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1 apagliflozin) and EMPEROR-Reduced (assessing 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 the likelihood of response to treatment with empagliflozin.
7 val: -0.14 to 0.32 l/min/m(2); p = 0.448) by empagliflozin.
8 arameters, and plasma NO were not altered by empagliflozin.
9 r hypotension occurred among those receiving empagliflozin.
10 ere [16%] and 11 serious [12%]), 86 (88%) on empagliflozin 10 mg (six severe [6%] and six serious [6%
11 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
12 c HFrEF patients (n = 84) were randomized to empagliflozin 10 mg daily or placebo for 6 months.
13 mized, placebo-controlled crossover study of empagliflozin 10 mg daily versus placebo.
14 alized for AHF were randomized 1:1 to either empagliflozin 10 mg once daily or placebo for 90 days.
15       Patients were randomly assigned 1:1 to empagliflozin 10 mg once daily or placebo, stratified by
16 0) were randomly assigned (1:1:1) to receive empagliflozin 10 mg or 25 mg or placebo once daily for 5
17 s and Results Individuals were randomized to empagliflozin 10 mg, 25 mg, or placebo.
18 stablished cardiovascular disease (1:1:1) to empagliflozin 10 mg, empagliflozin 25 mg, or placebo in
19 (-2) at screening were randomized to receive empagliflozin 10 mg, empagliflozin 25 mg, or placebo onc
20 on fraction <=40% were randomized to receive empagliflozin (10 mg daily) or placebo in addition to re
21 0% to double-blind treatment with placebo or empagliflozin (10 mg once daily), in addition to recomme
22          The participants were randomized to empagliflozin (10 mg/day, n=49) or placebo (n=48) for 6
23 ter 3 weeks, rats were randomized to receive empagliflozin (10 mg/kg per day) or water (vehicle) for
24 ure rat (mRen27/tetO-shIR) were treated with empagliflozin (10 mg/kg/d) or vehicle for 4 weeks.
25 mong 744 914 eligible patients, 28 075 began empagliflozin (15 976 [56.9%]) or dapagliflozin (12 099
26  ratio of relative change from baseline with empagliflozin: -22%, 95% CI -32 to -11; p=0.0003) or mac
27  [8%] and 23 serious [12%]) and 156 (83%) on empagliflozin 25 mg (18 severe [10%] and 22 serious [12%
28 flozin 10 mg and -0.68% (-0.88 to -0.49) for empagliflozin 25 mg (both p<0.0001).
29 e [6%] and six serious [6%]) and 78 (80%) on empagliflozin 25 mg (eight severe [8%] and seven serious
30 c at week 24 was -0.42% (-0.56 to -0.28) for empagliflozin 25 mg (p<0.0001).
31 regular loop diuretic who were randomized to empagliflozin 25 mg once daily or placebo for 6 weeks wi
32 374) were randomly assigned (1:1) to receive empagliflozin 25 mg or placebo for 52 weeks.
33 dium glucose cotransporter 2 inhibition with empagliflozin 25 mg QD on renal hyperfiltration in subje
34 ular disease (1:1:1) to empagliflozin 10 mg, empagliflozin 25 mg, or placebo in addition to standard
35 e randomized to receive empagliflozin 10 mg, empagliflozin 25 mg, or placebo once daily in addition t
36 stration of either 1) placebo, 2) the SGLT2i empagliflozin (25 mg), 3) the glucagon receptor antagoni
37 le dose, and following 4-week treatment with empagliflozin (25 mg).
38 e (NFG) and eight subjects with IFG received empagliflozin (25 mg/day) for 2 weeks.
39  validated, allowing sensitive estimation of empagliflozin (25-600 ng mL(-1)) in human plasma using d
40                       Compared with vehicle, empagliflozin 30 mg/kg/day for 2 weeks significantly red
41 es in patients with diabetes with the use of empagliflozin, a member of this new class of drugs.
42 ar disease with the antihyperglycemic agent, empagliflozin, a sodium glucose cotransporter 2 (SGLT2)
43                                              Empagliflozin, a sodium-glucose cotransporter 2 inhibito
44               In the EMPA-REG OUTCOME trial, empagliflozin, a sodium-glucose cotransporter 2 inhibito
45 pe 2 diabetes Mellitus Patients) showed that empagliflozin, a sodium-glucose cotransporter-2 inhibito
46     To determine whether glucose lowering by empagliflozin accelerates atherosclerosis regression in
47            Canagliflozin, dapagliflozin, and empagliflozin accounted for 53%, 42%, and 5% of the tota
48                              In both groups, empagliflozin administration raised EGP, lowered TGD, an
49                                              Empagliflozin administration to nondiabetic HFrEF patien
50 considered the pharmacokinetic evaluation of empagliflozin after administration to Egyptian volunteer
51            Canagliflozin, dapagliflozin, and empagliflozin, all recently approved for treatment of ty
52                                       In the empagliflozin-allocated group, there was significant low
53                                              Empagliflozin also caused significant reductions in body
54                                Unexpectedly, empagliflozin also reduced intestinal cholesterol absorp
55                               Interestingly, empagliflozin also reduces intestinal cholesterol absorp
56                                              Empagliflozin ameliorates adverse cardiac remodeling and
57  to determine the long-term renal effects of empagliflozin, an analysis that was a prespecified compo
58                               The effects of empagliflozin, an inhibitor of sodium-glucose cotranspor
59  repurpose the widely used antidiabetic drug empagliflozin, an inhibitor of the renal glucose cotrans
60 tration of the novel glucose lowering agent, empagliflozin, an SGLT2 inhibitor which targets the kidn
61 819 individuals who initiated treatment with empagliflozin and 17 464 with dapagliflozin were include
62 al of 3260 patients were assigned to receive empagliflozin and 3262 to receive placebo.
63 MPEROR-Preserved trials (9718 patients; 4860 empagliflozin and 4858 placebo), and patients were group
64 -glucose co-transporter-2 (SGLT2) inhibitors empagliflozin and canagliflozin have been shown to lower
65                               The effects of empagliflozin and dapagliflozin on hospitalisations for
66 led trial (the SUGAR-DM-HF trial [Studies of Empagliflozin and Its Cardiovascular, Renal and Metaboli
67                                              Empagliflozin and LY2409021 individually lowered fasting
68 transition pairs of m/z 449.01 to 371.21 for empagliflozin and m/z 407.00 to 328.81 for dapagliflozin
69 pitalization for heart failure in the pooled empagliflozin and placebo groups were analyzed in subgro
70 s were studied after 4 weeks' treatment with empagliflozin and placebo in a randomized, double-blind,
71  patients were randomized (95 each receiving empagliflozin and placebo), with a mean (SD) age of 64 (
72 .6 g/m(2) and 0.01 g/m(2) for those assigned empagliflozin and placebo, respectively (adjusted differ
73  consistent with the known safety profile of empagliflozin and were similar in the two trial groups.
74 me was for use of dapagliflozin, with 5% for empagliflozin, and 1% for canagliflozin.
75 r dapagliflozin, 2.52 (CI, 1.23 to 5.14) for empagliflozin, and 3.58 (CI, 2.13 to 6.03) for canaglifl
76  the trial, 43 (49%) received treatment with empagliflozin, and 44 (51%) received placebo.
77                            Oral semaglutide, empagliflozin, and liraglutide also reduced cardiovascul
78 ical trials of canagliflozin, dapagliflozin, empagliflozin, and sotagliflozin in patients with type 1
79 /-17.9 g/m(2) and 63.8+/-14.0 g/m(2) for the empagliflozin- and placebo-assigned groups, respectively
80                   In addition, in the heart, empagliflozin appears to inhibit sodium-hydrogen exchang
81       We assessed the efficacy and safety of empagliflozin as an add-on treatment in patients with ty
82  risk for cardiovascular events who received empagliflozin, as compared with placebo, had a lower rat
83 out baseline cardiovascular disease, and for empagliflozin at both the 10- and 25-mg daily doses; ana
84  m(2) of body-surface area to receive either empagliflozin (at a dose of 10 mg or 25 mg) or placebo o
85 the sodium glucose cotransporter 2 inhibitor empagliflozin attenuated renal hyperfiltration in subjec
86   In this model, blood glucose lowering with empagliflozin attenuated some molecular and histological
87 In male db/db mice, a 10-week treatment with empagliflozin attenuated the diabetes-induced upregulati
88 ar filtration rate stabilized over time with empagliflozin but gradually declined with placebo.
89                      These data suggest that empagliflozin, by switching energy metabolism from carbo
90 rters (eg, dapagliflozin, canagliflozin, and empagliflozin) can slow the rate of intestinal glucose a
91                                              Empagliflozin cardiac benefits in the EMPA-REG OUTCOME (
92                  The EMPA-REG OUTCOME trial (Empagliflozin Cardiovascular Outcome Event Trial in Type
93              Background In EMPA-REG OUTCOME (Empagliflozin Cardiovascular Outcome Event Trial in Type
94 in cardiac benefits in the EMPA-REG OUTCOME (Empagliflozin Cardiovascular Outcome Event Trial in Type
95 cular disease in the EMPA-REG OUTCOME trial (Empagliflozin Cardiovascular Outcome Event Trial in Type
96                                          The Empagliflozin, Cardiovascular Outcomes, and Mortality in
97                   In a landmark trial called Empagliflozin, Cardiovascular Outcomes, and Mortality in
98 inical outcomes, the EMPA-REG OUTCOME trial (Empagliflozin, Cardiovascular Outcomes, and Mortality in
99  observed in the EMPA-REG OUTCOME (BI 10773 [Empagliflozin] Cardiovascular Outcome Event Trial in Typ
100                 The EMPA-REG OUTCOME trial ([Empagliflozin] Cardiovascular Outcome Event Trial in Typ
101     In the EMPA-REG OUTCOME trial (BI 10773 [Empagliflozin] Cardiovascular Outcome Event Trial in Typ
102                                              Empagliflozin caused 50 +/- 4 and 45 +/- 4 g glucosuria
103                                              Empagliflozin caused a nonsignificant increase in fracti
104                       Compared with placebo, empagliflozin caused a significant increase in 24-hour u
105                                              Empagliflozin caused a significant increase in 24-hour u
106                    We sought to determine if empagliflozin causes a decrease in left ventricular (LV)
107                                              Empagliflozin causes significant natriuresis, particular
108                                 The EMPRISE (Empagliflozin Comparative Effectiveness and Safety) stud
109 EMPA-REG OUTCOME support the hypothesis that empagliflozin could reduce the risk of clinically releva
110                                  Addition of empagliflozin daily to standard medical treatment of acu
111 otransporter-2 (SGLT2) inhibitors, including empagliflozin, dapagliflozin, and canagliflozin, are now
112 Compared with sitagliptin, the initiation of empagliflozin decreased the risk of HHF-specific by 50%
113               Urinary glucose excretion with empagliflozin decreases with declining renal function, r
114                                              Empagliflozin did not affect myocardial free fatty acids
115 ct NHE3 inhibition using the SGLT2 inhibitor empagliflozin did not affect urinary calcium and phospha
116                                  At 6 weeks, empagliflozin did not cause a significant change in 24-h
117                                              Empagliflozin did not change myocardial oxygen consumpti
118     Across these 3 end points, the effect of empagliflozin did not differ in patients with prediabete
119  acute myocardial infarction, treatment with empagliflozin did not lead to a significantly lower risk
120                                              Empagliflozin did not lower HbA1c in patients with predi
121 dium-glucose cotransporter 2 inhibition with empagliflozin did not result in a meaningful reduction i
122 prandial PG excursion, which was annulled by empagliflozin during their combination (empagliflozin +
123  criteria, assessing three SGLT2 inhibitors: empagliflozin (EMPA-REG OUTCOME), canagliflozin (CANVAS
124                                              Empagliflozin enhanced beta-cell function only in subjec
125 art failure hospitalizations associated with empagliflozin, even though, by design, the hemoglobin A1
126            Among patients with stable HFrEF, empagliflozin for 12 weeks reduced PCWP compared with pl
127 itiated in 13 of 4687 patients (0.3%) in the empagliflozin group and in 14 of 2333 patients (0.6%) in
128 n 490 of 4687 patients (10.5%) in the pooled empagliflozin group and in 282 of 2333 patients (12.1%)
129 urred in 525 of 4124 patients (12.7%) in the empagliflozin group and in 388 of 2061 (18.8%) in the pl
130 ccurred in 70 of 4645 patients (1.5%) in the empagliflozin group and in 60 of 2323 (2.6%) in the plac
131 compared with placebo, fewer patients in the empagliflozin group reported intensification of diuretic
132 chemic myocardial injury in both groups, the empagliflozin group showed amelioration of adverse remod
133  myocardial infarction or stroke, but in the empagliflozin group there were significantly lower rates
134 -creatinine ratio (UACR) data for the pooled empagliflozin group versus placebo according to albuminu
135 r nonfatal stroke, as analyzed in the pooled empagliflozin group versus the placebo group.
136 Among MRA users at baseline, patients in the empagliflozin group were 22% less likely than those in t
137 ng MRA nonusers at baseline, patients in the empagliflozin group were 35% less likely than those in t
138 %) in the placebo group (hazard ratio in the empagliflozin group, 0.61; 95% confidence interval, 0.53
139 %) in the placebo group (hazard ratio in the empagliflozin group, 0.86; 95.02% confidence interval, 0
140 7-15.7 mL, P = 0.0015), respectively, in the empagliflozin group, compared with placebo.
141 epresenting a 55% lower relative risk in the empagliflozin group.
142 62 (9.9%) patients had HF in the placebo and empagliflozin groups, respectively.
143                          In EMPEROR-Reduced, empagliflozin had a beneficial effect on the key efficac
144 d with fluid restriction, those who received empagliflozin had a larger increase in plasma sodium lev
145                        Patients treated with empagliflozin had a significantly higher increase of med
146                        Patients who received empagliflozin had significant improvements in peak O(2)
147  260 assigned to placebo and 509 assigned to empagliflozin) had macroalbuminuria.
148 675 assigned to placebo and 1338 assigned to empagliflozin) had microalbuminuria, and 769 (11%; 260 a
149 382 assigned to placebo and 2789 assigned to empagliflozin) had normoalbuminuria, 2013 (29%; 675 assi
150 ith the lowest risk of glaucoma, followed by empagliflozin (HR 0.727, 95% CI 0.696, 0.759), dapaglifl
151 t-years of follow-up), and it was reduced by empagliflozin (HR, 0.70; 95% CI, 0.63-0.78; P<0.0001).
152                                              Empagliflozin improved clinical outcomes and reduced mor
153       In summary, plasma glucose lowering by empagliflozin improves plaque regression in diabetic mic
154                             Off-label use of empagliflozin in 4 GSD-Ib patients with incomplete respo
155 eath, suggesting that the benefits seen with empagliflozin in a randomized trial may be a class effec
156  The reductions in UACR were maintained with empagliflozin in all three groups compared with placebo
157                   TmG was further reduced by empagliflozin in both groups on day 14 (by 65 +/- 5 and
158 ssess the diuretic and natriuretic effect of empagliflozin in combination with loop diuretics.
159  the hyperglycemic clamp was not affected by empagliflozin in either IFG or NFG.
160 ly, none of these parameters were changed by empagliflozin in fed conditions.
161 milar characteristics as participants of the Empagliflozin in Heart Failure With a Preserved Ejection
162       Cardiovascular and renal outcomes with empagliflozin in heart failure.
163 orter 2 (SGLT2) inhibitors dapagliflozin and empagliflozin in HFrEF patients.
164 lure]) to investigate the cardiac effects of empagliflozin in patients in New York Heart Association
165 e prespecified a comparison of the effect of empagliflozin in patients with and without diabetes.
166                 The adverse event profile of empagliflozin in patients with eGFR <60 mL.min(-1).1.73
167                 The adverse-event profile of empagliflozin in patients with impaired kidney function
168 -glucose cotransporter-2 inhibitor (SGLT-2i) empagliflozin in patients with type 2 diabetes mellitus
169 ion of renal sodium-glucose cotransport with empagliflozin in subjects with IFG and NFG produces comp
170 n was attenuated by -33 mL/min/1.73m(2) with empagliflozin in T1D-H, (GFR 172+/-23-139+/-25 mL/min/1.
171     (Evaluating Comparative Effectiveness of Empagliflozin in Type 2 Diabetes Population With and Wit
172  including dapagliflozin, canagliflozin, and empagliflozin, increase glucose excretion and lower bloo
173                                              Empagliflozin increased myocardial ATP content and enhan
174  The mechanisms by which the SGLT2 inhibitor empagliflozin increases LDL cholesterol levels were inve
175               (Are the "Cardiac Benefits" of Empagliflozin Independent of Its Hypoglycemic Activity?
176            In patients with type 2 diabetes, empagliflozin-induced glycosuria improved beta cell func
177 demonstrated the largest treatment effect of empagliflozin: insulin-like growth factor-binding protei
178 abetes, initial therapy with finerenone plus empagliflozin led to a greater reduction in the urinary
179  renal benefit, the antihyperglycaemic drugs empagliflozin, liraglutide, and semaglutide-the latter b
180 und treatment (21 trials), oral semaglutide, empagliflozin, liraglutide, extended-release exenatide,
181                                              Empagliflozin lowered blood sugar levels compared to veh
182 d by empagliflozin during their combination (empagliflozin + LY2409021).
183 st LY2409021 (300 mg), or 4) the combination empagliflozin + LY2409021.
184 he sodium-glucose cotransporter 2 inhibitor, empagliflozin, markedly and rapidly reduced CV death and
185                         After treatment with empagliflozin, median serum sodium level rose to 134 mmo
186 etion of sodium increased significantly with empagliflozin monotherapy versus placebo (fractional exc
187 beyond therapy with metformin, ramipril, and empagliflozin (MRE).
188                             After 14 days of empagliflozin, natriuresis waned due to increased reabso
189                    Patients were assigned to empagliflozin of 10 mg or matching placebo once daily on
190 port the short-term and long-term effects of empagliflozin on albuminuria in patients with type 2 dia
191                We aim to study the effect of empagliflozin on cardiovascular and kidney outcomes acro
192  of sodium-glucose cotransporter-2 inhibitor empagliflozin on central hemodynamics in patients with H
193               We investigated the effects of empagliflozin on clinical outcomes in patients with type
194                       Post hoc, we evaluated empagliflozin on kidney outcomes in patients with or wit
195 se of this study was to assess the effect of empagliflozin on left ventricular (LV) function and volu
196 sodium-glucose cotransporter inhibition with empagliflozin on the fasting plasma glucose (FPG) concen
197                                The effect of empagliflozin on the primary composite outcome and key s
198 did not significantly modify the benefits of empagliflozin on the primary outcome (P-interaction=0.40
199                                   Effects of empagliflozin on these outcomes were consistent across c
200 did not differ with respect to the effect of empagliflozin on total hospitalizations for heart failur
201 support short-term and long-term benefits of empagliflozin on urinary albumin excretion, irrespective
202 tched pairs initiating treatment with either empagliflozin or liraglutide) were included in cohort 1,
203 losclerosis, however, were not improved with empagliflozin or metformin, and plasma and intra-renal r
204                   Animals were randomized to empagliflozin or placebo for 2 months.
205  of <1000 ml/24 h, a once-daily dose of oral empagliflozin or placebo for 4 days.
206 signed patients to receive 10 mg or 25 mg of empagliflozin or placebo once daily.
207      Of 3730 patients who were randomized to empagliflozin or placebo, 1978 (53%) had CKD.
208 rt of T2D patients >=18 years old initiating empagliflozin or sitagliptin from August 2014 through Se
209 tched pairs initiating treatment with either empagliflozin or sitagliptin) were included in cohort 2.
210 dentified 16,443 patient pairs who initiated empagliflozin or sitagliptin.
211              These mice then received either empagliflozin or vehicle for three weeks.
212 o any significant extent with dapagliflozin, empagliflozin, or phlorizin.
213                                             (EMPagliflozin outcomE tRial in Patients With chrOnic hea
214 n Fraction [EMPEROR-Preserved], NCT03057951; EMPagliflozin outcomE tRial in Patients With chrOnic hea
215                                             (EMPagliflozin outcomE tRial in Patients With chrOnic hea
216                                             (Empagliflozin Outcome Trial in Patients With Chronic Hea
217                                             (Empagliflozin Outcome Trial in Patients With Chronic Hea
218                                             (Empagliflozin Outcome Trial in Patients With Chronic Hea
219                          In EMPEROR-Reduced (Empagliflozin Outcome Trial in Patients With Chronic Hea
220                          In EMPEROR-Reduced (Empagliflozin Outcome Trial in Patients With Chronic Hea
221        At 14 days, the natriuretic effect of empagliflozin persisted, resulting in a reduction in blo
222 ealth care system was constructed to compare empagliflozin plus standard care to standard care alone
223 EMPA-REG Outcomes], long-term treatment with empagliflozin prevented fatal and nonfatal heart failure
224 um glucose cotransporter 2 (SGLT2) inhibitor empagliflozin promotes osmotic diuresis via urinary gluc
225 he sodium-glucose co-transporter 2 inhibitor empagliflozin provides cardiac protection.
226 jected intravenously by 20%, indicating that empagliflozin raises LDL levels through reduced cataboli
227 m-glucose co-transporter-2 (SGLT2) inhibitor empagliflozin reduced albuminuria in patients with type
228 art Failure With Reduced Ejection Fraction), empagliflozin reduced cardiovascular death or heart fail
229 s with type 2 diabetes and stage 2 or 3 CKD, empagliflozin reduced HbA1c and was well tolerated.
230                                              Empagliflozin reduced hemoglobin A1c significantly in bo
231                                              Empagliflozin reduced LV end-diastolic volume index by 8
232                  In comparison with placebo, empagliflozin reduced LV end-systolic volume index by 6.
233 The sodium-glucose cotransporter 2 inhibitor empagliflozin reduced LV volumes in patients with HFrEF
234                                              Empagliflozin reduced postprandial PG through increased
235                                              Empagliflozin reduced resting MBF by 13% (P < 0.01), but
236                             In the HF group, empagliflozin reduced risk of incident or worsening neph
237                                              Empagliflozin reduced the combined risk of death, hospit
238                                              Empagliflozin reduced the plasma glucose concentration t
239                                              Empagliflozin reduced the primary outcome and total HF h
240 art failure and a reduced ejection fraction, empagliflozin reduced the risk and total number of inpat
241 s with prevalent kidney disease at baseline, empagliflozin reduced the risk of cardiovascular death b
242                                              Empagliflozin reduced the risk of the primary outcome in
243 ascular disease, in comparison with placebo, empagliflozin reduced the risks of 3-point major adverse
244                                              Empagliflozin reduced the total number of heart failure
245                                              Empagliflozin reduces blood glucose levels via inhibitio
246 sodium-glucose transporter-2 inhibition with empagliflozin reduces both TmG and threshold for glucose
247                                              Empagliflozin reduces the risk of cardiovascular death o
248                      The hypothesis was that empagliflozin's cardiac benefits are mediated by switchi
249 fectiveness and Safety) study aims to assess empagliflozin's effectiveness, safety, and healthcare ut
250 he sodium-glucose-co-transporter 2-inhibitor empagliflozin seem to be especially advantageous with re
251                                              Empagliflozin showed beneficial effects on cardiovascula
252 art Failure With Reduced Ejection Fraction), empagliflozin significantly improved cardiovascular and
253                                              Empagliflozin significantly reduced the catabolism of (3
254  Trial in Type 2 Diabetes Mellitus Patients) empagliflozin significantly reduced the risk of cardiova
255                                              Empagliflozin slowed the slope of eGFR decline by 1.11 (
256                                              Empagliflozin switches myocardial fuel utilization away
257 nts with genital infections was greater with empagliflozin than placebo in all subgroups by UACR stat
258 efficacy results were driven by findings for empagliflozin (the only SGLT2 inhibitor for which data f
259                     Among patients receiving empagliflozin, there was an increased rate of genital in
260 tion in cardiovascular mortality would bring empagliflozin to $180 000 per QALY gained, the threshold
261 d be considered with administration of 25 mg empagliflozin to Egyptian population.
262               Atherosclerotic plaques in the empagliflozin treated mice were significantly smaller, s
263 ascular wall were significantly decreased in empagliflozin-treated mice.
264 ncreased risk of mycotic genital infections, empagliflozin-treated patients had fewer serious adverse
265                                              Empagliflozin-treated pigs did not consume glucose (redu
266                 Both single-dose and chronic empagliflozin treatment caused glycosuria during fasting
267                                              Empagliflozin treatment for 48 h reduced the TmG in both
268  hypertension and investigated the effect of empagliflozin treatment to test the hypothesis if empagl
269 apagliflozin) and EMPEROR-Reduced (assessing empagliflozin) trials showed that sodium-glucose co-tran
270 ummary, the glucose-lowering SGLT2 inhibitor empagliflozin, used for type 2 diabetes, was successfull
271 ined by 1.6+/-0.4 in patients withdrawn from empagliflozin versus placebo (P<0.0001).
272 dian of 34 or 35 days, UACR was lower in the empagliflozin versus placebo group in those with baselin
273 urohormones were similar (P<0.34) during the empagliflozin versus placebo period.
274  cardiovascular disease randomly assigned to empagliflozin versus placebo reported a 14% reduction in
275 y cardiovascular outcomes and mortality with empagliflozin versus placebo were consistent across the
276 E and hospitalization for heart failure with empagliflozin versus placebo were consistent in patients
277 ravenous treatment (415 versus 519 patients; empagliflozin versus placebo, respectively; hazard ratio
278 he risk of HHF among T2D patients initiating empagliflozin versus sitagliptin, a dipeptidyl peptidase
279 0- and 25-mg daily doses; analyses comparing empagliflozin versus the dipeptidyl peptidase-4 inhibito
280                         Absolute benefits of empagliflozin vs sitagliptin were larger in patients wit
281 edian (95% confidence interval) differences, empagliflozin vs. placebo, at Week 12 were -4.0 m (-16.0
282  (-25.1 +/- 26.0 ml vs. -1.5 +/- 25.4 ml for empagliflozin vs. placebo, respectively; p < 0.001) and
283 ss (-17.8 +/- 31.9 g vs. 4.1 +/- 13.4 g, for empagliflozin vs. placebo, respectively; p < 0.001) and
284 2.6 ml/min/kg vs. -0.5 +/- 1.9 ml/min/kg for empagliflozin vs. placebo, respectively; p = 0.017), oxy
285  (-26.6 +/- 20.5 ml vs. -0.5 +/- 21.9 ml for empagliflozin vs. placebo; p < 0.001).
286                  This finding indicates that empagliflozin warrants further study as a treatment for
287 mean ratio of UACR change from baseline with empagliflozin was -7% (95% CI -12 to -2; p=0.013) in pat
288 compared with sitagliptin, the initiation of empagliflozin was associated with a decreased risk of HH
289                            Across subgroups, empagliflozin was associated with a lower risk of the mo
290                                              Empagliflozin was associated with a significant reductio
291                                              Empagliflozin was associated with reductions in LV mass
292                                              Empagliflozin was associated with remarkable reduction o
293 ronary artery disease, SGLT2 inhibition with empagliflozin was associated with significant reduction
294 type 2 diabetes at high cardiovascular risk, empagliflozin was associated with slower progression of
295                                         Oral empagliflozin was rapidly absorbed as evidenced by a 27-
296                                              Empagliflozin was well tolerated in CKD patients.
297           Additionally, patients assigned to empagliflozin were 20% to 40% more likely to experience
298                        Patients treated with empagliflozin were more likely to experience a sustained
299 atic levels were further reduced by 84% with empagliflozin, while 3-hydroxy-3-methylglutaryl-CoA redu
300 liflozin treatment to test the hypothesis if empagliflozin will be protective in a heart failure mode

 
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