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1 n U87MG cells with and without an inhibitor (tariquidar).
2 g side effects associated with high doses of tariquidar.
3 or HM30181, which is structurally related to tariquidar.
4 h concurrent infusion of the ABCB1 inhibitor tariquidar.
5 d the use of a lower, more tolerable dose of tariquidar.
6 lacidar and 3.62 +/- 0.11 muSv/MBq for (11)C-tariquidar.
7 h a 3 or 15 mg/kg dose of the P-gp inhibitor tariquidar.
8 h concurrent infusion of the ABCB1 inhibitor tariquidar.
9 essing cells treated with the P-gp inhibitor tariquidar.
10 propoxy}quinoline trihydrochloride (DCPQ) or tariquidar.
11 injection of either (11)C-elacridar or (11)C-tariquidar.
12 op at baseline and after increasing doses of tariquidar (2, 4, and 6 mg/kg intravenously).
13 e in brain PET signal was observed for (11)C-tariquidar (+27% +/- 15%, P = 0.014, paired t test) and
14  min after radiotracer injection), unlabeled tariquidar (3 mg/kg) was intravenously administered.
15  intravenous infusion of the ABCB1 inhibitor tariquidar (3.75 mg/min, n = 5) or after oral intake of
16 or without P-gp inhibition using intravenous tariquidar (8 mg/kg).
17 inking between the NBDs was not inhibited by tariquidar, a drug transport inhibitor that stimulates P
18 ucted in humans, examined 2 P-gp inhibitors (tariquidar, a known inhibitor, and disulfiram, a putativ
19                                              Tariquidar, a P-gp inhibitor, aggregates at the lower ar
20 Lop PET during peak plasma concentrations of tariquidar, achieved with concurrent administration of i
21                            Results: Although tariquidar administration had no effect on (11)C-erlotin
22 more, the structurally dissimilar inhibitor, tariquidar, also increased brain uptake with potency equ
23 LLC-PK1+/-P-gp in the absence or presence of tariquidar, an inhibitor of P-gp.
24 function in humans after increasing doses of tariquidar, an inhibitor of P-gp.
25              In previous work, we found that tariquidar analogues lacking the tetrahydroisoquinoline
26 ir inability to visualize Pgp density, (11)C-tariquidar and (11)C-elacridar may find use as a new cla
27 f the radiolabeled Pgp/BCRP inhibitors (11)C-tariquidar and (11)C-elacridar to assess Pgp density in
28                The in vivo behavior of (11)C-tariquidar and (11)C-elacridar was consistent with that
29                                  In summary, tariquidar and [(11)C]dLop can be used in combination to
30                                     Although tariquidar and dLop compete for lysosomal trapping in th
31 t would disrupt hydrophobic interaction with tariquidar and inhibit its ability to rescue processing
32 splayed polarised P-gp transport, since both tariquidar and vinblasine selectively increased the apic
33                          The P-gp inhibitors tariquidar and vinblastine prevented the efflux of rhoda
34                    In P-gp-expressing cells, tariquidar (and another P-gp inhibitor) surprisingly dec
35 he subjects who received the highest dose of tariquidar (and had the highest brain uptake), regional
36 ild-type (with Abcb1a/b transport blocked by tariquidar) and Abcb1a/b(-/-) mice.
37 .8% increase of whole-brain K1 after 2 mg/kg tariquidar, and 57.9% for 3 mg/kg; in patients with phar
38 sfected HEK-293 cells treated with 1 micro M tariquidar, and ABCG2-transfected cells were 6-7-fold re
39     We found that the modulators zosuquidar, tariquidar, and elacridar stimulated the ATPase activity
40 ous tariquidar infusion, injected after oral tariquidar, and injected after disulfiram.
41                    (11)C-elacridar and (11)C-tariquidar are new PET tracers to assess the transport a
42 indicate that both (11)C-elacridar and (11)C-tariquidar are safe radiotracers, for which an injected
43                        Identification of the tariquidar-binding site has been the subject of intensiv
44 ng studies have identified several potential tariquidar-binding sites.
45                     The results suggest that tariquidar binds to a site within the drug-binding pocke
46 -like lipid bilayers, in both topotecan- and tariquidar-bound states, characterize the ligand size as
47 e that dLop is trapped in lysosomes and that tariquidar competes with dLop for lysosomal accumulation
48 dLop during tariquidar infusion, when plasma tariquidar concentrations reach their peak, resulted in
49 eased fairly linearly with increasing plasma tariquidar concentrations, but we are uncertain whether
50 aseline K1 and attenuated K1 increases after tariquidar correspond to high P-glycoprotein activity.
51 es, we suspect that plasma concentrations of tariquidar did not fully block P-gp; however, higher dos
52                                              Tariquidar differed from other drug substrates, however,
53 min infusion of the P-glycoprotein-inhibitor tariquidar followed by another (R)-[(11)C]verapamil PET
54  competition does not occur in brain because tariquidar has negligible entry into brain.
55 with a special modulator and slow substrate, tariquidar, in nanodiscs.
56 structures reveal that similar to topotecan, tariquidar induces two distinct ABCG2 conformations unde
57                   Injecting (11)C-dLop after tariquidar infusion also increased brain uptake, though
58 quidar infusion, injected during intravenous tariquidar infusion, injected after oral tariquidar, and
59 p inhibition, injected 1 h after intravenous tariquidar infusion, injected during intravenous tariqui
60                  Injecting (11)C-dLop during tariquidar infusion, when plasma tariquidar concentratio
61 d a second scan on the same day, but without tariquidar infusion.
62 or 1 micro M of the P-glycoprotein inhibitor tariquidar inhibited ABCG2-mediated PhA transport.
63                               In response to tariquidar injection, a moderate but statistically signi
64                                              Tariquidar is a unique P-gp inhibitor because it locks t
65 , we show through cross-linking studies that tariquidar most likely binds to sites within the transme
66 T scan of 120-min duration with either (11)C-tariquidar (n = 6) or (11)C-elacridar (n = 5) followed b
67                                 Neither oral tariquidar nor oral disulfiram increased brain uptake of
68                      In contrast, the larger tariquidar occupies most of the available volume in the
69 tudied the effects of a Pgp blocker (XR9576, tariquidar) on FPAC kinetics.
70 lation between distribution volumes of (11)C-tariquidar or (11)C-elacridar and distribution volumes o
71                     After injection of (11)C-tariquidar or (11)C-elacridar, the brain PET signal corr
72 plasma up to 60 min after injection of (11)C-tariquidar or (11)C-elacridar.
73 strates (cyclosporine A, FK506), modulators (tariquidar), or small corrector molecules.
74                   In contrast, 4 and 6 mg of tariquidar per kilogram increased brain uptake 2- and 4-
75 y slightly (approximately 30%) after 2 mg of tariquidar per kilogram.
76 e was similar with 2 and 4 mg of intravenous tariquidar per kilogram; however, the lower dose was bet
77 measured [(11)C]dLop uptake before and after tariquidar preadministration in lysosome-rich organs of
78                                        After tariquidar pretreatment in both species, radioactivity u
79  of temporal lobe epilepsy, with and without tariquidar pretreatment.
80 uced at 30 positions significantly inhibited tariquidar rescue of a processing mutant and activation
81                           This difference in tariquidar response was most pronounced in the sclerotic
82 ith concurrent administration of intravenous tariquidar, resulted in greater P-gp inhibition at the h
83                                              Tariquidar significantly enhanced microdose (11)C-metocl
84 ribution of the ABCG2/ABCB1 substrate [(11)C]tariquidar to the brain both in wild-type (with Abcb1a/b
85  tested in the presence of a P-gp inhibitor (tariquidar) to assess reversibility of transporter-media
86 d cerebral blood flow did not differ between tariquidar-treated and untreated subjects.
87                                              Tariquidar treatment also decreased flumazenil transport
88                           P-gp inhibition by tariquidar treatment increased brain concentrations of f
89  and kainate-treated rats, and the effect of tariquidar treatment was similar in both rat groups.
90 t fully block P-gp; however, higher doses of tariquidar would likely be associated with unacceptable