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1 etic-neuralgia patient abruptly discontinued pregabalin.
2 randomly assigned: 117 to placebo and 116 to pregabalin.
3 ain processing may respond to agents such as pregabalin.
4 te to precursors for GABA analogues, such as pregabalin.
5 cium-independent) dye release are reduced by pregabalin.
6                                     However, pregabalin 1 was active in the DBA/2 model after oral (a
7 0 mg/day of pregabalin (-9.2), 600 mg/day of pregabalin (-10.3), and lorazepam (-12.0) were significa
8 y disorder were randomly assigned to receive pregabalin (150 mg/day or 600 mg/day), lorazepam (6 mg/d
9 received daily treatment, 182 with 300 mg of pregabalin, 178 with 0.25 mg of pramipexole, 180 with 0.
10  point compared with placebo (-8.4 +/- 0.8): pregabalin, 300 mg (-12.2 +/- 0.8, P<.001), 450 mg (-11.
11 were randomized to 4 weeks of treatment with pregabalin, 300 mg/d (n = 91), 450 mg/d (n = 90), or 600
12 tine (nine of 14 studies); 7.7 (6.5-9.4) for pregabalin; 7.2 (5.9-9.21) for gabapentin, including gab
13 ven placebo (73%, N=50 of 69), 600 mg/day of pregabalin (71%, N=50 of 70), or 150 mg/day or pregabali
14 le score in the patients given 150 mg/day of pregabalin (-9.2), 600 mg/day of pregabalin (-10.3), and
15 egabalin (71%, N=50 of 70), or 150 mg/day or pregabalin (90%, N=62 of 69).
16 y adds to our understanding of the action of pregabalin, a drug used for treatment of partial seizure
17 igned to evaluate the efficacy and safety of pregabalin, a novel alpha(2)-delta ligand, for treatment
18 -5-phosphonopentanoic acid], suggesting that pregabalin action depends on NMDA receptor activation.
19               The central acting gabapentoid pregabalin affords a modest 12% pain reduction in patien
20 reating fibromyalgia, compared with placebo, pregabalin alone is associated with a small increase in
21 potent neuropathic analgesics gabapentin and pregabalin (alpha2delta-1 and alpha2delta-2), were also
22                                              Pregabalin, an alpha(2)delta-1/-2 ligand, and an alpha(2
23                                  A series of pregabalin analogues were prepared and evaluated for the
24 nderwent randomization, of whom 108 received pregabalin and 101 received placebo; after randomization
25                                              Pregabalin and alprazolam produced a significantly great
26  peripheral edema and burning sensation with pregabalin and capsaicin.
27 cing pain, and newly developed ones, such as pregabalin and duloxetine, while specifically marketed f
28 he most frequent adverse events reported for pregabalin and lorazepam were somnolence and dizziness.
29 he primary analyses involved a comparison of pregabalin and placebo over a period of 12 weeks with us
30                                     Doses of pregabalin and placebo were increased over 4 weeks.
31 d a comparison of rates of augmentation with pregabalin and pramipexole over a period of 40 or 52 wee
32 of the alpha-2-delta ligands (gabapentin and pregabalin) and the norepinephrine/serotonin reuptake in
33 serotonin-noradrenaline reuptake inhibitors, pregabalin, and gabapentin; a weak recommendation for us
34 us adverse events reported by patients given pregabalin, and no withdrawal syndrome was associated wi
35 vior, and could be rescued by the analgesic, pregabalin, and the libido-enhancing drugs, apomorphine
36                                        Acute pregabalin application reversibly dilated pressurized ar
37 ralgia compared with placebo, gabapentin and pregabalin are associated with a modest increase in the
38 tine and milnacipran--and the anticonvulsant pregabalin are encouraging.
39 in that all four manufacturing steps to make pregabalin are performed in water.
40                               Gabapentin and pregabalin are structurally related compounds with recog
41                                       In the pregabalin arm, 45 patients (38.8%) achieved the primary
42 (P = .009 and P = .007, comparing respective pregabalin arms to the placebo arm).
43 cities were significantly more common in the pregabalin arms, being more evident with the higher dose
44 get 75 mg twice daily and 150 mg twice daily pregabalin arms, respectively (P = .009 and P = .007, co
45 ovides support and a mechanism of action for pregabalin as a possible effective therapy in the treatm
46 n in patients with RLS who were treated with pregabalin as compared with placebo and pramipexole.
47                                              Pregabalin at 300 and 450 mg/day was associated with sig
48                                              Pregabalin at 450 mg/day improved several domains of hea
49                                              Pregabalin at 450 mg/day significantly reduced the avera
50                                              Pregabalin at 450 mg/day was efficacious for the treatme
51 nts were randomly assigned to receive either pregabalin at a dose of 150 mg per day that was adjusted
52 signed to receive 52 weeks of treatment with pregabalin at a dose of 300 mg per day or pramipexole at
53 -delta Type 1 substantially reduces specific pregabalin binding in CNS regions that are known to pref
54                              In mutant mice, pregabalin binding was robust throughout regions where t
55             In vitro studies have shown that pregabalin binds with high affinity to the alpha(2)-delt
56  three-step synthesis of the medicinal agent pregabalin (commercialized by Pfizer under the trade nam
57 the basis of preliminary promising data that pregabalin decreased hot flashes.
58                                              Pregabalin decreases hot flashes and is reasonably well
59                               Treatment with pregabalin did not significantly reduce the intensity of
60                     In short-term treatment, pregabalin does not appear to have the withdrawal sympto
61             However, the mechanisms by which pregabalin exerts its therapeutic effects are not yet co
62                                              Pregabalin exhibits robust activity in preclinical assay
63                          Prolonged (24-hour) pregabalin exposure did not alter total alpha(2)delta-1
64 l of 227 adverse events were reported in the pregabalin group and 124 in the placebo group.
65 sted leg-pain intensity score was 3.4 in the pregabalin group and 3.0 in the placebo group (adjusted
66 sted leg-pain intensity score was 3.7 in the pregabalin group and 3.1 in the placebo group (adjusted
67             Dizziness was more common in the pregabalin group than in the placebo group.
68 verse events was significantly higher in the pregabalin group than in the placebo group.
69        Of the 5 treatment groups, the 300-mg pregabalin group was the only medication group that diff
70 cebo; after randomization, 2 patients in the pregabalin group were determined to be ineligible and we
71 observation-carried-forward end point, the 3 pregabalin groups and the alprazolam group had significa
72 ntly (P<.02) improved by the 300- and 600-mg pregabalin groups, but not by the 450-mg pregabalin (wee
73                               Zonisamide and pregabalin have recently obtained licences as adjuvant t
74                                  The role of pregabalin in CIBP with a clinical neuropathic pain comp
75 um channels is the major binding protein for pregabalin in CNS.
76      Our findings do not support the role of pregabalin in patients with CIBP receiving radiotherapy.
77         The aim of this study was to examine pregabalin in patients with CIBP receiving radiotherapy.
78 d, double-blind, placebo-controlled trial of pregabalin in patients with sciatica.
79 atically reduces alpha(2)-delta 1 binding to pregabalin in vitro.
80             Acute systemic administration of pregabalin in vivo also selectively prevented the migrat
81 ral nervous system (CNS) binding protein for pregabalin in vivo, a mutant mouse with an arginine-to-a
82 ) mice, the acute systemic administration of pregabalin increased the threshold for SD initiation in
83 nstriction ("myogenic tone"), and attenuated pregabalin-induced vasodilation.
84                       At the cellular level, pregabalin inhibited glutamatergic synaptic transmission
85                                              Pregabalin inhibits release of excess excitatory neurotr
86                                              Pregabalin is a synthetic amino acid compound effective
87                  These results indicate that pregabalin is an effective, rapidly acting, and safe tre
88  the intraocular pressure-lowering effect of pregabalin is dependent on the Cacna2d1 haplotype.
89                                              Pregabalin is effective in the treatment of some types o
90                                The effect of pregabalin is not apparent in the presence of an N-methy
91 antiepileptic drugs (topiramate, lacosamide, pregabalin, levetiracetam), hypothermia, magnesium, pyri
92                                              Pregabalin (Lyrica(R)) is produced using a lipase based
93                            The antiepileptic pregabalin (Lyrica) shows clinical promise for migraine
94                                 Morphine and pregabalin markedly alleviated pressure hyperalgesia, wh
95                                              Pregabalin may be an effective alternative.
96 r, laboratory and clinical work suggest that pregabalin may be useful in treating CIBP.
97                  This study examined whether pregabalin may reduce the intensity of sciatica.
98 lds up to 74%, including the important drugs pregabalin, memantine, and the antimalarial artemisinin.
99                               The effects of pregabalin on dye release are masked in the presence of
100                       Finally, the action of pregabalin on dye release is most apparent before and ea
101 acebo with those of 150, 300, and 450 mg/day pregabalin on pain, sleep, fatigue, and health-related q
102           The authors examine the effects of pregabalin on presynaptic function of cultured hippocamp
103  [1-(aminomethyl)cyclohexaneacetic acid] and pregabalin (PGB) [(S)-(+)-3-isobutyl-GABA or (S)-3-(amin
104         The therapeutic drugs gabapentin and pregabalin (PGB), which are both alpha(2)delta ligands,
105         Asymmetric hydrogenation of CI-1008 (pregabalin) precursors, 39 and 40, provided good enantio
106                                              Pregabalin provided significantly improved treatment out
107                      The study revealed that pregabalin reduces the readily releasable pool of synapt
108             Previous studies have shown that pregabalin reduces the release of neurotransmitters in s
109                                              Pregabalin [S-[+]-3-isobutylGABA or (S)-3-(aminomethyl)-
110                          Additionally, while pregabalin significantly reduced deep dorsal horn evoked
111          As early as the week 1 observation, pregabalin significantly reduced the total Hamilton anxi
112 e CaV2.1 (P/Q-type) calcium channel subunit, pregabalin slowed the speed of SD propagation in vivo.
113  by 4.5 points, among participants receiving pregabalin than among those receiving placebo (P<0.001),
114 entation rates were significantly lower with pregabalin than with 0.5 mg of pramipexole.
115 roved or much improved was also greater with pregabalin than with placebo (71.4% vs. 46.8%, P<0.001).
116  40 or 52 weeks was significantly lower with pregabalin than with pramipexole at a dose of 0.5 mg (2.
117 the development of a new synthetic route for pregabalin that proceeds with an overall yield of 74%.
118  of suicidal ideation in the group receiving pregabalin, three in the group receiving 0.25 mg of pram
119                  Furthermore, the ability of pregabalin to alleviate mechanical hypersensitivity is l
120 FM4-64 to determine details of the action of pregabalin to reduce neurotransmitter release.
121 week 6 between the 150 mg twice daily target pregabalin treatment and placebo.
122 tings of pain intensity, between each of the pregabalin treatment groups and the placebo group.
123                    Our results indicate that pregabalin treatment, at concentrations that are therape
124 d no withdrawal syndrome was associated with pregabalin treatment.
125 ondary hot flash efficacy end points between pregabalin treatments and placebo.
126 ulticenter, double-blind randomized trial of pregabalin versus placebo was conducted.
127 ms, being more evident with the higher dose, pregabalin was generally well tolerated by most patients
128                                              Pregabalin was significantly more efficacious than place
129       In a controlled trial, the novel agent pregabalin was studied for the treatment of patients wit
130                                              Pregabalin was well tolerated and improved global measur
131 -mg pregabalin groups, but not by the 450-mg pregabalin (week 1, P = .06; week 4, P = .32) and the al
132 oembolic stroke patients, whereas gabapentin/pregabalin were favored in subarachnoid hemorrhage, intr
133 ocular pressure and a promising therapeutic, pregabalin, which binds to CACNA2D1 protein and lowers i
134            The interaction of gabapentin and pregabalin with conventional antiepileptic and analgesic

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