ライフサイエンスコーパス: DPP-4

1 tagliptin reduced the serum concentration of DPP-4.

2 to exogenous tumor necrosis factor-alpha and DPP-4.

3 compounds with subnanomolar activity against DPP-4 (42b- 49b), that is, 4-fluorobenzyl-substituted co

4 yl peptidase-4 (DPP-4); hence, inhibition of DPP-4 activity enables yet another pathway for potentiat

5 sm for DPP-4 inhibitors is that they inhibit DPP-4 activity in peripheral plasma, which prevents the

6 ivation of GLP-1R signaling or inhibition of DPP-4 activity produces a broad range of overlapping and

7 Blood DPP-4 activity, glucagon-like peptide-1 (GLP-1) levels,

8 Vildagliptin fully inhibited DPP-4 activity, reduced GLP-1 clearance by 40%, and incr

9 rtal GLP-1 receptors; 2) inhibition of islet DPP-4 activity, which prevents inactivation of locally p

10 ical mechanisms include 1) inhibition of gut DPP-4 activity, which prevents inactivation of newly rel

11 with vildagliptin on dipeptidyl peptidase-4 (DPP-4) activity, glucagon-like peptide 1 (GLP-1) concent

12 trials, along with the potential utility of DPP-4 and periostin as biomarkers of interleukin-13 path

13 nzymatic cleavage by dipeptidyl peptidase-4 (DPP-4) and through renal clearance.

14 on protein (FAP) and dipeptidyl peptidase-4 (DPP-4) are highly homologous serine proteases of the pro

15 , a new inhibitor of dipeptidyl peptidase 4 (DPP-4), as compared with placebo in patients with type 2

16 orter 2 (GLUT2), and dipeptidyl peptidase 4 (DPP-4), as well as that of the putative differentiation

17 ctural modeling suggests that FAP Ala657 and DPP-4 Asp663 confer their contrasting effects on TSS by

18 Conversely, DPP-4 Asp663 stabilizes dipeptidyl peptidase substrate b

19 FAP Ala657, which corresponds to DPP-4 Asp663, is important for endopeptidase activity; h

20 on of villin by 29% (6%), Cdx2 by 31% (10%), DPP-4 by 15% (6%), GLUT2 by 40% (11%), SLFN12 by 61% (14

21 LP-1 system by pharmacological inhibition of DPP-4 caused hyperinsulinemia, suppression of glucagon r

22 ecific dipeptidyl aminopeptidase IV (DPP IV, DPP-4, CD26), widely expressed in mammalians, releases X

23 nyl-, and peptidyl-Gly-Pro substrates, which DPP-4 cleaved poorly, suggesting an N-acyl-Gly-Pro motif

24 GLP-1 signaling is unclear, however, because DPP-4 cleaves other molecules as well.

25 alues for other prolyl peptidases, including DPP-4, DPP-7, DPP-8, DPP-9, prolyl oligopeptidase, and a

26 ion of compounds 34b and 46b in complex with DPP-4 enzyme revealed that (R)-stereochemistry at the 8-

27 ed as inhibitors of dipeptidyl peptidase IV (DPP-4) for the treatment of type 2 diabetes.

28 rmation of conserved residues FAP Glu204 and DPP-4 Glu206.

29 olyl peptidases like dipeptidyl peptidase-4 (DPP-4) have not been developed.

30 ts and inhibitors of dipeptidyl peptidase-4 (DPP-4) have shown pleiotropic effects on bone metabolism

31 are both cleaved by dipeptidyl peptidase-4 (DPP-4); hence, inhibition of DPP-4 activity enables yet

32 ent in vitro potency (IC50 = 4.3 nM) against DPP-4, high selectivity over other enzymes, and good pha

33 o had baseline serum dipeptidyl peptidase-4 (DPP-4) higher than the population baseline median, we no

34 In vitro and in vivo assays of DPP-4 inhibition (DPP-4i) on monocyte activation/migrati

35 These studies suggest that DPP-4 inhibition ameliorates hepatic steatosis and insul

36 The cardiovascular mechanisms engaged by DPP-4 inhibition are more complex, encompassing increase

37 iptin increased intact GLP-1 and GIP through DPP-4 inhibition but reduced total GLP-1 and GIP (feedba

38 rimary aims were to determine the effects of DPP-4 inhibition on GLP-1 clearance and on hepatic gluco

39 blockade, whereas the inhibitory effects of DPP-4 inhibition on glucagon and GE were abolished.

40 blood glucose is impaired; 2) the effect of DPP-4 inhibition on glycemia is likely to depend on adeq

41 DPP-4 inhibition reduced glycemia and enhanced insulin l

42 Furthermore, DPP-4 inhibition rescued WD-induced decreases in hepatic

43 antagonist, the glucose-lowering effects of DPP-4 inhibition were reduced by approximately 50%.

44 DPP-4 inhibition with saxagliptin did not increase or de

45 strongly preferred over (S) with respect to DPP-4 inhibition.

46 significantly to the therapeutic effects of DPP-4 inhibition.

47 d discusses these nonclassical mechanisms of DPP-4 inhibition.

48 es GLP mediating the antidiabetic effects of DPP-4 inhibition.

49 lin excursion after an OGTT with and without DPP-4 inhibition.

50 pic effects may contribute to the effects of DPP-4 inhibition.

51 erapeutic effects of dipeptidyl peptidase 4 (DPP-4) inhibition (vildagliptin) by using the GLP-1 rece

52 4 patients with T2D, dipeptidyl peptidase-4 (DPP-4) inhibition and its glucose-lowering actions were

53 GAT1 inhibition with dipeptidyl-peptidase-4 (DPP-4) inhibition led to further enhancements in active

54 ed to vehicle or alogliptin, a high-affinity DPP-4 inhibitor (40 mg . kg(-1) . d(-1)), for 12 weeks.

55 enyl)butanamide (6), a potent, orally active DPP-4 inhibitor (IC(50) = 6.3 nM) with excellent selecti

56 inedione (SMD, 0.16 [95% CI, 0.00 to 0.31]), DPP-4 inhibitor (SMD, 0.33 [95% CI, 0.13 to 0.52]), and

57 ion of the tricyclic structure of the potent DPP-4 inhibitor 1.

58 ovascular events were not increased with the DPP-4 inhibitor alogliptin as compared with placebo.

59 EXAMINE trial showed non-inferiority of the DPP-4 inhibitor alogliptin to placebo on major adverse c

60 hesis of sitagliptin, a potent and selective DPP-4 inhibitor for the treatment of type 2 diabetes mel

61 The DPP-4 inhibitor prevented WD-induced hepatic steatosis a

62 human GLP-1 analogue liraglutide versus the DPP-4 inhibitor sitagliptin, as adjunct treatments to me

63 thiazolidinedione, an SGLT-2 inhibitor, or a DPP-4 inhibitor to metformin to improve glycemic control

64 (5.6 +/- 1.7 mmol/mol) lower A1C response to DPP-4 inhibitor treatment in G-allele carriers, but ther

65 G) content was significantly attenuated with DPP-4 inhibitor treatment.

66 ay, development of diabetes, and response to DPP-4 inhibitor treatment.

67 ates of in-hospital heart failure in another DPP-4 inhibitor trial have been reported.

68 of 10,089 propensity score-matched pairs of DPP-4 inhibitor users and sulfonylurea users were examin

69 f exenatide (GLP-1 agonist) and sitagliptin (DPP-4 inhibitor) during periodontitis induction by ligat

70 Treatment with a DPP-4 inhibitor, alogliptin (AG), significantly reduced

71 half the effect seen with the addition of a DPP-4 inhibitor, and equated to a dose difference of 550

72 ose Western diet (WD) or a WD containing the DPP-4 inhibitor, MK0626, for 16 weeks.

73 sed imidazopyridine dipeptidyl peptidase IV (DPP-4) inhibitor 1 has been developed.

74 as as effective as a dipeptidyl peptidase-4 (DPP-4) inhibitor at reducing peak glucose levels in an a

75 Linagliptin is a dipeptidyl peptidase-4 (DPP-4) inhibitor in clinical use against type 2 diabetes

76 Linagliptin is a dipeptidyl Peptidase-4 (DPP-4) inhibitor that inhibits the degradation of glucag

77 potent and selective dipeptidyl peptidase 4 (DPP-4) inhibitor with an excellent pharmacokinetic profi

78 uding saxagliptin, a dipeptidyl peptidase 4 (DPP-4) inhibitor, are unclear.

79 ews the most recent CV outcome trials of the DPP-4 inhibitors (SAVOR-TIMI 53, EXAMINE, and TECOS) as

80 advances that reveal how GLP-1R agonists and DPP-4 inhibitors affect the normal and diabetic heart an

81 The results were similar for DPP-4 inhibitors and GLP-1 analogues.

82 DPP-4 inhibitors do not lower postprandial glucose conce

83 es demonstrate that both GLP-1R agonists and DPP-4 inhibitors exhibit cardioprotective actions in ani

84 DPP-4 inhibitors expand beta-cell mass, reduce alpha-cel

85 ay provide an impetus for the development of DPP-4 inhibitors for the prevention and treatment of str

86 nd metformin-based combinations, except that DPP-4 inhibitors had smaller effects.

87 ox models with exposure to sulfonylureas and DPP-4 inhibitors included as time-varying covariates wer

88 The classical mechanism for DPP-4 inhibitors is that they inhibit DPP-4 activity in

89 senatide in Acute Coronary Syndrom]) and the DPP-4 inhibitors saxagliptin (SAVOR-TIMI 53 trial [Saxag

90 The risk for hHF was not higher with DPP-4 inhibitors than with the other study drugs.

91 humans have found additional mechanisms for DPP-4 inhibitors that may contribute to their glucose-lo

92 effects on cardiovascular outcomes of adding DPP-4 inhibitors versus sulfonylureas to metformin thera

93 DPP-4 inhibitors were associated with lower risks for al

94 Compared with sulfonylureas, DPP-4 inhibitors were associated with lower risks for al

95 In our effort to discover DPP-4 inhibitors with added benefits over currently comm

96 Metformin was more efficacious than the DPP-4 inhibitors, and compared with thiazolidinediones o

97 ht was reduced or maintained with metformin, DPP-4 inhibitors, GLP-1 receptor agonists, and SGLT-2 in

98 nefits over currently commercially available DPP-4 inhibitors, MK-3102 (omarigliptin), was identified

99 ardiovascular actions of GLP-1R agonists and DPP-4 inhibitors, with a focus on the translation of mec

100 mpared with pioglitazone, sulfonylureas, and DPP-4 inhibitors.

101 sed drugs, including dipeptidyl peptidase 4 (DPP-4) inhibitors and glucagon-like peptide 1 (GLP-1) an

102 Dipeptidyl-peptidase 4 (DPP-4) inhibitors are increasingly used to accomplish gl

103 , and orally active dipeptidyl peptidase IV (DPP-4) inhibitors by extensive structure-activity relati

104 In this regard, dipeptidyl peptidase-4 (DPP-4) inhibitors have recently been reported to attenua

105 -1 activity, whereas dipeptidyl peptidase-4 (DPP-4) inhibitors increase concentrations of endogenous

106 glucose lowering by dipeptidyl peptidase-4 (DPP-4) inhibitors is unclear.

107 Dipeptidyl peptidase-4 (DPP-4) inhibitors prevent degradation of incretin hormon

108 udies concluded that dipeptidyl peptidase-4 (DPP-4) inhibitors provide glycemic control but also rais

109 GLP-1R) agonists and dipeptidyl peptidase-4 (DPP-4) inhibitors represent 2 distinct classes of incret

110 ones, sulfonylureas, dipeptidyl peptidase-4 (DPP-4) inhibitors, and sodium-glucose cotransporter-2 (S

111 hHF) associated with dipeptidyl peptidase-4 (DPP-4) inhibitors, creating uncertainty about the safety

112 ists (GLP-1 RAs) and dipeptidyl peptidase-4 (DPP-4) inhibitors, which inhibit the physiological inact

113 Binding of gliptins to DPP-4 is a rapid electrostatically driven process.

114 Because DPP-4 is expressed in inflammatory cells, we hypothesize

115 od was collected for analysis of glucose and DPP-4 levels.

116 which inhibitors of dipeptidyl peptidase-4 (DPP-4) lower postprandial glucose concentrations.

117 -36), a cardioactive metabolite generated by DPP-4-mediated cleavage.

118 Vildagliptin fully inhibited DPP-4 over the 4-h experimental period.

119 ion by inhibition of dipeptidyl peptidase-4 (DPP-4) promotes glycemic reduction for the treatment of

120 Thus, a significant DPP-4-sensitive glucose-lowering mechanism contributes t

121 e, Pro, or Arg at the P(2) residue; however, DPP-4 showed broad reactivity against this library, prec

122 ibrary, FAP cleaved only Ac-Gly-Pro, whereas DPP-4 showed little reactivity with all substrates.

123 unclear, and it is unknown whether conserved DPP-4 substrate binding residues support FAP endopeptida

124 e CP-induced increase in the levels of other DPP-4 substrates such as stromal cell-derived factor-1 a

125 DPP-4 was highly expressed in bone marrow-derived CD11b(

126 s, and inhibition of dipeptidyl peptidase-4 (DPP-4), which cleaves GLP-1, is renoprotective in rodent