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1 arameters, and plasma NO were not altered by empagliflozin.
2 fore and 48 h and 14 days after the start of empagliflozin.
3  after more chronic (14 days) treatment with empagliflozin.
4 or protein expression was also observed with empagliflozin.
5 intra-renal renin activity was enhanced with empagliflozin.
6 ere [16%] and 11 serious [12%]), 86 (88%) on empagliflozin 10 mg (six severe [6%] and six serious [6%
7 k 24 were -0.52% (95% CI -0.72 to -0.32) for empagliflozin 10 mg and -0.68% (-0.88 to -0.49) for empa
8 0) were randomly assigned (1:1:1) to receive empagliflozin 10 mg or 25 mg or placebo once daily for 5
9 stablished cardiovascular disease (1:1:1) to empagliflozin 10 mg, empagliflozin 25 mg, or placebo in
10 (-2) at screening were randomized to receive empagliflozin 10 mg, empagliflozin 25 mg, or placebo onc
11  ratio of relative change from baseline with empagliflozin: -22%, 95% CI -32 to -11; p=0.0003) or mac
12  [8%] and 23 serious [12%]) and 156 (83%) on empagliflozin 25 mg (18 severe [10%] and 22 serious [12%
13 flozin 10 mg and -0.68% (-0.88 to -0.49) for empagliflozin 25 mg (both p<0.0001).
14 e [6%] and six serious [6%]) and 78 (80%) on empagliflozin 25 mg (eight severe [8%] and seven serious
15 c at week 24 was -0.42% (-0.56 to -0.28) for empagliflozin 25 mg (p<0.0001).
16 374) were randomly assigned (1:1) to receive empagliflozin 25 mg or placebo for 52 weeks.
17 dium glucose cotransporter 2 inhibition with empagliflozin 25 mg QD on renal hyperfiltration in subje
18 ular disease (1:1:1) to empagliflozin 10 mg, empagliflozin 25 mg, or placebo in addition to standard
19 e randomized to receive empagliflozin 10 mg, empagliflozin 25 mg, or placebo once daily in addition t
20 le dose, and following 4-week treatment with empagliflozin (25 mg).
21 e (NFG) and eight subjects with IFG received empagliflozin (25 mg/day) for 2 weeks.
22  validated, allowing sensitive estimation of empagliflozin (25-600 ng mL(-1)) in human plasma using d
23                       Compared with vehicle, empagliflozin 30 mg/kg/day for 2 weeks significantly red
24 es in patients with diabetes with the use of empagliflozin, a member of this new class of drugs.
25 ar disease with the antihyperglycemic agent, empagliflozin, a sodium glucose cotransporter 2 (SGLT2)
26                                              Empagliflozin, a sodium-glucose cotransporter 2 inhibito
27               In the EMPA-REG OUTCOME trial, empagliflozin, a sodium-glucose cotransporter 2 inhibito
28            Canagliflozin, dapagliflozin, and empagliflozin accounted for 53%, 42%, and 5% of the tota
29                              In both groups, empagliflozin administration raised EGP, lowered TGD, an
30 considered the pharmacokinetic evaluation of empagliflozin after administration to Egyptian volunteer
31            Canagliflozin, dapagliflozin, and empagliflozin, all recently approved for treatment of ty
32                                Unexpectedly, empagliflozin also reduced intestinal cholesterol absorp
33                               Interestingly, empagliflozin also reduces intestinal cholesterol absorp
34  to determine the long-term renal effects of empagliflozin, an analysis that was a prespecified compo
35                               The effects of empagliflozin, an inhibitor of sodium-glucose cotranspor
36 tration of the novel glucose lowering agent, empagliflozin, an SGLT2 inhibitor which targets the kidn
37 -glucose co-transporter-2 (SGLT2) inhibitors empagliflozin and canagliflozin have been shown to lower
38 transition pairs of m/z 449.01 to 371.21 for empagliflozin and m/z 407.00 to 328.81 for dapagliflozin
39 me was for use of dapagliflozin, with 5% for empagliflozin, and 1% for canagliflozin.
40                   In addition, in the heart, empagliflozin appears to inhibit sodium-hydrogen exchang
41       We assessed the efficacy and safety of empagliflozin as an add-on treatment in patients with ty
42  risk for cardiovascular events who received empagliflozin, as compared with placebo, had a lower rat
43  m(2) of body-surface area to receive either empagliflozin (at a dose of 10 mg or 25 mg) or placebo o
44 the sodium glucose cotransporter 2 inhibitor empagliflozin attenuated renal hyperfiltration in subjec
45   In this model, blood glucose lowering with empagliflozin attenuated some molecular and histological
46 In male db/db mice, a 10-week treatment with empagliflozin attenuated the diabetes-induced upregulati
47                      These data suggest that empagliflozin, by switching energy metabolism from carbo
48 rters (eg, dapagliflozin, canagliflozin, and empagliflozin) can slow the rate of intestinal glucose a
49 cular disease in the EMPA-REG OUTCOME trial (Empagliflozin Cardiovascular Outcome Event Trial in Type
50                                          The Empagliflozin, Cardiovascular Outcomes, and Mortality in
51                   In a landmark trial called Empagliflozin, Cardiovascular Outcomes, and Mortality in
52 inical outcomes, the EMPA-REG OUTCOME trial (Empagliflozin, Cardiovascular Outcomes, and Mortality in
53                 The EMPA-REG OUTCOME trial ([Empagliflozin] Cardiovascular Outcome Event Trial in Typ
54                                              Empagliflozin caused 50 +/- 4 and 45 +/- 4 g glucosuria
55 otransporter-2 (SGLT2) inhibitors, including empagliflozin, dapagliflozin, and canagliflozin, are now
56               Urinary glucose excretion with empagliflozin decreases with declining renal function, r
57                                              Empagliflozin enhanced beta-cell function only in subjec
58 art failure hospitalizations associated with empagliflozin, even though, by design, the hemoglobin A1
59 itiated in 13 of 4687 patients (0.3%) in the empagliflozin group and in 14 of 2333 patients (0.6%) in
60 n 490 of 4687 patients (10.5%) in the pooled empagliflozin group and in 282 of 2333 patients (12.1%)
61 urred in 525 of 4124 patients (12.7%) in the empagliflozin group and in 388 of 2061 (18.8%) in the pl
62 ccurred in 70 of 4645 patients (1.5%) in the empagliflozin group and in 60 of 2323 (2.6%) in the plac
63  myocardial infarction or stroke, but in the empagliflozin group there were significantly lower rates
64 -creatinine ratio (UACR) data for the pooled empagliflozin group versus placebo according to albuminu
65 r nonfatal stroke, as analyzed in the pooled empagliflozin group versus the placebo group.
66 %) in the placebo group (hazard ratio in the empagliflozin group, 0.61; 95% confidence interval, 0.53
67 %) in the placebo group (hazard ratio in the empagliflozin group, 0.86; 95.02% confidence interval, 0
68 epresenting a 55% lower relative risk in the empagliflozin group.
69  260 assigned to placebo and 509 assigned to empagliflozin) had macroalbuminuria.
70 675 assigned to placebo and 1338 assigned to empagliflozin) had microalbuminuria, and 769 (11%; 260 a
71 382 assigned to placebo and 2789 assigned to empagliflozin) had normoalbuminuria, 2013 (29%; 675 assi
72                                              Empagliflozin improved clinical outcomes and reduced mor
73 eath, suggesting that the benefits seen with empagliflozin in a randomized trial may be a class effec
74  The reductions in UACR were maintained with empagliflozin in all three groups compared with placebo
75                   TmG was further reduced by empagliflozin in both groups on day 14 (by 65 +/- 5 and
76  the hyperglycemic clamp was not affected by empagliflozin in either IFG or NFG.
77 ly, none of these parameters were changed by empagliflozin in fed conditions.
78                 The adverse event profile of empagliflozin in patients with eGFR <60 mL.min(-1).1.73
79                 The adverse-event profile of empagliflozin in patients with impaired kidney function
80 -glucose cotransporter-2 inhibitor (SGLT-2i) empagliflozin in patients with type 2 diabetes mellitus
81 ion of renal sodium-glucose cotransport with empagliflozin in subjects with IFG and NFG produces comp
82 n was attenuated by -33 mL/min/1.73m(2) with empagliflozin in T1D-H, (GFR 172+/-23-139+/-25 mL/min/1.
83  including dapagliflozin, canagliflozin, and empagliflozin, increase glucose excretion and lower bloo
84  The mechanisms by which the SGLT2 inhibitor empagliflozin increases LDL cholesterol levels were inve
85            In patients with type 2 diabetes, empagliflozin-induced glycosuria improved beta cell func
86  renal benefit, the antihyperglycaemic drugs empagliflozin, liraglutide, and semaglutide-the latter b
87 he sodium-glucose cotransporter 2 inhibitor, empagliflozin, markedly and rapidly reduced CV death and
88 port the short-term and long-term effects of empagliflozin on albuminuria in patients with type 2 dia
89               We investigated the effects of empagliflozin on clinical outcomes in patients with type
90 sodium-glucose cotransporter inhibition with empagliflozin on the fasting plasma glucose (FPG) concen
91                                   Effects of empagliflozin on these outcomes were consistent across c
92 support short-term and long-term benefits of empagliflozin on urinary albumin excretion, irrespective
93 losclerosis, however, were not improved with empagliflozin or metformin, and plasma and intra-renal r
94 signed patients to receive 10 mg or 25 mg of empagliflozin or placebo once daily.
95 o any significant extent with dapagliflozin, empagliflozin, or phlorizin.
96 EMPA-REG Outcomes], long-term treatment with empagliflozin prevented fatal and nonfatal heart failure
97 jected intravenously by 20%, indicating that empagliflozin raises LDL levels through reduced cataboli
98 m-glucose co-transporter-2 (SGLT2) inhibitor empagliflozin reduced albuminuria in patients with type
99 s with type 2 diabetes and stage 2 or 3 CKD, empagliflozin reduced HbA1c and was well tolerated.
100                                              Empagliflozin reduced hemoglobin A1c significantly in bo
101                                              Empagliflozin reduced the plasma glucose concentration t
102 s with prevalent kidney disease at baseline, empagliflozin reduced the risk of cardiovascular death b
103 sodium-glucose transporter-2 inhibition with empagliflozin reduces both TmG and threshold for glucose
104 he sodium-glucose-co-transporter 2-inhibitor empagliflozin seem to be especially advantageous with re
105                                              Empagliflozin significantly reduced the catabolism of (3
106 nts with genital infections was greater with empagliflozin than placebo in all subgroups by UACR stat
107 efficacy results were driven by findings for empagliflozin (the only SGLT2 inhibitor for which data f
108                     Among patients receiving empagliflozin, there was an increased rate of genital in
109 d be considered with administration of 25 mg empagliflozin to Egyptian population.
110 ncreased risk of mycotic genital infections, empagliflozin-treated patients had fewer serious adverse
111                 Both single-dose and chronic empagliflozin treatment caused glycosuria during fasting
112                                              Empagliflozin treatment for 48 h reduced the TmG in both
113 dian of 34 or 35 days, UACR was lower in the empagliflozin versus placebo group in those with baselin
114  cardiovascular disease randomly assigned to empagliflozin versus placebo reported a 14% reduction in
115 mean ratio of UACR change from baseline with empagliflozin was -7% (95% CI -12 to -2; p=0.013) in pat
116                                              Empagliflozin was associated with remarkable reduction o
117 type 2 diabetes at high cardiovascular risk, empagliflozin was associated with slower progression of
118                        Patients treated with empagliflozin were more likely to experience a sustained
119 atic levels were further reduced by 84% with empagliflozin, while 3-hydroxy-3-methylglutaryl-CoA redu

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