ライフサイエンスコーパス: exenatide

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 raglutide, semaglutide, and extended-release exenatide.

6 in systolic blood pressure was observed with exenatide.

7 sensor in the porto-hepatic circulation with exenatide.

8 ht and body mass index than those not taking exenatide.

9 male Sprague Dawley rats were injected with exenatide (0.1, 0.5, 5 and 10 microg/kg) or saline intra

10 ts per patient per year) than in those given exenatide (0.3 events per patient per year).

11 mia less frequent with liraglutide than with exenatide (1.93 vs 2.60 events per patient per year; rat

12 ced mean HbA(1c) significantly more than did exenatide (-1.12% [SE 0.08] vs -0.79% [0.08]; estimated

13 ed mean fasting plasma glucose more than did exenatide (-1.61 mmol/L [SE 0.20] vs -0.60 mmol/L [0.20]

14 nal liraglutide 1.8 mg once a day (n=233) or exenatide 10 microg twice a day (n=231) in a 26-week ope

15 equence interactive voice-response system to exenatide, 10 microg twice daily, or placebo for 30 week

16 Sixteen subjects commenced exenatide, 12 continue (follow-up 214+/-57 days; range 1

17 y approximately 20% (saline 13.2 +/- 1.9 vs. exenatide 15.6 +/- 2.1 mg x kg(-1) x min(-1), P < 0.05)

18 d in the intention-to-treat analysis (160 on exenatide, 166 on sitagliptin, and 165 on pioglitazone).

19 atients were assigned to receive once weekly exenatide, 172 to receive sitagliptin, and 172 to receiv

20 web-response system, to receive once-weekly exenatide 2 mg by subcutaneous injection plus once-daily

21 (1:1) to receive subcutaneous injections of exenatide 2 mg or placebo once weekly for 48 weeks in ad

22 espite hyperglycemia (saline 2.9 +/- 0.6 vs. exenatide 2.3 +/- 0.3 mg x kg(-1) x min(-1), P = 0.29).

23 ntry and concomitant therapy) to once-weekly exenatide (2 mg subcutaneous injection) or once-daily gl

24 ce-daily liraglutide (1.8 mg) or once-weekly exenatide (2 mg).

25 Weight loss with exenatide (-2.3 kg, 95% CI-2.9 to -1.7) was significantl

26 milar weight losses (liraglutide -3.24 kg vs exenatide -2.87 kg).

27 ucose infusion rate (saline 15.9 +/- 1.6 vs. exenatide 20.4 +/- 2.1 mg x kg(-1) x min(-1), P < 0.001)

28 dial hyperinsulinemia and hyperglycemia with exenatide (20 microg) or saline injected at 0 min.

29 ast one dose of the assigned drug (233 given exenatide, 223 glargine).

30 mg/dL, and 2-h glucose of 177 +/- 11 mg/dL, exenatide (5 mug) or placebo was injected in double-blin

31 ts with type 2 diabetes received intravenous exenatide (7.5 mug) or saline (-30 to 240 min) in a doub

32 essed the safety and efficacy of once weekly exenatide, a glucagon-like peptide 1 receptor agonist, v

33 Exenatide, a glucagon-like peptide-1 (GLP-1) receptor ag

34 tion, whether the cardioprotective effect of exenatide, a glucose-lowering drug, is dependent on hype

35 Recent progress suggests that exenatide, a mimetic of glucagon-like peptide-1 (GLP-1),

36 Compound 10 is composed of an exenatide (AC2993) analogue, AC3174, and an amylinomimet

37 eutic polypeptides; insulin, calcitonin, and exenatide across the monolayer.

38 The GLP-1 receptor agonist exenatide activated SERCA but did not alter other Ca(2+)

39 intention-to-treat analysis indicating that exenatide, administered once weekly, was noninferior to

40 The coprimary hypotheses were that exenatide, administered once weekly, would be noninferio

41 Whether exenatide affects the underlying disease pathophysiology

42 Subjects on exenatide after ITx showed significantly lower weight an

43 HbA1c from baseline to week 28 compared with exenatide alone (-0.4% [95% CI -0.6 to -0.1]; p=0.004) o

44 eceive exenatide plus dapagliflozin (n=231), exenatide alone (n=231; n=1 untreated), or dapagliflozin

45 Incubation with exenatide also inhibited thrombus formation under flow c

46 rt, were prevented by exposure to exendin-4 (exenatide), an anti-diabetes agent.

47 of liraglutide, a human GLP-1 analogue, with exenatide, an exendin-based GLP-1 receptor agonist.

48 The HbA(c) level decreased by 1.74% with exenatide and 1.04% with placebo (between-group differen

49 s were enrolled and randomly assigned, 32 to exenatide and 30 to placebo.

50 Two patients taking both exenatide and a sulphonylurea had a major hypoglycaemic

51 -0.4% [95% CI, -0.7% to -0.2%]), once-weekly exenatide and albiglutide for fasting plasma glucose (-0

52 Co-initiation of exenatide and dapagliflozin improved various glycaemic m

53 risk, and to assess the interaction between exenatide and hyperglycemia.

54 Weight decreased by 1.8 kg with exenatide and increased by 1.0 kg with placebo (between-

55 Glucagon-like peptide-1 receptor agonists exenatide and liraglutide have been shown to improve gly

56 reated for 1 year with GLP-1R agonists, both exenatide and liraglutide increased energy expenditure.

57 Average increases in insulin dosage with exenatide and placebo were 13 U/d and 20 U/d.

58 Exenatide and sitagliptin treatments have led to a lower

59 The most frequent adverse events with exenatide and sitagliptin were nausea (n=38, 24%, and n=

60 co-initiation of the GLP-1 receptor agonist exenatide and the SGLT2 inhibitor dapagliflozin with exe

61 significantly between patients who received exenatide and those who received placebo.

62 ma glucose; taspoglutide, 20 mg, once-weekly exenatide, and dulaglutide, 1.5 mg, reduced body weight.

63 y GLP-1RAs, dulaglutide, 1.5 mg; once-weekly exenatide; and taspoglutide, 20 mg, showed a greater red

64 orted among patients who took sitagliptin or exenatide as compared with other therapies (P<.008, P<9x

65 nts for insulin resistance (pioglitazone and exenatide) as possible disease modifying drugs in Parkin

66 ents were fewer, and transit was slower with exenatide, as were the areas under the curves for serum

67 subcutaneous injections of extended-release exenatide at a dose of 2 mg or matching placebo once wee

68 In conclusion, exenatide augmented postprandial EF in subjects with dia

69 Nausea was greater in both groups with exenatide, but suppression of small intestinal motility

70 They were administered 17.4 mug exenatide (Byetta) or placebo over a 6-hour and 15-minut

71 peptide templates, such as the diabetes drug exenatide (Byetta).

72 he glucagon-like peptide-1 receptor agonist, exenatide (Byetta, Amylin Pharmaceuticals, CA) has prope

73 nction represents a novel mechanism by which exenatide can attenuate postprandial glycemia.

74 ls in vivo, glucose tolerance after an acute exenatide challenge was improved.

75 d all cancers associated with sitagliptin or exenatide, compared with other therapies.

76 cal utility is illustrated by a PEG hydrogel-exenatide conjugate that should allow once-a-month admin

77 her reduced in those initially randomized to exenatide (cumulative BMI reduction of 4%).

78 Exenatide did not reduce neuron-specific enolase levels

79 Exenatide directly stimulates glucose turnover by enhanc

80 ated to liraglutide and 12 (3%) allocated to exenatide discontinued participation because of adverse

81 Furthermore, the GLP-1 receptor agonist, Exenatide, dose-dependently enhanced phosphorylation of

82 als with induced periodontitis that received exenatide (EG); 2) animals with induced periodontitis th

83 Incubation with GLP-1 and the GLP-1R agonist exenatide elicited a cAMP response in MEG-01 cells, and

84 Exenatide elicited a greater reduction in percent change

85 Exenatide elicited eNOS activation and NO production in

86 Thus, we evaluated the acute effects of exenatide (EX) on hepatic (Hep-IR) and adipose (Adipo-IR

87 s study, we aimed to evaluate the effects of exenatide (EXE) treatment on exocrine pancreas of nonhum

88 raftment and long-term graft function of SI, exenatide (EXN) and etanercept treatment at islet infusi

89 ptin and the glucagon-like peptide-1 mimetic exenatide, from 2004-2009; data on adverse events associ

90 of this study is to evaluate the effects of exenatide (GLP-1 agonist) and sitagliptin (DPP-4 inhibit

91 Based on data on XTEN fusions to exenatide, glucagon, GFP and human growth hormone, we ex

92 -1.48%, SE 0.05; n=386) than in those in the exenatide group (-1.28%, 0.05; 390) with the treatment d

93 s who reported serious adverse events in the exenatide group (36 patients [15%]) was the same as that

94 primary analysis included 31 patients in the exenatide group and 29 patients in the placebo group.

95 .4%; 3.7 events per 100 person-years) in the exenatide group and in 905 of 7396 patients (12.2%; 4.0

96 Six serious adverse events occurred in the exenatide group and two in the placebo group, although n

97 [4%]), which occurred less frequently in the exenatide group and with decreasing incidence over time

98 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)

99 ocardial area at risk the data points of the exenatide group lay significantly lower than for the pla

100 Single-blinded rating of the exenatide group suggested clinically relevant improvemen

101 ean HbA1c change was -1.01% (SE 0.07) in the exenatide group versus -0.81% (0.07) in the glargine gro

102 ] in the liraglutide group vs 43 [9%] in the exenatide group), diarrhoea (59 [13%] vs 28 [6%]), and v

103 gliflozin group, -1.6% (-1.8 to -1.4) in the exenatide group, and -1.4% (-1.6 to -1.2) in the dapagli

104 ozin group, 124 (54%) of 230 patients in the exenatide group, and 121 (52%) of 233 patients in the da

105 ese events did decrease after week 26 in the exenatide group.

106 INTERPRETATION: Exenatide had positive effects on practically defined of

107 TEN to the exenatide peptide should increase exenatide half-life in humans from 2.4 h to a projected

108 Exenatide has been demonstrated to be cardioprotective a

109 old half-life extension of the 39-aa peptide exenatide in rats, and a noncirculating s.c. hydrogel co

110 analysis study was to evaluate the effect of exenatide in relation to system delay, defined as time f

111 ffects of the glucagon-like peptide-1 analog exenatide in resuscitated OHCA patients.

112 e safety, efficacy, and metabolic effects of exenatide in subjects with type 1 diabetes mellitus and

113 nt studies have been published on the use of exenatide in the management of pediatric obesity and new

114 Adverse events of exenatide included nausea, diarrhea, vomiting, headache,

115 Exenatide increased CMRglu in areas of the brain related

116 Intravenous exenatide increased fasting EF, and exendin-9 abolished

117 Exenatide increased Fos-LI dose-dependently in the myent

118 Once-weekly exenatide increased heart rate compared with albiglutide

119 Subcutaneous exenatide increased postprandial EF independent of reduc

120 Use of sitagliptin or exenatide increased the odds ratio for reported pancreat

121 , reducing hyperinsulinemia to basal levels, exenatide-increased total glucose turnover was completel

122 ury model, a single intravenous injection of exenatide inhibited thrombus formation in normoglycemic

123 ke peptide (GLP-1) and its receptor agonist, Exenatide, inhibited palmitate-mediated caspase 3 activa

124 n, pretreatment with exendin (9-39) prior to exenatide injection blocked the activation in both locat

125 ), randomly assigned to receive subcutaneous exenatide injection for 12 months or to act as controls.

126 Adding twice-daily exenatide injections improved glycemic control without i

127 Exenatide is a synthetic agonist of the glucagon-like pe

128 Exenatide is a type 2 diabetes treatment that has been s

129 Efficacy of once-weekly exenatide is sustained for 3 years.

130 1 (GLP-1) receptor via the antidiabetic drug exenatide led to improvements in both ERK and AKT signal

131 Both once daily liraglutide and once weekly exenatide led to improvements in glycaemic control, with

132 Both once daily liraglutide and once weekly exenatide led to improvements in glycaemic control, with

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

134 Activation of the enteric neurons by exenatide may be part of the pathway by which this pepti

135 Transport of insulin, calcitonin, and exenatide measured at different loading concentrations s

136 of hyperglycemia versus hyperinsulinemia in exenatide-mediated glucose disposal was studied.

137 Only 4 drugs (brain natriuretic peptide, exenatide, metoprolol, and esmolol) stand unchallenged t

138 -IV inhibitors were given 6 months GLP-1 RA (exenatide, n = 19; liraglutide, n = 6).

139 effects of a single injection of the GLP-1RA exenatide on cerebral and peripheral glucose metabolism

140 tudy determined the effect of GLP-1R agonist exenatide on postprandial EF in type 2 diabetes and the

141 randomly assigned to receive: 2 mg injected exenatide once weekly plus oral placebo once daily; 100

142 Addition of exenatide once weekly to metformin achieved this goal mo

143 In DURATION-3, exenatide once weekly was compared with insulin glargine

144 We compared the efficacy and safety of exenatide once weekly with liraglutide once daily in pat

145 e and the SGLT2 inhibitor dapagliflozin with exenatide or dapagliflozin alone in patients with type 2

146 Furthermore, Exenatide or forskolin reversed the inhibition by diazox

147 ients were randomized to receive intravenous exenatide or placebo before percutaneous coronary interv

148 ow 0/1 were randomly assigned to intravenous exenatide or placebo continuous infusion.

149 s with type 2 diabetes received subcutaneous exenatide or placebo for 11 days and EF, and glucose and

150 on counseling and were equally randomized to exenatide or placebo injection, twice per day.

151 caling suggests that a fusion of XTEN to the exenatide peptide should increase exenatide half-life in

152 we randomly assigned 695 patients to receive exenatide plus dapagliflozin (n=231), exenatide alone (n

153 HbA1c was -2.0% (95% CI -2.1 to -1.8) in the exenatide plus dapagliflozin group, -1.6% (-1.8 to -1.4)

154 recorded in 131 (57%) of 231 patients in the exenatide plus dapagliflozin group, 124 (54%) of 230 pat

155 Exenatide plus dapagliflozin significantly reduced HbA1c

156 Exenatide plus dapagliflozin was significantly superior

157 concentrations of cAMP produced by GLP-1 and Exenatide preferentially activate the PKA pathway, where

158 With hyperinsulinemia and hyperglycemia, exenatide produced a significant increase in total gluco

159 Thirteen exenatide recipients and 1 placebo recipient discontinue

160 112 of 138 exenatide recipients and 101 of 123 placebo recipients c

161 ing medications, and HbA(c) levels, and more exenatide recipients than placebo recipients withdrew be

162 Treatment with exenatide reduced HbA(1c) (least square mean -1.5%, 95%

163 Exenatide reduced RaO0-60 min (4.6 +/- 1.4 vs. 13.1 +/-

164 All doses of exenatide reduced sucrose intake following the 20 min ti

165 of this work is to test the hypothesis that exenatide reduces food intake and activates the enteric

166 ing glucagon-like peptide 1 receptor agonist exenatide reduces postprandial glycemia, partly by slowi

167 Exenatide represents a major new avenue for investigatio

168 delay </=132 minutes (n=74), treatment with exenatide resulted in a smaller infarct size (9 grams [i

169 Treatment with exenatide resulted in increased salvage index both among

170 licited a cAMP response in MEG-01 cells, and exenatide significantly inhibited thrombin-, ADP-, and c

171 ducing systemic hyperglycemia to euglycemia, exenatide still increased total glucose turnover by appr

172 We aimed to investigate whether exenatide stimulates glucose turnover directly in insuli

173 ment with the glucagon-like peptide-1 analog exenatide, streptozotocin injection, partial pancreatect

174 reversed the protective effects of GLP-1 and Exenatide, suggesting that PKA may play a role in the pr

175 -1 receptor agonists were more frequent with exenatide than glargine (nausea: 36 [15%] of 233 patient

176 d constipation (10% vs. 2%) were higher with exenatide than with placebo.

177 lin concentrations were initially lower with exenatide than with saline and subsequently higher.

178 In contrast, subjects on exenatide therapy had significantly higher HSQ 2.0 score

179 to be a risk associated with sitagliptin or exenatide therapy in humans.

180 PAM (S)-9b potentiated low-dose exenatide to augment insulin secretion in primary mouse

181 Acute administration of exenatide to comatose patients in the intensive care uni

182 effects of adding once-weekly treatment with exenatide to usual care in patients with type 2 diabetes

183 Exenatide-treated patients had a mean improvement at 12

184 Also, cardioprotection by exenatide treatment is independent of glucose levels at

185 In this post hoc analysis, exenatide treatment was associated with a 30% decrease i

186 r improvements in glycaemic control than did exenatide twice a day, and was generally better tolerate

187 Exenatide usage had a positive effect whereas single isl

188 ptin, and -0.3% (-0.6 to -0.1, p=0.0165) for exenatide versus pioglitazone.

189 Exenatide versus placebo decreased food intake and food-

190 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

191 -down ECD experiment showed that the Asp9 in exenatide was converted to isoAsp9 to form the unknown i

192 Decreased RaO0-60 min after exenatide was inversely correlated to CMRglu.

193 hours after admission in patients receiving exenatide was lower than that in patients receiving plac

194 Exenatide was tolerated in this patient population after

195 Exenatide was well tolerated, although weight loss was c

196 Although antithrombotic effects of exenatide were partly lost in mice transplanted with bon

197 The antidiabetic drugs sitagliptin and exenatide, which inhibit GLP-1 breakdown and stimulate G

198 once-daily dapagliflozin 10 mg oral tablets, exenatide with dapagliflozin-matched oral placebo, or da

199 administration of the GLP-1 receptor agonist exenatide, with or without prior GLP-1 receptor blockade

200 had EF measured before and after intravenous exenatide, with or without the GLP-1R antagonist exendin

201 We confirmed the biological activity of the exenatide-XTEN fusion in mice.