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1 ned largely unchanged in those randomized to canagliflozin.
2 the majority of amputations were observed on canagliflozin.
3 lozin, with 5% for empagliflozin, and 1% for canagliflozin.
4 ted by the synthesis of the SGLT2 inhibitor, canagliflozin.
5 lied to the synthesis of the alpha-anomer of canagliflozin.
6 umin-to-creatinine ratio decreased more with canagliflozin 100 mg (31.7%; 95% CI, 8.6% to 48.9%; P=0.
7 ed at least one dose of glimepiride (n=482), canagliflozin 100 mg (n=483), or canagliflozin 300 mg (n
9 the glimepiride group versus 24 (5%) in the canagliflozin 100 mg group and 26 (5%) in the 300 mg gro
10 tive voice or web response system to receive canagliflozin 100 mg or 300 mg, or glimepiride (up-titra
13 n and randomly assigned to either once-daily canagliflozin 100 mg, canagliflozin 300 mg, or glimepiri
15 In 666 T2DM patients randomized to receive canagliflozin 100 or 300 mg or placebo, the study assess
17 ted by the synthesis of the SGLT2 inhibitor, canagliflozin (1a), from commercially available 10 in on
18 mg (31.7%; 95% CI, 8.6% to 48.9%; P=0.01) or canagliflozin 300 mg (49.3%; 95% CI, 31.9% to 62.2%; P<0
21 eiving glimepiride, canagliflozin 100 mg, or canagliflozin 300 mg had reductions in HbA1c of 0.81%, 0
22 fference -0.01% [95% CI -0.11 to 0.09]), and canagliflozin 300 mg was superior to glimepiride (-0.12%
23 d to either once-daily canagliflozin 100 mg, canagliflozin 300 mg, or glimepiride uptitrated to 6-8 m
29 nergy calculations and inhibition assays for canagliflozin, an antidiabetic agent verified its effect
32 ence in median percent change between pooled canagliflozin and placebo were -15.0%, -16.1%, and -26.8
33 s for these transporters (eg, dapagliflozin, canagliflozin, and empagliflozin) can slow the rate of i
34 pecific inhibitors, including dapagliflozin, canagliflozin, and empagliflozin, increase glucose excre
35 including empagliflozin, dapagliflozin, and canagliflozin, are now widely approved antihyperglycemic
37 ypertension and diabetes, aliskiren-based or canagliflozin-based drug design against HIV-1 PR may eli
40 hort, the primary end point was reduced with canagliflozin compared with placebo (26.9 versus 31.5/10
46 dium-glucose cotransporter 2 inhibition with canagliflozin decreases HbA1c, body weight, BP, and albu
48 und of the 95% CI for the difference of each canagliflozin dose versus glimepiride of less than 0.0%.
50 , urinary tract infections (31 [6%] for both canagliflozin doses vs 22 [5%]), and osmotic diuresis-re
51 he previously reported risks associated with canagliflozin except for an increased risk of amputation
54 ardiovascular disease, patients treated with canagliflozin had a lower risk of cardiovascular events
55 orter-2 (SGLT2) inhibitors empagliflozin and canagliflozin have been shown to lower cardiovascular mo
60 years in patients with type 2 diabetes, and canagliflozin may confer renoprotective effects independ
61 of this study was to examine the effects of canagliflozin on cardiovascular biomarkers in older pati
63 each trial were randomly assigned to receive canagliflozin or placebo and were followed for a mean of
67 oteins (DeltaG(pred) = -9.1 kcal mol(-1) for canagliflozin-renin; K(i,exp)= 628 nM for canagliflozin-
68 e rate of the primary outcome was lower with canagliflozin than with placebo (occurring in 26.9 vs. 3
69 ta suggest a potential additional benefit of canagliflozin therapy compared with other SGLT2 inhibito
70 ctin-3 modestly increased from baseline with canagliflozin versus placebo, with significant differenc
71 nt, the results showed a possible benefit of canagliflozin with respect to the progression of albumin
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