ライフサイエンスコーパス: beta-CIT

1 Iodine-123-beta-CIT has been used as a probe of dopamine transporte

2 Iodine-123-beta-CIT has been used as a probe of monoamine transport

3 puted tomography and the radioligand [(I)123]beta-CIT ([(I)123]methyl 3beta-(4-iodophenyl) tropane-2-

4 oses, such as Parkinson's disease with (123I)beta-CIT single photon emission computed tomography, and

5 d transmission scans after injection of 123I-beta-CIT.

6 emission 123I scans after injection of 123I-beta-CIT.

7 thoxy-3beta-(4-123I-iodophenyl)tropane (123I-beta-CIT); nine healthy human control subjects who under

8 disease, the Parkinson Study Group used 123I-beta-CIT SPECT.

9 y ratios, as is commonly performed with 123I-beta-CIT, these outcome measures showed only small diffe

10 /- 13.2 yr; H&Y Stage I-II) with both [123I] beta CIT-FP and [18F]FDOPA.

11 We compared [123I] beta CIT-FP/SPECT and [18F]FDOPA/PET in the assessment o

12 1,25] = 52.1 and 53.0, p < 0.0001 for [123I] beta CIT-FP and [18F]FDOPA, respectively).

13 es (r = -0.69 and -0.60, p < 0.04 for [123I] beta CIT-FP and [18F]FDOPA, respectively).

14 These results indicate that [123I] beta CIT-FP/SPECT can provide quantitative descriptors o

15 ine in striatal uptake was noted with [123I] beta CIT-FP (r = -0.56, p < 0.04) but not with [18F]FDOP

16 [123I] beta-CIT and single photon emission computed tomography

17 lunteers was measured with the use of [123I] beta-CIT and single photon emission computed tomography,

18 med at either 0-7 hr or 18-24 hr after [123I]beta-CIT injection permits calculation of reliable and r

19 I]beta-CIT-FP and a faster washout for [123I]beta-CIT-FE (14.7% +/- 6.9%).

20 [123I]beta-CIT-FP and 7.7 +/- 0.7 for [123I]beta-CIT-FE, showing high in vivo selectivity for the do

21 midbrain activity was 9.1 +/- 1.8 for [123I]beta-CIT-FP and 7.7 +/- 0.7 for [123I]beta-CIT-FE, showi

22 30 min, with little or no washout for [123I]beta-CIT-FP and a faster washout for [123I]beta-CIT-FE (

23 ited to the most commonly used ligand, [123I]beta-CIT, stratification by affection status dramaticall

24 4 hr postinjection of 370 MBq (10 mCi) [123I]beta-CIT.

25 ures obtained after bolus injection of [123I]beta-CIT 0-7 hr (Day 1) and 18-24 hr (Day 2) after admin

26 assumptions about the reversibility of [123I]beta-CIT in striatum.

27 ng performed at 24 hr postinjection of [123I]beta-CIT permits calculation of reliable and reproducibl

28 participated in two kinetic studies of [123I]beta-CIT uptake.

29 post injection of 360 MBq (9.7 mCi) of [123I]beta-CIT.

30 tients the mean percent decline in the [123I]beta-CIT uptake was significantly greater with levodopa

31 omethoxy-3beta-(4-iodophenyl) tropane ([123I]beta-CIT) for measurement of central SERT availability.

32 ymethoxy-3-beta-(4-iodophenyl)tropane ([123I]beta-CIT) uptake.

33 ymethoxy-3 beta-(4-iodophenyl)tropane ([123I]beta-CIT), were used to determine DA transporter density

34 en; aged 19-74 yr) participated in two [123I]beta-CIT SPECT scans separated by 7-14 days.

35 y control subjects participated in two [123I]beta-CIT SPECT scans separated by 7-21 days.

36 and supports the feasibility of using [123I]beta-CIT in serial evaluation of human neuropsychiatric

37 and supports the feasibility of using [123I]beta-CIT in the evaluation of disease progression in Par

38 FP and another four were injected with [123I]beta-CIT-FE.

39 controls obtained after injection of [123I])beta-CIT in part to assess the utility of this tracer fo

40 Both [123I]-FPCIT and [123I]-beta-CIT demonstrated decreased striatal uptake in Parki

41 e of the present study was to compare [123I]-beta-CIT with [123I]-FPCIT in a within-subject design.

42 ls with a mean of V"3=3.5 and 6.7 for [123I]-beta-CIT (Parkinson's disease and controls, respectively

43 For [123I]-beta-CIT, the mean Parkinson's disease values represente

44 were higher for [123I]-FPCIT than for [123I]-beta-CIT.

45 t 24 hr postinjection 222 MBq (6 mCi) [123I]-beta-CIT and serially from 1-6 hr postinjection 333 MBq

46 fluoropropyl (FP)CIT is an analog of [123I]-beta-CIT and has been shown to achieve peak tracer uptak

47 control subjects participated in one [123I]-beta-CIT and one [123I]-FPCIT SPECT scan separated by 7-

48 riatal tissue 15-20 times faster than [123I]-beta-CIT, and estimates of dopamine transporter loss in

49 uctions in striatal uptake similar to [123I]-beta-CIT.

50 healthy volunteers were injected with [123I]-beta-CIT-FP and another four were injected with [123I]be

51 ompeting dopamine transporter binding agent, beta-CIT (RTI-55, 2 beta-carbomethoxy-3 beta-(4-iodophen

52 finities for serotonin or the cocaine analog beta-CIT.

53 l and fluoroethyl compounds (beta-CIT-FP and beta-CIT-FE, respectively), characterized by faster kine

54 s a significant negative correlation between beta-CIT binding to serotonin transporters in the brains

55 instem serotonin transporters as measured by beta-CIT binding.

56 the fluoropropyl and fluoroethyl compounds (beta-CIT-FP and beta-CIT-FE, respectively), characterize

57 propyl ester analog (1) of beta-CIT exceeded beta-CIT (2, an N-methyl-2 beta-carbomethoxy ester) in D

58 ymethoxy-3 bet-(4'-iodophenyl)nortropane (FP-beta-CIT, 5) support their use as improved markers for D

59 Animals with greater beta-CIT binding and low CSF 5-HIAA concentrations displ

60 -chloropropyl (4) > or = N-bromopropyl (3) > beta-CIT (2) > N-3'-phtalimidopropyl (11), with particul

61 A total of 101 (123)I-beta-CIT SPECT scans were obtained of subjects recruited

62 healthy comparison subjects by using [(123)I]beta-CIT and single photon emission computed tomography.

63 Striatal [(123)I]beta-CIT binding did not differ significantly between th

64 maging showed a decline in mean (SD) [(123)I]beta-CIT striatal uptake from baseline of 10.3% (9.8%) a

65 es in striatal, putamen, and caudate [(123)I]beta-CIT uptake after 22 and 34 months were also assesse

66 age change from baseline in striatal [(123)I]beta-CIT uptake after 46 months.

67 ean (SD) percentage loss in striatal [(123)I]beta-CIT uptake from baseline was significantly reduced

68 ntage loss from baseline in striatal [(123)I]beta-CIT uptake was correlated with the change from base

69 ated a reduction in loss of striatal [(123)I]beta-CIT uptake, a marker of dopamine neuron degeneratio

70 methoxy-3beta-(4-iodophenyl)tropane ([(123)I]beta-CIT) were used to assess dopamine transporter avail

71 on emission computed tomography with [(123)I]beta-CIT.

72 mpared to only 3.o-fold 5-HTT selectivity in beta-CIT itself.

73 expressing these mutants, but it inactivated beta-CIT binding in membrane preparations.

74 MTSET inactivated beta-CIT binding to I172C and Y176C, but only slightly i

75 ropyl)-2 beta- isopropyl ester analog (1) of beta-CIT exceeded beta-CIT (2, an N-methyl-2 beta-carbom

76 N-Substituted analogs of beta-CIT with a 2 beta-carbomethoxy ester moiety showed

77 arbomethoxy(iodophenyl)nortropane analogs of beta-CIT with the N-substituents difluoroethyl, mesoxypr

78 Two N-omega-fluoroalkyl analogs of beta-CIT, the fluoropropyl and fluoroethyl compounds (be

79 stabilised SERT mutants bound [(125)I]RTI55 (beta-CIT) with affinity similar to that of the wild-type

80 Several N-haloalkyl-substituted beta-CIT analogs yielded high 5-HTT affinity (Ki < 0.6 n

81 ester moiety showed lower DAT affinity than beta-CIT for the DAT, and some were more selective for t

82 ll yielded > 10-fold lower DAT affinity than beta-CIT itself, whereas the N-(fluoropropyl)-2 beta- is

83 ta-carbomethoxy-3beta-(4-iodophenyl)tropane (beta-CIT) for measurement of striatal DAT protein availa

84 bomethoxy-3beta-(4-[125I]iodophenyl)tropane (beta-CIT) in intact cells expressing these mutants, but

85 a-carbomethoxy-3 beta-(4-iodophenyl)tropane (beta-CIT) is a useful SPECT tracer for imaging the dopam

86 bomethoxy-3beta-(4-[125I]iodophenyl)tropane (beta-CIT).

87 -carbomethoxy-3 beta-(4'-iodophenyl)tropane (beta-CIT, 2) analogs and their neuropharmacological eval