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1 tion-to-treat analysis (450 liraglutide, 461 exenatide).
2 tion-to-treat analysis (450 liraglutide, 461 exenatide).
3 (semaglutide), and EXSCEL (extended-release exenatide).
4 -1R agonists (liraglutide, lixisenatide, and exenatide).
5 in systolic blood pressure was observed with exenatide.
6 sensor in the porto-hepatic circulation with exenatide.
7 ht and body mass index than those not taking exenatide.
8 ced risks were predicted for weight loss and exenatide.
9 raglutide, semaglutide, and extended-release exenatide.
11 male Sprague Dawley rats were injected with exenatide (0.1, 0.5, 5 and 10 microg/kg) or saline intra
13 mia less frequent with liraglutide than with exenatide (1.93 vs 2.60 events per patient per year; rat
14 ced mean HbA(1c) significantly more than did exenatide (-1.12% [SE 0.08] vs -0.79% [0.08]; estimated
15 ed mean fasting plasma glucose more than did exenatide (-1.61 mmol/L [SE 0.20] vs -0.60 mmol/L [0.20]
16 nal liraglutide 1.8 mg once a day (n=233) or exenatide 10 microg twice a day (n=231) in a 26-week ope
17 bA1c 5.76%) were assigned (1:1) to diet with exenatide 10 mug twice daily treatment (n = 15) or witho
18 equence interactive voice-response system to exenatide, 10 microg twice daily, or placebo for 30 week
20 y approximately 20% (saline 13.2 +/- 1.9 vs. exenatide 15.6 +/- 2.1 mg x kg(-1) x min(-1), P < 0.05)
21 d in the intention-to-treat analysis (160 on exenatide, 166 on sitagliptin, and 165 on pioglitazone).
22 atients were assigned to receive once weekly exenatide, 172 to receive sitagliptin, and 172 to receiv
23 web-response system, to receive once-weekly exenatide 2 mg by subcutaneous injection plus once-daily
24 e and study site to receive extended-release exenatide 2 mg by subcutaneous pen injection once per we
25 (1:1) to receive subcutaneous injections of exenatide 2 mg or placebo once weekly for 48 weeks in ad
26 Lowering) assessed the impact of once-weekly exenatide 2 mg versus placebo in patients with type 2 di
27 (1:1) to receive subcutaneous injections of exenatide 2 mg weekly for 48 weeks, or as controls, foll
28 espite hyperglycemia (saline 2.9 +/- 0.6 vs. exenatide 2.3 +/- 0.3 mg x kg(-1) x min(-1), P = 0.29).
29 ntry and concomitant therapy) to once-weekly exenatide (2 mg subcutaneous injection) or once-daily gl
33 ucose infusion rate (saline 15.9 +/- 1.6 vs. exenatide 20.4 +/- 2.1 mg x kg(-1) x min(-1), P < 0.001)
36 ticipants, more frequently with placebo than exenatide (38.1% versus 28.8%), with metformin (6.1% ver
37 mg/dL, and 2-h glucose of 177 +/- 11 mg/dL, exenatide (5 mug) or placebo was injected in double-blin
38 ts with type 2 diabetes received intravenous exenatide (7.5 mug) or saline (-30 to 240 min) in a doub
40 EXSCEL evaluated the effects of once-weekly exenatide (a GLP-1 [glucagon-like peptide-1] receptor ag
41 etrant, pegylated, longer-lasting version of exenatide (a glucagon-like peptide-1 receptor agonist) t
42 , double-blind trial to assess the effect of exenatide, a GLP-1 receptor agonist, on intracranial pre
43 essed the safety and efficacy of once weekly exenatide, a glucagon-like peptide 1 receptor agonist, v
46 tion, whether the cardioprotective effect of exenatide, a glucose-lowering drug, is dependent on hype
48 formulations with and without encapsulating exenatide, a pH-labile peptide that is known to be unsta
54 intention-to-treat analysis indicating that exenatide, administered once weekly, was noninferior to
59 HbA1c from baseline to week 28 compared with exenatide alone (-0.4% [95% CI -0.6 to -0.1]; p=0.004) o
60 eceive exenatide plus dapagliflozin (n=231), exenatide alone (n=231; n=1 untreated), or dapagliflozin
66 The HbA(c) level decreased by 1.74% with exenatide and 1.04% with placebo (between-group differen
69 -0.4% [95% CI, -0.7% to -0.2%]), once-weekly exenatide and albiglutide for fasting plasma glucose (-0
73 Glucagon-like peptide-1 receptor agonists exenatide and liraglutide have been shown to improve gly
74 reated for 1 year with GLP-1R agonists, both exenatide and liraglutide increased energy expenditure.
78 gon-like peptide-1 receptor (GLP-1R) agonist exenatide and the calcitonin gene-related peptide recept
79 co-initiation of the GLP-1 receptor agonist exenatide and the SGLT2 inhibitor dapagliflozin with exe
81 empagliflozin, liraglutide, extended-release exenatide, and dapagliflozin reduced all-cause mortality
82 ma glucose; taspoglutide, 20 mg, once-weekly exenatide, and dulaglutide, 1.5 mg, reduced body weight.
83 y GLP-1RAs, dulaglutide, 1.5 mg; once-weekly exenatide; and taspoglutide, 20 mg, showed a greater red
85 orted among patients who took sitagliptin or exenatide as compared with other therapies (P<.008, P<9x
86 nts for insulin resistance (pioglitazone and exenatide) as possible disease modifying drugs in Parkin
87 ents were fewer, and transit was slower with exenatide, as were the areas under the curves for serum
88 subcutaneous injections of extended-release exenatide at a dose of 2 mg or matching placebo once wee
90 by right censoring, but the favorable HR for exenatide became nominally significant in the sulfonylur
92 rst, generated steady-state plasma levels of Exenatide, but with PT320 producing continuous therapeut
95 he glucagon-like peptide-1 receptor agonist, exenatide (Byetta, Amylin Pharmaceuticals, CA) has prope
100 uated from the area under the time-dependent Exenatide concentration curve, was similar for equivalen
101 cal utility is illustrated by a PEG hydrogel-exenatide conjugate that should allow once-a-month admin
102 stablish whether the GLP-1 receptor agonist, exenatide, could slow the rate of progression of Parkins
106 ated to liraglutide and 12 (3%) allocated to exenatide discontinued participation because of adverse
108 Furthermore, the GLP-1 receptor agonist, Exenatide, dose-dependently enhanced phosphorylation of
109 efficacy of an infusion of the GLP-1 agonist exenatide during and after open-heart surgery in reducin
111 als with induced periodontitis that received exenatide (EG); 2) animals with induced periodontitis th
112 Incubation with GLP-1 and the GLP-1R agonist exenatide elicited a cAMP response in MEG-01 cells, and
117 Thus, we evaluated the acute effects of exenatide (EX) on hepatic (Hep-IR) and adipose (Adipo-IR
119 s study, we aimed to evaluate the effects of exenatide (EXE) treatment on exocrine pancreas of nonhum
120 In this study, we investigated the effect of exenatide (EXE), a glucagon-like peptide (GLP)-1 recepto
121 raftment and long-term graft function of SI, exenatide (EXN) and etanercept treatment at islet infusi
122 a profile of PT320, a sustained-release (SR)-Exenatide formulation under clinical development for tre
124 ents initiating liraglutide, dulaglutide, or exenatide from January 1, 2015, to December 31, 2021, an
125 ptin and the glucagon-like peptide-1 mimetic exenatide, from 2004-2009; data on adverse events associ
126 of this study is to evaluate the effects of exenatide (GLP-1 agonist) and sitagliptin (DPP-4 inhibit
128 with saline (-14.0-[-16.7]%) to -16.6% with exenatide:glucagon (-14.1-[-17.6]%), n = 8, z=-1.54, r=-
129 f 0.9% saline, glucagon (12.5 ng/kg/min) and exenatide:glucagon co-infusion (exenatide loading dose 5
131 umol/g/min (5.4-98 x 10(-3) umol/g/min) with exenatide:glucagon, n = 8, z = 2.24, r = 0.79, P < 0.05.
132 -1.48%, SE 0.05; n=386) than in those in the exenatide group (-1.28%, 0.05; 390) with the treatment d
133 s who reported serious adverse events in the exenatide group (36 patients [15%]) was the same as that
134 x; 2.5-8.3 years), 170 (24%) patients in the exenatide group and 165 (24%) patients experienced a pri
135 primary analysis included 31 patients in the exenatide group and 29 patients in the placebo group.
137 interval [CI] = 3.0 to 9.3, SD = 6.9) in the exenatide group and by 13 3 points (95% CI = 9.2 to 17.3
138 .4%; 3.7 events per 100 person-years) in the exenatide group and in 905 of 7396 patients (12.2%; 4.0
139 Six serious adverse events occurred in the exenatide group and two in the placebo group, although n
140 [4%]), which occurred less frequently in the exenatide group and with decreasing incidence over time
141 ed by 1.0 points (95% CI -2.6 to 0.7) in the exenatide group and worsened by 2.1 points (-0.6 to 4.8)
143 ocardial area at risk the data points of the exenatide group lay significantly lower than for the pla
145 ean HbA1c change was -1.01% (SE 0.07) in the exenatide group versus -0.81% (0.07) in the glargine gro
146 irst, plus recurrent, HHF was reduced in the exenatide group versus placebo (HR, 0.82 [95% CI, 0.68-0
147 ] in the liraglutide group vs 43 [9%] in the exenatide group), diarrhoea (59 [13%] vs 28 [6%]), and v
148 gliflozin group, -1.6% (-1.8 to -1.4) in the exenatide group, and -1.4% (-1.6 to -1.2) in the dapagli
149 ozin group, 124 (54%) of 230 patients in the exenatide group, and 121 (52%) of 233 patients in the da
150 ed) by a mean of 5.7 points (SD 11.2) in the exenatide group, and by 4.5 points (SD 11.4) points in t
153 TEN to the exenatide peptide should increase exenatide half-life in humans from 2.4 h to a projected
154 raglutide), SUSTAIN-6 (semaglutide), EXSCEL (exenatide), Harmony Outcomes (albiglutide), REWIND (dula
156 7; 95% CI: 0.79-1.19), or liraglutide versus exenatide (HR: 1.08; 95% CI: 0.83-1.38), nor were differ
158 old half-life extension of the 39-aa peptide exenatide in rats, and a noncirculating s.c. hydrogel co
160 analysis study was to evaluate the effect of exenatide in relation to system delay, defined as time f
162 e safety, efficacy, and metabolic effects of exenatide in subjects with type 1 diabetes mellitus and
163 nt studies have been published on the use of exenatide in the management of pediatric obesity and new
171 , reducing hyperinsulinemia to basal levels, exenatide-increased total glucose turnover was completel
172 ury model, a single intravenous injection of exenatide inhibited thrombus formation in normoglycemic
173 ke peptide (GLP-1) and its receptor agonist, Exenatide, inhibited palmitate-mediated caspase 3 activa
175 n, pretreatment with exendin (9-39) prior to exenatide injection blocked the activation in both locat
176 ), randomly assigned to receive subcutaneous exenatide injection for 12 months or to act as controls.
184 1 (GLP-1) receptor via the antidiabetic drug exenatide led to improvements in both ERK and AKT signal
185 Both once daily liraglutide and once weekly exenatide led to improvements in glycaemic control, with
186 Both once daily liraglutide and once weekly exenatide led to improvements in glycaemic control, with
187 with PT320 producing continuous therapeutic Exenatide levels and more rapidly reaching a steady-stat
188 , reached and maintained steady-state plasma Exenatide levels more rapidly, without dipping to a sub-
189 c exposure increased across PT320 doses, and Exenatide levels were maintained above the therapeutic t
192 /kg/min) and exenatide:glucagon co-infusion (exenatide loading dose 50 ng/min for 30 min then 25 ng/m
197 Only 4 drugs (brain natriuretic peptide, exenatide, metoprolol, and esmolol) stand unchallenged t
198 paring patients who initiated treatment with exenatide (n = 14 076, median follow-up 969 days; interq
201 kidney 293 cells and studied the effects of exenatide on action potential (AP) and other cardiac ion
202 effects of a single injection of the GLP-1RA exenatide on cerebral and peripheral glucose metabolism
203 ng system was used to explore the effects of exenatide on electrical properties and AF activity in is
204 lamp technique to investigate the effects of exenatide on hKv1.5 and hNav1.5 channels expressed in hu
205 tudy determined the effect of GLP-1R agonist exenatide on postprandial EF in type 2 diabetes and the
206 randomly assigned to receive: 2 mg injected exenatide once weekly plus oral placebo once daily; 100
210 e and the SGLT2 inhibitor dapagliflozin with exenatide or dapagliflozin alone in patients with type 2
212 ients were randomized to receive intravenous exenatide or placebo before percutaneous coronary interv
214 e intervention was an infusion of 17.4 ug of exenatide or placebo during cardiopulmonary bypass and t
215 s with type 2 diabetes received subcutaneous exenatide or placebo for 11 days and EF, and glucose and
219 caling suggests that a fusion of XTEN to the exenatide peptide should increase exenatide half-life in
220 we randomly assigned 695 patients to receive exenatide plus dapagliflozin (n=231), exenatide alone (n
221 HbA1c was -2.0% (95% CI -2.1 to -1.8) in the exenatide plus dapagliflozin group, -1.6% (-1.8 to -1.4)
222 recorded in 131 (57%) of 231 patients in the exenatide plus dapagliflozin group, 124 (54%) of 230 pat
225 concentrations of cAMP produced by GLP-1 and Exenatide preferentially activate the PKA pathway, where
227 With hyperinsulinemia and hyperglycemia, exenatide produced a significant increase in total gluco
231 ing medications, and HbA(c) levels, and more exenatide recipients than placebo recipients withdrew be
237 of this work is to test the hypothesis that exenatide reduces food intake and activates the enteric
238 ing glucagon-like peptide 1 receptor agonist exenatide reduces postprandial glycemia, partly by slowi
243 delay </=132 minutes (n=74), treatment with exenatide resulted in a smaller infarct size (9 grams [i
247 -1 RAs were used (lixisenatide, liraglutide, exenatide, semaglutide, efpeglenatide, dulaglutide, albi
249 licited a cAMP response in MEG-01 cells, and exenatide significantly inhibited thrombin-, ADP-, and c
250 suppressed lipolysis equal to baseline, but exenatide significantly lowered free fatty acid clearanc
252 secondary peak at 5 days, and achievement of Exenatide steady-state plasma levels from day 10-28.
253 ducing systemic hyperglycemia to euglycemia, exenatide still increased total glucose turnover by appr
255 ment with the glucagon-like peptide-1 analog exenatide, streptozotocin injection, partial pancreatect
257 for heart failure (HHF) in the EXSCEL study (Exenatide Study of Cardiovascular Event Lowering), with
259 reversed the protective effects of GLP-1 and Exenatide, suggesting that PKA may play a role in the pr
260 -1 receptor agonists were more frequent with exenatide than glargine (nausea: 36 [15%] of 233 patient
262 lin concentrations were initially lower with exenatide than with saline and subsequently higher.
263 n, RNase H that actively hydrolyzed RNA, and exenatide that is a commercial therapeutic peptide.
268 e combination of electrostatic adsorption of exenatide to the membrane surface and its self-associati
269 effects of adding once-weekly treatment with exenatide to usual care in patients with type 2 diabetes
275 r improvements in glycaemic control than did exenatide twice a day, and was generally better tolerate
277 [HR]) of composite treatment for DME or PDR: exenatide versus dulaglutide (HR 0.90; 95% confidence in
280 with rates of MACE, LEA, and the effects of exenatide versus placebo in patients with and without PA
281 literature-derived risk reductions, but the exenatide versus placebo MACE effect size and statistica
283 re -0.6% (95% CI -0.9 to -0.4, p<0.0001) for exenatide versus sitagliptin, and -0.3% (-0.6 to -0.1, p
287 -down ECD experiment showed that the Asp9 in exenatide was converted to isoAsp9 to form the unknown i
289 hours after admission in patients receiving exenatide was lower than that in patients receiving plac
294 once-daily dapagliflozin 10 mg oral tablets, exenatide with dapagliflozin-matched oral placebo, or da
295 les enabled the oral delivery of insulin and exenatide, with 10 U kg(-1) orally delivered insulin sus
296 administration of the GLP-1 receptor agonist exenatide, with or without prior GLP-1 receptor blockade
297 had EF measured before and after intravenous exenatide, with or without the GLP-1R antagonist exendin