ライフサイエンスコーパス: SGLT2 inhibitor

1 SGLT2 inhibitors also reduced end-stage kidney disease (

2 SGLT2 inhibitors are antihyperglycemic drugs that protec

3 SGLT2 inhibitors are proximal tubule and osmotic diureti

4 SGLT2 inhibitors attenuate the proximal reabsorption of

5 SGLT2 inhibitors improve glomerular hemodynamic function

6 SGLT2 inhibitors lower glomerular capillary hypertension

7 SGLT2 inhibitors may mimic systemic hypoxia and stimulat

8 SGLT2 inhibitors might modulate glucose influx into rena

9 SGLT2 inhibitors protected against the risk of major adv

10 SGLT2 inhibitors provide multiple benefits, including de

11 SGLT2 inhibitors reduced the risk of dialysis, transplan

12 SGLT2 inhibitors reverse this maladaptive signaling by t

13 SGLT2 inhibitors should be used when possible by people

14 SGLT2 inhibitors substantially reduced the risk of dialy

15 ucose with a sodium-glucose cotransporter 2 (SGLT2) inhibitor could improve insulin-mediated tissue g

16 hypoglycemic sodium-glucose cotransporter 2 (SGLT2) inhibitor dapagliflozin and the insulin sensitize

17 The sodium glucose cotransporter 2 (SGLT2) inhibitor empagliflozin promotes osmotic diuresis

18 gliflozin, a sodium-glucose cotransporter 2 (SGLT2) inhibitor, had positive cardiorenal effects in pa

19 iflozin, the sodium-glucose cotransporter 2 (SGLT2) inhibitor, on renal hemodynamics and tubular func

20 gliflozin, a sodium glucose cotransporter 2 (SGLT2) inhibitor.

21 onse to the sodium-glucose co-transporter 2 (SGLT2) inhibitor dapagliflozin, which has been shown to

22 nt with the sodium-glucose co-transporter-2 (SGLT2) inhibitor empagliflozin reduced albuminuria in pa

23 benefits of sodium-glucose cotransporter 2 (SGLT2) inhibitors and key lifestyle measures could play

24 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a new class of antidiabetic drugs.

25 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are a newer class of antihyperglycemic

26 g effects of sodium-glucose cotransporter 2 (SGLT2) inhibitors are already established, guidance is n

27 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are effective antidiabetic therapies i

28 Carbasugar sodium-glucose cotransporter 2 (SGLT2) inhibitors are highly promising drug candidates f

29 Sodium-glucose cotransporter 2 (SGLT2) inhibitors are the most recently approved class o

30 re recently, sodium-glucose cotransporter 2 (SGLT2) inhibitors have further improved disease outcomes

31 treated with sodium glucose cotransporter 2 (SGLT2) inhibitors have improved cardiovascular (CV) outc

32 Sodium-glucose cotransporter 2 (SGLT2) inhibitors improve glycaemia in patients with typ

33 s (ARBs) and sodium-glucose cotransporter 2 (SGLT2) inhibitors in adults with CKD (estimated glomerul

34 implicating sodium-glucose cotransporter 2 (SGLT2) inhibitors in glucagon secretion by pancreatic al

35 gon release, sodium-glucose cotransporter 2 (SGLT2) inhibitors induce stimulation of endogenous gluco

36 Sodium-glucose cotransporter 2 (SGLT2) inhibitors lower glycemia by enhancing urinary gl

37 mormalities, sodium glucose cotransporter 2 (SGLT2) inhibitors may improve these impairments.

38 ts with CKD, sodium-glucose cotransporter 2 (SGLT2) inhibitors provide cardiorenal protection, but wh

39 Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce the risk of hospitalization for

40 ctiveness of sodium-glucose cotransporter 2 (SGLT2) inhibitors vs sulfonylureas-the second most widel

41 Sodium/glucose cotransporter 2 (SGLT2) inhibitors were developed to lower blood glucose

42 cohorts: (1) sodium-glucose cotransporter 2 (SGLT2) inhibitors, (2) glucagon-like peptide 1 (GLP1) re

43 a) agonists, sodium glucose cotransporter 2 (SGLT2) inhibitors, and farnesoid X receptor (FXR) agonis

44 inhibitors, sodium-glucose cotransporter 2 (SGLT2) inhibitors, and sulfonylureas were created.

45 n the era of sodium-glucose cotransporter 2 (SGLT2) inhibitors, population-wide screening for chronic

46 ng ERAs with sodium-glucose cotransporter 2 (SGLT2) inhibitors, which have diuretic effects, offers a

47 ering agents-sodium-glucose cotransporter 2 (SGLT2) inhibitors-has been reported to decrease the risk

48 eported with sodium-glucose cotransporter 2 (SGLT2) inhibitors.

49 andomized to sodium-glucose cotransporter 2 (SGLT2) inhibitors.

50 117,989) or sodium-glucose cotransporter-2 (SGLT2) inhibitors (n = 258,614), a control group compose

51 ; p < 0.01), sodium-glucose cotransporter-2 (SGLT2) inhibitors (OR 0.68, 95% CI 0.58-0.79; p < 0.001)

52 es recommend sodium-glucose cotransporter-2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP1) rec

53 agonists and sodium-glucose cotransporter-2 (SGLT2) inhibitors are increasingly used as second-line a

54 2 diabetes, sodium-glucose cotransporter-2 (SGLT2) inhibitors are known to reduce glucose concentrat

55 istration of sodium-glucose cotransporter-2 (SGLT2) inhibitors could lead to ketoacidosis in patients

56 Use of sodium-glucose cotransporter-2 (SGLT2) inhibitors has been associated with Fournier gang

57 e effects of sodium-glucose cotransporter-2 (SGLT2) inhibitors may be related primarily to enhanced S

58 Sodium-glucose cotransporter-2 (SGLT2) inhibitors prevent glucose reabsorption and lower

59 own that the sodium-glucose cotransporter-2 (SGLT2) inhibitors, a newer generation of antihyperglycem

60 Sodium-glucose cotransporter-2 (SGLT2) inhibitors, including empagliflozin, dapagliflozi

61 benefit from sodium-glucose cotransporter-2 (SGLT2) inhibitors.

62 Sodium-glucose transport protein 2 (SGLT2) inhibitors are a class of anti-diabetic agents; h

63 use of the sodium-glucose co-transporter 2 (SGLT2) inhibitors dapagliflozin and empagliflozin in HFr

64 lockers and sodium-glucose co-transporter 2 (SGLT2) inhibitors.

65 rofile, the sodium-glucose co-transporter-2 (SGLT2) inhibitors empagliflozin and canagliflozin have b

66 ases (e.g., sodium-glucose co-transporter-2 (SGLT2) inhibitors for type 2 diabetes-interaction term f

67 Sodium-glucose co-transporter-2 (SGLT2) inhibitors have several beneficial effects in pat

68 Sodium-glucose co-transporter-2 (SGLT2) inhibitors have shown beneficial effects on renal

69 effects of sodium-glucose co-transporter-2 (SGLT2) inhibitors on kidney failure, particularly the ne

70 gonists and sodium-glucose co-transporter-2 (SGLT2) inhibitors reduce glycaemia and weight, and impro

71 [ARNIs], and sodium/glucose cotransporter 2 [SGLT2] inhibitors) reduce mortality in patients with hea

72 gonists, and sodium-glucose cotransporter 2 [SGLT2] inhibitors) using routinely available clinical fe

73 his analysis of U.S. data from 2022 to 2023, SGLT2 inhibitor prescription among people with a Class 1

74 P4 inhibitor (aHR, 1.36; 95% CI, 1.17-1.58), SGLT2 inhibitor (aHR, 1.14; 95% CI, 1.02-1.28), or sulfo

75 care [adjusted OR, 1.82; 95% CI, 1.14-2.91]; SGLT2 inhibitors and/or GLP-1RAs: from 12.3% to 60.4% fo

76 In addition, SGLT2 inhibitors doubled the risk for genital infections

77 As first-line agents, SGLT2 inhibitors and GLP1 receptor agonists would improv

78 Unlike other agents, SGLT2 inhibitors act on the kidney to promote urinary gl

79 Compared with other agents, SGLT2 inhibitors reduced body weight (mean difference, -

80 .0%) received an ACEI or ARB; 194 (4.6%), an SGLT2 inhibitor; and 885 (21.0%), neither therapy.

81 P-1 receptor agonist) with canagliflozin (an SGLT2 inhibitor) in patients with type 2 diabetes.

82 the efficacy and safety of canagliflozin, an SGLT2 inhibitor, with glimepiride in patients with type

83 el glucose lowering agent, empagliflozin, an SGLT2 inhibitor which targets the kidney to block glucos

84 If an SGLT2 inhibitor or GLP-1 receptor agonist is considered

85 In this cohort study, use of an SGLT2 inhibitor treatment increased among patients with

86 2 years after the FDA's first approval of an SGLT2 inhibitor, although the phenomenon had been known

87 usted HR, 0.87 [95% CI, 0.78 to 0.97]) or an SGLT2 inhibitor (adjusted HR, 0.80 [95% CI, 0.73 to 0.88

88 rate was lower among patients prescribed an SGLT2 inhibitor (4.9 events per 1000 person-years) than

89 Adults with type 2 diabetes prescribed an SGLT2 inhibitor had a lower rate of gout than those pres

90 abetes mellitus who were newly prescribed an SGLT2 inhibitor or a GLP1 agonist.

91 ons with type 2 diabetes newly prescribed an SGLT2 inhibitor were 1:1 propensity score matched to pat

92 KD and albuminuria, 21.0% did not receive an SGLT2 inhibitor or an ACEI or an ARB, despite compelling

93 onomic status were less likely to receive an SGLT2 inhibitor, suggesting that interventions to ensure

94 s; 122 096 [95.17%] men), 23 870 received an SGLT2 inhibitor and 104 423 received a sulfonylurea.

95 osis of heart failure, had never received an SGLT2 inhibitor previously, and were newly started on em

96 th metformin alone or in combination with an SGLT2 inhibitor for at least 3 months before screening.

97 atients with type 2 diabetes treated with an SGLT2 inhibitor increased from 3.8% to 11.9%.

98 2) or higher on metformin with or without an SGLT2 inhibitor were randomly assigned (1:1:1) to once-w

99 In this meta-analysis, SGLT2 inhibitors were associated with a reduced risk of

100 ation use of an ARNI, beta blocker, MRA, and SGLT2 inhibitor as a new therapeutic standard.

101 ogical therapy (ARNI, beta blocker, MRA, and SGLT2 inhibitor) versus conventional therapy (ACE inhibi

102 P-4 inhibitors, GLP-1 receptor agonists, and SGLT2 inhibitors, respectively.

103 with established, cardiovascular disease and SGLT2 inhibitors considered for patients with heart fail

104 n HF With Preserved Ejection Fraction]), and SGLT2 inhibitors (DAPA-HF [Dapagliflozin and Prevention

105 nitiating sulfonylureas, DPP4 inhibitors and SGLT2 inhibitors (n = 536,068), and a control group of 1

106 ril 1, 2022, and March 31, 2023, we assessed SGLT2 inhibitor prescription rates, stratified by presen

107 tes mellitus and chronic heart failure), but SGLT2 inhibitors activate SIRT1/PGC-1alpha/FGF21 signali

108 ide decrease in environmental nutrients, but SGLT2 inhibitors may also upregulate SIRT1, PGC-1alpha,

109 scular events without effect modification by SGLT2 inhibitor use (HR: 0.77; 95% CI: 0.68-0.87 without

110 ketogenic nutrient deprivation signaling by SGLT2 inhibitors may explain their cardioprotective effe

111 ynthetic route towards some novel carbasugar SGLT2 inhibitors, featuring an underexploited, regiosele

112 he way towards the development of carbasugar SGLT2 inhibitors as potential antidiabetic/antitumor age

113 However, the clinical usage of carbasugar SGLT2 inhibitors has been underexplored, due to the leng

114 ealed the unexpected SAR of these carbasugar SGLT2 inhibitors, and enabled the discovery of a highly

115 rm long-term efficacy and safety of combined SGLT2 inhibitor and MRA treatment.

116 xamine the safety and efficacy of continuing SGLT2 inhibitors in HF when the estimated glomerular fil

117 inuric CKD with and without type 2 diabetes, SGLT2 inhibitors facilitate the use of RAS blockade.

118 ar outcome trials in patients with diabetes, SGLT2 inhibitors improve cardiovascular and renal outcom

119 ts), which provided data for seven different SGLT2 inhibitors.

120 In patients with chronic kidney disease, SGLT2 inhibitors and endothelin A receptor antagonists (

121 Each SGLT2 inhibitor user was matched with three users of oth

122 al cohort study with target trial emulation, SGLT2 inhibitors were associated with a decreased risk o

123 Among people with heart failure, SGLT2 inhibitors reduce hospitalizations for heart failu

124 In patients with heart failure, SGLT2 inhibitors will likely be coprescribed with a loop

125 Finally, SGLT2 inhibitors have been shown to reduce myofilament s

126 The first SGLT2 inhibitors have been approved as a new class of an

127 the crucial role for selecting patients for SGLT2 inhibitor therapy and highlight several crucial qu

128 etes, 6.2% had a Class 1a recommendation for SGLT2 inhibitor therapy, and 3.1% (3.0%-3.2%) of those r

129 tes, 63.4% had a Class 1a recommendation for SGLT2 inhibitor therapy.

130 For SGLT2 inhibitors and GLP1 receptor agonists, there was a

131 summarizes proposed mechanisms of action for SGLT2 inhibitors, integrates these data with results of

132 Changes in hematological parameters for SGLT2 inhibitors and GLP-1 RAs throughout the 3-year fol

133 ndividuals with an incident prescription for SGLT2 inhibitors or GLP-1 RAs were included, with the fi

134 t a concise synthetic approach to gliflozin (SGLT2 inhibitors) aglycones from generating regioselecti

135 ta-analysis of patients hospitalized for HF, SGLT2 inhibitors reduced the early risk of cardiovascula

136 d lower proportions with Medicare had higher SGLT2 inhibitor prescription rates.

137 However, SGLT2 inhibitors do not alter regional tissue oxygen ten

138 However, SGLT2 inhibitors in clinical development inhibit only 30

139 ure and diabetic glomerular hyperfiltration, SGLT2 inhibitors may induce protective effects on the ki

140 If SGLT2 inhibitors protect the kidneys by reducing albumin

141 scontinuation, defined as an interruption in SGLT2 inhibitor or GLP-1 RA prescription for >=90 days,

142 Recent developments include SGLT2 inhibitors, vericiguat, and transcatheter mitral v

143 s with acceptable safety profiles, including SGLT2 inhibitors, endothelin receptor blockers, targeted

144 During this period, the use of open-label SGLT2 inhibitors was similar in the two groups (43% in t

145 First-line SGLT2 inhibitors and GLP1 receptor agonists had lower li

146 First-line SGLT2 inhibitors cost $43 000 more and added 1.8 quality

147 First-line SGLT2 inhibitors or GLP1 receptor agonists.

148 In summary, the glucose-lowering SGLT2 inhibitor empagliflozin, used for type 2 diabetes,

149 s may not be limited to diabetes management: SGLT2 inhibitors have also shown therapeutic promise in

150 Matched SGLT2 inhibitor (n=22 830) and other glucose-lowering dr

151 ecause of their unique glycosuric mechanism, SGLT2 inhibitors also reduce weight.

152 ucose-dependent and -independent mechanisms: SGLT2 inhibitors prevent both hyper- and hypoglycemia, w

153 synthetic route towards some small-molecule SGLT2 inhibitors by a chemo- and diastereospecific palla

154 Moreover, SGLT2 inhibitor therapy induces serious adverse events,

155 Our aim was to study the effects of SGLT2 inhibitor on circulating ZAG and ADI in nT2DM.

156 duced cardiovascular events independently of SGLT2 inhibitor use.

157 ardiovascular or kidney disease, the rate of SGLT2 inhibitor use increased but was lower than that am

158 50 000) was associated with a higher rate of SGLT2 inhibitor use.

159 82-0.85) were associated with lower rates of SGLT2 inhibitor use, whereas higher median household inc

160 ceptor agonists are consistent regardless of SGLT2 inhibitor use.

161 artiles of OOP costs for a 1-month supply of SGLT2 inhibitor and GLP-1 RA based on their health plan

162 Alternatively, the established ability of SGLT2 inhibitors to enhance SIRT1 might be the mechanism

163 ipal statistical mediators of the ability of SGLT2 inhibitors to reduce the risk of heart failure and

164 uest to determine the mechanism of action of SGLT2 inhibitors is ongoing, this therapeutic class of d

165 responses can be explained by the action of SGLT2 inhibitors to promote cellular housekeeping by enh

166 tentially indicative of a diuretic action of SGLT2 inhibitors) did not track each other closely in th

167 fraction may be mitigated by the actions of SGLT2 inhibitors to reduce blood pressure, body weight,

168 ute importantly to the consistent benefit of SGLT2 inhibitors to slow the deterioration in glomerular

169 or metabolism cannot explain the benefits of SGLT2 inhibitors either experimentally or clinically.

170 The benefits of SGLT2 inhibitors in heart failure may be mediated by the

171 of the potential cardiovascular benefits of SGLT2 inhibitors.

172 Discontinuation of SGLT2 inhibitors and GLP-1 RA was associated with recent

173 However, maximal doses of SGLT2 inhibitors fail to inhibit >50% of the filtered gl

174 ome evidence that the proportional effect of SGLT2 inhibitors might attenuate with declining kidney f

175 y physiology predicts the salutary effect of SGLT2 inhibitors on hard renal outcomes, as shown in lar

176 Observations: The beneficial effect of SGLT2 inhibitors on heart failure cannot be explained by

177 Effect of SGLT2 inhibitors on heart failure outcomes and cardiovas

178 dy used male SS rats only, and the effect of SGLT2 inhibitors on hypertension in females has not been

179 Effectiveness of SGLT2 inhibitors was derived from the Dapagliflozin and

180 way, sodium-related physiological effects of SGLT2 inhibitors and clinical correlates of natriuresis,

181 hanism underlying the cardiorenal effects of SGLT2 inhibitors and summarizes clinical trial evidence

182 summarize the key pharmacodynamic effects of SGLT2 inhibitors and the clinical evidence that support

183 studies that have shown that the effects of SGLT2 inhibitors are likely related to actions on the he

184 ociated ketosis and the ketogenic effects of SGLT2 inhibitors occur almost entirely independent of gl

185 We aimed to establish the effects of SGLT2 inhibitors on cardiovascular events, death, and sa

186 large-scale trials assessing the effects of SGLT2 inhibitors on cardiovascular outcomes in patients

187 w and meta-analysis to assess the effects of SGLT2 inhibitors on major kidney outcomes in patients wi

188 ponsible for the cardioprotective effects of SGLT2 inhibitors remain incompletely understood.

189 a signaling; this can explain the effects of SGLT2 inhibitors to promote ketonemia and erythrocytosis

190 organ-specific anti-inflammatory effects of SGLT2 inhibitors using evidence from animal and human st

191 ach of the beneficial and harmful effects of SGLT2 inhibitors-with the exception of their effect to l

192 However, the safety and efficacy of SGLT2 inhibitors when initiated soon after an episode of

193 iven to the balance of benefits and harms of SGLT2 inhibitors and risk mitigation strategies.

194 f randomized trials evaluating initiation of SGLT2 inhibitors in patients hospitalized for HF was per

195 data suggests that in-hospital initiation of SGLT2 inhibitors may reduce the early risk of cardiovasc

196 ut not Sglt2-knockout mice, and injection of SGLT2 inhibitors prevented this binding.

197 r government regulators nor manufacturers of SGLT2 inhibitors evinced an awareness of this extensive

198 Additional mechanisms of SGLT2 inhibitors that might be beneficial include a redu

199 estions about the risk-to-benefit profile of SGLT2 inhibitors when used as adjunctive therapy in pati

200 rmacokinetic and pharmacodynamic profiles of SGLT2 inhibitors in clinical trials and examine possible

201 These data suggest net protection of SGLT2 inhibitors against cardiovascular outcomes and dea

202 Important risks of SGLT2 inhibitors include euglycemic ketoacidosis, genita

203 1.73 m(2) To clarify and support the role of SGLT2 inhibitors for treatment of T2DM and CKD, the Nati

204 en done to assess the efficacy and safety of SGLT2 inhibitors in combination with insulin therapy in

205 ls designed to demonstrate the CVD safety of SGLT2 inhibitors in type 2 diabetes mellitus (T2DM), con

206 accounts for the high kidney specificity of SGLT2 inhibitors.

207 Preclinical studies and clinical trials of SGLT2 inhibitors have consistently demonstrated reductio

208 -controlled CV and kidney outcomes trials of SGLT2 inhibitors in patients with type 2 diabetes were i

209 , cardiovascular or kidney outcome trials of SGLT2 inhibitors that reported effects on major kidney o

210 total of 23 870 individuals with new use of SGLT2 inhibitors and 104 423 individuals with new use of

211 ntify significant differences between use of SGLT2 inhibitors and use of other glucose-lowering drugs

212 uing evidence gap for considering the use of SGLT2 inhibitors early following an acute MI to reduce c

213 idence and safety data related to the use of SGLT2 inhibitors for cardiovascular and renal protection

214 ce that support the rationale for the use of SGLT2 inhibitors in patients with HF who have T2D.

215 rong rationale to expect benefit from use of SGLT2 inhibitors in patients with type 2 diabetes at hig

216 e substantive evidence supporting the use of SGLT2 inhibitors to prevent major kidney outcomes in peo

217 ment of Veterans Affairs compared the use of SGLT2 inhibitors vs sulfonylureas in individuals receivi

218 ed with other glucose-lowering drugs, use of SGLT2 inhibitors was associated with a decreased risk of

219 In per-protocol analyses, continued use of SGLT2 inhibitors was associated with a reduced risk of d

220 ed with other glucose-lowering drugs, use of SGLT2 inhibitors was associated with decreased risk of c

221 onal per-protocol analyses, continued use of SGLT2 inhibitors with metformin was associated with a re

222 Patients were divided into new users of SGLT2 inhibitors and new users of other glucose-lowering

223 ular mortality and morbidity in new users of SGLT2 inhibitors versus new users of other glucose-lower

224 tify other possible mechanisms of benefit of SGLT2-inhibitor therapy.

225 Time to onset after initiation of SGLT2-inhibitor therapy ranged from 5 days to 49 months.

226 Rather, patients on SGLT2 inhibitor therapy adjust to the reduction in energ

227 onsistent with data from clinical studies on SGLT2 inhibitors and provide a rationale for the mode of

228 iven by findings for empagliflozin (the only SGLT2 inhibitor for which data from a dedicated long-ter

229 nd 20% less likely to initiate a GLP-1 RA or SGLT2 inhibitor, respectively, when compared with those

230 ey disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo.

231 of canagliflozin therapy compared with other SGLT2 inhibitors.

232 t of the five trials of 21 947 participants, SGLT2 inhibitors reduced the risk of composite cardiovas

233 In particular, SGLT2 inhibitors lower risk of congestive heart failure,

234 Compared with placebo, SGLT2 inhibitors reduced the risk of first HFH/CV death

235 e discovery of a highly selective and potent SGLT2 inhibitor.

236 discovery of two highly selective and potent SGLT2 inhibitors, thereby paving the way towards the dev

237 kely than White individuals to be prescribed SGLT2 inhibitors (OR 0.50, 95% CI 0.39-0.65; p < 0.001)

238 icipants from DELIVER and EMPEROR-Preserved, SGLT2 inhibitors reduced composite cardiovascular death

239 tes and a broad cardiovascular risk profile, SGLT2 inhibitor use was associated with reduced cardiova

240 rticipants with type 2 diabetes who received SGLT2 inhibitors.

241 10 038 and 1077 T2D patients newly receiving SGLT2 inhibitors (mean [SD] age, 59.5 [12.1] years; 5689

242 o identify patients with T2D newly receiving SGLT2 inhibitors or glucagonlike peptide-1 receptor agon

243 effects in those receiving and not receiving SGLT2 inhibitors at baseline (HR, 0.77 [95% CI, 0.54-1.0

244 55 unique cases of FG in patients receiving SGLT2 inhibitors between 1 March 2013 and 31 January 201

245 w-up period of 2.5 years, patients receiving SGLT2 inhibitors had lower incidence of composite anemia

246 for genital infection in patients receiving SGLT2 inhibitors.

247 ntified safety concern in patients receiving SGLT2 inhibitors.

248 nately, these benefits are not without risk: SGLT2 inhibitors predispose to euglycemic ketoacidosis i

249 We treated db/db mice with a selective SGLT2 inhibitor JNJ 39933673.

250 ecursors was synthesized and tested as SGLT1/SGLT2 inhibitors using a cell-based fluorescence assay o

251 the current knowledge on the use of SGLT2is (SGLT2 inhibitors) in pulmonary hypertension.

252 In dedicated kidney outcome studies, SGLT2 inhibitors reduced the incidence of kidney failure

253 Compared with sulfonylureas, SGLT2 inhibitors were associated with a reduced risk of

254 Compared with sulfonylureas, SGLT2 inhibitors were associated with reduced risk of al

255 These data indicate that SGLT2 inhibitor elicits direct tubular effects in non-di

256 ge pancreatic and prostate cancers, and that SGLT2 inhibitors, currently in use for treating diabetes

257 tudies in people with T2DM demonstrated that SGLT2 inhibitors reduce cardiovascular death and hospita

258 e adenocarcinomas, and provide evidence that SGLT2 inhibitors block glucose uptake and reduce tumor g

259 nical practice guidelines now recommend that SGLT2 inhibitors with proven cardiovascular benefit be p

260 Clinical studies have also shown that SGLT2 inhibitors promote gluconeogenesis, ketogenesis, a

261 herapeutic SGLT2 inhibition, we suggest that SGLT2 inhibitors induce aestivation-like metabolic patte

262 age x treatment interactions suggested that SGLT2 inhibitors were more cardioprotective in older tha

263 clusion, we provide evidence suggesting that SGLT2 inhibitors may offer renal protection and did not

264 the GLP-1 receptor agonist exenatide and the SGLT2 inhibitor dapagliflozin with exenatide or dapaglif

265 Here, we investigate the effect of the SGLT2 inhibitor dapagliflozin on haematocrit, red blood

266 n 58) studied the efficacy and safety of the SGLT2 inhibitor dapagliflozin versus placebo in 17 160 p

267 blood pressure and glycaemic effects of the SGLT2 inhibitor dapagliflozin with placebo in patients w

268 thod is demonstrated by the synthesis of the SGLT2 inhibitor, canagliflozin (1a), from commercially a

269 hod was demonstrated by the synthesis of the SGLT2 inhibitor, canagliflozin.

270 Here we show that the SGLT2 inhibitor (SGLT2i) dapagliflozin promotes ketoacid

271 betic HF rats tested the hypothesis that the SGLT2 inhibitor empagliflozin (EMPA) inhibits proximal t

272 Acutely, indirect NHE3 inhibition using the SGLT2 inhibitor empagliflozin did not affect urinary cal

273 FpEF (NCT03030235), we evaluated whether the SGLT2 inhibitor dapagliflozin improves the primary endpo

274 The mechanisms by which the SGLT2 inhibitor empagliflozin increases LDL cholesterol

275 pe 1 diabetes (n = 22) were treated with the SGLT2 inhibitor dapagliflozin (5 mg daily) or placebo fo

276 e report analyses of renal outcomes with the SGLT2 inhibitor dapagliflozin in the DECLARE-TIMI 58 car

277 zibotentan alone and in combination with the SGLT2 inhibitor dapagliflozin.

278 ing the GLP1 receptor agonist group with the SGLT2 inhibitor group, the hazard ratio for thyroid canc

279 type 2 diabetes receiving metformin therapy, SGLT2 inhibitor treatment was associated with a reduced

280 met our inclusion criteria, assessing three SGLT2 inhibitors: empagliflozin (EMPA-REG OUTCOME), cana

281 , 0.57-0.98]) also did not vary according to SGLT2 inhibitor use (P-heterogeneity=0.53 and 0.94, resp

282 the treatment effect estimates according to SGLT2 inhibitor use.

283 o interindividual differences in response to SGLT2 inhibitors.

284 ecretion by human alpha-cells in response to SGLT2 inhibitors.

285 94% of the total SGLT2 inhibitor exposure time was for use of dapaglifloz

286 d 13,538 patients, of whom 1,193 (8.8%) used SGLT2 inhibitors.

287 t of SGLT2 to prevent renal glucose wasting, SGLT2 inhibitors have been developed to treat diabetes a

288 We therefore investigated whether SGLT2 inhibitors could also reduce the risk of AF/AFL.

289 produced, it is important to understand why SGLT2 inhibitors inhibit <50% of the filtered glucose lo

290 advanced CKD stage were also associated with SGLT2 inhibitor discontinuation.

291 d with a reduced risk of death compared with SGLT2 inhibitor treatment without metformin.

292 bitors; and HR: 0.78; 95% CI: 0.49-1.24 with SGLT2 inhibitors) (P for interaction = 0.95) and reduced

293 nital tract infections were more common with SGLT2 inhibitors (odds ratios, 1.42 [CI, 1.06 to 1.90] a

294 e on the cardiorenal protective effects with SGLT2 inhibitors and GLP-1 receptor agonists in patients

295 cose lowering with DPP4 inhibitors than with SGLT2 inhibitors.

296 Treatment with SGLT2 inhibitors is distinguished by 2 intriguing featur

297 clinical trials, large clinical trials with SGLT2 inhibitors are now investigating the potential use

298 f ongoing cardiovascular outcome trials with SGLT2 inhibitors.

299 tor use (HR: 0.77; 95% CI: 0.68-0.87 without SGLT2 inhibitors; and HR: 0.78; 95% CI: 0.49-1.24 with S

300 emia due to chronic kidney disease, and yet, SGLT2 inhibitors produce an unattenuated erythrocytic re