PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 17116661-8 2007 A significant increase in the accumulation of ATV was noticed in the presence of P-glycoprotein and MRP1 inhibitors (dipyridamole, inter alia). Dipyridamole 117-129 ATP binding cassette subfamily B member 1 Homo sapiens 81-95 12545143-0 2003 Dipyridamole enhances digoxin bioavailability via P-glycoprotein inhibition. Dipyridamole 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 50-64 12545143-1 2003 BACKGROUND: On the basis of in vitro studies indicating that dipyridamole is an inhibitor for the MDR1 efflux membrane transporter P-glycoprotein, we postulated that dipyridamole could increase the bioavailability of digoxin, a P-glycoprotein substrate. Dipyridamole 61-73 ATP binding cassette subfamily B member 1 Homo sapiens 98-102 12545143-1 2003 BACKGROUND: On the basis of in vitro studies indicating that dipyridamole is an inhibitor for the MDR1 efflux membrane transporter P-glycoprotein, we postulated that dipyridamole could increase the bioavailability of digoxin, a P-glycoprotein substrate. Dipyridamole 61-73 ATP binding cassette subfamily B member 1 Homo sapiens 131-145 12545143-1 2003 BACKGROUND: On the basis of in vitro studies indicating that dipyridamole is an inhibitor for the MDR1 efflux membrane transporter P-glycoprotein, we postulated that dipyridamole could increase the bioavailability of digoxin, a P-glycoprotein substrate. Dipyridamole 61-73 ATP binding cassette subfamily B member 1 Homo sapiens 228-242 12545143-1 2003 BACKGROUND: On the basis of in vitro studies indicating that dipyridamole is an inhibitor for the MDR1 efflux membrane transporter P-glycoprotein, we postulated that dipyridamole could increase the bioavailability of digoxin, a P-glycoprotein substrate. Dipyridamole 166-178 ATP binding cassette subfamily B member 1 Homo sapiens 98-102 12545143-1 2003 BACKGROUND: On the basis of in vitro studies indicating that dipyridamole is an inhibitor for the MDR1 efflux membrane transporter P-glycoprotein, we postulated that dipyridamole could increase the bioavailability of digoxin, a P-glycoprotein substrate. Dipyridamole 166-178 ATP binding cassette subfamily B member 1 Homo sapiens 131-145 12545143-1 2003 BACKGROUND: On the basis of in vitro studies indicating that dipyridamole is an inhibitor for the MDR1 efflux membrane transporter P-glycoprotein, we postulated that dipyridamole could increase the bioavailability of digoxin, a P-glycoprotein substrate. Dipyridamole 166-178 ATP binding cassette subfamily B member 1 Homo sapiens 228-242 12545143-4 2003 MATERIAL AND METHODS: (1) The effect of dipyridamole on in vitro P-glycoprotein-mediated, polarized transport of tritium-labeled digoxin was investigated in Caco-2 cell monolayers. Dipyridamole 40-52 ATP binding cassette subfamily B member 1 Homo sapiens 65-79 12545143-11 2003 CONCLUSION: Dipyridamole is an in vitro and in vivo P-glycoprotein inhibitor that increases intestinal digoxin absorption and digoxin plasma concentrations. Dipyridamole 12-24 ATP binding cassette subfamily B member 1 Homo sapiens 52-66 10505047-3 1999 Dexniguldipine-HCl, its analogues B9203-009 and B9303-036, and the dipyridamole derivative BIBW22BS could reverse vincristine (VCR) resistance in BRO/mdr1.1 cells (transfected with full-length MDR1 cDNA) and 2780AD cells (selected for doxorubicin resistance) in vitro. Dipyridamole 67-79 ATP binding cassette subfamily B member 1 Homo sapiens 150-154 10838122-3 2000 Results showed that the accumulation of P-gp substrates calcein-AM and vinblastine by BeWo cells or primary cultures of human cytotrophoblasts was significantly enhanced in the presence of a typical P-gp inhibitor, cyclosporin-A, or other inhibitors such as quinidine, verapamil, and dipyridamole. Dipyridamole 284-296 ATP binding cassette subfamily B member 1 Homo sapiens 40-44 10838122-3 2000 Results showed that the accumulation of P-gp substrates calcein-AM and vinblastine by BeWo cells or primary cultures of human cytotrophoblasts was significantly enhanced in the presence of a typical P-gp inhibitor, cyclosporin-A, or other inhibitors such as quinidine, verapamil, and dipyridamole. Dipyridamole 284-296 ATP binding cassette subfamily B member 1 Homo sapiens 199-203 10543726-8 1999 Dipyridamole and dilazep, two nucleoside membrane transport inhibitors, appear to be P-gp inhibitors. Dipyridamole 0-12 ATP binding cassette subfamily B member 1 Homo sapiens 85-89 10505047-3 1999 Dexniguldipine-HCl, its analogues B9203-009 and B9303-036, and the dipyridamole derivative BIBW22BS could reverse vincristine (VCR) resistance in BRO/mdr1.1 cells (transfected with full-length MDR1 cDNA) and 2780AD cells (selected for doxorubicin resistance) in vitro. Dipyridamole 67-79 ATP binding cassette subfamily B member 1 Homo sapiens 193-197 7654751-5 1995 The ability of DIP to localize near the membrane surface with the substituents immersed into a hydrophobic moiety could be essential for the drug interaction with P-glycoprotein, which is responsible for mediation of the effects of several antitumour drugs. Dipyridamole 15-18 ATP binding cassette subfamily B member 1 Homo sapiens 163-177 27283486-0 2016 Imaging the impact of cyclosporin A and dipyridamole on P-glycoprotein (ABCB1) function at the blood-brain barrier: A [(11)C]-N-desmethyl-loperamide PET study in nonhuman primates. Dipyridamole 40-52 ATP binding cassette subfamily B member 1 Homo sapiens 56-70 8094005-4 1993 Inhibition of PGP efflux function with dipyridamole increased the influx rate constant by 4.0-fold in the KB-GRC1 cells but only 2.1-fold in the KB-3-1 cells. Dipyridamole 39-51 ATP binding cassette subfamily B member 1 Homo sapiens 14-17 27283486-0 2016 Imaging the impact of cyclosporin A and dipyridamole on P-glycoprotein (ABCB1) function at the blood-brain barrier: A [(11)C]-N-desmethyl-loperamide PET study in nonhuman primates. Dipyridamole 40-52 ATP binding cassette subfamily B member 1 Homo sapiens 72-77 27283486-1 2016 Cyclosporin A (CsA) and dipyridamole (DPy) are potent inhibitors of the P-glycoprotein (P-gp; ABCB1) in vitro. Dipyridamole 24-36 ATP binding cassette subfamily B member 1 Homo sapiens 72-86 27283486-1 2016 Cyclosporin A (CsA) and dipyridamole (DPy) are potent inhibitors of the P-glycoprotein (P-gp; ABCB1) in vitro. Dipyridamole 24-36 ATP binding cassette subfamily B member 1 Homo sapiens 88-92 27283486-1 2016 Cyclosporin A (CsA) and dipyridamole (DPy) are potent inhibitors of the P-glycoprotein (P-gp; ABCB1) in vitro. Dipyridamole 24-36 ATP binding cassette subfamily B member 1 Homo sapiens 94-99 27283486-1 2016 Cyclosporin A (CsA) and dipyridamole (DPy) are potent inhibitors of the P-glycoprotein (P-gp; ABCB1) in vitro. Dipyridamole 38-41 ATP binding cassette subfamily B member 1 Homo sapiens 72-86 27283486-1 2016 Cyclosporin A (CsA) and dipyridamole (DPy) are potent inhibitors of the P-glycoprotein (P-gp; ABCB1) in vitro. Dipyridamole 38-41 ATP binding cassette subfamily B member 1 Homo sapiens 88-92 27283486-1 2016 Cyclosporin A (CsA) and dipyridamole (DPy) are potent inhibitors of the P-glycoprotein (P-gp; ABCB1) in vitro. Dipyridamole 38-41 ATP binding cassette subfamily B member 1 Homo sapiens 94-99 27283486-4 2016 In this study, the P-gp inhibition potency at the BBB of therapeutic doses of CsA or DPy was evaluated in baboons using Positron Emission Tomography (PET) imaging with [(11)C]-N-desmethyl-loperamide ([(11)C]dLop), a radiolabeled P-gp substrate. Dipyridamole 85-88 ATP binding cassette subfamily B member 1 Homo sapiens 19-23