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17 results for “cholinesterase inhibitor”
Dataset for article: Pro-cognitive effects of dual tacrine derivatives acting as cholinesterase inhibitors and NMDA receptor antagonists
<p>Figure 1. Chemical structures of tacrine (<strong>a</strong>) and its derivatives created by introducing substituents on the aromatic core and/or altering the size of the cycloalkyl moiety attached to the aromatic region: 7-MEOTA (<strong>b</strong>), K1578 (7-chloro-1<em>H</em>,2<em>H</em>,3<em>H</em>-cyclopenta[<em>b</em>]quinolin-9-amine; <strong>c</strong>), K1592 (1-chloro-6<em>H</em>,7<em>H</em>,8<em>H</em>,9<em>H</em>,10<em>H</em>-cyclohepta[<em>b</em>]quinolin-11-amine; <strong>d</strong>), K1594 (6-methyl-1,2,3,4-tetrahydroacridin-9-amine; <strong>e</strong>), and K1599 (7-methoxy-1<em>H</em>,2<em>H</em>,3<em>H</em>-cyclopenta[<em>b</em>]quinolin-9-amine; <strong>f</strong>). Compounds in this study were used in the form of hydrochloride salts.</p> <p>Figure_2_values. Test results. Morris water maze: scopolamine-induced model of cognitive deficit in the acquisition and reversal phases. The graphs show the effects of K1578 (<strong>a</strong>), K1592 (<strong>b</strong>), K1594 (<strong>c</strong>), and K1599 (<strong>d</strong>) on escape latency during the acquisition phase, where none of the compounds ameliorated the deficit of spatial learning. The remaining graphs display the effects of K1578 (<strong>e</strong>), K1592 (<strong>f</strong>), K1594 (<strong>g</strong>), and K1599 (<strong>h</strong>) in the reversal phase, where K1578 (1 mg/kg) and K1599 (at both doses), and marginally K1592 (1 mg/kg; see in the text), mitigated the scopolamine-induced deficit of reversal learning. VEH – vehicle, the numbers in brackets denote the dose applied (mg/kg). Data are presented as the mean + SEM, * vs. VEH, * p < 0.05, ** p < 0.01, *** p < 0.001. <em>n</em> = 6–9 animals per group. Statistical significance was determined using two-way repeated measures ANOVA (a–d) or ANOVA (e, f, h) followed by Dunnett’s multiple comparisons tests.</p> <p>Figure-3_values. Test results. Morris water maze: MK-801-induced model of cognitive deficit in the acquisition phase. The graphs illustrate the effects of the compounds K1578 (<strong>a</strong>), K1592 (<strong>b</strong>), K1594 (<strong>c</strong>), and K1599 (<strong>d</strong>) on escape latency. Only K1599 (1 mg/kg) ameliorated the MK-801-induced deficit of spatial learning. VEH – vehicle, the numbers in brackets denote the dose (mg/kg). Data are presented as the mean + SEM, * vs. VEH, * p < 0.05, ** p < 0.01. <em>n</em> = 5–7 animals per group. Statistical significance was determined using two-way repeated measures ANOVA followed by Dunnett’s multiple comparisons tests.</p> <p>Figure_4_values. Open field test. The results demonstrate the effects of K1578 (<strong>a</strong>), K1592 (<strong>b</strong>), K1594 (<strong>c</strong>), and K1599 (<strong>d</strong>) on the distance moved by intact and MK-801-treated animals. VEH – vehicle, the numbers in brackets denote the dose (mg/kg). Data are presented as the mean + SEM, * vs. VEH group of the corresponding phenotype, * p < 0.05, ** p < 0.01, **** p < 0.0001. <em>n</em> = 6–14 animals per group. A significant effect of both factors (treatment and phenotype) was determined using two-way ANOVA, followed by Dunnett’s multiple comparisons tests.</p> <p>Figure-5_values. Acetylcholinesterase activity. The results document the effect of the compounds (1 mg/kg ip) on AChE activity in the hippocampus (<strong>a</strong>), prefrontal cortex (<strong>b</strong>), striatum (<strong>c</strong>), and whole brain sample (<strong>d</strong>). K1578 and K1599 decreased AChE activity in the striatum. VEH – vehicle. Data are presented as the median with minimum to maximum range, * vs. VEH, *** p < 0.001, **** p < 0.0001. VEH samples AChE enzyme activities reached the following absolute values (a) 15.19 ± 3.09 U/mg protein, (b) 9.810 ± 1.54 U/mg protein, (c) 26.05 ± 3.27 U/mg protein, and (d) 27.38 ± 3.36 U/mg protein. Significance was determined by ANOVA (graphs c, d), followed by Dunnett’s multiple comparisons tests.</p> <p>Figure_6_values. Electrophysiology: Inhibition of GluN1/GluN2A receptors by K1599. Representative whole-cell patch-clamp recordings measured from HEK293 cells expressing the GluN1/GluN2A receptors held at a membrane voltage of −80 mV and +60 mV; 30 μM K1599 was applied as indicated. Results summarizing the relative inhibition induced by 30 µM K1599, measured at the indicated membrane potentials. <em>n</em> ≥ 5 cells per each condition.</p> <p>Table_1. The rats were pseudo-randomly assigned to one of the 18 treatment groups listed in. Each group received two injections: one containing the study compound and another containing either MK-801 or scopolamine, as indicated by the group name. The vehicle group (VEH) received the DMSO vehicle (2.5 mL/kg) and saline. The “scopolamine” and “MK-801” groups received scopolamine or MK-801, respectively, along with the DMSO vehicle (2.5 mL/kg).</p> <p>Table 2. Treatment groups and <em>n</em> in biochemical experiments - AChE activity assay.</p>
Tabular and image data of article "Morphing cholinesterase inhibitor amiridine into multipotent drugs for the treatment of Alzheimer's disease"
<p>The search for novel drugs to address the medical needs of Alzheimer’s disease (AD) is an ongoing process relying on the discovery of disease-modifying agents. Given the complexity of the disease, such an aim can be pursued by developing so-called multi-target directed ligands (MTDLs) that will impact the disease pathophysiology more<br>comprehensively. Herewith, we contemplated the therapeutic efficacy of an amiridine drug acting as a cholinesterase inhibitor by converting it into a novel class of novel MTDLs. Applying the linking approach, we have paired amiridine as a core building block with memantine/adamantylamine, trolox, and substituted benzothiazole moieties to generate novel MTDLs endowed with additional properties like N-methyl-D-aspartate (NMDA) receptor affinity, antioxidant capacity, and anti-amyloid properties, respectively. The top-ranked amiridine-based compound 5d was also inspected by in silico to reveal the butyrylcholinesterase binding differences with its close structural analogue 5b. Our study provides insight into the discovery of novel amiridinebased drugs by broadening their target-engaged profile from cholinesterase inhibitors towards MTDLs with potential implications in AD therapy.</p> <p><strong>Table 1. </strong>hBChE inhibitory activities of 5c-d, 7c and 7 g and reference compounds (amiridine hydrochloride and THA); their cytotoxicity profile on SH-SY5Y cell line, and predictions of BBB penetration.</p> <p>T<strong>able 2</strong>. Relative inhibitions (RIs) of 5c-d and 7 m and reference compound memantine at recombinant human GluN1/GluN2B NMDA receptor expressed in HEK293 cells.</p> <p><strong>Fig_1</strong>. Chemical structures of rivastigmine, galantamine, and tacrine as representatives of cholinesterase inhibitors. Approaches to novel drugs for AD treatment on the selected candidates are displayed.</p> <p><strong>Fig_2</strong>. Examples of previously published amiridine-based derivatives and design strategy applied in the current study below, using various pharmacophores.</p> <p><strong>Fig_3</strong>. Top scored docking pose of 5b (A) and 5d (B) highlighting the key findings responsible for compound activity/inactivity. For the sake of clarity, superimposed ligands are aligned in the Fig. C with respect to key amino acid residue W82 to demonstrate the binding difference. Compounds 5b and 5d are colored in salmon and yellow, respectively. Essential amino acid residues responsible for ligand anchoring are rendered in green. Important interactions of different origin are displayed with dashed black lines. The figure was created with The PyMOL Molecular Graphics System, v. 2.5.2.</p> <p><strong>Scheme 1</strong>. Preparation of the amiridine-based compounds 5a-d. Reagents and conditions: <strong>a)</strong> 2-chloroacetyl chloride (4 eq.), CHCl3, 90 ◦C, overnight, 8, 54%, 11, 90%, 12, 52%; <strong>b)</strong> CH3CN, K2CO3, KI, reflux, 3 h, 5a, 54%, 5b, 54%; <strong>c)</strong> amiridine (1.1 eq), CH3CN, K2CO3, KI, reflux, overnight, 5c, 48%, 5d, 41%.</p> <p><strong>Scheme 2</strong>. Preparation of intermediate 13 and final compound 6. Reagents and conditions: <strong>a)</strong> potassium phthalimide, CH3CN, reflux, 3 h, then an excess of NH2NH2⋅H2O, reflux, overnight, 57%; <strong>b)</strong> DMF, TEA, BOP, room temperature, 2 days, 86%.</p> <p><strong>Scheme 3</strong>. Preparation of amiridine-benzothiazole derivatives 7a-m. Reagents and conditions: <strong>a)</strong> for 7a: 2-chlorobenzothiazole, 110 ◦C, overnight, 32%; for 7b-m: corresponding 2-chlorobenzothiazole, DIPEA, 100 ◦C, overnight, 21–77%.</p>
Discontinuation of Cholinesterase Inhibitors for the Treatment of Severe Alzheimer's Disease
ClinicalTrials.gov study NCT02035982. IPD Sharing: Not stated. Countries: 1. Publications: 1.
CHIEF-PD (CHolinesterase Inhibitor to prEvent Falls in Parkinson's Disease)
ClinicalTrials.gov study NCT04226248. IPD Sharing: NO. Countries: 1. Publications: 1.
Supplementary materials for: Long term effects of cholinesterase inhibitors on cognitive decline and mortality
Open the record for dataset details and reuse information.
Impact of Cholinesterase Inhibitors on Driving Ability in Healthy Older Adults
ClinicalTrials.gov study NCT00482001. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Cholinesterase Inhibitor Discontinuation
ClinicalTrials.gov study NCT02248636. IPD Sharing: NO. Countries: 1. Publications: 0.
Transcriptional profile of injured hearts treated with the cholinesterase inhibitor pyridostigmine (PYR) at Day 5
GEO Series GSE116988. Mus musculus. 24 samples. Type: Expression profiling by high throughput sequencing.
The Ric-8b protein (resistance to inhibitors of cholinesterase 8b) is key to preserving contractile function in the adult heart.
GEO Series GSE265903. Mus musculus. 11 samples. Type: Expression profiling by high throughput sequencing.
Efficacy, Safety and Tolerability of Rivastigmine Patch in Patients With Mild to Moderate Alzheimer's Disease Switched From Cholinesterase Inhibitors
ClinicalTrials.gov study NCT01529619. IPD Sharing: Not stated. Countries: 1. Publications: 0.
To Evaluate the Safety and Effectiveness of Atorvastatin Plus a Cholinesterase Inhibitor in AD Patients.
ClinicalTrials.gov study NCT00151502. IPD Sharing: Not stated. Countries: 10. Publications: 0.
Good Rate of Clinical Response to Cholinesterase Inhibitors in Alzheimer's Disease After Three Months of Treatment
ClinicalTrials.gov study NCT02007291. IPD Sharing: Not stated. Countries: 0. Publications: 0.
Comparison of Therapeutic Strategies With Cholinesterase Inhibitors (SOS TRIAL)
ClinicalTrials.gov study NCT03454646. IPD Sharing: NO. Countries: 1. Publications: 0.
Rivastigmine Monotherapy and Combination Therapy With Memantine in Patients With Moderately Severe Alzheimer's Disease Who Failed to Benefit From Previous Cholinesterase Inhibitor Treatment
ClinicalTrials.gov study NCT00234637. IPD Sharing: Not stated. Countries: 1. Publications: 0.
Cholinesterase Inhibitors to Slow Progression of Visual Hallucinations in Parkinson&Apos;s Disease
ClinicalTrials.gov study NCT01856738. IPD Sharing: Not stated. Countries: 1. Publications: 0.
The Predictive Factors of Good Clinical Response to Cholinesterase Inhibitors in Alzheimer Disease and Mixed Dementia
ClinicalTrials.gov study NCT02187276. IPD Sharing: Not stated. Countries: 0. Publications: 0.
EEG-cholinergic Index and Clinical Response to Treatment With Cholinesterase Inhibitors
ClinicalTrials.gov study NCT02623764. IPD Sharing: Not stated. Countries: 0. Publications: 0.
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Allen Brain Atlas
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