PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 31305009-11 2019 A combination of cyclosporine A with DNR prolonged survival of NSG mice inoculated with P-gp-positive t(17;19)-ALL cell line. Cyclosporine 17-31 phosphoglycolate phosphatase Mus musculus 88-92 33676539-8 2021 METHODS: In our study, hAPP mice were treated with vehicle, nocodazole (NCZ, microtubule inhibitor to block P-gp internalization), or a combination of NCZ and the P-gp inhibitor cyclosporin A (CSA). Cyclosporine 178-191 phosphoglycolate phosphatase Mus musculus 163-167 30679998-11 2019 However, the protective effects of Nrf2 overexpression on PQ-challenged A549 cells were abrogated following cyclosporine A treatment, a competitive inhibitor of P-gp, which also increased intracellular PQ levels. Cyclosporine 108-122 phosphoglycolate phosphatase Mus musculus 161-165 28707509-9 2018 The P-gp inhibitors cyclosporine significantly enhanced Pallidifloside D absorption in all four intestinal segments (duodenum, jejunum, ileum and colon) and the fold change ranged from 5.5 to 15.3. Cyclosporine 20-32 phosphoglycolate phosphatase Mus musculus 4-8 29986516-8 2018 P-glycoprotein inhibitors cyclosporine A and verapamil fail to restore JC-1 loading of the R and T cells to an extent similar to that observed in S cells. Cyclosporine 26-40 phosphoglycolate phosphatase Mus musculus 0-14 24980806-8 2014 The net efflux ratio of GA (C15:1) and GA (C17:1) in both cell models was greater than 2 and markedly reduced by the presence of Cyclosporin A (CsA) or GF120918, inhibitors of P-gp and BCRP, suggesting that GAs are P-gp and BCRP substrates. Cyclosporine 144-147 phosphoglycolate phosphatase Mus musculus 176-180 26324318-6 2015 These cytokines and LPS can induce P-gp expression through the STAT3/Nf-kappab pathway, contributing to a decrease of cyclosporine A retention, which can be reversed by the application of a P-gp inhibitor. Cyclosporine 118-132 phosphoglycolate phosphatase Mus musculus 35-39 26324318-6 2015 These cytokines and LPS can induce P-gp expression through the STAT3/Nf-kappab pathway, contributing to a decrease of cyclosporine A retention, which can be reversed by the application of a P-gp inhibitor. Cyclosporine 118-132 phosphoglycolate phosphatase Mus musculus 190-194 25264342-8 2015 These results indicated that P-gp strictly limited the intestinal absorption of aliskiren in mice and monkeys, and also that the effects of intestinal P-gp inhibition by CsA or zosuquidar on the pharmacokinetics of aliskiren were sensitively reproduced in monkeys. Cyclosporine 170-173 phosphoglycolate phosphatase Mus musculus 151-155 26324318-5 2015 The results revealed reduced retention of cyclosporine A in PMBC over-expressing P-gp in a TNBS-treated group and enhanced secretion of the cytokines IL-1beta, IL-6, IL-17, and TNF-alpha as well as LPS in plasma. Cyclosporine 42-56 phosphoglycolate phosphatase Mus musculus 81-85 24980806-8 2014 The net efflux ratio of GA (C15:1) and GA (C17:1) in both cell models was greater than 2 and markedly reduced by the presence of Cyclosporin A (CsA) or GF120918, inhibitors of P-gp and BCRP, suggesting that GAs are P-gp and BCRP substrates. Cyclosporine 144-147 phosphoglycolate phosphatase Mus musculus 215-219 20460505-5 2010 Pretreatment with topical cyclosporin A (CsA), verapamil, or XR9576, modulators of P-glycoprotein (P-gp), prevented Ing3A-induced hemorrhage but not neutrophil infiltration. Cyclosporine 26-39 phosphoglycolate phosphatase Mus musculus 83-97 24492412-8 2014 On day 7 of DSS treatment, the concentrations of cyclosporine A (CsA), a substrate of both CYP3A and P-gp, were significantly higher than controls. Cyclosporine 65-68 phosphoglycolate phosphatase Mus musculus 101-105 24492412-9 2014 These results indicated the existence of a second inflammatory response in the liver and upper small intestine of mice with DSS-induced colitis, and bioavailability of CsA was increased by the dysfunction of CYP3A and P-gp in these organs. Cyclosporine 168-171 phosphoglycolate phosphatase Mus musculus 218-222 24011632-5 2013 RESULTS: The result showed that RE of gefitinib at the concentrations of 1 muM and 10 muM was 4.12 and 4.05, respectively, but significantly decreased to 1 and 1.35 after adding a P-glycoprotein (P-gp) inhibitor, cyclosporine A. Cyclosporine 213-227 phosphoglycolate phosphatase Mus musculus 180-194 24280122-3 2014 The aim of the current study was to investigate if similar effects occur with another P-gp inhibitor, cyclosporin A (CsA). Cyclosporine 117-120 phosphoglycolate phosphatase Mus musculus 86-90 24280122-5 2014 P-gp inhibition by CsA enhanced the brain distribution of escitalopram by 70-80%. Cyclosporine 19-22 phosphoglycolate phosphatase Mus musculus 0-4 23285492-10 2004 Similar results were obtained with the WT rodents when they were intravenously infused with rhodamine-123 in the presence of cyclosporine A, an inhibitor of P-gp (6). Cyclosporine 125-139 phosphoglycolate phosphatase Mus musculus 157-161 22644589-10 2012 However, CsA treatment increased (18)F-MPPF free fraction, which is responsible for a misleading, P-gp unrelated enhanced brain uptake. Cyclosporine 9-12 phosphoglycolate phosphatase Mus musculus 98-102 22768295-7 2012 In wild-type mice, the co-administration of cyclosporin A, a known P-gp inhibitor, resulted in a 6-fold increase in the accumulation of quinacrine in the brain. Cyclosporine 44-57 phosphoglycolate phosphatase Mus musculus 67-71 20460505-5 2010 Pretreatment with topical cyclosporin A (CsA), verapamil, or XR9576, modulators of P-glycoprotein (P-gp), prevented Ing3A-induced hemorrhage but not neutrophil infiltration. Cyclosporine 26-39 phosphoglycolate phosphatase Mus musculus 99-103 20460505-5 2010 Pretreatment with topical cyclosporin A (CsA), verapamil, or XR9576, modulators of P-glycoprotein (P-gp), prevented Ing3A-induced hemorrhage but not neutrophil infiltration. Cyclosporine 41-44 phosphoglycolate phosphatase Mus musculus 83-97 20460505-5 2010 Pretreatment with topical cyclosporin A (CsA), verapamil, or XR9576, modulators of P-glycoprotein (P-gp), prevented Ing3A-induced hemorrhage but not neutrophil infiltration. Cyclosporine 41-44 phosphoglycolate phosphatase Mus musculus 99-103 15638123-4 2004 To detect the activity of Pgp, verapamil (Ver) or cyclosporine A (CsA) has to be used as Pgp inhibitors. Cyclosporine 50-64 phosphoglycolate phosphatase Mus musculus 89-92 20447559-6 2010 RESULTS: Modulation of P-gp with CsA (50 mg/kg) as well as mdr1a gene depletion resulted in significant increase in cerebral uptake of [(123)I]-FMIP with only minor effect on blood activity. Cyclosporine 33-36 phosphoglycolate phosphatase Mus musculus 23-27 17204702-3 2007 METHODS: Modulation of 8 radioligands by P-gp was assayed in mice by evaluating the effect of treatment with cyclosporine A (CsA) on uptake into the brain (assay 1) and the effect of treatment with a cold ligand of the corresponding radioligand on uptake of (11)C-verapamil, a representative radioligand for P-gp (assay 2). Cyclosporine 109-123 phosphoglycolate phosphatase Mus musculus 41-45 17204702-3 2007 METHODS: Modulation of 8 radioligands by P-gp was assayed in mice by evaluating the effect of treatment with cyclosporine A (CsA) on uptake into the brain (assay 1) and the effect of treatment with a cold ligand of the corresponding radioligand on uptake of (11)C-verapamil, a representative radioligand for P-gp (assay 2). Cyclosporine 125-128 phosphoglycolate phosphatase Mus musculus 41-45 16939683-0 2006 Site-dependent contributions of P-glycoprotein and CYP3A to cyclosporin A absorption, and effect of dexamethasone in small intestine of mice. Cyclosporine 60-73 phosphoglycolate phosphatase Mus musculus 32-46 16939683-1 2006 We examined whether the oral bioavailability of cyclosporin A is controlled primarily by P-glycoprotein (P-gp) or CYP3A in the small intestine. Cyclosporine 48-61 phosphoglycolate phosphatase Mus musculus 89-103 16939683-1 2006 We examined whether the oral bioavailability of cyclosporin A is controlled primarily by P-glycoprotein (P-gp) or CYP3A in the small intestine. Cyclosporine 48-61 phosphoglycolate phosphatase Mus musculus 105-109 16939683-8 2006 These results suggest that, under physiological conditions, the oral bioavailability of cyclosporin A is mainly controlled by CYP3A in the upper intestine, rather than liver, but when P-gp is induced by steroid, the intestinal absorption of cyclosporin A may be inhibited. Cyclosporine 88-101 phosphoglycolate phosphatase Mus musculus 184-188 16939683-8 2006 These results suggest that, under physiological conditions, the oral bioavailability of cyclosporin A is mainly controlled by CYP3A in the upper intestine, rather than liver, but when P-gp is induced by steroid, the intestinal absorption of cyclosporin A may be inhibited. Cyclosporine 241-254 phosphoglycolate phosphatase Mus musculus 184-188 20230790-4 2010 In vitro, the P-gp antagonist PSC833, a non-calcineurin-inhibitory cyclosporine A analogue, specifically inhibited cellular efflux of the P-gp substrate rhodamine-123 in wild-type CD3(+) T cells and MHC class II(+) APCs but not their P-gp knockout counterparts that lacked rhodamine-123 efflux capacity. Cyclosporine 67-81 phosphoglycolate phosphatase Mus musculus 14-18 20230790-4 2010 In vitro, the P-gp antagonist PSC833, a non-calcineurin-inhibitory cyclosporine A analogue, specifically inhibited cellular efflux of the P-gp substrate rhodamine-123 in wild-type CD3(+) T cells and MHC class II(+) APCs but not their P-gp knockout counterparts that lacked rhodamine-123 efflux capacity. Cyclosporine 67-81 phosphoglycolate phosphatase Mus musculus 138-142 20230790-4 2010 In vitro, the P-gp antagonist PSC833, a non-calcineurin-inhibitory cyclosporine A analogue, specifically inhibited cellular efflux of the P-gp substrate rhodamine-123 in wild-type CD3(+) T cells and MHC class II(+) APCs but not their P-gp knockout counterparts that lacked rhodamine-123 efflux capacity. Cyclosporine 67-81 phosphoglycolate phosphatase Mus musculus 138-142 18445990-5 2008 The uptake of olopatadine in LLC-GA5-COL150 was increased in the same level as that in LLC-PK1 in the presence of cyclosporine A, a P-gp inhibitor. Cyclosporine 114-128 phosphoglycolate phosphatase Mus musculus 132-136 16384676-0 2006 Contributions of intestinal P-glycoprotein and CYP3A to oral bioavailability of cyclosporin A in mice treated with or without dexamethasone. Cyclosporine 80-93 phosphoglycolate phosphatase Mus musculus 28-42 15802827-1 2005 The contribution of P-glycoprotein (P-gp) to the intestinal absorption of cyclosporin A (CsA) was investigated by comparing the in vivo pharmacokinetics of CsA in P-gp knockout mice versus wild-type mice following both oral and intravenous administration and by examining the transport of CsA across Caco-2 cell monolayers. Cyclosporine 89-92 phosphoglycolate phosphatase Mus musculus 20-34 15802827-1 2005 The contribution of P-glycoprotein (P-gp) to the intestinal absorption of cyclosporin A (CsA) was investigated by comparing the in vivo pharmacokinetics of CsA in P-gp knockout mice versus wild-type mice following both oral and intravenous administration and by examining the transport of CsA across Caco-2 cell monolayers. Cyclosporine 156-159 phosphoglycolate phosphatase Mus musculus 163-167 15802827-1 2005 The contribution of P-glycoprotein (P-gp) to the intestinal absorption of cyclosporin A (CsA) was investigated by comparing the in vivo pharmacokinetics of CsA in P-gp knockout mice versus wild-type mice following both oral and intravenous administration and by examining the transport of CsA across Caco-2 cell monolayers. Cyclosporine 156-159 phosphoglycolate phosphatase Mus musculus 163-167 15802827-2 2005 The apparent oral bioavailability of CsA in P-gp knockout mice was 1.55-fold larger than in wild-type mice, leading to an apparent absolute bioavailability of 41.8%. Cyclosporine 37-40 phosphoglycolate phosphatase Mus musculus 44-48 15802827-4 2005 These results suggest that the involvement of P-gp in the intestinal absorption of CsA is not as profound as was previously thought. Cyclosporine 83-86 phosphoglycolate phosphatase Mus musculus 46-50 15638123-4 2004 To detect the activity of Pgp, verapamil (Ver) or cyclosporine A (CsA) has to be used as Pgp inhibitors. Cyclosporine 66-69 phosphoglycolate phosphatase Mus musculus 26-29 15638123-4 2004 To detect the activity of Pgp, verapamil (Ver) or cyclosporine A (CsA) has to be used as Pgp inhibitors. Cyclosporine 66-69 phosphoglycolate phosphatase Mus musculus 89-92 15110893-2 2004 We have investigated whether the Pgp inhibitors cyclosporin A, valspodar (PSC833) and elacridar (GF120918) increase the accumulation of docetaxel in the brain. Cyclosporine 48-61 phosphoglycolate phosphatase Mus musculus 33-36 15110893-5 2004 Cyclosporin A, valspodar and elacridar significantly increased the brain concentrations of docetaxel in wild-type mice to 38%, 56% and 59%, respectively, of those achieved in Pgp knockout mice. Cyclosporine 0-13 phosphoglycolate phosphatase Mus musculus 175-178 12855665-2 2003 We have determined the efficacy of several (putative) inhibitors of Pgp (cyclosporin A, PSC833, GF120918, and Cremophor EL) on the penetration of paclitaxel into the mouse brain. Cyclosporine 73-86 phosphoglycolate phosphatase Mus musculus 68-71 14534356-2 2003 For daunorubicin as a transport substrate, Kapp was independent of [P-gp] for verapamil but increased strictly linearly with [P-gp] for vinblastine, cyclosporin A, and XR9576. Cyclosporine 149-162 phosphoglycolate phosphatase Mus musculus 126-130 15176436-8 2004 In the presence of P-glycoprotein (P-gp) inhibitor, cyclosporine or verapamil, the apical-to-basolateral transport of quinacrine increased. Cyclosporine 52-64 phosphoglycolate phosphatase Mus musculus 19-33 14534356-1 2003 The apparent inhibition constant, Kapp, for the blockade of P-glycoprotein (P-gp) by four drugs, verapamil, cyclosporin A, XR9576 (tariquidar), and vinblastine, was measured by studying their ability to inhibit daunorubicin and calcein-AM efflux from four strains of Ehrlich cells with different levels of drug resistance and P-gp content. Cyclosporine 108-121 phosphoglycolate phosphatase Mus musculus 60-74 14534356-1 2003 The apparent inhibition constant, Kapp, for the blockade of P-glycoprotein (P-gp) by four drugs, verapamil, cyclosporin A, XR9576 (tariquidar), and vinblastine, was measured by studying their ability to inhibit daunorubicin and calcein-AM efflux from four strains of Ehrlich cells with different levels of drug resistance and P-gp content. Cyclosporine 108-121 phosphoglycolate phosphatase Mus musculus 76-80 12003193-7 2002 These studies were performed in the presence or absence of cyclosporin A (CsA), a competitive inhibitor of Pgp. Cyclosporine 74-77 phosphoglycolate phosphatase Mus musculus 107-110 12673668-2 2003 In this study, we aimed to investigate whether cyclosporin A (CsA), a P-gp inhibitor, potentiates EPS induced by DOM. Cyclosporine 62-65 phosphoglycolate phosphatase Mus musculus 70-74 12673668-8 2003 These results suggest that CsA increases the brain distribution of DOM by inhibiting P-gp at the BBB, and potentiates catalepsy by increasing the occupancies of the D(1) and D(2) receptors. Cyclosporine 27-30 phosphoglycolate phosphatase Mus musculus 85-89 12069596-5 2002 Furthermore, the ECARs correlated with the expression level of Pgp in the two different cell lines and were reduced in a concentration-dependent manner by cyclosporin A, a potent inhibitor of the Pgp-ATPase. Cyclosporine 155-168 phosphoglycolate phosphatase Mus musculus 63-66 12069596-5 2002 Furthermore, the ECARs correlated with the expression level of Pgp in the two different cell lines and were reduced in a concentration-dependent manner by cyclosporin A, a potent inhibitor of the Pgp-ATPase. Cyclosporine 155-168 phosphoglycolate phosphatase Mus musculus 196-199 12128165-3 2002 This efflux was concentration dependent and subject to inhibition by the P-gp substrates verapamil and cyclosporin A. Cyclosporine 103-116 phosphoglycolate phosphatase Mus musculus 73-77 12107549-2 2002 METHODS: Three sublines were developed from the sensitive Ehrlich ascites tumour cell line (EHR2) and six sublines from the EHR2/DNR cell line positive for P-glycoprotein (PGP) by treatment with daunorubicin (DNR), a combination of DNR and verapamil (VER), or a combination of DNR and cyclosporin A (CsA). Cyclosporine 285-298 phosphoglycolate phosphatase Mus musculus 172-175 12107549-2 2002 METHODS: Three sublines were developed from the sensitive Ehrlich ascites tumour cell line (EHR2) and six sublines from the EHR2/DNR cell line positive for P-glycoprotein (PGP) by treatment with daunorubicin (DNR), a combination of DNR and verapamil (VER), or a combination of DNR and cyclosporin A (CsA). Cyclosporine 300-303 phosphoglycolate phosphatase Mus musculus 172-175 11880334-9 2002 Exposure of cells from WT mice to the hyperosmotic mannitol solution including the P-gp inhibitor cyclosporin A increased J(H) (at pH(i) 6.30) to an extent similar to that in cells from KO mice exposed to hyperosmotic mannitol alone. Cyclosporine 98-111 phosphoglycolate phosphatase Mus musculus 83-87 11718240-2 2001 ADM ototoxicity may be induced by combination therapy with CsA because extrusion of ADM from the inner ear by p-glycoprotein (p-gp), which acts as an extrusion pump and is expressed on the surface of endothelial cells of capillary blood vessels, might be inhibited by CsA. Cyclosporine 59-62 phosphoglycolate phosphatase Mus musculus 110-124 11739114-4 2002 The hyperosmotic solution in the presence of the P-gp inhibitors (verapamil or cyclosporin A) elicited RVI in the tubules from the WT mice but not from the KO mice. Cyclosporine 79-92 phosphoglycolate phosphatase Mus musculus 49-53 11718240-2 2001 ADM ototoxicity may be induced by combination therapy with CsA because extrusion of ADM from the inner ear by p-glycoprotein (p-gp), which acts as an extrusion pump and is expressed on the surface of endothelial cells of capillary blood vessels, might be inhibited by CsA. Cyclosporine 59-62 phosphoglycolate phosphatase Mus musculus 126-130 11718240-2 2001 ADM ototoxicity may be induced by combination therapy with CsA because extrusion of ADM from the inner ear by p-glycoprotein (p-gp), which acts as an extrusion pump and is expressed on the surface of endothelial cells of capillary blood vessels, might be inhibited by CsA. Cyclosporine 268-271 phosphoglycolate phosphatase Mus musculus 110-124 11718240-2 2001 ADM ototoxicity may be induced by combination therapy with CsA because extrusion of ADM from the inner ear by p-glycoprotein (p-gp), which acts as an extrusion pump and is expressed on the surface of endothelial cells of capillary blood vessels, might be inhibited by CsA. Cyclosporine 268-271 phosphoglycolate phosphatase Mus musculus 126-130 11718240-10 2001 However, ADM ototoxicity was induced by combination therapy with CsA, indicating that CsA has an inhibitory action on p-gp function in the auditory pathway, including the inner ear. Cyclosporine 86-89 phosphoglycolate phosphatase Mus musculus 118-122 11212278-10 2001 This is in contrast to P-gp substrates such as cyclosporin A and verapamil, which lose their activity within 60 min, suggesting that XR9576 is not transported by P-gp. Cyclosporine 47-60 phosphoglycolate phosphatase Mus musculus 23-27 11368976-1 2001 Cyclosporin A (CsA) inhibits the membrane transport protein p-glycoprotein (p-gp) and can enhance the accumulation of vinblastine (VBL) and doxorubicin (Dx) in the inner ear of mice. Cyclosporine 15-18 phosphoglycolate phosphatase Mus musculus 60-74 11368976-1 2001 Cyclosporin A (CsA) inhibits the membrane transport protein p-glycoprotein (p-gp) and can enhance the accumulation of vinblastine (VBL) and doxorubicin (Dx) in the inner ear of mice. Cyclosporine 15-18 phosphoglycolate phosphatase Mus musculus 76-80 11489261-7 2001 In mice treated with MPTP and a P-GP inhibitor (quinidine, trans-flupentixol or cyclosporine A), the elimination of MPP(+) from the striatum was significantly delayed. Cyclosporine 80-94 phosphoglycolate phosphatase Mus musculus 32-36 10661503-6 2000 Furthermore, inhibition of p-gp function by co-administration of cyclosporin A (CsA) with doxorubicin (ADM) in mdr1a(+/+) mice resulted in increased accumulation of ADM in inner ear tissues and hearing impairment similar to that noted in mdr1a(-/-) mice. Cyclosporine 65-78 phosphoglycolate phosphatase Mus musculus 27-31 10661503-6 2000 Furthermore, inhibition of p-gp function by co-administration of cyclosporin A (CsA) with doxorubicin (ADM) in mdr1a(+/+) mice resulted in increased accumulation of ADM in inner ear tissues and hearing impairment similar to that noted in mdr1a(-/-) mice. Cyclosporine 80-83 phosphoglycolate phosphatase Mus musculus 27-31 11741243-9 2000 [3H]-Cyclosporin A uptake by TM-BBB was significantly increased in the presence of 100 micromol/l verapamil and vincristine, suggesting that TM-BBB exhibits efflux transport activity via P-gp. Cyclosporine 5-18 phosphoglycolate phosphatase Mus musculus 187-191 10206323-7 1999 The steady-state uptake of BTL by LLC-GA5-COL300 cells, expressing human P-gp, was significantly increased in the presence of 20 microM cyclosporin A (another P-gp inhibitor), which had no effect in the LLC-PK1 host cells. Cyclosporine 136-149 phosphoglycolate phosphatase Mus musculus 159-163 10220486-4 1999 Intestinal excretion of [3H]IVM and [3H]CSA was enhanced in PGP (+/+) animals. Cyclosporine 40-43 phosphoglycolate phosphatase Mus musculus 60-63 8172879-3 1994 We wished to determine if Ser939/941 is also important for efficient interaction of P-gp with structurally different modulating agents, a cyclic peptide (cyclosporin A, CsA), a diaminoquinazoline (CP100356), and a chiral, tricyclic structure (CP117227). Cyclosporine 154-167 phosphoglycolate phosphatase Mus musculus 84-88 9732409-3 1998 G185 cells, which highly express P-gp, are resistant to saquinavir-mediated cytotoxicity, and co-administration of cyclosporine reversed this resistance. Cyclosporine 115-127 phosphoglycolate phosphatase Mus musculus 33-37 8620476-2 1996 The function of P-gp was analyzed by the accumulation and efflux of rhodamine 123 (Rh123) in the presence or absence of cyclosporin A (CSA) and a non-immunosuppressive analog of CSA (CSA-1). Cyclosporine 120-133 phosphoglycolate phosphatase Mus musculus 16-20 9723952-14 1998 [11C]verapamil accumulation in the brain of mdr1a(+/+) mice was increased by cyclosporin A to levels comparable with those in mdr1a(-/-) mice, indicating that reversal of P-gp mediated efflux can be monitored by PET. Cyclosporine 77-90 phosphoglycolate phosphatase Mus musculus 171-175 9723952-16 1998 We conclude that cyclosporin A can fully block the P-gp function in the blood brain barrier and the testes and that PET enables the in vivo measurement of P-gp function and reversal of its function non-invasively. Cyclosporine 17-30 phosphoglycolate phosphatase Mus musculus 51-55 8949985-3 1996 The sequels were suggestive of CsA- or ivermectin-induced central nervous system dysfunction; they were interpreted as caused by the neutralization of the Pgp at the blood-brain barrier level, implying that CsA and ivermectin were Pgp substrates. Cyclosporine 31-34 phosphoglycolate phosphatase Mus musculus 155-158 8949985-3 1996 The sequels were suggestive of CsA- or ivermectin-induced central nervous system dysfunction; they were interpreted as caused by the neutralization of the Pgp at the blood-brain barrier level, implying that CsA and ivermectin were Pgp substrates. Cyclosporine 31-34 phosphoglycolate phosphatase Mus musculus 231-234 8949985-3 1996 The sequels were suggestive of CsA- or ivermectin-induced central nervous system dysfunction; they were interpreted as caused by the neutralization of the Pgp at the blood-brain barrier level, implying that CsA and ivermectin were Pgp substrates. Cyclosporine 207-210 phosphoglycolate phosphatase Mus musculus 155-158 8949985-4 1996 CsA was already known to display both Pgp substrate and Pgp inhibitor properties. Cyclosporine 0-3 phosphoglycolate phosphatase Mus musculus 38-41 8949985-4 1996 CsA was already known to display both Pgp substrate and Pgp inhibitor properties. Cyclosporine 0-3 phosphoglycolate phosphatase Mus musculus 56-59 8647944-1 1996 The mouse mdr1a (also called mdr3) P-GP is abundant in the blood-brain barrier, and its absence in mdr1a (-/-) mice leads to highly increased levels of the drugs ivermectin, vinblastine, digoxin, and cyclosporin A in the brain. Cyclosporine 200-213 phosphoglycolate phosphatase Mus musculus 35-39 8845485-5 1995 Cyclosporin A (CsA) is a widely used immunosuppressant which has been demonstrated to be a potent inhibitor of Pgp in vitro at concentrations which are clinically achievable. Cyclosporine 15-18 phosphoglycolate phosphatase Mus musculus 111-114 7628053-12 1995 The mechanism responsible for this enhanced toxicity has not yet been elucidated but is likely to be related to an increased tissue retention of Dx due to inhibition of the P-glycoprotein (Pgp) pump by PSC 833, as has recently been proposed for cyclosporin A. Cyclosporine 245-258 phosphoglycolate phosphatase Mus musculus 189-192 8104444-8 1993 In the EMT6 parent line, which expresses very low levels of Pgp, 10-30-fold sensitisation to doxorubicin may be achieved using 0.1-5 microgram/ml of CsA. Cyclosporine 149-152 phosphoglycolate phosphatase Mus musculus 60-63 8169829-1 1994 Cyclosporin A (CsA) inhibits the membrane transport protein Pgp and can thus restore sensitivity to doxorubicin (Dx) and other antineoplastic agents in multidrug resistant cancer cells. Cyclosporine 0-13 phosphoglycolate phosphatase Mus musculus 60-63 8169829-1 1994 Cyclosporin A (CsA) inhibits the membrane transport protein Pgp and can thus restore sensitivity to doxorubicin (Dx) and other antineoplastic agents in multidrug resistant cancer cells. Cyclosporine 15-18 phosphoglycolate phosphatase Mus musculus 60-63 8169829-2 1994 Because Pgp is not expressed only in resistant tumor cells but also in normal tissues, CsA may modify the distribution of a concomitantly given antitumor agent which is a substrate for Pgp-mediated transport. Cyclosporine 87-90 phosphoglycolate phosphatase Mus musculus 8-11 8169829-2 1994 Because Pgp is not expressed only in resistant tumor cells but also in normal tissues, CsA may modify the distribution of a concomitantly given antitumor agent which is a substrate for Pgp-mediated transport. Cyclosporine 87-90 phosphoglycolate phosphatase Mus musculus 185-188 1363723-2 1992 This T-cell proliferative response displays a much higher DOX sensitivity in the presence of novel potent inhibitors of P-glycoprotein (Pgp)-mediated multidrug resistance (MDR), the cyclosporin (Cs) derivative, SDZ PSC 833, and the semi-synthetic cyclopeptolide, SDZ 280-446. Cyclosporine 195-197 phosphoglycolate phosphatase Mus musculus 120-134 1363723-2 1992 This T-cell proliferative response displays a much higher DOX sensitivity in the presence of novel potent inhibitors of P-glycoprotein (Pgp)-mediated multidrug resistance (MDR), the cyclosporin (Cs) derivative, SDZ PSC 833, and the semi-synthetic cyclopeptolide, SDZ 280-446. Cyclosporine 195-197 phosphoglycolate phosphatase Mus musculus 136-139 1363723-6 1992 Our results may open the way to a novel form of immunomodulation combining classical antineoplastic agents with Pgp-blocking Cs analogs (even non-immunosuppressive ones), which may be particularly useful when treating acute graft rejection. Cyclosporine 125-127 phosphoglycolate phosphatase Mus musculus 112-115 35397430-8 2022 However, pretreatment with unlabelled Seltorexant and P-gp competitor CsA observed significantly increased brain uptake of (18F)Seltorexant, indicating (18F)Seltorexant could interact P-gp at the blood-brain barrier. Cyclosporine 70-73 phosphoglycolate phosphatase Mus musculus 54-58 35397430-8 2022 However, pretreatment with unlabelled Seltorexant and P-gp competitor CsA observed significantly increased brain uptake of (18F)Seltorexant, indicating (18F)Seltorexant could interact P-gp at the blood-brain barrier. Cyclosporine 70-73 phosphoglycolate phosphatase Mus musculus 184-188