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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 e comparison of each canagliflozin dose with glimepiride.
4 and after administration of the sulfonylurea glimepiride.
5 polipoprotein A-I (r = -0.20, p = 0.01) with glimepiride.
6 on of coronary atherosclerosis compared with glimepiride.
7  hypoglycaemia, and blood pressure than does glimepiride.
8 all thickness compared with the sulfonylurea glimepiride.
9 one slowed progression of CIMT compared with glimepiride.
10 as not released from cells by treatment with glimepiride.
11 ed progression of maximum CIMT compared with glimepiride (0.002 mm vs 0.026 mm, respectively, at 72 w
12 n of mean CIMT was less with pioglitazone vs glimepiride (-0.001 mm vs +0.012 mm, respectively; diffe
13 ]), and canagliflozin 300 mg was superior to glimepiride (-0.12% [-0.22 to -0.02]).
14   Pioglitazone hydrochloride (15-45 mg/d) or glimepiride (1-4 mg/d) as an active comparator.
15 th 50 mg to -0.65% [0.114] with 6.25 mg) and glimepiride (-1.05% [SE 0.111]) groups versus placebo (-
16 trasonography and were randomized to receive glimepiride, 1 to 4 mg, or pioglitazone, 15 to 45 mg, fo
17 , TAK-875 (6.25, 25, 50, 100, or 200 mg), or glimepiride (4 mg) once daily for 12 weeks.
18 bo and, on a separate occasion, ingestion of glimepiride (4.0 mg) at 0 min (with glucose infused to p
19 lutide (1.2 mg [n=251] or 1.8 mg [n=247]) or glimepiride 8 mg (n=248) for 52 weeks.
20 ucose tolerance after a mixed meal and after glimepiride administration in the absence of a differenc
21 agon concentrations declined similarly after glimepiride administration.
22 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
23 ncreased 0.73% (95% CI, 0.33% to 1.12%) with glimepiride and decreased 0.16% (95% CI, -0.57% to 0.25%
24 n provides greater HbA1c reduction than does glimepiride, and is well tolerated in patients with type
25 abetes compounds tolbutamide, glibenclamide, glimepiride, and nateglinide and identified glibenclamid
26 change in CIMT was less with pioglitazone vs glimepiride at all time points (weeks 24, 48, 72).
27 ne and 0.36% (95% CI, -0.48% to -0.24%) with glimepiride (between-group P = .03).
28                                              Glimepiride, canagliflozin 100 mg, and canagliflozin 300
29                           Patients receiving glimepiride, canagliflozin 100 mg, or canagliflozin 300
30 , HbA(1c) decreased by 0.51% (SD 1.20%) with glimepiride, compared with 0.84% (1.23%) with liraglutid
31 ry disease were treated with pioglitazone or glimepiride for 18 months in the PERISCOPE (Pioglitazone
32           Mice were treated with linagliptin/glimepiride for 7 weeks.
33 pproach is demonstrated by the extraction of glimepiride from a water sample, followed by LC-MS analy
34                                              Glimepiride (Glim) is a new sulfonylurea reported to aff
35 nificantly higher rates were reported in the glimepiride group (19% [n=12]; p value range 0.010-0.002
36 groups (48%, n=29) and was lower than in the glimepiride group (61%, n=38).
37          Hypoglycemia was more common in the glimepiride group and edema, fractures, and decreased he
38 ent because of vomiting, whereas none in the glimepiride group did so.
39 ) patients had serious adverse events in the glimepiride group versus 24 (5%) in the canagliflozin 10
40 liflozin 100 mg and 300 mg groups versus the glimepiride group, we recorded a greater number of genit
41     In the pioglitazone group, compared with glimepiride, high-density lipoprotein levels increased 5
42 y of canagliflozin, an SGLT2 inhibitor, with glimepiride in patients with type 2 diabetes inadequatel
43 ioglitazone slowed progression compared with glimepiride in this population.
44 albiglutide, placebo, or active comparators (glimepiride, insulin glargine, insulin lispro, liragluti
45 ks, canagliflozin 100 mg was non-inferior to glimepiride (least-squares mean difference -0.01% [95% C
46 mised patients received at least one dose of glimepiride (n=482), canagliflozin 100 mg (n=483), or ca
47 gned to TAK-875 (n=303), placebo (n=61), and glimepiride (n=62).
48 difference of each canagliflozin dose versus glimepiride of less than 0.0%.
49 creased with pioglitazone and increased with glimepiride (P < .001).
50                                Compared with glimepiride, pioglitazone has been shown to slow the pro
51  in type 2 diabetic and normal mice, whereas glimepiride proved efficacious against stroke in normal
52 smooth muscle types), whereas glibenclamide, glimepiride, repaglinide, and meglitinide block both typ
53 canagliflozin 100 or 300 mg/d, compared with glimepiride, slowed the progression of renal disease ove
54 eactive protein between the pioglitazone and glimepiride treatment groups.
55 o receive canagliflozin 100 mg or 300 mg, or glimepiride (up-titrated to 6 mg or 8 mg per day) orally
56 nagliflozin 100 mg, canagliflozin 300 mg, or glimepiride uptitrated to 6-8 mg.
57 gulation, a comparison with the sulfonylurea glimepiride was done.

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