ライフサイエンスコーパス: brimonidine

1 ecurrence of inflammation after cessation of brimonidine.

2 reater efficacy than concomitant timolol and brimonidine.

3 cular hypertensive retinas was attenuated by brimonidine.

4 ries after application of nitroglycerine and brimonidine.

5 e common with BBFC than with brinzolamide or brimonidine.

6 % with brinzolamide, and 20.6% to 31.3% with brimonidine.

7 one of three arms: placebo, somatostatin, or brimonidine.

8 They were treated with brimonidine 0.15% for 8 weeks and designated for retesti

9 BFC (n = 193), brinzolamide 1% (n = 192), or brimonidine 0.2% (n = 175) BID.

10 results and large number of drop-outs in the brimonidine 0.2% arm suggest that more research is neces

11 Brinzolamide 1% and brimonidine 0.2% fixed combination administered BID had

12 While randomization to brimonidine 0.2% was protective compared to timolol 0.5%

13 ed to topical treatment with timolol 0.5% or brimonidine 0.2%.

14 and brimonidine, 0.2%; brinzolamide, 1%; or brimonidine, 0.2%) 1 drop 3 times daily for 3 months.

15 and brimonidine, 0.2%; brinzolamide, 1%; or brimonidine, 0.2%, 3 times daily for 3 months.

16 e fixed combination of brinzolamide, 1%, and brimonidine, 0.2%, can safely and effectively lower IOP

17 t fixed combination of brinzolamide, 1%, and brimonidine, 0.2%.

18 ion (fixed-combination brinzolamide, 1%, and brimonidine, 0.2%; brinzolamide, 1%; or brimonidine, 0.2

19 with fixed-combination brinzolamide, 1%, and brimonidine, 0.2%; brinzolamide, 1%; or brimonidine, 0.2

20 Patients were treated with 10 g of brimonidine, 0.33%, gel applied under occlusion for hemo

21 Topical brimonidine, 0.33%, gel can result in systemic central n

22 Topical brimonidine, 0.33%, gel has been reported for the use of

23 he risk of systemic toxic effects of topical brimonidine, 0.33%, gel when used for hemostasis.

24 Rats were treated intraperitoneally with brimonidine (1 mg/kg) or phosphate-buffered saline (PBS)

25 Next, brimonidine (100 ug/kg, IP) was administered either one

26 After the 8-week course with brimonidine, 14 of the 17 patients who completed the stu

27 brimonidine, 22.9%; brinzolamide, 18.6%; and brimonidine, 17.3%; P = .31), most of which were ocular.

28 eatment-related adverse effect (brinzolamide-brimonidine, 22.9%; brinzolamide, 18.6%; and brimonidine

29 0.19 mmHg; brinzolamide, 25.9 +/- 0.20 mmHg; brimonidine, 26.0 +/- 0.19 mmHg).

30 .37 (2.94; 5.83), timolol 3.70 (3.16; 4.24), brimonidine 3.59 (2.89; 4.29), carteolol 3.44 (2.42; 4.4

31 by the antiglaucoma drugs dipivefrine (72%), brimonidine (70%), and carbachol (78%).

32 Brimonidine, a selective alpha(2)-adrenoceptor agonist,

33 Brimonidine administration initiated 10 days after IOP e

34 Anterior uveitis secondary to topical brimonidine administration is rare and not well-defined.

35 nd CBSM cells indicates the possibility that brimonidine affects uveoscleral outflow.

36 -lowering effect than either brinzolamide or brimonidine alone and displayed a safety profile consist

37 the present study, we examined the effect of brimonidine (alpha(2)-adrenoceptor agonist) on RGC survi

38 tifunctional peptide (HR97) is conjugated to brimonidine, an intraocular pressure lowering drug that

39 Other alpha(2)-adrenoceptor agonists, brimonidine and apraclonidine, acted in a similar way to

40 2+ mobilization in the Pe in response to the brimonidine and carbachol combination was either blocked

41 The suppressive action of brimonidine and medetomidine was completely blocked by c

42 ion of synaptic transmission at IPL and that brimonidine and other alpha2 agonists may protect RGCs u

43 lso suppressed in a dose-dependent manner by brimonidine and other alpha2 receptor agonists, such as

44 up (P < 0.001) but remained unchanged in the brimonidine and somatostatin groups.

45 administration of two neuroprotective drugs (brimonidine and somatostatin) could prevent or arrest re

46 initial drug of choice, but latanoprost and brimonidine are now being recommended by many as alterna

47 However, latanoprost and brimonidine are often given as monotherapy as well as ea

48 he beneficial effect of randomization to the brimonidine arm was independent of possible differences

49 , therefore, urge against the use of topical brimonidine as a hemostatic agent until its safety is fu

50 patients (26 eyes) with consultant diagnosed brimonidine-associated anterior uveitis in a tertiary re

51 ted using poly(lactic acid) (PLA) to release brimonidine at a constant rate for 35 days and microneed

52 There is high-quality evidence that topical brimonidine, azelaic acid, and ivermectin, as well as or

53 Brimonidine, but not timolol, showed significant protect

54 not possible to define a quantity with which brimonidine can be used safely, nor can a safe wound siz

55 rostone concomitant therapy, and timolol and brimonidine concomitant therapy.

56 Concomitant latanoprost and brimonidine demonstrated better efficacy than the dorzol

57 icantly affect tissue permeability at either brimonidine dose.

58 t of rabbits receiving twice daily, standard brimonidine drops.

59 erase (PDE4) inhibitor, indicating that this brimonidine effect is mediated by the alpha2 receptor th

60 carbachol, the alpha 2-adrenoceptor agonist brimonidine elicited large Ca2+ increases (> 10-fold) in

61 ministration of a glaucoma medication (i.e., brimonidine) formulated for sustained release in the sup

62 In vitro release of brimonidine from the GMS drops and gel properties were q

63 IOP reduction in rabbits receiving a single brimonidine GMS drop was comparable to that of rabbits r

64 t 3 months, the mean IOP of the brinzolamide-brimonidine group (16.3-19.8 mm Hg) was significantly lo

65 e group (19.3-20.9 mm Hg; P </= .002) or the brimonidine group (17.9-22.5 mm Hg; P < .001) across all

66 nt study was that patients randomized to the brimonidine group were statistically less likely to have

67 This indicates that brimonidine has a neuroprotective activity unrelated to

68 alpha2 Agonists, such as brimonidine, have been shown to protect retinal ganglion

69 onidine was introduced for this use in 1966, brimonidine in 1974, and apraclonidine in 1978.

70 The transport of [3H]-brimonidine in bovine RPE-choroid explants was evaluated

71 A carrier-mediated transport process for brimonidine in RPE was demonstrated in bovine RPE-choroi

72 l ganglion cells by alpha2 agonists, such as brimonidine, in animal models of glaucoma and retinal is

73 Brimonidine increased C by 0.005 +/- 0.0005 muL/min/mm H

74 Brimonidine increased pro-MMP-9 an average of 116% +/- 3

75 determine how the alpha2-adrenergic agonist brimonidine influences loss of Thy1 promoter activation.

76 g effect increases ~17-fold compared to free brimonidine injection.

77 The transport of brimonidine into (choroid-to-retina transport [inward])

78 gnificant role in modulating the movement of brimonidine into and out of the eye.

79 Currently, brimonidine is classified as a category B medication wit

80 file and risk of systemic toxic effects when brimonidine is used topically for hemostasis is unknown.

81 A single brimonidine-loaded GMS drop was administered to 5 normot

82 t time, that the highly-targeted delivery of brimonidine-loaded microspheres into the supraciliary sp

83 To test this hypothesis, brimonidine-loaded microspheres were formulated using po

84 fference: -1.4 mmHg; P < 0.0001; t test) and brimonidine (LS mean difference: -1.5 mmHg; P < 0.0001).

85 ce, 0.035; 95% CI, 0.008-0.061; P = .02) and brimonidine (mean difference, -0.015; 95% CI, -0.082 to

86 l progressed faster than those randomized to brimonidine (mean rates of progression, -0.38 +/- 0.9 vs

87 ctivity compared with either brinzolamide or brimonidine monotherapy while providing a safety profile

88 here were 449 eligible patients allocated to brimonidine (n = 152), somatostatin (n = 145), or placeb

89 The brimonidine neuroprotective effect was abolished by an a

90 In glaucoma patients using brimonidine, one must consider this phenomenon to avoid

91 Brimonidine or NMDA receptor blockers protected RGCs in

92 cant changes in elevated IOP was found after brimonidine or PBS treatment when compared with the nont

93 e did not find any neuroprotective effect of brimonidine or somatostatin.

94 Systemic administration of brimonidine or timolol caused little decrease in IOP.

95 Systemic application of brimonidine or timolol had little effect on IOP.

96 Brimonidine or timolol was administered, either at the t

97 he control with elevated IOP but without any brimonidine/PBS treatment.

98 Brimonidine pretreatment also significantly reduced NMDA

99 dence suggests that alpha2 agonists, such as brimonidine, protect retinal ganglion cells (RGCs) from

100 This brimonidine protection is also enhanced significantly by

101 Brimonidine protects RGCs in the rabbit excitotoxicity m

102 Brimonidine reduced the progressive loss of ganglion cel

103 ed with progression whereas randomization to brimonidine revealed a protective effect (HR = 0.26, 95%

104 Brimonidine significantly improved impaired retinal vasc

105 Brimonidine significantly protected RGCs from elevated I

106 Pretreatment with brimonidine significantly reduced NMDA-elicited currents

107 ratories Inc., Fort Worth, TX], brinzolamide/brimonidine [Simbrinza; Alcon Laboratories Inc.], and la

108 Rate analysis showed that brimonidine slowed the initial rate of fluorescent cell

109 5 different human donors received control or brimonidine tartrate (45 nM) for 1, 3, or 7 days.

110 rochloride, apraclonidine hydrochloride, and brimonidine tartrate constitute the three topical alpha

111 eight healthy subjects was treated with 0.2% brimonidine tartrate ophthalmic solution to induce pupil

112 ophthalmic medication bottles were included: brimonidine tartrate, dorzolamide-timolol, latanoprost,

113 e advantages, but triple-therapy dorzolamide/brimonidine/timolol (dorz/brim/tim) is only available in

114 Both inward and outward brimonidine transport decreased at 5 microM compared wit

115 amount of cell death gradually increased in brimonidine-treated animals.

116 stimulus intensity was compared between the brimonidine-treated, miotic eye and the untreated eye.

117 Time between initiation of brimonidine treatment and presentation was 1 week to 49

118 one brimonidine treatment, and 55+/-6% after brimonidine treatment every other day (P<0.05 for both b

119 Almost all RGCs were protected following brimonidine treatment for 3 weeks both in groups A and B

120 e treatment every other day (P<0.05 for both brimonidine treatment groups compared to the control gro

121 BRIMONIDINE TREATMENT PRODUCED SIGNIFICANT REDUCTION IN

122 Brimonidine treatment was stopped immediately.

123 baseline in control mice, 51+/-6% after one brimonidine treatment, and 55+/-6% after brimonidine tre

124 always be considered in glaucoma patients on brimonidine treatment.

125 RGCs, these findings indicate that repeated brimonidine treatments may protect RGC health following

126 Repeated brimonidine treatments protect against loss of fluoresce

127 neurons in the group that received repeated brimonidine treatments was greater than the control grou

128 cts on the fellow untreated eye, compared to brimonidine twice-daily eye drops.

129 NPE, 10 microM acetylcholine (ACh), 1 microM brimonidine (UK 14304), or 1 microM epinephrine each eli

130 laucoma patients not previously treated with brimonidine underwent retinal vascular autoregulation te

131 l (representing choroid-to-retina transport) brimonidine uptake in ARPE-19 cells showed temperature d

132 Basolateral brimonidine uptake increased by 35% at extracellular pH

133 This suppressive action of brimonidine was blocked by alpha2 antagonists, cAMP anal

134 The uptake of [3H]brimonidine was evaluated in differentiated ARPE-19 cell

135 This suppressive effect of brimonidine was substantially enhanced by background add

136 y lower with brinzolamide than with BBFC and brimonidine, whereas blurred vision and ocular discomfor