 1 drug, propranolol, shows a high passive permeability at concentrations unrestricted by solubility that can overwhelm any potential transporter effects. Here we reinvestigate the effects of passive diffusion and carrier-mediated transport on S-propranolol.&lt;h4>Methods&lt;/h4>Bidirectional permeability and inhibition of efflux transport studies were carried out in MDCK, MDCK-MDR1 and Caco-2 cell lines at different concentrations. Transcellular permeability studies were conducted at different apical pHs in </description><dates><release>2015-01-01T00:00:00Z</release><publication>2015 Aug</publication><modification>2025-04-04T02:35:54.176Z</modification><creation>2019-03-27T02:15:11Z</creation></dates><accession>S-EPMC4891189</accession><cross_references><pubmed>25690341</pubmed><doi>10.1007/s11095-015-1640-3</doi></cross_references></HashMap>