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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
14 alized for AHF were randomized 1:1 to either empagliflozin 10 mg once daily or placebo for 90 days.
16 0) were randomly assigned (1:1:1) to receive empagliflozin 10 mg or 25 mg or placebo once daily for 5
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
23 ter 3 weeks, rats were randomized to receive empagliflozin (10 mg/kg per day) or water (vehicle) for
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%
29 e [6%] and six serious [6%]) and 78 (80%) on empagliflozin 25 mg (eight severe [8%] and seven serious
31 regular loop diuretic who were randomized to empagliflozin 25 mg once daily or placebo for 6 weeks wi
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
39 validated, allowing sensitive estimation of empagliflozin (25-600 ng mL(-1)) in human plasma using d
42 ar disease with the antihyperglycemic agent, empagliflozin, a sodium glucose cotransporter 2 (SGLT2)
45 pe 2 diabetes Mellitus Patients) showed that empagliflozin, a sodium-glucose cotransporter-2 inhibito
50 considered the pharmacokinetic evaluation of empagliflozin after administration to Egyptian volunteer
57 to determine the long-term renal effects of empagliflozin, an analysis that was a prespecified compo
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
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
66 led trial (the SUGAR-DM-HF trial [Studies of Empagliflozin and Its Cardiovascular, Renal and Metaboli
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.
75 r dapagliflozin, 2.52 (CI, 1.23 to 5.14) for empagliflozin, and 3.58 (CI, 2.13 to 6.03) for canaglifl
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
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
90 rters (eg, dapagliflozin, canagliflozin, and empagliflozin) can slow the rate of intestinal glucose a
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
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
101 In the EMPA-REG OUTCOME trial (BI 10773 [Empagliflozin] Cardiovascular Outcome Event Trial in Typ
109 EMPA-REG OUTCOME support the hypothesis that empagliflozin could reduce the risk of clinically releva
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%
115 ct NHE3 inhibition using the SGLT2 inhibitor empagliflozin did not affect urinary calcium and phospha
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
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
125 art failure hospitalizations associated with empagliflozin, even though, by design, the hemoglobin A1
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
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
144 d with fluid restriction, those who received empagliflozin had a larger increase in plasma sodium lev
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).
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
161 milar characteristics as participants of the Empagliflozin in Heart Failure With a Preserved Ejection
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.
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
174 The mechanisms by which the SGLT2 inhibitor empagliflozin increases LDL cholesterol levels were inve
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,
184 he sodium-glucose cotransporter 2 inhibitor, empagliflozin, markedly and rapidly reduced CV death and
186 etion of sodium increased significantly with empagliflozin monotherapy versus placebo (fractional exc
190 port the short-term and long-term effects of empagliflozin on albuminuria in patients with type 2 dia
192 of sodium-glucose cotransporter-2 inhibitor empagliflozin on central hemodynamics in patients with H
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
198 did not significantly modify the benefits of empagliflozin on the primary outcome (P-interaction=0.40
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
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.
214 n Fraction [EMPEROR-Preserved], NCT03057951; EMPagliflozin outcomE tRial in Patients With chrOnic hea
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
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.
233 The sodium-glucose cotransporter 2 inhibitor empagliflozin reduced LV volumes in patients with HFrEF
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
243 ascular disease, in comparison with placebo, empagliflozin reduced the risks of 3-point major adverse
246 sodium-glucose transporter-2 inhibition with empagliflozin reduces both TmG and threshold for glucose
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
252 art Failure With Reduced Ejection Fraction), empagliflozin significantly improved cardiovascular and
254 Trial in Type 2 Diabetes Mellitus Patients) empagliflozin significantly reduced the risk of cardiova
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
260 tion in cardiovascular mortality would bring empagliflozin to $180 000 per QALY gained, the threshold
264 ncreased risk of mycotic genital infections, empagliflozin-treated patients had fewer serious adverse
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
272 dian of 34 or 35 days, UACR was lower in the empagliflozin versus placebo group in those with baselin
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
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
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
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
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