ライフサイエンスコーパス: acamprosate

1 onclude that calcium is the active moiety of acamprosate.

2 macogenomic mechanism related to response to acamprosate.

3 in agreement with the established profile of acamprosate.

4 s) would have a better treatment response to acamprosate.

5 altrexone, and the Mayo Clinic CITA study of acamprosate.

6 st 1 medication for AUD: 132 (54.7%) covered acamprosate, 203 (84.2%) covered oral naltrexone, 175 (7

7 Most assessed acamprosate (27 studies, n = 7519), naltrexone (53 studi

8 nt with 16 weeks of naltrexone (100 mg/d) or acamprosate (3 g/d), both, and/or both placebos, with or

9 ment for 16 weeks with naltrexone, 100 mg/d, acamprosate, 3 g/d, or both, and/or placebo; 4 groups re

10 their drinking behavior was not affected by acamprosate, an FDA-approved drug for the treatment of a

11 s were made when the cells were treated with acamprosate-an FDA approved drug for AUD therapy.

12 g to any drinking were 11 (95% CI, 1-32) for acamprosate and 18 (95% CI, 4-32) for oral naltrexone at

13 o significant differences were found between acamprosate and naltrexone for controlling alcohol consu

14 tment-specific pharmacogenomic predictors of acamprosate and naltrexone response.

15 The PREDICT study tested acamprosate and naltrexone vs placebo in 426 randomly as

16 comparing combinations of medications (i.e., acamprosate and naltrexone) and behavioral interventions

17 data from the COMBINE and PREDICT studies of acamprosate and naltrexone, and the Mayo Clinic CITA stu

18 Both acamprosate and oral naltrexone were associated with red

19 ipt of FDA-approved medications (disulfiram, acamprosate, and naltrexone), psychotherapy (individual,

20 cent reports documenting that naltrexone and acamprosate are more effective than placebo in the treat

21 nd long-acting injectable formulations), and acamprosate-are underprescribed, despite being considere

22 rt the use of oral naltrexone at 50 mg/d and acamprosate as first-line pharmacotherapies for alcohol

23 Along with a few other medications, acamprosate (Campral-calcium-bis (N-acetylhomotaurinate)

24 Specifically, our previous open-label acamprosate clinical trial recruited 442 patients with A

25 ly inactive molecule and that the effects of acamprosate described in more than 450 published origina

26 ncluded higher gastrointestinal distress for acamprosate (diarrhea: risk ratio, 1.58; 95% CI, 1.27-1.

27 nd Drug Administration (FDA)-approved MAUDs (acamprosate, disulfiram, and oral and injectable naltrex

28 horization, quantity limit requirements) for acamprosate, disulfiram, and oral and injectable naltrex

29 In particular, acamprosate does not interact with NMDA receptors or met

30 Here we show that acamprosate does not interact with proposed glutamate re

31 442 patients with AUD who were treated with acamprosate for three months.

32 n Drugbank, two potential therapeutic drugs, Acamprosate (GABBR1 inhibitor) and Bryostatin 1 (CASP8 i

33 Acamprosate (grade A, from large-scale studies in Europe

34 reduce alcohol intake such as naltrexone and acamprosate have central nervous system action, disulfir

35 Intervention Four weeks of acamprosate (initial oral loading followed by 1998 mg da

36 here is accumulated evidence suggesting that acamprosate interferes with the glutamate system, the mo

37 Acamprosate is a Food and Drug Administration (FDA) appr

38 Acamprosate is approved for the treatment of alcoholism,

39 Surprisingly, calcium salts produce acamprosate-like effects in all three animal models.

40 s to the pathogenesis of alcoholism and that acamprosate may exert its actions by intervening in this

41 ments [baclofen (n = 6), metadoxine (n = 1), acamprosate (n = 1), and fecal microbiota transplant (n

42 defined as the documented use of disulfiram, acamprosate, naltrexone, gabapentin, topiramate, or bacl

43 ly; risk was not significantly increased for acamprosate or topiramate.

44 D initiation was defined as oral naltrexone, acamprosate, or disulfiram pharmacy fills within 2 days

45 can include pharmacotherapy with naltrexone, acamprosate, or disulfiram; however, these medications a

46 h fared better on drinking outcomes, whereas acamprosate showed no evidence of efficacy, with or with

47 Acamprosate showed no significant effect on drinking vs

48 n aid in reducing alcohol consumption, while acamprosate supports abstinence; however, not all patien

49 atient), and MM plus combined naltrexone and acamprosate therapy ($1003 per patient).

50 ntral glutamate are reduced across time when acamprosate therapy is initiated at the onset of alcohol

51 ocusing only on effectiveness, MM-naltrexone-acamprosate therapy is not significantly better than MM-

52 g cost and cost-effectiveness, MM-naltrexone-acamprosate therapy may be a better choice, depending on

53 e glutamate to creatine ratio across time by acamprosate (time x treatment interaction: F(,) = 13.5,

54 Meta-analyses of trials comparing acamprosate to naltrexone found no statistically signifi

55 mes (naltrexone THR: rs12749274, p = 3.9E-8; acamprosate TR: rs77583603, p = 3.1E-9).

56 tinal symptoms were significantly greater in acamprosate-treated individuals, in agreement with the e

57 rmined that TSPAN5 SNPs were associated with acamprosate treatment outcomes in AUD patients.

58 variants in IL17RB that were associated with acamprosate treatment outcomes.

59 IL17RB genetic variants might contribute to acamprosate treatment outcomes.

60 dentify potential biomarkers associated with acamprosate treatment outcomes.

61 d to gain insight into mechanisms underlying acamprosate treatment response phenotypes.

62 The models predicted acamprosate treatment response with a mean sensitivity a

63 ation and serum metabolite levels to predict acamprosate treatment response.

64 dentify potential biomarkers associated with acamprosate treatment response.

65 ukin-17 receptor B (IL17RB), associated with acamprosate treatment response. A GWAS for IL17RB concen

66 ients with high plasma calcium levels due to acamprosate treatment showed better primary efficacy par

67 egulation of TSPAN5 expression by ethanol or acamprosate treatment was also associated with decreased

68 e (no alcohol consumption during 3 months of acamprosate treatment) while nonresponse was defined as

69 measures are utilized to predict response to acamprosate treatment.

70 he NNT to prevent return to any drinking for acamprosate was 12 (95% CI, 8 to 26; risk difference [RD