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1  (P<0.01 for each canagliflozin group versus glimepiride).
2 ; 95% CI, 31.9% to 62.2%; P<0.001) than with glimepiride.
3 as not released from cells by treatment with glimepiride.
4 e comparison of each canagliflozin dose with glimepiride.
5 and after administration of the sulfonylurea glimepiride.
6 polipoprotein A-I (r = -0.20, p = 0.01) with glimepiride.
7 4 inhibitor linagliptin and the sulfonylurea glimepiride.
8 on of coronary atherosclerosis compared with glimepiride.
9  hypoglycaemia, and blood pressure than does glimepiride.
10 all thickness compared with the sulfonylurea glimepiride.
11 one slowed progression of CIMT compared with glimepiride.
12 abetic effect (% potency = 218%) compared to glimepiride.
13 ed progression of maximum CIMT compared with glimepiride (0.002 mm vs 0.026 mm, respectively, at 72 w
14 n of mean CIMT was less with pioglitazone vs glimepiride (-0.001 mm vs +0.012 mm, respectively; diffe
15 ]), and canagliflozin 300 mg was superior to glimepiride (-0.12% [-0.22 to -0.02]).
16 emic clamps with coadministration of: 1) SU (glimepiride 1 mg) or placebo, combined with 2) infusions
17   Pioglitazone hydrochloride (15-45 mg/d) or glimepiride (1-4 mg/d) as an active comparator.
18 th 50 mg to -0.65% [0.114] with 6.25 mg) and glimepiride (-1.05% [SE 0.111]) groups versus placebo (-
19 trasonography and were randomized to receive glimepiride, 1 to 4 mg, or pioglitazone, 15 to 45 mg, fo
20 per year for patients receiving sitagliptin; glimepiride, -1.92 (95% CI, -2.08 to -1.75) mL/min/1.73
21  135 (10.6%) patients receiving sitagliptin; glimepiride, 155 (12.4%); liraglutide, 152 (12.0%); and
22 ]), 18 147 started glipizide, 14 282 started glimepiride, 1887 started glyburide, and 13 849 started
23 26.1) were similar and lower than those with glimepiride (30.4) and sitagliptin (38.1).
24 , TAK-875 (6.25, 25, 50, 100, or 200 mg), or glimepiride (4 mg) once daily for 12 weeks.
25 bo and, on a separate occasion, ingestion of glimepiride (4.0 mg) at 0 min (with glucose infused to p
26 95% confidence interval 394 to 480 days) for glimepiride, 764 (741 to not calculable) days for liragl
27 lutide (1.2 mg [n=251] or 1.8 mg [n=247]) or glimepiride 8 mg (n=248) for 52 weeks.
28 ucose tolerance after a mixed meal and after glimepiride administration in the absence of a differenc
29 agon concentrations declined similarly after glimepiride administration.
30 ite sides of and could not exclude the null (glimepiride: aHR(Medicaid) 1.17, 95% CI 0.96-1.42; aHR(O
31 in PAV of 0.64% (95% CI, 0.23% to 1.05%) for glimepiride and a decrease of 0.06% (-0.47% to 0.35%) fo
32 ncreased 0.73% (95% CI, 0.33% to 1.12%) with glimepiride and decreased 0.16% (95% CI, -0.57% to 0.25%
33 t-specific associations with SCA/VA for both glimepiride and glyburide (vs.
34  for glipizide, 1.07 (95% CI, 0.96-1.16) for glimepiride, and 1.04 (95% CI, 0.83-1.24) for glyburide.
35  for glyburide, 8.6% (95% CI, 7.9%-9.2%) for glimepiride, and 9.1% (95% CI, 8.7%-9.7%) for glipizide.
36 n provides greater HbA1c reduction than does glimepiride, and is well tolerated in patients with type
37 abetes compounds tolbutamide, glibenclamide, glimepiride, and nateglinide and identified glibenclamid
38 change in CIMT was less with pioglitazone vs glimepiride at all time points (weeks 24, 48, 72).
39 ne and 0.36% (95% CI, -0.48% to -0.24%) with glimepiride (between-group P = .03).
40                                              Glimepiride, canagliflozin 100 mg, and canagliflozin 300
41                           Patients receiving glimepiride, canagliflozin 100 mg, or canagliflozin 300
42 , HbA(1c) decreased by 0.51% (SD 1.20%) with glimepiride, compared with 0.84% (1.23%) with liraglutid
43 o establish noninferiority of linagliptin vs glimepiride, defined by the upper limit of the 2-sided 9
44                                 In contrast, glimepiride enhanced T2D-induced angiogenesis and increa
45 ry disease were treated with pioglitazone or glimepiride for 18 months in the PERISCOPE (Pioglitazone
46  mice was treated with either linagliptin or glimepiride for 3 months before sacrifice.
47           Mice were treated with linagliptin/glimepiride for 7 weeks.
48 pproach is demonstrated by the extraction of glimepiride from a water sample, followed by LC-MS analy
49                                              Glimepiride (Glim) is a new sulfonylurea reported to aff
50 Initiation of treatment with a sulfonylurea (glimepiride, glipizide, or glyburide) or a DPP4i (refere
51 ng users of second-generation sulfonylureas: glimepiride, glyburide, and glipizide.
52 nificantly higher rates were reported in the glimepiride group (19% [n=12]; p value range 0.010-0.002
53 groups (48%, n=29) and was lower than in the glimepiride group (61%, n=38).
54 he linagliptin group and 1132 (37.7%) in the glimepiride group (HR, 0.23 [95% CI, 0.21-0.26]).
55 gliptin group and 362 of 3010 (12.0%) in the glimepiride group (HR, 0.98 [95.47% CI, 0.84-1.14]; P <
56          Hypoglycemia was more common in the glimepiride group and edema, fractures, and decreased he
57 ent because of vomiting, whereas none in the glimepiride group did so.
58 ) patients had serious adverse events in the glimepiride group versus 24 (5%) in the canagliflozin 10
59 in the linagliptin group vs 16 (0.5%) in the glimepiride group with adjudicated-confirmed acute pancr
60 rgine group, 1.1 (95% CI, 0.9 to 1.4) in the glimepiride group, 0.7 (95% CI, 0.6 to 0.9) in the lirag
61 liflozin 100 mg and 300 mg groups versus the glimepiride group, we recorded a greater number of genit
62 he linagliptin group and 2856 (94.9%) in the glimepiride group, with 15 participants (0.5%) in the li
63 isk of reaching HbA(1c) >=7.0% compared with glimepiride (hazard ratio 0.57, 95% confidence interval
64     In the pioglitazone group, compared with glimepiride, high-density lipoprotein levels increased 5
65 s is demonstrated for the microextraction of glimepiride, imipramine, and carbamazepine.
66 y of canagliflozin, an SGLT2 inhibitor, with glimepiride in patients with type 2 diabetes inadequatel
67 o in the CARMELINA trial, and linagliptin or glimepiride in the CAROLINA trial.
68 ioglitazone slowed progression compared with glimepiride in this population.
69 as rare but significantly more frequent with glimepiride (in 2.2% of the participants) than with glar
70 albiglutide, placebo, or active comparators (glimepiride, insulin glargine, insulin lispro, liragluti
71 ks, canagliflozin 100 mg was non-inferior to glimepiride (least-squares mean difference -0.01% [95% C
72 with 1.9, 1.9, 1.4, and 2.0 in the glargine, glimepiride, liraglutide, and sitagliptin groups, respec
73 nsulin glargine U-100 (hereafter, glargine), glimepiride, liraglutide, and sitagliptin.
74                Addition of insulin glargine, glimepiride, liraglutide, or sitagliptin to metformin, w
75 pants randomly assigned to insulin glargine, glimepiride, liraglutide, or sitagliptin, added to basel
76 mised patients received at least one dose of glimepiride (n=482), canagliflozin 100 mg (n=483), or ca
77 gned to TAK-875 (n=303), placebo (n=61), and glimepiride (n=62).
78 difference of each canagliflozin dose versus glimepiride of less than 0.0%.
79 hazard ratio (HR) of linagliptin relative to glimepiride of less than 1.3.
80 liptin once daily (n = 3023) or 1 to 4 mg of glimepiride once daily (n = 3010) in addition to usual c
81 fective at maintaining glycemic control than glimepiride or sitagliptin when added to metformin monot
82 r risk, the use of linagliptin compared with glimepiride over a median 6.3 years resulted in a noninf
83 creased with pioglitazone and increased with glimepiride (P < .001).
84                                Compared with glimepiride, pioglitazone has been shown to slow the pro
85  in type 2 diabetic and normal mice, whereas glimepiride proved efficacious against stroke in normal
86 6 events occurred in the groups treated with glimepiride (rate ratio, 1.61 [95% CI, 1.13-2.29]) or si
87                     However, linagliptin and glimepiride recovered the BBB integrity and restored the
88                               Interestingly, glimepiride reduced microglial activation, increased mic
89 smooth muscle types), whereas glibenclamide, glimepiride, repaglinide, and meglitinide block both typ
90 canagliflozin 100 or 300 mg/d, compared with glimepiride, slowed the progression of renal disease ove
91 ed cardiovascular outcomes of linagliptin vs glimepiride (sulfonylurea) in patients with relatively e
92  glipizide) and low-affinity (gliclazide and glimepiride) sulfonylureas combined with metformin.
93 ater benefit with glargine, liraglutide, and glimepiride than with sitagliptin.
94 -100 (hereafter, glargine), the sulfonylurea glimepiride, the glucagon-like peptide-1 receptor agonis
95 eactive protein between the pioglitazone and glimepiride treatment groups.
96 o receive canagliflozin 100 mg or 300 mg, or glimepiride (up-titrated to 6 mg or 8 mg per day) orally
97 nagliflozin 100 mg, canagliflozin 300 mg, or glimepiride uptitrated to 6-8 mg.
98 gulation, a comparison with the sulfonylurea glimepiride was done.
99                               Linagliptin or glimepiride were administered daily from 3 days after tM
100 4 inhibitor linagliptin and the sulfonylurea glimepiride, which restore T2D-induced brain vascular pa