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NICOTINIC ACETYLCHOLINE RECEPTOR LIGANDS

Compounds of formula (I), wherein D, Ar1, E and Ar2 are as defined in the specification, processes for preparing them, pharmaceutical compositions containing them and their use in therapy, especially in the treatment or prophylaxis of psychotic and intellectual impairment disorders.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H105N | ChemSpider

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Thermochemical stability: A comparison between experimental and predicted data

The first step to be performed during the development of a new industrial process should be the assessment of all hazards associated to the involved compounds. Particularly, the knowledge of all substances thermochemical parameters is a primary feature for such a hazard evaluation. CHETAH (CHEmical Thermodynamic And Hazard evaluation) is a prediction software suitable for calculating potential hazards of chemicals, mixtures or a single reaction that, using only the structure of the involved molecules and Benson’s group contribution method, is able to calculate heats of formation, entropies, Gibbs free energies and reaction enthalpies. Because of its ability to predict the potential hazards of a material or mixture, CHETAH is part of the so-called “desktop methods” for early stage chemical safety analysis. In this work, CHETAH software has been used to compile a complete risk database reporting heats of decomposition and Energy Release Potential (ERP) for 342 common use chemicals. These compounds have been gathered into classes depending on their functional groups and similarities in their thermal behavior. Calculated decomposition enthalpies for each of the compounds have also been compared with experimental data obtained with either thermoanalytic or calorimetric techniques (Differential Scanning Calorimeter – DSC – and Accelerating Rate Calorimeter – ARC).

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Quinuclidine – Wikipedia,
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Some scientific research about (R)-3-Aminoquinuclidine dihydrochloride

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Chemistry is the experimental and theoretical study of materials on their properties at both the macroscopic and microscopic levels.In a patent£¬Which mentioned a new discovery about 123536-14-1, molcular formula is C7H16Cl2N2, introducing its new discovery. , 123536-14-1

NICOTINIC ACETYLCHOLINE RECEPTOR LIGANDS

Compounds of formula (I), wherein D, Ar1, E and Ar2 are as defined in the specification, processes for preparing them, pharmaceutical compositions containing them and their use in therapy, especially in the treatment or prophylaxis of psychotic and intellectual impairment disorders.

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Quinuclidine – Wikipedia,
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Novel serotonin type 3 receptor partial agonists for the potential treatment of irritable bowel syndrome

Serotonin type 3 (5-HT3) receptor partial agonists are being targeted as potential new drugs for the treatment of irritable bowel syndrome (IBS). Two new chemical series bearing indazole and indole cores have exhibited nanomolar binding affinity for the h5-HT3A receptor. A range of partial agonist activities in HEK cells heterologously expressing the h5-HT 3A receptor were measured for the indazole series. Excellent 5-HT3 receptor selectivity, favorable in vitro metabolic stability and CYP inhibition properties, and good oral in vivo potency in the murine von Bezold-Jarisch reflex model is exemplified thereby indicating the series to have potential utility as improved IBS agents.

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Quinuclidine – Wikipedia,
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Brief introduction of Quinuclidin-4-ylmethanamine

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Discovery of highly potent and selective type I B-Raf kinase inhibitors

A series of pyrazolo[1,5-alpha]pyrimidine analogs has been prepared and found to be potent and selective B-Raf inhibitors. Molecular modeling suggests they bind to the active conformation of the enzyme.

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Application of 827-61-2, Catalysts function by providing an alternate reaction mechanism that has a lower activation energy than would be found in the absence of the catalyst. In some cases, the catalyzed mechanism may include additional steps.In a article, 827-61-2, molcular formula is C9H15NO2, introducing its new discovery.

Development of a high-throughput screen to identify small molecule enhancers of sarcospan for the treatment of Duchenne muscular dystrophy

Background: Duchenne muscular dystrophy (DMD) is caused by loss of sarcolemma connection to the extracellular matrix. Transgenic overexpression of the transmembrane protein sarcospan (SSPN) in the DMD mdx mouse model significantly reduces disease pathology by restoring membrane adhesion. Identifying SSPN-based therapies has the potential to benefit patients with DMD and other forms of muscular dystrophies caused by deficits in muscle cell adhesion. Methods: Standard cloning methods were used to generate C2C12 myoblasts stably transfected with a fluorescence reporter for human SSPN promoter activity. Assay development and screening were performed in a core facility using liquid handlers and imaging systems specialized for use with a 384-well microplate format. Drug-treated cells were analyzed for target gene expression using quantitative PCR and target protein expression using immunoblotting. Results: We investigated the gene expression profiles of SSPN and its associated proteins during myoblast differentiation into myotubes, revealing an increase in expression after 3 days of differentiation. We created C2C12 muscle cells expressing an EGFP reporter for SSPN promoter activity and observed a comparable increase in reporter levels during differentiation. Assay conditions for high-throughput screening were optimized for a 384-well microplate format and a high-content imager for the visualization of reporter levels. We conducted a screen of 3200 compounds and identified seven hits, which include an overrepresentation of L-type calcium channel antagonists, suggesting that SSPN gene activity is sensitive to calcium. Further validation of a select hit revealed that the calcium channel inhibitor felodipine increased SSPN transcript and protein levels in both wild-type and dystrophin-deficient myotubes, without increasing differentiation. Conclusions: We developed a stable muscle cell line containing the promoter region of the human SSPN protein fused to a fluorescent reporter. Using the reporter cells, we created and validated a scalable, cell-based assay that is able to identify compounds that increase SSPN promoter reporter, transcript, and protein levels in wild-type and dystrophin-deficient muscle cells.

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Quinuclidine – Wikipedia,
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Top Picks: new discover of (R)-3-Aminoquinuclidine dihydrochloride

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5-SUBSTITUTED IMIDAZOLES

Compounds of formula I: wherein A and R1 are as defined in the specification, processes for preparing them, pharmaceutical compositions containing them and their use in therapy, especially in the treatment or prophylaxis of psychotic and intellectual impairment disorders.

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Quinuclidine – Wikipedia,
Quinuclidine | C7H102N | ChemSpider

Simple exploration of Quinuclidin-4-ylmethanamine

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BRIDGED, BICYCLIC HETEROCYCLIC OR SPIRO BICYCLIC HETEROCYCLIC DERIVATIVES OF PYRAZOLO[1,5-A]PYRIMIDINES, METHODS FOR PREPARATION AND USES THEREOF

Compounds of formula A: Formula (1) pharmaceutically acceptable salts thereof are described, which selectively inhibit Raf kinase activity and are useful for treating disorders mediated by Raf kinases.

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Quinuclidine – Wikipedia,
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The Absolute Best Science Experiment for Quinuclidin-3-yl acetate

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COMPOSITIONS AND METHODS FOR THE TREATMENT OF PRESBYOPIA

The invention provides compositions and methods for the treatment of presbyopia. The compositions preferably use aceclidine separate or together with a cycloplegic agent and/or with a nonionic surfactant and viscosity enhancer, and or with low concentrations of a selective a-2 adrenergic receptor agonist.

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The Absolute Best Science Experiment for APR-246

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SLMP53-2 restoreswild-type-like function to mutant p53 through hsp70: Promising activity in hepatocellular carcinoma

Half of human cancers harbor TP53 mutations that render p53 inactive as a tumor suppressor. In these cancers, reactivation of mutant p53 (mutp53) through restoration of wild-type-like function constitutes a valuable anticancer therapeutic strategy. In order to search for mutp53 reactivators, a small library of tryptophanol-derived oxazoloisoindolinones was synthesized and the potential of these compounds as mutp53 reactivators and anticancer agents was investigated in human tumor cells and xenograft mouse models. By analysis of their anti-proliferative effect on a panel of p53-null NCI-H1299 tumor cells ectopically expressing highly prevalent mutp53, the compound SLMP53-2 was selected based on its potential reactivation of multiple structuralmutp53. In mutp53-Y220C-expressing hepatocellular carcinoma (HCC) cells, SLMP53-2-induced growth inhibition was mediated by cell cycle arrest, apoptosis, and endoplasmic reticulum stress response. In these cells, SLMP53-2 restored wild-type-like conformation and DNA-binding ability of mutp53-Y220C by enhancing its interaction with the heat shock protein 70 (Hsp70), leading to the reestablishment of p53 transcriptional activity. Additionally, SLMP53-2 displayed synergistic effect with sorafenib, the only approved therapy for advanced HCC. Notably, it exhibited potent antitumor activity in human HCC xenograft mouse models with a favorable toxicological profile. Collectively, SLMP53-2 is a new mutp53-targeting agent with promising antitumor activity, particularly against HCC.

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Quinuclidine | C7H169N | ChemSpider