PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 34742027-8 2021 In addition, the possible recognition mechanism of compound 5 and verapamil (VRP) with P-gp was predicted by molecular docking. Verapamil 66-75 ATP binding cassette subfamily B member 1 Homo sapiens 87-91 34668334-2 2022 This study aimed to investigate an IVIVE for intestinal P-glycoprotein (Pgp, ABCB1)-mediated DDIs between three Pgp substrates, digoxin, dabigatran etexilate and quinidine, and two Pgp inhibitors, itraconazole and verapamil, via PBPK modeling. Verapamil 214-223 ATP binding cassette subfamily B member 1 Homo sapiens 56-70 34668334-2 2022 This study aimed to investigate an IVIVE for intestinal P-glycoprotein (Pgp, ABCB1)-mediated DDIs between three Pgp substrates, digoxin, dabigatran etexilate and quinidine, and two Pgp inhibitors, itraconazole and verapamil, via PBPK modeling. Verapamil 214-223 ATP binding cassette subfamily B member 1 Homo sapiens 72-75 34668334-2 2022 This study aimed to investigate an IVIVE for intestinal P-glycoprotein (Pgp, ABCB1)-mediated DDIs between three Pgp substrates, digoxin, dabigatran etexilate and quinidine, and two Pgp inhibitors, itraconazole and verapamil, via PBPK modeling. Verapamil 214-223 ATP binding cassette subfamily B member 1 Homo sapiens 77-82 34668334-2 2022 This study aimed to investigate an IVIVE for intestinal P-glycoprotein (Pgp, ABCB1)-mediated DDIs between three Pgp substrates, digoxin, dabigatran etexilate and quinidine, and two Pgp inhibitors, itraconazole and verapamil, via PBPK modeling. Verapamil 214-223 ATP binding cassette subfamily B member 1 Homo sapiens 181-184 34668334-4 2022 For Pgp inhibitors, PBPK models utilized the reported in vitro values of Pgp inhibition constants (Ki ), 1.0 muM for itraconazole and 2.0 muM for verapamil. Verapamil 146-155 ATP binding cassette subfamily B member 1 Homo sapiens 73-76 34935100-8 2022 RESULTS: The data showed that drugs which are known P-gp inhibitors, including cyclosporin A, ketoconazole, and verapamil, caused great increases in rhodamine 123 retention, whereas noninhibitors did not affect the intracellular accumulation of the P-gp substrate. Verapamil 112-121 ATP binding cassette subfamily B member 1 Homo sapiens 52-56 34959345-6 2021 We tested the effect of 15 polyphenols of sour cherry origin on the basal and verapamil-stimulated ATPase activity of Pgp, calcein-AM and daunorubicin transport as well as on the conformation of Pgp using the conformation sensitive UIC2 mAb. Verapamil 78-87 ATP binding cassette subfamily B member 1 Homo sapiens 118-121 34907862-9 2021 Out of 24 AAs, Annonacin A (-8.10 kcal/mol) and Annohexocin (-10.49 kcal/mol) docked with a greater binding affinity at the ATP binding site than the first-generation inhibitor of ABCB1 (Verapamil: -3.86 kcal/mol). Verapamil 187-196 ATP binding cassette subfamily B member 1 Homo sapiens 180-185 34313784-8 2021 Uptake of both Rho123 and paclitaxel was decreased in SNAI1-transfected cells, and this decrease was blocked by verapamil, a P-gp inhibitor. Verapamil 112-121 ATP binding cassette subfamily B member 1 Homo sapiens 125-129 34959345-11 2021 We also investigated the effect of quercetin, naringenin and ellagic acid added in combination with verapamil on the transport activity of Pgp. Verapamil 100-109 ATP binding cassette subfamily B member 1 Homo sapiens 139-142 34794239-6 2021 Cinnamophilin uncompetitively inhibited the efflux of doxorubicin and rhodamine 123 and exhibited a distinct binding behavior compared with verapamil, the P-gp standard inhibitor. Verapamil 140-149 ATP binding cassette subfamily B member 1 Homo sapiens 155-159 34794239-8 2021 In regard to P-gp energy consumption, verapamil-stimulated ATPase activity was further enhanced by cinnamophilin at concentrations of 0.1, 1, 10, and 20 muM. Verapamil 38-47 ATP binding cassette subfamily B member 1 Homo sapiens 13-17 34753107-6 2021 Interestingly, the competitive inhibitor verapamil had lower IC50 values than newer generation inhibitors that are designed to allosterically modulate mammalian P-glycoprotein. Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 161-175 34745981-8 2021 The mechanism underlying Paclitaxel resistance resides in a significant increase in P-glycoprotein expression and, when this drug efflux pump was blocked with Verapamil, cells re-acquired Paclitaxel sensitivity. Verapamil 159-168 ATP binding cassette subfamily B member 1 Homo sapiens 84-98 35471238-2 2022 Recent developments in the studies of drug resistance have identified compounds such as verapamil and tamoxifen that specifically target ABCB1-expressing multidrug resistant (MDR) cells, through an ATP-dependent ROS-generating mechanism. Verapamil 88-97 ATP binding cassette subfamily B member 1 Homo sapiens 137-142 34238184-15 2022 The P-glycoprotein (P-gp) inhibitor, verapamil, and the multidrug resistance resistance-associated proteins (MRPs) inhibitor, MK571, significantly decreased the cellular uptake of fluoxetine. Verapamil 37-46 ATP binding cassette subfamily B member 1 Homo sapiens 4-18 34238184-15 2022 The P-glycoprotein (P-gp) inhibitor, verapamil, and the multidrug resistance resistance-associated proteins (MRPs) inhibitor, MK571, significantly decreased the cellular uptake of fluoxetine. Verapamil 37-46 ATP binding cassette subfamily B member 1 Homo sapiens 20-24 35366514-6 2022 Drug combination studies in PANC-1 cells with C1 and Verapamil hydrochloride (VRP), which is the established inhibitor of efflux transporter P-glycoprotein (Pgp), revealed enhancement of antiproliferative action of the complex in a dose-dependent manner, and slight arrest of cell cycle in the S phase. Verapamil 53-76 ATP binding cassette subfamily B member 1 Homo sapiens 141-155 35366514-6 2022 Drug combination studies in PANC-1 cells with C1 and Verapamil hydrochloride (VRP), which is the established inhibitor of efflux transporter P-glycoprotein (Pgp), revealed enhancement of antiproliferative action of the complex in a dose-dependent manner, and slight arrest of cell cycle in the S phase. Verapamil 53-76 ATP binding cassette subfamily B member 1 Homo sapiens 157-160 35366514-6 2022 Drug combination studies in PANC-1 cells with C1 and Verapamil hydrochloride (VRP), which is the established inhibitor of efflux transporter P-glycoprotein (Pgp), revealed enhancement of antiproliferative action of the complex in a dose-dependent manner, and slight arrest of cell cycle in the S phase. Verapamil 78-81 ATP binding cassette subfamily B member 1 Homo sapiens 141-155 35366514-6 2022 Drug combination studies in PANC-1 cells with C1 and Verapamil hydrochloride (VRP), which is the established inhibitor of efflux transporter P-glycoprotein (Pgp), revealed enhancement of antiproliferative action of the complex in a dose-dependent manner, and slight arrest of cell cycle in the S phase. Verapamil 78-81 ATP binding cassette subfamily B member 1 Homo sapiens 157-160 34516973-5 2021 The docking of triterpenoids 1 and 2 into the drug binding site of P-gp revealed a similarity between the conformation of the tested triterpenoids and that of classical inhibitor verapamil, thus assuming these compounds to be more likely the inhibitors than the substrates of P-gp. Verapamil 179-188 ATP binding cassette subfamily B member 1 Homo sapiens 67-71 34516973-5 2021 The docking of triterpenoids 1 and 2 into the drug binding site of P-gp revealed a similarity between the conformation of the tested triterpenoids and that of classical inhibitor verapamil, thus assuming these compounds to be more likely the inhibitors than the substrates of P-gp. Verapamil 179-188 ATP binding cassette subfamily B member 1 Homo sapiens 276-280 34268580-6 2021 For digoxin, verapamil and quinidine, in vitro kinetic data on their transport by Pgp were derived from literature and used to scale to in vivo parameters. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 82-85 34217736-7 2021 Eleven selected flavonoids significantly induced the basal P-gp-ATPase activity but much lower than that induced by verapamil. Verapamil 116-125 ATP binding cassette subfamily B member 1 Homo sapiens 59-63 35471238-3 2022 In this report, we demonstrate that treatment of ABCB1-expressing multidrug resistant cells (CHORC5 or MDA-Doxo400) or individual clones of the latter with sub-lethal concentrations of tamoxifen or verapamil down-regulates ABCB1 protein and mRNA expression in surviving clones. Verapamil 198-207 ATP binding cassette subfamily B member 1 Homo sapiens 49-54 35471238-3 2022 In this report, we demonstrate that treatment of ABCB1-expressing multidrug resistant cells (CHORC5 or MDA-Doxo400) or individual clones of the latter with sub-lethal concentrations of tamoxifen or verapamil down-regulates ABCB1 protein and mRNA expression in surviving clones. Verapamil 198-207 ATP binding cassette subfamily B member 1 Homo sapiens 223-228 35063459-0 2022 Deregulation of the CD44-NANOG-MDR1 associated chemoresistance pathways of breast cancer stem cells potentiates the anti-cancer effect of Kaempferol in synergism with Verapamil. Verapamil 167-176 ATP binding cassette subfamily B member 1 Homo sapiens 31-35 35350768-5 2022 Furthermore, the resistance of ABCB1-overexpressing cells to palbociclib was reversed by 3 muM of the ABCB1 inhibitor, verapamil. Verapamil 119-128 ATP binding cassette subfamily B member 1 Homo sapiens 31-36 35350768-5 2022 Furthermore, the resistance of ABCB1-overexpressing cells to palbociclib was reversed by 3 muM of the ABCB1 inhibitor, verapamil. Verapamil 119-128 ATP binding cassette subfamily B member 1 Homo sapiens 102-107 35063459-5 2022 We hypothesized that the pathway involved in chemoresistance could be effectively addressed through Kaempferol (K), alone or in combination with Verapamil (V), which is an inhibitor of MDR1. Verapamil 145-154 ATP binding cassette subfamily B member 1 Homo sapiens 185-189 2570070-9 1989 Net transepithelial transport of all these cytotoxic drugs and of verapamil was much higher in epithelia formed by MDCK cells infected with a human MDR1 virus (MDR-MDCK) which is expressed on the apical surface of MDR-MDCK monolayers. Verapamil 66-75 ATP binding cassette subfamily B member 1 Homo sapiens 148-152 2573357-6 1989 An 125I-labeled photoaffinity analog of verapamil labeled P-glycoprotein contained in membranes of HL60/Vinc cells. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 58-72 2569930-0 1989 Reversal mechanism of multidrug resistance by verapamil: direct binding of verapamil to P-glycoprotein on specific sites and transport of verapamil outward across the plasma membrane of K562/ADM cells. Verapamil 46-55 ATP binding cassette subfamily B member 1 Homo sapiens 88-102 2569930-0 1989 Reversal mechanism of multidrug resistance by verapamil: direct binding of verapamil to P-glycoprotein on specific sites and transport of verapamil outward across the plasma membrane of K562/ADM cells. Verapamil 75-84 ATP binding cassette subfamily B member 1 Homo sapiens 88-102 2569930-0 1989 Reversal mechanism of multidrug resistance by verapamil: direct binding of verapamil to P-glycoprotein on specific sites and transport of verapamil outward across the plasma membrane of K562/ADM cells. Verapamil 75-84 ATP binding cassette subfamily B member 1 Homo sapiens 88-102 2569930-5 1989 The Mr 170,000-180,000 verapamil acceptor was immunoprecipitated by monoclonal antibody MRK16 specific for P-glycoprotein associated with multidrug resistance, indicating that P-glycoprotein in the plasma membrane is a major target of verapamil in K562/ADM cells. Verapamil 23-32 ATP binding cassette subfamily B member 1 Homo sapiens 107-121 2569930-5 1989 The Mr 170,000-180,000 verapamil acceptor was immunoprecipitated by monoclonal antibody MRK16 specific for P-glycoprotein associated with multidrug resistance, indicating that P-glycoprotein in the plasma membrane is a major target of verapamil in K562/ADM cells. Verapamil 23-32 ATP binding cassette subfamily B member 1 Homo sapiens 176-190 2569930-5 1989 The Mr 170,000-180,000 verapamil acceptor was immunoprecipitated by monoclonal antibody MRK16 specific for P-glycoprotein associated with multidrug resistance, indicating that P-glycoprotein in the plasma membrane is a major target of verapamil in K562/ADM cells. Verapamil 235-244 ATP binding cassette subfamily B member 1 Homo sapiens 107-121 2569930-5 1989 The Mr 170,000-180,000 verapamil acceptor was immunoprecipitated by monoclonal antibody MRK16 specific for P-glycoprotein associated with multidrug resistance, indicating that P-glycoprotein in the plasma membrane is a major target of verapamil in K562/ADM cells. Verapamil 235-244 ATP binding cassette subfamily B member 1 Homo sapiens 176-190 2569930-7 1989 In addition, the photolabeling was partially blocked by Adriamycin, vincristine, and colchicine, suggesting that the specific binding sites for verapamil on P-glycoprotein are closely related to the binding sites for these calcium channel blockers and antitumor agents. Verapamil 144-153 ATP binding cassette subfamily B member 1 Homo sapiens 157-171 2569930-9 1989 The accumulation of [3H]verapamil in the multidrug-resistant cells was 30% of K562 cells and increased when K562/ADM cells were treated with vincristine and nicardipine at 5 microM, indicating that the P-glycoprotein transports verapamil as well as other antitumor agents in the multidrug-resistant cells. Verapamil 24-33 ATP binding cassette subfamily B member 1 Homo sapiens 202-216 2569930-10 1989 These results suggest that verapamil enhances antitumor agent retention through competition for closely related binding sites on P-glycoprotein. Verapamil 27-36 ATP binding cassette subfamily B member 1 Homo sapiens 129-143 35059317-14 2021 In cells stably overexpressing Gli2, treatment with gradient concentrations of verapamil, an MDR1 inhibitor, significantly inhibited MDR1 expression. Verapamil 79-88 ATP binding cassette subfamily B member 1 Homo sapiens 93-97 35059317-14 2021 In cells stably overexpressing Gli2, treatment with gradient concentrations of verapamil, an MDR1 inhibitor, significantly inhibited MDR1 expression. Verapamil 79-88 ATP binding cassette subfamily B member 1 Homo sapiens 133-137 2790792-8 1989 These results demonstrate the importance of duration of exposure to verapamil in reversing multidrug resistance, not only in cells that overexpress P-glycoprotein but also in cells, such as HL-60/AR, that express little, if any, P-glycoprotein. Verapamil 68-77 ATP binding cassette subfamily B member 1 Homo sapiens 148-162 2790792-8 1989 These results demonstrate the importance of duration of exposure to verapamil in reversing multidrug resistance, not only in cells that overexpress P-glycoprotein but also in cells, such as HL-60/AR, that express little, if any, P-glycoprotein. Verapamil 68-77 ATP binding cassette subfamily B member 1 Homo sapiens 229-243 2572588-11 1989 In contrast, in the HCT-15 cell line, a 5-fold increase of mdr-1/Pgp was accompanied by a comparable fall in vinblastine accumulation which was reversed by verapamil. Verapamil 156-165 ATP binding cassette subfamily B member 1 Homo sapiens 59-64 2572588-11 1989 In contrast, in the HCT-15 cell line, a 5-fold increase of mdr-1/Pgp was accompanied by a comparable fall in vinblastine accumulation which was reversed by verapamil. Verapamil 156-165 ATP binding cassette subfamily B member 1 Homo sapiens 65-68 2565823-2 1989 We show that drugs, such as verapamil, which reverse multidrug resistance (MDR), in P-glycoprotein-overexpressing tumor cells, increased the rate of lactate production in four human MDR cell lines, but not in the parent, sensitive cell lines. Verapamil 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 84-98 2565404-2 1989 The elevated pHi in the most resistant (2,000-fold) variant dropped to the control level upon addition of verapamil, a known inhibitor of P-glycoprotein activity. Verapamil 106-115 ATP binding cassette subfamily B member 1 Homo sapiens 138-152 2565823-7 1989 Verapamil induced an extra amount of ATP consumption in P-glycoprotein-expressing 2780AD cells of approx. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 56-70 2896069-9 1988 However, while net accumulation studies in the presence of 5 micrograms/ml verapamil reversed DOXR to parental values in LoVo colon adenocarcinoma cells, it only minimally decreased DOX resistance (12.6%) in HT1080/DR4 cells. Verapamil 75-84 ATP binding cassette subfamily B member 1 Homo sapiens 94-98 2564428-11 1989 Verapamil increased the intracellular accumulation of doxorubicin and vincristine in vitro for both a P-gly-positive myeloma cell line and tumor cells from two patients with end-stage myeloma which over-expressed P-gly. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 102-107 2564428-11 1989 Verapamil increased the intracellular accumulation of doxorubicin and vincristine in vitro for both a P-gly-positive myeloma cell line and tumor cells from two patients with end-stage myeloma which over-expressed P-gly. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 213-218 2564428-15 1989 The administration of verapamil along with VAD chemotherapy may partially circumvent drug resistance in patients whose tumors over-express P-gly. Verapamil 22-31 ATP binding cassette subfamily B member 1 Homo sapiens 139-144 2900677-14 1988 In contrast, verapamil and trifluoperazine, agents which inhibit active drug efflux and restore drug sensitivity in resistant cells, caused an increase in the P-glycoprotein ATPase activity suggesting that P-glycoprotein might be the target molecule of these agents. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 159-173 2900677-14 1988 In contrast, verapamil and trifluoperazine, agents which inhibit active drug efflux and restore drug sensitivity in resistant cells, caused an increase in the P-glycoprotein ATPase activity suggesting that P-glycoprotein might be the target molecule of these agents. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 206-220 3681376-3 1987 Two criteria suggest that primary multidrug resistance in human adenocarcinomas of the kidney results, at least in part, from expression of the mdr1 gene: (1) mdr1 mRNA levels are elevated in four unselected kidney adenocarcinoma cell lines that show a multidrug-resistant phenotype; and (2) multidrug resistance in these kidney cancer cell lines is reversed by verapamil and quinidine, agents known to reverse mdr1-associated drug resistance in cell lines selected for multidrug resistance in vitro. Verapamil 362-371 ATP binding cassette subfamily B member 1 Homo sapiens 144-148 32229058-18 2021 Isopetasin and S-isopetasin increased the ATPase activity of human P-gp in a comparable fashion as verapamil used as control P-gp inhibitor. Verapamil 99-108 ATP binding cassette subfamily B member 1 Homo sapiens 67-71 33965440-3 2021 This is particularly relevant for compounds such as verapamil that are believed to trap P-gp in a futile transport process that requires continuing ATP consumption. Verapamil 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 88-92 33735724-10 2021 The docking results showed that 5-hydroxy-7,8-dimethoxyflavanone and verapamil exhibited similar binding affinity to P-gp. Verapamil 69-78 ATP binding cassette subfamily B member 1 Homo sapiens 117-121 33514009-1 2021 In this study, the amino acid arginine (ARG) and P-glycoprotein (P-gp) inhibitors verapamil hydrochloride (VER), piperine (PIP) and quercetin (QRT) were used as co-formers for co-amorphous mixtures of a Biopharmaceutics classification system (BCS) class IV drug, furosemide (FUR). Verapamil 82-105 ATP binding cassette subfamily B member 1 Homo sapiens 49-63 33714442-3 2021 In addition, the inhibitory effect of verapamil (Ver), a prototype P-glycoprotein inhibitor, was examined in the module, demonstrating an enhanced Rho123 transfer and accumulation into cells as well as the applicability of the module for P-glycoprotein inhibitor testing. Verapamil 49-52 ATP binding cassette subfamily B member 1 Homo sapiens 238-252 33459729-0 2021 P-glycoprotein inhibition with verapamil overcomes mometasone resistance in Chronic Sinusitis with Nasal Polyps. Verapamil 31-40 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 33459729-3 2021 This study aims to determine whether P-gp inhibition using verapamil enhances mometasone retention and efficacy in nasal polyp explants. Verapamil 59-68 ATP binding cassette subfamily B member 1 Homo sapiens 37-41 33459729-12 2021 This P-gp mediated resistance was successfully reversed by addition of the P-gp inhibitor verapamil. Verapamil 90-99 ATP binding cassette subfamily B member 1 Homo sapiens 5-9 33459729-12 2021 This P-gp mediated resistance was successfully reversed by addition of the P-gp inhibitor verapamil. Verapamil 90-99 ATP binding cassette subfamily B member 1 Homo sapiens 75-79 32852057-2 2021 Verapamil has been shown to be able to reverse development of the multidrug resistance mediated by P-glycoprotein. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 99-113 32852057-5 2021 The results showed that the P-glycoprotein-mediated chemotherapy drug resistance was significantly reversed by verapamil in resistant SW620/Ad300 cells. Verapamil 111-120 ATP binding cassette subfamily B member 1 Homo sapiens 28-42 33714442-3 2021 In addition, the inhibitory effect of verapamil (Ver), a prototype P-glycoprotein inhibitor, was examined in the module, demonstrating an enhanced Rho123 transfer and accumulation into cells as well as the applicability of the module for P-glycoprotein inhibitor testing. Verapamil 38-47 ATP binding cassette subfamily B member 1 Homo sapiens 67-81 33714442-3 2021 In addition, the inhibitory effect of verapamil (Ver), a prototype P-glycoprotein inhibitor, was examined in the module, demonstrating an enhanced Rho123 transfer and accumulation into cells as well as the applicability of the module for P-glycoprotein inhibitor testing. Verapamil 38-47 ATP binding cassette subfamily B member 1 Homo sapiens 238-252 33714442-3 2021 In addition, the inhibitory effect of verapamil (Ver), a prototype P-glycoprotein inhibitor, was examined in the module, demonstrating an enhanced Rho123 transfer and accumulation into cells as well as the applicability of the module for P-glycoprotein inhibitor testing. Verapamil 49-52 ATP binding cassette subfamily B member 1 Homo sapiens 67-81 32885413-3 2021 Using PET imaging, we have shown that BBB P-gp activity is reduced in AD, as quantified by the in vivo brain distribution of the P-gp probe, [11 C]-verapamil. Verapamil 148-157 ATP binding cassette subfamily B member 1 Homo sapiens 42-46 32885413-3 2021 Using PET imaging, we have shown that BBB P-gp activity is reduced in AD, as quantified by the in vivo brain distribution of the P-gp probe, [11 C]-verapamil. Verapamil 148-157 ATP binding cassette subfamily B member 1 Homo sapiens 129-133 33514009-1 2021 In this study, the amino acid arginine (ARG) and P-glycoprotein (P-gp) inhibitors verapamil hydrochloride (VER), piperine (PIP) and quercetin (QRT) were used as co-formers for co-amorphous mixtures of a Biopharmaceutics classification system (BCS) class IV drug, furosemide (FUR). Verapamil 82-105 ATP binding cassette subfamily B member 1 Homo sapiens 65-69 33514009-1 2021 In this study, the amino acid arginine (ARG) and P-glycoprotein (P-gp) inhibitors verapamil hydrochloride (VER), piperine (PIP) and quercetin (QRT) were used as co-formers for co-amorphous mixtures of a Biopharmaceutics classification system (BCS) class IV drug, furosemide (FUR). Verapamil 107-110 ATP binding cassette subfamily B member 1 Homo sapiens 49-63 33514009-1 2021 In this study, the amino acid arginine (ARG) and P-glycoprotein (P-gp) inhibitors verapamil hydrochloride (VER), piperine (PIP) and quercetin (QRT) were used as co-formers for co-amorphous mixtures of a Biopharmaceutics classification system (BCS) class IV drug, furosemide (FUR). Verapamil 107-110 ATP binding cassette subfamily B member 1 Homo sapiens 65-69 32505850-6 2020 Hydantoin derivatives (5-7) were significantly more effective than the reference inhibitor verapamil (up to 2.6-fold at a 10-fold lower concentration) modulating ABCB1-efflux pump, also possessing a good drug-drug interaction profile. Verapamil 91-100 ATP binding cassette subfamily B member 1 Homo sapiens 162-167 32569926-3 2020 These P-gp inhibitors were dramatically effective than verapamil in sensitizing the human ABCB1-overexpressing ABCB1/Flp-In -293 cells and MDR KBvin cells to a series of chemotherapeutic agents, including vincristine and paclitaxel, as manifested by multi-fold decreases in the respective IC50 values to therapeutically attainable levels. Verapamil 55-64 ATP binding cassette subfamily B member 1 Homo sapiens 6-10 32569926-3 2020 These P-gp inhibitors were dramatically effective than verapamil in sensitizing the human ABCB1-overexpressing ABCB1/Flp-In -293 cells and MDR KBvin cells to a series of chemotherapeutic agents, including vincristine and paclitaxel, as manifested by multi-fold decreases in the respective IC50 values to therapeutically attainable levels. Verapamil 55-64 ATP binding cassette subfamily B member 1 Homo sapiens 90-95 32569926-3 2020 These P-gp inhibitors were dramatically effective than verapamil in sensitizing the human ABCB1-overexpressing ABCB1/Flp-In -293 cells and MDR KBvin cells to a series of chemotherapeutic agents, including vincristine and paclitaxel, as manifested by multi-fold decreases in the respective IC50 values to therapeutically attainable levels. Verapamil 55-64 ATP binding cassette subfamily B member 1 Homo sapiens 111-116 33397267-6 2021 RESULTS: Quercetin combined with vincristine showed an effect similar to verapamil (an ABCB1 inhibitor), and the docking showed that bind to ABCB1 in a similar region. Verapamil 73-82 ATP binding cassette subfamily B member 1 Homo sapiens 87-92 33397267-6 2021 RESULTS: Quercetin combined with vincristine showed an effect similar to verapamil (an ABCB1 inhibitor), and the docking showed that bind to ABCB1 in a similar region. Verapamil 73-82 ATP binding cassette subfamily B member 1 Homo sapiens 141-146 33315404-0 2021 Pharmacokinetic Modeling of (R)-[11C]verapamil to Measure the P-Glycoprotein Function in Nonhuman Primates. Verapamil 37-46 ATP binding cassette subfamily B member 1 Homo sapiens 62-76 33383667-9 2020 Inhibiting P-gp activity using verapamil and nicardipine impaired Abeta40 and Abeta42 secretion from both cell types, as determined by ELISA. Verapamil 31-40 ATP binding cassette subfamily B member 1 Homo sapiens 11-15 33197430-0 2020 Efflux mechanism and pathway of verapamil pumping by human P-glycoprotein. Verapamil 32-41 ATP binding cassette subfamily B member 1 Homo sapiens 59-73 33363626-8 2020 The nanoparticles also enhanced in vitro cytotoxicity and downregulation of P-gp expression in MDA-MB 453 cells compared to the commercial inhibitor verapamil hydrochloride, thus promising a piece of exciting evidence for the development of BioPerine based nano-drug delivery system in combination with traditional therapies as a crucial approach to tackling multi-drug resistance in cancers. Verapamil 149-172 ATP binding cassette subfamily B member 1 Homo sapiens 76-80 32377003-9 2020 The flexibility of that loop and the binding of a CS agent like verapamil could favor a particular conformation for the massive transport of GSH, not related to other transport activities of MRP1. Verapamil 64-73 ATP binding cassette subfamily B member 1 Homo sapiens 191-195 32849878-6 2020 all other subpopulations), but verapamil, an inhibitor of ABCB1, only partially mitigated the DXR resistance. Verapamil 31-40 ATP binding cassette subfamily B member 1 Homo sapiens 58-63 32627849-0 2020 P-glycoprotein overactivity in epileptogenic developmental lesions measured in vivo using (R)-[11 C]verapamil PET. Verapamil 100-109 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 32744702-4 2020 Previous studies have demonstrated that verapamil (VER) can reverse drug resistance by inhibiting the P-glycoprotein (P-gp), which is one of the main targets of VER. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 102-116 32744702-4 2020 Previous studies have demonstrated that verapamil (VER) can reverse drug resistance by inhibiting the P-glycoprotein (P-gp), which is one of the main targets of VER. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 118-122 32566390-4 2020 Comparing root mean square deviation (RMSD) of P-gp bound with SECO with that bound to its standard inhibitor verapamil showed that fluctuations in RMSD were lower in P-gp bound to SECO demonstrating higher stability of the complex of P-gp with SECO. Verapamil 110-119 ATP binding cassette subfamily B member 1 Homo sapiens 47-51 32566390-4 2020 Comparing root mean square deviation (RMSD) of P-gp bound with SECO with that bound to its standard inhibitor verapamil showed that fluctuations in RMSD were lower in P-gp bound to SECO demonstrating higher stability of the complex of P-gp with SECO. Verapamil 110-119 ATP binding cassette subfamily B member 1 Homo sapiens 167-171 32566390-4 2020 Comparing root mean square deviation (RMSD) of P-gp bound with SECO with that bound to its standard inhibitor verapamil showed that fluctuations in RMSD were lower in P-gp bound to SECO demonstrating higher stability of the complex of P-gp with SECO. Verapamil 110-119 ATP binding cassette subfamily B member 1 Homo sapiens 167-171 32566390-5 2020 In addition, the superimposition of P-gp structures after MD simulation showed that the nucleotide-binding domains of P-gp bound to SECO undertook a more central closer position compared with that bound to verapamil. Verapamil 206-215 ATP binding cassette subfamily B member 1 Homo sapiens 36-40 32566390-5 2020 In addition, the superimposition of P-gp structures after MD simulation showed that the nucleotide-binding domains of P-gp bound to SECO undertook a more central closer position compared with that bound to verapamil. Verapamil 206-215 ATP binding cassette subfamily B member 1 Homo sapiens 118-122 32627353-4 2020 The patient brains displayed substantial loss of xenobiotic clearance ability, as demonstrated by [11 C]verapamil positron emission tomography (PET) study, linking this phenotype with ABCB1 function. Verapamil 104-113 ATP binding cassette subfamily B member 1 Homo sapiens 184-189 32329770-3 2020 Verapamil hydrochloride and diltiazem hydrochloride are combined P-glycoprotein (P-gp) and CYP3A4 inhibitors and may be associated with increases in the risk of bleeding with DOACs. Verapamil 0-23 ATP binding cassette subfamily B member 1 Homo sapiens 65-79 32431612-4 2020 Pharmacological studies have shown that verapamil has a wide therapeutic spectrum, including antihypertensive, anti-inflammatory, and antioxidative effects, regulation of the blood-brain barrier function, due to its effect on P-glycoprotein, as well as adjustment of cellular calcium homeostasis, which may result in the delay of AD onset or ameliorate the symptoms of patients. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 226-240 32056006-7 2020 ABCB1 function was studied via calcein influx assay under treatment with known ABCB1 inhibitors (verapamil, tariquidar) as well as the kinase inhibitor bosutinib. Verapamil 97-106 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 32329770-3 2020 Verapamil hydrochloride and diltiazem hydrochloride are combined P-glycoprotein (P-gp) and CYP3A4 inhibitors and may be associated with increases in the risk of bleeding with DOACs. Verapamil 0-23 ATP binding cassette subfamily B member 1 Homo sapiens 81-85 32329770-18 2020 This study found increased bleeding risk associated with dabigatran when used concomitantly with the P-gp inhibitors verapamil and diltiazem in individuals with normal kidney function. Verapamil 117-126 ATP binding cassette subfamily B member 1 Homo sapiens 101-105 31936160-7 2020 In terms of P-gp ATPase activity, caffeic acid exhibited stimulation in both basal and verapamil-stimulated activity. Verapamil 87-96 ATP binding cassette subfamily B member 1 Homo sapiens 12-16 32050000-9 2020 These findings indicate that low baseline 99mTc-MIBI uptake that is markedly increased by verapamil represents cancer cells with high levels of MDR1 expression. Verapamil 90-99 ATP binding cassette subfamily B member 1 Homo sapiens 144-148 31704064-6 2020 Moreover, cytotoxicity studies were conducted in the presence of verapamil (20 mg/L), a P-gp inhibitor. Verapamil 65-74 ATP binding cassette subfamily B member 1 Homo sapiens 88-92 32200996-4 2020 Three radiolabeled substrates of the P-gp have been developed for clinical use: [11C]verapamil, [11C]-N-desmethyl-loperamide and [11C]metoclopramide. Verapamil 85-94 ATP binding cassette subfamily B member 1 Homo sapiens 37-41 31751870-8 2020 Although 21 neither affected the P-gp distribution nor expression in HepG2/ADR cells, the amount of P-gp monomer was induced by 21 and verapamil. Verapamil 135-144 ATP binding cassette subfamily B member 1 Homo sapiens 100-104 31715358-7 2020 Compared to the P-glycoprotein (P-gp) inhibition of verapamil, the transport mechanism of CR PMs across intestinal epithelial cells may bypass P-gp efflux. Verapamil 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 16-30 31715358-7 2020 Compared to the P-glycoprotein (P-gp) inhibition of verapamil, the transport mechanism of CR PMs across intestinal epithelial cells may bypass P-gp efflux. Verapamil 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 32-36 31810909-10 2019 Additionally, HCT116RFK866 cells showed improved sensitivity to FK866 when co-treated with verapamil, an ABCB1 inhibitor. Verapamil 91-100 ATP binding cassette subfamily B member 1 Homo sapiens 105-110 31452210-7 2019 In addition, verapamil increased the rate and amount of GA and GB entering cellular/subcellular compartments through inhibition of P-glycoprotein activity, and promoted the protective effect of GDL. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 131-145 31311995-4 2019 Functional inhibition of ABCB1 using vardenafil or verapamil significantly (p <= 0.05-0.001) potentiated the response to three chemotherapeutic drugs (vincristine, etoposide and methotrexate). Verapamil 51-60 ATP binding cassette subfamily B member 1 Homo sapiens 25-30 30353640-5 2019 In this assay, fluorescent reporter substrates (Calcein-AM for MDR1 and MRP1 and mitoxantrone for BCRP, respectively) are trapped in the cytoplasm and pumped out by MDR proteins depending on the presence or absence of specific inhibitors (verapamil for MDR1 and MRP1, indomethacin for MRP1 and KO134 for BCRP, respectively), allowing for quantitative, standardized assessment. Verapamil 239-248 ATP binding cassette subfamily B member 1 Homo sapiens 63-67 30353640-5 2019 In this assay, fluorescent reporter substrates (Calcein-AM for MDR1 and MRP1 and mitoxantrone for BCRP, respectively) are trapped in the cytoplasm and pumped out by MDR proteins depending on the presence or absence of specific inhibitors (verapamil for MDR1 and MRP1, indomethacin for MRP1 and KO134 for BCRP, respectively), allowing for quantitative, standardized assessment. Verapamil 239-248 ATP binding cassette subfamily B member 1 Homo sapiens 253-257 31506301-10 2019 Notably, transporter-mediated DDI simulations between rivaroxaban and P-gp inhibitors (verapamil and ketoconazole) yielded minimal increases in rivaroxaban"s systemic exposure when P-gp-mediated efflux was solely inhibited. Verapamil 87-96 ATP binding cassette subfamily B member 1 Homo sapiens 70-74 31506301-10 2019 Notably, transporter-mediated DDI simulations between rivaroxaban and P-gp inhibitors (verapamil and ketoconazole) yielded minimal increases in rivaroxaban"s systemic exposure when P-gp-mediated efflux was solely inhibited. Verapamil 87-96 ATP binding cassette subfamily B member 1 Homo sapiens 181-185 31127007-6 2019 Compound 8 significantly inhibited boron-dipyrromethene (BODIPY)-verapamil transport mediated by human P-gp (IC50 2.4 +- 0.6 microM); however, the BODIPY-conjugated derivative of 8 (compound 24) was not transported by P-gp. Verapamil 65-74 ATP binding cassette subfamily B member 1 Homo sapiens 103-107 31810909-6 2019 In addition, we analyzed the sensitivity of FK866 in parental HCT116 cells and HCT116RFK866 cells by co-treatment with MDR1 inhibitor verapamil. Verapamil 134-143 ATP binding cassette subfamily B member 1 Homo sapiens 119-123 31585733-6 2019 Moreover, transport of both Ado and Tes was significantly suppressed by verapamil, a typical P-gp inhibitor. Verapamil 72-81 ATP binding cassette subfamily B member 1 Homo sapiens 93-97 31084979-7 2019 The most frequent interactions were amiodarone-statin for CYP3A4 and atorvastatin-verapamil-diltiazem for P-gp. Verapamil 82-91 ATP binding cassette subfamily B member 1 Homo sapiens 106-110 30638237-6 2019 Moreover, DTX-S-OA showed a comparable ability with verapamil in inhibiting P-gp efflux. Verapamil 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 76-80 30959046-8 2019 On the other hand, GBD can downregulate the activity of P-gp ATPase when cotreated with DOX or verapamil, revealing that GBD was a substrate of P-gp. Verapamil 95-104 ATP binding cassette subfamily B member 1 Homo sapiens 56-60 30959046-8 2019 On the other hand, GBD can downregulate the activity of P-gp ATPase when cotreated with DOX or verapamil, revealing that GBD was a substrate of P-gp. Verapamil 95-104 ATP binding cassette subfamily B member 1 Homo sapiens 144-148 31081816-8 2019 For this reason, the P-gp expressing cell line (MDCKII-hMDR1) is either used without or with blocking prior to experiments by means of the P-gp substrate (+-)-verapamil and the results are compared to the ones observed for the wildtype cells. Verapamil 154-168 ATP binding cassette subfamily B member 1 Homo sapiens 21-25 30650062-5 2019 H295R, HAC15, and SW13 cells were treated with mitotane, doxorubicin, etoposide, cisplatin, and streptozotocin, with or without the P-glycoprotein inhibitors verapamil and tariquidar. Verapamil 158-167 ATP binding cassette subfamily B member 1 Homo sapiens 132-146 29428540-9 2018 Additionally, etamicastat was identified as P-gp and BCRP dual substrate, as demonstrated by net flux ratios of 5.84 and 3.87 and decreased >50% by verapamil and Ko143. Verapamil 151-160 ATP binding cassette subfamily B member 1 Homo sapiens 44-48 30659778-3 2019 We conducted virtual drug-drug interactions studies between DABE and the P-glycoprotein inhibitor verapamil in RI populations using physiologically based pharmacokinetic modeling. Verapamil 98-107 ATP binding cassette subfamily B member 1 Homo sapiens 73-87 29338533-9 2019 The p-glycoprotein pump was inhibited by Igepal CO-890 in Caco-2 cells comparable to verapamil. Verapamil 85-94 ATP binding cassette subfamily B member 1 Homo sapiens 4-18 30350627-9 2018 Rh123 was transported in a luminal direction ( Papp,efflux/ Papp,influx = 7) and was blocked by verapamil, a known inhibitor of P-glycoprotein. Verapamil 96-105 ATP binding cassette subfamily B member 1 Homo sapiens 128-142 30572191-6 2019 Obtained results showed that the UA could increase amount of doxorubicin (Dox) entering the cell to accumulate in nuclei, decrease the efflux ratio of digoxin comparable to the effects of the known inhibitor verapamil by acting as a P-gp substrate, decrease the content of intracellular alanine, lactate, pyruvate, glucose, alpha-ketoglutarate, glutamate, glutamine, aspartate, serine, and glycine. Verapamil 208-217 ATP binding cassette subfamily B member 1 Homo sapiens 233-237 30194155-5 2018 RESULTS: First-generation P-glycoprotein (P-gp) inhibitor verapamil required a dose that was nearly four-fold higher than that of ARI for P-gp inhibition, which suggested that ARI had a high specificity for P-gp binding to prevent efflux of anti-mitotic drugs. Verapamil 58-67 ATP binding cassette subfamily B member 1 Homo sapiens 26-40 30194155-5 2018 RESULTS: First-generation P-glycoprotein (P-gp) inhibitor verapamil required a dose that was nearly four-fold higher than that of ARI for P-gp inhibition, which suggested that ARI had a high specificity for P-gp binding to prevent efflux of anti-mitotic drugs. Verapamil 58-67 ATP binding cassette subfamily B member 1 Homo sapiens 42-46 29428540-10 2018 Conversely, nepicastat revealed to be a P-gp-only substrate, with a net flux ratio of 2.01, reduced to 0.92 in the presence of verapamil. Verapamil 127-136 ATP binding cassette subfamily B member 1 Homo sapiens 40-44 28895074-7 2018 Verapamil, a strong inhibitor of P-gp, decreased DOAC efflux in the Caco-2 cell model by 12-87%, depending on the drug tested. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 33-37 29599328-5 2018 Verapamil, an inhibitor of P-glycoprotein, partially enhanced the antiproliferative effects of the agents. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 27-41 29174985-7 2018 In the presence of the selective Pgp inhibitors verapamil (Ver) and valspodar (PSC 833) the effect was, respectively, distinctive and significant. Verapamil 48-57 ATP binding cassette subfamily B member 1 Homo sapiens 33-36 29635947-7 2018 P-gp inducers, carbamazepine, and inhibitors such as itraconazole and verapamil show greater effects on the pharmacokinetics of (S)-fexofenadine. Verapamil 70-79 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 28401570-0 2017 Effect of P-glycoprotein inhibition at the blood-brain barrier on brain distribution of (R)-[11 C]verapamil in elderly vs. young subjects. Verapamil 98-107 ATP binding cassette subfamily B member 1 Homo sapiens 10-24 28560774-9 2017 The effect of verapamil as Pgp inhibitor on DRE requires further evaluation and research. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 27-30 28528287-3 2017 Here we describe the influence of the P-glycoprotein (P-gp) inhibitor verapamil, on the disposition of oxcarbazepine and MHD enantiomers, both of which are P-gp substrates. Verapamil 70-79 ATP binding cassette subfamily B member 1 Homo sapiens 38-52 28528287-3 2017 Here we describe the influence of the P-glycoprotein (P-gp) inhibitor verapamil, on the disposition of oxcarbazepine and MHD enantiomers, both of which are P-gp substrates. Verapamil 70-79 ATP binding cassette subfamily B member 1 Homo sapiens 54-58 28528287-3 2017 Here we describe the influence of the P-glycoprotein (P-gp) inhibitor verapamil, on the disposition of oxcarbazepine and MHD enantiomers, both of which are P-gp substrates. Verapamil 70-79 ATP binding cassette subfamily B member 1 Homo sapiens 156-160 29121121-6 2017 Importantly, rhodamine 123 could increase the Kintrinsic (Ki) value of emodin linearly, whereas, verapamil could not, implying that emodin competitively bound to the R site of P-gp and noncompetition existed between emodin and verapamil at the M site, in a good accordance with the results of molecular docking that emodin bound to the R site of P-gp with higher affinity. Verapamil 227-236 ATP binding cassette subfamily B member 1 Homo sapiens 176-180 29018094-7 2017 Pgp was labeled with LRET probes, reconstituted in lipid nanodiscs, and the distance between the NBDs was measured at 37 C. In the presence of verapamil, a substrate that activates ATP hydrolysis, the NBDs of Pgp reconstituted in nanodiscs were never far apart during the hydrolysis cycle, and we never observed the NBD-NBD distances of tens of A that have previously been reported. Verapamil 144-153 ATP binding cassette subfamily B member 1 Homo sapiens 0-3 29018094-7 2017 Pgp was labeled with LRET probes, reconstituted in lipid nanodiscs, and the distance between the NBDs was measured at 37 C. In the presence of verapamil, a substrate that activates ATP hydrolysis, the NBDs of Pgp reconstituted in nanodiscs were never far apart during the hydrolysis cycle, and we never observed the NBD-NBD distances of tens of A that have previously been reported. Verapamil 144-153 ATP binding cassette subfamily B member 1 Homo sapiens 210-213 29187454-11 2017 Our results showed that JAK2 inhibitors inhibited P-gp action via a direct binding mechanism, which was similar to that of verapamil. Verapamil 123-132 ATP binding cassette subfamily B member 1 Homo sapiens 50-54 29299132-7 2017 Colchicine was used as the substrate for P-glycoprotein (Pgp) and multidrug resistance protein (MRP) 1, cisplatin was used as the substrate for Mrp2 and organic cation transporters 2 (Oct2), and verapamil and MK571 were used as inhibitors of Pgp and MRP1, respectively. Verapamil 195-204 ATP binding cassette subfamily B member 1 Homo sapiens 41-55 28301084-0 2017 The Effect of Verapamil, a P-Glycoprotein Inhibitor, on the Pharmacokinetics of Peficitinib, an Orally Administered, Once-Daily JAK Inhibitor. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 27-41 28301084-3 2017 The effects of verapamil, an inhibitor of the efflux pump P-gp, on the pharmacokinetic profile of peficitinib were assessed in this open-label, single-center, single-sequence, crossover drug-interaction study. Verapamil 15-24 ATP binding cassette subfamily B member 1 Homo sapiens 58-62 28805879-12 2017 Treatment of the resistant cells with verapamil, a known inducer of MDR1, was followed by increased copper-induced toxicity. Verapamil 38-47 ATP binding cassette subfamily B member 1 Homo sapiens 68-72 28943850-7 2017 To determine whether P-glycoprotein (P-gp) efflux affected the cytostatic activity of WND, P-gp was inhibited with verapamil and results indicated that the WND cytostatic effect in MM-CSCs was independent of P-gp efflux. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 37-41 28943850-7 2017 To determine whether P-glycoprotein (P-gp) efflux affected the cytostatic activity of WND, P-gp was inhibited with verapamil and results indicated that the WND cytostatic effect in MM-CSCs was independent of P-gp efflux. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 91-95 28943850-7 2017 To determine whether P-glycoprotein (P-gp) efflux affected the cytostatic activity of WND, P-gp was inhibited with verapamil and results indicated that the WND cytostatic effect in MM-CSCs was independent of P-gp efflux. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 91-95 28669723-8 2017 Our results suggested that the JAK2 inhibitors were able to inhibit P-gp pump-action via a direct binding mechanism, similar to verapamil. Verapamil 128-137 ATP binding cassette subfamily B member 1 Homo sapiens 68-72 28401570-4 2017 METHODS: We performed positron emission tomography scans using the model ABCB1 substrate (R)-[11 C]verapamil in five young [26 +- 1 years, (mean +- standard deviation)] and five elderly (68 +- 6 years) healthy male volunteers before and after intravenous administration of a low dose of the ABCB1 inhibitor tariquidar (3 mg kg-1 ). Verapamil 99-108 ATP binding cassette subfamily B member 1 Homo sapiens 73-78 28385544-1 2017 The purpose of this study was to establish physiologically based pharmacokinetic models to predict in humans the brain concentration-time profiles and P-glycoprotein (Pgp)-mediated brain drug-drug interactions between the model Pgp substrate (R)-[11C]verapamil (VPM), the model dual Pgp/breast cancer resistance protein (BCRP) substrate [11C]tariquidar (TQD), and the Pgp inhibitor tariquidar. Verapamil 251-260 ATP binding cassette subfamily B member 1 Homo sapiens 151-165 28385544-1 2017 The purpose of this study was to establish physiologically based pharmacokinetic models to predict in humans the brain concentration-time profiles and P-glycoprotein (Pgp)-mediated brain drug-drug interactions between the model Pgp substrate (R)-[11C]verapamil (VPM), the model dual Pgp/breast cancer resistance protein (BCRP) substrate [11C]tariquidar (TQD), and the Pgp inhibitor tariquidar. Verapamil 251-260 ATP binding cassette subfamily B member 1 Homo sapiens 167-170 28385544-1 2017 The purpose of this study was to establish physiologically based pharmacokinetic models to predict in humans the brain concentration-time profiles and P-glycoprotein (Pgp)-mediated brain drug-drug interactions between the model Pgp substrate (R)-[11C]verapamil (VPM), the model dual Pgp/breast cancer resistance protein (BCRP) substrate [11C]tariquidar (TQD), and the Pgp inhibitor tariquidar. Verapamil 251-260 ATP binding cassette subfamily B member 1 Homo sapiens 228-231 28385544-1 2017 The purpose of this study was to establish physiologically based pharmacokinetic models to predict in humans the brain concentration-time profiles and P-glycoprotein (Pgp)-mediated brain drug-drug interactions between the model Pgp substrate (R)-[11C]verapamil (VPM), the model dual Pgp/breast cancer resistance protein (BCRP) substrate [11C]tariquidar (TQD), and the Pgp inhibitor tariquidar. Verapamil 251-260 ATP binding cassette subfamily B member 1 Homo sapiens 228-231 27504932-6 2017 While pharmacological inhibition of either MDR1, ABCG2, Bcl-2 with Verapamil, Sorafenib, or Obatoclax, respectively decreased the levels of their target proteins under routine culture conditions as expected, such inhibition did not reverse PX resistance in PPSS conditions. Verapamil 67-76 ATP binding cassette subfamily B member 1 Homo sapiens 43-47 30108713-8 2017 Five compounds in group A, bearing a 2-pyridyl methyl ester substituent at the C3 position, significantly increased rhodamine accumulation at 25 muM comparable to verapamil, a well-established P-gp inhibitor, while only 2 compounds in group B bearing 3-pyridyl methyl ester at the same position had this effect. Verapamil 163-172 ATP binding cassette subfamily B member 1 Homo sapiens 193-197 28536971-2 2017 METHODS: DOX resistant K562 (K562R) cells were developed and reversal of resistance by P-gp inhibitor was validated by co-treatment with verapamil. Verapamil 137-146 ATP binding cassette subfamily B member 1 Homo sapiens 87-91 28530401-4 2017 Here, zeolitic imidazolate framework ZIF-8, as one of the biocompatible metal organic frameworks (MOFs), is reported for the first time as the multidrug carrier to realizing the efficient codelivery of verapamil hydrochloride (VER) as the P-glycoprotein inhibitor as well as doxorubicin hydrochloride (DOX) as an anticancer drug to overcome the MDR in addition to realize the active targeted ability for an efficient anticancer effect. Verapamil 202-225 ATP binding cassette subfamily B member 1 Homo sapiens 239-253 28533092-9 2017 Similarly, the presence of DM did not alter the locations of other drug-binding sites since the thiol reactive forms of the substrates verapamil or rhodamine labeled the same sites in transmembrane segments 5 (I306C for verapamil) and 6 (F343C for rhodamine) whether P-gp was in native membranes or in detergent micelles. Verapamil 135-144 ATP binding cassette subfamily B member 1 Homo sapiens 267-271 28385544-1 2017 The purpose of this study was to establish physiologically based pharmacokinetic models to predict in humans the brain concentration-time profiles and P-glycoprotein (Pgp)-mediated brain drug-drug interactions between the model Pgp substrate (R)-[11C]verapamil (VPM), the model dual Pgp/breast cancer resistance protein (BCRP) substrate [11C]tariquidar (TQD), and the Pgp inhibitor tariquidar. Verapamil 251-260 ATP binding cassette subfamily B member 1 Homo sapiens 228-231 28126516-2 2017 The most potent derivatives (1, 9-11) inhibited the ABCB1 efflux pump much stronger than the reference compound verapamil. Verapamil 112-121 ATP binding cassette subfamily B member 1 Homo sapiens 52-57 28389777-7 2017 A similar effect has been reported by the p-glycoprotein inhibitor verapamil. Verapamil 67-76 ATP binding cassette subfamily B member 1 Homo sapiens 42-56 27813130-5 2017 When verapamil, a P-gp inhibitor, was combined with the proteasome inhibitor MG132, bortezomib, or carfilzomib, the cytotoxic effects and apoptosis in TNBC MDA-MB-231 cells were enhanced, compared to each treatment alone. Verapamil 5-14 ATP binding cassette subfamily B member 1 Homo sapiens 18-22 28028729-7 2017 A number of in vitro and in vivo studies have already demonstrated DDIs from several cardiovascular ion channel inhibitors with human Pgp and its animal analogs, including verapamil, digoxin, and amiodarone. Verapamil 172-181 ATP binding cassette subfamily B member 1 Homo sapiens 134-137 27926506-5 2017 When scar fibroblasts were pre-treated with PSC833 or probenecid, a P-glycoprotein or MRP1 inhibitor respectively, the resistance to verapamil or etoposide was strongly attenuated. Verapamil 133-142 ATP binding cassette subfamily B member 1 Homo sapiens 68-82 27325447-5 2016 Transport studies across Caco-2 cell monolayers in the presence and absence of a P-glycoprotein (P-gp) inhibitor, verapamil, indicated that the para-iodo-substituted analog was not a P-gp transport substrate; this feature is a prerequisite for potential in vivo brain imaging compounds. Verapamil 114-123 ATP binding cassette subfamily B member 1 Homo sapiens 81-95 27538919-6 2016 The best predictability of FaFg was achieved when considering both SFCYP3A and SFP-gp The simulation also clarified the relative importance of CYP3A and P-gp in determining FaFg In particular, the nonlinear intestinal absorption of verapamil was caused by the saturation of intestinal CYP3A, whereas that of quinidine was governed by the saturation of both CYP3A and P-gp. Verapamil 232-241 ATP binding cassette subfamily B member 1 Homo sapiens 81-85 27538919-6 2016 The best predictability of FaFg was achieved when considering both SFCYP3A and SFP-gp The simulation also clarified the relative importance of CYP3A and P-gp in determining FaFg In particular, the nonlinear intestinal absorption of verapamil was caused by the saturation of intestinal CYP3A, whereas that of quinidine was governed by the saturation of both CYP3A and P-gp. Verapamil 232-241 ATP binding cassette subfamily B member 1 Homo sapiens 153-157 30475507-5 2016 To test the effects of Maldi 531.2[M+H](+) on MDR activity, an attempt to combine Maldi 531.2[M+H](+) with a potent P-gp substrate such as verapamil was performed. Verapamil 139-148 ATP binding cassette subfamily B member 1 Homo sapiens 116-120 30475507-8 2016 Verapamil is a strong substrate to P-gp. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 35-39 30475507-10 2016 On the one hand, verapamil and Maldi 531.2[M+H](+) exerted cooperative stimulation on P-gp. Verapamil 17-26 ATP binding cassette subfamily B member 1 Homo sapiens 86-90 27531061-0 2016 Cooperativity between verapamil and ATP bound to the efflux transporter P-glycoprotein. Verapamil 22-31 ATP binding cassette subfamily B member 1 Homo sapiens 72-86 27531061-3 2016 The cardiovascular drug verapamil is one of the most widely studied Pgp substrates and therefore, represents an ideal drug to investigate the drug-induced ATPase activation of Pgp. Verapamil 24-33 ATP binding cassette subfamily B member 1 Homo sapiens 68-71 27531061-3 2016 The cardiovascular drug verapamil is one of the most widely studied Pgp substrates and therefore, represents an ideal drug to investigate the drug-induced ATPase activation of Pgp. Verapamil 24-33 ATP binding cassette subfamily B member 1 Homo sapiens 176-179 27531061-4 2016 As previously noted, verapamil-induced Pgp-mediated ATP hydrolysis kinetics was biphasic at saturating ATP concentrations. Verapamil 21-30 ATP binding cassette subfamily B member 1 Homo sapiens 39-42 27531061-6 2016 To further understand this switch in kinetic behavior, the Pgp-coupled ATPase activity kinetics was checked with a panel of verapamil and ATP concentrations and fit with the substrate inhibition equation and the kinetic fitting software COPASI. Verapamil 124-133 ATP binding cassette subfamily B member 1 Homo sapiens 59-62 27531061-8 2016 Fluorescence spectroscopy of Pgp revealed that cooperativity between verapamil and a non-hydrolyzable ATP analog leads to distinct global conformational changes of Pgp. Verapamil 69-78 ATP binding cassette subfamily B member 1 Homo sapiens 29-32 27531061-8 2016 Fluorescence spectroscopy of Pgp revealed that cooperativity between verapamil and a non-hydrolyzable ATP analog leads to distinct global conformational changes of Pgp. Verapamil 69-78 ATP binding cassette subfamily B member 1 Homo sapiens 164-167 27531061-9 2016 NMR of Pgp reconstituted in liposomes showed that cooperativity between verapamil and the non-hydrolyzable ATP analog modulate each other"s interactions. Verapamil 72-81 ATP binding cassette subfamily B member 1 Homo sapiens 7-10 27306525-8 2016 MRP1 and P-gp targeted therapy using MK571, Verapamil, CoCl2 or ambient hypoxia appeared to be promising in abolishing the DOX efflux and DOX resistance of the NSCLC cells. Verapamil 44-53 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 27306525-8 2016 MRP1 and P-gp targeted therapy using MK571, Verapamil, CoCl2 or ambient hypoxia appeared to be promising in abolishing the DOX efflux and DOX resistance of the NSCLC cells. Verapamil 44-53 ATP binding cassette subfamily B member 1 Homo sapiens 9-13 29521222-4 2017 RESULTS: We observed that quinidine, a substrate for MDR1 transporter, showed efflux ratio (Papp B-A/ Papp A-B) of 838 in MDCKII-MDR1 cells which plummeted to 14 in presence of verapamil, a known inhibitor of MDR1. Verapamil 177-186 ATP binding cassette subfamily B member 1 Homo sapiens 53-57 29521222-4 2017 RESULTS: We observed that quinidine, a substrate for MDR1 transporter, showed efflux ratio (Papp B-A/ Papp A-B) of 838 in MDCKII-MDR1 cells which plummeted to 14 in presence of verapamil, a known inhibitor of MDR1. Verapamil 177-186 ATP binding cassette subfamily B member 1 Homo sapiens 129-133 29521222-4 2017 RESULTS: We observed that quinidine, a substrate for MDR1 transporter, showed efflux ratio (Papp B-A/ Papp A-B) of 838 in MDCKII-MDR1 cells which plummeted to 14 in presence of verapamil, a known inhibitor of MDR1. Verapamil 177-186 ATP binding cassette subfamily B member 1 Homo sapiens 129-133 28421447-3 2017 P-gp blocker verapamil suppressed doxorubicin accumulation leading to cell death induction. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 27883364-5 2017 Phloridzin and verapamil as inhibitors of sodium glucose transport protein (SGLT1) and P-glycoprotein, respectively, were not responsible for cellular uptake of SMM. Verapamil 15-24 ATP binding cassette subfamily B member 1 Homo sapiens 87-101 27836711-4 2016 In type I-like cells, rhodamine 123 (Rho123) accumulation was enhanced by various P-gp inhibitors such as verapamil and cyclosporine A. Verapamil 106-115 ATP binding cassette subfamily B member 1 Homo sapiens 82-86 27286705-8 2016 The decrease of DOX uptake was blocked by verapamil, a P-gp inhibitor. Verapamil 42-51 ATP binding cassette subfamily B member 1 Homo sapiens 55-59 27318188-13 2016 The control P-gp inhibitor, verapamil, partially increased doxorubicin uptake in CEM/ADR5000 cells. Verapamil 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 12-16 27415012-4 2016 MTT assays were used to assess chemosensitivity to paclitaxel and olaparib in drug-sensitive and drug-resistant cells+-the ABCB1 inhibitors verapamil and elacridar and cross-resistance to cisplatin, carboplatin, doxorubicin, rucaparib, veliparib and AZD2461. Verapamil 140-149 ATP binding cassette subfamily B member 1 Homo sapiens 123-128 27415012-7 2016 Resistance correlated with increased ABCB1 expression and was reversible following treatment with the ABCB1 inhibitors verapamil and elacridar. Verapamil 119-128 ATP binding cassette subfamily B member 1 Homo sapiens 37-42 27415012-7 2016 Resistance correlated with increased ABCB1 expression and was reversible following treatment with the ABCB1 inhibitors verapamil and elacridar. Verapamil 119-128 ATP binding cassette subfamily B member 1 Homo sapiens 102-107 27499787-8 2016 Digoxin and verapamil were used as a known substrate and inhibitor of P-gp, respectively. Verapamil 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 70-74 27060927-11 2016 CDX2 induced MDR1-dependent resistance to vincristine and paclitaxel, which was reversed by treatment with the MDR1-specific inhibitor verapamil. Verapamil 135-144 ATP binding cassette subfamily B member 1 Homo sapiens 13-17 27060927-11 2016 CDX2 induced MDR1-dependent resistance to vincristine and paclitaxel, which was reversed by treatment with the MDR1-specific inhibitor verapamil. Verapamil 135-144 ATP binding cassette subfamily B member 1 Homo sapiens 111-115 27177126-2 2016 Verapamil can enhance the cytotoxic effects of chemotherapeutic drugs and multidrug resistance by targeting the transport function of the P-glycoprotein (P-gp). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 138-152 27177126-2 2016 Verapamil can enhance the cytotoxic effects of chemotherapeutic drugs and multidrug resistance by targeting the transport function of the P-glycoprotein (P-gp). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 154-158 27177126-7 2016 A pro-apoptotic effect of verapamil was observed in L3.6pl cells, but not in L3.6plGres cells, which was linked to their differential expression of P-gp and equilibrative nucleoside transporter-1 (ENT-1). Verapamil 26-35 ATP binding cassette subfamily B member 1 Homo sapiens 148-152 26514967-1 2016 PURPOSE: Oxcarbazepine (OXC), a second-generation antiepileptic, and its chiral metabolite 10-hydroxycarbazepine (MHD) are substrates of P-glycoprotein, which can be inhibited by verapamil. Verapamil 179-188 ATP binding cassette subfamily B member 1 Homo sapiens 137-151 26585254-2 2016 To evaluate the brain expression of p-glycoprotein in patients with drug-resistant epilepsy, including neocortical epilepsy, we developed a noninvsive quantitative analysis including asymmetry indices based on (R)-[(11)C]-verapamil PET/MR imaging with cyclosporin A, a p-glycoprotein inhibitor. Verapamil 222-231 ATP binding cassette subfamily B member 1 Homo sapiens 36-50 26836364-5 2016 Analogues 6, 24, 28, 59, and 66 were identified as having higher potency than compound 1 and verapamil, a first-generation P-gp modulator. Verapamil 93-102 ATP binding cassette subfamily B member 1 Homo sapiens 123-127 27114800-10 2016 Adding verapamil, a P-glycoprotein inhibitor caused a further increase in the percentage of apoptotic cells when the cells were treated with both agents. Verapamil 7-16 ATP binding cassette subfamily B member 1 Homo sapiens 20-34 26514967-9 2016 CONCLUSION: Verapamil increased the AUC values of both MDH enantiomers, which is probably related to the inhibition of intestinal P-glycoprotein. Verapamil 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 130-144 26823559-0 2016 Unravelling the complex drug-drug interactions of the cardiovascular drugs, verapamil and digoxin, with P-glycoprotein. Verapamil 76-85 ATP binding cassette subfamily B member 1 Homo sapiens 104-118 26823559-3 2016 The calcium channel antagonist, verapamil and the cardiac glycoside, digoxin, exhibit DDIs with Pgp through non-competitive inhibition of digoxin transport, which leads to elevated digoxin plasma concentrations and digoxin toxicity. Verapamil 32-41 ATP binding cassette subfamily B member 1 Homo sapiens 96-99 26823559-4 2016 In the present study, verapamil-induced ATPase activation kinetics were biphasic implying at least two verapamil-binding sites on Pgp, whereas monophasic digoxin activation of Pgp-coupled ATPase kinetics suggested a single digoxin-binding site. Verapamil 22-31 ATP binding cassette subfamily B member 1 Homo sapiens 130-133 26823559-4 2016 In the present study, verapamil-induced ATPase activation kinetics were biphasic implying at least two verapamil-binding sites on Pgp, whereas monophasic digoxin activation of Pgp-coupled ATPase kinetics suggested a single digoxin-binding site. Verapamil 103-112 ATP binding cassette subfamily B member 1 Homo sapiens 130-133 26823559-6 2016 Higher concentrations of verapamil caused significant disruption of digoxin-Pgp interactions that suggested overlapping and competing drug-binding sites. Verapamil 25-34 ATP binding cassette subfamily B member 1 Homo sapiens 76-79 26823559-8 2016 Also, Pgp-coupled ATPase activity kinetics measured with a range of verapamil and digoxin concentrations fit well to a DDI model encompassing non-competitive and competitive inhibition of digoxin by verapamil. Verapamil 68-77 ATP binding cassette subfamily B member 1 Homo sapiens 6-9 26823559-8 2016 Also, Pgp-coupled ATPase activity kinetics measured with a range of verapamil and digoxin concentrations fit well to a DDI model encompassing non-competitive and competitive inhibition of digoxin by verapamil. Verapamil 199-208 ATP binding cassette subfamily B member 1 Homo sapiens 6-9 26565618-6 2016 Cancer cell viability screening confirmed 1-8 were cytotoxic to human colorectal carcinoma cells (IC50 > 3 muM), and were inhibitors of the ABC transporter efflux pump P-glycoprotein (P-gp), with 5 being comparable in potency to the positive control verapamil. Verapamil 253-262 ATP binding cassette subfamily B member 1 Homo sapiens 171-185 27494065-5 2016 PET imaging of P-gp function was first demonstrated in 1998 with the substrate tracer racemic [11C]verapamil. Verapamil 99-108 ATP binding cassette subfamily B member 1 Homo sapiens 15-19 27022464-5 2015 To this end, the present study investigates whether chronic treatment with the P-gp inhibitor verapamil and the antidepressant escitalopram results in enhanced brain distribution and antidepressant-like effects of escitalopram. Verapamil 94-103 ATP binding cassette subfamily B member 1 Homo sapiens 79-83 26455657-5 2015 Bidirectional transport cellular studies using Caco-2 cell culture model in the presence of the P-glycoprotein (P-gp) inhibitor, verapamil, showed that P-gp did not have a significant effect on the efflux of the para-methoxy substituted analog. Verapamil 129-138 ATP binding cassette subfamily B member 1 Homo sapiens 96-110 26455657-5 2015 Bidirectional transport cellular studies using Caco-2 cell culture model in the presence of the P-glycoprotein (P-gp) inhibitor, verapamil, showed that P-gp did not have a significant effect on the efflux of the para-methoxy substituted analog. Verapamil 129-138 ATP binding cassette subfamily B member 1 Homo sapiens 112-116 26352530-9 2015 In addition, the transportation of BER on the BL-AP surface was significantly faster (P<0.01), compared with that on the AP-BL surface and, following the addition of verpamil (a P-gp inhibitor), the Papp (AP-BL) of the four alkaloids increased, whereas the Papp (BL-AP) was significantly decreased (P<0.01). Verapamil 169-177 ATP binding cassette subfamily B member 1 Homo sapiens 181-185 27022464-2 2015 Specifically, acute administration of P-gp inhibitors, such as verapamil and cyclosporin A (CsA), has been shown to augment brain concentrations and functional activity of the antidepressant escitalopram in rodents. Verapamil 63-72 ATP binding cassette subfamily B member 1 Homo sapiens 38-42 26272936-7 2015 The resistance was reversed in the presence of the P-gp inhibitor verapamil. Verapamil 66-75 ATP binding cassette subfamily B member 1 Homo sapiens 51-55 26357852-5 2015 In addition, verapamil, a calcium ion channel blocker known to reverse P-glycoprotein (P-gp) mediated drug resistance, was used in combination with multiple cytochalasin congeners to determine whether drug sensitivity could be increased. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 71-85 26357852-5 2015 In addition, verapamil, a calcium ion channel blocker known to reverse P-glycoprotein (P-gp) mediated drug resistance, was used in combination with multiple cytochalasin congeners to determine whether drug sensitivity could be increased. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 87-91 26295572-4 2015 Following co-treatment of these cells with each CLA enantiomer and verapamil as a P-gp inhibitor, the (+)-isomer clearly antagonized the inhibitory effects of verapamil on P-gp efflux, whereas the (-)-isomer had slightly synergistic or additive effects. Verapamil 67-76 ATP binding cassette subfamily B member 1 Homo sapiens 82-86 26295572-4 2015 Following co-treatment of these cells with each CLA enantiomer and verapamil as a P-gp inhibitor, the (+)-isomer clearly antagonized the inhibitory effects of verapamil on P-gp efflux, whereas the (-)-isomer had slightly synergistic or additive effects. Verapamil 159-168 ATP binding cassette subfamily B member 1 Homo sapiens 172-176 25932627-8 2015 The Kp for digoxin, verapamil and docetaxel were 2, 16 and 2-times higher in the hMDR1 compared to the C57BL/6 WT mice. Verapamil 20-29 ATP binding cassette subfamily B member 1 Homo sapiens 81-86 26287374-10 2015 The expression of P-gp and the cell toxicity was determined in colistin with or without dexamethasone (P-gp inducer) and verapamil (selective P-gp inhibitor). Verapamil 121-130 ATP binding cassette subfamily B member 1 Homo sapiens 18-22 26171231-2 2015 Verapamil has been described as a P-glycoprotein (P-gp, ABCB1) substrate. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 34-48 26171231-2 2015 Verapamil has been described as a P-glycoprotein (P-gp, ABCB1) substrate. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 50-54 26171231-2 2015 Verapamil has been described as a P-glycoprotein (P-gp, ABCB1) substrate. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 56-61 26171231-3 2015 We wished to evaluate in vitro whether co administration of a P-gp inhibitor with verapamil could be a feasible strategy for increasing CNS uptake of verapamil. Verapamil 150-159 ATP binding cassette subfamily B member 1 Homo sapiens 62-66 26171231-4 2015 Fluxes of radiolabelled verapamil across MDCK II MDR1 monolayers were measured in the absence and presence of the putative P-gp inhibitor telmisartan (a clinically approved drug compound). Verapamil 24-33 ATP binding cassette subfamily B member 1 Homo sapiens 49-53 26171231-5 2015 Verapamil displayed a vectorial basolateral-to-apical transepithelial efflux across the MDCK II MDR1 monolayers with a permeability of 5.7 x 10(-5) cm sec(-1) compared to an apical to basolateral permeability of 1.3 x 10(-5) cm sec(-1). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 96-100 26171231-8 2015 The presence of telmisartan, however, only caused a slight reduction in P-gp-mediated verapamil transport to an efflux ratio of 3.4. Verapamil 86-95 ATP binding cassette subfamily B member 1 Homo sapiens 72-76 26219569-8 2015 Transfection with siRNA directed against P-gp or treatment with verapamil, an inhibitor of P-gp, restored the sensitivity to the drug in all cells with acquired resistance to 17-DMAG. Verapamil 64-73 ATP binding cassette subfamily B member 1 Homo sapiens 91-95 26182353-8 2015 We verified the overexpression of P-glycoprotein and confirmed its function by reversing the drug resistance with P-gp inhibitor Verapamil. Verapamil 129-138 ATP binding cassette subfamily B member 1 Homo sapiens 34-48 26182353-8 2015 We verified the overexpression of P-glycoprotein and confirmed its function by reversing the drug resistance with P-gp inhibitor Verapamil. Verapamil 129-138 ATP binding cassette subfamily B member 1 Homo sapiens 114-118 26149173-8 2015 K562DOX cells showed the lowest intracellular level of bosutinib, while K562DOX cells treated with the ABCB1 inhibitor verapamil showed intracellular bosutinib levels comparable with parental K562S. Verapamil 119-128 ATP binding cassette subfamily B member 1 Homo sapiens 103-108 26121397-6 2015 The results of P-glycoprotein (P-gp) inhibitor (verapamil) experiments showed that the transport of coumarin 4 was affected by the transport protein P-gp. Verapamil 48-57 ATP binding cassette subfamily B member 1 Homo sapiens 15-29 26121397-6 2015 The results of P-glycoprotein (P-gp) inhibitor (verapamil) experiments showed that the transport of coumarin 4 was affected by the transport protein P-gp. Verapamil 48-57 ATP binding cassette subfamily B member 1 Homo sapiens 31-35 26121397-6 2015 The results of P-glycoprotein (P-gp) inhibitor (verapamil) experiments showed that the transport of coumarin 4 was affected by the transport protein P-gp. Verapamil 48-57 ATP binding cassette subfamily B member 1 Homo sapiens 149-153 25824830-4 2015 Both inhibition of P-gp function by verapamil and inhibition of its transcription using mRNA silencing led to a reduction in the magnitude of the type I response in infected cells. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 19-23 25779097-9 2015 Molecular docking model displayed that the positions of ganoderenic acid B binding to ABCB1 were different from the region of verapamil interacted with ABCB1. Verapamil 126-135 ATP binding cassette subfamily B member 1 Homo sapiens 152-157 26125482-6 2015 We observed reproducible transport of two substrates, daunorubicin and verapamil, by an average of 11-12 A through the plane of the membrane as P-gp progressed through a catalytic cycle. Verapamil 71-80 ATP binding cassette subfamily B member 1 Homo sapiens 144-148 26026084-6 2015 The inhibition of the ABCB1 transporter was greater in the presence of the phenothiazine derivatives than for the known ABCB1 inhibitor verapamil. Verapamil 136-145 ATP binding cassette subfamily B member 1 Homo sapiens 22-27 26026084-6 2015 The inhibition of the ABCB1 transporter was greater in the presence of the phenothiazine derivatives than for the known ABCB1 inhibitor verapamil. Verapamil 136-145 ATP binding cassette subfamily B member 1 Homo sapiens 120-125 25596698-8 2015 The combination of PGRMC1 knockdown and the P-glycoprotein inhibitor verapamil significantly decreased the viability of P-glycoprotein-overexpressing MES-SA/DxR-8 muM cells after doxorubicin treatment. Verapamil 69-78 ATP binding cassette subfamily B member 1 Homo sapiens 44-58 25596698-8 2015 The combination of PGRMC1 knockdown and the P-glycoprotein inhibitor verapamil significantly decreased the viability of P-glycoprotein-overexpressing MES-SA/DxR-8 muM cells after doxorubicin treatment. Verapamil 69-78 ATP binding cassette subfamily B member 1 Homo sapiens 120-134 25695368-4 2015 Four compounds from this series were discovered as potent chemosensitizers for MDR1-G185 NIH-3T3 murine cells (3, 4, 6, and 7), showing higher efficacies than the classical P-glycoprotein inhibitor verapamil, a first-generation chemosensitizer, when reversing resistance to daunomycin and vinblastine at the lowest concentration tested of 1 muM. Verapamil 198-207 ATP binding cassette subfamily B member 1 Homo sapiens 173-187 25590413-6 2015 The resistance was reversed by co-treatment of MG132 and the ABCB1 inhibitor verapamil. Verapamil 77-86 ATP binding cassette subfamily B member 1 Homo sapiens 61-66 25689592-5 2015 RESULTS: Results showed that HZ08 was more potent than verapamil in MDCK-MDR1 monolayer transportation model. Verapamil 55-64 ATP binding cassette subfamily B member 1 Homo sapiens 73-77 25450342-7 2015 For P-gp liposomes, the kT value was significantly higher in the presence of ATP than in its absence or in the presence of ATP and the competitive inhibitor verapamil. Verapamil 157-166 ATP binding cassette subfamily B member 1 Homo sapiens 4-8 25510604-2 2015 Also, it was reported that verapamil (VP) could inhibit p-gp efflux. Verapamil 27-36 ATP binding cassette subfamily B member 1 Homo sapiens 56-60 25510604-2 2015 Also, it was reported that verapamil (VP) could inhibit p-gp efflux. Verapamil 38-40 ATP binding cassette subfamily B member 1 Homo sapiens 56-60 24621440-12 2015 The docking study indicated that cabozantinib and verapamil may partially share a binding site on P-gp. Verapamil 50-59 ATP binding cassette subfamily B member 1 Homo sapiens 98-102 25437111-4 2015 Active inhibition of efflux pumps was achieved by encapsulating first and third generation P-gp inhibitors- verapamil and elacridar respectively in non-ionic, anionic and cationic surfactant-based NPs. Verapamil 108-117 ATP binding cassette subfamily B member 1 Homo sapiens 91-95 25594233-5 2015 Demethoxycurcumin inhibited P-glycoprotein-mediated ATP hydrolysis under concentrations of <1 muM and efficiently inhibited 200 muM verapamil-stimulated ATPase activity, indicating a high affinity of demethoxycurcumin for P-glycoprotein. Verapamil 135-144 ATP binding cassette subfamily B member 1 Homo sapiens 28-42 25594233-5 2015 Demethoxycurcumin inhibited P-glycoprotein-mediated ATP hydrolysis under concentrations of <1 muM and efficiently inhibited 200 muM verapamil-stimulated ATPase activity, indicating a high affinity of demethoxycurcumin for P-glycoprotein. Verapamil 135-144 ATP binding cassette subfamily B member 1 Homo sapiens 225-239 24801141-5 2014 The intestinal availability after oral administration of CAM and TEL increased by 1.3- and 1.6-fold, respectively, after concomitant oral administration of verapamil as a P-glycoprotein (P-gp) inhibitor. Verapamil 156-165 ATP binding cassette subfamily B member 1 Homo sapiens 171-185 26046259-4 2015 There was a synergistic enhancement of growth inhibition with the combination of the Pgp inhibitor verapamil and both analogs in SF-295 cells. Verapamil 99-108 ATP binding cassette subfamily B member 1 Homo sapiens 85-88 26046259-6 2015 Verapamil increased the intracellular concentration of 3dSB-PNBS in both SF-295 and A549 cells in a Pgp-independent manner. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 100-103 25251877-6 2014 In vitro, the ABCB1-substrate CPA was cytotoxic for Treg cells at a 100-fold lower dose than for nonregulatory counterparts, and, inversely, verapamil, an inhibitor of ABC transporters, increased CPA-toxicity in nonregulatory CD4(+) T cells but not Treg cells. Verapamil 141-150 ATP binding cassette subfamily B member 1 Homo sapiens 14-19 25429230-8 2014 Early initiation of rituximab plus cyclophosphamide, doxorubicin, vincristine, and prednisone therapy and drug interactions between anticancer agents and verapamil as a p-glycoprotein inhibitor were considered the possible reasons for favorable outcome in the present case. Verapamil 154-163 ATP binding cassette subfamily B member 1 Homo sapiens 169-183 24687250-2 2014 An in vitro experimental model was established by treating human leukemia K562 and breast cancer MCF-7 cells with different schedules of DOX with or without surface P-glycoprotein (P-gp) inhibitor verapamil (VER). Verapamil 197-206 ATP binding cassette subfamily B member 1 Homo sapiens 181-185 24734954-5 2014 MDR-1 function was assessed by Rhodamine efflux in presence or absence of verapamil. Verapamil 74-83 ATP binding cassette subfamily B member 1 Homo sapiens 0-5 25186858-1 2014 OBJECTIVES: To study the functional activity of the multidrug efflux transporter P-glycoprotein (Pgp) at the blood-brain barrier of patients with temporal lobe epilepsy using (R)-[(11)C]verapamil (VPM)-PET before and after temporal lobe surgery to assess whether postoperative changes in seizure frequency and antiepileptic drug load are associated with changes in Pgp function. Verapamil 186-195 ATP binding cassette subfamily B member 1 Homo sapiens 81-95 25186858-1 2014 OBJECTIVES: To study the functional activity of the multidrug efflux transporter P-glycoprotein (Pgp) at the blood-brain barrier of patients with temporal lobe epilepsy using (R)-[(11)C]verapamil (VPM)-PET before and after temporal lobe surgery to assess whether postoperative changes in seizure frequency and antiepileptic drug load are associated with changes in Pgp function. Verapamil 186-195 ATP binding cassette subfamily B member 1 Homo sapiens 97-100 25065443-7 2014 Our results pointed to a possible binding competition of archazolid B with verapamil on P-glycoprotein. Verapamil 75-84 ATP binding cassette subfamily B member 1 Homo sapiens 88-102 24801141-5 2014 The intestinal availability after oral administration of CAM and TEL increased by 1.3- and 1.6-fold, respectively, after concomitant oral administration of verapamil as a P-glycoprotein (P-gp) inhibitor. Verapamil 156-165 ATP binding cassette subfamily B member 1 Homo sapiens 187-191 24907976-7 2014 While plumbagin did not affect calcein-AM transport by P-glycoprotein the derivatives 1c and 2a exhibited a 50% or 80% inhibition of the P-glycoprotein-mediated calcein-AM efflux relative to the clinically established sensitizer verapamil. Verapamil 229-238 ATP binding cassette subfamily B member 1 Homo sapiens 137-151 25145685-8 2014 RESULTS: The intracytoplasmic prednisone concentration was significantly greater relative to control following P-gp inhibition with Verapamil (155.28% +- 22.48%, p < 0.05) and Zosuquidar (125.81% +- 12.41%, p < 0.05). Verapamil 132-141 ATP binding cassette subfamily B member 1 Homo sapiens 111-115 25034865-11 2014 When the P-gp inhibitor verapamil was present, the efflux ratios of 21- and 7-day systems were 1.37 and 0.86, respectively, suggesting the comparability of the P-gp functional activity in both systems. Verapamil 24-33 ATP binding cassette subfamily B member 1 Homo sapiens 9-13 25034865-11 2014 When the P-gp inhibitor verapamil was present, the efflux ratios of 21- and 7-day systems were 1.37 and 0.86, respectively, suggesting the comparability of the P-gp functional activity in both systems. Verapamil 24-33 ATP binding cassette subfamily B member 1 Homo sapiens 160-164 24921920-4 2014 RESULTS: Verapamil and the MDM2-p53 antagonists potentiated vincristine-mediated growth inhibition in a concentration-dependent manner when used in combination with high MDR-1-expressing p53 mutant neuroblastoma cell lines at concentrations that did not affect the viability of cells when given alone. Verapamil 9-18 ATP binding cassette subfamily B member 1 Homo sapiens 170-175 25518327-11 2014 NPB304 exerted itself and synergy with verapamil activity on reversing tumor resistance via inhibiting the P-gp function. Verapamil 39-48 ATP binding cassette subfamily B member 1 Homo sapiens 107-111 24921920-5 2014 Liquid chromatography-mass spectrometry analyses showed that verapamil, Nutlin-3, MI-63 and NDD0005, but not RG7388, led to increased intracellular levels of vincristine in high MDR-1-expressing cell lines. Verapamil 61-70 ATP binding cassette subfamily B member 1 Homo sapiens 178-183 24321342-9 2014 Furthermore, considering the binding site of P-glycoprotein, verapamil performed as a competitive inhibitor with HZ08. Verapamil 61-70 ATP binding cassette subfamily B member 1 Homo sapiens 45-59 24641346-4 2014 Accumulation decreased in spheroids overexpressing Pgp (HEK-MDR) and was increased in the presence of Pgp inhibitors (verapamil, loperamide, cyclosporin A). Verapamil 118-127 ATP binding cassette subfamily B member 1 Homo sapiens 51-54 24641346-4 2014 Accumulation decreased in spheroids overexpressing Pgp (HEK-MDR) and was increased in the presence of Pgp inhibitors (verapamil, loperamide, cyclosporin A). Verapamil 118-127 ATP binding cassette subfamily B member 1 Homo sapiens 102-105 24641346-7 2014 The dose response curves of verapamil"s inhibition of Pgp and GJIC were similar (IC50: 8 muM). Verapamil 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 54-57 24887326-7 2014 Inhibition of ABCB1 using vardenafil or verapamil resulted in a significant increase in sensitivity to etoposide in ABCB1-expressing MB cell lines. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 116-121 24459178-3 2014 Using a bidirectional transport assay in human colon adenocarcinoma Caco-2 cell monolayers, we observed the vectorial transport of [(14)C]edoxaban, which was completely inhibited by verapamil, a strong P-glycoprotein (P-gp) inhibitor. Verapamil 182-191 ATP binding cassette subfamily B member 1 Homo sapiens 218-222 24362044-7 2014 The efflux mechanism related with P-glycoprotein also existed with the polar flavonoids; verapamil could enhance the permeation of rutin and quercetin via inhibition of P-glycoprotein. Verapamil 89-98 ATP binding cassette subfamily B member 1 Homo sapiens 34-48 24362044-7 2014 The efflux mechanism related with P-glycoprotein also existed with the polar flavonoids; verapamil could enhance the permeation of rutin and quercetin via inhibition of P-glycoprotein. Verapamil 89-98 ATP binding cassette subfamily B member 1 Homo sapiens 169-183 24231527-6 2014 The inhibition of ABCB1, ABCC1, or ABCG2 with verapamil, MK-571, or Ko-143, respectively, did not augment the cytotoxicity of jadomycins DNV, B, L, SPhG, F, S, or T in drug-resistant MCF7 cells. Verapamil 46-55 ATP binding cassette subfamily B member 1 Homo sapiens 18-23 24875445-2 2014 GSH efflux mediated by MRP1 can be stimulated by verapamil. Verapamil 49-58 ATP binding cassette subfamily B member 1 Homo sapiens 23-27 24875445-3 2014 In cells overexpressing MRP1, we have previously shown that verapamil induced a huge intracellular GSH depletion which triggered apoptosis of the cells. Verapamil 60-69 ATP binding cassette subfamily B member 1 Homo sapiens 24-28 24459178-3 2014 Using a bidirectional transport assay in human colon adenocarcinoma Caco-2 cell monolayers, we observed the vectorial transport of [(14)C]edoxaban, which was completely inhibited by verapamil, a strong P-glycoprotein (P-gp) inhibitor. Verapamil 182-191 ATP binding cassette subfamily B member 1 Homo sapiens 202-216 24524365-6 2014 P-gp function was assessed by monolayer release and bidirectional transport studies using rhodamine 123 (Rh123) and the inhibitors verapamil and LY335979. Verapamil 131-140 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 24380838-6 2014 However, 18beta-GA and 20(S)-GF1 exhibited significant inhibition on both basal and verapamil-stimulated P-gp ATPase activities at high concentration. Verapamil 84-93 ATP binding cassette subfamily B member 1 Homo sapiens 105-109 24135452-5 2014 Notably, nitensidine A was clearly found to stimulate the ATPase activity of ABCB1 as strongly as the control drug, verapamil. Verapamil 116-125 ATP binding cassette subfamily B member 1 Homo sapiens 77-82 24135452-10 2014 Molecular docking studies on human ABCB1 showed that, guanidine alkaloids from P. nitens dock to the same binding pocket as verapamil. Verapamil 124-133 ATP binding cassette subfamily B member 1 Homo sapiens 35-40 23784266-11 2013 CONCLUSION: Coadministration of the P-gp inhibitors quinidine, verapamil, and dronedarone increased edoxaban exposure. Verapamil 63-72 ATP binding cassette subfamily B member 1 Homo sapiens 36-40 24438524-7 2014 Compound 6 and verapamil (a well-known P-glycoprotein inhibitor) docked with similar binding energies to the same binding pocket. Verapamil 15-24 ATP binding cassette subfamily B member 1 Homo sapiens 39-53 24239173-0 2014 By inhibiting Src, verapamil and dasatinib overcome multidrug resistance via increased expression of Bim and decreased expressions of MDR1 and survivin in human multidrug-resistant myeloma cells. Verapamil 19-28 ATP binding cassette subfamily B member 1 Homo sapiens 134-138 24239173-1 2014 The calcium channel blocker verapamil inhibits the transport function of multidrug resistance protein 1 (MDR1). Verapamil 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 73-103 24239173-1 2014 The calcium channel blocker verapamil inhibits the transport function of multidrug resistance protein 1 (MDR1). Verapamil 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 105-109 24239173-4 2014 We found that verapamil suppresses MDR1 and survivin expressions and increases Bim expression via suppression of Src activation. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 35-39 24596624-7 2014 [(3)H]Paclitaxel uptake was markedly inhibited by cyclosporine and verapamil, well-known substrates of P-glycoprotein (P-gp) transporter. Verapamil 67-76 ATP binding cassette subfamily B member 1 Homo sapiens 103-117 24596624-7 2014 [(3)H]Paclitaxel uptake was markedly inhibited by cyclosporine and verapamil, well-known substrates of P-glycoprotein (P-gp) transporter. Verapamil 67-76 ATP binding cassette subfamily B member 1 Homo sapiens 119-123 24120885-5 2013 Additionally, the P-gp inhibitors, verapamil and cyclosporin A, significantly decreased the efflux of AC. Verapamil 35-44 ATP binding cassette subfamily B member 1 Homo sapiens 18-22 24120885-10 2013 In silico docking analyses suggested that AC and verapamil possess similar P-gp recognition mechanisms. Verapamil 49-58 ATP binding cassette subfamily B member 1 Homo sapiens 75-79 24066110-12 2013 Interestingly, combining verapamil, a P-gp modulator, significantly improved pharmacokinetic behaviour of enrofloxacin in all birds. Verapamil 25-34 ATP binding cassette subfamily B member 1 Homo sapiens 38-42 23670590-7 2013 Pre-treatment with the P-gp inhibitor verapamil enhanced the response to escitalopram in the TST. Verapamil 38-47 ATP binding cassette subfamily B member 1 Homo sapiens 23-27 23731657-4 2013 Verapamil, a known P-gp inhibitor, was used as a positive control drug. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 19-23 23686764-2 2013 The overall aim of our study was to investigate the inhibitory potential of both verapamil and norverapamil on the P-gp-mediated efflux of digoxin in both gut and liver. Verapamil 81-90 ATP binding cassette subfamily B member 1 Homo sapiens 115-119 23686764-5 2013 The range of values obtained for the 10 trials indicated that increases in area under the plasma concentration-time curve (AUC) profiles and maximum plasma concentration observed (Cmax ) values of digoxin following administration of verapamil were more comparable with in vivo observations, when P-gp inhibition by the metabolite, norverapamil, was considered as well. Verapamil 233-242 ATP binding cassette subfamily B member 1 Homo sapiens 296-300 23703021-1 2013 A prerequisite for the prediction of the magnitude of P-glycoprotein (P-gp)-mediated drug-drug interactions between digoxin and P-gp inhibitors (e.g. verapamil and its metabolite norverapamil) or P-gp inducers (e.g. rifampicin) is a predictive pharmacokinetic model for digoxin itself. Verapamil 150-159 ATP binding cassette subfamily B member 1 Homo sapiens 54-68 23703021-1 2013 A prerequisite for the prediction of the magnitude of P-glycoprotein (P-gp)-mediated drug-drug interactions between digoxin and P-gp inhibitors (e.g. verapamil and its metabolite norverapamil) or P-gp inducers (e.g. rifampicin) is a predictive pharmacokinetic model for digoxin itself. Verapamil 150-159 ATP binding cassette subfamily B member 1 Homo sapiens 70-74 23703021-1 2013 A prerequisite for the prediction of the magnitude of P-glycoprotein (P-gp)-mediated drug-drug interactions between digoxin and P-gp inhibitors (e.g. verapamil and its metabolite norverapamil) or P-gp inducers (e.g. rifampicin) is a predictive pharmacokinetic model for digoxin itself. Verapamil 150-159 ATP binding cassette subfamily B member 1 Homo sapiens 128-132 23703021-1 2013 A prerequisite for the prediction of the magnitude of P-glycoprotein (P-gp)-mediated drug-drug interactions between digoxin and P-gp inhibitors (e.g. verapamil and its metabolite norverapamil) or P-gp inducers (e.g. rifampicin) is a predictive pharmacokinetic model for digoxin itself. Verapamil 150-159 ATP binding cassette subfamily B member 1 Homo sapiens 128-132 23731657-5 2013 Results shown that, 10 muM verapamil and SLE (0.5, 2.0, and 10.0 mug/ml) were observed to significantly enhance the uptake and inhibit the efflux ratio of P-gp substrates in Caco-2 and L-MDR1 cells. Verapamil 27-36 ATP binding cassette subfamily B member 1 Homo sapiens 155-159 23707228-6 2013 Functionally, incubation with darunavir led to a marked inhibition of P-gp activity measured by the efflux of rhodamine-123 similar to that observed by verapamil, a specific P-gp inhibitor. Verapamil 152-161 ATP binding cassette subfamily B member 1 Homo sapiens 70-74 23743668-12 2013 This effect on tacrolimus pharmacodynamics was associated with ABCB1 3435C>T SNP in renal transplant patients: verapamil reduced the percentage of IL-2-producing CD4 and CD8 T cells by 14% and 22% in patients with the CC genotype (P < 0.05) but not in patients with the TT genotype. Verapamil 114-123 ATP binding cassette subfamily B member 1 Homo sapiens 63-68 23735077-8 2013 Furthermore, the ABCB1 inhibitor verapamil (10 muM) effectively reversed doxorubicin and paclitaxel resistance by 90- and 200-fold, respectively. Verapamil 33-42 ATP binding cassette subfamily B member 1 Homo sapiens 17-22 23665114-5 2013 Experimental results revealed that HZ08 is the most probable substrate of p-gp and may share the same modulation sites located at the p-gp with verapamil. Verapamil 144-153 ATP binding cassette subfamily B member 1 Homo sapiens 134-138 23562926-8 2013 Cyclosporin A and verapamil, both inhibitors of P-glycoprotein (P-gp), significantly decreased the efflux of AC. Verapamil 18-27 ATP binding cassette subfamily B member 1 Homo sapiens 48-62 23562926-8 2013 Cyclosporin A and verapamil, both inhibitors of P-glycoprotein (P-gp), significantly decreased the efflux of AC. Verapamil 18-27 ATP binding cassette subfamily B member 1 Homo sapiens 64-68 23466650-7 2013 Docking analysis also implied that DABB and DHBB bind directly to ABCB1 at a site partly overlapped with that of verapamil. Verapamil 113-122 ATP binding cassette subfamily B member 1 Homo sapiens 66-71 22946890-1 2013 AIM: To investigate the effect of the P-glycoprotein inhibitor verapamil on the pharmacokinetics and pharmacodynamics of dabigatran etexilate (DE). Verapamil 63-72 ATP binding cassette subfamily B member 1 Homo sapiens 38-52 23520057-11 2013 P-gp is sensitive to inhibition by both PSC 833 and verapamil in a dose-dependent fashion. Verapamil 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 23593196-6 2013 Validation of the assay was performed with known ABCB1 inhibitors, XR9576, verapamil, and cyclosporin A, all of which displayed dose-dependent inhibition of ABCB1-mediated calcein AM efflux in this assay. Verapamil 75-84 ATP binding cassette subfamily B member 1 Homo sapiens 157-162 23435914-4 2013 Compared with MDCKII or MCF-7, intracellular distribution of [(3)H]-menadione was significantly lower in MDCKII/MDR1 or NCI/ADR-RES cells, which could be restored by the P-gp inhibitors, verapamil and quinidine. Verapamil 187-196 ATP binding cassette subfamily B member 1 Homo sapiens 170-174 22946890-12 2013 CONCLUSION: Verapamil increased DE bioavailability, likely due to inhibition of P-glycoprotein. Verapamil 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 80-94 23359659-8 2013 CONCLUSION: We propose that on deliberate or inadvertent P-gp inhibition, the upper boundary of increase in human brain (or fetal) distribution of lipophilic drugs such as verapamil will be limited by tissue blood flow. Verapamil 172-181 ATP binding cassette subfamily B member 1 Homo sapiens 57-61 23340958-3 2013 Recently, positron emission tomography studies with P-gp substrates, such as [(11)C]verapamil, [(11)C]N-desmethyl loperamide, and [(11)C]loperamide, together with potent P-gp inhibitors, have indicated that increases in the influx rate constant for brain entry were observed in humans. Verapamil 84-93 ATP binding cassette subfamily B member 1 Homo sapiens 52-56 23340958-5 2013 In vitro P-gp inhibition assays using verapamil, N-desmethyl loperamide, and loperamide as P-gp probe substrates were performed in human multidrug resistance protein 1-expressing LLC-PK1 cells. Verapamil 38-47 ATP binding cassette subfamily B member 1 Homo sapiens 9-13 23380628-11 2013 The inhibition of the P-gp efflux pump by some BOnEOmBOn copolymers, similar to that measured for the common P-gp inhibitor verapamil, favored the retention of DOXO inside the cell increasing its cytotoxic activity. Verapamil 124-133 ATP binding cassette subfamily B member 1 Homo sapiens 22-26 23380628-11 2013 The inhibition of the P-gp efflux pump by some BOnEOmBOn copolymers, similar to that measured for the common P-gp inhibitor verapamil, favored the retention of DOXO inside the cell increasing its cytotoxic activity. Verapamil 124-133 ATP binding cassette subfamily B member 1 Homo sapiens 109-113 23313612-6 2013 The elimination of [(3)H]paclitaxel was inhibited by unlabeled paclitaxel and verapamil, suggesting a carrier-mediated transport process via P-gp. Verapamil 78-87 ATP binding cassette subfamily B member 1 Homo sapiens 141-145 24107783-3 2013 METHODS: Caco2 cells were treated with various concentrations of aspirin for 24 h. After treatment of Caco2 cells with verapamil, a specific inhibitor of MDR1, we assessed the extent of cell injury using a WST-8 assay at 24 h after aspirin-stimulation. Verapamil 119-128 ATP binding cassette subfamily B member 1 Homo sapiens 154-158 23399671-4 2013 [11C]verapamil is the first probe used to evaluate P-gp function at the BBB because verapamil is a substrate of P-gp and is usually extruded from the brain via active transport by P-gp. Verapamil 5-14 ATP binding cassette subfamily B member 1 Homo sapiens 51-55 23399671-4 2013 [11C]verapamil is the first probe used to evaluate P-gp function at the BBB because verapamil is a substrate of P-gp and is usually extruded from the brain via active transport by P-gp. Verapamil 5-14 ATP binding cassette subfamily B member 1 Homo sapiens 112-116 23399671-4 2013 [11C]verapamil is the first probe used to evaluate P-gp function at the BBB because verapamil is a substrate of P-gp and is usually extruded from the brain via active transport by P-gp. Verapamil 5-14 ATP binding cassette subfamily B member 1 Homo sapiens 112-116 23399671-4 2013 [11C]verapamil is the first probe used to evaluate P-gp function at the BBB because verapamil is a substrate of P-gp and is usually extruded from the brain via active transport by P-gp. Verapamil 84-93 ATP binding cassette subfamily B member 1 Homo sapiens 51-55 23399671-4 2013 [11C]verapamil is the first probe used to evaluate P-gp function at the BBB because verapamil is a substrate of P-gp and is usually extruded from the brain via active transport by P-gp. Verapamil 84-93 ATP binding cassette subfamily B member 1 Homo sapiens 112-116 23399671-4 2013 [11C]verapamil is the first probe used to evaluate P-gp function at the BBB because verapamil is a substrate of P-gp and is usually extruded from the brain via active transport by P-gp. Verapamil 84-93 ATP binding cassette subfamily B member 1 Homo sapiens 112-116 23399671-5 2013 However, many studies have shown that [11C]verapamil uptake is altered on administration of P-gp inhibitors and in neuropsychiatric diseases. Verapamil 43-52 ATP binding cassette subfamily B member 1 Homo sapiens 92-96 23126604-5 2013 The presence of verapamil and Pluronic both improved the intestinal absorption of PTX, which further certified the effect of Pluronic on P-gp inhibition. Verapamil 16-25 ATP binding cassette subfamily B member 1 Homo sapiens 137-141 23229154-3 2013 In the present study, we examined the effects of verapamil, a classic chemosensitizer whose reported mechanisms of action include inhibiting the transport function of P-glycoprotein (MDR1) or stimulating glutathione (GSH) transport by multidrug resistance-related protein 1 (MRP1), in combination with cisplatin (CDDP), carboplatin (CBP) or oxaliplatin on the GBC cell lines, SGC996 and GBC-SD. Verapamil 61-70 ATP binding cassette subfamily B member 1 Homo sapiens 191-205 23229154-3 2013 In the present study, we examined the effects of verapamil, a classic chemosensitizer whose reported mechanisms of action include inhibiting the transport function of P-glycoprotein (MDR1) or stimulating glutathione (GSH) transport by multidrug resistance-related protein 1 (MRP1), in combination with cisplatin (CDDP), carboplatin (CBP) or oxaliplatin on the GBC cell lines, SGC996 and GBC-SD. Verapamil 61-70 ATP binding cassette subfamily B member 1 Homo sapiens 207-211 23519262-5 2012 In the presence of verapamil, an inhibitor of P-glycoprotein (P-gp), the absorptive permeability (P(AB)) of paeoniflorin and liquiritin increased significantly (p < 0.05) and efflux ratios decreased, while the absorption of glycyrrhizic acid did not change significantly, which indicated that paeoniflorin and liquiritin might be P-gp substrates. Verapamil 19-28 ATP binding cassette subfamily B member 1 Homo sapiens 46-60 23527191-6 2013 Methadone also stimulated P-gp ATPase and inhibited verapamil-stimulated P-gp ATPase activity under therapeutic concentrations. Verapamil 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 73-77 23326571-13 2013 The best effect of SF was obtained after 72 h when it attained the effect of known P-gp inhibitors (Dex-verapamil and tariquidar). Verapamil 100-113 ATP binding cassette subfamily B member 1 Homo sapiens 83-87 23072916-9 2012 In the case of 3TC-Etha, the permeability of the intact compound (P(app) 0.093 +- 0.010 x 10(-4) cm/min) was impaired by a P-glycoprotein (P-gp) mediated efflux, evidenced by the higher permeability coefficient (6.933 +- 0.586 x 10(-4) cm/min) determined in the presence of verapamil on the apical side of the enterocyte. Verapamil 274-283 ATP binding cassette subfamily B member 1 Homo sapiens 123-137 23072916-9 2012 In the case of 3TC-Etha, the permeability of the intact compound (P(app) 0.093 +- 0.010 x 10(-4) cm/min) was impaired by a P-glycoprotein (P-gp) mediated efflux, evidenced by the higher permeability coefficient (6.933 +- 0.586 x 10(-4) cm/min) determined in the presence of verapamil on the apical side of the enterocyte. Verapamil 274-283 ATP binding cassette subfamily B member 1 Homo sapiens 139-143 23519262-5 2012 In the presence of verapamil, an inhibitor of P-glycoprotein (P-gp), the absorptive permeability (P(AB)) of paeoniflorin and liquiritin increased significantly (p < 0.05) and efflux ratios decreased, while the absorption of glycyrrhizic acid did not change significantly, which indicated that paeoniflorin and liquiritin might be P-gp substrates. Verapamil 19-28 ATP binding cassette subfamily B member 1 Homo sapiens 62-66 23519262-5 2012 In the presence of verapamil, an inhibitor of P-glycoprotein (P-gp), the absorptive permeability (P(AB)) of paeoniflorin and liquiritin increased significantly (p < 0.05) and efflux ratios decreased, while the absorption of glycyrrhizic acid did not change significantly, which indicated that paeoniflorin and liquiritin might be P-gp substrates. Verapamil 19-28 ATP binding cassette subfamily B member 1 Homo sapiens 333-337 22734651-5 2012 In accordance with these observations, carfilzomib-resistant H23 and DLD-1 cells showed marked upregulation of P-glycoprotein (Pgp) as compared to their parental controls, and coincubation with verapamil, a Pgp inhibitor, led to an almost complete restoration of cellular sensitivity to carfilzomib. Verapamil 194-203 ATP binding cassette subfamily B member 1 Homo sapiens 127-130 23046348-5 2012 In addition, BBA inhibited the verapamil-stimulated ABCB1 ATPase activity and the photolabeling of ABCB1 with [(125)I] iodoarylazidoprazosin in a concentration-dependent manner, indicating that BBA directly interacts with ABCB1. Verapamil 31-40 ATP binding cassette subfamily B member 1 Homo sapiens 52-57 23134497-0 2012 P-glycoprotein imaging in temporal lobe epilepsy: in vivo PET experiments with the Pgp substrate [11C]-verapamil. Verapamil 103-112 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 23134497-0 2012 P-glycoprotein imaging in temporal lobe epilepsy: in vivo PET experiments with the Pgp substrate [11C]-verapamil. Verapamil 103-112 ATP binding cassette subfamily B member 1 Homo sapiens 83-86 23134497-2 2012 To explore this hypothesis, positron emission tomography (PET) scans were performed with the Pgp substrate-verapamil (VPM) in animal models before and after status epilepticus (SE) and in patients with temporal lobe epilepsy (TLE) and healthy controls. Verapamil 107-116 ATP binding cassette subfamily B member 1 Homo sapiens 93-96 22584255-5 2012 To define the mechanisms responsible for this low bioavailability, two P-glycoprotein (P-gp) inhibitors, verapamil and cyclosporine A, were used, and their presence substantially decreased C-K"s efflux ratio in Caco-2 cells (from 26.6 to <3) and significantly increased intracellular concentrations (by as much as 40-fold). Verapamil 105-114 ATP binding cassette subfamily B member 1 Homo sapiens 71-85 22584255-5 2012 To define the mechanisms responsible for this low bioavailability, two P-glycoprotein (P-gp) inhibitors, verapamil and cyclosporine A, were used, and their presence substantially decreased C-K"s efflux ratio in Caco-2 cells (from 26.6 to <3) and significantly increased intracellular concentrations (by as much as 40-fold). Verapamil 105-114 ATP binding cassette subfamily B member 1 Homo sapiens 87-91 22764578-3 2012 P-gP functionality of PBMEC/C1-2 cells grown on Transwell filter inserts was proven by transport studies with P-gP substrate rhodamine 123 and P-gP blocker verapamil. Verapamil 156-165 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 22588188-1 2012 Decreased blood-brain barrier P-glycoprotein (Pgp) function has been shown in Alzheimer"s disease (AD) patients using positron emission tomography (PET) with the radiotracer (R)-[(11)C]verapamil. Verapamil 185-194 ATP binding cassette subfamily B member 1 Homo sapiens 30-44 22588188-1 2012 Decreased blood-brain barrier P-glycoprotein (Pgp) function has been shown in Alzheimer"s disease (AD) patients using positron emission tomography (PET) with the radiotracer (R)-[(11)C]verapamil. Verapamil 185-194 ATP binding cassette subfamily B member 1 Homo sapiens 46-49 22405646-3 2012 Compound 4i more potently reversed P-gp-mediated multidrug resistance (MDR) than DDB and verapamil (VRP) by blocking P-gp mediated drug efflux function and increasing drug accumulation in K562/A02 MDR cells, and persisted longer chemo-sensitizing effect (>24 h) than VRP (<6 h). Verapamil 89-98 ATP binding cassette subfamily B member 1 Homo sapiens 117-121 22258826-9 2012 This study also demonstrated that CuNG has a drug interaction site different from verapamil-, vinblastine- and progesterone-binding sites on P-gp. Verapamil 82-91 ATP binding cassette subfamily B member 1 Homo sapiens 141-145 22411726-6 2012 Furthermore, the backwards transport of MA and HA was inhibited by the P-gp inhibitor verapamil. Verapamil 86-95 ATP binding cassette subfamily B member 1 Homo sapiens 71-75 22545578-7 2012 The roles of P-gp activity in irradiation-induced drugs resistance were studied by using verapamil, an inhibitor of P-gp activity. Verapamil 89-98 ATP binding cassette subfamily B member 1 Homo sapiens 116-120 22145750-4 2012 In K562/MDR1 and K562/A02, the calcium channel blocker verapamil reduced the 50% inhibitory concentration and apoptosis rate of DNR, a P-gp protein substrate, but not of bortezomib. Verapamil 55-64 ATP binding cassette subfamily B member 1 Homo sapiens 8-12 22764578-6 2012 Moreover, effects after addition of P-gP inhibitor verapamil were investigated. Verapamil 51-60 ATP binding cassette subfamily B member 1 Homo sapiens 36-40 22764578-8 2012 Verapamil increased the transport rates of all second generation antihistamines, which suggested involvement of P-gP during their permeation across the BBB model. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 112-116 22792804-2 2012 METHOD: 3H-digoxin (Dig), a substrate of P-glycoprotein, was used as a probe to measure the P-gp-mediated drug efflux transport, which indicated the function of P-gp in Caco-2 cells, while Verapamil (Ver) was used as a positive P-gp inhibitor. Verapamil 189-198 ATP binding cassette subfamily B member 1 Homo sapiens 41-55 22792804-2 2012 METHOD: 3H-digoxin (Dig), a substrate of P-glycoprotein, was used as a probe to measure the P-gp-mediated drug efflux transport, which indicated the function of P-gp in Caco-2 cells, while Verapamil (Ver) was used as a positive P-gp inhibitor. Verapamil 189-198 ATP binding cassette subfamily B member 1 Homo sapiens 92-96 22792804-2 2012 METHOD: 3H-digoxin (Dig), a substrate of P-glycoprotein, was used as a probe to measure the P-gp-mediated drug efflux transport, which indicated the function of P-gp in Caco-2 cells, while Verapamil (Ver) was used as a positive P-gp inhibitor. Verapamil 189-198 ATP binding cassette subfamily B member 1 Homo sapiens 161-165 22792804-2 2012 METHOD: 3H-digoxin (Dig), a substrate of P-glycoprotein, was used as a probe to measure the P-gp-mediated drug efflux transport, which indicated the function of P-gp in Caco-2 cells, while Verapamil (Ver) was used as a positive P-gp inhibitor. Verapamil 189-198 ATP binding cassette subfamily B member 1 Homo sapiens 161-165 22365753-2 2012 Of the 30 analogs synthesized, N(alpha),N(epsilon)-[(CH(3))(2)Mle-Tic](2)Lys-NH(2) and its D-Lys analog were found to exhibit potent P-gp inhibitory activity, twice that of verapamil, in doxorubicin-resistant K562 cells. Verapamil 173-182 ATP binding cassette subfamily B member 1 Homo sapiens 133-137 22361742-5 2012 The SP population was reduced by co-incubation with MDR1 inhibitor Verapamil, while the ABCG2 inhibitor FTC failed to decrease the number of SP cells. Verapamil 67-76 ATP binding cassette subfamily B member 1 Homo sapiens 52-56 20824508-5 2011 The property of being a Pgp substrate was tested by comparison of the tracers uptake in R-3327 Dunning prostate carcinoma AT1 cells in presence and absence of the Pgp-inhibitor verapamil. Verapamil 177-186 ATP binding cassette subfamily B member 1 Homo sapiens 24-27 20641759-8 2004 Verapamil, a calcium channel blocker, is also a transport substrate for the P-gp efflux pump (7). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 76-80 20641759-9 2004 [(11)C]Verapamil is being developed as a positron emission tomography (PET) agent for studying P-gp function non-invasively. Verapamil 7-16 ATP binding cassette subfamily B member 1 Homo sapiens 95-99 22120145-6 2012 The aim of this study was to assess blood-brain barrier P-glycoprotein function in patients with Alzheimer"s disease compared with age-matched healthy controls using (R)-[(11)C]verapamil and positron emission tomography. Verapamil 177-186 ATP binding cassette subfamily B member 1 Homo sapiens 56-70 21757611-4 2011 Two P-glycoprotein (P-gp) inhibitors, verapamil and cyclosporine A, substantially decreased the efflux ratio of Rh2s from 28.5 to 1.0 and 1.2, respectively, in Caco-2 cells. Verapamil 38-47 ATP binding cassette subfamily B member 1 Homo sapiens 4-18 21757611-4 2011 Two P-glycoprotein (P-gp) inhibitors, verapamil and cyclosporine A, substantially decreased the efflux ratio of Rh2s from 28.5 to 1.0 and 1.2, respectively, in Caco-2 cells. Verapamil 38-47 ATP binding cassette subfamily B member 1 Homo sapiens 20-24 21692796-12 2011 The transport of these drugs was blocked by Pgp inhibitors tariquidar and verapamil. Verapamil 74-83 ATP binding cassette subfamily B member 1 Homo sapiens 44-47 22181075-7 2012 alpha-Turmerone and verapamil (a P-gp inhibitor) significantly inhibited the efflux of rhodamine-123 and digoxin (i.e., inhibited the activity of P-gp). Verapamil 20-29 ATP binding cassette subfamily B member 1 Homo sapiens 33-37 22181075-7 2012 alpha-Turmerone and verapamil (a P-gp inhibitor) significantly inhibited the efflux of rhodamine-123 and digoxin (i.e., inhibited the activity of P-gp). Verapamil 20-29 ATP binding cassette subfamily B member 1 Homo sapiens 146-150 22044878-7 2012 The best P-gp inhibitor found was 1-[2-(1H-benzimidazol-2-yl)ethanamine]-4-propoxy-9H-thioxanthen-9-one (45), which caused an accumulation rate of rhodamine-123 similar to that caused by verapamil in the K562Dox resistant cell line, and a decrease in ATP consumption by P-gp. Verapamil 187-196 ATP binding cassette subfamily B member 1 Homo sapiens 9-13 21903258-0 2011 Synergistic effect of folate-mediated targeting and verapamil-mediated P-gp inhibition with paclitaxel -polymer micelles to overcome multi-drug resistance. Verapamil 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 71-75 21903258-3 2011 Verapamil (VRP), a P-gp inhibitor, has been reported to be able to reverse completely the resistance caused by P-gp. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 19-23 21903258-3 2011 Verapamil (VRP), a P-gp inhibitor, has been reported to be able to reverse completely the resistance caused by P-gp. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 111-115 21721007-12 2011 In the ileum and colon, the P*(eff) for AP was significantly increased by verapamil, a P-glycoprotein (P-gp) inhibitor. Verapamil 74-83 ATP binding cassette subfamily B member 1 Homo sapiens 87-101 21721007-12 2011 In the ileum and colon, the P*(eff) for AP was significantly increased by verapamil, a P-glycoprotein (P-gp) inhibitor. Verapamil 74-83 ATP binding cassette subfamily B member 1 Homo sapiens 103-107 21636258-1 2011 The expressions of P-glycoprotein (P-gp) and multidrug resistance-associated proteins (MRPs) in the blood-brain barrier (BBB) were regulated by verapamil and probenecid. Verapamil 144-153 ATP binding cassette subfamily B member 1 Homo sapiens 19-33 21636258-1 2011 The expressions of P-glycoprotein (P-gp) and multidrug resistance-associated proteins (MRPs) in the blood-brain barrier (BBB) were regulated by verapamil and probenecid. Verapamil 144-153 ATP binding cassette subfamily B member 1 Homo sapiens 35-39 20824508-5 2011 The property of being a Pgp substrate was tested by comparison of the tracers uptake in R-3327 Dunning prostate carcinoma AT1 cells in presence and absence of the Pgp-inhibitor verapamil. Verapamil 177-186 ATP binding cassette subfamily B member 1 Homo sapiens 163-166 20824508-12 2011 Direct intratumoral injection of verapamil increased the tracer concentration by ~25% reflecting the functional Pgp activity. Verapamil 33-42 ATP binding cassette subfamily B member 1 Homo sapiens 112-115 21128075-5 2011 The involvement of MDR1 in amrubicinol resistance was evaluated by treatment with P-gp inhibitor verapamil and small interfering RNA (siRNA) against MDR1. Verapamil 97-106 ATP binding cassette subfamily B member 1 Homo sapiens 19-23 21538216-8 2011 This effect is prevented by Pgp inhibitors verapamil and cyclosporin A, as well as siRNA to ABCB1, with concomitant re-sensitization to silvestrol. Verapamil 43-52 ATP binding cassette subfamily B member 1 Homo sapiens 28-31 21634011-3 2011 We recently reported that the calcium channel blocker verapamil can activate massive GSH efflux in MRP1-overexpressing cells, leading to cell death through apoptosis. Verapamil 54-63 ATP binding cassette subfamily B member 1 Homo sapiens 99-103 21763326-7 2011 KEY FINDINGS: MDR1 blockade by the specific inhibitor verapamil reduced the percentage of rhodamine 123(low) cells in LDCs (from 31.8+-6.3% to 11.8+-2.8%, p<0.02). Verapamil 54-63 ATP binding cassette subfamily B member 1 Homo sapiens 14-18 21716273-3 2011 Verapamil and quinidine are good substrates of both the multidrug resistance 1 transporter (MDR1) and the cytochrome P450 (CYP) 3A4 enzyme (CYP3A4). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 56-78 21716273-3 2011 Verapamil and quinidine are good substrates of both the multidrug resistance 1 transporter (MDR1) and the cytochrome P450 (CYP) 3A4 enzyme (CYP3A4). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 92-96 21440934-6 2011 In the Caco-2 transport studies, the presence of verapamil and NOSC both improved the transport of Taxol( ), which further certified the effect of NOSC on P-gp inhibition, and PTX-M enhanced the permeability of PTX compared with Taxol( ). Verapamil 49-58 ATP binding cassette subfamily B member 1 Homo sapiens 155-159 21439263-6 2011 Effects were concentration dependent, as shown for the P-glycoprotein substrate verapamil, and were associated with cellular acidification and respiration. Verapamil 80-89 ATP binding cassette subfamily B member 1 Homo sapiens 55-69 21439263-7 2011 P-glycoprotein ATPase activation by verapamil could be described by a Michaelis-Menten type kinetic profile showing saturation at high substrate concentrations. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 21491921-9 2011 Binding assays revealed that Lipodox competed with verapamil for binding Pgp and hampered the interaction of colchicine with this transporter. Verapamil 51-60 ATP binding cassette subfamily B member 1 Homo sapiens 73-76 21289467-6 2011 The elevation of the oocyte Pgp level was associated with increased activity of rhodamine 6G efflux from the oocyte, and its efflux was suppressed by verapamil, an inhibitor of Pgp. Verapamil 150-159 ATP binding cassette subfamily B member 1 Homo sapiens 28-31 21289467-6 2011 The elevation of the oocyte Pgp level was associated with increased activity of rhodamine 6G efflux from the oocyte, and its efflux was suppressed by verapamil, an inhibitor of Pgp. Verapamil 150-159 ATP binding cassette subfamily B member 1 Homo sapiens 177-180 20563580-0 2011 Effect of MDR modulators verapamil and promethazine on gene expression levels of MDR1 and MRP1 in doxorubicin-resistant MCF-7 cells. Verapamil 25-34 ATP binding cassette subfamily B member 1 Homo sapiens 81-85 21229388-3 2011 The goal of this study is to evaluate whether copper pyrithione (CuPT), Sea-Nine 211, dichlofluanid and tolylfluanid, four widely used antifouling agents, can be transported by P-gp in embryos of sea urchin Strongylocentrotus intermedius in the presence and absence of the P-gp inhibitor verapamil. Verapamil 288-297 ATP binding cassette subfamily B member 1 Homo sapiens 177-181 21229388-7 2011 With this model, a flexible docking is performed and the results indicate that Sea-Nine 211 and dichlofluanid share the same binding site with verapamil, composed of key residues Lys677, Lys753, Thr756, Ala780, Met1033 and Phe1037, whereas tolylfluanid and CuPT display totally different binding modes to P-gp. Verapamil 143-152 ATP binding cassette subfamily B member 1 Homo sapiens 305-309 21336515-7 2011 In the further inhibition experiment in MDR1-MDCKII cells, the absorption was greatly increased and the efflux of phillyrin was competitively inhibited by verapamil and GF120918, which confirmed the involvement of P-gp in the efflux of phillyrin. Verapamil 155-164 ATP binding cassette subfamily B member 1 Homo sapiens 40-44 21336967-8 2011 The Pgp effect on miR-16/Bcl-2 was suppressed by Pgp blocker verapamil indicating the importance of the efflux of Pgp substrates. Verapamil 61-70 ATP binding cassette subfamily B member 1 Homo sapiens 4-7 21336967-8 2011 The Pgp effect on miR-16/Bcl-2 was suppressed by Pgp blocker verapamil indicating the importance of the efflux of Pgp substrates. Verapamil 61-70 ATP binding cassette subfamily B member 1 Homo sapiens 49-52 21336967-8 2011 The Pgp effect on miR-16/Bcl-2 was suppressed by Pgp blocker verapamil indicating the importance of the efflux of Pgp substrates. Verapamil 61-70 ATP binding cassette subfamily B member 1 Homo sapiens 49-52 21371443-7 2011 Notably, the P-gp inhibitor, verapamil, also directly interacted with P-gp but significantly diminished KNG-I-322-induced anti-proliferative activity. Verapamil 29-38 ATP binding cassette subfamily B member 1 Homo sapiens 13-17 21371443-7 2011 Notably, the P-gp inhibitor, verapamil, also directly interacted with P-gp but significantly diminished KNG-I-322-induced anti-proliferative activity. Verapamil 29-38 ATP binding cassette subfamily B member 1 Homo sapiens 70-74 21589945-8 2011 The identified binding site in the non-energized state is overlapping with, but not identical to, known binding areas of cyclic P-gp inhibitors and verapamil. Verapamil 148-157 ATP binding cassette subfamily B member 1 Homo sapiens 128-132 20563580-11 2011 It has also been shown that treatment of the cells with verapamil results in significant decrease in MDR1 mRNA levels. Verapamil 56-65 ATP binding cassette subfamily B member 1 Homo sapiens 101-105 21308736-5 2011 Furthermore, EFL1 could enhance the ATP hydrolysis activity of ABCB1 stimulated by verapamil. Verapamil 83-92 ATP binding cassette subfamily B member 1 Homo sapiens 63-68 20563580-6 2011 This study focuses on the effect of verapamil and promethazine on the expression levels of MDR1 and MRP1 genes and the drug transport activity in doxorubicin-resistant MCF-7 breast carcinoma cell line. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 91-95 21804948-5 2011 Non-selective ABCC-transport inhibition with probenecid significantly increased intracellular dFdU concentrations, with a similar trend observed with verapamil, a non-selective ABCB1 and ABCG2 transport inhibitor. Verapamil 150-159 ATP binding cassette subfamily B member 1 Homo sapiens 177-182 21062675-3 2011 P-gp function can in vitro be inhibited by cyclosporine A (CSA) and verapamil; moreover, P-gp reduction by CSA in systemic lupus erythematosus and rheumatoid arthritis has been demonstrated. Verapamil 68-77 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 21062675-5 2011 P-gp function on patient cells was analyzed by measuring the changes in rhodamine-123 (Rh-123) fluorescence after verapamil incubation. Verapamil 114-123 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 20969446-5 2010 Epithelial cells were isolated from the material and in in vitro conditions were preincubated with P-gp blocker-verapamil-before ALA-PDT. Verapamil 112-121 ATP binding cassette subfamily B member 1 Homo sapiens 99-103 21733412-10 2011 The rank order of these drugs potencies to up-regulate P-gp activity was as following: hyperforin >>> dexamethasone ~ beta-estradiol > caffeine > rifampicin ~ pentylenetetrazole > verapamil. Verapamil 198-207 ATP binding cassette subfamily B member 1 Homo sapiens 55-59 20623213-8 2010 The effects of the Cys431Leu variation, due to MDR1 (GT1292-3TG) nucleotide transition, on P-gp-dependent intracellular substrate accumulation appeared to be substrate dependent where doxorubicin, vinblastine, and paclitaxel exhibit an increased accumulation (p < 0.05), while verapamil and Hoechst33342 exhibit a decreased intracellular concentration compared with wild type (p < 0.05). Verapamil 280-289 ATP binding cassette subfamily B member 1 Homo sapiens 47-51 20623213-8 2010 The effects of the Cys431Leu variation, due to MDR1 (GT1292-3TG) nucleotide transition, on P-gp-dependent intracellular substrate accumulation appeared to be substrate dependent where doxorubicin, vinblastine, and paclitaxel exhibit an increased accumulation (p < 0.05), while verapamil and Hoechst33342 exhibit a decreased intracellular concentration compared with wild type (p < 0.05). Verapamil 280-289 ATP binding cassette subfamily B member 1 Homo sapiens 91-95 21128720-5 2010 RESULTS: The most active anti-P-gp poloxamines (which enhanced two- to three-fold doxorubicin accumulation compared with verapamil) resulted to be pristine medium-to-high hydrophobic T304, T904, T1301, T901 and T150R1. Verapamil 121-130 ATP binding cassette subfamily B member 1 Homo sapiens 30-34 21104926-8 2010 This effect was reversed when verapamil or ketoconazole, compounds known to interact with P-glycoprotein, were added together with digoxin into the donor compartment. Verapamil 30-39 ATP binding cassette subfamily B member 1 Homo sapiens 90-104 20735140-8 2010 While 2-4 showed either no or very weak inhibition of cellular P-glycoprotein (P-gp) activity, they either activated or inhibited the actions of the first generation P-gp inhibitors verapamil or cyclosporin, respectively. Verapamil 182-191 ATP binding cassette subfamily B member 1 Homo sapiens 166-170 20862795-5 2004 Calcium channel blockers (such as verapamil), cyclosporine (CsA, P-gp inhibitor) and CsA"s non-immunosuppressive analog PSC 833 (other mechanism) are MDR modulators that inhibit the transport of P-gp substrates out of the cells (6, 7). Verapamil 34-43 ATP binding cassette subfamily B member 1 Homo sapiens 195-199 20621639-3 2010 They were confirmed to be substrates of MDR1 and to compete with each other, as well as with verapamil for transport via this transporter. Verapamil 93-102 ATP binding cassette subfamily B member 1 Homo sapiens 40-44 20862794-5 2004 Calcium channel blockers (such as verapamil), cyclosporine (CsA, P-gp inhibitor) and CsA"s non-immunosuppressive analog PSC 833 (other mechanism) are MDR modulators that inhibit the transport of P-gp substrates out of the cells (6, 7). Verapamil 34-43 ATP binding cassette subfamily B member 1 Homo sapiens 195-199 20595016-12 2010 The higher sensitivity of VB-Caco-2 culture is also supported by the test results of NCEs, where 37% of NCEs were found to be P-gp substrate in VB-Caco-2 verified by verapamil, but only 9% by native Caco-2. Verapamil 166-175 ATP binding cassette subfamily B member 1 Homo sapiens 126-130 20944142-4 2010 RESULTS: The expression of P-gp was clearly inhibited by verapamil in all four cell lines. Verapamil 57-66 ATP binding cassette subfamily B member 1 Homo sapiens 27-31 20699370-10 2010 Overexpression of CDX2 in HT-29 cells revealed increased resistance to the known substrate of MDR1, vincristine and paclitaxel, which was reversed by an MDR1 inhibitor, verapamil. Verapamil 169-178 ATP binding cassette subfamily B member 1 Homo sapiens 94-98 20691599-0 2010 Iodination of verapamil for a stronger induction of death, through GSH efflux, of cancer cells overexpressing MRP1. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 110-114 20691599-1 2010 The multidrug resistance protein 1 (MRP1), involved in multidrug resistance (MDR) of cancer cells, was found to be modulated by verapamil, through stimulation of GSH transport, leading to apoptosis of MRP1-overexpressing cells. Verapamil 128-137 ATP binding cassette subfamily B member 1 Homo sapiens 4-34 20691599-1 2010 The multidrug resistance protein 1 (MRP1), involved in multidrug resistance (MDR) of cancer cells, was found to be modulated by verapamil, through stimulation of GSH transport, leading to apoptosis of MRP1-overexpressing cells. Verapamil 128-137 ATP binding cassette subfamily B member 1 Homo sapiens 36-40 20691599-1 2010 The multidrug resistance protein 1 (MRP1), involved in multidrug resistance (MDR) of cancer cells, was found to be modulated by verapamil, through stimulation of GSH transport, leading to apoptosis of MRP1-overexpressing cells. Verapamil 128-137 ATP binding cassette subfamily B member 1 Homo sapiens 201-205 20691599-2 2010 In this study, various iodinated derivatives of verapamil were synthesized, including iodination on the B ring, known to be involved in verapamil cardiotoxicity, and assayed for the stimulation of GSH efflux by MRP1. Verapamil 48-57 ATP binding cassette subfamily B member 1 Homo sapiens 211-215 20699370-10 2010 Overexpression of CDX2 in HT-29 cells revealed increased resistance to the known substrate of MDR1, vincristine and paclitaxel, which was reversed by an MDR1 inhibitor, verapamil. Verapamil 169-178 ATP binding cassette subfamily B member 1 Homo sapiens 153-157 20466050-5 2010 A well-known P-glycoprotein (ABCB1/P-gp) antagonist verapamil did not affect the transfer more than it did in the case of antipyrine, indicating that ABCB1/P-gp does not have a role in BP transfer. Verapamil 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 29-34 20620031-0 2010 Regional increase in P-glycoprotein function in the blood-brain barrier of patients with chronic schizophrenia: a PET study with [(11)C]verapamil as a probe for P-glycoprotein function. Verapamil 136-145 ATP binding cassette subfamily B member 1 Homo sapiens 21-35 20620031-7 2010 The decrease of [(11)C]verapamil uptake correlates with an increased activity of the P-gp pump. Verapamil 23-32 ATP binding cassette subfamily B member 1 Homo sapiens 85-89 20651984-10 2010 Furthermore, verapamil decreased MDR1 expression. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 33-37 20682982-1 2010 Iodinated derivatives of verapamil were synthesized and tested as P-glycoprotein (Pgp)-mediated multidrug resistance (MDR) reversal agents. Verapamil 25-34 ATP binding cassette subfamily B member 1 Homo sapiens 66-80 20682982-1 2010 Iodinated derivatives of verapamil were synthesized and tested as P-glycoprotein (Pgp)-mediated multidrug resistance (MDR) reversal agents. Verapamil 25-34 ATP binding cassette subfamily B member 1 Homo sapiens 82-85 20071452-7 2010 The ATP-dependent transport was inhibited by the model inhibitors verapamil (P-gp), benzbromarone (MRP2), and sulfasalazine (BCRP). Verapamil 66-75 ATP binding cassette subfamily B member 1 Homo sapiens 77-81 20121715-8 2010 Inhibitors of P-gp, including cyclosporine A (CsA) and verapamil (Vpa), increased the intracellular level of IB-MECA and reversed the resistance of K562/HHT cells to this drug. Verapamil 55-64 ATP binding cassette subfamily B member 1 Homo sapiens 14-18 20121715-8 2010 Inhibitors of P-gp, including cyclosporine A (CsA) and verapamil (Vpa), increased the intracellular level of IB-MECA and reversed the resistance of K562/HHT cells to this drug. Verapamil 66-69 ATP binding cassette subfamily B member 1 Homo sapiens 14-18 20336065-3 2010 Regional P-gp inhibition was expressed as cyclosporine A-induced percentage change in the distributional clearance of verapamil (K(1)) in the brain, normalized to the regional blood flow (rCBF). Verapamil 118-127 ATP binding cassette subfamily B member 1 Homo sapiens 9-13 20069466-1 2010 OBJECTIVE: To investigate the effects of the clinical dose of clarithromycin, a substrate of P-glycoprotein (P-gp), on P-gp function using positron emission tomography (PET) with [11C]verapamil. Verapamil 184-193 ATP binding cassette subfamily B member 1 Homo sapiens 109-113 23960725-6 2010 RESULTS: The absorption of furosemide was significantly influenced by the P-gp as confirmed by the everted vis the non-everted sacs together with the verapamil study in which the transport of furosemide was inhibited by verapamil. Verapamil 150-159 ATP binding cassette subfamily B member 1 Homo sapiens 74-78 23960725-6 2010 RESULTS: The absorption of furosemide was significantly influenced by the P-gp as confirmed by the everted vis the non-everted sacs together with the verapamil study in which the transport of furosemide was inhibited by verapamil. Verapamil 220-229 ATP binding cassette subfamily B member 1 Homo sapiens 74-78 20012601-2 2010 Verapamil is a substrate of both P-gp and CYP3A4. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 33-37 20012601-11 2010 CONCLUSION: Lovastatin increased the absorption of verapamil by inhibiting P-gp and inhibited the first-pass metabolism of verapamil by inhibiting CYP3A4 in the intestine and/or liver in humans. Verapamil 51-60 ATP binding cassette subfamily B member 1 Homo sapiens 75-79 20010957-1 2010 We attempted to assess regional differences in cerebral P-glycoprotein (P-gp) function by performing paired positron emission tomography (PET) scans with the P-gp substrate (R)-[(11)C]verapamil in five healthy subjects before and after i.v. Verapamil 184-193 ATP binding cassette subfamily B member 1 Homo sapiens 72-76 20135207-4 2010 METHODS: The previously reported concentration-dependent permeability of verapamil, quinidine, and vinblastine in MDR1-MDCKII, P-gp-highly induced Caco-2, P-gp-induced Caco-2, normal Caco-2, and MDR1-knockdown Caco-2 cells data were analyzed using a model in which the Km value was defined for the intracellular substrate concentration. Verapamil 73-82 ATP binding cassette subfamily B member 1 Homo sapiens 114-118 20135207-4 2010 METHODS: The previously reported concentration-dependent permeability of verapamil, quinidine, and vinblastine in MDR1-MDCKII, P-gp-highly induced Caco-2, P-gp-induced Caco-2, normal Caco-2, and MDR1-knockdown Caco-2 cells data were analyzed using a model in which the Km value was defined for the intracellular substrate concentration. Verapamil 73-82 ATP binding cassette subfamily B member 1 Homo sapiens 127-131 20135207-4 2010 METHODS: The previously reported concentration-dependent permeability of verapamil, quinidine, and vinblastine in MDR1-MDCKII, P-gp-highly induced Caco-2, P-gp-induced Caco-2, normal Caco-2, and MDR1-knockdown Caco-2 cells data were analyzed using a model in which the Km value was defined for the intracellular substrate concentration. Verapamil 73-82 ATP binding cassette subfamily B member 1 Homo sapiens 155-159 20135207-4 2010 METHODS: The previously reported concentration-dependent permeability of verapamil, quinidine, and vinblastine in MDR1-MDCKII, P-gp-highly induced Caco-2, P-gp-induced Caco-2, normal Caco-2, and MDR1-knockdown Caco-2 cells data were analyzed using a model in which the Km value was defined for the intracellular substrate concentration. Verapamil 73-82 ATP binding cassette subfamily B member 1 Homo sapiens 195-199 19944135-7 2010 Furthermore, verapamil (VER), an inhibitor of ABCB1 and an L-type calcium channel blocker, is capable of reversing the resistance in all drug-resistant sublines independent of ABCB1 expression. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 46-51 19944135-7 2010 Furthermore, verapamil (VER), an inhibitor of ABCB1 and an L-type calcium channel blocker, is capable of reversing the resistance in all drug-resistant sublines independent of ABCB1 expression. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 176-181 20069466-1 2010 OBJECTIVE: To investigate the effects of the clinical dose of clarithromycin, a substrate of P-glycoprotein (P-gp), on P-gp function using positron emission tomography (PET) with [11C]verapamil. Verapamil 184-193 ATP binding cassette subfamily B member 1 Homo sapiens 93-107 19631272-5 2010 Quinidine and verapamil, known MDR1 substrates/inhibitors, showed trans-inhibition on MDR1-mediated [(3)H]vinblastine and [(3)H]digoxin efflux. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 31-35 19726755-6 2010 SMDR2-mediated transport is inhibited by the Pgp modulators verapamil (IC(50)=12.1 muM) and nifedipine, and also by praziquantel, the current drug of choice against schisotosomiasis (IC(50)=17.4 muM). Verapamil 60-69 ATP binding cassette subfamily B member 1 Homo sapiens 45-48 19949935-5 2010 The calcium blocker verapamil was the first drug shown to be a modulator of Pgp, and since many different chemical compounds have been shown to exert the same effect in vitro by blocking Pgp activity. Verapamil 20-29 ATP binding cassette subfamily B member 1 Homo sapiens 76-79 19949935-5 2010 The calcium blocker verapamil was the first drug shown to be a modulator of Pgp, and since many different chemical compounds have been shown to exert the same effect in vitro by blocking Pgp activity. Verapamil 20-29 ATP binding cassette subfamily B member 1 Homo sapiens 187-190 19914261-2 2010 MAIN METHODS: We performed an inhibition study on the vectorial transport of digoxin, a typical substrate for P-gp, using a human colonic adenocarcinoma cell line, Caco-2 cells, and verapamil-stimulated ATPase activity using human multidrug resistance 1 (hMDR1)-expressing membrane. Verapamil 182-191 ATP binding cassette subfamily B member 1 Homo sapiens 231-253 19914261-2 2010 MAIN METHODS: We performed an inhibition study on the vectorial transport of digoxin, a typical substrate for P-gp, using a human colonic adenocarcinoma cell line, Caco-2 cells, and verapamil-stimulated ATPase activity using human multidrug resistance 1 (hMDR1)-expressing membrane. Verapamil 182-191 ATP binding cassette subfamily B member 1 Homo sapiens 255-260 20834157-6 2010 P-glycoprotein (MDR1), encoded by ABCB1, was elevated in the RPMI-8226/TP-110 cells, and the MDR1 inhibitor verapamil overcame their resistance to TP-110. Verapamil 108-117 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 20834157-6 2010 P-glycoprotein (MDR1), encoded by ABCB1, was elevated in the RPMI-8226/TP-110 cells, and the MDR1 inhibitor verapamil overcame their resistance to TP-110. Verapamil 108-117 ATP binding cassette subfamily B member 1 Homo sapiens 16-20 20834157-6 2010 P-glycoprotein (MDR1), encoded by ABCB1, was elevated in the RPMI-8226/TP-110 cells, and the MDR1 inhibitor verapamil overcame their resistance to TP-110. Verapamil 108-117 ATP binding cassette subfamily B member 1 Homo sapiens 34-39 20834157-6 2010 P-glycoprotein (MDR1), encoded by ABCB1, was elevated in the RPMI-8226/TP-110 cells, and the MDR1 inhibitor verapamil overcame their resistance to TP-110. Verapamil 108-117 ATP binding cassette subfamily B member 1 Homo sapiens 93-97 19947891-4 2010 Both in vitro and in vivo studies have demonstrated that both itraconazole and verapamil are potent P-glycoprotein inhibitors. Verapamil 79-88 ATP binding cassette subfamily B member 1 Homo sapiens 100-114 19947891-7 2010 Co-administration of itraconazole and/or verapamil significantly increased the AUC(0 - 24) of both enantiomers; their influence on the P-glycoprotein-mediated transport of (S)-fexofenadine was greater than that of the (R)-enantiomer. Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 135-149 19631272-5 2010 Quinidine and verapamil, known MDR1 substrates/inhibitors, showed trans-inhibition on MDR1-mediated [(3)H]vinblastine and [(3)H]digoxin efflux. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 86-90 19910428-3 2009 The aim of this study was to measure P-gp function at the human blood-brain barrier (BBB) after tariquidar administration using PET and the model P-gp substrate (R)-(11)C-verapamil. Verapamil 171-180 ATP binding cassette subfamily B member 1 Homo sapiens 37-41 20024113-5 2009 Six compounds from these series (, , , , and ) showed an effectiveness that was similar to (or higher than) the classical Pgp reversal agent verapamil for the reversal of resistance to daunomycin and vinblastine. Verapamil 141-150 ATP binding cassette subfamily B member 1 Homo sapiens 122-125 19952421-7 2009 The degree of inhibition in the presence of verapamil, a P-gp substrate, showed a significant correlation with that in the absence of verapamil. Verapamil 44-53 ATP binding cassette subfamily B member 1 Homo sapiens 57-61 19910428-3 2009 The aim of this study was to measure P-gp function at the human blood-brain barrier (BBB) after tariquidar administration using PET and the model P-gp substrate (R)-(11)C-verapamil. Verapamil 171-180 ATP binding cassette subfamily B member 1 Homo sapiens 146-150 19772851-0 2009 P-glycoprotein (ABCB1) modulates collateral sensitivity of a multidrug resistant cell line to verapamil. Verapamil 94-103 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 19772851-0 2009 P-glycoprotein (ABCB1) modulates collateral sensitivity of a multidrug resistant cell line to verapamil. Verapamil 94-103 ATP binding cassette subfamily B member 1 Homo sapiens 16-21 19772851-2 2009 However, the over-expression of P-glycoprotein in some tumor cells has been associated with increased sensitivity, or "collateral sensitivity", of multidrug resistant cells to specific drugs, including the calcium channel blocker verapamil. Verapamil 230-239 ATP binding cassette subfamily B member 1 Homo sapiens 32-46 19233288-5 2009 The purified MDR1 exhibited specific ATP hydrolase activity (1.7 micromol/min/mg) in the presence of a substrate, verapamil. Verapamil 114-123 ATP binding cassette subfamily B member 1 Homo sapiens 13-17 19684997-2 2009 Exposure to a known mammalian inhibitor (verapamil, 10 1M) and inducer (rhodamine 123, 3 1M) on the transport protein P-glycoprotein (Pgp) was investigated in the liver of the western mosquitofish and bluegill sunfish. Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 118-132 19684997-2 2009 Exposure to a known mammalian inhibitor (verapamil, 10 1M) and inducer (rhodamine 123, 3 1M) on the transport protein P-glycoprotein (Pgp) was investigated in the liver of the western mosquitofish and bluegill sunfish. Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 134-137 19740397-0 2009 Influence of ABCB1 gene polymorphisms on the pharmacokinetics of verapamil among healthy Chinese Han ethnic subjects. Verapamil 65-74 ATP binding cassette subfamily B member 1 Homo sapiens 13-18 19740397-1 2009 AIMS: To assess the association between polymorphisms of the ABCB1 gene and the pharmacokinetics of verapamil among healthy Chinese Han ethnic subjects. Verapamil 100-109 ATP binding cassette subfamily B member 1 Homo sapiens 61-66 19740397-11 2009 CONCLUSIONS: Our study showed for the first time that verapamil pharmacokinetics may be influenced by particular genetic polymorphisms of the ABCB1 gene among healthy Chinese Han ethnic subjects. Verapamil 54-63 ATP binding cassette subfamily B member 1 Homo sapiens 142-147 19224656-0 2009 Locally increased P-glycoprotein function in major depression: a PET study with [11C]verapamil as a probe for P-glycoprotein function in the blood-brain barrier. Verapamil 85-94 ATP binding cassette subfamily B member 1 Homo sapiens 18-32 19224656-4 2009 Positron emission tomography was used to measure brain uptake of [11C]verapamil, which is normally expelled from the brain by P-gp. Verapamil 70-79 ATP binding cassette subfamily B member 1 Homo sapiens 126-130 19224656-8 2009 The decreased [11C]verapamil uptake correlates with an increased function of the P-gp protein and may be related to chronic use of psychotropic drugs. Verapamil 19-28 ATP binding cassette subfamily B member 1 Homo sapiens 81-85 19617341-3 2009 We have previously demonstrated P-gp activity at the human BBB using PET of (11)C-verapamil distribution into the brain in the absence and presence of the P-gp inhibitor cyclosporine-A (CsA). Verapamil 82-91 ATP binding cassette subfamily B member 1 Homo sapiens 32-36 19617341-11 2009 CsA modulation of P-gp increased blood-brain transfer (K(1)) of verapamil into the brain by 73% (range, 30%-118%; n = 12). Verapamil 64-73 ATP binding cassette subfamily B member 1 Homo sapiens 18-22 19617341-14 2009 CONCLUSION: (11)C-verapamil and compartmental analysis can estimate P-gp activity at the BBB by imaging before and during P-gp inhibition by CsA, indicated by a change in verapamil transport (K(1)). Verapamil 18-27 ATP binding cassette subfamily B member 1 Homo sapiens 68-72 19617341-14 2009 CONCLUSION: (11)C-verapamil and compartmental analysis can estimate P-gp activity at the BBB by imaging before and during P-gp inhibition by CsA, indicated by a change in verapamil transport (K(1)). Verapamil 18-27 ATP binding cassette subfamily B member 1 Homo sapiens 122-126 19617341-15 2009 Inhibition of P-gp unmasks verapamil trapping in brain tissue that requires a 2C model for long imaging times; however, transport can be effectively measured using a short scan time with a 1C(10) model, avoiding complications with labeled metabolites and tracer retention. Verapamil 27-36 ATP binding cassette subfamily B member 1 Homo sapiens 14-18 19562680-6 2009 In the presence of cyclosporin A and verapamil, potent inhibitors of P-glycoprotein (P-gp), the P(ratio) decreased from 3.8 to 2.3 and 1.8, respectively, and permeation of apical to basolateral was enhanced. Verapamil 37-46 ATP binding cassette subfamily B member 1 Homo sapiens 69-83 19562680-6 2009 In the presence of cyclosporin A and verapamil, potent inhibitors of P-glycoprotein (P-gp), the P(ratio) decreased from 3.8 to 2.3 and 1.8, respectively, and permeation of apical to basolateral was enhanced. Verapamil 37-46 ATP binding cassette subfamily B member 1 Homo sapiens 85-89 19564743-3 2009 P-gp function was measured using the verapamil-sensitive Rhodamine efflux. Verapamil 37-46 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 18358568-4 2009 We studied cerebrovascular P-gp function using [(11)C]-verapamil positron emission tomography (PET) in seventeen healthy volunteers with age 18-86. Verapamil 55-64 ATP binding cassette subfamily B member 1 Homo sapiens 27-31 19638344-10 2009 Verapamil, a P-gp inhibitor, could reverse P-gp substrate (epirubicin) but not non-P-gp substrate (5-fluorouracil and cisplatin) resistance in GAS1-suppressed gastric cancer cells. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 13-17 19638344-10 2009 Verapamil, a P-gp inhibitor, could reverse P-gp substrate (epirubicin) but not non-P-gp substrate (5-fluorouracil and cisplatin) resistance in GAS1-suppressed gastric cancer cells. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 43-47 19638344-10 2009 Verapamil, a P-gp inhibitor, could reverse P-gp substrate (epirubicin) but not non-P-gp substrate (5-fluorouracil and cisplatin) resistance in GAS1-suppressed gastric cancer cells. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 43-47 19303743-6 2009 The verapamil vVg-CCB, which crosses the blood-brain barrier (BBB): (a) inhibits the P-glycoprotein, an active efflux transporter protein expressed in normal tissue, including the brain, which is believed to contribute to the in situ phenomenon of multidrug resistance; and (b) may regulate membrane depolarization induced by abnormal sodium channels functions by modulating the abnormal Ca++ influxes into neurons with subsequent cell resting. Verapamil 4-13 ATP binding cassette subfamily B member 1 Homo sapiens 85-99 19172664-6 2009 Procyanidine significantly inhibited the verapamil-induced P-gp ATPase activity by 78% when pretreated with 10 micromol/L in a concentration-dependent manner. Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 59-63 19319690-6 2009 The IC(50) of verapamil on nizatidine P-gp secretion was 1.2 x 10(-2) mM. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 38-42 19552748-9 2009 CONCLUSION: This study indicates that P-gp plays a key role in the stereoselectivity of fexofenadine pharmacokinetics, since the pharmacokinetics of fexofenadine enantiomers were altered by the P-gp inhibitor verapamil, and this effect was greater for S-fexofenadine compared with R-fexofenadine. Verapamil 209-218 ATP binding cassette subfamily B member 1 Homo sapiens 38-42 19552748-0 2009 Enantioselective disposition of fexofenadine with the P-glycoprotein inhibitor verapamil. Verapamil 79-88 ATP binding cassette subfamily B member 1 Homo sapiens 54-68 19552748-1 2009 AIMS: The aim was to compare possible effects of verapamil, as a P-glycoprotein (P-gp) inhibitor, on the pharmacokinetics of each fexofenadine enantiomer, as a P-gp substrate. Verapamil 49-58 ATP binding cassette subfamily B member 1 Homo sapiens 65-79 19552748-1 2009 AIMS: The aim was to compare possible effects of verapamil, as a P-glycoprotein (P-gp) inhibitor, on the pharmacokinetics of each fexofenadine enantiomer, as a P-gp substrate. Verapamil 49-58 ATP binding cassette subfamily B member 1 Homo sapiens 81-85 19552748-1 2009 AIMS: The aim was to compare possible effects of verapamil, as a P-glycoprotein (P-gp) inhibitor, on the pharmacokinetics of each fexofenadine enantiomer, as a P-gp substrate. Verapamil 49-58 ATP binding cassette subfamily B member 1 Homo sapiens 160-164 18937360-1 2009 Cholesterol promotes basal and verapamil-induced ATPase activity of P-glycoprotein (P-gp). Verapamil 31-40 ATP binding cassette subfamily B member 1 Homo sapiens 68-82 18937360-1 2009 Cholesterol promotes basal and verapamil-induced ATPase activity of P-glycoprotein (P-gp). Verapamil 31-40 ATP binding cassette subfamily B member 1 Homo sapiens 84-88 18937360-10 2009 In contrast, verapamil stimulation of P-gp ATPase activity was not only enabled by cholesterol but also by alpha-Toc and DPPC. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 38-42 19530439-7 2009 After treatment of the MDR1-expressing HeLa cells with MDR1 substrate vinblastin or inhibitors cyclosporin A and verapamil, the amount of R-123 retained in the cells was increased to 2 to 2.3 times the level in untreated MDR1-expressing HeLa cells. Verapamil 113-122 ATP binding cassette subfamily B member 1 Homo sapiens 23-27 19409044-10 2009 Only verapamil was effective in the inhibition of MRP1; however, the effects were more pronounced with [(99m)Tc]sestamibi, when compared to [(99m)Tc]tetrofosmin. Verapamil 5-14 ATP binding cassette subfamily B member 1 Homo sapiens 50-54 19139163-6 2009 It is interesting to note that transport of 17beta-estradiol 17beta-d-glucuronide (control), gimatecan, and BNP1350 by OATP1B1 could be completely inhibited by the classic ABCB1 and/or ABCG2 inhibitors elacridar, valspodar, pantoprazole, and, to a lesser extent, zosuquidar and verapamil. Verapamil 278-287 ATP binding cassette subfamily B member 1 Homo sapiens 172-177 19051210-6 2009 In particular, compound 1 markedly enhanced [(3)H]-DNM accumulation and significantly reduced [(3)H]-DNM efflux compared with the control, and this effect was more potent than that of verapamil, a well-known P-gp inhibitor. Verapamil 184-193 ATP binding cassette subfamily B member 1 Homo sapiens 208-212 19552748-9 2009 CONCLUSION: This study indicates that P-gp plays a key role in the stereoselectivity of fexofenadine pharmacokinetics, since the pharmacokinetics of fexofenadine enantiomers were altered by the P-gp inhibitor verapamil, and this effect was greater for S-fexofenadine compared with R-fexofenadine. Verapamil 209-218 ATP binding cassette subfamily B member 1 Homo sapiens 194-198 19095843-2 2009 P-glycoprotein (P-gp) efflux transporter and organic anion transport protein inward transporters (OATP, human; Oatp, rat) have been implicated in fentanyl and verapamil (only P-gp) transport across the blood-brain barrier. Verapamil 159-168 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 19280517-3 2009 Atorvastatin and verapamil have interesting clinical pharmacology attributes in that both agents are substrates and/or inhibitors of the dual cytochrome P450 (CYP) 3A4 and P-glycoprotein (Pgp) efflux transporter interplay. Verapamil 17-26 ATP binding cassette subfamily B member 1 Homo sapiens 172-186 19280517-3 2009 Atorvastatin and verapamil have interesting clinical pharmacology attributes in that both agents are substrates and/or inhibitors of the dual cytochrome P450 (CYP) 3A4 and P-glycoprotein (Pgp) efflux transporter interplay. Verapamil 17-26 ATP binding cassette subfamily B member 1 Homo sapiens 188-191 19040611-7 2009 Blocking the function of P-gp with verapamil, cyclosporine A or the anti-P-gp-antibody MRK16 had no impact on their complement resistance, whereas blocking of mCRP enhanced their susceptibility to complement. Verapamil 35-44 ATP binding cassette subfamily B member 1 Homo sapiens 25-29 18623213-8 2009 However, resistance to ptx was reversed by verapamil, which indicated that a sustained inhibition of Pgp was required for ptx to induce cytotoxicity in MDR cells. Verapamil 43-52 ATP binding cassette subfamily B member 1 Homo sapiens 101-104 19881253-5 2009 The uptake of [(3)H]paclitaxel and rhodamine 123 increased by verapamil, a P-gp inhibitor. Verapamil 62-71 ATP binding cassette subfamily B member 1 Homo sapiens 75-79 19082471-4 2009 Treatment with ABCB1/MDR1 inhibitor verapamil and ABCC10/MRP7 inhibitor sulfin-pyrazone altered the sensitivity of SK-LC6/VNB cells to vinorelbine. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 15-20 19470292-10 2009 The effects produced by some of these components are found to be comparable to those of well-known P-gp inhibitors verapamil and cyclosporine. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 99-103 20053600-2 2009 P-glycoprotein activity in lymphocytes was measured by the Rhodamine 123 efflux assay using flow cytometry, in the presence and absence of verapamil, a P-glycoprotein inhibitor. Verapamil 139-148 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 20093732-3 2009 The process of P-gp-mediated MDR seems to be related to intracellular calcium homeostasis, at least indirectly, for the following reasons: i. substances blocking calcium influx through L-type of calcium channels like verapamil were often found to antagonize P-gp-mediated MDR; ii. Verapamil 217-226 ATP binding cassette subfamily B member 1 Homo sapiens 15-19 20093732-3 2009 The process of P-gp-mediated MDR seems to be related to intracellular calcium homeostasis, at least indirectly, for the following reasons: i. substances blocking calcium influx through L-type of calcium channels like verapamil were often found to antagonize P-gp-mediated MDR; ii. Verapamil 217-226 ATP binding cassette subfamily B member 1 Homo sapiens 258-262 19082471-4 2009 Treatment with ABCB1/MDR1 inhibitor verapamil and ABCC10/MRP7 inhibitor sulfin-pyrazone altered the sensitivity of SK-LC6/VNB cells to vinorelbine. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 21-25 18851949-3 2008 The acidification resulted in the decreased P-gp activity with increased Rhodamine 123 (Rh123) accumulation in K562/DOX cells, which could be blocked by the P-gp inhibitor verapamil. Verapamil 172-181 ATP binding cassette subfamily B member 1 Homo sapiens 44-48 18851949-3 2008 The acidification resulted in the decreased P-gp activity with increased Rhodamine 123 (Rh123) accumulation in K562/DOX cells, which could be blocked by the P-gp inhibitor verapamil. Verapamil 172-181 ATP binding cassette subfamily B member 1 Homo sapiens 157-161 19003953-4 2008 The question is also raised whether a minimum effect of a reference P-gp inhibitor as verapamil should be demanded. Verapamil 86-95 ATP binding cassette subfamily B member 1 Homo sapiens 68-72 19026953-2 2008 The positron emission tomography (PET) ligand, [(11)C]-verapamil, has been used to measure in vivo P-gp activity at various tissue-blood barriers of humans and animals. Verapamil 55-64 ATP binding cassette subfamily B member 1 Homo sapiens 99-103 18951251-8 2008 Co-treatment with P-glycoprotein and organic cation transporter inhibitors, verapamil and phenoxybenzamine, resulted in reduced B to A permeability and slower basolateral intracellular uptake rate of cimetidine. Verapamil 76-85 ATP binding cassette subfamily B member 1 Homo sapiens 18-32 18661126-0 2008 Dual drug interactions via P-glycoprotein (P-gp)/ cytochrome P450 (CYP3A4) interplay: recent case study of oral atorvastatin and verapamil. Verapamil 129-138 ATP binding cassette subfamily B member 1 Homo sapiens 27-41 18661126-0 2008 Dual drug interactions via P-glycoprotein (P-gp)/ cytochrome P450 (CYP3A4) interplay: recent case study of oral atorvastatin and verapamil. Verapamil 129-138 ATP binding cassette subfamily B member 1 Homo sapiens 43-47 19026953-3 2008 Since verapamil is extensively metabolized in vivo, it is important to quantify the extent of verapamil metabolism in order to interpret such P-gp activity. Verapamil 6-15 ATP binding cassette subfamily B member 1 Homo sapiens 142-146 19026953-3 2008 Since verapamil is extensively metabolized in vivo, it is important to quantify the extent of verapamil metabolism in order to interpret such P-gp activity. Verapamil 94-103 ATP binding cassette subfamily B member 1 Homo sapiens 142-146 18636179-4 2008 Pgp activity can be measured by the efflux of the dye Rhodamine 123 (Rho 123) and can be blocked by verapamil. Verapamil 100-109 ATP binding cassette subfamily B member 1 Homo sapiens 0-3 18703021-8 2008 Various non-Pgp substrates demonstrated inhibition of digoxin secretion (verapamil, mifepristone, clotrimazole, mevastatin, diltiazem and isradipine) but did not induce Pgp-mediated digoxin secretion. Verapamil 73-82 ATP binding cassette subfamily B member 1 Homo sapiens 12-15 18204840-7 2008 The verapamil-stimulated P-glycoprotein ATPase activity was inhibited by glycyrrhetinic acid. Verapamil 4-13 ATP binding cassette subfamily B member 1 Homo sapiens 25-39 18690712-9 2008 Sav1866-mediated resistance and transport were inhibited by the human ABCB1 and ABCC1 modulator verapamil. Verapamil 96-105 ATP binding cassette subfamily B member 1 Homo sapiens 70-75 18535159-11 2008 Both assays were carried out in presence of verapamil (20-60 microM) or MK-571 (12.5-50 microM) inhibitors of MDR-1 and MRPs, respectively in presence of verapamil or MK-571. Verapamil 44-53 ATP binding cassette subfamily B member 1 Homo sapiens 110-115 18673531-8 2008 MTT assay showed that Pgp inhibitors such as cyclosporine A, verapamil and PSC833 sensitized Colo320HSR (colon, highest MDR1 expression) but not SNU-668 (gastric, highest) and SNU-C5 (gastric, no expression) to paclitaxel. Verapamil 61-70 ATP binding cassette subfamily B member 1 Homo sapiens 22-25 18673531-8 2008 MTT assay showed that Pgp inhibitors such as cyclosporine A, verapamil and PSC833 sensitized Colo320HSR (colon, highest MDR1 expression) but not SNU-668 (gastric, highest) and SNU-C5 (gastric, no expression) to paclitaxel. Verapamil 61-70 ATP binding cassette subfamily B member 1 Homo sapiens 120-124 18200532-5 2008 The P-glycoprotein substrate, verapamil, prevented otilonium bromide efflux and, conversely, otilonium bromide inhibited P-glycoprotein activity. Verapamil 30-39 ATP binding cassette subfamily B member 1 Homo sapiens 4-18 18625294-2 2008 MDR1 expression reduced intracellular levels of the Hexyl-ALA metabolite, protoporphyrin IX (PpIX) to a limited degree and could be reversed with a P-gp inhibitor, verapamil. Verapamil 164-173 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 18625294-2 2008 MDR1 expression reduced intracellular levels of the Hexyl-ALA metabolite, protoporphyrin IX (PpIX) to a limited degree and could be reversed with a P-gp inhibitor, verapamil. Verapamil 164-173 ATP binding cassette subfamily B member 1 Homo sapiens 148-152 18636179-10 2008 The low retention of Rho 123 could be modified by verapamil, indicating that the measurements reflected dye efflux due to Pgp activity. Verapamil 50-59 ATP binding cassette subfamily B member 1 Homo sapiens 122-125 18668443-7 2008 The reproducibility of the [(3)H]-digoxin or verapamil data determined from replicate monolayers across different cell passages indicates that the functional expression of P-gp is consistent across the range of passages (25-40) utilized for transport experiments and that the determination of bi-directional apparent permeability, or IC(50) for inhibition of P-gp, respectively, need only be performed on one occasion for a test compound. Verapamil 45-54 ATP binding cassette subfamily B member 1 Homo sapiens 172-176 18478216-6 2008 In the rhodamine accumulation assays, 30 microM PER produced a 429% increase of the cellular Rhd 123 concentration, which exceeded the inhibitory effect of the well-known Pgp inhibitor verapamil. Verapamil 185-194 ATP binding cassette subfamily B member 1 Homo sapiens 171-174 18265929-7 2008 Lower [11C]-verapamil uptake in midbrain and frontal regions of de novo PD patients could indicate a regional up-regulation of P-gp function. Verapamil 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 127-131 18193210-1 2008 AIM: It has been reported that verapamil and atorvastatin are inhibitors of both P-glycoprotein (P-gp) and microsomal cytochrome P450 (CYP) 3A4, and verapamil is a substrate of both P-gp and CYP3A4. Verapamil 31-40 ATP binding cassette subfamily B member 1 Homo sapiens 81-95 18513966-2 2008 Using a concentration of 4mug/mL, these compounds possess 11-43 times the potency of verapamil in reversing MDR in murine L-5178 lymphoma cells transfected with the human MDR1 gene. Verapamil 85-94 ATP binding cassette subfamily B member 1 Homo sapiens 171-175 18451514-4 2008 Their effects on the P-glycoprotein (P-gp), one of the major drug transporters, were also evaluated by the ATPase assay using human P-gp membranes and verapamil as a substrate. Verapamil 151-160 ATP binding cassette subfamily B member 1 Homo sapiens 21-35 18451514-4 2008 Their effects on the P-glycoprotein (P-gp), one of the major drug transporters, were also evaluated by the ATPase assay using human P-gp membranes and verapamil as a substrate. Verapamil 151-160 ATP binding cassette subfamily B member 1 Homo sapiens 37-41 18193210-8 2008 CONCLUSION: The above data suggest that atorvastatin could inhibit the absorption of verapamil via inhibition of P-gp and/or the metabolism of verapamil by CYP3A4 in humans. Verapamil 85-94 ATP binding cassette subfamily B member 1 Homo sapiens 113-117 18423116-2 2008 However, verapamil (VRP), the inhibitor of P-gp, can not totally reverse the drug resistance, indicating that additional mechanisms must contribute to the MDR phenotype. Verapamil 9-18 ATP binding cassette subfamily B member 1 Homo sapiens 43-47 18423116-2 2008 However, verapamil (VRP), the inhibitor of P-gp, can not totally reverse the drug resistance, indicating that additional mechanisms must contribute to the MDR phenotype. Verapamil 20-23 ATP binding cassette subfamily B member 1 Homo sapiens 43-47 17805981-11 2008 This effect was similar to that of VP, a known prototype of MDR1 reversal agent. Verapamil 35-37 ATP binding cassette subfamily B member 1 Homo sapiens 60-64 18195111-5 2008 Maternofetal permeability was increased by the ABCC2 inhibitor probenecid (0.59 +/- 0.15 versus 0.68 +/- 0.13, p = 0.028) and the nonspecific inhibitor verapamil (0.53 +/- 0.09 versus 0.66 +/- 0.16, p = 0.028) but was not influenced by the ABCB1 inhibitor valspodar (PSC833) (0.48 +/- 0.11 versus 0.46 +/- 0.09, p = 0.345). Verapamil 152-161 ATP binding cassette subfamily B member 1 Homo sapiens 240-245 18249061-9 2008 The increased expression of MDR1 and BCRP1 in leukemic cells correlated with increased cellular daunorubicin resistance, which could be reversed by the ABC transporter inhibitors verapamil and PSC-833. Verapamil 179-188 ATP binding cassette subfamily B member 1 Homo sapiens 28-32 18340565-5 2008 Moreover, the ABCB1 haplotypes did not alter the impact of dietary salt, although ABCB1 2677TT/3435TT subjects had slightly, but not significantly, higher C(max) and area under the curve (AUC) and lower T(max) for the verapamil enantiomers than did 2677GG/3435CC subjects in each salt phase. Verapamil 218-227 ATP binding cassette subfamily B member 1 Homo sapiens 82-87 18201958-5 2008 P-glycoprotein expression and MDR-function was detected in 82 cases by flow cytometry (by use of anti-P-glycoprotein monoclonal antibody and calcein-verapamil functional test). Verapamil 149-158 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 18193210-1 2008 AIM: It has been reported that verapamil and atorvastatin are inhibitors of both P-glycoprotein (P-gp) and microsomal cytochrome P450 (CYP) 3A4, and verapamil is a substrate of both P-gp and CYP3A4. Verapamil 31-40 ATP binding cassette subfamily B member 1 Homo sapiens 97-101 18193210-1 2008 AIM: It has been reported that verapamil and atorvastatin are inhibitors of both P-glycoprotein (P-gp) and microsomal cytochrome P450 (CYP) 3A4, and verapamil is a substrate of both P-gp and CYP3A4. Verapamil 31-40 ATP binding cassette subfamily B member 1 Homo sapiens 182-186 17947497-6 2008 Pgp inhibitors verapamil, cyclosporine A, or PSC833 increased doxorubicin accumulation in the MDR cells up to 79%, and it reversed drug resistance in these cells. Verapamil 15-24 ATP binding cassette subfamily B member 1 Homo sapiens 0-3 18277615-4 2008 Moreover, the BL-AP transport in the Caco-2 cells was significantly reduced by the cis-presence of P-glycoprotein (P-gp) inhibitors such as cyclosporine A, verapamil, and digoxin. Verapamil 156-165 ATP binding cassette subfamily B member 1 Homo sapiens 99-113 17912240-5 2007 This ability to reverse the P-gp-mediated resistance is comparable to that of another frequently used reversal agent known as verapamil. Verapamil 126-135 ATP binding cassette subfamily B member 1 Homo sapiens 28-32 18057712-5 2007 Downregulation of the expression of the Pgp with the specific inhibitor verapamil could markedly suppress the survivin mRNA expression, whereas the reverse impact was not observed. Verapamil 72-81 ATP binding cassette subfamily B member 1 Homo sapiens 40-43 18338644-5 2007 The results showed that the amount of BYZX accumulation in Bcap37/MDR1 cells were as many as those in Bcap37 cells (P > 0.05), and the concentrations of BYZX accumulated in the Bcap37/MDR1 cells did not increase when co-incubated with P-gp inhibitor verapamil. Verapamil 253-262 ATP binding cassette subfamily B member 1 Homo sapiens 66-70 18338644-5 2007 The results showed that the amount of BYZX accumulation in Bcap37/MDR1 cells were as many as those in Bcap37 cells (P > 0.05), and the concentrations of BYZX accumulated in the Bcap37/MDR1 cells did not increase when co-incubated with P-gp inhibitor verapamil. Verapamil 253-262 ATP binding cassette subfamily B member 1 Homo sapiens 187-191 17497080-9 2007 CONCLUSIONS: Cholesterol influences P-gp in three ways: (a) it enhances its basal ATPase activity, (b) it renders P-gp sensitive towards the modulators verapamil and progesterone and (c) it affects the modulator concentration at half maximal ATPase activation. Verapamil 152-161 ATP binding cassette subfamily B member 1 Homo sapiens 36-40 17497080-9 2007 CONCLUSIONS: Cholesterol influences P-gp in three ways: (a) it enhances its basal ATPase activity, (b) it renders P-gp sensitive towards the modulators verapamil and progesterone and (c) it affects the modulator concentration at half maximal ATPase activation. Verapamil 152-161 ATP binding cassette subfamily B member 1 Homo sapiens 114-118 17917277-6 2007 Analysis of verapamil-stimulated ATPase activity in membrane vesicles expressing human P-gp suggested that the increased daunorubicin accumulation by M4 was at least partly due to ATPase inhibition of P-gp. Verapamil 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 87-91 17917277-6 2007 Analysis of verapamil-stimulated ATPase activity in membrane vesicles expressing human P-gp suggested that the increased daunorubicin accumulation by M4 was at least partly due to ATPase inhibition of P-gp. Verapamil 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 201-205 17958337-6 2007 P-glycoprotein inhibitors such as cyclosporine, tariquidar and verapamil significantly increased the influx of udenafil and decreased the efflux of udenafil. Verapamil 63-72 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 17475454-5 2007 MDR1 functionality was studied using rhodamine123 and verapamil as a substrate-inhibitor pair. Verapamil 54-63 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 17475454-8 2007 Verapamil inhibited MDR1 efflux except at higher passage Caco-2WT cells, where no MDR1 activity could be observed. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 20-24 16959878-7 2006 In addition, the measure of raloxifene-glutathione adducts in the cryopreserved hepatocytes showed that the formation of the adducts increased in the presence of verapamil, which supports the idea that blocking Pgp in the liver increases metabolism and, therefore, the bioactivation of raloxifene. Verapamil 162-171 ATP binding cassette subfamily B member 1 Homo sapiens 211-214 17094122-3 2007 The purpose of the present study was to evaluate the species differences in the inhibitory effects of typical P-gp inhibitors, quinidine and verapamil, on P-gp-mediated drug transport using MDR1 transfected cell lines. Verapamil 141-150 ATP binding cassette subfamily B member 1 Homo sapiens 110-114 17094122-3 2007 The purpose of the present study was to evaluate the species differences in the inhibitory effects of typical P-gp inhibitors, quinidine and verapamil, on P-gp-mediated drug transport using MDR1 transfected cell lines. Verapamil 141-150 ATP binding cassette subfamily B member 1 Homo sapiens 155-159 17094122-3 2007 The purpose of the present study was to evaluate the species differences in the inhibitory effects of typical P-gp inhibitors, quinidine and verapamil, on P-gp-mediated drug transport using MDR1 transfected cell lines. Verapamil 141-150 ATP binding cassette subfamily B member 1 Homo sapiens 190-194 17094122-5 2007 On daunorubicin transport, the relative IC(50) value (quinidine IC(50)/verapamil IC(50)) of human P-gp was 5.25 and those from other species ranged from 0.89 to 10.70. Verapamil 71-80 ATP binding cassette subfamily B member 1 Homo sapiens 98-102 21783769-6 2007 The complete inhibition of Pgp by verapamil increased the cytotoxicity of DEHP, but neither DEP nor DBP had this effect, suggesting that DEHP alone may be a possible substrate for the Pgp. Verapamil 34-43 ATP binding cassette subfamily B member 1 Homo sapiens 27-30 21783769-6 2007 The complete inhibition of Pgp by verapamil increased the cytotoxicity of DEHP, but neither DEP nor DBP had this effect, suggesting that DEHP alone may be a possible substrate for the Pgp. Verapamil 34-43 ATP binding cassette subfamily B member 1 Homo sapiens 184-187 17134887-7 2007 They all inhibited the basal and decreased the verapamil-stimulated P-gp ATPase activity. Verapamil 47-56 ATP binding cassette subfamily B member 1 Homo sapiens 68-72 17003230-7 2007 The P-glycoprotein (P-gp) inhibitor verapamil reduced the efflux ratios and enhanced the absorptive transport of the chloro BZT analogs. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 4-18 17003230-7 2007 The P-glycoprotein (P-gp) inhibitor verapamil reduced the efflux ratios and enhanced the absorptive transport of the chloro BZT analogs. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 20-24 16997449-8 2006 Efflux of verapamil across the brush-border membrane by P-glycoprotein was very rapid. Verapamil 10-19 ATP binding cassette subfamily B member 1 Homo sapiens 56-70 17667930-21 2007 Pgp efflux was blocked by the Pgp inhibitor verapamil (positive control) but not impeded by hypericin. Verapamil 44-53 ATP binding cassette subfamily B member 1 Homo sapiens 0-3 17667930-21 2007 Pgp efflux was blocked by the Pgp inhibitor verapamil (positive control) but not impeded by hypericin. Verapamil 44-53 ATP binding cassette subfamily B member 1 Homo sapiens 30-33 17637191-5 2007 Analysis of verapamil-stimulated ATPase activity in membrane vesicles expressing human P-gp suggested that inhibition of P-gp function by tannic acid and pentagalloylglucose was at least partly due to ATPase inhibition of P-gp. Verapamil 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 87-91 17637191-5 2007 Analysis of verapamil-stimulated ATPase activity in membrane vesicles expressing human P-gp suggested that inhibition of P-gp function by tannic acid and pentagalloylglucose was at least partly due to ATPase inhibition of P-gp. Verapamil 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 121-125 17637191-5 2007 Analysis of verapamil-stimulated ATPase activity in membrane vesicles expressing human P-gp suggested that inhibition of P-gp function by tannic acid and pentagalloylglucose was at least partly due to ATPase inhibition of P-gp. Verapamil 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 121-125 16870476-2 2007 The present in vitro study has primarily focused on the evaluation of the chemosensitising drug model, verapamil, as a P-glycoprotein antagonist not only to overcome chemoresistance in non-Hodgkin"s lymphoma (NHL) chemoresistant cells (p53(+) i.e. over-expressing p53 mutant protein NHL cells) but also to evaluate and suggest the use of the single cell gel electrophoresis (SCGE) assay in the clinical setting. Verapamil 103-112 ATP binding cassette subfamily B member 1 Homo sapiens 119-133 17982279-7 2007 Furthermore, cobalamin potentiated cell sensitivity to vinblastine to the same range as that of the Pgp blocker verapamil and prevented methotrexate-induced up-regulation of mdr-1 gene expression. Verapamil 112-121 ATP binding cassette subfamily B member 1 Homo sapiens 100-103 16410038-10 2006 Both novel RMAs overcame drug resistance more efficiently than verapamil, a well-known P-gp inhibitor. Verapamil 63-72 ATP binding cassette subfamily B member 1 Homo sapiens 87-91 16460798-6 2006 PGP inhibition with verapamil or MRP inhibition with indomethacin did not affect [(3)H]-glyburide accumulation in the PGP or MRP2 over-expressing cell lines and only limited changes were seen in the MRP1 over-expressing cell line. Verapamil 20-29 ATP binding cassette subfamily B member 1 Homo sapiens 0-3 16877510-0 2006 Interaction of verapamil with lipid membranes and P-glycoprotein: connecting thermodynamics and membrane structure with functional activity. Verapamil 15-24 ATP binding cassette subfamily B member 1 Homo sapiens 50-64 16877510-10 2006 Using a functional phosphate assay we have measured the affinity of verapamil, amlodipine, and nimodipine for P-glycoprotein, and have calculated the free energy of drug binding from the aqueous phase to the active center of P-glycoprotein in the lipid phase. Verapamil 68-77 ATP binding cassette subfamily B member 1 Homo sapiens 110-124 16450357-6 2006 Indeed, the MDR1 inhibitor verapamil only partially restored sensitivity to drugs, confirming that P-glycoprotein-mediated drug efflux was not responsible for 100% resistance. Verapamil 27-36 ATP binding cassette subfamily B member 1 Homo sapiens 12-16 16837925-9 2006 Verapamil-induced inhibition of Pgp led to a significant increase in cellular concentration of cyclosporine (P<0.05). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 32-35 16530756-11 2006 Rhodamine uptake after treatment with verapamil was significantly greater in D407 and MDCK-MDR1, indicating functional expression of P-gp in these two cell lines. Verapamil 38-47 ATP binding cassette subfamily B member 1 Homo sapiens 86-95 16530756-11 2006 Rhodamine uptake after treatment with verapamil was significantly greater in D407 and MDCK-MDR1, indicating functional expression of P-gp in these two cell lines. Verapamil 38-47 ATP binding cassette subfamily B member 1 Homo sapiens 133-137 16616818-6 2006 The internalization of PEG(2000)-PE/TPGS micelles loaded with P-glycoprotein (P-gp) substrate, rhodamine-123 (RH-123), opposite to the internalization of the free RH-123, was not influenced by the inhibition of the P-gp pump with verapamil hydrochloride, which assumes a P-gp-independent micelle internalization. Verapamil 230-253 ATP binding cassette subfamily B member 1 Homo sapiens 78-82 16740770-3 2006 EXPERIMENTAL DESIGN: ABCB1-mediated transport in leukemic CD34+ CD38- cells compared with their normal counterparts was assessed by quantitating the effect of specific ABCB1 modulators (verapamil and PSC-833) on mitoxantrone retention [defined as efflux index (EI), intracellular mitoxantrone fluorescence intensity in the presence/absence of inhibitor]. Verapamil 186-195 ATP binding cassette subfamily B member 1 Homo sapiens 21-26 16765142-7 2006 Because (R)-[(11)C]verapamil is a substrate for P-gp, the volume of distribution of (R)-[(11)C]verapamil in the brain inversely reflects P-gp function in the BBB. Verapamil 95-104 ATP binding cassette subfamily B member 1 Homo sapiens 137-141 16260035-3 2006 Depsipeptide-resistant KU812 cells expressed P-glycoprotein (P-gp) and their resistance was abolished by co-treatment with verapamil. Verapamil 123-132 ATP binding cassette subfamily B member 1 Homo sapiens 45-59 16260035-3 2006 Depsipeptide-resistant KU812 cells expressed P-glycoprotein (P-gp) and their resistance was abolished by co-treatment with verapamil. Verapamil 123-132 ATP binding cassette subfamily B member 1 Homo sapiens 61-65 16713148-6 2006 Resistance to nanoparticle-encapsulated paclitaxel was reversed by verapamil, a P-gp inhibitor. Verapamil 67-76 ATP binding cassette subfamily B member 1 Homo sapiens 80-84 16713148-8 2006 Inhibition of P-gp by verapamil did not significantly affect the uptake or retention of nanoparticles in drug-resistant cells. Verapamil 22-31 ATP binding cassette subfamily B member 1 Homo sapiens 14-18 16492138-3 2006 Drug substrates such as verapamil bind in a common drug-binding pocket at the interface between the TM (transmembrane) domains of P-gp and stimulate ATPase activity. Verapamil 24-33 ATP binding cassette subfamily B member 1 Homo sapiens 130-134 16450357-6 2006 Indeed, the MDR1 inhibitor verapamil only partially restored sensitivity to drugs, confirming that P-glycoprotein-mediated drug efflux was not responsible for 100% resistance. Verapamil 27-36 ATP binding cassette subfamily B member 1 Homo sapiens 99-113 16513446-0 2006 The effect of short- and long-term administration of verapamil on the disposition of cytochrome P450 3A and P-glycoprotein substrates. Verapamil 53-62 ATP binding cassette subfamily B member 1 Homo sapiens 108-122 16765142-0 2006 Effect of age on functional P-glycoprotein in the blood-brain barrier measured by use of (R)-[(11)C]verapamil and positron emission tomography. Verapamil 100-109 ATP binding cassette subfamily B member 1 Homo sapiens 28-42 16406207-5 2006 The inhibitory potencies (apparent IC50) of known Pgp inhibitors astemizole, GF120918, ketoconazole, itraconazole, quinidine, verapamil and quinine were determined over at least a 1000-fold concentration range. Verapamil 126-135 ATP binding cassette subfamily B member 1 Homo sapiens 50-53 16513446-1 2006 BACKGROUND: Verapamil has the capability to inhibit and induce cytochrome P450 (CYP) 3A and P-glycoprotein (P-gp), but the relative extent and time course of these events in vivo are unclear. Verapamil 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 92-106 16513446-1 2006 BACKGROUND: Verapamil has the capability to inhibit and induce cytochrome P450 (CYP) 3A and P-glycoprotein (P-gp), but the relative extent and time course of these events in vivo are unclear. Verapamil 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 108-112 16513446-2 2006 The effect of verapamil on CYP3A and P-gp activity was determined by examining its effect on its own disposition and on the disposition of fexofenadine, respectively. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 37-41 16513446-13 2006 Short-term administration of verapamil caused net inhibition of intestinal P-gp, whereas long-term administration of verapamil induced P-gp activity. Verapamil 29-38 ATP binding cassette subfamily B member 1 Homo sapiens 75-79 16513446-13 2006 Short-term administration of verapamil caused net inhibition of intestinal P-gp, whereas long-term administration of verapamil induced P-gp activity. Verapamil 117-126 ATP binding cassette subfamily B member 1 Homo sapiens 135-139 16490820-13 2006 This approach resulted in a significantly higher transcellular transport of verapamil, a substrate for both OCTN2 and ABCB1. Verapamil 76-85 ATP binding cassette subfamily B member 1 Homo sapiens 118-123 16490770-7 2006 Verapamil, reported to inhibit P-glycoprotein but not ABCG2, had insignificant activity. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 31-45 16187976-1 2005 AIMS: We sought to define the influence of verapamil, an inhibitor of CYP3A and P-glycoprotein, on the pharmacokinetics of everolimus, a substrate of this enzyme and transporter. Verapamil 43-52 ATP binding cassette subfamily B member 1 Homo sapiens 80-94 16049968-6 2006 A P-gp inhibitor (verapamil) and an MRP1 inhibitor (MK571) could independently reverse the resistance to FK228 and apicidin in the drug-resistant clones. Verapamil 18-27 ATP binding cassette subfamily B member 1 Homo sapiens 2-6 15993035-3 2006 The P-gp function was assessed by means of the rhodamine 6G (R6G) efflux from oocytes with P-gp inhibitors such as verapamil and PSC-833. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 4-8 15993035-3 2006 The P-gp function was assessed by means of the rhodamine 6G (R6G) efflux from oocytes with P-gp inhibitors such as verapamil and PSC-833. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 91-95 16491453-2 2006 Among the active lathyrane derivatives 1 - 3, compound 2 displayed the highest inhibition of rhodamine 123 efflux of human MDR1 gene transfected mouse lymphoma cells when compared to the untreated cells or the positive control verapamil. Verapamil 227-236 ATP binding cassette subfamily B member 1 Homo sapiens 123-127 16531326-0 2006 Verapamil induces upregulation of P-glycoprotein expression on human monocyte derived dendritic cells. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 34-48 16531326-13 2006 Evaluation of other normal cells showed that P-glycoprotein upregulation in the presence of verapamil was also a characteristic of macrophages. Verapamil 92-101 ATP binding cassette subfamily B member 1 Homo sapiens 45-59 16531326-14 2006 This novel observation of the upregulation of P-glycoprotein in the presence of verapamil appears to be a characteristic of activated myeloid derived antigen presenting cells and suggest that P-glycoprotein is essential for these cells as when it is blocked, they respond by increasing expression of this protein. Verapamil 80-89 ATP binding cassette subfamily B member 1 Homo sapiens 46-60 16531326-14 2006 This novel observation of the upregulation of P-glycoprotein in the presence of verapamil appears to be a characteristic of activated myeloid derived antigen presenting cells and suggest that P-glycoprotein is essential for these cells as when it is blocked, they respond by increasing expression of this protein. Verapamil 80-89 ATP binding cassette subfamily B member 1 Homo sapiens 192-206 16531326-15 2006 In summary, this work describes that human dendritic cells generated from plastic-adherent monocytes rapidly upregulate expression of P-glycoprotein as they mature, and in the presence of inflammatory stress and the pharmacological agent verapamil, which blocks P-glycoprotein activity, suggesting that P-glycoprotein may play a role in activation as well as in migration of dendritic cells. Verapamil 238-247 ATP binding cassette subfamily B member 1 Homo sapiens 134-148 16531326-15 2006 In summary, this work describes that human dendritic cells generated from plastic-adherent monocytes rapidly upregulate expression of P-glycoprotein as they mature, and in the presence of inflammatory stress and the pharmacological agent verapamil, which blocks P-glycoprotein activity, suggesting that P-glycoprotein may play a role in activation as well as in migration of dendritic cells. Verapamil 238-247 ATP binding cassette subfamily B member 1 Homo sapiens 262-276 16531326-15 2006 In summary, this work describes that human dendritic cells generated from plastic-adherent monocytes rapidly upregulate expression of P-glycoprotein as they mature, and in the presence of inflammatory stress and the pharmacological agent verapamil, which blocks P-glycoprotein activity, suggesting that P-glycoprotein may play a role in activation as well as in migration of dendritic cells. Verapamil 238-247 ATP binding cassette subfamily B member 1 Homo sapiens 262-276 16289483-12 2005 Uptake studies with daunomycin and the P-gp inhibitor verapamil showed functional activity of P-gp. Verapamil 54-63 ATP binding cassette subfamily B member 1 Homo sapiens 39-43 16289483-12 2005 Uptake studies with daunomycin and the P-gp inhibitor verapamil showed functional activity of P-gp. Verapamil 54-63 ATP binding cassette subfamily B member 1 Homo sapiens 94-98 16259774-6 2005 In the experiments verapamil (VER) and P-gp specific monoclonal antibodies (mAb) (clone 17F9) were used to inhibit P-gp function. Verapamil 19-28 ATP binding cassette subfamily B member 1 Homo sapiens 115-119 16259758-5 2005 In the presence of ciclosporin and verapamil, potent inhibitors of P-glycoprotein (P-gp)/MRP2, the absorptive transport was enhanced and secretory efflux was diminished. Verapamil 35-44 ATP binding cassette subfamily B member 1 Homo sapiens 67-81 16259758-5 2005 In the presence of ciclosporin and verapamil, potent inhibitors of P-glycoprotein (P-gp)/MRP2, the absorptive transport was enhanced and secretory efflux was diminished. Verapamil 35-44 ATP binding cassette subfamily B member 1 Homo sapiens 83-87 16189799-5 2005 In the presence of verapamil, a specific inhibitor of P-glycoprotein, cellular uptake was increased by almost threefold after 5 min, and P(app) was doubled after 30 min. Verapamil 19-28 ATP binding cassette subfamily B member 1 Homo sapiens 54-68 16020127-4 2005 The aim of this study was to analyze the P-gP-modulating effects of PSC 833, a cyclosporine derivate, and verapamil on the chemotherapy of HB in vivo. Verapamil 106-115 ATP binding cassette subfamily B member 1 Homo sapiens 41-45 16077962-9 2005 Sensitivity to DXR was enhanced by treatment with the Pgp inhibitor, Verapamil, in proportion to the Pgp expression level, and the sensitivity to CDDP was increased by the gammaGCS inhibitor, Buthionine sulfoximine, in proportion to the gammaGCS expression level (corresponding to GSH content). Verapamil 69-78 ATP binding cassette subfamily B member 1 Homo sapiens 54-57 16077962-9 2005 Sensitivity to DXR was enhanced by treatment with the Pgp inhibitor, Verapamil, in proportion to the Pgp expression level, and the sensitivity to CDDP was increased by the gammaGCS inhibitor, Buthionine sulfoximine, in proportion to the gammaGCS expression level (corresponding to GSH content). Verapamil 69-78 ATP binding cassette subfamily B member 1 Homo sapiens 101-104 16043202-12 2005 Inhibitors such as calcium-channel blockers (verapamil), cyclosporin A, ONT-093, and XR9576 can modulate the P-gp functionality. Verapamil 45-54 ATP binding cassette subfamily B member 1 Homo sapiens 109-113 16084852-2 2005 To test whether certain ABCB1 haplotypes contribute to interindividual differences in central nervous system drug distribution, brain distribution of a model P-glycoprotein substrate, the calcium channel inhibitor verapamil, was measured by positron emission tomography (PET) in 2 groups of healthy volunteers. Verapamil 214-223 ATP binding cassette subfamily B member 1 Homo sapiens 158-172 16278191-7 2005 Treatment with verapamil as a PGP inhibitor did not affect the transport of ketobemidone in Caco-2 cells, indicating that PGP is not involved. Verapamil 15-24 ATP binding cassette subfamily B member 1 Homo sapiens 30-33 16003291-2 2005 The aim of this study was to confirm the effects of verapamil, a P-glycoprotein inhibitor, on the pharmacokinetics of risperidone. Verapamil 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 65-79 16003291-9 2005 CONCLUSION: This study demonstrated that the bioavailability of risperidone was increased by verapamil, suggesting in vivo involvement of P-glycoprotein in the pharmacokinetics of risperidone. Verapamil 93-102 ATP binding cassette subfamily B member 1 Homo sapiens 138-152 15693753-2 2005 Our observation of the opposite effect of verapamil on P-gp ATPase activity from DRM and solubilized-membrane fractions of CEM-resistant leukaemia cells, and results from Langmuir experiments on membrane monolayers from resistant CEM cells, strongly suggest that two functional populations of P-gp exist. Verapamil 42-51 ATP binding cassette subfamily B member 1 Homo sapiens 55-59 15974580-5 2005 Six compounds from this series (1, 8, 11, 12, 13 and 14) showed similar effectiveness to the classical P-glycoprotein modulator verapamil when reversing resistance to daunorubicin, but it is up to sixteen times greater than that of verapamil when reversing resistance to vinblastine. Verapamil 128-137 ATP binding cassette subfamily B member 1 Homo sapiens 103-117 15693753-3 2005 The first is located in DRM regions: it displays its optimal P-gp ATPase activity, which is almost completely inhibited by orthovanadate and activated by verapamil. Verapamil 154-163 ATP binding cassette subfamily B member 1 Homo sapiens 61-65 15693753-4 2005 The second is located elsewhere in the membrane; it displays a lower P-gp ATPase activity that is less sensitive to orthovanadate and is inhibited by verapamil. Verapamil 150-159 ATP binding cassette subfamily B member 1 Homo sapiens 69-73 15640379-7 2005 ATP-dependent uptake of [3H]vinblastine in vesicles was osmotically sensitive, suggesting intravesicular accumulation, and was inhibited by verapamil, an ABCB1 inhibitor. Verapamil 140-149 ATP binding cassette subfamily B member 1 Homo sapiens 154-159 15961982-2 2005 To determine the importance of P-gp at the human BBB, we developed a state-of-the-art, noninvasive, quantitative imaging technique to measure P-gp activity by use of carbon 11-labeled verapamil as the P-gp substrate and cyclosporine (INN, ciclosporin) as the P-gp inhibitor. Verapamil 184-193 ATP binding cassette subfamily B member 1 Homo sapiens 142-146 15961982-2 2005 To determine the importance of P-gp at the human BBB, we developed a state-of-the-art, noninvasive, quantitative imaging technique to measure P-gp activity by use of carbon 11-labeled verapamil as the P-gp substrate and cyclosporine (INN, ciclosporin) as the P-gp inhibitor. Verapamil 184-193 ATP binding cassette subfamily B member 1 Homo sapiens 142-146 15961982-2 2005 To determine the importance of P-gp at the human BBB, we developed a state-of-the-art, noninvasive, quantitative imaging technique to measure P-gp activity by use of carbon 11-labeled verapamil as the P-gp substrate and cyclosporine (INN, ciclosporin) as the P-gp inhibitor. Verapamil 184-193 ATP binding cassette subfamily B member 1 Homo sapiens 142-146 15914037-7 2005 A P-gp inhibitor, verapamil, could completely reverse the cellular drug resistance when applied to the QGY-7703G cells. Verapamil 18-27 ATP binding cassette subfamily B member 1 Homo sapiens 2-6 15764714-10 2005 P-gp inhibition was also observed in Caco-2 cells, causing an effect comparable to that observed for the known P-gp inhibitor verapamil (50% of control). Verapamil 126-135 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 15764714-10 2005 P-gp inhibition was also observed in Caco-2 cells, causing an effect comparable to that observed for the known P-gp inhibitor verapamil (50% of control). Verapamil 126-135 ATP binding cassette subfamily B member 1 Homo sapiens 111-115 15953199-6 2005 Secretory transport of [3H]-ivermectin and [3H]-selamectin was blocked by the P-gp inhibitor, verapamil. Verapamil 94-103 ATP binding cassette subfamily B member 1 Homo sapiens 78-82 15826803-5 2005 In the second part of this work, we studied the functional expression of the drug efflux pump multidrug resistance P-glycoprotein after long-term exposure to cadmium by immunoblotting with the monoclonal antibody F4 and measurement of calcein-AM+/-the P-gp inhibitor verapamil. Verapamil 267-276 ATP binding cassette subfamily B member 1 Homo sapiens 115-129 15598974-9 2005 In addition, cyclosporin A had no effect on the basal or prazosin-stimulated ATPase activity of ABCG2, whereas both the basal and verapamil-stimulated ATPase activities of P-gp were inhibited markedly. Verapamil 130-139 ATP binding cassette subfamily B member 1 Homo sapiens 172-176 15738623-8 2005 The inhibitory effects of QPA on P-gp were more effective than those of the typical P-gp inhibitors cyclosporin A and verapamil. Verapamil 118-127 ATP binding cassette subfamily B member 1 Homo sapiens 84-88 15683866-3 2005 The different aminopentol distribution between the two compartments of the culture system, and its variation in presence of verapamil or probenecid (P-gp and MRP inhibitors respectively), strongly suggests the involvement of P-glycoprotein in the influx/efflux mechanisms of aminopentol in the intestinal cells, reducing its oral bioavailability. Verapamil 124-133 ATP binding cassette subfamily B member 1 Homo sapiens 225-239 15746064-7 2005 Inhibition of the drug efflux protein P-glycoprotein with verapamil resensitized SW480 cells to treatment with low doses of paclitaxel alone and in combination with IR. Verapamil 58-67 ATP binding cassette subfamily B member 1 Homo sapiens 38-52 15668963-7 2005 We used positron emission tomography to measure brain uptake of [(11)C]-verapamil, which is normally extruded from the brain by P-gp. Verapamil 72-81 ATP binding cassette subfamily B member 1 Homo sapiens 128-132 15567300-7 2005 The uptake level was increased approximately three times in the presence of verapamil, a P-gp inhibitor, and the increased level was not affected by any IFN treatment, indicating that the efflux activity mediated by P-gp in the monolayers is not altered by these cytokines. Verapamil 76-85 ATP binding cassette subfamily B member 1 Homo sapiens 89-93 15567300-7 2005 The uptake level was increased approximately three times in the presence of verapamil, a P-gp inhibitor, and the increased level was not affected by any IFN treatment, indicating that the efflux activity mediated by P-gp in the monolayers is not altered by these cytokines. Verapamil 76-85 ATP binding cassette subfamily B member 1 Homo sapiens 216-220 15494300-8 2004 In clinical trials in MDS, first-generation Pgp blockers, such as cyclosporin-A and verapamil, were minimally effective, non-specific, and toxic. Verapamil 84-93 ATP binding cassette subfamily B member 1 Homo sapiens 44-47 15808585-5 2005 P-gp activity was determined for each subpopulation of cells by the ratio of the mean Rhodamine 123 fluorescence (MFI Rh123) in the presence of verapamil divided by the MFI Rh123 in the absence of verapamil. Verapamil 144-153 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 15808585-5 2005 P-gp activity was determined for each subpopulation of cells by the ratio of the mean Rhodamine 123 fluorescence (MFI Rh123) in the presence of verapamil divided by the MFI Rh123 in the absence of verapamil. Verapamil 197-206 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 15618625-3 2004 Verapamil, a potent P-glycoprotein inhibitor, increased the cellular accumulation of sphingoid bases, except for sphingosine, in a dose-dependent manner. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 20-34 15328394-0 2004 Use of verapamil as a potential P-glycoprotein inhibitor in a patient with refractory epilepsy. Verapamil 7-16 ATP binding cassette subfamily B member 1 Homo sapiens 32-46 15547738-5 2004 MDR1 functional activity was performed by a rhodamine (Rhd)-123 efflux test with or without verapamil. Verapamil 92-101 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 15544355-7 2004 Verapamil-induced ECARs were specific for MDR1-transfected cells and increased with the expression level of P-glycoprotein. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 42-46 15328394-1 2004 OBJECTIVE: To describe a patient in whom we used adjunctive verapamil therapy was used for its P-glycoprotein inhibitory effects. Verapamil 60-69 ATP binding cassette subfamily B member 1 Homo sapiens 95-109 15328394-6 2004 The calcium-channel blocker verapamil is a known inhibitor of P-glycoprotein and may function to block P-glycoprotein-modulated efflux of antiepileptic drugs in the brain, thereby raising the intracellular concentration of antiepileptic drugs and ultimately decreasing seizure burden in patients with refractory epilepsy. Verapamil 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 62-76 15328394-6 2004 The calcium-channel blocker verapamil is a known inhibitor of P-glycoprotein and may function to block P-glycoprotein-modulated efflux of antiepileptic drugs in the brain, thereby raising the intracellular concentration of antiepileptic drugs and ultimately decreasing seizure burden in patients with refractory epilepsy. Verapamil 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 103-117 15328394-7 2004 CONCLUSIONS: Verapamil may offer pharmacoresistant patients hope of improved seizure control due to its potential P-glycoprotein inhibitory effects. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 114-128 15274333-6 2004 RESULTS: Five of the 24 compounds showed greater P-gp inhibition than the control compound verapamil with AC50 values (concentration of the compound eliciting 50% of the maximal rhodamine 6G accumulation) significantly lower than that of verapamil. Verapamil 91-100 ATP binding cassette subfamily B member 1 Homo sapiens 49-53 15239129-5 2004 Furthermore, using rhodamine-123 efflux assays, we observed a significant decrease in P-glycoprotein activity in caveolin-1 overexpressing cells, similar to that observed with 5 microM cyclosporine A or 10 microM verapamil, 2 inhibitors of P-glycoprotein activity. Verapamil 213-222 ATP binding cassette subfamily B member 1 Homo sapiens 86-100 15359574-8 2004 The IC50 of verapamil was 8.44 microM on the P-gp-mediated secretion of fexofenadine. Verapamil 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 45-49 15276086-1 2004 P-glycoprotein (PGP) substrates with high membrane permeability, such as propranolol and verapamil, are considered to be essentially "transparent" to PGP since the transporter does not significantly limit their absorption or elimination. Verapamil 89-98 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 15276086-1 2004 P-glycoprotein (PGP) substrates with high membrane permeability, such as propranolol and verapamil, are considered to be essentially "transparent" to PGP since the transporter does not significantly limit their absorption or elimination. Verapamil 89-98 ATP binding cassette subfamily B member 1 Homo sapiens 16-19 15276086-7 2004 The induction of PGP by propranolol and verapamil was rapid with significant increases occurring within 3h with maximal stimulation after 6h exposure. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 17-20 15276086-9 2004 In conclusion, verapamil and propranolol, whose trans-epithelial permeability are unaffected by PGP, appear to be effective inducers of PGP expression in gut epithelial cells in vitro. Verapamil 15-24 ATP binding cassette subfamily B member 1 Homo sapiens 136-139 15453960-9 2004 The enhanced doxorubicin chemosensitivity of MDR+ cells in the presence of verapamil, a modulator of P-glycoprotein, was reflected by the reduced uptake of 18F-deoxyglucose, 125I-deoxyuridineribose, and 125I-methyltyrosine. Verapamil 75-84 ATP binding cassette subfamily B member 1 Homo sapiens 101-115 15274333-6 2004 RESULTS: Five of the 24 compounds showed greater P-gp inhibition than the control compound verapamil with AC50 values (concentration of the compound eliciting 50% of the maximal rhodamine 6G accumulation) significantly lower than that of verapamil. Verapamil 238-247 ATP binding cassette subfamily B member 1 Homo sapiens 49-53 15315328-9 2004 The functional activity of P-gp could be inhibited by 10 microg/ml verapamil. Verapamil 67-76 ATP binding cassette subfamily B member 1 Homo sapiens 27-31 15112361-13 2004 After P-gp inhibitor verapamil was administered, the concentration of quercetin in model cells was increased. Verapamil 21-30 ATP binding cassette subfamily B member 1 Homo sapiens 6-10 15033264-7 2004 The homologous LmrA protein featured the same stress-protective pattern than OmrA when expressed in E. coli, and the contribution to resistance of both OmrA and LmrA transporters was decreased by verapamil, a well-known inhibitor of the human MDR1 protein. Verapamil 196-205 ATP binding cassette subfamily B member 1 Homo sapiens 243-247 14985103-3 2004 In the case of cyclosporin A, vinblastine or valinomycin, this up-shift was found to be concomitant with the near-complete suppression of labeling with other mAbs specific for Pgp epitopes overlapping with UIC2, while pre-treatment with verapamil or Tween 80 brings about a modest suppression. Verapamil 237-246 ATP binding cassette subfamily B member 1 Homo sapiens 176-179 14726695-7 2004 Verapamil, an inhibitor for P-gp, could reverse the effects of ZNRD1 on drug sensitivity and drug accumulation in SGC7901 cells to a great extent. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 28-32 15110230-3 2004 In contrast, many other compounds such as calcium channel blockers (verapamil) and immunosupressors (cyclosporine-A) are able to inhibit P-gp function. Verapamil 68-77 ATP binding cassette subfamily B member 1 Homo sapiens 137-141 14655754-4 2003 Inhibition of PGP activity by verapamil or PSC 833 enhanced the cytotoxic effects of vincristine, doxorubicin, teniposide and taxol. Verapamil 30-39 ATP binding cassette subfamily B member 1 Homo sapiens 14-17 12954186-4 2003 Based on the transport data of domperidone and verapamil it was found that the Pgp efflux transporter was expressed in the Caco-2 cells. Verapamil 47-56 ATP binding cassette subfamily B member 1 Homo sapiens 79-82 12888645-7 2003 Additionally, two typical p-glycoprotein substrates, daunomycin and verapamil, both inhibited choline accumulation. Verapamil 68-77 ATP binding cassette subfamily B member 1 Homo sapiens 26-40 12948013-5 2003 RESULTS: In situ experimental results revealed that the extent to which the intestinal absorption is affected by P-gp was in the following order: quinidine > ritonavir > loperamide, verapamil, daunomycin > digoxin, cyclosporin A > dexamethasone, and vinblastine. Verapamil 188-197 ATP binding cassette subfamily B member 1 Homo sapiens 113-117 12948015-9 2003 The rank order in P-gp inhibitory potency for terfenadine, verapamil, ritonavir. Verapamil 59-68 ATP binding cassette subfamily B member 1 Homo sapiens 18-22 14522974-0 2003 Methanethiosulfonate derivatives of rhodamine and verapamil activate human P-glycoprotein at different sites. Verapamil 50-59 ATP binding cassette subfamily B member 1 Homo sapiens 75-89 12932699-13 2003 The efflux of rhodamine B was reduced by verapamil, which is, considered evidence for cell membrane p-gp activity, thus the accuracy of the method was confirmed. Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 100-104 12739760-3 2003 Functionality of P-gp was determined by bidirectional transport of rhodamine-123 with and without a P-gp inhibitor, verapamil. Verapamil 116-125 ATP binding cassette subfamily B member 1 Homo sapiens 17-21 12477351-1 2002 A general pharmacophore model of P-glycoprotein (P-gp) drugs is proposed that is based on a highly diverse data set and relates to the verapamil binding site of the protein. Verapamil 135-144 ATP binding cassette subfamily B member 1 Homo sapiens 33-47 12586499-6 2003 Microgels exhibited synergism of the doxorubicin transport enhancement with Verapamil, a known inhibitor of the P-gp. Verapamil 76-85 ATP binding cassette subfamily B member 1 Homo sapiens 112-116 12609962-7 2003 Retroviral-mediated transfection of the BCR-ABL(+) AR230 cell line with the MDR1 gene decreased its sensitivity to imatinib, an effect that was also reversed by verapamil. Verapamil 161-170 ATP binding cassette subfamily B member 1 Homo sapiens 76-80 12737312-5 2003 It induces a much higher chemosensitization than the well-known P-glycoprotein modulator verapamil, which is itself more efficient than RU38486. Verapamil 89-98 ATP binding cassette subfamily B member 1 Homo sapiens 64-78 12653670-11 2003 Evidence of clinical reversal of drug resistance by verapamil suggests a functional role of Pgp in drug resistance, although the significance of the evidence is generally weakened by poor trial designs. Verapamil 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 92-95 12740641-5 2003 Blockade of P-glycoprotein with verapamil led to a decrease in HLA class I expression in RMS resistant cell lines. Verapamil 32-41 ATP binding cassette subfamily B member 1 Homo sapiens 12-26 12608532-1 2003 PURPOSE: In an attempt to improve the oral bioavailability of paclitaxel, a novel P-glycoprotein inhibitor, KR30031, which is verapamil analog with fewer cardiovascular effects, was coadministered with paclitaxel, and to elucidate other possible causes of the low oral bioavailability of paclitaxel, an inhibitor of hepatic metabolism, ketoconazole, was also coadministered with paclitaxel. Verapamil 126-135 ATP binding cassette subfamily B member 1 Homo sapiens 82-96 12608532-8 2003 The ability of KR-30031 to reduce this efflux transport is equal to that of verapamil, a well-known P-glycoprotein inhibitor. Verapamil 76-85 ATP binding cassette subfamily B member 1 Homo sapiens 100-114 12477351-1 2002 A general pharmacophore model of P-glycoprotein (P-gp) drugs is proposed that is based on a highly diverse data set and relates to the verapamil binding site of the protein. Verapamil 135-144 ATP binding cassette subfamily B member 1 Homo sapiens 49-53 12477351-6 2002 On the basis of the obtained results, a hypothesis is proposed to explain the broad structural variety of the P-gp substrates and inhibitors: (i) the verapamil binding site of P-gp has several points that can participate in hydrophobic and HB interactions; (ii) different drugs can interact with different receptor points in different binding modes. Verapamil 150-159 ATP binding cassette subfamily B member 1 Homo sapiens 110-114 12477351-6 2002 On the basis of the obtained results, a hypothesis is proposed to explain the broad structural variety of the P-gp substrates and inhibitors: (i) the verapamil binding site of P-gp has several points that can participate in hydrophobic and HB interactions; (ii) different drugs can interact with different receptor points in different binding modes. Verapamil 150-159 ATP binding cassette subfamily B member 1 Homo sapiens 176-180 12434394-6 2002 p-Glycoprotein (p-gp)inhibitors, such as verapamil (100 microM) and cyclosporin A (CsA, 20 microM) significantly (p < 0.05) inhibited P(BA) but significantly (p < 0.05) enhanced P(AB). Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 12553571-6 2002 A variety of modulators known to interfere with mammalian P-glycoprotein function perturbed resorufin excretion from male adult schistosomes, including cyclosporin A, Ro11-2933, verapamil, or nifedipine. Verapamil 178-187 ATP binding cassette subfamily B member 1 Homo sapiens 58-72 12500571-11 2002 It was show that verapamil is able to induce changes of the surface of Pgp-containing monolayers, and these modifications are maximal at the Pgp:verapamil 1:1 molar ratio. Verapamil 17-26 ATP binding cassette subfamily B member 1 Homo sapiens 71-74 12500571-11 2002 It was show that verapamil is able to induce changes of the surface of Pgp-containing monolayers, and these modifications are maximal at the Pgp:verapamil 1:1 molar ratio. Verapamil 17-26 ATP binding cassette subfamily B member 1 Homo sapiens 141-144 12500571-11 2002 It was show that verapamil is able to induce changes of the surface of Pgp-containing monolayers, and these modifications are maximal at the Pgp:verapamil 1:1 molar ratio. Verapamil 145-154 ATP binding cassette subfamily B member 1 Homo sapiens 71-74 11967284-3 2002 Among these substances, Bodipy-FL-Verapamil, a fluorescent conjugate of the drug efflux blocker verapamil, has been used to study P-glycoprotein activity in different cell types. Verapamil 96-105 ATP binding cassette subfamily B member 1 Homo sapiens 130-144 12499874-3 2002 Inhibition of Pgp function using the antibody MRK16 and verapamil displayed a dose-dependent prevention of T cell mediated endothelial cell death and barrier breakdown. Verapamil 56-65 ATP binding cassette subfamily B member 1 Homo sapiens 14-17 12359058-6 2002 Cell survival assay revealed that verapamil and cepharanthine, conventional P-gp modulators, could completely overcome paclitaxel resistance. Verapamil 34-43 ATP binding cassette subfamily B member 1 Homo sapiens 76-80 12127970-8 2002 Azidopine-binding assay showed that cyclosporin A or verapamil inhibited azidopine binding on Pgp partially but sinensetin did not. Verapamil 53-62 ATP binding cassette subfamily B member 1 Homo sapiens 94-97 12183111-9 2002 Therefore, we have developed a method to measure the P-gp functionality in vivo with PET and [(11)C]verapamil as a positron-emitting P-gp substrate. Verapamil 100-109 ATP binding cassette subfamily B member 1 Homo sapiens 53-57 12183111-9 2002 Therefore, we have developed a method to measure the P-gp functionality in vivo with PET and [(11)C]verapamil as a positron-emitting P-gp substrate. Verapamil 100-109 ATP binding cassette subfamily B member 1 Homo sapiens 133-137 12608534-9 2003 In the presence of a Pgp inhibitor such as verapamil, cyclosporine A, or progesterone, the ATP-dependent uptakes of [3H]digoxin and [3H]vinblastine into BBMVs were significantly reduced. Verapamil 43-52 ATP binding cassette subfamily B member 1 Homo sapiens 21-24 12608535-8 2003 Cotreatment with a Pgp inhibitor, verapamil, abolished the difference in intracellular accumulation of doxorubicin as well as the differences in apoptosis between MCF7 and BC19 cells. Verapamil 34-43 ATP binding cassette subfamily B member 1 Homo sapiens 19-22 12388638-2 2002 Both drugs exhibited greater permeability in the basolateral (BL) to apical (AP) direction than in the AP to BL direction, indicating apically directed secretion; BL to AP transport was inhibited by P-glycoprotein (P-gp) inhibitors verapamil and cyclosporin A. Verapamil 232-241 ATP binding cassette subfamily B member 1 Homo sapiens 199-213 12388638-2 2002 Both drugs exhibited greater permeability in the basolateral (BL) to apical (AP) direction than in the AP to BL direction, indicating apically directed secretion; BL to AP transport was inhibited by P-glycoprotein (P-gp) inhibitors verapamil and cyclosporin A. Verapamil 232-241 ATP binding cassette subfamily B member 1 Homo sapiens 215-219 21782616-7 2002 P-Glycoprotein-mediated transport was characterised in Caco-2 cells by an enhanced transport of vincristine and rhodamine 123 in the basolateral to apical direction and by the inhibition of this transport by verapamil. Verapamil 208-217 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 12067980-5 2002 P-Glycoprotein function was studied by analysis of verapamil-inhibitable efflux of digoxin and rhodamine 123 in intact T84 cells and revealed that hypoxia enhances P-glycoprotein function by as much as 7 +/- 0.4-fold over normoxia. Verapamil 51-60 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 12067980-5 2002 P-Glycoprotein function was studied by analysis of verapamil-inhibitable efflux of digoxin and rhodamine 123 in intact T84 cells and revealed that hypoxia enhances P-glycoprotein function by as much as 7 +/- 0.4-fold over normoxia. Verapamil 51-60 ATP binding cassette subfamily B member 1 Homo sapiens 164-178 11911975-5 2002 In fact, the P-gp inhibitor verapamil reversed only partially the resistance to Dox-induced apoptosis of the MDR cells. Verapamil 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 13-17 12031686-4 2002 The activity of P-gp towards four atypical and two conventional antipsychotics and a proven substrate, verapamil, was examined by their P-gp ATPase activity, a putative measure of P-gp affinity. Verapamil 103-112 ATP binding cassette subfamily B member 1 Homo sapiens 16-20 12031686-4 2002 The activity of P-gp towards four atypical and two conventional antipsychotics and a proven substrate, verapamil, was examined by their P-gp ATPase activity, a putative measure of P-gp affinity. Verapamil 103-112 ATP binding cassette subfamily B member 1 Homo sapiens 136-140 12031686-4 2002 The activity of P-gp towards four atypical and two conventional antipsychotics and a proven substrate, verapamil, was examined by their P-gp ATPase activity, a putative measure of P-gp affinity. Verapamil 103-112 ATP binding cassette subfamily B member 1 Homo sapiens 136-140 11961114-3 2002 In the present study, 16 inhibitors of verapamil binding to P-gp were predicted using these models. Verapamil 39-48 ATP binding cassette subfamily B member 1 Homo sapiens 60-64 12415630-7 2002 Addition of verapamil, by inhibiting P-gp, reversed resistance thereby increasing drug cytotoxicity and allowing the appearance of drug induced cell-cycle perturbations. Verapamil 12-21 ATP binding cassette subfamily B member 1 Homo sapiens 37-41 11961114-6 2002 The degree of similarity in rank ordering prediction by these inhibitor pharmacophore models generated to date confirms a likely overlap in the sites to which the three P-gp substrates used in these studies (verapamil, vinblastine, and digoxin) bind. Verapamil 208-217 ATP binding cassette subfamily B member 1 Homo sapiens 169-173 11913542-5 2002 When verapamil (0.1 mm), a potent modulator of MDR1, was added to both apical and basolateral sides of Caco-2 cells, the absorptive permeation of methylprednisolone was increased and its secretory permeation was decreased. Verapamil 5-14 ATP binding cassette subfamily B member 1 Homo sapiens 47-51 11836114-3 2002 The activity of P-glycoprotein (Pgp) response for MDR in tumor cells was reduced by some of derivatives (3, 4, 8, 12), verapamil (VP) and nifedipine (NP). Verapamil 119-128 ATP binding cassette subfamily B member 1 Homo sapiens 16-30 11836114-3 2002 The activity of P-glycoprotein (Pgp) response for MDR in tumor cells was reduced by some of derivatives (3, 4, 8, 12), verapamil (VP) and nifedipine (NP). Verapamil 119-128 ATP binding cassette subfamily B member 1 Homo sapiens 32-35 11809535-4 2002 These inhibitory potencies for P-gp were more potent than typical P-gp inhibitors, cyclosporine A and verapamil. Verapamil 102-111 ATP binding cassette subfamily B member 1 Homo sapiens 31-35 11913542-12 2002 It was further found that apically-added verapamil demonstrated a modulating effect on MDR1 function even at 5 microM. Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 87-91 11970764-9 2002 Recently, radiopharmaceuticals including carbon 11-labeled colchicine, verapamil, and daunorubicin have been used in cell line and animal studies for the evaluation of Pgp-mediated transport functions using PET technology. Verapamil 71-80 ATP binding cassette subfamily B member 1 Homo sapiens 168-171 11836167-13 2002 A statistically significant correlation (p<0.001) was observed between P-gp protein expression as measured by FACScan analysis and the reversal of efflux activity by either PKC412 or verapamil. Verapamil 186-195 ATP binding cassette subfamily B member 1 Homo sapiens 74-78 11469885-13 2001 CONCLUSIONS: Intrinsic and acquired TXT resistance is primarily mediated by P-gp, but not by MRP or LRP, and is markedly reversed by the P-gp modulator verapamil. Verapamil 152-161 ATP binding cassette subfamily B member 1 Homo sapiens 76-80 11762554-7 2001 CD4+ and CD8+ T cells from patients and control subjects eliminated Rh123, and this activity was inhibited by verapamil, a known P-gp substrate. Verapamil 110-119 ATP binding cassette subfamily B member 1 Homo sapiens 129-133 11724091-8 2001 Both drugs are potent inhibitors of CYP3A4 and of P-glycoprotein; this may be the basis for the pharmacokinetic interaction between erythromycin and verapamil. Verapamil 149-158 ATP binding cassette subfamily B member 1 Homo sapiens 50-64 11676863-6 2001 In addition, the intracellular accumulation of valspodar was found to be 3 - 6 fold higher than that of cyclosporin A in four sublines and verapamil, an inhibitor of P-glycoprotein-mediated transport, enhanced the accumulation of cyclosporin A, but not valspodar. Verapamil 139-148 ATP binding cassette subfamily B member 1 Homo sapiens 166-180 11683237-6 2001 Our results also indicated that ultrasound exerted a much greater effect on cellular accumulation of R123 and DOX and cytotoxicity enhancement of DOX in the MDR variants than putative P-gp antagonist such as verapamil. Verapamil 208-217 ATP binding cassette subfamily B member 1 Homo sapiens 184-188 11739235-11 2001 Cells chronically treated with SJW had decreased accumulation of rhodamine 123, a P-gp substrate, that was reversed with acute verapamil, a P-gp inhibitor. Verapamil 127-136 ATP binding cassette subfamily B member 1 Homo sapiens 82-86 11739235-11 2001 Cells chronically treated with SJW had decreased accumulation of rhodamine 123, a P-gp substrate, that was reversed with acute verapamil, a P-gp inhibitor. Verapamil 127-136 ATP binding cassette subfamily B member 1 Homo sapiens 140-144 11469885-13 2001 CONCLUSIONS: Intrinsic and acquired TXT resistance is primarily mediated by P-gp, but not by MRP or LRP, and is markedly reversed by the P-gp modulator verapamil. Verapamil 152-161 ATP binding cassette subfamily B member 1 Homo sapiens 137-141 11376603-1 2001 Analogues Dmt-Tic (2",6"-dimethyl-L-tyrosine-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid) pharmacophore, a potent delta-opioid receptor antagonist, inhibited hMDR1 P-GP expressed in a G-185 fibroblast cell line in a manner similar to verapamil. Verapamil 239-248 ATP binding cassette subfamily B member 1 Homo sapiens 163-168 11668581-5 2001 However, heightening the Taxol sensitivity of GFP-EMTB-TC-7 cells by pre-incubating cells with the p-glycoprotein inhibitor, verapamil, did result in selective killing of cells highly expressing GFP-EMTB. Verapamil 125-134 ATP binding cassette subfamily B member 1 Homo sapiens 99-113 11351295-5 2001 In the resistant HEp2A cells, cytotoxicity was markedly enhanced by the Pgp/MRP inhibitor verapamil at low doxorubicin concentrations. Verapamil 90-99 ATP binding cassette subfamily B member 1 Homo sapiens 72-75 11351295-6 2001 The GST inhibitor curcumin also enhanced cytotoxicity in HEp2A cells when the Pgp/MRP efflux barrier had been reversed by verapamil or overcome by high doxorubicin concentrations. Verapamil 122-131 ATP binding cassette subfamily B member 1 Homo sapiens 78-81 11331075-5 2001 Our results indicate that LY335979 was 500-1500 times more potent than cyclosporin A or verapamil in restoring Pgp substrate accumulation in the MDR cell line HL60/VCR. Verapamil 88-97 ATP binding cassette subfamily B member 1 Homo sapiens 111-114 11403175-2 2001 Verapamil has been shown to be a competitive inhibitor of Pgp, and was one of the first multidrug-resistant reversing agents identified. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 58-61 11318771-8 2001 Furthermore, the interaction of CBZ with drugs that modulate both CYP3A4 and Pgp function such as verapamil is probably due to inhibition of CYP3A4 and not Pgp. Verapamil 98-107 ATP binding cassette subfamily B member 1 Homo sapiens 77-80 11279063-0 2001 Defining the drug-binding site in the human multidrug resistance P-glycoprotein using a methanethiosulfonate analog of verapamil, MTS-verapamil. Verapamil 119-128 ATP binding cassette subfamily B member 1 Homo sapiens 65-79 11279063-2 2001 Because verapamil is the most potent stimulator of P-gp ATPase activity, we synthesized a thiol-reactive analog of verapamil (MTS-verapamil) and used it with cysteine-scanning mutagenesis to identify the reactive residues within the drug-binding domain of P-gp. Verapamil 8-17 ATP binding cassette subfamily B member 1 Homo sapiens 51-55 11279063-2 2001 Because verapamil is the most potent stimulator of P-gp ATPase activity, we synthesized a thiol-reactive analog of verapamil (MTS-verapamil) and used it with cysteine-scanning mutagenesis to identify the reactive residues within the drug-binding domain of P-gp. Verapamil 8-17 ATP binding cassette subfamily B member 1 Homo sapiens 256-260 11279063-2 2001 Because verapamil is the most potent stimulator of P-gp ATPase activity, we synthesized a thiol-reactive analog of verapamil (MTS-verapamil) and used it with cysteine-scanning mutagenesis to identify the reactive residues within the drug-binding domain of P-gp. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 51-55 11279063-2 2001 Because verapamil is the most potent stimulator of P-gp ATPase activity, we synthesized a thiol-reactive analog of verapamil (MTS-verapamil) and used it with cysteine-scanning mutagenesis to identify the reactive residues within the drug-binding domain of P-gp. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 256-260 11279063-2 2001 Because verapamil is the most potent stimulator of P-gp ATPase activity, we synthesized a thiol-reactive analog of verapamil (MTS-verapamil) and used it with cysteine-scanning mutagenesis to identify the reactive residues within the drug-binding domain of P-gp. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 51-55 11279063-2 2001 Because verapamil is the most potent stimulator of P-gp ATPase activity, we synthesized a thiol-reactive analog of verapamil (MTS-verapamil) and used it with cysteine-scanning mutagenesis to identify the reactive residues within the drug-binding domain of P-gp. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 256-260 11279063-3 2001 MTS-verapamil stimulated the ATPase activity of Cys-less P-gp and had a K(m) value (25 microM) that was similar to that of verapamil. Verapamil 4-13 ATP binding cassette subfamily B member 1 Homo sapiens 57-61 11279063-3 2001 MTS-verapamil stimulated the ATPase activity of Cys-less P-gp and had a K(m) value (25 microM) that was similar to that of verapamil. Verapamil 123-132 ATP binding cassette subfamily B member 1 Homo sapiens 57-61 11379779-3 2001 Calcium channel blockers such as verapamil, nifedipine and nicardipine have been shown to reverse cellular drug resistance by inhibiting P-gp drug efflux. Verapamil 33-42 ATP binding cassette subfamily B member 1 Homo sapiens 137-141 11379779-5 2001 Verapamil, and even more markedly, lomerizine, increased cellular uptake of calcein transported by P-gp in a P-gp-expressing erythroleukemia cell line, K562-Dox. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 99-103 11379779-5 2001 Verapamil, and even more markedly, lomerizine, increased cellular uptake of calcein transported by P-gp in a P-gp-expressing erythroleukemia cell line, K562-Dox. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 109-113 11498403-6 2000 A wealth of recent experimental data shows that many of the previously tested P-glycoprotein inhibitors, including verapamil, cyclosporin A, and valspodar (SDZ PSC 833), are substrates and/or potent inhibitors of cytochrome P450 3A4 (CYP3A4). Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 78-92 11125025-2 2001 The resulting Pgp-stationary phase was used in frontal and zonal chromatographic studies to investigate the binding of vinblastine (VBL), doxorubicin (DOX), verapamil (VER), and cyclosporin A (CsA) to the immobilized Pgp. Verapamil 168-171 ATP binding cassette subfamily B member 1 Homo sapiens 14-17 11336351-6 2001 The potency of inhibition of P-gp was cyclosporine > tacrolimus > quinidine > verapamil > vinblastine. Verapamil 87-96 ATP binding cassette subfamily B member 1 Homo sapiens 29-33 11118294-4 2000 Similar results were obtained with verapamil, progesterone, and GF120918 in the MDR1-overexpressing cells MCF7/ADR. Verapamil 35-44 ATP binding cassette subfamily B member 1 Homo sapiens 80-84 11157479-4 2001 Although all progenitors expressed P-gp protein and GST mRNA, verapamil treatment significantly, and selectively, increased the toxicity of paclitaxel and carboplatin to CFU-Meg, suggesting an important role for P-gp in megakaryocyte drug resistance. Verapamil 62-71 ATP binding cassette subfamily B member 1 Homo sapiens 212-216 11159725-12 2001 In addition, lumenal but not cellular fluorescence intensity was significantly decreased when capillaries were incubated with PSC-833, Cyclosporin A or Verapamil, all inhibitors of p-glycoprotein. Verapamil 152-161 ATP binding cassette subfamily B member 1 Homo sapiens 181-195 11159725-13 2001 Conversely, unlabelled Ivermectin reduced the p-glycoprotein (Pgp)-mediated secretion of a fluorescent derivative of Verapamil, (BODIPY-Verapamil). Verapamil 117-126 ATP binding cassette subfamily B member 1 Homo sapiens 46-60 11159725-13 2001 Conversely, unlabelled Ivermectin reduced the p-glycoprotein (Pgp)-mediated secretion of a fluorescent derivative of Verapamil, (BODIPY-Verapamil). Verapamil 117-126 ATP binding cassette subfamily B member 1 Homo sapiens 62-65 11159798-9 2001 In CEM/VLB100 cells, this saturable component was inhibited by verapamil and was temperature-sensitive, consistent with Pgp-mediated transport. Verapamil 63-72 ATP binding cassette subfamily B member 1 Homo sapiens 120-123 27419877-8 2001 Moreover, radiopharmaceuticals including carbon-11-labeled colchicine, verapamil and daunorabicin have been used for the assessment of Pgp-mediated transport functions in vivo using PET technology. Verapamil 71-80 ATP binding cassette subfamily B member 1 Homo sapiens 135-138 11108806-8 2000 Surprisingly, in these non-P-glycoprotein expressing cells, verapamil increased both Dox and Rho 123 retention. Verapamil 60-69 ATP binding cassette subfamily B member 1 Homo sapiens 27-41 11108806-10 2000 These results should be considered when Rho 123 and verapamil are used to detect P-glycoprotein. Verapamil 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 81-95 11139374-11 2000 The functionality in vivo of P-gp can be measured with positron emission tomography and [(11)C]-verapamil or with single photon emission computer tomography and(99m)Tc-sestamibi. Verapamil 96-105 ATP binding cassette subfamily B member 1 Homo sapiens 29-33 11042226-4 2000 Polarised transport of doxorubicin in the Caco-2 and the LLC-PK1:MDR1 cell lines could be inhibited by the P-gp inhibitors SDZ-PSC 833 (PSC 833), cyclosporin A (CsA), verapamil and quinine, but not by the inhibitors for the organic cation carrier systems cimetidine and tetraethylammonium (TEA). Verapamil 167-176 ATP binding cassette subfamily B member 1 Homo sapiens 107-111 10947968-4 2000 Inhibition of MRP1 by verapamil or indomethacin resulted in a shift in the amount of probe that was internalized: approx. Verapamil 22-31 ATP binding cassette subfamily B member 1 Homo sapiens 14-18 10744311-3 2000 Displacement studies using other known PGP ligands, verapamil and cyclosporin A, demonstrated that there was selective binding between vinblastine and the immobilized PGP transporter. Verapamil 52-61 ATP binding cassette subfamily B member 1 Homo sapiens 167-170 10841824-5 2000 Enzyme assays were used to determine the effects of disulfiram on the verapamil-stimulated adenosine triphosphatase (ATPase) activity of P-gp. Verapamil 70-79 ATP binding cassette subfamily B member 1 Homo sapiens 137-141 10841824-8 2000 RESULTS: Disulfiram increased the sensitivity of P-gp-transfected cells to vinblastine and colchicine and inhibited P-gp"s verapamil-stimulated ATPase activity. Verapamil 123-132 ATP binding cassette subfamily B member 1 Homo sapiens 116-120 10837354-2 2000 Aldosterone secretion is significantly decreased by the PGP inhibitors verapamil, cyclosporin A (CSA), PSC-833, and vinblastine. Verapamil 71-80 ATP binding cassette subfamily B member 1 Homo sapiens 56-59 10837354-6 2000 In BC19/3 cells (MCF7 cells transfected with MDR1), the efflux of FL-aldosterone was rapid and it was inhibited by verapamil, indicating that transfection with MDR1 cDNA confers the ability to transport FL-aldosterone. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 45-49 10837354-6 2000 In BC19/3 cells (MCF7 cells transfected with MDR1), the efflux of FL-aldosterone was rapid and it was inhibited by verapamil, indicating that transfection with MDR1 cDNA confers the ability to transport FL-aldosterone. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 160-164 10912954-13 2000 In Vl cells drug removal was sensitive to the P-gp inhibitor verapamil or energy starvation. Verapamil 61-70 ATP binding cassette subfamily B member 1 Homo sapiens 46-50 10805101-10 2000 We conclude that (i) glioma cells exhibit constitutive mdr-like drug resistance that is not significantly altered by chronic drug exposure in vitro; (ii) endothelial cells may play an important role in Pgp-mediated drug resistance of gliomas in vivo; (iii) radiotherapy and repeated chemotherapy cycles do not modulate Pgp expression in human malignant gliomas in vivo; (iv) there is preliminary evidence for a non-Pgp, verapamil-sensitive drug transport activity in glioma cells. Verapamil 420-429 ATP binding cassette subfamily B member 1 Homo sapiens 202-205 10772630-5 2000 Known Pgp inhibitors, such as cyclosporin A, nicardipine, verapamil, quinidine, terfenadine, tamoxifen, and vinblastine were demonstrated to inhibit the Pgp-mediated efflux of daunorubicin. Verapamil 58-67 ATP binding cassette subfamily B member 1 Homo sapiens 6-9 10772630-5 2000 Known Pgp inhibitors, such as cyclosporin A, nicardipine, verapamil, quinidine, terfenadine, tamoxifen, and vinblastine were demonstrated to inhibit the Pgp-mediated efflux of daunorubicin. Verapamil 58-67 ATP binding cassette subfamily B member 1 Homo sapiens 153-156 10773005-0 2000 Characterization of the major metabolites of verapamil as substrates and inhibitors of P-glycoprotein. Verapamil 45-54 ATP binding cassette subfamily B member 1 Homo sapiens 87-101 10773005-2 2000 Furthermore, verapamil is known to be a potent inhibitor of P-glycoprotein function. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 60-74 10773005-4 2000 The aim of the present study was to investigate P-glycoprotein-mediated transport and inhibition properties of verapamil and its metabolites norverapamil, D-620, D-617, and D-703. Verapamil 111-120 ATP binding cassette subfamily B member 1 Homo sapiens 48-62 10773005-9 2000 Moreover, verapamil, norverapamil, and D-703 inhibited P-glycoprotein-mediated digoxin transport with IC(50) values of 1.1, 0.3, and 1.6 microM, respectively, whereas D-617 and D-620 did not (at concentrations up to 100 microM). Verapamil 10-19 ATP binding cassette subfamily B member 1 Homo sapiens 55-69 10773005-10 2000 We conclude that verapamil phase I metabolites exhibit different P-glycoprotein substrate and inhibition characteristics, with the N-dealkylated metabolites D-617 and D-620 being P-glycoprotein substrates and norverapamil and D-703 being inhibitors of P-glycoprotein function, which may influence P-glycoprotein-dependent drug disposition and elimination. Verapamil 17-26 ATP binding cassette subfamily B member 1 Homo sapiens 65-79 10773005-10 2000 We conclude that verapamil phase I metabolites exhibit different P-glycoprotein substrate and inhibition characteristics, with the N-dealkylated metabolites D-617 and D-620 being P-glycoprotein substrates and norverapamil and D-703 being inhibitors of P-glycoprotein function, which may influence P-glycoprotein-dependent drug disposition and elimination. Verapamil 17-26 ATP binding cassette subfamily B member 1 Homo sapiens 179-193 10773005-10 2000 We conclude that verapamil phase I metabolites exhibit different P-glycoprotein substrate and inhibition characteristics, with the N-dealkylated metabolites D-617 and D-620 being P-glycoprotein substrates and norverapamil and D-703 being inhibitors of P-glycoprotein function, which may influence P-glycoprotein-dependent drug disposition and elimination. Verapamil 17-26 ATP binding cassette subfamily B member 1 Homo sapiens 179-193 10773005-10 2000 We conclude that verapamil phase I metabolites exhibit different P-glycoprotein substrate and inhibition characteristics, with the N-dealkylated metabolites D-617 and D-620 being P-glycoprotein substrates and norverapamil and D-703 being inhibitors of P-glycoprotein function, which may influence P-glycoprotein-dependent drug disposition and elimination. Verapamil 17-26 ATP binding cassette subfamily B member 1 Homo sapiens 179-193 10783826-0 2000 Affinities at the verapamil binding site of MDR1-encoded P-glycoprotein: drugs and analogs, stereoisomers and metabolites. Verapamil 18-27 ATP binding cassette subfamily B member 1 Homo sapiens 44-48 10783826-0 2000 Affinities at the verapamil binding site of MDR1-encoded P-glycoprotein: drugs and analogs, stereoisomers and metabolites. Verapamil 18-27 ATP binding cassette subfamily B member 1 Homo sapiens 57-71 10783826-5 2000 RESULTS: Whereas some stereoselectivity was detected for the high-affinity P-gp substrates verapamil and carvedilol, little or no differences were observed in the case of other beta-blockers. Verapamil 91-100 ATP binding cassette subfamily B member 1 Homo sapiens 75-79 10783826-7 2000 CONCLUSIONS: Metabolites of verapamil, gallopamil, carvedilol and omeprazole are characterized by having higher IC50 values (lower P-gp affinity) than the respective parent compounds. Verapamil 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 131-135 10870315-3 2000 Verapamil, a calcium antagonist, inhibits the efflux function of gp-170 and cytoskeletal transportation. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 65-71 10870315-4 2000 The aim of this study was to determine the effect of verapamil on gp-170 expression and intracellular drug accumulation in RCC tumor cells and the modulation of cytotoxicity of various chemotherapeutic drugs on native RCC cell lines and acquired MDR sublines by verapamil. Verapamil 53-62 ATP binding cassette subfamily B member 1 Homo sapiens 66-72 10870315-5 2000 METHODS: Using cultured cell lines of RCC and their MDR sublines as target cells, the effect of verapamil on gp-170 expression was analyzed by immunofluorescence flow cytometry. Verapamil 96-105 ATP binding cassette subfamily B member 1 Homo sapiens 109-115 10870315-8 2000 RESULTS: From flow cytometric measurement, the expression of gp-170 was significantly decreased in A704 and Caki-1 tumor cells after verapamil treatment. Verapamil 133-142 ATP binding cassette subfamily B member 1 Homo sapiens 61-67 10870315-15 2000 CONCLUSIONS: These results suggest that verapamil plays an important role in the circumvention of native and acquired chemoresistance of RRC because it suppresses membranous gp-170 expression and cytoplasmic drug transportation. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 174-180 10727237-4 2000 The maximal basal-, verapamil-, and vinblastine-stimulated ATPase activities of the trypsinized Pgp were approximately 1.8-, 1.5-, and 1.75-fold higher than the activities of the native Pgp, respectively. Verapamil 20-29 ATP binding cassette subfamily B member 1 Homo sapiens 96-99 10727237-4 2000 The maximal basal-, verapamil-, and vinblastine-stimulated ATPase activities of the trypsinized Pgp were approximately 1.8-, 1.5-, and 1.75-fold higher than the activities of the native Pgp, respectively. Verapamil 20-29 ATP binding cassette subfamily B member 1 Homo sapiens 186-189 10978781-6 2000 Verapamil, an effective resistance modulator in P-glycoprotein MDR cells, restored the DNR distribution closer to that in the parent cells. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 48-62 10773025-0 2000 Verapamil stimulates glutathione transport by the 190-kDa multidrug resistance protein 1 (MRP1). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 58-88 10773025-0 2000 Verapamil stimulates glutathione transport by the 190-kDa multidrug resistance protein 1 (MRP1). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 90-94 10773025-3 2000 Moreover, agents such as verapamil that reverse P-glycoprotein-mediated resistance are often poorly, or not at all, effective in MRP1-overexpressing cells. Verapamil 25-34 ATP binding cassette subfamily B member 1 Homo sapiens 48-62 10773025-3 2000 Moreover, agents such as verapamil that reverse P-glycoprotein-mediated resistance are often poorly, or not at all, effective in MRP1-overexpressing cells. Verapamil 25-34 ATP binding cassette subfamily B member 1 Homo sapiens 129-133 10773025-4 2000 In the present study, we investigated the effects of verapamil on MRP1-mediated transport processes. Verapamil 53-62 ATP binding cassette subfamily B member 1 Homo sapiens 66-70 10773025-5 2000 We found that verapamil inhibited LTC(4) transport into inside-out membrane vesicles prepared from MRP1-transfected cells in a competitive manner, but only in the presence of reduced glutathione (GSH) or its nonreducing S-methyl derivative. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 99-103 10773025-8 2000 However, verapamil strongly stimulated MRP1-mediated GSH uptake by membrane vesicles in a concentration-dependent and osmotically sensitive manner that was inhibitable by MRP1-specific monoclonal antibodies. Verapamil 9-18 ATP binding cassette subfamily B member 1 Homo sapiens 39-43 10773025-8 2000 However, verapamil strongly stimulated MRP1-mediated GSH uptake by membrane vesicles in a concentration-dependent and osmotically sensitive manner that was inhibitable by MRP1-specific monoclonal antibodies. Verapamil 9-18 ATP binding cassette subfamily B member 1 Homo sapiens 171-175 10773025-10 2000 It is proposed that the variable ability of verapamil to modulate MRP1-mediated resistance in different cell lines may be more closely linked to its effect on the GSH status of the cells than on its ability to inhibit the MRP1 transporter itself. Verapamil 44-53 ATP binding cassette subfamily B member 1 Homo sapiens 66-70 10773025-10 2000 It is proposed that the variable ability of verapamil to modulate MRP1-mediated resistance in different cell lines may be more closely linked to its effect on the GSH status of the cells than on its ability to inhibit the MRP1 transporter itself. Verapamil 44-53 ATP binding cassette subfamily B member 1 Homo sapiens 222-226 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. Verapamil 269-278 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. Verapamil 269-278 ATP binding cassette subfamily B member 1 Homo sapiens 199-203 10727524-10 2000 Phe(335) also plays a role in the coupling of verapamil binding and modulation of daunorubicin intracellular accumulation in wild-type P-gp. Verapamil 46-55 ATP binding cassette subfamily B member 1 Homo sapiens 135-139 10677583-6 2000 The co-presence of verapamil, one typical P-glycoprotein (P-gp) substrate, and Deo-Na or Cap-Na demonstrated further reduction of epirubicin efflux. Verapamil 19-28 ATP binding cassette subfamily B member 1 Homo sapiens 58-62 10744311-6 2000 The Kd values obtained on the PGP-IAM for cyclosporin A and verapamil were 492+/-21 and 172+/-29 microM, respectively. Verapamil 60-69 ATP binding cassette subfamily B member 1 Homo sapiens 30-33 10636889-4 2000 When mdr1 inhibitors (PSC833, cyclosporine A, verapamil) were transiently added to cells with mdr1 up-regulation by pretreatment for 72 h with cadmium, cadmium-induced apoptosis increased significantly and to a percentage similar to that obtained in cells with no mdr1 up-regulation (72-h cadmium: 5.2 +/- 0.9% versus 72-h cadmium + 1-h PSC833: 7.2 +/- 1.4%; p < or = 0.001). Verapamil 46-55 ATP binding cassette subfamily B member 1 Homo sapiens 5-9 10636889-4 2000 When mdr1 inhibitors (PSC833, cyclosporine A, verapamil) were transiently added to cells with mdr1 up-regulation by pretreatment for 72 h with cadmium, cadmium-induced apoptosis increased significantly and to a percentage similar to that obtained in cells with no mdr1 up-regulation (72-h cadmium: 5.2 +/- 0.9% versus 72-h cadmium + 1-h PSC833: 7.2 +/- 1.4%; p < or = 0.001). Verapamil 46-55 ATP binding cassette subfamily B member 1 Homo sapiens 94-98 10636889-4 2000 When mdr1 inhibitors (PSC833, cyclosporine A, verapamil) were transiently added to cells with mdr1 up-regulation by pretreatment for 72 h with cadmium, cadmium-induced apoptosis increased significantly and to a percentage similar to that obtained in cells with no mdr1 up-regulation (72-h cadmium: 5.2 +/- 0.9% versus 72-h cadmium + 1-h PSC833: 7.2 +/- 1.4%; p < or = 0.001). Verapamil 46-55 ATP binding cassette subfamily B member 1 Homo sapiens 94-98 10769682-4 2000 The activity of P-glycoprotein (Pgp) responsible for MDR in tumor cells was reduced by compounds [G2, 3, 6, 5, 8, 1, 11], verapamil [VP] and nifedipine [NP]. Verapamil 122-131 ATP binding cassette subfamily B member 1 Homo sapiens 16-30 10769682-4 2000 The activity of P-glycoprotein (Pgp) responsible for MDR in tumor cells was reduced by compounds [G2, 3, 6, 5, 8, 1, 11], verapamil [VP] and nifedipine [NP]. Verapamil 122-131 ATP binding cassette subfamily B member 1 Homo sapiens 32-35 11036469-5 2000 Modulation of P-glycoprotein function was performed by verapamil or Cremophor EL. Verapamil 55-64 ATP binding cassette subfamily B member 1 Homo sapiens 14-28 11036469-11 2000 Reversal of P-glycoprotein function by verapamil or Cremophor EL enhanced the growth inhibitory effects of paclitaxel and further supported the role of P-glycoprotein for paclitaxel sensitivity of human RCCs. Verapamil 39-48 ATP binding cassette subfamily B member 1 Homo sapiens 12-26 10554093-6 1999 This polarized efflux was concentration dependent (saturable kinetics with Km = 207 microM, Vmax = 0.275 nmol cm(-2) min(-1)) and could be reduced in the presence of verapamil (300 microM), an inhibitor of p-glycoprotein. Verapamil 166-175 ATP binding cassette subfamily B member 1 Homo sapiens 206-220 11144235-5 2000 The combination of EPADI (10 microg/ml) with verapamil (1 microM) resulted in a considerable increase in the [A] and [R] of the model P-gp substrate rhodamine-123 within drug-resistant cells compared to when either agent were used alone. Verapamil 45-54 ATP binding cassette subfamily B member 1 Homo sapiens 134-138 10571255-3 1999 The calcium channel blocker verapamil has been shown to reverse cellular drug resistance by inhibiting P-gp drug efflux. Verapamil 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 103-107 10571255-5 1999 Verapamil (10 micromol/L), and even more markedly, carvedilol (10 micromol/L) increased cellular uptake of P-gp-transported calcein of a P-gp-expressing breast cancer cell line (Hs578T-Dox). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 107-111 10571255-5 1999 Verapamil (10 micromol/L), and even more markedly, carvedilol (10 micromol/L) increased cellular uptake of P-gp-transported calcein of a P-gp-expressing breast cancer cell line (Hs578T-Dox). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 137-141 10491157-1 1999 The ATPase activity of the multiple drug resistance transporter Mdr1 (P-glycoprotein, gp170) depended on the concentration of ATP with both positive and negative co-operativity both in the absence and in the presence of verapamil. Verapamil 220-229 ATP binding cassette subfamily B member 1 Homo sapiens 64-68 10491157-1 1999 The ATPase activity of the multiple drug resistance transporter Mdr1 (P-glycoprotein, gp170) depended on the concentration of ATP with both positive and negative co-operativity both in the absence and in the presence of verapamil. Verapamil 220-229 ATP binding cassette subfamily B member 1 Homo sapiens 70-84 10491157-1 1999 The ATPase activity of the multiple drug resistance transporter Mdr1 (P-glycoprotein, gp170) depended on the concentration of ATP with both positive and negative co-operativity both in the absence and in the presence of verapamil. Verapamil 220-229 ATP binding cassette subfamily B member 1 Homo sapiens 86-91 10491158-1 1999 Suramin, a known inhibitor of ATP binding enzymes with six negatively charged sulfonic acid groups, stimulated the ATPase activity of the multiple drug resistance transporter Mdr1 in low concentrations by acting as a substrate and by increasing the affinity for both verapamil and ATP. Verapamil 267-276 ATP binding cassette subfamily B member 1 Homo sapiens 175-179 10491158-4 1999 Verapamil itself activated the ATPase activity of Mdr1 only at moderate concentrations, but showed substrate inhibition at higher concentrations. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 50-54 10491158-5 1999 This was also observed for progesterone, which decreased the Ki of Mdr1 for verapamil but increased the Km. Verapamil 76-85 ATP binding cassette subfamily B member 1 Homo sapiens 67-71 10491158-6 1999 Additionally, verapamil increased the Hill coefficient of Mdr1 for progesterone from 1.1 to 3.2. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 58-62 10576649-7 1999 Binding of [3H]-vinblastine to P-gp in MES-Dx5 membranes was inhibited by GF120918 (K = 5+/-1 nM), verapamil (Ki = 660+/-350 nM) and doxorubicin (Ki = 6940+/-2100 nM). Verapamil 99-108 ATP binding cassette subfamily B member 1 Homo sapiens 31-35 10514357-3 1999 In particular, observations need to be clarified in which substrates showing high affinity to P-glycoprotein, e.g., verapamil, apparently do not seem to be greatly influenced by P-gp in their permeability and consequently also with respect to their extent of GI-absorption after oral administration, whereas weaker substrates of P-gp, e.g., talinolol, have clearly shown P-gp-related absorption phenomena such as nonlinear intestinal permeability and bioavailability. Verapamil 116-125 ATP binding cassette subfamily B member 1 Homo sapiens 94-108 10514357-3 1999 In particular, observations need to be clarified in which substrates showing high affinity to P-glycoprotein, e.g., verapamil, apparently do not seem to be greatly influenced by P-gp in their permeability and consequently also with respect to their extent of GI-absorption after oral administration, whereas weaker substrates of P-gp, e.g., talinolol, have clearly shown P-gp-related absorption phenomena such as nonlinear intestinal permeability and bioavailability. Verapamil 116-125 ATP binding cassette subfamily B member 1 Homo sapiens 329-333 10514357-3 1999 In particular, observations need to be clarified in which substrates showing high affinity to P-glycoprotein, e.g., verapamil, apparently do not seem to be greatly influenced by P-gp in their permeability and consequently also with respect to their extent of GI-absorption after oral administration, whereas weaker substrates of P-gp, e.g., talinolol, have clearly shown P-gp-related absorption phenomena such as nonlinear intestinal permeability and bioavailability. Verapamil 116-125 ATP binding cassette subfamily B member 1 Homo sapiens 329-333 10514357-12 1999 It was shown that a combination of high P-gp affinity with good passive membrane permeability, e.g., in the case of verapamil, will readily compensate for the P-gp-mediated reduction of intestinal permeability, resulting in a narrow range in which the permeability depends on the apical drug concentration. Verapamil 116-125 ATP binding cassette subfamily B member 1 Homo sapiens 40-44 10514357-12 1999 It was shown that a combination of high P-gp affinity with good passive membrane permeability, e.g., in the case of verapamil, will readily compensate for the P-gp-mediated reduction of intestinal permeability, resulting in a narrow range in which the permeability depends on the apical drug concentration. Verapamil 116-125 ATP binding cassette subfamily B member 1 Homo sapiens 159-163 10527640-0 1999 P-glycoprotein system as a determinant of drug interactions: the case of digoxin-verapamil. Verapamil 81-90 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 10527640-7 1999 Reports from oncology research show that verapamil can interact with P-glycoprotein as a modulator. Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 69-83 10527640-8 1999 Also taking into account that digoxin, like many anticancer drugs, is a substrate for P-glycoprotein, it is likely that P-glycoprotein modulation accounts for the digoxin-verapamil interaction. Verapamil 171-180 ATP binding cassette subfamily B member 1 Homo sapiens 86-100 10527640-8 1999 Also taking into account that digoxin, like many anticancer drugs, is a substrate for P-glycoprotein, it is likely that P-glycoprotein modulation accounts for the digoxin-verapamil interaction. Verapamil 171-180 ATP binding cassette subfamily B member 1 Homo sapiens 120-134 10527640-9 1999 Current knowledge suggest that the non-competitive digoxin-verapamil interaction is due to inhibition of P-glycoprotein activity by verapamil resulting in a decreased renal tubular elimination of digoxin. Verapamil 59-68 ATP binding cassette subfamily B member 1 Homo sapiens 105-119 10527640-9 1999 Current knowledge suggest that the non-competitive digoxin-verapamil interaction is due to inhibition of P-glycoprotein activity by verapamil resulting in a decreased renal tubular elimination of digoxin. Verapamil 132-141 ATP binding cassette subfamily B member 1 Homo sapiens 105-119 10374847-7 1999 The Pgp-inhibitor verapamil affected IDA uptake only in the most resistant cell line 8226-Dox40. Verapamil 18-27 ATP binding cassette subfamily B member 1 Homo sapiens 4-7 10511059-1 1999 OBJECTIVE: To examine the secretion of the beta1-adrenergic receptor antagonist talinolol into the small intestine during its intravenous administration and to show the relevance of the P-glycoprotein-modulating drug verapamil for this secretory transport mechanism in humans. Verapamil 217-226 ATP binding cassette subfamily B member 1 Homo sapiens 186-200 10511059-8 1999 This secretion is reduced by the intraluminal supply of the P-glycoprotein modulating drug R-verapamil. Verapamil 91-102 ATP binding cassette subfamily B member 1 Homo sapiens 60-74 10510888-11 1999 One of these strategies is to reverse MDR by using such P-gp inhibitors as verapamil and cyclosporine A. Verapamil 75-84 ATP binding cassette subfamily B member 1 Homo sapiens 56-60 10448079-5 1999 Treatment with the MDR1 P-gp inhibitor, verapamil, altered the kinetics of C12-NBD-PC in the resistant cells to more closely follow the pattern of C12-NBD-PC handling by sensitive cells. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 19-23 10463770-6 1999 Verapamil could not reverse the resistance of KBr to HePC although it is a well-known reversing agent against MDR1. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 110-114 10467374-3 1999 Furthermore, the resistance to doxorubicin was abolished by preincubation with the MDR1 inhibitor verapamil while resistance to MNU was ablated by the specific ATase inactivator, O6-benzylguanine (O6-beG) confirming that resistance to doxorubicin and MNU was conferred by MDR1 and ATase, respectively. Verapamil 98-107 ATP binding cassette subfamily B member 1 Homo sapiens 83-87 10399954-6 1999 Resistance to a P-gp-associated drug, doxorubicin, could be reversed with P-gp circumventing agents such as cyclosporin A and verapamil, but these substances had no effect on resistance to 5-fluorouracil. Verapamil 126-135 ATP binding cassette subfamily B member 1 Homo sapiens 16-20 10399954-6 1999 Resistance to a P-gp-associated drug, doxorubicin, could be reversed with P-gp circumventing agents such as cyclosporin A and verapamil, but these substances had no effect on resistance to 5-fluorouracil. Verapamil 126-135 ATP binding cassette subfamily B member 1 Homo sapiens 74-78 10418960-0 1999 Partial inhibition of the P-glycoprotein-mediated transport of anthracyclines in viable resistant K562 cells after irradiation in the presence of a verapamil analogue. Verapamil 148-157 ATP binding cassette subfamily B member 1 Homo sapiens 26-40 10418960-2 1999 The effect on P-gp-mediated transport of anthracyclines of cell irradiation in the presence of 2,2-diphenyl-5-[N-1-(o-azidophenyl)ethylamino]valeronitrile (VP*), a photoactivable analogue of verapamil was studied in viable K562/ADR cells. Verapamil 191-200 ATP binding cassette subfamily B member 1 Homo sapiens 14-18 10418960-4 1999 It was observed that the irradiation in the presence of the verapamil analogue was unable to completely inhibit the P-gp-mediated efflux of anthracyclines and we estimated that P-gp retained 10-20% of its ability to pump these toxins. Verapamil 60-69 ATP binding cassette subfamily B member 1 Homo sapiens 177-181 10511474-6 1999 Verapamil (25 microM), a P-glycoprotein inhibitor, markedly increased (approximately 40% increase) the accumulation of a non-saturating concentration of L-DOPA (2.5 microM) at both initial rate of uptake (IRU, 6 min incubation) and at steady-state (SS, 30 min incubation). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 25-39 10368654-0 1999 Combinations of P-glycoprotein blockers, verapamil, PSC833, and cremophor act differently on the multidrug resistance associated protein (MRP) and on P-glycoprotein (Pgp). Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 150-164 10334913-3 1999 MDR1 gene expression was associated with the expression of functional P-glycoprotein (gp-170); the function was reversed by verapamil and cyclosporin A. Verapamil 124-133 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 10334913-3 1999 MDR1 gene expression was associated with the expression of functional P-glycoprotein (gp-170); the function was reversed by verapamil and cyclosporin A. Verapamil 124-133 ATP binding cassette subfamily B member 1 Homo sapiens 70-84 10334913-3 1999 MDR1 gene expression was associated with the expression of functional P-glycoprotein (gp-170); the function was reversed by verapamil and cyclosporin A. Verapamil 124-133 ATP binding cassette subfamily B member 1 Homo sapiens 86-92 10225448-4 1999 However, in MDR cells treated with either 10 microM DNR or 1 microM DNR in association with the P-glycoprotein (P-gp) blocker verapamil (treatment conditions which yield an intracellular DNR concentration similar to that achieved with 1 microM in the parental cells), we were unable to detect SM hydrolysis, ceramide generation and apoptosis. Verapamil 126-135 ATP binding cassette subfamily B member 1 Homo sapiens 96-110 10225448-4 1999 However, in MDR cells treated with either 10 microM DNR or 1 microM DNR in association with the P-glycoprotein (P-gp) blocker verapamil (treatment conditions which yield an intracellular DNR concentration similar to that achieved with 1 microM in the parental cells), we were unable to detect SM hydrolysis, ceramide generation and apoptosis. Verapamil 126-135 ATP binding cassette subfamily B member 1 Homo sapiens 112-116 10344751-4 1999 Therefore, P-gp function was measured in vivo with positron emission tomography (PET) and [11C]verapamil as radiolabeled P-gp substrate. Verapamil 95-104 ATP binding cassette subfamily B member 1 Homo sapiens 11-15 10344751-4 1999 Therefore, P-gp function was measured in vivo with positron emission tomography (PET) and [11C]verapamil as radiolabeled P-gp substrate. Verapamil 95-104 ATP binding cassette subfamily B member 1 Homo sapiens 121-125 10344751-7 1999 [11C]Daunorubicin and [11C]verapamil accumulation were higher in GLC4 than in GLC4/P-gp cells. Verapamil 27-36 ATP binding cassette subfamily B member 1 Homo sapiens 83-87 10075817-5 1999 The fluorescein-colchicine transport was found to be dependent on the presence of P-glycoprotein, required ATP, and was inhibited by vanadate and the reversal agent, verapamil, in a dose-dependent manner. Verapamil 166-175 ATP binding cassette subfamily B member 1 Homo sapiens 82-96 10368654-0 1999 Combinations of P-glycoprotein blockers, verapamil, PSC833, and cremophor act differently on the multidrug resistance associated protein (MRP) and on P-glycoprotein (Pgp). Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 166-169 10368654-5 1999 Clinically optimal plasma levels of verapamil, cremophor, and PSC833 have been shown to completely block the function of Pgp in Pgp-over expressing cells. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 121-124 10368654-5 1999 Clinically optimal plasma levels of verapamil, cremophor, and PSC833 have been shown to completely block the function of Pgp in Pgp-over expressing cells. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 128-131 11741214-6 1999 The ratio of IC50for P-gp to that for CYP3A4 was more than 200 for L-754,394, 60 ~ 150 for ketoconazole, 1.5 for verapamil, and 0.05 for PSC 833. Verapamil 113-122 ATP binding cassette subfamily B member 1 Homo sapiens 21-25 10079321-9 1999 The results suggest that radiolabelled colchicine, verapamil and daunorubicin are feasible substrates with which to image Pgp function in tumours. Verapamil 51-60 ATP binding cassette subfamily B member 1 Homo sapiens 122-125 10079321-10 1999 Uptake of [11C]colchicine and [11C]verapamil is relatively high in the chest area, reducing the value of both tracers for monitoring Pgp-mediated drug transport in tumours located in this region. Verapamil 35-44 ATP binding cassette subfamily B member 1 Homo sapiens 133-136 10321958-3 1999 YT-INDY, a human NK-like cell line, was transfected with the MDR 1 gene, then tested for Pgp activity the presence of various concentrations of R-verapamil, a potent Pgp inhibitor. Verapamil 144-155 ATP binding cassette subfamily B member 1 Homo sapiens 166-169 10321958-4 1999 We showed that, unlike control YT-INDY, the Pgp activity of the transfectants (YT-mdr(+)) was only partially inhibited by R-verapamil. Verapamil 122-133 ATP binding cassette subfamily B member 1 Homo sapiens 44-47 9920858-4 1999 Herein we show that cells induced to express P-glycoprotein either by drug selection or by retroviral gene transduction with MDR1 cDNA are resistant to cell death induced by a wide range of death stimuli, such as FasL, tumor necrosis factor (TNF), and ultraviolet (UV) irradiation, that activate the caspase apoptotic cascade.However, P-glycoprotein-expressing cells were not resistant to caspase-independent cell death mediated by pore-forming proteins and granzyme B.MDR P-glycoprotein-expressing cells were made sensitive to caspase-dependent apoptosis by the addition of anti-P-glycoprotein antibodies or verapamil, a pharmacological inhibitor of P-glycoprotein function. Verapamil 609-618 ATP binding cassette subfamily B member 1 Homo sapiens 45-59 9920858-4 1999 Herein we show that cells induced to express P-glycoprotein either by drug selection or by retroviral gene transduction with MDR1 cDNA are resistant to cell death induced by a wide range of death stimuli, such as FasL, tumor necrosis factor (TNF), and ultraviolet (UV) irradiation, that activate the caspase apoptotic cascade.However, P-glycoprotein-expressing cells were not resistant to caspase-independent cell death mediated by pore-forming proteins and granzyme B.MDR P-glycoprotein-expressing cells were made sensitive to caspase-dependent apoptosis by the addition of anti-P-glycoprotein antibodies or verapamil, a pharmacological inhibitor of P-glycoprotein function. Verapamil 609-618 ATP binding cassette subfamily B member 1 Homo sapiens 125-129 10211547-3 1999 Verapamil or 2-deoxyglucose/Na azide enhanced only the retention of the free drug and the small (<70 kDa) conjugates, indicating that P-glycoprotein (P-gp) is not effective against large conjugates. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 137-151 10211547-3 1999 Verapamil or 2-deoxyglucose/Na azide enhanced only the retention of the free drug and the small (<70 kDa) conjugates, indicating that P-glycoprotein (P-gp) is not effective against large conjugates. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 153-157 9862789-0 1999 Characterization of binding properties to human P-glycoprotein: development of a [3H]verapamil radioligand-binding assay. Verapamil 85-94 ATP binding cassette subfamily B member 1 Homo sapiens 48-62 9862789-11 1999 Kinetics as well as specificity of the binding of verapamil to the P-gp preparation were demonstrated. Verapamil 50-59 ATP binding cassette subfamily B member 1 Homo sapiens 67-71 9862789-6 1999 Because of the reversible and competitive interaction of numerous substrates with P-gp, a radioligand-binding assay was developed by taking [3H]verapamil and [3H]vinblastine as radioligands and the human intestinal Caco-2 cells, overexpressed with P-gp by culturing in the presence of vinblastine or transfecting with multidrug resistance gene MDR-1 as receptor preparation. Verapamil 144-153 ATP binding cassette subfamily B member 1 Homo sapiens 82-86 9862789-13 1999 The binding properties of [3H]verapamil and [3H]vinblastine to a P-gp preparation derived from induced Caco-2 cells are described. Verapamil 30-39 ATP binding cassette subfamily B member 1 Homo sapiens 65-69 9756763-2 1998 The P-gp inhibitors verapamil and progesterone significantly increased the epithelial cell accumulation of both vinblastine and sparfloxacin. Verapamil 20-29 ATP binding cassette subfamily B member 1 Homo sapiens 4-8 9778376-4 1998 Preincubation of human Pgp expressed in Sf9 insect cells with vanadate in the presence of Mg2+, ATP, and verapamil resulted in nearly complete and stable inhibition of the drug-stimulated ATPase function. Verapamil 105-114 ATP binding cassette subfamily B member 1 Homo sapiens 23-26 9778376-5 1998 In contrast, the Pgp ATPase function was nearly unaffected when Mg2+, ATP, or verapamil was omitted. Verapamil 78-87 ATP binding cassette subfamily B member 1 Homo sapiens 17-20 9778376-8 1998 In support of this conclusion, vanadate, in the presence of Mg2+ and verapamil, caused selective trapping of 8-azido [alpha-32P] ATP and covalent labeling of ATP-binding site in the Pgp. Verapamil 69-78 ATP binding cassette subfamily B member 1 Homo sapiens 182-185 9822896-3 1998 The basal-to-apical transport of rhodamine 123, a P-glycoprotein substrate, was inhibited by erythromycin, midazolam and ketoconazole, as well as by P-glycoprotein inhibitors such as verapamil. Verapamil 183-192 ATP binding cassette subfamily B member 1 Homo sapiens 50-64 9822896-3 1998 The basal-to-apical transport of rhodamine 123, a P-glycoprotein substrate, was inhibited by erythromycin, midazolam and ketoconazole, as well as by P-glycoprotein inhibitors such as verapamil. Verapamil 183-192 ATP binding cassette subfamily B member 1 Homo sapiens 149-163 9732409-6 1998 Transport in the basolateral to apical direction was 3-fold greater than apical to basolateral flux for both saquinavir and saquinavir mesylate and was blocked by co-incubation with the established P-gp reversal agents cyclosporine and verapamil. Verapamil 236-245 ATP binding cassette subfamily B member 1 Homo sapiens 198-202 9765504-8 1998 Inhibitors of Pgp, including verapamil and cyclosporin A, were less effective in reversing resistance of the chimeric Pgp compared with wild-type Pgp, for certain drugs. Verapamil 29-38 ATP binding cassette subfamily B member 1 Homo sapiens 14-17 9765504-8 1998 Inhibitors of Pgp, including verapamil and cyclosporin A, were less effective in reversing resistance of the chimeric Pgp compared with wild-type Pgp, for certain drugs. Verapamil 29-38 ATP binding cassette subfamily B member 1 Homo sapiens 118-121 9765504-8 1998 Inhibitors of Pgp, including verapamil and cyclosporin A, were less effective in reversing resistance of the chimeric Pgp compared with wild-type Pgp, for certain drugs. Verapamil 29-38 ATP binding cassette subfamily B member 1 Homo sapiens 118-121 9751076-7 1998 When the effects of these two modulators on the formation of the enzyme-nucleotide complex important in the catalytic cycle were examined, verapamil increased the amount of vanadate-trapped 8-azido-[alpha-32P]ATP bound to Pgp by two-fold, whereas TMBY had no effect. Verapamil 139-148 ATP binding cassette subfamily B member 1 Homo sapiens 222-225 9751076-9 1998 Together, these data indicate that verapamil and TMBY bind to Pgp at a common site or overlapping sites, but only verapamil results in enhanced Pgp-ATP hydrolysis and formation of the vanadate-nucleotide-enzyme complex. Verapamil 35-44 ATP binding cassette subfamily B member 1 Homo sapiens 62-65 9751076-9 1998 Together, these data indicate that verapamil and TMBY bind to Pgp at a common site or overlapping sites, but only verapamil results in enhanced Pgp-ATP hydrolysis and formation of the vanadate-nucleotide-enzyme complex. Verapamil 114-123 ATP binding cassette subfamily B member 1 Homo sapiens 144-147 9818076-8 1998 In tissue cultures, SK-N-SH cells showed a relative resistance to vincristine and adriamycin (45.1 and 12.7-fold resp.) and reduced intracellular accumulation of rhodamine-123 which could be normalized by the Pgp blocker verapamil. Verapamil 221-230 ATP binding cassette subfamily B member 1 Homo sapiens 209-212 9528676-3 1998 The cardioactive drugs verapamil, quinidine, diltiazem, nifedipine, and a series of digitalis analogs, interacted directly with Pgp as shown on ATPase in both systems. Verapamil 23-32 ATP binding cassette subfamily B member 1 Homo sapiens 128-131 9657975-4 1998 P-Glycoprotein ATPase is activated by verapamil and by nicardipine but not by vinblastine. Verapamil 38-47 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 9657975-6 1998 The vinblastine-specific binding on P-glycoprotein is reported by the inhibitions of the verapamil- and the nicardipine-stimulated ATPase. Verapamil 89-98 ATP binding cassette subfamily B member 1 Homo sapiens 36-50 9657975-7 1998 These inhibitions are purely competitive, which means that the bindings of vinblastine and verapamil, or vinblastine and nicardipine, on P-glycoprotein are mutually exclusive. Verapamil 91-100 ATP binding cassette subfamily B member 1 Homo sapiens 137-151 9923970-0 1998 Effects of detergents on P-glycoprotein atpase activity: differences in perturbations of basal and verapamil-dependent activities. Verapamil 99-108 ATP binding cassette subfamily B member 1 Homo sapiens 25-39 9923970-2 1998 Using membrane vesicles prepared from the multidrug resistant cell line DC-3F/ADX, we studied the perturbation of the basal (i.e. in the absence of drug) and verapamil-dependent P-gp ATPase activities induced by various detergents, at non-solubilizing, as well as at solubilizing, concentrations. Verapamil 158-167 ATP binding cassette subfamily B member 1 Homo sapiens 178-182 9923970-5 1998 Analysis of the verapamil-induced P-gp activation reveals that P-gp ATPase activity is differently modulated by the various detergents at non-solubilizing concentrations. Verapamil 16-25 ATP binding cassette subfamily B member 1 Homo sapiens 34-38 9923970-5 1998 Analysis of the verapamil-induced P-gp activation reveals that P-gp ATPase activity is differently modulated by the various detergents at non-solubilizing concentrations. Verapamil 16-25 ATP binding cassette subfamily B member 1 Homo sapiens 63-67 9923970-8 1998 However, the verapamil-induced P-gp ATPase activation was lost during P-gp solubilization by CHAPS, but recovered after dilution of CHAPS below its critical micellar concentration. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 31-35 9923970-8 1998 However, the verapamil-induced P-gp ATPase activation was lost during P-gp solubilization by CHAPS, but recovered after dilution of CHAPS below its critical micellar concentration. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 70-74 9607955-6 1998 Previous drug exposure of the cells showed that verapamil, celiprolol, and vinblastine induced the P-gp expression, while metkephamid (MKA) decreased the P-gp expression level as compared to the control. Verapamil 48-57 ATP binding cassette subfamily B member 1 Homo sapiens 99-103 9531525-11 1998 K02 significantly inhibited the photoaffinity labeling of P-gp with azidopine and LU-49888, a photoaffinity analogue of verapamil. Verapamil 120-129 ATP binding cassette subfamily B member 1 Homo sapiens 58-62 9506530-6 1998 The P-glycoprotein-mediated multidrug resistance (MDR)-reversing agents verapamil, cyclosporin A, quinidine, sodium orthovanadate and tamoxifen significantly increased dox fluorescence at this depth, whereas genistein, indomethacin, probenecid and brefeldin A, which reverse multidrug-resistance-associated protein (MRP) function, exerted no effect. Verapamil 72-81 ATP binding cassette subfamily B member 1 Homo sapiens 4-18 9504633-6 1998 The efflux was blocked in the presence of verapamil, a PgP revertant agent. Verapamil 42-51 ATP binding cassette subfamily B member 1 Homo sapiens 55-58 9570481-2 1998 A variety of small molecules, such as verapamil and cyclosporin A, bind to P-glycoprotein and inhibit its ability to pump out antitumor drugs. Verapamil 38-47 ATP binding cassette subfamily B member 1 Homo sapiens 75-89 9570481-3 1998 The kinetics of P-glycoprotein-mediated efflux of various anthracycline derivatives was measured in multidrug-resistant (MDR) K562 cells in the presence of verapamil. Verapamil 156-165 ATP binding cassette subfamily B member 1 Homo sapiens 16-30 9618515-7 1998 Addition of anti-MDR-1 mAbs MRK16, UIC2, or the MDR-1 antagonist verapamil to skin explants at the onset of culture inhibited the appearance of DC, and accompanying T cells, in the culture medium by approximately 70%. Verapamil 65-74 ATP binding cassette subfamily B member 1 Homo sapiens 48-53 9618532-5 1998 Inhibition of P-gp function by the anti-P-gp mAb MRK-16 or verapamil could reverse resistance to these forms of cell death. Verapamil 59-68 ATP binding cassette subfamily B member 1 Homo sapiens 14-18 9626462-1 1998 The purpose of this study is to evaluate whether metastatic breast cancer that has progressed on an anthracycline-containing drug regimen will subsequently respond to that identical regimen if dexverapamil, a modulator of P-glycoprotein-mediated drug resistance, is given concomitantly. Verapamil 193-205 ATP binding cassette subfamily B member 1 Homo sapiens 222-236 9506534-9 1998 P-gp function modulators (verapamil and cyclosporin A) were able to modify DOX intracytoplasmic distribution and to increase drug intracellular concentration and cytotoxic effect in melanoma cells. Verapamil 26-35 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 9635488-2 1998 The presence of this ATP-dependent membrane P-glycoprotein (Pgp) pump was confirmed by biochemical ("binding"), molecular (immunohistochemical, Western, Northern), physiological (verapamil-sensitivity) and toxicological (modulation of toxicity) methods. Verapamil 179-188 ATP binding cassette subfamily B member 1 Homo sapiens 44-58 9635488-2 1998 The presence of this ATP-dependent membrane P-glycoprotein (Pgp) pump was confirmed by biochemical ("binding"), molecular (immunohistochemical, Western, Northern), physiological (verapamil-sensitivity) and toxicological (modulation of toxicity) methods. Verapamil 179-188 ATP binding cassette subfamily B member 1 Homo sapiens 60-63 9482283-9 1998 When MCS were incubated with verapamil, cyclosporin A, orthovanadate, and quinidine, which are known to reverse P-glycoprotein (Pgp)-mediated multidrug resistance (MDR), Dox accumulated also in deeper cell layers. Verapamil 29-38 ATP binding cassette subfamily B member 1 Homo sapiens 112-126 9488065-11 1998 Calcium-channel blockers (verapamil, quinidine) and protein kinase C inhibitors (tamoxifen) inhibited gp-170 activity and slowed the drug-efflux pump, with the acquired-MDR cells subsequently accumulating anticancer drugs. Verapamil 26-35 ATP binding cassette subfamily B member 1 Homo sapiens 102-108 9482283-9 1998 When MCS were incubated with verapamil, cyclosporin A, orthovanadate, and quinidine, which are known to reverse P-glycoprotein (Pgp)-mediated multidrug resistance (MDR), Dox accumulated also in deeper cell layers. Verapamil 29-38 ATP binding cassette subfamily B member 1 Homo sapiens 128-131 9507994-5 1998 Progesterone, verapamil, and trifluoperazine, inhibitors of p-glycoprotein which are known to inhibit cholesterol transport from the plasma membrane to the endoplasmic reticulum, reduced the amount of newly synthesized cholesterol reaching the plasma membrane. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 60-74 9476144-7 1998 In permeability studies with Caco-2 cell monolayers, the MDR-reversing agent verapamil inhibits secretion of P-glycoprotein substrates and, hence, increases apical-to-basolateral permeability. Verapamil 77-86 ATP binding cassette subfamily B member 1 Homo sapiens 109-123 9792953-2 1998 The Pgp substrate vinblastine and the modulator verapamil produced a reversible concentration-dependent block of swelling-activated Cl- currents in both a drug-sensitive cell line (MCF-7) and a Pgp-expressing derivative (BC19/3). Verapamil 48-57 ATP binding cassette subfamily B member 1 Homo sapiens 194-197 9651111-7 1998 The resistance displayed by KB-V cells is abrogated by co-administration of the P-gp inhibitor verapamil, whereas verapamil has no effect on CsA potency in control KB cells. Verapamil 95-104 ATP binding cassette subfamily B member 1 Homo sapiens 80-84 9405384-6 1997 The drug substrates verapamil, vinblastine, and colchicine protected these mutants against inhibition by dBBn, suggesting that these residues are important for interaction of substrates with P-glycoprotein. Verapamil 20-29 ATP binding cassette subfamily B member 1 Homo sapiens 191-205 9458331-5 1998 In the Pgp overexpressing cell lines, steady accumulation of 14C-taxol was defective and could be reverted by verapamil. Verapamil 110-119 ATP binding cassette subfamily B member 1 Homo sapiens 7-10 9815593-7 1997 Treatment also resulted in an increased resistance to epirubicin and decreased daunomycin accumulation, both of which were reversible by verapamil, a characteristic of the classical MDR phenotype in cells expressing P-glycoprotein. Verapamil 137-146 ATP binding cassette subfamily B member 1 Homo sapiens 216-230 9447822-7 1997 In contrast, 3.1- and 2.4-fold increases were found in uptake and retention of mitoxantrone in p-glycoprotein-positive cells (HL-60DOX) incubated with verapamil. Verapamil 151-160 ATP binding cassette subfamily B member 1 Homo sapiens 95-109 9287320-5 1997 However, wild-type MDR1, which is known to be phosphorylated in Sf9 membranes, and the 3E and 8E mutants, which mimic the charge of phosphorylation, achieved half-maximum activation of MDR1-ATPase activity at lower verapamil, vinblastine, or rhodamine 123 concentrations than the nonphosphorylatable 3A and 8A variants. Verapamil 215-224 ATP binding cassette subfamily B member 1 Homo sapiens 19-23 9370075-4 1997 It has been shown that p-glycoprotein can be circumvented in vitro by noncytotoxic agents such as verapamil and cyclosporin A, which interact pharmacologically with p-glycoprotein-mediated efflux. Verapamil 98-107 ATP binding cassette subfamily B member 1 Homo sapiens 23-37 9370075-4 1997 It has been shown that p-glycoprotein can be circumvented in vitro by noncytotoxic agents such as verapamil and cyclosporin A, which interact pharmacologically with p-glycoprotein-mediated efflux. Verapamil 98-107 ATP binding cassette subfamily B member 1 Homo sapiens 165-179 9408959-4 1997 Recently, clinical reversal of MDR by noncytotoxic P-gp modulators such as verapamil, cyclosporin A (CsA), and PSC 833 was explored in acute leukemia and multiple myeloma. Verapamil 75-84 ATP binding cassette subfamily B member 1 Homo sapiens 51-55 9353133-4 1997 The concentration dependence of the inhibition of P-gp by verapamil (Vp) was not influenced by PMA. Verapamil 58-67 ATP binding cassette subfamily B member 1 Homo sapiens 50-54 9287320-5 1997 However, wild-type MDR1, which is known to be phosphorylated in Sf9 membranes, and the 3E and 8E mutants, which mimic the charge of phosphorylation, achieved half-maximum activation of MDR1-ATPase activity at lower verapamil, vinblastine, or rhodamine 123 concentrations than the nonphosphorylatable 3A and 8A variants. Verapamil 215-224 ATP binding cassette subfamily B member 1 Homo sapiens 185-189 21227092-0 1997 Phase II evaluation of doxorubicin/vinblastine combined with inhibitors trifluoperazine/verapamil of P-glycoprotein in patients with advanced renal carcinoma. Verapamil 88-97 ATP binding cassette subfamily B member 1 Homo sapiens 101-115 9305607-10 1997 Verapamil did not increase DNR toxicity in four of these eight cases, but was more efficient in one other MDR1(+) case. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 106-110 9261121-5 1997 Initial uptake rates of vinblastine +/- verapamil measure the ability of P-glycoprotein to extract vinblastine from the plasma membrane before it enters the cell. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 73-87 9247172-8 1997 The purified human Pgp exhibits a verapamil-stimulated ATPase activity and the maximal activity is 2.5 +/- 0.5 micromol/min per mg of Pgp, suggesting that the purified Pgp from yeast is highly functional. Verapamil 34-43 ATP binding cassette subfamily B member 1 Homo sapiens 19-22 9322679-5 1997 P-gp activity was defined as a ratio of mean rhodamine 123 accumulation with/without verapamil. Verapamil 85-94 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 9110922-12 1997 The data presented advocate testing of new potential P-gp modulator combinations, such as RU-38486 and verapamil, with the aim of increasing efficacy and simultaneously reducing side effects. Verapamil 103-112 ATP binding cassette subfamily B member 1 Homo sapiens 53-57 9110922-3 1997 Additionally, the P-gp modulating potency of the combination of RU-38486 and verapamil was investigated. Verapamil 77-86 ATP binding cassette subfamily B member 1 Homo sapiens 18-22 9119038-4 1997 Vinblastine inhibits the activation of P-glycoprotein ATPase induced by verapamil or progesterone with an inhibition constant approximately 0.5 microM in both cases. Verapamil 72-81 ATP binding cassette subfamily B member 1 Homo sapiens 39-53 9235086-9 1997 Chemicals such as verapamil, nifedine, quinidine and calmodulin inhibitors are joined to pgp inhibiting it. Verapamil 18-27 ATP binding cassette subfamily B member 1 Homo sapiens 89-92 9119038-1 1997 P-glycoprotein, a plasma membrane protein overexpressed in multidrug-resistant (MDR) cells, exhibits in vitro an ATPase activity and is responsible for the energy-dependent efflux of structurally unrelated cytotoxic drugs (like vinblastine) and various MDR-reversing agents (like verapamil and progesterone) from these MDR cells. Verapamil 280-289 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 9119038-2 1997 To investigate the mechanism of P-glycoprotein interaction with various compounds, we measured the P-glycoprotein ATPase activity on membrane vesicles prepared from the MDR cell line DC-3F/ADX, and we studied the effects of vinblastine, verapamil and progesterone on this ATPase activity. Verapamil 237-246 ATP binding cassette subfamily B member 1 Homo sapiens 32-46 9119038-3 1997 The basal P-glycoprotein ATPase activity is increased by verapamil and progesterone, with respective half-maximal activating concentrations of approximately 1.5 microM and approximately 25 microM, and activation factors of approximately 1.7 and approximately 2.2. Verapamil 57-66 ATP binding cassette subfamily B member 1 Homo sapiens 10-24 9016791-3 1997 In this study, we have demonstrated that C219 inhibits the ATPase activity of P-glycoprotein based on the following findings: 1) the inhibition of total ATPase activity by C219 was selective to P-glycoprotein-positive membranes; 2) the C219-sensitive fraction of ATPase correlated the expression of P-glycoprotein; and 3) modulators of P-glycoprotein ATPase, verapamil and cyclosporin A, affected the C219-sensitive fraction of ATPase. Verapamil 359-368 ATP binding cassette subfamily B member 1 Homo sapiens 78-92 8980113-6 1996 The resistance to aureobasidin A conferred by the MDR2/Pgp as well as by the MDR1/Pgp was overcome by vinblastine, verapamil, and cyclosporin A, depending on their concentrations, but not by colchicine. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 55-58 8980113-6 1996 The resistance to aureobasidin A conferred by the MDR2/Pgp as well as by the MDR1/Pgp was overcome by vinblastine, verapamil, and cyclosporin A, depending on their concentrations, but not by colchicine. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 77-81 8980113-6 1996 The resistance to aureobasidin A conferred by the MDR2/Pgp as well as by the MDR1/Pgp was overcome by vinblastine, verapamil, and cyclosporin A, depending on their concentrations, but not by colchicine. Verapamil 115-124 ATP binding cassette subfamily B member 1 Homo sapiens 82-85 9044851-6 1997 The two resulting steroids, SA47 and SA450, were potent glucocorticoid receptor agonists also capable of inhibiting the human P-glycoprotein with an efficiency equal to that of verapamil. Verapamil 177-186 ATP binding cassette subfamily B member 1 Homo sapiens 126-140 8990381-11 1996 We speculate that the target of R-verapamil on resting NK cells is P-glycoprotein (Pgp), an ABC transporter that we recently reported was expressed on NK cells and whose functional activity is known to be inhibited by R-verapamil. Verapamil 32-43 ATP binding cassette subfamily B member 1 Homo sapiens 67-81 8990381-11 1996 We speculate that the target of R-verapamil on resting NK cells is P-glycoprotein (Pgp), an ABC transporter that we recently reported was expressed on NK cells and whose functional activity is known to be inhibited by R-verapamil. Verapamil 32-43 ATP binding cassette subfamily B member 1 Homo sapiens 83-86 8990381-11 1996 We speculate that the target of R-verapamil on resting NK cells is P-glycoprotein (Pgp), an ABC transporter that we recently reported was expressed on NK cells and whose functional activity is known to be inhibited by R-verapamil. Verapamil 218-229 ATP binding cassette subfamily B member 1 Homo sapiens 67-81 8990381-11 1996 We speculate that the target of R-verapamil on resting NK cells is P-glycoprotein (Pgp), an ABC transporter that we recently reported was expressed on NK cells and whose functional activity is known to be inhibited by R-verapamil. Verapamil 218-229 ATP binding cassette subfamily B member 1 Homo sapiens 83-86 9119038-6 1997 The combined modulation of P-glycoprotein ATPase by vinblastine and verapamil reveals that these two drugs are mutually exclusive. Verapamil 68-77 ATP binding cassette subfamily B member 1 Homo sapiens 27-41 9119038-9 1997 Since verapamil and progesterone are mutual inhibitors of P-glycoprotein ATPase stimulation in a non-competitive manner, these two molecules can also bind independently P-glycoprotein on separated sites. Verapamil 6-15 ATP binding cassette subfamily B member 1 Homo sapiens 58-72 9119038-9 1997 Since verapamil and progesterone are mutual inhibitors of P-glycoprotein ATPase stimulation in a non-competitive manner, these two molecules can also bind independently P-glycoprotein on separated sites. Verapamil 6-15 ATP binding cassette subfamily B member 1 Homo sapiens 169-183 9119038-10 1997 This is confirmed here by the observation of a synergistic effect when mixtures of verapamil and progesterone are tested for the modulation of P-glycoprotein ATPase. Verapamil 83-92 ATP binding cassette subfamily B member 1 Homo sapiens 143-157 8934230-7 1996 Thus, selection with colchicine at 5 ng/ml in combination with the P-gp inhibitors verapamil or PSC 833 produced a complete correction of the GC deficiency in the CA2-transduced fibroblasts. Verapamil 83-92 ATP binding cassette subfamily B member 1 Homo sapiens 67-71 8938148-7 1996 Photoaffinity labeling of Pgp by [3H]-azidopine was clearly inhibited by VLB, verapamil and EM. Verapamil 78-87 ATP binding cassette subfamily B member 1 Homo sapiens 26-29 8937469-2 1996 Mefloquine, a quinolinemethanol antimalarial drug, was shown to inhibit the labelling of P-glycoprotein with an efficiency similar to that for verapamil, a known chemosensitizer. Verapamil 143-152 ATP binding cassette subfamily B member 1 Homo sapiens 89-103 8855237-6 1996 LmrA and MDR1 extrude a similar spectrum of amphiphilic cationic compounds, and the activity of both systems is reversed by reserpine and verapamil. Verapamil 138-147 ATP binding cassette subfamily B member 1 Homo sapiens 9-13 9042229-0 1996 Effects of verapamil and S9788 on MDR-1 mRNA expression studied by in situ hybridization. Verapamil 11-20 ATP binding cassette subfamily B member 1 Homo sapiens 34-39 9042229-1 1996 The effects of Verapamil and S9788 (triazineaminopiperidine), a new modulator of multidrug resistance, on mdr-1 mRNA expression were determined using in situ hybridization. Verapamil 15-24 ATP binding cassette subfamily B member 1 Homo sapiens 106-111 9042229-3 1996 However, Verapamil only decreased mdr-1 mRNA expression in Human erythroleukemic resistant cells (ADM/k562) and in Human lymphoblastic resistant cells (VLB/CEM). Verapamil 9-18 ATP binding cassette subfamily B member 1 Homo sapiens 34-39 8782646-9 1996 Moreover, treatments of MCF-7/Adr cells with P-glycoprotein (P-gp) modulators, cyclosporin A and verapamil increased doxorubicin and vincristine-induced DNA fragmentation about 1.4- and 2.5-fold, indicating that P-gp is involved in the development of resistance to chemotherapy-induced apoptosis in this cell line. Verapamil 97-106 ATP binding cassette subfamily B member 1 Homo sapiens 45-59 8782646-9 1996 Moreover, treatments of MCF-7/Adr cells with P-glycoprotein (P-gp) modulators, cyclosporin A and verapamil increased doxorubicin and vincristine-induced DNA fragmentation about 1.4- and 2.5-fold, indicating that P-gp is involved in the development of resistance to chemotherapy-induced apoptosis in this cell line. Verapamil 97-106 ATP binding cassette subfamily B member 1 Homo sapiens 61-65 8782646-9 1996 Moreover, treatments of MCF-7/Adr cells with P-glycoprotein (P-gp) modulators, cyclosporin A and verapamil increased doxorubicin and vincristine-induced DNA fragmentation about 1.4- and 2.5-fold, indicating that P-gp is involved in the development of resistance to chemotherapy-induced apoptosis in this cell line. Verapamil 97-106 ATP binding cassette subfamily B member 1 Homo sapiens 212-216 8843701-5 1996 Verapamil, a substrate of MDR-1, increased the osmotically evoked taurine efflux. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 26-31 8794885-6 1996 Furthermore, BIBW22 BS, vinblastine, and verapamil, but not colchicine, inhibited the photolabeling of P-gp by [3H]azido-BIBW22 BS. Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 103-107 8695847-4 1996 The efflux of Rh123 could be inhibited by verapamil, suggesting that rhodamine efflux from primitive hematopoietic cells is primarily due to the P-glycoprotein (P-gp) pump or another intracellular transport system affected by verapamil. Verapamil 42-51 ATP binding cassette subfamily B member 1 Homo sapiens 145-159 8695847-4 1996 The efflux of Rh123 could be inhibited by verapamil, suggesting that rhodamine efflux from primitive hematopoietic cells is primarily due to the P-glycoprotein (P-gp) pump or another intracellular transport system affected by verapamil. Verapamil 42-51 ATP binding cassette subfamily B member 1 Homo sapiens 161-165 8911123-1 1996 To determine whether the cell cycle affects multidrug resistance (MDR) and its reversal, doxorubicin (DOX) cytotoxicity and the effect of inhibition of P-glycoprotein (Pgp) activity by verapamil (VER) were investigated in MDR LoVo cell lines (LoVo-R) in different phases of the cell cycle. Verapamil 185-194 ATP binding cassette subfamily B member 1 Homo sapiens 168-171 9067565-2 1996 In tissues over-expressing this protein, modulation with verapamil (an antagonist of p-glycoprotein) may be useful in reversing this form of treatment resistance. Verapamil 57-66 ATP binding cassette subfamily B member 1 Homo sapiens 85-99 8913319-6 1996 We conclude that the verapamil associated change in rhodamine 123 accumulation provides a sensitive functional assay for both P-glycoprotein- and MRP-mediated MDR. Verapamil 21-30 ATP binding cassette subfamily B member 1 Homo sapiens 126-140 8831211-5 1996 Adriamycin (ADM) and vinblastin (VLB) were used as anticancer drugs, and verapamil (Ver) and cyclosporin A (CsA) were as P-gp modulators. Verapamil 73-82 ATP binding cassette subfamily B member 1 Homo sapiens 121-125 8694845-0 1996 Study of P-glycoprotein functionality in living resistant K562 cells after photolabeling with a verapamil analogue. Verapamil 96-105 ATP binding cassette subfamily B member 1 Homo sapiens 9-23 8694845-6 1996 The irradiation of resistant cells, 10(6)/mL, in the presence of a verapamil analogue at concentrations equal to or higher than 3 microM yielded 70% inhibition of P-gp functionality. Verapamil 67-76 ATP binding cassette subfamily B member 1 Homo sapiens 163-167 8694845-7 1996 Our data provide the first evidence that the binding of a verapamil analogue to P-gp is not sufficient to completely inhibit the efflux of this anthracycline. Verapamil 58-67 ATP binding cassette subfamily B member 1 Homo sapiens 80-84 8667063-5 1996 The PgP reversing effect of verapamil was evaluated at different drug concentrations (50, 200, 500 microM). Verapamil 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 4-7 8713080-0 1996 Effects of steroids and verapamil on P-glycoprotein ATPase activity: progesterone, desoxycorticosterone, corticosterone and verapamil are mutually non-exclusive modulators. Verapamil 124-133 ATP binding cassette subfamily B member 1 Homo sapiens 37-51 8713080-6 1996 The effects of these steroids on verapamil-stimulated P-gp ATPase activity support a non-competitive mechanism, i.e. the binding sites for verapamil and steroids are mutually non-exclusive for P-gp ATPase modulation. Verapamil 33-42 ATP binding cassette subfamily B member 1 Homo sapiens 54-58 8713080-6 1996 The effects of these steroids on verapamil-stimulated P-gp ATPase activity support a non-competitive mechanism, i.e. the binding sites for verapamil and steroids are mutually non-exclusive for P-gp ATPase modulation. Verapamil 33-42 ATP binding cassette subfamily B member 1 Homo sapiens 193-197 8713080-6 1996 The effects of these steroids on verapamil-stimulated P-gp ATPase activity support a non-competitive mechanism, i.e. the binding sites for verapamil and steroids are mutually non-exclusive for P-gp ATPase modulation. Verapamil 139-148 ATP binding cassette subfamily B member 1 Homo sapiens 54-58 8713080-6 1996 The effects of these steroids on verapamil-stimulated P-gp ATPase activity support a non-competitive mechanism, i.e. the binding sites for verapamil and steroids are mutually non-exclusive for P-gp ATPase modulation. Verapamil 139-148 ATP binding cassette subfamily B member 1 Homo sapiens 193-197 8713080-8 1996 As expected from their mutually non-exclusive interactions on P-gp, progesterone and verapamil when mixed induce a synergistic modulation of P-gp ATPase activity. Verapamil 85-94 ATP binding cassette subfamily B member 1 Homo sapiens 62-66 8713080-8 1996 As expected from their mutually non-exclusive interactions on P-gp, progesterone and verapamil when mixed induce a synergistic modulation of P-gp ATPase activity. Verapamil 85-94 ATP binding cassette subfamily B member 1 Homo sapiens 141-145 8813556-3 1996 A complete inhibition of vincristine resistance by verapamil was observed in the vincristine-resistant HOB1/VCR cells, which suggests that acquired resistance may be mainly due to P-glycoprotein. Verapamil 51-60 ATP binding cassette subfamily B member 1 Homo sapiens 180-194 8792427-3 1996 P-GP efflux function was determined by measuring transmonolayer fluxes of cyclosporin A (CsA) and verapamil, while P-GP expression level was evaluated by Western blot analysis using monoclonal antibody C219. Verapamil 98-107 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 8635866-1 1996 Inhibitors of P-glycoprotein (P-gp) or chemosensitizers, such as verapamil, are used to reverse multi-drug resistance (MDR) in cancer patients. Verapamil 65-74 ATP binding cassette subfamily B member 1 Homo sapiens 14-28 8635866-2 1996 Clinical studies in patients with myeloma have shown that some patients with P-gp-positive cancer cells respond to the chemosensitizing effect of verapamil. Verapamil 146-155 ATP binding cassette subfamily B member 1 Homo sapiens 77-81 8635866-7 1996 Verapamil and cyclosporin A were only partially effective in blocking P-gp drug efflux in MDR10V compared to Dox40 cells. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 70-74 8635866-9 1996 [3H]Azidopine photoaffinity labeling of P-gp and its binding competition with unlabeled verapamil showed similar affinity for P-gp between Dox40 and MDR10V cell lines. Verapamil 88-97 ATP binding cassette subfamily B member 1 Homo sapiens 40-44 8635866-9 1996 [3H]Azidopine photoaffinity labeling of P-gp and its binding competition with unlabeled verapamil showed similar affinity for P-gp between Dox40 and MDR10V cell lines. Verapamil 88-97 ATP binding cassette subfamily B member 1 Homo sapiens 126-130 8635868-0 1996 Verapamil suppresses the emergence of P-glycoprotein-mediated multi-drug resistance. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 38-52 8635868-9 1996 Our results indicate that the inclusion of verapamil during drug selection with doxorubicin influences the drug-resistant phenotype by preventing the selection of MDR1/P-glycoprotein-positive cells. Verapamil 43-52 ATP binding cassette subfamily B member 1 Homo sapiens 163-167 8635868-9 1996 Our results indicate that the inclusion of verapamil during drug selection with doxorubicin influences the drug-resistant phenotype by preventing the selection of MDR1/P-glycoprotein-positive cells. Verapamil 43-52 ATP binding cassette subfamily B member 1 Homo sapiens 168-182 8605092-5 1996 In contrast, in human ovarian H134AD cells that are resistant to 1700 nM doxorubicin and used as P-gp-positive controls, the drug efflux was inhibited only by verapamil. Verapamil 159-168 ATP binding cassette subfamily B member 1 Homo sapiens 97-101 8600291-10 1996 Chlorpyrifos oxon stimulated P-gp ATPase activity 1.75 times that of the positive control (10 microM verapamil). Verapamil 101-110 ATP binding cassette subfamily B member 1 Homo sapiens 29-33 8642856-8 1996 One P-gp inhibitor (verapamil) slightly improved DNR-induced DNA fragmentation in KG1a cells whereas the combination of verapamil and buthionine-sulfoximine (BSO), which depletes glutathion store, further increased internucleosomal DNA fragmentation. Verapamil 20-29 ATP binding cassette subfamily B member 1 Homo sapiens 4-8 9772674-12 1996 Calcium antagonists and some calmodulin inhibitors such as verapamil, nifedepine, trifluorapine have effect on reversion of drug resistance, binding directly to PGP, but side effect of them is intolerable in clinical use. Verapamil 59-68 ATP binding cassette subfamily B member 1 Homo sapiens 161-164 8573197-4 1996 Although verapamil, an inhibitor of P-glycoprotein function, markedly increased the efficacy of taxol against the rodent cells (WS, WR, and CHO), the expression of P-glycoprotein was found only at low levels in the WR cells. Verapamil 9-18 ATP binding cassette subfamily B member 1 Homo sapiens 36-50 8616825-7 1996 Moreover we could correlate MDR1 gene expression and modulation of rhodamine 123 efflux from the leukaemic blasts by proven P-gp MDR chemosensitizing agents such as SDZ PSC 833, dexverapamil and dexniguldipine. Verapamil 178-190 ATP binding cassette subfamily B member 1 Homo sapiens 28-32 8713080-0 1996 Effects of steroids and verapamil on P-glycoprotein ATPase activity: progesterone, desoxycorticosterone, corticosterone and verapamil are mutually non-exclusive modulators. Verapamil 24-33 ATP binding cassette subfamily B member 1 Homo sapiens 37-51 8676093-4 1996 Complement resistance was reversed both by treatment with verapamil and with specific monoclonal antibodies (mAbs) capable of binding to P-glycoprotein and blocking its function. Verapamil 58-67 ATP binding cassette subfamily B member 1 Homo sapiens 137-151 8691629-3 1996 For example, verapamil or cyclosporin A may be useful for p-glycoprotein related multidrug resistance, and amphotericin B, docosahexaenoic acid or 8-chloro cAMP can be used for the modification of cisplatin-resistance. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 58-72 8648372-8 1996 The median peak and trough serum verapamil concentrations at the MTD were 5.1 micromol/L (range, 1.9 to 6.3), respectively, which are within the range necessary for in vitro modulation of Pgp-mediated multidrug resistance (MDR). Verapamil 33-42 ATP binding cassette subfamily B member 1 Homo sapiens 188-191 8648372-12 1996 CONCLUSION: r-Verapamil at 225 mg/m2 orally every 4 hours can be given safely with paclitaxel 200 mg/m2 by 3-hour infusion as outpatient therapy and is associated with serum levels considered active for Pgp inhibition. Verapamil 12-23 ATP binding cassette subfamily B member 1 Homo sapiens 203-206 8667063-9 1996 In the presence of verapamil, a known reverser of PgP functions, 99mTc-sestamibi uptake was increased by a factor of 2 in cells expressing no detectable levels of PgP and by a factor of 12 in cells with high PgP levels. Verapamil 19-28 ATP binding cassette subfamily B member 1 Homo sapiens 50-53 8667063-9 1996 In the presence of verapamil, a known reverser of PgP functions, 99mTc-sestamibi uptake was increased by a factor of 2 in cells expressing no detectable levels of PgP and by a factor of 12 in cells with high PgP levels. Verapamil 19-28 ATP binding cassette subfamily B member 1 Homo sapiens 163-166 8667063-9 1996 In the presence of verapamil, a known reverser of PgP functions, 99mTc-sestamibi uptake was increased by a factor of 2 in cells expressing no detectable levels of PgP and by a factor of 12 in cells with high PgP levels. Verapamil 19-28 ATP binding cassette subfamily B member 1 Homo sapiens 163-166 8567666-4 1996 Verapamil, cyclosporin A, and a number of other agents that compete with cytotoxic drugs for binding sites on P-glycoprotein can potently reverse MDR, but this is accompanied by severe toxicity in vivo. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 110-124 8593279-6 1996 At each fluorescence intensity, we calculated the P-gp mediated (verapamil-inhibitable) DNR transport rate from the rate of increase of the DNR fluorescence intensity in the absence of verapamil minus the rate of increase of the DNR fluorescence intensity in the presence of verapamil. Verapamil 65-74 ATP binding cassette subfamily B member 1 Homo sapiens 50-54 8593279-6 1996 At each fluorescence intensity, we calculated the P-gp mediated (verapamil-inhibitable) DNR transport rate from the rate of increase of the DNR fluorescence intensity in the absence of verapamil minus the rate of increase of the DNR fluorescence intensity in the presence of verapamil. Verapamil 185-194 ATP binding cassette subfamily B member 1 Homo sapiens 50-54 8593279-6 1996 At each fluorescence intensity, we calculated the P-gp mediated (verapamil-inhibitable) DNR transport rate from the rate of increase of the DNR fluorescence intensity in the absence of verapamil minus the rate of increase of the DNR fluorescence intensity in the presence of verapamil. Verapamil 185-194 ATP binding cassette subfamily B member 1 Homo sapiens 50-54 8672855-0 1996 [Expression of the MDR1 gene in five human cell lines of medullary thyroid cancer and reversion of the resistance to doxorubicine by ciclosporin A and verapamil]. Verapamil 151-160 ATP binding cassette subfamily B member 1 Homo sapiens 19-23 8562416-4 1996 Pgp functional activity was investigated by evaluation of verapamil influence upon rhodamine 123 efflux from the cells. Verapamil 58-67 ATP binding cassette subfamily B member 1 Homo sapiens 0-3 7591216-4 1995 Nitroanilino-azatoxin was the only compound for which resistance and reduced DNA damage observed in K562/ADM cells was partially reversed by verapamil, suggesting that nitroanilinoazatoxin was a substrate for P-glycoprotein. Verapamil 141-150 ATP binding cassette subfamily B member 1 Homo sapiens 209-223 8884813-0 1996 alpha-(3,4-dimethyoxyphenyl)-3,4-dihydro-6,7-dimethoxy-alpha- [(4-methylphenyl)thio]-2(1H)-isoquinolineheptanenitrile (CL 329,753): a novel chemosensitizing agent for P-glycoprotein-mediated resistance with improved biological properties compared with verapamil and cyclosporine A. Verapamil 252-261 ATP binding cassette subfamily B member 1 Homo sapiens 167-181 9275712-0 1996 Chemosensitizing effect of verapamil on Swiss-3T3 cells transfected with human MDR1 gene. Verapamil 27-36 ATP binding cassette subfamily B member 1 Homo sapiens 79-83 8548874-8 1996 In contrast, the P-glycoprotein inhibitors verapamil and cyclosporin A did not inhibit THP efflux. Verapamil 43-52 ATP binding cassette subfamily B member 1 Homo sapiens 17-31 7499263-5 1995 An inhibitor of P-glycoprotein-mediated pump activity, verapamil, was found to never affect the Cl- current. Verapamil 55-64 ATP binding cassette subfamily B member 1 Homo sapiens 16-30 7488154-6 1995 However, the verapamil concentration needed for the half maximal stimulation of the ATPase activity was found to be about hundred times higher than that for the wild type MDR1. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 171-175 8551799-7 1995 When the PGP-mediated drug efflux was blocked by verapamil (VRP), tubulin levels correlated linearly to VCR accumulation. Verapamil 49-58 ATP binding cassette subfamily B member 1 Homo sapiens 9-12 8551799-7 1995 When the PGP-mediated drug efflux was blocked by verapamil (VRP), tubulin levels correlated linearly to VCR accumulation. Verapamil 60-63 ATP binding cassette subfamily B member 1 Homo sapiens 9-12 8541114-3 1995 We examined the ability of verapamil, a reverser of P-glycoprotein (Pgp)-related resistance, to improve the efficacy of CyCAV combined chemotherapy (Cy, cyclophosphamide (CPA); C, cisplatin (CDDP); A, doxorubicin (ADM);V, etoposide (VP16)), as currently administered to SCLC patients at Institut Gustave-Roussy, France, and adapted to the treatment of nude mice implanted with these tumours. Verapamil 27-36 ATP binding cassette subfamily B member 1 Homo sapiens 52-66 8541114-3 1995 We examined the ability of verapamil, a reverser of P-glycoprotein (Pgp)-related resistance, to improve the efficacy of CyCAV combined chemotherapy (Cy, cyclophosphamide (CPA); C, cisplatin (CDDP); A, doxorubicin (ADM);V, etoposide (VP16)), as currently administered to SCLC patients at Institut Gustave-Roussy, France, and adapted to the treatment of nude mice implanted with these tumours. Verapamil 27-36 ATP binding cassette subfamily B member 1 Homo sapiens 68-71 8529475-3 1995 Several non-cancer therapy drugs (e.g., verapamil, phenothiazines) compete for the p-glycoprotein pump and thus can block efflux of a chemotherapeutic agent and overcome cellular resistance. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 83-97 7476894-2 1995 Because some P-gp inhibitors (e.g., verapamil and nifedipine) can increase mdr1 and P-gp expression in human colon carcinoma cell lines, we used our reserpine/yohimbine analogues to determine whether there was a structural requirement for this induction. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 13-17 7476894-2 1995 Because some P-gp inhibitors (e.g., verapamil and nifedipine) can increase mdr1 and P-gp expression in human colon carcinoma cell lines, we used our reserpine/yohimbine analogues to determine whether there was a structural requirement for this induction. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 75-79 7476894-2 1995 Because some P-gp inhibitors (e.g., verapamil and nifedipine) can increase mdr1 and P-gp expression in human colon carcinoma cell lines, we used our reserpine/yohimbine analogues to determine whether there was a structural requirement for this induction. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 84-88 7547962-7 1995 P-glycoprotein modulators generally demonstrated significantly greater potency (EC50; microM): SDZ PSC 833, 0.08; cyclosporin A, 1.3; verapamil, 4.1; quinidine, 6.4; prazosin, > 300. Verapamil 134-143 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 7643631-4 1995 Downmodulation of Pgp function in these cell lines could be demonstrated with different substances (verapamil, vinblastine, trifluoperazine, cyclosporin A, progesterone and quinidine) and was proven to be consistently higher in the vinblastine selected cells than in their non-selected drug sensitive counterparts. Verapamil 100-109 ATP binding cassette subfamily B member 1 Homo sapiens 18-21 7632959-2 1995 We evaluated mdr-1 expression by a quantitative polymerase chain reaction (PCR) assay in 78 biopsy samples from 48 patients with refractory lymphoma enrolled on a trial of infusional chemotherapy (EPOCH) in which R-verapamil was added as an antagonist of P-glycoprotein in a subset of patients whose tumors were unresponsive to treatment. Verapamil 213-224 ATP binding cassette subfamily B member 1 Homo sapiens 13-18 7646552-5 1995 TPA treatment caused an increase in P-glycoprotein, increased drug resistance and decreased rhodamine-123 accumulation which was verapamil sensitive, demonstrating that TPA induced a fully functional P-glycoprotein. Verapamil 129-138 ATP binding cassette subfamily B member 1 Homo sapiens 200-214 7640227-5 1995 In this study, we investigated whether chemosensitising agents of P-glycoprotein-mediated multidrug resistance such as verapamil, a biscoclaurine alkaloid (cepharanthine), and a dihydropyridine analogue (NIK250) could also reverse multidrug resistance in human glioma cells. Verapamil 119-128 ATP binding cassette subfamily B member 1 Homo sapiens 66-80 7636539-1 1995 PURPOSE: Dexverapamil is a competitive inhibitor of the P-glycoprotein (Pgp) efflux pump, a potent mechanism of multidrug resistance (mdr-1) in vitro. Verapamil 9-21 ATP binding cassette subfamily B member 1 Homo sapiens 56-70 7636539-1 1995 PURPOSE: Dexverapamil is a competitive inhibitor of the P-glycoprotein (Pgp) efflux pump, a potent mechanism of multidrug resistance (mdr-1) in vitro. Verapamil 9-21 ATP binding cassette subfamily B member 1 Homo sapiens 72-75 7636539-1 1995 PURPOSE: Dexverapamil is a competitive inhibitor of the P-glycoprotein (Pgp) efflux pump, a potent mechanism of multidrug resistance (mdr-1) in vitro. Verapamil 9-21 ATP binding cassette subfamily B member 1 Homo sapiens 134-139 7636539-15 1995 This dose was well tolerated on an outpatient basis and achieved plasma concentrations of dexverapamil and nor-dexverapamil within the effective range for Pgp inhibition in vitro. Verapamil 90-102 ATP binding cassette subfamily B member 1 Homo sapiens 155-158 7636540-2 1995 To study its role in lymphomas, we conducted a controlled trial of dexverapamil, an inhibitor of the mdr-1 gene product, P-glycoprotein (Pgp), in lymphomas refractory to etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (EPOCH) chemotherapy. Verapamil 67-79 ATP binding cassette subfamily B member 1 Homo sapiens 101-106 7636540-2 1995 To study its role in lymphomas, we conducted a controlled trial of dexverapamil, an inhibitor of the mdr-1 gene product, P-glycoprotein (Pgp), in lymphomas refractory to etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (EPOCH) chemotherapy. Verapamil 67-79 ATP binding cassette subfamily B member 1 Homo sapiens 121-135 7636540-2 1995 To study its role in lymphomas, we conducted a controlled trial of dexverapamil, an inhibitor of the mdr-1 gene product, P-glycoprotein (Pgp), in lymphomas refractory to etoposide, prednisone, vincristine, cyclophosphamide, and doxorubicin (EPOCH) chemotherapy. Verapamil 67-79 ATP binding cassette subfamily B member 1 Homo sapiens 137-140 7636540-14 1995 Of six patients with mdr-1 levels greater than 15 U, three responded to dexverapamil, while only one of eight patients with mdr-1 levels less than 15 U responded. Verapamil 72-84 ATP binding cassette subfamily B member 1 Homo sapiens 21-26 7636856-5 1995 For this initial series, verapamil (50 microM), the classical Pgp modulator, significantly enhanced cellular accumulation or displaced binding of Tc complexes of 1b, 1d, 1h, 2a, 2d, 3a, and 3b, indicative of targeted interactions with Pgp. Verapamil 25-34 ATP binding cassette subfamily B member 1 Homo sapiens 62-65 7636856-5 1995 For this initial series, verapamil (50 microM), the classical Pgp modulator, significantly enhanced cellular accumulation or displaced binding of Tc complexes of 1b, 1d, 1h, 2a, 2d, 3a, and 3b, indicative of targeted interactions with Pgp. Verapamil 25-34 ATP binding cassette subfamily B member 1 Homo sapiens 235-238 7756676-9 1995 In conclusion this MTC cell line exhibited over-expression of the MDR1 gene and its resistance to doxorubicin can be partially reversed by CSA, verapamil and S9788. Verapamil 144-153 ATP binding cassette subfamily B member 1 Homo sapiens 66-70 7608182-6 1995 Transport was prevented by omission of Mg2+, by substitution of nonhydrolyzable adenylyl-beta,gamma-imidodiphosphate for ATP, by inhibition of the ATPase activity of P-glycoprotein with vanadate and N-ethylmaleimide, and by the chemosensitizers verapamil and amiodarone. Verapamil 245-254 ATP binding cassette subfamily B member 1 Homo sapiens 166-180 9384669-3 1995 Drug resistance of these cells was due to P-glycoprotein expression, as confirmed by (1) staining with a monoclonal antibody (MRK16) specific for human P-glycoprotein, (2) decreased accumulation of [3H]vinblastine that was reversed by verapamil, and (3) enhanced cytotoxicity of vindesine in the presence of verapamil. Verapamil 235-244 ATP binding cassette subfamily B member 1 Homo sapiens 42-56 9384669-3 1995 Drug resistance of these cells was due to P-glycoprotein expression, as confirmed by (1) staining with a monoclonal antibody (MRK16) specific for human P-glycoprotein, (2) decreased accumulation of [3H]vinblastine that was reversed by verapamil, and (3) enhanced cytotoxicity of vindesine in the presence of verapamil. Verapamil 308-317 ATP binding cassette subfamily B member 1 Homo sapiens 42-56 7559918-0 1995 Inhibition of cell-mediated cytolysis and P-glycoprotein function in natural killer cells by verapamil isomers and cyclosporine A analogs. Verapamil 93-102 ATP binding cassette subfamily B member 1 Homo sapiens 42-56 7730340-5 1995 Drugs and chemosensitizers were able to block P-glycoprotein ATPase stimulation by verapamil, however, peptides and ionophores (with the exception of cyclosporine A) were unable to do so. Verapamil 83-92 ATP binding cassette subfamily B member 1 Homo sapiens 46-60 7738186-7 1995 Evidence that these compounds are P-glycoprotein substrates includes: (a) enhancement of cytotoxicity by verapamil; (b) demonstration of cross-resistance in a multidrug-resistant cell line, (c) ability to antagonize P-glycoprotein, increasing vinblastine accumulation by decreasing efflux; and (d) inhibition of photoaffinity labeling by azidopine. Verapamil 105-114 ATP binding cassette subfamily B member 1 Homo sapiens 34-48 7769842-5 1995 When P-gp function was assessed by Rhodamine 123 (Rh123) efflux kinetics, we found that only KG1a and KG1 cells, which have an early (immature) CD34+ CD33- CD38- phenotype, and to a lesser extent TF1, with an intermediate (CD34+ CD33+ CD38+) phenotype, displayed significant P-gp activity which could be inhibited by both verapamil and SDZ PSC 833. Verapamil 322-331 ATP binding cassette subfamily B member 1 Homo sapiens 5-9 7896810-3 1995 Verapamil- and colchicine-stimulated ATPase activities were markedly increased with concomitant increase in affinity for these compounds with Gly185-->Val substitution in the Pgp. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 178-181 7896810-5 1995 Because transport substrate-induced ATP hydrolysis is generally thought to reflect transport function, these data suggest that colchicine and verapamil are transported at an increased rate with Gly185-->Val substitution in the Pgp. Verapamil 142-151 ATP binding cassette subfamily B member 1 Homo sapiens 230-233 7896810-7 1995 Kinetic analyses indicate that cyclosporin A, an inhibitor of Pgp, binds to the verapamil and vinblastine binding/transport site(s) in the Pgp. Verapamil 80-89 ATP binding cassette subfamily B member 1 Homo sapiens 62-65 7896810-7 1995 Kinetic analyses indicate that cyclosporin A, an inhibitor of Pgp, binds to the verapamil and vinblastine binding/transport site(s) in the Pgp. Verapamil 80-89 ATP binding cassette subfamily B member 1 Homo sapiens 139-142 7896810-8 1995 Taken together, the results presented herein reveal that the verapamil and vinblastine binding/transport site(s) are in close proximity and that the cyclosporin A binding site spans the common region of these two drug binding/transport site(s) in the Pgp molecule. Verapamil 61-70 ATP binding cassette subfamily B member 1 Homo sapiens 251-254 7540903-2 1995 The efficacy of verapamil and cyclosporine A as modulators of P-glycoprotein, the multidrug resistance (MDR1) gene product, was studied in leukemic blast cells from 56 patients with de novo acute myeloid leukemia (AML) in vitro. Verapamil 16-25 ATP binding cassette subfamily B member 1 Homo sapiens 62-76 7540903-2 1995 The efficacy of verapamil and cyclosporine A as modulators of P-glycoprotein, the multidrug resistance (MDR1) gene product, was studied in leukemic blast cells from 56 patients with de novo acute myeloid leukemia (AML) in vitro. Verapamil 16-25 ATP binding cassette subfamily B member 1 Homo sapiens 104-108 7600845-12 1995 Prospective phase I, II, and III clinical trials using reversing agents in conjunction with chemotherapy in malignancies that express the MDR1 gene, such as the hematologic malignancies and breast cancer, are necessary before routine use of agents such as verapamil, quinidine, and cyclosporine, which carry innate toxicities. Verapamil 256-265 ATP binding cassette subfamily B member 1 Homo sapiens 138-142 7626853-5 1995 MDR resistance is mediated by GP170, a cell membrane protein, which can be inhibited by several pharmacological agents like verapamil, ciclosporine and S 9788 which are currently being clinically investigated. Verapamil 124-133 ATP binding cassette subfamily B member 1 Homo sapiens 30-35 7720780-5 1995 The cellular accumulation of [14C]pristinamycin IA was very low and was increased by P-glycoprotein inhibitors (verapamil, chlorpromazine and reserpine). Verapamil 112-121 ATP binding cassette subfamily B member 1 Homo sapiens 85-99 7733620-2 1995 We observed that low temperature or verapamil (a P-glycoprotein blocker) inhibited adriamycin efflux in multidrug resistant cells. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 49-63 7838133-0 1995 Evidence for transcriptional control of human mdr1 gene expression by verapamil in multidrug-resistant leukemic cells. Verapamil 70-79 ATP binding cassette subfamily B member 1 Homo sapiens 46-50 8698736-1 1995 Multidrug resistance (MDR) in a variety of human tumours such as renal cell carcinoma (RCC) is thought to be caused by expression of the MDR1 gene and may be reversed by applying modern chemosensitisers such as dexverapamil, which inhibit the MDR1 gene product P-glycoprotein. Verapamil 211-223 ATP binding cassette subfamily B member 1 Homo sapiens 137-141 8698736-1 1995 Multidrug resistance (MDR) in a variety of human tumours such as renal cell carcinoma (RCC) is thought to be caused by expression of the MDR1 gene and may be reversed by applying modern chemosensitisers such as dexverapamil, which inhibit the MDR1 gene product P-glycoprotein. Verapamil 211-223 ATP binding cassette subfamily B member 1 Homo sapiens 243-247 8698736-1 1995 Multidrug resistance (MDR) in a variety of human tumours such as renal cell carcinoma (RCC) is thought to be caused by expression of the MDR1 gene and may be reversed by applying modern chemosensitisers such as dexverapamil, which inhibit the MDR1 gene product P-glycoprotein. Verapamil 211-223 ATP binding cassette subfamily B member 1 Homo sapiens 261-275 8698739-10 1995 Among 6 patients with MDR-1 > 15, 3 responded to dexverapamil whereas only 1/8 patients with MDR-1 < 15 responded. Verapamil 52-64 ATP binding cassette subfamily B member 1 Homo sapiens 22-27 7838133-1 1995 We investigated the mechanism of verapamil (VRP) effects on mdr1 gene expression in two leukemic multidrug-resistant (MDR) cell lines, K562/ADR and CEM VLB100. Verapamil 33-42 ATP binding cassette subfamily B member 1 Homo sapiens 60-64 7964963-8 1994 Verapamil and cyclosporine (CsA) have been used as competitive inhibitors of the multidrug transporter P-gp in early clinical trials. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 103-107 8704279-6 1995 Verapamil enhanced the sensitivity of SKOV3/CIS to doxorubicin (260-fold), in conformity with the proposed mechanism of Pgp in multidrug resistance (MDR), but it did not potentiate cisplatin cytotoxicity in SKOV3/CIS cells. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 120-123 7727860-9 1994 These studies have employed "first generation" antagonists such as verapamil and cyclosporine which were toxic at concentrations needed to block P-glycoprotein. Verapamil 67-76 ATP binding cassette subfamily B member 1 Homo sapiens 145-159 7960246-9 1994 However, the cMDR-modifier verapamil (VP) significantly increased both parameters in those melanoma cells with the highest P-gp levels. Verapamil 27-36 ATP binding cassette subfamily B member 1 Homo sapiens 123-127 8835287-8 1995 Similarly to verapamil, dihydrocytochalasin B significantly stimulated the ATPase activity of P-glycoprotein, while other cytochalasins were ineffective. Verapamil 13-22 ATP binding cassette subfamily B member 1 Homo sapiens 94-108 7962123-11 1994 Verapamil (10 microM), which caused 80% reversal of Pgp-associated drug extrusion, failed to inhibit the HCS-evoked Cl- efflux of Pgp+ cells. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 52-55 7872686-0 1994 Effects of vinblastine, colchicine, and verapamil on rhodamine 123 accumulation in human P-glycoprotein-positive leukemia cells. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 89-103 7872686-2 1994 We addressed the question of whether R123 could compete with substrates or inhibitors (vinblastine, colchicine, verapamil) of P-glycoprotein (Pgp) overexpressed in MDR cells, using fluorescence image cytometry. Verapamil 112-121 ATP binding cassette subfamily B member 1 Homo sapiens 126-140 7872686-2 1994 We addressed the question of whether R123 could compete with substrates or inhibitors (vinblastine, colchicine, verapamil) of P-glycoprotein (Pgp) overexpressed in MDR cells, using fluorescence image cytometry. Verapamil 112-121 ATP binding cassette subfamily B member 1 Homo sapiens 142-145 7872686-6 1994 The results indicate that vinblastine, R123 and verapamil can compete for outward transport by Pgp. Verapamil 48-57 ATP binding cassette subfamily B member 1 Homo sapiens 95-98 7964963-9 1994 Although these studies show some activity in modulating clinical MDR, both verapamil and CsA manifest considerable toxicities at doses below those required for complete inhibition of P-gp function. Verapamil 75-84 ATP binding cassette subfamily B member 1 Homo sapiens 183-187 7945455-4 1994 The polarized transport of vinblastine in the basolateral to apical direction was temperature and energy dependent, and was reduced by P-glycoprotein inhibitors such as verapamil, chlorpromazine and reserpine. Verapamil 169-178 ATP binding cassette subfamily B member 1 Homo sapiens 135-149 7945455-7 1994 This polarized transport was inhibited by verapamil, chlorpromazine and reserpine, thus demonstrating that docetaxel is a substrate of P-glycoprotein. Verapamil 42-51 ATP binding cassette subfamily B member 1 Homo sapiens 135-149 7808368-13 1994 Our data suggest a synergy of verapamil and cyclosporine in the inhibition of multidrug resistance induced by gp170, without the occurrence of heavy toxicity. Verapamil 30-39 ATP binding cassette subfamily B member 1 Homo sapiens 110-115 7931593-6 1994 Primary chemoresistance was overcome by addition of the calcium antagonists verapamil or nimodipine to the cultures if the original tumor expressed p-glycoprotein (p < 0.01 for verapamil, p < 0.05 for nimodipine). Verapamil 76-85 ATP binding cassette subfamily B member 1 Homo sapiens 148-162 7914405-8 1994 Among these, progesterone is a potent inducer of the Pgp ATPase activity; at 50 microM, this hormone stimulated the Pgp ATPase activity as effectively as verapamil. Verapamil 154-163 ATP binding cassette subfamily B member 1 Homo sapiens 53-56 7915113-5 1994 Expression of P-gp in the transfected cells was associated with resistance to dolastatin 10 by a verapamil-sensitive mechanism. Verapamil 97-106 ATP binding cassette subfamily B member 1 Homo sapiens 14-18 7911330-3 1994 Evidence suggesting involvement of P-Glycoprotein (P-Gp), included (1) comparable transport of P-Gp substrate doxorubicin, (2) transport stimulation by ATP and (3) transport suppression by the P-Gp inhibitor, verapamil. Verapamil 209-218 ATP binding cassette subfamily B member 1 Homo sapiens 35-49 7919458-5 1994 In resistant cells, the ether phospholipid effect on DNR accumulation has also been found after blocking the PgP function by verapamil and cyclosporin A. Verapamil 125-134 ATP binding cassette subfamily B member 1 Homo sapiens 109-112 7912815-5 1994 The photoaffinity labeling of P-glycoprotein by ASA-Rh123 was specifically inhibited in the presence of vinblastine and verapamil but not in the presence of colchicine. Verapamil 120-129 ATP binding cassette subfamily B member 1 Homo sapiens 30-44 7908989-11 1994 Verapamil and quinidine lowered the IC50 values of doxorubicin for MDR1-positive cell lines. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 67-71 7749215-1 1994 Calcium channel inhibitors, such as verapamil, have been identified as having the ability to modulate the multidrug-resistant (MDR) phenotype due to overexpression of P-glycoprotein (Pgp). Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 167-181 7749215-8 1994 The effect of verapamil is therefore restricted to drug-selected lines presenting high levels of Pgp expression. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 97-100 7514263-2 1994 The macrolides FK506 and FK520 stimulate the Pgp-ATPase activity with affinities in the 100 nM range, nearly 10 times higher than that of verapamil, a well known Pgp substrate. Verapamil 138-147 ATP binding cassette subfamily B member 1 Homo sapiens 45-48 7514263-2 1994 The macrolides FK506 and FK520 stimulate the Pgp-ATPase activity with affinities in the 100 nM range, nearly 10 times higher than that of verapamil, a well known Pgp substrate. Verapamil 138-147 ATP binding cassette subfamily B member 1 Homo sapiens 162-165 7514263-4 1994 They do, however, act as potent competitive inhibitors of verapamil-stimulated Pgp-ATPase activity, with affinity constants in the 20-25 nM range. Verapamil 58-67 ATP binding cassette subfamily B member 1 Homo sapiens 79-82 7906729-5 1994 Verapamil (500 microM), the classical MDR modulator, produced an approximately 300% enhancement of 99mTc-sestamibi accumulation in Sf9 cells expressing MDR1 P-glycoprotein, but only a 50% enhancement in parental Sf9 cells, consistent with verapamil-induced inhibition of P-glycoprotein-mediated 99mTc-sestamibi efflux. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 152-156 7906729-5 1994 Verapamil (500 microM), the classical MDR modulator, produced an approximately 300% enhancement of 99mTc-sestamibi accumulation in Sf9 cells expressing MDR1 P-glycoprotein, but only a 50% enhancement in parental Sf9 cells, consistent with verapamil-induced inhibition of P-glycoprotein-mediated 99mTc-sestamibi efflux. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 157-171 7906729-5 1994 Verapamil (500 microM), the classical MDR modulator, produced an approximately 300% enhancement of 99mTc-sestamibi accumulation in Sf9 cells expressing MDR1 P-glycoprotein, but only a 50% enhancement in parental Sf9 cells, consistent with verapamil-induced inhibition of P-glycoprotein-mediated 99mTc-sestamibi efflux. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 271-285 7904185-0 1994 Non-competitive inhibition of P-glycoprotein-associated efflux of THP-adriamycin by verapamil in living K562 leukemia cells. Verapamil 84-93 ATP binding cassette subfamily B member 1 Homo sapiens 30-44 7904185-5 1994 Kinetic analysis indicates: (1) a saturation of the active efflux when the cytosolic free drug concentration increased (the Michaelis constant Km = 0.5 +/- 0.3 microM) and (2) that the inhibitory effect of verapamil on P-gp-associated efflux of THP-adriamycin in living cells is non-competitive. Verapamil 206-215 ATP binding cassette subfamily B member 1 Homo sapiens 219-223 7879670-5 1994 It has been demonstrated, at least in the laboratory, that resistance mediated by P-glycoprotein may be modulated by a wide variety of compounds, including verapamil and cyclosporine A. Verapamil 156-165 ATP binding cassette subfamily B member 1 Homo sapiens 82-96 7879670-9 1994 The detection of the P-glycoprotein in patient samples is very important in the design of these studies, as it appears that drug-resistant cells lacking P-glycoprotein will be unaffected by agents such as verapamil. Verapamil 205-214 ATP binding cassette subfamily B member 1 Homo sapiens 21-35 7896535-7 1994 Verapamil modulated docetaxel resistance only in sublines expressing resistance to the drug and overexpressing Pgp. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 111-114 7914405-5 1994 Antiestrogens such as tamoxifen, metabolites of tamoxifen (4-hydroxytamoxifen and N-desmethyltamoxifen), droloxifen, and toremifene stimulated the Pgp ATPase activity, and the maximum stimulation obtained with these agents equalled the maximal stimulation obtained by the best known MDR chemosensitizer, verapamil. Verapamil 304-313 ATP binding cassette subfamily B member 1 Homo sapiens 147-150 7914405-6 1994 Clomifene, nafoxidine and diethylstilbestrol also stimulated the Pgp ATPase activity, with maximal activations 75, 60 and 45% of the verapamil stimulation, respectively. Verapamil 133-142 ATP binding cassette subfamily B member 1 Homo sapiens 65-68 7909435-4 1994 We found that colchicine, vinblastine, daunomycin and verapamil (50 microM) caused block of a 40 pS outwardly-rectifying chloride channel in cells expressing P-glycoprotein. Verapamil 54-63 ATP binding cassette subfamily B member 1 Homo sapiens 158-172 7909520-0 1994 The multidrug-resistance-reverser verapamil interferes with cellular P-glycoprotein-mediated pumping of daunorubicin as a non-competing substrate. Verapamil 34-43 ATP binding cassette subfamily B member 1 Homo sapiens 69-83 7909520-1 1994 We examined P-glycoprotein-mediated verapamil transport, using two drug-sensitive and multi-drug resistant cell-line couples, i.e. A2780, 2780AD and SW-1573, SW-1573/1R500. Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 12-26 7909520-4 1994 In the P-glycoprotein-expressing cells, verapamil accumulation was increased by vinblastine and some known multidrug resistant (MDR) modifiers. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 7-21 7909520-6 1994 In this manner, we obtained evidence that verapamil is actively transported by the MDR-related P-glycoprotein. Verapamil 42-51 ATP binding cassette subfamily B member 1 Homo sapiens 95-109 7909520-11 1994 These and other observations are in agreement with a model in which daunorubicin and verapamil are non-competing substrates for P-glycoprotein. Verapamil 85-94 ATP binding cassette subfamily B member 1 Homo sapiens 128-142 7909520-12 1994 In conclusion, we obtained evidence that verapamil is actively transported by the MDR-related P-glycoprotein and that verapamil and daunorubicin are non-competing substrates for P-glycoprotein. Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 94-108 7909520-12 1994 In conclusion, we obtained evidence that verapamil is actively transported by the MDR-related P-glycoprotein and that verapamil and daunorubicin are non-competing substrates for P-glycoprotein. Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 178-192 7909520-13 1994 Consequently, the effectiveness of verapamil as an MDR antagonist may be compromised because it is extruded by P-glycoprotein. Verapamil 35-44 ATP binding cassette subfamily B member 1 Homo sapiens 111-125 7910786-0 1994 Inhibition of P-glycoprotein-mediated vinblastine transport across HCT-8 intestinal carcinoma monolayers by verapamil, cyclosporine A and SDZ PSC 833 in dependence on extracellular pH. Verapamil 108-117 ATP binding cassette subfamily B member 1 Homo sapiens 14-28 7910786-4 1994 P-gp-mediated rhodamine 123 efflux from dye-loaded single-cell suspensions of HCT-8 cells as measured by flow cytometry was not impeded at pHo 6.8 in comparison with pHo 7.5 in standard medium, but at low pHo the inhibitory activity of R-VPL (29% vs 60% rhodamine 123 efflux inhibition) was diminished significantly, again without a reduction in the effect of PSC 833 (rhodamine 123 flux inhibition, 75%). Verapamil 237-241 ATP binding cassette subfamily B member 1 Homo sapiens 0-4 7749215-1 1994 Calcium channel inhibitors, such as verapamil, have been identified as having the ability to modulate the multidrug-resistant (MDR) phenotype due to overexpression of P-glycoprotein (Pgp). Verapamil 36-45 ATP binding cassette subfamily B member 1 Homo sapiens 183-186 7749215-2 1994 We have studied the effect of verapamil on Pgp expression levels in a cell line originating from acute myeloblastic leukemia and resistant to adriamycin, K562/ADR. Verapamil 30-39 ATP binding cassette subfamily B member 1 Homo sapiens 43-46 7749215-3 1994 In this line, the addition of 15 microM verapamil in the culture medium gives a 3-fold decrease of Pgp expression after 72 hours of treatment. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 99-102 7749215-5 1994 The level of mdr1 mRNAs is decreased in the presence of verapamil (with a maximum effect obtained at the 24th hour), which suggests that the mechanism of action of verapamil is transcriptional and/or post-transcriptional. Verapamil 56-65 ATP binding cassette subfamily B member 1 Homo sapiens 13-17 7749215-5 1994 The level of mdr1 mRNAs is decreased in the presence of verapamil (with a maximum effect obtained at the 24th hour), which suggests that the mechanism of action of verapamil is transcriptional and/or post-transcriptional. Verapamil 164-173 ATP binding cassette subfamily B member 1 Homo sapiens 13-17 7749215-6 1994 We have also studied the effect of verapamil on the level of expression of mdr1 mRNAs in non-drug selected cells such as the HEL line (human acute myeloblastic leukemia) and the parental K562 line, which present a very low level of expression of Pgp, detectable only by PCR. Verapamil 35-44 ATP binding cassette subfamily B member 1 Homo sapiens 75-79 7941591-5 1994 Resistance to cytostatic drugs due to the p-glycoprotein coded by the MDR-gene is treated by a combination of cyclosporin-A or verapamil and VAD. Verapamil 127-136 ATP binding cassette subfamily B member 1 Homo sapiens 42-56 7820144-1 1994 Multidrug resistance (MDR) in a variety of human tumors such as renal cell carcinoma (RCC) is thought to be caused by expression of the mdr1 gene and may be reversed by applying chemosensitizers such as Dexverapamil that inhibit the mdr1 gene product P-glycoprotein. Verapamil 203-215 ATP binding cassette subfamily B member 1 Homo sapiens 136-140 7820144-1 1994 Multidrug resistance (MDR) in a variety of human tumors such as renal cell carcinoma (RCC) is thought to be caused by expression of the mdr1 gene and may be reversed by applying chemosensitizers such as Dexverapamil that inhibit the mdr1 gene product P-glycoprotein. Verapamil 203-215 ATP binding cassette subfamily B member 1 Homo sapiens 233-237 7820144-1 1994 Multidrug resistance (MDR) in a variety of human tumors such as renal cell carcinoma (RCC) is thought to be caused by expression of the mdr1 gene and may be reversed by applying chemosensitizers such as Dexverapamil that inhibit the mdr1 gene product P-glycoprotein. Verapamil 203-215 ATP binding cassette subfamily B member 1 Homo sapiens 251-265 7903200-6 1993 A comparison between verapamil and Triton X-100 revealed that the latter was more effective in inhibiting azidopine photolabeling to P-glycoprotein while verapamil was more effective in potentiating [3H]vinblastine accumulation in drug-resistant cells. Verapamil 21-30 ATP binding cassette subfamily B member 1 Homo sapiens 133-147 8105865-7 1993 N/C ratios in highly resistant P-glycoprotein-containing cells could be increased with the resistance modifier verapamil to values of 1.3-2.7, a process that was paralleled by a decrease of the cellular doxorubicin amounts present at IC50. Verapamil 111-120 ATP binding cassette subfamily B member 1 Homo sapiens 31-45 8105110-11 1993 A verapamil-sensitive drug efflux has been demonstrated for the PC-3 and Du-145, but not for the LNCaP, cell lines, using flow cytometric measurements of the P-gp substrate rhodamine 123 efflux from preloaded cells. Verapamil 2-11 ATP binding cassette subfamily B member 1 Homo sapiens 158-162 7911345-11 1993 Reversal compounds specifically inhibiting Pgp were found, such as verapamil, cyclosporin or quinidine. Verapamil 67-76 ATP binding cassette subfamily B member 1 Homo sapiens 43-46 8093882-4 1993 The resistance of KB-V1 cells to both okadaic acid and calyculin A was completely reversed by verapamil, suggesting that the toxins may be transported by P-glycoprotein (P-gp). Verapamil 94-103 ATP binding cassette subfamily B member 1 Homo sapiens 154-168 7690250-6 1993 Transport of P-glycoprotein antagonists in SW620 Ad300 cells was also affected by calphostin C. Cyclosporin A transport decreased, while verapamil transport increased. Verapamil 137-146 ATP binding cassette subfamily B member 1 Homo sapiens 13-27 7690250-7 1993 Cyclosporin A in calphostin C-treated cells resulted in additive P-glycoprotein antagonism, while no additive effect could be demonstrated with verapamil, suggesting that the increase in verapamil transport makes it a poorer P-glycoprotein antagonist. Verapamil 187-196 ATP binding cassette subfamily B member 1 Homo sapiens 65-79 7690250-7 1993 Cyclosporin A in calphostin C-treated cells resulted in additive P-glycoprotein antagonism, while no additive effect could be demonstrated with verapamil, suggesting that the increase in verapamil transport makes it a poorer P-glycoprotein antagonist. Verapamil 187-196 ATP binding cassette subfamily B member 1 Homo sapiens 225-239 21573335-6 1993 The in vitro resistance of vincristine was reversed by verapamil for these NHL tumor cells, suggesting that the MDR1 resistance is a relevant mechanism in this model. Verapamil 55-64 ATP binding cassette subfamily B member 1 Homo sapiens 112-116 8099135-4 1993 Cyclosporin A (CsA, 1 microgram/ml) and verapamil (5 micrograms/ml), but not cefoperazone (10 mM), completely reversed (CsA) or partially reversed (verapamil) the DNR efflux from K562/DOX mdr1(+) cell line. Verapamil 40-49 ATP binding cassette subfamily B member 1 Homo sapiens 188-192 7906217-3 1993 This action could be reversed by verapamil through competition for closely related binding sites on P-glycoprotein. Verapamil 33-42 ATP binding cassette subfamily B member 1 Homo sapiens 100-114 8100632-3 1993 Inhibition of P-glycoprotein by a variety of modulators (verapamil, 1,9-dideoxyforskolin, nifedipine, and taxotere) is associated with an increased vinblastine absorptive permeability. Verapamil 57-66 ATP binding cassette subfamily B member 1 Homo sapiens 14-28 8100632-5 1993 Upon inhibition of P-glycoprotein by verapamil and 1,9-dideoxyforskolin, vinblastine absorption increased and was linearly dependent on vinblastine concentration. Verapamil 37-46 ATP binding cassette subfamily B member 1 Homo sapiens 19-33 7681059-3 1993 Cyclosporin A itself interacts with a common binding site of P-glycoprotein to which Vinca alkaloids and verapamil bind. Verapamil 105-114 ATP binding cassette subfamily B member 1 Homo sapiens 61-75 8093882-4 1993 The resistance of KB-V1 cells to both okadaic acid and calyculin A was completely reversed by verapamil, suggesting that the toxins may be transported by P-glycoprotein (P-gp). Verapamil 94-103 ATP binding cassette subfamily B member 1 Homo sapiens 170-174 8094005-5 1993 Verapamil, another inhibitor of PGP-mediated efflux, increased the initial influx rate constant by 2.7-fold in the KB-GRC1 cells but only 1.4-fold in the KB-3-1 cells. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 32-35 8099844-5 1993 P-Glycoprotein inhibitors such as quinidine, verapamil, vincristine, and cyclosporine increased the net A-B flux and inhibited the total B-A flux without affecting the nonspecific flux significantly. Verapamil 45-54 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 8100040-2 1993 These findings suggest that verapamil inhibits the digoxin active secretory transport at the apical membranes, supporting the theory that P-glycoprotein mediates digoxin secretion in the renal tubular cells. Verapamil 28-37 ATP binding cassette subfamily B member 1 Homo sapiens 138-152 1358437-4 1992 Evidence supporting the involvement of P-gp included the inhibition of azidopine binding to P-gp benzo(alpha)pyrene and the inhibition of benzo(alpha)pyrene efflux by Adriamycin and verapamil. Verapamil 182-191 ATP binding cassette subfamily B member 1 Homo sapiens 39-43 1360820-2 1992 The effect of verapamil (VRP) as a chemosensitizer was studied in relation to the expression of the membrane efflux pump P-glycoprotein (PGP) as determined by a semiquantitative flow-cytometric proceder. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 121-135 1360820-2 1992 The effect of verapamil (VRP) as a chemosensitizer was studied in relation to the expression of the membrane efflux pump P-glycoprotein (PGP) as determined by a semiquantitative flow-cytometric proceder. Verapamil 14-23 ATP binding cassette subfamily B member 1 Homo sapiens 137-140 1363515-1 1992 Cyclosporin A and verapamil are substrates for P-glycoprotein. Verapamil 18-27 ATP binding cassette subfamily B member 1 Homo sapiens 47-61 1350903-5 1992 The dimeric P-glycoprotein was photolabeled with [3H]azidopine like the 180K monomeric P-glycoprotein and the photolabeling was inhibited by excess amount of vincristine and verapamil. Verapamil 174-183 ATP binding cassette subfamily B member 1 Homo sapiens 12-26 1387586-3 1992 In contrast, two of the drug-resistant variants selected with DOX plus verapamil, an agent which inhibits P-glycoprotein-mediated multidrug resistance, displayed a collateral sensitivity to STZ and BCNU. Verapamil 71-80 ATP binding cassette subfamily B member 1 Homo sapiens 106-120 1356264-8 1992 Several other drugs that are known to be transported by P-glycoprotein enhanced the ATPase activity in a dose-dependent manner with relative potencies as follows: doxorubicin = vinblastine greater than daunomycin greater than actinomycin D greater than verapamil greater than colchicine. Verapamil 253-262 ATP binding cassette subfamily B member 1 Homo sapiens 56-70 1352877-6 1992 The inhibitory effect of UIC2 in vitro was as strong as that of verapamil (a widely used Pgp inhibitor) at its highest clinically achievable concentrations. Verapamil 64-73 ATP binding cassette subfamily B member 1 Homo sapiens 89-92 8094079-1 1993 We observed increased levels of mdr-1 mRNA and its protein product P-glycoprotein (Pgp) in the human colon carcinoma cell line, LS 180, and its drug-resistant sublines, LS 180-Ad50 and LS 180-Vb2, after treatment with the Pgp antagonists, verapamil, nifedipine, and cyclosporin A. Verapamil 239-248 ATP binding cassette subfamily B member 1 Homo sapiens 32-37 8094079-1 1993 We observed increased levels of mdr-1 mRNA and its protein product P-glycoprotein (Pgp) in the human colon carcinoma cell line, LS 180, and its drug-resistant sublines, LS 180-Ad50 and LS 180-Vb2, after treatment with the Pgp antagonists, verapamil, nifedipine, and cyclosporin A. Verapamil 239-248 ATP binding cassette subfamily B member 1 Homo sapiens 83-86 8094079-6 1993 Treatment with verapamil or nifedipine was associated with electron microscopic changes consistent with increased differentiation and resulted in increased carcinoembryonic antigen expression, suggesting that the increase in mdr-1 expression was associated with the process of differentiation. Verapamil 15-24 ATP binding cassette subfamily B member 1 Homo sapiens 225-230 1350903-5 1992 The dimeric P-glycoprotein was photolabeled with [3H]azidopine like the 180K monomeric P-glycoprotein and the photolabeling was inhibited by excess amount of vincristine and verapamil. Verapamil 174-183 ATP binding cassette subfamily B member 1 Homo sapiens 87-101 1348241-2 1992 The action of Pgp in tumor cells can be detected by measuring the increase of daunorubicin accumulation upon blocking Pgp with drugs such as verapamil. Verapamil 141-150 ATP binding cassette subfamily B member 1 Homo sapiens 14-17 1350280-8 1992 Cytoplasts from P-glycoprotein containing multidrug-resistant K562 cells demonstrated a verapamil-reversible, decreased daunorubicin accumulation that was observed in resistant whole cells. Verapamil 88-97 ATP binding cassette subfamily B member 1 Homo sapiens 16-30 1349044-8 1992 These low levels of mdr-1/Pgp are capable of conferring MDR, which can be antagonized by verapamil. Verapamil 89-98 ATP binding cassette subfamily B member 1 Homo sapiens 20-25 1349044-10 1992 IMPLICATIONS: In vitro sensitization by the addition of verapamil in cell lines with these low levels of mdr-1/Pgp suggests that clinically detected levels may confer drug resistance in vivo. Verapamil 56-65 ATP binding cassette subfamily B member 1 Homo sapiens 105-110 1348241-2 1992 The action of Pgp in tumor cells can be detected by measuring the increase of daunorubicin accumulation upon blocking Pgp with drugs such as verapamil. Verapamil 141-150 ATP binding cassette subfamily B member 1 Homo sapiens 118-121 1682041-6 1991 The reduced cytotoxicity of topotecan in KB V1 cells was due to the overexpression of MDR1 in KB V1 cells since verapamil restored both topotecan accumulation and cytotoxicity. Verapamil 112-121 ATP binding cassette subfamily B member 1 Homo sapiens 86-90 1387586-4 1992 Verapamil was included in the selection protocol because it has been shown to inhibit the P-glycoprotein-mediated multidrug resistance phenotype and is now in clinical trials as a chemosensitizing agent. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 90-104 1346631-8 1992 The resistance to actinomycin D was attenuated in the presence of verapamil, a known inhibitor of P-glycoprotein. Verapamil 66-75 ATP binding cassette subfamily B member 1 Homo sapiens 98-112 1346496-6 1992 A finding of interest is that vinblastine and verapamil compete more effectively than daunorubicin for [3H]AB-DNR binding to Pgp, suggesting that vinblastine and verapamil have similar structural features not shared by daunorubicin. Verapamil 46-55 ATP binding cassette subfamily B member 1 Homo sapiens 125-128 1346496-6 1992 A finding of interest is that vinblastine and verapamil compete more effectively than daunorubicin for [3H]AB-DNR binding to Pgp, suggesting that vinblastine and verapamil have similar structural features not shared by daunorubicin. Verapamil 162-171 ATP binding cassette subfamily B member 1 Homo sapiens 125-128 1394818-3 1992 Verapamil was used as an inhibitor of P-glycoprotein. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 38-52 1352696-5 1992 Treatments based on the gp170 inhibitory property of verapamil were developed that allowed abrogation of resistance in MDR cell lines, a strategy that may be applicable to therapy treatments. Verapamil 53-62 ATP binding cassette subfamily B member 1 Homo sapiens 24-29 1364132-0 1992 P-glycoprotein expression in refractory hematological neoplasms and circumvention of resistance with verapamil or cyclosporine A containing protocols. Verapamil 101-110 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 1681887-6 1991 N/C ratios could be restored partly with verapamil only in Pgp/+ cells. Verapamil 41-50 ATP binding cassette subfamily B member 1 Homo sapiens 59-62 1682280-3 1991 In the first, including a series of Adriamycin-resistant SW620 and DLD-I sub-lines, and in parental HCT-15 cells, P-glycoprotein has a major role in Adriamycin resistance, as evidenced by a correlation between Adriamycin resistance, expression of the multidrug-resistance gene mdr-I and its product, P-glycoprotein (Pgp), decreased drug accumulation and reversibility by verapamil. Verapamil 371-380 ATP binding cassette subfamily B member 1 Homo sapiens 114-128 1677057-0 1991 P-glycoprotein expression and in vitro reversion of doxorubicin resistance by verapamil in clinical specimens from acute leukaemia and myeloma. Verapamil 78-87 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 1679346-7 1991 Total inhibition of photolabeling of the P-glycoprotein was observed with verapamil, nifedipine, diltiazem, and vinbalastine, and partial inhibition was observed with colchicine and cytochalasin B. Verapamil 74-83 ATP binding cassette subfamily B member 1 Homo sapiens 41-55 1677434-0 1991 New potent verapamil derivatives that reverse multidrug resistance in human renal carcinoma cells and in transgenic mice expressing the human MDR1 gene. Verapamil 11-20 ATP binding cassette subfamily B member 1 Homo sapiens 142-146 1677057-4 1991 Verapamil, a calcium channel blocker, has been demonstrated to circumvent the multidrug resistance in cell lines, possibly by interfering with P-glycoprotein function. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 143-157 1677057-7 1991 We conclude that high non-cytotoxic concentrations of verapamil were able to increase the in vitro doxorubicin sensitivity of fresh acute leukaemia and myeloma cells without detectable expression of the P-glycoprotein. Verapamil 54-63 ATP binding cassette subfamily B member 1 Homo sapiens 203-217 1977745-6 1990 Importantly, our results show that under our conditions vinblastine and verapamil are better able to compete with [3H]PRG for binding to Pgp than are other steroids, including testosterone, corticosteroids, and mineralocorticoids. Verapamil 72-81 ATP binding cassette subfamily B member 1 Homo sapiens 137-140 1977745-3 1990 The anticancer drug vinblastine and multidrug resistance reversing agent verapamil as well as several steroidal hormones were examined for their ability to interfere with [3H]PRG binding to Pgp. Verapamil 73-82 ATP binding cassette subfamily B member 1 Homo sapiens 190-193 1976255-7 1990 Unexpectedly, the mutant P-glycoprotein showed increased binding of photoactive analogs of vinblastine and verapamil and the photoactive compound azidopine and decreased binding of a photoactive colchicine analog. Verapamil 107-116 ATP binding cassette subfamily B member 1 Homo sapiens 25-39 1972154-2 1990 Pgp-mediated drug resistance can be overcome by the calcium channel blocker verapamil (Vp), which acts as a competitive inhibitor of drug binding and efflux. Verapamil 76-85 ATP binding cassette subfamily B member 1 Homo sapiens 0-3 1972154-2 1990 Pgp-mediated drug resistance can be overcome by the calcium channel blocker verapamil (Vp), which acts as a competitive inhibitor of drug binding and efflux. Verapamil 87-89 ATP binding cassette subfamily B member 1 Homo sapiens 0-3 1972771-1 1990 The interaction of etoposide (VP-16), Vinca alkaloids, and verapamil with the P-glycoprotein (P-gp) was studied in human breast (MCF-7) and Chinese hamster lung (DC3F) cell lines and the corresponding multidrug-resistant MCF-7/ADR and DC3F/ADX tumor cell lines, selected for resistance to Adriamycin and actinomycin D, respectively, and overexpressing P-gp. Verapamil 59-68 ATP binding cassette subfamily B member 1 Homo sapiens 78-92 1972771-1 1990 The interaction of etoposide (VP-16), Vinca alkaloids, and verapamil with the P-glycoprotein (P-gp) was studied in human breast (MCF-7) and Chinese hamster lung (DC3F) cell lines and the corresponding multidrug-resistant MCF-7/ADR and DC3F/ADX tumor cell lines, selected for resistance to Adriamycin and actinomycin D, respectively, and overexpressing P-gp. Verapamil 59-68 ATP binding cassette subfamily B member 1 Homo sapiens 94-98 1674435-4 1991 The potential therefore exists for new therapeutic studies aimed at circumventing resistance which develops through this mechanism, by using modulators, such as verapamil, quinidine and several others, which prevent cellular drug efflux by competitive binding to P-glycoprotein. Verapamil 161-170 ATP binding cassette subfamily B member 1 Homo sapiens 263-277 1671638-6 1991 The MDR modifiers verapamil, Cremophor EL, cyclosporin A and Ro 11-2933/001 had significant effects on DN cytotoxicity, total DN accumulation and efflux, only if P-gp was present. Verapamil 18-27 ATP binding cassette subfamily B member 1 Homo sapiens 162-166 1988684-1 1991 Aside from its more conventional uses as a cardiovascular drug, the calcium channel blocker verapamil has recently been added to chemotherapeutic regimens to reduce drug resistance in B-cell and other neoplasms that express the P-glycoprotein. Verapamil 92-101 ATP binding cassette subfamily B member 1 Homo sapiens 228-242 1671173-7 1991 Verapamil and quinine, both at levels suitable for human trials that produced only partial sensitization of the MDR1-transgenic mice, were fully sensitizing when used in combination. Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 112-116 1679277-3 1991 In vitro treatment of glioma cells with vincristine induced coordinate over-expression of both mdr1 and mdr3 genes associated with very high P-glycoprotein-mediated multidrug transport, resistant to the inhibitory activity of chemosensitizers like verapamil. Verapamil 248-257 ATP binding cassette subfamily B member 1 Homo sapiens 95-99 1679277-3 1991 In vitro treatment of glioma cells with vincristine induced coordinate over-expression of both mdr1 and mdr3 genes associated with very high P-glycoprotein-mediated multidrug transport, resistant to the inhibitory activity of chemosensitizers like verapamil. Verapamil 248-257 ATP binding cassette subfamily B member 1 Homo sapiens 141-155 1670642-0 1991 P-glycoprotein expression in malignant lymphoma and reversal of clinical drug resistance with chemotherapy plus high-dose verapamil. Verapamil 122-131 ATP binding cassette subfamily B member 1 Homo sapiens 0-14 1670642-5 1991 Based on prior reports suggesting that verapamil sensitizes drug-resistant cancer cells to chemotherapy by competitive inhibition of the P-glycoprotein, we tested the efficacy of verapamil as a chemosensitizer in 18 patients with drug-refractory disease. Verapamil 39-48 ATP binding cassette subfamily B member 1 Homo sapiens 137-151 1670642-12 1991 We conclude that the P-glycoprotein is uncommonly expressed in untreated lymphomas and frequently expressed in clinically drug-resistant disease, and that chemotherapy using CVAD plus maximally tolerated doses of verapamil results in a high response rate in patients carefully selected for clinical drug resistance. Verapamil 213-222 ATP binding cassette subfamily B member 1 Homo sapiens 21-35 1972761-4 1990 In vitro drug uptake studies by on-line flow cytometry showed that in leukemia cells expressing either mdr1 or mdr3, the steady-state accumulation of daunorubicin could be significantly increased by addition of cyclosporine and, to a lesser extent, by verapamil. Verapamil 252-261 ATP binding cassette subfamily B member 1 Homo sapiens 103-107 1972761-5 1990 Because cyclosporine and verapamil are known as inhibitors of the mdr1-encoded P-glycoprotein drug-efflux pump, and because the mdr1 and mdr3 genes are highly homologous, our data suggest that the mdr3 gene encodes a functional drug pump in B-cell lymphocytic leukemias. Verapamil 25-34 ATP binding cassette subfamily B member 1 Homo sapiens 66-70 1972761-5 1990 Because cyclosporine and verapamil are known as inhibitors of the mdr1-encoded P-glycoprotein drug-efflux pump, and because the mdr1 and mdr3 genes are highly homologous, our data suggest that the mdr3 gene encodes a functional drug pump in B-cell lymphocytic leukemias. Verapamil 25-34 ATP binding cassette subfamily B member 1 Homo sapiens 128-132 1972771-6 1990 Excess nonradioactive vinblastine or verapamil effectively competed with the P-gp photolabeling by either NASVP or NASV, with IC50 levels of 0.6 and 10 microM, respectively. Verapamil 37-46 ATP binding cassette subfamily B member 1 Homo sapiens 77-81 1970614-3 1990 The discovery that verapamil partially reverses chloroquine resistance in vitro led to the proposal that efflux may involve an ATP-driven P-glycoprotein pump similar to that in mammalian multidrug-resistant (mdr) tumor cell lines. Verapamil 19-28 ATP binding cassette subfamily B member 1 Homo sapiens 138-152 1968459-3 1990 Many agents, such as the calcium channel blocker verapamil, reverse multidrug resistance and also interact with P-glycoprotein. Verapamil 49-58 ATP binding cassette subfamily B member 1 Homo sapiens 112-126 1967551-0 1990 Binding of an optically pure photoaffinity analogue of verapamil, LU-49888, to P-glycoprotein from multidrug-resistant human leukemic cell lines. Verapamil 55-64 ATP binding cassette subfamily B member 1 Homo sapiens 79-93 1967551-1 1990 Verapamil enhances anticancer drug cytotoxicity in multidrug resistant (MDR) cells, apparently by competing with these agents for binding to P-glycoprotein (Pgp). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 141-155 1967551-1 1990 Verapamil enhances anticancer drug cytotoxicity in multidrug resistant (MDR) cells, apparently by competing with these agents for binding to P-glycoprotein (Pgp). Verapamil 0-9 ATP binding cassette subfamily B member 1 Homo sapiens 157-160 1967551-3 1990 We studied the binding of an optically pure photoaffinity analogue of verapamil, (S)-5-[(3-azidophenylethyl)-[N-methyl-3H]- methylamino]-2-(3,4,5-trimethoxyphenyl)-2-isopropylvaleronitrile (LU-49888), to Pgp from MDR cell lines. Verapamil 70-79 ATP binding cassette subfamily B member 1 Homo sapiens 204-207 1967551-7 1990 Modulators of Pgp-MDR also compete with LU-49888 for binding to Pgp: verapamil (82%), diltiazem (73%), quinidine (91%), reserpine (91%), rescinnamine (88%), and trimethoxybenzoylyohimbine (89%). Verapamil 69-78 ATP binding cassette subfamily B member 1 Homo sapiens 14-17 1967551-7 1990 Modulators of Pgp-MDR also compete with LU-49888 for binding to Pgp: verapamil (82%), diltiazem (73%), quinidine (91%), reserpine (91%), rescinnamine (88%), and trimethoxybenzoylyohimbine (89%). Verapamil 69-78 ATP binding cassette subfamily B member 1 Homo sapiens 64-67 1967551-10 1990 Our results demonstrate that the verapamil analogue LU-49888 specifically binds to Pgp and suggest that verapamil and some MDR modulators exert their effects by interacting with Pgp. Verapamil 33-42 ATP binding cassette subfamily B member 1 Homo sapiens 83-86 1967551-10 1990 Our results demonstrate that the verapamil analogue LU-49888 specifically binds to Pgp and suggest that verapamil and some MDR modulators exert their effects by interacting with Pgp. Verapamil 33-42 ATP binding cassette subfamily B member 1 Homo sapiens 178-181 1967551-10 1990 Our results demonstrate that the verapamil analogue LU-49888 specifically binds to Pgp and suggest that verapamil and some MDR modulators exert their effects by interacting with Pgp. Verapamil 104-113 ATP binding cassette subfamily B member 1 Homo sapiens 83-86 1967551-10 1990 Our results demonstrate that the verapamil analogue LU-49888 specifically binds to Pgp and suggest that verapamil and some MDR modulators exert their effects by interacting with Pgp. Verapamil 104-113 ATP binding cassette subfamily B member 1 Homo sapiens 178-181 2232849-6 1990 The leukemic blasts expressed very high levels of a 180 kd p-glycoprotein associated with multidrug resistance and daunomycin efflux could be blocked by verapamil. Verapamil 153-162 ATP binding cassette subfamily B member 1 Homo sapiens 59-73 1983720-3 1990 Anti-cancer drug sensitivity is restored by addition of other drugs (i.e., verapamil, reserpine) which are also P-glycoprotein substrates. Verapamil 75-84 ATP binding cassette subfamily B member 1 Homo sapiens 112-126