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1 gnificantly depending on the manufacturer of latanoprost.
2 d further increases after exposure to 200 nM latanoprost.
3 low that occurs after topical treatment with latanoprost.
4 eral outflow facility observed after topical latanoprost.
5  to the effect on the mechanism of action of latanoprost.
6 was noted 2 hours after treatment with 0.01% latanoprost.
7 veoscleral outflow pathway after exposure to latanoprost.
8 not meet the criterion for noninferiority to latanoprost.
9 r ocular hypertension who were intolerant of latanoprost.
10 3753380, rs6672484, rs11578155) responses to latanoprost.
11 for both concentrations of AR-13324 than for latanoprost.
12 and MMP-1, were related to refractoriness to latanoprost.
13 available and others who switched to generic latanoprost.
14 % KL, and 6.6 +/- 0.6 mm Hg (20%) for 0.005% latanoprost.
15 , greater than the effect produced by 0.005% latanoprost.
16            Transitioning from BAK-containing latanoprost 0.005 % to BAK-free travoprost 0.004 % prese
17 r ocular hypertension who were intolerant of latanoprost 0.005 % were transitioned to receive once-da
18 h a permuted block design, to receive either latanoprost 0.005% (intervention group) or placebo (cont
19 324 ophthalmic solution 0.02% daily (pm), or latanoprost 0.005% daily (pm) for 28 days.
20 nts were randomly assigned to treatment with latanoprost 0.005% or placebo.
21 on to treatment with a prostaglandin analog (latanoprost 0.005%) or placebo.
22 orms of bimatoprost (0.01 or 0.1 microg/mL), latanoprost (0.03 or 0.3 microg/mL), or unoprostone (0.1
23 ere treated with a commercial formulation of latanoprost (0.5 mug/mL) for 24 hours before imaging.
24 e as follows: bimatoprost 5.61 (4.94; 6.29), latanoprost 4.85 (4.24; 5.46), travoprost 4.83 (4.12; 5.
25  concentrations of latanoprost compared with latanoprost 50 mug/mL.
26 re -10.13, -9.59, -10.02, and -9.06 mmHg for latanoprost 50, 75, 100, and 125 mug/mL, respectively, a
27 18.6%, 20.8% and 15.9% of subjects receiving latanoprost 50, 75, 100, and 125 mug/mL, respectively.
28 ere randomized to receive an evening dose of latanoprost 50, 75, 100, or 125 mug/mL for 4 weeks.
29 M) > (+/-)-fluprostenol (EC(50) = 10.8 nM) > latanoprost acid (EC(50) = 34.7 nM) > bimatoprost acid (
30 were exposed to increasing concentrations of latanoprost acid (LA, 1 nM to 10 micro M) for 6, 18, and
31  90 and did not vary with 50, 100, or 200 nM latanoprost acid (P = 0.93, ANOVA).
32 (PG)F(2alpha) or to the PGF(2alpha) analogue latanoprost acid alters mRNA for matrix metalloproteinas
33 e cells with the prostaglandin (PG) analogue latanoprost acid alters transcription of mRNA for matrix
34 etermine the neuroprotective properties of a latanoprost acid derivative (ACS67) that donates the gas
35                                  Addition of latanoprost acid for 24 hours increased expression of MM
36                Addition of 8, 40, and 200 nM latanoprost acid for 24 hours increased MMP-1 mRNA in a
37  RNA from ciliary muscle cultures exposed to latanoprost acid for 24 hours revealed increased MMP-1,
38 M cells were treated with vehicle control or latanoprost acid for 24 hours.
39 ultures were treated with vehicle control or latanoprost acid for 24 hours.
40       Analysis of cultures exposed to 200 nM latanoprost acid for 4, 6, 12, or 24 hours revealed an i
41              The addition of PGF(2alpha) and latanoprost acid increased ERK1/2 activity by 117% +/- 1
42                        Exposure of sclera to latanoprost acid increases transscleral permeation by FG
43                              PGF(2alpha) and latanoprost acid induce coordinated alterations of MMP g
44                                              Latanoprost acid induced a dose-dependent increase of MM
45 n organ culture, and exposed to 50 to 200 nM latanoprost acid or vehicle for 3 days.
46 d for 24 hours with medium supplemented with latanoprost acid or vehicle.
47 6 Wilcoxon test) and that exposure to 100 nM latanoprost acid significantly increased mRNA for MMP-9
48 ion of sclera exposed to 50, 100, and 200 nM latanoprost acid was increased by an average of 48% +/-
49 dextran after exposure to 50, 100, or 200 nM latanoprost acid was significantly increased by 42% +/-
50 hours with medium supplemented with PGF(2a), latanoprost acid, or vehicle.
51                         The PGF(2alpha)- and latanoprost-acid-induced ERK1/2 activation was blocked b
52                                The effect of latanoprost after a single 0.01% dose was also measured
53  commonly as the initial drug of choice, but latanoprost and brimonidine are now being recommended by
54                                     However, latanoprost and brimonidine are often given as monothera
55                                  Concomitant latanoprost and brimonidine demonstrated better efficacy
56  MMP-3 and -10 mRNA after exposure to 100 nM latanoprost and further increases after exposure to 200
57 on, controlled on the unfixed combination of latanoprost and timolol or eligible for dual therapy bei
58  as that induced by bimatoprost and acids of latanoprost and travoprost.
59                               Apraclonidine, latanoprost, and pilocarpine had no measurable effect.
60 aqueous humor concentrations of bimatoprost, latanoprost, and their C-1 free acids indicate that lata
61  and vitreous concentrations of bimatoprost, latanoprost, and their C-1 free acids were determined by
62                                 Bimatoprost, latanoprost, and travoprost are among the most efficacio
63  prostaglandin analogues (PGAs) bimatoprost, latanoprost, and unoprostone.
64            Pharmacologic effects of timolol, latanoprost, and Y-39983 were studied in hypertensive mi
65  after treatment, there was no difference in latanoprost- and PBS-treated eyes.
66 n F2 alpha (PGF2 alpha) and analogs, such as latanoprost, are thought to lower intraocular pressure (
67 entrations of 0.0001%, 0.001%, and 0.01% and latanoprost at 0.005% were studied separately, with a mi
68 bruary 2011) and the 18 months after generic latanoprost became available (July 2011-December 2012).
69 ontinued to use brand-name PGAs once generic latanoprost became available and others who switched to
70 ed glaucoma drug use altogether when generic latanoprost became available.
71  all antiglaucoma interventions when generic latanoprost became available.
72                            Patients who used latanoprost binocularly were asked to return bottles to
73      TIMP-2 was unchanged by bimatoprost and latanoprost, but decreased by unoprostone (35% +/- 8%).
74 rost, and their C-1 free acids indicate that latanoprost, but not bimatoprost, is hydrolyzed in the m
75       AR-13324 0.02% was less effective than latanoprost by approximately 1 mmHg in patients with unm
76                        Sustained delivery of latanoprost by contact lenses is at least as effective a
77 terations in the aqueous dynamics induced by latanoprost can be measured reproducibly in the mouse an
78 th latanoprost have given no indication that latanoprost causes clinical CME.
79 favoring any of the higher concentrations of latanoprost compared with latanoprost 50 mug/mL.
80 sessed vision preservation in patients given latanoprost compared with those given placebo.
81                                              Latanoprost concentration in residual solution was analy
82                              The mean +/- SD latanoprost concentration measured in the residual solut
83                             No difference in latanoprost concentrations was found between the bottles
84                              Bimatoprost and latanoprost did not change MMP-2.
85 (2)-induced toxicity to RGC-5 cells, whereas latanoprost did not.
86 r CLLO, 3 weeks without treatment, 5 days of latanoprost drops, 3 weeks without treatment, and 1 week
87                                              Latanoprost-eluting low-dose contact lenses (CLLO) and h
88 derations indicate that the concentration of latanoprost expected in the posterior segment of the eye
89                        Patients treated with latanoprost for open-angle glaucoma or ocular hypertensi
90 r PGF(2alpha), or PhXA85 (the active form of latanoprost) for 1, 2, and 3 days.
91                    Four regionally available latanoprost formulations were measured.
92                           In contrast, 10 nM latanoprost free acid and fluprostenol caused membrane d
93  metabolite M1, trans-unoprostone isopropyl, latanoprost free acid, and fluprostenol were studied on
94 eated for 9 days with 10 microg/mL of either latanoprost (free acid) or prostaglandin F(2alpha) ethan
95                                              Latanoprost-free acid (LFA)-treated NTM cells were analy
96  mm Hg (4.0) in 231 patients assessed in the latanoprost group and 0.9 mm Hg (3.8) in 230 patients as
97 s 19.6 mm Hg (SD 4.6) in 258 patients in the latanoprost group and 20.1 mm Hg (4.8) in 258 controls.
98 preservation was significantly longer in the latanoprost group than in the placebo group: adjusted ha
99  18.7 mmHg in the AR-13324 0.01%, 0.02%, and latanoprost groups, respectively, representing a decreas
100                                              Latanoprost had no effect on IOP in the homozygous FP kn
101 linical trials and experimental studies with latanoprost have given no indication that latanoprost ca
102 cular edema (CME) in eyes being treated with latanoprost have led to concern regarding a possible cau
103  has been associated with a poor response to latanoprost in a healthy Japanese population.
104 ndicate that the early hypotensive effect of latanoprost in the mouse eye is associated with a signif
105  a crucial role in the early IOP response to latanoprost in the mouse eye.
106 ) or increase outflow facility (pilocarpine, latanoprost) in primates and humans lowered steady state
107                                              Latanoprost increased MMP-1 (in four of five cultures),
108                                              Latanoprost increased MMP-3 (in three of five cultures),
109                              Bimatoprost and latanoprost increased MMP-9 activity by 75% +/- 27% and
110           The array results also showed that latanoprost induced dose-dependent increases in the expr
111 ted changes could be expected to mediate the latanoprost-induced alteration of ECM in the ciliary bod
112 r topical treatment with 0.00015% or 0.0025% latanoprost, IOP increased by as much as 11% +/- 7%.
113                                              Latanoprost is a commonly used antiglaucomatous drug, an
114  too low to have a pharmacologic effect, and latanoprost is not known to exhibit vasoactive or inflam
115 oprost (isopropyl ester; EC(50) = 89.1 nM) > latanoprost (isopropyl ester; EC(50) = 778 nM) > bimatop
116 re the ocular hypotensive effects of 15-keto latanoprost (KL) with the commercial preparation of lata
117                              Pilocarpine and latanoprost, known to enhance aqueous humor outflow in h
118                   The reduction of IOP after latanoprost measurement was calculated by the comparison
119  nonrefrigerated storage, and those who used latanoprost monocularly were asked to return used bottle
120 l fixed combination was equal in efficacy to latanoprost monotherapy, timolol and unoprostone concomi
121 demonstrated modest additional efficacy over latanoprost monotherapy.
122 ncreases in TIMP-1 mRNA levels, as seen with latanoprost (n = 5).
123 eral studies have investigated the effect of latanoprost on intraocular pressure (IOP).
124 r of TIMPs may explain the limited effect of latanoprost on TM outflow.
125                    In an eye clinic setting, latanoprost ophthalmic solution 0.005% remains stable af
126  IOP-lowering effect of CLLO, CLHI, or daily latanoprost ophthalmic solution in the same monkeys.
127 CLHI demonstrated greater IOP reduction than latanoprost ophthalmic solution on day 3 (P = 0.001) and
128                                              Latanoprost ophthalmic solution resulted in IOP reductio
129 c solution compared with a positive control, latanoprost ophthalmic solution, in patients with open-a
130 at least as effective as delivery with daily latanoprost ophthalmic solution.
131 tion of 0.00015%, 0.0006%, 0.0025%, or 0.01% latanoprost or vehicle (phosphate-buffered saline [PBS])
132 sed on previous use of any PGA, any non-PGA, latanoprost, or travoprost monotherapies.
133 gnificant in eyes receiving 0.0025% or 0.01% latanoprost (P < 0.05, Student-Newman-Keuls test) and th
134   Compared with persons switching to generic latanoprost, patients who continued taking brand name PG
135 (CLHI) were produced by encapsulating a thin latanoprost-polymer film within the periphery of a metha
136 trations of KL and a 0.005% concentration of latanoprost produced significant (P < 0.05) reductions i
137                                              Latanoprost reduced IOP by increasing C by 0.009 +/- 0.0
138                                 In contrast, latanoprost reduced IOP in the treated eye of the hetero
139 r further determining the mechanism by which latanoprost reduces IOP and alters outflow facility.
140                                              Latanoprost reduces mouse IOP in a dose-dependent manner
141  the PTGFR and MMP-1 genes may determine the latanoprost response in a white European Spanish populat
142  This study identified 5 SNPs related to the latanoprost response; 1 SNP, rs3753380, already has been
143 sis of CARS/TPAF images of hTMC treated with latanoprost revealed multiple intracellular lipid membra
144             Contrary to the expected result, latanoprost seems to have a significant effect on TM cel
145 18 months before the introduction of generic latanoprost (September 2009-February 2011) and the 18 mo
146 cyclobutyl derivative is more efficient than Latanoprost, the most widely used glaucoma drug.
147 ect of bimatoprost and the fixed combination latanoprost-timolol (LTFC) on 24-hour systolic (SBP) and
148                                          The latanoprost-timolol fixed combination is available in ma
149                                          The latanoprost-timolol fixed combination provided greater e
150 te occasions, 2 hours after a 200-ng dose of latanoprost to the right eye of homozygous (n = 9) and h
151                       MMP-9 is present after latanoprost treatment and may also mediate ECM changes.
152  for MMP-1, -3, -17, and -24 is increased by latanoprost treatment.
153                      MMP-9 was present after latanoprost treatment.
154  the genes for MMP-3 and -17 is increased by latanoprost treatment.
155                     Bimatoprost, travoprost, latanoprost, unoprostone isopropyl ester, and their resp
156 ts of a possible association between CME and latanoprost use must be given serious consideration, and
157  those treated with higher concentrations of latanoprost versus those receiving 50 mug/mL.
158           A single 200-ng (4 microL) dose of latanoprost was applied to one eye 2 hours before measur
159     ACS67, its sulfurated moiety (ACS1), and latanoprost were tested for both their toxicity and abil
160                                 All doses of latanoprost were well tolerated.
161 ly used as pharmaceuticals and some, such as latanoprost, which is used to treat glaucoma, have becom
162 ng effects of three higher concentrations of latanoprost with the commercially available concentratio
163 rost (KL) with the commercial preparation of latanoprost (Xalatan; Pfizer, New York, NY) in monkey ey
164 ne [Simbrinza; Alcon Laboratories Inc.], and latanoprost [Xalatan; Pfizer, Inc., New York, NY]).

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