ライフサイエンスコーパス: tacrine

1 d acetylcholinesterase (AChE) in relation to tacrine.

2 as markedly reduced in comparison to that of tacrine.

3 being more potent than the parent inhibitor, tacrine.

4 of training, similar to the positive control tacrine.

5 a axis in underpinning the hepatotoxicity of tacrine.

6 r's disease before they began treatment with tacrine.

7 ice develop fewer jaw tremors in response to tacrine.

8 could be facilitated with different doses of tacrine (0.0003-10 mg/kg).

9 nary metabolic profiles in rats administered tacrine (1) suggested the presence of an unidentified me

10 of Alzheimer's disease (AD), a new family of tacrine-4-oxo-4H-chromene hybrids has been designed, syn

11 nano- and picomolar concentrations, the new tacrine-4-oxo-4H-chromene hybrids inhibit human acetyl-

12 Therapy with tacrine, a promising new treatment for Alzheimer's disea

13 These relative changes in propidium and tacrine affinities thus provided a sensitive molecular r

14 g metoprine, and the anticholinesterase drug tacrine (an early drug for Alzheimer's disease) are surp

15 mperature to perform the synthesis of chiral tacrine analogues in good yields (up to 93%) and excelle

16 es out of the cholinesterase (ChE) inhibitor tacrine and a benzimidazole-based human cannabinoid rece

17 In contrast, tacrine and donepezil, typical AChE inhibitors, could no

18 We found that our selected compounds tacrine and duloxetine significantly improved remyelinat

19 receptor epitopes involved in the binding of tacrine and Duo3 may not be identical.

20 By analyzing the interactions of tacrine and Duo3 with other allosteric muscarinic agents

21 alidated using the reference AChE inhibitors tacrine and galanthamine.

22 A5, syn-TA2PZ6, and syn-TA2PZ5, derived from tacrine and phenylphenanthridinium azides and acetylenes

23 The cholinesterase inhibitors, tacrine and physostigmine, and the mixed muscarinic m1 a

24 e, being superior to the physical mixture of tacrine and silibinin in all these regards.

25 including the acetylcholinesterase inhibitor tacrine and the bis-pyridinium derivative 4,4'-bis-[(2,6

26 A codrug of the anti-Alzheimer drug tacrine and the natural product silibinin was synthesize

27 Coupling of two distinct pharmacophores, tacrine and trolox, endowed with different biological pr

28 eral AChE inhibitors, including huperzine A, tacrine, and 1,5-bis(4-allyldimethylammoniumphenyl)penta

29 major route of metabolism and elimination of tacrine, and also catalyzes the pathway(s) involved in t

30 nhibitory activity, less hepatotoxicity than tacrine, and the best neuroprotective capacity, being ab

31 Association of the active center inhibitor, tacrine, and the peripheral site peptide inhibitor, fasc

32 Cholinesterase inhibition with tacrine appears to reduce deterioration in cognitive per

33 ) inhibitors by incubating a selected enzyme/tacrine azide combination with a variety of acetylene re

34 (PIQ) building blocks that combined with the tacrine azide within the active center gorge to form mul

35 A series of tacrine-based derivatives with amine/amino acid moieties

36 ws the same pro-cognitive effects in vivo as tacrine, being superior to the physical mixture of tacri

37 relation we observed between CBT results and tacrine blood levels is the first evidence supporting a

38 g during the study while they were receiving tacrine compared with placebo was 3.63 (95% CI, 2.80- 4.

39 ge scale (range, 1-7) for patients receiving tacrine compared with those receiving placebo was 1.58 (

40 Of these compounds, tacrine-coumarin heterodimer 7c and tacrine derivative 6

41 A series of novel tacrine derivatives and tacrine-coumarin heterodimers were designed, synthesized

42 mpounds, tacrine-coumarin heterodimer 7c and tacrine derivative 6b were found to be the most potent i

43 A series of novel tacrine derivatives and tacrine-coumarin heterodimers we

44 melatonin-like isocyanide, formaldehyde, and tacrine derivatives, according to the antioxidant additi

45 who are nonadherent, while recent trials of tacrine for Alzheimer disease and carvedilol for congest

46 Novel multifunctional tacrines for Alzheimer's disease were obtained by Ugi-re

47 The tacrine fragment was selected for its inhibition of chol

48 by combining a naphthoquinone function and a tacrine fragment.

49 We administered tacrine, galantamine or memantine to mouse cerebral cort

50 le-blind, placebo-controlled trials in which tacrine had been given for more than 1 day and that were

51 Tacrine has been called an atypical modulator because it

52 g the subset of patients most susceptible to tacrine hepatotoxicity.

53 A family of huprine-tacrine heterodimers has been developed to simultaneousl

54 Huprine-tacrine heterodimers take on added value in that they di

55 iracetam-huprine and levetiracetam-(6-chloro)tacrine hybrids to hit amyloid, tau, and cholinergic pat

56 , only one of them was less hepatotoxic than tacrine in HepG2 cells.

57 ing Wistar rats, the codrug was as potent as tacrine in reversing memory dysfunction.

58 strated 3.3-fold higher systemic exposure to tacrine in strong responders that experienced transamini

59 enterohepatic recycling of deglucuronidated tacrine in this subgroup, not attributable to variation

60 In contrast, the value of KI2 for tacrine increased substantially only when ligands had lo

61 s to elucidate and validate the mechanism of tacrine-induced hepatotoxicity in Lister hooded rats.

62 ice were hypersensitive to galanthamine- and tacrine-induced seizures and Straub tails.

63 ignificantly modulated the susceptibility to tacrine-induced transaminitis in vivo.

64 in gut microbial activities that mapped onto tacrine-induced transaminitis.

65 gic acetyltransferase (ChAT) neurons reduces tacrine-induced tremor.

66 s disease such as (-) huperzine A and E2020; tacrine inhibited the monomeric form 2-3-fold more poten

67 e inhibition constants KI2 for propidium and tacrine, inhibitors specific for the P- and A-sites, res

68 Tacrine is not atypical at monomers, which indicates tha

69 ith the logarithm of the steady-state plasma tacrine level obtained in 10 patients (R(2) = .69, P = .

70 f cationic trialkylammonium, acridinium, and tacrine ligands with tethers of varying length.

71 in identifying patients most susceptible to tacrine liver toxicity.

72 range, 0-50) showed a difference in favor of tacrine of 0.58 points (95% CI, 0.17-1.00; P= .006).

73 Fasciculin, but not tacrine, on the other hand, dramatically altered the dec

74 emorine), an acetylcholinesterase inhibitor (tacrine or E2020), or nicotine, increased the response l

75 cholinesterase (AChE) inhibitor derived from tacrine, prevented Abeta oligomers-induced inhibition of

76 Age, severity of dementia, and exposure to tacrine prior to randomization had no clear influence on

77 nfluences in modifying the hepatotoxicity of tacrine, providing insights for personalized medicine in

78 E inhibition, neuroprotective effects, lacks tacrine's hepatotoxicity in vitro and in vivo, and shows

79 The tacrine-silibinin codrug shows high AChE and BChE inhibi

80 inefungin, amodiaquine, diphenhydramine, and tacrine suggest differences in the active sites of these

81 esterase (AChE)/butyrylcholinesterase (BChE) tacrine templates.

82 nge, 0-30), was better in patients receiving tacrine than in patients receiving placebo by 0.62 point

83 For patients without prior exposure to tacrine, the odds of patients' withdrawing during the st

84 rats, in contrast to the effects seen after tacrine treatment, after administration of the codrug no

85 Finally, tacrine-trolox hybrids exhibited low in vivo toxicity af

86 A coumarin derivative with IC50 similar to tacrine was highlighted.

87 The structurally similar compound, tacrine, which is a known allosteric modulator of the mu

88 12 weeks, the progress of patients receiving tacrine would be expected to range between an improvemen