ライフサイエンスコーパス: tariquidar

1 h concurrent infusion of the ABCB1 inhibitor tariquidar.

2 g side effects associated with high doses of tariquidar.

3 or HM30181, which is structurally related to tariquidar.

4 lacidar and 3.62 +/- 0.11 muSv/MBq for (11)C-tariquidar.

5 d the use of a lower, more tolerable dose of tariquidar.

6 h concurrent infusion of the ABCB1 inhibitor tariquidar.

7 injection of either (11)C-elacridar or (11)C-tariquidar.

8 h a 3 or 15 mg/kg dose of the P-gp inhibitor tariquidar.

9 essing cells treated with the P-gp inhibitor tariquidar.

10 propoxy}quinoline trihydrochloride (DCPQ) or tariquidar.

11 op at baseline and after increasing doses of tariquidar (2, 4, and 6 mg/kg intravenously).

12 e in brain PET signal was observed for (11)C-tariquidar (+27% +/- 15%, P = 0.014, paired t test) and

13 min after radiotracer injection), unlabeled tariquidar (3 mg/kg) was intravenously administered.

14 or without P-gp inhibition using intravenous tariquidar (8 mg/kg).

15 inking between the NBDs was not inhibited by tariquidar, a drug transport inhibitor that stimulates P

16 ucted in humans, examined 2 P-gp inhibitors (tariquidar, a known inhibitor, and disulfiram, a putativ

17 Lop PET during peak plasma concentrations of tariquidar, achieved with concurrent administration of i

18 more, the structurally dissimilar inhibitor, tariquidar, also increased brain uptake with potency equ

19 LLC-PK1+/-P-gp in the absence or presence of tariquidar, an inhibitor of P-gp.

20 function in humans after increasing doses of tariquidar, an inhibitor of P-gp.

21 In previous work, we found that tariquidar analogues lacking the tetrahydroisoquinoline

22 ir inability to visualize Pgp density, (11)C-tariquidar and (11)C-elacridar may find use as a new cla

23 f the radiolabeled Pgp/BCRP inhibitors (11)C-tariquidar and (11)C-elacridar to assess Pgp density in

24 The in vivo behavior of (11)C-tariquidar and (11)C-elacridar was consistent with that

25 In summary, tariquidar and [(11)C]dLop can be used in combination to

26 Although tariquidar and dLop compete for lysosomal trapping in th

27 t would disrupt hydrophobic interaction with tariquidar and inhibit its ability to rescue processing

28 splayed polarised P-gp transport, since both tariquidar and vinblasine selectively increased the apic

29 The P-gp inhibitors tariquidar and vinblastine prevented the efflux of rhoda

30 In P-gp-expressing cells, tariquidar (and another P-gp inhibitor) surprisingly dec

31 he subjects who received the highest dose of tariquidar (and had the highest brain uptake), regional

32 .8% increase of whole-brain K1 after 2 mg/kg tariquidar, and 57.9% for 3 mg/kg; in patients with phar

33 sfected HEK-293 cells treated with 1 micro M tariquidar, and ABCG2-transfected cells were 6-7-fold re

34 We found that the modulators zosuquidar, tariquidar, and elacridar stimulated the ATPase activity

35 ous tariquidar infusion, injected after oral tariquidar, and injected after disulfiram.

36 (11)C-elacridar and (11)C-tariquidar are new PET tracers to assess the transport a

37 indicate that both (11)C-elacridar and (11)C-tariquidar are safe radiotracers, for which an injected

38 Identification of the tariquidar-binding site has been the subject of intensiv

39 ng studies have identified several potential tariquidar-binding sites.

40 The results suggest that tariquidar binds to a site within the drug-binding pocke

41 e that dLop is trapped in lysosomes and that tariquidar competes with dLop for lysosomal accumulation

42 dLop during tariquidar infusion, when plasma tariquidar concentrations reach their peak, resulted in

43 eased fairly linearly with increasing plasma tariquidar concentrations, but we are uncertain whether

44 aseline K1 and attenuated K1 increases after tariquidar correspond to high P-glycoprotein activity.

45 es, we suspect that plasma concentrations of tariquidar did not fully block P-gp; however, higher dos

46 Tariquidar differed from other drug substrates, however,

47 min infusion of the P-glycoprotein-inhibitor tariquidar followed by another (R)-[(11)C]verapamil PET

48 competition does not occur in brain because tariquidar has negligible entry into brain.

49 Injecting (11)C-dLop after tariquidar infusion also increased brain uptake, though

50 quidar infusion, injected during intravenous tariquidar infusion, injected after oral tariquidar, and

51 p inhibition, injected 1 h after intravenous tariquidar infusion, injected during intravenous tariqui

52 Injecting (11)C-dLop during tariquidar infusion, when plasma tariquidar concentratio

53 d a second scan on the same day, but without tariquidar infusion.

54 or 1 micro M of the P-glycoprotein inhibitor tariquidar inhibited ABCG2-mediated PhA transport.

55 In response to tariquidar injection, a moderate but statistically signi

56 Tariquidar is a unique P-gp inhibitor because it locks t

57 , we show through cross-linking studies that tariquidar most likely binds to sites within the transme

58 T scan of 120-min duration with either (11)C-tariquidar (n = 6) or (11)C-elacridar (n = 5) followed b

59 Neither oral tariquidar nor oral disulfiram increased brain uptake of

60 tudied the effects of a Pgp blocker (XR9576, tariquidar) on FPAC kinetics.

61 lation between distribution volumes of (11)C-tariquidar or (11)C-elacridar and distribution volumes o

62 After injection of (11)C-tariquidar or (11)C-elacridar, the brain PET signal corr

63 plasma up to 60 min after injection of (11)C-tariquidar or (11)C-elacridar.

64 strates (cyclosporine A, FK506), modulators (tariquidar), or small corrector molecules.

65 In contrast, 4 and 6 mg of tariquidar per kilogram increased brain uptake 2- and 4-

66 y slightly (approximately 30%) after 2 mg of tariquidar per kilogram.

67 e was similar with 2 and 4 mg of intravenous tariquidar per kilogram; however, the lower dose was bet

68 measured [(11)C]dLop uptake before and after tariquidar preadministration in lysosome-rich organs of

69 After tariquidar pretreatment in both species, radioactivity u

70 of temporal lobe epilepsy, with and without tariquidar pretreatment.

71 uced at 30 positions significantly inhibited tariquidar rescue of a processing mutant and activation

72 This difference in tariquidar response was most pronounced in the sclerotic

73 ith concurrent administration of intravenous tariquidar, resulted in greater P-gp inhibition at the h

74 Tariquidar significantly enhanced microdose (11)C-metocl

75 d cerebral blood flow did not differ between tariquidar-treated and untreated subjects.

76 Tariquidar treatment also decreased flumazenil transport

77 P-gp inhibition by tariquidar treatment increased brain concentrations of f

78 and kainate-treated rats, and the effect of tariquidar treatment was similar in both rat groups.

79 t fully block P-gp; however, higher doses of tariquidar would likely be associated with unacceptable