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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
8                                       In the canagliflozin 100 mg and 300 mg groups versus the glimep
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
11           For lowering of HbA1c at 52 weeks, canagliflozin 100 mg was non-inferior to glimepiride (le
12                                 Glimepiride, canagliflozin 100 mg, and canagliflozin 300 mg groups ha
13 n and randomly assigned to either once-daily canagliflozin 100 mg, canagliflozin 300 mg, or glimepiri
14              Patients receiving glimepiride, canagliflozin 100 mg, or canagliflozin 300 mg had reduct
15   In 666 T2DM patients randomized to receive canagliflozin 100 or 300 mg or placebo, the study assess
16                               In conclusion, canagliflozin 100 or 300 mg/d, compared with glimepiride
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
19 de (n=482), canagliflozin 100 mg (n=483), or canagliflozin 300 mg (n=485).
20       Glimepiride, canagliflozin 100 mg, and canagliflozin 300 mg groups had eGFR declines of 3.3 ml/
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
24                       Oral administration of canagliflozin activated AMPK in mouse liver, although no
25                     This study suggests that canagliflozin, aliskiren, and darunavir may induce profo
26                           We now report that canagliflozin also activates AMPK, an effect also seen w
27                                     Although canagliflozin also inhibited cellular glucose uptake ind
28                                              Canagliflozin also inhibited lipid synthesis, an effect
29 nergy calculations and inhibition assays for canagliflozin, an antidiabetic agent verified its effect
30       We compared the efficacy and safety of canagliflozin, an SGLT2 inhibitor, with glimepiride in p
31                Serum sST2 was unchanged with canagliflozin and placebo over 104 weeks.
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
36            These findings support the use of canagliflozin as a viable treatment option for patients
37 ypertension and diabetes, aliskiren-based or canagliflozin-based drug design against HIV-1 PR may eli
38                          The CANVAS Program (Canagliflozin Cardiovascular Assessment Study) randomly
39                            The CANVAS trial (Canagliflozin Cardiovascular Assessment Study) subsequen
40 hort, the primary end point was reduced with canagliflozin compared with placebo (26.9 versus 31.5/10
41                  AMPK activation occurred at canagliflozin concentrations measured in human plasma in
42 y weight, BP, and albuminuria, implying that canagliflozin confers renoprotection.
43                                              Canagliflozin, dapagliflozin, and empagliflozin accounte
44                                              Canagliflozin, dapagliflozin, and empagliflozin, all rec
45                        We determined whether canagliflozin decreases albuminuria and reduces renal fu
46 dium-glucose cotransporter 2 inhibition with canagliflozin decreases HbA1c, body weight, BP, and albu
47        Compared with placebo, treatment with canagliflozin delayed the rise in serum NT-proBNP and hs
48 und of the 95% CI for the difference of each canagliflozin dose versus glimepiride of less than 0.0%.
49 ty margin of 0.3% for the comparison of each canagliflozin dose with glimepiride.
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
52              Because of the disproportionate canagliflozin exposure in the database, the majority of
53 , 0.4 to 1.4), respectively (P<0.01 for each canagliflozin group versus glimepiride).
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
56 or canagliflozin-renin; K(i,exp)= 628 nM for canagliflozin-HIV-1 PR).
57 provide further insights into the effects of canagliflozin in these patient populations.
58                                              Canagliflozin is a sodium glucose cotransporter 2 inhibi
59                                   Background Canagliflozin is a sodium-glucose cotransporter 2 inhibi
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
62      We report the effects of treatment with canagliflozin on cardiovascular, renal, and safety outco
63 each trial were randomly assigned to receive canagliflozin or placebo and were followed for a mean of
64 articipants with type 2 diabetes mellitus to canagliflozin or placebo.
65                                              Canagliflozin provides greater HbA1c reduction than does
66                                              Canagliflozin reduced cardiovascular and renal outcomes
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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