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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.
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-
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
20 A5, syn-TA2PZ6, and syn-TA2PZ5, derived from tacrine and phenylphenanthridinium azides and acetylenes
23 including the acetylcholinesterase inhibitor tacrine and the bis-pyridinium derivative 4,4'-bis-[(2,6
25 Coupling of two distinct pharmacophores, tacrine and trolox, endowed with different biological pr
26 eral AChE inhibitors, including huperzine A, tacrine, and 1,5-bis(4-allyldimethylammoniumphenyl)penta
27 major route of metabolism and elimination of tacrine, and also catalyzes the pathway(s) involved in t
28 nhibitory activity, less hepatotoxicity than tacrine, and the best neuroprotective capacity, being ab
29 Association of the active center inhibitor, tacrine, and the peripheral site peptide inhibitor, fasc
31 ) inhibitors by incubating a selected enzyme/tacrine azide combination with a variety of acetylene re
32 (PIQ) building blocks that combined with the tacrine azide within the active center gorge to form mul
33 ws the same pro-cognitive effects in vivo as tacrine, being superior to the physical mixture of tacri
34 relation we observed between CBT results and tacrine blood levels is the first evidence supporting a
35 g during the study while they were receiving tacrine compared with placebo was 3.63 (95% CI, 2.80- 4.
36 ge scale (range, 1-7) for patients receiving tacrine compared with those receiving placebo was 1.58 (
38 A series of novel tacrine derivatives and tacrine-coumarin heterodimers were designed, synthesized
39 mpounds, tacrine-coumarin heterodimer 7c and tacrine derivative 6b were found to be the most potent i
41 melatonin-like isocyanide, formaldehyde, and tacrine derivatives, according to the antioxidant additi
42 who are nonadherent, while recent trials of tacrine for Alzheimer disease and carvedilol for congest
47 le-blind, placebo-controlled trials in which tacrine had been given for more than 1 day and that were
51 iracetam-huprine and levetiracetam-(6-chloro)tacrine hybrids to hit amyloid, tau, and cholinergic pat
54 strated 3.3-fold higher systemic exposure to tacrine in strong responders that experienced transamini
55 enterohepatic recycling of deglucuronidated tacrine in this subgroup, not attributable to variation
57 s to elucidate and validate the mechanism of tacrine-induced hepatotoxicity in Lister hooded rats.
62 s disease such as (-) huperzine A and E2020; tacrine inhibited the monomeric form 2-3-fold more poten
63 e inhibition constants KI2 for propidium and tacrine, inhibitors specific for the P- and A-sites, res
64 ith the logarithm of the steady-state plasma tacrine level obtained in 10 patients (R(2) = .69, P = .
67 range, 0-50) showed a difference in favor of tacrine of 0.58 points (95% CI, 0.17-1.00; P= .006).
69 emorine), an acetylcholinesterase inhibitor (tacrine or E2020), or nicotine, increased the response l
70 cholinesterase (AChE) inhibitor derived from tacrine, prevented Abeta oligomers-induced inhibition of
71 Age, severity of dementia, and exposure to tacrine prior to randomization had no clear influence on
72 nfluences in modifying the hepatotoxicity of tacrine, providing insights for personalized medicine in
73 E inhibition, neuroprotective effects, lacks tacrine's hepatotoxicity in vitro and in vivo, and shows
75 inefungin, amodiaquine, diphenhydramine, and tacrine suggest differences in the active sites of these
76 nge, 0-30), was better in patients receiving tacrine than in patients receiving placebo by 0.62 point
78 rats, in contrast to the effects seen after tacrine treatment, after administration of the codrug no
82 12 weeks, the progress of patients receiving tacrine would be expected to range between an improvemen
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