ライフサイエンスコーパス: dapagliflozin

1 en after displacement of kidney binding with dapagliflozin.

2 arxiga or any combination therapy containing dapagliflozin.

3 the reduction in AF/AFL events observed with dapagliflozin.

4 4.2 (95% CI, 1.0, 8.2; P=0.022) in favor of dapagliflozin.

5 -13.6; p=0.0022) for zibotentan 0.25 mg plus dapagliflozin.

6 reased by 2.8 kg (95% CI: -3.7 to -2.0) with dapagliflozin.

7 at may derive reduction in risk of MACE with dapagliflozin.

8 f prognostic importance, and were reduced by dapagliflozin.

9 h/HHF and progression of kidney disease with dapagliflozin.

10 nt pattern of incremental risk observed with dapagliflozin.

11 f the composite was reduced significantly by dapagliflozin.

12 dapagliflozin 3.7%; no PAD, placebo 0.4% vs. dapagliflozin 0.4%) (Pinteraction = 1.00).

13 h tracer equilibration, subjects received 1) dapagliflozin 10 mg (n = 26) or placebo (n = 12); 2) rep

14 assigned to receive balcinrenone 15 mg plus dapagliflozin 10 mg (n=108), balcinrenone 40 mg plus dap

15 lozin 10 mg (n=108), balcinrenone 40 mg plus dapagliflozin 10 mg (n=110), or dapagliflozin plus place

16 patients in the dapagliflozin 5 mg (n=277), dapagliflozin 10 mg (n=296), and placebo (n=260) groups,

17 fety analyses (dapagliflozin 5 mg [n=277] vs dapagliflozin 10 mg [n=296] vs placebo [n=260]; 778 of t

18 -10.7; p=0.0038) for balcinrenone 15 mg plus dapagliflozin 10 mg and -32.8% (-42.0 to -22.1; p<0.0001

19 Balcinrenone 15 mg plus dapagliflozin 10 mg and balcinrenone 40 mg plus dapaglif

20 In total, 263 patients were randomized to dapagliflozin 10 mg daily or placebo for 12 weeks.

21 e dapagliflozin 5 mg group, five (2%) in the dapagliflozin 10 mg group, and three (1%) in the placebo

22 and -0.84% (-0.98 to -0.70, p<0.0001) in the dapagliflozin 10 mg group.

23 stem, we randomly assigned (1:1) patients to dapagliflozin 10 mg once a day or to placebo, with rando

24 mg by subcutaneous injection plus once-daily dapagliflozin 10 mg oral tablets, exenatide with dapagli

25 cinrenone 40 mg plus dapagliflozin 10 mg, or dapagliflozin 10 mg plus placebo (double-dummy technique

26 10 mg were superior in reducing UACR versus dapagliflozin 10 mg plus placebo throughout the treatmen

27 At week 12, the UACR difference versus dapagliflozin 10 mg plus placebo was -22.8% (90% CI -33.

28 otentan 0.25 mg plus dapagliflozin 10 mg, or dapagliflozin 10 mg plus placebo, as adjunct to angioten

29 Dapagliflozin 10 mg significantly improved blood pressur

30 2% [95% CI -0.56 to -0.28; p<0.0001] and for dapagliflozin 10 mg vs placebo was -0.45% [-0.58 to -0.3

31 agliflozin 10 mg and balcinrenone 40 mg plus dapagliflozin 10 mg were superior in reducing UACR versu

32 07 (80%) patients in the dapagliflozin 5 mg, dapagliflozin 10 mg, and placebo groups, respectively; s

33 atment with combined balcinrenone 15 mg plus dapagliflozin 10 mg, balcinrenone 40 mg plus dapaglifloz

34 ment with zibotentan 0.25, 1.5, or 5 mg plus dapagliflozin 10 mg, changes in body weight (beta=0.36 [

35 in 2.5 mg, n=135; dapagliflozin 5 mg, n=133; dapagliflozin 10 mg, n=132; placebo, n=134).

36 dapagliflozin 10 mg, zibotentan 0.25 mg plus dapagliflozin 10 mg, or dapagliflozin 10 mg plus placebo

37 dapagliflozin 10 mg, balcinrenone 40 mg plus dapagliflozin 10 mg, or dapagliflozin 10 mg plus placebo

38 daily treatment with zibotentan 1.5 mg plus dapagliflozin 10 mg, zibotentan 0.25 mg plus dapaglifloz

39 -22.1; p<0.0001) for balcinrenone 40 mg plus dapagliflozin 10 mg.

40 te 25-75 mL/min/1.73m(2)) were randomized to dapagliflozin 10 mg/day matched to placebo (2152 individ

41 stem) to receive dapagliflozin (10 mg) only, dapagliflozin (10 mg) and saxagliptin (2.5 mg), or place

42 active voice-web response system) to receive dapagliflozin (10 mg) only, dapagliflozin (10 mg) and sa

43 inine ratio 200-5000 mg/g were randomized to dapagliflozin (10 mg/d) or placebo.

44 075 began empagliflozin (15 976 [56.9%]) or dapagliflozin (12 099 [43.1%]).

45 ith -0.67% (-0.81 to -0.53, p=0.0002) in the dapagliflozin 2.5 mg group, -0.70% (-0.85 to -0.56, p<0.

46 ncluded in analysis of the primary endpoint (dapagliflozin 2.5 mg, n=135; dapagliflozin 5 mg, n=133;

47 ed in similar proportions of patients in the dapagliflozin (2-4%) and placebo groups (3%).

48 ly assigned to receive one of three doses of dapagliflozin (2.5 mg, n=137; 5 mg, n=137; or 10 mg, n=1

49 pecific HRs were 1.86 (CI, 1.11 to 3.10) for dapagliflozin, 2.52 (CI, 1.23 to 5.14) for empagliflozin

50 pective of PAD status (PAD, placebo 4.2% vs. dapagliflozin 3.7%; no PAD, placebo 0.4% vs. dapaglifloz

51 2 to -5.51]; placebo-adjusted difference for dapagliflozin -4.28 mm Hg [-6.54 to -2.02]; p=0.0002).

52 Among patients in the dapagliflozin 5 mg (n=277), dapagliflozin 10 mg (n=296),

53 ment groups and included in safety analyses (dapagliflozin 5 mg [n=277] vs dapagliflozin 10 mg [n=296

54 up, -0.70% (-0.85 to -0.56, p<0.0001) in the dapagliflozin 5 mg group, and -0.84% (-0.98 to -0.70, p<

55 idosis occurred in four (1%) patients in the dapagliflozin 5 mg group, five (2%) in the dapagliflozin

56 sing an interactive voice response system to dapagliflozin 5 mg or 10 mg once daily, given orally, or

57 mean difference from baseline to week 24 for dapagliflozin 5 mg vs placebo was -0.42% [95% CI -0.56 t

58 %), 235 (79%), and 207 (80%) patients in the dapagliflozin 5 mg, dapagliflozin 10 mg, and placebo gro

59 imary endpoint (dapagliflozin 2.5 mg, n=135; dapagliflozin 5 mg, n=133; dapagliflozin 10 mg, n=132; p

60 = 22) were treated with the SGLT2 inhibitor dapagliflozin (5 mg daily) or placebo for 4 weeks in a r

61 Dapagliflozin, a selective inhibitor of sodium-glucose c

62 Dapagliflozin, a selective sodium-glucose cotransporter-

63 ac hypertrophy, was successfully targeted by Dapagliflozin, a sodium glucose cotransporter 2 inhibito

64 with higher baseline predicted risk for both dapagliflozin (absolute risk reduction: 2.1% vs 0.2%) an

65 We examined the effects of dapagliflozin according to age, given potential concerns

66 Clinical outcomes and the effect of dapagliflozin, according to AF status, were examined.

67 tion: Heart Failure evaluates the benefit of dapagliflozin across cohorts of duration of heart failur

68 and to test the consistency of the effect of dapagliflozin across the range of ejection fractions.

69 In vivo, dapagliflozin acutely induced renal glucose excretion in

70 verse-Outcomes in Heart Failure) showed that dapagliflozin added to other guideline-recommended thera

71 ntion of Adverse Outcomes in Heart Failure), dapagliflozin, added to guideline-recommended therapies,

72 ignificantly greater in patients assigned to dapagliflozin (adjusted mean change from baseline -0.63%

73 gnificantly reduced in the group assigned to dapagliflozin (adjusted mean change from baseline -11.90

74 (Dapagliflozin After Transcatheter Aortic Valve Implantat

75 1.10-1.62) but not among those randomized to dapagliflozin (aHR, 0.90; 95% CI, 0.74-1.09; P for inter

76 ne (-0.4% [95% CI -0.6 to -0.1]; p=0.004) or dapagliflozin alone (-0.6% [-0.8 to -0.3]; p<0.001).

77 , exenatide alone (n=231; n=1 untreated), or dapagliflozin alone (n=233).

78 T2 inhibitor dapagliflozin with exenatide or dapagliflozin alone in patients with type 2 diabetes ina

79 dapagliflozin/spironolactone combination and dapagliflozin alone sequences study primary outcome.

80 Dapagliflozin also reduced the total number (first and r

81 uced somatostatin secretion is suppressed by dapagliflozin (an inhibitor of sodium-glucose co-tranpor

82 g patients with HFmrEF or HFpEF treated with dapagliflozin, an initial eGFR decline was frequent but

83 -23.5; p<0.0001) for zibotentan 1.5 mg plus dapagliflozin and -27.0% (90% CI -38.4 to -13.6; p=0.002

84 , 2012, we randomly assigned 225 patients to dapagliflozin and 224 to placebo.

85 0 patients were randomly assigned to receive dapagliflozin and 637 to receive standard care alone aft

86 as 12.1 years (95% CI: 11.0-13.2 years) with dapagliflozin and 9.7 years (95% CI: 8.8-10.7 years) wit

87 inopenic conditions replicates the effect of dapagliflozin and causes ketoacidosis.

88 nths, similar proportions of patients in the dapagliflozin and control groups showed clinically meani

89 endpoints were change from baseline in UACR (dapagliflozin and dapagliflozin-saxagliptin groups) and

90 Dapagliflozin and dapagliflozin-saxagliptin reduced UACR

91 -glucose co-transporter 2 (SGLT2) inhibitors dapagliflozin and empagliflozin in HFrEF patients.

92 Albuminuria changes in response to dapagliflozin and eplerenone did not correlate, supporti

93 ody weight decreased by 0.92 to 1.61 kg with dapagliflozin and increased by 0.43 kg with placebo (mea

94 nsulin dose decreased by 0.63 to 1.95 U with dapagliflozin and increased by 5.65 U with placebo (mean

95 Adverse events were similar between dapagliflozin and placebo (44 (27.2%) versus 38 (23.5%)

96 fety outcomes between patients randomized to dapagliflozin and placebo across all age categories.

97 Adverse events were similar in the dapagliflozin and placebo groups (98 [44%] patients vs 9

98 ean diuretic dose did not differ between the dapagliflozin and placebo groups after randomization.

99 52 (2.5%) and 69 (3.2%) participants in the dapagliflozin and placebo groups, respectively (0.77 [0.

100 d in 36 (3.0%) and 53 (4.5%) patients in the dapagliflozin and placebo groups, respectively (HR, 0.66

101 n 115 (9.4%) and 122 (10.3%) patients in the dapagliflozin and placebo groups, respectively (HR, 0.91

102 d placebo, yet the difference in EGP between dapagliflozin and placebo persisted (+0.71 +/- 0.13 mg/k

103 nce in tolerability or safety events between dapagliflozin and placebo, even in elderly individuals.

104 rations was comparable in subjects receiving dapagliflozin and placebo, yet the difference in EGP bet

105 study drug discontinuation were similar with dapagliflozin and placebo.

106 The DAPA-HF (Dapagliflozin and Prevention of Adverse Outcomes in Hear

107 In the DAPA-HF trial (Dapagliflozin and Prevention of Adverse Outcomes in Hear

108 In the DAPA-HF trial (Dapagliflozin and Prevention of Adverse-Outcomes in Hear

109 time from diagnosis of HF in DAPA-HF trial (Dapagliflozin and Prevention of Adverse-outcomes in Hear

110 The DAPA-HF trial (Dapagliflozin and Prevention of Adverse-Outcomes in Hear

111 um-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin and the insulin sensitizer pioglitazone.

112 with or without diabetes: DAPA-HF (assessing dapagliflozin) and EMPEROR-Reduced (assessing empagliflo

113 Both DAPA-HF (assessing dapagliflozin) and EMPEROR-Reduced (assessing empagliflo

114 (SGLT2) inhibitors, including empagliflozin, dapagliflozin, and canagliflozin, are now widely approve

115 Canagliflozin, dapagliflozin, and empagliflozin accounted for 53%, 42%,

116 Canagliflozin, dapagliflozin, and empagliflozin, all recently approved

117 Dapagliflozin appears to robustly reduce the risk of bot

118 We have identified dapagliflozin as a potent and selective inhibitor of the

119 e aimed to assess the efficacy and safety of dapagliflozin as an add-on to adjustable insulin in pati

120 Our study shows a novel role for dapagliflozin as an inhibitor of ER stress and suggests

121 zin (25-600 ng mL(-1)) in human plasma using dapagliflozin as an internal standard (IS).

122 ndomized, placebo-controlled trial to assess dapagliflozin, as an adjunct to insulin, in youth with T

123 rience greater absolute risk reductions with dapagliflozin at 2 years: 2.1% (95% CI, -1.9% to 6.1%),

124 nsulin were randomised 1:1:1:1 to placebo or dapagliflozin at 2.5, 5 or 10 mg.

125 ng specificities for these transporters (eg, dapagliflozin, canagliflozin, and empagliflozin) can slo

126 T2, and SGLT2-specific inhibitors, including dapagliflozin, canagliflozin, and empagliflozin, increas

127 lobin A(1c) decreased by 0.79% to 0.96% with dapagliflozin compared with 0.39% with placebo (mean dif

128 of bladder and breast cancer was noted with dapagliflozin compared with control.

129 t in PAD patients, were not more common with dapagliflozin, compared with placebo, irrespective of PA

130 Dapagliflozin could benefit patients with type 2 diabete

131 Dapagliflozin (DAPA), a sodium-glucose cotransporter 2 i

132 Compared to dapagliflozin, dapagliflozin/spironolactone combination

133 Compared to dapagliflozin, dapagliflozin/spironolactone combination

134 gliflozin (CANVAS Program and CREDENCE), and dapagliflozin (DECLARE-TIMI 58).

135 Dapagliflozin decreased the incidence of reported episod

136 a sodium-glucose cotransporter 2 inhibitor (dapagliflozin), depleting neutrophils or Kupffer cells,

137 A higher proportion of patients assigned to dapagliflozin developed an initial eGFR decline greater

138 V and renal-specific composite outcomes with dapagliflozin did not significantly differ across the ra

139 DECLARE-TIMI 58 (Dapagliflozin Effect on Cardiovascular Events-Thrombolys

140 T2DM in the placebo arm of DECLARE-TIMI 58 (Dapagliflozin Effect on Cardiovascular Events-Thrombolys

141 DECLARE-TIMI 58 (Dapagliflozin Effect on Cardiovascular Events-Thrombolys

142 DEFINE-HF (Dapagliflozin Effects on Biomarkers, Symptoms and Functi

143 ents in the SGLT-2 inhibitor (canagliflozin, dapagliflozin, empagliflozin) and GLP-1 receptor agonist

144 from eight clinical trials of canagliflozin, dapagliflozin, empagliflozin, and sotagliflozin in patie

145 zin), but not to any significant extent with dapagliflozin, empagliflozin, or phlorizin.

146 (Dapagliflozin Evaluation to Improve the LIVEs of Patient

147 nts With Chronic Heart Failure) and DELIVER (Dapagliflozin Evaluation to Improve the Lives of Patient

148 ron emission tomography with 4-[(18)F]fluoro-dapagliflozin (F-Dapa).

149 Dapagliflozin (Farxiga), alone, or in the fixed dose com

150 The relative risk reductions with dapagliflozin for CV death/HHF (HR, 0.86, PAD; HR, 0.82,

151 rofile, have prompted clinical evaluation of dapagliflozin for the treatment of type 2 diabetes.

152 lumn life span and achieve the separation of dapagliflozin from potential interferences, especially i

153 event occurred in 91 patients (15.0%) in the dapagliflozin group and in 124 patients (20.1%) in the s

154 enal disease or renal death was lower in the dapagliflozin group than in the placebo group (11 [0.1%]

155 the mean decrease in eGFR was larger in the dapagliflozin group than in the placebo group.

156 ent therapy among 27 patients (10.9%) in the dapagliflozin group vs 39 (15.1%) in the control group.

157 (95% CI -2.1 to -1.8) in the exenatide plus dapagliflozin group, -1.6% (-1.8 to -1.4) in the exenati

158 atients with adverse events (79 [54%] in the dapagliflozin group, 104 [68%] in the dapagliflozin-saxa

159 (57%) of 231 patients in the exenatide plus dapagliflozin group, 124 (54%) of 230 patients in the ex

160 whom 461 were randomly assigned: 145 to the dapagliflozin group, 155 to the dapagliflozin-saxaglipti

161 up, 684 of 2371 (28.8%) patients and, in the dapagliflozin group, 527 of 2373 (22.2%) participants ex

162 group, and 121 (52%) of 233 patients in the dapagliflozin group.

163 atide group, and -1.4% (-1.6 to -1.2) in the dapagliflozin group.

164 etween groups, with one mild DKA case in the dapagliflozin group.

165 genital infections were more frequent in the dapagliflozin groups (2.5 mg, 11 patients [8%]; 5 mg, 18

166 serious adverse events (four in each of the dapagliflozin groups and five in the placebo group).

167 th the placebo group, patients in the pooled dapagliflozin groups had a higher rate of hypoglycemic e

168 These data suggest that dapagliflozin has the potential to be an efficacious tre

169 pagliflozin (HR 0.727, 95% CI 0.696, 0.759), dapagliflozin (HR 0.814, 95% CI 0.774, 0.855), and canag

170 Co-initiation of exenatide and dapagliflozin improved various glycaemic measures and ca

171 Dapagliflozin improves glycemic control, stabilizes insu

172 , neither was significantly more common with dapagliflozin in any age group.

173 ed Ejection Fraction (EMPEROR-Preserved) and Dapagliflozin in Heart Failure With Mildly Reduced or Pr

174 ectrometry (LC-MS/MS) bioanalytical assay of dapagliflozin in human plasma.

175 l pooled meta-analysis of two trials testing dapagliflozin in participants with heart failure and dif

176 We assessed the efficacy and safety of dapagliflozin in patients who have inadequate glycaemic

177 , which evaluated the efficacy and safety of dapagliflozin in patients with heart failure (HF) with r

178 e 2 inhibitors and the recent DAPA-HF trial (Dapagliflozin in Patients with Heart Failure and Reduced

179 We examined the efficacy and tolerability of dapagliflozin in relation to background diuretic treatme

180 s of renal outcomes with the SGLT2 inhibitor dapagliflozin in the DECLARE-TIMI 58 cardiovascular outc

181 cs, outcomes, and the efficacy and safety of dapagliflozin, in relation to time from diagnosis of HF

182 After inducing heart failure, dapagliflozin increased relative rates of ketone and fat

183 on in response to either 1 mmol/L glucose or dapagliflozin, indicating a functional impairment of the

184 sex, and frailty; and for canagliflozin and dapagliflozin individually.

185 h the sodium glucose transporter 2 inhibitor dapagliflozin induced production of GLP1 and IL6.

186 ) was also heterogeneous and correlated with dapagliflozin-induced glucagon secretion at 6 mmol/L glu

187 in plasma glucose concentration, and 2) the dapagliflozin-induced increase in EGP cannot be explaine

188 INTERPRETATION: Our results suggest that dapagliflozin is a promising adjunct treatment to insuli

189 Dapagliflozin is a sodium-glucose cotransporter-2 inhibi

190 r empagliflozin and m/z 407.00 to 328.81 for dapagliflozin (IS) was employed utilizing negative mode

191 SGLT2 inhibition with dapagliflozin leads to a sustained increase in haematocr

192 gliflozin 10 mg oral tablets, exenatide with dapagliflozin-matched oral placebo, or dapagliflozin wit

193 an inhibitor of ER stress and suggests that dapagliflozin might be useful for the prevention of DN.

194 abetic men were randomized to receive either dapagliflozin (n = 12) or placebo (n = 6) for 2 weeks.

195 s -21.0% (95% CI -34.1 to -5.2; p=0.011) for dapagliflozin (n=132) and -38.0% (-48.2 to -25.8; p<0.00

196 igned 695 patients to receive exenatide plus dapagliflozin (n=231), exenatide alone (n=231; n=1 untre

197 Benefits of dapagliflozin on clinically meaningful HF measures appea

198 The current study examined the effect of dapagliflozin on EGP while clamping plasma glucose, insu

199 In this study, we examined the effect of dapagliflozin on ER stress in the HK-2 proximal tubular

200 nvestigate the effect of the SGLT2 inhibitor dapagliflozin on haematocrit, red blood cell (RBC) count

201 ection Fraction)demonstrating the benefit of dapagliflozin on HF-related outcomes in patients with HF

202 The effects of empagliflozin and dapagliflozin on hospitalisations for heart failure were

203 Benefits of dapagliflozin on KCCQ-CSS were also consistent when anal

204 Additionally, we analyzed the effect of dapagliflozin on the composite of death or worsening HF

205 We explored the effect of dapagliflozin on the first and total number of AF/AFL ev

206 the DAPA-HF (Study to Evaluate the Effect of Dapagliflozin on the Incidence of Worsening Heart Failur

207 entation of oral therapy, and the effects of dapagliflozin on these additional events.

208 me to receive placebo or 2.5, 5, or 10 mg of dapagliflozin, once daily, for 48 weeks.

209 randomly assigned to receive 10 mg orally of dapagliflozin or matching placebo once daily for 48 week

210 mL/min were randomly assigned (1:1) to 10 mg dapagliflozin or placebo once daily.

211 Addition of once-daily 10 mg of dapagliflozin or placebo to guideline-recommended therap

212 atriuretic peptide levels were randomized to dapagliflozin or placebo.

213 e in diuretic therapy after randomization to dapagliflozin or placebo.

214 ailure and reduced ejection fraction, use of dapagliflozin over 12 weeks did not affect mean NT-proBN

215 18.0 (95% CI, 15.2-21.4) with corresponding dapagliflozin/placebo hazard ratios of 0.87 (95% CI, 0.6

216 e 40 mg plus dapagliflozin 10 mg (n=110), or dapagliflozin plus placebo (n=106).

217 At week 12, the difference in UACR versus dapagliflozin plus placebo was -33.7% (90% CI -42.5 to -

218 Dapagliflozin potently and selectively inhibited human S

219 Under pancreatic clamp conditions (study 3), dapagliflozin produced an initial large decrease in EGP

220 re we show that the SGLT2 inhibitor (SGLT2i) dapagliflozin promotes ketoacidosis in both healthy and

221 liraglutide, extended-release exenatide, and dapagliflozin reduced all-cause mortality.

222 In patients with previous MI (n=3584), dapagliflozin reduced the relative risk of MACE by 16% a

223 Across these subgroups, dapagliflozin reduced the relative risk of the primary o

224 Dapagliflozin reduced the risk of AF/AFL events by 19% (

225 Dapagliflozin reduced the risk of death and worsening he

226 Compared with placebo, dapagliflozin reduced the risk of the primary end point

227 the sodium-glucose cotransporter 2 inhibitor dapagliflozin reduced the risk of worsening heart failur

228 The sodium-glucose cotransporter 2 inhibitor dapagliflozin reduces the risk for hospitalization for h

229 The new type 2 diabetes drug, dapagliflozin, reduces blood glucose levels and body wei

230 st probability of benefit found was 0.90 for dapagliflozin regarding use of kidney replacement therap

231 We found that dapagliflozin regulated ER stress-mediated apoptosis in

232 were at high risk for heart-failure events, dapagliflozin resulted in a significantly lower incidenc

233 ng glucose analog uptake were used to assess dapagliflozin's ability to inhibit sodium-dependent and

234 The assay also quantifies dapagliflozin's major systemic circulating glucuronide m

235 2) and -38.0% (-48.2 to -25.8; p<0.0001) for dapagliflozin-saxagliptin (n=139).

236 HbA(1c) was reduced in the dapagliflozin-saxagliptin group (n=137) compared with th

237 pagliflozin-saxagliptin groups) and HbA(1c) (dapagliflozin-saxagliptin group) at week 24 in all rando

238 : 145 to the dapagliflozin group, 155 to the dapagliflozin-saxagliptin group, and 148 to the placebo

239 in the dapagliflozin group, 104 [68%] in the dapagliflozin-saxagliptin group, and 81 [55%] in the pla

240 nge from baseline in UACR (dapagliflozin and dapagliflozin-saxagliptin groups) and HbA(1c) (dapaglifl

241 e-4 inhibitor saxagliptin, and the effect of dapagliflozin-saxagliptin on glycaemic control in patien

242 Dapagliflozin and dapagliflozin-saxagliptin reduced UACR versus placebo th

243 Dapagliflozin seemed to prevent and reduce progression o

244 C57BL/6 mice treated with fructose or dapagliflozin showed markedly increased natriuresis afte

245 At week 24, both doses of dapagliflozin significantly reduced HbA1c compared with

246 Exenatide plus dapagliflozin significantly reduced HbA1c from baseline

247 The simulations predict that dapagliflozin slows cardiac remodeling by reducing prelo

248 ine and potassium increase was observed with dapagliflozin/spironolactone combination (SOGALDI-PEF [D

249 c peptide (NT-proBNP) difference between the dapagliflozin/spironolactone combination and dapaglifloz

250 Compared to dapagliflozin, dapagliflozin/spironolactone combination reduced LogNT-p

251 Compared to dapagliflozin, dapagliflozin/spironolactone combination reduced systoli

252 GlcNAcylated protein levels in SKO mice, and dapagliflozin successfully prevented the development of

253 ears the mean decrease in eGFR was less with dapagliflozin than with placebo.

254 rats were performed to assess the ability of dapagliflozin to improve fed and fasting plasma glucose

255 study was performed to assess the ability of dapagliflozin to improve glucose utilization after multi

256 mice exposed to fructose or a single dose of dapagliflozin to induce transient glycosuria showed incr

257 Addition of dapagliflozin to metformin provides a new therapeutic op

258 the number of patients needed to treat with dapagliflozin to prevent 1 experiencing an episode of fa

259 erse subsequent kidney composite outcomes in dapagliflozin-treated patients (aHR, 0.94; 95% CI, 0.49-

260 overall summary score or NT-proBNP, 61.5% of dapagliflozin-treated patients met this end point versus

261 correctly and non-randomly allocated to only dapagliflozin treatment groups were included in the safe

262 Dapagliflozin treatment in combination with insulin resu

263 Dapagliflozin treatment induced glucosuria and markedly

264 Once-daily dapagliflozin treatment over 2 weeks significantly lower

265 Surprisingly, following dapagliflozin treatment, EGP increased substantially and

266 reased by approximately 18% after 2 weeks of dapagliflozin treatment, while placebo-treated subjects

267 erage 6- and 12-week adjusted NT-proBNP with dapagliflozin versus placebo (1133 pg/dL (95% CI 1036-12

268 osite outcome was significantly reduced with dapagliflozin versus placebo (hazard ratio [HR] 0.76, 95

269 ecific composite outcomes were improved with dapagliflozin versus placebo across various prespecified

270 e efficacy and safety of the SGLT2 inhibitor dapagliflozin versus placebo in 17 160 patients with typ

271 ificant differences in any limb outcome with dapagliflozin versus placebo including limb ischemic adv

272 reatment effects on clinical end points with dapagliflozin versus placebo were assessed by baseline h

273 e randomized, double-blind 12-week trials of dapagliflozin versus placebo, recruiting participants wi

274 gon concentrations were 32% higher following dapagliflozin versus placebo, with a median within-parti

275 6974) or multiple risk factors (n=10 186) to dapagliflozin versus placebo.

276 ur of EGP measurement) in subjects receiving dapagliflozin was 22% greater (+0.66 +/- 0.11 mg/kg/min,

277 Among patients with HFimpEF, treatment with dapagliflozin was associated with lower rates of cardiov

278 The benefit of dapagliflozin was consistent across HF duration and on t

279 Beneficial response to dapagliflozin was consistent across prespecified subgrou

280 Exenatide plus dapagliflozin was significantly superior to either drug

281 Balcinrenone plus dapagliflozin was well tolerated, effects on potassium w

282 The C-aryl glucoside 6 (dapagliflozin) was identified as a potent and selective

283 the sodium-glucose cotransporter-2 inhibitor dapagliflozin were assessed by baseline HHF risk.

284 The benefits of dapagliflozin were consistent across HF duration.

285 The efficacy and safety of dapagliflozin were consistent across the diuretic subgro

286 cacy, and safety outcomes and treatment with dapagliflozin were evaluated in time-updated Cox proport

287 treatment with empagliflozin and 17 464 with dapagliflozin were included (median [IQR] age, 63 [54-71

288 initiators, those receiving canagliflozin or dapagliflozin were less likely to have diabetes-related

289 baseline covariates, patients randomized to dapagliflozin were more likely to experience a clinicall

290 cs associated with a >10% decline in eGFR on dapagliflozin were older age, lower eGFR, higher ejectio

291 Although relative risk reductions with dapagliflozin were similar for patients across the risk

292 m-glucose co-transporter 2 (SGLT2) inhibitor dapagliflozin, which has been shown to reduce heart fail

293 he sodium-glucose co-transporter-2 inhibitor dapagliflozin with and without the dipeptidyl peptidase-

294 Combining dapagliflozin with eplerenone resulted in a robust addit

295 or agonist exenatide and the SGLT2 inhibitor dapagliflozin with exenatide or dapagliflozin alone in p

296 with dapagliflozin-matched oral placebo, or dapagliflozin with exenatide-matched placebo injections.

297 Dapagliflozin with or without saxagliptin, given in addi

298 zin/spironolactone combination (SOGALDI-PEF [Dapagliflozin With or Without Spironolactone for HFpEF];

299 and glycaemic effects of the SGLT2 inhibitor dapagliflozin with placebo in patients with inadequately

300 SGLT2 inhibitor exposure time was for use of dapagliflozin, with 5% for empagliflozin, and 1% for can