ライフサイエンスコーパス: orlistat

1 n inhibition of fatty acid biosynthesis with orlistat.

2 of carbamazepine < diclofenac < fluoxetine < orlistat.

3 carbamazepine < diclofenac < fluoxetine and orlistat.

4 ompared with a more general lipase inhibitor orlistat.

5 s as well as acylation of various lipases by orlistat.

6 ll death and improved solubility compared to orlistat.

7 e AMP:ATP ratio, and this too was reduced by orlistat.

8 cy for FAS in biochemical assays relative to orlistat.

9 2 = 0%) for metformin and -0.50 to -0.94 for orlistat.

10 r target and a potential new application for Orlistat.

11 nly approximately 10-fold lower than that of orlistat (0.28 +/- 0.06 microM).

12 .5 mm Hg) and gastrointestinal distress with orlistat (1% to 37% of patients).

13 lus vitamin E (800 IU) daily with or without orlistat (120 mg three times a day) for 36 weeks.

14 Subjects treated with orlistat, 120 mg 3 times a day, during year 1 and year 2

15 ndomized to receive placebo 3 times a day or orlistat, 120 mg 3 times a day, for 52 weeks.

16 Treatment with orlistat, 120 mg 3 times a day, was associated with impr

17 The authors assessed in detail 50 studies of orlistat, 13 studies of fluoxetine, 5 studies of bupropi

18 in, 3.2 kg (95% CrI, -3.97 to -2.46 kg); and orlistat, 2.6 kg (95% CrI, -3.04 to -2.16 kg).

19 o, 30 mg orlistat, 60 mg orlistat, or 120 mg orlistat 3 times daily for 1 y in combination with a mai

20 After 1 y, subjects treated with 120 mg orlistat 3 times daily regained less weight than did pla

21 Use of metformin (8 studies, n = 616) and orlistat (3 studies, n = 779) were associated with great

22 45 kg; 35.2% regain) than those who received orlistat, 60 mg (4.26+/-0.57 kg; 51.3% regain), or place

23 to receive placebo 3 times a day (n = 138), orlistat, 60 mg (n = 152) or 120 mg (n = 153) 3 times a

24 randomly assigned to receive placebo, 30 mg orlistat, 60 mg orlistat, or 120 mg orlistat 3 times dai

25 In one approach, Orlistat, a drug approved for treating obesity, is used

26 Orlistat, a Food and Drug Administration-approved drug u

27 Orlistat, a gastrointestinal lipase inhibitor that reduc

28 udy was designed to test the hypothesis that orlistat, a gastrointestinal lipase inhibitor, is signif

29 acting reuptake inhibitor of monoamines, and orlistat, a pancreatic lipase inhibitor, have been appro

30 the fatty acid synthase/lipolysis inhibitor orlistat also sensitized leukemia cells to ABT-737, whic

31 inhibited with the general lipase inhibitor orlistat, AMPK activation by these agents was also parti

32 Orlistat, an antiobesity drug, is cytostatic and cytotox

33 The aim of this study was to determine if orlistat, an inhibitor of fat absorption, combined with

34 etine treatments and partial elimination for orlistat and diclofenac, with greater than 30% of the (1

35 from approximately 3% of initial weight for orlistat and lorcaserin to 9% for top-dose (15/92 mg) ph

36 e-stimulated secretion was less inhibited by orlistat and only at the highest concentration tested.

37 ese mice, alone or with the lipase inhibitor orlistat and parameters of AP induction (serum amylase a

38 Currently, two medications, orlistat and sibutramine, have been approved by the Unit

39 om 37% to 47% for lorcaserin, 35% to 73% for orlistat, and 67% to 70% for top-dose phentermine plus t

40 Sibutramine and orlistat are the 2 most-studied drugs.

41 Using the structure of orlistat as a starting point, which contains a beta-lact

42 The antitumor activity of orlistat can be attributed to its ability to inhibit the

43 These findings support the idea that an orlistat congener can be optimized for use in a preclini

44 Orlistat did not enhance weight loss or improve liver en

45 Twenty-three subjects in the orlistat/diet/vitamin E group and 18 in the diet/vitamin

46 The use of orlistat during periods of attempted weight maintenance

47 Drug Administration [FDA] approved in 1997), orlistat (FDA approved in 1999), and rimonabant (availab

48 The orlistat group lost a mean of 8.3% body weight compared

49 Moreover, more subjects in the 120-mg orlistat group than in the placebo group regained < or =

50 its ability to inhibit fatty acid synthase, Orlistat halts tumor cell proliferation, induces tumor c

51 rently approved medications, sibutramine and orlistat, have been shown to be safe and moderately effe

52 d carbamazepine, diclofenac, fluoxetine, and orlistat in soil-earthworm systems.

53 of REDD1; downregulation of REDD1 prevented orlistat-induced activation of caspase-2, as monitored b

54 e, primary indicators of cell death, whereas orlistat-induced cell death is rescued by coincubation w

55 er cell line incapable of inducing REDD1, to orlistat-induced cell death through caspase-2.

56 ve ovarian cancer cells (OVCA420 cells) from orlistat-induced death.

57 Orlistat inhibits endothelial cell FAS, blocks the synth

58 More significantly, orlistat inhibits human neovascularization in an ex vivo

59 Orlistat is a novel inhibitor of the thioesterase domain

60 Thus, orlistat is an antiangiogenic agent with a novel mechani

61 A or inhibition with the small molecule drug orlistat, leads to activation of the receptor-mediated a

62 Among overweight or obese adults, orlistat, lorcaserin, naltrexone-bupropion, phentermine-

63 s of screening or treatment (behavior-based, orlistat, metformin) for overweight or obesity in childr

64 ns approved in the USA or European Union are orlistat, naltrexone/bupropion, and liraglutide; in the

65 the present study was to test the effect of orlistat on endothelial cell proliferation and angiogene

66 th the chemically distinct lipase inhibitors orlistat or cetilistat.

67 meal replacements or weight-loss medication (orlistat or sibutramine), chosen by the participants in

68 CrI, 2.38-4.05; SUCRA, 0.39), and 44% taking orlistat (OR, 2.70; 95% CrI, 2.34-3.09; SUCRA, 0.22).

69 ed to receive placebo, 30 mg orlistat, 60 mg orlistat, or 120 mg orlistat 3 times daily for 1 y in co

70 erol sulfate and the antiobesity medications orlistat, phentermine hydrochloride, and sibutramine hyd

71 Sibutramine, orlistat, phentermine, probably diethylpropion, bupropio

72 Orlistat plus behavioral intervention resulted in 3-kg (

73 Two-year treatment with orlistat plus diet significantly promotes weight loss, l

74 these effects can be traced to the fact that orlistat prevents the display of the vascular endothelia

75 ng the concentration of the lipase inhibitor orlistat progressively and largely diminished the increm

76 nation of gemcitabine and the FASN inhibitor orlistat significantly diminished stemness, in part due

77 For orlistat, steatorrhea produces the principal gastrointes

78 ding that the FDA-approved antiobesity agent orlistat (tetrahydrolipstatin, Xenical) is a potent inhi

79 In the meta-analysis of orlistat, the estimate of the mean weight loss for orlis

80 ipation of (14)C varied by compound, and for orlistat, there was evidence of formation of nonextracta

81 ibitory activities than the lipase inhibitor Orlistat toward the same enzymes.

82 at, the estimate of the mean weight loss for orlistat-treated patients was 2.89 kg (CI, 2.27 to 3.51

83 During the first year orlistat-treated subjects lost more weight (mean +/- SEM

84 alysis, 223 placebo-treated subjects and 657 orlistat-treated subjects were evaluated.

85 p (n = 133) continued to receive placebo and orlistat-treated subjects were rerandomized to receive p

86 In addition, orlistat treatment (120 mg 3 times daily) was associated

87 sibutramine, which inhibits food intake, and orlistat, which blocks fat digestion.

88 Orlistat (Xenical) remains the single monotherapy that h