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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.
10 roup (adjusted coefficient for the effect of exenatide 0.92 [95% CI -1.56 to 3.39]; p=0.47).
11  male Sprague Dawley rats were injected with exenatide (0.1, 0.5, 5 and 10 microg/kg) or saline intra
12 ts per patient per year) than in those given exenatide (0.3 events per patient per year).
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
19                   Sixteen subjects commenced exenatide, 12 continue (follow-up 214+/-57 days; range 1
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
30 ce-daily liraglutide (1.8 mg) or once-weekly exenatide (2 mg).
31                             Weight loss with exenatide (-2.3 kg, 95% CI-2.9 to -1.7) was significantl
32 milar weight losses (liraglutide -3.24 kg vs exenatide -2.87 kg).
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)
34 dial hyperinsulinemia and hyperglycemia with exenatide (20 microg) or saline injected at 0 min.
35 ast one dose of the assigned drug (233 given exenatide, 223 glargine).
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
39         Exenatide significantly lowered ICP [exenatide: 9.74 (6.09) mmHg, n = 19, vehicle: 18.27 (6.6
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
44                                              Exenatide, a glucagon-like peptide-1 (GLP-1) receptor ag
45                                              Exenatide, a glucagon-like peptide-1 (GLP-1) receptor ag
46 tion, whether the cardioprotective effect of exenatide, a glucose-lowering drug, is dependent on hype
47                Recent progress suggests that exenatide, a mimetic of glucagon-like peptide-1 (GLP-1),
48  formulations with and without encapsulating exenatide, a pH-labile peptide that is known to be unsta
49                                              Exenatide, a promising cardioprotective agent, protects
50                          The interactions of exenatide, a Trp-containing peptide used as a drug to tr
51                Compound 10 is composed of an exenatide (AC2993) analogue, AC3174, and an amylinomimet
52 eutic polypeptides; insulin, calcitonin, and exenatide across the monolayer.
53                   The GLP-1 receptor agonist exenatide activated SERCA but did not alter other Ca(2+)
54  intention-to-treat analysis indicating that exenatide, administered once weekly, was noninferior to
55           The coprimary hypotheses were that exenatide, administered once weekly, would be noninferio
56       Our results show that the net cationic exenatide adsorbs electrostatically to liposomes contain
57                                      Whether exenatide affects the underlying disease pathophysiology
58                                  Subjects on exenatide after ITx showed significantly lower weight an
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
61                              Incubation with exenatide also inhibited thrombus formation under flow c
62                                              Exenatide also reduced some postprandial CERs, PCs, and
63                                              Exenatide also reversibly inhibited I(Nav1.5) with IC(50
64 rt, were prevented by exposure to exendin-4 (exenatide), an anti-diabetes agent.
65 of liraglutide, a human GLP-1 analogue, with exenatide, an exendin-based GLP-1 receptor agonist.
66     The HbA(c) level decreased by 1.74% with exenatide and 1.04% with placebo (between-group differen
67 s were enrolled and randomly assigned, 32 to exenatide and 30 to placebo.
68                     Two patients taking both exenatide and a sulphonylurea had a major hypoglycaemic
69 -0.4% [95% CI, -0.7% to -0.2%]), once-weekly exenatide and albiglutide for fasting plasma glucose (-0
70                             Co-initiation of exenatide and dapagliflozin improved various glycaemic m
71  risk, and to assess the interaction between exenatide and hyperglycemia.
72              Weight decreased by 1.8 kg with exenatide and increased by 1.0 kg with placebo (between-
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.
75     Average increases in insulin dosage with exenatide and placebo were 13 U/d and 20 U/d.
76                                              Exenatide and sitagliptin treatments have led to a lower
77        The most frequent adverse events with exenatide and sitagliptin were nausea (n=38, 24%, and n=
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
80  significantly between patients who received exenatide and those who received placebo.
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
84              We found no evidence to support exenatide as a disease-modifying treatment for people wi
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
89                               In conclusion, exenatide augmented postprandial EF in subjects with dia
90 by right censoring, but the favorable HR for exenatide became nominally significant in the sulfonylur
91       Nausea was greater in both groups with exenatide, but suppression of small intestinal motility
92 rst, generated steady-state plasma levels of Exenatide, but with PT320 producing continuous therapeut
93              They were administered 17.4 mug exenatide (Byetta) or placebo over a 6-hour and 15-minut
94 peptide templates, such as the diabetes drug exenatide (Byetta).
95 he glucagon-like peptide-1 receptor agonist, exenatide (Byetta, Amylin Pharmaceuticals, CA) has prope
96 nction represents a novel mechanism by which exenatide can attenuate postprandial glycemia.
97 ls in vivo, glucose tolerance after an acute exenatide challenge was improved.
98                              During fasting, exenatide, compared with control, reduced some ceramides
99 d all cancers associated with sitagliptin or exenatide, compared with other therapies.
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
103 her reduced in those initially randomized to exenatide (cumulative BMI reduction of 4%).
104                                              Exenatide did not reduce neuron-specific enolase levels
105                                              Exenatide directly stimulates glucose turnover by enhanc
106 ated to liraglutide and 12 (3%) allocated to exenatide discontinued participation because of adverse
107                    Here, we explored whether exenatide displayed anti-AF effects by inhibiting human
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
110                                              Exenatide during cardiopulmonary bypass and weaning ther
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
113                                              Exenatide elicited a greater reduction in percent change
114                                              Exenatide elicited eNOS activation and NO production in
115                                  Once-weekly exenatide (EQW) had a neutral effect on hospitalization
116 gon-like peptide receptor agonist (GLP-1 RA) exenatide (EQW) vs. placebo.
117      Thus, we evaluated the acute effects of exenatide (EX) on hepatic (Hep-IR) and adipose (Adipo-IR
118                                              Exenatide (Ex4), a GLP-1 incretin mimetic polypeptide, i
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
123                                      Both SR-Exenatide formulations proved well-tolerated and, follow
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
127             Based on data on XTEN fusions to exenatide, glucagon, GFP and human growth hormone, we ex
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
130                                              Exenatide:glucagon significantly increased the median le
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.
136                       92 participants in the exenatide group and 96 in the placebo group had at least
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)
142                Nine (9%) participants in the exenatide group had at least one serious adverse event c
143 ocardial area at risk the data points of the exenatide group lay significantly lower than for the pla
144                 Single-blinded rating of the exenatide group suggested clinically relevant improvemen
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
151 ese events did decrease after week 26 in the exenatide group.
152                              INTERPRETATION: Exenatide had positive effects on practically defined of
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
155                                              Exenatide has been demonstrated to be cardioprotective a
156 7; 95% CI: 0.79-1.19), or liraglutide versus exenatide (HR: 1.08; 95% CI: 0.83-1.38), nor were differ
157                                              Exenatide improved fasting and postprandial lipidomic pr
158 old half-life extension of the 39-aa peptide exenatide in rats, and a noncirculating s.c. hydrogel co
159 mployed to evaluate the anti-AF potential of exenatide in rats.
160 analysis study was to evaluate the effect of exenatide in relation to system delay, defined as time f
161 ffects of the glucagon-like peptide-1 analog exenatide in resuscitated OHCA patients.
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
164                            Adverse events of exenatide included nausea, diarrhea, vomiting, headache,
165                                              Exenatide increased CMRglu in areas of the brain related
166                                  Intravenous exenatide increased fasting EF, and exendin-9 abolished
167                                              Exenatide increased Fos-LI dose-dependently in the myent
168                                  Once-weekly exenatide increased heart rate compared with albiglutide
169                                 Subcutaneous exenatide increased postprandial EF independent of reduc
170                        Use of sitagliptin or exenatide increased the odds ratio for reported pancreat
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
174              These findings demonstrate that exenatide inhibits I(Kv1.5) and I(Nav1.5)in vitro and re
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.
177                           Adding twice-daily exenatide injections improved glycemic control without i
178  present article presents the results of the exenatide intervention.
179                                              Exenatide is a synthetic agonist of the glucagon-like pe
180                                              Exenatide is a type 2 diabetes treatment that has been s
181                    Our findings suggest that exenatide is safe and well tolerated.
182                      Efficacy of once-weekly exenatide is sustained for 3 years.
183 tinuous subcutaneous infusion of the GLP-1RA exenatide (ITCA 650) is unknown.
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
190 in) and GLP-1 receptor agonist (dulaglutide, exenatide, liraglutide, semaglutide) classes.
191                               Agents such as exenatide, lixisenatide, and liraglutide have demonstrat
192 /kg/min) and exenatide:glucagon co-infusion (exenatide loading dose 50 ng/min for 30 min then 25 ng/m
193 -matched oral placebo, or dapagliflozin with exenatide-matched placebo injections.
194         Activation of the enteric neurons by exenatide may be part of the pathway by which this pepti
195        Transport of insulin, calcitonin, and exenatide measured at different loading concentrations s
196  of hyperglycemia versus hyperinsulinemia in exenatide-mediated glucose disposal was studied.
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
199 ility, of whom 194 were randomly assigned to exenatide (n=97) or placebo (n=97).
200 -IV inhibitors were given 6 months GLP-1 RA (exenatide, n = 19; liraglutide, n = 6).
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
207                                  Addition of exenatide once weekly to metformin achieved this goal mo
208                               In DURATION-3, exenatide once weekly was compared with insulin glargine
209       We compared the efficacy and safety of exenatide once weekly with liraglutide once daily in pat
210 e and the SGLT2 inhibitor dapagliflozin with exenatide or dapagliflozin alone in patients with type 2
211                                 Furthermore, Exenatide or forskolin reversed the inhibition by diazox
212 ients were randomized to receive intravenous exenatide or placebo before percutaneous coronary interv
213 ow 0/1 were randomly assigned to intravenous exenatide or placebo continuous infusion.
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
216                        Patients treated with exenatide or placebo had similar rates of MACE and LEA,
217 on counseling and were equally randomized to exenatide or placebo injection, twice per day.
218 F and papilloedema) who receive subcutaneous exenatide or placebo.
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
223                                              Exenatide plus dapagliflozin significantly reduced HbA1c
224                                              Exenatide plus dapagliflozin was significantly superior
225 concentrations of cAMP produced by GLP-1 and Exenatide preferentially activate the PKA pathway, where
226                                              Exenatide prevented AF incidence and duration in rat hea
227     With hyperinsulinemia and hyperglycemia, exenatide produced a significant increase in total gluco
228                                 Furthermore, exenatide prolonged AP duration and suppressed the susta
229                                     Thirteen exenatide recipients and 1 placebo recipient discontinue
230                                   112 of 138 exenatide recipients and 101 of 123 placebo recipients c
231 ing medications, and HbA(c) levels, and more exenatide recipients than placebo recipients withdrew be
232                                              Exenatide recovered characteristic spreading depolarizat
233                               Treatment with exenatide reduced HbA(1c) (least square mean -1.5%, 95%
234                                              Exenatide reduced ICP, improving algetic thresholds and
235                                              Exenatide reduced RaO0-60 min (4.6 +/- 1.4 vs. 13.1 +/-
236                                 All doses of exenatide reduced sucrose intake following the 20 min ti
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
239                                 In contrast, Exenatide release from Bydureon exhibited a biphasic pro
240                                              Exenatide release from PT320 exhibited a triphasic pharm
241                                 Stability of exenatide remaining inside microspheres was evaluated by
242                                              Exenatide represents a major new avenue for investigatio
243  delay </=132 minutes (n=74), treatment with exenatide resulted in a smaller infarct size (9 grams [i
244                               Treatment with exenatide resulted in increased salvage index both among
245                                              Exenatide reversibly suppressed I(Kv1.5) with IC(50) of
246 GLP-1) receptor agonists (e.g., liraglutide, exenatide, semaglutide).
247 -1 RAs were used (lixisenatide, liraglutide, exenatide, semaglutide, efpeglenatide, dulaglutide, albi
248                                              Exenatide significantly and meaningfully lowered intracr
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
251                                              Exenatide significantly lowered ICP [exenatide: 9.74 (6.
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
254              We aimed to investigate whether exenatide stimulates glucose turnover directly in insuli
255 ment with the glucagon-like peptide-1 analog exenatide, streptozotocin injection, partial pancreatect
256                                      EXSCEL (Exenatide Study of Cardiovascular Event Lowering) assess
257 for heart failure (HHF) in the EXSCEL study (Exenatide Study of Cardiovascular Event Lowering), with
258 abetes mellitus and PAD in the EXSCEL trial (Exenatide Study of Cardiovascular Event Lowering).
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
261 d constipation (10% vs. 2%) were higher with exenatide than with placebo.
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.
264                     In contrast, subjects on exenatide therapy had significantly higher HSQ 2.0 score
265  to be a risk associated with sitagliptin or exenatide therapy in humans.
266              PAM (S)-9b potentiated low-dose exenatide to augment insulin secretion in primary mouse
267                      Acute administration of exenatide to comatose patients in the intensive care uni
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
270                                              Exenatide total exposure, evaluated from the area under
271                                              Exenatide-treated patients had a mean improvement at 12
272                    Thus, we investigated how exenatide treatment changes lipid metabolism and composi
273                    Also, cardioprotection by exenatide treatment is independent of glucose levels at
274                   In this post hoc analysis, exenatide treatment was associated with a 30% decrease i
275 r improvements in glycaemic control than did exenatide twice a day, and was generally better tolerate
276                                              Exenatide usage had a positive effect whereas single isl
277 [HR]) of composite treatment for DME or PDR: exenatide versus dulaglutide (HR 0.90; 95% confidence in
278 ptin, and -0.3% (-0.6 to -0.1, p=0.0165) for exenatide versus pioglitazone.
279                                              Exenatide versus placebo decreased food intake and food-
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
282 ere no differences in MACE or LEA rates with exenatide versus placebo.
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
284 ups had slight weight loss (-5.5% vs. -1.9%, exenatide vs. control; P = 0.052).
285 ificant proteins changed differentially with exenatide vs. placebo therapy.
286                                              Exenatide was associated with positive effects on partic
287 -down ECD experiment showed that the Asp9 in exenatide was converted to isoAsp9 to form the unknown i
288                  Decreased RaO0-60 min after exenatide was inversely correlated to CMRglu.
289  hours after admission in patients receiving exenatide was lower than that in patients receiving plac
290                                              Exenatide was tolerated in this patient population after
291                                              Exenatide was well tolerated, although weight loss was c
292           Although antithrombotic effects of exenatide were partly lost in mice transplanted with bon
293       The antidiabetic drugs sitagliptin and exenatide, which inhibit GLP-1 breakdown and stimulate G
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
298  We confirmed the biological activity of the exenatide-XTEN fusion in mice.

 
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